Dyspnea on exertion
Failure or CO to inc. during exercise.
-dyspnea = SOB
Culture negative causes of endocarditis:
HACEK organisms: Hemophilus Actinobacillus Cardiobacterium Eikenella Kingella
2 most common culture neg. causes of endocarditis.
Tricuspid valve endocarditis:
-which bugs besides S. aureus?
Pseudomonas, and Candida.
*S. aureus most common
-consequence of what?
-Group A strep pharyngitis!
Whats an Aschoff body?
-granuloma found in rheumatic fever.
What are Anitschkow cells?
-enlarged macrophages with ovoid, wavy, rod-like
-found in rheumatic fever.
Fusion of aortic/mitral commissures.
-found in which disease?
-rheumatic heart diseaes (late sequela of rheumatic fever).
Rheumatic fever Sxs:
FEVERSS Fever Erythema marginatum Valvular damage (vegetation and fibrosis) ESR Red-hot joints (migratory polyarthritis) Subcutaneous nodules St. Vitus’ dance (Sydenham chorea)
rheumatic fever: what are the early deaths due to?
SLE pericarditis: whats the fluid like?
serous, clear/yellow, protein rich w/few inflammatory cells.
Post MI pericarditis: whats the fluid like?
fibrinous, low protein count.
Acute pericarditis: more or less pain when leaning forward? During inspiration?
- less pain leaning forward
- more pain on inspiration
Causes of fibrinous pericarditis:
- Dressler syndrome
- uremia (etiology is poorly understood)
*Presents with loud friction rub.
Causes of serous pericarditis:
- viral pericarditis (often resolves spontaneously)
- noninfectious inflammatory diseases (e.g., rheumatoid arthritis, SLE).
Causes of Suppurative/purulent pericarditis:
- bacterial infections (e.g., Pneumococcus, Streptococcus).
* Rare now with antibiotics.
ECG of cardiac tamponade?
- low-voltage QRS
- electrical alternans (due to “swinging” movement of heart in large effusion - beat to beat alterations of QRS height).
Pulses paradoxus seen in which diseases?
- cardiac tamponade
- obstructive sleep apnea
What causes pulsus paradoxus?
- when you breath in the right ventricle filled more so expands into pericardial space & also into LV space. LV usually displaces but now it can’t due to constriction of cardiac tamponade.
- so LV is constricted, fills less. Less volume means less pressure (frank starling) so you get a drop in systolic BP on inspiration.
Tree bark appearance of syphillitic aorta due to what?
-irregular wrinkling of the tunica intima of the aorta.
- most common primary cardiac tumor in who?
- associated w/what disease?
- where does it usually arise?
- tuberous sclerosis
- Polypoid capillary hemangioma that can ulcerate and bleed.
- Associated with trauma and pregnancy.
- Benign, painful, red-blue tumor under fingernails.
- Arises from modified smooth muscle cells of glomus body.
- glomus body = modified smooth muscle cells invovled in temp. regulation.
Angiosarcoma: associated w/what risk factors?
- sun exposed areas
- PVC (liver)
- chronic lymphedema (skin)
Will kaposi sarcoma blanch?
Does a negative biopsy exclude Temporal arteritis?
- lesions are segmental.
Two most common signs of Temporal arteritis?
-what can it lead to?
- Unilateral headache, jaw claudication
- irreversible blindness due to ophthalmic art. occlusion.
-associated w/what disorder?
Takayasu arteritis Sxs:
- “Pulseless disease” (weak upper extremity pulses)
- night sweats
- skin nodules
- ocular disturbances.
Temporal & Takayasu arteritis:
- what type of inflammation?
- inc or dec. ESR?
- inc. ESR
Can calcific aortic stenosis lead to outflow obstruction?
- aortic stenosis murmur.
During systole, where is contraction force the strongest?
-endocardium. Hence its the most susceptible to ischemia.
What receptors modulate coronary flow?
- alphta 1
- beta 2
Osler node: type 3 HSR or septic emboli?
-type 3 HSR
Janeway lesion: type 3 HSR or sepetic emboli?
Which cells synthesize the fibrous cap of an atheroma?
- smooth muscle cell
- special SMCs that can produce collagen.
What lung problem can cause pulsus paradoxus?
-severe obstructive lung disease
What drugs prevent eosinophil degranulation?
Clinical definition of myopathy
-muscle pain w/serum CK 10x normal.
Bile acid sequesterants and statins
-take them 4 hours apart b/c the sequesterants may dec. absorption of the statin.
- first line med?
- what about if they have CHF or diabetes?
- If they have CHF or DM, give ACE inhibitor.
Beta blocker overdose
-will an atheroma form there?
-fatty streaks often occur in regions not particularly prone to atheroma formation. So answer is not necessarily.
Whats the most common cause of aortic stenosis?
Senile calcific aortic valve degeneration.
Acute onset heart failure in setting of recent viral infection:
- abdominal pain, melena
- HTN, neuro dysfunction
- cutaneous eruptions, levido reticularis
- renal damage (immune complexes)
- leukocytosis (neutros)
-lesions of varying stage
- Fever, cervical lymphadenitis, conjunctival injection, changes in lips/oral mucosa (“strawberry tongue” D ), hand-foot erythema, desquamating rash.
- coronary artery aneurysm, thrombosis => rupture, MI.
How does Kawasaki present?
acute febrile illness
- fever may persist after tylenol.
- only condition where you give a child w/fever aspirin.
What is the only circumstance where you give a feverish child aspirin?
-otherwise you dont to prevent reye syndrome
-what kind of inflammation?
-granulomatous and necrotizing vasculitis.
- anti-proteinase 3
- Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis.
- Lower respiratory tract: hemoptysis, cough, dyspnea.
- Renal: hematuria, red cell casts.
microscopic polyangitis vs wegeners
compared to Wegener’s. MP has:
- no nasopharyngeal involvement.
- no granulomas.
What are ANCAs?
-ANCA (Abs) can directly bind to leukocytes (neutros etc.) and stimulate them to release their granules which contain ROS and proteolytic enzymes.
Asthma, sinusitis, palpable purpura
- peripheral neuropathy (e.g., wrist/foot drop).
- Can also involve heart, GI, kidneys (pauci-immune glomerulonephritis).
What kind of inflammation is Churg Strauss?
-Granulomatous, necrotizing vasculitis with eosinophilia
- palpable purpura
- abdominal pain
Can you use beta-blockers in cardiogenic shock?
Can you use beta-blockers in vaso-spastic disease?
- no, they’re contraindicated.
- no, they’re contraindicated.
- name some
- verapamil, diltiazem.
- cardiac Ca channel blockers.
- the dihydropyridines are selective only for vascular smooth muscle.
- name some
- Amlodipine, nimodipine, nifedipine
- vascular smooth muscle
- lack cardiac depressant effects
- differs from other dihydropyridines
-subarachnoid hemorrhage (prevents cerebral vasospasm)
Calcium channel blockers
- Cardiac depression, AV block, peripheral edema, flushing, dizziness
What is first-line therapy for hypertension in pregnancy?
- potential side effect?
- inc. cGMP => relax smooth muscle.
- arterioles > venules.
- drug induced SLE, esp in slow acetylators.
- Its binds strongly to plasma proteins, so thats why it can cause sle-like syndrome and it can be used in pregnant women for HTN.
Hydralazine & peripheral neuritis
-Can cause B6 deficiency.
Hypertensive emergencies: commonly used drugs:
nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.
- HTN emergency, esp in pts w/renal insufficiency.
- coronary, peripheral, renal, and splanchnic vasodilation.
- dec. BP
- inc. natriuresis.
Minoxidil & diazoxide
- open K channels => hyperpolarization of smooth muscle.
- results in arterial vasodilation.
- used for HTN emergencies.
*minoxidil can be used for baldness.
endothelial cell M3 receptor
- non innervated receptors
- M3: Gq = cause release of NO
- you know its muscarinic so you know its gonna be dilatory and not constriction.
-its like nitroglycerin but for chronic use.
Statins: side effects
- rhabdo (esp if given w/fibrates or niacin).
- dec. lipolysis (inhibiting adenylate cyclase)
- dec. VLDL synth (blocks apoB-100 gene expression)
-flushing (give aspirin)
-hyperglycemia (acanthosis nigricans)
Bile acid resins
- name them
- side effects
- cholestyramine, colestipol, colesevelam
- bad taste, GI discomfort, dec. absorption of ADEK, cholesterol gallstones.
- Drugs that inc. hepatic chol. synthesis can lead to chol. gallstones. Like bile acid resins & fibrates.
What can leads to cholesterol gallstones
-as far as content of bile
- low bile salts.
- high cholesterol.
Cholesterol absorption blocker
- name it
- where does it work
- small intestine brush border
- side effects
- inc LPL which inc. TG clearance from blood.
- activates PPAR-alpha to induce HDL synth.
- may get fatter since ur storing more TGs via LPL.
- myositis (esp w/statins)
- hepatotoxicity, cholesterol gallstones (esp w/bile acid resin use).
Which two drugs used together will lead to cholesterol gallstones?
fibrates & bile acid resins.
-how does it work?
If you activate this you bypass insulin and just turn on insulin-related genes.
-hence the inc in LPL function due to fibrates which activate PPAR-alpha.
Which nerve does digoxin stimulate?
- basic mechanism?
- By blocking Na/K ATPase (competing w/K) you dec the gradient of Na. This inhibits the Na/Ca exchanger the pumps Ca out. So more Ca in myoctes = inc. inotropy.
- Stimulates vagus: Only squirts ACh at nodal tissue, which slows down nodal conduction. This dec. HR.
- so you’ve inc. inotropy and dec. HR!
-can be used for CHF & afib.
ECG changes due to cardiac glycosides
- Dec. AV nodal conduction = inc. PR interval.
- Speeds electrical impulse through atrial myocardium, so P wave would be narrowed.
- Speeds impulse conduction velocity through ventricles, so QRS complex would be narrowed.
- notable side effects
- how is it excreted?
- intracell. Na inc = you’re loading cations! Cell can hit threshold potential easier! Leads to Arrythmias.
- cholinergic, blurry yellow vision.
- ECG—ST scooping, T-wave inversion, arrhythmia, AV block.
- Excreted renally, so renal failure can lead to toxicity.
Which drugs can cause digoxin tox?
- verapamil, amiodarone, quinidine.
- they dec. digoxin clearance.
diuretics & digoxin
-what should you watch out for?
-diuretics can cause hypokalemia which can cause digoxin toxicity.
digoxin & hyperkalemia
- indicates a poor prognosis.
- digoxin competes w/K at the Na/K ATPase. So it blocks K from coming into cell. Causes hyperkalemia and dec. intracellular K.
antidote to digoxin tox
- normal potassium (it will probably be too high)
- anti-digoxin Fab fragments
- cardiac pacer
How does beta-1 stim. inc. inotropy?
beta1 = Gs = inc. cAMP = inc PKA activity = phosphorylates Ca channel = Ca influx = muscle contraction.
autonomic inn. of heart
- Beta receptors: nodal tissue and ventricular tissue,
- Muscarinic innervation only on nodal tissue.
How do fibrates and bile-acid-resins lead to chol. gallstones?
they inc. cholesterol content of bile.
Central venous pressure = measure of what?
pressure in RA
Do pt’s w/cor pulmonale have inc or dec renin/aldo?
- ANP/BNP is in effective but just lowers the already increased renin/aldo. So net effect is still inc. renin/aldo.
- whenever there is fluid backup you’re gonna have low blood pressure. Think about where the baroreceptors are: aortic arch, carotid artery, etc.
where are baroreceptors located?
In arteries! Not veins!