Acute Gastroenteritis - Yagupsky

Question 1

Water distribution in compartments (interacellular, interstitial and intravascular)

Answer 1

Intracellular water: 75%

Interstitial: 25%

Intravascular: 5%

Question 2

What is the composition of bacteria in the intestines

Defense mechanisms against offending bacteria

Answer 2

Normal flora: 10^11 microorganisms/g feces

99% anaerobic

pH (problems with antacids and gastrectomy)

Motility (stopped with opiates and increased mortality in dysentary because prolongs contact)

Question 3

Mechanisms of diarrhea (4)

Answer 3

Secretory:
Na/Cl pump is reveresed and water follows electrolytes into the lumen causing dehydration
V. Cholera, Shigella

Osmotic:
Enzymes destroyed at brush border and sugars can’t be absorbed after being broken down, increase osmotic pressure and water follows
Lactose intolerance

Entero-adherent
Physically blocks absorption, molecules can’t cross into mucosa
E. coli, Giardia

Invasive:
Destroy mucosal epithelium, inflammatory cells in stools. Candidate for antibiotics.
Salmonella, C. dificile, Shigella, Amoeba histolytica

Question 4

Degrees of water loss and electrolyte loss

Question 5

Mechanism of metabolic acidosis in dehydration

Answer 5

Tissue hypoperfusion–>renal failure–>fecal bicarbonate loss.

Kidney tries to save water by decreasing excretion.

Retained acid causes oliguria or aneuria.

Bicarbonate may be lost by diarrhea.8

Question 6

Treatment priorities in diarrhea

Answer 6

1: hypoperfusion and shock will kill patient first, correct luid, electrolyte and acid-base disturbances. Give large amounts at beginning to abolish shock and restore blood pressure. Then continue fluid supplied at a slower rate. In developing world: give oral rehydration salts.

2. Nutrition
3. Antibiotics (mostly not helpful except in shigella)

Question 7

How does hypernatremia and brain edema happen with mistreated diarrhea?

Answer 7

1. Natural course with no therapy but we compensate with water. More common in Western world where more nutrients available.
2. Volume loss and brain shrinkage to keep perfusion. More sodium outside than in the cell. Hemorrhage at initial stage of hypernatremia, microscopic bleeding from meningeal damage.
3. Protein breakdown inside the cell increases osmolarity with free amino acids. Outside water comes in to compensate and decreases blood pressure and brain enlarges again.
4. Fluid given at standard osmolarity which is actually hypoosmolar relative to the patient. Fluid rushes into the cell and creates swelling and pressure and brain edema. Serious neurological sequelae. Brain pressure occludes the vein and arteries causing hypoxia.