GIT Acidity Flashcards by Iseoluwa Ojo

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

break in the inner lining

esophagus, stomach, or duodenum.

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A peptic ulcer :

of the stomach is called a —————

of the duodenum, is called a _____________

of the esophagus, is called an _________

gastric ulcer

duodenal ulcer

esophageal ulcer.

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

infection

Helicobacter pylori

Chronic

nonsteroidal anti- inflammatory medications (NSAIDs),

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Gastric Defenses Against Acid

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

lower esophageal sphincter

reflux

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Gastric Defenses Against Acid

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

mucosal blood flow

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Gastric Defenses Against Acid

Stomach defense:

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

b) Secretion of _________ by ____________ cells.

mucus

bicarbonate ions

superficial gastric epithelial

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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.

prostaglandins E2 and I2

inhibit gastric acid secretion ; parietal

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Gastric Defenses Against Acid

Stomach defense:

Secretion of bicarbonate ions by superficial gastric epithelial cells.

Bicarbonate _________ HCl.

neutralizes

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

alcohol and NSAIDs

decr

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

T/F

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Regulatory molecules that stimulate acid secretion

_______
_______
_______

Acetylcholine

Histamine

Gastric

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Regulatory molecules that stimulate acid secretion

Acetylcholine:

Produced from nerve endings and stimulate ____ receptor on:

________ cells (produce HCl)

_________ cells and ______ cells (produce _______ )

_____ cells (produce ______)

Parietal; HCL

Enterochromaffin; Mast ; Histamine

G; gastrin

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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 _____

enterochromaffin; Mast

M3; CCK3

parietal; HCL

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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

stretch

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

2-________ stimulated acid secretion: stimulated by:

_______
_________
__________

Nocturnal; histamine

Meal

Gastrin Acetylcholine
Histamine

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Phases of gastric secretion

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

Cephalic

Gastric

Intestinal

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Phases of gastric secretion

Phase. Stimuli. Pathway

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

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

Stimulatory: Cephalic and gastric

Inhibitory: intestinal

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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 _______________

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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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 _____________

basolateral

bicarbonates; an antiport ; dependent

Actively ; cytoplasm of parietal cells

lumen of the canaliculus

the lumen of the stomach

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Management

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

Proton pump

Muscarine

Antacids

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Management

II- Mucosal protective agents

_________
_______________ agonists (________)
__________ compounds
__________

Sucralfate

Prostaglandin (PGE1); misoprostol

Colloidal bismuth

Carbenoxolone

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Prostaglandin (PGE1) agonists

Eg: ————

misoprostol

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Agents that reduce increased gastric acidity
1- Proton pump inhibitors

List 5

Pantoprazole

Esomeprazole

Omeprazole

Rabeprazole

Lansoprazole

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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 ________________

fasting (basal) and meal irreversible wall of parietal cells

_________ are the most potent suppressors of gastric acid secretion

Proton pump inhibitors

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

prodrugs; activation acidic secretory canaliculi SULFENIC ACID.

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

acid resistant; intestine Degraded in acid media parietal cells reversibly 24- to 48-hour; shorter

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

an empty ; food affects absorption 30 minutes to 1 hour ; an acidic pH stimulates

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

potentiate Not sure, I think I kept the wrong thing here

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 ________________)

3 to 4 days; inactivate the proton pumps 3 to 4 days synthesis of new proton pumps molecules

Proton pump inhibitors: Pharmacokinetics 8- Metabolized by the _____ 9- Minimal excretion by the ______

liver kidney

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

F dose reduction is necessary in severe liver impairment

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

T no dose reduction is necessary in renal impairment)

Proton pump inhibitors Adverse effects 1- The most common are _____ troubles in the form of _______, _______, _____, ________ and ______ 2- Subacute _______,_______,_________, and __________

GIT; nausea, abdominal pain, constipation, flatulence, and diarrhea myopathy, arthralgias, headaches, and skin rashes

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 ____________(___________)

B12; HCl is important for releasing vitamin B12 from food rebound hypersecretion of gastric acid growth of gastrointestinal tumors (carcinoid tumors )

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

2C19 and 3A4 warfarin, diazepam and cyclosporine

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.

Gastroesophageal reflux disease (GERD) Gastric and duodenal non-steroidal anti- inflammatory drug (NSAID); gastric ulcers; continue NSAID use. H. pylori

H2 receptor antagonists List 3

Ranitidine Famotidine Nizatidine

Muscarine receptor antagonists ______ __________

Pirenzepine Telenzepine

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).

meal Reversible

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

anticholinergic delay of gastric emptying

Agents that reduce increased gastric acidity Antacids Mechanism of action: 1- Reduction of intragastric acidity by _______________________ 2- Stimulate ___________

reacting with gastric HCl to form salt and water mucosal PG production

Agents that reduce increased gastric acidity Antacids Types: ________ - ___________ ________ - _______________ _________ - _________________ _______ - _____________

NaHCO3 - Sodium bicarbonate CaCO3 Calcium carbonate Al hydroxide Al(OH)3 Mg(OH)2 Magnesium hydroxide

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

1; 1 2; 2 3; 3 2; 2

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

excess HCl in the stomach unreacted products of the reaction

Effects of antacids Raising gastric pH from _____ to ____ neutralizes ___% of gastric acid. Raising gastric pH point from ___ to ___ neutralizes ___% of the gastric acid.

1.3 to 1.6 50 1.3 to 2.3 90

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)

rapid neutralization absorbed; metabolic alkalosis; impaired renal function. absorbed; fluid retention ; hypertension gastric distention; gastrin; rebound acidity hypercalcemia and renal insufficiency; milk-alkali

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)

less rapid gastric distention; gastrin; rebound acidity hypercalcemia and renal insufficiency; milk-alkali

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 _________

slow metabolic alkalosis constipation

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

slow metabolic alkalosis osmotic diarrhea kidney; renal insufficiency

Precautions with antacids Affect absorption of other drugs therefore should not _____________________

be given within 2 hours of tetracycline or iron

Mucosal protective agents 1- Sucralfate Sucralfate = complex _________ + ______ + ______

aluminum hydroxide sulfate sucrose

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

viscous paste ulcers or erosions 6 hours; physical barrier mucosal prostaglandins and bicarbonate

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.

stress ulcers; nosocomial infections. mucosal ulceration; acid production aphthous ulcers; rectal enema

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.

an empty 1 hour before meals antacids

Mucosal protective agents 1- Sucralfate Adverse Effects: __________

Constipation

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 ______

renal ; some aluminium is absorbed 2 hours forms a viscous layer in the stomach that may inhibit absorption of drugs)

agents 2-Misoprostol Action 1. Inhibit _____-stimulated gastric acid secretion 2. Stimulation of _____ and ______ secretion 3)Increase .—————-

histamine mucin and bicarbonate mucosal blood flow

agents 2-Misoprostol Therapeutic uses: Prevention of ________________________ (rarely used because __________ – ___ times daily)

NSAID-induced mucosal injury it needs frequent administration 4

agents 2-Misoprostol Adverse Effects: 1. _______, with or without abdominal pain and 2. Exacerbations of ___________ and should be avoided in patients with this disorder.

Diarrhea inflammatory bowel disease

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

Inflammatory bowel Pregnancy; abortion

Mucosal protective agents Colloidal bismuth compounds aka _____________

Bismuth subsalicylate

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

Rapid; Bismuth and salicylate Salicylates are absorbed Bismuth; prostaglandin and bicarbonate

Mucosal protective agents 3- Colloidal bismuth compounds Uses: -Treatment of __________ and _________

dyspepsia and acute diarrhoea

Mucosal protective agents 4- Cabenooxolone Mechanism of action: _____________

not known

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

aldosterone sodium Hypo Oedema hypertension

Specific acid dyspeptic disorders and therapeutic strategies Peptic ulcer

Proton pump inhibitors

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

Proton pump inhibitors H2 receptor antagonist Misoprostil

Specific acid dyspeptic disorders and therapeutic strategies Helicobacter pylori infection (H. pylori)

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

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

H2 receptor antagonists Proton pump inhibitors Antacids proton pump inhibitors ; H2 receptor antagonist

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 ______

mucus and bicarbonate. food and secretions. diffusion; stomach lumen; gastric mucosal lining E pancreatic juices and bile

DRUGS THAT REDUCE GASTRIC SECRETION •__________ Inhibitors •__________ Antagonist •_____________ DRUGS THAT PROTECT MUCOSAL SURFACE •_________ •________________ •______________ Analog •_________

Proton Pump; H2 Receptor; Antimuscarinics Sucralfate; Bismuth Subsalicylate Prostaglandin E ; Antacids

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

• Proton Pump Inhibitors • H2 Receptor Antagonist • Antimuscarinics

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

• Sucralfate • Bismuth Subsalicylate • Prostaglandin E Analog •Antacids

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

Irreversibly; H+/K+ ATPASE 95; 48

ADVERSE EFFECT of PPI Nausea Diarrhea Abdominal pain __________ __________ in long-term use Lightheadedness Headaches

Flatulence Osteoporosis

Examples of H2 receptors antagonist ?

Ranitidine Famotidine Nizatidine Cimetidine

H2 receptors antagonist Suppresses ____ hour gastric secretion by ___% Proton pumps inhibitor Decreases acid secretion by up to ___% for up to ____ h

24; 70 95; 48

ADVERSE EFFECT of H2 receptor antagonist ________,________. Headaches Lethargy Confusion Diarrhea Urticaria Sweating Flushing

Impotence Gynecomastia

Examples of Anti-muscarinics

Telenzepine Pirenzepine Dicyclomine

MECHANISM OF ACTION of Anti-muscarinics Binds and blocks Muscarinic _____ acetylcholine receptor antagonist. Blocks gastric acid secretions.

ADVERSE EFFECT of antacids Aluminum salt •_________ Magnesium salt •________ Sodium salt •__________, _________ Calcium salt •————,———,________

Constipation Diarrhea Metabolic alkalosis; Hypertension Constipation; Kidney stones ; Hyperacidity rebound

Prostaglandin E2 Analogue __________ Sucralfate _______________ + ______________

Misoprostol Sulfated Sucrose + Aluminum hydroxide

Triple Therapy ___ day treatment - Effective __-___ % _______________ + _________/_______ + _________/________

7; 80-85 PROTON PUMP INHIBITOR AMOXICILLIN/TETRACYCLINE METRONIDAZOLE/CLARITHROMYCIN

Quadruple Therapy ___________ + __________ A ____ day treatment, as efficacious as triple therapy

TRIPLE THERAPY + BISMUTH 3

PPI - (liver or kidney?) H2 receptor antagonist (liver or kidney?)

Liver Kidney

Muscarinic antagonist causes diarrhea or constipation?

Constipation