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Parkinsons Major clinical SX

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Title: Parkinsons Major clinical SX


1
Parkinsons Major clinical SX
  • Bradykinesia slowness of mvt, diffic
    initiationg movt
  • Muscular rigidity increase in mm tone
  • Resting tremor pill rolling
  • Stooping posture
  • Festinating gait shuffling gait, once initiate,
    rapid acc.
  • Due to deficit in DA in NSP, which contains 80
    DA in brain, SX appear after 80-90 DA depleted
  • Cause Unknown, genetics? Free-radicals?
  • Extrapyramidal System fine motor mvts, mm tone,
    posture
  • Cell bodies SN PC project fibers to
  • Nerve terminals NSP StriatumCaudatePutamen
  • NSP modifies output of desc motor pathway to
    turn gross mvt into fine mvt.

2
  • Indirect No-Go Cortex sends Glu to
    Caudate-Putmamen (Striatum), Glu excites Ach,
    which excites the GABA neuron going to LGP, which
    sends GABA to Subthalamic Nucleus, which sends
    Glu neuron to MGP/SNr, which sends GABA to
    thalamus, which inhibits Glu neuron leaving
    thalamus and going to Cortex. Result Mvt
    inhibited
  • Direct Cortes sends Glu to Striatum, which sends
    GABA to MGP/SNr, which sends GABA to thalamus,
    which sends Glu to Cortex. The GABA leaving the
    striatum inhibits the GABA leaving the thalamus,
    so that mvt is promoted, or disinhibited.

3
  • Nigrostriatal Pathway modifies mvt. Cortex
    sends neuron to SNc, which secretes Glu, which
    excites neuron w/in wihc secretes GABA, which
    inbigits neuron w/in which goes to Striatum, and
    has two branches w/in Striatum, both secreting
    DA. D2 secretes DA-, D1 secretes DA. THE DA-
    inhibits the No-Go pathway, and the D1 excites
    the Go pathway.
  • In PARK, NSP degenerated, causing DA deficit
    No-Go pathway predominates, Ach increases with
    breakdown of NSP

4
  • Most antipsychotics are D2R blockers, if you
    decrease DA, you increase Ach
  • Why Dopamine agonists, anti-muscarinics work with
    PARK.
  • Physiologic Tyrosine conc saturates toyrosine
    hydroxylase
  • L-tyr ? L-Dopa ? DA ? NE ? Epi
  • Enz tyrosine hydroxylase (RLS), Dopa
    Decarboxylase DA doesnt cross BBB, enzymes for
    NE, Epi not in brain
  • 10 neurons remaining are enough, takes several
    mos to see effects, degen continues, so effect
    diminishes with time. If tyrosine ?, l-dopa
    doesnt work as well

5
  • On-off effect fluctuation in response to l-dopa
    due to
  • DZ progression
  • Duration of TX, the longer youre on, the more
    likely
  • Fluctuations in dietary AAs, esp aromatics
  • 90 l-dopa converted to DA in periph, need large
    doses, ? SEFX
  • NV Stim Chemo-receptor Trigger Zone, in area
    postrema, floor of 4th ventricle, not portected
    by BBB
  • Many anti-emetics are phenothiazines,
    (prochlorperazine) D2 antagonists interfere w
    TX of l-dopa
  • Minimize with CARBIDOPA periph decarboxylase
    inhibitor keeps L-dopa from being converted to
    DA in periph,
  • LODOSYN Carbidopa alone

6
  • SINEMET 25mb Carbidopa/100 mg l-dopa 3X a day
    PRVN NV
  • SINEMET CR minimizes on-off effect
  • Also 5HT-3 antagonists
  • DOLASETRON
  • ONDANSETRON
  • GRANISETRON
  • Anti-histamines
  • BENZTROPINE
  • MECLIZINE
  • EMETROL phophrylated carbo soln, OTC
  • Can take l-dopa with food/milk, ? absorp, delay

7
  • DA can also stimulate alpha and beta R
  • Transient tachycardia CXN CV problems
  • DA stimulates B1 in heart
  • Give Propanalol beta blocker
  • Orthostatic hypotension changes in BP due to
    changes in posture
  • L-dopa psychosis elderly, meso-limbic pathway,
    cant use typical anti-psychs block DA R,
    interfere with TX.
  • Atypical CLOZAPINE, QUETIAPINE block 5HT-2
    receptors (Serotonin)
  • Orofacial dyskinesias tongue, face,
    supersensitive D2 Rs Degen of presyn term ?
    upregulation postsyn Rs,
  • Lactation ? DAPIF, TX with CARBIDOPA

8
RX Interactions w L-dopa
  • PYRIDOXINE Vit B6 Co-fctr for tyr Hase
  • PHENOTHIAZINES BYTYROPHENONES D2 Antagonists
  • NON-SELECTIVE MOA-Is MAO A, B
  • Phenelzine
  • Tranylcypromine
  • Isocarbozaxid
  • MAO-A in gut NE, EPI, 5-HT
  • MAO-B in brain DA
  • Tyramine, found in cheese, beer, metab by MAO-A,
    ? plasma levels enters NE terminals and adrenal
    medulla, metab to
  • NE, which is ? due to MAO-I,
  • Octopamine displaces NE
  • Net effects vasoconstriction, hypertensive
    crisis, () Inotropic/Chronotropic EFX

9
  • SELEGILINE relatively selectively INH
    MAO-B??HTN crisis Dose-dependent
  • Blocks DA uptake
  • ? activity catalase super oxide dismutase ?
    free radical scavenging
  • Metab to amphetamine and methamphetamine ?
    anxiety and insomnia
  • RX Interactions
  • MEPERIDINE(Demerol) Serotonin Syndrome stupor,
    rigidity, agitation, hyperthermia Mech blocks
    5HT uptake ??Serotonin transmission, perhaps
    Selegine also Inh MAO-A
  • TCAS AND SSRIS block Serotonin re-uptake
  • SELEGILINE gen taken with l-dopa or SINEMET

10
COMT Inhibitors
  • TOLCAPONE adjunct to l-dopa, selective inh of
    COMT ?DA
  • Do NOT use with non-select MAOI eliminates all
    mech of metab of catecholamines
  • Problem with Seleginine will INH MAO-B, so ? DA
  • SEFX 3 cases FATAL LIVER FAILURE
  • USE adjunct to l-dopa/carbidopa for On-Off
    phenom
  • ENTACAPONE Selective INH of COMT short t1/2
    2 hrs, so used onle with L-D/C
  • No sig HEPATOXICITY with this RX

11
Direct Acting DA Agonists
  • Conversion not required, longeracting drups, so
    no ON-OFF
  • BROMOCRIPTINE Ergot deriv LSD
  • Strong D2 agonist, partial D1 Agonist
  • Fewer dyskinesias stim D2 Rs but blox D1 Rs.
    Must stim D1 D2 to get full motor effect.
    Blocking D1 Rs diminishes dyskinesias
  • SEFX NV, Stim D2 in CTZ, confusion,
    hallucinations, hallucinosis persistent halluc.,
    HTN titrate dose slowly
  • TX Galactorrhea Acts on PIF

12
  • PERGOLIDE Ergot weakly stim D1 D2, adjunct
    for serious dyskinesias and On-Off phenom
  • SEFX ? Hallucinosis, ? Prolactin release
  • PRAMIPEXOLE non-ergot, D2 Selective
  • ROPINIROLE Non-ergot, D2 selective
  • Both do not cause HTN, but both cause SUDDEN
    SLEEP ATTACKS

13
  • MISC DAergic RX
  • AMANTADINE Sole agent in mild cases, anti-viral
    for flu
  • Mech ?DA release, ?DA uptake, Anti-muscarinic
    axn bc I PARK - ?Ach
  • CNS SEFX Confusion, dizziness, anxiety
  • PNS Constipation, dizziness, anxiety, LIVEDO
    RETICULARIS (1-5) benign red or blue patches on
    extremities

14
  • Anticholinergics block Ach-R, so ?Ach doesnt
    harm muscarinic antagonists
  • Nicotinic NMJxn, ganglia, adrenal medulla
  • Muscarinic others
  • TRIHEXYPHENIDYL prototype
  • BENZTROPINE
  • PROCYCLIDINE
  • BIPERIDIN
  • DIPHENHYDRAMINE Benadryl, anti-hist
  • SEFX CNS elderly confusion, depression,
    hallucinations PNS sedation, dry mouth, blurred
    vision, constipation, tachycardia all anti-PARA
    SX
  • CXN Narrow angle glaucoma PARA constricts
    ciliary mm, widens angle, block ciliary relaxes,
    no drainage, IOP up.

15
Barbituates
  • Sedative ? anxiety, calming effect w/o altering
    mental/motor fxn.
  • Hypnotic produce drowsiness
  • Into disfavor
  • Low TI (TITD50/ED50) Suicide
  • Tolerance RAPID work 3-4 nights MAX
  • Pharmacodynamic fxnal tolerance body changes
    hemoestoci mechs
  • Cross tolerance to ROH, opiods, benzodiazepies
    via down regulation receptors
  • Pharmcodynamic way body metab and disposes of
    drug Quick response enzyme indxn
    P450/microsomal enz
  • High abuse liability controlled substance DEA
    - withdrawl SX - FATAL
  • ?? Drug intrxn from Enz Indxn

16
Sleep cycles
  • 4 stages plus REM (paradoxical/fast wave)
  • Each stage deeper, REM subset of 1
  • Barbs supress REM, 1, 3, 4, but ? 2, ? total
    sleep time
  • Spontaneous awakening from REM
  • External Stimuls awakening non-REM, no brain
    filtering
  • Prolonged sleep latency cant fall asleep,
    shorter duration drug used for TX
  • Early morning awakenings cant sleep long
    enough longer action drug used for TX
  • Sudden discont BARBS REM-rebound ?nightmares
  • Tolerance due to sedative-hyponotic EFX, get
    hangover

17
Site of axn for BARBS
  • GABA A Receptor Complex ionotropic R directly
    linked to ion channles
  • 5 different subunits from total of 8 diff types
  • Each subunit exists in multiple isoforms
  • Min receptor requirements for BARB a, ß
  • ? subunit has 2 sites GABA and BARB
  • Binding GABA ? ? gCl ? hyperpolarization
  • Binding BARB ?GABA binding ? ? gCl ? etc
  • Benzos ? frequency channel opening
  • Net effect BARB prolong duration opening
  • All BARB anticonvulsant, but too sedating
  • TX doses REQUIRE GABA, Toxic directly open Cl
    channels
  • block Glu AMP Rs, allows inb ctrs to put brain to
    sleep

18
  • Ultra-short acting BARBs 20 min
  • Thiopental IV rapdi indxn, rapid recovery from
    anesthesia, pass by delirium (stage 2)
  • Venodilates ? venous capacitance ? ? BP by 20-30
    mm Hg ? ? HR (reflex)
  • Resp depression normally leads to ? ICP, but
    not with BARBs due to venodilation
  • Hyperalgesia - ? pain sensitivity.
  • HIST release
  • METHOHEXITAL
  • No Hist release still get bronchospasm
  • No venodilation thiopental only venodilator

19
  • Short-acting barbituates 3-4 hoursSedative-hypno
    tics, pre-anesthesia
  • PENTOBARBITAL anticonvulsant
  • SECOBARBITAL
  • Good for prolonged sleep latency
  • Intermed acting barbs 6-8 hours
  • Early morning awakening
  • AMOBARBITAL
  • BUTABARBITAL
  • Tuinal Secobarbital Amobarbital both

20
Long-acting 24 hoursnot good sedative too long
  • PHENOBARBITAL Antiepileptic, Status epilepticus
    (series of grand mals)
  • MEPHOBARBITAL N-methyl phenobarbital,
    demthylated by liver to phenobarb, contra liver
    DZ, not used much use sedative for anxiety,
    tension
  • BARBS Weak Acids so you alkalinize the urine
    to ionize the weak acid, so it can clear

21
SEFX BARBS
  • Paradoxical excitement inbibition of inhibitory
    process
  • Enzyme Indxn Pharmacokinetic ?p450
  • Leads to ?metab ??drug interxns
  • Resp depression depresses neurogenic drive with
    only 3X dose. Higher doses depress hypoxic and
    chemical drives to resp
  • Hangover effect daytime sedation
  • RX Interxn additive with other CNS depressants
  • CONTRA acute intermittent porphyria
    neuropathis, enzyme indxn toxic precursors

22
Benzodiazapines (BZ)
  • Uses S/H, anxiolytics, anesthetics,
    pre-anesthetics, anticonvulsants, musc relax
  • BZs do NOT cause
  • CNS depression
  • ENZ Induction leads to ?? drug
  • BZs have
  • High TI (LD50/ED50)
  • No signif resp depression
  • Caveats alcoholic, COPD BZs cause resp
    acidosis
  • Pts w OSA exaggerated EFX on albeolar hypoxia,
    pulmonary HTN, ventricular load
  • BZ snoring to OSA (Obstruc Sleep Apnea)
  • BZs suppress REM and all stages except stage 2,
    ?
  • ?Stage 4 Night terrors wake screaming from
    deep sleep, acts on RAS

23
Mech of axn of BZs
  • BZs bind at interface of a and b subunits of
    GABA-A Rcx, gama subunit REQUIRED. Binding to BZ
    site enhances binding of GAMA to beta subunit
    hyperpolarization
  • Net effect ? frequency
  • Without GABA, no effect on gCl
  • 2 types receptors omega BZ-1, BZ-2
  • Determined by Isoform of a subunit
  • BZs sed-hyp hi affinity BZ-1 Rs with a-1
    isoform
  • BZ-2 a-5 isoform anticonvulsant, mm relaxant
  • BZs nonselective unless otherwise stated, BZ -1,
    2
  • In proper dose ALL HAVE SED-HYP ACTIVITY
  • Allosteric relationships bt sites

24
BZs used as SED-HYPs
  • TRIAZOLAM t½ lt6h PSL
  • Quick tolerance, try intermittent use, amnesia
  • TEMAZEPAM - t½ 6-24 h, EMA
  • ESTAXOLAM -
  • FLURAZEPAM - t½ gt24h
  • Active metabolite desalkylflurazepam
  • Hangover effect, NIGHTMARES
  • QUAZEPAM long acting 2-oxo-quazepam
  • Both selective for BZ-1 receptor
  • MIDAZOLAM IV-preanesth, only anesth in some
    cases

25
  • FLUMAZENIL
  • only BZ Antagonist used clinically
  • Reverse the sedative effects of BZs
  • Pre-op or post-op
  • TX BZ OD
  • Clonidine Anti-HT
  • Causes sedation
  • ?2 agonist
  • Decrease sympathetic outflow

26
Misc sedative-hypnotics
  • ZOLPIDEM NON-BZ
  • Binds to BZ-1 sites on a subunit of GABA-A R Cx
    ?gCl-
  • Rapid onset, short dura PSL,
  • Doesnt alter sleep stages, not good for night
    terrors
  • ZALEPLON BZ-1 site, t½1hr, PSL
  • CHLORAL HYDRATE knock-out drug
  • Sed-Hyp, act metabtrichloroethanol,
  • BARB-like effect on GABA-A Receptor
  • NV, Hangover effect, sleep cycle like BARB, less
    ? in REM
  • PARALDEHYDE intox, tolerance, phys depen
  • Sedation in
  • Delirium tremors drug withdrawals
  • ER TX convulsions
  • DEXMEDETOMIDINE IV ICU mech vent
  • a2 agonist does not interfere w GABA,
  • ?1- Rap IV hypoTN, brdcardia, sinus arrest, ?
    vagal tone, barorflx

27
  • Factors governing sensitivity of nerve fibers to
    local anesthetic
  • Small diameter appear more sensitive
  • Pain fibers more sensitive
  • Non-myelinated more more susceptible
  • Myelinated blocked before non same diameter
  • Critical length length of neuon that must be
    exposed to Rx
  • 3 successive nodes must be blocked
  • The larger the fiber, the greater the the CL
  • Frequency and use dependance of neuron
  • ? Rx access to site of axn
  • MOA block voltage sensitive Na channels
  • Binding site for Rx inside a subunit.
  • The more frequently used, the more likely to be
    open

28
  • Na channel has 3 subunits, ß1, 2, a req for
    activity, 4 domains form ion channel w/in memb
    as neuron deopolarizes, ea domain will change
    charge and conform, causing channel to either
    open or close
  • After opening, channel enters inactivated state
    which is desensitized.
  • Local anesthetics prefer binding to OPEN and
    INACTIVATED states.
  • Binding to prefered states
  • STATE DEPENDENCE
  • Lipid soluble drugs go right in
  • Cationic form of Rx greatest affinity for R which
    must be accessed from intracellular side of
    channel must pass thru open channel

29
2 categories local anesth
  • Esters metab by plasma exterases shorter acting
  • Amides metab by LIVER longer acting
  • Hydrophillic grp 2ary or 3ry amine
  • Hydrophobic grp aromatic ring

30
Procaine short acting 15 min
  • Infiltration anesth minor surgery, dental
  • DX nerve blocks block plexus
  • Musc relax
  • DX spinal anesth
  • Intrathecal subarachnoid space lumbar level
  • Blocks sensory motor fibers below diaphragm
  • Control spread of anesth w/in SAS by
  • Adjusting specific gravity
  • Hyperbaric 10 glucose added
  • Hypobaric sterile water added
  • Adjusting tilt of patient
  • Many pts sensitive to esters, amides preferred
  • TOXIC EFX Resp ? - blocking Na channels

31
CHLOROPROCAINE
  • Rapid onset, short duration ? Toxicity
  • Uses infiltration, peripheral and epidural nerve
    block
  • Epidural associated with ? incidence of muscular
    back pain, possibly from tetany due to chelaiton
    of Ca2 by EDTA

32
COCAINE Intermediate acting
  • Topical use on mucous membranes
  • 4 and 10 solutions available
  • Vasoconstrictor blocks NE uptake
  • Advantages
  • ? systemic EFX from ? blood flow
  • ? duration
  • Control bleeding
  • CXN can slow wound healing
  • Other locals add vscnstr epi, phen
  • Systemic EFX
  • EUPHORIA block DA uptake mesolimbic
  • Tremors and convulsions ? excit tone, NE
  • Resp ?, death block Na channels
  • CV block NE uptake, beta at high dose
  • Hyperpyrexia block NE vasocon hypothal
    disrupt

33
TETRACAINE long acting 2-3 hours
  • CXN
  • Cardiotoxicity ext block Na chan
  • Vasodilates block Ca channels
  • ? risk to system
  • Uses No longer used
  • Pot SYS EFX all locals
  • Sys absorption from vasodilation via blocking Ca
    channels
  • Reflex ? HR, palpitations, chest pains,
  • Phenylephrine prfer bc no ß efx
  • Profound vasoconstriction reflex ? HR

34
PROPARACAINE Ophtalmic
  • Ester and ester link
  • Does not exhibit cross-sensitivity to other
    esters
  • Uses
  • Ophthalmic surgery
  • Removal of sutures
  • Removal foreign objects

35
Amide locals int act 30-90 min
  • LIDOCAINE
  • faster onset, longer than procaine
  • Topical pain, itch minor burns, hems, rash
  • Injexn infiltration, spinal, NN blocks,
  • Ventricular arrythmias block Na channels
  • SEFX seizures, coma, resp ?, resp arrest
  • MEPIVACAINE infiltr, epidural
  • Not OB lower Ph in neo blood ion trapping
  • PRILOCAINE 1.8 ML Dental cart only
  • Systemic TOX met Hbemia
  • Tx methylene blue

36
Long acting amides
  • BUPIVACAINE 2 4 hrs,
  • Varoius strengths w, w/o epi
  • Can be cardiotoxic
  • Uses similar to LIDOCAINE
  • LEVOBUPIVACAINE
  • Levorotary isomer of bupivacaine
  • Purified isomer
  • Uses
  • local and regional surgical anesthesia
  • Post-op pain management

37
Topical use skin, mucosa only, no eyes
  • DUBUCAINE cream, sunburn, rash, bites
  • DYCLONINE 2 ether links
  • Endoscopic procedures mucosa
  • PRAMOXINE 2 ether links sunburn
  • BENZOCAINE procaine wo NH2 grp
  • ?H2O solubility, ? systemic absorp
  • Topical dir to wound, sunburn, orajel lg area
    oral cav
  • BUTAMBEN OTC mucosa mouth sores
  • OPIODS morphine epi, intrathecal
  • ABSOLUTE ETOH
  • near NN trunks for intratractable pain Tic Delou

38
  • What are the four symptoms seen in Horners
    Syndrome?
  • Anhydrosis
  • Ptosis
  • Pigment changes (Lighter colored Iris) esp.
    congenital
  • Miosis
  • What is the most important part of the visual
    examination?
  • Visual acuity test

39
  • How would you treat a patient with orbital
    cellulitis?
  • Get them to the emergency room
  • Hospitalization
  • Massive I.V. antibiotics
  • Warm compresses to increase blood flow
  • Get sinus x-rays
  • Why is it important to get the patient to the ER
    quickly?
  • Patient can develop meningitis and die
  • Why do you need to hospitalize patients with
    orbital cellulits?
  • Because they need to start massive I.V.
    antibiotics and this is the only location that
    they can do this.
  • Why would you want to get sinus x-rays in orbital
    cellulitis?
  • Because infection can spread from the sinuses

40
  • Herpes Zoster if nose tip involved, elevated
    IOP, inflammation inside eye iritis,
  • Retinal detachments flashes, floaters,
    peripheral loss of vision,
  • Corneal abrasions Ab ointment, pressure patch,
    check the NEXT DAY, and the NEXT DAY, until it
    heals.

41
  • What are the two ocular changes seen in herpes
    zoster (vesicles seen on face)?
  • Ocular inflammation, also on nose
  • Secondary glaucoma (increase IOP) (so check eye
    pressure w/herpes-zoster pts)
  • What is the other name for ocular inflammation?
  • Iritis
  • What is the most common type of glaucoma?
  • Open-angle
  • What is not functioning properly in open-angle
    glaucoma?
  • Trabecular meshwork
  • Is the eye pressure in open angle high or
    moderate?
  • Moderate

42
  • Will the patient with open angle glaucoma
    typically have early symptoms?
  • No only after many years
  • Do patients with open angle usually lose
    peripheral or central vision?
  • Peripheral
  • How would a non-ophthalmologist measure eye
    pressure?
  • With a Shiots Stenometer
  • Where is aqueous humor produced?
  • Ciliary bodies
  • What of the population has open angle glaucoma?
  • 1 ½ gt 40 years of age

43
  • What is the high limit of normal eye pressure?
  • 21 mmHg (gt 21 look into a problem)
  • Where do the axons of the ganglion cells project?
  • They follow a course to the optic nerve
  • Which part of the eye has a more direct route to
    the optic nerve?
  • Macula
  • What happens (damage) with IOP?
  • Decreased blood flow to the optic nerve and you
    see cupping or indentation of the optic nerve
    which results in loss of vision (retrograde
    degeneration)
  • If the patient has inferior retinal loss, what
    area of the eye field is lost?
  • Superior eye field

44
  • What is the easiest way to lower IOP?
  • Eye drops timoptic (timolol)- a beta blocker
    that decreases aqueous production.
  • If patient is taking eye drops for glaucoma and
    continues to lose visual field, what is the next
    appropriate step?
  • Use laser surgery on the trabecular meshwork (
    open and stretch) allows aqueous to flow out
  • If laser surgery is not effective, what is the
    next appropriate step?
  • Perform a trabeculectomy

45
  • How is the trabeclulectomy performed?
  • Create a flap in the conjunctiva, then a
    superficial cut into the sclera then a full
    thickness cut into the second layer of sclera,
    and then remove a piece of the iris. Then suture
    the superficial flap followed by the conjunctiva
    flap. Aqueous flows under the trap door created
    instead of the trabecular meshwork.
  • Which type of glaucoma is rare but more serious?
  • Narrow angle or closed angle glaucoma

46
  • Instead of moderate pressure as in open angle,
    these patients can have pressure in the 70-80
    range. Besides acute pain, what else happens at
    these pressures?
  • 1. Cornea becomes cloudy or hazy (poor vision
    quickly)
  • 2. Eyes become very red
  • 3. Pupil no longer responsive
  • 4. Very often nauseated
  • 5. Eyes dilated
  • Is narrow angle glaucoma more common in men or
    women?
  • Women ( 3 fold higher)

47
  • What happens if the pressure in the eye stays at
    70 for more than 24-48?
  • Permanent vision loss if untreated
  • What are the two medical emergencies in
    opthamology?
  • 1. Alkaline burns
  • 2. Central retinal artery occlusion
  • Do vasoconstrictor eye drops alone work well in
    narrow angle glaucoma?
  • Not really ( dont penetrate the cornea)

48
  • How would you treat narrow angle glaucoma?
  • 1. Start on I.V. meds that pull fluid out of the
    eye via surrounding blood vessels (Mannitol or
    Diamox)
  • 2. Vasoconstrictor eye drops
  • 3. If patient is diagnosed ? laser surgery to
    burn a hole through the iris, to prevent likely
    reoccurrence. (patient no longer requires eye
    drops)
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