patho exam 2

Week 5

Chapter 16 Alterations in Blood Pressure

Determinants of systemic blood pressure:

The systemic arterial blood pressure is the physiologic result of the cardiac output (CO) and the resistance to the ejection of blood from the heart
CO = SV (stroke volume) X HR (heart rate)

Mechanisms of blood pressure regulation – short term and long term

Short Term: Short-term regulation primarily involves heart rate and systemic vascular resistance (SVR).
Long Term: Long-term regulation of systemic blood pressure Involves the influence of the nervous system, release of hormones, and responses of the kidneys to pressure changes Involves blood pressure variables: heart rate, stroke volume, and SVR.

Hypertension > or = 140/90:

prehypertension range
120-139 / 80-89
stage I hypertension range
140-159 / 90-99
stage II hypertension range
>160 / >100

Causes and risk factors of HTN:

Nonmodifiable Risk Factors
Increasing age
Family history
Ethnicity
Modifiable Risk Factors
Obesity
Sedentary lifestyle
Metabolic syndrome
Dietary factors
Increased fat intake
Increased sodium intake
Inadequate potassium intake
Inadequate calcium intake

Hypertension Effects on body

High BP (hypertension) & plaque build-up in arteries(atherosclerosis) affect different parts of the body: the heart and arteries, kidneys, brain, and eyes.
Heart and Arteries: High BP makes the heart work harder, leading to:
Thickening of the heart wall (left ventricular hypertrophy), which increases the heart’s oxygen needs.
This may result in stable angina (chest pain) or more serious conditions like heart attacks.
Kidneys: High pressure reduces blood flow to the kidneys, causing:
Damage to kidney function (autoregulatory failure).
This can lead to bleeding (hemorrhage), tissue death (ischemia), kidney shrinkage (atrophy), and eventually end-stage kidney failure.
Brain: High pressure affects brain blood vessels, leading to:
Hemorrhagic stroke (bleeding in the brain).
Temporary mini-strokes (TIA) & ischemic stroke (due to blocked blood flow).
Eyes: High pressure damages blood flow to the eyes, which can result in:
Retinal detachment (where the retina separates from its supporting tissue).
Hemorrhage in the eye, which can lead to blindness.

Hypertension treatments and goals of treatments

The main goals of treating hypertension are to:
Reduce morbidity and mortality related to heart, brain, and kidney diseases.
Lower blood pressure to target levels to decrease the risks of:
Stroke by 35–40%, Heart attack by 20–25%, Heart failure by over 50%
Target blood pressure levels: Under 60: Below 140/90 Older 60: Below 150/90
Treatment Interventions:
1) Lifestyle Changes
Exercise: 30 minutes exercise daily
Diet: The DASH diet, which is low in sodium and high in fruits, vegetables, and whole grains

Drug Classifications Used to Treat Hypertension

1. Reduce Stroke Volume - Decrease the volume of blood the heart pumps, thus lowering blood pressure:

Thiazide diuretics: Increase urine output, reducing blood volume.

Loop diuretics: Similar to thiazides, but more potent; often used in heart failure.

Potassium-sparing diuretics: Help retain potassium while promoting fluid loss.

Aldosterone receptor blockers: Inhibit the effects of aldosterone, leading to reduced sodium and water retention.

Angiotensin (ACE) inhibitors: Block the conversion of angiotensin I to angiotensin II, reducing fluid retention.

Angiotensin II receptor blockers (ARBs): Block the action of angiotensin II, leading to vasodilation and reduced blood volume.

Venodilators: Relax veins, decreasing venous return to the heart and reducing stroke volume.

2. Reduce Systemic Vascular Resistance - Decrease the resistance the heart must overcome to pump blood:

Combination α1- and beta-blockers: Reduce heart rate and relax blood vessels.

Angiotensin-converting enzyme (ACE) inhibitors: Lower resistance by inhibiting angiotensin II formation.

Angiotensin II receptor blockers (ARBs): Also lower vascular resistance by blocking angiotensin II.

Calcium channel blockers: Prevent calcium from entering cells of the heart and blood vessels, leading to relaxation and vasodilation.

α1-Blockers: Directly relax blood vessels, reducing resistance.

Central α2 agonists: Decrease sympathetic outflow, leading to lower vascular resistance.

Direct-acting vasodilators (arterial): Act directly on blood vessels to promote dilation and reduce resistance.

3. Decrease Heart Rate - Lower the heart rate, which can help reduce BP:

Beta-blockers: Block beta-adrenergic receptors, leading to decreased heart rate and contractility.

Combination α1- and beta-blockers: Provide dual action, reducing both heart rate and vascular resistance.

Hypotension causes, Signs/Symptoms, treatments

Orthostatic (postural) hypotension is a form of low blood pressure (LBP) that occurs when standing up from a sitting or lying position, leading to dizziness, lightheadedness, or even fainting due to a sudden drop in blood pressure.
Treatment for orthostatic hypotension includes making slow positional changes, avoiding hot environments and large meals, using compression stockings or abdominal binders, elevating the head of the bed, increasing salt and fluid intake (if safe), and reviewing medications. Squatting or crossing legs can help relieve symptoms when they start.

Chapter 18 Alterations in Cardiac Function

Etiology and risk factors for coronary artery disease

Main Cause: Atherosclerosis of coronary arteries.
Risk Factors:
Age
Family history
Abnormal lipid levels
Cigarette smoking
Hypertension
Diabetes
Obesity

Causes of cardiac ischemia

Cardiac ischemia occurs when the heart's demand for oxygenated blood exceeds its supply, often due to narrowed or blocked coronary arteries (atherosclerosis).

Stable angina vs. vasospastic angina vs. Acute Coronary Syndrome

Stable Angina: Predictable chest pain during physical activity or stress, relieved by rest or medication.
Vasospastic Angina: Caused by spasms in coronary arteries, can occur at rest, often unpredictable.
Acute Coronary Syndrome (ACS): A spectrum of conditions associated with sudden reduced blood flow to the heart, which includes:
Unstable angina & Myocardial Infarction (MI) (heart attack).

Signs/Symptoms of Myocardial Infarction (MI); biomarkers of MI

Myocardial infarction (MI), also heart attack, occurs when blood flow to the heart muscle is reduced or stopped.
Symptoms: Chest pain (often described as a pressure or squeezing sensation), shortness of breath, sweating, nausea, lightheadedness, or pain radiating to the arms, back, neck, or jaw.
Biomarkers:
Troponin: Protein found in heart muscle cells that’s released into the bloodstream when the heart is damaged, most sensitive and specific biomarker for myocardial injury. Elevated troponin levels indicate damage to the heart muscle.
Troponin I stops the muscle fibers in the heart from contracting and usually rises slightly earlier after a heart attack.
Troponin T helps attach heart muscle proteins and tends to stay elevated longer in the blood after a heart attack
CK-MB (Creatine Kinase-MB): Although less specific than troponin, CK-MB can also be elevated in MI. It's particularly useful when troponin levels are inconclusive or for assessing reperfusion injury.
Myoglobin: This is an early marker of myocardial injury and can rise within hours after the onset of symptoms. Lacks specificity compared to troponin.

Effects and treatments of MI

Effects: Damage to heart muscle leading to reduced cardiac function, which can result in heart failure.
Medications
Antiplatelets: Medications like aspirin and clopidogrel prevent platelet aggregation, reducing the risk of clot formation in arteries.
Anticoagulants: Drugs such as heparin and low molecular weight heparins inhibit clot formation and prevent existing clots from growing.
Beta-blockers: These reduce heart rate and myocardial oxygen demand, decreasing the heart's workload.
ACE Inhibitors: ACE inhibitors relax blood vessels, lowering blood pressure and reducing heart stress.
Surgical Interventions
Angioplasty: A catheter procedure that widens blocked coronary arteries to quickly restore blood flow.
Stenting: Placement of a mesh tube (stent) in the artery after angioplasty helps keep the artery open and maintain blood flow.
Coronary Artery Bypass Grafting (CABG): A surgical procedure that uses a grafted vessel to bypass the blocked artery, providing an alternate route for blood flow to the heart.

Clinical manifestations of valve disorders:

Mitral Valve Disorders: Problem with the valve located between the left heart chambers. The mitral valve is located between the left atrium and the left ventricle. 3 Types:
Mitral Stenosis: Impaired blood flow from left atrium to left ventricle.
Mitral Regurgitation: Backflow of blood into the left atrium during ventricular systole.
Mitral Valve Prolapse: Bulging of the mitral valves into the left atrium during ventricular contraction.
Aortic Valve Disorders: Aortic valve to narrow or leak. 2 Types:
Aortic Stenosis: Narrowing of the aortic valve due to calcium buildup.
Aortic Regurgitation: Backflow of blood from the aorta into the left ventricle.

Causes and Signs/Symptoms endocarditis vs. myocarditis vs. pericarditis

Endocarditis: Infection of the endocardium; symptoms include fever, heart murmurs, and signs of systemic infection. Often caused by bacteria.
Myocarditis: Inflammation of the heart muscle; symptoms include chest pain, heart failure signs, fatigue, and palpitations. Often viral in origin.
Pericarditis: Inflammation of the pericardium; symptoms include sharp chest pain, often worse with breathing or lying down, and pericardial friction rub on auscultation. Causes include infections, autoimmune diseases, and post-myocardial infarction.

Congenital heart defects: Acyanotic vs. cyanotic; which require surgery?

Acyanotic Defects: Include atrial septal defect, ventricular septal defect, patent ductus arteriosus, coarctation of the aorta, and aortic/pulmonary stenosis. These may or may not require surgery depending on severity.
Cyanotic Defects: Include tetralogy of Fallot, transposition of the great arteries, truncus arteriosus, and tricuspid atresia. These typically require surgical intervention early in life to correct or manage.

Classes of drugs used for HTN

Diuretics: Help the body eliminate excess sodium and water.
ACE Inhibitors: Block the formation of angiotensin II, relaxing blood vessels.
Angiotensin II Receptor Blockers (ARBs): Block the effects of angiotensin II on blood vessels.
Calcium Channel Blockers: Prevent calcium from entering heart and blood vessel cells, leading to lower blood pressure.
Beta-blockers: Reduce heart rate and output, decreasing blood pressure.
Vasodilators: Directly relax blood vessels.

Week 6

Chapter 19 Heart Failure and Dysrhythmias

Commonly used criteria for heart failure

Heart failure (HF) Clinical syndrome resulting from a primary condition which inhibits the heart’s inability to maintain sufficient cardiac output to optimally meet metabolic demands of tissues and organs.
Framingham Criteria and Minnesota Heart Failure Criteria are two sets of guidelines to help diagnose HF.
There’s no single diagnostic test for HF; instead, diagnosis is based on a combination of symptoms, clinical findings, and tests.

Heart failure with low ejection fraction vs. normal ejection fraction

HFrEF (Systolic Dysfunction): Heart can’t pump strongly enough, leading to reduced ejection fraction (EF), which means less blood is pushed out with each beat.
HFpEF (Diastolic Dysfunction): Heart’s pumping strength (EF) remains normal, but it struggles to fill with blood due to stiff heart muscle. Often occurs in elderly, women, and those without a history of MI.

Forward failure vs. backward failure

Forward Failure: The heart can't pump enough blood forward to meet the body’s needs, leading to low oxygen levels reaching tissues, including the brain.
Backward Failure: Blood backs up into the veins and lungs due to poor pumping, causing congestion and swelling.

Signs of decreased oxygenation to brain (forward failure)

Symptoms may include confusion, dizziness, fainting, and difficulty focusing due to reduced blood flow to the brain.

Diagnosis and goals of treatment for HF

Goal: Aims to improve cardiac output, minimize congestive symptoms, and prevent progression
Treatment:
ACE Inhibitors (ACEIs): Relax blood vessels, lowering blood pressure and reducing heart workload.
Angiotensin II Receptor Blockers (ARBs): Block angiotensin II effects to relax blood vessels and reduce blood pressure.
Aldosterone Antagonists: Block aldosterone to decrease fluid retention and reduce blood pressure.
β1-blocking Agents (Beta-blockers): Decrease heart rate and oxygen demand, easing heart strain.
Diuretics: Promote fluid loss through urine, reducing blood volume and lowering blood pressure.
Positive Inotropic Drugs: Increase heart muscle contraction strength, improving cardiac output.
Pacemakers: Regulate heart rhythm and improve heart function in cases of arrhythmias.
Antidysrhythmic Drugs: Control irregular heart rhythms to stabilize heart rate and function.

Normal sinus rhythm

NSR is the normal heart rhythm, with a rate between 60–100 beats per minute

Abnormal rates of sinus rhythm – know parameters for brady and tachy

Bradycardia: Heart rate below 60 beats per minute.
Tachycardia: Heart rate above 100 beats per minute.
Sinus Arrhythmia: The heart rate varies a bit with breathing, but this is generally normal.
Sick Sinus Syndrome: The heart’s natural pacemaker is off-balance, causing alternating slow (bradycardia) and fast (tachycardia) heart rates.
Sinus Arrest: The heart’s pacemaker pauses or stops for a moment, causing a missed beat (can lead to asystole, or no heartbeat, if it stops completely).

Atrial and ventricular fibrillation – heart action and treatments

Atrial Fibrillation (A-Fib): Rapid, irregular beating of the atria, causing poor blood flow. Treated with medications, cardioversion, or ablation.
Ventricular Fibrillation (V-Fib): Irregular, uncoordinated contraction of the ventricles, leading to loss of pulse. Emergency treatment includes defibrillation.

V-Tach – parameters, associated events, treatments

V-Tach: Rapid heartbeat originating from the ventricles, usually over 100 beats per minute. Can lead to V-Fib
Treatment:
Antiarrhythmic Drugs: Medications that help control or correct abnormal heart rhythms by stabilizing the electrical signals in the heart. Examples include amiodarone, flecainide, beta-blockers and potassium channel blockers
Electrical Cardioversion: A procedure where a controlled electric shock is delivered to the heart to "reset" its rhythm back to normal, commonly used for atrial fibrillation or other serious arrhythmias.

Classes of drugs for Heart Failure – how do they work?

ACE Inhibitors (ACEIs) and ARBs: Relax blood vessels to lower blood pressure and reduce workload on the heart.
Aldosterone Antagonists: Reduce salt and water retention, easing strain on the heart.
Beta-Blockers: Slow heart rate and lower blood pressure.
Diuretics: Help remove excess fluid, reducing congestion and swelling.
Positive Inotropic Drugs: Increase heart muscle contraction strength.
Pacemakers (in some cases): Regulate or stimulate heart rhythm if needed.

Week 7

Chapters 20 Shock

Types of shock – what is common denominator in all forms?

Shock: Imbalance between oxygen supply and oxygen requirements at the cellular level. 4 Types of Shock:
Cardiogenic Shock: Heart cannot pump enough blood.
Obstructive Shock: Blood flow is blocked due to an obstruction (e.g., pulmonary embolism).
Hypovolemic Shock: Loss of blood volume (e.g., due to bleeding or dehydration).
Distributive Shock: Blood vessels lose tone, causing low blood pressure (e.g., septic shock, anaphylactic shock).
Impaired Tissue Oxygenation: All forms of shock lead to inadequate oxygen supply to tissues, affecting cellular metabolism.

Clinical manifestations and Compensatory mechanisms of shock

Compensatory Stage: The body tries to maintain adequate blood flow despite reduced cardiac output, activating the sympathetic nervous system (SNS) to increase heart rate and constrict blood vessels.
Progressive Stage: Compensatory mechanisms fail, leading to hypotension, tissue hypoxia, lactate production, metabolic acidosis, and cell death.

Treatments based on clinical manifestations of shock – what is the goal?

Goal: Improving cardiac output and myocardial oxygen delivery while reducing cardiac workload
Pharmacotherapy:
Inotropic Agents: Medications that increase the strength of heart muscle contractions to improve cardiac output.
Afterload-Reducing Agents: Drugs that lower systemic vascular resistance, making it easier for the heart to pump blood (e.g., ACE inhibitors, ARBs).
Preload-Reducing Agents: Medications that decrease blood volume or venous return to the heart, reducing the heart's workload (e.g., diuretics, nitrates).
Mechanical Assist Devices
Impella and EMCO Devices: Temporary mechanical devices that help pump blood and support heart function during acute heart failure episodes.
Ventricular Assist Devices (VADs): Implantable devices that take over the pumping function of a weakened heart, providing long-term support for patients with severe heart failure.

Assessing adequate tissue oxygenation

Important factors determining adequate tissue oxygenation:
Cardiac output (amount of blood the heart pumps).
Arterial oxygen content (oxygen carried in the blood).
Distribution of blood flow to organs.

Possible complications of shock

Acute Respiratory Distress Syndrome (ARDS): Respiratory failure due to fluid in the lungs.
Disseminated Intravascular Coagulation (DIC): Abnormal clotting in the blood vessels throughout the body.
Acute Renal Failure: Sudden loss of kidney function/ kidney failure
Multiple Organ Dysfunction Syndrome (MODS): Failure of multiple organ systems, either primary or secondary.
Primary MODS: Direct organ failure due to an acute insult (such as sepsis, trauma, or severe injury).
Secondary MODS: Organ failure due to systemic responses to the initial insult, potentially developing later on.

Chapter 22 Obstructive Pulmonary Disorders

Asthma triggers and risk factors

Triggers and risk factors for asthma include allergens such as pollen, mold, and pet dander; irritants like smoke, pollution, and strong odors; respiratory infections (viral illnesses); physical activity (exercise-induced asthma); weather changes (cold air); stress or strong emotions; and a family history of allergies or asthma.

Clinical manifestations, treatment, and goals of treatment for asthma

Wheezing, Tightness in the chest, Dyspnea (shortness of breath), Cough, especially at night or early morning, Increased sputum production
Severe attacks may lead to accessory muscle use, agitation, tachypnea, and decreased peak expiratory flow rate (PEFR).
Treatment and Goals:
Goals: Control symptoms, prevent exacerbations, maintain normal lung function.
Pharmacotherapy:
Controllers:
Inhaled Corticosteroids: Medications that reduce inflammation in the airways, helping to prevent asthma attacks.
Leukotriene Modifiers: Drugs that block the action of leukotrienes, reducing airway inflammation and bronchoconstriction.
Rescue Medications:
Short-Acting Bronchodilators (e.g., Albuterol): Quick-relief medications that relax airway muscles to provide immediate relief from asthma symptoms.
Acute Treatment:
Bronchodilators: Medications that quickly open the airways during an asthma attack.
Corticosteroids: Anti-inflammatory drugs used to reduce severe inflammation in the airways during acute exacerbations.
Oxygen Therapy: Supplemental oxygen provided to improve oxygen saturation in patients experiencing respiratory distress.

Acute bronchitis diagnosis, treatment, goal of treatment

Diagnosis: Clinical presentation characterized by a recent onset of cough.
Treatment: Most cases resolve spontaneously (viral origin). Bacterial cases may require antibiotics.
Goal of Treatment: Symptom management.

Chronic bronchitis etiology, manifestations, diagnosis, treatment

Etiology: Chronic inflammation of the bronchial mucosa is often linked to smoking.
Clinical Manifestations: Patients may experience a chronic cough with sputum production. Shortness of breath on exertion is also common. Excessive mucus production can occur, and symptoms may include fever and fatigue.
Diagnosis: Diagnosis can be made through chest radiography, pulmonary function tests, and arterial blood gas testing.
Treatment:
Bronchodilators: Medications that quickly open the airways during an asthma attack.
Corticosteroids: Anti-inflammatory drugs used to reduce severe inflammation in the airways during acute exacerbations.
Oxygen Therapy: Supplemental oxygen provided to improve oxygen saturation in patients experiencing respiratory distress.

Emphysema etiology, manifestations, diagnosis, treatment

Etiology: Chronic inflammation of the bronchial mucosa is often linked to smoking.
Clinical Manifestations: Patients may experience a chronic cough with sputum production. Shortness of breath on exertion is also common. Excessive mucus production can occur, and symptoms may include fever and fatigue.
Diagnosis: Diagnosis can be made through chest radiography, pulmonary function tests, and arterial blood gas testing
Treatment:
Bronchodilators: Medications that quickly open the airways during an asthma attack.
Corticosteroids: Anti-inflammatory drugs used to reduce severe inflammation in the airways during acute exacerbations.
Oxygen Therapy: Supplemental oxygen provided to improve oxygen saturation in patients experiencing respiratory distress.

Emphysema Symptoms:

Shortness of Breath
Fatigue
Difficulty performing task
Feeling less alert
Blue or gray fingernails

Chronic Bronchitis:

Shortness of Breath
Fatigue
Fever
Cough
Excess mucus production
Symptoms that come & go

Bronchiolitis etiology, manifestations, diagnosis, treatment

Etiology: Bronchiolitis is caused by inflammation due to viral infections, most commonly respiratory syncytial virus (RSV).
Clinical Manifestations: Patients typically present with wheezing, crackles, dyspnea, and increased sputum production.
Diagnosis: Diagnosis can be confirmed through an elevated white blood cell count, chest radiograph, and pulmonary function tests.
Treatment: Treatment includes oxygen therapy, bronchodilators, corticosteroids, and hydration.

Cystic fibrosis etiology, diagnosis, treatment

Etiology: Cystic fibrosis is an autosomal recessive disorder caused by mutations in the CFTR gene, which affects chloride transport.
Diagnosis: Diagnosis involves ABG measurements, pulmonary function tests, sputum culture, and genetic testing.
Treatment: Treatment consists of bronchodilators, chest physiotherapy, nutritional support, antibiotics, and, in some cases, a possible lung transplant.

Classes of drugs for Asthma and COPD

Bronchodilators:
Short-acting beta-agonists (e.g., albuterol)
Long-acting beta-agonists (e.g., salmeterol)
Anticholinergics (e.g., ipratropium)
Anti-inflammatory Agents:
Inhaled corticosteroids (e.g., fluticasone)
Leukotriene modifiers (e.g., montelukast)
Other Treatments:
Mucolytics (for mucus clearance)
Antibiotics (for bacterial infections)