Lecture notes - parkinson, pituitary disorders, psoriasis, psychosis and schizophrenia PDF

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- - - merged files: PARKINSON.docx - Pituitary_Disorders.docx - Psoriasis.docx - Psychosis_and_schizophrenia.docx...

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PARKINSON’S DISEASE - Slow progressive neurodegenerative disorder where the dopaminergic neurons in substantia nigra. o i.e ↓DA in nigrostriatal pathway (in basal ganglia)-involved in movt o get imbalance with ↓DA, ↑Ach - Cause: 1*=genetic 2*= o Other neurodegenerative dis e.g structural lesions o Chemical toxins e.g pesticides o Meds: **dopamine antag  antipsychotics (as block DA recep) Antiemetics= Prochlorperazine, Metoclopramide  Droperidol, Haloperidol (also anti-psy first gen)  Tx: Domperidone- use instead as it doesn’t cross BBB so not block DA recep in nigrostraiatal pathway e.g Domperidone 10mg q8 hrs - Sx: - Non-motor sx: o autonomic disturbances e.g constipation, bladder dysfunction, sexual dysfunction o neuropsychiatric distubrances e.g depression, dementia, sleep disorder (REM sleep disorder), psychosis - Motor sx: TRAP o tremor, rigidity postural/gait abnormalities o Tremor: occurs at rest but goes away when do something,  is ‘rhythmic pill-rolling’ so like when roll pill w/ finger o muscle Rigidity:↑muscle tone, so not fluid motion (i.e resistant to movt e.g stiff limbs)  face is rigid infreq blinking, look unfriendly/reptilian stare o Akinesia/bradykinesia: suppression of vol movt (slow &↓movt), e.g o Postural instability: impaired balance/falls - Other: o pain (cuz muscle rigid) o Voice, writing changes= ↓ volume (hypophonia), monotone, wiritng gets maller and eligible  Due to muscle rigid o Autonomic dysfunction (NMS)  Loss of smell, orthostatic hypotension, drooling, bladder dysfunction, constipation, sexual dysfunction

Complication: depression, dementia, ↓Qol as can’t do simple activities like running Tx: Sx relief (no cure or agent to slow progession of dis) Initial tx of PD- early dis= levodopa or DA agonist - All med used to Tx PD can cause hallucination (due to too much DA in mesolimbic/mesocortical pathway) + PD itself can cause hallucination - All PD med start low dose & ↑(according to sx of PD) Levodopa (L) - MOA: Is the precursor of dopamine. It’s lipid sol so able cross BBB unlike DA hence why (L) is used. Its converted in body to DA by DA decarboxylase ↑DA in CNS - Tx: 1st line for >60yr w/ cognitive impairment o (not 1st line for 100g per week) Monitor: for hyperkalaemia so N,V constipation, polyuria (excessive urine as Ca), thirst (from ↑urine) o Ca2+ lvls 6. Dithranol (anthralin) e.g 0.5% d MOA: Antiproliferative effect Tx: mainly used for plaque psoriasis C/I for face, flexures, genitals ↑strength, ↓contact time e.g high strength >2% only for ½ hr then wash off. 7. Tazarotene (Topical retinoid) MOA: Anti-inflammatory and antiproliferative effective for plaque psoriasis ↑efficacy with CS use; Reduces tazarotene irritation and the development of atrophy with steroid use o Promising results with UV therapy Avoid in women of childbearing age as c/I preg a/e: redness, pruritus, burning,

Phototherapy - Natural – sunlight - Artificial: o UVB broadband – wavelength 290-320 nm (so covers larger range=braod) o UVB narrowband – wavelength 311-313 nm o UVA – wavelength 320-400 nm - PUVA (photochemotherapy)- Administration of a photosensitising agent before UVA exposure MOA: has immunosuppressive effects Tx: It is Reserved for patients: - Failed to respond to aggressive topical therapy - Widespread disease Dose: Controlled exposure to UV radiation to - Entire skin or restricted area - 2-3 times weekly at first then reduce to once every 2-4 weeks once remission achieved UVB Broad band (290-320nm) phototherapy Tx: May be used alone or in combination with tar OR for Monotherapy effective in mild psoriasis ( olanzapine>quetiapine  MONITOR FOR Sx OF METABOLIC SYNDROME: weight Hyperprolactinaemia  Can cause impotence, man boobs, ↓libido,  Amisulpride, risperidone, paliperidone, classical antipsychotics Neuroleptic malignant synfrom (NMS)  Similar to serotonin syndrome (occurs immediate) but takes longer time (days) to develop  HoLETHAL  NEED TO STOP ANTIPSYCHOTIC  Symptoms o EPSE: Muscle rigidity o Hyperthermia (fever) o ↑ HR, BP o CNS: Confusion, drowsiness  Lab findings o ↑ CK, WCC o Iron deficiency o Metabolic acidosis o Renal failure, hepatic impairment  Treatment - DISCONTINUE DRUG - Hydration and cooling

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Monitoring

Switching antipsychotics  For a non acute patient should have a 1-2 week washout period  If patient is acute  no washout, try cross tapering (i.e. reduce dose of first drug and gradually increase dose of second drug)  Depot take longer to washout than oral Polypharmacy (use more than 1 anti-psychotic) is not recommended but it is done Augmenting (not much evidence)  Antiepileptics- ↓mood, aggression e.g. sodium valproate, lamotrigine, carbamazepine  Lithium  Benzodiazepines  Beta Blockers Acute psychotic Agitation/arousal (e.g agitated, violent, noisy)  AIM = SEDATION (sue injection to bring them down quickly)

(classical more sedation than atypical hence 2nd line)

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Zuclopenthixol (classical antipsy) - Tx: Reserved for extremely agitated patient - Dose: 40-150mg IM every 2-3 days (Max 400mg a course) - Has high incidence of EPSE and risk of NMS

Key messages 1. Delusions vs hallucinations; positive vs negative symptoms 2. Significant relapse rates 3. Select an anti‐psychotic to suit the individual 4. Classical vs atypical anti‐psychotics 5. Consider depot anti‐psychotic for non‐compliant patients 6. Minimise ADR: monitor for NMS, EPSE and Metabolic Syndrome...