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NPLEX > Cardio > Flashcards

Cardio Flashcards

1
Q

What is the microscopic anatomical difference between layers of elastic and muscular arteries?

A

elastic arteries contain MORE elastic tissue in the tunica media than muscular arteries

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2
Q

What are the location/boundaries of the pericardium?

A

Lies within the mediastinum; inferior wall of fibrous pericardium attaches to diaphragm

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3
Q

What is the structure of the pericardium?

A

3 layers (outermost to inner):

  • Fibrous pericardium
  • Parietal layer of serous pericardium
  • Pericardial cavity
  • Visceral layer of serous pericardium
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4
Q

What nerve innervates the pericardium?

A

Phrenic nerve

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5
Q

What is the most posterior part of the heart?

A

Left atrium

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6
Q

What is the most anterior part of the heart?

A

Right ventricle

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7
Q

What is the most commonly injured part of the heart in trauma?

A

Right ventricle

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8
Q

Enlargement of the left atrium can cause what pathologies?

A

Mitral stenosis; compression of esophagus (dysphagia), compression of L laryngeal nerve causing hoarseness (Ortner syndrome)

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9
Q

Where is the best place to listen to the mitral valve?

A

5th L ICS MCL (apex)

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10
Q

Where is the best place to listen to the tricuspid valve?

A

5th L ICS

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11
Q

Where is the best place to listen to the pulmonic valve?

A

2nd L ICS

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12
Q

Where is the best place to listen to the aortic valve?

A

2nd R ICS

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13
Q

Where is Erb’s point?

A

3rd L ICS

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14
Q

What are the murmurs associated with the mitral valve and how do they sound?

A

Mitral regurgitation (holosystolic)

Mitral valve prolapse - systolic (midsystolic click)

Mitral stenosis (diastolic)

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15
Q

What pathology are associated with the tricuspid valve? For murmurs, know systolic vs diastolic.

A

Tricuspid regurgitation (holosystolic)

Ventricular septal defect (holosystolic)

Tricuspid stenosis (diastolic)

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16
Q

What pathology are associated with the pulmonic valve? For murmurs, know systolic vs diastolic.

A

All systolic ejection murmurs

Pulmonic stenosis
Atrial septal defect
Flow murmur

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17
Q

What pathology are associated with the aortic valve? For murmurs, know systolic vs diastolic.

A

All systolic murmurs

Aortic stenosis

Flow murmur (physiologic murmur)

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18
Q

What pathology are associated with the erb’s point? For murmurs, know systolic vs diastolic.

A

Aortic regurgitation (diastolic)

Pulmonic regurgitation (diastolic)

Hypertrophic cardiomyopathy (systolic)

At erb’s Point we get High

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19
Q

What pathology are associated with S3?

A

EARLY diastolic pathology

Mitral regurgitation
HF
Volume overload

Can be normal

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20
Q

What pathology are associated with S4?

A

LATE diastolic pathology

Hypertrophy
Pressure overload
Extreme HTN

ALWAYS ABNORMAL

S4 Dose Have Pretty Extreme Appetite

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21
Q

What causes the sound you hear for S1?

What part of the heart cycle occurs after S1 and before S2?

Where is it loudest?

A

Mitral and tricuspid valves closing

Systole

Mitral area

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22
Q

What causes the sound you hear for S2?

What part of the heart cycle occurs after S2 and before the next S1?

Where is it loudest?

A

Aortic and pulmonic valves closing

Diastole

L upper sternal area

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23
Q

Explain the pathway of conduction throughout the heart

A

SA node > atria > AV node > IV septum/Bundle of His > L+R bundle branches > purkinje fibers > ventricles

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24
Q

Explain how contraction of the heart is stimulated

A

Contraction stimulated by conduction system; ion flow across cardiac muscle cells initiates action potent ion and leads to contraction

Then, heart resets and returns to baseline and it all repeats

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25
Q

Where in the heart conduction pathway does the signal slightly delay? Why?

A

AV node; this is the only place there is no fibrous barrier between atria and ventricles, less gap junctions; allows time for atria to empty blood into ventricles prior to contraction

Control of the conduction pathway!

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26
Q

How does the cardiac conduction pathway begin?

A

Self excitation of SA node; caused by leaky sodium and calcium ions inward and rising resting membrane potential

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27
Q

How are purkinje fibers able to instantaneously transmit cardiac impulse through ALL of ventricular muscle?

A

Higher permeability of gap junctions at intercalated discs

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28
Q

What would you call a pacemaker anywhere else besides SA node?

A

Ectopic pacemaker

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29
Q

Explain the effect parasympathetic stimulation on the heart conduction pathway

A

Vagal n stimulation at SA/AV nodes > releases Ach at vagal endings, increasing permeability of membrane to K+ ions > increases membrane negativity (hyperpolarization) > tissue less excitable

Decreased SA node rhythm > decreased HR

Decreased excitability of AV junctional fibers b/w atrial muscle and AV node > slows transmission of cardiac impulses to ventricles

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30
Q

Explain the effect sympathetic stimulation on the heart conduction pathway

A

Sympathetic nerves most concentrated in ventricular muscle

NE released at nerve endings > stimulate beta-1 adrenergic receptors > increases cardiac rhythmicity and conduction > increased rate of SA node > increased rate of conduction and level of excitability throughout heart > increased force of contraction (esp ventricles)

Increased heart force + HR

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31
Q

What does the P wave of the cardiac cycle represent?

A

Atrial depolarization; followed by atrial contraction

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32
Q

What does the QRS complex of the cardiac cycle represent?

A

Ventricular depolarization; followed by ventricular contraction

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33
Q

What does the T wave of the cardiac cycle represent?

A

Ventricular repolarization; slightly before isovolumic relaxation, ventricles remain contracted until end of T wave

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34
Q

What does the R-R interval of the cardiac cycle represent?

A

Rate of one single cardiac cycle/heartbeat

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35
Q

What does the P-R/P-Q interval of the cardiac cycle represent?

A

Depolarization of atria to start of ventricle contraction

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36
Q

What does the Q-T interval of the cardiac cycle represent?

A

Depolarization and repolarization of ventricles

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37
Q

What would inversion of a T wave on an EKG indicate?

A

Ischemia or recent MI

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38
Q

What would a pathological U wave on an EKG indicate?

A

Hypokalemia

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39
Q

What does a long QTI predispose pts to? What is it caused by?

A

Torsades de pointes VTACH (wide QRS) > caused by drugs, low K or Mg, congenital abnormalities

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40
Q

Compare AV node fibers vs sinus nodal fibers

A

SA node fibers have less negative resting membrane potential, caused by leaky sodium and calcium ions > fast sodium channels blocking from opening due to higher resting membrane potential > slower action potential overall

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41
Q

Where does the myocardial action potential occur?

A

All cardiac myocytes, except those in SA and AV nodes

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42
Q

Briefly explain overview of myocardial action potential?

A

Depolarization (more positive membrane) > AP plateaus > repolarization (more negative membrane)

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43
Q

Describe phase 0 of the myocardial action potential

A

Depolarization

Fast Na channels open

Slow Ca channels open

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44
Q

Describe phase 1 of the myocardial action potential

A

Initial repolarization

Fast Na channels close
Fast K channels open

Slow Ca channels still open

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45
Q

Describe phase 2 of the myocardial action potential

A

Plateau

Fast K channels close

Slow Ca channels still open, increasing influx balance leaving K more and more

Calcium influx triggers: Ca release from sarcoplasmic reticulum + myocyte contraction via excitation-contraction coupling

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46
Q

Describe phase 3 of the myocardial action potential

A

Rapid repolarization

Slow Ca channels close
Slow K channels open

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47
Q

Describe phase 4 of the myocardial action potential

A

Resting membrane potential

High potassium permeability through leaky potassium channels

NaK ATPase and NaCa (Na in Ca out) exchanger at work

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48
Q

Where does the pacemaker action potential occur?

A

SA and AV nodes

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49
Q

Describe phase 0 of the pacemaker action potential

A

Opening of Ca channels causes upstroke

fVNaC permanently inactivated > slow conduction velocity used by AV node to prolong transmission from A > V

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50
Q

Describe phase 3 of the pacemaker action potential

A

Inactivation of Ca channels
Activation of K channels

> K efflux

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51
Q

Describe phase 4 of the pacemaker action potential

A

Slow spontaneous diastolic depolarization from funny current

Slow/mixed Na/K influx > accounts for automaticity of SA and AV nodes (slope determines HR) > Ach/adenosine will decrease HR, catecholamines will increase HR

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52
Q

What system controls HR and strength?

A

ANS

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53
Q

What is the basis of regulation of the cardiac cycle?

A

Intrinsic cardiac pumping regulation in response to changes in volume of blood flowing into the heart

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54
Q

What determines the amount of blood pumped into the heart each minute?

A

Venous return

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55
Q

What is the Frank-Starling Mechanism?

A

Ability for the heart to adapt to increasing volumes of blood

More heart muscle is stretched during filling > greater contraction force > greater quantity of blood pumped into aorta

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56
Q

Explain sympathetic stimulation and its role in ANS control of the heart

A

Increased CO > increases HR and force of contraction > increases volume of blood pumped and ejection pressure

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57
Q

Explain parasympathetic stimulation and its role in ANS control of the heart

A

Deceased CO >

minor decrease of contraction strength

major decrease of HR

vagal nerve fibers distributed more to atria than ventricles

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58
Q

Explain the effect of potassium ions on heart function

A

Excess extracellular K > dilated, flaccid heart > slow HR

Excess K could also block conduction of electrical impulse from atria to ventricle

Why?
Decreases resting membrane potential (less neg), decreases intensity of AP, decreased heart muscle contraction

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59
Q

Explain the effect of calcium ions on heart function

A

Excess intracellular Ca causes opposite effects of potassium

Excess leads to spastic contraction

Why?
Ca initiates the cardiac contractile process
Decreased Ca leads to cardiac weakness like the effects of high K

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60
Q

Where do the coronary arteries lie and where do they supply blood to?

A

CA and their branches lie in the epicardium and supply blood to the myocardium

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61
Q

During which heart phase do the coronary arteries fill?

A

Diastole

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62
Q

Describe the branching pattern of the coronary arteries

A

Aortic root > RCA + LCA

RCA > R marginal
RCA + LCA > PDA
LCA > LAD (widow)
LCA > circumflex > L marginal

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63
Q

What CA supplies blood to the SA node?

A

RCA

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64
Q

What CA supplies blood to the right ventricle?

A

RMA

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65
Q

Where does the LAD artery supply blood to?

A

Anterior 2/3 IV septum, anterior LV

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66
Q

Where does the circumflex artery supply blood to?

A

LA and posterior walls of LV

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67
Q

Where does the PDA supply blood to?

A

AV node, posterior 1/3 AV septum

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68
Q

Explain the branching of the aorta below the diaphragm

A

Inferior phrenic, celiac trunk (foregut), middle suprarenal arteries, renal arteries, SMA (midgut), testicular arteries, IMA (hind gut), lumbar arteries, common iliac arteries

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69
Q

What are the major lower extremity veins?

A

Anterior tibial, posterior tibial, peroneal veins, lower popliteal fossa, popliteal vein, superficial femoral vein

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70
Q

Explain the anatomy of the femoral and saphenous veins

A

Deep femoral v is lateral, joins superficial femoral and great saphenous in femoral canal, common femoral vein

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71
Q

In what pathologies would a high pulse pressure be present?

A

Hyperthyroid, aortic regurgitation, aortic stiffening, OSA, exercise

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72
Q

In what pathologies would a low pulse pressure be present?

A

Aortic stenosis, cardiogenic shock, cardiac tamponade, HF

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73
Q

What would cause high contractility?

A

B1R stim, increased intracellular Na/Ca

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74
Q

What would cause low contracility?

A

B1 blocker, HF, acidosis, hypoxia, NDHPCCB

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75
Q

What medication class would decrease preload?

A

Venous vasodilator (nitroglycerin, ACEis, ARBs)

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76
Q

What determines the amount cardiac muscles can contract in preload?

A

End diastolic volume

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77
Q

What determines afterload?

A

End systolic volume

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78
Q

What blood vessels have the highest total cross sectional area and lowest velocity?

A

Capillaries

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79
Q

Explain capillary fluid exchange

A

Cap pressure pushes fluids out, interstitial pressure pushes fluid in

Plasma osmotic and oncotic pressure pulls fluid in, interstitial fluid osmotic pressure pulls fluid out

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80
Q

What are starling forces and what do they determine?

A

Contraction force is proportional to preload; hearts ability to change contractions and SV in response to venous return. SV increase with increase in amount of blood that fills ventricles (EDV)

Starling forces determine fluid movement through cap membrane

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81
Q

Explain the acute effects of early exercise on the CV system.

A

CO maintained by increased HR and SV

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82
Q

Explain the adaptive effects of late exercise on the CV system.

A

CO maintained by HR only (as SV plateaus)

As HR increases > less filling time > decreased CO > diastole is shortened

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83
Q

Explain the function and biochem of atrial natiuretic peptide

A

Released from atrial myocytes in response to increased blood volume and atrial pressure

Caused vasodilation and decreased Na in the renal/medullary collecting duct

Dilates afferent renal arterioles and constricts efferent arterioles to promote diuresis

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84
Q

Explain the function and biochem of brain natriuretic peptide

A

Released from ventricular myocytes in response to increased tension

Longer half life than ANP

Used to Dx HF

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85
Q

Explain the function and biochem oF LDL

A

Transports cholesterol made in the liver to the tissues

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86
Q

Explain the function and biochem of HDL

A

Scavenges cholesterol from tissues and back to liver for disposal

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87
Q

Explain the unique relationship between the cardiovascular and pulmonary system

A

Pulmonary vasculature is the only one that vasoconstriction under hypoxia, so the well ventilated areas are perfused

Other areas of the body, hypoxia causes vasodilation

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88
Q

What is pulmonary HTN?

A

Increased pressure in pulmonary vasculature ONLY; elevated mean pulmonary artery pressure > 20 mmHg at rest

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89
Q

Explain the pathogenesis of pulmonary HTN and what it can lead to

A

Increased pulmonary vascular resistance > increased right ventricular pressure > increased right ventricular hypertrophy > right HF

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90
Q

What are the different possible causes of pulmonary HTN?

A

Idiopathic, inherited, drug induced, connective tissue disease

HD/HF (most common)

Lung disease and/or hypoxemia

Chronic thromboembolism

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91
Q

RF for pulmonary HTN

A

CHF, MI, chronic anemia, COPD/lung disease, chronic thromboembolism, pulmonary arterial HTN (genetic, idiopathic), lung fibrosis

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92
Q

Complications of pulmonary HTN

A

Arteriosclerosis, medial hypertrophy, intimal fibrous of pulmonary arteries, right HF

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93
Q

Clinical characteristics of pulmonary HTN

A

PLEXIFORM LESIONS (complex vascular formations originating from remodeled pulmonary arteries, like a spider vein in the lungs)

Fatigue, dyspnea, syncope, peripheral edema, palpitations, chest pain on exertion

Medial hypertrophy of muscular and elastic arteries

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94
Q

What is the most common type of systemic HTN and its causes?

A

1st degree: multi factorial

Increased CO: increased HR, contractility (exercise, anxiety), increased preload (amount of blood filling heart), decreased afterload

Increased TPR: amount of blood circulating and diameter of BVs

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95
Q

What is the most common cause of second degree systemic HTN?

A

Renal/renovascular disease

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96
Q

What is seen microscopically in pulmonary HTN?

A

Smooth muscle proliferation occurs due to decreased apoptosis; genetic connection to BMPR2 gene

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97
Q

RF for systemic HTN

A

Increased age, obesity, DM, physical inactivity, excess salt, excess alcohol, smoking, fhx

AA > caucasians > Asian

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98
Q

Complications of systemic HTN

A

CAD, HF, left ventricular hypertrophy, a fib, aortic dissection, aortic aneurysm, stroke, CKD, retinopathy

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99
Q

What defines a hypertensive crisis, hypertensive urgency, and hypertensive emergency?

A

Crisis: 180/110

Urgency: 180/120+ with NO sx end organ damage

Emergency: 180/120+ with evidence of end organ damage (encephalopathy, stroke, retinal hemorrhage, MI, HF, kidney injury)

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100
Q

Sx of systemic HTN

A

Commonly asymp

Fundoscopic exam showing hypertensive retinopathy (not required for dx)

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101
Q

What is congestive heart failure?

A

Cardiac pump dysfunction leads to congestion of the heart, decreased CO, and low perfusion

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102
Q

Types of left sided CHF

A

Systolic dysfunction: HF with reduced EF, increased EDV, decreased contractility

Diastolic dysfunction: HF with preserved EF, normal EDV, decreased compliance (increased EDP)

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103
Q

Etiology/causes of L CHF

A

Ischemic HD
HTN
Aortic and mitral valvular diseases
Myocardial disease

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104
Q

Common causes of R CHF

A

Left HF
Pulmonary HTN

Cor pulmonale - isolated right HF due to pulmonary causes

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105
Q

RF for CHF

A

Old age, CAD, HTN, DM, valvular heart disease, tobacco, obesity

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106
Q

Complications of L CHF

A

A fib, stroke/thrombosis, hypoxic encephalopathy, coma, death, right HF

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107
Q

Shared clinical characteristics of both types of CHF

A

S3 heart sounds, rales, JVD, pitting edema

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108
Q

L CHF clinical characteristics

A

S3, rales, JVD, pitting edema

pulmonary edema (increased pulmonary venous pressure > pulmonary venous distention and transduction of fluid) > HF CELLS IN LUNGS

Orthopnea (SOB when supine)

Paroxysmal nocturnal dyspnea

Dyspnea, orthopnea, fatigue

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109
Q

R CHF clinical characteristics

A

S3, rales, JVD, pitting edema

Congestive hepatomegaly (increased central venous pressure > increased resistance to portal flow) > NUTMEG LIVER on cadaver exam

Dyspnea, orthopnea, fatigue

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110
Q

what is angina pectoris?

A

Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm, no myocyte necrosis

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111
Q

Different types of angina pectoris

A

Stable angina

Vasospastic/variant

Unstable angina

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112
Q

Stable angina definition

A

most common

usually secondary to atherosclerosis (>70% occlusion)

triggered by: atherosclerosis, activity, BP, HR

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113
Q

Vasospastic/variant angina definition

A

occurs at rest secondary to CA spasm

triggered by: cocaine, alcohol, triptans

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114
Q

Unstable angina definition

A

Thrombosis with incomplete coronary artery occlusion

Triggered by: atherosclerosis, activity, BP, HR

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115
Q

RF for stable and unstable angina

A

HTN, HLD, tobacco, MI RF

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116
Q

RF for vasospastic/variant angina

A

Tobacco use

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117
Q

Clinical characteristics of stable angina

A

Pain on exertion, resolves with rest

No ECG changes

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118
Q

Are troponin levels elevated in any forms of angina?

A

No

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119
Q

Clinical characteristics of vasospastic angina

A

Pain at rest secondary to coronary artery spasm

Transient ST elevation on ECG

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120
Q

Clinical characteristics of chronic ischemic heart disease

A

Enlarged heavy heart with L ventricular hypertrophy and dilation

Obstructive ordinary atherosclerosis

Scars from healed infarcts

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121
Q

Complications of chronic ischemic heart disease

A

Leading cause of death worldwide

Progressive CHF leading to heart transplant

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122
Q

Clinical characteristics of unstable angina

A

Pain on mild extortion or at rest

Possible ST depression/T-wave inversion on ECG

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123
Q

What is chronic ischemic heart disease

A

Progressive onset of HF over many years due to chronic ischemic myocardial damage

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124
Q

What is myocardial ischemia

A

Imbalance between supply (perfusion) and demand of heart for oxygenated blood

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125
Q

Etiology of chronic ischemic heart disease

A

Reduced blood flow to obstructive atherosclerotic lesions in coronary artery, usually preceded by MI

Progression of CAD

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126
Q

Pathogenesis of chronic ischemic heart disease

A

Long and slow onset w/o sx

Syndrome of ischemic heart disease are late manifestations of coronary atherosclerosis

Appears post infarction due to functional decompensation of hypertrophied non infarcted myocardium

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127
Q

RF of chronic ischemic heart disease

A

HLD, HTN, MI, tobacco use, alcohol use, sedentary lifestyle, age, SAD diet

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128
Q

What is a myocardial infarction

A

Death of cardiac muscle due to prolonged severe ischemia

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129
Q

Most common cause of myocardial infarction

A

Rupture of coronary artery atherosclerotic plaque

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130
Q

Commonly occluded arteries with MIs

A

LAD > RCA > circumflex

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131
Q

Pathogenesis of MI

A

Initial event > sudden change in plaque > intraplaque hemorrhage, erosion, ulceration, rupture, fissuring

When exposed to subendothelial collagen and necrotic plaque contents, platelets adhere, become active, release granule contents, and aggregate to form microthrombi

Vasospasm is stimulated by mediators released from platelets

TF activates, activates coagulation pathway, increases bulk of thrombus, occludes complete lumen > leads to ischemia and myocyte death occurring at the location of the anatomical region supplied by artery in question

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132
Q

Biochem of MI

A

Loss of blood flow > cessation of aerobic metabolism within seconds

Inadequate production of ATP > accumulation of lactic acid

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133
Q

STEMI characteristics

A

Transmural

Full thickness

ST elevation, pathological Q waves

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134
Q

NSTEMI characteristics

A

Subendothelial

Subendocardium (inner 1/3)

ST depression

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135
Q

What is seen on microscopy at 0-24 hours, 1-3 days, 3-14 days, and 14+ days post MI

A

0-24 hrs: wavy fibers, coagulative necrosis, dark eosinophilic stripes

1-3 days: coagulative necrosis, neutrophils showing acute inflammation

3-14 days: macrophages, granulation tissue

14+ days: scar complete

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136
Q

RF for MI

A

Age, genetics, males, post menopausal women (drop in estrogen), atherosclerosis

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137
Q

Complications of MI

A

If caught late: necrosis of cardiac myocytes > chronic IHD, CHF, death

DARTH VADER: death, arrhythmia, rupture, tamponade, HF, valve disease, aneurysm, dressers, embolism, recurrence/regurgitation

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138
Q

Complications of MI by time frame (0-24 hours, 1-3 days, 3-14 days, 2+ weeks)

A

0-24 hours: ventricular arrhythmia, HF, cardiogenic shock
Vinny has constipation for 24 hours

1-3 days: postinfarction fibrinous pericarditis

3-14 days: cardiac tamponade, mitral regurgitation, LV, pseudoaneurysm

2+ weeks: dressier syndrome, HF, arrhythmia, ventricular aneurysm

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139
Q

Clinical characteristics MI

A

Elevated bio markers (CK-MB, troponins)

Chest/arm/back/neck/jaw pain

Trouble breathing

Lightheadedness

Diaphoresis/cold sweats

N/V

Severe chest pain

Malaise, fatigue

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140
Q

Aortic stenosis - S or D?

A

S

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141
Q

Aortic regurgitation / insufficiency - S or D?

A

D

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142
Q

Mitral stenosis - S or D?

A

D

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143
Q

Mitral insufficiency - S or D?

A

S

144
Q

Mitral valve prolapse - S or D?

A

S

145
Q

Etiology of aortic stenosis

A

Age-related calcification, bicuspid aortic valve

146
Q

RF aortic stenosis

A

Age, atherosclerosis, bicuspid aortic valve

147
Q

complications of aortic stenosis

A

SAD (syncope, angina, DOE), LV pressure is less than aortic pressure during systole

148
Q

Clinical characteristics aortic stenosis

A

Cresc-decresc ejection murmur

Pulses parvus et tartus (weak pulse)

Soft S2 and ejection click

149
Q

Etiology aortic regurgitation

A

BEAR (bicuspid aortic valve, endocarditis, aortic root dilation, rheumatic fever

150
Q

Complications aortic regurgitation

A

L CHF

151
Q

Clinical characteristics aortic regurgitation

A

Early diastolic decrescnedo

High, blowing murmur

Wide PP

Pistol shot femoral pulse

Pushing nail bed

152
Q

Mitral stenosis etiology

A

Rheumatic fever

153
Q

Mitral stenosis pathogenesis

A

L atrial pressure > ventricular pressure

154
Q

Mitral stenosis complications

A

Left atrial dilation, pulmonary congestion, a fib, ortner syndrome, hemopytsis, RCHF

155
Q

Mitral stenosis clinical characteristics

A

Follows opening snap, delayed rumbling mid-late murmur

156
Q

Mitral insufficiency etiology

A

Ischemic heart disease (post MI), MVP, LV dilation, rheumatic fever, infective endocarditis

157
Q

Mitral insufficiency clinical characteristics and sound

A

asymptomatic to shortness of breath, fatigue, and inability to exercise may arise (later in disease)

Holosystolic, high pitched blowing murmur

158
Q

Types of endocarditis

A

Infective/bacterial

No bacterial thrombotic endocarditis

159
Q

Etiology infective endocarditis

A

Infection of endocardial surface of heart, typically involves 1+ heart valves

Bacteria > fungi

Acute: S aureus; large destructive vegetation’s on normal valves; rapid onset

Subacute: strep Viridans; small vegetations on congenitally abnormal or diseased valves; gradual onset

160
Q

Pathogenesis infective endocarditis

A

Mitral valve affected more often than aortic

Tricuspid valve associated with IV drug use (Don’t Tri Drugs)

Endothelial injury > formation of vegetation’s consisting of platelets, fibrin, and microbes on heart valves

161
Q

Non bacterial thrombotic endocarditis etiology

A

Marantic endocarditis; rare

Vegetations arise on mitral or aortic valve, consists of sterile, platelet-rich thrombi that dislodge easily

162
Q

RF of infectious endocarditis

A

Subacute: dental procedure

RF by bacteria;
Prosthetic valves - s epidermis

GI/GU procedure - enterococcus

IV drug use - S aureus, pseudomonas, candida

163
Q

RF nonbacterial endocarditis

A

Hypercoagulable state from advanced malignancy (pancreatic adenocarcinoma) or SLE (Libman sacks endocarditis)

164
Q

Complications of bacterial endocarditis

A

Leads to valve regurgitation, septic embolism

165
Q

Complications of nonbacterial endocarditis

A

Embolism

166
Q

Clinical characteristics of infectious endocarditis

A 
FROM JANE
Fever
Roth spots
Osler nodes
Murmur
Jane way lesions
Anemia
Nail bed hemorrhages
Emboli

Vascular phenomena: septic embolism, petechiae, splinter hemorrhages, Jane way lesions

Immune phenomena: immune complex deposition, glomerulonephritis, Osler nodes, Roth spots

Modified duke criteria

167
Q

Nonbacterial endocarditis clinical characteristics

A

Asymptomatic

168
Q

Mitral valve prolapse etiology

A

Rheumatic fever, chordae rupture, myxomatous degeneration (primary or secondary due to connective tissue disease)

169
Q

Mitral valve prolapse complications

A

Typically benign, can predispose to infective endocarditis

170
Q

Mitral valve prolapse clinical characteristics

A

Late crescendo murmur with midsystolic click occurring after carotid pulse

171
Q

Rheumatic heart disease definition

A

Immune mediated (type II hypersensitivity)

Antibodies react to M protein, cross-react with self-antigens (often myosin)

172
Q

Rheumatic heart disease etiology

A

Pharyngeal infection with group A B-hemolytic strep

Not direct effect of bacteria

173
Q

Pathogenesis rheumatic heart disease

A

Affects heart disease mitral > aortic > tricuspid (MAT)

174
Q

Complications rheumatic heart disease

A

Early valvular regurgitation

Late valvular stenosis

175
Q

Clinical characteristics rheumatic heart disease

A

Aschoff bodies: granuloma with giant cells

Anitschkow cells: enlarged macrophages with ovoid, wavy, rod-like nucleus

J<3NES (major criteria):

Joint (migratory arthritis)

<3 carditis

Nodules in skin (subcutaneous)

Erythema marginatum (evansecent rash with ring margin)

Sydenham chorea (involuntary irregular movements of limbs/face)

176
Q

Carcinoid heart disease definition

A

Cardiac manifestation of systemic syndrome caused by carcinoid tumors (occurs in 50% of people)

177
Q

Carcinoid heart disease etiology

A

Involves endocardium and valves of right heart

Cardiac lesions: firm, plaque like endocardial fibrous thickening inside tricuspid and pulmonary valves (contain smooth muscle cells and collagen fibers)

178
Q

Carcinoid heart disease complications

A

Tricuspid insufficiency then pulmonary valve insufficiency

179
Q

Carcinoid heart disease clinical characteristics

A

Flushing of skin, cramps, N/V, diarrhea

180
Q

Types of cardiomyopathies

A

Dilated, Hypertrophic, Restrictive

181
Q

Dilated cardiomyopathy etiology

A

Most common, dilation of cardiac chambers (ventricles)

Idiopathic, genetic, drugs, infxn, ischemia, systemic

182
Q

Hypertropic cardiomyopathy etiology

A

Second most common; enlargement of cardiac muscle surrounding ventricles

Familial, autosomal dominant, chronic HTN, friedrich ataxia

183
Q

Restrictive cardiomyopathy etiology

A

Known as infiltrative, decreased ventricular compliance

PLEASe Help:
P: postradiation fibrosis
L: Loeffler endocarditis
E: endocardial fibroelastosis (kids)
A: amyloidosis
Se: sarcoidosis
Help: hemochromatosis
184
Q

Dilated cardiomyopathy complications

A

Systolic dysfunction

Clot formation

185
Q

Hypertrophic cardiomyopathy complications

A

Diastolic dysfunction
Sudden death in young athletes
Arrhythmias

186
Q

Restrictive cardiomyopathy complications

A

Diastolic dysfunction

187
Q

Dilated cardiomyopathy clinical characteristics

A

CHF, S3, systolic regurgitation murmur, dilated heart on echo

BALLOON APPEARANCE OF HEART ON CXR, ECCENTRIC HYPERTROPHY IN VENTRICLE, sarcomeres added in series

188
Q

Hypertrophied cardiomyopathy clinical characteristics

A

S4, systolic murmur, mitral regurgitation, dyspnea, syncope

VENTRICULAR CONCENTRIC HYPERTROPHY, MUSCLE TISSUE ENLARGED, sarcomeres added in parallel

189
Q

Restrictive cardiomyopathy clinical characteristics

A

Low voltage ECG

MUSCLE LESS COMPLIANT, LESS CONTRACTILE

190
Q

Myocarditis etiology

A

Inflammation of myocardium > global enlargement of heart and dilation of all chambers

Viral: coxsackie A and B virus

Parasitic; trypanosoma cruzi, toxoplasma gondii

Bacterial: borrelia burgdorferi, myoplasma pnemoniae, diphtheriae

Toxins: CO, black widow venom

Rheumatic fever

Drugs (cocaine)

Autoimmune disease

191
Q

Complications of myocarditis

A

SCD (Major cause in adults >40)

Arrhythmias, heart block, dilated cardiomyopathy, CHF, mural thrombus with systemic emboli

192
Q

Myocarditis clinical characteristics

A

Dyspnea, chest pain, fever, arrhythmias (persistent tachycardia out of proportion to fever)

If viral in etiology: lymphocytic infiltrate with focal necrosis

193
Q

Pericarditis definition

A

Inflammation of pericardium, fluid accumulates around heart

194
Q

Pericarditis etiology

A

Primary and secondary

SCCARR IIN pericardium

Surgery
Connective tissue disorder
CV events 
Autoimmune 
Radiation
Renal failure
Idiopathic (most common)
Infection (coxsackie B)
Neoplasm
195
Q

Pericarditis complications

A

Pericardial effusion

196
Q

Pericarditis clinical characteristics

A

Sharp pain, WORSE BY INSPIRATION, BETTER SITTING UP AND LEANING FORWARD

Friction rub
Diffuse ST elevation or depression

197
Q

Patent ductus arteriosis definition

A

Ductus arteriosis failes to close after birth; allows blood to flow back to lungs

198
Q

Patent ductus arteriosis etiology

A

Fetal period: normal (R to L) shunt

Neonatal period: decreased vascular resistance, shunt becomes L to R

Leads to RVH and/or LVH and HF

199
Q

Patent ductus arteriosis complications

A

Late cyanosis in lower extremities

200
Q

Patent ductus arteriosis clinical characteristics

A

No symptoms or cyanosis, fatigue, tachycardia

Continuous machine-like murmur

PDA is normal in utero, and normally closes after birth

201
Q

Tetralogy of fallot etiology

A

Anterosuperior displacement of infundibular septum

Most common cause of early childhood cyanosis

202
Q

Tetralogy of fallot complications

A

Pulmonary stenosis forces R to L flow across VSD > RVH

203
Q

Tetralogy of fallot clinical characteristics

A

Pulmonary infundibular stenosis

RVH - boot heaped heart on xray

Overriding aorta

VSD

“Tet spells” often caused by crying, fever, exercise

204
Q

Aneurysm definition

A

Dilation of aorta

205
Q

Types of aneurysm

A

Abdominal aortic

Thoracic aortci

206
Q

Abdominal aortic aneurysm pathogenesis

A

Transmural (all 3 layers)

Inflammation and extracellular matrix degradation

207
Q

Abdominal aortic aneurysm RF

A

Tobacco, age, males, Fhx

208
Q

thoracic aortic aneurysm pathogenesis

A

Aortic root dilation due to high pressure could lead to aortic valve regurgitation

209
Q

Thoracic aortic aneurysm RF

A

HTN, bicuspid aortic valve, connective tissue disease (Marfan), tertiary syphilis

210
Q

Abdominal aortic aneurysm Complications

A

Aortic dissection

211
Q

thoracic aortic aneurysm

A

Aortic dissection

212
Q

Abdominal aortic aneurysm clinical characteristics

A

Abdominal/back pain as sign of leaking, dissection, imminent rupture

Palpable pulsatilla abdominal mass

213
Q

Abdominal aortic aneurysm clinical characteristics

A

Abdominal/back pain as sign of leaking, dissection, imminent rupture

214
Q

Aortic dissection definition

A

Longitudinal intimal tear forming a false lumen

215
Q

Types of aortic dissection

A

Stanford type A: proximal, ascending aorta

Stanford type B: distal, descending aorta, below L subclavian artery

216
Q

Aortic dissection RF

A

HTN, bicuspid aortic valve, inherited CT disorders (Marfan syndrome)

217
Q

Aortic dissection complications

A

Organ ischemia, aortic rupture, death

Aortic regurgitation, cardiac tamponade

218
Q

Aortic dissection clinical characteristics

A

Tearing, sudden-onset chest pain radiating to back

Unequal BP in arms

CXR: mediastinal widening

219
Q

Arteriosclerosis definition

A

Hardening of arteries, arterial wall thickening, loss of elasticity

220
Q

How dose Arteriosclerosis affect blood vessels and which ones?

A

Affects small arteries and arterioles

Hyaline: thickening of vessel walls secondary to plasma protein leak into endothelium in essential HTN ad DM

Hyperplastic: onion skinning in severe HTN with proliferation of smooth muscle cells

221
Q

Atherosclerosis definition

A

Form of arteriosclerosis

Build up of cholesterol plaques in tunica intima

Elastic arteries and medium/large size muscular arteries

222
Q

Atherosclerosis Etiology

A

Location: A copy cat named Willis: abdominal aorta > coronary artery > popliteal artery > carotid artery > circle of Willis

Inflammation > endothelial cell dysfunction > macrophage and LDL accumulation > foam cell formation > fatty streaks > smooth muscle cell migration > proliferation and ECM deposition > fibrous plaque > complex atheromas > calcification

223
Q

Atherosclerosis complication

A

Atherosclerosis of CA (CAD) is #1 killer of M +F in US

CAD, MI

224
Q

Atherosclerosis RF

A

HTN, tobacco, HLD, DM

Age, males, postmenopausal status, Fhx

225
Q

Atherosclerosis clinical characteristics

A

Angina, claudication, asymptomatic

226
Q

Familial hypercholesterolemia definition

A

Receptor disease from mutation in gene encoding for LDL

227
Q

Familial hypercholesterolemia Pathophysiology

A

Loss of feedback > increased cholesterol levels

Premature atherosclerosis

Increased risk of MI

228
Q

Familial hypercholesterolemia RF

A

Fhx

229
Q

Familial hypercholesterolemia Complications

A

MI, CAD

230
Q

Familial hypercholesterolemia clinical characteristics

A

Very high LDL at young age

Nodules or raised bumps on skin, tendons, eyelids

White ring around cornea

Medications do not work for LDL

231
Q

Giant cell (temporal) arteritis etiology

A

Focal granulomatous inflammation

Increased ESR, IL-6 levels correlate with disease activity

Affects branches of carotid artery

232
Q

Giant cell (temporal) arteritis RF

A

Females, over 50, polymyalgia rheumatica

233
Q

Giant cell (temporal) arteritis complications

A

Irreversible blindness due to anterior ischemic optic neuropathy

234
Q

Giant cell (temporal) arteritis clinical characteristics

A

UL HD, temporal artery tenderness, jaw claudication

235
Q

Peripheral arterial disease (PAD) definition

A

Insufficient tissue perfusion due to narrowing or occlusion of aorta or peripheral branches

236
Q

Peripheral arterial disease (PAD) Etiology

A

Narrow arteries reduce blood flow to arms/legs

Buildup of fatty, cholesterol-containing deposits on artery walls (atherosclerosis), reduces blood flow through arteries

237
Q

Peripheral arterial disease (PAD) RF

A

Fhx, HTN, HLD, age, obesity, CAD

238
Q

Peripheral arterial disease (PAD) Complications

A

Critical limb ischemia, stroke, MI

239
Q

Peripheral arterial disease (PAD) clinical characteristics

A 
Coldness in LE or foot
LE numbness
Weakness
Loss of peripheral pulses 
Cramping
Skin color change
Sores that wont heal
ED
Hair loss
240
Q

Pulmonary embolism definition

A

Obstruction of pulmonary artery or one of its branches by thrombus

241
Q

Pulmonary embolism Etiology

A

Affected alveoli are ventilated but not perfused (V/Q mismatch)

242
Q

Pulmonary embolism RF

A 
THROMBOSIS
T: trauma, travel, thrombophilia
H: hypercoagulable state, hormone replacement 
R: rec drugs/IV drugs
O: old age
M: malignancy
B: birth control pills/patches
O: obesity, obstetrical (pregnancy- 6 wk postpartum)
S: surgery
I: immobilization, iatrogenic (CVC)
S: serious illness
243
Q

Pulmonary embolism Complications

A

Sudden death due to clot preventing blood from filling LV

Hypotension, shock, recurrent thromboembolism, pulmonary infarction, RHF

244
Q

Pulmonary embolism Clinical characteristics

A

Sudden onset dyspnea, pleuritic chest pain, cough, hemoptysis, tachyon ear, tachycardia, syncope, hypoxemia, respiratory alkalosis, sx of DVT,

Wells criteria for PE

ECG: R heart strain - S wave in 1, Q wave in 3, inverted T wave in 3

245
Q

Raynaud phenomenon definition

A

Color changes of skin due to decreased blood flow

246
Q

Raynaud phenomenon Etiology

A

Decreased blood flow to skin due to arteriolar (small vessel) vasospasm in response to cold or stress

Primary: idiopathic

Secondary: mixed connective tissue disease, SLE, CREST syndrome

247
Q

Raynaud phenomenon complications

A

Secondary: Digital ulceration

248
Q

Raynaud phenomenon clinical characteristics

A

Color change from white (ischemia) to blue (hypoxia) to red (reperfusion)

Most often to fingers/toes

249
Q

Thromboangitis Obliterans / Buerger disease definition

A

segmental, thrombosis, acute and chronic inflammation of medium sized and small arteries (tibial and radial)

250
Q

Thromboangitis Obliterans / Buerger disease Etiology

A

Direct endothelial cell toxicity by tobacco or immune response to the same agents

251
Q

Thromboangitis Obliterans / Buerger disease RF

A

Heavy cigarette smokers before age of 35

252
Q

Thromboangitis Obliterans / Buerger disease Complications

A

Vascular insufficiency

253
Q

Thromboangitis Obliterans / Buerger disease Clinical characteristics

A

Superficial nodular phlebitis, severe pain at rest, chronic ulceration of toes, fingers, feet

254
Q

Deep vein thrombosis definition

A

Blood clot within a deep vein (proximal LE veins - iliac, femoral, popliteal)

255
Q

DVT etiology

A 
Virchow triad (SHE)
Status - post op, long drive/flight 
Hypercoagulability - defect in coagulation cascade proteins, OCPs, pregnancy
Endothelial damage - exposed collagen triggers clotting cascade
256
Q

DVT RF

A

Obesity, contraceptives, pregnancy, fhx, previous venous thromboembolism, HRT

Inherited thrombophlebitis:
Factor V Leiden mutation
Protein C deficiency
Protein S deficiency

257
Q

DVT complication

A

PE

258
Q

DVT clinical characteristics

A

Leg swelling, pain, warmth, redness

Unilateral pitting edema in leg

D-dimer: rule OUT DVT

Wells criteria for DVT

259
Q

Varicose veins etiology

A

Prolonged increased intraluminal pressure and loss of vessel wall support

Superficial veins of LE

260
Q

Varicose veins RF

A

Obesity, FHx, females

261
Q

Varicose veins complications

A

Increased venous pressure, venous stasis, pedal edema, stasis dermatitis, ulcerations

262
Q

Varicose veins definition

A

Abnormally dilated, tortuous veins

263
Q

Vasculitis definition

A

Vessel wall inflammation

264
Q

Large vessel Vasculitis Etiology

A

aorta and large branches to extremities, head, neck

giant cell (temporal arteritis

Takayasu arteritis: granulomatous inflammation occurring in pts under 50

265
Q

Types of Vasculitis

A

Large vessel, medium vessel, small vessel

266
Q

Medium vessel Vasculitis etiology

A

Main visceral arteries and branches

Kawasaki disease: arteritis with mucocutaneous lymph node syndrome, in children. Coronary arteries involved with aneurysm or thrombosis

267
Q

Small vessel Vasculitis etiology

A

Arterioles, venues, capillaries, small arteries

Westerns granulomatosis: granulomatous inflammation involving respiratory tract and necrotizing vasculitis affecting small vessles

Churg-Strauss syndrome: same as wegeners but associated with asthma and blood eosinophilia

Microscopic polyangitis: necrotizing small vessel vasculitis with few or no immune deposits

268
Q

Viral myocarditis etiology

A

Adenovirus, coxsackie B, parvovirus B19, HIV, HHV-6

269
Q

Viral myocarditis clinical characteristics

A

Lymphocytes infiltrate with focal necrosis is highly indicative

270
Q

The truncus arteriosis gives rise to…

A

Asc aorta + pulmonary trunk

271
Q

Bulbus cordis gives rise to…

A

Outflow tract of LV and RV

272
Q

Primitive ventricle/aorta gives rise to…

A

Trabeculated part f R + L ventricles/aorta

273
Q

L horn of sinus venosus gives rise to…

A

Coronary sinus

274
Q

R horn of sinus venosus gives rise to…

A

Smooth part of R atrium (sinus venarum)

275
Q

When does the foremen ovale close? What causes this closure?

A

Immediately after birth, due to increased LA pressure

Breath > decreased pulm vasc resistance > increased LA pressure > fossa oval is > increase in O2 > decrease in PGEs > closure of ductus arteriosus

276
Q

What is patent foramen ovale

A

Failure of septum primum and secundum to fuse after birth

277
Q

What eventually develops into the arterial system?

A

Aortic arch derivatives

278
Q

1st aortic arch derivative

A

Maxillary arteries - branch of ext carotid

1st arch is max

279
Q

2nd aortic arch derivative

A

Stapedial and hyoid arteries

second stapedial

280
Q

3rd aortic arch derivative

A

Common carotid artery and proximal part of internal carotid artery

281
Q

4th aortic arch derivative

A

Aortic arch and proximal right subclavian artery

282
Q

6th aortic arch derivative

A

Proximal part of pulmonary arteries and ductus arteriosus (left)

283
Q

Endocardial cushion gives rise to…

A

Atrial septum, membranous IV septum, AV + semilunar valves

284
Q

R common cardinal + R anterior cardinal vein gives rise to…

A

SCV

285
Q

Posterior, subcardinal + supracardinal veins give rise to…

A

IVC

286
Q

Primitive pulm vein gives rise to…

A

Smooth part of LA

287
Q

What are the three roles of the lymphatic system

A

Returns interstitial fluid from tissues back to heart

Helps large molecules like hormones and lipids enter the blood

Helps with immune surveillance

288
Q

When does interstitial fluid become lymph?

A

Once in the lymphatic vessels

289
Q

Where is all of the collected lymph dumped?

A

Veins

290
Q

When do the one way mini valves of lymphatic capillary walls open?

A

When pressure in interstitial space is greater than pressure in lymphatic capillary, endothelial mini valves open

291
Q

Lymph vessel flow

A

Capillaries > bigger vessels > trunks > ducts

292
Q

What “pushes” lymph through the lymphatic system?

A

Smooth muscle in the lymph vessels react to pulsing of nearby arteries, then the squeezing of skeletal muscles exerts external pressure to keep lymph moving and reaching a lymphatic trunk

293
Q

What are the lymphatic trunks? What are they named after?

A

The lymphatic trunks are named after the regions of the body they drain the lymph into:

Two lumbar trunks
Two bronchomediastinal trunks 
Two subclavian trunks
Two jugular trunks 
One interstitial trunk
294
Q

what places does lymph go from the trunks?

A

Either the right thoracic duct (collects from right arm and right side of head and chest)

OR

Thoracic duct, much bigger (collects from rest of body)

295
Q

Where does the right lymphatic duct dump lymph into?

A

The junction of the right jugular vein and right subclavian vein

296
Q

Where does the thoracic duct dump lymph into?

A

The junction of the left jugular vein and left subclavian vein

Same junction as right duct but on L side of body

297
Q

Why do lymph ducts dump into the junction of jugular and subclavian veins?

A

Because the pressure is very low, easier for lymph to flow in

298
Q

What are lymph nodes in the intestinal wall called?

A

Peyer’s patches

299
Q

What types of cells detect pathogen in lymph nodes?

A

Dendritic cells

300
Q

Pathway of infection in lymph

A

Lymphatic capillary > vessel > node: sensed by dendritic cell and presented to B cells to make antibodies

Circulating T cells look for pathogens tagged with antibodies

301
Q

What are the three MAIN groups of lymph nodes?

A

Inguinal
Axillary
Cervical

302
Q

What group of lymph nodes drained abdominal wall below umbilicus, lower extremities, and genitalia

A

Inguinal

303
Q

What group of lymph nodes drains the posterior pharynx, tonsils, thyroid, and throat?

A

Anterior cervical

304
Q

What group of lymph nodes drains the scalp, neck, thorax, cervical, and axillary lymph nodes?

A

Posterior cervical

305
Q

What group of lymph nodes drains the Mediastinum, lungs, esophagus, and abdomen

A

Supraclavicular via thoracic duct

306
Q

What group of lymph nodes drains the Majority of the breast?

A

Axillary

307
Q

What are the great arteries of the heart that carry blood away from the heart?

A

Aorta + pulmonary arteries

308
Q

Describe the flow of blood to and from the heart, including when it is oxygenated and not.

A

LV pumps oxygenated blood > aorta > rest of body > deoxygenated loop comes back via RA > RV > to lungs via pulmonary artery > LA > LV

309
Q

What are the lymphaitc organs?

A

Diffuse lymphoid tissue, nodes/peyers patches, Thymus, spleen, tonsils

310
Q

Lymphatic function of tonsils

A

Form ring of lymphoid tissue around throat, trap pathogens from food eaten and air inhaled

311
Q

Lymphatic function of thymus

A

Development of T cells, making sure T cells that react to normal antigens are destroyed

Active neonatal and preadolescent then slowly atrophies and is replaced by fat after puberty

312
Q

Lymphatic function and location of spleen

A

L side of body below diaphragm, abovestomach

White pulp: antibodies generated by B cells, antibody coated bacteria filtered out

Red pulp: old and defective blood cells are destroyed, keeps RBC and platelets available

313
Q

What is the major relationship between the cardio and pulmonary systems?

A

They work together to circulate blood and oxygen throughout the body.

314
Q

What are the starling forces that affect lymph?

A

Govern passive exchange of water between capillary microcirculation and interstitial fluid

Determine directionality of net water movement between two compartments and the rate at which water exchange occurs

The direction of water exchange is determined by combo of relative hydrostatic and oncotic pressure of these two compartments, rate is governed by permeability of capillary itself

315
Q

What is the most common etiology of metastatic disease?

A

Lung tumors

316
Q

What is pericardial effusion?

A

Any fluid above normal 30-50mL found in pericardial space

317
Q

Pericardial effusion etiology

A

Typically due to hydrostatic or oncotic forces

318
Q

What is a hemopericardium? What causes it and what can it lead to?

A

Blood in pericardial sac

MI with rupture, traumatic perforation

Cases cardiac tamponade, death may occur

319
Q

Complications pleural effusion

A

Cardiac tamponade (fluid compresses heart, decreased CO)

320
Q

Pleural effusion clinical characteristics

A

Alternans on ECG, QRS alternating due to moving around in fluid

CXR-water bottle appearance
Echo- heart dancing in pericardium

321
Q

Bicuspid aortic valve etiology

A

Usually R + L coronary cusps are fused (common)

322
Q

Bicuspid aortic valve definition

A

2 instead of 3 lobes

323
Q

Complications bicuspid aortic valve

A

Ascending aortic aneurysm

324
Q

Bicuspid aortic valve clinical characteristics

A

Aortic stenosis and aortic regurgitation

Systolic ejection click just after S1

325
Q

Patent ductus arteriosis (PDA) RF

A

Prematurity

Rubella

326
Q

What is the most common septal congenital defect?

A

Interventricular septal defects

327
Q

Interventricular septal defects Complications

A

Increased risk of endocarditis

328
Q

Interventricular septal defects clinical characteristics

A

Asymptomatic holosystolic murmur

CHF

329
Q

What is the tetralogy in tetralogy of fallot

A

VSD
Pulmonic stenosis
RVH
Dextroposed aorta overriding VSD

330
Q

What are the four types of shock?

A

Hypovolemic, cardiogenic, obstructive, distributive

331
Q

What are causes of hypovolemic shock?

A

Hemorrhage, dehydration, burns

332
Q

What are causes of cardiogenic shock?

A

Acute MI, HF, valvular dysfunction, arrhythmia

333
Q

What are causes of obstructive shock?

A

Cardiac tamponade, PE, tension pneumothorax

334
Q

What are causes of distributive shock?

A

Sepsis, anaphylaxis, CNS injury

335
Q

What are sx of hypovolemic shock?

A

Cold, clammy skin

336
Q

What are sx of cardiogenic shock?

A

Cold, clammy skin

337
Q

What are sx of obstructive shock?

A

Cold, clammy skin

338
Q

What are sx of distributive shock?

A

Warm, dry skin

339
Q

What are hemangiomas?

A

Common vascular birthmarks made of extra blood vessels in the skin, benign

340
Q

What is kaposi sarcoma?

A

Endothelial malignancy most commonly affecting skin, mouth, GI tract, respiratory tract

Metastatic, dangerous

HHV-8, HIV

341
Q

RF kaposi sarcoma?

A

Old Eastern European males, AIDS, organ transplant, lindau von hipple disease (cavernous type)

342
Q

complications kaposi sarcoma

A

Pericardial effusion

Cardiac tamponade

343
Q

kaposi sarcoma clinical characteristics

A

Purple/black papules that may scale

344
Q

What is Chagas’ disease?

A

Parasite (trypanosoma cruzi)

“Kissing bug”

345
Q

What is the leading cause of infectious myocarditis worldwide?

A

Chagas’ disease

346
Q

RF Chagas’ disease

A

Central American, Mexico, southern US (rare)

347
Q

Complications Chagas’ disease

A

Dilated cardiomyopathy, HF, reduced EF, arrhythmias, heart block
Cardiac arrest
Enlarged esophagus
Enlarged colon

348
Q

Chagas’ disease clinical characteristics

A 
Swelling at bite sitefever
Fatigue
Rash
Body aches
Headache
349
Q

What is the etiology of Lyme disease?

A

Borrelia burgdorferi

Deer tick bite

350
Q

RF Lyme disease

A

NE US

351
Q

Lyme disease complications

A 
AV block
Carditis 
Bell’s palsy
Migratory myalgia
Encephalopathy
Chronic arthritis
352
Q

Lyme disease clinical characteristics

A

Erythema migrans rash - bullseye rash

Flu like sx

353
Q

Rocky Mountain spotted fever etiology

A

Rickettsia rickettsii

Tick vector

354
Q

Rocky Mountain spotted fever clinical characteristics

A

Headache, fever, rash (vasculitis)

Rash starts at wrists and ankles and spreads to trunk, palms, soles

355
Q

What are the three types of viral hemorrhagic fever?

A

Yellow fever, dengue fever, filoviruses

356
Q

Yellow fever (viral hemorrhagic fever) clinical characteristics

A

High fever, black vomitus, jaundice

May see councilman bodies on liver biopsy

357
Q

a deficiency B1 can lead to what

A

B1 deficiency (wet beriberi) can lead to high output cardiac failure (dilated cardiomyopathy)

NPLEX (28 decks)

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