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Clinical renal failure Flashcards

1
Q

Define clinical renal failure

A

A reduction in GFR

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2
Q

What is normal GFR

A

100 ml/min

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3
Q

What are the two main classifications of renal disease

A

Acute or chronic

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4
Q

What are the two main blood tests used in measuring renal function

A

Serum creatinine and serum urea

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5
Q

How is urea formed

A

When amino acids are catabolised the nitrogen that is released is further catabolised to ammonia which is converted into urea by the liver.

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6
Q

What are urea levels dependant on

A

dietary protein intake, protein catabolism which is increased in infection trauma and immobilisation

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7
Q

Describe renal handling of urea

A

Urea is easily filtered. When GFR is slow there is greater reabsorption from tubules increasing serum urea.

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8
Q

Why is serum urea less reliable as a marker of GFR?

A

Because levels are related to protein intake, hydration status, intestinal bleeding

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9
Q

Where is creatinine derived from

A

From creatine in muscles, solely a waste product

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10
Q

What is the rate of creatinine formation proportional to

A

Muscle mass

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11
Q

Why is creatinine clearance rate proportional to GFR and what is it’s effect on GFR

A

Because it is freely filtered and there is no tubular reabsorption, plasma creatinine rises as GFR falls

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12
Q

Why is plasma creatinine an insensitive index of renal function and what is it useful for

A

It is insensitive as an index marker due to the variety on muscle mass across the population. It is useful as a measurement of the course of renal disease.

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13
Q

When can plasma creatinine artificially rise?

A

After a protein rich meal.

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14
Q

What are factors to consider when measuring serum creatinine

A

Things that effect muscle mass. Weight, age, gender.

Calculations should be done on populations norms for demographic groups

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15
Q

What is the difference between eGFR and serum creatinine for measurement of GFR

A

eGFR also takes into account plasma creatinine, age and sex

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16
Q

Describe acute kidney failure including basic aetiology

A

A sudden rapid reduction in GFR, usually reversible, 70% due to non renal causes i.e. pre-renal and post-renal

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17
Q

Describe causes of pre renal failure

A

Low BP, reduced kidney perfusion from dehydration, septic shock, haemorrhage, cardiogenic shock, severe renal artery stenosis

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18
Q

What other serum markers might you get in acute renal failure

A

Hyperkalaemia (reduced kidney excretion), high phosphate (reduced kidney excretion), low calcium (kidneys turn Vitamin D into calcitriol which increases calcium absorption from intestines to the blood).

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19
Q

Treatment of pre-renal causes

A

Fix underlying problem, rehydrate, fix bleeding, antibiotics, fix heart

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20
Q

What are the two possible outcomes from pre-renal kidney failure?

A

Get better or develop acute tubular necrosis.

21
Q

What is the main cause of renal kidney failure

A

Acute tubular necrosis, 80% most of this is a progression of pre-renal.

22
Q

Signs and symptoms of acute tubular necrosis

A

Abnormal creatinine, phosphate, calcium, potassium, persistant oligouria after treating underlying cause.

23
Q

Treatments of acute tubular necrosis.

A

First ret underlying pre-renal cause. Patient may need dialysis to help filter blood/ maintain osmolality/ acid-base balance etc while tubules heal. Prevents death from hyperkalaemia.

24
Q

What percentage of patients recovers from Acute tubular necrosis

A

95%

25
Q

Another less common aetiology of acute tubular necrosis and what do patients with this typically present with

A

Glomerularnephritis

Proteinuria and haemataturia

26
Q

What are post-renal causes of kidney failure

A

Kidney stones, prostate, tumour, urinary retention

27
Q

Describe chronic kidney disease

A

Happens over months/ years. Irreversible. Considered in stages dependant on GFR

28
Q

List consequences of chronic kidney failure

A

Increased PTH (to release Ca as serum Ca low due to reduced Vit D metabolism to calcitriol)
Anaemia- low EPO (manufactured in the kidneys)
High phosphate
Acidosis
Hyperkalaemia
Uraemia

29
Q

Commonest cause of CKD

A

Diabetes (70%)

30
Q

Other causes of CKD

A

Glomerulonephritis, hypertension, loads of others

31
Q

Microscopic pathology seen in chronic kidney disease

A

Scarring of glomeruli and interstitium

32
Q

What are symptoms of uraemia

A

Anorexia, nausea, vomiting, pruritis, SOB due to anaemia or fluid overload, cold intolerance, swelling, seizures, coma

33
Q

Why would bone disease ensue in chronic kidney failure

A

Because the kidneys convert vitamin D to calcitriol which help to absorb Calcium from the intestines. In the presence of low serum Ca PTH is stimulated which causes excessive bone resorption of Ca. Causes fractures, and extra osseous calcification.

34
Q

What blood test readily distinguishes between chronic and acute kidney injury

A

Hb.
The kidneys produce erythropoietin, a hormone necessary for RBC production. In chronic injury production of erythropoietin is reduced and thus fewer RBC. This takes time to manifest as the life span of RBC is 120 days… so not evident in acute.

35
Q

Describe principles of treatment in chronic kidney injury

A 
Treat underlying cause of kidney injury
Treat hypertension
Treat anaemia
Monitor blood glucose
Monitor electrolytes
May need dialysis
36
Q

Why does K+ increase in kidney failure

A

Reduced renal excretion

37
Q

Describe the five mechanism for regulation of glomerular filtration

A

1) Tubuloglomerular feedback:
2) Myogenic
3) Renin-angiotensin-aldosterone
4) Sympathetic stimulation.
5) ANP and BNP

38
Q

Describe tubuloglomerular feedback for GFR regulation

A

MD cells sense NaCl and stimulate the JG cells to release NO if NaCl low- causing vasodilation of afferent arteriole, increased flow. If NaCl is high the MD cells release adenosine which causes the afferent arteriole to constrict decreasing flow.

39
Q

Describe Myogenic feedback for regulation of GFR

A

Increased stretch on the afferent arteriole cause it to constrict reducing flow

40
Q

Describe the RAAS for regulation of GFR

A

MD sense low NaCl causing JG to release renin, renin cleaves angiotensinogin to angiotensin I, ACE converts angiotensin I to angiotensin II. Angiotensin II causes constriction of efferent arteriole back pressure increases GFR. It also causes the adrenal gland to release aldosterone.Aldosterone results in NaCl retention, fluid retention,increased volume, increased flow.

41
Q

Describe sympathetic regulation of GFR

A

Peripheral baroreceptors detect low pressure decreased firing from these causes sympathetic stimulation resulting in vasoconstriction of the afferent arteriole decreasing flow (shock)

42
Q

Describe ANP and BNP in relation to regulation of GFR

A

Decreased stretch in atria of heart result in release of ANP causes dilatation of afferent arteriole increasing GFR

43
Q

Chronic kidney disease stage 1

A

Normal GFR >90

44
Q

Chronic kidney disease stage 2

A

GFR 60-89

Increased PTH

45
Q

Chronic kidney disease stage 3

A

Moderate absorption

GFR 30-59 decreased Ca,low EPO, increased CV risk

46
Q

Chronic kidney disease stage 4

A

Severe
High phosphate, acidosis, Hyperkalaemia, malnutrition
GFR 15-29

47
Q

Chronic kidney disease stage 5

A

ESRF GFR <15 Uraemia

48
Q

Describe the actions of ANP

A

ANP release inhibits release of ADH from the posterior pituitary gland, More water loss from collecting ducts. Inhibits aldosterone, more Na+ secretion and K+ retention (fluid loss), vasodilation of arteries, Vasodilation of afferent arteriole causing increased GFR.

49
Q

Name a drug that inhibits aldosterone and its mechanism of action

A

Spirolactone. Blocks aldosterone is a weak K+ sparing diuretic

GU (9 decks)

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