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Cardiovascular System Disorders Prof. Lorrie Hudd NURS1361  Today  CV System REVIEW: Structure & Function  Atherosclerosis  CAD  Dysrhythmias  PAD, PVD  Blood Pressure Dysregulation  Congestive Heart Failure  Valvular Disorders...

Cardiovascular System Disorders Prof. Lorrie Hudd NURS1361  Today  CV System REVIEW: Structure & Function  Atherosclerosis  CAD  Dysrhythmias  PAD, PVD  Blood Pressure Dysregulation  Congestive Heart Failure  Valvular Disorders Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 2  Structure & Function of the CV System REVIEW Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 3  REVIEW: The Circulatory System  The circulatory system is composed of:  Vessels, Fluid, Pump  Heart (muscular pump) contracts and pumps blood simultaneously into 2 loops of blood vessel system Pulmonary circulation Systemic circulation Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 4  REVIEW: Function of the Heart  Main function is transport.  Delivers oxygen and nutrients to tissues  Carries waste products from cellular metabolism to excretory organs  Circulates electrolytes and hormones  Transports immune substances that contribute to the body’s defense mechanisms  Helps to regulate temperature Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 5  REVIEW: Function of the Heart o Move deoxygenated blood from the venous system through the right heart & into the pulmonary circulation o Move the oxygenated blood from the pulmonary circulation through the left heart into the arterial system Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 6  Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 7 REVIEW: Anatomy of the Heart  Located in the mediastinum  Between the lungs  Enclosed in the pericardial sac  Parietal pericardium  Epicardium visceral pericardium  Pericardial cavity  Myocardium  Endocardium  Heart valves  Septum Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 8  REVIEW: Anatomy of the Heart  Pericardium  Forms a fibrous covering around heart  Holds it in a fixed position  Provides physical protection  Provides barrier to infection  Myocardium  Muscular portion  Forms the wall of atria and ventricles  Endocardium  Thin, three-layered membrane lining the heart  Continuous with lining of blood vessels Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 9  MORE ANATOMY: Coronary Circulation  Coronary arteries (R & L)  Branch of aorta immediately distal to the aortic valve  Part of the systemic circulation Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 10  REVIEW: Cardiac Cycle  Diastole  Systole  Semilunar valves have  Pressure mounts, AV valves shut shut (S2) and ventricles (S1) to prevent backflow and relax & fill. AV valves ventricles contract open Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 11  Heart Sounds  “Lubb-dupp”  S1 – closure of AV valves (M + T) “Lubb” Beginning of systole/contraction  S2 – Closure of semilunar valves (A + P)  “Dupp”  End of systole/beginning of diastole Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 12  REVIEW: Conduction System  Conduction pathway  Sinoatrial (SA) node Pacemaker Sinus rhythm  Atrioventricular (AV) node  Located in floor of the right atrium  Delay?  AV bundle (bundle of His)  Right and left branches  Purkinje fibers  Terminal fibers Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 13  Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 14  Heart: Conduction System (Cont.)  Electrocardiogram (ECG)  P wave Depolarization of atria  (loss of resting membrane potential due to alteration of cell membrane polarization)  QRS wave Depolarization of ventricles  T wave Repolarization of ventricles  (restoration of resting membrane potential) Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 15 How is the Heart Regulated? Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 16  Control of the Heart  Cardiac control center in medulla oblongata  Controls vital function incl. HR and force of contraction  Controls through sympathetic or parasympathetic nerves  Baroreceptors  Located in the aorta and internal carotid arteries  Detect changes in blood pressure  Send message to medulla oblongata  Sympathetic stimulation (cardiac accelerator nerve)  Increases heart rate (tachycardia), vasoconstriction  Parasympathetic stimulation (CN X vagus nerve)  Decreases heart rate (bradycardia) Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 17  Cardiac Function  Cardiac output Preload (CO) ◦ Amount of blood  Blood ejected by delivered to heart by a ventricle in one venous return minute Afterload  CO = SV × HR ◦ Force required to eject blood from ventricles Stroke volume (SV) ◦ Determined by  Volume of blood peripheral resistance pumped out of in arteries ventricle w each contraction Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 18  Cardiac Output  4-6 liters blood/min. Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 19  Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 20 Factors that Increase Heart Rate?? o Increased thyroid hormones or epinephrine o ↑ body temperature / infection (i.e. fever) o Increased environmental temperature (esp. high humidity) o Exertion or exercise o Smoking o Stress response o Pregnancy o Pain Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 21  Blood Pressure  Systolic pressure  Exerted when blood is ejected from ventricles (higher)  Diastolic pressure  Sustained pressure when ventricles relax (lower)  Blood pressure (BP) is altered by cardiac output, blood volume, and peripheral resistance to blood flow. Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 22  Blood Pressure (Cont.)  Changes in blood pressure  Sympathetic branch of ANS Increased output → vasoconstriction and increased BP Decreased output → vasodilation and decreased BP  BP is directly proportional to blood volume.  Hormones Antidiuretic hormone (↑ BP); aldosterone (↑ blood volume, ↑ BP); renin-angiotensin-aldosterone (vasoconstriction; ↑ BP) Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 23  Components & Function of the Vascular System  Function  Delivery of oxygen and nutrients and removal of wastes from the tissues  Components:  Arteries and arterioles  Capillaries  Venules and veins Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 24  Components & Function of the Vascular System Arterial System Large and medium size arteries/arterioles Thick-walled vessels with +++ elastic fibers Stretch during systole; recoil during diastole Arterioles act as control valves = blood is released as it moves into the capillaries Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 25  Components & Function of the Vascular System Capillaries (Microcirculation) Microscopic vessels Connect arterial / venous segments Have pores Fluids, electrolytes, gases, etc move across the endothelium by diffusion, filtration, pinocytosis Interstitial fluid exchange - controlled by hydrostatic / osmotic pressures Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 26  Components & Function of the Vascular System Venous System Low pressure system; returns blood to the heart Venules & veins Thin-walled, distensible, collapsible Valves prevent retrograde flow Skeletal muscle contraction helps blood flow Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 27  Diagnostic Tests for Cardiovascular Function  Auscultation  Determination of valvular abnormalities or abnormal shunts of blood that cause murmurs  Detected by listening through a stethoscope  Electrocardiography (ECG)  Useful in the initial diagnosis and monitoring of dysrhythmias, myocardial infarction, infection, pericarditis  Echocardiography (US of heart)  Used to record heart valve movements, blood flow, and cardiac output Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 28  Diagnostic Tests for Cardiovascular Function (Cont.)  Exercise stress tests  Used to assess general cardiovascular function  Fitness clubs, insurance companies, cardiac rehab  Chest x-ray films  Used to show shape and size of the heart Nuclear imaging (size of infarct in heart)  Cardiac catheterization  Measures pressure and assesses valve and heart function Determines central venous pressure and pulmonary capillary wedge pressure Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 29  Diagnostic Tests for Cardiovascular Function (Cont.)  Angiography  Visualization of blood flow in the coronary arteries  Doppler studies  Assess blood flow in peripheral vessels  Record sounds of blood flow or obstruction  Blood tests  Assess levels of serum triglycerides, cholesterol, sodium, potassium, calcium, other electrolytes  Arterial blood gas determination  Checks the current oxygen level and acid-base balance Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 30  General Treatment Measures for Cardiac Disorders  Dietary modifications  Cessation of smoking  Decrease total fat intake  Decreases risk of  General weight reduction coronary disease  Reduce salt intake  Smoking increases platelet adhesion  Regular exercise  Carbon monoxide displaces oxygen program  Increases high-density lipoprotein levels  Lowers serum lipid levels  Reduces stress levels Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 31  * Not testedTreatment Measures: Drug Therapy  Antihypertensive drugs  May be used to lower blood pressure  Many types Adrenergic or sympathetic-blocking agents Calcium blockers Diuretics Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blocking agents  Combinations of drugs from various classes effective  Some of these drugs do cause orthostatic Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 32  Treatment Measures: Drug Therapy  Vasodilators  Reduction of peripheral resistance  Beta blockers  Treatment of hypertension and dysrhythmias  Reduction of angina attacks  Calcium channel blockers  Decrease cardiac contractility  Antihypertensives and vasodilators  Prophylactic against angina Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 33  Treatment Measures: Drug Therapy  Digoxin  Treatment for heart failure  Antidysrhythmic drug for atrial dysrhythmias  Adrenergic blocking drugs  Act on SNS centrally or on the periphery  Beta blockers?  Angiotensin-converting enzyme (ACE) inhibitors  Block conversion of angiotensin I to angiotensin II Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 34  Treatment Measures: Drug Therapy  Diuretics  Remove excess sodium and/or water.  Treat high BP and congestive heart failure.  Anticoagulants  Reduce risk of blood clot formation  Cholesterol-lowering drugs  Reduce low-density lipoprotein and cholesterol levels Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 35 Heart Disorders Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 36  DISEASE OF THE CORONARY ARTERIES (AKA Coronary Artery Disease - CAD or Ischemic Heart Disease or Acute Coronary Syndrome) Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 37  1. Arteriosclerosis and Atherosclerosis  Arteriosclerosis  General term for all types of arterial changes (hardening of arterial walls) Degenerative changes in small arteries and arterioles Loss of elasticity Lumen gradually narrows and may become obstructed Cause of increased BP  Atherosclerosis  Presence of atheromas in large arteries (i.e. narrowed arteries due to plaque build up) Plaques consisting of lipids, calcium, and possible clots Related to diet, exercise, and stress Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 38  Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 39  Lipid Transport  Lipids are transported in combination with proteins.  Low-density lipoprotein (LDL)  Transports cholesterol from liver to cells  Major factor contributing to atheroma formation  High-density lipoprotein (HDL)  Transports cholesterol away from the peripheral cells to liver—“good” lipoprotein  Catabolism in liver and excretion Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 40 Atherosclerosis: Mechanism Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 41  Risk Factors for Atherosclerosis  Nonmodifiable  Age – common after 40  Gender – women HDL  Genetic or familial factors  Modifiable  Obesity  Sedentary lifestyle  Cigarette smoking  Diabetes mellitus  Poorly controlled hypertension  Combination of oral contraceptives and smoking Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 42  Atherosclerosis  Diagnostic tests  Serum lipid levels  Treatment  Weight loss  Increase exercise.  Dietary modification.  Reduce sodium intake.  Control hypertension.  Cessation of smoking  Antilipidemic drugs  Surgical intervention, such as coronary artery bypass grafting Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 43 ATHEROSCLEROSIS Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 44  2. Angina Pectoris  Occurs when there is a deficit of oxygen to meet myocardial needs  Chest pain may occur in different patterns.  Classic or exertional angina  Variant angina Vasospasm occurs at rest.  Unstable angina Prolonged pain at rest—may precede myocardial infarction Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 45 Angina: Imbalance of Oxygen Supply and Demand Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 46  2. Angina Pectoris  Relieved by rest and administration of coronary vasodilators  Example?? NTG - Nitroglycerin Primarily acts by reducing systemic resistance, decreasing the demand for oxygen Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 47 Emergency Treatment for Angina  Rest, stop activity  Patient seated in upright position  Administration of nitroglycerin—sublingual  Check pulse and respiration.  Administer oxygen, if necessary.  Patient known to have angina  Second dose of nitroglycerin  Patient without history of angina  Emergency medical aid Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 48  3. Myocardial Infarction  When coronary artery is totally obstructed  *Atherosclerosis = most common cause  *Thrombus from atheroma = obstruct artery  Vasospasm is cause in a small percentage.  Size / location of infarct determine damage  Most often left ventricle  Scar tissue Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 49  Warning Signs of Heart Attack  Feeling of pressure, heaviness, or burning in chest  Especially with increased activity  Sudden SOB, weakness, fatigue  Nausea, indigestion  Anxiety and fear  Pain may occur and, if present, is usually  Substernal  Crushing  Radiating Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 50  Myocardial Infarction (Cont.)  Diagnostic tests  Changes in ECG  Serum enzyme and isoenzyme levels (released from necrotic cells)  Serum levels of myosin and cardiac troponin are elevated.  Leukocytosis, elevated CRP and ESR common Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 51  Myocardial Infarction: Complications  Thromboembolism causing cerebrovascular accident (CVA; with left ventricular MI)  Congestive heart failure  Dysrhythmias  Sudden death  Cardiogenic shock  Rupture of necrotic heart tissue/cardiac tamponade Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 52 Myocardial Infarction: Treatment  Reduce cardiac demand.  Oxygen therapy  Analgesics  Anticoagulants  Thrombolytic agents may be used.  Tissue plasminogen activator  Medication to treat:  Dysrhythmias, hypertension, congestive heart failure  Cardiac rehabilitation begins immediately. Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 53 CARDIAC DYSRHYTHMIAS Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 54  Cardiac Dysrhythmias (Arrhythmias)  Deviations from normal cardiac rate or rhythm  Caused by electrolyte abnormalities, fever, hypoxia, stress, infection, drug toxicity  Electrocardiography (ECG) for monitoring the conduction system  Reduction of the efficiency of the heart’s pumping cycle  Many types of abnormal conduction patterns exist. Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 55  1. Sinus Node Abnormalities  SA node  Pacemaker of the heart; rate can be altered.  Bradycardia  Regular but slow heart rate  Tachycardia  Regular rapid heart rate  Sick sinus syndrome  Marked by alternating bradycardia / tachycardia Often requires mechanical pacemaker Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 56 2. Atrial Conduction Abnormalities  Premature atrial contractions/beats (PACs)  Extra contraction or ectopic beats Irritable atrial muscle cells outside conduction pathway Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 57 2. Atrial Conduction Abnormalities  Atrial flutter  Atrial heart rate of 160 to 350 beats/min Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 58 2. Atrial Conduction Abnormalities  Atrial fibrillation  Rate over 350 beats/min Causes pooling of blood in the atria = risk of thrombus Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 59 3. Atrioventricular Node Abnormalities  Heart blocks  Conduction excessively delayed or stopped at AV node or bundle of His  First-degree block Conduction delay between atrial and ventricular contractions  Second-degree block Every 2-3 atrial beats dropped at AV node  Third-degree block (slow rates) No transmission from atria to ventricles (dissociation) Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 60  Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 61  4. Ventricular Conduction Abnormalities  Bundle Branch Blocks  Premature ventricular contractions (PVCs) Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 62  4. Ventricular Conduction Abnormalities  Ventricular tachycardia  Ventricular fibrillation Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 63  4. Ventricular Conduction Abnormalities  Asystole Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 64  Treatment of Cardiac Dysrhythmias  Treat underlying cause  Antidysrhythmic drugs  SA nodal problems or total heart block require pacemaker  Defibrillator may be implanted for conversion of ventricular fibrillation. Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 65 Disorders of Blood Pressure Regulation Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 66  Blood Pressure  Control required to provide sufficient blood flow to organs  Arterial Higher pressure Propel blood to all other tissues of the body (i.e., systemic circulation)  Venous Lower pressure Propel blood through the lungs (i.e., pulmonary circulation) Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 67  Blood Pressure Regulation  Sympathetic branch of ANS  Increased output → vasoconstriction and ↑ BP  Decreased output → vasodilation and ↓ BP  Humoral Mechanisms  Hormones Antidiuretic hormone (↑ BP); aldosterone (↑ blood volume, ↑ BP); renin-angiotensin-aldosterone (vasoconstriction; ↑ BP)  Circadian Rhythms  Nocturnal “dipping” Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 68  Hypertension (HTN)  High blood pressure  Common  May occur in any age group  More common in individuals of African ancestry  Greater than 140/90  Sometimes classified as systolic or diastolic depending on measurement elevated  Categories: Primary and Secondary Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 69  Hypertension (cont’d) A. Primary  “Essential hypertension”  Blood pressure consistently above 140/90 mm Hg May be adjusted for age  Increase in arteriolar vasoconstriction  Over long period of time—damage to arterial walls Blood supply to involved area is reduced. Ischemia and necrosis of tissues, with loss of function Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 70  Hypertension (cont’d)  Non-Modifiable Factors? Modifiable / Lifestyle factors?  Age  Gender  Salt intake  Race  Other dietary habits  Family history  Smoking  Diabetes  Excessive alcohol intake Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 71  Hypertension (cont’d)  Areas most frequently damaged by long- standing or severe hypertension?  Kidneys  Heart  Brain  Retina Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 72  Hypertension (cont’d)  Frequently asymptomatic in early stages  Initial signs vague and nonspecific Fatigue, malaise, sometimes morning occipital headache  Treatment 1. Lifestyle modifications Physical activity Dietary modification, incl. sodium intake Weight reduction Reduction of stress Smoking cessation and decreased alcohol intake 2. Drugs Diuretics, ACE inhibitors, drug combinations Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 73  Hypertension (cont’d) B. Secondary hypertension  Results from renal or endocrine disease, pheochromocytoma (benign tumor of the adrenal medulla)  Oral contraceptives  Underlying problem must be treated to reduce blood pressure. Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 74  Hypertension (cont’d) C. Malignant or resistant hypertension  Uncontrollable, severe, and rapidly progressive form with many complications  Diastolic pressure is extremely high.  Hypertensive crisis - critical Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 75  Hypertension (cont’d) D. HTN in Special Populations  Pregnancy Pre-existing or Gestational (Preeclampsia)  Careful monitoring  Delivery is curative  Special medications needed – i.e. labetalol  Older Adults More common Treatment typical although meds initiated at smaller doses Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 76  Orthostatic HTN  Physical finding, not a disease  Abnormal drop in BP during change to upright position  Accompanied by decreased cerebral perfusion  Causes light-headedness, possible syncope, falls  Causes? Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 77 Vascular Disorders Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 78  Peripheral Arterial Disease  Disease in arteries (atherosclerosis) outside the heart  Femoral, popliteal arteries commonly affected  At risk: men, older women, age, lifestyle Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 79  Peripheral Arterial Disease  Signs and symptoms  Increasing fatigue and weakness in the legs  Intermittent claudication (leg pain) Associated with exercise caused by muscle ischemia  Sensory impairment (tingling, burning, numbness)  Peripheral pulses distal to occlusion = weak  Skin appearance on feet and legs changes? Marked pallor or cyanosis Skin dry and hairless Toenails thick and hard Dependent rubor? Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 80  Peripheral Arterial Disease  Signs and symptoms  Once blood flow severely reduced: Severe pain Ulceration Gangrene Limb amputation Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 81  Peripheral Arterial Disease  Diagnostic tests  Blood flow assessed by Doppler studies and arteriography, CT angio  Plethysmography measures the size of limbs and blood volume in organs or tissues.  PROBLEM? Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 82  Peripheral Arterial Disease  Treatment  to reduce symptoms and to decrease CV risk High risk of CAD, CVD and death Lifestyle modification  Blood sugar control  Weight loss  Diet, cholesterol levels  Smoking cessations  Exercise Meds – vasodilators, NTG, anticoagulants Bypass grafting, angioplasty/stent in severe cases Monitor ulcerations, possible amputation Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 83  Aortic Aneurysm  Aneurysm involving any part of aorta  2 most common causes:  Atherosclerosis  Degeneration of medial layer of the vessel  Also – trauma, infections, congenital defects  Risk high with HTN, older males, smokers** Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 84  Aortic Aneurysm  Localized dilation / weakening of arterial wall  Develops from a defect in the medial layer  Different shapes  Saccular (False) Bulging wall on the side  Fusiform (True) Circumferential dilation along a section of artery  Dissecting aneurysm Develops when there is a tear in the intima of the wall and blood continues to dissect or separate tissues Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 85 Types of Aortic Aneurysms Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 86  Aortic Aneurysm Signs and symptoms  Depend on size and location  Frequently asymptomatic until they become large or rupture  Bruit may be heard on auscultation.  Pulse may be felt on palpation of abdomen. Rupture may lead to moderate bleeding but usually causes severe hemorrhage and death Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 87  Aortic Aneurysm  Diagnostic tests  Radiography  Ultrasound  CT scanning  MRI  Treatment  Maintain blood pressure at normal level.  Prevent sudden elevations caused by exertion.  Prevent stress, coughing, constipation  Surgical repair Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 88 VASCULAR DISORDERS: VENOUS DISEASE Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 89  The Venous Circulation  Superficial Veins and Deep Veins  Disorders of venous system result in congestion, predispose to clot formation (stagnant blood flow) Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 90  1. Varicose Veins  Dilated, tortuous veins of lower extremities  Common  Lead to secondary problems = venous insufficiency  Risk factors: age, female gender, obesity, pregnancy, heredity  Primary (superficial veins)  Secondary (deep veins)  Most common cause is DVT Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 91  1. Varicose Veins  Mechanism  Prolonged standing Increased pressure in veins and dilates/stretches wall  Intra-abdominal pressure Pregnancy, lifting, hormones ↑ pressure on iliac/femoral valves/veins to support weight  Manifestations  Visible veins, aching, edema  Treatment  Prevention (stockings, exercise), surgical? Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 92  2. Chronic Venous Insufficiency  Consequence of DVT, valve incompetence or both  Effective unidirectional blood flow, emptying of veins cannot occur  S&S of impaired blood return  Edema  Skin atrophy  Hemosiderin staining  Stasis ulcers  Treatment  Compression  Medications for improving blood flow Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 93  3. Venous Thombosis  “Thrombophlebitis”  Thrombus development with accompanied inflammation in vein  Superficial or deep veins  Most common in deep veins in legs - “DVT”  Factors for thrombus development  Stasis of blood or sluggish blood flow?  Endothelial injury/vascular trauma?  Increased blood coagulability? Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 94  Venous Thombosis  Manifestations  Related to inflammatory process  Often unnoticed  Pain, swelling, deep muscle tenderness  Systemic signs—fever, malaise, leukocytosis  AT RISK FOR???? Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 95  Venous Thombosis  Diagnosis  D-dimer, doppler ultrasound  Treatment???  Preventive measures Early ambulation, exercise, compression, elevating legs, prophylactic anticoagulation  Anticoagulant therapy, thrombolytics  Surgical intervention Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. 96 Heart Failure Heart Failure Complex syndrome ◦Occurs when heart unable to pump sufficient blood to meet metabolic needs ◦Functional or structural disorder of the heart - any condition that reduces the pumping ability of the heart ◦One side of heart typically fails first ◦Pulmonary and/or systemic congestion  Burden of Disease o 400,000 Canadians/year o Affects approx. 10% over 65 o Incidence has doubled in past 30 years due to aging population and increased survival post –MI o Only major CV disease where incidence is increasing o Most prevalent acute care diagnosis and common cause of hospitalization (primarily elderly) o 1/3 require readmission within 90 days o 50% 5 year mortality Etiology of HF / Risk Factors Usually a complication from another condition ◦MI ◦Valve defect ◦HTN ◦Lung disease May present acutely but usually a chronic problem Etiology of HF / Risk Factors o CAD is leading cause of HF o MI impairs the pumping ability or conduction system o Hypertension o Valve defects (VHD) o Congenital heart defects o Increased demands on the heart due to o Obesity, Diabetes, Renal failure, excessive ETOH, smoking o Some genetic components increase risk Causes of Left-Sided HF  Acute myocardial infarction  Uncontrolled Hypertension  Cardiomyopathy  Causes of Right-Sided HF  Persistent left-sided failure  Conditions that restrict blood flow into lungs  Stenosis or regurgitation of the tricuspid or pulmonic valves  Right ventricular infarction  Cardiomyopathy  Acute or chronic pulmonary disease (cor pulmonale) Pathophysiology of CHF In response to functional or structural disorder of the heart (↓ pumping ability): o Chambers of the heard dilate o Cardiac muscle hypertrophies(cardiomegaly) o Ventricle walls become thicker o Needs of heart muscle increased (more blood supply needed for larger muscle) o Needs cannot all be met and some myocardial cells die and replaced with fibrous tissue  Pathophysiology of HF (RESULT)** 1. FORWARD EFFECT: Cardiac output or stroke volume decreases = ◦ Less blood reaches organs = hypoxia = ◦ Decreased cell function = ◦ Fatigue, dizziness, confusion and lethargy = ◦ Mild acidosis develops  Pathophysiology of HF (RESULT)** 1. FORWARD EFFECT: Cardiac output or stroke volume decreases = ◦ Less blood reaches organs = hypoxia = ◦ Decreased cell function = ◦ Fatigue, dizziness, confusion and lethargy = ◦ Mild acidosis develops 2. BACKWARD EFFECT: Backup and congestion = ◦ Output from ventricle less than inflow of blood ◦ Congestion in venous circulation behind affected ventricle (pulmonary or systemic) Pathophysiology of HF Helpful to refer to left sided heart failure or right-sided heart failure One side of the heart usually fails first Both result in low cardiac output Initially, compensation maintains cardiac output… ◦… but will aggravate the condition instead of providing assistance  Pathophysiology of HF: Compensatory mechanisms Reduced blood flow to systemic circulation and kidney (very impt**) ◦ ↑ renin and aldosterone secretion (RAAS) ◦ Vasoconstriction and increased blood flow add to heart’s workload = worsened CHF  SNS response ◦ ↑ HR (to try and ↑ CO) and peripheral resistance ◦ ↑ work for the heart  Left-sided Left-sided HF ◦ Most common ◦ Left ventricle cannot pump all blood into systemic circulation ◦ The normal volume of blood in the lungs cannot enter left side of the heart ◦ Eventually causes congestion in pulmonary circulation and possible pulmonary edema ◦ Fluid pushed into alveoli Right-sided Right sided HF ◦ Primary Cause: Left ventricular failure ◦ Right ventricle cannot maintain output ◦ “Back-up” of blood to right atrium and venous circulation = systemic congestion ◦ RESULT: increased blood volume in legs, feet, portal circulation, neck veins = ◦ peripheral edema, hepatomegaly, splenomegaly, vascular congestion of the GI tract, jugular vein distention ◦ (“cor pulmonale” if due to lung disease) Signs & Symptoms of Congestive Heart Failure (CHF) Forward effects (similar with failure on either side) ◦ Decreased blood supply to tissues, general hypoxia ◦ Fatigue and weakness ◦ Dyspnea and shortness of breath Compensation mechanisms ◦ Tachycardia ◦ Cutaneous and visceral vasoconstriction ◦ Daytime oliguria Signs & Symptoms Left-sided failure ◦ Related to pulmonary congestion** ◦ Dyspnea and orthopnea ◦ fluid accumulates in the lungs ◦ Cough ◦ fluid irritating the respiratory passages ◦ Paroxysmal nocturnal dyspnea ◦ Indicates the presence of acute pulmonary edema ◦ Usually develops during sleep ◦ Excess fluid in lungs frequently leads to infections such as pneumonia Signs and Symptoms Right-sided failure ◦ Related to Systemic Back-up** ◦ Edema in feet, legs, or buttocks ◦ Increased JVP = distended neck veins ◦ Hepatomegaly and splenomegaly ◦ Ascites ◦ Fluid accumulates in peritoneal cavity ◦ Marked abdominal distention Young Children with CHF Often secondary to congenital heart disease Feeding difficulties often first sign* ◦ Failure to gain weight or meet developmental guidelines Short sleep periods - irritability Tripod position to play Cough, rapid grunting respirations, flared nostrils, wheezing Radiographs show cardiomegaly Arterial blood gases used to measure hypoxia Diagnostic Tests for CV Function Auscultation Echocardiography ◦ Detection of valvular ◦ Used to record the abnormalities or abnormal heart valve shunts of blood that cause movements, blood murmurs flow, and cardiac output ECG ◦ Useful in initial diagnosis Exercise stress tests and monitoring of ◦ To assess general dysrhythmias, MI, infection, cardiovascular pericarditis function Diagnostic Tests for CV Function cont’d Chest x-ray films ◦ Shows shape and size of heart, pulmonary edema ◦ Nuclear imaging ◦ Tomographic studies Cardiac catheterization ◦ Measure pressure, assess valve & heart function ◦ Determination of central venous pressure and pulmonary capillary wedge pressure Angiography ◦ Visualization of blood flow in coronary arteries  Diagnostic Tests for Cardiovascular Function (Cont’d) Blood tests ◦Assess serum triglycerides, cholesterol levels, levels of sodium, potassium, calcium, other electrolytes Arterial blood gas determination ◦Check the current oxygen level and acid-base balance General Treatment Measures Dietary modifications ◦ Decrease total fat intake ◦ Reduce salt intake Weight loss Regular exercise program ◦ Increases HDL, lowers LDL, reduces stress/weight Cessation of smoking ◦ Decreases risk of coronary disease ↓ETOH Drug Therapy Digoxin ◦ Treatment for heart failure ◦ Increase cardiac contractility without increasing cardiac oxygen consumption Antidysrhythmic drug ◦ for atrial dysrhythmias Antihypertensive drugs (CCB, BB) ◦ Used to lower blood pressure Angiotensin-converting enzyme (ACE) inhibitors ◦ Block conversion of angiotensin I to angiotensin II Adrenergic-blocking drugs ◦ Act on SNS centrally or on the periphery Drug Therapy (Cont’d) Diuretics (decrease preload/intravascular volume) ◦ Remove excess sodium and/or water ◦ Treatment of high BP and congestive heart failure Anticoagulants ◦ Reduce risk of blood clot formation Cholesterol-lowering drugs ◦ Reduction of low-density lipoproteins and cholesterol content HF can be prevented by early detection and intervention… Health Promotion! Valvular Defects Heart Valves 4 chambers of heart separated by valves to prevent backflow of blood 4 valves: ◦ Atrioventricular valves (control blood flow from atria to ventricles) 1. Tricuspid (rt) 2. Mitral (bicuspid) (lt) ◦ Semilunar valves (3 cusps/half moons) (control blood flow out of ventricles) 3. Pulmonic valve 4. Aortic valve Heart Valves Heart Valves Heart Valve Function Valves function to maintain unidirectional blood flow within the heart Valves open one way only – open/close in response to pressure Closure of valves = heart sounds Heart Valve Dysfunction (Valvular Heart Disease) May be classified as stenosis or valvular incompetence (“insufficiency”, “regurgitation”, “leaky valve”) \ Heart Valve Dysfunction (Valvular Heart Disease) May be classified as stenosis or valvular incompetence (“insufficiency”, “regurgitation”, “leaky valve”) Stenosis o Valve opening is narrowed/constricted because the valve leaflets, or cusps, fail to open completely o i.e. mitral stenosis, aortic stenosis Heart Valve Dysfunction (Valvular Heart Disease) May be classified as stenosis or valvular incompetence (“insufficiency”, “regurgitation”, “leaky valve”) Stenosis o Valve opening is narrowed/constricted because the valve leaflets, or cusps, fail to open completely o i.e. mitral stenosis, aortic stenosis Regurgitation o Dysfunctional valve allows blow flow in the wrong direction due to: ◦ Failure of valve to close completely ◦ Blood leaks or regurgitates backwards o i.e. mitral regurgitation Effects of Heart Valve Defects  *don’t need to know Heart Valve Defect Types HVD CLINICAL MANIFESTATIONS Causes Exertional dyspnea, hemoptysis; fatigue; Adult cases primarily d/t rheumatic heart disease** Mitral valve palpitations Congenital stenosis Loud, accentuated S1; opening snap; low-pitched, SLE rumbling diastolic murmur May be asymptomatic for years until it becomes MI, chronic rheumatic heart disease, mitral valve Mitral valve acute with pulmonary edema and shock developing prolapse (MVP), ischemic papillary muscle dysfunction, regurgitation rapidly IE Systolic murmur Most asymptomatic Etiology unknown; Mitral valve Palpitations, dyspnea, CP, activity intolerance, MVP is one of the most common forms of VHD prolapse syncope; Late or holosystolic murmur Congenital Angina pectoris, syncope, exertional dyspnea, HF Aortic valve Similar to that of coronary artery disease or from Normal or soft S1, prominent S4, crescendo– stenosis calcification/scarring owing to rheumatic fever decrescendo murmur Acute: Sudden cardiovascular collapse: abrupt Aortic valve Acute AR is caused by IE, trauma, or aortic dissection onset of profound dyspnea, transient CP, regurgitation and constitutes a life-threatening emergency progression to shock Chronic AR is generally the result of rheumatic heart Chronic: fatigue, exertional dyspnea disease, syphillis or congential dx Peripheral edema, ascites, hepatomegaly; Tricuspid valve stenosis occurs almost exclusively in Tricuspid Diastolic low-pitched, decrescendo murmur with patients with rheumatic fever or in IV drug users stenosis and increased intensity during inspiration (stenosis), regurgitation Pansystolic murmur with increased intensity at Pulmonary stenosis is almost always congenital Diagnostics o Clinical Manifestations (PE/HHx) o Echocardiogram – valve structure, function, chamber size o Cardiac catheterization - detects chamber pressure changes, pressure gradients across the valves, size of valve openings o ECG – HR, rhythm, ischemia or chamber enlargement o CXR - heart size, alterations in pulmonary circulation, valve calcification Collaborative Care of VHD Conservative Therapy Prevention of recurrent rheumatic fever and IE (prophylaxtic antibiotics) Treatment depends on severity and valve involved. Focus on: ◦ Preventing exacerbations of HF, acute pulmonary edema, VTE, and recurrent endocarditis. ◦ Anticoagulant therapy – prevent/treat PE ◦ Medical mgmt – antiarrhythmia drugs, digoxin, diuretics, etc ◦ Sodium restriction ◦ Surgical Health Promotion Prophylaxis is key! ◦ Strep ◦ Hx rheumatic fever or endocarditis ◦ Valvular prosthesis References Gould, B. E., & Dyer, R. M. (2011). Pathophysiology for health professions (4th ed.). Philadelphia: Saunders. Gould, B. E. (2006). Pathophysiology for health professions (3rd ed.). Philadelphia: Saunders. Hannon, R.A., Pooler, C.P., & Porth, C.M. (2010). Porth pathophysiology: Concepts of altered health states (1st Canadian edition). Philadelphia: Wolters Kluwer. Huether, S.E., & McCance, K. L. (2012). Understanding pathophysiology (5th ed.). St. Louis: Mosby. VanMeter, K. & Hubert, R. Gould's Pathophysiology for the Health Professions (5th ed). Philadelphia: Saunders. Respiratory System Disorders Patho1361 Professor Lorrie Hudd  REVIEW: Respiratory System Function???  Respiratory System – Review  Two anatomic areas 1. Upper respiratory tract –Resident (normal) flora 2. Lower respiratory tract –Sterile Anatomy of the Respiratory System  Upper Respiratory Tract  Nasal cavity  Warming and moistening of air  Foreign material trapped by mucus secretions  Nasopharynx  Pharyngeal tonsils in posterior wall  Palatine tonsils  Lymphoid tissue in posterior portion of the oral cavity  Upper Respiratory Tract (Cont’d)  Oropharynx  Common passage for air and food  Epiglottis protects opening into larynx. Closes over glottis at swallowing to prevent aspiration  Larynx  Two pairs of vocal cords  Trachea  C-shaped rings of cartilage  Lower Respiratory Tract  Bronchial tree (continuous branching)  Trachea branches into: Right and left bronchi Secondary bronchi Bronchioles Alveolar ducts Alveoli – lined by surfactant to reduce surface tension and maintain inflation  End-point for inspired air  Site of gas exchange  Gas Exchange  Flow of gases between the alveolar air and the blood (external respiration)  Gas exchange depends on the relative concentrations (partial pressures) of the gases.  pO2 – partial pressure of oxygen  pCO2 – partial pressure of carbon dioxide  Each gas in a mixture which moves along its partial pressure gradient, independent of other gases (Dalton’s law). CIRCULATION Pulmonary Capillaries https://www.youtube.com/watch?v=8NUxvJS-_0k Diffusion of Gases  Factors Affecting Diffusion of Gases  Partial pressure gradient  Thickness of the respiratory membrane  Fluid accumulation in alveoli or interstitial tissue impairs gas exchange  Total surface area available for diffusion  If part of alveolar wall is destroyed, surface area is reduced – less exchange  Ventilation-perfusion ratio (V/Q ratio)  Ventilation (air flow) and perfusion (blood flow) need to match for maximum gas exchange.  Ventilation  Process of inspiration and expiration  Airflow depends on pressure gradient (Boyle’s law) Air always moves from high pressure area to low pressure area.  Atmospheric pressure higher than pressure in alveoli = inspiration Air moves from atmosphere into lungs  Pressure in alveoli higher than in atmosphere = expiration Air moves from lungs into atmosphere  Control of Ventilation  Primary control centers for breathing located in the medulla and pons  Chemoreceptors detect changes in carbon dioxide levels, hydrogen ions, and oxygen in blood or cerebrospinal fluid (CSF)  Central chemoreceptors are located in the medulla  Peripheral chemoreceptors are located in the carotid bodies  Control of Ventilation (Cont’d)  Hypercapnia  Carbon dioxide levels in the blood increase  Carbon dioxide easily diffuses into CSF i.e. Respiratory acidosis = low pH stimulates respiratory center (medulla) = increases rate and depth of respirations (hyperventilation) Normal Respiratory Control  Control of Ventilation (Cont’d)  Hypoxemia  Marked decrease in oxygen Chemoreceptors respond Important control mechanism in individuals with chronic lung disease – move to hypoxic drive Hypoxic Drive THEORY  Control of Ventilation (Cont’d)  Hypocapnia  Caused by low carbon dioxide concentration (low partial pressure of carbon dioxide) in blood May be caused by hyperventilation Excessive amounts of carbon dioxide expired Causes respiratory alkalosis  Pulmonary Volumes  Tidal volume  Amount of air exchanged with quiet inspiration and expiration.  Residual volume  Volume of air remaining in lungs after maximum respiration  Vital capacity  Maximal amount of air that can be moved in and out of the lungs with a single forced inspiration and expiration Pulmonary Volumes (Cont’d)  Respiratory Diagnostic Tests  Spirometry—pulmonary function test (PFT)  Test pulmonary volumes and airflow times  Arterial blood gas determination  Checks oxygen, carbon dioxide, bicarbonate, serum pH  Pulse Oximetry  Measures O2 saturation  Exercise tolerance testing  For patients with chronic pulmonary disease  Diagnostic Tests (Cont.)  Radiography  Helpful in evaluating tumors  Evaluate infections  Bronchoscopy  Perform biopsy.  Check site of lesion or bleeding.  Culture and sensitivity tests  Sputum testing for presence of pathogens  Determine antimicrobial sensitivity of pathogen General Manifestations of Respiratory Disease  General Manifestations of Respiratory Disease  Sneezing  Reflex response to irritation in upper respiratory tract Assists in removing irritant Associated with inflammation or foreign material  Coughing  Irritation caused by nasal discharge  Inflammation or foreign material in lower respiratory tract  Caused by inhaled irritants  Unproductive vs productive  General Manifestations: SPUTUM  Yellowish-green, cloudy, thick mucus Often indication of a bacterial infection  Rusty or dark-colored sputum Usually sign of pneumococcal pneumonia  Very large amounts of purulent sputum with foul odor May be associated with bronchiectasis  Thick, tenacious mucus Asthma or cystic fibrosis, blood-tinged sputum—may result from chronic cough; may also be sign of tumor or tuberculosis  Hemoptysis Blood-tinged (bright red), frothy sputum, pulmonary edema  General Manifestations of Respiratory Disease (Cont.)  Breathing patterns and characteristics  Eupnea, Tachypnea, Bradypnea  Kussmaul respirations Deep rapid respirations- typical for acidosis; DKA, CKD Labored respiration or prolonged inspiration or expiration Often associated with obstruction of airways  Wheezing or whistling sounds Indicate obstruction in small airways  Stridor High-pitched crowing noise Usually indicates upper airway obstruction Respiratory Patterns  General Manifestations of Respiratory Disease (Cont.)  Breath sounds  Crackles Light bubbly or crackling sounds, with serous secretions  Rhonchi Deeper or harsher sounds from thicker mucus  Absence Nonaeration or collapse of lungs  Friction rub Soft sound produced as rough, inflamed, or scarred pleura move against each other  General Manifestations (cont’d)  Dyspnea  Subjective feeling of discomfort May be caused by increased carbon dioxide or hypoxemia Often noted on exertion, such as climbing stairs  Respiratory distress (severe dyspnea)  Flaring of nostrils  Use of accessory respiratory muscles  Retraction of muscles between or above ribs  Orthopnea  Occurs when lying down  Usually caused by pulmonary congestion  General Manifestations (cont’d)  Paroxysmal nocturnal dyspnea (PND)  Sudden acute type of dyspnea  Common in patients with left-sided congestive heart failure  Cyanosis  Bluish coloring of skin and mucous membranes Caused by large amounts of unoxygenated hemoglobin in blood  Pleural pain  Results from inflammation or infection of parietal pleura CLUBBING Clubbed digits Result from chronic hypoxia Painless, firm, fibrotic enlargement at the end of the digit  Basic Therapies for Respiratory Disorders Respiratory Infections  Upper Respiratory Tract Infections  Common Cold  Sinusitis  Epiglottitis  Influenza  Scarlet Fever  URTI: Common Cold  AKA “infectious rhinitis” Viral infection  More than 200 possible causative agents  Spread through respiratory droplets  Hand-washing and respiratory hygiene important in prevention  Symptomatic treatment  Secondary bacterial infections may occur. Usually caused by streptococci Purulent exudate; systemic signs, such as fever  URTI: Common Cold Signs & Symptoms??  Slight fever  URTI: Common Cold Treatment:  Symptomatic and supportive  Unless bacterial infection develops secondarily  Antiviral drugs  May reduce symptoms and duration  Reduces risk to infect others Complications of Viral Respiratory Infection  Other Upper Respiratory Tract Infections  Sinusitis  Usually bacterial infection  Analgesics for headache and pain  Course of antibiotics often required to eradicate infection  Laryngotracheobronchitis (croup)  Common viral infection, particularly in children (3 months to 3 years old)  Common causative organism Parainfluenza viruses and adenoviruses  Infection usually self-limited  General Comparison of Respiratory Infections in Children  Other Upper Respiratory Tract Infections cont’d Epiglottitis  Acute infection  Common in children ages 3 to 7 years  Usually caused by Haemophilus influenzae B  Rapid onset; fever and sore throat  Tripod position, drooling, trouble swallowing, anxiety, stridor  Swelling/spasm of epiglottis may obstruct airway  Treatment  Oxygen and antimicrobial therapy  Upper RTIs: Influenza (Flu)  Viral infection  Three groups of influenza viruses  Type A (most prevalent), types B and C  Viruses constantly mutate.  Sudden, acute onset with fever, marked fatigue, aching pain in the body  May also cause viral pneumonia  Mild case of influenza may be complicated by secondary bacterial pneumonia.  Commonly, deaths in flu epidemics result from pneumonia.  Upper RTIs: Influenza (Cont.)  Treatment  Symptomatic and supportive Unless bacterial infection develops secondarily No Antibiotics!  Antiviral drugs May reduce symptoms and duration Reduces risk to infect others  Prevention  Respiratory hygiene!  Vaccination is recommended for most individuals.  Type A H1N1 Influenza  This virus contains genes from pig, bird, and human flu strains.  Usually affects children and teens younger than 20 years  Healthy young adults also at high risk  High mortality rate caused by acute respiratory syndrome  Pulmonary edema  Pneumonia  Requires ICU care  Scarlet Fever  Caused by group A β-hemolytic Streptococcus (S. pyogenes)  Symptoms  Typical “strawberry” tongue  Fever, sore throat  Chills, vomiting, abdominal pain, malaise  Treatment  Antibiotics Scarlet Fever (Cont.)  Lower Respiratory Tract Infections  Bronchiolitis  Pneumonia  Severe Acute Respiratory Syndrome  COVID-19  NOT COVERED IN PATHO 1:  Tuberculosis  Histoplasmosis  Anthrax  LRTIs: Bronchiolitis  Caused by the respiratory syncytial virus (RSV)  Transmitted by oral droplet  Virus causes necrosis, inflammation in small bronchi and bronchioles  Signs  Wheezing and dyspnea, rapid shallow respirations, cough, rales, chest retractions, fever, malaise  Treatment  Supportive and symptomatic  LRTIs: Pneumonia  Classification of pneumonias based on:  Causative agent (Viral, bacterial, fungal)  Anatomical location of infection Throughout both lungs, or consolidated in one lobe  Pathophysiological changes Changes in interstitial tissue, alveolar septae, alveoli  Epidemiological data Nosocomial (hospital-acquired) Klebsiella pneumoniae or Pseudomonas aeruginosa Community-acquired  Viral or bacterial Types of Pneumonia Types of Pneumonia (Cont.)  Lobar Pneumonia  Bacterial pneumonia  Community-based, often in healthy young adults  Usually caused by: Streptococcus pneumoniae Infection localized in one or more lobes. Inflammation and vascular congestion—exudate forms in the alveoli Exudate contains fibrin and forms a consolidated mass Exudate produces rusty sputum  Adjacent pleurae frequently involved  Infection may spread to pleural cavity—empyema  Lobar Pneumonia (Cont.)  Manifestations  Sudden onset  Systemic signs High fever with chills, fatigue, leukocytosis  Dyspnea, tachypnea, tachycardia  Pleural pain  Rales initially then disappears  Productive cough Typical rusty-colored sputum  Confusion and disorientation  Bronchopneumonia  Diffuse pattern of infection in both lungs lower lobes  Several species of microorganisms may be the cause.  Hypostatic pneumonia (supine position)  Inflammatory exudate forms in alveoli interfering with oxygen diffusion  Onset tends to be insidious  Moderate fever, cough, rales  Productive cough with purulent sputum—usually yellow or green  Antibacterial treatment  Other Types  Legionnaire’s Disease  Caused by Legionella pneumophila Thrives in warm, moist environments Often nosocomial infection  Difficult to identify—requires special culture  Untreated infections can be fatal  Primary Atypical Pneumonia  Caused by Mycoplasma pneumoniae (bacterial)  Pneumocystis carinii pneumonia  Opportunistic infection, often found in AIDS  Coronaviruses Causative agent of common colds Some in URTI Novel coronaviruses predominantly in LOWER respiratory tract 2 previous coronavirus-related outbreaks: SARS-CoV (Asia – 2002/2003) MERS-CoV (Saudi Arabia - 2012/2019) COVID-19 (SARS-CoV-2) is a new strain; less deadly but much more transmissible  Severe Acute Respiratory Syndrome (SARS-CoV)  Transmission by respiratory droplets - close contact  First signs  Fever, headache, myalgia, chills, anorexia, diarrhea x 3- 7 days  Later signs  Effect on lungs evident – cough, dyspnea, interstitial congestion, hypoxia; mechanical ventilation may be required  Lymphopenia, thrombocytopenia,  CRP,  liver enzymes  Severe Acute Respiratory Syndrome (SARS-CoV)  Treatment  Antivirals  Glucocorticoids  High fatality rate  Risk factors:  Travel to endemic areas, contact with such a traveler  Employment involving close contact with the virus High healthcare worker infection and other nosocomial spread Aerosolization during procedures (intubation, nebs, BiPAP, suctioning)  COVID-19: Coronavirus (SARS-CoV-2) SARS Co V-2 virus Cause of 2020 global pandemic Transmission - respiratory droplets, aerosols Pathophysiology Rapid attachment and damage to lung cells Can cause “cytokine storm” immune reaction Elderly, comorbidities, immunocompromised Newer variants infect upper respiratory  COVID-19 (Cont.) Most common symptoms: Cough, fever, SOB, taste loss, body aches, GI Spectrum of COVID-19 disease severity Asymptomatic to critical disease Treatments: Supportive care Antivirals Various therapeutic regimens (hydroxyquinilone, Remdesivir, Ivermectin, monoclonal antibodies) New drugs under development Prophylaxis is key DVT/ Pulmonary Embolus (PE)  Deep Vein Thrombosis (DVT)  Review from last week  Venous stasis, blood vessel damage, hypercoagulability increases chances deep vein thrombosis (DVT)  A thrombus may break away with movement or massage, resulting in a pulmonary embolus (PE)  Pulmonary Embolus  Blood clot or mass that obstructs pulmonary artery or any of its branches  Effect depends on material, size, and location  Small emboli might be “silent” unless they involve a large area of lung.  Large emboli may cause sudden death.  90% of pulmonary emboli originate from deep vein thromboses in legs; are preventable Pulmonary Embolus (Cont.)  Pulmonary Embolus (Cont.)  Signs and symptoms  Small emboli Transient chest pain, cough, dyspnea  Larger emboli Chest pain with coughing or deep breathing; tachypnea and dyspnea develop suddenly. Later—hemoptysis and fever Hypoxia—causes anxiety, restlessness, pallor, tachycardia  Massive emboli Severe crushing chest pain, low blood pressure, rapid weak pulse, loss of consciousness  Pulmonary Embolus (Cont.)  Prevention  Health teaching prior to surgery  Antiembolic stockings  Exercise to prevent thrombosis  Use of anticoagulant drugs  Diagnosis  Radiography, lung scan, MRI, pulmonary angiography  Pulmonary Embolus (Cont.)  Treatment  Assessment of risk factors  Prolonged bed rest and compression stockings  Heparin or streptokinase  Mechanical ventilation  Embolectomy  Some cases = Chronic Obstructive Pulmonary Disease (COPD)  Group of chronic respiratory disorders  Emphysema  Chronic Bronchitis  Chronic Asthma  Characterized by progressive tissue degeneration and obstruction in the airways  Causes irreversible and debilitating damage that may affect individual’s ability to work and function  Respiratory failure may occur  Only chronic disease with increasing mortality  4th leading cause of death  500,000 over age 35 diagnosed  Another 500,000 middle-aged Canadians have COPD and do not know   Quality of patient lives   Health service use   Economic burden  Cigarette smoking  Recurrent respiratory infections  Alpha-1 antitrypsin deficiency  Aging  Living in urban areas with smog  More than one out of every five deaths in the U.S. is the result of cigarette smoking  Incl. over 4,000 chemicals - many carcinogenic  Nicotine acts as a stimulant to the sympathetic nervous system resulting in:  Increased HR  Peripheral vasoconstriction  Increased BP and cardiac workload  Stimulate an inflammatory response in lungs 1. Hyperplasia of cells 2. Increased production of mucus 3. Narrows smaller airways  Increased difficulty in clearing secretions 4. Reduces ciliary activity 5. Dilates distal air spaces and destroys alveolar walls / capillary bed  Carbon monoxide  Decreases O2 carrying capacity  Impairs psychomotor performance and judgment  Second-hand smoke associated with:  Decreased pulmonary function  Increased risk of lung cancer  Increased mortality rates from IHD 2. INFECTION  Major contributing factor to the aggravation and progression of COPD  Recurring infections impair normal defense mechanisms 3. HEREDITY  ALPHA-1 Antitrypsin (AAT) deficiency is the only known genetic abnormality that leads to COPD  Accounts for < 1% of COPD  AAT is a produced by the liver and normally found in the lungs  AAT controlled by autosomal co-dominant genes  People with this type of emphysema are primarily of northern European origin  Some degree of emphysema common  Gradual loss of elastic recoil  Rib cage changes from osteoporosis and calcification of costal cartilages  Decreased compliance of chest wall  Increase work of breathing  Lungs become rounded and smaller  Thinner alveolar walls  Arterial O2 levels decrease EMPHYSEMA: PATHOPHYSIOLOGY 1. Breakdown of alveolar wall results in:  Loss of surface area for gas exchange  Loss of pulmonary capillaries  Loss of elastic fibers  Altered ventilation-perfusion ratio  Decreased support for other structures EMPHYSEMA: PATHO 2. Fibrosis / thickening of the bronchial walls from chronic irritation leads to:  Narrowed airways  Weakened walls  Interference with passive expiratory airflow EMPHYSEMA: PATHO 3. Progressive difficulty with expiration  Air trapping (increased residual volume)  Overinflation of the lungs  Fixation of ribs in an inspiratory position, increased anterior-posterior diameter of thorax (BARREL CHEST)  Flattened diaphragm (on radiographs) EMPHYSEMA: PATHO  Air goes into the lungs but is unable to come out on its own and remains in the lung  Causes bronchioles to collapse  Trapped air, hyperinflation and over- distention  As more alveoli collapse, blebs and bullae may develop EMPHYSEMA: PATHO 4. Advanced emphysema and loss of tissue  Adjacent damaged alveoli coalesce = large air spaces  Membrane around blebs/bullae rupture = Pneumothorax  Marked hypercapnia  Hypoxia becomes driving force of respiration (loss of hypoxic drive)  Frequent infections  Pulmonary hypertension and cor pulmonale may develop in late stage.. How??? EMPHYSEMA: PATHO (The downward spiral continues…) Recurrent infections = production and stimulation of neutrophils and macrophages Enzymes released by these neutrophils and macrophages cause FURTHER destruction of alveolar tissue  Inflammation  Exudate formation  Edema EMPHYSEMA: PATHO  Surface area for O2 diffusion in the blood decreases  Compensation occurs:  Body increases respiratory rate to increase alveolar ventilation  Hypoxemia usually only develops late in disease  Insidious onset  Dyspnea  Occurs first on exertion, then at rest  Hyperventilation with prolonged expiratory phase  Development of “barrel chest”  Tripod position  Patient is characteristically underweight even when the patient has adequate calorie intake (increased WOB)  Fatigue  Clubbed fingers  Inflammation, obstruction, repeated infection, chronic coughing twice for 3 months or longer in 2 years  History of cigarette smoking or of living in urban or industrial areas  Mucosa inflamed and swollen  Hypertrophy and hyperplasia of mucus glands  Chronic inflammatory changes and narrowing of small airways  Fibrosis and thickening of bronchial wall  Low oxygen levels  Altered function of alveolar macrophages leading to increased bronchial infections  Pulmonary hypertension and cor pulmonale may develop in later stages CHRONIC BRONCHITIS: PATHO (CONT’D)  Hyperplasia of mucus-secreting glands in the trachea and bronchi  Increase in goblet cells  Disappearance of cilia CHRONIC BRONCHITIS: PATHO (CONT’D)  Frequently airways are colonized with microorganisms  Excess amounts of mucus are found and may occlude small bronchioles  Alveolar structures and capillaries are normal CHRONIC BRONCHITIS: PATHO (CONT’D)  Chronic inflammation  Primary pathologic mechanism in causing changes  Causes vasodilation, congestion, mucosal edema  Mucous glands become hyperplasic  Causes narrowing of airway lumen and diminished airflow CHRONIC BRONCHITIS: PATHO (CONT’D)  Greater resistance to airflow = increased work of breathing  Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema  Mucus is a physical barrier to ventilation  Tendency to hypoventilate and retain CO2  Frequently patients require O2 both at rest and during exercise CHRONIC BRONCHITIS: PATHO (CONT’D)  Peribronchial fibrosis develops from the healing process secondary to inflammation  Cough ineffective to remove secretions because the person cannot breathe deeply enough to cause air flow distal to the secretions =  Bronchospasm frequently develops  Usually more common with history of smoking  Earliest symptoms:  Frequent, productive cough (esp during winter & in am)  Frequent respiratory infections  Bronchospasm can occur at end of paroxysms of coughing  Cough usually exacerbated by respiratory irritants or cold air  Dyspnea on exertion  Normal weight or heavyset  Ruddy appearance  Hypoxemia and hypercapnia  Result from hypoventilation and airway resistance in addition to problems with alveolar gas exchange  Cyanosis  Cor pulmonale  Infections / Pneumonia  Pulmonary hypertension  Acidosis  Polycythemia  Acute exacerbations of chronic bronchitis  Acute respiratory failure  Right side of the heart must increase to push blood into the lungs = Right-sided heart failure  Subsequent intravascular volume expansion  Systemic venous congestion  Distended neck veins  Hepatomegaly  Ascites  Peripheral edema  Weight gain  Can be caused by discontinuation of bronchodilator or corticosteroid medication  Beta-adrenergic blockers may exacerbate respiratory failure in patient with asthmatic component  Indiscriminate use of sedatives and narcotics may suppress respiratory drive and lead to respiratory failure  Peptic ulcer disease and GERD  Acid may get into lungs  Come COPD meds may make GERD symptoms worse  Chest radiograph  Pulmonary function tests (PFTs)  Spirometry, etc  Typical findings include reduced Forced Expiratory Volume and increased residual volume and total lung capacity  Labs such as ABGs  Exercise test to determine O2 saturation in the blood and pulse oximetry  ECG can show signs of right ventricular failure  pH less than 7.25  PaCO2 greater than 50 mm Hg  PaO2 less than 50 mm Hg  Reducing exposure to irritants  Treatment of infection, antimicrobials  Expectorants  Bronchodilators  Appropriate chest therapy  Including postural drainage and percussion  Low-flow oxygen for severe hypoxemia  Nutritional supplements  Appropriate breathing techniques (pursed lip breathing)  Adequate nutrition and hydration  Improves energy levels, resistance to infection  Lung reduction surgery  Remove 20 to 30% of damaged lungs  Surrounding tissue can work more efficiently Patient Education  smoking cessation, vaccinations, breathing techniques, adequate hydration and nutrition, etc) Cessation of smoking Limit exposure to irritants Vaccination for prophylaxis  References Gould, B. E., & Dyer, R. M. (2011). Pathophysiology for health professions (4th ed.). Philadelphia:Saunders. Gould, B. E. (2006). Pathophysiology for health professions (3rd ed.). Philadelphia:Saunders. Hannon, R.A., Pooler, C.P., & Porth, C.M. (2010). Porth pathophysiology: Concepts of altered health states (1st Canadian edition). Philadelphia: Wolters Kluwer. Huether, S.E., & McCance, K. L. (2012). Understanding pathophysiology (5th ed.). St. Louis: Mosby. Inflammation, Infection & Immunity Professor Lorrie Hudd NURS1361 Inflammation Composition of Blood What defenses does the body have against infection and disease??  Normal Body Defenses  First line of defense  Nonspecific  INNATE  Mechanical barrier Examples:  Skin  Mucous membrane  Secretions  Normal bacteria flora  Normal Body Defenses  Second line of defense  Nonspecific - defenses don’t differentiate between pathogens; respond same way each time  INNATE cellular and molecular responses Phagocytes migrate to infection, engulf foreign Phagocytosis bodies Increased capillary permeability at infected site Inflammation Recruitment of WBC/leukocytes Vasodilation (increased blood flow to site) Increased body temperatures to decrease Fever microbial growth  Normal Body Defenses  Third line of defense  Specific defense - B cells (lymphocytes) produce antibodies to specific antigens  ADAPTIVE Cell-mediated immunity These make memory cells to ensure long term immunity to a particular pathogen Example??  Normal Body Defenses https://study.com/academy/lesson/third-line-of-defense-in-the-body- definition-overview.html Defense Mechanisms in the Body  Inflammation A protective mechanism and important basic concept in pathophysiology  ***A NORMAL defense mechanism  GOALS: Eliminate CAUSE of injury Remove damaged tissue Generate NEW tissue  Inflammation (cont’d)  Not the same as infection = no microbe  Acute or Chronic  Many acute inflammatory disorders Ex; Artrhitis  Causes of Inflammation  Direct physical damage (cut, sprain)  Caustic chemicals (acid, drain cleaner)  Ischemia or infarction  Allergic reactions  Hot/cold extremes  Foreign body (splinter)  Infection  Acute Inflammation  Process of inflammation is the same, regardless of cause  Timing varies with specific cause  The ACUTE Inflammatory Response: 2 STAGES 1. Vascular  Blood vessels DILATE Promotes congestion, vascular permeability Movement of fluid into affected tissue Leads to redness, swelling, heat, pain, loss of function As fluid leaves capillaries, blood less viscous = more clotting The Acute Inflammatory Response: 2 STAGES 2. Cellular  Delivery of WBCs WBC (leukocytes) emigrate to site / into affected tissue Migrate to site of injury through chemotaxis The Acute Inflammatory Response: 2 STAGES 2. Cellular (cont’d)  Phagocytosis Leukocytes engulf / degrade cellular debris Intracellular killing Leads to exudates Cells of Inflammation  The Inflammatory Response: MEDIATORS  At same time as these responses, chemical mediators act to mediate the inflammatory response  Mediators come from the cells or plasma  The Inflammatory Response: MEDIATORS  Cell mediators  Plasma mediators  Secreted by cells in  Present in the plasma and response to must be activated stimulus  Kinins = stimulate pain  Histamine (inside receptors, dilation and mast cells) - causes vascular permeability (i.e. dilation/permeability bradykinin) of capillaries  Coagulation system/Clotting  Serotonin factors  Complement system Chemical Mediators in the Inflammatory Response  Acute Inflammation Chemical mediators affect blood vessels and nerves in the damaged area:  Vasodilation  Hyperemia = increase in blood flow to the area  Increase in capillary permeability  Leukocytes attracted by chemotaxis (chemicals stimulate the movement of organisms)  Diapedesis – leukocytes squeeze through capillary walls to get to site of injury  Cells destroy foreign material, cell debris (phagocytosis) Local Effects of Inflammation? Swelling: increased blood flow to the area Swelling: shift of protein and fluid into the interstititial space Pain Pus Loss of function  Local Effects of Inflammation (cont’d) Serous Fibrinous Purulent n Systemic Effects of Inflammation? Mild fever Malaise Fatigue Headache Anorexia Systemic Effects of Inflammation?  Leukocytosis  WBC response  Differential count –  Neutrophils, lymphocytes, eosinophils, basophils, etc.  Lymphadenitis  Painful palpable lymph nodes  Potential Complications of Inflammation  Infection  Microorganisms can more easily penetrate edematous tissues.  Some microbes resist phagocytosis.  Inflammatory exudate provides an excellent medium for microorganisms.  Skeletal muscle spasm  May be initiated by inflammation (tendinitis, fractures, sprains)  Protective response to pain  Spasm can force the bones of a joint out  Potential Complications  Deep ulcers may result from severe or prolonged inflammation  Caused by cell necrosis and lack of cell regeneration that causes erosion of the tissue Can lead to complications such as perforation of viscera Extensive scar tissue formation  Chronic Inflammation!  Chronic Inflammation  Follows acute episode of inflammation  NOT part of body’s natural healing process  Less swelling and exudate  Presence of more lymphocytes, macrophages, and fibroblasts  Continued tissue destruction  More fibrous scar tissue  Granuloma (small mass of cells with necrotic center) may develop around foreign object  Acute vs Chronic Inflammation Acute Chronic “Good” ; normal healing “Bad” ; abnormal healing Non-specific Specific Long-term inflammatory reaction caused Initial short term response to a threat by persistent acute inflammation (non- (pathogens, injured tissues) degradable pathogens, persistent foreign antibodies, autoimmune reactions) Onset Insidious/delayed and lasts Onset immediate and lasts a few days months t years Outcome may be resolution, abscess Outcome may be tissue destruction or formation, chronic inflammation fibrosis Cardinal signs include warmth, redness, No cardinal signs pain, fever, swelling Fundamental cells include neutrophils, Fundamental cells include macrophages, mast cells antibodies, B & T lymphocytes  Treatment of Inflammation  Acetylsalicylic acid (ASA) - Aspirin  Decreases prostaglandin synthesis  Allergy, stomach irritant  Blood thinning  Acetaminophen  Tylenol  Nonsteroidal anti-inflammatory drugs (NSAIDs)  Ibuprofen  Glucocorticoids (Corticosteroids)  Decrease capillary permeability and reduce immune response Drugs Used to Treat Inflammation  Treatment of Inflammation “RICE” Therapy  Rest?  Ice ?  Promotes vasoconstriction  Compression?  Encourages fluid back into vascular compartment and away from damaged area  Elevation?  Encourages fluid flow away from damaged area Healing  Tissue Repair  Overlaps inflammatory process  Can take form of tissue regeneration or replacement  Involves cellular migration, proliferation, differentiation and interaction with the extracellular matrix  Types of Healing 1. Resolution  Minimal tissue damage  Cells recover and return to normal Example???  Types of Healing 2. Regeneration  Damaged tissue regenerated (mitosis) and replaced with cells that are identical and functional  Organization of cells may be altered which can alter function Although usually little to no evidence of previous injury  Types of Healing 3. Replacement  Extensive tissue damage or cells incapable of mitosis  Losttissue replacement by fibrous/connective tissue (scar tissue)  Loss of function Brain or myocardium  Phases of Wound Healing 1. Hemostasis  Blood clotting, then vasodilation and increase permeability 2. Inflammation  Leukocytes migrate to the site and phagocytose bacteria and debris 3. Proliferative Phase  Fibroblasts help to build new tissue to fill the wound space 4. Remodelling Phase  Modelling of fibrous scar tissue  Longest Phase (may take over 1 year)  Factors Affecting Healing?? Factors Promoting Healing Factors Delaying Healing Youth - Age Good nutrition - Medications Adequate hemoglobin - Anemia Effective circulation - Circulatory problems Clean, undisturbed wound - Certain chronic diseases Infection  Microorganisms  Include bacteria, fungi, protozoa, viruses  Nonpathogenic  Usually do not cause disease unless conditions change  Part of normal flora  Often beneficial  Pathogens  Disease-causing microbes Types of Microorganisms  Common Pathogens 1. Viruses 2. Bacteria 3. Chlamydia, Ricketsia, etc 4. Fungi 5. Parasites 6. Prions  1. Viruses  Smallest pathogens  Can change (mutate) quickly  No organized cellular structure!  Protein coat (various shapes / sizes)  Surrounds nucleic acid core of RNA or DNA (not both)  Require a living host (to replicate) Active Viral Infection  Latent Viral Infection  Some active viruses enter host cell, insert their genome and remain latent (nonreplicating) for long periods without causing disease  Under appropriate conditions (suppressed immune system, etc), virus can begin replication and produce signs/symptoms (active disease)  2. Bacteria  Single cell organism  Classified as prokaryotes  NO organized nucleus!  Contain BOTH RNA and DNA  Function metabolically and reproduce  Do not require living host to survive  Vary in size and shape  Divide by binary fission  2. Bacteria: Basic Structure  Rigid cell wall  Protects and provides a specific shape  Two types  External capsule or slime layer  Offers additional protection  Flagellae  Provide motility; one or more attached to cell wall  Pili or fimbriae  Tiny hairlike structures—found in some bacteria  Assist with attachment; transfer DNA to other bacterium 2. Bacteria: Basic Structure (cont’d)  Classification of Bacteria  According to the microscopic appearance  Classification of Bacteria  According to staining of the cell (affected by chemical composition of the cell membrane)  Gram-positive organisms: stained purple by a primary basic dye (usually crystal violet)  Gram-negative organisms: not stained by the crystal violet but are counterstained red by a second dye (safranin)  2. Bacteria: Effects  Exotoxins Usually produced by gram-positive bacteria Diffuse through body fluids Variety of effects (make you feel unwell)  Endotoxins Released from cell wall on death of gram-negative bacteria Vasoactive compounds that can cause septic shock  Enzymes Damage tissues and promote spread of infection  Spores Formed by several species Dormant-latent form of bacterium, can survive long periods Highly resistant to heat and disinfectants Tetanus, botullism 3. Chlamydia, Rickettsia, Mycoplasmas  Have properties of Viruses and Bacteria  Chlamydia  Common cause of sexually transmitted disease  Can result in infertility, PID  Rickettsiae  Transmitted by insect vectors (lice, ticks)  Rash, small hemorrhages  Mycoplasmas  Lack cell wall – not affected by many antimicrobials  Cause of atypical type pneumonia  4. Fungi  Found throughout environment  On animals, plants, humans (microflora), food  Only a few are pathogenic (disease causing)  Cause primary infection on skin or mucous membranes but may spread systemically particularly in immunosuppressed individual  2 groups: yeasts and moulds  5. Parasites  Benefit from relationship with another organism  Method of Infecting  Infect and cause diseases in other animals; animals then transmit disease to humans.  Types  Protozoa  Helminths  Arthropods  5. Parasites (cont’d) Protozoa Helminths Many live independently Large multicellular organisms Transmitted through fecal-oral route that are visible to the naked (contaminated food, contact etc) or a eye vector Life cycle with at least three stages Examples: Trichomoniasis (STI), Ovum, larva, adult Malaria, Amebic dysentery (diarrhea) Enter body through skin or by ingestion, depending on Anthropods species Ectoparasites - attach or burrow into Infections commonly found in the skin and remain there for children, immunosuppressed. relatively long periods of time Examples: Examples: Insects/Arachnids - ticks, Pinworms, Hookworms, mosquitos, mites, lice Tapeworms, etc  6. Prions  No genome  Protein-like agents that change the shape of proteins within host cells  Transmitted by contaminated tissues  Ingestion of meat , infected blood or donor organs  Cause slow, progressive neuronal degeneration  Resistant to treatment, often fatal  Examples  Creutzfeldt-Jacob disease, mad cow disease  Nosocomial Infections  Occur in health care facilities  Hospitals, LTC, physician or dental offices  10-15% of patients acquire an infection in the hospital because of:  Transmission of Infection  Transmission from person to person  Agent  the microbe causing the infection  Reservoir  Source of infection Person with active infection or asymptomatic person Contaminated environmental source (water, soil)  Carrier  Person may never develop disease – still a carrier  Person with subclinical signs of the disease  Transmission of Infection  Mode of transmission  Method whereby agent reaches new susceptible host Direct contact Indirect contact Droplet transmission No intermediary Involves intermediary Respiratory or Touching infectious object or organism salivary secretions lesion Contaminated hand or are expelled from food infected individual Contact with infected blood or bodily Fomite—inanimate secretions object Aerosol transmission Vector-borne Involve small particles from the respiratory tract Insect or animal is an intermediate host Suspended in air, travel farther than droplets  Transmission of Infection  Portal of exit  Means whereby the agent leaves the reservoir  Portal of entry  Access to new host Penetration Direct contact Ingestion Inhalation Transmission of Infectious Agents  Transmission of Infection  Susceptible host - depends on:  Age (infants and older adults)  Pregnancy  Genetic susceptibility  Immunity  Nutrition  Health status: Chronic disease Severe physical or emotional stress Inflammation or trauma Impaired inflammatory responses  Disease Course in Infection  Incubation period  Time between entry of organism into the body and appearance of clinical signs of disease  Vary considerable with different organisms  Prodromal period  Fatigue, loss of appetite, headache  Nonspecific—“coming down with something”  Acute period  Infectious disease develops fully  Convalescent stage  Resolution stage Disease Course  Factors That Decrease Host Resistance  Age  Pregnancy  Malnutrition  Chronic disease  Stress  Inflammation or trauma  Virulence and Pathogenicity  Pathogenicity 