General psychiatry Flashcards
(25 cards)
Lithium - distribution in body after a dose?
Concentrated in thyroid and kidney
Lithium - excretion?
Almost wholly excreted in urine.
Depends on: GFR, reabsorption at proximal renal tubules, alkaline urine.
Lithium toxicities and association serum level:
Lithium toxicity:
0.6-1mmol/L - tremor
1.5-3mmol/L - diarhorrea, ataxia, thirst
>3mmol/L - confusion, spasticity, seizures, dehydration, coma.
Hypothyroidism and CKD are ASEs that are not serum level dependent.
Agents that reduce lithium clearance:
- THIAZIDE DIURETICS (classic interaction leading to toxicity)
- K+-sparing diuretics
- ACEi
- Most NSAIDs
- Loop diuretics can either increase or decrease serum levels!
Any condition causing volume depletion or renal impairment will increase reabsorption of lithium
(eg. GI losses, acute decompensated HF, cirrhosis, diuretics, NSAIDs, ACEi).
Agents that increase lithium clearance:
- Sodium bicarbonate - this works because increased plasma bicarb leads to greater urinary bicarb excretion. However, because bicarb is an ANION, there is need for a CATION to also be excreted, hence lithium is booted out.
- Loop diuretics
(though can decrease clearance by causing volume depletion - VERY IMPORTANT) - Osmotic diuretics
Renal toxicities of lithium:
- Nephrogenic diabetes insipidus (resistance to ADH)
- Distal RTA (incomplete) - increased backflow of H+ ions. urine pH >5.3, but extracellular pH and [HCO3-] are WNL
- Nephrotic syndrome (not common)
- Oedema during manic phase ?due to increased salt intake - Chronic interstitial nephritis, fibrosis and CKD (related to duration and cumulative dose)
- HyperPTH and HyperCa2+ (with hypocalciuria)
How do you treat nephrogenic DI due to lithium toxicity?
- CEASE LITHIUM if possible
- DI usually reversible
- but may have progressed to irreversible stage - If need to continue lithium then trial AMILORIDE
- decreases accumulation of lithium in collecting tubular cells by inhibiting the epithelial Na+ channels
- will not be effective if reached irreversible stage (ie. no longer lithium-dependent)
If amiloride is not successful, then try usual treatment for nephrogenic DI:
- Low Na+ diet
- Thiazide diuretic: to diminish distal water delivery or upregulate aquaporin receptors
- NSAIDs: to decrease the synthesis of prostaglandins
- DDAVP (desmopressin) - to provide supraphysiologic ADH levels and overcome partial resistance.
NOTE: VERY important to monitor lithium levels during use of amiloride, thiazide diuretics, and NSAIDs, as they all decrease clearance.
What effect will CO2 retention have on lithium levels?
Increased PaCO2
- -> acidification of blood and urine
- -> decrease in lithium excretion
- -> increase in serum lithium level
What distinguishes the atypical from the typical antipsychotics?
Give a few examples of each category.
Atypical antipsychotics are less likely to cause extrapyramidal side effects than the older typical antipsychotics.
This is because they cause less inhibition of D2 receptors (dopamine Rc type 2 - in substantia nigra), and act on other dopamine Rc subtypes (eg. 3, 4 - in mesolimbic system).
Typicals (work predominantly on D2-R): haloperidol, chlorpromazine, thioridazine, flupenthixol, zuclopenthixol.
Atypicals: risperidone, clozapine, olanzapine, quetiapine, amisulpride, apiprazole.
The atypical antipsychotics may be more sparing of dopamine pathways in the substantia nigra (and thus less likely to cause EPSEs), but they can cause other ASEs by affecting other dopaminergic pathways.
Give some examples.
Affect on projections to hypothalamus and pituitary.
–> Increased appetite (olanzapine = #1, clozapine) (hypothal)
–> increased prolactin –> gynaecomastia, sexual dysfunction (risperidone)
EPSEs which can be seen more commonly with older antipsychotics:
- Akithesia: restlessness
- Dystonia: muscle spasm
- Parkinsonism: rigidity, tremor
- Tardive dyskinesia: choreoathetoid movements - often orobuccal region.
Older antipsychotics can also have secondary negative symptoms.
Main ASEs of clozapine:
BM suppression
severe myocarditis
Cholinergic effects - hypersalivation
constipation and ileus
weight gain
Schizophrenia subtypes:
- Paranoid
- Disorganisned
- Catatonic
(organic brain syndrome: waxy flexibility, mutism, posturing) - Delusional disorder
“Older” antidepressants: main ASEs and some drug examples.
Drowsiness Blurred vision Confusion Constipation Urinary retention (anticholinergic effects)
Cardiotoxic in OD
Eg. Amitriptyline, imipramine, dothiepin.
withdrawal effect is usually over stimulation of the cholinergic (nausea, diarrhoea) and things like insomnia
their actual mech of action is likely blockade of the norAd reuptake
SSRIs: main ASEs and some drug examples.
Effects on sleep (insomnia), sex (impotence) and gut (N/V)
Not cardiotoxic in OD.
Fluoxetine (prozac)
Sertraline (zoloft)
Citalopram (cipramil)
Paroxetine
Examples and mechanisms of newer antidepressants:
- SSRIs
- SNRI (serotonin-noradrenaline reuptake inhibitors)
eg. venlafaxine (efexor), desvenlafaxine, duloxetine - Atypicals:
- Mirtazapine = pre-synaptic alpha-2 blocker
- Reboxetine = noradrenaline reuptake inhibitor
Serotonin syndrome: clinical presentation
TCA plus MOA-I
these days, it is more like SSRI + TCA or SSRI + SNRI
can also happen with tramadol and SSRI/SNRI or even with St John’s Wort
initially it is increased agitation
at worst it is with hypertonia, hyperreflexia (can look like NMS)
Neuroleptic malignant syndrome - clinical presentation:
.
Spectrum of anxiety disorders:
- Panic disorder (with or without agoraphobia)
- Generalised anxiety disorder
- Social phobia
- OCD
- PTSD
- Specific phobias
Treatment of anxiety disroders:
- SSRIs (beware initial agitation)
- Cognitive therapy - challenging irrational cognitions
- Behavioural therapy - visualisation, deep abdominal breathing, progressive muscular relaxation
- Systematic desensitisation of phobias (agoraphobia, specific phobias)
- Social skills training for social phobia
Risk factors for complicated grief (abnormal bereavement):
The college says: “history of prior conflict with the deceased” is more predictive of complicated grief than “Distress of bereaved at the time of death”* or “the fact that the bereaved lives alone”.
From UTD:
- Poor social supports
- Past history of psychiatric problems, especially depression
- Past history of childhood separation anxiety
- High initial distress*
- Unanticipated death, lack of preparation for death
- Other major concurrent stresses and losses
- History of abuse or neglect in childhood
- Lifestyle rigidity (aversiveness to lifestyle change)
- Highly dependent relationship with the deceased
- Death of a child
What is catalepsy?
this is called waxy flexibility, and is particularly associated with catatonic SCZ. It is when you move someone’s hands into an awkward position, and they just keep it there.
highly suggestive of an organic disease
Explain metabolism of clozapine.
What effect does tobacco use have?
…
What are the elements of the DSM-5 Criteria for Anorexia Nervosa?
Anorexia Nervosa
- Persistent restriction of energy intake leading to significantly low body weight
(in context of what is minimally expected for age, sex, developmental trajectory, and physical health) . - Either an intense fear of gaining weight or of becoming fat, OR
Persistent behaviour that interferes with weight gain (even though significantly low weight). - Disturbance in the way one’s body weight or shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.
Subtypes:
- Restricting type
- Binge-eating/purging type
