Gi 3 Sp

Front 1

Describe the processes involved in the control of emesis.

Back 1

A complex process controlled centrally in the chemoreceptor trigger zone and effected by responses in the gut, pharynx and thoracoabdominal wall (CTZ = chemorecptor trigger zone found in 'area postrema' just at the base of the skull outisde bbb, allowing for monitoring for toxins in blood stream).
Also, the cerebral cortex (anticipatory vomiting) and vestibular apparatus (in the ear involved in motion sickness)

Front 2

List different targets for antiemetic drugs and specift whether these affect the vestibular apparatus and local gut stimuli OR CTZ stimuli

Back 2

H1 Antagonist and anti-muscarinics work on Vestibular apparatus and local gut stimuli.
While D2 antagonists, 5HT3 Antagonist and NK-1 antagonist work on CTZ stimuli.

Front 3

Antihistamines for Emesis Tx, eg's and MOA

Back 3

Used for vestibular disorders (eg. motion sickness), use 1st gen so they cross BBB eg. pheniramine, promethazine and cyclizine.
S/E CNS effects such as sedation. Significant anti mACh effects contribute to their impact on motion sickness, less useful when emesis has commenced.

Front 4

Scopolamine, active ingredient, moa S/E

Back 4

Hyoscine hydrobromide (distinct from hyoscine butylbromide which was designed for peripheral action instead of CNS activity), acts on the CNS -depressed vestibular function helps to decrease reflexes from the chemoreceptor trigger zone that promote vomiting.
CNS S/E include drowsiness, amnesia, euphoria.

Front 5

Chemotherapy and nausea

Back 5

Different targets of emesis (CTZ vs. afferent) Different chemotherapy agents have different likelihood of emesis (cyclophosphomide >90%) so anti-emetics may be used in combo

Front 6

Anti-emetic combo

Back 6

5-HT3 and NK1 antags are used for "high risk" chemo regimens.
Act on both peripheral GI and CNS sites
5-HT3 better for acute and NK1 better for delayed sx
eg. Odansetron, aprepitant and dexamethasone.

Front 7

Moa of 5HT3 antags and S/E

Back 7

5-HT3 receptor is a ligand gated cation channel therefore blocking it causes rapid desensitating depol. located at vagus nerve terminal and CTZ, reduces response to visceral stim. eg. cytotoxics. Also inhibit colonic motility (via ACh leading to constipation.

Front 8

Metabolism and Examples of 5HT-3 Antags

Back 8

Rely on CYPs for metabolism (3A4, 2D6) have quite long MOA that does not reflect short t1/2 administer once daily.
Odansetron 4hr
Tropisetron (7hr except in poor metabolisers can be up to 45hrs)
Granisetron 9hr
Palonosetron 40hr

Front 9

Substance P/ NK1 antags eg's moa

Back 9

Tachykinin family of NTs, binds neurokinin-1 receptors, involved in neurogenic inflammation.
NK1 antags also metabolised by CYP3A4

Front 10

Dopamine antags

Back 10

more than of catecholamines in CNS are dopamine. D2 inhibits adenylyl cyclase and found in CTZ and peripherally (GI motility) many have Anti H and AntiACh activity "general purpose"

Front 11

Prochlorperazine, class, MOA and S/E

Back 11

antiDA phenothiazines act directly on the CTZ, they don't have anti-psychotic effects, but can cause extrapyramidal effects and akathisia, also risk of tardive dyskinesia increases with cumulative doses / increase duration of use.

another S/E of dopamine antags= can increase QT interval

Front 12

What are some of the advantages of using domperidone in px with nausea/ vomiting

Back 12

acts on peripheral D2 receptors to augment gastric emptying, more difficult to vomit when the stomach is empty, domperidone has less BBB penetration so EPSE are rare

Front 13

Usefulness of diphenhydramine

Back 13

used in combo with Dopamine antags, it has little antiemetic capacity but prevents or treats EPSE

Front 14

Cannabinoids

Back 14

can have antiemetic effects, CB1 (in CNS) and (CB2 in periphery) are endogenous receptors that binds arachidonic acid metabolites, inhibits NT release.
Botanical THC is a weak antiemetic but good for persistent nausea, has active metabolites, highly lipid soluble and large V so long t1/2

Front 15

Nabilone

Back 15

is a synthetic analogue of botanical THC, CNS side effects in >10%

Front 16

Pancreatitis, define it and what occurs, how is it treated

Back 16

Loss of endocrine (insulin and glucagon) and exocrine (digestive enzymes and Bicarb) functions. If loss >90% function, then -> steatorrhoea and protein malabsorption.
Tx= use porcine enzyme extracts - lipase, protease, amylase in different ratios.

Front 17

Cholestatic liver disease, define

Back 17

impairment of bile formation or flow. 'back-up' of bile can cause damage to liver leading to fibrosis.

Front 18

Ursodeoxycholic acid

Back 18

Ursodeoxycholic acid changes composition of bile (miscelles); stimulates hepatobiliary secretion; protection of hepatocytes against bile acid-induced apoptosis