Tardive Dyskinesia And Refeeding Syndrome Flashcards
(26 cards)
The hospitalized patient is prone to severe low phosphate levels due to what two things?
Decreased intestinal phosphate absorption and increased urinary phosphate excretion
2 reasons why we can have increased urinary phosphate excretion due to alcoholism?
Secondary hyperparathyroidism due to vitamin D deficiency
Alcohol causes proximal tubule dysfunction which reduces reabsorption capacity
What can happen because of IV therapy with dextrose continuing solutions for alcoholic patients coming in to the hospital and why?
Phosphate levels drop really low because the glucose stimulates insulin release which promotes phosphate to be taken up into the cells
Serial monitoring of what is required when alcoholic patients are admitted to the hospital?
Phosphate
When do we give oral phosphate or IV phosphate to treat low phosphate levels and when do we stop treatment?
Give oral when phosphate is between 1-1.9
Give IV phosphate when levels drop below 1
Stop when we get it back to 2
What is the clinical symptom we are looking for with low phosphate levels and what are these patients at risk for?
Myopathy due to both the low phosphate and alcohol toxicity
Rhabdo
Acute alcoholic myopathy is one of the most common causes of what?
What 2 things are commonly seen on chronic alcoholics that may potentiate the muscle toxicity?
Non traumatic Rhabdo and acute renal failure
Hypokalemia and low phosphate
What are three enzymes he talked about needing thiamine as a co factor in metabolism?
What is the scenario he described as to why thiamine deficiency patients experience wernickes?
Transketolase, alpha ketoglutarate dehydrogenase, and pyruvate dehydrogenase.
Thiamine depends on metabolic rate and the demand for it increases as demand goes up, especially in situations where glucose is high. So if a patient comes in who is an alcoholic and has low thiamine levels already and we decide to give IV fluids with glucose, we are increasing the metabolic demand for the patient and throwing them into wernickes.
What is the classic triad of wernickes?
Encephalopathy, oculomotor dysfunction, gait ataxia
What does he mean when he says presenting with the triad is the exception that her than the rule?
Most patients don’t present with all 3. Maybe 1 or 2 and in some they are just super lethargic and coma type.
In the study he mentioned what were the top 3 presenting symptoms?
Mental confusion, staggering gait and ocular problems was third
Changes in the cerebellum in wernickes are identical to what other condition?
Where is a less frequently affected area of the brain he mentioned?
Alcoholic cerebellar degeneration
Hippocampus, medial temporal lobe
Treatment for wernickes?
Immediate parenteral thiamine BEFORE any glucose
What is the lesion specific to Korsakoff?
Clinical sign/symptom of Korsakoff?
Medial temporal lobe
Selective anterograde and retrograde amnesia
How do we best define/describe tardive dyskinesia?
Movement disorder caused by exposure to dopamine receptor blocking agents that persist for at least a month after stopping the med.
Tardive, meaning later, presents later and lasts longer….and dyskinesia meaning involuntary abnormal movements of the mouth, face, trunk or limbs.
What is AIMS?
What does it assess?
What can we do to get a better prognosis of TD?
Abnormal involuntary movement scale for TD
Detects and assesses the severity of TD
Abnormal involuntary movements of face, mouth, trunk and limbs
The quicker you can get the patient off the medication the better the prognosis
How do we best describe the following types of TD?
Withdrawal emergent TD?
Withdrawal dyskinesia TD?
Masked TD?
Dyskinesia in kids that occurs less than 1 month after stopping the antipsychotic
Dyskinesia in adults immediately after stopping or reducing the dose of the drug
Tardive movements are resolved when the drug is resumed
What kind of drugs are most commonly causing TD?
All dopamine blocking agents can First and second generation antipsychotics Metoclopramide Prochlorperazine Chlorpromazine
What two second generation antipsychotics have the highest risk for TD?
Paliperidone and risperidone
3 conditions more at risk for TD?
Older, smokers and diabetes
What side effect comes with it a higher risk for TD from taking antipsychotics?
If you experience EPS then you are at higher risk
What was he big take home message as to why FGA have a higher risk for TD than SGA?
FGA block D2 receptors much more where as SGA, especially clozapine, block D1 receptors in the basal ganglia. Blocking leads to increased activity of D1 which is linked to susceptibility of TD.
What is another reason why they believe clozapine has such a low incidence for TD?
It is a 5HT2a antagonist and they have found this receptor linked to susceptibility for TD
What is the GABA hypothesis of TD?
Chronic blocking of D2 increases glutamate with the striatum causing excitotoxic destruction of GABA neurons in the striatum
