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MOD - 2 - Cells: Adaptation, Injury, and Death > Pathoma - Ch. 3 - Acute Inflammation > Flashcards

Pathoma - Ch. 3 - Acute Inflammation Flashcards

1
Q

what is the hallmark difference between acute and chronic inflammation?

A

actue - neutrophil heavy

chronic - lymphocyte heavy

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2
Q

what is acute inflammation characterized by?

A

edema and neutrophils in tissue

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3
Q

explain this picture

A

indicative of acute inflammation

note blood vessels on bottom corners; note the neutrophils; and note all the empty space in between the blood vessels and in the general area; that is edema

so edema and neutrophils : acute

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4
Q

what are the two stimuli that inflammation arises in response to?

what is the goal?

A
  • infection
  • necrosis
    goal: to eliminate pathogen or clear necrotic debris
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5
Q

know that acute inflammation is an Immediate response with limited specifity

A

* innate immunity

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6
Q

what is acute inflammation mediated by?

A

.

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7
Q

describe TLRs

A
  • present on cells of innate immune systems (macrophages and dendritic cells)
  • recognize PAMPs
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8
Q

what is an example of TLR?

A

CD14

  • present on macrophages

on macrophages that recgonizes the LPS on the outer membrane of Gram neg bacteria

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9
Q

what does activated TLR result in?

A

the upregulation of NF-kB;

this NFkB is like a switch, and it goes on to activate other immune response genes

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10
Q

describe Arachidonic Acid

A
  • released from phospholipid cell membrane by phospholipase A2
  • acted on by cyclooxygenase or 5-lipooxygenase
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11
Q

what happens when arachidonic acid is acted on by cyclooxygenase?

A

it produces PG (prostaglandins)

  • PGI2, PGD2, PGE2, (together) mediate vasodilation (at the level of arterial) AND Increased vascular permeability (specifically, at the post-capillary venule)
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12
Q

what does PGE2 also mediate?

A

fever and pain

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13
Q

what happens when arachidonic acid interacts with 5-lipooxygenase?

A

produces leukotrienes (LT)

  • LTB4

LTC4

LTD4

LTE4

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14
Q

*randomly: what 4 mediators attract and activate neutrophils?

A

-LTB4,

C5a,

IL-8,

and bacterial products

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15
Q

what do the 4 leukotrienes do?

A

LTB4: attract and activate neutrophils

LTC4, LTD4, LTE4: mediate vasoconstriction, bronchospasm, and increased vascular permeability

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16
Q

in general, what do LTs do?

A

contract smooth muscle

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17
Q

what 3 things activate mast cells?

A
  • tissue trauma
  • complement proteins: C3a and C5a
  • cross-linking of cell-surface IgE by antigen
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18
Q

what is the immediate response to mast cell activation?

A

**release of preformed histamine granules

- two primary fxs of histamine: vasodilation of arterioles and Increased vascular permeability (at the level of the post capillary venule)

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19
Q

what is the delayed response when a mast cell is activated?

A

production of arachidonic acid metabolites, particularly leukotrienes

  • this is for the maintenance of the mast-cell response
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20
Q

what is the compliment system?

A
  • proimflammatory serum proteins
  • circulate as inactive precursors
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21
Q

what are the 3 ways to activate the complement system?

A
  • classic pathway: C1 binds to IgG or IgM that is bound to the antigen
  • alternative pathway: microbial products directly activate complement
  • mannose-binding lectin pathway: MBL binds mannose on microorganisms and activates complement
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22
Q

what are the key products of complement system activation and what do they do?

A
  • C3a and C5a: trigger mast cell degranulation
  • C5a: chemotactic for neutrophils
  • C3b: opsonin for phagocytosis
  • MAC: lyses microbes by creating holes in the cell membrane
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23
Q

what is the Hagemen factor?

A
  • inactive proinflammatory protein produced in the liver
  • activated upon exposure to subendothelial or tissue collage

*plays a big role in DIC, esp. gram negative sepsis

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24
Q

what is the reaon hagemen factor plays an important role in DIC (disseminated intravascular coagulation)?

A

HF in turn activates:

  • coagulation and fribrinolytic system
  • complement
  • and kinin system: cleaves HMWK to bradykinin, which mediates vasodilation, incr vascular permeability and pain
25
what is the only difference between histamine and bradykinin?
they both mediate vasodilation and incr vascular permeability - but bk mediates **pain**
26
what mediates pain?
PGE2 and bradykinin
27
\*\*\*what are the cardinal signs of inflammation?
rubor (redness) and calor (warmth) swelling (tumor) pain (dolor) fever
28
what mediates the redness of the tissue? what are the key mediators?
- due to vasodilation, which results in incr blood flow (occurs via relaxation of arteriolar smooth m.) - key mediators: **histamine**, PGs, and bradykinin \*warmth is mediated by the exact same info\*
29
define swelling and its mediators
- due to leakage of fluid from postcapillary venules into interstitial space - mediators: histamine and tissue damage
30
what mediates pain and how?
bradykinin and PGE2 by sensitizing sensory nerve endings
31
how is fever caused?
- pyrogens cause macrophages to release IL-1 and TNF - they make their way in the blood to the perivascular cells of the hypothalamus, and increase COX (cyclooxigenase) activity - COX leads to incease in production of PGE2, which raises the temp set point \*high yield\*
32
----VIDEO 2: NETROPHIL----
three step process to inflammation (acute) 3 waves; fluid, neutrophil, macrophages n-phase peaks at 24 hours: m-phaseL peaks at 2-3 days
33
what happens in order for margination to occur?
neutrophils, being bigger components within the blood stream, ride the wave in the center due to lamilar flow; when vasodilation occurs, they are allowed to go to the edges of the blood vessel = margination
34
desribe Step 1 - Margination
- vasodilation slows blood flow in postcapillary venules - cells migrate from center to periphery of flow
35
describe Step 2 - Rolling
- endothelial cells begin to express Selectins (aka speed bumps), causing neutrophil to slow down - **P-**selectin is released from Weibel-**P**alade bodies (small bodies in the endothelial cells); mediated by **histamine** **- E-selectin:** Induced by TNF and IL-1
36
What do selectins bind?
- bind **sialyl Lewis X** on leukocytes (specifically neutrophils, but also macrophages, wbc, etc.) - interaction results in rolling of leukocytes
37
describe Step 3 - Adhesion
- Cellular Adhesion Molecules (CAMs) are upregulated on endothelium by **TNF and IL-1** - **INTEGRINS** upregulated on leukocytes by **C5a and LTB4** - interaction results in firm adhesion to vessel wall
38
describe Lukocyte Adhesion Deficiency and its clinical findings/ features (v important)
- AR defect of integrins (**CD18** subunit) CFs: *delayed separation of the umbilical cord* (this is cuz leukocytes help clean up necrotic tissue; and if there is a delay, it indicates that leukocytes never migrated) * - Incr circulating neutrophils* (marginated pool is not present, cuz theyre circulating due to lack of integrin) * - recurrent bacterial Infections that **lack pus formation***
39
why does it lack pus formation?
cuz pus is a pool of dead neutrophils. since they cant migrate, then no pool
40
Step 4 - Transmigration and Chemotaxis
- leukocytes transmigrate across endothelium of **postcapillary venules** - (Neutrophils) move towards chemical attractants: **bacterial products, C5a, IL-8, LTB4**
41
step 5 - phagocytosis
consumption of pathogens or necrotic tissue - enhanced by IgG and C3b (opsonins)
42
how does phagocytosis occur in this instance?
- pseudopods from leukocytes extend to form phagosomes - internalize stuff and merge it with lysosomes to form **phagolysosomes**
43
what is a defect that impairs the formation of phagolysosome?
Chediak-Higashi syndrome - protein trafficking defect (microtubules) - AR - characterized by impaired phagolysosome formation
44
what are the clinical features of Chediak-Higashi syndrome?
- incr risk of pyogenic infections (cuz phasgosome cant be desrtoyed) - neutropenia (because division cannot be pulled apart due to microtubule defect) - giant granules in leukocytes (cuz when the granules get made, they cant get sent nowhere, so they build up) - defective primary hemostasis - albinism (melanocyte produces melanin, then hands it off to surrounding cells; since it cant be moved along the railroad -microtubules-, it cant be distributed) - peripheral neuropathy
45
Step 6 - destruction of phagocytosed material
occurs in 2 ways: oxygen-dependent \>\>\> oxygen-independent
46
how does the oxygen dependent fashion occur?
O2 gets acted upon by NADPH-oxidase and turns it to SuperOxide (O2-) then SOD (super-oxide dismutase) acts on O2- and converts it into hydrogen peroxide (H2O2) then H2O2 is acted on by myeloperoxidase (MPO) and will be converted to bleach (HOCl) \*HOCl then destroys organism\* **high yield card**
47
what does HOCl do?
destroys phagocytosed microbes in phagolysosomes
48
what is chronic granulomatous disease?
you get poor O2-dependent killing - due to NADPH-oxidase defect **- X-linked or AR** pt gets granuloma diseases often
49
what particular organisms cause infection and granuloma formation in these pts with a defect in NADPH-oxidase?
**catalase-positive organisms** S Aureus P cepacia S marcescens Nocardia Aspergillus
50
why is it that catalase-positive organisms cause problems?
remember the pathway to make the bleach (HOCl-): O2 to O2- via NADPH-oxidase O2- to **H2O2** via SOD then H202 to HOCl- via MPO - So, you need hydrogen-peroxide (H2O2) to make the bleach. patients who lack NADPH-oxidase typically do not have a problem with other organism because **bacteria** within our body actually provide H2O2 as one of their byproducts. thus, we have bleach to destroy phagolysosomes **but!!** some bacteria ALSO produce **catalase**, which destroys H2O2 (the same H2O2 the bact produce). so if both these pathways get knocked out, no bleach.
51
how do you screen for CGD?
nitroblue tetrazolium test - turns blue if NADPH-oxidase can convert O2 to O2- - remains colorless if NADPH-oxidase is defective
52
whats with MPO deficiency?
results in defective conversion of H2O2 to HOCl- - increased risk for **Candida Infections;** most pts are actually asymptomatic - NBT test is normal
53
describe the O2-independent killing
- less effective - occurs via enzymes present in leukocyte secondary granules (lysozyme and major basic proteins)
54
step 7 - resolution
- netrophils undergo apoptosis - disappear within 24 hours after resulotion of inflammatory stimulus
55
what predominates after the neutrophil phase?
the macrophage phase - peaks 2-3 after inflammation begins
56
where do the macrophages come from?
- derived from monocytes in the blood - arrive the same way neutrophils do: margination, rolling, adhesion, and transmigration sequence
57
what do macrophages do once in their proper location?
ingest via phagocytosis destroy phagocytosed material using enzymes in **secondary granules (lysozyme)** (predominantly O2-independent)
58
what other roles do macrophages have?
they are managers: they determine the next step of the acute inflammatory response: - resolution and healing (via **IL-10 and TGF-Beta** - both of which are **anti-inflammatory**) - continued acute inflammation (if shits not good, and need more neutrophils, it send the signal aka **IL-8**) - Abscess (can create fibrous pocket) - chronic inflammation
59

MOD - 2 - Cells: Adaptation, Injury, and Death (10 decks)

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