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APP Part 2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

layers of vessel wall

A

Tunica Intima-endothelium, basement membrane
* internal elastic memb
Tunica Media - SM, elastic fibers
Tunica advetentia - areolar connective tissue.

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2
Q

Properties of vascular smooth muscle cells (VSMC)

A

Contractility
Secretory - ECM, GF, proteases
Plasticity - hypertrophy, prolif, angiogenesis (in response to ischemia, injury)

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3
Q

Virchow triad describes the formation of ___

A

Thrombosis

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4
Q

Virchow triad:

A

1) EC injury via HTN, shear stress, turbulent flow, bacterial infection.
2) disruption in laminar flow
3) Hypercoagulability -less frequent

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5
Q

alterations in blood flow occurs in ____ .

A
  • atherosclerotic plaques
  • aneurysms
  • MI
  • mitral valve stenosis
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6
Q

Edema is defined as ___

A

excess fluid in the interstitial spaces.

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7
Q

What maintains fluid balance inflow/outflow?

A
  • normally, fluid entering arterial end of microcirculation is balanced by inflow into venular end
  • excess fluid is drained by lymphatics, which returns to bloodstream via thoracic duct.
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8
Q

Increased Hydrostatic Pressure occurs in ___ (2)

A

impaired venous drainage, CHF

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9
Q

Decreased Oncotic Pressure occurs due to ___, seen in ____ (3 conditions).

A
  • reduced albumin

- nephrotic syndrome, cirrhosis, protein malnutrition (reduced production of plasma proteins).

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10
Q

Factors that contribute to the development of an infarct:

A
  1. presence of alternative blood supply (dual arterial supply–liver, lungs, hands VS. end arterial–renal, splenic)
  2. rate of development of occlusion - slow growing are less likely to infarct due to dev of alternative flow (pre-existing collaterals),
  3. vulnerability to hypoxia - neurons, myocardial cells, fibroblasts within myocardium,
  4. O2 content of blood - anemia, cyanotic patient, C
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11
Q

consequences of a systemic thromboembolism are dependent on ___ and ___.

A

the collateral supply and caliber (diameter) of the vessel occluded

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12
Q

Infarction is defined as ___

A

an area of ischemic necrosis due to occlusion of arterial supply or venous drainage.

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13
Q

Endothelium plays secretory and modulatory role for vascular SM tone and platelet function by producing….

A

vasodilators: NO, PGI2 (prostocyclins).
vasoconstrictors: Endothelin.
keeps platelets from aggregating
keeps vascular SM from doing mitosis

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14
Q

Metabolic role of endothelium includes processing of vasoactive factors including ___ and __

A
  • antiotensin converting enzyme production of Ang II (vasoconstrictor)
  • breakdown of bradykinin (inflammation)
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15
Q

Flow through a region is governed mainly by ____

A

resistance of the microcirculation

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16
Q

Factors that affect blood pressure

A 
P's law: deltaP= RQ = uLQ/r4
*r = radius of vessel is MOST important. 
R= resistance
Q= flow
L= length of vessel
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17
Q

3 types of regulation involved with local blood flow

A
  • Metabolic regulation – local metabolites cause vasodilation mostly
  • Auto-regulation – transmural pressure (against the wall) causes vasoconstriction mostly
  • Shear stress-induced vasodilation– caused by longitudinal pressure gradient
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18
Q

Vascular tone means __, which is controlled by ___ and ___

A
  • state of contractility
  • myogenic tone (intrinsic factors)
  • Neurologic and Humoral tone (extrinsic factors)-sym neurons
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19
Q

areas of bifurcation are more liekly to have aneurysms due to ___ and ___ induced injury

A

sheer stress and turbulance

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20
Q

If you increase radius by 2, flow …

A

r^4 is directly correlated with flow (Q). So if r doubles, flow is 16x higher!

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21
Q

Pressure fluctuations in formation of edema:

A
  • increased hydrostatic pressure or decreased plasma oncotic pressure (colloid onc P) leads to net acccumilation extravascular fluids. Causes edema when lymphatics cant drain this.
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22
Q

4 changes tht can cause edema:

A

1) INC capillary permeability (burns, allergic inflammation–loss of plasma prot)
2) DEC capillary oncotic pressure (dec plasma prot production– cirrhosis, malnutrition)
3) INC capillary Hydrostatic P (venous obstruction, renal Na/water retention, heart failure)
4) lymph obstruction (cant drain)

23
Q

Edema points to ___ and ___, which impairs ___ and ____

A
  • underlying disease, inflammation

- inflammation points to impaired wound healing and reduced ability to fight infection.

24
Q

4 things that can dec CO and lead to edema

A
  • Heart failure
  • malnutrition, neohrotic syndrome (dec. prot synth+ BV)
  • ascites, other effusions
  • primary renal failure
25
Q

Levels of Renin, AngII, ald, ADH are high in heart failure, why?

A

to compensate for low CO, by increasing salt and water retention => inc plasma volume.

26
Q

___ is often the cause of arterial thrombi.

A

Cardiac dysfunction

27
Q

Disseminated Intravascular Coagulation

A
  • forming excess clots due of widespread activation of thrombin. Thrombin doesn’t stay localized (everywhere)
  • not a primary disease, a complication.
  • a “consumptive coagulopathy”– consumes all the clotting factors, so none left to form a clot if there is hemorrhage.
  • manage it with anticoagulants and fresh frozen plasma (FFP).
  • Widespread ischemia, infarction, hypoperfusion
  • decreased fibrinolysis—not enough to keep up with clot formation.
28
Q

DIC is a major concern during pregnancy bc _____

A

risk of hemorrhage is high, but not enough clots can be formed in DIC (wasting clotting factors) = blood loss
*Bleeding is a sign of the inability to form a clot

29
Q

Why do we test for D-dimers to rule out DIC?

A

3rd step of normal thrombus formation (dissolution, fibrinolytic activity) requires fibrin degradation products (FDP)—particularly D-dimers. But in DIC, there isn’t enough D-diners to keep up with clot formation.

30
Q

A pulmonary thoromboemboli is most likely to originate from ___

A

a venous thrombi from a deep vein of the leg.

31
Q

PE in a (medium/small) vessel is more likely to cause an infarct.

A

small (mediums have collaterals).

32
Q

Complications of Pulmonary vs. systemic thromboembolism

A

PR: sudden death, CV collapse, cor polmonale

Systemic TE: complication in lower extrimities, brain, kidney, spleen (depends on size of vessel and collaterals).

33
Q

embolism

A

detached solid, liquid, or gaseous mass (usually a thrombus) travelling throuhgh vessels.

34
Q

infarct

A

zone of necrosis caused by blocked venous drainage OR arterial supply.

35
Q

initiating events for an infarct:

A
  • primarily embolus/thrombus
  • local vasospasm
  • swelling of a atheroma (hemorrhage within a plaque)
  • compression of a vessel (tumor)
36
Q

concentric vs. eccentric hypertrophy of heart walls

A 
concentric = muscular/buff
eccentric = baggy heart
37
Q

Causes of cardiogenic shock

A

pump failure due to:

  • intrinsic myocardial damage
  • ventricular arrhythmias
  • outflow obstructions
38
Q

Causes of hypovolumic shock

A
  • hemorrhage, burns, trauma
39
Q

Causes of septic shock

A

Gm Negative endotoxins (bacterial LPS released = inflammation)
Lead to: systemic vasodilation, pump failure/CV collapse, even DIC (EC injury, activation of coagulatory factors)

40
Q

Causes of neurogenic shock

A

anesthesia or spinal cord injury causes imbalance bw sympathetic and parasympathetic NS –> massive vasodilation

41
Q

intimal thickening forms ____. Exaggerated healing response to vascular injury leads to intimal thickening and may result in ____

A
  • neointima (ECM secreted by dedifferentiated SM cells)

- stenosis or occlusion.

42
Q

a progressive disease characterized by systolic dysfunction and simultaneous enlargement of ALL chambers of the heart

A

Dilated cardiomyopathy

43
Q
  • ventricular hypertrophy
  • strong, hyperkinetic contractions
  • impaired diastolic filling.
  • This heart is also incapable of stretching, so cannot effectively adjust stroke volume
A

Hypertrophic cardiomyopathy

asymmetric septal hypertrophy

44
Q

renal damage and decreased urine output starts in which stage of shock?

A

progressive stage

  • non progressive=compensations maintain perfusion
  • irreversible = renal shutdown, acute tubular necrosis. Cannot be corrected by hemodynamics.
45
Q

individuals with abdominal aortic aneurisms are at risk for ___ and ___

A

ischemic heart disease and stroke (due to systemic nature of atherosclerosis

46
Q

most common cause is ____ due to medial destruction, second is ___. Primary type of aneurism ___

A
  • atherosclerosis
  • plaque formation in the intima
  • abdominal aortic aneurism = most common.
47
Q

aneurism

A
  • localized abnormal dilation of vessel or heart

- primarily due to weakened wall.

48
Q

false aneurism vs. dissection

A 
FA = hematoma, extravasation of blood in extravascular connective tissue
Dissection = tear in intima, extravasation of blood into the wall, but no dilation.
49
Q

forward failure vs. backward failure

A 
forward = inadequate CO 
backward = venous backup
50
Q

Left side hrt failure can occur due to _____ vs. Rt side failure can occur due to ___

A

L=Systemic HTN, mitral/aortic valve disease, ischemic heart

R= Left Ventricular failure (with or without pulmonary congestion and disease)

51
Q

in CHF when sympathetics and myocyte hypertrophy is insufficient to compensate, ___ happens to inc PRELOAD, and achieve ___

A

dilation = chamber enlargement = inc preload.

Compensated heart failure.

52
Q

associated with CHF

A
  • backward failure: pulmonary congestion, edema, venous congestion, systemic edema
  • dyspnea due to dec lung compliance (congested remember)
  • ortopnea due to increased venous return
  • may become cyanotic and acidotic.
53
Q

Amount of activated thrombin > antithrombins in ____

A

DIC

APP Part 2 (9 decks)

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