Ward- Acute/chronic Inflammation Part 2

Front 1

_______ inflammation is marked by the outpouring of a thin fluid that is derived from either the plasma or secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities (called _______).

Back 1

Serous
effusion

Front 2

You can't see a virus in a light microscope, but you CAN see _______ caused by homogenized DNA

Back 2

inclusions

Front 3

Another name for serous inflammation above the basal layer of cell

Back 3

Suprabasal bullae
or
Intraepidermal bullae

Front 4

More severe injuries leave room for ______ to come out of bvs, that turns into ______. If it organizes, the exudate can turn to _______

Back 4

fibrinogen
fibrin
collagen (scar tissue)

Front 5

Bread and butter appearance of the heart is indicative of what inflammatory morphology?

Back 5

Fibrinous effusion - diagnostic of pericarditis

Front 6

What cells are almost always present in fibrillar effusion?

Back 6

Neutrophils (but you can also get fibrillar with a neutropenia)

Front 7

Exudate consisting of neutrophils, necrotic cells, and edema fluid is characteristic of what morphological pattern of inflammation?

Back 7

Suppurative or Purulent inflammation

Front 8

What type of bacteria is best known for it's pyogenic (pus-producing) capabilities?

Back 8

Staphylococcus

Front 9

Staph is a deep seeding bacteria so it causes _________ - localized collections of purulent tissue

Back 9

Abscesses

Front 10

An abscess has a central region of what?
What lines the center?
What is beyond that lining which indicates attempted repair and/or walling off?

Back 10

mass of necrotic leukocytes and tissue cells
zone of preserved neutrophils vascular dilation and parenchymal and fibroblastic proliferation occur

Front 11

One example of a purulent inflammatory reaction occurs from the bacteria ________, which is often misdiagnosed as fungus because of the formation

Back 11

Actinomyces

Front 12

What is a local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing of inflammatory necrotic tissue

Back 12

ulcerative inflammation

Front 13

Chronic reaction to ulcer: the ulcer develops _______ proliferation, scarring, and the accumulation of lymphocytes, _________, and plasma cells.

Back 13

fibroblastic
macrophages

Front 14

Ulcerative inflammation has both acute and chronic inflammation. Why?

Back 14

Epithelium worn out so acute at the exposed site, develops to chronic

Front 15

AML, drugs, irradiation, chediak-higashi syndrome, and mets? can all cause a defect in what part of the immune response?

Back 15

PMN production

Front 16

Diabetes, alcohol, steroids, beta chain of integrins can all lead to problems in what part of the immune response?

Back 16

Adherence

Front 17

Diabetes and immunodeficiencies can both lead to what problem in the immune system?

Back 17

Defective chemotaxis

Front 18

Diabetes, decreased immunoglobulin and decreased protein C (PSPB), and chediak-higashi syndrome all lead to defective what?

Back 18

phagocytosis

Front 19

MPO deficiency, chronic granulomatous disease, severe G6PD deficiency all lead to problems in what?

Back 19

Killing

Front 20

What genetic defect disease results in decreased oxidative burst (killing)?

Back 20

Chronic granulomatous disease
Recurrent bacterial infections are key to diagnosing the disease

Front 21

What enzyme is hereditarily defected in CGD patients?

Back 21

X-linked
NADPH oxidase

Front 22

There are 2 forms of CGD: X-linked which effects the _____-bound component and autosomal ______ which requires having 2 copies to functionally stop cytoplasmic components

Back 22

membrane
recessive

Front 23

Nitroblue Tetrazolium test: Increased NBT reduction implies ______ metabolic activity in the shunt

Back 23

Increased - so black pigment in normal neutrophils, none in neutrophils that don't convert NADPH to NADP

Front 24

CGD Pathogenic Organisms:
Staphylococci
Enteric organisms: _____, serratia, slamonella
Fungi: ______, aspergillus
NOTE: NO VIRUSES and NOT STREP

Back 24

E. Coli
Candida

Front 25

E. Coli produces some H202 but it also produces some _____ to break it down so in CGD patients it is able to survive in a phagolysosome. ______ produces H202 but no ________ so it gets rid of itself.

Back 25

catalase
Strep
catalase

Front 26

Organs involved in CGD: Membranes include skin, GIT, lungs. What part of the RES?

Back 26

liver

Front 27

2 histo things associated with CGD:
_______ inflammation with necrosis
Necrotizing _________ lesions

Back 27

suppurative
granulomatoid (invasive, half-assed granuloma... can have many giant cells)

Front 28

In severe G6PD deficiency you can't make _____, so essentially it is the same lesion as CGD. Pentose phosphate shunt blocked

Back 28

NADPH

Front 29

Severe G6PD has a:
More _____ defect (hemolytic anemia) and
_____ onset compared to CGD.
However, same net result - failure of resp burst and reduction in O2 dep killing.

Back 29

severe
later/delayed

Front 30

Exogenous bacterial products lead to endogenous release of ___ and ___ by WBC. This causes an increase in cyclooxygenase.

Back 30

IL-1, TNF (and IL-6 I think)

Front 31

An increase of cyclooxygenase leads to more _________ ____which can be converted to PGE2 (prostaglandin 2)

Back 31

arachidonic acid

Front 32

____ stimulates production of cyclic AMP which resets the temperature set point to avoid fever

Back 32

PGE2 (prostaglandin 2)

Front 33

NSAID and aspirin inhibit ________, thereby blocking PGE2 synthesis

Back 33

cyclooxygenase

Front 34

Pyrogens must reach the hypothalamus. This is done in 2 ways

Back 34

Cross BBB
Acquire access in regions lacking BBB

Front 35

Initiation of fever is marked by __ _____ increasing, vaso______in skin, shivering
Then plateau reached, shivering stops
Resolution - __ _____ decreases, vaso______ in skin, sweating

Back 35

set point
constriction
set point
dilation

Front 36

In acute phase reaction, the liver starts pumping out proteins: CRP and fibrinogen upregulated by ___, Serum albumin A upregulated by __ or ___

Back 36

IL-6
IL-1 or TNF

Front 37

CRP and SAA may act as _____ for capsulated bacteria

Back 37

opsonins

Front 38

Increased fibrinogen causes _____ formation

Back 38

rouleaux - strings

Front 39

Increased CRP levels in blood may indicate what?

Back 39

Imminent MI in patients with CAD because it measures inflammation (atherosclerosis)

Front 40

Prolonged SAA (serum albumin amyloidosis) causes what?

Back 40

secondary amyloidosis
ex: bronchiectasis, osteomyelitis, arthritis