respiratory

Question 1

chronic bronchitis defination

Answer 1

chronic productive cough for
atleast 3mnths
in 1 year
for 2 consecutive years

Question 2

effect of excess oxygen in COPD

Answer 2

In advanced chronic obstructive pulmonary disease (COPD), destruction of the terminal bronchioles and alveoli causes areas of physiologic dead space to develop. The affected regions have limited surface area available for gas exchange, which leads to ventilation/perfusion (V/Q) mismatch causing local hypoxia and hypercapnia.
Hypoxia induces selective vasoconstriction in these areas of the lung and redirects blood flow to better ventilated alveoli, reducing V/Q mismatch.
Supplemental oxygen improves hypoxia but can cause C02 retention by the following mechanisms:
• Loss of compensatory vasoconstriction in areas of ineffective gas exchange worsens V/Q mismatch
• Increase in oxyhemoglobin reduces the uptake of C02 from the tissues by the Haldane effect
• Decreased respiratory drive and slowing of the respiratory rate causes reduced minute ventilation The acidosis caused by an acute increase in C02 increases brain gamma-amino butyric acid and glutamine and decreases brain glutamate and aspartate, causing a change in level of consciousness. Hypercapnia also causes reflex cerebral vasodilation and may induce seizures, as seen in this patient

. Oxygen should be used cautiously with a goal Sa02 of 90%-93% or Pa02 60-70 mm Hg. Patients who develop significant acidosis or have severely reduced level of consciousness require mechanical ventilation.

Question 3

bohr effect

Answer 3

⬆️ pco2》⬆️H+》⬇️hb affinity for o2》⬆️o2 unloading

occurs at tissue level

Question 4

haldane effect

Answer 4

⬆️pO2⬆️unloading of CO2 at alveoli level

Oxygenation of blood in the lungs displaces carbon dioxide from hemoglobin which increases the removal of carbon dioxide. This property is the Haldane effect. Conversely, oxygenated blood has a reduced affinity for carbon dioxide.

Question 5

cause of leukocytosis after treatment of aasthma exacerbation

Answer 5

patient being treated for an asthma exacerbation now has leukocytosis with
neutrophilic predominance, which is a common effect of systemic glucocorticoids (eg,
methylprednisolone).
Glucocorticoid use causes a leukocytosis due to the following:
• Mobilization of marginated neutrophils into the bloodstream (predominant
mechanism
): Marginated neutrophils are attached to the endothelium of blood
vessels: glucocorticoid-induced mobilization of these neutrophils leads to a higher
number of circulating neutrophils
• Stimulation of release of immature neutrophils from the bone marrow (as evidenced
by the 3% band forms in this patient)
• Inhibition of neutrophil apoptosis
In contrast, glucocorticoids decrease the number of circulating lymphocytes and
eosinophils through a combination of increased apoptosis, increased emigration into the
tissues, and decreased production

Question 6

theophylline toxicity cause and symptoms

Answer 6

Theophylline has a
narrow therapeutic index, and toxicity can occur from accumulation by reduced clearance
or decreased metabolism due to saturation of metabolic pathways. Theophylline is
metabolized predominantly by the cytochrome oxidase system in the liver. Inhibition of
these enzymes by concurrent illness (eg, cirrhosis, cholestasis, respiratory infections with
fever) or drugs (eg, cimetidine, ciprofloxacin, erythromycin, clarithromycin, verapamil) can
raise serum concentration and cause toxicity.
Symptoms of toxicity usually manifest as central nervous system stimulation (eg,
headache, insomnia, seizures), gastrointestinal disturbances (eg, nausea, vomiting), and
cardiac toxicity (arrhythmia).

This patient recently began taking ciprofloxacin, a drug
known to decrease clearance of theophylline. Therefore, the best next step is to
measure serum theophylline levels to assess for toxicity.

Question 7

uses of non invasuve positive pressure ventilation

Answer 7

Noninvasive positive-pressure ventilation (NPPV) is ventilatory support delivered by
facemask rather than endotracheal tube; it can be delivered in several different modes,
including continuous positive airway pressure and bilevel positive airway pressure.
NPPV decreases work of breathing, improves alveolar ventilation, and is the preferred
method of respiratory support in patients with AECOPD. Physiologic benefits include a
decrease in respiratory rate and arterial carbon dioxide tension (PaCOzl, with an increase
in tidal volume, minute ventilation, and arterial oxygen tension (PaOzl. NPPV in patients
with AECOPD is associated with a decrease in mortality, intubation rate, treatment
failure, length of hospital stay, and incidence of nosocomial infection.
if it fails then⬇️

Invasive mechanical ventilation may be required in hypercapnic patients with
poor mental status (eg, somnolence, lack of cooperation, inability to clear secretions),
hemodynamic instability, or profound acidemia (pH <7.1 ). This patient’s pH of 7.32 and
PaC02 of 60 mm Hg suggest a mild to moderate acute respiratory acidosis on an existing
chronic respiratory acidosis. A trial of NPPV is warranted prior to intubation, especially
as advanced COPD may make weaning and extubation more challenging. If this patient
fails a 2-hour trial of NPPV (eg, h

Question 8

A-a pressure gradient

Answer 8

PE causes ventilation/perfusion (V/Q) mismatch, resulting in an increase from the expected alveolar-arterial (A-a) oxygen gradient.
Alveolar oxygen (PAOzl is calculated as follows:
PA02 = (Fi02 x [Patm-PH,Q))-(PaC0/0.8)
where Fi02 = fraction of inspired oxygen, Patm = atmospheric pressure, PH20 = water vapor pressure, and PaC02 = partial arterial pressure of carbon dioxide (obtained from arterial blood gas [ABG) results).
This simplifies to PA02 = 150-(PaC0/0.8) for patients breathing room air at sea level.
The A-a gradient is then calculated by subtracting PA02-Pa02, where Pa02 = partial arterial pressure of oxygen (also from ABG results). The A-a gradient is elevated if it is higher than the expected A-a gradient on room air, estimated by (2.5 + [0.21 x patient age)) or (patient age/4 + 4).
A-a gradient elevation occurs in processes that cause impaired gas exchange.

Question 9

tram track sign is seen in

Answer 9

Tram-track signmay be used in chest radiography or CT to denote the thickened non-tapering (parallel) walls ofcylindrical bronchiectasis.

Question 10

string of beads in radiology

Answer 10

String of beads in radiology-
Fibromuscular dysplasia
Chr. Pancreatitis (chain of lakes)
Small bowel obstruction
varicose bronchiectasis

Question 11

clinical features of sarcodosis

Answer 11

systemic granulomatous ds characterised by noncaseating granulomas 
constitutional symptoms of fever anorexia wht loss 
organs involved 
lungs 
     cough dyspnea
skin
         erythema nodosum
         lupus pernio
eyes
        ant and post uveitis 
heart
      arrythmias 
      heart block 
musculoskeletal 
       arthritis arthralgia 
nervous 
     cn paralysis

Question 12

diagnosis of sarcodosis

Answer 12

CXR - bilateral hilar adenopathy  hallmark of sarcoidoisis 
hypercalcemia 
hypercalciuria 
biopsy 
     noncaseating granulomas 
PFT 
   dec lung volume 
   dec diffusing capacity 
    dec FEV1/FVC ratio 

ace enzyme levels just to note ds progress

Question 13

stages of sarcoidoisis on chest xray

Answer 13

Stage I

bilateral hilar adenopathy without parenchymal infiltrates (highest rate of remission)
.
StageII

hilar adenopathy with parenchymal infiltrates 

StageIII

diffuse parenchymal infiltrates without hilar adenopathy (least favorable prognosis)

.StageIV

pulmonary fibrosis with honey combing and fibrocystic parenchymal changes

Question 14

treatment of sarcoidoisis

Answer 14

corticosteroids

Question 15

hallmark of sarcoidoisis

Answer 15

bilateral hilar lymphadenopathy

Question 16

causes of egg shell calcification

Answer 16

silicosis
sarcoidoisis
treated lymphoma
amyloidosis

Question 17

chest xray finding of asbestosis

Answer 17

typically involves lower lobes

pleural plaques

Question 18

chest xray finding of silicosis

Answer 18

typically involves upper lobes

and causes pleural plaques

Question 19

occupational increasing risk of silicosis

Answer 19

sandblasters
quartz
mining

Question 20

most common cancer caused by asbestosis

Answer 20

bronchogenic carcinoma

then malignant mesothelioma

Question 21

biopsy finding of asbestosis

Answer 21

dumbbell shaped asbestos bodies

Question 22

asbestosis increases risk of

Answer 22

bronchogenic carcinoma

malignant mesothelioma

Question 23

silicosis increases risk of

Answer 23

TB

Question 24

part of lung affected by asbestos

Answer 24

lower lobes

Question 25

part of lung affected by silicosis

Answer 25

upper lobes

Question 26

caplan syndrome

Answer 26

CWP + rheumatoid nodules in lung

Question 27

modified wells criteria

Answer 27

clinical decision rule for suspected acute pulmonary embolism ``` symptoms and signs of dvt alternative dx less likely thn PE HR>100 beats / min immobilization >3 days or surgery in previous 4 wks hemoptysis malignalcy ``` score <4 less likely PE score>4 indicates PE

Question 27

modified wells criteria

Answer 27

clinical decision rule for suspected acute pulmonary embolism ``` symptoms and signs of dvt alternative dx less likely thn PE HR>100 beats / min immobilization >3 days or surgery in previous 4 wks hemoptysis malignalcy ``` score <4 less likely PE score>4 indicates PE

Question 28

modified wells criteria

Answer 28

clinical decision rule for suspected acute pulmonary embolism ``` symptoms and signs of dvt alternative dx less likely thn PE HR>100 beats / min immobilization >3 days or surgery in previous 4 wks hemoptysis malignalcy ``` score <4 less likely PE score>4 indicates PE

Question 29

why warfarin causes skin necrosis

Answer 29

warfarin inactivates protein C more quickly than 2,7,9 ,10 factors thus creating a hypercoaguable state earlier leading to skin necrosis so heparin is given for first few days with warfarin so tht it effect can come and then warfarin continued alone for 6 months

Question 30

treatment of Pulmonary embolism

Answer 30

if pt is hemodynamically if pt is hemodynamically stable unstable ⬇️ ⬇️ IV heparin thrombolytic therapy ie 1-2 wks streptokinase ⬇️ ⬇️ anticoagulate anticoagulate with with heparin and warfarin for heparin and warfarin 6mths ⬇️ ⬇️ if C/I IVC filter if C/I IVC fillter + pul embolectomy

Question 31

diagnosis of pul embolism

Answer 31

``` non specific test ABG levels A-a gradient usually elevated CXRay hamptom hump westermark aigm ``` ecg- S1Q3T3 wave sinus tachycardia ``` specific test venous duplex USG helpful when positive but not when negative V/Q perfusion scan has been replaced by CT SCAN DONe when CT SCAN IS c/i ``` spiral CT test of choice disadv - may miss small segmental clots cannot be used in renal insufficiency due to contrast pulmonary angiography is the gold standard D dimer if normal them PE less likely

Question 32

gold standard for PE

Answer 32

pulmonary angiography

Question 33

test of choice for PE

Answer 33

spiral CT

Question 34

risk factors for DVT

Answer 34

``` age > 60 yrs malignacy prior history of dvt hereditary hypercoaguable states protein C ,S prolonged immobization obesity cardiac ds nephrotic syn due to loss of antithrombin 3 major surgery pregnancy and use of ocp ```

Question 35

lupus anticoagulant

Answer 35

antiphospholioid antibody syndrome has elevated PTT it does not mean tht it will increase bleeding it is a lab finding because of antiphospholioid antibody and use of phospholipd to calculate it false + ve VDRL can cause both venous and arterial thrombosis instead it is a hypercoaguable state spontaneous abortion occur

Question 36

triad of fat embolism

Answer 36

acute dyspnea petechiae over neck confusion

Question 37

treatment of fat embolism

Answer 37

supportive with O2 dont use heparin and coumarin

Question 38

hamptons hump

Answer 38

Hampton hump refers to a dome-shaped, pleural-based opacification in the lung most commonly due to pulmonary embolism and lung infarction (it can also result from other causes of pulmonary infarction (e.g. vascular occlusion due to angioinvasive aspergillosis). While a pulmonary embolism is expected to result in a wedge-shaped infarction, the expected apex of this infarction may be spared because of collateral supply from the bronchial arterial circulation, leading to the characteristic rounded appearance of a Hampton hump.

Question 39

westermark sign

Answer 39

focal oligemia seen in pulmonary embolism

Question 40

new 2012 berlin defination of ARDS

Answer 40

acute onset < 1week bilateral infilterates on chest imaging pulmonary edema not explained by fliud overload or CHF abnormal pao2/ Fio2 ratio

Question 41

treatment of Obstructive sleep apnea

Answer 41

Obstructive sleep apnea - weight losss CPAP surgery reserved for last uvuloplasty

Question 42

treatment of central sleep apnea

Answer 42

acetazolamide | progesterone

Question 43

types of lung cancer

Answer 43

``` small cell non small cell large cell squamous cell adenocarcinoma brochoalveolar carcinoma ```

Question 44

superior vena cava syndrome

Answer 44

Obstruction of SVC by mediastinal tumor facial fullness face and arm edema dilated veins over anterior chest arms face and jugular venous distention SVC syn with confusion, blurring of vision is a oncologic EMERGENCY

Question 45

signs of local invasion of lung cancer

Answer 45

``` svc syndrome phrenic nerve paralysis horner syndrome unlateral anhidrosis miosis ptosis pancoast tumor ```

Question 46

pancoast tumor

Answer 46

superior sulcus tumor apical tumor involving C8 T1-T2 nerve root causing shoulder pain radiating down the arm causes pain upper extremitiy weakness

Question 47

paraneoplastic syns with lung cancer

Answer 47

``` #occuring with SCC SIADH Ectopic ACTH eaton lambert #occuring with squamous cell carcinoma PTH like hormone hyoertrophic pulmonary osteoarthopathy ```

Question 48

treatment for NSCLC

Answer 48

surgery and radiation

Question 49

treatment of SCC

Answer 49

chemo and radiation