Pulmonology Flashcards
what are the three broad types of pneumonia source categories? which one is most common? which are most difficult to treat?
- community acquired pnuemonia (CAP)
**most common**
- healthcare/hospital acquired pneumonia (HCAP)
- most difficult to treat - ventilatror associated pneumonia (VAP)
what are four important ways to reduce ventalator associated pneumonia (VAP)?
- avoid ET tube
- keep head of bed elevated
- reduce sedation
- hand washing
what is important to do once you have finished treating pneumonia?
post treatment xray
want to make sure everything is cleared up and that the treatment has worked!
what is the most common organism seen in pneumoniae overall?
s. pneumoniae
what four patient populations make you at an increased risk for pneumonia?
- ETOH
- asthma
- immunosupressed
- elderly
Typical pneumonia
what are four common organisms associated with this and their characterist sputum color? how long do symptoms increase? what are some of the things on the long list of symptoms
“common symptoms”, usually responsive to B-lactams
#1 most common: streptococcus pneumoniae (rusty red color)
#2: haemophilis influenzae (green sputum)
staph aureus
klebsiella (currant jelly)
pseudomonas (foul smelling)
SX:
1-10 day increase in cough, purlulent sputum, SOB, dullness to precussion, rigors, tachycardia bronchial breath sounds, tactile fremitis (say 99), friction rub, pleuritic chest pain, night sweats
atypical pneumonia
“walking pneumonia”
usually unresponsive to beta lactam, use macrolide or fluorquinolone
1. mycobacteria pneumoniae (bullous myringitis..ear)
2. chlamydia pneumonia
3. legionella
4. viruses->
(RSV and parainfluenze in kids, and influenza in adults)
PE: often normal physical exam, can have extrapulmonary symptoms
DX: use macrolides (erythromycin, azithromycin, clarithromycin, doxycycline) or fluoroquinolones
what are the three most common organisms that cause community acquired pneumonia (CAP)?
#1: streptococcus pneumoniae
#2: haemophilis influenzae (esp in COPD)
#3 mycoplasma pneumoniae (atypical)
what are the three common organisms that cause hospital acquired pneumonia?
- gram negative pseudomonas
- ancinetobacter
- staph aureus
what is the mortality rate in hospital acquired pneumonia?
50-70%
what are the five tests you use to diagnose pneumonia?
- clinical syndrome, empirically
- gram stain- GCP
- sputum culture
- urine tests (only in legionella and pneumococcus)
- xray showing white infiltrate
streptococcus pneumoniae=
pneumococcus
they are the same thing, so if used in a test question, they mean the same thing, its just an abreviated name for this **important since this is the most common organism to cause pneumoniae**
if a patient has pneumonia with MRSA, what should you use to treat?
vancomycin
streptococcus pneumoniae in pneumonia
(what color is the sputum? what is it sensitive to? what can happen if this is systemic? is there a immunization for this?)
- rusty blood colored sputum
- beta lactam sensitivity
- if systemic can cause confusion
**immunizable** this is what the vaccine is for!
what is the treatment for patients with pneumonia? how long is the treatment regimen?
- 80% can be treated as outpatient with macrolide azithromycin/erythromycin/clarithromycin
(atypical or “walking pneumonia)
- if ths same patient has chronic illness combine with beta lactam
- if MRSA infection use vacomycin or fluroquinolone
**5- 14 day treatment**
Explain the new vaccine regimen that is reccomeded?
PVC13: childhood vaccination
PV23: used in 65 +
****new recommendations say 65+ recieve BOTH, adults get PCV13 first then PV23 second 8 weeks later***
if they have already had PV23, wait a year and give PVC13
explain which pneumonia organism these populations are at the most risk to get:
ETOH-
COPD-
CF-
Air-conditioning-
children
Children
ETOH- klebsiella
COPD- haemophilis influenzae
CF-pseudomonas
Air-conditioning-legionella
children
Children
what is the most common lung cancer seen in non smokers?
adenovirus
general bronchogenic carcinoma
“Lung cancer”
what is this the leading cause of? what are the two types? where are the four locations these mets are likely to spread? what is the main cause of these? what are 7 symptoms associated with lung cancer in general?
leading cause of cancer in men and women
made of two categories:
- small cell lung carcinoma
- non small cell lung carcinoma
mets to brain, bone, liver, lymph
SX:
****ASYMPTOMATIC, mostly incidental finding on CXR****
- ***change in nature of cough (squamous, small cell)
- hemoptosis
- vague nonpleuritic chest pain
- reccurent pneumonia
- WEIGHT LOSS ANOREXIA ASTHENIC (CLASSIC)
- HYPERCALCEMIA, don’t miss this
cigarette smoking is the main cause, 85% of lung cancer in smokers
small-cell carcinoma “oat cell”
is this fast or slow? WHERE IS IT LOCATED? what is the doubling time? what are the 6 paraneoplastic syndroms associated with it? what is the treatment? what is the difference between limited and extensive stage?
bad actor!!-grows quickyl metastasizes early!! assume m micrometasizes on presentation!
CENTRAL bronchial epithelium (near hilum because thats where all the vessels are so it can get a lot of nuitrients)
doubleing time: 30 day!!!
limited stage: tumor on the same side of chest, supraclavicular lymph nodes, or both (20% 2 year survival)
extensive stage: anyhting beyond limited stage (5% 2 year survival)
associated paraneoplastic syndromes: cushings, hyponaturemia, SAIDH, periphreal neuropathy, eaton lambert, cerebral degeneration
TX: since it matastasizes so quickly, CHEMO is the treatment
what are the three types of non small cell carcinoma?
(NSLC)
1. squamous, (smokers) central with cavitary lesions
2. adenocarcinoma (non smokers), periphreal, Asbestos
3. large cell very aggressive!
which is more common, small cell or non small cell lung carcinoma
non small cell carcinoma
80-85% of LC
where are four most common places for metastases for lung?
liver-common
bone-symptomatic
adrenal
brain
*****which cancer is associated with paraneoplastic type syndromes******
what are the 6?
SMALL CELL CARCINOMA
associated with:
cushings (buffalo hump), cortico levels, hyponaturemia, SAIDH, periphreal neuropathy, eaton lambert, cerebral degeneration
squamous cell cancer
which cells does this occur in? where is it located? how can you dianose/what is major symtom? what is a random paraneoplastic syndrome associated with this? what is interesting about the metastsis of this? who is this most common in?
MOST COMMON NON-SMALL CELL IN SMOKERS!!!
basal cells of bronchial epithelium
centrally located, frequency hemoptysis and change of cough, CAVITATION
hemoptosis diagnosed with cytology
late metastasis–so if you catch it early in the patient the prognosis is better!
paraneoplastic synderome: hypercalcemia
TX: surgical
adenocarcinoma
what is this the most common of? where does the cancer occur and where does it appear? what does it metastasize to? what is the treatment? what are two paraneoplastic syndromes? what can you get it from? smokers or nonsmokers?
most common bronchogenic CA
common in non-smokers
peripheral, lung parenchyma
originates in the mucous glands of tracheobrachial tree and appears in the periphreay of lung
moderate growth and metastatic rate
NON SMOKERS, can get from ASBESTOS!!!
paraneoplastic syndrome: thrombophlebitis, PTH-rp
TX: surgical
large cell cancer
where is this located? what is the doubling time? is there metastasis? what is the paraneoplastic syndrome? what is the treatment?
periphreal or centrally located
cavitation
rapid growth
early metastasis
doubling time 100 days
paraneoplastic syndrome: gynecomastic
TX: surgical
bronchial carcinoid tumor
what type of tumor is this? where else is it commonly found? describe what this tumor would look like if you saw it? what does it secrete (4), what are two symptoms you can have with this? what is the treatment?
CENTRAL neuroendocrine tumor, slow growth, slow mets
also commonly found in GI tract
typical: SESSILE (attached to base) or pedunulated (cylander)
atypical
pink/purple well vascularized central tumor, pedunculated or sessile
secretes SEROTONIN, ACTH, ADH, MSH
often asymptomatic, but can have hemoptosis and c_arcinoid syndrome_ (diareah from increased serotonin and left sided hear fibrosis)
TX: steroids and surgery, resistant to chemo and radiation
what is the #1 RF for lung cancer?
SMOKING
Lung cancer
what are the 4 keys sxs?
how do you initially dx? 3
and confirm dx? 3
2 major groups?
SXS:
1. new or changing cough
2. hemoptosis
- dyspnea
- pleural effusions
DX:
- CXR/CT
- PET
- Needle Bx/ bronchoscopy with bx/open lung bx
- small cell lung cancer (SCLC)
- NON-small cell lung cancer
Small cell lung cancer (SCLC)
what is the type of cancer that fulls under this?
4 qualities?
- when spreads?
- tx options?
- where spreads?
- find anything else?
OAT CELL CANCER
- spreads early
- can’t tx with surgery!!!
- Central to Periphreal
- AGGRESSIVE, micrometasis with presentation (hence no surgery)
Non-small cell lung cancer (NSCLC)
3 types?
speed?
tx?
slower grower
can have surgery!!
includes:
- squamous cell
- adenocarcinoma
- large cell
NSCLC
sqamous
location?
think what two things?
often presents with?
- occur centrally
- squamous=think “sentrally and SMOKING”
- often presents with hemoptosis
NSCLC
adenocarcinoma
what is the KEY fact to know about this one?
location?
speed?
metastasis?
**MOST COMMON TYPE OF LUNG CNACER**
- occur periphreal
- rapid
- metasizes to distant organs
NSCLC
large cell
- large cell
- VERY MALIGNANT
what lung cancer arises in nonsmokers?
adenocarcinoma
what are the metastasis palces for lung cancer?
5
Brain
Bone
Adrenals
Liver
kidney
carcinoid lung mass
what is a key characteristic of this?
what does it look like?
tx?
neuroendocrine tumor
*can also be in the GI tract*
bronchoscopy shows red, yellow, purple mass that is well vascularized
tx: surgical ressection
pulmonary coin lesions
what and where are these?
What is the most common cause?
appearance?
2 dx?
how do you determine what to do about them?
intraparenchymal lessions LESS THAN 3 cm
MC are infectious granulomas
if round and sharply demarkated don’t need to bx, usually found incidently on imaging
DX:
- CXR: popcorn calcicifications
- Chest CT
TX:
- if low malignancy likelihood round and sharply demarkated can watch and monitor
2. if begins to change or have poor margins then must EXCISE
acute bronchitis
What is this condition characterized by? how long does the cough last? what other symptoms might you see? what are 90% caused by (4)? what are the 3 bacteria that cause it in CHRONIC disease? when do you do a CXR?
inflammation of trachea, bronchi, and bronchioles resulting from RTI or chemical irritant characterized by COUGH, often follors URI
COUGH LASTS 10-20 DAYS!!, SEE EXPIRATORY RALES/RHONCHI
90% caused by viruses including rhinovirus, adenovirus, coronavirus, and RSV
in chronic lung disease, commonly caused by: haemophilis influenzae, strep pneumoniae, m cartillis
CXR: ONLY DO IF TRYING TO DISTINGUIS BETWEEN THAT AND PNEUMONIA
acute bronchitis
what are the four OTC treatments for this? what is the DOC for bacterial and what two types of patients qualify for this treatment?
- hydration
- expectorants
- analgesics
- cough suppressants (children)
for bacterial: DOC cephalosporin
-reccomended only for ELDERLY pt with underlying cardiopulmonary disease and a cough for >7-10 days and ANY IMMUNOCOMPRISED PT
***for acute exacerbations in otherwise healthy…..NO TREATMENT NEEDED****
acute bronchitis in normal host
do you treat this patient? what is the requirement for the length of time before giving them treatment? what are the two abx reccomended if they meet the criteria? what is the treatment for the different age groups?
THE TREATMENT WITH ABX IN NORMAL PATIENT HAS NOT BEEN CONFIRMED, use bronchodilators instead because they are more effective at getting rid of cough than abx
exception: >10-14 days, then can treat since this is beyond the viral process and happens in atypical pathogen like mycoplasma pneumoniae, chlamydophilia, pertussis
>55 years old= macrolide (mycins) or tetracycline
>8= doxycycline
idiopathic pulmonary fibrosis
aka idiopathic interstitial pneumonia
what type of pulmonary condition is this? what is caused by? how long does a patient typically have after diagnosis? what are the three types?
RESTRICTIVE!!
remodeling of the lung to look like honeycomb lung, fibroblasts come in and lay down fibrosis tissue, can be associated with age
dismal prognosis, 3 years from diagnosis
3 Types:
- usual interstitial fibrosis
- respiratory bronchiolitis, associated with this
- acute interstitial pneumonitis
idiopathic pulmonary fibrosis
what are 3 symptoms you would see of this? what are the 3 tests you would use diagnose this? what do you see on them?
SX:
-inspiratory “squeaks” crackles
- clubbing of digits
- progressive dyspnea with dry non productive cough
DX:
1. chest CT:
-diffuse reticular opacities with HONEYCOMBING, ground glass opacities
2. PFT shows decrease FEV1 and FVC, so FEV1/FVC appears normal
3. lung biopsy important for confirmation
idiopathic pulmonary fibrosis
what is the treatment
none, you’re out of luck!!
can give supplement O2 if needed but nothing has been shown to increase survival or quality of life.
lung transplant may be the only choice
who wants some pics of idiopathic pulmonary fibrosis?
these help to show honeycombing!!
bronchiectasis
explain the pathophys of this aka how does this happen? what are the two ways this can happen?
secondary disease that is caused by infection or other conditions that injure the walls of the airways or prevents the airways from clearing mucous. the mucous build up causes increased infection and each infection causes more damange and eventually the airways can’t move air in and out from damage and scarring.
*can be congenital with CF or from obstruction*
*as mucous builds up and stretches everything, the membranes become more floppy and can collapse easier, which is why this is obstructive, not just because of the mucous*
if a patient has bronchiectasis what four infections do you worry about?
1: haemophilis influenzae (most common in world)
the mucous build up creates a perfect breeding ground for pathogens
#2: pseudomonas (CF, #1 cause in US)
- aspergillis (brown sputum)
bronchiectasis
what are the 6 symptoms you would see with a pt with bronchiectasis? what are the 3 tests you would do to test patient for this? what would you see on these?
- recurrent pneumonia
- chronic cough
- hemoptysis (50-70%), bronchiectasis is main cause of this
- foul smelling mucopurlulent sputum
- clubbing (as seen with CF)
- crackles at base
DX:
- high resolution CT; imaging of choice, dilated tortuous airways
2. CXR; crowded bronch markings, basal cystic spaces, Tram Track markings (bronchial wall thickening), honeycombing, signet ring sign (pulmonary artery coupled with dilated bronchus)
3. bronchoscopy warrented to eval hemopytsis and remove secretions
bronchiectasis
what are the 4 treatment options?
- ABX for 10-14 days for infections
- supressive therapy
- bronchodilators
- lung transplant
solitary pulmonary nodules
what is the nickname for these? what makes it likely defined? what percent are benign/maligant? how do you diangnose? what are the three treatment for high, medium, and low maligancy risk?
“coin lesions”, KEEP IN MIND THIS IS THE FIRST MANIFESTATION OF ANY TYPE OF LUNG CANCER, THIS ISN’T A CANCER TYPE BUT THE CLASSIFICATION FOR ANY FIRST APPEARNCE OF CANCER
Defined:
Most at asymptomatic
60% benign, 40% malignant
often infectious granulomas from old reactive TB, fungal infection, or foreign body rxn
DX:
- CT for nodules
- PET for >1 cm and intermediate probability
TX: if high probability….RESECT LESION
if intermediate……biopsy
if low… can be watched, need CT every 3 months for a year, then decrease to every 6 months for two years
if
what are three symptoms that can help push you towards cancer?
- hemoptosis
- fever
- weight loss
what percent of solitary pulmonary nodules are primary lung cancer?
75%
sarcoidosis
what is this condition? what type of cells respond to this? what percent of people have lung involvment? what is the intial lesion called? and what about when its progressed? what are the 6 common parts of the body that it effects?
MULTISYSTEM DISEASE MADE OF NONINFECTIOUS NONCASEATING GRANULOMAS CAUSING INFLAMMATION IN INVOLVED ORGANS
the granumlomas form in response to exagerated T cell response, these granulomas “masses” take up space and disrupt organ function
90% have lung involvement
- initial lesion in lung called: CD4 T cell alveolitis*
- progression of disease: transforms into noncaseating granuloma*
most effected: 1. pulmonary 2. lymphadenopathy (_hilar lymph nodes_) 3. skin (erythema nodosa) 4. lupus pernio 5. PAROTID ENLARGEMENT 6. visual defects (20%)
what are the three tests you can do to confirm sarcoidosis?
1. serum blood tests
-Leukopenia
-eosinophilia
-elevated ESR
-hypercalcemia
-hypercalciuria
2. CXR
billateral hilar lymphadenopathy
2. elevated angiotensin (40-80%)
3. needle biopsy needed to confirm noncaseating granulomas
what percent of people with sarcoidosis can be asymptomatic?
what is the treatment?
50% can be asymptomatic
Very responsive to high dose corticosteroids!
what is the structure of influenza? what family? what types?
- single stranded RNA
- orthomyxovirdae family
- A, B, C types
what is the composition of influenza A? of these two, how many are there in humans?
hemagglutinin (HA)
neuramidase (NA)
3 HA types in humans
2 NA types in humans
what are 3 challenges of containment of influenza?
- short incubation time (1-7 days)
- ability for person with asymptomatic infection to transmit virus (can be contagious 1 day before symptoms)
- early symptoms of illness are likely to be non-specific, delaying recognition (need to get antivirals on board within 48 hours of onset)
influenza
what are the three types and which one is most pathogenic? what is the season for this disease, how is it spread and how long can it survive on a surface? how long does it incubate? how long do symptoms last? when is a person contagious? when is peak shedding and what does it correlate with? what is the definition? what is the best choice for diagnosis?
3 types; A (most pathogenic), B, C; neuramidase and hemmaglutinin make up the subtypes
Fall/winter outbreaks (october-november)
spread through aerosolized droplets, can live on surfaces 2-8 hours
- incubates 1-7 days, avg 3
- symptoms last 3-7 days, but up to 14
3. contagious 1 day before symptoms, 5-7 days after
4. peak shedding 3 days of illness, correlates with fever
fever >100 or 37.8C AND cough or sore throat in absence of know cause, ABRUPT onset, can have myalgia in legs and lumbosacral area. Emergency if CNS symptoms.
PCR is best choice for diagnosis, can do rapid from throat or nose, but not as good
what is the best way to prevent influenza?
what are the two mechanisms of this? which age groups should be considereded for these two methods? what form is the virus in? which patients should you NOT use this in???
IMMUNIZATION!!
- inactive intradermal vaccine: innactive, trivalent, quadrivalent, recombinant, higher antigen, contains 3-4 viruses, 70-90% effective everyone older than 6 months
2. intranasal: live attentuated, 2-49 year old, caution in >50 or pregnant
***don’t use if allergic to eggs or gelatin***
what are the treatment options for influenza?
how are they used?
when do they need to be started?
who don’t you use these in?
neuriamidase inhibitors
- oseltamivir
- zanamirvir
used for treatment and prophylaxis
need to be started within 48 hours
don’t use in
what do you worry about when a child has influenza and are given asprin? what is the fatality rate?
REYE SYNDROME
(fatty liver and encephalopathy)
happens when pt has viral infection and given asprin, occurs 2-3 weeks after with a 30% fatality rate
pleural effusion
what is an effusion? what are two causes? what are the four different types? what are four symptoms? what are the two radiology views you wanna do and what do they show?
abnormal accumulation of fluid in he pleural space
can occur from inflammation of the structures adjacent to the pleural space or lesions within the chest cavity
four types:
1. transudative
2. exudative
3. chylothorax
4. hemothorax
dyspnea, decrease breath sounds and dullness to percussion
DX:
AP view: blunting of costophrenic angle, loss of sharp demarcation of diaphram, mediastinal shift to uneffected side
lat decbutus view: patient lays on side, allows you to see smaller effusion and differentiate between free flow vs loculated fluid and empyema
thoracentsis: GOLD STANDARD, maximal removal 1.5 L in one session
transudative pleural effusion
how does a transudative pleural effusion occur? what type of fluid would you find? what is the most common cause of this? what percent of people are effected with this and what test do you do to confirm this? and second most common cause of this?
increase pressure in the capillaries causes it to push out into the lungs this is NOT INFLAMMATION, just fluid relocation
low protein serous fluid
#1 cause: Heart failure 90% of cases fluid backs up from right side of the heart and increases pressure and pushes it into the lungs right sided heart failure, BNP >1,500
#2 cause: cirrhosis/nephrotic syndrome
exudative pleural effusion
what is this caused from? what is another name for this? what does the fluid contain and what can form that needs surgical removal? what are the 4 lab characteristics for this? what are the four most common causes? what is the treatment, and the specific 3 treatments if malignancy related? what are the three common cancers that can cause this?
leaky capillaries are cause from INFLAMMATION FROM INFECTION, the inflammatory mediators cause the capillaries to be leaky and allow fluid into the lungs
also called “parapneumonic effusion”
fluid filled with cytokines, WBC, proteins, interleukins, the purlulent fluid can form an empyema that requires surgical removal “infected cyst”
PH
Cause #1: bacterial pneumonia
Cause #2: malignant cause aka lung cancer, metastic breast cancer, and lymphoma
Cause #3: PE
cause #4: TB (confirm with AFB stain)
TX: antibiotics specific for infection type, drainage and if malignant source portable catheter, chest tube or thoracostomy, sclerotic agent like talc or doxycycline to prevent it from happening again
pulmonary embolism evaluation
explain the pathway that is followed to rule in or out a PE and determine wha ttesting to do?
INITIAL:
low risk=PERC
everything else=HELICAL CT angiography
SECOND:
low PERC->WELLS
neg PERC=STOP
THIRD:
HIGH WELLS=helical CT
LOW WELLS=D-dimer
**keep in mind gold standard it pulmonary angriography**
what is the structure of influenza? what family? what types?
- single stranded RNA
- orthomyxovirdae family
- A, B, C types
what is the composition of influenza A? of these two, how many are there in humans?
hemagglutinin (HA)
neuramidase (NA)
3 HA types in humans
2 NA types in humans
what are 3 challenges of containment of influenza?
- short incubation time (1-7 days)
- ability for person with asymptomatic infection to transmit virus (can be contagious 1 day before symptoms)
- early symptoms of illness are likely to be non-specific, delaying recognition (need to get antivirals on board within 48 hours of onset)
what percent of pleural effusions are related to malignancy?
25%
HOLY MOLY
what are the requirements for thoracentesis for a pleural effusion? (3)
- pleural fluid protein to serum fluid protein ratio >.5
- pleural fluid LDH to serum LDH ratio >.6
- pleural fluid LDH greater than 2/3 the upper limit of normal serum LDH
what are 80% of malignant pleural effusions caused by?
asbestos exsposure
malignant mesothelioma
what are 3 risk factors for DVT? what is this collectively know as?
- venous stasis (immobility, post op, post stroke)
2. increased venous central pressure ( decreased cardiac output, CHF)
3. hypercoagubility (meds, malignancy, FACTOR V LEIDEN)
collectively known as virchows triad
- hypercoaguble
- venous stasis
- vascular intima inflammation or injury
**slight difference between two so I included both**
worry specifically about orthopedic, pelvic, or abdominal surgery or OCP
where is the most common site for development of a thrombus/embolus?
DVT is most common in
popliteal
iliofemoral
pelvic veins
90% arise here!
calf involvement alone is much less risky!
what is the test of choice for DVT?
venous ultrasound with doppler (non-invasive)
Pulmonary Embolism
explain the pathophysiology of this and what happens!
- pulmonary vascular bed by thrombus
- vasoconstriction in pulmonary artery, this mechanism isn’t well understood it just happens in the body as protective function, however, it actually has worse effects and harms the body
- increased pulmonary vascular resistance (PuVR) from vasoconstriction by neurohumoral reflexes and hypoxia
- continues to increase pulmonary artery pressure
- increased right heart strain from backed up fluid leading to right heart failure THIS IS OFTEN CAUSE OF DEATH
- increased alveolar dead space, ventilated but not profused, leads to decreased surfactant, atlectasis, and V/Q mismatch from impaired gas exchange
- V/Q mismatch leads to right to left shunting where blood is redirected to non obstructed lung for oxygenation
all of this causes decreased pulmonary compliance, increased work of breathing so the patient becomes tachypnea and has to work harder to inflate the lungs
pulmonary embolism
what are the 3 symptoms a patient with often present with ? what are 6 signs you may see on examination?
tachypnea, dyspnea, pleuritic chest pain (sharp stab) on inspiration
must have high suspicion because 50% of pt lack these characteristc symtoms
clinical signs:
1. crackles
2. S4 gallop (since right ventricle get stiff from the increase in pressure you hear right atrial contraction)
3. decreased S2 splitting
4. friction rub
5. positive homans sign (calf pain with dorsiflexion)
6. plasma D-Dimer (elvated in thrombus/degredation of fibrin)
pulmonary embolism
what are the four test you use to diagnose and what would you see on each test? Explain the flow chart for PE diagnosis?
1. CXR-atelectasis, pleural effusions, infiltrates
- westermarks sign (avascular markings distal to embolus)
-
hamptons sign (wedge shaped infiltrate that shows infarction)
2. Helical CT angiography
proximal vessel thromboembolism
3. EKG- S1Q3T3 classic for cor pulmonae
4. Pulmonary angiogram GOLD STANDARD
-the issue with this test is it is an invasive procedure that puts a catheter in the heart and injecting dye into a high pressure area, people can have a reaction to the dye or the kidney can be effected only indicated when VQ and CT scans are indeterminant and PE is still suspected
probability PE 4+
pulmonary embolism
what are the four treatment options and order for treating PE? when do you use each and explain them!
FULL ANTICOAGULATION FOR 3-6 MONTHS, LONG IS BETTER AND MOST DO 6 MONTHS **THIS PREVENTS FUTURE CLOTS**
1. LMWH or unfractioned heparin
low molecular weight heparin is usually preferred because it has a more predictive dose and is the same if not more effective that unfractioned heparin, but some people still use it 5-7 days while transitioning to warfarin
- warfarin
goal PTINR 2-3, can use new oral drugs like dabigatran, rivroxaban, apixaban they don’t need monitoring and may work better than warfarin, but more $$$
FULL ANTICOAGULATION FOR 3-6 MONTHS, LONG IS BETTER AND MOST DO 6 MONTHS **THIS PREVENTS FUTURE CLOTS**
- Streptokinase, urokinase, TPA
used in urgent situations to directly lyse intravascular thrombi and accelerate the 1st 24 hours, does not decrease mortality which is why it is used in URGENT cases
4. mechanical/surgical extraction
this is LAST RESORT when the patient is hemodynamically unstable and is bascailly going to die anyway because the surgery is a basic death sentence by opening them up and taking out the clot
when wouldn’t you do a mechanical/surgical intervention for PE? (5 things)
- if the patient is hemodynamically stable
- active internal bleeding
- stroke in prior two months
- trauma in the last 6 weeks
- uncontrolled hypertension
what can you do in a patient who has an absolute contraindication for coagulation for PE prophylaxis?
venal caval interruption filters
what is the criteria you use to determine the probabillity of DVT/PE?
wells score
over 2 mod probability
over 6 high prob
pulmonary hypertension
explain the sequence of event that cause this? what is the most potent stimulus of this pathway and explain why this happens?
patient with hypoxemia…
- increase pulmonary vascular resistance
- increase in pulmonary artery pressure
- increase in right ventrical, increases so much it can’t handle the pressure
- chronic right ventricle pressure causes right ventricle hypertrophy where it tries to thicken the walls to make it stronger so it can handle the increase in BV
- eventually this leads to right ventrical failure
hypoxia is the most important and potent stimulus of pulmonary vasoconstriction think about this…its really counterintuitive, if a patient is hypoxic, you would think the body would vasodilate to get more blood to the lungs to be oxygenated but for some strange reason the body decides to vasoconstrict, which only exacerbates the issues because it caues pulmonary hypertension in ADDITION to hypoxemia and creates a positive feedback loop where the body downward spirals into heart failure from hypoxemia
pulmonary hypertension
what are the two different causes of pulmonary hypertension? what are the examples under those categories that can cause them? (1/5)
idiopathic: unknown cause, rare, fatal within 5 years of diagnosis, some random correlation with anorexigens or fat burning pills fenflouramine, women 30-50, 20% familia
secondary: caused by pretty much any lund disease that causes hypoxemia because it inself is enough to vasconstrict the pulmonary arteries PE, vasculitis, SLE, emphysema chronically increase in venous pressure causes HF and mitral stenosis, can be congenital like in septal defect
explain three causes that can contribute to pumonary hypertension? what is the most important?
- hypoxemia ***most important** automatically stimualtes pulmonary arterial vasoconstriction
- acidosis
- venocclusive conditions
according to the clinical peals book, when looking at the heart, what are four causes of pulmonary hypertension?
1. left heart could have decreased forward flow so it backs up into the pulmonary system
2. increase in flow from the right side of the heart causing the pulmonary pressure to increase
3. issues with pulmonary vasculature
4. hypoxic vasoconstriction
**cause can be either cardiac or pulmonary**
pulmonary hypertension
what are 8 symptoms you would see with PH?
symtoms:
- dyspnea exertion and rest
- retrosternal CP that minics angina
- increase JVP
- increase right ventricle impulse
- loud s2
- S4 gallop
- TR murmers
- systolic ejection click
pulmonary hypertension
what are the 3 tests you use to diagnose PH? what are 2 things you find on the first? 3 on the second? and how does the last one work? what three drugs do you test?
1. CXR
- dilated/enlarged pulmonary arteries
- pruning vessels
2. echocardiogram
- right ventricular hypertrophy
- atrial hypertrophy
- right ventricular strain
3. cardiac cath (right heart)
-measure the pulmonary artery pressure, then do drug testing and see if using vasodilators or calcium channel blockers work to decrease hypertension so that you can figure out which drugs can help the patient adenosine, epoprostenol, nitric oxide
pulmonary hypertension
what are the 5 treatment options for pulmonary hypertension?
- calcium channel blockers if sensitive from cath, lower systemic arterial pressure
- phosphodiesterase-5 inhibitor sildenafil pulmonary vasodilation
- prostacyclins potent pulmonary vasodilator
- endothelin receptor antagonist bosentan
- heart-lung transplant usually needed
what are the four mediators of asthma? what do each of them do?
- acetylcholine- NT released via vagus nerve leading to bronchoconstriction
2. histamine-bronchoconstrictor in mast and basophils in lungs, in the present of inflammation it promots capillary leaking
3. kinins-bronchoconstrictor released by mast cells
4. leukotrienes-smooth muscle constrictor, increased mucous production
intrinsic vs. extrinsic asthma
explain the difference between the two? what are examples that can cause them? who are they most common in? is there a genetic link?
INTRINSIC:
1. NONallergic triggers infections (viral, bacterial), pharmocologic, emotional, occupation, stress, asprin, weather etc.
EXTRINSIC:
- ALLERGIES- largest risk factor for developing astma, ATOPY, most common in children/adolescents, there is genetic disposition (tabacco, smoke, GERD)
asthma
what are 3 symptoms you might see with asthma?
- highly variable presentation*
1. coughing/wheezing/chest tightness/SOB
2. note: in severe asthma, wheezing may decrease or stop because of decreased airflow
3. decreased FEV1 and FEV1/FVC
what is the admission and discharge criteria for a patient and the hospital?
admission criteria: Peak expiratory flow rate (PEFR)
discharge criteria: Peak expiratory flow rate (PEFR) >70% predicted
explain the four classifications of asthma severtiy and the treatment used for each step? WHAT SHOULD YOU NEVER DO???
Intermittent:
FEV1>80%, symptom frequency
-DOC SABA, albuterol
Mild persistent:
FEV1>80%, symtom frequency >2times/week
- SABA, albuterol +
- inhaled corticosteroid, fluticasone (if already taking this, increase dose)
- if unresponsive, oral corticosteroid, prednisone
moderate persistent:
FEV1 60-80
- above, +most warrent hospitalization/O2 supplementation
- repetitive/continous use of beta agonists in nebulizer with systemic corticosteroid IV
- continous monitoring PEFR and PCO2
severe persistent:
FEV1
-SAME AS ABOVE
**********NEVER SEDATE A PATIENT DURING ACUTE RESPIRATORY EXACERBATION BECAUSE IT CAN DECREASE THEIR RESPIRATORY DRIVE************
asthma
what are the 5 tests you can do to help diagnose asthma? what are the results you woudl expect to see?
1.
2.
- (3)
- (1)
- (4)
1. Peak expiratory flow rate (PEFR)
2. pulse oximetry
3. PFT GOLD STANDARD, proves reversible obstruction
-decreased FEV1
-decrease FEV1/FVC
**give bronchodilator, then this improves** postivie if >10% increase in FEV1 after bronchodilator
4. bronchoprovocation challenge test
give histamine/allergen OR METACHOLINE, and FEV1 decreases by 20%, this is DIAGNOSTIC
5. arterial blood gas
Respiratory alkalosis
hypoxemia
PaO2
PCO2
what is the atopic triad that you see with extrinsic (allergy induced) asthma?
**this is the greatest predisposing factor for asthma**
- wheeze
- eczema
- rhinnitis
(TYPICALLY AT NIGHT)
what weird condition is randomly assocaited with a persons risk for developing extrinsic (allergy) associated asthma?
ECZEMA
werid!!!
what is the single largest risk factor for developing asthma?
ATOPY
ALLERGIES!!!
asthma
what type of OBSTRUCTION is this? when does it typically develope? what are 5 things that can cause it to develope? what are the 3 main characteristics of asthma?
ACUTE REVERSIBLE OBSTRUCTION, can develope anytime but typically
-genetic, inflammatory infiltrates, injury to epithelium, thickening of airway, hyperresonsiveness
3 contirbutory causes:
1. airway obstruction-smooth muscle constriction, bronchial wall edema, thick mucous obstruction
2. bronchial hypersensitivity- stimulation from a mechanism either intrinsic (non IgE) or extrinsic (allergen stimulated)
3. inflammation of the airways-leukotrienes, histamine released from mast cells
explain the pulsus paradoxus that can be seen in asthma? why can asthma patients have decreased periphreal pulses?
- asthma is obstructive, so patients have a hard time getting air out, the increase in lung volume leads to an increased “sucking” effect where blood is pulled into the heart, the increase pressure and volume strains the right side of the hear and can push the intraventricular septum into left ventricle, causing less outflow and periphreal circulation= decreased periphreal pulses
- systolic pressure drop >10 mmHg during inspiration
in healthy: the decrease pressures in the chest during inspiration causes the blood to come back to the right side of the heart and go towards the right venticular wall, and there is only a small drop in systolic pressure
In tompenade: the increase blood flow and pressure on the right ventricle during inspiration can’t be distributed on the right ventricular wall, and instead is transmitted to the ventircular septum, causing a decrease in left ventricular filling and the reason you see the periphreal pulses decrease since decrease stroke volume and a lower systolic blood pressure
explain the receptors in asthma to understand how the medications work?
you want to activate the beta receptor because this causes relaxation
you want BLOCK the muscarinic receptor because this causes constriction
explain the receptors in asthma to understand how the medications work?
you want to activate the beta receptor because this causes relaxation
you want BLOCK the muscarinic receptor because this causes constriction
obstructive sleep apnea
what are the qualitifications to have this? what physical body part fails during this? what are the daytime symptoms and what are the nighttime symtoms? what test is most important for diagnosis?
repetitive cessation of airflow at the naso or oropharynx (caused by their passive collapse) that occurs during sleep
stop breathing for >10 secs or hypopnea decrease in airflow , must have at least 5 episodes
daytime symptoms: excessive sleepiness, sore throat, depressing, morning headache
nighttime symptoms: loud snoring, snort or gasp to wake up, apneic episode witnessed
DX: polysomnograph (PSG) sleep study!! can do EEG if brain is stimulated, or TSH
obstructive sleep apnea
what is the most important treatment for this? what are some lifestyle adjustments you can make?
nasal continous positive airway pressure (CPAP)
literally forces the air in so that way the airway can’t collapse
lifestyle changes: loose weight, avoid alcohol before bed, change sleeping positions, pharyngeal surgery
obstrucive sleep apnea
what are six RF and which is the most important one??
OBESITY (85%)…so loose weight
male
>40
alochol before bed
anatomic narrowing of nasopharynx
neck size, large tongue
COPD
what number cause of death is this? what is this characterized? what are the two conditions that contribute to this diagnosis? what is the pathophys of this disease and how it occurs?
3rd leading cause of death in US, rates increasing
progressive air flow obstruction
chronic bronchitis (cough) and emphysema(enlarged sacs) these two contribute to this, it can be one or both, depends on the person
1. loss of elastic recoil: smoking leads to chronic inflammation and decreased protective enzymes (alpha-trypsin) and increases damaging enzymes (elastase from neutrophils and macrophages), this causes alveolar capillary and wall destruction= decrease gas exchange surface area and elastic recoil *makes expiration active process*
2. increased air resistance from above
what is the most contributory cause of COPD?
smoking in 90%
what is the only genetic link with COPD?
alpha-1 antitrypsin deficiency
in patients younger than 40, associated with premature COPD
this enzyme protects the elastin in the lungs from being degrated by elastase released by WBC
what is really important to make sure the COPD patients do?
VACCINATION
- pnuemonia
- influenza
***they can get sicker faster! prefect breading gound**
what three bacteria are COPD patients particullarly suceptible to? what do you do for treatment?
- s. pneumoniae
2. hae influenzae
3. moraxella catarrhalis
***use antibiotics to treat these! don’t usually prescribe COPD patients antibiotics, doesn’t help underlying condtion**
COPD staging
explain the four stages of COPD and the medication classes you would use to treat or any other methods?
Stage 1:
mild, FEV1>80%, FEV1/FVC
-bronchodilators, vaccination
Stage 2:
moderate, FEV1 50-80
short term bronchodilators, long term bronchodilator
Stage 3:
severe, FEV1 30-50%
Short and long term bronchdilators, pulmonary rehab with inhaled glucocorticoids
stage 4:
very severe, FEV1 , cor pulmonale
-above plus O2 therapy, must consider surgical options or roflumilast
when would you hospitalize a patient for COPD? (5 things)
- rapid severity
- worsening hypoxemia
- advanced age
- arrythmias
- poor hom support
what do you need to watch for in a patient who has COPD?
cor pulmonale (esp with bronchitis)
multifocal atrial tachycardia, check with EKG
what lab results can suggest COPD? (2)
- PFT GOLD STANDARD
- FEV1/FVC - ABG
- normal early on
- decreased PO2 with progression
- PCO2, usually normal, but can decrease in progression
COPD TREATMENT
what is the most improtant factor? what is the goal of treatment? what are the two main classes you use and the drugs within those class? what do you need to do for COR pulmonale?!?!
most important is SMOKING CESSATION!!
goal of treatment: improve functional state and relieve symptoms
Anticholingerics
superior to B-agonists in achieving bronchodilation, since COPD has increase airway tone from acteylcholine, has less side effects ipratropium (short), tiotropium (long)
bronchodilators
most important agent to decrease symptoms albuterol, salmetrol
****if cor pulmonale, USE OXYGEN!!!! this is the only therapy proven to decrease mortality!!!****
emphysema-COPD
Name 8 symptoms you would see on PE. what would you see for the FEV1, FEV1/FVC, DLCO, CXR (2)?
- tachypnea, tachycardia
- barrel chested, increase AP diameter
- decrease breath sounds
- hypersonance/hyperinflation
- pursed lip breathing “pink puffers”
- respiratory alkalosis
- wheezing/whistling
- prolonged expiratory phase since obstructive
TESTS:
- FEV1-decreased
- FEV1/FVC- FVC stays the same just takes longer to get it out
2. increase RV (increase in RV since air trapping and can’t get air out)
- decreased DLCO in later stages, increased dead space!
- CXR: hyperinflation, flattened diaphram
what can you see in severe emphysema?
bullae or blebs
“large cystic areas in the lungs
INCREASED DEAD SPACE
chronic bronchitis-COPD
explain the pathophys of this and how it occurs?
cough and plegm for 3 months for 2 years
airways clog with mucous cause obstructed airflow, particularly obstructs expiration
- inflammation of conducting airways, damages the respiratory epithelium causing loss of cilia
- columnar cells may be replaced by squamous cells (metaplasia)
- airway narrowing (remember chronic bronchitis is an inflammatory issue!!!)->increases mucous secretion, hypertrophy of glands and smooth muscle, causing bronchospasm
- bronchospams increases the work of breathing and decreases ventilation of distal alveoli
- causes V/Q mismatch
positive feedback loop, continues
what often causes exacerbations of COPD caused from chronic bronchitis? what is the complication you really worry about?
minor URI, esp in winter months
complication: pulmonary hypertension leading to heart failure
COPD-chronic bronchitis
what are the 8 symtoms you would see?
- excessive “smokers” cough
- excessive phlegm
- crackles from mucous
- increased expiratory since obstructive
- wheezing/rhonchi
6. resipiratory alkalosis (the pt is breathing faster immediately as the CO2 rises, so…they are hyperventilating causing alkalosis…initially see patient increase CO2 that initiates the hyeprventilation, but this happens so quickly that you never actually see patient in acidosis)
- periphreal edema and cyanotic “blue bloaters”
- decreased FEV1, FEV1/FVC ratio
what is the treatment for COPD-chronic bronchitus?
the exact same as emphysema, so see that flashcard!
What is the 2 step process in emphysema causing
1st: obstructive issues
2nd: diffusion issues
in the green book how does it explain emphysema in one sentence ?
and what is alveolar septae
Step 1: Elastase startes to break down elastin in CT tissue around alveoli causing the alveoil to get really big! this casues obstructive resp issues because the air is gettig tapped in the huge alveoli. Usually expiration is a passive process due to recoil but with degredation of elastic in CT the alveoli got huge and lost a lot of its recoil causing air trapping and obstructive resp disease. This also negativly effects ventilation but perfusion is still okay (this is a prime example of V/Q mismatch)! because ventilation is affected we see shunting
Step 2: this is more rare in emphysema but still important to understand! The elastase does not stop its degradation of elastin in the CT it continues to the alveoli membrane and begins to degrade the membrane! this is very bad because this will now effect DIFFUSION because it is affecting the membrane. Since diffusion is now effected we have increase DEAD SPACE! this can lead to an area of dead space called a BULLAE and could lead to the patient needed a bullectomy !
IN the green book: it describes emphysema as a condition in which the air spaces are enlearged as a consequence of destruction of alveloar suptea
Alvelolar septum (sputae) separates adjacent alveoli in lung tissue (so this is what i talked about above with the elastase destroying destroying the elastin in the CT causing enlargment!)
explain the 3 surgical options considered if a patient has respiratory failure from COPD
- lung transplant
- lung volume reduction surgery for diffuse emphysema
- bullectomy, remove large bullae and reduce deadspace to increase V/Q mismatch (seen in pic, these are seen with emphysema, big floppy airs of the sacs that are huge from elastin destructio nand dn’t function. by rmoving this you decrease dead space!
emphysema-COPD
explain the pathophys of this and the two many things that happen? what does this cause?
OBSTRUCTIVE
abnormal and permanent enlargement of the air sacs, causing gradual destructon without fibrosis, the membrane gets damaged and becomes bigger, stretched out and floppier
- alveoli have decreased elastic recoil
- bronchioles more likely to collapse
THIS LEADS TO OBSTRUCTION FROM EXPANDED ALVEOLI, AIR TRAPPING=decreased ability for RECOIL and SHUNTING OCCURS due to issue with perfusion (diffusion)!
“floppy sacs”
Premature collapse of respiratory bronchioles in expiration results in air trapping; result is “obstructive picture” on PFT’s
the destruction of the alveoli and vasculature leads to V/Q mismatch with shunting and alveolar dead space
occupational lung disease
“pneumoconiosis”
what type of lung condition is this? what does the particulate matter cause? what percent of COPD patients have the influence of this? what are the 4 sources of this and where do you get them from?
RESTRICTIVE
inhalation of particulate matter that causes fibrosis of interstitial lung disease
duration of exsposure increases severity
15-20% of COPD patients have this involvement
asbestos-thermal and electrical insulating
silicosis-silica or quartz, stone cutting, glass factories
pneumoconiosis: “BLACK LUNG”, coal dusts
beryllium: nuclear reactor conductor
pneumoconiosis
“black lung”
what do you get from this? how does it happen? what are the two major things you would see on the CXR that would suggest this?
inhalation of coal dust
coal is inhaled by macrophages, release inflammatory mediators, fibroblast proliferation, and fibrosis and remodeling of intersitial lung
** nodules/nodular opacities in upper lobe**
**hyperinflation of lower lobes**
Leads to progressive massive FIBROSIS
silicosis
what exsposure caues this? where do you get it? what two things does it cause? and what specific three diseases does it make you at increases risk for?
silica or quartz exposure
stone cutting or glass factories, grantie quarries
leads to calcifications and fibrosis
increases risk for TB, and connective tissue diseases like RA and schleroderma
cystic fibrosis
what is this? what does it effect? 3
what does it cause?
average like expectancy?
genetic multisystem disease
abnormality in CFTR gene, in the Cl- channel found in lungs, intesting, pancreatic ducts, sweat glands causing mucous retention
38 years average life
abnormalities of salt and water transport across epithelial surfaces
cystic fibrosis
what are two organs that are particulalry effected??
- pancreatic dysfunction
- lungs
**mucous retention on both these two organs**
cystic fibrosis
4 key systems?
1 dx method?
SXS:
- postivie newborn screen
- reccurrent resp infections
- greasy foul smelling stool from fat malabsorption
- 99% males sterile
DX:
positive sweat test over 60
Cystic fibrosis
4 tx options
- mucous thinners/airway clearance
- lung transplant
- frequency abx
- supplemental pancreatic enzymes
what bacteria cause the most TB in the US? what are 4 other bacteria that can cause it?
mycobacterium tuberculosis
mycobacterium bovis
mycobacterium africanum
mycobacterium microti
mycobacterium canetti
what are the two populations of people that TB can be divided by?
hight risk for becoming INFECTED with TB
high risk for DEVELOPING TB DISEASE
what are 7 things that can put someone at high risk for TB INFECTION (not disease)
- close contact
- foreign born
- low income and homeless
- health care workers in high risk groups
- racial and ethnic minorities
- infants, children and adolescents
- IV drug users
name five areas of the world where TB is common?
- asia
- africa
- russia
- eastern europe
- latin america
what groups of people are at risk for developing TB disease!? (7)
- people with HIV (thats why prevalence increased in the 80s)
- infection of TB within last two years (5% risk, and 10% lifetime)
- infants and children <4 years old
4. prolonged therapy with corticosteroids
- IV drug use
- diabetes
- silicosis
what is the greatest risk factor for devloping TB?
HIV!!! 7-10% risk for devloping TB disease each year when infected with both TB and HIV
are people with LTBI infectious? what percent of these people will go on to develope the disease?
no they aren’t infectious!!
10% will go on to develope disease!
Explain the pathogenisis steps for TB (5 steps)
- tubercle bacilli are inhaled and travel to alveoli
- multiple in alveoli, infection begins
- small number of tubercle bacilli enter bloodstream and spread throughout body
- within 2-4 weeks macrophages survive bacilli, form a barrier shell that keeps the bacilli contained and under control know as LBTI
- if the immune system can’t keep tubercle bacilli under control, they multiple rapidly and cause TB DISEASE *it can occur in other places in the body too*
In TB, explain the differences between LTBI and TB disease in these characteristic:
- active/inactive bacilli
- chest xray findings
- sputum smears
- symptoms
- infectivity
- a case of TB or not
Is LTBI treated with medication?
YES IT IS
you want to prevent these patients from getting it in the future!!!
who is high priority treatment for LTBI with a TST >5 mm or postitive IGRA? (5 things)
- close contacts of those with infectious TB disease
- HIV
- chest xrays indicating previous TB
- organ donor transplants
- immunocomprimised patients
who is high priority for LTBI treatment >10 mm or positive IGRA test? (5 things)
- people who came to US within last 5 years where TB is common
- IV drug users
- live or work in high risk facilities
- micro labatories
- children <4 years old
multi-drug resistant TB is resistant to which drugs?
isoniazid and rifampin (2 first line drugs avaliable)
extensively drug resistant (XDR-TB), what drugs are they resistant to?
isoniazid and rifampin, PLUS fluoroquinolones and at least 1 of the 3 second line drugs
**this is a major issue around the world**
how long should a patient be treated for TB?
what if this person has pos sputum after 2 months of treatment?
at least 6 months
if cavities on chest xray and postitive sputum cultures at 2 motnhs then treatment should be extended for 9 months
what are the three phases of TB infection treatment?
1.initial phase: first 8 weeks of treatment, four drugs are used
isoniazid, rifampin, pyrazinamide, ethambutol
2. continuation phase: after first 8 weeks of treatment, bacilli remaining after initial phase are treated with at least two drugs
3. relapse phase: occurs when treatment is not continued for long enough, surviving bacilli may cause TB disease at a later time
in order to prevent drug resistance, TB disease must be treated with at least how many drugs?
2 ones the organism is suseptible to
Tuberculosis
what are the classic symptoms assosicated with TB (clinical and xray)?
clinical symptoms:
coughing >3 weeks
pleuritic chest pain
hemoptysis
positive rales
infiltrates (collection of fluid and cells in lung tissues)
cavities (hollow spaces within lung usually in the upper lobe)
caseating granuloms on biopsy (necrotizing granulomas)
what tests do you use to diagnose TB?
- tuberculin skin test (TST)
2. interferon gamma assays (IGRAS)-measures immune response to m. tuberculosis, less likely to be incorrect compared to TST
3. culture with AFB staining
-need 3 specimens, 8-24 hour collection intervals, can induce with inhaling saline mist spray
4. chest x-ray (infiltrates and cavities)
5. nucleic acid amplification test
6. bronchoscopy or gastric wash if having hard time getting sample
explain the tuberculin skin test? what can’t this test do? what are positive test results for the three groups of people?
in lastent infection positive 2-4 weeks after infection
-injected with inactive tubercle bacilli, read within 48-72 hours
**this test can’t differentiate between latent and active TB, just that a person has been infected at some point**
Positive test results:
15 mm in normal patients
10 mm in immigrants, children <4, high risk populations
5 mm in HIV, immunsuppressed, positive chest xray, primary TB exposure
explain the difference on chest xray between primary and reactivated TB?
primary: homogeous infiltrates, hilar/paratracheal lymph node englargement, middle/lower lobe consolidation
reactivation: fibrocavity apical disease, nodules, infiltrates **TB reactivation presents at the top of the lungs instead of wher eit happened originally**
what should you connect Ghon complexes and Ranke complexes? what are they?
TB
ghon complexes: calcified primary focus
ranke complexes: calcified primary focus and hilar lymph nodes
**these represent healed primary infection**
what does milliary TB look like?
millet seed like nodule lesions (2-4 mm)
what is the gold standard for TB testing?
acid fast bacilli tests
3 negative tests are considered negative!!
how long should a person be isolated and on treatment before being allowed in public when they have TB?
need to be isolated for a minimum of 2 weeks
what are the four drugs you use during the initial treatment phase for TB? what are their side effects? how do you treat someone if they have been exposed to someone with active TB? what is the treatment regiment for LBTI?
“RIPE acronym
- rifampin (hepatitis, flu, orange body secretions)
- isoniazid (hepatitis, periphreal neuropathy, give B6 to prevent risk)
- Pyrazinamide
- ethambutol (optic neuritis)
**for LBTI: treat with isoniazid and pyrazinamide for 9 months, or 12 months if HIV pos or granulomas present on CXR**
**if someone is exposed to patient with active TB, then treat them emipircally for 12 weeks until negative TB can be obtained**
