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Dr. Seva Visceral 1

Dr. Seva's 1st Visceral Pathology Exam

QuestionAnswer
What is a feature of hypertrophic response in the heart? enlargement of cardiac myocytes w/o an increase in the number of cardiac myocytes
What does hypertrophy initially reflect and what occurs with steady stress? Initially: a compensatory and potentially reversible mechanism but with persistent stress myocardium becomes irreversibly enlarged and dilated
What is concentric hypertrophy and what are risk factors? Enlargement of cardiocytes - thicker myocardium w/ no dilation of the chamber; hypertension and stenosis of valves.
What is eccentric hypertrophy and what are risk factors? enlargement of cardiocytes - thicker myocardium w/ dilation of the chamber; regurgitation or incompetence.
What is congestive heart failure? Accumulation of blood; unable to pump out.
What could heart failure be d/t? Weak ventricular contraction Abnormal ventricular relaxation Outflow and obstruction (AS & PS) Weak muscle (ischemia or infarction) Increased work from pressure or volume overload
What side of the heart is affected with backward failure? Right sided heart failure
What side of the heart is affected with forward failure? Left sided heart failure
What is the most common condition responsible for cardiac failure (accounts for 80% of heart disease deaths)? Ischemic heart disease or coronary artery disease. The remaining 20% are caused by heart muscle disease and congenital heart diseases
When are signs and symptoms prominent with heart failure? Symptoms: LVF Signs: RVF
What is the etiology of left heart failure? Ischemic heart disease Hypertension Valvular disease (low %age)
What are clinical features of LHF? Dyspnea on exertion (b/c decreased CO) Orhopnea Paroxysmal Nocturnal Dyspnea Cough (frothy, pink sputum) Hemoptysis
How does the body compensate for LHF? Left atrial pressure increases Pulmonary venous pressures increase Lung gets congested "wet" congested capillaries in the alveolar septum Heart failure cells or hemosiderin laden macrophages (HLM)
What changes can be noted in the heart, lungs, kidney, brain and skeletal m. with LHF? Heart: hypertrophy of LV Lungs: wet, HLM Kidney: decreased blood supply, decreased perfusion, decresed urine production, smaller in size Brain: inadequate cerebral perfusion Muscle: decreased perfusion of m. leads to fatigue and weakness.
What is the etiology of RHF (RVF, RSF)? MC is LVF Pulmonary HTN d/t left or right shunt Cor Pulmonale if RHF is d/t pulmonary dz (COPD)
What happens to compensate for RHF? Right atrial pressure increases and systemic venous pressure (SVC, IVC) increases
What are clinical features of RVF and the 4 seen first? 1. Neck vein distension 2. Elevated jugular venous pressure 3. Hepatomegaly and tender liver 4. Peripheral pitting edema Spleenomegaly Hepato-abdomino-jugular reflex Ascities
What is diastolic heart failure? As heart ages, ventricles become stiffer and need greater filling (diastolic) pressures. May be normal in size and normal systolic contractile function but exhibit s/s of heart
What would you expect to see microscopically with diastolic heart failure? Typically have interstitial fibrosis, causing decreased compliance of ventricular myocardium.
What is congenital heart disease and its prevalence? Results from faulty embryonic development. 7 per 1000
What can be causes of congenital heart disease? Genetic, Chromosomal anomalies (Turners and Downs), Maternal rubella infection, alcohol/ecstacy abuse, drugs in early pregnancy and maternal diabetes
What are types of congenital heart disease? (8) 1. MC: ventricular septal defects 2. atrial septal defects 3. patent ductus arteriosus 4. tetralogy of fallot 5. pulmonary stenosis 6. coarctation of the aorta 7. aortic stenosis 8. complete transposition of the great aa.
Describe the acyanotic group of congenital heart disease. No shunt and no cyanosis: abnormal passage/flow of blood; coarctation of the aorta, aortic stenosis
Describe the cyanose tardive group of congenital heart disease. An initial L-R shunt w/ late reversal of flow; d/t patent ductus arteriosus, atrial septal defect, ventricular septal defect. Cyanosis supervenes later, shunt L-R then goes R-L b/c increases in resistance cause R vent. pressure to exceed that of L vent.
Describe the cyanotic group of congenital heart disease. A permanent right to left shunt. Cyanosis in early stage itself. Includes tetralogy of fallot and complete transposition of great vessels.
How can CHD also be classified? Lt - Rt Rt - Lt No shunt
What condition(s) can be included in Lt - Rt CHD? ASD VSD PDA
What condition(s) can be included in Rt - Lt CHD? Tetrology of Fallot
What is the most common congenital heart lesion and what part is it commonly found in? Ventricular Septal Defect (VSD); Found in the membranous part of the IV septum
What is the significance of a small ventricular septal defect? No functional significance if the defect is small
What is the clinical significance of a big ventricular septal defect? Right ventricle hypertrophy; Fatigue, dyspnea on exertion (CO not enough); Palpitation d/t arrhythmia; Repeated Lower respiratory infection in childhood; Auscultation: pansystolic murmur
What is the Eisenmenger complex? A VSD can eventually result in thickening of pulmonary aa. and increased pulmonary vascular resistance causing the reversal of the shunt and goes from right to left. This reversal will cause deox. blood to mix with ox. blood -> cyanosis (tardive)
What does a patient presenting with Eisenmenger complex usually have? Late onset of cyanosis (tardive cyanosis), right ventricular hypertrophy and right-sided heart failure; Addn'l complications are infective endocarditis and paradoxical emboli
What is the most common type of atrial septal defect? Ostium secundum type (90% of all cases); Left to right shunt to cause dilation and hypertrophy of the right atrium and ventricle
What are the clinical features of a big Atrial Septal Defect? Fatigue, dyspnea on exertion Palpitation d/t arrhythmia Repeated LRI in childhood PHTN R ventricular hypertrophy Heart failure Paradoxical emboli Bacterial endocarditis Auscultation: ejection systolic murmur
What is Lutembacher syndrome? The combination of mitral stenosis and an ostium secundum atrial septal defect.
With whom is Patent Ductus Arteriosus common? Premature infants and infants whose mothers were infected with rubella virus early in pregnancy.
What are clinical features of patent ductus arteriosus? Left ventricular hypertrophy and heart failure, decreased CO PHTN Infective endocarditis Auscultation: Murmur in both systole and diastole = continuous machinery murmur.
What 4 changes define Tetrology of Fallot? 1. Pulmonary stenosis 2. Ventricular septal defect 3. Dextroposition of the aorta/overriding of aorta 4. Right ventricular hypertrophy
What are clinical features of Tetrology of Fallot? Severe cyanosis Surgical correction needed w/in 1st 2 years If surgery not done dyspnea on exertion quite noticeable Retarded physical dev. Cerebral thromboses Bacterial endocarditis and brain abscesses
What is transposition of the great arteries? Aorta arises from the right ventricle and pulmonary artery from the left ventricle
Who commonly will present with transposition of the great arteries? Males Offspring of diabetic mothers
When is Transposition of the great arteries not fatal? If there is an ASD or VSD or PDA
What is Coarctation of the aorta? A local constriction immediately below the origin of the left subclavian a. at the site of the ductus arteriosus.
What are clinical features of coarctation of the aorta? Male predominance Discrepancy of bp b/w UE & LE HTN in upper limb (LV hypertrophy, dizziness, HA, nosebleeds) Hypotension in lower limb (weakness, pallor, claudication/LE) Radiofemoral delay Vascular Bruit X ray: figure 3 appearance, rib notching
What are the 3 types of Aortic Stenosis? Congenital Senile Rheumatic
How does congenital stenosis present and when do symptoms appear? Bicuspid valve in children instead of 3 semilunar cusps; 4th and 5th decades of life
How does Senile Calcific AS present and when do symptoms appear? Degenerative cond'n of the aortic valve; 6th and 7th decades of life.
How does Rheumatic AS present? Almost always associated w/ mitral valve stenosis and aortic valve stenosis.
What are clinical features of AS? (4) 1. Angina (low blood supply to <3) 2. Syncope (low blood supply to brain = fainting) 3. Heart failure (left) 4. Soft S2 (absent A2, soft S2 being pulmonic component)
What is Endocardial Fibroelastosis? Fibroelastic thickening of the endocardium of the LV, which can also affect the valves. Valves may show collagenous thickening. Papillary mm. and chordae tendinae are thick and short. Dev. progressive heart failure.
What is Dextrocardia? Rightward orientation of the base-apex axis of the heart. Assoc. w/ a mirror image of the normal left-sided location and config. If situs inversus heart functions normal.
What is ischemic heart disease and when does it develop? In most cases a result of coronary artery atherosclerosis; when blood flow is to low to meet the O2 demands of the heart.
What is the leading cause of death and what are the principal effects? IHD (80% of deaths); Angina pectoris, MI, chronic congestive heart failure, sudden death
What is angina pectoris and when does it become symptomatic? Substernal pain radiating to the L arm, jaw and epigastrium; CAD becomes symptomatic only when the luminal cross sectional area of affected vessel is reduced by more than 75%.
What brings on chest pain, what is the duration and how is it relieved? recurrent episodes usually brought on by increased physical activity or emotional excitement; 1-15 min.; reducing physical activity or sublingual nitroglycerin (vasodilator).
What are other causes of angina and what is an atypical cause? Coronary vasospasm, AS, or aortic insufficiency; Prinzmetal angina (variant angina) occurs at rest and caused by coronary a. spasm occurs in structurally normal coronary aa.
What is unstable angina? Preinfarction angina, accelerated angina or crescendo angina; pain at work and rest and sublingual nitroglycerin won't work; not related to excersize, may occur during rest or sleep and assoc. w/ dev. of nonocclusive thrombi over atherosclerotic plaques.
How do unstable anginas look when tested and how can it progress? Normal EKG and no cardiac enzymes; w/o pharmacologic or mechanical intervention to "open up" coronary narrowing many pt.s progress to MI
How does an MI look on tests? Positive EKG and cardiac enzymes present in blood.
What are complications of MI? (7) 1. chronic CHF 2. Sudden death d/t ventricular fibrillation 3. Rupture - cardiac tamponade - hemopericardium 4. Ventricular aneurysm 5. Mural thrombus & embolism 6. Pericarditis 7. Postmyocardial infarction syndrome (Dressler syndrome)
What is pericarditis? Transmural MI involves epicardium -> inflam of pericardium; manifested as chest pain and may produce a pericardial friction rub. 1/4 w/ acute MI dev. pericardial effusion.
What is cardiac tamponade? Less frequently w/ anticoagulants appearance of hemorrhagic pericardial effusion; hypotensive, death d/t shock, decreased BP & CO.
What is Dressler syndrome? Post MI syndrome; delayed form of pericarditis that dev. 2-10 weeks after infarct. Antibodies to heart m. appear in these pt.s corticosteroids improve...may be immunologic.
What conditions influence the supply of blood to the heart? Atherosclerosis and thrombosis Thromboemboli Coronary artery spasm High BP, CO and HR Dissecting aneurysm
What conditions influence the availability of oxygen in the blood? Anemia Carbon Monoxide Cyanide (Don't drink the Kool-Aid or run the car in the garage)
What conditions increase oxygen demand/increase cardiac work? HTN Valvular stenosis or insufficiency Hyperthyroidism Fever Thiamine deficiency Catecholamines
What are the 3 locations of infarction? Posterior Anterior Lateral
What is a subendocardial infarct? Affects the inner 1/3 to 1/2 of the LV
What is LAD coronary artery infarct? Occlusion of this a. results in apical, anterior and anteroseptal walls of the left ventrical (anterior infarct)
What type of infarct results in the L circumflex coronary a.? Occlusion results in a lateral infarct.
How does MI develop? first in the subendocardium and progresses over several hours.
What occurs with transient coronary occlusion? May cause only subendocardial necrosis, persistent occlusion -> transmural necrosis. Thrombolytic drugs interrupt and limit myocardial necrosis
Why do infarcts involve the left ventricle? B/c of its workload much more commonly and extensively that the RV
What is seen with gross examination of acute MI? 24 hours pallor noticed 3-5 days: mottled and sharply outlined, w/ necrotic region bordered by hyperemic zone. 2-3 weeks: region depressed and soft w/ refractile, gelatinous appearance. Older are firm and have pale, gray appearance of scar tissue
What is Reperfusion of Ischemic Myocardium? Contraction band necrosis: contraction bands thick, irregular, transverse eosinophilic bands in neccrotic myocytes. Typically hemorrhagic d/t blood flow through damaged microvasculature.
What is HTN? A persistent increase of systemic BP above 120 mm systolic or 80 mm diastolic or both.
What is considered normal BP and prehypertension? Normal: 116/76 mm Hg PreHTN: >116/76, <120/80 mm Hg
What is the most prevalent and serious cause of IHD (&MI) in the U.S. and what are the stages? HTN; Stage 1 140-159 sys/90-99 diastolic; Stage 2 >160/100; Stage 3: >180/110
What does chronic HTN lead to? Pressure overload resulting first in compensatory LVH and eventually cardiac failure.
When is the term hypertensive heart disease used? Heart is enlarged in the absence of a cause other than HTN. (cardiomegaly)
What does HTN cause? LV concentric hypertrophy d/t increased cardiac workload. Weight increases.
What is BP the product of? CO X PR CO increases d/t high blood volume, high Na content and increased HR; PR raises d/t vasoconstriction.
What are the types of HTN? Primary or essential Secondary
What is Primary HTN? 95% of HTN >45 y/o Unknown etiology Insidious onset until target organs are involved. More common in balcks, male, familial Hx, smoking stress and obesity.
What are the end organs/target organs in primary HTN? Heart Kidney Brain Eyes
What are clinical symptoms and nonspecific signs of primary HTN? asymptomatic, in some pounding morning HA; LVH, shifted apical impulse (cardiomegaly) and S4
What is secondary HTN and what can it be d/t? Pt <35 y/o, secondary to something else: Kidney dz, adrenal cortex, adrenal medulla, pituitary, carctation of aorta, preeclampsia, thyroid
How do the specific etiologies of secondary HTN commonly present? Kidney dz: facial edema Adrenal cortex: high Na low K and aldosterone in plasma Adrenal medulla: high catecholamines in plasma and urine Pituitary: acromegaly Preeclampsia: pregnant Thyroid: hyperthyroidism (Grave's)
What are renal causes of secondary HTN? Polycystic kidney Rennin secreting tumor Renal a. stenosis Chronic glomerulonephritis
What are adrenal causes of secondary HTN? Medulla: Pheochromocytoma Cortex: excess aldosterone (Conn's) Cushing's syndrome: excess cortisol
What are complications of HTN? Diastolic dysfxn (MC) can lead to CHF LVH-increased O2 demand-MI Intracerebral hemorrhage-stroke Dissecting aneurysm of aorta Renal failure d/t nephrosclerosis if HTN severe Eye: retinal aa. constrict in response to HTN (copper wire appearance)
What are the progressive steps in acute and chronic cor pulmonale? 1. PHTN 2. RVH and diltation 3. Lungs effected
What is acute cor pulmonale? Sudden occurence of PHTN d/t sudden massive pulmonary embolism and adult respiratory distress syndrome; symptoms RVF along w/ pulmonary prob.s
What is chronic cor pulmonale? d/t COPD, pulmonary fibrosis and kyphoscoliosis; RV has thickness=LV, IV septum loses curvature toward LV and becomes straight; symptoms RVF along w/ pulmonary prob.s
What is rheumatic heart disease? d/t acute rheumatic fever; untreated pharyngitis A, B hemolytic srept. B produce antistrept. antibodies that w/ T cells react w/ cardiac antigens & may involve patho. effects on layers of heart.
What does acute rheumatic heart disease cause? Pancarditis: effects all layers of heart endocarditis, myocarditis, pericarditis
What is rheumatic fever? A multisystem childhood disease that follows a strept. infection involving heart, joints, CNS and skin.
How does myocarditis present? Aschoff body is granulomatous lesion. Anitschkow cells unusual cells in aschoff body whose nuclei have a band of chromatin. May become multinucleated termed Aschoff giant cells.
How does pericarditis present? Fibrin deposits found in pericardial space; bread and butter pericarditis; chest pain and fever; makes sound "scratchy" d/t fibrin deposits.
How does endocarditis present? Valvular Dz: Heart valves become inflamed and present fibrin nodules called "verrucae" Mitral valve (1st affected) and aortic valve (2nd) most affected than right sided valves.
What is required in Jone's criteria? Dx of RHD based on Jone's criteria: 2 major or 1 major and 2 minor clinical manifestations.
What are major manifestations in Jone's criteria Carditis: murmurs, cardiomegaly, pericarditis and CHF; Joints: polyarthritis; NS: chorea; Skin: erythema marginatum, subcutaneous nodules.
What are minor manifestations in Jone's criteria? Arthralgia Fever Raised ESR Leukocytosis Positive C reactive protein EKG changes
What are complications of Chronic Rheumatic Heart Disease? 1. Bacterial endocarditis follows bacteremia 2. Mural thrombi 3. Congestive cardiac failure 4. Adhesive pericarditis 5. Mitral stenosis, aortic stenosis or mitral valve prolapse
What causes Mitral Stenosis? Rheumatic Fever! Chronic RHD -> formation of fibrous adhesions b/w leaflets of MV and "fish mouthed" mitral stenosis
What are some s/s of Mitral stenosis? decreased CO, increased LA pressure, LVF then RVF; Emboli: LA enlargement-fibrillation=presses on L rec. laryngeal n.-hoarseness of voice
What is always associated w/ mitral stenosis? Aortic stenosis (rheumatic AS)
What is Mitral Valve Prolapse? Leaflets become enlarged, redundant, chorda tendinae become thinned, elongated and billowed leaflets prolapse into the L atrium during systole.
What are risk factors of mitral valve prolapse? Familial (#1), Marfan's, Hyperthyroidism, Rheumatic Fever
What are clinical features of mitral valve prolapse? Asymptomatic in most pt.s, systolic murmur (palpitation sx), atypical chest pain
What are complications of mitral valve prolapse? Mitral regurgitation, Infective endocarditis
What is bacterial endocarditis? Inflam. of cardiac valves by bacteria. Can be classified as acute or subacute bacterial endocarditis.
What are the clinical features of bacterial endocarditis? Fever (1st) New murmurs or changing murmurs Positive blood cultures
What can occur with infective thromboemboli? Emboli break up and lodge in small vessels, CNS: subarachnoid hemorrhage, CVS: acute congestive failure, Kidney: hematuria, Eye: Roth's spots, Nails: splinter hemorrhage.
What is Acute Bacterial Endocarditis? Infection of a normal cardiac valve by a highly virulent suppurative organisms (s. aureus and pyogenes)
What is Subacute Bacterial Endocarditis? Less virulent organisms affecting a structurally abnormal valve (MS, MVP)
What are risk factors for bacterial endocarditis? 1. RHD:Mitral valve:aortic valve (4:1) 2. IV drug abusers 3. Prosthetic valves 4. children with congenital heart disease
What is myocarditis? Inflam. of the myocardium associated w/ myocyte necrosis and m. degeneration.
What are primary and secondary myocarditis d/t? !. infectious etiology, either viral or protozoal 2. Rheumatic fever (SLE, TB, sarcoidosis)
What is viral myocarditis, what causes it and what are sx? Acute myocarditis; coxsachie and rubella viruses; asymptomatic but lead to debilitating loss of cardiac function mainly in children or young adult.
Describe hyperthyroidism. Causes increased HR (tachycardia) Increased workload & CO eventually leads to high output failure.
Describe hypothyroidism. Opposite hyper- Decreased HR (bradycardia) Impaired myocardial contractility Decreased CO Heart is flabby and dilated b/c of myxedema
What is Thiamine Deficiency: Wet Beriberi? In alcoholics or B12 deficient people Peripheral vasodilation - high CO - salt water retention - pedal edema - increased cardiac workload - tachycardia - edema - increased a. & v. pressure All lead to myocardial injury expressed as chest pain.
What are 3 metabolic diseases of the heart? 1. Hyperthyroidism 2. Hypothyroidism 3. Thiamine deficiency: Wet Beriberi
What is cardiomyopathy and the 5 types? Non-inflammatory disorder of myocardium 1. Idiopathic dilated cardiomyopathy 2. Toxic cardiomyopathy 3. Cardiomyopathy of pregnancy 4. Hypertrophic cardiomyopathy 5. Restrictive cardiomyopathy
What is the most common type of cardiomyopathy, what occurs and the etiology? Idiopathic dilated cardiomyopathy Symmetrical hypertrophy and biventricular dilatation, decreased contractile force of L & R ventricle -> CHF Et: mostly idiopathic, may be d/t alcohol, doxarubicin and thiamine deficiency (75% end up w/ CHF w/in 5 yrs)
What causes toxic cardiomyopathy? Alcohol: ethanol has an immediate negative inotropic effect on the heart.
When does cardiomyopathy of pregnancy develop, who is commonly affected and what is the result? Last trimester or 1st 6 mos after delivery MC in black race and multiparous women, some have spontaneous recovery rest end up w/ CHF.
What is hypertrophic cardiomyopathy also known as, how is it inherited and what part of the heart does it affect? Idiopathic hypertrophic subaortic stenosis Autosomal dominant type; no dilatation but asymmetrical hypertrophy (IV septum) that affects LV mostly.
What are clinical features of Hypertrophic cardiomyopathy? Apparent when pt young adult male. angina, atrial fibrillation, may result in sudden death.
What is restrictive cardiomyopathy? A group of diseases (sarcoidosis, hemochromatosis & amyloidosis) where contractile function of heart remains normal but limits diastolic filling.
What are 4 causes of sudden cardiac death? 1. Coronary artery disease (MI) 2. Aortic stenosis 3. Hypertrophic cardiomyopathy 4. Ventricular fibrillation
What are 3 types of cardiac tumors? 1. Cardiac myxoma 2. Rhabdomyoma 3. Metastatic tumor
What 2 cardiac tumors are benign and what are they? Cardiac Myxoma: 75% arise in LA as glistening gelatinous 5-6cm polypoid mass w/ a stalk; may obstruct mitral orifice. Rhabdomyoma: MC; in infants & children; nodular masses in myocardium.
Where do metastatic tumors of the heart usually originate? Lung, breast and malignant melanoma.
What is acute pericarditis? Inflammation of pericardium
What are symptoms of acute pericarditis, what relieves and aggravates it? sudden, sharp, substernal chest pain that may refer to the neck or shoulder and relieved by sitting forward. Aggravated by laying down & movement & respiration
What is pericardial effusion? Accumulation of excess fluid in the pericardial cavity in the form of transudate or exudates
What can serous pericarditis be d/t? CHF
What can chylous pericarditis be d/t? lymph exudate; could be from lymphoma
What can hemopericarditis be d/t? metastatic CA
What is cardiac tamponade and Beck's triad? Rushing of blood into pericardial cavity that restricts the venous filling; hypotension, increased JVP and muffled heart sounds
What is constrictive pericarditis? Chronic fibrosing disease evolved from TB or radiation therapy to mediastinum, pericardial cavity is obliterated. It compresses the heart and restricts blood flow.
What are clinical factors of constrictive pericarditis? Small, quiet heart, Restricted venous filling, High venous pressure, Low CO, Ascites, Pedal edema
What are pulmonary sequestrations? a portion of the lower lobe of lung receives blood supply from aorta but w/ no connection to rest of lung.
What is tracheoesophageal fistula? Communication b/w part of the esophagus and trachea can lead to aspiration pneumonia.
What is the result of Alfa1 antitrysin deficiency? emphysema
What is Allergic rhinitis? Type 1 hypersensitivity reaction; etiology can be pollen; nasal irritation, sneezing, watery rhinorrhea, itchy eyes, soft palate and ears.
What can cause laryngeal obstruction? Allergic edema, inhaled foreign body, inhaled vomitus, tumors of larynx.
What are tumors of the larynx? Squamous cell carcinoma; associated w/ tobacco (cigar) and alcohol use
What is pulmonary hypertension, where is it seen and what does it lead to? Increase in thickness of tunica media resulting in increased pressure in pulm. aa. seen in lt-rt shunt or MS or COPD; leads to respiratory failure.
What are clinical features of a pulmonary embolism? Dyspnea, sudden chest pain d/t lung infarction, hemoptysis
What are risk factors for acute bronchitis? air pollutants, allergies, chronic sinusitis, exposure to chemicals, fumes, dust and smoke inhalation.
What are s/s of acute bronchitis? persistent dry cough, then sputum prod'n, malaise, low-grade fever, insomnia, sx last 3-7 days and dry cough persists several weeks.
What is atelectasis? incomplete expansion of lung or collapse of already expanded lung; 2 types: acquired and congenital
Discuss Acute respiratory distress syndrome (ARDS). Sudden, life threatening lung failure, an acute diffuse alveolar damage; injury to alveoli or capillaries inflame the alveoli causing them to fill w/ liquid and collapse; gas exchange ceases; mechanical ventilation is tx.
What are causes of ARDS? 1. Serious infection of blood or other tissues (sepsis) 2. Severe lung infection 3. inhalation of smoke or other toxic fumes 4. Near drowning
What are s/s of ARDS and how is it diagnosed? Dyspnea, tachypnea, severe hypoxaemia, cyanosis; abnormalities in the arterial blood gas analysis [O2] and [CO2] and pH of blood
What is neonatal respiratory distress syndrome and what is evaluated in amniocentesis? Hyaline membrane disease; preterm infants (<34 weeks gestation) immaturity of type II pneumocytes, inadequate surfactant; lecithin and sphyngomyelin ratio measured for lung maturity.
What are clinical factors of bacterial pneumonia? Abrupt onset of high fever, malaise and productive cough; lead to lung abscess and brain abscess
What are clinical features of viral pneumonia? Caused by cytomegalo virus; low grade fever, dry cough, HA and malaise.
What is a lung abscess? Localized accumulation of pus with cough, fever and foul-smelling sputum.
What can cause a lung abscess? (3) 1. Alcoholic: aspiration MC cause 2. Pneumonia 3. Aspiration at dentist's office
What is primary TB? Caused by mycobacterium tuberculosis inhalation that replicates in alveoli and leads to form'n of Ghon's focus, Ghon's complex and may become secondary TB (5% of cases)
What is Ghon's focus w/ primary TB? Peripheral parenchymal granuloma in the upper lobes, 1-2cm in diameter w/ a central necrosis.
What is secondary TB? Reactivation of the primary TB or reinfection; mult. granulomas w/ extensive tissue necrosis in any part of lung
What can happen with secondary TB? May heal or calcify or may erode into a bronchus & cause a tuberculous cavity w/ caseous necrosis; complications: miliary TB and hemoptysis, can get in blood and then can travel anywhere (e.g. Pott's)
What is different w/ TB that is not seen in pulmonary embolism? Fever and organisms in sputum.
What is COPD and what is involved? Chronic OBSTRUCTIVE Pulmonary Disease; Tubes are involved w/ "obstructive"
What is included in COPD? Chronic bronchitis and Emphysema
What characterizes COPD? Decreased forced expiratory volume Decreased air flow either by an increase in resistance w/in the airways or a reduction in the outflow pressure.
What causes increased resistance in airways and reduction in outflow pressure? Narrowed airways in chronic bronchitis or asthma; Loss of elastic recoil as in emphysema
What is chronic bronchitis? Inflammation of the bronchi w/ persistent productive cough for at least 3 months for 2 successive years.
What can cause chronic bronchitis? Tobacco smoke, dust, fumes and pollution
What are clinical factors of chronic bronchitis? Begin as winter cough lasts 2 years (steady increase w/ lot of sputum); Wheeze, dyspnea & tightness in chest especially in the am; w/ progression exertional dyspnea, cyanosis &/or cor pulmonale.
What is emphysema? Enlargement of the alveoli distal to the terminal bronchioles w/ destruction of the interalveolar septum.
What causes emphysema? Alpha1 antitrypsin deficiency and cigarette smoking
How does a patient present with emphysema? Prolonged history of exertional dyspnea (low O2) and a minimal non-productive cough.
What is asthma? A chronic inflam disorder of the airways that causes recurrent episodes of expiratory wheezing, breathlessness, chest tightness and coughing esp. at night or early am. A cond'n where bronchial tubes in lungs react to different stimuli by becoming inflamed
What is recurrent and reversible asthma? Asthma usually associated w/ widespread but variable airflow obstruction that is often reversible
What is chronic and lethal asthma? Severe continuing attack of asthma (status asthmaticus) is a serious concern that can lead to respiratory failure and death.
What are stimuli/triggers for asthma? exercise, cold air, allergens, infections, emotional reactions and certain medications. Inflammation leads to bronchoconstriction. Type I hypersensitivity reaction.
What are s/s of asthma? Expirational wheezing, shortness of breath, tightness in chest and coughing.
What is Bronchiectasis? abnormal and irreversible dilatation of the bronchi and bronchioles proximal to the terminal brochioles w/ degeneration of elastic and muscular tissue d/t inflam. and accumulation of leukocytes.
What are clinical factors of bronchiectasis? chronic cough; foul-smelling, large volume of sputum; fever
What is cystic fibrosis? A hereditary disorder, abnormal viscous secretion of all the exocrine glands in the body.
What glands are affected in cystic fibrosis and what does this lead to? Lung - lower respiratory infections Pancreas - steatorrhea (fatty stools)
What are clinical factors of cystic fibrosis? increased thick mucus; decreased mucociliary clearance; increased bacterial infections
What is chronic restrictive lung disease (CRPD)? Non-infectious disorder caused by dust characterized by diffuse fibrosis involving lung parenchyma.
What is pneumoconiosis? An occupational dust Dz characterized by inhalation of organic dust, fumes, etc. a latent period b/w exposure and onset of clinical Dz
What are the 4 classifications of pneumoconiosis? 1. Anthracosis 2. Silicosis 3. Asbestosis 4. Berylliosis
What is anthracosis? MC pneumoconiosis; coal worker's pneumoconiosis, exposure to carbon dust.
What is Silicosis? Industrial worker's pneumoconiosis, exposure to grinding of stone, glass, sand, etc.
What is Asbestosis? Most important pneumoconiosis; in brake linings, insulation, shipyard workers; increased risk of malignant mesothelioma and bronchogenic carcinoma.
What is Beryllosis? A pneumoconiosis that is common in workers of the aerospace industry.
What is sarcoidosis? A systemic disorder of idiopathic origin; commonly manifests in the lungs and lymph nodes and is associated w/ abnormalities of the immune system
What are characteristics of sarcoidosis? non-casesating granulomas in lung and when they heal by organization lead to pulmonary fibrosis.
What are clinical factors of sarcoidosis? Gradual onset of increasing dyspnea w/ hilar lymph node involvements.
What 4 conditions have pulmonary fibrosis? 1. TB 2. Pneumoconiosis 3. Goodpasture syndrome 4. Sarcoidosis
What is Goodpasture syndrome? An interstitial lung and kidney disorder.
What is goodpasture syndrome characterized by? hemoptysis, hematuria, anemia, pulmonary fibrosis, presence of circulating anti-glomerular basement membrane antibodies.
What are risk factors for carcinoma of the lung? Cigarette smoking, beryllium, asbestose, radiation and a variety of genetic alterations.
What are the well differentiated types of lung carcinoma? Squamous cell carcinoma and Adenocarcinoma
Describe squamous cell carcinoma of the lung. MC type; near center of the lung; associated w/ smoking; silent until causes narrowing of bronchi; Arises from PSCC
Describe Adenocarcinoma of the lung. Arises from pneumocytes; chest x-ray shows peripheral coin lesions (alveolar cancer)
What are the undifferentiated types of lung carcinoma? Small cell carcinoma and Large cell carcinoma
Describe small (oat) cell carcinoma. Arises from the neuroendocrine cells - highly malignant, fast growing, strongly associated w/ smoking; secretes ectopic hormones like ADH and ACTH (paraneoplastic syndrome)
What are the pulmonary effects of undifferentiated types of lung carcinoma? cough, dyspnea, hemoptysis, chest pain, obstructive pneumonia, pleural effusion.
What is pancoast syndrome? Involvement of lung apex by tumor may involve C8, T1, T2 nerves and can lead to Horner's syndrome where cervical sympathetic ganglions are affected.
What is pneumothorax? Air in the pleural cavity.
What are the clinical features of pneumothorax? Sudden pain or feeling of tightness on the affected side; affected by deep inspiration, sudden onset of severe dyspnea. Lead to severe respiratory distress.
What is spontaneous pneumothorax? Air in the pleural cavity following the rupture of alveolus (inside - out)
What is traumatic pneumothorax? Air in the pleural cavity following penetrating injuries to the chest (i.e. rib Fx)
What is pleural effusion? collection of excess fluid in the pleural cavity d/t benign or malignant causes.
What are the different types of pleural effusions and their causes? (5) 1. Hydrothroax (heart failure patients) 2. Pyothorax (pus) and empyema (both complicated pneumonia) 3. Hemothorax (malignancy or trauma) 4. Chylothorax (lymphatic obstruction)
What is malignant mesothelioma? Cancer of the pleura, d/t asbestos exposure. 15-20 years may elapse b/w exposure and dev. of tumor
What are the predominant symptoms of malignant mesothelioma? Progressive chest pain and dyspnea; history of work
Created by: kabrown