Stomach Flashcards

1
Q

Chief Cells

A
  • Secrete pepsinogen, rennin, lipase
  • Lots of RER for enzyme production and storage in apical granules
  • Inc secretion if Ach and dec if somatostatin
  • Location: mainly fundus and body
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2
Q

Parietal Cells

A
  • Secrete HCl and Intrinsic Factor for Binding Vit B12
  • Round w/ central nucleus and homogeneous bright pink cyto b/c so much mito (need oxygen to pump H+ out via H-K-ATPase)
  • Many folds w/ intracellular canaliculi (microvilli) and tubulovesicular system to aid in acid secretion/inc SA (many H-K pumps on surface)
  • Stim by … histamine, gastrin, Ach (has receptors for these on basal side)
  • Inhib by… somatostatin, VIP, prostaglandins
  • Location: cardia, fundus, body
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3
Q

G Cells

A
  • Produce gastrin which stim parietal cells to inc HCl release by binding CCK receptors on parietal cells
  • Gastrin also inc histamine secretion; proliferation of mucosa; promotes peristalsis (gastro-colic reflex)
  • Inc secretion if proteins/AA in lumen –> Galpha Q -> IP3/DAG –> Ca++ and secondary messengers
  • look like pale fried eggs on histo
  • Location: esp in antrum and pylorus
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4
Q

ECL Cells

A
  • histamine release –> bind H2 receptors on parietal cells –> G alpha s –> inc cAMP –> up-reg kinases –> activate more H/K ATPases
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5
Q

D Cells

A
  • somatostatin release (FEEDBACK) –> inhibit G cells, ECL cells, parietal cells and chief cells
  • inhibit stomach contractions and initiate housekeeping MMC waves in duodenum
  • Somatostatin directly binds parietal cell membrane –> G alpha i –> dec cAMP –> down-reg kinases –> dec activation of H/K ATPase
  • Somatostatin indirectly binds G cells to inhibit gastrin release
  • Location: mainly antrum
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6
Q

Blood Supply + Venous Drainage (esophageal v. gastric varices)

A
  • Branches off celiac artery (rich and redundant so very rarely ischemic)
    • Lesser curve - L and R gastric
    • Greater curve - L and R gastoepiploic arteries
    • Fundus - short gastric arteries off splenic
  • Venous Drainage
    • Drains into portal system
      • Collaterals b/n gastric vein and esophageal vein –> esophageal varices in portal HTN
    • If short gastric veins that drain fundus and superior greater curve back up –> gastric varices (if splenic vein thrombosis)
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7
Q

3 Phases of Secretion Regulation

A
  • Cephalic Phase - sight, smell, thought of food stimulates acid secretion
    (vagus Ach release –> M3 receptors on parietal cell basolateral membrane –> G alpha q –> PIP2 –> Ca++ –> up-reg kinases –> activate more H/K ATPases)
  • Gastric Phase - distention in stomach, nutrients and chemicals stimulate acid secretion
    (gastrin and histamine effects on parietal cells)
  • Intestinal Phase - FEEDBACK INHIB of acid secretion based on fats, low pH, distention in SI
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8
Q

3 Ways to Inhibit Parietal Cells

A
  • Somatostatin - directly binds parietal cell membrane –> G alpha i –> dec cAMP –> down-reg kinases –> dec activation of H/K ATPase AND indirectly binds G cells to inhibit gastrin release

Prostaglandins - directly binds parietal cell membrane –> G alpha i –> dec cAMP –> down-reg kinases –> dec activation of H/K ATPase

VIP (from D1 cells)

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9
Q

3 Functions of Stomach Beyond Secretion

A

1- Filling - requires relaxation - vagal receptive relaxation in response to swallowing + local reflexes and paracrine factors

2- Mixing - powerful contractions (esp in antrum) to disintegrate food

3- Emptying

- Liquids empty quickly
- Solids - LAG phase then gradual emptying phase
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10
Q

Hypertrophic Pyloric Stenosis

A
  • congenital outlet obstruction due to loss of inhibitory NO neurons in pylorous
  • Infants projectile vomit; dx by barium swallow or ultrasound then repair surgically
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11
Q

Gastric Volvulus

A
  • RARE; abnormal rotation >180 degrees
  • Acute - due to compromise/block of blood supply
  • Chronic - causing vague discomfort
  • Tx - surgery
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12
Q

Zollinger Ellison Syndrome

A
  • Rare disease of excess gastrin secretion by endocrine tumor (usually in upper ab- in or near pancreas)
  • Gastrin secretion not down-reg by acid like normal G cells
  • Leads to hypertrophy of gastric folds, proliferation of parietal cells, excess acid secretion –> injury/ulcers/reflux
  • Can also cause high volume loos bowel movements
  • Dx and Tx - use somatostatin analogue (octreotide)
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13
Q

What is the most common gastric infection? (details and how to treat)

A

H Pylori

  • Gram neg, microaerophillic (hard to cx), spiral bacillus
  • Urease enzyme (dec acidity of stomach) so only colonizes stomach; urease breath test
  • Flagella, adhesins, catalase
  • Fecal-oral transmission
  • Histo - see band-like infiltrate (just affects superficial band of stomach along lumen)
  • Goal is to eradicate in all pts w/ or w/o ulcers due to role in peptic ulcer disease (triple treatment - 2 abx to avoid resistance and PPI esp if pH dep abx)
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14
Q

H Pylori Tx

A

Std -PPI + Clarithomycin + Amox

If PCN allergy - PPI + Clarithomycin + Metro

If PCN allergy or tx fails - PPI + Tetracycline + Metro + Bismuth

**All regimens for 10-14 days

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15
Q

Other Gastric Infections

A
  • Rarely mycobacterium tuberculosis or MAC or treponema pallidum (syphilitic gastritis)
  • Viral can be CMV and HSV in immune-comp
  • Fungi rare but can include Candida, aspergillus, histo and mucor
  • Parasites = cryptosporidium, Giardia, anisakis marina (in ingested fish) and Strongyloides stercoralis
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16
Q

Complications of Gastric Infection

A
  • Infection –> inflammatory infiltrate –> cytokines, ECL stimulation, more acid secretion –> mucosal injury and ulcerations eventually
  • MALT lymphadenopathy - low grade clonal proliferation of B cells in MALT (often total remission if eradicate H pylori)
  • Atrophic gastritis - atrophy –> less acid production –> more bacteria colonize –> inc conc of potential carcinogens
17
Q

Atrophic Gastritis (Types A and B)

A
  • Atrophy of mucosa epithelium –> may cause hypochlorhydria –> intestinal metaplasia (or even polyps, adenocarcinomas)
  • Type A - autoimmune anti-parietal cell antibodies (less HCl, less IF so pernicious anemia from less vit B12 absorbed)
    • Higher pH may cause high comp gastrin levels –> endocrine/ECL hyperplasia –> carcinoid tumor
  • Usually just occurs in body and fundus (antrum spared)
  • Type B- usually in antrum and associated w/ H pylori
    • Gastrin levels usually normal
    • Whole stomach
18
Q

Peptic Ulcer Disease (presentation, Dx, comp, causes)

A
  • Presentation - burning in epigastric area at night or few hours after meals (relived by antacids or more food)
  • Dx - w/ endoscopy
  • Imbalance b/n defenses and injurious influences
    • Defenses - blood flow, mucous layer, bicarb, tight junctions, phospholipids, repair
    • Injury - acid, cell injury, ischemia, dec mucous or dec bicarb
  • Complications - bleeding, perforation, stricture formation
  • Causes - commonly H pylori or NSAID use (dec prostaglandins from COX-1 that normally inc production of bicarb and mucous AND NSAIDs are weak acids so become protonated in stomach then diffuse and become trapped)
19
Q

Erosion v. Ulcer

A
  • Erosion - does not penetrate muscularis mucosa and usually heals w/o scars
  • Ulcer - beyond into submucosa so can erode vessels, penetrate into peritoneal cavity and cause scars/strictures
20
Q

Gastroparesis (presentation, causes, dx, tx)

A
  • Presentation - nausea, vomiting, bloating, ab distention, fullness, weight loss
  • Causes - neuro (most common), interstitial cells of Cajal problem, muscle effector cell prob
    • Ex) Diabetic neuropathy, infection, vagus nerve injury, scleroderma, amyloidosis, dermatomyositis
    • OR drug side effects
  • Dx - radionucleide solid phase emptying test; radio dye in food then measure time to half empty
  • Tx - restrict food/jejunal feeds +/- prokinetic drugs
21
Q

What 4 classes of drugs can cause gastroparesis?

A

anti-cholinergics

opioids

L-dopa

Ca++ channel blockers

22
Q

Chronic v Acute Gastritis

A
  • Acute - Neutrophils (usually H pylori, chemicals/NSAIDs, bile acid reflux, “stress”)
    - Tx - ulcer prophylaxis
  • Chronic - NO NEUTROPHILS; see lymphocytes and plasma cells (H pylori, autoimmune, radiation, injury from tubes)
23
Q

2 Types of Gastric Adenocarcinomas

A
  • Intestinal Type
    • Gross - solitary mass
    • Histo - gland-like w/ background of intestinal metaplasia and dysplasia
    • Associated w/ H pylori and autoimmune atrophic gastritis; HER2
  • Diffuse Type
    • Gross - diffuse thickening of wall
    • Histo - individual infiltrating cells w/ signet ring morphology
    • Not associated w/ H pylori and metaplasia
24
Q

3 Histo Features of MALT lymphoma

A
  • Thicker rugal folds
  • Dense lymphocytic infiltrate in lamina propria
  • Lymphoepithelial lesions