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Year 5 Chemical Pathology > 11: LFTs and Cases > Flashcards

11: LFTs and Cases Flashcards

1
Q

6 major functions of the liver

A
  1. Intermediary metabolism
  2. Xenobiotic metabolism
  3. Bile synthesis
  4. Protein synthesis
  5. Hormone metabolism
  6. Reticulo-endothelial
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2
Q

Intermediary metabolism: functions

A

enzyme-catalysed processes within cells that extract energy from nutrient molecules and use that energy to construct cellular components:

Functions:

  • glycolysis, glucose synthesis, FA synthesis, glycogen storage, AA synthesis, liporprotein metabolism
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3
Q

Consequences of acute liver failure (3)

A

Hypoglycaemia (due to lack of glycogen)

Lactic acidosis (as can no longer metabolise lactic acid)

Increase in ammonia (cannot process AAs)

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4
Q

Xenobiotic metabolism (chemical modification)

A
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5
Q

Xenobiotic metabolism (chemical modification)

A
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6
Q

Hormone metabolism

A

vit D hydroxylation (25-hydroxylase)

steroid hormones (conjugated and excreted)

peptide hormones (catabolism)

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7
Q

Bile synthesis: constituents, functions

A

Constituents

  • water, phospholipids, drugs and metabolites, bile salts/acids, cholesterol, BR, proteins

Functions

  • excretion
  • micelle formation
  • digestion

BR metabolism and transport

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8
Q

BR metabolism and transport

A
  • Red cells are broken down releasing heme, iron and globin
  • The heme then goes on to form bilirubin → bound to albumin in the plasma
  • This uBR goes to the liver and becomes glucuronidated (conjugated)
  • The conjugated bilirubin is released into the bile
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9
Q

Reticulo-endothelial

A

Kupffer cells:

  • clearance of infection and LPS
  • antigen presentation
  • immune modulation (i.e. cytokines, etc.)

Erythropoiesis

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10
Q

markers of liver damage

markers of synthetic function

tumour marker

A
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11
Q

markers of liver damage

markers of synthetic function

tumour marker

A
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12
Q

Liver architecture

A
  • blood comes up portal vein
  • goes throughs sinusoids
  • into central vein
  • bile canaliculi run in other direction
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13
Q

liver damage and zones

A
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14
Q

liver damage and zones

A
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15
Q

ALT and AST

A

Location

  • liver = hepatocytes
  • other = muscle, kidney, bone + pancreas but in small amounts

Catalyse transfer of alanine and aspartate to alpha-keto group of alpha-ketoglutarate → pyruvate and oxaloacetate formation

AST rises more in alcohol and cirrhosis

  • AST:ALT ratio >2 = alcoholic liver disease (S = SHOTS)
  • In absence of alcohol, AST:ALT >0.8 = advanced fibrosis or cirrhosis
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16
Q

GGT

A

Catalyses transfer of the gamma-glutamyl group from gamma-glutamyl peptides such as glutathione to other peptides and to L-amino acids

Locations:

  • liver = hepatocytes, bile duct (epithelium)
  • other = kidney, pancreas, spleen, heart, brain and seminal vesicles

Elevated in chronic alcohol use, in bile duct disease, and hepatic metastases

  • can also rise in response to medications
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17
Q

ALP

A

Catalyse hydrolysis of large number of organic phosphate esters at alkaline pH (precise function is UNKNOWN)

Locations:

  • liver (isoenzyme) = bile ducts (sinusoidal and canalicular membranes)
  • other = BONE, PLACENTA, small intestine, kidney, WBCs

Markedly elevated in…

  • obstructive jaundice
  • bile duct damage
  • pregnancy
  • bone disease
18
Q

Albumin: (amount synthesised and half-life), function, when is it low/raised, relation to clotting cascade

A

8-14g/day, 20 days (long half-life)

main contributor to ONCOTIC PRESSURE and BINDS to steroids/drugs/BR/calcium

low in:

  • low production states (CLD, malnutrition) - chronic course (not acute)
  • increased loss (nephrotic syndrome)
  • sepsis (3rd spacing - when endothelium leaky, to albumin leaks into tissues)

Raised in = causes of acute abdomen (i.e. acute pancreatitis)

clotting cascade:

  • PT (or INR) is a marker of ACUTE liver function (as BR half-life is 20 days)
19
Q

AFP: what is it, role, raised in?

A

Glycoprotein of the albumin superfamily

Involved in foetal transport, immune regulation/tolerance

In the FOETUS it is made by:

  • Yolk sac
  • GI epithelium
  • Liver

In ADULTS, the concentration is low, and it has no apparent function

Raised in:

  • Hepatocellular carcinoma (may rise late or not at all)
  • Hepatic damage/regeneration
  • Pregnancy
  • Testicular cancer
20
Q

BR

A

interpret in contact of other liver enzymes

also, image the biliary tree:

  • dilated ducts = gallstones, cancer, etc.
  • non-dilated ducts → other tests → ?biopsy
21
Q

Causes of jaundice

A
22
Q

Causes of jaundice

A
23
Q

Urine dipstick tests

A

BR = should be NONE in urine (only cBR can be found in urine when bile duct blocked or cBR spills back into circulation → dark urine)

Urobilinogen = breakdown of BR in intestines by bacteria. Soluble so enters enterohepatic circulation, some excreted in small amounts in urine

  • Urobilinogen in urine ABSENT in obstructive jaundice
  • Urobilinogen in urine PRESENT normally
  • Urobilinogen in urine INCREASED in haemolysis, hepatitis, sepsis (more BR -→ more uroBR)

Pale stools/dark urine = feature of obstructive jaundice

  • high cBR and no stercobilinogen
24
Q

What is in a liver panel?

A
25
Q

What is in a liver panel?

A
26
Q

ALT raised in isolation → fatty liver disease

A
26
Q

ALT raised in isolation → fatty liver disease

A
27
Q

3 ways of measuring liver function

A

Dye tests = indocyanine green/bromsulphalein

Breath tests = aminopyrine/galactose (carbon 14)

Serum bile acids = elevated esp. in cholestasis (10-100x in cholestasis of pregnancy, 25x in PBC/PSC)

28
Q

Causes of low urea

A

Severe liver disease, (synthesised in liver), malnutrition, pregnancy

29
Q

Causes of raised urea (x10 ULN)

A

Upper GI bleed (or large protein meal)

Dehydration/AKI (urea excreted renally)

30
Q

When is ALP normal in a bone condition?

A

Plasma cells suppress osteoblasts, hence ALP is normal in myeloma

31
Q

summary of liver enzymes

A
32
Q

summary of liver enzymes

A
33
Q
A

Gilbert’s syndrome

34
Q
A
  1. Drug-induced cholestasis from Augmentin
35
Q
A

pancreatic adenocarcinoma (head)

36
Q
A

acute hepatitis A

37
Q

3 things that make ALT go over 1000

A
  1. Toxins (paracetamol)
  2. Viruses (i.e. hepatitis viruses)
  3. Ischaemia (e.g. post-resuscitation)
38
Q

liver function test results in cirrhosis, acute liver failure, cholestasis, alcohol abuse

A
39
Q

Albumin and clotting factors summary (synthetic hepatocellular dysfunction)

A
40
Q

BR processing

A
41
Q

pre-hepatic, hepatic, post-he[atioc

A

Year 5 Chemical Pathology (18 decks)

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