Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Gen Path 300 > Classes 3-4 > Flashcards

Classes 3-4 Flashcards

0
Q

What are the possible outcomes of chronic inflammation?

A

Tissue destruction, fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

When does acute inflammation usually stop?

A

When injurious stimulus is removed, walled off, or broken down.

Outcomes: resolution, abscess formation, chronic inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 7 morphotypes of inflammation?

A 
Serous
Fibrinous
Purulent
Ulcerative
Pseudo membranous 
Chronic
Granulomatous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Serous inflammation

A

Mildest form of inflammation
Characterized by clear fluid
Occurs in early stage; typical in viral infections, burns, arthritis

Exudate mostly albumin and immunoglobulin

Self limiting

Generally resolves easily.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Fibrinous inflammation

A

Exudate rich in fibrin

Bacterial infections (strep throat, bacterial pneumonia, bacterial pericarditis).

Does not resolve easily. Often requires antibiotics.

Leads to growth of fibrous tissue (scarring) in parenchyma –> loss of function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Purulent inflammation

A

Typically formed by pus-forming bacteria. (Staph and strep)can accumulate on mucosa or in internal organs. May form abscess.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Abscess

A

Localized collection of pus within an organ or tissue

Does not heal spontaneously; must be surgically excised.

May lead to fistula or sinus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sinus

A

Cavity, usually occupied previously by an abscess that has ruptured, that drains through a tract to the surface of the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Fistula

A

A channel between preexisting cavities and/or hollow organs and/or surface of the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Empyema

A

Accumulation of pus in a preformed cavity (ex. gallbladder)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ulcerative Inflammation

A

Inflammation do body surfaces or mucosa.

Leads to ulceration or necrosis of epithelial lining.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ulcer

A

Defect involving the epithelium, which can also extend into connective tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pseudomembranous inflammation

A

Combination of ulcerative, fibrinous and purulent inflammation.

Ulcerative with fibronopurulent exudate (with mucus and cellular debris) which forms a pseudomembrane on surface of ulcer.

Diphtheria (pseudomembranes form on throat); C. Difficile in large intestines (secondary to antibiotic use)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chronic inflammation

A

Because of length of inflammation, produces more tissue destruction, heals less readily and associated with more serious functional deficiencies.

Exudate contains monocytes, lymphocytes, macrophages, plasma cells.

Secretory products stimulate proliferation of fibroblasts (–> scarring –> loss of function) and recruit new inflammatory cells (perpetuating inflammation)

Sm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Granulomatous inflammation

A

Not preceded by acute inflammation.

Not neutrophil driven.

T-lymphocytes and macrophages accumulate at site of injury.

Lymphocytes release cytokines, which transform macrophages into epithelioid cells.

Epithelial cells fuse with each other and form multinucleated giant cells.

Multinucleated giant cells, epithelium cells and lymphocytes form granulomas, which destroy cells and last long time.

Caseous and non caseous

TB, fungal infections, syphillis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical correlations of inflammation

A

Fever 37 degrees +
Leukocytosis
Constitutional symptoms (fatigue, weakness, depression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes fever?

A 
Pyrogenes cytokines (Tumour Necrosis Factor -- TNF -- and IL-1)
-- stimulate production of prostaglandins in hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cell categories based on ability to proliferate

A
  1. Continuously dividing/labile/mitotic
  2. Quiescent/facultative mitotic/stable
  3. Non-dividing/post-mitotic/permanent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Continuously Dividing Cell

A

Labile, mitotic, stem cells

Typically found in basal layer of skin or mucosa of internal organs.

Outcome: minimal tissue damage, short recovery time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Quiescent Cells

A

Facultative mitotic, stable

Do not divide regularly but can be stimulated to divide if necessary.

Form the parenchymal organs. (Eg liver, kidneys).

Outcome: regeneration, although may be limited.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Non-dividing Cells

A

Post-mitotic, permanent.

No capacity to divide period. Ex: neurons.

Outcome: replacement of parenchymal tissue with connective tissue leads to loss of function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Healing by First Intention.

A

When wound is clean, free of foreign material and necrotic tissue, and edge are close together.

Scab
PMNs scavenge debris
2-4 days later granulation tissue develops.
3-6 weeks scar develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Healing by Second Intention

A

Large break in tissue, inflammation, longer healing and more scarring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Granulation tissue

A

Vascularized connective tissue rich in macrophages, myofibroblasts and angioblasts.

Part of wound healing. Develops in 2-4 days.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
PMN's role in wound healing
Scavenge briefly at injury site
25
The role of connective tissue cells in wound healing
Produce scar tissue. Include myofibroblasts, angioblasts, fibroblasts
26
Epithelial cells and wound healing
Undergo mitosis and extend across wound.
27
Macrophages and wound healing
Stay at site and produce cytokines and growth factors.
28
Myofibroblasts and wound healing
Hybrids -- have properties of smooth muscle and fibroblasts. In first few days, contract reduces defect and holds margins together. Secrete matrix substances like fibroblasts.
29
Angioblasts and wound healing
Precursors of blood vessels Appear 2-3 days after incision and new blood vessels permeate site by 5-6th day. New vessels provide route for scavenger cells to remove scab and debris and allow influx of nutrients and O2
30
Fibroblasts and wound healing
Produce most of ECM Fibronectin- forms scaffold Collagens -- form fibrils in interstitial spaces
31
Healing Process
1. Blood clot formation 2. Inflammation develops 3. Cellular debris removed by phagocytes, monocytes and macrophages 4. Granulation tissue develops in gap 5. Epithelial cells insert mitosis and extend across wound 6. Fibroblasts produce collagen 7. Fibroblasts and macrophages produce cytokines which attract more fibroblasts. 8. Fibroblasts stimulate epithelial cell proliferation and migration and angiogenesis. 9. Cross linking and shortening of collagen fibres 10. Capillaries decease.
32
Contracture
Fixation and deformity of the joint
33
Adhesion
Bands of scar tissue that join two normally separated surfaces b
34
Immunity
Protection from disease, especially infectious disease. Natural and acquired.
35
Natural immunity
Primitive, nonspecific, inherited. Include mechanical factors like skin and cilia, and phagocytic and NK cells. Also includes protective proteins.
36
Natural immunity includes what protective proteins?
1. Complement 2. Properdin (plasma protein that activates alternative complement pathway) 3. Lysozome (bactericidal protein found in tears, and in nasal and intestinal secretions)
37
Acquired immunity
Based on body's ability to: 1. Distinguish self from non-self 2. Generate an immunologic memory 3. Mount an integrated reaction of various cells
38
Immune competence
The body's ability to mint and appropriate immune response
39
Cells of the immune system
1. Lymphocytes - - T lymphocytes (T helper and T suppressor/cytotoxic cells) - - B lymphocytes 2. Plasma cells
40
Primary lymphoid organs
Thymus | Bone marrow
41
Secondary lymphoid organs
Most notably lymph nodes and spleens. | Also GI tract and bronchial mucosa
42
MALT
Mucosa associated lymphoid tissue. | Formed by lymphocytes. Unencapsulated, integrated in mucosa.
43
T lymphocytes
Lymphocytes that have matured in thymus. Account for 2/3 lymphocytes in blood. Also found in lymph nodes and spleen. Include T helper (CD4) and T suppressor/cytotoxic cells (CD8) All T cells have a membrane T cell receptor (TCR) linked to CD3 protein. Used for recognition of antigens.
44
Natural Killer (NK) cells
T cells that do not express TCR-CD3 complex Mediate innate immune reactions; not involved in T & B cell mediated reactions. React against virus infected cells, and foreign and cancer cells
45
T Helper Cells
Help B cells produce antibodies Express CD4 on their surface. Secrete cytokines. Classified as Th1 or 2 depending on which cytokines produced
46
TH1 Cells
T helper cells that produce interleukin 2 (IL-2) and interferon gamma (IFN-gamma). Stimulate macrophages to become phagocytic Mediate formation of granulomas
47
TH-2 cells
T helper cells that make IL-4, IL-5 and IL-13 | Important for secretion if IgE and other immunoglobulins and activation of eisinophils
48
T Suppressor/Cytotoxic cells
Express CD8 on their surface Suppress unwanted antibody production Mediate killing of virus-infected and tumour cells.
49
Normal ratio of CD4:CD8 cells
2:1
50
B lymphocytes
Cells that mature in the bone marrow. When stimulated by antigens, differentiate into plasma cells
51
Plasma cells
Fully differentiated descendants of B cells Produce antibodies. Cytoplasm contains an abundance of ribosomes and RER.
52
Antibodies
Protiens of the immunoglobulin class secreted by plasma cells Made up of about 110 amino acids
53
IgM
``` Mega immunoglobulin (biggest) Composed of five basic units ``` Functions to neutralize microorganisms. First to appear after immunization. Natural antibody against ABO antigens Complement activator.
54
IgG
Gnomish. (Smallest immunoglobulin) Most abundant. Produced in small amounts on initial immunization but production is boosted upon re-exposure. Can cross placenta. Acts as opsonin.
55
IgA
Aw yucky Found in mucosal secretions (tears, nasal secretions), milk and intestinal secretions.
56
IgE
Evil (allergies) Secreted by plasma cells in tissues Locally attached to mast cells Mediates allergic reactions (Type 1 hypersensitivity reaction) Present in trace amounts in serum.
57
IgD
Doh! Cell-membrane bound; on B cells Participates in antigenic activation of B cells; not released into serum or body fluids.
58
Antibody production
Foreign antigen attaches to B-lymphocyte antigen receptor complex. B cells internalize antigen and function as Antigen Presenting Cells Present antigen to T cells. T helper cell produces cytokines, which transform B cell into plasma cell, which produces antibodies.
59
Major histocompatability complex
Proteins present on surface of cell that identify cell as self/other. The "identity" of pathogen that allows for specific immunity to be developed.
60
Ag-Ab reaction
Ab and Ag bind to form complexes. If large enough, may be phagocytosed in spleen/liver by fixed macrophages. If small, may bind on RBCs or endothelial cells, or filter through capillary walls. AbAg complexes on RBCs can cause agglutination --> hemolysis
61
Hypersensitivity Reaction
An abnormal immune response to exogenous antigen or endogenous auto-antigen
62
Types of hypersensitivity
I. Anaphylactic type reaction II. Cytotoxic Ab-mediated type reaction III. Immune complex mediated reaction IV. Cell-mediated, delayed type reactions.
63
Type I Hypersensitivity
Anaphylactic type IgE mediated. AgAb complex on mast cells trigger release of histamines Hay fever (allergic rhinitis) Eczema (atopic dermatitis) Bronchial asthma Anaphylactic shock.
64
Type II Hypersensitivity
Mediated by IgM or IgG Cytotoxic Abs react with Ags in cells or tissues. Activates complement system (MAC) then cell lysis, or attracts cytotoxic T cells Re exposure may lead to autoimmune disorders: Goodpastures, hemolytic anemia, Graves Disease, or Myasthenia gravies
65
Goodpasture's Syndrome
Type II hypersensitivity disorder Autoimmune reaction against Coolagen Type IV Leads to renal and pulmonary damage
66
Hemolytic Anemia
Type II hypersensitivity disorder Can occur as a result of acute hemolytic reaction (transfusion of mismatched blood) or SLE (systemic lupus erythematosus)
67
Epitope
Part of antigen that is recognized by immune system.
68
Graves Disease
Type II hypersensitivity disorder Form of hyperthyroidism in which antibodies to thyroid stimulating hormone receptors cause overproduction of thyroid hormones.
69
Myasthenia Gravis
Type II hypersensitivity disorder Antibodies to ACh receptors in NM junction prevent binding. Results in severe weakness and paralysis.
70
Type III Hypersensitivity Disorder
Mediated by AgAb complexes. Complexes get trapped in semipermeable membranes, and active complement system, triggering inflammation characterized by fibrotic necrosis.
71
Systemic Lupus Erythrematosus (SLE)
Lupus Involves Type III hypersensitivity Circulating AgAb complexes deposit on tissues and cause kidney disease, arthritis, skin disease, Eric.
72
Post streptococcal Glomerulonephritis
Type III hypersensitivity disorder Acute renal disease following URT strep infection. AgAb complex gets stuck in glomerular basement membrane, evoking complement mediated inflammation.
73
Polyarteritis Nodosa
Type III hypersensitivity disorder AgAb mediated Involves small to medium sized arteries. Acute: fibroid necrosis and acute inflammation Chronic: destruction of vessel wall; thrombosis and occlusion --> ischemia and infarcts
74
Type IV Hypersensitivity Reaction
Cell mediated or Delayed Type Immune Reaction Involves T cells and macrophages, which aggregate and form granulomas. Accounts for granulomas developing in response to tumours, and idiopathic granulomatous diseases. Response to M tuberculosis, mycobacterium Leprae, and fungi. Contact dermatitis most common clinical form.
75
Types of transplantation
Autograft -- self to self Isograft -- identical twin to twin Homografts: human to human Xenografts: nonhuman to human

Gen Path 300 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions