GIT Acidity Flashcards
A peptic ulcer (stomach or duodenal) is a ___________________ of the _______,________, or _________
break in the inner lining
esophagus, stomach, or duodenum.
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.
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),
Gastric Defenses Against Acid
Esophageal defense: the _________, which prevents _______ of acidic gastric contents into the esophagus.
lower esophageal sphincter
reflux
Gastric Defenses Against Acid
Stomach defense: require adequate __________ because of the high metabolic activity and oxygen requirements of the gastric mucosa
mucosal blood flow
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
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
Gastric Defenses Against Acid
Stomach defense:
Secretion of bicarbonate ions by superficial gastric epithelial cells.
Bicarbonate _________ HCl.
neutralizes
Drugs that inhibit prostaglandin formation (are _______ and _______ ) _____ease mucus secretion
alcohol and NSAIDs
decr
Drugs that inhibit prostaglandin formation predispose to the development of acid-peptic disease.
T/F
T
Regulatory molecules that stimulate acid secretion
_______
_______
_______
Acetylcholine
Histamine
Gastric
Regulatory molecules that stimulate acid secretion
Acetylcholine:
Produced from nerve endings and stimulate ____ receptor on:
________ cells (produce HCl)
_________ cells and ______ cells (produce _______ )
_____ cells (produce ______)
M3
Parietal; HCL
Enterochromaffin; Mast ; Histamine
G; gastrin
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
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
G
M3
stretch
Types of gastric HCl secretion
1-_______ (basal) acid secretion: depend on ________
2-________ stimulated acid secretion: stimulated by:
_______
_________
__________
Nocturnal; histamine
Meal
Gastrin Acetylcholine
Histamine
Phases of gastric secretion
1)_______ Phase
2) _______ Phase
3) _______ Phase
Cephalic
Gastric
Intestinal
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
Which Phases of gastric secretion are stimulators and which ones are inhibitory
Stimulatory: Cephalic and gastric
Inhibitory: intestinal
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.
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
Management
I- Agents that reduce gastric acidity
1. ________ inhibitors
2. ____ receptor antagonists
3. ______ receptor antagonists
4. ____________
Proton pump
H2
Muscarine
Antacids
Management
II- Mucosal protective agents
_________
_______________ agonists (________)
__________ compounds
__________
Sucralfate
Prostaglandin (PGE1); misoprostol
Colloidal bismuth
Carbenoxolone
Prostaglandin (PGE1) agonists
Eg: ————
misoprostol
Agents that reduce increased gastric acidity
1- Proton pump inhibitors
List 5
Pantoprazole
Esomeprazole
Omeprazole
Rabeprazole
Lansoprazole
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
- Inhibit _____-stimulated gastric acid secretion
- 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:
- _______, with or without abdominal pain and
- 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.
M1
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
