Unit 4 - Wk 8 Pathology

Front 1

Airspace disease

Back 1

Alveoli fill with fluid or exudate (displacing the air within them).
Areas of alveolar filling appear dense, white and radio opaque.

Front 2

Consolidation

Back 2

Means the lobe of the lung is essentially airless (as the alveoli are filled with inflammatory exudate).

Front 3

Air Bronchogram

Back 3

The larger central airways (still filled with air)
are surrounded by dense lung tissue and
stand out in bold relief

Front 4

What structures are included in the pulmonary interstitium?

Back 4

It includes the alveolar walls, interlobular septa and the peribronchovascular interstitium.

Front 5

Interstitial Lung Disease

Back 5

While the majority of these disorders do affect the airspaces, the predominant abnormality is thickening of the interstitium which may be due to the accumulation of fluid, cells or fibrous tissue.

(inflammation, infection,, fibrosis, fluid)

Front 6

Back 6

Normal

Front 7

Back 7

Lung metastases

Front 8

Back 8

Metastases from renal cell cancer

Front 9

Back 9

Thymoma. A chest x-ray (A) reveals an unusual contour over the right hilum That the hilum is not obscured (no silhouette sign) indicates that the mass must either be in front of or behind the hilum. If filling-in of the space behind the top of the sternum and the ascending aorta is seen, you are most likely dealing with an anterior mediastinal lesion.

Front 10

Differential diagnosis of mediastinal masses

Back 10

Back 11

Thymoma. A chest x-ray (A) reveals an unusual contour over the right hilum That the hilum is not obscured (no silhouette sign) indicates that the mass must either be in front of or behind the hilum. If filling-in of the space behind the top of the sternum and the ascending aorta is seen, you are most likely dealing with an anterior mediastinal lesion.
A computed tomography scan (B) reveals a soft tissue mass (arrow) just to the right of the aorta. This is the most common location of a thymoma.

Front 12

Back 12

Thymoma. A chest x-ray (A) reveals an unusual contour over the right hilum That the hilum is not obscured (no silhouette sign) indicates that the mass must either be in front of or behind the hilum. If filling-in of the space behind the top of the sternum and the ascending aorta is seen, you are most likely dealing with an anterior mediastinal lesion.
A computed tomography scan (B) reveals a soft tissue mass (arrow) just to the right of the aorta. This is the most common location of a thymoma.

Front 13

Back 13

Sarcoid; marked lymphatnopathy is seen in the region of both hila in the right paratracheal region

Front 14

Back 14

Lymphadenopathy at both hila; transverse contrast enhanced computer tomography scan of the upper chest

Front 15

Back 15

(PULMONARY PARENCHYMAL FIBROSIS) Asbestosis tends to be prominent in the lower lobes and in the subpleural areas. When disease is advanced, the lungs are small, streaks of fibrosis outline lobar and interlobar septa, and the visceral pleura is invariably thickened. "Honeycombing" may be prominent subpleurally and in the lower lobes. Pleural plaques are distinctive, smooth, white, raised, irregular lesions usually found on the parietal and rarely on the visceral pleura. They may vary from small to extensive (up to 50 cm2) and are usually nonadherent. Common sites are the posterolateral mid-lung zones, where they may follow the rib contour, and on the diaphragm.

Front 16

Back 16

The reticular pattern of end-stage fibrotic (honeycomb) lung is characterized by cystic airspaces surrounded by irregular walls. The distortion of normal lung morphology by extensive fibrosis results in irregular dilatation of segmental and subsegmental airways (traction bronchiectasis); in the periphery of the lung, it can be difficult to distinguish dilated airways from true honeycomb change.

Front 17

Back 17

fine reticular lines in both lower lobes suggestive of interstitial pneumoniae

Front 18

Back 18

Early findings of congestive heart failure. The major signs on upright posteroanterior chest x-ray (A) are cardiomegaly and redistribution of the pulmonary vascularity. Normally the vessels to the lower lobes are more prominent than those in the upper lobes; however, here they appear at least equally prominent. On a close-up view (B), small horizontal lines can be seen at the very periphery of the lung (arrows). These are known as Kerley B lines and represent fluid in the interlobular septa.

Front 19

Back 19

CT scan thorax with IV contrast , axial image Lung window of a patient with cardiac failure. CT scan shows bilateral pleural effusions (red arrows), and interlobular septal thickening ( yellow circles and yellow arrow heads) in keeping with pulmonary edema.

Front 20

DiGeorge's Syndrome

Back 20

DiGeorge Syndrome, also called congenital thymic aplasia, is caused by a
deletion in chromosome 22q11.2. A transcription factor called TBX1 (T box-1) is
encoded within this deleted chromosomal region. Mutations in the gene that encodes
TBX1 result in a similar defect in thymic development. In both cases, there is a
selective T cell deficiency which makes these patients susceptible to: viral infections
due to a lack in CTLs; mycobacterial infections due to a deficiency in cytokines from
TH1 cells, like IFN-γ, that are required for macrophage activation; and some fungal infections (Pneumocystis
jiroveci), also due to a deficiency in T-dependent responses.

Front 21

Double Negative Thymocytes

Back 21

Do not express CD4 or CD8; they are about to start rearranging the TCRB chain locus

Front 22

Double Positive

Back 22

Cd4+ and Cd8+

Front 23

Positive Selection

Back 23

While they are in the thymic cortex, double-positive thymocytes must bind self-MHC with self-peptides
on the cortical epithelial cells at least weakly or they will undergo apoptosis.

Front 24

Why are Ig levels decreased in DiGeorge's syndrome?

Back 24

Decreased in severe dz bc a lack of T cell help for T-dependent antibody response

Front 25

Association of thymic disorders with myasthenia gravis

Back 25

Mh is a NMJ dz; associated with thymic hyperplasia or thymoma

Front 26

Where does pleural fluid originate from?

Back 26

Systemic vessels of the pleural membranes, specifically the lymphatics of the parietal pleura

Front 27

Which pleural membrane is more important for normal pleural fluid formation?

Back 27

Parietal

Front 28

Back 28

P = visceral pleural
F = fibrous supporting tissue
S = fibrous septa
M = mesothelial cells
L = lymph vessels

Front 29

Pleural Cavity

Back 29

Front 30

Transudative Effusion

Back 30

Alterations in hydrostatic or oncotic pressure (without altering pleural permeability); MCM = heart failure but also cirrhosis or nephrotic syndrome

Front 31

Exudative Effusions

Back 31

Secondary to processes that result in increased capillary permeability; MANY causes including pneumoniae, cancer, embolism, viral infection, TB

Front 32

Chylous Effusion

Back 32

Milky white effusion; commonly due to neoplastic damage to thoracic duct

Front 33

Empyema

Back 33

Pus in pleural space

Front 34

Hemothorax

Back 34

Pleural fluid hematocrit greater than 50% of peripheral blood hematocrit; bloody fluid in pleural space

Front 35

Iatrogenic Effusion

Back 35

May be due to feeding tube or CVP perforating SVC; results in infusion of IV oslution or tube feedings into the pleural space

Front 36

Pleuritic Chest Pain

Back 36

Pain or discomfort that worsens on inspiration; can indicate inflammation of parietal pleura

Pain location can be over site of inflammation or referred to neck, shoulder, abdomen

Front 37

What symptoms indicate pleural effusion

Back 37

Pleuritic Pain (bc inspiration is compressing pleural fluid); unexplained dyspnea

cxr confirms

Front 38

Back 38

Normal chest xray

Front 39

Back 39

Large right pleural effusion

Front 40

Back 40

Interstitial pulmonary edema secondary to left heart failure' small left pleural effusion

Front 41

Pale yellow/straw colored pleural fluid

Back 41

Transudate

Front 42

Red pleural fluid

Back 42

Blood; due to malignancy, trauma, pulm infarct

Front 43

White (milky) pleural fluid

Back 43

Chylothorax/chylous pleural effusion

Front 44

Putrid odor to pleural fluid

Back 44

Anaerobic empyema

Front 45

Turbid pleural fluid

Back 45

Inflammatory exudate

Front 46

High lipid content pleural fluid

Back 46

Chylothorax

Front 47

Characteristics of mycobacterium

Back 47

Nonspore forming, aerobic rods
Complex lipid rich cell wall
Acid fast staining

Front 48

Sequence of events in primary pulmonary tuburculosis

Back 48

A. Time frame of first 3 weeks
B. Time frame greater than 3 weeks

Front 49

Which cells are mainly infected in TB

Back 49

Macrophages; early infection = unchecked proliferation. Late infection = macrophage stops proliferation and caseous granulomas develop

Front 50

What happens 3 weeks after a TB infection?

Back 50

Approximately 3 weeks after the infection a T helper (TH1) response develops and activates the macrophages
Mycobacterial antigens enter the draining lymph node and are displayed to T cells initiating the response


TH1 cells in the lymph nodes and lung produce IFN gamma
INF gamma stimulates the formation of the phagolysosome in the infected macrophages and is therefore critical in enabling the macrophage to control the TB infection


The TH1 response is also involved with granuloma formation and the development of caseous necrosis
Macrophages stimulated by IFN gamma can differentiate into “epithelioid histiocytes” which can then fuse to form giant cells
Activated macrophages also secrete TNF which can result in the recruitment of additional monocytes

The reactivation of infection or reexposure to the organism in a previously sensitized host results in a rapid immunological response but can also cause significant tissue destruction

Front 51

Primary Tuberculosis

Back 51

Develops in individuals who are previously unexposed

Elderly and immunosuppressed who lose immunity can develop primary TB again

Front 52

Secondary Tuberculosis

Back 52

Develops in previously sensitized hosts; reactivation of latent infection; exogenous reinfection

Classically involves the apices of the upper lobes of on eor both lungs

Brisk reactoin due to preexisting hypersensitivity and cavitation can readily occur; can result in erosion of the cavity airway causing increased infectivity through coughing of infected sputum

Front 53

Back 53

Ghon Complex; area of gray/white inflammation; combination of parenchymal lung lesion and nodal involvement; usually undergoes fibrosis; radiologically detectable as calcification

Front 54

Back 54

A and B: Tubercle. Note the central caseation and the surrounding epithelioid and multinucleated giant cells. This is the normal response seen in those who have cell-mediated immunity.
C: This is a tubercle without caseation
D) This is an example of a reaction in an immunosuppressed patient (without cellular immunity) – note sheets of macrophages packed with mycobacteria.

Front 55

Back 55

The initial lesion is typically an area of consolidation less than 2 cm diameter that is located within 1-2 cm of the apical pleura
; may heal w fibrosis or dz may progress

Front 56

Scrofula

Back 56

Tb involvement of hte cervical region

Front 57

Intestinal TB

Back 57

Swallowing of coughed up infectious material

Front 58

Potts disease

Back 58

Tb infection of vertebrae

Front 59

Back 59

Miliary TB involving the spleen; the cut surface shows gray white tubercles

Back 60

Acid fast stain; red rods of TB

Back 61

Acid fast stain; red rods of TB

Front 62

Back 62

Egg based mycobacterial culture; dry, granular, buff colored colonies