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Alimentary System: Pathology SA > Alimentary Pharmacology > Flashcards

Alimentary Pharmacology Flashcards

1
Q

What drugs affect acid suppression in the GI tract

A

Antacids
H2 receptor antagonists
Proton Pump inhibitors

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2
Q

What drugs affect GI motility

A

Anti-emetics
Anti-muscarinics/spasmodics
Anti-motility

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3
Q

What drugs help in bowel movement in the GI tract

A

Laxatives

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4
Q

What drugs are usedin the treatment of Inflammatory bowel disease

A

Aminosalicylates
Corticosteroids
Immunosuppressants
Biologics

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5
Q

What drugs affect intestinal secretion

A

Bile acid sequestrate
- Cholestyramine

Urosodeoxycholic acid

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6
Q

What is an example of an antacid drug, what is it composed of

A

Maalox

containing magnesium and aluminium

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7
Q

What is the mechanisms of antacids

A

Neutralising gastric acid

to relieve symptoms

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8
Q

What is an example of an Alginates and its mechanism in the treatment of acid suppression

A

Gaviscon

Forms a vicious gel that floats on the stomach contents and reduces reflux

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9
Q

Name three additional muscosal protectors in acid suppression

A

Bismuth
Sucralfate
Misoprostol

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10
Q

What is an example of a H2 receptor antagonist and its mechanism

A

Ranitidine

Blocks histamine receptor thereby reducing acid secretion (controlling acid production)

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11
Q

When is H2 receptor antagonist used

A

Indicated in GORD

Peptic ulcer disease

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12
Q

What is the administration of H2 receptor antagonist and proton pump inhibitors

A

Orally

IV

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13
Q

What is an example of a Proton Pump Inhibitor and it mechanism

A

Omeprazole

Blocks proton pump inhibitory thereby reducing acid secretion

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14
Q

What is the indication for the use of Proton pump inhibitor

A

Used in GORD
Peptic ulcer disease

Tripple therapy treatment for PU/DU associated with H.Pylori

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15
Q

What are the GI upset and predisposition that can occur due to Proton pump inhibitor s

A

C. Diff Infections
Hypomaganesaemia
B12 deficiency

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16
Q

What is the mechanism of pro kinetic agents

A

Increase gut motility and gastric emptying

by having parasympathetic nervous system control of smooth muscle and sphincter tone via ACh

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17
Q

What are examples of Prokinetic agents

A

Metoclopramide

Domperidone/dopamine antagonist

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18
Q

How does Domperidone increase gut motility and gastric emptying time

A

blocking dopamine receptors which inhibit post-synaptic cholinergic neurones

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19
Q

What is Pro-kinetics used in the treatment of

A

GORD

Gastroparesis - allows to empty quicker

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20
Q

What is anti emetics, give two examples

A

Prevent vomiting

5- HT3 antagonists

Anti Histamines

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21
Q

Where do 5-HT3 antagonist work to prevent vomiting

A

Chemoreceptor Trigger zone (drugs/toxin)

Vomiting centre/medulla

Pharynx and GIT
(gastroenteritis, radiotherapy, some drugs)

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22
Q

Where do antihistamine work in the prevention of vomiting

A

Vestibular nuceli (motion)

Vomiting centre/medulla

Chemoreceptor trigger zone

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23
Q

Where does dopamine antagonist work for increasing gut motility and gastric emptying

A

Chemoreceptor trigger zone

Pharynx and GIT (gastroenteritis, radiotherapy, some drugs)

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24
Q

What is examples of anti-motlity drugs

A

Loperamide (immodium)

Opiods

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25
Q

What is the mechanism of anti-motility drugs

A

antagonise optiate receptors in GI tract decreasing ACh release, thereby decreasing smooth muscle contraction and increasing anal spinchter tone

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26
Q

What is the clinical benefit of drugs which decrease GI motility

A

are anti-diarrhoea

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27
Q

Why does loperamide have few central opiate effects

A

Not well absorbed across the blood brain barrier

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28
Q

What doe antispasmodics reduce the symptoms of

A

IBS

Renal colic

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29
Q

What is the three mechanism od anti-spasmodics

A

anti-cholingeric muscarinic antagonists

Direct smooth muscle relaxants

Calcium channel blockers

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30
Q

What is examples if anti-cholinergic muscarinic antagonists

and there mechanisms

A
  • Hyoscine Buscopan
  • Meberverine

Inhibit smooth muscle constrictions in the gut wall, producing muscle relaxation and reduction in spasm

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31
Q

What is an example of a CCB and its mechanism

A

Peppermint oil

Reduce calcium required for smooth muscle contractions

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32
Q

What is the 4 types of laxatives, and examples

A

Bulk
(e.g. Isphagula)

Osmotic
(e.g. Lactulose)

Stimulant
(e.g. Senna)

Softeners
(e.g. Arachis oil)

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33
Q

What is the overall mechanism of laxatives

A

Work by increasing bulk or drawing fluid into the gut making it easier for stool to pass

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34
Q

What is potentially issues of laxatives

A

Can cause obstruction

Osmotic laxatives will not work without adequate fluid intake

Misuse

Route of administration: oral or rectal

35
Q

What is the problems of anti-motility drugs

A

Can cause constipation

Cannot take it there is an obstruction

Prevent diarrhoea - infection isn’t “flushed out”

36
Q

What drugs are used in treating inflammatory bowel disease

A

Aminosalicylates

Cortiscosteroids

Immunosuppressants (azathioprine)

Biologics
(Anti-TNFα antibodies)

37
Q

What is examples of aminosalicylates that treat IBD

and how are they administrated

A

Mesalazine

Olsalazine

(Sulfasalazine original drug but side effect problems)

Administrated either Orally or IV

38
Q

What is the mechanism of aminosalicylates in treating IBD

A

Unclear but has anti-infammatory properties

39
Q

What cautions should be taken when taking aminosalicylates for the treatment of IBD

A

Chemically related to salicylates so avoid if allergic

Be careful if have renal impairment

40
Q

What is the adverse effect of aminosalicylates

A

GI upset

Blood dyscrasias

Renal impairment

41
Q

What is the administration and mechanism of cortiscosterioids

A

Given: Orally, IV, Rectal

Anti-inflmammatory effects

42
Q

What is the concerns of taking corticosteroids in IBD

A

Can cause:
-Osteoporosis -Cushingoid features (weight gain, diabetes mellitus, HT)

Have an increased susceptibility to infection

If abrupt withdrawal causes addisonian crisis

43
Q

Define addisonian crisis

A

Medical emergency as symptoms that indicate severe adrenal insufficiency caused by insufficient levels of the hormone cortisol

44
Q

How does the immunosuppressant azathioprine work in the treatment of IBD

A

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

45
Q

What is the adverse effects of azathioprine that means it requires close monitoring

A

Bone marrow suppression

azathioprine hypersensitivity and organ damage to lung,liver, pancreatitis

Drug interaction

46
Q

What is an example of a Biologic that treats IBD, and its mechanism

A

Infliximab
- mouse human chimeric antibody to TNFα

Prevents the actions of TNFα preventing cytokine occurring in an inflammatory response

47
Q

What is infliximab also used in the treatment of

A

Psoriasus

Rheumatoid arthritis

48
Q

What are the cautions and contradictions of Infliximab treatment in IBD

A

Current TB/serious infection

Multiple sclerosis

Pregnancy/ breast feeding

49
Q

What is the adverse effect of Infliximab

A

Risk of infection,

Infusion reaction (fever, itch)

Anaemia, thrombocytopenia, neutropenia

Demyelination

Malignancy

50
Q

What should all patients taking Infliximab be screened for

A

TB

51
Q

What are 5 examples of other biologics that can be used in the treatment of IBD

A

Certolizumab

Adalimumab

Natalizumab

Golimumab

Vedolizumab

52
Q

What is the mechanism of Bile acid sequestrate’s

Cholestyramine

A

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

53
Q

What should be considered when taking Cholestyramine

A

May affect the absorption of other drugs - take separately

May affect fat soluble vitamin absorption so may decrease vitamin K levels (affecting clotting and warfarin)

54
Q

What does chlestyramine treat

A

Pruitits from biliary cause

55
Q

What does Ursodeoxycholic Acid treat

A

Gall stones

Primary Biliary cirrhosis

56
Q

What is the mechanism of Ursodeoxycholic Acid

A

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

57
Q

Gastrointestinal or liver disease can effect what process of drugs

A

Absorption
Distribution
Metabolism
Excretion

58
Q

What might change the route of administration of drugs

A

GI symptoms

59
Q

What facts affect the absorption of drugs in the GI

A

Change in pH

Gut length:

  • extra stomach time
  • slow time to small intestine

Transit time

  • dependant on bacteria
  • diarrhoea, increases transit time, decreases absorption
60
Q

What factor affect distribution of drug in the GI tract

A

Low albumin (decreased binding and increased free drug concentration)

61
Q

What factor affect the metabolism of drugs in the GI tract

A

Liver enzymes (decrease in disease, drugs toxicity increase)

Increased gut bacteria (metabolise drugs so increased dose needed)

Gut wall metabolism (disease may reduce first pass metabolism)

Liver blood flow (Blockage in flow means drugs will have a high extraction ratio)

62
Q

What factor affects the excretion of drugs in the GI tract

A

Biliary excretion due to an increased toxicity if hepatobilliary disease

63
Q

What are the pharmacodynamic effects with drug examples In Liver disease

A

Exaggerated response e.g. sedation with benzdiaepines

Reduced response e.g. reduced dieresis with loop diuretics

Increased toxicity e.g. nephrotoxicity with amino-glycosides

64
Q

What is the GI adverse effects of drug treatment

A

GI upset

Diarrhoea/constipation

GI bleeding/ulceration

Changes to gut bacteria

Drug induced liver injury

65
Q

What drugs causes the adverse reaction of diarrhoea/constipation

A

Cholinergics, NSAIDs, Antimicrobials

Opioids, Anticholinergics

66
Q

What are the mechanism of the drug treatment that cause diarrhoea

A

osmotic, secretory, shorted transit time,

protein losing, malabsorption,

67
Q

What is the main aetiology of drug induced diarrhoea

A

antimicrobials

68
Q

What are two example of drug induced GI bleeding/ulceration

A

Low dose aspirin/NSAIDS

Warfarin

69
Q

What is the mechanism of drug induced GI ulcers

A

Ulcer causation and increases bleeding tendency due to impaired platelet aggregation

Implication of other drugs e.g. SSRI and Platelet function

70
Q

What is NSAID pathology to GI Bleeding

A

Affect COX1 (Impairing the defence) and COX 2 (impairing the healing) and causes epithelial damage (impairing platelet aggregation)

resulting in local and systemic effect through prostaglandins

71
Q

Changes to the gut bacteria is mainly due to what drugs

A

Antibiotics

72
Q

What is the affect of changes to gut bacteria

A

Loss of oral contraceptive pill activity

Reduced Vitamin K absorption (increased prothrombin time)

Overgrowth pathogenic bacteria (eg C.diff infection)

73
Q

What is the two forms drug induced liver injury

A 
Intrinsic hepatoxocity
 (predictable, dose dependant)
Idiosyncratic hepatotoxicity 
(unpredictable, not dose dependant)
74
Q

What causes drug induced liver injury

A

The drug itself

or its active metabolite

75
Q

What is the diverse affect of the drug induced liver injury

A

From asymptomatic increase in LFTS to liver failure and death

Generally causes
- Acute/chronic hepatitis
- cholestasis
(gall stone in bile duct)

76
Q

What is the risk factors for drug induced liver disease

A

Age (elderly at risk)

Sex (female at risk)

Alcohol consumption

Genetic factors

Malnourishment

77
Q

What are examples of drugs causing drug induced liver disease (hepatotoxicity)

A

Paracetamol, isoniazid = acute

Diclofenac, methyldopa = chronic

ACE inhibitors, co-amociclav = acute cholestasis

Methotextrate = fibrosis/cirrhosis

78
Q

What is assessed for child-pugs classification scoring the severity of liver disease

A 
High Bilirubin 
Low albumin 
PTs 
Encephalopathy 
Ascites
79
Q

When prescribing in Liver disease what drug properties should be avoided

A

Drugs which can be toxic due to changes in pharmokinetics

Drugs which are hepatotoxic

Drugs which may worsen with non liver aspects of liver disease e.g. encephalopathy

80
Q

What are the pharmokinetics that change that can cause toxicity of drugs

A

Liver metabolism
Therapeutic index
Bilary excretion

81
Q

What is examples of drugs that are hepatotoxic

A

Methotrexate

Azathioprine

82
Q

What is an example of a drug which can worsen encephalopathy in liver disease

A

Benzodiazepine

83
Q

What particular drugs should be avoided when prescribing in liver disease and why

A

Warfarin/anti-coagulants
- clotting factors already low

Aspirin/NSAIDS

  • Increase bleeding time
  • worsen ascites due to fluid retention

Opiates/benzodiazepines
- precipitate encephalopathy by increasing sedation

Alimentary System: Pathology SA (27 decks)

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