renal injury and disease Flashcards

1
Q

what is more pink Pct or DCT

A

PCT - much pinker tubular epithelium than DCT due to packed through of mitochondria from a biopsy as 90% of solutes are reabsorbed in PCT

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2
Q

Formation or urine and eliminate of N2 waste
Control of water balance and serum osmolarity
Control electrolytes - sodium, potassium ,phosphate
Drug metabolism
Drug excretion
Hormone synthesis - renin and vit d EPO
Calcium and phosphate homeostasis
Acid base regulation
Blood pressure control

are all functions of what

A

kidney

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3
Q

where is urien collected

A

bowmans space

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4
Q

angiotensin 2 constrict which arteriole

A

efferent maintaining intraglomerular pressure - also noradrenaline and vasopressin

increase vasodilatory prostogladnisn on afferent side therefore increasing preload such as endothelial NO

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5
Q

preload

A

vol of blood in ventricles at end of diastole

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6
Q

after load

A

resistance left ventricle must overcome to circulate blood

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7
Q

the crockroft-gault equation evaluates creatinine clearance what mistake does ti assume

A

everyone is 70kg in weight

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8
Q

Renal injury definition

A

Reduced functional capacity ( principally diminished excretory function)

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9
Q

CKD defintion

A

kidney damage for over 3 months defined by strictly or functional abnormalities of the kidney with or without decreased GFR either pathological abnormalities or markers of kidney damage including blood or ruin

or GFR below 60 for 3 months or more

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10
Q

how many stages of kidney disease - chronic

A

5
1- 90 GRF - normal
2- 60-89 - middle reduced , blood monitor control
3- 30 - diagnosis
4-15 - several reduce mamnaegmtn of complications
5- under 15 - end stage kidney failure

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11
Q

acute kidney injury

A

An acute decline of renal function with risk of clinically significant toxicity which is potentially reversible and potentially required RRT
rise in creatine increases length of stay

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12
Q

the rifle criteria for acute renal dysfunction

A

increase creatine increased or GFR decreases in stages
1- Cr > 26.4
2 Cr > 200-300%
3- Cr> above 300%

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13
Q

impact of AKI

A
local production of inflammatory mediators 
cytokines ( IL-1) and chemokine (IL-8) 
compelmtn activation 
palette activating factor 
metabolites of arachidonic acid 
ROS
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14
Q

causes of AKI

A
Pre-renal - msot 
Intra renal 
ATN 
Glomerular 
micro/macro vascular 
Interstitial nephritis 
Post renal 
50% due to sepsis
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15
Q

what is a clinical consequence of AKI

how to treat it

A

hyperkalaemia - ECG - widening ORS complex and increased T waves

anagnoise the effect of potassium on heart with calcium
shift potassium back into cells usign beta agnostic and insulin
remove potassium from the body by diet and stop potassium retaining drugs like spironolactone and ACEI
dialysis

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16
Q

indications for dialysis

A

uremia
hyperkalaemia
fluid overload - resistant to diuretics especially pulmonary oedema
metabolic acidosis

17
Q

difference between AKI and CKD

A

kidney size goes small in chronic
carbamylated Hb goes high in chronic
broad casts on urinalysis present on chronic
history of kidney disease for chronic
anaemia and metboaci acids etc always present chronic
chronic is not really reversible

18
Q

lab abnorm in renal failure

A
sodium is low or high 
potassium high 
bicarbonate low 
pH low 
calcium low 
phosphate high 
Hb low