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GRACE Phase 2a Medicine > Liver > Flashcards

Liver Flashcards

1
Q

95% of paracetamol at a therapeutic concentration is excreted how? What happens to the other 5%?

A

Conjugated (sulfation or glucuronidation) to form a non-toxic metabolite which is readily excreted

Other 5% is oxidised by CYP450 to form NAPQI which is a toxic metabolite. This then undergoes conjugation to make it into a readily excretable substance

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2
Q

What happens in paracetamol overdose?

A

Build up of toxic metabolite NAPQI, leading to hepatic necrosis

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3
Q

Symptoms of paracetamol overdose?

A

Nausea, vomiting, RUQ pain

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4
Q

Mx of paracetamol overdose?

A 
Activated charcoal (gastric decontamination)
IV NAC (N-acetylcysteine)
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5
Q

6 types of hernia?

A

Inguinal, femoral, hiatus, epigastric, incisional, umbilical

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6
Q

Inguinal hernia - direct and indirect

A

Indirect (80%) - protruded through the opening of the inguinal canal (deep ring)
Direct (20%) - protrudes through a weak spot

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7
Q

Risk factors for inguinal hernia?

A

Male, chronic cough, heavy lifting, past abdo surgery

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8
Q

Px of inguinal hernia

A

Swelling of groin, painful, inducible

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9
Q

Ix for hernias?

A

Clinical, MRI, USS, CT

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10
Q

Femoral hernia Px

A

mass in medial upper thigh, irreducible and likely to strangulate

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11
Q

Hiatus hernia

A

Stomach protrudes through the oesophageal hiatus in the diaphragm - sliding (80%), rolling (20%)

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12
Q

Sliding hiatus hernia (80%)

A

Gastrooesophageal junction (GOJ) slides up through the hiatus, LOS is less competent

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13
Q

Rolling hiatus hernia (20%)

A

GOJ remains in the abdomen, part of the fundus rolls UP through the hiatus, therefore the LOS is intact, reflux is UNCOMMON

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14
Q

Px of rolling hiatus hernia?

A

Heartburn, GORD, dysphagia

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15
Q

Ix for hiatus hernia?

A

Barium swallow, endoscopy

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16
Q

MX for hiatus hernia?

A

Lose weight, PPI, surgery

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17
Q

What is acute pancreatitis?

A

Disease due to acute inflammation in the pancreas characterised by self-perpetuating pancreatic enzyme mediated auto-digestion

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18
Q

Epidemiology of acute pancreatitis?

A

80% mild cases, 20% –> life-threatening disease, 12% mortality

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19
Q

Causes of acute pancreatitis? (I GET SMASHED)

A 
Idiopathic
Gallstones (40%)
Ethanol (25%)
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidaemia
ERCP
Drugs e.g. NSAIDs
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20
Q

Pathophysiology of acute pancreatitis?

A

Release of precursor digestive enzymes which are activated within the pancreas and cause autodigestion of pancreatic tissue, triggering recruitment of inflammatory cells and release of inflammatory mediators. This increases vascular permeability –> oedema

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21
Q

Px of acute pancreatitis?

A

Nausea/vomiting, sudden epigastric pain (may radiate to back), diarrhoea, tachycardia

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22
Q

Ix for acute pancreatitis

A

Raised serum amylase/lipase, ABG, USS

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23
Q

Glasgow criteria

A

Predicts severity of pancreatitis - 3 or more factors –> transfer to ITU

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24
Q

Nutritional management for pancreatitis?

A

Nil by mouth, NJ feeding, urinary catheter

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25
Q

Mx for acute pancreatitis

A

Assess severity using Glasgow score, nil by mouth, urinary catheter, analgesia, monitor, ERCP if gallstone pancreatitis

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26
Q

Complications of acute pancreatitis?

A

Shock, ARDS, renal failure, hyperglycaemia

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27
Q

Px of chronic pancreatitis?

A

Epigastric pain radiates through to the back and is relieved by sitting forward/hot water bottles, severe weight loss, bloating, steatorrhoea, brittle diabetes

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28
Q

Ix for chronic pancreatitis?

A

US and CT scan - pancreatic calcifications

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29
Q

Mx of chronic pancreatitis?

A

analgesia, pancreatic enzyme supplements, no alcohol, surgical resection

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30
Q

What is hereditary haemochromatosis?

A

Autosomal recessive inherited disorder characterised by excessive iron storage in tissues –> organ failure, caused by mutation of human haemochromatosis gene

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31
Q

Px of hereditary haemochromatosis?

A

Hyperpigmentation (bronzed skin), painful joints, hair loss, sexual dysfunction, chronic fatigue, memory/mood disturbances

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32
Q

Dx of hereditary haemochromatosis?

A

Serum ferritin and transferrin saturation, genetic testing, liver biopsy

33
Q

Mx of hereditary haemochromatosis?

A

Venesection, genetic screening

34
Q

What is Wilson’s disease?

A

Autosomal recessive disorder characterised by abnormal copper deposition, presenting with liver and neuropsychiatric symptoms

35
Q

Cause of Wilson’s disease?

A

Mutation in the ATP7B gene which encodes for the copper-transporting P-type ATPase found in hepatocytes

36
Q

copper-transporting P-type ATPase

A

key protein in maintaining copper homeostasis, coded for on the ATP7B gene

37
Q

Px of Wilson’s disease

A

Hepatic problems - hepatitis, cirrhosis
Cognitive problems - memory loss, decreased IQ, depression, decreased libido
CNS problems - Parkinsonism (tremor, bradykinesia, dysarthria, rigidity - BUT symmetrical)
Kayser-Fleischer ring in eye

38
Q

Kayser-Fleischer ring

A

copper deposit in the cornea, ring around eye, sign of Wilsons disease

39
Q

Ix for Wilson’s disease

A

Serum caeruloplasmin (main carrier of Cu) serum copper, 24hr urinary copper excretion, liver biopsy

40
Q

Mx of Wilson’s disease

A

Copper chelation - penicillamine, liver transplants, genetic testing

41
Q

Alpha-1 antitrypsin

A

Enzyme released by hepatocytes that inhibits neutrophil elastase, breaking down bacteria, lines the alveoli

42
Q

Alpha-1 antitrypsin deficiency

A

autosomal recessive disorder causing liver/lung damage due to a mutation in the A1AT gene

43
Q

Mutation causing abnormal A1AT

A

Polymerises and forms deposits within hepatocytes –> cellular destruction –> cirrhosis

44
Q

Mutation causing lack of/no A1AT

A

Does not affect liver, lungs are are risk of elastase mediated damage since not inhibited by A1AT, breaks down elastin in alveoli –> emphysema –> COPD

45
Q

Ix for A1AT?

A

Low serum A1AT levels

46
Q

Mx for A1AT deficiency?

A

supportive, treat underlying disease, stop smoking

47
Q

What % of liver tumours are secondary? where do they commonly metastasise from?

A

90%, lungs, breast, stomach, colon

48
Q

two common primary malignant liver tumours?

A

HCC, cholangiocarcinoma

49
Q

two common primary benign liver tumours?

A

haemangioma, hepatic adenoma

50
Q

PX of liver tumours?

A

RUQ pain, fever, malaise, weight loss, late jaundice (except cholangiocarcinoma), hepatomegaly, abdominal mass

51
Q

Rapid development of liver tumour symptoms is indicative of which type of cancer?

A

HCC

52
Q

Ix for liver tumours?

A

Bloods - FBC, clotting, LFTs, alpha-fetoprotein
CT and biopsy
US

53
Q

When is alpha-fetoprotein raised?

A

In liver cancer due to high hepatocyte turnover

54
Q

What underlying disease is almost always present in HCC?

A

Cirrhosis

55
Q

Risk factors for HCC?

A

Cirrhosis, Hep B, C, Aflatoxin, Betel nut chewing, alcohol, smoking

56
Q

Mx of HCC?

A

Surgical resection, liver transplant

57
Q

Cholangiocarcinoma

A

Biliary tree cancer

58
Q

What is raised in cholangiocarcinoma?

A

Bilirubin –> jaundice, ALP

59
Q

haemangiomas

A

Commonest benign tumour, usually found incidentally, no treatment is required

60
Q

hepatic adenomas

A

associated with anabolic steroids, COCP, surgical resection only required if symptomatic or >5cm

61
Q

Pancreatic adenocarcinomas

A

Often inoperable by time of presentation, metastasise early, present late, asymptomatic through development, most common pancreatic cancer

62
Q

Pancreatic adenocarcinomas arise from what type of epithelium?

A

Ductal

63
Q

Where are pancreatic adenocarcinomas located within the pancreas?

A

70% head, 20% body/tail

64
Q

PX of pancreatic adenocarcinoma?

A

Head - obstructive jaundice, pale stools, dark urine

Body/tail - epigastric pain that radiates to the back

65
Q

Mx of pancreatic adenocarcinoma

A

analgesia, nutrition, emotional support, resectable if caught early

66
Q

Increased serum bilirubin is associated with

A

liver abnormalities

67
Q

Pale stools + dark urine =

A

cholestatic jaundice

68
Q

What is Budd-Chiari syndrome?

A

Vascular liver disorder due to obstruction of hepatic venous outflow, characterised by the classic triad of:
Ascites
Hepatomegaly
Abdominal pain
Syndrome due to a variety of underlying causes that cause obstruction anywhere from the small hepatic venules –> IVC at the R atrium

69
Q

Triad of symptoms in Budd-Chiari syndrome?

A

Ascites, hepatomegaly, abdominal pain

70
Q

Dx of Budd-Chiari syndrome?

A

Imaging - 1st line = doppler US, then CT/MRI

71
Q

Acute cholangitis - px (charcots triad)

A
  1. RUQ pain
  2. Fever
  3. Jaundice
72
Q

How would you treat alcohol withdrawal?

A

Diazepam

73
Q

What is primary sclerosing cholangitis?

A

Immune mediated disease causing progressive inflammation of the intra- and extra-hepatic bile ducts, –> cholestasis (poor flow), hepatic fibrosis (scarring) and bile duct strictures (narrowing)

74
Q

What disease is primary sclerosing cholangitis strongly associated with?

A

IBS

75
Q

Symptoms of primary sclerosing cholangitis?

A

Fatigue, itching, jaundice

76
Q

Why do you get itching with liver disease?

A

Increase in bile salts under your skin –> causes itching

77
Q

Pruritus?

A

itching

78
Q

mx of primary sclerosing cholangitis?

A

Liver transplant is the only effective tx

79
Q

What causes median arcuate ligament syndrome?

A

Compression of the coeliac artery by the MAL, causing abdominal pain, may be related to meals

GRACE Phase 2a Medicine (20 decks)

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