Pathology - Resp Flashcards

0
Q

List 6 causes of ALI or ARDS:

A

Infection, trauma (inc. fat embolism), toxic exposure, pancreatitis, uraemia, and immune reactions.

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1
Q

What are “heart failure” cells?

A

Haemosiderin-laden macrophages which occur with chronic congestion and are therefore indicative of heart failure.

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2
Q

Overall mortality rate in ARDS?

Compared to AIP?

A

40% compared with 50% in AIP, which is essentially ARDS with no identifiable cause.

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3
Q

What are the anatomical classifications of emphysema and what are the associated conditions/risk factors?

A

Centriacinar - heavy smokers

Panacinar - A1 anti-trypsin def

Distal acinar - near peripheral fibrosis.

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4
Q

Neutrophils mediate emphysema by releasing cellular proteases. Name them:

A

Elastase
Proteinase-3
Cathepsin-G

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5
Q

Why do NSAIDS trigger asthma?

A

These agents inhibit COX (without affecting LOX) and therefore tip the balance of arichidonic acid metabolism towards bronchoconstrictor leukotrienes.

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6
Q

Describe the acute, late, and remodelling phases of asthma:

A

Acute - IgE coated mast cells cause primary (leukotriene) and secondary (cytokine) mediator release which cause bronchospasm, oedema, mucus secretion, and leukocyte recruitment.

Late - mediated by leucocytes, this is characterised by persistent spasm and oedema with infiltration and epithelial loss.

Remodelling occurs due to SMC and mucus gland hypertrophy, increased vascularity, and increased collagen.

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7
Q

What is the most dangerous size bracket for respiratory particles?

Why?

A

1-5 micrometers. These particles can reach the terminal alveoli and settle in the lungs.

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8
Q

What is the hallmark of sarcoidosis?

3 histological features

A

Non-caseating granulomas.

Schaumann bodies and asteroid bodies commonly occur but are not pathognomonic.

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9
Q

Sarcoidosis is a diagnosis of…

A

Exclusion.

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10
Q

What is Loeffler’s syndrome?

A

Simple pulmonary eosinophilia.

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11
Q

95% of PE comes from DVT.

What are the other 5% from?

A

Pulmonary HTN
Pulmonary atherosclerosis
Heart failure

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12
Q

How frequent is pulmonary infarction in PE? Why is this? Who is at risk?

A

Occurs ~10%

Occurs in patients with heart failure as these patients fail to supply the tissue via the bronchial arteries.

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13
Q

What is the most common serotype of H. influenzae to cause pneumonia?

A

Serotype B (A-F).

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14
Q

Classification and virulence factors of H. influenzae?

A

Gram negative, encapsulated, pleomorphic organism.

Adhesive pili, a factor that dysregulates ciliary beating, and an IgA protease.

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15
Q

What is the most common Gram Negative pneumonia?

A

Klebsiella. Especially common in alcoholics.

H. influenzae more commonly affects children and patients with COPD.

16
Q

What are the 4 stages of lobar pneumonia?

A
  1. Congestion
  2. Red hepatization
  3. Grey hepatization
  4. Resolution.
17
Q

Asbestos + smoking =

A

50-90 fold increase in risk of lung cancers.

18
Q

Broad statements on SCC versus NSCC?

A

Small cell is metastatic at diagnosis with an initially high response to chemoradiation.

Non-small cell is les often metastatic but has a poorer response to treatment.

19
Q

Types and approximate frequencies of lung cancer?

A

Adenocarcinoma ~37%m 47%f

Squamous ~32%m 25%f

Small cell ~14%m 18%f

20
Q

Which subset of lung cancer is NOT associated with smoking?

Which is most closely associated with smoking?

A

Bronchioalveolar carcinoma.

Squamous cell carcinoma.

21
Q

Paraneoplastic syndromes occur in 1-10% of tumours. What are the causative substances?

A
ADH = SIADH
ACTH = Cushings
PTH = Hypercalcaemia
Calcitonin = Hypocalcaemia
Gonadotropins = Gynaecomastia
Serotonin = Carcinoid.
22
Q

Asbestos disease may manifest as:

A

Localised plaques and effusions
Parenchymal disease (asbestosis)
Lung carcinoma, malignant mesothelioma, laryngeal and other neoplasms.

23
Q

What are the two types of asbestos?

A

Straight stiff amphiboles reach the deep lung more readily than serpentine fibres, accounting for the former’s greater pathogenicity.

24
Q

What are asbestos bodies?

A

Ingested asbestos fibres, coated by iron containing material to form characteristic beaded, dumbbell shaped fibres that distinguish asbestosis from other disorders.

25
Q

What are the two common pre-cancerous lesions in the oral cavity?

A

Leukoplakia, occur in 3% of people; 5-25% of which are premalignant.

Erythroplakia, less common but more ominous.

26
Q

Most oral cancers are?

Overall 5-year survival?

A

95% are SCC

50% (early 80%; late 19%)

27
Q

50% of oropharyngeal cancers harbour which virus?

A

HPV

Patients with HPV associated cancers fare better.

28
Q

Risk factors for oral SCC beyond smoking, drinking, and HPV?

A

Pipe smoking
Betal nut and paan chewing
Actinic radiation
Family history.

29
Q

Nasopharyngeal carcinoma is associated with which virus?

Who does it affect?

Prognosis?

A

EBV

Children in Africa. Adults in southern China.

70% have nodes at presentation. 3-year survival is 50-70% with radiotherapy.

30
Q

Carotid body tumours are what?

A

Paragangliomas. Typically occur in patients between 50-70.

31
Q

Complications of xerostomia include?

A

Increased caries
Candidiasis
Difficulty swallowing
Difficulty taking.

32
Q

What is a ranula?

A

A mucocoele of the SUBLINGUAL gland.

33
Q

Sialadenitis is most commonly caused by which bacteria?

A

S. aureus or Strep. viridians

34
Q

What are pleomorphic adenomas?

What proportion of parotid tumours do they constitute?

What is their malignant potential?

A

Painless, slow growing, mobile, discrete benign tumours of mixed epithelial and mesenchymal differentiation.

Malignant transformation occurs in 10% after 15 years duration. 30-50% 5-year mortality if malignant.

35
Q

Which group is at risk for Warthin’s tumours?

A

Smokers are 8 times more likely to get this benign tumour.

36
Q

What is the most common primary malignancy of salivary glands?

A

Mucoepidermoid carcinoma.

15% of all salivary gland neoplasms. Poorly defined, 50% 5 year survival and high recurrence rates.