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GI > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What muscles contract to cause vomiting?

A

Abdominal muscles and diaphragm

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2
Q

What is retching?

A

Reverse peristalsis

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3
Q

What is regurgitation?

A

Effortless movement of swallowed food contents back into the mouth

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4
Q

Sickness signals through the vestibular pathway are generally caused by what?

A

Tinnitus or motion sickness

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5
Q

Through what nerve do signals from the vestibular pathway travel?

A

Vestibulocochlear nerve

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6
Q

Sickness signals through the vagal pathway are generally caused by what?

A

Bacteria/alcohol/smell and vision/pharynx i.e. excess cough

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7
Q

What is the central pathway with regards to vomiting?

A

Brainstem emetic control pathway

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8
Q

Where will all drugs acting on the chemoreceptor trigger zone act?

A

Outside the blood brain barrier

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9
Q

What do enterochromaffin cells in the mucosa do?

A

Release mediators e.g. 5HT

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10
Q

What do mediators released by enterochromaffin cells in the mucosa cause?

A

Depolarisation of sensory afferents in the mucosa and AP discharge in vagal afferents to the brainstem

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11
Q

What does AP discharge in vagal afferents to the brainstem cause?

A

Coordination of vomiting by the vomiting centre

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12
Q

In what state are the stomach, oesophagus and associated sphincters during vomiting?

A

Relaxed

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13
Q

Where is the vomiting centre found?

A

Medulla

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14
Q

What state is the glottis in during vomiting?

A

Closed to prevent aspiration

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15
Q

What usually precedes vomiting?

A

Profuse salivation, increased HR, sweating and nausea

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16
Q

Does the motor output of vomiting involve efferents or afferents?

A

Efferents

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17
Q

What do vagal efferents cause in vomiting?

A

Shortening of the oesophagus, relaxation of the stomach and contraction of small intestine

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18
Q

What do somatic motor neurones cause in vomiting?

A

Contraction of anterior abdominal muscles and diaphragm

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19
Q

What do autonomic and somatic efferents cause in vomiting?

A

Increase heart rate and force, increase salivary secretions, pallor and sweaty skin, constriction of bladder and anal sphincters

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20
Q

What are some consequences of vomiting?

A

Dehydration, metabolic alkalosis, hypokalaemia, Mallory Weiss tear, aspiration

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21
Q

What is a sign of a Mallory Weiss tear?

A

Reddish streaks of fresh blood in vomit

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22
Q

What are prochlorperazine and droperidol examples of?

A

Dopamine antagonists

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23
Q

What do dopamine antagonists work as at high doses?

A

Anti-psychotics

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24
Q

How do dopamine antagonists work?

A

Block chemoreceptor trigger zone

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25
Q

What are dopamine antagonists used to treat?

A

Vomiting associated with neoplastic disease, radiation and drug induced sickness

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26
Q

What are side effects of dopamine antagonists?

A

Sedation and dystonic reactions

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27
Q

Where do prokinetic drugs work?

A

Dopamine pathways

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28
Q

What do prokinetic drugs do?

A

Increase gastric peristalsis and lower oesophageal sphincter tone

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29
Q

What is a common anti-emetic in the prokinetic drug class?

A

Metoclopramide

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30
Q

What are granisetron and ondansetron examples of?

A

5HT3 Receptor antagonists

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31
Q

What is a frequent side effect of 5HT3 receptor antagonists?

A

Headaches, and sometimes GI effects

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32
Q

What do 5HT3 antagonists block?

A

Receptors in the GI tract and CNS

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33
Q

What are 5HT3 antagonists used for?

A

Management of CINV, radiation induced emesis, PONV

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34
Q

What are promethazine, cyclizine and cinnarize examples of?

A

H1 Antihistamines

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35
Q

What receptor do H1 antihistamines also often block?

A

Muscarinic

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36
Q

What effect does cinnazine also have?

A

Antivertigo (tinnitus and Meniere’s)

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37
Q

What are H1 antagonists most useful for?

A

Motion sickness, morning sickness, PONV

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38
Q

What can H1 antagonists cause and what is the rule associated with this?

A

CNS depression and sedation- cannot drive

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39
Q

What are hyoscine, dicyclomine examples of?

A

Muscarinic antagonists

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40
Q

What are anticholinergics given for?

A

Motion sickness

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41
Q

What can anticholinergics be associated with?

A

Blurred vision, dry mouth, urinary retention and sedation

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42
Q

What classes of drugs can be used as adjuvant anti-emetics?

A

NK1 receptor antagonists, corticosteroids, benzodiazepines, cannibinoids

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43
Q

What drugs are used in anticipatory nausea and vomiting?

A

Benzodiazepines

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44
Q

How long and wide is the large intestine?

A

1.5m long and 6cm wide

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45
Q

What controls opening of the ileocaecal valve?

A

Gastric distension to cause gastro-ileal reflex

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46
Q

What is the ileocaecal valve under control of?

A

Vagus nerve, sympathetic and enteric nerves

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47
Q

What does the ileocaecal valve allow?

A

Digested contents of small intestine to move into caecum

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48
Q

what does the ileocaecal valve prevent?

A

Colonic bacteria entering the ileum

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49
Q

What is absorbed in the large intestine?

A

H2O, Na+, Cl-, short chain fatty acids

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50
Q

what does the large intestine secrete?

A

K+, HCO3-, mucus

51
Q

What does host bacteria have a role in?

A

Increasing immunity, promoting motility, synthesising vitamin K2 and free fatty acids, activate some drugs, enterohepatic cyclone

52
Q

What class of drug is useful for long term maintenance of remission of IBD?

A

Amino salicylates

53
Q

Are aminosalicylates more useful in UC or CD?

54
Q

What do COX and LOX do?

A

Change lipids into inflammatory components

55
Q

What is the most commonly used aminosalicylate at the moment?

A

Mesalazine

56
Q

What are some adverse effects of Mesalazine?

A

Rashes, arthralgias, low folate

57
Q

What should be supplemented during use of aminosalicylates?

A

Folic acid

58
Q

What is a potent anti inflammatory used in IBD?

A

Corticosteroids

59
Q

Which IBD are corticosteroids used in?

60
Q

When are corticosteroids used for IBD?

A

Reserved for acute flares

61
Q

What does the increase of steroid dependent patients lead to the use of?

A

Immunosuppressants

62
Q

What do immunosuppressants do?

A

Inhibit T lymphocyte function

63
Q

What is the rate of onset of immunosuppressants?

64
Q

What is the immunosuppressant used in IBD?

A

Azathioprine

65
Q

What are adverse effects of immunosuppressants?

A

Bowel movement suppression and hepatotoxicity

66
Q

What are some other immunosuppressant drugs?

A

6-mercaptopurine and methotrexate

67
Q

What are biological agents?

A

Monoclonal antibodies

68
Q

When are biological agents only really used?

A

Patients unfit for surgery

69
Q

What do biological agents block the action of?

70
Q

What is a common side effect of biological agents and so what should be given in advance?

A

Hypersensitivity reactions- give antihistamines

71
Q

What is the common name ending for all biological agents?

72
Q

What is drug treatment secondary to in IBS?

A

Diet and lifestyle changes

73
Q

What drugs can be given in IBS?

A

Antispasmodics, laxatives or anti motility agents

74
Q

What do anti-spasmodic drugs reduce in IBS?

75
Q

What are the two types of anti-spasmodic drugs?

A

Anti muscarinic agents and direct smooth muscle relaxants

76
Q

Which anti-spasmodic drug is better tolerated?

A

Direct smooth muscle relaxants

77
Q

How do anti muscarinic anti-spasmodic drugs work?

A

Inhibit parasympathetic activity in the GI tract

78
Q

What are dicycloverine hydrochloride, propantheline bromide examples of?

A

Anti muscarinic anti spasmodics

79
Q

What are Alverine, mebeverine and peppermint oil examples of?

A

Direct smooth muscle relaxants

80
Q

When anti-spasmodic drugs fail, what can be used to relieve pain in IBS?

A

Tricyclic antidepressants at low doses

81
Q

Where does the majority of reabsorption occur?

A

Small intestine

82
Q

Which co-transporters are the major mechanisms of post-prandial Na+ reabsorption? What is especially useful about these transporters?

A

Na+/glucose and Na+/amino acids- remain in tact even in severe diarrhoea

83
Q

What type of transport occurs through Na+ co-transporters?

A

Secondary active transport

84
Q

What are neither the Na+/glucose or Na+/amino acid transporters regulated by?

A

cAMP or Ca++

85
Q

What is diarrhoea defined as?

A

Loos of fluids and solutes from the GI tract in excess of 500mls per day

86
Q

What is secretory diarrhoea?

A

Increase in adenyl cyclase

87
Q

What are the 3 key treatments involved in severe acute diarrhoea?

A

Maintenance of fluid and electrolyte balance
Use of antimicrobial agents when needed
Use of anti-motility and anti-spasmodic agents

88
Q

What is the most important treatment for diarrhoea?

89
Q

When is fluid loss classed as severe?

A

Lost more than 10% of body weight

90
Q

How many Na+ bind to the SGLT1 transporter and what does this cause?

A

2 Na+, increases affinity for glucose

91
Q

What do oral rehydration salts contain?

A

Glucose, NaCl, sodium bicarbonate, potassium chloride

92
Q

What do oral rehydration salts cause?

A

Absorption of Na+ and glucose by SGLT1 which causes absorption of water

93
Q

What antibiotics are used in C. diff colitis?

A

Less severe- oral metronidazole

More severe- oral vancomycin

94
Q

What antibiotic is used in protozoan infection?

A

Metronidazole

95
Q

Who should not receive anti-motility agents?

A

Under 12, acute infective diarrhoea, IBD, IBS and diverticulosis

96
Q

When cam anti-motility agents be used?

A

Short term measure in exhausting or idiopathic diarrhoea or mild traveller’s diarrhoea

97
Q

Opioid drugs have what kind of effect?

A

Constipating

98
Q

What are the main opioids used in diarrhoea?

A

Loperamide, diphenoxylate and codeine (rare)

99
Q

What makes loperamide the opioid of choice for diarrhoea?

A

Pretty selective for GI tract

100
Q

What are the side effects of diphenoxylate?

A

Nausea, headache, weakness, blurred vision

101
Q

What can cause constipation?

A

suppressing urge to defecate, decreased colonic activity, lack of exercise

102
Q

What do laxatives provide?

A

Mild action resulting in the passage of soft but formed stools

103
Q

What do purgatives produce?

A

Stronger action leading to more fluid evacuation

104
Q

When should neither laxatives or purgatives be used?

A

When there is physical obstruction to the bowel

105
Q

What can laxative abuse lead to?

A

Hypokalaemia

106
Q

What is a common side effect of stimulant purgatives?

A

Abdominal cramps

107
Q

What are the metabolic functions of the liver?

A

Protein, fat and carbohydrate metabolism

108
Q

The liver is the major site of degradation for which hormones?

A

Insulin, steroid hormones, glucagon and ADH

109
Q

Normal thyroid function is dependent n the hepatic formation of what?

A

T4-T3 thyroid hormones

110
Q

Liver is involved in the activation of which vitamin?

111
Q

The liver is involved in the storage of which vitamins?

A

A, D, E, K, B12

112
Q

What are Kupffer cells and what do they do?

A

Liver phagocytes which destroy cellular debris and invading bacteria

113
Q

What stimulates the gallbladder to contract and cause the Sphincter of Oddi to open?

A

Chime in the duodenum

114
Q

What allows the smooth muscle of the gallbladder to contract?

A

CCK and vagal impulses

115
Q

Ursodeoxycholic acid is only of use in which type of gallstones?

A

Cholesterol

116
Q

Why should you not use morphine in biliary colic?

A

Constricts sphincter of Oddi and increases heoatic pressure

117
Q

What analgesics should be used in biliary colic instead of morphine?

A

Buprenorphine or pethedine

118
Q

What drugs are used for relief of biliary spasm?

A

GTN or atropine

119
Q

Bile acid binding resins are a drug used for hypercholesterolaemia. What can they be used for in terms of GI and how?

A

Cholestatic jaundice by increasing the bile salts in the blood

120
Q

Why are bile acid binding resins not ideal drugs?

A

Large doses are required, have GI effects, and give a deficiency of fat soluble vitamins

121
Q

What drugs can be given for hepatic encephalopathy?

A

Lactulose and antibiotics

122
Q

What is the function of lactulose in hepatic encephalopathy?

A

It is not digested or absorbed in the ileum. Breakdown products in the colon are acidic which decreases pH

123
Q

Why are antibiotics used in hepatic encephalopathy?

A

Suppress colonic flora to inhibit ammonia generation

GI (17 decks)

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