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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

24
Q

Treatment of Nephritic syndrome

25
Nephrotic range proteinuria
> 3.5g/d
26
What condition produced "Cola coloured" urine?
Glomerulonephritis/ Nephritic syndrome
27
Causes of Raised anion gap metabolic acidosis
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
Causes of normal anion gap metabolic acidosis
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
Anion gap calculation and normal range
(Na+ + K+) - (Cl- + HCO-3) Normal = 10-18 mmol/L
30
CKD stage 1 definition
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
CKD stage 2 definition
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
CKD stage 3a definition
45-59 ml/min, a moderate reduction in kidney function
33
CKD stage 3b definition
30-44 ml/min, a moderate reduction in kidney function
34
CKD stage 4 definition
15-29 ml/min, a severe reduction in kidney function
35
CKD stage 5 definition
Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
36
Diuretic used for Ascites
Spironolactone
37
Features suggesting CKD rather than AKI
Hypocalcaemia (Due to lack of vitamin D)
38
Characteristics of Diabetes insipidus
high plasma osmolality and a low urine osmolality
39
Management of nephrogenic diabetes insipidus
thiazides low salt/protein diet
40
Treatment of central diabetes insipidus
desmopressin
41
What is renal tubular acidosis?
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
Most common types of Renal tubular acidosis
Type 1 - caused by pathology in distal tubule —> unable to excrete hydrogen ions Type 4 - caused by reduced aldosterone
43
What is acute tubular necrosis and what causes it?
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
What condition is associated with “muddy brown casts”
Acute tubular necrosis
45
Relevance of the anion gap?
Reveals whether your blood has an imbalance of electrolytes of if blood is too acidic/alkaline High +ve = acidosis
46
Why do patients with CKD develop anaemia?
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
Treatment of reduced erythropoietin levels due to CKD
Darbepoetin Alfa injections (EPO stimulating) (Check for other causes of anaemia first)
48
Extra renal features of autosomal dominant polycystic kidney disease
Hepatic cysts Diverticulosis Intracranial aneurysms Ovarian cysts
49
How is fluid challenge used to identify cause of oliguria?
Pre-renal uraemia - fluid challenge would cause increase in urine output Intra renal (e.g. acute tubular necrosis) - poor response to fluid challenge
50
Urine osmolality in acute tubular necrosis
< 359 mOsm/kg
51
What are Bence- Jones proteins?
Found in urine in multiple myeloma They are immunoglobulin light chains found in excessive quantities

FINALS (19 decks)

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