GI Part 1 Flashcards
1
Q
GI diseases
Esophagus –_____ (_____)
Stomach – _____, _____ (PUD)
Intestines –
-Acute: _____ (Bacteria, Viruses and Protozoa) / Traveler’s _____
Chronic: _____ (duodenum), _____ diseases (IBD- UC/Crohn’s), _____ (_____), and _____ disease
-_____
Rectum and Anus – Anal fissures, _____
A
Gastroesophageal reflux disease (GERD) gastritis peptic ulcer disease Gasteroenteritis diarrhea Peptic ulcer disease Inflammatory bowel Irritable bowel syndrome (IBS) Coeliac constipation Hemorrhoids
2
Q
GERD: a digestive disorder of the _____ (_____)
- symptoms: chronic _____, _____, _____, _____ pain and early _____
- Reflux – Excess _____ production, weakness of _____ at LES or _____
- > 9 million primary care visits annually in US
- Most common cause of _____
- If left untreated, esophagitis can cause _____, _____, and chronic _____
- Scarring narrows the esophagus and interferes with _____
- Long standing GERD symptoms may cause _____ (10-15%) increasing the likelihood of_____
A
lower esophageal sphincter (LES) heartburn dyspepsia regurgitation epigastric satiety acid muscular ring hiatal hernia esophagitis bleeding ulcers scarring swallowing Barrett's esophagus cancer
3
Q
GERD and extra-esophageal symptoms
- Refluxed gastric contents can go into the throat, airways and lungs causing irritation or damage:
- -Chronic _____
- -Chronic _____
- -_____
- -_____
- Progressive breathing problems
- Pulmonary diseases (adult-onset _____ or pulmonary _____)
-Distinguish _____ from _____ chest pain before diagnosing GERD
A
cough laryngitis aspiration pneumonia asthma fibrosis cardiac non-cardiac
4
Q
GASTRITIS: inflammation, irritation or erosion of _____
- acute/chronic
- causes:
- -excessive _____ use
- -chronic _____
- -_____
- -medications such as _____, other _____ and _____
- _____ pylori
- _____ reflux
- infections caused by _____ and _____
- if left untreated- severe loss of _____ and increased risk of developing _____
A
stomach lining alcohol vomiting stress aspirin NSAIDs bisphosphonates helicobacter bile bacteria viruses blood stomach cancer
5
Q
- _____: inflammation of superficial gastric mucosa
- _____: destruction of multiple small zones of superficial mucosa
- _____: destruction of full thickness of mucosa
A
superficial gastritis
erosive gastritis
gastric ulceration
6
Q
PUD: peptic ulcer disease (gastric/duodenal)
-_____ that develops on the _____ lining of the stomach and or the _____ portion of _____ (extends through _____ mucosa)
A
open sore inside upper SI muscularis
7
Q
symptoms of PUD
- _____ stomach pain
- feeling of _____
- _____ or _____
- _____ food intolerance
- _____
- _____
- gastric ulcer- pain is _____ after _____
- duodenal ulcer- _____ after meals
- etiology is similar to _____
- _____ alone do not increase the risk for PUD, can potentiate _____ risk in patients who use _____ concurrently
A
burning fullness bloating belching fatty heartburn nausea shortly meals 2-3 hours meals gastritis corticosteroids ulcer NSAIDs
8
Q
H. Pylori
- Gram _____, spiral bact, in _____ and _____
- Infection occurs by _____ route
- Oral cavity may be the permanent reservoir (found in dental plaque and saliva) and a _____ route is the most probable mode of transmission
- Several virulence factors are produced:
- _____- UREASE converts urea into _____ which buffers _____ and creates an _____ (allows to survive for years)
- Results in
- High levels of _____ and _____ and reduced levels of _____
- Impaired _____ secretion
A
–ve gastric antrum pyloric sphincter oral person-to-person Urease ammonia H+ ions ALKALINE CLOUD gastrin pepsinogen somatostatin duodenal bicarbonate
9
Q
“ALARM FEATURES” that warrant prompt gastroenterology referral
- _____
- _____
- early _____
- unexplained _____
- progressive _____ or _____
- recurrent vomiting and family history of _____
-patients with perforated PUD usually present with a sudden onset of severe, sharp _____ pain: _____!
A
bleeding anemia satiety weight loss dysphagia odynophagia GI cancer abdominal medical emergency
10
Q
NSAIDs
- NSAIDs are the most common cause of _____ in patients without _____ infection
- topical effects of NDAIDs cause _____. in addition, by inhibiting _____, NSAIDs inhibit the formation of _____ (PGE2) and their protective _____-2-mediated effects (i.e., enhancing gastric mucosal protection by stimulating _____ and _____ secretion and _____ proliferation and increasing mucosal _____)
- coexisting _____ infection increases the likelihood and intensity of _____- induced damage
- NSAID use is responsible for approximately one half of _____, which occur most commonly in older patients who are taking _____ or other _____ for _____ or _____
A
PUD H. Pylori submucosal erosions cyclooxygenase prostaglandins cyclooxygenase mucus bicarbonate epithelial cell blood flow H. Pylori NSAID perforated ulcers aspirin NSAIDs cardiovascular disease arthropathy
11
Q
PUD treatment
- Address the underlying cause
- Lifestyle changes:
- Reduction in _____ and _____ foods
- _____ loss
- Head of bed _____ & avoidance of meals _____ before _____
- Eradication of_____infection
- Withdraw _____
- Anti-secretory therapy
1: _____
2: _____ blockers
3: _____ inhibitors (PPIs)
A
fatty spicy weight elevation 2-3 hours bedtime H pylori NSAIDs Antacids H2 proton pump
12
Q
antacids: _____ + _____ = _____ + _____
- act as buffers to neutralize _____ (act within _____)
- therapeutic effect is by _____ or _____ properties
- salts of _____, _____, or _____
- available as chewable/dissolving tablets, liquid and gums
- examples: _____, _____, _____
- inhibit _____ activity by raising pH to _____
- side effects- _____ (_____ salts) and _____ (_____ salts)
- mixture of these two can preserve normal _____ function
- antacids impair the absorption of _____, oral _____, _____, _____, _____, _____ and _____
A
acid alkali salt water H+ ions mins physical chemical aluminum magnesium calcium alka-seltzer gelusil tums peptic 5 diarrhea Mg constipation Al bowel tetracycline iron fluoride ciprofloxacin erythromycin metronidazole thyroxine
13
Q
H2 blockers- inhibit _____ and _____ stimulated _____ secretion
- reversible competitive inhibitors of _____ at all H2- receptors
- highly selective for _____
- inhibit _____, _____, and _____ stimulated _____ secretion
- _____ secretion also falls with reduction in acid volume
- available both by OTC and prescription:
- _____ (Tazac, Axid)
- _____ (Pepcid)
- _____ (Zantac)
- _____ (Tagamet)
- _____ are likely to follow when treatment is stopped
- all agents are rapidly absorbed from _____
A
basal food gastric acid histamine H2 receptors histamine gastrin Ach acid pepsin Nizatidine Famotidine Ranitidine Cimetidine relapses intestine
14
Q
pharmacokinetics
- undergo _____ metabolism resulting in bioavailability of _____ (except _____)
- action starts within an _____ and DOA is _____ hours based on the dose administered
- ADRs: _____, _____, _____, _____, _____ and _____
- these drugs are cleared by combination of _____ metabolism, _____ filtration, and _____ secretion
- dose reduction is required in patients with moderate to severe _____ and _____ insufficiency
- in the elderly, a decrease in _____ and _____ decline in drug clearance occurs
A
first pass hepatic 50% Nizatidine hour 8-12 xerostomia diarrhea myalgia headache constipation fatigue hepatic glomerular renal tubular renal hepatic volume of distribution 50%
15
Q
clinical relevance
- use of H2 blockers before treatment ( _____ premedication/ _____) is beneficial in _____ patients
- _____ and _____ may occasionally cause _____
- GI pH is _____, concurrent use causes marked reduction in absorption of _____. advise patients to take at a different time.
- _____ alters the blood flow to the liver and is an enzyme inhibitor: can enhance DOA of other medications, especially _____
- cimetidine inhibits the metabolism of _____ and _____
A
anesthetic surgeries GERD cimetidine ranitidine thrombocytopenia increased antifungals cimetidine analgesics phenytoin warfarin
