Patho 2 Test 2

premature ventricular contraction (PVC)

a ventricular contraction preceding the normal impulse initiated by the SA node (pacemaker) -additional beats arising from a ventricular muscle cell or ectopic pacemaker. occasional PVCs do not interfere with heart function, but increasing frequency, multiple ectopic sites, or paired beats are of concern bc ventricular fib can develop from these, leading to cardiac arrest

pneumonia (lobar, broncho

**pneumonia** -develop as a primary acute infection in the lungs or may be secondary to another respiratory or systemic condition which tissue resistance is reduced -it is a risk following any aspiration or inflammation in the lung, when fluids pool or defense mech asuch as cilia is reduced -occasionally it is blood borne -may involve multiple microbes following aspirations -pathophysiologic changes occur primarily in the itnersitital tissue or avelor space -mixed bacteria are usually isolated from the resultant infection Legionnaires' disease Unknown until 1976 outbreak among American Legion convention attendees Legionella pneumophila (gram - bacteria) Resides in pulmonary macrophages Pneumocystis carinii pneumonia Fungus—often cause of fatality among AIDS patients Produces exudate (because of damaged tissues) Infectious inflammation of the lungs "...infectious Inflammation of lungs." (Inflammation of lungs: "pneumonitis") Bacterial & viral agents Breathed in Hematologic spread (septic bacteremia) → spread through the blood 2 categories dependent on exudate location Bronchopneumonia & lobar pneumonia → exudate collects in alveoli Interstitial pneumonia → edema in your tissues and does not get in alveoli Pneumonia is an infectious inflammation of the lungs. It can be caused by a variety of bacteria and some viral agents. The pathogens may be breathed in or may come from being transported in the blood stream. This can always be a complication from a hospital acquired infection. There are two main categories depending up the location of the exudate created (which often obstructs the airways)—broncho- and lobar pneumonia; and interstitial pneumonia. This poor person has every type of pneumonia in existence! Lobar pneumonia features a lobe in which the alveoli are filled with consolidation—a solidified exudate of debri, neutrophils, red blood cells, and fibrin. No gas is exchanged in these alveoli. Broncho pneumonia features consolidation in clumps of alveoli at the ends of bronchioles. It generally is more diffuse throughout the lungs. Interstitial pneumonia—usually of viral or mycoplasmic (see the infection chapter) origin, affects those interstitial cells that comprise the alveoli. The exudate usually causes swelling in the cells themselves. Some cases of this are termed walking pneumonia.

Discuss the causes and effects of CHF

-2 basic effects when the heart cannot maintain its pumping capability -cardiac output and stroke volume decreases, resulting in less blood reaching the various organs and tissues, a forward effect -- leading to dec cell function and fatigue and lethargy -backup congestion develops in the circulation behind the affected ventricle (output is less than the inflow of the blood) CAUSES: -MAY result from a problem in the heart itself, such as infarction or a valve defect -may arise from inc demands on the heart, such as hypertension or lung disease effects: -reduced blood flow into systemic circulation and this the kidneys leads to inc renin and aldosterone secretions -SNS response also inc heart rate and peripheral resistance

Venous disorders

Bluish purple skin discoloration Normal peripheral pulses Warm to touch Monitor for hx of DVT Slightly painful ulcers /w marked edema venous Circulation Passive Keeps blood from flowing back Disease process

Lower Respiratory Tract Infections

Bronchiolitis Pneumonia --Lobar Pneumonia --Bronchopneumonia --Legionnaire's Disease --Primary Atypical Pneumonia --Severe Acute Respiratory Syndrome --Tuberculosis --Histoplasmosis --Anthrax Lower respiratory tract infections are usually more serious than upper respiratory tract infections, and involve a variety of pathogens. lower Respiratory Tract Infections Affects bronchioles & lungs Viral, bacterial, fungal, and protozoan causes Often more serious than URIs Do not get gas exchange (inflammation in alveoli) Anything messes with the walls, you are in trouble with the gas exchange

Upper Respiratory Tract Infections

Common cold (infectious rhinitis) Allergic Rhinitis: Caused by exposure to antigen (allergen) upper Respiratory Tract Infections Involves: nose, throat, trachea, sinuses, etc. Viral cause Difficult to develop immunity Signs & symptoms: inflammation of mucous membranes (wet) Extra fluid production Spread via tubes (ears = otitis media) the common cold is caused by a viral infection of the URT -- most common pathogen is a rhinovirus We'll first look at infections in the lungs, starting at the top. Upper respiratory infections often carry similar signs and symptoms. Damage to the mucus membranes occur and there ia an inflammatory response. These affect nose, throat, trachea, even ears (through the Eustachian tubes).

ventricular tachycardia

A rapid heart rhythm in which the electrical impulse begins in the ventricle (instead of the atrium), which may result in inadequate blood flow and eventually deteriorate into cardiac arrest. Dangerous Can lead to Ventricular Fibrillation Very little filling of the heart and lousy cardiac output likely to reduce cardiac output b the filling time is reduced and the force of contraction is reduced 100-160/minutes -possibly reduced cardiac output

Discuss the development of respiratory failure

Acute Respiratory Failure Normal partial pressure (P) values are: PO2: 100 mm Hg PCO2: 40 mm Hg Respiratory Failure defined as: PO2: <50 mm Hg PCO2: >50 mm Hg May result from acute or chronic disorders Emphysema Combination of chronic and acute disorders Acute respiratory disorders Many neuromuscular diseases Signs may be masked or altered by primary problem Treatment Primary problem must be resolved. Supportive treatment to maintain respiratory function -ARF can be the result of many pulmonary disroders -indicated when the Pao2 is less than 50 mm Hg (severe hypoexmia) or Paco2 is greater than 50 mm Hg (hypercapnia) and serum pH is decreasing -normal values are approx 80-100 mm Hg for o2 and 35 to 45 mm Hg for co2 -respiratory insuff is applied to interim state which blood gases are abnormal but cell function can continue -primary problem may be complicated by reflex pulmonary vasoconstriction due to hypoxia or acidosis,which impairs lung perfusion and inc cardiac workload -acidosis of respiratory origin may become decompensated bc of failure in other systems, resulting in respiratory failure -respiratory arrest is when cessation of resp activity is quickly followed by cardiac arrest

Describe the pathophysiology of ARDS

Adult Respiratory Distress Syndrome (ARDS) Widespread lung tissue damage, especially the lining of alveoli Often secondary or even tertiary reaction to other disease states Lungs FAILING People would go into shock Can be caused by inhaling smoke Not getting gas exchange Causes of ARDS Non-infectious interstitial disease Affects interstitial tissue between alveoli Diffuse alveolar damage Septal wall thickening from inflammation Exudate into alveoli Shock Formally called "shock lung" Blood contents leak into interstitium and alveoli Try to do vasoconstriction; acidosis does vasodilation Miscellaneous causes Hypoxia, anoxia, inhalation of toxins, chemicals, drugs, DIC, and heat from fire Signs, Symptoms, and Treatment of ARDS Extreme dyspnea—gasping Low PO2 (hypoxemia) and high PCO2 (hypercapnia) CXR (Chest X-ray) shows diffuse consolidation End result: respiratory failure Must be placed on a ventilator About a 30-40% case fatality rate -aka shock lung, wet lung, stiff lung -restrictive lung disorder predisposing conditions -systemic sepsis, prolonged shok, burns, aspirations, and smoke -basic changes in the lungs results from injury to the alveolar walls and cap membrane, leading to elease of chemical mediators, inc perm of alevelor cap mem, inc fluid and protein in theintersitial area, and damge to the surf producing cells --these events result in dec diffusion of o2 reduced blood flow to the lungs, difficulty in expanidng the lungs, and diffuse atelcelasis -damage to the lung tissue progresses as inc numbers of neutrophils migrate to the lungs, releasing prtesases and other mediators -excess fluid in the lungs predisposes to pneumonia as a complications -chf may develop

tuberculosis

An infectious disease that may affect almost all tissues of the body, especially the lungs Mycobacterium tuberculosis TEST Airborne spread→ aerosol spread How it starts Primary TB (exposed and pretty healthy) → essentially asymptomatic Breathe in droplets Gets into lungs and attack lung tissues Make granuloma and wall bacteria off → it is still alive Delayed hypersensitivity response → helps w/ formation of granuloma (TYPE 4 HYPERSENSITIVITY) Clumps of bacteria (tubercles) start to kill surrounding tissue Area is walled off (granuloma) Calcifies and is called a Ghon complex (after it gets calcified) → more dense and what shows up in chest x-ray 'caseous necrosis' Dead tissue fluid severe coughing and possible blood vessel rupture (hemoptysis) Massive destruction of lung tissue (cavitation) Cavities in the lungs /dead tissue Coughing up their lungs Signs & symptoms Asymptomatic: +PPD (Purified Protein Derivative) Active disease: Fever Night sweats Weight loss (unexplained) Coughing (productive w. hemoptysis) → coughing up blood Can go to bones and liver (affects more than just lungs) Various stages of infection/outcomes Primary response Killed by body's immune response Secondary response Hypersensitivity to subsequent exposure to TB (PPD) Bacteria 'walled off' Miliary (extrapulmonary) TB immune response is poor or is overwhelmed by an extensive infection possible to see the gross pattern of granulomatous disease "miliary" pattern of granulomas because there are a multitude of small tan granulomas, about 2-4 mm in size, scattered throughout the lung parenchyma. TUBERCLE → WHERE WE GET THE NAME TUBERCULOSIS TEST ? There is a cure for TB (5 or 6 different drugs everyday for weeks) Directly observed therapy (DOT) Medical assistant to watch you take your medicine Tubercles that spread out rapidly through the lung tissue -diseaseof poverty and crowding -caused by mycobacterium tb and priamrily affects the lungs but the pathogen may invade other organs as well 2 stages: -primary (tb infection) and secondary (tb disease) -primary occurs when the microorganism first enters the lungs, engulfed by macrophages, ad cause a local inflamm rection -lymphocytes and macrophaes cluster together to form a granuloma contains the bacilli forming a tubercle -caseation necrosis develops in the center forming dead macrophages and necrotic tissue -secondary/reinfection is the stage of active infection -cavitation occurs with formation of a large open area in the lung and erosion into the bronchi and blood vessels -mycobacterium tb is transmitted by oral droplets released from a person with active infection that are inhaled into the lungs

Discuss the development of aortic aneurisms

Aneurysm Weakening in arterial wall Bulging or outpouching Fatty plaque buildup impairs artery's ability to dilate Hypertension Narrowing Tends to happen with ppl with athero and waterloo and hypertension Splits of arteries Aortic Aneurysm More common in abdominal aorta Much like a bulge on a car tire! -localized dilation and weakening of an arterial wall -most common location is either the abdominal or thoracic aorta -may take different shapes -fusiform shape (circumferential dilation along a section of artery) -dissecting aneurysms develop when there is a tear in the intima, allowing blood to flow along the length of the vessel between the layers of the arterial wall -the aneurysm develops from a defect in the medial layer, often associated with turbulent blood flow at the site, from a bifurcation, or from an atheroma -many aneurysms eventually rupture, causing a massive hemorrhage -common causes are atherosclerosis, trauma, syphillis, and other infections -rupture occassionally leads to moderate bleedings but most often causes severe hemorrhage and death (signs are severe pain and indications of shock)

anthrax

Anthrax Bacterial infection by gram-positive bacilli Inhalation anthrax Flulike symptoms Severe acute respiratory distress Shock caused by release of toxins High fatality rates Treatment with antimicrobial agent ciprofloxacin Animal vaccine available Recommended for people working with the organism or in other professions that might cause exposure Different types (GI tract, skin and blisters) Inhaled → destroy lung tissues, go into respiratory arrest, go into shock -bacterial infection of the skin, respiratory tract or gi tract -gram + bacillus that forms grayish white spores -causes flu-like synptoms -shock follows quickly due to release of toxins, and case fatality rates were 45% signs -cutaneous form (blisters, swelling around sore, sores on face) -inhalation form (fever, chills, cough, naseua, headache, sweats, SOB, confusion, etc) -GI form (hoarseness, diarrhea, swelling of tummy, tummy pain, fever and chills, sore throat, etc) -treated with antimicrobial

Describe the pathophysiology of aspiration

Aspiration (breathe stuff into your lungs) Breathing in foreign material into lungs Usually goes down right bronchus May cause obstruction to varying degrees Liquid aspiration produces complications Reflux or vomitus causes alveolar inflammation May lead to aspiration pneumonia and pulmonary abscesses -invovles the passage of food or fluid, vomitus, drugs, or other foreign material into the trachea and lungs -right lower lung is often the destination of aspirations material bc anatomically branching bronchus tends to continue straight down -common result is obstruction (whether the aspirate I s a solid object causing inflammation and swelling) -inflammation may interfere with swellin and gas exchange and predispose pneumonia -when liquids are aspirated, the effects are somewhat different -irritating liquids (like acids) tends to disperse into several bronchi -- they cause severe inflammation, leading to narrow airways and increased secretions, which make the lung more difficult to expand -alevoli is involved--> gas exchange may be impaired -aspiration pneumonia --> predisposes to the development of infection later other complications: -respiratory distress syndrome -pulmonary abscess -solvents may be absorbed into the blood

asthma (extrinsic/intrinsic)

Asthma (extrinsic) → caused by allergic response → you get bronchoconstriction Spasm of the airways Irritation, hypersensitivity Histamine—released when IgE encounters allergen vasoconstriction Mucous, constriction, swelling Dyspnea, wheezing Severe but reversible (inhalers) Allergic & exercise-induced states More seen in kids Non-Allergic Asthma (Book calls it intrinsic asthma) → intrinsic/non allergy Affects adults Psychogenic and irritant causes Possible autonomic nervous system imbalance Gets stressed Fight or flight response (overreaction of this / tightening of the airways) -disease that involves periodic epsiodes of severe but reversible brochial obstruction in which persons with hypersensitive airways -acute referring to a single episode -chronic referring to the long term condition -extrinsic asthma and involves acute epsiodes triggered by type I hypersensitivity reaction to an inhaled antigen -intrinsic asthma is onset during adulthood --> other types of stimuli target hyperresponsive tissues in the airway, initiating the acute attack (includes respiratory infections, exposure to cold, exercise, drugs) -bronchi respond to stimuli with three changes 1. inflammation of mucusa with edema 2. contraction of smooth musicle 3. inc secretion of thick mucus in passageays -- changes lead to obstructd airways -partial obstruction of the small bronchi results in air trapping and hyperinflation of the lungs --air passes I nthe areas distal to obstructuin -- partially expired -total obstruction of the airway results when mucus plugs completely block the flow of air in the already narrow passage

broncho

At higher magnification, the pattern of patchy distribution of bronchopneumonia is seen. Bronchopneumonia is classically a "hospital acquired" pneumonia seen in persons already ill from another disease process. Most common type Staphylococcus aureus, Streptococcus pneumoniae, and pneumococcus. patchy infiltrates consistent with bronchopneumonia from a bacterial infection. Lung Abscess two lung abscesses, one in the upper lobe and one in the lower lobe of this left lung. An abscess can be a complication of severe pneumonia, most typically from virulent organisms such as S. aureus. Abscesses also are complications of aspiration, where they appear more frequently in the right posterior lung. --Lung abscesses often are result of bacterial pneumonia and can also result from aspiration of food or stomach contents. Notice for bronchopneumonia the consolidation (light spots) is more spread out throughout the lung. See the light patches in what is suppose to be a dark lung field. That is consolidation blocking (attenuating) the X-rays. -scattered small patches -multiple bacteria -inflammation and purulent exudate in alveoli often arising from prior pooled secretions or irritations -insidious onset -muld fever -productive cough w yellow-green sputum and dyspnea -occurs as a diffuse pattern of infection in both lungs, more often in the lower lobes -begins at the bronchial mucuousa and soreads into the local alveoli -exudate interferes with o2 diffusion -recovery usually occurs without residual lung damage

Differentiate between arteriosclerosis and atherosclerosis

Atherosclerosis (cholesterol plaque deposits) → gets calcified Big chunk of big broad term (arteriosclerosis) Presence of atheromas Fatty plaques stick to arterial wall Hard & soft regions Hard = due to arteriosclerosis Soft = plaques (atheroma) Cause of: Myocardial infarction (MI) Strokes (CVA) Vascular disease Source of emboli Aneurysm

3rd degree (complete) heart block

Atria and ventricles beat independently of each other. Both P waves and Q-waves are present Heart block Something interrupts the conduction path from atrium to ventricle (ischemia? Drugs? PE?) Ventricles can take on bradycardic (40 bpm) rhythm (usually patient goes unconscious) three degrees 1st degree—delayed but eventually normal 2nd degree—complete intermittent obstruction 3rd degree—complete—ventricles on their own → total heart block (no signal) -heart block occurs when conduction is excessively delayed or stopped at the AV node or bundle of His 1. 1st degree is when the conduction delay prolongs the PR interval, the time bw the atrial and ventricular contractions 2. 2nd degree is when a longer delay leads periodically to a missed ventricular contraction 3. total/3rd degree blocks occur when there is NO transmission of impulses from the atria to the ventricles -the ventricles contract spontaneously at a slow rate of 30 to 45 BPM, totally independent of the atrial contraction, which continues normally. -cardiac output is greatly reduced, sometimes to the point of fainting (or causing cardiac arrest)

Describe the pathophysiology of congenital heart disorders

Congenital Heart Disease (Malformations) Exogenous (teratogens) Fetal Alcohol Syndrome Rubella Endogenous → from within Trisomy X 1 in a thousand people have this Exposures from things outside the baby (usually during the first 8 weeks of development. From fertilization → alcohol, rubella) Teratogen -cardiac anomalies are structural defects in the heart that develop during the first 8 weeks of embryonic life -congenital heart disease may include valvular defects that interfere with the normal flow of blood, septal defects that allow mixing of o2-ed blood from the pulmonary circulation with un-02-ed blood from the sustemic ciruculations, shunts or abnormalities in the position of the large vessel -these defects are often associated with chromosomal abnormalities, such as down syndrome large defects signs: -pallor and cyanosis -tachycardia -dyspnea -clubbed fingers or squatting position -intolerance for exercise and exposure to cold weather -delayed growth -surgical repair may be needed -ECG can be used to test this

test

Consolidation → mass that builds up alveoli (lung disease) TEST ? Consolidation occurs through accumulation of inflammatory cellular exudate in the alveoli and adjoining ducts. The liquid can be pulmonary edema, inflammatory exudate, pus, inhaled water, or blood (from bronchial tree or hemorrhage from a pulmonary artery).

myocardial infarction

Coronary artery occluded -Results in anoxia to tissues Affects Myocardium -Muscle necrosis (coagulation necrosis) -Inflammation/Granulation tissue -Fibrosis (myocardium doesn't regenerate) -Loss of muscle function Affects conduction tissues -Affected tissue loses conductivity -Arrhythmias develop Can result in heart failure and death MI can cause Ventricular Fibrillation which results in no cardiac output or even asystole (no rhythm). Both situations often lead to death. Collateral circulation may reduce damage. -Has neutrophils because of inflammation going on -Disrupts rhythm MI Consequences Eventual heart failure Brain damage if cardiac arrest occurred Infarct gets bigger if heart not rested Hypertrophy to make up for lost tissue Other problems: -Rupture of infarcted area -Ventricular aneurysm -Embolism with stroke MI Warning Signs Feeling of chest pressure, heaviness, or a burning sensation (particularly with increased exertion) SOB, perspiration, weakness, fatigue Nausea or feeling of indigestion Onset of anxiety or feeling of impending doom Manifestations of Progressing MI Pain -Unrelieved by ntg -Men—severe. Women—often milder Pallor, diaphoresis, nausea, dizziness , weakness, and dyspnea Marked anxiety or fear Hypotension (common) -CO decreases—rapid & weak pulse -Development of shock Low-grade fever -MI is also known as a heart attack, involves the death of the myocardial tissue due to ischemia (def of blood) -most common cause is atherosclerosis, usually with thrombus attached 1. thrombus may build up to obstruct the atery 2. vasospasm may occur 3. part of the thrombus may break away, forming an emboli -at point of obstruction, heart tissue becomes necrotic and the area of injury is inflammed -presence of collateral circulation may reduce the size of the infarct -signs: dizziness, pallor, nausea, dyspnea, low grade fever, weakness

Discuss the pathophsyiology of cardiomyopathy

Meaning "heart muscle disease" - not associated w/ischemia or inflammation **Three types:** Dilated CMP Enlarged, thinly-lined chambers Associated w/viral infections/alcohol/drug use Hypertrophic CMP Enlarged, thick left chamber Probably mostly hereditary Restrictive CMP Myocardium can't expand because of a restrictive substance, like amyloids Cardiomyopathy (kahr-dee-o-my-OP-uh-thee) is a disease of the heart muscle that makes it harder for your heart to pump blood to the rest of your body. Cardiomyopathy can lead to heart failure. The main types of cardiomyopathy include dilated, hypertrophic and restrictive cardiomyopathy DCM -The most common cause of heart failure (Weintraub et al, 2017), DCM is diagnosed on the basis that it cannot be explained by either abnormal loading conditions (increased blood pressure or volume) or coronary artery disease, where an ischaemic cardiomyopathy may occur (Elliott et al, 2008). DCM can develop at any age and is more common in males. In children, it accounts for around 60% of all cases of cardiomyopathy (Lipshultz et al, 2003). -The condition encompasses heterogeneous diseases characterised by inappropriate ventricular hypertrophy (thickening of the ventricle wall) or dilation of one or both ventricles (with thinning and enlargement). It occurs progressively (Weintraub et al, 2017) and can lead to decompensated heart failure. -DCM can also be secondary to systemic causes such as inflammation, malnutrition and infectious, autoimmune or endocrine diseases. In high-income countries, such as the UK, alcohol overuse contributes to 21-36% of cases (Weintraub et al, 2017). The risk of developing DCM as a result of alcohol misuse is influenced by various susceptibility factors, including those that are ethnic and genetic HCM -presented with asymmetrical cardiac septal thickening (hypertrophy) of the left ventricle, -HCM is a heterogeneous disorder characterized by left ventricular hypertrophy and, in some cases, left ventricular outflow tract obstruction (Houston and Stevens, 2015). In around 60% of adults and adolescents, the condition is caused by familial disease (Marian and Braunwald, 2017). A large number of genetic mutations in HCM have been described including those affecting proteins important for sarcomere function (a sarcomere is a basic unit of repeating contractile proteins that make up muscle cells). The normal mode of inheritance for such gene defects is autosomal dominant, although autosomal and sex-linked recessive patterns have also been described (Braunwald, 2017). -Some patients have few symptoms while others may experience chest pain, dyspnoea, palpitations and/or syncope. Patients with HCM can be at risk of sudden death in the absence of any previous symptoms -Age is an important clue in HCM as the inherited metabolic or neuromuscular causes are more common in newborns and infants than in older children and adults -patients may also have distended neck veins from raised jugular venous pressure. Palpation of the apex beat of the heart may reveal an increased left ventricular apical impulse or, rarely, a systolic thrill. There may also be a pan-systolic murmur resulting from mitral valve regurgitation. Another type of murmur may be present, caused by turbulent flow through the outflow tract, which is mid-systolic with a crescendo-decrescendo sound. RCM -Characterised by ventricular stiffness leading to reduced ventricular filling and diastolic volume during the cardiac cycle, RCM is suspected when patients have near-normal systolic function but diastolic dysfunction on echocardiography. -RCM may be associated with symptoms and signs of congestive heart failure, such as peripheral oedema, raised jugular venous pressure and gallop rhythm, as well as features of an underlying systemic disease.

Cardiac Dysrhythmias/Arrhythmias

Deviations from normal cardiac rate or rhythm --Caused by electrolyte abnormalities, fever, hypoxia, stress, infection, drug toxicity --Electrocardiography—for monitoring the conduction system -----Detects abnormalities Reduction of the efficiency of the heart's pumping cycle --Many types of abnormal conduction patterns exist. Dysrhythmia Bradycardia Beats too slow Tachycardia Beats too fast Arrhythmia Irregular HB May cause insufficient cardiac output By SA node→ 70-72 BPM (normal sinus rhythm) Depolarized → contracting (when atria contracts → P Wave) Depolarization of ventricle (QRS) → contraction --Happens within 0.04 seconds → very quick Repolarization of electrical in ventricle; build up of charge in atrium (T wave) 0.47 seconds (one square) 5 square→ 0.2 seconds Sinus Node Abnormalities -Bradycardia <60 bpm -Tachycardia >100 bpm -Sick sinus syndrome Alternating bradycardia and tachycardia -Ectopic beat (out of place → comes from somewhere else other than the natural pacemaker) Comes from somewhere besides SA node Will cause myocardium to pause Frequent—will lead to other arrhythmias May be due to damage from ischemia --Damage to myocardium -deviations from normal cardiac rate pr rhytm may result from damage to the heart's conduction system or system causes such as electrolyte abnormalities, fever, hypoxia, stress, infection, etc -dsy, reduce the efficiency of the heart's pumping cycle -irregular contractions are not eff. bc they interfere with the normal filling and emptying cycle

MI and CAD

Diagnosing MI & CAD -ECG (or EKG) -Elevated serum enzymes indicating damage to myocardium Creatinine phosphokinase (CK-MB, CPK-2) Rises at 6 hrs post MI, peaks at 24 hrs Aspartate aminotransferase (AST) Peaks at 48 hrs Lactic dehydrogenase (LDH) Peaks at 72 hrs and remains high for a while -Serum levels of myosin & troponin Elevated due to break down of myocardium -Misc. blood work: Leukocytosis (elevated WBCs) Elevated CRP Arterial blood gasses Echocardiography Nuclear perfusion imaging MRI -Cardiac Catheterization Cameras → inject dye/contrast and it blocks the x rays so we can see the coronary arteries light up Details about blood flow going up the artery Treating MI & CAD -PTCA (and stent) Inflate balloon→ opens up the artery Minimize damage that has been done to the heart -CABG (Coronary Artery Bypass Graft) When stenting does not restore circulation Takes out saphenous vein Others: Drugs Thrombolytic agents ASA Heparin Coumadin Streptokinase Urokinase Tissue plasminogen activator (TPA) Other drugs depending on nature of damage Digoxin (Know drugs on Table 18-1—use & action only) Cardiac rehabilitation → send them to gym (fitness trainer)

Explain the pathophysiology of valvular insufficiency (prolapse)

Diseases of the valves Valvular Insufficiency (regurgitative valve) → not closing all the way (floppy and leaking) → back flow to the chamber → inefficient Allows blood to regurgitate back into chamber Increases heart workload Hypertrophy develops Mitral Valve Prolapse 1-2% of Americans have this (most common) "floppy" regurgitation valve Blood leaks back into atrium instead of going out through aorta Regurgitation valve Build up pressure When left ventricle builds up pressure, shuts off (becomes inefficient) -incompetence is when there is a failure of the valve to close completely, allowing blood to regurigitate or leak backwards -mitral valve prolapse is a common occurence; it refers to abnormally enlarged and floppy valve leaflets that balloon backwards with pressure or to posterior displacement of the cusp, which permits regurgitation of blood -valvular defects reduce the efficiency of the heart to pump and reduce stroke volume -if valve leaks and blood regurgitates forwards, the heart must also increase its efforts to maintain cardiac output -treatment is surgical replacement

Complex Sleep Apnea

During a CPAP titration if Increasing the pressure eliminates Obstructive apnea but Central apneas begin to apear. Complex sleep apnea syndrome—both obstructive and central apneas are present → both of them

Discuss the pathophysiology and presentation of pulmonary emboli

Embolus flows in pulmonary circulation Obstructs potential infarction The closer to the beginning, the worse the case DVLT (deep vein leg thrombosis) Start to get infarctions in lung tissue (stopping process) closer you are to the heart, the worse the cases -a blood clot or a mass of other material that obstructs the pulmonary artery or branch of other material that obstructs the pulmonary artery or a branch of it, blocking the flow of blood through the lung tissue -most of them are thrombi or blood clots originating from the deep leg veins -due to deep vein thrombosis (DVT) is a leading cause of deaths -infarcation does not follow obstruction of the pulmonary circulation unlesss the general circulation is compromised or there is prior lung disease --usually invovles a segment of the lung and the pleural membrane in the area -small pulmonary emboli are silent -emboli that block moderate-sized arteries cause respiratory impairments bc fluid and blood fill the alveoli of the involved area -large emboli affects the cardiovascular system, causing right sided CHF and decreased cardiac output -resistance to the output from the right ventricle cuases acute cor pulmonale

Differentiate between the two groups of restrictive lung disorders

Group of disorders with impaired lung expansion and reduced total lung capacity → messing with the physics of breathing First group Abnormality of chest wall—limits or impairs lung expansion Kyphosis or scoliosis, poliomyelitis, amyotrophic lateral sclerosis, botulism, muscular dystrophy Second group (affects tissue of lungs) Diseases affecting the supporting framework of lungs Idiopathic pulmonary fibrosis, occupational diseases -applies to a group of diseases in which lung expansion is impaired and total lung cap is reduced -2 groups: 1. an abnormality of the chest wall limits lung expansion and those in which lung disease impairs expansion (includes kyphosis or scoliosisi -- affecting the thorax) or muscular dystrophy -- weak muscles 2. affecting the tissues providing the supportive framework of the lugns, rather than airway obstruction or alevolar destruction -idiophatic pulmonary fibrosis is an example of this -occupational diseases (inhaled irritants cause chornic, low grade but damaging inflammation over time) -ARDS --> stiff lung and reduced compliance reduce total lung capacity

Premature Atrial Contraction (PAC)

Heart Rate: Depends on underlying rhythm Regularity: Interrupts the regularity of underlying rhythm P-Wave: can be flattened, notched, or unusual. May be hidden within the T wave PRI: measures between .12-.20 seconds and can be prolonged; can be different from other complexes QRS: <.12 seconds Premature Atrial Contraction (PAC) Makes the ventricle contract too soon extra contraction/ectopic beats of the atria that usually arise from a focus of irritable atrial muscle cells outside the conduction pathway -interfere with the timing of the next beat

histoplasmosis

Histoplasma capsulatum Histoplasmosis Fungal infection Caused by Histoplasma capsulatum Spores can be inhaled on dust particles. Common opportunistic infection First stage often asymptomatic Second stage Granuloma formation and necrosis Cough, fatigue, fever, night sweats Treatment—antifungal agents KIND OF LIKE TB -fungal infection that is common in midwest -can be inhaled as dust particles -can occur as an opportinitisitic infection that is common in ppl w AIDS, which the fungus tends to disseminate or spread easily throughout the body -second stage (active infection) involves granuloma formation and necrosis and consolidation in the lungs as well as possible spread to other organs signs: -cought -marked fatigue -fever and night sweats -skin test -antigungal treatment

Describe the pathophysiology of IRDS (or NRDS)

Hyaline Membrane Disease Infant (or Neonatal) Respiratory Distress Syndrome (IRDS or NRDS) Newborns (usually premature) borne w/o surfactant Surfactant is what helps to keep alveoli 'open' Protein membrane forms lining bronchioles and alveoli (hyaline membrane in response to injury) Impairs gas exchange Untreated-death follows in 48 hrs Treatment: on ventilator until lungs mature Happens to premature babies → do not have the surfactant (cannot breathe) Protein membrane forms → to protect the alveoli No gas exchange ; can die -common cause of neonatal deaths -during 3rd trimester of fetal development, the alevelolar surface area and lung vascularity greatly inc in prep for indepent lung function after birth -surfacant -- reduced surface tension in the alevoli and promotes expansion -first few inspirations after birth are hard as the lungs are inflated; breathing becomes easier as residual air volume inc -poor lung perfusion and lack of surfacantant lead to inc alevlor cap perm, with fluid and protein leaking into the interstital area and alevoli, forming the hyaline membrane -viscious cycle develops as acidosis develops from the respiratory impairment and metabolic factors -stenous muscle activity needed to breathe requires more o2 than is available and leads to anaerobic metabolism and is inc lactic acid -acidosis causes pulmonary vasoconstriction and impairs cell metabolism, reducing the synthesis and secretion of surfactant

Explain the development of lower extremity arterial disease (Intermittent claudication)

IC -leg pain associated with exercise due to muscle ischemia, is a key indicator Hypertension (high blood pressure) Increased pressure through blood vessels Essential hypertension: 140/90 or more primary (essential) hypertension Unknown etiology More common Arterial plaques caused vessels to lose elasticity Cannot expand due to blood flow Hardened area = higher pressure Tends to run in families Secondary hypertension Due to other disease processes Kidney disease most common -Controlling your BP Pheochromocytoma (benign SNS tumor) -Make BP take off for no reason Malignant hypertension Uncontrollable severe hypertension Rapidly progresses Very high Diastolic pressure Lower extremity arterial disease is often attributed to smoking, obesity, and poor nutrition. People with unhealthy cholesterol levels—due to hereditary factors or a high-fat diet—can develop blocked arteries -Lower extremity arterial disease (LEAD) is one of the manifestations of systemic atherosclerosis. It is associated with a high risk of cardiovascular morbidity and mortality, functional impairment, and decreased quality of life. An early diagnosis of LEAD allows a more rapid initiation of lifestyle changes and specific treatment, with a better prognosis. LEAD has the same morbidity and mortality as coronary artery disease [1]. It has similar risk factors to coronary and cerebrovascular diseases, with which it is associated in most cases [1]. LEAD increases the general cardiovascular risk, patients with this disease having a fivefold to sixfold higher risk of morbidity or mortality than from other atherosclerotic causes, such as coronary artery disease or stroke. The initial evaluation of patients should focus on screening for specific risk factors, in order to diagnose the disease at an early stage, including asymptomatic patients and those with atypical symptoms.

Explain the pathophysiology of infectious endocarditis

Infective Endocarditis Inflammation of inner lining and valves Usually Streptococcus viridans or Staphylococcus aureus (acute type) "vegetations"—ulcers deform valves and chordae tendineae—valvular insufficiency Infection on the inside of the heart Can be caused by systemic infection brought on by: Tooth abscesses Skin infections UTI's Respiratory infections -two types: subacute type in which defective heart valves are invaded by organisms of low virulence such as strepto viridans; and the acute type in which normal heart valves are attacked by highly virulent organisms such as staphylo. aureus which tends to cause severe tissue damage and may be difficult to treat successfully -micororganisms in the general circulation attach to the endocardium and invade the heart valves, causing inflammation and formation of vegetations on the cusps --vegetations interefere with the opening and closing of the valves -pieces may break away, frming infecting septic emboli that then can cause infarction and infection in other tissues -heart murmors are a common indicator -presence of abnromal tissues in the heart and microbes in the blood and reduced host defenses -anorexia, and childsm and septic emboli, and CHF are some signs and symptoms -blood cultures are treatments -effects the valves which become edematus and verrucae form (rows of small vegetations along the outer dg of the valve cusps)

Inflammatory and Infectious Heart Disease

Inflammatory and infectious process involving the endocardium and pericardium Inflammation of heart is caused by known infectious agents, viruses, bacteria, fungi or parasites, and by toxic materials from the environment, water, food, air, toxic gases, smoke, and pollution, or by an unknown origin. Myocarditis is induced by infection of heart muscle by virus like sarcoidosis and immune diseases.

Describe the development of pneumoconioses

Inhalation of various foreign substances Usually a chemical in various dusts Fine dusts makes way into alveoli past all of the barriers/guardians Long-term occurrence, sometimes as much as 20 years! Removing culprit won't stop progression Continued inflammation causes fibrosis Silicosis (most common pneumoconiosis) -results from lung inhalation of irritating particles like abestos -inflammation and fibrous tissue develops with gradual destruction of connective tissue -immune responses may add to the damage in the case of more reactive particles, such as silica -as firbrosis expands, functional areas of the lugns are lost -tissue changes are irreversible and infections are common -abestos fibers cause pleural effusion and inc the risk of lung cancer -onset is insidious with dyspnea developing at first; cough is common -coal workers disease (coal dust, coal mines) -silicosis (silica, stone cutting) -asbestosis (asbestis, insulation and ship building) -farmer's lung (fungal spores and hay)

intersitital [or PAP]),

Interstitial pneumonia → edema in your tissues and does not get in alveoli -scattered small patches -influenza virus -mycoplasma -interstitial inflammation around alveoli -necrosis of bronchial epithelium -variable onset -variable fever, headache -aching muscles -nonproductive hacking cough primary atypical pneumonia -differes in both causative organisms, often viral or mycoplasmal and pathophysiology which involves interstitial inflammation -mycoplasma pneumoniae is a small bacterium that lacks a cell wall and can appear in varying shapes -common in older kids and young adutls -transmitted by aerosol but it is not considered highly contagious -viral pneumonia is often caused by flu a or b and rsv -chalmydia pneumonia is caused by the organism chlamydia pneumoniae -- caused by a PAP and pharyngititis

difference between LDL and HDL

LDL is the lipoprotein with high lipid content and transports cholestoral from liver to the cells; dangerous comp of elevated serum levels of lipids and chol. -binds to receptors -"bad" lipoprotein HDL is the "good" lipoprotein; it has a low lipid content and is used to transport cholesterol away from the peripheral cells to the liver, where it undergoes catabolism and excretion

lobar

LOBAR: -usually is bacterial -anatomic distribution of lesions may be diffuse and patchy throughout both lungs or lobar, meaning consolidated in one lobe -all of one or two lobes -inflammation of alveolar wall and leakage of cells, fibrin, and fluid into alveoli causing consolidation -pleura may be inflammed -sudden and acute onset -signs (high fever and chills, productive cough with rusty sputum, rales) -caused by strept. pneumoniae and is localized in one or more lobes -first stage in development is congestion and develops in the alveolar wall and exudate forms -second stage is consolidation (neutrophils RBCs and fibrin accumulare in the alveolar exudate forming a solid mass) -bc complete lobe is usually involved in inflam process the adjacent pleurae are frequently involved, producing pleuritic pain in affected site -empyema (can cause adhesions bw the pleural membranes restricting ventilation) -filling of alveoli with exudate reduces the diffusion of gases, with o2, and dec blood flow through the affected lobe -hypoxia results and is more marked bc the demand fir o2 increases with higher metabolic rate associated w the infection -o2 def leads to metabolic acidosis MANIFESTATIONS: -sudden onset -confusion and disorentation -treatment involves admin of antibacterial drugs Localized in one or more lobes Neutrophils, RBCs, Fibrin, mix w/alveolar exudate and form solid mass (consolidation) lobar pneumonia in which consolidation of the entire left upper lobe has occurred. Most lobar pneumonias are due to pneumococcus and for decades, these have responded well to penicillin therapy so that advanced, severe cases are not seen as frequently. However, pneumoccoci, like most other bacteria, are developing more resistance to antibiotics. Severe pneumococcal pneumonia still occurs, even in young to middle aged persons (not just the very young and the very old) and has a mortality rate of 20%!

Discuss the causes and effects of left-sided CHF

Left Ventricle Failure (take blood from lungs; pump to body) Shows up in the lungs.... Pulmonary edema (fluid leaking into alveoli out of capillaries) Drowning in your own fluids Pulmonary hypertension Dyspnea or orthopnea (dyspnea when reclining) Hypoxia Hemoptysis Blood coughed up due to ruptured lung vessels because of high pressure -If the left ventricle cannot pump all of its blood into the systemic ciruclation, the normal volume of blood returning from the lungs cannot enter the left side of the heart. this eventually causes congestion in the pulmonary circulation, increased capillary pressure, and possible pulmonary edema CAUSES: -infarction of left ventricle, aortic valve stenosis, hypertension, hyperthyroidism EFFECTS: -decreased cardiac output, pulmonary congestion BACKUP EFFECTS -orthopnea, cough, SOB, paroxysmal nocturnal dyspnea, rales FORWARD EFFECTS -fatigue, weakness, dyspnea, exercise, cold intolerance

development of right-to-left and left-to-right shunts (via VSDs)

Left-to-right shunt Of less consequence—blood gets oxygenated again Involve a hole in the heart Heart muscle and left ventricle is bigger and stronger Blood from left side of heart pumps into right side of the heart Shunt → transfer of the fluid Still get perfusion of o2 in the system Recycling blood that does not need to be recycled Acyanotic (o2-ed blood) (blue) or cyanotic (unoxygenated hemoglobin in the blood--> produces blueish color) -the blood from the left side of the heart is recycled to the right side and to the lungs, resulting in an increased volume in the pulmonary circulation, a decreased cardiac output, and an inefficient system -large opening promote this -blood can flow in only ONE direction, from high pressure and therefore blood flows through the septal defect from the left ventricle to the right ventricle -effect is that less blood leaves the left ventricle, reducing stroke volume and cardiac output to the systemic circulation -A diversion of blood from the left side of the heart to the right, as through a septal defect. A diversion of blood from the systemic circulation to the pulmonary circulation, as through a patent ductus arteriosus. Right-to-left shunt More serious—cyanosis—more oxygenated blood in systemic flow Stores o2 blood in left and back into right ventricle Builds up pressure from left side into right side Gets stronger, and over powering the left side of the heart Pushes blue blood into left ventricle (cyanosis) - unoxygenated blood from the right side of the heart bypasses the lungs directly and enters the left side of the heart **the direction and amount of the abnormal blood flow determines the effects on the individual -right-to-left shunt allows deoxygenated systemic venous blood to bypass the lungs and return to the body. Atrial Septal Defect (ASD) (hole b/w right and left atria) Blood usually flows from L to R due to higher pressure in left Produces a murmur Septum → dividing walls between the heart Ventricular Septal Defect (VSD) Increases workload of left ventricle Increases workload of right ventricle Increases circulation to lungs Results in pulmonary hypertension Gradually increases pressure in R Ventricle R pressure > L pressure R to L shunt Cyanosis develops Inefficient but will still work -most common congenital heart defect and is known as "hole in the heart" -opening in the interventricular septum -more blood enters the pulmonary circulation --> reduces the efficiency of the system and in time overloads damages to the blood vessels, causing pulmonary hypertension --this would lead to high BP in the right ventricle and a reversal of right to left shunt, leading to cyanosis -surgery for repairing

Legionnaires' disease

Legionnaires' disease Unknown until 1976 outbreak among American Legion convention attendees Legionella pneumophila (gram - bacteria) Resides in pulmonary macrophages -caused by gram - bacteriam -thrives in warm moist envirnments such as air conditioning systems and spas -arises as a nosocomial infection in hospitals or other places especially among those with lung disease -if untreated, the infection cuases severe congestion and consolidations, with necrosis in the lung and possibly fatal consequences

Describe the pathophysiology and clinical manifestations of chronic bronchitis

Lots of air pollution → lots of mucous production and edema Usually will get pulmonary hypertension pink puffers More blood cells (kind of pink) Blue bloaters (people with bronchitis) Inflammation, obstruction, repeated infection, chronic coughing twice for 3 months or longer in 2 years History of cigarette smoking or living in urban or industrial area Mucosa inflamed and swollen Hypertrophy and hyperplasia of mucous glands Fibrosis and thickening of bronchial wall Low oxygen levels Severe dyspnea and fatigue Pulmonary hypertension and cor pulmonale signs and Symptoms Constant productive cough Tachypnea and shortness of breath Frequent thick and purulent secretions Cough and rhonchi more severe in the morning Hypoxia, cyanosis, hypercapnia (lots of CO2) Caused by airway obstruction Polycythemia, weight loss, signs of cor pulmonale possible As vascular damage and pulmonary hypertension progress -significant changes in the bronchi resulting from constant irritation from smoking or exposure to industrial pollution -etiology: smoking and air pollution -located in the bronchi -increased mucous glands and secretions, inflammation, and infection, obstruction -early and constant cough, some dyspnea -large amoung and purulent sputum -there is cyanosis -frequent infections -cor pulmonale is common -o2 levels are low -pink puffer to summarize the dyspnea, hyperventilation, and over inflation that maintain o2 levels in the emphysema -blue bloater is wth low o2 levels

Describe the pathophysiology of lung cancer (primary and secondary)

Lung Cancer Etiology Often (but not always) smoking Exposure to carcinogens (work related) Genetic influence Signs & symptoms Onset often masked 'smoker's cough' → second hand smoke Hemoptysis Primary v. Secondary Originated in the lung vs originated somewhere else Types of Lung Cancer Bronchogenic (most common, develops in bronchial tree) majority of lung ca. Arising near bronchi Squamous cell carcinoma (SCC)-epithelium Adenocarcinoma-gland cells, periphery Small-cell ('oat-cell')-very aggressive, near major bronchus → spreads very quickly Metastases: from lung to other sites, most common=brain Goes to the bone and to the brain Possible Tumor Effects: Obstruction of air flow by tumor growth into bronchus Inflammation surrounding tumors (stimulates cough & predisposition to secondary inflamm). Pleural effusion, hemothorax (blood in the chest cavity) , or pneumothorax (air in the chest cavity → holes) Systemic effects Affect homeostasis Collapse of the lung (becomes nonfunctional and makes it harder to breathe) Cancer erodes into blood vessels Squamous Cell Cancer Squamous cell carcinomas are one of the more common primary malignancies of lung and are most often seen in smokers. Small Cell Ca (oat cell) oat cell carcinoma which is spreading along the bronchi. The speckled black rounded areas represent hilar lymph nodes with metastatic carcinoma. These neoplasms are more amenable to chemotherapy than radiation therapy or surgery, but the prognosis is still poor. Oat cell carcinomas occur almost exclusively in smokers. Problems with Diagnosing and Treating Lung Ca Only 20% of cases are diagnosed before spread Metastases: Bone (pain→ irradiate this) Brain Liver MRI showing Lung Ca metastasis to r. parietal lobe of the brain --develops from epithelial lining of the bronchus near the hilum and projects into the airway Secondary Lung Ca. aka Lung mets Malignancy arising from other sites Why is lung a primary site for mets? (Hint—why are the lungs prone to emboli?) Secondary lung ca originates from: Breast Colon Kidneys liver Tip: mets contain cells from the primary site. Biopsy is critical -secondary meta cancer develops in the lungs bc the venous return and lymphatics bring tumor cells from many distant sites in the body to the heart and then into the oulmonary circulation -bronchogenic arises from bronchial epithelium -mesothelioma has inc attention from media and legal firms -first change in lungs is metaplasia associ w smoking or chornic irritation -various chemical is cigarrette smoke are carcinogenic and act as intiators and promotoers -tumors in the lungs have effects (obstruction of airlow, inflammation, pleural effusion, paranelopslastic syndrome) Primary lung cancer starts in the lungs. The cancer cells are abnormal lung cells. Sometimes, people will have cancer travel from another part of their body or metastasize to their lungs. This is called secondary lung cancer because the lungs are a secondary site compared to the original primary location of the cancer. the lungs are common site for both primary and secondary lung cancer

Describe the pathophysiology and clinical manifestations of emphysema

Lungs become hyperinflated due to destruction 'trapped' (stale) air left in lungs Affects gas exchange (less O2, more CO2) Losing surface area Thorax will expand Common in smokers Alveoli may lose elasticity & eventually rupture Can introduce air into pleural space and decrease its pressure Lungs no longer expanded—collapse (pneumothorax) Air sits there / a lot of trapping of the gases here dilated airspaces Although some scarring with time because of superimposed infections, the emphysematous process is one of loss of lung parenchyma, not fibrosis Note large bullae Balloons, just kind of pops -destruction of the alveolar wals and septae, which leads to large, inflated alevolar air spaces -etiology: smoking and genetic -located in alveoli -destruction if alveolar walls, loss of elasticity, impaired expiration, barrel chest, hyperinflation -some coughing, marked dyspnea -little sputum, no cyanosis, some infections, and late cor pulomonale -proteases (destructive enzymes released by neutrophils during inflammatory response) -changes in lung tissue have many effects on the lung function 1. breakdown of the alveolar wall results in the (loss of surface area, erc) 2. fibrosis and thickening of bronchial walls have resulted from chronic irrirtation 3. progressive difficulty with expiration leads to air trapping and overinflation of the lungs 4. with advanced emphysema, sign loss of tissue

Discuss the possible consequences and complications of myocardial infarction

MI Consequences Eventual heart failure Brain damage if cardiac arrest occurred Infarct gets bigger if heart not rested Hypertrophy to make up for lost tissue Other problems: Rupture of infarcted area Ventricular aneurysm Embolism with stroke -sudden death shortly after MI occurs (ventricular arr. and fibrillation -area of necrosis and inflammation outside the conduction pathway may stimulate additional spontaneous impulses at an ectopic site, causing premature ventricular contrations that lead to tachy. -cocaine users may suffer fatal heart attacks -cardiogenic shock -CHF -rupture of necrotic heart tissue -thromboembolism

Explain the pathophysiology of myocarditis

Myocarditis Infection (usually viral) of myocardium Can kill myocardium Can lead to CMP & heart failure inflammation develops as localized lesions in the heart muscle, called Aschoff bodies, may interfere with conduction Myocarditis is inflammation of myocardium with necrosis of cardiac myocyte cells. Biopsy-proven myocarditis typically demonstrates inflammatory infiltrate of the myocardium with lymphocytes, neutrophils, eosinophils, giant cells, granulomas, or a mixture. Myocardial inflammation can be diffuse or focal

Differentiate between different types of cardiovascular drugs, their uses, and actions (pt 2)

Nitroglycerin -use: angina attacks and prophylaxis -actions: reduces cardiac workload, peripheral and coronary vasodilator metoprolol (Lopressor) -use: hyptertension, angina, antiarrhythmic -actions: blocks beta-adrenergic receptors, slows heart rate nifedeipine (Adalat) -use: angina, hypertension, peripheral vasodilator, antiarrhythmic -actions: calcium blockers, vasodilators digoxin (Lanoxin) -use: CHF, atrial arrhythmias -actionsL slows conduction through AV node and inc forces of contraction (cardiotonic) to increase efficiency enalapril (Vasotec) -use: hypertension -actions: ACE inhibitor-- blocks formation of angiotensin II and aldosterone furosemide (Lasix) hypertension -use: edema with CHF, hypertension -actions: diuretic -- inc. excretion of water and sodium simvastatim (Zocor) -use: hypercholesteremia (CHD) -actions: decreases cholesterol and LDL warfarin (Coumadin) -use: prophylaxis and treatment of thromboedmboli -actions: anticoagulant -- interferes with vitamin K in synthesis of clotting ASA (Aspirin) -use: prophylaxis of thromboedmboli -actions: prevents platelet adhesion, anti-inflamm Apizaban (Eliquis), Dabigatran (Pradaxa), Edoxaban (Savaysa), and Rivaroxaban (Xarelto) -use: blood-thinning dugs -actions: anticoagulant

Describe the pathophysiology of sleep apneas

Obstructive Sleep Apnea Increases w/age & obesity 3-5% of adults affected Chronic hypoxia Continuous Positive Airway Pump (CPAP) used to treat Also... Central sleep apnea—more of a neurological cause ("forgetting to breathe") sl→ brain Complex sleep apnea syndrome—both obstructive and central apneas are present → both of them Obstruction of the air way -sleep apnea is usually diagnosed when the sleeping partner notes loud snoring with intermittment gasps of loud air -complications are related to chronic hypoxia and fatigue and type 2 diabetes and pulmonary hypertension -treatment is CPAP machine,which delievers humidified air room air at a pressure that maintains an open airway

Explain the pathophysiology of infectious pericarditis

Pericarditis Infectious inflammation of pericardium or epicardium Exudate builds up in pericardial sac Painful heartbeats Can lead to cardiac tamponade (heart expansion restricted—"P.E.A.") -may be acute or chronic and usually secondary to another condition in either the heart of the surrounding structures -acute p. may involve a simple inflammation of the pericardium, in which the rough, swollen surfances cause chest pain and a friction rub --in some cases, an effusion may develop , with a large volume of fluid accumulating in the pericardial sac -large amount of fluid accumulates rapidy may compress the heart and impair its expansion and filling, thus decreasing cardiac output -right side of the heart is affected first(low pressure side), causing inc pressure in the systemic veins and if acute, distended neck veins -chronic p. results in formation of adhesions bw the pericardial membranes that may become constrictive, causing the pericardium to become a tight fibrous enclosure, thus limiting movement of the heart -tachy. can be a sign -inflammation of the outer layer may include effusion (excessive fluid accumulation) which impairs filling

Peripheral and other vascular Disorders

Peripheral Vascular Disease (PVD) Usually atherosclerotic Intermittent claudication Numbness, tingling in extremities Pallor & cyanosis in distal extremities (feet) The angina pectoris but now in your LEGS -refers to any abnormality in the arteries or veins outside the heart -most common sites are the abdominal aorta and femoral and iliac arteries, where partial occlusions may impair both muscle activity and sensory function in the legs -total occlusions may result from a thrombus obstructing the lumen or breaking off (an embolus) and eventually obstructing a smaller artery (loss of blood supply in a limb leads to necrosis, uclers, and gangrene)

Differentiate between thromboplebitis and phlebothrombosis

Phlebitis—inflammation of veins Deep veins thrombus formation (DVT) Results: poor circulation & possible embolus Vasculitis Inflammation of blood vessels Autoimmune disease Edema, thrombus, poor vascular functioning -thrombo and phlebo -thrombophlebitis refers to the development of a thrombus in a vein in which inflammation is present --the platelets adhere to the inflammed site, and a thrombus develops -may be present in superficial veins (aching or burning in affected leg, leg may be warm, thrombus in the deep veins may be causing pain, positive homans sign, fever, malaise) -phlebothrombosis, a thrombis forms spontaneously in a vein without prior inflammation, although inflammation may develop secondarily in response to thrombosis --the clot is less firmly attached in this case, and its development is asympotomatic or silent factos predisposing to thrombus development -stasis of blood / sluggish blood flow -endothelial injury -increased blood coagulation -problem: venous thrombosis may lead to pulmonary embolism treatment: exercise, anticoagulant therapy

Describe the basic pathophysiology of coronary artery disease

Plaques build up on inside of coronary arteries → opening of arteries get more narrow Artery loses flexibility Decreases the lumen of the arteries Results in ischemia of myocardium Eventually proceeds to heart failure Symptoms/signs: -Pain from oxygen deprived myocardium -Electrical conduction problems due to ischemic tissues -includes angina pectoris or temporary cardiac ischemia and MI (or heart attack) -MI results in damage to part of the heart muscle bc of the obstruction in a coronary artery -Insuff. o2 for the needs of the heart muscle -CAD may lead to heart failure, serious dysrhythmias, or sudden death

pleural effusion (hydrothorax, hemothorax, empyema)

Pleural Effusion → tumors can cause this (cancer) Hydrothorax Fluid is transudate CHF a frequent cause Pleural effusion (fluid in pleural space → exudate or water) Fluid is exudate Inflammation of the pleura or pleurisy (inflam. Of the pleura) → can be an infectious process Adhesions- scar tissue binding both sides of the pleura—limiting lung expansion Empyema—purulent exudate (ON THE TEST) -the presence of excessive fluid in the pleural vacity -pleurisy or pleuritis may preced or follow pleural effusion or occur independently -- inflamed swollen and rough -large amts of fluid first inc the pressure on the cavity and then cause separation of the membranes, preventing their cohesion during inspiration -a large amount of fluid causes atelectasis on the affected side and shift of the medsstinal contents towards the unaffected lungs -exudative effusions are a response to inflammation, perhaps from a tumor, in which inc capillary perm allows fluid containing protein and white blood cells to leak into the pleural cavity --transudates are watery effusions called HYDROTHORAX (result from inc hydrostatic pressure or dec osmotic pressure in the blood vessels, leading to a shift of fluid out of the blood vessels into the potential space in the pleural cavity) -hemothorax is when the fluid is blood resulting from trauma, cancer, or surgery -empyema occurs when the fluid is purulent as a result of infection often related to pneumonia

Discuss the pathophysiology and presentation of edema

Pulmonary Edema Fluid in septa and alveoli Fluid fills alveoli (which is supposed to be air) → fluid blocks capillaries Drowning in your own fluids Usually caused by L-sided heart failure and CHF Edema usually more severe in lungs Other tissues limit infiltrate Lungs are loose and spongy -refers to fluid collecting in the alveoli and itnerstitial area -accumulation of fluid reduces the amt of o2 diffusing into the blood and interferes with lung expansion, also reducing oxygenation of the blood -excess fluid in the alevolar tissue may develop when inflammation is present, plasma protein levels are low -pulmonart hypertesion develops -excessive amts of fluid in the intersitital areas and alveoli interfere with the diffsuion of o2, causing severe hypoexemia, as well as action of surfactant, elading to difficulty expanding lungs, which leads to collapsing -may result from left CHF backup of blood failing from the left ventricle causing high pressing in pul circulation

Discuss the pathophysiology and presentation of pulmonary hypertension

Pulmonary hypertension Lung circulation normally is at a relatively low pressure Pressure increase makes flow into system more difficult High BP in your lungs Pressure does not make it easy for the blood to get into the lungs Do not have flow of capillaries through alveoli (causes back pressure) CLD (lung disease) is cause Causes: Chronic lung disease L-sided heart failure → o2 blood is coming to left side but cannot get out (back up of blood → backs up into lungs and get back up of pulmonary) CHF Left and right sided heart failure → causes back pressure Mitral Valve Stenosis Valvular insufficiency It is restricted Between left atrium and left ventricle → causes PH Congenital heart defects → pulmonary stenosis Result: Cor pulmonale Right sided heart failure caused by pulmonary hypertension

Discuss the causes and effects of Cor Pulmonale

Pulmonary hypertension due to lung disease Can have secondary effects similar to right-sided heart failure People with emphysema (restricted/constricted, blood does not have easy time getting up to lungs) Back up on right side of heart (right sided CHF) -right sided CHF due to pulmonary disease is often referred to as cor pulmonale Cor pulmonale is defined as an alteration in the structure and function of the right ventricle (RV) of the heart caused by a primary disorder of the respiratory system. Pulmonary hypertension is often the common link between lung dysfunction and the heart in cor pulmonale -right sided CHF due to lung disease CAUSES: -blood clots in the lungs chronic obstructive pulmonary disease lung tissue damages sleep apnea cystic fibrosis EFFECT: Cor pulmonale is right ventricular enlargement secondary to a lung disorder that causes pulmonary artery hypertension. Right ventricular failure follows. Findings include peripheral edema, neck vein distention, hepatomegaly, and a parasternal lift.

Explain the pathophysiology of rheumatic heart disease

RHeumatic fever Acute systemic inflammatory condition May result from an abnormal immune reaction Can occur a few weeks after an untreated infection (usually group A β-hemolytic Streptococcus) Involves heart as well as joints Usually occurs in children ages 5 to 15 years Long-term effects Rheumatic heart disease May be complicated by infective endocarditis and heart failure in older adults Usually kids get this ; type of strep infection Abnormal immune reaction acute stage—inflammation of the heart Pericarditis Myocarditis—development of Aschoff bodies Endocarditis and incompetent heart valves (verrucae) → interior lining of heart Mitral valve stenosis it causes this Affects how the heart can contract other sites of inflammation Large joints Erythema marginatum Nontender subcutaneous nodules Involuntary jerky movement of the face, arms, legs Signs and Symptoms Low-grade fever Leukocytosis Malaise Anorexia, and fatigue Tachycardia Heart murmurs Epistaxis and abdominal pain may be present. -an acute systemic inflam. condition that appears to result from a abnormal immune reaction occuring a few weeks after an untreated infection, usually caused by certain strains of group A beta -occurs in kids ages 5-15 -remains a threat bc new strains of stretococcus, the cause of antecedent infection, continue to appear -antecedent infection appears as an upper respiratory infection, tonsilitis, etc -the heart is the only site where scar tissue occurs, causing RHD -during acute stage 1. pericardititis 2. myocardititis (inflam. develops as localized lesions in the heart muscle, called aschoff bodies, may interfere with conduction) 3. endocardititis, the most common problem, affects the valves which form cerrurcae -other sites of inflammation 1. large joints (in legs) 2. skin 3. wrists, elbows, knees, or ankles 4. basal nuclei in the brain -RHD develops years later in some ppl when scarred valves or arrhythmias compromise heart functions -to treat this --> antibacterial agents

Describe the development of radiation pneumonitis

Radiation Pneumonitis (inflammation by radiation to exposure by the lungs) Causes: Radiation exposure to lungs May result from external beam therapy or internal radiation therapy (such as shunted Y-90 from liver cancer treatment) Inflammation, edema, fibrosis, airway occlusions Signs/symptoms Fever Cough Congestion Shortness of breath (SOB) Chest pain radiation pneumonitis is inflammation of the lung caused by radiation therapy to the chest. It most commonly develops 1 to 3 months after treatment is over, but it can happen up to 6 months after treatment. Chronic pneumonitis can lead to permanent scarring of the lungs (called pulmonary fibrosis).

RSV infection (bronchiolitis)

Respiratory syncytial virus (RSV) Common among children age 2 to 12 months Varies in severity Can cause complete obstruction of smaller bronchioles Leads to "air trapping" and atelectasis Signs/Symptoms: Wheezing, dyspnea (hard time breathing), rapid shallow respirations, cough, rales (light bubbly sounds in lungs), fever, malaise common in young kids → in first year of life Obstructs the smaller bronchioles Air cannot get out with exhalation (build up pockets of air in the lungs) → respirations intensify and make it worse and it traps MORE air ! -respiratory syncytial virus infection -caused by RSV/myxovirus -transmitted directly by oral droplet and occurs a lot in the winter -predisposing factors include a familila history of asthma and cigarette smoke -causes a necrosis and inflammation in the small bronchi and bronchioles, with edema, inc secretions, and refelx bronchospasm --leads to obstruction of the small airways signs: -wheezing and dyspnea; rapid shallow respirations; cough; rales; chest retratctions and malaise -hyperinflation and air trapping due to partial obstructions -treatment to make sure o2 levels are adequate RSV virus affects children and can vary in severity. It can result in air trapping in the alveoli, which can then result in the lung tissues collapsing or ("atelectasis"). Rales are bubbling, rattling sounds heard in the lungs upon auscultation. A pregnant woman with a history of RSV exposure has a higher risk of having a baby with developmental problems (RSV is a teratogen).

Discuss the causes and effects of right-sided CHF

Right Ventricle Failure Distension of jugular vein Poor blood oxygenation Organs congested w/backed up blood Edema (in lower extremities) Pleural effusion (excess fluid in the pleura) -the right ventricle cannot maintain its output, so less blood proceeds to the left side of the heart and the systemic circulation (forwards effect) -backup effect/congestion (shown by inc blood volume) eventually also in the portal circulation and neck veins. CAUSES: -infarction of right ventricle, pulmonary valve stenosis, pulmonary disease (cor pulmonale) EFFECTS: -decreased cardiac output, systemic congestion, and edema of legs and abdomen BACKUP EFFECTS -dependent edema I n feet, hepatomegaly and splenomegaly, ascites, flushed face, headache, neck veins FORWARD EFFECTS -fatigue, weakness, exercise intolerance, cold intolerance

Differentiate between stable (book calls it exertional) and unstable angina pectoris

STABLE ANGINA PECTORIS IS BETTER THAN UNSTABLE -chest pain due to CAD -Stable Better of the two—predictable pain upon exertion which regularly subsides with rest -Unstable May follow no real pattern or intensities vary greatly High risk for myocardial infarction Treatment: -Nitroglycerin Vasodilators Effectiveness due to reducing systemic resistance Lessens heart's demands for oxygen -Ntg administration Tablet or spray under the tongue Skin patch -occurs when there is a deficit of o2 to the heart muscle (blood/o2 supply is impaired) -when the heart is working harder than usual and needs more o2 **chest pain may occur is patterns -exertional/stable (vasospasm occurs at rest) -unstable angina refers to the prolonged pain at rest and of recent onset, perhaps the result of a break in an atheroma (may cause MI) -episode of anginal pain occurs when the demand for o2 increases suddenly, with excretion -treated by coronary vasodilators

Describe the pathophysiology of hypertensive heart disease

Secondary to systemic hypertension L. Ventricular hypertrophy Cardiomegaly (to adjust for poor cardiac output) Increases atherosclertoic plaques in coronary arteries Hypertensive heart disease refers to heart conditions caused by high blood pressure. The heart working under increased pressure causes some different heart disorders. Hypertensive heart disease includes heart failure, thickening of the heart muscle, coronary artery disease, and other conditions.

Define shock and its effects on the body

Shock stops the heart and hoping the SA or AV node kicks in and starts making it work again Severe lack of tissue perfusion Lack of blood or BP to support organs BP plummets Poor oxygenation Loss of perfusion to tissues (loss of BP) Goes under insulin shock -shock/hypotension results from a decreased circulating blood volume, leading to decreased tissue perfusion and general hypoxia -may be caused by a loss of circulating blood volume (hypovolemic), inability of the heart to pump the blood through the circulation (cardiogenic shock), and its subcategoru, interference with blood flow through the heart (obstructive shock), or changes in peripheral resistance leading to pooling of blood in the periphery (distributive, vasogenic, neurogenic, septic, or anaphylactic) -BP is determined by blood volume, heart contraction, and PR TYPES OF SHOCK -hypovolemic loss of blood or plasma, heorrhage, burns, etc * results from loss of blood or plasma -cardiogenic dec pumping capability of the heart, MI of left ventricle, cardiac arrhythmias, pulmonary embolus, etc * associated with cardiac impairment -vasogenic vasodilation owing to loss of sympathetic and vasomotor tone, pain and fear, spinal cord injury, hypoglycemia *develop from pain or fear, drugs, or loss of SNS stimuli with spinal cord injury -anaphylactic systemic vasodilation and inc permeiability owing to severe allergic reaction, insert strongs * results from rapid general vasodilation due to release of large amounts of histamine in a severe allergic reaction -septic vasodilation owing to severe infection often with gram - bacteria, virulent microorganisms or multiple infection * develop in ppl w severe infection -pts with shock there is usually less cardiac output and blood flow through the microcirculation is decreased, leading to reduced o2 for the cells -vasoconstriction reduces arterial blood flow into the tissues and organs, causing ishemia and eventually necrosis -decompensation causes complication of shock (acute renal failure, shock lung, hepatic failure due to cell necorsis, etc) CHART: 1. decreased BP -compensations to maintain heart and braiin functions --> stimulate SNS (thirst, anxiety, tachy, vasoconstriction) --> renin- angiotensin- aldosterone (vasoconstriction, retention of na + and h20) --> inc adh secretion (retention of h20) 2. direct effects of dec BP -lethargy weakness -anaerobic metabolism metabolic acidosis leads to 3. vasodilation and dec cell function -slow blood flow in microcirculation (thrombus forms) -ishcemia in organs (dec function and necrosis) 4. decreased venous return 5. further dec I n cardiac output -severe acidosis -cns depression -organ damage (acute renal failure, lung damage) 6.. decompensation -early signs (anxiety and restlessness and hypotension--> stimulates SNS) -compensation (tachy, cool, pale, thirst, sns response stimulates heart) -progressive (lethargy, weakness, faintness, metabolic acidosis, dec blood flow and cardiac output) -prognosis is good in early stages but the mortality rate increases as decompensated shock develops in conjunction with renal failure, ARDS, or DIC

sinusitis

Sinusitis - usually bacterial developed in response to a viral infection -usually a bacterial infection secondary to a cold or an allergy that has obstructed the drainage of one or more of the paranasal sinuses into the nasal cavity -as the exudate accumulates, pressure builds up inside the sinus cavity, causing severe pain in the facial bone signs -nasal congestion -fever -sore throat -diagnosis is confirmed via radiograph or transilumination

pneumothorax (closed [spontaneous], open, and tension)

Spontaneous (basic) → don't know why it happens (air leaks out and fills space where lungs should be) The normal lung: negative pressure to make the pleura stick to the lungs Air enters through the lungs Open → air comes in from the outside (there is a hole in the chest) Lungs inflate ; space increases ; suck in air through the hole (not helping w gas exchange) Tension → hole; breathe and chest expands and sucks air through hole; flap of tissue (puncture injury); closes off flap so air cannot get out ; causing air to build up really quick ; big mediastinal shift (bending of the trachea) Medical attention asap Air in chest cavity Lung collapse Penetrating wound Painful Dangerous! Relieved by pleurocentesis (withdrawing air) -refers to air in the pleural cavity -fluid or blood may be present in the cavity CLOSED - air can enter the pleural cavity through an opening directly from the internal airways (no opening in the chest wall) -- can be simple of spontaneous -spon, idiopathic, ruptured bleb, from inside of lung, one lung is impaired, breath sounds are absent SIMPLE OR SPON - occurs when a tear on the surface of the lungs allows air to escape from the inside of the lung through a bronchus and visceral pleura -simple occurs in men who have no prior lung disease SECONDARY - associated with underlying respiratory disese resulting from rupture of an emhys bleb on the surface of the lung or erosion by a tumor OPEN - atmospheric air entering the pleural cavity through an opening in the chest wall -puncture wount through chest wall, air entry from outside of body through opening in thorax, mediastinal flutter impaurs venous return to the heart, sucking noise, tracheal swing, dec BP, moderate hypoxemia SUCKING WOUND -large opening in the chest wall where the sound of air moving in and out makes a typical sucking sound TENSION: -most serious form -results from an opening thoruh the chest wall and parietal plerua or from a tear in the lung itssue and viseral pleura that causes ateletaisi -damage creates a flap of tissue or a one way valve effect (opening enlarges on inspiration, promoting airflow into the pleural cavity) -on expiration, opening is sealed off preveting removal of air -severe hypoxia develops - open (pun through thorax) -close (tear in lung surface) -both with flap of one way valve -pleural paun -breth sounds absent on affected side -shock

scarlet fever

Streptococcus pyogenes Scarlet fever (β-hemolytic Streptococcus)--> treat with antibiotics Rash and high fever -an PRT infected caused by group A B hemo strepto. -incubation period I s 1-2 days -symptoms begin with fever and sore throat; chills and vomitting and ab pain and malaise also occur -strawberry tongue is caused by the exotoxin produced by the bacteria -find rash on the chest, neck, groin, and thights -can be treated with antibiotics

test question

Tetralogy of Fallot (TEST QUESTION) → which of these are included? VSD Ventricular septal defect Hole between the two ventricles Dextroposition of aorta Aorta shifted to the right Push up blue and red blood through aorta Pulmonary stenosis Pulm. artery is too narrow Compounds things A lot of back pressure R V Hypertrophy Because of all this back pressure

Explain the pathophysiology of valvular stenosis

Valvular Stenosis (scarring, calcium deposits) → scar is not as flexible Increased resistance to blood flow Heart works harder (to get blood through stiff valve) Hypertrophy develops Mitral Valve Stenosis Different from prolapse Blood impeded from filling left ventricle Can cause left sided congestion signs Can lead to thrombi It is a scarring / stiffening of the mitral valve Does not easily flow / not complete filling -stenosis is the narrowing of a valve, which restricts the forward flow of blood -if the opening is narrow, as in pulmonary stenosis, the myocardium must contract with more force to push the blood through -mitral stenosis and its effects are demonstrated in ECG --left atrium is enlarged from the backup pressure and the inc workload had produced the thickened atrial wall

Describe the development of varicose veins

Varicose veins Valves of veins no longer close off blood flow Stasis of blood (risks: edema, thrombus) Superficial (spider web) -varicosities are irregulare dilated and torturous areas of the superficial or deep veins (most common location is in the legs, but var. are also found in the esophogus and the rectum) -in the legs may develop from a defect or weakness in the vein walls or in the valves --long periods of standing during which the pressure within the vein is greatly elevated can also lead to var. -the weight of blood then damages the valve below, leading to backflow of blood into the section distal to the starting point -var. can predispose to thrombus formation in the presence of other contributing factors such as immobility -familial tendency to var veins walls -fatigue and aching are common and intersitital fluid interferes with arterial blood flow and nutrient supply -healing is slow bc of impaired blood flow -treatment is directed towards keeping the legs elevated and using support stocking to encourage venous return and relieve discomfort

Differentiate between different types of cardiovascular drugs, their uses, and actions

Vasodilators (Nitroglycerin or isosobride) -Reduction of peripheral resistance -Help flow blood vessels -workload of the heart also acts as coronary vasodilators -better o2 supply and demand in the heart muscles -decrease in BP (resulting in dizziness) Beta blockers (metamprolol or atenolol) -Treatment of hypertension and dysrhythmias -Reduction of angina attacks -block epinephrine stimulation -prevent SNS from increasing the heart activity Calcium channel blockers (diltiazem, verapamil, nifedipine, almodipine--> norvasc) -Decrease cardiac contractility -Antihypertensives and vasodilators -Prophylactic against angina -dec contractility / stabilizing -block the movement of calcium ions into the cardiac and smooth muscle fiber -verapamil slows the heart rate down by depressing the motion of the SA and AV nodes, preventing tachycardia and fibrillation Digoxin -Treatment for heart failure -Antidysrhythmic drug for atrial dysrhythmias -Stabilize the heart (more rhythmic) --slows conduction of impulses and heart rate -inotropic (inc. the contractility of the heart) Antihypertensive drugs -Used to lower blood pressure -some cause orthostatic hypotension Adrenergic blocking drugs -Act on SNS centrally or on the periphery -may act as direct vasodilator Angiotensin-converting enzyme (ACE) inhibitors (enalapril --> vasotec, ramipril --> altace, captopril --> capoten, perindopril --> coversyl) -Block conversion of angiotensin I to angiotensin II -Usually for BP; problems in kidneys (caused BP to go up) -treatment for pts with CHF or hypertension -result is a decrease in preload and after load Diuretics (hydrochlorothiazide, furosemide) -Remove excess sodium and/or water. -Treat high BP and congestive heart failure. -Lose some fluid in blood -HCT -increased urine output, reducing blood volume and edema Anticoagulants (warafind --> coumadine) -Reduce risk of blood clot formation -Aspirin -blood thinners Cholesterol-lowering drugs (simvastatin --> zocor, atorvastatin --> lipitor) -Reduce low-density lipoprotein and cholesterol levels -Decrease inflammation going on in inside of blood vessels - statins

obstructive sleep apnea

a disorder in which a person, while asleep, stops breathing because his or her throat closes; the condition results in frequent awakenings during the night Obstructive Sleep Apnea Increases w/age & obesity 3-5% of adults affected Chronic hypoxia Continuous Positive Airway Pump (CPAP) used to treat -sleep apnea results when the pharayngeal tissues collapse during sleep leading to repeated and momentary cessation of breathing -men are more affected than women, and incidence inc with age and obesity

Epiglottis

a flap of cartilage at the root of the tongue, which is depressed during swallowing to cover the opening of the windpipe. Epiglottitis Haemophilus influenzae (actually gram - bacteria) Does not cause the flu -acute infection usually caused by the bacterial organism, H influenzae type B -common in kids ages 3-7 -the infection causes swelling of the larynx, supraglottic area, and epiglottis, which appears as a round, red ball obstructing the airway -onset is rapid, fever and sore throat develop, and child refuses to swallow -drooling of saliva is apparent and inspiratory stridor is heard -appears anxious and pale and assumes sitting position with mouth open, struggling to breathe -treatment consists of o2 and antimicrobial therapy, with intubation or tracheotomy if needed

status asthmaticus

a severe, life-threatening asthma attack that is refractory to usual treatment and places the patient at risk for developing respiratory failure. Status Asthmaticus Less common form of asthma More dangerous Prolonged and won't stop on their own Require epinephrine injection May need tracheotomy May result in respiratory failure and death Does not respond to any treatments/can be life threatening -perisistant severe attack of asthma that does no respond to therapy -it is often related to inadequate medical treatment -may be fatal owing to severe hypoxia and acidosis leading to cardiac arrthymias or CNS depression -chronic asthma/chornic lung disease can develop from irreversible damage in the lungs with severe acutea asthmatic attacks

Pneumocystis carinii pneumonia

an opportunistic infection caused by the fungus Pneumocystis carinii Pneumocystis carinii pneumonia Fungus—often cause of fatality among AIDS patients -type of atypical pneumonia that occurs as an opportunitisc and often fatal infection in pts with acquired AIDS -caused in premature infants -was formarly known as a protozoan but now is a fungus -appears to be inhaled and attaches to alveolar cells, causing necrosis and diffuse interstitial inflammation -alveoli fill with exudate and fungi, including the cystic form -its onsent is difficulty breathin and nonproductive cough -for AIDS pts with low CD4 T-cell counts, prophylactic drugs such as a sulfamethozalole-tri. combination or pentiamidine aerosol are recommended

Obstructive Lung Diseases

asthma, emphysema, chronic bronchitis

Expansion disorders

atelectasis, pneumothorax Expansion Disorders Atelectasis → crushed lungs Lung collapse Usually the result of another condition Causes of collapse Obstruction of air passages (blocking air from filling in the alveoli) Compression of lung Air (pneumothorax) fluid (eg pleural effusion) Mass Atelectasis (compression and obstructive) Expansion Disorders Pleural Effusion → tumors can cause this (cancer) Hydrothorax Fluid is transudate CHF a frequent cause Pleural effusion (fluid in pleural space → exudate or water) Fluid is exudate Inflammation of the pleura or pleurisy (inflam. Of the pleura) → can be an infectious process Adhesions- scar tissue binding both sides of the pleura—limiting lung expansion **Empyema—purulent exudate (ON THE TEST)** Pneumothorax Spontaneous (basic) → don't know why it happens (air leaks out and fills space where lungs should be) The normal lung: negative pressure to make the pleura stick to the lungs Air enters through the lungs Open → air comes in from the outside (there is a hole in the chest) Lungs inflate ; space increases ; suck in air through the hole (not helping w gas exchange)

Describe the pathophysiology and clinical manifestations of bronchiectasis

caused by inflammation, swelling & mucous plugs Chronic cause TB, Cancer Necrosis causes: Saccular bronchiectasis (SACS) Bronchi form sacs Elongated (fusiform) bronchiectasis (bronchi forms long flexible tubes) Bronchi form tubes Cough produces foul-smelling combo of mucus, pus, and necrotic debris accompanied by halitosis. Bad breath demonstrates the focal area of dilated bronchi with bronchiectasis. Bronchiectasis tends to be localized with disease processes such as neoplasms and aspirated foreign bodies that block a portion of the airways. -usually a secondary problem that develops in pts with conditions such as cystic fibrosis of COPD -condition may be localized in one lobe or diffuses in both lungs -irreversible abnormal dilation or widening bronchi -may be saccular or elongated (fusiform) -- arise fro recurrent inflammation and infection in the airways that leads to obstruction in the airways or weakening of the muscle and elastic fibers in the bronchial wall -in dilated ballooning areas, large amounts of fluid collect and become infected -infections cause loss of cilia and metaplasian in the epithelium (interfere with the removal of fluids)

atelectasis

collapsed lung; incomplete expansion of alveoli Atelectasis → crushed lungs Lung collapse Usually the result of another condition Causes of collapse Obstruction of air passages (blocking air from filling in the alveoli) Compression of lung Air (pneumothorax) fluid (eg pleural effusion) Mass (compression and obstructive) -nonaeration or collapse of a lung or part of a lung leading to dec gas exchange and hypoxia -occurs as a complication of many primary conditions -ventilation and perfusion are altered and affects the o2 diffusion -the inc respiratory rate can control co2 levels bc this gas diffuses easily -if lungs are not reinflated quickly, the lung tissue can become necrotic and infected -obstructive it reabsorption atectasis develops when total obstruction of the airway -compression results when a mass such as a tumor exerts pressure -inc surface tension -fibrotic tissue in the lungs or pleura may restrict expansion -posteoperative

atherosclerosis

condition in which fatty deposits called plaque build up on the inner walls of the arteries Serum lipids Total cholesterol Triglycerides Low density lipoprotein (LDL cholesterol) → liver produces cholesterol and sends out to your muscles Transports cholesterol from liver to cells High cholesterol content "Bad" cholesterol High density lipoprotein (HDL cholesterol) → cleanses cholesterol and takes it back to liver (good cholesterol) Transports from cells to liver Low cholesterol content "Good" cholesterol Non-modifiable risk factors: (cannot help) -Age (40+, particularly men) -Gender (women have >HDL until menopause) -Familial tendencies Modifiable risk factors: Obesity High cholesterol diets Cigarette smoking -Decreases HDL -Increases LDL -Platelet adhesion -Fibrinogen production -Vasoconstriction Sedentary lifestyle DM (diabetes) Poorly controlled htn Combo: smoking & some oral contraceptives Combo: elevated cholesterol and high BP Diagnostic tests: Serum lipid levels (indicate presence of inflammation) Serum CRP levels Exercise stress testing (ETT) --> assess the degree of obstruction in the arteries Nuclear medicine myocardial perfusion imaging (MPI) --> used to determine the degree of tissue perfusion, the presence of collateral circulation, and degree of local cell metabolism Treatment -losing weight and maintaining health levels reduce onset -lowering serum chol. and ldl levels -sodium intake should be minimized -exercise -surgical intervention when it is advanced to reduce obstruction by means of invasive procedures Diet -Low cholesterol -High fiber diet Drugs -Statins Smoking cessation Anticoagulants -ASA -Warfarin (Coumadin) Advanced—PTCA or even CABG -differentiated by the presence of atheromas, plaques consisting of lipids, cells, fibrin, and cell debris, often with attached thrombi, which form inside the walls of large arteries -lipids and fats play a key role in this process -LDL (high lipid content and transports cholesterol from the liver to the cells is dangerous part of elevated serum levels of lipids and cholesteral) and also binds to receptors -HDL is the good lipoprotein; has a low lipid content and is used to transport cholesterol away from the peripheral cells to the liver where it undergoes catabolism and excretion -atheroma also damages the arterial wall, weakening the structure and decreasing its elasticity --> may calcify causing further rigidity of the wall (process may lead to an aneurysm or buldge in the arterial wall) -angina may occur; a total obstruction leads to MI -common cause of strokes, renal damage, and peripheral vascular disease

tetralogy of Fallot

congenital malformation involving four distinct heart defects -most common cyanotic congenital heart condition -includes four (tetra) abnormalities and is a cyanotic disorder -four defects are pulmonary valve stenosis, VSD, dextroposition of the aorta (to the right over the VSD), and right ventricular hypertrophy -this combo alters pressures within the heart and therefore alters blood flow -pulmonary valve stenosis restricts outflow from the right ventricle, leading to right ventricular hypertrophu and high pressure in the right ventricle -- this pressure leads to a right to left shunt of blood through the VSD -the flow of un-o2-ed blood from the right ventricle directly into the systemic ciruclation is promoted by the position of the aorta, over the septum or VSD -surgery is the only effective treatment for the t.o.f. --done during the first year of birth and involves a number of individual repairs: closing the VSD, reparing the pulmonary valve, and widening the pulmonary arteries to increase the flow

Describe the pathophysiology of cystic fibrosis

cystic Fibrosis Autosomal recessive disorder Defective protein involved with Cl- transport in cells Results in abnormally thick secretions from exocrine glands Involves pancreas and other secretory organs Avg age life expectancy is 37 -inherited disorder in kids -also called mucoviscidosis is a genetic disorder -relate to a protein involved in chloride ion trasprt in the cell membrane -defect in the exocrine glands causes abnormally thick secretions -primary effect is seen in lungs and pancreas, where the sticky mucous obstructs the passafes -in the lugns, the mucus obstructs the airflow in the bronchioles and small bronchi, causing air trapping with perm. damage to bronchial walls -organisms causing infections include p aeru a s aurous -in the digestive tract, the first indication may be meconium ileus in newborns -in the pancreas, the ducts of the exocrine gland becomes blocked, leading to dficit of pancreatic digestive enzymes in the intestine -bile ducts of the liver may be blocked by viscid mucus, preventing bile from reaching the duodenum and interefering with digestion -salivary glands --> midly affected with secretions that are abnormally high in na + chloride -sweat glands are also affected, producing sweat that is hgih in sodium chloride content -reproductive system may be affeted, w thock mucus obstructing the vas dererns in males or cervix in females leading to infertilitity

paroxysmal tachycardia

episode of tachycardia that occurs suddenly and then goes away without treatment Can be brought on by ectopic beats Episode of closely spaced and fast beats Chambers can't fill Probably due to ischemic damage Can lead to ventricular tachycardia So fast that the heart does not have time to fill → this affects cardiac output (it goes DOWN) → stroke volume goes down too

Influenza

flu -viral infection that may affect both the upper and lower RTs -influenza is presented as an ex of infection -type a, b, c --> these viruses mutate constantly, preventing effective immune defense for prolonged time periods -sudden and acute onset fever marked with fatigue and aching pains in the body -- causing pneumonia -treatment is antiviral drugs (useful to control the flu outbreaks in hospital or nursing homes) -incubation period for the virus is 1-4 days with an avg of 2 -prevention by vaccination

flail chest

fracture of two or more adjacent ribs in two or more places that allows for free movement of the fractured segment Ribs become separated (expansion of chest creates pressure gradient for air to come in) Wrecks boyle's law -falls and car accidents cause most injuries -resulys from fractures of the thorax and 3-6 ribs in two places or the sternum -chest wall rigidity is lost, resulting in paradoxical (opposite) movement during inspiration and expiration during inspiration -usual dec in pressure inside the lungs -flail is broken -compress adjacent lung on expiration -unstable flail secretion is arge -air is unaffected lung moves across into affected lung -mediastinal flutter occurs when the fail section is lare -hypoxia results from the limited expansion and dec inspiratory volume of the flail lung; the shunting of stale air bw the lungs, which lowers the o2 content o the air; and the dec venous return

arteriosclerosis

hardening of the arteries May refer to all types of tissue arterial tissue changes Generally-hardening of the arteries Tissue loses elasticity, becomes rigid Brittle vessels Rupture possible Thickening of arterioles & small arteries. Hypertrophy (bigger muscle) due to high BP --Heart muscle gets really big More resistance, less blood flow Involves the arteries; sclerosis is the closing in of arteries / hardening of arteries Artery disease Lose some elasticity (arteries do not really expand) → high BP -can be used as a general term for all types of arterial changes -degenerative changes in the small arteries and arterioles, occurring in those 50 + with diabetes -elasticity is lost, the walls becomes thick, and hard, and the lumen gradually narrows and may become obstructed -- leads to diffuse ischemia and necrosis in various tissues

Congestive Heart Failure

heart is unable to pump its required amount of blood Insufficiency of cardiac output Usually starts with one side (L or R) and ends up involving both Causes? CAD (ischemia, MI) → heart attack Myocarditis and cardiomyopathy (not CAD) → inflammation of the heart tissue Excessive cardiac burden Anemia, heart valve problems, hyperthyroidism (overactive thyroid → tachycardia) Arrhythmias Hypertrophy Either left sided or right sided (insufficient output) Left side gets backed up; then goes to right side (both sides not working= CHF) -occurs when the heart is unable to pump sufficient blood to meet the metabolic needs of the body. usually CHF occurs as a complications of another condition **Young Children with CHF** Often secondary to congenital heart disease Feeding difficulties often first sign Failure to gain weight or meet developmental guidelines (to "thrive") Short sleep periods Tripod position to play Cough, rapid grunting respirations, flared nostrils, wheezing Radiographs show cardiomegaly. Arterial blood gases used to measure hypoxia Get it from congenital heart disease

Laryngotracheobronchitis (Croup)

inflammation of the upper airways with swelling; creates a funnel-shaped elongation of tissue causing a distinct "seal bark" cough Laryngotracheobronchitis (Croup) Children of 1-2 years of age -common viral infection -common causes are parainfluenza viruses and adenoviruses -begins as an URC with nasal congestion and coughing -larnyx and subglottic area become inflamed with swelling and exudate, leading to obstruction and a characteristic barking cough (croup) -becomes severe at night time -cool air from a humidifier or shower relieves the obstruction -infection is self limited

atrial fibrillation

occurs when the normal rhythmic contractions of the atria are replaced by rapid irregular twitching of the muscular heart wall Atrial Fibrillation Quivering of atrium Patient may complain of "feeling bad" Cause?? Ischemia Hypertension Immediate treatment required Includes heparin therapy since AF can cause thrombi Long term treatment to stabilize Digitalis to regulate heart beat -rate of more than 350 delays conduction, and therefore causes pooling of blood in the atria and is treated with anticoagulant meds to prevent clotting and potential cerebrovascular accident (stroke)

Chronic Obstructive Pulmonary Disease (COPD)

permanent, destructive pulmonary disorder that is a combination of chronic bronchitis and emphysema OPD--Umbrella term for various disorders Reaction to primary disease or chronic irritation Considered a secondary condition Bronchi & bronchioles obstructed (or plugged) Inflammation due to debris & irritation Mucus production as response obstruction Changes to lung, destruction → changes in structure (form of the lungs) All forms result in ineffective ventilation (affects air getting down into lungs) Can be life long and is usually a destructive process going on Is irreversible -group of common chronic respiratory disorders that are characterized by progessive tissue degeneration and obstruction in the airways of the lungs -restrictive lung diseases (irritant causes interstitial inflammation and fibrosis, resulting in the loss of compliance of stiff lung) -causes irreversible and progressive damage to the lungs -repsiratory failure may result because of severe hypoxia -leads to the development of cor pulmonale (right sided CHF due to lung disease) COPD diseases Emphysema Chronic Bronchitis 90% due to cigarette smoke Defined as productive cough 3 months in a year for 2 consecutive years Bronchiectasis → associated with CB Also asthma is often included in this category (your text seems confused about this)

patent ductus arteriosis

persistence, after birth, of a communication between the main pulmonary artery and the aorta -Ductus Arteriosus Fetal lungs are collapsed until birth Provides route for mother's oxygenated blood to reach baby's systemic circulation Patent Ductus Arteriosus (PDA) DA doesn't close after birth --O2 is not getting in your lungs, getting it through mom's placenta Others Coarctation of the aorta (two great blood vessels switched positions) Transposition of the great arteries Patent ductus arteriosus (PDA) is a medical condition in which the ductus arteriosus fails to close after birth: this allows a portion of oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta, which has a higher pressure, to the pulmonary artery. Patent ductus arteriosus (PDA) is an opening between two blood vessels leading from the heart. A small PDA may cause no symptoms, but a large one may cause poor eating, failure to thrive, or breathlessness. Treatments include monitoring, medications such as anti-inflammatories (NSAIDs), and surgery. The ductus arteriosus is a normal connection between the pulmonary artery and aorta; it is necessary for proper fetal circulation. At birth, the rise in Pao2 and decline in prostaglandin concentration cause closure of the ductus arteriosus, typically beginning within the first 10 to 15 h of life. If this normal process does not occur, the ductus arteriosus will remain patent (see figure Patent ductus arteriosus). Patent ductus arteriosus Pulmonary blood flow, LA and LV volumes, and ascending AO volume are increased. AO = aorta; LA = left atrium; LV = left ventricle; PA = pulmonary artery. Physiologic consequences depend on ductal size. A small ductus rarely causes symptoms. A large ductus causes a large left-to-right shunt. Over time, a large shunt results in left heart enlargement, pulmonary artery hypertension, and elevated pulmonary vascular resistance, ultimately leading to Eisenmenger syndrome.

SARS

severe acute respiratory syndrome Severe Acute Respiratory Syndrome (SARS) SARS-CoV or SARS-associated coronavirus Initially flu-like-damages liver-causes fatal respiratory distress 10% fatal in general population, 50%+ in those >60 years -advent is triggered extensive global efforts to quickly identify the previously unknown microorganism and its mode of tranmission, then develop a system to contain and control spreading -causative microbe is a cornoavirus, an rna virus that is transmitted by respiratory droplets during close contact -first stage involves flulike symptoms -effects on the lungs are evident with a dry cough and marked dyspnea -lymphopenia and thrombocytopenia are oresent

central sleep apnea

sleep disorder with periods of interrupted breathing due to a disruption in signals sent from the brain that regulate breathing Central sleep apnea—more of a neurological cause ("forgetting to breathe") sl→ brain

Infectious Rhinitis (common cold)

the common cold is caused by a viral infection of the URT -- most common pathogen is a rhinovirus 'common cold' (infectious rhinitis) -the common cold is spread through respiratory droplets, which either are directly inhaled or are spread by secretions on hands or contaminated objects such as facial tissue -infectious is highly contagious bc the virus is shed in large numbers from the infected nasal mucousa during the first few days of the infection and can survive for several hours outside of the body -signs include: nasal congestion, mouth breathing, sore throat, headache, slight fever, cough, malaise -treatment is symptomatic (acteamenophin and a cold is self limiting) -secondary infections like strep throat are usually caused by streptococcus invading inflamed and necrotic mucous membrane -purulent exudate forms and systemic signs such as a fever develop Infectious rhinitis—the common cold, is typically caused by viral strains (there are an estimated 200 strains that cause the common cold). It's common because it takes a while to develop immunity to all the different strains, plus the strains are always mutating—trying to beat our immune system.

ventricular fibrillation

the rapid, irregular, and useless contractions of the ventricles the heart muscles contract independently and rapidly (uncoordinated quivering) and therefore are ineffective in ejecting blood. the lack of cardiac output causes severe hypoxia in the myocardium, and contraction ceases -rate over 300/min; uncoordinated muscle contractions -no filling, no output-- cardiac standstill Ventricular Fibrillation Ventricle is quivering No cardiac output Death imminent This is when you use the paddles (defibrillation) Shock stops the heart and hoping the SA or AV node kicks in and starts making it work again