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CPTP > Prescribing in Liver > Flashcards

Prescribing in Liver Flashcards

1
Q

1st pass metabolism

A

Orally injected drugs are metabolised by the liver before they enter the systemic circulation. Hence only some of the dose is converted to the active metabolite which will have a therapeutic effect. If the 1st pass metabolism is impaired may = toxicity

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2
Q

Hypoalbuminemia

A

Some drugs are highly plasma protein bound drugs such as phenytoin, CBZ and diazepam. In liver disease albumin levels are often low this may lead to increased free drug concentrations

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3
Q

Reduced clotting factor production

A

Care is needed for pt on anticoagulants, also prescribing NSAIDs with caution due to their increased risk of GI bleeding

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4
Q

Fluid overload

A

NSAIDs, corticosteroids and anticholingeric drugs can all promote urinary retention

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5
Q

Encephalopathy

A

sedatives and opiates may precipitate coma, drugs such as NSAIDs or ACEi that may lower eGFR may lead to uraemia

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6
Q

Dyspepsia

A

Indigestion + a spectrum of intermittent upper GI symptoms including epigastric pain, heartburn, N/V

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7
Q

Causes of dyspepsia

A

Non ulcerative (60%), PUD, gastritis, oesophagitis, gastric/oesophageal malignancy, GORD
alcohol/smoking
drug induced

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8
Q

Pathology of dyspepsia

A

Parietal cells in the stomach produce HCL when stimulated by gastrin produced by G cells. They are also crucial to produce intrinsic factor for B12 absorption

Lining of the stomach is protected by mucosa cells which use carbonic anhydrase to produce HCO3 and H+ from h20 and co2. H+ leaves into the blood stream and the HCO3 buffers the acidic ph and protects the cells

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9
Q

NSAIDs

A

Inhibit COX-1 which is crucial to produce prostaglandins , they also irritate the gastric mucosa

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10
Q

H.pylori

A

Gram -ve bacteria. Uses flagella to burrow into epithelial cells. Produces urease which breaks down urea to NH3 and c02 protecting it from the acidic environment. Direct cytotoxins damage the cells and weaken tight junctions leading to inflammation. This up regulates gastrin production and leads to more acid potentiating ulcers

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11
Q

ALARM symptoms

A 
Anaemia
Loss of wt
Anorexia
Recent onset and progression
Melena/haematemasis
Dysphagia
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12
Q

Mx ALARM symptoms

A

2wk wait endoscopy if any of these new onset >55y/o

Don’t prescribe PPI prior to endoscopy may mask

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13
Q

Drug induced dyspepsia

A

NSAIDs + steroids = reduced prostaglandins preventing buffer and irritate mucosa
Bisphosphanates - oesophageal irritation and ulceration
Theophylline - gastritis
Nitrates - reflux

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14
Q

Mx dyspepsia

A

stop drugs - NSAIDs, CCB
lose wt, reduce alcohol, stop smoking
smaller meals, less spicy/fatty food
OTC antacids

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15
Q

GORD

A

PC = retrosternal chest pain, dysphagia

waterbrash, nocturnal asthma. Can progress to oesophagitis strictures and Barrett’s

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16
Q

Causes of GORD

A

hiatus hernia, pregnancy, obesity, systemic sclerosis

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17
Q

Gastritis

A

Inflammation of the stomach lining commonly due to h.pylori, NSAID’s, alcohol and smoking. PC abdo pain, dyspepsia, N/V can progress to PUD

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18
Q

Gastric ulcers

A

worse @ eating

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19
Q

Duodenal ulcers

A

4x more common, relieved by eating, worse at night/ 2-3hrs post prandial

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20
Q

PC PUD

A

abdo pain, N/V, wt loss, reduced appetite

emergency = upper GI bleed

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21
Q

Causes of PUD

A

H.pylori, NSAID’s, alcohol

Gastric specific
Cushing ulcers - increased ICP
Curlings ulcers - burns, sepsis and trauma

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22
Q

H.pylori testing

A

Carbon 13 urea breath test or stool sample

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23
Q

H.pylori eradication

A

Triple therapy of metronidazole, PPI - omeprazole and either clarithromycin/amoxicillin

Abx for 2 weeks, 8 weeks of PPI cover. Crucial to retest post therapy

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24
Q

H.pylori eradication

A

Triple therapy of metronidazole, PPI - omeprazole and either clarithromycin/amoxicillin 7 day course

8 wks of PPI crucial to retest post therapy

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25
Q

MX PUD

A

ensure all other causes are exclude. Stop drugs, test for h.pylori, rule out cancer!

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26
Q

Hepatotoxic drugs

A

Paracetamol, methotrexate, isoniazid, rifampacin, statins, valproate, carbamazepine,

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27
Q

Choleostatic drugs

A

Erythromycin, COCP, TCA’s, fluxcloxicillin, sulponylureas

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28
Q

Antibiotics to avoid in liver dysfunction

A

Nitrofurantonin, tetracycline and antitubuerclous therapy are all hetpatoxic. Erythromycin can induce cholestasis

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29
Q

Extraction ratio

A

Fraction or % of drug removed on passage through the liver. Clearance:blood flow

30
Q

Reduced dose calculation

A

normal dose x bioavailability (1-ER)

100

31
Q

Hepatic drug clearance

A

Defined as the volume of blood perfusing the liver that is cleared of the drug per unit time. Is is affected by blood flow, intrinsic clearance ability of the liver and fraction of the drug which in unbound in the circulation

32
Q

Emergency presentation of PUD

A

Acute upper GI bleed due to ulcer eroding through gastroduodenal artery or perforation leading to peritonitis

33
Q

MOA of PPI

A

Ompeprazole/lansoprazole = act to inhibit the H+/K+ atpase ion channel on the surface of the luminal parietal cells. Acts as an irreversible inhibitor preventing H+ movement into the gastric lumen reducing acid secretion

34
Q

Indications for PPI

A

PUD, NSAID’s / steroid induced ulcer, GORD, zollinger ellison, h.pylori eradication

35
Q

SE PPI

A

N/V, diarrhoea, abdo pain, interstitial nephritis, increased risk of c.diff and GI infections

36
Q

Interactions of PPI

A

CYP450 enzyme inhibitor

37
Q

H2 receptor antagonists

A

Ranitidine compete at the h2 receptor on the parietal cells to prevent action of histamine and reduce acid secretion

38
Q

OTC antacids

A

Aluminium hydroxide or magnesium carbonate act to increase the pH of stomach neutralising acid. The bind an inactivate pepsin

39
Q

Non pharmacological management of constipation

A

Hydration, exercise, high fibre diet

40
Q

Bulk forming laxatives

A

Bran and isphalga husk. These long chain polysaccharides aren’t broken down by digestion stay in the gut bulking up the stool. Increased faecal size leads to colonic distention and peristalsis

41
Q

CI and SE of bulking forming

A

Don’t use in bowel obstruction. SE - time to work, abdo distention

42
Q

Osmotic laxitives

A

Macrogol and lactulose. Poorly absorbed long chain polysaccharides which increase the osmolality of the gut lumen drowning water via osmosis. This increases transit time and colonic distention

43
Q

Stimulant laxitives

A

Senna, bisacodyl. Direct stimulation of the myenteric plexus leading to SM contraction and peristalsis

44
Q

Lactulose hepatic encephalopathy

A

Used frequently to remove NH3 producing bacteria which live in the colon

45
Q

SE stimulant laxitives

A

Can lead to atonic colon if used long term due to overstimulation of the myenteric plexus. Cramps and abdo discomfort

46
Q

Softeners

A

Sodium decussate and paraffin. Act as surfactants reducing surface tension allowing h20 to penetrate stool and soften faeces.

Used to reduce pain in those with anal pathology

47
Q

SE if softeners

A

Reduced absorption of fat soluble vitamins therefore not used in young children

48
Q

Prophylactic PPI

A

Give to pt over 65y/o who are on long term NSAIDs or steroid therapy

49
Q

Non ulcer dyspepsia

A

4 wks low dose PPI, dietary advice, reduce alcohol and NSAIDs

50
Q

Upper GI bleed PC

A

haematemesis, melana
shock - hypotension, tachycardia, CRT >2, cool/clammy
N/V, abdo pain
stigmata of chronic liver disease

51
Q

Causes of Upper GI bleed

A 
PUD - perforation/rupture
Variceal bleed
Mallory Weiss tear
Oesophageal/Gastric cancer
Acute gastritis
52
Q

History Upper GI bleed

A

Chronic liver disease Hx - past varices?
Drugs - steroids, NSAIDs, warfarin,
Dysphagia, wt loss
Retching ?

53
Q

Blatchford Score

A

Stratification of GI bleed if above 0 need medical intervention i.e. endoscopy/tranfusion

Haemoglobin, Urea
BP Pulse
Melena
Cardiac failure, liver failure and syncope

54
Q

Mx GI bleed

A

ABCDE, 2x large bore cannula, 100% o2
inv - urea, FBC, U+E,LFTs, ABG, coag, G+S

Endoscopy stat for all pt once resuscitated
- Use mechanical - clips,banding, thermal diathermy with adrenalin or haemospray

For variceal bleed = terlipressin and band ligation

55
Q

Haemodynamically unstable

A

Linked to poor prognosis HR >100, BP <100, <30ml of urine per hour

Transfusion, FFP and clotting factors can be used to stabilise

56
Q

Post endoscopy PUD

A

80mg PPI stat bolus -IV 8mg per hr for 72hrs + high dose PPI for 2 weeks
stop NSAID’s and steroids
endoscopy @6-8wks and h.pylori test

57
Q

Rockall score

A 
Risk of rebleeding post endoscopy. If >6 surgery and linked to poor outcome
Age
Blood pressure
Comorbidities
Diagnosis 
Evidence of bleed
58
Q

NSAIDs

A

Non selective inhibitors of COX1 and COX2 enzymes. They prevent the production of throboxanes and prostaglandins

59
Q

Effects of NSAIDs

A

COX2 - pro inflammatory mediators

  • PGE2 = pyretic and proinflammtory
  • PGI2 = vasodilator and platelet aggregator

COX1 = affects stomach and renal prostaglandins and thromboxanes.

  • Stomach - Prostaglandins act to inhibit acid secretion and synthesise mucus
  • Renal - Prostaglandins crucial for vasodilation of the afferent renal arteriole. reduced eGFR

Thromboxanes = normally promote platelet aggregation and vasoconstriction

60
Q

Indications for NSAIDs

A

Inflammatory arthritis
Gout
Mild-moderate pain - dental, facial, headache

61
Q

SE NSAIDs

A

Gastric - dyspepsie, ulceration - bleeding

Renal reduced eGFR, acclamation of drugs, AKI, HTN and peripheral oedema. Can = interstitial nephritis/ATN

Hypersensitivity - SJS, TEN
Increased CVD risk

Bronchospasm in asthmatic due to reduced prostaglandin production leukotriene synthesis is increased leading to bronchoconstriction

62
Q

CI to NSAIDs

A

PUD or GI bleed Hx
CKD or ESRF
Cardiac Hx

63
Q

Interactions NSAIDs

A

ACEi, ARB’s and aminoglycosides = increased AKI risk
Anticoagulant effect increased with warfarin
methotrexate,digoxin,lithium toxicity

64
Q

Causes of diarrhoea

A

Vascular - mesenteric ischemia
Infection - salmonella, campylobacter, viral, shigella, pancreatitis, any infection/sepsis
AI - hyperthyroid
Metabolic -
Inflammatory - IBD, IBS, Coeliac
Neoplastic - CRC, rectal cancer
Doctors - laxative abuse, overflow, alcohol, c.diff

65
Q

Inv diarrhoea

A

stool sample, microscopy and culture
c diff toxin
Check TFTs, U+E

66
Q

Mx diarrhoea

A

loperamide. Admit in isolation! Glove and gown

IV fluids if necessary biggest risk is dehydration

67
Q

Loperamide

A

Acts on mu opiod receptors in myenteric plexus to reduce smooth and longitudinal SM contraction leading to reduced peristalsis. Used for IBD, IBD or gastroenteritis

68
Q

Causes of constipation

A 
AI - hypothyroidism
Metabolic - hypercalcemia, hypokalemia
Trauma - stricture, anal pathology
Medication - opioids, dehydration, poor diet
CRC, prostate cancer
MS, PD, spinal cord compression
69
Q

C difficile

A

Anaerobic gram +ve spore forming bacteria that releases powerful enterotoxins. Can lead to pseudomembranous colitis - bloody diarrhoea and mucus PR leading to ileus, perforation and multi organ failure

70
Q

PC c diff and risks

A

diffuse diarrhoea, fever, rapidly rising CRP

Risks = old age, PPI, length of hospital stay
Abx! 4 C’s - co-amox, clindamycin, cephalosporins and ciprofloxacin

71
Q

Mx C.diff

A

Metronidazole 400mg TDS or Vancomycin 125mg QDS PO

Urgent colectomy if pseudomembranous colitis

72
Q

Drug induced dyspepsia

A

Nitrates, NSAIDs, steroids, calcium channel blockers, theophylline and bisphosphonates

CPTP (11 decks)

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