Nutritional Deficiency

Question 1

characterized by nystagmus, conjugate gaze palsies, ataxia of gait and mental confusion

Answer 1

Wernicke disease

Question 2

is a mental disorder in which retentive memory is impaired out of proportion to all other cognitive functions in an otherwise alert and responsive patient

Answer 2

Korsakoff amnesic state

Korsakoff psychosis

Question 3

there are common medical circwnstances in which a subclinical thiamine deficiency becomes manifest

Answer 3

carbohydrate load, intravenous glucose is given to a malnourished individual
unbalanced intravenous hyperalimentation
refeeding syndrome
thyrotoxicosis
hypomagnesemia

Question 4

triad features of Wernicke

Answer 4

opthalmoplegia (with nystagmus)
ataxia
disturbances in mentation and consciousness

Question 5

T/F

In Wernicke disease, in approximately one-third of cases, one component of the triad may be the sole manifestation of the disease.

Answer 5

True

Question 6

Ocular abnormalities in Wernicke Disease

Answer 6

1) nystagmus that is both horizontal and vertical and mainly evoked by gaze; this is the most common feature
(2) weakness or paralysis of the lateral rectus muscles, and
(3) weakness or paralysis of conjugate gaze

Question 7

Most Common ocular abnormality in Wernicke Disease

Answer 7

nystagmus

Question 8

Next to nystagmus, common eye abnormality in Wernicke disease

Answer 8

lateral rectus weaknes

Question 9

most common disturbance of mentation in Wernicke disease

Answer 9

global confusional state

Question 10

Patients with the Korsakoff amnesic state may have a demonstrably impaired olfactory discrimination. This deficit is probably attributable to a lesion of

Answer 10

mediodorsal nucleus of thalamus and its connections

Question 11

Acute lesions of Wernicke-Korsakoff as seen in MRI

Answer 11

The acute lesions of the Wernicke-Korsakoff syndrome in the mammillary bodies, and other medial thalamic and periaqueductal areas

Question 12

Before treatment with thiamine, patients with Wernicke disease show a marked reduction in _________. Restoration of these values and of thiamine di-and triphosphate toward normal occurs within a few hours of the administration of thiamine, and completely normal values are usually attained within _____h.

Answer 12

transketolase, 24 hrs

Question 13

True or False

The effect of thiamine is so constant that a failure of the nystagmus and ocular palsies to respond to it should raise doubts about the diagnosis of Wernicke disease.

Answer 13

True

Question 14

In wernicke disease, treatment with thiamine

Horizontal nystagmus sometimes disappears in ______. Sixth-nerve palsies, ptosis, and vertical gaze palsies recover completely within a _______ in most cases, but vertical nystagmus may sometimes persist for ________.

Answer 14

horizontal nystagmus - minutes
sixth nerve palsies, ptosis and vertical gaze palsies - a week or two
vertical nystagmus - several months

Question 15

patients with Wernicke disease have lesions in which parts of the brain

Answer 15

the paraventricular regions of the thalamus and hypothalamus, mammillary bodies,
periaqueductal region of the midbrain,
floor of the fourth ventricle (particularly in the regions of the dorsal motor nuclei of the vagus and vestibular nuclei),
and supenor cerebellar vermis

Question 16

hypothermia in wernicke disease is attributed to which affected region of brain

Answer 16

to lesions in the posterior and posterolateral nuclei of the hypothalamus

Question 17

why is magnesium being given when treating for wernicke disease

Answer 17

it acts as a cofactor for thiamine activity

Question 18

the chronic alocholic exhausts thiamine in how many weeks

Answer 18

7-8 weeks

Question 19

T/F

infantile wernicke -beriberi disease
affects only breastfed infants

Answer 19

True

usually in the 2nd to 5th months of life

Question 20

where is thiamine absorbed

Answer 20

jejunum

Question 21

Wernicke disease is a result of a deficiency of

Answer 21

thiamine

Question 22

Fatalities in wernicke disease were attributable mainly to (2)

Answer 22

hepatic failure and infection

Question 23

lesions responsible for the memory disorder - those seen in

Answer 23

thalami

predominantly parts of the medial dorsal nuclei

Question 24

it is essentially a disease of the heart and of the peripheral nerves, with or without edema

Answer 24

nutritional polyneuropathy

neuropathic beriberi

Question 25

Night blindness seems to be caused by which nutrient deficiency

Answer 25

riboflavin or B2

Question 26

triad of dementia-dermatitis-diarrhea

Answer 26

Pellagra

Niacin, nicotinic acid, B3 deficiency

Question 27

amino acid precursor of nicotinic acid

Answer 27

tryptophan

Question 28

spinal cord lesions in pellagra

Answer 28

symmetrical degeneration of dorsal columns (Goll), lesser extent of corticospinal tracts

posterior column degeneration is likely to be secondary to degeneration of the dorsal root ganglion cells or posterior roots

Question 29

True or False

Only the dermal, gastrointestinal, and neurasthenic manifestations respond to treatment with niacin and tryptophan.

Answer 29

True

Question 30

Refers to a common and uniform type of degeneration of the vermian and anterior lobes of the cerebellum in alcoholics

Answer 30

alcoholic cerebellar degeneration

Question 31

T/F

Nystagmus and dysarthria are frequent in alcoholic cerebellar degeneration.

Answer 31

FALSE

infrequent
p1179

Question 32

pathologic changes in Alcoholic cerebellar degeneration

Answer 32

degeneration of the neurocellular elements of the cerebellar cortex but particularly of the Purkinje cells in the anterior and superior aspects of the vermis

Question 33

associated with chronic alcoholism
symmetrical demyelination of corpus callosum
affecting most prominently the central portion
varying presentation: altered mentation and consciousness , seizures, gait disturbance, behavioral abnormalities, mild progressive dementia, disconnection syndromes, death

Answer 33

Marchiafava-Bignami disease

Question 34

T/F

Inflammatory changes in Marchiafava-Bignami disease are absent.

Answer 34

True

p1180

Question 35

What structures are spared in Marchiafava-Bignami disease

Answer 35

internal capsule
corona radiata
subcortical arcuate fibers
cerebellum