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Therapeutics > Final exam lecture 3 > Flashcards

Final exam lecture 3 Flashcards

1
Q

anatomy of stomach

A

Fundus is the top
two valves.
(pyloric valve and esophageal valve.)

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2
Q

Name the 4 kind of drugs affecting gastric secretion.

A

Antacids
H2 histamine receptor antaginists
PPIs
Protectants

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3
Q

drugs that increase GI motility

A

Laxatives
prokinetic drugs

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4
Q

Drugs that reduce GI motility

A

Antidiarrheal
Anti emetic

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5
Q

Explain the physiological control of GI secretions

A

We eat food
It activates G cells to make gastrin
gastrin acts on ECL to produce histamine
Histamine, AcH and gastrin act on parietal cells to activate proton pumps

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6
Q

Effect of parietal cells being acted upon by histamine, gastrin or Ach

A

Histamine, Ach and gastrin acidify the lumen of the stomach by activating parietal cells

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7
Q

how is the acid secretion is stomach halted

A

acid acts on D cells to produce somatostatin. Somatostatin feedsback and shuts down G cells.

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8
Q

What do D cells do?

A

Deaccelerate to shut down acid secretion via somatostatin.

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9
Q

mucus is produced by cells in stomach through

A

prostaglandins

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10
Q

How does aspirin cause ulcers of stomach

A

decrease prostaglandin production, decreasing mucus

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11
Q

Name 4 of the antacids

A

NaHCO3
CaCO3
AL(OH)3
MG(OH)2

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12
Q

What is the neutralizing capacity of the antacids

A

NaHCO3- High
CaCO3- moderate
AL(OH)3- High
MG(OH)2- High

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13
Q

Adverse effects of the antacids

A

NaHCO3- systemic alkilosis, fluid retention
CaCO3- hypercalcemia, nephrolithiasis, milk-alkali syndrome
AL(OH)3- constipation, hypophosphatemia
MG(OH)2- diarrhea

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14
Q

difference in side effects between AL(OH)3 and MG(OH)2

A

Al causes constipation
Mg causes diarrhea

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15
Q

Which cells produce histamine that acts on parietal cells

A

ECL cells

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16
Q

how do histamine receptor antagonists work? (H2RA)

A

They competitively inhibit H2 histamine receptors

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17
Q

H2RA drugs names

A

End with -tidine
(cimetidine, ranitidine, Nizatidine, Famotidine)

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18
Q

Mechanism of PPI inhibition of acid secretion

A

Directly binds and blocks ability of protein pump to exchange a proton for K+. Leading to profound inhibition of gastric acidification.

Leads to irreversible inhibition through disulfide bond.

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19
Q

PPI drug names

A

End with -prazole
(esomeprazole Purified S enantiomer), omeprazole S and R enantiomer)

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20
Q

Structure of PPI

A

Hexene next to 5 membered ring with two nitrogens

21
Q

How are PPIs activated

A

By acidic PH in the parietal cells

22
Q

What may occur during withdrawal of PPIs

A

Hypergastrinemia occurs and may result in rebound hypersecretion of gastric acid.

23
Q

compare H2 blockade and PPI

A

H2 blockade damps down peaks in acid production.
PPI completely prevents acid producton

24
Q

People who take PPIs chronically have

A

hypergastrinemia

25
Q

Why does hypergastrinemia happen on PPIs

A

Reduced gastric acid removes somatostatin inhibition of gastrin secretion.

26
Q

side effects of PPI

A

Increased risk of infection
Vit B12 deficiency
Decreased Ca 2+ absorption/ increased bone fractures (increased bone resorption)

27
Q

What are the two mechanisms of PPI therapy causing fractures

A

1) decreased calcium absorption causes a decline in Ca.
causes secondary hyperparathyroidism, increasing bone resorption

2) Hypergastrinemia causes Parathyroid hyperplasia

28
Q

______ are prodrugs that must be protonated to become active and form ______ bonds

A

PPIs, covalent disulfide bonds

29
Q

MOA of sucralfate

A

It is an AlOH complex of sucrose. It polymerizes and forms a protective barrier at ulcer site. Acidic PH activates complex.

30
Q

Name two mucosal protective agents

A

Misoprostol
Sucralfate

31
Q

Misoprostol MOA

A

Semisynthetic PGE derivative. Instead of mimicking mucus, it stimulates gastric cells to produce their own

32
Q

H. pylori combo treatment (with example)

A

BSS
Antibiotic (metronidazole, clarithromycin, tetracycline, amoxicillin)
H2 blocker or PPI

example- Metronidazole+ omeprazole+clarithromycin X 2 weeks

33
Q

Example of bulk and osmotic laxatives

A

Psyllium (metamucil)
PEG 3350 (MiraLAX )
Methylcellulose (citrucel)
Lactulose (duphalac)

34
Q

example of stimulant laxatives

A

Castor oil, bisacodyl (dulcolax), senna

35
Q

What situations would prokinetic drugs be used

A

Gastroparesis
parkinsons
opioid induced constipation

36
Q

What is Metoclopramide? What is it use for?

A

Metoclopramide is a dopamine receptor antagonist.
It is used for promotion of gastric emptying for post OP, diabetic, gastroparesis patients

37
Q

name opioid receptor antagonists that cant cross BBB

A

Naloxegol (movantik)
Alvimopan (entereg)
naldemedine (SYMPROIC)

38
Q

Opioid induced constipation can be avoided by ________

A

Biased agonists like olicerdine (instead of morphine)

39
Q

How do Prucalopride (motegrity) and tegaserod (zelnorm) work

A

5HT4 agonists, leading to increased cAMP, PKA activation and release of ACH

40
Q

What is prucalopride (motegrity) indicated for

A

Chronic idiopathic constipation in adults

41
Q

WHat is tegaserod (zelnorm)indicated for

A

Indicated for treatment of IBS with constipation in women UNDER 65

42
Q

Age range of zelnorm (tegaserod)

A

Under 65 and no prior heart conditions

43
Q

How do chloride channel activators work?

A

Increases amount of Cl in gut, leads to increased Na+ and increased H20

44
Q

Example of chloride channel activators

A

Lubiprostone (amatiza)
Linaclotide (linzess)
Plecanatide (Trulance)

45
Q

What are chloride channel activators used for

A

IBS+constipation

46
Q

how does Tenapanor work?

A

Inhibits Na/H exchanger in gut. This leaves more Na+ in lumen and h20 follows. Leads to increased movement in intestine

47
Q

How do anti-diarrheals work

A

Slow peristalisis to increase water and electrolyte absorption

48
Q

Name anti diarrheals

A

Diphenoxylate Active in CNS
loperamide (imodium)
both opiates, but loperamide poorly traverses BBB

Therapeutics (46 decks)

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