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Adv. Patho > Chapter 33: Alterations Of CV Function > Flashcards

Chapter 33: Alterations Of CV Function Flashcards

1
Q

Prevalence of CV dz

A

Leading cause of death in the United States and the world
Total percent of deaths from cardiovascular diseases in the United States: 24.6%
Develop from lifestyle choices: sedentary, smoking, diet

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2
Q

Mechanisms of CV dz

A

Genetic, neurohumoral, and inflammatory mechanisms:
Underlying tissue and cellular processes ->
Endothelial injury
Remodeling
Stunning -> plaque forms and cannot perfuse
Reperfusion injury
Inflammation

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3
Q

Varicose veins

A

Vein in which blood has pooled
Usually in the saphenous vein
Distended, tortuous, and palpable veins

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4
Q

Causes of VV

A

Trauma or gradual venous distention, rendering valves incompetent

Think pressure and weight

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5
Q

RF of VV

A

genetic predisposition, pregnancy, obesity, prolonged sitting or standing,

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6
Q

Manifestations of VV

A

Irregular, purplish, bulging veins
Pedal edema
Fatigue
Aching in the legs
Shiny, pigmented, hairless skin on the legs and feet
Skin ulcer formation

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7
Q

Dx of VV

A

physical examination, Doppler ultrasound, and venogram

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8
Q

tx of VV

A

rest with affected leg elevated, compression stockings, avoid prolong standing or sitting, exercise, sclerotherapy, and surgical removal

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9
Q

Chronic venous insufficiency

A

Inadequate venous return over a long period as a result of varicose veins and valvular incompetency

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10
Q

Manifestations of CVI

A

Lower-Leg swelling, skin color and texture changes -> yellow slough or ruddy skin, venous ulcers (ankles) with irregular borders, dull, achy pain, pulse present, drainage

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11
Q

Deep vein thrombosis

A

Thrombosis: Clot
Detached thrombus: Thromboembolus; can lead to pulmonary emboli
Clot in a large vein
Obstruction of venous flow leading to increased venous pressure

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12
Q

Virchow triad: DVT

A

Venous stasis:
Immobile -> sx, long airplane ride, VV, obesity

Venous endothelial damage:
Sx, trauma, VP, atherosclerosis

Hypercoagulable states:
Genetic, malignancy, oral contraception, smoking

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13
Q

Common places of DVT

A

Typically see in legs, pelvis is hospitalized pt, arms in sedentary person

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14
Q

Prevention of DVT

A

Mobilization soon after surgery, illness, bed rest, injury
Prophylactic low–molecular-weight heparin, antithrombin agents, warfarin, or pneumatic devices
Inferior vena cava filter -> screen placed in IVC to catch clots

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15
Q

Dx of DVT

A

D-dimer: test that looks at fibrin degradation products (FDPS) in the blood –increased = blood clot formation
US

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16
Q

Tx of DVT

A

Low–molecular-weight heparin, unfractionated intravenous heparin, antithrombin agents, or adjusted-dose subcutaneous heparin

Thrombolytic therapy: TPA

Aspirin: Antiplatelet

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17
Q

HTN

A

Prolonged elevation in blood pressure
Excessive cardiac workload due to increased afterload and vasoconstriction

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18
Q

RF for HTN

A

advancing age, ethnicity (AA and Hispanic), family history, being overweight or obese, physical inactive, tobacco use, high-sodium diet, excessive alcohol intake, stress, and other chronic conditions

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19
Q

Primary HTN

A

Most common form
Develops gradually over time

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20
Q

Causes of primary HTN

A

Essential or idiopathic

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21
Q

Secondary HTN

A

Tends to be more sudden and severe
Occurs secondary to another cause

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22
Q

Causes of secondary HTN

A

Causes: renal disease, adrenal gland tumors, certain congenital heart defects, certain medications, and illegal drugs, pregnancy dt estrogen

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23
Q

Malignant HTN

A

Intensified form
Does not respond well to treatment

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24
Q

Manifestations of HTN

A

“Silent killer”
Include: fatigue, headache, malaise, and dizziness

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25
Q

Most common cause of stroke

A

HTN

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26
Q

Complications of HTN

A

atherosclerosis, aneurysms, MI, heart failure, stroke, hypertensive crisis, renal damage, vision loss, metabolic syndrome, memory problems

HTN encephalopathy: confusion, HA, sz
HTN retinopathy
HTN cardiomyopathy: HF
HTN nephropathy: chronic RF

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27
Q

HTN crisis

A

180/120. Typically bc patient is not treating their BP

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28
Q

Dx of HTN

A

history, physical examination, multiple blood pressure readings at varying times of the day,

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29
Q

Tx of HTN

A

Early detection and management is essential to prevent complications
Pharmacologic treatments

Restrict diet to 2g/1 teaspoon NA, Dash diet, stop smoking, exercise

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30
Q

DASH diet

A

6-8 servings of grains per day
6 or less servings of lean protein per day
4-5 servings of fresh fruits and veg per day
4-5 servings of legumes or nuts/seeds per day
Limited fats and sweets
2-3 servings of low-fat dairy per day

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31
Q

Orthostatic (postural) hypotension

A

Decrease in the systolic and diastolic blood pressures on standing by SBP 20 mm Hg or more and by DBP 10 mm Hg or more, respectively
Lack of normal blood pressure compensation in response to gravitational changes on the circulation, leading to pooling and vasodilation
Acute vs. chronic

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32
Q

Acute orthostatic hypotension

A

Caused by certain antiHTN medications.

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33
Q

Manifestations of ortho hypotension

A

Fainting upon standing

Typically occurs in an older person with lack of vaso motor tone. When they stand up, all the blood goes tot heir feet instead of vasoconstriction and keeping blood up in core.

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34
Q

Tx of ortho hypotension

A

Liberalize salt intake, raise the head of the bed, wear thigh-high stockings, expand volume with mineralocorticoids (aldosterone), and administer vasoconstrictors (shunt blood to core and head)

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35
Q

Aneurysms

A

Weaken of an artery
Can occur in an artery: Common in the abdominal aorta (most common), thoracic aorta, and the cerebral (second most common), femoral, and popliteal arteries
Can rupture – exsanguination
True and false aneurysms

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36
Q

RF for aneurysms

A

congenital defect, atherosclerosis, hypertension, dyslipidemia, diabetes mellitus, tobacco, advanced age, trauma, and infection

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37
Q

3 types of true aneurysms

A

affect all three vessel layers
Saccular aneurysm – bulge on the side
Cerebral

Fusiform aneurysm – occurs the entire circumference
Aortic

Dissecting aneurysms - occurs in the inner layers
Inner layer breaks open an bleeding starts in the layers
Fast leak -> emergency sx
Slow leak -> manage with BP medications

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38
Q

False aneurysm

A

does not affect all three layers of the vessel

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39
Q

3 things to think for aneurysm

A
  1. Where is it located
  2. True or false
  3. Shape
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40
Q

Manifestations of aneurysm

A

Aortic aneurysm asymptomatic until it ruptures -> pulsating mass, tearing pain
thoracic aorta -> resp difficulty.
Neuro decline common in brain aneurysm -> sz, sudden headache, loss of consciousness.
An extremity could be impaired.
Rupture -> shock -> sx

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41
Q

Dx of aneurysm

A

physical examination, X-ray, echocardiogram, CT, MRI, and arteriography

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42
Q

Tx of aneurysm

A

eliminating or managing cause and surgery

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43
Q

Thrombus

A

Stationary blood clot.
Activation of the coagulation cascade.

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44
Q

Causes of thrombus

A

roughening of the tunica intima by atherosclerosis

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45
Q

Emboli

A

Emboli – traveling body
May be a thrombus, air, fat, tissue, bacteria, amniotic fluid, tumor cells, and foreign substances
Can become lodged in places like the lungs, brain, and heart

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46
Q

Peripheral vascular dz

A

Narrowing of the peripheral vessels
Decreased blood supply to extremities

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47
Q

Causes of PVD

A

atherosclerosis, thrombus, inflammation, and vasospasms

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48
Q

Raynauds dz

A

Vasospasms of arteries, usually in the hands, because of sympathetic stimulation
Associated with autoimmune dz

49
Q

Thomromboangitis obliterans - Bergers disease

A

An inflammatory condition of the arteries
Rare but BV inflamed and they swell and when they swell they’re blocked with clots -> necrosis, could gangrene

50
Q

Common cause of BD

A

Smoking

51
Q

Manifestations of PVD

A

pain, intermittent claudication, numbness, burning, non-healing wounds, skin color changes, hair loss, and impotency, black Eschar, round smooth sores on toes and feet, NO drainage or edema, cool to touch

“The pain gets better if I dangle my foot of the bed -elevating my feet makes the pin worse”

Intermittent Claudication: first s/sx, c/o pain and heaviness in legs, induced by exercise and relieved by rest.
Shiny, hairless skin
No pulse

52
Q

Dx of PVD

A

US or arteriography would be the most definitive: dye into artery and see how patent.

53
Q

tx of PVD

A

reducing contributing factors, angioplasty, bypass procedures, laser procedures, atherectomy, antiplatelet agents (clopidogrel), anticoagulants, thrombolytic, and lipid-lowering agents

Stop smoking!!!
Exercise -> walk 1 hr/day to stimulate collateral circ around those vessels. Can rest with pain, but restart
Weight reduction
Control DM and hyperlipidemia
If nothing else works -> amputation

54
Q

Dyslipidemia

A

High levels of lipids in the blood
Increases risk for many chronic diseases
Lipids come from dietary sources and liver production

Dietary sources
Cholesterol – animal products
Triglycerides – saturated fats

Very common

55
Q

Types of cholesterol

A

Classified based on density, which is based on the amount of triglycerides (low density) and protein (high density)
Very-low density lipoproteins
Low density lipoproteins AKA “bad” cholesterol -> lead to deposition of plaque in BV
High density lipoproteins – AKA “good” cholesterol

HDL grab LDL and take them to liver to eliminate them

56
Q

Manifestations of hyperlipidemia

A

asymptomatic until it develops into other diseases

57
Q

Dx of hyperlipidemia

A

cholesterol screening and lipid panels

58
Q

Tx of hyperlipidemia

A

dietary changes, weight reduction, routine exercise, tobacco cessation, lipid-lowering agents, and complication management

59
Q

Atherosclerosis

A

Chronic inflammatory disease characterized by thickening and hardening of the arterial wall
Inflammatory process is triggered by a vessel wall injury -> HTN, smoking, hyperlipidemia, hyperhomocysteinmia, Hemodynamic factors, toxins, viruses, immune rxn
Lesions develop on the vessel wall and calcify over time

Leads to vessel obstruction, platelet aggregation, and vasoconstriction

Leading case of heart dz, contributes to stoke
Occurs throughout body

60
Q

Mechanism of atherosclerosis

A

LDL enters vessel -> oxidized to inflammatory lipids and then these lipids causes adhesions and then these cells turn into foam cells and they cause fatty streak and fibrous plaque, they oxidize and lesions form and blood clots form on it.

61
Q

Complications of atherosclerosis

A

peripheral vascular disease, coronary artery disease, thrombi, hypertension, and stroke

62
Q

Manifestations of atherosclerosis

A

asymptomatic until complications develop

63
Q

Dx of atherosclerosis

A

identify contributing factors and complications

64
Q

Tx of atherosclerosis

A

similar to dyslipidemia with the addition of angioplasty, bypass, laser procedures, and artherectomy

65
Q

Coronary artery dz

A

Atherosclerotic changes of the coronary arteries
Impairs myocardial tissue perfusion
Angina – chest pain resulting from myocardium ischemia
Infarction – necrotic damage to the myocardium

66
Q

Causes of CAD

A

atherosclerosis, vasospasms, thrombus, and cardiomyopathy

67
Q

Complications of CAD

A

myocardial infarction, heart failure, dysrhythmias, and sudden death

68
Q

Manifestations of CAD

A

angina, indigestion-like sensation, nausea, vomiting, clammy extremities, diaphoresis, and fatigue

69
Q

Dx of CAD

A

H&P, identify contributing factors, exercise stress test, echocardiogram, and electrocardiogram

70
Q

Tx of CAD

A

similar to those used to treat dyslipidemia and atherosclerosis with the addition of nitrates, vasodilators and anti-hypertensive’s, and oxygen

71
Q

Angina

A

Intermittent chest pain resulting from myocardium ischemia
Stable – goes away with demand reduction
Goes away with nitro and rest

Unstable – increased intensity or frequency, does not go away with demand reduction, or occurs at rest
Medical emergency

Prizmentals Angina (variant angina)-occurs almost exclusively at rest
Caused by vasospasm with or without atherosclerosis
Coke, genetic

72
Q

Infarction

A

permanent necrotic damage to the myocardium

73
Q

MI

A

Death of the myocardium
Coronary artery blood flow is blocked due to atherosclerosis, thrombus, or vasospasms
Risk factors are the same as those for atherosclerosis

74
Q

Manifestations of MI

A

Some are asymptomatic – “Silent” MI
Includes: angina, fatigue, nausea, vomiting, shortness of breath, diaphoresis, indigestion, elevation in cardiac markers, ekg changes

Infarcted myocardium is surrounded by a zone of hypoxic injury, which may progress to necrosis or return to normal; adjacent to this zone is a zone of reversible ischemia.
Sudden severe chest pain
ECG changes
Troponin I: Most specific
Elevates in 2 to 4 hours
Creatine phosphokinase–MB (CPK-MB), LDH

75
Q

2 major types of MI

A

Subendocardial infarction (NSTEMI)
Transmural infarction (STEMI): Goes all the way through the myocardium

76
Q

Coronary syndrome

A

Unstable Angina- Pre infarction. Can have ST changes on ekg, but cardiac enzymes are normal

Non- STEMI- Smaller infarctions are not associated with ST segment elevations
Suggest that additional myocardium is still at risk for recurrent ischemia and infarction

ST segment elevations (STEMI) on the ECG requires immediate intervention.
Individuals at highest risk for complications

77
Q

EKG alterations for unstable angina and NSTEMI

A

St depression and t wave inversion

78
Q

EKG changes for zones of MI

A

Zone of ischemia: st segment depression with or without t wave inversion as a result of altered repolarization
Zone of injury: myocardial injury cases ST segment elevation with out without loss of R wave
Zone of infarction: MI causes deep Q waves as result of absence of depolarization current from dead tissue and receding currents from opposite side of heart

79
Q

Tx of MI

A

Hospitalization
Immediate administration of supplemental oxygen and aspirin -> anti plt an the chew it and within 10 min -> anti plt aggregation occurs.
Nitroglycerine -> vasodilation
Morphine -> pain
Beta Blockers > decrease HR and vasodilation
Anticoagulants -> warfarin or aixaban to prevent clotting
Bed rest
Thrombolytic candidate -> only STEMI
Percutaneous coronary intervention (PCI) -> NSTEMI and unstable angina
Surgery

80
Q

Pericarditis

A

Inflammation of the pericardium
Fluid accumulates - pericardial effusion
Swollen tissue creates friction

81
Q

Cause of pericarditis

A

Virus -most common
Open heart sx

82
Q

Constrictive pericarditis

A

Loss of elasticity
Results from chronic inflammation

83
Q

Cardiac tamponade

A

Cardiac compression from excessive fluid accumulation
Life-threatening

84
Q

Manifestations of cardiac tamponade

A

Manifestations: falling arterial pressures fall, rising venous pressures, narrowing pulse pressure, and muffled heart sounds
decrease CO, low BP, increase preload

85
Q

Complications of cardiac tamponade

A

heart failure, shock, and death

86
Q

Manifestations of pericarditis

A

Pericardial friction rub (grating sound heard when breath is held)
Sharp, sudden, severe chest pain that increases with deep inspiration and decreases when sitting up and leaning forward
Dyspnea
Tachycardia
Edema
Flulike symptoms

87
Q

Dx of Pericarditis

A

H&P, CBC, electrocardiogram, chest X-ray, echocardiogram

88
Q

Tx of pericarditis

A

identify and resolve the underlying cause,
nonsteroidal anti-inflammatory drugs, analgesics,
bed rest,
oxygen therapy, pericardiocentesis
pericardiectomy

89
Q

Infective endocarditis

A

Commonly caused by Streptococcus and Staphylococcus infections
Vegetation forms on internal structures and creates small thrombi
Micro emboli occur as they are dislodged, resulting in micro-hemorrhages

90
Q

RF for IE

A

intravenous drug use, valvular disorders, prosthetic heart valves, rheumatic heart disease, congenital heart defects

91
Q

IE manifestations

A

flulike symptoms, fever, embolization, heart murmur, petechiae, splinter hemorrhages, Janeway lesions, Osler’s nodes, Roth spot on retina

92
Q

Dx of IE

A

H&P, blood cultures, CBC, urinalysis, erythrocyte sedimentation rate, electrocardiogram, and echocardiogram

93
Q

Tx of IE

A

identification of causative agent, long-term AB, bed rest, antipyretics, surgical valve repair, and prosthetic valve replacement

94
Q

Valvular dz

A

Disrupt blood flow through the heart

95
Q

Stenosis

A

narrowing
Less blood can flow through the valve
Causes decreased cardiac output, increased cardiac workload, and hypertrophy

96
Q

Regurgitation

A

insufficient closure
Blood flows in both directions through the valve
Causes decreased cardiac output, increased cardiac workload, hypertrophy, and dilation

97
Q

Causes of valve dz

A

congenital defects, infective endocarditis, rheumatic fever, myocardial infarction, cardiomyopathy, and heart failure

98
Q

Manifestations of valve dz

A

Vary depending on valve involved
Reflect alteration in blood flow through the heart

99
Q

dx of valve dz

A

H&P, heart catheterization, chest X-rays, echocardiogram, electrocardiogram, and MRI

100
Q

Tx of valve dz

A

diuretics, anti-dysrhythmics, anti-hypertensives, anticoagulants, oxygen therapy, low-sodium diet, surgical valve repair, and prosthetic valve replacement

101
Q

Cardiomyopathy

A

Conditions that weaken and enlarge the myocardium
Classified into three groups—dilated, hypertrophic, and restrictive

102
Q

Dilated cardiomyopathy

A

Dilated is most common. Heart muscle dilates. Most are idiopathic, ischemia, MI, CAD, alc, pregnancy, drug use

103
Q

Hypertrophic cardiomyopathy

A

septum thicken. genetic -> autosomal dominant disorder. Usually goes into sudden cardiac death.

104
Q

Restrictive cardiomyopathy

A

muscle can’t relax, diastole dysfunction. Amyloidosis -> buildup of protein or fat in heart, build up of iron in heart

105
Q

S/sx of cardiomyopathy

A

S/sx of heart failure: fatigue, dspneic, activity intolerance.

106
Q

Tx of cardiomyopathy

A

Heart transplant

107
Q

Heart failure

A

1 case of hospital admissions in age 65 and older

Inadequate pumping

Leads to decreased cardiac output, increased preload, and increased afterload

Compensatory mechanisms activated
Activation of the sympathetic nervous system
Activation of the renin-angiotensin-aldosterone system
Ventricular hypertrophy

108
Q

Types of HF: systolic dysfunction

A

Systolic dysfunction:
Pump problem
HFrEF: Heart failure with reduced ejection fraction -> Decreased contractility, enlarged ventricles, results from reduced contraction of the L ventricle such that not enough blood is pumped into circ

109
Q

types of HF: dastolic dysfunction

A

Filling problems
HFpEF: heart failure with reserved EF, decreased filling, thicken vent mm, L vent becomes stiff and does not relax normally, as a result it cannot fill properly and pressure begins to increase in the L heart chambers and in the lungs

110
Q

Left-sided HF

A

Cardiac output falls
Blood backs up to the pulmonary circulation

111
Q

Causes f L HF

A

left ventricular infarction, hypertension, and aortic and mitral valve stenosis

112
Q

Manifestations of L HF

A

pulmonary congestion, dyspnea, and activity intolerance, lung cracked, wheezing, displaced cardiac apex, L sided heart murmurs

113
Q

Right-sided HF

A

Blood backs up to the systemic circulation

114
Q

Causes of R HF

A

pulmonary disease, left-sided failure, and pulmonic and tricuspid valve stenosis

115
Q

Manifestations for RHF

A

edema and weight gain, hepatomegaly, increase JVD, regurgitant murmur in tricuspid area

116
Q

Mixed dysfunction HF

A

Both systolic and diastolic dysfunction

117
Q

HF manifestations

A

Shared L and R sx: cool peripheries, cyanosis, orthopnea, delayed cap refill

May be acute or chronic
Manifestations:
Depend on type
Fluctuates in severity
Appear as compensatory mechanisms fail
Includes: indications of systemic and pulmonary fluid congestion

118
Q

HF dx

A

H&P, chest X-ray, echocardiogram, electrocardiogram.

119
Q

HF tx

A

Identify and manage underlying cause
Include: lifestyle modification, angiotensin-converting enzyme inhibitors, diuretics, anti hypertensives, biventricular pacemaker, and heart transplant

Adv. Patho (5 decks)

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