Lung Diseases 2&3 Flashcards
1
Q
Mention site of primary pulmonary tuberculosis
A
Lower part of upper lobe or upper part of lower lobe close to pleura
2
Q
Define Ghon’s complex
A
Parenchymal lesion (Ghon’s focus) and nodal involvement
3
Q
Define Ranke complex
A
Ghon’s complex after undergoing fibrosis followed by radiologically detectable calcification
4
Q
Mention cellular elements of tuberculous granuloma
A
Epithelioid cells, multi-nucleated giant cells, outer mantle of lymphocytes & fibroblasts
5
Q
Mention major consequences of primary tuberculosis
A
- Induction of hypersensitivity & increased resistance
- Foci of scarring harbouring viable bacilli which can be reactivated later.
- Progressive primary tuberculosis
6
Q
Progressive primary tuberculosis manifestations
A
- Progressive pulmonary tuberculosis resembles an acute bacterial pneumonia with lower/middle lobe consolidation, hilar lymphadenopathy & pleural effusion.
- Lymphohematogenous dissemination, tuberculous meningitis & miliary TB
7
Q
Mention causes of secondary TB
A
- Primary tuberculosis
- Reactivation of dormant primary lesions
- Exogenous reinfection
8
Q
Mention special features of secondary than primary TB
A
- Marked tissue response around focus due to preexistence of hypersensitivity
- Regional lymph nodes are less prominently involved than in primary tuberculosis
- Cavitation occurs readily & dissemination along airways
9
Q
Mention site of seconadry TB & why?
A
Apex of one or both upper lobes
High oxygen tension in apices
10
Q
Mention the most favourable outcome of reactivation TB
A
Progressive fibrous encapsulation occurs leaving only fibrocalcific scars
11
Q
Manifestations of progressive pulmonary tuberculosis
A
Erosion into bronchus leading to Irregular cavity lined by caseous material that is poorly walled off by fibrous tissue
Erosion of blood vessels results in hemoptysis
12
Q
Mention results of inadequate treatment of progressive pumonary TB
A
Direct expansion, dissemination in airways, lyphatic channels & vascular system.
13
Q
Mention complications of progressive pulmonary TB
A
Pleural complications Endobronchial, tracheal & laryngeal TB may develop Miliary pulmonary disease Systemic miliary TB Isolated-oragn tuberculosis Amyloidosis
14
Q
Describe clinical features of secondary TB
A
- Localized secondary tuberculosis may be asymptomatic
- Systemic symptoms apear early in course anrexia, low grade fever….due to cytokines.
- Progressive pulmonary TB with cavitation
- Extrapulmonary manifestations related to organ
15
Q
Mention factors worsening prognosis of TB
A
Aged, debilitated & immune-suppressed persons
16
Q
Mention causes of lung abscess
A
- Aspiration
- Local causes: complications of lobar/bronchopneumonia, in obstructive lung diseases, chronic bronchitis, bronchial obstruction by tumour.
- Systemic causes due to septic emboli or due to disseminated pyogenic infection
17
Q
Abscesses due to aspiration are ….., while peumonic or pyemic are ….. .
A
Single
Multiple
18
Q
Describe cellular elements of lung abscess
A
Suppurative exudate containing neutophils & pus cells
Chronic abscess will be surrounded by proliferated fibroblasts, lymphocytes, plasma cells & macrophages.
19
Q
C/P of lung abscess
A
- Cough with expectoration, foul smelling sputum
- Hempotysis
- Fever, malaise & loss of weight
- Clubbing of fingers & amyloidosis when abscess is chronic
20
Q
Mention complications of lung abscess
A
- Pleural complications: pyo-pneumothorax, empyema, bronchopleural fistula
- Chronicity with later amyloidosis
- Septic embolization to the brain giving rise to brain abscess & meningitis
21
Q
Mentuon predisposing factirs & direct cause of lung gangrene
A
- Lung abscess, bronchiectasis, severe necrotizing pneumonia & Diabetes, senility, chronic nephriti
- Superimposed infection by saprophytic bacteria
22
Q
Mention suppurative lung diseases
A
- Bronchpneumonia
- Lung abscess
- Empyme/gangrene
- Bronchiectasis
23
Q
Classification of pneumonia anatomically
A
Lobar, bronchopneumonia, interstitial
24
Q
Classification of pneumonia aetilogically
A
Viral, bacterial, fungal, rickettsial, chlamydial
25
Classification of pneumonia according to nature of hast reaction
Fibrinopurulent, mononuclear interstitial, granulomatous & nectrotizing
26
Classification of pneumonia according to clinical setting
Community acquired, nosocomial, immunocompromised
27
Predisposing factors to community acquired pneumonia
-Chronic diseases, immunodeficiency, aspiration of nasopharyngeal flora, splenectomized parients, impaired muco-ciliary clearance, depressed cough/epiglottic reflexes, loss of cough reflex in coma.
28
Contrast gross apearnace of lobar vs bronchopneumonia
Lobar: whole lobe or large portion of lobe
BP: patchy consolidation of lung
29
Mention age group & stages of lobar pneumonia the wite a short note on each
Young adults
1. Congestion: vascular engorgement, intra-alveolar fluid with little neutophils
2. Red hepatization: liver-like consistency, the alveoli are filled with neutrophils, red blood cells& fibrin.
3. Grey hepatization: RBCs disintegrate, remaining fibrinous exudate persists, greyish brown appearance, fibrinous pleuritis.
4. Resolution: consolidtion exudate is liquefied resorbed and ingested by macrophages & expectorated.
OR, Organization may occur in the alveolar spaces, also pleuritis may undergo fibrosis & permenent adhesions
30
Describe microscopic features of bronchopneumonia
- Suppurative exudate fills the bronchi
| - Epithelium lining is desroyed, walls are infiltrated by polymorphs
31
C/P of lobar/bronchpneumonia
1. Sudden onset of fever, shaking chills, dyspnea, severe cough RUSTY SPUTUM
2. Pleuritis, chest pain friction rub.
3. Whole lobe is opaque in bronchopneumonia, FOCAL opacities in bronchpneumonia
4. Sudden recovery
32
Mention complications of bacterial pneumonia
1. Lung abscess
2. Spread to pleura/pericardium
3. Bronchiectasis
4. Organization
5. Bacteraemia: arthritis, meningitis, endocarditis…etc
33
Mention the seprataing feature between typical & atypical pneumonia
Inflammmation of the alveolar septa and interstitial tissue without alveolar inflammatory exudate
Moderate amounts of sputum, absence of physical findings of consolidation & moderate elevation of WBCs
34
Gross appearnce of interstitial pneumonia
Patchy ot may involve whole lobe bilateral or unilateral with trachea & bronchi congestion. Red-blue, congested & subcretiptant lobes.
35
Microscopic appearnce of viral community acquired pneumonia
- Confined to the walls with mononuclear inflammatory infiltrate.
- Alveolar spaces are free
- Hyaline membrane can form
- Hyperplasia of type II pneumocytes
- Intracytoplasmic/intrenuclear viral inculsion bodies.
- Secondary bac inf
36
C/P of atypical pneumonia
1. Similar to URTI or life-threatening in immunocompromised patients.
2. Acute nonspecific febrile illness, fever, headache & later with cough & sputum
3. Respiratory distress, V/Q mismatch
37
Predisposing factor to atypical pneumonia development
1. Viral infections
2. Smoking inhibit ciliary clearnce
3. Alcohol depress cough reflex
4. Chronic diseases
5. Cold weather
38
How can micro-organisms reach the lung
1. Inhalation
2. Aspiration
3. Direct contact with patients
4. Blood
5. Throat commensals
39
Describe X-ray appearnce & microscopic appearnce of lung hamartoma
Coin shadow small spherical 3-4 cm
| Mature cartilage, fibrous tissue, blood vessels & fat
40
Age of bronchogenic carcinoma
50-60 yrs
41
At the time of diagnosis, 50% of patients have ….., while 25% of …….
Distant metastases
| Regional LN metastases
42
Mention risk factors of bronchogenic carcinoma
1. Tobacco smoking: polycyclic aromatic hydrocarbon, benzopyrene.
2. Industrial hazards: radiation/asbestos
3. Air pollution
4. Genetic factors: p53 & p16 inactivation, EGFR & k-ras activation.
43
Contrast SCLC vs NSCLC in treatment
SCLC all metastatized at diagnosis, chemotherapy with(out) radiation is used.
NSCLC, chemotherapy is ineffective. Surgery & new targeted therapy are used.
44
Site & gross appearnce of bronchogenic carcinoma
S: arises mostly in & arounf hilum, adenoc is peripheral
G: small firm greyish mucosal lesion at beginning, grow as intraluminal mass, invades the bronchial wall pushing adjacent lung tissue, extend into pleural & spread to LN
45
Mention precursor lesion of SSC and prigression
Squamous metaplasia, dysplasia then carcinoma in situ
46
Describe microscopic features of SSC
Well-differentiated to poorly, sheets & masses of malignant squamous epithelial cells, may show central keratin formation.
47
Target population of lung adenocarcinoma
Females & nonsmokers
48
Precursor lesion of lung adenocarcinoma
Atypical adenomatous hyperplasia, proliferation of low-columnar cells & cytologic atypia.
49
Mention microscopic variants of adenocarcinoma
1. Acinar
2. Papillary
3. Mucinous
4. Solid masses & sheets
50
Mention the other name of adenocarcinoma in situ & its mucroscopic features.
Brinchiolo-alveolar carcinoma
| Tall columnar to cuboidal cells in a monolayer along the alveolar septa, no stronal invasion or desmoplasia.
51
Mention the most likely explanation of LCC pathogenesis
SCC or adenocarcinoma that is so undifferentiated & can no longer be recongnized.
52
Mention microscopic features of SCLC
Sheets of round/fusiform cells with scant cytoplasm, mitotic figures are frequent.
Neurosecretory graules responsible for paraneoplastic syndromes
53
Describe spead of SCLC
1. Bronchial: ulcerative bronchitis, bronchiectasis, abscess & bronchopneumonia.
2. Pleural
3. SVC compression/ invasion
4. Pericardium
5. Bone invovlement
6. Eosophagus: dysphagia/fistula
7. Nerves
54
Rank favourite sites of metastasis for lung carcinoma
1. Adrenals (50%)
2. Liver (30-50%)
3. Brain (20%)
4. Bone: thoracic vertebrae by retrograde venous route
55
C/P of bronchogenic carcinoma
1. Silent
2. Chronic cough & expectoration
3. Paraneoplastic syndromes
4. SVC sydrome
5. Pancoast’s tumour
56
Write a shirt note on paraneoplastic syndromes
1. Hypercalcemia, parathyroid hormone like substance secreation by SSC, may be due to metastataic osteolytic lesions
2. Migratory thrombophlebitis, endocarditis, DIC (adenocarcinoma)
3. Cushing sydrome due to adrenocorticotrophic hormone by SCLC
4. Syndrome of inappropriate secretion of ADH
5. Mysthinic sundome, polymyositis, peripheral neuropathy.
6. Clubbing
57
Compare microscopic features of typical & atypical carcinoid tumours
Typical: nests, cords & masses of monotonous cells, salt & pepper chromatin seperated by delicate fibrous stroma. Mit.figures are rare.
Atypical: higher miotic rates & higher rate of metastasis
58
Gross features of bronchial carcinoma
polypoid masses project into the lumen covered by intact mucosa, collar-button or dumbbell appearnace may occur if tumour produces little intraluminal mass the penetrate into the bronchial wall.
59
Mention immunostaining of carcinoid tumour
Chromogramin & synaptophysin
60
C/P of carcinod tumour
1. Asymptomatic
2. Partial bronchial obstruction, cough, repeated infection & hemoptysis
3. Carcinoid sydrome (flushing, diarrhea, cyanosis)
5. Rare distant meta.
61
Mention tumours which metastatize to the lung by direct spread
Eosophageal carcinomas
| Mediastinal lymphomas
62
Describe patterns of metastatic growth in the lung
1. Multiple, discrete nodules scattered in all lobes esp at periphery.
2. Cannon-ball metastases from renal cell carcinoma/testicular tumors.
63
Mention causes of pulmonary embolism
1. Prolonged bed rest
2. Othopedic surgery
3. Severe trauma
4. Congestive heart failure
5. Period of labour, OCP
6. Disseminated cancers
7. Hypercoagulability
64
Pathophysiology of pulmonary embolism
1. Increase pulmonary arterial pressure, vasospasm by neurogenic mechanism & release of thrombaxane A2 & seretonin.
2. Downstream ischemiadepending on ebolus size & cardiopulmonary status of patient.
Diminished cardiac output, right-sided heart failure (acute cor pulmonale) or even death.
65
Mention consequences, morphology & clinical features of large pulmonary embolus
C: acute right-sided heart failure.
M: saddle emolus
CF: sudden death, shock, acute right-sided heart failure (acute cor pulmonale)
66
Mention consequences, morphology & clinical features of medium embolus
C: haemorrahge in adequate bronchial circulation otherwise, haemorrhagic infarction.
M: haemorrhage due to ischemic damage of endothelial cells, haemorrhagic infaction (coagulative haemorrhagic necrosis)
CF: Dyspnea
67
Mention consequences, morphology & clinical features of small pulmonary emobli
C: pulmonary hypertension
M: pulmonary vascular changes
CF: silent unless multiple, the chronic right-sided heart failure, progressive dyspnea.
68
Define pulmonary hypertension
Pulmonary arterial pressue more than 25 mmHg at rest, or more than 30 mmHg during exercise.
69
Mention the classification of pulmonary hypertension.
1. Pulmonary arterial hypertension
2. P.H. due to left sided heart failure
3. P.H. due to lung diseases and/or hypoxia
4. chronic thromoembolic pulmonary hypertension
5. With unclear or multifactorial mechanisms
70
Pathogenesis of primary pulmonary hypertension
Increase in endothelial cells & pulmonary smooth muscle cells proliferation.
71
Mention causes of secondary pulmonary hypertension
1. Destruction of lung parechyma
2. Reduction of cross-sectional area
3. Increase in left atrial pressure due to mitral stenosis, incread blood flow due to right to left shunts.
72
Mention endothelial cell dyfunction resulting in PH
- decreased nitric oxide & prostacyclin
- increased endothelin
- growth factors & cytokines which cause proliferation & migration of SM
73
Describe morphology of vessels in PH
Large arteries: atheroma with intimal thickening by lipid laden macrophages, proliferated SM & fibrosis
Medium/small arteries: medial hypertrophy & intimal fibrosis
Plexiform lesions, tuft of capillaries, due to endothelial cell proliferation & multiple lumina.
74
Mention C/P of primary pulmonary hyp
Woman 20-40 yrs, fatigue, syncope esp on exercise, dypnea on exertion & chest pain.
75
Mention late complications of PH
Respiratory distress, cyanosis, right ventricular hypertrophy & decompensated cor pulmonale.
76
Drug therapy of PH
1. Prostaglandin analogues
2. Endothelin receptor antagonists
3. Phosphodiesterase 5 inhibitors
4. High does Ca channel blockers, diuretics
