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Y2 - BRS - Uro > Renal Failure > Flashcards

Renal Failure Flashcards

(51 cards)

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1
Q

What are the 4 main roles of the kidneys?

A

Homeostatic
Endocrine
Excretory
Glucose metabolism

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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
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3
Q

What are the endocrine functions of the kidney?

A

Erythropoietin

1 alpha hydroxylase

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4
Q

What are the homeostatic functions of the kidneys?

A

Electrolyte balance
Acid-base balance
Volume homeostasis

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5
Q

What are the glucose metabolism functions of the kidney?

A

Gluconeogenesis

Insulin clearance

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6
Q

What can go wrong during kidney failure?

A

Each of the 4 functions can be affected

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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
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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+

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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

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10
Q

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

A

Impaired glucose metabolism

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11
Q

What risk is increased with kidney failure?

A

CVD risk

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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

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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

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14
Q

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

A

Respiratory compensation for metabolic acidosis

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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

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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

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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

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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

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19
Q

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

A

CKD

Acute presentation of a chronic kidney disease

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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

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21
Q 
What will be the effect on the concentration of:
Urea
Creatinine
Sodium
Potassium
Haemoglobin

in the blood tests?

Study These Flashcards
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
Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
A

USS - normal sized kidneys with no obstruction

25
What is interesting about salt and water balance?
Can cause kidney failure OR Can be a symptom of kidney failure
26
What happens to the salt water balance in kidney failure? When may water loss be seen?
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
Why does hyponatremia not always lead to reduced total body sodium?
Fluid balance is affected (i.e. hypo/hypernatremia), total amount may still remain within range
28
What occurs in kidney failure acidosis?
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
Why might hyperkalaemia occur in kidney failure? How might this present clinically? What do the symptoms depend on?
Less postassium secretion in the distal tubule Acidosis Symptoms = cardiac arrhythmias, neural and muscular activity, vomiting Symptoms depend on chronicity
30
How may arrhythmias caused by hyperkalaemia show up on an ECG ?
Peaked T waves P wave = broadened, reduced amplitude, amy disappear completely QRS widening Heart block Asystole VT (ventricular tachycardia) / VF (ventricular fibrillation)
31
What do you give to treat hyperkalaemia?
Bicarbonate To reduce H+ So potassium can return to cell
32
How can metabolism in the kidneys be affected during kidney failure?
Reduced erythropoietin = anaemia Reduced 1-25 Vit D levels = reduced intestinal calcium absorption, hypocalcaemia, and hyperparathyroidism
33
Why may patients with kidney failure present with hyperparathyroidism?
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
What is a predictor of end stage renal failure?
CV (cardiovascular) risk - Higher CV risk = higher CKD risk
35
Why is CV risk more important than the CKD risk calculated from CV risk?
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
What are the standard factors that can affect CVD risk? What are the additional CV risks in renal failure?
Hypertension Diabetes Lipid abnormalities Inflammation Oxidative stress Mineral/bone metabolism disorder
37
What is the initial management for kidney failure?
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
How do gut absorption potassium binders work?
Bind to potassium in the gut that comes from food etc. Stops potassium from being absorbed into the body via the gut
39
What are the long-term management options for kidney failure?
Conservative Home therapy In centre therapy Transplantation
40
What are the long term conservative management strategies for kidney failure?
Erythropoietin injections to correct anaemia Diuretics to correct salt water overload Phosphate binders 1.25 vit d supplements Symptom management
41
What are the home and in centre therapies for long term management for kidney failure?
Home therapy = haemodialysis; peritoneal dialysis / assisted programmes In centre therapy = haemodialysis, 4hrs 3x / week
42
What is the ultimate aim in renal failure?
Transplantation if fit enough
43
Why may dialysis not be appropriate?
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
How does haemodialysis work?
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
What is a fistula? How is it created?
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
Why should transfusions be avoided in patients that are eligibile for kidney transplants?
Blood transfusions = sensistisation against blood = transplant failure (body more likely to reject the donor)
47
As a renal patient, what should be avoided clinically?
Avoid taking blood or IV lines into the veins in the ante-cubital fossa Due to need for fistula in the future
48
What are the traditional methods of assessing GFR (glomerular filtration rate)?
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
So how is eGFR calculated clinically nowadays (for MDRD)? Modification of diet in renal disease
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
How is eGFR calculated for CKD epidemiology collaboration?
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
How can patients with renal issues be classified?
Using eGFR AND proteinurea Increased proteinuria = reaching end stage renal failure

Y2 - BRS - Uro (8 decks)

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