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ADAMS > Metabolic > Flashcards

Metabolic Flashcards

1
Q

Serum Osmolality Formula

A

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

in mg/dL

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2
Q

Normal serum osmolality

A

270-290 mOsm/L

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3
Q

Ultimate determinant of the adequacy of oxygen supply to the organs

A

product of blood oxygen content and cardiac output

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4
Q

vulnerable to anoxia

A

hippocampus

deep folia of the cerebellum

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5
Q

resistant to anoxia and hypotension

A

brainstem and spinal cord

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6
Q

conditions with isoelectric EEG but permit recovery

A

anesthesia
intoxication with certain drugs
hypothermia

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7
Q

Posthypoxic Neurologic Syndromes

A
  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
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8
Q

Watershed syndromes

A
  1. Visual Agnosias including Balint syndrome and cortical blindness (Anton Syndrome)
  2. Proximal arm and shoulder weakness sometimes by hip weakness
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9
Q

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

A

delayed postanoxic encephalopathy and leukoencephalopathy

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10
Q

Prognosis in HIE

in a study by Levy

A

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

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11
Q

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

A

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

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12
Q

affinity of carbon monoxide to hemoglobin

A

more than 200x that of oxygen

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13
Q 
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
A

Carbon monoxide posioning

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14
Q

Treatment for Carbon Monoxide exposure

A

hyperbaric oxygen at 2-3 atmospheres

3 hyperbaric sessions in the first 2 4hrs after exposure

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15
Q

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,

A

high-altitude (mountain) sickness

extreme altitude sickness: fatal cerebral edema
VEGF has been implicated

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16
Q

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

A

Chronic Mountain Sickness

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17
Q

meds/condition that reduce tolerance to high altitude

A

sedatives
alcohol
slightly elevated PCO2

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18
Q

Tx for hypercapnic pulmonary disease

A

positive pressure ventilation

oxygen supplementation

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19
Q

level of blood glucose and clinical syndrome

A

30mg/dL - confusional state, seizures

10 mg/dL - coma, rreparable injury

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20
Q

glucose reserve in a normal brain

A

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

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21
Q

glucose utilization rate

A

60-80 mg/min

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22
Q

T/F

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

A

True

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23
Q

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

A

6

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24
Q

causes of hypolglycemic encephalopathy

A
  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
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25
Q

in hypoglycemic iencephalopathy, major damage is to the

A

cerebral cortex

26
Q

2 syndromes identified in diabetics from hyperglycemia

A

hyperglycemia with ketoacidosis

hyperosmolar nonketotic hyperglycemia

27
Q

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

A

sorbitol

28
Q

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

A

corticosteroids and phenytoin

29
Q

EEG findings in hepatic encephalopathy

A

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

30
Q

MRI in portal systemic encephalopathy

A

high signal intensity in the globus pallidus

results from manganese deposition

31
Q

Pathologic findings in hepatic encephalopathy

A

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

32
Q

EEG in uremic encephalopathy

A

diffusely and irregularly slow

33
Q

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

A

True

34
Q

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

A

<120, 500mL per 24 hrs

<130, 1000,L per 24 hrs

35
Q

T/F

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

A

True

36
Q

True or FalseCongenital hypothyroidism is usually recognized at birth.

A

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

37
Q

signs that raise suspicion of thyroid deficiency

A

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

38
Q

two types of early life hypothyroidism

A

sporadic and endemic

39
Q

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

A

sporadic cretinism

40
Q

2 types of endemic cretinism

A

myxedematous and neurologic

41
Q

neurologic form of endemic cretinism

A

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

42
Q

myxedematous form of endemic cretinism

A

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

43
Q

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

A

second

44
Q

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

A

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

45
Q

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

A

dendritic-axonal development and organization

46
Q

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.

A

true

47
Q

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

A

cretinismor neonatal myxedema

48
Q

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.

A

True

p1132

49
Q

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

A

incomplete infarctions in the border zones between major cerebral arteries

50
Q

with predominant anoxia, neurons in __________ are particularly vulnerable

A

hippocampus and deep folia of cerebellum

51
Q

“no-reflow” phenomenon

A

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

52
Q

most common early change in cases of severe anoxic encephalopathy

A

loss of distinction between teh cerebral gray and white matter

53
Q

EEG in brain death syndrome

A

EEG is isoelectric

54
Q

instances of CO poisoning

A

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

55
Q

half life of carbon monoxide

A

5 hrs

56
Q

T/F

Hypoxemia at high altitudes is intensified during sleep.

A

True

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

57
Q

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.

A

True

p1141
Epidemiology of Diabetes Interventions and Complications Study Research Group

58
Q

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

A

cerebral cortex

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

59
Q

T/F

The cerebellar cortex is more vulnerable to hypoglycemia than to hypoxia.

A

False

cerebellar cortex is less vulnerable to hypoglycemia

60
Q

most plausible view of the pathogenesis of dialysis encephalopathy

A

aluminum intoxication

61
Q

proposed causes in Septic Encephalopathy

A

altered phenylalanine metabolism and circulating cytokines

ADAMS (29 decks)

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