CVS_Copilot_Week 7 to 11 Notes_2nd Flashcards
(175 cards)
1
Q
What is myocardial ischemia?
A
Reduced blood flow to heart muscle, limiting oxygen supply.
2
Q
What determines myocardial oxygen demand?
A
Heart rate, contractility, wall tension, metabolic activity.
3
Q
What are causes of myocardial ischemia?
A
Atherosclerosis, coronary spasm, thrombosis, embolism, dissection, anemia, hypotension.
4
Q
What are the types of angina?
A
Stable: Exertional, relieved by rest. Unstable: Occurs at rest, unpredictable. Prinzmetal’s: Coronary spasm, transient ST elevation.
5
Q
What are ECG changes in angina?
A
Stable: ST depression, T wave inversion. Prinzmetal’s: Transient ST elevation. Unstable: Non-specific changes.
6
Q
What is the management of angina?
A
Lifestyle (quit smoking, exercise), medications (nitrates, beta-blockers, CCBs, antiplatelets), revascularization (PCI, CABG).
7
Q
What are risk factors for atherosclerosis?
A
Smoking, hypertension, hyperlipidemia, diabetes, obesity, age, sex, family history.
8
Q
What is the pathogenesis of atherosclerosis?
A
Endothelial injury → Lipid accumulation → Foam cells → Fibrous cap → Plaque formation.
9
Q
What are microscopic features of plaques?
A
Lipid core, fibrous cap (collagen, muscle cells), inflammatory cells, neovascularization.
10
Q
Plaque rupture vs. erosion in MI?
A
Rupture: Exposes thrombogenic core, occlusive thrombosis. Erosion: Less fibrous disruption, also leads to thrombosis.
11
Q
What are anti-atherosclerotic therapies?
A
Lifestyle (diet, exercise, smoking cessation), medications (statins, antihypertensives, antidiabetics).
12
Q
What are types of lipids?
A
Triacylglycerols (energy), phospholipids (membranes), cholesterol (hormone precursor).
13
Q
What are types of lipoproteins?
A
Chylomicrons, VLDL, LDL, HDL.
14
Q
What is LDL’s role in atherosclerosis?
A
Transports cholesterol to tissues; oxidized LDL triggers endothelial damage, foam cell formation.
15
Q
What are apolipoproteins?
A
Lipoprotein structural components, receptor ligands (e.g., ApoB-100 for LDL).
16
Q
What is HDL’s protective role?
A
Reverse cholesterol transport, anti-inflammatory, antioxidant effects.
17
Q
What are lipid-lowering agents?
A
Statins (HMG-CoA reductase inhibitors), ezetimibe (blocks intestinal absorption), PCSK9 inhibitors (increase LDL receptor recycling).
18
Q
What is ischemic heart disease (IHD)?
A
Coronary artery narrowing, leading to myocardial ischemia.
19
Q
What are MI risk factors?
A
Smoking, hypertension, hyperlipidemia, diabetes, metabolic syndrome.
20
Q
What is MI pathophysiology?
A
Plaque rupture → thrombosis → coronary occlusion → myocardial necrosis.
21
Q
What are ECG findings in STEMI vs. NSTEMI?
A
NSTEMI: ST depression, T wave inversion. STEMI: ST elevation, new LBBB, later Q waves.
22
Q
What are cardiac biomarkers for MI?
A
Troponin I/T (most sensitive), CK-MB (detects reinfarction).
23
Q
What are diagnostic imaging modalities?
A
Echocardiogram, cardiac MRI, coronary angiography, CT angiography.
24
Q
What are MI medical treatments?
A
MONA: Morphine, oxygen, nitrates, aspirin. Beta-blockers, anticoagulants, statins.
25
What are drug mechanisms in MI management?
Aspirin/clopidogrel (platelet inhibition), nitrates (vasodilation), beta-blockers (↓ oxygen demand), heparin (thrombus prevention).
26
What are MI interventions?
PCI (preferred for STEMI), CABG for high-risk cases, thrombolysis if PCI unavailable.
27
What are complications of MI?
Arrhythmias (most common early death cause), heart failure, shock, rupture, embolism, ventricular aneurysm, Dressler’s syndrome.
28
What are lifestyle modifications post-MI?
Smoking cessation, exercise, healthy diet, weight control, adherence to medications.
29
What embryonic layer forms the heart?
Mesoderm (cardiogenic mesoderm).
30
Which cells contribute to heart development?
Neural crest (outflow tract), proepicardial (epicardium, coronary vessels).
31
What initiates heart conduction?
SA node develops as pacemaker; AV node, bundle of His, Purkinje fibers follow.
32
What forms the atrial septa?
Septum primum grows, leaving foramen primum; foramen secundum forms before closure; septum secundum completes partitioning.
33
How does the AV canal partition?
Endocardial cushions grow and fuse, forming right and left AV canals.
34
What forms the ventricular septum?
Interventricular septum grows upward; endocardial cushions and bulbus cordis contribute.
35
What forms heart valves?
Endocardial cushions remodel and thin into valve leaflets.
36
What forms the aorta and arches?
Aortic sac and dorsal aortae; aortic arches remodel into adult arteries.
37
What forms coronary arteries?
Epicardium and endothelial cells contribute.
38
What forms cranial arteries?
Aortic arches and plexuses in the head region.
39
What forms the lymphatic system?
Endothelial sacs arise from veins.
40
What veins form early circulation?
Cardinal (embryo drainage), vitelline (yolk sac), umbilical (placental oxygenation).
41
What are key fetal circulation features?
Placenta oxygenates blood; foramen ovale and ductus arteriosus bypass lungs.
42
What are fetal blood oxygenation levels?
Oxygenated: Umbilical vein. Mixed: Right atrium, ventricle, aorta. Deoxygenated: Umbilical arteries.
43
What fetal circulation adaptations exist?
Foramen ovale (RA to LA shunt), ductus venosus (placenta bypass), ductus arteriosus (PA to aorta shunt).
44
What changes occur at birth?
Closure of foramen ovale, ductus arteriosus, ductus venosus; umbilical vessels obliterate.
45
What causes these changes?
Increased LA pressure closes foramen ovale; oxygen ↑ and ↓ prostaglandins close ductus arteriosus.
46
What is a congenital heart defect?
Structural abnormality of the heart present at birth.
47
What are left-to-right shunt defects?
PDA, VSD, ASD, PFO (increased pulmonary flow).
48
What are right-to-left shunt defects?
Tetralogy of Fallot, transposition of great arteries (cyanosis).
49
What causes PDA?
Failure of ductus arteriosus to close; leads to pulmonary overload.
50
What is PDA management?
Indomethacin (closure), surgery (if needed).
51
What causes TGA?
Aorta and PA switched; survival depends on mixing via shunts.
52
What is TGA management?
Prostaglandins (maintain ductus arteriosus), septostomy, surgical correction.
53
What causes VSD?
Failure of interventricular septum to close; left-to-right shunting.
54
What is VSD management?
Small defects may close spontaneously; larger ones need surgery.
55
What causes ASD?
Failure of interatrial septum to close; left-to-right shunting.
56
What is ASD management?
Small ASDs may close; larger ones need closure devices or surgery.
57
What causes Tetralogy of Fallot?
Four defects: VSD, overriding aorta, pulmonary stenosis, RV hypertrophy.
58
What is TOF management?
Surgical repair, possible staged procedures.
59
What causes coarctation of the aorta?
Aortic narrowing; leads to hypertension above the narrowing.
60
What is coarctation management?
Surgery or balloon angioplasty.
61
What are cardiovascular changes in pregnancy?
↑ CO (30-50%), ↑ plasma volume (40-50%), vasodilation, right axis ECG shift.
62
What is pre-eclampsia?
Hypertension + proteinuria after 20 weeks; can involve thrombocytopenia, organ dysfunction.
63
What are pre-eclampsia risk factors?
Nulliparity, multiple gestation, hypertension, diabetes, obesity.
64
What are pre-eclampsia symptoms?
Hypertension, proteinuria, edema, headache, visual disturbances.
65
What is pre-eclampsia management?
Monitoring (mild); hospital care, antihypertensives, magnesium sulfate, delivery (severe).
66
What complications does pre-eclampsia cause?
Maternal: HELLP, eclampsia, stroke. Fetal: Prematurity, IUGR, stillbirth.
67
What is endocarditis?
Inflammation of the heart's inner lining, primarily affecting valves.
68
What are risk factors for endocarditis?
Valvular disease, prosthetic valves, IV drug use, congenital defects, catheters, immune compromise.
69
What bacteria commonly cause infective endocarditis?
Staphylococcus aureus, Streptococcus viridans, Enterococci, HACEK group.
70
What are the main fungal causes of endocarditis?
Rare, seen in immunocompromised patients or prosthetic valves.
71
Describe the pathogenesis of infective endocarditis.
Endothelial damage → platelet-fibrin thrombus → bacterial colonization → vegetation formation.
72
What are key symptoms of infective endocarditis?
Fever, new/changing murmur, fatigue, malaise, anorexia, weight loss.
73
What embolic events occur in endocarditis?
Stroke, splenic infarct, renal infarct, pulmonary emboli (right-sided IE).
74
What immunologic signs appear in endocarditis?
Osler nodes, Janeway lesions, Roth spots, glomerulonephritis.
75
What investigations confirm endocarditis?
Blood cultures (≥3 sets), echocardiography (TTE/TEE).
76
What lab findings support endocarditis diagnosis?
Elevated ESR, CRP, anemia, leukocytosis.
77
What criteria are used to diagnose endocarditis?
Duke Criteria: Blood cultures + echocardiography + minor signs.
78
What is the medical treatment for infective endocarditis?
IV antibiotics for 4-6 weeks tailored to organism.
79
When is surgery needed in infective endocarditis?
Severe valve dysfunction, high embolic risk, uncontrolled infection.
80
What monitoring is needed during endocarditis treatment?
Serial blood cultures, echocardiograms, clinical assessment.
81
What are cardiac complications of endocarditis?
Heart failure due to valve destruction.
82
What are systemic complications of endocarditis?
Stroke, embolic infarcts, abscess formation, renal failure.
83
What is myocarditis?
Inflammation of the heart muscle.
84
What causes myocarditis?
Viruses (Coxsackie B, adenovirus, HIV), bacteria, fungi, parasites, autoimmune diseases, toxins.
85
What is the pathogenesis of viral myocarditis?
Direct infection of heart cells, immune attack causing damage.
86
What are symptoms of myocarditis?
Flu-like symptoms, chest pain, dyspnea, palpitations, syncope, arrhythmias.
87
What investigations confirm myocarditis?
ECG (ST/T wave changes), troponin, echocardiography, cardiac MRI, biopsy.
88
What are microscopic findings in myocarditis?
Inflammatory infiltrates, myocyte necrosis, edema.
89
What is myocarditis management?
Supportive care, HF treatment, arrhythmia management, avoid NSAIDs/alcohol.
90
What complications arise from myocarditis?
Dilated cardiomyopathy, arrhythmias, heart failure.
91
What is acute pericarditis?
Inflammation of the pericardium.
92
What causes pericarditis?
Viral (Coxsackie, adenovirus), bacterial, autoimmune (SLE), uremia, trauma, post-MI.
93
What are symptoms of pericarditis?
Pleuritic chest pain relieved by leaning forward, pericardial friction rub.
94
What ECG changes occur in pericarditis?
Widespread ST elevation, PR depression.
95
What is the treatment for pericarditis?
NSAIDs, colchicine, steroids (if refractory), treat underlying cause.
96
What are complications of pericarditis?
Pericardial effusion, cardiac tamponade, constrictive pericarditis.
97
What is acute rheumatic fever?
Autoimmune reaction post-Strep throat, affecting heart, joints, brain, skin.
98
What is rheumatic heart disease?
Chronic valve damage from repeated rheumatic fever episodes.
99
What is the pathogenesis of rheumatic fever?
Molecular mimicry—antibodies against strep attack heart, joints, brain.
100
What are signs of acute rheumatic fever?
Migratory arthritis, carditis, Sydenham's chorea, erythema marginatum, subcutaneous nodules.
101
What are major criteria for rheumatic fever diagnosis?
Carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules.
102
What are minor criteria for rheumatic fever?
Fever, arthralgia, elevated ESR/CRP, prolonged PR interval.
103
What tests confirm recent strep infection in RF?
Throat culture, anti-streptolysin O titers.
104
What is the management for rheumatic fever?
Penicillin, aspirin, corticosteroids, long-term antibiotic prophylaxis.
105
What are complications of rheumatic fever?
Rheumatic heart disease, heart failure, arrhythmias, stroke.
106
What is myxoma?
Most common primary heart tumor, usually benign.
107
What are symptoms of myxoma?
Obstruction (syncope, dyspnea), embolism (stroke, infarcts), systemic (fever, weight loss).
108
What is the best test for myxoma?
Echocardiography for visualization.
109
What is the treatment for myxoma?
Surgical excision.
110
What is cardiomyopathy?
Disease of the heart muscle impairing its ability to pump blood effectively.
111
What are the main types of cardiomyopathy?
Dilated (DCM), Hypertrophic (HCM), Restrictive (RCM), Arrhythmogenic Right Ventricular (ARVC).
112
What is dilated cardiomyopathy (DCM)?
Ventricular dilation and impaired systolic function, leading to reduced ejection fraction.
113
What causes DCM?
Idiopathic (most common), genetic mutations, infections, toxins (alcohol, drugs), metabolic disorders.
114
What are symptoms of DCM?
Heart failure signs: Dyspnea, fatigue, edema, palpitations, syncope.
115
What is the primary diagnostic tool for DCM?
Echocardiography: Shows ventricular dilation and reduced ejection fraction.
116
What is the treatment for DCM?
Heart failure management: ACE inhibitors, beta-blockers, diuretics, lifestyle modifications, possible device therapy.
117
What is hypertrophic cardiomyopathy (HCM)?
Genetic disorder causing unexplained left ventricular hypertrophy.
118
What causes HCM?
Autosomal dominant mutations in sarcomere protein genes (e.g., MYH7, MYBPC3).
119
What are symptoms of HCM?
Dyspnea, syncope, chest pain, palpitations, sudden cardiac death risk.
120
What is the primary diagnostic tool for HCM?
Echocardiography: Shows asymmetric LV hypertrophy (>15mm).
121
What is the treatment for HCM?
Beta-blockers, calcium channel blockers, activity restriction, possible surgery (myectomy).
122
What is restrictive cardiomyopathy (RCM)?
Stiff ventricular walls impairing diastolic filling, leading to heart failure with preserved ejection fraction.
123
What causes RCM?
Infiltrative diseases (amyloidosis, sarcoidosis), fibrosis, radiation therapy.
124
What are symptoms of RCM?
Dyspnea, edema, fatigue, signs of diastolic heart failure.
125
What is the diagnostic tool for RCM?
Echocardiography: Shows normal/increased ventricular wall thickness with restrictive filling pattern.
126
What is the management for RCM?
Supportive treatment, managing underlying cause, diuretics for symptom relief.
127
What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?
Genetic disease causing RV myocardium replacement with fibrofatty tissue, leading to arrhythmias.
128
What causes ARVC?
Genetic mutations in desmosomal proteins (e.g., PKP2, DSG2).
129
What are symptoms of ARVC?
Palpitations, syncope, ventricular tachycardia (often exertion-related).
130
What is the primary diagnostic tool for ARVC?
Echocardiography: Shows RV dilation and dysfunction.
131
What is the treatment for ARVC?
Beta-blockers, activity restriction, ICD placement for sudden death prevention.
132
What is pericardial effusion?
Abnormal fluid accumulation in the pericardial space.
133
What are causes of pericardial effusion?
Pericarditis (viral, bacterial), malignancy, trauma, autoimmune diseases, post-MI (Dressler’s syndrome).
134
What are symptoms of pericardial effusion?
Dyspnea, chest discomfort, muffled heart sounds, pericardial friction rub.
135
What is the diagnostic tool for pericardial effusion?
Echocardiography: Detects fluid in pericardial space.
136
What is the treatment for pericardial effusion?
Observation (small effusions), NSAIDs/colchicine, pericardiocentesis (large/symptomatic effusions).
137
What is cardiac tamponade?
Life-threatening condition due to rapid/excessive pericardial fluid accumulation, compressing the heart.
138
What are symptoms of cardiac tamponade?
Beck’s Triad: Hypotension, muffled heart sounds, jugular venous distension.
139
What is the treatment for cardiac tamponade?
Emergency pericardiocentesis to relieve compression.
140
What is constrictive pericarditis?
Thickened pericardium restricting ventricular filling, leading to right heart failure signs.
141
What are causes of constrictive pericarditis?
Idiopathic, tuberculosis, radiation therapy, cardiac surgery.
142
What are symptoms of constrictive pericarditis?
Progressive dyspnea, peripheral edema, ascites, hepatomegaly.
143
What is the treatment for constrictive pericarditis?
Definitive treatment: Pericardiectomy.
144
What is peripheral vascular disease (PVD) and acute limb ischemia (ALI)?
PVD affects blood vessels outside the heart and brain; ALI is a sudden drop in limb blood flow, threatening viability.
145
What are causes and symptoms of acute limb ischemia?
Caused by embolism/thrombosis. Symptoms: Pain, Pallor, Pulselessness, Paresthesia, Paralysis, Poikilothermia.
146
How is acute limb ischemia diagnosed and managed?
Clinical exam, Doppler ultrasound, angiography. Managed with urgent revascularization (embolectomy, thrombolysis, bypass).
147
What causes chronic limb ischemia, and what are its symptoms?
Atherosclerosis; symptoms include claudication, rest pain, non-healing ulcers, gangrene.
148
How is chronic limb ischemia diagnosed and treated?
ABI, Doppler ultrasound, angiography. Treated with lifestyle changes, medications (antiplatelets), revascularization.
149
What is aortic dissection (AD), and how common is it?
A tear in the inner aortic layer leading to separation of wall layers; rare but life-threatening.
150
What are AD risk factors and the role of cystic medial degeneration?
Hypertension, Marfan syndrome, Ehlers-Danlos, bicuspid aortic valve; medial degeneration weakens aortic wall.
151
What are the Stanford and DeBakey classifications of AD?
Stanford: Type A (ascending aorta), Type B (descending aorta). DeBakey: Type I (extends), Type II (ascending only), Type III (descending).
152
What are symptoms of AD?
Sudden severe tearing chest/back pain that may migrate, neurological deficits, limb ischemia.
153
How is AD diagnosed and treated?
CT angiography (gold standard). Type A: Surgery; Type B: Blood pressure control, possible surgery.
154
What is an aneurysm and its epidemiology?
Localized vessel dilation; AAA common in older men, often linked to atherosclerosis.
155
How are aneurysms classified?
True (all three wall layers: fusiform/saccular) vs. False (pseudoaneurysm with hematoma).
156
What is the pathogenesis of aortic aneurysm?
Arterial wall weakening via atherosclerosis, genetic disorders, infection, or inflammation.
157
What are symptoms and diagnostic tools for aortic aneurysm?
Often asymptomatic; when symptomatic, pulsatile mass, back pain. Diagnosed via ultrasound, CT, MRI.
158
How are aneurysms managed?
Small: Monitoring, risk control. Large/symptomatic: Open surgery or EVAR. Ruptured: Emergency repair.
159
What are varicose veins?
Dilated, tortuous superficial veins, often in the legs due to valve failure.
160
What is the pathogenesis and symptoms of varicose veins?
Valve incompetence → reflux → venous hypertension → vein dilation. Symptoms: Visible bulging veins, heaviness, swelling, skin changes.
161
What investigations diagnose varicose veins?
Clinical exam, duplex ultrasound (assesses reflux and rules out DVT).
162
How are varicose veins managed, and what are complications?
Compression stockings, sclerotherapy, endovenous ablation, surgery. Complications: Thrombophlebitis, bleeding, ulcers.
163
What is deep vein thrombosis (DVT)?
Formation of thrombus in deep veins, commonly in the legs.
164
What causes DVT, and what are symptoms?
Virchow’s Triad: Stasis, endothelial injury, hypercoagulability. Symptoms: Unilateral swelling, pain, warmth.
165
What investigations diagnose DVT?
D-dimer (rule out), compression ultrasound (gold standard).
166
How is DVT managed, and what are complications?
Anticoagulation (heparin, LMWH, oral drugs). Complications: PE, post-thrombotic syndrome.
167
What is chronic venous insufficiency (CVI)?
Impaired venous return due to valve dysfunction, causing chronic venous hypertension.
168
What is the pathogenesis and symptoms of CVI?
Venous reflux causes sustained hypertension. Symptoms: Edema, pain, itching, skin changes, ulcers.
169
What investigations diagnose CVI?
Clinical exam, duplex ultrasound (assesses reflux and obstruction).
170
How is CVI managed, and what are complications?
Compression therapy, leg elevation, wound care; possible surgery. Complications: Venous ulcers, cellulitis, recurrent DVT.
171
What is vasculitis?
Inflammation of blood vessel walls.
172
What are the types of vasculitis?
Large-vessel (GCA, Takayasu), medium-vessel (PAN, Kawasaki), small-vessel (ANCA-associated, IgA vasculitis).
173
What are the pathogenic mechanisms of vasculitis?
Non-infectious: Immune-mediated (autoantibodies, immune complexes). Infectious: Direct pathogen invasion.
174
What are symptoms of vasculitis?
Fever, weight loss, skin rashes, arthralgia, kidney failure, neurological deficits.
175
How is vasculitis diagnosed and treated?
Clinical assessment, lab tests (ANCA, CRP), imaging (angiography), biopsy. Treated with immunosuppressants (steroids, cyclophosphamide).
