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
Q

how does chronic renal failure cause hyperparathyroidism

A

causes PO4 3- retention which leads to low levels of calcitriol, which can cause hypocalcaemia and directly/indirectly hyperparathyroidism

26
Q

what is the major predictor of end stage renal failure

A

chronic kidney disease

27
Q

what is the major outcome for a patient with chronic kidney disease

A

cardiovascular disease

28
Q

4 ways in which there is an increased CV risk

A

hypertension, secondary cardiac effects, endothelial effects, lipid abnormalities

29
Q

differences in consequences of acute and chronic loss of kidney function (ultrasound and history)

A

acute: renal size unchanged, previously normal creatine; chronic: renal size often reduced, previously abnormal creatine, chronic uraemic symptoms

30
Q

initial management of patient (4 things)

A

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
Q

traditional poor, laborious or expensive methods of assessing GFR

A

urea, creatinine, creatinine clearance, inulin clearance (best test but laborious), radionuclide studies (e.g. EDTA)

32
Q

why is urea a poor indicator of GFR

A

confounded by diet, catabolic state, GI bleeding, drugs, liver function

33
Q

why is creatinine a poor indicator of GFR

A

affected by muscle mass, age, race (afro-caribbean, caucasian, asian), sex

34
Q

why is creatinine clearance a poor indicator of GFR

A

difficult for elderly patients to collect accurate samples, overestimates GFR at lot GFR

35
Q

how is GFR assessed

A

serum creatinine equation presenter ml/min per 1.73^2 using age and ethnicity

36
Q

when is the GFR equation unreliable

A

if >60ml/min, or patient very obese or very thin

37
Q

NICE guideline classification for chronic kidney disease

A

albumin:creatinine ration

38
Q

long term management of kidney dysfunction (4) causing poor quality of life

A

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