CAM part 2 exam 1

3 cardinal features of asthma

1. intermittent airflow caused by obstruction

2. bronchial hyperresponsiveness

3. airway inflammation

muscles tighten causing lining to get inflamed and mucus to build up

allergen/irritant exposure in asthma

allergen causes airway inflammation

IgE antibodies are made against the trigger and when exposed the antibodies bind mast cells that cause histamine to be released which causes an increase in eosinophiles, mucus hypersecretion and airway hyperresponsiveness

how can airway obstruction in asthma occur?

smooth muscle contractions

mucosal edema

and mucus hypersecretion

airways remodeling

chronic inflammation, mucus production, bronchospasm, protease activity cause goblet cell hypertrophy, SM hypertrophy, and scarring of bronchial endothelium- means a stiff thick bronchi

the increase in eosinophiles (eosinophiles release protease) - that causes scarring and thickening

histamine and leukotrienes cause constriction and increase mucus production

asthma changes in lumen cause what

as the lumen narrows there is turbulent air flow (expiration) = wheezing

and air trapping cause hypercapnia and hyperinflation

extrinsic triggers of asthma

means allergic IgE mediated

animals: cats, dogs, cockroaches, and mice

mold

dust mites

pollen - trees and grass

Intrinsic triggers of asthma

non allergic

exercise

cold/ dry air

pollutant like tobacco and smoke

respiratory infections

medications: aspirin, NSAID, beta blocker

asthma worse with what kind of living

urban

asthma development

interplay between:

genetic susceptibility

environmental exposure

developmental risk factors

asthma phenotypes

there is heterogeneity (state in being diverse) in pathogenesis and response to treatment

1. allergic (atopic)

   1. associated with triad of eczema and rhinitis

2. non allergic

   1. more often adult onset, neutrophils predominance and variable response to tx

3. eosinophilic asthma

   1. needs corticosteroids early

sx of asthma

often worse at night or early morning

episodic wheezing

SOB

chest tightness

cough

vary by degreeas

asthma on PE

acute

tachycardia

could be using accessory muscle use, tripoding

wheezing

tachypnea

silent

chronic ( in between attacks)

often normal

allergic rhinitis, eczema, mild wheezing

what is required for asthma diagnosis

asthma sx plus variable expiratory airflow obstruction the gold standard is spirometry

others are bronchoprovocation testing, peak expiratory flow (helpful in management)

all three test are PTFs pulmonary function testing

spirometry

measure of volume inhaled and exhaled over time

help differentiate obstructive and restrictive lung disease

FEVI

is the max volume of air exhaled in the first sec

FCV (forced vital capacity)

total amount of air exhaled

normal results from spirometry

what would restrictive and obstructive disease look like

FEV1/FVC= 80%

restrictive disease normal or increase ration

obstructive less than 70% (issue with exhalation)

spirometry asthma vs COPD

get baseline PTF then do the bronchodilator test where albuterol is administer and if FEVI or FVC increase by 10% then asthma cause it is showing airflow limitation that is reversible with bronchodilator

testing for asthma if pt is asymptomatic during spirometry

establish baseline FEVA/FVC then administer bronchoconstrictive agent such as histamine or methacholine and if FEV1 drops by 20 % or more than asthma

TEST CONTRAINDICATED in pt with baseline FEV1 less than 65% predicated

peak flow meter

measures the peak expiratory flow

use in the morning before bronchodilator and then again after using it and above 20% means inadequately controlled asthma

helpful tool in managing but involves adherent pt

green good

yellow not good control getting worse

red asthma is severe

goal of asthma tx

decrease sx that interfere with normal activity

reduce future risk like ED visits

prevent permanent airway remodeling

non pharm tx of asthma

aviod triggers/ irritants

increase physical activity

breathing exercises

pharm tx of asthma focus on what two issues

bronchospasm aka relievers

bronchial inflammation aka controllers

types of bronchodilators

anticholinergics

beta 2 agonist

theophylline

beta agonis

SABA- albuterol

LABA0 salmeterol and formoterol

anticholinergics

SAMA- ipratropium

LAMA- tiotropium

medications for bronchial inflammation

corticosteroids

leukotrienes modifiers

mast cell stabilizers

biologics

corticosteroids

systemic= prednisone, prednisolone, and methylprednisolone

ICS= budesonide, fluticasone, momentasone

leukotrienes modifiers

Montelukast

mast cell stabilizer

cromolyn

biologics

omalizumab

mepolizumab

relizumb

combination medications

• ICS/ SAB= albuterol and budesonide

• ICS/ LABA= budesonide/ formoterol and fluticasone/ salmeterol

low dose ICS

can be used as manteance and reliever

max 12 a day

medium dose

daily maintenance

can not be used as reliever too

go back to chart on slide 36

what can be done to reduce risk of exacerbations

using the ICS-formoterol as the reliver according to GINA but in NAEPP they rec only using SABA PRN for step 1

cycle of asthma tx

1. assessment of asthma control- eval based on sx of the last 4 weeks

2. treatment adjustment

3. periodic review

classifications for asthma control

one point for each of the following:

daytime sx more than 2x a week

nighttime awaken

interference with norm activity

reliver medication needed more than 2 a week

0 points= well controlled

1=2 partly controlled

3-4 not controlled

step up/ step down

when uncontrolled despite adherence and good inhaler technique

step down to find the minimum effective dose

monitor for 2-3 months prior to change

asthma severity

is classified retroactively

mild: step 1 or 2
mod: step 3

severe 4 or 5 - can not be diagnosed until inhaler technique, comorbidities, ongoing exposure to allergens looked at and med adherence confirmed all severe cases need referral to pulm

acute exacerbation of asthma

sudden worsening of asthma sx

bronchial SM contraction

step to take:

• R/O other possible causes- make sure asthma

• severity

• O2'

• give rapid acting inhaled bronchodilators via nebulizer or IV magnesium if severe

• start systemic glucocorticoids

asthma exacerbation severity catagorization

1. mild/moderate:

   1. mild= pulse less 100 & PEF/ FEV1 less than 70%

   2. mod= pulse 100-120& PEF/ FEV1 40-69%

2. severe- pulse over 120 and less than 40%

3. respiratory arrest imminent bradycardia and less than 25% of PEF FEV1, wheezing absent

mild moderate tx

1. inhaled SABA via nebulizer ot meter dose inhaler with holder chamber

2. systemic corticosteriods if peak flow less than 70 % or did not respond to SABA

severe tx

goal to maintain SPO2 above 90%

use inhaled SABA + SAMA- albuterol +ipratropium every 20 minutes or continuous for an hour and repeat assessment after 3 doses

inhaled bronchodilators

act on the SM by enhancing or blocking the affects of the autonomic NS

beta agonist bind to enhance relax

anticholinergics block the activity of Ach to suppress PNS and block SM contraction

admit/ transfer if

pt does not feel better

O2 below 94%

PEF less than 60%

fails the road test

boderline okay but no follow up plane

when to discharge

O2 above 94

pt feels better

PEF above 70

passes road test

make sure to have close follow up

asthma prevention and pt education

asthma action plan is written document with instruction with what medication to take, when each medication is appropriate and when to seek help

sleep apnea

apnea mean breath cessation for over 10 sec

hypopnea is decrease airflow with decrease in O2 greater than 4 %

types of sleep apena

1. obstructive - physical blockage of the airway despite respiration effort

2. central sleep - decrease or absent respiration drive

3. mixed

obstructive sleep apnea OSA

collapse of the pharynx during inspiration due to loos of normal muscle tone

upper airway obstruction during sleep

more common in men and obesity

increase in neck circumference strongest correlation of OSA

signs: excessive daytime somnolence and fatigue

ask partner if they have loud cyclical snoring or breath cessation

on PE: bull neck and may see narrowed oropharynx

OSA complications

cardiac arrthmias, HTN, and pulm hypertension

screening of OSA

STOP=BANG survey

use when pt has sx or pre op

score 0-2 no work up

3+ testing recommended

OSA labs

CBC can have erythrocytosis, increase hemoglobin/ hemocrit due to hypoxia

exclude hypothyroidism

OSA definitive diagnostics

1. polysomnography - sleep study and will show apneic episode with hypoxemia

OSA tx

weight loss

CPAP

aviod sedatives like alcohol

MRD mandibular repositioning

obesity hypoventilation syndrome OHS

development of daytime hypercapnia triad of:

1. obesity above 30

2. awake daytime hypercapnia above 45 paCO

3. sleep disordered breathing

diagnosis of exclusion

compilications: HTN, CHF, coronary artery disease

patho of obesity hypoventilation syndrome OHS

• respiratory mechanical impairment: increase adipose tissue along the chest wall and abdomen reduces function residual capacity, lung compliance, and expiratory reserve increase the total work of breathing

• blunted central respiratory drive: the neural stimulation to remain eucapnic fails and this starts as REM sleep but extends to daytime hypercapnia

same tx plan

what is COPD chacterized by

it is an obstructive disease

1. chronic bronchitis - a mucus problem blue bloaters

2. emphysema - a structural prob pink puffers

with persistent respiratory sx and airflow obstruction with history of significant noxious exposure and largely irreversible and progressive

main noxious stimuli for COPD

tobacco smoke

biomass fuel for cooking and heating

chronic bronchitis patho

• repeated noxious stimuli

• chronic inflammation and irritation

• hyperplasia increase in gland size and destruction of cillia

• bronchial thickening with excessive mucus production and retention

• airway obstruction

• chronic cough and phlegm

chronic bronchitis consequences

1. airway obstruction leads to decrease tidal volume and will cause air trapping and hyperinflation

2. damage to the mucociliary defense and increase risk of infection due to reduced clearance

emphysema patho

chronic irritant exposure cause an increase in protease and a decrease in anti means there is more alveolar destruction of the capillaries and alveolar wall with air space enlargement (dilation)

alpha 1 antitrypsin deficiency

increase risk of emphysema even with limited air pollutant exposure

emphysema consequences

aveolar wall and capillary destruction means the the SA is decreased and there is an increase in dead space and due to the elastin destruction it impairs ability to recoil which leads to air trapping and decrease tidal volume

clinical presentation of COPD

SOB

septum production

cough

productive cough is the bronchitis and the SOB is emphysema

acute exacerbation is worsening of any of these sx and is precipited by infection often times

COPD on PE

chachexia (wasting)

hypoxic or tachypnea

increase AP diameter, decrease breath sounds, hyperresonant to percussion, wheezing, rhonchi, crackles

diagnosis critera for COPD

1. COPD sx

2. persistent airflow limitation soj post bronchdilator FEVA/FVC<70%

   1. no alternative explanation of sx

COPD initial assessment

1. spirometry (needed for diagnosis)

2. asses severity via GOLD which is spirometry, questionnaire (CAT or Mmrc) AND EXACERBATION HX

3. CBC with diff

4. CXR

5. test for alpha def

spirometry of obstructive pattern

FEV1/FVC less than 70%

what can you use to asses severity of COPD on spirometry

FEV1 the degree of airflow obstruction is a prognostic factor

1- above than 80%

2- between 50-80

3-severe between 30 and 50

4- very severe less than 30 %

GOLD ABE assessment tool

if one or more exacerbation in the last year = E

if no exacerbation and mMRC0-1 or CAT less than 10=A

if no and mMRC equal or above 2 and CAT equal or greater than 10=B

CBC with diff in COPD

polycythemia

anemia (of chronic disease)

eosinphil count used to guide tx iICS if above 300

CXR findings in COPD

most reliable: hyperinflation and flattening of the diaphragms

others: hyperlucency of lungs, prominent pulm arteries, and bullae

chronic bronchitis cause increase in pulm vascular and right heart enlargement

emphysema cause decrease in vascular, hyperinflation, flatten diaphragms, hyperlucent, bullae/blebs, and both cause an increase in AP diameter

bullea increase risk of pneumothorax

stable COPD management

stop smoking, make sure they get vaccinations, aviod envirnmental triggers. pulm rehab, physical activity, good sleep and diet

oxygen th via nasal cannula 1-3 L /min if less than 88%, ABG above 55mmHg, cor pulmonale (RH failure). titrate o2 92% to not decrease respiration drive

everyone gets rescue inhaler -= SABA+ SAMA and th is dependent of group

bronchodilators for COPD

anticholinergics: block Ach from muscarinic receptor means less bronchoconstriction and decrease secretions. SE: dry everything, blurred vision, hard time swallowing

SAMA- ipratropium

LAMA- tiotropium, aclidinium, umeclidinium, glycopyrrolate

beta agonist for COPD

se: tremor, tachycardia, restlessness, hypokalemia, CNS stimulation

SAMA- albuteral

LAMA- formoterol and salmeterol

oral corticosteroids for COPD

ICS= budesonide, fluticasone, momentasone

helps reduce exacerbation use when EOS above 300

oral- tx for exacerbations long term affects: osteoporosis, weight gain, cataracts, glucose intolerance, increase risk of infection

COPD tx based on groups

all get rescue inhaler that is SAMA, SABA

group A= LAMA

group B- LAMA+LABA+ICS

COPD exacerbation management

1. o2 th to 88-93%

2. nebulize SABA/SAMA (albuterol and ipratropium)

3. systemic corticosteroids for airway inflammation'

4. empiric antibiotics for five days if they are hospitalized or if two of the cardinal sx are present

   1. no risk factor: azithro and cefpodoxime

   2. risk factor: amox-calvulanate, levofloxacin

smoke inhalation

slide 60

acute bronchitis

self limiting respiratory tract infection causing bronchial inflammation (of the large airways) when there is no evidence of pneumonia or chronic obstructive pulm disease. highest occurrence in late fall and winter along with viral peak.

virus caused thickening, increase mucus production (blockage), and airway hyperresponsivity (like asthma)

chronic cough is the cardinal sx is 18 days to 8 wks can be purulent or not, +/- hemoptysis but should bot be febrile

clinical dx

tx: supportive can use dextromorphan and guaifenesin as need for cough

indications for cxr for chronic bronchitis

abnormal vital

pulse above 100

RR above 24

temp above 100.4

o2 sat below 95 %

or if there is mental confusion with a patient above 75 y

respiratory syncytial virus

paramyxovirus outbreak in october-jan

aka RSV

can affect adult older than 60, severe immunodef

prodrome=1-3 days (URI sx like nasal congestion and cough) then progress to lower resp infection 2-3 days later with sx like wheezing, tachypnea, and worsening cough, peaks on 3-5 days

clincal dx: winter season less than 24 months, RSV PCR is gold standard only test if tx changes

RSV tx

supportive

hydrate, humidification of inspired air, nasal suction…

admit if they are hypoxic, respiratory distress, unable to tolerate PO

Ribavirin is antiviral when hospitalized

RSV prevention

1. Nirsevimab: all for infants less than 8 months entering first RSV season. Children 8-19 months at increase risk entering 2 season (prematurity. CF)

2. clesroviman: also first line for infant less than 8 months before RSV season no approved for second season

3. palivizumab- alt tx

4. arexvy- adults over 60

5. arbyso pregno pt 35-39 wks antibodies are transmitted to fetus.

pneumonia transmission

aerosol inhalation

colonizes in the nasopharynx and then reaches the alveoli and infection leads to inflammation and damage

legionella disease

through infected water such as AC units, ventilation systems (planes)

CM: extrapulmonary like watery diarrhea with neurological sx headache, confuson

PCR testing labs will show hyponatremia, increase ALT/AST & LDH, CK

tx: macrolides

different site of acquisition for pneumonia

1. community acquired - outside the hospital (or within 48 hrs of admission)

2. nosocomial (hospital acquired) after 48 hrs also includes VAP

3. aspiration pneumonia - aspiration of oropharyngeal or upper GI contents

Etiology of pneumonia

typical

atypical

fungi

virus

mycobacterium

CM of typical pneumonia

fever, productive cough, chest pain, dyspnea, rigors (chills and violent shaking)

atypical pneumonia

extrapulmonary symptoms

low grade fever

dry non-productive cough

physical exam for pneumonia findings

signs of consolidation:

inspiration crackles

bronchial breath sounds

dullness to percussion

increase tactile fremitus

egophony

atypical is often normal

bacteria that cause typical

kleb

strep pneumonia

staph pneumonia

h. influenza

Moraxella catarrhalis

atypical organism

mycoplasma pneumonia

legionella

chlamydia pneumonia

CAP

MC- strep pneumoniae gram + cocci in pairs (pairs strep down)

2nd MC h influenza gram - rod, often older adults

sudden onset chills and rigors with rusty blood-tinged sputum

staph aureus influenza

post influenza infection

gram + cocci in cluster

cxr: bilateral infiltrates multoloblar and can cause cavitary lesionsl

klebsiella pneumoniae

CAP in DM, alcoholics and impaired host defenses

gram - rods

has currant jelly sputum due to marked inflammation and necrosis cause the thick mucus that is blood tinged

cxr: can be cavity will be upper lobar consolidation with bulding

mycoplasma pneumoniae

walking pneumoniae

in young health collage students

URI prodrome followed by persistent cough

DX: CXR shows reticulonodular pattern or interstitial infiltrates and cold agglutinin titers will not be able to PCR

tx: macrolide or doxy

2 levofloxacin

CAP viruses

influenza

PCR testing or respiratory pathogen panel

tx: supportive care

influenza - oseltamivir

COVID- nirmatrelvir-ritonavir