Dr. Gerald Diaz @GeraldMD
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Board Certified Internal Medicine Hospitalist, GrepMed Editor in Chief πŸ‡΅πŸ‡­ πŸ‡ΊπŸ‡Έ - Sign up for an account to like, bookmark and upload images to contribute to our community platform. Follow us on IG: https://www.instagram.com/grepmed/ | Twitter: https://twitter.com/grepmeded/
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Autoimmune Hemolytic Anemia (AIHA) - Differential Diagnosis Table

Warm AIHA (48-70%)
Cold AHA (16-32%)
 β€’ Donath-Landsteiner HA (paroxysmal
Autoimmune Hemolytic Anemia (AIHA) - Differential Diagnosis Table Warm AIHA (48-70%) Cold AHA (16-32%) β€’ Donath-Landsteiner HA (paroxysmal cold hemoglobinuria) β€’ Cold Agglutinin Disease Mixed-type AIHA (7-8%) DAT-negative AIHA Matthew Ho, MD PhD @MatthewHoMD #Autoimmune #Hemolytic #Anemia #AIHA #Differential #Diagnosis #Table #hematology
Tongue Pathology 

Geographic tongue, fissured tongue, and hairy tongue are the most common tongue problems and
Tongue Pathology Geographic tongue, fissured tongue, and hairy tongue are the most common tongue problems and do not require treatment. Median rhomboid glossitis is usually associated with a candidal infection and responds to topical antifungals. Atrophic glossitis is often linked to an underlying nutritional deficiency of iron, folic acid, vitamin B12, riboflavin, or niacin and resolves with correction of the underlying condition. Oral hairy leukoplakia, which can be a marker for underlying immunodeficiency, is caused by the Epstein-Barr virus and is treated with oral antivirals. Tongue growths usually require biopsy to differentiate benign lesions (e.g., granular cell tumors, fibromas, lymphoepithelial cysts) from premalignant leukoplakia or squamous cell carcinoma. Burning mouth syndrome often involves the tongue and has responded to treatment with alpha-lipoic acid, clonazepam, and cognitive behavior therapy in controlled trials. Tongue lesions of unclear etiology may require biopsy or referral to an oral and maxillofacial surgeon, head and neck surgeon, or a dentist experienced in oral pathology. Recognition and diagnosis of tongue abnormalities require examination of tongue morphology and a thorough history, including onset and duration, antecedent symptoms, and tobacco and alcohol use. A complete head and neck examination, with careful assessment for lymphadenopathy, is essential. Satyendra Dhar MD, @DharSaty #tongue #Geographictongue, #fissuredtongue, #hairytongue #Medianrhomboidglossitis #candida #Atrophicglossitis #Oralhairyleukoplakia
Strangulated herniated lung after penetrating thoracic trauma

Dr. Mohammed Mar'ae Asiri @Asiritrauma1

#hernia #lung #herniated #trauma #clinical #video
Strangulated herniated lung after penetrating thoracic trauma Dr. Mohammed Mar'ae Asiri @Asiritrauma1 #hernia #lung #herniated #trauma #clinical #video #physicalexam
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Hepatojugular (Abdominojugular) Reflux on Physical Exam

Dr. Bruno Farnetano @bruno.farnetano

#Hepatojugular #Reflux #HJR #PhysicalExam #clinical #video #cardiology #abdominojugular
Hepatojugular (Abdominojugular) Reflux on Physical Exam Dr. Bruno Farnetano @bruno.farnetano #Hepatojugular #Reflux #HJR #PhysicalExam #clinical #video #cardiology #abdominojugular #AJR
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Chronic SVC Stenosis with Caudal Blood Flow of Dilated Abdominal Veins

60 y/o hx of seizures &
Chronic SVC Stenosis with Caudal Blood Flow of Dilated Abdominal Veins 60 y/o hx of seizures & cirrhosis presenting after seizure & found to have distended abdominal wall veins. What is the cause? Pay Attention to the direction of Venous Flow -> may suggest site of venous obstruction. Normal venous flow in the abdomen is typically Cephalad (towards the head) above the navel and Caudad (towards the feet) below the navel. For practical use: the maneuver should be performed both above and below the umbilicus. - Portal HTN- flow is always AWAY from the umbilicus 2/2 development of the portosystemic collaterals - SVC & IVC obstructions can also lead abdominal vein distention! - IVC obstruction - flow will be cephalad (towards SVC) - SVC obstruction - flow will be caudad (towards IVC) Though this pt does have cirrhosis, venous flow was dominantly caudad not typical for portal hypertension suggesting a possible SVC obstruction. CT imaging showed chronic stenosis of his SVC and additional lumbar & paraseophageal collaterals. Dr. Patrick Fadden @ptfaddenMD #Milking #SVC #syndrome #Stenosis #obstruction #abdominal #veins #Clinical #Video #Chest #PhysicalExam #Epigastric #Veins
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Demonstrating Rostral Venous Flow of Caput Medusae in Portal Hypertension

We do the milking method as depicted
Demonstrating Rostral Venous Flow of Caput Medusae in Portal Hypertension We do the milking method as depicted in the video. The direction of relatively quicker flow is the direction! In this case the direction of flow is away from the umbilicus. Dr. Arun Valsan @DrArunKValsan #Caput #Medusae #Portal #Hypertension #PhysicalExam #Milking #abdominal #clinical #video #flow #direction #veins #cirrhosis #hepatology
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Cryofibrinogenemia Summary

Cryofibrinogenemia Epidemiology:
 β€’ 40-70 years with a modest female predominance

Cryofibrinogenemia:
 β€’ The precipitation of a
Cryofibrinogenemia Summary Cryofibrinogenemia Epidemiology: β€’ 40-70 years with a modest female predominance Cryofibrinogenemia: β€’ The precipitation of a complex when plasma is cooled from the normal body temperature of 37Β°C to the near-freezing temperature of 4Β°C. β€’ This precipitating complex contains fibrinogen, fibrin, fibronectin, small amounts of fibrin split products, albumin, immunoglobulins and other plasma proteins which can plug blood vessels. β€’ Cryofibrinogen is distinguished from cryoglobulin (CG) since, it precipitates only in plasma and not in serum. β€’ Cryoglobulins precipitate in serum + plasma Cryofibrinogen - Cryofibrinogen is a cold insoluble complex of: β€’ Fibrin β€’ Fibrinogen β€’ Fibrin split products with: - Albumin - Cold insoluble globulin - Factor VIII - Plasma proteins Cryofibrinogenemia Symptoms: β€’ Asymptomatic or combination of: - Hyperviscosity, - Vascular reactivity (Skin necrosis) - Thrombosis (Thrombotic vasculopathy) β€’ Paradoxical spontaneous bleeding may occur due to the depletion of clotting factors Cryofibrinogenemia Can Be Divided Into Two Types: 1. Primary (essential) 2. Secondary form associated with autoimmune diseases, malignancies, vasculitis, sepsis or cryoglobulinemia Associated Disorders: β€’ Malignancy β€’ Infections including coronavirus disease 2019 (COVID-19) β€’ Inflammatory processes: β€’ Systemic rheumatic diseases β€’ Thromboembolic conditions Cryofibrinogenemia Clinical Manifestations - Findings may include: β€’ Cold sensitivity β€’ Painful ulcers β€’ Skin necrosis β€’ Purpura β€’ Livedo reticularis β€’ Painful or pruritic erythema (perniosis) of the extremities β€’ Arthralgias β€’ Raynaud phenomenon β€’ Simulates calciphylaxis clinicopathologically, - Related conditions: Stroke, myocardial infarction, limb and bowel ischemia or infarction, thrombophlebitis, pulmonary emboli, and ocular thrombi including retinal arterial and/or venous occlusions, as well as gangrene Cryofibrinogenemia Diagnosis: β€’ + Clinical findings/Presentation β€’ Asymptomatic: Plasma (CF) cryofibrinogen levels < than 50 mg/L - Significant levels >1g/L β€’ Negative cryoglobulins β€’ Negative causes of secondary cryofibrinogenemia. β€’ Biopsy: Typical pathologic findings on biopsy of affected tissue β€’ Angio: Occlusion of small to medium-sized arteries β€’ Secondary CF: Presence of associated disease Cryofibrinogenemia DDX: β€’ Calciphylaxis β€’ Cryoglobulinemia β€’ TTP, HUS and HIT β€’ Antiphospholipid syndrome β€’ Warfarin-induced skin necrosis β€’ DIC β€’ Septic emboli β€’ Frostbite β€’ Atherosclerotic PVD β€’ Atheroemboli #Cryofibrinogenemia #diagnosis #rheumatology #hematology
Weakness - Differential Diagnosis Framework

Approach To Weakness:
 β€’ Non-neuromuscular disorder (Cardiac, pulmonary etc)
 β€’ CNS ->
Weakness - Differential Diagnosis Framework Approach To Weakness: β€’ Non-neuromuscular disorder (Cardiac, pulmonary etc) β€’ CNS -> PNS -> NMJ -> Muscle β€’ Muscle weakness (generalized, distal, proximal, or localized) 1. Upper Motor Neuron Impairment: β€’ Acute stroke syndromes β€’ Space occupying lesions of the central nervous system: Brain tumor β€’ Lesions of the spinal cord β€’ Inflammatory: Vasculitis β€’ Infectious: Brain abscess β€’ Toxic/drug: Radiation β€’ Metabolic/endocrine: Vitamin B12 deficiency β€’ Congenital leukodystrophies 2. Lesions Of The Peripheral Nervous System: β€’ Symmetric polyneuropathy: DM β€’ Mononeuropathy: Nerve compression β€’ Mononeuritis multiplex (DM, Vasculitis-polyarteritis nodosa) β€’ Toxic/drug: Lead β€’ Neoplastic: Paraneoplastic syndrome β€’ Inflammatory: Myeloma/amyloid β€’ Infectious: Leprosy 3. Neuromuscular Junction: β€’ Exercise-induced weakness: Fatiguability - Consider NMJ β€’ Nerve Side Presynaptic: - Lambert-Eaton - Isaacs' syndrome - Tick-paralysis - Botulism - Aminoglycosides - Envenomation (venom from animal bites) β€’ Synaptic Cleft: - Organophosphate toxicity - Carbamate toxicity β€’ Muscle Side: - Postsynaptic: Myasthenia Gravis - Lack of UMN/LMN signs - Lack of sensory changes - Common pattern: Symmetric proximal weakness Myopathy: β€’ Inflammatory disorders: Polymyositis β€’ Immune mediated necrotizing myopathy β€’ Autoimmune: Inclusion body myositis β€’ Endocrinopathies: Hypothyroid β€’ Metabolic myopathies: Hypoglycemia β€’ Drugs and toxins: Steroids, Statins, amiodarone, Alcohol β€’ Infections: - Viral - Influenza, parainfluenza, Coxsackie, HIV, CMV, EBV - Bacterial - Pyomyositis, Lyme myositis β€’ Rhabdomyolysis β€’ Neoplastic: Malignancy-associated myositis β€’ Genetic: Muscular dystrophies Work Up: β€’ Chem: CPK aldolase, lactate dehydrogenase, and the aminotransferases β€’ Serology: - Anti-Ro/SSA, anti-La/SSB, anti-Sm, and anti-RNP - (Myositis) anti-histidyl-t-RNA synthetase [anti-Jo-1] - (Vasculitis) ANCA titers, hepatitis B and C serologies, and cryoglobulins β€’ PNS, NMJ, Nerve: Nerve conduction and electromyographic (EMG) studies β€’ MRI: Inflammation of the muscle β€’ Muscle Biopsy: Dermatomyositis, polymyositis, inclusion body myositis, certain drug-induced myopathies, the muscular dystrophies, or vasculitis #Weakness #Differential #Diagnosis #neurology
Irritable Bowel Syndrome (IBS) Treatment Options
Amitiza (Lubiprostone)
Antidepressants: Celexa, Wellbutrin, Prozac, Paxil, Nortriptyline, and Zoloft
Bentyl (Dicyclomine)
Creon
Ducolax
Imodium, Maalox,
Irritable Bowel Syndrome (IBS) Treatment Options Amitiza (Lubiprostone) Antidepressants: Celexa, Wellbutrin, Prozac, Paxil, Nortriptyline, and Zoloft Bentyl (Dicyclomine) Creon Ducolax Imodium, Maalox, Kaopectate (Loperamide) Levsin (Hyoscyamine) Librax (Chlordiazepoxide and Clidinium) Linzess (Linaclotide) Lotronex (Alosetron) Marijuana Miralax (Polyethylene glycol) Nexium (Esomeprazole), Protonix (Pantoprazole), Prevacid (Lansoprazole), Prilosec (Omeprazole) Reglan (Metoclopramide) Rifaxamin (Xifaxan) Viberzi (Eluxadoline) Zantac (Ranitidine) #irritable #bowel #syndrome #ibs #diarrhea #constipation #management #pharmacology #table
Modified penicillin binding proteins as mechanism of resistance to antibiotics.
Penicillin Binding Proteins (Transpeptidases) cross link peptidoglycan
Modified penicillin binding proteins as mechanism of resistance to antibiotics. Penicillin Binding Proteins (Transpeptidases) cross link peptidoglycan which stabilizes the cell wall - Beta-lactam antibiotics like PCN and cephalosporins bind PBPS active site and block this function - Vancomycin blocks the process by binding the terminal D-Ala, D-Ala Resistance: - Streptococcus pneumoniae will modify the PBPS so that PCN does not bind as well. THIS CAN BE OVERCOME: - Giving more antibiotic (e.g. high dose amox for an ear infection) - Switch to cephalosporin (e.g. CTX for a complicated pneumonia or pneumonia in unvaccinated) - Add vancomycin to CTX (e.g. pneumococcal meningitis) RESISTANCE: - Methicillin resistant Staphylococcus aureus makes a different transpeptidase which functions even in presence of PCNs or cephalosporins. - Vancomycin again remains active as it works at a different site. #Penicillin #Binding #Proteins #AMR #PBP #pharmacology #antibiotics #resistance