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Pathology 2 > Kidney shit > Flashcards

Kidney shit Flashcards

1
Q

4 major kidney structures susceptible to disease

A
  • glomeruli
  • tubules
  • interstitium
  • vasculature
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2
Q

pathogenesis of CRF

A
  • nephrons gradually lost –> remaining ones must handle glomerular filtration
  • undergo hypertrophy
  • 1/3 nephrons left –> can’t compensate, total filtration declines (GFR decreases)
  • increase in BUN/serum creatinine (azotemia)
  • loss of 2/3+ nephrons leads to isosthenurua, 3/4+ leads to azotemia
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3
Q

factors in development of polyuria CRF

A
  • “critical mass” of functioning nephrons no longer present to maintain medullary solute gradient and countercurrent exchange
  • solute diuresis occurs because few functioning nephrons must handle increased solute load –> solutes normally removed remain in ultrafiltrate in lumen
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4
Q

how many nephrons left when uremia develops

A

1/4

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5
Q

dehydration CRF

A
  • due to impairment of renal concentrating ability with excretion of large volumes of water
  • polydipsia not enough to correct it
  • vomiting and diarrhea
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6
Q

salt and water retention CRF

A
  • volume depletion from dehydration causes increased renin secretion
  • renin –> angiontensinogen –> angiotensin I –> angiotensin II
  • angiotensin II causes vasoconstriction –> hypertension, aldosterone secretion
  • aldosterone causes Na retention
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7
Q

metabolic acidosis CRF

A

-reduced total renal ammonia production, decreased bicarb uptake

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8
Q

abnormalities in Ca, P, bone metabolism (6) CRF

A
  • GFR falls below 25% –> P excretion reduced (serum P levels rise)
  • elevated P enhances Ca entry into tissues (hypocalcemia)
  • hypocalcemia triggers PTH secretion –> secondary renal hyperparthyroidism (also reduced PTH clearance)
  • PTH causes bone demineralization (renal osteodystrophy)
  • reduced production of vitamin D –> reduced Ca absorption (hypocalcemia)
  • metastatic mineralization
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9
Q

hematopoietic manifestations CRF

A
  • uremia characterized by normocytic, normochromic anemia (non-regenerative) from reduced erythropoietin production
  • uremic toxins
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10
Q

gastrointestinal manifestations CRF

A
  • oral ulcers

- erosive gastritis

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11
Q

how much does GFR have to be reduced to progress to end-stage renal failure

A

when GFR is 30-50% of normal

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12
Q

glomerulosclerosis CRF

A
  • blood flow to remaining glomeruli increased
  • dilation of afferent arteriole greater than that of efferet arteriole
  • increased glomerular BP (glomerular hypertension)
  • damage to cells –> increased permeability
  • increased mesangial production of matrix/mesangium
  • can be multifocal or generalized, global or segmental
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13
Q

tubulointerstitial damage CRF

A
  • interstitial fibrosis and tubular damage/loss

- ischemic damage, increased ammoniagenesis, proteinuria

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14
Q

what is acute renal failure characterized by

A
  • oliguria or anuria of rapid onset
  • azotemia
  • metabolic acidosis, hyperkalemia, hypophosphatemia
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15
Q

nephrosis

A

a form of acute tubular injury that is not caused by inflammation (usually ischemia, nephrotoxins)

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16
Q

ischemic acute tubular necrosis

A
  • usually associated with sever hypotension or renal hypoperdusion due to shock
  • “shock kidney”
  • multifocal or patchy necrosis along nephron
17
Q

toxic ATN

A
  • nephrotoxins, organic solvents, antibiotics, NSAISs, pesticides, vitamin D, hypercalcemia, ethylene glycol
  • kidneys are swollen and pale, perirenal edema
18
Q

pathogenesis of acute renal failure in ATN

A
  • tubule epithelial cell injury (vulnerable):
    1) cells are highly metabolically active –> high energy and O2 requirements
    2) large, highly charged surface area and active transport systems for reabsorption of ions and organic acids (and toxins)
    3) effectively concentrate toxins intracellularly
19
Q

principal mechanisms causing oliguria (4)

A
  • endothelial dysfunction (vasoconstriction and reduced GFR)
  • tubuloglomerular feedback (increased Na in distal tubules, increased renin, vasoconstriction)
  • tubular damage/necrosis (leakage/backflow of filtrate)
  • increased tubular pressure (obstruction) leads to leakage
20
Q

other causes of ARF (3)

A
  • acute glomerulonephritis
  • acute massive renal infarction
  • complete bilateral urinary tract outflow obstruction
21
Q

renal papillary (medullary crest) necrosis

A
  • primary disease in animals treated with NSAIDs
  • horses, dogs, cats
  • medullary interstitial cells are primary targets of papillotoxins
  • coagulation necrosis of medullary crest/inner medulla with hemorrhage
22
Q

renal infarcts

A
  • areas of coagulative necrosis from local ischemia of vascular occlusion (thromboembolism)
  • initially swollen and red, become pale tan with zone of hyperemia and hemorrhage
  • usually involve cortex
23
Q

what is glomerular filtration barrier composed of

A
  • pedicles (foot proesses) of podocytes
  • basal lamina
  • fenestrated epithelium of glomerular capillaries
24
Q

what is primary glomerulonephritis

A

inflammatory and/or immune mediated condition in which the renal glomerulus is the primary site of injury

25
Q

immune/inflammatory mechanisms of primary glomerulonephritis (5)

A
  • in situ immune complex formation
  • circulating immune complex deposition (antigen-antibody complexes)
  • cytotoxic antibodies
  • cell-mediated injury
  • activation of alternate complement pathway
26
Q

mediators of immunologic injury in primary glomerulonephritis (6)

A
  • neutrophils
  • C5b-9
  • monocytes/macrophages
  • platelets
  • glomerular cells
  • coagulation system
27
Q

consequences of glomerular injury (3)

A
  • changes in renal plasma flow and glomerular filtration rate
  • Na and fluid retention
  • proteinuria
28
Q

changes in renal plasma flow/GFR in glomerular injury

A
  • RPF and GFR may initially be increased, normal, or decreased (compensatory mechanisms) –> both decrease eventually
  • damage to glomeruli result in ischemia –> atrophy and/or necrosis
  • loss of nephrons and reduced GFR –> renal failure
29
Q

Na/fluid retention in glomerular injury

A
  • acute GN –> hypertension and edema –> acute renal failure
  • Na retention from reduced GFR or enhanced resorption
  • Na retention may be increased by low plasma volume –> RAAS
30
Q

proteinuria in glomerular injury

A
  • damage to filtration barrier affects protein permeability

- hemoglobin passes freely into filtrate, albumin retained

31
Q

4 findings in nephrotic syndrome

A
  • proteinurua
  • hypoalbuminemia
  • generalized edema
  • hyperlipidemia
32
Q

thrombotic diathesis in nephroic syndrome

A
  • mainly due to loss of antithrombin III in urine

- increases in clotting factors and fibrinogen

33
Q

what is amyloid

A

insoluble fibrillar protein with b-pleated sheet conformation

34
Q

AL amyloidosis

A
  • occurs in patients with plasma cell myelomas or other b cell lymphocyte dyscrasias
  • amyloid deposits are composed of fragments of light chains of immunoglobulins
35
Q

AA amyloidosis

A
  • reactive amyloidosis
  • most common form of spontaneously occurring amyloidosis in domestic animals
  • chronic inflammatory conditions
  • amyloid deposits composed of fragments of a serum acute-phase reactant protein called serum amyloid-associated protein (SAA)
36
Q

most common site in kidney for deposition of amyloid and what happens

A

glomeruli (renal medullar interstitium in cats) –> glomerular amyloidosis can result in nephrotic syndrome

Pathology 2 (8 decks)

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