Chapter 3: Inflammation & Repair Flashcards by Robin Sautter

What are the cardinal signs of inflammation? What are they caused by?

rubor (redness) and calor (heat) - d/t histamine-mediated vasodilation of arterioles

tumor (swelling) - d/t histamine-mediated increase in ventral permeability

dolor (pain) - PGE2 sensitizes specialized nerve endings to the effects of bradykinin

functio laesa (loss of function)

How well did you know this?

Not at all

Perfectly

What degrades bradykinin?

ACE

How well did you know this?

Not at all

Perfectly

What is a complication of an ACE inhibitor?

ACE inhibitor inhibits the metabolism of bradykinin –> increases vessel permeability –> angioedema

How well did you know this?

Not at all

Perfectly

What are the sequential cellular steps involved in acute inflammation?

emigration (includes margination, rolling of neutrophils, firm adhesion in venules d/t expression of intern adhesion molecules such as beta2-integrins)
transmigration (diapedesis) of neutrophils
chemotaxis
phagocytosis via opsonization
intracellular microbial killing

How well did you know this?

Not at all

Perfectly

What inactivates beta2-integrins and produces neutrophilic leukocytosis?

catecholamines and corticosteroids

How well did you know this?

Not at all

Perfectly

Name some chemotaxis mediators

C5a
leukotriene B4 (LTB4)
bacterial products
IL-8

How well did you know this?

Not at all

Perfectly

What is the purpose of exudates?

dilates bacterial toxins

2. provides opsonins

How well did you know this?

Not at all

Perfectly

Macrophages and dendritic cells that have encountered microbes produce which cytokines to activate the endothelial cells of nearby venules to produce selectins?

TNF and IL-1

How well did you know this?

Not at all

Perfectly

What are the two main opsonins?

IgG and C3b

How well did you know this?

Not at all

Perfectly

In acute inflammation, what is the main cell present?

neutrophil

How well did you know this?

Not at all

Perfectly

In chronic inflammation, what is the main cell present?

macrophage/monocyte

How well did you know this?

Not at all

Perfectly

How does a neutrophil or monocyte kill bacteria or fungi?

O2-dependent myeloperoxidase (MPO) system

How well did you know this?

Not at all

Perfectly

What is the process of the MPO system?

NADPH oxidase enzyme complex converts molecular O2 to superoxide FRs –> releases energy (respiratory burst)

How well did you know this?

Not at all

Perfectly

How can you diagnose chronic granulomatous disease?

no color change from clear to blue when conducting an NBT dye test

How well did you know this?

Not at all

Perfectly

What are macrophages in the CNS called?

microglial cells

How well did you know this?

Not at all

Perfectly

What are macrophages outside the CNS called?

dendritic cells

How well did you know this?

Not at all

Perfectly

What is the MC precipitation of hemolysis in G6PD deficiency?

infection

How well did you know this?

Not at all

Perfectly

What causes Chronic Granulomatous Disease?

Deficiency in NADPH oxidase

How well did you know this?

Not at all

Perfectly

What else should you know about CGD?

X-linked R
NBT dye test is negative (doesn’t change color b/c no respiratory burst)
missing peroxide b/c no NADPH oxidase

How well did you know this?

Not at all

Perfectly

What kind of bacteria CAN pts with CGD kill?

catalase negative (e.g. Strep. pyogenes)

How well did you know this?

Not at all

Perfectly

What kind of bacteria CAN’T pts with CGD kill?

catalase positive (e.g. Staph)

How well did you know this?

Not at all

Perfectly

G6PD deficiency results in a lack of what molecule?

NADPH –> therefore this interferes with normal function of the O2 dependent MPO system

How well did you know this?

Not at all

Perfectly

What is the most important chemical mediator in acute inflammation?

histamine

How well did you know this?

Not at all

Perfectly

What does histamine do to arterioles?

vasodilates

How well did you know this?

Not at all

Perfectly

What does histamine do to venules?

increases vessel permeability

What amino acid makes serotonin?

tryptophan

What effect does serotonin have on vasculature?

vasodilator and increases vascular permeability

What are the 2 anaphylatoxins? What do they do?

C3a and C5a Stimulate mast cells to release histamine --> vasodilation and increased vessel permeability

What is made by endothelial cells and is a potent vasodilator?

What is the function of IL-1?

associated with fever b/c stimulates the hypothalamus to make PG's --> stimulates thermoregulatory system to produce fever

What enzymes is blocked by corticosteroids?

phospholipase A2

What enzymes are blocked by aspirin?

COX 1 and 2 irreversibly

What medication blocks the enzyme 5-LOX?

Zileuton

What medication blocks receptors for LTB4, LTC4, LTD4, and LTE4?

Montelukast

If taking a corticosteroid, would you see an increase or decrease in neutrophils?

You would see an INCREASE in neutrophils on CBC b/c corticosteroids block the adhesion molecule LTB4 from being formed.

What affect does epinephrin have on adhesion molecule synthesis and neutrophil count?

DECREASES adhesion molecule synthesis | neutrophil count INCREASES

MCC of skin abscess

S. aureus

What is fibrinous inflammation?

exudate that covers serial surfaces (heart, lungs, peritoneum)

What is serous inflammation?

thin watery exudate (e.g. blister, viral pleuritis)

What percent of peripheral blood lymphocytes are T cells?

60%

What is the ratio of helper to suppressor T cells (CD4:CD8)?

CD4:CD8 = 2:1

What is a unique characteristic of eosinophils?

They have Charcot-Leiden crystals (seen in sputum of asthmatic pts)

What is the effector cell in a Type II hypersensitivity reaction?

Eosinophils

What is the effector cell in a Type I hypersensitivity reaction?

mast cells

What is the benefit of a fever?

O2 binding curve shifts to the right | decreased bacterial/viral reproduction

What disease is associated with pseudomembranous inflammation?

C. difficile

Name the markers on the following cell types: Helper T cell Cytotoxic T cell Marker for Ag recognition site for all T cells Marker for histiocytes Marker only on B cells (name virus that utilizes this marker) Marker found on all leukocytes

Helper T cell - CD4 Cytotoxic T cell - CD8 Marker for Ag recognition site for all T cells - CD3 Marker for histiocytes - CD1 Marker only on B cells (name virus that utilizes this marker) - CD21 (EBV) Marker found on all leukocytes- CD45

What mediators cause fever?

IL-1 and PGE2

What is the cause of osteomyelitis?

S. aureus

What is the common cause of cellulitis?

Group A Strep. pyogenes

What are causes of fibrous pericarditis?

1. SLE 2. first week of MI then again in 6 wks later (Dresser's Syndrome) 3. Coxsackie virus

MC organism producing infxn in 3rd degree burns

Pseudomonas auruginosa (pus is green d/t pyocyanin)

Those who suffer from poor wound healing should be checked for what deficiency?

Zn deficiency

What is the pathogenesis of Marfans?

Defect in fibrillin --> poor wound healing

What is the pathogenesis of Ehlers-Danlos?

defect in collagen d/t breaking down --> poor wound healing

What is pathogenesis of Scurvy?

Vitamin C deficiency --> defect in hydroxylation of lysine and proline --> no crossbridging --> abnormal collagen --> poor wound healing, hemorrhaging, hemarthroses

What type of collagen is the initial collagen in wound repair?

Type III collagen

What day does granulation tissue begin to form?

Day 3

What enzyme breaks down type III collagen and replaces it with type I collagen?

collagenase (tensile strength returns to 80% normal w/in 3 months)

What causes keloid formation?

excess Type III collagen deposition

In white individuals, what is keloid formation often due to?

3rd degree burns

What do surgeons inject into sounds in order to prevent excessive scar tissue formation?

glucocorticoids

MCC of impaired wound healing

infections

MC pathogen causing sound infection

S. aureus

How does diabetes increase susceptibility to infection?

decrease blood flow | increase tissue glucose levels

What is the difference between a keloid and hypertrophic scar?

Keloid- raised scars extending beyond borders of original wound Hypertrophic scar- raised scar remaining in confines of original wound

Scenario: Chronically draining sinus tract of the skin, the physicians tried to put abs on it (didn't work). There was an ulceration lesion at the orifice of this chronically draining tract. What is it?

squamous cell carcinoma

What cell is involved in lung injury repair?

Type II pneumocyte

What cell in the brain proliferations in response to injury and which one removes the debris?

Astrocytes proliferate Microglial cells remove debris

In peripheral nerve transection, which cell is key to reinnervation?

Schwann cells

Cardiac muscle damage is permanent or temporary? What kind of repair occurs?

permanent damage repair by fibrosis

What immunoglobulin is predominantly seen in acute inflammation?

IgM

What cells and immunoglobulins are seen in chronic inflammation?

absolute monocytosis | increased serum IgG

What findings on blood smear are seen in severe inflammatory conditions?

toxic granulation | Dohle bodies

What findings would you see with corticosteroid therapy?

increased plasma neutrophils | decreased B and T cells

What cell types are seen in each scenario? Acute inflammation Acute allergic reactions Viral infections Chronic inflammation

Acute inflammation - neutrophil Acute allergic reactions- eosinophil Viral infections - lymphocytes Chronic inflammation - monocytes/macrophages but also see a lot of plasma cells and lymphocytes

A granuloma results from an acute or chronic infection?

chronic

What cytokine (released by a T helper cell) activates a macrophage?

gamma INF

What two cells are key players in granuloma formation?

T helper cell and macrophage (Type IV hypersensitivity)

What cell is responsible for a positive PPD test?

T helper cell

What two areas of the kidney are most susceptible to tissue hypoxia?

1. straight portion of proximal tubule b/c most of oxidative metabolism located there 2. medullary segment of thick ascending limb

What happens to the ESR when you have increased immonoglobulins? Why?

immunoglobulins decrease the negative charge that normally keeps RBCs from sticking to each other --> clumping of RBCs --> increased ESR *seen in cold agglutination with IgM and multiple myeloma (cryoglobulins)