Disorders Flashcards

1
Q

Pre-hepatic: cause, serum bilirubin levels, stool colour, signs & symptoms

A
  • hemolytic anemia or internal hemorrhage; increase in RBC breakdown = increase in unconjugated bilirubin production
  • ^^^ unconj, ^ conj.
  • brown
  • anemia: fatigue, dizzy, pale skin; ? enlarged spleen
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2
Q

Gilbert’s Syndrome: cause, serum bilirubin levels, stool colour, signs & symptoms

A
  • defect in UDPGT so decrease in bilirubin conjugation
  • ^ unconj, v conj.
  • light clay
  • mild jaundice from time to time, no other symptoms
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3
Q

Dubin-Johnson Syndrome: cause, serum bilirubin levels, stool colour, signs & symptoms

A
  • defect in conj bilirubin transportation to canaliculi
  • ^ conj (buildup)
  • light clay
  • lifelong jaundice, no other symptoms
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4
Q

Hepatocellular dmg & necrosis: cause, serum bilirubin levels, stool colour, signs & symptoms

A
  • 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
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5
Q

Post-hepatic (OBD): cause, serum bilirubin levels, stool colour, signs & symptoms

A
  • 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
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6
Q

Inflammatory Bowel Disease: causes, pathophysiology, signs & symptoms

A

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

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7
Q

Ulcerative Colitis: pathophysiology, signs & symptoms

A

Pathophysiology:
- “shallow” inflammation = mucosa only
- only affects colon and rectum

Signs & symptoms:
- often bloody diarrhea
- cts area of mucosal inflammation seen in colonoscopy

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8
Q

Crohn’s Disease: pathophysiology, signs & symptoms

A

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

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9
Q

Lactose Intolerance: causes, pathophysiology, signs & symptoms

A

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

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10
Q

Malabsorption Syndromes: causes, pathophysiology, signs & symptoms

A

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

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11
Q

Celiac Disease: causes, pathophysiology, signs & symptoms

A

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

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12
Q

Tropical Sprue: causes, pathophysiology, signs & symptoms

A

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

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13
Q

Pernicious Anemia: causes, pathophysiology, signs & symptoms

A

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

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14
Q

Zollinger-Ellison Syndrome: causes, pathophysiology, signs & symptoms

A

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

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15
Q

Peptic ulcers: causes, pathophysiology, signs & symptoms

A

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

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16
Q

Nephritic syndrome: causes, pathophysiology, clinical findings

A

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

17
Q

Nephrotic syndrome: causes, pathophysiology, clinical findings

A

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

18
Q

Acute Kidney Injury (AKI): causes, pathophysiology, clinical findings

A

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

19
Q

Chronic Kidney Disease (CKD): causes, pathophysiology, clinical findings

A

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!)