NURS 301 RESPIRATORY 1 Test WEEK 3.pdf

Medsurg Test 3

RESPIRATORY 1

Allergic Rhinitis

-Seasonal: Intermittent allergic reactions

oSymptoms < 4 days/weak or < 4 weeks per year

oPollen, trees, grass, ragweed

-Perennial: Year-round allergies

oSymptoms > 4 days/weak or > 4 weeks per year

oGenetic component; different IGE response

-Agrivating factors (Type 1 Immuno Reaction)

oRed blotchy areas of skin

oItchiness

oWatery eyes

oIgE response; mast cells produce histamine, leukotrienes, cytokines,

prostaglandins (causing all symptoms)

oMigration into nasal passages- symptoms will continue—headaches could occur

when developed

oBradykinin; itch, vessel dilation- causing red blotchy areas

oSee snoring in a patient that doesn’t normally snore (inflammation, edema)

oCough that worsens when you lay down

oDust- 80% of Americans have dust mites

Allergic to feces

Minimalist décor

Damp dust

oSymptom control via drugs

Stuffiness and occlusion, stasis of secretions… NOT a good idea to tough

it out

oYou are the eyes for your patient. Stasis of mucous you get a sinus infection, so

look for problems

oVIRUS PARALYZES CILIA: they don’t cause infection themselves, but they effect

flow of secretions

-Treatment:

oAvoid the fricken aggravating factor

Dairy maybe help

Dust

Pets

Pollen

Minimalistic décor

Don’t use long heavy curtains

oSymptom control drugs

-Medications:

oAllergies/cold over the counter meds on pg. 479 table 26-2

DON’T just leave to immune system

oAntihistamines (SYMPTOM control drugs)

1st generation: Benadryl- makes you sleepy, patient safety

2nd generation: first line, no sedation

Be careful—these are drying

Maintain adequate fluid intake for patients

Don’t want to see thick secretions

oIntranasal corticosteroids

Cortisol: raises blood glucose, decrease wound healing, increase

infection, thin skin, bruising, osteoporosis

Locally NOT systemically

A pregnisone pill is systemic- COPDers on pregnisone tend to

have osteoporosis, thin skin, easy bruising, code yellow (Falls)

Two weeks prior to expected allergy and use all the way through allergy

sease

Can cause local tissue damage—watch for sores in nose

Don’t use chronically unless benefits outweighs risk (advanced COPD or

brutal asthma, low quality of life)

Redistribution of fat from extremities to core

oLeukotriene antagonists

Inhibit inflammation response

When things aren’t going well with corticosteroid, once a day, on empty

stomach, not first line

Monitor liver function periodically, discontinue if elevated

Singulair (Montelukast)

oNasal decongestants

Drippy nose, sympathomimetic

Sympathetic nervous system vasoconstricting agent

Pseudoephedrine

Dries up nose via vasoconstricts

Good for 1-4 days, between day 4-5, REBOUND DILATION, symptoms

worsen. Should not be used more than 4 days.

Acute Viral Rhinitis

-common cold is a VIRUS

-Only lasts 7-10 days, then should be good for a while

-Slow onset

oEarly stage: nose starts to run, scratchy throat

oIntermediate stage: Increased nasal stuffiness, crummy

oRecover stage: Nose dries up. Symptoms go away

-Give antibiotics for BACTERIAL infections NOT VIRAL

-A lot of questions on prophylaxis of infection and pneumonia

-Think echinacea (a root), zinc, and high dose vitamin C, Elderberry

oCuts it off at the knees

oZican

oDon’t drink vitamin C in pharyngitis… take pill form

-Let immune system mount to take care of this

- Airborne virus

-Winter months

-STRESS

-Signs and Symptoms

oScratchiness of throat

oElevated temp

oMyalgia

oSneezing

oWatery nose

oWater eyes

oCrumminess

oHeadache

-Meds and help

oGive fluids (keep secretions thin so they can flush), rest (immune system mount),

alternate Tylenol (harm to liver) and ibuprofen (harm to kidney) (too much of

one or the other is NOT GOOD)

oOver-counter decongested

-Nasal occlusion and stasis, causing bacterial infections

oUncomplicated viral- don’t have a high temperature, and secretions are clear or

white

oSymptoms of bacterial infection- high fever, green or colorful secretions

-Worried of pharyngitis due to traveling virus, sinus infection, tonsil infection, lower

respiratory tract infection, middle ear infection

- Viruses don’t CAUSE infection, can contribute

oOLDER patients with COPD and viral infection will die!

Doctor would be GOOD to give prophylactic antibiotics in this case

One of the only situations you give prophylactic antibiotics

oUpper respiratory tract most that develops to bacterial presents symptoms that

are more pronounced

Influenza

-October 1-end of May FLU SEASON

-3 main strains are A, B, and C

oA and B cause problems in humans

A mutates over time, governing how we change our vaccine

This year covered two A strains and two B strains

Type A has two types

H-hemaglutanin- facilitates virus entering the cell

N-neurominidase- allow cell to cell replication

A numeric designation after

Neurominidase inhibitor medication! (Tamiflu)

H1N1= swine flu

H3N2= updated that we got coverage for

2 B strains updated

People usually die from this when it enters the lower air way—

POPPING, WET NOISES, CRACKLES are the danger signs

-Hits you like a truck

-S/Sx

oABRUPT

oFever

oHeadache

oCrumminess

oCough- dry and non

oSore throat

-When one or more immunity responses fail and influences invades lower respiratory

tract, paralyzing cilia, TURNS into pneumonia

oHave patients cough and deep breathe, and constantly be assessing for crackles

in the lung fields or rhonchi

-Worried about the elderly folks

-We do have a pen injector, inhalant, egg free

-Symptoms

oVery pronounced

oFever is high in adults- not normal in viral infections

oSwine flu- a lot more GI complications

-Rapid flu test

oViral culture is gold standard, but can take up to three days

oThroat swab- takes 15 minutes

-Get an antiviral in the incubation period! Cuts it off before symptoms occur

-Incubation period 1 to 4 days, then symptoms last 7 days

oYou can pass the flu to someone up to 4 days before you have it

Vaccines

-2 Main types of vaccines

oDEAD- totally inactivated

More broadly given- anyone over 6 months should be getting this

Immunocompromised

Pulmonary issues

Babies 6 months – 2 years

Cardiac issues

Pregnant- 2nd or 3rd trimester

Health Care worker

If you are over 65, you need a higher dose to allow your immune system

to make antibodies

oLive attenuated- weak

Between 2 and 49

Don’t like needles

Pediatric populations

- Takes 2 weeks for antibodies to form

-Certain populations need multiple doses

-Egg free options!!

HOW allergic to eggs are you? If nothing airway, we still encourage

vaccination

oRecombinant= no real dose at all

oGuillon-Barre

Post vaccination neuro condition- involves autoimmune, body attacking

myelin sheath

oMUST be fever free 24 hours before vaccination—has to do with your immune

system

-Rest, fluids, prevention of secondary infections

-Airborne precautions

-Fluid in the alveoli=pneumonia has developed

-4 antiviral drugs approved FDA

oTamiflu- neurominidase inhibitor- does not allow for cell-cell replication

Go for this—we know this

oRelenza- neurominidase inhibitor- dry powder inhalant

oRapivab- IV, one dose, over 30 mins

oXofluza- pill that prevents cell-cell replication

Over 12 age

NOT neurominidase inhibitor

oRISK VS BENEFIT

By day 3 of symptoms, you will not receive these meds because your

immune system will have already started to mount. Let it run its course

(if you have a healthy immune system)

Sinusitis

-Difficult to treat

-Multiple different strains of bacteria

-Patient compliance!

-Come after colds or influenza or allergies

-Caused by SWELLING, OCCLUSION, STASIS OF MUCOUS

-Bacterial strains:

oH influenza bacteria

oStrep pneumonia bacteria

oFungal infections in immunocompromised patients

-SWIMMING POOLs- virus hangs around

-Really look sick- needs good course of antibiotics

-S/sx

oDependent headache (movement, tender to palpation)

Frontal, maxillary—sinus pressure and pain to palpation

oFever

oColorful secretions

oHeadache (pressure)

oMalaise

-TREAT:

oWarm compresses on sinuses – OPENS EVERYTHING UP

oSteam shower –COUGH in shower because humidity is loosening secretions

oNETTY POT

Don’t use tap water (sterile water or normal saline)

oPushing fluids

oDecongestants

Musinex- thins secretions so they can move

oAnalgesics

oSaline Nasal spray

oIf temp is greater than 100.4 NOTIFY MD

Nasal Polyps

-TONS of irritants

-Patients may not know

-Bluish/geryish round benign mass in the pink tuberacle mucosa

-Inhalation of cocaine

-Blocks upper airways

-Local corticoid steroid in injection form

-Clear, watery drainage

-Sound nasal-y

Foreign bodies

-Usually seen in children

-Don’t try to blow it out

-Pinchers, attempt to grasp

-No symptoms or local inflammation

oFoul smelling, purulent nasal discharge

-Avoid instilling water to flush out

Pharyngitis

- 4 defining characteristics

o1. Fever greater than 100.4

o2. Anterior cervical lymph node enlargement

o3. Tonsillar or pharyngeal exudate

o4. Absence of cough

- 90% of upper respiratory tract infections are viral

-Your health care provider might assume this

oYOU CAN NOT TELL if it is viral or strep with just a pen light

oPatches can happen with both viral or bacterial

oRapid strep test to really know

- REST, FLUIDS, ULTERNATE IBPROFEN AND TYLENOL, VITAMIN C

-GABHS- Group A Beta Hemolytic Strep

oLooks like Strep throat, impatego on skin (Red, swollen, acne-like areas)

oMulti-drug resistant

oTravels

oPrimary site of infection then, if misdiagnosed or antibiotics are not working,

we can see traveling and strep on cardiac valves, travel kidneys, joints

(arthritis)

oREEKS HAVOCK

-False negatives with rapid stress test!

oPatient education of what could happen

-Fungal

oAcute skin compromise

oIncreased risk for further infection

oTOO MANY ANTIBIOTICS (due to sepsis, possibly)

oNiastatin

Swish and spit into purple kidney bean

Swish and swallow

-Presentation

oScratchy throat

oPatchy yellow

oSwollen lymph nodes

oPart of viral syndrome

Peritonsillar abscess

-One of worst things that can happen with antibiotic

- Abscess= POCKET OF INFECTION, walls off, avascular

oPoor direct blood supply= hard to treat

-Strep throat, walled off infection in tonsils

oTonsil displaces uvula, obstruction of breath

-leukocytosis, fever, chills, drooling, difficulty swallowing

-Move to IV antibiotic therapy

-Removal of tonsil or drain

Head/Neck cancer

-Usually squamous in nature

-Slow growing

-Symptoms come later

-Oropharyngeal cancer is largest subgroup effected

oHappens to men 2x more than women

oALCOHOL AND TOBACCO together

-Can mean potential loss of voice

- Permanent trach

-Permanent disfigurement

- TRACH AND PEG for nutrition

-Over 50

-Oral human papilloma virus

-Patient does not know what is happening till we have immunological escape

- Smokers get Squamous Cell (SS

-Clinical Manifestations

oMouth ulcers that don’t hear- erythro/leukoplaquia

Ulcerations that don’t heel, which cause , need biopsy

oUnilateral soreness and pain referred to ear

oLumps

oVoice might sound different

oLate stages

Pain with chewing and eating, dysphagia

WEIGHTLOSS due to high metabolic state

Anorexia- loss of appetite

Mechanical discomfort (dentures)

Tracheal deviation/airway obstruction/dyspnea

-Diagnosing

oGold Standard-CT, MRI

oPet scan for Spread

oBronchoscopy, Laryngoscopy

NPO, numbing area, looking at vocal cord lesions

LOOK AT BOOK FOR TESTS

oBiopsy,

Monitor for return of gag reflex, looks for signs of internal bleeding

Throat is highly vasculary- risk for bleeding is high

-If we can diagnose this on stage 1 or 2, we can simply go in and remove tumor

-Higher stages could mean radiation and chemotherapy

oRadiation is fatiguing, when we radiate locally, we can cause local effect

Hyperthyroidism

Fluids to increase saliva production (due to dry mouth)

Have patients carry water

6-8 glasses of water in peg tube daily

oStomatitis

Irritations, pain, ulcerations

Eat soft foods

Avoid spicy foods, go bland

Rinse with water to avoid pockets of food

Causes ulceration

1:1:1 solution Antacid, Benadryl, Lidocaine

MAGIC WASH

oRadiations

Avoid lotions use 2 hours before surgery (burning)

oCordectomy

Removal of part of a cord

oLaryngectomy

Partial: temporary trach, voice remains

TOTAL: Removal of entire voice box

Permanent trach, voice prostethis

Cancer of larynx or disfunction

oVocal cords close TIGHTLY when you swallow

No longer happening

First line defense LOST

oLoss of function of turbinates

Need a home nebulizer and humidifier

oPeople with trach need a lot of fluids!!!

oRadical Neck

Usually is performed with laryngectomy

A LOT of node dissection, big incision, cutting spinal accessory nerve (REAAAD)

oModified

Done as alternative to radical

Preserves nerves and muscles

oPREOP

Talk to patient about what coming back from this will look like- will not be able to

communicate as normal

Show different communication methods

Suction set up at bed side, show patient how to manage oral secretions to avoid

aspiration

Aspiration from saliva is NOT benign—think of bacteria that are above the sterile

field can cause infection… saliva in lower tract= BAD

oPOSTOP

Priorities: maintaining airway

In the first 24 hours they can swell! (STICU or ICU for intubation if needed)

Bleeding-highly vascular, internal bleeding is huge here

Tachycardia, poor perfusion (pedal pulses weak), low H&H, BP drop,

problems with abdomen

Checking vitals frequently

Hemo-vac drain- Round accordian style drain

Frank red blood, to serosanguinous, to serous

Output from drain should be decreasing as healing happens

Nutrition: NG tube, TPN, PEG until they can (if they can) pass

Speech therapy, occupational therapy, psychosocial support

Aspiration precautions—every single patient on your own precautions

Gloves… use them

oPatient teaching

READ on TRACHS (Chapter 26)

Sterile suctioning- check it!! Will be tested

Don’t worry about peg

Scarf over trach when shaving or applying make up

DO. NOT. SWIM.

Medical alert bracelet

O2 therapy to neck

CPR TO NECK

Humidified air! Not getting it from nose

Patient cannot smell… so make food look good 

Tissue repair=protein in diet

-Rib Fractures

oPredisposing factors: osteoporosis

oMost common chest injury from trauma

oEtiology: blow to chest pathological fracture

oSHALLOW BREATHING—Breathing deeply and sigh

CO2 release, and surfactant into air

Collapsed airless alveoli is dead space—no gas exchange (surfactant

decreases surface area

Secretions hang around. STASIS = INFECTIONS

oReceive NSAIDS, opioid, nerve block

-Flail chest

oParadoxical chest wall movement

oUnstable chest wall because of multiple rib fractures

o2 or more ribs in 2 or more separate places

oNot a stable chest wall

oIncreased work of breath

oPresentation

Rapid shallow respirations

Tachycardia

Abnormal resp movement

Air in crepitis tissue

oDiagnosis

Arterial blood gas

Chest X-Ray

Evaluate for crepitis near fractured ribs

oTreatment

Pain control

Air per breath 500mL

Airway management (possible mechanical)

Allow for healing

-Lung Cancers

oCIGARETTE SMOKING NUMBER 1

oNumber 1 cause of cancer related deaths in US

oLOCATION, LOCATION-axillary nodes, chance of metastatic spread is greater 

oDivided non-small cell and small cell

Non-small cell- what we want

Slow growing

More common

Problematic because smokers cough grey sputum and blood—

don’t report symptoms

Small cell

Rapidly proliferating

Ya killing me smalls

oSigns/Symptoms

Cough worsens-persistent

Sputum is usually grey from smoking

Shortness of breath increased

Bronchial obstruction-wheeze

Highly metabolic state cancer

Loss of appetite

Fatigue

N/V

oDiagnosis

Bronchoscopy

CT

Chest X-Ray

Evaluating gag reflex

oTreatment

Stage 1-3a- SURGERY

VATS

Wedge resection

Remove segment of lobe, lobe, whole lung

Radiation

Chemo

Neutropenic precautions

THINK OF PD4 BLOCKERS- cancers hide from immune system

oNursing Care

Assess smoking history

Pack year history- number of smoke packs per day x years of smoking

1 pack of day for 15 years= 15

Nutrition

High calorie

High protein

Fluids

High fowlers

Monitoring for hemorrhage

Monitoring of chest tube

80-90% of lung cancer patients are smokers!!!

It is never too late to encourage quitting

MedSurg Test 3; Power Point 2

-Most respiratory tract infections are 90% viral

-Talking about structures below Carina

oAll sterile

oIf one or more of your body’s defense mechanisms fail, then we get infection of

this sterile area

oStrep Pneumonia, H flu bacteria, or Microplasmo (atypical offender that mimics

bacteria)

-Acute Bronchitis

oInflammation and infection involving the bronchi

Hangs around for about 21 days (ACUTE form)

oEtiology: usually viral, may be bacterial

oPresentation

Hallmark is an infection that worsens at night and worsens when you lay

down

Wheezing (squeaking)

Dyspneic exertion

Low grade fever- viral

Viral- secretions are clear or white

Symptoms are less

BACTERIAL: fever goes higher, more pronounced symptoms, white count

higher

Colorful secretions

Chest X ray

Should not be consolidation nor infiltrations

Consolidation or infiltrates= pneumonia

oPus, junk in alveoli, fluid

oHow will consolidation look in assessments?

oNursing implications

Rest- immunity mounts

Anti-inflammatory drugs

Encourage fluids- thin the secretions

Vaporizer or moisture—humidity

Cough suppressor at night

If bacterial, antibiotics

Renal failure or heart failure= fluid restrictor, we can’t push fluids

Because it is lower resp, we do give neuro-base inhibitors

Tamiflu- blocks cell to cell replication

-Pneumonia

oAcute inflammation in lungs that produces excess fluid from microbial organism

or aspirated irritant

Adventitious lung sounds

Ronchi= mucous

Crackles= wetness

oEdema and Exudate in alveoli

oCan be primary disease or complication of another condition

Hospital acquired

o***When you call respiratory therapy for bronchodilation—they HAVE to be

wheezing! Make every intervention first

Have patient cough, sigh, and deep breath

Sit head of bed all the way up

Nasal Canula

oWe have many primary mechanisms that keep things from getting into lower

respiratory tract

Turbinates in nose

Cilia (cilia escalator)

Cough reflex

Epiglottis

ImgA

If one or more of these mechanisms fail, we see infection

oAspirate flora

oIf there is ronchi, you HAVE to remove it (suction)

oReview P 501, table 27-1 for risk factors for PNA

oCURB 65 p 501 27-1

oExudate in alveoli does not let CO2 leave

Respiratory acidosis

Decreased level in consciousness- drunk, stuporess

KNOW oxygen pirameters

oDivided into CAP and HAP:

oCommunity Acquired Pneumonia

Onset is in community or during first two days of hospital stay

Altered pharyngeal flora

Diabetes or alcoholism

Increased gram-negative flora

A1C—long term measure of blood glucose control

Bedrest

Turn q2h in order to prevent pneumonia—moves secretions,

encourage thoracic expansion

Choking on vomit—ASPIRATION IS HUGE

Urinary tract infection=urinosepsis= triple antibiotic therapy= Causing a

alteration in normal oropharyngeal glora

HIV-immunocompromise

Immunosuppressant drugs (organ transplants)

oHospital Acquired Pneumonia

Health care-associated pneumonia

Bedrest

Turn q2h in order to prevent pneumonia—moves secretions,

encourage thoracic expansion

CHAIR is better than BED for preventative measures

oAspiration Pneumonia

Tube feed-document on this q4h

When abnormal secretions or substances enter lower airway

Mouth or stomach secretions enter trachea

TUBE FEED MONITORING

Safety check (auscultate, aspirate, flush)

High risk in patients with decreased LOC and decreased swallowing

ORAL CARE- document q4h

Head injury

oOpportunistic Pneumonia

Occurs in patients that have suppressed immune systems

Fungal pneumonia, cytomegaly virus

Organ transplant recipients

HARDCORE ANTI VIRALS AND ANTIFUNGALS- amphoterrasins

oClinical Manifestations

Typical

Sudden onset of fever, chills, SOB, productive cough, possible

pleuritic pain, crackles

Older adults may only present with confusion or stupor

Atypical

Gradual onset, dry cough, extra pulmonary manifestations

Headache, sore throat, nausea, vomiting, diarrhea, fatigue,

crackles

Not good gas exchange, air trapping

Viral

Chills, fever, dry, nonproductive cough

oComplications

Inflammation changes at the level of the lungs

Cytokines, Interleukin 1, Compliment cascade, tumor necrosis

factor

Pleuressy= puffy and inflammation of pleural sac, might hear pleural rub

Risky medications

Poor prognosis

Atelectasis

Collapsed, airless, alveoli

Need surfactant to lower surface tension

Sepsis= pneumonia spreads in blood stream (60% mortality)

Lung abscess (in reading)

Walled off pocket of infection

Poorly vascularity, IV antibiotics

VATS procedure

Empyema

infection that invades the pleural space

purulent exudate

Pericarditis

Lung infection, inflammation cascade, moves to heart

Meningitis

100% fatal not treated

Nuccal rigidity and headache

Endocarditis

oInfection in blood gets to heart

oDiagnostics

Chest X-ray

History

Physical exam

Sputum for culture gram stain

Broad spectrum antibiotics

Pulse ox and ABGs

Low- retaining CO2, O2 will be low, PACO2, will be elevated

Labs

Leukocytes > 15000

oNursing Interventions

Prevent aspiration

Asepsis

Standard precautions

ORAL CARE

Monitor ABGs, oximetry, oxygen

TCDB

Limit activity and rest

Antipyretics for increased temperature

Limit activity and rest

Encourage mobility

Hydration

Except if on fluid restrictions (HF, kidney failure)

Calorie dense foods

Things we woudn’t have them eat

High protein

6 times a day instead of 3 big meals

Pneumovax

50-80% effective against pneumonia

Influenza

Percussions 

Helps move secretions up

-Tuberculosis

oAgent- Mycobacterium tuberculosis

oSites of involvement

Primarily lung, can involve other parts

oIncrease risk for TB if person is immunocompromised

oThose at risk

Foreign born, inner city, hawaiins, americans, Asians

oSeen a resurgence of TB

oTransmitted by CLOSE, REPEATED contact- float for minutes to hours

Can’t spread by inanimate objects

oAlveolar macrophages that ingest cilli fuse to form epithelial cell tubercles (tiny

nodules) surrounded by WBCs to capture bacteria

oPerson who has latent TB infection, might not have active disease

oGranulomas not typically viable

Infection remains encapsulated, disease is contained

Lesion can form scar tissue, necrosis of organ

Desemination, granulomas become inflamed and rupture, therefore

exposing surrounding tissue to infection of TB

Now in blood stream, can travel to other drugs

oLatent TB:

Can live in body

Not sick

Not asymptomatic

Not infectious

Fought off by immune system

Negative sputum

Need special blood test

At any given point TB can become activated and move to active TB

TB test

oActive TB:

Become active, immune system can’t stop it from growing

Immunocompromised

SICK

Fatigue

Weight loss

Chills

Low grade fever

Night sweats

Can spread to organs

If patient is immunocompromised already, their risk for getting TB is much

higher

Cough is productive

Contains Blood

Infectious

Abnormal chest x ray

We do NOT diagnose active TB unless it is positive in the sputum

o3 levels of diagnostics in millimeters

Induration—hardening, raised lung. Larger than 5mm, then that’s

positive PPD for immunocompromised patient

Greater than 10: positive for health care worker

Greater than 15: positive for rest of non-health care population

oRead on tests

QFT test tells of if TB is present (does not decifer between latent and

active)

3 morning sputum tests

oNursing implications

Treated on outpatient basis

Hospitalized use airborne isolation- conduct 3 morning sputum tests

Active treatment

Four drug treatment in initial phase

oIsoniazid

oRifampin

oEthambutol

oPyraxinamide

oPG 509 TB 29-11

oSide effect of PZA and rifampin is non-viral hepatitis

Monitor liver function

Masks

HEPA (high efficiency particulate air

N95

-Asthma

oConsidered reversible

oChronic inflammation airway

oMucosal edema and thick secretions block airway

oHyperactivity

oSpasms

oWheezing, tight chest, cough hard to catch breath (sometimes burning)

oRESULT: Airway obstruction

oHR should be up- if it starts slowing this is pretty terrible

oA lot of inflammatory mediators are seen

Exaggerated IgE

oAvoid triggers

oDo not want to see silent chest- CARDIAC PULMONARY ARREST, NO O2 TO BRAIN

oTreat with B2-agaonist

oHypocapnic (due to short rapid breaths, anxiety), getting rid of a lot CO2

o4 classifications of asthma

1. Intermittent

No more than 2 a week

2. Mild

2/week

3. Moderate

Daily symptoms

4. Severe persistent

Severe persistent

oTRIPODING- leaning over, on something, one hand on chest

Requires investigation

oComplications

Status asthmaticus

LIFE THREATENING

Unresponsive to common treatment

Dyspnea at rest, speaks in words only

RR OVER 30, HR OVER 120

If progresses, silent chest, bradycardia, and impending respiratory

failure

IV corticosteroids—for inflammatory problem like refracted asthma or

COPD, increased risk of infection, delayed wound healing

oDiagnosing asthma

History and physical exam

Does your family have allergies, asthma, exercise, what triggers

Peak flow variability or spirometry

FEV1 (REEEEAD***)

Forced expiratory volume in 1 second

Pulmonary function test

Finding out if air trapping is reversible

With hold medication for 6-12 hrs

Perform spirometry

Then look at FEV1-when air is trapped, they fail miserably

BRONCHODILATING TREATMENT wait 15-20 minutes, re-evaluate

oIf test results improved=asthma

oIf test results stayed the same=COPD

Chest X-ray

oArterial blood gas will show a decreased O2

oAt first will release too much CO2 (respiratory alkalosis)

After air trapping starts to occur, retaining of CO2 begins to happen,

which causes acidosis

oNursing implications

Give O2 AS PRESCRIBED

IV access, for corticosteroid therapy in exacerbation of asthma

Monitor FEFR daily at home

Blow green= asthma under control

Blow yellow= adjustment of meds

Blow red= GO TO ED

Exercise induced= educate to premedicate

oDrug Therapy

Antti-inflammatory

Corticosteroids (given immediately)

Leukotriene modifiers

oSingulair

SubQ called Xolair

oAnti IgE

oGiven for asthma that is not being treated by the

conventional

Bronchodilators (Long acting)

Long-acting inhaled or oral Beta-2

Anticholinergics

Bronchodilators (Short acting)

Albuterol

Anticholinergic

Short acting

Long acting

Combination agents

Bronchodilator and anti-inflamatory in one

SEE 28-6 AND 28-8 for the rest

-COPD (Chronic Obstructive Pulmonary Disorder)

oChronic air trapping

oNor fully reversible

oDevelops over years (progressive)

oEncompasses 2 types of obstructive disorders

Emphysema

Chronic Bronchitis

oResults in decreased gas exchange

oCO2 retention

oInability to fully expire

o80-90% caused by smoking

o15-20% caused by other

oChronic Bronchitis

Presence of chronic, productive cough for 3 months in 2 years back to

back in someone whom other causes of cough were ruled out

oEmphysema

Abnormal, irreversible, destructive, enlargement of air spaces distal to

terminal bronchioles with destruction of alveoli walls resulting in

decreased elastic recoil properties

Causing permanent over extension of alveolar walls

Loss of recoil ability

oMost COPDers have both

oRisk Factors

Smoking

Hyperplasia of goblet cells—increased mucous—narrowed airway

Decreases ciliary action

Destroys alveolar walls—dilate distal air space

Occupational hazards

Air pollution

Recurring lung infections

Damage and change mucociliary mechanisms

Heredity

Seen in patients who are young with no history of smoking

AAT (Alpha 1 antitrypsin) deficiency

Serum protein, produced in liver, found in lungs, protective of

proteolytic enzymes and macrophages

Prevents immune system from destroying lung tissue

Autoimmuninty

Given drug called prolastin (high dose)

Aging

oS/Sx

Barrel chest

Trapped air

Pulmonary hypertension

Hypertrophy of right side of heart

Leads to pulm hypertension

Chronically hypoxic—stimulating eurythropoesis, over production of

RBCs, Polycypenia—viscosity of blood increases, alveoli become stiff,

increased pulmonary pressures, right side of heart works harder (carido

muscle becomes hard and thickened, RIGHT SIDED FAILURE)

Polycypenia= unoxygenated hemoglobin, anemia

Cough worsens

Dyspnea worsens

Teached pursed lip breathing (28-13)

Cor Pulmonale (please read….)

Hypoxia, Hypoxemia

Enlarged and tender liver

Distended neck veins

Dependent Edema

Weight Gain

Treatment: LOW flow, continuous, CO2

oDiagnostics

Normal PACO2 35-45—end stage COPD if at 50

Chest X-rays (increased AP diameter)

AAT deficiency?

ABGs are monitored

Fail pulmonary function test

FEV1 is terrible and doesn’t improve with bronchodilators

oNursing Care

PNA and Flu vaccines

Smoking cessation

Position to maximize ventilation

Drug therapy—stepwise fashion

Air way clearance techniques

Effective huff coughing (tb 28-23)

Promotion of sleep

Humidified air

Nutrition= eat 5-6 small meals

High calorie and high protein

Chest physiotherapy

Percussion, vibration, and postural therapy

Exercise

15-20 minutes/three times weekly

RENAL

Kidney Function

-Renal stimulates vitamin D synthesis

oWithout vitamin D, calcium will be reabsorbed, causing decalcification

-Acid/Base balancing- potassium balancing via renal system

-Excrete waste

-Regulate BP

-Produce erythropoietin

oNo erythropoietin = no stimulation of red blood cell production (ANEMIA.COM)

-Activate Vitamin D

-Regulate acid-base balance

-RAAS- Renin-Angiotensin-aldosterone system

oRenin is secreted

oActivates angiotensinogen to Angiotensin

oAngiotensin I is converted to Agiotensin II BUY ACE (in the lungs)

oAngiotensin II stimulates release of aldosterone

oAldosterone causes vasoconstriction

RESPONSE TO HYPOTENSION

-The kidneys…

oOne major arteries going in

oLots of protection for kidneys

-The nephrons

oFunctional unit of kidney

oContain glomulerus

oEach kidney has about 1 million

oGFR= 90-120 mL of fluid/minute being pushed through

VERY RAPID

oNormal is 125? NO

-NORMALS: (need to know )

oSerum BUN: 6-20

oSerum Creatine 0.6-1.3

More sensitive indicator than BUN

BUN to creatine ration: 10-20:1

When BUN and Creatine go up, the glomeruli are not doing what they

should be doing

oCreatine Clearance level: 70-135

Creatine clearance= 24 hr specimen, take to lab, measure concentration

of BUN and Creatine to the total volume (percentage)

Approxamates GFR

Diagnostics table: 44-8

oYou will need to calculate this stuff (ugh)

Renal Calculi

oStones

oNephrolithiasis=kidney stones

o#1 reason= DEHYDRATION

oApprox. 1-2million cases annually in US

Highest incidence in the US southeast & southwest followed by Midwest

More common in summer

More common in Caucasians than in African Americans

Most prevalent between ages 20-55

More prevelent if genetic history is present

oMajor prophylaxis of this is simply fluid replacement

oEtiology

Two components:

Urinary pH

the more basic (higher, alkaline) the less soluble calcium and

phosphate are- give patient’s fluids that will make pH more acidic

(cranberry juice)

oCITRIC MAKES PATIENT’S URINE MORE ALKALINE

The lower the pH, the less soluble are uric acid cystine

oGive citric juices

Classifies kidney stones

Bacterial infections

We can see urea—splitting bacteria

Contributes to stone formation

Infected stones can be seen (indwelling caths, neurogenic bladder, urinary

retention)

oTypes of renal calculi

Calcium Phosphate

Calcium NOT the phosphate that is forming stone

Remove calcium as much as possible from diet

oMilk, cheese, dairy

oAll beans except green beans

oLentils

oFish with small bones

oDried fruit

oNuts

oChocolate, cocoa

oFruit juices

Grow in alkaline urine (give cranberry juice)

Increase Hydration ALWAYS

Primary Hyperparathyroidism

oIncreased excretion of calcium into blood

Calcium Oxalate

The oxalate, not the calcium causing problem

Therapeutic effects:

oGet rid of oxalating causing foods (spinach, rhubarb,

asparagus, cabbage, tomato, beats, nuts, chocolate, tea,

Worcestershire sauce, parsley

oIncrease hydration

oThiazide diuretics

oCholestyramine to bind to oxylate

oCalcium lactate to precipitate oxalate in GI tract

Independent from serum pH

1st LINE: Calcium lactate-binds to oxalate and takes it to GI

2nd LINE: Anti-cholesterol drugs that bind to oxalate

3rd LINE: Thiazide diuretics- gets rid of oxalate

oEffects blood pressure, some patients may have fragile blood

pressure

Uric Acid

Patients with Gout have this

Taking in too much purine, OR not being able to excrete uric acid

Acidic urine

Increase Hydration

Decrease urinary concentration of uric acid

Give allopurinol

Decrease urinary purines

oTake away lots of red meats, organ meats, fish, and birds

Potassium citrate- alkalizes and

Cystine

Genetic predisposition

Defective absorption of cystine in GI tract and kidney

SMALL number of cases

Therapeutic interventions:

oIncrease hydration

oAlpha Penicillamine and Tiopronin to prevent cysteine

crystallization

oK citrate and Alkalinize the urine

Struvite

Predisposing factors

o3-4 times more common in women than men

oALWAYS occurs after UTI!!!

Therapeutic interventions

oHyrdration

oAntimicrobials

oAcetohyroxamic acid (Listhostat)—drug that indirectly lowers

oUrine pH

oSurgical removal

oAcidify urine—Cranberry Juice

Symptoms

Severe or back flank pain

Renal Colic

Hemoturia

May see nausea, vomiting

Colicky, intense pain as it passes through ureter

oSome have described

May see signs of shock

oCool, moist skin

oBecause of pain being so intense

oBP drops

oHR fast

Ureterovesical junction (UVJ)

oPain radiates into testicles, labia, or groin

DESIRE IS TO HAVE STONES PASS ON THEIR OWN, unless too large

-Diagnosis of Renal Calculi

oUrinalysis

Checking pH, WBCs, RBCs

oIVP- site of obstruction, done with dye

Gold standard

Iodine and shellfish allergies

oUltrasound

oCystoscopy

oLabs

BUN

Creatine

Creatine clearance

Culture

-Removal by Endourologic procedures

oLazor action, cystoscopy, break it up

oStones in the renal pelvis Percutaneous Nephrolithotomy

Inserted through sinus tract- goes through skin

Stones crushed using using ultrasound

Wash to remove fragments

Leave a stent in (usually) so residual stone that weren’t able to come out

do not block up ureter

Very days to few weeks

Inflammation may occur, so stents help relieve swelling

oLithoripsy

Shock waves aimed directly at stones

Through patient’s back

Antibiotics for two weeks

Setiment that remains

Self-retaining stent in place for 1-2 weeks to promote passage of sand

May need re-treatment if stone is large

Bright red urine at first (due to trauma) should turn brown and dusty)

Large bruising

Strain urine

Nursing care:

Plan for pain management, ID obstructions, patients education

to reduce re-occurance

Nursing Implementations

Bed, rest, hyrdration

oTurn q2h to facilitate moving the stone

oPatient education to regarding diet, testing urine for pH

oMay require regular urinalysis

Urinary Tract Infections

-Typically the urinary tract above urethra is STERILE

-Women have shorter UTIs than men… therefore more predisposed

-E. Coli is most common

-UTI umbrella

oUrethritis

oCystitis

oPyelonephritis

Cystitis

-Pain urination

-Puss in urine

-Suprabubic pain

-Foul smelling urine

-Dysuria

-Labs (Clean catch)

oWBC and Blood

oUrine culture

oIf all negative, may be caused by irritants

Chemical cystitis—inflammation due to non-bacterial factors

-Subjective assessment

oPrevious UTI, kidney stones, structural problems, pregnancy, stds, bladder cancer,

oMeds: use of antibiotics, anticholinergic, and antispasmodics

oSurgical procedures or foley catheter insertions

oHistory of elimination problems

oTEACHING OF THESE THINGS

-Relief from dysuria

oMedications

oABX (sulfa drugs)

oAntispasmodics

oPain Meds

o#1 BEST PAIN MED IS PYRIDIUM (will turn tears orange)

oApply heat

-No reoccurance of UTI

oTake all meds as prescribed

oGood hygiene

oSEVERAL UTIS= Polionephritis

oAdequate hydration

oAvoid tight clothing

oQuick follow up for recurrent symptoms

Pyelonephritis

-Inflammation of the renal parenchyma and collection system to include renal pelvis

-Presentation

oMild malaise

oFever

oChills

oVomiting

oFlank pain

oDysuria

oLeukocytosis and a shift to

oCast cells: created in urine when WBCs are present

-SYSTEMIC ISSUE

-1-2 IV antiobiotics

-Worry of sepsis

Immune disorders of Kidney:

BIG TWO: Glomerulonephritis and good-pasture’s syndrome

Glomerulonephritis

-Inflammation of glomeruli

-Can be acute or chronic

-There is antigen antibody created within glomeruli that is acting as an autoimmune issue

-May be irrevirsable damage

-Host of things that causes this (See book)

-3 most common

oStreptococcal infections—STREP THROAT

oGood pastures

oLupus

-Signs and Symptoms

oRBCs, WBCs and casts in urine

oProteinurea

oIncreased BUN

oMassive Edema—Filtration not happening like it should

oLethargic

oLittle urine output

oIncreased blood pressure

-Treat

oRest

oSodium and Fluid restrictions

oDiuretics

oAntihypertensives

DIURTEICS

oAdjust protein as needed

oMight need TPN, Central line, PICC line

oDECREASE AMOUNT OF THINGS THAT NEED TO BE FILITERED

Goodpasture’s syndrome (Read)

-Cytotoxic autoimmune disease attack not only glom.s but also the alveolar membrane

-Rare, mostly young male smokers

-S/Sx

oGU

Hematuria

Proteinurea

Renal failure

Elevated BUN and Cr

oPulmonary

Pulmonary insufficiency

Crackles

Rhonchi

Blood in lungs

-Treatment

oImmunosuppressant on outpatient basis—keeps in remission (corticosteroids)

oFor Flare-up; corticosteroids is first treatment (decrease inflammation)

Followed by immunosuppressant

oIf corticosteroids do not work, you will give plasmaphoresis

Plasmaphoresis and Diaphoresis

DI= filters and diffuses the whole blood

PP= filters and diffuses the plasma

Usually used for patients who can’t get back into remission

Bladder Cancer

-Very specific to bladder cells

oTransitional cell carcinoma

-Classified by Jewett-Strong-Marshall system

oSystem of superficial, invasive, and metastatic based on invasion of tumor into

bladder wall

-Treatment

oChemotherapy, Radiation, Immunotherapy

oSurgery

oIntravesical therapy

Route

Bladder tissue is unique and responds well with contact with

chemotherapy and immunotherapy

Bladder Incontinence

-More common in women

-Men- usually overflow secondary to urinary retention

-Bladder pressure is exceeding urethral closure pressure

-Anything that interferes with bladder or urethral sphincter control

-DRIP- Delerium, Dehydration, Depression, Restricted mobility, Rectal impaction,

Infection, Inflammation, Polyuria, Polypharmacy

-Pelvic floor muscle training

-Biofeedback

-Surgery

Urinary retention

-Inability to empty bladder

-Occurs with or without retention

-Two Causes

oBladder outlet obstruction

oDeficient Detrusor Contraction

-Drugs that cause urinary retention

oAnti-hypertensives, anti-parkinsonian, antihistamines, anticholinergics,

antispasmodics, sedatives, anesthetics

-Causes of urinary retention post-operative

oHypovolemia

oAtropines

oAnesthesia

oSedatives

oSwelling and Irritation post foley

oSupine position

-Indications of urinary catheterization

oRelief of retention

oBladder decompression prior to surgery

oSurgical repair of urethra and other structures in that area or to facilitate healing

oInstill meds into bladder

oResidual urine can be measured

oAssess for structural problems

oUrodynamic testing

oSterile sample

oMeasure of I&Os

-Acute Kidney Injurry

oRapid decline of kidney function

oUremia—symptomatic azotemia

BUN and Cr are going up

oProgressive elevation in potassium

o30mL/hr or 240mL/8hr

IF NOT CALL MD

Oliguria is first stage of kidney disease

Not adequately perfusing- not getting enough blood to perfuse

them

GFR is dropping

oPre-renal Causes

Thinks that are happening with blood flow to kidneys

Hypovolemia

Decreased Cardiac Output

Decreased peripheral vascular resistance

oIntra-renal cause

Things that are happening in the bean

Nephrotoxicity injury

Interstitial nephritis

Malignant HTN, prolonged renal ischemia, thrombus formation

oPost-Renal

Blockage between beans and urethra

BPH, bladder cancer, renal calculi

oThree phases

1. Oliguria—less than 400mL/24hr, fluid and electrolytes (increased K,

decreased Na), uremia, fluid retention, neck veins distended, bounding

pulses, edema

2. Diuretic phase

Loops are overwhelmed by access fluid, and start getting rid of

fluid

Nephrons are functioning but not at the diuretic phase

Manifested

Increased of urine to 1-3 L/day

STILL SEE LOW CREATINE CLEARANCE—nephrons are

overwhelmed

High BUN, high serum creatine

Due to fluid loss, may see hyponatremia, dehydration, changes in

potassium levels decreased

oONLY TIME WHEN BOTH N AND K ARE DECREASED—loops

are working, filters are not

oWonkie-Donkie

3. Recovery Phase

Begins when GFR returns to normal, Cr and BUN come down

Manifested by marked improvement in 1-2 weeks

May take up to 12 months to fully recover

oDiagnosis

History and exam

Look at blood flow through kidneys

Identify the precipitating cause

Cr, BUN, electrolytes

Urinalysis

Renal ultrasound, pyelogram, renal scan, CT

oNursing Care

Treat precipitating cause

Fluid restriction (500-600mL and 24-hour monitoring of output)

Equation: if patient 600+300 (Output)= 900mL next 24 hr

Nutritional therapy

Lower K

Calcium supplements

Prevent bone breakdown

TPN or enteric feeding if necessary

Dialysis if needed (oliguria phase and diuretic phase)

oNutritional therapy

DO NOT give sodium during oliguria phase—will avoid hypertension and

CHF

Low protein (1-1.5)

When it is broken down, a biproduct is POTASSIUM

Will cause metabolic acidosis

35-55 Kcal/kg of body weight—non-protein energy source food

Fat good 

oImpact on patient

Altered mental status secondary to _______

Sensory perception alteration

Altered thought process

Fatigue

Anxiety

High risk of infection due to lines, altered immune system, uremic toxins

oThe elderly

More prone to this because decreased renal reserve and impaired

function of other organs secondary to aging

Hypotension, dehydration, diuretics, aminoglycoside therapy, obstruction

such as BPH

-Chronic Kidney Disease

oProgressive, Irreversible

oNephrons die, do not heal!

oDiabetes is leading cause

oHigh blood pressure

oGenetics

oTobacco use greater than 60 years

oObesity

oFamily History

oHeart Problems or stroke

oStage 1

GFR 90% or higher

oStage 2

GFR 60-80

Moderate loss

oStage 3A

Mild to Moderate loss

45-59

oStage 3B

Moderate to severe loss

30-44

oStage 4

15-29

oStage 5

Kidney failure

Less than 15

oDecreased activation of VD

oImpaired Calcium absorption from gut

oDecreased serum calcium

oOSTEOPOROSIS IS A BIG DEAL

oKey intervention: protect from hyperkalemia

As this rises, creates environment of metabolic acidosis

HOW TO LOWER:

Regular insulin, moves K into cells

Sodium bicarbonate—also corrects acidosis

Remember bicarb is a BASE and K is an ACID

oKayexalate draws fluid into gut and electrolytes are

decreased via diarrhea

Calcium Gluconate IV—used in advanced cardiac toxicity

Dialysis—hemodialysis (1), can drop levels in 30 minutes to 2

hours, peritoneal dialysis (2)

oGFR is 15 or less- STAGE 5

oDiffusion is the way peritoneal dialysis works, getting rid of

excessive biproducts

Putting a tube into perineum, then patient can do it

at home in a few months

Put fluid in belly via tube, let it mix, then filter it

Tube can be left in and then used at home

oComplications of peritoneal dialysis

Lower back problems

Bleeding

Pulmonary complications

Protein loss

Exit site infection

Peritonitis

WORST THING that could happen

SHOCK

Die from hypovolemia very quickly

Firm abdomen, pain, BP drop, HR elevating

Hernias

Left sided heart failure if there is not a good

exchange of fluid

oHemodialysis

Fistula or graft

Heparin added—prevent clotting (watch for

bleeding)

oComplications of hemodialysis

Hypotension

Muscle cramps

Loss of blood

Volume issues

READ ABOUT

Sodium Polystyrene sulfonate (Kayexalate)

oMagnesium tends to be elevated—doesn’t usually cause problems

oSodium can be low to normal

oKILLER with kidney disease: INFECTION

oClinical Manifestations

Waste production accumulation

Altered carbohydrate metabolism

Elevated Triglyceride

Anemia, Bleeding tendency, increased risk of infection, increased risk of

cancer, skin issues

oDialysis: movement of fluid/molecules across a semipermeable membrane from

one compartment to another

Used to correct fluid and electrolyte imbalances and to remove waste

products

Can be used to treat drug overdose

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