GI + HPB Flashcards

1
Q

name some common drugs that undergo extensive FPM

A
aspirin
levodopa
lidocaine
morphine
propranalol
salbutamol
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2
Q

name 3 ways in which liver impairment can affect drug metabolism

A

1) drug accumulation due to less metabolic activity
2) decreased active drug availability due to decreased active-metabolite
3) increase in free active drug due to hypoalbunaemia

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3
Q

phenytoin is not a hepatotoxic drug - T or F

A

F

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4
Q

it is safe to give anti TB drugs in liver failure - T or F

A

F

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5
Q

what is extraction ratio?

A

the % of drug in the blood that is removed each time it goes through the liver.

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6
Q

how does extraction ratio affect drug doses in liver failure

A

in oral medication

if high extraction ratio - must reduce both loading dose and maintenance dose

if low extraction ratio - reduce maintenance dose, but keep loading dose same

in IV medication

keep loading dose the same, but reduce maintenance dose

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7
Q

how to investigate suspected c diff

A

c diff stool test

flexi sig

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8
Q

management of C diff

A

14 days metronidazole, if not vancomycin

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9
Q

differentials diarrhea

A
gastroenteritis
c diff
pancreatitis
alcoholic gastritis
IBD
ischaemic bowel
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10
Q

further investigations of diarrhea if suspecting cancer

A

flexi sig
faecal calprotectin
faecal elastase
CT abdomen

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11
Q

causes of secondary constipation

A
opiates, iron, CCB
neurological damage
dietary
mechanical obstruction - cancer, stricture, painful anus
metabolic 
endocrine
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12
Q

what are metabolic causes of constipation

A

high or low calcium
low potassium
low mg

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13
Q

2 endocrine causes of constipation

A

hypothyroidism

diabetes

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14
Q

when to investigate further in constipation

A

if over 40 years old or

iron def anaemia, associate red flag symptoms

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15
Q

4 types of laxatives

A

bulk forming - ispaghula husk
osmotic - macrogol
stimulant - senna
stool softeners - docusate

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16
Q

how to go about management constipation

A

1st line - ispaghula husk
2nd line - macrogol
if not then add stimulant

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17
Q

how to manage opioid induced constipation?

A

osmotic and stimulant laxative

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18
Q

what must patient be encouraged to do when given bulk forming laxative?

A

drink water

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19
Q

what is a common contraindication of laxatives

A

intestinal obstruction

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20
Q

what blatchford score is indicative of further investigation needed

A

> 0

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21
Q

what is dyspepsia

A

loose term describing symptoms of

epigastric pain (heartburn)
nausea, vomiting
bloating, fullness

22
Q

what are some redflags in dyspepsia

A
weight loss
upper GI bleed
vomiting
anorexia
dysphagia
haematemesis
23
Q

causes of peptic ulcer disease

A
h pylori
nsaid use
stress
long term steroid use
smoking
alcohol
24
Q

symptoms of PUD

A
dyspepsia
epigastric pain
gastric bleeding
weight loss
anaemia
25
Q

how can upper GI bleeding present

A

haematemesis

malaena

26
Q

what 2 scoring systems used in pud/gastric bleeding

A

blatchford and rockall

27
Q

differential diagnoses of PUD

A
ulcer
pancreatitis
gastric cancer
reflux
gall stones
MI
28
Q

how to manage PUD?

A

if under 55

test and treat - if clinical assessment suggests, do H pylori test, and if positive, treat

if over 55 - do endoscopy

29
Q

how is h pylori tested for

A

urea breath test
stool antigen testing
HP antibody serum test
endoscopic biopsy tests

30
Q

how is PUD managed if under 55, +veHP and on NSAIDs, incld monitoring

A

give 2 months of PPI first, then eradication therapy

7 days

PPI + amox + clarithro/metro

repeat endoscopy 6-8 weeks later

31
Q

how is PUD managed if under 55, +ve HP, and not on NSAIDs, incld monitoring

A

eradication therapy, retest for HP after

32
Q

how to manage if HP -ve?

A

4-8 weeks of PPI

33
Q

what should be done if someone has PUD but needs to take NSAID?

A

give PPI also, consider switching to COX2 if low CDVS risk

34
Q

how is alcohol metabolised in the liver?

A

ethanol —(ethanol dehydrogenase)–> acetyldehyde —(aldehyde dehydrogenase)—> acetic acid

35
Q

what causes fatty acid accumulation in ALD?

A

increased ethanol metabolism causes depletion of NAD+ and increase in NADH, this causes decrease in fatty acid oxidation and increased hepatic fatty acid synthesis. fatty acids then esterified into glyceride

36
Q

how does ALD cause damage to hepatocytes

A

increase in NADH causes necrosis of hepatic acinus, causing release of TNF-alpha and free radicals

37
Q

what role does inflammation play in ALD

A

release of cytokines cause inflammation, neutrophil infiltration and cirrhosis

38
Q

what are the stages of ALD

A

steatosis
alcohol steatohepatitis
alcohol cirrhosis

39
Q

hepatic steatosis from alcohol is reversible - T or F

A

T, with abstinence

40
Q

symptoms of ALD

A

can be asymptomatic, otherwise signs of liver damage incl. jaundice, RUQ pain, vomiting/nausea, hepatomegaly, ascites, fatigue, complications of cirrhosis

41
Q

what are compliations of liver cirrhosis

A

jaundice, ascites, portal hypertension, bleeding varices, SBP, encephalopathy

42
Q

biochemical marker picture in ALD

A

raised bili, ast, alt, alk phos, PT, low albumin

43
Q

specific investigations in ALD

A

ultrasound
CT
biopsy

44
Q

management of ALD

A

alcohol cessation - managed
thiamine
steroids
liver transplant

45
Q

what is NAFLD associated with

A

metabolic syndrome

46
Q

what is metabolic syndrome

A
hypertension
insulin resistance
central obesity
hyperlipidaemia
nafld
47
Q

what is nafld

A

fatty liver causing inflammation, fibrosis and cirrhosis

48
Q

what does nafld increase the risk of

A

cirrhosis, hcc, liver failure

49
Q

what are symptoms of nafld

A

often asymptomatic, picked up incidentally

50
Q

what are signs of nafld

A

abnormal lfts
hepatomegaly
ultrasound showing fatty liver

51
Q

how is nafld diagnosed

A

raised alt/ggt
imaging evidence of steatosis
raised alt and evidence of metabolic syndrome

with no other possible causes of liver disease (alcohol, viral, autoimmune etc)

52
Q

how is nalfd managed

A

lifestyle, exercise, diet, weight loss, alcohol cessation, treat metabolic syndrome