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What is atherosclerosis?
Chronic inflammatory disease of medium and large arteries that begins with endothelial injury or dysfunction
What is the pathogenesis of atherosclerosis?
Endothelial injury → LDL enters intima and oxidizes → inflammatory cells migrate in → macrophages become foam cells → fatty streaks form → smooth muscle proliferates and deposits connective tissue → fibrous plaques narrow lumen and may rupture causing thrombosis or embolization
What are the risk factors for atherosclerosis?
Hypercholesterolemia, dyslipidemia, elevated LDL, age (men 45 and older; women 55 and older), family history of premature coronary disease, smoking, obesity, hypertension, diabetes mellitus, inactivity, stress
What are the manifestations of atherosclerosis?
Often asymptomatic for years; manifestations depend on artery affected such as angina, neurologic deficits, claudication, diminished pulses, cool tissues, delayed capillary refill, ischemic pain
What are 7 complications of atherosclerosis?
Ischemic heart disease
myocardial infarction
stroke
peripheral vascular disease
chronic tissue ischemia
plaque rupture with thrombosis/emboli
aneurysm formation
What is atherosclerotic peripheral vascular disease?
Atherosclerotic blockage of large leg arteries that reduces distal tissue perfusion
What is the pathogenesis of atherosclerotic peripheral vascular disease?
Large artery blockages reduce leg perfusion; with exercise oxygen demand rises but supply cannot increase adequately, causing ischemic pain; chronic poor perfusion causes trophic skin changes and poor wound healing
What are the risk factors for atherosclerotic peripheral vascular disease?
Smoking, diabetes, hypertension, hyperlipidemia, obesity, older age, inactivity; smoking and diabetes are especially important
What are 9 manifestations of atherosclerotic peripheral vascular disease?
Intermittent claudication
cool extremities
weak pulses
blanching with elevation, dependent rubor
shiny skin
brittle toenails
hair loss
ulcers
delayed wound healing
What is deep vein thrombosis (DVT)?
Formation of a thrombus in a deep vein, usually in the legs
What is the pathogenesis of DVT?
Virchow’s triad (venous stasis, hypercoagulability, vessel wall injury) allows clotting factors and platelets to accumulate in stagnant blood; thrombus may remain or embolize to lungs causing pulmonary embolism
What are the risk factors for DVT?
Immobility, bed rest, spinal cord injury, surgery, trauma, pregnancy, cancer, obesity, smoking, acute MI, heart failure, shock, venous obstruction, estrogen exposure, inherited clotting tendencies
What are the manifestations of DVT?
Mild/no symptoms
Common signs: swelling, pain, tenderness, warmth, red/discolored skin, enlarged superficial veins
Sometimes first sign is pulmonary embolism → sudden SOB, chest pain, rapid HR
What is the management of DVT?
Prevention with early ambulation, leg exercises, compression devices/stockings, hydration, prophylactic anticoagulation; treatment with anticoagulation and monitoring for PE such as sudden dyspnea or pleuritic chest pain
What is hypertension?
Persistent elevation in arterial pressure
What is the pathogenesis of hypertension?
Persistent elevation in arterial pressure caused by increased cardiac output, increased total peripheral resistance, or both.
Primary (essential) hypertension is multifactorial and linked to genetics, age, race, obesity, diet, dyslipidemia, smoking, alcohol, sedentary lifestyle, insulin resistance, and obstructive sleep apnea.
Secondary hypertension results from specific causes such as renal disease, endocrine disorders, pheochromocytoma, aortic coarctation, oral contraceptives, decongestants, or illicit drugs
What are the risk factors for hypertension?
Genetics, age, race, obesity, poor diet, dyslipidemia, smoking, alcohol, sedentary lifestyle, insulin resistance, obstructive sleep apnea
secondary causes include renal disease, endocrine disorders, pheochromocytoma, aortic coarctation, oral contraceptives, decongestants, illicit drugs
What are the manifestations of hypertension?
Often asymptomatic, which is why hypertension is called a silent condition.
When symptoms occur they may include headache, dizziness, visual changes, or nonspecific fatigue.
Severely elevated pressures may present as hypertensive crisis, urgency, or emergency.
What is the management of hypertension?
Treat secondary cause if present; lifestyle measures such as weight control, exercise, smoking cessation, lower sodium intake, diet improvement; medications include diuretics, ACE inhibitors, calcium channel blockers; patient education and long-term adherence are essential
What are the complications of hypertension?
Heart: left ventricular hypertrophy and heart failure.
Brain: stroke, cognitive impairment, and dementia.
Kidneys: nephrosclerosis and chronic kidney damage.
Peripheral vasculature: accelerated atherosclerosis.
Eyes: retinal damage and possible blindness.
Hypertensive crisis is defined in the slides as BP greater than 180/120 mm Hg and may be urgency or emergency depending on acute organ injury.
What are important older adult considerations in hypertension?
Older adults commonly develop hypertension because vessels stiffen with age and are less able to buffer systolic pressure.
Isolated systolic hypertension is especially common in aging adults.
Older adults also carry higher risk of stroke, heart failure, and silent or atypical presentations
What is orthostatic hypotension?
Drop in systolic BP greater than 20 mm Hg or diastolic BP greater than 10 mm Hg on standing
What is the pathogenesis of orthostatic hypotension?
Autonomic and vascular compensation fails after position change, causing inadequate cerebral perfusion
worsened by volume depletion, prolonged bed rest, or medications that blunt vasoconstriction
What are the risk factors for orthostatic hypotension?
Age, reduced blood volume, bed rest, drugs, autonomic nervous system disorders
What are the manifestations of orthostatic hypotension?
Dizziness, lightheadedness, blurred vision, weakness, near-syncope, syncope, fall risk on standing
What is heart failure?
Clinical syndrome in which the heart cannot pump enough blood to meet metabolic needs or can do so only at elevated filling pressures
What are the 3 ways heart failure is classified?
Pump function
Systolic dysfunction (HFrEF): weak contraction, EF < 40%, blood is not ejected well
Forward failure: decreased cardiac output → poor tissue perfusion
Diastolic dysfunction (HFpEF): stiff ventricle, impaired filling, EF preserved/near normal
Backward failure: blood backs up behind the failing ventricle
Side effected
Left-sided HF: backs up into lungs
Right-sided HF: backs up into systemic circulation
Cardiac output
Low Output: heart cannot pump enough blood (common)
High output: CO is normal/increased but insufficient for body’s demands
What are the risk factors for heart failure?
Hypertension, coronary artery disease, prior MI, diabetes, valvular disease, cardiomyopathy
Systolic failure is commonly caused by MI and dilated cardiomyopathy
Diastolic failure is commonly caused by hypertension, LV hypertrophy, aging
What are the manifestations of heart failure?
Fatigue, weakness, exercise intolerance, dizziness, confusion later
left-sided failure causes dyspnea, orthopnea, crackles, pulmonary congestion, pulmonary edema
right-sided failure causes peripheral edema, JVD, hepatomegaly, ascites;
high-output failure causes warm extremities and bounding pulses,
low-output causes cold pale extremities and weak pulses
What tests help diagnose heart failure?
Staging
Stage A: at risk (HTN, CAD, diabetes)
Stage B: structural disease, no symptoms
Stage C: structural disease with symptoms
Stage D: end-stage/refractory HF
Blood tests
BNP / NT-proBNP: elevated in HF
Electrolytes
BUN/creatinine
Troponin if acute
Diagnostic tests
Echocardiogram: most important; measures EF, structure, systolic vs diastolic dysfunction
Chest X-ray: cardiomegaly, pulmonary congestion
ECG
Cardiac MRI if needed
What is the management of heart failure?
Nonpharmacologic: sodium restriction, fluid restriction, smoking cessation, cardiac rehab, monitor for worsening HF
Medications: ACEI, beta blockers, aldosterone antagonists, diuretics
Advanced therapy: mechanical support, heart transplant
What is dilated cardiomyopathy?
Ventricles enlarge and weaken, causing poor systolic function and reduced ejection fraction
What is the pathogenesis of dilated cardiomyopathy?
Ventricular dilation → decreased contractility → reduced ejection fraction → heart failure (blood remains in ventricle + backs up blood)
What are the risk factors/causes of dilated cardiomyopathy?
Mixed genetic and nongenetic causes; may be associated with myocarditis, toxins, alcohol, pregnancy, or idiopathic disease depending on etiology.
What are the 6 manifestations of dilated cardiomyopathy?
Fatigue
dyspnea on exertion + orthopnea
peripheral edema
S3 heart sound
arrhythmias
signs of heart failure
What is hypertrophic cardiomyopathy?
Genetic disease causing thickened myocardium, especially the interventricular septum, with impaired filling
What is the pathogenesis of hypertrophic cardiomyopathy?
Genetic defects in contractile proteins cause myocardial thickening, smaller chamber size, impaired filling, and possible outflow obstruction
What are the risk factors for hypertrophic cardiomyopathy?
Inherited genetic mutations, family history
What are the manifestations of hypertrophic cardiomyopathy?
Exertional syncope
dyspnea
chest pain
arrhythmias
reduced exercise tolerance
What are the complications of hypertrophic cardiomyopathy?
Sudden cardiac death, especially in young athletes, left ventricular outflow obstruction, dysrhythmias
What is coronary artery disease (CAD)?
Atherosclerotic narrowing or blockage of coronary arteries that reduces myocardial oxygen supply
What is the pathogenesis of CAD?
Plaque buildup narrows or blocks coronary arteries, creating a supply-demand mismatch; the endocardium is especially vulnerable to ischemia
What are the risk factors for CAD?
Hyperlipidemia, smoking, hypertension, diabetes, obesity, inactivity; stress, exercise, cold exposure, tachycardia, and hypertension increase oxygen demand and worsen ischemia
What are the manifestations of CAD?
Stable angina: predictable pain with exertion, stress, or cold; relieved by rest or nitroglycerin.
Silent ischemia: ischemia without chest pain, more common in older adults and people with diabetes.
Variant (vasospastic) angina: occurs at rest, often at night or early morning, due to coronary spasm.
If blood flow reduction becomes severe, patients may develop MI, arrhythmias, conduction defects, heart failure, or sudden cardiac death.
What are the complications of CAD?
MI, arrhythmias, conduction defects, heart failure, sudden cardiac death
What is acute coronary syndrome (ACS)?
Sudden decrease in coronary blood flow ranging from unstable angina to myocardial infarction
What is the pathogenesis of ACS?
Plaque rupture → platelet aggregation → thrombus formation over damaged plaque → reduced coronary blood flow
What are the risk factors for ACS?
Smoking, diabetes, hypertension, dyslipidemia, obesity, prior atherosclerotic disease
What are the manifestations of ACS?
Unstable angina: pain at rest/minimal exertion, new or worsening pattern, lasts longer than 20 minutes, may not be fully relieved by nitroglycerin
STEMI: severe, crushing substernal pain, not relieved by nitroglycerin
Associated symptoms may include dyspnea, diaphoresis, nausea, anxiety, and restlessness
What tests help diagnose ACS?
History of the pain pattern and response to nitroglycerin.
ECG variables: T-wave inversion, ST depression, or ST elevation depending on severity.
Serum cardiac markers: troponin is most sensitive and specific; CK-MB and myoglobin may also be used.
What is shock?
Inadequate tissue perfusion causing insufficient oxygen/nutrient delivery, anaerobic metabolism, lactic acidosis, cell death, and organ dysfunction
What is the pathogenesis of shock?
Decreased cardiac output, loss of circulating volume, severe vasodilation, or mechanical obstruction reduce perfusion; compensatory SNS and RAAS activation occurs
What are the risk factors/causes of shock?
Hypovolemic shock: hemorrhage, dehydration, severe fluid loss, third spacing.
Cardiogenic shock: acute MI, severe heart failure, cardiomyopathy, dysrhythmias, valve failure.
Obstructive shock: pulmonary embolism, cardiac tamponade, tension pneumothorax, aortic dissection.
Distributive shock: sepsis, anaphylaxis, neurogenic causes.
What are the manifestations of shock?
General: tachycardia, anxiety/restlessness, cool pale skin in many forms, decreased urine output, delayed capillary refill, hypotension late.
Hypovolemic: cool clammy skin, restlessness, low urine output, weak pulses, metabolic acidosis late.
Cardiogenic: poor perfusion with evidence of pump failure, often pulmonary congestion.
Obstructive: signs vary with the obstruction but include low cardiac output and severe hypoperfusion.
Distributive/septic shock may have warm flushed skin early due to vasodilation.
What is the management of shock?
Restore circulating volume with IV fluids and blood products when indicated.
Correct the cause: stop bleeding, give antibiotics for sepsis, remove obstruction such as PE or tamponade, revascularize cardiogenic shock from MI when possible.
Improve oxygen delivery with supplemental oxygen or mechanical ventilation as needed.
Support hemodynamics with vasopressors if fluids are insufficient; inotropes such as dobutamine are used for cardiogenic shock.
What are the complications of shock?
ARDS: fluid leaks into alveoli which impairs gas exchange
acute renal failure: decreased urine output and accumulation of waste products
GI ischemic injury: loss of gut barrier, ulcers, possible bleeding
DIC: simultaneous clotting and bleeding
MODS: multi organ failure
Aortic valve stenosis and regurgitation
What is the pathogenesis of aortic stenosis?
Valve does not open fully, obstructing forward flow from the LV into the aorta, increasing workload and often causing a systolic murmur
What is the pathogenesis of aortic regurgitation?
Valve does not close fully, so blood flows backward from the aorta into the LV during diastole, causing volume overload and increased LV workload
What are the manifestations of aortic stenosis?
Murmur, exertional dyspnea, chest pain/angina, fatigue, syncope, reduced forward flow
What are the manifestations of aortic regurgitation?
Murmur, fatigue, dyspnea, palpitations, signs of volume overload or heart failure over time
What is myocardial infarction (MI)?
Myocardial cell death caused by prolonged ischemia from complete coronary artery blockage
What is the pathogenesis of MI?
Plaque rupture and thrombus formation commonly cause complete blockage; infarct size depends on location, area supplied, duration of occlusion, collateral circulation, hemodynamic status
What are the risk factors for MI?
Smoking, hypertension, hyperlipidemia, diabetes, obesity, age, family history
What are the manifestations of MI?
Abrupt crushing substernal pressure not relieved by nitroglycerin, pain radiating to left arm/neck/jaw/back, nausea, vomiting, SOB, fatigue, weakness, diaphoresis, pale cool clammy skin, anxiety, impending doom; women, older adults, and diabetics may have atypical symptoms
What tests help diagnose MI?
ECG changes (ST elevation/depression, T-wave changes, abnormal Q waves), troponin, CK-MB, myoglobin, echocardiography, perfusion imaging
What is cardiac tamponade?
Life-threatening accumulation of fluid or blood in the pericardial sac that prevents normal heart filling
What is the pathogenesis of cardiac tamponade?
Rising pericardial pressure impairs diastolic filling, decreasing stroke volume and cardiac output, causing hypotension and shock
What are the manifestations of cardiac tamponade?
Hypotension, jugular venous distention, muffled heart sounds, tachycardia, weak thready pulse, diaphoresis, anxiety, decreased urine output
How is cardiac tamponade diagnosed and treated?
Echocardiogram confirms diagnosis; treatment is emergent pericardiocentesis or surgical drainage
What are the risk factors for tuberculosis?
Close exposure to airborne droplets, older age, immunocompromised states such as HIV/chemotherapy/chronic steroids, crowded living conditions, inability to contain infection
What are the manifestations of tuberculosis?
Primary infection may be asymptomatic or mild and may become latent in a granuloma/Ghon focus.
Reactivation (secondary TB) commonly causes chronic cough, hemoptysis, night sweats, weight loss, fatigue, muscle wasting, pallor, and weak appearance.
Military TB can cause widespread systemic illness when organisms spread through the bloodstream.
What is pneumonia?
Inflammation of lung tissue involving alveoli and bronchioles that fills alveoli with fluid or pus and decreases gas exchange
What is the pathogenesis of pneumonia?
Lung tissue becomes inflamed → alveoli fill with fluid, pus, and inflammatory cells → gas exchange becomes impaired → oxygen levels drop
What are the risk factors for pneumonia?
Older age, smoking, immunocompromise, aspiration risk, hospitalization, ventilator exposure, preceding viral infection; HAP has higher resistant organism risk
What are the manifestations of pneumonia?
Fever
productive cough
crackles
dyspnea
decreased oxygen saturation, pleuritic chest pain
chills,
tachypnea
tachycardia
increased tactile fremitus
dullness to percussion
atypical pneumonia may cause dry cough
What is the management of pneumonia?
Treat the cause with antibiotics for bacterial pneumonia and supportive care for viral causes; oxygen therapy, hydration, pulmonary hygiene, monitor respiratory status, watch for deterioration or secondary bacterial pneumonia after influenza
What are the complications of pneumonia?
Hypoxemia, respiratory failure, sepsis, systemic spread of infection, pleural effusion, worsened gas exchange
What is hypoxemia?
Arterial oxygen lower than normal
What is the pathogenesis of hypoxemia?
mechanisms include hypoventilation, impaired diffusion, inadequate pulmonary perfusion, and V/Q mismatch.
Low inspired oxygen, respiratory disease, neurologic depression, circulatory problems, pulmonary embolism, heart failure, and shock can all contribute.
V/Q mismatch is emphasized as the most common cause
What are the risk factors for hypoxemia?
Pneumonia, COPD, ARDS, pulmonary edema, pulmonary embolism, shock, high altitude, opioid overdose, neuromuscular disease
What are the manifestations of hypoxemia?
Early: tachycardia, peripheral vasoconstriction, diaphoresis, restlessness, slight confusion, reduced concentration, and decreased visual acuity.
Chronic: increased ventilation, pulmonary vasoconstriction, pulmonary hypertension, polycythemia, cyanosis, and clubbing in prolonged disease
What is the management of hypoxemia?
Treat underlying cause, provide supplemental oxygen, support ventilation/perfusion, monitor for respiratory failure especially with hypercapnia or altered mental status
What is COPD?
Progressive, largely irreversible airflow obstruction disorder that includes chronic bronchitis and emphysema
What is the pathogenesis of COPD?
Major structural changes include inflammation and fibrosis of bronchial walls, hypertrophy of submucosal glands with mucus hypersecretion, loss of elastic fibers, and destruction of alveolar tissue.
Chronic bronchitis is dominated by mucus hypersecretion and productive cough from enlarged mucus glands and inflamed bronchi.
Emphysema is dominated by alveolar wall destruction, loss of recoil, air trapping, and reduced surface area for gas exchange
What are the risk factors for COPD?
Cigarette smoking, air pollution, chronic irritant exposure, alpha-1 antitrypsin deficiency
What are the manifestations of COPD?
Dyspnea, chronic cough, sputum, wheezing, prolonged expiration, decreased breath sounds; emphysema causes barrel chest, weight loss, severe dyspnea, accessory muscle use, air trapping; chronic bronchitis causes productive cough for at least 3 months in each of 2 consecutive years, early cyanosis, possible edema/cor pulmonale; CO2 retention causes headache, drowsiness, confusion, CO2 narcosis
What oxygen saturation goal is used for chronic CO2 retainers with COPD?
88% to 92% to reduce risk of oxygen-induced hypercapnia
What is asthma?
Chronic inflammatory airway disease with reversible obstruction
What is the pathogenesis of asthma?
Airway inflammation, increased airway responsiveness, and mucus plugging; histamine and leukotrienes cause edema, epithelial injury, and mucus production; hyperreactive airways constrict in response to triggers, especially during exhalation
What are the risk factors for asthma?
Respiratory infections, exercise, cold air, hyperventilation, smoke, pollution, aspirin/NSAID sensitivity, atopy, allergen exposure
What are the manifestations of asthma?
Wheezing, chest tightness, dyspnea, cough, tachycardia, decreased oxygen levels, accessory muscle use; airway is swollen, narrowed, and full of thick mucus during attack
What is pneumothorax?
Air in the pleural space causing partial or complete lung collapse
What is the pathogenesis of pneumothorax?
Air enters pleural space and prevents full lung expansion; spontaneous pneumothorax often follows ruptured bleb, traumatic follows chest injury, tension pneumothorax traps air and raises pressure compressing lung, heart, and great vessels
What are the risk factors for pneumothorax?
COPD, ruptured blebs, chest trauma, invasive procedures, positive-pressure ventilation
What are the manifestations of pneumothorax?
Sudden dyspnea, pleuritic chest pain, decreased or absent breath sounds on affected side; tension pneumothorax may cause hypotension, decreased cardiac output, tracheal deviation
What is the management of pneumothorax?
Small cases may be observed with oxygen; large or symptomatic cases need needle decompression or chest tube drainage; sudden dyspnea after thoracentesis suggests post-procedure pneumothorax
What is pulmonary embolism (PE)?
Blockage of a pulmonary artery branch, usually by thrombus from the leg
What is the pathogenesis of PE?
Thrombus travels to lungs and blocks perfusion, creating dead-space ventilation and V/Q mismatch; severe emboli can cause acute right-heart strain, shock, sudden death