Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory Medicine Midterm > The Lung Part 9 > Flashcards

The Lung Part 9 Flashcards

1
Q

Pneumonia in the immunocompromised host

A
  • most common serious complication in immunocompromised=pulmonary infiltrate w/ or without signs of infection
  • opporunistic infections w/high mortality
  • Diff Dx of infiltrates: drug reactions and involvement of lung by tumor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bacteria that cause pneumonia in the immunocompromised host causing pulmonary infiltrates

A
  • P. aeruginosa
  • Mycobacterium sp.
  • L. pneumophila
  • Listeria monocytogenes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Viruses that cause pneumonia in the immunocompromised host causing pulmonary infiltrates

A

-CMV and HSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Fungi that cause pneumonia in the immunocompromised host causing pulmonary infiltrates

A
  • P. jiroveci
  • Candida sp.
  • Aspergillus sp.
  • Phycomycetes
  • Cryptococcus neoformans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Common causes of DIFFUSE pulmonary infiltrates

A
  • CMV
  • Pneumocystis jiroveci
  • Drug reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Uncommon causes of DIFFUSE pulmonary infiltrates

A
  • Bacterial pneumonia
  • Aspergillus
  • Cryptococcus
  • Malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Common causes of FOCAL infiltrates

A
  • Gram-neg bacterial infections
  • Staph. aureus
  • Aspergillus
  • Candida
  • Malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Uncommon causes of FOCAL infiltrates

A
  • Cryptococcus
  • Mucor
  • Pneumocystis jiroveci
  • Legionella pneumophila
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Bacterial lower respiratory tract infections caused by ____ pathogens are among the most serious pulmonary disorders in HIV

A
  • “usual” rather than opportunistic organisms like S. pneumoniae, S. aureus, H. influenzae, and gram-neg rods
  • pneumonias in HIV pts are more common, more severe and more associated w/bacteremia than in those without
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

NON-INFECTIOUS causes of pulmonary infiltrates in HIV individuals

A
  • Kaposi sarcoma
  • non-Hodgkin lymphoma
  • Lung cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diseases and associated CD4+ count in HIV patients

A
  • Higher CD4+ >200=bacterial and tubercular infxns
  • Less than 200=Pneumocystis pneumonia
  • Less than 50=CMV, fungal, Mycobacterium avium complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pulmonary disease in HIV patients may result from

A

-more than one cause leading to atypical presentation requiring more extensive diagnostic workup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Indications for Lung Transplantation

A
  • all non-neoplastic terminal lung disease
  • End-stage emphysema, idiopathic pulmonary fibrosis, cystic fibrosis, idiopathic/familial pulmonary arterial hypertension
  • bilateral transplant possible, but usually only single done;
  • when bilateral lung chronic infnx present (cystic fibrosis, bronchiectasis), both lungs replaced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Two major complications of lung transplant

A
  • Pulmonary infections

- Rejection (Acute and chronic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pulmonary infections in lung transplant patients

A
  • early posttransplant–bacterial infxn most common
  • w/ganciclovir prophylaxis and matching donor-recipient CMV status, CMV pneumonia less common/less severe but some resistant strains emerging
  • Most infxns occur in 3RD-12TH month after transplant
  • Pneumocystis=RARE bc of Bactrim prophylaxis
  • Common fungal infxns= Aspergillus, Candida involving brachial anastomotic site and/or lung
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acute rejection in Lung transplant patients

A
  • occurs to some degree in all patients despite immunosuppression
  • usually WEEKS TO MONTHS after surgery but can be years later or whenever immunosuppression is decreased
  • S/S: fever, dyspnea, cough and infiltrates
  • Dx WITH TRANSBRONCHIAL BIOPSY
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Chronic rejection in Lung transplant patients

A
  • problem in at least 50% of pts by 3-5 yrs poststranplant

- S/S: cough, dyspnea and irreversible decrease in lung function tests due to pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Rejection morphology in Lung transplant patients

A

-Acute rejection=inflammatory infiltrates (lymphocytes, plasma cells, few neutrophils and eosinophils) in blood vessels and/or submucosa of airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Major morphologic correlate of chronic rejection is

A
  • BRONCHIOLITIS OBLITERANS
  • partial or complete occlusion of small airways by fibrosis, with or without active inflammation
  • patchy and hard to Dx via transbronchial biopsy
  • Bronchiectasis and pulmonary fibrosis may develop in long-standing cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Acute cellular airway rejection (fibrous obliteration) treatment

A

-responsive to therapy–progress can slow but cannot be reversed!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Infrequent complications of lung transplantation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

lung transplant prognosis

A
  • short term outcome has improved a lot but still not as good as that for renal or cardiac
  • One yr survival=79%, 5yr=53%, 10 yr.=30
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Most frequent tumors in the lung are?

A

CARCINOMAS–90-95%!!

-next common is bronchial carcinoids and then mesenchymal and other

24
Q

Most frequently diagnosed major cancer in the world and the most common cause of cancer mortality worldwide

A

LUNG CANCER!

  • poor prognosis–incidence=mortality
  • incidence and mortality have been decreased in men due to decreased smoking rates; in women lung cancer mortality higher than breast cancer mortality
  • most often bw ages of 40-70 with peak at 50s or 60s
25
Q

Etiology and Pathogenesis of lung cancers–broad categories

A
  • Tobacco smoking
  • Industrial hazards
  • Air pollution
  • Molecular genetics
26
Q

Etiology and Pathogenesis of lung cancers–tobacco smoking

A
  • 80% of lung CA occur in smokers or recent ex-smokers
  • linear correlation bw pack years and cancer frequency
  • risk is 60x higher in smoker with Hx of 2 packs for 20 yrs
  • women= higher susceptibility to tobacco carcinogens
  • cessation lowers risk but never to baseline–genetic changes in bronchial epithelium persist in ex- smokers
  • passive smoking increases risk to 2x and pipes/cigars only modestly increase risk
27
Q

How come not all smokers/ppl exposed to tobacco develop cancer?

A
  • Bc mutagenic effect of carcinogens is modified by genes
  • Increased risk in those w/ polymorphisms in P-450 that increases capacity to activate procarcinogens
  • Ppl whose blood lymphocytes show more chromosomal breakages after tobacco exposure (mutagen-sensitivity genotype) have more than 10x increased risk for lung CA bc of variation in DNA-repair genes
28
Q

Order of morphological events in epithelial cell changes from cigarette smoke

A
  • 1) basal cell hyperplasia
  • 2) squamous metaplasia
  • 3) squamous dysplasia
  • 4) carcinoma in situ
  • 5) invasive cancer
29
Q

Industrial hazards associated with lung cancer

A
  • asbestos, arsenic, chromium, uranium, nickel, vinyl chloride, mustard gas, ionizing radiation
  • Latent pd before lung cancer in asbestos exposure is 10-30 yrs; Lung CA=most frequent malignancy in ppl exposed to asbestos, esp in smokers
  • Asbestos+smoker=55x > risk; asbestos+no smoke=5x>
30
Q

Air pollution and lung CA; radon gas

A
  • likely adds to risk in smokers/ppl exposed to 2nd hand smoke
  • Chronic exposure to smog may cause lung irritation, inflammation and repair, increasing risk for CA
  • Radon gas–radioactive and linked to increased lung CA in uranium miners, esp in those who smoke
31
Q

Molecular Genetics and Lung CA

A
  • smoking related carcinomas arise by a stepwise accumulation of oncogenic driver mutations that result in neoplastic transformation of pulm epithelial cells
  • genetic changes found in “benign” bronchial epithelium of smokers w/o lung CA suggesting that large areas of resp. mucosa are mutagenized by exposure to carcinogens in tobacco smoke (“field effect”); cells that accumulate driver mutations develop into invasive carcinomas
32
Q

Squamous cell carcinoma

A
  • associated with tobacco smoke exposure
  • chromosome deletions w/tumor suppressor loci–losses in 3p, 9p (CDKN2A) and 17p (TP53)=early events in tumor evolution–can be detected in normal resp mucosal cells of smokers
  • has highest frequency of TP53 mutations than any other lung carcinoma!
  • p53 over expression is also an early event–seen in squamous dysplasia and carcinoma in situ
  • Loss of RB tumor suppressor also seen in some sqcc
33
Q

CDKN2a in squamous cell carcinoma

A
  • cyclin dependent kinase inhibitor gene

- is inactivated and its protein product p16 is lost in 65% of tumors

34
Q

Many squamous cell carcinomas have amplification of

A

-FGFR1–gene encoding fibroblast growth factor receptor tyrosine kinase

35
Q

Small cell carcinoma

A
  • shows the strongest association with smoking
  • diff histology but shares many molecular features with squamous cell CA like LoF of TP53 (75-90%!), RB and chromosome 3p deletions
  • Also common is amplification of genes of MYC family
36
Q

Adenocarcinoma

A
  • oncogenic GAIN of FNX mutations in GF signaling pathways–receptor tyrosine kinases–EGFR, ALK, ROS, MET and RET
  • tumors without tyrosine kinase mutations have mutations in KRAS gene which lies downstream of receptor tyrosine kinases in GF signaling pathways
37
Q

Lung cancer in Never Smokers

A
  • more common in women
  • most are adenocarcinomas
  • more likely to have EGFR mutations and almost NEVER have KRAS mutations!
  • TP53 not uncommon but less frequent than in smoking related cancers
38
Q

Precursor (Preinvasive lesions)–4 types

A

1) squamous dysplasia and carcinoma in situ
2) atypical adenomatous hyperplasia
3) adenocarcinoma in situ
4) diffuse idiopathic pulmonary neuroendocrine cell hyperplasia

39
Q

Relative proportions of the types of carcinomas

A
  • Adenocarcinomas–38%
  • Squamous cell carcinoma–20%
  • Small cell carcinoma–14%
  • Large cell carcinoma–3%
  • Other-25%
  • can have mix of any of the above like adenocarcinoma+scc and sqcc+scc=10%
40
Q

Most common form of lung cancer in women–why?

A

Adenocarcinoma

  • probably due to increase in women smokers
  • changes in cigarette type (filter tips, lower tar and nicotine) have caused smokers to inhale more deeply and expose more peripheral airways and cells (with predilection to adenocarcinoma) to carcinogens
41
Q

_____ carcinomas arise in the peripheral lung and _____ arise in the central/hilar region

A
  • peripheral lung=adenocarcinomas

- central/hilar region=squamous cell carcinomas

42
Q

Atypical adenomatous hyperplasia

A
  • small lesion (<5mm); dysplastic pneumocytes lining alveolar walls that are mildly fibrotic
  • can be single or multiple and can be in the lung adjacent to invasive tumor or away from it
43
Q

Adenocarcinoma in situ morphology

A
  • also called brochioalveolar carcinoma
  • lesion less than 3 cm and made of entirely dysplastic cells growing along preexisting alveolar septae
  • cells have more dysplasia than atypical adenomatous hyperplasia and may or may not have intracellular mucin (mutinous or nonmucinous)
44
Q

Adenocarcinoma morphology

A
  • invasive malignant epithelial tumor w/glandular differentiation or mucin production by tumor cells
  • Many patterns: acinar, lepidic, papillary, micro papillary, and solid with mucin formation
  • in contrast to squamous cancers, these are more PERIPHERALLY located and SMALLER
  • spectrum from well-differentiated w/glandular elements to papillary lesions similar to papillary carcinomas to solid masses w/only occasional mucin producing glands/cells
45
Q

Majority of adenocarcinomas express what transcription factor?

A
  • thyroid transcription factor-1

- first identified in thyroid–required for normal lung dev.

46
Q

At the periphery of the adenomatous tumor, there is often a ____pattern of spread

A

-Lepidic pattern–where tumor cells crawl along normal-appearing alveolar septae

47
Q

What is a microinvasive adenocarcinoma?

A
  • tumors less than or=3 cm w/small invasive component (<5mm) associated with scarring and a peripheral lepidic growth pattern
  • Much better prognosis than invasive carcinomas of same size!!!
48
Q

Mucinous adenocarcinomas

A
  • spread aerogenously, forming satellite tumors
  • present as solitary nodule or multiple nodules or entire lobe may be consolidated by tumor resembling lobar pneumonia (less likely to be cured by surgery)
49
Q

Squamous cell carcinoma

A
  • mostly found in MEN

- STRONGLY ASSOCIATED WITH SMOKING

50
Q

Precursor lesions to squamous cell carcinoma

A
  • squamous metaplasia or dysplasia in bronchial epithelium which transforms into carcinoma in situ
  • CIS can last for years–by this time can see atypical cells in sputum or in bronchial lavage fluids/brushings; but lesion is still asymptomatic and undetectable on Xray
  • Eventually develops into squamous cell carcinoma
51
Q

Various paths that squamous cell carcinoma call follow

A
  • 1) grow exophytically into bronchial lumen producing intraluminal mass eventually obstructing bronchus leading to atelectasis and infection
  • 2) penetrate wall of bronchus and infiltrate along peri-bronchial tissue into adjacent carina or mediastinum
  • 3) grow along broad front to produce cauliflower like intraparenchymal mass that pushes lung substance ahead of it
52
Q

Color and texture of neoplastic tissue in squamous cell carcinoma

A
  • Gray-white and firm to hard
  • Esp when tumors are bulky, focal areas of hemorrhage or necrosis may appear to produce red or yellow-white mottling and softening;
  • sometimes these necrotic foci cavitate
53
Q

Histologically, squamous cell carcinomas are characterized by

A
  • presence of keratinization and/or intercellular bridges
  • Keratinization may take form of squamous pearls or individual cells with markedly eosinophilic dense cytoplasm
  • these features prominent in well-differentiated tumors, easily seen but not extensive in moderately differentiated tumors and focally seen in poorly differentiated tumors
54
Q

Mitotic activity is higher in what kind of squamous cell carcinomas (well-differentiated or poorly differentiated?)

A

-poorly differentiated tumors

55
Q

What is seen adjacent to the squamous cell carcinoma tumor mass?

A

-squamous metaplasia, epithelial dysplasia and foci of frank carcinoma in situ

Respiratory Medicine Midterm (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions