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Cardiology
FA complete review
| Question | Answer |
|---|---|
| What structures are originated from the Endocardial cushion? | Atrial septum, membranous interventricular septum; AV and semilunar valves |
| The primitive pulmonary vein gives to --> | Smooth part of the Left atrium |
| The left horn of the sinus venosus gives rise to the: | Coronary sinus |
| What structure is derived from the right horn of the sinus venosus? | Smooth part of the right atrium |
| What veins give rise to the Superior vena cava (SVC)? | Right common cardinal vein and right anterior cardinal vein |
| The Bulbus cordis gives rise to the: | Smooth parts (outflow tract) of left and right ventricles |
| What gives rise to the Ascending aorta and pulmonary trunk? | Truncus arteriosus |
| At what week of development does the heart beat spontaneously? | Week 4 |
| Another name for Kartagener syndrome? | Primary ciliary Dyskinesia |
| Defect in left-right Dynein leads to: | Dextrocardia |
| What is the cause of the Patent Foramen Ovale? | Failure of septum primum and septum secundum to fuse after birth |
| What is a common complication in PFO? | Paradoxical emboli |
| What is Paradoxical emboli? | Venous thromboemboli that enter systemic arterial circulation |
| Where does VSD is most commonly occuring? | Membranous septum |
| What are some conotruncal abnormalities associated with failure of neural crest cells to migrate? | 1. Transposition of great vessels 2. Tetralogy of Fallot 3. Persistent truncus arteriosus |
| What is the percentage of oxygen saturation in blood in umbilical vein? | 80% |
| What is the PO2 in Umbilical vein? | 30 mmHg |
| The ductus venosus provides bypassing of: | Hepatic circulation |
| What is the postnatal derivative of the Allantois? | Median umbilical ligament |
| What is the Urachus? | Part of allantoic duct between bladder and umbilicus |
| The Notochord becomes the ____________________ after birth. | Nucleus pulposus |
| Which fetal structure gives rise the the Medial umbilical ligaments? | Umbilical arteries |
| The fetal umbilical vein becomes the ____________________________ after birth, and it contains the ______________________. | Ligamentum teres hepatis (round ligament); Falciform ligament. |
| What coronary artery supplies the right ventricle? | Right (acute) marginal artery |
| What areas are irrigated by the PDA? | -AV node - Posterior 1/3 of interventricular septum - Posterior 2/3 walls of ventricles - Posteromedial papillary muscle |
| What areas are irrigated by the LAD? | - Anterior 2/3 of interventricular septum - Anterolateral papillary muscle - Anterior surface of the left ventricle |
| The LCX supplies: | Lateral and Posterior walls of the left ventricle and anterolateral papillary muscle. |
| What is the most posterior part of the heart? | Left atrium |
| What are possible complications of Left atrium enlargement? | 1. Dysphagia (compression of the esophagus) 2. Hoarseness (compression of the Left recurrent Laryngeal nerve) |
| What is a branch of the Vagus nerve, that causes hoarseness upon compression by the left atrium? | Left Recurrent Laryngeal Nerve |
| The pericardial cavity is between which Pericardium layers: | Parietal and Visceral layers |
| Pulse pressure = | Systolic pressure - Diastolic pressure |
| Which conditions are seen with increased pulse pressure? | Hyperthyroidism, aortic regurgitation, aortic stiffening (isolated systolic hypertension in elderly), obstructive sleep apnea (increase sympathetic tone), anemia, exercise (transient) |
| A decrease in pulse pressure is seen with: | Aortic stenosis, cardiogenic shock, cardiac tamponade, advanced heart failure (HF). |
| What condition can cause a decrease in Diastole? | Increase in heart rate |
| Less filling time (diastole) ---> | Decreased CO |
| How is CO maintained in late stages of exercises? | Increased heart rate only (SV plateaus) |
| MAP = | CO x TPR |
| SV = | EDV - ESV |
| CO = | SV x HR |
| CO = | rate of O2 consumption -------------------------------------------------------- (arterial O2 content - venous O2 content) |
| Which conditions decrease Contractility? | - B1-blockade (decrease cAMP) - HF with systolic dysfunction - Acidosis - Hypoxia/Hypercalcemia - Non-dihydropyridine Ca2+ channel block |
| What condition increase Contractility? | 1. Catecholamine stimulation via B1 receptor 2. Increase intracellular Ca2_+ 3. Decrease in extracellular Na+ 4. Digitalis |
| What value can approximate Preload? | Ventricular EDV |
| Preload depends on: | Venous tone and circulating blood volume |
| Venous vasodilators ---> | Decrease preload |
| What is a very common venous vasodilator? | Nitroglycerin |
| Afterload can be approximated by: | MAP |
| What is a common arterial vasodilator? | Hydralazine |
| Arterial vasodilators ---> | Decrease Afterload |
| Which type of medications can decrease both preload and afterload? | ACE inhibitors and ARBs |
| In relation to afterload pressure, how is LV hypertrophy developed? | Chronic hypertension (increase MAP) |
| Increase in all the following lead to myocardial O2 demand increase: | Contractility, Afterload, Heart rate, and Diameter of ventricle |
| An increase of diameter of ventricle means = | Increase wall tension |
| How is Ejection Fraction affected in Systolic HF? | Decrease |
| What anatomical structure has the highest cross-sectional area and lowest flow velocity? | Capillaries |
| What structure account for most of TPR? | Arterioles |
| Viscosity depends mostly on ____________________. | Hematocrit |
| What conditions increase viscosity? | Hyperproteinemia states (multiple myeloma), polycythemia |
| What condition leads to a decrease in viscosity? | Anemia |
| Resistance in series is added : | R t = R1 + R2 + R3...... |
| Total resistance of vessels in parallel are added in: | 1/Rt = 1/R1 + 1/R2 +1/R3...... |
| What are common examples of things that Increase Inotropy? | Catecholamines, digoxin (+), and exercise |
| An increase in Inotropy causes an ____________________ shift in the Cardiac function curve. | Increase |
| What are examples of activities that cause a negative Inotropy change? | HF with reduced EF, narcotic overdose, and sympathetic inhibition. |
| Changes in Inotropy basically mean: | Changes in contractility --> change in preload |
| What are some things that cause an increase in venous return? | Fluid infusion, sympathetic activity |
| Acute hemorrhage and spinal anesthesia (-) are examples of actions that cause: | A decrease (downward shift) in the Venous return curve |
| The use of vasopressors cause what changes in the Cardiac and vascular function curves? | Increase in in TPR |
| What are examples of things that cause a decrease in TPR? | Exercise, and AV shunt (-) |
| Compensatory changes in the Cardiac and Vascular function curves: | HF decreases inotropy -----> fluid retention to increase preload and maintain CO |
| What is the ultimate goal of reinforcing changes in the Sterling curve? | Maximize CO |
| What specific changes will maximize CO? | Exercise to increase inotropy and a decrease in TPR. |
| What changes accompany an increase in Contractility? | Increased SV and EF, and a decrease in ESV |
| An increase in Afterload is seen with which other changes? | Increase in Aortic pressure and ESV, and a decrease in SV. |
| Increase in preload also indicates an increase in: | Stroke volume |
| Isovolumetric contraction: | Period between mitral valve closing and Aortic valve opening |
| Which phase of the Pressure-Volume Loop is characterized with the highest O2 consumption? | Isovolumetric Contraction |
| What closedure indicate Isovolumetric relaxation? | Period between aortic valve closing and mitral valve opening |
| To which ventricle is the Pressure-Volume loop directed? | Left Ventricle |
| What causes the S1? | Mitral and Tricuspid valve closure |
| Where is the S1 the loudest? | Mitral area |
| What caused the S2? | Aortic and pulmonary valve closure |
| Best area to auscultate for an S2 is ---> | Left upper sternal border |
| At what stage of the Pressure volume loop is the S3 found? | In early diastole during rapid ventricular filling phase |
| What pathological heart sound is associated with increased filling pressures? | S3 |
| What conditions are typical of showing a S3? | Mitral regurgitation and HF; especially in DCM. |
| Which population is normal to develop and S3? | Children, young adults, and pregnant woment |
| The "atrial kick" is referred to the _______. | S4 |
| Which abnormal heart sound is found at late diastole? | S4 |
| What is the best way to listen to a S4? | At apex of heart with patient in left lateral decubitus positon |
| Why is there an S4 in HCM? | Left atrium must push against still LV wall |
| In the JVP, which wave represents atrial contraction? | a wave |
| In the JVP, the c-wave depicts? | RV contraction |
| Patient with AFIB, is probably missing which wave in the JVP tracing? | a wave |
| Increase in Right Atrial pressure due to filling against Tricuspid valve, is indicated in JVP with: | v-wave |
| Which condition depicts a prominent y-descent in the JVP? | Constrictive Pericarditis |
| Absent y-descent on JVP is often seen in patients with: | Cardiac tamponade |
| What is the direct effect of inspiration? | Drop in intrathoracic pressure |
| Normal splitting is due to: | Delayed closure of pulmonic valve |
| What conditions are seen with Wide Splitting? | Pulmonic stenosis, RBBB |
| Wide splitting is due to: | Delay RV emptying |
| What can increase the intensity of Wide Splitting? | Inspiration |
| What kind of split is associated with ASD? | Fixed split |
| The ASD causes: | Left-to-right shunt ---> Increase in RA and RV volumes ---> Increase flow through the pulmonic valve, regardless of respiration. |
| What is the cause of the conditions that cause Paradoxical splitting? | Delay aortic valve closure |
| What are some conditions associated with Paradoxical splitting? | Aortic stenosis, LBBB |
| In which type of splitting the order order of valve closure is reversed? | Paradoxical splitting |
| Which sounds occurs first in Paradoxical splitting? | P2 |
| What action can "eliminate" Paradoxical splitting? | Inspiration |
| Inspiration causes: | Increase venous return to right atrium |
| What bedside maneuver can be performed to increase the volume reaching the Right atrium? | Inspiration |
| Inspiration increases the intensity of ________ heart sounds | Right |
| Hand grip causes an: | Increase in afterload |
| Which murmurs are increased in intensity by Hand grip? | MR, AR, and VSD |
| How is Preload affected by Valva Phase II and Standing up? | Decrease |
| What actions can increase the intensity of Hypertrophic cardiomyopathy murmur? | Valsalva II and Standing up |
| What happens to Preload, Afterload and venous return with Rapid Squatting? | All three increase |
| What murmurs are intensified with Rapid squatting? | AS, MR, and VSD |
| HCM murmur decreases intensity with? | Rapid Squatting |
| Which are the Systolic murmurs? | 1. Aortic/Pulmonary stenosis 2. Mitral/Tricuspid regurgitation 3. VSD, MVP, HCM |
| Which are the Diastolic murmurs? | 1. Aortic / Pulmonic regurgitation 2. Mitral/Tricuspid stenosis |
| Which are the 3 Holosystolic Murmurs? | TR, VSD, and MR |
| Which 3 murmurs are best heard in the Left Sternal border? | AR, PR, and HCM |
| Crescendo-decrescendo systolic ejection murmur and soft S2 + Ejection click | Aortic Stenosis |
| Which murmur radiates to the carotids? | Aortic Stenosis |
| What is "Pulsus parvus et tardus"? | Pulses are weak with a delayed peak |
| What characteristic pulse is associated with Aortic Stenosis? | Pulsus parvus et tardus |
| Holosystolic, high-pitched "blowing murmur" | Mitral/Tricuspid regurgitation |
| Loudest at apex and radiates toward axilla | Mitral regurgitation |
| What murmur is due to RV dilation? | Tricuspid regurgitation |
| What are the MCC of MR? | Ischemic heart disease (post-MI), MVP, and LV dilation |
| Late systolic crescendo murmur with midsystolic click | Mitral valve prolapse |
| What is the MCC of MVP? | Sudden tensing of chordae tendineae |
| When is MVP the loudest? | Just before S2 |
| What are some conditions associated with the development of MVP? | Myxomatous degeneration (Primary or secondary connective tissue disease such as Marfan or Ehlers-Danlos syndrome), Rheumatic fever, chordae rupture |
| Holosystolic , harsh-sounding murmur | VSD |
| VSD is best hear te the _______________ area. | Tricuspid |
| High-pitched "blowing" early diastolic decrescendo murmur | Aortic regurgitation |
| Long diastolic murmur, hyperdynamic pulse, and head bobbing are seen in: | Aortic regurgitation |
| What are the MCC of Aortic regurgitation? | Aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever |
| Untreated AR may lead to ----> | Left Heart Failure |
| Which murmur follows an Opening Snap? | Mitral Stenosis |
| What is the cause of the Opening Snap in MS? | Abrupt halt in leaflet motion in diastole, after rapid opening due to fusion a t leaflet tips |
| What is a common and highly specific sequelae on untreated Rheumatic fever? | Mitral Stenosis |
| Chronic MS causes _________________________, leading to hoarseness and dysphagia. | LA dilation |
| What is the MCC of PDA? | Congenital rubella or prematurity |
| Continuous machine-like murmur | Patent ductus arteriosus |
| Phase 0 is in myocardial AP: | rapid upstroke and depolarization |
| What channels are open in Phase 0 in myocardial AP? | Voltage gated Na+ channels |
| Initial repolarization in cardiac muscle AP? | Phase 1 |
| The inactivation of voltage-gated Na+ channels, and the beginning of voltage-gated K+ opening, in cardiac muscle | Phase 1 |
| Phase 2 of Myocardial AP is: | Plateau; Ca2+ influx through voltage-gated Ca2+ channels balance K+ efflux |
| What occurs with the Ca2+ influx to myocyte? | Triggers Ca2+ release from Sarcoplasmic reticulum and myocyte contraction. |
| Phase 3 of Myocardial action potential is known as: | Rapid repolarization |
| Which is the Resting potential phase in cardiac AP? | Phase 4 |
| High K+ permeability through K+ channels | Phase 4 |
| Why does rapid repolarization occurs? | massive K+ efflux due to opening of voltage-gated slow K+ channels and closedure of voltage-gated Ca2+ channels. |
| Which action potential cell type, has a "platuem" ? | Cardiac muscle |
| What ion is required by cardiac muscle in order to produce contraction? | Calcium |
| The sentence "Ca2+-induced Ca2+ release" most relates to which type of muscle Action Potential? | Cardiac muscle contraction |
| How are Cardiac myocytes electrically coupled to each other? | Gap junctions |
| What value is normal for cardiac muscle Effective Refractory period? | 200 msec |
| Where does the pacemaker action potential occurs? | SA and AV nodes |
| In Pacemaker AP, which ion voltage channel opening is responsible for Phase 0 (upstroke)? | Calcium |
| How are the Fast voltage-gated Na+ channels in Pacemaker AP? | Permanently inactivated |
| Which phases are missing in Pacemaker AP? | Phase 1 and Phase 2 |
| Phase 3 in Pacemaker AP is known as: | Repolarization |
| Inactivation of Ca2+ channels and increased activation o K+ channels ---> K+ efflux. Describes? | Phase 3 of Pacemaker AP |
| Phase 4 in Pacemaker AP is due to: | slow spontaneous diastolic depolarization due to If |
| What is the roles of If channels? | Slow, mixed Na+/K+ inward current |
| Which phase accounts for the AUTOMATICITY of SA and AV nodes? | Phase 4 |
| What in the Pacemaker AP determines the heart rate? | The slope of Phase 4 in the SA node |
| What would ACh/Adenosine cause to heart rate? | Decrease the rate of diastolic depolarization leading to decreased HR |
| What substances can be used to increase rate of Pacemaker AP depolarization and increase heart rate? | Catecholamines |
| What are the divisions of the Left Bundle branch? | Left anterior and Left Posterior fascicles |
| Which "pacemaker" is inherent dominance with slow phase of upstroke? | SA node |
| Which artery supplies the AV node? | RCA |
| What is the rates of the pacemaker? | SA node > AV node > bundle of His/Purkinje/ ventricles |
| Which pacemaker has the fastest speed of conduction? | Purkinje > atria > ventricles > AV node |
| What wave in the ECG represents atrial depolarization? | P-wave |
| The PR interval represents? | Time from start of atrial depolarization to start of ventricular depolarization |
| Ventricular depolarization in the ECG is represented with: | QRS complex |
| T-wave on ECG represents: | ventricular repolarization |
| What conditions lead to creation of a U wave in the EKG? | Hypokalemia and bradycardia |
| Torsades de pointes: | Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG |
| What is the most severe complication of Torsades de Pointes? | Ventricular fibrillation |
| What are the main causes of Torsades de Pointes? | Drugs, hypokalemia, decreased Mg2+, and congenital abnormalities |
| What is the MC treatment for Torsades de Pointes? | Magnesium sulfate |
| What antiarrhythmics are related to development of Torsades de pointes? | Class IA and III |
| Which kind of antibiotics often have Torsades de pointes as a SE? | Macrolides |
| Person on Haloperidol should be monitored for which ECG abnormality? | Torsade de Pointes |
| Ondansetron is often used to control chemotherapy-induced emesis, but it can cause ____________________ in ECG. | Torsade de Pointes |
| What are the two most common disorders that cause and abnormally long QT interval? | 1. Romano-Ward syndrome 2. Jervell and Lange-Nielsen syndrome |
| What is the most common cause of death in patients with Congenital long QT syndrome? | Torsade de Pointes |
| What is the the main clinical difference in a patient with Romano-Ward syndrome and one with Jervell and Lange-Nielsen syndrome? | Jervell and Lange-Nielsen syndrome have sensorineural deafness. |
| ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3. | Brugada syndrome |
| What kind of population is MC to be affected by Brugada Syndrome? | Asian males |
| What is the best treatment for Brugada syndrome? | Implantable cardioverter-defibrillator (ICD) |
| What is the MC type of ventricular pre-excitation syndrome? | Wolff-Parkinson-White syndrome |
| ECG delta wave is characteristic of which syndrome? | Wolff-Parkinson-White syndrome |
| Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node? | Wolff-Parkinson- White syndrome |
| What is a severe complication of WPW syndrome? | SVT |
| What is a associated disease with the development of 3rd degree AV block? | Lyme disease |
| What is the function of ANP? | Increase blood volume and atrial pressure |
| ANP causes: | Vasodilation and decreased Na+ reabsorption at the renal collecting tubule |
| What are the effects on the efferent and afferent arterioles by ANP? | Dilates afferent renal arterioles and constricts efferent renal arterioles |
| What substance promotes and contributes the "aldosterone escape"? | ANP |
| BNP is secreted by ventricular myocytes in response to? | Increased ventricular tension |
| What is good negative predictive value for diagnosis HF? | Elevated BNP levels |
| Aortic arch receptors transmit via? | Vagus nerve to solitary nucleus of medulla |
| Aortic arch receptors respond to: | a decrease or increase in Blood pressure |
| Carotid sinus receptors transmit via the: | Glossopharyngeal nerve to solitary nucleus of medulla |
| What is the normal pressure in the Right Atrium? | < 5 mm Hg |
| What is the normal pressure in the Right Ventricle? | 25/5 mm Hg |
| What area in the heart has a pressure of 25/10 mm Hg? | Pulmonary vein |
| What is the normal pressure of PCWP? | 4-12 mm Hg |
| What is the normal pressure seen in a healthy Left atrium? | < 12 mm Hg |
| What is the recorded pressure in the Left ventricle? | 130/10 mm Hg |
| What is autoregulation in relation to blood circulation? | Blood flow to an organ remains constant over a wide range of perfusion pressures |
| What heart factors determine autoregulation? | Local metabolites (vasodilatory); adenosine, NO, CO2, and decreased Oxygen. |
| What factors determine autoregulation in the lungs? | Hypoxia causes vasoconstriction |
| What is unique about pulmonary vasculature ? | During hypoxia causes vasoconstriction so teha only well-ventilated areas are persuasive. |
| In most orgasn, except the lungs, hypoxia causes? | Vasodilation |
| What is the most important factor in skin autoregulation? | Sympathetic stimulation to control temperature. |
| What are local metabolites, used by skeletal muscle, that determine blood autoregulation? | Lactate, adenosine, K+, H+, and CO2. |
| Pc (capillary pressure) causes: | pushes fluid out of capillary |
| What force is in charge of pushing fluid into capillary? | Pi (interstitial fluid pressure) |
| Heart failure causes edema due to changes in what Starling force? | Increased capillary pressure |
| Which syndromes are characterized by a decrease in plasma proteins? | Nephrotic syndrome, liver failure, and protein malnutrition |
| A decrease in plasma colloid osmotic (oncotic) pressure is represented by: | rr c (pi c); which pulls fluid into capillary |
| What is the cause of Persistent truncus arteriosus? | Truncus arteriosus fails to divide into pulmonary truck and aorta due to lack of aorticopulmonary septum formation |
| What kind of septum defect is often seen with Persistent truncus arteriosus? | VSD |
| Failure of the aorticopulmonary septum to spiral | D-Transposition of great vessels |
| Tricuspid atresia requires of ________________________ to survive. | VSD and ASD |
| What is the MCC of Tetralogy of Fallot? | Anterosuperior displacement of the infundibular septum. |
| What is the MCC of childhood cyanosis? | Tetralogy of Fallot |
| What are the main four symptoms seen in ToF? | 1. Pulmonary infundibular stenosis 2. Right Ventricular hypertrophy 3. Overriding aorta 4. VSD |
| What is the main determinant of prognosis in ToF? | The degree of Pulmonary stenosis |
| Pulmonary stenosis in ToF causes: | 1. Forces R-to-L flow across the VSD --> RVH |
| Why does squatting help cyanosis in a ToF patient? | It increases SVR and decreases the Right to Left shunt |
| What condition is characterized by the Pulmonary veins draining into the right heart circulation? | Total anomalous pulmonary venous return |
| What kind of anomaly is associated with Lithium use during pregnancy? | Ebstein anomaly |
| What conditions are associated with Ebstein anomaly? | Tricuspid regurgitation and Right HF |
| Ebstein anomaly is: | Displacement of tricuspid valve leaflets downward into RV, artificially "atralizing" the ventricle. |
| Right-to-Left shunts cause "blue ______________" | babies |
| Left-to-Right shunts cause "blue _______________" | kids |
| Right to left shunts produce ---> ________________ cyanosis | Early |
| Left to right shunts produce -----> _______________ cyanosis | Late |
| VSD oxygen saturation is: | Increased in RV and pulmonary artery |
| What is the MC congenital heart defect? | VSD |
| What congenital heart defect is due to abnormal interatrial septum? | ASD |
| What anatomical areas of the heart have increased O2 saturation in ASD? | RA, RV and pulmonary artery |
| Which Left to Right shunt defect has a Loud S1; wide, fixed split S2? | ASD |
| Ostium secundum defects are most common cause of: | ASD |
| What is an uncorrected Left-to-Right shunt complication? | Eisenmenger syndrome |
| Why is there development of Pulmonary arterial hypertension in an uncorrected L-to-R shunt? | The increased pulmonary blood flow due to the ASD, VSD, or PDA, cause pathologic vascular remodeling, leading to Pulmonary HTN. |
| What is the compensation mechanism for Eisenmenger syndrome? | Right Ventricular hypertrophy, which causes the "functional" reversal of the shunt. |
| What are some clinical complications of Eisenmenger syndrome? | Late cyanosis, clubbing, and polycythemia |
| What condition is associated with Turner syndrome? | Coarctation of the aorta |
| Hypertension in the upper extremities and weak, delayed pulse in lower extremities? | Brachial-Femoral delay seen in Coarctation of the aorta |
| Notched ribs appearance on CXR? | Coarctation of aorta |
| What are some complications of Coarctation of the aorta? | HF, cerebral hemorrhage (berry aneurysms), aortic rupture, and possible endocarditis. |
| What congenital cardiac defects are associated with Fetal alcohol syndrome? | VSD, PDA, ASD, and tetralogy of Fallot |
| Congenital rubella is seen with: | PDA, pulmonary artery stenosis, and septal defects |
| Infant of diabetic mother often develops? | Transposition of the great vessels |
| A patient with Williams syndrome is associated with which congenital heart defects? | Supravalvular aortic stenosis |
| The 22q11 syndromes are associated with: | Truncus arteriosus and tetralogy of Fallot |
| What differentiates hypertensive urgency from Hypertensive emergency? | Emergency shows evidence of acute end-organ damage |
| What are examples of acute end-organ damage in hypertension? | Encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia. |
| Plaques or nodules composed of lipid-laden histiocytes in skin? | Xanthomas |
| Eyelid xanthoma is known as: | Xanthelasma |
| What are Tendinous xanthoma? | Lipid deposit in tendon, especially Achilles |
| What is the MC reason for appearance of Corneal arcus in a young patient? | Hypercholesterolemia |
| What are the two types of Arteriosclerosis? | Hyaline arteriosclerosis and Hyperplastic arteriosclerosis |
| What is and associated diseases of Hyaline arteriosclerosis? | Thickening of vessel walls in essential hypertension or diabetes mellitus |
| Hyperplastic arteriolosclerosis? | "Onion skinning" in severe HTN with proliferation of smooth muscle cells |
| What types of vessels are affected by Arteriosclerosis? | Small arteries and arterioles |
| Form of arteriosclerosis caused by buildup of cholesterol plaques. | Atherosclerosis |
| Atherosclerosis pathogenesis: | Endothelial cell dysfunctin ---> macrophage and LDL accumulation ---> foam cell formation --> fatty streaks --> smooth muscle cell migration, proliferation, and extracellular matrix deposition --> fibrous plaque --> complex atheromas. |
| Which type of aortic aneurysm is associated with Atherosclerosis? | Abdominal aortic aneurysm |
| What condition is related with palpable pulsatile abdominal mass? | Abdominal aortic aneurysm |
| What type of aortic aneurysm is associated with cystic medial degeneration? | Thoracic aortic aneurysm |
| What are risk factors are associated with Thoracic aortic aneurysm? | Hypertension, bicuspid aortic valve, connective tissue disease (Marfan syndrome). |
| What area is at most risk of an traumatic aortic rupture? | Aortic isthmus |
| Where is the aortic isthmus? | Proximal descending aorta just distal to origin of the Left Subclavian artery. |
| Longitudinal inteama tear of the aorta foring a false lumen? | Aortic dissection |
| What are the associated clinical features seen in a patient with presenting aortic dissection? | Tearing chest pain, of sudden onset, radiating to the back +/- markedly unequal BP in arms. |
| What is the Stanford type A aortic dissection? | Proximal; involves the Ascending aorta |
| What is the treatment for Stanford A dissection? | Surgery |
| What is the treatment for Stanford B dissection? | B-blockers, followed by vasodilators |
| What area is involved in a Stanford B aortic dissection? | Distal; involves descending aorta and/or aortic arch. |
| Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm; no myocyte necrosis | Angina |
| What is the MCC of Stable angina? | Secondary to atherosclerosis |
| What is the MCC of Variant (Prinzmetal) angina? | Secondary to coronary artery spasm |
| What are common triggers of Variant angina? | Ca2+ channel blockers, nitrates, and smoking cessation. |
| Type of angina that is due to thrombosis with incomplete coronary artery occlusion: | Unstable angina |
| Free wall rupture: | Produces tamponade; 5-14 days after initial MI |
| What is a key characteristic of Papillary muscle rupture? | Mitral regurgitation |
| Chronologically, usually which occurs first as a Post MI complication, Papillary Muscle rupture or Ventricular free wall rupture? | Papillary Muscle rupture |
| What post-MI complication is seen with friction rub? | Postinfarction fibrinous pericarditis |
| What are the common findings seen in Dilated cardiomyopathy? | HF, S3, systolic regurgitant murmur, dilated heart on echocardiogram, ballon appearance of heart on CXR. |
| Which viral agent often causes DCM? | Coxsackie B virus |
| Which are some common causes of DCM? | Chronic alcohol abuse, wet Beri beri, Coxsackie B virus, chronic cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis, sarcoidosis, peripartum cardiomyopathy. |
| Dilated cardiomyopathy is seen with __________________ dysfunction. | Systolic |
| What kind of hypertrophy is associated in DCM? | Eccentric (added in series) |
| Hypertrophic cardiomyopathy is autosomal ___________________ inheritance. | Dominant |
| Marked ventricular hypertrophy, often septal predominance. Myofibrillar disarray and fibrosis. | Hypertrophic cardiomyopathy |
| What is the mutation that causes HCM? | B-myosin heavy-chain mutation |
| Sudden death in young athletes? | Hypertrophic cardiomyopathy |
| What are the common findings in Hypertrophic Cardiomyopathy? | S4, systolic murmur. |
| Which two cardiomyopathies have diastolic dysfunction? | Hypertrophic and Restrictive |
| What is Loffler syndrome? | A common cause of Restrictive cardiomyopathy, seen with endomyocardial fibrosis with a prominent eosinophilic infiltrate |
| What cardiomyopathy is most associated with amyloid deposition? | Restrictive/Infiltrative cardiomyopathy |
| What are the main 3 signs of Left Heart failure? | Orthopnea, Paroxysmal nocturnal dyspnea, and Pulmonary edema |
| What are the 3 main signs of Right Heart failure? | Hepatomegaly (nutmeg liver), Jugular venous distension, and Peripheral edema |
| What's orthopnea? | Shortness of breath when supine |
| What is Paroxysmal nocturnal dyspnea? | Breathless awakening from sleep |
| What are "HF cells"? | Seen in LHF pulmonary edema; made up of hemosiderin-laden macrophages |
| What are common causes for an Hypovolemic shock? | Hemorrhage, dehydration, and burns |
| What are the MCC of Cardiogenic Shock? | Acute MI, HF, valvular dysfunction, and arrhythmia |
| Obstructive shock is due to: | Cardiac tamponade, pulmonary embolism |
| Sepsis, anaphylaxis, and CNS injury are common causes of __________________ shock. | Distributive shock |
| What is the main change in Hypovolemic shock? | A decrease in PCWP (preload) |
| Cardiogenic and obstructive shock main deficit is due to a decreased: | Cardiac output |
| Which type of shock has the greatest decrease in SVR (afterload)? | Distributive shock |
| What is the most common cause of Dry Distribute shock? | CNS injury |
| How is the skin in Hypovolemic, Cardiogenic, and Obstructive shock? | Cold and clammy |
| What is the treatment for cardiogenic shock? | Inotropes and diuresis |
| FROM JANE: | Fever Roth spots Osler nodes Murmur Janeway lesions Anemia Nail-bed hemorrhage Emboli |
| What is the most common organism to cause Subacute bacterial endocarditis? | viridans streptococci |
| What is a common heart sequelae of dental procedures | Subacute bacterial endocarditis |
| Which type of bacterial endocarditis has a gradual onset? | Subacute |
| What are Osler nodes? | Tender raised lesions on finger or toe pads |
| Small, painless, erythematous lesions on palm or sole | Janeway lesion |
| What are Roth spots? | Round white spots on retinal surrounded by hemorrhage |
| HACEK include: | Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella. |
| FROM JANE describes the MC symptoms of _________________. | Bacterial endocarditis |
| What is the most commonly involved valve in bacterial endocarditis? | Mitral valve |
| Which valve develops bacterial endocarditis in an IV user? | Tricuspid valve |
| Rheumatic fever is a consequence of: | Pharyngeal infection with group A B-hemolytic streptococci |
| Which type of valves are affected the most in Rheumatic fever? | High-pressure valves (mitral >>> aortic >> tricuspid) |
| What is the early lesion of Rheumatic fever? | Mitral regurgitation |
| Untreated MR due to Rheumatic Fever may turn into: | Mitral stenosis |
| What is the major criteria mnemonic of Rheumatic fever? | JONES |
| What does JONES criteria encloses? | Joint (migratory polyarthritis) O (carditis) Nodules in skin (subcutaneous) Erythema marginatum Sydenham chorea |
| What kind of Erythema is associated with RF? | Marginatum |
| What two histological findings are characteristic of Rheumatic fever? | Aschoff bodies and Anitschkow cells |
| What are Aschoff bodies? | Granuloma with giant cells in Rheumatic fever |
| What are the Anitschkow cells? | Enlarged macrophages with ovoid, wavy, rod-like nucleus in Rheumatic fever |
| What titers are elevated in RF? | ASO titers |
| Rheumatic fever is considered a type ______ hypersensitivity reaction. | II |
| What condition is due to antibodies of M protein cross-react with self antigens? | Rheumatic fever |
| What is the main treatment for Rheumatic fever? | Penicillin |
| Inflammation of the pericardium is known as: | Pericarditis |
| What is the clinical presentation of Pericarditis? | Sharp pain, aggravated by inspiration, and relieved by siting up and leaning forward |
| What condition is commonly seen with friction rub? | Pericarditis |
| What is the common findings on the ECG of pericarditis? | Widespread ST-segment elevation and/or PR depression |
| Which are common autoimmune disorders that cause pericarditis? | SLE, rheumatoid arthritis |
| Inflammation of myocardium leads to: | Global enlargement of heart and dilation of all chambers |
| What is the major cause of sudden cardiac death in adults over 40 years old? | Myocarditis |
| What is the term used for inflammation of the myocardium? | Myocarditis |
| What is the typical presentation of arrhythmias in a patient with myocarditis? | Tachycardia out of proportion to fever |
| Which are the most common viral causes of myocarditis? | Adenovirus, coxsackie B, parvovirus B19, HIV, and HHV-6 |
| What histological finding is highly indicative of viral myocarditis? | Lymphocytic infiltrate with focal necrosis |
| What drugs are often associated with myocarditis development? | Doxorubicin and cocaine |
| What is a cardiac tamponade? | Compression of the heart by fluid leading to a decrease in Cardiac output. |
| Which condition is seen with equilibration of diastolic pressures in all four chambers? | Cardiac tamponade |
| What triad is known to describe some symptoms of cardiac tamponade? | Beck triad |
| What are the components of the Beck triad? | Hypotension, distended neck veins, distant heart sounds |
| What characteristic pulse is seen in Cardiac tamponade? | Pulsus paradoxus |
| What are the findings of ECG in cardiac tamponade? | Low-voltage QRS and electrical alternans |
| What is the pulsus paradoxus? | decrease in amplitude in systolic BP by > 10 mm Hg during inspiration |
| What conditions are commonly seen with pulsus paradoxus? | Cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, and croup. |
| What is Syphilitic heart disease? | Tertiary syphilis disrupts the vasa vasorum of the aora with consequence atrophy of vessel walls and dilation of aorta and valve ring. |
| What are some consequences of Syphilitic heart disease? | Aneurysm of the ascending aorta or aortic arch, aortic insufficiency. |
| What condition is seen with "tree bark" appearance of aorta? | Syphilitic heart disease |
| What are the two main Large vessel vasculitis? | 1. Giant cell (temporal) arteritis 2. Takayasu arteritis |
| What is the MC population to develop Giant cell arteritis? | Elderly females |
| What are the most typical symptoms of Giant cell arteritis? | Unilateral headache, possible temporal artery tenderness, and jaw claudication |
| What condition is associated with possible irreversible blindness? | Giant cell (temporal) arteritis |
| Which artery is involved in the possible development of irreversible blindness in Giant cell arteritis? | Ophthalmic artery |
| What is a strong and common muscular association to Giant cell arteritis? | Polymyalgia rheumatica |
| What are the vessels most commonly affected by Giant cell arteritis? | Branches of Carotid artery |
| Vasculitis seen with Focal granulomatous inflammation and increased ESR? | Giant cell (temporal) arteritis |
| What is the treatment in GCA to prevent blindness? | High-dose corticosteroids |
| What is referred as the "Pulseless disease"? | Takayasu arteritis |
| What population is often seen with Takayasu arteritis? | Asian females < 40 years old |
| What is referred as weak upper extremity pulses? | "Pulseless disease" |
| What is the MC treatment for Takayasu arteritis? | Corticosteroids |
| What vascular structures are most commonly affected in Takayasu arteritis? | Aortic arch and proximal great vessels |
| What lab result is shared/common in Takayasu and Giant cell arteritis? | Increased ESR |
| Granulomatous narrowing and thickening of aortic arch and proximal great vessels? | Takayasu arteritis |
| What are the 3 MC Medium-vessel vasculitis? | 1. Polyarteritis nodosa (PAN) 2. Kawasaki Disease 3. Buerger disease |
| What is another name for Kawasaki disease? | Mucocutaneous lymph node syndrome |
| What is another way to refer to Buerger disease? | Thromboangiitis obliterans |
| What is the most common population to develop PAN? | Middle-aged men |
| What is a commonly associated infection with PAN? | Hepatitis B |
| Which arteries are usually affected in PAN? | Renal and visceral arteritis |
| Which vessels/arteries are spared in PAN? | Pulmonary arteries |
| What is the pathological changes seen in PAN? | Transmural inflammation of arterial wall with fibrinoid necrosis of the renal and visceral vessels |
| What vascularity is seen or described with different sates of inflammation coexinging in different vessels? | Polyarteritis nodosa (PAN) |
| What is a common arteriogram in a patient with PAN? | Innumerable renal microaneurysms and spams |
| What is the treatment of PAN? | Corticosteroids and Cyclophosphamide |
| Cyclophosphamide is used to treat which vascularity? | Polyarteritis nodosa (PAN) |
| What are the most significant symptom of PAN? | Systemic - fever, weight loss, and headache GI: abodominal pain, melena Other: HTN, neurologic dysfinction, cutaneous eruptions, and renal damage |
| Which population is commonly affected by Kawasaki disease? | Asian children < 4 years old |
| What is the common mnemonic used to describe the most significant features of Kawasaki disease? | CRASH and BURN |
| What is a common complication of Kawasaki disease? | Coronary artery aneurysms |
| Coronary artery aneurysms are often seen as an complication of which vasculitis? | Kawasaki disease |
| What is the treatment for Kawasaki disease? | IV immunoglobulin and aspirin |
| What does CRASH and BURN stand for in Kawasaki disease? | C- Conjunctival injection R- Rash A- Adenopathy S- Strawberry tongue H- Hand-foot changes Burn- Fever |
| What is the rash seen in Kawasaki disease? | Polymorphous ---> desquamating |
| Which lymph nodes are most affected in Kawasaki? | Cervical (adenopathy) |
| What is the simple term to describe Oral mucositis in Kawasaki disease? | Strawberry tongue |
| What changes are seen in Kawasaki by "Hand-foot changes" description? | Edema and erythema |
| What population is most affected by Buerger disease? | Heavy smokers, males < years old |
| What is the vessel pathology or changes in Buerger disease? | Segmental thrombosing vasculitis with vein and nerve involvement |
| Buerger disease involves the ______ and ______, along with arteries. | Vein and Nerve |
| What key phenomenon is seen in Buerger disease? | Raynaud phenomenon |
| What is the clinical presentation of Buerger disease? | Gangrene, autoamputation of digits, and superficial nodular phlebitis |
| What is the reason of the clinical symptoms of Buerger disease? | Intermittent claudication of affected vascular structures |
| What is the treatment for Buerger disease? | Smoking cessation |
| Which are the Small-vessel vasculitis? | 1. Granulomatosis with polyangiitis (Wegener) 2. Microscopic polyangiitis 3. Behcet syndrome 4. Eosinophilic granulomatosis with polyangiitis 5. Immunoglobulin A vasculitis |
| What is the triad of Wegener disease? | - Focal necrotizing vasculitis - Necrotizing granulomas in the lung and upper airway - Necrotizing glomerulonephritis |
| What are the Granulomatosis with polyangiitis upper respiratory tract symptoms? | Perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis |
| What are lower respiratory tract symptoms seen with Wegener disease? | Hemoptysis, cough, dyspnea |
| What type of renal features are seen with Wegener disease? | Hematuria and red blood cell casts |
| What antibodies are positive in Granulomatosis with polyangiitis? | PR3-ANCA/c-ANCA |
| CXR- large nodular densities + c-ANCA positive. Dx? | Wegener disease |
| What is the treatment of Wegener disease? | Cyclophosphamide, corticosteroids |
| What is another name for MPO-ANCA/p-ANCA? | Anti-myeloperoxidase |
| What vasculitis p-ANCA positive? | Microscopic polyangiitis |
| What is Microscopic polyangiitis? | Necrotizing vasculitis commonly involving lungs, kidneys, and skin with pauci-immune glomerulonephritis and palpable purpura. |
| What is the cutaneous involvement of Microscopic polyangiitis? | Palpable purpura |
| What are the most commonly involved organs in Microscopic polyangiitis? | Lung, kidneys, and skin |
| Which small vessel vasculitis is characterized by the absence of granulomas? | Microscopic polyangiitis |
| How to distinguish between Microscopic polyangiitis and Granulomatosis with polyangiitis? | Microscopic polyangiitis has no NASOPHARYNGEAL involvement. |
| What population is commonly affected with Behcet syndrome? | Turkish an eastern Mediterranean descent |
| Immune complex vasculitis? | Behcet syndrome |
| What vasculitis is associated with HLA-B51? | Behcet syndrome |
| Clinical features of Behcet syndrome? | Recurrent aphthous ulcers, genital ulcerations, uveitis, erythema nodosum. |
| What viral infections are associated with development of Behcet syndrome? | HSV or Parvovirus |
| What is a common name of Eosinophilic granulomatosis with polyangiitis? | Churg-Strauss syndrome |
| p-ANCA (+) and increased levels of IgE level. Most common vasculitis? | Churg-Strauss syndrome |
| Granulomatous, necrotizing vasculitis with eosinophilia? | Churg-Strauss syndrome |
| What is the most common neurological manifestations of Churg-Strauss syndrome? | Wrist/foot drop |
| What kind of kidney involvement is seen in Eosinophilic granulomatosis with polyangiitis? | Pauci-immune glomerulonephritis |
| What is another name of IgA vasculitis? | Henoch-Schonlein purpura (HSP) |
| Vasculitis secondary to IgA immune complex deposition? | Immunoglobulin A vasculitis |
| What glomerular condition is associated with HSP? | IgA nephropathy |
| Berger disease is associated with _______________ vasculitis. | Immunoglobulin A vasculitis. |
| What is the classic triad of Immunoglobulin A vasculitis? | 1. Skin: palpable purpura on buttocks/legs 2. Arthralgias 3. GI: abdominal pain |
| What is the GI complication is often resulting in IgA vasculitis? | Intussusception |
| What is the most common precipitating factor of IgA vasculitis? | URI |
| What is the MC heart tumor? | Metastasis |
| What is the most common primary heart tumor of adults? | Myxoma |
| Where is the MC location for a myxoma? | Atria (Left atrium MC) |
| What is a common associated symptom of myxoma? | Multiple syncopal episodes |
| What is the common auscultation finding of a Myxoma? | Early diastolic "tumor plop" sound |
| Myxoma histology is described as: | Gelatinous material, myxoma cells immersed in glycosaminoglycans |
| "ball valve" obstruction in atrium. Dx? | Myxoma |
| What is the most frequent primary cardiac tumor in children? | Rhabdomyomas |
| What Autosomal Dominant disorder is associated with Rhabdomyomas? | Tuberous Sclerosis |
| What is the common histological description used in Rhabdomyomas? | Hamartomatous growths |
| What is the Kussmaul sign? | Increase in JVP on inspiration instead of a normal decrease |
| What are some common conditions that exhibit Kussmaul sign? | Constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors |
| What is another named for Hereditary hemorrhagic telangiectasia? | Osler-Weber-Rendu syndrome |
| What is an AD inherited disorder of blood vessels? | Osler-Weber-Rendu syndrome |
| What are the most significant clinical features of Osler-Weber-Rendu syndrome? | 1. Blanching lesions (telangiectasias) on skin and mucous membranes 2. Recurrent epistaxis 3. Skin discolorations, 4. Arteriovenous malformations (AVMs) 5. GI bleeding 6. Hematuria |
| List of medications used for Primary (essential) hypertension: | Thiazide diuretics, ACE inhibitors, ARBs, dihydropyridine Ca2+ channel blockers |
| What kind of Calcium channel blockers are used in the treatment of essential HTN? | Dihydropyridine Ca2+ channel blockers |
| Hypertension with Heart failure (HF) is commonly treated with: | Diuretics, ACE inhibitors/ARBs, B-blockers (compensated HF), aldosterone antagonists |
| B-blockers are completely contraindicated in HTN with HF treatment in patients presenting with what kind of shock? | Cardiogenic |
| B-blockers in treating HTN with HF are to be used carefully in pts with: | Decompensated heart failure (HF) |
| In HF, ARBs may be combined with what? | Neprilysin inhibitor (sacubitril) |
| What is a commonly used Neprilysin inhibitor in combination with Valsartan? | Sacubitril |
| Which antihypertensive medications are protective against diabetic nephropathy? | ACE inhibitors and ARBs |
| What does ARBs stand for? | Angiotensin II receptor blockers |
| What kind of beta-blockers can be used in treatment of HTN in a person with asthma? | Selective B-blockers |
| Which kind of B-blocker category should be avoided in a Asthmatic person? | Non-selective B-blocker |
| Why are non-selective beta-blockers not used in asthmatic patients? | They induce bronchoconstriction |
| Hypertension in asthma should avoid two types of medications: | 1. Non-selective B-blockers 2. ACE inhibitors |
| Why are ACE inhibitors to be avoided in Asthma patients? | To prevent confusion between drug or asthma-related cough |
| What are the antihypertensives used in pregnancy? | Hydralazine, Labetalol, methyldopa, and Nifedipine |
| What are the dihydropyridine Calcium channel blockers? | Amlodipine, Clevidipine, Nicardipine, Nifedipine, and Nimodipine |
| Where do dihydropyridine Calcium channel blockers work on? | Vascular smooth muscle |
| Which Ca2+ Channel blockers work on the vascular smooth muscle? | Dihydropyridine |
| Which are the two most common Non-dihydropyridine Ca2+ channel blockers? | Diltiazem and Verapamil |
| Where do Non-Dihydropyridine Calcium channel blockers act on? | Heart |
| Verapamil and Diltiazem are: | Non-dihydropyridine Calcium channel blockers |
| What is the MOA of Calcium channel blockers? | Block voltage-dependent L-type calcium channels of cardiac and smooth muscle |
| What is the result of calcium channel blockade by Calcium channel blockers? | Decrease muscle contractility |
| What are the clinical uses of non-dihydropyridine Ca2+ channel blockers? | Hypertension, angina, atrial fibrillation/flutter |
| With the exception of Nimodipine, what are the general clinical uses for dihydropyridine CCBs? | HTN, angina (including Prinzmetal), Raynaud phenomenon |
| What medication is used to treat Raynaud phenomenon? | Dihydropyridine calcium channel blockers |
| What is the most important clinical use for Nimodipine? | Subarachnoid hemorrhage |
| Why is Nimodipine used in SAH? | Prevent cerebral vasospasm |
| Which dihydropyridine Calcium channel blockers are used in Hypertensive urgency or emergency? | Nicardipine and Clevidipine |
| What are the associated adverse effects of Non-dihydropyridine CCBs? | Cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia |
| What is a common oral/buccal side effect of Verapamil therapy? | Gingival hyperplasia |
| Prolonged use of Diltiazem can cause what hormonal imbalance? | Hyperprolactinemia |
| What is the general mechanism of action of Hydralazine? | Increase cGMP ----> smooth muscle relaxation |
| Hydralazine has a greater vasodilatory effect on arteries or veins? | Arteries |
| The arterial vasodilation caused by Hydralazine causes what to the afterload? | Reduction |
| Hydralazine potential reflex tachycardia is often prevented with coadministration of a ___________________. | B-blocker |
| What are the two main uses for hydralazine? | Severe (acute) hypertension |
| What are the adverse effects seen with Hydralazine? | 1. Compensatory tachycardia 2. Fluid retention, headache, angina 3. SLE-like syndrome |
| SLE-like syndrome is an adverse effect of: | Hydralazine |
| What are the common medication used to treat Hypertensive emergency? | Clevidipine, Fenoldopam, Labetalol, Nicardipine, or Nitroprusside |
| What is an associated toxicity seen with Nitroprusside therapy in HTN emergency? | Cyanide toxicity |
| What is the MOA of Nitroprusside? | Short acting; Increase cGMP via direct release of NO |
| Quick acting and the increase of cGMP via direct release of Nitric monoxide, descries the mode of action of _______________. | Nitroprusside |
| Dopamine D1 receptor agonist used in Hypertensive emergency. | Fenoldopam |
| What is the function of Fenoldopam? | Vasodilation of coronary, peripheral, renal , and splanchnic arteries due to Dopamine D1 stimulation. |
| Which dopamine receptor is stimulated by Fenoldopam? | D1 |
| What is a common antihypertensive used postoperative? | Fenoldopam |
| What are the MC nitrates? | Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate |
| What is the MOA of nitrates? | Vasodilate by increase NO in vascular smooth muscle ---> increase in cGMP and smooth muscle relaxation. |
| Which vessels (vein or artery) are more affected with Nitrates? | Veins |
| The vasodilation caused by nitrates causes a ________ in preload. | Decrease |
| Hydralazine decreases the _________________, while Nitrates decrease the __________________. | Hydralazine --> decrease afterload Nitrates ----> decrease preload |
| What are the 3 main uses of Nitrates? | Angina, Acute coronary syndrome, and Pulmonary edema |
| What is "Monday disease"? | Development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend |
| What are the effects of the "loss" of tolerance over the weekend seen in Monday disease? | Tachycardia, dizziness, headache upon exposure |
| Mine worker complains of palpitations, headache, and N/V on several Monday mornings last month. Dx? | Monday Disease |
| What condition contraindicates the use of Nitrate on a patient? | History of Right ventricular infarction |
| What are some Adverse effects of Nitrates? | Reflex tachycardia (tx with Beta blockers), hypotension, flushing and "Monday disease". |
| What is the ultimate goal of Antianginal therapy? | Reduction of myocardial O2 consumption (MVO2) |
| What are the determinants of MVO2? | End-diastolic volume, Blood pressure, Heart Rate, and Contractility |
| What therapeutic combination has the greatest decrease in MVO2? | Nitrates + B-blockers |
| What antiarrhythmic type causes an increase in Ejection time? | B-blockers |
| What calcium channel blocker has similar effect to B-blockers? | Verapamil |
| When is Ranolazine used? | Angina refractory to other medical therapies |
| What is the MOA of Ranolazine? | Inhibits the LATE phase of Sodium current thereby reducing diastolic wall tension and oxygen consumptions |
| How is HR and Contractility affected by Ranolazine? | Unaffected |
| What is an important adverse ECG effect of Ranolazine? | QT prolongation |
| Selective PDE-3 inhibitor? | Milrinone |
| Milrinone is an ___________________________________. | Selective PDE-3 inhibitor |
| What is accumulated in the use of Milrinone? | cAMP |
| What is the ultimate effect/result of the use of Milrinone on Cardiomyocytes? | Increase inotropy and chronotropy |
| What is the ultimate result of the use of Milrinone on vascular smooth muscle? | General vasodilation |
| What is the main clinical use for Milrinone? | Short-term use in acute decompensated HF |
| What are the two classes of Lipid-lowering agents that decrease the most LDL levels? | 1. HMG-CoA reductase inhibitors 2. PCSK9 inhibitors |
| What is the MOA of Statins? | Inhibit conversion of HMG-CoA o mevalonate,a cholesterol precursor |
| Which type of lipid-lowering agent as proven to decrease mortality in CAD patiens? | HMG-CoA reductase inhibitors |
| What are the main side effects of Statin therapy? | 1. Hepatotoxicity 2. Myopathy |
| Myopathy is often an adverse effect of Statin therapy, especially when co-administered with? | Fibrates or Niacin |
| What are common Bile acid resins? | Cholestyramine, Colestipol, and Colesevelam |
| What is the MOA of Bile acid resins? | Prevent intestinal reabsorption of bile acids |
| What are the associated side effects of Bile acid resins? | 1. Decrease absorption fat-soluble vitamins 2. GI upset |
| What is the mode of action of Ezetimibe? | Prevents cholesterol absorption at small intestine brush border |
| What is the main type of lipid decrease when using Fibrate? | Triglycerides |
| What are some commonly referred Fibrates? | Gemfibrozil, Bezafibrate, and Fenofibrate |
| What are the MOA of fibrates? | 1. Upregulate LPL --> Increase TG clearance 2. Activates PPAR-a to induce HDL synthesis |
| What kind of lipid lowering drug acts by activating the PPAR-a ? | Fibrates |
| Upregulation of the LPL is seen with the use of ____________. | Fibrates |
| What are the most common adverse effects of fibrate therapy? | 1. Myopathy (increase risk with statins), 2. Cholesterol gallstones |
| A person with cholesterol gallstones is very likely to be using ____________, as a lipid lowering agent. | Fibrates |
| What is the method by which cholesterol gallstones appear in fibrate therapy? | Via inhibition of cholesterol 7a-hydroxylase |
| What is the mode of action of Niacin? | Inhibits lipolysis in adipose tissue |
| What enzyme activity is inhibited by Niacin? | Hormone-sensitive lipase |
| What are the associated adverse effects associated with Niacin? | Flushed face, hyperglycemia, and hyperuricemia |
| What arthritic-condition is possibly developed in long term Niacin therapy? | Gout due to hyperuricemia |
| What two substances are overly secreted as an adverse effect of Niacin? | Uric acid and glucose |
| What lipid lowering agent reduces hepatic VLDL levels? | Niacin |
| MOA of PCSK9 inhibitors? | Inactivation of LDL-receptor degradation --> increased removal of LDL from bloodstream |
| Common adverse effects of PCSK9 inhibitors | Myalgias, delirium, dementia, and other neurocognitive defects |
| What are the benefits of Fish oil and marine omega-3 fatty acids therapy? | Slightly increase in HDL and slight decrease in Triglycerides |
| Which lipid lowering agents work on the liver directly? | Statins and PCSK9 inhibitors |
| Adipose lipolysis is done by __________, a common lipid lowering agent. | Niacin |
| Which lipid lowering agents are categorized as LPL-upregulators? | Fibrates |
| Where do Bile acid resins and Ezetimibe exert their actions? | Intestinal lumen |
| Which lipid-lowering drugs are referred as Mevalonate synthesis agents? | Statins |
| Which 2 types of lipid lowering agents work in the Blood? | Niacin and Fibrates |
| Which lipid lowering agent is categorized as "cholesterol absorption" agent? | Ezetimibe |
| Which type of lipid lowering medication is said to be a "LDL-receptor degradation"? | PCSK9 Inhibitors |
| Which are some common PCSK9 inhibitors? | Alirocumab and Evelocumab |
| Most common cardiac glycoside? | Digoxin |
| What is the direct inhibition in the MOA of Digoxin? | Inhibition of NA+/K+ ATPase |
| What is the INDIRECT inhibition of Digoxin mode of action? | Inhibition of Na+/Ca2+ exchanger |
| The increased levels of Ca2+ concentration by the use of Digoxin, ultimately cause? | Positive inotropy |
| Besides the positive inotropic effects of Digoxin, what is another mechanism of action displayed by such cardiac glycoside? | Stimulation of Vagus nerve to decrease Heart rate |
| Stimulation of the Vagus nerve causes ---> | Decrease heart rate (bradycardia) |
| Positive inotropy by Digoxin means = | Increase cardiac contraction |
| What is the most common type of arrhythmia treated with Digoxin? | Atrial fibrillation |
| Why is Digoxin used to treat AFIB? | Decrease conduction at AV node and depression of SA node |
| What are some significant adverse effects of Digoxin? | 1. Cholinergic effects (N/V, diarrhea) 2. Blurry yellow vision, 3. Arrhythmias 4. AV block 5. Hyperkalemia |
| Hyperkalemia in the setting of Digoxin toxicity indicates --> | Poor prognosis |
| What are some factors that predispose to Digoxin toxicity? | 1. Renal failure (decrease excretion) 2. Hypokalemia 3. Drugs: 3a. Displace Digoxin binding site, and, 3b. Decreased clearance (verapamil, amiodarone, quinidine) |
| What are 3 common drugs that predispose to Digoxin toxicity due to its interaction leading to a decrease clearance rate of digoxin? | Verapamil, Amiodarone, and Quinidine |
| Why does hypokalemia increase the risk of Digoxin toxicity? | Creates environment permissive for Digoxin binding at K+-binding site on Na+/K+ ATPase. |
| What is the treatment and antidote to Digoxin toxicity? | Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments (antidote), and Mg2+. |
| What is the main function of Sodium channel blockers? | 1. Slow or block conduction in depolarized cells 2. Decrease slope 0 depolarization |
| Which cells are especially preferencial to Sodium channel blockers? | Depolarized cells |
| A depolarized cell has a less ____________ charge _________. | Negative; Inside |
| What is meant by Na+ channel blocker been State dependent? | Selectively depress tissue that is frequently depolarized |
| What is the most basic and clear manifestation of a tissue been frequently depolarized? | Tachycardia |
| What are the Class IA sodium channel blockers? | Quinidine, Procainamide, Disopyramide |
| What phase is affected by Na+ channel blockers? | Slope of phase 0 (I Na) |
| Which Na+ channel blocker has the strongest blockage/change in slope 0 of the actin potential? | Class IC |
| What is the magnitude order, from weakest to strongest, sodium channel blockage of slope 0? | Class IB < Class IA <<Class IC |
| Which type of Na+ channel have the most significant increase in AP duration? | Class IA |
| Which sodium channel blocker category has some Potassium channel blocking effects? | Class IA |
| What are the clinical uses of Class IA sodium channel blockers? | Atrial and ventricular arrhythmias, especially SVT and V-TACH |
| What are the two most significant arrhythmias treated with Class IA Na+ channel blockers? | SVT and V-TACH |
| What are the associated adverse effects of Quinidine? | Cinchonism (headache and tinnitus) |
| What are the components of Cinchonism? | Headache and Tinnitus in patients on Quinidine |
| What is the most important adverse effect of Procainamide antiarrhythmic? | reversible SLE-like syndrome |
| Reversible SLE-like syndrome is seen with the use of __________. | Procainamide |
| What is the specific adverse effect seen with Disopyramide? | Heart failure |
| What are some adverse effects seen with all Class IA Sodium channel blockers? | Thrombocytopenia, torsades de Pointes due to Incrased QT interval |
| The increase in QT interval induced by sodium channel blockers is responsible for the development of: | Torsades de pointes |
| Which are the main 2 Class IB sodium channel blockers? | Lidocaine and Mexiletine |
| Which is a common anti-convulsive that may be consider a Class IB Na+ channel blocker? | Phenytoin |
| What is the effect on AP with Class IB sodium channel blockers? | Decrease |
| What tissue is preferably affected by Class IB sodium channel blockers? | Ischemic or depolarized Purkinje and ventricular tissue. |
| Ischemic or depolarized Purkinje or ventricular tissue, is best targeted by which Na+ channel blocker class? | Class IB |
| What are the two most common arrhythmias treated with Class IB sodium channel blockers? | - Acute ventricular arrhythmias - Digitalis-induced arrhythmias |
| A patient develops a fast arrhythmic heart rate after a mistakenly doubling the dosage of digitalis. What is a common drug used to treat that arrhytmia? | Class IB Na+ channel blockers |
| What class of Na+ blocker is best for Post-MI ventricular arrhythmias? | Class IB |
| What are the two most common Class IC Na+ channel blockers? | Flecainide and Propafenone |
| Flecainide and Propafenone are: | Class IC Sodium channel blockers |
| In which tissue do Class IC sodium channel blockers have their strongest effect? | Significantly prolongs ERP in AV node and accessory bypass tracts |
| What is the most significant change by using Class IC Na+ channel blockers? | Prolongation of ERP |
| What are the adverse effects associated with Class IC sodium channel blockers? | Proarrhythmic, especially post-MI |
| A patient with a recent Hx of and MI, should never be treated with what class of Na+ channel blockers? | Class IC |
| What can be use as last resort in refractory V-Tach? | Class IC Sodium channel blockers |
| What are the Class II antiarrhythmics? | B-blockers |
| What phase is affected by the use of B-blockers? | Decrease slope of phase 4 |
| Which cardiac node (AV or SA) is more sensitive to the actions/effects of B-blockers? | AV node |
| What ECG change is seen by the use of a beta-blocker? | Increase in PR interval by stimulating the AV node. |
| Which a very short acting beta blocker? | Esmolol |
| What is the MOA of Beta blockers? | Decrease SA and AV nodal activity by decreasing cAMP, and decrease in Ca2+ currents |
| Which type of currents are decreased in activity by the use of Class II antiarrhythmics? | Calcium ion currents |
| cAMP is __________________ by the use of beta blockers. | Decreased |
| Arrhythmic uses of Beta-blockers | 1. SVT 2. Ventricular rate control for AFIB and A-flutter |
| What sort of antiarrhythmics are used to control the ventricular rate of AFIB/AFLUTTER? | B-blockers |
| May mask signs of hypoglycemia | B-blockers |
| What are the important adverse respiratory effects seen with B-blockers? | Exacerbation of COPD and asthma |
| Which Beta blocker is known to cause dyslipidemia? | Metoprolol |
| What is an important and specific adverse effect of Propranolol? | Exacerbate vasospasm in vasospastic angina |
| What is the risk of administering B-blockers to a patient with Pheochromocytoma? | Unopposed alpha-1 - agonism |
| What type of antiarrhythmic is must be avoided in a patient with a cocaine addiction? | B-blockers |
| Why are B-blockers contraindicated in a patient with cocaine overdose/abuse? | Unopposed alpha-1 - agonism |
| What is the treatment of B-blocker overdose? | Saline, atropine, and glucagon. |
| Decrease slope of phase 4 depolarization is seen with: | B-blockers |
| Which are the non-selective beta blockers? | Carvedilol and Labetalol |
| What are the 4 most important Class III antiarrhythmics? | Amiodarone, Ibutilide, Dofetilide, and Sotalol |
| What channel is blocked by Class III antiarrhythmics? | Potassium channels |
| Which two arrhythmias are treated by all Class III antiarrhythmics? | Afib and A flutter |
| V-Tach can be treated with which 2 Potassium channel blockers? | Amiodarone and Sotalol |
| What 3 features of the AP and ECG are increased by K+channel blockers? | AP duration, ERP, and QT interval |
| Which are the specific adverse effects of Sotalol? | Torsades de pointes and excessive B-blockade |
| Which two K+ channel blockers are associated with development of torsades de pointes? | Sotalol and Ibutilide |
| What is the reason by which Amiodarone can have Class I, II, III, and IV antiarrhythmic properties? | Lipophilic |
| Which antiarrhythmic is said to be a "lipid lover"? | Amiodarone |
| Markedly prolonged repolarization is seen with? | Class III Potassium channel blockers |
| Which function tests are to be monitored in a patient on Amiodarone? | Pulmonary (PFTs), Hepatic (LFTs), and Thyroid (TFTs) |
| What are the main 3 adverse effect of Amiodarone, that require function test revision? | Pulmonary fibrosis, hepatotoxicity, and hypo-or hyperthyroidism |
| What are the ocular side effects of Amiodarone therapy? | Corneal deposits |
| Reason to which the ocular and skin adverse effects of Amiodarone? | It acts as a hapten |
| What is the cutaneous manifestations of Amiodarone adverse effects? | Blue-gray skin deposits resulting in photodermatitis |
| What are two common calcium channel blockers? | Diltiazem and Verapamil |
| What are class IV antiarrhythmics? | Calcium channel blockers |
| What is the mechanism of action of Calcium channel blockers? | Decrease conduction Velocity, Increase ERP, and Increase PR interval |
| What are the common adverse effects of Ca2+ channel blockers? | Constipation, flushing, edema, cardiovascular effects |
| Calcium Channel blockers cause: | 1. Slow rise of action potential 2. Prolonged repolarization at AV node |
| What is the MOA of Adenosine? | Increase K+ out of cells --> hyperpolarizing the cell and decrease Calcium current, decreasing AV node conduction |
| What is the drug of choice used to diagnose SVT? | Adenosine |
| What medications or compounds can blunt the effects of Adenosine? | Theophylline and caffeine |
| What are the most common side effects of Adenosine? | Flushing, hypotension, chest pain, sense of impending doom, and bronchospasm |
| What is the action exerted by Ivabradine? | Prolongs the slow depolarization (phase IV) |
| How does Ivabradine prolong phase IV? | Selectively inhibiting "funny" sodium channels (I f) |
| When is Ivabradine used? | In patients unable to tolerate B-blockers and those with HF with reduced Ejection fraction |
| What are characteristic adverse effects seen with Ivabradine? | Luminous phenomena/ visual brightness, HTN, and bradycardia |
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