Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Jugular Venous Pulse graph

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Myxoma

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Heart Normal pressures

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Familial dysbetalipoproteinemia (type II hyperlipoproteinemia)

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Apolipoproteins

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pulses paradoxus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Class 1 antiarrhythmic

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Heart embryology

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Coronary artery anatomy

A

FA 266

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cardiac output

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cardiac and vascular function curves

A

FA 269

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pressure-volume loops and cardiac cycle

A

FA 270

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Aortic area

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Left sternal border

A

Diastolic murmur - Aortic regurgitation, pulmonic regurgitation

Systolic murmur - Hypertrophic cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pulmonic area

A

Systolic ejection murmur - Pulmonic stenosis, flow murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tricuspid area

A

Pansystolic murmur - Tricuspid regurgitation, ventricular septal defect

Diastolic murmur - Tricuspid stenosis, Atrial septal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Mitral area

A

Systolic murmur - Mitral regurgitation

Diastolic murmur - Mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Heart murmurs

A

FA 273

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Speed of conduction

A

Purkinje > atria > ventricles > AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Some Risky Meds Can Prolong QT

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Congential long QT syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Wolf-Parkinson-White syndrome

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Atrial fibrillation

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Atrial flutter

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Ventricular fibrillation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

1st degree av block

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

2nd degree AV block

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3rd degree AV block

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Atrial natriuretic peptide

A

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

30
Q

B-type (brain) natriuretic peptide

A

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.

31
Q

Receptors:

A

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)

32
Q

Right-to-left shunts

A

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

33
Q

Persistent truncus arteriosus

A

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

34
Q

D-transposition of great vessels

A

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.

35
Q

Tricuspid atresia

A

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

36
Q

Tetralogy of Fallot

A

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

37
Q

Total anomalous pulmonary venous return (TAPVR)

A

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.

38
Q

Ventricular septal defect

A

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.

39
Q

Atrial septal defect

A

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

40
Q

Patent ductus arteriosus

A

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)

41
Q

Eisenmenger syndrome

A

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.

42
Q

Hypertensive emergency

A

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

43
Q

Atherosclerotic progression

A

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

44
Q

Aortic dissection

A

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.

45
Q

ECG diagnosis of MI

A

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

46
Q

Dilated cardiomyopathy

A

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.

47
Q

Hypertrophic cardiomyopathy

A

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.

48
Q

Restrictive/infiltrative cardiomyopathy

A

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).

49
Q

CHF

A

FA 291

50
Q

Aschoff bodies

A

Associated with rheumatic fever (granuloma with giant cells).

51
Q

Kussmaul sign

A

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.

52
Q

Strawberry hemangioma

A

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.

53
Q

Cherry hemangioma

A

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

54
Q

Pyogenic granuloma

A

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

55
Q

Cystic hygroma

A

Cavernous lymphangioma of the neck. Associated with Turner syndrome.

56
Q

Glomus tumor

A

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

57
Q

Bacillary angiomatosis

A

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

58
Q

Angiosarcoma

A

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.

59
Q

Lymphangiosarcoma

A

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

60
Q

Kaposi sarcoma

A

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.

61
Q

Temporal (giant cell) arteritis

A

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.

62
Q

Takayasu arteritis

A

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.

63
Q

Polyarteritis nodosa

A

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.

64
Q

Kawasaki disease

A

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.

65
Q

Buerger disease

A

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.

66
Q

Granulomatosis with polyangiitis (Wegener)

A

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.

67
Q

Microscopic Polyangitis

A

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.

68
Q

Churg-Strauss syndrome

A

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.

69
Q

Henoch-Schonlein purpura

A

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.

70
Q
A

Step 1 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions