Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
41 Cards in this Set
- Front
- Back
|
What is normal?
|
The ability to meet the demands placed on the body and to adapt to those changes in the external environment so as to maintain reasonable constancy of the internal environment.
|
|
|
What is disease?
|
Any deviation from or interruption of the normal structure of function of a part, organ, or system of the body.
|
|
|
What is atrophy?
|
cells are smaller, or are fewer in tissue
|
|
|
What is hypertrophy?
|
cells increase in size, occurs when there is an increase in workload
|
|
|
hyperplasia?
|
increase in number of cells in tisse
|
|
|
Metaplasia?
|
cells are in an environment where they can't function/survive well, changes cell type so they can survive. in response to chronic inflammation
|
|
|
dysplasia?
|
also in response to chronic inflammation, much greater, eventually presence of cancer, can revert back
|
|
|
process of ATP depletion
|
tissue hypoxia->V intracellular ATP->NA/K pump failure->altered cell membrane permeability
|
|
|
Heterozygous
|
one mutated gene in pair
|
|
|
Homozygous
|
both genes are mutated
|
|
|
What is infection?
|
Invasion of the human body by microorganisms leading to harmful and potentially lethal consequences.
|
|
|
What is a benign tumor?
|
Cells are well-differentiated, slow growing, cohesive, encapsulated, does not spread to distant sites
|
|
|
What is a malignant tumor?
|
Cells are undifferentiated, grow rapidly, uncohesive, unencapsulated, invasive, metastasis
|
|
|
Acute functions of stress response
|
-mobilization of energy
-sharpened focus and awareness -increased cerebral blood flow -enhanced utilization of glucose -enhanced cardiac and respiratory function -redistribution of blood flow to the brain and muscles -inhibition of reproductive function -decreased appetite |
|
|
Acute stress
|
Etiology: physically psychologically threatening events
Pathogenesis: activation of ANS Effect: Arousal, vigilance, alertness, enhanced cognition, focused attention |
|
|
Chronic stress
|
chronic activation of the stress response, becomes maladaptive
|
|
|
What are the stages in Acute inflammation?
|
Vascular response, cellular response, inflammatory mediators
|
|
|
Explain vascular response.
|
-brief vasoconstriction followed by venous and arterial vasodilation
-increased capillary permeability -fluid movement into interstitial fluid-exudates SIGNS: erythema, warmth, edema/swelling, pain |
|
|
Explain cellular response.
|
Margination: cells move the the edge of the blood vessel
Emigration: cells leave blood vessel into interstitial space Chemotaxis: releases chemicals to bring WBCs to area (cytokines) Phagocytosis: WBCs phagocytize whatever was brought in |
|
|
Explain inflammatory mediators.
|
Histamine, Plasma proteases, Arachidonic Acid Metabolites, Platelet aggravating factor, cytokines, nitric oxide
|
|
|
What are the two patterns of chronic inflammation?
|
Nonspecific and Granulomatous
|
|
|
What is nonspecific chronic inflammation?
|
-macrophage and lymphocyte infiltration
-fibroblast proliferation -greater scarring and deformity |
|
|
What is granulomatous chronic inflammation?
|
-foreign body or poorly controlled organism
-macrophage infiltration -lymphocyte encasement |
|
|
There are three stages of Wound healing. What are they? and what does each stage entail?
|
Inflammatory, Proliferation, remodeling
Proliferation: fibroblast and vascular endothelial cell proliferation->granulation tissue and angiogenesis->epithelialization "scar formation" Remodeling: fibroblast synthesis and lysis of collagen-> increase scar tensile strength can lead to keloid formation |
|
|
Explain type I hypersensitivity disorders (IgE mediated disorders).
|
Etiology:
Binding of an allergen to a specific IgE on a sensitized mast cell or basophil Reactions: initial- 5-30 minutes, vasodilation, vascular leakage, smooth muscle spasm secondary- 2-8 hours, swelling of mucosal tissues, mucous production, leukocyte infiltration, bronchospasm |
|
|
Explain type II hypersensitivity disorders (Antibody-mediated cytotoxic disorders).
|
IgG or IgM antibodies bind with cell or tissue specific antigens - cell/tissue destruction
|
|
|
Explain type III hypersensitivity disorders (Immune-complex disorders).
|
formation of A-A complexes, deposited in vessel walls (or joints, kidneys, heart) and activates complement
|
|
|
Explain type IV hypersensitivity disorders (cell mediated disorders).
|
antigen binds to a cell (APC)
either direct cell mediated toxicity (CD8-kill APC) OR delayed type hypersensitivity (APC+CD4)--secretion of cytokines, attract WBCs, increased vascular permeability |
|
|
How does HIV replicate?
|
1. Attachment
2. Internalization & Uncoating 3. DNA synthesis 4. Integration 5. Transcription 6. Translation 7. Cleavage 8. Assembly |
|
|
Explain the primary infection phase.
|
appears 1-4 weeks after exposure, lasts 2-4 weeks
acute mono-like symptoms, fever and malaise, high viral load, decrease CD4 count(<800), low viral load |
|
|
Explain the chronic asymptomatic of latent phase.
|
lasts ~10 years
no signs/symptoms of illness, decrease CD4 (800-200), lymphadenopathy |
|
|
Explain the overt AIDS phase.
|
CD4 <200, AIDS defining illness, opportunistic infections
without antiviral therapy, death in 2-3 years |
|
|
What are clinical manifestations of AIDS?
|
HIV wasting syndrome (fever, diarrhea, weight loss), generalized lymphadenopathy, opportunistic infections, esophagitis, malignancy, CNS dysfunction
|
|
|
What are the opportunistic infections of AIDS?
|
Pneumocystis carinii pneumonia (PCP), Candidiasis (Thrush), Cytomegalovirus (CMV), Mycobacterium avium-intracellulare complex (MAC), Tuberculosis
|
|
|
What are the malignancies of AIDS?
|
Kaposi's Sarcoma, Non-Hodgkin's Lymphoma, Cervical carcinoma
|
|
|
Explain Acute Myelocytic Leukemia (AML or ANLL(Acute Nonlymphocytic Leukemia)).
|
80% affected are adults
etiology-unknown, toxins, chromosome abnormalities Pathogenesis-malignant transformation of myeloblast line and monoblast line clinical manifestations-infection, anemia, bleeding, bone pain, fatigue, weight loss, easy bruising and bleeding, opportunistic infections Diagnosed-bone marrow aspiration, RBCs low, platelets low |
|
|
Explain Acute Lymphocytic Leukemia (ALL)
|
common cancer among children
Etiology-unknown, toxins, chromosomal abnormalities Pathogenesis-malignant transformation of lymphoblast line, CNS involvement Clinical manifestations-same as ANLL, lymphadenopathy, malaise, lethargy, hepatosplenomagaly, CNS symptoms (headache, vomiting, seizures, visual disturbances) |
|
|
Explain Chronic Myelocytic Leukemia (CML).
|
etiology-Philadelphia chromosome
ALL cell lines affected clinical manifestations-WBC>30,000, anemia, splenomegaly |
|
|
Explain Chronic Lymphocytic Leukemia (CLL).
|
Lymphoproliferative, age>60, 2:1 male
clinical manifestations-painless lymphadenopathy, splenomegaly |
|
|
Explain Hodgkin's Lymphoma.
|
etiology-unknown
clinical manifestations-nontender rubbery feeling node, dry cough, anorexia, weight loss, cachexia, fatigue, splenomegaly, immunocompetence diagnosis-Reed-Sternberg cell |
|
|
Explain Non-Hodgkin's Lymphoma.
|
Nodular-cohesive aggregation of cells
Diffuse-absence of aggregation Manifestations-painless diffuse lymphadenopathy, NO hilar adenopathy, GI symptoms, immunocompetence diagnosis-lymph node biopsy |
