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GI > Alimentary Pharmacology > Flashcards

Alimentary Pharmacology Flashcards

1
Q

drugs for acid suppression

A

antacids

H2 Receptor antagonists

PPI

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2
Q

drugs affecting GI motility

A

anti-emetics

antimuscarinics/ other anti-spasmodics

antimotility

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3
Q

drugs for inflammatory bowel disease

A

aminosalicylates

corticosteroids

immunosuppressants

biologics

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4
Q

drugs affecting intestinal secretions

A

bile acid sequestrates

ursodeoxycholic acid

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5
Q

describe antacids (e.g. Maalox)

A

contains Mg or Aluminium

neutralises gastric acid

taken when symptoms occure

not preventative or curative, purely symptomatic treatment

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6
Q

describe alginates (e.g. gaviscon)

A

form a viscous gel that floats on stomach contents and reduces reflux

acid suppression

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7
Q

describe H2 receptor antagonists mechanism and use (e.g. ranitidine)

A

blocks histamine receptor therefore reducing acid secretion

indicated in GORD/ peptic ulcer disease

given orally or IV

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8
Q

describe PPI mechanism and use (e.g. omeprazole)

A

irreversibly block proton pump and therefore reduce acid secretion

indicated in GORD/ peptic ulcer disease

oral or IV administration

widely used (over used?)

triple therapy if associated with H Pylori

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9
Q

problems associated with PPI

A

-GI upset

predisposition to:

  • C.Diff
  • Hypomagnesaemia
  • B12 Deficiency
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10
Q

function of pro kinetic agents on the gut

A

increase gut motility and gastric emptying

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11
Q

describe the mechanism of action of GI motility drugs

A

not clear

involves parasympathetic nervous systems control of smooth muscle and sphincter tone (via ACh)

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12
Q

examples of drugs that decrease GI motility

A

loperamide (ammonium)

opiods

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13
Q

mechanism of action of drugs that decrease GI motility

A

via opiate receptors in GI tract to decrease ACh release.
decrease in smooth muscle contraction
increase anal sphincter tone

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14
Q

explain caution associated with GI motility reduction

A

don’t want to use it cause want to get rid of the organism causing it

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15
Q

use of anti-spasmodics

A

reduce symptoms associated with IBS, renal colic

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16
Q

mechanisms of action of anti-spasmodics

A
  • anti-cholinergic muscarininc antagonists
  • direct smooth muscle relaxants
  • calcium channel blockers
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17
Q

how do anti-cholinergic muscarinic antagonists work

A

inhibit smooth muscle constriction in the gut wall, producing muscle relaxation and reduction spasm

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18
Q

how do calcium channel blockers work as anti-spasmodics

A

reduce calcium required for smooth muscle contraction

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19
Q

4 types of laxatives

A

bulk

osmotic

stimulant

softeners

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20
Q

how do laxatives work

A

work by increasing bulk or drawing fluid into gut

21
Q

issues with laxatives

A

obstruction

route administration

need for other measures (e.g. osmotic laxatives will not work without adequate fluid intake)

Misuse

22
Q

mechanism of action of aminosalicylayes

A

unclear but but anti-inflammatory

23
Q

use of aminosalicylayes

A

IBD

oral or rectal administration

24
Q

adverse effects aminosalicylayes

A

GI upset

blood dycrasias

renal impairment

25
Corticosteroids
anti-inflammatory effects given orally or rectally
26
concerns and contraindications of Corticosteroids
osteoperosis cushingoid features including weight gain Increased susceptibility to infection addisonian crisis with abrupt withdrawal
27
use and mechanism of action of immunosuppresents
IBD prevents the formation of purines required for DNA synthesis so reduces immune cell proliferation
28
adverse effects of immunosuppressents
bone marrow suppression azathioprine hypersensitivity organ damage (lung, liver, pancreas) numerous DD interactions
29
how do biologics work when treating IBD
addresses inflammatory response but not underlying disease process so course of disease after discontinuation is unclear
30
what is the primary biologic used for treating IBD
anti-TNFa antibodies
31
anti-TNFa antibodies e.g. infliximab
primary biologic used for treating IBD
32
Cautions/ contraindications of infliximab
current TB or other serious infection multiple sclerosis pregnancy/ breast feeding
33
infliximab
type of anti-TNFa antibody prevents action of TNFa
34
adverse effects of infliximab
risk of infection (particularly TB) infusion reaction (e.g. fever, itch) anaemia thrombocytopenia neutropenia malignancy
35
cholestyramine function
reduces bile salt by binding them in the gut and then excreting them as an insoluble complex
36
possible effects of cholestyramine
- absorption of other drugs may be effected | - fat soluble vitamin absorption might be effected, so may decrease vitamin K levels
37
purpose of Ursodeoxycholic Acid
used to treat gallstones and primary biliary cirrhosis
38
mechanism of action Ursodeoxycholic Acid
inhibits an enzyme involved in the formation of cholesterol, altering amount in bile and slowly dissolving non-calcified stones
39
what is absorption dependant on
pH gut length transit time
40
what happens to gut function when theres low albumin
decreased binding and increased free drug concentration
41
features of metabolism that can be effected by ADME drugs
liver enzymes gut bacteria gut wall infection liver blood flow
42
what percentage of hospital admissions are due to ADRs
6.5%
43
what percentage of hospital admissions are killed due to ADRs
0.1-0.2%
44
effects of changes to gut bacteria
loss oF OCP activity reduced vit K absorption overgrowth of pathogenic bacteria
45
GI adverse effects of drug induced liver injury
intrinsic hepatotoxicity idiosyncratic hepatotoxicity
46
risk factors for ADRs
age (elderly) female high alcohol consumption genetic factors malnourishment
47
caution to be considered when prescribing warfarin to a patient with liver disease
clotting factors are already low
48
caution to be considered when prescribing aspirin/NSAIDs to a patient with liver disease
can increase bleeding time, in combination with a deficiency in clotting factors NSAIDs can worsen ascites due to fluid retention
49
caution to be considered when prescribing opiates/benzodiazepines to a patient with liver disease
may precipitate encephalopathy by increasing sedation

GI (35 decks)

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