Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > Alimentary Pharmacology > Flashcards

Alimentary Pharmacology Flashcards

1
Q

drugs for acid suppression

A

antacids

H2 Receptor antagonists

PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

drugs affecting GI motility

A

anti-emetics

antimuscarinics/ other anti-spasmodics

antimotility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

drugs for inflammatory bowel disease

A

aminosalicylates

corticosteroids

immunosuppressants

biologics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

drugs affecting intestinal secretions

A

bile acid sequestrates

ursodeoxycholic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe alginates (e.g. gaviscon)

A

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

acid suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

problems associated with PPI

A

-GI upset

predisposition to:

  • C.Diff
  • Hypomagnesaemia
  • B12 Deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

function of pro kinetic agents on the gut

A

increase gut motility and gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

examples of drugs that decrease GI motility

A

loperamide (ammonium)

opiods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

use of anti-spasmodics

A

reduce symptoms associated with IBS, renal colic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

mechanisms of action of anti-spasmodics

A
  • anti-cholinergic muscarininc antagonists
  • direct smooth muscle relaxants
  • calcium channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do anti-cholinergic muscarinic antagonists work

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how do calcium channel blockers work as anti-spasmodics

A

reduce calcium required for smooth muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

4 types of laxatives

A

bulk

osmotic

stimulant

softeners

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Corticosteroids

A

anti-inflammatory effects

given orally or rectally

26
Q

concerns and contraindications of Corticosteroids

A

osteoperosis
cushingoid features including weight gain
Increased susceptibility to infection
addisonian crisis with abrupt withdrawal

27
Q

use and mechanism of action of immunosuppresents

A

IBD

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

28
Q

adverse effects of immunosuppressents

A

bone marrow suppression

azathioprine hypersensitivity

organ damage (lung, liver, pancreas)

numerous DD interactions

29
Q

how do biologics work when treating IBD

A

addresses inflammatory response but not underlying disease process so course of disease after discontinuation is unclear

30
Q

what is the primary biologic used for treating IBD

A

anti-TNFa antibodies

31
Q

anti-TNFa antibodies e.g. infliximab

A

primary biologic used for treating IBD

32
Q

Cautions/ contraindications of infliximab

A

current TB or other serious infection

multiple sclerosis

pregnancy/ breast feeding

33
Q

infliximab

A

type of anti-TNFa antibody

prevents action of TNFa

34
Q

adverse effects of infliximab

A

risk of infection (particularly TB)

infusion reaction (e.g. fever, itch)

anaemia

thrombocytopenia

neutropenia

malignancy

35
Q

cholestyramine function

A

reduces bile salt by binding them in the gut and then excreting them as an insoluble complex

36
Q

possible effects of cholestyramine

A
  • absorption of other drugs may be effected

- fat soluble vitamin absorption might be effected, so may decrease vitamin K levels

37
Q

purpose of Ursodeoxycholic Acid

A

used to treat gallstones and primary biliary cirrhosis

38
Q

mechanism of action Ursodeoxycholic Acid

A

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

39
Q

what is absorption dependant on

A

pH

gut length

transit time

40
Q

what happens to gut function when theres low albumin

A

decreased binding and increased free drug concentration

41
Q

features of metabolism that can be effected by ADME drugs

A

liver enzymes

gut bacteria

gut wall infection

liver blood flow

42
Q

what percentage of hospital admissions are due to ADRs

A

6.5%

43
Q

what percentage of hospital admissions are killed due to ADRs

A

0.1-0.2%

44
Q

effects of changes to gut bacteria

A

loss oF OCP activity

reduced vit K absorption

overgrowth of pathogenic bacteria

45
Q

GI adverse effects of drug induced liver injury

A

intrinsic hepatotoxicity

idiosyncratic hepatotoxicity

46
Q

risk factors for ADRs

A

age (elderly)

female

high alcohol consumption

genetic factors

malnourishment

47
Q

caution to be considered when prescribing warfarin to a patient with liver disease

A

clotting factors are already low

48
Q

caution to be considered when prescribing aspirin/NSAIDs to a patient with liver disease

A

can increase bleeding time, in combination with a deficiency in clotting factors

NSAIDs can worsen ascites due to fluid retention

49
Q

caution to be considered when prescribing opiates/benzodiazepines to a patient with liver disease

A

may precipitate encephalopathy by increasing sedation

GI (35 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions