4-Hemodynamics, Thromboembolitics, and Shock Flashcards

1
Q

What is edema?

A

when the movement of water into tissues exceeds lymphatic drainage, fluid accumulates

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2
Q

What causes edema?

A

results when either increased capillary pressure or diminished colloid pressure causes an increased interstitial fluid

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3
Q

What prefix do we use to tell that there is edema in various cavities?

A

Hydro- (hydrothorax, hydropericardium, and hydroperitoneum (ascites))

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4
Q

What is anasarca?

A

severe and generalized edema with widespread subcutaneous tissue swelling

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5
Q

Why does increased hydrostatic pressure cause edema?

A

when veins are blocked or arterioles dilate, the increased hydrostatic pressure in the arteries squeezes more fluid into the interstitial fluid, causing edema

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6
Q

Why does reduced plasma osmotic pressure cause edema?

A

when there is less proteins in the blood, the osmotic pressure will be smaller than the osmolarity in the interstitial fluid, drawing water into the interstitial fluid causing edema

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7
Q

Why does blocked lymphatics cause edema?

A

If the lymphatics are blocked, they can’t drain the interstitial fluid, causing edema

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8
Q

Edema from increased hydrostatic pressure or reduced protein results in what type of fluid to leak into tissues?

A

Transudate

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9
Q

What medical conditions cause transudate in edema?

A

This is seen in heart failure, renal failure, hepatic failure, and certain forms of malnutrition.

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10
Q

Inflammatory edema is causes what type of fluid to leak into the interstitum

A

exudate

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11
Q

What is hyperemia?

A

it’s an active process in which arteriolar dilation leads to increased blood flow

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12
Q

What is the morphology of hyperemia?

A

Affected tissues turn red (erythema) because of all oxygenated blood accumulation

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13
Q

What is congestion?

A

it’s a passive process from reduced outflow of the blood from a tissue. It can be systemic, from like cardiac failure, or local like in a vein obstruction

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14
Q

What is the morphology of congestion?

A

Tissues turn cyanotic due to RBC stasis and accumulation of deoxygenated blood

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15
Q

The accumulation of what specific cells present in congestion?

A

hemosiderin-laden macrophage clusters

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16
Q

What is a hemorrhage?

A

extravasation of blood into the extravascular space. This may be external or contained within a tissue

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17
Q

What is a hematoma?

A

any accumulation of blood within a tissue.

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18
Q

What are petechiae?

A

1-2mm hemorrhages (“pindots”) on the skin, mucous membranes or serosal surfaces

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19
Q

What causes petechiae?

A

Often from increased intravascular pressure or low/defective platelets

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20
Q

What are the size of purpura?

A

larger (>3mm) hemorrhages

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21
Q

What causes purpura?

A

from trauma, vasculitis, or vascular fragility (amyloidosis).

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22
Q

What are ecchymoses?

A

1-2cm subcutaneous hematomas (bruises)

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23
Q

What prefix do we use to show where blood is accumulating?

A

Hemo- (hemothorax, hemopericardium, hemoperitoneum, or hemoarthosis)

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24
Q

What is normal hemostatis?

A

this is the first stage of wound healing, when the rapid formation of a hemostatic clot is formed

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25
Q

What is the first thing that happens in normal hemostasis, after injury?

A

local secretion of endothelin causes arteriolar vasoconstriction

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26
Q

What occurs during primary hemostasis?

A

platelet activation and aggregation

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27
Q

Where is the tissue factor/factor III/thromboplastin released from?

A

endothelial cells

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28
Q

What does the tissue factor do?

A

makes thrombin

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29
Q

What does thrombin do?

A

Cleaves fibrinogen to fibrin

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30
Q

What does fibrin do?

A

Gets poured onto the platelets to form the platelet plug (this is secondary hemostasis)

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31
Q

What is the main counter-regulatory mediator that down-regulates the clotting cascade?

A

tissue plasminogen activator (t-PA)

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32
Q

What is the most important coagulation factor?

A

Thrombin

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33
Q

What is the intrinsic coagulation pathway?

A

aka “contact activation pathway,” involved with many factors that are activated when polyanionic surfaces are encountered

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34
Q

What is the extrinsic coagulation pathway?

A

aka “tissue factor pathway,” involved solely with tissue factor (thromboplastin) getting activated by factor VII. This occurs when tissues are damaged

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35
Q

Which coagulation pathway is Hageman factor (XII) involved in?

A

intrinsic pathway

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36
Q

Which pathway does the prothrombin time (PT) measure?

A

Extrinsic pathway

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37
Q

Which factors does the PT measure?

A

factors II, V, VII and X

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38
Q

How do we activate the PT test?

A

using exogenous Ca++

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39
Q

<p>

| What factors does the PTT measure?</p>

A

<p>

| factors II, V, VIII-XII</p>

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40
Q

What pathway does the PTT measure?

A

intrinsic pathway

41
Q

How do we activate the PTT test?

A

Uses negative charged particles to activate Hageman (XII) factor

42
Q

What is thrombosis?

A

The formation of a blood clot inside a blood vessel. This obstructs the flow of blood

43
Q

How does endothelial injury lead to thrombosis?

A

endothelial tissues maintain the balance between the formation and degradation of clots. Any disruption in the endothelium can lead to local clotting events

44
Q

How does abnormal blood flow lead to thrombosis?

A

Promotion of endothelial activation- enhances pro-coagulation activity

45
Q

A mutation in which factor leads to the most common cause of inherited hypercoagulability?

A

point mutations in factor V (prothrombin)

46
Q

What is heparin-induced thrombocytopenia?

A

A acquired hypercoagulability where administration of unfractionated heparin causes antibodies to bind to platelets and activate them

47
Q

What is antiphospholipid antibody syndrome (AAS)?

A

Autoantibodies cause endothelial injury –> activates platelets and complement

48
Q

What are the main complications with AAS?

A

recurrent thromboses, repeated miscarriages, cardiac valve vegetations, PE’s, stroke, and fetal loss

49
Q

When do we determine that AAS is primary in nature?

A

lack evidence of other autoimmune diseases, often associated with certain drugs or infections

50
Q

When do we determine that AAS is secondary in nature?

A

when other autoimmune diseases exist (systemic lupus erythematosus)

51
Q

What is the cause and direction of thrombi formation in arteries?

A

begin at the sits of turbulence, grow retrograde from the point of attachment

52
Q

What is the cause and direction of thrombi formation in veins?

A

begin at sites of stasis, extend in the direction of blood flow

53
Q

If a thrombus was examined and was determined that it formed AFTER the patient had died, what would it look like?

A

if a clot formed post-mortem, the RBC’s settle to the bottom of a test tube and the buffy coat “chicken fat” layer comes up at the top

54
Q

What would it look like if a thrombus formed while the patient was alive? What is this called?

A

if the clot formed when the patient was alive, there are alternating layers of dark to light areas. These are called Lines of Zahn

55
Q

What is it called when a thrombus forms in the heart wall?

A

Mural thrombi

56
Q

What are the causes of mural thrombi?

A

arrhythmias, dilated cardiomyopathy, MI or any endomyocardial injury (myocarditis or catheter trauma)

57
Q

What is it called when thrombi form on the heart valves?

A

Vegetations

58
Q

What causes vegetations?

A

these are blood-borne bacteria or fungi damage the heart valves, causing infective endocarditis

59
Q

What are the main complications with arterial thrombi?

A

Strokes, MI

60
Q

What are the main complications with venous thrombi?

A

DVT’s

61
Q

Where do DVT’s start (usually)?

A

large leg veins AT or ABOVE the knee

62
Q

What are the main problems with DVT’s?

A

If they break off and form a PE

63
Q

What is disseminated intravascular coagulation (DIC)?

A

condition where blood clots form throughout the body’s small blood vessels. The clots reduce or block blood flow and damage the body’s organs

64
Q

Is DIC a primary disease?

A

No, it’s a potential complication of any condition associated with widespread activation of thrombin

65
Q

What are the main complications with DIC?

A

petechiae on skin and organs, circulatory insufficiency, particularly in brain, lungs, heart, and kidneys

66
Q

What can DIC eventually progress into?

A

they activate platelets and fibrinolytic mechanisms, which can evolve into a bleeding catastrophe

67
Q

What is an embolism?

A

detached intravascular solid, liquid or gaseous mass. It’s carried by the blood to a distant site

68
Q

Where do we see PE’s?

A

Seen in immobilized patients, hypercoagulable states, or heart failure

69
Q

Where do 95% of PE’s come from?

A

Deep leg veins

70
Q

What is the special name of the emoli formed in the pulmonary arteries that wrap around a bend?

A

Saddle emboli

71
Q

Where do most arterial thrombi come from?

A

Mural thrombi of the heart

72
Q

Fat/marrow emboli- etiology

A

Soft tissue trauma and burns, post-CPR, post-bone Fx

73
Q

Fat/marrow emboli- morphology

A

fat globules

74
Q

Air emboli- etiology

A

deep sea diving (mainly)

75
Q

Air emboli- morphology

A

frothy masses

76
Q

How many cc’s of air do you need before you can have significant clinical affects with air emboli?

A

100

77
Q

What are the bends?

A

rapid formation of gas in SkM and tissues

78
Q

What are the chokes?

A

gas bubbles in vasculature

79
Q

What is Caisson disease?

A

gas emboli in skeletal system (femur, humerus, tibia)

80
Q

Amniotic Fluid Embolism- etiology

A

Infusion of amniotic fluid into maternal circulation via a tear in the placental membranes or rupture of uterine veins.

81
Q

Amniotic Fluid Embolism- morphology

A

Squamous cells from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from fetal respiratory or GI tract in the maternal pulmonary microvasculature

82
Q

Amniotic Fluid Embolism- clinical problems

A

Sudden severe dyspnea, cyanosis, and shock

83
Q

What is an infarction?

A

an area of ischemic necrosis caused by occlusion of either the arterial supply or venous drainage

84
Q

What is a red infarct?

A

occur with venous occlusions or any disorder that causes arterial blood pooling

85
Q

What is a white infarct?

A

occur with arterial occlusions in solid organs with end-arterial circulation (heart, spleen, kidney)

86
Q

What are septic infarcts?

A

occur when infected cardiac valve vegetations embolize or when microbes seed necrotic tissues

87
Q

Define shock

A

a life-threatening condition when there is an inadequate level of oxygen delivery to a tissue.

88
Q

Hypovolemic shock- cause

A

Insufficient circulating volume. From hemorrhage, vomiting, diabetes, burns, or excess urine loss.

89
Q

Hypovolemic shock- Sx

A

Tachycardia, cool clammy skin, tachypnea, hypothermia

90
Q

Cardiogenic shock- cause

A

Failure of the heart to pump effectively. From damage to the heart (MI), arrhythmias, CHF, or other problems.

91
Q

Cardiogenic shock- Sx

A

Jugular vein distension, weak pulse, arrhythmias

92
Q

Septic shock- cause

A

Overwhelming systemic infection. From gram negative bacteria

93
Q

Septic shock- Sx

A

Fever, tachycardia. Low WBC count, tachypnea. Progreses to renal failure, liver dysfunction, ALOC, or elevated serum lactate.

94
Q

Neurogenic shock- cause

A

Severe CNS damage causes a sudden loss of sympathetic stimulation to the blood vessels. This results in vasodilation and thus hypotension.

95
Q

Neurogenic shock- Sx

A

Hypotension, bradycardia

96
Q

What occurs during the first (nonprogressive) stage of shock?

A

reflex mechanisms maintain perfusion to vital organs is maintained

97
Q

What occurs during the second (progressive) stage of shock?

A

tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances

98
Q

What occurs during the third (irreversible) stage of shock?

A

the cellular and tissue injury is so severe that even if it’s corrected, survival is not possible