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Cardiac Conduction System and Understanding ECG, Animation.
 
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This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia The cardiac conduction system consists of the following components: - The sinoatrial node, or SA node, located in the right atrium near the entrance of the superior vena cava. This is the natural pacemaker of the heart. It initiates all heartbeat and determines heart rate. Electrical impulses from the SA node spread throughout both atria and stimulate them to contract. - The atrioventricular node, or AV node, located on the other side of the right atrium, near the AV valve. The AV node serves as electrical gateway to the ventricles. It delays the passage of electrical impulses to the ventricles. This delay is to ensure that the atria have ejected all the blood into the ventricles before the ventricles contract. - The AV node receives signals from the SA node and passes them onto the atrioventricular bundle - AV bundle or bundle of His. - This bundle is then divided into right and left bundle branches which conduct the impulses toward the apex of the heart. The signals are then passed onto Purkinje (pur-KIN-jee) fibers, turning upward and spreading throughout the ventricular myocardium. Electrical activities of the heart can be recorded in the form of electrocardiogram, ECG or EKG. An ECG is a composite recording of all the action potentials produced by the nodes and the cells of the myocardium. Each wave or segment of the ECG corresponds to a certain event of the cardiac electrical cycle. When the atria are full of blood, the SA node fires, electrical signals spread throughout the atria and cause them to depolarize. This is represented by the P wave on the ECG. Atrial contraction , or atrial systole (SIS-toe-lee) starts about 100 mili-seconds after the P wave begins. The P-Q segment represents the time the signals travel from the SA node to the AV node. The QRS complex marks the firing of the AV node and represents ventricular depolarization: - Q wave corresponds to depolarization of the interventricular septum. - R wave is produced by depolarization of the main mass of the ventricles. - S wave represents the last phase of ventricular depolarization at the base of the heart. - Atrial repolarization also occurs during this time but the signal is obscured by the large QRS complex. The S-T segment reflects the plateau in the myocardial action potential. This is when the ventricles contract and pump blood. The T wave represents ventricular repolarization immediately before ventricular relaxation, or ventricular diastole (dy-ASS-toe-lee). The cycle repeats itself with every heartbeat. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Cardiac Output, Stroke volume, EDV, ESV, Ejection Fraction
 
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Cardiac Physiology Basics. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia CARDIAC OUTPUT is the amount of blood pumped by each ventricle in one minute. It is the product of STROKE VOLUME – the amount of blood pumped in one heartbeat, and HEART RATE – the number of beats in one minute. An INcrease in either stroke volume or heart rate results in INcreased cardiac output, and vice versa. For example, during physical exercises, the heart beats faster to put out more blood in response to higher demand of the body. It is noteworthy that the ventricles do NOT eject ALL the blood they contain in one beat. In a typical example, a ventricle is filled with about 100ml of blood at the end of its load, but only 60ml is ejected during contraction. This corresponds to an EJECTION fraction of 60%. The 100ml is the end-DIASTOLIC volume, or EDV. The 40ml that remains in the ventricle after contraction is the end-SYSTOLIC volume, or ESV. The stroke volume equals EDV minus ESV, and is dependent on 3 factors: contractility, preload, and afterload. Contractility refers to the force of the contraction of the heart muscle. The more forceful the contraction, the more blood it ejects. PRELOAD is RELATED to the end-diastolic volume. Preload, by definition, is the degree of STRETCH of cardiac myocytes at the end of ventricular filling, but since this parameter is not readily measurable in patients, EDV is used instead. This is because the stretch level of the wall of a ventricle INcreases as it’s filled with more and more blood; just like a balloon - the more air it contains, the more stretched it is. According to the Frank-Starling mechanism, the greater the stretch, the greater the force of contraction. In the balloon analogy, the more inflated the balloon, the more forceful it releases air when deflated. AFTERLOAD, on the other hand, is the RESISTANCE that the ventricle must overcome to eject blood. Afterload includes 2 major components: - Vascular pressure: The pressure in the left ventricle must be GREATER than the systemic pressure for the aortic valve to open. Similarly, the pressure in the right ventricle must exceed pulmonary pressure to open the pulmonary valve. In hypertension for example, higher vascular pressures make it more difficult for the valves to open, resulting in a REDUCED amount of ejected blood. - Damage to the valves, such as stenosis, also presents higher resistance and leads to lower blood output. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Temporomandibular Joint (TMJ) Anatomy and Disc Displacement Animation
 
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TMJ made easy. everything you need to know. This video and variations (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/dental-videos ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. The temporomandibular joint -- the TMJ - is the joint between the lower jawbone - the mandible - and the temporal bone of the skull. The TMJ is responsible for jaw movement and is the most used joint in the body. The TMJ is essentially the articulation between the condyle of the mandible and the mandibular fossa - a socket in the temporal bone. The unique feature of the TMJ is the articular disc - a flexible and elastic cartilage that serves as a cushion between the two bone surfaces. The disc lacks nerve endings and blood vessels in its center and therefore is insensitive to pain. Anteriorly it attaches to lateral pterygoid muscle - a muscle of chewing. Posteriorly it continues as retrodiscal tissue fully supplied with blood vessels and nerves. The mandible is the only bone that moves when the mouth opens. The first 20 mm opening involves only a rotational movement of the condyle within the socket. For the mouth to open wider, the condyle and the disc have to move out of the socket, forward and down the articular eminence, a convex bone surface located anteriorly to the socket . This movement is called translation. The most common disorder of the TMJ is disc displacement, and in most of the cases, the disc is dislocated anteriorly. As the disc moves forward, the retrodiscal tissue is pulled in between the two bones. This can be very painful as this tissue is fully vascular and innervated, unlike the disc. The movements made by chewing or even talking cause a chronic bruise to the tissue resulting in inflammation and pain. The forward dislocated disc is an obstacle for the condyle movement when the mouth is opening. In order to fully open the jaw, the condyle has to jump over the back end of the disc and onto its center. This produces a clicking or popping sound. Upon closing, the condyle slides back out of the disc hence another "click" or "pop". This condition is called disc displacement with reduction . In later stage of disc dislocation, the condyle stays behind the disc all the time, unable to get back onto the disc, the clicking sound disappeared but mouth opening is limited. This is usually the most symptomatic stage - the jaw is said to be "locked" as it is unable to open wide. At this stage the condition is called disc displacement without reduction Fortunately, in majority of the cases, the condition resolves by itself after some time. This is thanks to a process called natural adaptation of the retrodiscal tissue, which after a while becomes scar tissue and can functionally replace the disc. In fact, it becomes so similar to the disc that it is called a pseudodisc.
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Cardiac Action Potential, Animation.
 
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Cardiac action potential in pacemaker cells and contractile myocytes, electrophysiology of a heartbeat. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: https://www.patreon.com/AlilaMedicalMedia/posts The heart is essentially a muscle that contracts and pumps blood. It consists of specialized muscle cells called cardiac myocytes. The contraction of these cells is initiated by electrical impulses, known as action potentials. The impulses start from a small group of myocytes called the PACEMAKER cells, which constitute the cardiac conduction system. The cells of the SA node fire SPONTANEOUSLY, generating action potentials that spread though the contractile myocytes of the atria. The myocytes are connected by gap junctions. This enables electrical coupling of neighboring cells. Pacemaker cells and contractile myocytes exhibit different forms of action potentials. The pacemaker cells of the SA node SPONTANEOUSLY fire about 80 action potentials per minute, each of which sets off a heartbeat. Pacemaker cells do NOT have a TRUE RESTING potential. The voltage starts at about -60mV and SPONTANEOUSLY moves upward until it reaches the threshold of -40mV. This is due to action of so-called “FUNNY” currents present ONLY in pacemaker cells. Funny channels open when membrane voltage becomes lower than -40mV and allow slow influx of sodium. The resulting DE-polarization is known as “pacemaker potential”. Calcium channels open, calcium ions flow into the cell further DE-polarizing the membrane. This results in the rising phase. At peak, potassium channels open, calcium channels inactivate, potassium ions leave the cell and the voltage returns to -60mV. This is falling phase of the action potential. Contractile myocytes have a different set of ion channels. Their sarcoplasmic reticulum, the SR, stores a large amount of calcium. They also contain myofibrils. The contractile cells have a stable resting potential of -90mV and depolarize ONLY when stimulated. When a cell is DE-polarized, positive ions leak through the gap junctions to the adjacent cell and bring the membrane voltage of this cell up to the threshold of -70mV. FAST sodium channels open creating a rapid sodium influx and a sharp rise in voltage. This is the depolarizing phase. L-type, or SLOW, calcium channels also open at -40mV, causing a slow but steady influx. Sodium channels close quickly, voltage-gated potassium channels open and these result in a small decrease in membrane potential, known as EARLY RE-polarization phase. The calcium channels remain open and the potassium efflux is eventually balanced by the calcium influx. This keeps the membrane potential relatively stable for about 200 msec resulting in the PLATEAU phase, characteristic of cardiac action potentials. Calcium is crucial in coupling electrical excitation to physical muscle contraction. The influx of calcium from the extracellular fluid triggers a MUCH greater calcium release from the SR, in a process known as “calcium-induced calcium release". Calcium sets off muscle contraction by “sliding filament mechanism”. Calcium channels close, potassium efflux predominates and membrane voltage returns to its resting value. The absolute refractory period is much longer in cardiac muscle. This is essential in preventing summation and tetanus. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
Просмотров: 395562 Alila Medical Media
The Cardiac Cycle, Animation
 
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Phases of the cardiac cycle. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia The cycle is initiated with the firing of the SA node that stimulates the atria to depolarize. This is represented by the P-wave on the ECG. Atrial contraction starts shortly after the P-wave begins, and causes the pressure within the atria to increase, FORCING blood into the ventricles. Atrial contraction, however, only accounts for a FRACTION of ventricular filling, because at this point, the ventricles are ALREADY almost full due to PASSIVE blood flow DOWN the ventricles through the OPEN AV valves. As atrial contraction completes, atrial pressure begins to FALL, REVERSING the pressure gradient across the AV valves, causing them to CLOSE. The closing of the AV valves produces the first heart sound, S1, and marks the beginning of SYSTOLE. At this point, ventricular depolarization, represented by the QRS complex, is half way through, and the ventricles start to contract, RAPIDLY building UP pressures inside the ventricles. For a moment, however, the semilunar valves remain closed, and the ventricles contract within a CLOSED space. This phase is referred to as isovolumetric contraction, because NO blood is ejected and ventricular volume is UN-changed. Ventricular ejection starts when ventricular pressures EXCEED the pressures within the aorta and pulmonary artery; the aortic and pulmonic valves OPEN and blood is EJECTED out of the ventricles. This is the RAPID ejection phase. As ventricular repolarization, reflected by the T-wave, begins, ventricular pressure starts to FALL and the force of ejection is REDUCED. When ventricular pressures drop BELOW aortic and pulmonary pressures, the semilunar valves CLOSE, marking the end of systole and beginning of diastole. Closure of semilunar valves produces the second heart sound, S2. The first part of diastole is, again, isovolumetric, as the ventricles relax with ALL valves CLOSED. Ventricular pressure drops RAPIDLY but their volumes remain UNchanged. Meanwhile, the atria are being filled with blood and atrial pressures RISE slowly. Ventricular FILLING starts when ventricular pressures drop BELOW atrial pressures, causing the AV valve to open, allowing blood to flow DOWN the ventricles PASSIVELY. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Animation of Protein Synthesis (Translation) in Prokaryotes.
 
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Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/medical-genetics ©Alila Medical Media. All rights reserved. Initiation of translation in prokaryotes: The small ribosomal subunit is separated from the large subunit with the help of two initiation factors: IF1 and IF3. This complex then binds a to purine-rich region -- the Shine-Dalgarno sequence -- upstream of the AUG start codon on the mRNA. The Shine-Dalgarno sequence is base-paired to a complementary sequence on the 16S rRNA - a component of the small subunit. This alignment ensures that the start codon is in the right position within the ribosome. Another initiation factor - IF2 - brings in the initiator tRNA charged with the initiator amino acid N-formyl-methionine. The large ribosomal subunit joins the complex and all initiation factors are released. The ribosome has three sites: the A-site is the entry site for new tRNA charged with amino-acid or aminoacyl-tRNA; the P-site is occupied by peptidyl-tRNA - the tRNA that carries the growing polypeptide chain; the E-site is the exit site for the tRNA after it's done delivering the amino acid. The initiator tRNA is positioned in the P-site. Elongation: A new tRNA carrying an amino acid enters the A-site of the ribosome. On the ribosome, the anticodon of the incoming tRNA is matched against the mRNA codon positioned in the A-site. During this proof-reading, tRNA with incorrect anticodons are rejected and replaced by new tRNA that are again checked. When the right aminoacyl-tRNA enters the A-site, a peptide bond is made between the two now-adjacent amino-acids. As the peptide bond is formed, the tRNA in the P-site releases the amino-acids onto the tRNA in the A-site and becomes empty. At the same time, the ribosome moves one triplet forward on the mRNA. As a result, the empty tRNA is now in the E-site and the peptidyl tRNA is in the P-site. The A-site is now unoccupied and is ready to accept a new tRNA. The cycle is repeated for each codon on the mRNA. Termination: Termination happens when one of the three stop codons is positioned in the A-site. No tRNA can fit in the A-site at that point as there are no tRNA that match the sequence. Instead, these codons are recognized by a protein, a release factor. Binding of the release factor catalyzes the cleavage of the bond between the polypeptide and the tRNA. The polypeptide is released from the ribosome. The ribosome is disassociated into subunits and is ready for a new round of translation. The newly made polypeptide usually requires additional modifications and folding before it can become an active protein.
Просмотров: 282911 Alila Medical Media
Development of Glaucoma Animation, Open Angle vs Angle Closure Glaucoma.
 
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Complete and concise tutorial of glaucoma. This video and other ophthalmology videos are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/all-animations/eyes-and-vision-videos ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Glaucoma is a group of eye diseases in which the optic nerve is damaged leading to irreversible loss of vision. In most cases, this damage is due to an increased pressure within the eye. The eye produces a fluid called aqueous humor which is secreted by the ciliary body into the posterior chamber - a space between the iris and the lens. It then flows through the pupil into the anterior chamber between the iris and the cornea. From here, it drains through a sponge-like structure located at the base of the iris called the trabecular meshwork and leaves the eye. In a healthy eye, the rate of secretion balances the rate of drainage. In people with glaucoma, the drainage canal is partially or completely blocked. Fluid builds up in the chambers and this increases pressure within the eye. The pressure drives the lens back and presses on the vitreous body which in turn compresses and damages the blood vessels and nerve fibers running at the back of the eye. These damaged nerve fibers result in patches of vision loss, and if left untreated, may lead to total blindness. There are two main types of glaucoma: open-angle and angle-closure. Open-angle glaucoma , or chronic glaucoma, is caused by partial blockage of the drainage canal. The angle between the cornea and the iris is "open", meaning the entrance to the drain is clear, but the flow of aqueous humor is somewhat slow. The pressure builds up gradually in the eye over a long period of time. Symptoms appear gradually, starting from peripheral vision loss, and may go on unnoticed until the central vision is affected. Progression of glaucoma can be stopped with medical treatments, but part of vision that is already lost can not be restored. This is why it's very important to detect signs of glaucoma early with regular eye exams. Angle-closure glaucoma, or acute glaucoma, is caused by a sudden and complete blockage of aqueous humor drainage. The pressure within the eye rises rapidly and may lead to total vision loss quickly. Certain anatomical features of the eye such as narrow drainage angle, shallow anterior chamber, thin and droopy iris, make it easier to develop acute glaucoma. Typically, this happens when the pupil is dilated and the lens is stick to the back of the iris. This prevents the aqueous humor from flowing through the pupil into the anterior chamber. Accumulation of fluid in the posterior chamber presses on the iris causing it to bulge outward and block the drainage angle completely. Acute angle-closure glaucoma is a medical emergency and requires immediate attention.
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Muscle Contraction - Cross Bridge Cycle, Animation.
 
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Molecular basis of the sliding filament theory (skeletal muscle contraction) - the cross bridge cycle. This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/all-animations/cell-molecular-biology-genetics-videos Voice by: Sue Stern ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Muscle contraction is at the basis of all skeletal movements. Skeletal muscles are composed of muscles fibers which in turn are made of repetitive functional units called sarcomeres. Each sarcomere contains many parallel, overlapping thin (actin) and thick (myosin) filaments. The muscle contracts when these filaments slide past each other, resulting in a shortening of the sarcomere and thus the muscle. This is known as the sliding filament theory. Cross-bridge cycling forms the molecular basis for this sliding movement. - Muscle contraction is initiated when muscle fibers are stimulated by a nerve impulse and calcium ions are released. - To trigger muscular contraction, the troponin units on the actin myofilaments are bound by calcium ions. The binding displaces tropomyosin along the myofilaments, which in turn (and) exposes the myosin binding sites. - At this stage, the head of each myosin unit is bound to an ADP and a phosphate molecule remaining from the previous muscular contraction. - Now, the myosin heads release these phosphates and bind to the actin myofilaments via the newly exposed myosin binding sites. - In this way, the actin and myosin myofilaments are cross-linked. - The two myofilaments glide past one another, propelled by a head-first movement of the myosin units powered by the chemical energy stored in their heads. As the units move, they release the ADP molecules bound to their heads. - The gliding motion is halted when ATP molecules bind to the myosin heads, thus severing the bonds between myosin and actin. - The ATP molecules bound to myosin are now decomposed into ADP and phosphate, with the energy released by this reaction stored in the myosin heads, ready to be used in the next cycle of movement. - Having been unbound from actin, the myosin heads resume their starting positions along the actin myofilament, and can now begin a new sequence of actin binding. - Thus, the presence of further calcium ions will trigger a new contraction cycle
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12 Lead ECG Explained, Animation
 
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Understanding the standard 12-lead EKG - Basics of electrocardiography explained. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Electrical activities of the heart can be picked up on the skin via electrodes. An ECG machine records these activities and displays them graphically. The graphs show the heart’s OVERALL electrical potential, or voltage, as it changes over time during a cardiac cycle. The 12 leads of the ECG represent 12 electrical views of the heart from 12 different angles. The conventional 12-lead procedure involves attaching 10 electrodes to the body: one to each limb and six across the chest. There are 6 limb leads and 6 chest leads. The 6 limb leads look at the heart in a vertical plane and are obtained from three electrodes attached to the right arm, left arm, and left leg. The electrode on the right leg is an earth electrode. The measurement of a voltage requires 2 poles: negative and positive. The ECG machine uses the negative pole as zero reference. Thus, the position of the positive pole is the “point of view”, and the line connecting the 2 poles is the “line of sight”. Leads I, II, and III are BI-polar - they measure electrical potential between 2 of the 3 limb electrodes: Lead I represents the voltage between the right arm – negative pole - and the left arm – positive pole, and thus looks at the heart from the left. Lead II sees signal movements between the right arm – negative - and the left leg –positive - forming the INFERIOR LEFT view. Similarly, lead III measures electrical potential between the left arm – negative - and the left leg –positive, looking at the heart from an INFERIOR RIGHT angle. Leads aVR, aVL, and aVF, or “augmented limb leads”, are UNIpolar. They use ONE limb electrode as the positive pole, and take the average of inputs from the OTHER two as the zero reference. Hence, aVR looks at the UPPER RIGHT side of the heart; aVL looks at the UPPER LEFT side of the heart; and aVF looks at the INFERIOR wall of the heart. The chest leads, or precordial leads, view the heart in a HORIZONTAL plane. These are unipolar leads. The corresponding chest electrodes serve as the positive poles. The reference negative value is the same for all chest leads and is calculated as the average of inputs from the three limb electrodes. DE-polarization TOWARD a lead produces a POSITIVE deflection; DE-polarization AWAY from a lead gives a NEGATIVE deflection. The REVERSE is true for RE-polarization. Thus, leads that look at the heart from different angles may have waves pointing in different directions.
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Micturition Reflex - Neural Control of Urination Animation Video.
 
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This video and other urinary system animation (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/urinary-system-videos ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Neural control of urination - micturition reflex. When the bladder is full, stretch receptors in the wall of the bladder send nerve impulses to the sacral region of the spinal cord. By way of a parasympathetic response, signals return to the bladder and stimulate contraction of the muscle of the bladder and relaxation of the internal urethral sphincter. This part of the reflex is involuntary and is predominant in infants and young children. As the central nervous system matures, it acquires voluntary control over the external urethral sphincter. Urination is controlled mainly by the micturition center in the pons. This center receives sensory signals from the bladder and communicates with the cortex about the appropriateness of urinating at the moment. At times when it's not convenient to urinate, the center sends back an inhibitory signal to keep the sphincters closed and prevent voiding. When you wish to urinate, this inhibition is removed; the spinal cord instructs the muscle of the bladder to contract and the sphincters to open to let the urine out. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Trabeculectomy Surgery for Glaucoma, Animation.
 
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This video and related images/videos are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/eyes-and-vision-videos ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Trabeculectomy, also called Filtration Surgery, is a surgical procedure performed for treatment of glaucoma. The treatment involves removing part of the trabecular meshwork and creating a new escape route for the aqueous humor. When successful, it allows the aqueous fluid to drain from the eye into an area underneath the conjunctiva where it is subsequently absorbed by the body's circulatory system or filtered into tears. In this procedure: - A conjunctival pocket is created and maybe treated with Mitomycin or other antimetabolites for a few minutes. These drugs are used to prevent scarring of the operation site. Scarring, if occurs, may clog the new drainage canal, and is therefore the major reason the procedure may fail. - A half thickness flap is then made in the sclera and is dissected all the way to the clear cornea. - A block of scleral tissue including part of the trabecular meshwork and Schlemm's canal is then removed to make a hole into the anterior chamber of the eye. - As the iris may plug up this hole from the inside, a piece of the iris maybe removed at this time. This is called iridectomy. - The scleral flap is then sutured loosely back in place. These sutures can be released gradually during a couple of weeks after surgery. This allows adjustment of the aqueous flow in order to achieve target pressure and to avoid the complication of having a too low intraocular pressure. - The conjunctiva is sewn back in place to cover the area. After surgery, aqueous humor drains into a filtering area called a "bleb" under the conjunctiva. Since the surgery is usually performed near the top of the eye, the bleb can easily be concealed behind the upper eyelid.
Просмотров: 146391 Alila Medical Media
Eukaryotic Translation (Protein Synthesis), Animation.
 
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This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/medical-genetics ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia The translation process involves the following components: - mRNA or messenger RNA containing the genetic information to be translated. - tRNA or transfer RNA bringing in the amino acids – the building blocks of the protein. - Ribosome – the machine that performs the translation. The ribosome has two subunits: small and large. - Several initiation factors, elongation factors, and release factors. These factors assist with initiation, elongation and termination of the process, respectively. Steps of the translation process: Initiation (eukaryotes) : The small ribosomal subunit binds to the initiator tRNA carrying the initiator amino acid methionine. This complex then attaches to the cap structure at the 5’ end of an mRNA and scans for the start codon AUG. The process is mediated by several initiation factors. At the start codon, the large ribosomal subunit joins the complex and all initiation factors are released. The ribosome has three sites: the A-site is the entry site for new tRNA charged with amino-acid or aminoacyl-tRNA; the P-site is occupied by peptidyl-tRNA - the tRNA that carries the growing polypeptide chain; the E-site is the exit site for the tRNA after it’s done delivering the amino acid. The initiator tRNA is positioned in the P-site. Elongation: A new tRNA carrying an amino acid enters the A-site of the ribosome. On the ribosome, the anticodon of the incoming tRNA is matched against the mRNA codon positioned in the A-site. During this proof-reading, tRNA with incorrect anticodons are rejected and replaced by new tRNA that are again checked. When the right aminoacyl-tRNA enters the A-site, a peptide bond is made between the two now-adjacent amino-acids. As the peptide bond is formed, the tRNA in the P-site releases the amino-acids onto the tRNA in the A-site and becomes empty. At the same time, the ribosome moves one triplet forward on the mRNA. As a result, the empty tRNA is now in the E-site and the peptidyl tRNA is in the P-site. The A-site is now unoccupied and is ready to accept a new tRNA. The cycle is repeated for each codon on the mRNA. Termination: Termination happens when one of the three stop codons is positioned in the A-site. No tRNA can fit in the A-site at that point as there are no tRNA that match the sequence. Instead, these codons are recognized by a protein, a release factor. Binding of the release factor catalyzes the cleavage of the bond between the polypeptide and the tRNA. The polypeptide is released from the ribosome. The ribosome is disassociated into subunits and is ready for a new round of translation. The newly made polypeptide usually requires additional modifications and folding before it can become an active protein.
Просмотров: 237790 Alila Medical Media
Heart Sounds and Heart Murmurs, Animation.
 
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Basic hearts sounds and common heart murmurs. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. When a healthy heart beats, it makes a “lub-dub” sound. The first heart sound “lub”, also known as S1, is caused by the closing of the AV valves after the atria have pumped blood into the ventricles. The second heart sound “dub”, or S2, originates from the closing of the aortic and pulmonary valves, right after the ventricles have ejected the blood. The time interval between S1 and S2 is when the ventricles contract, called SYSTOLE. The interval between S2 and the NEXT S1 is when the ventricles relax and are filled with blood, called DIASTOLE. Diastole is longer than systole, hence the lub-dub, lub-dub, lub-dub… Heart sounds are auscultated at 4 different sites on the chest wall which correspond to the location of blood flow as it passes through the aortic, pulmonic, tricuspid, and mitral valves, respectively. This is how SIMILAR defects associated with DIFFERENT valves are differentiated. Heart murmurs are whooshing sounds produced by turbulent flow of blood. Murmurs are diagnosed based on the TIME they occur in the cardiac cycle, their changes in INTENSITY over time, and the auscultation SITE where they are best heard. Examples of conditions associated with common systolic murmurs include: - MITRAL valve regurgitation, when the mitral valve does NOT CLOSE properly and blood surges back to the left atrium during systole. The murmur starts at S1, when the AV valves close, and maintains the same intensity for the entire duration of systole. This holosystolic murmur is best heard at the mitral region -the apex, with radiation to the left axilla. Because the valve closure in mitral regurgitation is INcomplete, S1 is often quieter. On the other side of the heart, a TRICUSPID valve regurgitation has similar timing and shape, but it is loudest in the tricuspid area and the sound radiates up, along the left sternal border. - AORTIC valve stenosis, when the aortic valve does NOT OPEN properly and blood is forced through a narrow opening. The blood flow starts small, rises to a maximum in mid-systole at the peak of ventricular contraction, then attenuates toward the end of systole. This results in a crescendo-decrescendo, or a diamond-shaped, murmur which starts a short moment after S1. It is often preceded by an ejection click caused by the opening of the STENOTIC valve. Aortic stenosis murmur is loudest in the aortic area and the sound radiates to the carotid arteries in the neck following the direction of blood flow. Again, on the other side of the heart, a PULMONIC stenosis has the same characteristics but is best heard in the pulmonic area and does NOT radiate to the neck. Other conditions that cause audible systolic murmurs include ventricular septal defect and mitral valve prolapse. An example of diastolic murmurs is aortic valve regurgitation. This is when the aortic valve does NOT CLOSE properly, resulting in blood flowing back to the left ventricle during diastole- the filling phase. As the blood flows in the REVERSE direction, the murmur is best heard NOT in the aortic area, but rather along the left sternal border. It peaks at the beginning of diastole when the pressure difference is highest, then rapidly decreases as the equilibrium is reached. Other common diastolic murmurs are associated with pulmonic regurgitation, mitral stenosis and tricuspid stenosis.
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Cardiac Arrhythmias
 
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Cardiac Arrhythmias Overview: Sinus, Atrial and Ventricular Rhythms, Anatomy and ECG, Animation. This video and other related images/videos (in HD) are available for licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Abbie Drum Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Cardiac arrhythmias classified by site of origin: Sinus rhythms, from the SA node; Atrial rhythms the atria; Ventricular rhythms from the ventricles. Sinus bradycardia and sinus tachycardia may be normal or clinical depending on the underlying cause. For example, sinus bradycardia is considered normal during sleep and sinus tachycardia may be normal during physical exercises. Cardiac arrhythmias that originate from other parts of the atria are always clinical. The most common include: atrial flutter, atrial fibrillation and AV nodal re-entrant tachycardia. These are forms of supraventricular tachycardia or SVT. Atrial flutter or A-flutter is caused by an electrical impulse that travels around in a localized self-perpetuating loop, most commonly located in the right atrium. This is called a re-entrant pathway. For each cycle around the loop, there is one contraction of the atria. The atrial rate is regular and rapid - between 250 and 400 beats per minute. Ventricular rate, or heart rate, however, is slower, thanks to the refractory properties of the AV node. The AV node blocks part of atrial impulses from reaching the ventricles. In this example, only one out of every three atrial impulses makes its way to the ventricles. The ventricular rate is therefore 3 times slower than the atrial rate. This is an example of a “3 to 1 heart block”. Ventricular rate in A-flutter is usually regular, but it can also be irregular. On an ECG atrial flutter is characterized by absence of normal P wave. Instead, flutter waves, or f-waves are present in saw-tooth patterns. Atrial fibrillation is caused by multiple electrical impulses that are initiated randomly from many ectopic sites in and around the atria, commonly near the roots of pulmonary veins. These un-synchronized, chaotic electrical signals cause the atria to quiver or fibrillate rather than contract. The atrial rate during atrial fibrillation can be extremely high, but most of the electrical impulses do not pass through the AV node to the ventricles, again, thanks to the refractory properties of the cells of the AV node. Those do come through are irregular. Ventricular rate or heart rate is therefore irregular and can range from slow - less than 60 - to rapid -more than 100 - beats per minute. On an ECG, atrial fibrillation is characterized by absence of P-waves and irregular narrow QRS complexes. The baseline may appear undulating or totally flat depending on the number of ectopic sites in the atria. In general, larger number of ectopic sites results in flatter baseline. AV nodal re-entrant tachycardia or AVNRT is caused by a small re-entrant pathway that involves directly the AV node. Every time the impulse passes through the AV node, it is transmitted down to the ventricles. The atrial rate and ventricular rate are therefore identical. Heart rate is regular and fast, ranging from 150 to 250 beats per minute. Ventricular rhythms are the most dangerous. In fact, they are called lethal rhythms. Ventricular tachycardia or V-tach is most commonly caused by a single strong firing site or circuit in one of the ventricles. It usually occurs in people with structural heart problems such as scarring from a previous heart attack or abnormalities in heart muscles. Impulses starting in the ventricles produce ventricular premature beats that are regular and fast, ranging from 100 to 250 beats per minute. On an ECG V-tach is characterized by wide and bizarre looking QRS complexes. P wave is absent. V-tach may occur in short episodes of less than 30 seconds and cause no or few symptoms. Sustained v-tach lasting for more than 30 seconds requires immediate treatment to prevent cardiac arrest. Ventricular tachycardia may also progress into ventricular fibrillation. Ventricular fibrillation or v-fib is caused by multiple weak ectopic sites in the ventricles. These un-synchronized, chaotic electrical signals cause the ventricles to quiver or fibrillate rather than contract. The heart pumps little or no blood. V-fib can quickly lead to cardiac arrest. V-fib ECG is characterized by irregular random waveforms of varying amplitude, with no identifiable P wave, QRS complex or T wave. Amplitude decreases with time, from initial coarse v-fib to fine v-fib and ultimately to flatline.
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Swallowing Reflex, Phases and Overview of Neural Control, Animation.
 
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This video and other related videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/digestive-system-videos ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Swallowing, or deglutition, is the process by which food passes from the mouth, through the pharynx and into the esophagus. As simple as it might seem to healthy people, swallowing is actually a very complex action that requires an extremely precise coordination with breathing since both of these processes share the same entrance - the pharynx. Failure to coordinate would result in choking or pulmonary aspiration. Swallowing involves over twenty muscles of the mouth, throat and esophagus which are controlled by several cortical areas and by the swallowing centers in the brainstem. The brain communicates with the muscles through several cranial nerves. Swallowing consists of three phases: 1. Oral or buccal phase: this is the voluntary part of swallowing, the food is moistened with saliva and chewed, food bolus is formed and the tongue pushes it to the back of the throat (the pharynx). This process is under neural control of several areas of cerebral cortex including the motor cortex. 2. Pharyngeal phase starts with stimulation of tactile receptors in the oropharynx by the food bolus. The swallow reflex is initiated and is under involuntary neuromuscular control. The following actions are taken to ensure the passage of food or drink into the esophagus: - The tongue blocks the oral cavity to prevent going back to the mouth. - The soft palate blocks entry to the nasal cavity. - The vocal folds close to protect the airway to the lungs. The larynx is pulled up with the epiglottis flipping over covering the entry to the trachea. This is the most important step since entry of food or drink into the lungs may potentially be life threatening. - The upper esophageal sphincter opens to allow passage to the esophagus. 3. Esophageal phase: food bolus is propelled down the esophagus by peristalsis - a wave of muscular contraction that pushes the bolus ahead of it. The larynx moves down back to original position.
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Bundle Branch Block, Animation.
 
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Understanding ECGs of Left and Right Bundle Branch Blocks (LBBB and RBBB). This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Bundle branch blocks happen when there is an obstruction in one of the bundle branches. The names “left bundle branch block” and “right bundle branch block” indicate the side that is affected. In a normal heart, the two ventricles are depolarized simultaneously by the two bundles and contract at the same time. In bundle branch blocks, the UN-affected ventricle depolarizes first. The electrical impulses THEN move through the myocardium to the other side. This results in a DELAYED and SLOWED depolarization of the affected ventricle, hence a broader QRS complex – typically longer than 120 milliseconds; and a loss in ventricular synchrony. Left and right bundle branch blocks are diagnosed and differentiated by looking at ECG recordings obtained from the CHEST leads, which register signal movements in a horizontal plane. Of these, the most useful are leads V1 and V6 as they are best located to detect impulses moving between the left and right ventricles. Activation of the ventricles starts with the interventricular septum. In normal conduction, depolarization of the septum is initiated from the left bundle going to the right, TOWARD V1 and AWAY from V6. This results in a small positive deflection in V1 and a negative deflection in V6. The signals then move both directions to the two ventricles, but as the left ventricle is usually much larger, the NET movement is to the left, AWAY from V1, TOWARD V6. This corresponds to a negative wave in V1 and a positive wave in V6. In RIGHT bundle branch block the initial septal activation is unchanged. The left ventricle depolarizes NORMALLY toward V6, away from V1, producing a positive deflection in V6, negative in V1. The impulses then REVERSE the direction spreading to the right ventricle, hence a subsequent negative wave in V6, positive in V1. Lead V1 gives a characteristic M shape with a terminal R wave, while V6 sees a broader S wave. In LEFT bundle branch block septal depolarization is REVERSED, from right to left, giving a negative wave in V1. The right ventricle activates first, with the signals moving to the right, generating a small upward deflection. Depolarization then spreads to the larger left ventricle, resulting in a large downward deflection. Lead V6 sees the opposite, producing a wide, characteristic “bunny ears” QRS complex with two R waves. In some cases, right ventricular depolarization may not be visible. Some people with bundle branch blocks are born with this condition. They usually do not have any symptoms and do not require treatments. Others acquire it as a consequence of another heart disease. These patients need monitoring, and in severe cases, a pacemaker may be required to restore ventricular synchrony
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Diabetes Type 1 and Type 2, Animation.
 
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This video and more updated versions of similar images/videos are available for instant download licensing here https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/endocrinology ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Diabetes refers to a group of conditions characterized by a high level of blood glucose, commonly referred to as blood sugar. Too much sugar in the blood can cause serious, sometimes life-threatening health problems. There are two types of chronic diabetic conditions: type 1 diabetes and type 2 diabetes. Pregnant women may acquire a transient form of the disease called “gestational diabetes” which usually resolves after the birth of baby. Pre-diabetes is when the blood sugar level is at the borderline: higher than normal, but lower than in diabetics. Prediabetes may or may not progress to diabetes. During food digestion, carbohydrates - or carb - break down into glucose which is carried by the bloodstream to various organs of the body. Here, it is either consumed as an energy source - in muscles for example - or is stored for later use in the liver. Insulin is a hormone produced by beta cells of the pancreas and is necessary for glucose intake by target cells. In other words, when insulin is deficient, muscle or liver cells are unable to use or store glucose, and as a result, glucose accumulates in the blood. In healthy people, beta cells of the pancreas produce insulin; insulin binds to its receptor on target cells and induces glucose intake. In type 1 diabetes, beta cells of the pancreas are destroyed by the immune system by mistake. The reason why this happens is unclear, but genetic factors are believed to play a major role. Insulin production is reduced; less insulin binds to its receptor on target cells; less glucose is taken into the cells, more glucose stays in the blood. Type 1 is characterized by early onset, symptoms commonly start suddenly and before the age of 20. Type 1 diabetes is normally managed with insulin injection. Type 1 diabetics are therefore “insulin dependent”. In type 2 diabetes, the pancreas produces enough insulin but something goes wrong either with receptor binding or insulin signaling inside the target cells. The cells are not responsive to insulin and therefore cannot import glucose; glucose stays in the blood. In other words, type 2 diabetics are “insulin resistant”. Here again, genetic factors predispose susceptibility to the disease, but it is believed that lifestyle plays a very important role in type 2. Typically, obesity, inactive lifestyle, and unhealthy diet are associated with higher risk of type 2 diabetes. Type 2 is characterized by adult onset; symptoms usually appear gradually and start after the age of 30. Type 2 diabetes accounts for about 80 to 90% of all diabetics. Management focuses on weight loss and includes a low-carb diet.
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Action Potential in Neurons, Animation.
 
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What is Action Potential? How is it Generated in Neuron? Clear and Concise Explanation of Phases. This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Cells are polarized, meaning there is an electrical voltage across the cell membrane. In a resting neuron, the typical voltage, known as the RESTING membrane potential, is about -70mV (millivolts). The negative value means the cell is more negative on the INSIDE. At this resting state, there are concentration gradients of sodium and potassium across the cell membrane: more sodium OUTSIDE the cell and more potassium INSIDE the cell. These gradients are maintained by the sodium-potassium pump which constantly brings potassium IN and pumps sodium OUT of the cell. A neuron is typically stimulated at dendrites and the signals spread through the soma. Excitatory signals at dendrites open LIGAND-gated sodium channels and allow sodium to flow into the cell. This neutralizes some of the negative charge inside the cell and makes the membrane voltage LESS negative. This is known as depolarization as the cell membrane becomes LESS polarized. The influx of sodium diffuses inside the neuron and produces a current that travels toward the axon hillock. If the summation of all input signals is excitatory and is strong enough when it reaches the axon hillock, an action potential is generated and travels down the axon to the nerve terminal. The axon hillock is also known as the cell’s “trigger zone” as this is where action potentials usually start. This is because action potentials are produced by VOLTAGE-gated ion channels that are most concentrated at the axon hillock. Voltage-gated ion channels are passageways for ions in and out of the cell, and as their names suggest, are regulated by membrane voltage. They open at some values of the membrane potential and close at others. For an action potential to be generated, the signal must be strong enough to bring the membrane voltage to a critical value called the THRESHOLD, typically about -55mV. This is the minimum required to open voltage-gated ion channels. At threshold, sodium channels open quickly. Potassium channels also open but do so more slowly. The initial effect is therefore due to sodium influx. As sodium ions rush into the cell, the inside of the cell becomes more positive and this further depolarizes the cell membrane. The increasing voltage in turn causes even more sodium channels to open. This positive feedback continues until all the sodium channels are open and corresponds to the rising phase of the action potential. Note that the polarity across the cell membrane is now reversed. As the action potential nears its peak, sodium channels begin to close. By this time, the slow potassium channels are fully open. Potassium ions rush out of the cell and the voltage quickly returns to its original resting value. This corresponds to the falling phase of the action potential. Note that sodium and potassium have now switched places across the membrane. As the potassium gates are also slow to close, potassium continues to leave the cell a little longer resulting in a negative overshoot called hyper-polarization. The resting membrane potential is then slowly restored thanks to diffusion and the sodium-potassium pump. During and shortly after an action potential is generated, it is impossible or very difficult to stimulate that part of the membrane to fire again. This is known as the REFRACTORY period. The refractory period is divided into absolute refractory and relative refractory. The absolute refractory period lasts from the start of an action potential to the point the voltage first returns to the resting membrane value. During this time, the sodium channels are open and subsequently INACTIVATED while closing and thus unable to respond to any new stimulation. The relative refractory period lasts until the end of hyper-polarization. During this time, some of the potassium channels are still open, making it difficult for the membrane to depolarize, and a much stronger signal is required to induce a new response. During an action potential, the sodium influx at a point on the axon spreads along the axon, depolarizing the adjacent patch of the membrane, generating a similar action potential in it. The sodium currents diffuse in both directions on the axon, but the refractory properties of ion channels ensure that action potential propagates ONLY in ONE direction. This is because ONLY the unfired patch of the axon can respond with an action potential; the part that has just fired is unresponsive until the action potential is safely out of range.
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Cardiac Axis Interpretation, Animation.
 
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What is the heart axis? How to calculate cardiac axis on an ECG strip? Methods for estimation/determination of cardiac axis. This video (updated with real voice) and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Cardiac axis is the net direction of electrical activity during depolarization. In a healthy heart, the net movement is downward and slightly left. This axis is altered, or deviated, in certain conditions. For example, in left ventricular hypertrophy the axis is skewed further left; while right ventricular hypertrophy results in a deviation to the right. Cardiac axis can be determined by examining the 6 limb leads, which look at the heart from different angles in a vertical plane. The QRS axis is the most important, and also the easiest to be determined, as it represents ventricular depolarization. The QRS axis is considered normal when it is between -30 and +90 degrees. Left axis deviation is between -30 and -90 degrees. Right axis deviation goes between +90 and +180 degrees. The rest is known as northwest axis or extreme axis deviation. Remember that depolarization TOWARD a lead produces a POSITIVE deflection; depolarization AWAY from a lead gives a NEGATIVE deflection. Impulses moving at a 90 degree angle relative to a lead produce an isoelectric, or equiphasic result with positive and negative deflections of similar amplitude. There are several methods to estimate the QRS axis; we here discuss 2 of them. The quadrant method. This method looks at the QRS complex in lead 1 and lead aVF. If the QRS complex is mostly positive in both leads, the axis is somewhere in between the 2 leads, which is in the normal range. If it’s negative in lead I and positive in aVF, the axis is running away from lead I but toward aVF and is thus in the lower right quadrant. The diagnosis is right axis deviation. A positive value in lead I and negative in lead aVF, place the axis in the upper left quadrant, which interprets as possible left axis deviation. A more accurate method will be needed to further determine if it is borderline normal or left deviation. Negative values of the QRS complex in both leads are indicative of extreme axis deviation. The isoelectric lead method: this method consists of finding the isoelectric or equiphasic lead – the one with equal, or closest to equal, negative and positive deflections. In other words, the one with zero, or nearest to zero, net amplitude. The axis line is perpendicular to the direction of the isoelectric lead. Now, look at the lead that runs nearest to this line. If the QRS complex is positive in that lead, the axis points to roughly the same direction as the lead. If it is negative, the axis points to the opposite direction.
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Myofascial Pain Syndrome and Trigger Points Treatments, Animation.
 
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This animation and many other pain management related videos/images (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/pain-management-images-and-videos ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Perfect for patient education. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Myofascial pain syndrome is a common chronic pain disorder that can affect various parts of the body. Myofascial pain syndrome is characterized by presence of hyperirritable spots located in skeletal muscle called trigger points. A trigger point can be felt as a band or a nodule of muscle with harder than normal consistency. Palpation of trigger points may elicit pain in a different area of the body. This is called referred pain. Referred pain makes diagnosis difficult as the pain mimics symptoms of more well-known common conditions. For example, trigger point related pain in the head and neck region may manifest as tension headache, temporomandibular joint pain, eye pain, or tinnitus. Symptoms of myofascial pain syndrome include regional, persistent pain, commonly associated with limited range of motion of the affected muscle. The pain is most frequently found in the head, neck, shoulders, extremities, and lower back. Trigger points are developed as a result of muscle injury. This can be acute trauma caused by sport injury, accident, or chronic muscle overuse brought by repetitive occupational activities, emotional stress or poor posture. A trigger point is composed of many contraction knots where individual muscle fibers contract and cannot relax. These fibers make the muscle shorter and constitute a taut band -- a group of tense muscle fibers extending from the trigger point to muscle attachment. The sustained contraction of muscle sarcomeres compresses local blood supply, resulting in energy shortage of the area. This metabolic crisis activates pain receptors, generating a regional pain pattern that follows a specific nerve passage. The pain patterns are therefore consistent and are well documented for various muscles. Treatment of myofascial pain syndrome aims to release trigger points and return the affected muscle to original length and strength. Common treatment options include: - Manual therapy, such as massage, involves application of certain amount of pressure to release trigger points. The outcome of manual therapy strongly depends on the skill level of the therapist. - The Spray and Stretch technique makes use of a vapor coolant to quickly decrease skin temperature while passively stretching the target muscle. A sudden drop in skin temperature provides a pain relief effect, allowing the muscle to fully stretch, and thus releasing the trigger points. - Trigger point injections with saline, local anesthetics or steroids are well accepted as effective treatments for myofascial trigger points. - Dry needling -- insertion of a needle without injecting any solution - is reported to be as effective as injections.
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Neuroscience Basics: GABA Receptors and GABA Drugs, Animation
 
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Mechanism of action of GABA-A, GABA-B and GABA-C. Allosteric modulators. Action of Benzodiazepines (benzos) and Flumazenil. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology Voice by: Sue Stern ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Gamma-aminobutyric acid, or GABA, is the primary INHIBITORY neurotransmitter in the mature brain. It REDUCES neuronal activity of target cells through its binding to GABA receptors present on the cell surface. Nearly half of all synapses of the brain express some kind of GABA receptor and are thus responsive to GABA. There are at least 3 types of GABA receptors: GABA-A, GABA-B and GABA-C. GABA-A and GABA-C are ligand-gated chloride channels. Upon transmitter binding, they open and allow chloride ions to flow into the neuron, making it more NEGATIVE, or HYPER-polarized, and thus LESS likely to generate action potentials. GABA-B acts through a G-protein to activate potassium channels, which allow positively-charged potassium to flow OUT of the cell, again resulting in membrane HYPER-polarization and a subsequent decrease in neuron responsiveness. GABA is believed to play a major role in controlling neuronal hyperactivity associated with fear, anxiety and convulsions. GABA-A receptor is composed of 5 protein subunits. In addition to binding sites for GABA, it has allosteric binding sites for other substances known as GABA modulators. These are molecules that can INCREASE or DECREASE the action of GABA, but have no effect in the absence of GABA. For example, benzodiazepines, a class of drugs used to treat anxiety, bind to GABA-A receptor and facilitate its binding to GABA, thus potentiating GABA inhibitory effect. Other positive modulators include barbiturates, alcohol, propofol, among others. Examples of negative modulators are convulsants, such as Flumazenil. Flumazenil reverses the effects of benzodiazepines by competing with them at the same binding site on GABA-A. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Long Term Potentiation and Memory Formation, Animation
 
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Role of the hippocampus, synaptic plasticity, the 2 phases of LTP, connection with short-term and long-term memory. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology Voice by: Sue Stern ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia The process of learning begins in the cortex. Sensory signals are then transmitted to the hippocampus. If a signal is strong, or repeated, a long-term memory is established and wired back to the cortex for storage. Lesions in the hippocampus impair formation of new memories, but do not affect the older ones. The brain consists of billions of neurons. Neurons communicate with each other through a synapse. Synaptic connections can change over time, a phenomenon known as synaptic plasticity. Synaptic plasticity follows the “use it or lose it” rule: frequently used synapses are strengthened while rarely used connections are eliminated (synaptic pruning). Synaptic plasticity is believed to underlie the process of learning and memory retention. High-frequency signals or repeated stimulations STRENGTHEN synaptic connections over time. This is known as long-term potentiation, or LTP, and is thought to be the cellular basis of memory formation. LTP can occur at most excitatory synapses all over the brain, but is best studied at the glutamate synapse of the hippocampus. When a glutamatergic neuron is stimulated, action potentials travel down its axon and trigger the release of glutamate into the synaptic cleft. Glutamate then binds to its receptors on the post-synaptic neuron. The 2 main glutamate receptors that often co-exist in a synapse are AMPA and NMDA receptors. These are ion channels that activate upon binding to glutamate. When the pre-synaptic neuron is stimulated by a WEAK signal, only a small amount of glutamate is released. Although both receptors are bound by the glutamate, only AMPA is activated by weak stimulation. Sodium influx through the AMPA channel results in a SLIGHT DE-polarization of the post-synaptic membrane. The NMDA channel remains closed because its pore is blocked by magnesium ions. When the pre-synaptic neuron is stimulated by a STRONG or REPEATING signal, a large amount of glutamate is released; the AMPA receptor stays open for a longer time, admitting more sodium into the cell, thus resulting in a GREATER DE-polarization. Increased influx of positive ions EXPELS magnesium from the NMDA channel, which NOW activates, allowing not only sodium but also CALCIUM into the cell. Calcium is the mediator of LTP induction. There are 2 distinct phases of LTP. In the early phase, calcium initiates signaling pathways that activate several protein kinases. These kinases enhance synaptic communication in 2 ways: they phosphorylate the existing AMPA receptors, thereby increasing AMPA conductance to sodium; and help to bring more AMPA receptors from intracellular stores to the post-synaptic membrane. This phase is thought to be the basis of short-term memory, which lasts for several hours. In the late phase, NEW proteins are made and gene expression is activated to further enhance the connection between the 2 neurons. These include newly synthesized AMPA receptors, and expression of other proteins that are involved in the growth of NEW dendritic spines and synaptic connections. The late phase may correlate with formation of long-term memory. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Atrial Fibrillation Anatomy, ECG and Stroke, Animation.
 
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This video and similar images/videos are available for instant download licensing here https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Atrial fibrillation is the most common type of cardiac arrhythmia. In a healthy heart, the sinoatrial node or SA node initiates all electrical impulses in the atria. In atrial fibrillation, electrical impulses are initiated randomly from many other sites called ectopic sites in and around the atria, commonly near the roots of pulmonary veins. These un-synchronized, chaotic electrical signals cause the atria to quiver or fibrillate rather than contract. Although the atrial rate during atrial fibrillation can be extremely high, most of the electrical impulses do not pass through the atrioventricular – the AV - node to the ventricles. This is due to refractory properties of the cells of the AV node. Those do come through are irregular. Ventricular rate or heart rate is therefore irregular and can range from slow - less than 60 - to rapid -more than 100 - beats per minute. On an ECG (EKG), atrial fibrillation is characterized by absence of P-waves and irregular narrow QRS complexes. Reminder: P-wave represents electrical activity of the SA node that is now obscured by activities of multiple ectopic sites. The baseline may appear undulating or totally flat depending on the number of ectopic sites in the atria. In general, larger number of ectopic sites results in flatter baseline. As the atria do not function properly, the heart puts out less blood, and heart failure may occur. The most common complication of atrial fibrillation, however, is the formation of blood clots in the atria. As the atria do not empty completely into the ventricles, the blood may stagnate inside the atria and blood clots may form. These clots may then pass into the bloodstream, get stuck in small arteries and block them. When a blood clot blocks an artery in the brain, a stroke may result.
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How Respiratory Pump Affects Venous Return, Animation.
 
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Thoracic pump (or effect of breathing) on the rate of venous return. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Venous return is the flow of blood from the periphery back to the heart’s right atrium. Blood from the upper body returns via the superior vena cava, blood from the lower body returns via the inferior vena cava. The rate of venous return is determined by two factors: the pressure gradient between venous pressure and right atrial pressure; and venous resistance. A decrease in right atrial pressure leads to an increase in venous return, and vice versa. Breathing is one of the mechanisms that facilitate venous return. This is known as thoracic pump, or respiratory pump. During inspiration, the diaphragm moves down, expanding the thoracic cavity, resulting in a decreased intra-thoracic pressure and a subsequent expansion of the lungs. Part of this change in pressure is transmitted across the walls of the heart, lowering right atrial pressure and thus facilitating venous return. Another aspect of the diaphragmatic descent is the concomitant increase in abdominal pressure. As the inferior vena cava passes through both abdominal and thoracic cavities, an increase in abdominal pressure together with a decrease in thoracic pressure squeeze the blood upward - toward the heart. On the other hand, left ventricular stroke volume is decreased during inspiration. This is because the expansion of the lungs causes pulmonary blood volume to increase and the blood flow from the lungs to the left atrium to decrease. During expiration, the diaphragm moves up, the pressure in the thoracic cavity reverses. Venous return decreases. Pulmonary blood vessels shrink pumping more blood through the pulmonary veins into the left atrium. Stroke volume increases as a result. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Autonomic Nervous System: Sympathetic vs Parasympathetic, Animation
 
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Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia The divisions of the ANS: Sympathetic, SNS, versus parasympathetic, PSNS. This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology ©Alila Medical Media. All rights reserved. Voice by: Ashley Fleming All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. The autonomic nervous system, or ANS, is the part of the nervous system that regulates activities of internal organs. The ANS is largely AUTONOMOUS, acting independently of the body’s consciousness and voluntary control. It has two main divisions: sympathetic, SNS, and parasympathetic, PSNS. In situations that require alertness and energy, such as facing danger or doing physical activities, the ANS activates its sympathetic division to mobilize the body for action. This division INcreases cardiac output, accelerates respiratory rate, releases stored energy, and dilates pupils. At the same time, it also inhibits body processes that are less important in emergencies, such as digestion and urination. On the other hand, during ordinary situations, the parasympathetic division conserves and restores. It slows heartbeats, decreases respiratory rate, stimulates digestion, removes waste and stores energy. The sympathetic division is therefore known as the “fight or flight” response, while the parasympathetic division is associated with the “rest and digest” state. Despite having opposite effects on the same organ, the SNS and PSNS are NOT mutually exclusive. In most organs, both systems are simultaneously active, producing a background rate of activity called the “autonomic tone” - a balance between sympathetic and parasympathetic inputs. This balance SHIFTS, one way or the other, in response to the body’s changing needs. Some organs, however, receive inputs from ONLY ONE system. For example, the smooth muscles of blood vessels only receive sympathetic fibers, which keep them partially constricted and thus maintaining normal blood pressure. An increase in sympathetic firing rate causes further constriction and INcreases blood pressure, while a DEcrease in firing rate dilates blood vessels, lowering blood pressure. The autonomic nerve pathways, from the control centers in the central nervous system to the target organs, are composed of 2 neurons, which meet and synapse in an autonomic ganglion. Accordingly, these neurons are called PREganglionic and POSTganglionic. In the SNS, the preganglionic neurons arise from the thoracic and lumbar regions of the spinal cord; their fibers exit by way of spinal nerves to the nearby sympathetic chain of ganglia. Once in the chain, preganglionic fibers may follow any of 3 routes: some fibers synapse immediately with postganglionic neurons; some travel up or down the chain before synapsing; some pass through the chain without synapsing - this third group continues as splanchnic nerves to nearby collateral ganglia for synapsing instead. From the ganglia, LONG POSTganglionic fibers run all the way to target organs. The SNS has a high degree of neuronal DIVERGENCE: one preganglionic fiber can synapse with up to 20 postganglionic neurons. Thus, effects of the SNS tend to be WIDESPREAD. In the PSNS, the preganglionic neurons arise from the brainstem and sacral region of the spinal cord. Preganglionic fibers exit the brainstem via several cranial nerves and exit the spinal cord via spinal nerves before forming the pelvic splanchnic nerves. Parasympathetic ganglia are located near or within target organs, so postganglionic fibers are relatively short. The degree of neuronal divergence in the PSNS is much lower than that of the SNS. Thus, the PSNS produces more SPECIFIC, LOCALIZED responses compared to the SNS.
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Laser Trabeculoplasty for Glaucoma: ALT vs SLT, Animation.
 
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This video and other ophthalmology images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/ophthalmology-optometry ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Trabeculoplasty is a laser treatment for primary open-angle glaucoma. The laser is used to treat the trabecular meshwork, through which the aqueous humor drains. In this procedure: - The eye is numbed with eye drops. - A special laser lens is placed on the eye to help control the direction of the laser beams. - The laser burns a small area in the trabecular meshwork, opening up the drainage canal. - About 50 spots over 180 degrees of the meshwork circle are treated in one therapy. The original laser trabeculoplasty procedure applies argon laser of 514-nm (nano meter) wavelength on half of the meshwork circle in one treatment. Although a second treatment can be performed on the other half of the circle, the procedure is generally not repeatable as it causes extensive scarring of the trabecular meshwork. The newer technique -- Selective Laser Trabeculoplasty or SLT -- uses a solid-state laser of 532-nm wavelength. The pulse energy of SLT is about 100 times lower than the traditional argon laser trabeculoplasty. SLT selectively targets pigmented cells while leaving the rest of the trabecular meshwork tissue intact. For this reason, it can be applied to 360 degrees of the meshwork in one treatment and is considered safe to be repeated. In term of efficiency, the two techniques return similar results in lowering intraocular pressure. Laser trabeculoplasty treatment is effective in about 75% of patients. The effect may take a few weeks to kick in and can last for several years.
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Hyperkalemia: Causes, Effects on the Heart, Pathophysiology, Treatment, Animation.
 
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How serum potassium levels affect resting membrane potential and cardiac action potential; ECG (EKG) changes in hyperkalemia. How hyperkalemia causes bradycardia. Electrolytes disorders This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Hyperkalemia refers to abnormally high levels of potassium in the blood. The ratio of INTRAcellular to EXTRAcellular potassium is important for generation of action potentials and is essential for normal functions of neurons, skeletal muscles and cardiac muscles. This is why potassium levels in the blood are strictly regulated within a narrow range between 3.5 and 5mmol/L. As the normal daily dietary intake of potassium varies widely and can be as much as 100mmol a day, the body must keep blood potassium levels within the normal limits. This is achieved by 2 mechanisms: - Excretion of potassium through the kidneys and intestines - Shifting of potassium from the extracellular fluid into the cells by the sodium/potassium pump. The pump is mainly regulated by hormones such as insulin and catecholamines. Hyperkalemia is defined as a serum potassium concentration HIGHER than 5mmol/L. Hyperkalemia may result from decreased excretion, excessive intake, or shift of potassium from INSIDE the cells to EXTRA-cellular space. The most common scenario is a RENAL INsufficiency combined with excessive potassium supplements OR administration of certain drugs. Impaired kidney function is most prominent Mild hyperkalemia is often without symptoms, some patients may develop muscle weakness. Slow or chronic increase in potassium levels is less dangerous, as the kidneys eventually adapt by excreting more potassium. Sudden onset and rapid progression of hyperkalemia can be fatal. Primary cause of mortality is the effect of potassium on cardiac functions. As potassium levels INcrease in the EXTRAcellular space, the MAGNITUDE of potassium gradient across the cell membrane is REDUCED, and so is the ABSOLUTE value of the resting membrane potential. Membrane voltage becomes less negative, moving closer to the threshold potential, making it EASIER to initiate an action potential. The effect this has on excitability of myocytes, however, is complex. While initial changes seem to increase myocyte excitability; further rise of potassium has the OPPOSITE effect. This is because the value of membrane potential at the onset of an action potential DETERMINES the number of voltage-gated sodium channels activated during depolarization. As this value becomes less negative in hyperkalemia, the number of available sodium channels DEcreases, resulting in a SLOWER influx of sodium and subsequently SLOWER impulse conduction. ECG changes produced by hyperkalemia follow a typical pattern that correlates with serum potassium levels: peaked T-wave, P wave widens and flattens, PR interval lengthens, QRS complex widens and eventually blends with T-wave. Diagnosis on the basis of ECG alone very difficult. Acute hyperkalemia must be suspected in any patient having new bradycardia or conduction block, especially in those with renal problems. Severe hyperkalemia is treated in 3 steps: - Calcium infusion is given to rapidly REVERSE conduction abnormalities. - Insulin to stimulate the sodium/potassium pump, promoting INTRA-cellular shift - Hemodialysis to remove potassium
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Congestive Heart Failure: Left-sided vs Right-sided, Systolic vs Diastolic, Animation.
 
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This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Heart failures can be due to an inability to PUMP effectively during systole - SYSTOLIC heart failure, or inability to FILL properly during diastole - DIASTOLIC heart failure. Heart failure can be right-sided or left-sided . In systolic heart failure, ventricular contraction is compromised. This may be caused by any condition that weakens the heart muscle: - Coronary artery disease/Ischemic HD: - Dilated cardiomyopathy - Hypertension: - Valvular heart disease: Damage to the valves, such as stenosis The effectiveness of ventricular contraction is measured by the EJECTION fraction. The normal range of the ejection fraction is between 50 and 70%. In systolic heart failure, it drops below 40%. In DIASTOLIC heart failure, the ventricle is filled with LESS blood. This may be because it is smaller than usual, or it has lost the ability to relax. The ejection fraction may be normal, but the blood output is reduced. The ejection fraction is therefore commonly used to differentiate between SYSTOLIC and DIASTOLIC dysfunction. Examples of conditions that can lead to diastolic heart failure include: - Hypertrophic cardiomyopathy - Restrictive cardiomyopathy: - Hypertension Regardless of being systolic or diastolic in nature, left-sided heart failures share a common outcome: LESS blood pumped out from the heart. As a result, blood flows back to the lungs, where it came from, causing CONGESTION and INCREASED pulmonary pressure. As this happens, fluid leaks from the blood vessels into the lung tissue, resulting in PULMONARY EDEMA, a hallmark of left-sided heart failure. Accumulation of fluid in the alveoli IMPEDES the gas exchange process, resulting in respiratory symptoms such as shortness of breath, which worsens when lying down, and chest crackles. RIGHT-sided heart failure is most commonly caused by LEFT-sided heart failure. This is because the INCREASED pulmonary pressure caused by left-sided heart failure makes it harder for the right ventricle to pump INTO the pulmonary artery. This results in SYSTOLIC dysfunction. In compensation, the right ventricle grows thicker to pump harder, which reduces the space available for filling, eventually leading to DIASTOLIC dysfunction. Other common causes of right-sided heart failure include chronic lung diseases which also raise pulmonary blood pressure. As the right ventricle pumps out less blood, the blood, again, backs up to where it came from, and in this case, the SYSTEMIC circulation. This results in abnormal fluid accumulation in various organs, most notable in the feet when standing, sacral area when lying down, abdominal cavity and liver. The fluid status can be assessed by examining the distension level of the jugular vein. Heart failure is usually managed by treating the underlying condition, together with a combination of drugs. ACE inhibitors, beta blockers are used to reduce blood pressure in patients with systolic dysfunction. Diuretics are used to reduce water retention.
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Bankart Lesion and Repair Surgery Animation
 
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Arthroscopic surgery for repair of bankart lesions. This video and other orthopaedic animations (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/bones-joints-and-muscles-videos ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Dislocated shoulder causes labral tear and detachment. Sometimes an injury can cause the humeral head (top of the arm bone) to come out of glenoid (the socket). Most shoulder dislocations are anterior dislocations meaning the humeral head comes forward as it leaves the socket. The labrum is a rim of cartilage that attaches around the edge of the glenoid and contributes to the stability of the shoulder joint. Sometimes the humeral head tears part of the labrum as it dislocates. This is known as a Bankart lesion. The Bankart lesion can result in the shoulder joint becoming unstable and requiring surgery. A Bankart repair involves reattachment and tightening of the torn labrum. The torn edges of the labrum are removed to reveal fresh labrum. Small holes are drilled in the glenoid to receive a special fixation device called an anchor. Attached to the anchor are sutures which are used to pull the labrum back on to the glenoid. This process is repeated until the labrum is completely reattached to the glenoid. After the procedure the arm is placed in a sling for a few weeks. Physical therapy will be required to regain shoulder motion and strength.
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Diabetic Ketoacidosis (DKA) Pathophysiology, Animation
 
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Diabetic ketoacidosis (one of the hyperglycemic crises), DKA, pathophysiology, causes, clinical presentation (signs and symptoms) and treatment. This video and similar images/videos are available for instant download licensing here https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/endocrinology Voice by: Penelope Hammet ©Alila Medical Media. All rights reserved. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Diabetic ketoacidosis, DKA, is an ACUTE and potentially life-threatening complication of diabetes mellitus. DKA is commonly associated with type 1 but type 2 diabetics are also susceptible. DKA is caused by a critically LOW INSULIN level and is usually triggered when diabetic patients undergo further STRESS, such as infections, inadequate insulin administration, or cardiovascular diseases. It may also occur as the FIRST presentation of diabetes in people who did NOT know they had diabetes and therefore did NOT have insulin treatment. Glucose is the MAJOR energy source of the body. It comes from digestion of carbohydrates and is carried by the bloodstream to various organs. Insulin is a hormone produced by beta-cells of the pancreas and is responsible for DRIVING glucose INTO cells. When insulin is DEFICIENT, glucose can NOT enter the cells; it stays in the blood, causing HIGH blood sugar levels while the cells are STARVED. In response to this metabolic starvation, the body INcreases the levels of counter-regulatory hormones. These hormones have 2 major effects that are responsible for clinical presentation of DKA: - First, they produce MORE glucose in an attempt to supply energy to the cells. This is done by breaking down glycogen into glucose, and synthesizing glucose from NON-carbohydrate substrates such as proteins and lipids. However, as the cells CANNOT use glucose, this response ONLY results in MORE sugar in the blood. As blood sugar level EXCEEDS the ability of the kidneys to reabsorb, it overflows into urine, taking water and electrolytes along with it in a process known as OSMOTIC DIURESIS. This results in large volumes of urine, dehydration and excessive thirst. - Second, they activate lipolysis and fatty acid metabolism for ALTERNATIVE fuel. In the liver, metabolism of fatty acids as an alternative energy source produces KETONE bodies. One of these is acetone, a volatile substance that gives DKA patient’s breath a characteristic SWEET smell. Ketone bodies, unlike fatty acids, can cross the blood-brain barrier and therefore can serve as fuel for the brain during glucose starvation. They are, however, ACIDIC, and when produced in LARGE amounts, overwhelm the buffering capacity of blood plasma, resulting in metabolic ACIDOSIS. As the body tries to reduce blood acidity by EXHALING MORE carbon dioxide, a deep and labored breathing, known as Kussmaul breathing may result. Another compensation mechanism for high acidity MOVES hydrogen ions INTO cells in exchange for potassium. This leads to INcreased potassium levels in the blood; but as potassium is constantly excreted in urine during osmotic diuresis, the overall potassium level in the body is eventually depleted. A blood test MAY indicate too much potassium, or hyperkalemia, but once INSULIN treatment starts, potassium moves BACK into cells and hypokalemia may result instead. For this reason, blood potassium level is monitored throughout treatment and potassium replacement is usually required together with intravenous fluid and insulin as primary treatment for DKA.
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ECG Interpretation Basics continued - ST Segment Changes, Animation.
 
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How to read EKG strips. Recognize ST segment elevation and depression. This video (updated with real voice) and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. The ST segment extends from the end of the S wave to the start of the T wave. A normal ST segment is mostly flat and level with the baseline. Elevation of more than two small squares in the chest leads or one small square in the limb leads, indicates the possibility of myocardial infarction. The infarction may be localized based on the leads with ST elevation. There is usually a reciprocal ST depression in the electrically opposite leads. For example, ST elevation in leads I and aVL typically produces ST depression in lead III. Pericarditis causes a characteristic “saddleback” ST segment elevation and PR segment depression in all leads except aVR and V1, where the reverse - ST depression and PR elevation – are seen. ST depression is diagnostic of ischemia. ST depression may be of various morphology and may be seen in a variable number of leads, and therefore cannot be used to localize the lesion.
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Myocardial Infarction and Coronary Angioplasty Treatment, Animation.
 
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Anatomy of Heart Attacks. This video and related animations are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/heart-and-blood-circulation-videos. ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Myocardial infarction, commonly referred to as heart attack, is the sudden death of part of the heart muscle due to loss of blood flow. This occurs when one of the coronary arteries -- the arteries that supply blood to the heart -- is blocked. The blockage is commonly due to atherosclerosis - cholesterol plaques/fat deposits on the wall of blood vessels. As the plaque builds up, the vessel becomes narrow restricting blood flow. Under stress, the plaque may rupture. This triggers formation of blood clot on top of the plaque leading to complete blockage of blood flow. When this happens in a coronary artery, the downstream patch of the myocardium dies from lack of oxygen. Weaken heart muscle may disrupt electrical activity of the heart and subsequently cause cardiac arrest. Coronary angioplasty is a non-surgical procedure used to open narrowed or blocked coronary arteries. It can also be performed as an emergency treatment for myocardial infarction. The first part of the procedure is to localize the site of blockage. This part is called cardiac catheterization. A guiding catheter is inserted through the femoral artery at the groin and threaded all the way to the aorta. The tip of the catheter is placed at the beginning of the coronary artery to be investigated. A radio-opaque dye is injected through the catheter into the coronary artery. This enables real-time visualization of the artery using X-ray imaging. A narrowed part of an artery would appear as a bottle neck on an x-ray image. After the location of narrowed artery is identified, angioplasty can begin. A guidewire with a deflated balloon is inserted and pushed to the location of blockage. The balloon is inflated to crush the plaque. At the end of procedure, the balloon is again deflated and removed together with all catheters and guidewire. In some cases, a stent is inserted together with the balloon, inflated and left on place of the plaque to keep the artery open permanently.
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Neuroscience Basics: Neuroglia Functions, Animation.
 
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Functions of major glia (glial cells) in the brain: oligodendrocytes, microglia, and astrocytes (the other cells of the brain). This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology Voice by: Sue Stern ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia A human brain contains billions of neurons. Neurons are probably the more important and better-known cells of the brain as they carry out the brain’s communication function. Less known are some trillions of support cells called glia, or glial cells. The glia may not be the center of attention, but without them, neuron functions would be impossible. The major types of glial cells in the brain include: oligodendrocytes, microglia, and astrocytes. Oligodendrocytes are specialized cells with long processes that wrap around axons of neurons to form the myelin sheath. The myelin sheath acts like an electrical insulator around a wire. It helps to speed up the electrical signals that travel down an axon. Without oligodendrocytes, an action potential would propagate 30 times slower! Microglia are special macrophages found only in the central nervous system. They wander through the brain tissue, phagocytizing dead, injured cells and foreign invaders. High concentrations of microglia are an indication of infection, trauma or stroke. Astrocytes are the most abundant and functionally diverse glia. These star-shaped glial cells provide supportive frameworks to hold neurons in place. They provide neurons with nutrients such as lactate. They also produce growth factors that promote neuron growth and synapse formation. It’s been suggested that astrocytes can control how a neuron is built by directing where to make synapses or dendrites. Through their processes, known as perivascular feet, astrocytes induce endothelial cells of blood vessels to form tight junctions. These tight junctions are the basis of the blood brain barrier that restricts the passage of certain substances from the bloodstream to the brain tissue. Astrocytes help to maintain the chemical composition of the extracellular fluid. They express membrane transporters for several neurotransmitters such as glutamate, ATP and GABA, and help to remove them from synaptic spaces. Astrocytes also absorb potassium ions released by neurons at synapses. This helps to regulate potassium concentrations in the extracellular space. Abnormal accumulation of extracellular potassium is known to cause epileptic neuronal activity. Recently, it has been shown that astrocytes can also communicate electrically with neurons and modify the signals they send and receive. In a manner similar to neurons, astrocytes can release transmitters, called gliotransmitters, upon stimulation. This suggests that astrocytes maybe involved DIRECTLY in the communication functions of the brain. From the clinical viewpoint, neurons have little capacity for renewal and therefore rarely form tumors. On the contrary, glial cells are capable of dividing throughout life and are the primary source of brain tumors. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Sciatica:  signs and symptoms, causes, treatment, animation
 
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Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Pathology of sciatica. This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/pain-management-images-and-videos ©Alila Medical Media. All rights reserved. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Sciatica or sciatic neuralgia is a common condition in which one of the spinal nerve roots of the sciatic nerve is compressed resulting in lower back, b. and leg pain. Sciatic nerve is a large nerve derived from 5 spinal nerve roots: L4, L5, S1, S2 and S3. It runs from the lumbar spine through the b. down the leg and the foot on the posterior aspect. There is one sciatic nerve on each side of the body. Typically, only one side of the body is affected. A typical sciatica pain is described as a sharp shooting pain in the lower back, down the b., thigh and leg on one side of the body. There may also be numbness, burning and tingling sensations. The pain can get worse with sitting, moving, sneezing, or coughing. The patterns of pain depend on which nerve root is compressed, and follow the dermatome distribution. The most common cause of sciatica is a herniated spinal disc. The spinal disc is a soft elastic cushion that sits in between the vertebrae of the spine. With age, the discs become rigid and may crack; the gel-like center of the disc may protrude out and become a herniation outside the normal boundaries of the disc. Disc herniation presses on the nerve root as it exits the spine. In majority of the cases the condition resolves by itself after a few weeks of rest and conservative treatment. Pain relief, nonsteroidal anti-inflammatory drugs and muscle relaxants may be prescribed. Stretching exercises and physical therapy may be recommended. Surgery may be needed if the pain doesn’t go away after 3 months or more of conservative treatments. The herniated disc may be removed in a procedure called discectomy. Or, in another procedure called laminotomy, part of the bone of the vertebrae may be cut to make room for the nerve.
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Physiology of Pain, Animation.
 
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Pain pathways: Spinothalamic and Spinoreticular pathway, Visceral and Referred pain. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology ©Alila Medical Media. All rights reserved. Voice by: Ashley Fleming All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Basically, noxious signals send impulses to the spinal cord, which relays the information to the brain. The brain interprets the information as pain, localizes it, and sends back instructions for the body to react. Pain sensation is mediated by pain receptors, or nociceptors, which are present in the skin, superficial tissues and virtually all organs, except for the brain. These receptors are essentially the nerve endings of so-called “first-order neurons” in the pain pathway. The axons of these neurons can be myelinated, A type, or, unmyelinated, C type. Myelinated A fibers conduct at FAST speeds and are responsible for the initial SHARP pain perceived at the time of injury. Unmyelinated C fibers conduct at SLOWER speeds and are responsible for a longer-lasting, dull, diffusing pain. First-order neurons travel by way of spinal nerves to the spinal cord, where they synapse with second-order neurons in the dorsal horn. These second-order neurons cross over to the OTHER side of the cord, before ascending to the brain. This is how information of pain on the left side of the body is transmitted to the right side of the brain, and vice versa. There are two major pathways that carry pain signals from the spinal cord to the brain: - The spinothalamic tract: second-order neurons travel up within the spinothalamic tract to the thalamus where they synapse with third-order neurons; third-order neurons then project to their designated locations in the somatosensory cortex. This pathway is involved in LOCALIZATION of pain. - The spinoreticular tract: second-order neurons ascend to the reticular formation of the brainstem, before running up to the thalamus, hypothalamus, and the cortex. This tract is responsible for the EMOTIONAL aspect of pain. Pain signals from the face follow a DIFFERENT route to the thalamus. First-order neurons travel mainly via the trigeminal nerve to the brainstem, where they synapse with second-order neurons, which ascend to the thalamus. Pain from the skin, muscles and joints is called SOMATIC pain, while pain from INTERNAL organs is known as VISCERAL pain. Visceral pain is often perceived at a DIFFERENT location in a phenomenon known as REFERRED pain. For example, pain from a heart attack may be felt in the left shoulder, arm or back, rather than in the chest, where the heart is located. This happens because of the CONVERGENCE of pain pathways at the spinal cord level.
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Hypokalemia: Causes, Symptoms, Effects on the Heart, Pathophysiology, Animation.
 
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How hypokalemia causes tachycardia; how it affects resting membrane potential. Electrolytes disorders. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. The ratio of INTRAcellular to EXTRAcellular potassium is important for generation of action potentials and is essential for normal functions of neurons, skeletal muscles and cardiac muscles. This is why potassium levels in the blood are strictly regulated within a narrow range between 3.5 and 5mmol/L. As the normal daily dietary intake of potassium varies widely and can be as much as 100mmol a day, the body must keep blood potassium levels within the normal limits. This is achieved by 2 mechanisms: - Excretion of potassium through the kidneys and intestines - Shifting of potassium from the extracellular fluid into the cells by the sodium/potassium pump. The pump is mainly regulated by hormones such as insulin and catecholamines. Hypokalemia is defined as a serum potassium concentration LOWER than 3.5 mmol/L. Hypokalemia may result from INCREASED excretion, INadequate intake or shift of potassium from the extracellular fluid into the cells. Most commonly, hypokalemia is caused by excessive loss of potassium in the urine, from the GI tract, or skin. The cause is usually apparent by the patient’s history of predisposing diseases or medication. Urine potassium levels are measured to differentiate between RENAL and NON-renal causes. Symptoms may include muscle weakness, cramping, tremor, intestinal obstruction, hypotension, respiratory depression and abnormal heart rhythms. As potassium levels DEcrease in the EXTRAcellular space, the MAGNITUDE of the potassium gradient across the cell membrane is INCREASED, causing hyperpolarization. This moves the membrane voltage FURTHER from the threshold, and a GREATER than normal stimulus is required to generate an action potential. The result is a REDUCED excitability or responsiveness of the neurons and muscles. In the heart, however, HYPER-excitability is observed. This is because HYPER-polarization ENHANCES the “FUNNY” currents in cardiac pacemaker cells, resulting in a FASTER phase 4 depolarization and thus a FASTER heart rate. The effect is greatest in Purkinje fibers as these are more sensitive to potassium levels, as compared to the SA node. Increased automaticity of Purkinje fibers may lead to the development of one or more ECTOPIC pacemaker sites in the ventricles, causing ventricular premature beats, tachycardia and fibrillation. Reduced extracellular potassium also inhibits the activity of some potassium channels, and thus DELAYS ventricular repolarization. As hypokalemia becomes more severe, especially in patients with other heart conditions, the inward current may exceed the OUTward current, resulting in early afterdepolarization and consequently extra heartbeats. Prolonged repolarization may also promote re-entrant arrhythmias. Early ECG changes in hypokalemia are mainly due to delayed ventricular repolarization. These include flattening or inversion of T wave, increasingly prominent U wave, ST-segment depression, and prolonged QU interval. Hypokalemia-induced arrhythmias require immediate potassium replacement. Oral administration is safer but may not be effective in severe cases. If potassium infusion is indicated, continuous cardiac monitoring and hourly serum potassium determinations must be performed to avoid HYPERkalemia complications.
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Mitral Valve Prolapse and Regurgitation, Animation
 
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Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Mitral (bicuspid) valve diseases: pathology, complications, diagnosis and treatment. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. The mitral valve serves to ensure ONE-WAY blood flow from the left atrium to the left ventricle of the heart. It OPENS during diastole when the left atrial pressure is higher than the left ventricular pressure, allowing blood to fill the left ventricle; and CLOSES during systole, when the pressure gradient is reversed, to prevent blood from flowing BACK to the atrium as the ventricles contract. The mitral valve has 2 flaps, known as anterior and posterior mitral leaflets, which are supported by a fibrous ring, called mitral annulus. During ventricular contraction, the leaflets are kept from opening in the wrong direction by the action of papillary muscles which attach to the leaflets via cord-like tendons called chordae tendineae, or tendinous chords. The most common of all heart valve diseases is mitral valve prolapse, or MVP. In MVP, the mitral leaflets bulge into the left atrium every time the ventricles contract. In many people, the reason why this happens is unclear. In others, it is linked to connective tissue disorders such as Ehlers-Danlos or Marfan syndrome. Connective tissue problems are believed to weaken the leaflets, INcrease leaflet area and cause elongation of the chordae tendineae. In most people, MVP is Asymptomatic and does not require treatment. However, it does increase the risks of developing other heart diseases such as arrhythmias, endocarditis, and most frequently, mitral valve regurgitation. In fact, mitral valve prolapse is the most common cause of mitral regurgitation. The billowing leaflets may not fit together properly; elongated chords may also rupture, resulting in a LEAKY valve, which permits BACKflow of the blood to the left atrium when the ventricles contract. When the volume of regurgitated blood is significant, the left side of the heart experiences volume OVERLOAD and eventually fails; blood is backed up to the lungs, causing pulmonary congestion, a hallmark of left-sided heart failure. Mitral valve prolapse and regurgitation produce characteristic ABNORMAL heart sounds, such as clicks and murmurs, which can be heard during auscultation. Diagnosis is usually confirmed by echocardiography, a procedure in which heart valves and blood flows can be visualized LIVE using ultrasound. A leaky valve requires surgical repair or replacement. In a typical valve repair surgery, the floppy portion of the valve is removed and the remaining parts are REconnected. The procedure may also include tightening or replacing the mitral annulus, known as annuloplasty. Valve replacement is considered when repair is not possible. Artificial valves can be mechanical or bio-prosthetic. Mechanical valves last longer but usually require life-long administration of anticoagulant medications to prevent formation of blood clots.
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Thyroid Gland, Hormones and Thyroid Problems, Animation
 
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Regulation of thyroid hormone, hyper- and hypothyroidism: causes, symptoms and treatment, goiter. This video and similar images/videos are available for instant download licensing here https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/endocrinology Voice by: Sue Stern ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. The thyroid is a butterfly-shaped ENDOCRINE gland located in the neck. It is wrapped around the trachea, just below the thyroid cartilage –the Adam’s apple. The two major hormones of the thyroid are triiodothyronine, T3 and thyroxine, T4. The numbers 3 and 4 indicate the number of iodine atoms present in a molecule of each hormone. T3 and T4 are collectively referred to as THYROID hormones. Thyroid hormone secretion is under control of thyroid-stimulating hormone, TSH, from the anterior pituitary. TSH, in turn, is induced by thyrotropin-releasing hormone, TRH, produced by the hypothalamus. The amount of circulating thyroid hormones is regulated by a negative feedback loop: when their levels are too high, they SUPPRESS the production of TSH and TRH, consequently INHIBITING their own production. Thyroid hormones act to INCREASE the body’s metabolic rate. They stimulate appetite, digestion, breakdown of nutrients and absorption. They also increase oxygen consumption, raise the breathing rate, heart rate and contraction strength. As a result, the body’s HEAT production is INCREASED. Thyroid hormone secretion usually rises in winter months to keep the body warm. Thyroid hormones are also important for bone growth and fetal brain development. There are 2 major groups of thyroid problems: HYPOthyroidism: when the thyroid does NOT produce ENOUGH hormones, resulting in a LOW metabolic rate, combined with SLOW respiratory and cardiovascular activities. Common symptoms include fatigue, weight gain despite poor appetite, cold intolerance, slow heart rate, heavy menstrual bleeding and constipation. Iodine deficiency and Hashimoto's thyroiditis are the most common causes. Hashimoto's thyroiditis is an autoimmune disease in which the thyroid gland is gradually destroyed by the body’s own immune system. Hypothyroidism, especially when caused by iodine deficiency, may lead to swelling of the thyroid gland, known as GOITER. In an attempt to fix the low levels of thyroid hormones, the pituitary produces MORE TSH to further stimulate the thyroid gland. The thyroid, while UNable to make hormones WITHOUT iodine, responds to TSH by GROWING in size. Hypothyroidism is managed with thyroxine hormone replacement. HYPERthyroidism: when the thyroid gland produces TOO MUCH hormones, resulting in a TOO ACTIVE metabolism, together with respiratory and cardiovascular rates that are HIGHER than necessary. Common symptoms include irritability, insomnia, weight loss despite good appetite, heat intolerance, heart racing and diarrhea. Hyperthyroidism is most commonly caused by Graves' disease, another autoimmune disorder characterized by presence of an antibody, called thyroid stimulating immunoglobulin, TSI. TSI, similar to TSH, stimulates the thyroid gland to produce hormones. Unlike TSH, however, TSI is NOT regulated by negative feedback mechanisms, leading to UNcontrolled production of thyroid hormones. TSI also stimulates the thyroid gland to grow, which MAY lead to formation of a goiter. Hyperthyroidism may be managed with drugs that suppress thyroid function, radioactive iodine that selectively destroys the thyroid gland, or surgery that removes part of the gland.
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Neuroscience Basics: Human Brain Anatomy and Lateralization of Brain Function, 3D Animation.
 
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Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology ©Alila Medical Media. All rights reserved. The human brain is divided into three major parts : - The cerebrum (SER-eh-brum) – the largest part of the human brain. The cerebrum enables sensory perception and controls voluntary motor actions. - The cerebellum (SER-eh-BEL-um) – the cerebellum lies inferior to the cerebrum at the back of the head. It is mostly involved in coordination of movement and fine tuning of motor activities. - The brainstem - the brainstem is located at the base of the brain and is continuous to the spinal cord. It houses all nerve connections between different parts of the central nervous system. The brainstem provides innervation to the head and neck via cranial nerves. It also contains nuclei associated with important body functions such as regulation of blood pressure, respiration, swallowing, bladder control, sleep cycle, … among others. On top of the brainstem, and sometimes classified as part of it, is the diencephalon. The main components of the diencephalon are: - The thalamus – the thalamus serves as a gateway relaying sensory signals originated throughout the body to the cerebral cortex. It is also involved in emotional and memory functions. - The hypothalamus – the hypothalamus is the major control center of the autonomic nervous system and plays essential role in homeostatic regulation. The hypothalamus links the nervous system to the endocrine system via the pituitary gland. It also contains nuclei involved in regulation of body temperature, food and water intake, sleep and wake cycle, memory and emotional behavior. The cerebrum consists of two cerebral hemispheres. The left hemisphere controls the right half of the body. The right hemisphere controls the left half of the body. The two hemispheres are separated by a deep groove called the longitudinal fissure. Each hemisphere has a number of folds called gyri (JY-rye) separated by grooves called sulci (SUL-sye). A major landmark is the central sulcus. The cerebrum has four major lobes. The frontal lobe is situated anterior to the central sulcus. It is associated mainly with voluntary motor functions, planning, motivation, emotion and social judgment. Posterior to the central sulcus is the parietal lobe. This lobe is mainly concerned with sensory functions of the somatosensory category such as touch, stretch, movement, temperature and pain. The temporal lobe is separated from the frontal and parietal lobes by the lateral sulcus. The temporal lobe is associated with hearing, learning, visual memory and language. The occipital lobe is located at the rear of the cerebrum. This is the visual processing center of the brain. At first glance, the two hemispheres look identical, but research has found a number of differences between them. This is called lateralization of brain function. For example, the language formation areas - the Wernicke’s (WUR-ni-keez) and Broca’s areas - are usually located in the left hemisphere of right-handed people. Lesions to these areas result in language comprehension deficits or speech disorders. The corresponding areas in the right hemisphere are responsible for emotional aspect of language. Lesions to these areas do not affect speech comprehension and formation, but result in emotionless speech and inability to understand the emotion behind the speech such as sarcasm or a joke. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Baroreflex Regulation of Blood Pressure, Animation.
 
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How heart rate is controlled by the parasympathetic and sympathetic divisions of the autonomic nervous system, with overview of baroreceptor resetting. This video (updated with real voice) and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Baroreflex, or baroreceptor reflex, is one of the mechanisms the body uses to maintain stable blood pressure levels or homeostasis. Baroreflex is a rapid negative feedback loop in which an elevated blood pressure causes heart rate and blood pressure to decrease. Reversely, a decrease in blood pressure leads to an increased heart rate, returning blood pressure to normal levels. The reflex starts with specialized neurons called baroreceptors. These are stretch receptors located in the wall of the aortic arch and carotid sinus. Increased blood pressure stretches the wall of the aorta and carotid arteries causing baroreceptors to fire action potentials at a higher than normal rate. These increased activities are sent via the vagus and glossopharyngeal nerves to the nucleus of the tractus solitarius – the NTS - in the brainstem. In response to increased baroreceptor impulses, the NTS activates the parasympathetic system – the PSNS - and inhibits the sympathetic system – the SNS. As the PSNS and SNS have opposing effects on blood pressures, PSNS activation and SNS inhibition work together in the same direction to maximize blood pressure reduction. Parasympathetic stimulation decreases heart rate by releasing acetylcholine which acts on the pacemaker cells of the SA node. Inhibition of the sympathetic division decreases heart rate, stroke volume and at the same time causes vasodilation of blood vessels. Together, these events rapidly bring DOWN blood pressure levels back to normal. When a person has a sudden drop in blood pressure, for example when standing up, the decreased blood pressure is sensed by baroreceptors as a decrease in tension. Baroreceptors fire at a lower than normal rate and the information is again transmitted to the NTS. The NTS reacts by inhibiting parasympathetic and activating sympathetic activities. The sympathetic system releases norepinephrine which acts on the SA node to increase heart rate; on cardiac myocytes to increase stroke volume and on smooth muscle cells of blood vessels to cause vasoconstriction. Together, these events rapidly bring UP blood pressure levels back to normal. Baroreflex is a short-term response to sudden changes of blood pressure resulted from everyday activities and emotional states. If hypertension or hypotension persists for a long period of time, the baroreceptors will reset to the “new normal” levels. In hypertensive patients for example, baroreflex mechanism is adjusted to a higher “normal” pressure and therefore MAINTAINS hypertension rather than suppresses it. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Antiarrhythmic Drugs, Animation
 
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Support us on Patreon and get FREE downloads and other great rewards: https://www.patreon.com/AlilaMedicalMedia/posts The 5 classes of agents according to Vaughan Williams classification, mechanism of action. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. ANTI-Arrhythmic agents are drugs used to SUPPRESS abnormal rhythms of the heart. They act to either: - interfere with the dynamics of cardiac action potentials by blocking a certain ion channel, or - block the sympathetic effects of the autonomic nervous system on the heart, to slow down heart rate. There are 5 classes of antiarrhythmic drugs: - Class I: Sodium-channel blockers: these drugs bind to and block the fast sodium channels that are responsible for the DE-polarizing phase in contractile myocytes. The result is a SLOWER depolarization with a smaller amplitude. This REDUCED conduction velocity helps to SUPPRESS formation of re-entrant circuits, hence the use of these drugs for treating re-entrant tachycardias. Class I agents are divided further into subclass IA, IB and IC. These subclasses differ in the STRENGTH of sodium channel blockage, and in their effect on the duration of action potentials and the effective refractory period, the ERP. While subclass IC has no effect on ERP, IA prolongs and IB shortens ERP, respectively. Changes in ERP may have different outcomes for different types of arrhythmias. A longer ERP generally reduces cardiac excitability, but prolonged repolarizations may increase the risk of torsades de pointes, a type of tachycardia caused by afterdepolarizations. - Class II: Beta-blockers: these drugs bind to beta1-adrenergic receptors and block the sympathetic influences that act through these receptors. Sympathetic nerves release catecholamines which act to increase SA node firing rate and cardiac conductibility, especially at the AV node. Useful in treatment of tachycardias that originate upstream of the AV node, known as supraventricular tachycardias, or SVT. - Class III: Potassium-channel blockers: these agents block the potassium channels responsible for the repolarizing phase. The result is a SLOWED repolarization, hence a PROLONGED duration of action potentials and refractory period. This reduces the heart’s excitability and suppresses re-entrant tachycardias. However, these drugs may also CAUSE arrhythmias because slow repolarizations are associated with LONGER QT intervals and INcreased risks of torsades de pointes. - Class IV: Calcium-channel blockers: these drugs block calcium channels that are responsible for DE-polarization in SA and AV nodal cells. Blocking these channels results in a LOWER sinus rate and SLOWER conduction through the AV node. However, because calcium is also involved in cardiac myocyte contraction, these agents also reduce contractility of the heart and should not be used in case of systolic heart failures. - Class V includes all drugs that act by other or unknown mechanisms.
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Mechanism of Drug Addiction in the Brain, Animation.
 
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This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Addiction is a neurological disorder that affects the reward system in the brain. In a healthy person, the reward system reinforces important behaviors that are essential for survival such as eating, drinking, sex, and social interaction. For example, the reward system ensures that you reach for food when you are hungry, because you know that after eating you will feel good. In other words, it makes the activity of eating pleasurable and memorable, so you would want to do it again and again whenever you feel hungry. Drugs of abuse hijack this system, turning the person’s natural needs into drug needs. The brain consists of billions of neurons, or nerve cells, which communicate via chemical messages, or neurotransmitters. When a neuron is sufficiently stimulated, an electrical impulse called an action potential is generated and travels down the axon to the nerve terminal. Here, it triggers the release of a neurotransmitter into the synaptic cleft - a space between neurons. The neurotransmitter then binds to a receptor on a neighboring neuron, generating a signal in it, thereby transmitting the information to that neuron. The major reward pathways involve transmission of the neurotransmitter dopamine from the ventral tegmental area – the VTA - of the midbrain to the limbic system and the frontal cortex. Engaging in enjoyable activities generates action potentials in dopamine-producing neurons of the VTA. This causes dopamine release from the neurons into the synaptic space. Dopamine then binds to and stimulates dopamine-receptor on the receiving neuron. This stimulation by dopamine is believed to produce the pleasurable feelings or rewarding effect. Dopamine molecules are then removed from the synaptic space and transported back in to the transmitting neuron by a special protein called dopamine-transporter. Most drugs of abuse increase the level of dopamine in the reward pathway. Some drugs such as alcohol, heroin, and nicotine indirectly excite the dopamine-producing neurons in the VTA so that they generate more action potentials. Cocaine acts at the nerve terminal. It binds to dopamine-transporter and blocks the re-uptake of dopamine. Methamphetamine – a psychostimulant – acts similarly to cocaine in blocking dopamine removal. In addition, it can enter the neuron, into the dopamine-containing vesicles where it triggers dopamine release even in the absence of action potentials. Different drugs act different way but the common outcome is that dopamine builds-up in the synapse to a much greater amount than normal. This causes a continuous stimulation, maybe over-stimulation of receiving neurons and is responsible for prolonged and intense euphoria experienced by drug users. Repeated exposure to dopamine surges caused by drugs eventually de-sensitizes the reward system. The system is no longer responsive to everyday stimuli; the only thing that is rewarding is the drug. That is how drugs change the person’s life priority. After some time, even the drug loses its ability to reward and higher doses are required to achieve the rewarding effect. This ultimately leads to drug overdose.
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LASIK or PRK? Which is right for me? Animation.
 
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This video and related videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/eyes-and-vision-videos Voice by: Sue Stern. ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia Perfect for patient education purposes. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. LASIK, or "laser-assisted in situ keratomileusis," is the most commonly performed laser eye surgery to treat myopia, hyperopia and astigmatism. The goal of the treatment is to reshape the cornea to correct the refractive error of the eye. The cornea is the transparent dome-shaped structure in front of the eye. The cornea refracts light and accounts for about two-thirds of the eye's total optical power. Altering the curvature of the cornea changes the way light rays enter the eye. As a result, the light rays can be focused properly onto the retina for clearer vision. For nearsighted people, the laser is used to flatten the cornea. For farsighted people, the cornea is made steeper. For patients with astigmatism, the laser is used to smooth the irregularly-shaped cornea into a more regular shape. The outer layer of the cornea - the epithelium – is capable of replacing itself within a few days after being damaged or removed. The deeper layer of the cornea – the stroma, on the contrary, is a permanent corneal tissue with very limited regenerative capacity. The stroma, if reshaped by a laser, will remain that way permanently. In this procedure, a thin, circular "FLAP" is created in the surface of the cornea to gain access to the permanent corneal tissue. This can be done with a mechanical cutting tool called a microkeratome, OR, for a blade-free experience, by a femtosecond laser. An excimer laser is then used to remove some corneal tissue to reshape the cornea. Excimer laser uses cool ultraviolet light beams to vaporize microscopic amounts of tissue in a precise manner to accurately reshape the cornea. The excimer laser is computer-controlled and is programmed based on the patient’s refractive error. The flap is then laid back in place and is allowed to heal. LASIK eye surgery is mostly painless and can be completed within minutes. Improved vision can usually be seen overnight. PRK, or photorefractive keratectomy, was the first type of laser eye surgery for vision correction and is the predecessor to the popular LASIK procedure. In PRK, NO flap is created. Rather, the epithelial cells on the eye surface are simply removed. An excimer laser is then used to reshape the cornea just like it does in LASIK. The vision correction outcomes of PRK surgery are comparable to those of LASIK, but the recovery period is longer. This is because the epithelium is completely removed in PRK and it takes a few days to regenerate. PRK patients also have more discomfort and haziness of vision in the first few days after the surgery. Improved vision also takes longer to achieve. PRK does, however, offer certain advantages. Because PRK does not involve creation of a flap, which contains both epithelial and deeper stromal tissue, the entire thickness of the stroma is available for treatment. The treatment range is therefore higher. This is particularly useful for patients with high levels of myopia or for those whose cornea is too thin for LASIK. PRK is also free of flap-related complication risks.
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Atrioventricular Block (AV block) - Types of Heart Block Part 2, Animation.
 
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This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. There are three degrees of AV block: First-degree AV block: the electrical signals are SLOWED as they pass from the SA node to the AV node, but all of them eventually reach the ventricle. On an ECG, this is characterized by a longer PR interval of more than 5 small squares. First-degree AV blocks rarely cause symptoms or problems and generally do NOT require treatment. Second-degree AV blocks are divided further into type I and type II: - In type I, the electrical signals are delayed further and further with each heartbeat until a beat is missing completely. On an ECG, this is seen as PROGRESSIVE prolongation of PR interval followed by a P wave WITHOUT a QRS complex. This is known as a “blocked” P wave or a “dropped” QRS complex. The cycle then re-starts over. As this usually repeats in regular cycles, there is a fixed ratio between the number of P waves and the number of QRS complexes per cycle. The number of QRS complexes always equals the number of P waves MINUS one. In this example, there are four P waves for every three QRS complexes. This is a “4 to 3” heart block. Second-degree type I blocks are usually mild and no specific treatment is indicated. - In type II second degree blocks, some of the electrical signals do NOT reach the ventricles. On an ECG, this is seen as intermittent non-conducted P-waves. The PR interval, however, remains CONSTANT in conducted beats. In majority of cases, the successfully conducted QRS complexes may appear broader than usual. In some type II blocks, there is a fixed number of P waves per QRS complex. In this example, there are three P waves for every QRS complex and the condition is described as “3 to 1” heart block. However, as the nature of type II block is unstable, this ratio is likely to change over time. Second- degree type II is less common than second-degree type I but is much more dangerous as it frequently progresses to complete heart block or cardiac arrest. Implantation of an artificial pacemaker is recommended for treatment of this type of AV blocks. Third-degree AV blocks are also referred to as complete heart blocks. In this condition, NONE of the electrical signals from the atria reach the ventricles. With NO input coming from the atria, the ventricles usually try to generate some impulses on their own. This is known as an “ESCAPE rhythm”. On an ECG, two independent rhythms can be seen: a regular P wave pattern represents atrial rhythm; and a regular, but UNUSUALLY slow QRS pattern represents the escape rhythm. The PR interval is variable as there is NO relationship between the 2 rhythms. Patients with third-degree heart blocks are at high risk of cardiac arrest. They require immediate treatment, cardiac monitoring and pacemaker implantation.
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Neuroscience Basics: GABA and Glutamate, Animation
 
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Basics of inhibitory and excitatory networks of the brain. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology Voice by: Sue Stern ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia The brain is a complex network of billions of neurons. Neurons can be excitatory or inhibitory. Excitatory neurons stimulate others to respond and transmit electrical messages, while inhibitory neurons SUPPRESS responsiveness, preventing excessive firing. Responsiveness or excitability of a neuron is determined by the value of electrical voltage across its membrane. Basically, a neuron is MORE responsive when it has more POSITIVE charges inside; and is LESS responsive when it becomes more NEGATIVE. GABA is a major INHIBITORY neurotransmitter. Upon binding, it triggers GABA receptors, ligand-gated chloride channels, to open and allow chloride ions to flow into the neuron, making it more NEGATIVE and LESS likely to respond to new stimuli. Glutamate receptors, another type of ion channel, upon binding by glutamate, open to allow POSITIVELY-charged ions into the cell, making it more POSITIVE and MORE likely to generate electrical signals. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
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Effects of Alcohol on the Brain, Animation, Professional version.
 
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Depressant effect of alcohol: action on GABA and Glutamate synapses and how this leads to over-drinking, addiction, withdrawal syndrome and relapse. This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/neurology ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Alcohol, or more specifically, ethanol, affects brain functions in several ways. Alcohol is generally known as a DEPRESSANT of the central nervous system; it INHIBITS brain activities, causing a range of physiological effects. The pleasurable feeling associated with drinking, on the other hand, is linked to alcohol-induced dopamine release in the brain’s reward pathway. Alcohol also increases levels of brain serotonin, a neurotransmitter implicated in mood regulation. Neurons can be excitatory or inhibitory. Responsiveness or excitability of a neuron is determined by the value of electrical voltage across its membrane. A balance between excitation and inhibition is essential for normal brain functions. Short-term alcohol consumption DISRUPTS this balance, INCREASING INHIBITORY and DECREASING EXCITATORY functions. Specifically, alcohol inhibits responsiveness of neurons via its interaction with the GABA system. GABA is a major INHIBITORY neurotransmitter. Upon binding, it triggers GABA receptors, ligand-gated chloride channels, to open and allow chloride ions to flow into the neuron, making it more NEGATIVE and LESS likely to respond to new stimuli. Alcohol is known to POTENTIATE GABA receptors, keeping the channels open for a longer time and thus exaggerating this inhibitory effect. GABA receptors are also the target of certain anesthetic drugs. This explains the SEDATIVE effect of alcohol. At the same time, alcohol also inhibits the glutamate system, a major excitatory circuit of the brain. Glutamate receptors, another type of ion channel, upon binding by glutamate, open to allow POSITIVELY-charged ions into the cell, making it more POSITIVE and MORE likely to generate electrical signals. Alcohol binding REDUCES channel permeability, LOWERING cation influx, thereby INHIBITING neuron responsiveness. GABA ACTIVATION and glutamate INHIBITION together bring DOWN brain activities. Depending on the concentration of ethanol in the blood, alcohol’s depressant effect can range from slight drowsiness to blackout, or even respiratory failure and death. Chronic, or long-term consumption of alcohol, however, produces an OPPOSITE effect on the brain. This is because SUSTAINED inhibition caused by PROLONGED alcohol exposure eventually ACTIVATES the brain’s ADAPTATION response. In attempts to restore the equilibrium, the brain DECREASES GABA inhibitory and INCREASES glutamate excitatory functions to compensate for the alcohol’s effect. As the balance tilts toward EXCITATION, more and more alcohol is needed to achieve the same inhibitory effect. This leads to overdrinking and eventually addiction. If alcohol consumption is ABRUPTLY reduced or discontinued at this point, an ill-feeling known as WITHDRAWAL syndrome may follow. This is because the brain is now HYPER-excitable if NOT balanced by the inhibitory effect of alcohol. Alcohol withdrawal syndrome is characterized by tremors, seizures, hallucinations, agitation and confusion. Excess calcium produced by overactive glutamate receptors during withdrawal is toxic and may cause brain damage. Withdrawal-related anxiety also contributes to alcohol-seeking behavior and CONTINUED alcohol abuse.
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Corrective Jaw (Orthognathic) Surgery, Animation.
 
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This video and variations (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/dentistry Voice by: Sue Stern ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Corrective jaw surgery, or orthognathic surgery, is a group of procedures performed to correct dentofacial irregularities, most commonly manifested as misalignments of the jaws. These deformities not only cause malocclusion or bad bite, but also create problems in the temporomandibular joint - the TMJ- and the airway, resulting in difficulties chewing, swallowing, speaking and breathing. While the surgery is performed to correct functional problems, patient's appearance may be dramatically improved as a result. Open bite is a condition where the upper and lower front teeth do not touch when the mouth is closed or at rest. An open bite can lead to a number of oral health conditions including tooth wear, tooth breakage and TMJ disorders. It may also cause speech problems known as ‘lisping’ in some individuals. Open bite surgery involves removing some of the bone of the upper jaw to move it to a new position. Once the jaws are aligned, plates and screws are used to secure the bones in place. Protruding lower jaw is corrected in a procedure called mandibular setback surgery. The tooth-bearing portion of the lower jaw is separated from its base and moved backward for proper alignment. In a similar way, receding lower jaw, or “weak chin”, is corrected with mandibular ADVANCEMENT surgery. In this case, the tooth-bearing portion of the lower jaw is repositioned FORWARD. Orthognathic surgeries are commonly performed in combination with orthodontic treatments and may take several years to complete.
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Acid Base Balance, Animation.
 
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Acid base regulation basics, pulmonary regulation and renal handling of acid-base balance. This video and other related images/videos (in HD) are available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/urology ©Alila Medical Media. All rights reserved. Voice by Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: https://www.patreon.com/AlilaMedicalMedia/posts All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. pH is an indicator of acidity. The body’s blood pH is strictly regulated within a narrow range between 7.35 and 7.45. This is because even a minor change in acidity may have devastating effects on protein stability and biochemical processes. Normal cellular metabolism constantly produces and excretes carbon dioxide into the blood. Carbon dioxide combines with water to make carbonic acid which dissociates into hydrogen ions and bicarbonate. This equilibrium is central to understand acid-base regulation. CONTINUED carbon dioxide production by all cells of the body drives the equilibrium to the right to generate more hydrogen ions. Because pH is basically a function of hydrogen ion concentration, more hydrogen means higher acidity and lower pH. Normal metabolism, therefore, constantly makes the blood more acidic. The body must react to keep the blood pH within the normal limits. This is achieved by 2 mechanisms: - Elimination of carbon dioxide through exhalation. The amount of carbon dioxide exhaled by the lungs is regulated in response to changes in acidity. A decrease in pH is sensed by central or arterial chemoreceptors and leads to deeper, faster breathing; more carbon dioxide is exhaled, less hydrogen is made, blood acidity decreases and blood pH returns to normal. Pulmonary regulation is fast, usually effective within minutes to hours. - Excretion of hydrogen ions and reabsorption of bicarbonate through the kidneys. The kidneys control blood pH by adjusting the amount of excreted acids and reabsorbed bicarbonate. Renal regulation is slower; it usually takes days to respond to pH disturbances. Pathologic changes may cause acid-base disturbances. Acidosis refers to a process that causes increased acidity, while alkalosis refers to one that causes increased alkalinity. It’s not uncommon for a patient to have several processes going on at once, some of them in opposite directions. The resulting plasma pH may be normal; too acidic, called acidemia; or too basic, called alkalemia. Acidosis may result from inadequate function of the lungs which causes arterial carbon dioxide to accumulate. This is RESPIRATORY acidosis. On the other hand, METABOLIC acidosis may result from excessive production of metabolic acids, decreased ability of the kidneys to excrete acids, ingestion of acids, or loss of alkali. Metabolic acidosis is characterized by primary decrease in plasma bicarbonate.
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Heart Blocks, Anatomy and ECG Reading, Animation.
 
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This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Voice by: Sue Stern. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Heart block is a group of diseases characterized by presence of an obstruction, or a “BLOCK” in the heart electrical pathway. A block may slow down the conduction of electrical impulses, OR, in more severe cases, completely stop them. Heart blocks are classified by location where the blockage occurs. Accordingly, there are: SA nodal blocks, AV nodal blocks, intra-Hisian blocks, bundle branch blocks and fascicular blocks. Of these, AV nodal blocks, or AV blocks, are most clinically significant. In fact, very commonly, the term “heart block “, if not specified otherwise, is used to describe AV blocks. In AV blocks, the electrical signals are slow to reach the ventricles, or completely interrupted before reaching the ventricles. There are three degrees of AV block: First-degree AV block: the electrical signals are SLOWED as they pass from the SA node to the AV node, but all of them eventually reach the ventricle. On an ECG, this is characterized by a longer PR interval of more than 5 small squares. First-degree AV blocks rarely cause symptoms or problems and generally do NOT require treatment. Second-degree AV blocks are divided further into type I and type II: - In type I, the electrical signals are delayed further and further with each heartbeat until a beat is missing completely. On an ECG, this is seen as PROGRESSIVE prolongation of PR interval followed by a P wave WITHOUT a QRS complex. This is known as a “blocked” P wave or a “dropped” QRS complex. The cycle then re-starts over. As this usually repeats in regular cycles, there is a fixed ratio between the number of P waves and the number of QRS complexes per cycle. The number of QRS complexes always equals the number of P waves MINUS one. In this example, there are four P waves for every three QRS complexes. This is a “4 to 3” heart block. Second-degree type I blocks are usually mild and no specific treatment is indicated. - In type II second degree blocks, some of the electrical signals do NOT reach the ventricles. On an ECG, this is seen as intermittent non-conducted P-waves. The PR interval, however, remains CONSTANT in conducted beats. In majority of cases, the successfully conducted QRS complexes may appear broader than usual. In some type II blocks, there is a fixed number of P waves per QRS complex. In this example, there are three P waves for every QRS complex and the condition is described as “3 to 1” heart block. However, as the nature of type II block is unstable, this ratio is likely to change over time. Second- degree type II is less common than second-degree type I but is much more dangerous as it frequently progresses to complete heart block or cardiac arrest. Implantation of an artificial pacemaker is recommended for treatment of this type of AV blocks. Third-degree AV blocks are also referred to as complete heart blocks. In this condition, NONE of the electrical signals from the atria reach the ventricles. With NO input coming from the atria, the ventricles usually try to generate some impulses on their own. This is known as an “ESCAPE rhythm”. On an ECG, two independent rhythms can be seen: a regular P wave pattern represents atrial rhythm; and a regular, but UNUSUALLY slow QRS pattern represents the escape rhythm. The PR interval is variable as there is NO relationship between the 2 rhythms. Patients with third-degree heart blocks are at high risk of cardiac arrest. They require immediate treatment, cardiac monitoring and pacemaker implantation.
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QRS Transitional Zone (ECG), R Wave Progression Explained, Animation
 
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Transition of the QRS complex in the chest leads of the 12-lead EKG. Clinical significance. This video and other related images/videos (in HD) are available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/cardiology-and-vascular-diseases ©Alila Medical Media. All rights reserved. Support us on Patreon and get FREE downloads and other great rewards: patreon.com/AlilaMedicalMedia All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. The chest leads look at the heart in a horizontal plane. V1 represents the rightmost view, and V6 - the leftmost. The QRS complex represents depolarization of the ventricles which starts with the interventricular septum. In normal conduction, depolarization of the septum is initiated from the left bundle going to the right, TOWARD V1 and AWAY from V6. This results in a small positive deflection in V1 and a negative deflection in V6. The signals then move both directions to the two ventricles, but as the left ventricle is usually much larger, the NET movement is to the left, AWAY from V1, TOWARD V6. This corresponds to a negative wave in V1 and a positive wave in V6. Thus, the QRS complex starts as predominantly negative in V1, and ends as predominantly positive in V6. Somewhere in between, usually from V3 to V4, it is isoelectric, with equal positive and negative deflections. This is known as the transitional zone. In addition, there is a gradual increase in amplitude of R wave from V1 to V5. This is known as R wave progression. The normal transitional zone is between V3 and V4. When transition happens at or before V2, it is referred to as early transition, rightward shift, or counter-clockwise rotation. This is because these ECG patterns would have been generated if the heart had rotated counter-clockwise around the longitudinal axis. Reversely, when the transition occurs after V4, it is referred to as late transition, leftward shift, or clockwise rotation. These shifts may or may not be signs of heart diseases. In many cases, these are simply artefacts, resulting from incorrect placement of the chest electrodes - too low or too high. In other cases, they are due to normal anatomical variations of the heart’s shape and orientation. Clockwise rotation is more commonly associated with cardiovascular diseases while counter-clockwise rotation is more common in healthy individuals. Some clinical causes of clockwise rotation include: - Physical rotation of the heart in conditions such as chronic obstructive pulmonary disease - Conduction problems due to anterior myocardial infarction - Heart chambers dilatation (Dilated cardiomyopathy) Some clinical causes of counter-clockwise rotation include: - Conduction problems due to posterior myocardial infarction - Electrical shift to the right in conditions such as right ventricular hypertrophy When the transitional zone is absent, or is not clear, it is usually clinical. In this case it may be helpful to look at R wave progression. Non-progression or poor progression of R wave - R wave stays low and S wave remains deep throughout all chest leads. This is an extreme case of clockwise rotation and is suggestive of extensive anterior myocardial infarction. Reverse progression of R wave - tall R wave in V1, tallest in V1 or V2 - is usually seen in right ventricular hypertrophy. Increased muscle mass in the right ventricle results in net electrical movement towards the right chest leads.
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