Patho lower (Big ass deck)

Question 1

What happens with altitude?

Answer 1

• With altitude, barometric pressure decreases
  
  • sea lelve 760mmhg
  • denver 633mmHg - 83% of sea level
  • pikes peak 457 - 60% of sea level
  • mt everest 253 - 33% of sea level.
• The percent of oxygen in the air is still 20% but the partial pressure of O2 is lower, thus decreasign the O2 partial pressure in the lungs and the blood.

Question 2

Partial pressure of oxygen, alveolar-arterial gradient

Answer 2

1. Normal A-a gradient is about 5-20mmHg
2. Hypoxemia is a decrease in the PaO2
3. Hypoxemia secondary to a pulmonary cause will increase the A-a gradient by 30 or more mmHg
4. Hypoxemia secondary to extrapulmonary casue will have a normal A-a gradient.

Question 3

Hypoexemia a-a gradient based on a pulmonary/cardiac problem.

Answer 3

• Hypoxemia secondary to a pulmonary or cardia cause will increase the a-a gradient by 30mmHg.
  
  • entitites which will block gas exchange or shunt deoxygenated blood from the systemic venous to arterial side.
• causes
  
  • ventilatin defect: alvoli perfused, but o2 not delivered to alveoli - atelectasis
  • perfusion defect: alveoli ventilated but no perfusion of the alveoil - pulmonary embolism
  • diffusion defect: o2 cannot diffuse thorugh alveolar capillary interface- interstitial fibrosis, pulmonary edema, pneumonia
  • right to left cardiac shunts - tetraology of fallot, transposition of the great vessels, truncus arteriosus

Question 4

Why does partial pressure of oxygen change comparing the atmoshperic to alveolar air.

Answer 4

Because of the partial pressure of water vapor and Co2 goes to 47 and 40 compared to 0 in the atmospheric air.

Question 5

Compare diffusion of Co2 o2 and CO

Answer 5

carbon dioxide diffuses 20x faster than oxygen, and carbon monoxide diffuses 200x faster than oxygen

Question 6

What is normally the limiting factor of oxygen diffusion in capillaries

Answer 6

1. normal conditions
   
   1. oxygen diffusion from the alveolar air to the pulmonary capillary blood is perfusion limited, the ability of gas tto fidufse depends on the amount of blood flow through the capillary adjacent to the alveolus
2. Under abnormal conditions
   
   1. oxygen diffusion becomes diffusion limited.
   2. Diffusion capacity decreases in
      
      1. conditions that increase the alveolar capillary membrane thickness
         
         1. pulmonary fibrosis, pulmonary edema
      2. conditions that decrease the effective area for diffusion
         
         1. atelectasis, emphysema, ARDS, pulmonary embolus

Question 7

What is normal A-a gradient? What is hypoxemia? Pulmonary hypoxemia a-a vs nonpulmonary hypoxemia a-a

Answer 7

Normal A-a gradient is 5-20

• hypoxemia is a decrease in the PaO2
  
  • hypoxemia secondary to a pulmonary cause will increase the a-a gradient by 30 or more mmHg
  • nonpulmonary a-a stays the same.

Question 8

What does the oxygen-hemoglobin dissociation curve show.

Answer 8

1. at low oxygen concentrations, Pv02 (tissues and venous blood) there is uncombined hemoglobin in the blood and low oxyhemoglobin
2. at high oxygen concentrations, Pa02 (lungs and arterial blood), there is Hemoglobin saturated with O2, oxyhemoglobin.
3. Also shows that in the plateau part that o2 will load onto hemoglobin molecule even if the PO2 falls slightly
4. it also means that with increasing levels of Po2 there will not be significant increase in the Hb saturation.

Question 9

What does the Bohr effect describe

Answer 9

At lower pH tissues, o2 is released from the hemoglobin, facilitating the uptake of O2 in tissues

at lower co2 and h+ concentrations like the lung, there is an increased affinity for hemoglobin for o2 and o2 goes into hemoglobin

Question 10

What is the haldane effect?

Answer 10

the haldane effect: facilitates the release of Co2 from the rbcs in the lungs. when hemoglobin takes up oxygen, H+ is released and drives the bicarbonate reaction to release Co2 which is then expired.

At low concentrations of o2, the loading of co2 onto hemoglobin is enhanced.

Question 11

What might cherry red skin imply?

Answer 11

Hemoglobin saturated with CO, aka carbon monoxide poisoning

Question 12

What are the two important values to know in the alveolar gas equation?

Answer 12

The atmospheric pressure at altitude and the partial pressure of arterial Co2 (PaCo2)

Question 13

What can acclimitization add in terms of PaO2?

Answer 13

10-13mmHg more Pao2 partial pressure of alveolar air.

Question 14

What is the color of cyanosis dependent on?

Answer 14

• blue color secondary to low oxygen saturaiton, usually less than 85 to 75%
• the color is dependent on an absolute quantity of deoxyhemoglobin. Seen more easliy in patients with high hemoglobin count than in anemic pts.

Question 15

what are the three automatic (involuntary) brainstem centers for respiration?

Answer 15

• Medullary respiratory center
  
  • has two components. A rhythm generator
    
    • inspiratory center
    • expiratory center
• apneustic center
  
  • stimulates the medullary inspiratory center and the depth of inspiration
• pneumotaxic center
  
  • turns off inspiration

Question 16

What does the medullary inspiratory center do?

Answer 16

1. its the rhythm generator for breathing getting senosry input from cn 9 and 10, chemoreceptors and pulmonary mechanoreceptors via the vagus nerve. Motor output is via the phrenic n.
   
   1. expiratory center is not active in normal breathing, but is in active expiration
2. central medullary chemoreceptors are most important determinants for normal breathing and respond to changes in pH or the CSF
   
   1. if Co2 increases, there is an increase in CSF Pco2. a decrease in CSF pH and increased ventilation. Hypercapnia leads to hyperventilatoin. The goal is to keep the arterial pH within the normal range
3. decreased pao2 stimualtes the peripheral carotid and aortic chemoreceptors to increase ventilation. This is the most sensitive peripheral mechanism for breathing.
4. the pons regulates the medulla: apneustic center stimultates prolonged inspiration, the penumnotaxic center turns off inspiratoin.

Question 17

co2 and cerebral blood flow

Answer 17

with every mmHg decrease in Paco2 there is a 3-4% decrease in cerebral blood flow secondary to vasoconstriction.

Question 18

What does pulmonary surfactant do?

Answer 18

1. surface tension is the tendency for liquid surfaces to shrink to the minimum surface area
2. thus alveoli, lined with liquid surface tend to collapse, preventing gas exchange
3. Surfactants reduce surface tesnsion and thus preven thte alveoli from collapsing
4. Surfactant is a lipoprotein made by type ii cells that reduces surface tensin within alveoli
5. This increases pulmonary compliance
   
   1. loss of surfactant will make lungs stiffer, decreased compliance
6. prevents atelectasis
7. re-expands collapsed airways.

Question 19

When does production of surfactant begin in utero?

Answer 19

28 weeks. NRDS - no surfactant

Question 20

Elasticity and compliance, when does compliance decrease?

Answer 20

1. elasticity is the recoil property of the lungs and chest wall. this is inversely related to compliance
2. compliance is a measure of the ability of the lungs and chest wall to expand/distend, this is the change in volume for a given change in pressure
3. compliance will decrease in restrictive pulmonary conditions (lungs become stiffer)
   
   1. any condition that results in the reduction in the ability of the lung or chest wall to inflate, ie ARDS, restrictive lung dz, diffuse fibrosis or infiltrates.
4. diffusion of oxygen across the alveoli in to the blood is decreased if
   
   1. the surface area of the lungs is decreased (emphysema),
   2. the interface is thickened as in fibrosis,
   3. or there is a decreased partial pressure gradient between the alveoli and the pulmonary capillaries

Question 21

Elasticity of lungs is related how to compliance?

Answer 21

elasiticity is the ability of the lungs to recoil theri resting volume after stretching force is released

inversely related to compliance

in emphysema, the lung compliance may be increased, patients have no problem inflating lungs but have extreme difficulty exhaling because of narrowing of the bronchi from increased intrathoracic pressure.

Question 22

What is compliance? how is it related to elasticity?

Answer 22

Compliance is defined as the change in volume for any given applied pressure. Volume chagne per unit pressure change

this ia measure of distensibility (stretchability) and stiffness of the lung

clinically it inlcudes both the lunga nd chest wall in combination

low compliance, stiff lungs, as seen in restrictive disease, more effort is requierd to inflate alveoli

in a stiffer lung, more pressure is needed than normal to breath in a given volume of air and inflate alveoli.

surfactant in the lung will increase pulmonary compliance.

Question 23

What happens in obstructive lung disease, asthma and COPD

Answer 23

increased inspiratory effort to overcome airway resistance to a degree and move air into the alveoli

However, during expiration, intrathoracic pressures will act to compres airways proximal to the alveoli leading to further obstruction, decreased expiratory flow and distal air trapping.

Question 24

What happens in increases in intrathroacic pressure?

Answer 24

This will decrease the diamter of the airways and result in increased expiratory resistance

Compression of airways secondary to expiratory effort and increased intra-thoracic intrapleural and intrapulmonary pressures

aggravates obstructive airway disease

Question 25

Describe V/q ratios

Answer 25

1. one liter of blood holds 200ml of oxygen 2. one liter of humidified air holds about 200ml of oxygen 3. thereofre ideal v/q ratio is 1.0 4. however in real life 1. there are regional variations in the v/q ratios given the anatomy and the lungs and gravity 2. normal v/q ratio is 0.8 3. oveall in the lungs, the alveolar ventilation in L/min is 80% of the value for pulmonary blood flow in liters per minute. this is an average value for the lungs as a whole. 5. Upper lungs have lowest blood flow and ventilation. Lower lungs have the greatest 6. with respiration , ventilation and perfusion is greatest in the lower lungs.

Question 26

Pathological v/q ratios

Answer 26

1. pathological conditions occur where there is abnormal gas exchange or no gas exchange 1. Perfusion but not ventilation, no gas exchange --\> right to left pulmonary shunt 2. pulmonary shunt could be secondary to obstruction of the trachea or bronchi and conditions in which the alvoeli are filled with fluid, blood or pus 2. In a right to left pulmonary shunt, there is always hypoxemia because the blood bypassees the lungs an is not oxygenated. 3. In this PaCo2 is usually normal because Co2 is blown off quicky.

Question 27

Describe Dead space V/q

Answer 27

pathological conditions result in abnormal gas exchange when there is ventilation but no perfusion, dead space occurs ie pulmonary embolism.

Question 28

what is physiological deadspace and anatomic deadspace?

Answer 28

physiological is volume not participating in gaseous exchange. Anatomic dead space and functional dead space (alveoli not contributing ot gas exchange) anatomic dead space is the volume of the trachea, bronchi, ~150ml Normally funcitnoal deadsapce is very small this occurs/can be secondary to ventilation perfusion mismatch, ie ventilated alveoli are not perfused by pulmonary capillary blood or it could be secondary to blood, fluid or pus filling the alveoli.

Question 29

what comprises an acinar unit

Answer 29

bronchioles, alveoli, pulmonary blood vessels.

Question 30

Disease of bronchioles, alveoli/respiratory capacity/, alveoli, and pulmonary vascularity

Answer 30

* bronchioles * obstructive lung disease * alveoli/respiratory capacity * restrictive lung disease * alveoli * fluid, blood, pus * pulmonary vascularity * pulmonary emboli, pulmonary HTN *

Question 31

Obstructive lung diseases

Answer 31

* resistance to expiration, decreased alveolar elastic recoil --\> retention of carbon dioxide * emphysema * chronic bronchitis * asthma * CF * mechanical obstruction of an airway.

Question 32

What is FEV1 and what is FVC

Answer 32

1. FEV1, forced expiratory volume in one second 2. FVC - forced vital capacity. 1. biggest breath and biggest expiratoin .

Question 33

obstructive and restrictive FEV1

Answer 33

1. FEV1 - forced expiratory volume in one second is decreaed in obstructive diseases

Question 34

Restirctive lung diseases

Answer 34

* resistance to inspiration - alveoli don't adequately open * stiff lungs with thick alveolar walls (inflammatory, connective tissue disease) * stiff chest wall * respiratory muscle weakness * central sleep apnea FEV1 is reduced, FEF is 25-75% reduced or normal total lung capacity is decreased, major decrease in inspiratory reserve volume.

Question 35

Alveoli filled with fluid, blood or pus

Answer 35

* fluid * pulmonary edema, ARDS * blood * good pasture syndrome * pus * pneumonia *

Question 36

what is atelectasis?

Answer 36

collapse of lung with loss of lung volume resulting in decrease or absence of gas exchange Types - resorption, compression, surfactant loss

Question 37

what is resorption atelectasis?

Answer 37

1. pathogenesis 1. airway obstruction by mucus secretions or plugs in cystic fibrosis, asthma, post surgery; malignancies; or foreign bodies 2. Resorpption of air distal to the obstruction by circulating blood in the pulmonary capillaries causes the collapse of lung within hours. 1. ther eis a perufsed lung without gas exchange, ie V/q mismatch, there is a resutling intrapulmonary shhunting of blood right to left 2. obstruction can occur in a bronchi, segmental bornchi, terminal bronchioles. obstruction of a bronchus with fluid filling th ebronchus distal to the obstruction presents as a drowned lung, no airin the bronchus distal to a bronchial obstruction 3. symptoms depend on degree of atelectasis, occuring within 24 to 46 hours of collpase 3. signs include absent breath sounds, absent tactile fremitus 4. atelectatic lung can become infected 5. Tx 1. after surgery, incentive spirometry 2. CPAP by facemask 3. PEEP on mechanical ventilation

Question 38

What is plate like atelectasis?

Answer 38

atelectasis of small portions of the lungs, commonly seen in hospital secondary to decreased ventilation

Question 39

what is compression atelectasis?

Answer 39

air, pneumothorax or fluid (plueral effusion, empyema) compressing lung tension pneumothorax - air enters pleural cavity through open, sucking chest wound, negative pleural pressure is lost permitting collapse of ipsilateral lung and reducing venous return ot the heart. Mediastinum shifts and compresses opposite lung. on expiration - as well contracts and diaphragm rises, air is expelled from the pleural cavity via the wound, medistinum shifts to affected side and mediastinal flutter further impairs venous return by disortion of the vena cava.

Question 40

what is atelectasis secondary to loss of surfactant?

Answer 40

surfactant reduces surface tension in the avleoli and thus prevents collapse during the expiration when collapsing rpessure is greatest seen in Neonatal respiratory distress syndrome alveoli collapse due to no surfactnat to decrease surface tension

Question 41

Neonatal respiratory distress syndrome = hyaline membrane disease

Answer 41

* found in premies before 28 weeks gestation * also seen in poorly controlled maternal diabestes and cesarian deliveries * glucocorticoids are given to mothers to incrase fetal surfactant synth * patho: widespread atelectasis results in massive intrapulmonary shunting (perfusion wihtout ventilation) * proteins leaking out of damaged vessels cause alveolar membraens (hyaline membranes * tx: CPAP with endotracheal tube with oxygen and surfactant * CXR: ground glass appearence of lungs and air bronchograms

Question 42

What is pulmonary edema?

Answer 42

1. edema secondary to alterations in the starling pressures - transudates (ultrafiltrate of plasma - clear, low proteins, low specfiic gravity, low monocytes 1. increased hydrostatic pressure - in pulmonary capillareis secondary to heart failure 2. decreased oncotic pressure - secondary to loss of plasma proteins, especially albumin 2. others: microvascular or alvoelar injury 1. infections 2. aspirtation 3. durgs - heroins 4. high altititude pe 5. ards 3. Exudates are inflammtory or neopalsitc fluid, cloudy, high specific gravity, high protein, high monocyte.

Question 43

Chronic bronchitis

Answer 43

Productive cough for at least 3 months for two consecutive years caused by CF and smoking

Question 44

Whats the pathogenesis in chronic bronchitis and changes in the bronchi

Answer 44

* Hypersecretion of mcuus occurs in the bronchus and its subdivisions * obstruction to airflow occurs from mucus plugs located in segmental bronchi and proximal bronchioles * irreversible fibrosis may occur in chroncially inflmaed segmental bronchi and bronchioles changes in bronchi * Hypersecretion of submucosal mucus secreting glands in trachea dn bronchi primarily responsible for sputum overproduction * chronic as well as acute inflammation * loss of ciliated epitehlium and squamous metaplasia * changes in bronchioles, mucus plugs, goblet cell metaplasia, chronic inflammation and fibrous narrowing of lumen.

Question 45

Clincal findings in COPD

Answer 45

* productive cough * dyspnea late in disease * hypoxemia and respiratory acidosis early in disease * cyanosis of skin and mucous membraens * o2 saturation is decreased from hypoexmia * stocky or obese - blue bloaters * expiratory wheezing, * cor pulmonae present * CXR * large horizontal heart * increased bronchial markings * PFTs and Blood gasses * less increase in TLC and RV than emphysema * chronic resp acidodos * arterial PCO2 is greater than 45 * Bicarbonate is more than 30 * moderate to severe hypoexmia early in disease

Question 46

CXR on chronic bronchitis?

Answer 46

1. extensive fine strandy interstitital markings 2. hyperinflation and rapid tapering of pulmonary vessels.

Question 47

emphysema

Answer 47

* permanent enlargement of all or part of the respiraotry unit, resp bronciholes, alveoli ducts and alvoli. * epidemiology * cigarette smokking * alpha 1 antitrypstin deficiency * types * centrilobular (centriacinar) emphysema * panacinar emphysema * increased compliance (secondary to loss of alveolar and elastic tissue, decreased elasticty) * chemical imbalance between elastase and antielastases, oxidants and antioxidants with resultant destruction of elastic tissue * cigarette smoking is chemotactic to neutrophils and macropahges which accumulate in the resp unit and release free radicals * free radicals inactivate AAT and antioxidants producing functional AAT deficiency * destruction of elastic tissue * keeps small airways open, resulting in small airway collapse esp during expiratoin . *

Question 48

centriacinar/centriolobular emphysema

Answer 48

* mc in smokers * apical segments of upper lobes * distal terminal broncioels and resp brionchiles * trapped air behind the distal terminal bronchioles distends the resp bronchioles and incrases residual volume and TLC\>

Question 49

Panacinar/panlobular emphysema

Answer 49

* associated with alpha 1 antitrypsin ATT deficiency * genetic: autosomal dominant * aquired * cigarette smoke inactives ATT * primarily lower lobes * distal terminal bronchioles and all parts of respiraotyr units are sites of elastic tissue destruction * air trapping behind collapsed terminal bronchioles distends entire resp unit.

Question 50

radiology emphysema

Answer 50

* hyperexpansion of lungs, increased AP diameter * small heart * flattened diagphragms * standry pulmonary desnities * hilar pulmonary arteries will become prominent with superimposed pulmonary htn. * Massive air sacs in bullous emphysema

Question 51

clinical findings - emphysema

Answer 51

* progressive dyspnea and hyperventilation * dyspnea occurs early in disease * hypoxemia occurs late in disease * breath sounds diminisehd because of hyperinflation - tympany on percussion * cor pulmonale uncommon.

Question 52

PFT emphysema

Answer 52

* increased total lung capacity due to increase residual volume * decreaed FEV1 * decreased FEF * decreased FVC * Decreased FEV1 FVC * Decreaesd PAo2 occurs late in disease - destruction of the capillary bed matches destruction of respiratory unit. * normal to decreased PCo2 - resp alkalosis, pink puffer.

Question 53

emphysema tx

Answer 53

* stop smoking * pulmonary rehab * oxygen via nasal prongs to maintain 02 sat 90% * bronchodilators * catecholamine inhalers/nebulizers * anticholingerics * Current recomendations * long term oxygen therpay - will improve survival in patients with COPD when * PAo2 is less than 55 or pulse ox sat is 88% * pao2 of 56-60 with erythrocytosis or cor pulmonale

Question 54

TX beware-

Answer 54

1. patients with acute exacerbations of COPD may develop worsenign hypercapnia with application of supplemental oxygen, particularly at high concentrations 2. This may be secondary to 1. worsening ventilation perfusion mismatch secondary to attenuation of hypoxic pulmonary vasoconstriction 2. the haldane effect which involves displacement of carbon dioxide bound to hemoglobin by increased oxygen concentration 3. hypoventilation - central chemoreceptors for o2 are not sensitive as those for co2 and are not activated until pao2 is less than 60, if greater than 60, decrease in ventilatory drive.

Question 55

Bronchial asthma - extrinsic

Answer 55

1. extrinsic asthma 1. type 1 hypersensitivity reaction 2. atopic family history 3. IL-4 stimulates isotype switching to IgE production. IL-5 stimulates eosinophil activation 4. inhaled antigens cross link ige antibodies on mucosal surface mast cells 5. release of histmaine and mediators which stimulate bronchoconstricotrs, mucus production, influx of leukocytes 6. late phase reaction can occur, activation of eosinophils and major basic protein cuasing damge to epithelial cells an dairway constriction 7. leukotrienes cause prologned bronchodconstriction 8. acetylcholine causes airway muscle contraction

Question 56

bronchial asthma

Answer 56

* histological changes in bronchi * thickening of basement membrane * edema and inflammaotyr infiltrates * hypertorphy of submucosal glands * hypertorphy/hyperplasia of smooth muslce - bronchospasm * Histological bronchilar changes * mucus plug production * goblet cell metaplasia * thick basement membrane * smooth muscle hyperropyh and hyperplasia - bronchospasm

Question 57

Bronchial asthma clinical findings

Answer 57

* episodic expiratory wheezing * inspiratory wheezing when severe * nocturnal cough * hyperaeration of lungs * initial resp alkalosis - resp acidosis if bronchospams not relieved * FEV1 is best measure of severtiy * eosinophilia * tx * mild disease * saba * advanced disease * ICS * leukotriene inhibtors * SABA

Question 58

intrinsic asthma

Answer 58

* nonimmune * causes * virus induced respiratory infection * air pollutants * aspirin or NSAIDs drug sensitivity * stress, exercise, cigarette smoke, cold air.

Question 59

Bronchiolitis (acute viral bronchiolitis)

Answer 59

* inflammation of the bronchioles * occurs in children less than 3, common, occuring in up to a third of children in first year of life * clinical * coughing * wheezing * dyspnea * rapid resp rate * physical exam * crackles and wheezing * etiology * major respiratory syncytial virus, others are influenza, parainfluenza, corona virus, adenovirus, rhinovirus * This disease can be severe * acute inflammaotyr exudate occluding the lumen of the bronchiole and inflammatoin of the bronchiolar wall.

Question 60

Restrictive lung diseases

Answer 60

1. disorderds characterized by reduced total lung capacity (TLC) in the presence of a normal or reduced expiratory flow rate 2. cauess 1. chest wall disorders, kyphoscoliosis, pleural disease, obesity 2. acute or chronic instersitital ung diseases 3. ARDS 4. chronic intersitital lung disesae 1. idiopathic pulmonary fibrosis 2. autoimmune: sle, RA, systemic sclerosis 3. medications: amiodarone, bleomycin, methotrexate 4. radiation therapy 5. pneumoconiosies: silicosis, asbesots, berylliosis 6. granulomatous disesas - sarcoidosis 7. hypersensitivity pneumonitis

Question 61

Idiopathic pulmonary fibrosis

Answer 61

* MCC of restrictive lung diseases * more common in smokers * individuals 40-70, males more common * interstitial fibrosis - generally restrictive lung dz * begins iwht alveolitis * leukocytes release cytokines that stimulate fibrosis * fibrosis cuases functional loss of alveolar and capillary untis * fibrosis decreases lung compliance * decreased expansion of lungs during inspiration * increased elasticity on expiration. * clinical findings * dry cough and exterional dyspnea * crackles * potential for cor pulmonale * PFTs * all volumes and capacities decreased * decreaed FEV1 * decreased FVC (forced vital capacity) * Increased FEV1/FVC ratio * respiratory alkalosis PAco2 \<33 * Decreased Pao2 * clinical findings * fever * DOE * chronic, non productive cough * late inspiratory crackles. * Honeycomb lung

Question 62

Sarcoidosis

Answer 62

Multisystem noninfectious granulomatous disease causing interstitial fibrosis 25% of interstitial lung dz african americans, non smokers, women more common pathogenesis: disorders of immune regulation , genetic risk factor, CD4 TH cells interact with unkown airborne antigens releasing cytokines causing non-caseating granulomas pathogenesis: disorder of immune regulation, genetic risk factor, Cd4 tH cells interat with unkown airborne antigens releasing cytokines causing non-caseating granulomas.

Question 63

Clinical findings of sarcoidosis

Answer 63

1. dyspnea 2. nodular skin lesions 3. violaceious rash on nose and cheeks 4. erythema nodosum - painful nodules on lower extremities 5. inflammation of subcutaneous fat 6. uveitis with blurry vision, glaucoma, corneal opacities 7. granulamtous hepatits 8. enlarged parotid and salivary glands 9. renal tones and nephrocalcinosis 10. lab findings 1. increased angiotensin converting enzyme 2. hypercalcemia 3. polycloncal gammopathy 4. cutaneous anergy to common skin antigens 11. approximately 50% will have spontaenous remission in 3 years, 5 % die. CXR: interstital fibrosis, honeycomb, 1 2 3 sign.

Question 64

ARDS

Answer 64

Noncardiogenic pulmonary edema resulting from avute alveolar capillary damage secondary to direct pulmonary damage or systemic diseases * causes * gram negative sepsis * gastric aspiration * severe trauma with shock * diffuse pulmonary infections * severe acute respiratory syndrome * hantavirus * heroin, smoke inhalation, acute pancreatitsi, cardiopulmonary bypass, DIC, amniotic fluid emoblism, fat embolism * patho * acute damage to alveolar epithelial cells and capillary walls * alveolar macropahges and other cells release cytokines. Cytokines attract neutrophils. Neutrophils damge type 1 and 2 pneumocytes decreasing * chronically may lead to proressive interstitial fibrosis

Question 65

ARDS clinical findings

Answer 65

* dyspnea and tachypnea * inspiratory crackles * lab findings * severe hypoxemia not responsive to oxygen therapy - pa o2 \<50mmHg * pulmonary arterial wedge pressure less than 18, normal * respiratory acidosis or normal PaCo2 * Increased A-a gradient * intrapulmonary shunting secondary to atelectasis * diffusion abnormalities secondayr to hyaline membranes and alveolar infiltrates. * tx * treat underlying condition * hemodynamic monitorign * mechanical ventilation * nitric oxide inhalation, corticoisteroids * prone positioning was helpful in covid 19 * poor prognosis - 40-50% mortality

Question 66

What are the 3 types of pneumoconioses

Answer 66

* occupational exposure to mineral dust leading to interstitial fibrosis * 1-5 microns deposit in respiratory bronchioles and alvolar ducts * less than 0.5 microns deposit in alveoli and are phagocytized by macrophages * coal dust least fiibrogenic * silicia, asbestosis, beryllium very firbogenic * about 25% of interstitial lung dz.

Question 67

Coal worker pneumoconiosis CWP

Answer 67

* pulmonary anthracosis * usually asymptomatic * pulmonary athracosis (desposition of coal dust) in interstitial tissue and lymph nodes * simple CWP * fibrotic opacites small * complicated * black lung diseaes * crippling * cor pulmonale

Question 68

Silicosis

Answer 68

1. mc occupational dz in the world 2. quartz most common implicated 3. foundaries, sand blasting, mining 4. highly fibrogenic, esp in upper lungs 5. silica is cytolytic to alveolar macrophages \> cytokines \> fibrogenesis 6. interluekin 1 - pro inflammatoyr cytokine 7. increased incidence of SLE and autoimmune dz 8. complications 1. cor pulmonale 2. TB and lung cancer 9. CXR 1. egg shell calcifications of lymph nodes

Question 69

Asbestosis

Answer 69

* local immune and inflammatory response to asbestos * firbous silicate cyrstals * most common chagnes are benign plueral plaques * diffuse interstitial fibrosis in lower lungs * calcified plaques on pelura and diaphragm * increased incidence of * mesotheliolma * primary bronchogenic carcinoma * complications * cor pulmonale

Question 70

Pneumonia

Answer 70

* majority are secondary to bacterial pathogens, especially streptococcal pneumoniae * patho * microaspiratoin of oropharyngeal contents during sleep * mcc * inhalation of aerosol drops * 0.5 to 1 micron * blood stream infection * bronchopneumonia * begins as acute bronchitis and spreads locally * lower lobes or right middle lobe * patchy areas of consolidation * microabscesses in areas of consolidation * lobar pneumonia * complete or almost complete consolidation of a lobe * complications * abscesses * empyema * sepsis * presentation * sudden onset of high fever and productive cough * chest pain * tachycardia * signs of consolidation * dullness to percussion * increased tactile fremitius * late inspiratory crackles * bronchial breath sounds, bronchophony, egophany * diagnosis * chest film is gold standard * patchy infiltrates (bronchopneumonia) or lobar consolidatoin (lobar pneumonia) * sensitivity is 50-85% - beware dehydration * lab findings * positive gram stains * more useful than culture * sensitivity 80% * neutrophilic leukocytosis * blood cultures * consolidation is * lung tissue filled with fluid, water, blood, pus * sound transmitted more easily through water than air

Question 71

Pneumonia consolidation clinical findings

Answer 71

1. percussion - dullness to percussion, decreased tympany 2. auscultation: vocal resonance increased through fluid medium 1. bronchial breath sounds 2. egophany (goat sond) transmittion of high pithced but not low pitched osunds 3. tactile premitus - sounds felt over areas/ vibration over consolidation 4. whispered pectrioloquy - 99 normally not heard, heard in consolidation 5. crackles, rales

Question 72

TB

Answer 72

* mycobacterium tuberculosis * lives in phagosomes of alveolar macrophages * screening: ppd * drug resistance: chromosomal mutations * primary TB * first infection occurs in the upper part of the lower lobes or lower part of the upper lobes * Ghon Focus: caseous necrosis in the lung periphery * ghon complex: caseuous necrosis in hilar lymph nodes * usually resolves and produces a scar and calcification * may be a nidus for secondary (reactivation) TB

Question 73

Secondary (reactivation) tuberculosis

Answer 73

* reactivation of earlier infection * usually involves apices of the upper lobes * if you see a lesion in the upper lobes apices, think TB * Mycobacterium tb is a strict aerobe, therefore it likes oxygen, ie the apices of the upper lobes * clinically: fever, drenching night sweats, weight loss * phthisis and consumption were old terms for TB, wasting away * complications * hemoptysis, bronchiectasis, scar carcinoma * massive pulmonary hemorrhage - rasmussen's aneuysm * miliary spread in lungs and extrapulmonary sites * adrenal involvenet may cause addissons dz * granulomatous hepatits * diagnosis * bronchoalveolar lavage * sputum cultures * therapy * isoniazid, rifampin, pyrazinamide, ethambutol * long term therapy with close follow up and strict compliance

Question 74

Atypical tb

Answer 74

* mycobacterium avium-intraceullulare MAC * most common TB in AIDS * tx * clarithomycin, rifabutin, ethambutol

Question 75

What is hypersensitivity pneumonitis?

Answer 75

* extrinsic allegic alveolitis secondayr to exposure to inhaled antigen * not mediated by ige - antibodies or with eosinophilia * ex * farmers lung - thermophilic actinomycetes - moldy hay * first exposure develops igg antibodies * second epxosure - immune complexes form and cause inflammatoyr alvolitis * silofillers diseaes - inhalatin of nitrogen oxides from plants * byssinosis: bacterial endotoxin in cotton *

Question 76

Pulmonary neoplasia

Answer 76

* Classification * non small cell lung carcinoma - 80% of lung cancers, relatively insensitive to chemo * squamous cell 30% * large cell * adenocarcinoma 30% * bronchoalveolar carcinoma * small cell lung carcinoma - 20% of lung cancers - oat cell carcinoma * sensitive to chemo, but aggressive and worse prognosis * strongly associated with smoking * Other- carcinoid tumor * Classification * nonsmall cell - better prog * adenocarcionoma * squamous cell * small cell - oat - poor prognosis * large cell carcinoma * bronchial carcinoid * squamous and small cell carcinomas * mostly associated with smoking * centrally located * adenocarcinomas * weakest smoking associatoin * peripherally located. * clinical findings * cough 75% persistent dry * weight loss * chest pain * hemoptsys * dyspnea * dx * cxr * ct/pet determine local and distant metastases * TMN classification - set up tx protocols * sputum cytology * biopsy * can present with * superior vena cava syndrome * virchows node * horner syndrome * clubbing * muscle weakness * eaton lambert syndrome * paraneoplastic syndromes

Question 77

pancoast tumor?

Answer 77

* primary small cell carcinoma * destruction of cervical sympathetic ganglion --\> horner syndrome

Question 78

paraneoplastic syndromes

Answer 78

* corticotropic effects - cushing syndrome * adh effects - * parathyroid like effects * Metastses * most common * colon * renal cell * melanoma * if you see single mass in lung wihtout known primary - likely primary malig * if u see multiple - most likely metas