Renal Overview Flashcards

1
Q

What is polyuria

A

pee too much

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2
Q

What is dysuria

A

pain on passing urine

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3
Q

What is haemapuria

A

passing blood in urine

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4
Q

What is proteinuria

A

protein in urine

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5
Q

What is uremia

A

when waste products should be excreted by the kidney are starting to accumulate in the blood

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6
Q

How is renal function measured

A

serum urea
serum creatine
24 hour urine collection

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7
Q

How is serum urea used to measure renal function

A

o goes up in renal dysfunction but also rises with dehydration meaning it isn’t a good indicator

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8
Q

How is serum creatine used to measure renal function

A

o good general guide to renal function
o should be relatively low
o if kidney is not working then it will rise

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9
Q

How is urine collection used to measure renal function

A

o creatine clearance – best measure

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10
Q

What are the consequences of renal failure

A
loss of renal excretory function 
loss of water and electrolyte balance 
loss of acid base balance
loss of renal endocrine function 
calcium metabolism 
renin secretion
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11
Q

Why is there a loss of water and electrolyte balance in renal failure

A

o unable to modify electrolytes within the collecting duct and so losing more than you should do

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12
Q

Why is there a loss of acid base balance in renal failure

A

o losing hydrogen ions
o this can upset the acid base balance
o can be compensated by ventilation (breathing more acid)

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13
Q

What renal endocrine functions are lost

A

erythropoietin
calcium metabolism
renin secretion

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14
Q

What are the two types of renal failure

A

acute and chronic

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15
Q

What is acute renal failure

A

o happens suddenly
o often due to infection, trauma or damage to the kidneys
o rapid loss of renal function
o usually over hours or days

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16
Q

What is chronic renal failure

A

o gradual loss of renal function

o usually over many years

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17
Q

What can causes of renal failure be split into

A

prerenal
renal
post renal

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18
Q

What are the prerenal causes

A

hypoperfusion of the kidney
shock
renal artery or aorta diseases

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19
Q

What are the renal causes

A

chronic disease
drug damage
trauma
rhabdomyolysis

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20
Q

What is rhabdomyolysis

A

o protein taken from muscle round to kidney blocking glomerulus

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21
Q

What are post renal causes

A

 renal outflow obstruction

o stones

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22
Q

How is acute renal failure defined

A

It is the rapid loss of renal function resulting in a Creatine > 200umol/L. The normal is usually 80.

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23
Q

How does acute renal failure present

A

anuric initially with volume overload
gradually progresses to polyuria
development of hyperkalaemia
development of uremia and acidosis

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24
Q

What does anuric and volume overload result in

A

 ankle oedema (if ambulatory), sacral oedema (if bed bound)
 pulmonary oedema and breathlessness
 raised jugular venous pressure (JVP)
 weight gain

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25
Q

What does hyperkalaemia result in

A

can lead to cardiac arrest as it alters the nerves excitability

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26
Q

What does the development of uremia and acidosis result in

A

 high urea
 low bicarbonate
 increased respiratory excretion of CO2
o raised respiratory rate

27
Q

What are the causes of acute renal failure

A

usually prerenal

28
Q

Is acute renal failure reversible

A

Usually reversible with time
Renal support is required until recovery
 dialysis
 nutrition

29
Q

What are the primary causes of chronic renal failure

A

 glomerulonephritis

 polycystic kidney disease

30
Q

What are the secondary causes of chronic renal failure

A
	diabetes (30%)
	hypertension (20%)
	drug therapy 
	vasculitis 
	renal artery disease/aorta disease
31
Q

What is seen in glomerulonephritis

A

Haematuria/proteinuria in an otherwise healthy individual
There will be a gradual progression to hypertension and chronic renal failure due to the damage to the glomerulus system meaning that you will not be producing angiotensin and renin

32
Q

What is nephrotic syndrome due to

A

Complications of glomerulonephritis

33
Q

What happens in nephrotic syndrome

A

Complications of glomerulonephritis:
 excessive loss of protein in the urine
 loss of plasma oncotic pressure
 tissue swelling (oedema) due to the lack of oncotic pressure to draw the fluid back into the vessels

hypercoagulable state

34
Q

Why is there a hypercoaglulable state in glomerulonephritis

A

antithrombin is lost in the urine, leading to a higher activity of Factor II and Factor X and in increased tendency to thrombosis.

35
Q

Why are NSAIDs bad for renal disease

A

NSAIDs inhibit glomerular blood flow and cause interstitial nephritis due to their inhibition of prostaglandins
They should be avoided in renal disease if possible.

36
Q

What other drugs can result in renal disease

A

Nephrotoxic drugs can also result in renal disease e.g cyclosporin.

37
Q

What are different renal vascular diseases

A

reduced blood flow to kidney

microangiopathy

38
Q

What is reduced BF to kidney due to

A

 atheroma of renal artery and aorta

 hypertension – narrowing of renal artery

39
Q

What is micrangiopathy

A

 immune reaction causing small blood vessel damage, RBC damage and thrombosis
o E.Coli 0157 association

40
Q

What is polycystic kidney disease due to

A
	gene mutation (PKD 1,2 or 3)
o	inherited (AD or AR) or spontaneous
41
Q

what can polycystic kidney disease lead to

A

o enlarged kidney
o progressive destruction of normal kidney
o gradual renal failure

42
Q

What is end stage renal disease defined by

A

 eGFR <15ml/min

 creatine 800-1000umol/L

43
Q

What is the time taken for end stage renal disease dependent on

A

 underlying cause

 modifying factors

44
Q

What is the grading for kidney disease

A

The kidney damage can be graded

1 is normal and 5 is kidney failure

45
Q

How is chronic renal failure managed

A
reduce rate of decline
correct fluid balance
correct deficiencies 
remove outflow obstruction
treat infection
46
Q

how do you reduce rate of decline of chronic renal failure

A
	eliminate the nephrotoxic drugs
	control hypertension
	control diabetes
	control vasculitis disease 
o	steroids/other immune suppressant drugs
47
Q

How do you correct fluid balance

A

 restrict fluid intake

 restrict salt, potassium and protein

48
Q

How do you correct deficiencies

A

 anaemia (erythropoietin)

 calcium (vitamin D)

49
Q

How do you remove outflow obstruction

A

 renal stones (calculi)

 prostate enlargement

50
Q

What infections do you treat when managing chronic renal failure

A

 chronic renal system infection

51
Q

What are the signs of chronic renal failure

A

 anaemia
 hypertension
 renal bone disease

52
Q

What are the causes of renal bone disease in chronic renal failure

A

o low Ca, high PO4
o hyperparathyroidism
o osteomalacia

53
Q

What are the symptoms of renal failure

A
	insidious 
o	may be a few
	polyuria
	nocturia
	tired and weak
	nausea
54
Q

What is renal replacement therapy

A

Have to replace the functions of the kidney but it is not a cure as the kidneys still do not work

55
Q

When should be care taken in dentistry regarding renal disease

A

Care should be taken with prescribing
 check all drugs with renal physician
 avoid NSAIDs and tetracyclines
 reduce dose of most others

56
Q

What is the effect of renal disease in children

A

Growth may be slow in children and tooth eruption may be delayed

57
Q

What are the secondary effects of anaemia

A

 oral ulceration

 ‘dysaesthesias’ – painful mucosa and tongue

58
Q

Why may white patches be seen in the mouth

A

 uraemic stomatitis

59
Q

What may be seen in patients with renal disease

A

oral opportunistic infections
dry mouth and taste disturbances
bleeding tendencies
renal osteodystorphy

60
Q

Why may you see a dry mouth and taste disturbance

A

o fluid restriction and electrolyte disturbance

61
Q

What are the oral opportunistic infections

A

o fungal and viral infections/reactivations

o prone to post-op infections

62
Q

Why is there bleeding tendencies

A

o platelet dysfunction

63
Q

What will be seen in the mouth regarding renal osteodystrophy

A

o lamina dura lost
o bony radiolucency
 secondary hyperparathyroidism increases osteoclast activity