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PAEDIATRICS > Nephrology > Flashcards

Nephrology Flashcards

1
Q

4S of nephrotic syndrome

A
  • Proteinuria
  • Hypoalbuminemia
  • Generalised edema
  • Hyperlipidemia
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2
Q

Protein/ creatinine ratio in nephrotic syndrome is

A

High

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3
Q

Proteinuria levels in nephrotic syndrome

A

> 3g/d

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4
Q

DDs for edema

A
  • Trauma
  • Allergies ( Drugs, Food)
  • Insect bite
  • Hypothyroidism
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5
Q

Pathophysiology of edema in nephrotic syndrome

A

Reduced albumin in blood cause water to leak out of the blood vessels. Causing cells to enlarge. ( Albumin is hydrophilic)

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6
Q

How to exclude nephritic syndrome before Dx nephrotic Syndrome

A
  • BP high?
  • UOP reduced?
  • Blood in urine?
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7
Q

Protenuria in nephrotic syndrome is due to

A

Increased glomerular permeability causing proteins to leak into filtrate

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8
Q

Types of protein lost due to nephrotic syndrome

A
  • Albumin
  • Immunoglobulin
  • Anti- thrombin
  • Lipoproteins
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9
Q

ADRS of reduced lipoprotein in nephrotic syndrome

A

Lipoprotein brings lipid from blood to liver. Reduced Lipoprotein levels cause serum lipid levels to increase (Hypercholesterolemia)

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10
Q

Typical features of Nephrotic syndrome

A
  • Periorbital edema
  • Scrotal or vulval, leg, ankle edema
  • Ascites
  • Breathlessness due to pleural effusion and abdominal distension.
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11
Q

Periorbital edema is seen at

A

Morning

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12
Q

Main cause of nephrotic syndrome

A

Idiopathic

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13
Q

Secondary causes of Nephrotic syndrome

A
  • Henoch- schonlein purpura
  • Vasculitis, SLE
  • Infections- Malaria, Hepatitis
  • HIV
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14
Q

Acute complications of Nephrotic syndrome

A
  • Hypovolemia
  • Thrombosis
  • Infections
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15
Q

Cause of thrombosis in nephrotic syndrome

A
  • urinary loss of anti- thrombin
  • Thrombocytosis (exacerbated by steroid therapy)
  • Increased synthesis of clotting factors
  • Increased blood viscosity
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16
Q

Sx and signs of hypovolemia

A
  • Abd pain
  • Faintishness
  • Low volume pulse
  • High PCV
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17
Q

Sx of thrombosis (DVT)

A
  • One limb swollen
  • Child refuses to let the swollen limb to touch
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18
Q

Main infections nephrotic child is at risk of getting infected

A

encapsulated bacteria
Pneumococcus

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19
Q

Main risk of infections in nephrotic syndrome

A

Spontaneous bacterial peritonitis

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20
Q

Long term complications of nephrotic syndrome

A
  • Due to steroid therapy
  • Social and psychological problems to child and the family
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21
Q

Complications of steroid therapy

A
  • Failure to thrive
  • Increased susceptibility to infections
  • weight gain
  • Increased BP
  • Diabetes
  • Cataracts
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22
Q

Causes of abd pain in Nephrotic syndrome

A
  • Infections
  • UTI
  • Renal vein thrombosis
  • Reduced BP causing gut ischemia
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23
Q

Sx of Renal vein thrombosis

A
  • Abd pain
  • Abd lump
  • Hematuria
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24
Q

Ix of nephrotic syndrome

A
  • Proteinuria
  • Serum albumin <25g/L
  • serum cholesterol increased
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25
Q

Proteinuria is Dx by

A
  • 3+ or more
  • 24h urine protein excretion
  • Urine protein/creatinine ratio increased
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26
Q

Ix to detect complications in nephrotic syndrome

A
  • FBC,Hb,PCV - Dehydration, infections
  • CRP, Blood culture
  • Urine microscopy for pus cells, pus cells casts, RBC, RBC casts
  • Serum electrolytes
  • Serum creatinine & blood urea
  • Urine culture & ABST
  • USS KUB- Renal V thrombosis
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27
Q

Ix to detect a cause in nephrotic syndrome

A
  • HIV test
  • ESR ( increased in SLE)
  • C3 & C4
  • ANA, dsDNA
  • Hep B SAg
  • Renal Biopsy
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28
Q

Indications for a renal biopsy in nephrotic syndrome

A
  • Onset <6months of age
  • Initial macroscopic hematuria before the onset of proteinuria
  • Persistent microscopic hematuria with HTN
  • Renal failure not attibutable to hypovolemia
  • Persistently low C3, C4 levels
  • Steroid resistance
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29
Q

General Mx of nephrotic syndrome

A
  • normal protein diet
  • Daily weight chart
  • IP/OP chart
  • Temp chart
  • Steroids
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30
Q

Prednisolone dose for nephrotic syndrome

A
  • 60mg/m2/d (6 weeks)
  • then 40mg/m2/d EOD (8 weeks)
  • Then taper the dose
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31
Q

dose of prednisolone

A

5mg (white pills)

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32
Q

Mx of a relapse in nephrotic

A
  • 60mg/m2/d until proteinuria settles
  • then 40mg/m2/d EOD for 2months
  • then taper the dose
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33
Q

Mx of Acute hypovolemia in nephrotic syndrome

A
  1. Saline IV bolus (10mL/kg)
  2. Then Cryo-poor precipitate 10mL/kg
    OR albumin can be used 4.5% albumin
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34
Q

Mx of infections in nephrotic syndrome

A
  • Peritonitis - IV penicillin + 3rd gen cephalosporin
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35
Q
A
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36
Q

Sx of UTI

A

Fever
Burning type abdominal pain
Burning sensation upon passing urine
Increased frequency
Increased urgency

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37
Q

Incidence of UTI

A

Before 1 yr of age - UTI more common in boys (structural abnormalities are common)
After 1yr of age - UTI more common in girls (Urethra & anus are close, contamination is more)

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38
Q

Causative Organisms of UTI

A

E-coli (most common)
Proteus
Klebsiella
Pseudomonas

They are gram negative

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39
Q

Predisposing factors of UTIs

A
  1. Vesico Ureteric reflex (VUR)
  2. Urinary tract obstruction -
    Unilateral obstruction: Pelviureteric junction obstruction, Vesicoureteric juncton obstruction
    B/L Obstruction: Bladder neck obstruction, Posterior urethral valves
  3. Infrequent voiding habits
  4. Voiding dysfunction - Due to nerve abnormalities. Eg: Meningo myelocoele
  5. Constipation
  6. Urethral instrumentation - Catheters
  7. Poor personal hygiene - Inappropriate, prolonged use of diapers, wiping of the perineum from front to back
  8. Impaired host immunity
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40
Q

D/d of abdominal pain + Fever

A

Peritonitis
Diarrhoea
Appendicitis
UTI

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41
Q

Complications of Kidney failure that can lead to death

A

Uremia - Itching, uremic encephalopathy
HTN
Vitamin D will not be activated - Ca not absorbed, weak bones
Metabolic acidosis - Enzymatic processes will be disrupted due to low pH
Pulmonary oedema - due to fluid retention
Hyperkalemia - Heart changes
Decreased EPO - Anemia

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42
Q

C/F of Upper UTI (Pyelonephritis)

A

High fever
May have chills and rigor
Back/Loin pain/tenderness
Ill looking child
Haematuria
Offensive, cloudy urine
May have febrile convulsions

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43
Q

C/F of Lower UTI (Cystitis, urethritis)

A

Dysuria
Increased frequency of urine
Burning Lower abdominal pain
Child is otherwise well looking
No/Mild Fever

44
Q

Why is Upper UTI/ pyelonephritis more dangerous in children?

A

It can damage the growing kidney by forming a scar, predisposing to HTN and Chronic renal failure if the scarring is B/L

45
Q

Upto half of the patients have a structural abnormality of their urinary tract. T/F?

A

T

46
Q

Presentation of UTI in an infant

A

Fever, V, Lethargy/irritability, Poor feeding/failure to thrive, jaundice, septicemia, offensive urine, febrile convulsions (>6M)

47
Q

Ix in UTIs

A

FBC - High WBC (Neutrophils)
Urine Full Report - Pus cells (>10), Hematuria (>5 cells)
Urine culture and ABST - Gold standard. Colony count >10^5 is considered +
USS KUB - For pyelonephritis/pyonephrosis and for structural abnormalities predisposing to infection (VUR, PUV)
Micturating cysto-urethrography (MCUG) - For PUV, VUR
DMSA scan - To look for renal scarring. Done atleast 6M after UTI, cause acute infection might mimic a scar.
DTPA scan - To see renal function ofeach kidney.

48
Q

How is MCUG carried out?

A

Catheter is inserted, a dye is put in. Patient is asked to urinate.

49
Q

Method of urine collection

A

1.Wash external genitalia with water and soap.
Clean catch mid-stream urine sample into culture bottle.
2. Suprapubic aspiration (esp in neonates) - Needle into bladder, A single organism present is considered +
3. Catheter sample -
If + : Doesn’t mean child has UTI
If - : Child does not have UTI

50
Q

How long can a sample of urine being kept before been tested?

A

In room air - 2-4hrs
in fridge - 24hrs
If further delayed than 24hrs, discard sample

51
Q

Mx of an UTI

A
  1. Rx with antibiotics for 7 days
    Upper UTI: IV antibiotics - Cefotaxime, cefuroxime or gentamycin (Nephrotoxic)
    Lower UTI: Oral antibiotics - co-amoxiclav, co-trimoxazole, urinary antiseptics (nalidixic acid (not given if <6M) or nitrofurantoin (not given in infants <3M))
  2. Advice about preventive measures
    High Fluid intake
    Regular voiding, double micturition in PUV
    Treat constipation
    Good perineal hygiene
    Advise to check urine culture, if c/f of non-specific illness develops (Like fever)
    Rx structural abnormalities if present
  3. Low dose antibiotic prophylaxis (Co-trimazole, cephalexin, nitrofurantoin, nalidixic acid) to prevent a 2nd UTI
    Monitor BP, Renal growth and function
    Manage complications which may develop (HTN, RF)
52
Q

Causes of headache in kidney failure

A

Anemia
HTN leading to intracranial bleeding
Uremia

53
Q

Pathophysiology of Vesico-ureteric reflex (VUR)

A

Developmental anomaly of the vesicoureteric junctions.
Ureters are laterally displaced and enter directly into the bladder rather than at an angle, with a shortened or absent intramural course.

54
Q

Causes of VUR

A

Familial
Secondary to bladder pathology
After UTI (temporary)

55
Q

VUR associated with ureteric dilatation can result in?

A

Urine returning to the bladder from the ureters after voiding results in incomplete bladder emptying, which encourages infection.
Kidneys can get infected (pyelonephritis), if there is an intrarenal reflux leading to renal scarring and chronic renal failure.
Bladder voiding pressure is transmitted to the renal papillae, can contribute to renal damage if voiding pressures are high.

56
Q

Ix and Mx of VUR

A

Ix - USS Abdomen, MCUG
Mx - Some VUR gets better when child is aging.
Surgery - Ureteric reimplantation

57
Q

Sites where Urinary tract obstruction can occur

A

Pelviureteric junction
Vesicoureteric junction
At the bladder neck (due to disruption of the nerve supply, neuropathic bladder)
Posterior urethral valve at the posterior urethra.

58
Q

What is PUV?

A

Posterior urethral valve
A mucosal fold arising from posterior urethra.

59
Q

T/F regarding PUV
1. PUV only occurs in males
2. PUV associated with VUR
3. B/L hydronephrosis on antenatal USS in a male infant warrants an USS shortly after birth
4. Associated with a trabeculated bladder wall
5. Mother will have polyhydroamnios

A
  1. T
  2. T
  3. T (To exclude PUV)
  4. T (Due to increased bladder pressure)
  5. F (Oligohydramnios)
60
Q

Presentation of a child with PUV

A

Intermittent stream
Poor urine stream
Dribbling of Urine
Bladder, ureters, kidneys and urethra proximal to obstruction dilates.

61
Q

PUV Ix and MX

A

Ix - MCUG
Mx - Cystoscopic Ablation (Burning of ablation with a cystoscope)

62
Q

Causes of Chronic Renal Failure (CRF)/CKD

A

Recurrent UTI
Structural malformations (40%) - Cysts, PCKD
Glomerulonephritis (25%)
Hereditary nephropathies (20%) - Alport Xd
Systemic diseases - SLE (10%)
Miscellaneous/Unknown (5%)
HTN
Toxins - Agrochemicals

63
Q

Kidney failure + Vision & Hearing impairment

A

Alport Xd

64
Q

C/F of CKD

A

Anorexia and lethargy
Polydipsia and polyuria - Kidneys cannot concentrate urine
Failure to thrive/ Growth failure - GH may not act properly due to kidney dysfunction
Bone deformities from renal osteodystrophy (Renal rickets) - Due to impaired vit. D causing hypocalcemia and hyperphosphatemia leading to secondary hyperparathyroidism
HTN - due to impaired rennin secretion
Acute-on-Chronic RF - Precipitated by infection or dehydration
Incidental finding of protenuria
Unexplained normochromic, normocytic anemia (due to decreased EPO)

65
Q

Ix of CKD

A

Renal function tests - Blood urea, creatinine
USS KUB
ESR, ANA, dsDNA, C3 and C4 levels

66
Q

CKD Mx

A

Prevent Sx and metabolic abnormalities of CKD, to allow normal growth and development and to preserve residual renal function

1.High caloric diet, NG tube feeding if appetite is very low.
2. Prevention of renal osteodystrophy -
Phosphate restriction by decreasing the dietary intake of milk products, CaCO3 as a phosphate binder, activated Vit D supplement help to prevent renal osteodystrophy.
3. Control of salt and water balance and acidosis (HCO3)
4. Anaemia - Recombinant human EPO
5. Hormonal abnormalities -
Recombinant human GH
6. Dialysis and renal transplantation - In end stage renal failure.
7. Potassium containing food should be avoided - fruits, king coconut

67
Q

CKD complications

A

Hyperkalemia - Heart changes
Acidosis
HTN
Anemia
Hypocalcemia
Uremia
Pulmonary edema

68
Q

Pathophysiology of renal osteodystrophy

A

Normal process,
Vitamin D is hydroxylated in the Liver forming 25-OH-Cholecalciferol.
It enters the kidney for further hydroxylation by 1-alpha hyrdoxylase forming 1-alpha-25-dihydroxycholecalciferol (Activated Vit. D).
This allows gut absorption of Ca2+.

In Kidney failure, The second hydroxylation does not occur due to the absence of 1-alpha hydroxylase. Activated Vit. D is not formed leading to hypocalcemia.
This leads to the release of PTH activating osteoclasts releasing Ca in bones leadinf to osteomalacia, rickets, osteitis fibrosa. Secondary hyperparathyroidism.

Since Phosphate cannot be excreted by the kidney, it causes hyperphosphatemia. When phosphate is high it binds with Ca2+ in gut, therefore Ca2+ will not get absorbed.

69
Q

What is Acute Kidney Disease?

A

A sudden, potentially reversible reduction in renal function.
Oliguria is usually present (0.5ml/kg/hour)

70
Q

Types of AKD?

A

Pre-renal
Renal-renal
Post-renal

71
Q

Causes of pre-renal RF

A

Hypovolaemia - Gastroenteritis, Burns, sepsis, hemorrhage, Nephrotic Xd
Circulatory failure
Poor oral intake

72
Q

Causes of Renal-Renal RF

A

Vascular - HUS, Vasculitis (SLE), Embolus, Renal vein thrombosis
Tubular - Acute tubular necrosis (ATN, due to decreased kidney blood supply), ischaemic, toxin (Snake bites), obstructive
Glomerular - Glomerulonephritis
Interstitial - Interstitial nephritis (Rare in children), Pyelonephritis

73
Q

Causes of Post-renal Rf

A

Obstruction:
Congenital - PUV
Acquired - Blocked urinary catheter

74
Q

Ix of AKD

A

S. Electrolytes
USS if obstruction is suspected
BU
Creatinine
Blood gas
pH

75
Q

Mx of AKD

A

Pre-renal : Fluid replacement, circulatory support if ATN is to be avoided.

Renal-renal : Fluid restriction if circulatory overload is present, Diuretic challenge (Frusemide), High caloric, normal protein diet. Manage metabolic abnormalities. Avoid Potassium containing diets like fruits.

Post-renal : Assessment of the site of obstruction and relief by nephrostomy or bladder catheterization.
Surgery can be performed once fluid volume and electrolyte abnormalities have been corrected.

76
Q

Types of metabolic abnormalities in ARF and their Mx

A

Metabolic acidosis - Sodium Bicarbonate
Hyperphophatemia - Calcium Carbonate (phosphate binder), Dietary restriction (Milk, water melon)
Hyperkalemia -
Calcium Gluconate - To stabilize heart
Salbutamol (nebulized/IV)
Glucose and Insulin/ Insulin and Dextrose
Calcium exchange resin
Dietary restriction
Dialysis

77
Q

Indication for dialysis in ARF

A

Failure of conservative Mx
Severe hyperkalemia
Severe hypo/hypernatremia
Pulmonary edema or HTN
Severe acidosis
Multisystem Failure

78
Q

Triad of HUS

A

Hemolysis (Hemolytic anemia)
Uremia (ARF) - Due to decreased blood supply to kidney, kidney function decreases.
Thrombocytopenia

79
Q

Types of HUS

A

Typical and atypical

80
Q

Cause of Typical HUS

A

Secondary to GI infections (Blood and mucous diarrhoea) with verocytotoxin producing E-coli O157:H7 acquired through contact with farm animals or eating uncooked beef.
Less often Shigella.

81
Q

Pathophysiology of Typical HUS

A

Toxins from the organisms enters and damages the GI mucosa and enter into the blood vessels, localises into the endothelial cells of the kidney and damages where it causes the formation of blood clots activating the coagulation cascade.
Platelets deplete due to the formation of microthrombi.
Microangiopathic hemolytic anemia results from damage to RBC as they cross microthrombi on the circulation.
Other organs such as brain (Seizures, unconciousness), pancreas (Insulin secretion problems) and heart may also maybe involved.

82
Q

HUS Ix

A

Renal Function Tests - BU, Creatinine
FBC - Low Hb, Low platelets
Blood picture - Broken down red cells (Schistocytes)

83
Q

Typical HUS Mx

A

Supportive Mx including dialysis.
Good prognosis.
Follow up is needed.

84
Q

C/F of Atypical HUS

A

No diarrhoeal prodrome
Maybe familial
Frequently relapses.
High risk of HTN and CRF
High mortality
Prognosis is not good

85
Q

Childhood HTN Cutoff

A

BP more than the 95th percentile for the age, sex and height

86
Q

How is BP measured in children?

A

Choose correct cuff length - Should cover 2/3rd of the child’s arm.
Child should be seated.
To confirm HTN, Bp should be measured at least 2 times, 15mins apart.
Any arm can be used.

87
Q

Presentation of children with HTN

A

Incidental finding
Headaches
Tiredness due to HF

88
Q

Complications of HTN if not Rx

A

Brain Bleeding
HF
Kidney damage

89
Q

Causes of HTN in childhood

A

1.Renal - Renal parenchymal disease, Renovascular (Renal artery stenosis), PCKD (AR and AD), Renal tumors (Wilm’s tumor)
2. COA - Turner Xd
3. Catecholamine Excess - Phaeochromocytoma (Adrenal gland tumor), Neuroblastoma
4. Endocrine - Congenital adrenal hyperplasia (Ambiguous genitalia, AR), Cushing Xd or corticosteroid therapy, Hyperthyroidism
5. Essential HTN - Idiopathic. A dx of exclusion
6. Artherosclerosis - Common in adults

90
Q

Ix for childhood HTN

A

Renal function tests - BU, Creatinine
USS KUB - Structural kidney problems (Cysts)
Echo - COA
Hormonal assay
Lipid profile

91
Q

Childhood HTN Mx

A

Treat underlying problem if present
Anti-hypertensives:
A - ACEI (Captopril)
B - B-blockers (Proponalol/atenalol)
C - Ca channel blockers (Nifedipine) Commonly given
D - Diuretics (Frusemide)

92
Q

A child presents with an abdominal mass. USS revealed PCKD. Later the child developed liver failure as well. What’s the most likely dx?

A

AR PCKD

93
Q

Causes of Palpable kidneys

A

Unilateral:
Multicystic Kideny
Compenstaory hypertrophy
Obstructed hydronephrosis
Renal tumor (Wilm’s tumor)
renal vein thrombosis

B/L:
AR (infantile) PCKD
AD (Adult) PCKD
Tuberous sclerosis
Renal Vein thrombosis

94
Q

Phaechromocytoma C/F

A

Intermittent HTN
Tachycardia
Profuse sweating
Palpitations

95
Q

Tuberous sclerois C/F

A

Shagreen patches
Ash-leaf macules
Adenoma sebaceum
Kidney tumor

96
Q

AR and AD PCKD C/F

A

AR PCKD - HTN, hepatic fibrosis, progression to CRF

AD PCKD - Adult type, Bengin prognosis in childhood with onset of RF in adulthood.

97
Q

Non-glomerular causes of hematuria

A

Infections (Bacterial, viral, TB, schistosomiasis), UTI - Painful
Stones - Painful
Trauma to genitalia, Urinary tract or kidneys - Painful
Tumors - Painless
Sickle cell disease - Painless/Painful
Bleeding disorders - Painless
Renal Vein thrombosis - Painless/Painful
Hypercalciuria - Can cause stones

98
Q

Glomerular causes of Hematuria

A

Acute glomerulonephritis (Usually with proteinuria)
Chronic glomerulonephritis Usually with proteinuria)
IgA Nephropathy
Familial nephritis eg: Alport Xd
Thin basement membrane disease

99
Q

Ix in hematuria

A

UFR and urine culture
Protein and Ca excretion
USS kidney and urinary tract
Plasma urea, electrolytes, creatinine, Ca, phosphate, albumin
FBC, platelets, clotting screen, sickle cell screen

If suggestive of glomerular hematuria (Eg:SLE)
ESR, complement levels, anti-DNA antibodies
Throat swab and ASO/Anti-DNA B titres - PSGN
Hep B and C Screen and HIV
Renal Biopsy if indicated
Test mother’s urine for blood (If Alport Xd suspected)
Hearing and vision test (If Alport Xd suspected)

100
Q

Glomerular heamaturia presentation

A

Brown urine
Presence of deformed/dysmorphic red cells and casts and is often accompanied by proteinuria.

101
Q

Henoch-Schnonlein Purpura (HSP) is a combination of the following..

A

Characteristic rash
Arthralgia
Periarticular oedema
Abdominal pain
Glomerulonephritis

102
Q

T/F on HSP
1. Common in girls
2. Occurs between 3 and 10 years of age
3. Often preceded by an Upper respiratory infection

A
  1. F. Boys
  2. T
  3. T
103
Q

C/F of HSP

A
  1. Non-blanching (Rash doesn’t disappear on pressing) is the most obvious feature.
    Symmetrically distributed over the buttocks, the extensor surfaces of the arms and legs and the ankles.
    Trunk is spared unless lesions are induced by trauma
    Rash maybe urticarial, rapidly becoming maculopapular and purpuric.
    It is characteristically palpable and may recur over several weeks.
  2. Joint pain (esp knees & ankles) and periarticular oedema. No long term damage
  3. Fever
  4. Colicky abdominal pain (corticosteroids if severe)
    GI petechiae can cause hematemesis and melena.
    Intussusception can occur.
    Ileus, Protein losing enteropathy, orchitis are rare complications.
  5. Renal Involvement (Common but rarely the 1st Sx)
    Over 80% have microscopic or macroscopic hematuria or mild proteinuria.
    Can result in nephritic or nephrotic Xd.
104
Q

HSP commonly have hematuria. T/F?

A

T

105
Q

Most common vasculitis in children.

A

HSP
Due to IgA immune complex deposition

106
Q

Mx of HSP

A

Supportive MX
Mx nephrotic/nephritic Xd if present
Steroids and USS abdomen in abdominal pain.

107
Q

Why are the Lower limbs and buttocks predominantly affected in HSP?

A

Because antibodies and complexes are gravity dependant.

PAEDIATRICS (15 decks)

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