Medical Disorders of the Liver (old version, with sound) - CRASH! Medical Review Series

[@pwbmd]

@ - I am referring here to an exudation, not a transudation. A transudation is a hydrodynamic process resulting in ascites w/ a SAAG > 1.1. An exudation is caused by, among other things, failed integrity of the vasculature, resulting in fluid and other components making their way into the ascitic fluid. Hence the SAAG in an exudate will be < 1.1 (ascitic fluid is more like serum).

[@kay5667-u2h]

You are awesome... God richly bless you... You raising a generation of brilliant doctors world wide... Your work is highly appreciated.. Pls know that..

[@Khaled-io9bz]

13:40 When the vessels leak not only fluid but protein and cells as well (as in cases of infection and tumour) it's called EXUDATION, not transudation.

[@kegsl4639]

PBC affects mainly the intra-hepatic bile ducts,whereas PSC affects both the extra-hepatic and intra-hepatic ducts. This is another important distinguishing point between both

[@heyitsmedima]

i think spider angioma is due excess estrogen in circulation (failure of liver to metabolize estrogen), not due to portal hypertension. caput medusae is due to portal hypertension.

[@vaibhavsharma4529]

Don't you mean that the SMV and IMV together with the Splenic Vein form the Portal Vein and it is the Hepatic Vein that leaves the Liver draining into IVC ?

[@lenkaanderson6875]

Thank you Paul! Getting ready for my NP boards. Great help - I can listen to your videos while driving or waiting somewhere. Thank you so much!!!

[@ildikotorok7529]

Excellent videos - Thanks so much!! I especially like the review questions of each subject.

[@ishratjahan5594]

Excellent presentation... so helpful!!!

[@meto2854]

Brilliant vids, thank you! Just one important thing, I think it is safe to say you meant EXUDATE, instead of TRANSUDATE? An exudation is one caused by TB, cancer or inflammation. I didn't hear you correct it in your narration.

[@kay5667-u2h]

Yeah it true.. I realized that as well... Slip of mind probably.. But excellent all true out

[@aimeequaifes175]

My health was horrible because I was diagnosed with Hepatitis B and I felt like there was no hope for my health because I was told there was no cure. But today I am here to let everyone know that there is a herbal medicine to cure Hepatitis B and other diseases because I was able to get rid of my Hepatitis B with the help of Dr.Auchi on KZbin channel herbal remedies..✅

[@ShazWorkout]

Thank you so much for the clear cut differentiation between PBC and PSC!

[@tjenzinger10]

thank you so much for all these videos!!!! you have helped me so much!!! this will help me help my patients. paying it forward!!! thank you so much!!

[@woloabel]

Thursday, October 27, 2022. Gastroenterology: Medical Disorders of the Liver (Hepatopathy [Cirrhoses]): Anatomy and Physiology of the Liver. The Liver is Localized to the Right Upper Quadrant of the Abdomen where it serves the functions of 1) Detoxification (Nitrogen Waste Metabolism and Deactivation of Pharmacologic Agents) and 2) Synthesis of Albumin (Most Abundant Serum Protein and vital for Oncotic Pressure Maintenance), 3) Coagulation Factor Synthesis (II, V, VII, X), 4) Portal Tract Venous Hub (Lower Body Venous Return to Right Atrium). Pathology of the Liver is Multiple, but the End-Stage Disease is Usually Characterized by Fibrosis of the Liver Tissue (Parenchyma) called Cirrhosis, pathogenesis of Acute Inflammation progressing to Chronic Inflammation and multiple possible Complications therein. This Pathologic State interferes with Proper, normal Liver function and Manifests with Portal Hypertension. US Epidemiology of Cirrhosis attributes Alcoholism as the Primary Aetiologic Factor of End-Stage Liver Disease, an irreversible and uncurable state (Treatment is usually Symptomatic only) along with other less common Causes. There is an undeniable Association of Hepatocellular Carcinoma Malignancy in Cirrhosis. SSx: 1) Ascites (Fluid in the Peritoneum/Cx: Spontaneous Bacterial Peritonitis [SBP] has Fever And/or Abdominal Pain), 2) Edema (Fluid in the Interstitium), 3) Hemorrhage/Bleeding, 4) Asterixis (Hand Flapping on Px; Cx: Hepatic Encephalopathy [Hyperammonemia/Azotemia]), 5) Decreased Capacity to Metabolize Pharmacologic Agents, 6) Splenomegaly (Portal Hypertension is Venous Blood Backup in the Liver), 7) Hemorrhoids, 8) Spider hemangiomata, 9) Varices, 10) Susceptibility to Vibrio vulnificus and Yersinia spp Infections (Opportunistic Infections). The Serum Albumin-Ascites Gradient (SAAG) is the difference between Albumin in the Serum and Albumin in the Ascitic Fluid. The SAAG Assessment is via a Periocentesis Procedure. When the SAAG is High (> 1.1) the cause of Ascites is Portal Hypertension (A High Portal Pressure). If SAAG is Low (< 1.1), then Transudation (Multiple Possible Causes: TB, Cancer, Infection, amongst others) is the ongoing Pathophysiology, where Albumin is Free to Enter the Ascitic Fluid, usually due to Exudation/Extravasation of Cells and Protein. Cirrhosis has a High SAAG Score (> 1.1) due to the Portal Hypertension. In SBP, Periocentesis with White Blood Cell (WBC) Analysis (Positive if WBC > 500) is the Modality of Diagnosis. Tx is via 1) Third Generation Cephalosporins IV Antibiotics (Ceftriaxone or Cefotaxime) for 10-14 Days. 2) Albumin Transfusion is also Available. 3) ICU Admission is Standard of Care. 4) Repeat Periocentesis. Diseases with Cirrhosis: 1) Alcoholic Cirrhosis is due to Alcoholism (MCC), 2) Chronic Hepatitis is an Infection Localized to the Liver (Ax: HBV and HCV are MCC) which progress to Chronic Inflammation and Fibrosis (Hepatocyte Necrosis). SSx: 1) Asymptomatic until Cirrhotic Stage. Risk Factors for these Bloodborne Infections are 1) IV Drug Use, 2) High-Risk Sexual Practices, 3) Needle sticks and 4) Occupational Hazards of Healthcare. Dx is via Hepatitis Titers (Serology; aka Hepatitis Panel [Antigen/Antibody Assessment]) where the Presence of Hepatitis B Surface Antigen (HBsAg) for Hepatitis B is Diagnostic; and for HCV Infection the Presence of Anti-Hepatitis C Virus Antibodies (Anti-HBV Abs) and a Positive Viral Load is Diagnostic for HCV Infection. Tx for both HBV and HCV Infection involves Interferon-Alpha, a therapeutic recombinant cytokine. HBV gets Antivirals Lamivudine, an Antiretroviral/Nucleoside Reverse Transcriptase Inhibitors (NRTI)/Hepatitis B Treatment/Nucleoside Analogs (Antiviral), and Adefovir, a Hepatitis B Treatment Nucleotide Analogs (Antiviral). HCV get Ribavirin, a Hepatitis C Nucleoside Analog. HBV Prophylaxis is also available for the Prevention of HBV Infection via Vaccination (HCV has no Prophylactic Therapy). 3) Primary Sclerosing Cholangitis (PSC) is an Idiopathic Inflammation of the Biliary Ductal System resulting in Cholestasis (Elevation of Alkaline Phosphatase) and is Associated with Inflammatory Bowel Disease (IBD), an Indirect Cause of Fibrosis of the Liver. SSx: 1) Non-specific Symptomatology, 2) Fatigue, 3) Pruritus (Hypersensitivity to Hyperbilirubinemia), 4) Jaundice 5) Malabsorption (Diarrhea/Steatorrhea) is Possible due to the Inability to Emulsify Lipids, and 6) Cirrhotic Symptoms are Possible. Laboratories: 1) Normal Aspartate Aminotransferase/Aspartate Transferase and Alanine Aminotransferase (AST/ALT in BMP/CMP) because initially Hepatocytes are unaffected, 2) Elevated Alkaline Phosphatase (ALP) and Gamma-Glutamyltransphosphatase (GGTP). Dx: Antimitochondrial Antibodies (AMA) Titers are Negative. Endoscopic Retrograde Cholangiopancreatography (ERCP), an endoscopic and minimally invasive procedure (with X-Ray Visualization) or Transhepatic Cholangiogram are definitive Examinations. Tx is Bile Acid-Binding Resins (Cholestyramine with Sugar) or Antihyperlipidemia/Bile Acid Sequestrants, and 2) Liver Transplant (Curative). SSx: 4) Primary Biliary Cirrhosis (PBC) is an Autoimmune Inflammatory Disorder of the Biliary Duct System similar to PSC. The Cholestasis ultimately involves the Liver and has an End-Stage Pathogenesis of Cirrhosis. The Epidemiology is predominately middle-aged Females and has an Association with other Autoimmune Pathologies (Sjögren’s Syndrome [Gland Involvement], Rheumatoid Arthritis, Systemic Lupus Erythematosus, Hashimoto's Thyroiditis, et al). SSx: 1) Non-specific Symptomatology, 2) Fatigue, 3) Pruritus (Hypersensitivity to Hyperbilirubinemia), 4) Jaundice 5) Malabsorption (Diarrhea/Steatorrhea) is Possible due to the Inability to Emulsify Lipids, and 6) Cirrhotic Symptoms are Possible. This pathology maybe Asymptomatic. Laboratories: 1) Normal Aspartate Aminotransferase/Aspartate Transferase and Alanine Aminotransferase (AST/ALT in BMP/CMP) because initially Hepatocytes are unaffected, 2) Elevated Alkaline Phosphatase (ALP) and Gamma-Glutamyltransphosphatase (GGTP). Dx: 1) Antimitochondrial Antibodies (AMA) Titers are Positive (Unlike PSC) and 2) Liver Biopsy will make the definitive Diagnosis. Tx is Identical to PSC. 5) Hemochromatosis is Autosomal Recessive Congenital Disease of Iron Metabolism leading to excessive Absorption and Deposition of Iron Primarily in the Liver, Heart and Pancreas. Iron in Excess will damage Hepatocytes and ultimately cause Fibrosis/Cirrhosis of the Liver amongst other Organ Systems (Multiple Organ Dysfunction [MOD] is Possible via this Disease Process). SSx: 1) Cirrhosis and other Cirrhotic Symptoms, 2) Restrictive Cardiomyopathy involves the Heart; 3) Arthralgia when Deposition of Iron is in the Joints; 4) Hyperpigmentation of the Skin; 5) Diabetes Mellitus (DM) when Iron is Excessively Deposited in the Pancreas; 6) Hypogonadism if this Disease Process Involves the Gonads. A Family History (FHx) of 1) Cirrhosis, 2) Liver Cancer (Malignancy), 3) Liver Problems/Disease is Important in the Investigation Process of this Pathology. Dx is via Iron Studies, namely 1) Iron Levels (High), 2) Ferritin (High), 3) Total Iron-Binding Capacity/Transferrin (TIBC) will be Low. 2) Liver Biopsy will be a Definitive Examination (Extensive Hepatocellular Siderosis and Iron Staining shows Extensive Iron Accumulation). Tx is via 1) Phlebotomy (Most Effective Measure) is the withdrawing of Blood via a Venipuncture (Ferritin Level Reduction), 2) Iron Chelation via Chelating Agents (Deferoxamine) is also a viable Treatment. The Subjects with Hemochromatosis are at Increased Risk of Infections with Vibrio vulnificus and Yersinia spp (Diarrhea causing Bacteria). 6) Alpha-1 Antitrypsin Deficiency, 7) Wilson's Disease is a Rare Autosomal Recessive Congenital Disease (Genetic Aetiology [ATP7B Copper Transporter Gene]) of Copper Absorption, Secretion, and Deposition. Excessive Copper Deposition occurs in all Tissues of the Body (Liver, Eyes and Brain are best Known Organs). Copper overload and Deposition is toxic to the Liver yielding a Fibrotic Liver (Cirrhosis). SSx: 1) General Cirrhotic Symptoms, 2) Kayser-Fleischer Ring is Pathognomonic for Wilson's Disease (A Brown to Green Pericorneal and Iris Ring on Eyes). It is visible via a Slit Lamp Illumination; 3) Brain Deposition Leads to Movement Symptoms (Parkinson-like Gait or Tremor, Muscle Cramps) and Psychoses (Depression, Irritability, Anger et al). Therefore, a clinical Scenario of 1) Cirrhosis/Hepatocellular Carcinoma (HCC), and 2) Psychiatric Symptoms should alert the Medical Indagator of this Pathology. Family History (FHx) is an essential Diagnostic Modality: 1) Psychiatric History, 2) Liver Pathology (Problems), and/or 3) Liver Cancer (Malignancy) can assist the Diagnostic Process. Dx is via Copper Studies: 1) Serum Ceruloplasmin (Low) Level, a Copper Transporter Protein, 2) Serum Copper Level (High). 3) Liver Biopsy will be the Definitive Diagnostic Method (1) Micro- and Macrovesicular Hepatic Steatosis, 2) Glycogenated Nuclei in the Periportal Hepatocytes, and 3) Focal Hepatocellular Necrosis. Pathogenesis: 1) Progression of parenchymal Damage and Inflammation, 2) Fibrosis, and subsequently Cirrhosis, invariably develop [End-Stage Liver Disease]). Tx is via Penicillamine (Copper Chelation), A Chelating Agent of Copper. Complications of Cirrhosis: 1) Hepatocellular Carcinoma, 2) Hepatorenal Syndrome (HRS). MD Paul Bolin, es geht gut aber Googlatu schwach kann nur sein. Heil!

[@luysion]

Hey paul, thanks again for the video been going through all of yours! just a question regarding the low ceruloplasmin levels, I've read this is due to reduced synthesis of ceruloplasmin by the liver due to the damage to the liver that occurs in Wilson's disease as a consequence of copper accumulation (due to defective transport into the bile)? some sources also state - "High serum copper is not an indication of Wilson disease. Since most Wilson patients have a low ceruloplasmin they actually have a lower than normal serum copper. Ceruloplasmin is the protein that binds with copper to remove it from the body. It is the unbound (to ceruloplasmin) copper that is free to roam around the body and accumulate in organs causing Wilson disease damage." Just wanted your opinion on this, thanks :)

[@luysion]

***** Thank you! :)

[@aimeequaifes175]

My health was horrible because I was diagnosed with Hepatitis B and I felt like there was no hope for my health because I was told there was no cure. But today I am here to let everyone know that there is a herbal medicine to cure Hepatitis B and other diseases because I was able to get rid of my Hepatitis B with the help of Dr.Auchi on KZbin channel herbal remedies..✅

[@luysion]

Hey thanks so much for doing these videos! they really are an incredible resource - - was just wondering if we could get a copy of the powerpoints too to print off and annotate while we listen to your videos? I understand if you wish to not share these just thought id ask. Thanks :)

[@Mirak7]

U r Awesome!! Thanks alot!! ur all videos are amazing!

[@rreshidi6301]

Awesome video but KF rings or on Decemt's membrane of cornea not iris

[@ThePokemon098]

i see a lot of people pointing out 2,5,7 and 10 as the factors produced by the liver. doesnt it produce every single one except 8 and, obviously, calcium?

[@surendrakanankege]

A very good lecture

[@samualloy]

**SAAG

[@kay5667-u2h]

Yeah I just realized that was a mistake

[@goksusaygili9280]

I think it should've been primary biliary cholangitis instead of sclerosis at 28:30 (formerly known as primary biliary cirrhosis)

[@aronautodidacte8419]

Think you for the lectures , please can you do some one about dermatology

[@ripalripal7550]

hi poul as you said in the intial part in SAAG lecture REGARDING THE trasudation,both fluid and albumin leaks through capillaries.BUT I dont think so,,in transudative due to increase in starling forces lots of fluid escape from vascular compartment to interstitial compartment without injury to endithelial cells(no permeability) that fluid is protein poor fluid..

[@a311yaga4]

Hey! Paul bolin why ur new versions have no sound

[@ShazWorkout]

The labs are what kill me in hepatobiliary disease. I was wondering if you could please enlighten me on what the AST, ALT, Alk phos, GGTP, bilirubin are for Hemochromatosis, Wilsons dx, alpha 1 antitrypsin deficiency. Oh and also the bilirubin for PSC and PBC.

[@mushihussain6633]

perfect thank you

[@nobushinoworwolski5062]

Thank you!

[@Wargoat6]

Typo @ 30:19 , in the slide title. Should be "PBS."

[@DrPompiliu]

Exudate* Great videos though! Thanks!