PBL 2 Flashcards

1
Q

What factors determine the amount of blood pumped out of the heart?

A
  • CO=HRxSV
  • CO is determined by filling pressure/central venous pressure, peripheral venous pressure.
    • must be a change in pressure for flow to occur.
  • Starling’s law: “the heart pumps what it receives”
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2
Q

What factors determine the amount of blood pumped through a given tissue?

A
  • Q=ΔP/R
  • Arteriole constriction is the most important factor in tissue resistance.
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3
Q

What are the components of a normal electrocardiogram (ECG)?

How does each component of the ECG relate to the mechanical events of the cardiac cycle?

A
  • P wave = Atrial Depolarization (contraction)
  • PRI = impulse traveling from SA to AV Node
  • QRS Complex = Ventricular Depolarization
  • ST segment = Plateau phase of Myocardial AP
  • T wave = Ventricular repolarization
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4
Q

What makes the heart beat in a regular fashion?

A
  • Pacemaker cells
    • have the funny channels which allow in Na+, but allow out K+ (Overall net increase of Na+ in, and thus slow depolarization).
    • Transient Ca+2 channels allow calcium in to reach threshold for full depolarization
    • Transient channels then close
    • Slow channels of Ca+2 allow for sustained entry of calcium and for the cell to remain in a depolarized state until contraction, and influx of K+ hyperpolarize the cell again.
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5
Q

What alterations in pacemaker cell structure and function can lead to an irregular heartbeat?

A
  • Disturbance of either impulse FORMATION or impulse CONDUCTION = arrhythmia
  • Irregular heartbeats can happen in times of sympathetic innervation.
    • NE acts on alpha 1 receptors to increase Na+ permeability and decrease K+ permeability
      • PVC/PACs
  • When there is damage to parts of the heart, like the AV node, it can have conduction re-entry block (A-fib, A-flutter, or 2° blocks)
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6
Q

How do you explain the pain associated with myocardial infarction?

A
  • Viscerosomatic Convergence
  • Heart → innervated by the Vagus (CNX) Nerve (parasympathetic), Cervical & Thoracic Sympathetic Trunk.
    • central nervous system (CNS) perceives pain from the heart as coming from the somatic portion of the body supplied by the thoracic spinal cord segments T1-4(5) because the dermatomes of this region of the body wall and upper limb have their neuronal cell bodies in the same dorsal root ganglia (T1-5) and synapse on the same second order neurons in the spinal cord segments (T1-5) as the general visceral sensory fibers from the heart.
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7
Q

What is the classic presentation of a myocardial infarction?

A
  • Chest pain described as sensation of tightness, pressure, or squeezing
    • Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and upper abdomen, where it may mimic heartburn
  • Dyspnea, diaphoresis, weakness, light-headedness, nausea, vomiting, and palpitations
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8
Q

How does MI presentation differ in women?

A
  • Women are more likely than men to experience some of the other uncommon symptoms, such as jaw or back pain, shortness of breath, and nausea or vomiting.
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9
Q

What biochemical markers can be measured to assess the likelihood of a myocardial infarction?

A
  • Troponin
    • highly sensitive and specific for damage to the myocardium
  • NTproBNP
    • detects heart failure, indicative of excess ventricular stretching
  • D-dimer
    • rule out PE, DVT, DIC
  • CK
    • measure of reinfarction
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10
Q

What is the basic biochemistry and physiology of NTproBNP?

A
  • N-terminal pro B-type Natriuretic Peptide, or BNP
  • pro form gets cleaved by an enzyme → Brain Natriuretic Protein aka Ventricular Natriuretic Protein
    • which is secreted by the ventricles in response to excessive stretching in the cardiac tissue.
    • The half-life of these proteins are 10x longer than that of ANP (atrial natriuretic protein) so it helps to interpret the pathophysiology.
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11
Q

What is the basic biochemistry and physiology of Troponin?

A
  • Troponin is a protein made of three smaller proteins: c, i, and t
    • found in striated muscles.
  • Gets released into circulation as a result of myocardial death/damage → loss of membrane stability → leak contents of the cell
  • Troponins i and t are highly sensitive and specific for damage to the myocardium, and most notably myocardial infarctions.
    • can remain high up to two weeks
    • can also be high due to other strains on the heart e.g. SVT
  • Troponin I = most sensitive and specific marker
    • rises 2-4 hours after infarction
    • peaks at 24 hours
    • returns to normal by 7-10 days
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12
Q

What is the basic biochemistry and physiology of Creatine Kinase?

A
  • A measure of reinfarction.
    • Because Troponin remains elevated 7-10 days post MI and CK normalized 48-72 hours post-infarct
    • CK can be used to rule in a reinfarction before Troponin normalizes.
  • Rises 4-6 hours after infarction
  • Peaks at 24 hours
  • Returns to normal in 48-72 hours
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13
Q

What is the basic biochemistry and physiology of D-dimer?

A
  • Plasmin breaks cross-linked Fibrin into D-dimers
    • They are not normally in circulation unless there has been some kind of coagulation event.
    • When there is an abnormal level it is indicative of:
      • Pulmonary Embolism
      • Deep Vein Thrombosis
      • DIC
      • IF NEGATIVE, RULE OUT.
      • IF POSITIVE… You don’t know shit.
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14
Q

What is the epidemiology (deaths/yr, incidence, prevalence) of coronary artery disease and MI in the US?

A
  • Epidemiology: Heart disease=~600,000 Deaths/year.
    • NUMBER 1 KILLER IN THE US
  • Incidence: 735,000 people will have an MI each year.
    • 525,000 will have their first
    • 210,000 will have their second
  • Prevalence: 6.2% in persons ≥ 20 years old
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15
Q

What is a coronary angiogram?

A
  • X-ray with radiocontrast in the coronary arteries
  • Fluorescent dye is injected into coronary vessels via catheterization and X-Rays are taken
  • Used to determine which coronary arteries are blocked and the extent of the blockage, and what treatment is best.
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16
Q

What is the MOA of morphine?

A
  • works on mu receptors to decrease pain
  • analgesic
17
Q

What is the MOA of Nitroglycerin?

A

forms free radical NO → activates guanylyl cyclase → increases cGMP → activates MLC phosphatase → dephosphorylation of MLC → smooth muscle relaxation → vasodilation (mostly veins) → decrease blood returning to heart (central venous pressure) → decrease preload → decrease stress on myocardium → decrease oxygen demand

(antihypertensive)

18
Q

What is the MOA of Clopidogrel (Plavix)?

A
  • Irreversibly blocks ADP receptors on platelet cell membranes→ blocks platelet activation
    • anticoagulant
19
Q

What is the MOA of Heparin?

A

Potentiates activity of antithrombin III → inactivates thrombin → prevents conversion of fibrinogen to fibrin

Anticoagulant

20
Q

What is the MOA of Eptifibatide?

A

Binds to GPIIb/IIIa receptor on activated platelets → prevents fibrinogen from binding → prevents aggregation

ANTICOAGULANT

21
Q

What is the MOA of thrombolytics like tPA?

A

Directly or indirectly aid conversion of plasminogen → plasmin, which cleaves thrombin and fibrin clots.

(Examples: Alteplase (tPA), reteplase, tenecteplase)

22
Q

What is the MOA of “Statins”?

A
  • inhibit cholesterol synthesis by inhibiting HMG-CoA reductase
    • reduce plaque formation in the vessels
    • decrease mortality post-MI

(Examples: anything that ends in ***-statin)

23
Q

What is the MOA of Beta Blockers?

A
  • block β1-adrenergic receptors located mainly in the heart and in the kidneys and β2-adrenergic receptors located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle
  • used for the management of cardiac arrhythmias, protect the heart from a second heart attack (myocardial infarction) after a first heart attack (secondary prevention), and, in certain cases, hypertension
  • Examples: Atenolol, Metoprolol, anything -olol
24
Q

What is the MOA of ACE Inhibitors?

A
  • inhibit the angiotensin-converting enzyme, an important component of the renin-angiotensin-aldosterone system (RAAS)
  • cause relaxation of blood vessels, as well as decreased blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart
  • Examples: perindopril, captopril, enalapril, lisinopril, and ramipril.
25
Q

What are the common drugs included in drug-eluding stents?

A
  • Antiproliferative drugs:
    • sirolimus (blocks mTOR)
    • paclitaxel (interferes with normal breakdown of microtubules)
26
Q

What are the pathologic changes associated with the subtypes (stages) of atherosclerosis?

A
  • ↑LDL in intima → inflammation → macrophage recruitment → foam cells = fatty streak
  • foam cell accumulation → necrosis → ↑inflammation → fibrous tissue forms cap = fibrofatty plague
  • Plaque growth and remodeling leads to:
    • aneurysm and rupture
    • occlusion by thrombus
    • critical stenosis
27
Q

What is the pathology of myocardial infarction including the gross and microscopic
features?

A
  • A coronary artery atheromatous plaque undergoes an acute change consisting of intraplaque hemorrhage, erosion or ulceration, or rupture or fissuring.
  • When exposed to subendothelial collagen and necrotic plaque contents, platelets adhere, become activated, release their granule contents, and aggregate to form microthrombi.
  • Vasospasm is stimulated by mediators released from platelets.
  • Tissue factor activates the coagulation pathway, adding to the bulk of the thrombus.
  • Within minutes, the thrombus can expand to completely occlude the vessel lumen.
  • Under 4 hours, no changes are seen, micro or macro
  • 4-24 hours, coagulative necrosis and a darker discoloration of the tissue is seen
  • > 24 hours Neutrophils followed by macrophages are seen
28
Q

What are common complications of therapies for MI and the mechanisms by which they occur?

A
  • Fibrinolysis or angioplasty: open up blocked vessel with medication or in cath lab
    • 1.Reperfusion of irreversibly damaged cells results in calcium influx, leading to hypercontraction of myofibrils → contraction band necrosis
    • 2.Return of oxygen and inflammatory cells may lead to free radical generation → further damaging mycocytes → reperfusion injury
  • Anticoagulants/Thrombolytics risk bleeding.
29
Q

What is the difference between bare-metal and drug-eluting stents for the management of coronary artery disease?

A
  • Drug-eluting stents are preferred to bare metal if the patient can tolerate and comply with the dual antiplatelet therapy and if the risk of restenosis is increased (left main disease, small vessels, long lesions, diabetes, multiple lesions)
  • Bare-metal stents are preferred in patients with a high risk of bleeding, inability to comply with antiplatelet therapy, or anticipated invasive surgical procedure in the next 12 months
30
Q

Who decides whether organs and/or tissues are donated following a person’s death?

A
  • Legally: organ donor status overrides family’s wishes
  • Actually: not many ER docs will overrule family, even if the donor status is on the license
31
Q

What is the phenotype, possible genotype, and mode of inheritance of familial hypercholesterolemia (also called hyperlipidemia type IIA)?

A
  • Autosomal Dominant
  • Homozygotes have SEVERE cardiovascular disease
    • cholesterol between 500-1,000 mg/dL (13-25.9 mmol/L)
    • LDL-C > 600 mg/dL (15.5 mmol/L)
  • heterozygotes have LESS severe problems
    • total cholesterol between 310-550 mg/dL (9-14 mmol/L)
    • low-density lipoprotein cholesterol (LDL-C) between 190-400 mg/dL (5-10 mmol/L)
    • normal triglycerides
  • LDLR receptor (ATM Machine) gene is mutated OR
  • APOB (apolipoprotein B) gene mutated OR
  • pro-protein convertase subtilisin/kexin 9 (PCSK9) gene mutated
32
Q

What is Prinzmetal’s angina?

A
  • Prinzmetal’s angina is a vasospasm in a coronary artery, which leads to ischemia and chest pain.
  • It typically occurs at rest and in cycles and can occur in a diseased artery or a healthy one.
  • It can be seen on an EKG as ST segment elevation.