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PATH MAGIC > Key 2- Inflammation, Apoptosis and necrosis > Flashcards

Key 2- Inflammation, Apoptosis and necrosis Flashcards

1
Q

The alternative pathway, which can be triggered by…………………

A

microbial surface molecules (e.g., endotoxin, or LPS), complex polysaccharides, cobra venom, and other substances, in the absence of antibody.

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2
Q

Leukotriene B4 = FUNCTION?

A

Chemotaxis

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3
Q

Leukotriene C4, D4, E4 …FUNCTIONS? (AGGRAVATED IN ASPIRIN USE)

A

Broncho Constriction- smooth muscle

(NON-ATOPIC ASTHMA)

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4
Q

THROMBOXANE a2- FUNCTION?

A

PROMOTE PLATELET AGGREGATION

STOP THIS MEDICATION TO PREVENT CLOT!!

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5
Q

CONTRACTION OF SMOOTH MUSCLE IS CAUSED BY?

A

PG

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6
Q

MUSCLE WASTING, DEATH IN CANCER PATIENT (MEDIATOR)?

A

Tumor necrosis factor-alpha

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7
Q

PROSTACYCLIN FUNCTION?

A

VASODILATATION

(ALSO NITRIC OXIDE)

and

Inhibit platelet Aggregation

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8
Q

Interleukin-1 FUNCTION?

A
  1. Acute phase reaction (eg: fever)
  2. Endothelial effect (Leukocyte adhesion, pro & anticoagulant effect)
  3. Fibroblast Effect (collagen synthesis – scar)

BAD!!!, IS NOT IT?

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9
Q

MEDIATOR ACTIVATE MACROPHAGE?

A

Interferon-gamma FROM CD4 CELLS

(ALSO IL-12 CAUSES INCREASED PRODUCTION OF INF)

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10
Q

MEDIATOR, THAT INCREASES SAA, FIBRINOGEN, CRP IS?

A

IL-6

TEST ESR!

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11
Q

NEUTROPHIL’S Specific (or secondary) granules PRODUCE?

A

Lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, and alkaline phosphatase.

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12
Q

NEUTROPHIL’S Azurophil (or primary) granules PRODUCE?

A

Myeloperoxidase (THINK P-ANCA), bactericidal factors (lysozyme=THINK ABSCESS FORMATION), defensins).

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13
Q

MACROPHAGE AND LIQUIFRACTIVE NCROSIS IN BRAIN- DISCUSS

A

– acid proteases (only active within lysosomes).

– neutral proteases such as elastase and collagenase are destructive in ECM.

Typical in Liquefactive necrosis- BRAIN

​

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14
Q

C3a, C5a: ==?

A

stimulate histamine release from mast cells and thereby increase vascular permeability and cause vasodilation

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15
Q

C5a:===?

A

chemotactic agent for neutrophils, monocytes, eosinophils, and basophils

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16
Q

Opsonization and phagocytosis: ?

A

C3b AND IG

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17
Q

MAC (MEMBRANE ATTACH COMPLEX)- deficiency of the terminal components of complement predisposes to ………………..infections.

A

Neisseria

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18
Q

MAC•This tube LIKE STRUCTURE forms a channel allowing the passage of ions and small molecules. Water enters the cell by ……………and the cell lysis.

THIS PROCESS SEEN IN WHICH CONDITIONS?

A

….Osmosis

A-In immune hemolysis (MISMATCHED BLOOD TRANSFUSION)

A-PNH

​​

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19
Q

•C1 inhibitor (C1 INH)

–blocks the activation of C1, the first protein of the classical complement pathway. Inherited deficiency of this inhibitor is the cause of …………………….

A

hereditary angioedema

20
Q

•Decay-accelerating factor (DAF) and CD59

–DAF prevents the formation of ……………………..and CD59 inhibits the formation of the ………………………

•An acquired deficiency of the enzyme leads to excessive …………………activation and lysis of red cells in the disease called ………………………..

A

C3 convertases, membrane attack complex (C5b-9)

complement, paroxysmal nocturnal hemoglobinuria (PNH)

21
Q

HISTAMINE (Mast CELL-DERIVED/PREFORMED GRANULES)- FUNCTIONS?

A

EARLY VASODILATION AND PERMEABILITY

OTHER FUNCTIONS=

–physical injury, such as trauma, cold, or heat, BEE STRING,

–binding of antibodies to mast cells, which underlies immediate hypersensitivity (allergic) reactions [(ASTHMA EARLY PHAGE MEDIATOR)] and

–products of complement called anaphylatoxins (C3a and C5a)

–Neuropeptides (e.g., substance P) and cytokines (IL-1, IL-8) may also trigger the release of histamine

22
Q

PAF FUNCTION-…………?

A

PLATELET ACITIVATION, VASODILATION AND PERMEABILITY

23
Q

Kinins FUNCTIONS?

A

Increased vascular permeability, smooth muscle contraction, vasodilation, pain

24
Q

Lipoxygenase inhibitors. 5-lipoxygenase is not affected by …………………

A

NSAIDs

25
Q

DIAGNOSIS?

A

COAGULATIVE NECROSIS

FATE- SCAR

26
Q

MECHANISM?

A

NEUTROPHIL LYSOZYME INDUCED NECROSIS

27
Q

HISTOLOGICAL FINDING: COAGULATIVE NECROSIS AND BLOOD=…?

A

REPERFUSION INJURY

28
Q

DIAGNOSIS?

A

NON CASEATING GRANULOMA

29
Q

The destruction of cells during embryogenesis…?

A

APOPTOPSIS

30
Q

Involution of hormone-dependent tissues upon hormone withdrawal…?

A

APOPTOSIS

31
Q

Formation of cytoplasmic blebs IN SINGLE CELL..?

A

APOPTOSIS

32
Q

Phagocytosis of apoptotic cells or cell bodies, usually by ………………

A

macrophages

33
Q

Anti-apoptotic. …..GENES?

A

BCL2, BCL-XL

34
Q

Pro-apoptotic………………..

A

BAX and BAK

35
Q

APOPTOSIS: The best-known death receptors are the …………….receptor

A

type 1 TNF

36
Q

The mitochondrial pathway leads to activation of the initiator caspase-……

A

9

37
Q

Executioner caspases, such as ……………………, act on many cellular components

A

caspase-3 and -6

38
Q

However, if the DNA damage is too great to be repaired successfully, ……………..triggers apoptosis.

A

p53

39
Q

Once released into the cytosol, …………………….binds to a protein called APAF-1 (apoptosis-activating factor-1), forming a multimeric structure called the apoptosome AND START THE PROCESS OF APOPTOSIS

A

cytochrome c

40
Q

FasL is expressed on T cells that recognize self-antigens (and functions to eliminate self-reactive lymphocytes). AN EXAMPLE OF THIS PROCESS IS?

A

cytotoxic T lymphocytes (which kill virus-infected and tumor cells).

41
Q

(Steps of apoptosis =intrinsic)?

IMPORTANT TO KNOW!!!

A

DNA DAMAGE- BCL2 INACTIVATION- BAX ACTIVATION- RELEASE OF CYTOC- ACTIVATION OF CASPASE 9- ACTIVATION OF CASPASE 3/6- ENDONUCLEASE ACTIVATION- APOPTOSIS

SAD!!!

42
Q

VIRUS INFECTION- FAS+TNF1 INTEGRATION- ACTIVATION OF CASPASE 8/10- ACTIVATION OF CASPASE 3/6- ENDONUCLEASE ACTIVATION- APOPTOSIS

RECALL CD8 CELL FUNCTION :)

= THIS PROCESS IS KNOWN AS—?

A

The Extrinsic (Death Receptor-Initiated) Pathway of Apoptosis!

KNOW THIS!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

43
Q

SUN EXPOSED SKIN BIOPSY FINDING.

WHATS THE MECHANISM OF THIS FORMATION OF THIS PINK CELL

A

APOPTOSIS VIA INTRINSIC PATHWAY!!!

44
Q

PINK CELLS- SEEN IN HEPATITIS B VIRAL INFECTION (IMAGE).

NAME THE CELL?

MECHANISM?

A

COUNCILMAN BODY

APOPTOSIS EXTRINSIC PATHWAY!!!

45
Q

Steps of the vascular event of acute inflammation?

A
  1. The release of mediators, notably histamine
  2. Vasodilation
  3. Increased blood flow
  4. Increased permeability of the microvasculature
  5. Slowing of blood flow
  6. Stasis
  7. Loss of axial flow
  8. Margination
46
Q

Steps of the cellular event of acute inflammation?

A
  1. Margination-
  2. Rolling
  3. Activation (Neutrophils)
  4. Adhesion (Including firm adhesion)
  5. Diapedesis of neutrophils- transmigration (part of migration)
  6. Chemotaxis (part of migration))
  7. and Phagocytosis

PATH MAGIC (21 decks)

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