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124 Cards in this Set
- Front
- Back
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What are the structures inside the carotid sheath?
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1. Internal jugular vein (lateral)
2. Common carotid Artery (medial) 3. Vagus Nerve (posterior) |
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What factors (4) cause increase of contractility (and stroke volume) ?
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1. Catecholamines - increase activity of Ca2+ pump in sarcoplasmic reticulum.
2. Increase in intracellular calcium 3. Decrease in extracellular sodium 4. Digitalis - increase intracellular Na by blocking Na-K pump --> decrease activity of Na/Ca exchanger --> resulting in increases of Ca (cell does not pump in more Na+ so Ca2+ accumulates) |
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What 5 factors decrease contractility and stroke volume?
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1. Beta blockade
2. Heart failure 3. Acidosis 4. Hypoxia/hypercapnea 5. Non-dihydropyridine Ca2+ blockers |
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The 4 factors that increase myocardial O2 demand are
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1. Inc afterload (proportional to increase in arterial pressure)
2. inc contractility 3. Inc heart rate 4. Inc heart size (inc wall tension) |
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Name the three differences between cardiac and skeletal muscle
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1. Cardiac muscle action potential has a plateau, due to Ca2+ influx
2. Cardiac muscle contraction requires Ca2+ influx to release Ca2+ from sarcoplasmic reticulum 3. Cardiac myocytes are electrically coupled via gap junctions |
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Congenital Heart Disease
5 Causes of Right to Left Shunt Early cyanosis Number of vessels |
1. Tetrology of Fallot - most common (4)
2. Transposition of great vessels (2) 3. Truncus arteriosus (1) 4. Tricuspid atresia (3) 5. Total anomalous pulmonary venous return TAPVR |
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Congenital Heart Disease
3 Causes of Left to Right Shunt |
1. VSD - most common congenital cardiac anomaly
2. ASD - loud S1; wide, fixed split S2 3. PDA close with indomethacin. Frequency VSD > ASD > PDA causes increase in pulm resistance because of arteriolar thickening, leading to progressive right-to-left shunt (Eisenmenger's) |
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Tetrology of Fallot
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1. Pulmonary stenosis (imp prognostic factor)
2. RVH 3. Overriding aorta 4. VSD boot-shaped heart caused by anterosuperior displacement of the infundibular septum squatting relieves symptoms |
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What's the deal with transposition of the great vessels? hmm?
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Aorta leaves RV and pulm trunk leaves LV = separation of systemic and pulm circulations. Not compatible with life unless a shunt is present to allwo adequate mixing (VSD, PDA or PFO)
Due to failure of the articopulmonary septum to spiral. Die w/in a few months unless surgery. |
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Coarctation of the aorta
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Infantile type - aortic stenosis proximal to insertion of ductus arteriosis (preductal)
Adult type - stenosis is distal to ductus arteriosus (postductal). associated with notching of ribs due to collateral circulation, hypertension in upper extremities, weak pulses in lower extremities Assoc w/ Turner's syndrome Male 3 : Female 1 Check Femoral pulses |
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Patent Ductus Arteriosus
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In fetal period, shunt is right to left (normal). In neonatal period, lung resistance decreases and shunt becomes left to right with subsequent RVH and failure (abnormal).
Associated with a continuous, "machine-like" murmur. Patency is maintained by PGE synthesis and low O2 tension |
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cardiac defects w/ 22q11 syndromes
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truncus arteriosus,
tetrology of fallot |
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cardiac defects in down's syndrome
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ASD, VSD, AV septal defect (endocardial cushion defect)
incomplete atria/ventricular septum and abnormal tricuspid valve |
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cardiac defects assoc w/ congenital rubella
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Septal defects, PDA, pulm artery stenosis
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cardiac defects w/ Turner's syndrome
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coarctation of the aorta, biscupid aorta
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cardiac defects w/ Marfans
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MVP, thoracic aortic aneurysm and dissection,aortic regurgitation (late)
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cardiac defects in offspring w/ diabetic mother
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transposition of great vessels
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Monckeberg arteriosclerosis
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Calcification in the internal elastic lamina and media of medium sized arteries that leads to vascular stiffening without obstruction. Esp radial or ulnar. Usually benign. Pipestem arteries on X-ray
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Gross and Micro findings: 0-24 hours after MI
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Gross: None; Dark mottling, pale with tetrazolium stain
Micro: Early coagulative necrosis,release of necrotic cellcontents into blood; edema,hemorrhage, wavy fibers.Neutrophils appear. Reperfusion injury,associated with generationof free radicals, leads tohypercontraction of myo brilsthrough increased free calcium influx. |
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Gross and Micro findings: 1-3 days after MI
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Gross: Hyperemia
Micro: Extensive coagulative necrosis.Tissue surrounding infarct shows acute inflammationwith neutrophils. |
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Gross and Micro findings: 3-14 days after MI
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Gross: Hyperemic border;central yellow-brownsoftening—maximally yellowand soft by 10 days
Micro: Macrophages, then granulationtissue at margins |
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Gross and Micro findings: 2 weeks to several months days after MI
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Gross: Recanalizedartery, gray-white fibrotic scar
Micro: Contracted scar complete |
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Dilated (congestive) cardiomyopathy
-Causes (hint: ABCCCD) -Murmur |
Most common cardiomyopathy 90%, idiopathic or familial
Etiologies: Alcohol abuse, Beriberi, Coxsackie B viral myocarditis, Cocaine use, Chagas disease, Doxorubicin toxicity, peripartum cardiomyopathy Heart dilates and looks like a ballon on CXR S3, systolic murmur |
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Hypertrophic cardiomyopathy
-Causes |
Hypertrophy often asymmetric and involving interventricular septum. Near normal heart size.
50% cases are familial, autosomal dominant. Sudden death in young athletes. Loud S4, apical impulses, systolic murmur. Rx - beta-blocker or non-dihydropyridine Ca channel blocker (verapamil) Diastolic dysfunction ensues |
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Restrictive/obliterative cardiomyopathy
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Major causes: sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler's syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate) and hemochromatosis (dilated cardiomyopathy may also occur)
Diastolic dysfunction. |
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Libman-Sacks endocarditis
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Verrucous vegetations on both sides of the valve. Can be associated with mitral regurg and less commonly, mitral stenosis. Seen in lupus.
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Rheumatic heart disease
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consequence of group A strep. Early deaths due to myocarditis. Late sequelae include rheumatic heart disease that affects heart valves - mitral > aortic >> tricuspid. (high pressure areas affected most)
Associated with Aschoff bodies (granuloma w/ giant cells), Anitschkow's cells (activated histiocytes), migratory polyarthritis, erythema marginatum, elevated ASO titers. Immune mediated (type II hypersensitivity), not direct effect of bacteria. |
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Cardiac tamponade
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Compression of heart by fluid in pericardium, leading to decrease CO. equilibriation of diastolic pressures in all 4 chambers.
Hypotension, inc venous pressure JVD, distant heart sounds, inc HR, pulsus paradoxus, ECG shows electrical alternans (beat to beat alterations of QRS complex height) Pulsus paradoxus Kussmaul's pulse - decrease in amplitude of pulse during inspiration. also seen in asthma, obstructive sleep apnea, pericarditis and croup. |
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Pericarditis
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Serous - caused by SLE, RA, viral infxn, uremia
Fibrinous - caused by uremia, MI (Dressler's), rheumatic fever Hemorrhagic - TB or malignancy Sx - pericardial pain, friction rub, pulsus paradoxus, distant heart sounds. ECG changes w/ diffuse ST elevation. resolves w/o scarring, chronic adhesives or chronic constrictive pericarditis |
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Syphilitic heart disease
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Tertiary syphilis disrupts vaso vasorum of the aorta resulting in dilation od the aorta and valve ring.
May lead to calcification of aortic root and ascending arch. Leads to tree bark appearance of the aorta. |
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What abnormalities can be heard at the left sternal border?
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Diastolic murmur
Aortic regurgitation Pulmonic regurgitation |
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The many equations for Cardiac output
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CO = SV x HR
CO = (rate of O2 consumption) / (arterial O2 - venous O2 content) MAP = CO x TPR CO = (135 x BSA) / ( 13 x Hb x SaO2 - SvO2) SV = EDV - ESV |
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Ejection fraction
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EF = SV/ EDV = (EDV - ESV) / EDV
EF is an index of ventricular contractility EF is normally >= 55% |
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Resistance, pressure, flow
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delta P = Q x R
Resistance = (viscosity x length) / (radius^4) Viscosity mostly depends on hemotocrit. Increased in polycythemia, hyperproteinemic states, hereditary spherocytosis |
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S3 Heart Sound occurs when?
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Early in diastole during rapid ventricular filling phase
Associated with increased filling pressures and more common in dilated ventricles Normal in children |
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S4 Heart Sound occurs when?
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Atrial kick - high atrial pressure.
Associated with ventricular hypertrophy Abnormal in all ages |
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When do you get S2 splitting?
-Normal pattern -Wide -Fixed -Paradoxical |
Normally, the aortic valve closes before the pulmonic
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Mitral/tricuspid regurgitation sounds like...
radiates to? |
Holosystolic, high-pitched blowing murmur
Mitral - loudest at apex and radiates toward axilla Tricuspid - loudest at tricuspid and radiates to right sternal border |
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Aortic stenosis sounds like...
radiates to? |
crescendo-decrescendo systolic ejection murmur following ejection click (maximal aortic opening)
LV >> aortic pressure during systole Radiates to carotids/apex Pulsus parvus et tardus - pulses weak compared to heart sounds If severe - Syncope, Angina, Dyspnea |
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VSD sounds like...
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Holosystolic, harsh-sounding murmur.
Loudest at tricuspid area |
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Mitral prolapse sounds like...
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Late systolic murmur with midsystolic click (being held down by chordae, papillary muscle).
Most frequent valvular lesion. Loudest at S2 |
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Aortic regurgitation sounds like...
Risk factor? |
Immediate high-pitched blowing diastoic murmur
Wide pulse pressure when chronic Bicuspid valve |
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Mitral stenosis sounds like..
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Follows opening snap
Delayed rumbling late diastolic murmur. LA >> LV pressure during diastole Tricuspid stenosis differs because it gets louder with inspiration (more blood flows into RA w/ inspiration) elevates LAEDP and PCWP > LVEDP - should be equal shorter A2 to opening snap interval = more severe |
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PDA sounds like...
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Continuous machine-like murmur
Loudest at time of S2 Prematurity or congenital rubella |
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Wolff-Parkinson-White Syndrome
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Accessory conduction pathway from atria to ventricle (bundle of Kent)
Bypasses the AV node Ventricles begin to partially depolarize earlier, giving rise ot delta wave on ECG May result in reentry current leading to supraventricular tachycardia WPW triad: 1. Delta wave 2. Shortened PR interval 3. Widened QRS |
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First degree AV block
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PR interval is prolonged > 200 ms
Asymptomatic |
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2nd degree AV block
Mobitz type I Wenckeback |
Progressive lengthening of PR interval until a beat is dropped (P wave not followed by QRS complex)
Usually asymptomatic |
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2nd Degree AV block
Mobitz type II |
Dropped beats that are not preceded by a change of length in PR interval
Abrupt, nonconducted P waves result in pathologic condition. Often found as 2:1 block, where there are 2 P waves to 1 QRS response. May progress to 3rd degree block |
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3rd degree AV block
complete |
The atria and ventricles beat independently of each other
Both P waves and QRS complexes are present, although P waves bear no relation to QRS complexes. The atrial rate is faster than the ventricular rate Usually treat with pacemaker |
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What factors do the peripheral chemoreceptors respond to?
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pO2 less than 60
Inc pCO2 Dec pH of blood |
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What factors do Central chemoreceptors respond to?
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changes in pH and pCO2 of brain interstitial fluid, which are influenzed by arterial pCO2
Does not directly respond to pO2 Cushing rxn - Inc intracranial pressure constricts arterioles, leads to cerebral ischemia, hypertension (sympathetics), reflex bradycardia Cushing's triad - hypertension, bradycardia, respiratory depression |
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Factors causing edema
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1. Inc capillary pressure - heart failure
2. Dec plasma proteins - nephrotic syndrome, liver failure 3. Inc capillary permeability - toxins, infections, burns 4. Inc interstitial fluid colloid osmotic pressure - lymphatic blockage |
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Ebstein's anomaly
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Apical displacement of tricuspid valve leaflets increased volume of right atrium, atrialization of RV
linked to in utero lithium for bipolar disorder |
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Cardiac tumors
-Children -Adults |
Myxomas are most common in adults
Occur in mostly LA, "ball-valve" obstruction associated w/ multiple syncopal episodes Rhabdomyomas are most frequent cardiac tumor in children - assoc w/ tuberous sclerosis Mets to heart from melanoma, lymphoma |
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Churg-Strauss
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Granulomatous vasculitis w/ eosinophilia
Involves lung, heart, skin, kidneys, nerves Often seen in atopic patients p-ANCA |
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Granulomatosis with polyangitis (Wegner was a nazi)
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Triad :
Focal necrotizing vasculitis Necrotizing granulomas in lung and upper airway Necrotizing glomerulonephritis Sx - perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea, hemoptysis, hematuria cANCA CXR w/ nodular densities; hematuria and red cell casts Cyclophosphamide and corticosteroids small vessels |
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Sturge-Webber
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Congenital vascular disorder that affects capillary sized blood vessels
port-wine stain of face and leptomeningeal angiomatosis (intracerebral AVM) |
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Henoch-Schonlein purpura
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Most common form of childhood systemic vasculitis
Skin rash (palpable purpura), arthralgia, intestinal hemorrhage, abd pain, melena Follows URIs, multiple lesions of same age IgA immune complexes deposit on BV's and vessel mesangium Skin, joints, GI |
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Buerger's disease
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Aka thromboangiitis obliterans.
idiopathic, segmental, thrombosing vasculitis of small and medium peripheral arteries and veins. Seen in heavy smokers. Sx - intermittent claudication, superficial nodular phlebitis, cold sensitivity (Raynaud's), severe pain, maybe gangrene |
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Kawasaki's disease
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Acute, self-limiting disease of infants/kids
necrotizing vasculitis of small/medium-sized vessels. Fever, congested conjuctiva, changes in lips/oral mucosa "strawberry tongue", lymphadenitis May develop coronary aneurysms |
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Polyarteritis nodosa
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Characterized by necrotizing immune complex inflammation of medium-sized muscular arteries
Sx - fever, weight loss, malaise, abd pain, melena, HA, myalgia, HTN, neurologic dysfunction, cutaneous eruptions Medium arteries - usually renal and visceral HBV in 30% Multiple anuerysms and constrictions on arteriograms typically not associated w/ ANCA Corticosteroids, cyclophosphamide |
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Takayasu's arteritis
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Pulseless disease
granulomatous thickening of aortic arch and/or proximal vessels. Elevated ESR Asian females < 40. Fever, Arthritis, Night sweats, Myalgia, Skin nodueles, Weak pulses in extremities |
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Temporal giant cell arteritis
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Common vasculitis that affects medium and large arteries, branches of the carotid
Focal, granulomatous inflammation Elderly females Unilateral HA, jaw claudication, impaired vision (occlusion of ophthalmic artery) Elevated ESR Polymyalgia rheumatica Medium and large vessels |
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Treatment for malignant hypertension
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Nitroprusside - short acting
Fenoldopam - D1 agonist - relaxes renal smooth muscle Diazoxide - K channel opener - hyperpolarizes and relaxes vascular smooth muscle |
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HMG-CoA reductase
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Decrease LDL a lot
Inc HDL Dec TG Inhibit cholesterol precursor, mevalonate Expensive, reversible LFTs, myositis |
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Niacin
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Dec LDL
Inc HDL a lot Dec TG Inhibits lipolysis in adipose tissue reduces hepatic VLDL secretion into circulation Red flushed face, dec by aspirin use |
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Bile acid resins
cholestyramine, colestipol |
Dec LDL
Inc HDL slightly Inc TG slightly Prevents intestinal reabsorption of bile acids Liver must use cholesterol to make more Gi discomfort, decreased vit ADEK |
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Cholesterol absorption blockers
Ezetimibe |
Dec LDL
No effect on HDL/TG Preven cholesterol reabsorption at small intestine brush border Rare LFTs |
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Fibrates
gemfibrozil, clofibrate, bezafibrate, fenofibrate |
Dec LDL
Inc HDL Dec TG a lot! Upregulate LPL, inc TG clearance Myositis, LFT inc |
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Class IA antiarrhythimcs
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quinidine, amiodarone, procainamide, dysopyrimide
Inc AP, Inc refractory period, Inc QT Na channel blockers |
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Class IB
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lidocaine, mexilitien, tocainide
Dec AP duration CNS/cardiovascular depression |
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Class IC
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Flecainide, encainide, propafenone
no effect on AP duration proarrhythmic, esp post MI |
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Class III
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Sotalol, ibutilide, bretylium, amiodarone
Inc AP duration, Inc refractory, Inc QT interval pulm fibrosis, hepatotoxicity, hypothyroidism, hyperthyroidism |
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Embryology-truncus arteriosus |
ascending aorta and pulmonary trunk |
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Embryology-bulbis cordis |
Smooth parts (outflow tract) of left and right ventricles |
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Embryology-right common cardinal vein and right anterior cardinal vein |
SVC |
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Embryology- Endocardial cushion |
Atrial septum, membranous interventricular septum, AV and semilunar valves |
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Fetal derivatives-Ligamentum teres |
Umbilical vein |
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Fetal derivatives-Medial umbilical ligaments |
Umbilical arteries |
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Fetal derivatives-Median umbilical ligaments |
Allantois---> urachus |
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Blood supply to SA and AV nodes |
RCA (infarct--> heart block) |
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When does coronary blood flow peak? |
Diastole (heart relaxation) |
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In heart cross section, which chamber is anterior? |
Right ventricle |
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In heart cross section, which chamber lateral to the right? (looking down from the head) |
Right atrium |
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In heart cross section, which chamber is posterior? |
Left atrium |
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In heart cross section, which chamber is lateral to the left? |
Left ventricle |
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Pulse pressure= |
Systolic pressure-diastolic pressure |
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Pulse pressure is directly proportional to? inversely proportional to? |
Directly-Systolic volume Inversely-arterial compliance |
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Systolic volume= |
End diastolic volume-end systolic volume |
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In early exercise, CO is maintained by? |
HR and SV |
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In late exercise, CO is maintained by? |
HR (SV plateaus!) |
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What factors (3) affect stroke volume? |
Contractility, Afterload, Preload |
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LaPlace Law for wall tension |
Pressure x radius/2x wall thickness (explains hypertrophy as compensation for increasing after load) |
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Holosystolic murmur at mitral valve |
Mitral regurgitation |
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Diastolic murmur at mitral valve |
Mitral stenosis |
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Systolic murmur at left sternal border |
Hypertrophic cardiomyopathy |
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Effect on heart sounds-Inspiration |
Increases venous return to right atrium Increases intensity of right heart sounds |
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Effect on heart sounds-Hand grip |
Increases afterload Increases intensity of MR, AR, VSD murmurs Decreases hypertrophic cardiomyopathy murmurs Later click in MVP |
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Effect on heart sounds-Valsalva, standing up |
Decreases preload Decreases intensity of most murmurs Increases intensity of hypertrophic cardiomyopathy murmur Earlier click in MVP |
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Effect on heart sounds-rapid squatting |
Increases venous return, increases preload, increases afterload Decreases intensity of hypertrophic cardiomyopathy murmur Increases intensity of AS murmur Later click in MVP |
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What type of heart sounds are: aortic/pulmonic stenosis, mitral/tricuspid regurgitation, VSD, MVP |
Systolic |
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What type of heart sounds are: aortic/pulmonic regurgitation, mitral/tricuspid stenosis |
Diastolic |
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U wave |
Hypokalemia |
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Fastest and slowest conduction speed: AV node, SA nodes, purkinje fibres, ventricles |
Fastest: Purkinje fibres Slowest: AV node |
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Order of cardiac conduction |
SA node --> atria --> AV node --> bundle of His --> right andleft bundle branches --> Purkinje fibers--> ventricles |
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Right atrium pressure |
5 mm Hg (<5) |
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Right ventricle pressure |
25/5 mm Hg (sys/dia) |
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Left atrium pressure |
10 mm Hg (<12) |
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Left ventricle pressure |
100 mm Hg (130/10) |
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Pulmonary trunk pressure |
25/10 mm Hg |
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Normal pulmonary wedge pressure |
4-12 mm Hg |
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In what conditions do you see hyaline arteriosclerosis (small vessels)? Defining feature? |
HTN and DM Thickening of walls |
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What defines hyper plastic arteriosclerosis? |
“Onion skinning” in severehypertension with proliferation of smooth muscle cell |
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MI complications 0-24 hours |
Ventricular arrhythmia, HF,cardiogenic shock |
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MI complications 1-3 days |
Postinfarction brinouspericarditis (friction rub) |
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MI complications 3-14 days |
Free wall rupture --> tamponade Papillary muscle rupture --> mitral regurgitation Interventricular septal rupturedue to macrophage-mediatedstructural degradation LV pseudoaneurysm (risk ofrupture) |
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MI complications 2 weeks to several months |
Dressler syndrome, HF,arrhythmias, true ventricularaneurysm (risk of muralthrombus) |
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What is Dressler Syndrome? |
Autoimmune fibrous pericarditis |
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EKG localization: V1–V2 |
Anteroseptal (LAD) |
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EKG localization: V3–V4 |
Anteroapical (distal LAD) |
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EKG localization: V5–V6 |
Anterolateral (LAD or LCX) |
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EKG localization: I, aVL |
Lateral (LCX) |
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EKG localization: II, III, aVF |
InFerior (RCA) |
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EKG localization: V7–V9, ST depression in V1–V3 with tall R waves |
Posterior (PDA) |
