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
How can distribution of drug be affected
– Low albumin (decreased binding and increased free drug concentration) • e.g. Phenytoin
26
How can metabolism affect drug action
– 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
How can excretion affect drug action
– Biliary excretion (increased toxicity if hepatobiliary disease) • e.g. Spironolactone
28
What ways can NSAIDs causes mucosal injury & bleeding
``` Reduced mucosal flow Reduce mucus & bicarbonate secretion Impaire platelet aggregation Epithelial damage Reduced angiogenesis Increases leukocyte adherence ```
29
What is involved with changes to gut bacteria
– Mainly antibiotics – Loss of OCP activity – Reduced vitamin K absorption (increased prothrombin time) – Overgrowth of pathogenic bacteria (e.g. Clostridium difficile)
30
Name drugs that can cause acute hepatitis
Paracetamol Isoniazid Ritonavir Troglitazone
31
Name drugs that can cause chronic hepatitis
Diclofenac Methyldopa Minocycline Nitrofurantoin
32
Name drugs that cause acute cholestasis
ACE inhibitors Co-amoxiclav Chlorpromazine Erythromycins
33
Names drugs that cause mixed pattern or atypical hepatitis
Phenytoin | Sulfonamides
34
Name drugs that can cause nonalcoholic steatohepatitis
Amiodarone | Tamoxifen
35
Name a drug that can cause fibrosis/cirrhosis
Methotrexate
36
Name drugs that can cause microvascular stenosis
NRTIs, Valproic
37
Name a drug that can cause veno-occlusive disease
Cyclophosphamide
38
Risk factors for induced liver injury
* Age (elderly at risk) * Sex (female at risk) * Alcohol consumption * Genetic factors * Malnourishment
39
What classification is used for liver disease classification
``` Child-Pugh classification Bilirubin Albumin PT Encephalopathy Ascites ```
40
Child-Pugh classification >9
C
41
Child-Pugh classification 7-9
B
42
Child-Pugh classification <7
A
43
Particular drugs to avoid in liver disease
• 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