Clinical renal failure Flashcards

1
Q

Define clinical renal failure

A

A reduction in GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is normal GFR

A

100 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the two main classifications of renal disease

A

Acute or chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Serum creatinine and serum urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are urea levels dependant on

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is creatinine derived from

A

From creatine in muscles, solely a waste product

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the rate of creatinine formation proportional to

A

Muscle mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When can plasma creatinine artificially rise?

A

After a protein rich meal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Treatment of pre-renal causes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

25
Another less common aetiology of acute tubular necrosis and what do patients with this typically present with
Glomerularnephritis | Proteinuria and haemataturia
26
What are post-renal causes of kidney failure
Kidney stones, prostate, tumour, urinary retention
27
Describe chronic kidney disease
Happens over months/ years. Irreversible. Considered in stages dependant on GFR
28
List consequences of chronic kidney failure
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
Commonest cause of CKD
Diabetes (70%)
30
Other causes of CKD
Glomerulonephritis, hypertension, loads of others
31
Microscopic pathology seen in chronic kidney disease
Scarring of glomeruli and interstitium
32
What are symptoms of uraemia
Anorexia, nausea, vomiting, pruritis, SOB due to anaemia or fluid overload, cold intolerance, swelling, seizures, coma
33
Why would bone disease ensue in chronic kidney failure
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
What blood test readily distinguishes between chronic and acute kidney injury
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
Describe principles of treatment in chronic kidney injury
``` Treat underlying cause of kidney injury Treat hypertension Treat anaemia Monitor blood glucose Monitor electrolytes May need dialysis ```
36
Why does K+ increase in kidney failure
Reduced renal excretion
37
Describe the five mechanism for regulation of glomerular filtration
1) Tubuloglomerular feedback: 2) Myogenic 3) Renin-angiotensin-aldosterone 4) Sympathetic stimulation. 5) ANP and BNP
38
Describe tubuloglomerular feedback for GFR regulation
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
Describe Myogenic feedback for regulation of GFR
Increased stretch on the afferent arteriole cause it to constrict reducing flow
40
Describe the RAAS for regulation of GFR
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
Describe sympathetic regulation of GFR
Peripheral baroreceptors detect low pressure decreased firing from these causes sympathetic stimulation resulting in vasoconstriction of the afferent arteriole decreasing flow (shock)
42
Describe ANP and BNP in relation to regulation of GFR
Decreased stretch in atria of heart result in release of ANP causes dilatation of afferent arteriole increasing GFR
43
Chronic kidney disease stage 1
Normal GFR >90
44
Chronic kidney disease stage 2
GFR 60-89 | Increased PTH
45
Chronic kidney disease stage 3
Moderate absorption | GFR 30-59 decreased Ca,low EPO, increased CV risk
46
Chronic kidney disease stage 4
Severe High phosphate, acidosis, Hyperkalaemia, malnutrition GFR 15-29
47
Chronic kidney disease stage 5
ESRF GFR <15 Uraemia
48
Describe the actions of ANP
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
Name a drug that inhibits aldosterone and its mechanism of action
Spirolactone. Blocks aldosterone is a weak K+ sparing diuretic