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Cardiology
New set 2023 UWORLD only
| Question | Answer |
|---|---|
| In fetal circulation, is PVR high or low? | High PVR |
| Why is PVR high in fetal circulation? | Lungs are filled with amniotic fluid --> diffuse vasoconstriction of pulmonary capillary beds |
| In fetal circulation, is SVR high or low? | Low SVR |
| Why is SVR low in fetal circulation? | Fetal systemic circulation is connected in parallel to the low resistance placental vascular bed via the umbilical arteries and vein. |
| What is the result or benefit of ↑PVR and ↓SVR in Fetal circulation? | Facilites the R -->L shunt through the ductus arteriosus |
| Which ventricle contributes more to systemic blood flow in fetal circulation? | Both contribute the same |
| What is the result of PVR and SVR just after birth? | ↓ PVR and ↑ SVR |
| What causes the ↓ PVR at birth? | Oxygenation and ventilation of the lungs |
| What causes the ↑ SVR at birth? | Umbilical cord clamping --> reverse the shunt (R-->L to L-->R via the ductus arteriosus) |
| Which ventricle is the only one that contributes to systemic blood flow after birth? | Left ventricle |
| How is S4 best auscultated or heard? | Near apex of heart at point of maximal impulse with the patient in the Left Lateral Decubitus position |
| If a patient is positioned in the Left Lateral decubitus position, is it safe to assume that what murmur/sound is been auscultate? | S4 |
| What causes S4? | Atrial contraction --> forces blood into the LV that has had react its limit of compliance. |
| What condition is often associated with the development of S4? | Chronic hypertension as it causes LV hypertrophy |
| What is the MOA of fibrates? | Activate PPAR-α --> ↓↓↓ VLDL and ↑↑ Lipoprotein Lipase (LL) activity |
| What is the histology of Atrial myxoma? | Amorphous extracellular matrix with scattered stellate or globular myxoma cells and abundant mucopolysaccharide substance. |
| What are the local/endogenous substances that mediate resting coronary blood flow? | Adenosine and Nitric oxide (NO) |
| Adenosine and NO trigger coronary arteriolar vasodilation or vasoconstriction? | Vasodilation |
| What are common drugs that cause coronary arteriolar vasodilation? | Adenosine and Dipyridamole |
| What action resembles using pharmacologic arteriolar dilators? | Exercise |
| What is coronary Steal? | Redistribution of blood flow from ischemic to non-ischemic areas of the myocardium |
| What are the hemodynamic changes of an AV fistula? | 1. ↓↓ SVR (afterload) 2. ↑↑↑ Venous return (preload) & SV 3. LV contractility remains the same |
| What hemodynamic changes occur by the use of nitrates? | ↓ preload and LV-End diastolic volume and pressure |
| Why are preload, LVEDV, and LVEDP decreased with the use of nitrates? | Due to ↑↑↑ in peripheral VENOUS capacitance |
| Where are the most common foci for development of AFIB? | Ectopic electrical foci in the PULMONARY VEINS |
| Where is the ablation done in treating AFIB? | Foci in the pulmonary veins near their ostia onto the left atrium |
| Why does Aortic Stenosis develop angina? | Chronic ↑↑ LV pressure leads to LV hypertrophy and ventricular wall stress --> ↑↑ myocardial oxygen demand due to ↑ ventricular mass |
| Which receptors are stimulated by Clonidine? | α-2 |
| Which α-2 receptors does Clonidine specifically target? | Central α-2 receptors |
| Central α-2 adrenergic receptor agonist used as antihypertensive. | Clonidine |
| MOA of Clonidine | Stimulation of central α-2 receptors leads to PRESYNAPTIC ↑ release of NE and ↓↓↓ sympathetic outflow. |
| What is a serious and common adverse effect of Clonidine? | Orthostatic syncope |
| Why does Clonidine cause Orthostatic syncope? | The ↓↓ sympathetic outflow prevents normal baroreceptor-mediated ↑ in peripheral vascular resistance and heart rate during standing up |
| Which reflex is inhibited by Clonidine? | Baroreceptor-reflex |
| What is the role of the baroreceptor-reflex? | Increase peripheral vascular resistance and HR during standing up |
| Which drug is known to block or inhibit the Baroreceptor-reflex? | Clonidine |
| What are the causes of Orthostatic hypotension? | 1. Drugs (α-1 antagonists [Doxazosin, Terazosin]), diuretics. 2. Volume depletion 3. Autonomic dysfunction |
| How do α-adrenergic agonists ↑ systolic and diastolic blood pressure? | Stimulating α-1 receptors in vascular walls --> vasoconstriction |
| What is the response to ↑BP due to α-1 vascular receptor stimulation? | Reflexive ↑ in Vagal tone ===> ↓HR and slowed AV node conduction |
| What are common α-1 agonists? | Midodrine and Phenylephrine |
| What is the MC α-2 agonist? | Clonidine |
| What are common α-1 antagonists? | Doxazosin and Terazosin |
| MC α-1/α-2 antagonist | Phenoxybenzamine |
| Which adrenergic receptor is stimulated by Isoproterenol? | ß-adrenergic receptors (1 & 2) |
| What drug classes (sympathomimetics) can be used to ↓ heart rate? | α-1 agonists, α-2 agonists, and ß-1 antagonists |
| Histologic description of an Aortic aneurysm | Myxomatous changes, with pooling of mucopolysaccharides in the media layer of large arteries |
| Which layer of arteries is affected by aneurysms? | Medial layer |
| The buzzwords "myxomatous changes and pooling of mucopolysaccharides" refers to: | Aortic aneurysm |
| Which type of calcium channel blockers are most associated with the development of heart blocks? | Non-dihydropyridine Ca2+ channel blockers [diltiazem, verapamil] |
| What are the 2 most common non-dihydropyridine calcium channel blockers? | Diltiazem and Verapamil |
| What is the ß-1 response to abrupt ↑ in BP by α-1 agonism (phenylephrine)? | The ↑ PNS activity + ↓ SNS activity ==> ↑↑ cAMP in the heart (via ß-1 and M2 receptors) --> ↓↓ HR & contractility |
| A reduction of inward Ca2+ into SA cells will cause | Reduction in Heart Rate (HR) |
| What is the MCC of Down syndrome? | Maternal meiotic nondisjunction |
| Is Dobutamine an α or ß-adrenergic agonist? | ß-agonist |
| For which ß-receptor does Dobutamine have predominance? | ß-1 adrenoreceptor activity |
| Which drug can mimic (replace) a treadmill stress test in people unable to walk/run? | Dobutamine |
| What is the result of ß-1 agonism by Dobutamine? | ↑ HR & contractility --> ↑↑ myocardial oxygen consumption |
| What is the compensatory hormonal mechanism seen in CHF with low CO? | Neuroendocrine mechanism, which include ↑ Sympathetic outflow and activation of RAAS |
| What is the result, in compensated HF, of ↑ sympathetic outflow and ↑RAAS activity? | Vasoconstriction and volume retention in order to maintain organ perfusion |
| Common non-selective vasodilatory ß-blocker of receptors ß1, ß2 and α1? | Labetalol |
| In Labetalol, which receptor outweighs the other, between ß2 and α-1? | α-1 outweighs ß-2 blockade ---> peripheral vasodilation with ↓ venous return and ↓↓↓ SVR |
| What is the role of ß-1 blockade in Labetalol? | Overrides the expected baroreflex-mediated ↑ in HR -->--->---> overall ↓ HR. |
| What determines Coronary dominance? | Coronary artery supplying the PDA (Posterior Descending artery) |
| Which is the most common coronary dominance? | Right dominance |
| A person with Right Dominance in coronaries will have: | 1. PDA originates from RCA |
| Which CORONARY artery supplies the blood to the AV node? | Dominant coronary artery via the AV nodal artery |
| A person with left dominant coronary dominance, the PDA is derived from which artery? | Left Circumflex artery |
| What happens to Hematocrit and Albumin in the setting of Hypovolemia? | ↑[Hct] and ↑[Albumin] |
| Why is Albumin and Hct increased in hypovolemia? | Both blood components are trapped within the intravascular space. |
| What happens to uric acid concentration in hypovolemic situations? | ↑ absorption of Uric acid in the PCT --> ↑↑↑ serum uric acid level |
| What are the initial and MC symptoms of early Mitral Stenosis? | Exertional dyspnea |
| What are the hemodynamic changes in mild Mitral Stenosis (MS) vs severe MS? | At rest, LVDP, afterload, and contractility remain normal until MS is severe. |
| What is the MC underlying pathology for Mitral Stenosis? | Rheumatic Heart disease |
| What pathological or abnormal sound is seen with Mitral Regurgitation (MR)? | S3 |
| What are cardiac findings seen in severe MR? | Left-sided volume overload + S3 due to large volume of the regurgitant flow reentering the ventricle during mid-diastole |
| What is a key sign to distinguish btw severe and mild MR? | Prescence of S3 is indicative of severe MR |
| What is the auscultatory description of Pulmonic Stenosis? | Crescendo-decrescendo systolic murmur best heard at LUSB |
| What causes the wide splitting of S2 in Pulmonic stenosis? | Delay closure of the pulmonic valve |
| What is the MCC of MVP? | Defects in connective tissue proteins that predispose to myxomatous degeneration of the mitral leaflets and chordae tendineae |
| What is the key auscultation finding of MVP? | Midsystolic click |
| What maneuver could make the midsystolic click disappear and why? | Squatting due to ↑↑↑ LV End-Diastolic Volume |
| What is the overall effect on preload and afterload by Heart failure compensatory mechanisms? | ↑↑ afterload & preload |
| How is the ↓ in CO compensated in a patient? | Activation of RAAS and sympathetic nervous system. |
Created by:
rakomi
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