renal 1-3 Flashcards

(78 cards)

1
Q

what are the four main functions of the kidney?

A
  1. maintenance of normal fluid balance
  2. excretion of metabolic waste (esp. protein breakdown byproducts)
  3. phosphate and potassium homeostasis (and other electrolytes)
  4. production or activation of certain hormones (renin, rythropoietin (EPO), active vitamin D)
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2
Q

what goes where?

A

like this

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3
Q

normal dog kidney - which is the cortex and which is the medulla?

A

cortex - outside
medulla - inside

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4
Q

The nephrons are arranged in a specific way within the kidney.
a. glomeruli are mostly in the cortex, tubules mostly in medulla
b. tubules mostly in the cortex, glomeruli are mostly in the medulla

A

a. glomeruli are mostly in the cortex, tubules mostly in medulla

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5
Q

which is NOT one of the 3 main conditions that need to be present to allow urine concentration:
a. The tubule wall must be permeable to water
b. There must be a concentration gradient whereby the solute concentration in the interstitium is higher than in the tubular fluid
c. There have to be enough functioning nephrons to ‘cope’ with the load of urine
d. both kidneys need to be present

A

d. both kidneys need to be present - all the rest are true

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6
Q

The net movement of water out of the tubules is driven by…..

A

medullary hypertonicity - the fact that the interstitium in the medulla has a high concentration of sodium and urea.

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7
Q
  • is released when blood volume or blood pressure drops, or when blood potassium increases
    a. anti-diuretic hormone (ADH)
    b. aldosterone
A

b. aldosterone

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8
Q
  • acts on the distal convoluted tubules by increasing the activity of Na/K+ pumps in the membrane (promotes sodium reabsorption, and therefore increases water reabsorption via osmosis = concentrated urine)
    a. anti-diuretic hormone (ADH)
    b. aldosterone
A

b. aldosterone

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9
Q

which is released from the pituitary gland?
a. anti-diuretic hormone (ADH)
b. aldosterone

A

a. anti-diuretic hormone (ADH) - (aldosterone is released from the adrenal cortex)

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10
Q

When _____ is released from the pituitary gland it opens up pores in the collecting duct membrane so that more water moves out of the tubule into the medullary interstitium. _____ also activates urea pumps in the membrane, pumping more urea into the interstitium.
a. anti-diuretic hormone (ADH)
b. aldosterone

A

a. anti-diuretic hormone (ADH)

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11
Q

is it the thick or thin part of the loop of henle permeable?

A

decending thick = impermeable
thin = permeable
ascending thick = impermeable, but contains Na pump

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12
Q

what is it called when there is a slow progressive loss of nephrons?

A

chronic kidney disease:
renal insufficiency at 2/3 nephrons lost
renal failure at 3/4

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13
Q

what would happen to urine volume and urine concentration in an animal with renal failure compared to an animal with normal renal function?

A

volume would increase, concentration would decrease - kidneys will produce an increased volume of urine because the tubules are no longer able to drive water reabsorption

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14
Q

what does polyurea mean?

A

the excessive production and excretion of urine, resulting in frequent urination and potentially large volumes of urine per day

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15
Q

what does polydypsia mean?

A

Polydipsia is the medical term for excessive thirst, characterized by an abnormal and persistent desire to drink

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16
Q

what does Isosthenuria mean?

A

a condition where the kidneys produce urine with a specific gravity (concentration) that is equal to that of blood plasma - meaning it hasn’t been concentrated/diluted at all

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17
Q

he two main protein breakdown byproducts are….

A
  • urea (comes from all protein breakdown)
  • creatinine (from muscle protein breakdown)
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18
Q

what is azotaemia?

A

increased levels of creatine and/or urea in the blood

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19
Q

Could the person depicted on the right produce concentrated urine?

A

yes - kidneys don’t lose the ability to concentrate urine until 75% of nephrons are damaged or lost, this guy still has 50% (if the remaining kidney is healthy)

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20
Q

Chronic kidney disease will lead to:
a. Hyperkalaemia
b. Hypokalaemia

A

b. Hypokalaemia - with chronic kidney disease there will be large amounts of urine flowing through the tubules, therefore more K+ will be lost in the urine

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21
Q

true or false - High tubular flow rates lead to excessive loss of potassium in the urine, while the opposite happens when tubular flow rates are low.

A

true

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22
Q

Acute kidney disease will lead to:
a. Hyperkalaemia
b. Hypokalaemia

A

a. Hyperkalaemia - acute kidney disease results in decreased urine production involving low (or no) urine flow through the tubules. decreased tubular flow rate causes decreased K+ excretion

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23
Q

in the early stages of acute kidney injury the kidneys actually produce very little urine (oliguria) or none at all (anuria) - true or false?

A

true

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24
Q

Healthy kidneys are net excretors of phosphate. When blood flow to the kidneys decreases to around 25% normal, phosphate excretion is impaired and hyperphosphataemia develops… except for in what species?
a. dogs
b. cows
c. sheep
d. horses

A

d. horses - it’s always fucking horses (horses get hypercalcaemia instead)

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25
In non-equine species, hyperphosphataemia occurs in both acute and chronic kidney failure. When it is prolonged (i.e. chronic kidney disease) and severe, phosphate ions in serum (PO43-) can combine with calcium ions (Ca2+) to form insoluble calcium phosphate which can then precipitate in soft tissues. This process is known as..... a. bladder stones b. metastatic calcification c. dystrophic calcification
b. metastatic calcification
26
using your knowledge of haematology and the mechanism of action of EPO, which type of anaemia do you think will be present in chronic renal failure: a. Haemolytic b. Non-regenerative c. Regenerative
b. Non-regenerative - loss of functional kidney tissue in chronic kidney disease results in decreased EPO production = lack of reticulocyte production
27
Would you expect to see anaemia in acute kidney disease? a. No b. Yes
a. No - erythrocytes have a lifespan of about 3 months, so it takes a while to lose enough of them to cause anaemia. anaemia = chronic kidney disease
28
what does uraemia mean?
"urine in the blood" - in vet med, used to describe the whole spectrum of abnormalities that develop when the kidneys fail
29
what is uraemia ("urine in the blood") caused by?
buildup of a bunch of stuff (urea, ammonia, hormone breakdown products and toxins) that should have been excreted by the kidneys
30
what is a kidney's functional reserve?
The ability of the kidney to compensate for loss of function. When some nephrons fail, the remaining ones work harder in order to compensate (pov: my braincells right now)
31
which kidney (or kidneys) below would have a decreased ability to concentrate (or dilute) urine? a. left b. middle c. middle and right d. right
c. middle and right middle - This kidney would not be able to produce optimally concentrated urine, but it could produce concentrations above that of plasma right - kidney can't concentrate urine even slightly. Urine from this kidney would be isosthenuric.
32
which kidney (or kidneys) below that would be associated with azotaemia (the increased creatine/urea in blood one) a. left b. middle c. middle and right d. right
d. right - Patients become azotaemic once they lose 3/4 of their nephrons. This patient would be azotaemic (and isosthenuric). *note - concentration is lost earlier than urea/creatine excretion)
33
which is NOT a symptom of circulating uraemic toxins in the bloodstream? a. loss of appetite, lethargy and vomiting b. inhibited platelet function (severely uraemic patients are predisposed to bleeding c. volatile toxins are breathed out, can smell on breath of uraemic patients d. eyes fall out e. caustic to endothelial and mucosal cells (ulcers)
d. eyes fall out (lol i couldn't think of anything better), does everything else
34
what is glomerular filtrate?
the fluid that passes into Bowman's capsule in the glomerulus *not the same as urine output, most of the water component is reabsorbed from the tubules and goes back into the blood
35
what is the glomerular filtration rate (GFR) of a kidney?
the total amount of filtrate produced by all the nephrons over time - strongly correlated with kidney function, chronic kidney disease is caused by the progressive loss of nephrons (decline in GFR)
36
true or false - failing kidneys can't excrete protein breakdown products quickly enough to stop them building up in the blood
true - we can then use these protein breakdown products (eg creatinine, urea, SDMA) to diagnose kidney disfunction
37
what is creatinine?
a small soluble protein fromed from the muscle protein phosphocreatine *muscle proteins are continually turned over and renewed at a constant rate, so an animal with stable muscle mass will steadily release creatinine into the blood
38
what are the two problems with using creatinine to measure kidney function?
1. serum creatinine levels don't start to rise above normal till 75% of kidney function is lost 2. if an animal is sick and losing muscle mass (eg with chronic kidney disease) the amount of creatinine they form will slowly decrease bc there's less muscle to make it - might not reflect the severity of the kidney disease
39
what is SDMA (symmetric dimethyl arginine)?
a compound that is produced by all nucleated cells at a constant rate - level in blood is almost fully dependent of glomerular excretion, and level changes quite quickly when GFR decreases
40
what tool to you use to measure the concentration of urine (urine specific gravity/USG)?
a refractometer
41
what does urine specific gravity (USG) measure?
the amount of dissolved solute present - ie, the concentration of the urine
42
which is elevated in both acute and chronic kidney disease? a. potassium (K+) b. phosphate (PO4^3-)
b. phosphate (PO4^3-)
43
which is normal with chronic kidney disease but elevated with acute kidney injury? a. potassium (K+) b. phosphate (PO4^3-)
a. potassium (K+)
44
what does isosthenuric mean? a. very dilute urine b. same dilution as plasma - kidneys neither diluting or concentrating c. minimally concentrated
b. same dilution as plasma - kidneys neither diluting or concentrating
45
what does hyposthenuric mean? a. very dilute urine b. same dilution as plasma - kidneys neither diluting or concentrating c. minimally concentrated
a. very dilute urine
46
how dilute does urine specific gravity need to be to be classified as hyposthenuric for dogs, cats, and large animals (all the same value)? a. <1.001 b. <1.008 c. 1.008-1.012
b. <1.008 = hyposthenuric
47
how dilute does urine specific gravity need to be to be classified as isosthenuric for dogs, cats, and large animals (all the same value)? a. <1.001 b. <1.008 c. 1.008-1.012 d. 1.013-1.030
c. 1.008-1.012
48
which is the minimally concentrated urine specific gravity value for dogs, which is cats, and which is large animal? a. 1.013 - 1.025 b. 1.013 - 1.030 c. 1.013 - 1.035
a. 1.013 - 1.025 = large animal b. 1.013 - 1.030 = dogs c. 1.013 - 1.035 = cats
49
which is the optimally concentrated urine specific gravity value for dogs, which is cats, and which is large animal? a. >1.025 b. >1.030 c. >1.035
a. >1.025 = large animal b. >1.030 = dogs c. >1.035 = cats
50
categorise the urine specific gravity (USG) in this cat: a. Hyposthenuric b. Isosthenuric c. Minimally concentrated d. Optimally concentrated
d. Optimally concentrated - it's above 1.035
51
a cat has a urine specific gravity seen in the image - does this tell us anything about the kidney function of this cat?
USG - >1.035 = optimally concentrated this means the kidney must be functioning normally (there must be 2/3 of nephrons working in order to concentrate urine)
52
categorise the urine specific gravity (USG) in this dog: a. Hyposthenuric b. Isosthenuric c. Minimally concentrated d. Optimally concentrated
c. Minimally concentrated - between 1.013 and 1.030
53
if a dog's USG was minimally concentrated - between 1.013 and 1.030, can you say it has normal renal funtion?
not from USG alone - you'd need to know it's hydration status to see if it was appropriate *however, it's not in severe renal failure, it can still concentrate some urine (hasn't lost 75% of nephrons)
54
if a dog's USG was minimally concentrated - between 1.013 and 1.030 - but it's clinically dehydrated (hypovolaemic), what does that day about renal function?
concentration mechanism is not working to full capacity (a dehydrated animal should be making optimally concentrated urine) - maybe renal insufficiency? (lost between 2/3 and 3/4 of nephron function)
55
what are the four mechanisms of increased urea/creatinine in the blood (azotaemia)?
1. Non-renal azotaemia 2. Pre-renal azotaemia 3. Renal azotaemia 4. Post-renal azotaemia
56
which category would gastrointestinal haemorrhage, post-prandial sampling (done after eating), catabolic state (body protein breakdown), and a high protein diet fall under? 1. Non-renal azotaemia 2. Pre-renal azotaemia 3. Renal azotaemia 4. Post-renal azotaemia
1. Non-renal azotaemia
57
which category would dehydration fall under? 1. Non-renal azotaemia 2. Pre-renal azotaemia 3. Renal azotaemia 4. Post-renal azotaemia
2. Pre-renal azotaemia
58
which category would severe chronic kidney disease and severe acute kidney injury fall under? 1. Non-renal azotaemia 2. Pre-renal azotaemia 3. Renal azotaemia 4. Post-renal azotaemia
3. Renal azotaemia
59
which category would a ruptured bladder or urethral obstruction fall under? 1. Non-renal azotaemia 2. Pre-renal azotaemia 3. Renal azotaemia 4. Post-renal azotaemia
4. Post-renal azotaemia
60
is dash azotaemic? a. no b. yes
b. yes - urea and creatinine levels are both above normal range
61
could this be non-renal azotaemia? a. yes b. no c. not sure
b. no - we can rule out non-renal because dash has elevated urea AND creatinine, non renal only results in elevated urea with creatinine in the normal range
62
could this be pre-renal azotaemia? a. yes b. no c. not sure
a. yes - dehydration is by far the main cause of pre-renal azotaemia (bc it decreases blood volume and therefore renal blood flow, less urea and creatinine are delivered to the kidneys for excretion and their concentrations progressively increase in the blood).
63
could this be renal azotaemia? a. yes b. no c. not sure
b. no - he's producing optimally concentrated urine, which means he must have normal renal function
64
could this be post renal azotaemia? a. yes b. no c. not sure
c. not sure
65
true or false - can you have more than one kind of azotaemia happening at once?
true - ALWAYS work through all four types
66
what is non-renal azotaemia?
when increased amounts of urea/creatinine are PRODUCED. does not involve the kidney (non-renal), usually mild. only urea concentration increases.
67
which form of azotaemia results in only increased urea, not creatinine? 1. Non-renal azotaemia 2. Pre-renal azotaemia 3. Renal azotaemia 4. Post-renal azotaemia
1. Non-renal azotaemia
68
what is pre-renal azotaemia?
decreased DELIVERY of urea/creatinine to the kidney. happens before the kidney, usually decreased blood flow due to dehydration - mild, and should be able to rule out renal with USG
69
what is renal azotaemia?
where the kidney is unable to keep up with the excretion of urea and creatinine (loss of > 75% of nephrons). look for USG issues to confirm
70
what is post renal azotaemia?
when urea/creatinine is unable to be excreted in the urine, happens AFTER the kidney. check patient for trauma/blockages of urinary bladder/urethra etc
71
what is the pathogenesis behind haemorrhage in the stomach?
uraemic toxins secreted into stomach > caustic damage to mucosal epithelial cells > ulceration > bleeding PLUS: uraemic toxins > inhibited platelet plug formation > predisposed to bleeding from mucosal surfaces
72
what is the pathogenesis behind pale mucous membranes?
kidney failure > loss of EPO > failure to stimulate red blood cell production in bone marrow > no reticulocytes released > run out of erythrocytes (non-regenerative anaemia)
73
what is the pathogenesis behind ulcerated mucous membranes?
caustic uraemic toxins excreted in saliva > necrosis of oral mucosa > ulceration
74
what is the pathogenesis behind body cavity effusions, e.g. pericardium, thoracic cavity, alveolar spaces
Uraemic toxins damage endothelial cells in serosal surfaces and alveoli > leaky vessels > buildup of proteinaceous fluid in cavities
75
what is the pathogenesis behind pathological fractures? hint - related to hyperphosphataemia and renal secondary hyperparathyroidism
Renal failure > decreased GFR > decreased PO4 excretion > hyperphosphataemia > PO4 combines with Ca ions > calcium phosphate > precipitates in soft tissues (metastatic calcification) > lowers serum Ca conc. > detected by parathyroid gland > releases parathyroid hormone (PTH) > stimulates osteoclasts in bone > osteoclasts dissolve mineral (calcium phosphate) in bone (to increase serum calcium) BUT > weak bones > predisposed to fractures
76
what is the pathogenesis behind vomiting up material that looks like coffee grounds?
Uraemic toxins in blood > cause nausea and vomiting PLUS Uraemic toxins in blood > inhibit platelet plug formation > mucosal bleeding AND uraemic toxins secreted into stomach > cause mucosal necrosis (ulceration) > bleeding into stomach >> blood in stomach reacts with gastric acid > forms brownish granular material > combined with vomiting > coffee-ground material in vomit
77
azotaemia severity classification - how does it work? *important
- mildly elevated = up to 3 x normal range - moderately elevated = 3 - 10x normal range - severely elevated = >10x normal range
78
if you see hyperproteinaemia but A:G ratio is normal, what's going on
hyperproteinaemia - increased production or relative due to dehydration. if A:G ratio normal = dehydration