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Week 6 Foundations of Medicine > Inflammation Lecture Oct 2 > Flashcards

Inflammation Lecture Oct 2 Flashcards

1
Q

What are the 5 cardinal signs of inflammation?

A

redness

swelling

heat

pain

loss of function

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2
Q

What are the four main stimuli for actue inflammation?

A

Infections (receptors recognize microbe/microbe products)

Tissue necrosis (trauma, ischemia, chemical/thermal, irradiation release molecules from dead cells)

Foreign bodies

Immune reactions (hypersensitivity reactions)

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3
Q

What are the three major components (what happens) in acute inflammation?

A
  1. vasodilation to increase blood flow
  2. Increased permeability of blood vessels allowing fluid, proteins, and leukocytes to enter the tissues
  3. Emigration of the leukocytes from the circulation, accumulation at the site of injury, and removal of offending agent
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4
Q

What is an exudate? What is a transudate? How are they different?

A

An exudate is a buildup of fluid in the extracellular space with a HIGH PROTEIN CONCENTRATION (high cellular debris and high specific gravity)

A transudate is a buildup of fluid in the extracellular space WITH LOW PROTEIN CONCENTRATION (no cellular debris, low specific gravity).

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5
Q

What does the presence of an exudate imply?

What does the presence of a transudate imply?

A

Presence f an exudate implies an increase of normal permeability of small vessels in an area of injury - allowing both fluid AND protein to enter the tissues.

Presence of a transudate implies an imbalance betwee nthe osmotic or hydrostatic forces across the vessel wall WITHOUT an icnrease in vascular permeability - only fluid will leak out.

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6
Q

What’s edema? WHat’s effusion?

A

Edema is an excess of fluid in the interstitial tissue

An effusion is excess of fluid in a serous cavity (like in the lungs or pericardial space)

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7
Q

Is pus a transudate or an exudate?

A

an exudate - it has a high level of neutrophils, cell debris and microbes

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8
Q

What are the blood vessel reactions to inflammation?

A
  1. vasodilation (increased blood flow)
  2. . Increased vascular permeability (escape of protein rich exudate into tissues - edema)
  3. stasis (dilated vessels packed with slowly moving RBCs because of fluid loss, resulting in fascular congestion)
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9
Q

What are three mediators of blood vessel vasodilation in the inflammatory response?

A

histamine

nitric oxide

prostacylin

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10
Q

What are the three mechanisms of increased vascular permeability?

A
  1. constriction of endothelial cells — increased interendothelial spaces (mediated by histamine, serotonin, complement, bradykinin, leukotrienes, substance P)
  2. ENdothelial injury
  3. increased transport of fluids and proteins
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11
Q

What causes stasis?

A

if the small vessels are dilated and fluid loss is occuring, then the vessels will be packed with slowly moving RBCs which can result in vascular congestion visible to the eye in affected tissues - redness

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12
Q

How do the lymphatic vessels participate in the vascular response of inflammation?

A

DUring inflammation, the increase in extracellular fluid will lead to increase lymph flow.

THerefore, the lymphatics can become secondarily inflamed (the red streaks een in lymphangitis)

THe draining lymph nodes will swell and becoem painful (lymphadenitis)

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13
Q

What are the three main steps of extravasation of leukocytes from the blood into the extracellular space?

A
  1. Leukocyte adhesion to endothelium: through marginalization (leukoctyres near the wall), rolling (transient adherence to endothelial wall), and adhesion (stop rolling and bind to I-CAM)
  2. Leukocyte migration through the endothelium into the extracellular space (transmigration or diapedesis)
  3. Chemotaxis of leukocytes to the area of infection
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14
Q

What mediates the adherence of leukocytes to the endothelial wall?

A

Margination occurs secndary to the effects of stasis

Rollin ginteractions are mediated by proteins called selectins which bind to silalylated oligosaccharide ligands (the expression of these are mediated by cytokines like TNF and IL1)

Firm adhesion is mediated by surface proteins on the leukocyte called INTEGRINS (expression enhanced by cytokines) binding to I-CAM on the endothelial wall with the help of chemokines like CXCL8

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15
Q

What mediates leukocyte migration through the endothelium and into the extracellualr space?

A

The binding of the leukocyte integrin to the endothelial wall I-CAM

plus chemokines

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16
Q

What mediates chemotaxis of leukocytes?

A

It’s locomotion oriented along a chemical gradient of the chemokines

The chemotactic agents will then bind to the surface of the leukocyte, including the polymerization of intracellular actin and resulting in leukocyte locomotion

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17
Q

What are some examples of exogenous and endogenous chemoattractants?

A

Exogenous: bacterial products

Endogenous: cytokines, complement components, arachidonic aci metabolites (mainly leuokotriene B4)

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18
Q

What blood cells predominate in the early stages of inflammation? What are they later replaced by?

A

Neutrophils predominate at first (wihthint 6-12 hours), but they die off quickly and are replaced by monocytes (macrophages)

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19
Q

What three sets of receptors allow leukoctyes to recognize external stimuli?

A
  1. Receptors for microbial produccts (TLRs for PAMPs)
  2. GPCRs for PAMPs, chemokines, breakdown products of complement, prostaglanding, leukotrienes, etc.
  3. receptors of opsonins (so Fc and C3 receptors)
  4. Receptors for cytokines like INF-gamma (which are secreted by NK cells and T cells to activate macrophages)
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20
Q

How is the degradation within the neutrophil or macrophage largely accomplished?

A

Mostly through ROS and reactive nitrogen species. This requires rapid oxidative reactions called the respiratory or oxidative burst.

THey also use digestive enzymes

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21
Q

In addition to eliminating microbes and dead cells, what else can macrophages do?

A

THey can produce growth factors that drive the process of repair

However,t hey can also cause injury to normal cells if the microbe is difficult to eradicate or if the inflammatory response is inappropriately directed or excessive

22
Q

How can defects in leukocyte function arise and what problem does this cause?

A

This causes an increased vulnerability to infections

inherited defects in: leukocyte adhesion, phagolysosome function (chediak-higashi), inherited defects in the microbicidal activity within the leukocyte, and ACQUIRED DEFICIENCY FROM destruction of bone marrow in chemotherapy

23
Q

How is the actue inflammatory response controlled/terminated?

A
  1. chemical mediators like histamine are produced rapidly but also degrade quickly
  2. neutrophils have a short life span
  3. Inflammatory process also triggers a variety of stop signals such as change in arachidonic acid metabolism, liveration of anti-inflammatory cytokines, production of anti-inflammatory lipid mediators, and neurl impulses that inhibit production of TNF from macrophages
24
Q

What are the mediators of inflammation?

A

Vasoactive amines (histamine and seratonin)

Arachidonic Acid Metabolites (prostaglandinds and leukotrienes, also lipoxins)

Platelet aggregating factor (PAF)

ROS

Nitric oxide

Cytokines (especially TNF and IL-1)

Chemokines

Lysosomal constituents of leukocytes

Neuropeptides

25
Q

How do arachidonic acid metabolites mediate inflammation?

A

WHen activated, cells can convert membrane-bound AA into prostaglandins and leukotriends

Prostaglandins (from mast cells, macrophages, and endothelial cells): vascular response + pain and fever

Leukotrienes (from leukocytes): chemoattractant and vascular affects

Lipoxins: actually inhibit inflammation

26
Q

How do COX1 and COX2 inhibitors work to lower inflammation?

How do steroids work to control inflammation?

A

STeroids blod the phospholipases that cleave arachidonic acid from the membrane.

THe COX inhibitors block cyclooxygenase so you don’t get the production of prostaglandins from arachidonic acid

27
Q

Where does platelet aggregating factor come from and what does it contribute to?

A

It’s secreted by platelets, leukocytes, mast cells and endothelial cells.

It elicits most of the vascular and cellular reactions of inflammation as well as vasoconstriction, boncohspasm and platelet aggregation

28
Q

What are some of the main inflammatory effects of cytokines? Particularly IL1 and TNF?

A
  1. expression of leukocyte adhesion molecules to aid in extravasation
  2. increase leukocyte activation and further production of cytokines
  3. increase coagulation
  4. increase proliferation of fibroblasts and collagen synthesis for repair purposes
  5. Results in fever
  6. Production of acute phase proteins in the liver
29
Q

What family of proteins act as chemoattractants for leukocytes?

A

chemokines (through concentration gradients and GPCRs)

30
Q

What is the complement system involved in?

A

THey are involved in the inflammation itself because C3, C5 and C4 stimulate histamine release from mast cells. C5 is a chemoattractant and activates arachidonic acid conversion into inflammatory mediators

THey are involved in opsonization for phagocytosis: C3b when bound to microbial cell wall will promot phagocytosis by neutrophils and macrophages

They are involves in cell lysis: C9 complexes on microbrial cell walls create membrane attack complexes resulting in influx of ions and water - cell lysis

31
Q

WHat does the inflammatory response look like in an actue MI?

A

You get the formation of coagulative necrosis which recruits a neutrophil response,

Later, macrophages will arive to scavenge the debris

32
Q

What is acute suppurative inflammation?

A

acute inflammation which is rich in neutrophils, forming pussy discharge.

33
Q

What is a localized collection of purulent inflammatory tissue called?

A

and abscess

34
Q

What do serous effusions arise from?

A

First of all, serous effusions are transudative effusion and do not arise form non-inflammatory mechanims

35
Q

WHat develops if you have fibrinogen passing through the vessles during inflammation?

A

you get fibrin being deposited int he extracellular space, which is later replaced by fibrous tissue

36
Q

What is empyema? WHen does it occur?

A

Empyema is a word for suppurative (purulent) inflammation within a pleural cavity - this is an exudative effusion that ariese from inflammatory mechanisms

37
Q

What are the three situations when chronic inflammation can arise?

A
  • with persistent infections like TB
  • with immune-mediated inflammatory disease - autoimmune or allergies
  • prolonged exposure to a toxic agent (liike silicosis)
38
Q

WHat is chronic inflammation characterized by? 3 things…

A
  1. Inflammation with MONONUCLEAR cells (macrophages, lymphocytes, plasma called) as opposed to neutrophils in acute inflammation
  2. Tissue destruction (without the vascular changes adn edema)
  3. Attempts at healing with CT replacement of damaged tissue (fibrosis) and proliferation of small vessels (angiogenesis)
39
Q

What cell tryps are involved in chrinic inflammation?

A

macrophages

lymphocyts

plasma cells

eosinophils

mast cells

40
Q

Describe the feedback loop between macrophages and lymphocytes.

A

So the macrophages present antigen to the T cells to activate them, which then secrete cytokines to activate macrophages.

This is why you end up with chromic inflammation if an infectiond doesn’t clear.

41
Q

WHy are eosinophils effective against parasites but not bacteria?

A

their granules contain major basic prtoein which is toxic to worms but not to bacteria

42
Q

What stimulates the growth of blood vessels and lymphatics in chronic inflammation?

A

growth factors released by macrophages and endothelial cells

43
Q

What is a granuloma and when does it form?

A

During infections that are hard to eradicate, a granuloma will form - it’s a form of chornic inflammation consisting of an aggreagation of macropahges

the macrophages first become more like epithelial cells - histiocytes - and then join together to form multinucleated giant cells.

They surround the infection

44
Q

WHat are the three forms of granulomas and when do they occur?

A

Foreign body granulomas - around indigestible material

Caseating granulomas - induce necrosis inside (as in TB or fungal infections)

Non-caseating granulomas - induce the cell mediated immune response without central necrosis (sarcoidosis or crohn’s)

45
Q

When might you see a non-caseating granuloma in a TB infection?

A

if the person is immune compromised and can’t develop the necrosis inside the granuloma

46
Q

WHat is the acute phase response? Characteristics?

A

the systemic changes in inflamation:

fever, synhtesis of acute phase proteins, leukocytosis, hypotension, rigors, chills, anorexia, somnolence, malaise, septic shock

47
Q

What are some of the acute phase proteins and what d othey do?

A

These are plasma proteins synthesized in the liver that increase greatly as a result of inflammation:

C-reactive protein

Fibrinogen

Serum amyloid A protein

48
Q

What is the erythrocyte sedimentation rate? What does it tell you?

A

THe ESR is a nonspecific test for inflammation:

Acut phase proteins like fibrinogen and antibodies will bind to RBCs and make them stack - rouleaux - which makes them sediment out faster in a tube of blood.

So elevated ESR means inflammation.

49
Q

What is C-reactive protein and what does it tell you?

A

C-reactive protein is an acute phase protein, so it can be tested for in the bloo das a marker for inflammation.

This is very sensitive but not specific for inlammation.

50
Q

WHat can the WBC differential tell you?

A

Which specific WBC is elevated can give you an idea of what kind of inflammation they have:

Neutrophili: acute inflammation from new infection or MI

Eosinophilia: allergic reaction or parasite infection

Basophili: chronic myeloid leukemia

Monocytosis: chronic infections

Lymphocytosis: viral infections

51
Q

Does a negative WBC and no fever rule out bacteremia?

A

No. People with immune compromise may not have a WBC or fever. THe patient may have a defect in the fever pathway. Their WBCs may just be entering the tissues too quickly so they’re not noticed in the blood.

52
Q
A

Week 6 Foundations of Medicine (12 decks)

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