Exam 2 Flashcards by Chelsea curry

 What vascular and cell processes commonly occur in inflammation?  

Increased blood flow
Increased vascular permeability
Leukocytic exudation through vessels
(Margination/rolling, Adhesion and migration, Chemotaxis and activation)

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List 5 signs that often accompany inflammation and describe the pathophysiologic basis of these signs.  

a. Rubor (redness): increased blood to the area
b. Tumor (swelling)- increased permeability
c. Calor (heat): body temp goes up due to cytokine mediators and increased BF
d. Dolor (pain): stimulation of free nerve endings
e. Functiolaesa (loss of function)

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The process of reaction of living vascularized tissue to injury

Inflammation

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List 5 chemicals mediators that can mediate an increase in vascular permeability at a site of inflammation?

histamine
C3a, C5a
Bradykinin, 
Leukotrienes (C4/D4/E4)
Platelet Activating factor (PAF)

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List 3 chemical mediators of cells

Vasoactive amines: histamine, serotonin
Prostaglandins and leukotrienes: PGE2, LTB4
Cytokines/chemokines: TNF alpha, IL-1, IL-8, MIP-1
Nitric Oxide

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How does C5a contribute inflammatory reactions?

Increase vascular permeability
Chemotactic for neutrophils, eosinophils, and macrophages
Cause mast cell degranulation, smooth muscle contraction, secretion of neutrophil granules
Stimulates oxygen radical production in neutrophils and macrophages, and arachadonic acid metabolism

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How do Coagulation/Fibrinolytic products contribute inflammatory reactions?

chemotactic for PMN’s and macrophages through fibrinopeptide formation

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What cells release vasoactive amines and arachidonic metabolites and are important in regulating  inflammation?  

Vasoactive amines: Mast cells, basophils, platelets

AA metabolites:
resident cells, leukocytes, and mast cells (PGE2) and
Neutrophils, Macrophages, eosinophils (leukotrienes)

???

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What pathogenic mechanisms are responsible for edema in inflammatory reactions?  

Increased vascular permeability and vasodilation allows plasma proteins to leak into the ECM, altering oncotic pressure, allowing fluid to follow

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Why are neutrophils often the first inflammatory cells to reach a site of injury during an acute  inflammatory reaction?  

Highly motile and high phagocytic rate

Respond to a wide variety of chemotactic stimuli, which enables them to respond quickly and efficiently

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What properties of macrophages allow for them to function effectively in a chronic inflammatory  process?

Much longer life, can phagocytize more than once

effective in destruction and long-term digestion of phagocytosed particulates

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C3a’s role in inflammation

increase vascular permeability

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What are the 2 vasoactive amines

histamine and serotonin

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What is the role of vasoactive amines in inflammation?

vasodilation
Increased venular permeability
Bronchial and other smooth muscle contraction

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Source of prostaglandins

resident cells, leukocytes, mast cells

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Inflammatory effects of Prostaglandins

Increase vascular permeability (PGE2)
Increase blood flow
Inhibit fibroblast and lympho proliferation
Increase body temp
Stimulate pain receptors

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Source of leukotrienes

neutrophils, macrophages, and eosinophils

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Inflammatory effects of LTB4

chemotactic for neutrophils and eosinophils and chemokinesis for monocytes/macrophages

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MOST potent neutrophil chemotactic substance

leukotrienes (LTB4)

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Inflammatory effects of LTD4/C4/E4

smooth muscle contraction, increase vascular permeability

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What cell surface molecules on leukocytes and endothelial cells play a role in regulating leukocyte rolling and margination?

a. E selectins: endothelial cells (upregulated by TNF alpha and IL 1)
b. P selectins: endothelial cells
c. Sialylated oligosaccharides: leukocytes

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List 2 stimuli that can upregulate E selectins  and the process of migration and margination of leukocytes

TNF alpha and IL 1

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How do neutrophils and macrophages mediate tissue injury during an inflammatory reaction?  

Via release of lysosomal enzymes and oxygen radicals

Macrophages, also, release their cytokines which can induce damage

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An inflammatory cell that is long-lived, can divide locally in tissue and regulates immune and repair responses:

a) Neutrophil
b) Eosinophil
c) Macrophage
d) Platelet
e) B and C

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Histamine increases vascular permeability at the level of capillaries and venules through the mechanism of: a) Endothelial cell contraction b) Endothelial cell damage c) Increased transcytosis d) Induce endothelial proliferation

Which cell surface molecules on leukocytes and endothelial cells mediate leukocyte rolling?

E and P selectins on endothelial cells (upregulated by TNF alpha and IL 1)binding to sialylated oligosaccharides on leukocytes

Which cell surface molecules on leukocytes and endothelial cells mediate leukocyte adhesion?

ICAM-1 and VCAM-1 on endothelial cells | Integrins (LFA-1, Mac-1, VLA-4) on leukocytes, which are stimulated by TNF alpha, IL-8 and IL-1

Which cell surface molecules on leukocytes and endothelial cells mediate leukocyte transmigration?

Co expression of PECAM-1 (CD31) on both endothelial cells and leukocytes (homophilic adhesion molecule)

Bovine leukocyte adhesion deficiency is caused by a defect in which gene? How would you detect the abnormality in a carrier animal?  

a. CD18 gene b. Calves have poor neutrophil response to infection by bacteria and common fungi c. Enteritis and pneumonia

Leukocyte adhesion deficiency in Irish Setter Dogs is associated with a genetic defect in which gene?  

CD18 missense mutation

Why do bacterial infections often lead to neutrophil-dominated inflammatory reactions?  

Neutrophils are highly motile, high phagocytic capacity, and are the most effective killers of bacteria (strong neutrophil chemotactic factor is the bacterial cell wall)

How do lymphocytes, macrophages, and mast cells amplify or produce inflammatory response?

Release inflammatory mediators (IFN gamma, leukotrienes, interleukins, chemokines, prostaglandins). Can amplify a reaction by releasing chemicals like oxygen radicals, superoxide anions and lysosomes. This can cause tissue damage too

Neutrophil-Endothelial surface molecules mediating rolling a) Integrin (CD11/CD18)- selectin b) Siayl lewis X-selectin c) Integrin (CD11/CD18)- ICAM-1 d) PECAM-1 (CD31)-PECAM-1 (CD31)

Holstein cattle and Irish Setter dogs have mutations in which molecules to develop leukocyte adhesion molecule deficiency a) Selectin b) ICAM-1 c) Integrin (CD18) d) PECAM-1 (CD31) e) Siayl-Lewis X glycoprotein

How are inflammatory reactions commonly classified morphologically?  

Duration :acute, sub-acute, chronic Distribution: focal, multifocal, locally-extensive, diffuse Type of exudate Tissue Involved

What are histologic indicators of a chronic inflammatory reaction?  

fibrosis

necrotic inflammatory reaction on an epithelial surface down to the basement membrane

erosion

necrotic inflammatory reaction on an epithelial surface that involves LOSS of the basement membrane

ulcer

What pathogenetic events are important in the stimulation of a granulomatous inflammatory reaction?  

Inciting stimuli-substances that resist lysosomal  degradation and substances that induce T-cell hypersensitivity

``` Suppurative inflammatory reactions are often induced by? A. Fungi B. Nematode parasites C. Bacteria (non-mycobacterial) D. Mycobacteria E. Toxins ```

C. Bacteria (non-mycobacterial)

``` Eosinophilic inflammatory reactions are often induced by a. fungi b. nematode parasites C. Mycobacteria E. Toxins ```

``` Macrophage dominated inflammatory reactions are often induced by: a. Fungi B. Nematode parasites C. Bacteria (non-mycobacteria) D. Mycobacteria E. Toxins ```

A and D

``` Which type of inflammatory cell is often associated with liquefactive necrosis? a. Lymphocyte B. Neutrophil C. Macrophage D. Eosinophil E. Mast cell ```

B. neut

What role does delayed type hypersensitivity play in the pathogenesis of granulomatous inflammation?  

Hypersensitivity is NOT a requirement but CAN accelerate and intensify the inflammation response via lymphokines released from T cells.

True or False | Granulomatous inflammation is almost always a chronic process unless there is a pre-existing T cell hypersensitivity.

TRUE

Inflammatory reaction dominated by macrophages

Granulomatous

Compact and organized collection of mononuclear inflammatory cells dominated by macrophages

granuloma

highly organized fibrovascular tissue that often replaces necrotic cells and areas where poor regeneration has occurred

Granulation tissue

Granuloma with central necrosis +/- calcification

complex granuloma

Inciting stimuli of granulomatous inflammation are? a) Particulates resisting lysosomal degradation b) Persisting molecules that stimulate T-cell hypersensitivity c) Stimuli that are chemotactic for macrophages and neutrophils d) A, B e) A, B, C

Granulomatous inflammation is almost always: a) Acute b) Chronic

Inflammatory cells central to granulomatous inflammation a) Macrophages b) Epithelial cells c) Multinucleated giant cells d) A,B,C e) A, C

process resulting in increase of collagen in tissue; often an important and sometimes necessary component of the repair process

Fibrosis usually results in fibrous connective tissue

Cells that have latent capacity to regenerate; normally quiescent in G0 state; have long life spans and don’t turnover quickly

Stable

epithelial cells in liver, kidney, lung, endocrine glands; smooth muscle cells, fibroblasts, endothelial cells (also skeletal muscle to an extent) are examples of this kind of cell

stable

Cells that continue to multiply throughout life (never leave cell cycle to G0 state) and replenish those lost due to normal turnover

Liable

epidermal/intestinal epithelial cells, lymphoid and hematopoietic cells are examples of these kind of cells

liable

cells w/ no capacity to regenerate additional cells

Permanent or non-dividing cells

neurons and cardiac cells are examples of these kind of cells

permanent

Cell migration along a concentration gradient of chemical mediatory

chemotaxis

Random migration stimulated by a mediator

chemokinesis

What do non-dividing cell do in response to injury

limited capacity to regenerate some cell cytoplasm therefore only repair by scaring

Process by which lost or necrotic cells are replaced by vital cells

repair

replacement of cells by cells of the same type aka good

regeneration

damage cells are replaced by connective tissue

fibrosis aka bad

small chemotactic cytokines produced by macrophages, stroll cells, and epithelial cells

chemokines

Two examples of broad chemokines and their spectrum of biological activities

CXC chemokines- primarily for neutrophils and endothelial cells (e.g. IL8 and factor 4) CC chemokines- chemotactic for mononuclear cells (lymphs, mono) and eos (MIP1, Rantes, Eotaxin)

4 cytokines that regulate the inflammatory and/or repair process

TNF alpha IL-1 IFN gamma Chemokines

Released from macrophages and other inflammatory cells and fibroblasts in response to viral and fungal infections, endotoxins and chemical injury. Upregulates endothelial adhesion molecules, promotes production of cytokines and mediators and induces acute phase proteins

TNF alpha and IL-1

Has similar actions to TNF alpha and cachexia

IL-1

Produced by T cells and NK cells during Ag driven inflammatory response. Upregulates macrophage function, increases macrophage killing capacity and giant cell fusion

IFN gamma

What general molecular events might explain why transforming growth factor-beta stimulates  fibroblast proliferation and inhibits epithelial proliferation and repair?  

Both fibroblasts and epithelial cells have TGF beta, but their second messenger systems must differ. Allowing for upregulation in one cell and down in another.

List three cytokines or growth factors that are released from macrophages that modulate fibrosis and angiogenesis

Fibroblast growth factor (FGF) Vascular endothelial growht factor (VEGF) Platelet derived growth factor (PDGF)

Once collagen in a scar is formed is it inert to further change and collagen modification?

No, eventually the scar can resolve and the tissue goes back to almost normal. Collagen is degraded and resynthesized over time

What type of injuries and pathologic processes commonly lead to fibrosis?

* Severe/prolonged injury * Loss of basement membrane * Large amount of exudate * Lack of renewable cells (non-dividing cells)

What type of injuries and pathologic processes commonly lead to regeneration?

* Mild/brief injury * Maintenance of BM/microvascular/tissue framework * Small amounts of exudate * Available renewable cells (stem cells)

Which conditions favor tissue repair by fibrosis following injury? a) Lack of renewable population b) Prolonged/severe injury c) Minimal exudate d) A,B e) A,B,C

Which tissues are highly susceptible to repair by fibrosis or scarring because they lack dividing renewable cell populations? a) Renal tubular epithelium b) Myocardial myocytes c) Cerebral corticol neurons d) A,B,C e) B,C

Growth factors and cytokines that lead to epithelial proliferation.migration

b-EGF, HGF KGF basic, Epithelial growth factor Hepatocyte Growth Factor aka Scatter Factor (HGF) Keratinocyte growth factor

Give examples of diseases that are dependent on type IV hypersensitivity phenomena?

TB, contact derm, fungal disease, tissue rejection transplants

Which of the following are potent inducers of angiogenesis? a) VEGF b) B-FGF c) HGF d) A,B e) A,B,C

ALWAYS ASKS THIS QUESTION | D

Which of the following is a potent inducer of fibrosis? a) TGF-beta b) TNF- alpha c) PDGF d) A,B e) A,B,C

What is a morphologic diagnosis, and how does it differ from an etiologic diagnosis?

Morphologic- dx purely on morphology | Etiologic- dx that includes the causative agent

What are IL-8 and eotaxin? What are their functions?

IL-8 CXC chemokine, attracts neutrophils to wound | Eotaxin- CCchemokine, attracts eosinophils to wound

LIST two growth factors that are released by macrophages that strongly promote endothelial growth and angiogenesis. 

Here is 3 | VEGF, beta- FGF, PDGF

List two growth factors / cytokines released by macrophages that strongly promote fibroblast proliferation and collagen synthesis.

There are several: | TGF-beta, PDGF, TNF, collagenase, MMPs

List two mediators released by macrophages that are strongly chemotactic for neutrophils.

IL-8 and LTB4

How do neutrophils contribute to tissue damage in immune complex injuries? 

mediate tissue injury via lysosomal enzymes and oxygen radicals

How do complement fragments (C3a and C5a) contribute to immune complex disease? 

Type II Hypersensitivity | May lyse cells or the cells are phagocytized and eliminated by cells of the mononuclear phagocyte series

``` Which of the following inflammatory mediators induces increases vascular permeability, fever and pain? A. LTB4 B. LXA4 C. C5a D. PGE2 E. Histamine ```

PGE2 (note that in chart it says just vasodilation, but then on his slide it says it causes vascular perm too) LTB4, C5a, histamine- just perm LXA4- have no idea what that is

``` Which of the following inflammatory mediators is strongly chemotactic for neutrophils? A. LTB4 B. LXA4 C. C5a D. PGE2 E. A and C ```

E. LTB4 and C5a

``` Which of the following mediators is produced by sensitized lymphocytes and is strongly chemotactic for eosinophils?  A. Histamine B. LXA4 C. C5a D. PGE2 E. Eotaxin (CCL11) ```

Eotaxin Sensitized- therefore a hypersensitive response

List three growth factors that stimulate epithelial proliferation in repair. 

EGF, HGF (aka scatter factor), KGF (FGF-7)

Which of the four types of hypersensitivity diseases according to the classification of Gell and Coombs are dependent on T-lymphocytes versus immunoglobulin? 

Type IV hypersensitivity

Generalized anaphylaxis is dependent upon which inflammatory mediators? 

Histamine and serotonin: Increase venular permeability, induce smooth muscle contraction in pulmonary airways, cause arteriolar dilation

How do neutrophils contribute to tissue damage in immune complex injuries? 

Formation of antigen-antibody complex in tissue Fixation of complement and liberation of chemotactic fragments Neutrophils accumulation at site of immune complex deposition and mediation of tissue injury through release of lysosomal enzymes and toxic oxygen radicals

What form of antigen-antibody complex is necessary for immune complex disease to develop?

Just need excess antigen

How do complement fragments (C3a and C5a) contribute to immune complex disease? 

Released during the complement cascade and act as chemotactic factors for neutrophils

 How do sensitized T-cells contribute to tissue damage in type IV hypersensitivity disease?

lymphokine mediated effects and CD8 mediated toxicity

3 components of cytotoxic T cell action

* Perforin cell membrane lysis (necrosis) * Perforin-granzyme induced apoptosis * FASL-FAS induction of apoptosis

Type I anaphylactic hypersensitivity reactions can be mediated by: a) IgG b) IgM c) IgE d) A,B e) A, C

Type III hypersensitivity reactions can be mediated by: a) IgG b) IgM c) IgE d) A,B e) A,C

D | SAID THIS ONE IS IMPORTANT

Tissue injury type IV hypersensitivity/allergic reactions is mediated via? a) Immune complex formation b) T-call induction of granulomatous inflammation c) Direct- T cell cytotoxicity d) A, B,C e) B,C

Type III immune complex hypersensitivity reactions occur most commonly in a state of a) Ag excess b) Ab excess c) Ag-Ab equivalence

A !!!!!

Examples of Type I hypersensitivity

anaphylaxis, allergic dermatitis

Mechanism of Type I hyper.

mediator release

Examples of Type II hypersensitivity

autoimmune hemolytic anemia

Examples of Type III hypersensitivity

glomerulonephritis

Mechanism of Type II hyper.

cytotoxic via complement and cells

Mechanism of Type III hyper.

immune complexes

Mechanism of Type IV hyper.

cell mediated immunity

Immunologic mediator for type I hyper

IgE (IgG in dogs)

Immunologic mediator for type II hyper

IgM, IgG

Immunologic mediator for type III hyper

IgM, IgG

Immunologic mediator for type IV hyper

T-lymphocytes

Developmental disturbance that results in Complete absence of an organ and associated primordium

agenesis

Developmental disturbance that results in refers to the absence of an organ due to failure of growth of the existing primordium (have the precursor cells)

aplasia

Absence of an opening, usually of a hollow organ | o Developmental growth disturbance

Atresia (usually GI tract)

Developmental disturbance that results in failure to develop to normal size • Can be secondary to in utero viral infection

hypoplasia

Development to bigger than normal size

hyperplasia

Increase in cell size (resulting from increased production of cellular proteins)

hypertrophy

Often in response to increased workload (physiologic, e.g. exercise and pathologic, e.g. cardiac hypertrophy)

hypertrophy

Main cellular adaptation in cells incapable or with limited ability for cell division

hypertrophy

Increase in cell number | o Causes: a lot, hormonal, compensatory, irritation, infection, etc.

hyperplasia

Cells must be able to divide in this disturbance of growth

hyperplasia

2 examples we say in class that demonstrated hyperplasia and hypertrophy

Chronic giant hypertrophic gastropathy • Basenji beagle, boxer, bull terrier • Cause is unknown • Weight loss, diarrhea, vomiting, hyoproteinemia Dogs, adrenal glands, secondary to functional pituitary adenoma→increase ACTH→cortical hypertrophy and hyperplasia

Decreased cell and organ size | Can just be the cell and rest of tissue is fine

atrophy

decreased nutrient supply, disuse (decreased workload or denervation), loss of endocrine stimulation, pressure causes...

atrophy

Is metaplasia classified as reversible or irreversible?

reversible | If persists, can produce malignant transformation

Change in phenotype of differentiated cells

Metaplasia

Metaplasia can be caused by...

chronic irritation

Loss of uniformity of cells and loss of orientation

Dysplasia, usually epithelial cells

variation in size and shape of cells

pleomorphism

Is dysplasia reversible?

Yes, especially if not full thickness and removal of inciting cause "flirting with neoplasm"

New growth

neoplasia or neoplasm

disorder of cell growth that is triggered by a series of mutations that give the cells a survival and growth advantage that is independent of growth regulation signals (autonomous)

Neoplasia or neoplasm

2 basic components of tumors

parenchyma and stroma

neoplastic cells that constitute the tumor

parenchyma

reactive tissue surrounding neoplastic cells(parenchyma) composed of connective tissue, BV, and +/- cells from the adaptive and innate immune system

stroma

abundant fibrous stroma, carcinomas

Schirrous response or desmoplasia

Gross and microscopic appearance are considered relatively “innocent” Can have an intact capsule or no capsule Remain localized No spread to other sites Amendable to surgical removal Can still result in significant morbidity and still be lethal!

Benign neoplasms, location is often key for these

Benign tumor that is derived from glands

adenoma | Epithelial tumor

Benign tumor that is micro or macroscopic fingerlike or warty projections arising from an epithelia surface

papilloma

benign (or malignant) raised projection above a mucosal surface and projects into lumen

polyp

Fibroma and chondroma are what classification of tumor

mesenchymal bengin tumor

List 4 types of injuries or pathologic processes that lead to fibrosis

1) large amounts of exudate 2) loss of basement membrane 3) lack of renewable cell population 4) severe and prolonged tissue injury

List two major pathogenic mechanisms that contribute to the development of granulomatous inflammatory reactions.

1) substances that induce T-cell hypersensitivity | 2) substances that resist lysosomal degradation

``` Which of the following is a chemokine that is a potent chemotactic factor for neutrophils? A. IL-8 B. TNF-α C. IL-14 D. PDGF E. TGF-β ```

IL-8

Which of the following is a cytokine that promotes macrophage activation and differentiation to giant cells and epithelioid cells in granulomatous inflammation? ``` A. PDGF B. TNF-α C. Interferon-α D. Interferon-β E. Interferon-γ ```

``` One of the most reliable indicators of chronicity in an inflammatory reaction is: A. Plasma cells B. Lymphocytes C. Macrophages D. Lack of neutrophils E. Fibrosis ```

Fibrosis

All of the following events or conditions favor repair by fibrosis, rather than by regeneration: 1. Severe and prolonged injury 2. Acute neutrophilic inflammatory response 3. Loss of basement membranes 4. Large amounts of necrotic and/or fibrinous exudates 5. Lack of renewable cells ``` A. 1,2 B. 1,2, 3 C. 1,2,3,4 D. 1,2,3,4,5 E. 1,3,4,5 ```

Which of the following are mechanisms that account for neutrophils generally being the first cells to reach an inflammatory site during an acute inflammatory reaction? 1. Neutrophils are rapidly motile 2. High circulating number of neutrophils in peripheral blood 3. Neutrophils are responsive to a wide array of chemotactic substances 4. Neutrophils have a 7 to 14 day half life in tissue ``` A. 1 B. 1,2 C. 1,2,3 D. 1,2,3,4 E. 2,3,4 ```

Leukocyte rolling in vessels during an inflammatory cell response is mediated by: ``` A. Immunoglobulin and complement fragments B. Integrins C. Intercellular adhesion molecules D. Selectins E. B and C ```

D | Note that integrins only come to play in the later steps

Leukocyte adhesion and migration during an inflammatory cell response is mediated by: A. Immunoglobulin and complement fragments B. Integrins C. Intercellular adhesion molecules D. Selectins E. B and C

E ICAM is intercellular adhesion molecule on endo cells Integrins are on leuks

Which of the following factors released by macrophages stimulate fibroblast proliferation? 1. Vascular endothelial growth factor (VEGF) 2. Basic fibroblast growth factor (b-FGF) 3. Tumor necrosis factor-alpha (TNF-α) 4. Transforming growth factor beta (TGF-β) 5. Platelet derived growth factor (PDGF) ``` A. 1, 2 B. 1,2,3 C. 1,2,3,4, 5 D. 2,3,4,5 E. 3,4,5 ```

D | ??

All inflammatory reactions are characterized by: 1. Increase blood flow 2. Increased vascular permeability 3. Fibrin exudation 4. Leukocytic exudation 5. Parenchymal cell necrosis ``` A. 1 B. 1,2 C. 1,2,3 D. 1,2,3,4,5 E. 1,2,4 ```

``` Pain in an inflammatory reaction is mediated by release of: A. Bradykinin B. Prostaglandin E2 C. Histamine D. Leukotriene B4 E. A and B ```

E. Brady and PGE2

Which of the following factors are released by activated neutrophils in an inflammatory reaction to augment recruitment of additional neutrophils? 1. Leukotriene B4 2. IP-10 3. Fibrinogen 4. Serum amyloid A ``` A. 1 B. 1,2 C. 1,2,3 D. 2 E. 2,4 ```

Which of the following molecular interactions is responsible for leukocyte adhesion to endothelial cells during an inflammatory reaction? A. ICAM-1 / Integrin (CD11/CD18) B. P-selectin / Sialyl Lewis X modified protein C. Antigen / IgE D. P-selectin / E-selectin E. VCAM-1 / P-selectin

Which of the following is the best indicator of chronicity when examining inflammatory reactions by light microscopy? A. Plasma cells in the tissue exudate B. Macrophage number in the tissue exudate C. Endothelial cell proliferation and hemorrhage. D. Fibroblast proliferation and collagen synthesis E. Epithelial cell proliferation and mucus production

``` Epithelioid cells and multinucleated giant cells in granulomatous inflammatory reactions are derived from: A. Mast cells B. Neutrophils C. Eosinophils D. Lymphocytes E. Macrophages ```

Which of the following cells is considered to be a stable cell capable of contributing to regeneration? ``` A. Neuron B. Cardiac myocyte C. Nonciliated bronchiolar epithelial cell D. Bone marrow progenitor cell E. Basal epithelial cell in epidermis ```

``` .Which of the following is a chemokine that is a potent chemotactic factor for monocytes/macrophages? A. LTB4 B. TNF-α C. Macrotactin D. Interferon-γ E. MIP-1α ```

The growth factor released from macrophages in chronic inflammatory reactions that has the paradoxical effect of promoting fibroblast proliferation and inhibiting epithelial proliferation is: ``` A. TGF-β B. TNF-α C. b-FGF D. PGDF E. VEGF ```

Which of the following is commonly generated during thrombosis and is chemotactic for macrophages? ``` A. C5a B. Leukotriene C4 C. Leukotriene B4 D. Fibrinopeptides E. Plasminogen activator ```

Which of the following are growth factors for endothelial cells that are produced by macrophages? ``` A. Vascular endothelial growth factor B. Basic fibroblast growth factor C. Tumor necrosis factor D. A and B E. A, B and C ```

D (was a precious answer) BUT NOT SURE, thinking it may be all. Will check tomorrow

In granulation tissue, blood vessels often are arranged parallel to one another and in which orientation to the exudates surface? A. Parallel B. Perpendicular

Which of the following is an etiologic diagnosis? A. Pasteurella multocida B. Protozoal encephalitis C. Chronic multifocal suppurative encephalitis D. Johnes Disease E. Lymphosarcoma

B | a. is cause, c is morphological, d and e is name of disease

Which of the following is a disease cause? A. Pasteurella multocida B. Cutaneous habronemiasis C. Chronic diffuse eosinophilic and granulomatous dermatitis D. Johnes Disease E. Cerebral nematodiasis

``` Which of the following mechanisms is most commonly responsible for edema that occurs at the site of an inflammatory reaction? A. Increased hydrostatic pressure B. Increased vascular permeability C. Decrease oncotic pressure D. Obstruction of lymphatics E. Increased sodium retention ```

``` Which of the following are growth factors that are produced by macrophages and strongly promote endothelial growth and angiogenesis? A. Interleukin-5 B. Vascular endothelial growth factor C. Transforming growth factor – β D. Fibroblast growth factor E. B and D ```

E. B and D

Which of the following inflammatory mediators induces vasodilation, fever and pain? ``` A. LTB4 B. LXA4 C. C5a D. PGE2 E. Histamine ```

Firm binding of neutrophils to endothelial cells prior to migration out of vessels into sites of inflammation is mediated by upregulation of which of the following molecules on neutrophils? ``` A. VCAM-1 B. ICAM-1 C. Integrins (e.g., CD11/CD18) D. E-selectins E. A and B ```

C VCAM and ICAM are responsible for adhesion BUT is on endothelial cells, E-selectin is on endothelial cell during rolling

``` The histologic hallmark of a chronic inflammatory reaction is: A. Macrophages B. Plasma cells C. Neutrophils D. Fibrinous exudate E. Fibrosis ```

Acute inflammatory reactions are often characterized histologically by accumulation of large numbers of both necrotic and non-necrotic neutrophils due to all of the following EXCEPT: A. Neutrophils are highly motile B. Neutrophils respond to a wide array of chemotactic factors C. Neutrophils have a half life less than 24 hours D. Neutrophils release chemotactic factors that can recruit other neutrophils E. None of the above

e???

All of the following cells can be derived from monocytes EXCEPT: ``` A. Macrophages B. Multinucleated giant cells C. Epithelial cells D. Epithelioid cells E. C and D ```

. C5a contributes to immune complex injury by mediating: ``` A. Neutrophil chemotaxis B. Increased vascular permeability C. Activation of kallikrein D. A and B E. A, B and C ```

d Note kallikrein is activated by Hageman

Which of follow mediators is produced by lymphocytes and strongly chemotactic for eosinophils? ``` A. Eotaxin B. LXA4 C. C5a D. PGE2 E. Histamine ```

Which of the following mediators is/are released by macrophages and is/are strongly chemotactic for neutrophils? ``` A. Eotaxin B. LTB4 C. C5a D. PGE2 E. B and C ```

B? C5a is chemotactic for neut but not released by macrophages

Type IV (delayed type) hypersensitivity contributes to acceleration or augmentation of granulomatous inflammation mediated largely by lymphocyte production of which of the following? ``` A. IL-1 B. TNF-α C. Interferon-γ D. MCP-1 E. TGF-β ```

``` Which of the following cells is highly effective in killing nematode larvae mediated in part by major basic protein? A. Neutrophil B. Macrophage C. Lymphocyte D. Eosinophil E. Mast cell ```

Which of the following is a morphologic diagnosis? ``` A. Cutaneous acariasis B. Johne’s disease C. Acute multifocal suppurative hepatitis D. Escherichia coli E. A and C ```

C A. Cutaneous acariasis – etiological diagnosis (includes causative agent) B. Johne’s disease - disease C. Acute multifocal suppurative hepatitis - morph D. Escherichia coli – cause (agent) E. A and C

``` Necrosis in which of the following tissues is most likely to lead to repair by fibrosis? A. Myocardium B. Lung C. Liver D. Epidermis E. Bone marrow ```

``` Which of the following cells releases both vasoactive amines and arachidonic acid metabolites to regulate inflammation? A. Neutrophil B. Macrophage C. Lymphocyte D. Eosinophil E. Mast cell ```

E | VA: histamine, serotonin, AA: PGE2, PGD2, COX-2 inhib, leukotriene , LXA

Which of the following cytokines or growth factors stimulates proliferation of fibroblasts and can inhibit division of epithelial cells? ``` A. IL-1 B. TNF-α C. Interferon-γ D. MCP-1 E. TGF-β ```

``` Which of the following events promote repair by fibrosis? A. Loss of basement membrane B. Abundant necrotic exudate C. Lack of renewable cell population D. Long duration of tissue injury E. All of the above ```

Which of the following is a small chemotactic cytokine for neutrophils? ``` A. C5a B. LTB4 C. IL-8 D. A and B E. A, B and C ```

All are chemotactic for neutr, BUT the only one that is a small cytokine is C

Necrosis of epithelium and associated defect below the basement membrane defines: ``` A. Erosion B. Ulcer C. Infarct D. Granuloma E. Arthus reaction ```

Activation or enzymatic cleavage of which of the following leads to generation of serum-derived inflammatory mediators? ``` A. Hageman factor B. Kallikrein C. Fibrinogen D. A and B E. A, B and C ```

E A. Hageman factor (activates prok->kallikrein) B. Kallikrein (becomes bradykinin, plasma md) C. Fibrinogen (fibrinolytic pdts – plasma md)

``` Pulmonary tuberculosis in rhesus monkeys is characterized by which of the following inflammatory lesions? A. Granulomatous inflammation B. Simple granulomas C. Complex granulomas D. Caseation necrosis E. All of the above ```

E (in lab)

``` Which of the following chemicals mediates pain during an inflammatory reaction? A. Bradykinin B. LTE4 C. TNF-α D. IL-8 E. A and B ```

``` Which of the following is synthesized and released by macrophages and is chemotactic for neutrophils? A. Eotaxin B. C5a C. IL-1 D. LTB4 E. Histamine ```

``` Which of the following are released by neutrophils and macrophages during a chronic inflammatory process to mediate cell and tissue damage? A. Superoxide anion B. Hydoxyproline C. Type IV collagen D. Heparin sulfate E. Transforming growth factor beta ```

``` Which of the following is a cytokine that promotes macrophage activation and differentiation to giant cells and epithelioid cells in granulomatous inflammation? A. PDGF B. TNF-α C. Interferon-α D. Interferon-β E. Interferon-γ ```

``` Leukocyte adhesion deficiency in Irish Setter Dogs is associated with a genetic defect in which of the following genes? A. CD11 B. CD18 C. ICAM-1 D. CD34 E. PECAM-1 ```

``` Which of the following changes in tissue is the most reliable indicator that an inflammatory reaction is chronic? A. High numbers of lymphocytes B. High number of macrophages C. Endothelial cell hypertrophy D. Low number of neutrophils E. Fibrosis ```

``` An intestinal mucosal defect characterized by epithelial necrosis and loss is classified as an erosion, rather than an ulcer if it doesn’t go deeper than the A. Mucularis mucosa B. Lamina propria C. Tunica muscularis D. Basement membrane E. Mesenteric plexus ```

Epithelioid cells and multinucleated cells in granulomatous inflammatory reactions derive from: ``` A. Macrophages B. Lymphocytes C. Neutrophils D. Mast cells E. Eosinophils ```

Which of the following molecular interactions is responsible for leukocyte rolling on endothelial cells during an inflammatory reaction? A. ICAM-1 / Integrin (CD11/CD18) B. P-selectin / Sialyl Lewis X modified protein C. Antigen / IgE D. P-selectin / E-selectin margination/rolling)

``` Which of the following upregulate expression of integrins on leukocytes? A. TGF-β B. IL-1 C. TNF-α D. A, B, C E. B, C ```

``` . All inflammatory reactions are characterized by: 1. Increase blood flow 2. Increased vascular permeability (plus vascular changes in blood flow, leukocytic events) 3. Fibrin exudation 4. Leukocytic exudation 5. Parenchymal cell necrosis A. 1 B. 1,2 C. 1,2,3 D. 1,2,3,4,5 E. 1,2,4 ```

``` Eosinophils are effective in killing nematode larvae at least in part because they synthesize and release: A. LTC4 B. PGE2 C. Myeloperoxidase D. Superoxide anion E. Major basic protein ```

Which of the following is a morphologic diagnosis? A. Habronema microstoma B. Cutaneous habronemiasis C. Chronic diffuse eosinophilic and granulomatous dermatitis D. A, B E. A, B, C

C A is agent B is etiological C is morph

``` Which of following cells is considered to be a stable cell capable of contributing to regeneration? A. Neuron B. Cardiac myocyte C. Renal tubular epithelial cell D. Bone marrow progenitor cell E. Basal epithelial cell in epidermis ```

Which cell cycle stages are in the correct order beginning at the “start” of the cycle? a. G1, G2, S, M b. G1, G2, M, S c. G1, M, G2, S d. G1, S, G2, M e. S, M, G1, G2

LIST three cytokines or growth factors that are released from macrophages that modulate fibrosis and/or angiogenesis.

1. PDGF (both) 2. FGF (both) 3. VEGF (angio) Also: TNF-alpha (fibrosis)

B | Going to check on this one

``` Which of the following inflammatory mediators induces vasodilation, fever and pain? A. LTB4 B. LXA4 C. C5a D. PGE2 E. Histamine ```

``` The histologic hallmark of a chronic inflammatory reaction is: A. Macrophages B. Plasma cells C. Neutrophils D. Fibrinous exudate E. Fibrosis ```

``` Firm binding of neutrophils to endothelial cells prior to migration out of vessels into sites of inflammation is mediated by upregulation of which of the following molecules on neutrophils? A. VCAM-1 B. ICAM-1 C. Integrins (e.g., CD11/CD18) D. E-selectins E. A andB ```

``` All of the following cells can be derived from monocytes EXCEPT: A. Macrophages B. Multinucleated giant cells C. Epithelial cells D. Epithelioid cells E. C and D ```

``` C5a contributes to immune complex injury by mediating: A. Neutrophil chemotaxis B. Increased vascular permeability C. Activation of kallikrein D. A and B E. A, B and C ```

``` Which of the following mediators is produced by lymphocytes and is strongly chemotactic for eosinophils? A. Eotaxin (CCL11) B. LXA4 C. C5a D. PGE2 E. Histamine ```

``` Which of the following mediators is/are released by macrophages and is/are strongly chemotactic for neutrophils? A. Eotaxin (CCL11) B. LTB4 C. C5a D. PGE2 E. B and C ```

B | Note that C5a is chemotactic for neutrophils but not released by macrophages

``` Type IV (delayed type) hypersensitivity contributes to acceleration or augmentation of granulomatous inflammation mediated largely by lymphocyte production of which of the following? A. IL-1 B. TNF-α C. Interferon-γ D. MCP-1 E. TGF-β ```

``` Which of the following cells is highly effective in killing nematode larvae mediated in part by major basic protein? A. Neutrophil B. Macrophage C. Lymphocyte D. Eosinophil E. Mast cell ```

Which of the following is a morphologic diagnosis? A. Cutaneous acariasis B. Johne’s disease C. Acute multifocal suppurative hepatitis D. Escherichia coli E. A and C

``` Necrosis in which of the following tissues is most likely to lead to repair by fibrosis? A. Myocardium B. Lung C. Liver D. Epidermis E. Bone marrow ```

``` Which of the following cells releases both vasoactive amines and arachidonic acid metabolites to regulate inflammation? A. Neutrophil B. Macrophage C. Lymphocyte D. Eosinophil E. Mast cell ```

``` Which of the following cytokines or growth factors stimulates proliferation of fibroblasts and can inhibit division of epithelial cells? A. IL-1 B. TNF-α C. Interferon-γ D. MCP-1 E. TGF-β ```

``` Which of the following is a small chemotactic cytokine for neutrophils? A. C5a B. LTB4 C. IL-8 D. A and B E. A, B and C ```

C | All are chemotactic for them, but IL8 is the only small cytokine (chemokine)

``` Necrosis of epithelium and associated defect below the basement membrane defines: A. Erosion B. Ulcer C. Infarct D. Granuloma E. Arthus reaction ```

``` Activation or enzymatic cleavage of which of the following leads to generation of serum-derived inflammatory mediators? A. Hageman factor B. Kallikrein C. Fibrinogen D. A and B E. A, B and C ```

E (was in lab)

``` An increase in cell number associated with an increase in organ size is? (2 points) A. Hypertrophy B. Atrophy C. Hypoplasia D. Metaplasia E. Hyperplasia ```

hyperplasia

``` An increase in cell size associated with an increase in organ size is? A. Hypertrophy B. Atrophy C. Hypoplasia D. Metaplasia E. Hyperplasia ```

``` A three day old foal with a small thymus might have which thymic disturbance of growth? A. Atrophy B. Hypoplasia C. Metaplasia D. A or B E. A or C ```

``` Testicular Sertoli cell tumors in dogs occasionally induce which of the following disturbances of growth in prostatic epithelium? A. Hypertrophy B. Atrophy C. Hypoplasia D. Metaplasia E. Hyperplasia ```

Which of the following processes regresses with stimulus removal? (2 points)(p163) A. Neoplasia B. Hyperplasia

``` Which of the following is a malignant neoplasm of smooth muscle? (2 points)(p165) A. Hemangioma B. Leiomyoma C. Leiomyosarcoma D. Rhabdomyoma E. Rhabdomyosarcoma ```

All of the following are important diagnostic criteria for benign and malignant tumors EXCEPT? (2 points)(p166) A. Compression/disturbance of function in surrounding tissue B. Differentiation / anaplasia C. Rate of growth D. Local invasiveness E. Metastasis

``` A malignant neoplasm of urinary bladder epithelium is called? (2 points)(p165) A. Mesothelioma B. Teratoma C. Cystandenocarcinoma D. Transitional cell carcinoma E. Choriocarcinoma ```

``` Common mutations in genes associated with cancer include all of the following EXCEPT? (2 points)(p169) A. Apoptosis regulating genes B. Cytochrome P450 expression genes C. Proto‐oncogenes D. Tumor suppressor genes E. DNA repair genes ```

``` Which of the following are proto‐oncogenes that are commonly mutated in cancer? (2 points)(?) A. RAS B. PDGFB C. ERBB1 (EGFR) D. p53 E. A, B, C ```

Have to look up, person answered D but technically that is a tumor suppressor gene

``` Which of the following is highly expressed in malignant neoplastic cells to promote angiogenesis? (2 points)(p173) A. TNF‐alpha B. VEGF C. Collagenase D. p53 E. TGF‐alpha ```

``` The gene that serves as the “Guardian of the Genome” to block growth of mutated cells and control DNA repair is? (2 points)(p171) A. p53 B. K‐RAS C. Cytochrome c D. VEGF E. Telomerase ```

Which of the following enzymes play a role in tumor cell breakdown of extracellular matrix in invasion and metastasis? (2 points)(p174) A. Plasminogen activator B. Matrix metalloproteases C. Phospholipases D. A, B E. A, B, C

D... (havent gotten to)

Which of the following proteins is broken down in epithelial cells to mediate loosening of intercellular junctions prior to invasion/metastasis? (2 points)(p174) A. TP53 B. ICAM‐1 C. CD11 D. E‐cadherin E. Fibronectin

``` Tumor cells evade immunologic destruction by all of the following mechanisms EXCEPT? (2 points)(p175) A. Produce immunosuppressive molecules B. Upregulate tumor suppressor genes C. Develop antigen negative variants D. Reduce MHC molecule expression E. A, B ```

``` Hypercalcemia in apocrine gland adenocarcinoma of the anal sac in dogs is mediated by? (2 points)(p178) A. PGE2 B. IL‐1 C. IL‐2 D. PTH E. PTHrP ```

E.. havent gotten to yet

``` Which of the following proteins is important in mediating cancer cachexia? (2 points)(p178) A. TNF‐α B. Proteolysis inducing factor C. p53 D. KRAS oncogene protein E. A,B ```

E | Have not gotten to yet

``` Chronic inflammatory reactions in most tissues in the body are usually characterized by which of the following processes? (2 points)(p115) A. Neutrophil chemotaxis B. Basophil infiltration C. Mast cell hyperplasia D. Fibrinous response E. Fibrosis ```

``` One of the mechanisms contributing to effective parasite larval killing by eosinophils is? (2 points)(p102) A. Superoxide anion B. Hydroxyl radical C. Lipid peroxides D. Major basic protein E. Ferrous iron production ```

``` Macrophages can differentiate into which of the following cells? (2 points)(p102) A. Epithelial cells B. Epithelioid cells C. Multinucleated giant cells D. A, B, C E. B, C ```

``` Which of the following mediators is strongly chemotactic for lymphocytes? (2 points)(p114) A. CCL3/MIP‐1alpha B. CCL11/Eotaxin C. C5a D. PGE2 E. LTB4 ```

``` Which of the following mediators is strongly chemotactic for neutrophils? (2 points)(p114) A. CCL3/MIP‐1alpha B. CCL11/Eotaxin C. CXCL8/IL‐8 D. LTB4 E. C and D ```

Type IV hypersensitivity reactions contribute to tissue damage via which of the following mechanisms? (2 points)(p134) A. Complement fixation and neutrophil chemotaxis and cytotoxicity B. CD8 T‐cell cytotoxicity C. Cell mediated immunity with cytokine/lymphokine mediated indirect effects D. A and B E. B and C

``` Which of the following growth factors stimulates epithelial proliferation in repair? (2 points)(p129) A. TGF‐beta B. EGF C. PDGF D. A, B, C E. B, C ```

Histamine increases vascular permeability at the level of capillaries and venules via which mechanism? (2 points)(in-class question) A. Endothelial cell contraction B. Endothelial cell damage C. Increased transcytosis D. Induces endothelial proliferation

``` Which is an inflammatory cell that is long‐lived, can divide locally in tissue and regulates immune and repair responses? (2 points)(p102) A. Neutrophil B. Eosinophil C. Macrophage D. Platelet E. B and C ```

``` Which of the following mediate pain in an inflammatory reaction? (2 points)(p114) A. CXCL8/IL‐8 B. C5a C. LTC4 D. PGE2 E. TNF‐alpha ```

``` Which of the following growth factors stimulates endothelial proliferation in repair? (2 points) A. VEGF B. basic‐FGF C. TNF‐alpha D. A,B E. A,B,C ```

Which of the following cells release vasoactive amines and arachidonic acid metabolites to upregulate inflammatory reactions? (2 points)(p111 & p 102) A. Mast cell B. Neutrophil C. Lymphocyte D. Macrophage E. A and B

``` Leukocyte adhesion deficiency has been described in which of the following? (2 points)(p101) A. Holstein cattle B. Labrador Retriever dogs C. Irish Setter dogs D. A and B E. A and C ```

``` Which of the following pathogenetic mechanisms of edema contribute most significantly to protein-rich edema fluid in inflammatory reactions? (2 points) A. Increased hydrostatic pressure B. Increased vascular permeability C. Decrease capillary oncotic pressure D. Lymphatic obstruction E. Increased sodium retention ```

Which molecules on leukocytes (L) and endothelial cells (E) respectively mediate leukocyte rolling on endothelial cells during inflammation? (2 points)(p100) A. L:integrin (CD11/CD18) and E: ICAM‐1 B. E: integrin (CD11/CD18) and L: ICAM‐1 C. L:Sialy‐Lewis X‐modified glycoprotein and E: E‐selectin D. E:Sialy‐Lewis X‐modified glycoprotein and L: E‐selectin E. A and C

Which molecules on leukocytes (L) and endothelial cells (E) respectively mediate leukocyte adhesion on endothelial cells preceding transmigration during inflammation? (2 points)(p100) A. L:integrin (CD11/CD18) and E: ICAM‐1 B. E: integrin (CD11/CD18) and L: ICAM‐1 C. L:Sialy‐Lewis X‐modified glycoprotein and E: E‐selectin D. E:Sialy‐Lewis X‐modified glycoprotein and L: E‐selectin E. A and C

Inciting stimuli of granulomatous inflammation are? (2 points)(p115) A. Particulates resisting lysosomal degradation B. Persisting molecules that stimulate T‐cell hypersensitivity C. Stimuli that are chemotactic for neutrophils D. A, B E. A, B, C

Histamine increases vascular permeability via:

endothelial cell contraction

An inflammatory cell that is long-lived, can divide locally in tissue, and regulates immune and repair responses:

Macrophages

Suppurative inflammatory rxns are often induced by:

Bacteria

Macrophage-dominated (granulomatous) inflammatory rxns are often induced by:

Fungi and mycobacteria

Which type of inflammatory cells is often associated with liquefactive necrosis?

neutrophil

Growth factors and cytokines affecting stages of tissue repair by monocyte/macrophage chemotaxis

Growth factors and cytokines affecting stages of tissue repair

Growth factors and cytokines affecting stages of tissue repair by fibroblast migration/replication and collagen synthesis

PDGF, EGF, FGF, TGF-beta, TNF, IL-1

Growth factors and cytokines affecting stages of tissue repair by epithelial proliferation/migration

EGF, HGF AND KGF

Growth factors and cytokines affecting stages of tissue repair by angiogenesis

VEGF, FGF, PDGF

Growth factors and cytokines affecting stages of tissue repair by connective tissue myofibroblast contraction and remodeling

TGF-beta, PDGF, collagenase, MMPs

Which of the following are potent inducers of angiogenesis? a. VEGF b. Beta-FGF c. HGF d. A and B e. A,B,C

Which of the following is a potent inducer of fibrosis? a. TGF-beta b. TNF-alpha c. PDGF d. A and B e. A, B, C

``` Type I anaphylactic hypersensitivity rxns can be mediated by: a.IgG b.IgM c.IgE dA,B e.A,C ```

Which of the following inflammatory mediators play a central role in anaphylaxis? a. Histamine b. LTC4, LTD4, LTE4 c. C5a d. A,B e. A,B,C

Tissue injury in a type IV hypersensitivity rxn/allergic rxn is mediated via: a. Immune complex formation b. T-Cell induction of granulomatous inflammation c. Direct T-cell toxicity d. B,C

Type III hypersensitivity reactions can be mediated by: a. IgG b. IgM c. IgE d. A,B e. A,C

Lab question: From which cells are the epitheloid and multinucleated giant cells derived from?

Monocytes and macrophages

Lab question: what mechanisms can explain the central caseation necrosis in granulomas, and is this sometimes diagnostically useful?

Central necrosis may be due to toxic molecules released by macrophages (superoxide anion and lysosomal enzymes) and hypoxemia. The necrosis may undergo secondary dystrophic calcification to result in radiodense lesions that are readily detectable in radiographs

Lab: what was the etiologic diagnosis for changes present in the stallion penis?

penile habronemiasis

Note the zones of granulation tissue around a hematoma (lab)

center-->outward fibrin zone of macrophages, capillaries, and fibroblasts growing inward zone of proliferating capillaries and fibroblasts Zone of maturing fibrous connective tissue

LAb wueston: what is the possible stimulus for the granulation tissue to form in the dog hematoma (mast cell was removed and reaction to the sutures)

Persistence of fibrin in the hematoma and failure of fibrinolysis to completely lyse the clot. Persistence release chemotactic substances and growth factors from fibrin and platelets (fibrinopeptides, PDGF, TGF beta) induces infiltration of macrophages, fibroblasts, and release of other growth factors (VEFE, b-FGF, PDGF, TGF-beta) that promotes granulation tissue and angiogenesis

Lab question: what would have been the likely long-term outcome of the granulation tissue process had the mass not been removed surgically?

cyst would clot and been replaced by dense fibrous connective tissue which would have matured and formed dense scar tissue

Lab question: Organization by granulation tissue occurs in what other processes or types of lesions?

chronic inflammatory process where there is continued generation of necrotic exudate Large areas of necrosis (e.g. infarct) Areas of chronic ulceration where there is accumulation of necrotic exudate

Lab question: what mechanisms can account for the influx of macrophages, fibroblasts, and endothelial cells into the thrombus?

fibrinopeptides are chemotactic for macrophages. Then macrophages and platelets release other chemotactic substances for other inflammatory cells and growth factors for endothelial cells and fibrosis

Exam 2 Flashcards

(288 cards)