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Respiratory Medicine Midterm > Respiratory System Pathology 4 - Galbraith > Flashcards

Respiratory System Pathology 4 - Galbraith Flashcards

1
Q

Defense mechanisms in the lung compromised in infections

A 
Cough reflex
Impaired or diminished ciliary function
Mucus stasis
Decreased macrophage activity
Pulmonary edema
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2
Q

Community-acquired bacterial pneumonia (CAP)

A

CRP and procalcitonin levels higher in bacterial pneumonia

May follow viral URI

Predisposing conditions:
Young or old
COPD, DM, CHF
Absent splenic function - encapsulated bacterial infections

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3
Q

Streptococcus pneumoniae

A 
most common cause of CAP
Gram +
Elongated diplococci
Seen in sputum
*false positives
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4
Q

Haemophilus influenzae

A 
cause of CAP
Gram -
encapsulated type b most virulent
pediatric bacterial pneumonia, OM
most common cause of bacterial acute exacerbation of COPD
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5
Q

Moraxella catarrhalis

A

cause of CAP
Elderly: bacterial pneumonia, exacerbation of COPD

Pediatric: OM

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6
Q

Staphylococcus aureus

A

cause of CAP
secondary bacterial pneumonia following viral

higher incidence of complications - abscess, empyema

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7
Q

Klebsiella pneumoniae

A

cause of CAP
Gram - bacterial pneumonia
chronic alcoholics, malnourished

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8
Q

Pseudomonas aeruginosa

A

cause of CAP
pneumonia in CF, neutropenic
Hematogenous spread

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9
Q

Legionella pneumophila

A

cause of CAP
water tanks, pipes
Immunosuppressed, chronic disease
Urine Legionella antigen

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10
Q

Mycoplasma pneumoniae

A

cause of CAP

children, young adults

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11
Q

pneumonia morphology

A

alveolar filling with inflammatory cells and exudate
–> consolidation (solidification) of lung tissue

Patterns:
bronchopneumonia
Lobar pneumonia

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12
Q

Bronchopneumonia morphology

A

patchy involvement of lung parenchyma
Consolidated areas may coalesce
Formed of acute suppuration
Basal, often mutlilobar and frequently bilateral

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13
Q

Lobar pneumonia morphology

A

consolidation of an entire lobe

Stages:
Congestion - vascular engorgement, cell-poor intra-alveolar fluid with bacteria
Red hepatization - robust exudate with neutrophils, erythrocytes, fibrin
Grey hepatization - fibrinosuppurative material, erythrocyte disintegration, early organization
Resolution - organizing fibrosis admixed with macrophages

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14
Q

Clinical course of CAP

A

Abrupt fever, shaking chills, productive cough - rust colored sputum

Lobar: CXR opaque lobe
Bronchopneumonia: CXR focal opacities

Abx: culture and sensitivity

Complications:
Abscess
Empyema - pleural involvement
Bacteremia

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15
Q

Community acquired Viral pneumonia - organisms, predisposing factors

A 
Influenza A, B, C
RSV
Human metapneumovirus
Adenovirus
rhinoviruses

Predisposing factors:
Very young, elderly
Malnutrition/alcoholism
Chronic disease

Inflammation and damage to ciliary mechanism –> bacterial superinfection

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16
Q

Influenza A virus

A

Virus virulence factors (Ab response targets):
Hemagglutinin (H1-H3) bind to respiratory epithelial cells allowing cellular infection

Neuraminidase (N1-N2) - allows release of newly created virions

Genome: 8 RNA segments

Viral RNA polymerase lacks error detection –> antigenic drift

Recombination of segment genome when connected with different types
-antigenic shift leading to new strain –> pandemic

17
Q

Influenza virus infection morphology

A 
Upper respiratory tract
Infects respiratory epithelium causing:
-Intraalveolar fluid accumulation
-cell death
-inflammation

Lung infection patchy or extensive

Vascular congestion
Inflammation in alveolar wall interstitial tissue
-edema
-lymphocytes and macrophages

18
Q

Influenza virus clinical course

A

variable

Extent of disease affected by:

  • Host immune status
  • Virulence of strain
  • presence/absence of other complicating conditions
19
Q

Histoplasma capsulatum

A

intracellular fungal pathogen
Inhaled soil particles contaminated with bird/bat droppings

US: endemic along Mississippi and Ohio rivers - much of the Midwest

Targets macrophages

20
Q

Histoplasmosis clinical course

A

Self-limited pulmonary infection

Chronic, progressive lung infection

  • apical
  • night sweats, fever, coughing

extra pulmonary involvement
-liver, adrenal glands, mediastinum, meninges

wide dissemination

21
Q

Histoplasmosis morphology

A

Granulomas - often caseating

May coalesce and consolidate lung focally or form cavities

resolve and form nodular calcified scars

Silver stain: 3-5 um yeast

Disseminated disease: within clusters of macrophages, caveating granulomas not seen

22
Q

Blastomyces dermatiditis

A

soil dwelling dimorphic fungus

Central and Southern US

In tissue form 5-15 um yeast with double wall and visible nucleus

Broad Based Budding

Forms granulomas with superimposed suppuration

May resolve spontaneously

23
Q

Pulmonary blastomycosis

A

productive cough, chest pain
headache
Anorexia, weight loss, fever, chills, night sweats

24
Q

Coccidioides immitis

A

Southwest US

Infective form - arthroconidia which are inhaled

Taken up by macrophages - resist intracellular killing

Lung granulomas - giant cells containing large spherules (20-60um) filled with endospores

Rupture of spherules may induce recruitment of neutorphils

25
Q

Coccidiomycosis

A

subclinical and self limiting

Minority: San Joaquin Valley Fever
-fever, cough, detectable lung granulomas, pleuritic pain, skin lesions - erythema nodosum, erythema multiforme

26
Q

Etiologic factors and incidence of lung carcinomas

A

Most between 40-70 yo, peak 50s-60s

Smoking:

  • direct relationship between cancer frequency and pack-year history
  • genetically susceptible to tobacco smoke - polymorphisms of CYP450 mono-oxygenase

Environmental exposure:
-Asbestos, uranium, vinyl chloride

27
Q

Squamous cell carcinoma

A

Strong association with tobacco smoke

p53 mutations and over expression

preceded in bronchial epithelium by squamous metaplasia, dysplasia, CIS

Often arise in central lung/hilar region

28
Q

Adenocarcinoma

A

Smokers or nonsmokers
likely peripheral

Gain of function mutations:
EGFR, ALK, ROS, MET, RET, KRAS

Precursor lesions:

  • atypical adenomatous hyperplasia (less than or = 5mm)
  • adenocarcinoma in situ (less than 3 cm) - cells are more atypical and may be mutinous

Invasive positive TTF-1 staining for lung origin (primary site, rather than mets)

29
Q

Small cell carcinoma

A

Strongest association with smoking

TP53 and RB mutations

Aggressive, very high fatality rate

Central or peripheral, likely from neuroendocrine cells in bronchial epithelium
-Immunostains for chromogranin, synpatophysin, CD57+

Tumor cells small, little cytoplasm, closely arranged with “molding” and absent nuclei

Cells grow in clusters without architectural pattern

Marked necrosis

30
Q

Metastatic carcinoma of lung

A

Any type of lung CA may spread to pleural space

Spread hematogenously or within lymphatics
-mediastinal, bronchial, paratracheal nodes

Mets to:
Adrenal glands, liver, brain, bone

31
Q

Carcinoid tumor

A

arise from bronchial neuroendocrine cells
-neuroendocrine tumorlets, carcinoid tumors, small cell carcinoma

under 40 yo

Low grade malignant neoplasm - typical and atypical forms

32
Q

carcinoid tumor morphology

A

central or peripheral
-central carcinoids protrude into bronchial lumen

organoid Nexus of regular cells
-moderately abundant cytoplasm and regular round nuclei

Atypical carcinoids show cell variability and higher mitotic activity
-invade lymphatic vessels

33
Q

Carcinoid tumor clinical course

A

symptoms related to bronchial obstruction
-coughing, hemoptysis, impaired drainage

Carcinoid syndrome - tumors secreting vasoactive amines (serotonin):
Flushing
Diarrhea
Cyanosis

95% 5 year survival for typical carcinoids
70% for atypicals

34
Q

Tumors metastatic TO the lung

A

most common site of tumor mets

via blood or lymphatics

Growth pattern is multiple, scattered nodules

Common primary sites:
Breast, colon, kidney, prostate, urinary bladder

35
Q

Malignant mesothelioma

A

asbestos exposure NOT compounded by smoking

homozygous deletion of p16

arises in visceral or parietal pleura, spreads to pleural space –> ensheathing and compressing lung

May invade adjacent thoracic structures

36
Q

Malignant mesothelioma morphology and course

A

epithelioid and sarcomatoid types

IHC differentiates MM from adenocarcinoma

Present with CP, dyspnea, recurrent pleural effusions

Concurrent asbestos-related interstitial fibrosis

1 yr survival 50%, most do not survive 2 years

Respiratory Medicine Midterm (11 decks)

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