Week 3 Flashcards
Which region of the heart is most likely affected in this patient, based on the ECG leads?
A. Anteroapical left ventricle
B. Anteroseptal left ventricle
C. Anterolateral left ventricle
D. Inferior wall of left ventricle
C. Anterolateral left ventricle
The patient exhibits signs and symptoms consistent with acute transmural myocardial infarction (MI). Typical symptoms include severe chest pain not relieved by rest or nitroglycerin, diaphoresis, dyspnea, nausea, lightheadedness, palpitations. Peaked T waves are the first ECG sign, reflecting localized hyperkalemia, then ST-segment elevation follows within minutes to hours.
The patient has most likely suffered a transmural infarct of the anterolateral left ventricle (C is correct), as evidenced by ECG changes in the anterior (V1-V3) and lateral (I, aVL) chest leads.
Card from 2018 - 2019 lectures
Cardiac catheterization in this patient will most likely show which of the following?
A. Atherosclerotic plaque obstructing 50% of the lumen, no thrombus
B. Atherosclerotic plaque obstructing 80% of the lumen, no thrombus
C. Significant coronary artery vasospasm causing flow obstruction
D. Ruptured atherosclerotic plaque with fully obstructive thrombus
D. Ruptured atherosclerotic plaque with fully obstructive thrombus
Explanation:
Transmural infarction is most commonly caused by an acute plaque change (rupture) which produces a superimposed thrombus that completely occludes the involved coronary artery (D is correct).
An atherosclerotic plaque obstructing 50% of lumen with no thrombus would be unlikely to produce symptomatic myocardial ischemia. Symptoms of stable angina do not become proeminent until at least 75% of the cross-sectional area of the coronary artery lumen is occluded (A incorrect).
Lesion described in B is a stable plaque producing a fixed obstruction. Patient would most likely be suffering from stable angina, with chest pain induced by exercise and stabilized by rest or sublingual nitroglycerin.
Finally, coronary artery vasospasm (C) occurs in Prinzmetal’s or variant angina, an uncommon condition of episodic angina that occurs at rest. The spasm may occur at sites of coronary atherosclerosis and can result in transient transmural ischemia with ST elevation on ECG. However, the spasm of Prinzmetal’s responds promptly to vasodilators like nitroglycerin.
Card from 2018 - 2019 lectures
A 52-year old male presents to your office complaining of periodic substernal chest pain that is precipitated by fast walking, especially uphill and against the wind. The pain remits following 5 minutes of rest. The patient has a history of HTN and smokes a pack of cigarettes a day. Which of the following is the most likely pathophysiologic mechanism of this patient’s condition?
A. Atherosclerotic plaque obstructing 50% of the lumen, no thrombus
B. Atherosclerotic plaque obstructing 80% of the lumen, no thrombus
C. Significant coronary artery vasospasm causing flow obstruction
D. Ruptured atherosclerotic plaque with fully obstructive thrombus
B. Atherosclerotic plaque obstructing 80% of the lumen, no thrombus
Explanation:
- The patient has symptoms characteristic of typical stable angina pectoris: deep, poorly localized chest or arm discomfort (angina) + angina reproducibly associated with physical exertion or emotional stress + relieved within 5 minutes by rest or sublingual nitroglycerin.
- He also has 2 major risk factors for atherosclerosis : HTN and smoking.
- Lesion most often underlying stable angina is a fixed atheromatous obstruction of one or more coronary arteries occluding at least 75% of the luminal cross sectional area. B is correct.
A is no symptoms, C is Prinzmetal’s angina, D is acute MI
Card from 2018 - 2019 lectures
A 59-year old woman presents to the ER with crushing chest pain, sweating and lightheadedness. BP is 90/60 and heart rate 48. ECG shows sinus bradycardia and ST segment elevation in leads II, III, aVF. Occlusion of which of the following coronary arteries is most likely responsible for this patient’s condition?
A. Left main coronary artery
B. Left anterior descending artery
C. Left circumflex artery
D. Right coronary artery
A. Left main coronary artery – gives rise to LAD and LCX, so ST elevations for leads corresponding to both.
B. Left anterior descending artery – V1-V4 mainly
C. Left circumflex artery – V5-V6, I, aVL
D. Right coronary artery – II, III, aVF
Explanation: Patient presents with symptoms and ECG findings consistent with MI of the inferior wall of the heart, which in 90% of individuals is supplied by the posterior descending branch of the right coronary artery (D is correct). Of note, the patient’s bradycardia and hypotension suggests that there may have been ischemic injury to the SA node as well.
Card from 2018 - 2019 lectures
A 68-year old man comes to the ER due to lightheadedness, weakness and palpitations. BP is 110/60, pulse 144/min and irregular. ECG shows an irregularly irregular rhythm and absent P waves. Long-term anticoagulation is initiated to prevent atrial thrombus formation and he is eventually discharged home on warfarin. Which of the following is the best test to monitor the anticoagulation effect of warfarin in this patient?
A. Activated partial thromboplastin time
B. Bleeding time
C. Fibrin split products
D. Fibrinogen levels
E. Prothrombin time
E. Prothrombin time
Explanation: The patient’s ECG suggests A Fib, which makes thrombus formation more common (especially LA appendage). If this thrombus detaches from the atrial wall, there is a risk of stroke. The oral anticoagulant warfarin reduces thrombus formation risk by inhibiting the activation of Vit K dependent clotting factors II, VII, IX and X. This leads to decreased levels of these factors, particularly Factor VII, therefore prolonging the prothrombin time (E is correct).
- aPTT is used to monitor heparin therapy, which primarily affects the intrinsic coagulation pathway. (A is incorrect).
- Bleeding time is used to assess platelet function. Increased bleeding time can be seen with thrombocytopenia, von Willebrand disease, aspirin therapy etc. (B is incorrect)
- The combination of decreased fibrinogen levels and fibrin split products (D-Dimer) is characteristic of disseminated intravascular coagulation (DIC). (C, D are incorrect).
Card from 2018 - 2019 lectures
A 56-year old man comes to the clinic for a routine checkup. PMH includes HTN, Type 2 DM, hyperlipidemia. His blood pressure is 152/101 and pulse 87/min. Waist circumference is 110 cm (43 inches). Laboratory studies show: LDL 161 mg/dL. Fasting blood glucose 201 mg/dL. Hemoglobin A1c: 7.4%.
Which of the following vascular beds is most likely to carry the highest atherosclerotic burden in this patient?
A. Carotid arteries
B. Coronary arteries
C. Mesenteric arteries
D. Renal arteries
B. Coronary arteries
Explanation:
- Patient has multiple risk factors that contribute to atherosclerosis: HTN, DM, hyperlipidemia. Pathophysiology: focal intima thickening due to accumulation of lipid-laden macrophages and extracellular matrix (fatty streaks). With advancing age, there is transition of fatty streaks to atherosclerotic plaques and more advanced lesions develop a lipid-rich necrotic core and regions of calcification.
- The most susceptible vascular regions involve bends and branch points, which cause turbulence and local flow disruption. Of all the major vascular beds, the lower abdominal aorta and coronary arteries (B is correct) are the most susceptible to atherosclerosis. Atherosclerotic lesions occur in these vessels as early as the second decade of life.
Card from 2018 - 2019 lectures
A 12-year old boy experiences excessive bleeding following a tooth extraction. PMH includes episodes of painful joint swellings from minor trauma. Laboratory results are as follows:
- Bleeding time: 5 minutes (normal = 2-9 minutes)
- Prothrombin time: 23 seconds (normal = 11-14 seconds)
- Activated partial thromboplastin time: 25 seconds (normal = 25-40 seconds)
Patient most likely has a deficiency involving which of the following factors?
A. Factor VII
B. Factor VIII
C. Factor XI
D. Von Willebrand factor
A. Factor VII
Explanation:
Patient’s hemarthroses and excessive bleeding following tooth extraction are suggestive of a coagulopathy (clotting factor deficiency). Lab results show normal bleeding time, normal aPTT and prolonged PT.
- Normal bleeding time indicates adequate platelet function (vWF is mediator of platelet adhesion to endothelium, therefore deficiency of vWF results in increased bleeding time, D is incorrect). Normal aPTT indicates an intact intrinsic coagulation system (deficiency in either factor VIII and factor XI will result in normal bleeding time, normal PT, prolonged aTT). (B and C are incorrect).
- The prolonged PT indicates a defect in the extrinsic coagulation pathway, most commonly factor VII (A is correct).
Card from 2018 - 2019 lectures
Question: What is atypical angina, and what are the types of patients more likely to present with atypical angina?
Answer: Atypical angina does not have the classic presentation and may be atypical in location and not necessarily associated with provoking factors (not brought on by stress or exertion). Presenting symptoms of atypical angina are anginal “equivalents” or other symptoms of myocardial ischemia: dyspnea, nausea, fatigue, faintness. Women, elderly patients, and diabetics are more likely to present with atypical angina
Angina is defined as pain or discomfort in the chest or adjacent areas caused by insufficient blood flow to the heart. Its clinical types are: chronic/stable, atypical, anginal equivalents and silent ischemia, and others (Decubitus, nocturnal, refractory, unstable, microvascular, vasospastic)
Learning objective: SM 128a – Ischemic Heart Disease: Pathophysiology (State the definition, characteristics, and epidemiology of angina)
Question: Which of these is true about the release of cardiac enzymes during an acute coronary event?
- Peak values of Troponin-I occur at around 24 hours when blood flow is not restored; if blood is restored, then the peak of Troponin-I is delayed to 36 hours
- If a patient had a cardiac event prior to 48 hours ago, their CK-MB level should be elevated
- Troponins are continuously released for 1-2 weeks after the inciting cardiac event
- MIs can occur without the release of troponin-I, which is why it is crucial to also check levels of CK-MB
Answer: C. Troponins are continuously released for 1-2 weeks after the inciting cardiac event. When there is damage to the myocardium, structural components of the myocyte including troponin-I and -T and CK-MB are released. The levels of these enzymes rise in the blood and can be detected within 4-6 hours after injury. Peak values occur at 24 hours if blood flow is not restored, and 12 hours if blood flow is restored (A is incorrect). CK-MB then decreases gradually over 2-3 days, while troponins persist for 1-2 weeks. Therefore, troponins can be used to detect events that have occurred at least 48 hours ago (B is incorrect). Myocardial infarction does not occur without troponin-I release (D is incorrect). Currently, any myocardial release of troponin-I in the setting of an episode of chest pain and/or ECG changes is considered as evidence of myocardial necrosis and an indicator of worse prognosis.
Learning objective: SM 129a – Acute Coronary Syndromes: Pathophysiology (Explain the various diagnostic tools to detect and quantify myocardial injury and necrosis)
Question: Which of the following describes a mechanism that regulates blood pressure that can contribute to hypertension?
A) Increased bradykinin
B) Increased firing of afferent baroreceptors (in the carotid sinus and aortic arch, etc.)
C) Decreased intracellular calcium levels
D) Increased aldosterone
Explanation: The correct answer is D). Aldosterone, which is secreted by the adrenal gland, leads to increased sodium absorption which leads to an increase in intravascular volume that leads to higher blood pressure. Increased aldosterone can happen through stimulation by the renin-angiotensin system (increased angiotensin II). Primary aldosteronism can also be caused by an adrenal adenoma or from bilateral hyperplasia of the adrenal glands.
A is not correct. Bradykinin is a vasodilator, so increased bradykinin will lead to vasodilation and a decrease in peripheral vascular resistance and a lower blood pressure. This can be seen in Pouiselle’s Law, where increasing the vessel radius leads to a decrease in blood pressure. Decreases in Angiotensin II levels can lead to increased bradykinin levels.
B is not correct. The afferent baroreceptors in the carotid sinus, aortic arch, left ventricle, and juxtaglomerular apparatus in the kidney senses effective arterial blood volume and fires when high blood pressures are detected. Increased firing of afferent baroreceptors leads to decreased sympathetic tone which leads to decreased blood pressures through decrease in cardiac contractility, heart rate, and arterial constriction.
C is not correct. Increased, not decreased, intracellular calcium levels in the vascular endothelium leads to vasoconstriction which increases peripheral vascular resistance and increases blood pressure. Calcium channel blockers that decrease intracellular calcium levels thus are used to treat hypertension.
Learning objective: SM 133: Hypertension Pathophysiology and Pharmacology (Explain the mechanisms responsible for the pathogenesis of hypertension)
(Question from old MSTP review sessions)
Question: Fill in the blanks about microvascular resistance (R2) in the coronary vasculature.
- Under basal conditions, microvascular resistance (R2) is normally low or high
- R2 is adjusted on a global or local basis
- R2 follows Poiseuille’s law and is directly or inversely proportional to the vessel radius doubled or tripled or quadrupled
Learning objective: SM 134: Coronary Blood Flow (Explain the major factors governing coronary vascular resistance and coronary blood flow, Explain coronary flow reserve and factors affecting its magnitude)
Learning objective: SM 134: Coronary Blood Flow (Explain the major factors governing coronary vascular resistance and coronary blood flow, Explain coronary flow reserve and factors affecting its magnitude)
Explanation:
- Under basal conditions, microvascular resistance (R2) is normally high
- R2 is normally high and is adjusted on a local basis via metabolic and endothelial factors to achieve vasodilation (resulting in lowered R2)
- R2 is adjusted on a local basis
- This adjustment of R2 is governed by mainly metabolic factors (adenosine, PO2) as well as endothelial factors (EDRF, EDHF, prostacyclines) and neurohumoral factors
- R2 follows Poiseuille’s law and is inversely proportional to the vessel radius quadrupled
Question: Name the following components of an ECG tracing. What are the normal ranges for the: PR interval, QRS interval, and QT interval?
Explanation:
- P-wave
- PR interval: 0.12-0.20 seconds
- QRS complex: up to 0.10 seconds
- ST segment
- T-wave
- QT interval: must be corrected for heart rate.
Upper limit of normal for men = 0.45 seconds, women = 0.46 seconds
Learning objective: SM 130: ECG II (Describe the principles behind basic measurements: PR interval, QRS interval, QT interval, QRS and T axis (normal or abnormal), heart rate)
Question: A patient with a history of MI is prescribed an antibody-based drug that interferes with platelet aggregation. Which molecule does it target?
- ADP P2Y12 receptor
- TXA2
- Intracellular ADP
- Intracellular cAMP
- GPIIb/IIIa
Explanation: the correct answer is E – GPIIb/IIIa
- ADP P2Y12 receptor - Thienopyridines
- TXA2 - Aspirin
- Intracellular ADP - none
- Intracellular cAMP - Dipyridamole
- GPIIb/IIIa – abciximab
Learning objective: SM 132: CAD pharmacology (Describe the various types of antiplatelet agents, how their targeted receptors differ, and how they affect platelet function)
Question from old MSTP review sessions
Question: In which leads would you likely see ST segment elevation in during a:
Anterior MI
Lateral MI
Inferior MI
Explanation:
Anterior MI: V1-V4
Lateral MI: I, aVL, V5-V6
Inferior MI: II, III, aVF
Learning objective: SM 131: ECG III (Explain how to localize an ischemic process (including MI) to an area of the heart and, by extension, to a specific coronary artery)
