Disorders Flashcards
Pre-hepatic: cause, serum bilirubin levels, stool colour, signs & symptoms
- hemolytic anemia or internal hemorrhage; increase in RBC breakdown = increase in unconjugated bilirubin production
- ^^^ unconj, ^ conj.
- brown
- anemia: fatigue, dizzy, pale skin; ? enlarged spleen
Gilbert’s Syndrome: cause, serum bilirubin levels, stool colour, signs & symptoms
- defect in UDPGT so decrease in bilirubin conjugation
- ^ unconj, v conj.
- light clay
- mild jaundice from time to time, no other symptoms
Dubin-Johnson Syndrome: cause, serum bilirubin levels, stool colour, signs & symptoms
- defect in conj bilirubin transportation to canaliculi
- ^ conj (buildup)
- light clay
- lifelong jaundice, no other symptoms
Hepatocellular dmg & necrosis: cause, serum bilirubin levels, stool colour, signs & symptoms
- hepatitis: mostly viral infections, cirrhosis: irrev scarring, leading cause is alcohol
- ^ unconj, ^^ conj. (hepatocytes functional but bilirubin goes to diff pathways)
- light clay
- ? abdominal pain, ? enlarged liver, +/- enlarged spleen
Post-hepatic (OBD): cause, serum bilirubin levels, stool colour, signs & symptoms
- obstruction causes impaired bilirubin excretion e.g. from gallstones, cysts & tumours, pancreatic cancer compressing bile duct
- ^ conj.
- light clay
- gallstones: pain, pancreatic cancer: pain, weight loss
Inflammatory Bowel Disease: causes, pathophysiology, signs & symptoms
Causes:
1. cause is poorly understood
2. seems to have a genetic predispostion -> impaired immune function
Pathophysiology:
genetic predisposition + exogenous factors + host factors -> dysregulated immune system
*typical onset in adolescence and early adulthood
Signs & symptoms:
1. abdominal pain
2. loss of appetite
3. fatigue
4. diarrhea (bloody if ulcers perforate)
5. possibly anemia
6. possibly leukocytosis
Ulcerative Colitis: pathophysiology, signs & symptoms
Pathophysiology:
- “shallow” inflammation = mucosa only
- only affects colon and rectum
Signs & symptoms:
- often bloody diarrhea
- cts area of mucosal inflammation seen in colonoscopy
Crohn’s Disease: pathophysiology, signs & symptoms
Pathophysiology:
- inflammation extends entire thickness of intestinal wall
- affects all of GI tract; commonly in proximal colon & ileum
Signs & symptoms:
1. diarrhea (mostly non-bloody)
2. small intestine villi damaged -> malabsorption
3. endoscopy shows: patches of inflammation, deep ulcers, swelling & scarring = obstruction
Lactose Intolerance: causes, pathophysiology, signs & symptoms
Causes:
decreased lactase production
Pathophysiology:
decreased lactose breakdown, lactose accumulates in GI lumen
Symptoms:
1. diarrhea (water stays in lumen due to presence of disaccharide)
2. gas/bloating/cramps: gut microbiome breaks down lactose and produces methane and hydrogen gas
Malabsorption Syndromes: causes, pathophysiology, signs & symptoms
Causes:
1. Impaired mucosal absorption mechanism or brush boarder (microvilli) enzymes
2. pancreatic disorder: decrease in digestive enzymes
3. liver disorder: low bile output
4. infection causes intestinal damage
Pathophysiology:
involves dmg to intestinal mucosal lining or decreased nutrient digestion (lack of enzymes)
Symptoms:
1. abdominal discomfort
2. diarrhea
3. weight loss
4. Specifics depend on which nutrient is not absorbed e.g. decreased fat absorption can result in steatorrhea
Celiac Disease: causes, pathophysiology, signs & symptoms
Cause:
HSR to gluten
Pathophysiology:
Immune-mediated dmg to small intestinal mucosa leads to malabsorption:
1. dmg to intestinal epithelial cells
2. blunted villi
3. damaged intestinal microvilli
Symptoms:
1. abdominal pain
2. diarrhea
3. weight loss
4. possibly anemia if B12 not absorbed
Tropical Sprue: causes, pathophysiology, signs & symptoms
Cause:
Poorly understood
Pathophysiology:
Observed to be caused by ova, parasites, and bacteria (E. coli, Enterobacter, Klebsiella). Occurs in residents or visitors of tropical and sub-tropical areas
Symptoms:
Same as celiac disease
Pernicious Anemia: causes, pathophysiology, signs & symptoms
Causes:
- autoimmune disease that produces antibodies against parietal cell components and intrinsic factor
- dmg to terminal ileum
Pathophysiology:
1. antibodies againts IF prevent B12 from being absorbed properly
2. decreased in RBC production
Symptoms:
1. anemia: fatigue, shortness of breath, pale skin
2. if parietal cells destroyed, gastric pH > RR
3. esp in elderly: degeneration of nervous system
Zollinger-Ellison Syndrome: causes, pathophysiology, signs & symptoms
Cause:
Gastrinoma - G-cell tumour in dudoenum and pancreas
Pathophysiology:
- G cells produce too much gastrin -> parietal cells make more HCl
- stomach: hyperplasia of parietal cells
- small intestine: villi dmg causes malabsorption
Symptoms:
1. recurring/severe ulcers -> bloody diarrhea
2. tumor
3. ^ HCl, ^ gastrin
4. possibly steatorrhea if fat malabsorption
Peptic ulcers: causes, pathophysiology, signs & symptoms
Cause:
1. H.pylori infection
2. long-term NSAID use (e.g. ibuprofen)
3. physiological stress, severe illness, major surgery
4. genetics
Pathophysiology:
Damaged mucosal lining (HCl, pepsin, inflammation) or impaired mucosal protection (less mucous, bicarbonate)
Symptoms:
1. abdominal pain/discomfort
2. bloating
3. weight loss/loss of appetite
4. nausea & vomiting
5. often bloody diarrhea
6. obstruction due to scarring or swelling
7. ^ HCl, ^ pepsin, ^ gastrin
Nephritic syndrome: causes, pathophysiology, clinical findings
Cause:
Glomerulonephritis - inflammation of the glomeruli due to immune defects like immune complex deposits (e.g. Goodpasture’s syndrome: Ab attack glomerular basement membrane)
Pathophysiology:
1. dmg to glomeruli results in RBC in filtrate
2. dmg to glomeruli results in small amt of protein in filtrate
3. inflammation and dmg causes fenestrated endothelial cells to proliferate and podocyte epithelium fibrosis
4. occlusion in capillary lumen -> decreased GFR
5. decreased GFR activates RAAS, causes blood volume to increase
6. increased blood in arteries = vasoconstriction = increased vascular resistance
Symptoms:
1. hematuria
2. proteinuria (0, +, or ++) in urine dipstick
4. oliguria, uremia
5. ^BP, HTN, maybe mild edema
Nephrotic syndrome: causes, pathophysiology, clinical findings
Causes:
Damage to glomeruli via
1. diabetic kidney disease
2. minimal change disease
3. infection (HIV, Hepatitis) or autoimmune disease (lupus)
Pathophysiology:
1. dmg to glomeruli increases permeability to protein
2. “pores” in glomeruli
3. increased permeability to lipoproteins
4. liver increases cholesterol production
5. protein loss from blood decreases oncotic pressure, so fluid moves from vascular to interstitial space
Symptoms:
1. hypoproteinemia, hypoalbuminemia
2. proteinuria (++++), frothy urine
3. lipiduria
4. hypercholesterolemia, hyperlipidemia
5. Major edema
Acute Kidney Injury (AKI): causes, pathophysiology, clinical findings
Cause:
1. Physical, toxic, or infectious dmg to kidney
2.vascular dmg leads to decreased kidney perfusion
3. hypoxic insults due to septic shock or cardiac failure can ause kidney failure
Pathophysiology:
1. sudden decrease in renal function within 48 hrs
2. reversible as long as damaging stimulant is removed and regeneration occurs
3. dmg glomeruli or decrease in kidney perfusion decreases GFR
4. dmg tubules decreases secretion
5. low GFR/decrease in kidney perfusion activates RAAS and increases blood volume
Symptoms:
1. oliguria
2. uremia, high creatinine levels, acidosis, hyperkalemia, nausea & vomit if severe
3. HTN, edema
Chronic Kidney Disease (CKD): causes, pathophysiology, clinical findings
Cause:
long-standing
1. vascular dmg -> HTN
2. glomeruli dmg -> diabetes, glomerulonephritis
3. tubule dmg -> toxicity, infection, obstuctive dmg
Pathophysiology:
progressive over >3 months or years
1. irreversible dmg to nephrons -> end stage renal disease
2. kidney dmg -> low GFR
3. tubule dmg -> decreased reabsorption
4. tubule dmg -> decreased secretion
5. low GFR activates RAAS -> increased blood volume
6. destruction of renal parenchymal fibroblasts -> decreased EPO
Symptoms:
1. urine volume variable
2. hypernatremia
3. waste retention increases: uremia, high creatinine, hyperkalemia, acidosis
4. HTN, maybe edema
5. anemia (not seen in AKI!)
