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Patho-Workbook-Test 2 Chapters > Chapter 32 Alterations of Cardiovascular Function in Adults > Flashcards

Chapter 32 Alterations of Cardiovascular Function in Adults Flashcards

1
Q

Distended and tortuous superficial veins in which blood has pooled because of damaged valves.

A

Varicose Veins

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2
Q

Sustained inadequate venous return due to valvular damage

A

Chronic venous insufficiency

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3
Q

Ischemic pain in the lower extremities that occurs while walking but disappears when resting.

A

Intermittent claudication

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4
Q

Inflammatory disease of peripheral arteries that usually is associated with smoking

A

Thromboangitis obliterans

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5
Q

Vasospastic disease of peripheral arteries in which episodes of ischemia and pallor are followed by rubor and paresthesias.

A

Raynaud disesase

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6
Q

Inflammation of the membranous sac that surrounds the heart

A

Pericarditis

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7
Q

Compression of the heart by pericardial fluid

A

tamponade

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8
Q

Post-thrombotic syndrome is characterized by chronic persistent pain and (pallor & atrophy OR edema & ulceration) of a limb that had a deep venous thrombosis.
(pallor & atrophy OR edema & ulceration).

A

edema & ulceration

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9
Q

A major danger of DVT is development of (cerebral OR PULMONARY) thromboembolism; a danger of an arterial thrombus is development of (systemic OR pulmonary) thromboembolism.

A

pulmonary; systemic

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10
Q

Superior vena cava (SVC) syndrome occurs when a tumor or other mass (ruptures OR compresses) the SVC causing (severe hypertension OR venous distention) in the upper extremities and head.

A

compress; venous distention

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11
Q

Factors that cause primary hypertension increase peripheral vascular (responsiveness OR resistance) and/or cause sustained (increase OR decrease) in blood volume.

A

resistance; increase

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12
Q

In HTN, the pressure-natriuresis relationship shifts so that the hypertensive individual excretes (more OR less) sodium in the urine.

A

less

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13
Q

Persons who have uncomplicated hypertension usually have (no OR many) signs and symptoms in addition to their elevated BP; treatment usually begins with (antihypertensive medications OR lifestyle modifications).

A

no; lifestyle modifications

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14
Q

The term “dissecting aneurysm” means that blood enters an artery wall and (runs between the layers of the wall OR bursts through the wall & causes hemorrhage).

A

runs between the layers of the wall

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15
Q

Risk for MI increases with low blood levels of (LDL or HDL) and with high blood levels of (LDL or HDL).

A

HDL; LDL

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16
Q

Cardiac valve damage in rheumatic fever is caused by (group A B-hemolytic streptococci OR an abnormal immune response) whereas cardiac valve damage in infective endocarditis is caused by (streptococci or other organisms OR an abnormal immune response).

A

an abnormal immune response; streptococci or other organisms

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17
Q

Orthopnea is often seen in (left heart failure OR right heart failure)?

A

Left heart failure

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18
Q

Ankle edema is often seen in (left heart failure OR right heart failure)?

A

Right heart failure

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19
Q

Jugular venous distention is often seen in (left heart failure OR right heart failure)?

A

Right heart failure

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20
Q

Dyspnea is often seen in (left heart failure OR right heart failure)?

A

Left heart failure

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21
Q

Decreased urine output is often seen in (left heart failure OR right heart failure)?

A

Left heart failure

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22
Q

Coughing pink, frothy sputum is often seen in (left heart failure OR right heart failure)?

A

Left heart failure

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23
Q

Crackles upon auscultation is often seen in (left heart failure OR right heart failure)?

A

Left heart failure

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24
Q

Hepatomegaly is often seen in (left heart failure OR right heart failure)?

A

Right heart failure

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25
Q

A clot in a blood vessel that breaks loose and circulates is called a

A

thromboembolis

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26
Q

Sluggish circulation from chronic venous insufficiency may cause a venous __________ ulcer.

A

stasis

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27
Q

Sustained hypertension causes left ventricular _________ and coronary atherosclerosis, thus increasing the risk for _____________ ____________.

A

hypertrophy; myocardial infarction

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28
Q

Rapidly progressive hypertension with a diastolic pressure above 140 mmHg is called ____________ hypertension and can damage the ____________.

A

malignant; brain

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29
Q

Postural hypotension, aslo called ____________ hypotension , is a systolic blood pressure decrease of at least __ mmHg or a diastolic blood pressure decrease of at least __mmHg within 3 minuets of standing and is a significant risk factor for ___________.

A

orthostatic; 20; 10; falls

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30
Q

Persons who have subacute bacterial endocarditis are at risk ________ embolism, whereas persons who have trauma to long bones are at risk ____________ embolism.

A

bacterial; fat

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31
Q

The risk factors for peripheral arterial disease are the same as the risk factors for _______; the risk factors for contrary artery disease are the same risk factors for _________.

A

atherosclerosis; atherosclerosis

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32
Q

Clot formation at the site of rupture of an atherosclerotic plaque causes tissue __________ , which leads to ________ if blood flow is not restored.

A

ischemia; infarction…remember, 20 minutes for ischemia to turn into infarction

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33
Q

Persons who are obese have decreased levels of ______, an antiatherogenic adipokine.

A

adiponectine

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34
Q

Risk for myocardial infarction increases with factors that increases myocardial oxygen _________ or reduce myocardial oxygen ________.

A

demand; supply

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35
Q

Tissue healing after myocardial infarction creates a noncontractile _______.

A

scar

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36
Q

The ischemic injury from a sudden blockage of a coronary artery can be exacerbated by _______ injury when blood flow is restored.

A

reperfusion - toxic oxygen radicals are released, a calcium flux and pH changes occur w/sustained opening of mitochondrial permeability transition pores (mPTP).

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37
Q

Acute rheumatic fever is characterized by carditis, acute migratory ________ , chorea, and _______ marginatum, which occur 1 to 5 weeks after streptococcal infection of the _______.

A

polyarthritis ;erythema; pharynx

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38
Q

Heart failure in which the cardiac output is increased but still insufficient to meet the body’s oxygen and nutrient needs is called _______ heart failure.

A

high-output

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39
Q

Right atrial and right ventricular dilation and hypertrophy

A

tricuspid regurgitation

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40
Q

Left atrial hypertrophy and dilation

A

mitral stenosis

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41
Q

Left ventricular hypertrophy and dilation

A

aortic stenosis

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42
Q

Left atrial and left ventricular dilation and hypertrophy

A

mitral regurgitation

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43
Q

Acronym for clot formation in a large vein, usually in lower extremities

A

DVT

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44
Q

Nonspecific marker of inflammation measured to asses cardiac risk

A

CRP

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45
Q

Another term for Peinzmetal angina

A

variant

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46
Q

Localized outpouching or dilation of a vessel wall or cardiac chamber

A

aneurysm

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47
Q

Blood clot that is attached to the endothelium in a blood vessel or cardiac chamber

A

thrombus

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48
Q

type of angina caused by a clot temporarily occluding a coronary artery, resolving before necrosis occurs

A

unstable

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49
Q

Valve cusps billow backward into valve opening when valve should be closed

A

prolapse

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50
Q

Acronym for type of lipoprotein that migrates into arterial walls in atherosclerosis

A

LDL

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51
Q

Cardiac biomarker measured in blood to detect myocardial infarction

A

troponin

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52
Q

Disturbance of cardiac rhythm

A

dysrhythmia

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53
Q

A bolus of matter circulating in the blood

A

embolus

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54
Q

Lack of oxygen in tissue due to a lack of blood supply

A

ischemia

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55
Q

The lesion of atherosclerosis

A

plaque

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56
Q

Acronym foe a myocardial infarction that shows ST-segment elevation on ECG

A

stemi

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57
Q

Acronym for elevated systolic blood pressure accompanied by normal diastolic blood pressure

A

ISH

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58
Q

Name three factors that promote venous thrombosis (triad of Virchow)

A

1) VENOUS STASIS due to immobility (i.e. during air travel), age, heart failure or spinal cord injury
2) VENOUS ENDOTHELIAL DAMAGE (trauma & IV meds), and
3) HYPERCOAGULABLE STATES (pregnancy, malignancy, OCPs, & genetic coagulopathies).

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59
Q

Treatment for DVT:

A

heparin (IV or subq) & antithrombin agents, then ASA to reduce recurrence after heparin is D/C

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60
Q

Conditions that affect cardiovascular system (strokes, heart failure) are detrimental because

A

reduces the CV carrying power, most important in hemostasis because carries O2 & nutrients to all cells.

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61
Q

Xanthelasmas (small fat deposits around eyelids) or arcus senilis of the eyes (a yellow lipid ring around cornea) suggests

A

dyslipidemia & possible atherosclerosis

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62
Q

Peripheral or carotid arterial bruits suggests

A

probable atherosclerosis and increases likelihood that CAD is present

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63
Q

Characteristic signs of subendocardial ischemia on EKG include:

A

transient ST-segment depression & T-wave inversion

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64
Q

Characteristic signs of transmural ischemia (ST-segment elevation on EKG)

A

seen in variant (Prinzmetal angina) & MI

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65
Q

Determination of the presence of atherosclerotic plaques requires the use of what imaging studies?

A

CT w/ and w/o angiography, MRI, or intravascular ultrasound but these are high risk and expensive; used primarily for evaluation for possible PTCI or CABG.

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66
Q

For what amount of time do cardiac cells stay viable in ischemic conditions?

A

20 minutes

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67
Q

After 20 minutes of ischemia and blood flow is not restored, what condition ensues?

A

Myocardial infarction

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68
Q

Primary aim of therapy for myocardial ischemia?

A

Increase delivery of O2 by improving coronary artery blood flow AND
Reduce myocardial oxygen consumption

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69
Q

Methods to improve coronary artery blood flow are

A

reverse vasoconstriction, prevent clotting, & reduce plaque growth & rupture.

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70
Q

Methods to decrease myocardial oxygen consumption are

A

manage BP, HR, & contractility, and

manage left ventricular volume

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71
Q

Which drug class available in the management of stable angina improves coronary blood flow and reduces myocardial demand by reducing cardiac workload (decreasing peripheral vascular resistance & venous return to heart i.e. preload)?

A

Nitrates

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72
Q

How do beta blockers, considered first-line therapy for stable angina, reduce myocardial oxygen requirements (like during physical exertion)?

A

They diminish catecholamine-induced elevations of HR, myocardial contractility, and BP. By reducing heart rate, additional diastolic filling time for coronary perfusion is possible enhancing oxygen delivery to the heart.

73
Q

Which drug class for treatment of stable angina meant to decrease myocardial oxygen demand works by reducing influx of calcium into myocardial cells & vascular smooth muscle, modify SA node pacemaker activity, and conduction properties of AV node?

A

Calcium-channel blockers ( aka calcium antagonists)

74
Q

What harmful effects do calcium-channel blockers have on the heart?

A

May impair cardiac contractility and heart rate.

75
Q

Unstable angina patients may have symptom relief but not reversal of atherosclerotic process. What medications are indicated to stabilize or regress plaques and prevent clotting?

A

ACE inhibitors or ARBs, statins, & anti-thrombotics

76
Q

Coronary revascularization with percutaneous coronary intervention (PCI) and CABG is indicated when ______

A

patients fail to respond adequately to antianginal drugs (refractory angina), have high-risk atherosclerotic lesions, or present hemodynamic instability

77
Q

A form of acute coronary syndrome that indicates an atherosclerotic plaque has ruptured and infarction is likely is called____________.

A

unstable angina - occurs when fissuring or superficial erosion of a plaque leads to transient episodes of thrombotic vessel occlusion & vasoconstriction at site of plaque damage, occlusion lasts no more than 10-20 minutes, reperfusion occurs before necrosis ensues.

78
Q

Clinical manifestations of unstable angina are:

A

new onset angina,
angina occurring at rest, or
angina that is increasing in severity or frequency. Pts experience dyspnea, diaphoresis, & anxiety as angina worsens.

79
Q

EKG findings in unstable angina:

A

ST-segment depression & T-wave inversion during pain

80
Q

What percentage of patients with unstable angina will progress to MI or death within hours or days of onset of symptoms?

A

20%

81
Q

Serum cardiac biomarkers such as troponins, creatine phosphokinase-myocardial bound (CK-MB) & lactate dehydrogenase (LDH-1) are NORMAL or ABNORMAL in unstable angina?

A

normal, markers become abnormal when infarction (myocyte necrosis) occurs

82
Q

Primary cause of myocardial infarction is decreased coronary flow as a result of ________?

A

atherosclerotic CAD, other causes include coronary spasm & coronary artery embolism.

83
Q

What are the two categories of MI?

A

non-STEMI (subendocardial) and

STEMI (transmural MI)

84
Q

Which type of MI is this describing?
thrombus breaks up before complete distal tissue necrosis occurs; infarction only involves myocardium directly beneath the endocardium where infarction occurs, usually presents with ST-depression and T-wave inversion

A

non-STEMI (subendocardial)

85
Q

Which type of MI is this describing?
thrombus lodges permanently in the vessel, infarction extends through the myocardium (from endocardium through to the epicardium), resulting in severe cardiac dysfunction; usually presents with marked elevations in ST-segement on EKG.

A

STEMI (transmural)

86
Q

Which one is a higher risk for serious complications and requires immediate intervention, non-STEMI or STEMI?

A

STEMI, although non-STEMI will also need intervention since disrupted plaque is high risk for recurrent clot formation

87
Q

As a result of oxygen deprivation, ischemic myocardial cells lose contractility and release _____________ predisposing the patient to serious imbalances of sympathetic and parasympathetic function like _______.

A

catecholamines (epi and norepi); dysrhythmias & heart failure

88
Q

Norepinephrine raises blood glucose levels how?

A

stimulation of gluconeogenesis by liver and skeletal muscles & suppression of beta-cell activity (reducing insulin) and results in hyperglycemia noted 72 hours after MI increasing risk of death.

89
Q

Angiotensin II released during myocardial ischemia contributes to pathogenesis of MI how?

A

systematic effects of angiotensin II (peripheral vasoconstriction & fluid retention)
increase cardiac workload AND
locally causes coronary artery vasospasm

90
Q

What type of wave is found on EKG that is characteristic of an STEMI a few hours after infarction?

A

Q-wave

91
Q

Which laboratory test is the most specific indicator of myocardial infarction?

A

Cardiac troponin I (cTnI), detectable 2-4 hrs after onset of symptoms.

92
Q

At what time intervals should troponin I levels be obtained in suspected MI patients?

A

upon initial presentation, within 6-9 hrs, and again 12-24 hours after presentation, especially if initial tests were negative.

93
Q

Troponin I levels can be used to estimate infarct size and likelihood of complications, TRUE or FALSE?

A

True

94
Q

Other laboratory findings, aside from elevated troponin levels, common in MI patients include:

A

elevation of cardiac biomarkers (CPK-MB & LDH), leukocytosis and elevated C-reactive protein (indicating inflammation), elevated BS levels, & hypoxemia.

95
Q

When is the time of highest risk of cardiac death following an MI?

A

First 24 hours

96
Q

Myocardial repair following MI results in the formation of scar tissue, that at __________ is often stressed when individuals feel they are more capable of increasing activities following MI, but is not strong yet until ______ weeks following an MI.

A

10-14 days; 6 weeks…although this new scar tissue is unable to contract & relax like healthy myocardial tissue.

97
Q

After a STEMI & initial PCI, thrombolytic, or antithrombotic therapy, continued pharmacologic management is necessary with what classes of drugs?

A

ACE inhibitors, statins, & beta-blockers

98
Q

Risk factors that contribute to the likelihood of death or reduce the chances of long-term survival after an MI include:

A

1) degree of left ventricular dysfunction
2) degree of left ventricular ischemia
3) potential for ventricular dysrhythmia, and
4) individual’s age

99
Q

What are the most important predisposing factors for heart failure?

A

Hypertension and ischemic heart disease

100
Q

Most common cause of decreased myocardial contractility

A

MI, other causes include cardiomyopathies and myocarditis

101
Q

What 3 major factors influence stroke volume?

A

contractility, preload, & afterload

102
Q

What are consequences of ventricular remodeling that occurs as a result of inflammatory, immune, and neurohumeral changes in the myocardium in patients with heart failure?

A

Disruption of normal myocardial extracellular structure causing progressive myocyte contractile dysfunction over time, diminishing contractility, stroke volume falls, & left ventricular end-diastolic volume (LVEDV) = dilation of heart & increase in preload.

103
Q

Weakness of cardiac muscle due to hypertension-induced hypertrophy is called ________?

A

hypertensive hypertrophic cardiomyopathy

104
Q

Neurohumoral changes in heart failure involve what two processes?

A

1) RAA - Renin-angiotensin-aldosterone system and

2) SNS- sympathetic nervous system

105
Q

Cardiac cachexia is

A

Weight loss and weakness in individuals with heart failure

106
Q

The clinical manifestations of HFrEF (heart failure with reduced ejection fraction, a.k.a. left sided heart failure) are:

A

dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urinary output, & edema (as a result of pulmonary vascular congestion & inadequate perfusion of systemic circulation)

107
Q

What is the principle cause of acute onset left heart failure?

A

MI

108
Q

The administration of oxygen, nitrates, & morphine in treatment of heart failure helps by:

A

1) improving myocardial oxygenation,
2) relieves coronary spasm, and
3) lowers cardiac preload through systemic vasodilation.

109
Q

Diuretics are the mainstay of heart failure therapy, why?

A

They reduce cardiac preload by reducing circulating volume.

110
Q

How do ACE inhibitors help in the treatment of heart disease and heart failure?

A

They reduce preload and afterload by inhibiting conversion of angiotensin I to angiotensin II (ang II causes Na and H20 retention and is toxic to myocardium).

111
Q

How do beta blockers help in the treatment of heart disease and heart failure?

A

They reduce myocardial demand (myocardial oxygen requirements).

112
Q

ARBs are used in heart failure patients who cannot tolerate what class of drugs?

A

ACE inhibitors

113
Q

Digoxin is what type of drug & how does it work?

A

Inotropic - acts on cardiac cells, causes excitation-contraction coupling triggering membrane depolarization, inhibits Na-K pump causing increased intracellular Na which increases Na/Ca exchange resulting in increased calcium in sarcoplasmic reticulum = activation of cardiac contractile proteins (actin & myosin) =

1) INCREASED FORCE OF CONTRACTION OF CARDIAC MUSCLE
2) Depressed SA node, prolonged AV conduction, increased refractory period of AV node, increased peripheral resistance all work to SLOW THE HEART RATE.

114
Q

Digoxin is most effective in what kind of heart failure?

A

Failure caused by left ventricular dysfunction, added effect in these patients is brought about by the increased cardiac output leading to improved renal perfusion and increase in diuresis.

115
Q

Primary causes of diastolic heart failure (also called heart failure with preserved ejection fraction- HFpEF)?

A

Major causes of diastolic dysfunction in these patients is hypertension-induced myocardial hypertrophy & MI w/resultant ventricular remodeling, and left ventricular hypertrophy.

116
Q

Diastolic heart failure accounts for ____% of all cases of left heart failure and is more common in _________.

A

50%; women. This type of heart failure does not call for use of inotropic drugs (digoxin) since contractility and ejection fraction are not affected.

117
Q

Decreased ventricular compliance in HFpEF causes an increase in left atrial pressure that leads to _____

A

pulmonary edema from pulmonary congestion made worse by tachycardia

118
Q

Symptoms of HFpEF upon presentation include

A

dyspnea on exertion & fatigue…because any activity that induces exerts the heart increases left atrial pressure leading to increased pulmonary congestion and pulmonary edema.

119
Q

Increased pulmonary congestion and pulmonary edema may lead to _________

A

right ventricular failure.

120
Q

Current guidelines recommend treating underlying cause of heart failure with diastolic dysfunction (HFpEF) which most often is

A

hypertension or valvular disease. Nonpharmacologic recommendations include physical training (aerobic & weight training),

121
Q

Right heart failure most often results from ________

A

left heart failure, leading to increased pulmonary circulation and pulmonary pressures which increase resistance to right ventricular emptying.

122
Q

Because the right ventricle is not anatomically prepared to deal with increased pulmonary resistance in right sided failure, the right ventricle fails leading to increased systemic venous circulation and clinical manifestations of right-sided heart failure such as _____

A

jugular venous distention, peripheral edema, & hepatosplenomegaly.

123
Q

Treatment of right sided heart failure is reliant on treatment of ______________

A

left sided heart failure.

124
Q

What are other etiologies of right-sided heart failure when left-sided heart failure is not the cause?

A

pulmonary hypertension resulting from diffuse hypoxic pulmonary disease (COPD, cystic fibrosis, & ARDS), ventricular MI, cardiomyopathies, & pulmonic valve disease.

125
Q

What is high-output heart failure?

A

The inability of the heart to adequately supply the body’s needs despite adequate blood volume and normal or elevated myocardial contractility.

126
Q

What are the causes of high output heart failure?

A

In this type of heart failure, although the heart increases output, body’s metabolic needs are still not met, common causes include anemia, septicemia, hyperthyroidism, & beriberi.

127
Q

How does septicemia cause high output heart failure?

A

Septicemia leads to disturbed metabolism, bacterial toxins, & inflammatory processes which cause vasodilation & fever, all these lead to lowered systemic vascular resistance & elevated metabolic rate…despite hearts attempts to increase cardiac output and prevent acidosis, yet it is unable to meet the body’s needs & body’s tissues show signs of inadequate blood supply despite very high cardiac output.

128
Q

Beriberi (thiamine deficiency) is associated with high output heart failure. It is often seen in what type of patients?

A

Those with malnutrition secondary to chronic alcoholism. Thiamine deficiency affects cardiac muscle cells and blood vessels causing insufficient contractile strength and peripheral vasodilation = decreased systemic vascular resistance (SVR) which triggers increased cardiac output which impaired myocardium is unable to deliver.

129
Q

Hypertension is? Primary hypertension is? Secondary hypertension is?

A 
Consistent elevation of systemic arterial blood pressure caused by increases in cardiac output or total peripheral resistance, or both.
Primary hypertension accounts for 95% of cases of HTN and has no known cause but thought to be due to genetics and environment.
Secondary hypertension (5% of cases) caused by altered hemodynamics due to underlying primary disease.
130
Q

Risk factors for primary HTN include

A

1) family hx of HTN, 2) advancing age, 3) gender (men 70), 4) black race, 5) high dietary Na intake, 6) glucose intolerance (DM), 7) cigarette smoking, 8) obesity, 9) heavy alcohol consumption, and 10) low dietary intake of potassium, calcium, & magnesium.
All of these are risk factors for other disorders, like dyslipidemia & glucose intolerance, that together with HTN is known as metabolic syndrome.

131
Q

Cardiac output is increased by

A

any condition that increased HR or stroke volume

132
Q

Peripheral resistance is increased by

A

any factor that increases blood viscosity or reduces vessel diameter (vasoconstriction) like inflammation, endothelial dysfunction, obesity-related hormones, & insulin resistance.

133
Q

HTN is mediated by effects of what pathophysiologic mechanisms?

A

sympathetic nervous system, RAAS, & natriuretic peptides.

134
Q

Pressure-natriuresis relationship is

A

the relation of increased vascular volume to decreased renal excretion of salt, for a given BP, individuals with HTN tend to secrete less salt in their urine.

135
Q

How does increased SNS activity raise BP?

A

increases HR & systemic vasoconstriction, increases insulin resistance causing endothelial dysfunction, increased vascular remodeling & procoagulant effects all which lead to narrowing of vessels & vasospasm = increased SVR

136
Q

In HTN pts, overactivity of the RAAS (renin-angiotensin-aldosterone system) causes

A

salt & water retention & increased vascular resistance

137
Q

How do ACE (angiotensin-converting enzyme) inhibitors and ARBs (angiotensin-receptor blockers) help in treatment of HTN?

A

They oppose the activity of the RAAS, effective in reducing BP and protecting against end organ damage (atherosclerosis, renal disease, cardiac hypertrophy, angina, CHF).

138
Q

Preload means?

A

refers to the load or tension on a muscle as it begins to contract. In the heart, this term refers to the pressure or quantity of blood in the ventricle at the end of diastole.

139
Q

Afterload means?

A

resistance against which the heart must pump

140
Q

In hypertensive patients, an increase in ANP & BNP levels is linked to an increased risk for what other pathophysiological changes?

A

ventricular hypertrophy, atherosclerosis, & heart failure.

141
Q

Target organs for hypertension include:

A

kidney, brain, heart, extremities, & eyes

142
Q

If elevated BP is not detected and treated, it becomes established and begins to accelerate its effect on tissues by what age of the individual?

A

30 to 50 years of age.

143
Q

How is diagnosis of HTN made?

A

Diagnosis requires measurement of BP on at least 2 separate occasions averaging two readings at least 2 minutes apart, with individual seated, arms supported at heart level, after 5 minutes of rest, no smoking or caffeine intake 30 min prior to reading.

144
Q

Joint National Committee Classifications of HTN in adults are:

A

Normal SBP 160 or DBP >100

145
Q

Pharmacologic management for Stage 1 HTN

A 
SBP >140-159  or DBP >90-99
START WITH: 
Thiazide-type diuretics for most 
MAY CONSIDER: 
ACEI, ARB, BB, CCB, or combination
THEN:
If not at goal BP, optimize dosages or add additional drugs until goal BP is achieved, consider consultation with HTN specialist.
146
Q

Pharmacologic management for Stage 2 HTN

A

SBP >160 or DBP >100
START WITH:
two-drug combination for most (usually thiazide-type diuretic & ACE or ARB or BB or CCB)
THEN
If not at goal BP, optimize dosages or add additional drugs until goal BP is achieved, consider consultation with HTN specialist.

147
Q

First line pharmacologic treatment of HTN in pts with heart failure, CKD, post MI, recurrent CVA includes what classes of drugs?

A

ACE inhibitor, ARB, or aldosterone antagonist (goal is to manage RAAS as first line intervention).

Diuretics & BB are first line choice for pts without these conditions.

148
Q

Low dietary intake of what nutrients is considered a risk factor for HTN?

A

potassium, magnesium, & calcium

149
Q

Substance released by kidneys that contributes to some cases of HTN

A

Renin

150
Q

Modifiable risk factor for HTN estimated with BMI

A

Obesity

151
Q

High dietary intake of this electrolyte is a factor in HTN.

A

Sodium

152
Q

Traditional risk factors for for atherosclerosis include age, family hx, gender, smoking, dyslipidemia, HTN & DM. Novel risk factors include:

A

elevated CRP, increased serum fibrinogen, oxidative stress, infection, & periodontal disease.

153
Q

Emboli as a result of defective fat metabolism after trauma to long bones are what type?

A

Fat emboli…usually from release of fat globules from bone marrow of long bones exposed by fractures.

154
Q

Coronary artery obstruction that results in recurrent predictable chest pain is called _______ ________?

A

Stable angina

155
Q

Abnormal vasospasm of coronary vessels resulting in unpredictable chest pain is called ______ _____?

A

Prinzmetal angina, or variant angina

156
Q

Myocardial ischemia that does not cause detectable symptoms is called ______ __________.

A

Silent ischemia

157
Q

Reversible myocardial ischemia as a result of transient episodes of thrombotic vessel occlusion & vasoconstriction at the site of plaque damage that is a harbinger to myocardial infarction is called _______ __________.

A

Unstable angina. Reperfusion prior to significant myocardial necrosis can prevent MI.

158
Q

Prolonged ischemia causing irreversible damage to heart muscle is known as _______ ___________.

A

Myocardial infarction

159
Q

Interruption of coronary blood flow for extended period resulting in myocyte necrosis is called

A

myocardial infarction (MI).

160
Q

Dysrhythmias, CHF, & sudden death are the most common complications of ___________ ___________ ___________.

A

acute coronary syndromes

161
Q

Collection of fluid in the pericardial sac is called _______ ____________.

A

pericardial effusion

162
Q

Prolapsed or stenotic heart valves are at greater risk for developing infective endocarditis. True or False?

A

True

163
Q

Cardiomyopathy categorized as dilated is ________.

A

congestive

164
Q

Cardiomyopathy categorized as restrictive is _______ and __________.

A

rigid and noncompliant

165
Q

Cardiomyopathy categorized as hypertrophic is ________.

A

asymmetric

166
Q

Mitral valve prolapse is more common in men or women?

A

women

167
Q

Rheumatic fever is a delayed autoimmune response to what?

A

streptococcal infection, most often pharyngeal, resolves without sequelae if treated early.

168
Q

A patient presenting with carditis, acute migratory polyarthritis, chorea, and erythema marginatum should be assessed for what type of disorder if they voice a history of sore throat and fever a month prior to visit?

A

Acute rheumatic fever, usually 1-5 weeks after streptococcal pharyngitis.

169
Q

Severe heart valve abnormalities, chronic bacteremia, and systemic emboli can result from untreated __________ ________.

A

infective endocarditis, occurs when vegetation breaks off valve surface & travels through bloodstream.

170
Q

Cardiac output is dependent on ______ and ________.

A

stroke volume and heart rate.

171
Q

Stroke volume is influenced by three things which are???

A

contractility, preload, & afterload.

172
Q

What is the most common cause of decreased contractility?

A

MI, causes ventricular remodeling that leads to progressive myocyte contractile dysfunction from scar formations.

173
Q

What types of conditions cause an increase in preload?

A

Decreased contractility and increased plasma volume

174
Q

What causes an increase in afterload?

A

increased peripheral resistance, which leads to decreased ventricular emptying and increased left ventricular workload, causing LVH & ventricular remodeling which further decreases contractility leading to increased preload, & increased afterload causing further increase in peripheral resistance!! (viscious cycle)

175
Q

Clinical manifestations of left heart failure (dyspnea, orthopnea, frothy sputum, fatigue, decreased urinary output, edema, cyanosis, inspiratory crackles, pleural effusion, S3 gallop) are caused by what?

A

pulmonary vascular congestion & inadequate systemic perfusion

176
Q

Goals of treatment for left heart failure are?

A

increase contractility, reduce preload & afterload

177
Q

What are causes of right heart failure?

A

Left heart failure & diffuse hypoxic pulmonary disease (e.g. COPD, cystic fibrosis, ARDS).

178
Q

Dysrhythmias occur because of conditions that impair the _________ of impulse generation or the __________ of impulses through the myocardium.

A

rate of impulse generation or abnormal conduction of impulses.

Patho-Workbook-Test 2 Chapters (1 decks)

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