Miscellaneous Lectures Flashcards
(64 cards)
Give an systematic overview of how to examine an abdominal radiograph fully.
“**View Patients Adequately, And Give Very Many Chances to Be Living”
https://drive.google.com/file/d/16eneW0nmwgXi9bVNQ_2JGIS94hTpvjqg/view?usp=sharing
(Above for detailed slides of lecturer)
What are the four types of carbohydrate metabolism executed by the liver?
Glycogenesis: Glucose ⟶ glycogen Stimulated by insulin
Glycogenolysis: Glycogen ⟶ glucose Stimulated by glucagon and adrenaline
Gluconeogenesis: Lactate/amino acids/glycerol ⟶ glucose
(when glycogen reserves are depleted)
Glycolysis: Glucose ⟶ pyruvate
(releases energy in the form of ATP and NADH)
What is emulsification (of ingested fats)?
The breakdown of fat globules in the duodenum into tiny droplets, which provides a larger surface area on which the enzyme pancreatic lipase can act to digest the fats into fatty acids and glycerol.
Emulsification is assisted by the action of the bile salts:
3 types of which:
- Cholic Acid
- Taurocholic Acid
- Deoxycholic Acid
Give an outline of the breakdown and excretion of Bilirubin
1: Macrophages destroy old or damaged erythrocytes in the spleen and liver
2: Haem is oxidised to biliverdin via haem oxygenase
3: Biliverdin is reduced to unconjugated bilirubin via biliverdin reductase
4: Unconjugated bilirubin + albumin → Conjugated bilirubin
(Unconjugated bilirubin is water insoluble, so Albumin binds to unconjugated bilirubin in the bloodstream to make it soluble)
5: Conjugated bilirubin is then modified by gut bacteria (Glucuronic Acid is removed) to form urobilinogen
6:
- 80% urobilinogen is excreted in faeces as stercobilin (brown colour)
- 18% urobilinogen returns to enterohepatic circulation
- 2% urobilinogen is excreted in urine as urobilin (yellow colour)
What is Jaundice? And when is it detectable?
Jaundice describes a yellow discoloration of the sclera and skin.
It is detectable clinically when serum bilirubin > 50 µmol/L
Draw a table of the most common causes - primary and secondary - of jaundice, and the types of jaundice they case
What are the main roles of the Liver?
- Carbohydrate Metabolism
- Protein Metabolism
- Lipid Metabolism
- Clotting Factor Synthesis
- Drug Metabolism
- Production of Bile
- Bilirubin Metabolism
- Alcohol Metabolism
Give an overview of protein synthesis:
- Deamination and transamination of amino acids
- Synthesis of various plasma proteins, including:
- Albumin
- CRP (an infection marker)
- Blood clotting factors
- Angiotensinogen
- Transferrin
- Opsonin
- Complement Proteins
- Thrombopoietin
Synthesis of glucose and lipids from the carbohydrate backbone of amino acids
- Excretion of ammonia (toxic) via urea cycle
- Ammonia buildup ⟶ hepatic encephalopathy*
Draw a table outlining the metabolism of paracetamol
NOTES
Glucuronidation is a conjugation reaction whereby glucuronic acid, is covalently linked to a substrate containing a nucleophilic functional group.
Sulfation is a conjugation reaction that entails the addition of SO₃ group
Outline the treatment for Paracetamol poisoning
What are the signs and symptoms of paracetamol poisoning?
Explain the pathogenesis of Liver cirrhosis
Cirrhosis Definition
- Chronic liver injury leading to chronic inflammation
- Extensive fibrosis (scar tissue)
- Presence of regenerative nodules
Inflammation/Fibrosis
Alcohol consumption increases numbers of gram -ve bacteria in GI lumen
Leads to increase in LPS in blood stream
Kupferr cells in the liver have TLR (Toll-like receptors), activated by LPS
They secrete the following cytokines:
TNF-a
IL 1a/b
IL 6
IL 12
This attracts macrophages, and activates Hepatic Stellate cells
The HS cells produce collagen, whilst also secreting IL 8 , attracting neutrophils
Neutrophils + Macrophages + Collagen:
INFLAMMATION/FIBROSIS
Steatosis
Alcohol/ethanol is converted to acetaldehyde by alcohol dehydrogenase.
Acetaldehyde is then converted to acetate.
This process produces excess NADH which:
- Shunts carbohydrate pathway: Pyruvic acid converted to lactic acid
- Shunts lipogenic pathway: ↑ production of lipids, fatty acids and glycerol.
Chronic alcohol consumption (>10 years) leads to:
↑ Fatty acid synthesis, ↓ fatty acid oxidation Formation of scar tissue + STEATOSIS (excess fat build-up)
INFLAMMATION + FIBROSIS + STEATOSIS leads to irreversible cirrhosis.
What are the main roles of the liver?
How is Acute Liver Injury defined?
Severe liver injury with hepatocyte necrosis, with rapid onset
Tested by: Diminished hepatic function
- Coagulopathy (INR > 1.5)
- Hepatic encephalopathy
Assumes no pre-existing liver disease
Draw the diagram to explain in basic terms the onset of Hepatic Encephalopathy
What constitutes stages 1-4 of hepatic encephalopathy, and what three types of it are there in terms of severity/timing?
What is the difference in complications of Acute and Chronic Liver failure?
Chronic includes: Ascites, Varices, and Renal involvement becomes hepatorenal syndrome
What are different features and prognosis for Acute, Hyperacute and Subacute Liver failure?
Draw a diagram of the effects of Liver failure on different areas of the body
Give an overview of the Child-Pugh scoring system. What does each element measure?
What is the difference between compensated and decompensated cirrhosis?
Compensated: An asymptomatic phase
Decompensated: The development of complications from portal hypertension and/or liver dysfunction, termed decompensated cirrhosis.
The transition has been estimated to occur at a rate of 5%-7% per year. I
n recent years this process has been proposed as a series of critical steps that if unchecked, culminate in hepatic decompensation[1].
Draw the demeaco classification of liver failure with accompanying mortality rate percentages
What does the MELD score include that the Child-Pugh score doesn’t?
It includes Serum Creatinine measurements, to assess renal involvement
Give an overview of the development of Ascites
Liver Cirrhosis leads to an increase in portal venous pressure
In addition, NO production leads to vasodilation of the splanchnic arterial system
Lymph production is increased proximal to the point of arterial obstruction, eventually overwhelming the capacity of lymphatic drainage and transudate moves across the liver, mesentery and intestines and into the peritoneal cavity.
Splanchnic vasodilation leads to renal hypoperfusion, activating the RAAS system leading to the development of hyperaldosteronism
This leads to increased sodium and water retention, and as the excess fluid is continuously leaking into the peritoneal cavity, the process of underfilling continues in a vicious cycle.
