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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
MX PUD
ensure all other causes are exclude. Stop drugs, test for h.pylori, rule out cancer!
26
Hepatotoxic drugs
Paracetamol, methotrexate, isoniazid, rifampacin, statins, valproate, carbamazepine,
27
Choleostatic drugs
Erythromycin, COCP, TCA's, fluxcloxicillin, sulponylureas
28
Antibiotics to avoid in liver dysfunction
Nitrofurantonin, tetracycline and antitubuerclous therapy are all hetpatoxic. Erythromycin can induce cholestasis
29
Extraction ratio
Fraction or % of drug removed on passage through the liver. Clearance:blood flow
30
Reduced dose calculation
normal dose x bioavailability (1-ER) | 100
31
Hepatic drug clearance
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
Emergency presentation of PUD
Acute upper GI bleed due to ulcer eroding through gastroduodenal artery or perforation leading to peritonitis
33
MOA of PPI
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
Indications for PPI
PUD, NSAID's / steroid induced ulcer, GORD, zollinger ellison, h.pylori eradication
35
SE PPI
N/V, diarrhoea, abdo pain, interstitial nephritis, increased risk of c.diff and GI infections
36
Interactions of PPI
CYP450 enzyme inhibitor
37
H2 receptor antagonists
Ranitidine compete at the h2 receptor on the parietal cells to prevent action of histamine and reduce acid secretion
38
OTC antacids
Aluminium hydroxide or magnesium carbonate act to increase the pH of stomach neutralising acid. The bind an inactivate pepsin
39
Non pharmacological management of constipation
Hydration, exercise, high fibre diet
40
Bulk forming laxatives
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
CI and SE of bulking forming
Don't use in bowel obstruction. SE - time to work, abdo distention
42
Osmotic laxitives
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
Stimulant laxitives
Senna, bisacodyl. Direct stimulation of the myenteric plexus leading to SM contraction and peristalsis
44
Lactulose hepatic encephalopathy
Used frequently to remove NH3 producing bacteria which live in the colon
45
SE stimulant laxitives
Can lead to atonic colon if used long term due to overstimulation of the myenteric plexus. Cramps and abdo discomfort
46
Softeners
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
SE if softeners
Reduced absorption of fat soluble vitamins therefore not used in young children
48
Prophylactic PPI
Give to pt over 65y/o who are on long term NSAIDs or steroid therapy
49
Non ulcer dyspepsia
4 wks low dose PPI, dietary advice, reduce alcohol and NSAIDs
50
Upper GI bleed PC
haematemesis, melana shock - hypotension, tachycardia, CRT >2, cool/clammy N/V, abdo pain stigmata of chronic liver disease
51
Causes of Upper GI bleed
``` PUD - perforation/rupture Variceal bleed Mallory Weiss tear Oesophageal/Gastric cancer Acute gastritis ```
52
History Upper GI bleed
Chronic liver disease Hx - past varices? Drugs - steroids, NSAIDs, warfarin, Dysphagia, wt loss Retching ?
53
Blatchford Score
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
Mx GI bleed
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
Haemodynamically unstable
Linked to poor prognosis HR >100, BP <100, <30ml of urine per hour Transfusion, FFP and clotting factors can be used to stabilise
56
Post endoscopy PUD
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
Rockall score
``` Risk of rebleeding post endoscopy. If >6 surgery and linked to poor outcome Age Blood pressure Comorbidities Diagnosis Evidence of bleed ```
58
NSAIDs
Non selective inhibitors of COX1 and COX2 enzymes. They prevent the production of throboxanes and prostaglandins
59
Effects of NSAIDs
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
Indications for NSAIDs
Inflammatory arthritis Gout Mild-moderate pain - dental, facial, headache
61
SE NSAIDs
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
CI to NSAIDs
PUD or GI bleed Hx CKD or ESRF Cardiac Hx
63
Interactions NSAIDs
ACEi, ARB's and aminoglycosides = increased AKI risk Anticoagulant effect increased with warfarin methotrexate,digoxin,lithium toxicity
64
Causes of diarrhoea
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
Inv diarrhoea
stool sample, microscopy and culture c diff toxin Check TFTs, U+E
66
Mx diarrhoea
loperamide. Admit in isolation! Glove and gown | IV fluids if necessary biggest risk is dehydration
67
Loperamide
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
Causes of constipation
``` AI - hypothyroidism Metabolic - hypercalcemia, hypokalemia Trauma - stricture, anal pathology Medication - opioids, dehydration, poor diet CRC, prostate cancer MS, PD, spinal cord compression ```
69
C difficile
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
PC c diff and risks
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
Mx C.diff
Metronidazole 400mg TDS or Vancomycin 125mg QDS PO Urgent colectomy if pseudomembranous colitis
72
Drug induced dyspepsia
Nitrates, NSAIDs, steroids, calcium channel blockers, theophylline and bisphosphonates

CPTP (11 decks)

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