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FINALS > Nephrology & Urology > Flashcards

Nephrology & Urology Flashcards

1
Q

Causes of renal disease following URTI

A

IgA nephropathy
Post-streptococcal glomerulonephritis

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2
Q

Raised anti-streptolysin O titre - meaning

A

it is likely that the person tested has had a recent strep infection.

ASO titers that are initially high and then decline suggest that an infection has occurred and may be resolving.

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3
Q

What is post-streptococcal glomerulonephritis

A

Occurs 1 – 3 weeks after a β-haemolytic streptococcus infection, such as tonsillitis

Immune complexes made up of streptococcal antigens, antibodies and complement proteins get stuck in the glomeruli of the kidney and cause inflammation –> AKI

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4
Q

What is IgA Nephropathy?

A

AKA Berger’s disease. Related to Henoch-Schonlein Purpura (IgA vasculitis)

IgA deposits in the nephrons of the kidney causes inflammation (nephritis).

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5
Q

Two most common causes of nephritis in children

A

post-streptococcal glomerulonephritis IgA nephropathy (Berger’s disease)

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6
Q

Similarities and differences between IgA Nephropathy and post-streptococcal glomerulonephritis

A

Similarities:
- Recent URTI
- Haematuria

Differences:
- PSGN develops 1-2 weeks after URTI.
- IgA nephropathy develops 1-2 days after URTI

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7
Q

Testicular problem associated with mumps

A

Orchitis

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8
Q

Indications for dialysis in AKI

A

Life threatining, refactory AKI with complications:

I) Severe hyperkalemia / acidaemia / uraemia
II) Refactory pulmonary oedema
III) toxins / drugs

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9
Q

Treatment of severe hyperkalaemia

A

Stabilise myocardium:
1. 10ml 10% calcium gluconate

Drive K+ into cells:
2. IV insulin + 25g glucose
3. Salbutamol nebs

Correct acidosis:
4. 1.4% sodium bicarbonate

  1. Treat cause
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10
Q

Components of nephritic screen - if unexplained AKI/CKD

A

ANCA (vasculitis)
ANA/ ds DNA (SLE)
Complement (Low in infection/SLE)
Hep B/C screen

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11
Q

Primary causes of Nephrotic syndrome

A

= immune complex deposition &/or complement activation

Minimal change disease (most common in children)

Focal segmental glomerulonephritis

Membranous glomerulonephritis

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12
Q

Characteristics of nephrotic syndrome

A

Mean features:
1. Proteinuria
2. Hypoalbuminaemia
3. Oedea - periorbital, legs, scrotal/vaginal

N.B. Periorbital oedema is often noticed first and mistaken for allergy

Others:
- hyperlipidemia
- hypercoagulability
- infections

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13
Q

Consequences of reduced albulin in nephrotic syndrome

A

Peripheral/periorbital OEDEMA –> Ascites, abdo pain

PLEURAL EFFUSIONS –> SOB, Orthopnoea

Retaining of Na+ and water

Decreased oncotic pressure also a driver for increased lipid synthesis and production of clotting factors

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14
Q

Secondary causes of nephrotic syndrome

A

= damage due to underlying disease

  • Diabetic nephropathy
  • SLE
  • Infection - hepatitis B/C, HIV, malaria, syphilis
  • Drugs (penicillamine, NSAIDs, iron)
  • Myeloma
  • Pre-eclampsia
  • Henoch schonlein purpura (HSP)
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15
Q

What is Minimal change disease?

A
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16
Q

What is Focal segmental glomerulonephritis?

A
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17
Q

What is Membranous glomerulonephritis?

A
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18
Q

What is nephritis?

A

= inflammation of glomerulus
A specific form of glomerulonephritis

Inflammation –> damage to glomerular capillaries (RBC loss), damage to podocytes (protein loss), reduced GFR

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19
Q

What is glomerulonephritis?

A

= group of diseases causing immune-mediated inflammation in the glomerulus

A spectrum of Nephrotic and Nephritic syndromes

Nephritis = a specific form of glomerulonephritis

Causes are either:
1. Post-infectious: malaria/staph/salmonella/strep
2: Systemic autoimmune diseases / vasculitis e.g. SLE

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20
Q

Features of nephritis

A
  1. Haematuria
  2. Oliguria (<0.5-1ml /kg/hr)
  3. Proteinuria
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21
Q

What are red cell casts?

A

Reflects microscopic bleeding / damage to glomerulus
RBC clump together

22
Q

Investigations for glomerular disease

A
  1. Confirm diagnosis:
    - urine dip & MCS
    - bloods: U&Es, Cr, Albumin, FBC, ESR, CRP, LFTs
    - RENAL BIOPSY - shows microscopic changes to glomerulus
  2. Determine cause:
    - autoimmune screen
    - Serum & urine immunoglobulins / electrophoresis
    - infection screen
  3. Assess complications
    - CXR, lipid profile, TFTs, Coag screen
23
Q

Treatment of nephrotic syndrome

A
24
Q

Treatment of Nephritic syndrome

A
25
Q

Nephrotic range proteinuria

A

> 3.5g/d

26
Q

What condition produced “Cola coloured” urine?

A

Glomerulonephritis/ Nephritic syndrome

27
Q

Causes of Raised anion gap metabolic acidosis

A
  1. lactic acidosis:
    - A: sepsis, shock, hypoxia, burns
    - B: metformin
  2. ketones:
    - diabetic ketoacidosis
    - alcohol
  3. urate: renal failure
  4. acid poisoning: salicylates, methanol
28
Q

Causes of normal anion gap metabolic acidosis

A
  1. GI bicarbonate loss:
    - prolonged diarrhea (may also result in hypokalemia)
  2. Ureterosigmoidostomy fistula
  3. Renal tubular acidosis
  4. Drugs: e.g. acetazolamide
  5. Treatment of metabolic alkalosis (ammonium chloride injection)
  6. Addison’s disease
29
Q

Anion gap calculation and normal range

A

(Na+ + K+) - (Cl- + HCO-3)

Normal = 10-18 mmol/L

30
Q

CKD stage 1 definition

A

Greater than 90 ml/min, with some sign of kidney damage on other tests

*if all the kidney tests (proteinurea/U&Es) are normal, there is no CKD

31
Q

CKD stage 2 definition

A

60-90 ml/min with some sign of kidney damage

*if all the kidney tests (proteinurea/U&Es) are normal, there is no CKD

32
Q

CKD stage 3a definition

A

45-59 ml/min, a moderate reduction in kidney function

33
Q

CKD stage 3b definition

A

30-44 ml/min, a moderate reduction in kidney function

34
Q

CKD stage 4 definition

A

15-29 ml/min, a severe reduction in kidney function

35
Q

CKD stage 5 definition

A

Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

36
Q

Diuretic used for Ascites

A

Spironolactone

37
Q

Features suggesting CKD rather than AKI

A

Hypocalcaemia (Due to lack of vitamin D)

38
Q

Characteristics of Diabetes insipidus

A

high plasma osmolality and a low urine osmolality

39
Q

Management of nephrogenic diabetes insipidus

A

thiazides
low salt/protein diet

40
Q

Treatment of central diabetes insipidus

A

desmopressin

41
Q

What is renal tubular acidosis?

A

Metabolic acidosis due to pathology in the tubules of the kidney
Tubules are responsible for balancing hydrogen and bicarbonate ions and maintaining normal pH
Different types of RTA based upon where along the tubule is affected

42
Q

Most common types of Renal tubular acidosis

A

Type 1 - caused by pathology in distal tubule —> unable to excrete hydrogen ions

Type 4 - caused by reduced aldosterone

43
Q

What is acute tubular necrosis and what causes it?

A

Necrosis of epithelial cells of the renal tubules
Most common cause of AKI

Damage occurs due to:
- ischaemia (E.g. shock, sepsis, dehydration)
- Toxins (e.g. contrast dye, gentamicin, NSAIDs)

44
Q

What condition is associated with “muddy brown casts”

A

Acute tubular necrosis

45
Q

Relevance of the anion gap?

A

Reveals whether your blood has an imbalance of electrolytes of if blood is too acidic/alkaline

High +ve = acidosis

46
Q

Why do patients with CKD develop anaemia?

A

Reduced erythropoietin levels - most sig. factor

Others
- Reduced erythropoiesis due to toxic effects of uraemia on bone marrow
- Reduced absorption of iron
- Anorexia/nausea due to uraemia
- reduced RBC survival (esp. haemodialysis)
- Blood loss due to capillary fragility and poor platelet function

47
Q

Treatment of reduced erythropoietin levels due to CKD

A

Darbepoetin Alfa injections (EPO stimulating)

(Check for other causes of anaemia first)

48
Q

Extra renal features of autosomal dominant polycystic kidney disease

A

Hepatic cysts
Diverticulosis
Intracranial aneurysms
Ovarian cysts

49
Q

How is fluid challenge used to identify cause of oliguria?

A

Pre-renal uraemia - fluid challenge would cause increase in urine output

Intra renal (e.g. acute tubular necrosis) - poor response to fluid challenge

50
Q

Urine osmolality in acute tubular necrosis

A

< 359 mOsm/kg

51
Q

What are Bence- Jones proteins?

A

Found in urine in multiple myeloma

They are immunoglobulin light chains found in excessive quantities

FINALS (19 decks)

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