GI disorders: intro and gerd Flashcards

1
Q

Parietal cells can be stimulated to release acid by what 3 things:

A

Gastrin
Acetylcholine (Ach)
Histamine

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2
Q

Stimuli for gastrin secretion?

A
  1. Small peptides and amino acids in the lumen of the stomach
  2. Distention of the stomach
  3. Vagal stimulation
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3
Q

what inhibits gastrin?

A

H+ in the lumen of the stomach

Somatostatin

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4
Q

acid production: cephalic response

A

Response to sight, smell, taste, and anticipation of food (mediated by Ach)

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5
Q

acid production: gastric

A

Induced by the presence of food in the stomach

Distention of the stomach  vagal response  gastrin release

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6
Q

acid production:intestinal

A

Due to entry of food into the lumen of the small intestine

Amino acids have positive feedback on gastrin release

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7
Q

epidemiology of Gerd

A

more common in whites and blacks

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8
Q

Gastro esophageal reflux disease

A

Effortless movement of gastric contents from the stomach to the esophagus leading to symptoms and signs of injury to the esophagus, oropharynx, larynx, and respiratory tract

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9
Q

pathophysiology of Gerd

A

Develops when acidic contents reflux into the esophagus and remain there long enough to cause damage . common in the first trimester of pregnancy due to relaxation of LES

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10
Q

for reflux to occur

A

LES (lower esophageal sphincter) must be relaxed enough to allow passage of fluid and
Pressure must be greater in the stomach than the esophagus must allow this flow

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11
Q

risk factors for Gerd increasing intragastric

A

Delayed gastric emptying  increase gastric volume and frequency of reflux
Smoking and high fat meals  increased gastric volume and emptying

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12
Q

risk factors for Gerd: intra-abdominal pressure

A

Obesity and pregnancy

Tight fitting clothes

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13
Q

Foods that decrease LES pressure

A
Fatty meal
Carminatives (peppermint, spearmint)
Ethanol
Garlic 
Chocolate 
Caffeine (coffee, tea, cola)
Chili Peppers 
Onions
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14
Q

foods that increase LES pressure

A

High protein meals

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15
Q

drugs that decrease LES pressure

A
Anticholinergics (TCAs)
Barbituates 
Caffeine 
DHP CCBs
Dopamine
Estrogen
Ethanol  
Nitrates
Progesterone 
Tetracycline 
Theophylline
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16
Q

Direct Irritants to the esophageal mucosa:foods

A
Foods 
Spicy foods 
Orange juice 
Tomato juice 
Coffee
17
Q

Direct Irritants to the esophageal mucosa ;medications

A
Medications: NSAIDs / Aspirin 
Alendronate 
Iron 
Quinidine 
Potassium Chloride
18
Q

clinical presentation of Gerd

A

Heartburn
Burning retroperitoneal pain
Can occur anytime of day, but most frequently after meals
Water brash
Reflex salivary hypersecretion in response to esophagitis
Belching
Regurgitation
Gastric contents are returned to the mouth in the absence of nausea

19
Q

alarming symptoms of Gerd

A
May be indicative of complications 
Dysphagia
Difficulty swallowing 
Odynophagia 
Pain on swallowing 
Bleeding
Unexplained weight loss
Choking 
Chest Pain
20
Q

complications Gerd

A

Esophageal stricture
Esophageal ulceration, perforation, or bleeding
Barrett’s esophagus and esophageal adenocarcinoma

21
Q

diagnosis of Gerd

A
Clinical History 
Heartburn / acid regurgitation 
Pts with mild symptoms 
Endoscopy 
Preferred technique 
Allows exclusion of other diseases and confirms diagnosis 
Ambulatory pH / impendence monitoring 
Esophageal Manometry 
PPI Test 
Short course of PPI
22
Q

therapy for Gerd:lifestyle changes

A

Lifestyle modifications
Avoid laying down for several hours following a meal
Limit tight fitting clothes
Eat smaller meals
Avoid foods/drugs that decrease LES pressure
Weight loss
Smoking cessation
Elevating the head of the bed 6-8 inches with a foam wedge under the mattress

23
Q

antacids

A
Mechanism of action
Neutralizes gastric acid 
Dosing 
PRN 
Place in GERD therapy 
Fast symptom control 
Poorly suited for regular use 
Agents
Calcium carbonate  
Aluminum Hydroxide 
Magnesium Hydroxide 
Sodium Bicarbonate .Pepcid AC has aluminum hy and mag to counter act GI
effects

Fluroquinolones and tetracyline calcium mag ad
Alum can bind to these products and not allow them to
Absorb. Levothroxine also can not be absorbed

24
Q

antacids

A
Adverse Effects
Constipation 
More common with aluminum and calcium 
Diarrhea 
More common with magnesium 
Aluminum and magnesium containing antacids can accumulate in renal failure 
Pregnancy Category C
Drug Interactions 
In general, schedule around other medications by 2-4 hours to avoid interactions don't work on receptor stressed
25
Q

histamine 2 agonists

A
Mechanism of action: 
Blocks H2 receptor activation on parietal cells and prevents histamine-stimulated acid production
Better at blocking nocturnal acid production than food-stimulated secretion  
Dosing: 
BID to QID
Place in GERD Therapy 
Mild to moderate GERD
Agents
Cimetidine
Usually avoided due to higher incidence of ADEs and drug interactions 
Ranitidine
Famotidine 
Nizatidine (rarely used)

Might not be good choice for those who have problems
After meals

Ranitidine-zantac
Famotidine-pepcid
Most commonly used

26
Q

proton pump inhibitors: mechanism of action and dosing

A
Mechanism of action 
Irreversibly inhibits the H+/K+ ATPase (proton pump) of the parietal cell 
Blocks all acid production 
Only inhibits activated pumps 
Takes 3-5 days to reach clinical effect 
Dosing 
Dosed daily to BID
Administer before meals
27
Q

proton pump inhibitors: drug interactions and adverse effects

A

Place in GERD Therapy

Adverse Effects
Diarrhea or constipation
Vitamin B12 deficiency
Controversial association with C. Diff infection
Drugs Interactions
Clopidogrel  decreases pro-drug activation
Less with pantoprazole

28
Q

Prokinetics: mechanism of action, adverse effects, place in therapy

A

Metoclopramide
Mechanism
Antidopaminergic and stimulation of cholinergic receptors
Increases LES pressure
Accelerates gastric emptying
Adverse effects
EPS (extrapyramidal symptoms)
Akathesia
Contraindicated in patients with GI bleed, perforation or obstruction, pheochromocytoma, other drugs that cause EPS, and/or seizure disorders
Place in therapy
Great for adjunctive therapy in select patients – not ideal for monotherapy

29
Q

treatment of intermittent and mild heartburn

A

LSM
Antacids: PRN or after meals/at bedtime
Over-the-counter doses of PPIs or H2 Blockers
If symptoms persist  move to mild treatment

30
Q

mild symptoms no warning signs

A

LSM
H2 Blockers for 6-12 weeks or PPI for 4-8 weeks
If no relief with H2 Blocker  try PPI
If no relief with PPI  increase dose or refer for endoscopy

31
Q

moderate to severe symptoms no warning signs

A

LSM
PPI for 4-16 weeks (full doses)
If no relief  increase PPI dose or add-on H2 blocker or refer for endoscopy

32
Q

warning signs or known erosive esophagitis

A

LSM
Refer patient with warning signs for endoscopy
PPI at healing doses for 4-16 weeks

33
Q

H2 blockers

A

H2 blockers will not keep you from getting
Acid production because there are multiple
Ways that acid gets produced

Histamine is going to work on parietal cell
And cause it to release acid
M3 and gastrin in atrum can also produce acid

Stools less fluid. Unknow why it causes diarrhea
Sometimes more diarrhea

/more studies to back up use of zantac in preg

Pregnancy some use tums although cate B