BRS MOCK 3 - Liver failure, genitourinary, regulation gut, physiology and pulmonary Flashcards

1
Q

What is cholestasis?

A

Slow/cessation of bile flow.

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2
Q

What does cholestasis cause?

A

Jaundice.

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3
Q

What causes prehepatic jaundice?

A

Haemolysis, massive transfusion, large haematoma reabsorption, ineffective erythropoiesis

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4
Q

What are the 3 principle causes of intrahepatic jaundice?

A

Decreased uptake of bilirubin, decreased conjugation of bilirubin (decreased processing) and decreased secretion of bilirubin.

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5
Q

What can cause intrahepatic cholestasis?

A

Sepsis, total parenteral nutrition.

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6
Q

What is liver failure?

A

Rate of hepatocyte death is greater than regeneration.

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7
Q

What are the two ways in which hepatocytes can die?

A

Apoptosis and necrosis.

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8
Q

What can liver failure cause?

A

Hepatic encephalopathy, coagulopathy, ascites, hypoglycemia (due to impaired glycogen production), increased risk of infection (due to lack of globulin production).

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9
Q

Biomarkers for liver failure?

A

Reduced albumin and increased prothrombin time.

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10
Q

2 causes of acute liver failure?

A

Toxins, inflammation.

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11
Q

2 causes of chronic liver failure?

A

Inflammation and alcohol abuse.

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12
Q

Liver cirrhosis mechanism?

A

Factor (e.g alcohol abuse) causes necrosis of hepatocytes. Enzyme leak (e.g lysosomal enzymes) causes release of cytokines. This results in activation of kupffer cells, granulocytes and lymphocytes which results in release of cytokines and growth factors. Hepatic stellate cells gets converted to myofibroblasts and macrophages form fibroblasts. Extracellular matrix deposit which results in fibrosis.

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13
Q

What causes ascites in liver failure?

A

Low albumin production.

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14
Q

What can ascites result in?

A

Reduction in plasma volume causes second degree hyperaldosteronism which causes hypokalemia which causes intracellular acidosis, this activates ammonium formation in proximal tubules, and this results in systemic alkalosis.

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15
Q

What coagulation factors does hepatocytes not make?

A

VWF, factor VIII.

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16
Q

Why does liver failure cause coagulopathy which can lead to bleeding?

A

Reduction in clotting factor synthesis.

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17
Q

How does cholestasis result in coagulopathy?

A

Decrease in fat absorption and fat soluble vitamins due to lack of bile in intestine. Reduced absorption of vitamin K which is a fat soluble vitamin can result in reduced carboxylation of vitamin K depending clotting factors which leads to coagulopathy and bleeding.

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18
Q

What are the mechanisms that lead to cholestasis?

A

Canalicular dilation, decreased cell membrane fluidity of hepatocytes, biliary transporter insertion on wrong side of hepatocyte, increase in tight junction permeability and decreased mitochondrial ATP synthesis.

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19
Q

Consequences of cholestasis?

A

Pruritus (itching), cholesterol deposition around eyes and cholangitis (inflammation of bile duct system).

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20
Q

What does portal hypertension in liver failure cause?

A

Splenomegaly which results in thrombocytopenia (caused by platelet pooling). Oesophageal varices. Exudative enteropathy.

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21
Q

What are 3 thing that cause bleeding in liver failure?

A

Decrease in active clotting factors, thrombocytopenia and varices.

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22
Q

What is exudative enteropathy?

A

When albumin and other protein-rich materials leak into your intestine.

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23
Q

What does exudative enteropathy result in?

A

Bacteria feed on plasma proteins leading to liberation of ammonium which can cause hyperammoniemia which leads to encephalopathy and alkalosis.

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24
Q

What is a prehepatic cause of portal hypertension?

A

Portal vein thrombosis.

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25
Q

What is a post hepatic cause of portal hypertension?

A

Right heart failure, constrictive pericarditis.

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26
Q

How does your body counterregulate portalhypertension? What is the consequence of this?

A

Secretes vasodilators. Drop in blood pressure but increase in cardiac output resulting in hyperperfusion of abdominal organs and varices.

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27
Q

Why does varices occur?

A

Blood not being taken away by portal vein and so pressure builds up in thin wall collateral vessels (close by vessels) and these can rupture.

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28
Q

What is child pugh score used for?

A

To assess severity of liver disease and peri-operative mortality.

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29
Q

How to treat liver failure?

A

Reduce protein intake and phosphate enemas (empties bowels) for encephalopathy. Dextrose and calcium gluconate for hypoglycaemia and hypocalcaemia. Haemofiltration for renal failure. Albumin and vasoconstrictors for hypotension. Vitamin K, FFP and platelets for bleeding. Antibiotics for infection.

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30
Q

What cells are found in the late distal convoluted tube and collecting duct?

A

principal and intercalated cells

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31
Q

Which parts of a nephron are low in mitochondria?

A

Thin descending and ascending loop of henle, principal cells.

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32
Q

What nephron has its loop of henle extends deep into inner medulla?

A

juxtamedullary nephron.

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33
Q

What cells are present in the juxtaglomerular apparatus?

A

Juxtaglomerular cells, extraglomerular mesangial cells, macula densa.

34
Q

What are the macula densa cells part of?

A

Distal convoluted tube

35
Q

What are the cell junctions between podocytes in the bowman’s space called? What can pass through these junctions?

A

Slit diaphragm. Water and small solutes.

36
Q

How does myogenic autoregulation regulate GFR if arterial pressure increases?

A

Afferent arteriole experiences stretch. Smooth muscle in afferent arteriole contracts and resistance in blood vessel increases. Blood flow reduces and so GFR stays the same.

37
Q

How does tubulo-glomerular feedback mechanism regulate GFR if GFR rises?

A

Increase in GFR. Increase in sodium chloride in loop of henle. Change detected by macula densa. Increase in ATP release. Adenosine removed from ATP and so increase in adenosine released. This signal results in constriction of arteriole. Blood flow reduces and GFR therefore stays the same.

38
Q

Why is creatinine not as good as inulin?

A

Small amount of creatinine is secreted into nephron. Needs to be adjusted when calculating GFR.

39
Q

Creatinine levels that can indicate renal failure?

A

High plasma creatinine or low creatinine clearance.

40
Q

What does a molecule need to fulfil to be used for renal plasma flow?

A

Molecule is removed from plasma via filtration and secretion.

41
Q

What molecule is used for renal plasma flow?

A

Para aminohippurate

42
Q

How to calculate filtration fraction?

A

GFR / RPF

43
Q

What is filtration fraction?

A

Ratio of plasma which is filtered.

44
Q

What will be the concentration of creatine in the efferent arteriole if the concentration in the afferent arteriole is 1.5 mmol/L?

A

1.5 mmol/L.

45
Q

How does sodium and bicarbonate reabsorption occur in early proximal convoluted tube?

A

Carbonic acid converted to carbon dioxide and water by carbonic anhydrase in tubular fluid. CO2 enters duct cell by diffusion. Carbon dioxide and water in duct cell is converted to H+ and bicarbonate in cell by carbonic anhydrase. H+ diffuses out into tubular fluid and sodium diffuses into cell by Na+H+ antiporter. Sodium and bicarbonate enter blood by sodium bicarbonate symporter.

46
Q

What allow for passive movement of water into medullary interstitum in descending portion of henle’s loop?

A

Hyperosmotic due to lots of salt.

47
Q

Osmotic nature of fluid in ascending portion of loop of henle? Why?

A

Hypoosmotic as only sodium moves out into medullary interstitum as ascending portion is impermeable to water.

48
Q

How is sodium and chloride reabsorbed in the thick ascending limb?

A

Sodium, chloride and potassium ions enter via symporter into duct cell. Potassium and chloride exit into blood via symporter on basolateral membrane. Sodium reabsorbed into blood via sodium potassium atpase.

49
Q

What is the function of intercalated cells?

A

Maintaining acid-base balance

50
Q

What is the function of alpha intercalated cells?

A

Bicarbonate reabsorption and H+ secretion.

51
Q

What is the function of beta intercalated cells?

A

Bicarbonate secretion and H+ reabsorption.

52
Q

What pumps are involved in intercalated cells?

A

Chloride bicarbonate antiporter and H+ ATPase.

53
Q

What is the function of principal cells?

A

Sodium reabsorption and potassium secretion.

54
Q

What is hirschsprung’s disease? What does it result in?

A

Congenital absence of ganglion of myenteric and submucosal. Enlarged colon.

55
Q

What stimulates release of gastrin?

A

Amino acids and peptides present in the lumen of the stomach. Gastric distention and vagus nerve.

56
Q

What does gastrin do?

A

Stimulates gastric acid secretion by parietal cells. Trophic (growth) effects on mucosa layer.

57
Q

What would you seen in a gastrinoma?

A

Ulcer (too much acid) and hypertrophy of stomach wall.

58
Q

What does secretin do?

A

Pancreatic and biliary bicarbonate secretion. Inhibits gastrin. Inhibition of gastric emptying. Trophic effect on the exocrine pancreas.

59
Q

What stimulates release of CCK?

A

Fat and peptides in upper small intestine.

60
Q

What does CCK do?

A

Stimulates pancreatic enzyme release. Stimulates gallbladder contraction and relaxation of sphincter of oddi. Delays gastric emptying and decreases food intake.

61
Q

What stimulates release of GIP?

A

All 3 macronutrients.

62
Q

What cells secretes GIP and where are these cells located?

A

K cells in duodenum and jejunum.

63
Q

What does GIP do?

A

Stimulates insulin secretion.

64
Q

What cells release GLP-1 and where is it released?

A

L cells and small intestine.

65
Q

What stimulates release of GLP-1?

A

Hexose and fat.

66
Q

What does GLP-1 do?

A

Increases sensitivity of pancreatic beta cells to glucose. Induce satiety.

67
Q

What does pancreatic polypeptide do?

A

Induce satiety.

68
Q

What stimulates pancreatic polypeptide release?

A

Fat

69
Q

What does peptide YY do?

A

Reduce intestinal motility, gallbladder contraction and pancreatic exocrine secretion.

70
Q

What cells release peptide YY? When is it released?

A

L cells after digestion.

71
Q

What does vasoactive intestinal peptide do?

A

Relaxation of gut smooth muscle.

72
Q

What do enkephalins do?

A

Increase smooth muscle tone.

73
Q

Blood tests that indicate thromobosis?

A

D dimer and fibrinogen levels.

74
Q

How to calculate heart rate using small squares method?

A

1500 / number of small squares between consecutive R waves.

75
Q

Normal FVC and low FEV1 indicate what?

A

Restrictive lung disease.

76
Q

What does a crescendo decrescendo murmur indicate?

A

Atrial stenosis (valve narrowing).

77
Q

Key difference in flow volume loops in obstructive and restrictive?

A

Indented curve in obstructive.

78
Q

Normal flow volume loop with blunted inspiratory curve is known as what?

A

Variable extrathoracic obstruction.

79
Q

Normal flow volume loop with blunted expiratory curve is known as what?

A

Variable intrathoracic obstruction.

80
Q

Normal flow volume loop with blunted expiratory curve and inspiratory curve is known as what?

A

Fixed airway obstruction.