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Cardiology 1.1
UWORLD Cardio Review
| Question | Answer |
|---|---|
| Defective type 1 collagen | Osteogenesis imperfecta |
| What organs/tissues are made of Collagen type 1? | Dermins, Bones, Tendons, Dentin, Cornea, blood vessels, and scar tissue. |
| Cartilage, vitreous humor, and nucleus pulposus | Type 2 cartilage |
| What organs/tissues are made of Collagen type 3? | Skins, lungs, intestines, blood vessels, bone marrow, lymph nodes and granular tissue |
| Basement membrane is made of Collagen type _______. | Collagen type 4 |
| Alport syndrome | Autoimmune disease against to collagen type 4 |
| Defective collagen 4 synthesis. Dx? | Goodpasture Syndrome (RPGN) |
| What is the cause of Decompensated heart failure? | Left-ventricular Systolic/Diastolic dysfunction. |
| What are unique characteristics of CXR decompensated heart failure? | 1. Cephalization of Pulmonary vessels 2. Peripheral Alveolar edema 3. Blunting of costovertebral angles |
| Where does a Pulmonary artery catheter to diagnose? | Pulmonary HTN |
| The pressure recorded at the end of a pulmonary artery catheter, it closely resembles? | Left PCWP |
| What is the MC site for Aortic rupture? | Aortic ISTHMUS |
| How is the IVC formed? | Junction of the Right and Left common iliac veins at the L4-L5. |
| At vertebral level is the IVC formed? | L4-L5 |
| The _________ is formed by the junction or joining of the _________ and _________ ___________________ veins. | IVC: Right and Left Common Iliac veins. |
| A 3 AV Block is due to dysfunction of? | Complete dysfunction of the PURJINKE fibers. |
| What node or area has the lowest conduction? | AV Node |
| 45-55 bpm is seen commonly at: | AV Node |
| The ________ node has a velocity of __________________ bpm. | SA; 60-100 bpm |
| What is the approximate pressure of the right atrium? | 1-6 mm Hg |
| the right ventricle has an approximate pressure of ______________ mm Hg. | 15-30 |
| What is the approximate pressure of PCWP? | 6-12 mm Hg |
| A pressure of 9 mm Hg, mostly would indicate which location? | Pulmonary artery prior entrance to Left Atrium |
| What is the approximate pressure of the normal Left ventricle (LV)? | 90-140/6-12 |
| How many days after an MI, is a Left free wall rupture commonly seen? | 5-14 days |
| After 9 days of MI, the patient is a risk of development of? | Left Free Wall rupture |
| How is Left Free Wall rupture clinically manifested? | Sudden onset of chest pain, profound shock and rapid death |
| Why is the Left Free wall prefered than the right? | The rupture is seen in the left due to higher pressure than the right. |
| The ______________ flow is the _________________ to the power of _____. | blood flow; radius; 4 |
| Resistance is ________________________ proportionately to blood flow. | Inversely |
| The reduction of the ____________ by factor of _______, leads to a _________ decrease of original _____________ size. | radius; 16; 50%; radius |
| What proteins is produced by Strep Viridans, that help to colonize dental and heart valves? | Dextrans |
| The MCC of Subacute Bacterial Endocarditis is? | Infection by Strep Viridians |
| Common procedure associated with S. viridans infection, leading to Subacute Bacterial endocarditis? | Dental procedures |
| Strep Viridans is an ________-hemolytic and _________________ _________________. | alpha; bacitracin-resistant |
| What is the MCC of Rheumatic Heart disease? | Streptococcus pyogenes |
| What murmur is acutely developed in Rheumatic Heart disease? | Mitral Regurgitation (MR) |
| Holosystolic murmur with radiation to the AXILLA and best heard at the APEX of the heart. | Mitral Regurgitation (MR) |
| Mitral Stenosis (MS) is a ____________________ murmur, with a _____________ at the beginning of _______________. | Diastolic; OPENING SNAP; DIASTOLE |
| Low-pitch and mid-systolic rumbling, diastolic murmur, and long secuela of rheumatic fever disease. | Mitral Stenosis (MS) |
| Aortic Stenosis (AS): | Associated bicuspid Aortic valve. Radiation carotids. Crescendo-decrescendo |
| crescendo-decrescendo | Aortic Stenosis (AS) |
| What is the mutation seen in Pulmonary HTN? | BMPR2 gene |
| What does a BMPR2 gene mutation causes? | Excessive proliferation of endocardial and smooth muscle proliferation, which is the 1st hit in Pulmonary HTN pathogenesis. |
| What is the second "hit" in the 2-hit hypothesis of Pulmonary HTN pathogenesis? | D2 activation |
| Asymmetric ventricular septal hypertrophy is seen in which cardiomyopathy? | HYPERTROPHIC |
| Hypertrophic cardiomyopathy causes: | dynamic left ventricular outflow tract obstruction |
| What pathology causes the "pushing" toward to the INTERVENTRICULAR SEPTUM by the anterior mitral leaflet. | Hypertrophic cardiomyopathy |
| Blood reaching the heart defines the principle of _____________ | Preload |
| What decreases preload? Why? | 1. Sudden standing 2. Valsalva (straining) 3. Nitroglycerin Less blood reaches the heart |
| What actions increase preload? Pathogenesis? | 1. Squatting 2. Sustained handgrip 3. Passive leg raise More blood reaches the RIGHT atrium |
| A _____________________ infusion increases the ____________________. | Phenylephrine; AFTERLOAD |
| Increased afterload leads to a : | 1. Increase in End Systolic Volume (ESV) 2. Decrease in Stroke Volume (SV) |
| Afterload is due to: | 1. increased vascular resistance (HTN) 2. Semilunar valve damage |
| Which are the SEMILUNAR valves: | Aortic and Pulmonary valves |
| The Atrioventricular valves are: | Mitral (bicuspid) and Tricuspid valves |
| Damaged Aortic valve will lead to a probable increase in: | Afterload |
| What are the main reasons for increased Preload? | 1. Fast filling time 2. Increased venous return |
| Increased preload causes: | Increased End Diastolic Volume (EDV) and increased stroke volume. |
| Hypothyroidism is a cause of: | decreased Preload |
| Afterload increased is seen with ___________________________. | Handgrip |
| A sustained ______________________, raises both ___________________ and ________________, but the _________________ effects are dominant. | Handgrip; afterload and preload; Afterloads |
| Increase in afterload leads to a decrease in intensity of which murmur? | Hypertrophic cardiomyopathy |
| Which murmurs increase with Expiration? | Left sided murmurs, such as Aortic regurgitation |
| Murmurs that increase with INSPIRATION are _____________ sided | Right |
| Where is Aortic regurgitation best heard? | Left-sternal border, at the 4th/5th intercostals, and by sitting up and leaning forward. |
| MCC of aortic stenosis | Calcific degeneration of the aortic valve |
| Harsh, systolic murmur, best heard at the 2nd intercostal with carotid radiation? | Aortic Stenosis (AS) |
| MTHFR deficiency? | Most common cause of elevated levels of HOMOCYSTEINE |
| What vitamin cofactors are used in the Folic and Methionine cycles? | Vitamin B12 and Vitamin B6 |
| What type of diseases or condition increase the risk of developing Infective endocarditis? | Rheumatic Fever disease, Prosthetic valves, and congenital heart disease, as these cause damage to heart valves. |
| What is Beck's Triad? | The triad of symptoms seen with Cardiac TAMPONADE 1. hypotension 2. Pulsus paradoxus 3. Muffled heart sounds |
| What are common disorders that lead to developing a cardiac tamponade? | Malignancy and Radiation therapy, Viral and Bacterial infections, medication (INH/hydralazine), and connective tissue diseases such as SLE and RA. |
| Where is DIGOXIN cleaved in the body? | Kidneys |
| It is fine to assume ______________________ in the elderly, leading to increased risk of intoxication with a renal metabolism drug. | mild kidney deficiency |
| Digoxin side effects in the cardiac, GI, and Neurological systems? | Cardiac --> arrhythmias due to Hyperkalemia GI --> Nausea, vomiting, abdominal pain Neuro --> Yellow-vision, fatigue, weakness |
| Hypokalemic patient is at increased risk of __________________ toxicity. | Digoxin |
| Digoxin's clearance is decrease as it interacts with: | Verapamil, quinidine, and amiodarone |
| What is the treatment for Digoxin toxicity? | 1. Normalize K+ level, 2. Cardiac Pacer, 3. ANTI DIGOXIN Fab-fragments, 4. Mg2+ |
| How does digoxin treat Heart Failure (HF)? | Increase contractility |
| What is the action of Digoxin that helps the treatment of Atrial fibrillation? | Decrease conduction of the AV node and depression of the SA node |
| Overdose of Beta blockers is treated with? | Glucagon |
| Glucagon: | Raises heart rate and contractility, without any adrenergic effects |
| What is Digoxin's direct MoA? | Inhibition of the Na+/K+ - ATP pump, leading to increased [Na] |
| What is DIgoxin's INDIRECT effect? | Inhibition of the Na+/Ca2+ exchange, leading to an increase in [Ca2+] |
| The resultant decrease in AV conduction by digoxin causes: | An increase in PS (parasympathetic) vagal tone ( decreased HR) |
| A CT of the heart depicts the _________________ as the most anterior part of the heart. | Right Ventricle |
| Which chamber of the heart is most likely to be injured in a knife wound directly in the anterior chest? | Right Ventricle |
| Which chamber is in closest proximity to the esophagus? | Left Atrium |
| Dysphagia and hoarseness of the voice may be due to enlargement of the ____________, leading to ____________________ of the _____________ and ___________________, respectively. | Left Atrium; COMPRESSION; Esophagus; Left recurrent Laryngeal nerve |
| Which muscles are penetrated in a anterior chest knife wound? | Pectoralis major, Transverse Thoracic muscle, and Pericardium |
| Sterile thrombi (platelet) on cardiac valve | Non-bacterial Thrombotic Endocarditis (NBTE) |
| NBTE is associated with malignancies and inflammatory diseases such as: | SLE, antiPhospholipid syndrome, and sepsis. |
| A damaged cardiac muscle lead to a decreased _________________, which activates 3 neuronal responses: | Cardiac Output; 1. SNS activation --> Increased HR and contractility + Vasoconstriction 2. Renin-Angiotensin activation --> Vasoconstriction + Increased extracellular volume 3. ADH secretion --> Increased extracellular volume |
| The long term neuronal activations and its immediate physiologic responses help to maintain _________________________. | Blood pressure |
| What are the numbers for hypertensive Crisis? | Persistent DIASTOLIC pressure exceeding 130 mm Hg |
| Onion-like concentric thickening of arteriolar walls of vasculature, describes histology seen in what cardiac pathology? | Hypertensive crisis with Diastolic hypertension |
| Hyperplastic arteriosclerosis is associated with: | Hypertensive crisis |
| What is dystrophic calcification? | Damaged or necrotic tissue in setting of normal calcium levels |
| What is a hallmark of all types of necrosis? | Dystrophic calcification |
| Dystrophic calcification + Hypercalcemia --> | Metastases |
| Mitral regurgitation (MR) is a _________________ murmur best heard at the heart's _____________, and associated with _______ gallop. | Holosystolic; Apex: S3 |
| A functional MR is successfully treated if there is a reduction of _________________________________ after treatment. | LV preload (LVEDV) |
| What is a complication shared by Infective endocarditis and severe mitral regurgitation? | Chordae tendinae rupture |
| Decreased ventricular COMPLIANCE + elevated LV pressures. Dx? | Diastolic Heart Failure |
| What are common causes of DHF? | HTN, obesity, and infiltrative disorders such as Amyloidosis and Sarcoidosis. |
| What type of Heart failure is most often secondary to myocardial hypertrophy? | Diastolic Heart Failure |
| Systolic Heart failure (SHF) is mostly secondary to: | Isquemia/MI or dilated cardiomyopathy |
| What function (levels) are preserved or normal in Diastolic HF? | Preserved EF, and normal EDV |
| How is EF and EDV in Systolic HF? | reduced EF and increased EDV |
| What does an increase EDV mean? | Increased filling volume of ventricle; Increase in venous return --> overly stretched cardiac muscle fibers (DCM) |
| Increased preload causes an _____________________ in _________ & ______. | Increase in Stroke Volume and EDV |
| Formula for Stroke Volume: | SV = EDV - ESV |
| Main decrease in Diastolic HF? | Decrease in COMPLIANCE |
| Main decrease in Systolic HF? | Decrease in CONTRACTILITY |
| Most common cause of Right heart failure? | Left Heart failure |
| Isolated cause of right heart failure is known as: | Cor pulmonale |
| What is Cor pulmonale? | isolated right HR due to pulmonary cause |
| What drugs have shown decrease mortality in HF patients? | ACE-inhibitors, ARBs, Beta-blockers (except on acute Decompensated HF), and Spironolactone. |
| Thiazides and Loop diuretics are mainly used in HF for? | symptom relief |
| What are the 3 most characteristic symptoms of Left HF? | 1. Orthopnea 2. Paroxysmal Nocturnal Dyspnea 3. Pulmonary edema |
| What is orthopnea? It is an highly associated symptom of? | Shortness of breath when supine (laying down, face up); Highly associated with LHF |
| Breathless awakening from sleep? Associated symptom of? | Paroxysmal Nocturnal Dyspnea; Association with Left Heart Failure |
| Pulmonary edema seen Left HF, is associated with what cells? Found in which organ? | Hemosiderin-laden macrophages or known as "HF" cells found in the LUNGS |
| What are the 3 main symptoms that indicate Right HF? | 1. Hepatomegaly (nutmeg liver) 2. Jugular venous distention (JVD) 3. Peripheral Edema |
| Left HF is associated with ____________________ edema, while Right HF is associated with _______________________ edema. | Pulmonary Edema; Peripheral Edema |
| Increased central venous pressure leads to development of ______________________ seen in RHF. | Hepatomegaly |
| RHF increases venous pressure, which lead to occurrence of? | JVD and Peripheral edema |
| Increased pulmonary venous pressure is causal of _______________ edema seen in ________________ failure. | Pulmonary edema; Left Heart failure |
| What EKG changes are seen in TRANSMURAL MI? | ST elevation + Q-wave formation |
| What is the common pathogenesis of Transmural MI? | 1. Fully obstructive thrombus 2. Ruptured atherosclerotic coronary artery plaque |
| STEMI: | Transmural MI; ST elevation |
| NSTEMI: | Subendocardial MI; ST depression |
| EKG changes shared by STEMI and NSTEMI? | Hyperacute (peaked) T waves, T-wave inversion, new LBBB, pathologic Q- waves |
| Distal LAD MI is seen in which EKG leads the best? | V3 - V4 |
| Distal LAD indicates what location? | anteroapical |
| The anteroseptal area of the heart is the ___________ area, and its MI is recorded best with leads ________________. | LAD; V1 - V2 |
| STEMI seen best in EKG leads II, III, and aVF? | RCA (inFerior) MI |
| LCX STEMI is seen best in ___________________ EKG recordings. | I, and aVL (Lateral) |
| PDA STEMI is seen in leads? what is characteristically seen with PDA STEMI R-waves in V1 -V3? | V7-V9; ST depression in V1-V3 with tall R-waves. |
| Diltiazem and Verapamil are: | Non-dihydropyridine Calcium channel blockers |
| Side effects of Non-dihydropyridine Ca-channel blockers? | Constipation, bradycardia, AV block |
| What is the cause of AV block development in usage of Verapamil? | Non-dihydropyridine ca-channel blockers, have negative chronotropic effects and a decrease sinus rate. |
| What are the 2 most common Non-dihydropyridine Calcium channel blockers? | Verapamil and Diltiazem |
| What is the MoA of Verapamil and Diltiazem? | Exert action on L-type Ca2+ channels during Phase 0 and decrease conductance velocity. |
| What are some disorders or conditions for which Diltiazem and Verapamil are used for? | HTN, angina, Supraventricular arrhythmias (A-flutter, A-fib, and PSVT) |
| What type of channels are used by Non-dihydropyridine antiarrhythmics? | L-type Calcium channels |
| On what phase do non-dihydropyridine Ca2+ channel blockers work? | Phase 0 |
| Decreased conduction velocity, increase ERP, and increase PR interval, describes the mechanism of action of? | Class IV antiarrhythmics (Calcium channel blockers) |
| What are the Class IV antiarrhythmics? | Calcium channel blockers (Verapamil and Diltiazem) |
| Changes seen in Action potential in Class IV antiarrhythmics? | Slow rise of Action potential, Prolonged repolarization at AV node, and decreased threshold potential |
| Markedly prolonged repolarization is seen in what kind of antiarrhythmics? | Class III - Potassium channel blockers |
| What are some Class III antiarrhythmics? | Amiodarone, Ibutilide, Sotalol, Dofetilide |
| What are the main side effects of Sotalol? | Torsades de Pointes and excessive Beta-blockade |
| The use of Ibulitide is associated with possible development of _________________________ (fatal arrhythmia) | Torsades de Pointes |
| Pulmonary fibrosis, Hyper/Hypothyroidism, and liver dysfunction, are associated side effects of which antiarrhythmic? | Class III antiarrhythmic - K+ channel blocker AMIODARONE |
| What K+channel blocker acts as an HAPTEN? What does it cause? | Amiodarone; results in development of blue/gray deposits in skin leading to photodermatitis, and to corneal deposits. |
| Increased AP duration, Increased ERP, Increased QT interval, is the mechanism of action seen in? | Class III antiarrhythmics |
| Decreased slope of Phase 0 depolarization is seen in: | Class I antiarrhythmics: Na + channel blockers |
| Class I antiarrhythmics have a preference for: | tissue that is frequently depolarized |
| Depolarized cells in heart will be affected with preference by what antiarrhythmics? | Sodium channel blockers (Class I) |
| Class IA antiarrhythmics? | Quinidine, Procainamide, and Disopyramide |
| Class IB antiarrhythmics? | Lidocaine and Mexiletine |
| Flecainide and Propafenone are? | Class IC antiarrhythmics |
| What side effect is seen with Quinidine? | Cinchonism |
| What is cinchonism? | Side effect of Class I antiarrhythmic QUINIDINE; it is tinnitus induced by Quinidine |
| Reversible SLE-like syndrome is seen with the use of: | Procainamide |
| Development of HF is often associated with __________________, a Class ____ antiarrhythmic. | Disopyramide: I |
| Antiarrhythmic: 1. Quinidine 2. Procainamide 3. Disopyramide | SE: 1. Cinchonism 2. reversible SLE-like syndrome 3. Heart failure |
| What SE effects are seen in all Na-channel blockers? | Thrombocytopenia and increased risk of Torsades de pointes |
| Why is there in and increased risk for Torsades de pointes in the use of Class I antiarrhythmics? | Increased QT interval |
| Main two arrhythmias treated with Class IA antiarrhythmics? | SVT and V-Tach (atrial and ventricular arrhythmias) |
| What seizure medication may be considered a Class IB antiarrhythmic? | Phenytoin |
| What type of tissue has Class IB antiarrhythmic preference? | Ischemic or depolarized Purjinke and ventricular tissue |
| Digoxin overdose, lead to the development of arrhythmias. What class of antiarrhythmic is classically used to treat the arrhythmia? | Class IB antiarrhythmic, such as Lidocaine. |
| Patient with chronic AFIB is treated with Digoxin. Few days after starting medication is admitted to local ER, and EKG shows sustained VTACH. What drugs is commonly used. | Lidocaine is often used to treat Digoxin-induced arrhythmias. Common treatment of AFIB is digoxin. |
| What kind of drugs are the LAST RESORT to treat SVT and AFIB? | Class IC antiarrhythmics |
| What are the associated side effects of Class IC antiarrhythmics? | Proarrhythmic especially in post- MI |
| Class IC antiarrhythmics are contraindicated in what type of patients? | Structural and ischemic heart disease patients |
| What type of antiarrhythmic is used as__________________ RATE CONTROL of AFIB and AFLUTTER? | VENTRICULAR; Beta blockers (Class II) |
| Beta blockers cause a decrease in cAMP and Calcium current which is manifested with: | Decreased SA and AV nodal activity |
| In use of Beta blockers, the ______ node is found to have greater sensitivity causing an increased _________ interval. | AV node; PR |
| AV node beta blocker stimulation leads to: | Increased PR interval |
| Why are B-blockers, such as propranolol, to be used very carefully in diabetic patients? | May mask signs of hypoglycemia |
| Impotence is associated the toxicity of ___________ antiarrhythmic. | Class II |
| The chronic use of B-blockers may lead to: | 1. Exacerbation of ASTHMA and COPD 2. CNS --> sedation and sleep alterations 3. Cardio --> HF, AV block and bradycardia |
| A __________________ drug addict cannot be given ______________, as it would cause UNOPPOSED ________________________. | COCAINE; B-blocker; alpha-1 agonist |
| What are common treatments for B-blocker toxicity? | Saline, atropine, glucagon |
| What MEN2A - associated malignancy is cannot be treated with purely B-blockers? | Pheochromocytoma (cause unopposed a-1 agonism) |
| What is a distinctive side effect of metoprolol? | Dyslipidemia |
| What B-blocker may exacerbate vasospasm in Prinzmetal angina? | Propranolol |
| Which are the non-selective B-blockers? | Labetalol and Carvedilol |
| Which B-blockers have both alpha and beta antagonistic effects? | Non-selective B-blockers (Labetalol and Carvedilol) |
| Where are B-1 receptors found? | Cardiac tissue and Renal Juxtaglomerular cells |
| Stimulation of B-1 receptors lead to a decreased level of ___________ | cAMP |
| Which are the Adrenergic receptors? | alpha-1, alpha-2, B-1 and B-2 |
| M1, M2, and M3 are? | Cholinergic receptors |
| The ultimate result of the Carotid Sinus massage is to _______________________. | Decrease heart rate |
| Massaging the Carotid sinus initially increases ______ tone, leading to a ____________ inhibition of the _____________. This results in _______ conduction through the _____________ causing a prolongation of _________________ of _______ node, causing ultimately a decreased ________________. | PS; temporary; SA node; slow; AV node; Refractory Period of AV Node; Heart Rate |
| What is the result of the slow conduction through the AV node seen in Carotid Sinus massage? | Prolongation of the Refractory period of AV node. |
| MC site of clot causing sudden loss of vision? | Retinal artery |
| Occlusion of the _______________ artery causes sudden loss of vision. | Retinal |
| The ophthalmic artery branches off the ________________ ___________. | Internal Carotid |
| Path of Ocular artery | Internal Carotid --> Ophthalmic artery --> retinal artery |
| Development of AFIB is due to: | The loss of AV function |
| In AFIB, the AV function is lost, thus it is replaced by: | SA node, resulting in irregular pattern and rapid impulses. |
| What is a varicocele? | Tortuous formation of renal vein due to increased renal pressure. |
| Which side renal vein is most commonly seen with varicocele development? | Left Renal vein |
| Causes of Varicoceles? | Renal vein stenosis, leading to retrograde blood flow. |
| Retrograde blood flow of the left renal vein, is associated with development of ____________________, due to ___________________. | Varicocele: Left Renal vein stenosis |
| What is the "Nutcracker" effect? | Pain elicited by a varicocele. |
| Pain in the flank and gross hematuria, HTN, and very tender scrotum. | Nutcracker effect indicating possible Varicocele. |
| Varicocele Hx in a patient may be associated with: | Low sperm production and low sperm quality, leading to infertility. |
| "Bag of worms" description of the scrotum. Dx? | Varicocele |
| Which vein on the Left side becomes more commonly tortuous leading to development of varicocele? | Gonadal (spermatic) vein |
| Crescendo - Decrescendo, harsh systolic ejection murmur | Aortic Stenosis (AS) |
| Best heard at 2nd intercostal space, radiation to the carotids. Associated commonly with old age. | Aortic Stenosis (AS) |
| Bicuspid aortic valve is a common cause of___________________ murmur. | Aortic Stenosis (AS) |
| What are the most common causes of Aortic Root Disease? associated with what syndrome? | 1. Aneurysmal dilation 2. Aortic Regurgitation 3. Aortic Dissection Associated with Marfan syndrome |
| Collective cardiovascular syndrome, causing damage to aortic valve such as thickening, stiffness, dilaton. | Aortic Root Disease |
| Mid-systolic click and eventual late-systolic murmur | MVP |
| Where is an MVP best heard? | Apex of heart |
| VSD is a ________murmur, commonly seen in __________ syndrome. It is required in neonates with ________________ for survival. | Systolic; Down Syndrome: Transposition of Great Vessels. |
| Dobutamine uses the _____ pathway and increases the level of ______ and ____________. | Gs; cAMP and adenylyl cyclase |
| Dobutamine shows stronger affinity to which type of Beta receptors? | B1 receptors have stronger affinity to dobutamine than B2. |
| What are the cardiac effects of Dobutamine? | Affects cardiac muscle causing positive chronotropy and increases inotropy. |
| What is chronotropy? | Action of affecting the heart rate. Positive refers to accelerate HR. Negative chronotropy meas lowering HR. |
| What is the action of Aldosterone inhibitors? | Increased renal Na+ reabsorption |
| Where in the RAAS does renin enter ? | Enzyme that works in conversion of Angiotensinogen into AT 1 |
| ACE: | Enzyme in charge of converting AT 1 into AT II |
| What antihypertensives work on AT II? | ARBs |
| What stimulates the release of Renin? | 1. Decreased Renal blood flow (RBF) 2. Sympathetic stimulation |
| What drugs have the suffix -pril? Examples. | The ACE inhibitors such as CaptoPRIL, or LisinoPRIL. |
| What is a common serious side effects of ACE inhibitors.? | 1st dose syncope |
| The co-administration of _________________ with new start on ACE inhibitors, increase the risk of developing ___________________, thus it must be prevented by starting with ____________. | Diuretics; 1st dose syncope; low doses |
| BUN of 36 and Cr of 5.3 is started with low doses of Captopril. Why? | Patients with chronic renal failure, may develop ACE inhibitor - induced 1st dose syncope. It is prevented by staring with low dosages. |
| On the jugular venous tracing, which wave represents Right Atrial contraction? | a-wave |
| The x-descent on JV tracing represents which cardiac contraction moment? | Right-atrial relaxation. |
| X-decent depicts RA ___________________ and the a-wave indicates RA _____________________. | Relaxation; Contraction |
| Which feature on JV tracing represents the PASSIVE RA emptying after the TV has opened? | y-descent |
| Continuous blood inflow of the venous blood | represented with the "v-wave" on the JV tracing. |
| The pressure (building) on the TV during Right Ventricular contraction is depicted with the ______-wave, on the jugular venous tracing. | c-wave |
| Patient with chronic AFIB is missing which JV tracing feature? | a-wave |
| Constrictive Pericarditis is associated with: | Stepper y-descent on JV tracing. |
| What part of the JV tracing represents the Atrial Portion? | From end of y-decent, all a-wave to the benging of c-wave |
| x, v and y points on JV tracing are part of the __________________ portion. | Ventricular |
| Which part represents Ventricular Diastole? | From v-wave to the end of y-descent. |
| the area covered from x-descent to start of v-wave on JV tracing is? | Ventricular systole |
| Atrial Diastole is enclosed in JV tracing by? | Max point at a-wave to max point of c-wave. |
| The first half (minimum to max point) of a-wave represents? | Atrial systole |
| Thickened and calcified pericardium describes what type of cardiac condition? | Constrictive Pericarditis |
| Triad of progressive dyspnea, peripheral edema, and ascites, plus absent y-descent on JV tracing? | Constrictive Pericarditis |
| Hx of TB and radiation to the chest, and cardiac surgery are risk factor for the development of ___________________. | Constrictive Pericarditis |
| Systolic pressure decreased > 10 mmHg on inspiration | Pulsus Paradoxus |
| Pulsus paradoxus is most commonly associated with? | Cardiac tamponade |
| What part of the respiratory cycle is associated with Pulsus Paradoxus? | Inspiration |
| What is the second most common cause of Pulsus paradoxus? | severe COPD and ASTHMA, and constrictive pericarditis |
| First line of treatment for HTN in DM patients? Second? | ACE inhibitors, as these are protective of the kidneys. Second line are the ARBs. |
| What is an advantage of ARBs over ACE inhibitors? | ARBs do not cause increase levels of bradykinin, thus no edema or cough |
| MC side effect of ACE inhibitors? | Cough and angioedema due to increased levels of Bradykinin |
| Granulomatous inflammation of the media (vessel) | Morphological transformation of vessel structure seen in: 1. Takayasu's Arteritis 2. Temporal (Giant Cell) arteritis |
| Microscopic polyangiitis, Microscopic polyarteritis, and Hypersensitive vasculitis, are _________________________ vasculitis, seen in the first _______________ wit _____________________________. | Leukoclastic; 24 hours; Fragmented Neutrophils |
| What are the two most common large vessel vasculitis? | Temporal (Giant cell) arteritis and Takayasu's arteritis |
| Unilateral headache associated vasculitis? | Temporal (Giant cell) arteritis |
| Ophthalmic artery occlusion is seen as irreversible complication of _________________________ arteritis. | Temporal (Giant cell) arteritis |
| Temporal arteritis is often associated with: | 1. Polymyalgia rheumatica 2. Increased ESR 2. Unilateral headaches 4. Affects females > males |
| What is the treatment of Giant cell arteritis? Why is the treatment before ophthalmic artery biopsy? | High dose glucocorticoids prior to Ophthalmic artery biopsy in order to prevent irreversible blindness. |
| Granulomatous thickening and narrowing of aortic arch and proximal great vessels? | Takayasu's arteritis |
| "Pulseless disease" otherwise known as: | Takayasu's arteritis |
| Asian female 44 years old, almost absent radial and brachial pulses bilaterally, complains of night sweats, arthralgias, and vision problems. Dx? Treatment? | Takayasu's arteritis is treated with corticosteroids |
| Increased ESR is a lab result seen in which type of vasculitis? | Large cell vasculitis |
| What viral agent is highly associated with PAN? | Hepatitis B virus |
| In Polyarteritis nodosa (PAN), which vessels are affected, and which are spared? | PAN mostly sees affected medium sized vessels, involving the renal and visceral, while sparing the pulmonary arteries. |
| Corticosteroids and ___________________ are drugs used in the treatment of PAN. | Cyclophosphamide |
| Which medium sized vasculitis is seen with different stages of inflammation coexisting in same vessel? | Polyarteritis Nodosa (PAN) |
| CRASH and burn, mnemonic of? | Kawasaki Disease |
| Kawasaki Disease is a _________ size vasculitis, affecting primarily ____________ _______________ of less than 4 years old. | Medium; Asian children |
| Another name for Kawasaki Disease? | Mucocutaneous Lymph Node Syndrome |
| Kawasaki Disease main clinical manifestations: | Conjunctiva injection, Rash (desquamating), Adenopathy (cervical), Strawberry tongue (oral mucositis), Hand and Foot changes, Fever |
| What is the treatment of Kawasaki disease? | IV immunoglobulin and aspirin |
| Common name of Thromboangiitis obliterans? | Buerger disease |
| Buerger disease is strongly associated with ______________________, with segmental thrombosing vasculitis ________________ and _________________ involvement. | smoking; vein and nerve. |
| Raynaud phenomenon is often present in __________________ disease. | Buerger |
| What is the product of lipid peroxidation? | Lipofuscin |
| In what organ is lipofuscin is often found? Description. | Lipofuscin is found in the HEART. It is found in aging cells seen in malnutrition and cachexia and is of yellow-brown color. |
| Systolic Ejection click, loudest in base of heart, soft S2 | Aortic Stenosis (AS) |
| Which channels are preferred to bind Lidocaine? | Inactive Na+ channels and rapidly dissasiociates |
| Exercise in the Frank-Starling Curve will cause an _______________ in cardiac output and increase in ____________________. | Increase; inotropy |
| No change in normal path of Cardiac output, but negative inotropy? | Myocardial Infarct |
| Negative Inotropy and a decrease in TPR, Dx? | Hemorrhage |
| Change in inotropy means | changes in contractility |
| What conditions cause positive inotropy? | Catecholamines, exercise, digoxin |
| What disorders cause negative inotropy? | Heart failure, narcotic OD, and sympathetic inhibition |
| Fluid infusion, sympathetic activation | Increase in Venous return |
| What can cause a decrease in venous return? | Acute hemorrhage |
| What causes a decrease in TPR? increase TPR? | Exercise decrease TPR; Vasopressors increase TPR. |
| Anterior leaflet of the mitral valve push toward the interventricular hypertrophied septum, Dx? | Hypertrophic Cardiomyopathy |
| Hypertrophic cardiomyopathy is associated with _____ sound. | S4 |
| Holosystolic, high-pitch, "blowing murmur" best heard at the apex of heart, Dx? | Mitral Regurgitation (MR) |
| What murmur is associated with radiation to the axilla? | Mitral Regurgitation (MR) |
| What two diseases are often cause of secondary development of MR? | Rheumatic Fever and Infective endocarditis |
| A reduced Preload and Afterload is accomplished by what medication? | Nitroprusside |
| Nitroprusside decreases ______________________ and ________________. | Preload and Afterload |
| What vessel and blood flow characteristics increase risk of developing atherosclerosis? | Vessels that branch and twist constantly, which produce TURBULENT flow. |
| Which are the two most susceptible vessels for developing atherosclerosis? | Lower abdominal aorta and coronary arteries |
| When is Hibernating myocardium present? | LV dysfunction due to reduced coronary blood flow. |
| What can prevent the effects on IV NE on vasculature? | Phentolamine injection (alpha-1 blocker) |
| What are the extravasation effects of IV NE? | Blanching of the vein, and leads to vasoconstriction. |
| How is the flow of a fistula between the aortic root and the Right ventricle? | Continuous blood flow from the Aortic root to the RV. |
| WHat is the MCC of Enterococcal Endocarditis? | Genitourinary instrumentation such as CYSTOSCOPY or CATHETERIZATION. |
| Bacteria that grows on hypertonic (6.5%) saline and bile, PYR +, and causes NO (gamma) hemolysis. | Entococcal bacteria |
| What are the two common species of Enterococcal bacteria often cause Endocarditis? | E. faecalis and E. faecium |
| Effects of cardiac physiological forces after an MI: | 1. Reduced blood pressure 2. Increased distended Jugular vein --> Elevated Central Venous Pressure 3. Decreased PCWP with decreased filling pressures. |
| Why is the central venous pressure elevated after an MI? | There's a backflow of blood, as the heart inability of heart to push blood forward. |
| Medial degeneration of aorta? | Aortic aneurysm |
| Myxomatous changes with pooling of proteoglycans in the media layer of large arteries found in cystic medial degeneration, produces a predisposition to? | Aortic dissection |
| Pulsatile abdominal mass | Abdominal Aortic Aneurysm |
| Where is the abdominal aortic aneurysm most commonly located? | Infrarenal (distal to the origin of renal arteries) |
| Defective fibrillin-1 glycoprotein | Marfan Syndrome |
| The ingestion of sweat peas is associated to development of __________________ syndrome. | Marfan Syndrome |
| What enzyme is important in the cross linking of elastic fibers, involved in Marfan syndrome? | LYSYL OXIDASE |
| Chronic, repetitive endothelial injury causes ---> | Atherosclerosis |
| Foam cell formation and fatty streaks and endothelial cell damage is part of pathogenesis of which pathology? | Atherosclerosis |
| Thoracic Aortic aneurysm has a association to? | Tertiary syphilis |
| Hyperplastic arteriosclerosis most commonly involves which arteries? | Renal arteries |
| "Onion-skinning" of the renal arteries + Malignant Hypertension, often indicate what diagnosis? | Hyperplastic Arteriosclerosis |
| How else is Malignant Hypertension known? | Accelerated hypertension |
| rapid microvascular damage with necrosis in the walls of small arteries and arterioles + intravascular thrombosis, Dx? | Malignant Hypertension |
| What type of heart failure is often a complication of malignant HTN? | Left Heart Failure |
| What is the clinical presentation of Stable Angina? | Exertional chest pain relieved by rest or nitroglycerin |
| What level of vessel occlusion is required to develop Stable Angina? | 70% occlusion |
| Atherosclerosis is most often associated with _____________ angina. | Stable |
| Secondary to coronary Vasospasm | Prinzmetal (Variant) Angina |
| Stable angina depicts an ___________________, and Prinzmetal angina shows a ______________________, on EKG. | ST depression seen in Stable angina ST elevation seen in Variant angina |
| HTN and hypercholesterolemia are NOT associated risk factors of ____________ angina. | Prinzmetal (Variant) Angina |
| ST elevation and T-wave inversion with no cardiac enzymes, indicates? | Unstable Angina |
| What is the MC treatment of Variant Angina? | Ca2+ blockers, nitrates, and smoking cessation. |
| What is the most common risk factor of Prinzmetal angina? | Smoking |
| Chest pain not relieved with rest or nitrates | Unstable angina |
| Order of worsening anginas: | Stable< Variant (Prinzmetal) < Unstable |
| Cocaine, EtOH, and triptans are triggers of which kind of angina? | Prinzmetal (Variant) Angina |
| Atherosclerotic plaque is made by the _____________________, which releases _______________________, in order to breakdown __________. | Fibrous cap; METALLOPROTEINASES; collagen |
| B-1 receptors use the _________ pathway. | Gs |
| Common ARTERIOLAR vasodilators? | Hydralazine and Minoxidil |
| Side effect of arteriolar vasodilators, such as Hydralazine? | Reflex Tachycardia |
| Pathogenesis of Reflex tachycardia | Stimulation of baroreceptors cause a reflex sympathetic stimulation , leading to increased HR, contractility, and CO. |
| What are the two main SE of arteriolar vasodilators? | 1. Reflex activation sympathetic system 2. Peripheral edema by activation of RAAS axis |
| Stiff heart is commonly seen in ______________________ cardiomyopathy. | Restrictive |
| What kind of diseases demonstrate a increased ventricular cavity size? | Ischemic heart disease and dilated cardiomyopathy |
| Poor ventricular wall compliance leads to impaired Left ventricular filling, such describes? | Diastolic dysfunction |
| What condition depict left dynamic outflow tract obstruction? | 1. Left Hypertrophic cardiomyopathy |
| A right dynamic flow obstruction is seen in: | Tetralogy of Fallot |
| What is the common presentation of Peripheral Arterial disease (PAD)? | fatigue, leg pain, discolored with exertion, and poor distal pulses |
| What is a common drug used in PAD? | Citalozol |
| MoA of Citalozol? | Phosphodiesterase inhibitor, that inhibits platelet aggregation and acts a direct arterial vasodilator. |
| What substances are to be raised in order to cause inhibition of platelet aggregation in the treatment of PAD? | Protein Kinase A |
| Only cells capable of synthesize collagen in atherosclerosis | Vascular Smooth Muscle cells (VSMC) |
| The VSMCs are responsible for producing what structure? | Fibrous cap |
| Metalloproteinases are releases or secreted by the _______________, which was produced by the _______________. | Fibrous cap; VSMC |
| Common condition seen in patient with Malignant HTN? | Persistent Diastolic Hypertension |
| Persistent Diastolic HTN | >130 mm Hg |
| A complication of Malignant HTN is Hypertensive Encephalopathy, which can be accompanied by: | Retinal hemorrhages, exudates, or papilledema. |
| Verapamil can decrease the conduction velocity of the: | SA and AV nodes |
| Embryological deficit or error, in the development of ToF | Anterior and Cephalad deviation of the Infundibular septum |
| VSD, overriding aorta, pulmonary stenosis, | symptoms seen in ToF |
| Kid that squats in order to feel relieved from fatigue or weakness, borned with early cyanosis. Dx? | Tetralogy of Fallot |
| Squatting : | Increases PRELOAD, leading to an increase in Peripheral vascular resistance |
| What are the cardiac abnormalities seen in SLE? | SEROSITIS, which is characterized by: 1. Pleurisy, 2. Pericarditis, 3. Peritonitis |
| What lipid lowering agent is used to reduce LDL and triglycerides? | Niacin |
| Most common and characteristic side effect of Niacin therapy | Cutaneous flushing due to Prostaglandins |
| How is the flushing caused by Niacin may be prevented? | Pre-treatment with Aspirin |
| Mechanisms of action of Niacin: | 1. Inhibits hormone-sensitive Lipase --> inhibit lipolysis 2. Reduction of VLDL synthesis |
| Gout or gout-like symptoms are seen with use of _____________. | Niacin |
| Besides flushing of face, what other side effects are seen with Niacin therapy? | Hyperglycemia and Hyperuricemia |
| Which lipid-lowering agent increases the risk of developing cholesterol gallstones? | Fibrates |
| Decreased fat soluble vitamin absorption is seen as a side effect of _________________________ therapy in lipid lowering treatment. | Bile acid resins |
| What enzyme is inhibited by statins? | HMG-reductase |
| What product is prevented from synthesis by actions of statins? | Mevalonate |
| What are the most important side effects seen statin therapy? | Hepatotoxicity and Myopathy |
| Side effects of statins are seen even more pronounced by co-administration with? | Niacin and Fibrates |
| Why are cholesterol gallstones formed in Fibrate therapy? | Inhibition of cholesterol 7a-hydroxylase |
| Which kind of lipid-lowering agent has similar LDL, HDL, and TG profile as statins? | PCSK9 inhibitors |
| Alirocumab and Evolucumab | PCSK9 inhibitors |
| Which lipid lowering agents decrease the most LDL? | Statins and PCSK9 inhibitors |
| All kind of lipid lowering agents, which are known to cause focal and nonfocal neurological deficits as a side effect? | PCSK9 inhibitors |
| Using Naproxen in Niacin therapy may help to reduce the risk of: | Red, flushing face |
| How is TG clearance achieved in Fibrate therapy? | Upregulation of LPL |
| Besides the upregulation of LDL to increase TG clearance by fibrates, this lipid-lowering agent has another MoA, which is? | Activation of PPAR-alpha to induce HDL synthesis |
| Activation of PPAR-a --> | Fibrate therapy MoA |
| Fibrates' activation of PPAR-a is to ____________________, and the upregulation of _________, is to ______________________. | make more HDL; LPL; get rid of Triglycerides |
| Which lipid-lowering agent type, forces the liver to use more cholesterol to synthesize bile acid? | Bile acid resins |
| Bile acid is made of ________________________ | cholesterol |
| Actions of PGI2 opposes those of ___________________ | Thromboxane A2 |
| Prostacyclin (PGI2): is produced by _____________. It ________________ and INHIBITS _______________________, leading to increased vascular ______________. | Prostacyclin H2 by Prostacyclin synthase; vasoDILATES; Inhibits platelet aggregation; Increase vascular permeability |
| If PGI2 produces vasodilation arteries and does not allow plt aggregation, then Thromboxane A2: | Vasoconstriction and stimulates clotting. |
| What is a common vitamin K dependent factor made in the liver, and involved in the coagulation cascade? | Protein C |
| Protein C function | Inactivation of factors 5a and 8a |
| Myosin binding to Protein C mutation is seen: | Hypertrophic cardiomyopathy |
| Activated Protein C participates in | Anticoagulation by cleaving factors 5a and 8a |
| Inactive Protein C is part of the ____________________ process | Coagulation |
| Thrombotic skin necrosis after administration of Warfarin. Suspect what Hypercoagulability disorder? | Protein C or S deficiency |
| Inability to inactive factors 5a and 8a is seen in __________________, leading to increased risk of _____________________ events. | Protein C or S deficiency; Thrombotic |
| Common cause of Secondary (functional) Mitral Regurgitation | Decompensated HF |
| Signs of LOW PERFUSION in Decompensated Heart failure include: | 1. Cold Extremities 2. Low urine Output 3. Altered mental status 4. Poor response to IV diuretics 5. Prerenal azotemia |
| What are some signs/clinical manifestations of CONGESTION seen in acute Decompensated HF? | Increased JDV, Peripheral Edema, S3, Orthopnea, Rales, and weight gain |
| Decompensated HF seen with Low Perfusion and High congestion? | Wet and Cold HF |
| Decompensated HF seen with High Perfusion and Congestion? | Wet and Warm HF |
| Increasing the CONGESTION in HF, means making Decompensated HF more _______. | Wet |
| Increasing the HF PERFUSION status, means labeling Decompensated HF more and more ___________. | Warm |
| In the LV Pressure vs LV volume loop graph, the changes seen in Aortic stenosis, resemble the most those seen with: | Increased AFTERLOAD |
| When is the maximum intensity of AS? | At maximum level of gradient between the LV and the Aorta pressures |
| Mutation to the Potassium-channel protein is seen in which congenital disorder? | Congenital Long QT syndrome |
| What occurs to the movement of K+ in Long QT syndrome? | Reduction in K+ - efflux, producers prolongation of the ACTION POTENTIAL leading to elongation of the QT interval. |
| What are risk of complication seen in Long QT syndrome? | Ventricular arrhythmias such as Torsades de Pointes and VTACH |
| What color do Psammoma bodies stain? | Dark purple |
| Rheumatic heart disease occurrence of dysphagia is mostly seen because of: | Left atrium compression of the Esophagus. |
| The _______________ is the most __________________ heart chamber, as seen in a CT scan. | Left Atrium; POSTERIOR |
| In relation to a CT view of the heart, describe the anatomical(cardinal) position of the heart chambers. | Right Ventricle -- NORTH (most anterior chamber) Left Atrium --SOUTH (most posterior chamber) Right Atrium -- WEST Left Ventricle -- EAST |
| The esophagus compression by LA enlargement causes dysphagia, but the LA can also compress the __________________ provoking _________________. | Recurrent Left Laryngeal Nerve; hoarseness of the voice. |
| Arginine and nitric oxide synthase, produce? | Nitric Oxide |
| Pretreatment with which amino acid, has been beneficial in Stable angina? | Arginine as it may cause Vasodilation |
| Nitric Oxide (NO) is made by: | ARGININE and NO synthase |
| Hypotension, muffled heart sounds, elevated JVD | Beck's Triad |
| Becks triad + Pulsus paradoxus | Cardiac Tamponade |
| X-ray of heart described as" Water bottle" | Cardiac Tamponade |
| Anatomical point for Pericardiocentesis? | Paraxiphoid area |
| Ultrasound finding in Cardiac Tamponade | Late diastolic collapse of the right atrium, due to primordial fluid |
| Pericardial rub described in auscultation, most commonly seen in? | Cardiac tamponade |
| Aortic Regurgitation, Mitral Stenosis, and Continuous PDA | Diastolic Murmurs |
| Decrescendo at LUSB indicates: | Aortic Regurgitation, most likely of valvular origin |
| What valvular condition predispose development of AR? | Bicuspid aortic valve, and Rheumatic Heart disease |
| Marfan Syndrome is associated to ___________________ conditions, that predispose to the development of ___________ best heard at the ____________. | Aortic Root disease; Aortic Regurgitation; RUSRB |
| Mitral Stenosis auscultation description: | OPENING SNAP followed by mid-systolic rumble with presystolic accentuation. |
| Mitral Stenosis --_____________________________. Aortic Stenosis -- ____________________________. ASD --________________________________. | OPENING SNAP - MR EJECTION CLICK -- AS WIDE & FIXED S2 SPLIT --ASD |
| Machine-like sound murmur | PDA |
| Radiation to Carotids murmur | Aortic Stenosis (AS) |
| Radiation to the Axilla murmur | Mitral Regurgitation (MR) |
| Very small crescendo - decrescendo, best heard at mid-sternal border | Hypertrophic cardiomyopathy |
| Mid Systolic click + late systolic murmur | MVP |
| Holosystolic murmur best heard at Left sternal border | VSD |
| Midsystolic murmur with a wide-fixed S2 split | ASD |
| Systolic Murmurs: | AS, MR, IHSS, MVP, ASD, and VSD |
| What disorders are associated to cause Restrictive Cardiomyopathy? | Amyloidosis, Sarcoidosis, and Hemochromatosis |
| Spironolactone effect on cardiac functions: | Increase ventricular ejection fraction |
| Which diuretic increases the ventricular EF? | Spironolactone |
| Spironolactones effect on ventricular EF, is due to: | ventricular remodeling |
| What drugs cause Coronary "Steal"? | Adenosine and Dipyridamole |
| When is Coronary Steal seen in cardiac muscle? | MI as blood flow is limited and perfusion is affected. |
| The use of adenosine in Coronary Steal, causes: | No change in blood flow, and an increase in perfusion. |
| 62 yo male, hypertensive, seen with a palpable pulsating abdominal mass. Dx? | Abdominal Aortic aneurysm |
| Transmural inflammation and matrix degeneration within wall of aorta, leading to weakening and expansion of aorta, specifically below the renal arteries. Most common Dx? | Abdominal Aortic aneurysm |
| Focal intimal tear, tearing chest pain, with radiation to the back? | Aortic Dissection |
| Overall increase in heart rate and contractility, leads to an increase in: | Myocardial oxygen consumption |
| tPA: | Converts PLASMINOGEN into PLASMIN |
| What is the role of Plasmin? | Breakdown of CLOTS |
| What are some tPA- analogues? | Alteplase, Teneplase, and Streptokinase. |
| Pulsus Paradoxus occurs during ___________________ | Inspiration |
| What are Korotkoff sounds? | Sounds recorded while taking BP |
| Low frequency sound just before S1 at the end of diastole. | S4 |
| Murmur that radiates to the axilla best heard at the heart's apex. | Mitral Regurgitation (MR) |
| The joining of the Cardinal veins create the ________________. | Superior Vena Cava (SVC) |
| What vessels during embryology form the IVC? | Right and Left common Iliac veins at the L4-L5 level. |
| Patient develops endocarditis after surgical repair of a prosthetic valve. Which organism is associated with that infective endocarditis? | Staph epidermidis |
| Orthopnea is a classic symptom of ____________________________. | Left-sided Heart failure |
| Common complication 2-4 days after MI | Pericarditis |
| Sharp, pleuritic pain, increased by swallowing and relieved by leaning forward. | Pericarditis |
| Diastolic decrescendo murmur, widened pulse pressure and abrupt carotid distension | Aortic Regurgitation (AR) |
| "Head-bobbing" | Aortic Regurgitation (AR) |
| Which artery is commonly accessed to reach the lower extremity? | Common Femoral artery |
| Cannulation of the Common Femoral artery increases the risk of ___________________________. | Retroperitoneal hemorrhage |
| Baroreceptors of the neck stimulate which cranial nerve? | CN 9 Glossopharyngeal |
| The ______________ baroreceptors are associated with cranial nerve _________. | Aortic; 10 |
| What normal changes are expected in normal aging? | 1. Decreased LV chamber size 2. "S"-shaped Ventricular Septum 3. Accumulation of Lipofuscin |
| When is AR seen with the highest intensity? | Just after A2 |
| AR is best heard right after ________________________. | Expiration |
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