Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Cardiology
UWORLD Round 2 Part 1
| Question | Answer |
|---|---|
| What are two common cardiac pathologies associated with Thiamine deficiency? | Beriberi and Wernicke-Korsakoff syndrome |
| What vitamin deficiency lead to Wernicke-Korsakoff syndrome and Beri Beri? | Thiamine deficiency |
| What can be expected to develop in a patient with vitamin B1 deficiency? | Beriberi and Wernicke-Korsakoff syndrome |
| What are the two categories of Beri Beri? | Wet and Dry Beriberi |
| What is the main feature of Dry Beri Beri? | Symmetrical peripheral neuropathy |
| What is the difference between Wet Beriberi and Dry Beriberi? | Wet Beri Beri includes the addition of high-output congestive heart failure |
| Which type of Beri Beri is associated with high-output congestive heart failure? | Wet Beriberi |
| What are the main features of "high-output" congestive heart failure? | Elevated cardiac output, low systemic vascular resistance , and low arterial-venous oxygen content difference |
| What causes the low systemic vascular resistance (SVR) in High-output heart failure? | Due to peripheral vasodilation or arteriovenous shunting |
| - Increased CO - Low SVR - Low A-V oxygen content difference Dx? | High-output heart failure |
| Granulomatosis polyangiitis is (+) for c-ANCA or p-ANCA? | c-ANCA |
| Common (+) c-ANCA vasculitis | Granulomatosis polyangiitis |
| PR3-ANCA is another way to refer to: | c-ANCA |
| What is Granulomatosis polyangiitis? | ANCA-associated systemic vasculitis that typically presents with upper and lower respiratory manifestations and renal insufficiency due to glomerulonephritis |
| What are the two main organ systems affected in Granulomatosis polyangiitis? | Respiratory and Renal systems |
| What causes the renal insufficiency seen in Granulomatosis polyangiitis? | Rapidly Progressive Glomerulonephritis |
| What are the upper respiratory manifestations Granulomatosis polyangiitis? | Sinusitis/Otitis, saddle-nose deformity |
| What are the lower respiratory manifestations of Granulomatosis polyangiitis? | Lung nodules/ cavitation |
| What are some common skin features seen with Granulomatosis polyangiitis? | Livedo reticularis, and non-healing ulcers |
| To which areas of the world is Chagas disease endemic to? | Central and South America |
| What type of cardiomyopathy is developed due to Chagas disease? | Dilated cardiomyopathy |
| What is the differentiating histological features between most cause of dilated cardiomyopathy and Chagas-induced DCM? | Chagas cardiomyopathy is seen with localized apical wall thinning with large apical aneurysm development |
| What is the most common histological change seen in most cause of DCM except for DCM secondary to Chagas disease? | Diffuse ventricular thinning |
| If the thinning of the ventricular wall is localized and in the apical zone of the heart, what is the most common cause of this DCM? | Chagas disease |
| Clinical description of VSD | Low-pitched, holosystolic murmur at the mid to lower left sternal border |
| Where is a VSD best heard or auscultated? | Mid to lower left sternal border |
| What is a common low-pitched, holosystolic murmur best heard at the LLSB? | VSD |
| Sound of VSD is accentuated with maneuvers that increase: | Afterload |
| What produces the symptoms in VSD? | Higher interventricular pressure gradient |
| What are maneuvers that increase afterload? | 1. Squatting and, 2. Handgrip |
| A patient that is ask to make a fist (handgrip motion) while auscultating the heart, is done to: | Increase afterload |
| What are known maneuvers that increase Preload? | Squatting and Passive leg raise |
| What is increase by passive leg raise that allows for better auscultating some murmurs? | Increase in preload |
| What maneuvers cause a decrease in Preload? | 1. Valsalva strain phase 2. Abrupt standing |
| What effect does abrupt or quick standing has on preload? | Sudden decrease in preload |
| What murmurs are known to increase intensity with handgrip maneuver? | AR, MR, and VSD |
| What does a decrease in Preload mean? | Decrease in Left Ventricular volume |
| What does an increase in Afterload mean? | Increase in LV and Aortic pressure |
| What is the effect on Preload and Afterload in cases of increase blood flow through stenotic or regurgitant valve? | Increase in preload and afterload |
| What are the blood flow to the heart effects upon inspiration? | 1. Increase venous return to the RIGHT heart 2. Decrease venous return to the LEFT heart |
| Which side of the heart experiences a decrease in venous return during inspiration? | Left side of heart |
| Which side of the heart, Right or Left, has an increase in venous return during inspiration? | Right side of heart |
| Which phase of Valsalva causes a decrease in Preload? | Valsalva strain phase |
| Squatting is known to cause an _____________ in preload and afterload. | Increase |
| What are the effects seen with chronic heart failure? | 1. Decreased CO in HF triggers --> 2. Neuroendocrine compensatory mechanisms to maintain organ perfusion, however, the compensatory mechanisms are maladaptive over a long term |
| What are the neuroendocrine mechanisms overly activated in chronic heart failure? | 1. Increased sympathetic output, and, 2. Activation of RAAS |
| What are the overall results of activated neuroendocrine compensatory mechanisms in heart failure? | Vasoconstriction and volume retention |
| What is represented by an increased sympathetic output? | Baroreceptors sense decreased perfusion and stimulate epinephrine and NE release to increase heart rate and contractility |
| How is vasoconstriction achieved by compensatory mechanisms seen in chronic heart failure? | Increasing arteriolar resistance and raising afterload |
| What are the cardiac hemodynamic results of chronic aortic regurgitation? | Reduction in Diastolic blood pressure and compensatory increase in LV stroke volume |
| Is Diastolic or Systolic blood pressure affected by chronic AR? | Diastolic blood pressure |
| What is the compensatory response of diastolic blood pressure dysfunction due to AR? | Increase in LV stroke volume |
| List of hemodynamic changes due to chronic aortic regurgitation: | 1. High-amplitude 2. Rapid rise-rapid fall pulsation (widened pulse pressure) 3. Head-bobbing 4. "pistol-shot" femoral pulses |
| What does the rapid rise and fall of pulsatio due to aortic regurgitation produces? | Widened pulse pressure |
| What produces the widened pulse pressure seen in AR? | The rapid rise-rapid fall of pulsation |
| What is a key feature of AR that is clinically visible? | Head bobbing |
| What is the common descriptio used for the femoral pulses in AR? | "pistol-shot" pulses |
| What is a common accompanying auscultation finding of ASD? | Wide, fixed splitting of the S2 |
| What causes the wide, fixed S2 sound in ASD? | Right-sided volume overload from the Left--> Right shunting. |
| What is the result of uncorrected ASD? | Irreversible medial hypertrophy of the pulmonary arteries with pulmonary hypertension and reversal to Right--> Left shunting |
| What is the name of the reversal of Left to Right shunt into Right---Left shunting? | Eisenmenger syndrome |
| Which anatomical part of the cardiac system suffers of irreversible changes due to uncorrected ASD? | Pulmonary arteries |
| What is the result of Right-sided heart overload from a L--->R shunt in ASD? | Wide, fixed splitting of the S2 |
| S4, precedes S1 or S2? | S1 |
| What is an S4 heart sound? | Low-frequency, late diastolic sound on cardiac auscultation that immediately precedes S1 |
| What causes an S4 heart sound? | Sudden rise in End-diastolic pressure with atrial contraction |
| What is the result of sudden rise in ED-pressure with atrial contraction? | S4 |
| What are conditions (examples) that present with S4? | Hypertensive heart disease, Aortic stenosis, and HCM |
| What type of conditions lead to development of abnormal S4? | Reduced ventricular compliance |
| Which abnormal heart sound usually emerges due to reduced ventricular compliance? | S4 |
| What are the main features of S4? | 1. Atrial gallop sound (before S1) 2. Heard immediately after atrial contraction as blood is forced into a stiff ventricle |
| What abnormal heart sound is expected in cases that blood is passed into a stiff (poor compliance) heart ventricle? | S4 |
| Abnomal S4 is associated with: | 1. Younger adults and children 2. Diastolic dysfunction patients |
| What patients are normal to develop and S4? | Healthy older adults |
| What are the main features of an S3? | 1. Ventricular gallop sound (after S2) 2. Heard during rapid passive filling of ventricles in diastole 3. Sudden cessation of filing as ventricle reaches its elastic limit |
| Heard during rapid passive filling of the ventricles in diastole | S3 |
| Ventricular gallop sound after S2 | S3 |
| S4 : atrial or ventricular gallop? | Atrial gallop |
| S3: atrial or ventricular gallop? | Ventricular gallop |
| When is S3 normally to be heard? | 1. Age < 40 2. Pregnant women |
| Which conditions lead to abnormal S3? | 1. Systolic heart failure 2. Mitral regurgitation 3. High-output states |
| What murmur is strongly associated with S3? | Mitral regurgitation |
| Systolic heart failure is most likely to develop a S3 or S4? | S3 |
| Is S3 heard before or after S2? | After S2 |
| What are the main structures that mediates the Calcium efflux from cardiac cells? | Na+/ Ca2+ exchange pump and Sarcoplasmic reticulum Ca2+-ATPase pump |
| What is Dobutamine? | B-adrenergic agonists with predominant activity on B1-receptors and weak activity of B2 and a-1 receptors |
| On which, B1 or B2, does Dobutamine exerts greater agonist effects? | B1>>B2 |
| What is the result of Dobutamine increase stimulation of B1 receptors? | Increase cAMP preociton and increase cytosolic Ca2+ concentration |
| What is the result of increased cAMP and Calcium cytosolic contract due to Dobutamine therapy? | Facilitation of interaction between ACTIN and MYOSIN leading to increased myocardial contractility |
| Which proteins' activity is directly affected by the use of Dobutamine? | Actin and Myosin |
| What is the result of increased interaction between Actin and Myosin? | Increased myocardial contractility |
| Increased myocardial contractility may be produced by the use of which B-1 (preferred) sympathomimetic? | Dobutamine |
| Are the levels of AT I and AT II increased or decreased with the use of ARBs? | Both are increased |
| What is Isoproterenol? | A B1 and B2 adrenergic receptor agonist that causes increased myocardial contractility and decreased SVR |
| What is the B1 effect of Isoproterenol? | Increased myocardial contractility |
| What does (+) inotropic effect means? | Increased myocardial contractility |
| What is the B2 effect of Isoproterenol? | Decreased SVR |
| What condition is commonly treated with Niacin? | Hyperlipidemia |
| What are the intended cholesterol effects of Niacin therapy? | Increases HDL and decrease LDL and triglycerides |
| What is an important and common adverse effect of Niacin? | Cutaneous flushing |
| What is the main mediator of cutaneous flushing due to Niacin? | Prostaglandins (PGD2 and PGE2) |
| How is Niacin-induced cutaneous flushing diminished or preventable? | Pretreatment with Aspirin |
| Which medication is often used to diminish the cutaneous flushing induced by Niacin? | Aspirin |
| What is the initial presentation of Mitral Stenosis? | Usually due to underlying Rheumatic heart disease and presents with exertional dyspnea |
| Patient with history of Rheumatic heart disease complains of difficulty breathing with exercise. Possible diagnosis? | Mitral stenosis |
| At rest, a patient with mild MS, will have: | Normal ventricular diastolic pressure, afterload, and contractility |
| What does cardiac and smooth muscle contraction initiation depend on? | Extracellular calcium influx through L-type Ca2+ channels |
| What types of channels are blocked in SM and cardiac muscle by Calcium channel blockers? | L-type Ca2+ channels |
| Which type of muscle in the body is resistant to Calcium channel blockers? | Skeletal muscle |
| Why are Calcium channels blockers ineffective in Skeletal muscle? | Calcium release in skeletal muscle by the Sarcoplasmic reticulum is triggered by an interaction between L-type and RyR calcium channels |
| RyR channels and L-type calcium channel interaction is seen in which type of muscle: skeletal, cardiac, and/or smooth muscle? | Skeletal muscle |
| Mutated TTN gene. Dx? | Familial Dilated cardiomyopathy |
| What is encoded by the TTN gene? | Sarcomere protein titin |
| What is the MCC of Familial DCM? | Mutated TTN gene |
| Autosomal dominant mutation of TTN gene, leading to a abnormal sarcomere protein titin. Dx? | Familial Dilated cardiomyopathy |
| DCM is associated with Systolic or Diastolic dysfunction? | Systolic dysfunction |
| What are common condition associated with Systolic dysfunction? | Ischemic heart disease and DCM |
| What valvular conditions are associated with DCM development? | AR and MR |
| What type of cardiomyopathy is most often seen with patients with AR or MR? | Dilated cardiomyopathy |
| Which condition is seen with dilation of the Left Ventricular cavity due to systolic dysfunction? | Dilated cardiomyopathy |
| What type of hypertrophy is seen with DCM? | Eccentric hypertrophy |
| Eccentric or Concentric hypertrophy. DCM? | Eccentric hypertrophy |
| Eccentric or Concentric hypertrophy. HCM? | Concentric |
| What is the long term consequence of chronic volume overload due to DCM? | Progressive eccentric hypertrophy leads to reduced ventricular contractility and decompensated heart failure |
| Is DCM associated with compensated or decompensated heart failure in the long run? | Decompensated heart failure |
| When do most Thoracic Aortic aneurysms become symptomatic? | As they become large enough to compress the surrounding structures or cause rupture |
| What are the most common symptoms or signs of symptomatic Thoracic aortic aneurysm? | Chest or back pain, with possible compression of nearby structures causing, dysphagia, hoarseness, cough or dyspnea |
| What are the compression signs of thoracic aneurysms? | Dysphagia, hoarseness of voice, cough and/or dyspnea. |
| What is systolic dysfunction? | Impaired ventricular contraction (loss of inotropy) |
| What is the difference between compensated and decompensated heart failure? | Compensated heart failure the clinical signs are not evident due to the heart's ability to "compensate" for the problem, while decomenasted the heart is not strong enough to overcome the condition |
| What is diastolic dysfunction? | Cardiac condition caused by a “stiffening” of the heart's ventricles (the major pumping chambers) |
| How Peripheral Vascular Disease clinically presented? | Intermittent claudication, which is described with muscle pain that is reproducibly caused by exercise and relieved by rest |
| What is the MCC of PVD? | Atherosclerotic stenosis in large arteries that prevent sufficient blood flow to the exercising muscle |
| Which extremities, lower or upper, are more often affected by Peripheral Vascular disease? | Lower extremities |
| Although distal lesions are more common, what is a common clinical profile of a PVD due to proximal lesion? | In aortoiliac occlusion it can cause Gluteal claudication and impotence |
| What are the clinical signs of PVD due to Aortoiliac claudication? | Gluteal claudication and impotence |
| What conditions are part of a complete AV canal defect? | ASD, VSD, and common AV valve defect |
| What type of patients are most often associated with AV canal defects? | Down syndrome |
| What is the MC cardiac congenital anomaly seen in Down syndrome patients? | AV canal defect, such as ASD, VSD, or AV valve defect |
| What is necessary to add to hypertension, in order to be considered a Hypertensive emergency? | End-organ damage |
| What is the kidney evidence of end-organ damage? | Malignant nephrosclerosis, characterized by fibroid necrosis and hyperplastic arteriosclerosis |
| What is the the common description of Malignant nephrosclerosis and hyperplastic arteriosclerosis? | "Onion-skin" appearance |
| What type or classification of anemia is often seen with Hypertensive emergency? | Microangiopathic Hemolytic anemia |
| What gives rise to the development of Microangiopathic Hemolytic anemia in Hypertensive emergency? | Erythrocyte fragmentation and platelet consumption at the narrowed arterial lumen |
| In heart failure, why does it often develop Cardiogenic Pulmonary edema as well? | Due to increased pulmonary venous pressure |
| What is the result of the increased pulmonary venous pressure in acute heart failure patients? | Development of Acute Cardiogenic Pulmonary edema |
| How does the Pulmonary edema due to heart failure appears in gross examination? | Pink, acellular material within the alveoli |
| What common cardiac conditions are associated with S4? | Restrictive cardiomyopathy and Left Ventricular hypertrophy |
| Low frequency sound heard at the end of diastole just before S1 | S4 |
| What are the major defects of Tetralogy of Fallot? | Right ventricular Outflow Tract obstruction and VSD |
| What is common to happen to ToF patients with some activities such as feeding? | Precipitate cyanotic episodes (tet spells) by causing a dynamic incree in RVOT obstruction |
| What does an increase in RVOT obstruction ToF cause? | Cyanotic episodes |
| What happens during Cyanotic episode in TOF patients? | RV pressure is increased, while pulmonary and LA pressures are decreased as blood is shunted away from the pulmonary circulation |
| Systolic ejection type, crescendo-decrescendo murmur that stars after the first heart sound and typically ends just before the A2 component of the S2? | Aortic stenosis |
| Peak intensity of AS would be at the point where: | Aortic pressure its is highest and Left Atrial pressure at its lowest |
| Common cause of syncope associated with tactile stimulation of the carotid sinus | Carotid Sinus hypersensitivity |
| What common daily activity may precipitate Carotid Sinus hypersensitivity? | Shaving |
| Syncope due to carotid sinus hypersensitivity is due to stimulation of which nerve? | Vagus nerve |
| What causes syncope in Carotid sinus hypersensitivity? | Exaggerated vagal response stimulated by the carotid baroreceptors, which leads to slower heart rate and maked peripheral vasodilation with a resulting transient loss of cerebral perfusion |
| What is the time frame in which Left ventricular wall rupture is expected after an MI? | Mostly within 5 days, but can take up to 2 weeks |
| What are the consequences or results of LV Free Wall rupture after an MI? | Cardiac tamponade that causes hypotension and shock with rapid progression to cardiac arrest |
| What is seen at the autopsy of a patient that died due to LV Free wall rupture? | Slit-like tear at the site of infarction in the LV wall |
| What adrenergic receptors are stimulated by Epinephrine? | a-1, B-1, and B-2 |
| Which receptors stimulated by Epinephrine increase systolic blood pressure? | a-1 and B-1 |
| Which receptor is stimulated by Epinephrine that increase heart rate? | B-1 |
| What is distinctive of Epinephrine in association of Diastolic blood pressure? | It is dose dependent, as it may have a-1 ro B-2 predominance |
| Which common sympathomimetic is known to possible cause a n increase of decrease in diastolic pressure depending on the dose? | Epinephrine |
| What happens to the hemodynamics of a patient that is given Epinephrine, but was pretreated with Propranolol? | The beta blocker eliminates all Epinephrine's beta effects, leaving only the alpha effet (vasoconstriction) |
| What are the B-effects of Epinephrine? | Vasodilation and tachycardia |
| Predominance of a-1 effects by Epinephrine will lead to vasoconstricción or vasodilation? | Vasoconstriction |
| How are the effects of Amiodarone on cardiac action potential reflected on the ECG? | QT interval prolongation |
| Common Class 1C antiarrhythmic agent | Flecainide |
| MOA of Flecainide: | Block the Fast Na+ channels responsible for Ventricular depolarization (phase 0), prolonged QRS duration with little effect on the QT interval |
| Which part of the ECG tracing is most affected by the use of Flecainide? | Increased QRS duration |
| Which antiarrhythmics (class) affect QT prolongation the most? | Class IA and Class III |
| What are some common Class III antiarrhythmics? | Amiodarone, Sotalol, and Dofetilide |
| MOA of Dofetilide: | Predominantly block K+ channels and ibnitir the outward K+ currents during phase 3 of the cardiac AP, thereby prolonging repolarization and total AP duration |
| Which phase of the cardiac AP is most affected by Class III antiarrhythmics? | Phase 3 |
| Which phase of the cardiac AP is affected mostly by Class IC antiarrhythmics? | Phase 0 |
| Class III antiarrhythmics prolonged repolarization or depolarization of the cardiac cell? | Repolarization |
| Which type of antiarrhythmic are known to affect the ventricular depolarization, leading othe a prolonged QRS duration? | Class IC antiarrhythmics |
| How do Beta-blockers reduce morbidity and mortality ? | Decreasing cardiac output and myocardial oxygen demand |
| Which type, cardioselective or non-selective, beta blockers are NOT indicated for Asthma or COPD patients? | Non-cardioselective beta blockers |
| Propranolol and Nadolol are selective or non-selective beta blockers? | Non-cardioselective beta blockers |
| Cardioselective Beta blockers are preferential to B1 or B2 receptor? | Beta -1 |
| If a beta blocker only works on B-1 receptors, is its commonly prefered to be use in what type of patients? | Asthmatic or COPD |
| What is the MCC of congenital long QT syndrome? | Mutation that slows the delayed rectifier K+ current that repolarized the cardiomyocyte action potential |
| What are some medications that are known to slow K+ repolarization current? | Macrolides, antispsychotics, and antiemetics |
| Slowed K+ current repolarization presents with: | Prolonged QT interval |
| What are some severe complications of prolonged QT intervals? | Cardiac arrhythmia, resulting in syncope or sudden cardiac death |
| What are the physiologic changes of Endurance training? | Increaed maximum CO via increae in Stroke volume |
| What type of hypertrophy is seen with Endurance training? | Eccentric hypertrophy of the LV wall |
| What is the result of eccentric hypertrophy of the LV in endurance training? | Increased left ventricular cavity size and improve diastolic filling capacity |
| What is the direct result of an increased EDV capacity, as seen in endurance training? | Increased stroke volume (SV) and cardiac output (CO) |
| Increased SV and CO, may be acquired after ___________ training. | Endurance training |
| What is the effect on ejection fraction if the EDV and SV are both increased? | Ejection fraction remains mainly UNCHANGED |
| Where is an S4 best heard? | Cardiac apex at point of maximal impulse with the patient in the Left Lateral Decubitus position |
| What produces the S4 heart sound? | Atrial contraction, which forces blood into on LV that has reached its limit on compliance |
| What is a possible consequences chronic hypertension? | Left ventricular hypertrophy, which itself may promote the generation of an S4 |
| Connection between pulmonary artery and aorta | PDA |
| What is the result in the Pulmonary artery in PDA? | Higher-than expected oxygen concentration in the Pulmonary artery |
| Which embryological congenital condition is seen with unchanged oxygenation of the right and left heart chambers? | PDA |
Created by:
rakomi
Popular USMLE sets