Cardio Path 2

Question 1

What can cause the most common type of cardiomyopathy?

Answer 1

Dilated cardiomyopathy is caused by ABCCCD. Alcohol abuse, Beriberi, Coxsackie B, Cocaine, Chagas disease, Doxorubinicin, and hemochormatosis and peripartum cardiomyopathy

Question 2

How do you treat dilated cardiomyopathy? What kind of dysfunction ensues if untreated?

Answer 2

Transplant is the only way (pathoma says so). It is systolic dysfunction b/c dilated so much.

Question 3

What is the cause of hypertrophic cardiomyopathy?

Answer 3

Autosomal dominance is 60-70%. Young athletes can have it and SUDDEND EATH from ahhrythmia

Question 4

How do you treat a young athlete with an S4 and possibly systolic murmur?

Answer 4

It is hypertrophic cardiomyopathy. Stop high intensity athletics and use Beta blocker or verapamil.

Question 5

Because we care so much about pictures, note that hypertrophic cardiomyabothy has a unique histology:

Answer 5

Myofibrillar disarray (fibers go every which way)

Question 6

What is obstructive HCM?

Answer 6

Hypertrophied septum interferes with mitral leaflet and outflow is obstructed and dyspnea, or syncope can happen

Question 7

When do you see low voltage ECG?

Answer 7

Restrictive/infiltrative cardiomyopathy b/c there is non-cardiac tissue in the heart that doesn’t conduct electricity well, despite thick appearing myocardium

Question 8

What causes restrictive/infiltrative cardiomyopathy?

Answer 8

sarcoid, amyloidosis, postradiation fibrosis and endocardial fibroelastosis and LOFFLER SYNDROME: (endomyocardial fibrosis with EOSINOPHILIC INFILTRATE) and hemochromatosis

Question 9

What cardiomyopathy can hemochromatosis cause?

Answer 9

There are 2 things! Dilated and restrictive

Question 10

What decreases mortality in CHF? (what is more for symptomatic relief and no evidence in mortality)?

Answer 10

ACEi, beta blockers, Angiotensin II receptor blockers, sprionolactone, diuretics are more for symptomatic relief

Question 11

What are hemosiderin-laden macrophage?

Answer 11

Heart failure cells in lungs

Question 12

What is arguably most important drug in CHF and why?

Answer 12

ACEi b/c low cardiac output causes more renin/angiotensin-aldosterone pathway so more volume which exacerbates problem from after load and preload affecting the heart

Question 13

What does orthopnea happen?

Answer 13

CHF. Laying means more venous b/c redistribution of blood and more pulmonary vascular congestion

Question 14

Acute vs subacute endocarditis organism

Answer 14

Acute: S aureus (BAD symptoms and IV users usually)
Subacute: S viridans is most common overall cause (low virulence) on valves that had already been damaged (s bovid if colon cancer or epidermis if prosthetic)

Question 15

Does endocarditis destroy heart valves?

Answer 15

Staph A does, otherwise no (remember IV drug users are hit on tricuspid, which makes sense)

Question 16

What organisms cause endocarditis with negative blood cultures?

Answer 16

HACEK. Haemophilus, Actinobacillus, Cardiobacterium (easy to remember that one), Eikenella, Kingella

Question 17

Which valves are affected by rheumatic heart?

Answer 17

Mitral>aortic»tricuspid (high pressure hit most)

Question 18

Rheumatically affected valve does what?

Answer 18

Early it is regurg, then mitral stenosis

Question 19

2 Histology markers of rheumatic carditis?

Answer 19

Aschoff bodies (granuloma with GIANT CELLS!) and Anitschkow cells (enlarged macrophage with wavy rod like nucleus) Pics on page 292 in FA 2014.

Question 20

Jones criteria?

Answer 20

Evidence of previous Group A infection. Minor criteria is fever and ESR
Major criteria: J<3 Pancarditis (all layers and can cause acute death)
Nodules of skin
Erythema marginatum (more red on border)
Sydenham chorea (dancing)

Question 21

What causes three types of pericaditis?

Answer 21

Fibrinous: Dressler syndrome, ureamia and radiaiton
Serous: Viral pericarditis (spontaneous resolution) or noninfectious inflame like rheumatoid arthritis and SLE
Supportive/purulent: caused by bacterial infections like Pneumococcus andstreptococcus(now rare with antibiotics)

Question 22

Pulses paradoxus?

Answer 22

lower in amplitude of systolec BP by more than 10 mmHg during inspiration. Happens with tamponade, asthma, obstructive sleep apnea, pericarditis and croup

Question 23

What is syphilitic heart disease?

Answer 23

tertiary syphilis disrupts vasa vesorum (vessels of the vessel) of aorta so atrophy of vessel an looks like “tree bark” appearance of aorta. Can result in aneurysm of ascending aorta and aortic insufficiency b/c of it

Question 24

Most common cardiac tumor for adults? how about children?

Answer 24

Overall most common is metastasis from melanoma or lymphoma
Adults most common cardiac tumor is myxoma which has BALL VALVE that can cause syncope
Children most common cardiac tumor is rhabdomyoma

Question 25

What is rhabdomyoma associated with?

Answer 25

tuberous sclerosis HIGH YIELD. Benign hamartomas (resembling tissue it came from, so makes sense that rhabdomyoma is a hamartoma) throughout body with this genetic mutation in tumor suppressor TSC1 and TSC2 (names for tuberosclerosis, TSC).

Question 26

Kussmaul sign?

Answer 26

High JVP with inspiration instead of lower like normally. HAPPENS when heart can’t pass on negative inthrathoracic pressure. So if there is restriction of the heart from restrictive cardiomyapothy, constrictive pericarditis or right atrial/ventricular tumors

Question 27

Skipping vascular tumors on page 295 of FA 14

Answer 27

hi

Question 28

What are the large vessel types of vasculitis and what is the difference between the two?

Answer 28

Temoral Giant Cell Arteritis (elderly females) and Takayasu arteritis (asian females less than 40 with aortic arch involvement)

Question 29

How do you treat every vasculitis except Kawasaki?

Answer 29

Corticosteroids! some other things have more stuff, but hey, its a good start

Question 30

What do you see on biopsy with Temporal arteritis?

Answer 30

Giant cells, duh! but might miss it because the disease is segmental, so negative biopsy does not mean it is a negative test

Question 31

Danger of temporal arteritis?

Answer 31

Blindness b/c branches of carotid is affected and can have occlusion of ophthalmic artery

Question 32

35 year old asian presents with ear upper extremity pules, fever, night sweats, arthritis, myalgia, skin nodule and ocular disturbances

Answer 32

Takayasu arteritis. Corticosteroids. Granulomatous thickening and narrowing of aortic arch

Question 33

25 year old, weight loss, mailaise, headache, abdominal pain, melena (blood in stool), HTN, neurologic dysfunction, cutaneous eruptions and renal damage? What is it? What would you see on exam and tests?and how do you treat it?

Answer 33

Polyerteritis NODOSA (nodes in many arteries) b/c immune complex mediated, makes sense that they are scattered everywhere. Transmural inflammation of arterial wall with fibrinoid necrosis that looks pink on histology. The fibrinoid is bumpy and feels like nodes and microaneuysms and spasm on arteriogram also look like nodes! SO NAME MAKES SENSE AND I LOVE IT. 30% have Hep B

Treat with Corticosteroids (duh) and Cyclophosphamide

Question 34

Asian 3 year old has a fever with fever, cervical lymphadenitis, conjunctival injection, strawberry tongue, hand-foot erythema and desquamating rash? disease and complications and tx?

Answer 34

Kawasaki: has vague symptoms. Imagine a kid riding a motor cycle with hand and foot erythema from holding bike so tight and heart racing from adrenaline.

Complications: Coronary artery aneurysm so MI/rupture

Treatment: IV immunoglobulin and aspirin (note this is the ONLY time you give aspirin to a little kid)

Question 35

What is causing a person to have chronic sinusitis with nose bleeds and hemoptysis and dyspnea and hameutria and red cell casts?

Answer 35

Granulomatosis with polyangiitis (wagerers!) C disease. C Shape of body symptoms (nose, lung kidney) and cyclophosphamide and corticosteroids and C-ANCA. (antiNEUTROPHIL c-ANCA (anti-proteinase 3). Granulomas are a key finding here (p-ANCA doesn’t have it) Granulomas are necrotizing in lung and upper airways with focal necrotizing vasculitis. CXR will have nodular densities

Question 36

Microscopic polyangiitis is different than granulomatosis how?

Answer 36

it is MPO-ANCA/pANCA meaning against myeloeroxidase and is perinuclear. No nasopharyngeal involvement. No granulomas. Still treat with cyclophoashmaide and corticosteroids. Relapse is common

Question 37

When do you have asthma, sinusitis with palpable purport and peripheral neuropathy (wrist/foot drop)? Also can involve heart, GI, kidneys. What antibodies will you find?

Answer 37

Churg-Strauss syndrome. Note palpable purpura. It is granulomatous necrotizing vasculitis with EOSINOPHILIA. MPO-ANCA/p-ANCA (that is like microscopic polyangiitis) with high IgE

Question 38

What is most common systemic vasculitis in children? What antibodies are present (High YIELD)

Answer 38

Henoch-Shonlein purpura. Palpable purpura on butt and legs, arthralgia, abdominal pain, melena and many lesions starting at same time. IgA complex exposition and is associated with IgA nephropathy

Question 39

How do you treat primary HTN?

Answer 39

Diuretic, ACE inibhitors, ARBs, calcium channel blockers

Question 40

How do you treat HTN with CHF?

Answer 40

ACEi/ARBs, Diuretics, Aldosterone antagonists. Beta blockers MUST BE CAUTIOUSLY USED in decompensated CHF and are contraindicated in cardiogenic shock (sympathetics are important to keep you alive, sometimes, ya know)

Question 41

How do you treat HTN in diabetes?

Answer 41

ACEi/ARBs are protective against diabetic nephropathy! others are kind of duh: Beta blockers, alpha blockers calcium channel blocker and diuretics