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Exam 2 APP > APP Module (GTown) - Cardiovascular Pathophysiology I (Hrs 1 and 2) > Flashcards

APP Module (GTown) - Cardiovascular Pathophysiology I (Hrs 1 and 2) Flashcards

1
Q

What are the three layers of the vessel wall, from innermost to outermost?

A

1) tunica intima
2) tunica media
3) tunica adventitia

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2
Q

Where does the internal elastic membrane lie?

A

Between the tunica intima and the tunica media.

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3
Q

What is in the tunica intimia?

A

1) endothelial layer

2) basement membrane

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4
Q

What is in the tunica media?

A

1) smooth muscle

2) elastic fibers

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5
Q

What is in the tunica adventitia?

A

areolar connective tissue

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6
Q

Does the structure of the vessel wall differ between different vessels?

A

Yes, there is a difference in components in each varying according to the size and type of vessel

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7
Q

What are the three characteristics of vascular smooth muscle cells?

A

1) contractility
2) secretion
3) plasticity

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8
Q

What is a key concept in most endothelial injury?

A

normal vascular smooth muscle cells will be mainly contractile, but will turn into secretory cells when injured

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9
Q

What are the ways in which vascular smooth muscle cells demonstrate plasticity?

A

1) hypertrophy
2) proliferation (hyperplasia)
3) change in phenotype (metaplasia)

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10
Q

What are the types of secretory components given off by vascular smooth muscle cells?

A

1) matrix formation
2) growth factors
3) proteases

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11
Q

How do you define vascular tone?

A

State of contraction due to myogenic and neurogenic factors

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12
Q

What are the two types of factors which control the contractile state of VSMC?

A

1) intrinsic factors (myogenic tone)

2) extrinsic factors (neurogenic tone)

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13
Q

How do you differentiate between neurogenic and myogenic tone?

A

Myogenic factors are determined by components that are in the vascular system. Neurogenic factors are those that are controlled and determined by hormones or extrinsic mechanisms outside the blood vessels.

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14
Q

What is vasomotion?

A

Change in the caliber of a blood vessel?

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15
Q

What are three characteristics of the endothelium?

A

1) secretory or modulatory
2) metabolic
3) plasticity

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16
Q

What are some molecules released by the endothelium?

A

endothelin, nitric oxide, and prostacyclin (PGI2)

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17
Q

What is the endothelium’s metabolic function?

A

Processing of factors which affect vasomotion

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18
Q

What are two metabolic processes the endothelium undergoes?

A

1) ACE production of Ang II

2) breakdown of bradykinin

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19
Q

How is the endothelium plastic?

A

through angiogenesis

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20
Q

What causes angiogenesis?

A

injury and ischemia

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21
Q

What mainly governs flow through a region of tissue?

A

The resistance of the microcirculation

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22
Q

What role does radius play in the change in pressure in a vessel?

A

Change in pressure is inversely proportion to the fourth power of the radius

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23
Q

If you double the length of a tube, everything else being equal, what is the pressure change?

A

Double the pressure

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24
Q

What does vasoconstriction cause generally in a blood vessel?

A

Turbulent flow

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25
Q

`What are the three regulators of local blood flow?

A

1) metabolic regulation (local metabolites)
2) autoregulation (myogenic regulation)
3) shear stress-induced vasodilation

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26
Q

In the microcirculation, what determines whether fluid is exudated or absorbed?

A

Hydrostatic pressure as it falls along the length of the vessel as oncotic pressure is largely the same.

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27
Q

What amount of protein is lost to the lymphatics/interstitium?

A

0.5%

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28
Q

Thinking about Starling forces, why might transudative forces prevail in the lower extremities?

A

In relation to the heart and while standing, there is a larger venous pressure such that is may favor filtration

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29
Q

In what situations can compensatory mechanisms fail to make up for the pressure difference in the lower extremities?

A

1) hypoalbuminemia
2) shock
3) venous thrombosis

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30
Q

Where does the thoracic duct drain into?

A

Left subclavian vein

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31
Q

What does increased hydrostatic pressure in the capillary bed lead to?

A

bulk flow of fluid into the interstitial space and edema

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32
Q

What is another name for interstitial fluid?

A

Extravascular fluid

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33
Q

Why might somebody have “relative hypovolemia”?

A

They might have a normal net amount of fluid in their body, but the distribution between the intravascular and extravascular compartments is abnormal

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34
Q

What are some of the mechanisms which cause edema?

A

1) lymph obstruction
2) increased capillary hydrostatic pressure
3) decreased capillary oncotic pressure
4) increased capillary permeability

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35
Q

Why is edema clinically relevant?

A

1) points to an underlying pathology
2) impairs wound healing
3) impairs ability to fight infection

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36
Q

What are some pathophysiological causes of edema?

A

1) primary heart failure
2) primary renal failure
3) nephrotic syndrome
4) liver cirrhosis
5) malnutrition

37
Q

What is the definition of circulatory shock?

A

Systemic hypoperfusion leading to impaired tissue perfusion and cellular hypoxia

38
Q

What is the common final pathway between the types of shock?

A

cardiovascular collapse; where the CV system cannot function

39
Q

What is cardiogenic shock?

A

Shock where a reduction in cardiac output is directly caused by cardiac damage or other factors that cause the heart to stop working

40
Q

What are two compensatory mechanisms for when cardiac output drops?

A

1) RAAS activation

2) catecholamine release (sympathetic activation)

41
Q

What is hypovolemic shock?

A

Systemic hypoperfusion due to reduced circulating BV due to loss of blood or plasma

42
Q

What does catecholamine release do to the systemic circulation?

A

Causes an increase in systemic vascular resistance

43
Q

What are three compensatory mechanisms to increase blood volume in response to the drop of cardiac output in hypovolemic shock?

A

1) shift of interstitial fluid
2) aldosterone, ADH production
3) splenic discharge

44
Q

What is neurogenic shock?

A

Systemic hypoperfusion due to a total loss in vascular tone

45
Q

What happens to the blood when you lose vascular tone?

A

It will pool in the peripheries

46
Q

What is anaphylactic shock?

A

Type I general IgE hypersensitivity causing systemic vasodilation and increased vascular permeability

47
Q

What is the common pathway for all the shocks?

A

Decrease in BV or CO –> decrease in tissue perfusion –> impaired cellular metabolism

48
Q

What is septic shock? What usually causes it?

A

Septic shock is the movement of a localized infection into the bloodstream and the associated systemic effects that the bacterial endotoxins have

49
Q

What are the three microbe-associated molecular patterns which cause sepsis?

A

1) gram negative bacteria carrying LPS
2) gram positive bacteria carrying toxic FA core (lipoteichoic acid)
3) fungi which carry a polysaccharide coat

50
Q

What does septic shock invariably lead to?

A

multi-organ dysfunction syndrome (MODS) or multi organ system failure

51
Q

What are the three most important vital organs?

A

Brain, heart, lungs

52
Q

What is the result of low quantities of LPS?

A

Local inflammation: activation of endothelial cells, immune response and complement

53
Q

What is the result of moderate quantities of LPS?

A

systemic effects such as fever, acute-phase reactant production by the liver, and leukocyte production by the bone marrow

54
Q

What happens at high concentrations of LPS?

A

You get septic shock with ADRS, DIC, decreased CO and peripheral resistance, endothelial injury, etc.

55
Q

What are the three stages of the progressive disorder otherwise known as shock?

A

1) nonprogressive stage
2) progressive stage
3) irreversible stage

56
Q

What is the irreversible stage composed of?

A

severe tissue injury in which recovery is not possible leading to feedback loops of decreased cardiac efficacy, ischemic bowel, renal failure, etc.

57
Q

What is the progressive stage?

A

Tissue hypoxia leads to the worsening of circulatory and metabolic disturbances

58
Q

What is made in the switch from aerobic to anaerobic metabolism?

A

lactic acid

59
Q

What is metabolic dilation?

A

The release of metabolites of injured tissue which leads to vasodilation of the vasculature

60
Q

What is the nonprogressive stage of septic shock?

A

Largely reversible changes which are defined by compensatory mechanisms that control neurohumoral regulation of CO and BP

61
Q

What is a hemorrhage?

A

extravasation of blood

62
Q

What is a hematoma?

A

accumulation of blood within tissue

63
Q

What are petechiae?

A

small spots of color on the skin/membranes which represent small hemorrhages

64
Q

What are purpuras?

A

these are large splotches of hemorrhaged tissue

65
Q

What are ecchymoses?

A

Ecchymoses are the the discoloration associated with bruises, although not necessarily having to do with trauma

66
Q

What determines the severity of hemorrhage?

A

1) size of the cavity in which the blood escapes
2) amount of blood lost
3) how quickly the blood is lost

67
Q

What is the main actor in the endothelium in regard to hemostasis?

A

thrombin

68
Q

What is a thrombosis?

A

an inappropriate clot

69
Q

What is an embolism?

A

the migration of an object, commonly a clot

70
Q

What is an infarction?

A

the downstream cellular effects of a thrombosis

71
Q

What is a hemorrhage?

A

the inability of the blood to clot and prevent blood leaking out

72
Q

What is Virchow’s triad?

A

1) endothelial injury
2) abnormal blood flow
3) hypercoagulability

73
Q

What causes endothelial injury?

A

perturbation of endothelial balance via hypertension, shear stress, turbulent flow, and/or bacterial infection leading to dysfunction and dysregulation

74
Q

What are two abnormal blood flow states?

A

1) stasis

2) turbulent flow

75
Q

What are the consequences of abnormal blood flow?

A

1) disruption of laminar flow
2) disruption of platelets in contact with EC
3) preventing of dilution of clotting factors
4) retards inflow
5) promotes EC/platelet activation

76
Q

What are some examples of abnormal blood flow?

A

1) atherosclerotic plaques
2) aneurysms
3) MI
4) mitral valve stenosis

77
Q

What is an example of a hypercoagulable state?

A

Genetic deficiency of a protease (ADAMTS13) which cleaves von Willebrand factor

78
Q

What is the clinical definition of thrombocytopenia?

A

A platelet count below 100k / mm3

79
Q

What two things factor into the presence and amount of platelets there are?

A

1) rate and amount of platelet formation

2) rate of platelet destruction

80
Q

What is ITP and TTP?

A

ITP is immune thrombocytopenic purpura. TTP is thrombotic thrombocytopenic purpura.

81
Q

What is the end result of immune thrombocytopenic purpura?

A

autoimmune platelet destruction resulting in hemorrhage and the formation of purpura

82
Q

What is the end result of TTP?

A

the aggregation of platelets in the circulation leading to a lack of available platelets

83
Q

What is disseminated intravascular coagulation?

A

DIC is a complication of septic shock in which there is widespread activation of thrombin within the microcirculation.

84
Q

What happens when there is widespread activation of thrombin in the microcirculation?

A

Diffuse circulatory insufficiency

85
Q

What is another name for DIC? Why?

A

consumptive coagulopathy. the amount of clots forming consumes the available clotting factors available

86
Q

What is TF? What does it do?

A

Tissue factor. TF cleaves prothrombin into thrombin initiating clotting

87
Q

What is a result of DIC?

A

widespread endothelial damage

88
Q

What is the treatment for DIC?

A

1) treating the underlying disorder
2) anticoagulation therapy
3) FFP (fresh frozen plasma)

89
Q

What is the primary fibrin degradation product?

A

D-dimer. Which tells you the level of fibrin degradation occurring

Exam 2 APP (5 decks)

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