Path 2 quiz 1

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nakomarose
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Path 2 quiz 1
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2010-08-17 13:12:12
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Path 2 lecture, quiz 1 (midterm)
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  1. Functions of kidneys
    • Excretion of waste products of metabolism
    • Regulation of the body's concentration of water & salt
    • Maintenance of appropriate acid balance of plasma (7.2-7.4)
    • Secretion of hormones
  2. Hormones secreted by the kidneys
    • Renin- regulates BP
    • Erythropoietin- increases RBC formation
    • Prostaglandins- mediators of inflammation
  3. 4 Compartments of the kidneys
    • Glomerulus
    • Tubules
    • Interstitial tissue
    • Kidney vessels
  4. Diseases of kidney glomerulus are almost always caused by _____.
    Immune system pathologies
  5. The kidney tubules are mainly affected by ______ & _______.
    Toxins, infections
  6. Kidney interstitial tissue is mainly affected by ______ & _____.
    Toxins, infections
  7. Kidney vessels are mainly affected by ________.
    Cardiovascular pathologies
  8. Glomerulus
    • Bundle of capillaries located within a Bowman's capsule
    • Highly permeable to water
    • Contains a network of afferent & efferent arterioles
  9. 3 layers of the capillaries of the glomerulus
    • Endothelial cells
    • Basement membran
    • Epithelial cells
  10. Endothelial cells of the capillaries of the glomerulus
    Innermost layer of capillary; have holes called pseudofenestrations between them
  11. Epithelial cells of the capillaries of the glomerulus
    • aka podocytes or visceral epithelial cells
    • Outermost layer of the capillaries with filtration slits between them
  12. Nephrin
    Glycoprotein located between the podocyte slits of the capillaries of the glomerulus that aids in selective filtration
  13. Parietal epithelial cells
    Similar in nature to the podocytes, but they line the internal surface of the Bowman's capsule
  14. Mesangial cells
    Fill in the spaces b/w bordering vessels in the glomeruli- account for scar tissue in the healing process
  15. Juxtaglomerular cells
    • Located in the area where the afferent arterioles enters the glomerulus
    • Function is to regulate BP
    • Produces renin when BP decreases
  16. Glomerulonephritis (GMN) or NephrItic syndrome
    Inflammation of all 3 layers of the glomeruli capillaries
  17. GMN/NephrItic syndrome is characterized by:
    • Hematuria
    • Oliguria
    • Azotemia
    • Hypertension
  18. Hematuria
    • Change in the permeability of the arterial wall in the glomerulus
    • Results in blood & RBC casts in the urine
  19. Oliguria
    Decreased urine production resulting from decreased GFR
  20. Azotemia
    • Nitrogen in the blood
    • Waste products of metabolism are not able to go from the bloo to the urine due to oliguria
    • Is a biochemical abnormality (not clinical) characterized by increased levels of creatine & blood urea nitrogen (BUN) in the bloodstream
    • There are no clinical symptoms until the process becomes advanced, in that case, it is referred to as uremia
  21. Hypertension due to GMN/NephrItic syndrome
    • Juxtaglomerular cells release renin due to a decrease in GFR
    • Renin-> angiotensinogen-> angiotensin 1-> angiotensin 2 (vasoconstrictor)-> increased BP
    • Angiotensin 2 also stimulates the release of aldosterone (increases salt & water reabsorption)-> increased BP
  22. 3 main pathogenic mechanisms of GMN
    • 1. Circulating immune complex deposition GMN
    • 2. Anti-Glomerular basement membrane GMN
    • 3. Heyman GMN
  23. Circulating immune complex deposition GMN
    • Type 3 hypersensitivity reaction
    • Antigen & antibody are both present in flowing blood-> binding takes place in circulating blood to form an immune complex-> immune complex settles in tissue
    • Phagocytes try to engulf the complex & release destructive enzymes against it
    • The immune complex is protected because it has settled within the wall of the glomerulus-> more enzymes are released which eventually begin to digest the wall of the glomerulus
    • Vasculitis occurs locally
  24. Anti-glomerular basement membrane GMN
    • Type 2 hypersensitivity reaction
    • BM becomes "non-self"-> the antigens are fixed & antibodies are released by the immune system-> an immune complex forms on the BM
    • Phagocytic cells cannot engulf this complex so they release destructive enzymes that destroy the BM & the immune complex
  25. Heymann GMN
    • Not a specific type of hypersensitivity
    • Marked by an autoimmune reaction against the podocytes as well as some antigens located wthin the podocytes-> leads to destruction of the podocytes
  26. Specific Causes of GMN
    • 1. Acute proliferative (post strep infectious) GMN
    • 2. Rapidly progressive crescentic GMN
    • 3. IgA nephropathy
    • 4. Alport syndrome
  27. Acute proliferative (post strep infection) GMN
    • Type 3 hypersensitivity
    • Occurs predominantly in children; 99% recover if treated on time
    • Caused by beta hemolytic streptococcus group A
    • Antibodies are produced & form a complex w/ the antigen that settles in the glomerular tissue in the subentimal layer of the membrane (layer b/w BM & endothelium)
    • Adults recover in 50% of cases (the other 50% switch to chronic GMN)
  28. Rapidly progressive crescentic GMN
    Group of disorders marked by hyperplasia of the parietal cells of the Bowman's capsule that merge to form a crescent shape-> the increased amount of cells compress the glomerulus & lead to pressure atrophy-> development of oliguria & death if not treated within weeks or months
  29. 3 types of rapidly progressive crescentic GMN
    • Type 1 anti-GBM
    • Type 2 immune complex deposition
    • Type 3 pauci-immune
  30. Type 1 anti-GBM (rapidly progressive crescentic GMN)
    • Type 2 hypersensitivity
    • Goodpastures syndrome
  31. Goodpastures syndrome
    • Development of antibodies against alveolar & glomerular basement membranes; in the lungs there is the accumulation of RBC's & hemoptosis
    • Idiopathic in more than 50% of cases
  32. Type 2 immune complex deposition (rapidly progressive crescentic GMN)
    • Type 2 hypersensitivity
    • idiopathic
    • SLE
    • Henoch-Schonlein purpura
  33. Systemic lupus erythromatosis (SLE)
    • Occurs in young women (3x more common in black women)
    • Kidneys are most involved organ
    • Butterfly rash on face
    • Anti-nuclear antibodies are produced against double stranded DNA
    • Exposure to UV radiation can trigger an episode
    • Also includes joint involvement (like RA) & hypertension
    • May also be triggered by post strep infection
  34. Henoch-Schonlein purpura (aka hemorrhagic vasculitis)
    • Develops in late adolescent males
    • 4 manifestations
    • Formation of purpura (subcutaneous hemorrhages) on the legs, abdomen, & buttocks
    • Duodenitis & gastritis
    • Arthritis
    • Nephritic syndrome (most dangerous)
  35. Type 3 pauci-immune (rapidly progressive crescentic GMN)
    • Not related to a specific type of hypersensitivity
    • Idiopathic vasculitis
    • Wegner's granulomatosis
  36. Wegner's Granulomatosis
    • Mostly affects middle-aged males
    • Anti-neutrophil cytoplasmic auto-antibodies are produced
    • Necrotic granulomas of the upper/lower respiratory tract
    • Necrotic vasculitis of arteries, arterioles, & capillaries
    • Facial bones may be destroyed (decay)
  37. Polyarteritis (periarteritis) nodosa
    • This used to be considered a type of rapidly progressive GMN type 3, but it has been found that this disease does NOT cause GMN
    • Vasculitis of middle & small arteries only w/o any aretriole or capillary involvement in all parts of the body except lungs
    • Involves pouching of the vascular walls
    • Kidney is the organ MC involved -> leads to destruction of vessels, ruptures/hemorrhages, microinfarction causing decreased lumen size, compression of surrounding tissue, & wet gangrene
  38. IgA nepropathy aka Berger's disease
    • Do NOT confuse w/ BUERGER's disease
    • MC cause of GMN in the world
    • Manifested as hematuria 1-2 days after a common cold, UTI, or intestinal infection
    • Caused by overproduction of IgA (which is normally only present in mucous membranes) -> immune complexes found in mesangial cells
    • Not related to a specific type of hypersensitivity
  39. Buerger Disease
    • Do NOT confuse with BERGER's disease
    • aka thromboagitis obliterans
    • Segmental thrombosing vasculitis of middle & small arteries AND veins & nerves in the vicinity
    • Has an affinity for the tibial & radial nerves
    • Strong association w/ smoking
    • Classic symptom is instep claudication- pain after walking
  40. Alport syndrome
    GMN w/ other symptoms such as lens dislocation, cataracts, corneal dystropy, & hearing/ear problems
  41. Chronic Glomerulonephritis
    • Typically the end stage of any glomerular disease
    • The kidney is not able to function properly because the functional tissue has been replaces w/ connective scar tissue-> a contracted kidney may develop-> the kidney becomes yellow, pale, & coarsely granular-> ends w/ the development of chronic renal failure
    • Symptoms may include crystal deposits on the skine, ammonia breath, nausea, CNS problems, secondary hyperparathyroidism leading to osteoporosis

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