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clinpath test 2 > Kidney > Flashcards

Kidney Flashcards

1
Q

1-4. What hormones does kidney make

PREH(eim)

A
  1. prostaglandins
  2. Renin
  3. Epo
  4. hydroxylation of vit D
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2
Q

(Pre-renal azotemia)

  1. caused by anything that does what?
A
  1. reduces blood flow to kidneys

(decreased perfusion pressure)

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3
Q

(Pores)

  1. albumin is smaller than pore - why doesn’t it go through normally?
  2. What is the hallmark of pore damage?
A
  1. cause of negative charge of pore
  2. proteinuria
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4
Q

(Tubule)

  1. What is the hallmark of tubule dysfunction?
A
  1. azotemia, electrolyte disturbance, glucosuria, proteinuria (to a much lesser extent), can’t conc urine
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5
Q
  1. When you have an abnormal glomerular barrier, albumin leaks - but if the tubules are normal will have normal USG and no azotemia
  2. Proteinuria (albumin) - is an indicator of what?
A
  1. glomerular damage **IF NOT OTHER **sources of portein in urinary tract (LUT dz - more common)
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6
Q
  1. GFR depends on renal plasma flow - affected by what?
  2. total GFR may decrease with what (if kidney completely normal)?
A
  1. blood vol, CO, #fx glomeruli, constriction/dilation of afferent/efferrent arterioles
  2. hypovolemia, cardiac dz, vasc disturbance
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7
Q

(tubular function)

  1. ion exchange, water balance, mineral balance, glucose/protein reabsorption
  2. if failure will lose regulation of all this –> isothenuric, glucosuria (if less than <200), proteinuria (usually from glomerular dmg)
A
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8
Q

memorize this chart

  1. how does Ca interfere?
  2. example of endocrine interference?
  3. What is medullay washout?
  4. With what condition does osmotic diuresis commonly occur?
A
  1. closes aquaporin doors –> PU/PD
  2. corticosteroids –> PU/PD
  3. when you take urea and salt away –> no gradient –> water will stay where it is
  4. DM
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9
Q

1-3. What are the three reasons Urine can’t be concentrated in renal failure? (KNOW THIS)

A
  1. dmg cells - less responsive to ADH
  2. medullary hypertonicity lost (tissue dmg/abnormal blood flow)
  3. high solute loads to remaining nephrons are overwhelming (can’t reabsorb all the solutes you need to reabsorb - usually solute)
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10
Q

(Causes of poorly conc urine)

1-10. What are they?

quadruple H, Dirty Projectors, Matt Preheim, Ray Liotta

A
  1. hyperadrenocorticism: corticosteroid interfere with ADH action
  2. hypoadrenocorticism: loss of mineralcorticoid fx (aldosterone -> kidney retains sodium)
  3. hypercalcemia (malignancy): interefre w/ ADH
  4. hypokalemia (dec tubular responsiveness to ADH)
  5. diabetes (insipidus and mellitus): solute diuresis (gluc/keto)
  6. pyometra: bac interfere w/ ADH
  7. medullary washout (loss of conc gradient)
  8. post-obstructive
  9. renal failure
  10. liver failure (dec urea prod, ^H20 consumption)
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11
Q
  1. What are the routing renal system tests?
A
  1. UA, serum biochem, urine protein/creatinine ratio, CBC
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12
Q

(urine color)

  1. yellow/amber = ?
  2. red/brown = ?
  3. yellow-orange/green-brwon =
A
  1. normal
  2. RBC, hemoglobin, myoglobin
  3. bilirubin
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13
Q

(Turbidity)

  1. normal is ?
  2. cloudiness due to what?
  3. why is horse urine normally turbid?
  4. cow urine normally turbid on standing from what?
A
  1. clear (can be a little cloudy)
  2. cells, bacteria, casts, mucus, lipid
  3. from mucus and CaCO3
  4. crystal formation
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14
Q

(USG)

  1. measured how?
  2. effect of protein and glucose?
  3. don’t memo chart - just know that cat is the highest
  4. how do you confirm persistent isosthenuria?
A
  1. refractometer
  2. minimally increase
  3. test throughout the day
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15
Q

(do memo this)

  1. maximally conc - hardly ever see this
  2. adequately conc - implies what?
  3. innappropriate - for who?
  4. hypothenuria = ?
A
  1. suff kindey fx
  2. azotemic/dehydrated patients
  3. below isosthenuria
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16
Q

(urine protein)

  1. small amount is normal
  2. what is best method of collection (cysto, catheter, free catch)?

(dipstick)

  1. affected by USG
  2. freq get what?
  3. more sens to albumin or globulins?

(urine protein/creatinine ratio)

  1. assumes what?
  2. ratios of what are abnormal?
A
  1. cysto (lower protein - but get blood)
  2. false pos
  3. albumin
  4. constant creatinine excretion over 24 hr period
  5. >1
17
Q

(proteinuria)

  1. can see in what non-pathologic situation?
A
  1. post strenuous exercise
18
Q

(proteinuria)

(pre-renal - hyperproteinemia - overflow - severe ^)

  1. increased what?
  2. see w/ what?
  3. will it cause hypoproteinemia?
A
  1. small proteins in blood that can pass through glomerulus
  2. plasma cell malignancy, colostrum, hemoglobin/myoglobin
  3. no
19
Q

(proteinuria)

(glomerular)

  1. selective loss of what?
  2. can also lose what?
A
  1. albumin
  2. clotting factors (ATIII)
20
Q

(proteinuria)

(tubular)

  1. failure to do what?
  2. severity compared to glomerular?
  3. usually from acute or chonic dmg?
  4. often times tubular dmg is 2° to what?
A
  1. absorb proteins
  2. milder
  3. acute
  4. glomerular dmg (proteins cause inflam)

if only tubule thin toxic, neoplastic, inflam

21
Q

(proteinuria - post-renal)

  1. caused by what?
  2. will it cause hypoproteinemia?
  3. presence of what supports this cause?
  4. ALWAYS rule out before presuming glomerular dz
A
  1. hemmorhage/inflam anywhere in GI tract (including kidney)
  2. no (unless massive/chronic hemorrhage or down-reg of albumin prod)
  3. leukocytes/blood
22
Q

(glucosuria)

  1. freely filtered - almost completely reabsorbed in first 20% of tubule (normal to have undetectable amount in urine)

2-3 what are two causes?

A
  1. tubule max for reabsorption is exceeded (~200)
  2. tubular dysfunction (usually acute tubular necrosis or toxin)
23
Q

(glucosuria - measurement)

  1. glucose oxidase method
  2. H2O2 and peroxidase + 0-toluidine indicator are oxidized to cause color change
  3. what can cause false +?
  4. what can cause false -?
A
  1. PEROXIDE or BLEACH
  2. absorbic acid or formaldehyde
24
Q

(acetonuria - ketone bodies)

  1. products of fat degradation that appear in the filtrate and are reabsorbed until capacity overwhelmed
  2. present in ruminant when?
  3. present in SA when?
A
  1. during starvation/energy deficit
  2. DM
25
Q

(Serum Biochemical tests of renal fx)

(Azotemia)

(pre-renal)

  1. caused by what?
  2. see what?

(renal)

  1. buidlup from renal dysfx

(post-renal)

  1. cause by what?

(uremia)

  1. what is it?
A
  1. dehydration, dec CO, hypoperfusion
  2. ^ in Cr and/or BUN, and conc urine
  3. outflow impairment (tubular P and dec GFR)
  4. cx from azotemia: lethary, anorexia, mucosal ulceration, vomiting, diarrhea, weight loss, anemia, altered urine output
26
Q

(REnal failure)

  1. what causes acute?
  2. chronic can be stable for long time - often won’t know original cause - what is it called when acute episode causes disaster in chronic?
  3. what are the effects of post-renal?
A
  1. toxins, ischemia, infectious agents
  2. “acute on chronic”
  3. renal outflow impairment, ^tubular pressure, dec GFR
27
Q

(BUN or Urea)

  1. most synth where?
  2. freely filtered in glomerulus, passive diffusion back into circ… therefore what does this mean?
  3. degraded by microbial flora in ruminants - what effect does this have in BUN vs Cr?
  4. horse does what than decreases elevation of BUN in renal failure?
A
  1. in the liver from ammonia
  2. dependent on tubular flow rate: ^rate –> dec absorbed
  3. ^BUN will lag behind Cr in renal insuff
  4. intestinal excretion

(so in LA, BUN not as good as Cr at indicating dec GFR)

28
Q

(decreased BUN)

1-4. name four causes

A
  1. liver failure/shunt
  2. low protein diet
  3. PU/PD (cause or effect)
  4. young animals (high fluid intake, rapid growth w/ anabolic state)
29
Q

(^BUN)

1-3. 3 causes

A
  1. dec GFR
  2. high protein diet/GI hemorrhage
  3. ^protein catabolism (starvation, prolonged exercise, fever, corticosteroids)
30
Q

(creatinine)

  1. most produced from what?
  2. why is it better than BUN?
  3. is decreased Cr significant?
A
  1. constant low level conv of musc creatinine to creatinine
  2. freely filtered - but NO REABSORPTION
  3. not really (maybe dec muscle mass or ^body water)
31
Q

(Creatinine)

1-3. what are the causes of increased?

A
  1. dec GFR
  2. high dietary protein
  3. non-creatinine chromagens (analyzer sees as creatinine) - not too significant
32
Q

(Sometimes change in BUN and Cr aren’t parallel)

  1. which is more sens to pre-renal or early renal factors?
  2. is creatinine or BUN more sens indicator in LA in some cases?
A
  1. BUN (cause affected by flow rate)
  2. Cr
33
Q

(Analytes in Azotemia)

(Phosphorus and azotemia)

  1. increase or decrease?
  2. Why may phosphorus be low in horses?
  3. cattle may have ^P cause of excretion of P in saliva and rumen…
A
  1. increase (failure of excretion)
  2. hypercalcemia
34
Q

(Analytes in Azotemia)

(Calcium)

  1. unpredictable - mostly normal, but dec more common than ^
  2. horses can often be what?
  3. dogs and cats w/ hypercalemia = ?
  4. horses with ^ Ca?
A
  1. hypercalcemic (usually high urinary excretion cause they take in all the calcium they can get)
  2. hypercalcemia of malig that causes azotemia (ADH interferecene)
  3. result of renal dz
35
Q

(Analytes in Azotemia)

(albumin)

  1. may increase why?
  2. may decrease why?
A
  1. dehydration
  2. glomerular dz

(dilution rarely)

36
Q

(Analytes in Azotemia)

(Na and Cl)

  1. usually normal until terminal phases
  2. hyper if?
  3. hypo if?
A
  1. loss of water greater than
  2. loss of water less than
37
Q

(Analytes in Azotemia)

(Potassium)

  1. often normal
  2. hyper when?
  3. hypo when?
A
  1. anuric/oliguric w/ post-renal - EMERGENCY
  2. polyuric renal failure from ^ losses +/- anorexia

clinpath test 2 (7 decks)

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