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Cardiovascular, Pulmonary, Renal, Genitourinary System: A Review with Exercises, Exams of Nursing

NURS 3366 EXAM 3 REVIEW/NURS 3366 EXAM 3 REVIEW/NURS 3366 EXAM 3 REVIEW/NURS 3366 EXAM 3 REVIEW/NURS 3366 EXAM 3 REVIEW/NURS 3366 EXAM 3 REVIEW

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2021/2022

Available from 06/16/2022

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EXAM 3 REVIEW: Cardiovascular, Pulmonary, Renal,
Genitourinary
Right atrium tricuspid valve right ventriclepulmonic valvepulmonary artery
pulmonary arteriolespulmonary capillaries [gas exchange with alveoli occurs here]
pulmonary venules pulmonary veinsleft atriummitral valveleft ventricle aortic
valve
aorta
part of this freshly oxygenated blood goes into coronary arteries,
which branch off the aorta just beyond the aortic valve.
part goes up to brain via carotids
rest goes to tissue beds of remainder of body
arterioles capillaries [gas exchange with tissue occurs here ] venules
veinsinferior vena cava (from body) or superior vena cava (from head) right
atrium
PERIPHERAL VASCULAR SYSTEM
Venous: vessels that carry deoxygenated blood from tissues to right side of heart
Healthy veins: Facilitate good venous return & prevent backflow;
Bad Veins: bad valves ⟶ backflow ⟶ venous congestion peripheral tissue edema;
stasis
& immobility
sluggish blood flow
Chronic Venous Insufficiency (CVI): backflow (congestion) of blood into distal
veins of legs & feet
Floppy valves ⟶ blood backflow ⟶ congestion & stasis of blood in legs & feet ⟶
increased hydrostatic pressure ⟶ engorged veins ⟶ pushes fluid into tissues ⟶
edema ⟶
S&S
S&S: edema
swollen, tight, dry, discolored skin; venous stasis ulcers
(tissue breakdown from edema/poor cell fxn), thrombi, varicose veins (+
hydrostatic pressure
backflow pressure to surface veins)
Risk factors: standing for too long, pregnancy, old people, genetics, immobility
Tx: encourage mobility, hydration, elevate legs for venous return, blood
thinners, look for skin breaks, TED hose
Deep Vein Thrombosis (DVT): clot on vein wall, usually deep vein in thigh/calf
S&S: Thrombophlebitis, redness/pain/erythema/warmth (inflammatory
signs), edema, unilateral
Risk factors: 1+ element of Virchow’s Triad
Virchow’s Triad: injury to endothelium of vein (ex. surgery), stasis of blood
flow (ex. muscles not pumping/venous insuff), hypercoagulability (ex.
Dehydration)
Couch potato, casts, bed-ridden, pregnant, obese,
diuretics/hormone therapy, CVI
Sequela of DVT ⟶ Pulmonary Embolus
Pulmonary Embolism (PE):
Thrombus breaks free & becomes venous emboli
goes to lungs
gets
stuck in pulm arterioles (PE)
blocks deoxy blood from getting to alveoli to
get Oxy
SOB, chest
pain, ⟶ irritates arterial intima ⟶ inflammation ⟶
leakage of blood into lung tissue ⟶
hemoptysis
S&S: chest pain, SOB, hemoptysis (blood in sputum), shock (from systemic
release of inflammatory mediators), death
Tx: encourage mobility, hydration, elevate legs for venous return, blood
thinners, look for
skin breaks, TED hose
VTE (venous thromboembolism) = DVT + PE
Arteries: vessels that carry oxygenated blood from heart to tissue beds all over body
Healthy arteries: good vasomotor tone & patent lumen (flexible, compliant,
patent, normal resistance)
good perfusion
no ischemia
Good Perfusion : delivery of O2 & nutrients to tissues
cap refill <2 seconds, skin pink, warm, pulse normal, norm BP range
(110/60 to 115/70), normal organ function (good urine output, good
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EXAM 3 REVIEW: Cardiovascular, Pulmonary, Renal, Genitourinary Right atrium tricuspid valve right ventriclepulmonic valvepulmonary artery pulmonary arteriolespulmonary capillaries [gas exchange with alveoli occurs here] pulmonary venules pulmonary veinsleft atriummitral valveleft ventricle aortic valve aorta part of this freshly oxygenated blood goes into coronary arteries, which branch off the aorta just beyond the aortic valve. part goes up to brain via carotids rest goes to tissue beds of remainder of body arterioles capillaries [gas exchange with tissue occurs here] venules veinsinferior vena cava (from body) or superior vena cava (from head)  right atrium ❖ PERIPHERAL VASCULAR SYSTEM ➢ Venous : vessels that carry deoxygenated blood from tissues to right side of heart ▪ Healthy veins: Facilitate good venous return & prevent backflow; Bad Veins: bad valves ⟶ backflow ⟶ venous congestionperipheral tissue edema ; stasis & immobilitysluggish blood flow ▪ Chronic Venous Insufficiency (CVI): backflow (congestion) of blood into distal veins of legs & feet

  • Floppy valves ⟶ blood backflow ⟶ congestion & stasis of blood in legs & feet ⟶ increased hydrostatic pressure ⟶ engorged veins ⟶ pushes fluid into tissues ⟶ edema ⟶ S&S
  • S&S: edema ⟶ swollen, tight, dry, discolored skin; venous stasis ulcers (tissue breakdown from edema/poor cell fxn), thrombi, varicose veins (+ hydrostatic pressure ⟶ backflow pressure to surface veins)
  • Risk factors: standing for too long, pregnancy, old people, genetics, immobility
  • Tx: encourage mobility, hydration, elevate legs for venous return, blood thinners, look for skin breaks, TED hose ▪ Deep Vein Thrombosis (DVT): clot on vein wall, usually deep vein in thigh/calf
  • S&S: Thrombophlebitis , redness/pain/erythema/warmth (inflammatory signs), edema, unilateral
  • Risk factors: 1+ element of Virchow’s Triad ◆ Virchow’s Triad: injury to endothelium of vein (ex. surgery), stasis of blood flow (ex. muscles not pumping/venous insuff), hypercoagulability (ex. Dehydration) ➢ Couch potato, casts, bed-ridden, pregnant, obese, diuretics/hormone therapy, CVI
  • Sequela of DVT ⟶ Pulmonary Embolus ▪ Pulmonary Embolism (PE): - Thrombus breaks free & becomes venous emboli ⟶ goes to lungs ⟶ gets stuck in pulm arterioles (PE) ⟶ blocks deoxy blood from getting to alveoli to get Oxy ⟶ SOB, chest pain , ⟶ irritates arterial intima ⟶ inflammation ⟶ leakage of blood into lung tissue ⟶ hemoptysis
  • S&S: chest pain, SOB, hemoptysis (blood in sputum), shock (from systemic release of inflammatory mediators), death
  • Tx: encourage mobility, hydration, elevate legs for venous return, blood thinners, look for skin breaks, TED hose ▪ VTE (venous thromboembolism) = DVT + PE ➢ Arteries : vessels that carry oxygenated blood from heart to tissue beds all over body ▪ Healthy arteries: good vasomotor tone & patent lumen (flexible, compliant, patent, normal resistance) ⟶ good perfusion ⟶ no ischemia
  • Good Perfusion: delivery of O2 & nutrients to tissues ◆ cap refill <2 seconds, skin pink, warm, pulse normal, norm BP range (110/60 to 115/70), normal organ function (good urine output, good

mentation, cardiac output)

overdrive of RAAS

◆ SNS overdrive: epinephrine elevated ⟶ stimulates beta receptors of heart ⟶ tachycardia and/or increased contractility of heart ⟶ greater cardiac output & ejection pressure ⟶ greater driving pressure ⟶ increase in BP ◆ RAAS overdrive: low BP or volume ⟶ RAAS always “in gear” ⟶ sustained vasoconstriction & larger blood volume (retention of NA+ and H2O) ⟶ high BP ➢ Sequela: chronic high BP ⟶ hypertrophy & hyperplasia of arterial muscles ⟶ smaller lumen ⟶ more HTN ⟶ intima (inner lining) damage ⟶ inflammatory response (mediators) ⟶ increase swelling & permeability of intima endothelial cells

  • S&S of HTN: secondary to vascular damage, stroke (ischemia from narrowed vessels & high BP), vision changes (ischemia/infarct of retina from narrowing), hematuria & proteinuria (spillage from dmg to renal arteries), renal failure, heart attack (increased LV ejection ⟶ increased workload ⟶ MI, HF, PAD) ▪ Aneurysm: Outpouching of arterial walls due to stiff/atherosclerosis + HTN (in brain, thoracic, femoral arteries)
  • atherosclerosis & HTN weaken arterial walls ⟶ local dilatation/outpouching of walls ⟶ intima lining injuries + blood seeps from lumen to muscle/tissue ⟶ increase aneurysm size ⟶ rupture
  • Brain S&S: stroke ⟶ unilateral weakness; change in consciousness; sudden horrible headache
  • Aorta S&S: AAA- Abdominal/back pain, palpable pulsatile mass; Thoracic aortic: chest/back pain
  • Other S&S: diminished pulse (on one side), ischemia to distal tissues, pain (if large and/or ruptures) ▪ Tx of arterial dz: manage stress, stop smoking, moderate alcohol, nutritious diet low in LDL’s & high HDL’s (exercise/niacin), Omega 3’s, beta blocker (prev overactivity of SNS), ACE inhibitors (prev overactivity RAAS), blood thinners (prev clots), aspirin (inflammation) ▪ Nurse interventions: monitor BP/pulse trends, check cap refill for tissue/oxy, watch for skin breaks ▪ NOTE: arterial dz would NOT want to elevate feet b/c it would be harder for arterial flow to get to distal ischemic areas ❖ CIRCULATORY SYSTEM ➢ Heart Cycle Review ▪ Electrical pathway: SA node ⟶ AV node ⟶ Bundle of HIS ⟶ L&R bundle branches ⟶ Purkinjie fibers ▪ Systole : RV & LV contracting & ejecting blood into pulm artery & aorta; between the “lub” (closure of AV/tricuspid&mitral valves--before systole) and “dub” (closure of pulm & aortic valves--before diastole); generated by SA node, stroke volume ▪ Diastole : RV & LV receive blood from RA & LA, “resting” period ➢ Cardiac Output (HR x SV): amount of blood the LV ejects per minute (norm= 4-6L/min) ▪ Normal Sinus Rhythm (NSR or SR): normal HR & Rhythm - Heart Rate (rate of impulses from SA node) 60-100bpm ◆ Tachycardia (>100bpm) causes: ➢ Neurohormonal influences of SNS: epinephrine (bind with beta receptors & increase HR) ➢ Electrolyte changes: Hyperkalemia ⟶ hypo-polarization ⟶ irritable myocardium ◆ Bradycardia: (<60bpm) causes: ➢ Neurohormonal influences of PNS: vagus nerve secretes acetylcholine ⟶ decrease HR ➢ Electrolyte changes: Hypokalemia ⟶ hyper-polarization ⟶ bradycardia, decrease contractility, weakness ➢ Ischemia from right coronary artery narrowing/blockage (RCA feeds

➢ Atrial fibrillation (A-fib): chaotic impulses in atria cause quivering (irregular heart beat); usually begins b/c myocardium has to endure long-term hypoxic strain or chronic HF ; common in elderly ▪ Sequela:

  • no “atrial kick” to propel blood into ventricles ⟶ atria quiver ⟶ diminished CO
  • Thrombi/emboli formation (from pooling of blood [sludge/lumpy] in atria); L. Atrium ⟶ arterial thrombi ⟶ brain emboli ⟶ stroke (unilateral weakness, confusion from brain ischemia); or R. Atrium ⟶ venous thrombi ⟶ lung emboli ⟶ Pulmonary Embolism (SOB, chest pain, hemoptysis, shock, death) ➢ Ventricular fibrillation (V-fib): chaotic impulses in ventricles cause quivering (ventricles like a bowl of jello); acute & deadly (3- 6 seconds until unconsciousness) ▪ Sequela: Deadly! No ventricular contractions ⟶ No CO at all ⟶ no blood flow, no pulse ⟶ no perfusion to brain & other organs ⟶ unconsciousness ⟶ death ▪ Stroke Volume (ability of heart to eject ~70 ml of blood per beat); contractility/preload/afterload
  • Contractility (PUMP ACTION): how toned, how well heart eject/squeeze/pumps blood ◆ Low contractility ⟶ low SV ⟶ low CO ⟶ S&S of diminished perfusion ➢ Causes (i.e. negative inotropic influences) of decreased contractility: ▪ Myocardial ischemia ▪ Neurohormonal effects; electrolytes: hypokalemia (hyperpolarized ⟶ bradycardia, decreased contractility, weakness); hyperkalemia (hypo- polarized ⟶ irritable myocardium) ◆ Positive inotropic effect—anything that increases contractility (med: digoxin)
  • Preload (VENOUS RETURN/VOLUME): volume of blood returning to heart ◆ High preload ⟶ fluid volume overload (from HF, SIADH); increased blood volume ◆ Low preload ⟶ fluid volume deficit (bleeding, dehydration, Diabetes Insipidus) or systemic vasodilation (from Anaphylaxis/sepsis); low amt of blood sent to heart ⟶ low SV ⟶ low CO, low BP, S&S of dehydration
  • Afterload (RESISTANCE TO FORWARD FLOW): ANY resistance to forward blood flow, arterial walls not too dilated/constricted; affects SV/CO/perfusion ◆ RV afterload (pulmonary vascular resistance—PVR) : ➢ HIGH PVR causes: athero/arteriosclerosis of pulm vasculature (narrow pulm artery ⟶ high resistance); from vasoconstriction or chronic bronchitis /lung probs LV afterload (systemic vascular resistance—SVR) ➢ HIGH afterload causes: from HTN (high BP ⟶ high resistance) arterio/atherosclerosis (narrowed/ vasoconstricted aorta & arteries ⟶ high resistance) ▪ S&S: Not enough pressure & volume to tissues ⟶ decreased perfusion ⟶ delayed cap refill, cold extremities, diminished pulse, low BP LOW SVR causes: from arterial vasodilation (ex: anaphylaxis/sepsis, heat, meds, endotoxins) ⟶ shock ▪ S&S: CO high from less resistance ⟶ pooling of blood in periphery, angioedema ⟶ less blood back to heart ⟶ low CO ⟶ low BP, shock ➢ Coronary Artery Disease (CAD): coronary arteries narrowed/occluded from plaques (athero/inflamm) ▪ Risk factors: same as HTN-- family hist, diet, obesity, Type 2 DM, smoking, high Na+ intake ▪ High homocysteine levels (free-radical behavior) and CRP (inflammatory component);

▪ S&S: angina (ischemic pain; chest pain, left arm, jaw, back pain) w/ exercise, cardiac ischemia (SOB, nausea, diaphoresis, dysrhythmias); can lead to MI if not reversed

  • LCA blockage ⟶ LV affected ⟶ low CO ⟶ S&S of decreased perfusion
  • RCA blockage ⟶ RV & SA node affected ⟶ bradycardia ⟶ low CO
  • Other S&S: ◆ N&V, diaphoresis (CNS reaction to pain)

fails)

- Dx: ANP & BNP secreted by RA & LV to lower blood vol but kidneys don’t listen ⟶ high BNP levels

  • Tx: vasodilators (NTG, ACE inhibitors) ⟶ decrease afterload; diuretics ⟶ decrease preload; decrease HR; increase contractility (positive inotrope/digoxin) ▪ Left Heart Failure
  • Etiology:

◆ LV decreased contractility/pumping, high afterload/SVR, high preload/vol ⟶ decreased CO/perfusion ⟶ RAAS triggered ⟶ peripheral arterial vasoconstriction ⟶ even more afterload ◆ Pulmonary edema CAUSED BY LFH & retrograde/backup flow (First HF ⟶ Then lung probs)

  • S&S: Can’t eject blood from LV to tissues ⟶ decreased CO/poor perfusion (fatigue, weakness, mental status change, hypotension, dyspnea/SOB, > cap refill, low UO) ⟶ fluid backup in lungs ⟶ cardiogenic pulmonary edema (crackles, hemoptysis, orthopnea/SOB upon lying down, increase RR, decrease SO2) ▪ Right Heart Failure
  • Etiology: ◆ RV decreased contractility/pumping, high afterload PVR, high preload/vol ⟶ decrease CO/perfusion ⟶ RAAS triggered ⟶ increase aldosterone ⟶ body hangs on to NA/H2O ⟶ even more preload ◆ Chronic bronchitis/PE/chronic lung dz/COPD ⟶ increased PVR ⟶ cor pulmonale ⟶ RHF (RHF specifically caused by increased PVR from PE/COPD/chronic lung dz ◆ Lung congestion CAUSES RHF & retrograde venous flow [First lung probs ⟶ Then HF] ◆ Can be caused by ischemia & MI but also increased PVR
  • S&S: RV fails to move blood forward⟶ decreased CO/poor perfusion (fatigue, weakness, mental status change, hypotension, dyspnea/SOB, > cap refill, low UO) ⟶ Backpressure/retrograde flow ⟶ peripheral venous congestion (jugular veins distended (JVD); enlarged liver; ascites; peripheral edema) ➢ Cardiogenic Shock ▪ Shock:
  • hypotension ⟶ inadequate perfusion to tissues ⟶ decreased perfusion ⟶ cell hypoxia ⟶ impaired cellular metabolism ⟶ S&S of decreased level of consciousness, dyspnea, low UO, pale cool skin, > cap refill, & compensatory S&S such as tachycardia (to make up for decreased CO) ▪ Cardiogenic Shock:
  • shock that is caused by a HEART PROBLEM (ischemia/MI/valve probs/pump prob) ⟶ weakened contractility ⟶ decreased CO ⟶ hypotension ⟶ S&S of low perfusion (decreased level of consciousness, dyspnea, low UO, pale cool skin, > cap refill) & compensatory S&S such as tachycardia (to make up for decreased CO) ▪ Tx: decrease afterload (vasodilate arteries) ❖ PULMONARY SYSTEM ➢ Arterial Blood Gases (ABG) “ROME – R espiratory O pposite, M etabolic E qual” ▪ pH: aciditiy of blood = 7.35-7.PO2: pressure O2 in blood (O2 gas dissolved in plasma) = 80-100mmHg (<80 ⟶ hypoxemia) ▪ SO2: O2 saturation (O2 carried by each Hgb) 97-100% (<97 ⟶ hypoxemia) ▪ PCO2: pressure of CO2 in blood (“acid gang”) = 35-45mm Hg (out of norm range ⟶ RESP prob) ▪ HCO3: bicarbonate in blood (“alkali guy”) = 22-26 mEq/l (out of norm range ⟶ METAB prob) ➢ Respiratory Acidosis ⟶ low pH, high PCO2, low PO2; decreased RR ▪ Unconscious/head injury/ pneumonia/impaired resp centers ⟶ Hypoventilation ⟶ not breathing out enough CO2 ( hypercapnea ) ⟶ Acidosis ⟶ kidneys hang on to or make more HCO ➢ Respiratory Alkalosis ⟶ high pH, low PCO2; increased RR ▪ Anxiety/panic attack/asthma attack ⟶ Hyperventilation ⟶ too much CO2 blown off ⟶ Alkalosis ⟶ kidneys excrete HCO3 in urine or hold on to H+ (paper bag breathing to breathe back CO2) ➢ Metabolic Acidosis ⟶ low pH, low HCO3; increased RR

▪ Vomiting ⟶ loss of HCl/accum of alkali ⟶ alkalosis ⟶ Hypoventilation ⟶ Lungs hang on to CO ➢ Inhalation & Restrictive Lung Diseases ▪ Inhalation norm: diaphragm drops ⟶ muscles pull outward ⟶ thorax enlarges ⟶ negative pressure ⟶ air sucked into bronchi & alveoli ⟶ O2 passes across membranes into blood & CO2 passes across membrane from blood into alveoli

  • Ventilation: where air passes into bronchi & alveoli (lung tissue)
  • Perfusion: where lung blood vessels bring CO2 to alveoli & take away O2 to pass to rest of body ▪ Respiratory Vocab:
  • Increased work of breathing: dyspnea (subjective SOB, can’t get enough air); DOE (dyspnea on exertion); orthopnea (SOB upon lying down, “three pillow”, LHF); PND/Paroxysmal nocturnal dyspnea (SOB at night)
  • Rate-related: hypoventilation (from CNS/neuro probs/intracranial bleeding); hyperventilation (from “air hunger” in pulm probs; fright/anxiety)
  • Depth-related: hypopnea (shallow breathing); hypernea (increased depth of respirations); apnea (no respirations at all); Cheyne-Stokes (“end of life breathing”; deep/fast breathing ⟶ decreases to temp stop in breathing; causes are HF, Stroke, sleep apnea) - Abnormal use of muscles to breathe: accessory muscles (diaphragm & intercostal muscle use during exhalation); nasal flaring - Cough and sputum: cough (acute=bronchitis; chronic = COPD, GERD); hemoptysis (coughing up blood from inflammation in alveoli); purulent sputum (=infection) ▪ Restrictive Lung Dz’s: can’t get air into blood (V/ventilation) or can’t get blood to alveoli to be oxygenated (Q/perfusion) ⟶ decreased O2 getting in ⟶ hypoxemia; increased work of breathing/S&S; low SO2 and/or low PO2; V/Q mismatch
  • V= ventilation (norm amt of air breathed in/out per min ~4 liters)
  • Q= perfusion (norm amt of blood in the lungs available for gas exchange per min ~5 liters)
  • Norm V/Q ratio = 0.8 or 4/ LOW V/Q DISORDERS: can’t get outside air to blood, low V (ex: Pneumonia ⟶ alveoli secretions & portions collapse ⟶ less air pass into alveoli ⟶ low ventilation/Vlow V/Q)
  • Chest wall restriction (low V/Q) ◆ Mechanical: from Kyphosis (deformity); flail chest; obesity ◆ Neuromuscular weakness: from Polio/myasthenia gravis/paralytic dz
  • Airway restriction (low V/Q) ◆ Etiology: foreign body, trachea/bronchi tumors, Croup (laryngotracheobronchitis— inflamm of larynx/bronchi) ◆ Croup S&S:—stridor (high-pitched, raspy sound during inspiration from narrowed airways), fever, increased RR, barking cough ◆ Tx: cool mist (decrease swelling), sometimes steroids
  • Pleural restrictions (Low V/Q) ◆ Pleural effusion: extra fluid in pleural space ➢ Etiology: pleura irritated/inflamed i.e. lung cancer, heavy coughing ⟶ edema ⟶ extra fluid into pleural space ➢ S&S: chills, fever (infection), pleuritic pain (upon deep breaths/cough), shallow breathing (to avoid pain of deep breaths) ◆ Pneumothorax (“collapsed lung”): air in pleural space ➢ Etiology: rupture in visceral or parietal pleura ⟶ disruption of negative pressure in thorax ⟶ air accumulation in thorax/positive pressure ⟶ lung collapses ➢ Open pneumothorax: trauma from outside; i.e. gunshot/broken rib ⟶

puncture to lung ⟶ air into thorax ⟶ positive pressure ⟶ collapses lung ⟶ chest pain, SOB ➢ Closed/tension pneumothorax: trauma from inside; i.e. rupture of dz alveoli ⟶ positive pressure ⟶ collapses lung ⟶ puts pressure on other lung ⟶ chest pain, SOB ➢ Tx: chest tube ⟶ water seal ⟶ air escapes thorax and can’t get back in ⟶ negative pressure re-established ⟶ lung re-expands

▪ Asthma: chronic inflammatory disorder of airways due to bronchial hyperresponsiveness to stimuli (allergens)

  • Patho: inhaled irritants ⟶ inflammatory mediators (histamines, leukotriene, PG’s) ⟶ vasodilation/increased permeability ⟶ infiltration by neutrophils/eosinophils ⟶ swelling of bronchial lining ⟶ edema; ALSO: bronchial smooth muscle reacts to mediators ⟶ spasm & constriction of bronchial musculature/narrowed airways ⟶ difficult exhalation
  • **Note: some hyperventilation in normal, but too much/exacerbation could lead to decompensation ⟶ tire out, unable to maintain higher rate ⟶ hypoxemia ⟶ retain CO2 (hypercapnia) ⟶ Resp Acidosis (decompensation) ⟶ Respiratory Failure
  • S&S: wheezing upon exhalation (possible inhalation if severe); accessory muscle use during exhalation; hyperventilation (SO2 drop/hypoxemia ⟶ increase RR); low baseline PF; respiratory alkalosis
  • Tx: monitor daily with PF readings, bronchodilators (Ventolin via nebulizer, inhalers), steroids (decrease swelling/stabilize cap membranes) ▪ COPD: Collective Obstructive Pulmonary Disease (from smoking)
  • Emphysema: cig smoke irritants ⟶ chronic inflamed airways ⟶ increased elastase activity ⟶ destroy of alveolocapillary membrance ⟶ stiff/hyperinflated alveoli ⟶ air trapping ⟶ large, hyperinflated, stiff lungs ⟶ hypoxemia/air hunger ⟶ chronic hyperventilation ◆ pH  PCO2  (little) HCO3 norm PO2/SO2  (hypoxemia) RR  (chronic hypervent) Resp Alkalosis ◆ S&S: chronic hyperventilation ⟶ “ pink puffer ” (i.e. fairly well oxygenated); thin & no appetite (hyperventilating takes energy); barrel- chested (air trapping ⟶ lungs huge); tripod position to maximize chest expansion; “pursed lip” breathing (increase pressure in chest & prolong expiratory time); wheezing (low air flow); chronic Respiratory Alkalosis (from hyperventilation) ◆ **Note: some hyperventilation in normal, but too much/exacerbation could decompensate ⟶ tire out, unable to maintain higher rate ⟶ hypoxemia ⟶ retain CO2 (hypercapnia) ⟶ Resp Acidosis (decompensation) ⟶ Respiratory failure ◆ Tx: smoking cessation, give O2 appropriately, bronchodilators, steroids
  • Chronic Bronchitis: hypersecretion of mucus & chronic cough for at least 3/mo for 2 yr. ◆ pH  PCO2  HCO3 norm SO2/PO2  (hypoxemia; mucus plug) RR normal Resp Acidosis ◆ Patho: cig smoke irritants ⟶ unable to expel due to altered cilia ⟶ irritated bronchial walls ⟶ inflammation & infiltration of neutrophils, macrophages into bronchial wall ⟶ bronchial edema ⟶ thick mucus & bronchospasm ⟶ obstruction ⟶ can’t get air out ◆ S&S: “blue bloaters” ; hypoxemia (from mucus plugs & bronchial narrowing ⟶ decreased surface area for O2 to diffuse); cyanosis (extra inhaled O cannot get through mucus plugs); clubbing of fingers (oxy probs from lung cancer/CF/CHD); overweight (don’t move to conserve energy); cor pulmonale (RV can’t get blood into stiff/mucus lungs ⟶ RV strained ⟶ RHF results ⟶ peripheral edema “bloat”); chronic hypercapnia (CO2 can’t diffuse through thick mucus ⟶ Respiratory Acidosis; does NOT hyperventilate ❖ GENITOURINARY SYSTEM ➢ Male disorders ▪ Prostate problems
  • BPH (benign prostatic hyperplasia) or “enlarged prostate”: proliferation of prostate tissue (seen in men over 50) ◆ S&S: compressed urethra ⟶ urgency, weak flow, slow to start flow, urinary retention ◆ Dx: digital rectal exam, history of S&S ◆ Tx: meds or TURP surgery (remove/resected tissue) to decrease prostate size
  • Prostate Cancer: malignant neoplastic condition (diet high in sat fat; high
  • Etiology: caused by chlamydia & gonorrhea ➢ Female disorders ▪ Uterine Disorders
  • Dysmenorrhea: painful, heavy periods; larger bleeding volume (hormonal) - Amenorrhea: absence of menses (anorexia; over-exercising) ⟶ onset of menopause
  • Endometriosis: presence of endometrium outside uterus Patho: Endometrial tissue escapes via fallopian tubes ⟶ attaches to outside of organs ⟶ ectopic (out of place) endometrium still responds to menstrual hormones ⟶ chronic bleeding irritates the area ⟶ adhesions/scarring to organs ⟶ obstructions and/or infertility ➢ S&S: dyspareunia (pain during intercourse); dysmenorrhea; pelvic pain ➢ Tx: hormonal therapy, surgery ▪ Ovarian cancer: malignant neoplastic condition; metastasizes intra-abdominally; most cancer deaths related to female reproductive system—often advanced when it’s found; “I feel bloated!”
  • S&S: (very vague ) bloating; mild abdominal discomfort; constipation; diminished appetite/weight loss; metastasis ⟶ pain; ascites (from liver involvement); dyspepsia; vomiting; alterations in bowel movement ▪ Pelvic Inflammatory Disease (PID): infection in reproductive tract
  • Patho: starts with STI/Chlamydia infecting/inflaming cervix ⟶ spreads to uterus ( endometritis and/or myometritis ), fallopian tubes ( salpingitis ); and ovaries ( oopheritis )— salpingo-oopheritis = infection of fallopian tubes AND ovaries
  • S&S: abnormal vaginal discharge; pelvic/abdominal pain that worsens with movement; can cause infertility
  • Tx: abx, pain killers ▪ Urologic infections: Cystitis (bladder); Pyelonephritis (kidney infection); UTI
  • Most common microbe is E. Coli due to closeness of anal and vagina os; short urethra
  • S&S: dysuria, urine frequency/urgency (from irritation of pressure-sensors of bladder), hematuria (from bladder irritation), pyuria (pus in urine; cloudy, foul-smelling), abdominal/back pain (where kidneys are), fever
  • Dx: UA, urine C&S
  • Tx: abx ▪ Menopause: ovaries atrophy, estrogen production ceases ⟶ no periods
  • No estrogen ⟶ no bone build-up or maintenance ⟶ osteoclastic activity ⟶ osteoporosis ▪ Non-Gender specific disorders
  • STI’s ◆ Chlamydia: caused by bacteria Chlamydia trachomatis ➢ S&S for MEN: urethritis, inflammation, discomfort in penis, dysuria, discharge ➢ S&S for WOMEN: vaginal discharge; pelvic pain ⟶ PID ◆ Gonorrhea: caused by bacteria Neisseria gonorrhea ➢ S&S for MEN: purulent discharge from penis; dysuria ➢ S&S for WOMEN: asymptomatic; vaginal discharge or bleeding; and/or full PID ◆ Syphilis: caused by spirochete Treponema pallidum ➢ S&S: lesions ( chancres ) on skin anywhere that microbe touches mucous membranes or skin (lips, labia, penis); later stages ⟶ neurosyphilis & other S&S ➢ Tx: abx if treated during stage 1 (Primary Syphilis); systemic if not treated ◆ Herpes Simplex Virus (HSV): HSV1: cold sore; HSV2: genital herpes (can

spread to anus) ➢ Patho: HSV penetrates local nerve fibers ⟶ travels to spinal ganglion & lies dormant ⟶ goes back down to genitals during times of stress ⟶ breakouts of lesions ➢ Note: once infection there is no cure; stays permanent in body & breaks out periodically ➢ S&S of HSV2: painful, red, crusty crops of lesions; systemic S&S fever and malaise ➢ Tx: antivirals to treat S&S but no cure