Brainscape's Knowledge GenomeTM

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


See full index

Pathology > 4-Hemodynamics, Thromboembolitics, and Shock > Flashcards

4-Hemodynamics, Thromboembolitics, and Shock Flashcards

1
Q

What is edema?

A

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

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

What causes edema?

A

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

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

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

A

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

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

What is anasarca?

A

severe and generalized edema with widespread subcutaneous tissue swelling

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

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

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

Why does blocked lymphatics cause edema?

A

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

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

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

A

Transudate

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is hyperemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the morphology of hyperemia?

A

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

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

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

What is the morphology of congestion?

A

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

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

The accumulation of what specific cells present in congestion?

A

hemosiderin-laden macrophage clusters

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

What is a hemorrhage?

A

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

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

What is a hematoma?

A

any accumulation of blood within a tissue.

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

What are petechiae?

A

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

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

What causes petechiae?

A

Often from increased intravascular pressure or low/defective platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the size of purpura?

A

larger (>3mm) hemorrhages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What causes purpura?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are ecchymoses?

A

1-2cm subcutaneous hematomas (bruises)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

local secretion of endothelin causes arteriolar vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What occurs during primary hemostasis?

A

platelet activation and aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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

A

endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does the tissue factor do?

A

makes thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does thrombin do?

A

Cleaves fibrinogen to fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does fibrin do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

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

A

tissue plasminogen activator (t-PA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the most important coagulation factor?

A

Thrombin

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

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

A

intrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which pathway does the prothrombin time (PT) measure?

A

Extrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which factors does the PT measure?

A

factors II, V, VII and X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do we activate the PT test?

A

using exogenous Ca++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

<p>

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

A

<p>

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

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

Pathology (4 decks)

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