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IHP 1001 > Ch.2 Acute Inflammation pt.3 > Flashcards

Ch.2 Acute Inflammation pt.3 Flashcards

1
Q

collection of soluble proteins (pre-made) and their membrane receptors that function mainly in host defense against microbes and in pathologic inflammatory reaction

A

Complement System

Innate

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2
Q

Inflamation will caused the trigger and release of chemokine TNF & Il-6 which will trigger an ____ ___ ____ in the liver. What does this response release?

A

Acute Phase response; releases pre-made complement protiens from the liver.

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3
Q

The critical step in complement activation is the _____ ____ of the third (and most abundant) component, C3

A

Proteolytic Cleavage

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4
Q

What complement pathway?

which is triggered by fixation of C1 to antibody (IgM or IgG formed adaptively) that has combined with antigen.

*req pre-formed antibodys

A

Classical

C1- antibody (IgM & IgG)

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5
Q

What complement pathway?

which is triggered by microbial surface molecules (e.g.,endotoxin, or lipopolysaccharide [LPS]), complex polysaccharides, and other substances, in the absence of antibody.

A

Alternative pathway

C3B innate ability to bind surface microbs

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6
Q

Which Complement pathway?

plasma mannose-binding lectin binds to carbohydrates on microbes and activates C1, also without a role for antibody

A

Lectin Pathway

MBL binds to mannose on microb

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7
Q

All three patways of the complement actiation lead to the formation of an enzyme called?

A

C3 convertase

Splits C3 into C3a & C3b

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8
Q

What does C3B go on to do?

A

Bind to other fragments and produce C5 Convertase.

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9
Q

What does C5 convertase do?

A

Cleaves C5 into C5a & C5b

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10
Q

C5b binds the late components (C6-C9), culminating in the formation of the ____

A

Membrane attack complex MAC

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11
Q

Function of Complement:

C3a and C5a are ____ they trigger mast cell degranulation resulting in histamine mediated vasodialation and increase in vascular permeability

Inflamation (1)

A

Anaphylotoxins

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12
Q

Function of complement:

When C3b and cleavage products are fixed to microbial walls, they act as ____ promoting phagocytosis by neutrophils & macrophages.

The leukocytes have receptors for the _____

A

Opsinins!

Opsinization & phagocytosis (2)

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13
Q

Function of complement:

assembly of the MAC on cells creates holes in the cell membrane that allow intracellular water and ions to leak out, resulting in the** death (lysis) of the cells**

A

Cell Lysis (3)

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14
Q

What kind of thin-walled microbes are verys suseptible to complement induced cell lysis?

A

Neisseria bacteria

Meningococci and Gonococci

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15
Q

Complement activation is heavily controled by ____ protiens that prevent healthy tissue from being injured at sites of complement activation

A

Regulatory Proteins

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16
Q

What complement regulatory protien?

blocks the activation of C1, the first protein of the classical complement pathway.

Inherited deficeny= hereditary angioedema

A

C1 inhibitor (C1 INH)

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17
Q

What complement regulatory protien?

____prevents formation of C3 convertases and ____ **inhibits formation of the membrane attack complex.**

paroxysmal nocturnal hemoglobinuria (PNH)

A

Decay accelerating factor (DAF) and CD59

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18
Q

What complement regulatory protien?

plasma protein that promotes the inactivation of the C3 convertase

Deficency causes what?

A

Factor H

Excessive complement activation

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19
Q

Proinflamatory protien produced by the live in an inacitve from APP

A

Hangeman Factor (XII)

Link btwn coagulation cascade & inflmation

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20
Q

What activate the Hangeman Factor?

A

Coming into contact with exposed sub-endothelium or collagen

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21
Q

Kinin clevaes high molecular weight kinogen (HMWK) to bradykinin which mediations vasodialation and increased vasculare permeability + pain

A

Kinin System

22
Q

Hageman factor promotes activity of what 3 things?

A
  1. coagulation (intrinsic) and fibronolytic systems
  2. activates complement
  3. kinin system
23
Q

Vasodialator of arterioles+ mild constrictor of post capillary venules

pooling of blood in capillaries to send lots of leukocyte rich blood to tissues.

Ties with PGE2 to lower pain threshold and chronic pain

A

Bradykinin

24
Q

Pt. with antihypertensive medications have lots of cough, what can this be linked to?

A

Bradykinin

25
Q

Similar to prostoglandis, ___ has a function in intial constriction of any feta vessles that eventually close

A

Bradykinin

26
Q

Work on nerve endings, lower pain threshold, more pain. Peripheral nervous syste.

A

Neuropeptides

27
Q

What common feature of inflmmation?

accelerated release of cells from the bone marrow postmitotic reserve pool (caused by cytokines, including TNF and IL-1) and is therefore associated with **increased numbers of immature neutrophils in the blood (“band” cells), referred to as a shift to the left

A

Leukocytosis

28
Q

Most bacterial infections induce an increase in the blood neutrophil count

A

Neutrophelia

29
Q

Viral infections, such as infectious mononucleosis, mumps, and German measles, cause an **absolute increase in the number of lymphocytes **

no fever BUT very Fatigued. Chronic inflmation

A

Lymphocytosis

30
Q

allergies and parasitic infestations, blood eosinophils increase

A

Eosinophillia

31
Q

Certain infections (typhoid fever and infections caused by rickettsiae, and certain viruses and protozoa) are associated with a **decreased number of circulating white cells

A

Leukopenia

32
Q

Protiens sythesized by the liver and released on a contiunous basis at a homeostatic level.

Pre-preared, released all at once during inflmatory reaction (TNF and IL-6 trigger this)

A

Acute Phase Reactants

33
Q

Ferritin, fibrogen, hepcidin, CRP, AA amyloid are all examples of what?

A

Actue phase protiens

34
Q

What acute phase protien?

Binds bacterial polysachrdes then activates complemenet.
Detected in serum= inflamation , prognosis!

A

C-Reactive Protien

less= less infection. NSAIDs mask reduce levels & mask

35
Q

What can be detected in the serum of patients with chronic inflmatory conditons like CAD, RA, obesity, cigarette smoker?

A

High levels of CRP

36
Q

What acute phase protien?

Binds to iron and takes it away from microbs so they can use it for oxygen. Stored in macrophages of liver+ bone.

A

Ferritin

37
Q

During an infection binding of Iron away from microbs by ferritin results in what?

A

Temporary iron defficency

38
Q

What acute phase protien?

Has antibactieral properties as well as iron trapping function.

Can cause anemia in chronic inflamation

A

Hepcidin

39
Q

4

The rate of accumulation of erythrocytes, if theres is ongoing inflammation elevation is proportionate to APPP secreation.

APP bind to cell membrane and neutralize (-) charge, causing stacks.

A

Erythrocyte Sedementation Rate

Chronic inflmation; vasculitis, endocarditis, surgery; all evelvate

40
Q

What are the two hallmarks of acute inflammatory reaction’s?

A
  1. Vasodialation of small blood vessles
  2. accumulation of leukocytes & fluid in extravascular tissues (exudate)
41
Q

What kind of accute inflammation?

marked by the accumulation of serumlike protein-rich exudates in body cavities lined by the peritoneum, pleura, or pericardium or spaces created by tissue injury.

A

Serous Inflamation

Blisters (white) btw dermis and epidermis
42
Q

What kind of accute inflammation?

characterized by the deposition of fibrin as a result of the local activation of coagulation.

large increases in vasccular permeability so high MW molecules like Fibrogen accumulate within exudates; fibrin forms.

A

Fibrinous Inflamation

Common in lining of body cavities; meningitis, pericardium, pleura
43
Q

What kind of accute inflammation?

Characterized by the production of pus, an exudate consisting of neutrophils, the liquefied debris of necrotic cells, and edema fluid.

A

Purulent (Suppurative) Inflammation, Abscess

44
Q

Infection with bacteria that cause liquifactive necrosis, ex. Staph, cause ____ inflamation

Pyogenic pathogens= pus producing

A

Purulent inflamation

View arrows
45
Q

A common example of an acute Purulent (suppurative) inflammation

A

appendicitis

46
Q

localized collections of pus caused by suppuration within a tissue, an organ, or confined space.

A

Abcesses

central region of necroses tissue, rig of preserved neutrophils
47
Q

What kind of accute inflammation?

a local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing (shedding) of inflamed necrotic tissue

only occure when tissue necrosis and inflamtion occur near surface.

A

Ulcers

Crater, Loss of epithelium, sub epithelium exposed

most common in mucosa of mouth stomach, intestine, GI tract, skin.

48
Q

What outcome of accute inflamation?

Tissue cleared of microbs, IL-1/6 no longer coming from macrophages, regeneraton capacity not exceeded

involves removal of cellular debris and microbes by macrophages and resorption of edema fluid mainly through lymphatics.

A

Compete reslution

49
Q

What outcome of accute inflamation?

Occurs after substantial tissue destruction, when the inflammatory injury involves tissues that are incapable of regeneration, or when there is abundant fibrin exudation in tissue or in serous cavities (pleura, peritoneum) that cannot be fully cleared. (TGF-Beta)

A

Scar Formation

Healing by connective tissue replacement (scarring, or fibrosis)

50
Q

What outcome of accute inflamation?

acute inflammatory response cannot be resolved because of either the persistence of the injurious agent or some interference with the normal process of healing.

A

Progression to chronic inflamation

IHP 1001 (18 decks)

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