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Pathophys > Alterations in the Cardiovascular System > Flashcards

Alterations in the Cardiovascular System Flashcards

1
Q

lymphatic capillaries openings are

A

larger than venous, because they pull in large proteins that can’t go back into veings

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2
Q

lymphatics return

A

protein, lipids, cellular debris from interstitium to vasculature

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3
Q

lymphedema occurs from

A
  • stagnation of fluid in interstitium due to blockage

- inflammatory response (macrophages) or fibrosis

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4
Q

s/s lymphedema

A

usually nonpitting edema

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5
Q

primary lymphedema

A

congenital

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6
Q

secondary lymphedema

A

damage to lymphatics due to non congenital causes

  • filiariasis = mosquito born parasite that damages lymph vessels
  • cancer or cancer tx
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7
Q

cause of Chronic Venous Insufficiency (CVI)

A

vein or valve blockage/malfunction

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8
Q

Risk Factors for CVI

A

female, pregnancey, obesity, aging, family hx, stasis

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9
Q

s/s CVI

A

vericosity, itching, burning, muscle cramp, pitting edema,

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10
Q

Virchow’s Triad

A

stasis, vascular injury, hypercoagulability

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11
Q

examples of vascular injury

A

venepuncture, atherosclerosis, heart valve disease, surgery, trauma

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12
Q

examples of circulatory stasis

A

A-Fib, Lft Ventricular syfunction, immobility, obesity

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13
Q

s/s of DVT

A

pain, tenderness, swelling, erythema, none

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14
Q

diagnosis of DVT

A

d-dimer, ultrasound

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15
Q

complications of DVT

A

thromboembolus, post-thrombotic inflammatory syndrome

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16
Q

arterial thrombus is caused by

A

activation of the coagulation cascade caused by the artherosclerotic roughening of the tunica intima

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17
Q

types of thromboembolism

A

arterial, pulmonary emboli, air embolism, amniotic fluid, bacterial, fat, foreign material

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18
Q

left hear delivers blood to

A

arteries

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19
Q

pulmonary emboli source

A

most commonly from the deep veins of the thigh

right heart or venous circulation

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20
Q

pathophys of pulmonary embolism

A

occlusion of part of pulmonary circulation => hypoxic vasoconstriction=>decreased surfactant=>release of neurohumoral response=>atelectasis in affected lung=> further hypoxemia=> pulmonary edema, HTN,shock, death

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21
Q

s/s pulmonary embolism

A

tachypnea, dyspnea, chest pain, dead space, V/Q imbalances, decrease PaO2, pulmonary infarction, HTN, decreased CO, systemic Hypotension due to decreased blood flow from heart

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22
Q

Superior Vena Cava Syndrome

A

venous distention in UE and head due to compression of SVC from lung cancer or lymphoma

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23
Q

Aneurysms

A

walls are still intact but fluid leaks btn layers resulting in ballooning or bulging

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24
Q

True Aneurysm

A

involve all 3 layers of the BV

fusiform, circumferential or dissecting

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25
Q

Pseudoaneurysm

A

extravascular hematoma that extends into the intravascular space

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26
Q

Risk factors for aneurysms

A

HTN
Atherosclerosis =erodes walls
inflammation = infection such as syphilis
collagen disorders = Marfan’s, EDS

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27
Q

complications of HTN

A

retina damage, Lft ventricle hypertrophy, kidney failure

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28
Q

Blood Pressure

A

CO + Peripheral Vascular Resistance

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29
Q

Stroke Volume

A

amt of blood pumped out of the L ventricle per beat

- affected by contractility, preload, and afterload

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30
Q

Cardiac Output

A

= Stroke Volume x HR

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31
Q

stage I HTN

A

130-139/80-89

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32
Q

stage II HTN

A

> 140/>90

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33
Q

mechanisms of vascular resistance

A

blood viscosity (water retention) and vascular diameter

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34
Q

two mechanisms for HTN

A

increased vascular resistance, increase CO

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35
Q

how does change in SNS affect HTN

A

Norepi is released and binds to alpha1 on BV and beta1 on heart = vasoconstriction and increase in HR = increase in CO and increase in vascular resistance

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36
Q

causes of Primary HTN

A

genetic + environment + neurohumoral

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37
Q

causes of Secondary HTN

A

systemic disease, renal artery disease, coarctation of aorta

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38
Q

malignant HTN

A

hypertensive crisis
rapidly progressive HTN = >180/>120
can lead to encephalopathy, and hypertensive emergency

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39
Q

Pulmonary HTN

A

Lft HF, hereditary, Phen-Phen, parenchymal lung disease

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40
Q

Juxtaglomerular Cells

A

release renin

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41
Q

mechanisms for renin release

A

> response to PG stimulus from macula densa cells
response to activation of Beta Adrenergic receptors by increased activity of SNS
response to barorecptrs directly sensing low blood pressure

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42
Q

macula densa cells

A

detects Na concentrations in distal tubule

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43
Q

Renin

A

converts Angiotensinogen into Angiotensinogen I

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44
Q

Angiotensinogen

A

hormone made by the liver secreted into blood stream

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45
Q

Angiotensinogen Converting Enzyme

A

secreted by the lungs

converts Angiontensinogen I into Angiotensinogen II

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46
Q

Angiotensinogen II

A

increases SNS activity
H2O retention by kidneys
Aldosterone secretion by Adrenal Cortex
Arteriole Vasoconstriction increasing BP
Post Pituitary release of Vasopressing/ADH
ADH increases H2O reabsorption which increases circulating volume

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47
Q

Aldosterone

A

released from the adrenal cortex by stimulation from Ang II, responsible for signalling kidneys to retain H2O, Na, and excreting K

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48
Q

Antidiuretic Hormone(ADH)/Vasopressin

A

Released from the posterior pituitary in response to Ang II ==> retain water by kidneys

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49
Q

Angiotensin Converting Enzyme (ACE)

A

enzyme found on mostly on the surface of the lungs and some on the kidneys
=> responsible for cleaving Ang I into Ang II
=> destroys bradykinin

50
Q

bradykinin

A

potent humoral modulator that is a powerful vasodilator

51
Q

naturetic hormones

A

activate excretion of Na into the urine
control renal sodium excretion and induce diuresis
improve renal blood flow/filtration
supress aldosterone and SNS

52
Q

obesity leads to increased Primary Hypotension thru

A 
increased adipokines (leptin)
overactive SNS and RAAS
Insulin Resistance - endothelial injury and inflammation
53
Q

preemclampsia

A

HTN in pregnancey and proteinuria after 20 weeks

54
Q

Primary Orthostatic Hypotension

A

neurogenic conditions

55
Q

Secondary Orthostatic Hypotension

A

medications, dehydration

56
Q

examples of vasculitis

A

inflammation of vessels due drugs, infection or autoimmune => thrombangitis obliterans, Kawasaki, temporal arteritis

57
Q

Temporal arteritis/Giant Cell Arteritis

A

T cell and macrophages attack arteries of the brain

58
Q

risk for Temporal arteritis/Giant Cell Arteritis

A

postmenopausal and scandinavian decent

59
Q

S/S Temporal arteritis/Giant Cell Arteritis

A

HA, Vision changes, tenderness, jaw pain

60
Q

Thromboangiitis Obliterans/Buerger’s Disease

A

autoimmune vasculitis where inflammation blocks peripheral arteries of LUE
=> strongly associated with smoking and male gender

61
Q

two categories of Raynaud’s

A

Primary Idiopathic Raynaud’s Disease

Secondary Raynaud’s Syndrome => hypersensitivity rxn associated with connective tissue diseases

62
Q

Raynaud’s

A

Vasospastic response in the small arteries /arterioles of fingers

63
Q

Criteria for Kawasaki Disease

A

Vasculitis seen in children need 5/6
> fever for 5 days
> bilateral conjuctival injection w/o exudate
> changes in oral mucous such as strawberry tongue
> polymorphous rash
> cervical lymphadenopathy
> changes in the extremities/peripheral edema

64
Q

coronary artery stenosis can be a result of

A

Kawasaki Disease

65
Q

Acute Kawasaki

A

fever, conjunctivitis, strawberry tongue, rash, lymphadenopathy, irritability

66
Q

Subacute Kawasaki

A

Begins when fever ends, ends when clinical signs resolve
Child is most at risk for coronary artery aneurism
Peeling of palms and soles, thrombosis

67
Q

Convalescent Kawasaki

A

continued elevation of erythrocyte sedimentation rate and platelet count, coronary artery stenosis, arthritis, thickening of the tunica intima

68
Q

mucocutaneous lymph node syndrom

A

Kawasaki Disease

69
Q

leading cause of coronary artery and cerebrovascular disease

A

Artherosclerosis

70
Q

atheroma

A

plaque development through the accumulation of lipid laden macrophages

71
Q

foam cells

A

macrophages that have consumed oxidized LDLs from microtears in tunica intima

72
Q

fatty streaks

A

accumulation of fatty streaks on BP roughened BV wall

73
Q

what happens to fatty streaks

A

calcify into fibours plaques, that are prone to rupture that can result in thrombus that may occlude artery

74
Q

HTN and Angiotensin

A

=> HTN creates microtears in BV endothelium due to shear pressures
=> HTN results in the release of ANGII
=> ANG II
> endothelial disfunction
> decreases apoptosis
> increases artherosclerosis
> increases thrombosis by increasing platelet aggregation and increasing vasoconstriction
> increases smooth muscle cell growth and migration

75
Q

PAD Peripheral Artery Disease

A

type of atherosclerosis in arteries that supply extremities

76
Q

S/S of PAD

A

intermittent claudication, diminished pulses

77
Q

Ankle Brachial Index

A

BP taken at ankles and calves to see if there is a differential = PAD

78
Q

intermittent claudication

A

leg pain during exercise due to narrowing of arteries

79
Q

How does endothelial dysfunction cause atherosclerosis?

A

Damage to the endothelium upsets the balance between vasoconstriction and vasodilation and initiates a number of events/processes that promote or exacerbate atherosclerosis; these include increased endothelial permeability, platelet aggregation, leukocyte adhesion, and generation of cytokines

80
Q

macrophages release enzymes to digest oxidated LDL and toxic oxygen radicals create oxidative stress

A

atherosclerosis

81
Q

LDL is primarily responsible for

A

delivering cholesterol to tissues

82
Q

excess LDL enters blood arteries

A

causing inflammation

83
Q

can be improved by diet and exercise

A

HDL

84
Q

Lp(a)

A

similar to LDL but has an apolipoprotein(a) attached

85
Q

Lp(a) may increase

A

Coronary Heart Disease and inhibit thrombolysis

86
Q

goal levels of LDL

A

<100-130

87
Q

goal levels of HDL

A

> 40 men

> 50 women

88
Q

function of cholesterol

A

hormone synthesis, cell membrane, bile acid synthesis

89
Q

Hyperlipidemia

A

elevated cholesterol, TG, or LDL

90
Q

Dyslipidemia

A

Hyperlipidemia and lo HDL

91
Q

apolipoprotein

A

protein taxi for cholesterol, w/o which cannot bind to liver receptor and be taken in for processing

92
Q

type of hyperlipidemia that increases patient’s risk for pancreatitis

A

secondary hypertriglyceridemia

93
Q

cardiac leading cause of death

A

coronary artery disease = atherosclerosis of coronary arteries

94
Q

modifiable risk factors of CAD

A

obesity, HTN, diet, diabetes mellitus

95
Q

Risk Factors for CAD

A

adipokines, CKD, pollution, meds, CA calcification, inflammation, microbiome

96
Q

Consisting of four defects, TOF is a congenital cardiac defect that:

A

Allows desaturated blood to enter the systemic system without passing through the lungs

97
Q

A stricture is present in the aorta which leads to restricted blood flow to the lower part of circulation. BP in head and UL’s is high, whilst that in the LL’s is low.

A

Coarctation of the Aorta

98
Q

most common cyanotic congenital cardiac defect

A

Tetralogy of Fallot

99
Q

Tet spells

A

Near occlusion of the right ventricular outflow tract with profound cyanosis

100
Q

Children with cyanotic congential heart disease often

A

squat, this kinks the femoral artery increasing peripheral resistance. This in turn increases left-sided ventricular resistance which lessens the burden of right-eft shunt.

101
Q

normally ductus arteriosus closes and becomes

A

ligamentum arteriosus

102
Q

Coarctation should be suspected in

A

an asymptomatic child with hypertension

103
Q

decrease in the systolic BP on standing by 20 mmHg

A

Orthostatic Postural Hypotension

104
Q

Causes for Orthostatic Hypotension

A

dysfunction of baroreceptors
elderly
beta blockers

105
Q

angina is a symptom

A

of CAD

106
Q

angina pectoris is similar to

A

intermittent claudication

107
Q

pain from angina and intermittent claudication is caused by

A

lactic acid build up from hypoxia in tissues

108
Q

transient myocardial ischemia types

A

Stable Angina = predictable chest pain
Unstable Angina = new onset or change in old pattern
Prinzmetal Angina = vasospasms causing unpredictable angina
Silent Ischemia = no detectable symptoms

109
Q

atherosclerosis is so pervasive that it is threatening to occlude bloodflow to heart

A

> life threatening
acute coronary syndrome
unstable angina

110
Q

Non-STEMI

A

no significant ST segment elevation
early MI
subendocardial ischemia
injury reversible

111
Q

ST elvevation MI

A

Ischemia of heart muscle has gone through wall = transmural

Significant ST segment elevation

112
Q

T Wave Inversion

A

Ischemia

113
Q

ST Segment Elevation

A

Myocardial Injury

114
Q

Q Wave Depression

A

Infarction/Necrosis

115
Q

Mr. PM As MVP

A

Mitral Regurgitation, Physiologic Murmur, Aortic Stenosis, Mitral Valve Prolapse - Systolic Murmurs

116
Q

ARMS

A

Aortic Regurgitation, Mitral Stenosis - Diastolic Murmurs

117
Q

first 24 hrs after MI

A

arrythmias, cardiogenic shock

118
Q

3 days after MI

A

inflammation of pericardium,inflammatory response due to hypoxia and cell death

119
Q

3-14 days after MI

A

scar begins, mushy tissue and easily reinjured, AVOID STRESS

120
Q

2 weeks and beyond

A

remaining muscle picks up slack and grows

121
Q

risk factors for heart failure

A

ischemic heart disease/MI, HTN, congenital disorders

Pathophys (3 decks)

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