The chemical pathology of renal disease Flashcards

1
Q

What are the four main homeostatic and three main endocrine functions of the kidney?

A
Homeostatic:
-Waste products of metabolism
-Fluid and salt balance
-Acid base balance
-Removal of drugs
Endocrine:
-Epo production
-Renin aldosterone angiotensin system
-Hydroxylation of vitamin D
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2
Q

What are the serum creatinine levels compared to baseline in the different stages of acute kidney injury?

A

Stage 1 - 1.5 to 1.9x baseline
Stage 2 - 2.0 to 2.9x baseline
Stage 3 - 3.0 or above

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3
Q

What are the main causes of pre renal AKI?

A

Hypovolaemia - haemorrhage or dehydration
Renal artery stenosis
Sepsis and vasodilation
Pump failure

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4
Q

What are the main causes of intrinsic AKI?

A
Ischaemia
Nephrotoxic drugs
Pyleonephritis
Early CKD, such as glomerulonephritis
Trauma
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5
Q

What are the main causes of post renal AKI?

A

Obstruction such as stones or tumour

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6
Q

What are the urine output findings in pre renal vs intrinsic AKI?

A

Pre renal - low

Intrinsic - initially high

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7
Q

What is the urine:plasma osmolality findings in pre renal vs intrinsic AKI?

A

Pre renal - >2:1

Intrinsic - <1:1

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8
Q

What is the urine Na in pre renal vs intrinsic AKI?

A

Pre renal - <15

intrinsic - >40

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9
Q

What is the plasma sodium in pre renal vs intrinsic AKI?

A

Pre renal - high

Intrinsic - low

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10
Q

What is the urea v creatinine in pre renal vs intrinsic AKI?

A

Pre renal - urea&raquo_space; creatinine

Intrinsic - urea = creatinine

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11
Q

How do you treat pre renal vs intrinsic AKI?

A

Pre renal give fluids to increase kidney perfusion

Intrinsic if you give fluids you can kill the patient

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12
Q

What are the earliest changes that occur in AKI and are potentially life threatening?

A

Metabolic acidosis as acid wastes not being excreted

Hyperkalaemia due to potassium not being excreted - life threatening above 8mmol/L

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13
Q

What are the clinical features of AKI?

A

They are non specific and occur late on
As nitrogenous waste products built up you get: nausea, malasie, confusion
Can get fluid overload as less blood is filtered

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14
Q

How is intrinsic AKI treated?

A

With dialysis to support renal function until the kidney has healed

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15
Q

What is the treatment for post renal AKI?

A

Removal of the obstruction

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16
Q

What are some of the main causes of CKD?

A
Diabetes
Hypertension
polycycstic kidneys
recurrent pyelonephritis
reflux nephropathy
glomerulonephritis
17
Q

What are the stages of CKD?

A
In eGFR ml/min
1 - >90
2 - 60-90
3 - 30-60
4 - 15-30
5 - <15
18
Q

What are some of the consequences of stage 3 CKD and above?

A

Hypertension due to water retention
Low calcium due to vitamin D, causes anaemia and anorexia
Get salt and water retention, acidosis and hyperkalaemia

19
Q

What endocrine changes occur at stage 3 and above CKD?

A

Patients will have to take 1,25 OH vitamin D due to decreased hydroxylation, this leads to low calcium levels and hyperparathyroidism.
Increased parathyroid hormone can cause osteomalacia (soft bones) from increased calcium reabsorption.
Epo production can drop and cause anaemia

20
Q

How is CKD managed?

A

Endocrine and metabolic abnormalities can be corrected with hormone replacement. Phosphate binders are given to prevent calcification. diet is modified to reduce potassium.
Acid - base balance corrected with bicarb
Dialysis for renal replacement

21
Q

What is renal glycouria?

A

Lack of uptake of glucose

22
Q

What is hypophosphataemic rickets?

A

Caused by decreased phophate uptake

23
Q

What are the three main forms of renal tubular acidosis?

A

Type 1 - (distal) failure to secrete H+ ions and excess K+ being lost, this causes hypokalaemia acidosis and kidney stones. Treated with bicarbonate and K+
Type 2 - (proximal) leads to alkalosis due to bicarbonate leak.
Type IV - Low renin and aldosterone - Causes hyperkalaemia