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FS II, Module I > 7. Acute Inflammation III > Flashcards

7. Acute Inflammation III Flashcards

1
Q

Review: Systemic effects of Inflammation (Acute phase reaction)

TNF, IL1, IL6 on brain: ____

IL1, IL6 on liver: ____

TNF, IL1, IL6 on bone marrow: ____

A

fever
acute phase proteins
leukocyte production/release

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2
Q

____ > neutrophils, eosinophils, basophils

____ > monocytes, lymphocytes

Platelets are not cells, they’re remnants of the ____

Basophils are the blood-counterpart of tissue ____ , unknown ____

Neutrophils: \_\_\_\_ 
Eosinophils: \_\_\_\_ 
Basophils: \_\_\_\_ 
Monocytes: \_\_\_\_ 
Lymphocytes: \_\_\_\_
A 
granulocytes
round cells
megakaryocytes
mast cells
function
50-70%
5%
1%
5-8%
20-40%
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3
Q

[TAKE A LOOK AT THE CELL IDENTIFICATION SLIDE]

A

YAY

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4
Q

Neutrophil Kinetics

____ is present in bone marrow (of 100B), only ____ is not in the bone marrow and circulating/marginating (loosely adhering) throughout the body

\_\_\_\_ = neutrophils in circulation
\_\_\_\_ = marginated neutrophils
A

93%
7%

3%
4%

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5
Q

Neutrophil Development

Nucleus gets smaller as you go from ____ to ____ (formation of granules) > myleocyte (more ____, and nucleus size is getting ____) > ____ (nucleus is becoming ____ shaped, the cytoplasm is increasing) > band (____ cell) > segmented/mature PMN

Blue background to yellow background > blue cells are all ____ (myeloblast, promyelocyte and myelocyte), and move to yellow (metamyelocyte, band, and segmented PMN) they stop ____ and mature into a neutrophil

Get into tissue and removed via ____; neutrophils are called ____ because they can only go one way > 1-2 hour they undergo apoptosis and removed via macrophages

Shift to the left > normally you do not expect to see ____ neutrophils, and if you do see a large amount > the reserve neutrophils in BM have been used up in the case of ____ for example

Regulated by ____ > released from fibroblasts and macrophages; when there is infection more of it is produced > causes more myeloblasts to enter the cycle and produce neutrophils and causes conversion of myelocytes into ____

A 
myeloblast
promyelocyte
granules
smaller
metamyleocyte
band
???

dividing
dividing

macrophages
end cells

band

infection

G-CSF

metamyleocyte

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6
Q

NEUTROPENIA

Neutropenia:

A

1500

500

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7
Q

NEUTROPENIA

  • BONE MARROW PATHOLOGY:
  • ____
  • Malignancies
  • ____
  • Drugs (Anti-cancer antibiotics)
  • Infection (____ and ____, ____)
  • INEFFECTIVE PRODUCTION:
  • ____
  • Vitamin B12

ENHANCED DESTRUCTION:
» ____
» ____

A 
congenital
radiation
hep A
B
measles

folic acid

septecemia
hypersplenism

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8
Q

NEUTROPENIA: ORAL MANIFESTATIONS

  • Susceptible to ____ infection
  • Middle ear, oral cavity, perirectal area
  • ____ infection (PMN<500/mm3).
  • Oral Cavity:(____, ____, ____ mucosa)
  • ____ most affected (Ulceration)
  • Premature bone loss/Exfoliation of Deciduous dentition
  • Treatment and Prognosis
  • ____
  • Oral ____
  • ____
A 
bacterial
pulmonary
lip
tongue
buccal
gingiva
antibiotic
hygiene
G-CSF
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9
Q

CYCLIC NEUTROPENIA:

•

A

200
3-6
ulceration

affected
periodontal bone
recession mobility

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10
Q

Cyclic Neutropenia

  • Mutation in ____ gene
  • Arrest at ____
  • ____
Diagnosis and Treatment
• Sequential WBC count
– \_\_\_\_ times/week for \_\_\_\_ weeks.
• \_\_\_\_ for infection when PMN counts are low.
• \_\_\_\_
• Oral \_\_\_\_

ELA2 > arrest promyelocyte > apoptosis > no neutrophil production

Can ____ test for mutation

A

Elastase (ELA2)
promyelocyte
apoptosis

2-3
8
antibiotics
G-CSF
hygiene

genetically

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11
Q

[TAKE A LOOK AT THE CASE REPORT]

A

YAY

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12
Q 
Agranulocytosis
• \_\_\_\_, (\_\_\_\_ are absent)
•Decreased production or increased destruction.
•Some cases are \_\_\_\_.
•\_\_\_\_ chemotherapeutic agents.
•\_\_\_\_ infection often develops.
•Deep oral ulcers:
\_\_\_\_ mucosa, \_\_\_\_, \_\_\_\_, \_\_\_\_ (infection)
Treatment
• If drug-induced, \_\_\_\_ ASAP
• \_\_\_\_ for infection. 
• \_\_\_\_
• Oral \_\_\_\_
A 
granulocytes
PMNs
idiopathic
anticancer
bacterial

buccal
tongue
palate
gingiva

discontinue
antibiotics
G-CSF
hygiene

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13
Q

Inflammation increased vascular permeability to proteins > ____ develops

As a result of inflammation > and the RBC clump > ____ (from fibrinogen, acute phase protein) > bigger, and they’re ____ on neutrophils, and then the neutrophil tumbles onto the surface of the endothelial cells and bounce off…

A

stasis
rouleaux
pushing

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14
Q

Neutrophil recruitment coincides with increased ____; even when there are not enough physical gaps, the neutrophils still ____ the endothelial cells > they produce their own gaps

[NOTES]

A

vascular permeability

transverse

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15
Q

Mast cell (he added)

[NOTES]

A

ADD HERE

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16
Q

Slowing of neutrophils mediated by selectins, and the ligands contain sugar molecules (carbohydrates)

L-selectin: L for ____, expressed on surface of leukocyte and ligand is on endothelial cells

P-selectin: present on surface of ____ and ____, and the ligand is on the leukocyte

E-selectin: present on ____, and the ligand is on the leukocyte

Normally, selectins are not ____ on surface of endothelial cells

A 
leukocyte
plasma cell
endothelial cells
endothelial cells
expressed
17
Q

P-selectin is pre-synthesized and stored in ____; and ____ from mast cells causes the redistribution of P-selectins from WP bodies from cytoplasm onto the surface of the endo cell

____ contributes to initial adherence of leukocytes to endo cells**

Cytokines (IL1, TNFalpha) induce expression of ____, takes longer than P-selectin (pre-synthesized), and induces ligand for ____

Following all this, interaction is ____ (bt neutrophils and endo cells) and is not sufficient to bring neutrophils to a halt on surface of endo cells; “slow brakes” on your car

Next: ____, mediated by different set of molecules

A

webel-palade bodies (WP bodies)
histamine

histamine

E-selectin
L-selectin

low-affinity

firm adhesion

18
Q

FIRM ADHESION OF NEUTROPHIL ON ENDOTHELIAL SURFACE

Integrins are receptors and LFA-1 contains two subunits (____), Mac1 (____), p150,95 (____)

All three have common subunit = ____, LFA-1 in all ____ cells, Mac-1 > most granulocytes, but mostly ____ and ____, p150,95 > more on ____ than monocytes

Ligands are present on endo cells > ____ > upon interaction > firm adhesion of neutrophil

Only occurs when ____ is present

A

CD11a/CD18
CD11b/CD18
CD11c/CD18

CD18
immune
macrophages monocytes
macrophages

ICAM1

inflammation

19
Q

FIRM ADHESION OF NEUTROPHILS ON ENDOTHELIAL SURFACES

Normally: no ICAM-1, add ____ (IL1, TNFalpha) during inflammations > induction of ICAM-1 > this induction is not sufficient for firm adhesion; neutrophils must be ____

Integrins are activated by ____ (chemotactic cytokines, produced from macrophages during infection/irritation, bind to PG on endothelial (???) cells; captures chemokines near where they are produced) > bind receptor on neutrophil there is activation of neutrophil > integrins become ____, and they have higher ____ for ICAM-1 > firm adhesion

Integrins are always ____ on neutrophils, but only once ____ the integrins align properly and interact with ICAM-1

A

cytokines
activated

chemokines
clustered
affinity

present
activated

20
Q

TRANSMIGRATION / EXTRAVASATION / DIAPEDESIS

Neutrophils are crossing endothelial cells and are being recruited extravascularly

Second group of adhesion molecules > ____ (expressed both on ____ and on ____; upregulated on neutrophils by ____; upregulated sequentially after ____ takes place)

A 
PECAM-1
neutrophils
endothelial cells
chemokines
firm adhesion
21
Q

Type of emigrating leukocytes depend on the nature of the etiology

• Most acute inflammation:
– Neutrophils first ____ h
– Monocytes ____ h

• Pseudomonas organisms:
– ____ several days

• Viral infection:
– ____

• Allergic asthma
– ____

A

6-24
24-48

neutrophils

lymphocytes

eosinophils

22
Q

Type of emigrating leukocytes depend on the age of the inflammatory response

Left: myocardial infarct; neutrophil firmly adhered to surface of BV > neutrophil removes dead tissue

Firstly, ____, then ____ recruitment, and then the recruitment of ____

Neutrophils > larger in number

Monocytes > smaller in number, expression of ____ molecules is smaller, they become macrophages and remain in the ____ tissue

[REWATCH]

A

edema
neutrophil
monocytes/macrophages

adhesion
EV

23
Q

Leukocyte Adhesion Deficiency (LAD-I)

• Etiology and Pathogenesis:
• Deficient expression of the integrins containing
____ (mutation in ____ gene, CD18)
• Decrease in ____ to the endothelium

• Clinical Manifestations
• Delayed separation of the ____ (Normal,
7-10 days; LAD-I ____ days)
• Recurrent ____ infection (skin/mucosal surfaces)
• ____ (later in life)
• Impaired ____ healing
• ____ (10,000 - 40,000/mm3)

Similar clinical representation to ____; neutrophils cannot be recruited to where they’re required because they cannot adhere and cannot transverse in the EV space

A

CD18
ITGB2
firm adhesion

umbilical cord
>30
bacterial
gingivitis/periodontitis
wound
leukocytosis

neutropenia

24
Q

Leukocyte Adhesion Deficiency (LAD-I)

Delayed separation of the ____

____/____

____

Impaired ____

Stump of umbilical cord > irritant > neutrophil recruited > inflammation > removed and heals; if LAD-1 > no number with total number of neutrophils, but no inflammatory response (the earliest sign of LAD-1 deficiency) > develop into ____

A 
umbilical cord
omphilitis
septicemia
gingivitis/periodontitis
healing

omphilitis/septicemia

25
Q

LEUKOCYTE ADHESION DEFICIENCY-I (LAD-I)

Diagnosis:
• Clinical presentation, history
• Reduced expression of \_\_\_\_ (CD11a and CD11b) on neutrophils (\_\_\_\_). 
• Elevated \_\_\_\_ count
• \_\_\_\_ testing

Treatment:
• ____
• Ustekinumab? (____)

A

CD18
flow cytometry
neutrophil
genetic

antibiotics
stelara

26
Q

LAD1 Case Report

• A 19-year-old man with LAD1 (mutation in ____ gene, CD18) presented for evaluation of severe periodontal disease.
• Had delayed umbilical cord separation, otitis, and skin infections in early childhood.
• ____ at 4 years of age, which led to the diagnosis of LAD1. Prophylactic treatment with trimethoprim–
sulfamethoxazole.
• Since then, recurrent oral ____ (treated with steroids), frequent skin infections and several cases of pneumonia.
• Severe periodontitis began in his early ____ and chronic non-healing wound
• On admission, the patient had severe periodontitis with generalized gingival inflammation and severe periodontal bone loss.

The patient’s CD18 expression ____ of the control (moderate LAD1).
• Biopsy of gingival and chronic cutaneous wound tissue; lymphocyte infiltrate and ____, ____

A

ITGB2
appendicitis
ulcers
teens

~34%
IL17, IL23

27
Q

____ > apoptotic neutrophils phagocytosed by macrophages in the wound

Infection > more ____ > more neutrophil production in BM

Efferocytosis > negative feedback on production of cytokines > no ____

…
In LAD-1; neutrophil cannot get out BV > no efferocytosis, so no feedback inhibition of ____ (macrophages have nothing to phagocytose)

TURN-OFF SIGNAL > not transverse migration of neutrophils, nothing for macrophage to phagocytose

IL17 > involved in oral ____, ____ wound, ____ and ____

Stelara/Ustekinumab > monoclonal ab binds to ____ subunit of ____ (IL-12 may participate in periodontal disease) > prevents production of ____ and ____

A

efferocytosis
G-CSF
IL23/17

cytokines

ulceration
chronic
gingivitis
periodontitis

P40
IL-23/IL-12

IL17
G-CSF

28
Q

Inflammation: Gingiva

Upon treatment with Ustekinumab/Stelara…

____ decreases upon treatment

Also had severe ____> would treatment regress the bone loss > in this patient, no change in ____

Chronic inflammation > ____ destruction > won’t regrow the tissue, but will treat the other issues

A

bleeding
bone loss
bone growth
tissue

29
Q

LEUKOCYTE ADHESION DEFICIENCY-II (LAD-II)

  • Etiology and Pathogenesis:
  • Absence of ____
  • ____ deficiency
  • Neutrophils do not bind to ____ on EC
  • Defective ____
  • Clinical Manifestations
  • Less severe than ____
  • No ____ in umbilical cord separation
  • ____ infection not life threatening
  • ____
A

sialyl lewis X-modified glycoprotein
GDP-fucose transporter
selectins
rolling

LAD-I
delay
bacterial
periodontitis

30
Q

LEUKOCYTE ADHESION DEFICIENCY-II (LAD-II)

  • Diagnosis:
  • ____ Stature, mental/growth ____
  • ____ (neutrophils, 10,0000 – 40,0000/mm3)
  • Absence of ____ expression (____)
  • Treatment
  • ____ (children)
  • ____
  • ____ supplementation
A 
short
retardation
leukocytosis
SLeX
flow cytometry

antibiotic prophylaxis
periodontitis
fucose

31
Q

LEUKOCYTE ADHESION DEFICIENCY-III (LAD-III)
• Etiology and Pathogenesis:
• Defect in integrin ____ by chemokines
• Mutation in the gene for the adapter protein ____ (which binds to beta ____, ____, and ____)
• Reduced ____
• Dysfunctional platelet ____

  • Clinical Manifestations
  • Similar to ____
  • ____ at birth
  • ____ disorders

Kindlin-3 protein is also found in ____, the mutation is global which results in hemorrhage

A 
activation
kindlin-3
1
2
3 integrins
firm adhesion
aggregation

LAD-I
cerebral hemorrhage
bleeding

platelets

32
Q

LEUKOCYTE ADHESION DEFICIENCY-III (LAD-III)

  • Diagnosis:
  • Intact integrin ____ but impaired ____
  • ____(neutrophils, 10,0000 – 40,0000/mm3)
  • ____ analysis for mutation in Kindlin-3
  • Treatment:
  • ____ or ____ cell transplantation
  • Prognosis poor unless treatment in early ____
A

expression
activation
leukocytosis
genetic

bone marrow
hematopoietic
infancy

33
Q

[REVIEW LAD TABLE]

A

YAY

FS II, Module I (14 decks)

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