Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

123 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
cd95; cell surface receptor that triggers apoptosis after binding to fasL -- essential in eliminating activated lymphycotes (limiting immune response)
produced by CTLs -- drills holes thru target cells, followed by injection of cytotoxic proteins like granzyme b
"guardian of the genome": blocks cell cycle at G1 after DNA damage until repaired, else activates apoptosis
apoptosis vs necrosis
apoptosis: cells shrink, organelles densely packed, cytoplasmic blebs, PERIPHERAL AGGREGATION OF CHROMATIN; necrosis: pale chromatin (karyolysis), irregular clumps, shrinking nucleus (pyknotic body), inflammation
follicular lymphoma
a type of small cleaved cell (b cell) lymphomas, t(14;18): b-cl2+IgH
bcl-1+igH; a/w lymphocytic lymphomas, myelomas, some mantle-cell lymphoma
Burkitt's lymphoma: c-myc+IgH
tumor with ganglion cells and rosettes
neuroblastoma (amplification of n-myc --> poor prognosis)
c-myc vs n-myc
c-myc in follicular lymphoma [t(14;18)]; n-myc in neuroblastoma
salicylate vs acetaminophen tox presentation
salicylate causes metabolic acidosis and respiratory alkalosis (RENAL problems); acetaminophen causes nausea, vomiting, abdominal pain, hepatic failure (GI problems)
CO tox presentation
hypoxia, cherry red coloration of lips / mucous membranes (CO-bound hemoglobin binds O2 very tightly, left-shift of hemoglobin curve)
lead vs mercury posioning
lead: anemia, neuropathy, GI problems; mercury: CNS atrophy, gingivitis, gastritis, RENAL tubular changes
reason for increased gastric adenocarcinoma risk in Japanese
diet: polycyclic hydrocarbons in smoked fish
liver/bladder/intestines injury (haematobium --> SCC of bladder;
ITP has no fragmented red cells (schistocytes) because it's immune mediated
platelet threshold for generalized bleeding
20000 platelets
tingible body macrophages
found in germinal center of lymph nodes, seen in benign reactive lymphadenitis (macrophages containing debris from apoptotic b cells)
benign vs malignant lymphadenopathy
benign is usually tender (!?)
causes of decreased ESR
cells settle slower: sickle cell anemia (altered cell shape), polycythemia (too many cells), CHF
DIC associated with which leukemia
AML type M3 (promyelocytic). t(15;17); auer rods contain tissue factor --> release --> clotting
excess fibrous tissue formation in stroam of tumor
erythroblastosis fetalis
newborn, Rh or ABO incompatibility (mom's Abs attack fetal RBCs) --> weakly positive coombs dest, microspherocytosis
Ames test
measures damage to DNA -- correlates well with carcinogenicity; cheap, used for screening
Watson-Schwartz test
detects porphobilinogen in urine, used in dx of porphyria
Widal test
used to dx typhoid fever
Woellner enzyme test
monospot test
porphyria steps
succinyl CoA + glycine --> dALA --> prophobilinogen --> uroporphyrinogen III --> protoporphyrin --> heme
rate limting step of heme synthesis
succinyl CoA + glycine --------dALAsynthetase-----------> dALA
fanconi anemia
congenital aplastic anemia --> pancytopenia, hypoplastic bone marrow; a/w short stature, microcephaly, hypogenitalism, strabismus
used to tx migraines (feverfew the band GIVES irun a migrane)
causes of nystagmus
PCP (not amphetamines), phenytoin
2 main causes of MAHA
DIC and prosthetic valve
primary amyloidosis
Ig light chains (AL protein = amyloid light chain) deposition; deposits in tissues of mesodermal origin (heart, muscle, tongue, kidney)
secondary amyloidosis
AA protein (formed from SAA, serum amyloid-asociated protein); involve parenchymal organs: KIDNEY, liver, adrenals, pancreas, lymph nodes, spleen; usu 2' to chronic inflam disease like RA, TB, osteomyelits, syphilis, leprosy, etc.
varying sizes
varying shapes
basophil vs mast cell
basophils in blood, mast cells in tissue; both involved in allergic (type I hypersensitivity) reaction -- release histamine and heparin
causes of eosinophilia
NAACP (Neoplasm, Asthma, Allergy, Collagen vascular diseases - eg Churg-Strauss, Parasites)
churg-strauss syndrome
type of PAN, aka 'allergic granulomatosis'; small/medium vessel autoimmune vasculitis --> necrosis; a/w eosinophils, granulomas, and pANCA
definition of serum
plasma - clotting factors
dense granules
ADP, Ca++, vasoactive amines
alpha granules
fibrinogen, vWF
serine protease formed from prekallikrein by factor XIIa; used to convert HMWK (kininogen) --> bradykinin and plasminogen --> plasmin
tumor grade vs stage
grade = degree of cellular differentiation; stage = degree of spread (TNM system: Tumor size, Node involvement, Metastases); stage generally has greater prognostic value
Brain mets
50% of brain tumors are mets. "Laura Bush's Skin Kills Glia" (Lung, Breat, Skin-melanoma, Kidney, GI)
Liver mets
"Cancer Sometimes Penetrates Benign Liver" (Colon > Stomach > Pancreas > Breast > Lung)
Bone mets
"P.T. Barnum Loves Kids:" Prostate, Thyroid, Testes, Breast (Both lytic and Blastic), Lung (Lytic), Kidney; Breast and Prostate are most common; Mets >> 1' bone tumors
Cancer Epi, Men
Incidence: Prostate > Lung > Colon/Rectum; Mortality: Lung > Prostate
Cancer Epi, Women
Incidence: Breast > Lung > Colon/rectum; Mortality: Lung > breast (replace male Prostate with Breast)
spur cell (liver damage, eg abetalipoproteinemia)
Burr Cell
Renal disease (TTP/HUS)
distribution of alpha vs beta thal
alpha in africa/asia; beta in mediterranean
HbBarts = gamma4, occurs in alpha thal major (4 missing alpha genes --> hydrops fetalis) -- "Bart's just a KID (hydrops fetalis) who plays with his SLINGSHOT (gamma globins)"
beta4 tetramers, seen in alpha thal minor (3 genes missing)
beta thal hemoglobins
major: HbF (alpha2gamma2 -- fetal hemoglobin); minor: HbA2 (alpha2delta2) + HbF
sickle-cell thal
HbS/B-thal heterozygote: mild to moderate disease
drug causes of aplastic anemia
benzene, chloramphenicol, NSAIDs, alkylating agents, anti-metabolites
non-drug causes of aplastic anemia
radiation, VIRAL (B19, EBV, HIV), Fanconi's anemia, idiopathic, post-ACUTE HEPATITIS
fanconi anemia
AR, defect in DNA repair --> marrow hypofunction, along with hypoplasia of kidney and spleen.
crew cut' on xrays
sickle cell or thal -- indicates extramedullary hematopoeisis
complications of sickle cell
1) aplastic crisis after parvovirus B19; 2) osteomyeltis from Salmonella; 3) autosplenectomy; 4) painful (vaso-occlusive) crisis in deoxygenated/cold/dehydrated environments
cold vs warm agglutinin HA
cold: IgM, ACUTE, triggered by cold, a/w recovery from mycoplasma pneumo / infections mononucleosis infection; warm: IgG, CHRONIC, a/w SLE, CLL, drugs (eg alpha-methyldopa); both cause spherocytosis, coombs positive
hereditary spherocytosis vs autoimmune anemia
both have spherocytosis; HS is coombs negative and can be detected by osmotic fragility test; HS due to ankyrin/spectrin defect
paroxysmal nocturnal hemoglobinuria -- defect in pig1 gene --> defective GPI anchor for proteins that inhibit complement-mediated destruction ==> hemolysis by complement, increased urine hemosiderin
causes of DIC
MCC: obstetric complications (toxemia, amniotic fluid embolus, abruptio placentiae); others: G- sepsis, transfusion, trauma, malignancy
Idiopathic/Immune Thrombocytopenic Purpura: self-limtiing in kids, chronic in adults; anti-platelet IgGs cause platelet destruction and increased production (increased megakaryocytes)
Thrombotic Thrombocytopenic Purpura: ADAMTS13 mutation (vWF metalloprotease deficiency) --> increased vWF --> clumping --> MAHA, depletion of platelets; a/w neuro abnormalities and renal dysfunction (like HUS)
platelet abnormalities
1) ITP; 2) TTP; 3) DIC; 4) Aplastic anemia; 5) Drugs (immunosuppressive); ==> microhemorrhage, increased BT
Coag factor defects
1) Hemophilia A (VIII); 2) Hemophilia B (IX); 3) vWD (defective platelet adhesion, \/ VIII); ==> MACROhemorrhage (hemarthroses, easy bruising, /\ PT and/or PTT)
Henoch-Schonlein Purpura
post-infectious, IgA hypersensitivity vasculitis, hemorrahagic urticaria; GI/renal involvement (IgA nephropathy)
Osler-Weber-Rendu syndrome
aka Hereditary Hemorrhagic Telangiectasia -- AD, localized venous malformations --> hemorrhage
defect of GP Ib
glanzmann's thrombasthenia
defect of GP Iib/IIIa
Hodgkin's lymphoma
Reed Sternberg cells (CD15+ CD30+), localized axial lymphadenopathy, extranodular nodes rare, constitutional sx seen in type B, EBV assoc, bimodal age distribution (young and old), more common in men; good progress: inc lymphocytes, dec RS cells
Non-Hodgkin's lymphoma
multiple lymphnodes, peripheral, noncontiguous spread; usus B-Cell, a/w HIV/immunodeficiency; fewer constitutional sx than HL, peak age 20-40 (inverse of HL)
Hodgkin's lymphoma epi
bimodal age distribution (young and old); more common in men except for nodular sclerosing (most common type -- women > men, young adults)
hodgkin's lymphoma Nodular Sclerosing subtype
NODULAR SCLEROSING: most common, f>m, 20s, excellent prognosis, collagen banding, no a/w EBV, *lacunar* variant of RS cell;
hodgkin's lymphoma, Non-NodularSclerosing subtypes
LYMPHOCYTE PREDOMINANT: young males, excellent prognosis, lots of lymphocytes; LYMPHOCYTE DEPLETED (rare): older males, poor prognosis; MIXED CELLULARITY (more common than both): in between in # lymphocytes and in prognosis
KIDS, most responsive to Tx, can spread to CNS / testes
adults, Auer rods; M3 subtype = APML, t(15;17), responsive to all-trans retinoic acid; a/w DIC (release of auer rods with treatment)
older adults, hepatosplenomegaly, indolent, SMUDGE CELLS, v.similar to SLL (small lymphocytic lymphoma)
Ph chromosome t(9;22); splenomegaly, elevated PMNs; can progress to AML (BLAST CRISIS);
CML vs leukemoid reaction
elevated leukocyte alk phosphatase in leukemoid reaction, very low in CML
ewing's sarcoma
Burkitt's lymphoma: c-myc+IgH
mantle cell lymphoma: bcl-1 / Cyclin D1
follicular lymphoma: bcl-2
M3 type of AML (responsive to all-trans retinoic acid)
Multiple myeloma vs Waldenstrom's
both have M-spike on SPEP, rouleux formations, bence jones proteins; waldenstrom's has hyperviscosity, NO lytic bone lesions
mab against GP Iib/IIIa receptors on activated platelets --> prevents aggregation
consequences of warfarin-induced inhibition of protein C
skin necrosis (seen in first week of warfarin tx)
steps of tumor invasion
1) detachment (downregulation of e-cadherins); 2) adherence to basement membranes (increased laminin, other adhesion molec); 3) invasion of BM (proteolytic secretions, including metalloproteinases, cathepsin D)
what binds integrins
collagen, fibronectin, and laminin
geographic types of burkitt's lymphoma
african: endemic, jaw involvement, a/w EBV; american: visceral organ involvement, sporadic
burkitt's vs follicular
burkitt's: kids, t(8;14), jaw involvement (african type); follicular: adults, t(14;18), generalized lymphadenopathy
dangerous vitamin deficiency in preterm infants
Vit K: hepatic immaturity, gut flora not well established, low vit k content of breast milk (also no vit D)
role or Rb
regulates G1 --> S transition; phosphorylation --> E2F --> goes through checkpoint
regulation of iron
enterocytes: absorbed iron either binds transferrin in blood or ferratin in enterocyte; when dietary iron is high, intestinal cells decrease the amt abosrbed
diff in labs of Factor V Leiden and Antiphospholipid Ab syndrome
antiphospholipid antibody syndrome has elevated PTT (paradoxically, since it's a thrombotic disorder) -- in vitro artifact
heme effects of folic acid deficiency
homocysteinuria (folic acid required for homocysteinuria --> methionine) ==> prothrombotic state
histo of follicular lymphoma
at low mag, aggregates of packed follicles that obscure normal lymph node architecture
lipofuscin vs hemosiderin
hemosiderin is from iron excess, lipofuscin is from "wear and tear"; both look yellow-brown
ALL seen in KIDS
anemia a/w placenta abruptiae
tests for DIC
platelet count (low), fibrinogen levels (low), fibrin degradation products (high)
ALL-B ("3 looks like a B")
AML M2 and M3
Megakaryocytic differentiation
Erythroid differentiation
monoblastic / monocytic
myeloid AND monocytic
AML M1 --> M7
increasing differentiation
mechanism of thrombolytics (streptokinase, urokinase, tPA)
bind and cleave plasminogen --> plasmin --> fibrin cleavage
type of anemia in renal failure
normochromatic, normocytic (decreased epo)
main component of eosinophil granules
major basic protein --> destruction of parasites
target cells a/w
liver disease, thalassemia, and HbC
WBC diff of pts with CML
increased PMNs and metamyelocytes, decreased eosinophils, basophils, and a few blasts
no CNS effects in HUS
DIC has elevated PT and PTT, decreased fibrinogen, and elevated fibrinogen split products; also, DIC doesn't have renal involvement?
lab effects of tPA administration
increased PT and PTT, no change in platelets
pathogenesis of EBV mono
EBV invades B-cells using CD-21 receptor, causes hyperproliferation --> lymphadenopathy and splenomegaly; in peripheral smear, would see elvated CD8+ CTLs