CV- FA Flashcards
C-ANCA targets what? what about P-ANCA?
C-ANCA: neutrophil proteniase 3
P-ANCA: neutrophil myeloperoxidase
weak pulse, fever, night sweats, myalgia, ocular disturbances. Diagnosis?
Takayasu
- Takayasu: PULSLESS disease
Rapid acting beta blokcer?
esmolol
Brugada syndrome
- inheritance pattern
- most commonly affected group
- ECG findings
- autosomal dominant
- asian male
- ST elevation on V1-V3, pseudo right bundle branch block
Aortic stenosis vs. Aortic regurgitation: at which location is murmur heard?
- AS: aortic area, RIGHT 2nd intercoastal
- AR: LEFT sternal border, 3rd/4th intercoastal
- this rule applies same for PS and PR
- PS: pulmonic area, LEFT 2nd intercoastal
- PR: left sternal border
Three heart manifestations of Marfan
- Aortic dissection
- Thoracic aortic aneurysm
- MVP
What is dextrocardia?
Heart in right side of chest
Kartgener syndrome
Ranolazine
- MOA
- indication
- major side effect
- inhibit late stage Na+ channel -> decrease wall tension, no effect on contractility or HR
- refractory angina
- QT prolongation
- BUT does NOT cause Torsades (this is UWORLD question)
BNP (B type natriuretic peptide)
- where is it released? in response to what?
- How is it used clinically
- What is name of recombinant form?
- BNP is released from VENTRICLE in response to increased VENTRICULAR TENSION (HF)
- BNP test can be used for HF diagnosis.
Very good NEGATIVE predictive value, meaning
negative BNP test means no HF (ruling out) - HF -> increased ventricular volume -> increased BNP
- Nesiritide (recombinant form) can be used for HF patient
- diuresis -> reduce congestion
MI diagnosis
- what is gold standard for first 6 hrs
- troponin I
- CK-MB
- ECG gold standard for first 6 hrs
- Troponin I: specific, peaks at 24 hrs, last 7-10 days
- CK-MB: less specific, peaks at 16-24 hrs, last only for two days => useful for re-infarction
Pt with osteopenia wants to avoid development of osteoporosis. what lipid lowering drug should be avoided?
cholestyramine
GI upset and malabsorption of fat soluble viatamins
-> less vitamin D -> less Ca2+ absorption
Kussmaul signs vs. Kussmaul respiration
- how is it different?
- example for each? 3 for Kussmaul signs and 1 for Kussmaul repisration
- Kussmaul sign: increase in JVP in respiration, meaning that there is defect in heart filling
=> constrictive heart pathology
1. pericarditis
2. cardiac temponade
3. RA or RV tumors (bulky tumors inhibiting filling) - Kussmaul respiration:
rapid/deep breathing= hyperventilation
seen in DKA
Three drugs that increase digoxin toxicity? by what mechanism?
- Quinidine
- Amiodarone
- Verapamil
Decrease renal clearance of digoxin
- Antiarrythmics; 1A, 3, 4
Hydralazine is co-administered with what drug? why?
to prevent reflex tachy, beta blocker is given
Contraindications for hydralazine? why?
angina and CAD
reflex tachy will overload heart
- hydralazine is normally indicated for
- hypertension
- HF
Triad of Cushing reaction? explain why
- hypertension
- bradycardia
- respiratory depression
increased ICP -> CNS vascular constriction
- > brain ischemia -> pCO2 -> central chemoreceptor to increase perfusion-> increased blood pressure
- > increased blood pressure sensed by baroreceptor
- > reflex bradycardia and respiratory depression
What cardiac condition show PR depression on ECG?
pericarditis (I have no fucking clue)
In pericarditis, widespread ST elevation will be also seen
Describe how cardiac output is changed over the course of exercise
- early phase
- late phase
- early phase: both HR and SV increases
- late phase: only HR is increased, while SV stays constant
- SV plateaus
What does inverted T wave on ECG mean?
recent MI
What two heart sounds are present in dilated cardiomyopathy? explain
- Systolic regurgitant murmur: dilated ventricle, blood flows back to atrium during systole
- S3: same reason of regurgitant murmur. Dilated ventricle, blood flows back to atrium during systole. In next round of filling, extra blood in atrium makes S3 sound
What causes closure of foramen ovale after birth?
increased LA pressure
Which two beta blockers are safe for treating pheocytochroma? Why?
carvedilol and labetalol
- these are non-selective alpha and beta blocker.
Other beta blockers are not safe for pheo, as selective beta blockade can result in unopposed alpha stimulation.
- Pheocytochroma is treated with alpha antagonist first (Phenoxybenzamine, irreversible alpha antagonist), followed by beta blocker (non-selective) to suppress reflex tachy
An infant is found to have a PDA and tetralogy of Fallot at birth. What treatment would you recommend until surgery is possible?
Prostaglandins E1 and E2 to keep PDA opened
=> Keeping PDA opened will reduce pulmonary stenosis effect in tetralogy of Fallot
*this is also true for transposition of great vessels. keeping PDA opened will allow communication between pulmonary artery and aortic artery.
Which class of antiarrhythmics can be used to treat digitalis (digoxin) induced arrythmia?
class 1B
- class 1B is also used for post MI ventricular arrythmia
Tricuspid pressure wave- x descent and y descent
- in which condition is X descent prominent? what about the condition where X descent is absent?
- in which condition is y descent prominent? what about the condition where y descent is absent?
- prominent x descent
1. tricuspid valve insufficiency: blood leaking into ventricle, more dramatic decrease in x descent
2. right HF: less RV pressure, more downward shift of tricuspid valve leaflet - absent x descent: tricuspid valve regurgitation
- prominent y descent: constrictive pericarditis
=> more squeezing, more RA emptying into RV - absent y descent: cardiac temponade
=> less RA blood initially, thus less RA emptying into RV
Familial hypertrophic cardiomyopathy
- inheritance pattern
- what gene is associated?
- autosmal dominant
- beta-myosin heavy chain mutation
cyanotic lower extremities, while upper extremities are normal. diagnosis?
PDA
: PDA inserts into aorta after 3 branches for upper extremities and brain
- this is called differential cyanosis
Ebstein anomaly: explain how tricuspid is messed up
tricuspid VALVE DISPLACEMENT
: valve leaflets DOWNWARD into RV, atrializing ventricle
Explain histologic finding on Buerger disease
segmental THROMBOSING vasculitis
- way to remember: another name for Buerger is thromboangitis obliterans. so THROBOSING
ECG finding of atrial fibrillation?
no p wave, irregular RR interval
FA p.278
Define Monckeberg sclerosis
calcification in MEDIA and INTERNAL ELASTIC LAMINA
intima NOT affected. Thus, NO OBSTRUCTION (clinically silent). just vascular stiffening.
X-ray: calcified blood vessels
Which pressure parameter is useful for estimating preload?
PCWP (also good indicator of LA pressure)
Which coronary arteries are susceptible to obstruction? ( from most likely to least likely) - circumflex - left anterior descending - right coronary artery
LAD >RCA > circumflex
- this makes sense: the bigger artery is, the more likely it is going to be obstructed.`
What two congenital heart defects are associated with DiGeorge syndrome?
- truncus arteriosus
- tetralogy of Fellot
Which nucleus of medulla receives vagus nerve signal from aortic baroreceptor?
solitary nucleus
What step in embryology is impaired in
- tetralogy of Fellot
- transposition of great vessels
- truncus arteriosus
- tetralogy of Fellot: deviation of intrafundibular septum
- transposition of great vessels: impaired spiraling of aorticopulmonary septum
- truncus arteriosus: absence of aorticopulmonary septum