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Paeds Exam > Nephrology > Flashcards

Nephrology Flashcards

1
Q

2008A Q22

Which of the following is the main site of potassium reabsorption in the nephron?
A. Proximal convoluted tubule.
B. Descending limb of the Loop of Henle.
C. Ascending limb of the Loop of Henle.
D. Distal convoluted tubule.
E. Collecting duct.

A

A. Proximal convoluted tubule.

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2
Q

In a patient in renal failure with acidosis and low Hb, should a blood transfusion be given?

How should pH be corrected?

A

No!!

Blood transfusion with also provide K+ which MUST BE AVOIDED IN PATIENTS IN RENAL FAILURE.

If you raise the pH with bicarbonate, K+ binds to albumin causing hypocalcemia.

Therefore don’t change the pH without first correcting calcium (with lots of yummy chewable tablets because IV calcium is dangerous).

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3
Q

What are the effects of hypocalcemia?

A
  • Fatigue
  • cramping
  • tetany
  • seizures
  • laryngospasm
  • arrythmia
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4
Q

If someone presents with microscopic haematuria and hearing loss, and there is a family history of haematuria, what diagnosis do you need to consider?

A

Alport Syndrome (hereditary nephritis)

X-linked in 80%

Inherited form of glomerular disease assoc with hearing loss and ocular abnormalities.

Patients with Alport disease and overt proteinuria can be treated with with angiotensin blockage therapy using ACE inhibitor or angiotensi receptor blocker.

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5
Q

How is IgA nephropathy different to post strep GN?

A
  • Gross haematuria concurrent with illness (c.f. approx 2/52 post)
  • Recurrent
  • Persistent microsopic haematuria
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6
Q

What are typical presentation features of a patient with post infectious GN?

A
  • Hx of strep or other infection
  • Present with acute onset gross haematuria
  • Oedema
  • Often hypertensive
  • Depressed C3
  • Haematuria up to 2 years
  • Does not recur
  • Can have “coca-cola” urine
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7
Q

What is a Wilms Tumour?

A

Renal malignancy.

  • Most common renal malignancy in children.
  • 4th most common childhood cancer.
  • 2/3 dx by 5 yrs, almost all by 10yrs.
  • Assoc with mutations in a number of tumour suppressor genes
  • Most have solitary tumour
  • Most common presentation is detection of abdominal mass or swelling without other signs or symptoms. May have abdo pain, haematuria, hypertension.
  • Dx on histology.
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8
Q

What is the survival rate of Wilms tumour?

A

Now 90 %.

Has improved from 20% in the late 1960s.

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9
Q

When is haematuria an emergency?

A

With…..

  • Hypertension
  • Oedema
  • Oliguria
  • Significant proteinuria
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10
Q

How is fractional excretion of sodium (FENa) calculated?

A

(Urine Na+/Urine creatinine) X (plasma creatinine/Plasma Na+) X100%

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11
Q

What is normal GFR of a term infant at birth?

A

25 ml/min per 1.73m2

This increases by 50-100% during the first week.

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12
Q

What may oligohydramnios or anhydramnios indicate?

A

Urinary tract obstruction and/or reduced prodution of urine by displastic kidneys.

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13
Q

On antenatal renal USS, what are some signs of fetal renal abnormality?

A

Bright echogenicity, lack of corticomedullary differentiation, cyst formation and hydronephrosis.

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14
Q

A fetus with severe oligohydramnios can develop a lung pathology secondary to congenital renal abnormalities. This abnormality is the major determinant in survival at delivery.

What is the lung pathology?

A

Pulmonary hypoplasia

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15
Q

What determines GFR?

A
  1. Transcapillary hydrostatic pressure gradient (favours glomerular filtration)
    (Pcb)
  2. Transcapillary oncotic pressure gradient (counters glomerular filtration)
    (Pπ)
  3. Permeability coefficient of the glomerular capillary wall, k

GFR= k(Pcb-Pπ)

GFR is expressed as a function of body surface area.

Correct GFR (ml/min/1/73m2)= Absolute GFR (ml/min) X 1.73/surface area

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16
Q

In the renal tubules, what are the sites of major reabsorption of mostof the glomerular filtrate?

A

Proximal tubule and loop of henley

17
Q

In the kidney,where does the “fine tuning” of the final composition of urine occur?

A

Distal tubule and collecting duct.

18
Q

What is the primary active transport system in the proximal tubule?

A

Na+/K+/ATPase enzyme reabsorbing 50% of filtered Na+

19
Q

What aborbs 90% of bicarb and where?

A

Na+/H+ antiporter in proximal tubule.

Some Cl- also reabsorbed.

20
Q

What is reabsorbed in the proximal tubule?

A
  • Na+
  • Glucose (completely, unless plasma level high then glycosuria)
  • Amino acids (completely)
  • Phosphate (80-90% under influence of PTH which reduces reabsorption and enhances excretion)
  • Calcium (95% in total, 60% proximal, 20%LOH, 10% DT, 5% CD)
  • Organic solutes (incl creatinine and urate, some drugs (trimethoprim and diuretics) secreted in proximal tubule.
21
Q

50% of Na+ is reabsorbed in the proximal tubule. How much is reaborbed in the Loop of Henle and how?

A

40% via the Na+/K+/2Cl- co-transporter in the thick ascending limb.

22
Q

Where is the concentration gradient generated in the nephron?

A

In the loop of Henle because it is impermeable to water.

23
Q

How do loop diuretics work?

A

By blocking the Cl- binding sites on the Na+/K+/2Cl- co-transporter

24
Q

Aldosterone-sensitive channels in the Distal Tubule are involved in regulating K+ secretion.

  1. What is natriuresis assocated with?
  2. What are conditions of elevated aldosterone associated with?
A
  1. Natriuresis is associated with increased K+ secretion and hypokalemia
  2. Elevated aldosterone associated with hypokalemia
25
Q

Where does spironolactone have its effects?

A

Spironolactone BINDS TO AND BLOCKS the aldosterone receptor.

The aldosterone-sensitive channels are involved in regulating K+ secretion. Elevated levels of aldosterone lead to hypokalemia. Spironolactone blocks K+ secretion. It is therefore a K+ sparing diuretic at the expense of Na+

26
Q

Describe the renin-angiotensin-aldosterone system

A

Decreased pefusion to kidney ⇒ renin release from JGA ⇒ increased Angiotensin II levels ⇒ vasoconstriction and increased aldosterone release ⇒ enhanced distal tubular Na+ and H2O conservation and therefore ECF volume expansion.

27
Q

What is Conn Syndrome?

A

Low renin hypertension.

Primary hyperaldosteronism - high aldosterone leading to to ECF volume expansion, hypertension, hypokalaemia and renin suppression.

28
Q

How does anaemia occur in renal disease?

A

EPO released by renal peritubular cells is deficient in renal disease.

29
Q

Vit D3 (cholecalciferol) mainly available from action of UV light on its precursor in the skin.

It is hydroxylated in the liver to 25(OH)-vitamin D3.

What is the kidneys involvement in Vit D metabolism?

A

After hydroxylation in the liver to 25 (OH)-vitamin D3, it is further metabolised in the kidney by 1-hydroxylase to produce calcitriol, 1, 25 (OH)2-vitamin D3. This is the most biologically active vitamin D metabolite.

30
Q

What effect does hypocalcaemia have on Vit D metabolism?

A

Hypocalcaemia leads to enhanced 1-hydroxylase activity

31
Q

What is primary mechanism causing oedema in nephrotic syndrome?

A

Decreased capillary oncotic pressure

32
Q

Which is hypertensive, nephrotic or nephritic syndrome?

A

nephritic

33
Q

Goodpastures syndrome presentation and diagnostic features

A

Anti-GBM antibody disease affecting type IV collagen in glomerular basement membrane and alveoli.

present with:

  • rapidly progressive glomerulonephritis: acute renal failure, nephritic urine sediment, and non-nephrotic proteinuria.
  • Pulmonary involvement (alveolar hemorrhage) is present in 50 to 60 percent of patients.

Diagnosis by anti-GBM antibodies either on biopsy or serum.

ANCA raised in 40%

34
Q

What happens to complement levels in post strep GN?

A

Decreased C3

35
Q

Why does creatinine overestimate GFR as GFR is declining?

A

Creatinine is secreted by the tubules.

36
Q

What are the causes of metabolic acidosis with high anion gap?

A

MUDPILES (methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates)

Paeds Exam (42 decks)

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