Cardiovascular

Cardiovascular US Medical PG Question 1: A 48-year-old male accountant presents to the family practice clinic for his first health check-up in years. He has no complaints, and as far as he is concerned, he is well. He does not have any known medical conditions. His blood pressure is 140/89 mm Hg and his heart rate is 89/min. Physical examination is otherwise unremarkable. What is the single best initial management for this patient?

• A. Treat the patient with beta-blockers.
• B. Try angiotensin-converting enzyme inhibitor.
• C. Start trial of calcium channel blockers.
• D. Return to the clinic for a repeat blood pressure reading and counseling on the importance of aerobic exercise. (Correct Answer)
• E. The patient does not require any treatment.

Cardiovascular Explanation: ***Return to the clinic for a repeat blood pressure reading and counseling on the importance of aerobic exercise.*** - The patient's blood pressure of **140/89 mm Hg** is considered **Stage 1 hypertension**. It is crucial to confirm sustained hypertension with **repeat measurements** over several weeks to avoid misdiagnosis and unnecessary medication. - Initial management for Stage 1 hypertension without other compelling indications typically involves **lifestyle modifications**, such as regular aerobic exercise, dietary changes, and weight management, before initiating pharmacotherapy. *Treat the patient with beta-blockers.* - **Beta-blockers** are generally not first-line agents for isolated hypertension unless there are specific indications such as **concomitant heart failure**, **post-myocardial infarction**, or **migraines**. - Without confirmed sustained hypertension and prior lifestyle interventions, initiating beta-blockers would be **premature**. *Try angiotensin-converting enzyme inhibitor.* - **ACE inhibitors** are effective first-line agents for hypertension, but only after proper diagnosis confirmation and a trial of **lifestyle modifications**. - Rushing to medication without confirming sustained hypertension and exploring non-pharmacological approaches is **not the recommended initial step**. *Start trial of calcium channel blockers.* - **Calcium channel blockers** are also effective antihypertensive agents, especially in older adults or those with **isolated systolic hypertension**. - However, similar to other pharmaceutical interventions, they should be considered **after confirming sustained hypertension** and attempting lifestyle changes. *The patient does not require any treatment.* - A blood pressure reading of **140/89 mm Hg** is elevated and indicates **Stage 1 hypertension**, which requires management. - While immediate medication might not be necessary, **monitoring and lifestyle interventions** are crucial to prevent progression to more severe hypertension and cardiovascular complications.

Cardiovascular US Medical PG Question 2: An 83-year-old male presents with dyspnea, orthopnea, and a chest radiograph demonstrating pulmonary edema. A diagnosis of congestive heart failure is considered. The following clinical measurements are obtained: 100 bpm heart rate, 0.2 mL O2/mL systemic blood arterial oxygen content, 0.1 mL O2/mL pulmonary arterial oxygen content, and 400 mL O2/min oxygen consumption. Using the above information, which of the following values represents this patient's cardiac stroke volume?

• A. 30 mL/beat
• B. 70 mL/beat
• C. 40 mL/beat (Correct Answer)
• D. 60 mL/beat
• E. 50 mL/beat

Cardiovascular Explanation: ***40 mL/beat*** - First, calculate cardiac output (CO) using the **Fick principle**: CO = Oxygen Consumption / (Arterial O2 content - Venous O2 content). Here, CO = 400 mL O2/min / (0.2 mL O2/mL - 0.1 mL O2/mL) = 400 mL O2/min / 0.1 mL O2/mL = **4000 mL/min**. - Next, calculate stroke volume (SV) using the formula: SV = CO / Heart Rate. Given a heart rate of 100 bpm, SV = 4000 mL/min / 100 beats/min = **40 mL/beat**. *30 mL/beat* - This answer would result if there was an error in calculating either the **cardiac output** or if the **arteriovenous oxygen difference** was overestimated. - A stroke volume of 30 mL/beat with a heart rate of 100 bpm would yield a cardiac output of 3 L/min, which is sub-physiologic for an oxygen consumption of 400 mL/min given the provided oxygen content values. *70 mL/beat* - This stroke volume is higher than calculated and would imply either a significantly **lower heart rate** or a much **higher cardiac output** than derived from the Fick principle with the given values. - A stroke volume of 70 mL/beat at a heart rate of 100 bpm would mean a cardiac output of 7 L/min, which is inconsistent with the provided oxygen consumption and arteriovenous oxygen difference. *60 mL/beat* - This value is higher than the correct calculation, suggesting an error in the initial calculation of **cardiac output** or the **avO2 difference**. - To get 60 mL/beat, the cardiac output would need to be 6000 mL/min, which would mean an avO2 difference of 0.067 mL O2/mL, not 0.1 mL O2/mL. *50 mL/beat* - This stroke volume would result from an incorrect calculation of the **cardiac output**, potentially from a slight miscalculation of the **arteriovenous oxygen difference**. - A stroke volume of 50 mL/beat at 100 bpm would mean a cardiac output of 5 L/min, requiring an avO2 difference of 0.08 mL O2/mL, which is not consistent with the given values.

Cardiovascular US Medical PG Question 3: A 70-year-old male presents for an annual exam. His past medical history is notable for shortness of breath when he sleeps, and upon exertion. Recently he has experienced dyspnea and lower extremity edema that seems to be worsening. Both of these symptoms have resolved since he was started on several medications and instructed to weigh himself daily. Which of the following is most likely a component of his medical management?

• A. Lidocaine
• B. Verapamil
• C. Carvedilol (Correct Answer)
• D. Aspirin
• E. Ibutilide

Cardiovascular Explanation: ***Carvedilol*** - The patient exhibits classic symptoms of **heart failure**, such as **dyspnea on exertion**, **orthopnea** (shortness of breath when he sleeps), and **lower extremity edema**. - **Beta-blockers** like carvedilol are essential for managing **chronic heart failure** by reducing myocardial oxygen demand and improving cardiac function. *Lidocaine* - **Lidocaine** is primarily an **antiarrhythmic drug** used for acute treatment of **ventricular arrhythmias**, not for chronic heart failure management. - It works by blocking sodium channels and has no direct benefit in addressing the underlying pathophysiology of heart failure. *Verapamil* - **Verapamil** is a **non-dihydropyridine calcium channel blocker** typically used for hypertension, angina, and supraventricular tachyarrhythmias. - It can have **negative inotropic effects**, which are generally contraindicated or used with extreme caution in patients with **systolic heart failure** due to its potential to worsen cardiac function. *Aspirin* - **Aspirin** is an **antiplatelet agent** used for primary or secondary prevention of **atherosclerotic cardiovascular disease** (e.g., in patients with coronary artery disease). - It does not directly manage the symptoms or pathophysiology of **heart failure** unless there is a coexisting ischemic etiology. *Ibutilide* - **Ibutilide** is an **antiarrhythmic drug** specifically used for the rapid conversion of **atrial flutter and atrial fibrillation** of recent onset to sinus rhythm. - It is not a medication used for the long-term management of **heart failure** symptoms described in the patient.

Cardiovascular US Medical PG Question 4: A 14-year-old boy who has been otherwise healthy presents to his doctor complaining of feeling easily winded and light-headed at basketball practice. He has never felt this way before and is frustrated because he is good enough to make varsity this year. He denies smoking, alcohol, or recreational drug use. His mother is very worried because her oldest son and brother had both died suddenly while playing sports despite being otherwise healthy. The transthoracic echocardiogram confirms the suspected diagnosis, which demonstrates a preserved ejection fraction and systolic anterior motion of the mitral valve. The patient is advised that he will need to stay hydrated and avoid intense exercise, and he will likely need an ICD due to his family history. Which of the following physical exam findings is consistent with this patient’s most likely diagnosis?

• A. Tricuspid regurgitation
• B. Systolic ejection murmur that radiates to the carotids
• C. S3 heart sound
• D. Mitral regurgitation
• E. Systolic ejection murmur that worsens with the Valsalva maneuver (Correct Answer)

Cardiovascular Explanation: ***Systolic ejection murmur that worsens with the Valsalva maneuver*** - The patient's presentation with **syncope/lightheadedness during exertion**, family history of **sudden cardiac death in athletes**, and echocardiogram findings of **systolic anterior motion (SAM) of the mitral valve** are classic for **hypertrophic cardiomyopathy (HCM)**. - The murmur of HCM is typically a **systolic ejection murmur** that **worsens with maneuvers that decrease preload**, such as the **Valsalva maneuver** or standing, because this reduction in ventricular volume exacerbates the left ventricular outflow tract (LVOT) obstruction. *Tricuspid regurgitation* - This is typically associated with **right heart failure** or **pulmonary hypertension**, which are not indicated by the patient's symptoms or echo findings. - While it can be heard as a **systolic murmur**, it usually accentuates with inspiration (Carvallo's sign) and does not worsen with the Valsalva maneuver in the context of hypertrophic cardiomyopathy. *Systolic ejection murmur that radiates to the carotids* - A systolic ejection murmur radiating to the carotids is characteristic of **aortic stenosis**, which involves a fixed obstruction of the aortic valve. - While both HCM and aortic stenosis cause systolic murmurs, HCM's murmur has different auscultatory behavior with preload-altering maneuvers (worsening with Valsalva) compared to aortic stenosis (which often softens or is unchanged). *S3 heart sound* - An **S3 heart sound** is typically a low-pitched diastolic sound associated with **volume overload** and **heart failure with reduced ejection fraction**, indicating rapid ventricular filling into a dilated ventricle. - The patient's echocardiogram shows a **preserved ejection fraction**, and his symptoms are related to outflow obstruction, not volume overload. *Mitral regurgitation* - While **mitral regurgitation (MR)** can occur in HCM due to systolic anterior motion (SAM) of the mitral valve causing malcoaptation, the primary murmur heard due to the **LVOT obstruction** is a **systolic ejection murmur**. - The murmur of MR is typically a **holosystolic murmur** that radiates to the axilla and usually **softens with the Valsalva maneuver** as reduced preload can decrease the severity of regurgitation.

Cardiovascular US Medical PG Question 5: A 71-year-old man presents to the emergency department for shortness of breath. The patient was returning from a business trip to China, when he suddenly felt short of breath during the taxi ride home from the airport. The patient has a past medical history of poorly controlled diabetes mellitus and a 50 pack-year smoking history. The patient is non-compliant with his medications and is currently only taking ibuprofen. An initial ECG demonstrates sinus tachycardia. A chest radiograph is within normal limits. Laboratory values are notable for a creatinine of 2.4 mg/dL and a BUN of 32 mg/dL as compared to his baseline creatinine of 0.9 mg/dL. His temperature is 98.8°F (37.1°C), pulse is 122/min, blood pressure is 145/90 mmHg, respirations are 19/min, and oxygen saturation is 93% on room air. On physical exam, you note an older gentleman in distress. Cardiac exam is notable only for tachycardia. Pulmonary exam is notable for expiratory wheezes. Which of the following is the best confirmatory test for this patient?

• A. Ventilation perfusion scan
• B. Lower extremity ultrasound with Doppler
• C. CT angiogram (Correct Answer)
• D. Arterial blood gas
• E. D-dimer

Cardiovascular Explanation: ***CT angiogram*** - This patient presents with multiple risk factors for **pulmonary embolism (PE)**, including a recent long-haul flight and acute onset of dyspnea with tachycardia and hypoxemia. CT pulmonary angiography (CTPA) is the **gold standard confirmatory test** for PE, directly visualizing thrombi in the pulmonary arteries with high sensitivity (>90%) and specificity. - While this patient has **acute kidney injury** (creatinine elevated from 0.9 to 2.4 mg/dL), raising concerns about contrast-induced nephropathy, the **high clinical probability of PE** (recent long flight, acute dyspnea, tachycardia, hypoxemia) makes urgent diagnosis critical. In hemodynamically stable patients with intermediate-to-high PE probability and renal insufficiency, CTPA with appropriate precautions (IV hydration, minimizing contrast dose, avoiding nephrotoxic agents) is still preferred as it provides the most definitive diagnosis. - The patient's hemodynamic stability (BP 145/90) allows time for renal protective measures before contrast administration. *Ventilation perfusion scan* - A V/Q scan is an important **alternative** for diagnosing PE, particularly valuable in patients with severe renal insufficiency (CKD Stage 4-5) or contrast allergy where CTPA is truly contraindicated. - However, in this patient with **expiratory wheezes** suggesting possible underlying obstructive lung disease (50 pack-year smoking history), a V/Q scan has higher likelihood of **indeterminate results** (intermediate probability), which would not confirm or exclude PE and might necessitate additional testing anyway. - V/Q scans also have lower sensitivity than CTPA and require the patient to cooperate with breathing maneuvers, which may be difficult in an acutely dyspneic patient. *Lower extremity ultrasound with Doppler* - This test diagnoses **deep vein thrombosis (DVT)**, the most common source of PE. While a positive DVT in a patient with suspected PE would support treatment, a **negative study does not rule out PE** since the thrombus may have already completely embolized. - This is a supportive test, not a confirmatory test for PE itself. The patient's symptoms require direct assessment of the pulmonary vasculature. *Arterial blood gas* - An ABG typically shows **hypoxemia and respiratory alkalosis** in PE due to V/Q mismatch and hyperventilation, but these findings are **non-specific** and occur in many cardiopulmonary conditions (pneumonia, asthma, COPD exacerbation, heart failure). - ABG is a supportive tool that may guide oxygen therapy but does not confirm PE diagnosis. *D-dimer* - D-dimer has excellent **negative predictive value** and is useful to exclude PE in patients with **low clinical probability** (Wells score <2 or PERC rule negative). - In this patient with **high clinical probability** of PE (recent long flight, acute symptoms, risk factors), D-dimer would almost certainly be elevated and thus **not helpful for confirmation**. Elevated D-dimer occurs in many conditions including infection, inflammation, malignancy, recent surgery, and advanced age, making it non-specific in this context.

Cardiovascular US Medical PG Question 6: A 74-year-old man comes to the physician for a 6-month history of progressively worsening fatigue and shortness of breath on exertion. He immigrated to the United States 35 years ago from India. His pulse is 89/min and blood pressure is 145/60 mm Hg. Crackles are heard at the lung bases. Cardiac examination shows a grade 3/6 early diastolic murmur loudest at the third left intercostal space. Further evaluation of this patient is most likely to show which of the following?

• A. Paradoxical splitting of S2
• B. Pulsus paradoxus
• C. Pulsus parvus et tardus
• D. Fixed splitting of S2
• E. Water hammer pulse (Correct Answer)

Cardiovascular Explanation: ***Water hammer pulse*** - The patient's presentation with **fatigue**, **dyspnea**, **crackles**, and a **grade 3/6 early diastolic murmur** loudest at the **third left intercostal space** is highly suggestive of **aortic regurgitation (AR)**. - A **water hammer pulse** (also known as a **Corrigan's pulse**) is a **bounding**, **collapsing pulse** characteristic of severe AR due to the rapid runoff of blood from the aorta into the left ventricle during diastole, causing a widened pulse pressure (145/60 mmHg in this case). *Paradoxical splitting of S2* - **Paradoxical splitting of S2** occurs when the aortic valve closes *after* the pulmonic valve, typically due to **left bundle branch block** or **severe aortic stenosis**, which are not indicated here. - In such cases, the split narrows or disappears during inspiration. *Pulsus paradoxus* - **Pulsus paradoxus** is an exaggerated drop in systolic blood pressure (>10 mmHg) during inspiration, commonly seen in **cardiac tamponade**, **severe asthma**, or **constrictive pericarditis**. - There are no features in the patient's history or examination to suggest these conditions. *Pulsus parvus et tardus* - **Pulsus parvus et tardus** (small and delayed pulse) is characteristic of **severe aortic stenosis**, where the pulse is weak and slow to rise due to obstruction of left ventricular outflow. - The murmur described, an **early diastolic murmur**, is indicative of **aortic regurgitation**, not stenosis. *Fixed splitting of S2* - **Fixed splitting of S2** is typically associated with an **atrial septal defect (ASD)**, where the split between the aortic and pulmonic components of S2 remains constant during respiration. - There is no clinical evidence to suggest an ASD in this patient.

Cardiovascular US Medical PG Question 7: A 51-year-old African American man presents to his primary care physician’s office for an annual visit. He has no major concerns and says that he has been healthy for the last year. His past medical history is significant for diabetes as well as long standing hypertension that has developed gradually since his 30's; however, he has refused to take any medications. Physical exam shows no abnormal findings. Routine laboratory testing reveals the following: Serum creatinine concentration: 1.5 mg/dL Blood urea nitrogen: 31 mg/dL Based on these results, urine studies are conducted that reveal mild proteinuria of less than 1 g/day and no casts. Which of the following is most likely associated with the cause of this patient's elevated creatinine?

• A. String of beads on angiography
• B. Kimmelstiel-Wilson lesions (Correct Answer)
• C. Apple-green birefringent lesions
• D. Renal cortex necrosis
• E. Flea-bitten kidney

Cardiovascular Explanation: **Kimmelstiel-Wilson lesions** - The patient has a history of long-standing diabetes and hypertension, which are the primary risk factors for **diabetic nephropathy**. - **Kimmelstiel-Wilson lesions** are nodular glomerulosclerosis pathognomonic for **diabetic nephropathy**, characterized by hyaline nodules in the mesangium. - This is the most likely cause given the combination of diabetes, mild proteinuria (<1 g/day), and chronic renal insufficiency. *String of beads on angiography* - This finding is characteristic of **fibromuscular dysplasia**, a non-inflammatory vascular disease that can cause **renal artery stenosis**. - While renal artery stenosis can cause hypertension and renal impairment, the patient's long-standing diabetes and gradual progression make diabetic nephropathy a more probable cause. *Apple-green birefringent lesions* - This describes the characteristic staining of **amyloid deposits** with **Congo red stain** under polarized light. - While amyloidosis can cause renal failure with proteinuria, it is less common than diabetic nephropathy in a patient with long-standing diabetes and the typical presentation described. *Renal cortex necrosis* - This is a rare and severe form of **acute kidney injury** often associated with conditions like severe sepsis, obstetric complications, or disseminated intravascular coagulation. - The patient's history of gradual onset hypertension and diabetes, along with mild proteinuria and elevated creatinine, points to a chronic rather than acute process. *Flea-bitten kidney* - This describes the gross appearance of kidneys in **malignant hypertension**, showing petechial hemorrhages on the renal surface. - While the patient has long-standing hypertension, the presentation suggests chronic kidney disease from diabetic nephropathy rather than acute malignant hypertension, which would present with markedly elevated blood pressure and acute kidney injury.

Cardiovascular US Medical PG Question 8: A 58-year-old woman who underwent urgent coronary artery bypass grafting develops sudden-onset of difficulty breathing shortly after postoperative transfusion of 1 unit of packed red blood cells because of moderate blood loss. She has alcohol use disorder, and has smoked one pack of cigarettes daily for 22 years. Her temperature is 38.3ºC (100.8ºF), respirations are 35/min, and blood pressure is 88/57 mmHg. Pulse oximetry on room air shows an oxygen saturation of 72%. Physical examination shows profuse sweating and cyanosis. There is no jugular venous distension and no peripheral edema. A chest x-ray shows bilateral alveolar and interstitial infiltrates and a normal cardiac silhouette. Which of the following is the most likely underlying mechanism of this patient's transfusion reaction?

• A. Activation of primed neutrophils (Correct Answer)
• B. Type I hypersensitivity reaction
• C. Excessive circulating blood volume
• D. ABO incompatibility
• E. Cytokine accumulation during blood storage

Cardiovascular Explanation: ***Activation of primed neutrophils*** - This clinical presentation of sudden-onset **dyspnea**, **hypoxemia**, **fever**, **hypotension**, and **bilateral pulmonary infiltrates** following a transfusion is highly characteristic of **Transfusion-Related Acute Lung Injury (TRALI)**. - The most commonly proposed mechanism for TRALI involves a "two-hit" model, where the first hit (e.g., surgery, sepsis, trauma) **primes neutrophils** in the recipient's pulmonary vasculature. The second hit occurs when donor antibodies (typically anti-HLA or anti-HNA) in the transfused blood activate these primed neutrophils, leading to degranulation, release of inflammatory mediators, and **non-cardiogenic pulmonary edema**. *Type I hypersensitivity reaction* - A Type I hypersensitivity reaction (e.g., **anaphylaxis**) would typically present with **bronchospasm**, **urticaria**, angioedema, and would not necessarily show bilateral alveolar and interstitial infiltrates specifically. - While it can manifest with hypotension and dyspnea, the prominent **pulmonary infiltrates** and absence of typical allergic skin manifestations make TRALI a more fitting diagnosis. *Excessive circulating blood volume* - **Transfusion-Associated Circulatory Overload (TACO)** involves fluid overload, which would present with signs of **congestive heart failure**, such as **jugular venous distension**, **peripheral edema**, and an enlarged cardiac silhouette on chest x-ray. - This patient explicitly has no jugular venous distension and no peripheral edema, and a normal cardiac silhouette, ruling out TACO. *ABO incompatibility* - Immediate **hemolytic transfusion reactions** due to ABO incompatibility typically cause fever, chills, flank pain, **hemoglobinuria**, and **renal failure**. - While it can lead to shock, the primary manifestations are centered on hemolysis, and it does not directly cause the severe, non-cardiogenic pulmonary edema characteristic of TRALI. *Cytokine accumulation during blood storage* - **Febrile non-hemolytic transfusion reactions (FNHTR)** are associated with accumulated cytokines in stored blood, leading to fever and chills. - However, FNHTR generally does not cause severe **hypoxemia**, **hypotension**, or diffuse **pulmonary infiltrates**, which are hallmark features of TRALI.

Cardiovascular US Medical PG Question 9: A 47-year-old man presents as a new patient at an outpatient clinic. He has never seen a physician before, but was motivated by his 40-year-old brother's recent heart attack and seeks to optimize his health. In particular, he read that uncontrolled atherosclerosis can lead to a heart attack. Which molecule is downregulated in response to the advent of atherosclerosis?

• A. Tumor necrosis factor
• B. Serotonin
• C. Nitric oxide (Correct Answer)
• D. Interleukin 1
• E. Thromboxane A2

Cardiovascular Explanation: ***Nitric oxide*** - **Nitric oxide (NO)** is a potent **vasodilator** and **anti-inflammatory** molecule produced by endothelial cells. In atherosclerosis, endothelial dysfunction leads to reduced NO bioavailability. - Decreased NO production contributes to vasoconstriction, increased platelet aggregation, and enhanced smooth muscle cell proliferation, all of which promote **atherosclerotic plaque formation** and progression. *Tumor necrosis factor* - **Tumor necrosis factor-alpha (TNF-α)** is a **pro-inflammatory cytokine** that plays a significant role in the pathogenesis of atherosclerosis. - It is **upregulated** in response to atherosclerotic plaque formation, contributing to endothelial activation, leukocyte recruitment, and smooth muscle cell proliferation. *Serotonin* - **Serotonin (5-hydroxytryptamine)** is primarily known for its role as a neurotransmitter but also acts as a **vasoconstrictor** and promotes platelet aggregation. - While it can be released from activated platelets in the context of vascular injury, it is not consistently **downregulated** in atherosclerosis; rather, its effects can contribute to disease progression. *Interleukin 1* - **Interleukin-1 (IL-1)**, particularly IL-1β, is a major **pro-inflammatory cytokine** critically involved in the immune response in atherosclerosis. - It is **upregulated** in atherosclerotic plaques, contributing to systemic inflammation, endothelial dysfunction, and vascular smooth muscle cell activation. *Thromboxane A2* - **Thromboxane A2 (TXA2)** is a potent **vasoconstrictor** and **platelet aggregator** produced by activated platelets. - Its levels are **increased** in atherosclerosis, contributing to hypercoagulability and increased risk of thrombotic events like myocardial infarction.

Cardiovascular US Medical PG Question 10: A 53-year-old woman presents to the emergency room with severe chest pain radiating to the back. She was diagnosed with acute aortic dissection. A few hours into the resuscitation, she was having oliguria. Laboratory findings show a serum creatinine level of 5.3 mg/dL. Which of the following casts are most likely to be seen on urinalysis?

• A. RBC casts
• B. Fatty casts
• C. Muddy brown casts (Correct Answer)
• D. Waxy casts
• E. Hyaline casts

Cardiovascular Explanation: ***Muddy brown casts*** - **Acute tubular necrosis (ATN)**, likely caused by **renal hypoperfusion** in the context of an aortic dissection, is characterized by the presence of **muddy brown granular casts** in urinalysis. The significantly elevated **creatinine (5.3 mg/dL)** and **oliguria** support a diagnosis of acute kidney injury with ATN. - These casts are pathognomonic for ATN and are formed from shed **epithelial cells** and debris accumulating in the renal tubules. *RBC casts* - **Red blood cell (RBC) casts** are indicative of **glomerulonephritis** or other causes of **glomerular injury**, which are not directly suggested by the presentation of aortic dissection and subsequent oliguria. - While hematuria can occur in various renal conditions, the presence of **RBC casts** points to bleeding originating from the glomerulus, which is a different pathology than ATN. *Fatty casts* - **Fatty casts** are typically associated with **nephrotic syndrome**, a condition characterized by significant proteinuria, hypoalbuminemia, and edema. - There is no clinical information to suggest nephrotic syndrome in this patient, whose acute renal failure is likely due to hypoperfusion. *Waxy casts* - **Waxy casts** are generally indicative of **chronic kidney disease** and highly advanced, severe tubular damage, representing a later stage of kidney injury. - While the patient has acute kidney injury, the timeline and acute nature of the insult make muddy brown casts more likely than waxy casts. *Hyaline casts* - **Hyaline casts** are composed primarily of Tamm-Horsfall mucoprotein, a normal protein secreted by renal tubule cells. - These casts can be seen in normal urine, especially after exercise or dehydration, and are not specific for any particular kidney pathology or acute kidney injury.

Cardiovascular Flashcard 1 of 10

Question: Concentric hypertrophy is often seen in _____ heart failure

Answer: diastolic

Extra Information:  * due to concentric hypertrophy & increased wall thickness Watch Congestive Heart Failure Pathophysiology [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-cardiac/videos/medical-pathophysiology-cardiac-heart-failure-congestive-heart-failure-pathophysiology?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/heart-failure?index=4] https://onlinemeded.org/spa/cardiology/heart-failure/acquire?ref=anki 

Cardiovascular Flashcard 2 of 10

Question: Pulmonary hypertension is characterized by _____ of the pulmonary trunk

Answer: atherosclerosis

Cardiovascular Flashcard 3 of 10

Question: Immobilization, cardiac wall dysfunction (arrhythmia, MI), and aneurysm increase risk of _____ due to disruption of blood flow

Answer: thrombosis

Cardiovascular Flashcard 4 of 10

Question: _____ is defined as the hardening of arteries, with arterial wall thickening and loss of elasticity

Answer: Arteriosclerosis

Cardiovascular Flashcard 5 of 10

Question: What microscopic changes occur during the first 4 hours of a myocardial infarction? _____

Answer: None :)

Extra Information:  Watch Acute Myocardial Infarction & Post MI Timeline [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-cardiac/videos/medical-pathophysiology-cardiac-ischemic-heart-disease-acute-myocardial-infarction-and-post-mi-timeline?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/myocardial-infarction?index=6] https://onlinemeded.org/spa/cardiac?ref=anki  

Cardiovascular Flashcard 6 of 10

Question: Atherosclerotic plaques thicken the intima and impair perfusion of the tunica media resulting in _____ of smooth muscle cells

Answer: cystic medial necrosis

Extra Information:   https://onlinemeded.org/spa/surgery-subspecialty/vascular/acquire?ref=anki 

Cardiovascular Flashcard 7 of 10

Question: Legg-Calvé-Perthes (LCP) and Slipped Capital Femoral Epiphyses (SCFE) are both causes of _____

Answer: Avascular Necrosis of the Femoral Head

Extra Information:  https://onlinemeded.org?ref=anki 

Cardiovascular Flashcard 8 of 10

Question: In response to fatty streaks in the intima, there is _____ cell migration/proliferation and extracellular matrix deposition

Answer: smooth muscle

Extra Information:   Watch Atherosclerosis Pathophysiology [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-vascular/videos/medical-pathophysiology-vascular-atherosclerosis-atherosclerosis-pathophysiology?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/stable-angina-and-atherosclerosis?index=4] https://onlinemeded.org/spa/surgery-subspecialty/vascular/acquire?ref=anki Atlas: 

Cardiovascular Flashcard 9 of 10

Question: Which arteries may be associated with anterolateral myocardial infarction? _____

Answer: LAD or LCX

Extra Information:  Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/myocardial-infarction?index=4] https://onlinemeded.org/spa/cardiac?ref=anki 

Cardiovascular Flashcard 10 of 10

Question: Late (chronic) lesions of rheumatic heart disease cause mitral _____

Answer: stenosis

Extra Information:   Watch Mitral Stenosis, Acute Rheumatic Fever & Rheumatic Heart Disease [https://dashboard.sketchy.com/study/medical/courses/medical-pathophysiology/units/medical-pathophysiology-cardiac/videos/medical-pathophysiology-cardiac-valvular-disorders-mitral-stenosis-acute-rheumatic-fever-and-rheumatic-heart-disease?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/valvular-disease?index=8] https://onlinemeded.org/spa/cardiac?ref=anki