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
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**
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
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
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
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
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
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**
