Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Written exam > Renal/urology > Flashcards

Renal/urology Flashcards

1
Q

Haemoglobinuria / myoglobinuria in UA

A

No RBCs on microscopy but dipstick pos for blood
Confirm with urine ammonium sulfate test - precipitates haemoglobin but not myoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

HUS pathophysiology

A
  • Thrombotic microangiopathy
  • Most commonly by Shiga toxin (esp E Coli aka typical HUS)
  • Less commonly by activation of alternate complement pathway (aka atypical HUS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Non AKI causes of creatinine variations

A
  • Low in infants
  • Low in kids with low muscle mass (DMD, spina bifida)
  • High in muscular adolescents
  • High in rhabdomyolysis
  • Drugs - probenecid, cimetidine, trimethoprim (high Cr due to impaired secretion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Fractional excretion of sodium (FENa)

A

= [(UNa x PCr) / UCr x PNa)] x 100
- Measures % Na excreted in urine
- Can’t be accurately interpreted in setting of diuretics (consider FE-Urea in that case - <30%=azotemia)
- If <1% -> due to prerenal azotaemia
- If >1% -> due to intrinsic causes of AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Total body water

A

70-80% term infants
60% at 1 yr
50% for females after puberty (M stay at 60%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Osmolarity v osmolality

A
  • Osmolarity - number of osmotically-active particles (osmoles) PER VOLUME of solute (Osm/L)
  • Osmolality - number of osmoles PER WEIGHT of solution (Osm/kg)
  • Normal serum osmolality ~280 mOsm/kg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ADH

A
  • Secreted by posterior pituitary
  • Acts on late distal tubule and CD to increase water permeability
  • Regulated by (among others)
    1) Osmoreceptors in hypothalamus
    2) Volume (stretch) receptors in left atrium and blood vessels
  • Strongest stimulant = low volume aka hypovolaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Clinical clues to hypovolaemia

A

Tachycardia
Narrowed pulse pressure
Orthostatic hypotension
Orthostatic tachycardia (increase of 15-20 beats)
Prolonged CR
Resting tachycardia with hypotension
Low central venous pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Liddle syndrome

A

Primary Na retention (affects principal cells of distal tubule and CD)
-> low renin and aldosterone levels
-> HTN
-> hypokalaemia metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Bartter and Gitelman - common features

A

Severe Na+ losses -> hypovolaemia
-> Elevated renin/aldosterone levels
-> Hypokalaemia and alkalosis
Rarely hypertensive due to increased prostaglandin production causing vasodilation of renal arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Bartter syndrome

A
  • AR inheritance
  • Abnormal solute transport in thick aLOH
  • Lose Na, Cl, Ca and Mg in urine
  • Similar labs to LOOP DIURETICs
  • Type 4 is associated with deafness
  • Sometimes presents with stones or nephrocalcinosis in neonatal period or early childhood due to Na wasting and hypercalciuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Gitelman syndrome

A
  • Defect in Na/Cl cotransporter in early distal tubule
  • Similar labs to THIAZIDE DIURETICs, but also have severe Mg wasting
  • Symptoms milder than Bartter
  • Usually present later in life with muscle weakness, cramps, sapsms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bartter v Gitelman

A
  • Both cause hypokalaemic metabolic alkalosis & salt wasting WITHOUT HTN
  • Bartter - affects aLOH, sometimes associated with deafness, HYPERcalciuria, NORMAL/LOW Mg, clinically = LOOP diuretics
  • Gitelman - affects distal convoluted tubule, HYPOcalciuria, HYPOmagnesaemia, clinically = THIAZIDE diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Thiazide diuretics - urinary Ca

A

DECREASES urinary Ca (can be used to treat kidney stones) and INCREASES serum Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Loop diuretics - affect on urinary Ca

A

INCREASES urinary Ca and DECREASES serum Ca (can be used to treat hypercalcaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

RTA type 1

A

Defective H+ SECRETION from DISTAL tubule
- Low K+, sometimes low Na
- Hypercalciuria
- +ve urinary anion gap (Na + K - Cl)
- AR and AD forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

RTA type II

A

Inability to reabsorb HCO3 in PROXIMAL tubule
- Low K+, normal Na+
- Normal urine Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Anion gap equation

A

Na - (HCO3 + Cl)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes of HAGMA - MUDPILES

A

Methanol
Ureamia
DKA
Propylene glycol
Iron/isoniazide/inborn error
Lactic acidosis
Ethylene glycol
Salicylates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

PUV - overview

A
  • Obstructing membranous folds within the lumen of the posterior urethra.
  • Caused by disruption in the normal embryologic development of the male urethra.
  • Most common cause of chronic renal disease due to urinary tract obstruction in children.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

PUV - presentation

A
  • Usually antenatal - bilateral hydronephrosis, dilated bladder, dilated posterior urethra
  • Postnatal - newborn with UTI, abdo distension, resp distress (lung hypoplasia)
  • Infant - FTT, urosepsis, poor urinary stream, straining while voiding
  • Older - UTIs, day and night incontinence, voiding dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

PUV - complications

A
  • VUR
  • Bladder dysfunction
  • Increased risk of CKD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

PUV - diagnosis

A

Micturating cystourethrogram (MCUG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

PUV - mgmt

A
  • Urgent urology consult
  • IDC (NGT, not balloon)
  • Manage sepsis, UEC abnormalities, uraemia, acidemia, fluid imbalance
  • Ablation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Potter sequence

A
  • Due to severe inutero oligohydramnios
  • Positional limb deformities (club feet and hip dislocation)
  • Typical facial appearance incl pseudoepicanthus, recessed chin, posteriorly rotated, flattened ears, flattened nose
  • Pulmonary hypoplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Ureteropelvic junction (UPJ) obstruction description

A
  • Partial or total intermittent blockage of urine flow that occurs where the ureter enters the kidney, resulting in hydronephrosis.
  • Most common pathologic cause of congenital hydronephrosis
  • Usually due to intrinsic narrowing of musculature between junction of the renal pelvis and ureter, but may be due to extrinsic compression
  • More common in males and on left side
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

UPJ obstruction - presentation

A
  • Usually identified on antenatal US - renal pelvis but not ureter dilated
  • Infants - abdo mass (enlarged kidney), UTI, haematuria, FTT
  • Older kids - intermittent flank pain and abdo pain (pain after drinking due to dilatation of renal pelvis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

UPJ obstruction - management

A
  • Aimed at preservation of renal parenchyma and function
  • Pyeloplasty if decrease function or significant dilatation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Renal embryology

A

Ureteric bud -> collecting system
Metanephric mesenchyme -> glomerulus and nephrons

Wk 9 - 1st nephrons
Wk 12 - urine excretion
Wk 36 - nephrogenesis complete (or 4 wks postnatally, whichever is sooner)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Urine osmolality (mOsm/kg) - neonates v kids

A

At birth - 500-600
6-12 mths - 1,200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Indications for renal imaging postnatally

A

Failure to urinate 1st 24 hrs
Low urine output
Weak urine stream
Suprapubic mass
HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Timing of postnatal renal US

A

After 48 hrs of age - before then will underestimate hydronephrosis due to physiological dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Nocturnal enuresis overview

A
  • Involuntary nighttime voiding after 5 yrs
  • By 5 yrs, 90-95% of kids almost completely continent during the day and 80-85% at night
  • Primary = nocturnal urinary control never achieved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Nocturnal enuresis - 1st line mx (30-60%) success

A

Restrict fluids after 6pm
Motivational therapy
Conditioning therapy – sensor alarm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Nocturnal enuresis - medical management

A

Desmopressin acetate
Oxybutinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Nephrotic syndrome - most common pathologies

A
  • Minimal change disease (MCD) - >70%
  • Mesangiocapillary / membranoproliferative GN (MPGN) – 8%
  • Focal segmental glomerulosclerosis (FSGS) – 7%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Nephrotic syndrome - presentation

A

Facial swelling
Proteinuria
HTN
+/- low C3 (MPGN, PIGN)
+/- strep titres positive (PIGN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Complement levels in nephrotic sydnromes

A

Low C3 – MPGN, PIGN
Low C3 & C4 – lupus nephritis
Normal – idiopathic nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Minimal Change Disease (MCD) - key features

A

Typical features
- < 6 yrs
- No HTN, no haematuria
- Normal C3&C4
- Normal renal function
- Usually responds to glucocorticoid therapy in 8 wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

MPGN - key features

A
  • Most common in 10-20 yrs
  • Most present with nephrotic syndrome
  • May also present with acute nephritic syndrome with gross haematuria or asymptomatic microscopic haematuria and proteinuria
  • Renal function normal or decreased
  • HTN common
  • Often low C3
41
Q

MPGN v PSGN

A
  • Both may have haematuria, HTN, low C3, positive strep titres
  • PSGN – improve within 2 mths
  • MPGN – nephritic syndrome, proteinuria & low C3 persist
42
Q

AIN causes

A
  • Drug induced immune response (esp NSAIDs, antimicrobials, anticonvulsants)
  • Infection
  • SLE
43
Q

AIN presentation

A
  • Classic triad – fever, rash, arthralgia (only present in minority)
  • Low grade haematuria and pyuria - typical
  • WC casts and urinary eosinophils – suggestive but not diagnostic
44
Q

AIN management

A
  • Stop medication
  • Supportive care
  • Occasionally corticosteroids
45
Q

RTA - key common feature

A
  • Disorders of tubule characterised by NORMAL anion gap (hyperchloremic) metabolic acidosis with relatively well preserved GFR
  • Either hypoK (type 1&2) or hyperK (type 4)
46
Q

RTA type I (dRTA) - key features

A

= Defective H secretion from DISTAL tubule
- Urine pH > 5.5 (no H+ in urine)
- PCT reabsorbs all alkali including citrate (normally makes Ca soluble) therefore HIGH urinary Ca +/- nephrolithiasis, nephrocalcinosis
- Low K+, sometimes low Na+
- +ve urinary anion gap (equation = Na + (K - Cl))
- NO FANCONI syndrome
- AR and AD forms
- Seen in Sjogren’s syndrome, SLE, primary biliary cirrhosis, autoimmune hepatitis
- TREATMENT - alkali and K+ replacement

47
Q

RTA type II (pRTA) - key features

A

= Wasting HCO3 in PROXIMAL tubule (aka inability to reabsorb)
- Urine pH < 5.5 (distal tubules secrete excess H+)
- Low K+, normal Na+
- Normal urine Ca - no renal stones
- Associated with Fanconi syndrome (PAGU - phosphaturia, aminoaciduria, uricaciduria, glycosuria)
- Also seen in Myeloma, drugs (tenofovir, acetazolamide)
- TREATMENT - alkali (large doses) and K+ replacement

48
Q

RTA type IV (aldosterone)

A
  • Decreased production or diminished responsiveness of CD to aldosterone
  • Most common type
  • Present with HYPERkalaemia
  • Associated with DM (most common), NSAIDs, ACE-I, calcineurin inhibitors (cyclosporine and tacrolimus), K sparing diuretics, high dose heparin
  • MANAGEMENT
    • if normotensive, fudrocortisone (mineralcorticoid)
    • if hypertensive - thiazide or loop diuretic -> increases distal delivery of Na causing urinary secretion of H+ and K+
49
Q

HUS triad

A
  • Microantiopathic haemolytic anaemia
  • Thrombocytopania
  • AKI
50
Q

HUS causes

A
  • Infection, drugs, genetics, systemic
  • Most common - E Coli (shiga like toxin O157:H7) - diarrhoea
  • 2nd most common - strep pneumonia
  • Other countries - Shigella toxin
51
Q

HUS presentation

A
  • Fever (low grade), N&V, abdo pain, BLOODY diarrhoea
  • HUS at ~6 days -> increasing pallor and AKI
  • Anaemia, low plts, hyperK+
  • CNS involvement (sz (20%), encephalopathy) due to microthrombi
52
Q

HUS diagnosis/labs

A
  • Haemolytic anaemia (PT and PTT normal, cf DIC)
  • High WCC
  • LOW plts
  • Schistocytes (fragments) on urine microscopy DIAGNOSTIC
  • Coombs neg (unless associated with strep pneumo - empyema etc)
53
Q

HUS treatment

A

Supportive care and dialysis:
- IVH
- Control HTN
- Transfusions (RBC, not plts) + electrolytes
- 50% need 2/52 dialysis
- Antibiotics contraindicated

54
Q

HUS recovery

A
  • Plts recover 1st, then AKI, then anaemia
  • Worse prognosis if strep pneumonia
  • Genetic form relapse and remit with a poorer prognosis and have low C3 (Eculizumab for genetic)
55
Q

Poor prognostic features HUS

A
  • Anuria > 2 wks
  • Initial neutrophil count > 20K cells/uL
  • Coma on admission
  • Atypical forms (diarrhoeal better)
56
Q

Age at which GFR ~reaches adult value?

A

2 yrs

57
Q

Electrolyte abnormality associated with unilateral renal artery stenosis and why

A

Hypokalaeamia
Due to activation of RAAS -> aldosterone causes Na reabsorption and K secretion (aka hypoK+)

58
Q

What is nephrotic syndrome?

A
  • Damage to GBM -> causes protein loss
  • Triad of proteinuria, hypoalbuminaemia and oedema
  • May have hyperlipidaemia due to liver’s compensatory synthesis of proteins (incl albumin and lipoproteins) in response to hypoalbuminaemia
  • May have microscopic haematuria
  • Diagnostic criteria:
    - Proteinuria (dipstick 3-4+ or Ur P/Cr ratio >0.2 gm/mmol (200 mg/mmol)
    - Hypoalbuminaemia (<25 g/L)
59
Q

Acute management for nephrotic syndrome

A
  • Admit
  • Treat sepsis if present (high risk of infection)
  • Manage oedema -> 1) no added salt 2) daily wts 3) daily dipstick 4) strict fluid balance 5) monitor input and output 6) +/- albumin infusion 7) +/- frusemide
  • Steroids (defer live vaccines while on high dose steroids)
  • Prophylaxis against infection
60
Q

Complications of nephrotic syndrome

A
  • Infection - due to IgG losses, steroids, oedema (esp SBP, cellulitis, sinusitis, pneumonia)
  • Thrombotic disease - due to hypercoagulable state and haemostatic abnormalities
  • Oedema, with risk of anascara (massive generalised oedema)
  • AKI -> CKD
  • Hyperlipidaemia
  • Cataracts and osteopaenia if long term steroid use
61
Q

Nephritic syndrome - core features

A
  • AKI
  • Haematuria (with RBC casts and dysmorphic RBCs)
  • HTN
  • Oedema
    + Oliguria
    + Variable proteinuria
62
Q

Commonest nephrotic and commonest nephritic syndromes

A

Nephrotic - MCD
Nephritic - IgA nephropathy

63
Q

Nephritic syndromes with LOW complement levels + DDx

A

Nephritic syndromes
- PIGN
- Membranoprolifiterative GN
- SLE

Ddx
- Subacute bacterial endocarditis
- Complement mediated thrombotic microangiopathy
- Shunt nephritis

64
Q

Nephritic syndromes with NORMAL complement levels

A
  • IgA nephropathy
  • IgA vasculitis (HSP)
  • Pulmonary-renal diseases eg anti-glomerular basement membrane disease with pulm haemorrhage
  • Granulomatosis with polyangitis
65
Q

Conditions with nephritic urine sediment

A

Nephritic urine sediment = RBC casts, WBC or granules

Conditions:
- IgA nephropathy
- PIGN
- Membranoproliferative GN
- SLE
- Rapidly progressive GN

66
Q

Tubular reabsorption of Na and water

A

Na
- 70% PCT
- 25% aLOH
- 5% DCT
- 1-2% CD (supported by aldosterone)

Water - independent of Na
- through ADH and aquaporin channels in CD

67
Q

Where ions are absorbed in renal tubules

A
68
Q

Diuretics - general mechanism of action

A
  • Inhibit tubular Na reabsorption
  • Causes secondary hyperaldosteronism -> low K, low H -> hypokalaemia and metabolic alkalosis
  • K sparing diuretics (aldosterone antagonists) -> K and H retention -> hyperkalaemia, metabolic acidosis
69
Q

Proximal convoluted tubule

A
  • Reabsorbs 65% Na (Na-H)
  • Key area for regeneration of HCO3 (via carbonic anhydrase)
  • Na reabsorption coupled to reabsorption of glucose (SGLT), amino acids, phosphate, uric acid
  • Defect causes RTA type II (proximal, impaired HCO3 regeneration)
70
Q

Barrter syndrome - overview

A
  • Defect in Na reabsorption in TAL of LOH
  • Presents with metabolic alkalosis and hypokalaemia with LOW to NORMAL BP
  • HIGH urinary Ca
  • Multiple types/genes
  • Type 4 associated with SNHL
  • May have normal to low Mg
  • Usually presents young
71
Q

Frusemide - site and MOA

A

Inhibits NKCC2 transporter in TAL
Therefore also inhibits paracellular reabsorption of Ca and Mg aka HYPOcalaemia

72
Q

Site and MOA Thiazides

A
  • DTC - inhibits NaCl cotransporter (NCCT)
  • Causes upregulation of NKCC2 in TAL, leading to Ca reabsorption aka HYPERcalaemia
  • Gitelman syndrome also due to impaired NCCT (hence similar affects)
73
Q

Gitelman

A
  • Impaired Na reabsorption by NCCT (NaCl cotransporter) in DCT
  • Similar to Thiazide
  • Presents with hypokalaemic metabolic alkalosis (highish bicarb) AND hypomagnesaemia AND lowish BP
  • LOW urinary Ca (due to reuptake of Ca++ in TAL)
  • Presents older, sometimes with tetany due to low Mg
74
Q

Causes of metabolic alkalosis with hypoK

A
  • Bartter, Gitelman (will have low BP)
  • Hyperaldosteronism (will have high BP)
  • Chronic vomiting (will have low Cl due to increased NaCl reabsorption)
  • Diuretic abuse (variable urinary Cl levels - depends on time of use)
75
Q

Water reabsorption in the collecting duct

A
  • Principal cells contain AQP2 (reabsorb water)
  • ADH moves AQP2 from endosomes to the otherwise water impermeable luminal surface
76
Q

Diabetes insipidus (excessive water loss) - types

A
  • Central - vasopressin deficiency
  • Nephrogenic - kidneys fail to respond to ADH
  • Lithium - nephrogenic DI due to decreased expression of AQP2 genes
77
Q

Action of Vasopressin receptors

A

V1 - located on vascular smooth muscle - cases vasoconstriction, increases SVR and increases BP
V2 - located on renal tubular cells - mediate water absorption through activating AQP2 channels

78
Q

RAAS overview

A
  • Macula densa cells in the DCT sense urinary Na and Cl -> when low stimulates juxtaglomerular cells
  • JG cells on afferent arterioles -> secrete renin
  • Renin cleaves angiotensinogen (liver) -> AGI
  • Angiotensin converting enzyme (ACE) in lung cleaves AI -> AII
  • AII = vasoconstrictor + increases aldosterone secretion
  • Nb AII constricts efferent arterioles > afferent
  • ACEI and ARB decrease intraglomerular pressure and therefore filtration (make less urine) -> less proteinuria BUT also may have resultant rise in creatinine
79
Q

Aldosterone action

A
  • Secreted by the zona glomerulosa of adrenal cortex
  • Causes Na reabsorption + K & H excretion
  • Upregulates basolateral Na-K-ATPase - causes concentration gradient with low intracellular Na
  • Upregulates epithelial Na channel (ENaCs - increases apical membrane permeability for Na+
  • Intraluminal movement of Na causes K secretion
  • Intraluminal negativity causes H secretion by alpha intercalated cells
80
Q

Cells in DCT

A

90% principal cells
10% - alpha (acid) and beta (bicarb) intercalated cells

81
Q

How hyper K+ potentiates metabolic acidosis

A
  • Excess K+ enters the cell and in exchange H+ is secreted
  • K+ competes with H+ for secretion at collecting duct
  • HyperK decreases renal ammonia production and so inhibits H+ excretion (ammonia is the chief buffer for H+)
82
Q

How hypoK potentiates alkalosis

A

Augments H-K-ATPase pumps in the collecting duct (type A intercalated cells) which secrete H+ and reabsorb K+

83
Q

Pathophysiology of hyperPTH in CKD

A
  • Phosphate retention (initial trigger)
  • Decreased Ca concentration
  • Decreased calcitriol concentration
  • Increased FGF 23 concentration
  • Reduced expression of CaSR, FGF23 receptors and klotho (co-receptors for FGF23)
84
Q

Proteinuria & albuminuria - levels

A
85
Q

Types of GN

A
86
Q

GN - investigations

A
87
Q

PIGN - management

A

Fluid/salt retention
Diuretics - frusemide
Antihypertensives - frusemide, CCB +/- ACEI

Proteinuria/haematuria may persist for 3-4 mths
Recheck C3 in 8 wks - if post infective will resolve in 8 wks (if still low ?MPGN)

88
Q

IgA nephropathy - treatment

A
89
Q

HSP (IgA vasulitis) treatment

A
90
Q

ANCA associated vasculitis - types

A
91
Q

ANCA-associated vasculitis - overview

A
92
Q

Tubular channels

A
93
Q

Fanconi syndrome - causes

A
94
Q

Cystinosis - overview

A
  • Storage disorder
  • AR
  • Defect in CTNS gene (chr 17) - encodes cystinosin protein (cystine transport protein)
  • > 50 diff mutations, single large gene deletion in ~50%
95
Q

Cystinosis - management

A
96
Q

14 yr boy, seizures, liver disease, renal calculi

A
97
Q

4 mth, Vit D resistant rickets, renal calculi. Elevated cysteine levels in leuks.

A
98
Q

8 yr boy, polyuria, microscopic haematuria, abdominal pain

A
99
Q
A

Written exam (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions