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88 Cards in this Set

  • Front
  • Back
schistocyte
microangiopathic hemolytic anemia
microangiopathic hemolytic anemia
TTP
HUS
DIC
HELLP
Prosthetic heart valves
aortic stenosis
ringed sideroblasts
sideroblastic (iron deficient anemia) iron trapped in mitochondria around nucleus
spherocytes, splenomegaly
hereditary shperocytosis (defect of spectrin/ankryn/band 3.1); IGG-mediated hemolytic anemia (SLE, CLL, some drugs)
Howell-Jolly bodies
present after splenectomy (nuclear fragments in RBCs) auto splenectomy of sickle cell anemia
Target cells
β-thalassemia minor and major; sickle cell disease
Dactylitis
swollen hands/feet due to vasoocclusive bone infarcts
(common presenting sign of sickle cell anemia)
“crewcut” skull xray,
chipmunk face,
hepatosplenomegaly
β-thalassemia major; sickle cell anemia
Megaloblastic anemia
with hypersegmented
neutrophils
folate or vitamin B12 deficiency
Heinz bodies and
Bite cells
G6PD deficiency. Leads to intravascular hemolysis.
Presents with hemoglobinuria and back pain hours
after exposure to oxidative stress.
Defect in ALAS
congenital sideroblastic anemia
Parvovirus B19
infects progenitor RBCs, halting erythropoiesis; leads
to significant anemia with preexisting marrow stress
Pancytopenia
Aplastic anemia (drugs, viral infections, autoimmune);
Myelophthisic process (pathogolic replacement of BM)
Autoimmune destruction
of parietal cells
Vitamin B12 deficiency (ileum can’t absorb vit b12
Unless it is bound to intrinsic factor)
E. coli O157:H7
HUS
Abnormal ristocetin test
Von Willebrand Disease
Auer rods
APL
Elevated D-dimer
DIC; Pulmonary infarction due to PE
Cellular swelling
reversible injury
AL amyloid
Primary amyloidosis
AA amyloid
Secondary amyloidosis
Non-mutated serum
transthyretin
Senile cardiac amyloidosis
Mutated serum
transthyretin
Familial amyloid cardiomyopathy
Aβ amyloid
Alzheimer disease
Amylin
T2DM (derived from insulin—deposits in islets)
Β2-microglobulin
in joints
Dialysis-associated amyloidosis
Giant granules in
Leukocytes
Chediak-Higashi syndrome (autosomal recessive)—also
affected with albinism, blood-clotting disorders, nerve problems (abnormal fusion of intracellular organelles)
Epithelioid histiocytes
Granulomatous inflammation
NADPH oxidase defect
Chronic granulomatous disease (prolonged Th1 activation; defecient respiratory burst)
Mutated Bruton
tyrosine kinase
X-linked Agammaglobulinemia (B cells are blocked at
the pre-B-cell stage); recurrent extracellular bacterial
infections—strep/staph/flu; absence of serum Ig
Hepatic vein thrombosis
Budd-Chiari Syndrome
Anticardiolipin Ab
SLE; false-positive syphilis test
Anti-ribonucleoprotein
antibodies
Sjogren Syndrome (Anti-SS-A/Ro and Anti-SS-B/La)
40% increased risk of developing lymphoma
Anti-DNA topoisomerase
I antibody
Anti-DNA topoisomerase
I antibody
Scleroderma (Scl-70 ab)
Serum Ab against U1
ribonucleoprotein
Mixed connective tissue disease
Anti-Jo-1 Ab
Polymyositis
Asbestos
lung carcinoma/ mesothelioma
EBV
Nasopharyngeal carcinoma; Burkitt lymphoma; B cell/
CNS lymphoma in AIDS
HHV-8
Kaposi sarcoma
HBV/HCV
Hepatocellular carcinoma
HTLV-1
Adult T-cell leukemia/lymphoma (ATLL); only
retrovirus associated with human cancer
High-risk HPV
SCC of vulva, vagina, anus, cervix; adenocarcinoma of
cervix (subtypes 16, 18, 31, 33)
9;22 translocation
CML (and some types of ALL)
8;14 translocation
Burkitt lymphoma (MYC overexpression)
11;14 translocation
Mantle cell lymphoma
14;18 translocation
Follicular lymphoma
Chromogranin
Neuroendocrine cells (small cell carcinoma of lung;
carcinoid tumors)
CD40/CD40L mutation
Hyper-IgM syndrome (no CD40-CD40L interaction
between T cells and B cells= no isotype switching
Persistent viral
infections
lack of cytotoxic T cells
caseating necrosis
TB; resistance to activated macrophages; granuloma
Fas/FasL mutation
ALPS (autoimmune lymphoproliferative syndrome
Damage to renal glomeruli
basement membrane
Goodpasture’s Syndrome (complement/granulocyte-
mediated) Type II HS
AutoAb against TSHR
Grave’s Disease (agonist autoAb) Type II HS
AutoAb against AchR
Myasthenia Gravis (antagonist autoAb) Type II HS
Splenomegaly and
anemia
Autoimmune hemolytic anemia—& lots of other things
Demyelination of
nerve cell axons
MS (Type IV HS)
Destruction of Islets
of Langerhans
T1DM (CD8 and DTH Type IV HS)
Destruction of
thyroid cells
Hashimoto’s thyroiditis (DTH Type IV HS)
AIRE gene mutation
Autoimmune polyglandular syndrome type I, aka
autoimmune polyendocrinopathy-candidiasis-
ectodermal dystrophy (APECED)—no negative selection of T cells in the thymus
FoxP3
IPEX (immune dyregulation, polyendocrinopathy,
Enteropathy, X-linked syndrome) lack of Treg cells
CTLA-4 gene
polymorphism
Graves’ disease, Hashimoto’s disease, T1DM
Poison ivy
Type IV HS; hapten
HLA matching
kidney allograft (not for heart, liver, pancreas, lung)
p53
small cell lung carcinoma, breast cancer
APC
colon cancer
Partial/complete absence
of thymus
DiGeorge Syndrome (absence of T cells)
B cells don’t differentiate
to plasma cells
Common Variable Hypogammaglobulinemia
Reduced platelets and
reduced ab response to
T-independent antigens
Wiskott-Aldrich Syndrome (eczema, thrombocytopenia,
immune deficiency
Bence Jones proteins
in urine
Multiple myeloma
• ADAMTS13
TTP
• GP1b
Bernard-Soulier syndrome (genetic)
• GPIIb/IIIa
Glanzmann thrombasthenia (genetic)
• Factor VIII
Hemophilia A (X-linked)—PTT corrects w mixing study
Coagulation factor Inhibitor (acquired)
• Factor IX
Hemophilia B (genetic)
• vWF
Von Willebrand Disease (aut. dom.= most common)
• CBS
Homocystinuria (thrombosis, MR, lens dislocation, long
slender fingers)
• Protein C/S
Warfarin skin necrosis (increased risk)
• ADA
low T & B cells; low serum Ig (deoxy ATP accumulation)
• MHCII
Bare lymphocyte syndrome (reduced CD4 cells)
• C1 inhibitor
Hereditary angioedema (esp. periorbital edema)
• C3/C4
SLE (hypocomplementemia)—immuno
• CR3/CR4/LFA-1/
MAC-1
LAD (impaired diapedesis) defective β2 integrin gene
• RAG
SCID (absence of T and B cells), Omenn syndrome
• γ5 gene
B-cell immunodeficiency (no surrogate light chain)
• Purine nucleoside
phosphorylase
low T cells (deoxy-GTP accumulation toxic to T cells)
• G6PD/MPO
reduction in respiratory burstgranulomatous disease
• IFNγ receptor
persistent mycobacterial infection; no TNFα in response
to IFNγ
• GPI (absent)
Paroxysmal Nocturnal Hemoglobinuria (DAF isn’t able
to be bound to blood cell surface to protect against
complement)