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Cardiology 2
UWORLD + FA Cardio Review
| Question | Answer |
|---|---|
| What is the most abundant type of collagen in human body? | Type 1 Collagen |
| What type of collagen is seen in mature scars? | Type 1 Collagen |
| Type 1 Collagen: | Dermis, Bones, Tendons, Ligaments, Dentin, Cornea, Blood vessels, and scar tissue |
| What condition is associated with defective Type 1 Collagen? | Osteogenesis Imperfecta |
| Type 2 Collagen makes up: | Cartilage, Vitreous humor, and Nucleus pulposus |
| What organs or tissues are made of Type 3 Collagen? | Skin, lungs, intestines, blood vessels, bone marrow, lymphatics, and granulation tissue |
| Ehlers-Danlo syndrome is due to defective __________________ collagen. | Type 3 |
| What type of collagen makes up the basement membranes? | Type 4 Collagen |
| Alport syndrome is due to defective ________________________. | Type 4 Collagen |
| Autoimmune disorder against Type IV collagen? | Goodpasture Syndrome |
| What kind of Cell-surface receptor is seen in collagen IV? | Laminin receptors |
| What is the cell-surface receptors of collagen 1, 2,3, and 5? | Integrin |
| Associated cells of Collagen I and Collagen II? | Collagen type I ---> Fibroblasts Collagen type II ---> Chondrocytes |
| What type of cells are associated with collagen IV? | All epithelial cells, endothelial cells, and regenerating hepatocytes |
| 1/3 of collagen structure is made of _________________. | Glycine |
| _______________ content best reflects collagen synthesis. | Glycine |
| What are the 6 steps of collagen synthesis? | 1. Synthesis 2. Hydroxylation 3. Glycosylation 4. Exocytosis 5. Proteolytic processing 6. Cross-linking |
| What is the second step in collagen synthesis? What disease is associated with this step? | Hydroxylation of Lysine and Proline residues; required Vitamin C. Deficeincy in Vitamin C -----> SCURVY |
| Scurvy is due to: | Deficiency of Vitamin C |
| The deficiency in Vitamin C causes: | 1. Development of Scurvy 2. Inhibition of Hydroxylation of Collagen synthesis process. |
| At which step of collagen synthesis is the TRIPLE HELIX formed? | 3rd step (GLYCOSYLATION) |
| Inability to form a triple helix collagen structure, is the basis of development __________________________. | Osteogenesis Imperfecta |
| Glycosylation of pro-a-chain hydroxylysine residues and formation of procollagen via formation of Hydrogen and disulfide bonds | Triple Helix formation in collagen synthesis |
| How is the triple helix of collagen composed? | 3 collagen alpha chains bonded with hydrogen and disulfide bonds |
| ____________________ is seen in defective Proteolytic processing of collagen in the ______________. | Ehlers-Danlos Syndrome; Extracellular space. |
| Disorders associated with defective cross-linking of collagen: | 1. Ehlers-Danlos Syndrome and, 2. Menkes disease |
| Copper-containing lysyl oxidase is involved in: | Collagen CROSS-LINKING with tropocollagen, in order to form collagen fibrils |
| Technique used to identify DNA mutations | Southern Blotting |
| What laboratory technique involves restriction ENDONUCLEASE digestion of sample DNA, gel electrophoresis, and gene identification with a labeled DNA probe? | Southern Blotting |
| Western blotting identifies | Proteins |
| Northern blotting identifies______________ mutations. | RNA |
| What hemodynamic effects are seen with Epinephrine? | 1. Increase in HR and contractility (B1 stimulation) 2. Increase in SYSTOLIC BP (B1 and a1 stimulation) 3. Diastolic BP: ----- low dose -----> decrease (B2>a1) ----- high dose -----> Increase (a1>B2) |
| How does a high or low dose of epinephrine causes opposing effects? | Diastolic Blood Pressure (BP). A high dose cause an increase due to higher a-1 stimulation than B-2, contrary to a low dose. |
| Pretreatment with a Beta-blocker such as Propranolol, in subsequent application of Epinephrine, would cause: | Blockage of B-receptors leads to inhibition of B-effects of epinephrine (Vasodilation and tachycardia), leaving only manifestation of the alpha-effects (Vasoconstriction) |
| Epinephrine has ________________ and ______________ agonist effects. | Alpha and Beta |
| Which adrenergic receptors are stimulated by epinephrine? | a-1, a-2, B-1, and B-2. |
| Stimulation of alpha(a)-1 adrenergic receptors cause: | Increase in Vasoconstriction and BP, and a decrease in mucosal edema. |
| B-1 receptor stimulation causes: | Increase in heart rate and contractility |
| B-2 receptor stimulation is manifested by: | Increase bronchodilation and decreased mediator release |
| Atropine is a _______________________________. | Muscarinic Receptor ANTAGONIST |
| What drug is associated by increasing heart rate by blocking parasympathetic vagal influence. | Atropine |
| Atropine is used in the _______________ to produce ________________. | Eye; MYDRIASIS |
| What drug is used to block the effects seen in Cholinesterase Inhibitor Effects? | Atropine |
| Organophosphate toxicity is treated with? | Atropine |
| What simplistic description is used to depict the overall effect of Atropine intoxication? | Dryness and Hot |
| Isoproterenol is: | Non-selective B-adrenergic receptor agonist |
| Isoproterenol + Epinephrine | Decrease in Diastolic BP and Increase in Tachycardia |
| What drug is non-specific a-1 and a-2 blocker, and has no Beta-effects? | Phentolamine |
| Selective alpha(a)-adrenergic agonist; associated with Increased BP (systolic and diastolic) and reflex bradycardia. | Phenylephrine |
| What is the best anatomical site to access the Great Saphenous Vein? | Inferolateral to the Pubic Tubercle |
| The Great Saphenous vein drains into the _____________________, in the ___________________. | Femoral vein in the Femoral Triangle |
| What vessels and nerves travel through the Popliteal fossa? | Popliteal artery and vein, and the Tibial nerve. |
| What disorders are associated with the Popliteal fossa? | Popliteal artery aneurysm, and Baker's cysts. |
| ASIS stands for? if damaged? | Anterior Superior Iliac Spine; Damage--> Lateral cutaneous nerve of the thigh. |
| What heart structure is crossed by venous (right side vein) catheter insertion, in order to reach the Left Atrium? | Interatrial septum through the Foramen Ovale. |
| Pathologic Spit of S2, may be described as __________________ or _________________. | Widened or Narrowed |
| What are the main reasons for a Widened Split of S2, and its associated pathologies? | 1. Delayed P2: -- Pulmonic Stenosis, Pulmonary HTN, ASD, and RBBB 2. Early A2 -- VSD |
| A delayed A2 causes a ________________ split of S2. | Narrowed |
| What are the causes for a Narrowed S2 split due to Delayed A2 closedure? | Aortic Stenosis, Systemic HTN, LBBB and HCM |
| What murmur's auscultation findings are described by a Crescendo-Decrescendo, with increased intensity in inspiration? | Pulmonic Stenosis |
| PS is best heard at the: | Upper Left Sternal border |
| Why is the intensity of PS (right-sided murmur) increased with Inspiration? | Increased blood to the Right-side of heart, furthering the P2 closedure. |
| Delayed P2 closedure causes? | Widened Split of S2 |
| VSD S2 split is due to? Narrow or widened split? | Widened split due to EARLY A2 closure |
| Loud S1 is mostly associated with: | Mitral Stenosis, TS, and ASD |
| Rupture of cortical bridging veins MC cause: | Subdural Hematoma |
| "Crescent-shaped" mass on CT of brain | Subdural Hematoma |
| Young male, arrives ER due to car accident. Presents with a progressive (gradual) onset of headache, and develops confusion. Abnorally shaped mass seen in CT. Most probable Dx? | Subdural Hematoma |
| Midline shift is seen in ______________________, and ________________ mass in CT of brain. | Subdural Hematoma; "Crescent-shaped" |
| Epidural hematoma is due to rupture of the __________________. | Middle Meningeal Artery |
| Brain CT of Epidural hematoma shows: | 1. Biconvex (lentiform), hyperdense blood collection, NOT crossing the suture lines. |
| Trauma involving the Pterion, should raise suspicion of? | Rupture of the MMA leading to possible Epidural Hematoma |
| Patient receives a lateral blow to the cranium. Rush to the hospital by ambulance, where the patient is lucid and cooperative, but soon after ER arrival patient is in-and-out of consciousness. Dx? | Epidural Hematoma |
| "Lucid interval" is associated with: | Epidural Hematoma |
| What vessels are ruptured in a Hypertensive crisis? | Penetrating branches |
| What kind of intracranial hemorrhage is related to systemic hypertension, and amyloid angiopathy (in elderly)? | Intraparenchymal (intracerebellar) hemorrhage |
| Subarachnoid hemorrhage is MCC by? | Rupture of cerebral aneurysm (Saccular or Berry) |
| "Worst headache of my life" + yellow spinal tap. Dx? | Subarachnoid Hemorrhage |
| Atrial fibrillation causes? | It is the loss of atrial contraction, which may lead to reduction of Left Ventricular filling causing hypotension and pulmonary edema |
| In severe cases of AS and Concentric LV hypertrophy, what structure is the main contributor for LV filling? | Atria contraction |
| High-pitch, blowing, diastolic murmur, with decrescendo intensity pattern? | Aortic Regurgitation (AR) |
| AR due to Aortic Root dilation disease is best heard at the ________________. | RUSB (right upper sternal border) |
| Where is AR murmur best heard if it is due to a valvular pathology? | Left 3rd intercostal space |
| An Opening Snap is most associated with __________________ | Mitral Stenosis (MS) |
| What is the pathogenesis of Congenital Long QT syndrome? | Mutation that SLOWS the delayed rectifier POTASSIUM current that repolarizes the cardiomyocyte action potential. |
| What medications are associated with worsening Congenital Long QT syndrome? | 1. Macrolides and Fluoroquinolones 2. Antiemetics (Ondansetron) 3. Azoles 4. Antipsychotics and TCA antidepressants 5. Class 1A antiarrhythmics (Quinidine) 6. Class 3 antiarrhythmics (Dolfetide) |
| Romano-Ward Syndrome and Jervell and Lange-Nielsen syndrome are associated with worsening of? | Congenital Long QT syndrome |
| What induced-arrhythmia is associated with fatal consequences in case of taking in a patient with Congenital Long QT syndrome? | Torsades de Pointes, which lead to syncope and sudden cardiac death |
| What is the clinical triad of a patient with hypovolemic shock? | 1. Severe hypotension 2. Tachycardia 3. Cool extremities |
| The infusion of IV fluids in patient with hypovolemic shock will cause an hemodynamic increase in: | 1. Intravascular EDV and, 2. Left ventricle EDV (LVEDV) |
| Hypovolemic Shock is described as: | Cold, clammy Decreased in PCWP (Preload) and CO Increase in Afterload (SVR) |
| What are the MCC of Hypovolemic shock? | Hemorrhage, dehydration, and burns |
| Shock caused by sepsis is described as ___________ and __________, and is known as _____________________ shock. | Warm and dry; Distributive shock. |
| If shock patient is been treated with Dobutamine, suspect? | Cardiogenic Shock |
| What is the most important way to prevent infection of central venous catheter insertion? | Proper hand hygiene prior the procedure |
| What vein is best to be avoided in placing a central venous catheter? | Femoral vein |
| What are the prefered venous vessels to insert a Central Venous catheter? | Subclavian and Internal Jugular veins |
| Phenylephrine is a: | 1. Selective alpha-1 adrenergic receptor AGONIST 2. Increases Peripheral Vascular resistance and Systolic BP 3. Decreased Pulse Pressure and HR |
| Dobutamine is a ______________________, which INCREASES _______ and ________________, but has _____________________. | B-receptor agonist; Increases HR and contractility; NO effect on Peripheral vascular resistance |
| Epinephrine: | Endogenous catecholamine with alpha and beta receptors. Increase HR and Pulse pressure Decreases Peripheral vascular resistance |
| Clonidine is an _______ - agonist. | Alpha-2; |
| What organism is causative of Lyme Disease? | SPIROCHETE Borrelia Burgdorferi |
| Early Lyme disease can be presented with: | Lyme Carditis: Varying severity of 3 degree AVB, and may be accompanied with Syncope, Dyspnea, and lightheadedness. |
| Myocarditis development is mostly caused by_________________ infection. | Viral (Coxsackie A virus) |
| What is a severe complication of ACE inhibitor therapy? | 1st-dose syncope in those with volume depletion conditions or Heart failure (HF) |
| Why a patient on HCTZ, should be carefully started on Captopril? | Prolonged diuretic therapy induces a hypovolemic status, which may precipitate 1st-dose syncope when started with high doses of ACE inhibitor. |
| What are the main risk factor for Abdominal Aortic Aneurysm? | 1. Age > 65 2. Smoking (increase risk by 15-fold) 3. Male sex |
| Focal dilation of abdominal aorta by more than 50% or >3cm in diameter? | Abdominal Aortic Aneurysm |
| When in AR heard with highest intensity? | Just after Aortic Valve closure |
| In AR pressure tracing, which are some characteristics? | 1. Loss of Aortic Dicrotic notch 2. Stepp diastolic decline of aortic pressure 3. High-peaking LV and aortic systolic pressures ---> Wide pulse pressure |
| Cardioselective Beta-blockers, prefer which receptor? | Beta-1 receptors |
| Cardioselective Beta-blockers include: | Metoprolol, atenolol, nebivolol, bisoprolol |
| Cardioselective B-blockers are safe to use in: | COPD patients |
| Why is propranolol not to be used in patient with emphysema? | Non-selective B-blockers may exacerbate COPD symptoms |
| Which adrenergic receptors are stimulated by NE and Epi? which is not? | NE and Epi stimulate A-1, A-2, and B-1 Epi stimulate a1, a2, b1, and b2 |
| Atropine causes _________________ effects. | Anticholinergic |
| What medication can be used to alleviate the bradycardia produced by Inferior wall MI? | Atropine |
| What leads are the best to depict Inferior Wall MI? | II, AVF, and III; |
| Common drug used to diagnose and treat SVT? | Adenosine |
| What drug has the opposing effects of Atropine? | Physostigmine |
| TTN gene mutation | Familial Dilated cardiomyopathy |
| Titin: | Protein coded by TTN gene; its mutation leads to Familial DCM |
| Decreased contractile function of one or both ventricles, and increased ventricular cavity size. Dx? | Dilated cardiomyopathy |
| What is the clinical presentation of DCM? | Decompensated HF symptoms, such as, fatigue, dyspnea, and orthopnea. |
| What are the related mutations of Hypertrophic cardiomyopathy? | Mutations of the B-heavy myosin chain or myosin-binding protein C. |
| Young athlete sudden death | Hypertrophic cardiomyopathy |
| Hypertrophic cardiomyopathy is associated with _____ sound, while dilated cardiomyopathy is related to a ______ cardiac sound. | S4 -- HCM S3 --- DCM |
| What is the best treatment options for HCM? | Beta-blockers and Non-dihydropyridine Calcium channel blockers, plus immediate cessation of all athletic activity. |
| Diastolic dysfunction development | Hypertrophic cardiomyopathy |
| Ventricular concentric hypertrophy is seen in ______________ cardiomyopathy | Hypertrophic |
| What kind of hypertrophy is seen in DCM? | Eccentric (sarcomeres added in series) |
| Ventricular sarcomeres are added in parallel in _________________. | Hypertrophic cardiomyopathy |
| Findings: HF, S3, systolic regurgitant murmur, dilated heart on echocardiogram, balloon appearance of heart on CXR. | Dilated cardiomyopathy |
| What are the best treatment options for DCM? | Sodium restriction, ACE inhibitors, Beta-blockers, diuretics, digoxin, ICD, and heart transplant. |
| From what embryonic vessels is the SVC derived from? | Common Cardinal Veins |
| What is the primary function of Thiamine (Vitamin B1)? | Decarboxylation of a-keto acids (carbohydrate metabolism) |
| What are the disorders associated with Thiamine deficiency? | 1. Wernicke-Korsakoff encephalopathy 2. Beriberi |
| What is the difference between dry and wet Beriberi? | Dry --> Symmetrical peripheral neuropathy Wet --> Dry beriberi + High-output heart failure |
| What are varicose veins? | SUPERFICIAL leg veins become dilated and tortuous |
| What is the pathogenesis (cause) of varicose veins? | Intraluminal pressure and/or loss of tensile strength in the vessel wall lead to incompetence of vessel valves. |
| What are the MC complications seen in Varicose veins patients? | Edema, Stasis dermatitis, SKIN ULCERATIONS, poor wound healing, and Infections |
| Deep venous thrombosis complication? | Pulmonary edema |
| Superficial venous thrombosis causes _______________ veins, compicating into __________________, while Deep venous thrombosis may cause ___________________. | Superficial veins ---> Varicose veins ----> Skin ulcerations and Edema. Deep veins --> Pulmonary edema |
| What is the main reason for Intermittent claudication in the legs? | Inadequate blood flow due to obstruction (atherosclerosis of Femoral vein MC) |
| Intermittent claudication of legs has more pain during times of ___________________, contrary to patients with _________________ and ___________. | Prolonged rest; Deep venous thrombosis and Varicose veins |
| Intermittent claudication increases the risk of developing ______________ and ______________. | Ischemic stroke and MI |
| The endogenous- or pharmacological-induced vasodilation that causes redistribution of BLOOD FLOW ischemic areas to non-ischemic areas of the myocardium. | Coronary steal syndrome |
| What drugs are used to provoke a Coronary Steal? | Adenosine, Dipyridamole, and Regadenoson |
| What is the difference in Endogenous-induced and Drug-induced Coronary steal? | In endogenous, the affected area is the one VASODILATED, in order to maintain proper blood flow, while Drug-induced coronary steal vasodilates the non-affected area, increasing its compliance large enough to maintain proper blood flow. |
| What are the endogenous substances that cause a Coronary steal? | Adenosine and NO |
| Principle behind pharmacologic stress test with coronary vasodilators.. | Coronary Steal syndrome |
| Poor cardiac reserve due to LV outflow tract obstruction. Dx? | Hypertrophic cardiomyopathy |
| What hemodynamic change is present in HCM, that worsen the symptoms? | Decreased LV blood volume |
| Why are beta-blockers used in the treatment of HCM? | Decrease HR and contractility, and increase blood volume, and decrease LV outflow tract obstruction |
| What are two main principles of B-blocker MoA? | 1. Reduce Heart rate 2. Reduce LV contractility |
| A reduction in heart rate is seen with __________________, which leads to an increase amount of blood to ____________________. | Beta-blockers; enter the heart every beat --> Increasing EDV |
| How is ESV increased by the use of Beta-blockers? | Reduces the amount of blood ejected during systole. |
| How are EDV and ESV changed with Beta-blockers? | Both are increased. leading to overall increase in blood volume. |
| The early stage of HF is usually __________________ of HF symptoms, but does present with a ________________________________. | asymptomatic; 50% reduction in LV ejection fraction |
| How are neurohormonal levels in early stages of HF? | In order to maintain blood pressure and homeostasis: 1. SNS activation ---> increase in NE 2. RAAS activation --> Increase in AT II and Aldosterone 3. Momentary elevation of ANP and BNP |
| Fixed coronary stenosis | Stable angina |
| How does a fixed coronary stenosis cause stable angina? | Limit blood flow to the downstream myocardium, preventing myocardial oxygen supply from increasing during exertion. |
| What drug mimics the effects of exercise and increases myocardial demand? | Dobutamine |
| Dobutamine is ______ receptor _________, that provokes a decrease in _____________ which is seen with a _______________________. | B-1 adrenergic receptor agonist; Contractility ---> decreased ejection fraction |
| Strong Positive Inotropic and Chronotropic effects, and a mild vasodilation. | Effects of Dobutamine |
| What drug is used to exacerbate myocardial ischemia? | Dobutamine |
| Why is dobutamine used to determine myocardial ischemia? | It provokes an increased in heart rate and contractility, which lead to an increase in myocardial oxygen consumption, which in case of myocardial ischemia cannot be compensated. |
| What are the 3 main clinical applications for the use of Dobutamine? | 1. Heart Failure 2. Cardiogenic Shock 3. Cardiac Stress testing |
| Isoproterenol is a ________________________. | B-1 = B-2, B3 agonist |
| Norepinephrine: | 1. alpha > beta affinity 2. Reflex bradycardia 3. Unopposed a-1 effect ---> Increase in Peripheral Resistance |
| Comparing NE vs Epi vs Isoproterenol: | 1. NE has the largest increment in Blood pressure, causes reflex bradycardia, and unopposed alpha-1 effects on peripheral resistance, and has higher alpha-adrenergic affinity than beta. 2. Epinephrine has almost equal alpha and beta affinity, increase HR, and decrease of peripheral resistance 3. Isoproterenol: greater beta affinity, reflex tachycardia, unopposed beta -2 effect, |
| Isoproterenol and Epinephrine __________________ heart rate, while _______________ has a ________________ heart rate. | Epi & Isoproterenol --> increase HR (epi due to B-1 stimulation); Norepinephrine decreases heart rate |
| What is the normal cardiac pacemaker? | SA node |
| How many bpm are seen in SA node? AV node? | SA node --- 60-100 bpm AV node --- 45-55 bpm |
| Besides the SA node cells, which are other possible cardiac pacemakers in case of SA dysfunction? | AV node, His bundle, Purjinke fibers |
| Atrial depolarization ----> | P-wave |
| Ventricular depolarization ----> | QRS complex |
| Ventricular repolarization -----> | T-wave |
| The T-wave on an ECG represents the ____________________. | Ventricular repolarization |
| The QRS in the ECG represents the _____________________. | Ventricular depolarization |
| P-wave on an ECG represents the ___________________________. | Atrial depolarization |
| Aberrant or deficient communication between the cells that connect the SA node and the AV node causes? | Third-degree AV block |
| Impulse generation (pacemaker cells) below the SA node and His Bundle, develop? | Heart rate as low as 20 bpm, and abnormally shaped QRS complexes. |
| A abnormally shaped QRS means: | - Pacemakers is below the AV node and His Bundle - Abnormal ventricular depolarization |
| In simple words, what is Pulmonary Arterial Hypertension? | Patient cannot pump blood through the lung and lung vasculature. |
| Pulmonary arterial HTN has: | 1. Increased: ----- Central venous pressure (CVP), RV ventricular size 2. Decreased: ------- PCWP and Cardiac output (CO) |
| What are the manifestations of the elevated CVP seen in pulmonary arterial HTN? | JVD, Hepatomegaly, and lower extremity edema |
| What are important findings in the Physical Exam of Pulmonary arterial HTN? | 1. Loud pulmonic component of S2 2. Accentuated, palpable impulse of the Left-sternal border (left parasternal lift due to RV heave) |
| How is the increased RV size in Pulmonary arterial HTN presented? | RV heave, Parasternal lift, and Loud P2 (pulmonic component of S2) |
| No pulmonary edema is associated with ____________________. | Pulmonary arterial HTN |
| What are the Dihydropyridine calcium channel blockers? | Amlodipine and Nifedipine |
| Side effects seen with Amlodipine and Nifedipine? | 1. PERIPHERAL EDEMA 2. Dizziness and lightheadedness |
| What is the most common trigger for AFIB development? | Ectopic Electrical foci in the PULMONARY VEINS |
| Which vessel is the most commonly involved in the development of AFIB? | Pulmonary Vein |
| In order to ablate AFIB, the catheter must reach the _____________. | Pulmonary Vein |
| What is an AV shunt? | Abnormal connections between the coronary arteries and a compartment in the venous side of the heart |
| What is instantly elevated or increased in developing an AV shunt? | Venous Return ---> right shift |
| Why is there an increase in Cardiac Output in AV shunt? | The AV fistula lowers the peripheral resistance, especially if it involves a large artery such as the abdominal aorta, which is compensated with an increase in cardiac output. |
| What other condition causes the same kind of shift in the cardiovascular curve as an AV fistula (shunt)? | Exercise |
| Heart failure and narcotic overdose, shows a ____________________ in cardiac output on the CV function curve, and _________________ in the venous return. | Decrease in CO; No change in Venous return |
| What is the mode of action of Fibrates? | 1. Activation of PPAR-g ------> decreased hepatic VLDL production and increase LPL activity ---> lowering of Triglycerides |
| What kind of lipid lowering agent is best for lowering Triglycerides? | Fibrates |
| Increase activation of PPAR-gamma receptors is seen in ____________, which causes a ________________ hepatic _______ production and __________________ ____________ activity. | Fibrates; decrease; VDLD; increase LPL |
| What is the first step in the pathogenesis of valvular vegetations seen in infective endocarditis? | Fibrin deposition on damaged endothelial surface. |
| Hemosiderin-laden cells | Stain blue with Prussian Blue |
| HF cells are? seen in? | Hemosiderin - laden cells; seen in pulmonary alveolar pathologies |
| Phenylephrine is a: | Selective Alpha-1 agonist |
| What are the effects produced by Phenylephrine? | 1. Increase in: Peripheral vascular resistance and Systolic BP 2. Decrease in: Pulse pressure and Heart rate |
| Systole accounts for the _____________ and _________________ in an ECG. | QRS complex and T-wave |
| QRS + T-wave = | Systole |
| In almost all tissues, the maximum blood flow is at _____________ _________, and minimum blood flow is during _______________, except for __________________________, which is reversed. | Max- ventricular systole Min - diastle Except Left Ventricular myocardium |
| Why is the blood flow in the Left Ventricular myocardium different for all tissues? | During ventricular systole (contraction), the vessels surrounding the LV myocardium are compressed, not allowing the passage of flow of blood. |
| Why is the right ventricular myocardium's blood flow not reversed as in LV myocardium? | The pressure in the RV is so low, that during contraction it still can flow with normality. |
| What kind of antiarrhythmics work in the AV nodes (atrial tissue)? | Class II and Class IV |
| Which kind of antiarrhythmics work on regular myocardium (ventricular)? | Class I and Class III |
| Decreased slope of phase 0 depolarization of ventricular muscle? | Class I antiarrhythmics |
| Class II antiarrhythmics mechanism of action? | 1. Decrease slope of phase 4 depolarization, 2. Prolong repolarization at the AV node |
| Prolonged repolarization at ventricular tissue | Class III antiarrhythmics |
| 1. Slows the rise in action potential, 2. Prolong repolarization of the AV node | Class IV antiarrhythmics |
| Neprilysin | Responsible for breakdown of Natriuretic peptides and AT II |
| What protein is responsible for the catabolism of ANP, BNP and AT II? | Neprilysin |
| The inhibition of Neprilysin causes? | Increased activity of natriuretic peptides and AT II |
| Neprilysin is co-administer with _________________, in the treatment of heart failure. | ARBs |
| What are the negative effects of AT II? | Vasoconstriction and fluid retention |
| What are the positive effects of Natriuretic peptides? | Vasodilation and Diuresis |
| Common neprilysin inhibitor? | Sacubitril |
| B-blocker therapy is to be used carefully in what kind of patients and contraindicated to what patients? | Carefully used in decompensated HF patients and contraindicated in cardiogenic shock patients. |
| What are the two key hemodynamic characteristics of Diastolic Heart Failure (dysfunction)? | 1. Preserved Ejection fraction (>50%) 2. Reduction of stroke volume due to reduced cardiac output |
| Describe the pathogenesis in Diastolic HF. | Prolonged HTN --> LV concentric hypertrophy --> LV wall becomes stiff and less complaint --> impaired diastolic relaxation + increased LVED pressure --> Pulmonary edema ---> Reduced LVEDV --> decreased CO --> decreased stroke volume |
| What substance is accumulated in Natriuretic peptides and Sildenafil? | cGMP |
| _________________ is a ________________________ which decreases the degradation of _________, leading to relaxation of vascular smooth muscle and vasodilation. | Sildenafil; Phosphodiesterase inhibitor; cGMP |
| Stimulation guanylyl cyclase increases the conversion of cGTP in to _________, and it is seen with _________, ________, and d__________. | cGMP; ANP, BNP, and NO |
| DMC results from direct damage to cardiomyocytes leading to: | 1. Myocardial contractile dysfunction (systole dysfunction) 2. Volume overload 3. Ventricular dilation |
| What are the MC organisms seem to cause a viral myocarditis? | Coxsackie A, adenovirus, and influenza virus |
| What kind of hypertrophy is seen in DCM? | Eccentric cardiomyocyte hypertrophy |
| Decompensated Heart Failure patient presents clinically as: | Dyspneic, lower extremity edema, JVD, and pulmonary crackles |
| Diastolic dysfunction is developed in _____________ and _________. | Hypertrophic cardiomyopathy and Restrictive cardiomyopathy |
| A "stiff" heart usually indicates _________________ cardiomyopathy. | Restrictive |
| A heart with increased intraseptal thickness is indicated of _________________ cardiomyopathy. | Hypertrophic |
| Coronary Steal syndrome involves the ____________________. | Coronary arterioles |
| What structures are referred as the epicardial vessels? | Large coronary vessels such as RCA and LCX |
| What are the only vessels that trigger a Coronary steal? | Coronary arterioles |
| What is the initial insult or change in Septic shock? | Peripheral vasodilation |
| Septic shock can be presented with ________________ or ____________________. | Hypothermia or Hyperthermia |
| What hemodynamic changes are seen in Septic shock with the initial peripheral vasodilation? | Decreased CVP, decreased systemic vascular resistance, and decreased PCWP. |
| How is cardiac output in Septic shock? how does it affect? | CO is increased, which causes high flow rates ---> incomplete oxygen extraction at the tissues ----> High mixed venous blood saturation (MvO2) |
| An increased SVR is the only elevated hemodynamic change in? | Hypovolemic shock |
| What changes are seen to be lowered in Cardiogenic shock? | LV output and MvO2 |
| How is the PCWP in Cardiogenic shock and Obstructive (if caused only by cardiac tamponade)? | Increased |
| Selective PERIPHERAL Dopamine-1 agonist | Fenoldopam |
| When is Fenoldopam used? | Treatment of Hypertensive crisis in patients with renal insufficiency. |
| What are the effects produced by Fenoldopam? | 1. Arteriolar dilation 2. Increases renal perfusion 3. Promotes diuresis and natriuresis |
| ARBs block the ___________, and cause an increase in ______________, and a decrease in ___________, with no changes in __________ levels. | ATII; Increase AT I, AT II, and Renin; Decrease in Aldosterone; no changes in Bradykinin |
| HCM presents a ____________________ which is worsen by _____________. | Left Ventricular Outflow tract obstruction (LVOT); Decreased LV volume. |
| How is LV volume diminished? in what non-valvular heart condition are these contraindicated? | 1. Diuretics --> Decrease the preload 2. Vasodilators (Dihydropyridine Ca2+ channel blockers, Nitroglycerin, and ACE inhibitors) ----> Reduce systemic vascular resistance. CI in HCM |
| What is the treatment of HCM? Why? | Negative Inotropic agents such as B-blockers, Non-dihydropyridine calcium channel blockers, and disopyramide. Reducers the LVOT obstruction |
| What is the MC deficiency leading to Homocysteine accumulation? | MTHFR mutation |
| What vitamin i6s used by MTHFR? | Vitamin B2 (riboflavin) |
| What vitamin is used in the Transsulfuration pathway? | Vitamin B6 |
| What enzymes in the homocysteine pathway use Vitamin B6? | Cystathionine synthase and Cystathionine |
| Methionine synthase is an enzyme that requires ___________ as cofactor, and aids in production of __________________. | Vitamin B12; Methionine |
| What enzyme is deficient or mutated, thus preventing Homocysteine to converting into Methionine? | MTHFR |
| What is the ejection fraction (EF) formula? | = SV/EDV |
| SV = | (EDV - ESV) / EDV |
| What is the most common side effect of Fibrinolysis? | Hemorrhage (GI bleed or intracerebral) |
| What are some important fibrinolytics? | Alteplase, Streptokinase, tPA |
| What is the difference between SVC vs Brachiocephalic vs Subclavian compression? | SVC ---> BILATERAL facial, neck, chest and arm edema Brachiocephalic ---> Unilateral facial, neck, chest and arm edema Subclavian ---> Unilateral arm edema |
| BILATERAL facial, neck, chest and arm edema | SVC mass compression/obstruction |
| Patient with a benign mass compressing the Subclavian vein will have? | Ipsilateral arm edema/swollen |
| Patient shows signs of tenderness, warm, and swolleness on the right side of face, neck and arm. Dx? | Right brachiocephalic vein compression/obstruction |
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rakomi
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