Esophageal Pathophysiology

Crohns Disease

-can occur anywhere in tract

-transmural inflammation (IBD) causing tears and skip lesions

Obstruction
Dysphagia: difficulty of swallowing

Muscle/Nerve Dysfunction
-failure to contract (scleroderma) or relax (mimics chest pain)
-altered PSNS control

Varices
-dilation of veins due to portal venous hypertension
-vomiting blood
-bumpy lining

Diverticula (Outpouching)
Pulsion = weakening of walls
Zenkers = regurgitation of undigested food
Hiatial Hernia = between esophagus and diaphragm

Gastroesophageal Reflux Disease

-contents of stomach > LES > esophagus
-due to increased gastric pressure leading to acid burn
-Barretts Esophagus = chronic

Sphincter Pathophysiology
Achalasia
-LES stays contracted
-peristalsis is lost
-Birds Beak appearance

Gastric Pathophysiology

Parietal Cells (+)

-acidify environment
-neural (Ach), Histamine (ECL), and endocrine (Gastrin) control

Gastrin (G cell)
ON = vagus nerve
OFF = somatostatin increased, pH decreased

Bicarbonate
-neutralizes acid by secretin
-slows down motility

Ulcers
-increased acid secretion leading to holes in stomach
1. H. Pylori (most common),
2. Decreased mucosal protection (NSAIDS, COX, Alcohol)
3. Stress
Gastric = at time of eating
Duodenal = after eating; 2+ hours
Secretin Test = stimulates gastrin when theres a gastrinoma

Gastroparesis
-paralysis of stomach so it does not function correctly

Pernicious anemia
-decrease in RBCs
-loss of intrinsic factor (VB12)
-loss of gastric parietal cells

Small Intestine Pathophysiology

CCK = release I cells (fats/peptides) for regulation in response to food

Malabsorption
Digestion = reduced enzyme and acid secretion
Absorption = reduced surface area, transport, or lymphatics

Celiac Sprue
-inflammation in response to gluten (wheat)

Mesenteric ischemia
-injury due to inadequate blood supply
-lining of wall is twisted and strangled up so you cant absorb

Large Intestine Pathophysiology

Diverticula

-outpouchings due to diet low in fiber

Secretory Diarrhea
-increased secretion = excess VIP or infection
-decreased absorption
cholera toxin > mast cells > histamine > increased Cl > increased motility

Osmotic Diarrhea
-too much water in bowels
-lactose intolerance dehydration

Hematochezia
-bright red bleeding from distal GI
-hemorrhoids in rectum

Liver Pathophysiology

Jaundice

-increase in unconjugated or conjugated bilirubin

-turn yellow

Unconjugated Bilirubin (lipid) = breakdown of RBCs = dark urine

Conjugated Bilirubin (water) = bile cant get into intestine = dark stool

Hepatitis
A = contaminated food and water
B = infected blood, fluids, needles
C = drug use

Portal Venous Hypertension

1.
2.
3.
4.

Ascites: edema in peritoneal cavity

Caput Medusa Veins
Varices
Hemorrhoids

Prehepatic = thrombosis
Intrahepatic = cirrhosis and fibrosis
Posthepatic = surrounding failures

Gallbladder Pathophysiology
Bile = pigments from bilirubin breakdown + cholesterol
Cholelithiasis
-excess pigment or cholesterol
-leads to gallstones
-leads to elevated alkaline phosphatase
-F.F.F.F.

Pancreas Pathophysiology

Trypsin = activates proenzymes (a lot when you eat)

Insulin = lowers blood glucose
Glucagon = raises blood glucose

VIPoman
-rare tumor increasing VIPs leading to WDDA

Malabsorption
-reduced acinar cell secretions
-cystic fibrosis (CFTR)

Renal Pathophysiology
Acute Renal Failure

Pre = Low Blood volume, Low albumin, BUN/Creatinine Ratio > 20:1
Intrinsic = Glomerulonephritis, ATN, FENa > 2%
Post = Collecting

Nephrotic

Nephritic

Proteinuria
Hyerplipidemia
Tubular Necrosis

Inflammation
HTN
Hematuria
Oliguria
Immune Complexes
1. Decreased GFR
2. Decreased blood flow

Pyelonephritis
-bacterial infection reaching pelvis

Acute Tubular Necrosis

Ischemia = hypotension, shock, sepsis

Acute Renal Failure

ESRF (worst) = Diabetes Mellitus and HTN = GFR <15 ml/min
Azotemia = increased BUN/Creatinine = Proinflammation
Loss of Ca = Loss of Vitamin D = Gain of PTH (bone)
Loss of EPO = Anemia