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clin med > heme > Flashcards

heme Flashcards

1
Q

major functions of blood

A

transport (O2, CO2, nutrients, hormones)

immunity (WBCs)

hemostasis (stop bleeding)

homeostasis (provide optimal environment to
maintain steady state (pH, ions, temp, nutrient supply)

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2
Q

main role of RBCs

A

transportation of oxygen

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3
Q

how long do RBCs survive?

A

4 months (120 days)

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4
Q

precursor RBC in bone marrow

A

erythroblast

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5
Q

what are platelets?

A

essential for blood coagulation
much smaller than leukocytes
represent bits of the cytoplasm of megakaryocytes
largest precursor cells in the bone marrow
short survival, about 10 days

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6
Q

most numerous of the WBCs in an adult

A

neutrophils

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7
Q

what are bands?

A

slightly less mature neutrophils that have a non-segmented or band-shaped nucleus - neutrophils which have just been released from the bone marrow

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8
Q

sites of hematopoiesis

A

yolk sac
liver and spleen
bone marrow

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9
Q

what is a granulocyte?

A

WBC that is filled with microscopic granules
little sacs containing enzymes that digest microorganisms

innate immune system

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10
Q

role of basophil

A

secretory cell which mediates the hypersensitivity reaction

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11
Q

what is the largest cell in the peripheral blood?

A

monocytes

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12
Q

which WBCs are referred to as mononuclear?

A

monocytes and lymphocytes

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13
Q

what is the flexible inner protein fiber in RBCs?

A

spectrin

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14
Q

hematopoiesis occurs in the red bone marrow of what?

A

axial skeleton and girdles

epiphyses of the humerus and femur

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15
Q

Erythropoietin (EPO) release by the kidneys is triggered by:

A

Hypoxia due to decreased RBCs
Decreased oxygen availability
Increased tissue demand for oxygen

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16
Q

where does the body get iron from?

A

stores iron in Hb, the liver, spleen, and bone marrow

intracellular iron is stored in protein-iron complexes such as ferritin and hemosiderin

circulating iron is loosely bound to the transport protein transferrin

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17
Q

where does RBC breakdown occur?

A

spleen - dying RBCs are engulfed by macrohages. heme and globin are seperated and the iron is salvaged for reuse

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18
Q

what is heme degraded into?

A

Fe recycled ot ferritin or hemosiderin

yellow pigment called bilirubin

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19
Q

what is hematocrit?

A

portion of total blood volume that is RBC

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20
Q

what is MCV?

A

mean corpuscular volume - average volume/size of a single RBC

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21
Q

abnormal variation in cell volume

A

anisocytosis

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22
Q

when will you see target RBCs?

A

iron deficiency
liver disease
spleen removal
thalassemia

*densely stained central area with a pale surrounding area

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23
Q

what are platelets?

A

cytoplasmic fragments of megakaryocytes - in adults megakaryocytes are exclusively in the bone marrow

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24
Q

what is thrombopoeitin?

A

promotes the grown of Meg-CFC
increases the rate of endomitosis
inhibits apoptosis
stimulates magakaryocyte maturation

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25
Q

does thrombopoeitin promote platelet release?

A

no

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26
Q

what inhibits platelet aggregation?

A

cyclic AMP

- Cyclic AMP increased by prostoglandins

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27
Q

what do anti-platelet drugs do?

A

interfere with prostaglandin synthesis
Aspirin, NSAIDS - COX1 inhibitor
Celebrex - COX 2 inhibitor

interfere with cyclic AMP, ADP binding, and inhibition of the GPIIb/IIIa receptor

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28
Q

acquired platelet dysfunction is from what?

A 
liver disease
cadiopulmonary bypass
uremia
dysproteinemia
myeloproliferative disorders (bone marrow)
alcohol toxicity
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29
Q

inherited platelet dysfunction

A 
giant platelet disorders 
Wiskott-aldrich syndrome
storage pool disorders
glanzmann thrombasthenia
platelet release disorders
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30
Q

what is thrombocytopenia?

A

reduced platelet count in peripheral blood

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31
Q

what causes thrombocytopenia?

A

increased destruction**
decreased production
abnormal pooling or distribution within the body
artifact

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32
Q

what is pseudothrombocytopenia?

A

conformational change in plt membrane
Immune clumps the platelets
cold dependent clumping

*evaluate with smear

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33
Q

what is ITP?

A

immune thrombocytopenic purpura
also called idiopathic autoimmune thrombocytopenic purpura
occurs in both children and adults
caused by platelet specific antibodies which bind to the platelets

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34
Q

this mediates adhesion of platelets to the collagen exposed on endothelial cell surfaces

A

von willebrand factor - acts as a bridge between a specific glycoprotein complex on the surface of platelets and collagen fibrils

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35
Q

vWF is required to bind to and stabilize coagulation factor what?

A

VIII

36
Q

what is aggregation?

A

binding to other platelets via fibrinogen

37
Q

aggregation is mediated by what?

A

fibrinogen receptors (GPIIb/IIIa)- undergo conformational change to active state

38
Q

goal of clotting cascade

A

form fibrin

39
Q

this is initiated when contact is made between blood and exposed negatively charged surfaces

A

intrinsic cascade

40
Q

this is initiated upon vascular injury which leads to exposure of tissue factor

A

extrinsic pathway

41
Q

what pathway does aPTT (activated partial thromboplastin time) evaluate?

A

intrinsic

42
Q

what pathways doe PT/INR (prothrombin time) evaluate?

A

extrinsic

43
Q

factors determining hemoglobin values

A 
age
gender
race
degree of sexual maturation
altitude
heredity
44
Q

what does a high retic count indicate?

A

bone marrow is trying to compensate for anemia

45
Q

symptoms of iron deficiency anemia

A 
asymptomatic
weakness, fatigue, SOB, pallor, dizziness, irritability, decreased exercise tolerance
pica - severe state (ice craving)
palor
koilonychia
tachycardic
glossitis
46
Q

what is sideroblastic anemia?

A

iron fails to bind to pophyrin ring in the erythroblast to produce heme

iron is retained in the mitochondria of the cell

ringed sideroblasts (normoblast with perinuclear halow of blue-stained material) seen on bone marrow smear with prussian blue staining

47
Q

what is sideroblastic anemia characterized by

A

anemia
low retic count
ineffective erythropoiesis with distinctive mophology

48
Q

treatment of sideroblastic anemia

A

remove offending agent

trial of pyridoxine to correct nutritional deficience

49
Q

what are folate and B12 required for?

A

DNA synthesis and regulation

50
Q

B12 and folate deficiency anemia results in what?

A

megaloblastic anemia due to reduced DNA replication

51
Q

clinical manifestations of folate deficiency

A

jaundice due to ineffective erythropoiesis

smooth tongue

52
Q

lab findings for folate and cobalamin deficiency

A 
macrocytosis
howell-jolly bodies
relatively low retic count
mild thrombocytopenia and/or neutropenia
hypersegmentation of neutrophils
megaloblastic changes in marrow
53
Q

will magaloblastic anemia of B12 deficiency respond to folic acid in high doses?

A

yes, but neurologic deficits do NOT respond

54
Q

what is anemia of chronic disease?

A

occurs in setting of chronic disease states associated with inflammatory cytokines or impaired marrow production

induce production of hepcidin - blocks iron absorption from gut

55
Q

causes of anemia of chronic disease

A 
acute and chronic infections
inflammatory and autoimmune diseases (T-cell mediated)
cancer
CKD
liver disease 
MDS (myelodysplastic syndromes)
aging
56
Q

what is aplatic anemia

A

failure of bone marrow due to injury or abnormal expression of pluripotent hematopoietic stem cell

hallmark: bone marrow shows hypocellularity and hypoplasia of all cell lines

57
Q

most common cause of non-immune hemolytic anemia

A

hereditary spherocytosis

58
Q

manifestations of sickle cell disease

A 
chronic hemolytic anemia
pain
dactylitis
acute chest syndrome 
chronic organ damage (spleen, brain, kidneys)
59
Q

most frequent reason for sickle cell hospitalization

A

vaso-occlusive pain crisis

severe, agonizing pain usually starting in limbs

60
Q

transfusion indications in sickle cell

A 
acute stroke or TIA
acute chest syndrome
priapism
splenic sequestration
pre-operative
sympotomatic anemia
aplastic crisis
abnormal transcranial doppler
61
Q

what is not indicated for a sickle cell transfusion?

A

pain crisis

anemia

62
Q

neonatal factor assays for hemophilia

A

should be performed on male infants with a family hstory of bleeding problems or prolonged bleeding after circumcision

hemophilia A - can be diagnosed from FVIII levels in CORD BLOOD collected immediately after delivery

hemophilia B- requires blood to be taken after 6 months of age since FIX is vitamin-K dependent and all neonates have low levels of vitamin K and FIX

63
Q

what should you avoid in patients with severe pain due to bleeding in joints?

A

aspirin and NSAIDS - can exacerbate bleeding

64
Q

what is DIC characterized by?

A

clotting and bleeding

systemic activation of coagulation system results in overactivation of the fibrinolytic system

  • clotting due to circulating thrombin
  • bleeding due to depletion of clotting factors and excessive fibrinolysis
65
Q

why do you have platelet dysfunction in coagulopathy of liver failure?

A

splenomegaly due to portal hypertension - sequesters platelets

ETOH cirrhosis- suppression of thrombopoeisis by toxicity of alcohol or concomitant folate deficiency

66
Q

where are you clotting factors made?

A

liver - except VWF

67
Q

what is the best prognostic indicator in Acute liver failure?

A

factor V level- helps determine need for urgent transplant in patient presenting with encephalopathy

68
Q

treatment of coagulopathy in liver failure

A

not curative, only supportive

novoseven (recombinant human factor VII) - off label use in liver disease but use is restricted due to limited data and excessive cost

69
Q

what coag factors are dependent on vitamin k?

A

II, VII, IX, X

70
Q

what is virchow’s triad?

A

pathrogenesis of a thrombus

endothelial injury
abnormal bloodflow
hypercoagulability (primary - genetic or secondary - acquired)

71
Q

what signs/symptoms are indicative of a DVT?

A

painful, swollen, warm and plethoric extremity with reduced pulse volume

72
Q

what signs/symptoms are indicative of a PE?

A

cough, SOB, hemoptysis, tachycardia

73
Q

hypercoagulable state workup for primary

A

protein C activity - impaired inactivation of factors V and VIII –>unregulated fibrin production

protein S activity - impaired inactivation of factors V and VIII –>unregulated fibrin production

antithrombin III - major inhibitor of thrombin and fibrin formation

factor V leiden

74
Q

hypercoagulable state workup for secondary

A

anticardiolipin antibody
lupus anticoagulant
homocysteine

75
Q

what is factor V leiden mutation?

A

activated protein C resistance

point mutation in gene for Factor V renders it unable to be inactivated by protein C

76
Q

primary HCS screening guidelines

A

VTE

77
Q

primary HCS treatment

A

heparin drip until therapeutic with warfarin

goals: 2-3

78
Q

primary HCS duration of tratment

A

first VTE episode: 6-12 months

recurrent VTE: lifelong therapy

79
Q

who is likely to have antiphospholipid syndrome

A

often associated with Lupus

recurrent pregnancy loss

80
Q

what is antiphospholipid syndrome?

A

autoantibodies directed against phospholipids in cell membranes lining blood vessels

induces endothelial cell damage, predisposing to thrombosis - starts coag cascade with no tissue damage

81
Q

what should you suspect in patients with prolonged aPTT with no clinical bleeding?

A

lupus antigoagulant - clinically not a bleeding disorder. just an antibody that prolongs aPTT by binding to phospholipid in the lab assay

82
Q

what are mixing studies used for?

A

performed on blood plasma used to distinguish factor deficiences from factor inhibitors

83
Q

what are the primary lymphoid organs?

A

thymus and bone marrow

84
Q

what are the secondary lymphoid organs

A

spleen
MALT
lymph nodes
tonsils

85
Q

what is the complication from tumor lysis syndrome (TLS)?

A

marked increase in uric acid excretion can result in ACUTE RENAL FAILURE

  • occurs with rapid release of intracellular potassium and phosphorous into blood stream
86
Q

diagnostic tests for tumor lysis syndrome

A 
LFT and LDH
uric acid
renal function test
serum electrolytes
EKG if hyperkalemic

clin med (12 decks)

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