cvs

Question 1

What is Vancomycin Infusion Reaction (VIR), and how is it managed?

Answer 1

Definition: VIR is a non-IgE-mediated reaction caused by rapid infusion of vancomycin.

Mechanism: Direct mast cell activation → massive histamine release

Symptoms: Flushing, erythema, pruritus, especially of face/neck (“Red Man Syndrome”)

Onset: Seconds to minutes after starting infusion

Question 2

What is reperfusion injury, and what are its main mechanisms?

Answer 2

Reperfusion Injury = Paradoxical cell death after blood flow is restored to ischemic tissue.

🔬 Mechanisms include:

Oxygen free radicals → from parenchymal, endothelial cells & leukocytes

Mitochondrial permeability transition → irreversible mitochondrial damage

Inflammation → neutrophil infiltration causes more injury

Complement activation → leads to further cell damage & inflammation

🧪 Clinical clue:

Leakage of creatine kinase (CK) into blood = marker of membrane damage in heart, brain, or muscle cells

Question 3

What defines a cardiomyopathy, and how is it different from myocardial disease caused by external factors

Answer 3

Cardiomyopathies involve intrinsic dysfunction of the myocardium.

They are primary diseases of the heart muscle itself.

Not classified as cardiomyopathies:

Myocardial dysfunction due to external causes, such as:

Coronary artery disease

Hypertension

Valvular disease

Question 4

What are the major causes of dilated cardiomyopathy (DCM)?

Answer 4

🦠 Infectious (Myocarditis):

Viral: Coxsackievirus, Adenovirus, Influenza

Mechanism: Direct cytotoxic effect or autoimmune destruction of cardiomyocytes

🧬 Genetic mutations

🤰 Peripartum cardiomyopathy (late pregnancy or postpartum)

🧫 Infiltrative diseases (late stage):

Amyloidosis

Hemochromatosis

🧪 Toxins/Drugs:

Chronic alcohol abuse

Anthracyclines (e.g., doxorubicin)

Question 5

What are the typical mitral valve manifestations of rheumatic heart disease by age group?

Answer 5

Age <25 years: Mitral regurgitation is more common

Age >30 years: Mitral stenosis is more common

Older adults: Mixed mitral valve disease (both regurgitation & stenosis) becomes more frequent

Etiology: Rheumatic heart disease is a common cause of both MR and MS

Epidemiology: Most common in patients from Latin America, Africa, or Asia

Question 6

How does cocaine intoxication lead to myocardial ischemia, and what is the treatment?

Answer 6

Mechanism:

↑ Sympathetic activity due to inhibition of norepinephrine reuptake

↑ HR, BP, contractility → ↑ myocardial O₂ demand (β1 effect)

Coronary vasoconstriction → ↓ myocardial O₂ supply (α1 effect)

Result: Myocardial ischemia (eg, chest pain, ST depression)

Symptoms:

Agitation, dilated pupils, tachycardia, hypertension, chest pain

Treatment:

Nitroglycerin: Reduces preload and improves ischemia

Benzodiazepines:

Question 7

What auscultatory findings help assess the severity of mitral regurgitation and mitral stenosis?

Answer 7

Mitral Regurgitation (MR):
S3 gallop = marker of severe chronic MR

Due to volume overload from regurgitant flow into the LV during diastole

Absence of S3 → makes severe MR unlikely

🔸 Mitral Stenosis (MS):
Opening snap = early diastolic sound after S2

Caused by abrupt halting of stenotic mitral valve leaflets

Shorter S2-to-opening snap interval = more severe MS

Reflects higher left atrial pressure

Question 8

Why is the diastolic murmur intensity in mitral stenosis not a reliable indicator of disease severity?

Answer 8

Because murmur intensity depends on:

The transvalvular pressure gradient

The amount of blood flow through the valve

In very severe MS, flow may be so low that the murmur is faint or absent, despite critical stenosis.

Question 9

What is the most common cause of coronary sinus dilation seen on echocardiography?

Answer 9

Elevated right atrial pressure, usually due to pulmonary hypertension.(Because the CS communicates freely with the right atrium, it will become dilated by any factor that causes dilation of the right atrium.)

Question 10

What are the immediate effects on the left ventricle after PDA ligation?

Answer 10

↓ LV preload (due to reduced pulmonary venous return)

↑ LV afterload (due to increased aortic diastolic pressure)
➡️ Leads to acute ↓ in LV stroke volume and cardiac output

How is the right ventricle affected by PDA closure?
No significant change

Question 11

What happens to myocardial contractility within the first minute of total ischemia, and why

Answer 11

Loss of contractility occurs within ~60 seconds

Due to localized ATP depletion in high-demand areas (e.g., near contractile fibers and ion pumps)

Also worsened by accumulation of toxic metabolites

Question 12

Major risk factors for development of AAA (>50% above normal or >3 cm in diameter) )

Answer 12

Age >65
Smoking (up to 15-fold risk increase)
Male sex
(screening for AAA with ultrasonography is recommended for men age 65-75 who have ever smoked)

Question 13

differential cyanosis in a newborn (lower extremity cyanosis with normal upper extremities) and strong femoral pulse

Answer 13

right-to-left shunting through the ductus arteriosus (pulmonary artery → aorta)

Condition: Persistent Pulmonary Hypertension of the Newborn (PPHN)
Mechanism:

High pulmonary vascular resistance (PVR) persists after birth

Pulmonary arterial pressure > systemic pressure

Strong femoral pulses help distinguish PPHN from other causes (e.g., critical coarctation → weak femoral pulses)

Question 14

Plasma renin activity (PRA

Answer 14

Valsartan (ARB) and hydrochlorothiazide (diuretic) should both increase PRA:

ARBs block angiotensin II, removing negative feedback → ↑ renin

Diuretics cause hypovolemia → ↓ renal perfusion → ↑ renin

If PRA remains low or unchanged, it suggests the patient is not taking the medications as prescribed

Question 15

What is the role of prostacyclin (PGI₂) in vascular homeostasis, and how is it clinically relevant?

Answer 15

Function of Prostacyclin (PGI₂):

Synthesized from prostaglandin H₂ via prostacyclin synthase

Derived from arachidonic acid

Secreted by vascular endothelium

Actions:
✅ Inhibits platelet aggregation
✅ Inhibits platelet adhesion to endothelium
✅ Causes vasodilation

Synergist:

Nitric oxide (NO) — also inhibits platelet function and promotes vasodilation

Pathology:

Atherosclerosis impairs PGI₂ and NO production → ↑ thrombosis risk

Clinical Use:

Epoprostenol (synthetic PGI₂) is used to treat:

Pulmonary hypertension

Peripheral vascular disease

Raynaud syndrome

Question 16

What are the most common cardiac abnormalities and leading causes of death in Marfan syndrome (MFS)?

Answer 16

Most Common Cardiac Abnormalities in MFS:

Mitral valve prolapse (MVP)

Cystic medial degeneration of the aorta → leads to aortic root dilation

Leading Causes of Death in MFS:

Aortic dissection (from aortic aneurysm due to cystic medial necrosis)

Cardiac failure (due to MVP and/or aortic regurgitation)

Question 17

What is coronary steal syndrome, how does it occur, and at what level of coronary occlusion is it seen

Answer 17

Coronary steal syndrome is a paradoxical decrease in blood flow to ischemic myocardium due to vasodilation of non-ischemic vessels.

Seen in ≥70% coronary artery occlusion

Distal vessels in ischemic zones are already maximally dilated due to chronic hypoperfusion

Administering vasodilators (eg, adenosine, dipyridamole) dilates normal vessels

This diverts blood away from ischemic zones (“steals” flow) → worsens ischemia

Question 18

What is atheroembolic disease, what triggers it, and how is it diagnosed histologically

Answer 18

Atheroembolic disease occurs when cholesterol crystals embolize from disrupted atherosclerotic plaques into the microvasculature.

Trigger:

Often follows invasive vascular procedures (e.g., catheterization, angiography, surgery)

Plaque disruption → cholesterol-rich microemboli “shower” into circulation

Histologic Diagnosis:

Needle-shaped cholesterol clefts in small arteries or arterioles

Commonly Affected Organs:

🩺 Kidneys → acute kidney injury (AKI)

🦶 Skin → livedo reticularis, blue toe syndrome

🍽 GI tract → bleeding, infarction

🧠 CNS → stroke, amaurosis fugax

Question 19

What are the 4 major mechanical complications of myocardial infarction, and how do they present?

Answer 19

1. Ventricular Free Wall Rupture
   Timing: 5–14 days post-MI

Presentation: Sudden hypotension, cardiac tamponade, PEA arrest

2. Interventricular Septal Rupture
   Timing: 3–5 days post-MI

Presentation: New loud holosystolic murmur, heart failure, shock

3. Papillary Muscle Rupture
   Timing: 2–7 days post-MI

Presentation: Acute mitral regurgitation, pulmonary edema, hypotension

4. Left Ventricular Aneurysm
   Timing: Weeks to months post-MI

Presentation: Heart failure, persistent ST elevations, embolic events

Question 20

What are the key findings and complications of an atrial septal defect (ASD), and how can it lead to Eisenmenger syndrome?

Answer 20

Right atrial and ventricular dilation (→ visible on chest x-ray)

Atrial fibrillation (from RA stretch)

Pulmonary hypertension (from chronic volume overload) (medial hypertrophy of the pulmonary arteries. This increases pulmonary vascular resistance (PVR))

Progression to Eisenmenger syndrome:
Shunt reverses to right-to-left
Causes late-onset cyanosis, clubbing, polycythemia

Question 21

What is Trousseau syndrome, and what does it indicate

Answer 21

Trousseau syndrome = migratory superficial thrombophlebitis — recurrent, migrating venous thromboses in superficial veins.

Clinical Clue:

Thromboses appear, resolve, and recur in different locations

Often tender, palpable cords under the skin

Associated With:

Paraneoplastic hypercoagulability

Most commonly seen with visceral adenocarcinomas,

Question 22

What type of cardiac damage is caused by anthracyclines (e.g., doxorubicin), and what are the biopsy findings?

Answer 22

Leads to dilated cardiomyopathy

Can be acute or chronic

Histologic Findings (Biopsy):
Patchy myocardial fibrosis
Myocyte vacuolization and lysis

Question 23

What are Aschoff bodies, and with which condition are they associated?

Answer 23

acute rheumatic fever (carditis phase)

Follows untreated group A streptococcal pharyngitis

Histologic Findings -Aschoff Bodies:
Interstitial myocardial granulomas
Contain Anitschkow cells:
Plump macrophages
Abundant cytoplasm
Central, slender, “caterpillar” chromatin ribbons

Question 24

why the murmur of aortic stenosis (AS) behaves differently than that of hypertrophic cardiomyopathy (HCM) during the Valsalva maneuver

Answer 24

Aortic Stenosis (AS) Murmur:
Cause: Fixed obstruction of the aortic valve due to calcified cusps — the valve opening is narrowed.

Murmur: Harsh, crescendo-decrescendo systolic murmur best heard at the right upper sternal border and radiates to the carotids.

➤ What happens during Valsalva?
Preload ↓ → less blood flows through the narrowed aortic valve.

So the murmur intensity decreases, because less flow = less turbulence across the calcified valve.

It’s a fixed obstruction, meaning that its severity doesn’t depend on ventricular size or wall motion.

Hypertrophic Cardiomyopathy (HCM) Murmur:
Cause: Asymmetric septal hypertrophy causes dynamic obstruction of the LV outflow tract — the anterior mitral leaflet gets sucked into the tract (SAM: systolic anterior motion).

Murmur: Also a crescendo-decrescendo systolic murmur, but best heard at the left lower sternal border and does not radiate to the carotids.

➤ What happens during Valsalva?
Preload ↓ → smaller LV cavity

Smaller LV → more obstruction from hypertrophied septum and SAM

So the murmur intensity increases

Question 25

What is myxomatous degeneration, and how does it contribute to both mitral valve prolapse (MVP) and aortic aneurysm formation

Answer 25

MYXAMATOUS degeneration = accumulation of mucopolysaccharides in connective tissue Leads to weakening of structural components in valves and arterial walls (CYSTIC MEDIAL degeneration) Often due to defects in connective tissue proteins (e.g., Marfan syndrome) Manifestations: 🔹 Mitral Valve Prolapse (MVP): Affected structures: Mitral leaflets, chordae tendineae Auscultation: Midsystolic click + late systolic murmur (mitral regurgitation) Maneuvers: Squatting ↑ LV volume → delays or eliminates click/murmur 🔹 Aortic Aneurysm: Affected structures: Media layer of large arteries Described as cystic medial degeneration

Question 26

What is peripartum cardiomyopathy, how does it cause dilated cardiomyopathy, and what are the compensatory changes in the heart?

Answer 26

peripartum cardiomyopathy is a rare cause of dilated cardiomyopathy occurring late in pregnancy or shortly after delivery. Possibly related to impaired angiogenic growth factor signaling. Pathophysiology: Leads to eccentric hypertrophy (sarcomeres added in series), which: Increases ventricular compliance Temporarily maintains cardiac output Progression: Chronic volume overload → increased wall stress Eventually leads to left ventricular failure, reduced ejection fraction, and symptomatic heart failure

Question 27

What are the major causes of aortic stenosis (AS), and how do they differ between developed and developing nations

Answer 27

Developed nations: Most common cause: Calcific degeneration of a trileaflet aortic valve Pathology: THIKINING AND CALCIFICATION → restricted leaflet mobility Bicuspid aortic valve (congenital) → accelerated degeneration Developing nations: Most common cause: Rheumatic valve disease Pathology: Commissural FUSION due to chronic inflammation Usually affects younger patients and involves mitral valve as well

Question 28

What is Takotsubo (stress-induced) cardiomyopathy, how does it present, and what is its typical prognosis?

Answer 28

Acute, reversible cardiomyopathy triggered by physical or emotional stress Pathophysiology: Catecholamine surge → myocardial stunning LV findings: Hypokinesis of mid & apical segments Hyperkinesis of basal segments Results in systolic dysfunction (resembles MI, but no obstruction) Epidemiology: Most common in postmenopausal women Prognosis: Self-resolving within weeks

Question 29

Match each cardiac-related condition with its inheritance pattern and affected gene/protein

Answer 29

Condition Inheritance Gene/Protein Affected Duchenne/Becker MD X-linked recessive Dystrophin cause Dilated cardiomyopathy familial Dilated cardiomyopathy autosomal dominant TTN gene, which encodes for the sarcomere protein titin Marfan Syndrome Autosomal dominant Fibrillin-1 cause Aortic root dilation, regurgitation Long QT Syndrome Autosomal dominant/recessive Inward rectifier K⁺ channels cause arrhythmia Cardiac Amyloidosis Acquired Transthyretin (TTR) cause restrictive Hypertrophic Cardiomyopathy (HCM) Autosomal dominant β-Myosin heavy chain, MyBP-C

Question 30

Cardiac hemochromatosis

Answer 30

IT MAY BE HERIDITARY Pathophysiology: Excess intestinal iron absorption Deposition of iron (ferritin, hemosiderin, free iron) in myocardium Oxidative injury to myocytes Cardiomyopathy: Early: diastolic left ventricular dysfunction (restrictive pattern) Later: cardiac remodeling & dilated cardiomyopathy Conduction system disease : Sinus node dysfunction (sick sinus syndrome) Atrial & ventricular arrhythmias Sudden cardiac death

Question 31

MI Complications by Timeline

Answer 31

Immediate (0–24 hours): Arrhythmias Heart failure Cardiogenic shock Right ventricular infarct: Hypotension, JVD, clear lungs Early (1–3 days): Pericarditis (fibrinous) :Sharp chest pain, friction rub, not Dressler’s yet Continued arrhythmias :Especially 2nd/3rd-degree AV block with inferior MI Intermediate (3–7 days): Free wall rupture → Tamponade → Interventricular septum rupture → VSD Papillary muscle rupture → Severe MR, pulmonary edema, 🧠 Note: Ruptures occur due to macrophage-mediated degradation of necrotic tissue → wall weakness ⌛ Late (Weeks after MI): Dressler syndrome :Autoimmune pericarditis LV aneurysm Mural thrombus Heart failure Due to permanent myocardial damage

Question 32

How do activated macrophages contribute to plaque rupture in atherosclerosis, leading to acute coronary syndrome?

Answer 32

Activated macrophages infiltrate the atheroma and secrete metalloproteinases. These enzymes degrade extracellular matrix (e.g., collagen) in the fibrous cap. Ongoing inflammation weakens the plaque’s mechanical stability. This leads to plaque rupture, thrombosis, and acute coronary syndrome (ACS).

Question 33

What is myocardial hibernation, and how does it differ from ischemic preconditioning?

Answer 33

Myocardial Hibernation سبات Chronic, moderate/severe ischemia ↓ Metabolism + ↓ contractility to match ↓ perfusion Prevents necrosis but causes LV systolic dysfunction Reversible with revascularization ⚡ Ischemic Preconditioning تحضير Brief, repeated ischemia + reperfusion Activates protective pathways → limits damage from future prolonged ischemia Prevents infarction by reducing ischemic injury

Question 34

Most common type of pericarditis

Answer 34

Most common type of pericarditis Fibrin-rich exudate in pericardial space Pleuritic chest pain (worse with inspiration, better sitting up) Classic triphasic friction rub on auscultation ⚠️ Common Causes Viral infections Post-MI (early: fibrinous; late: Dressler’s) Uremia Rheumatologic diseases (SLE, RA)

Question 35

Which neurologic manifestation is a major criterion of acute rheumatic fever and what is its significance?

Answer 35

Sydenham Chorea Major Jones criterion of acute rheumatic fever (ARF) Presents with involuntary, irregular, jerky movements of face, arms, and legs Occurs months after group A streptococcal pharyngitis Caused by autoimmune attack on basal ganglia 💔 Clinical Significance Indicates high risk of chronic rheumatic heart disease, especially mitral valve damage

Question 36

prolonged QT interval

Answer 36

1)medication 2)mutation 3)Electrolyte abnormalities ↓ Magnesium, ↓ potassium, ↓ calcium Jervell and Lange-Nielsen syndrome Autosomal recessive disorder Caused by mutations in potassium channel genes (e.g., KCNQ1, KCNE1) Leads to prolonged QT interval (congenital long QT syndrome) 🔑 Clinical Features Bilateral sensorineural hearing loss (congenital) Prolonged QT on ECG → risk of ventricular arrhythmias and sudden cardiac death Romano-Ward syndrome (the same but autosomal dominant) Medications are the most common cause of acquired LQTS and the most important exacerbating factor in patients with congenital LQTS many medications like: Macrolides (erythro)& fluoroquinolones Antiemetics (eg, ondansetron) Azoles (eg, fluconazole) Antipsychotics, TCAs & SSRIs Some opioids (eg, methadone, oxycodone) Class Ia antiarrhythmics (eg, quinidine) Class III antiarrhythmics (eg, dofetilide, sotalol)

Question 37

How does acute and chronic severe hypertension affect the renal vasculature, and what are the histologic features?

Answer 37

Acute (Hypertensive Emergency) Rapid BP rise → malignant nephrosclerosis Fibrinoid necrosis: Smudged, pink necrotic arteriolar walls Hyperplastic arteriolosclerosis: "Onion-skin" smooth muscle hyperplasia قاسي May cause microangiopathic hemolytic anemia, renal failure 🕰️ Chronic (Essential Hypertension) Long-standing mild/moderate HTN → benign nephrosclerosis Hyaline arteriolosclerosis: Homogeneous, pink hyaline in vessel walls اطرى شوي وتسكير اقل Leads to glomerulosclerosis, interstitial fibrosis, tubular atrophy

Question 38

What does the Prussian blue stain detect, and what are “heart failure cells”

Answer 38

Prussian Blue Stain Detects ferric iron (Fe³⁺) in ferritin and hemosiderin 🧫 Hemosiderin-Laden Macrophages Macrophages with golden-brown granules that stain blue with Prussian blue Called siderophages In alveolar spaces, they indicate chronic pulmonary congestion (e.g., in left heart failure) → nicknamed “heart failure cells”

Question 39

Chagas disease

Answer 39

Caused by protozoan Trypanosoma cruzi Vector: triatomine ("kissing") bug Endemic in Central & South America Cardiac manifestations Dilated cardiomyopathy with biventricular failure Apical wall thinning with aneurysm ± mural thrombus Ventricular arrhythmias Gastrointestinal manifestations Megaesophagus (secondary achalasia) Megacolon

Question 40

What lipid-lowering medication should be given if HDL is low,

Answer 40

Statins are still the first-line for CV risk reduction even though Niacin (Vitamin B3) Raises HDL more than any other drug but does not reduce cardiovascular events Used in patients who fail other lipid-lowering therapies

Question 41

Why are Class IB antiarrhythmics (e.g., lidocaine) effective in ischemia-induced ventricular arrhythmias?

Answer 41

Weakest Na⁺ channel blockers → fastest dissociation Bind preferentially to inactivated Na⁺ channels Minimal QRS prolongation in normal tissue ❤️ Why they target ischemic myocardium: Ischemic cells have less negative resting potential This delays Na⁺ channel recovery → channels stay inactivated longer → More drug binding = greater effect in ischemic tissue

Question 42

What are the renal and cardiac benefits of mineralocorticoid receptor antagonists (e.g., spironolactone) in heart failure?

Answer 42

Block aldosterone receptors in distal renal tubules → ↑ Na⁺ & water excretion, ↓ K⁺ excretion (K⁺-sparing diuresis) ❤️ Cardiac Benefits: Inhibit myocardial fibrosis Improve ventricular remodeling ↓ Morbidity & improve survival in HFrEF (↓ ejection fraction) Neurohormones (eg, norepinephrine, angiotensin II, and aldosterone) play a large role in the deleterious cardiac remodeling that occurs in heart failure with reduced ejection fraction. ACE inhibitors, angiotensin-receptor blockers, mineralocorticoid receptor antagonists, beta blockers, and angiotensin receptor-neprilysin inhibitors reduce mortality in these patients by reducing neurohormonal-mediated cardiac remodeling.

Question 43

nitrate

Answer 43

Nitrates → metabolized to nitric oxide (NO) in smooth muscle NO activates guanylate cyclase → ↑ cGMP ↑ cGMP → ↓ intracellular calcium ↓ myosin light-chain kinase activity ↑ myosin light-chain phosphatase → Dephosphorylation of myosin light chain → smooth muscle relaxation 🩸 Result: Vasodilation, especially venodilation → ↓ preload → ↓ myocardial oxygen demand

Question 44

Amiodarone

Answer 44

Amiodarone primarily functions as a class III antiarrhythmic, inhibiting the delayed rectifier potassium current to slow ventricular repolarization and prolong the QT interval. It also inhibits fast sodium channels (class I effect) to slow ventricular depolarization and prolong QRS complex duration. Beta blockade (class II effect) and inhibition of slow L-type calcium channels (class IV effect) slow conduction in the sinus node and atrioventricular node causing decreased sinus rate and a prolonged PR interval.

Question 45

which medications used in chronic HFrEF improve mortality, and which do not?

Answer 45

Angiotensin receptor-neprilysin inhibitor (ARNI), ACE inhibitors ARBs Beta blockers, including metoprolol succinate and carvedilol Mineralocorticoid receptor antagonists, such as spironolactone and eplerenone SGLT2 inhibitors, like dapagliflozin Diuretics (e.g., furosemide, metolazone) do not reduce mortality but are important for symptom relief. Digoxin does not provide a mortality benefit, but it can help reduce hospitalizations.

Question 46

What are the common adverse effects of major antihypertensive drug classes?

Answer 46

Thiazide diuretics: Acute kidney injury Hyponatremia, hypokalemia Hyperuricemia → gout Hyperglycemia, hyperlipidemia HYPERCALCEMIA - with low PTH 🔹 ACE inhibitors: Cough Angioedema Hyperkalemia 🔹 ARBs (Angiotensin II receptor blockers): Hyperkalemia Rare cough 🔹 Calcium channel blockers (eg, amlodipine, nifedipine): Peripheral edema Dizziness/light-headedness 🔹 Beta blockers: Bradycardia Bronchospasm Fatigue Sexual dysfunction

Question 47

How do NSAIDs (e.g., indomethacin, ibuprofen) help close a Patent Ductus Arteriosus (PDA)

Answer 47

inhibit cyclooxygenase (COX). COX normally converts arachidonic acid into prostaglandins, including PGE₂. PGE₂ maintains ductal patency by promoting relaxation of the ductus arteriosus. Inhibition of PGE₂ synthesis leads to ductal smooth muscle contraction, promoting closure of the PDA.

Question 48

What are the causes of Down syndrome

Answer 48

Most Common Cause (∼95%): Maternal meiotic nondisjunction → Trisomy 21 (three full copies of chromosome 21) Less Common Cause (<5%): Robertsonian translocation Break near the centromeres of two chromosomes (eg, 14 and 21) Fetus has 46 chromosomes but effectively 3 copies of chromosome 21

Question 49

MI scar collagen type

Answer 49

Type I collagen is the primary collagen in mature scars (eg, remote myocardial infarction). It is the most prevalent type of collagen and provides strength and support throughout the human body, particularly in bones, tendons, ligaments, and skin. and granulation tissue type 3

Question 50

List all water-soluble vitamins and their main deficiency symptoms. ( thiamine effect CVS )

Answer 50

Thiamine (B1) Beriberi (wet: heart failure, dry: peripheral neuropathy), Wernicke-Korsakoff syndrome (confusion, ataxia, ophthalmoplegia) Riboflavin (B2) Cheilosis (cracked lips, scaling at corners of mouth), corneal vascularization Niacin (B3) Pellagra: 3 D’s – Diarrhea, Dermatitis, Dementia Pantothenic acid (B5) Rare; dermatitis, enteritis, alopecia, adrenal insufficiency Pyridoxine (B6) Peripheral neuropathy, seizures, sideroblastic anemia Biotin (B7) Dermatitis, alopecia, enteritis (can occur with raw egg white consumption) Folate (B9) Megaloblastic anemia, neural tube defects in fetus, glossitis Cobalamin (B12) Megaloblastic anemia, neurologic symptoms (eg, paresthesias, subacute combined degeneration) Ascorbic acid (Vitamin C) Scurvy: bleeding gums, petechiae, poor wound healing, anemia

Question 51

What is the most common congenital heart defect in Turner syndrome

Answer 51

Bicuspid aortic valve

Question 52

Etiology of Syncope (Fainting)

Answer 52

REFLEX (VASOVAGAL) ORTHOSTATIC CARDIAC CEREBROVASCULAR 1. Reflex (Neurally Mediated) Syncope 🔹 MOST COMMON TYPE (VASOVAGAL) VASOVAGAL (emotional stress, pain, prolonged standing) SITUATIONAL (cough, urination, defecation, swallowing) CAROTID SINUS HYPERSENSITIVITY (tight collar, turning head) 🧬 MECHANISM: Transient AUTONOMIC REFLEX → DECREASES HR AND/OR BP → transient cerebral hypoperfusion 2. Orthostatic Hypotension 🔹 POSTURAL DROP IN BP (>20/10 mmHg) WITHIN 3 MINUTES OF STANDING CAUSES: HYPOVOLEMIA (dehydration, bleeding) AUTONOMIC DYSFUNCTION (e.g., diabetes, Parkinson's) DRUGS: antihypertensives (α-blockers, diuretics, nitrates) 🧬 MECHANISM: Inadequate vasoconstriction UPON STANDING → DECREASED CEREBRAL PERFUSION 3. Cardiac Syncope 🔹 OFTEN SUDDEN AND EXERTIONAL; HIGH RISK OF SUDDEN DEATH STRUCTURAL HEART DISEASE Aortic stenosis Hypertrophic cardiomyopathy Myxoma OR tamponade PE (pulmonary embolism) ARRHYTHMIAS Bradyarrhythmias (e.g., sick sinus, AV block) Tachyarrhythmias (VT, SVT) Long QT, WPW, Brugada 🧬 MECHANISM: ABRUPT DROP IN CARDIAC OUTPUT 4. Cerebrovascular (Rare) 🔹 USUALLY ASSOCIATED WITH FOCAL NEUROLOGIC SIGNS Vertebrobasilar insufficiency Subclavian steal syndrome TIA (RARELY CAUSES ISOLATED SYNCOPE)