Metabolic

Question 1

Serum Osmolality Formula

Answer 1

OSM = 2 x Na + (gluc/18) + (BUN/3)

in mg/dL

Question 2

Normal serum osmolality

Answer 2

270-290 mOsm/L

Question 3

Ultimate determinant of the adequacy of oxygen supply to the organs

Answer 3

product of blood oxygen content and cardiac output

Question 4

vulnerable to anoxia

Answer 4

hippocampus

deep folia of the cerebellum

Question 5

resistant to anoxia and hypotension

Answer 5

brainstem and spinal cord

Question 6

conditions with isoelectric EEG but permit recovery

Answer 6

anesthesia
intoxication with certain drugs
hypothermia

Question 7

Posthypoxic Neurologic Syndromes

Answer 7

1. persistent coma or stupor
2. dementia with or without extrapyramidal signs
3. extrapyramidal (parkinsonian) syndrome with cognitive impairment
4. choreoathetosis
5. cerebellar ataxia
6. intention or action myoclonus (Lance-Adams syndrome)
7. Amnesic state

Question 8

Watershed syndromes

Answer 8

1. Visual Agnosias including Balint syndrome and cortical blindness (Anton Syndrome)
2. Proximal arm and shoulder weakness sometimes by hip weakness

Question 9

common, unexplained phenomenon
with initial improvement followed by a variable period of time (1-4 weeks) by a relapse, characterized by apathy, confusion, irritability and occasionally agitation or mania

some progress to additional weakness, diffuse rigidity, spasticity, sphincteric incontinence, coma and detah after 1-2 weeks

Answer 9

delayed postanoxic encephalopathy and leukoencephalopathy

Question 10

Prognosis in HIE

in a study by Levy

Answer 10

13% state of independent function at 1 yr
25% absent pupillary reflexes - none regained independent fxn
50% - reactive pupils. with eye movements, motor response - better prognosis

Question 11

clinical signs at 1 day after cardiac arrest that predict poor outcome

Answer 11

absent corneal response
absent pupillary reactivity
no withdrawal to pain
absence of any motor response

Question 12

affinity of carbon monoxide to hemoglobin

Answer 12

more than 200x that of oxygen

Question 13

exposure to gasoline/fulty furnaces
headache, nausea, dyspnea, confusion,dizziness, clumsiness
cherry-red color of the skin 
cyanosis
blindness/visual field defects
papilledema
seizure
delayed neurologic deterioration 1-3 weeks after exposure
extrapyramidal features

Answer 13

Carbon monoxide posioning

Question 14

Treatment for Carbon Monoxide exposure

Answer 14

hyperbaric oxygen at 2-3 atmospheres

3 hyperbaric sessions in the first 2 4hrs after exposure

Question 15

occurs when a sea-level inhabitant abruptly ascends to a high altitude
headache, anorexia, nausea and vomiting, weakness, insomnia above 8000 ft

on reaching higher altitudes: ataxia, tremor, drowsiness, mild confusion, hallucinations

16,000 ft: asymptomatic retinal hemorrhages,

Answer 15

high-altitude (mountain) sickness

extreme altitude sickness: fatal cerebral edema
VEGF has been implicated

Question 16

observed in long-term inhabitant of high-altitude mountainous regions

main features: pulmonary hypertension, cor pulmonale, secondary polycythemia hypercarbia
mental dullness, slowness, fatigue, nocturnal headache and sometimes papilledema

Answer 16

Chronic Mountain Sickness

Question 17

meds/condition that reduce tolerance to high altitude

Answer 17

sedatives
alcohol
slightly elevated PCO2

Question 18

Tx for hypercapnic pulmonary disease

Answer 18

positive pressure ventilation

oxygen supplementation

Question 19

level of blood glucose and clinical syndrome

Answer 19

30mg/dL - confusional state, seizures

10 mg/dL - coma, rreparable injury

Question 20

glucose reserve in a normal brain

Answer 20

1-2 g (30mmol/100g of tissue) inthe form of glycogen

Question 21

glucose utilization rate

Answer 21

60-80 mg/min

Question 22

T/F

Glucose reserve may sustain cerebral activity for 30 min or less once blood glucose is no longer available.

Answer 22

True

Question 23

oxidation of 1 mole of glucose requires how many moles of O2

Answer 23

6

Question 24

causes of hypolglycemic encephalopathy

Answer 24

1. accidental or deliberate overdose of insulin or an oral diabetic agent
2. islet cell-insulin-secreting tumor of the pancreas
3. depletion of liver glycogen, which occasionally follows a prolonged alcoholic binge, starvation, or any form of severe liver failure
4. glycogen storage disease of infancy
5. idiopathic hypoglycemia in the neonatal period and infancy
6. subacute and chronic hypoglycemia from islet cell hypertrophy and islet cell tumors of the pancreasm carcinoma of the stomach, fibrous mesothelioma, carcinoma of the cecum, hepatoma

Question 25

in hypoglycemic iencephalopathy, major damage is to the

Answer 25

cerebral cortex

Question 26

2 syndromes identified in diabetics from hyperglycemia

Answer 26

hyperglycemia with ketoacidosis hyperosmolar nonketotic hyperglycemia

Question 27

according to Prockop, the cerebral edema seen in hyperglycemia is due to the accumulation of

Answer 27

sorbitol

Question 28

in hyperosmolar nonketotic hyperglycemia, what are the 2 drugs believed to inhibit the release of insulin

Answer 28

corticosteroids and phenytoin

Question 29

EEG findings in hepatic encephalopathy

Answer 29

paroxysms of bilaterally synchronous slow or triphasic waves in the delta range which at first predominate frontally and are interspersed with alpha activity

Question 30

MRI in portal systemic encephalopathy

Answer 30

high signal intensity in the globus pallidus results from manganese deposition

Question 31

Pathologic findings in hepatic encephalopathy

Answer 31

increase in the number and size of protoplasmic astrocytes in the deep layers of the cerebral cortex, lenticular nuclei, thalamus, substantia nigra, cerebellar cortex, red dentate, pontine nuclei NO VISIBLE ALTERATION IN THE NERVE CELLS PAS - astrocytes were seen to contain glycogen inclusions - Alzheimer Type II astrocytes

Question 32

EEG in uremic encephalopathy

Answer 32

diffusely and irregularly slow

Question 33

T/F As with many other metabolic derangements, the severity of the clinical effect is related to the rapidity of decline in serum Na

Answer 33

True

Question 34

restriction of fluid intake if serum Na level is <120mEq/L <130mEq/L

Answer 34

<120, 500mL per 24 hrs | <130, 1000,L per 24 hrs

Question 35

T/F Rapid elevations of sodium shrink the brain, especially in infants.

Answer 35

True

Question 36

True or FalseCongenital hypothyroidism is usually recognized at birth.

Answer 36

Falsebecome apparent only after a few weeksdiagnosis is usually made 6-12 months

Question 37

signs that raise suspicion of thyroid deficiency

Answer 37

physiologic jaundice tends to be severe and prolonged up to 3 monthswidening of posterior fontanellmottling of skin

Question 38

two types of early life hypothyroidism

Answer 38

sporadic and endemic

Question 39

at birth gland is either absent or represented by cysts indicating failure of development or destructive lesionlatter part of first yr - stunting of growth, delayed psychomotor developmentretarded but good naturedmovements are slow, hyporeflexivebody temp is low, extremities are cyanotichead is small but fontanelles may not close until 6th or 7th yr from delayed ossification

Answer 39

sporadic cretinism

Question 40

2 types of endemic cretinism

Answer 40

myxedematous and neurologic

Question 41

neurologic form of endemic cretinism

Answer 41

varying degrees of deaf-mutism or lesser degrees of hearing loss dysarthria, proximal limb and truncal rigid-spastic motor disorder involving mainly the lower extremities and mental deficiency severely affected: strabismus, kyphoscoliosis, underdevelopment of leg muscles, and frontal lobe release signs Bone age, head size, and height are normal and there are none of the coarse facial features

Question 42

myxedematous form of endemic cretinism

Answer 42

short stature, microcephal, coarse facial features and retarded psychomotor development are the main features, no deafness or spastic rigidity of the limb face is pale and puffy with dry skin dry, scanty and coarse hair, the eyelids thickened the thickened lips parted by the enlarged tongue the forehead low; and the base of the nose broad abdomen is protuberant, often with an umbilical hernia

Question 43

for congenital hypothyroidismIt is during the latter part of the ______ trimester, when the cochleas and the neuronal population of the cerebral cortex and basal ganglia are forming, that these structures suffer irreparable damage from lack of thyroid hormone

Answer 43

second

Question 44

True or FalseThe effects of this midfetal hypothyroidism and iodine deficiency CAN be corrected by giving thyroid hormone at birth and thereafter.

Answer 44

falseit can only be prevented by giving iodine therapy to the mother before and during the first trimester of pregnancy

Question 45

Thyroid hormone appears to be essential, NOT for neuronal formation and migration but for ______

Answer 45

dendritic-axonal development and organization

Question 46

true or falseIn sporadic cretinism, if the condition is recognized at birth and treated consistently with thyroid hormones, height and mental development can be stimulated to normal or near-normal levels.

Answer 46

true

Question 47

This form of severe intrauterine hypothyroidism (in mother and fetus) or postnatally as a hereditary or acquired thyroid disease, is probably the most frequent and potentially preventable and correctable metabolic mental defect in the world

Answer 47

cretinismor neonatal myxedema

Question 48

T/F The main features of the reversible metabolic encephalopathies are confusion, typified by disorientation and inattentiveness and accompanied in certain special instances by asterixis, tremor, and myoclonus, usually without signs of focal cerebral disease.

Answer 48

True p1132

Question 49

under conditions of transient ischemia, one pattern of damage takes the form of

Answer 49

incomplete infarctions in the border zones between major cerebral arteries

Question 50

with predominant anoxia, neurons in __________ are particularly vulnerable

Answer 50

hippocampus and deep folia of cerebellum

Question 51

"no-reflow" phenomenon

Answer 51

one of the irreversibility of ischemic lesions may be swelling of the endothelium and blockage of circulation into the ischemic cerebral tissues

Question 52

most common early change in cases of severe anoxic encephalopathy

Answer 52

loss of distinction between teh cerebral gray and white matter

Question 53

EEG in brain death syndrome

Answer 53

EEG is isoelectric

Question 54

instances of CO poisoning

Answer 54

burn units patients who have attempted suicide accidental exposure to a faulty furnace to a car exhaust in a closed garage

Question 55

half life of carbon monoxide

Answer 55

5 hrs

Question 56

T/F | Hypoxemia at high altitudes is intensified during sleep.

Answer 56

True p1139 as ventilation normally diminishes and also by pulmonary edema - another manifestation of mountain sickness

Question 57

T/F Recurrent hypoglycemic episodes in the course of treatment of diabetes over many years are very well tolerated and do not lead to cognitive decline.

Answer 57

True p1141 Epidemiology of Diabetes Interventions and Complications Study Research Group

Question 58

all forms of hypoglycemic encephalopathy, the major damage is to the

Answer 58

cerebral cortex Cortical nerve cells degenerate and are replaced by microglia cells and astrocytes

Question 59

T/F | The cerebellar cortex is more vulnerable to hypoglycemia than to hypoxia.

Answer 59

False cerebellar cortex is less vulnerable to hypoglycemia

Question 60

most plausible view of the pathogenesis of dialysis encephalopathy

Answer 60

aluminum intoxication

Question 61

proposed causes in Septic Encephalopathy

Answer 61

altered phenylalanine metabolism and circulating cytokines