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Pharmacology Flashcards

1
Q

which drug classes that influence acid secretion block competitively?

A
  • muscarinic receptor antagonist e.g. pirenzepine

- H2 histamine receptor antagonists e.g. ranitidine

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2
Q

which drug classes that influence acid secretion block irreversibly?

A

NSAIDs e.g. aspirin

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3
Q

which drug classes that influence acid secretion block by covalent modification?

A

proton-pump inhibitors e.g. omeprazole

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4
Q

How does drug treatment of peptic ulcers aim to promote ulcer healing by?

A
  • reducing acid secretion
  • increasing mucosal resistance
  • eradicating H. pylori
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5
Q

which types of drugs reduce prostaglandin formation?

A

Non-steroidal anti-inflammatory drugs e.g. NSAIDs

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6
Q

what may Non-steroidal anti-inflammatory drugs cause?

A

trigger gastric ulceration and cause bleeding

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7
Q

How can gastric damage due to long term NSAID treatment be prevented?

A

with a stable PCE1 analogue

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8
Q

what are drugs that reduce gastric acid secretion used in?

A
  • peptic ulcer
  • gastro-oesophageal reflux disease
  • acid hypersecretion
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9
Q

what are the mechanisms of anti-secretory activity?

A
  • irreversible inhibition of proton pump
  • competitive antagonism of histamine H2 receptors
  • competitive antagonism of muscarinic M1 and M3 ACh receptors
  • antagonism of gastrin receptors
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10
Q

How do proton pump (PPIs) work?

A
  • inhibit the active H+/K+-dependant ATPase
  • basic prodrugs that are inactive at neutral pH but which change conformation in a strongly acidic environment
  • are absorbed from the GI tract and delivered via the systemic circulation to the secretory canaliculi of the stomach where accumulation activation and covalent modification of lumenal sulphydral groups of the membrane inserted proton-pump occurs
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11
Q

how do histamine H2 receptor antagonists work?

A

block the histamine mediated component of acid secretion and reduce secretion evoked by gastrin and ACh

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12
Q

what are examples of mucosal strengtheners?

A

surcalfate and bismuth chealate

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13
Q

How does surcralfate work?

A

binds to ulcer base and forms complex gels with mucus - provides a mucosal barrier against acid and pepsin

increases mucosal blood flow, mucus, bicarbonate and prostaglandin production

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14
Q

what are laxatives?

A

agents that are used to treat constipation

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15
Q

what are purgatives?

A

agents that cause purging, or cleansing, of bowels by promoting evacuation

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16
Q

when should laxatives or purgatives not be used?

A

when there is a physical obstruction to the bowel

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17
Q

How do laxatives work?

A

increase peristalsis and/or soften faeces causing, or assisting, evacuation

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18
Q

when should laxatives/purgatives be used?

A
  • when ‘straining’ is potentially damaging to health (e.g. patients with angina) or when defaecation is painful predisposing to constipation (e.g haemorrhoids)
  • to purge bowel before surgery or endoscopy
  • to treat drug-induced constipation or constipation in bedridden or elderly patients
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19
Q

what are bulk laxatives?

A

indigestible polysaccharide polymers. improve stool consistency. slowly acting

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20
Q

what are osmotic laxatives?

A

poorly absorbed solutes, rapidly acting

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21
Q

what is the mechanism of action of bulk/osmotic laxatives?

A

retain H2O
increase bulk
increase peristalsis

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22
Q

what is a common side effect of stimulant purgatives?

A

abdominal cramping

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23
Q

what are faecal softeners?

A

detergent like action

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24
Q

how do stimulant purgatives/faecal softeners work?

A

increase H2O and electrolyte secretion
increase peristalsis
faecal softening

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25
Q

What is the treatment for irritable bowel syndrome (IBS)?

A

treatment is symptomatic with adjustments to diet and anti-diarrhoeals and anti-spasmodics or laxatives as requires

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26
Q

what is the treatment for inflammatory bowel disease (IBD)?

A
  • glucocorticoids for acute attacks

- aminosalicylates for maintenance and mild disease

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27
Q

what drugs cause nausea and vomiting?

A
  • cancer chemotherapy
  • general anaesthetic
  • agents with dopamine agonist properties
  • morphine and other opiate analgesics
  • cardiac glycosides (e.g. digoxin)
  • drugs enhancing 5-HT function
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28
Q

what are examples of 5-HT3 receptor antagonists?

A
  • ondansetron
  • palonosetron
    (drugs that end in - setron)
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29
Q

when are 5-HT3 receptor antagonists used?

A

used to suppress chemotherapy and radiation induced emesis and post-operative nausea and vomiting

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30
Q

how do 5-HT3 receptor antagonists work?

A

block peripheral and central 5-HT3 receptors

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31
Q

when are 5-HT3 receptor antagonists not effective?

A

against motion sickness or vomiting induced by agents increasing dopaminergic transmission

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32
Q

what are the most common unwanted effects of 5-HT3 receptor antagonists?

A

constipation and headaches

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33
Q

what are muscarinic acetylcholine receptor antagonists used for?

A

prophylaxis and treatment of motion sickness

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34
Q

what are examples of muscarinic acetylcholine receptor antagonists?

A

hyosine

scopolamine

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35
Q

how do muscarinic acetylcholine receptor antagonists work?

A

probably blodk muscarinic acetylcholine receptors at multiple sites
direct inhibition of GI movements and relaxation of the GI tract may contribute to anti-emetic effects

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36
Q

what unwanted effects do muscarinic acetylcholine receptor antagonists have? what are these a result of?

A

blurred vision
urinary retention
dry mouth
resulting from blockade of the parasympathetic ANS and centrally mediated sedation

37
Q

What are Histamine H1 receptor antagonists used for?

A

prophylaxis and treatment of motion sickness and acute labyrinthitis and nausea and vomiting caused by irritants in the stomach

38
Q

what are examples of Histamine H1 receptor antagonists?

A

cyclizine

cinnarizine

39
Q

how do Histamine H1 receptor antagonists work?

A

blockade of H1 receptors in vestibular nuclei and NTS

40
Q

what do Histamine H1 receptor antagonists normally cause?

A

CNS depression and sedation - drowsiness may affect performance of skilled tasks

41
Q

What are examples of dopamine receptor antagonists?

A

domperidone and metoclopramide

42
Q

what are dopamine receptor antagonists used for?

A

drug induced vomiting and vomiting in GI disorders

43
Q

how do dopamine receptor antagonists work?

A

centrally block dopamine D2 (and D3) rceptors in CTZ

peripherally exert a prokinetic action on the oesophagus, stomach and intestine

44
Q

what are phenothiazines used for?

A

severe nausea and vomiting

45
Q

what unwanted effects may arise metoclopramine but are less likely in domperidone and why?

A

disorders of movement

domperidone does not cross the BBB

46
Q

when are NK1 receptor antagonists used?

A

in combination to 5-HT3 receptor antagonists and dexamethasone in acute phase of highly emetogenic chemotherapy

47
Q

how do NK1 receptor antagonists work?

A

antagonism of substance P (which causes vomiting and is released by vagal afferents) is assumed

48
Q

what is an example of an NK1 receptor antagonist?

A

aprepitant

49
Q

when are cannabinoid (CB1) receptor agonists used?

A

used ideally in in-patient setting for treatment of cytotoxic chemotherapy that is unresponsive to other anti-emetics

50
Q

how do cannabinoid (CB1) receptor agonists work?

A

decrease vomiting induced by agents stimulating the CTZ.

51
Q

what unwanted effects of cannabinoid (CB1) receptor agonists are there?

A

drowsiness
dizziness
dry mouth
mood changes

52
Q

how do opioids work on the alimentary tract?

A
  • inhibition of enteric neurones
  • creased peristalsis, increased segmentation
  • increased fluid absorption
  • constriction of pyloric, ileocaecal and anal sphincters
  • increased tone of large intestine
53
Q

what are the major opioid agents used in diarrhoea?

A
  • codeine
  • diphenoxylate (low CNS penetration, low water solubility)
  • loperamide (low CNS penetration, low solubility in water)
54
Q

what is the best treatment for symptomatic stones?

A

laproscopic cholecystectomy

55
Q

who may ursodeoxycholic acid be suitable for?

A

patients with unimpaired gall bladder function who have small/medium sized radiolucent stones (CH stones) which it dissolves

56
Q

what is a adverse effect of ursodeoxycholic acid?

A

diarrhoea

57
Q

what may happen if morphine is given for biliary colic?

A

pain may worsen due to constriction of sphincter of oddi and increased intrabiliary pressure

58
Q

what are alternatives to morphine for biliary colic?

A

buprenorphine and pethidine

59
Q

what might biliary spasms be relived by?

A

atropine and glyceryltrinitrate (GTN)

60
Q

what are examples of bile acid sequestrants (resins)?

A

colveselam
colestipol
colestyramine

61
Q

how do bile acid sequestrants work?

A

act by binding to bile acids, preventing their reabsorption

62
Q

how do bile acid sequestrants indirectly lower plasma LDL-cholesterol?

A
  • promote hepatic conversion of cholesterol to bile acids
  • increase cell surface expression of LDL-Receptor in hepatocytes
  • increase clearance of LDL-cholesterol from plasma
63
Q

what are clinical uses of bile acid sequestrants?

A

hyperlipidaemia
cholestatic jaundice
bile acid diarrhoea

64
Q

what are limitations and adverse effects of bile acid sequestrants?

A
  • unpalatable, inconvenient (large dosages)
  • frequently causes diarrhoea
  • reduced absorption of fat-soluble vitamins and some drugs
65
Q

what is the main organ of drug metabolism?

A

liver, but the GI tract, lungs and plasma alos have activity

66
Q

what does drug metabolism act to do?

A
  • convert parent drugs to more polar metabolites that are not readily reabsorbed by the kidney, facilitating excretion
  • concert drugs to metabolites that are usually pharmacological less active than parent compound.
  • less frequently, metabolites may; be converted to active compounds or gain activity, have unchanged activity or posses a different type, or spectrum of action
67
Q

what are the two phases that are often present in drug metabolism?

A

phase I (oxidation, reduction, hydrolysis) - makes drug more polar, adds a chemically reactive group permitting conjunction

phase II (conjunction) - adds an endogenous compound increasing polarity

68
Q

what are the main gene families in the human liver?

A

CYP1, CYP2, CYP3

69
Q

What mediates oxidation reactions (phase I) in the liver?

A

haem proteins located in the endoplasmic reticulum of liver hepatocytes

70
Q

what is glucuronidation?

A

transfer of glucuronic acid to electron-rich atoms of the substrate

71
Q

how to you teat hepatic failure?

A
  • lactulose

- antibiotics (neomycin, rifamixin)

72
Q

what happens during hepatic failure?

A

detoxification of ammonia, via the urea cycle to urea fails, blood ammonia levels rise exerting toxic effect upon the CNS that causes incoordination, drowsiness, coma and death.

73
Q

how do you treat allergic oesophagitis?

A

steroids/chromoglycate/montelukast

74
Q

what drugs can be used for treatment of GORD?

A

antacids
H2 antagonists
proton pump inhibitors

75
Q

why are antacids used for GORD?

A

symptomatic relief

no benefit in healing/preventing complications

76
Q

what two H2 antagonists are used in GORD?

A

cimetidine - symptom relief

ranitidine - poor at preventing relapse and complications

77
Q

what drugs function is acid suppression?

A

intravenous omeprazole

78
Q

which methods achieve haemostasis?

A 
terlipressin
endoscopic variceal ligation
sclerotherapy
sengstaken-blakemore balloon
TIPS
79
Q

what is sulphasalazine?

A

a combination of sulphapyridine and 5-ASA

80
Q

what does 5-aminosalicyclic acid act as?

A

anti-inflammatory

81
Q

what side effects of sulphasazine are due to the sulphapyridine moiety?

A 
oligospermia
headache
heinz body aneamia
megaloblastic aneamia
lung fibrosis
82
Q

what are common 5-ASA side effects?

A 
GI upset
headache
agranulocytosis
pancreatitis
interstitial nephritis
83
Q

what types of 5-ASA drugs are there?

A

sulphasalazine
mesalazine
olsalazine

84
Q

what are the therapy options for ulcerative colitis?

A

5ASA (mesalazine)
steroids
immunosuppressants
anti-TNF therapy

85
Q

what are the therapy options for crohn’s disease?

A

steroids
immunosuppressants
anti-TNF therapy

86
Q

what do 5ASAs reduce the risk of?

A

colon cancer

87
Q

what are the steroid side effects?

A

muscoskeletal -avascular necrosis, osteoporosis
GI
cutaneous - acne, thinning of skin
metabolic - weight gain, diabetes, hypertension
neuropsychiatric - cataracts, growth failure

88
Q

what are the side effects of azathioprine?

A

pancreatitis
leucopaenia
hepatitis
small risk of lymphoma, skin cancer

GI (10 decks)

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