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PRIN > PRIN 13 Inflammation > Flashcards

PRIN 13 Inflammation Flashcards

1
Q

What does the Lymphatic System include?

A 
Lymph nodes
Lymphatic Vessels
Tonsils
Thymus
Spleen
Peyer's Patches
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2
Q

What IS Lymph?

A

An ultra filtrate of blood

contains tissue fluid, WBC, fats & chyle) from GI

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3
Q

What makes lymph flow through vessels?

A

Contraction of skeletal muscle

One-way valves

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4
Q

Superficial & Deep Drainages … what do they follow?

A

Superficial drainage follows the veins

Deep drainage follows the arteries

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5
Q

What are the 2 major deep lymph drainage pathways?

A

Right Lymphatic Duct

  • drains R side of head R side of thorax
  • drains into R subclavian vein

Thoracic Duct

  • drains all the rest of the body
  • drains into L subclavian vein
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6
Q

When are lymph nodes palpable?

A

Superficial Nodes are palpable when inflamed
(eg):
Cervical nodes > 1cm
Inguinal nodes > 1.5cm

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7
Q

Which are the palpable lymph nodes?

A

EPIC-Ap

Cervical
Axillary
Epi-trochlear
Inguinal (superfic)
Popliteal
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8
Q

Which are the NON-palpable lymph nodes?

A

Parasternal
Aortic
Iliac
Inguinal (deep)

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9
Q

Inflammation which lymph nodes is suggestive of cancer?

A

Supra-clavicular Nodes & Virchow’s/Sentinal Nodes

from abdomen & thorax

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10
Q

Pathway of lymph drainage in breasts

A

Lateral & Inferior regions … axillary nodes

Medial regions … Parasternal Nodes … Subclavian Nodes … Subclavian Veins

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11
Q

Pathway of lymph drainage in testes

A

Lumbar & aortic nodes

not palpable

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12
Q

Pathway of lymph drainage in scrotum

A

Superficial inguinal nodes

palpable

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13
Q

What are central/primary lymphoid organs?

A

Sites of generation & early maturation of WBC

Bone Marrow
Thymus

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14
Q

What are Secondary Lymphoid Organs?

A

Lymph nodes
Spleen
Tonsils
Mucosal Tissue …

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15
Q

What arises from Hematopoietic Stem Cells?

A

Lymphoid Progenitors
(B&T cells)
&
Myeloid Progenitors

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16
Q

What arises from Myeloid Progenitors?

A

Granulocyte / Macrophage Progenitor
*BEN, Monocytes (Macro & DCs)

Megakaryo & Erythrocyte Progenitor
*Platelets & RBC

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17
Q

What is pus?

A

Accumulation of dying neutrophils responding to the site of infection

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18
Q

What is left shift?

A

Sign of Early neutrophil release from BM

L Shift Products look more like monocytes and have not developed the normal multi-lobed nucleus

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19
Q

What are the 3 APCs?

A

“Big-MD”

Macrophages
DCs
B-cells

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20
Q

What is the function of the spleen?

A

Capture Ags from blood

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21
Q

What are germinal centers?

A

LOCATED IN LYMPH NODES
Region where lymphocytes have been stimulated by Ag

Result: Clonal expansion of activated B-cells

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22
Q

What is the Paracortical area of the lymph nodes?

A

Site where T-cells are interacting with APC & B-cells

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23
Q

Within the spleen, what is Red Pulp & White Pulp

A

RED: where aged RBCs are destroyed

WHITE: lymphoid areas

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24
Q

Which cells serves as the bridge between Innate and Adaptive Immune Systems?

A

Dendritic Cells

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25
Q

What do neutrophils respond to?

A

Chemotactic factors

Neutrophils migrate toward higher concentration of chemotactic factors

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26
Q

Which cells are phagocytic?

A

Nasty-MD

neutrophils
monocyte/macrophage
DCs

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27
Q

Within the complement system, what are the 3 pathways?

A

Classical
Lectin
Alternative

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28
Q

Within the complement system, when do all 3 pathways unite?

A

Cleavage of C3:
C3a - anaphylatoxin
C3b - cleaves C5

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29
Q

What do T cells do?

A

Circulate through system checking out antigens presented on the MHC of APCs

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30
Q

What do Abs do?

A

Bind to Ag of microbes & serve as a flag. Microbe cell becomes coated in Abs (ADCC)
(antibody coated cell)

Signals for destruction via phagocytosis by NK & Macrophages

NOTE: Abs kill INDIRECTLY by simply acting as an opsonin

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31
Q

What system kills via MAC?

A

Complement System
kills via Membrane Attack Complex
(lyses cells)

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32
Q

Which complement pathway is initiated by Ab-Ag complex?

A

Classical Pathway

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33
Q

What is the clinical result of not having a functional Complement System?

A

Infection

Autoimmunity

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34
Q

What do NK cells do?

A

Attack cells with intracellular disturbances that do not look normal

(eg) tumor cell, virus infected cell

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35
Q

What do Neutrophils do?

A

Devour extracellular pathogen. In the process of neutrophills sacrifice themselves

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36
Q

What is pus?

A

Dying / Dead neutrophils

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37
Q

What are PMNs?

A

aka Neutrophils

Polymorphic Nuclei

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38
Q

Why do cancer patients receiving treatment have poor immune response?

A

Cancer treatment targets quickly dividing cells. Neutrophil development is inhibited

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39
Q

What is ROS?

A

Reactive Oxygen Species
molecules produced in “oxidative bursts” that function in lysosomes
(eg) H2O2, radicals, HOCl

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40
Q

Which cells kill pathogens by production of ROS?

A

MEN

Neutrophils
Macrophages
Eosinophils

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41
Q

What is CGD?

A

Chronic Granulomatous Disease
Impaired innate immune system due to lack of oxidative bursts (ROS)

Results in recurrent bacterial infections

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42
Q

What is the primary, most IMPORTANT role of DCs?

A

Antigen Presentation

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43
Q

PAMP vs PRR

Which cell has what?

A

MICROBE-PAMP
(pathogen associated molecular pattern)

PHAGOCYTE-PRR
(pattern recognition receptor)

Note: each PRR only recognizes one PAMP

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44
Q

How is Homeostasis maintained in the Innate System?

A

EARLY:
Neutrophils & Macrohages act as the alarm signal & trigger inflammation

LATER:
DCs down-regulate inflammation & promote healing

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45
Q

What happens within a few minutes following tissue injury?

A 
Vasodilation
Increased Blood Flow
Increased Permeability
Resident Macrophages defend
Extravasation
46
Q

What happens within a few hours following tissue damage?

A

Neutrophil infiltration into tissues

47
Q

The first immune cells to attack pathogen is what?

How does it do it?

A

Resident Macrophages have PRR that recognize PAMP on pathogen.

  • **Phagocytosis …
  • **Call the alarm: Release Cytokines: IL1, IL6, TNFa
48
Q

What are the LOCAL effects of the released cytokines?

A

IL1, TNFa:
up-regulate adhesion molecule

NO, IL1, IL6, TNFa:
Vasodilate
Increase Vasc. Perm.

TNFa:
Promote chemotaxis & activation of neutrophils

49
Q

What releases NO?

A

Local endothelial cells

50
Q

What explains pain during acute inflammation?

A

Kinin Cascade
activated by contact with collagen & BM

FUNCTION: cleaves HMWK into Bradykinin

51
Q

What is Bradykinin ?

What does it do?

A

9aa peptide
Promotes vasodilation
Increase Vasc. Perm.
Stimulates pain nerve fibres

52
Q

What activates Mast Cells?

A

C3a
C5a
TLR

53
Q

What do Mast Cells Release?

A

Histamine
IL6
TNFa

(cytokines are released contributing to redundancy)

54
Q

What is Histamine?

What does it do?

A

Small amine molecule that binds to receptors on endothelial cells & smooth muscle cells

Causes:
Promotes vasodilation
Increase Vasc. Perm.

55
Q

By 6 hours following injury, what immune cells predominate?

A

Neutrophils (PMNs)

56
Q

Steps in Neutrophil Extravasation

A

(1) Rolling adhesion
(2) Tight Binding
(3) Diapedesis

57
Q

What mediates neutrophil tight binding?

A

LFA-1 on Neutrophil

ICAM-1 on endothelial cell

58
Q

Besides neurophils, what other immune cells respond to the cry for help?

A

Monocytes

Recruitment is more gradual than PMN recruitment

59
Q

What are the SYSTEMIC effects of cytokines?

A

IL-1, IL-6, TNFa:
To Brain … released prostaglandins … fever

To Liver … Secrete APRP (CRP) etc..

IL-6, TNFa:
To Bone Marrow … Leukocytosis … neutrophilia

60
Q

Exogenous

A

Bacterial Infection
MHC2
CD4+ T_helper

61
Q

Endogenous

A

Viral
MHC1
CD8+ CTL

62
Q

What are the 3 signals that activate T Cells?

A

(1) MHC-Ag to TCR
(2) Costimulation
(3) Cytokines help differentiation of T Cells

63
Q

What do CTLs do?

A

Cytoxic T Lymphocytes (when activated) kill by inducing the infected cell to undergo apoptosis

64
Q

Which cells can present via MHC1?

A

All cells in the body … any cell can become virally infected

65
Q

Which cells can present via MHC2?

A

APCs: “Big MD”
Macrophages
B-cells
DCs

66
Q

Which are the BEST APCs?

Why?
2 reasons

A

(1) have the most PRRs

(2) provide the best costimulation of Naive T cells

67
Q

What is an example of a co-stimulatory signal as presented by a DC?

A

B7 on DC interacts with

CD28 on T-Helper

68
Q

What is an example of cytokine release finishing the activation of a T-helper cell?

A

IL-2 via autocrine by T-helper

“self kick in the pants”

69
Q

What type of cytokines does the DC release?

A

IL-12, TNFa

70
Q

How do Abs kill a microbe?

A

INDIRECTLY:

*bind Ag of pathogen and act as flag calling NK cells to come and kill

71
Q

What do NK cells do?

A

Wander the system and hunt down cells that don’t look quite right ….
(eg) tumor cells, cells covered in Abs, infected cells

72
Q

Besides its role in complement activation, what does C3b do?

A

Acts as Opsonin

C3b binds to pathogen and enhances the ability of a macrophage to engulf it

73
Q

What does TH1 do?

A

secretes INFy which activates macrophage to up-regulate lysosome mechanisms

74
Q

Acute vs Chronic Inflammation

What are the predominant cells involved?

A

ACUTE:
Neutrophils

CHRONIC:
T Cells, Macrophages

75
Q

Acute vs Chronic Inflammation

What is a bacterial example of cause?

A

ACUTE:
S aureus

CHRONIC:
M. Tuberculosis

76
Q

HOW does M Tuberculosis cause chronic inflammation

A

Bacteria survive in lysosomes of macrophages

Macrophages accumulate and started going “crazy” whereby they spew out their proteolytic enzymes

77
Q

What is a Tuberculous granuloma?

A

Attempt to section off damaged area in lungs caused by exploded macrophages …. leads to loss of lung tissue function

78
Q

Which cell is involved in the clean up after infection and inflammation is resolved?

A

Macrophages

79
Q

What is Meningitis?

A

Inflammation of the meninges.

caused by N. meningitidis

80
Q

Why did the Meningitis patient get a rash that eventually led to necrosis?

MOA?

A

Bacteria had entered the blood stream (bacteremia) and circulated the system getting stuck in the smallest capillaries.

The rash was caused by the body mounting an inflammatory response. Bacteria damaged endothelial cells. Inflammatory response resulted in the vessels becoming extremely leaky.

81
Q

Why was Rifampin given to Anna’s roommates?

A

Rifampin = RNA polymerase inhibitor

Given as a chemo-prophylactic measure

82
Q

What is DIC?

A

Dessiminated Intravascular Coagulation

blood clots form throughout the body’s small blood vessels.

These blood clots can reduce or block blood flow through the blood vessels, which can damage the body’s organs.

Platelets get used up and internal bleeding occurs

83
Q

Anna’s acute phase response resulted in …

A

Fever
neutrophilia
high CRP

84
Q

What is vasculitis?

A

Inflammation of SMALL blood vessels in response to encounter with pathogen stuck in capillaries

85
Q

Which cell type infiltrates in large numbers into the rash sites:

A

Neutrophils

86
Q

Why is Neissaria Meningitis so dangerous?

A

gram - bacteria releases LPS toxin as it dies

87
Q

Signs of Sepsis

A

Bacteria present in blood stream accompanied by inflammatory response result in:

  • *Fever
  • *Elevated HR & RR
88
Q

What marks the entrance into Septic Shock?

A

BP drops even though we are administering fluids

89
Q

Disseminated Intravascular coagulation

What tests are done?

A

d-dimer
platelet count
prothrombin time

We must monitor our Meningitis patient for this!

90
Q

What are the three amigos?

A

IL-1
IL-6
TNFa

91
Q

Which cells present MHC-1?

Which cells present MHC-2?

A

MHC-1:
All nucleated cells

MHC-2:
APC’s only (B cells, DCs, Macrophages)

92
Q

What is the role of MHC I?

A

recognizing altered self and presents Ag to CTLs

i.e.: samples the intracellular milieu and presents intracellular antigens on the surface of cells

93
Q

What is SIRS?

A

systemic inflammatory response syndrome

94
Q

How do we diagnose Disseminated intravascular coagulation?

A

fall in blood platelet levels

95
Q

What induces immediate endothelial cell retraction?

A

NO

histamine

96
Q

What is the predominant immune cell type in granulomas

A

Macrophages

97
Q

Which one of the following phases of drug development is most likely to include healthy human subjects?

A

Phase 1

98
Q

Where does peptide loading of MHC Class I molecules with endogenous antigens occur?

A

ER

99
Q

What are the phagocytes?

A

neutrophils,
macrophages/monocytes
DCs

100
Q

Which cells are involved with resolving inflammation?

A

Macrophages

101
Q

Which complement protein also acts as an opsonin?

A

C3b

102
Q

Which complement proteins trigger mast cell degranaulation?

A

C3a, C5a

103
Q

Which cell types can produce reactive oxygen species via a respiratory burst?

A

MEN

Neutrophils
Eosinophils
Macrophages

104
Q

Which cell type takes up microbes via antigen-specific receptors, then processes and presents microbial antigens?

A

B-cells

note … Ag specific!!!

105
Q

Which cell type releases nitric oxide, a potent vasodilator?

A

Macrophages

106
Q

Are neutrophils phagocytic and Ag presenting?

A

Phagocytic only

They simply follow the trail of chemo tactic factors, gobble up cells and then die

106
Q

How do CTL kill?

A

Once in direct contact with affected cell, CTL releases Perforin & Granyme B into it … triggers Caspases … apoptosis

107
Q

In the case of persistent and localized antigenic stimulation (i.e.: mycobacterium, sutures, parasitic eggs etc) the immune system responds by walling off the antigen. What type of process is this?

A

Chronic Inflammation

108
Q

Which cells are involved in resolving inflammation.

A

Macrophages

109
Q

Which cell type presents antigen and activates naïve TH?

A

DCs

110
Q

Which cell type takes up microbes via antigen-specific receptors, then processes and presents microbial antigens?

A

B cell

111
Q

Which cell type releases nitric oxide, a potent vasodilator?

A

Macrophage, Endothelial Cells

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