lecture 7 Flashcards

1
Q

4 things that happen when kidneys stop working

A

loss of excretory function, homeostatic function, endocrine function, abnormality of glucose homeostasis

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2
Q

result of loss of excretory function

A

accumulation of waste products

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3
Q

result of loss of homeostatic function

A

disturbance of electrolyte balance, loss of acid-base control, inability to control volume homeostasis

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4
Q

result of loss of endocrine function

A

loss of erythropoeitin production, failure to 1-a hydroxylase vitamin D

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5
Q

result of abnormality of glucose homeostasis

A

decreased gluconeogenesis

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6
Q

what are clinical features of kidney dysfunction determined by

A

rate of deterioration

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7
Q

causes of lethargy and anorexia in patients with kidney disease: failure of excretion

A

accumulation of nitrogenous waste products, hormones, peptides and “middle-sized” molecules

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8
Q

causes of lethargy and anorexia in patients with kidney disease: failure of homeostasis

A

acidosis, hyponatraemia, volume depletion causing hypotension

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9
Q

causes of lethargy and anorexia in patients with kidney disease: failure of endocrine function

A

anaemia

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10
Q

normal salt and water imbalance in renal dysfunction

A

difficulty in excreting salt and water, causing Na+ retention and subsequent hypertension, oedema and pulmonary oedema

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11
Q

when can salt and water loss be present

A

tubulointerstitial disorders where concentrating mechanisms have been damaged

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12
Q

causes of salt and water imbalance (low)

A

inability to decrease Na+ excretion when Na+ depleted, osmotic diuresis caused by high concentration of small MW waste substances e.g. urea, resultant volume depletion causing hypotension

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13
Q

what are chronic kidney disease and acute kidney injury associated with

A

hyponatraemia (low blood Na+) - serum Na+ levels are not equal to total bod Na+

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14
Q

what causes metabolic acidosis

A

decreased excretion of H+ ions and retention of acid bases

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15
Q

what buffers metabolic acidosis and impact

A

H+ ions passing into cells in exchange for K+ ions, so tendency of hyperkalaemia

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16
Q

other compensation for metabolic acidosis (respiratory)

A

increasing loss of CO2 through lungs, causing Kussmahl respiration (air hunger)

17
Q

2 other central and local mechanisms caused by acidosis

A

exacerbation of anorexia and increased muscle catabolism

18
Q

cause of hyperkalaemia

A

failure of distal tubule to secrete K+

19
Q

how does metabolic acidosis exacerbate hyperkalaemia

A

causes shift of K+ from IC to EC space

20
Q

what can hyperkalaemia cause (CV)

A

asystole; cardiac arrythmias (initial loss of P waves and bradycardia), arrest

21
Q

what other activity can hyperkalaemia affect

A

neural, muscular

22
Q

hyperkalaemia ECG

A

tall, tented T-waves; lose P-waves; broadening of QRS complex until becomes asystole

23
Q

what causes anaemia in kidney dysfunction

A

decreased erythropoietin production

24
Q

what do low 1,25 vitamin D levels cause

A

poor intestinal Ca2+ absorption, hypocalcaemia (short term), hyperparathyroidism (long term)

25
how does chronic renal failure cause hyperparathyroidism
causes PO4 3- retention which leads to low levels of calcitriol, which can cause hypocalcaemia and directly/indirectly hyperparathyroidism
26
what is the major predictor of end stage renal failure
chronic kidney disease
27
what is the major outcome for a patient with chronic kidney disease
cardiovascular disease
28
4 ways in which there is an increased CV risk
hypertension, secondary cardiac effects, endothelial effects, lipid abnormalities
29
differences in consequences of acute and chronic loss of kidney function (ultrasound and history)
acute: renal size unchanged, previously normal creatine; chronic: renal size often reduced, previously abnormal creatine, chronic uraemic symptoms
30
initial management of patient (4 things)
IV normal saline to rehydrate, IV NaHCO3 to correct acidosis, IV insulin and dextrose to lower plasma K+ by driving K+ ions back into cells, transfer for dialysis
31
traditional poor, laborious or expensive methods of assessing GFR
urea, creatinine, creatinine clearance, inulin clearance (best test but laborious), radionuclide studies (e.g. EDTA)
32
why is urea a poor indicator of GFR
confounded by diet, catabolic state, GI bleeding, drugs, liver function
33
why is creatinine a poor indicator of GFR
affected by muscle mass, age, race (afro-caribbean, caucasian, asian), sex
34
why is creatinine clearance a poor indicator of GFR
difficult for elderly patients to collect accurate samples, overestimates GFR at lot GFR
35
how is GFR assessed
serum creatinine equation presenter ml/min per 1.73^2 using age and ethnicity
36
when is the GFR equation unreliable
if >60ml/min, or patient very obese or very thin
37
NICE guideline classification for chronic kidney disease
albumin:creatinine ration
38
long term management of kidney dysfunction (4) causing poor quality of life
remain on regular haemodialysis, low K+ diet and fluid restriction, erythropoietin injections to correct anaemia, 1,25 vitamin D supplements to prevent hyperparathyroid bone disease