Cardiology

Question 1

Jugular Venous Pulse graph

Answer 1

a- right atrial contraction

c- Bulging of tricuspid valve during right ventricular contraction

x- right atrial relaxation

v- continued inflow of venous blood

y- passive emptying of right atrium after tricuspid opening

Question 2

Myxoma

Answer 2

Histologically, these tumors are composed of scattered cells within a mucopolysaccharide stroma, abnormal blood vessels, and hemorrhagic. Myxomas produce large amounts of vascular endothelial growth factor, which contribute to angiogenesis hemorrhaging ( seen as hemosiderin deposition [brown]), and friability seen in these tumors. Myxomas also produce large amounts of interlukin 6, thus patients frequently present with constitutional symptoms (e.g. weight loss, fever).

Question 3

Heart Normal pressures

Answer 3

Right atrium (0,8), right ventricle (4,25), pulmonary artery (9,25), Left atrium (2,12), Left ventricle (9,130), Aorta (70,130)

Question 4

Familial dysbetalipoproteinemia (type II hyperlipoproteinemia)

Answer 4

characterized clinically by xanthomas and premature coronary and peripheral vascular disease. The primary defects in familial dysbetalipoproteinemia are in Apo E3 and ApoE4, apolipoproteins found on chylomicrons and VLDL that are responsible for binding hepatic apoliportein receptors. Without E3 and #4, the liver cannot effeciently remove chylomicrons and VLDL remnants from the circulation, causing their accumulation in the serum and resultant elevations in cholesterol and triglyceride levels.

Question 5

Apolipoproteins

Answer 5

ApoA-I: LCAT activation (cholesterol esterification)

ApoB-48: CHylomicron assembly and secreation by the intestine

ApoB-100: LDL particle uptake by extrahepatic cells.

ApoC-II: Lipoprotein lipase activation

ApoE-3&4: VLDL and chylomicron remnant uptake by liver cells

Question 6

Pulses paradoxus

Answer 6

Decreased systemic blood pressure during inspiration (acute cardiac tamponade, constrictive percarditis, sever obstructive lung disease, and restrictive cardiomyopathy.)

Question 7

Class 1 antiarrhythmic

Answer 7

Class 1 A (Disopyranide, Quinidine, Procainamide (Double Quarter Pounder) Intermediate ihib phase 0, prolonged effect on length of action potential; Class 1B (Lidocaine, Tocainide, Mexiletive (Lettuce, Tomato, May)) weak, shortened; Class 1 C (Marcizine, Flecainide, Propafenone (More Fries Please)) Strong, no change.

Question 8

Heart embryology

Answer 8

Truncus arteriosus (TA) - Ascending aorta and pulmonary trunk

Bulbus cordis - Smooth parts (outflow tract) of left and right ventricles

Primitive atria - Trabeculated part of left and right atria

Primitive ventricle - Trabeculated part of left and right ventricles

Primitive pulmonary vein - smooth part of left atium

Left horn of sinus venosus (SV) - Coronary sinus

Right horn of SV - Smooth part of right atrium

Right common cardinal vein and right anterior cardinal vein - SVC

Question 9

Coronary artery anatomy

Answer 9

FA 266

Question 10

Cardiac output

Answer 10

CO = stroke volum (SV) x heart rate (HR)

Fick principle: CO = rate of O2 consumption/ (arterial O2 content - venouse O2 conent)

Mean arterial pressure (MAP) = CO x TPR

MAP = 2/3 diastolic pressure + 1/3 systolic pressure

Pulse pressure = systolic pressure - diastolic pressure (increased in hyperthyroidism, aortic regurgitation, arteriosclerosis, obstructive sleep apnea, exercise (transient)). Pulse pressure is proportional to SV, inversely proportional to arterial compliance. (decrease pulse pressure in aortic stenosis, cardiogenic shock, cardiac tamponade, and advanced heart failure.)

SV = EDV - ESV

Question 11

Cardiac and vascular function curves

Answer 11

FA 269

Question 12

Pressure-volume loops and cardiac cycle

Answer 12

FA 270

Question 13

Aortic area

Answer 13

Systolic murmur - Aortic stenosis, flow murmur, aortic valve sclerosis

Question 14

Left sternal border

Answer 14

Diastolic murmur - Aortic regurgitation, pulmonic regurgitation

Systolic murmur - Hypertrophic cardiomyopathy

Question 15

Pulmonic area

Answer 15

Systolic ejection murmur - Pulmonic stenosis, flow murmur

Question 16

Tricuspid area

Answer 16

Pansystolic murmur - Tricuspid regurgitation, ventricular septal defect

Diastolic murmur - Tricuspid stenosis, Atrial septal defect

Question 17

Mitral area

Answer 17

Systolic murmur - Mitral regurgitation

Diastolic murmur - Mitral stenosis

Question 18

Heart murmurs

Answer 18

FA 273

Question 19

Speed of conduction

Answer 19

Purkinje > atria > ventricles > AV node

Question 20

Some Risky Meds Can Prolong QT

Answer 20

Sotalol, Risperidone (antipsychotics), Macrolides, Chloroquine, Protease inhibitors (-navir), Quinidine (class Ia; also class III), Thiazides

Question 21

Congential long QT syndrome

Answer 21

Inherited disorder of myocardial repolarization, typically due to ion channel defects; inc risk of sudden cardiac death due to torsades de points. Includes:

Romano-Ward syndrom - autosomal dominant, pure cardiac phenotype (no deafness).

Jervell and Lange-Nielsen syndrome - autosomal recessive, sensorineural deafness

Question 22

Wolf-Parkinson-White syndrome

Answer 22

Most common type of ventricular pre-excitation syndrome. Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave with shortened PR interval on ECG. May result in reentry circuit -> supraventricular tachycardia.

Question 23

Atrial fibrillation

Answer 23

Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly space QRS complexes. Can result in atrial stasis and lead to thromboembolic stroke. Treatment includes rate control, anticoagulation, and possible pharmacological or electrical cardioversion.

Question 24

Atrial flutter

Answer 24

A rapid succession of identical, back-to-back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves. Pharmacologic conversion to sinus rhythm: class IA, IC, or III antiarrhythmics. Rate control: b-blocker or CCB. Definitive treatment is catheter ablation

Question 25

Ventricular fibrillation

Answer 25

A completely erratic rhythm with no identifiable waves. Fatal arrhytmia without immediate CPR and defibrillation.

Question 26

1st degree av block

Answer 26

The PR interval is prolonged (\>200 msec). Benign and asymptomatic. No treatment required

Question 27

2nd degree AV block

Answer 27

Mobitz type I - Progressive lenghtening of the PR interval until a beat is "dropped" ( a P wave not followed by a QRS complex). Usually asymptomatic Mobitz type II - Dropped beats that are not preceded by a change in the length of the PR interval. It is often found as 2:1 block, where there are 2 or more P waves to 1 QRS response. May progress to 3rd-degree block. Often treated with a pacemaker.

Question 28

3rd degree AV block

Answer 28

The atria and ventricles beat independtly of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate. Usually treated with pacemaker. Lyme disease can result in 3rd-degree heart block.

Question 29

Atrial natriuretic peptide

Answer 29

Released from atrial myocytes in response to inc blood volume and atrial pressure. Causes vasodilation and dec Na reabsorption at the renal collecting tubule. Constricts efferent renal arterioles and dilates afferent arterioles via cGMP, promoting diuresis and contributing to "aldosterone escape" mechanism

Question 30

B-type (brain) natriuretic peptide

Answer 30

Released from ventricular myocytes in response to inc tension. Similar physiologic action to ANP, with longer half-life. BNP blood test used for diagnosisng heart failure (very good negative predictive value). Available in recombinant form (nesiritide) for treatment of heart failure.

Question 31

Receptors:

Answer 31

Aortic arch transmits via vagus nerve to solitary nucleus of medulla (responds only to Inc BP) Carotid sinus (dilated region at cartoid bifurcation) transmits via glossopharyngeal nerve to solitary nuclus of medulla (responds to dec and inc in BP)

Question 32

Right-to-left shunts

Answer 32

Early cyanosis - "blue babies". Often diagnosed prenatally or become evident immediately after birth. usually require urgent surgical correction and/or maintenance of a PDA. The 5 T's: 1. Truncus arteriosus 2. Transposition 3. Tricuspid atresia 4. Tetralogy of Fallot 5. TAPVR

Question 33

Persistent truncus arteriosus

Answer 33

Failure of truncus arteriosus to divide into pulmonary trunk and aorta; most patients have accompanying VSD.

Question 34

D-transposition of great vessels

Answer 34

Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior) -\> separation of systemic and pulmonary circulations. Not compatible with life unless a shunt is present to allow mixing of blood (e.g., VSD, PDA, or patent forament ovale). Due to failure of the aorticopulmonary septum to spiral.Without surgical intervention, most infacnts die within the first few months of life.

Question 35

Tricuspid atresia

Answer 35

Absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability

Question 36

Tetralogy of Fallot

Answer 36

Caused by anterosuperior displacement of the infundibular septum. Most common cause of early childhood cyanosis. 1. Pulmonary infundibular stenosis (most important determinant for prognosis) 2. RVH - boot-shaped heart on CXR. 3. Overriding aorta. 4. VSD Pulmonary stenosis forces right-to-left flow across VSD -\> early cyanotic "tet spells", RVH

Question 37

Total anomalous pulmonary venous return (TAPVR)

Answer 37

Pulmonary veins drain into right hear circulation (SVC, cornoary sinus, etc); assocated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO.

Question 38

Ventricular septal defect

Answer 38

Most common congenital cardiac defect. Asymptomatic at birth, may manifest weeks later or remain asymptomatic throught life. Most self resovle; larger lesions may lead to LV overload and heart failure.

Question 39

Atrial septal defect

Answer 39

Defect in interatrial septum; loud S1; wide, fixed split S2. Usually occurs in septum secundum; septum primum defects usually occur with other anomalies. Symptoms range from none to heart failure. Distinct from patent forament ovale in that septa are missing tissue rather than unfused

Question 40

Patent ductus arteriosus

Answer 40

In fetal period, shunt is right to left (normal). In neonatal period, dec lung resistance -\> shunt becomes left to right -\> progressive RVH and/or LVH and heart failure. Associated with a continous, "machine-like" murmur. Patency is maintained by PGE synthesis and low O2 tension. Uncorrected PDA can eventually result in late cyanosis in the lower extremities (differential cyanosis)

Question 41

Eisenmenger syndrome

Answer 41

Uncorrected left-to-right shunt (VSD, ASD, PDA) -\> inc pulmonary blood flow -\> pathologic remodeling of vasculature -\> pulmonary arteriolar hypertension. RVH occurs to compensate -\> shunt becomes right to left. Causes late cyanosis, clubbing, and polycythemia. Age of onset varies.

Question 42

Hypertensive emergency

Answer 42

Sever hypertension (\>180/120) with evidence of acute, ongoing target organ damage (e.g. papilledema, mental status changes)

Question 43

Atherosclerotic progression

Answer 43

Inflammation important in pathogenesis. Endothelial cell dysfunction -\> macrophage and LDL accumulation -\> foam cell formation -\> fatty streaks -\> smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition -\> fibrous plaque -\> complex atheromas Abdominal aorta\>coronary arter\>popliteal arter\>carotid arter

Question 44

Aortic dissection

Answer 44

Longitudinal intraluminal tear forming a false lumen. Associated with hypertension, bicuspid aortic valve, and inherited conective tissue disorders (e.g., Marfan syndrome). Can present with tearting chest pain, of sudden onset, radiating to the back +/- markedly unequal BP in arms. CXR shows mediastinal widening. The false lumen can be limited to the ascending aorta, propagate from the ascending aorta, or propagate from the descending aorta. Can result in pericardial tamponade, aortic rupture, and death.

Question 45

ECG diagnosis of MI

Answer 45

Anterior wall (LAD) - V1-V4 Anteroseptal (LAD) - V1-V2 Anterolateral (LAD or LCX) - V4-V6 Lateral wall (LCX) - I, aVL Inferior wall (RCA) - II, III, aVF

Question 46

Dilated cardiomyopathy

Answer 46

Most common cardiomyopathy (90% of cases). Often diopathic or congenital. Other etiologies include chronic alcohol abuse, wet beriberi, coxsackie B virus myocarditis, chronic cocaine use, Chagas disease, Docorubicin toxicity, hemocrhomatosis, and peripartum cardiomopathy. Findings: heart failure, S3, dilated heart on echocardiogram, balloon appearance of heart on CXR. Treatment: Na restriction, ACE inhibitors, B-blockers, diuretics, digoxin, implantable cardioverter defibrillator (ICD), heart transplant.

Question 47

Hypertrophic cardiomyopathy

Answer 47

60-70% of cases are familial, autosomal dominant (commonly a B-myosin heavy-chain mutation). Rarely can be associated with Friedreich ataxia. Cause of sudden death in young athletes, due to ventricular arrhythmia. Findings: S4, systolic murmur. Treatment: Cessation of high-intensity athletics, use of B-blocker or non-dihydropyridine calcium channel blockers (e.g., verapamil). ICD if patient is high risk.

Question 48

Restrictive/infiltrative cardiomyopathy

Answer 48

Major causes include sarcoidosis, amyloidosis, postradation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate), and hemochromatosis (dilated cardiomyopathy can also occur).

Question 49

CHF

Answer 49

FA 291

Question 50

Aschoff bodies

Answer 50

Associated with rheumatic fever (granuloma with giant cells).

Question 51

Kussmaul sign

Answer 51

Increase in JVP on inspiration instead of a normal decrease. Inspiration -\> negative intrathoracic pressure not transmitted to heart -\> impaired filling of right ventricle -\> blood back up into venae cavae -\> JVD. May be seen with constrictive pericardiits, restrictive cardiomyopathies, right atrial or ventricular tumors.

Question 52

Strawberry hemangioma

Answer 52

Genign capillary hemangioma of infancy. Appears in first few weeks of life (1/200 births); grows rapidly and regresses spontaneously at 5-8 years old.

Question 53

Cherry hemangioma

Answer 53

Benign capillary hemangioma of the elderly. Does not regress. Frequency inc with age

Question 54

Pyogenic granuloma

Answer 54

Polpyoid capillary hemangioma that can ulcerate and bleed. Assocated with trauma and pregnancy

Question 55

Cystic hygroma

Answer 55

Cavernous lymphangioma of the neck. Associated with Turner syndrome.

Question 56

Glomus tumor

Answer 56

Benign, painful, red-blue tumor under fingernails. Arises from modified smooth muscle cells of glomus body.

Question 57

Bacillary angiomatosis

Answer 57

Benign capillary skin papules found in AIDS patients. Caused by Bartonella henselae infections. Frequently mistaked for Kaposi sarcoma.

Question 58

Angiosarcoma

Answer 58

Rare blood vessel malignancy typically occuring in the head, neck, and breast areas. Usually in the elderly, on sun-exposed areas. Associated with radiation therapy and arsenic exposure. Very aggressive and difficult to resect due to delay in diagnosis.

Question 59

Lymphangiosarcoma

Answer 59

Lymphatic malignancy associated with persistent lympedema (e.g., post-radical mastectomy).

Question 60

Kaposi sarcoma

Answer 60

Endothelial malignancy most commonly of the skin, but also mouth, GI tract, and respiratory tract. Associated with HHV-8 and HIV. Frequently mistaken for bacillary angiomatosis.

Question 61

Temporal (giant cell) arteritis

Answer 61

Generally elderly females. Unilateral headache (temporal artery), jaw claudication. May lead to irreversible blindness due to ophthalmic artery occlusion. Associated with polymyalgia rheumatica. Most commonly affects branches of carotid artery. Focal granulomatous inflammation. inc ESR. Treat with high-dose corticosteoids prior to temporal artery biopsy to prvent vision loss.

Question 62

Takayasu arteritis

Answer 62

Asian females \<40 years old. "pulseless disease" (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances. Granulomatous thickening and narrowing of aortic arch and proximal great vessels. inc ESR. Treat with corticosteroids.

Question 63

Polyarteritis nodosa

Answer 63

Young adults. Hepatitis B seropositivity in 30% of patients. Fever, weight loss, malaise, headache. GI: abdominal pain, melena. Hypertension, neurologic dysfunction, cutaneous eruptions, renal damage. Typically involves renal and visceral vessels, not pulmonary arteries. Immune complex mediated. Transmural inflammation of the arterial wall with fibrinoid necrosis. Innumerable microaneurysms and spasm on arteriogram. Treat with corticosteroids, cyclophosphamide.

Question 64

Kawasaki disease

Answer 64

Asian children \<4 y.o. Fever, cervical lympadenitis, conjunctival injection, changes in lips/oral mucosa ("strawberry tongue"), had-foot erythema, desquamating rash. May develop coronary artery aneurysms, thrombosis -\> MI rupture. Treat with IV immunoglobulin and aspirin.

Question 65

Buerger disease

Answer 65

Heavy smokers, males \<40 years old. Intermitten claudication may lead to gangrene, autoamputation of digits, superficial nodular phlebitis. Raynaud phenomenon is often present. Segmental thrombosing vasculitis. Treat with smoking cessation.

Question 66

Granulomatosis with polyangiitis (Wegener)

Answer 66

Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis. Lower respiratory tract: hemoptysis, cough, dyspnea. Renal: hematuria, red cell casts. Triad: focal necrotizing vasculitis, necrotizing granulomas in the lung and upper airway, necrotizing glomerulonephritis. PR3-ANCA/c-ANCA (anti-proteinase 3). CXR: large nodular densities. Treat with cyclophosphamide, corticosteroids.

Question 67

Microscopic Polyangitis

Answer 67

Necrotizing vasculitis commonly involving lung, kidneys, and skin with pauci-immune glomerulonephritis and palpable purpura. Presentation similar to granulomatosis with polyangiitis but without nasopharyngeal involvement. No granulomas. MPO-ANCA/p-ANCA (anti-myeloperoxidase). Treat with cyclophosphamide and corticosteroids.

Question 68

Churg-Strauss syndrome

Answer 68

Asthma, sinusitis, palpable purpura, peripheral neuropathy (e.g., wrist/foot drop). Can also involve heart, GI, kidneys (pauci-immune glomerulonephritis). Granulomatous, necrotizing vasulitis with eosinophilia. MPO-ANCA/p-ANCA, inc IgE level.

Question 69

Henoch-Schonlein purpura

Answer 69

Most common childhood systemic vasculitis. Often follow URI. Classic triad: Skin: palpable purpura on buttock/legs; arthralgias; GI: abdominal pain, melena, multiple lesions of same age. Vasculitis secondary to IgA complex deposition. Associated with IgA nephropathy.