pathophysiology exam 4 - review

7/27/2019 Pathophysiology Exam 4 - Review

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Waqas A. Gil

Pathophysiology Exam 4 - Review

Ch. 15Brain & Spinal Cord Injury II

Acute spinal cord injury:o Prognosis:

Focuses on the degree of brain/spinal function, strength of reflexes, life expectancy, risks forother conditions (pneumonia, thrombosis, urinary disorders, etc), and mortality rates. Spinal shock:

Lesions and signs associated with severing of spinal cordo Sympathetic: Lesions along the spine commonly lead to very high BP, severe headaches, skin

irritation above the area of spinal injury, and severe convulsions.

o Parasympathetic: Slow heart rate, pale skin, and perfuse sweating. Autonomic dysreflexia:

o Manifestations:1-12 weeks afterSpinal injury at/above T-7 A potentially fatal complication that occurs in response to stimulation of internal organs (i.e.

expanded bladder) or of the skin, afterthe shock of a spinal injury has worn off.

o Reasons for Clinical Manifestations: Spinal lesions usually lead to afferentimpulses becomingblocked (no sensory input to the brain), and so in the example of urinary bladder distension, reflexesare activated below the lesion to increase sympathetic activity below the lesion Increased BP.


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As this happens, cardiac baroreceptors detect this BP shift and compensates by loweringheart-rate and dilating blood-vessels above the lesion. Since the brain still cannot sendsignals to regulate activity below the lesion, overall, BP is not regulated (up to 300mm Hg).

o Treatment and Management: Elevation of bed to 45o to help decrease BP, removal of noxious stimuli by providing

bladder/bowel relief & removal of tight clothing, and through ganglionic blockers.

Phantom paino Pain experienced despite the loss/realignment of sensory/synaptic pathways, release of excitatory or

accessory pain pathways, & dendriticsproutingin the area of injury as tissues heals.

Ch. 16Autonomic Nervous System

Understand the divisions of the nervous system particularly ANSo Nervous system CNS & PNS Sensory & Motor Somatic & ANSo ANS Sympathetic, Parasympathetic, and Enteric (digestive tractsmooth muscle contractions,

glandular secretions, & detect physical/ionic changes in lumen content).

Somatic: Skeletal muscle, Conscious & unconscious (step on tac) movement, Skeletal musclecontracts, 1-synapse mechanism, ACh,Nicotinic receptors, and myelinated axons.

Autonomic: Smooth/Cardiac muscle & glands, unconscious regulation, stimulation/inhibition, 2-synapse mechanism, ACh (pre-ganglionic) + ACh/Nor-Epineph (post-ganglionic), Myelinated axons

(pre-ganglionic) & Unmyelinated axons (post-ganglionic).

Sympathetic and parasympathetic system: Organizational and functional differenceso Sympathetic & parasympathetic divisions often supply thesame organs but differ in # of features

and will often exhibit opposingactions.

o Sympathetic Chain-Ganglion: Preganglionic cell bodies in lateral horns of spinal vertebrae T1-L2.(Thoracolumbardivision )

o Parasympathetic Division: Preganglionic cell bodies in nuclei of brainstem or lateral parts of spinalcord gray matter from S2-S4 (Craniosacraldivision).

o Preganglionic axons Cranial III, VII, IX, and X Pelvic splanchnic nerveso Terminal Ganglia: Located nearthe innervated organ or embedded in the organ-wall.

Routes of sympathetic axons (4)o Spinal nerves, Sympathetic nerves, Splanchnic nerves, & Innervation to adrenal gland.


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ANS receptors and neurotransmitters

o Parasympathetic only uses ACh for both pre and post-ganglionic bindingCholinergic receptors Nicotinic (always excitatory) &Muscarinic (Excitatory/Inhibitory) cholinergic receptors.o Sympathetic system only uses ACh for pre & eitherACh/NE for post Adrenergic receptors (NE)

Alpha (1 & 2) andBeta (1 & 2) adrenergic receptors (Excitatory/Inhibitory).

Influence of brain on ANS functions

ANS regulationo Autonomic reflexes control most

of activity of visceral organs,

glands, and blood vessels, and is:

o Influenced by the Hypothalamus(overallANS control) & higher

brain-centers.

o Brainstem: Survival functions(especially related toGlossopharyngealand Vagus

nerve, but others too).


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Visceral reflex arc and various autonomic reflexeso Visceral reflex: Always have polysynaptic

pathways & afferent fibers are found inspinal/autonomic nerves.

o Parasympathetic reflex:Vaguslowers heart rate.o Sympathetic reflex: Cardiac acceleratornerves

cause heart rate to increase.

o Baroreceptors in the carotid sinus and aortic archmonitor blood pressure.

o If BP inc., APs are conducted by Glossopharyngealand Vagus to cardioregulatory & vasomotor centers

in the medulla to initiate homeostatic mechanisms.

o Cushings response (Hypertension & Bradycardia) happens because of a disconnectb/w thebrainstem and middle of spine, which allows opposing reflexes to activate, simultaneously.

Functional generalization of ANSo Dual innervation: To most organs with sympathetic and parasympathetic having the opposite effects.o Coordination: Either division alone or both working together can coordinate activities of different

structures.

o Sympathetic prepares body for physical activity: or flight-or-fight response. At rest, thesympatheticsystem is responsible formaintainingBP. Exercise: Inc. heart-rate, skeletal/cardiac vessel + airway dilation, inc. glycolysis + -Oxid.,

body-temp. inc., sweat-gland secretions inc., & dec. in non-essential organ activities.

o Parasympathetic - Resting state: SLUDD: salivation, lacrimation, urination, digestion, defecation Various types of receptors in detail

o Cholinergic: Bind Acetylcholine (ACh)2 types, which are named after drugs that mimic ACh.i. Nicotinic:Found on somatic targets (post-synaptic), all ganglionic neurons of Sym/Parasym

divisions, & the hormone-producing cells of the adrenal medulla. (Always stimulatory). Works by opening Na+-gated channels on post-synaptic membranes.

ii. Muscarinic:Found on all effector cells stimulated by postganglionic cholinergic fibers.Induces indirecteffects through G-proteins. (StimulatoryorInhibitory). Works by activating G-protein coupled receptors.

o Adrenergic: Bind Epinephrine & Norepinephrine (NE)2 types, all mediated through G-proteinsi. Alpha: Generally stimulatory:

1Releases intracellularCa2+ from the E.R. (ExcitatoryVasoconstriction) 2Decreases cAMP levels (InhibitoryArterial dilation with venous constriction)

Mechanism: Endothelial cells make up blood vessels, which are surrounded by smoothmuscle cells. When you have a sympathetic (alpha) response, these smooth muscle cellscontract, thus constricting the blood vessels and increasing the blood pressure to increase O2transport. It will usually lead to vasoconstriction of peripheral blood vessels, thus increasing

the blood flow to essential skeletal muscles and the heart, and dec. blood flow to extremities.ii. Beta: Generally inhibitory, except for the heart, where -receptors arestimulatory.

This exception explains why -blockers (antagonists) reduceones heart-rate. 1Increases cAMP levels (Inc. metabolism, heart-rate, and force of contraction) 2Decreases cAMP levels (Relax respiratory smooth muscle to ease breaths 3Increases cAMP levels (Activation of lipolysis in Adipose [fat] tissue).


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Function of sympathetic and parasympathetic nerves on target organs

o Radial muscleradiates (spreads): Contraction leads to pupillary dilation Sympathetic systemRich in Alpha-1 receptors Small pupil to large pupil (Mydriasis)

o Sphincter muscle: Contraction leads to pupillary contraction Parasympathetic system Big pupil to small pupil (Miosis)

o Ciliary muscle:-2 activation leads to relaxation and lens flattening Helps with far-sight. Nightshade (flower) leads to pupillary dilation (but also super-hypertension), it was originally given

to female entertainers by the Romans to make their eyes more beautiful.

o The picture on the right shows the movement of SA-impulses as they travel from theSA-node AV-node Interventricular septum Left/Right Bundle branches Purkinje fibers

o For all vessels/glands/tissues, sympathetic activation commonly leads to constriction, whileparasympathetic activation usually leads to dilation.


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o Bronchial relaxation helps us breathe faster and more:

Relaxation is usually paired with less secretion, while Constriction is usually paired with more secretion.

o Sympathetic activation of the Liver leads to all functions that would increase glucose;vice-versa Effects of drugs:

o AtropineBlocksparasympathetic effects, and so helpful for pupillary dilation.o NeostigmineInhibits acetylcholinesterase & used to treatMyasthenia-Gravis (muscle weakness)

Influence Cholinergic receptor-activityo Tricyclic AntidepressantsProlong the activity of Norepinephrine on postsynaptic membranes.

InfluenceAdrenergic receptor-activityo OTC drugs for Colds, Allergies, and Nasal CongestionStimulate -Adrenergic receptorso Beta-blockersattach mainly to 1 receptors and reduce heart rate and prevent arrhythmias

ANS Disorderso Raynauds Disease: Constrictionof blood vessels in the periphery of the body,

especially the fingers. Symptoms: Pale cold hands prone to ulcerations & gangrene (dec.blood) Causes: High sensitivity of blood vessels to sympathetic innervation.

o Hyperhidrosis: excessive sweating, exaggerated sympathetic innervation of thesweat glands

o Achalasia: Difficulty swallowing/controlling contractions of esophagus whereit enter the stomach and therefore interrupting normal peristaltic contractions of

esophagus (bottom picsevere constriction in central region).

o Hirschsprung Megacolon Disease: Functional obstruction of lower colon andrectum. Ineffective parasympathetic function and a predominance of

sympathetic stimulation of colon inhibit peristaltic action.


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Ch. 17Integration of Nervous System

Sensation:

i. Senses and Sensory Receptors: Detect stimuli inside/outside the body and converts them into APs General receptors:All over body and generate APs (generatorpotentials) from primary

receptors and send them to the brain.

a) Somatic: Body & environment (touch, pressure, temp., proprioception, pain).b) Visceral: Internal organs (pain, pressure) Special senses: Smell, taste, sight, hearing, & balance. These receptors produce potentials

but also release neurotransmitters to secondaryreceptors that travel to the brain.

Types of receptors: Based onstimulia) Mechanoreceptors: Compression, bending, & stretching of cells.

o Touch, pressure, proprioception, hearing, and balanceb) Chemoreceptors: Chemicals attach to receptors on their membranes (Smell & taste)c) Thermoreceptors: Respond to changes in temperatured) Photoreceptors: Respond to light (vision)e) Nociceptors: Extreme mechanical, chemical, or thermal stimuli. (Pain-perception)

o Any of the above receptors, under extreme conditions, can act as a nociceptor Types of receptors: Based on locationa) Exteroreceptors: Associated with skinb) Visceroreceptors: Associated with organsc) Proprioceptors: Associated with joints/tendons

Responses to senses:a) Accommodation (adaptation): Decreased sensitivity to a continued stimulus.b) Proprioception: Provide info about the precise position/rate of movement of various

body parts, the weight of an object being held in hand, &joints range of movement.

o Slowly adapting (Tonic) receptors: Accommodate very slowly. Ex. Know where little finger is without looking

o

Rapidly adapting (Phasic) receptors: Accommodate rapidly. Ex. You know where hand is as it moves

ii. Ascending (Sensory) Nerve Tracts:Carry the APs from the receptors to the CNS & ganglions Nomenclature: 1st half of word (origin) & 2nd half (termination)Ex. SpinoCerebellar tract Spino-Thalamic Tract:3-neuron system:

i. Primary: Periphery posterior horn of spineii. Secondary: Decussate, enter Spinothalamic tract Ascend to Thalamus, &

iii. Tertiary: Thalamus Somatic sensory cortex This tract can detect pain, temp, touch, pressure, tickle, and itch.


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iii. Sensory Areas of the Cerebral Cortex:Translate the APs into perception of pain.Sensory

Primary somatic sensorycortex (general sensory area):

Posterior to the central sulcus. Generalsensory input:

Pain, pressure, &

temperature Taste area: Inferior end of

postcentral gyrus Olfactory cortex: Inferior

surface of frontal lobe

Primary auditory cortex:Superior part of temporal lobe

Sensory speech: WernickesArea senses speech APs and

transfers them to the Motor speech: Brocas area to translate those APs into

motor functions.Association Areas

Somatic sensory: posterior to primary somatic sensory cortex Visual association: anterior to visual cortex: present visual

information compared to past information.

o Somatic Sensory Cortex: Homunculus The relative size of each region correlates to the # of

sensory receptors in that area of the body. Projection: The processing of info from the point of

origin of the stimuli to _____

Receptors:


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o Muscle spindles: 3-10 specialized muscle cells providinginfo about muscle-length & involved in

the stretch-reflex.

o Golgi Tendon Organ: Proprioceptors associated w/tendons that respond to increased tension.

o Referred Pain: Sensation in one region of body that is notsource of stimulus. Organ pain usually referred to the skin.

Both the organ and that region of the skin input to the samespinal segment and converge on the same ascending

neurons.

o Phantom Pain: Occurs in people who have appendages amputated or structures removed (tooth). Gate-Control Theory: In an uninjured limb, pressure & touch sensation can inhibit pain

(i.e. massage). This explains why amputees can experiencephantompain, since the lack of

pressure & touch sensation also leads to the lack of pain-inhibition.

Control of Skeletal Muscles:o Motor Areas of the Cerebral Cortex:

Motor system: Maintains posture & balance, moves limbs, trunk, head, eyes, facialexpressions, & conducts speech. Contains 3 motorareas:

i. Precentral gyrus (primary motor cortex/area): 30% of upper motor neurons, another30% in premotor area, and the rest in the somatic sensory cortex.

ii. Premotor area: Anterior to primary motor cortex. Motor functions organized beforeinitiation

iii. Prefrontal area: Motivation, foresight to plan and initiate movements, emotionalbehavior, & mood.

Reflexes: Movements that occur without conscious thought Voluntary movements: Consciously activated to achieve a specific goal in 3 steps:

i. Initiation in thepremotorareas of the cerebralcortex and results in the stimulation of upper motorneurons.

ii. The axons of the upper motor neurons form thedescending nerve tracts. They stimulate lower motorneurons which stimulate skeletal muscles to

contract.

iii. The cerebral cortex interacts with the basal nucleiand cerebellum in the planning, coordination and

execution of movements.

o Motor Nerve Tracts: Direct pathways:Control muscle tone and conscious fine,skilled movements in the face and distal limbs through the

directsynapse of upper motor-neurons of the cerebralcortex w/ lower motor-neurons in the brainstem or spinal

cord.

i. Corticospinal Tract: Direct control of movementsbelow the head.

ii. Corticobulbar Tract: Direct control of movements inthe head and neck.


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Indirect pathways: Control (un)conscious musclemovements in trunk& proximal limbs through indirectsynapse in intermediate nucleus rather than directly w/ lower

motor neurons.

i. Rubrospinal: Upper neurons synapse in red nucleus.Similar to comparatorfunction of cerebellum.Regulates fine motor control of muscles in distal parts

of upper limbs.

ii. Vestibulospinal: Influence neurons innervatingextensor muscles in trunk and proximal portions of

lower limbs; help maintain upright posture.

iii. Reticulospinal: Maintenance of posture. Cerebellum:

o Helps maintain muscle tone in postural muscles, controls balanceduring movement, and coordinates eye movements.

o Purkinje cells help control fine motor movements through: Comparative Function: The cerebellum compares the bodys

actual movements to the motor signals being sent from the

brain and adjusts accordingly. Parkinsons disease: The experiencing of tremors at restdue to damaged basal nuclei Cerebellum damage (comparative function damage), leads to an intendedtremor,

meaning not at rest, but when performing simple tasks, they become exaggerated.

Brainstem Functions: Gives way to all ascending/descending pathways.o Cranial nuclei 2-12, and many important survival reflexes are located here:

Heart rate, blood pressure, respiration, sleep, swallowing, vomiting, coughing, and sneezingo Reticular activating system (RAS): Controls sleep/wake cycle

RAS receives input from cranial nerves II (Optic), VIII (Vestibulocochlear), ascendingtactile sensory pathways, & descending neurons from the cerebral cortex.

Wakefulness is maintained by info coming in from the eyes, ears, and because of infocoming in from the cerebral cortex.

Other Brain Functions:o Speech: Area normally in leftcerebral cortex, since the rightside isnt as developed:

Wernicke's area: SensoryUnderstanding what is heard & thinking of what one will say. Broca's area: MotorSending messages to the appropriate muscles to make the sounds. Sound is heard 1st in the 1oassociation area, then info travels to Wernicke's area.

Neuronal connections exist b/w Wernicke's area (sensory) and Broca's area (motor). Aphasia: Absent or defective speech or language comprehension.

Caused by a lesion somewhere in the auditory/speech pathway.

Pic 1: Occipital lobe activation (looking before speakingVisual cortex) Pic 2:Brocas area is activated as youspeakyour words Pic 3: Cerebral cortex activation leading to more fine-tuned speech. Pic 4:Wernickes area is activated as you thinkabout what youre going to say


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o Cerebral Cortex: Outermost layered structure of the Cerebrum that is split into 2 cortices: Left cortex (controls rightside of body): Math & Speech Right cortex (controls leftside of body): 3-D/Spatial perception, know faces, musical ability Both sides of info, however, issharedthrough commissures (Corpus Callosum).

Brain Waves and Sleep:o Electroencephalogram (EEG): Record of brains electrical activity, through the summation of all of

the APs occurring at a particular moment sensed by electrodes placed on the scalp. Patterns include:

Alpha: Wakeful, resting state with eyes closed. Beta: During intense mental activity (Test-taking) Theta: Occur in children, in adults experiencing frustration, or in brain disorders (Stress) Delta: Occur in deep sleep, infancy, and severe brain disorders (large deflecting waves)

Note the pattern of nREM and REM sleep (Nystagmus).

Memory:o Sensory: Very short-term retention of sensory inputo Short-term: Information retained for few seconds to minuteso Long-term: Explicit or declarative (Retention of facts)

Accessed by hippocampus (actual memory) and amygdaloid nucleus (emotional)o Implicit (procedural; reflexive) memory: Development of skills (Riding a bicycle).

Effects of Aging on the N.S.o Gradual decline in sensory/motor function, slower reflexes, brain-size/weight dec., dec. short-term

memory, and changes in sleep patterns. (Long-term memory unaffected or improved).


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Ch. 18Pain

Understand the conceptual basis of the following:o Pain: Unpleasant sensory & emotional experience associated with actual orpotentialtissue damage

Whatever the experiencing person says it is, existing whenever he says it does.o Pain theory:

Specificity theory: Amount of pain is related to the amountof tissue injury. Accounts for many types of injuries, but does not explain psychological contributions

Gate control theory: Developed to explain the complexities of the pain phenomenono Neuroanatomy:

Nociception: Perception of pain Nociceptors: Bare nerve endings in skin, muscle, joints, arteries, & viscera that respond to

chemical, mechanical, and thermal stimuli (A fibers, Unmyelinated C polymodal fibers).

Various Pathways of Nociception


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o Neuromodulation of pain: This is achieved by neurotransmittersthat are released by neurons into synaptic terminals, but notreabsorbed or metabolized and end up diffusing into the CSF,

where they modulate the activity of different neuronal pathways.

Neuromodulators: Serotonin, Acetylcholine, etc. Function: May besegmentalinhibition of periphery

sensory axons, spinal interneurons, or Top-down control

pathways on spinal dorsal-horn regions.

Direct excitation: Threshold depolarization fromdirectstimuli.

Indirect excitation: Threshold depolarizationfrom inflammatory mediators post-injury.

EndorphinResponse:

o Clinical Description:i. Pain threshold: Point at

which a stimulus is

perceived as pain

ii. Perceptual dominance:Pain at one location maycause an increase in thethreshold in another

location.

iii. Pain tolerance:Duration of time or theintensity of pain that a person will endure before initiation of pain responses

o Pain types: Nociceptive PainReceptor-mediated pain (Pain from normal injury).

Somatic & Visceral Non-Nociceptive PainNeuropathic pain (Ex.Trigeminal Neuralgia)

Peripheral pain: Linked to PNS Central pain: Linked to CNS

Psychogenic PainPsyalgia Pain induced by mental/emotional state, but not induced by physical injury

o Ex. Heart-brokennesso Manifestations:

Acute Pain: Triggers Sympathetic system (fear, anxiety)Leading to the symptoms below: Protective mechanism:

o Alerts an individual to conditions/experience that immediately harms the body Symptoms:Tachycardia, hypertension, fever, diaphoresis, dilated pupils, outward

pain behaviors, elevated blood sugar levels, decreased gastric acid secretion andintestinal motility, and a general decrease in blood flow.

i. Somatic: Very high in # (Connective tissue, muscle, bone, skin)o A fibersPain is sharp and well localizedo C fibersDull, aching, and poorly localized

ii. Visceral:Not very high in # (Internal organs)o Poorly localized due to the lesser# of nociceptors.

iii. Referred Pain: Pain that is present in an area removed/distant from its point of origin.Ex. Myocardial infarction pain that radiates down the left arm.


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Chronic Pain: A situation/state that may develop suddenly or slowly and last for at least 3months w/ varying response patterns, producing significant behavioral/psychological changes Usually leads patients intoDepression. Common typesinclude:

i. Myofascial pain syndromes: Injury to the muscle & fascia (connective-tissue that covers muscle)

Spasm, tenderness, and stiffness.ii. Chronic postoperative pain:

Immediately after a surgery (nerve damage from cutting flesh)iii. Cancer pain:

Due to multiple reasons: Cancer mass pressure, cancer treatment side-effects, & diasthesia/paresthesia (pins-n-needles sensation).

Neuropathic Pain:Mostly results from nerve-trauma/disease (Postherpetic-Neuralgia)i. Diabetic:Painful neuropathy

Leads to damage of retinal ganglia/neurons.ii. Deafferentation pain: Unnecessary activation of receptors (w/out stimuli)

Usually due to receptor damage/disease.iii. Sympathetically maintained pain:

iv. Complex regional pain syndromes (CRPS): Plexus damage

Ex.Brachialplexus damage from sleeping on ones arms too much.v. Central pain:

vi. Phantom limb pain: Pain experienced despite the loss/realignment of a limb.

o Pediatric pain: Pathways/chemicals assoc. w/ pain are functional in preterm & newborns.

Nociceptorsystem is functional by 24 weeks (end of2ndtrimester) Expressions: Crying, facial expressions, & body language

o Aging pain:i. Increase in pain threshold: Peripheral neuropathies & Skin thickness changes

ii. Decrease in pain tolerance: More sensitive to painiii. Alteration in metabolism of drugs and metabolites in patients: Require a higherdosage of

medication to remove pain because ofincreasedmetabolic enzymes.

o Drug therapy for pain: Non-steroidal anti-inflammatory drugs (NSAIDs):

The NSAIDs inhibit the biosynthesis of hyperalgesic and proinflammatory PGs. Pharmacologically, they exhibit anti-inflammatory, antipyretic, + analgesic activity. Adverse reactions: Gastric-bleeding/ulceration & reduced platelet aggregation. Mechanism: Tissue damage Activates phospholipase-AWhich cleaves lipid-

bilayers & releases arachidonic acid Leaving the acid susceptible to attack by:

o COX-1: Produces Prostaglandins & Thromboxane (causes clots) Aspirin: Acts as a Thromboxane-inhibitor (dissolves clots)

o COX-2: Synthesized in inflammatory cells (neutrophils, mast-cells) followingbacterial endotoxin/cytokine exposure, and works to generate only

Prostaglandins at the site of inflammation/tissue injury

Ex. Tumor Necrosis Factor (TNF), Interluken-1 Most NSAIDs show little or no selectivity as inhibitors of the two COX isoforms, w/

the exception ofMeloxicam (Mobic), which is a relatively selective inhibitor of

COX-2 and combines anti-inflammatory & antiociceptive activity in animals. NSAIDsinhibitCOX-1 & COX-2Inhibitthe production ofprostaglandins.


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Other uses of NSAIDs:i. Pain of cancer metastases and some types of headache, which are also

associated with an inflammatory reaction.

ii. Dysmenorrhea, which results from increased uterine PG formation. NSAIDs are generally given orally and the analgesic activity is likely to

persist for approximately 6-8 hrs, although the effect of some NSAIDs suchasPiroxicam andPhenylbutazone (withdrawn several years ago) can last

much longer (12 hours -to- several days).

o Analgesics: Are drugs designed to provide relief from pain (painkillers) by affecting the PNS/CNS Unlike opioids or anesthetics in the sense that they do not numb the patient from sensation.

o Opioids: Interact w/ specific opioid-receptors to producepharmacologic effects. 3 main classes:i. Mu functions: Analgesia, sedation, inhibit respiration Slow GI (addiction-potential).

ii. Kappa functions: Analgesia, modulation of hormone & neurotransmitter releaseiii. Delta functions: Analgesia and affective behavior Slow GI Drug Interactions: Full or Partial agonists, mixed agonists (Full & Partial), + Antagonists. Adverse Effects: Respiratory depression, constipation, which leads to nausea + vomiting,

pupillary constriction, rapiddevelopment of tolerance, & physical dependence (addiction).

Ex: Morphine, codeine, heroin, methadone, meperidine, papaveretum, etorpine, fentanyl Very useful for neuropathic pain: like Trigeminal Neuralgia & Phantom Limb-pain.

o Pain sensitive and insensitive structures: Sensitive: Skin, scalp, muscles, arteries, skull periosteum (layer along bone), cranial sinuses

(headache), intracranial venous sinuses, parts of dura and base of brain, & arteries w/in dura. Insensitive: Brain parenchyma (no pain receptors), meningeal tissue, & abdominal viscera.

Ch. 19Thermoregulation

Understand the mechanism ofo Thermoregulation: The ability of an organism to maintain internal body temperature, where the mainvariables to consider are location, activity, environment, circadian (bio-clock) rhythm, & gender.

Humans are consideredHomeotherms, because of their ability to maintain body-temp, whereour core-temp (highest in rectalregion) is about 0.5-1oF warmer than ourperipheries.

The lowest body-temp is recorded at night, particularly around 2am. Gender differentiatesregions during different hormonal activity, such as body-temp inc. during ovulation.

This balance is mediated by:Hypothalamus & Neural/Hormonal mechanisms.o Means of heat Production: Metabolism, muscle-contraction, chemical thermogenesis (mediated by

brown-fat), & vasoconstriction. Mechanism: Hypothalamus releases TSH-releasing hormoneMakes the Anterior pituitary

gland release TSH Causes Thyroid to secrete ThyroxinMakes Adrenal-medulla releaseEpinephrineWhich stimulates Glycolysis, inc. metabolic rate, & vasoconstriction ( heat)

o Means of heat Loss: Radiation, conduction, convection, vasodilation (inc. permeability), dec.muscle-tone (post-exercise), evaporation, inc. respiration (goes both ways depending on airs temp.),

adaptation to warmer climates (usually takes around 2 weeks to adapt).

o Thermoregulation in pediatric and aging population: Pediatrics: Produce sufficient heat, but cannot conserve (high body surface-to-weight ratio),

small body, and thin subcutaneous layer (bad insulation).

Aging: Slower blood circulation, vasoconstrictive response, & metabolic rate, coupled w/decreased sweating and perception of heat/cold (sensation dec.) as receptors are lost/dec. Ex. Our average body-temp decreases as we get older (Adult: 96.899.5oF)


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o Neural axis for thermoregulation: Temp. Sensors (Thermoreceptors) in skin, abdominal

organs, spinal cord, & hypothalamus.

Sensory Nerves carry impulses to the neurons of thePreoptic nucleus (hypothalamicthermostat) in the anterior

hypothalamus. Autonomic nerves mediate vasoconstriction/vasodilation,

sweating, piloerection, & short-term increases in basal

metabolic rate. Motor nerves initiate voluntary/involuntary muscle

movement (Ex. shivering).

o Role of hypothalamus:It detects the bodys temp. & makes adjustments to maintain it: Hypothalamic Thermostat (Preoptic nucleus): Controls theset-pointfor body temp. Manifestations:Shivering (makes heat), vasoconstriction (reroutes blood to core to warm)

Fever: Pyrogenic hyperthermia that causes an elevation in body-temperature through pyrogen activation.o 4 Stages:

i. Prodrome: Period where patient feels cold & heat-activation mechanisms predominate.ii. Chills: Heat activation mechanisms are even more pronounced and shivering is present.

iii. Flushing: Vasodilation occurs to enhance heat-loss (removal of the pyrogenic stimulus), &iv. Defervescence breaking offever: Heat loss accelerated by evaporative cooling (sweating). Febrile seizures: Pediatric condition where fever is >102.5 and lead to seizures.

(feel cold) | (feel hot)

o Types:Etiology Exogenous pyrogens include bacterialtoxins & cell wall components, while Endogenous pyrogens include many cytokines produced during inflammatory responses.

o Production: Exogenous pyrogens (endotoxins) are phagocytized Causing the phagocytes torelease cytokines (TNF, IL)Which act on the preoptic nucleusWhich releases Prostaglandins Causing the set-point to shift higher So body adjusts temp. & releases more cytokines, which

provide negative feedback in efforts to help the body eventually get back to its normal body-temp.

o Treatment: Should not be given too quickly, or else the pathogenic microorganisms causing thisfever will continue to proliferate. Intervention is ideally aimed at the underlyingcause.

o Prognosis: Fevers induce mechanisms that help kill microorganisms (beneficial), dec. serum levelsof zinc, iron, & copper, lead to lysosomal breakdown, lymphocytic transformation, &phagocytosis.


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Hyperthermia: Notmediated by pyrogenso Symptoms: Convulsions (105.8oF), Death (109.4oF)High internal heat lead to protein coagulation.

Heat cramps: Severe spasmodic cramps in the abdomen/extremities afterprolongedsweating and associated sodium loss. This is common in individuals not accustomed to heat

or those performing strenuous work in warm climates (fever, rapid pulse, and inc. BP). Heat exhaustion: Collapse due toprolongedhigh core/environmental temp. from prolonged

vasodilation & profuse sweating (dehydration, depressed plasma, hypotension, dec. cardiac

output, & tachycardia Dizziness, weakness, nausea, and syncope.

Heat stroke: Potentially lethal result of a breakdown in overstressed thermoregulatory center The brain cannot tolerate temperatures >104.9oF (40.5oC), so temp. is maintained by

blood flow through the veins in the head/face, because Cardiovascular&

thermoregulatory centers may shut down if the temp. gets too high.

o Rapid peripheral cooling will cause peripheral vasoconstriction & limitcore-cooling,meaning that cooling should be donegradually and not just on extremities.

o Children are more susceptible: More metabolic heat during exercise, greater surfacearea-to-mass ratio, and less sweating capacity than adults (so less cooling off).

Leads to:Cerebral edema, CNS degen., swollen dendrites, & renal tubular necrosiso Treatment: Move patient to a cool area and remove any tight clothing that would restrict heat loss.

MalignantHyperthermia:o Complication ofinheritedmuscular disorder that is precipitated by the administration of volatile

anesthetics and neuromuscular blocking agents

Increased Ca2+release or decreased Ca2+uptake in muscles (sustained contraction) Increased O2 consumption and lactic-acid production.

Hypothermia: Body temp. falls below95oF(35oC)o Symptoms: Vasoconstriction, alterations in microcirculation (inc. blood viscosity & slows

circulation), coagulation, & ischemic tissue damage. Ice crystals form inside the cells rupture/die

i. Accidental hypothermia: Sudden immersion in cold water or prolonged exposure to cold.ii. Therapeutic hypothermia: Used to slow metabolism and preserve ischemic tissue during surgery or

limb reimplantation. May lead to ventricular fibrillation and cardiac arrest.

Trauma-induced Temp. change:o CNS trauma, accidental injuries, hemorrhagic shock, major surgery, & thermal burns

Headache: A mixture of nociceptive & neuropathic pain that haveprimary disorders +secondary effectso Risk factors: Stress, Depression, Sinus infection, Fatigue, Hypertension, Constipation, Caffeine,

Hormonal cycles/therapy, Cigarettes, Alcohol, and some foods (cheese/chocolate)

o Types: Acute vs. Chronic or Vascular vs. Tension (Medicated w/ OTC analgesics & TCAs)i. Tension:Muscle contraction associated w/ stress or activities (assembly line, sewing, or

keyboard work) that may directly deform pain receptors or may compress blood vessels,

leading to ischemia (inadequate blood supply). Pain-band around head & down back of neck.ii. Vascular: Some degree of hyperemia (too much blood) within the cerebral and scalp vessels

which may or may not be preceded by a period of vasoconstriction.

o Pathophysiology: Neural tissue does not have pain-receptors, but there are many receptors in themeninges, skull, & blood vessels and in the muscles of the face, scalp, and neck.

o Mechanisms of headache: Distention/displacement/pulling of blood-vessels, contraction ofhead/neck muscles, stretching of periosteum, upper-spine degeneration, & encephalin deficiency.

High risk: Worst headache, vomiting, neck-stiffness, photophobia, & neuralgic deficits. New headache in older persons: Depression, subdural hematoma, & intracranial masses.


18/18

Migraine:Prototype headache that can be Classic (with aura) orCommon (without aura)o Symptoms: Unilateral, throbbing pain (4-72hrs), nausea, phonophobia & photophobia.

1/8 adults (age:25-34) have them, women

pathophysiology exam 4 - review

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