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Block 2 SD3 > Cardio Illa Block 2 > Flashcards

Cardio Illa Block 2 Flashcards

1
Q

How does Acute Rhematic Fever progress?

A

Over decades it progresses to Chronic Rhematic Heart Disease then Stroke, HF and Endocarditis

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2
Q

What are the signs of Acute Rheumatic Fever?

A

Migratory polyarthritis, carditis, subcutaneous nodules, erythema, marginatum and chorea dancelike movements

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3
Q

How do you prevent Acute Rheumatic Fever from progressing into Chronic Rhematic Fever?

A

Prophylactics antibiotics to prevent reoccurrences

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4
Q

How do you treat Acute Rheumatic Fever?

A

Antibiotics, Aspirin, Corticosteroids for carditis

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5
Q

What are some predisposing factors for Infective Endocarditis?

A

congenital heart defects, rheumatic valvular disease, bicuspid or calcific aortic valves, MVP, HCM, prior endocarditis, and or a prosthetic valve.

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6
Q

How does Infective endocarditis affect the body?

A

Systemic immune phenomena (eg, glomerulonephritis) and septic emboli, lungs (with right sided endocarditis), kidneys, spleen, CNS, skin, and retina (with left-sided endocarditis).

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7
Q

What are the clinical features of Infective Endocarditis?

A

Clinical- Janeway lesions, Roth’s spots, Osler’s nodes, Clubbing

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8
Q

How do you diagnose Infective Endocarditis?

A

Blood culture

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9
Q

Who is most likely to at risk with Infective Endocarditis?

A

IV drug abuse- Tricuspid regurgitation following endocarditis

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10
Q

What are the clinical features of Aortic Stenosis?

A

Senile calcification, Congenital bicuspid aortic valve , Rheumatic fever
‘SAD’ : Syncope, Angina, Dyspnea
“Pulsus parvus et tardus”

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11
Q

What type of murmur would you hear for AS and where would you hear it?

A

Harsh systolic ejection murmur, high-pitched, crescendo-decrescendo (diamond shaped), mid-systolic, aortic listening post, radiating to carotids; S4 heart sound, reverse splitting S2
↓Murmur intensity with ↓preload; ↑murmur intensity with ↑preload

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12
Q

What are the lab presentation with Aortic Stenosis?

A

Microangiopathic hemolytic anemia, schistocytes, hemoglobinuria

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13
Q

How would you diagnose Aortic Stenosis?

A

Echo- Concentric LVH, LV pressure overload

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14
Q

How would you treat Aortic Stenosis?

A

Trt- Balloon valvotomy, Valve replacement

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15
Q

What are the two most common causes of Aortic Regurgitation?

A

Most common Idiopathic dilation of the aortic root
Acute Infective Endocarditis

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16
Q

What can Aortic Regurgitation progress into in the developing countries?

A

Developing countries Chronic RHD

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17
Q

What are some clinical signs of Aortic Regurgitation?

A

Wide pulse pressure Water-hammer, Corrigan, Becker, Muller, Qunicke, deMusset

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18
Q

What would the murmur sound like in Aortic Regurgitation?

A

Early diastolic decrescendo murmur best heard with the diaphragm along the left sternal border. Lean pt. forward with breath held in full expiration.

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19
Q

Where is the murmur heard in Aortic Regurgitation?

A

; S3, S4, Austin Flint murmur at apex: Anteriormitral valveleaflet hit by rapid regurgitant flow into the LV.

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20
Q

How would you diagnose Aortic Regurgitation?

A

Echo- Dilated left ventricle, left atrium, LV volume and pressure overload

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21
Q

What is the common cause of Mitral Stenosis?

A

Rhematic fever

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22
Q

What are the clinical signs of Mitral Stenosis?

A

Dyspnea, Hemoptysis, Dysphagia, hoarseness of voice, Malar flush, LA enlargement
Lt. atrial thrombi , A-fib, Systemic emboli, Pulm HTN → RVH → RHF. Left ventricle spared.

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23
Q

What would the murmur sound like in Mitral Stenosis?

A

Auscultation- OS, early to mid-diastolic rumble, low-pitched, decrescendo-crescendo. Apex, left lateral decubitus, bell

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24
Q

What is the treatment of Mitral Stenosis?

A

Balloon valvotomy, RF prophylaxis, beta blockers, CCB

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25
Q

What is the most common cause of Mitral Valve Prolapse?

A

Mitral regurgitation

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26
Q

Who is most likely to have Mitral valve prolapse?

A

Female>male, lean pts, Marfan syndrome, Ischemia

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27
Q

What are some clinical features of Mitral Valve Prolapse?

A

Myxomatous Degeneration

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28
Q

What would the murmur sound like in Mitral Valve Prolapse?

A

Mid-systolic clicks. A late systolic murmur if MR present. Click moves closer to S1 on standing, moves away from S1 on squatting.

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29
Q

What are some complications of Mitral Valve Prolapse?

A

Complications: Infective endocarditis, MR, sometimes with chordal rupture, Stroke

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30
Q

How do you diagnose Mitral Valve Prolapse and what is the tx?

A

Diagnosis: Echo
Treatment: β-blockers, valve repair/replacement surgery

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31
Q

What is the most common cause of Mitral Regurgitation?

A

Most common cause – Mitral valve prolapse
2nd common: rupture/dysfunction of papillary muscle, Annular dilation, Infective endocarditis

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32
Q

What are the clinical features of Mitral Regurgitation?

A

Acute:dyspnea, fatigue, weakness, edema , cardiogenic shock
Chronic: DOE and fatigue, Palpitations, atrial fibrillation, LA and LV volume overload, palpitation

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33
Q

What would the murmur sound like in Mitral Regurgitation?

A

Murmur- Blowing, pansystolic, heard best over the apex (diaphragm) radiates to the axilla, Midsystolic click + late systolic murmur  MVP

34
Q

What is the tx for Mitral Regurgitation?

A

Valve replacement, Vasodilators, diuretics

35
Q

What is the Tx for Aortic Regurgitation?

A

Hydralazine, Nifedipine, valve replacement

36
Q

What causes a Dilated Heart?

A

Systolic Dysfunction, hypokinetic ventricle and Low CO

37
Q

What causes Hypertrophy?

A

Diastolic dysfunction and outflow obstruction , hypertrophy ventricles, mitral systolic anterior motion, asymmetric, normal to low CO

38
Q

What cause restriction of the heart?

A

Diastolic dysfunction, cavity obliteration, normal to low CO

39
Q

What are the right to left shunts?

A

5 T’s
Truncus arteriosus (1vessel)(associated with DiGeorge)
Transposition of the great vessels (2vessels are switched)
Tricuspid atresia (3= tri)
Tetralogy of Fallot (4= tetra)
Total anomalous pulmonary venous return (TAPVR= 5 letters)(pulmonary oxygen vein emptied in the RA) Exam question
Pulmonary atresia
Ebstein anomaly

40
Q

What are the left to right shunts?

A

Ventricular septal defect (VSD)
Atrial septal defect (ASD)
Patent ductus arteriosus (PDA)

41
Q

What er the obstructive congenital heart anomalies?

A

Pulmonary stenosis
Aortic stenosis
Aortic coarctation

42
Q

What happens in ASD?

A

Left to right shunt
Small -close spontaneously, but larger ones do not, causing right atrial and ventricular overload and ultimately PAH, elevated pulmonary vascular resistance, and RVH and RA; supraventricular tachycardia, atrial flutter, or atrial fibrillation
Paradoxical embolization

43
Q

What type of murmur would you hear in ASD?

A

Paradoxical embolization
Grade 2 to 3/6 midsystolic murmur and a widely split, fixed S2, can travel to the brain

44
Q

When would you hear the ASD murmur?

A

Moderate to large ASDs should be closed, typically between ages 2 yr and 6 yr, using a transcatheter device when possible.
Most common noticed later in life around 30 years

45
Q

Who will most likely have VSD?

A

VSD, more common in trisomy 21, 13

Over time- PAH, elevated pulmonary artery vascular resistance, RVH, which ultimately cause shunt direction to reverse, leading to Eisenmenger syndrome (shunt reversal).
Larger defects cause symptoms of heart failure at age 4 to 6 wk.

46
Q

What would the murmur for VSD sound like?

A

Grade 3 to 4/6 holosystolic murmur at the lower left sternal border.

47
Q

What are the clinical features of PDA?

A

Premature infants may have respiratory distress or other serious complications (eg, necrotizing enterocolitis).
Large shunt  left heart enlargementpulmonary artery hypertension  Eisenmenger syndrome, Differential Cyanosis if untreated

48
Q

What will the murmur sound like in PDA?

A

Left to right shunt, Continuous murmur, “machinery-sounding” quality.

49
Q

How do you keep the shunt opened and closed for PDA?

A

Hypoxia and prostaglandin (progesterone) and Indomethacin to close it

50
Q

What is Eisenmenger Syndrome?

A

Associated with VDD (shunt reversal) patients will present with hypoxia, clubbing of fingers and toes, secondary polycythemia

51
Q

When would you see Tetralogy of Fallot?

A

At birth or first few weeks of life, Right to left shunt. Boot shape appearance, Hyper cyanotic spells (TET) the baby will start crying then will turn blue (cyanosis)

52
Q

What would relieve the cyanosis with Teratology of Fallot?

A

Older childen- h/o squatting while playing to relieve cyanosis.
Severe cyanosis: infusion of prostaglandin E1 to open the ductus arteriosus. Place infant in the knee-chest position and give oxygen; sometimes, opioids (morphineorfentanyl), volume expansion,sodium bicarbonate, beta-blockers (propranololoresmolol),

53
Q

What are the symptoms of Tetralogy of Fallot?

A

Pulmonary valve stenosis RVH, an Overriding aorta, and VSD – (PROVe).

54
Q

What are the clinical features of Teratology of Fallot?

A

Severely affected neonates -marked cyanosis, dyspnea with feeding, poor weight gain, and a harsh grade 3 to 5/6 systolic ejection murmur at left upper sternal border (due to pulmonary stenosis) Repair surgically at 2 to 6 mo or earlier if symptoms are severe.- Closure of the VSD with a patch and reconstruction of the right ventricular outflow tract.

55
Q

What is Truncus arteriosus?

A

Single large vessel associated with Di George syndrome

56
Q

What is tricuspid atresia?

A

No tricuspid valve and Tx is prostaglandin

57
Q

What is Total anomalous pulmonary venous return?

A

Pulmonary veins drain into right heart circulation, ASD & PDA with a snowman appearance. Tx is prostaglandin

58
Q

What is Ebstein Anomaly?

A

Tricuspid regurgitation, associated with exposure to lithium and tx with prostaglandin E1

59
Q

What is Coarctation of the Aorta?

A

Localized narrowing of the lumen, typically in the proximal thoracic aorta just beyond the left subclavian artery and before the opening of the ductus arteriosus.
Pressure overload proximal to the coarctation heart failure, berry aneurysm
Hypoperfusion distal to the coarctation.

60
Q

What would you see in Coarctation of the Aorta?

A

BP gradient between upper and lower extremities, grade 2 to 3/6 ejection systolic murmur, sometimes most prominent in the left interscapular area.
CXR- Rib notching, figure of 3

61
Q

What are the clinical features of Pericarditis?

A

Inflammation
Abrupt/ Insidious chest pain: Sharp, Aggravated by supine posture, coughing, deep breathing = positional, pleuritic, Relieved by sitting up and leaning forward
Fever, tachycardia, and pericardial friction rub- heard better on leaning forward
Usually elevated ST segments, Concave upwards in most leads, PR depressions
ECG and echo are usually adequate. CT, or MRI for constrictive pericarditis.

62
Q

What is the tx for pericarditis?

A

Trt- NSAIDs and/orcolchicine; corticosteroids.

63
Q

Name the 4 clinical features of Cardiac Tamponade?

A

Beck’s triad- hypotension, muffled heart sounds, JVD
Pulsus Paradoxus
ECG: Electrical Alternans
Pericardiocentesis

64
Q

What is Cardiac Tamponade?

A

Massive fluid collection to the extent that it leads to decrease Cardiac output and may cause Shock and death

65
Q

What is Constrictive Pericarditis?

A

Marked inflammatory, fibrotic thickening of the pericardium leading to systemic venous congestion without myocardial dysfunction

66
Q

What are the clinical features of Constrictive Pericarditis?

A

Pericardial Knock, Kussmaul’s sign
Pericardiectomy

67
Q

What is the most common clinical feature in Aortic Dissection?

A

HT and connective tissue disorders

68
Q

How do you diagnose Aortic Dissection?

A

TEE

69
Q

What is an Aortic Aneurysm?

A

Abnormal dilations of thoracic or abdominal aorta caused by weakening of the arterial wall.

70
Q

What are the common causes of Aortic Aneurysms?

A

Common causes include HTN, atherosclerosis, infection, trauma, and or connective tissue disorders.

71
Q

What is Peripheral arterial disease?

A

Intermittent claudication (pain in legs while walking a few distance) Rest pain ischemic ulcers (often at toes), dependent rubor (dusky red color in one limb) Chronic PAD will also have thinning hair

72
Q

What are the common causes of Peripheral arterial disease?

A

Atherosclerosis, common in men, HTN, DM, dyslipidemia, smoking, tobacco

73
Q

What are some clinical signs of Peripheral arterial disease?

A

Almost always in the lower (distal and toes) extremities, cold, blue color, wet or dry gangrene, ulcers, Low ankle brachial index

74
Q

What is the tx for PAD?

A

rivaroxaban,pentoxifylline, orcilostazol

75
Q

What is Thromboangiitis obliterans (TAO)?

A

Inflammatory thrombosis, whole vessels, if the patient i a smokers, Claudication ischemic ulceration and gangrene

76
Q

Who will most likely have Thromboangiitis obliterans:
TAO and what is the cure?

A

Almost exclusively in Asian male smokers aged 20 to 40, smoking cessation

77
Q

What is a DVT?

A

Obstruction and insufficiently, clotting of blood in a deep vein, common in lower extremities

Complication: Pulmonary embolism, the femoral, popliteal veins, posterior tibial and peroneal veins

78
Q

How do you diagnose and treat a DVT?

A

D-dimer testing, Doppler ultrasonography.
Treatment :heparinfollowed by oralwarfarin

79
Q

What are the clinical features of DVT?

A

Virchow’s Triad- stasis, vessel damage, and hypercoagulability
Homan’s sign, pain in veins

80
Q

What is chronic venous insufficiency?

A

Disorders that result in venous hypertension impaired venous returnlower extremity discomfort, edema, and skin changes.Most common cause is after DVT, can occur in trauma, age, obesity

81
Q

What are the sings of Chronic Venous Insufficiency?

A

Heaviness, aching, and paresthesias. Skin changes range on a continuum from normal skin or mildly ectatic veins to severe stasis dermatitis and ulceration.

82
Q

Who is most likely to have Varicose Veins?

A

Occupation of standing, more common in females due to estrogen, can be genetic
Asymptomatic, or cause a sense of fullness, pressure, pain or hyperesthesia in the legs, venous ulcer and bleeding.

Block 2 SD3 (5 decks)

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