Pathoma - Respiratory Pathology Flashcards Preview

STEP 1 STUFF > Pathoma - Respiratory Pathology > Flashcards

Flashcards in Pathoma - Respiratory Pathology Deck (36)
Loading flashcards...
1
Q

allergic rhinitis

A

type I hypersensitivity reaction
inflammatory infiltrate with eosinophil
associated with asthma and eczema

2
Q

consequence of allergic rhinitis

A
  • nasal polyps occur in response to repeated bouts of rhinitis.

polyp is edematous inflamed nasal mucosa

3
Q

child with nasal polyps consider…

A

cystic fibrosis

4
Q

aspirin intolerant asthma

A

nasal polyps
aspirin induced bronchospasm
asthma

– triad, seen in 10 percent of asthamtic adults

5
Q

angiofibroma
pathology
presentation
epidemiology

A

benign tumor of the nasal mucosa, consists of large vessels and fibrous tissue.
seen in adolescent males
presents with profuse epistaxis

6
Q

Nasopharyngeal carcinoma

  • associated virus
  • epidemiology
  • histology
A
  • malignant tumor of nasopharyngeal epithelium
  • associated with EBV.
  • classically seen in african children and asian young adults.
  • will often present with involvement of the cervical lymph nodes. biopsy will show pleomorphic epithelial cells in the background of lymphocytes.
  • -> stain for keratin to determine presence of epithelial cells.
7
Q

Acute epiglottitis

- most common cause

A

H. Flu type B

8
Q

Acute epiglottitis - presentation

A
high fever 
sore throat 
drooling 
dysphagia 
muffled voice 
inspiratory stridor
9
Q

Laryngotracheobronchitis - AKA

A

Croup

10
Q

Laryngotracheobronchitis - most common cause

A

para influenza virus
hoarse barking cough
inspiratory stridor

11
Q

vocal cord nodules due to…

A

excessive use

myxoid degeneration of connective tissue

12
Q

laryngeal papilloma

  • associated virus
  • presentation adult vs child
A

due to HPV 6 and 11
- benign tumor.

presents usually as single lesion in adult but multiple lesions in child.

13
Q

laryngeal carcinoma

  • origin
  • presentation
  • risk factors
A

squamous cell carcinoma arising from lining of vocal cord.

  • presents with hoarseness, sometimes cough and stridor.
  • risk factors are alcohol and tobacco use
14
Q

pneumonia physical exam -
breath sounds?
percussion?

A

decreased breath sounds

dullness to percussion

15
Q

Chemical mediators of pleuritic chest pain in pneumonia

A

bradykinin

prostaglandin E2

16
Q

Reid index

A

thickness of mucus glands relative to bronchial wall thickness. > 50 percent Reid index in chronic bronchitis, < 40 percent is normal.

17
Q

PiZ mutation

A

most common clinically relevant mutation of alpha-1- antitrypsin deficiency. results in significantly low levels of circulating A1AT.

18
Q

PiMZ mutation

A

heterozygotes, usually asymptomatic. decreased circulating levels of A1AT. BUT there is a significant risk of emphysema with smoking.

19
Q

Pathophysiology of A1AT

A

accumulation of misfolded, mutated AIAT protein in ENDOPLASMIC RETICULUM of hapatocytes. stains pink, PAS +.

20
Q

PiZZ

A

significant risk for panacinar emphysema and cirrhosis. Homozygous for mutant protein.

21
Q

FRC in emphysema

A
  • FRC is increased as recoil of the lung is lost. Increased AP diameter.
22
Q

Pathogenesis of asthma

A

In genetically susceptible individuals, Th2 cells are activated and release
IL-4 - induces class switching of plasma cell to IgE
IL-5 - recruits eosinophils
Il-10 - ability to inhibit the production of Th1 helper T-cells, and stimulates Th2 (promotes this overall reaction)

  • upon rexposure to the allergen there is cross linking of mast cell (IgE) stimulating dumping of preformed histamine granules. This leads to histamine induced vasodilation and histamine induced vascular permeability. This is the early phase.

The second phase by which inflammation is perpetuated is by leukotriene C4, D4, E4 (arachdonic acid metabolite). This causes vasoconstriction, increased vascular permeability by constricting pericytes, and broncho constriction by constricting smooth muscle of the bronchus. –> take away point is that there is bronchoconstriction.

23
Q

Charcot-Leyden crystals

A
  • derived from eosinophils. can be seen in microscopy of the sputum.
24
Q

Patients at risk for bronchiectasis

A
cystic fibrosis 
kartagener syndrome 
tumor or foreign body
necrotizing infection 
allergic bronchopulmonary aspergillosis
25
Q

bronchiectasis

A
  • permanent dilation of the bronchioles and the bronchi. Due to necrotizing inflammation with damage to airway walls. As a result loss of airway tone results in air trapping.
26
Q

Pathophysiology of idiopathic pulmonary fibrosis

A

TGF-beta released from cyclical injury of pneumocytes that induces fibrosis.

interstitial pulmonary fibrosis can be caused by medications (classically bleomycin or amiodarone) or radiation. rule these out as causes first.

  • but we dont know what causes the cyclical damage, idiopathic.
27
Q

pneumoconioses

A

interstitial fibrosis due to occupational exposure to small particles that are fibrogenic.

  • induced by macrophage engulfing a very small particle.
28
Q

pneumoconioses examples

A
  • Coal workers pneumoconiosis from carbon dust
  • silicosis seen in sand blasters and silica miners. –> fibrotic nodules in the upper lobe of the lung. resides in macrophages preventing phagolysosome formation. increases risk for TB.
  • asbestosis from asbestos fibers seen in construction workers, plumbers, and shipyard workers. Increased risk of lung cancer. Pts with mesothelioma are more likely to get lung cancer than mesothelioma.
  • -> look for asbestos bodies long brown rods in the sample.
  • berylliosis beryllium seen in beryllium miners and workers in the aerospace industry –> forms non-caseating granulomas of the lung, hilar lymph nodes and other organs (do not confuse with sarcoidosis).
29
Q

Sarcoidosis pathophysiology

A

Non-caseating granulomas of multiple organs.

- grnaulomas most commonly involve the hilar lymph node and the lung leading to restricitve lung disease.

30
Q

Sarcoidosis other organs involved

A
  • uvea (uveitis)
  • skin (erythema nodosum)
  • salivary and lacrimal glands mimicking sjogrens syndrome
31
Q

Sarcoidosis clinical features

A
  • dyspnea or cough
  • elevated serum ACE
  • hypercalcemia (1-alpha hydroxylase activity of the epithelioid histiocytes converts Vitamin D to its active form)
32
Q

Hypersensitivity pneumonitis

A

pigeon breeders lung

  • presents with fever, cough, dyspnea hours after the exposure.
  • -> will see eosinophils since this is a hypersensitivity reaction.
  • symptoms resolve when the antigen is removed
  • with chronic exposure can get interstitial fibrosis leading to restrictive pattern.
33
Q

Primary pulmonary hypertension

A
  • etiology is unknown mostly
  • SOME FAMILIAL forms are related to a mutations of BMPR2 leading to proliferation of vascular smooth muscle and pulmonary hypertension.
34
Q

Plexiform lesions

A

are seen with severe long standing pulmonary hypertension. They are bundles of capillaries.

35
Q

ARDS Pathophysiology

A

damage to alveolar capillary interface leads to leakage of protein and formation of hyaline membrane around the air sac.

  • -> thickened diffusion barrier
  • -> increased surface tension of alveolar air sac leading to collapse of the lung.
  • recovery can be complicated by interstitial fibrosis due to loss of type pneumocytes (the stem cell of the alveoli).
36
Q

Cancers of the lung chart on page 96

A

see page 96 pathoma