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Heme/Genetics > Hemodynamics/Hemostasis > Flashcards

Hemodynamics/Hemostasis Flashcards

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1
Q

What are elastic vessels?

A

Those with great ability to expand/contract because of systolic pulse.
- ex. aorta, common carotid A

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2
Q

Describe the layers of muscular AA.

A

All arteries start with an intima that’s one cell lining thick.

  • Underneath that is a basement membrane.
  • Underneath that is an internal elastic lamina.
  • Between the two elastic lamina (internal and external) is the tunica media that contains smooth MM fibers that allows constriction or dilation.
  • Outside of that is the tunica adventitia which is continuous with the subQ tissue.
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3
Q

Describe the pressure in small arteries/arterioles and venules.

A

The vessel is under much lower pressure, therefore they don’t have much smooth muscle.

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4
Q

Do lymphatic channels have muscle?

A

No, they are a single layer thick. They rely on surrounding skeletal muscle and subcutaneous tissues pressing on the skin to move the lymph.

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5
Q

How wide is a capillary?

A

1 RBC wide - 7 microns

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6
Q

Why do sickle cell patients get joint pain?

A

Sickle cells get trapped in capillaries around the joint capsule.

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7
Q

What is the importance of tight junctions in epithelial cells?

A

They don’t allow movement between intravascular space and extravascular space.
*think of BBB and barriers in testes and ovaries.

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8
Q

Fenestrated capillary

A

Spaces between the endothelial lining that allow movement of water and ions between the intra and extravascular space.

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9
Q

Where are fenestrated capillaries seen?

A

In the kidneys.

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10
Q

Can albumin move in fenestrated capillaries?

A

No, its molecular weight is too large.

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11
Q

In sinusoids, what moves in/out of fenestra?

A

RBCs

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12
Q

Thrombus

A

Intravascular blood coagulum.

“Blood clot”

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13
Q

What are the 3 sizes of thrombi?

A
  1. Petechiae- 1-2mm often seen in epithelia
  2. Purpura => 3mm
  3. Ecchymosis > 1-2cm subcutaneous
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14
Q

Postmorten intravascular coagulum

A

Forms only from the plasma coagulation factors (no cellular factors at play)

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15
Q

Hemostasis

A

Involuntary mechanism that forms an intravascular blood coagulum (thrombus)

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16
Q

What is happening at the site of hemorrhage?

A
  1. Vasoconstriction (occurring immediately)
  2. Formation of platelet plugs (hemostasis mechanisms into play, primary + secondary)
  3. Fibrinolysis (dissolution of the clot)
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17
Q

Vasoconstriction functions (2)

A
  1. It slows the bleeding.

2. It hemoconcentrates the blood so that the clotting factors pile up at the site because of the reduced blood flow.

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18
Q

Which vessels have smooth muscle coat?

A

Arteries, arterioles, and large veins.

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19
Q

Which vessels do not have muscular coat?

A

Venules and small veins.

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20
Q

Steps to vasoconstriction.

A

Upon injury, the neurogenic and humoral stimuli cause transient vasoconstriction of the vessel lumen, thereby reducing blood flow.

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21
Q

Platelets are produce from…

A

Megakaryocytes

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22
Q

Where are platelets found?

A

Circulating in the blood.

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23
Q

Step after vasoconstriction.

A

Primary hemostasis.

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24
Q

What occurs in primary hemostasis?

A
  1. Receptor-mediated platelet adhesion to ECM
  2. Change in shape/activation
  3. Release of ADP by EC help change shape
  4. Thromboxane A2 helps to stimulate platelets and recruits more
  5. Platelets are stacking up - this is the formation of hemostatic plug.
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25
Q

What occurs in secondary hemostasis?

A
  • endothelial cells are releasing tissue factors (factor 3, thromboplastin, and pro-coagulant glycoprotein acting with factor 7 as an initiator of coagulation)
  • this results in thrombin generation
  • thrombin cleaves fibrinogen to form fibrin
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26
Q

Formation of the permanent plug

A
  • polymerized fibrin and platelet aggregates form the solid plug
  • now anticoagulant activities begin
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27
Q

Anticoagulant activities s/p permanent plug formation

A
  • t-PA (tissue plasminogen activator) is released to break down polymerized fibrin and start to limit the progression of the permanent plug
  • thrombomodulin changes thrombin to anticoagulant factor
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28
Q

Plasminogen activator (t-PA) function

A

It takes fibrin and starts to digest it. These chopped up threads re-enter the circulation and can be measured.

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29
Q

D-Dimer

A

Measures the fibrin splits in circulation. Elevated D-Dimer can signify a clot.

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30
Q

Steps in Platelet Adhesion and Aggregation

A
  • Platelet GpIb receptor attaches to vWF (von willebrand factor) in the extracellular matrix
  • Fibrinogen links GpIIb-IIIa receptors on the platelets
  • ADP from endothelial cells stimulates conformational changes
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31
Q

What does Plavix inhibit?

A

ADP, thus preventing coagulation (used in MI, stent, CABG patients)

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32
Q

What makes vWF?

A

Megakaryocytes in endothelial cells.

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33
Q

Where is factor VIII made?

A

Liver and kidney

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34
Q

von Willebrand-Factor VIII complex

A

Is circulating and can activate factor X

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35
Q

Fibrinolysis function

A
  • Opposes and counteracts coagulation

- Prevents coagulation of blood in areas where it’s not needed

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36
Q

Steps in fibrinolysis

A
  • Thrombin activates plasminogen to plasmin
  • Plasmin degrades fibrin into fibrin-split products
  • Split products can be measured in the blood (D-Dimer) to detect presence of “clot”
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37
Q

The most important PA…

A

t-PA (tissue plasminogen activator)

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38
Q

Functions of plasmin (3)

A
  1. Breaks down fibrin
  2. Interferes with fibrinogen polymerization to fibrin
  3. Is inactivated by plasmin activator inhibitor (PAI)
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39
Q

Activation of Factor 10

A

Continues the clotting cascade to the formation of fibrin.

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40
Q

2 pathways that get you to Factor 10

A

Intrinsic + extrinsic

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41
Q

Coagulation pathway

A

Is a cascade of amplified enzymatic reactions.

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42
Q

What factors require vitamin K as cofactor?

A

2, 7, 9, 10

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43
Q

Plavix vs. Coumadin

A

Plavix is anti-platelet.

Coumadin is an anti-coagulant, meaning it interferes with the clotting cascade.

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44
Q

Which pathway involves factor 7?

A

Extrinsic

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45
Q

How is factor 10 activated?

A

Thromboplastin converts factor 7 to factor 7a.

In the presence of calcium, factor 7a will convert factor 10 to factor 10a.

46
Q

PT (Prothrombin time) asses function of…

A

7, 10, 2, 5, and fibrinogen

47
Q

How is PT run?

A

Adding tissue factor and phospholipid to chelated serum, then adding calcium.

48
Q

Which pathway requires exposure of factor 12?

A

Intrinsic pathway

49
Q

PTT (Partial Thromboplastin time) tests for…

A

12, 11, 9, 8, 10, 5, 2 and fibrinogen (I)

50
Q

What delays the intrinsic pathway?

A

Heparin

51
Q

Define hemorrhage

A

Site of uncontrolled blood loss

52
Q

Direct methods of hemorrhage control

A
  • pressure on site of bleeding
  • application of tourniquets
  • suturing of damaged vessels
  • burning the blood vessel with cautery
  • vasoactive drugs (like epinephrine)
53
Q

You never use ________ with epinephrine when suturing up appendages.

A

Lidocaine

fingers, toes, penis, nose, ears

54
Q

Congenital coagulopathies

A
  • Hemophilia A & B

- von Willebrand Disease

55
Q

Hemophilia A is deficiency in what factor?

A

Factor 8

56
Q

Hemophilia A facts

A
  • sex-linked with high rate of spontaneous mutation (30%)

- Males&raquo_space;> females

57
Q

Hemarthrosis

A

Bleeding into joint space, common with hemophilia A.

- can lead to crippling arthropathy

58
Q

Platelet count, PT, and PTT in Hemophilia A

A
  • Platelet count: normal
  • PT: normal
  • PTT: increased
59
Q

Hemophilia A is deficiency in what factor?

A

Factor 9

60
Q

Hemophilia B factors

A
  • sex-linked

- less common

61
Q

von Willebrand Disease facts

A
  • autosomal dominant disease
  • affecting a coagulation factor produced by the endothelial cells
  • characterized by easy bruising
  • easy bleeding
62
Q

Using hemarthrosis to differentiate Hemophilia A and VWD

A

little to no bleeding into joints with VWD due to location of vWF

63
Q

Acquired bleeding disorders

A
  • vitamin K deficiency

- severe liver disease

64
Q

Coumadin interferes with…

A

Vitamin K, thus interfering with factors 2, 7, 9, 10

65
Q

Which factors are synthesized in the liver?

A

2, 7, 9, 10

66
Q

Sources of vitamin K deficiency

A
  • malnutrition due to ETOH
  • malabsorption
  • biliary obstruction
  • drug therapy
67
Q

Thrombocytopenia

A

Decrease in platelets

68
Q

Thrombocytopenia characteristics

A

Petechial bleeding into the skin, GI tract, mucous membranes, urinary tract, and/or brain.

69
Q

What platelet count impedes coagulation?

A

< 50,000/mL

70
Q

What platelet count may result in spontaneous hemorrhage?

A

< 20,000/mL

71
Q

How does aspirin interfere with function of platelets?

A

Inhibition of thromboxane A2

72
Q

Thrombosis

A

Formation of blood “clots”

73
Q

Virchow’s Triad

A
  1. Alteration of vascular endothelium
  2. Alteration of blood flow
  3. Alterations of blood components
74
Q

How does alteration of blood flow affect thrombi formation?

A

Stasis or turbulence will disrupt the normal laminar flow of blood, bringing platelets in direct contact with the endothelium.

75
Q

What contributes to disrupted vascular flow?

A
  • Atherosclerosis
  • Diabetes
  • Hypertension
  • Bacterial toxins
  • Chemical agents
  • Immunologic reaction
76
Q

Causes of hypercoagulability and inappropriate thrombosis.

A
  1. Excessively viscous blood
    - Polycythemia
    - Hyperproteinemia
  2. Abnormal presence of procoagulants
    - Systemic lupus
    - Various neoplasms
  3. Deficiencies of anticoagulants (Protein C, Protein S, Factor V Leiden)
77
Q

Arterial Thrombi

A
  • Form mostly in areas of atherosclerotic damage to the vessel wall
  • Also seen in the heart wall over areas of previous myocardial infarction
78
Q

Mural thrombus

A

A clot attached to the underlying chamber wall (generally nonocclusive).

79
Q

Occlusive arterial thrombi

A

In smaller arteries (coronary, cerebral, femoral).

80
Q

White (Arterial) Thrombi

A
  • Develop in alternating layers

- Particularly those in the heart and large arteries where there is high blood flow

81
Q

Lines of Zahn

A

Seen as layers of fibrin and aggregated platelets which grossly gives the thrombus a grey laminated appearance

82
Q

Red (Venous) Thrombi

A
  • These usually form in areas of blood stasis (less tendency to develop line of Zahn)
  • Typically found in the deep leg veins
  • Frequently occlusive
83
Q

Capillary Thrombi

A
  • usually due to local endothelial damage.

- generally consist of platelets and fibrin and are not grossly visible

84
Q

Postmortem clots

A
  • form a perfect cast of the vessel in which they form
  • Do not contain lines of Zahn
  • are not firmly attached to the vessel wall
  • have a “currant-jelly” and/or “chicken fat” appearance
  • do not break apart easily because they are mostly fibrous without cellular elements
85
Q

Thrombolysis

A

Neutrophils and monocytes trapped in a thrombus will degrade and phagocytize fibrin and cell debris

86
Q

Lysosomal enzymes from neutrophils and platelets function to…

A

Digest the coagulum and lead to softening

87
Q

Fibroblast & endothelial cell roles in thrombolysis.

A
  • Fibroblasts and endothelial cells from the underlying vessel will infiltrate the thrombus, and initiate fibrinolytic activity
  • Endothelial proliferation may reestablish vascular flow (recanalization) through an occlusive thrombus.
88
Q

Final step of thrombolysis

A

Eventually fibroblastic contraction will shrink the thrombus and it may become incorporated into the wall of the vessel

89
Q

Thromboembolus

A
  • During thrombolysis a thrombus may fragment or become completely detached from its place of origin
  • As it tumbles through the circulation it is referred to as a thromboembolus (because it started as an intravascular coagulum - thrombus)
  • Or just plane embolus (may be many kinds)
90
Q

Clinical manifestations of thrombosis

A

Depend on several factors:

  • The size
  • Number
  • Location
  • Rapidity of development
  • Availability of collateral circulation
91
Q

Infarction

A
  • refers to the process of tissue necrosis secondary to an abrupt reduction in tissue oxygenation.
  • brain infarctions result in liquefactive necrosis
  • tissues that are more highly specialized and/or are more metabolically active, are most sensitive to the effects of hypoxia/anoxia
92
Q

Infarctions are usually the result of…

A

sudden interference with the arterial blood supply to a tissue

  • in some instances, they may be due to obstruction of venous drainage or to conditions that decrease the oxygen carrying capacity of blood
  • slowly developing vascular occlusions are LESS prone to cause infarction since collateral circulation may develop around the obstruction
93
Q

Which tissues are somewhat protected against abrupt hypoxia?

A

Small bowel (rich anasmotic blood supply), lung, and liver (due to dual blood supply).

94
Q

Where do red infarcts occur?

A

Any time you have 2 different circulations.

95
Q

Infarction appearance

A

Grossly, infarcts due to arterial occlusion tend to be wedge-shaped with the apex located close the point of obstruction
- initially, somewhat ill-defined but become progressively demarcated with time

96
Q

White or pale infarction

A
  • occlusion of an artery will result in coagulation necrosis in those tissues that have a single blood supply without significant anastomoses (kidney, spleen, heart, etc.)
  • since blood profusion of the tissue is interrupted, the tissue becomes white/pale
97
Q

Infarction - Clinical Significance

A
  • effects of an infarct depends on the location and size.
  • A small infarct of the myocardium may be clinically insignificant, while one of the brainstem may be fatal.
  • Conversely, a large infarct of the cerebral cortex may result only in neurologic deficits, while a large infarct of the myocardium may cause sudden death
98
Q

3 kinds of emboli

A

Fat, air, and blood

99
Q

Define embolus

A

A free-floating mass that is carried through the vascular system to a point distant to its site of origin or entry.
- often a fragment of pre-existing thrombus (thromboembolus)

100
Q

Embolization

A

Emboli will impact and occlude vessels when the diameter of the vessel becomes smaller than the diameter of the embolus.

101
Q

Systemic (arterial) emboli

A

80-85% arise from thrombi that form on the wall of the atria or ventricle (mural thrombi) on the left side of the heart – potentiated by dysfunctional heart rhythms - A-fib

102
Q

Other sources of systemic (arterial) emboli

A
  • Valve infections with “vegetations”
  • Aortic mural thrombi
  • Fragments of atherosclerotic plaque
103
Q

What tissues are affected by systemic (arterial) emboli?

A

Tissues with high metabolic needs (brain, kidney, heart, intestines)
- others: lower extremities, intestines, spleen

104
Q

Pulmonary embolism from venous thrombus

A
  • Third most common cause of sudden death (after myocardial infarct and stroke)
  • 95% arise from thrombi in the deep LE veins (popliteal, femoral, iliac), travel through enlarging venous channels, through the right heart, and into the pulmonary arteries
105
Q

Pulmonary embolism clinical significance

A
  • depends on size, number and cardiovascular status of the patient
  • Presence should prompt investigation of underlying cause: hypercoagulability or malignancy
106
Q

Fat/Marrow Emboli

A
  • Occur after long-bone trauma when marrow fat is exposed to the venous circulation
  • Fat emboli >20 µm are filtered in the lung
  • Smaller aggregates may pass through the lung and lodge in brain and/or kidneys
107
Q

Fat/Marrow Emboli Clinical Syndrome

A

1-3 days after trauma:

  • progressive respiratory distress
  • CNS impairment (restlessness, confusion, incontinence, and coma)
  • possible renal dysfunction related to the mechanical and chemical effects of the fat
108
Q

Air Emboli

A

May result from trauma or procedures that access large veins:

  • Pelvic fracture
  • Gynecological procedures including delivery
  • Pneumothorax
  • COPD with emphysema
109
Q

Define Disseminated Intravascular Coagulation (DIC)

A
  • Can be acute, subacute or chronic

- Thrombus formation in microvascular channels throughout the body

110
Q

When does DIC occur and from what sites?

A
  • Can occur with sepsis, eclampsia, trauma, multisystem organ failure
  • Bleeding at multiple sites can occur
111
Q

DIC Mechanism

A
  • The coagulations use up platelets, fibrin and coagulation factors
  • Thrombolytic/fibrinolysis factors are triggered
  • Thrombin/thrombomodulin creates anticoagulant effect.
  • Coagulation gone wild
112
Q

How do you treat DIC?

A

With platelets and clotting factors.

Heme/Genetics (15 decks)

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