Term
|
Definition
| study of mechanisms by which disease occurs in living organisms, the responses of the body, and the effects of these diseases on normal function. |
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Term
|
Definition
| Genetic,Acquired, Multifactorial,Idiopathic |
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Term
|
Definition
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Term
|
Definition
| Development and course of a disease |
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Term
| Clinical Manifestations of pathogenesis |
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Definition
Signs-observable phenomena
Symptoms-subjective feelings
Syndrome-cluster of s/s |
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Term
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Definition
| rapid onset, usually short duration >2 weeks |
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Term
|
Definition
| longer duration (months or years), onset may be abrupt or insidious |
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Term
|
Definition
| Mortality, Morbidity, Incidence, Prevalence,Risk factors |
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Term
|
Definition
| deaths associated with a disease |
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Term
|
Definition
| disease occurrence, associated with disability caused by disease rather than death. |
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Term
|
Definition
| number of new cases over a time period |
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Term
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Definition
| total number of cases present at a point in time |
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Term
|
Definition
| total number of cases present at a point in time |
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Term
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Definition
| associated conditions, environmental, lifestyle, habits |
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Term
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Definition
| any adverse influence that deranges the cell's ability to maintain a steady normal or adaptive homeostasis. The reaction to injury is dependent upon the stimulus or stressor (type, duration, and severity) and the cell (type, state, and adaptability). |
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Term
| Is Cell injury is reversible? |
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Definition
up to a point, but if the stimulus persists or is severe enough from the
beginning, the cell reaches the point of no return (irreversible ). |
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Term
| Causes of Cell Injury/Death |
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Definition
| Hypoxia,Physical Agents, Chemical Agents and Drugs,Infections, Genetic Defect,Nutritional Imbalance |
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Term
|
Definition
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|
Term
| Most common cause of hypoxia? |
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Definition
| ischemia (loss of blood supply) |
|
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Term
What are the Physical Agents
associated with Cell injury |
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Definition
| Mechanical trauma, extremes of temperature, sudden changes in atmospheric pressure, radiation, electric shock. |
|
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Term
| Chemical Agents and Drugs associated with Cell injury |
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Definition
| Glucose or salt in hypertonic concentrations, oxygen in high concentration; Alcohol and narcotic drugs; insecticides, herbicides, pollutants. |
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Term
| Genetic Defect associated with cell injury |
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Definition
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Term
| Nutritional Imbalance associated with cell injury |
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Definition
| Protein - calorie deficiencies; Overnutrition |
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Term
| How does Hypoxia injure a cell |
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Definition
| When cells are deprived of oxygen. Oxidative metabolism and the creation of ATP are interrupted. Hypoxia causes ATP depletion or Power Failure. |
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Term
| How does Hypoxia injure a cell |
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Definition
| When cells are deprived of oxygen. Oxidative metabolism and the creation of ATP are interrupted. Hypoxia causes ATP depletion or Power Failure. |
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Term
| What happens when Aerobic metabolism stops |
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Definition
less ATP is produced
Na+/K+ ATPase cannot run fast enough
Cell swells up with water
Anaerobic metabolism used ‡ lactic acid produced
Acid damages cell membranes, intracellular structures, and DNA |
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Term
|
Definition
| Free radicals are highly reactive oxygen molecules |
|
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Term
| How are free radicals formed |
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Definition
| They are by-products of many normal reactions in the body. External factors that cause free radicals production include: tobacco smoke, pollutants and organic solvents, pesticides and radiation. |
|
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Term
| Free radicals are usually removed from the body by? |
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Definition
| Normally removed from body by antioxidants |
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Term
| How do free radicals injure cells |
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Definition
| Highly unstable molecules can react with cell walls and nucleic acids, damaging cells or turning them into more free radicals |
|
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Term
| What is Impaired Calcium Homeostasis |
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Definition
| Altered calcium levels produce damaging effects in cells by activating cellular enzymes. |
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Term
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Definition
| a state that lies between the normal, unstressed cell and the overstressed, injured cell. A change in environmental demands, various stressors and pathological states act as stimuli; cells must adapt or die. |
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Term
| Types of Cellular Adaptation |
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Definition
| Atrophy,Hypertrophy, Hyperplasia, Metaplasia, Dysplasia |
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Term
|
Definition
| shrinkage in the size of the cell by loss of cell substance; reduction in structural components of the cell. |
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Term
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Definition
| Diminished function or use, reduction in hormonal stimulation, or reduced blood supply. For example, when an arm is immobilized in a cast for a period of time, the skeletal muscles will become smaller or “atrophy”. Or a kidney can become smaller if its blood supply from the renal artery is less due to renal artery narrowing. |
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Term
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Definition
| an increase in the size of cells and an increase in size of the organ. Cells are larger. Not due to increased water content but to synthesis of more structural components |
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Term
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Definition
| Tissue becomes larger due to normal hormonal stimulation, i.e. uterine muscles during pregnancy |
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Term
|
Definition
| Muscles enlarge in response to weight lifting. |
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Term
|
Definition
| cells that get bigger in response to pathogenic stress, i.e. The heart of a person with high blood pressure (hypertension) can become hypertrophied because the heart must pump harder to order to eject blood out of the left ventricle against a higher systemic pressure |
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Term
|
Definition
| an increase in the number of cells in an organ or tissue which may then have increased volume; is induced by a known stimulus; stops when the stimulus has ceased. While there is an increase in the number of cells, cell structure and arrangement within the tissue is normal |
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Term
|
Definition
| hormonal hyperplasia-Breast tissue becomes hyperplastic during pregnancy to prepare for lactation |
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Term
|
Definition
| enables a tissue to regenerate |
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Term
|
Definition
| usually occurs from excessive hormonal stimulation. The thyroid gland may enlarge to increase its output of thyroid hormones. |
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Term
|
Definition
| continually proliferate throughout life. i.e. epidermis, intestinal epithelium, fibroblasts, bone marrow. Cells that rapidly proliferate are most susceptible to chemotherapeutic and therapeutic radiation treatments. These agents target rapidly growing cancer cells as well as labile cells since both rapidly proliferate |
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Term
|
Definition
| retain the capacity to replicate although they do not normally do so. i.e. bone, cartilage and smooth muscle |
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Term
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Definition
| cannot reproduce themselves after birth, i.e., nerve cells, skeletal muscle, cardiac muscle cells and lens cells of the eye. |
|
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Term
| What types of cells are capable of hyperplastic growth |
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Definition
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Term
|
Definition
| Reversible conversion of one adult cell type to another adult cell type in response to chronic stress. Represents adaptive cells better able to withstand the adverse environment. |
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Term
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Definition
| Deranged cell growth in which cells undergo changes in size, shape and appearance from their predecessors. Irritation is more severe and prolonged than metaplasia. |
|
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Term
| What cells are the most common cell type to exhibit dysplasia |
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Definition
| Epithelial cells, (uterine, oral cavity,GB, respiratory tract) |
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Term
| Type of cell adaptation thought to be precancerous |
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Definition
|
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Term
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Definition
| Normal process in the body, “cell suicide” Removes cells that are being replaced or have “worn out” Removes unwanted tissue |
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Term
|
Definition
death of cells in a living person. Occurs when a stimulus is too intense or
prolonged (Irreversible).
Unregulated death caused by injuries to cells
Cells swell and rupture
Inflammation results |
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Term
|
Definition
Cells turn on their own enzymes inside the cell, especially capsases
Digest their own cell proteins and DNA
Are then destroyed by white blood cells |
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Term
| Cell death and degradation associated with cell necrosis, cells may undergo: |
|
Definition
Liquefaction
Coagulation
Infarction
Caseous necrosis
Cell contents often released
Inflammation often results |
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Term
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Definition
|
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Term
|
Definition
| an area of tissue death due to a local lack of oxygen caused by obstruction of the tissue's blood supply |
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Term
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Definition
| a group of cells that begin to develop in an abnormal type of growth that is unresponsive to normal growth control mechanisms. |
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Term
|
Definition
| tumors that do not spread by invasion and metastasis so they grow locally. |
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Term
|
Definition
| tumors that are able spread by invasion and metastasis. Invasion is the direct extension and penetration by cancer cells into surrounding tissues. Metastasis is the ability of cancer cells to penetrate into lymphatic and blood vessels, circulate in the blood to other areas of the body where they can invade normal tissue and form tumors at new locations. Cancer refers to malignant tumors. |
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Term
| Normally, the number of cells produced are: |
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Definition
| = the number of cells that die, The total number of cells in the body remains constant |
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Term
| Cells divide only when they are told to do so by what? |
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Definition
|
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Term
|
Definition
| The normal genes that code for normal proteins used in cell division |
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Term
| When mutated proto-oncogenes become |
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Definition
|
|
Term
| Proteins that proto-oncogenes code for |
|
Definition
Growth factors
Growth factor receptors
G proteins
Enzymes that produce second messengers
Genes that turn the production of these proteins on and off |
|
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Term
| oncogenes still code for the proteins needed for cell division But they might produce |
|
Definition
| Too much of the protein An abnormal protein Protein that turns on all by itself Protein that is made when it is not needed Protein that cannot turn cell division off Protein that should be made by a different cell |
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Term
|
Definition
| make sure the cell has made the proteins needed to separate the chromosomes, check that the DNA has been correctly duplicated,measure whether the cell has grown large enough to divide |
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Term
| Tumor-Suppressor Proteins |
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Definition
| The checkpoints usually stop the division of mutated cells |
|
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Term
| tumor-suppressor proteins |
|
Definition
Cyclins
Cyclin-dependent kinases
Cyclin inhibitors (p53) |
|
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Term
|
Definition
| DNA sequences at the ends of the chromosomes |
|
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Term
|
Definition
| is the development of cancer |
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Term
|
Definition
| initiation, promotion, progression |
|
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Term
| Initiation in carcinogenesis |
|
Definition
| initial irreversible transformation of the genetic code of the cell (DNA) by a carcinogen |
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Term
| Promotion in carcinogenesis |
|
Definition
reversible stage that is poorly understood. It is believed to be a dose-response
type of effect to stimulation over time that alters the genetic expression of a cell. Promoters may affect cell proliferation by altering cell-to-cell communication or by producing oxygen free-radicals. |
|
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Term
| Progression in carcinogenesis |
|
Definition
| an irreversible stage that involves rapidly growing, highly malignant cells. |
|
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Term
| Initiation in oncogenesis |
|
Definition
|
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Term
|
Definition
| mutated cells are stimulated to divide |
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Term
| Progression in oncogenesis |
|
Definition
| tumor cells compete with one another and develop more mutations which make them more aggressive |
|
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Term
|
Definition
| Environmental factors capable of triggering the development of cancer |
|
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Term
| what percent of all cancer is related to environmental influences. |
|
Definition
|
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Term
|
Definition
| Process of cell maturation, the process of cell maturation and specialization. It is the extent to which cells resemble comparable normal cells in structure, organization, and function. |
|
|
Term
| tumor with will differentiated cells |
|
Definition
|
|
Term
| tumors that are variable with regard to differentiation |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| more rapidly than normal tissue but more slowly than malignant tumors |
|
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Term
| Malignant tumors growth rates |
|
Definition
| exhibit highly variable growth rates. Typically faster than benign. |
|
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Term
|
Definition
| developing a new blood supply |
|
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Term
| Loss of contact inhibition in cancer cells |
|
Definition
| cancer cells do not adhere to one another as normal cells do. |
|
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Term
| How does Failure to differentiate help the cancer cells |
|
Definition
|
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Term
|
Definition
| enclosed within a fibrous capsule. Such capsules tend to contain the benign tumor as a discrete, readily palpable, and easily movable mass that can be surgically removed. |
|
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Term
|
Definition
| invasion, and destruction of surrounding tissue (crab-like feet into adjacent tissues). |
|
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Term
|
Definition
Direct extension
Lymphatic spread
Vascular spread |
|
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Term
|
Definition
Spread of cancer cells from location of origin to other areas of the body.
Unequivocally marks a tumor as malignant, benign cannot metastasize. |
|
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Term
|
Definition
| Cancer cells spread from a primary site of origin to distant sites (secondary sites). Primary tumors have common sites of distant metastasis. |
|
|
Term
| Steps needed for development of metastasis |
|
Definition
a. Invasion of surrounding tissue
b. Penetration of blood and/or lymph or body cavity.
c. Release of tumor cells or emboli into the lymphatic fluid or blood.
d. Arrest and adherence of the emboli in small vascular channels.
e. Transport to a secondary site.
f. Invasion of the wall of the arresting vessel and seeks itself into the tissue.
g. Development of new blood vessels to support the secondary tumor (angiogenesis). |
|
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Term
|
Definition
| based on cytologic differentiation and number of mitoses within the tumor after microscopic examination. Aggressiveness and level of malignancy are graded on a I to IV scale. |
|
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Term
|
Definition
| based on size of primary lesion, extent of spread to regional lymph nodes, presence or absence of blood borne metastases. Important in the selection of the best form of therapy for the person. |
|
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Term
|
Definition
T = size of primary tumor (1-4)
N = regional lymph node involvement (0-3)
M = metastases (0-2) |
|
|
Term
| Local Effects of Tumor Growth |
|
Definition
Bleeding
Compression of blood vessels
Superior vena cava syndrome
Portal hypertension
Compression of lymph vessels
Edema, ascites, effusion
Compression of hollow organs
Compression of nerves
Pain, paralysis |
|
|
Term
Clinical Manifestations
Local (Benign and Malignant) |
|
Definition
a. Impingement on adjacent structures (Pain).
b. Functional activity such as hormone production.
c. Bleeding and secondary infections when they ulcerate through adjacent surfaces. |
|
|
Term
| components of Cancer cachexia syndrome |
|
Definition
Weight loss
Muscle wasting
Weakness
Anorexia
Anemia |
|
|
Term
|
Definition
| Loss of body fat and lean body mass, weakness, anorexia, and anemia which is common in terminal stages. Poorly understood but several theories. |
|
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Term
|
Definition
. Cancer releases peptides or other factors into the serum that derange the nutritional homeostasis of host.
Decreased intake due to anxiety, grief, and depression.
Increased catabolism due to infections in CA patients |
|
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Term
|
Definition
| syndromes that are not the direct result of the tumor or metastasis important because : May represent the earliest manifestation of a neoplasm. May represent significant clinical problems and be lethal. |
|
|
Term
| the most common paraneoplastic syndrome |
|
Definition
|
|
Term
| Ectopic hormone secretion |
|
Definition
| in paraneoplastic syndrome: ADH secretion in oat cell carcinoma |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Adrenocorticotropic hormone produced in response to biological stress (along with corticotropin-releasing hormone from the hypothalamus). Its principal effects are increased production and release of corticosteroids and, as its name suggests, cortisol from the adrenal cortex. |
|
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Term
|
Definition
| Parathyroid hormone, It acts to increase the concentration of calcium (Ca2+) in the blood, (leads to hypercacemia in pat with paraneoplastic syndrome. |
|
|
Term
|
Definition
| Messenger RNA copy of a gene |
|
|
Term
| Translation occurs in the cells |
|
Definition
|
|
Term
|
Definition
The mRNA acts as a pattern telling the cell how to line up amino acids to form a protein
Amino acids are carried into position by transfer RNA molecules
Ribosomes made of ribosomal RNA fasten the amino acids together to make a protein |
|
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Term
|
Definition
Transfer RNA, Carries an amino acid
Lines up by matching its anticodon to the mRNA’s codon |
|
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Term
|
Definition
Ribosomal RNA, Moves along the messenger RNA, moving transfer RNAs into position
Connects amino acids that the tRNAs have carried into
position |
|
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Term
|
Definition
| Replication of DNA in cell division |
|
|
Term
|
Definition
| Replication of DNA in the production of gametes. |
|
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Term
|
Definition
When chromosome pairs line up during meiosis, they can exchange ends
Each of the four resulting gametes will have a different combination of genes |
|
|
Term
|
Definition
Two genes that are close together on the chromosome are called “linked”
Linked genes are rarely separated by crossing-over, and therefore are usually inherited together |
|
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Term
|
Definition
|
|
Term
|
Definition
| your genes from mom and dad differ (Dd) |
|
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Term
|
Definition
| If you are heterozygous for a recessive trait and do not show it |
|
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Term
|
Definition
| If all your copies of a gene are alike, you are |
|
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Term
|
Definition
| a person’s genetic material |
|
|
Term
|
Definition
| a person’s physical characteristics |
|
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Term
|
Definition
| Gene on one of the autosomes that if present will almost always produce a specific trait or disease |
|
|
Term
|
Definition
| Genetic trait that appears only in people who have received 2 copies of a mutant gene, one from each parent |
|
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Term
|
Definition
| Genetic mutations cause en utero not by inheritance. |
|
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Term
|
Definition
| Sequential reaction to cell injury |
|
|
Term
| General steps in inflammation response |
|
Definition
It neutralizes the inflammatory agent
Removes necrotic material
Prepares an environment for healing and repair |
|
|
Term
|
Definition
| Inflammation is a rapid, nonspecific protective response to cellular injury. It usually is beneficial |
|
|
Term
| Causative factors for Acute Inflammation |
|
Definition
1.Microorganisms.
2.Physical agents - burns; radiation; trauma.
3.Chemicals - toxins; caustic substances.
4.Necrotic tissue (dead cells).
5.Immunologic reactions. |
|
|
Term
| Inflammatory Response triggered by |
|
Definition
| release of chemical mediators |
|
|
Term
| Primary aim of inflammation response |
|
Definition
| removing the injurious agent and limiting tissue damage |
|
|
Term
| Local Signs and Symptoms of inflammation |
|
Definition
redness
heat
pain
swelling - edema
loss of function |
|
|
Term
|
Definition
| Various mediators are released during both the vascular and cellular phases of inflammation that enhance the inflammatory response. The mast cell, which is present in connective tissue, releases chemical mediators and synthesizes additional mediators. Three other plasma protein systems (clotting, complement, kinin) are activated during inflammation and mediate the response. WBCs also secrete mediators. |
|
|
Term
| Lymphatics in inflammation response |
|
Definition
| assists venous system in returning blood and lymph to right side of heart. Acts to remove cellular debris. Lymphatic flow is increased in inflammation so as to drain edema, leukocytes, and debris from the extravascular space. |
|
|
Term
|
Definition
| enlarged, swollen lymph nodes, sign of a severe localized infection |
|
|
Term
| Vascular stage of inflammation |
|
Definition
Arterioles and venules dilate
Increasing blood flow to injured area
Redness and warmth result
Capillaries become more permeable
Allowing exudate to escape into the tissues
Swelling and pain result |
|
|
Term
| Cellular phase of inflammation |
|
Definition
| Margination, Emigration and chemotaxis |
|
|
Term
|
Definition
WBC slows down and sticks to the inner walls of blood vessels (the
endothelial lining). When the endothelium appears lined with WBCs, it is called
pavementing. WBCs adhere in great numbers to the endothelial surface. |
|
|
Term
|
Definition
| WBC slows down and sticks to the inner walls of blood vessels |
|
|
Term
|
Definition
| When the endothelium appears lined with WBCs,WBCs adhere in great numbers to the endothelial surface |
|
|
Term
|
Definition
| (also called diapedesis) and chemotaxis - Emigration refers to the movement of WBCs from blood vessels to the tissues.Neutrophils predominate in the first 6 to 24 hours but disintegrate and disappear. They are replaced by monocytes in 24 to 48 hours and which survive much longer in tissue |
|
|
Term
|
Definition
| is the unidirectional migration of cells toward an attractant |
|
|
Term
| The most significant chemotactic agents for neutrophils are |
|
Definition
| (1) products of tissue breakdown; (2) bacterial products; (3) activated complement factors; and (4) cytokines (chemicals produced by WBCs). |
|
|
Term
|
Definition
1.Recognition and attachment.
2.Engulfment
3.Killing or degradation (cytoplasmic granules destroy phagocytosed
material). |
|
|
Term
|
Definition
| neutrophils and macrophages. |
|
|
Term
| Serous Fluid of inflammation |
|
Definition
| thin fluid- dominant pattern in mild injuries |
|
|
Term
| Fibrinous Fluid of inflammation |
|
Definition
| large amounts of plasma proteins including fibrinogen. Can be thick and clotted. |
|
|
Term
| Purulent (Suppurative) Fluid of inflammation |
|
Definition
| exudate with pus and tissue damage from breakdown of neutrophils and macrophages. |
|
|
Term
|
Definition
| localized collections of pus in an organ |
|
|
Term
|
Definition
| local defect of the surface of an organ or tissue that is produced by shedding of inflammatory tissue. |
|
|
Term
| Outcomes of acute inflammation |
|
Definition
1.Complete resolution.
2.Healing by scarring.
3.Abscess formation.
4.Progression to chronic inflammation. |
|
|
Term
| Chronic inflammation is noted by |
|
Definition
a.Infiltration by macrophage, lymphocytes, and plasma cells.
b.Proliferation of fibroblasts.
c.Increased connective tissue (fibrosis).
d.Tissue destruction. |
|
|
Term
| Systemic Effects of Inflammation |
|
Definition
Fever and the acute phase response
Leukocytosis |
|
|
Term
| Fever-mediators released from WBC act in |
|
Definition
|
|
Term
Leukocytes release interleukins and tumor necrosis factor
Affect thermoregulatory center causing |
|
Definition
|
|
Term
| Leukocytes release interleukins and tumor necrosis factor affect the cns causing |
|
Definition
|
|
Term
| Leukocytes release interleukins and tumor necrosis factor causing skeletal muscle to |
|
Definition
|
|
Term
| Liver makes fibrinogen and C-reactive protein in order to: |
|
Definition
Facilitate clotting
Bind to pathogens
Moderate inflammatory responses |
|
|
Term
|
Definition
| number of circulating leukocytes increases |
|
|
Term
| When Inflammatory mediators cause WBC production what happens? |
|
Definition
| WBC count rises; Immature neutrophils (bands) released into blood. |
|
|
Term
|
Definition
| involves the restoration of original strength and function of tissue. |
|
|
Term
|
Definition
| replacement of lost or injured tissue by cells capable of regeneration.(labile or stable cells). |
|
|
Term
|
Definition
| Replacement of destroyed tissue by scar tissue; scar tissue is composed of collagen. |
|
|
Term
|
Definition
| Healing, Resolution, and Repair |
|
|
Term
| Fibrovascular granulation tissue |
|
Definition
| when fibroblasts accumulate and deposit collagen |
|
|
Term
|
Definition
healing by first intention, i.e., surgical incision. Edges are
approximated; healing occurs without significant bacterial contamination, and there is a minimal loss of tissue and a "small" scar. |
|
|
Term
|
Definition
healing by second intention. i.e., large tissue defect to fill or
pressure ulcer. Inflammation is more intense; more debris and exudate
present that must be removed; longer healing time; "larger" scar. |
|
|
Term
|
Definition
|
|
Term
|
Definition
abnormal amounts of collagen is present in connective tissue and
produces a large, bulging scar. It is a genetic characteristic. It can appear disfiguring. It may recur after excision. |
|
|
Term
|
Definition
| the binding of scar tissue to adjacent surfaces. Commonly occurs in the abdominal cavity. |
|
|
Term
| Local Wound Factors that Affect Healing |
|
Definition
| Presence of necrotic tissue,Presence of foreign bodies, Lack of moisture, Presence of infection,Improper approximation of wound edges |
|
|
Term
| Systemic Factors Influencing Healing |
|
Definition
| Age, Body Build,Health Status, Nutrition, Medications |
|
|
Term
| Nutritionally body tissues have a increased need for what? |
|
Definition
| Protein, calories, zinc, and vitamins |
|
|
Term
| Medications that impair healing |
|
Definition
| Steroids, immunosuppressants, anticoagulants |
|
|
Term
| how do medication impede healing |
|
Definition
a.Impair inflammatory phase.
b.Slow epithelialization.
c.Weaken collagen strength.
d.Clotting deficiencies |
|
|
Term
| chronic diseases that impede healing |
|
Definition
hypotension, hypovolemia, edema, pulmonary disease, atherosclerosis,
anemia, irradiated tissue, diabetes mellitus |
|
|
Term
| How could obesity impede healing? |
|
Definition
| Adipose tissue poorly vascularized. |
|
|
Term
|
Definition
| an invasion of the body by pathogens that results in adverse effects. |
|
|
Term
| How might the cells of the body may be destroyed by the pathogen |
|
Definition
| by a toxin released by the pathogen, or cell injury may occur indirectly as a result of the inflammatory or immune response to the microorganism. |
|
|
Term
| Microflora (normal Flora) |
|
Definition
| are organisms that normally live in or on the body |
|
|
Term
|
Definition
| ability of infecting organism to cause disease |
|
|
Term
|
Definition
Intact skin and mucosal surfaces
Inflammatory reaction
Immune system
Lymphatic system |
|
|
Term
| Risk Factors for Developing Infection |
|
Definition
Having one or more chronic diseases
Dehydration and malnutrition
Immobility, decreased alertness, and incontinence
Hospitalization or nursing home |
|
|
Term
|
Definition
| Obligate intracellular parasites whose effects on the host range from lytic destruction, with fast viral replication, to mutual integration, with long term persistence of infection. |
|
|
Term
| what pathogen Accounts for the majority of human infections |
|
Definition
|
|
Term
| What is the cellular structure of a Virus? |
|
Definition
| No cellular structure - have protein coat (capsid) around nucleic acid core of RNA or DNA (never both). |
|
|
Term
| Steps in viral replication |
|
Definition
1.Attachment
2.Penetration
3.Uncoating
4.Replication
5.Assembly
6.Release of new virions |
|
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Term
| Examples of common viral infections include |
|
Definition
| the common cold, influenza, mumps, hepatitis, measles, chicken pox, infectious mononucleosis, HIV – AIDS, warty growths, i.e., papillomavirus (HPV), and poliomyelitis. |
|
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Term
|
Definition
| Free-living, one-celled organisms that reproduce on their own, but use animal hosts for nutrient access |
|
|
Term
| Pathogenic effects of bacterial infection usually result from |
|
Definition
| substances such as enzymes or toxins produced by bacteria or from injury caused by the inflammatory response. |
|
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Term
|
Definition
Spherical - cocci
Rod shaped - bacilli
Spiral - spirochetes |
|
|
Term
| Gram positive bacteria stain |
|
Definition
|
|
Term
| Gram negative bacteria stain |
|
Definition
|
|
Term
|
Definition
| (usually pyogenic cocci) account for most suppurative lesions seen (staphylococcus; streptococcus; Pneumococcus). |
|
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Term
|
Definition
| they account for the majority of hospital acquired and opportunistic bacterial infections. (Escherichia coli, Klebsiella pneumonia, Enterobacter, Proteus, Serratia marcescens, Pseudomonas, Neisseria gonorrhea). |
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Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Structural characteristics of bacteria |
|
Definition
|
|
Term
| Lower Forms of Bacteria include |
|
Definition
| Mycoplamas, rickettsiae, chlamydiae |
|
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Term
|
Definition
|
|
Term
| characteristics of Chlamydial Diseases |
|
Definition
Obligate intracellular parasite-lacks enzymes to produce ATP
Transmitted by direct contact between hosts such as sexual contact
Main human disease: sexually transmitted urogenital infection
Very small gram negative bacteria |
|
|
Term
| Characteristics of Rickettsial Diseases |
|
Definition
| Small, obligate intracellular parasites that can peacefully perpetrate themselves in arthropod vectors (house flea, tick) and change to pathogenic mode when deposited in mammalian tissue. They begin to replicate at the bite and spread through the blood. Protective antibodies are produced resulting in lasting immunity. Examples: Typhus and Rocky Mountain Spotted Fever. All cause fever, most cause rash. |
|
|
Term
| Characteristics of Mycoplasma Diseases |
|
Definition
| The tiniest free-living organism known - difficult to isolate and identify. Lack a cell wall, and therefore are insensitive to antibiotics which act to destroy the cell wall. Infect surfaces and tissues of respiratory, GI, and GU tract. Example: Mycoplasma pneumonia. Occurs mostly in adolescents and young adults and is characterized by fever, pharyngitis, cough, pulmonary infiltration. |
|
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Term
|
Definition
| produced mainly by gram-positive bacteria and are contained within the bacterium. Their toxic effects are produced when they are released as metabolic products during bacterial growth |
|
|
Term
| Effects of the . tetani neurotoxin |
|
Definition
| acts on the central and sympathetic nervous systems by blocking motor inhibition. It also acts on the respiratory center of the brain causing spasm or depression of respiratory muscles thus respiratory distress and death. |
|
|
Term
| Effects of the C. botulinum exotoxin |
|
Definition
| causes severe food poisoning. It can cause paralysis of the eye orbit, pharynx, larynx, and respiratory muscles |
|
|
Term
|
Definition
| They are produced almost exclusively by gram negative bacteria. They are contained in the cell wall and are released during lysis or destruction of the bacteria |
|
|
Term
| General toxic effect of endotoxins? |
|
Definition
| fever, weakness, aches, shock |
|
|
Term
| Moderate fever helps fight infect by: |
|
Definition
1. Some bacteria and viruses have been shown to reproduce more slowly when temperature is elevated.
2.Phagocytes act more quickly to accomplish their purpose.
3.Stimulates interferon production thereby limiting the course of infection. |
|
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Term
|
Definition
|
|
Term
|
Definition
| refers to inadvertent adverse effects or complications caused by or resulting from medical treatment or advice |
|
|
Term
|
Definition
| Single-celled animals that normally exist as free living organisms that are capable of causing infections. Among the foremost causes of disease and death in developing countries. |
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|
Term
| Examples of protazoal diseases |
|
Definition
Entamoeba histolytica - dysentery.
Plasmodium vivax - malaria.
Cryptosporidium - diarrheal disease.
Trichomonas vaginalis - vaginitis. |
|
|
Term
|
Definition
| Hospital-Acquired Infections |
|
|
Term
| Function of immune response |
|
Definition
– to recognize and destroy what is foreign
– to tolerate self |
|
|
Term
|
Definition
any foreign substance that
stimulates the immune response |
|
|
Term
|
Definition
|
|
Term
| Mechanisms of innate immunity |
|
Definition
–Epithelial barriers
–Phagocytic cells
–Plasma proteins
–Cell messenger molecules |
|
|
Term
| Acquired or Adaptive Immunity |
|
Definition
|
|
Term
| How would you actively acquire adaptive immunity naturally |
|
Definition
|
|
Term
| How would you actively acquire adaptive immunity artificial |
|
Definition
| response to a vaccination |
|
|
Term
| Is the immunity you get from your mother as an infant Passive or active, Natural or artificial |
|
Definition
|
|
Term
| Active aquired immunity happens |
|
Definition
| Inside the body, via body processes |
|
|
Term
| passive aquired immunty happens |
|
Definition
| outside of the body and is put into it after the process has occurred. Isn't always sufficient and doesn't last as long as active. |
|
|
Term
|
Definition
(antibody proteins in the blood
that attack the specific antigen) |
|
|
Term
|
Definition
(phagocytic cells that
attack the specific antigen) |
|
|
Term
| What are the regulatory cells control the immune response |
|
Definition
– T helper cells
– T suppressor cells
– Antigen presenting cells |
|
|
Term
which cells are the Effector cells that carry out the attack on
the antigen |
|
Definition
– T cytotoxic (or T killer) cells
– B cells (produce antibodies |
|
|
Term
|
Definition
| Pieces of a antigen that have been broken down by an antigen presenting cell |
|
|
Term
| Once the antigen presenting cell has broken the antigen down, where does it put the epitopes |
|
Definition
on the cell
surface, attached to
MHC II proteins |
|
|
Term
| Where do stem cells originate |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Where do t cells mature, and where do they hang out once they have matured |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
Stimulate the T cytotoxic cells and
other phagocytic cells to attack the
antigen |
|
|
Term
|
Definition
Stimulate the B cells to create
antibodies against the antigen |
|
|
Term
|
Definition
chemicals that control
the immune response |
|
|
Term
|
Definition
| inflamitory mediators, growth factors, cell communication molecules |
|
|
Term
| B Lymphocytes activated by |
|
Definition
|
|
Term
|
Definition
cells remain
in the body
– In the future, they will fight
off the antigen without a
T helper cell telling them
to do so |
|
|
Term
|
Definition
create
antibodies, special
proteins designed to
attach to that antigen
and destroy it |
|
|
Term
|
Definition
|
|
Term
|
Definition
| circulates in body fluids, attacking antigens |
|
|
Term
|
Definition
circulates in body fluids; has five units to pull
antigens together into clumps |
|
|
Term
|
Definition
found in secretions on mucus membranes;
prevents antigens from entering the body |
|
|
Term
|
Definition
found on the surface of B cells; acts as an
antigen receptor |
|
|
Term
|
Definition
found on mast cells in tissues; starts an
inflammation |
|
|
Term
| Which Ig is passed from mother to infant? |
|
Definition
|
|
Term
| Which Ig is present at allergic response |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What is an example of a physiologic immune deficiency |
|
Definition
| newborn. (at 6 months, IgG -passive immunity from mom originally- from mom degrading, not sufficient, not a true deficiency syndrome, as they mature, it resolves. More likely if not bfing.) |
|
|
Term
| What is a Primary Immunodeficiency usually caused by |
|
Definition
|
|
Term
| 2 exapmles of primary immune-deficiency |
|
Definition
Agammaglobulinemia
DiGeorge Syndrome |
|
|
Term
| When does Agammaglobulinemia usually manifest |
|
Definition
| 6 months - 2 years marked by by recurrent infections |
|
|
Term
| What is Secondary or acquired immune-deficiency |
|
Definition
| caused by an illness, like cancer or viral infection. Complications of infection, malnutrition, aging, Side effect of immunosuppression, irradiation, chemotherapy. (iatrogenic, treatment related). Diabetes suppresses chemotaxis and white cell functioning |
|
|
Term
| Is aids primary, secondary or acquired |
|
Definition
| Secondary to viral infection, acquired by infection from another source. |
|
|
Term
|
Definition
| A virus that carries genetic material in RNA |
|
|
Term
| How do retroviruses infect cells |
|
Definition
| by binding to the surface of a target cell through a receptor and then inserting their RNA into the target cell. |
|
|
Term
| What cells are targeted by the aids virus |
|
Definition
|
|
Term
| What is the normal cd4 (thelper cell) count |
|
Definition
| 800-1200 CD4+/mcl of blood |
|
|
Term
| You are likely to remain healthy with what number of cd4's |
|
Definition
|
|
Term
| At what level of cd4 count are symptoms mostly likely to manifest |
|
Definition
|
|
Term
| What types of signs and symptoms would you see in the Primary infection phase |
|
Definition
Signs of systemic infection
Seroconversion: immune system responds and antibodies against HIV appear (1–6 months) |
|
|
Term
| What types of signs and symptoms would you see in the latent period |
|
Definition
Virus is replicating, TH cell count gradually falls
May last 10–11 years or longer More and more infections |
|
|
Term
| What types of signs and symptoms would you see in the Overt AIDS |
|
Definition
| TH cell count <200 cells/μL or AIDS-defining illness |
|
|
Term
| What is Peripheral neuropathy |
|
Definition
| numbness, tingling or painful |
|
|
Term
|
Definition
| -infection of blood stream |
|
|
Term
| Later symptoms, generally associated with decreased CD4 counts (200-499): |
|
Definition
fever/nite sweats
myalgia
mouth lesions
diarrhea
peripheral neuropathy
persistent Herpes simplex
recurrent bacteremias |
|
|
Term
| AIDS Defining Illnesses (CD4 < 200) |
|
Definition
opportunistic infections
neoplasms
neurologic symptoms |
|
|
Term
| Immune Hypersensitivity definition |
|
Definition
| Excessive or inappropriate activation of the immune response The body is damaged by the immune response, rather than by the antigen (allergen) |
|
|
Term
| Definition of allergic reaction |
|
Definition
| Rapidly developing immunologic reaction occurring within minutes of an antigen combining to an antibody bound to mast cells or basophils in a person previously sensitized to the antigen. Mediated by IgE. It may cause a systemic or local reaction |
|
|
Term
| What does the primary mediator of the immune response (Histamine) cause in allergic reactions |
|
Definition
a.Intense bronchial smooth muscle contraction.
b.Increased vascular permeability.
c.Increased secretions by nasal, bronchial and gastric glands. |
|
|
Term
| What are the 4 types of hypersensitivity |
|
Definition
Allergic reaction (type 1) and cytotoxic reactions (type 2) immuno-complex (type 3)
Cell-mediated reactions (type 4) |
|
|
Term
| What to antibodies are related to type 2 (cytotoxic) hypersensitivity reactions |
|
Definition
|
|
Term
| 2 examples of type 2 response |
|
Definition
| Rh incompatibility, transfusion reaction, Graves disease (thyroid incompatibility) |
|
|
Term
| What happens in the type 3 hypersensitivity response |
|
Definition
| Immune complexes formed and deposited in various tissues; acute inflammation triggered |
|
|
Term
| When a immuno-complex forms in the kindey it causes |
|
Definition
|
|
Term
| When a immuno-complex forms in the synovium of a joint cavity |
|
Definition
|
|
Term
| Immuno- complex (type 3 incompatibility) is usually what |
|
Definition
|
|
Term
| What cell is present in a cell mediated hypersensitivity response |
|
Definition
|
|
Term
| What are the two catalysts for cell mediated reactions |
|
Definition
| Direct (cytoxic t cells fail to recognize tissues and attack) and Delayed (something foreign or antigen triggers cellular reaction releases chemicals in the area, 2-3 days to see the T cell reaction. ) |
|
|
Term
| 3 examples of cell mediated hypersensitivity reaction |
|
Definition
| TB skin test, poison Ivy, Graft v host. |
|
|
Term
| Antibodies are produced by: |
|
Definition
|
|
Term
| Acquired or secondary immunodeficiency syndromes |
|
Definition
develop after birth
2. may be caused by viral infections
3. may develop after immunosuppressive therapy |
|
|
Term
| HIV is cytotoxic and its primary target is |
|
Definition
|
|
Term
| Individuals are diagnosed with AIDS when HIV is present and the CD4 T lymphocyte count drops below: |
|
Definition
|
|
Term
|
Definition
| antibody that attack own body (sometimes anitbody mediated or t cell mediated) |
|
|
Term
| definition of Rheumatoid Arthritis |
|
Definition
a chronic multisystem, inflammatory disease of unknown cause. RA primarily affects the
synovial joints, although skin, eyes, heart, and lungs may be affected. |
|
|
Term
|
Definition
| joint fixation and deformity |
|
|
Term
| Generally see onset at what age |
|
Definition
|
|
Term
| What type of hypersensitivity response do you see in RA |
|
Definition
| type III immune complex hypersensitivity. |
|
|
Term
|
Definition
| Tissue that forms when synovial lining is and inflamed from multiple attacks. |
|
|
Term
|
Definition
| worldwide is about 1%. Women are affected 3 times more often than men. The peak prevalence is the 3rd to 4th decades of life. Increased frequency of RA among first degree relatives. |
|
|
Term
|
Definition
| degenerative bone disease characterized by loss of articular (joint) cartilage, thatprimarily affects the weight bearing joints |
|
|
Term
| Incidence incidence of OA |
|
Definition
| Has been referred to as the single major cause of disability in the U.S. 80% of persons over age of 65 have it. Women affected two times greater than men. |
|
|
Term
|
Definition
Heberden's nodes at distal interphalangeal joints. Bouchard's nodes - at proximal interphalanged joints.
Pain worse throughout the day. |
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|
