Lesson 11 - Exam 2 Flashcards
Pain =
Dolar.
Heat =
Calor.
Redness =
Rubor.
Swelling =
Tumor.
Vasodilation due to release of vasoactive and chemotactic factors will present as -
- Dolar (pain)
- Calor (heat)
- Rubor (Redness)
Increased permeability due to release of vasoactive and chemotactic factors will present as -
Tumor (swelling)
Neutrophil emigration deu to release of vasoactive and chemotactic factors will present as -
Tumor (Swelling)
Release of vasoactive and chemotactic factors will directly result as -
Dolar (pain)
________ ________ will cause release of chemotactic and vasoactive factors.
Tissue damage.
True or false: Inflammation is a result of cell injury, that will have specific responses depending on the cause of injury.
FALSE: Inflammation is a result of cell injury, that will have a non-specific response regardless of causation.
3 healing types:
- Scar tissue - From fibrosis.
- Regeneration - Replacement with same type of tissue cells, following irreversible damage.
- Resolution - Damaged cells recover, following reversible damage.
The following are all potential causes for what condition?
1. extension of acute inflammation.
2. Prolonged healing of acute inflammation.
3. Persistence of a causative agent.
Chronic inflammation.
Histamine is a a chemical mediator in inflammatory response: Name its Source and action -
Source:
Mast cell granule.
Action:
imediate vasodialation and increased capillary permeability to form exudate.
Chemotactic factors are chemical mediators in inflammatory response - Name its source and action:
Source: Mast cell granules.
Action: Attract neutrophils to a site of inflammation.
Platelet-activating factor (PAF) is a chemical mediator in the inflammatory response - name its source and action:
Source: Cell membrane of platelets.
Action: Platelet aggregation.
Cytokines (interleukins and lymphokines) are mediators in the inflammatory response - name its source and action:
Source: T-Lymphocytes and macrophages.
Action: increased plasma proteins, Induces fever, chemotaxis, and leukocytosis.
Neutrophil specific granule contents:
- phospholipase A2. **
- Myeloperoxidase.
- Cationic proteins.
- Acid hydrolases.
- Elastase. **
- Cathepsins
Neutrophil azurophilic granule contents:
- Phospholipase A2.
- Lysozyme.
- Alkaaline phosphatase.
- Type IC collagenase.
- Lactoferrin.
- Vitamin B-12 binding proteins
Neutrophil tertiary granule contents:
- Metalloproteinases
Eosinophil specific granule contents:
Crystalloid contents:
1. Major basic protein.
2. eosinophil cationic protein.
3. eosinophil peroxidase.
4. Eosinophil-derived neurotoxin.
5. Histaminase.
6. collagenase.
Eosinophil azurophilic granule contents:
Acid hydrolases, collagenases, other eisonphil-specific hydrolases.
Basophil specific granule contents:
Pre-formed mediators of the inflammatory response, including histamine, heparin sulfate, and chondroitin.
Cause synthesis of other mediators upon stimulation.
Basophil azurophilic granule contents:
Acid hydrolases.
________________ are white blood cells that are found inside the blood vessels, that act on cells outside of the blood vessel.
Inflammatory cells.
Inflammatory cell names - In the blood vessel vs in the target tissue:
Basophil (blood) ———> Mast cell (tissue)
Monocyte (blood) ———-> Macrophage (tissue)
Lymphocytes (blood) ———–> Plasma cells (tissue)
How do we name white blood cells?
- Based on appearance in blood smears stained with Wright’s stain.
- Named based on shape, size, prescence of granules, and color of granules.
True or false: Basophils and monocytes have no major granules.
False - Monocytes and lymphocytes have no major granules, while basophils have significant granules.
Under high magnification in monocytes and lymphocytes, we can see small azurophilic granules, what are these?
These are lysosomes, called non-specific granules.
________________ Inflammatory chemical mediators, will circulate the blood in their inactive form and will need to be activated at the site of inflammation.
Plasma derives inflammatory chemical mediators.
_________________ Inflammatory chemical mediators, are pre-formed and stored in granules OR produced de novo (on demand)
Cell-derived inflammatory chemical mediators
List the heterogenous mediators of inflammation:
- Biogenic amines (histamine)
- Peptides (bradykinin and compliment)
- Arrachiodonic acid derivatives (prostagladins)
List the functions of multi-function mediators of inflammation:
- Vasodialation.
- Constriction of vessels.
- Activation of inflammatory cells.
- chemotaxis.
- cytotoxicity.
- pain and fever.
How fast does the late-phase inflammatory reaction take, in allergen exposure?
2-24 hours.
True or false: In the inflammatory response to allergen exposure, the vascular and smooth muscle reaction develops within minutes of exposure.
TRUE.
In the _______ inflammatory reaction to allergen exposure, inflammatory infiltrate will be rich in eosinophils, neutrophils, and T-lymphocytes.
Late-phase.
In the _______ inflammatory reaction ot allergen exposure, vasodilation, congestion, and edema will occur.
Immediate.
When stimulated, arachiodonic acid derivatives will be released from ______________, and be used as an important _______________ mediator.
- Phospholipids.
- Inflammatory.
What enzyme will act on the cell membrane to create the arachidonic acid pool?
Phospholipases.
Which of the following cannot inhibit the synthesis of arachidonic acid derivatives?
a. Steroids.
b. NSAIDS
c. COX 1/2 inhibitors.
d. Phospholipases.
D - Phospholipases.
Phospholipases will help create more arachidonic acid derivatives!
True or false: NSAIDS specifically inhibit phospholipases?
FALSE - Steroids specifically inhibit phospholipases.
NSAIDS are indiscriminate inhibitors of COX 1 and COX 2, meaning it will inhibit functions of both, what are the consequences of this?
Inhibition of COX-1 can cause gastric ulcers, renal ischemia, premature closure of the ductus arteriosus, and reye’s syndrome.
COX stands for:
Cyclooxygenase.
This is expressed in most tissues and does maintenance of the stomach, kidneys, intestines, platelets, and endothelium. It will be initiated by a physiological stimulus, and end with a physiological stimulus.
a. COX-1
b. COX-2
a - COX-1
This will be stimulated by an inflammatory stimuli, and attract macrophages and synoviocytes to the site of inflammation. Over-expression of this will result in gallbladder carcinoma.
a. COX-1
b. COX-2
b- COX-2
_______ is inducible by inflammatory stimuli and occur constitutively in the immune tissues like the kidneys, bones, and brain.
COX-2
What are the two important pathogenic factors of edema?
- Increased venous pressure.
- Reduced oncotic pressure, resulting from a low albumin concentration.
True or false: Edema can be caused by hydrostatic and oncotic pressure increases, while decreases in vascular permeability and causing blood vessel obstruction.
FALSE - Edema will increase hydrostatic pressure and vascular permeability, while decreasing oncotic pressure and causing blood vessel obstruction.
__________________ causing edema is typically due to venous thrombosis or heart failure.
Increased hydrostatic pressure.
_________________ causing edema is typically due to nephrotic syndrome enteropathy or liver failure.
Decreased oncotic pressure.
_________________ causing edema is typically due to inflammation, trauma, or burns.
Increased vascular permeability.
________________ causing edema is typically due to tumors, surgery, or parasites.
Obstruction of lymph vessels.
What is the role of neutrophils and macrophages?
Phagocytosis.
A side-effect of __________, using ________ or _________, is that free radicals will be produced - such as reactive O2 species and nitric oxide (NO)
- Phagocytosis.
- Neutrophils.
- Macrophages.
What will stimulate the immigration of neutrophils and macrophages to a tissue to begin phagocytosis?
Tissue injury causes release of chemical mediators that promote vasodilation and binding of neutrophils and macrophages to the capillaries.
True or false: Macrophage-derived IL-1 will stimulate the release of neutrophils from bone marrow, causing neutrophilia.
TRUE!
The first receptors activated during a host-pathogen interaction are part of what receptor family?
Toll-like-receptor (TLR) family
CD-14 serves as a co-receptor for TLP’s
What serves as a co-receptor for the TLR family?
CD-14.
What is the effect of cytokines inducing the liver to release acute-phase proteins?
Increases plasma fibrinogen levels, and works as a clotting factor by reducing the charge of RBCs.
_________ is a clotting factor created by acute-phase proteins.
Fibrinogen.
IL-1, IL-6, and TNF-a are all mediators of inflammation that will cause:
- Release of clotting factors from the liver (fibrinogen)
- Release of C-reactive proteins to facilitate phagocytosis.
- Release of serum amyloid a.
- Release of protease inhibitors (a1-antitrypsin)
True or false: IL-1, IL-6, and TNF-a are mediators of inflammation that are intended to further damage the tissue.
FALSE - These will function to prevent excessive damage to the injured tissue.
__________ __________ ____ provides a measure of the level of inflammation in an individual.
erythrocyte sedimentation rate (ESR)
Cytokines involved in the inflammatory response will enhance protein catabolism in skeletal muscle, for what purpose?
To provide a free amino acid pool, to use toward antibody production.
Increased body temp:
a. Disrupts the inflammatory response.
b. Has no effect on the inflammatory response.
c. Enhances the inflammatory repsonse.
c - enhances the inflammatory response.
______ diffuses into the hypothalamus and raises the set-point for thermoregulation and helps maintain ______ in the inflammatory response.
- PGE2
- Fever
In a healthy individual, the hypothalamic thermoregulatory center adjusts -
The peripheral loss of heat matches the heat production.
Wound healing - incision wound within hours of injury:
- Leukocytes surround the wound
- Scab forms on the epidermis.
Wound healing - incision wound days after being sutured:
- Macrophages and fibroblasts are at the site of injury.
- Granulation tissue forms.
- Blood flow is higher.
Wound healing - incision wound weeks after being sutured:
Scar tissue has formed, causing a primary intention scar.
Primary intention scar:
Matrix will change from fibronectin and fibrin to collagen III, and finally to collagen I.
Wound healing - Gaping wound soon after injury:
Foreign bodies and bacteria can invade the gaping wound.
Wound healing - Gaping wound a while after injury:
Abundant granulation tissue forms, as a temporary structure made of C.T to replace a fibrin blood clot. (wound does not close)
Secondary intention scar:
Due to excessive scarring making a hypertrophic scar made mostly of type III collagen.
