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STEP 2 KAPLAN > rhematology / renal > Flashcards

rhematology / renal Flashcards

1
Q

juvenile idiopathic arthritis (pathophysiology, HLA, presentation)

A
  • vascular endoth hyperplasia + cartilage erosion
  • DR5/8
  • Morning stiffness but pain later (no redness)
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2
Q

juvenile idiopathic arthritis - criteria

A
  1. less than 16 years 2. one or more joints, 3. more than 6 weeks 4. type by presentation in the first 6 months
  2. exclusion of other arthritis, vasculitis, and connect tis)
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3
Q

juvenile idiopathic arthritis - types and presentation

A
  1. pausiarticular: fewer than 5 joints, lower extremities (not hip), almost never upper
  2. polyarticular: 5 or more (large or small), like adults, Rheumatoid nobules (in severe) , may cervical
  3. systemic onset: visceral involvement, daily Q spikes (at least 39) for 2 or more wks, salmon migratory linear or circular rash (trank or extremities)
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4
Q

juvenile idiopathic arthritis - treatment

A
  1. NSAID 2. methotrexate (safest + most efficous 2nd line) 3. corticosteroids (overwhelming infl, systmemic illness, bridge treatment) 4. Opthalmol follow up
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5
Q

juvenile idiopathic arthritis - polyarticular - serology , major problems, outcome

A
  • RF(+): older gitls, hand + wrist erosions, unremitting nodules –> poor
  • ANA(+) –> younger girls –> good
  • seronegatice –> variable prognosis
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6
Q

juvenile idiopathic arthritis - pauciarticular- serology , major problems, outcome

A
  • RF(+): erosion + unremitting nodules –> poor
  • ANA (+) –> younger girls, chronic iridocyclitis –> excelent (except eyes)
  • HLAB27 –> older males –> good
  • Sero (-) –> good
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7
Q

juvenile idiopathic arthritis - systemic - serology , major problems, outcome

A

pauciarticular –> good

polyarticular –> poor

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8
Q

SLE - HLA/age/sex/treatment

A
  • HLA B8, DR2, DR3
  • onset before age 8 is unusual / females
  • NSAID (if no renal), methotrexate, biological drugs, anticoagulation in trombosis, steroids for kidney, cyclophosphamide for severe
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9
Q

pregnant woman with SLE

A

transfer IgG (usually anti-Ro) across placenta at 12-16 weeks –> variety of manifestations –> most important is congenital heart block –> all terminal except heart (permanent pacing)

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10
Q

Leading cause of acquired heart disease in US + japan / age of onset

A

Kawasaki (20% develop coron ar abnorm without treatment) / 80 are under 5 years old

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11
Q

Kawasaki - diagnostic criteria

A
  • fever for 5 or more days nor improved with ibuprofen or acetaminophen + 4 the the following 5
    1. not exudative conjuctivitis (bilateral)
    2. rash (polymorphous non-vesicular) (diapered children may have perineal desquamation)
    3. edema (or erythema of hands or feet)
    4. adenopathy (cervical, often unilateral, 1.5 cm or more)
    5. mucosal involvement (intraoral erythema, strawberry tongue, dry + cracked lips)
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12
Q

Kawasaki - other findings / cardiac findings?

A

irritability, asseptic mening, diarrhea, hepatitis, hydrops of gallbladder, urethritis, otitis media, arhtritis

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13
Q

Kawasaki - heart?

A 
early myocarditis (50%) with tachycardia + decreased ventr function, pericariditis, coronary aneyrysm (2nd to 3rd week
no evidence of long term hear disease if not coronary abnormalities within 2 months
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14
Q

Kawasaki - treatment + management

A 
acute: IV globulin + high dose aspirin
sabacute phase (no fever) low dose aspirin (3-5 mg/kg/day.     Inf vaccine if in winter (Reye) 
management: 2D echo, repeat at 3 wks + if normal at 7 wks. Also ecg + follow platelets
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15
Q

Kawasaki - labs

A

normal to increased wbc, increased ESR, anemia (chronic disease), STERILE pyuria, hepatic transaminases, CSF pleocytosis,
platelets: high/normal in wk 1, significant increase in 2-3 wk (more than a million)

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16
Q

MCC of of nonthrombocytopenic purpura in children? / mechanism / epidimiology / definitive diagnosis

A

Henoch-Schonlein purpura
IgA - mediated vasculitis of small vessels (IgA + C3)
males , 2-8, winter / definitive diagnosis by skin biopsy

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17
Q

Henoch-Schonlein purpura - hallmark presentation

A

pink, maculopapular rash below waist, progress to peteechiae + purpura (red –> purple, rusty brown) crops over 3-10 days (at times in intervals up to 3-4 months)

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18
Q

Henoch-Schonlein purpura - labs

A

increased platelets, wbcs, ESR, IgA, IgM, anemia
urine RBCs, wbc, casts, albumin
anticardiolipin or antiphospolipids antibodies

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19
Q

Henoch-Schonlein purpura - treatment

A
  • symptomatic for self limited
  • steroids (oral or IV) in intestinal complications (dramatic improvement)
  • same treatment for any renal disease if its involved
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20
Q

Henoch-Schonlein purpura - complications

A
  1. renal insufficiency/failure (less than 1% insufficiency
    - -> less than 0.1% to failure)
  2. bowel perforation
  3. scrotal edema
  4. testicular torsion
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21
Q

risk factors for urinary tract infection

A

female: wiping, sex, pregnancy
male: uncircumcised
both: vesicoulateral reflux, toilet-training, constipation, anatopic abnormalities

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22
Q

diagnosis for UTI

A
  1. urine culture (gold standard) 2. UA findings
    need a proper sample (if toiled trained midstream collection)
    possitive if more tan 50.000 (single pathogen) + pyuria
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23
Q

UTI treatment + follow up

A

cystitis: amoxicillin, TMP-SXM, nitrofurantoin
pyelon: oral antibiotics, unless hospitalization
follow up: urine culture in 1 wk after stopping antibiotics –> periodic reassessment for next 1-2 years
- US and cysteourethrogram in reccurent or other complications

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24
Q

vesiculateral reflex - pathogenesis / results

A

occurs when submucosal tunnel between mucosa + detrusor muscle is short or absent
- pyelonephritis –> scarring –> reflux neuropathy (hypertension, proteinria, end stage)

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25
Q

vesiculateral reflex - grading

A
  1. urine reflex into nondilated ureter (anyone)
  2. upper collecting system without dilation
  3. mild to moderate dilation of pelvis + ureter
  4. moderate dilation of ureter +/- tortuosity of ureter
  5. severe dilation + tortuosity of ureter, pelvis, calyces
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26
Q

vesiculateral reflex - diagnosis

A

VCUG for diagnosis + grading

renal scan for renal size, scarring + function (if scarring, follow creatinine

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27
Q

vesiculateral reflex - natural history

A
  • increased scar in grade 5 (less with bilateral 5)
  • majority of 1-4 regress (regardless age or uni/bilateral)
  • tendency to resolve (6-7 years) (lower grade –> better chances)
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28
Q

vesiculateral reflex - treatment

A
  1. medical: based on reflux resolving
  2. careful monitoring for UTIs
  3. surgery if: medical fails, scar, worsening on VCUG or renal scan
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29
Q

Obstructive uropathy - clinical presentation

A
  1. hydronephrosis 2. upper abd or flank pain
  2. recurrent UTI 4. weak + decreased urinary stream
  3. failure to thrive 6. diarrhea 7. other non-specific
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30
Q

MCC of abd mass in newborns (and also other causes)

A
  1. hydronephrosis ureteropelvic junction obstruction

2. multcystic kidney disease

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31
Q

obstructive uropathy - diagnosis

A
  1. palpable abd mass
  2. US (prenatally)
  3. VGUG (in all congenital hydronehrosis + iin any dilation –> to rule out posterior urethral valves)
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32
Q

obstructive uropathy - common etiologies

A
  1. ureteropelic junction obstruction (MC, uni or bilateral)
  2. ectopic ureter (drains outsied bladder –> incontinence + UTIs)
  3. ureterocele (mostly girls)
  4. posterior urethral valves (mostly boys)
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33
Q

posterior urethral valves - characteristics

A
  • MCC of severe obstructive uropathy
  • mostly in boys
  • can lead to end stage renal disease
  • mild hydronephrosis to severe renal dysplasias
  • palpable bladder and weak urinary stream
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34
Q

obstructive uropathy - diagnosis / treatment / complication

A
  • diagnosis: VCUG complication: Potter disease (lung)

- treatment: decompress bladder with catheter, antibiotic (iv), transurethral ablation or vesicostomy

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35
Q

acute poststreptococcal glomerulonephritis - follows (and when) / complement activation through / symptoms

A
  • follows: sore throat in cold weather (after 1-2 wks) or skin in warm (after 3-6 wks)
  • alternative pathway
  • classic triad: edema, hypertension, hematuria
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36
Q

acute poststreptococcal glomerulonephritis - diagnosis

A
  • urianalysis (RBC casts, polymorphonuclear, protein),
  • mild anemia (hemodilation + low hemolysis)
  • low C3 (normal in 7wks)
  • positive throat culture or increased antibodies to strep antigens
  • biopsy if: ARF, nephrotic, more than 2 months, absence of strep, normal Complement
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37
Q

acute poststreptococcal glomerulonephritis - complications + treatment

A
  • hypertension, ARF, CHF, electr abn, acidosis, seizures

- penicillin for 10d, sodium restriction, diuresis, fluid + elctr manegment, control hypertension

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38
Q

MC chronic glomerular disease worldwide - name/clinical presentation / treatment

A
  • Berger disease (IgA nephropathy)
  • Gross hematuria
  • associated with URI or GI infection
  • NORMAL C3
    treatment: control hypertension
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39
Q

Alport syndrome - pathology, mode of inheritance, symptoms,

A
  1. Foam cells 2. XD 3. Asympt hematuria 1-2 d after UTI, hearing defects, occular abnormalitis
40
Q

Alport syndrome - characteristics of hearing and occular abnormalities

A
  1. hearing: bilateral sensorineural, never congenital, females have subclinical
  2. occular: pathognomic is extrusion of central part of lens into anterior chamber
41
Q
  1. MCC of nephrotic sindrome in adults

2. MCC of chronic glomerulonephritis in older children and young adults

A
  1. Membranous glomerulopathy

2. Membranoproliferative glomerulonephritis

42
Q

MCC of ARF in young children (age) , manifestations, causes, pathophysiology

A

HUS less than 4 years old: microangiopathic hemolytic anemia, thrombocytopenia, uremua
causes: E.coli (also shigella, salmonella, campylobacter, viruses , drugs, idiopathic etc)
subendothelial + mesengial depositis of granular amorphous material –> vasc occlusion (endoth injury), glomerular sclerosis, cortical necrosis
5-10 DAYS AFTER INFECION

43
Q

HUS - labs + rare complications / prognosis

A

labs: hb 5-9, helmet cells, burr cells, gragmented cells, reticulocytosis, WBC up to 30000, platelets 20-10000
complications: colitis, intessusceptions, perforations, heart diseaes
more than 90% survivr acute stage.small number EDRD

44
Q

HUS - treatment

A
  1. fluid + electrolites monitor
  2. hypertension
  3. aggressive total parental nutrition
  4. early peritoneal dialysis
  5. no antibiotics if E.coli –> increased risk for HUS
  6. plasmapheresis or fresh frozen plasma - beneficial for HUS not associated with diarhea or severe CNS
45
Q

AR polycystic kidney disease - pathophysiology

A

microcysts –> progressive intestinal fibrosis + tubular atrophy –> renal failure
also liver disease (50): bile duct prolif + ectasia with hepatic fibrosis

46
Q

AR polycystic kidney disease - treatment / prognosis

A

more than 80% survive 10 years, ESRF in more than 50%, dialysis + transplantation

47
Q

AD polycystic kidney disease - treatment

A

control BP (disease progression correlates with degree of hypertension)

48
Q

types of proteinuria (and examples

A
  • transient (fever, exercise, dehydration, cold, CHF, seizures, stress)
  • orthostatic (mc in school aged, rule it out)
  • fixed: glomerulal or tubular disorder (suspect in any patients with more than 1 g/24h or with hypetension, hematuria, or renal dysfunction
49
Q

MC nephrotic syndrome in children and features of nephrotic syndrome

A

steroid-sensitive minimal change disease:

  1. more than 40/mg/m2/h protein
  2. hypalbuminemia (less than 2.5g/dL
  3. edema
  4. hyperlipidemia
50
Q

minimal change disease - age, symptoms, extra labs test (except albumin + protein)

A

age: 2-6,
sympoms: common (diarrhea, abd pain, anorexia), uncommon (hypertension, gross hematuria)
- urine protein/cr more than 2)
- serum creatinine normal or slightly increased
- normal C3/4

51
Q

minimal change disease - treatment, biopsy

A
  • prednisone for 4-6 wks, then taper 2-3 months withiut biopsy –> biopsy if: hematuria, hypertension, HF, no response in 8 wks prednisone
  • sodium restriction
  • if severe: hospitilize, fluid restriction, IV 25% albumin infusio + then diuresis
  • re-treat relapse: may be alternative agents (renal biopsy with evidence of steroid dependency)
52
Q

minimal change disease - complications, prognosis

A
  • infections (immunizations agains pneumonococcus, varieala , check PPD)
  • MC is spontaneous bacter peritonitis (S. pneum)
  • thromboembolism (if aggressive diuresis)
    prognosis: children have relapses but decreased with age
  • if steroid resistance or segmental glomerulscloeris –> poorer prognosis
53
Q

Undescended testes - common in, mechanisms, treatment, prognosis

A

common in preterm (inguinal canal or ectopic), should be descended by 4 months, surgery best at 6 months, but do it at 9-15 months (orchiopexy
if treated: bilateral 50-65% remain fertile, if unilateral 85%
if untreated or delay –> risk for malignancy (mc seminoma)

54
Q

MCC of test pain over 12 / presentation / diagnosis / treatment

A

testicular torsion: acute pain, swelling, tenderness, retracted testis, no cremateric reflex, diagnosis with dolpper color / emergent surgery (scrotal orchipexy) if witin 6h, and less than 360 degrees, more than 90% survives

55
Q

MCC of test pain at 2-11 / presentation / diagnosis / prognosis

A

appendix testes torsion: GRADUAL onset, 3-5 mm inflmaed mass at upper pole, resolves in 3-10 days with bed rest
diagnosis: blue spot seen through scrotal skin, US (if consider test torsion), scrotal exploration if still uncertain

56
Q

testicular tumors - malignant?

A

65%

57
Q

varicocele - age/ surgery if

A

age less than 10

surgery if significant different size of testes, pain o in contralateral testis is diseased or absent

58
Q

epididymitis - definition presentation / labs / treatment

A

ascending, retrograde urethral infection –> acute scrotal pain + swelling (rare before puberty eps male)

lab: pyuria (N. gon or chlamydia but mc undetermined)
treatment: bed-rest + antibiotics

59
Q

MCC childhood leukemia / poor progosis if / sign + symptoms / best test

A

ALL 77% / brief onset + nonspecific
poor prognosis if age less than 1 or more than 10 or more than 100.000 WBCs, chromosomal abnorm, slow response to therapy
- common: bone + joint pain (esp lower)
- bone marrow failure symptoms
- best test: bone marrow aspiration (lymph blasts)
- leukemic cells not see early

60
Q

ALL is both postitive to / progosis

A
  1. CALLA (common ALL antigen)
  2. TdT
    prognosis more than 80% survival in 5 yrs
61
Q

ALL - complications

A
  1. relapse (20%): a. increased ICP or isloated CN palsies, b. testicular relapse in 1-2% of boys
  2. Pnumocysts + other infections
  3. Tumor lysis syndrome (after initial chemo) –> hyperurichemia, K+, Pi (+ low Ca2+) –> treat with hydration + alkalinization + allopurinol
62
Q

ALL - treatment

A
  1. remission induction (98% remission in 4-5 wks with combination drugs
  2. second phase: CNS treatment (systemic + intrathecally)
  3. maintenance phase 2-3 years
63
Q

Hodgkin - age / predisposition / 4 major histologic subtypes / pr

A

age: 15-19, predisposition: EBV + immunodeficiency
types: Lymph predominant, nob scleosis, Mixed, Lympocyte depleted (now considered as high grade non Hodgkin)

64
Q

Hodgkin - clinical presentation

A

depends on location:

  • painless firm cervical or supraclavicular nodes (MC)
  • anterior mediastinam mass
  • β symptoms, lethargy, anorexia, pruritus
65
Q

Hodgkin - diagnosis / treatment / prognosis

A

diagnosis: extensional biopsy on node (preferred)
treatment: determined by stage, size, hilar nodes / chemo + radio
prognosis: overall cure 90% in early stage / 70 in more advance

66
Q

non-Hodgkin - 3 histological subtypes

A
  1. Lymphoblastic usually T cells (mostly mediastinal masses)
  2. Small noncleaved cell lymphoma - B cells
  3. Large cells - T, B, or indeterminate cells
67
Q

non-Hodgkin - presenation / diagnosis

A

presentation depends on location: respiratory symptoms in anterior mediasatinal mass, abdominal pain + mass, hemoatgenous spread
diagnosis: prompot because aggressive –> biopsu, any noninvasive test to determinate stage

68
Q

non-Hodgkin - treatment + prognosis

A

surgical excision of abdominal tumors, chemo, monoclanal antibodies, +/- radiation
90 % ccure for stages I + II (stage: I-IV)

69
Q

Rhabdomyosarcoma - site / increased frequency in

A 
almost any site 
1. head + neck - 40%
2. GI - 20%
3. Extremities - 20%
4. Trunk - 10%  5. Retroperitoneal + other - 10%
Increased frequency in Neurofibromatosis
70
Q

Rhabdomyosarcoma - types + features of every type

A
  1. Embryonal (60%) - intermediate prognosis
  2. Botryoid - vagina, uterus, bladder, naosopharynx (projects, graplike)
  3. Alveolar (15%) - very poor prognosis, trunk + extrem
  4. pleomorphic - adults, rare in children
71
Q

Rhabdomyosarcoma - presentation / diagnosis

A

mass (painful or not), displacement or destruction of normal tissue, easy disseminated to lung + bone
diagnosis: Biopsy, CT, MRI, U/S, bone scan

72
Q

Rhabdomyosarcoma - treatment

A

best prognosis with completely resected (most are not resectabele
chemo pre + postoperatively / radiation

73
Q

Brain tumors / epidimiology / age / site / diangosis / visual changes due to

A

2nd MC malignancy i children / mortality 45%
less than 7 ages
Most are infratentorial
best initial test: CT / best imaginig : MRI
visual changes: CN 3 + 6

74
Q

Infratentorial tumors - aggressiveness / types + locations / treatment + prognosis)

A

low grade / rarely invasive

  1. juvenila pilocytic astrocytoma (cerebellum, surgery radiation +/- chemo, resection –> 80-100% surv)
  2. Maligant astrocytoma (includes GBM)
  3. Medulloblastoma (midline cerebellar)
  4. Brain stem tumors (Diffuse instrict with very poor prognosis)
  5. Ependymoma (posterior fossa)
75
Q

types of suratentorial tumors - types / epidimiology / invasiveness - presentation

A
  1. Craniopharyngioma (7–10% MC) - minimal invasive (Calcification) - panhypopituitarism, growth failure, visuall loss
  2. optic glioma:MC tumor of optic nerve - benign, slowly progressive, increased with NF - Unilatera visual loss. proptosis, eye deviateion, optic atrophy, strabismus, nystagmus
76
Q

suratentorial tumors - treatment

A

craniopharyngioma - Surgery + radiation (NO CHEMO)

optic glioma - if chiasm: radiation/chemo / if proptosis with visual loss: surgery

77
Q

Phemochromocytoma is associated with / retinal examination / treatment

A
  • AD: NF, MEN, Tuberuous sclerosis, Strunger wber, ataxia telangiectasia
  • eye: papiledema, hemorrhages, exudate
  • treatment: removal (but high risk) / preoperative a+b blocker + fluids / need follow up
78
Q

Pheochromocytoma - diagnosis

A

Most tumor with CT (best initial + MRI) but extradrenal masses are difficult
Can use I-131 metaiodobenzylguanide (MBIG) scan –> taken by chromafin tissue anywhere in body

79
Q

Wilms tumor - aka / epidemiology / diagnosis

A

nephroblastoma: 2nd MC malignan abd tumor
age: 2-5, 7% is bilateral
best initial test: US
Abd CT for confirmation
prognosis: 54-97% have 4 year survival

80
Q

Wilms tumor (nephroblastoma) - presentation / treatment

A

most asymptomatic abd mass / Hypertension if renal ischemia
treatment: surgery / then chemo + radio
if blateral (7%) unilateral nephrectomy + partial contralateral

81
Q

neuroblastoma - gene / epidimiology / site

A

C-myc / 8%of childhood malignancies

site: any site, adrenal, retroperitoneal symp ganglia, cervical, thoracic, or pelvic ganglia

82
Q

neuroblastoma - presentation

A
  • firm palpable mass in flank or midlne, PAINFUL, with CALCIUM + hemorrhage
  • initial presentaton: metastasis (lung, bones + skull, orbita;, bone marrow, lymph, liver, skin)
  • ospomyoclonus + horner
83
Q

neuroblastoma - treatment / diagnosis / stage

A

surgery, chemo, radition, stem cells (definitive)

diagnosis: plain xray, CT. MRI (best), spread evaluation (bone scan, bone marrow)
stage: 1 (organ of origin) to 4 (disseminated)

84
Q

neuroblastoma vs pheo according to labs

A

pheo –> esp VMA + metanephrine (norepinephrine)

neuroblastoma –> esp HVA (dopamine)

85
Q

Hypopituitarism - definition / etiology / DDX

A

deficiency of GH +/- other hormones. Due to congenital (AD, AR, X) or acquired (MC is cranioph)
DDX: systemic conditions (weight is less than height), constituitonal delay, familiar short stature, 1ry hypothyroidism, emotional deprivation

86
Q

Congenital hypopituitarism - clinical presentation

A

normal size + weight at berth –> them severe Ggrowth failure in 1st year. Infants present with neonatal emergencies (apnea, hypogl seizures, hypothyroidism, hypoadrenalism in 1st wks) or boys with microphallus + small tests +/- cryptorchydis. Also variety of dysmorphic features

87
Q

hypopituitarism - labs

A
  • low serum IGF-1 or IGF binding-binding protein-3
  • definitive test is GH stimulation
  • other pituitary functions (other hormones)
  • x-rays for destructive lesions
  • Calcifications
  • Bone age - skeletal maturation ,arkedly delayed
  • MRI in all patients with hypopituitarism
88
Q

hypopituitarism - treatment / GH use indications

A

recombinant GF / need periodic thyroid evaluation
Indications for GH: a. documented deficiency b. Turner c. ESRD before transplant d. Prader willi
e. Idiopathic pathologic short stature
f. IUGR without catch up growth by 2 years age

89
Q

hyperpituitarism - etiology / test

A
  • 1ry is rare. MOST are hormone-secreting adenomas.
  • 2ry: Majortiy are deficiencies of target orgnas (negative feedback)
    labs: 1. high low serum IGF-1 or IGF binding-binding protein-3 2. MRI 3. glucose suppression test (to confirm) 4. Thryroid test 5. Chromosomes esp in tall males (XXY, frangile X)
90
Q

hyperpituitarism - management

A
  • treatment only if prediction of adult height (BA) more than 3SD above the mean or if evidence of severe psychosocial impairment
  • trial of sex steroids (accelerates puberty + epiphysial fusion)
91
Q

Precocious puberty - definition / etiology

A

girls: sexual develop less than 8, boys 9
etiology, sporadic + familial in girls, hamartomas in boys
clinical presentation: advanced height, weight, + bone age, early epiphysial closure + early fast advancement Tanner stage

92
Q

Precocious puberty - evaluation + treatment

A

screen: increased LH. Definitive: GnRH IV for a brisk LH respone. If (=) –> MRI
treatment: Leuprolide

93
Q

Incomplete precocious puberty - types / definition / etiology etc

A
  1. premature thelarche: usually isolated, transient (from birth due to maternal estronges). May be 1st sign of true precosious puberty
  2. Premature adrenarche: early adrenal androgen production –> axillary, inguinal + genital hair –> familiar
  3. Premature menarche - very rare
94
Q

causes of congenital hypothyroidism

A

most are 1ry / sporadic or familiar, with or without goiter a. MC is thyroid dysgenesis (hyposlasia, aplasia ectopia –> no goiter)

b. Defect in thryoid hormone synthesis (due to goitrous or AR)
c. transplacental passage of maternal TSH (transient / nmz antibodies)
d. Maternal antithyroid drugs e. Central
f. iodine deficiency or endemic goiter
g. Radioiodine exposure/fetal exposure to excessive iodine (typical iodine antiseptics) (rare in US)

95
Q
  • Hashimoto - age / 1st sign
A
  • adolescent / 1st sign: deceleration of growth
96
Q

Autoimmune polyglandular - types + manifestation

A 
type 1: hypoparathyroidism, addison, Mucocutaneous candidiasis, small number with autoimmune thyroditis 
type 2 (Schmidt syndrome)L addison, DM1, +/- thyroditis

STEP 2 KAPLAN (2 decks)

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