Kidney shit

Question 1

4 major kidney structures susceptible to disease

Answer 1

• glomeruli
• tubules
• interstitium
• vasculature

Question 2

pathogenesis of CRF

Answer 2

• 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

Question 3

factors in development of polyuria CRF

Answer 3

• “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

Question 4

how many nephrons left when uremia develops

Answer 4

1/4

Question 5

dehydration CRF

Answer 5

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

Question 6

salt and water retention CRF

Answer 6

• 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

Question 7

metabolic acidosis CRF

Answer 7

-reduced total renal ammonia production, decreased bicarb uptake

Question 8

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

Answer 8

• 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

Question 9

hematopoietic manifestations CRF

Answer 9

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

Question 10

gastrointestinal manifestations CRF

Answer 10

• oral ulcers

- erosive gastritis

Question 11

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

Answer 11

when GFR is 30-50% of normal

Question 12

glomerulosclerosis CRF

Answer 12

• 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

Question 13

tubulointerstitial damage CRF

Answer 13

• interstitial fibrosis and tubular damage/loss

- ischemic damage, increased ammoniagenesis, proteinuria

Question 14

what is acute renal failure characterized by

Answer 14

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

Question 15

nephrosis

Answer 15

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

Question 16

ischemic acute tubular necrosis

Answer 16

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

Question 17

toxic ATN

Answer 17

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

Question 18

pathogenesis of acute renal failure in ATN

Answer 18

• 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

Question 19

principal mechanisms causing oliguria (4)

Answer 19

• 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

Question 20

other causes of ARF (3)

Answer 20

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

Question 21

renal papillary (medullary crest) necrosis

Answer 21

• 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

Question 22

renal infarcts

Answer 22

• 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

Question 23

what is glomerular filtration barrier composed of

Answer 23

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

Question 24

what is primary glomerulonephritis

Answer 24

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

Question 25

immune/inflammatory mechanisms of primary glomerulonephritis (5)

Answer 25

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

Question 26

mediators of immunologic injury in primary glomerulonephritis (6)

Answer 26

- neutrophils - C5b-9 - monocytes/macrophages - platelets - glomerular cells - coagulation system

Question 27

consequences of glomerular injury (3)

Answer 27

- changes in renal plasma flow and glomerular filtration rate - Na and fluid retention - proteinuria

Question 28

changes in renal plasma flow/GFR in glomerular injury

Answer 28

- 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

Question 29

Na/fluid retention in glomerular injury

Answer 29

- 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

Question 30

proteinuria in glomerular injury

Answer 30

- damage to filtration barrier affects protein permeability | - hemoglobin passes freely into filtrate, albumin retained

Question 31

4 findings in nephrotic syndrome

Answer 31

- proteinurua - hypoalbuminemia - generalized edema - hyperlipidemia

Question 32

thrombotic diathesis in nephroic syndrome

Answer 32

- mainly due to loss of antithrombin III in urine | - increases in clotting factors and fibrinogen

Question 33

what is amyloid

Answer 33

insoluble fibrillar protein with b-pleated sheet conformation

Question 34

AL amyloidosis

Answer 34

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

Question 35

AA amyloidosis

Answer 35

- 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)

Question 36

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

Answer 36

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