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95 Cards in this Set
- Front
- Back
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This is composed of water, proteins, lipids, carbs, and electrolytes
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protoplasm
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all of these cells have a nucleus
and.. all of these cells do not |
eukaryotic
prokaryotic (bacteria) |
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the nucleus contains _________, which serve as the template for making the ______, which is later used to direct the synthesis of __________ in the cytoplasm
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DNA
RNA PROTEINS |
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Ribosomes serve as the site for __________ synthesis in the cytoplasm.
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protein
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________ endoplasmic reticulum is studded with ribosomes attached to specific binding sites on the membrane
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ROUGH
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The ______ complex modifies proteins and packages them into secretary granules bound for the membrane
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GOGLI
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___________ contain powerful hydrolytic enzymes that are used to break down excess and worn-out cell parts as well as foreign substances
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LYSOSOMES
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Peroxisomes contain a special enzyme that degrades __________
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peroxides
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mitochondria are the site of cellular _____________, the product of which is the formation of __________
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respiration
ATP (energy) |
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transport along the axon of neuronal cells takes place along the primary cytoskeletal component ____________
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microtubules
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actin and myosin are examples of functional ____________ within muscle cells
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microfilliments
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integral proteins span the entire lipid bi-layer, whereas _____________ proteins are bound to one side of membrane or the other
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peripheral
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what are the 4 tissues of the body
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epithelial
connective muscle neuronal |
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of the 4 types of tissue, what 2 are excitable
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muscle & neural
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This part of cell controls the shape and movement of cell
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cytoskeleton
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this part of cell separates inner cell and outer cell, regulates cell growth & proliferation, receptors for hormones, only allows specific substances across membrane, has lipid bi-layer
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plasma membrane
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what are the cellular organelles
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mitochondria
lysosomes/peroxisomes gogli apparatus ribosomes ER-endopalsmic reticulum (rough/smooth) |
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what is the protoplasm made up of, referred to as the matrix
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H2O, proteins, lipids, electrolytes
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what are the 3 types of cell communication
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autocrine- chemical released for own activity
paracrine- act mainly on nearby cells endocrine- relies on hormones through body |
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what are 2 ways cells communicate via
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electrical or chemical
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describe metabolism
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where fats, carbs, proteins, are broken down & converted to ATP needed for cell
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Electron transport chain?
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H+ & O2 = H20
energy released to bond to ATP 36 molecules from 1 glucose molecule (32 from ETC, 2 from citric acid cycle, 2 from glycolysis) |
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Diffusion
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High concentration to low concentration
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Passive movement
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does NOT require much energy, electrical gradient, passive movement of particles
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Cells may adapt to the environment by undergoing changes in __________, __________ and _______________.
3 ways |
size, # and type
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There are 2 types of genes involved in adapting to the environment: the _________ genes, for normal function of a cell
and the genes that control cellular _______ |
housekeeping
differentiation |
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Atrophy is seen as a decrease in cell ____________
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Size
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Denervation will result in cellular ________
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atrophy
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Hypertrophy is an ________ in cell size
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increase
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An increase in muscle mass associated with exercise is an example of _________
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hypertrophy
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Hyperplasia
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an increase in the number of cells in an organ or tissue
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Liver regrowth is an example of _____________ hyperplasia.
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compensatory
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pathological or non-physiologic hyperplasia is due to ?
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excessive hormonal stimulation or excessive grpwth factors
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Metaplasia
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one normal cell type replaces another normal cell
ie: psuedostratified epithelial changes to stratified |
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Dysplasia
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abnormal cells replace normal cells
(pre-cancerous stage) |
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anaplasia
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undifferentiated cells, variable structure, associated with cancer
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Ways cell INJURY occurs?
B iologic E lectrical N utritional T rauma T emp |
physical trauma
extreme temp electrical biologic nutritional factors |
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ALL injuries of a cell = ? loss of _______
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function
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what 3 things does the extent of a cell injury depend on? DIA
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duration
intensity agent |
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what are 3 basic problems with cell injury ? DIT
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Deficiency- MI/CVA (O2)
Intoxication- toxins decrease fx Trauma- altered structure = loss of fx |
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What are the stress factors of cell injury ? SBRN
(selina bickle registered nurse) |
Severity of insult
Blood supply Regenerative capacity Nutritional status |
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What is mechanism of injury?
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production of free radicals
hypoxia Ca+ imbalance |
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apoptosis
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programmed cell death
eliminates old/damaged cells via>>> cell membrane changes>> induces phagocytosis>>> degradation process w/macrophages |
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3 basic steps of apoptosis?
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1)nucleus shrinks
2)breaks apart 3)engulfed by phagocytic cell |
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2 types of hyperplasia due to hormonal stimulation or excessive growth factors
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pathologic or non physiologic
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metaplasia usually occurs on response to chronic _________ and _________ allows for substitution of cells that are better able to survive stressful or harmful conditions
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irritation
inflammation |
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dysplasia is strongly implicated as a precursor to _______
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cancer
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Deranged cell growth of a specific tissue tat results in cells that cary in size, shape, and organization is known as __________
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Dysplasia
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intracellular _________ represent the buildup of substances that cells cannot immediately use or eliminate
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accumulations
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________ radicals are highly reactive chemical species having an unpaired electron in the outer valence shell of the molecule
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Free radicals
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_______ deprives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP
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hypoxia
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how does necrosis differ from atoposis?
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it involves unregulated enzymatic digestion of cell components, loss of cell membrane integrity with uncontrolled release of the products of cell death into the intracellular space, and initiation of the inflammatory response
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The increased ______ levels may inappropriately activate a number of enzymes with potentially damaging effects
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calcium
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acidosis develops and denatures the enzymatic and structural proteins of the cell during _______ necrosis
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coagulation
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how can chemo drugs injure normal cells?
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the chemicals damage normal healthy cells as they are vulnerable and dividing to make new healthy cells
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one complication of hypoxia?
how can acidosis damage tissue? |
low arterial blood oxygen, inhibits metabolic fx
or low O2 needed for cellular respiration, and ATP production |
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2 pathways that apoptosis to occur
WHAT major protein is involved |
extrinsic pathway is death receptor dependant
intrinsic is independent & due to injury BOTH are initiated by proteolytic enzymes |
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list five categories of cellular injury
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1.physical
2.chemical 3.radiation 4.biologic 5.nutritional imbalance |
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Free radicals
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toxic
reactive to chemical species interfere with DNA, proteins & membranes |
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Ischemia
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restriction of O2
can= vasoconstriction, thrombosis, embolism sample: hepatocytes death in 4-5 minutes of ischemia |
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what does an enlarged heart result in ?
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pathology
problem except for major athletes heart cells do not replicate at all/hypertrophy of L heart ventricle = heart failure |
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State the five cardinal signs of inflammation
(local signs) |
1.erythema
2.edema 3.warmth 4.pain 5.loss of function (possibly) |
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Describe the vascular changes in an acute inflammatory response.
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1-momentary vasoconstriction(stop bleeding)
2-rapid vasodilation (blood flow=heat/redness) 3-incrased permeability (protein rich exudate) 4-increased capillary pressure (fluid buildup=swell/pain/decreased fx |
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list 4 types of inflammatory mediators and their function
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1) VASOACTIVE & smooth muscle-constrict. like histamine
2) PLASMA PROTEASES-activate complement/clotting cascade 3) CHEMOTACTIC: chemokines 4) REACTIVE molecule & cytokines from leukocytes |
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contrast acute inflammation and chronic
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Acute is short in duration/immediate response
Chronic- long duration/ self perpetuating |
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__________ is the primary phagocyte that arrives early at the site of inflammation
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neutrophil
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Hyperemia?
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erythemia and warmth
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Acute inflammation (key facts)
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short duration
early response constrict blood flow prevent spread of agent |
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Chronic inflammation(key facts)
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lasts longer weeks- years
self perpetuating |
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2 phases of acute inflammation?
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vascular and cellular
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what happens in the vascular phase of inflammation?
(steps) cellular phase? |
vasoconstriction > vasodilation > ^permeability > ^ capillary pressure > swelling & pain
cellular: migration of leukocytes > adhesion > margination > transmigration > chemotaxis |
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leukocyte activation?
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phagocytosis & cell killing
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what are the chemical mediators?
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leukocytes, platelets, mast cells
=secrete histamine & prostaglandin |
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histamine effects?
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capillary dialtion, increases capillary permeability
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prostaglandin effects?
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mediates pain response, capillary dilation, increased permeability
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transcapillary refill?
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movement of fluid out of capillary into tissue
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leukocyte activation & phagocytosis? 3 steps
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-antibody binds foreign particle to phagocyte receptor's surface
-phagocyte engulfs antibody bound particle -phagocyte digests foreign particle |
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3 things that move out of capillary into tissue?
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1-cells
2-proteins 3-plasma& serum |
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2 goals of acute inflammation?
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1-localize inflammation
2-phagocytosis (clear debris) |
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6 types of exudate?
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serous
purulent hemoragic fibrinous membraneous |
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serous exudate
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serum, no clotting factor
watery clear mild, acute inflammation |
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purulent exudate
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wbc, bacteria, necrotic cell debris
thick/fluid white cloudy severe infection/injury can have foul odour |
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hemoragic exudate
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contains whole blood
fluid blood red colour capillary rupture |
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fibrinous exudate
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high concentration of fibrinogen/fibrin
thick, sticky, meshwork severe injury |
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membranous exudate
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mucous membrane
embedded within, will have necrotic cells in fibre purulent exudate |
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local clinical signs of infection?
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fever
malaise fatigue muscle soreness headache |
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what does hypothalamus do in relation to fever?
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body's thermostat
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pyrogens?
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chemicals that bring on fever, stimulate the release of prostaglandins
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5 steps of pathogenesis of fever?
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1-exogenesis pyrogens cause body to change set temp
2-endogenous pyrogens now make own cells 3-trrigger prostaglandins E2, local hormones 4-hormones bind hypothalamus 5.increase temp set rate via cAMP |
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with pathogenesis of a fever what else will happen in body?
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increased temp= increases phagocytosis
increased rate of immune response |
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why take antipyretic medication?
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too high of fever causes;
-cell damage -protein denaturation -elderly & children have lower buffering capacity |
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Do fevers kill pathogens?
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NO
they decrease replication and slow bacterial growth |
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C-reactive proteins?
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non specific proteins
produced in liver serum marker for inflammation serum marker for athereoscelosis |
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non medical treatments for fever?
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non-
cold pack for edema, bandage for pressure, elevation for limiting blood flow against gravity heat to ^ metabolic rate and phagocytosis |
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medical treatments for fever
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ASA- acetylsalacitic acid- inhibits prostaglandin synthesis
NSAIDS-decrease every step of inflammation -decrease swelling -decrease pain -decrease rate of leukocytosis -decrease capillary permeability -decrease release of prostaglandins |
