CANCER/MORE GENES/HEME Flashcards
- hollow “ground glass” nuclei, 2. laminar calcified “psammoma bodies”
- nontender, fixed thyroid nodule
- “orphan annie eyes”
**associated with history of radiation exposure, BRAF mutations
*excellent prognosis
Papillary Carcinoma
- invades thyroid capsule (unlike adenoma)
- Hematogenous spread (skips LN)
- PAX8-PPARy mutations
Follicular Carcinoma
- originates from parafollicular “C” cells
- assoc w/ MEN2A, 2B, familial carcinoma
- RET proto oncogene mutation, Calcitonin tumor marker
Medullary Carcinoma
- MC affects elderly
- rapidly enlarging neck mass
- TP53 mutation
Anaplastic Carcinoma
Anti-nuclear (ANA)
anti-dsDNA
anti-smith
SLE
Anti-ribonucleoprotein (U1 RNP)
Mixed connective tissue disease (SLE, polymyositis, systemic sclerosis)
anticentromere (CREST)- calcinosis cutis, raynaud, esophageal dysmotility, sclerodactyl, telangictasias)
Systemic Sclerosis (limited cutaneous sys sclerosis)
Anti endomysial ab
small bowel villous atrophy
crypt hypertrophy
IDA, dermatitis herpetiforms
Celiac dz (AI intestine disorder)
antimitochondrial ab (AMA)
-anti gp210
-AI damage of small interlobular bile ducts
Primary biliary cholangitis (PBC)
P-ANCA
Primary sclerosing cholangitis (PSC)
anti-LKM1
anti-smooth muscle
AI hepatitis
-Pediatric AI neuropsychological disorder (PANDA)
-Scarlet fever
-
S. Pyogenes GAS
3 C’s
Koplik
rash face –> extremities
Acute dissem encephalitis (within 2 wks after)
Subacute sclerosis panenceph (7-10 YEARS after)
Measles (Rubeola)
Progressive Pancephalitis
Congenital RUBELLA
anti-histone ab
Drug induced lupus
Anti SS A Ro, Anti SS B La
Sjogren
*AI destruction of lacrimal/salivary glands
*dry mouth, eyes, swallowing, poor dental hygiene
columnar metaplasia replaces normal squamous epithelium
*barretts, GERD
esophageal adenocarcinoma
distal 1/3
“slightly raised non blanching rash on butt/extensor, abd pain, joint pain, tenderness. Previous URI last week.”
Urinalysis: INC RBC
Palpable purpura rash
Commonly follows a viral/strep URI in children
*SYSTEMIC VASCULITIS
what is it and what will renal biopsy show
Henoch-Schonlein Purpura: triad of hematuria withOUT any other urinalysis probs, join/abd pain, palpable purpura rash
“IgA immune complex deposits in mesangium”
differentiate from IgA nephropathy (berger): HSP is systemic, Berger is confined to kidneys
New onset hematuria in children, WITH protein in urine
“dense deposit tram track disease”
dense deposit of C3 in center of basement membrane
Membranoproliferative Glomerulonephritis type 2
Normal Light microscopy, with foot processes fusion on Electron microscopy with PODOCYTES
-Nephrotic syndrome: selective PROTEIN in urine, albumin lost
**NO HEMATURIA
Minimal Change disease
“spike and dome” evenly spaced
small IgG deposits along subepithelial aspect of glomerular basement membrane
Nephrotic syndrome in adults: PROTEIN in urine, hematuria is ONLY SEEN IF COMBINED WITH ANOTHER ILLNESS (hep B/C)
Membranous Glomerulopathy
detects presence of Ab AGAINST RBC’s in a recipients SERUM, PRIOR to receiving a transfusion (looks if there will be a possible reaction)
*also used to determine if a Rh- preg woman developed anti-Rh ab during previous preg, which would place current fetus at risk of hemolytic disease of newborn
Indirect coombs test (if there are any AGAINST)
Analyzes a person’s RBCs, To detect recipient antibodies BOUND to surface antigens on donor RBC’s. AFTER THE TRANSFUSION
**diagnoses acute hemolytic transfusion reaction.
DIRECT Coombs test (if there are any BOUND)
Spectrin deficiency
decreases mechanical stability of RBCs, prevents maintenance of normal RBC shape, and increasing susceptibility to lysis in a hypotonic solution
Hereditary spherocytosis
