LAB - Infectious Disease A, B, C, and D Flashcards Preview

Pathology - Quiz 2 > LAB - Infectious Disease A, B, C, and D > Flashcards

Flashcards in LAB - Infectious Disease A, B, C, and D Deck (16)
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1

Acute appendicitis: what changes are seen? (4) what layers are found in the normal appendix? (5)

Changes:
--Infiltration of neutrophils: can extend from mucosa all the way down to serosa
--Ulceration of mucosa
--Subserosal edema (white space between muscularis and serosa) with infiltration of neutrophils (and sometimes eosinophils)
--Edema/infiltrate pulling apart muscularis layer, infiltrating in between muscle layers

Layers:
Mucosa (normally has some lymphocytes)
Submucosa
Submucosal fat
Muscularis
Serosa: thin layer of flattened/low cuboidal cells

2

Acute pyelonephritis: what can cause this? what changes are seen? (7)

Causes: ascension of a bacterial infection from the bladder

Changes:
--Hypercellular, blue stripes/bands seen at low power
--Leukocytes in interstitium (between tubules, glomeruli, vascular elements)
--Tissue elements in stripes harder to recognize because of necrosis
--See lakes of NEUTROPHILS, MOs, necrotic debris
--Tubules filled with neutrophils, killed off
--Bacteria seen as basophilic haze
--Creation of pus-filled abscess over time

3

Acute pleuritis with empyema: what can cause this? what changes are seen in the lung (2), pleura (1), and outside of the pleura (5)?

Causes: initial insult = aspiration of mixed population of bacteria from mouth/respiratory tract (breathing in large amounts of spit/vomit)
--Initial inflammatory process + actions of bacteria -> destruction of tissue -> bacterial abscess -> pleuritis/empyema

Changes:
--Lung edematous
--Some alveolar spaces empty, others full of infiltrate and neutrophils (looks like very thick walls, but isn't)

--Pleura -> granulation tissue to wall off abscess (thin walled capillaries, highly activated fibroblasts, active endothelial cells)
----[Normal pleura = thin layer of cuboidal epithelium]

--Outside of pleura = PUS (neutrophils, inflammatory debris, bacteria, fibrin deposition [pinkish material])

--Outside of pus = hypocellular area
----Bacteria! (basophilic clumps)
----Few neutrophils/inflammatory cells
----Lots of inflammatory debris
----Polymerized fibrin (pink, lacy) from fibrin that leaked from blood vessels

4

Acute bacterial pneumonia in neonate: what can cause this? what changes are seen? (3)

Causes: bacterial infection in neonate

Changes:
--Fibrin accumulations (pink stringy/clumpy stuff)
--Sparse inflammatory infiltrate: few neutrophils/MOs
--Lots of hemorrhage (seen in lungs of neonates with inflammation)

5

Acute bacterial endocarditis: what can cause this? what changes are seen? (6)

Cause: Staphylococcus aureus

Changes:
--Tons of fibrin, bacteria (purple) and inflammatory cells
--Normal valve tissue = pink (lots of collagen)
----Mostly dissolved by inflammatory process
--May have vegetations hanging off the side or detached
--Granulation tissue forming between the valve and the myocardium
--Vegetation: LOTS of FIBRIN, degenerating leukocytes, bacteria

6

Acute mycotic aneurysm: what can cause this? what changes are seen?

Cause: primary site of Aspargillis fungal infection in lung -> pieces break off, go through LV -> circulation -> brain (in this example)
--Aspargillis loves to grow through vessel wall -> thrombosis
--Mycotic aneurysms can be of fungal, yeast, OR bacterial nature

Changes: (in immunosuppressed patient)
--Thrombus in vessel
--Neutrophils at inner surface of vessel where thrombus meets wall
--Blood vessel wall ballooned out, quite massive, purple
----Layered fibrin accumulates in ballooned out portion
--Vessel wall (smooth muscle) being infiltrated by densely packed hyphae of fungus
--Vessel wall dead
--Neutrophils attacking hyphae

7

Bacterial pneumonia: what can cause this? what changes are seen? (8ish)

Cause: Pneumococcus

Changes: hyperemia, then HEPATIZATION (lung firm, looks like liver)

Red hepatization stage: (first)
--Hyperemia with hemorrhage as capillaries lose integrity
--Edema - alveolar spaces full of eosinophilic fluid
--Tons of RBCs, fibrin
--Congested capillaries

Gray hepatization stage: (second)
--Lung firm, looks like liver
--Massive leukocyte (neutrophil) infiltration after RBCs break down
--Alveolar spaces filled with neutrophils and fibrin, NOT many RBCs or bacteria
--Very congested capillaries

8

Septic emboli of kidney: what can cause this? what changes are seen? (6)

Cause: fragments of vegetation from endocarditis vegetations can break off lodge in blood vessels

Changes:
--Changes seen in GLOMERULI
--Most glomeruli look deep blue
--Some glomeruli totally broken down, replaced with tons of neutrophils and bacteria as well as fibrin
--Some glomeruli have large blue dots = colonies of bacteria
--Bowman's capsules filled with neutrophils, which then dissolve glomeruli
--MICROABSCESSES can form: highly eosinophilic necrosis surrounded by neutrophils and bacteria

9

Opportunistic fungal infection of the lung: what can cause this? what changes are seen? (3)

Cause: severe immunosuppression
--Aspargillis: INFARCTION -> DEAD TISSUE -> FUNGUS FOOD in multiple organs

Changes:
--Extremely extensive necrosis, no normal parenchyma of lung
--45 degree branching hyphae of Aspargillis: kills lung tissue via infarction, then uses it as its culture medium
--Very little/no immune response

10

Opportunistic fungal infection of the placenta: what can cause this? what changes are seen? (4)

Cause: immunosuppression

Changes:
--Necrosis -> ghosts of vili
--Outside of placenta (inside embryonic sac), see tons of fungal forms
----Large and thick walled = Aspargillis
----Small and thin walled (pseudohyphae) = Candida

11

Candida infection of the esophagus: what can cause this? what changes are seen? (4)

Cause: severe immunosuppression

Changes:
--Along non-keratinized squamous epithelium, see thin or absent parts (ulcers) with Candida
--Very little inflammatory response (few MOs)
--Candida infiltrating into tissue, extending pseudohyphae
--Greenish-blue dots are the yeast form, or hyphae cut in cross section

12

Typhoid fever in ileum and liver: what can cause this? what changes are seen? (2)

Cause: S. typhi

Changes:
--Erythroid phagocytosis: phagocytes eating RBCs

Liver:
--Small, indistinct typhoid nodules: little areas where the hepatocytes have been replaced by phagocytes, which contain S. typhi

13

Cytomegalovirus infection of kidney: what can cause this? what changes are seen? (3)

Cause: CMV in immunosuppressed patient

Changes:
--Cells that are HUGE with large INTRAnuclear inclusions
--Massively dilated tubules with huge cells in them
--Intranuclear inclusions: dark pink blobs in nucleus, often have clear halo around them

14

Measles pneumonia in lung: what can cause this? what changes are seen? (7)

Cause: measles in a child that -> pneumonia

Changes:
--Large GIANT CELLS scattered throughout lung parenchyma (look for purple dots)
----Giant cells (and some parenchymal cells) have INTRAnuclear eosinophilic inclusions
--Large areas of consolidation with no visible parenchyma
--Thickening/neutrophilic infiltration of alveolar walls (interstitium)
--Bronchioles filled with neutrophils, possibly destroyed
--Proliferating pneumocytes, fibroblasts, and macrophages
--Lots of fibrin debris, hemorrhage

15

HSV hepatitis in liver: what changes are seen? (3)

Changes:
--Mottled appearance -> focal areas of necrosis with congested sinusoids full of RBCs
--In areas with living cells, see amphiphilic (blue and pink) nuclear inclusion bodies
----Chromatin in ring around nucleus, then clear zone around pink viral inclusion body

16

Herpes virus dermatitis in skin: what can cause this? what changes are seen? (2)

Cause: herpes infection of skin

Changes:
--Bulla: fluid-filled cyst on surface where epithelial tissue is lifted up
--At advancing edge of cleft, see herpes intranuclear inclusions: paler than in liver, but still herpes
--In bulla fluid, have shedded cells and proteinaceous fluid