12. Chronic Inflammation II Flashcards

1
Q

Cells in chronic inflam > ____ (neutrophils in acute inflam)

Macro’s need help > T cells

Macro engulfs, and will try to kill it themselves (not very good at it) > produce ____ > present on material of cell on surface > present antigens to T cells > activating ____: neutrophil recruitment and some monocyte; activate Th1: ____ > macrophages (classical); bi-directional mode of activation as long as etiology exists

A

macrophages
cytokines
TH17
IFNgamma

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2
Q

Chronic Sialadentitis

Histo of normal salivary gland in middle

Chronic: foci of ____ cells; stain with trichrome and parts would be blue > destruction, ____, and foci of inflam cells, and fibrosis all going on simultaneously

A

inflam

LOF

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3
Q

Rheumatoid Arthritis

Chronic > pannus formation (___ cells, ___ cells, ___ tissue, ___ connective tissue), and fibrous connective tissue > fibrous ankylosis (___ fused with fibrous tissue), and another example, which involves the use of bony joints

A

proliferating synovial lining
inflammatory
granulation
fibrous

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4
Q

Liver failure > most likely to be ___

A

transudate

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5
Q

Exposed to silica dust particles > lung tissue > normal lung parenchyma replaced with ___ > ___

A

fibrosis

LOF

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6
Q
Granulomatous Inflammation
• Infectious:
– \_\_\_ (Bacterial)
– \_\_\_, Blastomycosis (Fungal)
– \_\_\_ disease (Bacterial)

• Non-Infectious (foreign-body):
– ___, breast prosthesis,
– ___, food particles, ___

• Unknown:
– ___
– Orofacial granulomatosis

How is granulomatous different from non-specific chronic inflammation > in chronic: destruction taking place in a large area

Destruction here doesn’t occur uniformly, you begin to see small nodules

Where the inflam reaction is trying to contain the etiology > make sure that it doesn’t get out of hand

Most etiologic agents for GI are agents that are hard to remove, or agents that are very difficult to digest (macro’s take intracellularly, they can’t and then they induce granulomatous inflammation)

A
tuberculosis
histoplasmosis
crohn
suture
uric acid (gout)
metals

sarcoidosis

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7
Q

Granulomatous Inflammation

  • A distinct pattern of chronic inflammation characterized by the presence of ___
  • A small nodular collection in which the predominant cell is the activated ___
• Epithelioid cells
– Derived from \_\_\_
– \_\_\_ cytoplasm
– Long \_\_\_ nuclei
• Surrounded by a collar of \_\_\_ (and fibroblasts)

Activated macrophage > epithelioid cells > look like epithelial cells (have pink cytoplasm, but unlike epithelial, their nuclei is ___)

A
granulomas
macrophage
macrophages
pink
stringy
"round cells"

string-like

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8
Q

Granulomatous Inflammation

  • Giant Cells:
  • “Committee of ___ cells
  • > ___ um in diameter
  • Abundant Cytoplasm

• Langhan’s type
– ___ or more nuclei in periphery
– “___ pattern”

• Foreign body:
– Nuclei ___
– “___ Pizza”

  • ___ bodies
  • ___ bodies

Giant cells are not always present > base your assessment on presence of ___

When macrophages are trying to rid of inorganic material (suture) > you also see a committee, but arranged in a pepperoni pizza (foreign body)

___ contrition > schaumann body

___ > asteroid body

A
epitheloid
50
20
horse shoe
scattered
pepperoni
schaumann
asteroid

granuloma

calcium
asteroid/star-shaped

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9
Q

You see a lot of ___ in CGD

In biospy of proud flesh > ___ tissue

PA granuloma > chronic inflam ___ tissue

These are all misnomers; when you have a granulomotous inflammation > you see the structure of a physical ___, and not examples like this

These are not examples of ___ inflammation (must have giant cells, epitheliod cells, etc.)

A

neutrophils/macro’s

granulation

granulomatous

granuloma

granuolomatous

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10
Q

Tuberculosis

Tuberculosis:
It is a disease of poverty - people of lower socioeconomic status and overcrowding

◦ Now about 1.7 billion people worldwide have been infected
‣ But infection doesn’t automatically mean ___
• Ex: Septa can be crowded and if infected person with Tuberculosis sneezes around you, you can become ___ but not ___

A

disease
infected
diseased

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11
Q

Tuberculosis

Receptors are present on ___ (not many neutrophils in alveolar space)

Takes in the microbacterium and tries to digest it > MB has something in it that prevents the macrophage from digesting it > ___ is activated, however it is ineffective and you cannot release lysosomal enzymes

The microbes multiply within the phagolysosome, and then released into the ___ > bacteremia seeding into multiple sites; this occurs 1-3 weeks after infection (may have ___ symptoms, or ___)

If ___ immune is not activated in response > trouble

Cell-mediated response tries to now contain bacterium:
___ macro’s present on MHC II > T-cells > Th1 > IFNgamma > ___ > they’re able to kill microbes by producing more chemokines/cytokines > macrophages transform into ___ cells > granuloma > can undergo ___

A
macrophages
phagolysosome
lung
flu-like
asymptomatic

cell-mediated

alveolar
macrophages (classical)
epitheloid
caseation

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12
Q

Tuberculosis

Primary infection takes place in area where microbe’s first lodged and in draining lymph node > ___ > granulomas coalesce > ___ necrosis > ___ complex:
Infected with microbacterium, organisms in lung > alveolar macro’s trying to digest, but bacteria prevent and escape > activate T-cells; granuloma occuring at site of ___ and the ___

If you have a good immune system > T/macro’s > contains the microbe > healing by ___ (this is good, no symptoms or disease, do not want to remove)

Individuals who are infected with HIV/AIDs > defective T-cell number > not able to contain microbe, and the lesion becomes ___ Tb > can occur as a result of reinfection, or reactivation > disease-state >

Can now become progressive and spread to other areas > ___ Tb

No T cells > defense mechanism compromised > cavitation > localized ___ obstructive lesions

Lung biospy > ___ staining to detect organisms > other conditions may mimic symptoms associated with Tb > histoplasmosis, coccidoiodomycosis and blastomycosis > ___ infection

A
caseation
coag
Ghon
nucleation
lymph node

scar

secondary

milliary

caseating

acid-fast
fungal

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13
Q

Histoplasmosis, Coccidiodomycosis and Blastomycosis

• Histoplasmosis:
– Most ___ systemic fungal infection in the US
– ~500,000 new cases every year:
– ___ areas with soil enriched with bird or bat ___
– Fertile river valleys; ___, ___

• Coccidiodomycosis:
– ___ part of the US
– California’s San Joaquin Valley (“___”)

• Blastomycosis:
– Overlap with ___
– Relatively ___ (1/10th of Histoplasmosis)

Top-right > CM
Bottom-left > BM; bigger cell

A
common
humid
excrement
ohio
mississippi

southwestern
valley fever

histoplasmosis
uncommon

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14
Q

Histoplasmosis

• Primary:
– ___ (fever, headache, ___ cough)

• Chronic (granulomatous):
– ___ (less common than primary)
– Similar to ___ (cough, weight loss, fever, weakness)

• Disseminated:
– Spread of infection from lung
– \_\_\_, AIDS
– \_\_\_, GI, liver, \_\_\_
– Commonly affected: \_\_\_, \_\_\_, \_\_\_ mucosa

Ulcerated granular lesion; maxillary buccal vestibule. ___?

Ulceration: Ventral surface of the tongue. ___?

A

self-limited
non-productive

lung
Tb

immunosuppressed
kidneys
oral mucosa
tongue
palate
buccal

cancer
cancer

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15
Q

Histoplasmosis

Diagnosis, Treatment and Prognosis:
• Diagnosis:
– Identification of organism in tissue section or by culture
– Serologic testing: ___

• Primary:
– self-limiting-no ___ required

• Chronic (granulomatous):
– ___/Itraconazole

• Disseminated:
– Death in 80-90 % of \_\_\_ patients, if
untreated
– \_\_\_ then \_\_\_ (daily, 6 – 18 months)
– Despite therapy, mortality rate, (7 -23%)

Medium power: ___ containing organisms (arrows)

High power: yeasts of His. cap ___ stain

A

antibodies

amphotericin B

immuno-suppressed

amphotericin B
itraconazole

macrophages
grocott-gomori methenamine silver

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16
Q

Blastomycosis

• Primary:
– Resemble ___; high fever, chest pain,
night sweats, ___ sputum.

• Chronic (Granulomatous):
– Lung (More ___ than primary)
– Similar to Tb (cough, weight loss, fever, weakness)

• Disseminated:
– Spread of infection from lung
– \_\_\_
– Epithelial hyperplasia (\_\_\_ carcinoma?)
– Oral lesions (from \_\_\_ or local \_\_\_)

rregular ulceration of the tongue:
Chewing ___ “Kentucky field candy”

A

pneumonia
mucopurulent

common

severe cutaneous infection
squamous-cell
lung
inoculation

17
Q

Blastomycosis

Blastomycosis
• Oral lesions (continued…)
– Mass on ___ mucosa

• Diagnosis:
– Identification of organism in tissue section
– Culture specimen from sputum or fresh biopsy material
– ___ testing NOT helpful (lack of specific antibody)
– ___ probe

• Primary:
– self-limiting-no ___ required

• Chronic:
– ___/ Itraconazole

• Disseminated:
– Only occurs in a small percentage of infected patients.
– Prognosis ___ with treatment
– High mortality rate in ___ and patients with AIDS

Presence of ___ cell in high-power

Use ___agents to treat

High power: large yeast of ___. and multinucleated giant cell

A

buccal
serologic
DNA

treatment
amphotericin B

good
immunosuppressed

giant cell
anti-fungals

Blas. Derm.

18
Q

Crohn Disease

• Inflammatory bowel Disease (IBD):
• Ulcerative colitis
– ___ and rectum
– ___ and submucosa

• Crohn Disease
– May involve any are of the \_\_\_ tract
– Transmural
– Abdominal \_\_\_, diarrhea, \_\_\_
– \_\_\_ appearance
– \_\_\_ granuloma

Chron’s > any area of the GI tract > it crosses into the lower layers (___)

Unlike Tb, in Chron’s the granulomas are ___ > do not form cheese-like structure within the granuloma

A
colon
mucosa
GI
cramping
nausea
cobblestone
non-caseating

transmural
non-caseating

19
Q

Crohn Disease

Oral before \_\_\_ lesions in ~30% of cases.
• Swelling of the \_\_\_
• \_\_\_----buccal
mucosa
• \_\_\_ granuloma

If you think it’s Chron’s > ask for ___

A
buccal
lips
cobblestone
non-caseating
symptoms
20
Q

Crohn Disease
Autophagy/Inflammasome/Granulomatous inflammation?

  • Healthy ileum: ___ cells secrete antimicrobial peptides and lysozyme to control intestinal microbiota.
  • ___: cellular homeostatic process in which “autophagosomes” degrade captured proteins and cytoplasmic organelles
  • Loss of autophagy caused by ATG16L1 mutation, fewer granule content
  • Loss of autophagy in macrophages from ATG16L1 mutation results in overproduction of ___

LOA > interaction bt autophagy and inflammasome pathway > autophagy inhibits the ___ pathway

If autophagy is gone > inflammasome is ___ > macrophages produce IL-1b

A

paneth
autophagy
IL-1B

inflammasome
upregulated

21
Q

Granulomatous Inflammation

• Infectious:
– Tuberculosis (Bacterial)
– Histoplasmosis, Blastomycosis (Fungal)
– Crohn disease (Bacterial)

• ___ (foreign-body):
– Suture, breast prosthesis,
– Uric acid (gout), food particles, Metals

• Unknown Etiology: – Sarcoidosis
– Orofacial granulomatosis

A

Non-infectious

22
Q

GRANULOMATOUS INFLAMMATION

Non-infectious (foreign-body): ___

Breast implant leaks > ___ particles > macro’s try to digest and remove, however they are unable to do so > ___ inflam

Silica particles in cross-section; foreign body granuloma, and the giant cells are ___ shaped

A

breast prosthesis
silica
granulomatous
pepperoni

23
Q

GRANULOMATOUS INFLAMMATION (Non-Infectious)

Polarized light: Intravenous drug user (drug mixed with talc)

Cholesterol clefts with associated foreign-body giant cells

Giant cell (___)

___ > cells are dying and they are releasing lipid mediators

A

pepperoni

cholesterol clefts

24
Q
Granulomatous Inflammation
• Infectious:
– Tuberculosis (Bacterial)
– Histoplasmosis, Blastomycosis (Fungal)
– Crohn disease (Bacterial)
• Non-Infectious (foreign-body):
– Suture, breast prosthesis,
– Uric acid (gout), food particles, Metals
• \_\_\_: 
– Sarcoidosis
– Orofacial granulomatosis
A

unknown etiology

25
Q

Sarcoidosis

  • Multi-system disorder of ___ etiology characterized by ___ granulomatous inflammation in many tissues and organs
  • World-wide distribution
  • Age, <40; ___ Americans
  • ___ 10 times higher than whites

• Primary:
– Fever, fatigue, ___, weight loss

• Chronic (Granulomatous):
• \_\_\_ ~90%
– \_\_\_, dry cough, chest pain
• \_\_\_ ~20%
– Chronic \_\_\_, indurated lesions termed “\_\_\_”
– \_\_\_, nose, \_\_\_ and face
• Salivary gland enlargement:
– \_\_\_

Some sort of ___ involvement

Symptoms are similar to ___

Chronic violaceous > ___; indurated > hard

A

unknown
non-caseating
danish/swedish
african americans

anorexia

lung
dyspnea
cutaneous
violaceous
lupus perino
ear
lips
xerostomia

genetic
TB
red

26
Q

Sarcoidosis

• Oral:
– ___, ___ labial mucosa
• Salivary gland enlargement: – ___

Multiple ___ Macules

Erythematous macule with central ___

Macule > discolored lesion that is not raised (redness)

Lips > erythematous macule > central hyperkeratosis (area within the middle of the macule)

A

hard palate
lower
xerostomia

erythemetous
hyperkeratosis

27
Q

Sarcoidosis

• Histopathology:
• Classic granulomatous
inflammation
• \_\_\_ cells
• Do not typically undergo central \_\_\_ necrosis
• Asteroid bodies
– Entrapped fragments of \_\_\_
• \_\_\_ body
• Fungal or bacterial stains \_\_\_

Full blown Tb > cough out material; SD > the cough will be ___

Can differentiated from HP and fungal diseases and Tb (bc ___ for fungal and bacterial stains)

A
giant
caseous
collagen
schaumann
negative
dry
negative
28
Q

Diagnosis and Treatment of Sarcoidosis

  • Clinical and Radiographic
  • Histologic
  • ACE
  • Pulmonary involvement
  • Kveim Test
  • 60% resolve within 2 years
  • Corticosteriods
  • Methotrexate
  • TNF-a antagonists

Can see SD on ___

ACE > ___

Kveim test > injected sterile ___ (___) tissue into skin and waiting to see a development of a ___

Majority of patients resolve within ___ yrs

Bc of inflam > ___

Methotrexate > ___

TNFa antagonists do not always ___

A
x-ray
elevated
sarcoid
spleen
granuloma

2

corticosteroids
anti-metabolite
work

29
Q

OROFACIAL GRANULOMATOSIS
Melkersson-Rosenthal Syndrome

Non-___ Persistent swelling of one or both ___

Persistent enlargement of lower lips ___ PARALYSIS

___ tongue

A

tender
lips
facial
fissured

30
Q

OROFACIAL GRANULOMATOSIS

• Cheilitis Granulomatosa – Swelling of ___ only

Only swelling of lip, and on biopsy only on part of lip > cheilitis > granulomastose > no ___ paralysis or ___ tongue

A

lips
facial
fissured

31
Q

Diagnosis

  • ___ granulomatous inflammation
  • Edema
  • No ___ material

Granulomas contain multinucleated giant cells within granulomas

Presence of edema > swelling

Unknown etiology, no foreign material

Clinical manifestations, based on biopsy, and swelling is due to an edema (unknown which ___)

A

non-caseating
foreign
type

32
Q

Treatment

  • ___
  • Antibiotics?
  • Surgical ___

Unknown etiology > target the lesion directly

Will not use antibiotics (amox) because it’s not a typical ___ infection

___ > medium to high potent corticosteroid

A

intralesional steroid
recontouring
microbial
triamcinolone

33
Q

Inflammation and Wound Healing

 Inflammation
• Wall off the \_\_\_ agent,
• Eliminate the cause of \_\_\_,
• Minimize the extent of tissue damage, 
• \_\_\_ dead cells and debris,
• Initiate healing,

Inflammation > trigger: dead tissue, necrotic tissue, temperature and bacterial

Vascular response > ___, and ___; cellular response (neutrophils)

In order to initiate healing you need inflammation, which is also a vascular response (need ___ tissue formation) > ___

Wound healing and chronic inflammation > ___ tissue is wound healing, but it becomes extensive that affects function of organ > chronic inflammation > healing is complete until the etiology is removed

Non-specific inflam > neutro recruitment, tissue damage, fibrosis > foci of inflam cells and tissue destruction (chronic sialodentitis); silicosis

Granulomatose > have distinct phenotypes

A

injurious
injury
remove

vasodilation/constriction
vascular permeability

granulation
angiogenesis

scar