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289 Cards in this Set
- Front
- Back
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What do muscarinic antagonists do
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inhibit the actions of Ach
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Where do Muscarinic antagoinsts inhibit actions of Ach
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released from parasympathetic postganglionic, inhibit on neuronal and ganglionic receptors, and on tissues which do not receive a direct parasympathetic innervation
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Do muscarinic antagoinst exhibit nicotninic cholinoceptor antagoinst activity
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little, selective for muscarinic receptor
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Therapetuic actions depend on
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inhibition of parasympathetic drive
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What muscarinic antagoinsts have CNS activity
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scopolamine and benztropine
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What is muscarinic antagoinst have ganglionic blockade
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ipratropium
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What is muscarinic antagoinst that has neuromuscular blockade
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NONEq
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What are the muscarinic antagoinsts
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AS BITCH DOT DOT P
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What are special properties of benztropine
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CNS activity and parkinsonism extrapyrmaid SEs
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What are special properties of ipratropium (4)
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Ganglionic blockade, very poor absroption,, NO decrease mucociliary clearancw
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What do does mean that ipratropium have no decreased mucociliary celearance
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ipratropium conites to clear airways
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What are special properties of tiotropium
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M1/ and M3 antagoinst and longer duration
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What are special propteries of cyclopentolate
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decreased duration and decreased cylopelgia
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What are special properites of homatroprine
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decreased duration and decreased cylopelgia
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What are special properties of Dicylomine
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antispasmodic
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What are special properties of oxyphencyclimine
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antspamodic
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What are special properties of tropicamine
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decreased duration and decreased cycloplegia
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What are special properties of darifenacin
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urologic specfic
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What are special properties of oxybutyin
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antispasmodic, and urologic specfic
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What are special propteries of tolerodine
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urologic specific
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What special properties of pirenzeypine
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M1 antagoinst (blocks acid secretion) and petic ulcer
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The antispasmodic agents have
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WEAK antigcholingeric properties, and direct smooth muscle relaxant actions w/o SEs
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Are all the muscarinic agents COMPETITIVE inhibitiors
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YES--overcome blockade by increaings agoinst concentrations
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What antagoinst penetrates the BBB readily at therapetic levels
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scopolamine
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What antagoinst penetrate BBB at very high terapeutic levels
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atropine
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What are scopolamine effects on CNS (atropine at high levels) and benztropine
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DIE EAT
Depression (drowsiness fatigue, dreamless sleep) influences vestibular apparatus euphoria excitment anti-temor activity toxic doseses--CNS depression and coma paralysis |
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What is benfit of influence on vestibulat apparatus
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involve in balance---used for motion sickness (scopolamine)
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What is benefit of anti-temor activity by action on basal ganglia/stratum
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useful for parkinson's disease (benztropine)
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What condition is are the CNS muscarninc antagonists used for
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anesthetic premeidcation, anti-temor medications, and motion sickness
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What is benifit of scopolamine and atropine in anesthetic premedication
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tranquilizing and amnesia effects, and inhibitior of salivaiton and respiratory secretions
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What is an anti-tremor medication, and use in
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benztropine, scopolamine, and used in parkinsonism, adn extrapyramidal side effects of antipsychotic medications
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What is a medication used in moition sickness
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scopolamine
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When scopolamine best applied
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prophylactically
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What are side effects of scopolamine
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sedation and dry mouth
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What are Muscarinic antagoinst actions on the heart
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Positive chrontropic increases HR
Little on force of contraction Increases AV node conduction |
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How does Muscarinic antagoinsts have a positive chronotropic effect
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inhibition of vagal effects
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What do muscarinic antagoinst do to children
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cuase atrial dysrhytmias, even small doses decrease HR in children
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How does muscarinic antagoinst increase AV conduction
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decreasing relativie refractory period in AV node
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What effect does decrease releative refractory period of AV node affect
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patients with atrial fibrillation, can cause ventricular tachycardia
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What are affects of muscarinic antagoinsts on blood vessels and blood pressure
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NONE--no cholineric innvervation
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What can toxic doses of atropine cuases on blood vessels
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atropine fluce in face
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What conidtions of the heart would muscarnic antagoinsts treat
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vagal hyperactivity of heart
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What effects would an M2 antagonist have
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Increasing Ach release by blocking the presynaptic M2 receptor
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What do Muscarinic antagoinsts do to GI system
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inhbit but do not block GI smooth muscle activity
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What actions do muscarinic antagoinsts have on GI
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decrease amplitude of contractions
and decrease peristaltic activity of stomach and intestines decreased salivary secretion and gastic secretion |
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What is side effect of decreased peristalisi
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constipation
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What is a side effect of decreased salviary secretion
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xerostomia, difficulty swallowing and talking
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Muscarinic antagoinsts decrease gastric acid secretion from
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gastric parietal cells (M1)
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What are muscarninc antagoinsts used for in GI
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intestinal hypermotility
diarrhea associated with irrative conditions of lower bowel, and excessive salivation |
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What drugs are usefull for diarrhea assoicated with irritative conditions of lower bowel
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dicylomine and oxyphencyclimine ---less atropine SEs
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Are the antispasmodic actions UNreleated to muscarinic antagonism
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YES
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Antimuscarinic agents are often combined with what drugs
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opioids to prevent opiate abuse by producing SEs
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What is prolems with muscarinic antagoinsts in treating peptic/duodenal ucler
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pronounced SE's--like atropine (no see no pee, no spit no shit)
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Can gastric ulcer be aggravted by atropine like drugs, and how
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YES---by delaying gastric emptying you expose gastric muscosa to low pH for longer time
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What is a drug used for peptic/duodenal ulcer
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Pirenzepine
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Is Pirenezpine as efficcious as H2 antagoinsts
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YES, and may be synergistic with H2 antagoinsts
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What are muscarinic antagionsts effects on urniary tract
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dilates ureters adn relaxes detrusor muscle of bladder
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What is side effect of dilates ureters and relaxing detursor muscle of bladder
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urniary retnetion
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What are muscarinic antagoinsts use in urnairy tract
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unstable bladder conditions
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What receptors on bladder and trigone
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M3 and (m2)
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What drugs treat unstable bladder conditions
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darifenacin, oxybuting and tolterodine
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Dry mouth is a side effect of urnary tract drugs--what drug has a lower incide of dry mouth than oxybutynin
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tolerodine--hihger specficity for bladder muscarinic cholinceptors
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What receptor is darifenacin selective for
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M3 selective antagoinst
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What are muscarinic antagoinsts actions on airways
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relaxes airways smooth musce
decreases secretions in nose, pharxyn and bronchi, and decrease bronchial ciliary funciton |
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Muscarinic antagoinsts relaxes airways smooth muscle, when do they cause BRONCODILATION
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when parasymthatpetic cuases bronconstritions--if luketriones involved NO bronchodilation
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Muscarinic antagoinst result in decreased bronhcial cillary fuction which causes
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decreased muscus clearance from airways and airway obsturction
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What are use of muscarinic antagoinsts in airways
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decrease secretion in UPPER airways, bronchodilation, and anestethic premedication
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How do antihistamines decreases secretion in nose (upper airways) in rhinitis
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work though anticholinerigic activty
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What conditions is bronchodilation more effective in
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bronchitis and emphesema, THAN asthma (not)
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What are 2 drugs for treatment of bronchodilation
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ipatropium and tiotropium
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What limits the efficacy of ipratroium
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causes presynatic M2 inhbiition
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How are anestetic premedication treated in airways
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muscarninic antagoinsts decrease secretions in airways and decrease larynogospams by secretions
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What are effects of muscarinic effects on sweat glands
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decreases secretions by sweat glands
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What happens when mucarinic decreases secretions by sweat glands
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skin becomes dry and hot
inhibition of thermoregulatory mechanisms |
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When does the body temp increased b/c of inhibition of secretions by sweat gland
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only at high environmental temperatures
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Who is affected by atropine fever
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caused by moderate doses in infants and children
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What are actions of muscarinic antagoinsts on eye
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relax cicular muscle of iris
(atropa belladonna) relaxes ciliary muscle |
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What are effects of relaxes spinchter (cicular) muscle of iris
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blocks pupillary reflex to light-for photophobia
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What are effects of relaxing ciliary muscle
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cylopelgia
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What are side effects of muscasrinic antagoinsts on eye
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blurred , dry sandy eyes, and photophobia
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What are USES of muscarinic antagoinsts in eye
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mydriasis induction, and clyoplegia induction
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What drugs are to cause mydrasis induction
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cyclopentolate, homatropine, and tropicamide (short DOA and decrease cyloplegia
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When does cyclopelgia induction occur
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at doses taht exceed mydriatic dose
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If you obtian cylopeglia always get
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midrasisi and swelling
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WHat drugs are more effective than cylpentolate or torpicamine
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atropine and scopolamine
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Atropine and scopolamine are applie topically--what prevents symstemic absorption, what has worse side-effect on eye
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nasolacrim duct--scopoloamine--gets in CNS better
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What are muscarinic antagoinsts in eye contraindicated in
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narrow angle glucome
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What happens antimuscarinic drugs ROLE in antichlinesterase poisioning
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block excessive parasympathetic effects in muscarinic antagoinsts, broncoconstrictors and bradycardia
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Will musarinic antagoinsts affect NM poisoning of anticholinesterase
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no
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Why wouldnt a muscarinic antagoinst reverese the NM effecgt of Ach poisioning
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only nicotinic effect
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What is an adjust to anticholinestase therapy of myasthenia gravis
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blocks parasympathetic side effect of AchE inhibitor therapy--useful in ealy period
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What is an antidote for rapid type of mushroom poisoning
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atoprine
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What are actions of muscarinic antagoinism in eye
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relax spinchter musucle (mydrasis)
relax ciliary muscle (cyloplegia) |
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What are effects of muscarinic antagoinst of gall bladder, savilary glands and all GLANDS
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decreases secretions
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Do you need parsympatetic drive to see effects of antimuscarinic agents
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YES
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Is tissue suspceptibility to muscairnic antagoinsts dose-depenpendent
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YES
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What is order of tissue susceptiblity to dose-dependent
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Salvaryy glands,=broncial =sweat glands>eye =heart>bladder =GI>GI secretions
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What do nicotinic antagoinst do
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inhibit the actions of Ach
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Where do nicotinic antagionst inhibit the actions of Ach
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at autonomic ganglia
on SKM cells |
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What happens if you inhibit Nn receptors
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bloack ganglionic transmission
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What are ganglionic blocking drugs
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hexamethonium, trimethaphan, and mecamlamine
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What are pharmacolgocial actions of Nicontinc blockcade
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effects ANS--effect seen depends on inhibition of dominannt NS
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What are effects of autonomic blockade on eye
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para --relax ciliary musce-cyloplegia
relax circular-mydraisis |
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What are effects of heart when autonomic bloackage
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para-blockade--increases HR
sym blockade--decreases contractility |
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What effects of autonomic blockade of areterioles and veins
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sym.--dialtion
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What effects of autonomic blockade of GI tract
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para--decreases motility and tone
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What effects of autonomic blockade saviliary glands
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para--decreased secretion
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What effects of autonomic blockade of sweat glands
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sym--decreased secretion
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What are effects of autonomic bloackade of urinary bladder
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para--uninary retnetion
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What are USES of ganglionic blocking drugs
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blood pressure contorl, inudction of controlled hypotension, and management of autonomic hyperrreflexia
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What do ganglionic blocking drugs do in blood pressure control
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Decreases sympathetic outflow decreases BP, and rise of BP at site of tear
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What do ganglionic block drugs do in induction of controlled hypotensions
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inihbit symathetic control of BP--so BP controled by tilt table
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What is use of ganglionic blocking drugs in mangement of autonomic hyperreflexia
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bladder distenion activates spinal reflex, what increases autonomic discharge
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What drugs are chosen for BP control
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Trimethaphan--raid onset and short half life
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Mecamlamine is orally acitve-and can enter CNS adn
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cuase problems
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What are side effects of ganglionic blocking drugs
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para--block urination,constipation
sympathetic--no sweating ---drugs are bad!! |
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What do Neuromuscular blocking drugs inhibit
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NM receptors---paralysis-need ventialtion and rendal adjustments
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What are 2 classes of Neuromuscular blocking drugs
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competivie agents (non)
depolarizing agents |
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What are depolarizing agents
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succinylcholine
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What are the non-depolarizing agents (competitive0
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MAC RV DPPT
Mivacurium atracurium cisatracurium rocuronium vecuronium doxacurium pancuronium pipecuronium tubocurarine |
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What are properties of succinylcholine
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onset 1 min, duration 5-8, histmaine ++, no ganglionic blockade and plamsa and hepatic ChE
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Non-depolarizing or cometivie antagoinst compete with
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Ach for Nm receptor
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What are characteristics of blockade
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surmoutable, reversible by cholinesterase inhibitor and does not depolarize motor end plate
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What does it means surmountable
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Increasing conc of Ach in NMJ--can decrease bloackage
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What can reverse NM blockade
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chlinesterase inbhitor--increases Ach in NMJ
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Depolarizing antagoinsts the blockade comprises
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two phases---phase I and phase II
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What happens in phase I
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succinylchoile activates Nm receptors and inital depolarization of MEP--leads to muscle fasciculations
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What happens after inital depolarization of MEP
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persistant mebrane depolarization, and unable to initate AP
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What happens in Phase II
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motor endplate repolarizes,and converts to non-depolarizing competitive types
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What promotes conversion to Phase II competitive inhbitior
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fluroinated hydrocarbon anestetics
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What are characteristics of Phase I
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insurmountable
ChE inhibition increases Block MEP depolarizted |
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What are characterstics of Phase II
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surmountable
ChE inhibition decreases block MEP not depolarized |
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What is end result of use of non-depolarizing and depolarizing agents
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bloackae of NM transmission and paralysis of SKM (diaphragm
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What is ordoer of activity of paralysis of SMK
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small rapidly acting to first
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What is affected Last
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respiraotry and diaphragm, and first to recover
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What are therapetic uses of Neuromuscular blocking agents
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muscle relaxation during survery, adn decreased muscle spasms in orthopedic proceudres and relaxation during ECT
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Why would you relax msucel durign ECT
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seizures could lead to dislocations and fractures, b/c high amnts of somatic outflow
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What are characteristic of IDEAL neuromuscular blocking drug
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non-depolarizing
rapid onset short life idenpendent of renal hepatic metabolism |
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What are side effects of histamine release
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Decrease BP, increase bronchial and salivary secretions, and BRONCHOCONSTRCTION
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What are other side effects of NM blocking drugs
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GAP HI
ganglionic actions post-operative muscle pain aytpical butrylcholinestase interactions hyperkalemia intergastic pressure |
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What are side effects of ganglionic actiosn
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tubocuraine>>>pancuronium result in decrease BP (blocking symp) and decrease GI motility (para)
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What are side effects of aytpical butyrylcholinesterase interactions
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succinylchoine metabolized by in liver and plasma--prolonged use results in liver dysfuction--decreased hepatic blood flow, and abnormal butyrylcholinesterase
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What causes Hyperkalemia (succinylcholine)
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increased K+ into blood and can cause arrest in susceptible patients
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What causes Increase intragastric pressure (succinylcholine)
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fasciculation increase pressure, adn increased probability of vomititng
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What are drug interactions with Neuromuscular blocking agents
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Anticholinesteases agents (endrophonium, neogstigmine, adn pyridostigmine), inhalation anesthetics, antibiotics, Ca+ cannel antagoinsts
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What do antighcolinesase agents do
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1. increased dopolarization in phase I
2. reverse non-depolarizing blockade in phase I |
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What do inhalation anesthetics do
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act synergistcailly wtih non-depolarizing drugs, adn reduce dose of succinylcholine
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What do Ca+ channels do
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act synergergistically with NM blocking drugs
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What does succinylcholine and halogenated hydrocarbons do
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maliganant hyperthemia
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Maligant hyperthermia involves mutation of Ca++ release channels and what
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excessive Ca+ release from SR--causing muscle rigidity, and heat production, metabolic acidosis, and death
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What is main causes of death to anesthersia
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syccinylchloine, and inhaled anestthetics (hlogenated hydrocarbons)
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What is treatment of maligant hypertermia caused from succinylchloine and halogenated hydrocarbons (inhaled anestethics)
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dantrolene--inhibits Ca++ release from SR
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What are normal ways cell respond to stress
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autocrine
paracrine and endocrine signaling |
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A normal cells is in homeostatis with its environment, if there is a stress of increased demands on cell what happens
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either adapts, of if it is inabile to adapt it results in cell injury and death
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What are signal transduction mechanisms of cell
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cyclic nucleotides
-camp, cGMP proteins kinases EFG receptor ras MAPK |
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What a key concept to all regulation
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phosphorlayion and dedephophorlation
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Epidermal Growth factors is a example of phosphorlation to be active it was 1st succesful molecular target to
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reat lung cancer 9Iressa, Tarceba, inhibit EGF receptor
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What are stressful stimuli that affect cells
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PACE GIIN
phyical agents (mechaninal, thermal) anoxia (lack of O2) chemical agnets endocrine (deficient/excessive) genetic imuune infective nutritional |
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What is a reversible cell injury
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when the environment influence evoke a cellular response that remain within the range of homeostatis
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What type of injury is reversible, and what happens at injury cessation
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injury mild or short lived (low toxin concetionat or brief hypoxia/anoxia)--cessation cells revets to normal
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What is most common response of cell to low toxin concentration or breif hypoxia/anoxia
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celluar swelling
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What causes swelling of cell
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any damage to cell decreases ATP, which decrease ATPase activyt, Na+ Cl- and water influx into cell and cause swelling
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What happens as a result of swollen mitochondria
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swollen mitochondira generate less energy, produces ATP by anerobic glycolysis, and increase lactic acid production, and the increase pH slow down cell metabolism
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What also swells beside mitochonria
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swelling of RER, decreases protein synthetsis, and swollen cells lose contact with adjuacent cells as a result of desmosomes
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What causes an irrversible cell injury, and length
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high toxin conc, and severe hypoxia/anoxia--overwhelimg or long=liver
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What happens after injury cessation
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cell is irrversbile damage
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What are characteristics of irrversible cell injury
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loss of cell integrity, cell membrane rupture, and nuclear changes, and mitoochrondira damage
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What happens as a result of damaged mitochondria
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Loss of ATP production, loos of cellular function and plasma membrane fuction, rupture of cell membrane
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What happens after cell membranes rupture
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release of cytoplasmic enzymes,such as LDH, which can be measured in blood
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What are nucelar changes of irrversbile cell injury
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Pyknosis-condenstion of chromatin
Karyorhexi--framgentation into smaller particles Karyolysis--dissoluciton of nuculear structure and lysis of chormiatin by enzymes |
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What is an exmaple of reversible injury
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hypoxia from a thrombus causing ischemia
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What happens after post-perfusion of ijnury
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increased oxygen form Oxygen radials form forming Hydrogen peroxide, and superoxide result in necrotic cell
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How can you prevent death of cell by perfperfusion
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give antioxidants
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What are some damaging effects of Super oxide anion and Hydrogen peroxidase on cell
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perodiation of lipids--membrane damge, DNA damge--imparied protein systneh and mitochonrdiral damge reulst in Ca+ influx into cell
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What happens there is mitochorndiral damge from radicals
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Increased cytoplasmic Ca+ from ER and Mitochondira, and pumped out is block by decreased ATP,
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When Ca+ levels get high enough what happens
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activates phopholiases and proteases which degrade membrane, and actiavte nucuelase which degraded DNA
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What are cellular defenses
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GAP PH
glutathione antioxdiant enzymes p53 proteosome heat shock proteins |
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What are some antioxidant enzymes
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Superoxide dismutase
catalase glutahione peroxidase, and reductase |
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What does SOD do
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catalyzes the conversion of superoxide to hydrogen peroxide
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What does catalase to
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catalyzes the breadown of hydrogen perosixe to H20
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What does gluathione peroxidase do
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catylzes clearance og H202 by alllowing glutahione to bind to it
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What is P53
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main protect of DNA, when DNA is damaged p53 attaches to DNA and prevents it from replicating, and increase expression of proteins taht inhibit cell growth
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P53 arrest cell division for until repair, if not reapir then
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apoptosis
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What happens when mutant p53
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implications for cancer
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Explain the cellular defense the proteosome
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A damage or misfolded protein binds and activates ubiqution, and the unuqinated protein is recognized by the protease to be destoryed
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Explain the cellular defense Heat-shock proteins
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newly made client protein assoicates with a muti-protein complex chaperones--chaperone comlexes prevent its aggregation, and assists in its intracellular trafficking, and phosphorlayted to be active, and also target for degration through ubiqtoine
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What are cellular acummulation examples
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Fatty change
Lipofuscin Melanin |
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What happens with fatty change
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alcohol stimualtes accumlation of fat in liver if reversible--but chonric and frequent =chirrosis
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What happens with lipofuscin
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incomplete oxidzed mas of membrane remants, that is a linear function of AGE
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What is Melanin function in
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inadequate function of the adrenal cortex causes increased ACTH (MSH-like activity), causes skin darkeneing
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Are cellular acummulations always harmful
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NO--often just indiciate a problem
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What are reversible changes in tissue size is controled by
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cell cycle
and cell cycle regulation by cyclin kinases |
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What are the 4 phases of the cell cycle
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G1, S (synthesis of DNA), G2 M (mitosis)
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What happens during G1, S, and G2
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mitotic cylin concentration gradually increases,
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What happens near the end of G2
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mitotic cyclin and CDK form a active comlplex with phosphorlation, allow entrance in M phases
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Where is the restriction point on the cell cycle
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G1--cell cycle is halted until condition are suitable for pregession into S phase
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What does Rb protein normally do
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prevents cells from passing though the restirction point in S phase
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What happens when growth factors bind to cell membrane
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tirgger production of ACTIVE Cdk-Cylin complexes which phosphorlate Rb
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What happens after Rb is phosphorlated
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Rb no longer exert its inhibitor influence on the resitrction point and cells are free to pass into S phase
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The response of a tissue to reversible damage depneds on
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the ability of its cells to divide
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What are 3 cells types
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Permanent cells (cannot replicate)
Stable cells-normally quiesent-injury Labile--continue to replicate |
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If cells can divide changes that can occur are
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cell number
differentiation cell size |
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Cell number changes
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involuntion (decrease cell #)
hyperplasmis (increase cell #) |
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What are type cell differentitaion
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metaplasia (another cell type)
dysplasia-degraned archiecture) neoplasia-unregulated growth |
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What are changes in cell size
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atrophy--decrease cell size
hypertrophy--increase in cell size |
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What is an example of increase in cell number
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nestrual cycle
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What is an example of differntiation
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smoking changes columuar epithetal to squamous epthielum
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Atropy can cells get smaller by paritally digesting itself-to perserve energy
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YES
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What is an example of increase in cell size
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ahterle's increase in muscle size--person loses kidney, thyroid gland
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What is reponse of tissue to irrversilbe damage
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increase cellular permeability and death
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What are 2 types of cellular death
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apoptosis and necorosis
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What is differance between nerosis and apoptosis
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necrosis--expogensouly--accdient cell death
apoptosis is programed cell death |
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What happens in necrosis
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cell and organlelg swell, cell repturse
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What happens in apoptosis
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cell cytoplasm shrinks and forms cell blebs, and apoptic bodies and engulfed by phagocytes
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2 types of pathways that trigger apoptosis, the external pathway, and internal the external pathway, external moclcules bind to
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death receptors, and triggers caspase cascade-to active Apoptosis
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Apoptosis affect sinlge cell, what does necrosis affect
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sheets or groups of cell dies together
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Which has inflammation apoptosis or nerosis
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necrosis
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What is teh phosphadtidylserine (PS) signal
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moves to outside of cell, and tells negihobring to "eat me"
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What is histology of inflammation and repiar
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epithelium
mescenchme basement membrane blood flow blood cels |
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Epthelium secretes protein to make
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basement membrnae
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What is the conncetive tissue layer made of cells, fibers, and ground substances
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mescenchme
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What are types of mesenchyme
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1. Loose, Dense, estic ,reticular and adipose
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What are all cells of blood dervied form
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Bone marrow
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Where in adults are main site of bone marrow
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ribs, skull, sternum
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What is dervied from a pleuripotential stem cell
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B-lymphocytes
T-lymphoctes Myeloid stem cell--RBC, Granuclocyte or Monocyte, or Platletes |
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In general epithelium do not move, mechencyme does, what happens to epithelium in disease
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eats through basement membrane to get out
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Where are toll-like receptors
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on macrophages--floating aournd in body--bind to bacteria--and stimulate inital inflammation---
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Macrophages active the immune response how
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Toll-like recptors bind to LPS--and triggers synthesis and release of cytokines, which trigger inflammation
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What is one mechanism that bacterial species have evoled to evading phagocytosis
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large pollysaccharide coat
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What is order of inflammation
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1. Changes in circulation of blood
2. Change vesssel permeabiltiy 3. White blood cell response 4. release of mediators |
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What is bodys first response to injury
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relaxation of smooth muscle allowing blood to rush into capillaries, binding of neutrophils and platelets release mediators of inflammation for chemotaxis
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Cells mvoe along the concentration gradient of the
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chemotactic simulus
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What is release from plateles and mast cells
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histamine--increases blood vessel permaabily
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Histmaine is an example of a
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pre-formed mediator
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Bradykinin is formed in the plasma through activation of
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Hageman factor which causes vascular peremabiltiy and clotting
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What is main chemoattractant for neurophils
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endotoxin
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The neurophils are 1st to arrive, and what attracts them to bind to endothelial cells
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chemotactic substances
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After neutophils bind to endothelial cells what happens
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insert their cytoplasmic pseudopohs bettwen juctions of endothelial cells, adn pass through basement membrane
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Area of tissue damge, causes vasodilation, then increased cappillary permeability, what happens
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neuotropils and platelets adehere release medaitors of inflammation--attrached to inflammatory cells
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Once neutrophils binds to bacteria, how does it recognize
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the bacterium was opsonized--binds to Fc complememt
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What is opsonized
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coated with IgG, and complements C3b
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What happens after Neutophil binds to the oponins
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engulf the bacterium, and attached to lysosome which releases enzymes that detory the bacteria
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Is the pH in the lyosome acidic, and why
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YES, enyzmes are only active in acdic pH,cytosol is pH of 7,1
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Also neutrophiles can genetic toxic oxygen radials that kill bacteria, what are most potent
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hydroxyl radical from fenton reaction, >>>hydropohilate ions from myeloperoidase, >>>hydogen peroxide from SOD
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What converts the moecular oxygen to superoxide ion raidal and other radials
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NADPH
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What are the 4 cardinal signals of inflammation
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heat, redness, swelling and pain
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Where do macrophaes reside
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in all cell tissue of body
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What are 2 main properies of neutrophils
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release inflammaotry mediators, and phaocytosis of bacteria
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Macorphages are last to appear at site of inflammation and what do they do
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Phocytosis of bacter,and release inflammatory mediatiors, INIATE immune response, cleanup dead neutrophils,
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Is there overlapping fuction--with alternative, classical and lectin pathways which deposit C3b on microbe
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YE
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What are eicosanoids
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newly-formed mediatorys
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What do eicosanoids comprise
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protaglinsts, thromboxanes, and leukotrines
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What are eicosanoids dervied from
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neutrophiles and macrophages in inflammation
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How is arachidonic acid formed
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phospholipases of membrane
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Anachiodinic acid it is further metabolized to
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lipoxygenase pathway, and cyclocooxygenase pathway
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What does Lipoxtgenase form
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Leukotriens- and Lipoxin
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What do luekotrienes do
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promotes chemotaxis and inflmamation
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What does Cyloccogenase form
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forms prostaglandins, and thromboxane A2
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What do progstagalinds promte
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vasodialtiion, and inflmamation
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What do Thromboxane A2 promote
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platlet aggreation and vasoconstrition
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What do COX 1 and Cox 2 inhbitiors inhibit
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Cylooxygnease--COX2 induceable--inflammation
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Where do steriods inbhit
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phospholipases
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Do leukotrienes and prostaglinds completment each other
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YES---by themselves poor mediatior of inflamamtory
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WHat is Platlet activating factor
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newly-formed mediator--DOES everything
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Where is Platelt activating factor dervived from
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a variety of cell types
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What are most cytokines
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simple polypetides or glycoproteins
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What causes the production of cytokines
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reuglatoed by inducing stimulat at level of transcriptin and translations
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The production is transietn and action of radius is short--cytokinase act by
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bind to high-affity cell surface receptors
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What are actions of cytokines attributed to
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altered gene expression in raget cells
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What are the major cytokines
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IL1
Il-6 TNF-a |
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How do cytokine receptors work
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cytokine binds and JAK phosphorlate each other, then stat binds are phosphorlated by JAK, then move into nucleus and modifty transcription genes
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Is the inflammatory response more inactive >>>active
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YES
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Is the inflammatory response short lived
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YES
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What are options after acute inflammation
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resolution, fibrosis, or chronic inflammation
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What is resolution after aute inflmmation
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clearance of injouris stimulate and replace of injured cells--result in normal function
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What is function of lyphatics
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fluid drained from the tissue by lymph capillares
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What is granulation tissue
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wound-healing tissue
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What is the key cell in wound healing
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macrophage
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What do macrophages signal
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fibroblasts, angioblasts and collagen
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Macrophages secrete fibrogenic and angiogenic factors taht
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cause cappilary buds to grow and fibrobalsts depost collagen makingm tissue stronger
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In order for cappilary sprouting, what is needed so new blood vessels grow
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proteases destory tissue, adn macrophages sense hypoxic area and make HIF to enable blood vessel repair to go on
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What are fibroblast differentiate from
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mesenchymal cells
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What are properties of fibroblasts
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proliferate in chonric inflammation, adn synthezie and secrete collagen
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Angiogensis produces VEG-F vasuclar endothelia growth factor do
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stimualte cell division of endothelial cells and ability to move
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What does wound repair depend on
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extent and location, diet, and internal factors such herdiety age blood flow and disease
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Chronic inflammation is best defined by its
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duration--a long time
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What are possible outcomes of an ulcer
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1. healing
2. perrformation 3. chronicity |
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Does perforation put a whole in the stomach linign
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YES
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What is chronicc inflammatory disease
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some healing is going on, but does not overcome acid---ulcer can persist for many years
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