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STEP 1 (1) > Respiratory-Pathology > Flashcards

Respiratory-Pathology Flashcards

1
Q

What is rhinosinusitis?

A

Obstruction of sinus drainage into the nasal cavity leading to inflammation and pain over the affected (most commonly the maxillary sinuses which drain to the middle meatus)

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2
Q

What is the most common cause of rhinosinusitis?

A

viral UTI (can be superimposed on a bacterial infection)

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3
Q

Most common bacterial infection causing rhinosinusitis?

A

S. pneumo, H. influenzae, and M catarrhalis

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4
Q

What is epitaxis?

A

Nose bleed

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5
Q

Where does epitaxis most commonly occur?

A

in the anterior segment of the nostril (Kiesselbach plexus)

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6
Q

Potentially life-threatening nose bleeds occur where?

A

The posterior segemnt (sphenopalatine artery, a branch of the maxillary a.)

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7
Q

What are the most common causes of head and neck cancer?

A

tobacco and alcohol

HPV-16 (oropharyngeal)

EBV (nasopharyngeal)

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8
Q

What is the Virchow triad?

A

These are a triad of symptoms related to increased risk of thromboembolism, including:
SHE

Stasis

Hypercoagulability

Endothelial damage

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9
Q

What test can be used to rule out a DVT?

A

D-dimer test

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10
Q

How should a DVT be treated prophylatically?

A

Unfractionated heparin or LMW heparin (e.g. enoxaparin) for prophylaxis and acute management

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11
Q

How should a DVT be treated?

A

oral anticoagulatns (e..g warfarin, rivaroxaban) for treatment or long-term prevention

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12
Q

What is the best imaging test for a DVT?

A

compression ultrasound

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13
Q

What is the imaging test of choice for a pulmonary embolism?

A

CT pulmonary angiography

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14
Q

What histologic finding is indicative of an embolis?

A

Lines of Zahn - interdigitating areas of pink (platelets, fibrin), and red (RBCs)

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15
Q

T or F. Lines of Zahn are only found in thrombi formed before death

A

T.

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16
Q

What are the main types of emboli?

A

FAT BAT

Fat

Air

Thrombus

Bacteria

Amniotic fluid

Tumor

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17
Q

Describe fat emboli and their CLASSIC presentation

A

These commonly form after fracture of long bones (in older people usually) and present with the classic triad of:

hypoxemia

neurologic confusion

petechial rash

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18
Q

An amniotic fluid embolus most commonly leads to what?

A

DIC, especially in post-partum

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19
Q

What are obstructive lung diseases?

A

these are diseases that result in air flow obstruction leading to air being trapped in the lungs

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20
Q

What is FVC? FEV1?

A

Forced vital capacity, or FVC, is the amount of air which can be forcibly exhaled from the lungs after taking the deepest breath possible. FVC is used to help determine both the presence and severity of lung diseases.

FEV1 is this volume expelled in 1 second

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21
Q

What is the hallmark of an obstructive lung disease on a PFT?

A

decreased FEV1/FVC ratio (both decrease but FVC decreases more)

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22
Q

What are some types of obstructive lung disease?

A
  • chronic brinchitis
  • emphysema
  • asthma
  • bronchiectasis
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23
Q

What is chronic bronchitis?

A

defined as a productive cough for 3+ months per year (doesnt have to be consecutive) for 2+ consecutive yrs

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24
Q

What causes chronic bronchitis?

A

There is marked hyperplasia of mucus-secreting glands in the bronchi, as defined as greater than 50% via the Reid Index

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25
Q

What are the findings of chronic bronchitis?

A

wheezing, crackles, cyanosis (early-onset hypoxemia due to shunting), and late-onset dyspnea and Co2 trapping

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26
Q

What is emphysema?

A

loss of alveolar walls leading to enlargement of air spaces and thus, less surface area for gas exchange

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27
Q

How do compliance and recoil change in emphysema?

A

compliance increases (this is due to increased elastase activity due to less a1-antitrypsin) and recoil decreases

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28
Q

What are the main types of emphysema?

A
  • centriacinar
  • panacinar
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29
Q

Describe centriacinar emphysema

A

this is most commonly found in the upper lobe and is associated with smoking (smoke rises),

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30
Q

Describe panacinar emphysema

A

this is more common in the lower lobes and is associated with a1-antitrypsin deficiency

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31
Q

What are the classic findings of emphysema on CXR?

A

barrel-chest, increased AP diameter, and a flattened diaphragm

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32
Q

How might a person with emphysema breath?

A

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

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33
Q

What is asthma?

A

An obstructive lung disease caused by bronchial hyperresponsiveness that results in reversible bronchoconstriction

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34
Q

What are some classic histological findings of asthma?

A
  • smooth muscle hypertrophy
  • Curschmann spirals (below)- shed epithelium that forms whorled mucus plugs
  • Charcot-Leyden crystals
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35
Q

What are Charcot Leyden crystals?

A

eosinophilic, hexogonal, needle-like crystals that form from breakdown of eosinophils in suptum

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36
Q

What is bronchiectasis?

A

a chronic necrotizing infecvtion of bronchi that results in permanent dilation

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37
Q

What are some common causes of bronchiectasis?

A
  • bronchial obstruction
  • cystic fibrosis
  • smoking

Kartagener syndrome

-allergic aspergillosis

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38
Q

What are restrictive lung diseases?

A

diseases that are marked by restricted lung expansion causing decreased lung volume (FEV1:FVC ratio is still above 80%)

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39
Q

What are the main categories of types of restrictive lung disease?

A
  • poor breathing mechanics
  • interstitial lung disease
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40
Q

What are some causes of poor breathing mechanics?

A
  • poor muscular effort- polio, myasthenia gravia, Guillian-Barre syndrome
  • poor structural apparatus- scoliosis, morbid obesity
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41
Q

What are some causes of ILD?

A
  • ARDS and NRDS (hyaline membrane)
  • Pneumoconiosis
  • Sarcoidosis
  • IPF
  • Goodpasture syndrome
  • Wegener Polyangiitis
  • Langerhan Cell Histiocytosis
  • Hypersensitivity Pneumonitis
  • Drug toxicity (bleomycin, busalfan, amiodarone, methotrextae)
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42
Q

Once you diagnosis restrictive lung disease via a PFT, how can you determine whether the cause is mechanical or interstitial lung disease?

A

Check the A-a gradient

Normal in mechanical issues and elevated in ILD

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43
Q

What is the most common cause of ARDS?

A

premature birth before surfactant is fully developed (surfactant is mature at 35 weeks)

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44
Q

What are some common types of pneumoconioses?

A
  • anthracosis/coal miners pneumoconiosis
  • silicosis
  • abestosis
  • berylliosis
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45
Q

What causes coal miners pneumoconiosis (aka black lung disease?

A

typically prolonged coal dust exposure

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46
Q

What is this?

A

Coal miners pneumoconiosis marked by carbon laden macrophages that can significant interstital inflammation and fibrosis

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47
Q

What lung lobes are most commonly affected by coal miners pneumoconiosis?

A

upper

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48
Q

Asbestosis is most common in what types of jobs?

A

shipbuilding, roofing, and plumbing

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49
Q

What is this?

A

Pleural plaques which are pathgnomonic to asbestosis

50
Q

What lung lobes are most commonly affected by asbestosis?

A

lower

51
Q

What are these?

A

Asbestos (ferruginous) bodies- golden-brown fusiform rodes resembling dumbbells found in alveolar suptum samples

52
Q

How can asbestos bodies be best seen?

A

Prussion blue stain

53
Q

Describe berylliosis

A

This is common in aerospace and manufacturing industries and commonly affected the upper lobes

54
Q

Where is siliocosis most common?

A

foundries, sandblasting, and mines

55
Q

Pts with silicosis are at an increased risk of what?

A

TB- silica interrupts phagolysosomes and impairs macrophages

56
Q

What lung lobe in silicosis most common in?

A

upper

57
Q

What is hypersensitivity pneumonitis?

A

mixed type III/IV hypersensitivity reaction to an environmental antigen leading to dyspnea, cough, chest tightness, and HA

Often seen in farmers and those exposed to birds

58
Q

What are some common causes of ARDS?

A

SPARTAS

Sepsis

Pancreatitis

Pneumonia

Aspiration

uRemia

Trauma

Amniotic Fluid Embolism

Shock

59
Q

What is a classic finding of ARDS (and NRDS) and what causes it?

A

hyaline membranes (below)- endothelial damage caused increased capillary permaebility leading to leakage of protein-rich exudate into the alveoli and the formation of noncardiogenic pulmonary edema (normal PCWP)

60
Q

How should ARDS be managed?

A

Go to deck

61
Q

What is a common cause of increased EPO in the blood?

A

Sleep apnea, which results in hypoxia induced synthesis of EPO

62
Q

What is the normal pulmonary a. pressure?

A

10-14 mm Hg

63
Q

How is pulmonary HTN defined?

A

25+ mm Hg at rest

64
Q

What are the most common causes of pulmonary HTN?

A
  • Idiopathic PAH
  • Left heart disease
  • chronic TE
65
Q

What is the genetic cause of hereditary PAH?

A

inactivating mutation in BMPR2 gene (which normally inhibits vascular smooth muscle proliferation)- poor prognosis

66
Q

Keep in mind that anything that induces pulmonary hypoxemia will result in vasoconstriction and potential formation of PAH

A

I.e. High altitude

67
Q

How would a pleural effusion look on a CXR?

A
68
Q

How does a pleural effusion affect breath sounds? percussion? Fremitus?

A

breath sounds are decreased and percussion is dull

Fremitus also decreases

69
Q

Does the trachea deviate in a pleural effusion?

A

Typically no but may deviate away from the effusion if its large enough

70
Q

How does atelectasis (bronchial obstruction causing lung collapse) affect breath sounds? percussion? Fremitus?

A

breath sounds are decreased and percussion is dull

Fremitus also decreases

71
Q

How would the treachea deviate in atelectiasis?

A

toward the side of the lesion

72
Q
A
73
Q

How does spimple pneumothorax affect breath sounds? percussion? Fremitus?

A

breath sounds and fremitus are decreased and percussion is hyperresonant (same in tension)

74
Q

What is this?

A

Tension pneumothorax.. notice how the trachea deviates to the opposite side

75
Q

Does the trachea deivate in simple pneumothorax?

A

NO

76
Q

What is a pleural effusion?

A

Accumulation of fluid between the pleural alyers lining the lungs leading to restricted lung expansion during inspiration

77
Q

What are the main categories of ‘materials’ found in pleural effusions?

A

transudate,

exudate,

lymphatic

78
Q

What causes transudate?

A

This kind of fluid is low in protein content and is typically driven by increased hydrostatic pressure in the inter-ventricular capillaries of the lung

79
Q

What are the main causes of a transudative pleural effusion?

A

HF

nephrotic syndrome

hepatic cirrhosis

80
Q

What are the main causes of a exudate in a pleural effusion, which is marked by increased protein content?

A

typically things that increase vascular permeability such as malignancy, pneumonia, collagen vascular disease, or trauma

81
Q

What pt. population is typical for a spontaneous pneumothorax?

A

tall, thin, young males

82
Q

What are the main categories of pneumonia?

A
  • lobar
  • bronchopneumonia
  • interstitial (atypical)
83
Q

What are the most common causes of lobar pneumonia?

A
  • S pneumo (most common)
  • Legionella, Klebsiella
84
Q

S. pneumo is _____-hemolytic

A

alpha

85
Q

What is ‘alpha’ hemolysis?

A

partial hemolysis in which the surrounding zone if hemolysis has a green hue from oxidation of hemoglobin

86
Q

What is the major virulence factor of strep pneumo?

A

a polysaccharide capsule

87
Q

Is Strep pneumo Optochin resistant or sensitive?

A

sensitive

88
Q

How does strep pneumo appear?

A

lancet-shaped gram-positive diplococci

89
Q

How does strep pneumo lobar pneumonia present?

A

production of a rust-colored sputum

90
Q

What else does strep pneumo very commonly cause besides pneumonia?

A

MOPS

Meningitis

Otitis Media

Pneumonia

Sinusitis

91
Q

What other virulence determinant does Strep pneumo use?

A

IgA protease

92
Q

Who has a particularly increased risk of infection with strep pneumo?

A

those with no spleen (SCD, trauma, etc.)

93
Q

How should Strep pneumo be treated?

A

Azithromycin, a macrolide

Ceftriaxone, or other 3rd-gen cephalosporin

94
Q

What are the main causes of bronchopneumonia?

A

S. pneumo

S. aureus

H. influenzae

Klebsiella

95
Q

What are the most common causes of Interstitial (atypical) pneumonia?

A

viruses (influenza, CMV, RSV, adenovirus),

Mycoplasma

Legionella

Chlamydia

96
Q

What is a pancoast tumor?

A

a carcinoma that occurs in the apex of the lung

NOTE: Most Pancoast tumors are squamous cell carcinomas (SCCs) or adenocarcinomas; only 3-5% are small cell carcinomas.

97
Q

How might a pancoast tumor?

A

may cause dyspnea, nonproductive cough, etc.

  • voice hoarseness
  • Pancoast syndrome
  • Horner Syndrome
  • SVC syndrome
98
Q

Why would a pancoast tumor cause voice hoarseness?

A

The tumour can also compress the recurrent laryngeal nerve and from this a hoarsevoice and bovine cough may occur

99
Q

What is Pancoast syndrome?

A

Pancoast syndrome is characterized by a malignant neoplasm of the superior sulcus of the lung with destructive lesions of the thoracic inlet and involvement of the brachial plexus and cervical sympathetic nerves (stellate ganglion). This is accompanied by the following:

Severe pain in the shoulder region radiating toward the axilla and scapula along the ulnar aspect of the muscles of the hand

Atrophy of hand and arm muscles

Horner syndrome ( ptosis, miosis, hemianhidrosis, enophthalmos)

Compression of the blood vessels with edema

100
Q

Pancoast tumor presentation

A

-referred pain over the scapula to the shoulder as the result of damage to the afferent pain fibers of the sympathetic trunk.

Initially, localized pain occurs in the shoulder and vertebral border of the scapula. Pain may later extend along an ulnar nerve distribution of the arm to the elbow and, ultimately, to the ulnar surface of the forearm and to the small and ring fingers of the hand (C8).

If the tumor extends to the sympathetic chain and stellate ganglion, Horner syndrome and anhidrosis develop on the ipsilateral side of the face and upper extremity.

The pain is frequently relentless and unremitting, and adequate relief often requires administration of narcotics. The patient usually supports the elbow of the affected arm in the hand of the opposite upper extremity to ease the tension on the shoulder and upper arm.

The hand muscles may become weak and atrophic, and the triceps reflex may be absent.

101
Q

What is Horner syndrome?

A

It is characterized by miosis (a constricted pupil), ptosis (a weak, droopy eyelid), apparent anhidrosis (decreased sweating), with or without enophthalmos (inset eyeball).

102
Q

What is SVC syndrome?

A

Compression of the SVC, typically due to malignancy, that blocks drainage from the head leading to:

edema (swelling due to excess fluid) of the face and arms and development of swollen collateral veins on the front of the chest wall.

blanching of skin after fingertip pressure

Shortness of breath and coughing are quite common symptoms.

103
Q

What is this?

A

Psamomma body

104
Q

What are some diseases associated with psamomma bodies?

A

Papillary thyroid carcinoma

Papillary renal cell carcinoma

Micropapillary subtype of lung adenocarcinoma

Ovarian papillary serous cystadenoma and cystadenocarcinoma

Endometrial adenocarcinomas (Papillary serous carcinoma ~3%-4%)

Meningiomas, in the central nervous system

Peritoneal and Pleural Mesothelioma

Somatostatinoma (pancreas)

Prolactinoma of the pituitary

105
Q

Where does lung cancer like to MET to?

A

BABeL

Brain

Adrenals

Bone (can lead to pathological fracture)

Liver

106
Q

What cancers like to MET to the lungs?

A

Everywhere fluid comes out of:

Breast

Colon

Prostate

Bladder

107
Q

What are the five main types of lung cancer?

A
  • small cell (oat cell) carcinoma
  • adenocarcinoma
  • squamous cell carcinoma
  • large cell carcinoma
  • bronchial carcinoid tumor
108
Q

What lung cancers can consistently be found centrally in the lungs?

A

small cell and squamous cell

109
Q

Describe small cell carcinomas

A

these are undifferentiated and very aggressive.

110
Q

What are some associations of small cell carcinomas?

A
  • may produce ACTH (Cushing Syndrome)
  • SIADH
  • Lambert-Eaton Syndrome
  • paraneoplastic myelitis/encephalitis
111
Q

How might SIADH present?

A

hyponatremia leading to brain swelling and

concentrated urine

112
Q

What is Lambert-Eaton Syndrome?

A

A rare presynaptic disorder of neuromuscular transmission in which quantal release of acetylcholine (ACh) is impaired due to binding of Abs to Ca2+ channels

113
Q

How does Lambert-Eaton syndrome present?

A

Symptoms of Lambert-Eaton myasthenic syndrome (LEMS) usually begin insidiously and progress slowly. Many patients have symptoms for months or years before the diagnosis is made. Weakness is the major symptom. Weak muscles may ache and are occasionally tender. Proximal muscles are more affected than distal muscles; lower extremity muscles are affected predominantly.

Patients typically have difficulty rising from a chair, climbing stairs, and walking.

114
Q

Amplification of the ____ proto-oncogene is commonly seen in a small cell carcinoma

A

MYC

115
Q

How does a small cell carcinoma look histologically?

A

Kulchitsky cells (small dark blue cells) common

116
Q

What stains can be used to diagnose small cell carcinoma?

A

chromogranin A

117
Q

Histologically, squamous cell carcinomas of the lung are marked by what?

A

keratin swirls and intercellular bridges

118
Q

SSC of the lung typically is seen at bronchi bifurcations

A
119
Q

What is one common manifestation of SCC of the lung?

A

hypercalcemia due to secretion of PTHrP

120
Q

What cancers of the lung are commonly found in the periphery?

A

adenocarcinoma and large cell carcinoma

121
Q

What mutations are common in adenocarcinomas?

A

activating mutations in KRAS, EGFR, and ALK

122
Q

What is the main paraneoplastic syndrome of adenocarcinoma?

A

hypertrophic osteoarthropathy (clubbing)

STEP 1 (1) (28 decks)

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