Complications of CKD Flashcards

1
Q

What are the complications of CKD?

A

Accumulation of waste products

Salt and water retention

High blood pressure

Metabolic acidosis

Hormone disturbaces

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2
Q

Examples of hormonal disturbances triggered by CKD

A

Secondary hyperparathyroidism

Bone disease

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3
Q

Why does fluid accumulate in CKD?

A

The ability for the tubule to filter water and sodium breaks down

Water and salt retention leads to fluid accumulation

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4
Q

What are clinical ways to pick up fluid accumulation?

A

Press on skin - leaves dent due to presence of water

Pulmonary oedema - can hear crackles via stethoscope

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5
Q

How does CKD affect blood pressure?

A

CKD leads to secondary hypertension

Secondary hypertension causes more kidney injury

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6
Q

What causes secondary hypertension in CKD?

A

Fluid retention

Activation of the renin-angiotensin system

Excess renin production

Increased sympathetic activity

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7
Q

What are the consequences of hypertension?

A

Left ventricular hypertrophy

Heart failure - many patients with CKD die from heart failure rather than kidney failure

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8
Q

What is metabolic acidosis?

A

When kidney are not removing enough acids from the body, so there is a build up of acid in the blood

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9
Q

Why does CKD lead to metabolic acidosis?

A

There is diminished excretion of non-volatile acids

Increased loss of bicarbonate ions

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10
Q

What do patients with metabolic acidosis present wit clinically?

A

Hyperventilation

To remove the carbon dioxide from the system - pushes to form less carbonic acid

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11
Q

Which hormones do kidneys control?

A

EPO

Vitamin D

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12
Q

What stimulates EPO production from the kidney?

A

Decreased blood oxygen

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13
Q

What is the role of EPO?

A

Acts in the bone marrrow to increase numbers of RBC precursors

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14
Q

What happens to EPO production during CKD?

A

EPO concentration decreases

There is less RBC precursor production

Less RBC in the blood

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15
Q

What condition stems from the decreased EPO synthesis?

A

Normochromic normocytic anaemia

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16
Q

What does normochromic normocytic anaemia mean?

A

Normochromic - normal shape

Normocytic - normal size

The RBC are normal, there are just less produced than what is needed

17
Q

How is vitamin D metabolised in the body?

A

Vitamin D is obtained from the gut or skin

FIrst it is hydroxylated in the liver to form 25(OH)D

Then it passes to the kidneys and is hydroxylated to 1,25(OH)2D - active form

18
Q

What does PTH do?

A

Maintains bone turnover

19
Q

What do patients with CKD have in context to PTH?

A

Secondary/ tertiary hyperthyroidism

20
Q

What is the pathogenesis of secondary/ tertiary hyperthyroidism?

A

Kidneys diseases and becomes smaller

Therefore it releases less active form of vitamin D -> 1,25(OH)2D

Parathyroid gland has receptor for this molecule -> negative feedback loop

There is a compensatory increase in the PTH released

The parathyroid gland becomes hypertrophied and autonomous -> releases PTH regardless of stimulus

21
Q

What is the condition called when the parathyroid gland releases PTH regardless of the stimulus?

A

Tertiary hyperthyroidism

22
Q

What are the clinical presentations of hyperthyroidism?

A

Bone erosion

Bone fracturing

Hypercalcemia

23
Q

What other hormone does the parathyroid release?

A

FGF23

24
Q

What is FGF23?

A

A fibroblast growth factor

25
Q

How does FGF23 affect 1,25-vitD levels?

A

Decreases the release of the vitamin D intermediate

26
Q

What stimulus causes FGF23 to be released?

A

An increase in blood concentration of vitamin D active intermediate

An increase in phosphate concentration in the blood

27
Q

How does CKD affect FGF23 release?

A

Inhibits reabsorption of phosphate from the urinary tract

Blood concentration of phosphate decreases

FGF decreases 1,25-vitD release - there is an increase in PTH release (negative feedback loop)

Phosphate also binds directly to receptors on the parathyroid - increases PTH release