Lecture 34 Clinical Pharmacology of Alimentary Flashcards

1
Q

What drugs are used for acid suppression

A

o Antacids
o H2-receptor antagonists
o Proton pump inhibitors

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2
Q

What drugs are used to control GI motility

A

o Anti-emetics
o Anti-muscarinics/other anti-spasmodics
o Anti-motility

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3
Q

What drugs are used for IBD

A

o Aminosalicylates
o Corticosteroids
o Immunosuppressants
o Biologics

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4
Q

What drugs affect intestinal secretions

A

o Bile acid sequestrants and ursodeoxycholic acid

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5
Q

What is the action and use of antacids

A

Contain magnesium or aluminium and neutralised gastric acid

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6
Q

What is the action of alginates and give an example of one

A

Forms viscous gel that floats on stomach contents and reduces reflux

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7
Q

What is the action of H2-receptor antagonists and what’s its use

A

– Block histamine receptor thereby reducing acid secretion
– Indicated in GORD/Peptic ulcer disease
Ranitidine

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8
Q

What is the action and use of a PP inhibitor and name an example

A

– Block proton pump and thereby reduce acid secretion
– Indicated in GORD/peptic ulcer disease
– Oral or IV administration
Omeprazole
– Triple therapy for treatment of PU/DU associated with H pylori

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9
Q

What is the function of Prokinetic agents

A

Increase gut motility and gastric emptying

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10
Q

What drugs are used to treat vomiting

A
Anti-muscaranics
Anti-histamines
Dopamine antagonists
5HT3 antagonists
Cannabinoids
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11
Q

Where does anti-histamines act on

A

Vestibular nuclei

Medulla

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12
Q

Where does anti-muscaranics act on

A

Medulla

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13
Q

Where does dopamine antagonists act on and what does it involve

A

Chemoreceptor trigger zone
Pharynx and GIT
involves parasympathetic nervous system control of smooth muscle and sphincter tone (via ACh)

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14
Q

Where does 5HT3 act on

A

Chemoreceptor trigger zone

Pharynx and GIT

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15
Q

Where does cannabinoids act on

A

Chemoreceptor trigger zon

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16
Q

How do anti-spasmodics help relieve symptoms of IBS, renal colic

A
  • Anti-cholinergic muscarinic antagonists (hyoscine buscopan, mebeverine)
  • inhibit smooth muscle constriction in the gut wall, producing muscle relaxation and reduction spasm.
  • Direct smooth muscle relaxants
  • Calcium-channel blockers (peppermint oil) reduce calcium required for smooth muscle contraction
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17
Q

Name the 4 types of laxatives and how they work

A
–	Bulk (e.g. Isphagula)
–	Osmotic (e.g. Lactulose)
–	Stimulant (e.g. Senna)
–	Softeners (e.g. Arachis oil) 
–	Work by increasing bulk or drawing fluid into gut
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18
Q

Issues with laxatives

A
–	Obstruction
–	Route of administration
•	Oral or Rectal
–	Need for other measures
•	Osmotic laxatives will not work without adequate fluid intake
–	Misuse
19
Q

Concerns or contraindications for corticosteroids

A
  • Osteoporosis
  • Cushingoid features including weight gain, DM, HT,
  • Increased susceptibility to infection
  • Addisonian crisis with abrupt withdrawal
20
Q

What are the mechanisms of immunosuppressants

A

– Prevents the formation of purines required for DNA synthesis so reduces immune cell proliferation

21
Q

Whats the mechanism of Biologics

A

– Prevents action of TNFα (key cytokine in inflammatory response)

22
Q

Mechanism of Cholestyramine

A

– Reduces bile salts by binding with them in the gut and then excreting as insoluble complex

23
Q

Mechanism of Ursodeoxycholic Acid

A

– Inhibits an enzyme involved in the formation of cholesterol, altering amount in bile and slowly dissolving non-calcified stones

24
Q

Drug effect on absorption

A

o Tend to reduce absorption, but not always depending on drug properties
o Rate more affected than total absorption

25
Q

How can distribution of drug be affected

A

– Low albumin (decreased binding and increased free drug concentration)
• e.g. Phenytoin

26
Q

How can metabolism affect drug action

A

– Liver enzymes (variability in effects but generally toxicity)
– Increased gut bacteria (metabolise drugs so increased dose needed)
– Gut wall metabolism (disease may reduce first pass metabolism)
• e.g. Morphine
– Liver blood flow (drugs with a high extraction ratio)

27
Q

How can excretion affect drug action

A

– Biliary excretion (increased toxicity if hepatobiliary disease)
• e.g. Spironolactone

28
Q

What ways can NSAIDs causes mucosal injury & bleeding

A
Reduced mucosal flow
Reduce mucus & bicarbonate secretion
Impaire platelet aggregation
Epithelial damage
Reduced angiogenesis
Increases leukocyte adherence
29
Q

What is involved with changes to gut bacteria

A

– Mainly antibiotics
– Loss of OCP activity
– Reduced vitamin K absorption (increased prothrombin time)
– Overgrowth of pathogenic bacteria (e.g. Clostridium difficile)

30
Q

Name drugs that can cause acute hepatitis

A

Paracetamol
Isoniazid
Ritonavir
Troglitazone

31
Q

Name drugs that can cause chronic hepatitis

A

Diclofenac
Methyldopa
Minocycline
Nitrofurantoin

32
Q

Name drugs that cause acute cholestasis

A

ACE inhibitors
Co-amoxiclav
Chlorpromazine
Erythromycins

33
Q

Names drugs that cause mixed pattern or atypical hepatitis

A

Phenytoin

Sulfonamides

34
Q

Name drugs that can cause nonalcoholic steatohepatitis

A

Amiodarone

Tamoxifen

35
Q

Name a drug that can cause fibrosis/cirrhosis

A

Methotrexate

36
Q

Name drugs that can cause microvascular stenosis

A

NRTIs, Valproic

37
Q

Name a drug that can cause veno-occlusive disease

A

Cyclophosphamide

38
Q

Risk factors for induced liver injury

A
  • Age (elderly at risk)
  • Sex (female at risk)
  • Alcohol consumption
  • Genetic factors
  • Malnourishment
39
Q

What classification is used for liver disease classification

A
Child-Pugh classification 
Bilirubin
Albumin
PT
Encephalopathy
Ascites
40
Q

Child-Pugh classification >9

A

C

41
Q

Child-Pugh classification 7-9

A

B

42
Q

Child-Pugh classification <7

A

A

43
Q

Particular drugs to avoid in liver disease

A

• Warfarin/anti-coagulants
– In liver disease, clotting factors are already low
• Aspirin/NSAIDs
– Can increase bleeding time, in combination with deficiency in clotting factors;
– NSAIDs can worsen ascites due to fluid retention
• Opiates/benzodiazepines
– May precipitate encephalopathy by increasing sedation