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Lungs/Respiratory > Respiratory Pathology > Flashcards

Respiratory Pathology Flashcards

1
Q

What causes rhinosinusitis?

A

Obstruction of sinus drainage into the nasal cavity leading to inflammation and pain over the affected area

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2
Q

What is the most common site of inflammation causing rhinosinusitis?

A

Maxillary Sinuses (because the drainage orifice is superiorly placed near the roof, which impedes drainage)

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3
Q

What is the most common cause of acute rhinosinusitis?

A

Viral URI

a viral URI can lead to a superimposed bacterial infection

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4
Q

What are the three most common bugs associated with rhinosinusitis?

A
  1. S. pneumoniae
  2. H. influenzae
  3. M. catarrhalis
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5
Q

What is epistaxis?

A

Nose bleed

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6
Q

What is the most common site of epistaxis (nose bleed)?

A

Anterior Segment of nostril (Kiesselbach plexus, where 4 arteries anastomose)

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7
Q

Where do life-threatening hemorrhages in the nostril occur?

A

Posterior Segment (sphenopalatine artery, a branch of the maxillary artery)

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8
Q

What are the three components of Virchow’s Triad that predispose patients to DVTs?

A

Virchow Triad (SHE):

  1. Stasis (Venous)
  2. Hypercoaguability (e.g. defect in coagulation cascade proteins, such as factor V leiden)
  3. Endothelial Damage (exposed collagen triggers clotting cascade)
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9
Q

What is Homan’s sign?

A

Calf pain with passive stretching (i.e. dorsiflexion of foot)

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10
Q

What is a Deep Venous Thrombosis (DVT)?

A

Blood clot within a deep vein causing swelling, redness, warmth and pain

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11
Q

How do you treat a Deep Venous Thrombosis (DVT)?

A

Use fractionated heparin or low-molecular weight heparins (eg. enoxaparin) for prophylaxis and acute management

Use oral anticoagulants (eg. warfarin, rivaroxaban) for treatment (long-term prevention)

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12
Q

What patient populations are predisposed to DVTs?

A
  1. ortho trauma
  2. immoblization
  3. pregnant/post-pardum
  4. Cancer patients
  5. Older patients
  6. Patients taking long plane rides or car rides
  7. Women on birth control pills
  8. Lupus (hypercoaguability)
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13
Q

What are the signs of a pulmonary emboli (PE)?

A

Sudden onset dyspnea, chest pain, tachypnea, tachycardia (may present as sudden death)

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14
Q

What is the imaging test of choice for evaluating a pulmonary emboli (PE)?

A

CT pulmonary angiography (look for filling defects)

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15
Q

What histological finding helps to distinguish pre and postmortem thrombi?

A

Lines of Zahn, which are interdigitating areas of pink (platelets, fibrin) and RBCs (light pink then darker pink/red then light pink again, layers are alternating). This is only found in thrombi formed before death.

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16
Q

What are the different types of pulmonary emboli (PE)?

A

FAT BAT

Fat
Air
Thrombus
Bacteria
Amniotic Fluid
Tumor
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17
Q

What are the two associations with forming fat emboli and what is the classic triad of symptoms for fat emboli?

A

Associated with long bone fractures and liposuction

Triad:

  1. Hypoxemia
  2. Neurologic Abnormalities
  3. Petechial Rash
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18
Q

What is the most common sequelae associated with Amniotic emboli?

A

Can lead to DIC (widespread activation of the clotting cascade, leading to bleeding, bruising, and kidney failure) especially post pardum

See shistocytes and helmet cells in peripheral smear in DIC

Classic boards tip off to DIC: blood oozing from all IV sites

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19
Q

What can lead to air emboli and how is it treated?

A

Nitrogen bubbles precipitate in ascending divers

Treat with hyperbaric O2

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20
Q

Where is the most common site of origin for pulmonary emboli?

A

Femoral Vein

even though the most common site of DVT is the calf

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21
Q

What is the result of obstructive lung disease and what are some examples?

A

Obstruction of air flow resulting in air trapping in lungs

Ex: Chronic Bronchitis, Emphysema, Asthma, Bronchiectasis

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22
Q

What happens to RV in obstructive lung disease?

A

RV increases

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23
Q

What happens to FEV1 in obstructive lung disease?

A

FEV1 decreases

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24
Q

What happens to FVC in obstructive lung disease?

A

FVC decreases

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25
Q

What happens to the FEV1/FVC ratio in obstructive lung disease?

A

FEV1/FVC ratio decreases (hallmark of obstructive lung disease)

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26
Q

What are the common sequelae of obstructive lung disease?

A

V/Q mismatch leads to chronic, hypoxic pulmonary vasoconstriction, which can lead to cor pulmonale

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27
Q

What is the classic presentation of Chronic Bronchitis?

A

“Blue Bloater”

Productive cough for > 3 months (not necessarily consecutive) for > 2 years

Findings: wheezing, crackles, cyanosis (early onset hypoxemia due to shunting), late-onset dyspnea, CO2 retention ( hypercapnia), 2° polycythemia (body tries to compensate for poor oxygenation)

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28
Q

What is the pathology of chronic bronchitis?

A

Hypertrophy/Hyperplasia of mucus glands

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29
Q

What is the Reid index and what is the value of the Reid Index in chronic bronchitis?

A

Thickness of gland layer/total thickness of bronchial wall

> 50 in chronic bronchitis

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30
Q

What is the pathology of emphysema?

A

Enlargement of air spaces, decreased recoil, increased compliance, and decreased diffusing capacity resulting from destruction of alveolar walls

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31
Q

What are the two types of emphysema and what are each type associated with?

A
  1. Centriacinar - associated with smoking
  2. Panacinar - associated with alpha 1 antitrypsin deficiency (inhibits neutrophil elastase from breaking down, w/ mutation increased elastase activity, causes loss of elastic fibers and increases lung compliance; look for a young patient with liver problems and lung problems)
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32
Q

What is the classic presentation of a patient with emphysema?

A

“Pink Puffer” who is barrel chested and breathing through pursed lips (exhalation through pursed lips causes an increase in airway pressure and prevents airway collapse during respiration)

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33
Q

What is the pathology of asthma?

A

Bronchial hyperresponsiveness causes reversible bronchoconstriction

(Type 1 Hypersensitivity reaction)

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34
Q

What are common triggers of asthma?

A

Viral URIs, allergens, stress

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35
Q

What are the findings associated with asthma?

A

Nighttime cough, wheezing, tachypnea, dyspnea, hypoxemia, decreased inspiratory/expiratory ratio, pulsus paradoxes and mucous plugging

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36
Q

What are common histological findings for asthma?

A
  1. Smooth muscle hypertrophy
  2. Curschmann spirals (shed epithelium forms whorled mucus plugs)
  3. Charcot-Leyden crystals (eosinophilic hexagonal, double pointed, needle-like crystals formed from the breakdown of eosinophils in the sputum)
  4. Eosinophils (release major basic protein)
  5. Creola Bodies
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37
Q

What cytokines are triggered in asthma?

A

Th2 cytokines (IL-4, IL-5, IL-10, IL-13)

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38
Q

What test do you do to rule asthma in or out?

A

Methacholine challenge

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39
Q

What is the pathology of bronchiectasis?

A

Chronic necrotizing infection of bronchi:

  • permanently dilated airways
  • purulent sputum
  • recurrent infections
  • hemoptysis
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40
Q

What are common associations for bronchiectasis?

A

Associated with:

  • bronchial obstruction
  • poor ciliary motility (e.g. smoking, Kartangener syndrome)
  • cystic fibrosis
  • allergic bronchopulmonary aspergillosis
  • Klebsiella
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41
Q

What are the histological findings associated with bronchiectasis?

A
  1. mucoid exudate
  2. goblet cell metaplasia
  3. epithelial basement
  4. membrane thickening
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42
Q

What is the pathology of restrictive lung disease?

A

Restricted lung expansion causes a decrease in lung volumes (decreased FVC and TLC)

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43
Q

In restrictive lung disease is the FEV1/FVC ratio increased or decreased?

A

FEV1/FVC ratio > or = 80%

It is either preserved or increased

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44
Q

What are the two types/causes of restrictive lung disease?

A
  1. Poor Breathing mechanics (extra pulmonary, peripheral hypoventilation, normal A-a gradient)
    - poor muscular effort (polio, myasthenia gravis)
    - poor structural apparatus (scoliosis, morbid obesity)
  2. Interstitial Lung Diseases (decreased diffusion capacity, increased A-a gradient)
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45
Q

What are some examples of interstitial lung diseases?

A
  1. Acute Respiratory Distress Syndrome (ARDS)
  2. Neonatal Respiratory Distress Syndrome (NRDS; hyaline membrane disease)
  3. Pneumoconioses (e.g. anthracosis, silicosis, asbestosis)
  4. Sarcoidosis: bilateral hilar lymphadenopathy, noncaseating granuloma: increased ACE and Ca2+
  5. Idiopathic pulmonary fibrosis (repeated cycles of lung injury and wound healing with collagen deposition)
  6. Goodpasture Syndrome
  7. Granulomatous with polyangitis (Wegener)
  8. Langerhands cell histiocytosis (eosinophilic granuloma)
  9. Hypersensitivity Pneumonitis
  10. Drug Toxicity (bleomycin, busulfan, amiodarone, methotrexate)
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46
Q

How are lung volume changes different in restrictive vs. obstructive lung diseases?

A

Restrictive: lung volumes normal

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47
Q

How does FEV1 and FVC change in restrictive vs. obstructive lung diseases?

A

Reduced in BOTH restrictive and obstructive

In obstructive, FEV1 is more dramatically reduced compared to FVC resulting in a DECREASE FEV1/FVC ratio

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48
Q

What hypersensitivity is involved in Hypersensitivity Pneumonitis?

A

Mixed Type III and Type IV hypersensitivity reaction to environmental antigen

IgG Ab = Type III
CD8+ = Type IV

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49
Q

When and how does Hypersensitivity Pneumonitis present?

A

4-6 hours after mold or droppings exposure (Aspergillus and Actinomyces). Often seen in farmers and those exposed to birds.

Symptoms: dyspnea, cough, chest tightness, and headache

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50
Q

What are two risks associated with Pneumoconioses (coal worker’s pneumoconiosis, silicosis and asbestosis)?

A
  1. Increased risk of cor pulmonale

2. Caplan Syndrome (rheumatoid arthritis and pneumoconiosis with intrapulmonary nodules)

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51
Q

What findings are pathonomonic of asbestosis?

A

“Ivory white” calcified pleural plaques

Asbestos (ferruginous) bodies are golden brown fusiform rods resembling dumbbells (found in alveolar septum)

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52
Q

What are jobs associated with asbestos exposure?

A

shipbuilding, roofing, plumbing

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53
Q

What are the risks associated with asbestos?

A

Increased risk of lung cancer (bronchogenic carcinoma > mesothelioma)

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54
Q

Which pneumoconioses affects the lower lobes of the lung?

A

Asbestosis

Asbestos is from the roof (was common in insulation), but affects the base (lower lungs)

Silica and Coal are from the base (earth), but affect the roof (upper lungs)

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55
Q

Which industries are associated with Berylliosis?

A

Aerospace and manufacturing

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56
Q

What is the histology associated with Berylliosis?

A

Granulomatous, and therefore, occasionally responsive to steroids

(affects upper lobes)

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57
Q

What is Anthracosis?

A

Asymptomatic condition found in many urban dwellers exposed to sooty air

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58
Q

What is the pathology of Coal worker’s pneumoconiosis?

A

Prolonged coal dust exposure leads to macrophages laden with carbon leading to inflammation and fibrosis

(affects upper lobes)

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59
Q

What industries are associated with Silicosis?

A

Associated with foundries, sandblasting, mines

60
Q

What is the pathology of Silicosis?

A

H2O2 production damages tissue, macrophages respond to silica and release fibrogenic factors + release of cytokines (TNF, IL-1, LTB4)

(affects upper lobes)

61
Q

Silicosis increases someone’s risk for which two conditions?

A
  1. Tuberculosis

2. Bronchogenic Carcinoma

62
Q

What finding is pathonomonic of silicosis?

A

“Eggshell” calcification of hilar lymph nodes

63
Q

What is the pathology of Neonatal Respiratory Distress Syndrome?

A

Surfactant deficiency leads to increased surface tension leads to decreased compliance and increased work of breathing

Increased surface tension can cause alveolar collapse (“ground glass” appearance of lung fields)

64
Q

What lecithin/sphingomyelin ratio in the amniotic fluid is predictive of NRDS?

A

is low risk)

65
Q

What are risk factors for NRDS?

A
  1. Prematurity
  2. Maternal Diabetes (due to increased fetal insulin)
  3. C-section delivery (decreased release of fetal glucocorticoids)
66
Q

What are complications associated with NRDS?

A
  1. metabolic acidosis
  2. PDA (persistently low O2 tension)
  3. Necrotizing enterocolitis
67
Q

What is the treatment for NRDS?

A

Maternal steroids before birth
or
Artificial surfactant for infants

68
Q

What are the risks associated with therapeutic supplemental O2?

A

RIB:

Retinopathy of prematurity
Intraventricular hemorrhage
Bronchopulmonary dysplasia

69
Q

What is Acute Respiratory Distress Syndrome (ARDS) and what are some potential causes?

A

Clinical syndrome characterized by acute onset respiratory failure, bilateral lung opacities, decreased PaO2/FiO2, no HF

May be caused by trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, amniotic fluid embolism

70
Q

What is the pathology of Acute Respiratory Distress Syndrome (ARDS)?

A

Initial damage is due to release of neutrophilic substances toxic to the alveolar wall, activation of coagulation cascade, and oxygen derived free radicals.

Diffuse alveolar damage leads to increased alveolar capillary permeability and protein leakage into alveoli and noncardiogenic pulmonary edema (normal PCWP)

71
Q

What is the common histological finding associated with ARDS?

A

Intra-alveolar hyaline membranes

72
Q

What is the management for ARDS?

A

Mechanical ventilation with low tidal volumes

73
Q

What is sleep apnea?

A

Repeated cessation of breathing > 10 seconds during sleep

Normal PaO2 during the day

74
Q

What are the classic signs/complaints indicating sleep apnea?

A

disrupted sleep & daytime somnolence

75
Q

What are potential sequelae of sleep apnea/nocturnal hypoxia?

A

systemic/pulmonary hypertension, arrhythmias (atrial fibrillation/flutter), sudden death

76
Q

What is Obstructive Sleep Apnea?

A

Respiratory effort against airway obstruction. Caused by excess parapharyngeal tissue in adults and adenotonsillar hypertrophy in children.

It is associated with obesity and loud snoring.

77
Q

What is the treatment for Obstructive Sleep Apnea?

A

Weight loss, CPAP, surgery

78
Q

What is Central Sleep Apnea?

A

No respiratory effort (due to CNS injury/toxicity)

Narcotics, HF, Renal Failure, Rapid Ascent to High Altitudes

79
Q

What is Obesity Hypoventilation Syndrome?

A

Obesity (BMI > 30 kg/m2)

Hypoventilation (decreased respiratory rate) with decreased PaO2 and increased PaCO2 during sleep

Increased PaCO2 during waking hours too (daytime hypercapnia is the way to distinguish this from OSA)

80
Q

What are the long term sequelae of pulmonary hypertension?

A

Cor pulmonale and right ventricular failure

81
Q

What is normal mean pulmonary artery pressure and at what value are you concerned about pulmonary hypertension?

A

Normal PA pressure = 10-14 mm Hg

Pulmonary Hypertension > 25 mm Hg at rest

82
Q

What is the gene involved in heritable pulmonary arterial hypertension (PAH)?

A

Due to an inactivating mutation in BMPR2 gene (normally inhibits vascular smooth muscle proliferation); poor prognosis

83
Q

On examination, what do bilateral dullness to percussion and decreased breath sounds at the lung bases suggest?

A

Pleural Effusion

84
Q

On examination, what does hyper resonant percussion suggest?

A

Pneumothorax

85
Q

On examination, what does increased tactile fremitus, bronchial breath sounds and late inspiratory crackles suggest?

A

Consolidation (pneumonia or pulmonary edema)

86
Q

What is a pleural effusion?

A

Excess accumulation of fluid between pleural layers (restricted lung expansion during inspiration)

87
Q

How can a pleural effusion be treated?

A

thoracocentesis to remove the fluid

88
Q

What is a transudate pleural effusion and what causes it?

A

decreased protein content

due to increased hydrostatic pressure or decreased oncotic pressure (eg. HF, nephrotic syndrome, hepatic cirrhosis)

serum/fluid protein ratio

89
Q

What is a exudate pleural effusion and what causes it?

A

increased protein content, cloudy

due to malignancy, pneumonia, collagen vascular disease, trauma (occurs in states of increased vascular permeability)

**must be drained due to risk of infection

serum/fluid protein ratio > 0.5
serum/ fluid LDL > 0.6

90
Q

What is a lymphatic pleural effusion (chylothorax) and what causes it?

A

Milky-appearing fluid; increased triglycerides

Due to thoracic duct injury from trauma or malignancy

91
Q

What is a pneumothorax?

A

Accumulation of air in pleural space

92
Q

What are the clinical signs of a pneumothorax?

A

Unilateral chest pain and dyspnea, unilateral chest expansion, decreased tactile fremitus, HYPERRESONANCE, diminished breath sounds all on the affected side

93
Q

What is the cause of primary spontaneous pneumothorax and who gets this?

A

Due to rupture of apical blebs or cysts

Occurs most frequently in tall, thin, young males

94
Q

What is the cause of secondary spontaneous pneumothorax and who gets this?

A

Due to a diseased lung (eg. bullae in emphysema, infections), mechanical ventilation with use of high pressures (barotrauma)

95
Q

What is the cause of traumatic pneumothorax and who gets this?

A

Caused by blunt trauma (rib fracture) or penetrating trauma (gun shot or needle puncture)

96
Q

What is a tension pneumothorax?

A

Air enters the pleural space and cannot exit

(increased trapped air = tension pneumothorax)

EMERGENCY, must do a needle decompression before a scan

97
Q

Which way does the trachea deviate in a tension pneumothorax?

A

Away from the side of the lesion

98
Q

Which way does the trachea deviate in atelectasis (bronchial obstruction)?

A

Toward the side of the lesion

99
Q

What organisms cause lobar pneumonia?

A

S. pneumoniae most frequently, also Legionella and Klebsiella

100
Q

What are the characteristics of a lobar pneumonia?

A

Intra-alveolar exudate / consolidaton

May involve entire lobe or lung

101
Q

What organisms cause bronchopneumonia?

A
  1. S. pneumoniae
  2. S. aureus
  3. H. influenzae
  4. Klebsiella
102
Q

What are the characteristics of a bronchopneumonia?

A

Patchy distribution involving 1 or more lobes

Acute inflammatory infiltrates from bronchioles into adjacent alveoli

103
Q

What organisms cause interstitial pneumonia?

A

Viruses (influenza, CMV, RSV, adenoviruses)

Mycoplasma, Legionella, Chlamydia

104
Q

What are the characteristics of an interstitial pneumonia?

A

Diffuse patchy inflammation localized to interstitial areas at the alveolar walls

involving 1 or more lobes

generally follows a more indolent course (“walking pneumonia”)

105
Q

What is a lung abscess?

A

Localized collection of pus within parenchyma

106
Q

What causes lung abscesses?

A

Aspiration of oropharyngeal contents (especially in patents predisposed to loss of consciousness, e.g. alcoholics or epileptics)

or

Bronchial obstruction (cancer)

107
Q

What is the CXR finding for lung abscesses?

A

air-fluid levels (common in cavities, suggests cavitation)

108
Q

What organisms cause lung abscesses?

A

Anaerobes (eg. Bacteroides, Fusobacterium, Peptostreptococcus) or S. Aureus

109
Q

What is the treatment for lung abscesses?

A

Clindamycin

110
Q

What is mesothelioma?

A

Malignancy of the pleura; associated with asbestos (smoking makes it worse, but is not an independent risk factor)

May result in hemorrhagic pleural effusion (exudative) and pleural thickening

111
Q

What histological finding is associated with mesothelioma?

A

Psammoma bodies (laminated calcifications)

112
Q

Where are pan coast tumors located?

A

Also called Superior Sulcus Tumors

Located in the apex of the lung

113
Q

What are the sequelae of pan coast tumors and what syndromes do they cause?

A

May cause Pancoast Syndrome by invading the cervical sympathetic chain, which causes Horner’s Syndrome (ipsilateral ptosis, mitosis, anhidrosis), SVC syndrome, sensorimotor deficits and hoarseness

114
Q

What is SVC syndrome?

A

An obstruction of the SVC that impairs blood drainage from the head

Signs include:

  • facial plethora
  • JVD
  • Edema in the upper extremities

Commonly caused by malignancy (pan coast tumor) and thrombosis from indwelling catheters

It’s a medical emergency bc it can raise intracranial pressure (look for headaches, dizziness, increased risk of aneurysm/rupture of cranial arteries)

115
Q

What is the presentation of lung cancer?

A

Cough, hemoptysis, bronchial obstruction, wheezing, pneumonic “coin lesion” on CXR or non-calcified nodule on CT

116
Q

What are the sites of metastases of lung cancer?

A

Adrenals, brain, bone (pathologic fracture), liver (jaundice, hepatomegaly)

117
Q

In the lung, what are more common, metastases or primary neoplasms?

A

Metastases (usually multiple lesions) are more common than primary neoplasms

Most often breast, colon, prostate and bladder cancer

118
Q

What are the sequelae of lung cancer?

A

SPHERE

SVC Syndrome
Pancoast tumor
Horner syndrome
Endocrine (paraneoplastic)
Recurrent laryngeal nerve compression (hoarseness)
Effusions (pleural and pericardial)
119
Q

What are the risk factors for lung cancer?

A

smoking, second hand smoke, radon, asbestos, family history

120
Q

What is the most common type of lung cancer?

A

Adenocarcinoma is the most common lung cancer in non-smokers and overall (except for metastases)

121
Q

Where does adenocarcinoma of the lung occur?

A

Periphery

122
Q

What mutations should you expect in adenocarcinoma of the lung?

A

Activating mutations in KRAS, EGFR, and ALK

123
Q

What physical finding is associated with adenocarcinoma of the lung?

A

Hypertrophic osteoarthropathy (clubbing)

124
Q

What is the histology associated with adenocarcinoma of the lung?

A

Glandular pattern on histology; often stains with mucin

clara cells + type 2 pneumocytes

125
Q

What is the prognosis for adenocarcinoma of the lung?

A

excellent prognosis

126
Q

What is are the CXR and histological findings of the bronchioalveolar subtype of adenocarcinoma of the lung?

A

CXR shows hazy infiltrates similar to pneumonia

Histology: grows along alveolar septae and see thickening of alveolar walls

127
Q

Where does squamous cell carcinoma of the lung occur?

A

Central (hilar mass arising from the bronchus)

128
Q

What finding is associated with squamous cell carcinoma of the lung?

A

Hypercalcemia (mass can produce PTHrp)

129
Q

What is the major risk factor for developing squamous cell carcinoma of the lung?

A

Smoking

130
Q

What histological finding is associated with squamous cell carcinoma of the lung?

A

Keratin Pearls and intercellular bridges

131
Q

What is the prognosis for small cell carcinoma of the lung?

A

undifferentiated tumors; very aggressive

worst 5 year prognosis

132
Q

Where does small cell carcinoma of the lung occur?

A

Central

133
Q

What small molecules can small cell carcinoma of the lung produce and what syndromes do these cause?

A
  1. ACTH (Cushing syndrome)
  2. ADH (SIADH leads to fluid retention and hyponatremia)
  3. Antibodies against presynaptic Ca2+ channels (Lambert-Eaton myasthenia syndrome)
  4. neurons (paraneoplastic myelitis/encephalitis)
134
Q

What genetic mutation is common in small cell carcinoma of the lung?

A

Amplification of myc oncogenes

135
Q

What are the histological findings associated with small cell carcinoma of the lung?

A

Neoplasm of neuroendocrine Kulchitsky cells, which are small dark blue cells on histology

Chromogranin A +

136
Q

What is the treatment for small cell carcinoma of the lung?

A

Inoperable; treat with chemotherapy

137
Q

Where does large cell carcinoma of the lung occur?

A

Peripheral

138
Q

What is the prognosis of large cell carcinoma of the lung?

A

Highly anapestic undifferentiated tumors; poor prognosis

139
Q

What can large cell carcinoma of the lung secrete?

A

Beta-hCG

140
Q

What histological finding is associated with large cell carcinoma of the lung?

A

Pleomorphic giant cells

141
Q

What is the treatment for large cell carcinoma of the lung?

A

Less responsive to chemotherapy; remove surgically

142
Q

What is the prognosis for bronchial carcinoid tumors?

A

Excellent prognosis; grow slowly and metastasis is rare

143
Q

How do bronchial carcinoid tumors present?

A

Symptoms are usually due to the mass effect: bronchial obstruction, hemoptysis, coughing

144
Q

What syndrome can be associated with bronchial carcinoid tumor and what hormone causes it?

A

Carcinoid Syndrome (serotonin/5-HT secretion)

leads to flushing, diarrhea, wheezing (sometimes right heart failure)

145
Q

What are the histological findings of bronchial carcinoid tumors?

A

Nests of neuroendocrine cells

Chromogranin A +

Lungs/Respiratory (4 decks)

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