Kidney

Question 1

1-4. What hormones does kidney make

PREH(eim)

Answer 1

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

Question 2

(Pre-renal azotemia)

1. caused by anything that does what?

Answer 2

1. reduces blood flow to kidneys

(decreased perfusion pressure)

Question 3

(Pores)

1. albumin is smaller than pore - why doesn’t it go through normally?
2. What is the hallmark of pore damage?

Answer 3

1. cause of negative charge of pore
2. proteinuria

Question 4

(Tubule)

1. What is the hallmark of tubule dysfunction?

Answer 4

1. azotemia, electrolyte disturbance, glucosuria, proteinuria (to a much lesser extent), can’t conc urine

Question 5

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?

Answer 5

2. glomerular damage **IF NOT OTHER **sources of portein in urinary tract (LUT dz - more common)

Question 6

1. GFR depends on renal plasma flow - affected by what?
2. total GFR may decrease with what (if kidney completely normal)?

Answer 6

1. blood vol, CO, #fx glomeruli, constriction/dilation of afferent/efferrent arterioles
2. hypovolemia, cardiac dz, vasc disturbance

Question 7

(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)

Question 8

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?

Answer 8

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

Question 9

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

Answer 9

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)

Question 10

(Causes of poorly conc urine)

1-10. What are they?

quadruple H, Dirty Projectors, Matt Preheim, Ray Liotta

Answer 10

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)

Question 11

1. What are the routing renal system tests?

Answer 11

1. UA, serum biochem, urine protein/creatinine ratio, CBC

Question 12

(urine color)

1. yellow/amber = ?
2. red/brown = ?
3. yellow-orange/green-brwon =

Answer 12

1. normal
2. RBC, hemoglobin, myoglobin
3. bilirubin

Question 13

(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?

Answer 13

1. clear (can be a little cloudy)
2. cells, bacteria, casts, mucus, lipid
3. from mucus and CaCO3
4. crystal formation

Question 14

(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?

Answer 14

1. refractometer
2. minimally increase
3. test throughout the day

Question 15

(do memo this)

1. maximally conc - hardly ever see this
2. adequately conc - implies what?
3. innappropriate - for who?
4. hypothenuria = ?

Answer 15

2. suff kindey fx
3. azotemic/dehydrated patients
4. below isosthenuria

Question 16

(urine protein)

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

(dipstick)

3. affected by USG
4. freq get what?
5. more sens to albumin or globulins?

(urine protein/creatinine ratio)

6. assumes what?
7. ratios of what are abnormal?

Answer 16

2. cysto (lower protein - but get blood)
3. false pos
4. albumin
5. constant creatinine excretion over 24 hr period
6. >1

Question 17

(proteinuria)

1. can see in what non-pathologic situation?

Answer 17

1. post strenuous exercise

Question 18

(proteinuria)

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

1. increased what?
2. see w/ what?
3. will it cause hypoproteinemia?

Answer 18

1. small proteins in blood that can pass through glomerulus
2. plasma cell malignancy, colostrum, hemoglobin/myoglobin
3. no

Question 19

(proteinuria)

(glomerular)

1. selective loss of what?
2. can also lose what?

Answer 19

1. albumin
2. clotting factors (ATIII)

Question 20

(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?

Answer 20

1. absorb proteins
2. milder
3. acute
4. glomerular dmg (proteins cause inflam)

if only tubule thin toxic, neoplastic, inflam

Question 21

(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

Answer 21

1. hemmorhage/inflam anywhere in GI tract (including kidney)
2. no (unless massive/chronic hemorrhage or down-reg of albumin prod)
3. leukocytes/blood

Question 22

(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?

Answer 22

2. tubule max for reabsorption is exceeded (~200)
3. tubular dysfunction (usually acute tubular necrosis or toxin)

Question 23

(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 -?

Answer 23

3. PEROXIDE or BLEACH
4. absorbic acid or formaldehyde

Question 24

(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?

Answer 24

2. during starvation/energy deficit
3. DM

Question 25

(Serum Biochemical tests of renal fx) (Azotemia) (pre-renal) 1. caused by what? 2. see what? (renal) 3. buidlup from renal dysfx (post-renal) 4. cause by what? (uremia) 5. what is it?

Answer 25

1. dehydration, dec CO, hypoperfusion 2. ^ in Cr and/or BUN, and conc urine 4. outflow impairment (tubular P and dec GFR) 5. cx from azotemia: lethary, anorexia, mucosal ulceration, vomiting, diarrhea, weight loss, anemia, altered urine output

Question 26

(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?

Answer 26

1. toxins, ischemia, infectious agents 2. "acute on chronic" 3. renal outflow impairment, ^tubular pressure, dec GFR

Question 27

(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?

Answer 27

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)

Question 28

(decreased BUN) 1-4. name four causes

Answer 28

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)

Question 29

(^BUN) 1-3. 3 causes

Answer 29

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

Question 30

(creatinine) 1. most produced from what? 2. why is it better than BUN? 3. is decreased Cr significant?

Answer 30

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)

Question 31

(Creatinine) 1-3. what are the causes of increased?

Answer 31

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

Question 32

(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?

Answer 32

1. BUN (cause affected by flow rate) 2. Cr

Question 33

(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...

Answer 33

1. increase (failure of excretion) 2. hypercalcemia

Question 34

(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?

Answer 34

2. hypercalcemic (usually high urinary excretion cause they take in all the calcium they can get) 3. hypercalcemia of malig that causes azotemia (ADH interferecene) 4. result of renal dz

Question 35

(Analytes in Azotemia) (albumin) 1. may increase why? 2. may decrease why?

Answer 35

1. dehydration 2. glomerular dz (dilution rarely)

Question 36

(Analytes in Azotemia) (Na and Cl) 1. usually normal until terminal phases 2. hyper if? 3. hypo if?

Answer 36

2. loss of water greater than 3. loss of water less than

Question 37

(Analytes in Azotemia) (Potassium) 1. often normal 2. hyper when? 3. hypo when?

Answer 37

2. anuric/oliguric w/ post-renal - EMERGENCY 3. polyuric renal failure from ^ losses +/- anorexia