Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y2 - BRS - Uro > Renal Failure > Flashcards

Renal Failure Flashcards

1
Q

What are the 4 main roles of the kidneys?

A

Homeostatic
Endocrine
Excretory
Glucose metabolism

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

What are the excretory functions of the kidney?

A 
Nitrogenous waste
Hormones
Peptides
Middle sized molecules (Mr of 2-5000)
Salt and water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the endocrine functions of the kidney?

A

Erythropoietin

1 alpha hydroxylase

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

What are the homeostatic functions of the kidneys?

A

Electrolyte balance
Acid-base balance
Volume homeostasis

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

What are the glucose metabolism functions of the kidney?

A

Gluconeogenesis

Insulin clearance

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

What can go wrong during kidney failure?

A

Each of the 4 functions can be affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens when homeostatic function of the kidneys is affected?

A

The electrolyte balance is disturbed due to lack of excretion of potassium

Increasde potassium
Decreased bicarb
Decreased pH
Increased phosphate
Salt and water imbalance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens when endocrine function of the kidneys is affected?

A

Loss of ability to process vitamin D

Leads to decreased Ca2+ levels, anaemia

Increased PTH to try and compensate for low serum Ca2+

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

What happens when excretory function of the kidneys is affected?

A

Lack of excretion of urea, creatinine and insulin

Increased urea
Increased creatinine
Decreased insulin requirement

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

What happens when glucose metabolism function of the kidneys is affected?

A

Impaired glucose metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What risk is increased with kidney failure?

A

CVD risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can affect clinical presentation of kidney failure? i.e. why might kidney failure symptoms display differently in clinic

A

Rate of deterioration

Cause of kidney failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q 
75F - Mrs EH
Presents to A&E
3 week history of feeling of 'having the flu'
Increasingly weak
No appetite
Drinking only 2 cups of tea/ day
24hr history of being too weak to move

PMH = kidney issues after birth of 2nd child, reflux, MI 2 years ago, high plasma creatinine (163 umol.L) at time of MI, and eGFR of 138 mol/min

Examination = 
Very unwell, pale, cold hands
Capillary refill decreased
Lungs clear on auscultation
HR = 50/min; low BP of 67/35 mmHg; O2 sats 100%
JVP not visible, tachypnoeic

What will be the patient’s blood volume status?

A

Hypovolemic - due to low BP, cannot see jugular venous pressure at the clavicle, cool hands (vasoconstriction) and reduced capillary refill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why is Mrs EH tachypnoeic with normal O2 sats and clear lungs on auscultation?

A

Respiratory compensation for metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q 
What will be the effect on the concentration of:
Urea
Creatinine
Sodium
Potassium
Haemoglobin

in the blood tests?

A 
Urea = increased
Creatinine = increased
Sodium = anywhere
Potassium = increased
Haemoglobin = decreased

Blood results due to lack of excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q 
What will be the effect on the concentration of:
pH
pCO2
pO2
Bicarbonate ions
Base excess
A 
pH - decreased (acidotic)
pCO2 - decreased
pO2 - increased (good O2 sats)
Bicarbonate ions - decreased
Base excess - decreased

Due to metabolic acidosis with respiratory compensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why is pCO2 decreased and O2 normal in Mrs EH’s blood gas results?

A

Hyperventilation to compensate for metabolic acidosis = breathes off CO2 = low pCO2
Ventilation = good = normal pO2

CO2 + H2O H2CO3 HCO3- + H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Summary of Mr EH’s clinical findings =
Symptoms of extreme lethargy, weakness and anorexia
Clinical volume depletion = severe hypotension
Elevated plasma urea and creatinine make diagnosis of renal failure

What would be the next investigation?

A

Ultrasound (USS) - shows 2 small shrunken kidneys

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

What does it mean clinically to find 2 small shrunked kidneys?

A

CKD

Acute presentation of a chronic kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

54 -
Previously fit and well
Admitted with 2 day history of nausea, vomiting
1 day history of reduced urinary output after eating wild mushrooms

Examination:
Alert and orientated
Temp = 36.4 degrees
HR = 79; RR = 16; BP = 143/81 mmHg
Normal skin turgor

What will be the patient’s blood volume status?

A

Euvolemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q 
What will be the effect on the concentration of:
Urea
Creatinine
Sodium
Potassium
Haemoglobin

in the blood tests?

A 
Urea - increased
Creatinine - increased
Sodium - anywhere
Potassium - normal / increased
Haemoglobin - normal / decreased (not too much)
22
Q

What will be the effect on the concentration of:

pH
pCO2
pO2
Bicarbonate ions
Base excess
A

pH = decreased
pCO2 = decreased
pO2 = normal / high
Bicarbonate ions = decreased

Mild metabolic acidosis with respiratory compensation

23
Q

Why might Hb not be low in this patient?

A

Acute kidney failure - not enough time for erythropoetin levels to go down and show up in the blood work

24
Q

What would be the next investigation?

A

USS - normal sized kidneys with no obstruction

25
Q

What is interesting about salt and water balance?

A

Can cause kidney failure
OR
Can be a symptom of kidney failure

26
Q

What happens to the salt water balance in kidney failure?

When may water loss be seen?

A

Kidney failure tends to reduce secretion of salt and water - leads to hypertension, oedema, pulmonary oedema

BUT - salt and water loss may be seen in tubulointerstitial disorders – damage to concentrating mechanism in the kidneys
Leads to hypovolemia, which may be the cause of AKI (acute kidney injury)

27
Q

Why does hyponatremia not always lead to reduced total body sodium?

A

Fluid balance is affected (i.e. hypo/hypernatremia), total amount may still remain within range

28
Q

What occurs in kidney failure acidosis?

A

CO2 + H2O H2CO3 HCO3- + H+

So if acid (H+) increased, there is retention of bases as H+ combines with HCO3- to decrease acidosis

Acidosis causes symptoms of anorexia and muscle catabolism

29
Q

Why might hyperkalaemia occur in kidney failure?

How might this present clinically? What do the symptoms depend on?

A

Less postassium secretion in the distal tubule
Acidosis

Symptoms = cardiac arrhythmias, neural and muscular activity, vomiting
Symptoms depend on chronicity

30
Q

How may arrhythmias caused by hyperkalaemia show up on an ECG ?

A

Peaked T waves
P wave = broadened, reduced amplitude, amy disappear completely
QRS widening
Heart block
Asystole
VT (ventricular tachycardia) / VF (ventricular fibrillation)

31
Q

What do you give to treat hyperkalaemia?

A

Bicarbonate
To reduce H+
So potassium can return to cell

32
Q

How can metabolism in the kidneys be affected during kidney failure?

A

Reduced erythropoietin = anaemia

Reduced 1-25 Vit D levels = reduced intestinal calcium absorption, hypocalcaemia, and hyperparathyroidism

33
Q

Why may patients with kidney failure present with hyperparathyroidism?

A

There is low 1-25 vit D and phosphate retention in chronic renal failure

Calcium binds with phosphate so it is pooped out rather than absorbed by the body

Therefore increased PTH release to compensate for low serum Ca2+

34
Q

What is a predictor of end stage renal failure?

A

CV (cardiovascular) risk -

Higher CV risk = higher CKD risk

35
Q

Why is CV risk more important than the CKD risk calculated from CV risk?

A

In the elderly, more likely to die from increased CV risk (so CVDs e.g. stroke, MI etc.) rather than end stage renal failure

36
Q

What are the standard factors that can affect CVD risk?

What are the additional CV risks in renal failure?

A

Hypertension
Diabetes
Lipid abnormalities

Inflammation
Oxidative stress
Mineral/bone metabolism disorder

37
Q

What is the initial management for kidney failure?

A

Restore fluid balance -
Hypovolemic = give fluids
Hypervolemic = trial of dieuretics / dialysis

Treat hyperkalaemia =
Drive K+ into cells via sodium bicarbonate and insulin dextrose
Drive K+ out of the body using diuretics (if there is sustained fluid output)/ dialysis, laxatives would buy time if dialysis machines were busy (potassium pooped out instead of being absorbed)
Gut absorption - potassium binders

38
Q

How do gut absorption potassium binders work?

A

Bind to potassium in the gut that comes from food etc.

Stops potassium from being absorbed into the body via the gut

39
Q

What are the long-term management options for kidney failure?

A

Conservative
Home therapy
In centre therapy
Transplantation

40
Q

What are the long term conservative management strategies for kidney failure?

A

Erythropoietin injections to correct anaemia

Diuretics to correct salt water overload

Phosphate binders

1.25 vit d supplements

Symptom management

41
Q

What are the home and in centre therapies for long term management for kidney failure?

A

Home therapy = haemodialysis; peritoneal dialysis / assisted programmes

In centre therapy = haemodialysis, 4hrs 3x / week

42
Q

What is the ultimate aim in renal failure?

A

Transplantation if fit enough

43
Q

Why may dialysis not be appropriate?

A

The side effects are awful - nausea, fatigue
Must come in 3x a weak
Some patients will live just as long with conservative management as they would with dialysis

44
Q

How does haemodialysis work?

A

Haemodialysis = blood removed from patient, filtered, put back into patient

Blood travels through tubes to dialysis machine

Blood is pumped in a counter current direction on one side of a semi-permeable membrane, whilst the other side contains a carefully balanced fluid

High osmotic drag pulls in fluid from the blood

Waste and extra fluid is drained out of the patient

45
Q

What is a fistula? How is it created?

A

Created by connecting artery to vein - vein swells up and becomes ‘juicy’

Allows for easier insertion of needle

Useful for dialysis machine where blood is being taken out of the body to be filtered

46
Q

Why should transfusions be avoided in patients that are eligibile for kidney transplants?

A

Blood transfusions = sensistisation against blood = transplant failure (body more likely to reject the donor)

47
Q

As a renal patient, what should be avoided clinically?

A

Avoid taking blood or IV lines into the veins in the ante-cubital fossa

Due to need for fistula in the future

48
Q

What are the traditional methods of assessing GFR (glomerular filtration rate)?

A

Urea = poor indicator, confounded by many factors e,g. diet, catabolic state, GI bleeding (bacterial breakdown of blood in the gut), drugs, liver function etc.

Creatinine = affected by muscle mass, age, race. Need to look at the patient when interpreting the result and use trends

Creatinine clearance = labourious and overestimates GFR at low GFR rates as it takes into account the secreted creatinine, Also difficult for elderly to collect an accurate sample

Insulin clearance = laborious and so only used for research purposes

Radionuclide studies = EDTA clearance etc. It is reliable but expensive, so only used for donated kidneys to check function prior to transplantation

49
Q

So how is eGFR calculated clinically nowadays (for MDRD)?

Modification of diet in renal disease

A

Using serum creatinine conc.

GFR (mL/min/1.73m2) = 175 x (SCr)-1.154 x (Age)-0.203 x (0.742 if female) x (1.212 if Afr American)

50
Q

How is eGFR calculated for CKD epidemiology collaboration?

A

CDP - EPI = epidemiolgy collab

GFR = 141 x min (SCr/K,1)-α x max (SCr/K,1)-1.209 x 0.993Age x 1.018 [if female] x 1.159 [if black]

51
Q

How can patients with renal issues be classified?

A

Using eGFR AND proteinurea

Increased proteinuria = reaching end stage renal failure

Y2 - BRS - Uro (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions