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Patho Exam 1 > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

___ is the increased interstitial fluid which produces swelling and is initially painless

A

edema

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2
Q

___ is the accumulation of fluid in the body cavities

A

effusion

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3
Q

What are the 4 causes of edema?

A

1-too much leakage–increased vascular permeability
2-too little reabsorption–lymphatic obstruction
3-increased capillary hydrostatic pressure
4-reduced plasma oncotic pressure

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4
Q

Retention of sodium and thus water like in kidney disease results in what cause of edema?

A

increased hydrostatic pressure

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5
Q

___ determines extracellular fluid volume and osmolarity

A

sodium

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6
Q

Hydrostatic pressure from arterioles results in an outflow of ___ of fluid into extracellular space normally

A

14 ml/min

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7
Q

Oncotic pressure in venules results in inflow of ___ of fluid into vasculature

A

12 ml/min

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8
Q

What accounts for the extra 2ml/min of fluid not involved in hydrostatic or oncotic pressure?

A

lymphatics

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9
Q

What increases hydrostatic pressure? 3 things

A

1-increased venous pressure (thrombosis, clot, CHF)
2-hypervolemia-sodium retention, acute renal failure
3-arteriolar dilation-inflammation, heat

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10
Q

What causes decreased oncotic pressure?

A

hypoproteinemia-nephrotic syndrome, cirrhosis, malnutrition

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11
Q

What are the causes of localized edema? 3

A

1- DVT
2- lymphatic obstruction
3- acute inflammation

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12
Q

What are the causes of generalized edema? 5

A
  • cardiogenic
  • nephrogenic
  • cirrhosis
  • hypoalbumininemia
  • steroids
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13
Q

___ is extreme generalized edema

A

anasarca

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14
Q

___ is an active process with increased diameter or number of vessels typically due to increased blood supply such as in inflammation

A

hyperemia

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15
Q

___ is a passive process and is due to outflow of blood from an area and it presents blue/red

A

congestion

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16
Q

___ is seen with inflammation and infection, is protein rich, and is seen with increased vascularity and hyperemia

A

exudate

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17
Q

__ is seen with CHF and hypoalbumininemia, is non-inflammatory and is a filtrate of plasma seen with congestion

A

transudate

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18
Q

___ are minute hemorrhages caused by rupture of capillaries or arterioles or low platelet counts

A

petechiae

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19
Q

___ are larger hemorrhages that are caused by rupture of capillaries or arterioles, low platelet counts, trauma, vasculitis, and increased fragility of vessels

A

purpura

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20
Q

___ are bruises

A

ecchymoses

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21
Q

a ___ is a rounded mass hemorrhage with a mass effect on tissue surrounding

A

hematoma

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22
Q

initiation and formation of the platelet plug occur in ___ hemostasis

A

primary

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23
Q

propagation of the coagulation cascade occurs in ___ hemostasis

A

secondary

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24
Q

Fibrinolysis is very important to minimize ___ of tissue distal to the clot

A

ischemia

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25
Q

coumadin affects the ____ pathway of the coagulation cascade

A

extrinsic

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26
Q

heparin affects the ___ pathway of coagulation cascade

A

intrinsic

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27
Q

both heparin and coumadin affect the ___ pathway of coagulation cascade

A

common

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28
Q

Factor ___ is part of the extrinsic pathway

A

VII

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29
Q

Factor ___ is part of the intrinsic pathway

A

XII

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30
Q

___ is the most important coagulation factor

A

Thrombin

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31
Q

The intrinsic pathway is measured by the ____ lab test

A

PTT

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32
Q

The extrinsic pathway is measured by the ___ lab test

A

PT

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33
Q

a ___ is a stationary intravascular blood clot

A

thrombus

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34
Q

___ is an intravascular blood clot that travels

A

embolus

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35
Q

an ___ blood clot causes ischemia and infarction in tissue distal to it

A

arterial

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36
Q

a ___ blood clot causes emboli somewhere else

A

venous

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37
Q

Virchow’s triad refers to the classic causes/predispositions for ___ formation; what are the 3 factors?

A

thrombus formation; hypercoaguable state, endothelial injury, altered blood flow (usually stasis)

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38
Q

a venous thrombus usually starts at the ___

A

valves

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39
Q

A ___ thrombus restricts the lumen but does not occlude it

A

parietal

40
Q

a red thrombus is from ___

A

venous

41
Q

a white thrombus is from ___

A

arterial

42
Q

What are Virchow’s triad factors in venous blood clots?

A

1-endothelial injury from trauma or surgery
2-abnormal blood flow-stasis
3-hypercoagulability-OCPs and older folks

43
Q

What are Virchow’s triad factors in arterial blood clots?

A

1-endothelial injury from atherosclerosis
2-abnormal blood flow-turbulence
3-hypercoagulability

44
Q

What are the 3 consequences of arterial occlusion?

A

1-infarction or dysfunction of tissue perfused by that artery
2-infarcted tissue will undergo scarring and atrophy
3-can embolize to next capillary bed

45
Q

What are the 4 consequences of venous occlusion?

A

1-edema and pain
2-infarction from embolism to next capillary bed,
3-infarction from back pressure of arterial supply
4-leakage of fibrin that retards oxygen perfusion

46
Q

Venous emboli are usually from the deep veins of ___ and ___ system that go into the pulmonary arteries

A

thigh and popliteal

47
Q

a ___ embolus gets to systemic circulation through an abnormal communication between the venous and arterial systems at the level of the heart

A

paradoxical embolism

48
Q

What are the risk factors for arterial thrombi/emboli? 4

A

atrial fibrillation, endocarditis, MI, valve abnormalities

49
Q

The arterial thrombi usually arise in what 3 places?

A

1-arteries complicated with atherosclerotic plaques
2-heart chambers
3-site of atherosclerosis/aneurysm

50
Q

Arterial thrombi may embolize to arteries in almost any part of the body with ____ and ___ most common

A

lower extremities and brain

51
Q

a ___ emboli is a special form of emboli resulting from bone fracture especially in the pelvis which usually affects the pulmonary and CNS

A

fat

52
Q

a ___ emboli is a special form of emboli from atheromas–atherosclerotic debris–and may resemble a fat embolus

A

cholestrol

53
Q

a ___ embolus is a special form of emboli that is usually iatrogenic–from injections or surgery–often from acute decompression sickness

A

gas

54
Q

____ embolus is a special form of emboli in which fetal cells and debris enter the maternal circulation–it is often seen at the end of labor and is often catastrophic–can cause DIC

A

amniotic fluid

55
Q

___ like talc and cement can also cause special forms of emboli

A

foreign materials

56
Q

What are the 5 causes of arterial obstruction?

A 
1-atherosclerosis
2-arteriosclerosis
3-arterial spasm
4-compartment syndrome
5-torsion
57
Q

arterial spasm is caused by

A

intense vasoconstriction

58
Q

____ is when an arteriole cannot relax in absence of endothelium due to lack of NO

A

Furchgott phenomenon

59
Q

Raynaud’s phenomenon is often seen in the fingers and is an example of ____

A

arterial spasm

60
Q

What is the path of compartment syndrome?

A

perfusion pressure falls below tissue pressure in closed anatomic site –> veins are affected first –> arteries are then affected –> leads to tissue necrosis or functional deficits

61
Q

What are the 5/6 ‘P’s of compartment syndrome?

A 
Pain
Paresthesia
Pallor
Paralysis
Pulselessness
Polar/poikilothermia
62
Q

____ is a deformation of forearm with flexion at the wrist that follows muscle infarction and replacement with fibrous tissue

A

Volkmann’s contracture

63
Q

___ can cause infarction–it is a twisting that first causes venous obstruction and with further twisting causes arterial obstruction

A

torsion

64
Q

____ is similar to torsion but usually occurs due to a hernia or in the colon or small bowel

A

strangulation

65
Q

___ is decreased blood supply to organ

A

ischemia

66
Q

damage from infarction depends on what 4 things?

A

1-type of vascular supply–terminal, dual
2-rate of development of occlusion (acute or chronic)
3-vulnerability of tissue to hypoxia
4-oxygen content of blood

67
Q

Acute infarcts are often ___ due to damage to the endothelium

A

red

68
Q

___ infarcts are often seen in the heart, kidneys, and spleen from arterial occlusion of terminal arteries

A

white

69
Q

___ infarcts may be due to either arterial or venous blood system and hemorrhage into the infarct

A

red

70
Q

___ is a kind of cardiovascular collapse where the blood supply to the body is insufficient to meet the body’s demands

A

shock

71
Q

What are two factors for decreased cardiac output?

A

1-pump failure–LV is not pumping out enough blood

2-decreased effective circulating volume–volume is remaining in periphery instead of returning to central

72
Q

In early shock, skin is cold and clammy–why?

A

the heart tries to compensate by vasoconstricting peripheral blood vessels to shunt blood to necessary organs

73
Q

Later on in shock the skin returns to warm and pink–why?

A

the pt has reached the point of no return where the compensatory mechanisms fail and vasodilation returns peripheral blood

74
Q

When the kidneys are not perfused the patient becomes ___ which damages the heart further

A

acidotic

75
Q

___ shock is due to myocardial pump failure as in MI, arrhythmias, cardiac tamponade, PE

A

cardiogenic

76
Q

___ shock is due to reduced amounts of blood volume as may happen with bleeding, dehydration, burns, and diarrhea

A

hypovolemic

77
Q

___ shock is due to peripheral vasodilation and increased permeability as well as microbial infection

A

septic

78
Q

___ shock is due to Type 1 IgE mediated hypersensitivity

A

anaphylactic

79
Q

___ shock is due to severe brain or spinal cord injury which impairs vasomotor control—can’t vasoconstrict

A

neurogenic

80
Q

sepsis is “_____”–a systemic response to infection

A

SIRS plus signs of infection

81
Q

The leading cause of septic shock is now considered to be

A

gram positive bacteria, followed by gram negative bacteria, and then fungi

82
Q

What happens in septic shock?

A

1-bacteria have structural components of cell walls that cause immune and endothelial cell activation which release cytokines and activate complement which causes a hyperinflammatory state with leaky blood vessels

83
Q

Induction of a procoagulant state in septic shock leads to systemic activation of ___ and deposition of fibrin-rich thrombi in small vessels which leads to ___

A

thrombin; DIC

84
Q

Death of alveolar cells, acute tubular necrosis of the kidney, liver failure, myocardial cell death, bowel necrosis, and brain ischemia are all consequences of ____

A

multiple organ dysfunction syndrome

85
Q

In general, how is multi-system organ failure caused?

A
  • -microbial product starts it
  • -an inflammatory response is activated globally
  • -cytokines, etc. cause vasodilation, increased permeability and decreased perfusion
86
Q

the ____ stage of shock has a compensatory mechanism that is activated and perfusion of vital organs is maintained

A

nonprogressive

87
Q

the ___ stage of shock has tissue hypoperfusion which leads to worsening circulatory and metabolic imbalances including lactic acidosis

A

progressive

88
Q

the ___ stage of shock is when there is so much cell and tissue injury that survival is not possible

A

irreversible

89
Q

In shock the ____-____-___ system is activated which leads to sodium and water retention; then ___ and ___ cause selective constriction of peripheral vessels to shunt blood to vital organs (heart and brain)

A

renin-angiotensin-aldosterone; norepinephrine and angiotensin 2

90
Q

How do the vessels respond to norepinephrine and angiotensin 2?

A

the vessels constrict

91
Q

The vasoconstriction induced by compensatory mechanisms of shock require ATP and when the ATP is depleted there is a switch to anaerobic glycolysis which produces lactic acidosis—what does that result in?

A

acidosis blunts the vasomotor response and the sodium/potassium pump doesn’t function and there is a point of no return where blood pressure can no longer be raised

92
Q

____, released from the posterior pituitary gland, is rapidly poured out and leads to increased water retention and decreased urine output

A

vasopressin

93
Q

Hypotension, tachycardia, cool clammy skin, tachypnea, oliguria, change in mental status, metabolic acidosis, and multi-system organ failure are all clinical signs of

A

shock

94
Q

___ is a systematic hypersensitivity involving basophils and mast cells that release cytokines and things like histamine

A

immediate, type 1 hypersensitivity

95
Q

____ is an autosomal dominant disease with a C1 esterase inhibitor deficiency—can cause asphyxiation and death, follows mild trauma or stress

A

hereditary angioedema

Patho Exam 1 (5 decks)

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