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Respiratory Pathology 1 Flashcards

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USMLE® Step 1 flashcards
1
Q

what is the function of meatus?

A

meatus connects sinuses to nasal cavities

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2
Q

which meatus drains sphenoid and posterior ethmoid ?

A

superior meatus

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3
Q

what drains inferior meatus?

A

nasolacrimal duct

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4
Q

what is mnemonic SSPIN for?

A

superior meatus drains sphenoid and posterior ethmoid, inferior drains nasolacrimal duct

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5
Q

what does middle meatus drain ?

A

Frontal, maxillary and anterior ethmoid

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6
Q

what is the result of meatus obstruction?

A

secretion build up and inflammation and pain over affected area.

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7
Q

which sinuses are typically affected in rhino-sinusitis and what is the reason of it?

A

Maxillary. it has superior medial ostium and during obstruction drainage of this sinus is particularly impossible.

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8
Q

what is the most common cause of rhinosinusitis?

A

viral - rhinovirus, may lead to superimposed bacterial infection

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9
Q

what are the most common bacterial causes of rhinosinusitis and what are they also known for?

A
  1. streptococcus pneumoniae
  2. haemophilus influenzae
  3. moraxella catarrhalis

also known for causes of otitis media

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10
Q

what are fungal causes of rhinosinusitis and in which patients?

A

Aspergillus and Mucormycosis in immunocompromised patients

diabetes, neutropenia secondary to chemotherapy

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11
Q

which diseases are predisposing for rhinosinusitis?

A

CF, primary ciliar dyskinesia, granulomatosis polyangiitis

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12
Q

how does patient with chronic sinusitis present?

A

facial pain,
nasal congestion/ rhinorrhea,
+/- fever

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13
Q

how does patient with rhinosinusitis caused by mucormycosis looks like?

A

dark red necrotic ulcers in very ill patient

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14
Q

what are complications of rhinosinusits?

A
  1. extend to the orbits and cause orbital cellulitis
  2. spread along facial veins to the cavernous sinus and cause cavernous sinus thrombosis
  3. extend to the brain and cause meningitis
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15
Q

what is epistaxis?

A

AKA - nose bleed

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16
Q

what makes kiesselbach plexus??

A
  1. anterior and posterior ethmoid artery
  2. 2nd branch of superior labial artery
  3. great palatin artery
  4. branch of sphenopalatin artery (maxillary art branch)
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17
Q

where does nose bleed occur most commonly

A

in anterior segment of nostrils ( kiesselbach plexus)

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18
Q

where does life threatening hemorrhage occur during nose bleeding and which pateints are predisposed to it?

A

in posterior segment of sphenopalatine artery.

it is lifethreatening esp. in pts with coagulopathies or pts on warfarin (anticoagulants)

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19
Q

what are common causes of epistaxis?

A
  1. foreign body
  2. trauma
  3. allergic rhinitis
  4. nasal angiofibromas
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20
Q

which cause of epistaxis is common in adolescent males?

A

nasal angiofibromas

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21
Q

what cell type lines URT and UGT?

A

mostly squamous cell type

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22
Q

what type of cancers are mostly in head and neck?

A

squamous cell carcinoma

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23
Q

what are the risk factors of head and neck cancers?

A
  1. tobacco
  2. alcohol
  3. HPV 16
  4. EBV
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24
Q

which cancer is predisposed by HPV-16 in head and neck?

A

oropharyngeal squamous cell carcinoma

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25
Q

which cancer is predisposed by EBV in head and neck?

A

nasopharyngeal carcinoma

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26
Q

what is field cancerization?

A

carcinogens damage wide mucosal area that causes multiple tumors in that area to develop independently.

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27
Q

what is deep venous thrombosis?

A

it is thrombotic clot in deep veins of lower extremities such as iliac, popliteal and superficial femoral veins.

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28
Q

predisposion of DVT

A

Virchows’ triad : venous stasis, hyper coagulability and endothelial damage.

other words : inappropriate activation of coagulation cascade (vs arteries - atherosclerosis)

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29
Q

what are the risk factors of DVT caused by stasis?

A

immobility caused by
1. post-operative, long travel/flight
2. paralysis (Guilian barre)
trauma ortho (femoral fracture - also endothelial)
3. chronic venous insufficiency - varicose veins
4. CVI (cortical visual impairment)

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30
Q

what are the risk factors of DVT caused by endothelial damage

A

exposed collagen triggers clotting cascade

  1. trauma
  2. surgery
  3. smoking
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31
Q

what are the risk factors of DVT caused by hyper coagulability? ?

A
  1. malignancy
  2. sepsis
  3. genetic
  4. nephrotic syndrome
  5. high estrogen (pregnancy/OCP)
  6. autoimmune
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32
Q

what are the genetic risk factors of DVT?

A

factor V leiden, antithrombin deficiency

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33
Q

which nephrotic syndrome is most commonly associated with hyper coagulable state and what mc is its outcome?

A

membranous nephropathy and renal venous thrombosis

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34
Q

why is pregnancy risk of venostasis?

A

gravity of uterus compresses iliac vein and causes stasis of blood

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35
Q

what is the clinical representation of patient with DVT ?

A

pts unilateral, painful, red, not swollen extremity

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36
Q

what are the differentials of DVT?

A

cellulitis and popliteal baker’s cyst (arthritis of the knee and rheumatoid arthritis)

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37
Q

what test is used for ruling our DVT in low -to moderate risk patients ?

A

d-dimer lab test (high sensitivity low specificity)

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38
Q

how isDVT diagnosed?

A

compression ultrasound with doppler .

compress ultrasound on normal veins they are easily compressible if there is no clot.

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39
Q

what is the prophylaxis and acute managment of DVT ?

A

Unfractionated heparin or low-molecular weight heparin (enoxaparin ) for

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40
Q

what is used for treatment and long term prevention of DVT?

A

oral anticoagulants (rivaroxaban, apixaban)

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41
Q

why do we use for treatment of DVT firstly UFH/LMWH and then warfarin? what is time in between?

A

cause ewarfarin inhibits synthesis as procoagulants (factor 2, 7, 9, 10) as well as anticoagulants (protein C and S). half life of anticoagulants are short so firslty for short time when pt starts treatment with warfarin body is in hypercoagulable state .
use heparin with warfarin for 3-5 day but if you really need to know check PT and INR ( it should be 2-3 before stoping heparin)

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42
Q

what are DVT complication/ why we need to treat DVT?

A

pulmonary emboli (life threatening)

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43
Q

what is venous thromboembolism (VTE)?

A

risk factors for Pulmonary embolism (PE) and DVT are same so they are often coupled and called together VTE

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44
Q

what are causes of pulmonary emboli ?

A 
Fat
Air
Thrombus
Bacteria
Amnionic fluid
Tumor
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45
Q

what are fat emboli related to?

A
  1. long bone fractures
  2. surgery (orthopedic procedures)
  3. liposuction
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46
Q

what is pathophysiology of fat emboli ?

A
  1. small fat particles leak in venous system
  2. fat is hydroxylated by lipoprotein lypase to FFA
    3/ FFA damage endothelium
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47
Q

what is the most common manifestation of fat emboli?

A

FFA damage lung endothelium and cause Acute respiratory distress syndrome (dyspnea and hypoxemia)

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48
Q

what are common sites and results of fat emboli?

A
  1. lung - ARDS - hypoxemia
  2. skin - petechial rash
  3. neuro-vesseles - neurologic/cognitive deficits’
    classic triad and also,
  4. blood cells - anemia, thrombocytopenia
  5. renal failure
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49
Q

how does fat emboli reach from venous system to systemic circulation?

A

25 % of population has patent foramen ovale.

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50
Q

in which stain appears fat white ?

A

HE, cause alcohol dissolve fat

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51
Q

what are air emboli related to?

A
  1. surgical procedurs
  2. decompression syndrome - caisson’s disease - nitrogen bubbles
  3. iatrogenic causes
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52
Q

which surgical procedures are most common cause of air emboli and why?

A
  1. neurosurgery cause patient hat sitting position and pressure in brain vessels is negative , sucks the air from surrounding
  2. laparoscopic surgery insufflation cavities with gas
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53
Q

what are iatrogenic causes of air emboli?

A
  1. mechanical ventilation

2. central line

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54
Q

what is presentation of patient if air gets in venous system?

A

mc pulmonary circulation obstruction that causes hypoxia, sudden hypotension and distended jugular veins

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55
Q

what is presentation of patient if air gets in systemic circulation?

A
  1. shock
  2. MI
  3. renal failure
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56
Q

what is the tx of air emboli in RV ?

A

we place pt in left decubitus position with the head down, it trapes emboli at the apex of the RV, which moves away from pulmonary outflow and the place central line to aspirate embolus

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57
Q

what is the most common source of septic emboli?

A

bacterial infection - endocarditis

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58
Q

how to treat decompression disease?

A

hyperbaric O2

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59
Q

what are the causes of amnionic fluid emboli ?

A

disruption of amnionic membrane : labor or uterine trauma

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60
Q

what causes fetus cells in maternal ciruclation?

A
  1. inflammatory cascade - anaphylactoid reaction - cardiac-respiratory collapse - hypotension, shortness of breath
  2. systemic reaction -activation of clotting cascade - DIC -
    - 1st thrombosis 2nd bleeding
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61
Q

what are the risk factors of amnionic fluid emboli?

A
  1. always peripartum
    2.maternal age > 30
  2. multiparity
  3. trauma (placental abruption)
    (waek amnionic membrane)
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62
Q

what is the diagnosis of DIC?

A

schistocytes and helmet cells

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63
Q

what is dx tool for amniotic fluid emboli?

A

autopsy - fetal squamous cells with in the mother’s pulmonary circulation.

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64
Q

what is the MC site of thrombus in PE?

A

proximal illiofemoral vein

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65
Q

what are the risk factors of Pulmonary thromboemboli?

A

virchow’s triad

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66
Q

what is the pathophysiology of Pulmonary thromboemboli?

A

V/Q mismatch, effected portion dead space- hypoxemia - chemo r - hyperventilation - blown up CO2- respiratory alkalosis. meanwhile hypoxemia causes vasoconstriction of vessels (shunt) - massive vasoconstriction will lead to RV failure - hypotension (syncope) and shock.

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67
Q

how is massive emboli obstruction of main pulmonary trunk called?

A

saddle embolism

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68
Q

what do we call the type of shock caused by pulmonary emboli?

A

obstructive shock

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69
Q

what kind of infarction happens in lungs?

A

pulmonary infarction is very rare cause of collaterals, but if it happens it is haemorrhagic and will cause hemoptisis and pleuritic chest pain that worsens with inspiration

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70
Q

what is the clinical representation of pt with PE?

A

1) dispnea
2. +/- chest pain, hemoptisis, syncope
3) hypoxemia, tachypnea not corrected with O2
4. hypotension
5) respiratory alkalosis
6. JVD

) always

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71
Q

how is PE dx made?

A
  1. CT pulmonary angiogram

2. ECG

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72
Q

what do we see in ECG of PE patient?

A
  1. sinus tachycardia always

2. sometimes characteristic S1Q3T3 (S in lead 1, Q wave in lead 3 and inverted T in lead 3)

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73
Q

how to tell in autopsy if thrombus was formed before or after death?

A

lines of zahn - interdigitating areas of pink (platelets, fibrin) and red (RBC) - pt died because of PE.

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74
Q

how is mediastinum devided?

A

by imaginary line from sternum angle to T4.
UP - superior mediastinum
down - inferior mediastinum.

inferior mediastinum is further divided into anterior, middle (heart and pericardium) and posterior mediastinum.

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75
Q

what can go wrong in mediastinum?

A
  1. masses
  2. inflammation
  3. gases
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76
Q

recall anterior mediastinal masses

A
  1. thymic neoplasms - myasthenia gravis
  2. thyroid mass (substernal goiter)
  3. teratoma
  4. terrible lymphoma
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77
Q

recall middle mediastinal massses

A

bronchogenic cyst
esophageal carcinoma
metastases
hiatal hernia

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78
Q

recall posterior mediastinal masses

A

vertebral - neurogenic tumor (neurofibroma), multiple myeloma

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79
Q

what is the causes of mediastinitis?

A
  1. cardiothoracic procedure
  2. esophageal perforation
  3. nearby infection
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80
Q

what is the most common cause of medaistinitis?

A

postoperative complications due to coronary artery by pass - appears < 14 days

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81
Q

what is boerhaare syndrome?

A

esophageal perforation

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82
Q

what nearby infections may cause mediastinits and which bugs are common cause of this infections?

A

dental and retropharyngeal abscess infiltrates.

gram + cocci

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83
Q

what is the clinical presentation of mediastinits?

A

fever, tachycardia, tachypnea, lukocytosis and sternal wound dranaige if opstoperative

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84
Q

what is characteristic of chronical mediastinitis?

A

it happens more gradually and will cause fibrosis. AKA fibrosing mediastinitis

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85
Q

to which infection is classically linked fibrosing mediastinitis?

A

fungal infection - histoplasmosis

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86
Q

what are causes of fibrosing mediastinitis?

A
  1. histoplasmosis
  2. TB
  3. radiation therapy
  4. inflammation disease such as sarcoidosis and behcet disease
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87
Q

what are causes of pneumomediastinum?

A

spontaneous - pulmonary bleb rupture and 2ndary to

  1. iatrogenic
  2. trauma
  3. esophageal perforation
88
Q

what is pulmonary bleb?

A

Pulmonary blebs are small subpleural thin walled air containing spaces congenital.

89
Q

what is clinical presentation of pt with pneumomediastinum?

A

chest pan,
dyspnea,
voice change
subcutaneous empysema

90
Q

how is crepitus on cardiac auscultation called otherwise and when do we hear it?

A

Hamman’s sign in

spontaneous mediastinal emphysema

91
Q

what happens to flow -volume parameters and loop in obstructive lung disease?

A

both FEV1 and FVC both decrease but FEV1 decreses proportionally more so ratio is also decreased. lung volumes : RV, TLC, FRC are all increased.
loop shifts to the left

92
Q

what happens to flow -volume parameters and loop in restrictive lung disease?

A

both FEV1 and FVC decrease but ratio remains normal or lightly increased.
lung volumes all decrease : RV, TLC< FRC.
loop shifts tot he right

93
Q

what is normal FEV1/FVC ratio and what does that mean?

A

FEV1/FVC = 80%, this means that in 1s forcely blown out air will be 80% of total air we can exhale

94
Q

what parameters does spirometry measure?

A

Vital capacity (VC), Forced vital capacity (FVC), Forced expiratory volume (FEV).

we ask pt to inhale as much as possible and exhale as much as possible (FVC). FEV1 is similar but in 1 s (75-80% is normal)

95
Q

what is hallmark of obstructive disease?

A

low fev1/fvc ratio

96
Q

what does v/q mismatch cause?

A

hypoxia - vasoconstriction - chronic HTN in pulmonary circulation - cor pulmonale - RHF.

this pts are chronically hypercarbic - ventilate poorly which causes chronic respiratory acidosis that leads to compensatory chronic metabolic alkalosis

97
Q

what disease are united in obstructive lung disease?

A
  1. COPD (emphysema and chronic bronchitis)
  2. asthma
  3. bronchiectasis
98
Q

what do we call patients with chronic bronchitis?

A

blue bloaters; cyanosis from shunting (blue) air trapping (bloater)

99
Q

what is hallmark of chronic bronchitis?

A

hypertrophy of mucous gland and high Reid index. DLCO normal.

100
Q

what is Reid index and what parameter is pathologic?

A

Reid index is diagnostic criteria of chronic bronchitis. it is the ratio of gland layer/total bronchial wall thickness. >50 % is pathognomic for chr bronchitis. can be detected in autopsy

101
Q

what is presentation of pt with chronic bronchitis?

A
  1. cough, wheezing, crackles, cyanosis (shunting), dyspnea

2. RHF, CO2 retention, 2ndary polycythemia

102
Q

what are diagnostic criteria for chronic bronchitis?

A

productive cough (sputum) for more than 3 months in a year for more that 2 consecutive years. no other causes of cough present , strongly ass with smoking.

103
Q

what causes emphysema?

A

imbalance between proteases and anti proteases causes alveolar tissue destruction
high proteases level in smoking emphysema, low anti proteases in alpha1 def.

104
Q

how do we call patients with emphysema and why ?

A

pink puffer;
loss of alveoli, loss of surface area for O2 absorption (dead space), hyperventilation to compensate (puffer) initially maintains O2 level (pink)

105
Q

which type of emphysema is caused by smoking tobacco?

A

centriacinar upper lobes

106
Q

how does smoke destruct alveolar tissue?

A

smoke activated macrophages that recruit neutrophils , which than release proteases.

107
Q

what happens to lung recoil, compliance and DLCO and blood volume in capillaries in emphysema ?

A

decreased recoil which causes small airway collapse during exhalation and high compliance, DLCO is decreased from destruction of alveolar walls and blood volume also decreased.

108
Q

what is hallmark and clinical presentation of emphysema?

A

barrel chested pt breathing with pursed lips (to increase airway pressure and prevent airway collapse).

dyspnea, cough (less sputum then in chronic bronchitis), hyperventilation - weight loss, decreased breath sounds, tachycardia, hypoxemia, cor pulmonale, right heart failure.

109
Q

what is acinus?

A

bronchiole plus alvoli

110
Q

what are morphologic types of emphysema?

A
  1. panacinar emphysema - lower lobes - alpha 1 antitrypsin

2. centriacinar emphysema - upper lobes - smoking

111
Q

what are histological findings in emphysema?

A

thin septae and large airways. if smokers lung - black spots/ dirty holes

112
Q

what does alpha 1 antitrypsin do?

A

inhibits neutrophil elastase, so its deficiency will cause more breakdown of elastin in lungs.

113
Q

what is clinical presentation of pt with alpha 1 antitrypsin deficiecy?

A

typical COPD (cough, sputum, wheeze) but young (<40) pt + liver problems + lung problems, unexplained emphysema and abnormal liver function tests

114
Q

why does alpha 1 antitrypsin def causes liver damage?

A

abnormal alpha1 builds up in liver and only occurs in phenotypes with pathologic polymerization.

115
Q

what alpha 1 def patients must never do?

A

smoke

116
Q

what are diagnostic criteria for emphysema?

A

cxr: high AP diameter, flattened diaphragm, high lung field lucency.

117
Q

what is asthma

A

asthma is reversible bronchoconstriction caused by bronchiole hypersensitivity

118
Q

in which population is asthma c

A

children

119
Q

what is asthma associated with ?

A

other T1HS/ allergic reactions like allergic rhinitis, eczema

120
Q

what may trigger asthma?

A

URI, allergens (animal dander, dust mites, mold, pollen) ,stress, exercise, cold, aspirin

121
Q

what are classical findings in asthma?

A

smooth muscle hypertrophy and hyperplasia, curshman spirals, charcot-leyden crystals, DLCO normal r high

122
Q

what are curshman spirals?

A

shed of epithelium that forms whorled usous plugs

123
Q

what are charcot-leyden crystals?

A

eosinophilic, hexagonal, double-pointed crystals formed from breakdown of eosinophils in sputum.

124
Q

what role do eosinophils have in asthma?

A

eosinophils release major basic protein that causes epithelial damage and bronchospasm in asthma.

125
Q

what do we see in allergic asthma ?

A

we can see Th2 cytokines: IL4, IL5, IL10, IL13

126
Q

what is clinical representation of asthmatic patient?

A

episodic cough at night, wheezing dyspnea, tachypnea, hypoxia, decreased inspiratory/expiratory ratio, decreased peak flow pulsus paradoxus

127
Q

what is pulsus paradoxus?

A

systolic BP decreases by 10 mm Hg during inspiration, seen in asthma, pericardial fusion, tamponade

128
Q

what is normal ratio of inspiration/expiration and what happens if pt has asthma?

A

normal is 1/2, in asthmatic patients because of prolonged expiratory phase it becomes 1/4 or even 1/5

129
Q

what does peak flow show?

A

highest velocity of airflow patient can create

130
Q

what is rare but life-threatening complication of asthma?

A

status asthmaticus - death

131
Q

how we dx asthma?

A
  1. 1st spirometry (generalized obstructive pattern)

2. 2nd metacholine challenge to induce exacerbated of asthma

132
Q

what is metacholine test and how do we do it?

A

metacholine is muscarinic agonist, it causes bronchoconstriction. we should administer increasing amounts of nebulized drug and check with spirometry each dose. look for dose at which FEV1 falls significantly, if dose is low positive test.

133
Q

what is AERD?

A

aspirin/nsaid exarcerbated respiratoy disease

134
Q

how does aspirin exacerbate asthma attack?

A

in this patient there is dysregulation of arachidonic acid metabolism, aspirin inhibits cox and causes overproduction of leukotriens that induces airway constriction.

135
Q

what is commonly associated pathology with AERD?

A

nasal polyps and chronic rhinosinusitis

136
Q

what is treatment of AERD?

A

leukotrien r antagonist (for overporducted leukotriens) - Montelukast and Zafirlukast

137
Q

what is bronchiectasis?

A

chronic inlammation or necrotizing infection of bronchi or obstruction will cause irreversible dilation of large airways, the small and medium airways are characterized by airflow obstruction predominantly arising from thickening of the bronchial wall

138
Q

what are the causes of bronchiectasis ?

A
  1. necrotizing infections with bugs like Klebsiella and staph.
  2. bronchial obstruction (tumor)
  3. decreased ciliar motility (Kartagener syndrome, ICF, smoking, cystic fibrosis, allergic bronchipulmonary aspergillosis)
139
Q

what is clinical presentation of bronchiectasis?

A
  1. cough with excessive purulent sputum (foul smelling)
  2. infections
  3. hemoptysis
  4. cor pulmonale
  5. digital clubbing
  6. amyloidosis
140
Q

what is primary ciliary dyskinesia?

A

AKA immotile-cilia syndrome is inherited (autosomal recessive) mutation of motor protein dynein structure/function that causes cilia unable to beat normally.

141
Q

what is kartagener’s syndrome and how it manifests?

A

one of the ciliary disorders; chronic sinusitis, bronchiectasis (chronic cough, recurrent infections), male infertility, situs inversus

142
Q

what is classic case of kartagener’s syndrome?

A

child with recurrent sinus/ear infections, chronic cough, bronchiectasis on chestCT, obstruction on PFTs and situs inversus

143
Q

what is ABPA?

A

AKA allergic bronchopulmonary aspergillosis is a hypersensitivity (allergic) reaction to aspergillus (which is low virulence fungus and infects only immunocomropmised or debilitated lungs)

144
Q

in which patients does ABPA present predominnatly?

A

in Asthma and CF patients

145
Q

what findings do we have in ABPA patients

A
  1. increases Th2 Cd4+ cells
  2. synthesis interleukins
  3. eosinophilia
  4. IgE antibody production
146
Q

what is classical case scenario in ABPA

A
  1. asthma or CF patient
  2. recurrent episodes cough, fever, malaise
  3. brownish mucus plugs, hemoptysis
  4. peripheral blood eosinophilia
  5. high IgE level
  6. bronchiectasis on imaging
  7. PFTs with obstruction
147
Q

how we Dx and Tx ABPA?

A

skin testing aspergillosis and steroids

148
Q

what is the hallmark of restrictive lung disease?

A

normal or high FEV1/FVC ratio, decrease lung volumes, patient presents with short, shallow breaths

149
Q

what are two group of causes of restrictive lung disease?

A
  1. poor breathing mechanisms

2. interstitial lung disease

150
Q

what are extra pulmonary causes of restrictive lung disease?

A
  1. poor muscular effort - neuromuscular disorders - polio, myasthenia gravis, guillain barre syndrome
  2. poor structural apparatus - scoliosis, morbid obesity
151
Q

how we distinguish interstitial lung disease vs poor breathing mechanism?

A

in poor breathing mechanism there is normal DLCO and normal A-a gradient

152
Q

what are interstitial lung diseases?

A

AKA diffuse parenchymal lung diseases , group of diseases with similar clinical, radiologic, pathologic manifestation that cause inflammation/fibrosis of lung interstitium and decrease lungs ability to inflate fully, cant get air in lung

153
Q

recall interstitial lung diseases list

A
  1. idiopathic pulmonary disease
  2. systemic diseases
  3. pneumoconiosis
  4. drug toxicities
  5. hypersensitivity reactions
  6. pulmonary langerhans cell histiocytosis (eosinophilic granuloma)
154
Q

which systemic diseases cause interstitial lung disease?

A
  1. RA
  2. scleroderma
  3. goodpasture’s disease
  4. wegeners granulomatosis
  5. sarcoidosis
155
Q

how do we measure diffusion capacity?

A 
with CO which is diffusion limited gas (vs NO, O2) .
1. patient inhale small amount of CO
2.machine measures CO exhaled
3. normal =75-140%
sever disease <40%
156
Q

what does DLCO measure?

A

diffusion capacity of CO , measures ability of lungs to transfer gas to RBCs

157
Q

what causes decrease of DLCO?

A
  1. interstitial lung diseases
  2. emphysema
  3. abnormal vasculature : Pulmonary hypertension, pulmonary embolism
  4. prior lung resection
  5. anemia - corrects when adjusted by Hb level.
158
Q

what is classical radiologic presentation of interstitial lung disease?

A
  1. bilateral diffuse pattern
  2. small irregular opacities (reticulonodular)
  3. honeycomb lung appearance
159
Q

what is the most common interstitial lung disease?

A

idiopathic pulmonary fibrosis

160
Q

what is IPF?

A

repeated cycles of lung injury and wound healing that leads to slow onset dyspnea collagen deposition and honeycomb lung appearance, tractional bronchiectasis and digital clubbing.

161
Q

in which population is classic IPF?

A

older adults > 40 y

162
Q

what is hypersensitivity pneumonitis?

A

it is mixed type III/IV hypersensitivity reaction to environment antigen most commonly :

  1. agricultural dust
  2. microorganisms (fungal,bacterial or protozoa) actinomyces, aspergillus
  3. chemicals
163
Q

what is difference between asthma and hypersensitivity pneumonitis?

A

asthma is T1Hs, and also pathology is in bronchioles not in alveoli

164
Q

what is presentation of hypersensitivity pneumonitis?

A

dyspnea, cough, chest tightness, fever, headache

165
Q

what is classical population in Hypersensitivity pneumonitis?

A
  1. Farmers Lung (moldy hay, grain exposure)

2. bird/poultry handler (proteins in bird droopings -dried - dust)

166
Q

what is classical case in Hypersensitivity pneumonitis

A

farmer or bird handler with dyspnea, cough and chest tightness, diffuse crackles symptoms come out in 4-6 h after exposure , Xray may look like atypical pneumonia or interstitial lung disease

167
Q

how do we dx Hypersensitivity pneumonitis?

A
  1. bronchioalveolar lavage
  2. inhalation challange
  3. lung biopsy
168
Q

what is tx for Hypersensitivity pneumonitis?

A
  1. avoid exposures (early stage reversible)

2. may use steroids

169
Q

what is sarcoidosis?

A

noncaseating granulomatous disease

170
Q

how does noncaseating granuloma on histology looks like?

A

tightly packed central area of macrophages, epitheloid cells, multinucleated giant cells, surrounded by lymphocytes, monocytes, mast cells, fibroblasts

171
Q

what is pathology of sarcoidosis

A

it is cell mediated immune process characterized by high CD4:CD8 ratio, key players : CD4, IL2, IFNy. accumulation of TH1 Cd4+ cells that secrete IL2 and interferon y. Il2 stimulates Th1 proliferation, while IFNy activates macrophages that ultimately leads to granuloma formation

172
Q

what is characteristic finding in sarcoidosis?

A
  1. schaumann body (calcium and protein collection in giant cells)
  2. asteroid body (lipid + calcium in giant cells)
  3. high ACE level (ACH is produced in lung)
  4. hypercalcemia
  5. low PTH
173
Q

what leads to hypercalcemia in sarcoidosis?

A

elevated 1-alpha hydroxylase activity in alveolar macrophages that increases Vitam D levels ( it converted 25-OH VitD to active form 1,25 Oh2 VitD)

174
Q

what organs are involved in sarcoidosis?

A
  1. lungs most common
  2. skin
  3. eye
  4. heart
  5. renal
  6. CNS
    any system can be involved
175
Q

what is classical finding on CXRay of patient with sarcoidosis?

A

bilateral hilar lymphadenopathy and coarse reticular opacities

176
Q

what is cardiac involvement in sarcoidosis?

A

conduction disease (heart block), cardiomyophathy

177
Q

renal involvement in sarcoidosis may lead to?

A

renal fialure

178
Q

what is characteristic neural involvement in sarcoidosis?

A

bells palsy, neurosarcoid, motor loss

179
Q

what is classic lesion in sarcoidosis?

A
  1. erythema nodosum, inflammation of fat cells under skin that leads to tender red nodules and is usually manifested on both shins
  2. lupus pernio - skin lesions on face resembling lupus
180
Q

what is consequence of eye involvement in sarcoidosis?

A

uveitis (may be anterior (iris, ciliary), posterior (choroid)) ,it has often mild symptoms such as dry eye and blurry vision so is often detected on routine exam

181
Q

what is classical presentation of patient with sarcoidosis?

A

african american female, with lymphadenopathy, cough, dyspena and who is often asymptomatic and may be detected n routine chest xray

182
Q

what is treatment of sarcoidosis?

A
  1. steroids

2. other immunosuppressants : methotrexate, azathioprine, mycophenolate

183
Q

what is inhalation injury?

A

complication of inhalation of noxious stimuli, mc - smoke consequence of fire

184
Q

what are 3 potential mechanisms of injury in inhalation injury?

A
  1. burn of respiratory tract (hot)
  2. particles called soot (carbon) can obstruct respiratory tract and cause asphyxiation, ards (inflammation/edema), good environment for bugs so pneumonia as well
  3. noxious gases
185
Q

which noxious gases can be inhaled in inhalation injury?

A
  1. CO and CN
  2. if plastic and rubber are burn chemicals like NH3
  3. also common industry gas ATO (arsenic trioxide)
186
Q

what are signs to suspect inhalation injury?

A
  1. facial burns
  2. singed nasal hairs
  3. oropharyngeal soot
  4. hypoxemia as well
  5. hoarseness of voice that may mean vocal cords burn
187
Q

what we do if we suspect inhalation injury?

A

bronchoscopy
1. there may not be aiway soot or edema cause it takes while to develop (18 h after injury)
2. if there is edema we should prevent obstruction and do tracheal intubation as soon as possible
resolution at 11 days after injury)

188
Q

what means if patient after fire has headache and altered mental status?

A

CO posoning or CN poisoning

189
Q

what appears postpartum on Co injured patient?

A

cherry red skin

190
Q

what shall we do in CO poisoning?

A

give 100% O2 and measure carboxyhemoglobin

191
Q

how CN causes AMS and headache?

A

it inhibits cytochrome oxidase in complex 4 transport chain

192
Q

what are pneumoconioses?

A

broad group of lung diseases caused by exposure to coal, silica, asbestos

193
Q

which diseases are united in pneumoconiosis?

A
  1. asbestosis
  2. berylliosis
  3. coal worker’s pneumoconiosis
  4. silicosis
194
Q

what is berylliosis?

A

pneumoconiosis associated with exposure to beryllium in aerospace and manufacturing industries (NASA)

195
Q

what are characteristics of berylliosis?

A
  1. granulomatous (nonceaseating),
  2. high risk of cancer and cor pulmonale,
  3. affects upper lobes,
  4. occasionally responsive to steroids
196
Q

what is coal workers pnuemoconiosis?

A

AKA black lung disease , prolonged exposure to coal dust leads to inflammation and fibrosis of upper lobes, and macrophages full of coal - i

197
Q

what is anthracosis?

A

asymptomatic coal workers pneumoconiosis in patients who live in cities and have chronic exposure to sooty polluted air

198
Q

what is characteristic finding in black lung disease?

A

small rounded nodular opacities

199
Q

for what do patient with coal workers pneumoconiosis have increased risk?

A

Caplan syndrome : RA+ pneumoconiosis+ intraparenchymal nodules

200
Q

where is silica found?

A

in rock particles : qaurtz , granate, sandstone (beach-wind, sand -silica inhalation)

201
Q

how do we call silicosis otherwise?

A

potter’s rot, grinder’s disease

202
Q

who gets silicosis?

A

who work in

  1. foundries (metal production - what shapes metals is made of silica)
  2. mines
  3. sandblasting - abrasive blasting
203
Q

what makes silica inbody?

A

h2o2 production and other oxygen radicals that damage lung tissue, mainly upper lobes

204
Q

which cells respond to silica inbody?

A

macrophages , they take up this particles and release cytokines : TNFalpha, IL1, LTB4, which leads to inflamation - firboblasts- collagen

205
Q

what is characteristic for silicosis?

A

egg shell calcifications of lymph nodes on CXRay and high risk for TB, bronchogenic cr, cor pulmonale and caplan syndrome

206
Q

what is asbestosis associated with?

A

it is associated with shipbuilding, roofing, plumbing

insulation, fireproofing, soundproofing

207
Q

what is histologic finding in asbestosis ?

A

golden brown ferruginous bodies (asbestos bodies) resemling dumbbells that are formed when asbestos particles got coated by ferritin in alveoli. visualized using prussian blue stain, often obtained by bronchoalveolar lavage.

208
Q

what i characteristic for asbestosis vs other pneumoconiosis?

A

it mainly affects lower lobes

209
Q

what is classical pathognomical CXray presentation of patient with asbestosis?

A

ivory white, calcified , supradiaphragmatic and pleural plaques

210
Q

what pulmonary manifestations asbestosis includes?

A
  1. benign pleural plaques (CT) - MC
  2. asbesotis / diffuse ILD - chronic exposure
  3. cancers : bronchogenic cr > mesothelioma
211
Q

what do pt with asbestosis have high risk for?

A

bronchogenic cr, caplan syndrome and pleural effusions

212
Q

what is mesothelioma?

A

it is pleural malignancy that leads to pleural thickening and sometimes hemorrhagic pleural effusions. asbestosis exposure increases risk and smoke doesn’t (vs bronchogenic cr.)

213
Q

what shows histology in mesothelioma ?

A

psammoma bodies

214
Q

how to dif dx mesothelioma vs cr?

A

check cytokeratin and calretinin; + in mesothelioma

215
Q

what is presentation and prognosis of mesothelioma?

A

slow onset symptoms : dyspnea, cough, chest pain with poor prognosis (median survival 4-13 months untreated; 6-18 months treated with chemo)

216
Q

which drug toxicities cause restricitve lung disease ?

A
  1. bleomycin and busulfan - anticancer
  2. amiodarone - antiarrithmic
  3. metothrexate -anti-inflammatory

respiratory usmle (4 decks)

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