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Year 1: Patho/Pharm > GI Patho > Flashcards

GI Patho Flashcards

1
Q

GERD Etiology

A
  1. Decrease LES tone
    - anticholinergics
    - nicotine
  2. Increased intra-abdominal pressure
    - obesity
    - pregnancy
  3. decreased motility
    - gastroparesis
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2
Q

GERD Pathophysiology

A
  1. Reflux gastric contents into esophagus
    - HCl acid
    - pepsin
    - bile salts
  2. Direct irritation of esophageal mucosa
  3. Inflammatory response
    - erythema
    - Increase vascular permeability, edema
    - esophageal erosions
    - Barrett’s esophagus
  4. Adenocarcinoma
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3
Q

GERD
Clinical manifestations

A

Pyrosis (heart burn)
Dyspepsia
Dysphagia
Pain (worse lying down, after eating)
Cough
Laryngitis
Worsening asthma

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4
Q

GERD
Pharmacological treatment

A

PPI - omeprazole
H2 receptor antagonists - cimetidine
antacids - calcium carbonate
pro kinetic agents - metoclopromide

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5
Q

GERD
Non-pharmacological treatment

A
  1. LES sphincter
    - stop smoking (nicotine)
  2. Intraabdominal pressure
    - lose weight
    - lose clothing
    - HOB elevated
  3. GI motility
    - walking after eating
    - staying upright
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6
Q

GERD
Diagnosis

A
  1. physical assessment
  2. clinical history
  3. endoscopy with biopsy (r/o eosinophilic esophagitis)
  4. R/O cardiac (angina? MI?)
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7
Q

Two types of GERD

A
  1. erosive
  2. non-erosive (heart burn, no esophageal injury)
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8
Q

Gastritis
Definition

A

Inflammation of the stomach

  1. Acute
  2. Chronic (1. autoimmune type A ; 2. chronic non-immune type B)
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9
Q

Acute Gastritis
Pathophysiology

A

Direct injurious agent
Damage and inflammation to superficial mucosa (fundus, antrum, both)

  • Nicotine
  • NSAIDs
  • H. pylori
  • histamine
  • Alcohol
  • Urea
  • digoxin
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10
Q

Acute Gastritis
Treatment

A

H2 receptor blockers

Antacids

Remove injurious agent (D/C alcohol, smoking, NSAID etc.)

Self resolves in a couple of days

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11
Q

Chronic Gastritis
Pathophysiolgy

A
  1. Type A - autoimmune
    - Antibodies against H/K ATPase
    - destruction parietal cells
    - no Intrinsic factor –> Vitamin B12 deficiency –> pernicious anemia
    - no HCl
  2. Type B - non-immune
    - H. pylori infection (NSAIDs, smoking, alcohol)
    - chronic inflammation -> damage
    - HCl normal
    - can lead to pan gastritis (autoimmune gastritis)
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12
Q

Chronic Gastritis
Clinical symptoms

A

Non-specific
epigastric pain
fullness
anorexia
N/V
fatigue
anemia
bleeding

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13
Q

Diagnosis
Chronic Gastritis

A
  1. physical examination
  2. history
  3. biopsy
  4. achlorhydria
  5. Intrinsic Factor
  6. Vitamin B12
  7. other autoimmune disorders - thyroid, RA, type I DM
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14
Q

Treatment
Chronic Gastritis

A

H. pylori
- quadruple / triple antibiotic therapy

D/C causative agent
- D/C NSAIDs, smoking, alcohol
- if non-immune

Rx
- Vitamin B12 if autoimmune
- iron supplmentation

Small regular meals

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15
Q

Risk Factors
Peptic Ulcer Disease

A

NSAIDS
H. pylori infeciton
Chronic diseases (emphysema, RA, cirrhosis, obesity, diabetes)
Age
Smoking
Alcohol
Stress
Type O blood

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16
Q

Defintion
Peptic Ulcer Disease

A

Erosion (superficial - mucosal layer) / ulceration (deep - muscularis) of the mucosal lining of
1. esophagus
2. stomach
3. duodenum

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17
Q

Complications
Peptic Ulcers

A
  1. Hemorrhage
  2. perforation
  3. obstruction
18
Q

Zollinger-Ellison Syndrome

A

PUD
Tumor secretes gastrin

Gastrin
hormone secreted by G cells (stomach, duodenum)
increase HCl secretion
increase GI motility

19
Q

Etiology
Duodenal ulcers

A

most common ulcer
1. H. pylori
2. NSAIDS
3. idiopathic (rare)

20
Q

Pathophysiology
Duodenal Ulcer
NSAID

A

Trigger (NSAID, H. pylori) –> acid/pepsin in duodenum –> penetration mucosal barrier –> erosion –> ulceration

NSAID
direct irritant, damage mucosal lining
also decrease mucous secretion, bicarbonate secretion, and blood flow to the mucosal barrier

21
Q

Pathophysiology
Duodenal Ulcer
H. Pylori

A

H. pylori

urease - neutralizes pH, decrease viscosity mucous

Cag A virulence factor - elongation epithelial cells, disruption tight junction

Cag A immunogenic –> inflammation, infiltration

VacA virulence factor - pores, vacuolation, apoptosis

VacA virulence factor –> inhibit proliferation T cells, apoptosis T cells –> adaptive immune evasion

Change flagella –> evade TLR recognition innate immune system

22
Q

Clinical manifestations
Duodenal ulcer

A

NSAID
- asymptomatic
- painless hemorrhage and perforation
- melena stool
- hematemesis
- anemia

H. pylori
- chronic intermittent epigastric pain
- urea breath test
- wakes up at night
- nocturnal pain
- relieved with eating (reoccurs 2-3 hours after eating)
- pain - antacid/food- relief pattern
- anemia
- remission to relapse
- heals more quickly

23
Q

Pharmacological Treatment
Duodenal ulcers

A

H. pylori

  • quadruple therapy (metronidazole + tetracycline + bismuth + PPI)
  • triple therapy (metronidazole/amoxicillin + clarithromycin + PPI)
  • antacids (calcium carbonate, aluminum hydroxide, magnesium hydroxide, sodium bicarbonate)
  • H2 receptor antagonists (cimetidine, famotidine, ranitidine)
  • PPI (omeprazole, lansoprazole)
  • Sucrafalate (ulcer protection)

NSAID

  • D/C NSAID
  • PPI (omeprazole, lansoprazole)
  • H2 receptor antagonist (cimetidine, famotidine)
  • antacids
  • sucrafalate
24
Q

Pathophysiology
Gastric Ulcers

A

Break in mucosal barrier

  • NSAID ( no prostaglandins )
  • H. pylori infection ( virulence factors, urease)
  • reflux from SI (bile, pH, mucous viscosity decrease)
  • decreased parietal cells (chronic gastritis)
  • decrease mucus production

Exposure epithelium to H+ and pepsin –> erosions

25
Q

Clinical Symptoms
Gastric Ulcers

A

intermittent epigastric pain
pain when food in stomach
pain- antacid-relief pattern
chronic ulcer without remission
heals more slowly
more weight loss, vomiting, anorexia

26
Q

Diagnosis
Gastric Ulcers

A
  1. physical examination
  2. history
  3. endoscopy with biopsy
  4. gastrin to r/o cancer
  5. urea breath test, H. pylori stool test
27
Q

Treatment
Gastric ulcer

A
  • PPI
  • H2 receptor antagonist
  • Antacid
  • Antibiotic if H. pylori (quadruple or triple therapy)
  • sucrafalate
28
Q

Pathophysiology
Stress Ulcers

A

Physiological stress (multi-system trauma, TBI, sepsis, ventilation > 48 hours) –> activation SNS –> vasoconstriction –> ischemia –> decreased blood flow to GI mucosal barrier –> disruption barrier –> exposure H+ and pepsin –> erosions, ulceration

Cushing ulcer

29
Q

Treatment
Stress ulcers

A

prophylactic treatment
PPI
H2 receptor antagonists

30
Q

Cellular pathophysiology
Gastric ulcers

A
  • abnormal mucus
  • normal/low parietal cell mass
  • normal/low acid production
  • high gastrin
  • normal pepsinogen
  • H. pylori 80%
31
Q

Cellular pathophysiology
duodenal ulcers

A
  • abnormal mucus
  • high parietal cells
  • high acid production
  • normal gastrin
  • high pepsinogen
  • H. pylori 95-100% time
32
Q

Pathophysiology
PUD

A

Trigger (NSAID, h. pylori, alcohol, smoking, schema)

Disruption mucosal barrier
- decrease mucus
- decrease tight junctions
- gastric acid direct contact with mucosa

Conversion pepsinogen to pepsin
- erosion

Histamine
- vasodilation, permeability, edema, pain, infalmmation
- increase acid secretion
- erosions
- muscle spasms (acid)

33
Q

Infantile Hypertrophic Pyloric Stenosis
Pathophysiology

A

Narrowing of pyloric sphincter (ingrowth of muscles) prevents food from passing from stomach to small intestine

34
Q

Hypertrophic pyloric stenosis
Clinical Signs and Symptoms

A

projectile vomiting
palpable olive mass RUQ
demands to be re-fed
weight loss
occurs 2-8 weeks neonate

35
Q

Hypertrophic pyloric stenosis
Treatment

A

Laparoscopic pyloromyotomy

36
Q

Paediatric
Gastric Esophageal reflux
Normal for first 12 months?

A

True

37
Q

Paediatric GERD
Clinical Manifestations

A

food refusal
dysphagia
epigastric pain
wheezing
sinusitis, pharyngitis, otitis media

38
Q

Paediatric GERD
Treatment

A

R/O milk allergy
endoscopy with biopsy R/O barren esophagus and adenocarcinoma

pro kinetics - metoclopromide
feed - thicken

39
Q

Paediatric GERD
Causes

A

LES sphincter tone low

anatomy

40
Q

Cells and secretions
Stomach

A

Chief cells - pepsinogen
mucousal cells - gastrin
D cells - somatostatin
Enterocromaffen cells - histamine
parietal cells - HCl

41
Q

Stimulation secretions

A

Acetylcholine
- stimulates Gastrin
- pepsinogen
- HCl

Gastrin
- stimulates histamine
- HCl
- pepsinogen release

Histamine
- stimualtes HCl release

Prostaglandins/NO
- protective of mucosal barrier
- increase mucous, bicarb, and decrease HCl secretions

Year 1: Patho/Pharm (39 decks)

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