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Gastrointestinal Block > GI Pharmacology > Flashcards

GI Pharmacology Flashcards

1
Q

Strength of ___ wave determines escape of chyme through ____

A

antral, pyloric sphincter

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2
Q

Gastric factors that determine stomach emptying?

A

DISTENSION

  • STRETCH promotes motility of smooth muscle
  • Simulates activity of INTRINSIC NERVE PLEXUSES
  • Simulates VAGUS NERVE activity
  • Stimulates GASTRIN release
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3
Q

Rate of emptying is proportional to?

A

Volume and consistency of chyme (causes distension)

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4
Q

Enterogastrones ____ contractile forces of stomach

A

decrease

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5
Q

Examples of enterogastrones?

A

Cholycystkinene, secretinin, gastric inhibitory peptides

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6
Q

Enterogastrones released inresponse to?

A

fatty hypertonic acidic chyme in duodenum

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7
Q

fatty hypertonic acidic chyme in duodenum will stimulate…

A

1) duodenal enterendocrine cells
2) chemoreceptors and stretch receptors (activate enteric neurones, inc. SNS activity dec. PNS activity)

These will inhibit contractile force and rate of emptying in stomach

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8
Q

D cells secrete ____ , this ____ HCL secretion. D cells are found in the ______ of the ______

A

SOMATOSTATIN, inhibits, mucosa, pyloric gland area

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9
Q

G cells secrete ____ , this ____ HCL secretion. G cells are found in the ______ of the ______

A

Gastrin, inhibits, mucosa, pyloric gland area

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10
Q

Enterochromaffin-like cells secrete ____ , this ____ HCL secretion. Enterochromaffin-like cells are found in the ______ of the ______

A

Histamine, stimulates, OXYNTIC MUCOSA, fundus and body

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11
Q

Parietal cells secrete ____ & _____. Parietal cells are found in the ______ of the ______

A

Hydrocholric acid, intrinsic factor, OXYNTIC MUCOSA, fundus and body

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12
Q

Chief cells secrete ____ . chief cells are found in the ______ of the ______

A

pepsinogen, OXYNTIC MUCOSA, fundus and body

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13
Q

What does intrinsic factor do?

A

Binds to vitamin B12 allowing it to be absorbed in terminal ileum

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14
Q

What does pepsinogen do?

A

Precursor of pepsin - an enzyme that breaks down proteins

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15
Q

What does HCL do?

A

Activates pepsinogen to pepsin
Denatures protein
Kills most (not all) micro-organisms ingested with food

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16
Q

What does oxyntic mean

A

secretory cells which produce hydrochloric acid in the main part of the stomach, or the glands which they compose.

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17
Q

How is HCL secreted from gasrtic parietal cells?

A

Water and C02 makes carbonic acid.
Carbonic acid breaks down releasing one H+ ion and hydrogen carbonate.
H+ leaves the cell via an antiporter which transfers K+ into the cell
hydrogen carbonate goes into an antiporter.
Antiporter allows entry of Cl- into cell
Cl- diffuses out of cell into lumen of gastric pit
H+ and Cl- become HCL

18
Q

Which pumps are involbed in HCL secretion?

A 
K+ channel
Cl- channel
Cl-/hydrogen carbonate antiporter
H+/K+ ATPase (PROTON PUMP)
Na+/K+ ATPASE
19
Q

How is secretion of HCL regulated? Which receptors?

A
  • Gastrin (CCk2) receptor - expressed on enterochromaffin like cell and parietal cells
  • Muscarininc M1 or M3 Ach receptor expressed enterochromaffin like cell and PARIETAL CELLS
  • Histamine H2 receptor expressed on PARIETAL CELLS
20
Q

GASTRIN ACTS ON

A

Gastrin CCK receptor expressed on enterochromaffin like cell and parietal cells

21
Q

Ach from postganglionic parasympathetics acts on

A

Muscarininc M1 or M3 Ach receptor expressed enterochromaffin like cell and PARIETAL CELLS

22
Q

Histamine from ____ cells acts on ____, expressed on _____

A

enterochromaffin like, H2 receptor on parietal cells

23
Q

T/F

Somatostatin inhibits gastrin sceretion between meals. This has the ffect of increasing HCL secretion

A

F

Somatostatin DOES inhibit gastrin sceretion between meals. This has the ffect of DECREASING HCL secretion

24
Q

Prostaglandin inhibits ..?

A

The effect of stimulating Gastrin CCK2 receptors, M1, M3 and H2 receptors on parietal cells

25
Q

Receptors M1,M2.H2 and G on parietal cells specifically stimulate the ____

A

K+/H+ antiporter!

26
Q

Secretion from M1,M2.H2 and G on parietal cells results in (detail)

A
  • Extended microvilli in cannaculi of pRIETAL CELL
  • Release of protein kinases
  • Protein kinases cause TRAFFICKING of K+/H+ antiporter from INSIDE cell to the surface of the extended microvillus
27
Q

What are the three phases of gastric secretion?

A
  • cephalic : sight/smell vagal stimulation acting on Parietal cells and G cells
  • Gastric : mechanical and chemical factors (distensin and digestion products)
  • Intestinal
28
Q

Intestinal phase gastric secretion?

A
  • less distension , less stimuli for secretion
  • secretion of somatostatin resumes between miles
  • factors from intestine switch off acid secretion
29
Q

NSAIDS block _____, this is ____ binding, this ____ acid secretion

A

Cyclooxygenase ( stops creation of prostaglandin),

irreversible, increases

30
Q

Ranitidine is a ____, it blocks _____

this is ____ binding, this ____ acid secretion

A

Histamine receptor antagonist, H2 receptor

competitive, decreases

31
Q

Pirenzepine is a ____, it blocks _____

this is ____ binding, this ____ acid secretion

A

Muscarinic receptor anatgonis, M1 m3,

competitive, decreases

32
Q

Omeprazole is a ____, it binds to _____

via ____ , this ____ acid secretion

A

proton pump (H+/K+) inhibitor, proton pump, covalent modification, decreases

33
Q

Localle produced prostaglandins protect the mucosa from attack by HCl and pepsin by..

A

reduce acid secretion
increase mucus and bicarbonate secretion
increase mucosal blood flow

34
Q

Gastric damage due to longterm NSAID use can be prevented with…

A

a stable PGE analogue - stimulates PGE receptors MISOPROSTOL

35
Q

H Pylori causes peptic ulcer because…

A

Lives in mucus gel and secretes agents tht cause persistent inflammation
weakens mucosal barrier
Breakdown mucosal barrier exposed to pepsin and HCL

36
Q

Drugs that reduce gastric acid secretion are used in the treatment of

A
  • peptic ulcer
  • GORD (inapprop relaxation of LOS, reflux gastric acid secretion)
  • Acid hypersecretion (Zollinger-Ellison syndrome, Cushing’s)
37
Q

How do PPIs respond to changes in pH?

A
  • They are BASIC PRODRUGS
  • Inactive at NEUTRAL pH
  • Conformational chnage and ACTIVATION in LOW ph(strongly acidic)
38
Q

T/F

Omeprazole’s full effect is only achieved after repeated dosing

A

T

39
Q

T/F

Ranitidine has many common side effects

A

F

side effects rare

40
Q

What is sucralfate?

A

MUCOSAL strengthener

41
Q

How does sucralfate work?

A
  • binds to the ulcer base (positively charged proteins) - forms complex gels with mucus
    – provides a mucosal barrier against acid and pepsin

Increases mucosal blood flow, mucus, bicarbonate, prostaglandin

42
Q

What are examples of Mucosal strengtheners?

A

Sucralfate

Bismuth chealate

Gastrointestinal Block (13 decks)

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