Gen Path - Class 13

Front 1

What are three categories/causes of environmental & occupational lung disease?

Back 1

(1)INORGANIC DUSTS (PNEUMOCONIOSIS), (2)ORGANIC DUSTS (HYPERSENSITIVITY PNEUMONITIS), (3)FUMES, GASES, SMOKE

Front 2

What is pneumoconiosis?

Back 2

“dusty lungs” - lung dz resulting from permanent deposition of inhaled industrial inorganic dust

Front 3

What is the etiology of pneumoconiosis?

Back 3

Inhalation of iron ore (siderosis), coal, sand/silica(silicosis), asbestos, aluminum, agricultural dust, cadmium

Front 4

What are the risk factors of pneumoconiosis?

Back 4

High-risk workplaces (mines, construction sites, etc.); greater risk if a smoker. Severity depend on: exposure pattern, particle size (small is bad) and insolubility (bad), presence of underlying pulmonary disease, smoking history

Front 5

What is the pathogenesis of pneumoconiosis?

Back 5

Particles deposit in lungs -- pierce lung lining -- ingesting macrophages are activated -- secrete fibroblast stimulating factor -- fibrosis -- coal macules, thickened calcified pleural plaques. More specific pathogenesis with each specific dz. Generally it’s common for the dz process to take over 10 years, up to 40 years, to develop and produce symptoms

Front 6

What are six clinical manifestations of pneumoconiosis?

Back 6

(1)progressive dyspnea, (2)chest pain, (3)chronic cough/expectoration, (4)exacerbation of asthma/new onset of asthma, (5)loss of appetite, (6)blood tinged mucous

Front 7

What is hypersensitivity pneumonitis?

Back 7

Extrinsic allergic alveolitis dt chronic inhalation of organic dusts & chemicals (eg. molds, fungal spores, wood dust. Occupational also – prolonged exposure to mushroom compost, moldy hay, plant/tree fibers, coffee beans, bird feathers, etc

Front 8

What are four clinical manifestations of hypersensitivity pneumonitis?

Back 8

(1)abrupt onset dyspnea, (2)fever, (3)chills, (4)non-productive cough comes/goes w exposure

Front 9

What five conditions do have an increased risk in children exposed to second hand smoke?

Back 9

(1)Ear infections, (2)More frequent and severe asthma attacks, (3)Respiratory symptoms (for example, coughing, sneezing, and shortness of breath), (4)Respiratory infections (bronchitis and pneumonia), (5)Sudden infant death syndrome (SIDS)

Front 10

What is the result of intrauterine exposure to second hand smoke?

Back 10

low birth weight, premature birth, changes to lung development -- increased. Also correlated with increased risk of ADHD

Front 11

In adults who have never smoked, second-hand smoke can cause:

Back 11

(1)Heart disease - immediate harmful effects on the heart and blood vessels, (2)Lung disease: heart disease deaths, lung cancer deaths, (3)Stroke

Front 12

What can occur in a person who has survived drowning (near drowning)?

Back 12

Surviving (24 h. or longer) the physiologic effect of hypoxemia and acidosis which result from submersion in fluid

Front 13

What are the dry and wet injuries that can occur with near drowning?

Back 13

Dry: little or no fluid in the lungs b/c of laryngeal spasm – minimal lung injury(10-15%)

Wet: aspiration of fluid with asphyxia(85%)

Front 14

With near drowning, what is respiratory distress secondary to?

Back 14

Aspiration pneumonia or pulmonary edema, within 1-2 days of a near-drowning incident

Front 15

What are the risk factors of near drowning?

Back 15

Male (80% of drowning victims); epilepsy, mental disability, heart attack, alcohol consumption, head/cord injury at time of accident, poor use of safety measures

Front 16

What is the pathogenesis of near drowning?

Back 16

wet – severe pulm injury, persistent arterial hypoxia, metabolic acidosis -- damage to brain, kidney, and lungs -- may be irreversible

Front 17

What are two clinical manifestations of near drowning?

Back 17

(1)respiratory (cough, tachypnea, maybe ARDS, pulm edema, pneumonia), (2)neurological (seizures, altered mental status, agitation, coma)

Front 18

What is cystic fibrosis?

Back 18

Genetically inherited disorder of ion transport (Na +Cl) in exocrine glands affecting many systems (Hepatic, Digestive, Male reproductive, respiratory). Predisposes to chronic bacterial airway infections -- almost always leads to COPD.

Front 19

What is the etiology of cystic fibrosis?

Back 19

genetic – CF gene on chromosome 7; most common inherited genetic dz in caucasians

Front 20

In cystic fibrosis, what can impermeability of epithelium to chlorideand reabsorption of sodium and water across epithelialcells leads to?

Back 20

(1)Abnormal mucus (lungs, pancreas, intestines, sweat glands), (2)Increased NaCl, (3)Pancreatic enzyme insufficiency

Front 21

What is the pathogenesis of cystic fibrosis?

Back 21

obstruction of bronchi and bronchioles by abnormal mucous -- infection and patchy atelectasis -- progression to bronchiectasis, pneumonia -- fibrosis, large bronchial cysts. Blockages in the pancreas -- pancreatic lipases, insulin obstructed -- fat & glucose problems.

Front 22

What are six clinical manifestations of cystic fibrosis?

Back 22

(1)“salty kiss”, (2)chronic cough w/ purulent sputum, (3)chronic pulmonary infections, (4)hypoxia, hypercapnia, clubbing, cyanosis, (5)GI (poor fat absorption), (6)glucose regulation problems. Almost all CM’s are a result of overproduction of mucous and deficiency of pancreatic enzymes.

Front 23

How is cystic fibrosis diagnosed?

Back 23

skin sweat test

Front 24

What is the prognosis of cystic fibrosis?

Back 24

Bronchitis, bronchiectasis, atelectasis, pneumonia, pulmonary abscess, pulmonary failure (MCC of CF death)

Front 25

What are five types of parenchymal diseases?

Back 25

(1)Atelectasis, (2)Pulmonary Edema, (3)Acute Respiratory Distress Syndrome (ARDS), (4)Sarcoidosis, (5)Lung cancer

Front 26

What is atelectasis?

Back 26

collapse of normally expanded and aerated lung at any tissue level (Parenchyma, Alveoli, Pleura, Chest wall, bronchi)

Front 27

What is the etiology of atelectasis?

Back 27

i. bronchial obstruction (MCC) -- reabsorption - slow collapse as trapped air is absorbed into bloodstream, ii. direct compression – pressure from air (pneumothorax),blood (hemothorax), or edema (hydrothorax) in pleural space, iii. Rt middle lobe syndrome - secondary to lymph node cancer compression

Front 28

What is pulmonary edema?

Back 28

excessive fluid accumulation in interstitial tissues or alveoli dt: cardiac - Lt-ventricular failure, acute HTN, mitral valve dz, kidney or liver disorders (esp w ↑ Na / water retention, eg. Cushing’s dz), IV narcotics, smoke/toxin inhalation

Front 29

What is Acute Respiratory Distress Syndrome (ARDS)?

Back 29

acute respiratory failure secondary to systemic or pulmonary insult. Often a fatal complication of serious illness, trauma or major surgery.

Front 30

What are the risk factors and etiology of ARDS?

Back 30

Injury causing severe trauma, septic shock, pancreatitis, bypass surgery, infection, burns, aspiration, blood transfusion

Front 31

What is the pathogenesis of ARDS?

Back 31

damage to capillary endothelial cells &alveolar epithelial cells -- alveolar pulmonary edema -- increased vasc. perm. & decreased surfactant -- alveolar collapse). Decreases lung compliance and impairs gas exchange

Front 32

What are five clinical manifestations of ARDS?

Back 32

(1)shallow, rapid breaths, (2)dyspnea, (3)hyperventilation, (4)cyanosis, (5)multiple organ distress syndrome (MODS)

Front 33

What is the outcome of ARDS?

Back 33

multiple organ distress syndrome (MODS)

Front 34

What is sarcoidosis?

Back 34

Systemic idiopathic dz with widespread, diffuse nodular granulomatous inflammation (a collection of macrophages surrounded by lymphocytes, forming nodules). Mainly in women 20-40 y.old; 3-4x more prevalent in blacks than whites. In the lung 90% of the time, and LN’s; also skin, eyes, liver, spleen, heart, small bones.

Front 35

What is the pathology of sarcoidosis?

Back 35

exaggerated immune response to a foreign antigen

Front 36

What are seven clinical manifestations of sarcoidosis?

Back 36

(1)dyspnea, (2)dry cough, (3)fever, (4)wt loss, (5)erythema nodosum, (6)chest pain, (7)hemoptysis

Front 37

What is lung cancer?

Back 37

bronchogenic carcinoma - MCC cancer death inUSA. Malignancy of the epithelium of the respiratory tract. Small cell (oat cell) - 20%. Non-small cell (squamous cell carcinoma, adenocarcinoma, large cell carcinoma) – 80%.

Front 38

What are the risk factors for lung cancer?

Back 38

smoking and environmental pollutants (radon, diesel exhaust, radiation) - urban ↑risk; also nutrition, genetics, age, fam hx.

Front 39

What is the pathogenesis of lung cancer?

Back 39

DNA mutations; direct damage; possible interactions b/t estrogen and epidermal growth factors; all lung cancer arises from common bronchial precursor cell. Metastasis to long bones, vertebrae (esp thoracic), chest wall by direct invasion.

Front 40

What are five clinical manifestations of lung cancer?

Back 40

at first – similar to smoker’s sx’s; Then: (1)bone pain, paravertebral pain (from SNS), (2)night pain, (3)shoulder pain dt ulnar n. (C8-T1 brachial plexus) involvement, (4)Horner’s syndrome (ptosis, myosis, anhydrosis – cervical plexus involvement), (5)poss paraneoplastic syndrome – hormone secreting tumors (hypercalcemia, digital clubbing, osteoarthopathies)

Front 41

What are three pulmonary vasculature disorders?

Back 41

(1)Pulmonary embolism, (2)Pulmonary Hypertension, (3)Cor Pulmonale

Front 42

What is a pulmonary embolism?

Back 42

Obstruction of pulmonary artery by embolus, (90% thromboembolus) -- obstructed blood supply to lung parenchyma. Also: fat, air, bone, vegetations on heart valves (from endocarditis), tumours. MCC is DVT = MCC sudden hospital death & pregn-related death in US

Front 43

What are three major risk factors for a pulmonary embolism?

Back 43

(1)BLOOD STASIS (prolonged travel, spinal cord injury, bed rest in hospital, fracture with casting), obstetrics, age, obesity– prolonged immobilization, (2)ENDOTHELIAL INJURY of the legs or pelvis– surgery, trauma, fractures, (3)HYPERCOAGUABILITY thrombocytic disorders– surgery, trauma, fractures – BC pills, cancer, genetic.

Front 44

What are four other risk factors for a pulmonary embolism?

Back 44

(1)HTN, (2)CHF, (3)trauma, (4)hip/femur fracture

Front 45

What are nine clinical manifestations of pulmonary embolisms?

Back 45

(1)DVT (leg pain, T2P, swelling); (2)dyspnea, SOB, (3)pleuritic pain, (4)hemoptysis, (5)persistent cough, (6)apprehension, (7)tachypnea, tachycardia, (8)rales, (9)fever

Front 46

How is a pulmonary embolism treated?

Back 46

meds (anticoagulants: aspirin, heparin; thrombolytics, pulm vasodilators); surgery

Front 47

What is pulmonary hypertension?

Back 47

HIGH BP IN THE PULMONARY ARTERIES (5-10MM ABOVE NORMAL)

Front 48

What is cor pulmonale?

Back 48

Pulmonary heart disease. Enlargement of right ventricle secondary to pulm HTN (doesn’t include Rt failure secondary to Lt failure, vascular dysfn or congenital heart disease)

Front 49

What are two clinical manifestations of cor pulmonale?

Back 49

(1)Chronic productive cough, exertional dyspnea, fatigability, weakness, (2)occ sudden severe chest pain (large thrombus) -- LOC, death in minutes poss avoided by pounding on chest

Front 50

What are three pleural space disorders?

Back 50

(1)Pneumothorax, (2)Pleurisy/Pleuritis, (3)Pleural Effusion,

Front 51

What is pneumothorax?

Back 51

accumulation of air in pleural cavity dt defect in visceral pleura or chest wall. Lung collapses (atelectasis) on the affected side.

Front 52

What is the etiology and risk factors of pneumothorax?

Back 52

(1)traumatic, (2)spontaneous – tall, slim boys, dtemphysematous bleb defects, (3)tension – dangerous; pleural rupture acts as check valve (one way valve) -- pumping air into pleural space compressing lung

Front 53

What are five clinical manifestations of pneumothorax?

Back 53

(1)dyspnea, (2)sudden sharp pleural chest pain, (3)decreased BP, weak/rapid pulse, (4)decreased resp mvmt on affected side, (5)tension -- severe hypoxemia, dyspnea, hypotension -- shock -- bradycardia

Front 54

What is pleurisy/pleuritis?

Back 54

Inflammation of the pleura caused by infection, injury or trauma. “wet” and “dry” forms

Front 55

What is etiology and risk factors of pleurisy/pleuritis?

Back 55

Complication of lung dz (i.e. pneumonia or TB), abscesses, influenza, SLE, RA, or pulmonary infarction.

Front 56

What is the pathogenesis of wet and dry pleurisy/pleuritis?

Back 56

wet -- abnormal increased in intrapleural fluid -- exudate covers pleura/ interferes w breathing.

dry -- pleural layers become congested and swollen -- rubbing -- friction pain

Front 57

What are four clinical manifestations of pleurisy/pleuritis?

Back 57

(1)sharp chest pain (worse on inspiration or w/ coughing, sneezing), (2)rapid shallow breathing, (3)possibly referred pain (lower chest wall, abdomen, neck, upper traps, shoulder), (4)auscultation -- decreased breathing sounds, rubs

Front 58

What is pleural effusion?

Back 58

Accumulation of fluid in pleural space; transudate or exudate – no inflammation!

Front 59

What is the etiology of pleural effusion?

Back 59

heart failure, lymphatic obstruction dt neoplasm. Also drugs, pancreatitis, collagen-vascular dz, intraabdominal abscess.

Front 60

What is the clincal manifestation of pleural effusion?

Back 60

dyspnea on exertion