N211 -Health Differences Across the Life Span 1 Flashcards
HTN
28-31% adults in US
of this , 90-95% PRIMARY HTN (unidentified cause)
remaining 5-10% SECONDARY HTN (identified cause)
Identified Causes for HTN
-narrowing renal arteries, renal parenchymal dis, hyperaldosteronism (mineralocorticoid HTN), Pregnancy, coarctation of aorta, certain meds
ETOH and HTN linked to
UP triglycerides, sugars, weight gain, LDLs, cardiac function
Dx someone with HTN elevation on one round. Must have average of
2 or more contacts w health care provider
Normal BP
<120/<80
Pre HTN
120-139/80-89
PIH (pregnancy induced HTN usually resolves after placenta expelled)
Stage 1
140-159 / 90-99
Stage 2
160 up / 100 up
Stage 1 TX
Medication, MD until stable
Stage 2 Tx
doctor and workups
?250 - 400
Moderate Cardio Vas dis.
UnTx HTN
.UP workload to heart
.thickening of arterial wall
. etc
HTN Emergency
BP 180/120
.pressure in head
HTN Crisis Tx.
Short lived meds (minutes - 4hrs)
Nitroglycerin (Nitro-Bid)
Socium Nitroprusside (nipride or nitropress)
nicardipine hydrocholoride (cardene)
enalaprilat (vasotec)
Vasodilator: Fendolopam
Fendoldopam (Corlopam)
1.action
Alpha Adrenergic Clocker
WORK DIRECTLY ON BLOOD VESSELS
keeps hormone from tightening muscles and walls. counter epi and nor epi.
SE: V/N/D, urinary freq, cardio vascular collaps
Alpha Adrenergic Clocker
WORK DIRECTLY ON BLOOD VESSELS
keeps hormone from tightening muscles and walls. counter epi and nor epi.
SE: V/N/D, urinary freq, cardio vascular collaps
Beta Adrenergic Blocker
COREG
ALPHA and BETA
Dry Cough - BAD, change meds
Slow transition to get used to
SE: cardiovascular. can worsen ss. not for newly HTN patients Not first line drug.
Contracindicated in Heart failure, COPD and ?
Beta Adrenergic Blocker: Inderol
Propanolol
for Stage Fright, BP control,
slows HR, reduces cardiac output, fatigue, bizarre dreams
SE bradycardia, insomnia, fatigue,
Calcium Chan Blocker
Diltiazem
Inhibit calcium ion influx and reduce after load.
inhibit na, inhibit water.
Procardia: CHF, resistant Angina,
Some people chew to get emergency fast effects. not for normal pt as it can bottom out pressure fast.
Beta Adrenergic Blocker
Lopressor, Corguard, Inderol, Toprolol
slow HR. they get breathless, can’t excercise on this drug.
decrease contractions and AV signal,
SE bradycardia, insomnia, fatigue, bad dreams, sex dysf, LO HDL, GI probs, LO BP, depresson
ACE Inhibitors
Angio 1 - 2.
lowers resistanece of peripheral vascular syste =less risistance
SS proteinurea, dry cough, hyperkalemia, renal damage
Catapress
Aldamet
diminish periphera outflow from brain. brain action to neurons.
dose at bedtime. monitor 30-90min for syncopy
Diuretics
Thiazides
pulling fluid from extra vascular to intra vascular spaces to rebalance lo plasma.
affect smooth muscle.
Burn patients
hi K levels. As they stabilize, K drawn back into cells.
Loop Diuretics
can cause volume depletion . NOT first line. After Thiazines tried.
K sparing Diurents
can cause Hyper Kalemia.
Vasodialiators
Hydralazine
Hydralazine (Apresoline)
DASH Diet
reduce cholestoerol in blood
Chart textbook P15
MAKE CARDS
PTT (partial prothrombin time)
eficacy of Heparin
PT(C) (prothrombin time)
Efficacy of Coumadin
when we have a venus problem, DO NOT add heat
it will increase circulation. If arterial problem, yes warm. you want blood to go down to extremeties. in venous, the blood is pooling and we need to elevate legs to help move up blood.
intermitent caudicatoin
when person walks, not enough blood flow to legs. sever pain, heavy , sharp.
they stand still , then it goes away, then it starts again when they walk
Abdominal Aortic Aneurysm
-asymptomatic
Watch for
clotting
emboli
rx for clotting
SS:
Abdominal pain, low back pain, feel heart beat
Assessing AAA
Bruit, swooshing over consicted artery.
Pain: abdominal/loabdomin
Calcium Channel Blockers
Tx Angina, HBP
affect movement of ca in cells of heart
Digoxin/Linoxin
stronger heart contraction
Beta Blockers
Control catacholoamines
Beta Blockers
Control catacholoamines
Digoxin Antagonist
digoxinase ?
Hyperkalemia Antagonist
Kayexalate
Heparin
protamin sulfate
Coumadin antagonist
vit k
Pulse Pressure
diff between top and bottom
Pump Problems
cardiomyopathy
Cardiogenic shock
loss of hearts ability to pump enough blood to heart
hypovolemic shock
loss of large amount of blood or fluid
Distributive Shock
loss of vascular tone causing decreased peripheral resistance, larger vascular bed, result in hypovolemia
Class 3
9/6/18
Problems of intake and supply of O2
.
beta blockers
Inderol?
non selective vs selective
classic angina comes from
exertion or stress
unstable angina pre infarction
frequent times daily with increasing severity
classic dysrythmias result from
hypoxia and hypercapnia
Digitalis preps effective in treating
CHF
cardiac glycoside aka
dig glycoside
digitalis
allows heart to work less but beat stronger
strted from page 24
review ABG
Sudden hypercapnia causes
.UP Pulse, resp, BP
.Mental cloud
see rest
Acute Respiratory Acidosis
inadequate excretion of CO2 w inadequate vent
Chronic Resp Acidosis
occurs w pulmonary diiseases
Nursing Interventions
.lo flo O2
.monitor consiousnee, abg, ekg for dysrythmias
SLIDE 9
HCO3 is Bicarb not H2CO3
when you rae chronically aciic, hi CO2
body become used to it. It’s stops becoming the hi CO2 that makes the breath, but the lo O2 levels.
go over respiratory vs metabolism
k
Respiratory Alkalosis
Carbonic Acid deficit
.body loses CO2, decrease in acid, increases ph level
.occurs w hyperventilation, leads to loo CO2
……
Causes
.
SS
.
.
.
.
.
.
.
Nursing Intervention
.tx underlying cause
Metabolic Acidosis
.ABG
.lo bicarb
.lo ph
Metabolic Alkalosis
.hi ph > 7.45
.hi plasma bicarb (HCO3 > 26)
.paCO2 INC as lungs attempt to compensate for excess bicarb by retaining CO2
compensate by blowing it off
Acidotic complication
.peripheral vasodilation and decrease cardiac output w Ph drops to <7.0
.chronic metabilic acidosis usually seen wtih chronic renal failure
.closemonits K leves. hypokalemia
LOOK at old ABG slides
look at old ABG slides
metabolic acidosis
.see P57 in book
. lo bicarb
.hyperkalemia
SEE pg 57 in book
MAKE SLIDES
Adult Respiratory Failure
Slide 97
pg 61
beta antagonist
corticosteroids
Atropine
drying secretions
…….
PNA clsassification
community hospita incompromised host aspiration pna ? ?
ended at laryngeal obstructino
slide 182
Factors Causing Hypertension
.INcreased Sympathetic stimulation
.UP blood volume d.t increased renal reabsorption of Na+, CL- and H2o retention
.UP activity of RAAS system, caused expansion of extracellular fluid volume. causing systemic vascular resistance
.Dysfx of vascular endothelium causing decreased vasodilation of arterioles
.resistance to Insulin
most gastric cancers are
adenocarcinomas
will go through stomach and into other organs
most gastric cancers are
adenocarcinomas
will go through stomach and into other organs
Ovarian Ca SS
bloating
to take the ovaria
.
Capoten
Captopril
ACE inhibitor
Lotensin
Benazepril
Zestril
Lisinopril
Aldactone
Spironolactone
ARB - Aldosterone Receptor Blocker
Cozaar
Losartin
ARB
what does epinephrine do?
vasoconstrict
Lopressor
Metaprolol
Beta Blocker
Tenormin
Atenolol
BB
Norvasc
Amlodipine
CCB
Plendil
Felodipine
CCB
Procardia
Nifedipine
Catapres
Clonidine
Central Alpha 2 agonist
Coreg
Carvedilol
alpha and BB
Apresoline
Hydralazine (direct vasodilator) helps body loose excess water by releasing excess salt
Esidrix
Hyrochlorothiazide
Diuretic
Prinzide
Lisinopril / HCTZ
(Lisinopril/HCTZ) {=Thiazide diuretic and ACE inhibitor} causes the blood vessels to loosen and dilate. This decreases the strain on the arterial walls. Therefore, the speed and pressure inside the artery walls decreases {=Vasodilators}
Prinzide
Lisinopril / HCTZ
(Lisinopril/HCTZ) {=Thiazide diuretic and ACE inhibitor} causes the blood vessels to loosen and dilate. This decreases the strain on the arterial walls. Therefore, the speed and pressure inside the artery walls decreases {=Vasodilators}
Systolic heart failure
most common
alteration in ventricular contractoin
Diastolic heart failure
stiff noncompliant heart muscle
Type of Heart Failure determined by EF
Ejection Fraction, vol blood ejected w each contraction of ventricular volume (normal 55-65%)
determines Systolic or Diastolic heart
failure
HF = low EF
Left Sided HF
Pulmonary Edema
SS: dyspnea, wet lung, cough, fatigue, tachy, anxiety, restlessness, confusion, paroxysmal nocturnal dyspnea (sudden attacks at nght), orthopnea (diff breathing lying down)
Frothy pink sputum = severe Pulm Edema
Dominant feature of heart failure is decreased tissue
perfusion to kidney, brain, and GI system
Right Sided HF
Peripheral Edema
SS: peripheral edema, weight gain, distended neck vain, anorexia, nausea, nocturia, weakness
HF
.decreased cardiac output .impaired urinary elim d/t decreased perfusion .activity intolerance .anxiety .ineffective tissue perfusion
Tx: restrict Na, to reduce salt and water retention, reducing vascular volume
.assess/monitor q4hrs
.assess/mon apical hr
.assess for hypoxia (restlessness, tachy, chest pain)
.auscultate lungs for pulmon edema (crackles/wet sounds)
.admin O2
HF Interentions
.observe ss of edema (daily weight, monitor i&O, measure abdom girth, observe ankles/fingers for swelling.
.elevate HOB to assist w breathing and limit Na intake.
.check apical HR before Digitalis, HOLD if <60.
.diuretics in AM
.periods of rest after activity
Cardiomyopathy, 3 types
Disease of myocardium
- Dilated (most common)
• Causes diffuse cellular necrosis and fibrosis
• Leads to decreased contractility (systolic failure) - Hypertrophic (rare)
• A chronic disorder in which the heart muscle becomes abnormally
thick. - Restrictive cardiomyopathies lead to decreased
distensibility and ventricular filling (diastolic failure)
HF NURSING DX
• Altered cardiac and peripheral circulation related to
decreased cardiac output
• Ineffective tissue perfusion from altered circulation
• Anxiety related to lack of knowledge and fear of the
unknown
• Activity intolerance related to decreased cardiac
output
PAC
Preatrial Contraction
normal electrophysiological phenomenon
frequent PACs may cause palpitations, or sense of “skipping a beat”
can trigger afib, aflutter etc.
Atrial Fibrillation (Afib)
Electrocardiogram
– Chaotic activity from the AV node
– No true P wave visible
– Irregular ventricular rhythm
TX:
– Anticoagulant therapy due to risk of stroke
– Antidysrhythmic drugs
– Cardioversion to treat atrial dysrhythmia
– Ablation of atria
Preventricular Contraction
Ectopic firing
Ventricular Tachycardia
Electrocardiogram
– Wide bizarre QRS
– Pulse erratic and with impaired cardiac output
Treatment:
– Synchronized cardioversion if pulse present
– If no pulse, treat as ventricular fibrillation
– Antidysrhythmics
Ventricular Fibrillation
Cardiac Emergency Electrocardiogram – Irregular undulations of varyious amplitudes from coarse to fine – No cardiac output Treatment: – CPR – Defibrillation as quickly as possible – Antidysrhythmic drugs
Myocardial Infaction
Part of myocardium permanently destroyed
• Caused by reduced blood flow in coronary artery • Due to rupture of atherosclerotic plaque • Subsequent occlusion of artery by thrombus
ACS, Acute Coronary Symdrome
Unstable Angina: plaque rupture, but artery not completely occluded
or also
• Vasospasm (sudden narrowing) • Decreased oxygen supply (from acute blood loss, anemia, or low BP) • Increased demand for 02 (rapid heart rate, thyrotoxicosis, or ingestion of cocaine)
Cardiac Markers for Dx and MI
- Troponin (cTc1 and cTnT) – will be evident 3-4 hours after a
heart attack, peak in 12-16 hrs and stay elevated for 2 – 3
weeks - Myoglobin (Mb) can elevate in other conditions; troponin
level is taken to confirm MI (1-3 hrs and peaks in 12 hrs) - Creatine kinase (CK), an enzyme found in heart muscle cells
and other cells of the body, so a more specific level of
elevation in cardiac cell must be obtained (peaks in 24 hrs)
3 Cardiac Markers for MI
- Troponin, 3-4 hrs after attack
- Myoglobin
- Creatine Kinase
Electrocardiogram
note dysrhythmias, changes in T wave and SG segment and presence of Q wave
Echocardiogram
to assess cardiac muscular function and valves
Types of Schock
Cardiogenic: loss of heart ability to pump
Hypovolemic: loss of blood
Distributive: loss of vascular tone
Cardiogenic Shock SS
.sinus tachycardia, weak, thready pulse, tachypnea
.S3 and S4 heart sound
.hypotension
.Oliguria (<30ml/hr)
NI: NPO, reduce risk of aspiration .admin/monitor fluids to avoid fluid overload .admin 02 to maximize cardiac .mon pulmonary and renal fx .monitor intra-aortic balloon pump (IABP) .Digitalis .Vasoconstriction agents .dopamine
Iron Deficiency Anemia
MEN: Normal 13-31 Umole/L
WOMEN: 11-29 umole/L
Megaloblastic Anemia
.caused by deficiencies of Vit B12 or Folic Acid
.changes in bone marrow, peripheral blood
.abnormally large Erythrocytes called Megaloblastic red cells
SS: weakness, listlessness, fatigue
NI: DO NOT admin RBC transfusion because body w compensate and go into fluid overload.
Low Hemoglobin
heart compensates by pumping faster/harder to deliver more blood to hypoxic tissue
SS: tachy, palpitation, dyspnea, dizzy, orthopnea, exertional dyspnea
Sickle Cell Disease
.inherited Autosomal Recessive disorder of HgB
.African/eastern mediterranean descent
.after 6 mos age
.hemoglobin S replace all or part of normal HgB, causes RBCs to sickle w O2 is released into tissue
Sickle Cell Anemia
if both parents have sickle cell train, children may inheri 2 abnormal HbS genes and w have sickle cell anemia, most severe form of disease
Sickle Cell Anemia SS
.bone marrow expand in childhood, compensate to offset anemia
.anemia (7-10 g/dL)
.jaundice
.enlarged facial bones and skull
.tachy, enlarged heart, murmurs
Hand-Foot Syndrome
swollen hands
Sickle Cell Crisis
- Sickle cell crisis: tissue hypoxia and necrosis in tissue or organ
- Aplastic crisis: infec w human parvovirus
- Sequestration crisis: other organs pool sickled cells
Most kids with SC will have a Splenic Infarction by age 10 and it becomes non functional (liver and lungs in adults)
Splenic infaction
a condition in which oxygen supply to the spleen is interrupted, leading to partial or complete infarction (tissue death due to oxygen shortage) in the organ. Splenic infarction occurs when the splenic artery or one of its branches are occluded, for example by a blood clot.
Acute Chest Syndrome
Rapid decrease in hemoglobin, fever, tachi, bilateral inflitrates
.mimics infection but are infarctions withing pulmonary
Image result for acute chest syndromethorax.bmj.com
Pulmonary HTN
sequel to sickle cell disease
4 Sickle Cell Txs
.Bone Marrow Trans .Hydroxyurea: (Hydrea): chemotherapy agent – increases hemoglobin F levels and decreased formation of sickled cells .Arginine: antisickling properties; used in combination with Hydrea to manage pulmonary hypertension .Long-term RBC transfusions
Sickle Cell NI’s
manage pain, swollen joints, elevate extremities
.relaxation
.manage infection
.promote coping skills
Chronic myeloproliferative disorder
• Increased RBCs • .Leukocytosis • Thrombocytosis • Increased hemoglobin concentration • Occurs between ages 40-60 in males of Jewish ancestry (mortality high if not treated)
Polycythemia SS & TX
SS: • Clubbing of digits • Dizziness • Headache • Hypertension • Ruddy cyanosis of nose • Thrombosis of smaller vessels • Visual disturbances
Tx: • Phlebotomy • Chemotherapy • Myelosuppressive drugs • Anti-gout agents (Allopurinol) • Replace fluid volume lost during procedure
Polycythemia SS & TX
SS: • Clubbing of digits • Dizziness • Headache • Hypertension • Ruddy cyanosis of nose • Thrombosis of smaller vessels • Visual disturbances
Tx: • Phlebotomy • Chemotherapy • Myelosuppressive drugs • Anti-gout agents (Allopurinol) • Replace fluid volume lost during procedure
Idiopathic Thrombocytopenic Purpura (ITP)
Auto Immune
.Idiopathic
SS:
– Too few platelets
– Bruising, petechiae, and internal
bleeding
TX:
– Steroids
– Immune globulins
– Splenectomy
Thrombocytopenio: Low Platelet Count
.lo platelet production in marrow
.up destruction of platelets
.up consumption of platelets
SS: .<20K/mm3 petechiae
.nasal/gum bleeding
.hi menstrual bleed
.monitor dental and Sx.
Tx:
.teach avoid substance that lo platelet fx. (i.e. otc meds, herbs, supplements etoh)
.inform med providors
Disseminated Intravascular Coagulation (DIV)
massive amt of tiny clots form in microcirculatotion
triggered by: trauma, sepsis, shock, ca, abruptio placentae, toxins, allerg reactions
Initially normal clotting time, then as the many clots forming use u the plateletes and clotting factors, coag time starts to fail.
PARADOXICAL result of up clotting is bleeding
DIC more
pt bleed from mucous membranes, venipuncture site, gi, urinary tract
Hemophelia
bleeding disorder, males
contracted by x-linked recessive chromosome (mother carrier)
normla factor activity 50-200%, Hemophelia 0-25%
Dx: PTT prolonged, factor VIII assays <25% of normal factor
class 2, pg 80
.
AICD:Automatic Implanted Cardioverter Defibrillator:
A
device that detects and terminates life-threatening
episodes of ventricular tachycardia (VT) or fibrillation
(VF)
Pacemaker
an electronic
instrument that supplies
electrical stimuli to the heart
muscle
Intra-Aortic Balloon Pump (IABP)
.facilitate UP myocardial O2 supply
.LO myocardial O2 demand
IABP Compmlications
Transient loss of peripheral pulse Limb ischemia; compartment syndrome Thromboembolism; cardiac tamponade Compartment syndrome Aortic dissection Local vascular injury— false aneurysm, hematoma, bleeding from the wound Infection Balloon rupture (can cause gas embolus) or balloon entrapment Hematological changes, i.e., thrombocytopenia Malpositioning causing cerebral or renal compromise
IABP NI
.monitor pulmonary pressure
.treat arrhythmias. >106
.monitor HgB and Hct for anemia
.monitor complication of cardiogenic shock
.monitor for impending renal compromise <30cc/hr
Intracoronary Stent
stent placed in artery to maintain patency.
Stent complication
.bleeding/hematoma .weak pulse distal to insertion site .pseudoaneurysm and arteriovenous fistula .retroperitoneal bleeding .acute renal failure
Normal ABGs
pH 7.35 – 7.45 Kids 7.36 – 7.44
PCO2 34 – 45 mmHg (ACID)
PO2 80 – 100 mmHg
HCO3 21 – 28 mEq/L (BASE)
Respiratory Acidosis
response to HYPOventilation
- pH < 7.53
- PaCO2 > 45mmHg
- UP CO2, UP Carbonic Acid
- Hyperkalemia
COMPENSATION:
.UP respirations to blow off CO2
.Bicarb UP to compensate
Med Tx:
Calcium, Insulin, glucose, NaO2, Dialysis
Acidosis SS
h/a, sleepiness, confusion, loc, coma, sob, cough, seizure, weakness, diarrhea, arrhythmia, up hr, N/V
Causes of Resp Acidosis
Hypoventilation
.severe pna, ards, impairment of resp muscles, pulmonary edema, aspiration of foreign object, atelectasis, pneumothorax, od sedatives, sleep apnea, non therapeutic O2, COPD pts
COPD and Chronic Hypercapnia
COPD pts gradually accumulate CO2 over time, may not develop hypercapnia d/t compensatory renal changes.
Respiratory Alkalosis
Carbon Acid deficit
lo CO2, decrease in acid, UP pH >7.45, PaCO2 < 38mmhg
.HYPERventilation, LO CO2
.Lo Carbonic Acid
Causes of Respiratory Alkalosis
.extreme anxiety . blow off excess CO2 .Hypoxemia .Gram Neg bacteremia .salicylate intox, ventilator settings
SS of Respiratory Alkalosis
ha, sleepy, confusion, loc, coma, sob, cough, arrhythmia, up hr, seizures, weakness, n/v/d, light headed, stupor, coma, hand tremor, parestesia, twitching, spasms,
Respiratory Alkalosos
Dx:
.UP Ph >7.45
.
continue on Pg 25
pg 25
Adult Respiratory Failure (ARF)
sudden, life threat
deterioration of gas exchange of O2 for CO2 in lungs
can not keep up w rate of O2 consumption and CO2 production
CONDITION not a disease.
any disease w disorder of nerves, spinal cord, muscles or neuromuscular junction involved in respiration
Muscular dystrophy, myasthenia gravis, poliomyelitis,
ALS (amyotrophic lateral sclerosis, Guillain-Barre
syndrome, and cervical spinal cord injuries
Chronic Respiratory Failure (CRF)
CRF is a deterioration in the gas exchange function of the
lung, which develops insidiously, OR has persisted for a long
period after an episode of ARF
Acute Respiratory Distress Syndrome
severe form of acute lung injury
Major cause of death: non pulmonary multiple system organ failure
Suctioning
.apply suction ONLY when REMOVING catheter, gently rotating while withdraw
.NO more than 10-15sec, 3-4 times
.O2 1-2 min before and after suction
O2 Administration
Nasal Cannula, Simple face mask, non rebreather mask, partial rebreather mask, , venturi mask
PNA risks
pt w
.alteration in LOC
.LO/NO gag reflex
.immobile
Raise head of bed when feeding.
PNA
Inflammation of lower resp track.
Bacterial, Viral, Fungal (rare), Chemical
Types of PNA
.community acquired
. hospital acquired
.PNA in immunocompromised host
.aspiration pna
CAP
Community Aquired PNA
.reside naturally in upper resp tract, then colonizes.
.causes lobar or bronchopneumonia
. after recent resp illness
PNA SS
Streptoccal (pneumococcal) PNA: .sudden onset of chills .rapid fever (101-105) .patient severely ill .tachypnea (25-45bmp) .UP plulse
VAP
Ventilator Assisted PNA
VAP SS
.bradycardia (viral) .mycoplasma infection .legionella organim .may URI, Mucopurulent sputum .h/a, lo fever, pleuritic pain, myalgia, rash, pharyngitis
.SEVERE: flushed cheeks,
OLDER adults: .lethargy, confusion, anorexia, rapid hr
.pain/dullness during percussion over affected lung area
.bronchial breath sounds, crackles
Xray: infiltrates w consolidation or pleural effusion
PNA NIs
.monitor abx .deep breathing q 2hrs .humidity to loosen secretions .suction airway PRN .up to 3L/day fluid .encourage flu shot
Chronic Bronchitis
.chronic sputum w cough production on daily basis for min of 3 mos - 1yr .chronic hypoxemia . UP mucous .UP bronchial wall thickness .
Blue bloater
chronic bronchitis .excessive mucous .airway obstruction .hypoxia .residual lung volume UP
Pink Puffer
emphysema .hyperventilation .muscle wasting .weight loss .less hypoxia, work neck and chest muscles
Tripod Position
sitting in chair, hands on knees (tripod)
TB
infection w Mycobacterium Tuberculosis bacteria
.AIRBORNE
.after initial exposure, bacteria encapsulates (form GHON lesion)
.bac dormant until later when ss appear.
TB SS
.asymptomatic .fever, night sweats .anorexia .malaise .cough, sputum .dyspnea, pleuritic chest pain .cavitation or calcification per Xray .positive sputum culture
TB Skin Test
Bacillus Calmette Guerin (BCG) vaccine test w be positive
positive = induratio 10mm or greater in 48-72hrs
TB NIs
• Risk for infection • Ineffective Airway Clearance • Activity Intolerance • Anxiety • Imbalanced nutrition: less than body requirements • Impaired Gas Exchange • Knowledge deficit
TB Interventions
.H, isolation .cough into tissue and dispose immediately in to special basket .meds for 9-12mos .hand washing .report ss of deteriorating/hemorrhage .collect sputum culture .return to work after 3 neg cultures
Cystic Fibrosis
.Autosomal recessive disease, cause dysfx of exocrine gland
.tenacious mucus production, obstructs vital structures
.lung insufficiency
.pancreatic insuff
.UP los of Na+ and Cl- in sweat
Cystic Fibrosis SS
usually dx in white infant or child
.meconium ileus at birth (10-20%) .chronic resp infection .pulmonary congestion .steatorrhea (fatty stool) .foul smelling stool .LO growth and weight .skin salty when kissed
Cystic Fibrosis NIs
.monitor respiration
.IV abx
.pancreatic enzymes
.fat soluble vits A, D, E, K in water soluble form
.nebulizer and O2 tx
.percussion and postural drainage
.DIET: HI cal, HI protein, MOD/HI fat, MOD/LO carbs
child needs 150% of usual calorie intake for normal growth and dev.
Sleep Apnea
sleeping, loud snoring, breathing cessation for 10sec or longer
.awaken abruptly w loud snort as O2 level drops
.5-several hundred events per night.
.HI risk for CAD, cerebrovascular disease, premature death
.repeated apneic events cause hypoxia and hypercapnia
.daytime sleepiness and fatigue
Types of Sleep Apnea
Central and Obstructive
Obstructive Sleep Apnea
most common
.reduced diameter of upper airway or reduced upper airway muscle tone
TX: nasal CPAP or BiPAP w supplemental O2 for severe hypoxia and hypercapnia
.weight loss recommended for obese
.no ETOH and sedatives
Central Sleep Apnea
simultaneous suspension of both airflow and respiratory mvmt
Sx:
– Uvulopalatopharyngoplasty to correct obstruction
– Tracheostomy to bypass obstruction for respiratory failure
or life-threatening dysrhythmias; unplugged during sleep
NI:
.avoid ETOH and respiratory suppressive drugs
.weight loss
.notify re potential daytime sleepiness
Sleep Apnea MEDS
• Modafinil (Provigil) to reduce daytime sleepiness
• Protriptyline (Triptil) HS to increase respiratory drive;
improve upper airway muscle tone
• Patient may require nasal continuous positive airway
pressure (CPAP)
Childhood Upper Airway Disorders
.Croup .Epiglottis tis .Laryngotracheobronchitis .Spasmodic Laryngitis .Tracheitis
Epiglottitis
infection of epiglottis. caused by H. Influenzae type B
SS: .sudden onset .restlessness .hi fever .dysphagia .drooling .muffled voice .child assumes upright position w chin out and tongue protruding
Epiglottitis
• Epiglottis cherry red, swollen and edematous and
can obstruct airway
• Secretions pool in pharynx and larynx above
epiglottis
• Child has sore throat and unable to swallow
• Can have airway obstruction within 2-6 hours
• Hib vaccine has reduced incidence
Bronchiolitis
RSV, Respiratory Syncytial Virus
.young infants
. HIGHLY contagious
.thick secretions
.paroxysmal coughing, nasal flaring, prolonged expiratory phase, wheezing, rales
.deteriorates to rapid, shallow respiration
Bronchitis NIs
.upright position .intubation/Trach .IV abx .NPR, I7o .antipyretics, cotiscosteroids to decrease edema .manage sore throat pain
Croup in kids
Laryngotracehobronchitis
Laryngotracheobrochitis
viral infection
inflammation, edema and narrowing of larynx, trachea and bronchi
.3mos - 8yrs
.most common croup syndrome
.inspiratory stridor and suprasternal retractions upon inhalation (barking cough)
Tonsilitis ss
sore throat fever snoring diff swallow enlarged adenoids cause mouth breathing, head colds, earaches
SARS
Severe Acute Respiratory Syndrome
SARS
.discovered asia, 2/2003
.RESPIRATORY, droplet
.spread by contaminated surfaces then touching mucous membranes
SARS SS
.HI fever .H/a body aches .mild respiratory ss . 10-20% have diarrhea .after 2-7 days, dry cough
SARS Contaigion
• More contagious when symptoms present • Most contagious during second week of illness • Limit contact until ten days after fever no longer present and respiratory symptoms improved • Treatment same as CAP
Nursing Process
ADPIE
Assess Dx Planning Implementation Evaluation
Leading Cause death for MEN
Lung, Prostrate, Colorectal
Leading Cause death for WOMEN
Lung, Breast, Colorectal
Cell membrane of malignant cells contain
proteins tha develop over tikme called “tumor-specific antigens” i.e. prostate-specific antigen (psa)
Malignant Cells
.grow and divind w glucose, O2
.mali`gnant cells us ANEROBIC metabolism
Malignant cells attatch to endothelium and
attract fibrin, platelets and clotting factors to seal off from immune system.
Endothelium retracts, mal cells secret LYSOSOMAL ENZYME tha destroys body sys and allow implantation
Angiogenesis
development of new capillaries from host tissue by release of growth factors and enzymes
such as vascular endothelial growth factor (VEGF)
.These proteins rapidly stimulate formation of new
blood vessels that help malignant cells obtain
nutrients and oxygen
• Through vascular network, the tumor emboli enter
systemic circulation and travel to distant sites.
Therapies target VEGF or its receptors.
Carcinogenesis
malignant transformation
.Imitation: chemicals, physical factors, biologic agents, escape normal enzymatic mechanisms
and alter genetic structure of cellular DNA
.Promotion: repeated exposure to promoting agents (co-carcinogens) causes expression of
abnormal or mutant genetics information (different latency periods)
.Progression: • cells that changed during imitation and promotion invade adjacent tissues and
metastasize
