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Cardiology 2

UWORLD + FA Cardio Review

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
Created by: rakomi



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When you need a break, try one of the other activities listed below the flashcards like Matching, Snowman, or Hungry Bug. Although it may feel like you're playing a game, your brain is still making more connections with the information to help you out.

To see how well you know the information, try the Quiz or Test activity.

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