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Step 1 Miscellanous > Pathoma Respiratory High Yield > Flashcards

Pathoma Respiratory High Yield Flashcards

1
Q

What do you think about an adult with asthma, nasal polyps, and bronchospasm?

A

Likely aspirin-induced asthma - seen in 10% of adults

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2
Q

What causes nasal polyps and what is a typical cause in children?

A

Caused by repeated bouts of edema / inflammation due to rhinitis
-> classically seen in children with Cystic fibrosis

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3
Q

A patient comes in with a locally aggressive and destructive benign neoplasm of the nasopharynx causing epistaxis. Name and describe his condition, and what demographics he most likely is?

A

Nasopharyngeal angiofibroma (it is aggressive despite being benign)

Highly vascular neoplasm which causes profuse bleeding and has a high recurrence rate

Almost exclusively in adolescent males, especially with fair skin and red hair

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4
Q

What typically causes nasopharyngeal carcinoma and who is it seen in?

A

Seen in African children and Chinese adults

Associated with EBV infection classically, also nitrosamines and tobacco / fumes

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5
Q

What does nasopharyngeal carcinoma look like microscopically?

A

Poorly differentiated squamous cell carcinoma (pleomorphic, keratin-positive), surrounded by lymphocytes (mostly T cells to fight EBV infection)

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6
Q

What radiologic sign is descriptive of epiglottitis and what is your major worry? What organism causes this?

A

Thumbprint sign -> inflamed epiglottis shows up on X-ray

Risk of airway obstruction is the major worry
-> caused by hemophilus influenzae b

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7
Q

Where do Singer’s nodules arise and what do they look like histologically?

A

Arise on the true vocal cord, usually bilateral due to excessive use

Appear as degenerative (myxoid) connective tissue -> resolves with rest

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8
Q

What causes laryngeal papilloma and how does the presentation differ between kids and adults?

A

HPV 6/11

Adults - only one papilloma (wart)
Children - usually multiple

-> presents with hoarseness

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9
Q

What is the usual cause of laryngeal vs pharyngeal/oropharynx squamous cell carcinoma?

A

Laryngeal - usually due to alcohol / tobacco

Oropharynx - usually due to HPV 16
-> includes tonsils, soft palate, base of tongue, pharynx

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10
Q

How do patients typically get Klebsiella pneumoniae? How does this relate to who is most susceptible?

A

It is enteric flora which has been aspirated

-> people most susceptible to aspiration include elderly, diabetics, and alcoholics

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11
Q

Who gets Moraxella catarrhalis?

A

Second most cause of exacerbation of COPD, behind Haemophilus influenzae

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12
Q

What is the most common cause of atypical pneumonia in infants? Prophylaxis?

A

Respiratory syncytial virus

Prophylaxis with palivizumab

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13
Q

What type of disease does Coxiella burnetii cause and why can it be thought of as an atypical atypical?

A

Causes atypical (interstitial) pneumonia, but also causes high fever

Also does not require arthropod vector for transmission like most Rickettsial organisms, and does not produce a skin rash.

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14
Q

What happens when TB involves the kidneys?

A

Causes a sterile pyuria

Dr. Sattar says it’s common

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15
Q

What is the clinical diagnostic criteria for chronic bronchitis?

A

Productive cough for >3 months in a year for >=2 consecutive years.

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16
Q

What is the classic pathologic finding in Chronic Bronchitis?

A

Increase in thickness of the mucinous glands >50% - from the epithelium to the cartilage

Normal is <40%

The % occupied is the Reid Index

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17
Q

Why do patients with Chronic Bronchitis turn blue?

A

Mucus plugs trap carbon dioxide in alveoli -> increases PACO2 -> automatically drops PAO2 -> drop in PaO2 -> cyanosis

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18
Q

What is the consequence of chronic hypoxia in the alveoli in chronic bronchitis?

A

Generalized pulmonary vasoconstriction -> cor pulmonale

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19
Q

Where does protein accumulate in A1AT deficiency?

A

In the endoplasmic reticulum of hepatocytes -> PAS positive

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20
Q

Why does the AP diameter increase in emphysema?

A

Because there is a loss of elastic recoil of the lung to pull the chest wall inward -> FRC equilibrates further outward, more towards chest wall’s desired point.

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21
Q

Are hypoxemia and cor pulmonale more common in emphysema or chronic bronchitis?

A

More common in chronic bronchitis, where air trapping behind mucus plugs is more likely to lead to hypercapnia -> hypoxia -> vasoconstriction. This leads to early cor pulmonale.

Hypoxemia is a LATE complication of emphysema due to elastase destroying blood vessels in the interstitium -> reduction in gas exchange -> pulmonary hypertension and subsequent cor pulmonale.

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22
Q

What airway remodeling occurs in asthma in the bronchi / bronchioles?

A

From top to bottom:

  1. Globlet cell metaplasia / mucous gland hyperplasia
  2. Sub-basement membrane fibrosis
  3. Edema of submucosa with inflammatory cell infiltrate with eosinophils, increased vascularity
  4. Smooth muscle hyperplasia / hypertrophy (chronic bronchoconstriction)
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23
Q

What diagnostic things of asthma are contained in the mucous plugs?

A

Curschmann spirals - mucoid swirls of epithelial cells

Charcot-Leyden crystals - needle-like structures formed by extruded and coalesced granules of eosinophils, next to eosinophils

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24
Q

What is the cause of airway obstruction in bronchiectasis?

A

Dilation of the airways -> airflow becomes more easily turbulent in the large airways -> air just begins to swirl around in the open tube when attempted to exhale and never leaves

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25
Q

What obstructive lung disease is associated with allergic bronchopulmonary aspergillosis? Who gets it?

A

Bronchiectasis

Occurs in asthmatics and patients with cystic fibrosis

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26
Q

What is thought to be the underlying pathogenesis of idiopathic pulmonary fibrosis (IPF / UIP)?

A

Cyclical lung injury -> wound healing with fibrosis

-> increased collagen deposition in the interstitium via TGFbeta

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27
Q

What is the common pathology of UIP?

A

subPLEURAL and bibasilar accentuation of tissue damage (extensive fibrosis)
->heterogeneity of tissue damage with “fibroblastic foci” - extensive fibroblast proliferation with ECM

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28
Q

What is the common late stage of UIP?

A

Honeycomb lung. Much more likely to progress than other Interstitial lung diseases.

  • > dilated airspaces from destroyed lung alternating with fibrous scars
  • > septae are extremely thick with poor gas exchange due to fibrosis of interstitium
29
Q

What is the general pathogenesis of a pneumoconiosis?

A

Small occupational exposure particles reach the distal airways
-> macrophages engulf the particles and try to wall off the crap by inducing fibrosis via TGFbeta

30
Q

What is Caplan syndrome?

A

The combination of rheumatoid nodule interstitial lung disease + pneumoconiosis (typically silicosis or Coal Worker’s pneumoconiosis)

31
Q

Where does centrilobular emphysema usually occur?

A

Upper lobes of the lung -> smoke rises

32
Q

What are two characteristic pathologic findings of Sarcoidosis which are not non-caseating granulomas?

A
  1. Asteroid bodies - look like little spokes in a stellate shape - a funny configuration of giant cells
  2. Schaumann bodies - calcium and protein inclusions as part of a giant cell reaction -> basically look like DCIS or Psammoma bodies within a noncaseating granuloma
33
Q

What are the possible ocular, and skin manifestations of sarcoidosis?

A

Ocular - anterior and posterior uveitis

Skin - lupus pernio (skin lesions looking like lupus butterfly rash), erythema nodosum (usually on shins, like due to endemic mycoses)

34
Q

What are the possible nervous system and heart manifestations of sarcoidosis?

A

Nervous system: **Bell’s palsy, neuropathy, hypothalamic and pituitary lesions which can lead to SIADH or diabetes insipidus

Heart involvement: Sudden death due to complete heart block

35
Q

What condition might you confuse with Sjogren’s syndrome?

A

Sarcoidosis - since it can involve the salivary and lacrimal glands

36
Q

What is extrinsic allergic alveolitis? What happens in the lungs?

A

A pseudonym for Hypersensitivity pneumonitis
-> basically an asthmatic reaction but at the level of the alveoli -> Type III / Type IV hypersensitivity reaction i.e. to bird droppings (pigeon breeder’s lung)

-> extended exposure leads to restrictive lung disease with interstitial fibrosis

37
Q

What characterizes the Type III / Type IV hypersensitivity rxn of hypersensitivity pneumonitis?

A

Type III - early -> flu-like symptoms with immune complex deposition and complement activation

Type IV - later -> CD4 T cells and poorly formed granulomas, with progressive fibrosis being induced by macrophages

38
Q

Other than intimal fibrosis, medial hyperplasia, and atherosclerosis of the pulmonary trunk, what is one important pathological finding of pulmonary HTN and why does it happen?

A

Plexiform lesions - tufts of capillary-sized arteries which grow around the pulmonary artery to divert blood around thinkened pulmonary artery passageways

https://www.youtube.com/watch?v=VCvBh41OyZs

39
Q

What is the definition of pulmonary hypertension?

A

Mean pulmonary arterial pressure >25 mmHg at rest. Normal is 10 mmHg.

40
Q

What is the function of BMPR2?

A

Gene which normally inhibits vascular smooth muscle proliferation
-> inactivating mutation causes heritable pulmonary arterial hypertension

41
Q

What can result in the lungs due to recurrent pulmonary emboli?

A

Decreased cross-sectional area of the pulmonary vascular bed -> pulmonary HTN

42
Q

Why might ARDS lead to interstitial fibrosis?

A

Damage and loss of Type II pneumocytes -> loss of stem cells -> healing by fibrosis

43
Q

What is the pathogenesis of ARDS?

A

Endothelial damage -> activation of endothelium -> infiltration of neutrophils and macrophages -> damage to Type I / Type II pneumocytes + endothelial cells -> protease and free radical mediated damage -> leakage of exudate into the alveoli -> formation of hyaline membranes

44
Q

How do you know when the lung has reached adequate levels of surfactant?

A

Lecithin (phosphatidylcholine) : sphingomyelin ratio > 2

45
Q

What are two major risk factors for NRDS other than prematurity?

A
  1. C-section delivery -> reduced stress leads to less sympathetic / cortisol-mediated surfactant production in lungs
  2. Maternal diabetes -> insulin decreases surfactant production -> baby will produce more insulin in response to high sugar crossing the placenta.
46
Q

What congenital heart defect can result from NRDS?

A

Patent ductus arteriosus -> hypoxemia increases the risk of persistence of PDA since increasing oxygen is one of the factors which closes the PDA (along with a drop in PGE2)

47
Q

What are the four complications of NRDS supplemental oxygen or prematurity?

A 
RIB
1. Retinopathy of prematurity
2. Intraventricular hemorrhage 
3. Bronchopulmonary dysplasia
Also necrotizing enterocolitis
48
Q

Why does retinopathy of prematurity happen?

A

Equilibration to high oxygen levels -> massive angiogenesis once ventilator is removed -> VEGF-mediated hyperproliferation of vessels and possible retinal detachment may occur

49
Q

Why does intraventricular hemorrhage occur? What can happen to survivors?

A

Germinal matrix is a hemodynamically unstable area of the brain and premature infants have poor cerebral autoregulation of blood flow

Between 24 and 32 weeks the germinal matrix loses its cellularity and decreases in size -> decreased risk of hemorrhage

Survivors may develop hydrocephalus or permanent neurological defects

50
Q

What are the features and results of bronchopulmonary dysplasia?

A

Increased oxygen tension -> increased free radical production -> alveolar damage. Leads to squamous metaplasia of alveolar airways

Increased oxygen also stunts development / branching -> alveolar hypoplasia -> loss of alveolar septations

51
Q

Why are uranium miners at increased risk of lung cancer? Why is this relevant?

A

Radon is formed by radioactive decay of uranium, an abundant radioactive element in soil

  • > Radon also accumulates in closed spaces such as basements
  • > it is the second most common cause of lung cancer in the US behind cigarette smoke
52
Q

Which type of lung cancer is not amenable to surgical resection?

A

Small cell lung cancer is NOT amenable to surgical resection -> it’s as if the cells are so small that the surgeon can’t see them
-> treat with chemotherapy

53
Q

What paraneoplastic syndrome is squamous cell carcinoma of the lung associated with? What other cancers do this?

A

P is next to Q in the alphabet
sQuamous = PTHrP

Includes squamous cell carcinomas of the lung, head and neck + urinary tract + BRCA

  • > renal cell carcinoma + bladder cancer
  • > breast and ovarian carcinoma
54
Q

What is the most common cause of lung cancer in male vs female smokers? Which is most common overall?

A

Most common overall - adenocarcinoma
Female smokers - adenocarcinoma
Male smokers - squamous cell carcinoma

55
Q

What lung cancer forms intercellular bridges?

A

Squamous cell carcinoma - desmosomal connections between tumor cells

Also generally seen with keratin pearls

56
Q

What are the two defining pathologic features of adenocarcinoma?

A

Characteristic histology of glands or mucin

57
Q

What type of adenocarcinoma has a pneumonia-like presentation? Where does it grow?

A

BronchiOLOalveolar subtype of adenocarcinoma in
situ:
Grows along alveolar septae with apparent thickening of alveolar walls. Tall, columnar cells containing mucus

Pneumonia-like presentation because CXR shows hazy infiltrates and patients often present with bronchorrhea (copious amounts of watery sputum from mucus production)

58
Q

Are bronchioloalveolar carcinoma, large cell carcinoma, small cell carcinoma, and carcinoid tumor related to smoking

A

Bronchioloalveolar subtype of AIS - NOT related to smoking

Carcinoid tumor - NOT related to smoking

Small cell carcinoma - starts with S - YES related to smoking

Large cell carcinoma - the exception - YES! related to smoking

59
Q

What is the classic presentation of carcinoid tumor?

A

Centrally growing polyp-like mass, low grade malignancy

May be central or peripheral however.

60
Q

Are metastases to the lung common? Which two cancers most frequently metastasize there?

A

More common than primary tumors

  1. Breast
  2. Colon
61
Q

What are the key places where lung cancer metastases to?

A
  1. Adrenals - unique
  2. Brain - also has metastases from breast cancer and melanoma
  3. Bone - pathologic fractures
62
Q

What are two situations in which DLCO may actually be increased?

A
  1. Increased hemoglobin in alveoli - i.e. Goodpasture syndrome -> alveolar hemorrhage
  2. Increased pulmonary capillary blood volumes
    - > i.e. congestive heart failure, polycythemia, etc
63
Q

Is DLCO increased in asthma / COPD?

A

Asthma may be normal or increased (if blood volume / congestion increased)

COPD - normal or decreased - since COPD pretty much always co-exists with emphysema

64
Q

What does a decreased PaCO2 automatically imply?

A

Hyperventilation

Hypocapnia implies ongoing hyperventilation
Hypercapnia implies ongoing hypoventilation
#528

65
Q

What is the primary driving force for respiration in normal people vs people with COPD?

A

Normal people - amount of CO2, until PO2 drops < 70 mmHg

COPD - amount of PO2 is primary driver of respiration, since their central chemoreceptors become desensitized to increased CO2 levels.

66
Q

What receptors are primarily responsible for sensing CO2 / O2 levels?

A

CO2 - major contribution is by central chemoreceptors in the medulla (detect a rise in H+ when CO2 diffuses across BBB)

O2 - major contribution is peripheral chemoreceptors (carotid and aortic bodies). Note that these also respond to pH and CO2.

67
Q

Give two useful tumor markers for mesothelioma?

A
  1. Cytokeratin - also called tonofilaments
  2. Calretinin - in the Troponin C family

Taken together, can differentiate mesotheliomas from other peripheral / pleural lung cancers or things which would spread to the region

68
Q

What will be seen on the cell surface of mesothelioma?

A

Long, slender microvilli can be seen via EM

Step 1 Miscellanous (40 decks)

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