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STEP 1 (2) > Heme Anatomy > Flashcards

Heme Anatomy Flashcards

1
Q

Erythrocytes- what is their lifespan?

A

120 days

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2
Q

What is the source of energy for RBCs?

A

glucose (90% used in glycolyssis, 10% used in HMP shunt)

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3
Q

What is polycythemia?

A

a disease state in which the proportion of blood volume that is occupied by red blood cells increases. Blood volume proportions can be measured as hematocrit level. A hematocrit of >55% is seen in polycythemia.

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4
Q

What is anisocytosis? Poikilocytosis?

A

anisocytosis- varyng RBC sizes

poikilocytosis- varying RBC shapes

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5
Q

What are these?

A

platelets

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6
Q

Describe the function of platelets

A

these are derived from megakaryocytes and when activated by endothelial cell injury, aggregate and interact with fibrinogen to form a platelet plug

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7
Q

What is the life span of platelets?

A

8-10 days

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8
Q

What are the contents of dense granules in platelets?

A

adenosine diphosphate (ADP), adenosine triphosphate (ATP), ionized calcium (which is necessary for several steps of the coagulation cascade), histamine and serotonin

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9
Q

What are the contents of alpha granules in platelets?

A

insulin-like growth factor 1, platelet-derived growth factors, TGFβ, platelet factor 4 (which is a heparin-binding chemokine) and other clotting proteins (such as thrombospondin, fibronectin, fibrinogen, factor V, and von Willebrand factor).

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10
Q

Approximatly 1/3 of the platelet pool is stored where?

A

the spleen

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11
Q

Thrombocytopenia or decreased platelet function results in ______

A

petechiae

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12
Q

What is the receptor for vWF?

A

GpIb

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13
Q

What is the receptor for fibrinogen?

A

GpIIb/IIIa

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14
Q

What are the types of leukocytes?

A
  • granulocytes (neutrophils, eosionphils, basophils)
  • mononuclear cells (monocytes, lymphocytes)
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15
Q

What is a normal WBC?

A
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16
Q

What is a normal WBC differential?

A

Neutrophils (54-62%)

Lymphocytes (25-33%)

Monocytes (3-7%)

Eosinophils (1-3%)

Basophils (0-0.75%)

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17
Q

What are these?

A

Neutrophils

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18
Q

Neutrophil granules (not azurophilic granules) contain what?

A

ALP, collagenase, lysozyme, and lactoferrin

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19
Q

Neutrophil azurophilic granules (aka lysosomes) contain what?

A

MPO

B-glucuronidase

proteinases

acid phosphatase

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20
Q

Hypersegemented polys (5+ lobes) are seen in what?

A

vit B12/folate deficiency

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21
Q

Increased neutrophil bands reflect what?

A

states of increased myeloid proliferation (bacterial infection, CML)

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22
Q

What are the important neutrophil chemotractants?

A

C5a, IL-8, kallikrein, PAF

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23
Q

What is this?

A

monocyte

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24
Q

Monocytes differentiate into ________ in tissue

A

macrophages

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25
What is this?
macrophage
26
How are macrophages invovled in septic shock?
Lipid A from bacterial LPS binds to CD14 on macrophages to initiate septic shock
27
What are the roles of eosinophils?
-defend against helminthic infections (major basic protein and histaminase)
28
What are the main causes of eosinophilia?
**NAACP** **N**eoplasia **A**sthma **A**llergic processes **C**hronic adrenal insufficiency **P**arasites
29
Basophilia is uncommon but can be a sign of \_\_\_\_\_\_\_\_\_\_
myeloproliferative disease, particularly CML
30
How do mast cells work?
They can bind the Fc portion of IgE to its membrane, and cross-linking causes degranulation, which releases histamine, heparin, and eosinophil chemotactic factors
31
T cells can differentiate into what?
- Cytotoxic T cells (express CD8, recognize MHC I) - Helper T cells (express CD4, recognize MHC II) - Treg cells
32
Lymphocyte
Plasma cell
33
T or F. IgM crosses the placenta
F. Only IgG
34
Describe erythroblastosis fetalis
Rh (D)- mothers exposed to Rh+ blood from babies (often during delivery) may make anti-D IgG Abs. In subsequent pregnancies, these Abs can cross the placenta causing hemolytic disease of the newborn if it is Rh+
35
How is erythroblastosis fetalis prevented?
RhoGam in 3rd trimester (28 weeks) to bind any fetal blood before maternal IgG can be made
36
Describe the kinin cascade
kallikrein activates bradykinin (ACE inactivates bradykinin) from HMWK resulting in: - vasodilation - increased permaebility - pain
37
Describe the intrinsic coagulation pathway
collagen, BM, platelets, and HMWK can activate XIIa from XII XIIa activates XIa XIa activates IXa IXa complexes with VIIIa
38
How is VIIIa activated?
thrombin (IIa)
39
Describe the extrinsic coag pathway
VIIa is activated (aka tissue factor)
40
Describe the common coag pathway
VIIa activates Xa, which complexes with some Va and together they activate thrombin (IIa) from prothrombin. Thrombin then activates more Va and VIIIa, activates XIIIa and converts fibrinogen to fibrin (Ia) which cross-links XIIIa molecules
41
What things prevent the activation/action of Xa?
- LMWH (heparin) and heparin - Direct Xa inhibitors (apixaban, and rivaroxaban) - fondaparinux
42
What things prevent the activation/action of IIa (aka thrombin)?
- heparin (best) - LMWH (daltepan, enoxaparin) - direct thrombin inhibitors (argatroban, bivalirudin, dabigatran)
43
How is plasmin activated?
tPA alte**plase**, rete**plase**, tenecte**plase** streptokinase
44
What does plasmin do?
breaks down fibrin to destabilize clots
45
What steps of the coag pathway require Ca2+ and phospholipids?
-activation of: VIIa, Xa (by both VIIa and IXa/VIIIa), IIa
46
What inhibits activation of plasmin?
aminocaproic acid
47
What coag rxns require reduced K+?
activation of II, VII, IX, X, proteins C and S
48
How does warfarin work?
it inhibits the enzyme vitamin K epoxide reductase, which is needed to reduce K for coag activation
49
What is hemophilia A? B? C?
lack of: A: factor VIII B: factor IX C: factor XI
50
How is protein C activated?
thrombin-thrombomodulin complex on endothelial cells
51
What does protein C do?
binds to protein S and cleaves and inactivates Va and VIIIa
52
What does antithrombin do?
inactivates II, VII, IX, X, XI, and XII (heparin enhances this action)
53
What is a Factor V Leiden?
mutation making factor V resistant to protein C
54
What is the first step in coagulation?
endothelial injury causes transient vasoconstriction via neural stimulation reflex and endothelin
55
What is the second step in coagulation?
vMF (from Weibel-Palade bodies of endothelial cells and a-granules of platelets) binds to exposed collagen
56
What is the third step in coagulation?
platelets bind vMF via GpIB at the site of injury and undergo a conformational change, releasing ADP and Ca2+
57
What is the role of ADP in coag?
it allows platelets to adhere to endothelium and causes expression of GpIIb/IIIa expression on platelets
58
What is the fourth step in coagulation?
fibrinogen binds to GpIIb/IIIa and links platelets (this completes primary hemostasis; secondary hemostasis then occurs via the coag pathway)
59
Again one of the initial parts of hemostasis is the binding of vMF to damaged endotheium and then binding of platelets via GpIb. Lack of vMF is seen in what disease?
von Willebrand disease
60
Again one of the initial parts of hemostasis is the binding of vMF to damaged endotheium and then binding of platelets via GpIb. Lack of GpIb is seen in what disease?
Bernard-Soulier syndrome
61
What drugs prevent ADP from binding to the platelet and inducing expression of GpIIb/IIIa?
clopidogrel, prasugrel, ticlopidine
62
Again, GpIIb/IIIa on platelets bind fibrinogen to link platelets to each other. Lack of GpIIb/IIIa is seen in what disease?
Glanzmann thrombasthenia
63
What drugs inhibit the action of GpIIb/IIIa?
abciximab eptifibatide tirofiban
64
TXA2 is also a pro-coagulant released during platelet activation. Formation of TXA2 from arachidonic acid is inhibited by what drug?
Aspirin
65
\_\_\_\_\_ activates vMF to bind GpIb
Ristocetin

STEP 1 (2) (16 decks)

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