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NURS 617 EXAM 5 (NEW 2025/ 2026 UPDATE) PHARMACOTHERAPEUTICS GUIDE| QS & AS| GRADE A+, Exams of Pharmacology

University of Southern Indiana (USI)Pharmacology

3 factors governing blood flow - ANS ✓pressure, resistance, flow -increase in viscosity and decrease in temp=decrease in blood flow Compliance - ANS ✓-total quantity of blood that can be stored in a given portion of circulation for each mm HG increase in pressure -compliance=increase in volume/increase in pressure; ability to increase of decrease depending on BP -most distended=veins Pre load vs after load vs inotropy - ANS ✓-pre-load: ventricular filling/enddiastolic pressure; volume of blood prior to systole, largely determined by venous return to heart -after-load: resistance of ejection of blood from the heart; pressure muscles are exerted to move blood into aorta and around body; aortic stenosis can increase afterload -inotropy: force of cardiac contractility; increase in inotropy=increase in ejection fraction + SV Heart Sounds S1 S2 S3 S4 - ANS ✓S1 - normal; lub, produced by closure of the mitral valve S2 - norma; dub, produced by closure of the aortic valve

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NURS
NURS617
NURS617/ NURS 617 EXAM 5 (NEW 2025/ 2026
UPDATE) PHARMACOTHERAPEUTICS GUIDE| QS & AS|
GRADE A| 100% CORRECT (VERIFIED ANSWERS)-
3 factors governing blood flow - ANS ✓pressure, resistance, flow
-increase in viscosity and decrease in temp=decrease in blood flow
Compliance - ANS ✓-total quantity of blood that can be stored in a given portion
of circulation for each mm HG increase in pressure
-compliance=increase in volume/increase in pressure; ability to increase of
decrease depending on BP
-most distended=veins
Pre load vs after load vs inotropy - ANS ✓-pre-load: ventricular filling/end-
diastolic pressure; volume of blood prior to systole, largely determined by
venous return to heart
-after-load: resistance of ejection of blood from the heart; pressure muscles are
exerted to move blood into aorta and around body; aortic stenosis can increase
afterload
-inotropy: force of cardiac contractility; increase in inotropy=increase in ejection
fraction + SV
Heart Sounds
S1
S2
S3
S4 - ANS ✓S1 - normal; lub, produced by closure of the mitral valve
S2 - norma; dub, produced by closure of the aortic valve
S3 - abnormal; early diastole, occurs after the mitral valve opens; rapid
ventricular fillingsyss
S4 - abnormal; late diastole, occurs during atrial contraction
**S3 + S4=indicative of resistance of ventricular filling
Law of laplace - ANS ✓-pressure is directly proportional to surface tension and
inversely proportional to radius of alveolus
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Partial preview of the text

Download NURS 617 EXAM 5 (NEW 2025/ 2026 UPDATE) PHARMACOTHERAPEUTICS GUIDE| QS & AS| GRADE A+ and more Exams Pharmacology in PDF only on Docsity!

NURS

NURS617/ NURS 617 EXAM 5 (NEW 2025 / 2026

UPDATE) PHARMACOTHERAPEUTICS GUIDE| QS & AS|

GRADE A| 100% CORRECT (VERIFIED ANSWERS)-

3 factors governing blood flow - ANS ✓pressure, resistance, flow

  • increase in viscosity and decrease in temp=decrease in blood flow Compliance - ANS ✓-total quantity of blood that can be stored in a given portion of circulation for each mm HG increase in pressure
  • compliance=increase in volume/increase in pressure; ability to increase of decrease depending on BP
  • most distended=veins Pre load vs after load vs inotropy - ANS ✓-pre-load: ventricular filling/end- diastolic pressure; volume of blood prior to systole, largely determined by venous return to heart
  • after-load: resistance of ejection of blood from the heart; pressure muscles are exerted to move blood into aorta and around body; aortic stenosis can increase afterload
  • inotropy: force of cardiac contractility; increase in inotropy=increase in ejection fraction + SV Heart Sounds S S S S4 - ANS ✓S1 - normal; lub, produced by closure of the mitral valve S2 - norma; dub, produced by closure of the aortic valve S3 - abnormal; early diastole, occurs after the mitral valve opens; rapid ventricular fillingsyss S4 - abnormal; late diastole, occurs during atrial contraction **S3 + S4=indicative of resistance of ventricular filling Law of laplace - ANS ✓-pressure is directly proportional to surface tension and inversely proportional to radius of alveolus

NURS

  • wall tension increases as wall becomes thinner, wall tension decreases as wall becomes thicker Frank-Starling Mechanism - ANS ✓-A mechanism by which the stroke volume of the heart is increased by increasing the venous return of the heart (thus stretching the ventricular muscle).
  • allows heart to adjust pumping ability to accommodate venous return
  • increase in force of contract=increase in ventricular end diastolic volume Pulmonary vs. Systemic Circulation: pressure/resistance - ANS ✓pulmonary=low pressure, low resistance; avg 90mm Hg; right side of heart Systemic=high pressure, high resistance; avg 12mm Hg; left side of heart Blood flow through the heart - ANS ✓ 1 - Superior & Inferior Vena Cava, 2-Rt Atrium, 3-Tricuspid Valve, 4- Rt Ventricle, 5-Pulmonary Valve, 6-Pulmonary Artery, 7- Lungs-pick up oxygen, 8-Pulmonary Veins, 9- Lt Atrium, 10- Mitral Valve (Bicuspid), 11-Lt Ventricle, 12- Aortic Valve, 13-Aorta, 14- Body, repeat Lub vs dub - ANS ✓lub=mitral and tricuspid valves shutting Dub=shutting of aortic and pulmonary (semilunar) valves Pericardium - ANS ✓-A loose-fitting membrane that encloses the heart, consisting of a superficial fibrous layer and a deep serous layer
  • holds heart in fixed position
  • protects from infection and physical trauma Myocardium - ANS ✓-muscular, middle layer of the heart; cardiac muscle, behaves as a single unit
  • regulated by tropomyosin and troponin complex (T and I)
  • calcium retrieved from skeletal muscles for contraction Endocardium - ANS ✓-innermost layer of the heart; 3 thin layers
  • inner=smooth endocardium 4 heart valves and roles - ANS ✓R ventricle: pumps blood to lungs L ventricle: pumps blood to systemic circulation R atrium: receives blood returning to heart from circulatuin L atrium: receives oxygenated blood from lungs Fibrous skeleton of the heart - ANS ✓-4 interconnecting valve rings

NURS

  • s/s: chest pain relieved by leaning forward, pericardial friction rub, increased ESR & CRP Tx: nsaids, abx, corticosteroids, colchicine Pericardial Effusion and Cardiac Tamponade - ANS ✓-accumulation of fluid in the pericardial cavity
  • extensive pericardial effusion leads to cardiac tamponade; excess fluid in the pericardial cavity limit the expansion of the heart during cardiac filling
  • s/s: pulsus paradoxus (weak pulse during inspiration, strong during exhalation; compressed L ventricle=less output & ventricle filling), cushing's triad (tachy, narrowed pulse pressure, jugular vein distention), shock
  • tx: pericardiocentesis, nsaids, corticosteroids, colchicine Constrictive pericarditis - ANS ✓-causes: tuberculosis (developing world); systemic lupus erythematosus (developed world)
  • calcified scar tissue develops on pericardium, causes decrease in diastolic filling; causes equalization of end-diastolic pressures in all 4 chambers (R side filling pressures normally lower than L side)
  • s/s: ascites, jugular vein distention, weight loss, muscle wasting, pedal edema, dyspnea on exertion
  • tx: pericardiectomy Coronary artery disease (CAD) - ANS ✓-a condition affecting arteries of the heart that reduces the flow of blood and the delivery of oxygen and nutrients to the myocardium; most often caused by atherosclerosis
  • development is usually slow, progressive
  • dx: exercise stress test (CAD=chest pain, SOB, ST-segment changes, decrease in BP), echo, EKG, arteriography, cardiac cath Stable vs unstable angina - ANS ✓stable - a pattern of symptoms that has unchanged for 6 or more weeks; more during stress/exercise Unstable - a pattern of symptoms that is new in onset, changing in severity or frequency, occurring at rest, or lasting longer than 20 minutes. 3 factors controlling coronary circulation - ANS ✓HR, L ventricular contractility, systolic pressure
  • HR=most important; increase HR=increase O2 consumption, decreased diastolic filling time
  • regulated by O2 needs

NURS

Vasodilator drugs - ANS ✓1. Adenosine

  1. Nitric oxide
  2. Dopamine/dobutamine - increases myocardial contractility and SV Acute coronary syndrome (ACS) - ANS ✓-sudden symptoms of insufficient blood supply to the heart indicating unstable angina or acute myocardial infarction d/t unstable atherosclerotic plaques
  • s/s: increased troponin I/T/creatine kinase, abnormal Q wave/T wave inversion/ST segment elevation, angina at rest >20min ST-segment elevation MI: s/s + tx - ANS ✓-ischemic death of myocardial tissues; usually abrupt, or chronic is progressed from unstable angina/NSTEMI
  • s/s: substernal pain that radiates to L arm/neck/jaw, N/V, frothy pink mucous...eventually leads to shock d/t low CO
  • death d/t MI happens within 1h of s/s onset d/t arrythmias
  • results in scar tissue & decreased ability to contract heart
  • tx: thrombolytic agent within 60-90min, nitro, o2, nitrates, aspirin, pain (morphine), beta-blockers, reperfusion therapy (re-establish blood flow to heart to prevent necrosis, eg: CABG), fibrinolytic therapy (TPA) to dissolve unstable plaques Chronic ischemic heart disease: types of angina - ANS ✓-Chronic stable angina, silent myocardial ischemia, and variant or vasospastic angina
  • stable=fixed coronary obstruction; less blow flow=increased metabolic needs of myocardium
  • silent MI=no anginal pain, shorter episodes, less area effected; diabetes=increased risk d/t neuropathy
  • variant angina=d/t vasospasm; happens more @ night and w/ rest, EKG changes & arrythmias during attack
  • pectoris=pain precipitated by stress, cold, exercise *dx: EKG, stress test, echo; usually have high ldls, low hdls, insulin resistance Ischemic cardiomyopathy - ANS ✓-a weakness in the muscle of the heart due to coronary artery disease because of inadequate oxygen delivery to the myocardium
  • usually results in congestive heart failure, but ischemia can be reversed if treated in time Cardiomyopathy types - ANS ✓-Hypertrophic, Dilated, Restrictive
  • Due to: Ischemia, Genetic problems, Systemic Disease (primary d/t genetics or secondary d/t diabetes, cancer drugs, pregnancy, infection, HTN)

NURS

Fetal heart development + circulation (fetal + perinatal) - ANS ✓-heart develops between 4-7 weeks of gestation; first functioning organ in embryo

  • fetal=o2 through placenta; fetal cardiac output +HR=higher d/t lower spo
    • perinatal=o2 in lungs Heart disease in pediatrics: prophylactic measures - ANS ✓-prophylactic abx before dental procedures d/t risk of IE and RF Patent ductus arteriosus (PDA) - ANS ✓-common in kids; an abnormal opening between the pulmonary artery and the aorta caused by failure of the fetal ductus arteriosus to close after birth
  • failure to divert blood from R side of heart away from lungs; leads to pulmonary HTN and congestion
  • s/s: machine like murmor continuous through systole + diastole, widened pulse pressure
  • if untreated=results in congestive HF, IE, calcification, thrombus formation, aneurysm formation Arterial septal defect - ANS ✓-Increased pulmonary blood flow, risk for pulmonary vascular disease; increase in blood volume that must be ejected from R side; prolongs closure of pulmonary valve and produces separation of aortic + pulmonary components
  • there is a hole between the atria; oxygenated blood from the left atrium is shunted to the right atrium and lungs
  • do not compromise children seriously; surgical closure is recommended before school age; can lead to congestive heart failure or atrial dysrhythmias later in life if not corrected Tetralogy of Fallot (TOF) - ANS ✓-set of 4 congenital heart defects occurring together; blood shunted from R to L
  • ventricular septal defect, dextroposition of the aorta, R ventricular outflow obstruction, R ventricular hypertrophy
  • s/s: hypercyanotic "tet" spells (d/t crying, feeding, pooping d/t increased pulmonary resistance causing decreased pulmonary blood flow)
  • tx: surgery, knee to chest position Transposition of the great vessels - ANS ✓-a congenital abnormality where the aorta is attached to the right ventricle and the pulmonary artery to the left ventricle (this is backwards and leads to two separate blood routes)
  • surgery needed

NURS

Coarctation of the aorta (coa) - ANS ✓-severe congenital narrowing of the aorta

  • s/s: weak distal lower extremity pulses, bounding proximal (ex: carotid and brachial), BP higher in arms than in legs (normally higher in legs by 10-20 mm Hg)
  • surgery needed; risk for HTN post-op Kawasaki disease - ANS ✓-immune response causes inflammation of blood vessels (hence the strawberry tongue) & coronary artery aneurysms
  • effects skin, brain, eyes, heart, liver, and lymph nodes
  • acute phase=4-8 weeks; abrupt fever, conjuctivitis, rash, swelling/edema, unresponsiveness to abx
  • can lead to pericarditis, mitral regurgitation, myocarditis
  • subacute=8 weeks-4y; peeling skin, s/s slowly disappear Pathophysiology of shock - ANS ✓Decreased Blood Volume Decreased Venous Return Decreased Stroke Volume Decreased Cardiac Output Decreased Tissue Perfusion Impaired cellular metabolism/death Cardiogenic shock - ANS ✓-not enough oxygen is delivered to the tissues of the body d/t low CO/hypotension/hypoxia
  • severe complication of a large acute myocardial infarction or DVT Hypovolemic shock - ANS ✓shock resulting from blood or fluid loss, most common Obstructive shock - ANS ✓-Shock that occurs when there is a block to blood flow in the heart or great vessels, causing an insufficient blood supply to the body's tissues
  • ex: DVT, atherosclerosis Distributive shock - ANS ✓-Shock due to a shift of fluid from blood to tissues; results in low BP, loss of blood vessel tone, or enlarged vascular compartment
  • ex: serious burns, hypothermia Complications of shock - ANS ✓Acute renal failure Shock lung, acute lung injury, or adult respiratory distress syndrome

NURS

  • EKG detects early ischemia and prevents early MI complications
    • improper lead placement can change QRS Mechanisms of arrhythmias and conduction dx - ANS ✓1. Automaticity: specific cells spontaneously initiating an impulse
  1. Excitability: cells ability to respond to an impulse
  2. Conductivity: cells ability to conduct impulses
  3. Refractoriness: extent of cells to respond to stimulus *cardiac scar tissue slowens conduction, increases chance of unilateral block & arrythmias Respiratory sinus arrythmia - ANS ✓-normal P, QRS and T waves but the heart rate varies with respiration - the rate increases on inspiration and decreases on expiration
  • more common in kids Sinus bradycardia - ANS ✓< Normal sinus rhythm, origin=SA node Can be d/t rx, athletes Sinus Tachycardia - ANS ✓>100 bpm Normal sinus rhythm, origin=SA node Can be d/t fever, blood loss, anxiety, exercise, SNS stimulation, loss of vagal tone Supraventricular vs ventricular arrythmias - ANS ✓-supraventricular=dx of atrial rhythm or conduction above the ventricles (ex: afib, a flutter, PAC)
  • ventricular=dx of ventricular rhythm or conduction; can be life threatening (ex: vtach, vfib) Premature arterial contraction (PAC) - ANS ✓-arrhythmia in which atria contract earlier than they should; SA node does not reach AV
  • additional P wave Atrial Tachycardia - ANS ✓Rate: 150- 250 beats per minute Regularity: regular P-waves: may be upright or inverted will appear different from underlying rhythm; up to 3 P waves QRS-complex: Normal PR interval- may be normal, shortened, or prolonged

NURS

Atrial flutter - ANS ✓-irregular beating of the atria (240-450 bpm); re-entry of rhythm in R atria

  • sawtooth pattern; no observable p wave Atrial Fibrillation (A-Fib) - ANS ✓-an irregular and often very fast heart rate originating from abnormal conduction in the atria; atrial cells cannot repolarize in time for next stimulus
  • atria=400-600bpm, ventricles=80-180bpm
  • can occur w and w/o cardiac disease
  • absent p wave, widened QRS
  • pulse deficit: difference in apical rate and peripheral pulses **need anticoag rx Paroxysmal Supraventricular Tachycardia (PSVT) - ANS ✓-A regular, narrow- QRS tachycardia that starts or ends suddenly
  • can be d/t AV node re-entry
  • HR 140-240 BPM Premature ventricular contraction (PVC) - ANS ✓-a ventricular contraction preceding the normal impulse initiated by the SA node (pacemaker)
  • QRS occurs before P wave Ventricular tachycardia (V-tach) - ANS ✓-A life-threatening heart rhythm in which there is very rapid contraction of the ventricles, and the heart does not pump blood at all
  • wide, tall, bizarre QRS; absent p wave. 70-250bpm
  • origin=bundle of his Ventricular fibrillation (V-fib) - ANS ✓-abnormal heart rhythm which results in quivering of ventricles
  • no cardiac output, no palpable/audible pulses
  • VFIB=DEFIB!
  • BPM=150- 500 First degree AV block - ANS ✓Prolonged PR interval (>0.20); delayed AV conduction Second degree AV block - ANS ✓-missed beats; action potential is not reaching the AV node, failure of conduction from atria to ventricles
  • causes more p waves

NURS

  • alveoli: terminal air space for resp tract; gas exchange between air and blood. Contains brush cells (monitor air quality of lungs) and macrophages (remove debris from lungs) Alveoli: type I vs II pneumocytes - ANS ✓I: 95% of cells; create barrier between air and alveoli wall, cannot divide II: 5%; synthesize surfactant, which decreases surface tension of alveoli to aid in expansion/inflation; starts maturing at 26-27 weeks, betamethasone used for pre-term babies to prevent ards Pulmonary vs bronchial circulation - ANS ✓Pulmonary Circulation=deoxygenated blood that flows from the right ventricle to the alveoli to be oxygenated. It returns to the heart via the pulmonary vein. Bronchial Circulation=oxygenated blood that flows from the left ventricle (via the thoracic aorta) to supply the tissues of the lungs and tracheobronchial tree; some of the now-deoxygenated blood returns to the heart via the pulmonary vein, some by the bronchial veins, and some by the bronchopulmonary veins.
  • can undergo angiogenesis (formation of new vessels) Lymphatic circulation: resp system - ANS ✓-superficial vessels: drains surface of the lungs, travels through connective tissue of visceral pleura
  • deep lymphatic vessels: drains the pulmonary artery/veins, bronchial tree through bronchioles **aids in removal of particulates/plasma proteins to prevent excess fluid in the pleural cavity Pleura of the lungs - ANS ✓-serous membrane that lines the lungs; outer surface adheres to thoracic wall, inner adheres to lungs
  • serous fluid between the 2 layers help protect the pleura
  • inflammation of pleura = pleural effusion; produces machine-like sound **pleura=only part of lung w/ pain receptor Lung volumes - ANS ✓-tidal volume=500ml
  • inspiratory reserve volume=air inspired in excess of the tidal volume
  • expiratory reserve volume=volume of air expired in excess of tidal volume
  • residual volume=volume of air remaining in lungs after max expiration Pulmonary function tests: forced vital capacity - ANS ✓-max air that is rapidly/forcefully exhaled after full inspiration
  • lower in obstructive diseases

NURS

Pulmonary function tests: maximal voluntary ventilation - ANS ✓volume of air moved in and out max effort for 12-15 sec Pulmonary function tests: forced expiratory volume - ANS ✓-air expired in the first second of forced vital capacity

  • used in diagnosis of obstructive disorders Pulmonary function tests: forced inspiratory volume - ANS ✓-respiratory response during maximal inspiration
  • mid-expiratory flow rate=measurement of respiratory muscle dysfunction
  • inspiratory flow relies more on effort Pulmonary function tests: minute volume - ANS ✓-amount of air exchanged in 1 min; dependent on metabolic needs
  • minute volume: 6,000ml=500ml (tidal volume) X RR
  • stiff/noncompliant: decreased VT and increased RR to meet needs
  • obstructive: increased VT and decreased RR to meet needs Dead air space - ANS ✓-air that occupies the space between the mouth and alveoli (conducting airways) but that does not actually reach the area of gas exchange
  • increase in anatomic (150-200ml=normal) and alveolar (5-10ml=normal), dead space=increased lung disease
  • ventilation w/o perfusion in dead space can result in pulmonary embolism Inspiration and expiration: impact on intrathoracic pressure - ANS ✓- inspiration=decrease in intrathoracic pressure
  • expiration=increase in intrathoracic pressure Pulmonary shunt - ANS ✓-blood moves from L to R side of circulation without being oxygenated
  • anatomic: venous to arterial side without passing through lungs; congenital heart defect
  • physiologic: insufficient ventilation to provide o2 to blood in alveolar capillaries (ex: HF, destructive lung disease)
  • perfusion w/o ventilation can result in atelectasis or airway obstruction Gas exchange in lungs - ANS ✓-Occurs via diffusion
  • O2 concentration is higher in the lungs than in the blood, so O2 diffuses into blood

NURS

Tuberculosis - ANS ✓-Mycobacterium tuberculosis - enters lungs via air, triggers cell-mediated hypersensitivity response

  • lytic enzymes released in lung and causes damage; result in ghon complex (lung lesion)
  • healed dormant lesion=latent TB; can be reactivated
  • s/s: fatigue, fever, weight loss, night sweats, chest pain, dry cough, anemia, dyspnea Small cell lung cancer - ANS ✓- 20 - 25% of lung cancers; rapidly growing tumor in bronchioles that tends to metastasize quickly, oftenly to brain
  • strong association w/ tobacco
  • causes neoplastic syndrome - tumor secretions (hormones, cytokines, TNF, Interleukin-1), may cause hypercalcemia, hypoglycemia, SIADH Non-small cell lung cancer - ANS ✓-Squamous cell carcinoma (25-40%); common in men and smokers; originates in central bronchi, spreads centrally; causes neoplastic syndrome
  • Adenocarcinoma (20-40%): common in women and non-smokers; originates in bronchiolar or alveolar tissue
  • Large cell carcinoma (10-15%): metastasizes early, originates in outer edge of lung, invades bronchi and large airways S/s of lung cancer - ANS ✓-dry hacking cough
  • hoarseness
  • dyspnea
  • haemoptysis/rust coloured sputum
  • pain in chest area
  • diminished breath sounds/wheezing
  • pleural effusion
  • common areas of metastasis: brain, liver, bone RDS in infants - ANS ✓-most common in pre terms born gestation < 34 weeks
  • s/s: nasal flaring, grunting, tachypnea, accessory muscle use
  • betamethasone (surfactant) used in infants up to 36 weeks of gestation Role of surfactant in the lungs - ANS ✓coats inner surface of alveoli and reduces surface tension in alveoli to prevent collapse during expiration Signs of respiratory distress in newborn - ANS ✓Nasal flaring, cyanosis, retractions (ribs)- supra sternal, substernal and intercostal, see saw breathing or abnormal movement of chest/abdomen, increased RR + HR, confusion

NURS

Viral vs spasmodic croup - ANS ✓-aka laryngotracheobronchitis; impacts upper

  • lower airway
  • viral=barking cough & inspiratory stridor; treat with racemic epinephrine & glucocorticoids if stridor at rest
  • spasmodic croup=acute onset of stridor croup at night, resolves without treatment; usually d/t allergies Epiglottitis - ANS ✓-severe, life-threatening infection of the epiglottis and supraglottic structures that occurs most commonly in children between 2 and 12 years of age
  • upper airway bacterial infection; d/t Haemophilus influenzae type B (HIB)
  • tx: IV ABX, fluids, corticosteroids Respiratory Syncytial Virus (RSV) - ANS ✓-A virus that causes an infection of the lungs and breathing passages; can lead to other serious illnesses that affect the lungs or heart, such as bronchiolitis and pneumonia
  • highly contagious and spread through droplets
  • usually URI but can spread to lower resp Signs of impending respiratory failure in children - ANS ✓-size of airways in infants/small children results in respiratory distress being more serious
  • s/s:cyanosis not relieved by oxygen administration, HR 150+, RR 60+ in newborns/30+ in children, retractions of intercostal spaces/sternum, fatigue, extreme anxiety/agitation, grunting, decreased chest movement Chylothorax pleural effusion - ANS ✓-Collection of chylous (lymph fluid) usually d/t local infection OR trauma
  • most common in fetus/neonates
  • white, milky fluid in lymph (chyle) Parapneumonic pleural effusion - ANS ✓-exudates that accompany bacterial pneumonias; can cause lung abscess
  • common after tx w/ pneumonia; if pt is stable and asymptomatic there is no more testing needed Transudative pleural effusion - ANS ✓-LDH and protein levels increase; fluid in pleural space
  • d/t bacterial pneumonia and viral infections

NURS

  • most common causes=recurrent infections and smoking Chronic interstitial (restrictive) lung disease - ANS ✓-group of lung disorders producing inflammatory and fibrotic changes; effect collagen/elastic connective tissues of alveolar walls, which causes decreased lung volume/hypoxemia/decreased diffusion
  • insidious; 1st sign=SOB w/ exercise, non-productive cough, wheezing, hypoxemia @ rest, hypercapnia/resp acidosis
  • examples: pulmonary fibrosis, interstitial pneumonia, asbestosis, sarcoidosis Acute lung injury (ALI)/Acute respiratory distress syndrome (ARDS) - ANS ✓-rapid onset within 12-18h after event (infection, trauma, chronic lung disease or neuromuscular disease)
  • respiratory system fails gas exchange and/or ventilation
  • local and systemic inflammatory response; causes widespread endothelial injury, increases permeability of alveolar membrane and becomes filled with fluid...lungs become stiff and difficult to inflate
  • results in hypoxemia, hypercapnia, respiratory acidosis Acute respiratory failure: ventilation vs perfusion/vent mismatching - ANS ✓ventilation=normal perfusion w/ inadequate ventilation d/t insufficient o2 to alveoli and retained co2; d/t upper airway obstructions, chest wall injury, or weakness/paralysis of respiratory muscles Perfusion/ventilation mismatching=adequate ventilation w/ inadequate perfusion OR perfused but not ventilated; hypoxemic failure; d/t advanced COPD, severe pneumonia, or atelectasis Cystic fibrosis - ANS ✓-two copies of recessive allele (transmembrane conductance regulator (CFTR) gene)
  • characterized by an excessive secretion of mucus and consequent vulnerability to infection; fatal if untreated
  • GI manifestations (fatty stool) Right ventricular hypertrophy with cor pulmonale - ANS ✓-causes pulmonary HTN, results in hypertrophy of R ventricle and eventually R side HF
  • severe fluid build up in lungs can lead to shock Atherosclerosis development: 3 stages - ANS ✓1. Endothelial injury (smoking, obesity, HTN); causes increase in adhesion of platelets + phagocytic monocytes

NURS

  1. Migration of inflammatory cells; macrophages engulf lipoproteins (ldls) and creates "foam-like" cells
  2. Fibrous plaque forms; central core=lipid-laden foam cells. Can result in haemorrhage into plaque or thrombotic occlusion Atherosclerosis vs arterial sclerosis - ANS ✓atherosclerosis=type of arterial sclerosis Arterial sclerosis=hardening/thickening of vessel wall; loss of elasticity Arterial vs venous disease - ANS ✓arterial=decreased blood flow to tissues Venous=decreased blood return + removal of waste products Arterial circulation: 3 diseases - ANS ✓1. Atherosclerosis: progressive dx d/t formation of fibrofatty plaques in large or medium arteries. Risk factors=hyperlipidemia & inflammation
  3. Vasculities: inflammation of blood vessels (arteries/veins/capillaries); d/t direct injury, infection, or immune process
  4. Aneurysms: dilation of artery d/t weakness in vessel wall; as size increases, % of rupture increases Lipid levels + role: total, LDL, HDL - ANS ✓total: <200 (high risk=240+) LDL: <100; carries cholesterol to peripheral tissues HDL: 40+; protective; removes cholesterol from tissues to liver for disposal **liver=major role in LDL metabolism; poor liver function=increased ldls Atherosclerosis: risk factors + arteries effected - ANS ✓-HTN, smoking, AA race, diabetes, age, genetic predisposition (low LDL receptors=increase risk d/t increased need for macrophages to digest lipids; forms foam cells)
  • birth control, HIV meds, beta-blockers, estrogens
  • arteries supplying heart, brain, kidneys, lower extremities, small intestine Athersclerosis: 3 types of lesions - ANS ✓1. Fatty streak - yellow
  1. Fibrous plaque - grey/pearly
  2. Complicated lesion - scar tissue, ulceration, thrombosis risk Giant Cell Arteritis (Temporal Arteritis) - ANS ✓-granulomatous inflammation of aorta + its major branches (ex: carotid); autoimmune panarteritis d/o frequently affecting the temporal artery (lupus, RA)
  • s/s: blurred vision or diplopia, fever, myalgia, arthralgia. Increased CRP & ESR
  • risk for aortic aneurysm
  • tx: high dose corticosteroids