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Aneesha Flashcards BRS 2 > Chronic kidney disease and renal failure > Flashcards

Chronic kidney disease and renal failure Flashcards

1
Q

What are the basic functions of the kidneys?

A

Homeostatic functions
Excretory functions
Endocrine functions
Glucose metabolism functions

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2
Q

What homeostatic functions do the kidneys have?

A

Electrolyte balance
Acid-base balance
Volume homeostasis

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3
Q

What homeostatic derangements occur in kidney disease?

A

Potassium increases
Phosphate increases
Bicarbonate decreases
pH decreases (metabolic acidosis)
Salt and water imbalance

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4
Q

What excretory functions do the kidneys have?

A

Nitrogenous waste (urea, creatinine)
Hormones
Peptides
Middle-sized molecules
Salt and water

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5
Q

What types of excretory derangement occurs in kidney disease?

A

Increase in urea
Increase in creatinine
Decrease in insulin requirement (due to low insulin clearance so more stays in system)

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6
Q

What types of excretory derangement occurs in kidney disease?

A

Increase in urea
Increase in creatinine
Decrease in insulin requirement (due to low insulin clearance so more stays in system)

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7
Q

What endocrine functions does the kidney have?

A

synthesis of:
erythropeitin
1-alpha hydroxylase for vitamin D

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8
Q

What happens when endocrine functions of kidney are compromised?

A
  • Decrease in calcium
  • Anaemia
  • Increase in parathyroid hormone (to compensate for low calcium)
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9
Q

What glucose metabolism functions do the kidneys have?

A

Gluconeogenesis
Insulin clearance

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10
Q

In kidney disease, what is there an increased overall risk of?

A

Cardiovascular risk

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11
Q

How does rate of deterioration affect clinical presentation?

A
  • If rate of deterioration is slow, body is very good at adapting e.g. some patients present with urea of 50 (which for a normal person is really bad) but their body is used to it since it’s developed over years so they don’t feel unwell
  • Acute renal failure presents quicker because body hasn’t adapted
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12
Q

Give 2 examples of how the cause of kidney failure can dictate the clinical presentation

A

If you have Goodpasture’s disease where body makes antibodies against glomerular basement membrane, you might present with haemoptysis (lung involvement of Goodpasture’s since antibodies are made against lung too) and then you do blood test and find renal failure in the patient too

If you have skin rash (purpura) and do blood test and find they have renal failure

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13
Q

What can indicate hypovolemia?

A

Pallor
Decreased capillary refill
Hands cold
Poor skin turgor
Low heart rate
Low BP
JVP not visible
Tachypnoeic

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14
Q

What can cause tachypnoea with normal O2 sats and clear lungs on auscultation?

A

Respiratory compensation- Kussmaul respiration

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15
Q

What changes will there be in concentrations of urea, creatinine, sodium, potassium and haemoglobin in a hypovolemic patient with chronic kidney injury?

A
  • Urea higher
  • Creatinine higher
  • Sodium can go up or down
  • Potassium higher
  • Haemoglobin lower
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16
Q

What changes will there be in pH, pCO2, pO2, HCO3- and base excess in a hypovolemic chronic kidney injury?

A
  • pH will be lower
  • pCO2 will be lower as she’s hyperventilating so she’s expelling CO2
  • pO2 will be up a bit as she’s hyperventilating so she’s bringing in O2
  • HCO3- will be lower
  • Base excess will be lower or normal
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17
Q

What causes changes to acid base status in kidney injury

A

They have increased H+ because less is excreted because of the kidney failure so the patient has metabolic acidosis which is compensated by resp rate increasing to decrease CO2 to shift equation left

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18
Q

What changes will there be in concs of urea, creatinine, sodium, potassium, haemoglobin in acute kidney injury?

A
  • Urea higher
  • Creatinine higher
  • Sodium could be either
  • Potassium higher
  • Haemoglobin normal (because it’s acute renal failure so there’s still some EPO around)
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19
Q

What changes will there be in pH, pCO2, pO2 and HCO3- in acute kidney injury?

A
  • pH lower
  • pCO2 lower
  • pO2 higher
  • HCO3- lower

Mild metabolic acidosis with respiratory compensation

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20
Q

Kidney failure leads to reduced secretion of salt and water, leading to?

A

Hypertension
Oedema
Pulmonary oedema

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21
Q

In what kind of circumstances (kidney injury) can salt and water loss be seen though?

A

In tubulointerstitial disorders- damage to the concentrating mechanism of urine
Seen right after kidney transplant- there’s a bit of damage to the tubules and you pee out a lot of water
Seen also after kidney obstruction is relieved, kidney can’t concentrate urine and you get kidney failure

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22
Q

What may be a cause of AKI?

A

Hypovolemia

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23
Q

What does hyponatremia mean and what does it not mean?

A

-It does not mean reduced total body sodium
- It’s to do with how much free water you have- you’ll have more in hyponatremia

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24
Q

Why is it important to understand that hyponatremia does not mean does not mean reduced total body sodium when treating hyponatremia?

A

You may not want to give them salt but instead remove the excess free water

25
Q

Describe how acidosis happens in renal failure.

A
  • Reduced secretion of H+ ions which means you become acidotic
  • Cells take up this H+
26
Q

What happens to K+ when cells take up H+?

A

The cells taking up the H+ also forces K+ out of the cells leading to hyperkalaemia

27
Q

What are the 2 causes of hyperkalaemia?

A
  • Acidosis
  • Reduced distal tubule potassium secretion
28
Q

What are the symptoms of hyperkalaemia?

A
  • Cardiac arrhythmias
  • Neural and muscular activity
  • Vomiting
29
Q

What does symptom presentation in hyperkalemia depend on?

A

Chronicity of the disease- if it’s acute hyperkalaemia then these symptoms show but if its chronic then body adapts and they don’t show

30
Q

What ECG changes come up in hyperkalaemia?

A
  • Peaked T waves
  • P waves broaden, have reduced amplitude and disappear
  • QRS widening
  • Heart block
  • Asystole
  • VT/VF (ventricular tachycardia/ventricular fibrillation)
31
Q

What health consequences does hyperkalemia have?

A

Anorexia
Catabolism

32
Q

What effects does reduced EPO and reduced 1-25 Vit D levels have?

A

Reduced EPO–> anaemia
Reduced 1,25 Vit-D–>
-Reduced intestinal calcium absorption
-Hypocalcaemia
-Hyperparathyroidism

33
Q

What is the result of phosphate retention in chronic renal failure?

A
  • Phosphate is usually excreted by kidneys
  • Phosphate retention contributes to low levels of 1-25 vit D and hypocalcaemia and therefore hyperparathyroidism
34
Q

Chronic renal failure increases the overall risk of what group of conditions?

A

Cardiovascular

35
Q

What is the major predictor of end stage renal failure?

A

CKD

36
Q

What is the major outcome for a patient with CKD?

A

Cardiovascular disease- A patient with CKD is more likely to die from cardiovascular disease than end stage renal failure

37
Q

Diagram of cardiovascular risk during progression of CKD

A
38
Q

What standard cardiovascular risk is there for kidney failure patients?

A

Hypertension
Diabetes
Lipid abnormalities

39
Q

What additional risks are there for kidney failure patients (non-standard)?

A

Inflammation
Oxidative stress
Mineral/ bone metabolism disorders

40
Q

What are the 2 main things we want to treat in initial management of renal failure?

A

Fluid balance
Hyperkalemia

41
Q

How do we manage hypovolaemia vs hypervolaemia in renal failure?

A
  • Hypovolaemia- give fluids
  • Hypervolaemia- trial of diuretics/dialysis
42
Q

What are the 3 ways we manage hyperkalemia?

A

Drive it into cells
Drive it out of the body
Reduce gut absorption

43
Q

How do we drive potassium into cells?

A

Sodium bicarbonate
Insulin dextrose

44
Q

How does sodium bicarbonate work?

A
  • Binds to H+ to push equation to the right
  • H+ come out of cell into blood to equalise this and K+ goes back into cell
45
Q

Why do we need to be careful with insulin dextrose?

A
  • There are fatalities associated with it due to hypoglycaemia
  • We only use it when potassium >6.5 or there are ECG changes
46
Q

Why do we need to be careful with insulin dextrose?

A
  • There are fatalities associated with it due to hypoglycaemia
  • We only use it when potassium >6.5 or there are ECG changes
47
Q

How do we drive K+ out of the body?

A

Diuretics/ dialysis

48
Q

How do we reduce gut absorption of K+?

A

Potassium binders

49
Q

What different long term management options are there for kidney failure?

A

Conservative
Home therapy
In-centre therapy
Transplantation

50
Q

Conservative treatment for renal failure

A
  • EPO injections to correct anaemia
  • 1,25 vit D supplements for hypocalcaemia
  • Diuretics to correct salt water overload
  • Phosphate binders- for hyperphosphataemia so reduces itching
51
Q

Home therapy for renal failure

A
  • Haemodialysis
  • Peritoneal dialysis/assisted programmes
52
Q

In centre therapy for renal failure

A

Haemodialysis, 4 hours 3 times a week

53
Q

Kidney failure risk equation

A
54
Q

What is important to keep in mind for managing patients in hospital with kidney disease in terms of taking blood from them?

A

Take it from the back of the hand and not anterior cubital fossa or cephalic vein at wrist level because we need it for the fistula and it can scar up (stenosis) and we can’t do the fistula

55
Q

If a patient is fit for transplantation, why do we need to avoid transfusions?

A

Transfusions sensitise patients to the antigens in the blood of the donor and then if they then get a kidney donation from someone else who shares similar antigens to the blood donor there’s increased risk of transplant failure

56
Q

What different methods are there for assessing kidney function?

A
  • Urea
    • it’s a poor indicator
    • Confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function etc
  • Creatinine
    • It’s affected by muscle mass, age, race, sex etc
    • We need to therefore look at the patient when interpreting the result (if they’re small/big, M/F etc)
    • We look at the trend of creatinine (if we know what normal creatinine is) which is useful
  • Radionuclide studies
    • EDTA clearance etc
    • Very reliable but expensive
    • Used for donors
  • Creatinine clearance
    • Difficult for elderly patients to collect an accurate 24 hour urine sample
    • Overestimates GFR at low GFR (as a small amount of creatinine is also secreted into urine)
  • Inulin clearance
    Laborious so used for research purposes only
  • We mainly calculate estimated GFR (eGFR)- Serum creatinine is main factor here
57
Q

These graphs show difference between actual GFR and eGFR- what does this show?

A

As kidneys get better and actual GFR goes up, the eGFR becomes less accurate

Therefore, in patients with normal/high eGFR in kidney disease-We look at creatinine trend e.g. someone could have increase in creatinine 30 → 60 but still have eGFR >90 so it won’t be picked up

58
Q

What do we use to classify CKD

A
  • Proteinuria
  • ACR (albumin:creatinine ratio)
  • GFR

More protein means more risk of end stage renal failure

Aneesha Flashcards BRS 2 (47 decks)

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