Tardive Dyskinesia And Refeeding Syndrome

Question 1

The hospitalized patient is prone to severe low phosphate levels due to what two things?

Answer 1

Decreased intestinal phosphate absorption and increased urinary phosphate excretion

Question 2

2 reasons why we can have increased urinary phosphate excretion due to alcoholism?

Answer 2

Secondary hyperparathyroidism due to vitamin D deficiency

Alcohol causes proximal tubule dysfunction which reduces reabsorption capacity

Question 3

What can happen because of IV therapy with dextrose continuing solutions for alcoholic patients coming in to the hospital and why?

Answer 3

Phosphate levels drop really low because the glucose stimulates insulin release which promotes phosphate to be taken up into the cells

Question 4

Serial monitoring of what is required when alcoholic patients are admitted to the hospital?

Answer 4

Phosphate

Question 5

When do we give oral phosphate or IV phosphate to treat low phosphate levels and when do we stop treatment?

Answer 5

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

Question 6

What is the clinical symptom we are looking for with low phosphate levels and what are these patients at risk for?

Answer 6

Myopathy due to both the low phosphate and alcohol toxicity

Rhabdo

Question 7

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?

Answer 7

Non traumatic Rhabdo and acute renal failure

Hypokalemia and low phosphate

Question 8

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?

Answer 8

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.

Question 9

What is the classic triad of wernickes?

Answer 9

Encephalopathy, oculomotor dysfunction, gait ataxia

Question 10

What does he mean when he says presenting with the triad is the exception that her than the rule?

Answer 10

Most patients don’t present with all 3. Maybe 1 or 2 and in some they are just super lethargic and coma type.

Question 11

In the study he mentioned what were the top 3 presenting symptoms?

Answer 11

Mental confusion, staggering gait and ocular problems was third

Question 12

Changes in the cerebellum in wernickes are identical to what other condition?
Where is a less frequently affected area of the brain he mentioned?

Answer 12

Alcoholic cerebellar degeneration

Hippocampus, medial temporal lobe

Question 13

Treatment for wernickes?

Answer 13

Immediate parenteral thiamine BEFORE any glucose

Question 14

What is the lesion specific to Korsakoff?

Clinical sign/symptom of Korsakoff?

Answer 14

Medial temporal lobe

Selective anterograde and retrograde amnesia

Question 15

How do we best define/describe tardive dyskinesia?

Answer 15

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.

Question 16

What is AIMS?
What does it assess?
What can we do to get a better prognosis of TD?

Answer 16

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

Question 17

How do we best describe the following types of TD?
Withdrawal emergent TD?
Withdrawal dyskinesia TD?
Masked TD?

Answer 17

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

Question 18

What kind of drugs are most commonly causing TD?

Answer 18

All dopamine blocking agents can
First and second generation antipsychotics
Metoclopramide
Prochlorperazine
Chlorpromazine

Question 19

What two second generation antipsychotics have the highest risk for TD?

Answer 19

Paliperidone and risperidone

Question 20

3 conditions more at risk for TD?

Answer 20

Older, smokers and diabetes

Question 21

What side effect comes with it a higher risk for TD from taking antipsychotics?

Answer 21

If you experience EPS then you are at higher risk

Question 22

What was he big take home message as to why FGA have a higher risk for TD than SGA?

Answer 22

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.

Question 23

What is another reason why they believe clozapine has such a low incidence for TD?

Answer 23

It is a 5HT2a antagonist and they have found this receptor linked to susceptibility for TD

Question 24

What is the GABA hypothesis of TD?

Answer 24

Chronic blocking of D2 increases glutamate with the striatum causing excitotoxic destruction of GABA neurons in the striatum

Question 25

How can we best treat TD?

Answer 25

Take the offending drug away. Switching from a first generation to a second like clozapine or quetiapine.

Using benzos, Botox, valbenazine or tatrebenazine to control TD symptoms.

Question 26

What treatment did he share at the end that was effective in treating TD in china?

Answer 26

Gingko biloba extract