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Brain Power: Adam and Victor's Neurology > Acquired Metabolic Disease > Flashcards

Acquired Metabolic Disease Flashcards

1
Q

With BUN and Glucose in mg/dl how does one compute for osmolality in a patient with a Na of 150, Glucose of 100mg/dl, BUN of 10mg/dl?

A

OSM 2xNa + Glucose/18 + BUN/3

300+5.5+3.3 = 308.3 mOsm/L

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2
Q

OSM? Na 155 Glucose 180 BUN 30

A

310 + 10 + 10 = 330 mOsm/L

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3
Q

What is normal serum osmolality?

A

270-290mOsm/L

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4
Q

What part of the brain is most affected during: 1. Anoxia 2. Ischemia

A
  1. Hippocampus (CA1; CA2 is sometimes spared) and the deep folia of the cerebellum
  2. Incomplete infarctions at the border zones between the arteries
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5
Q

Beyond how many minutes of CPR is there usually permanent injury?

A

5

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6
Q

What are the main syndromes associated with watershed infarctions from hypoperfusion?

A
  1. Balint syndrome– inability to perceive the visual field as a whole (simultanagnosia), difficulty in fixating the eyes (oculomotor apraxia), and inability to move the hand to a specific object by using vision (optic ataxia) – Lesion in the inferior parietal lobule in the dorsal stream of the visal cortex output
  2. Proximal arm and shoulder weakness– man in a barrel syndrome
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7
Q

How do the landmark trials of Bernard and Nielsen differ? Re: Hypothermia after cardiac arrest

A

Bernard 32-34 degrees celsius target

Nielsen Less than 36 degrees celsius target

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8
Q

What are the distinct lesions associated with CO poinsoning?

A

Discrete lesions centered in the globus pallidus bilaterally and sometimes the inner portion of the putamina

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9
Q

What is the treatment for CO poisoning?

A

Administration of hyperbaric oxygen at 2-3 atmospheres (2 sessions in 24 hours)

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10
Q

At what altitude:

  1. 50% of individuals develop retinal hemorrhages
  2. Headache, weakness, insomnia, weakness all first appear?
A
  1. 16,000 ft

2. 8,000 fit

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11
Q

What are the 3 main features of chronic mountain sickness?

A
  1. Pulmonary htn
  2. Cor pulmonale
  3. Secondary polycythemia
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12
Q

What is the most effective preventive measure for chronic mountain sickness?

A

2-4 day stay at intermediate altitudes

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13
Q

What are the key features of hypercapnic pulmonary disease?

A 
Headache
Papilledema
Mental Dullness/ Confusion
Decrease sensorium
Asterixis and tremor
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14
Q

What is the rate of glucose utility of the brain?

A

60-80mg per minute

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15
Q

What CA is linked to hypoglycemia?

A

Islet cell tumor of the pancreas

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16
Q

What glucose level is associated with deep coma, dilation of pupils, slow pulse and hypotonia?

A

10mg per dl

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17
Q

What glucose level do symptoms of nervousness, hunger, flushed facies, sweating and headache occur?

A

30mg per dl

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18
Q

What happens to diabetic patients who use steroids and phenytoin?

A

Both drugs inhibit insulin release hence there is possibility of developing hyperosmolar nonketotic hyperglycemia

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19
Q

How does an Eck fistula lead to encephalopathy?

A

It is a surgical portosystemic shunt leading to hepatic stupor and coma.

Remember THE LIVER CAN BE NORMAL BUT IF THERE IS A SHUNT PROTEIN CAN INDUCE EPISODIC HEPATIC COMA

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20
Q

The movement disorder characterized by intermittency of sustained muscle contraction was originally described in what form of encephalopathy?

A

Hepatic. This is asterixis– elicited by sustaining postures such as in holding arms in front with wrists extended.

21
Q

Where do triphasic waves of hepatic encephalopathy start?

A

Frontal region. Bilateral synchronous int he delta range

22
Q

What are the neurohistopathologic changes associated with hepatic coma?

A

Diffuse increase in the number and size of protoplasmic astrocytes (Midbrain, pontine, cerebellum, lenticular nuclei, deep cerebral layers).

23
Q

What is the eponym attached to the astrocytes that are identified in hepatic coma? Describe them.

A

Alzheimer type 2 astrocytes.

  1. Swollen termina processes
  2. Cytoplasmic vacuolation
  3. Increased number of mitochondria and enzymes that catabolize ammonia
24
Q

What neurotransmitter predominates in the brains of hepatic encephalopathy patients?

A

Ammonia inhibits GABA metabolism thereby enhancing neurotransmission by the compound

25
Q

What are the 4 treatment options for hepatic failure?

A
  1. Limitatioon of dietary protein
  2. Antibiotics: Rifamixin working by reduction of bowel flora
  3. Oral lactulose
  4. Transplant
26
Q

How does lactulose work in hepatic encephalopathy?

A

It is metabolized by colonic bacteria that produced hydrogen ions that shift the formation from ammonia to ammonium– a nontoxic product eliminated in the stool

27
Q

What are the two main clinical features main features and preceding clinical event in patients who develop Reye-Johnson syndrome, a type of non icteric haptic encephalopathy?

A

Acute brain swelling and fatty infiltration of the viscera particularly the liver

Intake of aspirin in children

28
Q

How would an MRI of uremic and hepatic encephalopathy vary?

A

Hepatic: cerebral edema
Renal: cerebral shrinkage

29
Q

What are the two theories for Dialysis disequilibrium?

A
  1. Rapid urea lowering with dialysis causes more urea in the brain than in the plasma
  2. SIADH– water intoxication
30
Q

What metal is responsible for dialysis dementia?

A

Aluminum in dialysate

31
Q

What characteristic MRI feature can accompany administration of cyclosporine and other immunosuppressants after renal transplant?

A

PRES

32
Q

T or F: Paratonia is common in septic encephalopathy but NOT myoclonus or asterixis

A

T

33
Q

What is the main treatment for SIADH associated hyponatremia?

A

Fluid restriction
If Na <120, 500 ml in 24h
If Na <130, 1000 in 24h

34
Q

How to compute for the amount of NaCl to be infused?

A

(Target Na-starting Na)x0.6xweight = total infused Na load (mEq)

35
Q

What is the sodium concentration found in 0.9% PNSS? How about 3% PNSS?

A

0.9% 154 mEq/L

3% 513 mEq/L

36
Q

What degree of Calcium evelation causes neuro symptoms?

A

If CHON normal, more than 12mg/dl

37
Q

How is the histopath of ODS differentiated from MS or infarct?

A

Selective destrucitno of the myelinated sheaths with relative sparing of the axons and intactness of the nerve cells of the pontine nuclei. ALSO SIGNS OF INFLAMMATION ARE MISSING.

38
Q

What 3 main features distinguish Wilson Disease from Chronic Acquired (Non wilsonian) Hepatocerebral Degeneration?

A
  1. Familial occurrence: autosomal recessive
  2. Kayser-Fleishcer rings
  3. Abnormal labs: Diminished serum ceruloplasmin, elevated serum copper and elevated urinar copper excretion
39
Q

Chronic neurologic disorder in patients with disturbed hepatic functions correlate with what level of serum ammonia?

A

> 200mg dl

40
Q

What e abnormalities are associated with hypoparathyroidism?

A

HypoCa2

HyperPO4

41
Q

What part of the brain is exquisitely sensitive to hyperthermia (such as in heat strokes)

A

Cerebellum: Degeneration of the purkinje cells with gliosis throughout the cerebellar cortex (These finding are NOT found in infective fevers or neuroleptic syndrome)

42
Q

Besides peripheral neuropathy what other neurologic syndrome accompany celiac disease?

A

Cerebellar syndromes

43
Q

What dose of prednisone will there usually be psychiatric symptoms of emotional lability, inability to sleep?

A

60-100mg per day.

44
Q

What antibodies are seen in steroid responsive encephalopathy syndrome?

A

Anti thyroid peroxidase
Anti thyroglobulin

THIS IS HASHIMOTO ENCEHAPHALOPATHY– most have had normal thyroid function

Diagnosis of Hashimoto encephalopathy can be made when all six of the following criteria have been met:[3]

  1. Encephalopathy with seizures, myoclonus, hallucinations, or stroke-like episodes
  2. Subclinical or mild overt thyroid disease (usually hypothyroidism)
  3. Normal brain MRI or with non-specific abnormalities
  4. Presence of serum thyroid (thyroid peroxidase, thyroglobulin) antibodies
  5. Absence of well-characterized neuronal antibodies in serum and CSF
  6. Reasonable exclusion of alternative causes
45
Q

What movement disorders are common in Hashimoto encephalopathy?

A

Myoclonus

Patients also have tremors, transient aphasia, seizures and ataxia

46
Q

What is the most frequent and potentially preventable and correctable metabolic mental defect in the world?

A

Cretinism

Congenital thyroid deficiency

47
Q

What are the two forms of cretinism?

A

Neurologic

Myxedema (NO DEAFNESS OR SPASTIC LIMBS)

48
Q

Which type of early life hypothyroidism is still treatable at birth? Endemic or sporadic?

A

Sporadic can be treated with supplementation with thyroid hormones.

Endemic can only be prevented by supplementation of iodine to the mother

49
Q

What are histopath changes in cretinism?

A

Reduction in the number of nerve cells especially in the 5th cortical layer– porverty of dendritic branchings and crossings

THYROID HORMONE NOT ESSENTIAL FOR NEURONAL FORMATION AND MIGRATION BUT ESSENTIAL FOR DENTRITIC AXONAL DEVELOPMENT AND ORGANIZAITON

Brain Power: Adam and Victor's Neurology (19 decks)

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