Cardiolovascular Final

Front 1

Familia Hypercholesterolemia type 2

Back 1

Defect-LDL receptor and apo b100

Hint 1

Patient with xantomas

Front 2

Most common cause of Mitral stenosis

Back 2

Rheumatic fever

Some have symptoms of left heart failure. Hemoptysis too if there is rupture of high pressure bronchial veins.

Front 3

Immigrant from eastern europe with symptoms of left sided heart failure

Back 3

Look out for rheumatic heart disease.

Front 4

Systolic murmur that increases in intensity with maneuvers that's increases lv volume

Back 4

Hypertrophic Cardiomyopathy

Hint 4

Sometimes with symptoms of Mi.diff the murmur from dilated cm. Which decreases in intensity

Front 5

Biventricular dilation with symptoms of heart failure

Back 5

Dilated Cardiomyopathy

Hint 5

Systolic murmur that decreases in intensity with maneuvers that increases lv volume

Front 6

Widened splitting

Back 6

Anything that delays closure of pulmonary valve.Right bundle branch block,pulmonic stenosis

Hint 6

A2 then p2

Front 7

When acute ischemia causes depletion of ATP stores and dysfunction of Na_k_atpase what happens

Back 7

Extracellular Na leaks in and intracellular k leaks out .extracellular k increases

Front 8

Patient with metabolic acidosis, use of k sparing diuretics eg spironolactone, use of beta adrenergic antagonist and ekg peaked t wave,no p wave,prolong qrs and slowed heart rate

Back 8

Hyperkalemia

Front 9

In jugular venous curve

Back 9

Upward slopes indicate contractions and downward slope indicates relaxation

A- right Atrial contraction

C-tricuspid bulge

X- right atrial relaxation

V-Continuous inflow of venous blood

Y-right atrial emptying.

Front 10

Diff Isolated vsd and tetralogy of fallot

Back 10

Isolated vsd do not cause early cyanosis but large may do in older patient due to einsenmenger.left to right shunt. Unlike tof- right to left shunt

Front 11

Decreased na concentration outside the cell will

Back 11

Decrease depolarization

Front 12

Massive pulmonary embolism leads to

Back 12

Obstructive shock due to impedance of right ventricular forward flow

Hint 12

Elevated cardiac output,pcwp,decreased left ventricular preload.Elevated central venous pressure(jugular venous) due to impaired forward flow.

Front 13

Intestinal lipase inhibitor that inhibits absorption of dietary fat. Causes weight loss with significant Gastrointestinal side effect

Back 13

Orlistat

Hint 13

Diff from Ezetimibe which decreases small intestinal cholesterol absorption.does not cause weight loss.

Front 14

Most beneficial life style in reducing risk of myocardial infarction

Back 14

Smoking cessation.cigarette smoke generates free radical that oxidizes ldl and lead to accelerated arteriosclerosis.

Front 15

ST elevation

Back 15

Damage to the entire wall

Front 16

Cardiac enzyme used to detect reinfarction days after MI

Back 16

Ck-MB. Goes down after 72hrs. Rises 4 to 6 hrs.2nd enzyme

First to appear is Troponin I - rises 2 to 4 hrs after Mi Goes down after 7 to 10 days

Front 17

Contraction band

Back 17

Returning calcium in blood back to dead tissue.fibrinolysis.reperfusion injury also seen when oxygen(free radical) is returned with blood

Front 18

Microscopic changes in mi loop

Back 18

1 day(coagulative necrosis)-(neutrophil then macrophage)1 week-(granulation tissue)1 month-(Scar)

<4 hrs- normal

Coagulative necrosis -4 to 24 hrs

Inflammation

Healing(scar formation)

Front 19

Dressler syndrome

Back 19

Antibody against pericardium

Front 20

Perivascular infiltrate with abundant eosinophils

Back 20

Hypersensitivity myocarditis. Usually due to new drug therapy

Front 21

Patchy necrosis with granulation tissue

Back 21

Ischemic damage to the donor heart

Front 22

Collagen subtypes and their location

Back 22

Type1-(bone,tendon,dermis,ligament,dentin,cornea,scar tissue)asss disease-osteogenesis imperfecta

Type2-Cartilage,vitreous humor, nucleus polposus.

Type3-skin,lung, intestine,granulation tissue. Bone marrow,lymphatic.-ehler danlos .

Type4- basement membrane(Alport syndrome)

Front 23

Unilateral renal artery stenosis

Back 23

The contralateral kidney is exposed to high blood pressure(hypertensive nephrosclerosis-arterial wall thickening due to hyaline arteriolosclerosis . And onion skinning.

Front 24

Drugs that cause QT prolongation

Back 24

Class 1A(procainamide)-sodium channel blocker inhibits depolarization and class 3(amiodarone,sotalol,dofetilide) blacks potassium channel and inhibit repolarization

Front 25

Sick sinus syndrome

Back 25

Age related degeneration of sino atrial node(right atrial wall). First delayed p wave then dropped p wave. Light headedness and near syncope.

Front 26

Degrees of av block

Back 26

1st -prolonged pr interval

2nd- dropped QRS.

3rd- dissociation of p wave and qrs complex.

Conduction abnormality of his bundle. Inferior portion of interatrial septum.

Hint 26

Interatrial septum while bundle of his block is inter ventricular septum.

Front 27

Bundle branch block.

Back 27

Impaired synchronization of ventricular depolarization. Widened QRS. Interventricular septum.

Front 28

Reduced left ventricular compliance

Back 28

Diastolic dysfunction . Seen in decompensated congestive heart failure

Front 29

Mutation in transthyretin

Back 29

Amyloid protein infiltrating the myocardium

Front 30

Things that lead to diastolic heart failure

Back 30

Restrictive cardiomyopathy (amyloidosis,sarcoidosis,hemochromatosis etc

Front 31

Left ventricular end diastolic pressure is determined by

Back 31

Blood volume in the left ventricle and compliance.

Decrease compliance leads to increases left ventricular pressure but volume remains the same.

Front 32

Neprilysin

Back 32

Breaks down ANP AND BNP. Neprilysin inhibitors allows for Enhanced activity of ANP AND BNP which stimulates diuresis and peripheral vasodilation to alleviate volume overload. Inhibits RAAS.

Front 33

Squatting

Back 33

Increases systemic vascular resistance forcing blood from the right ventricular output through the pulmonary vasculature .

Front 34

Aorta and right ventricular pressure during normal cardiac cycle

Back 34

Aorta pressure is higher.

Front 35

Unique flow of left ventricular myocardium

Back 35

Maximum flow during diastole(when the coronary vessels are not compressed by the ventricular wall pressure created by myocardial contraction)and minimum flow during systole.

Front 36

Drug that Improves symptoms in HCM

Back 36

Beta blocker

1)Decreases heart rate allows more blood to flow into the heart

2) reduces contractility which reduces stroke volume out of the heart.

Both allow increases in end systolic and end diastolic volume.

Hint 36

Murmur increases in intensity with anything that decreases blood flow to the left ventricle.

Front 37

Anaerobic metabolism and ATP

Back 37

Anaerobic metabolism cannot maintain proper ATP due to failure of NA/K-ATPASE AND CA-ATPASE. accumulation of intracellular calcium leads to cellular swelling.Digozin has the same effect-NA/K ATPASE BLOCK.

Front 38

amiodarone and torsade

Back 38

class 3(POTASSSIUM CHANNEL) drug that prolongs action potential but has less risk of torsade than other class 3 antiarrythmic drugs(ONLY QT).class 1a also prolongs AP and affects both QT and QRS..Macrolide,antiemetic,antipsychitic,azole.fluoroquinolone

Front 39

impairs hepatic clearance of statin thereby increases myopathy

Back 39

fibrate.

Front 40

preferred drugs for rate control

Back 40

calcium channel or beta blocker.digoxin is sometimes used increasing parasympathetic tone..

Front 41

Parameters in shock

Back 41

Hypovolemic- everything is decreased except SVR

Cardiogenic- everything is increased except Cardiac output and svo2

Septic-opposite of cardiogenic.

Obstructive- same as cardiac except pcwp.

Front 42

Heart Failure with preserved ejection fraction

Back 42

Diastolic dysfunction eg chronic hypertension. Increased systemic vascular resistance due to decreased cardiac output.

Front 43

Site of origin of atrial fibrillation

Back 43

Pulmonary vein. While tachycardia is sino atrial node.

Front 44

Derived from the common cardinal vein

Back 44

Superior vena cava.

Umbilical vein degenerates nd vitelline vein forms the portal system.

Front 45

ST elevation signifies

Back 45

Damage to the entire wall

Front 46

Brachiocephalic trunk

Back 46

The left common carotid and subclavian come directly off the aortic arch while the right come off brachiocephalic trunk.

Front 47

Carotid sinus

Back 47

Efferent limb carries parasympathetic fiber to the sino atria and av node via vagus which increases av node refractory period and slows down conduction.

*Affarent through glossopharyngeal.

Paroxysmal supraventricular tachycardia and vagal maneuver

Front 48

Sudden onset palpitations plus rapid regular tachycardia

Back 48

Parasysmal supraventricular tachycardia

Front 49

Flutter vs fibrillation

Back 49

Flutter-Regular,saw tooth

Fibrillation-Irregular varrying R-R interval, absent p wave.

Front 50

Target organ of beta blockers

Back 50

Beta 1- heart and kidney

Beta 2- many organs.

Avoid b2 in patients with copd

Front 51

Location of coronary sinus

Back 51

Atrioventricular groove at the posterior part of the heart. In 3 lead biventricular pacemaker placement the 3rd lead is placed there.at the left ventricle.

Front 52

Isolated decrease in cardiac output(normal venous return)-

Back 52

Decreased contractility that's Not a result of decreased preload. Decreased contractility due to inhibited contraction from negative inotropes or myocardial injury eg M.I

Front 53

Class 1 Na blocker anti arrhythmic drug binding activity.

Back 53

CAB.Class 1B has the weakest binding send strongest dissociation that's y it has a Minimal cumulative effect leading to decreases use dependence.

Front 54

Severe mitral stenosis diagnosis

Back 54

A2 to opening snap time. The shorter the time the more severe it is.

Front 55

Patients with severe aortic stenosis depends on

Back 55

Atrial contraction for filling the stiffened ventricle.severe aortic stenosis impairs lv output leading to lv hypertrophy.at

Front 56

Norepinephrine extravasation

Back 56

Swelling and necrosis around injection site due to alpha 1 vaso constriction effect.Give phentolamine an alpha blocker with vasodilation effect.

Front 57

Isoproterenol

Back 57

Increases cardiac contractility and relaxation of vascular smooth muscle. Decreasing vascular resistance. B1 and B2 effect.

Front 58

Methicillin resistant until proven otherwise

Back 58

Most coagulase -ve staph. Vancomycin initial therapy

Front 59

Heart failure cells in congestive heart failure

Back 59

rupture of pulmonary cappilary from the congestion gets into the alveoli.(hemosiderin laden macrophages from Iron in the blood consumed by the alveoli air sacs)

Front 60

Ductus arteriosus

Back 60

connects the aorta and the pulmonary trunk.PDA left to right shunt(pulmonary hypertension over time leads to right to left shunt)'cyanosis later in life bcos deoxygenated blood goes to the lower extremity.Treat with indomethasin

Front 61

congenital heart defect ass with maternal diabetes

Back 61

transposition of great vessels.PE2 keeps the PDA open.

Front 62

Difference BTW infantile and adult coarctation of aorta

Back 62

infantile lies proximal to the pda Bcos of the low pressure above the coatctation deoxygenated blood from the right side of the heart will go to the lower extremity and cause cyanosis:

Adult form is not ass with pda.obstruction by the coarctation leads to backflow into the upper extremity and hypertension in upper and hypotension in lower extremity.

Front 63

The most deoxygenated blood in the body

Back 63

Coronary sinus.

Front 64

Type A and B aortic dissection originates from

Back 64

Type A =Sinotubular junction(ascending aorta.

Type B=Left Subclavian artery.

Front 65

ivc filter is used for

Back 65

prevent embolization of DVT from the egs to the lung vasculature(pulmonary embolism) in patients contraindicated to anticoagulant.

Front 66

drugs that increases systolic and diastolic blood pressure and decreases heart rate

Back 66

alpha 1 .reflexive increase in vagal tone leads to decreased heart rate.

Front 67

young patient who develop heart failure following symptomatic viral prodrome

Back 67

Dilated cardiomyopathy

Front 68

symptoms similar to SVC but only on one side

Back 68

Brachiocephalic vein.Bilateral brachiocephaic vein combine to form the SVC.

Front 69

Endocarditis with negative blood cultures

Back 69

HACEK Organism.Hemophilus,actinobacillus,Cardiobacterium,Eikenella,Kingella.

Front 70

Non bacterial thrombotic endocarditis

Back 70

Hypercoagulable state or underlying adenocarcinoma. Usually involves the mitral valve(regurgitation)

Front 71

large vessel vasculitis

Back 71

involves aorta and its branches

1)Temporal(giant cell)arteritis>50yrs..ESR often >100,ass with polymyalgia rheumatica

2)Takayasu <50yrs. pulseless disease.

they are both granulomatous .

Front 72

medium vessel vasculitis

Back 72

1)Polyarteritis nodosa-Lung is spared.string of pearl appearance.fibrinoid necrosis.

2)Kawasaki.young child with M.I

3)Buerger(smokers) affects digits.raynaud

Front 73

small vessel vasculitis

Back 73

nasopharynx,lungs, kidney

wegener granulomatosis.key treatment is cyclophosphamide

2)Microscopic polyangitis(similar to wegener granulomatosis but without granuloma and nasopharynx involvement also has p anca.

3)churge strauss

4)HSP-palpable purpura

Front 74

Aortic dissection location

Back 74

proximal 10 cm of the aorta with preexisting weakness of the media-HTN and inherited defect(marfan and ehler danlo.

Front 75

vasa vasorum

Back 75

tiny blood vessels that feed the adventitia bcos the proximal aorta wall is thick so the oxygen from the regular blood vessel is insufficient.

Tertiary syphilis-endarteritis of vasa vasorum-thoracic aneurism

Front 76

hemangioma and kaposi sarcoma

Back 76

not present in an actual channel but its in an endothelium ,it does not blanch.hemangioma blanches

Front 77

Atherosclerosis formation of fibrous cap.

Back 77

1)Stress or hyperlipidemia

2)Endothelial injury

3)vcam

4)monocytes and lymphocyte migration to intima

5) engolfment of oxidized ldl.

6)foam cells

7)growth factor and cytokines

8) migration of smoothmuscle cells to intima induced by growth factor.

9) synthesize collagen,elastin,proteoglycan that form the fibrous cap.

Front 78

Maintaining cardiac output in the setting of valvular abnormality(aortic regurgitation)

Back 78

Increase in left ventricular stroke volume.

Front 79

Calcium channel blockers do not affect skeletal muscle contractility because

Back 79

Because skeletal muscle is not dependent on extracellular calcium influx. Mechanical coupling between type and RyR calcium channel

Front 80

Inferior wall M.I can lead to

Back 80

Right ventricular infarction, decreased flow to the left ventricle.

Front 81

Inspiration and venous return

Back 81

During inspiration there is increase in venous return. (Ass. Pulsus paradoxus)

Front 82

Fixed splitting

Back 82

Pulmonic valve closure is greatly delayed. ASD. Left to right shunt.

Front 83

No difference in gradient between ventricles and aorta

Back 83

Aortic regurgitation. Normal ventricle 120 and normal aorta 80 to 120.

Front 84

Spider like lesion on nasal and oral mucosa, face, arm and nose bleed

Back 84

Osler Weber rendu

Front 85

Flow direction of venous blood

Back 85

Superficial to deep vein of extremities to IVC. Backward flow leads to varicose veins. Incompetent venous valves

Front 86

Plaque stability is reduced by?

Back 86

Metaloproteinases (secreted by macrophages)which degrades collagen

Front 87

Drug induced long qt(torsades de pointes)

Back 87

Antiarrythmic(1a and class 3)

Antibiotics(macrolide)

Antipsychotic (Haloperidol)

Antidepressants (TCA)

Antiemetics(ondasetron)

Front 88

Shortened pr interval, delta wave with widened qrs.

Back 88

Wolff parkinson white-

Front 89

Conduction pathway

Back 89

Sinoatria->atria->av node->bundle of his->left and right bundle branch->purkinje fibre->ventricle.

Left bundle branch divides into anterior and posterior fascicles.

Front 90

Normal pr interval

Back 90

<200msec. Normal qrs <120

Front 91

3rd degree av block can be caused by

Back 91

Lyme disease

Front 92

What stimulates central and peripheral chemoreceptors

Back 92

Central(located in medulla)-ph and pCo2 of brain interstitial fluid

Peripheral(located in carotid body and aortic body)- decreased po2 <60mmhg), decreased ph of blood and increased pco2 .

Peripheral senses pa02 and central senses pc02

Front 93

Hypertensive urgency vs emergency

Back 93

Emergency has acute end organ damage.

Front 94

Po2 are lowest and highest where in the heart

Back 94

Lowest in deoxygenated blood of three svc,right side. And highest in the left heart

Front 95

Free wall rupture

Back 95

LAD.5 to 14 days

Front 96

Papillary muscle rupture

Back 96

2 to 7 days. RCA

Front 97

Additional treatment in STEMI

Back 97

Reperfusion therapy.PCI over fibrinolysis.

Front 98

Best indicator of severe mitral regurgitation

Back 98

S3

Front 99

Differences between infective endocarditis and rheumatic fever

Back 99

Large friable vegetation rather than fibrosis seen in rheumatic fever.

Front 100

Baroreceptor firing rate and sympathetic outflow

Back 100

Always opposite. Eg hypervolemia ->Increased blood pressure->increased baroreceptor

Front 101

Thickening of the right ventricle is not seen in pulmonary embolism

Back 101

As there is no time for compensatory hypertrophy to occur in response to increased pressure load

Front 102

Complication of chronic venous insufficiency

Back 102

Stasis dermatitis- hemosiderin deposition due to extravasation of RBC