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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
Clinical Symptoms Gastric Ulcers
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
Diagnosis Gastric Ulcers
1. physical examination 2. history 3. endoscopy with biopsy 4. gastrin to r/o cancer 5. urea breath test, H. pylori stool test
27
Treatment Gastric ulcer
- PPI - H2 receptor antagonist - Antacid - Antibiotic if H. pylori (quadruple or triple therapy) - sucrafalate
28
Pathophysiology Stress Ulcers
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
Treatment Stress ulcers
prophylactic treatment PPI H2 receptor antagonists
30
Cellular pathophysiology Gastric ulcers
- abnormal mucus - normal/low parietal cell mass - normal/low acid production - high gastrin - normal pepsinogen - H. pylori 80%
31
Cellular pathophysiology duodenal ulcers
- abnormal mucus - high parietal cells - high acid production - normal gastrin - high pepsinogen - H. pylori 95-100% time
32
Pathophysiology PUD
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
Infantile Hypertrophic Pyloric Stenosis Pathophysiology
Narrowing of pyloric sphincter (ingrowth of muscles) prevents food from passing from stomach to small intestine
34
Hypertrophic pyloric stenosis Clinical Signs and Symptoms
projectile vomiting palpable olive mass RUQ demands to be re-fed weight loss occurs 2-8 weeks neonate
35
Hypertrophic pyloric stenosis Treatment
Laparoscopic pyloromyotomy
36
Paediatric Gastric Esophageal reflux Normal for first 12 months?
True
37
Paediatric GERD Clinical Manifestations
food refusal dysphagia epigastric pain wheezing sinusitis, pharyngitis, otitis media
38
Paediatric GERD Treatment
R/O milk allergy endoscopy with biopsy R/O barren esophagus and adenocarcinoma pro kinetics - metoclopromide feed - thicken
39
Paediatric GERD Causes
LES sphincter tone low anatomy
40
Cells and secretions Stomach
Chief cells - pepsinogen mucousal cells - gastrin D cells - somatostatin Enterocromaffen cells - histamine parietal cells - HCl
41
Stimulation secretions
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 (45 decks)

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