Metabolic Flashcards
Serum Osmolality Formula
OSM = 2 x Na + (gluc/18) + (BUN/3)
in mg/dL
Normal serum osmolality
270-290 mOsm/L
Ultimate determinant of the adequacy of oxygen supply to the organs
product of blood oxygen content and cardiac output
vulnerable to anoxia
hippocampus
deep folia of the cerebellum
resistant to anoxia and hypotension
brainstem and spinal cord
conditions with isoelectric EEG but permit recovery
anesthesia
intoxication with certain drugs
hypothermia
Posthypoxic Neurologic Syndromes
- persistent coma or stupor
- dementia with or without extrapyramidal signs
- extrapyramidal (parkinsonian) syndrome with cognitive impairment
- choreoathetosis
- cerebellar ataxia
- intention or action myoclonus (Lance-Adams syndrome)
- Amnesic state
Watershed syndromes
- Visual Agnosias including Balint syndrome and cortical blindness (Anton Syndrome)
- Proximal arm and shoulder weakness sometimes by hip weakness
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
delayed postanoxic encephalopathy and leukoencephalopathy
Prognosis in HIE
in a study by Levy
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
clinical signs at 1 day after cardiac arrest that predict poor outcome
absent corneal response
absent pupillary reactivity
no withdrawal to pain
absence of any motor response
affinity of carbon monoxide to hemoglobin
more than 200x that of oxygen
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
Carbon monoxide posioning
Treatment for Carbon Monoxide exposure
hyperbaric oxygen at 2-3 atmospheres
3 hyperbaric sessions in the first 2 4hrs after exposure
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,
high-altitude (mountain) sickness
extreme altitude sickness: fatal cerebral edema
VEGF has been implicated
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
Chronic Mountain Sickness
meds/condition that reduce tolerance to high altitude
sedatives
alcohol
slightly elevated PCO2
Tx for hypercapnic pulmonary disease
positive pressure ventilation
oxygen supplementation
level of blood glucose and clinical syndrome
30mg/dL - confusional state, seizures
10 mg/dL - coma, rreparable injury
glucose reserve in a normal brain
1-2 g (30mmol/100g of tissue) inthe form of glycogen
glucose utilization rate
60-80 mg/min
T/F
Glucose reserve may sustain cerebral activity for 30 min or less once blood glucose is no longer available.
True
oxidation of 1 mole of glucose requires how many moles of O2
6
causes of hypolglycemic encephalopathy
- accidental or deliberate overdose of insulin or an oral diabetic agent
- islet cell-insulin-secreting tumor of the pancreas
- depletion of liver glycogen, which occasionally follows a prolonged alcoholic binge, starvation, or any form of severe liver failure
- glycogen storage disease of infancy
- idiopathic hypoglycemia in the neonatal period and infancy
- 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
in hypoglycemic iencephalopathy, major damage is to the
cerebral cortex
2 syndromes identified in diabetics from hyperglycemia
hyperglycemia with ketoacidosis
hyperosmolar nonketotic hyperglycemia
according to Prockop, the cerebral edema seen in hyperglycemia is due to the accumulation of
sorbitol
in hyperosmolar nonketotic hyperglycemia, what are the 2 drugs believed to inhibit the release of insulin
corticosteroids and phenytoin
EEG findings in hepatic encephalopathy
paroxysms of bilaterally synchronous slow or triphasic waves in the delta range which at first predominate frontally and are interspersed with alpha activity
MRI in portal systemic encephalopathy
high signal intensity in the globus pallidus
results from manganese deposition
Pathologic findings in hepatic encephalopathy
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
EEG in uremic encephalopathy
diffusely and irregularly slow
T/F
As with many other metabolic
derangements, the severity of the clinical effect is related
to the rapidity of decline in serum Na
True
restriction of fluid intake if serum Na level is
<120mEq/L
<130mEq/L
<120, 500mL per 24 hrs
<130, 1000,L per 24 hrs
T/F
Rapid elevations of sodium shrink the brain, especially in infants.
True
True or FalseCongenital hypothyroidism is usually recognized at birth.
Falsebecome apparent only after a few weeksdiagnosis is usually made 6-12 months
signs that raise suspicion of thyroid deficiency
physiologic jaundice tends to be severe and prolonged up to 3 monthswidening of posterior fontanellmottling of skin
two types of early life hypothyroidism
sporadic and endemic
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
sporadic cretinism
2 types of endemic cretinism
myxedematous and neurologic
neurologic form of endemic cretinism
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
myxedematous form of endemic cretinism
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
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
second
True or FalseThe effects of this midfetal hypothyroidism and iodine deficiency CAN be corrected by giving thyroid hormone at birth and thereafter.
falseit can only be prevented by giving iodine therapy to the mother before and during the first trimester of pregnancy
Thyroid hormone appears to be essential, NOT for neuronal formation and migration but for ______
dendritic-axonal development and organization
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.
true
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
cretinismor neonatal myxedema
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.
True
p1132
under conditions of transient ischemia, one pattern of damage takes the form of
incomplete infarctions in the border zones between major cerebral arteries
with predominant anoxia, neurons in __________ are particularly vulnerable
hippocampus and deep folia of cerebellum
“no-reflow” phenomenon
one of the irreversibility of ischemic lesions may be swelling of the endothelium and blockage of circulation into the ischemic cerebral tissues
most common early change in cases of severe anoxic encephalopathy
loss of distinction between teh cerebral gray and white matter
EEG in brain death syndrome
EEG is isoelectric
instances of CO poisoning
burn units
patients who have attempted suicide
accidental exposure to a faulty furnace to a car exhaust in a closed garage
half life of carbon monoxide
5 hrs
T/F
Hypoxemia at high altitudes is intensified during sleep.
True
p1139
as ventilation normally diminishes and also by pulmonary edema - another manifestation of mountain sickness
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.
True
p1141
Epidemiology of Diabetes Interventions and Complications Study Research Group
all forms of hypoglycemic encephalopathy, the major damage is to the
cerebral cortex
Cortical nerve cells degenerate and are replaced by microglia cells and astrocytes
T/F
The cerebellar cortex is more vulnerable to hypoglycemia than to hypoxia.
False
cerebellar cortex is less vulnerable to hypoglycemia
most plausible view of the pathogenesis of dialysis encephalopathy
aluminum intoxication
proposed causes in Septic Encephalopathy
altered phenylalanine metabolism and circulating cytokines
