Inflammatin for Pathology by Spicer, Bastyr
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| What are the three Durations of disease? | Acute: hours to a few days
Chronic: weeks to years
Insidious: Unknown
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| Define Etiology: | The cause and progression of illness.
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| Etiology: what are the three causes of the illness? | a) idiopathic: Unknown, Autoimmune, Autosensitivity,
b) known/suspected: Disease that is diagnosed.
c) iatrogenic: (medical interventions)
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| Define Pathogenesis: | history and development of disease:
beginning with the initial event, tracing the ongoing development of abnormal structure/function in an organ or system.
Also, how the body is acting and reacting to the disease and treatment.
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| Define Pathophysiology: | how is the incorrect/abnormal function expressed?
Which functions switch from normal to abnormal. How does this effect the person.
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| What are the two Levels of pathology? | a) Anatomic pathology:
b) Clinical pathology:
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| Define Anatomic pathology: | looking for structural abnormalities, use of many different tools
Gross exam: clinical exam/office visit, scans and xrays
Observation: unaided eye/ear aided scans and xrays
Microscopic: tissue samples (blood tests, tissue biopsy to spot abnormal cells)
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| Define Clinical pathology: | study of functional aspects of disease by lab study of tissue, blood, urine, cerebrospinal fluid, etc.
Example: blood glucose levels to diagnose diabetes
Example: microbiology workup of urine to detect or rule out bacterial infection
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| What is the Relationship between structure and function in Pathology? | This relationship is important in understanding pathogenesis of a disease.
1. Structural defect leads to functional disorder:
Example: a bacterial infection of a heart valve destroys the normal architecture, leading to a functional abnormality: mitral v
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| What is the importance of measurements? | Defects in performance (function) can be assessed by taking measurements (blood pressure, pulse) or collecting samples/specimens for lab analysis.
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| Describe medical history: | Medical history is a combination of objective and subjective data, taken to determine the presence/absence of wellness.
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| Define Symptoms: | Symptoms are "complaints" reported by patient (or a proxy, based upon patient's words). These are subjective, and can be verified only by the patient's direct experience. Ex: pain, nausea, light headedness, tingling, etc.
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| Define Sighns: | Signs: objective observations by someone else. These are verifiable, and can sometimes be quantified: Ex: fever, high blood pressure, discolorations.
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| Can a physical problem be both a sign and a symptom? | a physical problem can be both a symptom and a sign. Ex: the patient reports feeling feverish, and the physician uses a thermometer to record a body temperature of 101F - both of them are noting the same event, but from 2 different perspectives.
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| Are all signs verifiable? | Some symptoms are non-verifiable; the same is not true for signs.
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| Define Syndrome: | Syndrome is a collection of clinical signs, symptoms, and data which add up to a particular diagnosis.
Example: AIDS, where "S" stands for syndrome
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| What is normal anyway? | Definition of normal: in a clinical setting, it refers to the results of measurements or observations used to determine whether disease is present.
- Based on clinical results, you are defined as either normal (implying that you are healthy), or abnormal
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| Describe the Problems with the use of "normal" values: | positive result means abnormal
a) tests may be inaccurate
False positive "You are sick!": but not really
False negative "You are well!": but not really
b) sometimes sick patients have normal test results
"clean bill of health" given after a physical
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| Define a Clinically Silent disease: | Clinically silentdisease is not advanced enough to be detected yet (small tumors of the lung, pancreas, ovary remain clinically silent for a long time)
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| Describe human error in Lab tests: | lab mix-ups, computer malfunctions, lost records, etc.
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| Why are normal ranges important? | Normal ranges show human variations must be taken into account (height, weight, activity level, genetics, life cycle stages, diet, occupation, lifestyle choices) when interpreting results of tests.
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| Describe a Referance Range of clinical tests: | A "reference" range has been established for most quantitative tests (numerical values).
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| What is the range for Qualitative tests? | For qualitative results, there is no range - the test is either positive (abnormal) or negative (normal). Example: you either do or do not have antibodies to hepatitis virus. This is not to say that you can't quantitate the amount of antibodies, but it is
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| Describe the Normal Distribution curve for test results: | Normal distribution curve: measure a lot of healthy people, record their values, and distribute the values to see a curve which shows that most healthy people cluster around certain values. The "tails" of the curve will show outliers, where abnormality ex
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| DefineTest sensitivity: | Sensitivity: how accurately can the test detect the disease? Example: a test is 99% sensitive, meaning it will miss only 1 in every 100 cases of disease.
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| Define Test specificity: | Test Specificity shows how well the test avoids false positives. Example: a test which is 99% specific will be negative in 99 out of 100 people who do not have the disease.
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| In regards to test specificity and sensitivity demonstrate an effective clinical strategy: | first use a very sensitive test. Then follow up on a positive result by using a very specific test to rule out a false positive result. Test sensitivity gives you a strong positive while test specificity reduces the margin of error.
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| Take-home message: | medical tests are not perfect predictors of disease. Good clinicians realize this, and choose tests carefully, then interpret them cautiously. Second opinions are always a good idea.
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| Structural defect leads to: | Functional Disorder
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| Functional disorder leads to: | Structural Change
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| Anatomy = | Structure
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| Physiology = | Physiology
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| Define Tissue: | collection of similar cells.
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| What are the four types of tissue? | a) epithelial tissue: classified by structure (shape);
b) connective tissue: classified by structure;
c) muscle tissue: classified by functional and structural characteristics;
d) nervous tissue: as for muscle.
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| Define Organ: | Organ: composed of 2 or more tissue types that perform common functions.
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| Define Parenchyma: | Parenchyma are specialized cells of an organ (the functional unit);
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| Define Stroma: | Stroma: holds together specialized cells (fibrocytes, collagen, elastic fibers).
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| What are three Common features of a normal animal cell: | Nucleus
Cytoplasm
Plasma Membrane
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| Describe the Nucleus of a cell: | Structures:
*Chromosomes contain DNA.
*Nucleolus contains RNA.
*Nuclear membrane segregates these from the cytoplasm.
Functions:
*Oversees all major cytoplasmic events (protein synthesis for respiration, cellular growth, metabolism).
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| Describe the Cytoplasm of a cell: | Cytoplasm: cytosol (water containing minerals, proteins, carbohydrates, lipids) + organelles
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| Describe the Cytoplasm of a cell: | Cytoplasm: cytosol (water containing minerals, proteins, carbohydrates, lipids) + organelles
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| Describe the Organells in the Cytoplasm: | Organelles: structures with accompanying functions:
a) Mitochondria: generate energy
b) Ribosomes: protein synthesis
c) Endoplasmic reticulum: if "rough" (studded with ribosomes), the site of protein synthesis; if "smooth", the site of catabolic react
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| Describe the Plasma Membrane: | Plasma membraneStructure: polarized bilayer of lipids with proteins and carbohydrates embedded in it; requires active maintenance and energy expenditure by the cell.
Function: serves as a semi-permeable barrier; contains receptors, adhesion molecules, tr
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| Define HORMONE: | chemical messenger
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| What are the 3 types of HORMONES: | Autocrine, Paracrine, Endocrine.
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| Describe Autocrine Hormones: | Autocrine: Self-stimulation of a cell via growth factors. Example: T lymphocytes secrete interleukin-2 (IL-2); interacts with own surfacereceptors to stimulate cell growth.
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| Describe Paracrine Hormones: | Transmission of signals from 1 adjacent cell to another, Example: Release of hydrochloric acid from chief gastric cells in the gastric mucosa, under the influence of gastrin (neuropeptide hormone) released by neuroendocrine G cells.
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| Describe Endocrine Hormones: | Endocrine: Hormones are released from one tissue into the bloodstream and travel to a distant receptor site in another tissue.
Example: insulin secreted from the islet cells of the pancreas travels through the blood to affect the liver, muscles, and fat
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| What type of hormones stimulate cell growth within the cell? | Autocrine. Auto=Self
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| What type of hormone is used for communication foe adjacent cells? | Paracrine
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| What type of Hormone is used for communication to a distant part of the body? | Endocrine
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| Define Homeostasis: | HOMEOSTASIS is the maintenance of a very narrow range of physiologic parameters by a cell. The body strives to maintain a balanced, steady state of equilibrium.
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| Define Apopotosis: | Apoptosis is planned or programmed cell death. ie: Skin, GI tract
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| Define Necrosis: | Necrosis: cell death caused by disease.
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| Define Stressors: | Stressors: All disease occurs because of injury. (see page 24) Stressors cause injury.
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| What are the nine stressors? | 1) Oxygen deprivation
2) Physical action or trauma
3) Ionizing Radiation
4) Toxic mollecular injury
5) Microbes
6) Inflammatory and immune reactions
7) Nutritional imbalances
8) Genetic Defects
9) Aging
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| Describe Oxygen deprivation: | Lack of Oxygen...
Examples: Hypoxia - due to ISCHEMIA (loss of arterial bloo supply), inadequate oxygenation of the blood (as in pneumonia), or reduced oxygen-carrying capacity of red cells (anemia, or carbon monoxide poisoning). Consider the type of ce
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| What are examples of Physical Action or Trauma? | Example: mechanical force: hemorrhage, ischemia may result from this.
Example: pH changes due to ingestion of acids or alkalis.
Example: temperature fluctuations (extreme heat or cold) can damage cells.
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| What are examples of Ionizing radiation? | Example: acute radiation injury: hydroxyl group attached to DNA and prevents cell reproduction; very serious to rapidly dividing cells.
Example: chronic radiation injury causes DNA mutations that could lead to neoplasia.
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| What are examples of Toxic molecular injury? | Toxic molecular injury
Example: chemicals, heavy metals disrupt enzymes & their biochemical pathways.
Example: Water Hemlock, the most deadly toxin in North America!
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| What are examples of Microbes? | Example: bacteria produce toxins that interfere with cell protein synthesis or cell oxygen utilization.
Example: Viral invasion lyses cells or causes immune reaction that kills the cell to stop the invaders.
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| What are examples of Inflammatory and immune reactions? | Example: autoimmune disease attacks the body's own cells as foreign tissue. EX: Lupus, RA, Bee Stings.
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| Examples of Nutritional imbalances? | Example: over nutrition - obesity is an epidemic in the developed world, leading to health complications including heart disease, cancer, and diabetes.
Example: undernutrition - calorie deficiency, protein deficiency robs cells of normal structure and fu
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| Examples of Genetic defects: | Example: mutations in base sequences permanently change the message of DNA.
Example: cytogenetic disease is a change in the number of chromosomes, or the amount of genetic information on parts of chromosomes. Original message is lost.
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| Examples of Aging: | Example: progressive, mild injury which weakens or kills the cell. NOTE:
Biologic aging is a normal, physiologic process distinct from disease.
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| Give Examples of other intracellular accumulations due to mild chronic injury: | 1. Fat
Example: chronic alcoholism
2. Cholesterol
Example: atherosclerosis: deposition of cholesterol in cells of arteries
3. Protein
Example: alcoholic liver disease
Example: Alzheimer disease
4. Glycogen
Example: diabetic hepatocytes
5. P
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| What are 5 adaption methods of cells? | Atrophy
Hypertrophy
Hyperplasia
Dysplasia
Metaplasia
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| Describe ATROPHY: | -decrease in cell size & function due to loss of cell substance; if enough cells atrophy, the entire tissue shrinks.
Examples: The thymus atrophies after childhood; the female reproductive system atrophies during menopause (normal), or smaller, flaccid l
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| Describe HYPERTROPHY: | -increase in cell size, resulting in increased organ size & function. Example: body building (normal) or enlarged left ventricle due to hypertension (pathologic). General rule of thumb: cells that are "permanent" will hypertrophy.
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| Describe HYPERPLASIA: | -increase in the number of cells in an organ or tissue (may occur with hypertrophy). Example: number of endometrial cells increases during female puberty; high altitude living increases the number of circulating red cells to carry oxygen more efficiently.
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| Describe DYSPLASIA: | -premalignant change which is reversible.
Example: abnormal Pap smear shows cells with atypical size or shape
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| Describe METAPLASIA: | -reversible change that replaces one adult cell type (epithelial) with another
Example: respiratory epithelium in a smoker changes from ciliated columnar cells to stratified squamous cells (the smoker gains protection from the assault of smoking, but los
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| Describe IRREVERSIBLE INJURY: | Stress of the cell where the cell can not adapt.
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| Define Apoptosis: | apoptosis - programmed cell death ("cellular suicide")
The body uses this mechanism as part of normal physiologic processes. Example: destruction of cells during fetal development
Example: deletion of auto-reactive T cells in the thymus (>95% of your t
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| Define Necrosis: | necrosis - sequence of morphologic changes that follow cell death in a living tissue
Example: coagulative necrosis, featuring cell swelling, denatured cytoplasmic proteins, and damaged organelles.
Other types of necrosis: see p.25
-liquefactive necrosi
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| Define INFLAMMATION: | a protective, nonspecific response to limit the extent/severity of injury, to eliminate the initial cause of cell injury, and clean up the necrotic cells & tissues resulting from the original damage.
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| Purpose of inflammation: | to deliver WBC's to site of injury, where they will "munch" microbes or break down necrotic tissue.
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| What causes Inflammation: | Anything external (exogenous) or internal (endogenous) that causes cell injury can cause this complex reaction in vascularized connective tissues.
- Exogenous: External Cuts, Sliver of wood, virus.
- Endogenous, Internal, appendicitis, broken bone.
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| What are the good qualities of Inflammation? | - Neutralizes toxins,
- Repairs damaged tissue,
- Clears infections,
- Makes wound healing possible.
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| What are the bad qualities of Inflammation? | -life-threatening anaphylactic reactions (insect bites, food, drugs)
-chronic diseases:rheumatoid arthritis and atherosclerosis;
-cause intestinal obstruction due to fibrous bands of tissue
-impairs cardiac function due to scar tissue; (heart attacks,
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| What does "itis" mean? | inflammation.
Ex: appendicitis means an inflamed appendix.
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| Describe the basic players in Inflammation: | A team of VASCULAR and CELLULAR players work together to resolve a local injury and restore normal tissue function.
- Circulating cells
- Plasma proteins
- Vascular wall cells
- Connective tissue cells & matrix
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| What Circulating cells are involved in Inflammation? | -White blood cells
-Platelets
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| What Plasma proteins cells are involved in Inflamation? | -Coagulation/clotting factors
-Kinins
-Complement components
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| What Vascular wall cells are involved in Inflammation? | -Endothelial cells directly contacting the blood
-Underlying smooth muscle cells
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| What Connective tissue cells & matrix cells are involved in Inflammation? | -Mast cells, macrophages
-Fibroblasts
-Extracellular matrix (ECM): collagen & elastin, proteoglycans, adhesive glycoproteins
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| Who is already there at the site of in flammation and who shows up? | Vascular wall cells, Connective tissue & Matrix already there, Circulating and Plasma proteins show up.
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| What are the four steps in the Broad outline of inflammation process: | Step 1: Initial inflammatory stimulus (noxious agent, microbes, Cut, etc.) occurs.
Step 2: Chemical mediators are released in response (from plasma or connective tissue cells).
Step 3: Vascular and cellular changes occur, in response to the mediators.
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| What are the two basic patterns on Inflammation?: | ACUTE: short duration; a few minutes to a few days; will see influx of fluids to the area.
CHRONIC: longer duration; days to years; will see increased blood supply & scar tissue.
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| Describe ACUTE INFLAMMATION: | Starring: Neutrophils
Acute inflammation is the fast, nonspecific, early response to injury that delivers leukocytes to the sites of injury. Injury could include microbial infections, physical or chemical injury or immune injury.
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| What are the 2 big jobs of the cells during ACUTE inflammation? | 1) clear the area of invading microbes (if any), and 2) begin to break down necrotic tissue.
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| What are the basic components of ACUTE inflammation? | Chemicals, + Cells, + Blood vessels = Acute inflamation.
Chemicals: (Chemical Signals)
Cells: Phagocytes, diapedesis
Blood Vessels: Dilation
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| Define diapedisis: | Cells all going to the injury, think Lemmings.
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| Descrtibe the three functional elements of Acute Inflammation: | 1) Abnormal Chemical Signals,
2) Dilation
3) Phagocytosis
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| What are the The 2 big things that occur in Blood Vessels during Acute Inflammation? | -(Vascular Changes) Changes in vascular caliber (diameter) and flow
-(Hemodynamic Changes) Increased vascular permeability ("leakiness")
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| During Acute Inflamation, what are the VASCULAR CHANGES: | changes in blood flow in response to the local release of chemical mediators; VASODILATION begins quickly but develops at variable rates, depending on the type and severity of the original injury.
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| During Acute Inflamation what are the HEMODYNAMIC CHANGES: | Increased vascular permeability allows proteins to leave the bloodstream.
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| Describe the basic CELLULAR EVENTS of Acute Inflammation: | recruiting and activating the necessary cells. (macrophages)
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| What are the 5 cardinal signs of Acute Inflammation? | There are 5 cardinal signs of acute inflammation (identified by Celsus and Galen 2000 years ago)
Tumor: swelling
Rubor: redness
Calor: heat
Dolor: pain
Loss of function (function laesa)
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| Define VASODILATION: | diameter of arterioles increases.
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| Describe INCREASED VASCULAR PERMEABILITY: | vessels become leaky; protein-rich fluid moves into tissue spaces
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| Define ERYTHEMA: | redness, accompanied by heat
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| Define EDEMA: | fluid accumulation in the interstitial spaces.
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| Define INFLAMMATORY EXUDATE: | Accumulation of fluid, WBCs is INFLAMMATORY EXUDATE: 3 types
1) SEROUS INFLAMMATION
2) FIBRINOUS
3) SUPPARATIVE (PURULENT, PYOGENIC)
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| What are the three types of INFLAMMATORY EXUDATE? | 1) SEROUS INFLAMMATION
2) FIBRINOUS
3) SUPPARATIVE (PURULENT, PYOGENIC)
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| Describe SEROUS INFLAMMATION: | Copious amounts of watery fluid that is relatively low in protein compared to other inflammatory exudate and contains relatively few inflammatory cells. Ex: Fluid in burn blisters
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| Describe FIBRINOUS: | Higher protein content than is found in serrous. Many proteins from coagulation proteins that clot to form fibrin.Contains more inflammatory cells than serous fluid. Ex: Crust of a Scab.
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| Describe SUPPARATIVE (PURULENT, PYOGENIC): | Characterized by creamy fluid, pus, composed of fluid, necrotic debris, and overwhelming numbers of neutrophils.
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| What is The big Cellular Event that occurs in Acute Inflammation: | Neutrophils arrive at the scene, attracted by chemicals, to perform a "clean up operation" via phagocytosis.
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| What are the cell types in Acute Inflammation? | - POLYMORPHONUCLEAR (PMNs) leukocytes, a.k.a. NEUTROPHILS
- EOSINOPHILS
- BASOPHILS
- LYMPHOCYTES:
- MONOCYTES
- MACROPHAGES
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| Describe the function of POLYMORPHONUCLEAR (PMNs) leukocytes, a.k.a. NEUTROPHILS in Acute Inflammation: | phagocytosis of microbes; these are the 1st to arrive on the scene & dominate for 1st 6-24 hours. p37 They also call other cells to the scene via chemicals. Pus is the accumulation of dead PMNs.
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| Describe the function of EOSINOPHILS in Acute Inflammation: | present in allergic responses (hayfever, asthma); involved in parasitic infections; appear 2-3 days after PMNs.
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| Describe the function of BASOPHILS in Acute Inflammation: | attracted during allergic reactions & attract other cells; release histamine, leading to inflammation. Mast cells are closely related, perform the same functions, but hang out in tissues as opposed to the blood.
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| What is the relationship between Basophil and Mast Cell? | Basophil in Blood = Mast cell in different location.
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| Define Granulocyte: | The general name for neutrophils, eosinophils, and basophils is GRANULOCYTE.
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| Describe the function of LYMPHOCYTES in Acute Inflammation: | Have minor function in Acute Inflamation. Have major function in Chronic Inflammation.
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| Describe the function of MONOCYTES in Acute Inflammation: | perform phagocytosis after 24 hours, up to 48 hours. Will be discussed in chronic inflammation, for their role in presenting antigen (foreign protein) to lymphocytes.
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| What is the relationship between Monocyte and Macrophage? | Monocytes in blood = Macrophage in different location.
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| Describe the function of MACROPHAGES in Acute Inflammation: | phagocytosis; these are mature monocyte-like cells; permanent residents of organs; long-lived & have more important roles in chronic inflammation
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| 6 Basic facts for chemical/molecular mediators in Acute Inflammation: | 1. There are plasma-derived and cell-derived chemical substances.
2. Plasma-derived mediators circulate in an inactive form until needed.
3. Cell-derived mediators are stored in intracellular granules that are secreted when needed.
4. Most mediators m
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| What is the Functions of chemical/molecular mediators in Acute Inflammation? | Mediators Cause
- Vasodilation
- Increased Vascular permeability
- Leukocyte recruitment and activation
- Fever
- PAIN
- Tissue Damage
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| What are the Groups of PLASMA derived mediators in Acute Inflammation? | - Clotting system: Stops blood loss
- Complement system: Recruits other cells
- Kinin system: Pain, Vasodilation, leakyness
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| Describe the Clotting System: | Plasma derived mediator of Acute Inflamation. Dozen proteins that interact with one another in a complex cascade to cause blood to clot. Stimulates Kinin and Complement System.
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| Describe the Kinin System? | Closely related to the clotting system and consists of more than a dozen blood proteins that interact to generate molecules that cause vasodilation and increased endothelial cell permeability.
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| Describe the Complement System: | About two dozen proteins that react with one another in a chain reaction initiated by the immune system or by the presence of certain products derived from microbes. These interactions cause vasodilation, attract WBC's and directly attack and destroy micr
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| What are the Groups of CELL derived molecular mediators in Acute Inflammation? | 1. Vasoactive amines
2. Cell membrane factors
3. Cytokines
4. Reactive oxygen compounds
Not mentioned in the book, but very important: arachidonic acid metabolites (such as prostaglandins)
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| Describe Vasoactive amines? | Small preformed molecules that are stored in granulocyte cytoplasmic lysosomes and act to cause local capillaries to dilate and become leaky. Release Histamine and Serotonin.
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| Describe Histamin: | Cell derived Amine that is released from the cytoplasm of Mast Cells, basophils, and platelets. Causes local dilation and leakiness.
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| Describe Serotonin: | Cell derived Amine that is released from platelets. Causes local dilation and leakiness.
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| Describe Cell membrane factors: | formed from phospholipids in the cell membranes of injured cells and act as local hormones to attract leukocytes and cause vasodilation.
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| Describer Cyotokines: | hormone like protein molecules secreted by other cells that act to enhance immune reactions by attacking leukocytes, stimulating phagocytosis, and causing vasodilation.
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| What is the communication process of Cytokines: | Activated WBC's "talk" to other cells via:
- Colony stimulation factors
- Growth Factors
- Interleukins
- Chemokines
- Tumor necrosis factors (TNF)
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| What is the Generalized response of Cytokines? | Cause generalized response:
- Fever,
- Lethargy
- Cachexia
- PMN Release
- Corticosteroid release
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| Describe Reactive Oxygen Compounds: | Powerful vasodilator, increases membrane permeability, bacteriocidal. O2- (oxygen superoxide) is bacteriocidal
*EX: nitric oxide (No) gas-
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| What are the OUTCOMES OF ACUTE INFLAMMATION dependent upon? | The outcome is dependent on factors such as:
- Type of injury or noxious agent
- Intensity of tissue damage
- Site of damage
- Type of tissue affected (liver & kidney cells don't divide unless some are lost; heart and nerve cells cannot divide so any
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| What are the Possible Outcomes of Acute Inflammation? | There are 3 possible outcomes of acute inflammation:
RESOLUTION
SCARRING
PROGRESSION TO CHRONIC INFLAMMATION
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| Describe the RESOLUTION outcome of Acute Inflamation: | A limited or brief injury, with minimal tissue damage, in a strong healthy body will result in restored cell structure and function. The body is able to neutralize or remove the chemical mediators, restore normal vascular permeability, and stop leukocyte
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| Describe SCARRING/FIBROSIS outcome of Acute Inflamation: | Substantial tissue destruction leads to scarring when connective tissue attempts to fill in the damaged areas. If the injury occurred in tissue that does not regenerate, scars will form. Abscesses and collections of pus (dead white cells) may be left behi
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| Describe PROGRESSION TO CHRONIC INFLAMMATION outcome of Acute Inflamation: | The good news is that chronic inflammation can by followed by regeneration, or the not-so-good outcome, scarring.
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| What are some Clinical indicators of acute inflammation: | (visualize yourself with the flu)
- General malaise & fatigue; drowsiness
- Fever (elevated body temperature exceeding 37 degrees Celsius)
- Pain (may be localized, as in appendicitis, or systemic, as in the flu)
- Rapid pulse rate
- Lack of appetit
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| What are Laboratory results of Acute Inflammation? | Elevated white cell count,
Increased level of C-reactive protein.
Increased Fibrinogen:
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| Describe Elevated white cell count: | when microscopic exam of blood sample is made; called LEUKOCYTOSIS (15-20,000 white blood cells per microliter of blood, as opposed to 5-10,000 normally).
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| Describe Increased level of C-reactive protein: | C-reactive protein from the liver is usually elevated in acute inflammation and is nonspecific marker for defining "sick".
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| Desceribe increase in Fibrinogen protein: | Fibrinogen protein is another liver protein, coagulation protein, that causes RBCs to settle rapidly in their own plasma, an effect measured by a generalized test called erythrocyte sedimentation rate (ESR). An increased "sed rate" indicates the presence
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| Describe ESR: | Erythrocyte sedimentation rate. Increased SED rate indicates the presence of large amounts of plasma proteins, indicating inflammation.
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| What are two drugs given for Acute Inflammation? | Steroids and Asprin.
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| Describe Steroid Drug therapy for acute inflammation: | - Steroids may be given to inhibit the production of phospholipases, which will short circuit the production of arachidonic acid and its metabolites that cause symptoms.
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| How does Asprin effect Acute Inflammation? | - Aspirin inhibits the cyclo-oxygenase pathway, preventing production of prostaglandins and thromboxane.
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| Describe some Local & systemic factors that influence healing: | - Nutritional status: protein, vitamin C, and zinc are required for collagen synthesis to rebuild tissues.
- Inadequate vascular circulation drastically impairs healing.
- Avoidance of infection will speed up healing times, so proper hygiene is essentia
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| Describe CHRONIC INFLAMMATION | - Starring Macrophages and Lymphocytes
- Has prolonged duration (weeks to months), and produces more extensive tissue destruction and loss of function.
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| Differences of Acute Inflammation and Chronic Inflammation | In contrast to the vascular changes, edema, and neutrophil influx of acute inflammation, chronic inflammation's hallmarks are:
- Infiltration with mononuclear cells: lymphocytes, macrophages, plasma cells;
- Tissue destruction, directed by the inflammat
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| Basic appearance of Chronic Inflammation: | Chronic inflammation will look less intense: rather than hot, swollen, red, tender tissue you might see scars, atrophy, or necrosis.
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| Describe Granulosis: | Special kind of Chronic Inflammation that is the hallmark of tuberculosis. Massive accumulations of macrophages (and some lymphocytes) which aggregate to form inflammatory nodules.
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| What are some of the common causes Chronic inflammation: | - VIRAL INFECTIONS
- PERSISTENT MICROBIAL INFECTIONS
- AUTOIMMUNE DISEASE
- PROLONGED TOXIC EXPOSURE
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| What is the Underlying cause of Chronic Inflammation? | Persistent causative factors.
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| Describe VIRAL INFECTIONS: | Chronic Inflammation where Infected cells require the work of lymphocytes and macrophages to target and destroy infected cells.
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| Describe PERSISTENT MICROBIAL INFECTIONS: | Chronic Inflammation where The human body deals with certain microbes by using a hypersensitivity mechanism (to be discussed later). Tuberculosis, syphilis, and certain fungi are examples.
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| Describe AUTOIMMUNE DISEASE: | Chronic Inflammation where A person can react to self-antigens and tissues, creating a constantly renewable source of inflammation. Examples: rheumatoid arthritis, multiple sclerosis.
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| Describe PROLONGED TOXIC EXPOSURE: | Classic example of Chronic Inflammation: smokers, silicosis in lung tissue of miners & stone cutters, and atherosclerosis as a response to chronically elevated plasma lipids.
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| What are CHRONIC INFLAMMATORY CELLS AND MEDIATORS: | Macrophages
Lymphocytes
Plasma cells
Neutrophils (PMNs)
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| Describe Macrophages: | These cells circulate in the blood as monocytes, then migrate from the bloodstream into the tissues and are renamed "big eaters". Their jobs are to filter out particulate matter & microbes, and to act as guards ready to alert the immune system to injury.
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| What are Areas where macrophages hang out in low numbers normally: | - Liver (Kupffer cells)
- Spleen
- Lymph nodes (sinus histiocytes)
- CNS (microglial cells)
- Lungs (alveolar macrophages)
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| What is the relationship between Monocytes and Macrophages? | Monocytes are in the blood and move to the injury site. Once they become ACTIVATED, they become Macrophages.
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| Describe how Macrophages react to injury: | Monocytes migrate to the site of injury within 24-48 hours post-trauma.
Once in the extravascular tissue, monocytes respond to cytokines secreted by sensitized T cells, or bacterial endotoxins, or mediators from acute inflammation, or extracelular matrix
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| What happens to these hard working macrophages? | - In acute inflammation, they die, or wander off into lymphatics.
- In chronic inflammation, they accumulate and proliferate, following the steady release of chemical factors from lymphocytes. Sometimes the macrophages fuse into large, multinucleated cel
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| Describe Lymphocytes in relation to Chronic Inflammation: | Both B & T cells migrate into inflammatory sites. T cells have a reciprocal relationship with macrophages: T cells are activated when macrophages present antigen fragments to them. Activated lymphocytes produce chemical mediators for activating monocytes
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| Describe Plasma cells in relation to Chronic Inflammation | These are B lymphocytes that are terminally differentiated (committed to producing antibodies directed against specific antigens).
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| Describe Neutrophils (PMNs) in relation to Chronic Inflammation: | It is possible to detect these cells far beyond the timeline of acute inflammation.
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| Describe the Consequences of chronic inflammation: | - Resolution to scar
- Persistent chronic inflammation
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| Function of Lymphatic System: | to filter and patrol extravascular fluids, returning clean fluids to the bloodstream.
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| Describe Lymphatics: | tiny channels with no muscular support, valves to force one-way flow, and very thin walls.
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| Function of Lymphatics: | to move extravascular fluid from distal to proximal tissues, eventually back to the heart.
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| Describe Distant effects of Chronic inflammation: | During inflammation, lymphatic flow increases and helps drain edema from tissue spaces. Leukocytes & cell debris accumulate in the lymphatic channels, arriving at lymph nodes to be filtered and processed.
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| Define LYMPHANGITIS: | Lymphangitis occurs when the lymphatics themselves become inflamed; presents as red streaks.
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| Describe Lymph nodes: | small, oval, capsulized structures containing sinuses.
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| Function of Lymph Nodes: | to receive, filter and purify lymph, then return it to venous bloodstream. Fixed macrophages in the sinuses engulf debris/pathogens.
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| Describe LYMPHADENITIS: | LYMPHADENITIS is inflamed lymph nodes. Painful enlargement of nodes is a clinical warning sign.
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| Describe LYMPHADENOPATHY: | LYMPHADENOPATHY is a general term applied to enlarged/tender nodes.
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| Describe LEUKOCYTOSIS: | LEUKOCYTOSIS is Increases WBC in peripheral blood.
-- Clinical correlates: The type of white blood cell that increases during inflammation gives a clue about what is causing it.
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| Describe LEUKOCYTOSIS: | LEUKOCYTOSIS is the general word for increased white blood cell count. Normally, we have 5 - 10,000 white cells per microliter of blood. Your body can make as many as 100,000 cells per microliter, if need be.
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| Describe Neutrophilia: | Increase in PMNs (neutrophils), Usually Indicates a Bacterial infection
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| Describe Eosinophilia: | Increase in Eosinophils Usually Indicates a Parasitic infections; allergies
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| Describe Lymphocytosis : | Increase in Lymphocytes Usually Indicates a Viral infections: specifically, mononucleosis, mumps, rubella
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| Describe Leukopenia: | Circulating white cells in general are decreased in number Viral infections (other than above), rickettsial infections, protozoan infections, typhoid fever (bacterial)
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