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Pulmonary > Diseases > Flashcards

Diseases Flashcards

0
Q

Central Sleep Apnea

A

Cessation of all breathing efforts
Less reticular input to Vagal Root Ganglion and reduced CO2 chemosensing leads to reduced hypercapnic drive
No neural activity to effector muscles

Causes: neuromuscular disease, encephalitis, myasthenia gravis, brainstem infarct

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1
Q

Sleep Apnea Diagnosis and complications

A

Apnea: cessation of breathing for 10 seconds or more
hypopnea: decreased airflow leads to 4% decrease in SO2

Respiratory Disturbance Index=#apneas +hypopneas/hr
RDI> 15 diagnostic of sleep apnea

usually in light slow wave or REM sleep

results in SO2 to 75% or less
PaO2 to 40 mmHg or less
PaCO2 to 55 mmHg or more

Causes: chronic hypoxia, hypercapnia can lead to polycythemia, pulmonary hypertension, right sided heart failure, arrythmias, CHF

Complications: excessive daytime sleepiness, morning headaches, impotence, poor judgement and depression

Treatment: nasal continuous positive airway pressure (CPAP) for obstructive
Central: CPAP with supplemental O2
Complex: servo-adapt ventilation

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2
Q

Obstructive Sleep Apnea

A

Good breathing efforts but upper airway collapse (pharyngeal dilator tone decreases)
Defective chemoreceptor activity

Not hypercapnic during the day

Associated with obesity, loud snoring

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3
Q

Obesity hypoventilation Syndrome

A

90% coexist with obstructive sleep apnea
BMI>30 kg/m2
AND awake hypercapnia (PaCO2 >45 mmHg without other explanation)

Abnormal central ventilation drive related to obesity

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4
Q

Rhinitis

A

Common cold
Inflammation of the nasal mucosa
Edema and thickening of nasal mucosa, increased mucous secretions, narrowing of nasal cavities, sneezing, sometimes sore throat
Earache in children
Viruses: Rhiniviruses, adenovirsuses, coronaviruses, parainfluenza, influenza, RSV, coxasackie A, echoviruses

No vaccine: treatment is supportive

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5
Q

Pharyngitis/Tonsillitis

A

Sore throat, erythema, and swelling of tonsils and pharynx

“Strep throat”-from Strep Pyogenes
acute sore throat, fever, headache, tonsils, uvula, soft palate red, swollen, often covered with yellow-white exudate, swollen cervical lymph nodes

Viral or bacterial in origin, most commonly viral

Viral causes: epstein Barr virus, adenoviruses, parainfluenza, influenza, rhinoviruses, Coxsackie A or B, herpes simplex virus

Bacterial Causes: Strep. pyogenes, Corynebacterium diphtheriae, Neisseria gonorrhoeae

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6
Q

Rheumatic fever

A

Type II hypersensitivity
Caused by post-streptococcal infection
Fever, carditis, migratory polyarthritis, cardiac enlargment and valvular damage
Anti-M protein Abs cross react with heart tissue=molecular mimicry

Treatment with penicillin of streptococcal infection can decrease risk of rheumatic fever

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7
Q

Post streptococcal Glomerulonephritis

A

Type III hypersensitivity
edema, hypertension, hematuria, proteinuria, due to kidney damage
Depsotion of Ag-Ab complexes (Ab to M protein) in kidneys leads to nephritis

Not prevented by treatment with penicillin

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8
Q

Infectious Mononucleosis

A

Mono= fever, fatigue, sore throat, cervical lymphadenpathy, ofen heaptosplenomegaly

Epstein Barr virus-replicates in B lymphocytes

Lymphocytosis and Downey cells
Downey Cell: atypical lymphocyte (cytotoxic T cell) with basophilic vacuolated cytoplasm, lobulated nucleus and indented cell margins

Heterophile Abs-agglutination of sheep or horse RBCs (monospot test)

Also caused by CMV in immunocompromised with - Monospot test

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9
Q

Pharyngoconjunctival fever

A

Swimming pool conjunctivitis or epidemic kertoconjunctiviits

Sore throat, cervical lympadenopathy, and conjunctivitis
Other people in similar circumstances infected

Caused by Adenovirus

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10
Q

Otitis Media

A

Symptoms: fever, ear pain, redness and swelling of tympanic membrane fluid in middle ear

Most common causes: Strep. pneumo, H. influenza, Moraxella catarrhalis

less common causes: strep. pyogenes, staph. aureus

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11
Q

Epiglottitis

A

Rare but life threatening inflammation of the epiglottis

Most common in young children

Symptoms: fever, difficulty swallowing, drooling, hoarseness, stridor

Most frequently caused by H. influenzae B

incidence has decreased since introduction of Hib vaccine for Hib meningitis

Conjugated protein to diptheria toxoid which increases immunogenicity in infants

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12
Q

Laryngitis and Tracheitis

A

In conjunction wit common cold or influenza

Symptoms: hoarseness, throat pain, inspiratory stridor, harsh barking cough

Primarily viral: parainfluenza, influenza, rhinovirus, adenovirus

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13
Q

Croup

A

Acute laryngotracheitis
Inflammation of subglottic area

Symptoms: hoarseness, barking cough, dyspnea with inspiratory stridor

children 3 months to 3 years

Viral especially parainfluenza

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14
Q

Bronchitis

A

Inflammation of the tracheobronchial tree associated with upper respiratory infection

Cough but no evidence of pneumonia

Coarse bubbling rhonchi due to fluid in larger airways

80% viral in origin: influenza, parainfluenza, RSV, adenovirus

Bacterial causes: Bordetella pertussis=whooping cough, H. influenza, Mycoplasma pneumoniae, chlaymdophila pneumoniae

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15
Q

lobar Pneumonia

A

Inflammation and fibrinosuppurative consolidation of a distinct region or lobe of the lung-done by neutrophils
Spreads via pores of Kohn-holes in adjacent alveoli
With polymorponuclear exudate in alveoli
Looks like liver: hepatization

Strep. Pneumo: Most common, middle aged adults and elderly
Klebsiella: Aspiration, malnourished and debilitated individuals (nursing homes, alcoholics, and diabetics), complicated by abscess, thick currant jelly sputum
legionella

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16
Q

Bronchopneumonia

A

More diffuse patchy suppurative consolidation starting in small airways with PMN exudate in the alveoli adjacent to airways
Spreads along airways

S. Aureus: secondary pneumonia, abscess or empyema complicate it
H. influenza: superimposed on COPD
Pseudomonas: cystic fibrosis
Moraxella: superimposed on COPD and community acquired
Legionella: Superimposed on COPD, immunocompromised, transmitted via water source, intracellular, visualized using silver stain

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17
Q

Interstitial pneumonia

A

Invasion of the lung alveolar septa and interstitial tissue

Mycoplasma: atypical, young adults, hemolytic anemia, cold agglutinin, no cell wall
Chlamydia: atypical in young adults
RSV: Atypical in infants
CMV: Atypical with immunosuppression
Influenza: Atypical in elderly and immunocompromised, increased risk of S. Aureus and H. influenza pneumonia
Coxiella burnetii: HIGH fever, farmers and veterinarians

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18
Q

Acute bacterial pneumonia

A

Symptoms: rapid onset, productive cough, fevers, chills, dyspnea, increased RR sometimes chest pain

Bacterial invasion of lung parenchyma
Alveoli SPACES filled with inflammatory exudate, with fibrin and PMNs

Lobar or bronchopneumonia

Diagnosis: gram stain and sputum, blood culture
Sputum should contain PMNs and a preponderance of a single type of bacterium,
presence of squamous cells and mixed normal flora means poor specimen

Common causes: strep. pneummo, S. aureus, H. influenza, Klebsiella (enterobacteriaceae), S. pyogenes, Moraxella catarrhalis, Legionella

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19
Q

Primary Atypical pneumonia

A

Symptoms: slower onset of fever, headache, malaise, less severe symptoms, non-productive cough
“walking pneumonia”

Lymphocytic repsonse
Caused by intracellular bacteria and viruses

Monocytic infiltrate within thickened alveolar SEPTA
Often interstitial

Common causes: mycoplasma pneumoniae, influenza virus, Chlamydia pneumoniae

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20
Q

Bubonic Plague

A

Pneumonic plauge

Caused by Yersinia pestis

Usually vector borne (fleas) but can be via aerosol

Infected rats, prairie dogs and other rodents

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21
Q

Tuberculosis

A

Primary: asymptomatic or fever and malaise. Radiographs show infiltrates in mid-zones and enlarged draining lymph nodes around hilum
Lymph modes fibrose and sometimes calcify they produce characteristic picture (Ghon complex)
Can disseminate into many organs cause necrotic tubercle

Secondary (reactivation): period of immunosuppresion precipitated by malnutrition, alcoholism, diabetes, old age, and dramatic change in life
Cough is universal symptom: initially dry, but later becomes mixed with blood
Fever, malaise, fatigue, swearing, and weight loss all progress with continuing disease
Radiograph infiltrates in spices of lung cause progressive destruction of lung tissue
Potts disease: demineralization of vertebral bodies

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22
Q

AIDS and TB

A

Poorly disseminated granulomas
GI tract and lymph nodes
Macrophages contain many M. avium and M. intracellulare

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23
Q

Miliary Tuberculosis

A

Hematogenous spread to many organs
tiny yellow-white granulomas resemble millet seeds
Via pulmonary ARTERY to lungs
Via pulmonary VEINS to bone marrow, liver, spleen, kidney, adrenals, prostate and heart

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24
Q

Lung abscess/Aspiration pneumonia

A

Clinical: cough, fever, chest pain

Morphology: infections resulting in central suppuration + necrosis
Surrounding wall of chronic inflammation
R Lobe more common due to aspiration

Presdisposing factors: altered consciousness (impairing cough reflex), Neurologic defects resulting in dysphagia, GERD, mechanical compromise, vomiting
Secondary to sepsis (from endocarditis), prior pneumonia, bronchiectasis

Sputum: foul smelling, abundant, bloody
Weight loss
Clubbed fingers and toes

Diagnosis: Chest X-ray
Exclude malignancy

Anaerobic bacteria of oropharynx: Peptostretococcus, Bacteroides, Prevotella, Fusobacterium)
Complications: hemorrhage, extension to pleural cavity, seeding of brain, secondary amyloidosis (Abs),

Abscess cavity forms:
BV-hemorrhage
Airway-air/fluid level
Empty space-secondary saprophytic infection (esp. Aspergillus)

Treat with clindamycin!

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25
Q

> 200 CD4 Cells

A

usual bacteria, tuberculosis

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26
Q

Less than 200 CD4 count

A

Pneumocystis jirovecii, TB usual bacteria

27
Q

Less than 50 CD4 count

A

CMV, Mycobacterium avium-intracellulare pneumonia

28
Q

less than 100 CD4

A

Toxoplasma abscesses

29
Q

Chronic Bronchitis

A

Blue Bloater
Productive cough for >3 months per year for >2 years
Obstructive disease
Normal DLCO

Pathologic findings: hypertrophy/hyperplasia of mucus glands (thickness of gland layer/total thickness of bronchial wall greater than 50%)
Goblet cell metaplasia
inflammation (neutrophil infiltration)
Patchy squamous cell metaplasia

exam findings: wheezing, crackles, cyanosis (early onset hypoxemia due to shunting), late onset dyspnea, CO2 retention
Frequent respiratory infections

Etiology: tobacco smoke/air pollution

Immunology: infiltration of CD8+ lymphocytes, macrophages and neutrophils
IL-13 mucus hypersecretion
Transcription of mucin gene MUC5AC and neutrophil elastase are increased

Symptoms: cough, sputum production (cups)
Cyanosis: Increase PaCO2 due to mucus plugs trapping CO2
Increased risk of infection and cor pulmonale

30
Q

Cystic Fibrosis

A

Autosomal recessive
Defect in CFTR gene on Chromosome 7 (deletionof Phe508 most common)

CFTR encodes an ATP gated Cl- channel that normally secretes Cl- in lungs and GI tract and reabsorbs CL- in sweat glands

Mutations lead to increase intracellular Cl- and compensatory Na+ and H2O reabsorption leading to abnromally thick mucus

Diagnosis: Increased CL- concentration in sweat
Contract alkalosis and hypokalemia

Complications: Recurrent pulmonary infections, chornic bronchitis and bronchiectasis, pancreatic insufficiency, malabsorption and steatorrhea, nasal polyps, and meconium ileusin newborns
Infertility in males
Fat soluble vitamins (ADEK) deficiencies

Treatment: N-acetylcysteine to loosen mucus plugs and dornase alfa to clear leukocytic debris
pancreatic lipase increased macornutrient and vitamin absorption

31
Q

Kartagener Syndrome

A

Immotile cilia due to a dynein arm defect

Results in male and female infertility due to immotile sperm and dysfunctional fallopian tube cilia

increase risk of ectopic pregnancy

Can cause bronchiectasis, recurrent sinusitis, and situs inversus

Diagnosis: low nasal nitric oxide level

32
Q

Idiopathic Pulmonary Fibrosis

A

Males affected more than females
Fibrosis of lung interstitium

Clinical: dyspnea and cough,

Etiology is unknown-most likely related to cyclical lung injury: TGF-B from injured pneumocytes induces fibrosis

High resolution CT: bilateral interstitial lines, traction broncheictasis, honeycomb change
Most prominent in periphery and lung bases

usual interstitial pneumonia morphology: temporal heterogeneity (fibroblastic lesions of different ages), fibroblastc foci, honeycomb fibrosis

Mean survival

33
Q

Non-specific intersitial pneumonia

A

chronic bilateral lung disease of unknown etiology

Better prognosis than idiopathic

Clinical: cough of several months duration

Pathology: cellular and fibrosing
Cellular-chronic inflammation
Fibrosing-diffuse of patchy fibrosis
NO fibroblastic foci or honeycombing 
Use corticosteroids
34
Q

Coal Worker’s Pneumoconiosis

A

Anthracosis; asymptomatic with no inflammatory reaction, carbon laden macrophages accumulate along lymphatics (PERILYMPHATIC) and in lymph nodes

Upper lobes-simple (centrilobular ephysema)

Progressive massive fibrosis-years to develop
leads to diffuse fibrosis ( black lung)

Can be associated with Rheumatoid arthritis

35
Q

Silicosis

A

Most prevalent occupational hazard in world-foundries, sandblasting, and mines

Upper lobes

Inhalation of crystalline silica-sand blasting and hard rock mining (quartz most common)

Release of IL-1 from macrophages leads to fibrosis

Histology: silicotic nodules containing birefringent silica
Eggshell calcifications
Hilar adenopathy

increased susceptibility to TB- impair macrophages phagylysosome formation
Also increased risk of bronchogenic carcinoma

36
Q

Asbestosis

A

Associated with shipbuilding, roofing and plumping

Four manifestations:
1. pleural plaques: parietal pleura along lower lungs and diaphragm
Composed of circumscribed areas of dense collagen that become calcified
Asymptomatic unless collapse of adjacent lung parenchyma
2. Asbestosis: progressive pulmonary fibrosis
Smoking is synergistic
3. bronchiogenic carcinoma: most common malignancy
Smoking is synergistic
Mesothelioma: malignancy of pleura
more specific for asbestos exposure

Amphiboles more pathogenic-furruginous bodies-golden brown fusiform rods resembling dumbbells have transluecent asbestos center with iron containing material (Prussian blue stain)

Oncogenic effects on mesothelium-free radicals generated by asbestos fibers
Adsorption of carcinogens from tobacco

begins in Lower lobes

eventual honeycombing
Pleural plaques of dense collagen sometimes calcified (not asbestos bodies) can lead to bloody pleural effusions

37
Q

Sarcoidosis

A

Younger adults

38
Q

Hypersenstivity Pneumonitis

A

Affects alveoli usually caused by inhaled organic antigens

Risk factors: amount of exposure, nonsmoking, pregnancy, labor

Manifests as a restrictive lung disease with decreased diffusion capacity, lung compliance, and total lung volume
Interstitial infiltrates

Noncaseating Granulomas-CD8

Acute-fever, cough, dyspnea and constitutional signs 4-8 hours after exposure
Physical findings: fever, tachypnea, tachycardia, crackles
Laboratory: leukocytosis (neutrophils and lymphopenia), hypoxemia
PFTs-restrictive, decreased FVC and Decreased DLCO

Chronic: insidious onset of cough, dyspnea and weight loss may lead to interstitial fibrosis
PFT-combined

Bronchioalveolarlavage: increased CD4 and CD8 T lymphocytes
Patients have precipitating Abs in their serum
Complement and immunoglobulins are found in vessel walls indicating a Type 3 immune reaction
Mixed type II/Type IV hypersenstivity

Radiographs: diffuse patchy infiltrates
Subacute: ground glass attenuation, chronic-50% honey combing

39
Q

Aspirin Induced Asthma

A

Typical onset is the 3rd to 4th decade
Chronic nasal congestion with nasal polyps

Acute symptoms 1 hour after ingestion of aspirin
Asthma attack is accompanied by rhinorhea, conjunctival irritation and scarlet flush of the head and neck

Aspirin decreases prostaglandins and increase leukotrienes

Aspirin patients do not react to COX-2 inhibitors

40
Q

Allergic bronchopulmonary aspergillosis

A

Aspergillus fumigatus colonizes sputum plugs in the bronchi of asthmatics
Immune response to Ags released from the fungus
Fleeting pulmonary infiltrates, eosinophilia, and A. fumigatus in sputum cultures

Associated with asthma and cystic fibrosis
May cause bronchiectasis and eosinophilia

Skin and serologic tests (IgE Abs to Aspergillus) are used for diagnosis

treatment: oral steroids

41
Q

Tension Pneumothorax

A

Symptoms: tachycardia, hypotension, tachypnea, hypoxemia, absent breath sounds, hyperresonance on affected side
X-ray: lucent area with no lung markings located laterally or at the apex of the thoracic cavity
Border of collapsed lung is seen as a sharp line

Increased air pressure in the pleural space
Displacement of medistinum away from affected side
Flattened or inverted hemidiaphragm at side of pneumothorax

Usually occurs due to trauma or infection
Air capable of entering pleural space but not exiting

42
Q

Spontaneous pneumothorax

A

Symptoms: tachycardia, hypotension, tachypnea, hypoxemia, absent breath sounds, hyperresonance on affected side

X-ray: lucent area with no lung markings located laterally or at the apex of the thoracic cavity
Border of collapsed lung is seen as a sharp line

Increased air pressure in the pleural space
Displacement of medistinum away from affected side
Flattened or inverted hemidiaphragm at side of pneumothorax
Accumulation of air in pleural space.

Occurs most frequenlty in tall, thin, young males because of rupture of apical blebs (continuous distended air spaces that can form cyst like sacs) or with emphysema

43
Q

Aspirations

A

While upright: most likely lower right inferior lobe

While Supine: posterior superior portion of right inferior lobe or posterior inferior segment of right superior lobe

44
Q

Trachea/bronchus Lesion

A

Decreased breath sounds on affected side
Trachea deviates toward affected side
Atelectasis leads to decreased lung volume

Cancerous lesions lead to prevention of ventilation then alveolar collapse which causes unilateral pulmonary opacification

45
Q

Methehemoglobinemia

A

Cyanosis and chocolate colored blood

46
Q

Carbon Monoxide poisoning

A

CO has greater for Hb than O2
Competitively binds to hemoglobin altering hemoglobin into a relaxed state
Forms Carboxyhemoglobin

Causes: decreased oxygen binding capacity with left shift in O2-hemoglobin dissociation curve
Decreased O2 unloading in tissues

47
Q

Nitrite poisoning

A

Oxidizes Fe2+ to Fe3+ (Fe3+ does not bind to O2)

Normal PaO2 of arterial blood
Leftward shift of curve

48
Q

Cyanide Poisoning

A

Cyanide binds to cytochome a-a3 complex of ETC
Inhibits aerobic metabolism and rapidly causes death

Clinical: facial flushing, tachypnea, headache and tachycardia, nausea, vomiting, confusion, weakness,
Respiratory distress and cardiac dysfunction follow
Lactic acidosis and oxygenated veins due to decreased unloading
High affinity for Fe3+ on deoxygenated hemoglobin

Treatment: nitrites oxidize Hb to methemoglobin which binds to cyanide
Then use thiocyanate to renally excrete

49
Q

Obstructive Lung disease general characteristics

A

Airways close prematurely at high lung volumes resulting in air trappin in lungs

PFTs: decreased FEV1/FVC ratio (both FEV1 and FVC decreased but FEV1 decreased more)
Increased TLC, Increased RV (increased RV/TLC ratio), decreased DLCO
V/Q mismatch

Increased EPO
Chronic hypoxic pulmonary vasoconstriction leads to cor pulmonale
Increased R. ventricular afterload due to pulmonary hypertension

O2 supplementation leads to respiratory suppression and coma (O2 is the respiratory drive instead of CO2)

50
Q

Emphysema

A

Pink puffer, barrel shaped chest

Enlargement of air spaces-distal to terminal bronchioles
Decreased recoil, increased compliance, decreased DLCO due to destruction of alveolar walls

Centriacinar: upper lobe (smoke rises) smoking enhances macrophage elastase
Panacinar: associated with a1-antitrypsin deficiency (lower lobe due to increased perfusion and neutrophil infiltration)

Minimize airway resistance by maintaining hyperinflated state

Increased elastase (from macrophages and neutrophils) leads to loss of elastic fibers and increased lung compliance, decreased lung capacity leads to compression during exhalation
Increased proteinase:antiprotease activity

Exhalation through pursed lips to increase airway pressure and prevent collapse during respiration

51
Q

Asthma

A

Bronchial hyperresponsiveness causes reversible bronchoconstriction
Smooth muscle hypertrophy

Findings: cough, wheezing, tachypnea, dyspnea, hypoxemia, decreased I/E ratio, pulsus paradoxicus, mucus plugging
Can be triggered by viral URIs, allergens and stress

Family history of allergic triad: allergic rhinitis, atopic dermatitis, asthma

Decreased peak expiratory rate

Increased TH2 leads to increased risk of developing asthma (second hand smoke)

Curschmann spirals (epithelium from mucus plugs)
Charcot Leyden crystals (formed from breakdown of eosinophils in sputum)
Eosinophils activated by IL-5

Diagnosis: methacholine challenge: test bronchial hypersensitivity
Decreased FEV1 by more than 20% indicates asthma
Treatment: acutely with B-agonists that increased cAMP

52
Q

Bronchiectasis

A

Chronic necrotizing infection of bronchi leading to permanently dilated airways
Purulent sputum, recurrent infections, hemoptysis

Associated with bronchial obstruction, poor ciliary motility (smoking), Kartagener syndrome, cystic fibrosis, allergic bronchopulmonary aspergillosus

53
Q

Restrictive Lung Disease

A

restricted lung expansion causes decreased lung volume (decreased FVC and TLC)
FEV1/FVC ratio is normal or increased (above 80%)
Decreased DLCO
Increased elastic recoil-fiborsis keeps airways open during expiration (radial traction)

Symptoms: exertional dyspnea, crackles, honeycombing and ground glass, clubbing

X-Ray: small irregular reticulonodular opacities most pronounced in lower lobes

Types:
Poor breathing mechanics: polio, myasthenia gravis, scoliosis, morbid obesity (peripheral hypoventilation, normal A-a gradient)

Interstitial lung disease (decreased diffusing capacidty, increased A-a gradient)
ARDS
NRDS
Pneumoconioses
Sarcoidosis
Idiopathic-repeated cycles of injury and wound healing with increased collagen deposition (lined by type II pneumocytes)
Goodpasture syndrome
Wegeners syndrome
Langerhans cell histiocytosis (eosinophilic granuloma)
Hypersensitivity pneumonitis
Drug toxicity: busulfan, bleomycin, amioradone, methotrexate

54
Q

Neonatal Respirator Distress Syndrome

A

Surfactant deficiency leading to increased surface tension and alveolar collapse (hyaline membrane disease)
Lecithin: sphingomyelin ratio

55
Q

Berrylliosis

A

Dyspnea and ill defined nodular or irregular opacities on chest X-Ray
40% hilar adenopathy

Non-caseating granulomas (similar to sarcoidosis)

Enlarged LNs

56
Q

Acute Respiratory Distress Syndrome

A

May be caused by trauma, sepsis, gastric aspiration, uremia, acute pancreatitis (increased serum amylase and lipase, necrotizing), amniotic fluid embolism

Diffuse alveolar damage leads to increased alveolar capillary permeability leading to protein rich leakage into alveoli and non cardiogenic pulmonary edema (normal PCWP)

Results in formation of intra-alveolar hyaline membrane

initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade and oxygen derived free radicals
Sepsis/shock produce endothelial damage from release of endotoxin induced release of adherent leukocytes and cytokines

Decreased lung compliance, increased work of breathing, increased decreased oxygen diffusing capacity

Can lead to atelectasis of regional alveoli leading to V/Q mismatch

Will have interstitial edema with alveolar infiltrates
Acute stage lung will be heavy, red and boggy

57
Q

Pulmonary Hypertension

A

Normal primary artery pressure=10=14 mmHg, pulmonary hypertension>25 mmHg

Pathogenesis: Muscularization of small arteries leading to medial hypertrophy and intimal hyperplasia causing intimal fibrosis lastly formation of capillary tufts plexiform lesion

Primary: due to an inactivating mutation in the BMPR2 gene (proapoptotic) normally function to inhibit vascular smooth muscle proliferation
Poor prognosis
Increased endothelin, decreased NO, decreased prostacyclin

Secondary: due to COPD (destruction of lung parenchyma), mitral stenosis (increased resistance leads to increased pressure), recurrent thromboemboli (decreased Cross Sectional area of pulmonary vascular bed), autoimmune disease (systemic sclerosis, inflammation in intimal fibrosis and medial hypertrophy), L to R (shear stress leads to endothelial injury), sleep apnea or living at high altitude (hypoxic vasoconstriction), Left heart failure, chronic hypoxia, HIV
Ingestion of appetite suppressants (fenfluramine, dexfenfluramine, phentermine)

Course: severe respiratory distress leading to cyanosis and RVH leading to death from decompensated cor pulmonale

Symptoms: dyspnea on exertion, chest pain, and distended neck veins
Accentuated pulmonary component of second heart sound, tricuspid regugitation accentuated with inspiration, hepatomegaly, peripheral edema
Dilation of Right atrium leading to dilation of coronary sinus

Treatment: Bosentan (endothelin antagonist), somewhay vasodilator epoprostenol

58
Q

Superior Vena Cava Syndrome

A

Obstruction of SVC that impairs blood drainage from the head (both sides) neck (JV distension) and upper extremities (wekaness and loss of sensory)

Commonly caused by malignancy and thrmobosis from indwelling catheters (mediastinal mass)
lung cancer and non-hodgkin lymphoma

Medical emergency

Can raise intracranial pressure leading to headaches, dizziness, and increased risk of aneurysm/rupture of intracranial arteries

Symptoms: dyspnea, cough, and swelling of face, neck, upper extremities

59
Q

Obstruction of Brachiocephalic vein

A

Similar to SVC syndrome but only ONE side

Due to external compression, apical lung tumor, thrombotic occlusion or central catheter in place for a prolonged period of time

R. brachiocephalic is internal jugular and subclavian veins

Drains R. lympatic duct which drains r. upper extremity, r. face and neck, r. hemithorax, and r. upper quadrant

Face and arm swelling

60
Q

Fat Emboli

A

Associated with long bone and pelvic fractures and liposuction, orthopedic surgeries

Classic Triad: 1. respiratory distress (hypoxia, dyspnea, tachypnea)
2. Neurologic symptoms (altered mental status seizures)
Emboli escape via pre capillary AV shunts then occlude microessels impairing gas exchange leading to microvascular occlusion in cerebral white matter, brain stem and SC
3. petechial rash on head, neck, thorax and axilla

Can be stained with osmioum tetraoxide (black)

Pulmonary and CNS dysfunction may be promoted by:

  1. release of mediators form platelets which adhere and coat fat emboli
  2. systemic activation of lipoprotein lipase and intravascular release of oleic acid

Anemia due to increased RBC aggregation and destruction and maybe pulmonary hemorrhage

61
Q

Rhinosinusitits

A

OBstruction of sinus drainage into nasal cavity leading to inflammation and pain over affected area (typically maxillary sinuses in adults)

Most common cause is viral URI
Can cause superimposed bacteria infection most commonly S. pneumo, H. influenza, and Moraxella catarrhalis

61
Q

Deep Vein Thrombosis

A

Leads to pulmonary emobli

Stasis: risk factors-older age, lower extremity surgery, immobility
Hypercoagulability: defect in coagulation cascade proteins (Factor V Leiden)
Endothelial damage: exposed collagen triggers clotting cascade

Pregnancy-increased clotting factors, decreased fibrinolysis, decreased anticoagulant levels, decreased venous tone, pressure on gravid uterus leads to stasis (USE HEPARIN)

Symptoms: unilateral leg pain, swelling and warmth
Tenderness of calf on dorsiflexion

Treatment: heaprin for prevention and acute management
Warfarin (teratogenic) for long term prevention of DVT recurrence

Diagnosis: doppler ultrasound

61
Q

Pulmonary Emboli

A

Increased pulmonary resistance and increaesed R. ventricular afterload leads to R. heart failure
decreased blood through affected alveoli, increased blood everywhere else leading to V/Q mismatch and hypoxemia (due to increased perfusion to underventilated areas)

Symptoms: sudden onset dyspnea, chest pain, tachypnea
may present as sudden death (post surgery)

Type: Fat, Air, Thrombus, Bacteria, Amniotic fluid, tumor

Large emboli lodge in pulmonary artery bifurcation
Small emboli occlude peripheral branches

CT pulmonary angiography is imaging test of choice for PE

Risk factors: immobilization (venous stasis), recent surgery (hypercoagulable state)

61
Q

Amniotic fluid emboli

A

Can lead to DIC, especially postpartum

61
Q

Gas emboli

A

Nitrogen bubbles precipitate in ascending divers

Treat with hyperbaric oxygen

62
Q

Sarcoidosis

A

African American females

Characterized by immune mediated, widespread noncaseatign granulomas (can be found in liver)

Often asymptomatic except for enlarged LNs (can have fever, malaise, weight loss, cough, dyspnea)

Indcidental finding on chest X-ray is bilateral hilar adenopathy and/or reticular opacities

Associated with restrictive lung disease (interstitial fibrosis), erythema nodosum, lupus pernio (hardened raised purple lesion), Bell’s palsy, epitheliod granuloms, microscopic Scaumann and asteroid bodies (eosinophilic calcium and protein inclusion in phagocytes), uveitis, and hypercalcemia (decreased PTH)

Hypercalcemia due to 1a hydroxylase activation of Vitamin D in macrophages
Diagnosis: increased CD4/CD8 ratio

Pulmonary (1 decks)

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