Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MCC Part 1 > Hematology > Flashcards

Hematology Flashcards

1
Q

Fever of unknown origin

A
  • body temp >38.3 on >1 occasion
  • duration >3wk
  • no dx after 3d inpatient eval or 3 outpt apt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hyperpyrexia

A

excessive fever >41.5 caused by increase in body’s thermal set point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hyperthermia

A

increase in body temperature beyond the body’s thermal set point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Exogenous pyrogens

A
  • substances (microbial cell wall components, Lipopolysaccharides on bacteria) that induce formation of endogenous pyrogens from host cells (macrophages)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pyrogenic cytokines

A

cytokines (IL-6) that act on hypothalamus to increase body temperature by releasing PGE2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Antipyretics mechanism of action

A

Inhibit synthesis of PGE2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Corticosteroids mechanism of action

A

Inhibit phospholipase A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ASA and NSAID mechanism of action

A

Inhibit cyclooxyrgenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cell-mediated immunity

A
  • composed of T lymphocytes, macrophages, and NK cells
  • major defence against intracellular pathogens
  • cytotoxic T cells directly attack and lyse host cells expressing foreign antigens
  • helper T cells stimulate B cell proliferation and production of immunoglobulin (Ab)
  • reticuloendothelial system = monocyte-derived phagocytes in liver, spleen, LN, lung that clear circulating microorganisms
    defects predispose to intracellular pathogen infection - bacteria, fungi, parasitic, viral (various species)
    vs. hypogammaglobulinemia and asplenia predispose to infection with encapsulated bacteria (S. pneumonia, H. influenza, N. meningitidis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Humoral immune system

A
  • Ab, complement system, phagocytes
  • defends against extracellular pathogens (encapsulated bacteria)
  • Ab produced by mature B cells that recognize and bind foreign antigens
  • proteins of complement system can act as opsonins, ‘tagging’ pathogens for destruction by phagocytes - terminal complement proteins can directly kill some pathogens via membranes attack complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Neutrophils re: immunity

A
  • engulf and destroy pathogenic microbes
  • circulating neutrophils localize sites of infection via adhesion molecules expressed by endothelial cells
  • diapedesis into extravascular space and further localize via chemokine and chemoattractants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Vaccinations in asplenic patients

A

S. pneumo
HiB
N. meningitides
Influenza

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

T cells

A
  • primary mediators of CMI

- Ab production requires intact T-cell number and function (stimulation of B cell proliferation by IL2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Leukocytosis

A

high WBC count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Leukopenia

A

low WBC count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Neutrophils and what are derived from the same common progenitor?

A

erythrocytes, megakaryocytic, monocytes
proliferation from common progenitor via IL-3 and GM-CSF
later differentiation via granulocyte colony-stimulating factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Migration of neutrophils

A

To sites of infection or inflammation via paracellular and transcellular routes through endothelial cell layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Are polymorphonuclear leukocytes (PML) granules toxic?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Neutropenia

A
  • ANC <1.5 x1^9/L
  • decreased production (primary marrow disorder, B12/folate deficiency, infection/sepsis, drugs)
  • increased destruction (autoimmune disease, drugs)
  • sequestration (splenomegaly)
  • constitutional/normal variant (African descent)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Neutrophilia

A
  • ANC >7.5 x10^9/L
  • increased production (reactive, myeloproliferative disease)
  • decreased destruction (hyposlenism, asplenism)
  • decreased margination (drugs, vigorous physical exertion, stress)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Lymphocytosis

A

> 4 x10^9/L

  • infection (often viral, pertussis, toxoplasmosis)
  • hypersensitivity (drug induced, serum sickness)
  • neoplastic (ALL, CLL, lymphoma)
  • stress (cardiac, trauma, status epileptics, post-splenectomy)
  • autoimmune (RA, malignant thymoma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Leukemoid reaction

A
  • persistent neutrophilic with ABC 30,000-50,000/ microL; circulating neutrophils tend to be mature, not globally derived (vs. leukaemia)
  • often with septicaemia and severe bacterial infections (shigellosis, salmonellosis, meningococcemia)
  • if 12% all cells immature then LEFT SHIFT (rapid release of cells from bone marrow)
  • may see increased band forms
  • higher degree of left shift = more immature neutrophil precursors = serious bacterial infection, trauma, burns, surgery, acute hemolysis, hemorrhage
23
Q

BCR-ABL

A

aka Philadelphia chromosome

CML

24
Q

Primary hemostasis

A
  • platelets and vWF
  • endpoint = platelet plug formation
    bleeding - mucocutaneous (epistaxis, gingival, menorrhagia, petechia/ecchymoses)
  • immediate onset of bleeding after injury
25
Q

Secondary hemostasis

A
  • coagulation cascade
  • result in fibrin cross linking = reinforcement and stabilization of platelet plug
    bleeding - deep tissue (hemarthrosis, intramuscular hematoma)
  • delayed onset of bleeding after injury
26
Q

Intrinsic coagulation pathway

A 
collagen (injured vessel) = XII -> XIIa
XIIa = XI -> XIa
XIa = IX -> IXa
platelet phospholipids, calcium, VIIIa 
to common pathway
27
Q

Extrinsic coagulation pathway

A

Tissue factor = VII -> VIIa
platelet phospholipids, calcium
to common pathway

28
Q

Common coagulation pathway

A 
IXa + VIIa = X -> Xa
platelet phospholipids, calcium, Va 
= II -> IIa (thrombin) -> XIII 
IIa = fibrinogen -> fibrin
XIIIa = fibrin -> cross linked fibrin
29
Q

Tests for hemostasis

A

primary
- platelet count, platelet function test
secondary
- PTT: intrinsic pathway factors (VII, IX, XI, XII), monitors heparin tx
- PT/INR: extrinsic pathway factor (VII), monitors warfarin tx
- TT (thrombin time): measures fibrinogen deficiency or reduced prothrombin activation

30
Q

PTT 1:1 dilution

A
  • if PTT corrects with 1:1 dilution = absolute deficiency in factor level
  • if PTT remains high = factor inhibitor present
31
Q

Ddx hypercoagulable state

A

inherited - thrombopilia

  • antithrombin deficiency
  • protein c & s deficiency
  • factor V Leiden
  • prothrombin 20210 mutation

acquired

  • cellular elements (hypercoagulability) - malignancy, pregnancy, OCP, HRT, HIT, DIC, TTP, other
  • vascular endothelium - surgery, trauma
  • circulatory - pregnancy, immobilization, a. fib
32
Q

HIT with subsequent thrombosis

A
  • patient has Ab to PF4-heparin complex
  • reduction in platelet count and 30-fold increase risk of thrombosis
  • d/c heparin and cannot replace with LMWH (cross reactivity) or warfarin (skin necrosis)
  • switch to direct thrombin inhibitor or heparinoid anticoagulation
33
Q

Diagnostic testing re: VTE/ hypercoagulable

A
  • compression U/S gold standard veins above calf
  • V/Q scan if PE (not if parenchymal lung disease present)
  • spiral CT if PE (not if reduced renal function or pregnancy)
  • pulmonary angiography is fold standard for PE (rarely used - CI if compromised renal function)
34
Q

Ddx splenomegaly

A

Increased splenic function demand

  • clearance of abnormal RBC (thalassemia major, abnormal RBC shape)
  • infection (bacterial, viral, fungal, parasitic)
  • autoimmune (RA - Felty syndrome, SLE, collagen vascular disease, drug rxn)

Altered splenic circulation
- cirrhosis, portal HTN, protein vein obstruction, hepatic vein obstruction, splenic vein obstruction, CHF

Splenic infiltration
- Myeloproliferative disorders, malignancy, amyloidosis, sarcoidosis, storage disease

35
Q

Major causes splenomegaly acronym

A

ICE MASS

  • infectious
  • congestive splenomegaly
  • chronic liver disease
  • extra medullary hematopoesis
  • malignancy
  • amlyoidosis
  • sarcoidosis, storage disease
36
Q

Castell sign

A
  • percussion in 8-9 intercostal space in left anterior axillary line of supine patient elicits resonant note throughout respiratory cycle if spleen normal
  • > castell sign = percussion on full inspiration produces dull note (splenic enlargement)
37
Q

Anemia

A
  • decrease in number of circulating RBC
  • result from reduced production, increased destruction, or blood loss
  • MCV must be taken into account
38
Q

B12 (cobalamin) absorption

A
  • cobalamin-protein complex from diet enters stomach -> stomach acid release cobalamin from protein
  • cobalamin + R proteins (parietal cells)
  • pancreatic enzymes in stomach release cobalamin from R-protein
  • cobalamin binds intrinsic factor -> to terminal ileum
  • cobalamin-IF complex binds cubuilin (R on mucosal cells in ileum) = endocytosis
  • cobalamin binds transport proteins -> TCII-cobalamin complex endocytose; cobalamin released and converted to coenzymes
39
Q

B12 deficiency causes

A

Decreased intake - vegans
Altered metabolism
- pernicious anemia (antibodies to parietal cells or IF)
- achlorhydria (acid needed to release cobalamin from protein)
- H2 blockers (decrease IF secretion)
- postgastrectomy
- pancreatic insufficiency (can’t digest R-binders off)
Decreased absorption
- ileal disease
- celiac disease
- pancreatic insufficiency

40
Q

Neuro sx B12 deficiency

A 
dementia
peripheral neuropathy (esp. lower limbs)
subacute combined degeneration - cortocospinal tract (spasticity, hyperreflexia) and dorsal column (decreased proprioception and vibration sense)
41
Q

Fe-deficiency labs

A
  • ferritin = ++ decreased
  • serum iron = decreased/normal
  • TIBC = increased/high normal
  • % saturation = ++decreased
42
Q

Ddx microcytic anemia

A

MCV <80fL

  • iron deficiency
  • thalassemia
  • anemia of chronic disease
  • lead poisoning
  • siberoblastic anemia
43
Q

Ddx normocytic anemia

A 
MCV 80-100fL
Low/normal reticulocytes
- anemia of chronic disease
- renal failure
- combined iron and B12/folate deficiency
- marrow infiltration
- aplastic anemia

High reticulocytes

  • acute blood loss
  • hemolysis
  • splenic sequestration
44
Q

Ddx microcytic anemia

A

MCV >100fL

  • megaloblastic (B12/folate deficiency, drugs)
  • liver disease
  • EtOH
  • MDS
  • hypothyroidism
  • reticulocytosis (response to hemorrhage or hemolysis)
45
Q

Polycythemia

A

Increase in hemoglobin (increase RBC mass or decrease plasma volume)

  • primary = polycythemia vera
  • secondary = increased EPO
46
Q

Ratio of RBC mass to plasma volume

A

Hemoglobin and hematocrit

- sensitive to changes in either RBC mass or plasma volume

47
Q

Polycythemia vera characteristics

A
  • absolute increase of RBC mass and decreased EPO
  • median age dx 60
  • venous and arterial thrombosis in unusual sites
  • headache
  • blurry vision
  • erythromelagia
  • gouty arthritis
  • pruritus
  • splenomegaly
  • easy bleeding (GI bleed, epistaxis)
48
Q

Polycythemia vera dx

A

Dx requires both major criteria and one minor criterion OR first major criterion and two minor criteria:
Major criteria
- elevated hemoglobin (>185 males, >165 females)
- JAK2 mutation
Minor criteria
- hyper cellular bone marrow with trilineage myeloproliferation (panmyelosis)
- decreased serum EPO
- endogenous erythroid colony growth in vitro

49
Q

EPO stimulation, production, action

A

Stimulation - reduced oxygenation of blood
Production - peritubular kidney cells
Action - bone marrow, increase RBC production

50
Q

Lymphadenopathy and ddx

A

LN >1cm = abnormal
- LN have cortex and medulla (germinal enters in cortex)

DDx

  • infectious - viral, bacterial, fungal, parasitic
  • malignancy - lymphoma, leukaemia, metastatic CA
  • immunologic/ inflammatory - serum sickness, collagen vascular disease, drug hypersensitivity
  • other - sarcoidosis, amyloidosis, endocrine (hyperthyroidism), storage disease
51
Q

Lymphatic system constituents

A

LN and vessels
Thymus
Spleen
Peyer patches in gut

52
Q

Activation of adaptive immunity

A

Recognition stage
- antigens recognized by lymphocytes and macrophages
Proliferation stage
- dominant lymphocytes proliferate and differentiate into cytotoxic (killer) T cells or B cells
Response stage
- cytotoxic T and B cells perform cellular and hum oral functions
Effector stage
- antigens destroyed or neutralized through action of antibodies, complement, macrophages, and cytotoxic T cells

53
Q

LN characteristics (normal, inflammation, lymphoma, metastatic)

A

normal - soft, discrete, mobile
inflammation - tender, mobile
lymphoma - large, rubbery, non-tender, mobile
metastatic cancer - hard,non-tender, matted, non-mobile

MCC Part 1 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions