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House Pharmacology > GIT Acidity > Flashcards

GIT Acidity Flashcards

1
Q

A peptic ulcer (stomach or duodenal) is a ___________________ of the _______,________, or _________

A

break in the inner lining

esophagus, stomach, or duodenum.

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2
Q

A peptic ulcer :

of the stomach is called a —————

of the duodenum, is called a _____________

of the esophagus, is called an _________

A

gastric ulcer

duodenal ulcer

esophageal ulcer.

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3
Q

The two most important initiating causes of ulcers are _______ of the stomach by a bacterium named “____________” and (acute or chronic?) use of _________________

A

infection

Helicobacter pylori

Chronic

nonsteroidal anti- inflammatory medications (NSAIDs),

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4
Q

Gastric Defenses Against Acid

Esophageal defense: the _________, which prevents _______ of acidic gastric contents into the esophagus.

A

lower esophageal sphincter

reflux

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5
Q

Gastric Defenses Against Acid

Stomach defense: require adequate __________ because of the high metabolic activity and oxygen requirements of the gastric mucosa

A

mucosal blood flow

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6
Q

Gastric Defenses Against Acid

Stomach defense:

A) Secretion of a ______ layer that protects gastric epithelial cells.

b) Secretion of _________ by ____________ cells.

A

mucus

bicarbonate ions

superficial gastric epithelial

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7
Q

Gastric Defenses Against Acid

Stomach defense:

a)Secretion of a mucus layer that protects gastric epithelial cells.

Mucus production is stimulated by _______ and ________ , which also directly ___________ by _____ cells.

A

prostaglandins E2 and I2

inhibit gastric acid secretion ; parietal

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8
Q

Gastric Defenses Against Acid

Stomach defense:

Secretion of bicarbonate ions by superficial gastric epithelial cells.

Bicarbonate _________ HCl.

A

neutralizes

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9
Q

Drugs that inhibit prostaglandin formation (are _______ and _______ ) _____ease mucus secretion

A

alcohol and NSAIDs

decr

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10
Q

Drugs that inhibit prostaglandin formation predispose to the development of acid-peptic disease.

T/F

A

T

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11
Q

Regulatory molecules that stimulate acid secretion

_______
_______
_______

A

Acetylcholine

Histamine

Gastric

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12
Q

Regulatory molecules that stimulate acid secretion

Acetylcholine:

Produced from nerve endings and stimulate ____ receptor on:

________ cells (produce HCl)

_________ cells and ______ cells (produce _______ )

_____ cells (produce ______)

A

M3

Parietal; HCL

Enterochromaffin; Mast ; Histamine

G; gastrin

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13
Q

Regulatory molecules that stimulate acid secretion

Histamine

Produced by ________ cells and _____ cells in response to stimulation of _____ receptors (by acetylcholine) and _____ receptors by gastrin.

It stimulates _______ cells to produce _____

A

enterochromaffin; Mast

M3; CCK3

parietal; HCL

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14
Q

Regulatory molecules that stimulate acid secretion

Gastrin:

Produced by ____ cells in response to stimulation of ____ receptors by acetylcholine and ______ and by chemical substances in food

A

G

M3

stretch

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15
Q

Types of gastric HCl secretion
1-_______ (basal) acid secretion: depend on ________

2-________ stimulated acid secretion: stimulated by:

_______
_________
__________

A

Nocturnal; histamine

Meal

Gastrin Acetylcholine
Histamine

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16
Q

Phases of gastric secretion

1)_______ Phase
2) _______ Phase
3) _______ Phase

A

Cephalic

Gastric

Intestinal

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17
Q

Phases of gastric secretion

Phase. Stimuli. Pathway

Cephalic. _________. 1,2,3
Gastric __________. 1,2,3
Intestinal ___________

A

Sight, smell, taste or thought of food;

1)Vagus (M3 receptors).2) Histamine (H2 receptor). 3)Gastrin

Food in the stomach

1)Stretch: local reflex (M3 receptors)
2)Chemical substances in food (gastrin)
3)Increase pH: Inhibition of somatostatin release

Chyme in the duodenum

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18
Q

Which Phases of gastric secretion are stimulators and which ones are inhibitory

A

Stimulatory: Cephalic and gastric

Inhibitory: intestinal

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19
Q

Steps of gastric acid secretion by parietal cells

STEP1: Hydrogen ions are produced in the ______ cells by the action of the enzyme ________ which catalyses the reaction between _______ and _____, in which _______ is produced.

This acid immediately ________ into ________ and _________

• Hydrogen ions __________ by the aid of _______________

A

parietal; carbonic anhydrase

carbon dioxide and water; carbonic acid

dissociates; hydrogen ions and carbonate ions.

leave the cell ; H+/K+ ATPase pump.

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20
Q

Steps of gastric acid secretion by parietal cells

STEP2: Chloride ions are transported across the ________ membrane of the parietal cells into the parietal cells in exchange with __________, aid of ___________ (ATP ________ carrier).

• Chloride (Cl ̄) and hydrogen ions are secreted (passively or actively?) from the _________________ into the ____________ where they combine into HCl which is then secreted into _____________

A

basolateral

bicarbonates; an antiport ; dependent

Actively ; cytoplasm of parietal cells

lumen of the canaliculus

the lumen of the stomach

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21
Q

Management

I- Agents that reduce gastric acidity
1. ________ inhibitors
2. ____ receptor antagonists
3. ______ receptor antagonists
4. ____________

A

Proton pump

H2

Muscarine

Antacids

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22
Q

Management

II- Mucosal protective agents

_________
_______________ agonists (________)
__________ compounds
__________

A

Sucralfate

Prostaglandin (PGE1); misoprostol

Colloidal bismuth

Carbenoxolone

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23
Q

Prostaglandin (PGE1) agonists

Eg: ————

A

misoprostol

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24
Q

Agents that reduce increased gastric acidity
1- Proton pump inhibitors

List 5

A

Pantoprazole

Esomeprazole

Omeprazole

Rabeprazole

Lansoprazole

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25
Q

Agents that reduce increased gastric acidity
1- Proton pump inhibitors

Action: Inhibit both ———- and ________ - stimulated HCl secretion by (reversible or irreversible?) inactivation of the proton pump in the ________________

A

fasting (basal) and meal

irreversible

wall of parietal cells

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26
Q

_________ are the most potent suppressors of gastric acid secretion

A

Proton pump inhibitors

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27
Q

Proton pump inhibitors: Pharmacokinetics

Proton pump inhibitors are _____ that require _______ in the ________ of parietal cells, where its converted to its active form: ___________

A

prodrugs; activation

acidic secretory canaliculi

SULFENIC ACID.

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28
Q

Proton pump inhibitors: Pharmacokinetics

1- Oral forms are prepared as __________ formulations that release the drug in the __________ (because they are _____________________ )

2- After absorption, they are distributed by blood to __________

3-They (reversibly or irreversibly?) inactivate the proton pump molecule (providing ___________ suppression of acid secretion, despite the much (shorter or longer?) plasma half-lives of the

A

acid resistant; intestine

Degraded in acid media

parietal cells

reversibly

24- to 48-hour; shorter

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29
Q

Proton pump inhibitors: Pharmacokinetics

4- they should be given on _______ stomach because __________

5- They should be given ______ to _______ before food intake because _______ in the parietal cell acid canaliculi is required for drug activation, and food ______ acid production

A

an empty ; food affects absorption

30 minutes to 1 hour ; an acidic pH

stimulates

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30
Q

Concomitant use of other drugs that inhibit acid secretion, such as H2-receptor antagonists, might be predicted to (lessen or potentiate?) the effectiveness of the proton pump inhibitors

A

potentiate

Not sure, I think I kept the wrong thing here

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31
Q

Proton pump inhibitors: Pharmacokinetics

6- Maximal effect is reached after ____________ of administration (the time required to fully ______________)

7- Their effects persists for _______ after stopping the drug (the time required for the ________________)

A

3 to 4 days; inactivate the proton pumps

3 to 4 days

synthesis of new proton pumps molecules

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32
Q

Proton pump inhibitors: Pharmacokinetics

8- Metabolized by the _____

9- Minimal excretion by the ______

A

liver

kidney

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33
Q

dose reduction of proton pump inhibitors is not necessary in severe liver impairment

T/F

A

F

dose reduction is necessary in severe liver impairment

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34
Q

no dose reduction of proton pump inhibitors is necessary in renal impairment

T/F

A

T

no dose reduction is necessary in renal impairment)

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35
Q

Proton pump inhibitors Adverse effects

1- The most common are _____ troubles in the form of _______, _______, _____, ________ and ______

2- Subacute _______,_______,_________, and __________

A

GIT; nausea, abdominal pain, constipation, flatulence, and diarrhea

myopathy, arthralgias, headaches, and skin rashes

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36
Q

Proton pump inhibitors Adverse effects

3- Prolonged use leads to vitamin _____ deficiency (because _____________).

4-Hypogastrinemia which may predispose to _____________ upon discontinuation of therapy and may promote the ____________(___________)

A

B12; HCl is important for releasing vitamin B12 from food

rebound hypersecretion of gastric acid

growth of gastrointestinal tumors (carcinoid tumors )

37
Q

Proton pump inhibitors: Drug interactions

Metabolized by cytochrome P450 enzymes (CYP _____ and ———- ) and may interfere with the metabolism of drugs metabolized with cytochrome P450 such as ———,———-, _______ increasing their levels and producing toxicity

A

2C19 and 3A4

warfarin, diazepam and cyclosporine

38
Q

Proton pump inhibitors: Therapeutic uses

_________________

______ and _______ ulcers

Prevention of recurrence of ________-associated ________ in patients who _________

Reducing the risk of duodenal ulcer recurrence associated with _______ infections.

A

Gastroesophageal reflux disease (GERD)

Gastric and duodenal

non-steroidal anti- inflammatory drug (NSAID); gastric ulcers; continue NSAID use.

H. pylori

39
Q

H2 receptor antagonists

List 3

A

Ranitidine
Famotidine
Nizatidine

40
Q

Muscarine receptor antagonists

______
__________

A

Pirenzepine
Telenzepine

41
Q

Muscarine receptor antagonists

Mechanism of action:
reduce ______ stimulated HCl secretion by (reversible or irreversible?) blockade of muscarinic (M3) receptors on the cell bodies of the intramural cholinergic ganglia
( receptors on parietal cells are M3).

A

meal

Reversible

42
Q

Muscarine receptor antagonists

Adverse effects:
They produce ________ side effects at doses that block HCl secretion

Because of poor efficacy, side effects and ____________, they are not used in treating acid

A

anticholinergic

delay of gastric emptying

43
Q

Agents that reduce increased gastric acidity

Antacids
Mechanism of action:
1- Reduction of intragastric acidity by _______________________
2- Stimulate ___________

A

reacting with gastric HCl to form salt and water

mucosal PG production

44
Q

Agents that reduce increased gastric acidity

Antacids
Types:

________ - ___________

________ - _______________

_________ - _________________

_______ - _____________

A

NaHCO3 - Sodium bicarbonate

CaCO3 Calcium carbonate

Al hydroxide Al(OH)3

Mg(OH)2 Magnesium hydroxide

45
Q

Chemical reactions of antacids with HCl in the stomach

NaHCO3 + __HCL —-> NaCl_ + H2O + CO2

CaCO3 + ___HCL —-> CaCl__+ H2O + CO2

Al(OH3) + ___HCL —-> AlCl__ + H2O + CO2

Mg(OH)2 + __HCL —-> MgCl__ + H2O + CO2

A

1; 1

2; 2

3; 3

2; 2

46
Q

Effects of antacids

1- Neutralize _________ in the ______ (by the reacted part)
2- Effect of the ______ part
3- Effects of the _____________

A

excess HCl in the stomach

unreacted

products of the reaction

47
Q

Effects of antacids

Raising gastric pH from _____ to ____ neutralizes ___% of gastric acid.

Raising gastric pH point from ___ to ___ neutralizes ___% of the gastric acid.

A

1.3 to 1.6

50

1.3 to 2.3

90

48
Q

Effects of antacids 1- Sodium bicarbonate

1- Effect of the reacted part: __________ of the gastric HCL

2- Unreacted sodium bicarbonate could be ________ causing _______ if given in high doses or in patients with ________

3- NaCl produced by the reaction could be _______ causing _________ and aggrevating ________

4- CO2 produced causes _______ and increased production of ____ which causes ________

5- High doses given with dairy products can lead to ________ and ________ (_________ syndrome)

A

rapid neutralization

absorbed; metabolic alkalosis; impaired renal function.

absorbed; fluid retention ; hypertension

gastric distention; gastrin; rebound acidity

hypercalcemia and renal insufficiency; milk-alkali

49
Q

Effects of antacids 2- Calcium carbonate

1- Effect of the reacted part: _______ neutralization of the gastric HCL

2- CO2 produced causes _______ and increased production of ____ which causes ________

3- High doses given with dairy products can lead to ________ and ________ (_________ syndrome)

A

less rapid

gastric distention; gastrin; rebound acidity

hypercalcemia and renal insufficiency; milk-alkali

50
Q

Effects of antacids 3- Aluminum hydroxide

1- Effect of the reacted part: ______ neutralization of the gastric HCL

2- No ____________

3- Unabsorbed aluminum salts may cause _________

A

slow

metabolic alkalosis

constipation

51
Q

Effects of antacids 4- Magnesium hydroxide

1- Effect of the reacted part: _____ neutralization of the gastric HCL

2- No __________

3- Unabsorbed magnesium salts may cause ________

4- Magnesium could be absorbed and excreted by the ______ and therefore should not be given to patients with ______ for a long tine

A

slow

metabolic alkalosis

osmotic diarrhea

kidney; renal insufficiency

52
Q

Precautions with antacids

Affect absorption of other drugs therefore should not _____________________

A

be given within 2 hours of tetracycline or iron

53
Q

Mucosal protective agents
1- Sucralfate

Sucralfate = complex _________ + ______ +
______

A

aluminum hydroxide

sulfate

sucrose

54
Q

Mucosal protective agents
1- Sucralfate

Mechanism of action:
1- in acidic environment of the stomach, it forms a ____ that binds to ——— or ____ for ______ forming a _______ against hydrolysis of mucosal proteins by pepsin.

2- stimulates _______ and _______ production

A

viscous paste

ulcers or erosions

6 hours; physical barrier

mucosal prostaglandins and bicarbonate

55
Q

Mucosal protective agents 1- Sucralfate

Therapeutic uses:
Prophylaxis of ________ in critically ill patients (increased pH of the stomach increases the possibility of ___________)

Conditions associated with _______ not due to _________ as ______ and by ________ solitary rectal ulcers.

A

stress ulcers; nosocomial infections.

mucosal ulceration; acid production

aphthous ulcers; rectal enema

56
Q

Mucosal protective agents 1- Sucralfate
Administration:

Since it is activated by acid, sucralfate should be taken on _____ stomach _____________

The use of _______ within 30 minutes of a dose of sucralfate should be avoided.

A

an empty

1 hour before meals

antacids

57
Q

Mucosal protective agents 1- Sucralfate

Adverse Effects: __________

A

Constipation

58
Q

Mucosal protective agents 1- Sucralfate

Precautions:
1)should be avoided in patients with ______ failure (because __________).

2)Should be taken at least _____ after the administration of other drugs as phenytoin and digoxin (because it __________________________ that may ______

A

renal ; some aluminium is absorbed

2 hours

forms a viscous layer in the stomach that may inhibit absorption of drugs)

59
Q

agents 2-Misoprostol

Action

  1. Inhibit _____-stimulated gastric acid secretion
  2. Stimulation of _____ and ______ secretion

3)Increase .—————-

A

histamine

mucin and bicarbonate

mucosal blood flow

60
Q

agents 2-Misoprostol

Therapeutic uses:
Prevention of ________________________ (rarely used because __________ – ___ times daily)

A

NSAID-induced mucosal injury

it needs frequent administration

4

61
Q

agents 2-Misoprostol
Adverse Effects:

  1. _______, with or without abdominal pain and
  2. Exacerbations of ___________ and should be avoided in patients with this disorder.
A

Diarrhea

inflammatory bowel disease

62
Q

agents 2-Misoprostol

Contraindications:
1. __________ disease
2. _______ (may cause _______)

A

Inflammatory bowel

Pregnancy; abortion

63
Q

Mucosal protective agents

Colloidal bismuth compounds aka _____________

A

Bismuth subsalicylate

64
Q

Mucosal protective agents
3- Colloidal bismuth compounds

Pharmacological actions:
1- Undergoes (slow or rapid?) dissolution in the stomach into ______ and ______

2- _______ are _______

3- ______ coats ulcers and erosions protecting them from acid and pepsin and increases ______ and _______ production

A

Rapid; Bismuth and salicylate

Salicylates are absorbed

Bismuth; prostaglandin and bicarbonate

65
Q

Mucosal protective agents
3- Colloidal bismuth compounds

Uses:
-Treatment of __________ and _________

A

dyspepsia and acute diarrhoea

66
Q

Mucosal protective agents
4- Cabenooxolone

Mechanism of action: _____________

A

not known

67
Q

Mucosal protective agents
4- Cabenooxolone

Adverse reactions:
It has _______ like action and may cause:
1-______ retention
2- _____kalemia
3- ________
4- Exacerbates ________

A

aldosterone

sodium

Hypo

Oedema

hypertension

68
Q

Specific acid dyspeptic disorders and therapeutic strategies

Peptic ulcer

A

Proton pump inhibitors

69
Q

Specific acid dyspeptic disorders and therapeutic strategies
NSAID-related Ulcers
1-__________ (best)
2- _________
3- _________

A

Proton pump inhibitors

H2 receptor antagonist

Misoprostil

70
Q

Specific acid dyspeptic disorders and therapeutic strategies

Helicobacter pylori infection (H. pylori)

A

Triple therapy for 14 days:
[Proton pump inhibitor + clarithromycin + (metronidazole or amoxicillin)] twice a day.

71
Q

Specific acid dyspeptic disorders and therapeutic strategies

Gastro-esophageal reflux disease

If it’s mild:

If it’s severe:

______are recommended only for the patient with mild, infrequent episodes of heartburn.

If it’s Severe with nocturnal acid breakthrough: _________ twice daily. If symptome persist, ________ is added at night

A

H2 receptor antagonists

Proton pump inhibitors

Antacids

proton pump inhibitors ; H2 receptor antagonist

72
Q

MUCOSA DEFENSE MECHANISM

•Secretion of ______ and ______

•Dilution of gastric acid by ______ and ______

•Prevention of _______ of HCl from the _______ back into the __________.

•Release of Prostaglandin ____.

•Alkalization of gastric secretions by _____ and ______

A

mucus and bicarbonate.

food and secretions.

diffusion; stomach lumen; gastric mucosal lining

E

pancreatic juices and bile

73
Q

DRUGS THAT REDUCE GASTRIC SECRETION
•__________ Inhibitors
•__________ Antagonist
•_____________

DRUGS THAT PROTECT MUCOSAL SURFACE
•_________
•________________
•______________ Analog
•_________

A

Proton Pump; H2 Receptor; Antimuscarinics

Sucralfate; Bismuth Subsalicylate

Prostaglandin E ; Antacids

74
Q

DRUGS THAT REDUCE GASTRIC SECRETION

•__________ Inhibitors
•__________ Antagonist
•_____________

A

• Proton Pump Inhibitors • H2 Receptor Antagonist • Antimuscarinics

75
Q

DRUGS THAT PROTECT MUCOSAL SURFACE
•_________
•________________
•______________ Analog
•_________

A

• Sucralfate
• Bismuth Subsalicylate
• Prostaglandin E Analog
•Antacids

76
Q

MECHANISM OF ACTION of PPI

(Reversibly or Irreversibly?) bind and blocks the __________ ENZYME

This results in achlorhydria; all gastric acid secretion is blocked.

Decreases acid secretion by up to _____% for up to ____ h

A

Irreversibly; H+/K+ ATPASE

95; 48

77
Q

ADVERSE EFFECT of PPI

Nausea
Diarrhea
Abdominal pain
__________
__________ in long-term use
Lightheadedness
Headaches

A

Flatulence

Osteoporosis

78
Q

Examples of H2 receptors antagonist ?

A

Ranitidine
Famotidine
Nizatidine
Cimetidine

79
Q

H2 receptors antagonist
Suppresses ____ hour gastric secretion by ___%

Proton pumps inhibitor
Decreases acid secretion by up to ___% for up to ____ h

A

24; 70

95; 48

80
Q

ADVERSE EFFECT of H2 receptor antagonist

________,________. Headaches Lethargy Confusion Diarrhea Urticaria Sweating Flushing

A

Impotence Gynecomastia

81
Q

Examples of Anti-muscarinics

A

Telenzepine Pirenzepine Dicyclomine

82
Q

MECHANISM OF ACTION of Anti-muscarinics

Binds and blocks Muscarinic _____ acetylcholine receptor antagonist.

Blocks gastric acid secretions.

A

M1

83
Q

ADVERSE EFFECT of antacids

Aluminum salt
•_________

Magnesium salt
•________

Sodium salt
•__________, _________

Calcium salt
•————,———,________

A

Constipation

Diarrhea

Metabolic alkalosis; Hypertension

Constipation; Kidney stones ; Hyperacidity rebound

84
Q

Prostaglandin E2 Analogue
__________

Sucralfate
_______________ + ______________

A

Misoprostol

Sulfated Sucrose + Aluminum hydroxide

85
Q

Triple Therapy

___ day treatment - Effective __-___ %

_______________ + _________/_______ + _________/________

A

7; 80-85

PROTON PUMP INHIBITOR

AMOXICILLIN/TETRACYCLINE

METRONIDAZOLE/CLARITHROMYCIN

86
Q

Quadruple Therapy

___________ + __________

A ____ day treatment, as efficacious as triple therapy

A

TRIPLE THERAPY + BISMUTH

3

87
Q

PPI - (liver or kidney?)

H2 receptor antagonist (liver or kidney?)

A

Liver

Kidney

88
Q

Muscarinic antagonist causes diarrhea or constipation?

A

Constipation

House Pharmacology (50 decks)

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