- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
121 Cards in this Set
- Front
- Back
|
In DPLD, describe the change in RR and tidal volume
|
RR increases
Tidal volume decreases |
|
Pathologic classificaitons of idiopathic interstitial pneumonitides
|
1. Usual interstitial pneumonitis (IPF)
2. NSIP (more inflammation) 3. Acute interstitial pneumonitis 4. Desquamative interstitial pneumonitis |
|
Histology of IPF
|
Fibroblastic foci
*pallisades of myofibrobplasts into the lumen * no inflammatory cells * number of FF correlates w/ prognosis |
|
Pathogenesis of IPF
|
injury/toxin damages epithelial cells
stimulates TGF-beta & PDGF which are profibrotic May be a genetic link --> gene polymorphisms predispose |
|
Clinical features of IPF
|
Histo: fibroblastic foci
CXR: Reticulonodular shadows, lower lobes Exam: velcro crackles, loud P2, edema, finger clubbing Outcome: poor prognosis Treatment: poor response to steroids (unlike AIP, NSIP, DIP) which have better respone to corticosteroids |
|
How does ground glass appearance vs honeycombing reflect treatment of IPF?
|
ground glass will repsond, honeycomb no
|
|
What is BOOP?
|
Plugs of CT in the terminal airways
Caused by virus, fume exposure, CT dz CXR: patchy consolidations |
|
What is COP?
|
Idiopathic version of BOOP
|
|
What are the key characteristics of Chronic Eosinophilic Pnuemonia?
|
CXR: negative image of pulmonary edema
Timing: Acute or subacute Sx: cough, fever, weight loss Treatment: corticosteroids NOT IgE mediated Biopsy: tissue infiltrate has eosinophils |
|
DDx of BOOP
|
Nitrofurantoin, Ascaris
|
|
Pulmonary Alveolar proteinosis
|
Alveolar spaces fill with surfactant
|
|
Lymphangio-leiomyomatosis
|
Obstruciton of lymp by smooth muscle proliferation
Childbearing-age women |
|
Pulmonary langerhas-cell histiocytosis ("Eosinophilic granuloma"
|
Stellate scars and cysts in upper lobes
X bodies Pneumothorax Smokers disease |
|
Common epidemiology of Sarcoidosis
|
Black females or scandanavians
|
|
Systems involved in sarcoidosis
|
Cholestatic defect
Bells palsy Erythema nodosum Anterior uveitis Cardiomyopahty Arthralgias Hypercalcemia |
|
Sarcoidosis
-pathognominic -CXR |
Non-caseating granuloma
Bilateral hilar adenopathy and interstitial infiltrates |
|
Sarcoidosis pathophysiology
|
Involves macrophages and T cells
T cell over activation in affected tissues leads to depletion in peripheral blood --> skin test anergy B cell activation - hyper gammaglobulinemia |
|
what disease has increased ACE levels
|
sarcoidosis
|
|
Common lung manifestations of the following CT diseases:
RA SLE Scleroderma |
RA:
Pleuritis/plerual effusion DPLD PH bronchiolitis SLE: Pleural efusion, DPLD, PH Scleroderma: DPLD & PH |
|
When do you know to treat sarcoidosis?
How treat? |
If ocular, neurologic, or cardiac involvement, treat with corticoteroids
also if you have persistent cough, dypsnea, abnormal PFTs |
|
Wergener's clinical manifestations
|
ENT: facial pain, sinusitis, ulceration
Kidney: uremia, proteinuria, hematuria Lung: fever, coughhemoptysis |
|
Pathology of Wergeners
how treat |
Necrotizing granulomatous vasculitis in upper airway, lung, kidney
corticosteroids |
|
Churg Strauss
|
Starts out as asthma, then get blood eosinophila to lung and gi tract
Affects heart as well: |
|
Goodpastrues syndomre
|
Anti-GBM antibody, crossreact against type IV collage on alveolar BM
Clinical presentation: Acute, lung hemorrage, hematuria Setting: After influenza or other airway injury Pathology: Linear immune complex deposits on the glomerular BM |
|
Unique clinical features:
Asbestosis HP Beryllium Silicosis |
Asbestosis: clubbing, pleural plaques
HP: no lymphadenopathy Beryllium: lymphocyte proliferation test (looks like sarcoid) Silicosis: calcified nodes |
|
Malignant mesothelioma Characteristics
|
Unilatearl
Fatal |
|
Asbestosis CXR and occupations
|
Basilar Linear opacities
Interstital fibrosis occupations: pipe fitters, brake-lining, pulmbers, insulation, shipwuilders |
|
Possible coal related diseases
|
Chronic bronchitis
Emphysema Caplan's syndrome CWP |
|
Specific pneumoconiosis that predisposes for MTb infection
|
Silicosis
toxicity of macrophages |
|
HP pathology
|
Monocyte infiltrates with loose granulomas
IgG mediated |
|
HP on CXR
|
Increased interstitial markings
Ground glass on CT |
|
Types of HP
|
Acute: 4-12 hrs after exposure. Cough, dyspnea, chest tightness, fevers, chills, malaise, myalgias.
rales, tacycardia, tachypnea, inc WBC Sub-Acute Chronic Dyspnea on exertion, wheezing rales, RV fail |
|
Clinical prediciton for HP
|
*Exposure to known offending agent
*Recurrent episodes *Sx 4-8 hrs after exposure *Weight loss *Serum percipitins *Inspiratory crackles |
|
Beryllium dose response?
|
NOT dose response.
Very little amt can cause the disease Cell mediated res;ponse |
|
Beryllium Disease
|
Granulomatous disease
|
|
How do you test for beryllium disease?
|
Lymphocyte transformation.
Lymphocytes have been sensitized when exposure first occurs. On second exposure, they transform into blasts and proliferate. Positive even w/o clinical symptoms. |
|
Etiology of work related asthma
|
Immune mediated: isocyantates, animal dander, latex
Irritant mediated: High dose gives you reactive airways dysfunction syndrome |
|
Bronchiolitis Obliterans
|
* Fixed airway obstruciton
*Air trapping on CT *usually seen in post-transplant *can also be due to large exposures of ammonia, chlorine, diacetyl |
|
normal amt of fluid in pleural space
|
1-10cc
|
|
Pressure of vascular supply to parietal and visceral pleura
|
Visceral --> bronchail vessels (lower pressure)
Parietal --> intercostals (higher pressure) |
|
Pressure in pleural space at rest
|
Negative (-5)
there are no normal situations with a positive Ppl |
|
Palv pressure on expiration is
|
Positive
|
|
Pleural fluid is genearlly moved (in/out) of the pleural space on the (parietal/visceral) surface
|
out/visceral
|
|
Spontaneous pneumothorax
|
Primary:
Tall, smokers, males Blebs pop Secondary: Bullae pop, emptying air into pleural space Due to COPD, asthma or b/c of inflammation, or b/c of lung fibrosis |
|
Most common clinical sx of pneumothorax
|
Chest pain
Dyspnea |
|
Why give O2 to a pneumothorax pateitn
|
Increase gradient between Ppl gas pressure and venous capillary pressure to promote gas absorpiton into venous side
|
|
Tension pneumothorax described as
who at risk |
Ppl positive
people on mechanical venitlators, b/c you are pumping positive pressure into them |
|
During forced expiration, Ppl is
|
Positive
|
|
Relationship of Ppl to Patm in stab wound
|
Ppl = Patm
|
|
Ppl in tension pnuemorthorax is...
|
positive
|
|
Criteria for pleural effusion
|
1) LDHpl/LDHserum <.6
2) proteinpl/proteinserum <.5 3) total LDH 200 IU or >.6 upper normal serum limit |
|
What is loculation and when do you see it?
|
Pleural effusion with fibrosis.
Usually because of an inflammatory process |
|
Most common symptom of sarcoidosis
|
Dyspnea
|
|
Most common noninfectious granulomatous disease of teh liver
|
Sarcoidosis
|
|
Why are babies more prone to respiratory distress and fatigue?
|
More type 2 fibers (fast twitch)
Flatter diaphragm |
|
During what stage are terminal air sacs formed
|
Saccular
|
|
What is the signifcicange of pores of kohn in relation to peds
|
They dont develop until 1 year old, so peds are more prone to atelectasis
|
|
Canals of lambert
|
connect bornchioles
develop when 7 years of age |
|
Bronchopulmonary dysplasia defined as
|
oxygen dependency for at least 28 days after birth
|
|
Reasons for hypoxia in BPD
|
Hypoventilation
V/Q mismatch Shunt Diffusion abnormalities |
|
Sound worse than they are
|
Croup
|
|
Stridor
|
Croup
|
|
Clinical triad of eppligotitis
what causes this |
Drooling (b/c unable to swallow)
Dysphagia Respiratory distress HIB *no cough present |
|
Look worse than they sound
|
Epiglottitis
|
|
Thumb sign
|
Epiglottitis
|
|
Steeple sign
|
Croup
|
|
RSV
Pathogeneiss CXR |
Pathogenesis:
RSV -->inflamation and necrosis --> edema --> air trapping --> V/Q mismatch & hypoxia CXR: Hyperinflation, peribronchial thickening, atelectasis |
|
Classic CF
|
*Excessive Cl in sweat
*Fat malabsorption *Chronic bacterial infection of airways and sinuses *Infertilitiy |
|
Most common CF mutation
what chromosome |
DeltaF508
phenylalanine deletion chomosome 7 |
|
Pulm manifestations of CF
|
Mucus plugs in lungs
If secretions cannot be cleared, they are at risk for bacterial infections. Chronic infections --> chronic inflammatory response and therefroe lung damage |
|
Why do CF patients have defective mucociliary transport?
|
Absence of periciliary liquid layers (PCL) with formation of mucus plaques
|
|
most common infections in CF patients
|
S aureus
P aeruginosa |
|
Treatment for CF
|
DNase
Bronchodilators Hypertonic saline --> inc mucociliary clearance Macrolides (azythromicin) as immunemodulator |
|
Why is there pancreatic insufficiency in CF?
|
pancreatic ducts obstructed by thick secretions
|
|
Cutoff levels to define CF (sweat test)
|
<40 mml/L normal
40-60 mmol/L bornderline abornomar (atypical) >60 mmol/L abnormal |
|
Neonatal screenign of CF looks for
|
Trypsinogen
|
|
Normal MPAP
|
10-18
|
|
PH --> what is the MPAP
|
25
|
|
Normal RVP
|
20-30/2-8
|
|
iPH most common in...
|
women
|
|
A PaO2 less than what will stimulate breathin
|
60 mmHg
|
|
Discuss the interaction between ventilatory response and relationship of PO2 and PCO2
|
If you dec PCO2 you will dec response to hypoxia...this is DANGEROUS
|
|
Acute Mountain Sickness:
Description Risk Factors Clinical features |
Person goes up a mountain and doesnt ahve the ventilaory drive to compensate for dec PiO2
RF: Rate of descent, extreme altitude CF: Headache, dizzineess, anorexia, fatigue, insomnia, pulm edema, cerebral edema |
|
PaO2 response is central or peripheral
|
Peripheral
|
|
Differnen response of body to metabolic vs respiratory acidosis
|
fast for resp b/c co2 can diffuse across BBB
slow for metabolic |
|
What is Ondine's Curse?
|
No ventilatory drive.
So problem when awake |
|
What are causes of Hyperventilation?
|
Anxiety
Asprin Fibrosed lung Acute hypoxia (asthma attack) |
|
Ashtmatics usually have a respiratory acidosis or alkalosis?
|
Alkalosis
|
|
What is Shock?
|
Diminished delivery of oxygen and nutrients to vital organs
Compromised renal fxn and imparied abiltiy to remove wastes |
|
Shock: Effect
|
Anaerobic meetabolism --> lactic acidosis
poor organ fxn (espeically brain and kidney) death |
|
Shock
Signs |
Hypotension
Fever Cold, clammy hands Tachycardia Tachypnia Confusion |
|
What is livido reticularis
|
poor perfusion due to plugging of capillaries
|
|
Microvascular effect of shock?
|
Activation of endothelial cells, coag, immune system, cytokine response
Results in leukocyte adhesion, DIC, coagulation, capillary leak, altered rbc morphology |
|
Sepsis vs. severe spesis vs spetic shock
|
sepsis is SIRS w/ infeciton
severe sepsis is SIRS w/ infection and organ dysfxn, hypoperfusion, or hypotension Septic shock - hypotension despite adaquet fulid resuscitation |
|
Types of emphysema
which types are asociated w/ smokign or loss of AAT |
Centrolobular
Paraseptal Panacinar Irregular Centriacinar and panacinar |
|
Emphysema affects what part of airway
|
Respiratory unit
|
|
Centrilobular ephysema
pathogenesis |
Most common type in smokers
Apical segments of upper lobes Distal terminal bornchioles and RBs |
|
Where does centrilobualr emphysema affect more and why?
|
upper lobes, b/c distance from bronchi to bronchioles is shorter
|
|
Emphysema that contributes to spontaneous pneumothorax
|
Paraseptal
|
|
Emphysema in lower lubes
|
Panacinar
|
|
Bulla vs. bleb
|
Bulla is part of emphysema
Bleb is like a blister; spont pneumothorax |
|
why is a ghon focus usually visible on CXR?
|
It is calcified
|
|
Classic location for TB primary infection
|
Lobar fissure
|
|
Loose granulomas refers to...
|
Wergeners Granulomatosis
|
|
Treat sleep apnea w/ what resp care
|
CPAP
|
|
How do we practice EBM?
|
1) Ask an answerable question, using info from the patient
2) Track down best evidence to answer question 3) Critically appraise question: Validity, impact, applicability 4) Integrate w/ clinical expertise and patient values and circumstance 5) Evaluate how well you did the above steps |
|
Quantity of which inflammatory cell is a marker for the severity of COP?
|
Macrophage
|
|
Specific pathogens that trigger asthma
|
RSV and rhinovirus
|
|
Fungus that survives inside the phagocyte
|
Histoplasmosis
|
|
Most aggressive lung cancer
|
Small cell carcinoma
|
|
Pathology of adenocarcinoma
|
•Found at periphery
•Spiculated parenchymal •Ultrastructure: Short, plump microvilli |
|
Cancer with large promient nucleoli
|
Large Cell carcinoma
Rarely seen Aggressive |
|
Hamartoma
periphery or central? |
Peripheral
|
|
Most common primary lung tumor in children
|
Carcinoid
|
|
Types of Carcinoid tumors
|
Typical:
Central and stains for synaptophysin Atypical Periphery, high mitotic activity, necrosis |
|
Most common places to metastazie (Lung cancer)
|
o Hilar lymph nodes
o Adrenal o Lung/pleura o Liver o Brain o Bone |
|
Lung Cancers not associated with smoking
|
Adenocarcinoma
Large Cell carcinoma Carcinoid |
|
K-Ras associated with
|
Adenocarcinoma
|
|
Sputum of pnuemococcus
|
rust, red, mucopululent
|
|
Process S is regulated by...
|
homeostasis
|
|
Biggest dec in HR, BP, and CO comes in which phase of sleep?
lesat dec? |
Biggest Dec --> Tonic REM
Least --> Phasic REM |
