Final Flashcards
cystic fibrosis
- autosomal recessive disorder
- most common fatal of this type among Caucasians
cystic fibrosis pathophysiology
- mutation of cystic fibrosis transmembrane receptor (CFTR)
- prevents chloride transport in exocrine tissues
- results in thick mucus and increased salt content in sweat
- can effect pancreas, GI tract, liver, reproductive
cystic fibrosis diagnosis
- elevated sweat chloride > 60 mmol/L
- two tests of this level = confirmation
cystic fibrosis treatment goals
- clear secretions
- reverse bronchoconstriction
- treat respiratory infection
- replace pancreatic enzymes
- nutritional support
community acquired pneumonia
- streptococcus pneumonia most common cause
- right middle lobe most common site
- x-ray gold standard for diagnosis
atypical pneumonia
- mycoplasma pneumoniae most common (walking pneumonia) with CXR bilateral patchy infiltrate
- pneumocystis jiroveci in HIV positive
tools to admit pneumonia patient
- PORT score to assess outpatient CAP Tx
- CURB score for admission decision
hospital acquired pneumonia
develops 48 hours after admission
ventilator associated pneumonia
develops 48 hours after intubation
viral pneumonia
- flu like
- patchy infiltrates on CXR
- most common in kids
strep pneumonia
- red-brown rusty sputum
- lobar
- gram + diplococci
H influenzae pneumonia
- COPD patients
- small gram - rods
klebsiella pneumonia
- alcoholics, aspiration
- currant jelly sputum
- encapsulated gram - rod
staph pneumonia
- pink salmon colored sputum
- often nosocomial
- gram + cocci in cluster
mycoplasma pneumonia
- young adults
- CXR looks worse than patient
pseudomonas pneumonia
ICU
immunocompromised
CF patients
legionella pneumonia
- air conditioners
- GI and CNS symptoms that start later
pneumocystitis jiroveci
- HIV patients
- white out CXR
- Tx with bactrim
TB pneumonia
fever, night sweats, weight loss, bloody sputum
occupational disease
need to identify source so that it can be avoided to prevent worsening disease from more exposure
pertussis
- respiratory tract infection caused by bordetella pertussis
- consider for cough lasting more than 3 weeks
- 50% in <2 years old
- no lasting immunity from vaccine or active infection
pertussis catarrhal stage
- 7-10 days
- insidious onset
- mild fever
- hacking cough at night
- coryza
- conjunctivitis
pertussis paroxysmal stage
7-28 days
- spasmodic rapid coughing
- followed by inspiratory stridor
pertussis convalescent stage
- several months
- decreasing severity and frequency of symptoms
pertussis diagnosis
nasopharyngeal culture swab = gold standard
pertussis treatment
-macrolides for all suspected cases
(end in -thromycin)
-prophylaxis for those exposed within 3 weeks
RSV
- form of paramyxovirus
- leading cause of hospitalization of children
- highly contagious
RSV presentation
fever rapid breathing cough possible accessory muscle runny nose nasal flaring
RSV treatment
- O2
- hydration
- treat the fever
- ribavirin in extreme cases
- clear nasal passages
bronchiolitis
- generic term for inflammatory processes that affect the bronchioles
- usually caused by RSV
- most common in under 2
- clinical diagnosis
bronchiolitis treatment
- majority can be discharged
- deep nasal suctioning
croup causes
- parainfluenza most common
- also RSV and flu
- bacterial pneumonia may be secondary
children 3-36 months
croup clinical findings
- gradual onset of symptoms
- barking cough
- hoarse voice
- inspiratory stridor
- mild fever
- often at night
croup severity
westley croup score
croup treatment
- mild: humidified air, antipyretics, fluid
- moderate: single dose dexamethasone, nebulized Epi
- severe: repeated nebulized epi with admission if no improvement
- impending respiratory failure: O2, ICU, scheduled epi, IV steroids
epiglottitis
- inflammation of epiglottis and adjacent supraglottic structures
- in children primarily caused by H. influenza type B, strep, and staph
epiglottitis clinical findings
- febrile toxic appearing children with rapid onset
- dysphagia
- drooling
- tripoding
- hot potato voice
epiglottitis treatment
- defer pharyngeal exam
- stabilize airway
- draw labs before ABX
- empiric ABX cefotaxime or ceftriaxone plus clindamycin or vancomycin
mild westley score
0-2
- at home care
- humidified air
- antipyretics
- fluid
moderate westley score
3-7
- single dose PO steroid
- racemic epi nebulized
severe westley score
8-11
- repeated doses racemic epi
- admission unless marked improvement
impending respiratory failure westley score
12+
- supplemental O2
- scheduled racemic epi
- IM/IV steroid
- ICU admission
Virchow’s Triad
- hypercoagulability
- vessel injury
- venous stasis
sensitive findings for PE
- dyspnea
- pain on inspiration
- tachypnea
- tachycardia
types of emboli with PE
- most common is thrombus
- PE develop with 50-60% patients with proximal DVT
Wells score for DVT
stratifies risk for DVT
0 = low
1-2 = moderate probability
3 or more = high probability
Wells score for PE
stratifies risk of PE
0-1.5 = low probability
2-6 = moderate probability
> 6 = high probability
testing for PE/DVT
pulmonary angiography = gold standard
- V/Q scan no radiation = good for pregnant
- CT scan
- CXR
- EKG
- ultrasound
- ABG/VBG
- D dimer
- CBC
D-dimer
- degradation product of cross linked fibrin that are elevated in presence of a thrombus
- have a high negative predictive value
PERC criteria
- if all are negative can rule out PE for the patient
- can only be used for low risk Wells score patients
positive PERC = perform D dimer
- negative: rule out PE
- positive: CT scan
doppler ultrasound
- test of choice for DVT detection*
- indicated for patients with high pretest probability of DVT and positive D dimer
ABG and PE
- acute respiratory alkalosis from hyperventilation
- profound hypoxia
CXR and PE
- rule out other lung diseases
- Westermark’s sign
- Hampton’s hump
DVT prophylaxis
- low risk: mechanical or Rx
- high risk: mechanical and Rx
PE treatment with anticoagulation
-not definitive therapy but form of secondary prevention that allows endogenous fibrinolytics to clear the existing clot
PE treatment duration with anticoagulation
- first episode w/ reversible cause: 3 months
- first episode w/ idiopathic cause: at least 3 month
- all others long term
nodule versus mass size
- nodule < 3cm
- mass > 3cm
benign nodule characteristics
- size: <1-2 cm
- shape: spherical
- margins: well defined
malignant nodule characteristics
- size: > 1-2 cm
- shape: lobulated
- margins: spiculated
Intermittent asthma
- symptoms: less than or equal to 2 days/week
- night awakenings: less than or equal to 2/month
- use of SABA: less than or equal to 2 days/week
- ADL interference: none
- FEV1: >80% predicted
- FEV1/FVC: normal
- treatment: step 1
mild persistent asthma
- symptoms: >2 days/week but not daily
- night awakenings: 3-4/month
- SABA use: >2/week but not daily and no more than 1/day
- ADL interference: minor
- FEV1: >80% predicted
- FEV1/FVC: normal
- treatment: step 2
moderate persistent asthma
- symptoms: daily
- night awakenings: >1/week, but not nightly
- SABA use: daily
- ADL interference: some limitation
- FEV1: >60% but <80% predicted
- FEV1/FVC: reduced 5%
- treatment: step 3
severe persistent asthma
- symptoms: throughout the day
- night awakenings: often 7/week
- SABA use: several times per day
- ADL interference: extreme limitation
- FEV1: <60% predicted
- FEV1/FVC: reduced >5%
- treatment: step 4 or 5
obstructive PFT
- FEV1: reduced
- TLC: normal or increased
- FEV1/FVC: reduced
restrictive PFT
FEV1: normal or reduced
TLC: reduced
FEV1/FVC: normal or increased
PFT reversible obstruction definition
increase of 12% or more and 200mL increase in FEV1 or FVC
5 components of asthma management
- assess control and severity
- severe versus uncontrolled
- appropriate pharmacology
- address modifiable risk factors and environmental concerns
- self management and education
LABA
- indicated for bronchodilation maintenance
- helps with nocturnal symptoms
short acting anticholinergic
- reduces vagal tone of the airway
- useful for severe exacerbation when combined with SABA
long acting muscarinic agent
- reduces vagal tone of the airway
- works well in COPD
- slow onset of action 60-90 minutes
inhaled corticosteroids
- suppress acute and chronic airway inflammation
- inhibit inflammatory cell migration
- block late phase reaction
- first line maintenance therapy for persistent asthma
leukotriene receptor antagonist
- decreases airway smooth muscle activity
- decreases mucus production
- used in long term control but with variable effect
- alternative to ICS in mild persistent
mast cell stabilizers
- prevent bronchoconstriction
- for prevention and maintenance
- trial of 6-8 weeks needed before effectiveness known
methylxanthines
- causes bronchodilation
- suppresses response of airway to stimuli
- 2nd/3rd line treatment for moderate to severe
- can cause toxicity and drug interactions
step 1 treatment
SABA
step 2 treatment
- low dose ICS
- SABA
step 3 treatment
-low dose ICS and LABA combo
step 4 treatment
-medium dose ICS and LABA
step 5 treatment
medium to high dose ICS/LABA and LAMA
emphysema
- permanent enlargement of airspace due to alveolar destruction
- increased CO2 retention
- pursed lip breathing
- thin with barrel chest
- accessory muscle use
chronic bronchitis
- extensive bronchial mucus
- daily productive cough for 3 consecutive months
- cyanotic/dusky
- hypoxic
- digital clubbing
- exertional dyspnea
- accessory muscle use
COPD causes
- smoking #1
- occupational dust/chemicals
- air pollution
- genetic factors
- Hx allergies and recurrent bronchitis
- alpha1 antitrypsin deficiency
COPD GOLD 1
- mild
- FEV1 greater than or equal to 80% predicted
COPD GOLD 2
-moderate
FEV1: 50-80% predicted
COPD GOLD 3
-severe
FEV1 30-50% predicted
COPD GOLD 4
-very severe
FEV1: <30% predicted
COPD group A treatment
- 0-1 moderate exacerbation but no admission
- mMRC 0-1
- CAT <10
bronchodilator
COPD group B treatment
- 0-1 moderate exacerbation but no admission
- mMRC 2 or more
- CAT 10 or more
LABA or LAMA
COPD group C treatment
- 2 or more moderate exacerbation or 1 or more exacerbation with admission
- mMRC 0-1
- CAT <10
LAMA
COPD group D treatment
- 2 or more moderate exacerbation or 1 or more exacerbation with admission
- mMRC 2 or more
- CAT 10 or more
LAMA
LAMA + LABA (highly symptomatic CAT>20)
ICS + LABA (eos >300)
COPD treatment steroids
- inhaled reduce exacerbation frequency in combination with LABA
- not responsive to oral steroids but a subset of steroid responsive may warrant a trial
COPD treatment when hospitalized
- oxygen
- broad spectrum antibiotics (levofloxacin, ceftriaxone, piperacillin tazobactam)
- usually nebulizers/IV steroids
pH normal
7.35 - 7.45
PaCO2 normal
35 - 45
HCO3 normal
22 - 26
PaO2 normal
> 80
SaO2 normal
> 95
respiratory acidosis
decreased pH
increased pCO2
respiratory acidosis with compensation
decreased pH
increased HCO3
respiratory alkalosis
increased pH
decreased pCO2
respiratory alkalosis with compensation
increased pH
decreased HCO3
alpha 1 antitrypsin deficiency
genetic cause of COPD
influenza diagnosis
- rapid antigen test
- often clinical diagnosis
influenza Rx treatment
- neuraminidase inhibitors
- give within 48 hours of symptom onset
- for high risk patients and prophylactically for high risk patients that were close contact to diagnosed
wegner’s granulomatosis
“granulomatosis with polyangiitis”
-idiopathic
clinical triad
- glomerulonephritis
- necrotizing & inflammatory vasculitis of upper respiratory tract
- necrotizing & inflammatory vasculitis of lower respiratory tract
wegner’s granulomatosis labs
“granulomatosis with polyangiitis”
- normochromic normocytic anemia
- elevated C-ANCA in 90% of patients
wegner’s granulomatosis treatment
“granulomatosis with polyangiitis”
- corticosteroids
- immunosuppressant
churg-strauss syndrome
“eosinophilic granulomatosis with polyangiitis”
-idiopathic
three phases
- prodromal: allergic rhinitis, asthma
- eosinophilic: eosinophilic infiltration of lungs and GI
- vasculitic: life threatening systemic vasculitis
churg-strauss labs
“eosinophilic granulomatosis with polyangiitis”
- elevated IgE
- elevated P-ANCA
churg-strauss treatment
“eosinophilic granulomatosis with polyangiitis”
- corticosteroids
- immunosuppressant
high risk individuals for TB
- close contacts
- foreign born where TB common
- visits TB prevalent country
- high risk congregate settings
- health care workers
- medically underserved
- low income who abuse drugs or alcohol
multidrug resistant TB
-resistant to isoniazid and rifampin
extensively drug resistant TB
-resistant to isoniazid and rifampin
plus
-fluoroquinolones and at least 1 of the 3 injectable 2nd line drugs
≥ 5mm induration TST positive patients
- HIV infected
- recent infectious TB contact
- fibrotic changes on CXR consistent with prior TB
- immunosuppressed
≥ 10mm induration TST positive patients
- recent arrival from TB prevalent country
- injection drug user
- resident/employee high-risk congregate area
- mycobacteriology lab personnel
- have condition that increase risk for progressing to TB
- children under 5
- children and youth exposed to high risk adults
≥ 15 mm induration TST positive patient
has no known risk factors
TB diagnosis
culture is gold standard for confirming TB diagnosis
- all specimens get cultured even if acid fast smear and NAA are negative
- patient is negative with 2 consecutive negative cultures
latent TB treatment
- isoniazid for 9 months
- before treatment check LFT and screen for HIV
isoniazid adverse reaction
- peripheral neuropathy can be treated with vitamin B6
- fatal hepatitis (pregnant/postpartum = higher risk)
TB treatment
"RIPE" Rifampin Isoniazid Pyrazinamide Ethambutol
gets directly observed therapy
pulmonary hypertension
pathologic elevation of pulmonary arterial pressure
mean > 20 mmHg
or
systolic > 30 mmHg
pulmonary hypertension and HIV
treatment of pulmonary HTN can interfere with HIV treatment
-always get HIV test
pulmonary hypertension scoring
NYHA classes I-IV
group 1 pulmonary hypertension
primary pulmonary hypertension
group 2 pulmonary hypertension
due to left heart disease
group 3 pulmonary hypertension
due to lung disease or hypoxia
group 4 pulmonary hypertension
due to chronic PE
group 5 pulmonary hypertension
multifactorial
right sided heart failure signs
- JVD
- pedal edema
- possible systolic ejection murmur
- loud or split S2
transudate pleural effusion
- increased hydrostatic pressure or low plasma oncotic pressure
- low protein and LDH
- CHF, cirrhosis, nephrotic syndrome, PE, hypoalbuminemia
exudate pleural effusion
- due to inflammation and increased capillary permeability
- high protein and LDH
- pneumonia, cancer, TB, viral infection, PE, autoimmune
lights criteria
- determine if fluid is exudative
- looks at serum protein and serum LDH
lofgren’s syndrome
associated with sarcoidosis
- erythema nordosum
- bilateral hilar adenopathy
- polyarthralgia and fever
sarcoidosis labs
- increased ACE
- restrictive PFT
sarcoidosis imaging staging
stage 1: bilateral hilar adenopathy
stage 2: bilateral hilar adenopathy and infiltrates
stage 3: infiltrate only
stage 4: honeycomb
spontaneous pneumonthorax
- primary: no lung disease
- secondary: lung disease
traumatic pneumothorax
simple: blunt trauma
tension: penetrating trauma
iatrogenic pneumothorax
provider caused (central line placement)
ARF criteria
dysfunction of oxygenation and ventilation
PO2 < 60
PCO2 > 50
Sa O2 < 88
ARF presentation
- dyspnea
- headache
- cyanosis
ARF respiratory support
supplemental O2 to keep PO2 >60 or SaO2 >90
assist control ventilation
-inspiratory attempt triggers mechanical breath
synchronized intermittent mechanical ventilation
-patient can breath spontaneously between synchronized mechanical breath
ARDS
- acute onset hypoxemic respiratory distress after clinical insult
- new bilateral pulmonary infiltrate
- impaired oxygenation of arterial blood not caused by HF
