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Medicine - Circulatory System
A mind map about medicine - circulatory system, including knowledge about pathology, disease, pharmacology, circulatory system, cardiovascular system diseases, cardiac insufficiency, related drugs, etc.
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Medicine - Circulatory System
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- Outline
circulatory system
cardiovascular system diseases
Atherosclerosis (AS)
Mainly affects large and medium-sized arteries (increased collagen fibers, hyalinization, calcification)
Risk factors: smoking, hyperlipidemia, hypertension, diseases causing secondary hypertension (DM, hyperinsulinemia, hyperthyroidism, nephrotic syndrome), genetic factors, gender and age
Injury-response theory: LDL penetrates into the subendothelial space and is engulfed by macrophages to form foam cells (macrophage-derived); SMC enters to form foam cells (myocyte-derived foam cells); cholesterol crystallizes
Pathological changes
Basic pathological changes
Lipid streaks: the earliest lesions, punctate or striped yellow irregular bulges with accumulation of foam cells (derived from SMC, macrophages)
Fibrous plaque: grayish yellow or porcelain white, fibrous cap (SMC), internal (extracellular lipid mass) hyaline degeneration
Atheromatous plaque: cholesterol crystals
Secondary lesions: hemorrhage, ulcer, thrombosis, calcification, aneurysm
Major arterial pathological changes
Aortic atherosclerosis: It commonly occurs in the posterior wall of the aorta and the openings of its branches, with the abdominal aorta being the most serious disease.
Coronary atherosclerosis and coronary heart disease
Coronary atherosclerosis: the left anterior descending coronary artery is the highest
Main clinical manifestations of CHD (coronary atherosclerosis is the most common cause)
Angina pectoris: acute, temporary ischemia and hypoxia, manifested by paroxysmal precordial pain that can radiate to the left upper limb (stable, unstable, variant)
MI: Sustained ischemia leads to large myocardial necrosis, severe and long-lasting retrosternal pain
Subendocardial MI: Involves the inner 1/3 of the ventricular wall and the three major branches of the coronary arteries
Transmural MI: the ventricular wall is full thickness or as deep as 2/3 of the ventricular wall, mostly in the left anterior descending coronary artery
Pathological changes (avascular necrosis) granulation tissue → scar tissue
Complications: heart failure (the most common cause of death), heart rupture (the most serious complication), etc.
Renal atherosclerosis: AS pyknotic kidney at the opening of the renal artery and the proximal end of the aorta
Hypertension (hardening of the arteries)
benign hypertension
Dysfunction stage: intermittent spasm and contraction of small arteries and increased blood pressure
Arteriopathy stage: arteriosclerosis (main feature, manifested as hyaline degeneration of arterioles), arteriosclerosis
visceral disease stage
Heart: The heart chambers are not dilated (centripetal hypertrophy), the heart chambers are dilated (centrifugal hypertrophy)
Kidney: Hyalinization of the renal afferent artery, glomerular fibrosis, sclerosis, and hyalinization; renal tubular atrophy, interstitial proliferation, glomerular compensatory hypertrophy, and compensatory dilation of the renal tubules (the lesions are mild). idiopathic granular pyknotic kidney
brain
Cerebral edema or hypertensive encephalopathy (increased permeability) hypertensive crisis (severe headache, disturbance of consciousness, convulsions)
Encephalomalacia
Cerebral hemorrhage: the most serious, often occurs in the basal ganglia and internal capsule, and the lenticulostriate artery is the most susceptible to rupture and bleeding.
Malignant hypertension: fibrinoid necrosis of arterioles, proliferative arteriolar sclerosis
Rheumatism: Group A beta-hemolytic streptococci (serous inflammation, recurrent attacks of valvular heart disease)
installment
Deterioration and exudation stage: myxoid degeneration, collagen fibrinoid necrosis
Proliferative phase or granulomatous phase: myocardial interstitial granulomatous lesions. Rheumatoid bodies (diagnostic significance) are composed of groups of rheumatoid cells and a small amount of lymphocytes and plasma cells, mostly located next to small blood vessels. Owl-shaped in cross section; caterpillar in longitudinal section.
Fibrosis or sclerosis stage
Organ disease
rheumatic heart disease
Rheumatic endocarditis: Mitral valve most commonly affected Verrucous vegetations
Rheumatic myocarditis: Involves the myocardial interstitial connective tissue, has Aschoff bodies, is common in the left ventricle
Rheumatic epicarditis: Involves the visceral layer of the epicardium, a large amount of serous fluid exudes to form an effusion, covered by fibrin → villous heart organization → constrictive epicarditis
Rheumatoid Arthritis: Invasion of large joints, with recurrent migratory attacks, local redness, swelling, heat, pain and dysfunction, and serous fluid and fibrin protein exudation in the joint cavity
Skin lesions: annular erythema (exudative lesions, more common on the skin of the trunk and limbs), subcutaneous nodules (proliferative lesions)
Rheumatic encephalopathy (minor chorea)
Infective endocarditis (purulent inflammation involving mitral valve and aortic valve, white thrombus)
Acute infective endocarditis: pyogenic bacteria (Staphylococcus aureus)
Subacute infective endocarditis: viridans streptococci can cause localized or diffuse glomerulonephritis and Osler's nodes
valvular heart disease
Mitral valve stenosis: the main cause is rheumatic fever, the valve is fish-shaped, and there is a rumble-like murmur in the apical area. In the late stage, it becomes a "pear-shaped heart"
Mitral regurgitation: consequence of rheumatic endocarditis, systolic blowing murmur
Aortic stenosis: the heart becomes shoe-shaped
Aortic regurgitation: diastolic wind-like murmur, patients may have carotid pulse, water pulse, water pipe shooting sound and capillary pulse.
Cardiomyopathy: cardioectasis (significant enlargement of the heart chambers), hypertrophic cardiomyopathy (hypertrophy of the left and/or right ventricle, smaller ventricular cavity, characteristic change is asymmetric ventricular septal hypertrophy), Keshan disease (selenium deficiency)
Myocarditis: coxsackievirus (most common), echovirus, influenza virus, adenovirus
cardiac insufficiency
Causes and incentives (the most common are infections, especially respiratory infections; childbirth, too rapid or excessive infusion, potassium ion metabolism disorders, acidosis): decreased myocardial contractility, ventricular overload, ventricular diastole and restricted filling (see details P194)
compensatory response
Neuro-humoral regulatory mechanisms (RAAS, sympathetic-adrenomedullary system, natriuretic peptide system)
The heart itself compensates (accelerated HR, cardiac tensogenic dilation, enhanced myocardial contractility, ventricular remodeling: concentric hypertrophy, pressure load, eccentric hypertrophy, volume load)
Extracardiac compensation: increased blood volume, blood flow redistribution
The mechanism
Decreased myocardial contractile function: changes in myocardial contraction-related proteins (denaturation, necrosis), myocardial energy metabolism disorders (energy generation, energy reserves, energy utilization), myocardial excitation-contraction coupling disorders (sarcoplasmic reticulum calcium transport dysfunction, extracellular Calcium ion influx disorder, troponin and calcium ion binding disorder)
Myocardial diastolic dysfunction: active diastolic dysfunction (insufficient ATP supply), passive diastolic dysfunction (reduced ventricular compliance)
Uncoordinated diastolic and systolic activities of various parts of the heart
The pathogenesis of clinical manifestations (reduced heart pumping function, redistribution of organ blood flow), venous congestion (systemic circulation congestion, pulmonary circulation congestion)
Related drugs
antiarrhythmic drugs
Ia (sodium ion blocking drug)
Moderate blockade: quinidine (cinchona reaction, torsade de pointes), procainamide (lupus-like syndrome)
Mild block: lidocaine (ventricular), phenytoin (competes sodium potassium ATPase, ventricular arrhythmias caused by cardiac glycoside poisoning)
Significant blockade: propafenone (broad spectrum, not suitable for combination with other antiarrhythmic drugs)
Ib (beta blocker drug)
Propranolol: Supraventricular arrhythmias (sympathetic hyperexcitability, hyperthyroidism, pheochromocytoma), easy to induce boating, dyslipidemia, DM, use with caution
Ic (drug that prolongs action potential duration, potassium ion blockade)
Long-term use of amiodarone (broad-spectrum thyroxine) may cause corneal brown particle deposition, hyperthyroidism or hypothyroidism, interstitial pneumonia or pulmonary fibrosis, and T3 and T4 need to be monitored.
ID (calcium channel blocker)
Verapamil: first choice for paroxysmal supraventricular tachycardia
Drugs that act on the RAAS system
ACEI (Puri): protects the heart, kidneys, and blood sugar, reverses cardiovascular remodeling (preferred), causes irritating dry cough, hyperkalemia (not combined with potassium-sparing diuretics), angioedema, severe renal failure, and bilateral Renal artery stenosis, contraindicated in pregnant women
AT1-R (-) (Satan): No dry cough, can promote uric acid excretion
high blood pressure medicine
A (ACEI, ARB) Pril, Sartan
B (β-receptor blocker) Lorol: patients with angina pectoris and tachycardia; young people with hypertension
C (calcium channel blocker) dipine
D (diuretics): reduce blood volume in the early stage, relax smooth muscles in the later stage, and inhibit sodium and calcium exchange
Central antihypertensive drugs: excite α2 receptors on the postsynaptic membrane of the nucleus tract solitarius in the dorsal medulla, and imidazoline I1 receptors in the ventrolateral region of the rostral medulla.
Clonidine: a detoxification drug for morphine addicts. ADR is dry mouth, constipation, and drowsiness. It is not suitable for high-altitude operations, motor vehicle drivers, and the elderly.
Sodium nitroprusside: caused by hypertensive crisis, controlled hypotension during surgical anesthesia, hypertension combined with MI, and pheochromocytoma
Heart failure drugs (diuretics, vasodilators, beta-blockers, ACEI, ARB, inotropes)
Cardiac glycosides: positive inotropy, negative frequency, negative conduction, oxygen-reducing sodium-potassium ATPase, treatment of atrial fibrillation and atrial flutter ADR: gastrointestinal reactions (most common), central nervous system reactions (visual disturbance, redness) (indications for drug withdrawal), sinus tachycardia (indications for drug withdrawal), bradycardia, atrioventricular block (rescued by atropine), sinus tachycardia, ventricular fibrillation (rescued by phenytoin)
Lipid-adjusting drugs
Statins (lowering TC LDL) HMG-CoA reductase Myalgia, myositis, rhabdomyolysis Not suitable for use by pregnant women and patients with abnormal liver and kidney function
Cholestyramine: Promote Ch consumption, reduce lipid absorption, gastrointestinal symptoms, hyperchloraemia
Fibrates: Comprehensive reduction of blood lipids. Rhabdomyolysis (combined with statins), pregnant women and children, and those with renal insufficiency are prohibited.
Antianginal drugs (propranolol, nitroglycerin, nifedipine)
Nitroglycerin dilates blood vessels and can cause reflex hypertension (combined with propranolol). Nifedipine is suitable for variant angina.