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Mechanisms of Disease > Inflammation & Repair - Friedlander > Flashcards

Inflammation & Repair - Friedlander Flashcards

1
Q

Inflammation

A

The response of vascularized tissue to injury

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2
Q

Acute inflammation

A

Vessels dilate - histamine - red and hot
Vessels leak protein
(albumin, IgG and fibrinogen depending on severity)
Neutrophils pass through venues and damage anything they think is bacteria - pain, loss of function

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3
Q

If you hurt a little what comes out?

A

Albumin - swelling

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4
Q

If you hurt worse what comes out?

A

IgG

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5
Q

If you hurt real bad what comes out?

A

Fibrinogen/fibrin for mesh

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6
Q

Chronic inflammation

A

Orchestrated mostly by T-cells
B cells become plasma cells and make antibodies
Macrophages gobble things up

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7
Q

What do eosinophils kill?

A

Worms

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8
Q

Granulomas

A

Pissed off macrophages form walls

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9
Q

What does a scar do?

A

CONTRACTS

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10
Q

What happens to the fibrin meshwork?

A

If not destroyed by plasmin, will be organized into granulation tissue by endothelial cells and fibroblasts

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11
Q

What do fibroblasts make?

A

Collagen fibers

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12
Q

How does the body defend itself?

A

Inflammation

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13
Q

What cell type has 3 segments with 2 bridges?

A

Neutrophils

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14
Q

What cell type has a kidney bean shaped nucleus with a dent?

A

Monocyte

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15
Q

What is a band cell?

A

Immature neutrophil

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16
Q

What cell has a nucleus that takes up almost the entire cell?

A

Lymphocyte

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17
Q

What changes to a macrophage when it leaves the bloodstream?

A

Monocyte

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18
Q

What are the commandos of acute inflammation?

A

Neutrophils

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19
Q

What is diapedesis?

A

Transmigration of neutrophils through a blood vessel

-not through the capillary, too big, would damage it

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20
Q

What are azurophil granules?

A

Myeloperoxidase
Elastase
Cathepsins
Lysozyme

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21
Q

What are specific granules in neutrophils?

A

Alkaline phosphatase, lactoferrin and collagenase

Lysozyme

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22
Q

Myeloperoxidase

A

A heme based protein that produces hypochlorite like in household bleach

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23
Q

Free radical pathway

A

Oxygen —-(NADPH oxidase)—> Superoxide –(superoxide dismutase)—-> H2O2 —-(myeloperoxidase)—-> Hypochlorite (OCl-)

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24
Q

What is the effect of ongoing inflammation on neutrophils?

A

Makes neutrophils stick better and get through the endothelium

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25
Q

If you see an single inflamed joint, what should you expect?

A

Gonococcal infection

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26
Q

Hyperemia

A

Extra blood flow through dilated arteries

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27
Q

Neutrophils and all human tissue are gram____

A

Negative

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28
Q

What is the adjective for pus?

A

Purulent

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29
Q

What is the verb for making pus?

A

Suppurate

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30
Q

Abscess

A

Pus surrounded by more normal tissue

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31
Q

Empyema

A

Pus filling a body cavity

ie. pleural space, gall bladder

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32
Q

What happens to neutrophil nuclei after death?

A

Lose segmentation

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33
Q

Why does pus build up pressure?

A

Because of the osmotic pull of the small molecules produced by hydrolysis of big proteins

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34
Q

Gum abscess

A

From a deep root infection
Feels great when it ruptured outward
Used to be a common killer

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35
Q

The greenish tinge of pus on exposure to air is due to?

A

Neutrophil myeloperoxidase

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36
Q

Pseudomonas infections? What is the pigment

A

Fluorescent green pus that smells like grapes

Pigment is pyocyanin

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37
Q

Clostridial infections

A

Thin (hyrolyzed), gray (lipolyzed) dishwater pus

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38
Q

What is a toxic granulation?

A

A powered up neutrophil

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39
Q

Left shifted

A

When a peripheral smear shows a lot of immature neutrophils (child soldiers)

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40
Q

What is a leukemoid reaction?

A

> 50,000 WBC in the absence of true leukemia

High leukocyte alkaline phosphatase, toxic granulation and will lack the chromosome markers for leukemia

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41
Q

What is the alk phos level in leukemia?

A

Low

vs. high in leukemoid reaction

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42
Q

Systemic inflammatory response

A

Current term for multiple organ failure developing as a result of a bad infection
Extreme elevations of IL-1 and TNF-a
–treating the cause may not save the patient

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43
Q

How does staphylococci try to evade host defense?

A

Sequester and hide themselves

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44
Q

How does streptococci try to evade host defense?

A

Try to outrun them

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45
Q

Meningitis

A

Pus at the base of the brain

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46
Q

Chediak-Higashi

A

Problems with organelles (lysosomes, melanocytes) and thus impaired neutrophil killing of microbes

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47
Q

Chronic granulomatous disease

A

Several defects in neutrophil killing of common staphylococci
-body walls off staph using granulomas instead

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48
Q

The fluid released from vessels in inflammation is called?

A

An exudate

-protein rich

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49
Q

Friction blister

A

Epidermis detached from dermis

-very mild inflammatory cellular reaction

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50
Q

Reactive oxygen species

A

ROS - free radicals

Need these to kill germs

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51
Q

How long do neutrophils last? And then what do they do?

A

72 hours or so and then turn into traps

-neutrophil extracellular traps

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52
Q

Sunburn is an example of

A

Vessel dilaltion

–the molecular and cellular mediators of inflammation aren’t even involved

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53
Q

After a scratch what is the triple response of Lewis?

A
  1. local redness
  2. a flare surrounding the scratch - cap dilate
  3. swelling (a wheal) surrounds the scratch
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54
Q

Which step of the triple response of Lewis is dependent on an intact nerve supply?

A

Flare (2)

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55
Q

Histamine and functions in inflammation

A 
Major mediator
Dilate blood vessels
Make them leaky to proteins, especially albumin
Contribute to pain and itching
Bronchoconstriction
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56
Q

Serotonin

A

Released from platelets
Constricts vessels
Emotional health

57
Q

Bradykinin

A

Inflammatory protein that dilates vessels, partly by producing PGI2/prostacyclin
Produced in the blood by kinin-kallikrein system
Bronchoconstrictor and inflames the airway mucosa

58
Q

How are prostaglandins and thromboxanes made?

A

From arachidonic acid by means of cycle-oxygenase

59
Q

Prostaglandin E2 (and D2)

A

Variety of effects in acute inflammation
Fever
Vessels permeable and dilate

60
Q

Prostacyclin (PGI2)

A

Inhibits platelet aggregation and dilates blood vessels

-keep the vessels open for the troops

61
Q

Thromboxane A2

A

Promotes platelet aggregation and constricts blood vessels

-let’s not have a hemorrhage right now, troops

62
Q

When cyclo-oxygenase is inhibited pharmacologically what happens to AA?

A

Gets shunted into the lipo-oxygenase pathway instead - this favors production of neutrophils and macrophages
-leukotrienes and lipoxins

63
Q

Leukotriene B4

A

Famous promoter of neutrophil attachment and chemotaxis

64
Q

Leukotrienes C4, D4 and E4

A

Generally constrict vessels, permeable and constrict airway smooth muscle
–meds for asthmatics

65
Q

5-HETE

A

Also produced by neutrophils and lymphocytes via the lipoxygenase pathway is a powerful chemotactic agent

66
Q

Lipoxins

A

Produced by neutrophils and macrophages when inflammation is about to end

67
Q

C3a

A

Powerful chemotactic agent

-second only to C5a

68
Q

C3b

A

Binds to microbes via Abs and allows more complement activation nearby
Promotes opsonization and therefore phagocytosis

69
Q

C5a

A

Promotes chemotaxis
Makes more adhesion molecules on endothelium
Makes vessels dilate
Makes vessels leak

70
Q

Membrane attack complex

A

MAC
Produced at end of complement cascade
Punches holes in membranes

71
Q

IL-1

A

Produce by macrophages, and others

Effects:
Fever
Increased neutrophil production
Increase in adhesion molecules
recruit lymphocytes
Fatigue and sensitivity to pain
Dilates blood vessels
72
Q

Anakinra

A

Blocks IL-1Ra

Works against RA

73
Q

IFN-y

A

Made by T cells mostly
Proinflammatory cytokine
-recruit neutrophils and macro
-activate macros and make more deadly
-make cells produce more IL-1, IL-12, IL-23
Used for chronic granulomatous disease and osteopetrosis

74
Q

IL-2

A

Regulate whether T-cells respond to antigens or tolerate them
Tx of malignant melanoma and renal cell carcinoma

75
Q

IL-4 and IL-13

A

Anti-inflammatory

Produced in macrophages and tell them to produce other anti-inflammatory mediators - TGF-B, IL-10

76
Q

Which macrophages are the ‘nicer’ ones?

A

Alternatively activated - M@

Oriented toward healing, pump out osteopontin

77
Q

IL-5

A

From Th2 and mast cells

Attracts and activates eosinophils

78
Q

IL-6

A

Some pro-inflammatory - fever, neutrophil production
Some anti
When produced from muscle has anti-inflammatory properties

79
Q

What is the one major cytokine produced by skeletal muscle?

A

IL-6

80
Q

Which cytokine is credited for much of the acute phase reaction?

A

IL-6

81
Q

IL-12

A

From stimulated dendritic macrophages and stimulated b-cells

Turns undifferentiated T cells into T-helper cells

82
Q

IL-17

A

Produced mostly by T-helper 17 cells

Promote recruitment of neutrophils, macrophages and Th17 cells to sites of inflammation

83
Q

Tumor necrosis factor

A

Produced by macrophages and has pro inflammatory effects

  • fever
  • neutrophil production
  • activates neutro and macro
  • mediates acute phase reaction
  • promotes thrombosis
  • promotes insulin resistance
84
Q

Which cytokine is most important for treating asthma, RA, ankylosing spondylitis, IBD, psoriasis
What are the chief risks of these meds?

A

TNF

TB and fungal infections are chief risks

85
Q

Platelet derived growth factor

A

Powerfully promotes growth of new vessels

–granulation tissue/young scar

86
Q

TGF-B

A

Key to effective collagen production in scar and is blamed for fibrosis in chronic inflammation
Slows inflammation, promotes fibrosis and restoration of damaged epithelial populations

87
Q

CRP

A

C Reactive Protein
Produced in liver in response to the acute phase reaction
‘Pop’ blood test for coronary risk factor
Clear value in rheumatology

88
Q

SAA

A

the protein that is often beta-pleated to amyloid in chronic inflammation
ie. leprosy

89
Q

what is the disease that can mimic anyting

A

Familial mediterranean fever

90
Q

The acute phase reaction

A

The quantities of various proteins in the plasma change when significant inflammation has been going on for a while
This causes the red blood cells to sink faster in the plasma

91
Q

Neutrophils

A

Classic bacteria infection, candida, bad injury

92
Q

Lymphocytes

A

Autoimmunity, viruses, pertussis

93
Q

Monocytes

A

Mycobacteria, other fungi, typhoid

94
Q

Eosinophils

A

Worms, asthma, Hodgkin’s, dermatits herpetiformis

They have extremely alkaline granules

95
Q

Plasma cells/activated B cells

A

Especially abundant with spirochetes

-syphilis, Lyme disease

96
Q

What has no inflammatory cells?

A

Prions
Gas gangrene - very aggressive clostridia
The very immunocompromised

97
Q

A lymphocyte with a nuclear mini-dent is often what type of cell?

A

T killer

98
Q

The inflammatory reaction in most viral infections is mostly what?

A

Lymphocytes

99
Q

What do plasma cells look like?

A

Nucleus to one side, looks like a soccer ball

100
Q

The hardness of a chancre in primary syphilis is due to what?

A

Great abundance of mostly plasma cells

101
Q

Where is tattoo ink located?

A

In fixed macrophages

102
Q

In an infection, what comes first and then later on?

A

Neutrophils first

Monocytes/macrophages later

103
Q

Talk to me about splinters

A

Epithelium doesn’t tolerate free edge, so grows along splinters
Macrophages adhere to splinter and to one another forming a granuloma

104
Q

Epithelioid

A

Macrophages are called this because they stick together
Mimic epithelium
Aka granuloma

105
Q

Foreign body giant cells

A

Are fused clusters of macrophages with nuclei distributed throughout

106
Q

Langhans giant cells

A

Fused macrophages with nuclei in a horseshoe around the edge

107
Q

What is the sealant for abrasions?

A

Fibrin

108
Q

Fibrous means

A

Collagen

109
Q

Fibrinous means

A

Fibrin

110
Q

Ulcer

A

The epithelium and a significant amount of the CT underneath have been lost to necrosis
Crater of an ulcer is always inflamed and fibrin-sealed

111
Q

Erosion

A

Loss of epithelium without significant damage to the underlying CT

112
Q

Pseudomembrane

A

Very broad, very shallow ulcer
Common in diphtheria and C. difficult
Often looks like a mushroom cloud

113
Q

Scab

A

Fresh clot
Factor 13 crosslinks fibrin
Ready to fall off, immature scar tissue underneath

114
Q

Law of epithelium? What eventually stops it?

A

Does not tolerate free edge

Stopped by contact inhibition

115
Q

Scar

A

New collagen laid down at a site of healing injury

116
Q

When do you get a scar?

A

If you damage the CT below the lamina propria

117
Q

Labile cell populations

A

Always renewing themselves

-bone marrow, gut epithelium, epidermis

118
Q

Stable cell populations

A

Renew themselves if some members die

-liver, other glands, fibroblasts

119
Q

Permanent cell populations

A

Very limited ability to replace lost members

-brain, heart

120
Q

4 steps of wounds healing

A

Fibrin
Becomes granulation tissue
Becomes scar
Scar contracts

121
Q

Who are budding pathologists?!

A

Maybe not us….but we are gonna kick some path ass on this test!!!!

122
Q

Exuberant granulation tissue

A

After injury
An exaggeration of healing, not sure why
May require surgical debridement

123
Q

Most famous angiogenic factor?

A

VEGF-A

124
Q

What color is dense collagen?

A

Deep blue

125
Q

Wounds heal by primary intention

A

When they are well-approximated, well-nourished, no diabetes, not on glucocorticoids, clean

126
Q

Healing by secondary intention

A

When it is complicated

Ie. motorcycle wreck

127
Q

Keloid

A

Scar that is overly large, tends to expand over time and has thick ‘glassy’ collagen fibers
The related hypertrophic scar lacks the serrated edge and has tendency to keep oxpanding

128
Q

What happens in healing bone?

A

Fibroblasts to cartilage to new bone

Just like in kids

129
Q

-tomy

A

cut something

130
Q

-ectomy

A

cut something out

131
Q

-ostomy

A

made a mouth to outside/between two organs

132
Q

-plasty

A

reshaped

133
Q

-pexy

A

moved something to the right place

134
Q

-rraphy

A

sewed something up

135
Q

-desis

A

made two things stick together

136
Q

Aching pain

A

Periosteum, tooth, dura, circuit in brain

137
Q

Burning pain

A

Mucosal injury

Nerve injury

138
Q

Crampy pain

A

Hollow organ

139
Q

Stabbing pain

A

Serosal membrane

Mechanisms of Disease (8 decks)

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