what happens when the kidneys stop working Flashcards

1
Q

what happens when the kidneys stop working

A

loss of excretory functioin
loss of homeostatic function - K/H/Na
loss of endocrine function
abnormality of glucose homeostasis - endogenous producer of glucose and metaboliser of insulin

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2
Q

effect of loss of excretory functioin

A

accumulation of waste products

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3
Q

consequence of loss of homeostatic function

A

disturbacnce of electrolyte balance
loss of acid-base control
inability to control vol

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4
Q

consequence of loss of endocrine function

A

failure of erythropoietin production

and 1 alpha hydroxylase vit D to make it active

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5
Q

consequence of abnormality of glucose homeostasis

A

decreased gluconeogenesis

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6
Q

what affects the symptoms of renal failure

A

time frame - GFR falls really quick = feel really ill

falls over years = only feel ill at very end

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7
Q

what is a cystogram and what does it show

A

inject dye into the bladder
shows reflex into the kidney that shouldn’t be there
- Vesicoureteral reflux -> Chronic pyelonephritis-> scarred kidneys - the reflux is repaired but still get high BP

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8
Q

what does a GFR of 28ml/min mean

A

only running at 28%

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9
Q

signs that show the intervascular volume is low `

A
pale 
cold hands 
capillary refill prolonged
slow pulse 
poor skin turgor 
low BP 
JVP not visible
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10
Q

signs of renal failure from blood results

A

high urea and creatinine

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11
Q

signs of chronic kidney disease

A

lethargy, weakness, anorexia
low vol = hypotension
elevated plasma urea and creatine - diagnosis of renal failure
ultrasound confirm

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12
Q

what causes symptoms of lethargy and anorexia

A

failure of excretion - accumulation of waste products, hormones, peptides
failure of homeostatsis - acidosis = nausea, hyponatraemia, volume depletion - low BP
failure of endocrine - anaemia

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13
Q

what causes a salt and water imbalance

A

difficulty excreting more common - hypertension, oedema, pulmonary oedema

excess loss - in pt with tubointestinal disorders - concentrating mechanisms have been damaged = dry

osmotic diuresis - high conc small molecular weight eg urea = low bp

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14
Q

are serum Na and total body Na levels different

A

yes

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15
Q

what salt dysregulation is associated with kidney disease

A

hyponatraemia

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16
Q

what are the implications of acidosis

A

caused - decreased excretion of H+ ions and retention of acid bases
buffered by H enter cell - exchange for K = hyperkalaemia
buffer by increasing CO2 loss through lungs - kussmahl respiration - air hunger

worsen anorexia and muscle catabolism = weakness

17
Q

implication of hyperkalaemia

A

cause - failure of DCT to secrete K
worsened by acidosis

results in arrhythmia - initial loss P wave and bradycardia and arrest
affect neuronal and muscular activity - weakness

clinical features depend on the chronicity of hyperkalaemia

18
Q

ECG with hyperkalaemia

A

tall tented T wave
lose P wave
broad QRS
-> bradycardia -> asystole `

19
Q

hwo do you treat hyperkalaemia

A

give Ca intravenously
insulin to drive K into cell
treat acid base

20
Q

effect on metabolic function of kidney

A

decrease erythropoietin

CKD = low 1-25 Vit D = intestinal Ca absorption, hypocalcaemia (short term) and hypercalcaemia (long term)

increased CHD risk

21
Q

how does CKD -> hyperparathyroidism

A

phosphate retention -> hypocalcaemia and hyperparathyroidism and low levels of calcitriol

hypocalcaemia and low levels of calcitriol -> hyperparathyroidism

22
Q

what CV risks does CKD cause

A

hypertension
secondary cardiac effects
endothelial effects
lipid abnormalities

23
Q

difference between acute and chronic kidney disease

A

acute - renal size unchanged, previously normal creatinine

chronic - renal size OFTEN reduced, previously abnormal creatinine, chronic uraemic symptoms - look at the history

24
Q

how can CKD have normal sized kidneys

A

DM, myeloma and amyloid preserve size

25
Q

urea to measure GFR

A

poor
confounders: diet (high - meat), catabolic state, GI bleed (high - protein broken by bacteria), drugs, liver func, urine output (urea high if output low)

26
Q

creatinine to measure GFR

A
affected by:
muscle mass 
age
race - afro Caribbean>Caucasian > Asian 
sex 

need to look at the patient when interpreting the result `

27
Q

creatinine clearance for GFR

A

difficult to collect sample - especially if elderly

overestimates in value is low - because small amout is secreted into urine

28
Q

inulin clearance to measure GFR

A

gold standard

laborious - invasive and complicated so only used in research

29
Q

radionucleotide studies for measuring GFR

A

EDTA clearance
reliable
expensive

best gold standard now

30
Q

calculations for GFR

A
eqn automatically calculates GFR from serum creatinine 
presented ml/min per 1.73 squared 
easiest eqn uses age and ethnicity 
variety eqns used - CKD, epi, MORD
some eqn use weight, albumin

reliable when GFR>60ml/min
unreliable in V thin/obese pt

31
Q

describe a table of GFR and ACR categories and risk of adverse outcomes

A

the risk increases towards the bottom R

32
Q

what are the dietary modifications required

A

low K diet
fluid restriction
vit D supplements - prevent hyperparathyroid bone disease

33
Q

ACE inhibitors

A

reduce ANG2

lower bp

34
Q

osmotic diuretics

A
glucose and mannitol 
when in urine increase osmolarity 
not reabsorbed in distal part 
smaller osmotic gradient 
less water reabsorbed
35
Q

examples of diuretics

A
osmotic diuretics 
carbonic anhydrase inhibitors 
loop diuretics - furosemide 
thiazides - block Na/cl cotransport 
K sparing diuretics - amiloride - block Na channels, spironolactone - aldosterone antagonist
36
Q

action of carbonic anhydrase inhibitors

A

inhibit production of protons
less to be exported
less na reabsorbed in exchange
cause increased urinary acidity

37
Q

loop diuretics

A
in ascending limb of loop of henle 
inhibit triple transporter of Na, cl, k 
more na in tubular fluid 
also affect interstitial Na because of this 
affect 25% diuresis
38
Q

thiazides

A

inhibit Na, Cl transporter

affect 5-10% filtered load

39
Q

K sparing diuretic

A

inhibit Na Cl cotransporter in principle cell in DCT and collecting duct
reduce Na entry
reduce Na into blood - through Na K ATPase - less K in
inhibit aldosterone = Na not enter or then leave and kl channel inhibited