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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
`What are the three regulators of local blood flow?
1) metabolic regulation (local metabolites) 2) autoregulation (myogenic regulation) 3) shear stress-induced vasodilation
26
In the microcirculation, what determines whether fluid is exudated or absorbed?
Hydrostatic pressure as it falls along the length of the vessel as oncotic pressure is largely the same.
27
What amount of protein is lost to the lymphatics/interstitium?
0.5%
28
Thinking about Starling forces, why might transudative forces prevail in the lower extremities?
In relation to the heart and while standing, there is a larger venous pressure such that is may favor filtration
29
In what situations can compensatory mechanisms fail to make up for the pressure difference in the lower extremities?
1) hypoalbuminemia 2) shock 3) venous thrombosis
30
Where does the thoracic duct drain into?
Left subclavian vein
31
What does increased hydrostatic pressure in the capillary bed lead to?
bulk flow of fluid into the interstitial space and edema
32
What is another name for interstitial fluid?
Extravascular fluid
33
Why might somebody have "relative hypovolemia"?
They might have a normal net amount of fluid in their body, but the distribution between the intravascular and extravascular compartments is abnormal
34
What are some of the mechanisms which cause edema?
1) lymph obstruction 2) increased capillary hydrostatic pressure 3) decreased capillary oncotic pressure 4) increased capillary permeability
35
Why is edema clinically relevant?
1) points to an underlying pathology 2) impairs wound healing 3) impairs ability to fight infection
36
What are some pathophysiological causes of edema?
1) primary heart failure 2) primary renal failure 3) nephrotic syndrome 4) liver cirrhosis 5) malnutrition
37
What is the definition of circulatory shock?
Systemic hypoperfusion leading to impaired tissue perfusion and cellular hypoxia
38
What is the common final pathway between the types of shock?
cardiovascular collapse; where the CV system cannot function
39
What is cardiogenic shock?
Shock where a reduction in cardiac output is directly caused by cardiac damage or other factors that cause the heart to stop working
40
What are two compensatory mechanisms for when cardiac output drops?
1) RAAS activation | 2) catecholamine release (sympathetic activation)
41
What is hypovolemic shock?
Systemic hypoperfusion due to reduced circulating BV due to loss of blood or plasma
42
What does catecholamine release do to the systemic circulation?
Causes an increase in systemic vascular resistance
43
What are three compensatory mechanisms to increase blood volume in response to the drop of cardiac output in hypovolemic shock?
1) shift of interstitial fluid 2) aldosterone, ADH production 3) splenic discharge
44
What is neurogenic shock?
Systemic hypoperfusion due to a total loss in vascular tone
45
What happens to the blood when you lose vascular tone?
It will pool in the peripheries
46
What is anaphylactic shock?
Type I general IgE hypersensitivity causing systemic vasodilation and increased vascular permeability
47
What is the common pathway for all the shocks?
Decrease in BV or CO --> decrease in tissue perfusion --> impaired cellular metabolism
48
What is septic shock? What usually causes it?
Septic shock is the movement of a localized infection into the bloodstream and the associated systemic effects that the bacterial endotoxins have
49
What are the three microbe-associated molecular patterns which cause sepsis?
1) gram negative bacteria carrying LPS 2) gram positive bacteria carrying toxic FA core (lipoteichoic acid) 3) fungi which carry a polysaccharide coat
50
What does septic shock invariably lead to?
multi-organ dysfunction syndrome (MODS) or multi organ system failure
51
What are the three most important vital organs?
Brain, heart, lungs
52
What is the result of low quantities of LPS?
Local inflammation: activation of endothelial cells, immune response and complement
53
What is the result of moderate quantities of LPS?
systemic effects such as fever, acute-phase reactant production by the liver, and leukocyte production by the bone marrow
54
What happens at high concentrations of LPS?
You get septic shock with ADRS, DIC, decreased CO and peripheral resistance, endothelial injury, etc.
55
What are the three stages of the progressive disorder otherwise known as shock?
1) nonprogressive stage 2) progressive stage 3) irreversible stage
56
What is the irreversible stage composed of?
severe tissue injury in which recovery is not possible leading to feedback loops of decreased cardiac efficacy, ischemic bowel, renal failure, etc.
57
What is the progressive stage?
Tissue hypoxia leads to the worsening of circulatory and metabolic disturbances
58
What is made in the switch from aerobic to anaerobic metabolism?
lactic acid
59
What is metabolic dilation?
The release of metabolites of injured tissue which leads to vasodilation of the vasculature
60
What is the nonprogressive stage of septic shock?
Largely reversible changes which are defined by compensatory mechanisms that control neurohumoral regulation of CO and BP
61
What is a hemorrhage?
extravasation of blood
62
What is a hematoma?
accumulation of blood within tissue
63
What are petechiae?
small spots of color on the skin/membranes which represent small hemorrhages
64
What are purpuras?
these are large splotches of hemorrhaged tissue
65
What are ecchymoses?
Ecchymoses are the the discoloration associated with bruises, although not necessarily having to do with trauma
66
What determines the severity of hemorrhage?
1) size of the cavity in which the blood escapes 2) amount of blood lost 3) how quickly the blood is lost
67
What is the main actor in the endothelium in regard to hemostasis?
thrombin
68
What is a thrombosis?
an inappropriate clot
69
What is an embolism?
the migration of an object, commonly a clot
70
What is an infarction?
the downstream cellular effects of a thrombosis
71
What is a hemorrhage?
the inability of the blood to clot and prevent blood leaking out
72
What is Virchow's triad?
1) endothelial injury 2) abnormal blood flow 3) hypercoagulability
73
What causes endothelial injury?
perturbation of endothelial balance via hypertension, shear stress, turbulent flow, and/or bacterial infection leading to dysfunction and dysregulation
74
What are two abnormal blood flow states?
1) stasis | 2) turbulent flow
75
What are the consequences of abnormal blood flow?
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
What are some examples of abnormal blood flow?
1) atherosclerotic plaques 2) aneurysms 3) MI 4) mitral valve stenosis
77
What is an example of a hypercoagulable state?
Genetic deficiency of a protease (ADAMTS13) which cleaves von Willebrand factor
78
What is the clinical definition of thrombocytopenia?
A platelet count below 100k / mm3
79
What two things factor into the presence and amount of platelets there are?
1) rate and amount of platelet formation | 2) rate of platelet destruction
80
What is ITP and TTP?
ITP is immune thrombocytopenic purpura. TTP is thrombotic thrombocytopenic purpura.
81
What is the end result of immune thrombocytopenic purpura?
autoimmune platelet destruction resulting in hemorrhage and the formation of purpura
82
What is the end result of TTP?
the aggregation of platelets in the circulation leading to a lack of available platelets
83
What is disseminated intravascular coagulation?
DIC is a complication of septic shock in which there is widespread activation of thrombin within the microcirculation.
84
What happens when there is widespread activation of thrombin in the microcirculation?
Diffuse circulatory insufficiency
85
What is another name for DIC? Why?
consumptive coagulopathy. the amount of clots forming consumes the available clotting factors available
86
What is TF? What does it do?
Tissue factor. TF cleaves prothrombin into thrombin initiating clotting
87
What is a result of DIC?
widespread endothelial damage
88
What is the treatment for DIC?
1) treating the underlying disorder 2) anticoagulation therapy 3) FFP (fresh frozen plasma)
89
What is the primary fibrin degradation product?
D-dimer. Which tells you the level of fibrin degradation occurring

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