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Cyanotic Congenital Heart Diseases
 
06:23
This is a brief video on five cyanotic congenital heart diseases. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Cyanotic Congenital Heart Defects Defects in which deoxygenated blood bypasses the lungs, mixes with oxygenated blood, and enters the systemic circulation (1) Truncus Arteriosus (2) Transposition of the Great Arteries (3) Tricuspid Atresia (4) Tetralogy of Fallot (5) Total Anomalous Pulmonary Venous Connection (1) Truncus Arteriosus (2) Transposition of the Great Arteries (3) Tricuspid Atresia (4) Tetralogy of Fallot (5) Total Anomalous Pulmonary Venous Connection Most patients have VSD Persistent Truncus Arteriosus Transposition of the Great Arteries (1) Truncus Arteriosus (2) Transposition of the Great Arteries (3) Tricuspid Atresia (4) Tetralogy of Fallot (5) Total Anomalous Pulmonary Venous Connection Requires at least one shunt (ASD, VSD, and/or PDA) Tricuspid Atresia (1) Truncus Arteriosus (2) Transposition of the Great Arteries (3) Tricuspid Atresia (4) Tetralogy of Fallot (5) Total Anomalous Pulmonary Venous Connection Must have ASD and VSD Tetralogy of Fallot (1) Truncus Arteriosus (2) Transposition of the Great Arteries (3) Tricuspid Atresia (4) Tetralogy of Fallot (5) Total Anomalous Pulmonary Venous Connection Total Anomalous Pulmonary Venous Connection (1) Truncus Arteriosus (2) Transposition of the Great Arteries (3) Tricuspid Atresia (4) Tetralogy of Fallot (5) Total Anomalous Pulmonary Venous Connection Associated with ASD and sometimes PDA
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Salivary Gland Neoplasms
 
03:11
This is a short video on the most common neoplasms (tumors and cancers) of the salivary glands. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Neoplasms of the salivary glands Pleomorphic adenoma Warthin's tumor Mucoepidermoid carcinoma Adenoid cystic carcinoma By Ed Uthman, MD - http://web2.airmail.net/uthman/specim..., Public Domain, https://commons.wikimedia.org/w/index... Pleomorphic adenoma Most common benign salivary gland tumor Usually in parotid gland Pleomorphic: variable appearance architecturally Parenchymatous glands with myoepithelium Stroma with epithelial tissue Diagnose with fine needle aspiration (best: 90% sensitivity), US, CT, or MRI Treat with surgical resection (parotidectomy), but it's a recurrent issue; can become carcinoma Pleomorphic adenoma Warthin's tumor Mucoepidermoid carcinoma Adenoid cystic carcinoma BOTTOM: By Schomynv - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index... LEFT: CC BY-SA 3.0, https://commons.wikimedia.org/w/index... Warthin’s tumor AKA papillary cystadenoma lymphomatosum Second most common benign salivary gland tumor Usually in parotid Histo: germinal centers, cystic spaces, many lymphocytes, condensed chromatin (pyknotic) nuclei Associated with smoking, older people Tumor is slow growing, often painless Pleomorphic adenoma Warthin's tumor Mucoepidermoid carcinoma Adenoid cystic carcinoma CC BY-SA 3.0, https://commons.wikimedia.org/w/index... Mucoepidermoid carcinoma Most common malignant salivary gland tumor Usually starts in parotid, can also be found outside of salivary gland Histo: contains mucinous cells and squamous cells Tumor is slow growing, often painless Associated with CMV Pleomorphic adenoma Warthin's tumor Mucoepidermoid carcinoma Adenoid cystic carcinoma By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index... By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index... Adenoid cystic carcinoma Second most common malignant salivary gland tumor Common tumor of the submandibular gland Can also involve other tissues Slow growing Can have distant metastases: eye, lung, brain, sinuses, trachea, breast Treatment is surgical resection, radiation Pleomorphic adenoma Warthin's tumor Mucoepidermoid carcinoma Adenoid cystic carcinoma TOP: By Jto410 - In my clinical work as a diagnostic radiologist, CC BY-SA 3.0, https://commons.wikimedia.org/w/index... BOTTOM: By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index...
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Drugs for Asthma Treatment
 
06:49
This is a short video on drugs used to treat the obstructive airway disease asthma. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Antigen/Irritant/Trigger INFLAMMATION -prolif/invasion of lymphocytes, eosinophils, macrophages, mast cells -mediators (IgE, IL5, leukotrienes) Reflex Parasympathetic Bronchospasm mucus secretion, vasodilation, collagen deposition, alveolar remodeling, hyperplasia, etc Sympathetic (β2-mediated) Bronchospasm Mediators DRUGS FOR ASTHMA Antigen/Irritant/Trigger Mediators INFLAMMATION -prolif/invasion of lymphocytes, eosinophils, macrophages, mast cells -mediators (IgE, IL5, leukotrienes) Sympathetic (β2-mediated) Bronchospasm Reflex Parasympathetic Bronchospasm mucus secretion, vasodilation, collagen deposition, alveolar remodeling, hyperplasia, etc β2-agonist (albuterol) long acting β2-agonist (salmeterol, formoterol) Muscarinic antagonist (ipratropium, tiotropium, umeclidinium) antibodies (omalizumab for IgE, mepolizumab for IL5) Inhaled Corticosteroids (ICS) PDE inhibitor (theophylline) Leukotriene blockers (zafirlukast, montelukast, zileuton) Antigen/Irritant/Trigger Mediators INFLAMMATION -prolif/invasion of lymphocytes, eosinophils, macrophages, mast cells -mediators (IgE, IL5, leukotrienes) Sympathetic (β2-mediated) Bronchospasm Reflex Parasympathetic Bronchospasm mucus secretion, vasodilation, collagen deposition, alveolar remodeling, hyperplasia, etc β2-agonist (albuterol) long acting β2-agonist (salmeterol, formoterol) Muscarinic antagonist (ipratropium, tiotropium, umeclidinium) antibodies (omalizumab for IgE, mepolizumab for IL5) Inhaled Corticosteroids (ICS) PDE inhibitor (theophylline) Leukotriene blockers (zafirlukast, montelukast, zileuton) Antigen/Irritant/Trigger Mediators INFLAMMATION -prolif/invasion of lymphocytes, eosinophils, macrophages, mast cells -mediators (IgE, IL5, leukotrienes) Sympathetic (β2-mediated) Bronchospasm Reflex Parasympathetic Bronchospasm mucus secretion, vasodilation, collagen deposition, alveolar remodeling, hyperplasia, etc β2-agonist (albuterol) long acting β2-agonist (salmeterol, formoterol) Muscarinic antagonist (ipratropium, tiotropium, umeclidinium) antibodies (omalizumab for IgE, mepolizumab for IL5) Inhaled Corticosteroids (ICS) PDE inhibitor (theophylline) Leukotriene blockers (zafirlukast, montelukast, zileuton) Antigen/Irritant/Trigger Mediators INFLAMMATION -prolif/invasion of lymphocytes, eosinophils, macrophages, mast cells -mediators (IgE, IL5, leukotrienes) Sympathetic (β2-mediated) Bronchospasm Reflex Parasympathetic Bronchospasm mucus secretion, vasodilation, collagen deposition, alveolar remodeling, hyperplasia, etc β2-agonist (albuterol) long acting β2-agonist (salmeterol, formoterol) Muscarinic antagonist (ipratropium, tiotropium, umeclidinium) antibodies (omalizumab for IgE, mepolizumab for IL5) Inhaled Corticosteroids (ICS) PDE inhibitor (theophylline) Leukotriene blockers (zafirlukast, montelukast, zileuton) short acting beta two agonist beta2 betatwo b2 btwo agonist short acting muscarinic cholinergic agonist
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Types of Laxatives
 
04:18
This is a brief video describing the four types of laxatives along with examples of each. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS Laxatives Bulk-forming agents Hyperosmotic agents Stool softeners Stimulant agents By Connormah Raster: en:User:User:Dflock - Based off File:Intestine.png, Public Domain, https://commons.wikimedia.org/w/index... Bulk-forming agents Work in the small and large intestines, where they resist enzymatic digestion Increase stool volume and bacterial mass Absorbs water Fiber Plant-based foods Polycarbophil Methylcellulose Psyllium By Scott Bauer - USDA Image Number K5267-7, Public Domain, https://commons.wikimedia.org/w/index... Hyperosmotic agents Work in the colon; retain water in the lumen in colon by creating osmotic pressure Saline: MgCitrate; NaPO4 Sugars: lactulose, PEG, sorbitol Alcohol: glycerin By Shattonbury - Shattonbury, Public Domain, https://commons.wikimedia.org/w/index... Bulk-forming agents Hyperosmotic agents Stool softeners Allow water and fats to be added to stool, softens, making passage through small/large intestines tract easier Examples Docusate Lowers surface tension of stool Mineral oil Minimally digested By Angela Mabray - originally posted to Flickr as Mineral Oil, Front, CC BY-SA 2.0, https://commons.wikimedia.org/w/index... Bulk-forming agents Hyperosmotic agents Stool softeners Stimulant agents Stimulant agents Stimulate peristaltic action Act on intestinal mucosa and/or nerve plexus Exact MoA unclear Examples Senna glycoside Bisacodyl BISACODYL By MarinaVladivostok - Own work, CC0, https://commons.wikimedia.org/w/index... Bulk-forming agents Hyperosmotic agents Stool softeners Stimulant agents
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Neurotransmitters of the human body
 
11:07
This is a overview of some common neurotransmitters found in the human body. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Neurotransmitters An introduction to chemicals that transmit information across the body, their functions, and their receptors Acetylcholine Serotonin Dopamine Norepinephrine Glutamate GABA Glycine Amino acids Monoamines Catecholamines Acetylcholine (ACh) Acetylcholine Serotonin Dopamine Norepinephrine Glutamate GABA Glycine Found in: Motor neurons Brain: basal ganglia and nucleus basalis of Meynert Autonomic nervous system (ANS) Sympathetic (ganglion neurotransmitter) Parasympathetic (both ganglion and final product) Used in treatment of: Alzheimer’s disease Dementia Receptors: Ionotropic → nicotinic receptors, excitatory Metabotropic → muscarinic receptors, excitatory or inhibitory Serotonin (5-HT) Acetylcholine Serotonin Dopamine Norepinephrine Glutamate GABA Glycine Found in: Brain and brainstem Pineal gland Raphe nuclei in the pons Limbic function (emotions/mood, hunger, sex, instincts, temperature) sleep Used in treatment of: Depression Sleep regulation Receptors: Ionotropic → 5-HT3 receptor, excitatory Metabotropic → 5-HT1-7 receptors, excitatory or inhibitory Dopamine Acetylcholine Serotonin Dopamine Norepinephrine Glutamate GABA Glycine Found in: Brain and brainstem Substantia nigra (reward, addiction, movement) Hypothalamus (inhibits prolactin release) Used in treatment of: Schizophrenia, psychosis Parkinson’s disease Receptors: Ionotropic → none Metabotropic D1 → excitatory (K+/Ca2+) D2 → inhibitory (K+/Ca2+) Norepinephrine Acetylcholine Serotonin Dopamine Norepinephrine Glutamate GABA Glycine Found in: Brain: Locus ceruleus, projecting to cortex, for arousal, attention, and anxiety ANS: sympathetic neurons (final product, postganglionic neurons) Used in treatment of: ADHD Anxiety Cardiac failure Receptors: Ionotropic → none Metabotropic α1 and β1 are excitatory α2 and β2 are inhibitory Glutamate Acetylcholine Serotonin Dopamine Norepinephrine Glutamate GABA Glycine Found everywhere in CNS: Excites the cerebral cortex, spinal cord, brainstem, hippocampus, cerebellum Used in treatment of: Amyotrophic lateral sclerosis (ALS), Lou Gehrig's disease Excites motor, sensory, and cognitive neurons Receptors (all excitatory): Ionotropic NMDA receptor AMPA receptor Kainate receptor Metabotropic gamma-Aminobutyric acid Acetylcholine Serotonin Dopamine Norepinephrine Glutamate GABA Glycine Found everywhere in CNS: Inhibits the cerebral cortex, spinal cord, brainstem, hippocampus, cerebellum, basal ganglia Predominately found in interneurons Used in treatment of: Anxiety and rehab for drug abuse Inhibits motor, sensory, and cognitive neurons → sedation, muscular/cardiorespiratory relaxation, inhibits pain/reflexes Receptors (all inhibitory): Ionotropic GABAA receptor → Cl- channel (ligand-gated) Metabotropic GABAB receptor → decrease cAMP and increase K channels Glycine Acetylcholine Serotonin Dopamine Norepinephrine Glutamate GABA Glycine Found in the spinal cord: Inhibits spinal cord interneurons Used in treatment of: Spasticity Receptors (all inhibitory): Ionotropic Cl- channel
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Mental status exam
 
13:53
This is a brief video on the mental status exam in psychiatry. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Appearance: “general appearance of a patient, including apparent age, height, weight, and manner of dress and grooming.” Eg, disheveled, proper/poor hygiene, appears (older/younger than) staged age Behavior: “observations of specific abnormal movements, as well as more general observations of the patient's level of activity and arousal, and observations of the patient's eye contact and gait.” Eg, (un)cooperative with exam, proper/poor eye contact, proper/poor engagement, repetitive movements (perhaps indicating OCD) Motor: psychiatric disturbances manifesting in changes/deficiencies in motor function Eg, psychomotor agitation, psychomotor retarded, tremors, restlessness (perhaps indicating parkinsonism) Speech: “concerned with the production [rather than content] of speech” Eg, speed, rate, volume, pressured, fluent/understandable versus impoverished speech, tone, delay/latency Mood: description of patient's internal emotional state in their own words (report in quotes) Eg, happy, sad, OK, good, great, depressed Affect: description of patient’s “apparent emotion conveyed by the person's nonverbal behavior (anxious, sad etc.), and also by using the parameters of appropriateness, intensity, range, reactivity and mobility” Eg, neutral, euthymic, dysphoric, euphoric, angry, anxious, apathetic, irritable, guarded, inappropriate (out of context) Eg of range: flat (nothing elicits reactivity) → blunted → restricted / constricted (mild/moderate depression) → full / normal → labile / expansive (pt apparently not in control of emotions) Congruence with reported mood Thought process: description of “quantity, tempo (rate of flow) and form (or logical coherence) of thought” Eg, linear, logical, goal-directed, disorganized, flight of ideas (thoughts so rapid → incoherent), tangential, circumferential Tangential - thought process that goes off on a tangent and never returns to the matter at hand Circumferential - thought process that goes off with extraneous details but does circle back to the matter at hand Thought content: description of “a patient's delusions, overvalued ideas, obsessions, phobias, and preoccupations” Eg, comments endorsing or denying suicidal ideations, homicidal ideations, and paranoid ideations; ideas of reference; any fixations or preoccupations Perceptual disturbances: description of disruption in one’s organization, identification, or interpretation of sensory information Eg, auditory / visual hallucinations and illusions, whether or not patient responds to them; other internal stimuli Insight: understanding of his or her mental illness, evaluated by exploring his or her explanatory account of the problem and available treatment options Eg, good, fair, poor Judgement; patient's capacity to make sound, reasoned, and responsible decisions Eg, good, fair, poor; (un)cooperative with plan, forced by family to come, handling treatment well/poorly Memory: three words to remember for later Concentration: ability to concentrate assessed by serial 7s or spelling world backwards Orientation: to person (name, date of birth), place (state, town, current location/building/floor), time (season, year, month, date, day of the week)
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Cellular adaptations
 
12:00
See full presentation with speaker notes at: https://docs.google.com/presentation/d/1FZoUrbFwul2PXSzUQC087IKkpSbRdV1d_MbDFXdX234/edit?usp=sharing SCRIPT: Alright so today I’ll be talking about how organs and tissues respond to environmental changes. These changes occur at the cellular level, so we call them cellular adaptations. As you know, many of our organ systems are regulated to maintain homeostasis, and in this video, I’m going to discuss changes that result from excess stress or prolonged disuse. In the image we have in the middle here, we can see an organ, in this case, the bicep muscle in the arm. If the bicep muscle is constantly stressed, such as during strength training, the muscle can experience hypertrophy in which it increases in size to the larger bicep on the left. If muscles aren’t used for extended periods of time, which might be the case for the handicapped or bedridden patients, the muscles might undergo atrophy, which is a decrease in size to the muscle on the right. I’ll be discussing the mechanisms that can causes changes like the ones shown here. Let’s start with mechanisms in which tissues and thus organs are enlarged or become bigger. There are two ways this can happen. The first is hypertrophy, literally meaning over-nourishment, which is an increase in size of the cells making up a tissue or organ. You can see this left side of the diagram where the same four cells are increased in size during hypertrophy The second way an organ can become enlarged is through hyperplasia, which literally means over-formation of cells; so the cells are becoming more numerous. On the right side of this diagram you can see the cells multiplying as they go from four to twelve cells. There is an increase in the NUMBER of cells. Again, this is in contrast to the cells increasing in SIZE during hypertrophy on this side. One last thing to note is that oftentimes hypertrophy and hyperplasia occur together. So when an organ increases in size in the body, we are really seeing an increase in the size and number of cells. An example of hypertrophy and hyperplasia occurring together is in the growth of the uterus during pregnancy. Now in order to have hypertrophy, the cell volume needs to physically increase. In a normal animal cell, a protein structure known as a cytoskeleton is what holds up the cell membrane to maintain cell shape and rigidity. This is a microscope image of cells where the cytoskeleton components are stained red and green, and you can see how they kind of stretch out that plasma membrane and define the cell size and volume. So, to increase the cell size, this cytoskeleton needs to become bigger. Because the cytoskeleton is made of proteins, the process of hypertrophy requires increased protein production, which of course means the activation of more genes to synthesize those proteins. A larger cell also requires more organelles spread about the cell to produce ATP, remove wastes, synthesize molecules, and do everything that organelles do. This means that organelle production increases during hypertrophy as well. An example of pathologic hypertrophy is in the ventricles of the heart, as shown in this picture here. We see a substantial increase in the walls of the right ventricle in this heart right here. This occurs when the heart struggles to pump blood to the body during heart failure, or when a person has chronic hypertension. Hypertrophy in the walls of a hollow organ or chamber is called eccentric hypertrophy, and the word “eccentric” here means “away from the center.” The walls surrounding the chamber -- in this case, the right ventricle -- are enlarged because of the increased stress on the right ventricle. The right ventricle pumps blood to the pulmonary circulation, so a patient with this condition might have pulmonary hypertension or COPD. Hyperplasia, or the increase in cell number, is a bit simpler to explain. Hyperplasia is essentially increased cell proliferation or mitosis, and the cells are usually dividing and differentiating themselves from a set of stem cells. Normal (or physiologic) hyperplasia occurs in the body and is often triggered by hormones, cytokines, or other signaling molecules. One example of normal hyperplasia is the proliferation of the milk ducts in response to increased estrogen during pregnancy. Estrogen and progesterone also trigger the milk-producing alveolar epithelium for breastfeeding. Pathological hyperplasia includes benign prostate hyperplasia or BPH, more commonly known as prostate enlargement, which cases urinary issues in men. And of course, cancer metastasis are a form of hyperplasia, and this moving image here is a proliferation of skin cancer cells from mice. ... SEE REST OF SCRIPT AT ABOVE LINK I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor.
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Chemotherapeutic agents
 
16:29
This is a brief overview of chemotherapeutic agents, their mechanism of action, and some related side effects. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Chemotherapeutic agents Classes of chemical agents used in the treatment of cancer Alkylating agents Antimetabolites Microtubule targeting agents Topoisomerase inhibitors Anthracyclines Monoclonal antibodies Other agents Alkylating agents Attach alkyl groups to DNA, allows cross linking of base pairs, damaging DNA; cell cycle nonspecific Typical alkylating agents: cyclophosphamide, ifosfamide, melphalan, busulfan, mechlorethamine, chlorambucil, thiotepa Side effects: myelosuppression drop in WBC, Hb, crit, nausea/vomiting, secondary malignancies, infertility/impaired fertility, hemorrhagic cystitis hematuria, dysuria from direct irritation of bladder by acrolein metabolite Atypical alkylating agents Platinum compounds covalently bind purine DNA bases. Drugs and side effects: cisplatin causes nephrotoxicity and n/v carboplatin causes thrombocytopenia oxaliplatin causes cold sensitivity all cause peripheral neuropathies, paresthesia Nitrosoureas: BCNu, CCNu both cause pulmonary toxicity, phlebitis. CNS Alkylating agents Antimetabolites Microtubule targeting agents Topoisomerase inhibitors Anthracyclines Monoclonal antibodies Other agents Antimetabolites Inhibit DNA replication or repair by mimicking normal cell compounds; S phase specific Folate inhibitor: Methotrexate inhibits DHFR, prevents regeneration of THF Adjuvant leucovorin to protect healthy cells adjuvant Side effect is mucositis, myelosuppression Pyrimidine inhibitors 5-fluorouracil inhibits thymidylate synthetase Bolus dose causes myelosuppression Continuous dose causes GI problems mucositis, diarrhea Synergistic leucovorin potentate mechanism of action synergistic Capecitabine is essentially an oral prodrug for 5-FU Side effect: hand-foot syndrome - palms and hands and feet become red, can start blistering Cytarabine AraC is a DNA chain terminator Side effects: conjunctivitis and cerebellar neural defects The 7 in 7+3 chemotherapy Purine analog is 6-mercaptopurine Alkylating agents Antimetabolites Microtubule targeting agents Topoisomerase inhibitors Anthracyclines Monoclonal antibodies Other agents Microtubule targeting agents These drugs inhibit mitosis, specifically M phase Vinca alkaloids destroy microtubules, obviously preventing their function Vincristine, vinblastine, and vinorelbine Side effects: peripheral neuropathy, myelosuppressive blast others Fatal if given intrathecally Taxanes stabilize microtubules, preventing their function Paclitaxol, docetaxol Side effects: myelosuppression, peripheral neuropathies Hypersensitivity from diluent: Cremophor diluent in paclitaxel Tween80 in docetaxel Avoid hypersenitivity with abraxane, protein-bound paclitaxol particles less sensitivity but more neuropathy Topoisomerase inhibitors Topoisomerase I inhibitors prevent relaxation of supercoiled DNA Topotecan, irinotecan Both have side effect of myelosuppression Irinotecan causes diarrhea: “I ran to the can” Topoisomerase II inhibitors prevent recoiling of DNA after transcription Etoposide, teniposide Both have side effects of myelosuppression, mucositis, secondary malignancies AML Etoposide also causes hypotension Anthracyclines Various mechanisms of action: intercalate DNA, inhibit topo II, generate ROS, perhaps alkylation -rubicins: doxorubicin, daunorubicin, idarubicin, epirubicin Side effects: biventricular heart failure, necrotic with extravasation The 3 in 7+3 chemotherapy Monoclonal antibodies Origin determined from suffixes: -omab from mouse; -ximab is chimeric cross between human/mouse; -umab is humanized; -mumab is fully human mAb Target Treats: Toxicity Rituximab CD20 lymphoma - Trastuzumab Her-2 breast cancer - Cetuximab EGFR solid tumors initially for colorectal cancer Acneiform rash Bevacizumab VEGF solid tumors initially for colorectal/lung cancers GI perforation, Other chemotherapeutic agents Bleomycin causes lung toxicity Side effects: pulmonary fibrosis, interstitial pneumonitis, hypersensitivity pneumonitis cough, infiltrates Hormonal therapies Antiestrogens block estrogen stimulation of breast cancer Tamoxifen, fulvestrant, megestrol acetate Aromatase inhibitors block synthesis of estrogen Anastrozole, letrozole Antiandrogens block androgen stimulation of prostate cancer Other targets for prostate cancer are LHRH agonists prevent testosterone production, GnRH antagonist, CYP17 inhibitor
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Pharyngeal arches and their derivatives
 
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This is a brief summary of the pharyngeal arches present during human embryonic development and their skeletal, muscular, and arterial derivatives. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS Pharyngeal Arches Arch 1 Arch 2 Arch 3 Arch 4 Arch 6 Pharyngeal arches, their skeletal, muscular, and arterial derivatives Arch 1 - “mandibular arch” Innervated by V3 of the trigeminal nerve (CN5) Skeletal derivatives are in two subdivisions: Maxillary process (upper jaw) Maxilla, zygomatic bone, squamous part of temporal bone Maxillary processes fuse with medial nasal process to form upper lip and jaw. Abnormalities here causes Cleft lip - anterior to incisive foramen Cleft palate - posterior to incisive foramen Mandibular process (lower jaw) derived from Meckel cartilage Mandible, sphenomandibular ligament, incus, malleus Mandibular process fuses in midline to form lower jaw Muscle derivatives Muscles of mastication (temporalis, masseter, medial/lateral pterygoid), mylohyoid, anterior belly of digastric, tensor veli palatini, tensor tympani Aortic arch 1 becomes part of the maxillary artery Arch 1 Arch 2 Arch 3 Arch 4 Arch 6 Bilateral complete lip and palate Unilateral complete lip and palate Incomplete cleft palate Arch 2 - “hyoid arch” Innervated by the facial nerve (CN7) Skeletal derivatives derived from Reichert cartilage Parts of hyoid bone (lesser horns and upper body), styloid process, stylohyoid ligament, stapes Muscle derivatives Muscles of facial expression, posterior belly of digastric, stylohyoid, stapedius Aortic arch from arch 2 becomes the stapedial artery By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See "Book" section below)Bartleby.com: Gray's Anatomy, Plate 979, Public Domain, https://commons.wikimedia.org/w/index... Arch 1 Arch 2 Arch 3 Arch 4 Arch 6 Bilateral complete lip and palate Unilateral complete lip and palate Incomplete cleft palate Arch 3 Innervated by the glossopharyngeal nerve (CN9) Skeletal derivative: body and greater horn of the hyoid bone Muscle derivative: the stylopharyngeus Aortic arch 3 becomes common carotid and part of internal carotid Arch 4 Innervated by the vagus nerve (CN10) Skeletal derivative: thyroid cartilage Muscle derivative: cricothyroid, pharyngeal constrictor, levator veli palatini Right aortic arch 4 becomes subclavian and left becomes arch of aorta Arch 6 Innervated by the vagus nerve (CN10) Skeletal derivative: cricoid, arytenoid, corniculate, & cuneiform cartilages Muscle derivative: all laryngeal muscles except cricothyroid Aortic arch 6 becomes pulmonary arteries Arch 1 Arch 2 Arch 3 Arch 4 Arch 6 Bilateral complete lip and palate Unilateral complete lip and palate Incomplete cleft palate Arch 1 Arch 2 Arch 3 Arch 4 Arch 6 arch alt name subdivision innervation derivatives skeletal muscular aortic 1 mandibular arch maxillary process V3 of trigeminal nerve (CN5) maxilla, zygomatic bone, squamous part of temporal bone muscles of mastication (temporalis, masseter, medial/lateral pterygoid), mylohyoid, anterior belly of digastric, tensor veli palatini, tensor tympani part of the maxillary artery mandibular process mandible, sphenomandibular ligament, incus, malleus 2 hyoid arch facial nerve (CN7) Parts of hyoid bone (lesser horns and upper body), styloid process, stylohyoid ligament, stapes muscles of facial expression, posterior belly of digastric, stylohyoid, stapedius stapedial artery 3 glossopharyngeal nerve (CN9) body and greater horn of the hyoid bone stylopharyngeus common carotid and part of internal carotid 4 vagus nerve (CN10) thyroid cartilage cricothyroid, pharyngeal constrictor, levator veli palatini left → aortic arch; right → subclavian 6 vagus nerve (CN10) cricoid, arytenoid, corniculate, & cuneiform cartilages all laryngeal muscles except cricothyroid pulmonary arteries Summary Bilateral complete lip and palate Unilateral complete lip and palate Incomplete cleft palate
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Thyroid Cancers
 
09:51
This is a video on the most common cancers that originate in the thyroid tissue. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Thyroid cancers The most common carcinomas that originate in the thyroid tissue Epi: Frequency of 80 percent (most common); good prognosis (10 year survival 95%); F:M 3:1; peak incidence in 30s to 50s Gross: irregular contours, no capsule around it Histo: nuclear clearing (nuclei appear empty - “Orphan Annie eye”), nuclear grooves, intranuclear pseudoinclusions, psammoma bodies (calcifications) , reduced colloid, crowded cells, papillary architecture (sometimes present) Derived from follicular cells Increased risk: mutations (RET and BRAF), radiation exposure as child Spread: often by lymphatic invasion to cervical nodes, neck; slow growth Secretes thyroglobulin; takes up radioiodine Treat: lobectomy (maybe total thyroidectomy with lymph node removal) High risk pts get radioiodine tx TSH suppression with thyroid hormone replacement Epi: Frequency of 10 percent; more aggressive than papillary with early metastases; also F:M 3:1; peak in 40s to 60s Histo: monotonous/uniform population, overlapping follicular cells, microacinar formation, reduced colloid, might contain Hurthle cells Derived from follicular cells Increased risk: mutations in RAS Spread: often by vascular invasion; locally invasive, invades thyroid capsule Distal spread more common than papillary Invades blood vessels and invades through the capsule Differentiate from follicular adenoma: Secretes thyroglobulin; takes up radioiodine (except Hurthle cells) Same treatment: lobectomy (maybe total thyroidectomy with lymph node removal) High risk pts get radioiodine tx TSH suppression with thyroid hormone replacement Epi: Frequency of 5%; more aggressive than follicular with early metastases; Sporadic (80%) → F:M 3:2, peak in 40s to 60s Familial (20%) → F:M 1:1, peak onset at early age Histo: neuroendocrine appearance, ‘packets’ of uniform cells; stroma made of amyloid (stains w Congo red) Derived from parafollicular cells (C (clear) cells); produces calcitonin Increased risk: family with MEN 2A and 2B (association), mutation in RET (proto-oncogene) Spread: early metastases Does not secrete thyroglobulin; does not take up radioiodine Same treatment: lobectomy (maybe total thyroidectomy w lymph node removal) Thyroid hormone replacement for normal TSH (no TSH suppression) Anaplastic carcinoma Left of image is amyloid, right of image is near normal thyroid follicles Anaplastic carcinoma AKA undifferentiated carcinoma (because it’s poorly differentiated) Epi: Frequency of 3 percent; very aggressive, poor prognosis, most deadly; M:F 2:1, peak in 60s to 80s Histo: several variants, but all high grade Spread: infiltrative into local structures, soft tissue of neck; widespread metastases, early mortality Does not take up radioiodine Papillary carcinoma Follicular carcinoma Medullary carcinoma Anaplastic carcinoma
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Nervous System Tumors
 
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This is a summary of the major tumors of the nervous system. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Medulloblastoma Pilocytic astrocytoma Diffuse astrocytoma Anaplastic astrocytoma Glioblastoma Oligodendrogliomas Ependymomas Meningiomas Neurofibromas Schwannomas By James Heilman, MD - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=16272952 Embryonal tumor Meningeal tumor Peripheral tumor Astrocytoma Gliomas Medulloblastoma Grade IV malignant tumor Arises from external granular layer in cerebellum Histo: small round blue cells; Homer-Wright rosettes; mitotically active Located in the cerebellum Can drop metastases to seed the CSF Well-circumscribed (non diffuse, solid) By Jensflorian - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/wiki/File:Neuroblastoma_Homer_Wright_rosettes_HE.jpg Pilocytic astrocytoma Grade I Imaging: Solid nodule with cystic component Common in cerebellum, hypothalamus, and optic nerve Well-circumscribed (non diffuse) Histo: Rosenthal fibers, eosinophilic granular bodies BRAF mutation Tumor in hypthalmic region - By The Armed Forces Institute of Pathology - http://peir2.path.uab.edu/scripts/acdis.dll?cmd=see&fp=/dbih/AFIP/00405615.tif&fmt=jpg&q=100&h=512, Public Domain, https://commons.wikimedia.org/w/index.php?curid=6182037 ROSENTHAL FIBERS - By Marvin 101 - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=5766818 Diffuse and anaplastic astrocytoma Diffuse astrocytoma Grade II malignant tumor Diffuse Most common in cerebral hemispheres Histo: hypercellular Molecular: no 1p/19p codeletion Anaplastic astrocytoma Grade III malignant tumor Diffuse Common location is cerebral hemispheres Histo: hypercellular, increased mitotic activity Molecular: no 1p/19p codeletion Glioblastoma Grade IV malignant tumor Diffuse, infiltrative mass Common location is cerebral hemispheres Ring enhancement on imaging; internal necrosis Histo: hypercellular, increased mitotic activity, microvascular proliferation, necrotizing, pseudopalisading Molecular: EGFR, PTEN Ring enhancing- By Christaras A - Created myself from anonymized patient MR, CC BY 2.5, https://commons.wikimedia.org/w/index.php?curid=1247038 Hypercellularity - By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=516831 Oligodendrogliomas Grade II-III malignant tumor Common location is cerebral hemispheres Histo: hypercellular, perinuclear halo (fried-egg appearance), negative for astrocyte marker Molecular: 1p/19q co-deletions Perinuclear halo - By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=7437415 Ependymomas Grade II-III malignant tumor Common in cerebellum and spinal cord Well-circumscribed (non diffuse) Can drop metastases to seed the CSF Histo: perivascular rosettes, ependymal rosettes Rosettes - By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=10714428 meningiomas Grade I benign tumor Tumor of adults, not children More common in females Might respond to hormone growth (progesterone/estrogen receptors) Dural tails; extra-axial location Can invade bone and less-commonly brain Histo: cellular whorls, psammoma bodies (calcium deposits) Whorls - By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=10728713 Dural tails By Glitzy queen00 - http://en.wikipedia.org/wiki/Image:Contrast_enhanced_meningioma.jpg, Public Domain, https://commons.wikimedia.org/w/index.php?curid=2359385 Neurofibromas Associated with neurofibromatosis type I Cafe-au-lait spots, lisch nodules in eye Histo: “shredded carrot appearance” of collagen strands Lisch nodules - By Dimitrios Malamos - Own work, CC BY 4.0, https://commons.wikimedia.org/w/index.php?curid=45193921 Histo - By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=443285 Schwannomas Can be associated with NF2 Histo: verocay bodies (palisading cells surrounding acellular zone) biphasic neoplasm with Antoni A (hypercellular) and Antoni B (hypocellular) regions Common: Vestibular schwannoma (aka acoustic neuroma) from CN VIII Hearing problems and disequilibrium Medulloblastoma Pilocytic astrocytoma Diffuse astrocytoma Anaplastic astrocytoma Glioblastoma Oligodendrogliomas Ependymomas Meningiomas Neurofibromas Schwannomas Biphasic histo - By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=17748282
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Eukaryotic Translation Initation
 
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Rough script of mechanism: This is a general scheme of translation initiation. We start with the small subunit of the ribosome, the 40S subunit. Now, normally we see this subunit paired with the larger 60S subunit. In this case, the ribosomal subunits are kept separate by initiation factor 3. This is important for initiating translation -- we want to keep the 40S unit separate until we are bound to the mRNA. The next step is the delivery of the first tRNA, which is of course, carrying the amino acid methionine. Initation factor 2 delivers this tRNA directly to the P site of the ribosome. Next, we have initiation factor 4 come in and guide the entire complex, called the pre-initiation complex, to the mRNA. Now, the preinitation complex doesn’t bind directly to the AUG start codon -- its actually nonspecific in binding, and it proceeds to scan the transcript to find the first start codon, which is an AUG. Once the complex finds the AUG, the GTP attached to initiation factor 2 can be hydrolyzed, and eIF2 can dissociate. eIF3 dissociates next, allowing the large 60 subunit of the ribosome to bind. We’re now ready for elongation to begin. elongation factor 1 alpha comes in carrying the second tRNA into the A site, and peptidyl transferase, a ribozyme, can create peptide bonds. This last step is repeated, and each subsequent tRNA is brought in with elongation factor 1 to continue to form a growing polypeptide chain https://docs.google.com/presentation/d/1nhfd2hwFewB36RNl_oFy8o2TqrbzJ3q5Bay2g2E7xtQ/edit?usp=sharing I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor.
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Antiretroviral agents for HIV / AIDS treatment
 
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This is a brief overview of the HIV life cycle and the various antiretroviral agents for HIV / AIDS treatment Maraviroc Allosterically inhibits CCR5 co-receptor Zidovudine (Retrovir, “AZT”) Competitively binds RT; terminates DNA chain elongation Raltegravir Inhibits integrase; prevent viral DNA integration in host genome Lopinavir / Ritonavir (Kaletra) Protease inhibitor; prevents cleavage of viral proteins I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor.
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Antiarrhythmic Drugs
 
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This is a brief overview of antiarrhythmic agents, or drugs used to resolve abnormal cardiac rhythms. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS Class IA antiarrhythmic agent Moderate sodium s, which s action potential duration Quinidine side effects blocks hERG , which results long QT and can cause torsades de pointes Procainamide Less prolongation QT segment, less TdP Disopyramide s force contraction heart Side effects: constipation, urinary retention, glaucoma IB antiarrhythmic Mild sodium s, which s action potential duration Lidocaine Intravenous only Mexiletine Can be administered orally IC antiarrhythmic Marked sodium s, doesn’t change action potential duration Flecainide Possibly produces an ventricular arrhythmias Propafenone Some beta er effects (bradycardia and cardiac inotropy) addition to changing AP duration by changing Na influx, Is also: phase 4 depolarization threshold potential sub degree Na+ AP duration change Beta-adrenergic receptor ers (beta ers) catecholamines (norepinephrine, epinephrine, dopamine) Reduces myocardial need for oxygen, can ischemia slope phase 4 depolarization s self-generated rhythmic firing heart (s automaticity) Prolong repolarization AV node → reentry Effectively s refractory period III antiarrhythmic s potassium s (delayed-rectifier potassium (DRK) s) Prolongs repolarization (phase 3) Amiodarone, Sotalol, Ibutilide, D etilide, Dronedarone III: Amiodarone Wide range effects through many mechanisms s sinus node firing s automaticity s reentrant circuits s Na, K, and Ca s ( I, III, IV antiarrhythmics) s alpha and beta ( II) adrenergic receptors → vasodilation and d intropy Treats many tachyarrhythmias: atrial flutter, atrial fibrillation, vtach, ventricular flutter, SVT Pharmacokinetically unique: absorbed slowly, deposits adipose tissue Half life 25-60 days → cannot easily diminish or reverse effects Side effects: pulmonary (pneumonia, pul fibrosis); cardiac (brady, arrhythmias, long QT, TdP); thyroid (due to iodine); GI; CNS Amiodarone Wide range effects through many mechanisms sinus node firing; s automaticity; s reentrant circuits; Na, K, and Ca alpha and beta adrenergic receptors vasodilation and intropy Treats many tachyarrhythmias: atrial flutter, atrial fibrillation, vtach, ventricular flutter, SVT Pharmacokinetically unique: absorbed slowly, deposits adipose tissue Half life 25-60 days Side effects: pulmonary (pneumonia, pul fibrosis); cardiac (brady, arrhythmias, long QT, TdP); thyroid (due to iodine); GI; CNS High rates torsades de pointes Dronedarone (amiodarone analog without iodine) Gastrointestinal side effects but not TdP Sotalol Calcium L-type Ca2+ Most effective cells dependant on Ca (SA, AV nodes) transmission through AV node (for rapid atrial pulses) Terminates reentrant rhythms Treats AV nodal reentrant tachycardia (primary treatment) Side effects: hypotension and heart failure pts taking beta-ers Diltiazem and Verapamil Digoxin Inhibits activity sodium potassium pump (Na+-K+ ATPase inhibitor) Treats heart failure complicated with atrial fibrillation (by decreasing heart rate) s vagal tone; reduces sympa tic activity Opens potassium (K+ activator) Intravenously with saline flush (short 10 s half life) Hyperpolarizes cells Allows for rapid termination reentrant supraventricular tachycardia chemical defibrillator
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Digestive hormones of the GI tract
 
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This is a brief video detailing the main hormones in the GI tract, where they are localized, and their primary functions. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: HORMONE LOCALIZATION MAIN PHYSIOLOGIC ACTIONS Gastrin Gastric antrum, duodenum (G cells) -stimulate secretion of gastric acid and intrinsic factor from parietal cells -stimulate secretion of pepsinogen from chief cells -promotes gastric and intestinal motility, mucosal growth Cholecystokinin (CCK) Duodenum, jejunum (I cells) -stimulate gallbladder contraction -stimulates release of pancreatic enzymes -relaxes sphincter of Oddi for release of bile and enzymes -role in inducing satiety Secretin Duodenum, jejunum (S cells) -stimulate secretion of HCO3 from pancreas -inhibits gastrin and gastric acid secretion Vasoactive intestinal peptide (VIP) Enteric nerves -increases water and electrolyte secretion from pancreas and gut -relaxes smooth muscles (via nitric oxide) of the gut Gastric inhibitory polypeptide (GIP) Duodenum, jejunum (K cells) -reduces gastric acid secretion and intestinal motility -stimulates insulin release Motilin Throughout the gut (Mo cells and ECL cells) -increases small bowel motility (MMC during fasting) and gastric emptying Somatostatin Stomach, small intestine, and pancreas (D cells) -inhibits secretion and action of many hormones, including all of the above Digestive hormones in the GI tract
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Anticoagulant Drugs
 
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CORRECTION - Spoken mistake in the first minute of the video -- The oldest drug on this video is heparin, NOT Warfarin. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS Anticoagulant Drugs Commonly used blood thinners for treating venous thromboses Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Warfarin Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Inhibits Vitamin K regeneration Therefore, inhibits Vit K-dependant factors Coag factors II, VII, IX, and X and protein C and S Warfarin Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Vitamin K Vit K epoxide reductase Vitamin K epoxide Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Warfarin Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Inhibits Vitamin K regeneration Therefore, inhibits Vit K-dependant factors Coag factors II, VII, IX, and X and protein C and S Requires bridging with use Warfarin blocks II, VII, IX, X, C, and S C, a coagulation cascade inhibitor, runs out first So if used alone, Warfarin has a COAGULATIVE effect at first Use with other coagulant for first five days Otherwise, skin necrosis Can be taken orally, effects require a few days NOT compatible with pregnancy Heparin Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Very negatively charged carbohydrate Polysaccharide with sulfate groups Binds to antithrombin Inhibits thrombin (IIa) and coag factor Xa Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Heparin Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Very negatively charged carbohydrate Polysaccharide with sulfate groups Binds to antithrombin Inhibits thrombin (IIa) and coag factor Xa Heparin must be 5 sugars long to bind AT and 18 sugars to inhibit thrombin in the heparin-AT complex Heparin monitored with Anti-Xa levels Coag factor Xa activity measured based on decrease in rate of: X → Xa Antidote is positively-charged protamine sulfate Administered subcutaneously, incurs effects immediately Enoxaparin (Low Molecular Weight Heparin) Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Polymers approximately one third the size of big Heparin Cannot complex with antithrombin to inhibit thrombin Enoxaparin is not the required 18 sugars long Affects coag factor Xa, as measured with Anti-Xa test Improved effects against VTE associated with cancer Fondaparinux (“tiny Heparin”) Pentasaccharide portion of heparin binds to antithrombin Cannot complex with antithrombin to inhibit thrombin Affects coag factor Xa, as measured with Anti-Xa test Synthetically made, unlike others that are animal extracts Does not induce HIT, unlike the others New Oral Anticoagulants Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban NOACs cause fewer intracranial bleeds NOT used in patients with mechanical heart valves Rivaroxaban and Apixaban Inhibit factor Xa Metabolized in the liver Dabigatran Direct thrombin inhibitor Cleared through kidneys Argatroban Warfarin Heparin Enoxaparin (LMWH) Fondaparinux (tiny Heparin) NOACs Argatroban Direct thrombin inhibitor No need for antithrombin Therefore it inhibits all three coagulation tests TT, PT, and PTT Used in cases of HIT Metabolized in the liver
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Hepatitis B serologies
 
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This is a short video describing three serologic markers for Hepatitis B and how they can be used to describe a persons Hep B infection status. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: remote infx (cleared) inactive chron. carrier acute infx Hepatitis B serologies Marker Meaning Acute infection Window period Chronic infection Remote infection (cleared) Immun- ization Inactive chronic carrier HBcAb Exposure + + + + - + HBsAg Infection + - + - - - HBsAb Immunity - - - + + - Time after exposure Titer window per. The easiest way to remember the signfiicance of each of these serologic markers is with the words in teh second column. HBcAb indicates that a patient has been EXPOSED to hepatitis B. HBsAg indicates that a patient has been INFECTED with Hep B. And HBsAb indicates that a person is IMMUNE to HepB. So, using these three terms, it’s easy to fill out the rest of the chart. In an acute infection, a person has been exposed (that’s how they got infected) and they’re obviously infected. They are not immune -- they still have the infection. This actue infection phase is indicated in the table below.. The person just got infected, and the body responds by making the core Ab that it will keep forever, and there is still viral antigen around . Next is the window period, which is after the
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Mood disorders (depression, mania/bipolar, everything in between)
 
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This is a brief video on mood disorders in psychiatry, including depression, mania/bipolar, and everything in between. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Mood disorders Low mood Neutral High mood Major depressive disorder: 5 or more of the following, and must have depressed mood or anhedonia Depressed mood: S = sleep changes I = interest loss (anhedonia) G = guilt (worthless) E = energy lack C = concentration reduced A = appetite change P = psychomotor change S = suicide ideation or thoughts For at least 2 weeks Not attributable to substances or medical conditions Treat with psychotherapy, meds (SSRI, SNRI, MAOi, TCA), and ECT in refractory cases Depression Hypomania: 3 or more of DIGFAST For at least 4 days. No significant impairment Hypomania Mania: 3 or more of the following D = Distractible I = Irresponsibility / irritable / impulsive G = Grandiose F = Flight of ideas A = Activity increase S = Sleep decrease T = Talkative For at least one week Causing significant impairment. Not attributable to substances or medical conditions Mania Bipolar I: Requires only one episode of mania, although often includes hypomania and major depression Bipolar II: Requires at least one episode of hypomania and one episode of major depression Treatment includes mood stabilizers (lithium/valproate first line, also lamotrigine/quetiapine; add atypical antipsychotic for acute mania Cyclothymic disorder: alternating periods of hypomanic symptoms and depressive symptoms without actually meeting criteria for hypomania and depression; persisting for 2+ years Treat with CBT and lithium, atypical antipsychotics Persistent depressive disorder: (aka dysthymic d/o) depressed mood and SIGECAPS symptoms without meeting full MDD criteria for 2+ years; described as baseline sadness; still enjoy some things Treat with CBT first, then meds like SSRIs Adjustment disorder: mood and anxiety symptoms 3 months after a stressor, typically resolving within 6 months Treatment: supportive psychotherapy and meds for symptoms (insomnia, nausea)
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Anti-diabetic medications
 
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This is a short video on medications used to treat diabetes mellitus by lowering blood glucose levels I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Insulin Bind insulin receptor, activate tyrosine kinase receptor pathway All used for DM1, DM2, GDM Rapid acting insulin: Lispro, Aspart, Glulisine Monomeric insulin analogs → monomers in solution Peak time in 1 hour → no LAG Used for post-prandial glucose control Short acting insulin: regular insulin Same insulin found in human body → dimer/hexamer in sol’n Peak in 2 to 4 hours Administered IV for DKA Intermediate acting insulin: NPH Peak in 4 to 10 hours Long acting insulin: glargine, detemir Insulin analog → precipitates at body pH Doesn’t really peak, relatively flat Good for mimicking basal insulin secretion Biguanides METFORMIN Sensitizes to insulin Thought to stimulate liver enzyme AMPK → exact MoA unclear Does not require functioning beta cells More effective in liver than muscle Administered orally Decreases HbA1c by 1-2% Mild weight loss SEs: diarrhea, nausea, vit B12 deficiency, lactic acidosis Contraindicated in kidney/liver/heart failure First line for DM2 Insulin Thiazolidinediones TZDs or -glitazones: pioglitazone and rosiglitazone Sensitizes to insulin → increases number and sensitivity Bind to peroxisome proliferator-activated receptor gamma (PPARγ) More effective in periphery (muscle/fat) than liver Does not require functional beta cells Administered orally Decreases HbA1c by 1-1.5% Mild weight gain, increases LDL, expensive, slow onset SEs: weight gain, edema, heart failure, liver toxicity, fractures Safe with renal failure Increases secretion of insulin Decreases HbA1c by 1-2% SEs: weight gain, hypoglycemia, allergies (sulfa drugs) Administered orally Sulfonylureas: tolbutamide, chlorpropamide, glipizide, glyburide, glimepiride Binds to SU on the ATP-activated potassium of beta cells → requires functional beta cells Blocks K channel → Ca influx → activate insulin release Meglitinides: repaglinide, nateglinide Bind to another receptor to block K channel → Ca influx → activate insulin release Faster onset, slower duration, more expensive than sulfonylureas Anti alpha glucosidase Acarbose, miglitol Slows absorption of carbohydrates in the proximal gut Alpha glucosidase is an enzyme that hydrolyzes carbs in the brush border of the GI tract Delays carb breakdown and thus absorption Decreases postprandial hyperglycemia Administered orally Decreases HbA1c by 0.5-1% SEs: flatulence (causes poor adherence), other GI disturbance, liver enzyme elevation Expensive Incretin mimetics Incretins GLP-1 and GIP are gut-derived hormones that: (1) stimulate insulin secretion, (2) inhibit glucagon secretion, (3) slow gastric emptying, and (4) promote satiety Incretin release stimulated by eating GLP-1 receptor analogs: exenatide, liraglutide, dulaglutide Mimick GLP-1 and produce same incretin effects Cause weight loss Dipeptidyl peptidase-4 (DPP4) is the enzyme that breaks down incretins DPP4 inhibitors increase blood conc of incretins -agliptins: sitagliptin, saxagliptin, linagliptin Administered orally Amylin analogues Synthetic amylin analogue: pramlintide Co-secreted with insulin, deficient in diabetes, and has the following effects: (1) inhibit glucagon secretion, (2) slow gastric emptying, (3) promote satiety Decreases HbA1c by 0.5-1% SEs: nausea, hypoglycemia Promotes moderate weight loss Administered orally or subcutaneously Cause weight loss Glycosurics Promote renal excretion of glucose Sodium-glucose cotransporter 2 (SGLT2) is a channel in the proximal tubule responsible for 90% of glucose reabsorption SGLT2 inhibitors: canagliflozin, dapagliflozin, empagliflozin Decreases HbA1c by 0.5-1% SEs: UTIs, vuvlvovaginal candidiasis (vaginal yeast infxns), glycosurea, renal failure, decrease blood pressure, hyperkalemia, dehydration Promotes substantial weight loss Colesevelam Bile acid sequestrant → exact MoA unknown Decreases HbA1c by 0.3-0.4% SEs: constipation, dyspepsia, nausea, hypertriglyceridemia Bromocriptine Dopamine agonist → exact MoA unknown Decreases HbA1c by 0.4-0.5% SEs: headache, dizziness, nausea, vomiting
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Cancers of the lung
 
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This is a short video describing the four most common carcinomas of the lung. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Cancers of the lung The most common carcinomas that originate in the lung parenchyma Squamous cell carcinoma Adenocarcinoma Large-cell undifferentiated carcinoma Small-cell carcinoma Non-small-cell carcinomas Squamous cell carcinoma Smokers (98%) Often arises centrally/proximally in larger bronchi more than peripheral lung Occurs in bronchi more than larynx and trachea bc flow more turbulent Associated with hypercalcemia (secretes PTH-like cmpd); causing weakness, dehydration, AMS Might see desmosomes and/or keratin accumulation (keratin pearls) Can cause obstruction of airway, atelectasis, collapse of lung Can invade lymphatics Can cause clubbing Squamous cell carcinoma Adenocarcinoma Large-cell undifferentiated carcinoma Small-cell carcinoma Adenocarcinoma Most common carcinoma in nonsmokers (but 80% are smokers) More likely to be peripheral than central/proximal Might see glands and/or mucin production on histology Hypertrophic osteoarthritis (HPO) triad has clubbing, long bone swelling, and arthritis Adenocarcinoma in situ (formerly: "Bronchioloalveolar carcinoma" (BAC)) Lepidic growth pattern, replaces type I pneumocytes, but no invasion of interstitium Can be solitary nodule, multiple nodules (multifocal, bilateral) Presents as cough and dyspnea, again +/- mucinous Squamous cell carcinoma Adenocarcinoma Large-cell undifferentiated carcinoma Small-cell carcinoma Large-cell undif. carcinoma Large cells with prominent nuclei No desmosomes, no keratin, no mucin staining Expression analysis on cDNA microarray Squamous cell carcinoma Adenocarcinoma Large-cell undifferentiated carcinoma Small-cell carcinoma Small-cell carcinoma Exclusively smokers Paraneoplastic syndromes: Secretes hormones: ACTH (can cause Cushing’s), ADH (Na abnormality) Eaton-Lambert (neurologic disorder) Fast-growing, rapid progression, early metastases, often high stage at presentation Highly responsive to chemo/rad treatment Limited → Extensive staging as metastasis outside of hemithorax High N/C ratios, frequent mitotic figures, high percentage of cells in division, salt and pepper chromatin, cells aren’t that small Squamous cell carcinoma Adenocarcinoma Large-cell undifferentiated carcinoma Small-cell carcinoma
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Disorders of sexual development
 
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This is a brief video on congenital disorders affecting biological gender, the genitalia, and reproductive health. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Disorders of sexual development Congenital disorders affecting traits of gender, the genitalia, and reproductive health McCune-Albright syndrome Turner’s syndrome Klinefelter syndrome Androgen insensitivity syndrome 5 alpha reductase deficiency Kallmann syndrome McCune-Albright syndrome Genetic disorder causing precocious puberty Pathophysiology: defect in G3 alpha subunit protein makes it constitutively active Chimeric, so several/various tissues affected Gonadotropin-independent Clinical: early breast development, early puberty Hyperthyroidism, hyperparathyroidism, café-au-lait spots with “coast of Maine” borders Treat with aromatase inhibitors to limit estrogen Genetic disorder of delayed puberty and no periods (primary amenorrhea) Result of ovarian failure; streak gonads PE: short stature; shield chest with widely spaced nipples; webbed neck; and prepubertal vagina, uterus, and cervix Lab tests: high FSH, high LH, low estradiol Karyotype: 45 XO Associated: renal problems, autoimmune (Hashimoto's thyroiditis), cardiac (aortic coarctation, aortic aneurysm, mitral valve prolapse, bicuspid aortic valve) Treatment: growth hormone, hormone replacement, egg donation for childbirth (with significant risks) Neck webbing Genetic disorder affecting testicles Testicular atrophy causes dysfunction of leydig cells and seminiferous tubules Clinical: tall, gynecomastia, female hair distribution, long extremities, developmental delays Lab tests: increases LH and FSH, decreased testosterone, increased estrogen, decreased inhibin B Karyotype 47 XXY Androgen insensitivity syndrome AKA testicular feminization Caused by inactivating mutation in androgen receptor gene in end organs Male genotype, female phenotype, appears normal until pubertal age when menstruation doesn’t happen Short vagina with little sexual hair; no cervix, no uterus bc testes produce anti mullerian hormone during development Lab tests: FSH normal, LH normal, estrogen normal, LH:FSH is high, testosterone very high Treat with HRT, testes removal (usually in labia majora), expansion of vagina 5 alpha reductase deficiency 5 alpha reductase converts testosterone to dihydrotestosterone Genetic disorder, affects genetic males Internal genitalia are male; ambiguous external genitalia until puberty, when increase in testosterone causes sudden testicular enlargement, phallus/clitorus enlargement, deepening of voice, increased muscle mass “Penis at 12” syndrome Lab tests: high testosterone, high testo/DHT ratio, 46 XY karyotype Caused by “impaired migration of neurons” due to disorder in adhesion protein anosmin-1 Impaired migration of GnRH secreting neurons in the hypothalamus Impaired migration of olfactory neurons → anosmia Hypogonadotropic hypogonadism Clinical: delayed puberty, anosmia, amenorrhea/low sperm count Lab tests: low GnRH, low FSH, low LH, low estrogen Treat with HRT for most symptoms; treat with recombinant FSH for fertility By Neil Smith - Created ny a medical illustrator for the production of a booklet on Kallmann syndrome, CC BY-SA 3.0, https://en.wikipedia.org/w/index.php?curid=36507233 McCune-Albright syndrome Turner’s syndrome Klinefelter syndrome Androgen insensitivity syndrome 5 alpha reductase deficiency Kallmann syndrome
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Opioids
 
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This is a brief summary of medicines that target the opioid receptors. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS Opioids Drug Mechanism of action Indication Notes Heroin Strong μ agonist Manage pain, suppress cough, antimotility for diarrhea Contraindication: phenothiazine, MAO inhibitors, and tricyclic antidepressants (depressant effects); alcohol and benzodiazepine (respiratory effects); hepatic metabolism Often abused IV; not legal in US; Morphine Strong μ agonist Prototypical opioid; various routes of admin Fentanyl Strong μ agonist Rapid onset and offset with small doses; CV stability; 100x more potent than morphine Methadone Strong μ agonist Also used for opioid/heroin withdrawal; racemic mixture of NMDA antagonist and mu agonist Meperidine Strong μ agonist No biliary SE, doesn't constrict sphincter of Oddi; seizures Codeine Moderate μ agonist Less potent morphine Hydrocodone Moderate μ agonist Most prescribed opiate; often combined with NSAIDs/acetaminophen Oxycodone Moderate μ agonist Similar to hydrocodone Tramadol Weak μ agonist Synthetic codeine; lower addiction risk; can cause seizures and serotonin syndrome Buprenorphine μ agonist; κ antagonist Analgesic; deterrent, detoxification High affinity, low efficacy at mu receptor → partial agonist Nalbuphine κ agonist; μ antagonist Treats opioid-induced pruritus Originally hoped to be less addictive, less side effects than other opioids → no Naloxone μ antagonist (short acting) Treat opioid addiction, overdose, and toxicity; reverses mu agonist effects; increases respiratory rate within 1-2 min Better for opioid overdose; half-life is 1 hour Naltrexone μ antagonist (long acting) Treats alcoholism; lasts 24 hours after moderate dose
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Leukodystrophies (ALD, MLD, and GLD)
 
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This is a brief video on three hereditary leukodystrophies: ALD, MLD, and GLD (Krabbe diease). I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Leukodystrophies Disorders that cause degeneration of white matter in brain Show diffuse white pattern on MRI Usually present in children with developmental disabilities Subcortical U fibers connecting gyri of the brain are typically well-preserved This is NOT an exhaustive list ALD MLD GLD Adrenoleukodystrophy Aka X-linked ALD or adrenomyeloneuropathy X-linked inheritance Deficiency in ATP binding cassette transporter (ABCD1) Diagnose with elevated very long chain fatty acid Peroxisomal disorder Demyelination in occipital lobe (ALD) and brainstem/spinal cord (AMN) In addition to myelin in CNS/PNS, also affects adrenal cortex and Leydig cells in the testes Macrophages containing long chain fatty acid Treatment Lorenzo’s oil (triglyceride mixture) is controversial and unproven By Frank Gaillard - http://radiopaedia.org/images/318699 and http://radiopaedia.org/uploads/radio/0031/8699/T2.jpg, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=9783483 ALD MLD GLD Metachromatic leukodystrophy Autosomal recessive Deficiency in arylsulfatase A Sulfatide accumulates in CNS/visceral cells Lysosomal storage disease; sphingolipidoses (sphingolipid metabolism) Variable presentation: ataxia, dementia Starts after 6 months of age in late infantile, juvenile, and adult forms Macrophages containing sulfatide (metachromatic material) By Shoyrudude555 at English Wikipedia - Transferred from en.wikipedia to Commons., Public Domain, https://commons.wikimedia.org/w/index.php?curid=2819137 ALD MLD GLD Krabbe disease Aka globoid cell leukodystrophy (GLD) or galactosylceramide lipidosis Autosomal recessive Deficiency in galactocerebroside-b-galactosidase Lysosomal storage disease; sphingolipidoses (sphingolipid metabolism) Presents as irritability, peripheral neuropathy, optic atrophy, decerebrate posture (extension of upper extremities), developmental delay Generally fatal before age two Histo shows characteristic multinucleated globoid cells Macrophages containing galactocerebroside ALD MLD GLD
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Personality disorders by clusters
 
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This is a brief video on personality disorders listed by clusters A, B, and C. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Personality disorders by clusters Cluster C: “worried,” anxious, fearful Avoidant: social inhibition and inadequacy; intense fear or rejection; extreme sensitivity to negative evaluation; but desire companionship Dependant: psychological need to be cared for by other people; poor confidence; need others to take care, make decisions; fear of being alone Obsessive-compulsive: rigid conformity to rules, perfectionism, control, inflexibility, orderliness; to the point of satisfaction (egosyntonic) and exclusion of leisurely activities and friendships; successful professionally but not socially Cluster B: “wild,” dramatic, emotional Antisocial: disregard for and violation of the rights of others, lack of empathy, bloated self-image, impulsive behavior; break rules/laws; understand social cues → manipulative; often criminals; socio/psychopaths; conduct disorder is precursor in less than 18 y/o Borderline: abrupt mood swings, unstable relationships, self-image, identity, behavior and affect, often leading to self-harm and impulsivity; often experience splitting; physical, emotional, and sexual abuse in childhood; treated with dialectical behavioral therapy (DBT) Histrionic: attention-seeking behavior and excessive emotions; provocative, flamboyant, extroverted, sexually inappropriate; can’t form long-lasting, meaningful relationships Narcissistic: grandiosity, superiority, inflated ego, entitled, need for admiration; perceived or real lack of empathy, exploit others, criticize others; often have underlying low self-esteem Cluster A: “weird,” odd, eccentric Paranoid: irrational suspicion and mistrust of others, interpreting motivations as malevolent; often accusatory without evidence; blame problems on others; pathologically jealous Schizoid: prefer to be alone; lack of interest and detachment from social relationships, apathy, and restricted emotional expression; voluntary social withdrawal and isolation; reclusive, quiet, unsociable Schizotypal: odd, eccentric thoughts and behavior; magical thinking, peculiar appearance; pattern of extreme discomfort interacting socially, and distorted cognitions and perceptions https://en.wikipedia.org/ wiki/Personality_disorder
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Anticonvulsants (antiepileptic drugs)
 
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This is a brief summary of anticonvulsants, or medicines used to treat epilepsy. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Anticonvulsants Drug Mechanism of action Modern approach Other indications Side effects (unique/notable listed first) Interaction Metab Carbamazepine Na+ channel blocker: binds inactive Na channel, extend inactivation simple partial, complex partial, secondary generalized (narrow) bipolar disorder, trigeminal neuralgia Hyponatremia... bone marrow suppression; hepatotox; sedation; dizziness; n/v; double vision; ataxia; fetal malform; bone demineraliz; Stevens-Johnson syndrome p450 induction hepatic Phenytoin Na+ channel blocker: complex actions simple partial, complex partial, secondary generalized (narrow) n/a Bone demineralization; gingival hyperplasia (long term use); hypotension, arrhythmias, tissue necrosis ( IV admin)... bone marrow suppression; hepatotox; sedation; dizziness; n/v; double vision; ataxia; fetal malform; Stevens-Johnson syndrome p450 induction hepatic Lamotrigine Na+ channel blocker: selective for excitatory neuron NT like glutamate all seizure types (broad spectrum) bipolar disorder; antidepressant effects Stevens-Johnson syndrome (life threatening rash)... sedation; dizziness; n/v; double vision; ataxia; fetal malform; bone demineraliz; Stevens-Johnson syndrome p450; OCPs decrease efficacy hepatic Ethosuximide Ca2+ channel blocker (α subunit, T type, thalamic) absence seizures (narrow spectrum) n/a; just first line for absence seizures sedation; dizziness; n/v; double vision; ataxia; fetal malform; bone demineraliz; Stevens-Johnson syndrome n/a hepatic Phenobarbital GABA antagonist: augments GABA receptor (Cl channel) simple partial, complex partial, secondary generalized (narrow) Tremors (similar to primidone for essential tremor) Hyperactivity, addiction, sedation... bone marrow suppression; hepatotox; dizziness; n/v; double vision; ataxia; fetal malform; bone demineraliz; Stevens-Johnson syndrome p450 induction hepatic Valproate many: blocks Na, enhance GABA, block Ca all seizure types (broad spectrum) Migraine prophylaxis, bipolar disorder fetal malformation (strongest teratogen); weight gain, tremor, hair loss, fulminant hepatic failure (limits use in kids); bone marrow suppression... sedation; dizziness; n/v; double vision; ataxia; fetal malform; bone demineraliz; Stevens-Johnson syndrome p450 inhibitor hepatic Topiramate many: blocks Na, enhance GABA, block glutamate (NMDA) receptor all seizure types (broad spectrum) Migraine prophylaxis Cognitive impairment, weight loss, kidney stones... sedation; dizziness; n/v; double vision; ataxia; fetal malform; bone demineraliz; Stevens-Johnson syndrome Decreases efficacy of OCPs 70:30 hepatic: renal Gabapentin unknown or partially known mechanism simple partial, complex partial, secondary generalized (narrow) Neuropathic pain, chronic pain Ankle edema, weight gain... sedation; dizziness; n/v; double vision; ataxia; fetal malform; bone demineraliz; Stevens-Johnson syndrome Antacids (limit bioavailability) renal Pregabalin unknown or partially known mechanism simple partial, complex partial, secondary generalized (narrow) Neuropathic pain; fibromyalgia Ankle edema, weight gain... sedation; dizziness; n/v; double vision; ataxia; fetal malform; bone demineraliz; Stevens-Johnson syndrome Antacids (limit bioavailability) renal Levetiracetam unknown or partially known mechanism all seizure types (broad spectrum) n/a Depression, behavioral/psychiatric issues (up to 15%)... sedation; dizziness; n/v; double vision; ataxia; fetal malform; bone demineraliz; Stevens-Johnson syndrome n/a renal
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Anatomy of Cranial Nerve Nuclei
 
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This is a brief video on the cranial nerve nuclei, including their anatomy and the nerves/functions that synapse at them. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Anatomy of cranial nerve nuclei By Gray696.png: User:mcstrotherderivative work: Mcstrother - Gray696.png, Public Domain, https://commons.wikimedia.org/w/index.php?curid=15058610 Posterior view of brain without thalamus or cerebellum Anatomy of cranial nerve nuclei Posterior view of brain without thalamus or cerebellum III and Edinger Westphal Parasympathetic to pupils IV trochlear V trigeminal (motor) V trigeminal (sensory) VI abducens VII facial VIII vestibular and cochlear Nucleus solitarius Taste and baro/ chemoreceptors (CNs VII, IX, & X) X vagus (motor) parasympathetic to viscera Nucleus ambiguus Swallowing (CN IX & X) and phonation (CN X) XII hypoglossal IX glossopharyngeal X vagus (sensory) Sensory Motor By Gray696.png: User:mcstrotherderivative work: Mcstrother - Gray696.png, Public Domain, https://commons.wikimedia.org/w/index.php?curid=15058610
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Antipsychotics (neuroleptics)
 
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This is a brief video on antipsychotics, also called neuroleptics, including their mechanisms, their indications, and side effects I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Anti- psychotics (neuroleptics) First-generation antipsychotics First-gen side effects Extrapyramidal side effects Neuroleptic malignant syndrome Atypical antipsychotics By Unknown - http://www.flickr.com/photos/x-ray_delta_one/4298034735/, Public Domain, https://commons.wikimedia.org/w/index.php?curid=16041923 First generation (typical) antipsychotics Haloperidol and -azines High potency: haloperidol, trifluoperazine, fluphenazine Medium potency: perphenazine Low potency: chlorpromazine, thioridazine MoA: high affinity antagonist for dopamine (D2) receptor, thus increasing concentration of cAMP Indications: schizophrenia positive symptoms (and brief psychotic disorder, schizophreniform), schizoaffective, other psychoses, bipolar, delirium, Tourette, Huntington’s First-generation antipsychotics First-gen side effects Extrapyramidal side effects Neuroleptic malignant syndrome Atypical antipsychotics First generation (typical) antipsychotics: Side effects Delay cardiac conduction (prolong QTc interval), risk of torsades de pointes Anticholinergic effects → Blurred vision, constipation, dry mouth, urinary retention Worse with lower potency antipsychotics Antihistamine effect → sedation Anti alpha1 effect → orthostatic hypotension Endocrine: hyperprolactinemia → osteoporosis, amenorrhea, galactorrhea, gynecomastia, and sexual side effects Caused by D2 blockage on tuberoinfundibular pathway Extrapyramidal symptoms Neuroleptic malignant syndrome First-generation antipsychotics First-gen side effects Extrapyramidal side effects Neuroleptic malignant syndrome Atypical antipsychotics First generation (typical) antipsychotics: SEs: extrapyramidal side effects Caused by D2 blockage on nigrostriatal pathway Hours to days: acute dystonic rxn (sustained muscle contraction); tx with IM diphenhydramine or benztropine Days to weeks: akathisia (restlessness) Weeks to months: parkinsonism (tremor, cogwheel rigid, hypokinesia); tx with lower dose antipsychotic or diphenhydramine or benztropine Months to years: tardive dyskinesia (hyperkinetic movement of head, limbs, trunk → perioral movements (tongue, facial grimacing, and lip puckering) are common) Tx by switching 1st-gen→2nd-gen or 2nd-gen→clozapine First-generation antipsychotics First-gen side effects Extrapyramidal side effects Neuroleptic malignant syndrome Atypical antipsychotics First generation (typical) antipsychotics: SEs: neuroleptic malignant syndrome Idiosyncratic reaction presenting with confusion, vital sign (autonomic) instability, hyperpyrexia (high fever), rhabdomyolysis (myoglobinuria), renal failure, cardiovascular collapse Fever Encephalopathy Vitals unstable Enzyme increase Rigidity of muscles Treat with dantrolene Don’t confused with malignant hyperthermia! First-generation antipsychotics First-gen side effects Extrapyramidal side effects Neuroleptic malignant syndrome Atypical antipsychotics Atypical (2nd generation) antipsychotics Aripiprazole, -apines, -idones aripiprazole, asenapine, clozapine, olanzapine, quetiapine, iloperidone, lurasidone, paliperidone, risperidone, ziprasidone MoA: weaker D2 antagonist and serotonin (5-HT2a) agonist Indications: schizophrenia (positive and negative symptoms) Side effects: Delay cardiac conduction (prolong QTc interval), risk of torsades de pointes Less anticholinergic and EPS effects Metabolic (weight gain, diabetes, high lipid) → -apines Agranulocytosis → clozapine (very potent) Hyperprolactinemia → risperidone First-generation antipsychotics First-gen side effects Extrapyramidal side effects Neuroleptic malignant syndrome Atypical antipsychotics
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Red Blood Cell Morphological Abnormalities
 
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This is a video describing various morphological abnormalities found in red blood cells, including changes in red cell size, shape, color, and distribution. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Macrocytosis Large As measured with MCV altered DNA synthesis MCV, things that alter DNA synthesis , B12/folate deficiency Liver disease Thyroid disease Chemotherapy Anti-retrovirals (AZT) Microcytosis Small Measured with MCV iron deficiency, thalassemia, lead poisoning measured with MCV, Iron deficiency, Thalassemias, Lead poisoning, Sideroblastic anemia Anisocytosis Wide range of RBC sizes High red cell distribution width (RDW) Hypochromasia with too little hemoglobin Measured with mean corpuscular Hb (MCH) hypochromic cells, central cell diameter caused by lack of hemoglob (iron defiiciency, thalassemia, liver problems) Polychromasia that are shaded grayish blue often reticulocytes (immature ) Anisocytosis, large RDW Poikilocytosis that vary widely shape Analogous anisocytosis anisocytosis - vary size poikilocytosis - vary shape Target cells codocytes Related liver disease, thalassemias, hemoglob C, post-splenectomy Normal RBC cross section Target cell Anisocytosis, large RDW Spherocytes Spherical (instead of biconcave disk-shaped Appears on blood smear as loss of central pallor Hereditary spherocytosis Autoimmune hemolysis Normal RBC Spherocyte cross section cross section (biconcave disk) (more spherical) Ab attack membrane of RBC, if you pull out chunks of membrane, surface area of RBC membrane decreases Schistocytes fragments Sharp edges Can be caused by plaque on arterial walls that shear Also Microangiopathic Hemolytic Anemia (MAHA) Sickle cells fragments sickle cell anemia Hemoglob molecules with Point mutation that changes glutamic acid valine Polymerization of Hb at low pH, low pO2, high temperature Anisocytosis, large RDW Echinocytes burr cells Projections that are regular renal disease Acanthocytes spur cells Projections that are irregular large liver disease Teardrop cells dacrocytes Caused by infiltration of bone marrow (myelophthisic processes) Something body ( lymphocytes, scar tissue, cancer) enters grows bone marrow Linear aggregations or “stacks” of are high levels of immunoglobulins usually have similar surfaces charges that keep them from sticking together Immunoglobulins neutralize these charges, allow attract with charge-charge interactions a normal patient, you might see this on dense side of a blood smear, bc RBC conc is more concentrated Agglutination collect clumps Less orderly than rouleaux are coated with IgM, which bridge together cause aggregation Howell-Jolly Bodies Remnants of nucleic acids that found postsplenectomy Look like little purple dots
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Eating disorders (anorexia, bulimia, and binge-eating disorder)
 
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This is a brief video on eating disorders in the DSM-5, specifically focused on how to similarities and differences between anorexia, bulimia, and binge-eating disorder. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Eating disorders in the DSM-5 Anorexia nervosa Bulimia nervosa Binge- eating disorder Preoccupation with weight and body image resulting in low food absorption → low BMI (BMI 18.5) Restrictive: patient severely limits food intake Binge eating/purging: food intake followed by compensation (vomit, laxative/diuretic, and/or exercise) Coexist with perfectionism; depression Associated medical issues: starvation, osteoporosis → fractures, amenorrhea, anemia, electrolyte disturbances (refeeding syndrome, hypophosphatemia), hypothyroidism (euthyroid sick syndrome) with low T3/T4 but low/nl TSH, IUGR/prematurity in pregnancy, Treat with psychotherapy, low dose olanzapine (SSRIs ineffective unlike bulimia) Anorexia nervosa Bulimia nervosa Binge- eating disorder Anorexia nervosa Binge eating followed by compensatory behavior: Purge: vomit, laxative, diuretic Teeth and enamel erosion, esophageal tears, parotitis, thickened knuckles Non-purge: exercise or diet Patients are normal weight or overweight (BMI 18.5) Treat with psychotherapy and SSRIs (fluoxetine); bupropion is contraindicated Anorexia nervosa Bulimia nervosa Binge- eating disorder Bulimia nervosa The erosion on the lower teeth was caused by bulimia. For comparison, the upper teeth were restored with porcelain veneers. Binge eating WITHOUT compensatory behavior Therefore does not fit qualifications of bulimia At least three of the following: Eating quickly Eating alone out of embarrassment Eating until uncomfortably full Binge eating when not hungry Feelings of guilt/depression/disgust after eating Patients are often overweight / obese and suffer from metabolic syndrome, cardiovascular disease, and diabetes Treatment: psychotherapy, strict diet/exercise, stimulants and orlistat (pancreatic lipase inhibitor) may help Anorexia nervosa Bulimia nervosa Binge- eating disorder Binge-eating disorder Anorexia nervosa Bulimia nervosa Binge- eating disorder Anorexia nervosa Low food absorption (either restrict diet or binge/purge) → Low BMI Bulimia nervosa Binge then purge Tx: SSRIs Binge-eating disorder Binge WITHOUT purge Tx: stimulants, orlistat Binge eating Tx: psychotherapy Compensatory behavior Signs of purging/vomiting Bupropion contraindicated nl/high BMI
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Summary of Leukemias
 
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This is a brief summary of four leukemias: CML, CLL, AML, ALL. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS Leukemia CML CLL AML ALL Chronic Myelogenous Leukemia Chronic Lymphocytic Leukemia Acute Myeloid Leukemia Acute Lymphoblastic Leukemia Chronic Myelogenous Leukemia Neoplasm of progenitor stem cell → considered myeloproliferative Malignant cells can still differentiate → morphological heterogeneity Clinical: ambiguous symptoms (fever, sweats, weight loss) or asymptomatic; occurs in adults (median 66); hepatosplenomegaly; high WBC (neutro/baso/eosinophils), low RBC, high plts Characteristic translocation t(9;22) forming the Philadelphia chromosome New BCR-ABL fusion protein codes for an oncogenic tyrosine kinase Diagnose with FISH for t(9:22) or PCR for BCR-ABL transcript Chronic phase → accelerated phase → blast phase (AML, ALL) Treat with imatinib (tyrosine kinase inhibitor), cure with allogeneic stem cell transplant CML CLL AML ALL Chronic Myelogenous Leukemia CML CLL AML ALL Peripheral blood (MGG stain): marked leucocytosis with granulocyte left shift Chronic Myelogenous Leukemia CML CLL AML ALL Peripheral blood (MGG stain): marked leucocytosis with granulocyte left shift Chronic Lymphocytic Leukemia Malignancy of mature (but naive) B cells; which are differentiated → morphological homogeneity, clonal Clinical: ambiguous symptoms (fever, sweats, weight loss); occurs in adults (median 72); hepatosplenomegaly; lymphadenopathy; high WBC (neutro/baso/eosinophils), low RBC, low plts; hypogammaglobulinemia → frequent infections (respiratory by encapsulated bacteria) Autoimmune hemolytic anemia; immune thrombocytopenia (2%) Spherocytes, smudge cells Flow cytometry: CD19+, CD20+, CD23+, CD5+, Zap-70, CD38+, gamma OR lambda but not both CD10- (unlike follicular, burkitt, ALL); CyclinD1- (unlike mantle cell) Rai: stage 0 is leukocytosis only; stages I, II, III, IV has lymphadenopathy, splenomegaly, anemia, thrombocytopenia, respectively (I,II,III,IV=L,S,A,T) Not curable, but good long-term prognosis CML CLL AML ALL zap70 is the itams associated with TCR, usually on T-cells but its on CLL B cells… CD38 is white blood cells in general Chronic Lymphocytic Leukemia CML CLL AML ALL Peripheral blood (MGG stain): marked leucocytosis with granulocyte left shift Chronic Lymphocytic Leukemia CML CLL AML ALL Acute Myeloid Leukemia Malignancy of immature myeloid progenitor; proliferation of granulocyte blast cells; cannot differentiate → morphological homogeneity, clonal Smear: large blasts; 20% blasts; Auer rods (crystallization of mpo, DIC) Clinical: high WBCs, low RBCs, low neutrophil, low plts Arise from t(15;17) → Acute Promyelocytic Leukemia (APL) Disrupts RAR, which inhibits maturation, because retinoic acid (RA) is a differentiator → treat with ATRA, good prognosis Arise from FLT3 mutation (de novo), which makes tyrosine kinase → bad Other bad prognoses → deletion of chr 5 or 7, old age, AML from previous MDS or treatment (chemo/rad) Curable: treat with 7+3 chemo → 7 d cytarabine and 3 d anthracycline; potential for allogeneic stem cell transplant CML CLL AML ALL Acute Myeloid Leukemia CML CLL AML ALL Peripheral blood (MGG stain): marked leucocytosis with granulocyte left shift Acute Myeloid Leukemia CML CLL AML ALL Acute Lymphoblastic Leukemia Malignancy of immature lymphoid progenitor; proliferation of B or T blast cells; cannot differentiate → morphological homogeneity, clonal Clinical: low RBCs, low neutrophil, low plts, hepatosplenomegaly Tumor lysis syndrome: high K, high uric acid, high LDH, high PO43-, low Ca → renal failure Lymph node, mediastinal mass Most common cancer in children (peak incidence ages 2 to 5) Risk factors: chemo/rad, down’s, NF, Bloom synd, ataxia telangiectasia B cell ALL is more common, expresses CD10+, TdT+, CD19+, CD20+ Good prognosis if: hyperdiploid, age 1-10, t(12;21), Bad prognoses if: hypodiploid, high WBC, t(9;22), abn(11q23) T cell ALL is less common, represents as thymic mass in teenagers CML CLL AML ALL young - median age is 11 Acute Lymphoblastic Leukemia CML CLL AML ALL
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Female breast pathology
 
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This is a brief video on neoplastic and nonneoplastic diseases of the breast in females (excluding gynecomastia) I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Breast pathology Neoplastic and nonneoplastic diseases of the breast in females Fibroadenoma Phyllodes tumor Fat necrosis Acute mastitis Periductal mastitis Mammary duct ectasia Fibrocystic changes Intraductal papilloma Ductal carcinoma in situ Paget disease Invasive ductal carcinoma Lobular neoplasia Invasive lobular carcinoma Benign conditions Malignant conditions Def: Noncancerous breast tumor consisting of stromal and epithelial tissues Epi: women in 20s to 30s, most common benign neoplasm Clinical: painless, firm, rubbery, mobile lump might enlarge based on menstrual cycle (estrogen-sensitive) Gross: solid, lobulated, tan/pink, firm, no necrosis, no hemorrhage; well-circumscribed US: solid, round, homogenous mass; well-circumscribed Histo: gland structures with stromal and ductal proliferation, no cytologic atypia Phyllodes tumor AKA cystosarcoma phyllodes, cystosarcoma phylloides and phylloides tumor Def: Masses arising from stromal cells surrounding ducts of the breast Fibrous neoplasia pushes out tissue→ gross and histologic changes Epi: older (40+ and postmenopausal), African American, rare tumor Clinical: large mass, bulky, mobile, firm as a “wooden log” -- twice as large as the other breast Gross: blue veins on skin surrounding tumor, well-circumscribed Histo: fibrous gland and tissues with intermittent cystic spaces, epithelial leaf-lined structure; cytologic atypia and mitotic figures are rare Spread: might recurs after excision, 5-10 percent undergo malignant transformation Treatment: excise surgically (wide local excision or mastectomy) Fat necrosis AKA fatty lumps Def: normal fat cells of the breast become round lumps through necrosis Caused by trauma, radiation, or surgery involving breast Epi: women post trauma, radiation, or surgery Clinical: painful, induration with irregular contours, retraction of skin Mammogram: eggshell calcification (results from saponification) Gross: necrotic fat tissue → must biopsy to rule out cancer; induration Histo: necrotic fat with calcifications, giant cells, granulation tissue, lipid-laden macrophages Spread: no malignant potential Although confused with cancer bc of calcification, induration, skin retraction, irregular contours Treatment: not necessary Fibroadenoma Phyllodes tumor Fat necrosis Acute mastitis Periductal mastitis Mammary duct ectasia Fibrocystic changes Intraductal papilloma Ductal carcinoma in situ Paget disease Invasive ductal carcinoma Lobular neoplasia Invasive lobular carcinoma Fibroadenoma Phyllodes tumor Fat necrosis Acute mastitis Periductal mastitis Mammary duct ectasia Fibrocystic changes Intraductal papilloma Ductal carcinoma in situ Paget disease Invasive ductal carcinoma Lobular neoplasia Invasive lobular carcinoma Histo: necrotic fat with calcifications, giant cells, granulation tissue, lipid-laden macrophages Acute mastitis Def: bacterial infection of the breast Typically caused by skin organisms Staph aureus (or Strep), when breastfeeding → stress on skin allows bacteria to enter breast Epi: breastfeeding women Clinical: purulent discharge from breast; warm, erythematous breast; engorgement; loss of nipple integrity Spread: no malignant potential dicloxacillin for beta-lactamase-producing organisms such as S aureus) and drainage Periductal mastitis Def: inflammation of breast tissue beneath the nipple Epi: smokers AKA duct ectasia of breast or plasma cell mastitis Def: lactiferous duct becomes blocked or clogged Inflammation of the duct leads to duct dilation → debris piles up and goes into nipple → discharge Epi: postmenopausal, multiparous women; rare Clinical: green/brown nipple discharge Mammogram: typical rod-like calcifications Histo: chronic inflammation, plasma cells Fibrocystic changes AKA fibrocystic breasts or fibrocystic breast disease or fibrocystic breast condition (FBC)
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Antidepressants
 
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This is a brief video on antidepressants, including their mechanisms, indications, and side effects. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Antidepressants Monoamine oxidase inhibitors: Tranylcypromine, phenelzine, isocarboxazid, selegiline MoA: inhibits monoamine oxidase, which breaks down monoamine NTs (5-HT, dopa, norepi) First line treatment for atypical depression; also for anxiety, MDD after other tx fails SE: orthostatic hypotension, sedation, sexual dysfunction Serotonin syndrome (with other serotonergic agents) → diarrhea, restless, hyperreflexia, hyperthermia, rigidity Hypertensive crisis (with tyramine containing foods) → vasoconstriction, elevated BP, n/v, headache, sweating MAOIs: tranylcypromine, phenelzine, isocarboxazid, selegiline SSRIs: fluoxetine, paroxetine, sertraline, (es)citalopram, fluvoxamine SNRIs: (des)venlafaxine, duloxetine, (levo)milnacipran TCAs: amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine Atypical: bupropion, mirtazapine, amoxapine, trazodone, varenicline Selective serotonin reuptake inhibitors: Fluoxetine, paroxetine, sertraline, (es)citalopram, fluvoxamine MoA: blocks presynaptic neuron from absorbing serotonin from the synapse (increasing serotonin levels/effectiveness) Fluoxetine has longest half-life Paroxetine and fluvoxamine have shortest half-lives Treats MDD, anxiety, and other related disorders SE: GI (n/v/d), sex (decreased libido, ejaculation; anorgasmia) Risk of serotonin syndrome Hepatic metabolism Serotonin-norepinephrine reuptake inhibitors: (des)venlafaxine, duloxetine, (levo)milnacipran MoA: blocks presynaptic neuron from absorbing serotonin AND norepinephrine from the synapse (increasing their effectiveness) Treats MDD, neuropathic pain, anxiety Venlafaxine used for other related disorders, including OCD, PTSD, and social anxiety SE: GI (n/v/d), sex (decreased libido, ejaculation; anorgasmia), sedation, hypertension Risk of serotonin syndrome Hepatic metabolism Tricyclic antidepressants: Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine MoA: blocks serotonin and norepinephrine transporters (increasing their effectiveness in the synapse) Also blocks histamine and muscarinic cholinergic receptors Treats MDD, neuropathic pain, and headaches Also prophylaxis for headaches/migraines SE: anticholinergic (constipation, dry mouth, orthostatic hypotn, urinary retention), cardiovascular (tachycardia, prolonged QT) Risk of serotonin syndrome Atypical antidepressants: Bupropion: inhibits dopa and norepi reuptake; treats seasonal affective disorder, preferred bc lack of sex SEs; also used for smoking cessation Mirtazapine: increases norepi and 5-HT concentration; causes sedation, increased appetite, weight gain, dry mouth Amoxapine: increases norepi and 5-HT concentration; causes sedation, increased appetite, weight gain Trazodone: increases serotonergic effect via complex mechanism; causes sedation thus used for insomnia; risk of priapism, nausea, postural hypotension Varenicline: partial agonist for nicotinic cholinergic receptor; also used for smoking cessation; can cause trouble sleeping
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Fungi and Antifungal Agents
 
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This is a brief overview of antifungal agents, their mechanisms of action, and some fungi that they affect. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: anti-fungal, anti fungal glycoproteins containing mannose β1,3 β1,6 glucans chitin ergosterol DNA synthesis Antifungal Agents Echinocandins (such as caspofungin, anidulafungin, micafungin) inhibit the enzyme that synthesizes β-glucans, called the "penicillin of antifungals" Polyenes (such as amphotericin B) bind ergosterol, weaken the membrane, cause pore formation, leakage of K+ and Na+, fungal cell death; also confers mammalian toxicity. Azoles (such as fluconazole, ketoconazole, itraconazole) inhibit the enzyme that synthesizes ergosterol 5-flucytosine (5-FC) is converted to 5-FU to inhibit DNA synthesis as a pyrimidine analog; side effect is myelosuppression Fungi and Antifungal Agents Fungi and Antifungal Agents Yeasts Candida Cryptococcus Molds Aspergillus Zygomycetes Fusarium Dimorphics Histoplasma Blastomyces Coccidioides Paracoccidioides Echinocandins (inhibits β-glucans synthesis) Works in Candida and Aspergillus Doesn’t work in dimorphism Polyenes (inhibits ergosterol activity) Works in all except Aspergillus terreus Azoles (inhibits ergosterol synthesis) Works in all except Candida glabrata Fluconazole ineffective in Candida krusei and molds 5-flucytosine → 5-FU (inhibits DNA synthesis) Works in all yeasts, but there is resistance Doesn’t work in molds or dimorphics
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Psychotic disorders
 
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This is a brief video on psychotic disorders, including schizophrenia and related disorders. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Involvement of mood → Duration of symptoms → Schizophrenia Need 1, 2, or 3 and 1 more of: Delusions Hallucinations Disorganized speech Disorganized / catatonic behavior Negative symptoms (flat affect, anhedonia, flat speech, cognitive def) For at least one month Total disease length 6 months including prodromal/residual phases Brief psychotic disorder Same criteria as schizophrenia but total disease length 1 day and 1 month Can be caused by major stressor; termed post-partum psychosis if following pregnancy Schizophreniform Same criteria as schizophrenia but total disease length 1 month and 6 months Upgrade from brief psychotic disorder, precursor to schizophrenia Schizoaffective Meet criteria for schizophrenia PLUS criteria for mood disorder (depression or bipolar) for majority of illness WITH Delusions/hallucinations are present for at least two weeks without mood disorder Psychosis in absence of mood disorder Mood disorder with psychotic features Meet criteria for mood disorder (SIGECAPS for major depressive disorder or DIGFAST for mania in bipolar I) with additional symptoms of psychoses. BUT Delusions/hallucinations are NOT present for two weeks without mood disorder. Constant mood disorder with intermittent psychosis MDD: Depressed mood + 4 of: S = sleep changes I = interest loss G = guilt (worthless) E = energy lack C = cognition/concentration reduced A = appetite change P = psychomotor change S = suicide ideation or thoughts BPAD 1: for mania, 3 or more of: D = Distractible I = Irresponsibility / irritable / impulsive G = Grandiose F = Flight of ideas A = Activity increase S = Sleep decrease T = Talkative Psychotic disorders Psychotic disorders Schizophrenia treatment: Antipsychotics First generation (typical) for positive symptoms Haloperidol + -azines (thiazine, chlorpromazine) Delusions, hallucinations disorganized speech, disorganized / catatonic behavior Second generation (atypical) for negative symptoms Risperidone, ziprasidone, quetiapine, olanzapine, aripiprazole, clozapine Flat affect, anhedonia, poverty of speech, cognitive deficits Related disorders not to be confused: Schizoid personality disorder Lack of interest and detachment from social relationships, apathy, and restricted emotional expression. Schizotypal personality disorder A pattern of extreme discomfort interacting socially, distorted cognitions/perceptions, strange beliefs, and/or magical thinking. Delusional personality Fixed false beliefs that are believable but unrealistic in that person’s culture No prominent hallucinations, thought disorder, mood disorder, or significant flattening of affect
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Anesthetics
 
06:14
This is a short summary of medicines used for anesthesia. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Anesthesia Drug Administration Mechanism of action Advantage Disadvantages Etomidate Intravenous Bind GABA receptor, enhance effects of GABA (main inhibitory neurotransmitter) Cardiovascular stability Many side effects, can't use in septic shock Ketamine Antagonize NMDA receptor, reduce effects of glutamate (main excitatory neurotransmitter) → dissociative anesthetic Potent without respiratory depression Increases heart rate and cardiac output; can cause hallucinations and nightmares Propofol Enhance GABA Rapid onset, rapid recovery → very widely used Can cause respiratory depression and bradycardia Thiopental Enhance GABA Can decrease intracranial pressure Can cause respiratory depression and bradycardia Nitrous oxide Inhalation Enhance GABA transmission; inhibit glutamate receptors Causes analgesia, depersonalisation, derealisation, dizziness, euphoria Low potency (high minimum alveolar concentration) → cannot achieve surgical anesthesia Halothane Low cost → widely used worldwide Risk of arrhythmias and immune hepatitis → no longer used in US Fluranes: desflurane, isoflurane, sevoflurane Potent, enough for general anesthesia for surgery Can cause malignant hyperthermia (fatal hypermetabolic dz, treat with dantrolene) Side effects: -CV (dec heart contraction, SVR, and BP) -respiratory (inc rate, dec TV and CO2 response to CO2) -renal (dec blood flow and GFR)
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Glomerular diseases
 
18:01
This is a summary of diseases that affect the glomerulus of the kidney, including those that case nephrotic and nephritic syndromes. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Glomerular diseases Minimal change disease Focal segmental glomerulosclerosis Membranous glomerulonephritis Diabetic nephropathy Amyloid nephropathy Lupus nephritis Membranoproliferative glomerulonephritis IgA nephropathy Acute postinfectious glomerulonephritis Anti-GBM disease ANCA glomerulonephritis Nephrotic Nephritic Systemic Primary glomerular disease with nephrotic syndrome Most common in children, especially young children LM: “minimal change” -- looks normal IF: negative (no immune complex deposition) EM: foot process effacement, see figure secondary causes: cancer, infection, drugs, atopy (hyperallergic) Associated with lymphoma and use of NSAIDs Primary glomerular disease with nephrotic syndrome Focal means some glomeruli, segmental means not all of glomerulus LM: segmental glomerular scarring, see hyaline material (deposits from plasma) IF: positive for Ig and complement, granular appearance EM: segmental effacement Primary FSGS is idiopathic Secondary causes: genetic, infection (HIV, parvovirus), drugs (heroin), sickle cell, obesity Most common in blacks Primary glomerular disease with nephrotic syndrome LM: capillary wall thickening with IgG and C3 immune complexes IF: positive for IgG and C3 in the capillary, granular EM: immune complexes in subEPIthelial space Primary cause: Ab against anti-phospholipase A2 receptor Secondary causes: cancer, lupus, NSAIDs, HBV, Hep B, syphilis… Ag can be Hep B or cancer Secondary nephropathy with nephrotic syndrome; DM is primarily systemic disease Caused by DM types I and II → accumulation of glycosylated plasma protein in GBM and mesangium LM: mesangial expansion and KW nodules IF: linear staining of IgG EM: thickened GBM Treatment is reduce blood sugar, lower blood pressure, avoid nephrotoxins Most common cause for end stage renal disease in United States Secondary nephropathy with nephrotic syndrome; amyloidosis is primarily a systemic disease Caused by accumulation of polypeptides (especially AL and AA amyloid) LM: thickening of mesangium amorphous pale pink stuff in glomerulus, confirm with Congo Red stain IF: monoclonal staining of accumulated amyloid protein EM: randomly arranged fibrils Associated with rheumatoid arthritis and multiple myeloma Ranked by class: I (best) to VI (worst) Antigen antibody complexes deposit in gloms, activate complement which leads to proliferation of mesangium and infiltration of PMNs LM: endocapillary and mesangial proliferation and sometimes crescents IF: granular pattern, everything lights up! “full house pattern” EM: deposits anywhere and everywhere Hypocomplementemia - both C3 and C4 blood levels are low Presents with nephritic and/or nephrotic syndrome; kind of in between Type I is immune complex and C3 deposits Caused by bacterial infection, hep C infection, malignancies Type II is just C3 deposits but no Ig Caused by complement dysregulation LM: capillary wall thickening with hypercellularity IF: immune complexes and/or C3 granular deposits causing hypocomplementemia EM: same deposits (subendo and BM) Deposits of IgA alone or with other Igs, in mesangium Activates complement, which causes proliferation of mesangial cells LM: mesangial hypercellularity IF: IgA positive, granular pattern in the mesangium EM: mesangial deposits Primary IgA nephropathy is idiopathic Can be part of systemic disease IgA vasculitis; related to Henoch– Schönlein purpura Occurs few weeks after infection; most often follows strep or staph LM: endocapillary and mesangial hypercellularity and PMNs IF: pos for C3 in capillary walls, granular EM: subepithelial humps Hypocomplementemia; low C3 levels Treatment is supportive Nephritic Caused by autoAb to glomerular basement membrane Abs recruit complement and lymphocytes → damages capillary → proliferation and accumulation in Bowman’s space → crescent LM: crescent formation IF: pos for IgG in linear pattern EM: normal Disease is called Goodpasture’s syndrome when presents with both kidney and lung involvement LM: crescents, necrosis IF: pauci-immune; not much lights up EM: normal Associated diseases: Granulomatosis with polyangiitis (GPA); Wegener's; PR3 Eosinophilic granulomatosis with polyangiitis (eGPA); Churg–Strauss churg Strauss Microscopic polyangiitis (MPA)
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Renal Tubule Acidosis
 
07:16
This is a short video on the different types of renal tubule/tubular acidosis, or disorders in which the body cannot acidify urine. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Renal Tubule Acidosis Acidification of the body due to inability of the kidneys to acidify urine Type 1 Distal Type 2 Proximal Type 3 Combined Type 4 Hyperkalemic Type 1: Distal Type 4: Hyperkalemic Type 2: Proximal Type 1: Distal tubule RTA Failure of the alpha-intercalated cells in distal convoluted tubule to secrete acid (H+) Cannot acidify urine… urine pH 6ish Decreased H+ in tubule lumen draws out K+ causing hypokalemia Associated with Sjögren Sjogren syndrome (autoAb against CAII, which generates H+ in DCT) Calcium phosphate kidney stones Caused by decreased citrate excretion and hypercalciuria Salts more likely to precipitate at higher pH Type 1 Distal Type 2 Proximal Type 3 Combined Type 4 Hyperkalemic Type 2: Proximal tubule RTA Failure of the proximal tubule to reabsorb filtered bicarbonate Initial insult: Excess bicarb excretion; urine pH is 6.5 After insult: Bicarb serum levels drop, impaired absorption sufficient to can still acidify urine to 5.5 Distal nephron still functions normally NaHCO3 loss → hypoaldosteronism → mild hypokalemia Other associated proximal tubule defects, including glucose, uric acid, phosphate, and AAs in urine (Fanconi syndrome) Bone demineralization due to phosphate excretion; Type 2 RTA can be caused by multiple myeloma Type 1 Distal Type 2 Proximal Type 3 Combined Type 4 Hyperkalemic Type 3: Combined RTA Patients share features of distal and proximal RTAs (types 1 and 2) Rarely discussed Type 1 Distal Type 2 Proximal Type 3 Combined Type 4 Hyperkalemic Type 4: Hyperkalemia RTA Caused by decreased aldosterone release or activity (hypoaldosteronism) Decreased ENaC activity in distal tubule Tubular lumen is less negative Decreased excretion of K+ and H+ Hyperkalemia and acidosis Acidosis in principal cells of DCT prevents ammoniagenesis, and NH3 is main carrier of thus urine pH is 5.5 Type 1 Distal Type 2 Proximal Type 3 Combined Type 4 Hyperkalemic Summary Type 1 Distal Type 2 Proximal Type 3 Combined Type 4 Hyperkalemic Type 1 Type 2 Type 3 Type 4 Affected physiology: Distal convoluted tubule Proximal convoluted tubule PCT and DCT Aldosterone effects on DCT serum pH: acidosis acidosis acidosis acidosis serum pH: hypokalemia hypokalemia hypokalemia hyperkalemia urine pH: 6 initially 6, then 5.5 - 5.5 Associated: High urine Ca2+, stones Bone disorders, multiple myeloma - Hypoaldosteronism
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Hypolipidemic Agents
 
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This is a brief overview of hypolipidemic agents, or drugs that alter the levels of lipids in the body. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS Hypolipidemic Agents Statins Bile Acid Sequestrants Niacin Fibrates Statins Inhibit the enzyme HMG-CoA reductase, which is the rate limiting step in cholesterol synthesis Decrease LDL, increase HDL, decrease TGs Proven to reduce risk of coronary artery disease Side effects: Liver toxicity (most metabolized by cytochrome P450), muscle toxicity (rhabdomyolysis) Contraindications: liver disease, CYP450 inhibitor drugs, pregnancy (birth defects) Lovastatin, Pravastatin, Simvastatin, Atorvastatin, Rosuvastatin Statins Bile Acid Sequestrants Niacin Fibrates Bile Acid Sequestrants Binds bile acid in the gut and prevents reuptake, thus promoting excretion of bile acid Cholesterol is typically converted to bile acid and secreted into the GI tract; 99% of this bile acid is then reabsorbed into the body Loss of 1% of bile acid is typically the only method of removing cholesterol from the body Bile acid sequestrants allow for more than 1% of bile acid to excreted from the body, forcing body to produce more bile acid from cholesterol Decrease LDL, increase HDL, no effect on TGs Side effects: GI distress (nausea, constipation, bloating → since it’s inhibiting fat absorption, resolved with fiber intake) Malabsorption of other drugs and fat-soluble vitamins (DEAK) Avoid use in people with familial dysbetalipoproteinemia with very high TG Colestipol (Colestid), Colesevelam (Welchol), Cholestyramine (Questran) Statins Bile Acid Sequestrants Niacin Fibrates Niacin Prevents release of free fatty acid into the bloodstream from adipocytes Increases HDL by decreasing hepatic excretion of a major protein in HDL (apoA-I) Increase HDL, decreases LDL, decreases TGs Side effects: skin flushing (resolved with aspirin), hyperuremia, hyperglycemia, GI distress (n/v and peptic ulcers), and hepatotoxicity Contraindications: patients with gout and liver disease (monitor liver enzymes) Niacin (Niaspan, Niacor) is also known as nicotinic acid or vitamin B3 Niacin has a number of other functions, and lack of niacin causes pellagra, degenerative disease causing skin lesions (shown) and mental disturbance Statins Bile Acid Sequestrants Niacin Fibrates Fibrates Activate a transcription factor (peroxisome proliferator-activated receptors (PPARs)) that increases lipoprotein lipase, which converts VLDL to LDL and therefore reduces VLDL and triglyceride levels PPARs are regulators that transport from cytoplasm to nucleus to bind regulatory regions of target genes Decrease TGs, decrease LDL, increase HDL Side effects: GI distress, skin rash, muscle toxicity (also worsened by statins, too), hypokalemia, arrhythmias Avoid use in patients with liver and renal disease Gemfibrozil Fenofibrate Statins Bile Acid Sequestrants Niacin Fibrates
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Anxiety, OCD, PTSD, and related psychiatric disorders
 
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This is a brief video on psych disorders related to nervousness, rumination, and related somatic complaints. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Generalized anxiety disorder 5-10 percent lifetime prevalence; 2:1 W:M Definition: Excessive worrying and anxiety for 6 months Worry about school/grades, job, money, relationships, events, life Pathophys: “disrupted functional connectivity of the amygdala and its processing of fear and anxiety” At least 3 of symptoms: Restlessness, Tires easily, Problems concentrating, Irritability, Muscle tension, Problems with sleep Specific phobias 10 percent lifetime prevalence; W M, approx 2:1 Definition: Irrational fear of a specific object, place, situation, or concept for 6+ months Fear out or proportion to imminent threat Fear interferes with functioning in society Exposure induces immediate fear; removal reduces anxiety Fear might have developed from related trauma Social phobia: fear of embarrassment in public situation Agoraphobia: fear of public places due to lack of ability to escape; fear of unsafe environment Treatment: Separation anxiety disorder Definition: “excessive anxiety regarding separation from home or from people to whom the individual has a strong emotional attachment” for 4w in children or 6mo in adults May include anxiety/fear/distress when separated; reluctance to be alone/leave home/school/work; worry about harm to attachment figures Symptoms cause dysfunction in society Treat with CBT, family therapy, and possibly adjunct SSRIs Similar anxiety during normal child development: Stranger anxiety at 6 months Separation anxiety at 1 year Panic attacks 4% lifetime prevalence; W:M 2:1 Definition: “sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling that something bad is going to happen” Occurrence of at least one attack Constant worry about recurrence Other symptoms … trembling, unsteadiness, depersonalization, palpitations, abdominal pain, chest pain Must rule out medical etiologies: hyperthyroidism, afib, pheochromocytoma, drugs (amphetamines, sympathomimetics) Obsessive compulsive disorder 2 to 3 percent lifetime prevalence; M=F Obsessions: recurrent thoughts that persist despite trying to ignore them Compulsions: explicit rituals that either reduce anxiety or that patients feel they have to perform OCD is associated/comorbid with other psychiatric disorders: other anxieties, depression/bipolar, OCPD Treatment: Psychotherapy: CBT Pharmacotherapy: SSRI clomipramine (TCA) ECT Generalized anxiety d/o Specific phobias Separation anxiety d/o Panic attacks OCD OCD-related d/o PTSD Acute stress d/o Adjustment d/o OCD-related disorders Body dysmorphic disorder WM, higher in derm and cosmetic sx pts Perceived flaws in physical appearance Excoriation disorder - compulsive skin picking Hoarding disorder Cannot discard possessions, regardless of value Typically accumulate trash Treat with specialized CBT Trichotillomania - hair pulling disorder Treat with specialized CBT: habit reversal training; SSRIs, atypical antipsychotics Post traumatic stress disorder Mental disorder occurring after exposure to trauma, such as sexual assault, warfare, violence, traffic collisions Symptoms of increased reactivity, irritability, difficulty concentrating, hypervigilance, exaggerated startle, sleep difficulties Avoidance of triggers of symptoms Symptoms lasting 1 month Acute stress disorder: PTSD-like condition with trauma occurring 1 mo ago symptoms lasting 1 mo Treatment: Psychotherapy: CBT (exposure therapy, cognitive processing therapy) Adjustment disorder Very common; up to 20 percent in outpatient clinics Patient unable to cope with stress or major life event Symptoms include loss of interest, crying, feeling of hopelessness Symptoms occur within 3 mo of stressor and should resolve by 6 mo Symptoms resolve when pt adapts to new situation “Situational depression” Treat with supportive therapy Can consider temporary medications for some symptoms (insomnia, anxiety, or depression)
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Lumbar plexus and derivative nerves, muscles, and lesions of the lower extremity
 
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This is a brief video on the neuromusculature of lower extremity, specifically the lumbar plexus and derivative nerves, muscles, and lesions of the lower extremity. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Scrotum/labia majora Through inguinal canal Ilioinguinal n. (L1) (sensation) Lateral femoral cutaneous n. (L2, L3)→ beneath inguinal ligament Sensation to anterolateral thigh Genitofemoral n. (L1, L2) Genital branch Femoral branch → under inguinal l. Sensation to area on proximal/ anterior thigh Femoral n. (L2-L4) with psoas and iliacus branches Beneath inguinal ligament, thru femoral triangle Anterior thigh muscles: Hip flexors: pectineus, sartorius, psoas major + iliacus = iliopsoas (deep to inguinal lig., to lesser trochanter of hip) (also laterally rotate hip) Knee extensors: quadriceps (rectus femoris, vastus medialis (branch thru adductor canal), vastus lateralis, vastus intermedius) → continue as patellar tendon into tibial tuberosity Obturator n. (L2-L4) Through obturator canal Medial thigh muscles: Hip adductors: adductor longus, adductor brevis, gracilis, adductor magnus (except hamstring portion) Lat hip rotator: obturator externus Sacral nerves Lumbosacral trunk (L4-5) Hip fracture (femur neck fracture) → leg is shortened and laterally rotated bc of iliopsoas muscle Femoral a and v pass through adductor magnus → adductor hiatus Pectineus - flexes and adducts the hip Sartorius - long, thin hip abduct, ext rot, flex Gracilis - long, thin hip adductor, used for muscle grafts Insert into pes anserinus: “goose foot” Anterior branch → sensory to medial thigh region Meralgia - entrapment causes burning pain and/or paresthesia to outer thigh Terminates as saphenous (longest sensory nerve) Saphenous and vastus medialis branch go thru adductor canal
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Antiemetics and Prokinetics
 
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This is a short video describing commonly used drugs that increase GI motility. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: ACh ACh NANC D2R 5HT3R 5HT4R Serotonin Metoclopramide Dope Bethanechol 5HT3R antagonist: -ex: ondansetron -few side effects Phenothiazine -ex: promethazine -SE: sedation, drowsiness Motilin Smooth muscle Macrolides -ex: erythromycin -tachyphylaxis -SE: diarrhea Domperidone Cisapride Dronabinol -δ-9-THC -unknown MoA ANTIEMETICS and PROKINETICS
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Premature rupture of membranes
 
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This is a brief video on premature rupture of membranes, or the leakage of amniotic fluid before labor. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Premature rupture of membranes 10-week-old human fetus surrounded by amniotic fluid and fetal membranes By drsuparna http://www.flickr.com/photos/74896762@N00/ - http://www.flickr.com/photos/74896762@N00/3167352760/, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=5658338 Leakage of amniotic fluid before labor Overview Risk factors and causes Diagnosis Management Chorio- amnionitis PROM = premature rupture of membranes Amniotic sac rupture / fluid spillage more than one hour before onset of labor Labor = regular contractions + cervical change PPROM = preterm premature rupture of membranes Amniotic sac rupture before 37 weeks Prolonged rupture of membranes Amniotic sac rupture for longer than 18 hours before delivery “Gush of fluid” vs steady leakage of fluid Note color and consistency of fluid Thick vs watery Clear, cloudy, meconium, blood-tinged Overview Overview Risk factors and causes Diagnosis Management Chorio- amnionitis Vaginal or cervical infections: UTIs, STIs, bacterial vaginosis Smoking or drug use during pregnancy PROM or preterm deliveries in previous pregnancies Nutritional deficiencies; underweight mothers Polyhydramnios (too much amniotic fluid) Multiple gestation Cervical insufficiency (short or prematurely dilated cervix) Invasive procedures (amniocentesis, cerclage, etc) Pathophysiology: Weak fetal membranes Infections (sometimes subclinical) Genetics Risk factors and causes Overview Risk factors and causes Diagnosis Management Chorio- amnionitis Three classic tests Pooling: Collection of fluid in the vagina (posterior fornix) Nitrazine: Neutral fluid turns nitrazine paper blue; vaginal fluid usually acidic. Amniotic fluid is mildly acidic → blue nitrazine paper False positives: blood, semen, infections, antiseptics, lubricant Ferning: Dry amniotic fluid on glass slide has crystallization pattern called arborization that resembles fern plant on light microscopy Ultrasound can detect low levels of fluid (low residual fluid levels) Other new tests detect chemicals or proteins in amniotic fluid By Paul_012 - originally posted to Flickr as Positive fern test, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=5223846 Management Overview Risk factors and causes Diagnosis Management Chorio- amnionitis Previable 24 weeks Watchful waiting; no tocolytics, steroids, MgSO4, or abx Induction of labor to end pregnancy Preterm 24-33 weeks Tocolytics to prevent labor; steroids twice 24 hrs apart for lung maturity; MgSO4 as tocolytic while lungs mature; abx for GBS prevention Amnioinfusion to replace lost fluid is controversial Late preterm 34-36 weeks Induce labor; abx for GBS prevention Term 37 weeks Induce labor; abx for GBS prevention Definition: infection of chorion, amnion, and/or amniotic fluid surrounding fetus Diagnosis: Signs and symptoms: fever, rupture of membranes, leakage of fluid, uterine tenderness, elevated maternal heart rate ( 100 bpm), elevated fetal heart rate (160 bpm) Fever: exclude maternal URI and UTI Labs: increased white count ( 15,000 cells/mm³) Treat with ampicillin, gentamicin, and clindamycin Induce delivery Covers gram negatives and anaerobes Afebrile for 24 hours Chorioamnionitis Overview Risk factors and causes Diagnosis Management Chorio- amnionitis By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=16158284
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Somatic symptom and factitious disorders
 
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This is a brief video on somatic symptom and factitious disorders. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Somatic symptom and factitious disorders in the DSM-5 Somatic symptom disorder Illness anxiety disorder Conversion disorder Factitious disorder Malingering Also/previously called somatoform disorder, somatization disorder At least one somatic symptom (such as pain) along with excessive fear, worry, stress, or behavioral change regarding this pain Duration of 6 months Similar to illness anxiety in the fear/stress but with actual somatic symptoms Symptom(s) is/are subconsciously driven; patients actually believe they has a disorder EPI: F M; 5-7% prevalence; risk factors include low SES, low education, older age, unemployment Prognosis: symptoms can get better or worse over time based on mood and/or stress Patients often present frustrated having seen many doctors all not believing their symptoms with many negative workups Management: Acknowledge symptoms (because they are real) Schedule regular follow-ups with a single PCP Build rapport Allows you to monitor any changes in symptoms Avoid unnecessary workup and treatment Somatic symptom disorder Somatic symptom disorder Illness anxiety disorder Conversion disorder Factitious disorder Malingering Also/previously called hypochondriasis, hypochondria, health anxiety Excessive and undue fear, worry, stress, and/or behavioral change regarding having or being diagnosed with a serious illness Duration of 6 months Somatic symptoms are absent or very minor Preoccupation with illness severely impacts their daily functioning Sometimes caused by recent psychological stressor Such as death in family → worry about same disease in self Reassurance is often ineffective Epi: M=F; ⅔ have another psychiatric illness; most prevalent in 20s-30s Management: Acknowledge concerns Schedule regular follow-ups with a single PCP Psychotherapy (CBT) Screen for comorbid anxiety and depression, consider SSRI If source is psychological stressor, resolve that stressor Also called functional neurological symptom Patient presents with at least one symptom (usually neurologic, such as numbness, blindness, mutism, or paralysis) that cannot be explained neurologically (not in normal stroke pattern) Symptom onset is usually abrupt and following significant life stress or event (death of family member, bereavement) Patient’s are often indifferent to or unconcerned with their symptom(s) La belle indifference Epi: WM; most frequent in adolescence and early adulthood Pseudoseizures, or psychogenic nonepileptic seizures, can be the symptom of conversion disorder Differentiate from epileptic seizure with prolactin level (elevated in epileptic) and EEG (normal in pseudoseizure) Management: Education about conversion disorder; reassurance that symptom will resolve Consider CBT if symptoms persist Spontaneous recovery usually occurs Also known as Munchausen's syndrome when severe Patient acts as if he has an illness by deliberately producing, feigning, or exaggerating symptoms, purely to attain a patient's role with no secondary gain or external reward Patient often creates symptoms in dangerous ways, such as injecting themselves with feces (infection) or insulin (hypoglycemia) or ingesting blood and inducing vomiting (hematemesis) Can also create less serious symptoms: abd pain, depression, hallucinations Patient can present themselves as patient or present another as a patient (Munchausen’s by proxy) Parent making child sick is child abuse Epi: WM; higher incidence in healthcare workers Management: Confront in nonthreatening manner Document and contact PCP and other providers to avoid unnecessary procedures Patient fabricates symptoms of mental or physical disorders for secondary gain or external reward Secondary gain is oftentimes getting out of work/school, obtaining drugs, clearing charges/legal record, free room and board, etc Malingering is NOT a mental illness or psychiatric pathology Oftentimes present as ill-defined, nonspecific complaints that don’t add up; often unsatisfied with reassurance or negative workup Symptoms improve once secondary gain is achieved Epi: MW; often in patients with antisocial personality disorder Management: Present the patient with discrepancies between objective findings and their subjective report Give patient opportunity to admit malingering Do not confront with hostility
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Psychoactive Drugs: pharmacology, intoxication, withdrawal, and treatment
 
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This is a brief video on psychoactive drugs, including the pharmacology of these drugs, intoxication symptoms, withdrawal symptoms, and relevant treatments. Errata: error at 3:27; misspoke, should have said "agonize" not "antagonize"; proper word listed on slide. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Anti addiction medications 1. cocaine 2. crack cocaine 3. methylphenidate (Ritalin) 4. ephedrine 5. MDMA (Ecstasy) 6. mescaline (cactus) 7. LSD blotter 8. psilocybin mushroom (Psilocybe cubensis) 9. Salvia divinorum 10. diphenhydramine (Benadryl) 11. Amanita muscaria mushroom 12. Tylenol 3 (contains codeine) 13. codeine with muscle relaxant 14. pipe tobacco 15. bupropion (Zyban) 16. cannabis 17. hashish Depressants / sedatives Alcohol, barbiturates, benzodiazepines MoA: enhancement of GABA receptor Intoxication: incoordination, ataxia, slurred speech, euphoria, nystagmus, attention impairment, behavior inhibition, coma, blackouts, AST = 2*ALT Hypotension, respiratory depression → benzos and barbs Treatment: flumazenil for benzo OD, supportive for others Withdrawal: hallucinations, seizures, hypertension, nausea, sweating, insomnia, anxiety, agitation, tremors Muscle cramps, twitches, tachycardia → benzos and barbs Delirium tremens (2-4 days after last drink)→ fluctuating consciousness, high HR, seizures, tremors, anxiety Treatment: benzodiazepines Can be fatal Opioids Heroin, prescription pain meds (oxycodone, hydrocodone, etc) MoA: agonize opioid receptor, especially mu subtype Intoxication: motor slowness, slurred speech, euphoria, impaired attention and sedation, miosis, respiratory depression Treatment: naloxone, naltrexone (opioid antagonists) Withdrawal: depression/anxiety, diarrhea, cramps, sweating, piloerection, pupillary dilation, yawning, muscle aches Treatment: supportive for pain and GI distress; methadone and buprenorphine (weaker agonists) can help Not fatal Heroin and oxycodone are most widely abused opioids → responsible for many deaths Depressants / sedatives Opioids Stimulants Cannabinoids (marijuana) Hallucinogens (LSD) Dissociatives (PCP) Anti addiction medications Stimulants Cocaine, amphetamines, methamphetamines, MDMA (ecstasy), cathinone (bath salts), caffeine, nicotine MoA: Cocaine → block norepi and DA reuptake Amphetamine → increase synaptic [norepi] and [DA] Nicotine → agonize PNS/CNS cholinergic receptors Caffeine → enhance DA effect by blocking ADO receptors Intoxication: Amphetamines → behavioral (grandiose, euphoric, hypervigilant, paranoia, agitation); autonomic (inc BP/HR, chills, sweating, n/v) Cocaine → add hallucinations of bugs on skin Treatment: lorazepam (anxiety); haloperidol (psychosis); vitals Withdrawal: Amphetamines/cocaine → appetite, low HR, depression, fatigue Nicotineappetite, low HR, dysphoria, anxiety, irritability Caffeine mild dysphoria, headaches, anxiety Treatment: supportive Cannabinoids Marijuana, hashish, synthetic blends (e.g., K2, spice) MoA: delta-5-tetrahydrocannabinol (THC) binds to cannabinoid receptor, which inhibits adenylate cyclase and cAMP production Intoxication: conjunctivitis, dry mouth, high BP/HR, appetite, euphoria, hallucinations at high doses, agitation Treatment: lorazepam for agitation Withdrawal: irritability, agitation, insomnia, nausea Treatment: supportive Unnecessary because not fatal Social implications: maybe amotivational syndrome, gateway drug Physiological changes: low testosterone in men, decreased ovulation in females, low birth weights in neonates, increased neonatal malformations Medical form (dronabinol) used as supportive addition to with chemo (antiemetic) or AIDS treatment (stimulate appetite) Hallucinogens LSD (acid), psilocybin (shrooms), mescaline (peyote) MoA: LSD activates serotonin receptors in the limbic system, neocortex, and brainstem Intoxication: hallucinations, delusions, mydriasis, tachycardia, sweating, ataxia, tremor Euphoria, paranoia → psilocybin Psychosis, flashbacks → LSD Treatment: lorazepam for agitation, haloperidol for psychosis Withdrawal: none Dissociatives PCP, ketamine MoA: both PCP and ketamine block glutamate NMDA receptors Ketamine is used as an anesthetic (NMDA antagonist) Intoxication: dissociation, hallucinations, impulsivity, analgesia, often violent behavior, high BP/HR, miosis, nystagmus, delusions, seizures Benzodiazepines and antipsychotics → PCP Monitor for serotonin syndrome and rhabdomyolysis Alcohol addiction Disulfiram (blocks aldehyde dehydrogenase) Acamprosate (analog of GABA, NMDA receptor antagonist) Naltrexone (opioid antagonist) Endogenous opioid pathways play a key role in pathway that leads to reinforcement for alcohol addiction Opioid addiction Naltrexone (opioid antagonist) Buprenorphine/naltrexone
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Foramina at base of skull
 
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This is a brief video on the foramina at the base of the skull and the important structures that run through them. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Foramina at the base of the skull By Schädelbasis1.jpg: Welleschikderivative work: Mcstrother (talk) - Schädelbasis1.jpg, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=12036569 Inferior view of the skull Anterior cranial fossa Middle cranial fossa Posterior cranial fossa I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. Cribriform plate → olfactory nerve (CN1) Optic canal → optic nerve (CN2), ophthalmic artery Foramen magnum → medulla oblongata, meninges, accessory nerve (CN11), anterior and posterior spinal nerves, vertebral arteries Hypoglossal canal → hypoglossal nerve (CN12) Superior orbital fissure → ophthalmic veins; CN 3, 4, 5.1, and 6 Foramen rotundum → trigeminal nerve, maxillary division (CN5.2) Foramen ovale → trigeminal nerve, mandibular division (CN5.3) Foramen spinosum → middle meningeal artery Jugular foramen → glossopharyngeal, vagus, and accessory (CN 9, 10, and 11), internal jugular vein, occipital artery
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Classes of antibiotics that target bacterial ribosomes
 
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This is a brief overview of antibacterials that target the bacterial ribosomes Aminoglycosides (e.g. streptomycin and gentamicin) Binds 30S subunit, bactericidal Resistance conferred by (1) drug phosphorylation, adenylation, or acetylation; (2) altering ribosome (rRNA methylation or protein mutation); (3) increased efflux Tetracyclines (e.g. tetracycline and doxycycline) Binds 30S subunit, bacteriostatic Resistance conferred by (1) increased efflux or (2) production of ribosome protection proteins Chloramphenicol Binds 50S subunit, bacteriostatic Resistance conferred by inactivating antibiotic with methylation Macrolides (e.g. erythromycin and azithromycin) Binds 50S subunit, bacteriostatic Lincosamides (e.g. clindamycin) Binds 50S subunit Unique because effective against anaerobes Streptogramins A and B Bind 50S subunit, individually bacteriostatic but together they are bactericidal MLSB resistance: erm gene expression to methylate ribosome Oxazolidinones (e.g. linezolid) Bind 50S subunit, bacteriostatic I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor.
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Cardiac Imaging Modalities
 
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This is a brief overview of cardiac imaging modalities and clinical methods of visualizing the heart I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Cardiac Imaging Modalities An overview of the clinical methods of visualizing the heart Chest X-ray Echocardiogram (TTE / TEE) Myocardial Perfusion Imaging MRI Catheterization Cardiac CT Chest X-ray (CXR) Dates back to early 1900s → first used for diagnosing TB Differentiate/resolve objects based on density High density objects (solids: bone, metal) appear white Low density objects (gas, lungs) appear black Water-based tissues somewhere in between Cannot resolve cardiac structures, but see silhouette Use to calculate cardiac ratio Can find lung manifestations of heart disease Pleural edema, pulmonary effusion Cheap, small radiation exposure → used frequently with chest pain presentations Chest X-ray Echocardiogram (TTE / TEE) Myocardial Perfusion Imaging MRI Catheterization Cardiac CT Echocardiogram Ultrasound waves emitted from piezoelectric transducer bounce off tissues; reflected waves are measured → no risk/toxicity, low cost Transthoracic echocardiogram (TTE) or transesophageal echocardiogram (TEE) TEE is gold standard for excluding intracardiac thrombus M mode (one beam) or 2D (multiple beans in arc to capture a beama) or 3D (similar multibeam reconstruction) Doppler echocardiography Visualize blood flow → identify turbulent regions Gold standard for find valvular abnormalities Chest X-ray Echocardiogram (TTE / TEE) Myocardial Perfusion Imaging MRI Catheterization Cardiac CT Myocardial Perfusion Imaging Heavy element radioisotopes (such as thallium-201) are used to mark areas of myocardial perfusion Perfusion is ability to deliver blood to capillaries Imaging the heart when exposed to these markers allows us to identify areas of low perfusion (indicating ischemia) Nuclear stress test → imaging before and after stress Chest X-ray Echocardiogram (TTE / TEE) Myocardial Perfusion Imaging MRI Catheterization Cardiac CT Cardiovascular MRI Noninvasive use of magnetic fields and radio waves to form images of structures in the heart Downside: expensive, exposure to contrast Produces moving and still images Gold standard for assessing cardiac structure and function Chest X-ray Echocardiogram (TTE / TEE) Myocardial Perfusion Imaging MRI Catheterization Cardiac CT Cardiac Catheterization Involves insertion of catheter into the chambers of vessels of the heart Allows for therapy (stents) and diagnostics Downsides: radiation exposure, expensive, invasive (albeit minimally) Right heart cath → insert through vein (femoral) to measure right heart, pulmonary artery pressures Gold standard for assessing intracardiac pressures and cardiac output Left heart cath → insert through artery to measure left heart pressures, insert dye for coronary angiography Coronary angiography is gold standard for visualizing coronaries and identifying stenosis Chest X-ray Echocardiogram (TTE / TEE) Myocardial Perfusion Imaging MRI Catheterization Cardiac CT Cardiac CT Computed tomography of the heart: extensive heart x-ray Used to assess extent of coronary stenosis Visualize thoracic aorta Benefits: less invasive than catheterization, produces 3D models Drawbacks: still requires radiation exposure, contrast that damages kidneys Chest X-ray Echocardiogram (TTE / TEE) Myocardial Perfusion Imaging MRI Catheterization Cardiac CT
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Anti-obesity medication
 
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This is a brief video on pharmacologic agents that help reduce weight or control weight. I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Anti-obesity medication Pharmacological agents that reduce weight or help control weight Phentermine Orlistat Phentermine/ topiramate Lorcaserin Bupropion/ naltrexone Liraglutide By James Heilman, MD - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=4854133 Phentermine Approved by FDA in 1959 Mechanism: releases norepinephrine Short term use (3 to 6 months) Not approved for long term use Cheap Phentermine Orlistat Phentermine/ topiramate Lorcaserin Bupropion/ naltrexone Liraglutide Orlistat Approved by FDA in 1999 Mechanism: inhibits lipase (gastric and pancreatic) Therefore, decrease in fat breakdown and absorption Side effects: GI disturbance (cramps, fecal incontinence, diarrhea (specifically steatorrhea)), fat soluble vitamin deficiency (vitamins DEAK) → give multivitamins Good for CAD patients or those at risk for CVD Available over-the-counter Phentermine Orlistat Phentermine/ topiramate Lorcaserin Bupropion/ naltrexone Liraglutide Phentermine/topiramate Approved by FDA in 2010 Phentermine mechanism: releases norepinephrine Topiramate mechanism: blocks Na channels, modulates GABA receptor to increase action Used for migraine prophylaxis and seizures (simple, complex, tonic-clonic) Side effects: mental sedation, kidney stones Phentermine Orlistat Phentermine/ topiramate Lorcaserin Bupropion/ naltrexone Liraglutide Lorcaserin Approved by FDA in 2012 Mechanism: agonists serotonin (5-HT2C) receptor Side effects: dizziness, dry mouth, GI disturbance (nausea, vomiting, diarrhea), fatigue, headaches Phentermine Orlistat Phentermine/ topiramate Lorcaserin Bupropion/ naltrexone Liraglutide Bupropion/naltrexone Approved by FDA in 2014 Bupropion mechanism: increase norepinephrine and dopamine levels Naltrexone mechanism: opioid antagonist Side effects: anxiety, headaches Good for patients also struggling with smoking cessation (bupropion approved for smoking cessation) Phentermine Orlistat Phentermine/ topiramate Lorcaserin Bupropion/ naltrexone Liraglutide Liraglutide Approved by FDA in 2015 Mechanism: agonizes the GLP-1 receptor (GLP-1 analog) Subcutaneous injection Side effects: pancreatitis, nausea, vomiting Phentermine Orlistat Phentermine/ topiramate Lorcaserin Bupropion/ naltrexone Liraglutide
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Cause of Huntington's disease
 
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Genetic basis of Huntington's disease Slides: https://docs.google.com/presentation/d/1WREGKnFosqjF7V2v0AKQaxymvGMA7E0bgQ6Ic3-WHyE/edit?usp=sharing I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Huntington’s disease Cause of the genetic neurodegenerative disorder Cause of Huntington’s disease Repetitive sequences in the human genome Microsatellite instability Severity depends on repeat count Repetitive sequences in human genome Satellite DNA Section of repeated base pair sequence GCG ATC GCG ATC GCG ATC GCG ATC Microsatellite Repeat sequence of four or less base pairs CAG CAG CAG CAG CAG CAG CAG CAG Cause of Huntington’s disease Repetitive sequences in the human genome Microsatellite instability Severity depends on repeat count Microsatellite instability Microsatellite at beginning of huntingtin gene: Repeat of CAG codon produces poly-glutamine Microsatellite expansion → unstable ... aag tcc ttc cag cag cag cag cag cag cag cag ... ... Lys Ser Phe Gln Gln Gln Gln Gln Gln Gln Gln ... Cause of Huntington’s disease Repetitive sequences in the human genome Microsatellite instability Severity depends on repeat count instability is thought to occur from polymerase slippage during DNA replication Severity depends on repeat count Higher repeat count results in earlier onset Hereditary Considered autosomal dominant (50%) Cause of Huntington’s disease Repetitive sequences in the human genome Microsatellite instability Severity depends on repeat count
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Ectopic pregnancy
 
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This is a brief video on ectopic pregnancies, or a pregnancy occurring outside the uterus. I created this presentation with Google Slides. Images were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor. ADDITIONAL TAGS: Ectopic pregnancy Ectopic pregnancy in open Fallopian tube, ~7 weeks gestational age By Ed Uthman, MD (Flickr, Wikipedia) - (2014). "Tubal pregnancy with embryo". WikiJournal of Medicine 1 (2): 7. DOI:10.15347/wjm/2014.007., Public Domain,https://commons.wikimedia.org/w/index.php?curid=840032 Pregnancy outside of the uterus Definition: embryo attaches outside the uterus Most commonly occur in the ampulla of fallopian tube, but can occur in other parts of tube, ovary, cervix, myometrium or within the abdomen Ectopic embryos can grow and create pressure or invade surrounding tissues Overview Overview Presentation Causes Diagnosis Management Symptoms: Classic symptoms: abdominal/pelvic pain, vaginal bleeding Pain can be sharp, dull, and/or crampy, often mimicking appendicitis Bleeding 6 weeks after last menstrual period Tender cervix, adnexal mass, or adnexal tenderness Symptoms of pregnancy: nausea, vomiting, urination, fatigue, breast tenderness Destruction / rupture of fallopian tubes: Rupture: abdominal distention, generalized tenderness, peritonitis, and hypovolemic shock (low BP, high HR, feeling cold) Presentation Overview Presentation Causes Diagnosis Management Damage to Fallopian tubes and/or hair-like cilia in internal surface of tubes Pelvic inflammatory disease / salpingitis resulting in scarring (most common) Infertility IUD use Exposure to DES Tubal surgery (ligation) Intrauterine surgery (D&C) Smoking Previous ectopic pregnany Endometriosis Causes / risk factors Overview Presentation Causes Diagnosis Management Overview Presentation Causes Diagnosis Management By Mikael Häggström, from original by BruceBlaus - File:Blausen 0602 Laparoscopy 02.png, CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=32779153 Overview Presentation Causes Diagnosis Management A "blob sign", which consists of the ectopic pregnancy. The ovary is distinguished from it by having follicles, whereof one is visible in the field. This patient had an intrauterine device (IUD) with progestogen, whose cross-section is visible in the field, leaving an ultrasound shadow distally to it. By Mikael Häggström.When using this image in external works, it may be cited as:Häggström, Mikael (2014). "Medical gallery of Mikael Häggström 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 2002-4436. Public Domain.orBy Mikael Häggström, used with permission. - Own work, CC0, https://commons.wikimedia.org/w/index.php?curid=32779152 Perform transabdominal/transvaginal ultrasound: ↪ If intrauterine gestational sac present in uterus → not ectopic pregnancy ↪ If gestational sac present elsewhere (ring of fire with color Doppler d/t increased vascular flow to adnexa) → ectopic pregnancy ↪ If no gestational sac seen, perform quantitative serum hCG: ↪ If serum hCG 1500-2000 → treat like ectopic pregnancy (should be able to see intrauterine pregnancy) ↪ If serum hCG 1500-2000 → too soon to tell → perform serial hCG: ↪ Repeat hCG in 48 hours: ↪ If hCG doubles → intrauterine pregnancy → routine care, evaluate other causes of symptoms ↪ If hCG fails to double → ectopic pregnancy Ruptured ectopic pregnancy: Stabilize with fluids, blood, pressors OR for salpingectomy (remove tube) Unruptured ectopic pregnancy: Stabilize, OR for salpingostomy (unblock tube) If hCG 3000, gestational size 3.5 cm, no fetal heart tones Medical management: methotrexate +/- leucovorin Management Overview Presentation Causes Diagnosis Management Uterus in blue arrows Bleeding ectopic pregnancy in red arrows By Mikael Häggström - File:Ectopic pregnancy1981.jpg by Urskalberer81, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=31193206 By Urskalberer81 - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=29204493 Salpingectomy
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