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BRS 2 > Chronic Kidney Disease & Renal Failure > Flashcards

Chronic Kidney Disease & Renal Failure Flashcards

1
Q

What is CKD?

A

CKD is defined as abnormalities of kidney structure or function, present for >3 months.

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2
Q

What GFR parameter defines CKD?

A

• GFR <60mL/minute/1.73m2

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3
Q

What are the symptoms of CKD?

A

Albuminuria/proteinuria, haematuria, electrolyte abnormalities detected by imaging.

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4
Q

What endocrine functions are performed by the kidneys?

A

Erythropoietin synthesis

1-alpha hydroxylase vitamin D

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5
Q

What homeostatic are performed by the kidneys?

A

Electrolyte balance
Acid-base balance
Volume homeostasis

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6
Q

What are the excretory functions of the kidneys?

A

Nitrogenous waste
Middle sized molecules
Hormones, peptides
Salt and Water

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7
Q

What are the functions of the kidney regarding glucose metabolism?

A

Gluconeogenesis

Insulin clearance

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8
Q

Disruptions to the homeostatic balance of the kidneys can manifest as what?

A

Hyperkalaemia
Reduced bicarbonate - decreases pH and manifests as metabolic acidosis
Increased phosphate
Salt want water imbalance

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9
Q

What are the endocrine imbalances that occur in kidney dysfunction?

A

Increased PTH
Anaemia - reduced EPO production
Hypocalcaemia- reduced calcitriol synthesis

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10
Q

Why is there parathyroid hyperplasia associated with kidney dysfunction?

A

There is a reduction of calcitriol synthesis, due to insufficient activity of renal 1-alpha hydroxylase, manifesting as chronic hypocalcaemia, this increases PTH secretion to potentiate bone resorption

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11
Q

Why does anaemia occur in kidney dysfunction?

A

Reduced erythropoeitin production

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12
Q

What are the symptoms associated with kidney failure and reduced secretion of sodium chloride?

A

Hypertension
Oedema
Pulmonary Oedema

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13
Q

Why is salt and water loss evident in tubulointestinal disorders?

A

Damage int he concentrating mechanism of the juxtamedullary interstitial - water reabsorption decreased

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14
Q

Why does metabolic acidosis occur in kidney failure?

A

Reduced excretion of hydrogen ions from the distal convoluted tubule into the filtrate, manifests as acid retention

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15
Q

Why does hyperkalaemia occur in kidney failure?

A

Reduced potassium excretion

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16
Q

What is used to treat hyperkalaemia in an acute setting?

A

Sodium bicarboante- neutralises the hydrogen ions, such that potassium can re-enter the cells

17
Q

What can acidosis cause?

A

Anorexia and muscle catabolism

18
Q

What are the symptoms of hyperkalaemia?

A

Cardiac arrhythmias
Neural muscular activity
Vomiting

19
Q

What features on an ECG suggest hyperkalaemia?

A 
Peaked T waves
P-waves: Broadens, reduced amplitude
QRS widening
Heart block
Asystole
VT/VF
20
Q

What type of hyperparathyroidism is linked with chronic kidney failure?

A

Tertiary hyperparathyroidism

21
Q

Why is there an increased cardiovascular risk with chronic kidney disease?

A

There is an increased cardiovascular risk, since cardiac ventricular myocyte contraction is directly related to extracellular concentrations of calcium (arrythmias) + increased calcification risk.
• Predictor of end stage renal failure is CKD
• Outcome for a patient with CKD  Cardiovascular disease

22
Q

What are the standard cardiovascular risk?

A

Hypertension
Diabetes
Lipid abnormalities

23
Q

What is the immediate treatment in a patient with hypovolaemia?

A

Give fluids

24
Q

What is the immediate treatment for a patient with hypervolaemia?

A

Fluid restriction, consider diuretics/dialysis

25
Q

What is the treatment for hyperkalaemia?

A

Drive into cells – sodium bicarbonate
Insulin dextrose (caution) – carries hypoglycaemic risk. Insulin is a potassium drive (short term solution)
Drive out of the body – Diuretics/dialysis
Gut absorption – Potassium chelating agents

26
Q

How does insulin dextrose treat hyperkalaemia?

A

Insulin induces a potassium drive (short-term solution).

27
Q

What is the long term management for CKD?

A
  • Erythropoietin injections to correct anaemia
  • Diuretics to correct salt-water overload
  • Phosphate binders
  • 1-25 Vitamin D supplements
28
Q

What home therapy is available for CKD?

A
  • Haemodialysis
  • Peritoneal dialysis/assisted programmes  The peritoneum behaves as a semipermeable membrane and a dialysate is delivered with specific concentrations (hyperosmolar to generate drive, fluid into the peritoneal cavity)
29
Q

What is a fistula in terms of CKD?

A

A fistula is created by connecting an artery directly to the vein – vein swells for ease of access.

30
Q

Where should taking blood be avoided in patients with renal failure?

A

avoid taking blood or inserting IV lines into the veins of the antecubital fossa or cephalic vein at wrist level

31
Q

Which veins should be used when taking blood or IV lines for patients with renal failure?

A

Dorsal venous structures

32
Q

Why should transfusions be avoided in patients with renal failure?

A

• Transfusions will sensitise anaemia (haemolytic anaemia, as foreign antigens are detected, and antibodies are formed)  Autoimmune mediated rejection of transplanted kidney).

33
Q

Why is urea a poor indicator of GFR?

A

Poor indicator

Confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function

34
Q

What factors affect creatinine within patients with renal failure?

A

Affected by muscle mass ,age, race and sex

35
Q

What is the most appropriate radionucleotide studies in patients with renal failure?

A

EDTA

36
Q

What calculation is used, to estimate GFR in patients?

A

Modification of Diet in Renal Disease (MDRD)
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)

or
CKD Epidemiology Collaboration (CKD-EPI)
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]

37
Q

Which GFR-CKD classification is recommended by NICE and why?

A

NICE guidelines to use CKD-EPI (At high GFR, it is more accurate)

BRS 2 (62 decks)

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