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Res Quizzes > Metabolic Diseases > Flashcards

Metabolic Diseases Flashcards

1
Q

Formula for serum osmolality

A

OSM=2Na+Glucose/18+BUN/3 in mg/dL

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2
Q

What is the normal serum osmolality?

A

270-290 mOsm/mL

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3
Q

True or False. the brain may be damaged, even to an irreparable degree, by a disturbance of blood chemistry (e.g., hypoglycemia, hypoxia) that has vanished by the time the patient is examined

A

TRUE

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4
Q

What are the medical conditions that lead to ischemic-hypoxic encephalopathy?

A
  1. global reduction in cerebral blood flow
  2. Hypoxia from suffocation
  3. diseases that paralyze the respiratory muscles ( or damages the medulla and leads to
    failure of breathing
  4. carbon monoxide (CO) poisoning
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5
Q

What is the ultimate determinant of the adequacy of oxygen supply to organs?

A

product of blood oxygen content & cardiac output

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6
Q

What determines blood oxygen content?

A

Hemoglobin concentration &

O2 saturation %

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7
Q

How much is the hemoglobin O2 saturation at normal pH and temperature, partial pressue of 60mmHg? At 40mmHg?

A

@ 60mmHg = 90%

@ 40mmHg = 75%”

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8
Q

The parts of the nervous system which are most vulnuerable to hypoxia are:

A

1 CA1 of hippocampus
2 cerebellar Purkenje cells
3 striatal neurons
4 Cortical Layers 3 5 6

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9
Q

The parts of the nervous system which are resistent to hypoxia are:

A

nuclear structures of the brainstem and spinal cord

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10
Q

True or False. degrees ofhypoxia that at no time abolish consciousness rarely, if ever, cause permanent damage to the nervous system.

A

TRUE

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11
Q

True or False. Subnormal body temperatures, greatly prolong the tolerable period of hypoxia

A

TRUE

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12
Q

What connotes a more favorable prognosis for patients with anoxia?

A

intact brainstem function as indicated by normal pupillary light and ciliospinal responses, induced by passive head turning (doll’s eye movements), and other
vestibula-ocular reflexes

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13
Q

4 Signs of grave prognosis in anoxic patients:

A 
after Day 1 absence of the following:
1 absent corneal response
2 absent pupillary reactivity
3 no withdrawal to pain
4 absence of any motor response
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14
Q

The most common early change in neuroimaging studies of patients with severe hypoxic injury:

A

loss of gray-white matter distinction

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15
Q

The 7 permanent neurologic sequelae or posthypoxic syndromes observed most frequently are as follows:

A
  1. Persistent comaor stupor
  2. With lesser degrees of cerebral injury, dementia with
    or without extrapyramidal signs
  3. Extrapyramidal (parkinsonian) syndrome with cognitive
    impairment (discussed in relation to CO poisoning)
  4. Choreoathetosis
  5. Cerebellar ataxia
  6. Intention or action myoclonus (Lance-Adams syndrome)
  7. An amnesic state
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16
Q

Syndrome of initial improvement after hypoxia/anoxia followed by apathy, confusion, irritability, agitation or mania after 1-4 weeks

A

Delayed Postanoxic Encephalopathy and Leukoencephalopathy

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17
Q

What is Lance Adams Syndrome?

A

delayed movement-induced myoclonic and ataxic tremor after an anoxic episode

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18
Q

Carbon Monoxide affinity to hemoglobin is ____ times more than oxygen

A

200x

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19
Q

Half life of carbon monoxide?

A

5 hours

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20
Q

Symptoms of carbon monoxide poisoning when the carboxyhemoglobin reaches 20-30%

A

headache, nauseam dyspnea, confusion, dizziness, clumsiness

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21
Q

Symptoms of carbon monoxide poisoning when the carboxyhemoglobin reaches 50-60%

A

coma, decerebrate, decorticate, seizures

generalized EEG slowing

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22
Q

Symptoms of carbon monoxide poisoning when the carboxyhemoglobin reaches slightly higher than 30%

A

blindness, visual defects papilledema

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23
Q

Delayed neurologic deterioration after CO poisoning

A

extrapyramidall symptoms (parkinsonian, bradykinesia)

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24
Q

Characteristic lesions in neuroimaging of patients with CO poisoing

A

can be normal
globus pallidus
putamen

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25
Q

Treatment of CO poisoning

A

hyperbaric oxygen

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26
Q

The protein that is said to be responsible of cerebral edema in acute mountain sickness

A

VEGF

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27
Q

Main features of Monge Disease

A

aka chronic mountain sickness

pulmonary hypertension
cor pulmonale
secondary polycythemia
hypercarbia

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28
Q

Most effective preventive measure for acute mountain sickness

A

acclimatization by a 2- to 4-day stay at intermediate altitudes

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29
Q

the brain rapidly adapts to respiratory acidosis through:

A

the generation and secretion of bicarbonate by the choroid plexuses

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30
Q

the mechanism of hypercapnic pulmonary disease in inducing cerebral disorder

A

direct CO2 narcosis

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31
Q

Symptoms of hypoglycemia at

1) 30mg/dL
2) 10mg/dL

A

1) 30mg/dL - confusional state, seizure
2) 10mg/dL - “medullary phase”, coma, irreparable injury, dilated pupils, pale skin, shallow respiration, hypotonia, slow pulse

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32
Q

What is the rate of glucose utilization in the brain?

A

60-80mg/min

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33
Q

The normal brain has a glucose reserve of ______________, mostly in the form of
glycogen.

A

1 to 2 g (30 mmol/ 100 g of tissue)

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34
Q

How many moles of O2 is required for the oxidation of 1 glucose molecule

A

6

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35
Q

What happens to the 10-15% of glucose taken up by the brain if it isnt oxidized?

A

used for the formation of neurotransmitters, particularly GABA

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36
Q

Nonglucose substances that can be utilized by the brain

A

keto acids, lactate, pyruvate, fructose, other hexoses

37
Q

The convulsions in hypoglycemia has been attributed to?

A

an altered integrity of neuronal membranes and to elevated NH3 and depressed GABA and lactate levels

38
Q

The most common causes of hypoglycemic encephalopathy are (6):

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) an idiopathic hypoglycemia in the neonatal period and infancy
(6) subacute and chronic hypoglycemia from islet cell hypertrophy and islet cell tumors of the pancreas, carcinoma of the stomach, fibrous mesothelioma, carcinoma of the cecum, and hepatoma

39
Q

Ultrastructural changes in the brain seen in hypoglycemia

A

mitochondrial changes, first in dendrites and then in nerve cell soma, followed by nuclear membrane disruption leading to cell death

40
Q

Pathogenesis of Hepatic Encephalopathy or Porto Sytemic Encephalopathy

A

1 abnormality of NH3 metabolism - NH3 not converted to urea because the brain does not have urea enzymes– intereferes with cerebral metabolism

2 ATP depletion - removal of NH3 depends on glutamine formation which depends on ATP dependent glutamine synthetase

3 manganese accumulation in the pallidum

4 NH3 inhibits GABA metabolism –> increased GABA

41
Q

West Haven Grading of Hepatic Encephalopathy

A

Grade 0 - Minimal hepatic encephalopathy; lack of detectable changes in personality or behavior; minimal changes in memory, concentration, intellectual function, and coordination; asterixis is absent.
Grade 1 - Trivial lack of awareness; shortened attention span; impaired addition or subtraction; hypersomnia, insomnia, or inversion of sleep pattern; euphoria, depression, or irritability; mild confusion; slowing of ability to perform mental tasks
Grade 2 - Lethargy or apathy; disorientation; inappropriate behavior; slurred speech; obvious asterixis; drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, and intermittent disorientation, usually regarding time
Grade 3 - Somnolent but can be aroused; unable to perform mental tasks; disorientation about time and place; marked confusion; amnesia; occasional fits of rage; present but incomprehensible speech
Grade 4 - Coma with or without response to painful stimuli

42
Q

Mainstay of treatment of hepatic encephalopathy

A

lactulose - inert sugar metabolized by bacteria which produces H+ covnverting ammonia to ammonium, non toxc product eliminated in the stool

43
Q

Given to suppress the urease-producing organisms in the bowel

A

kanamycin

neomycin

44
Q

Neuropathologic changes in hepatic encephalopathy

A

diffuse increase in the number and size of the protoplasmic astrocytes in the deep layers of the cerebral cortex, lenticular nuclei, thalamus, substantia nigra, cerebellar cortex, and red, dentate, and pontine nuclei, with little or no visible alteration in the nerve cells or other parenchymal elements

Alzheimer Type II astrocytes

45
Q

a special type of nonicteric hepatic encephalopathy occuring in children and adolescents characterized by ACUTE BRAIN SWELLING in association with fatty liver

A

Reye Syndrome

or Reye Johnson Syndrome

46
Q

Implicated pathogenesis of Reye Syndrome and aspirin toxicity

A

mitochondrial dysfunction

47
Q

EEG finding in Reye Syndrome

A

diffuse arrhythmic delta activity

progressing to electrocerebral silence

48
Q

True or False. The myoclonic-twitch syndrome is a component of hypertensive encephalopathy

A

FALSE

49
Q

True or False. Cerebral edema is seen in uremic encephalopathy

A

FALSE

in fact neuroimaging would usually show cerebral shrinkage

50
Q

True or False. All every level of the nervous system is affected in uremia

A

TRUE

51
Q

Possible biochemical basis of uremic encephalopathy

A

retention of organic acids
phosphate elevation in the CSF
urea and other toxins like parathyroid hormone

52
Q

Reason for the shift of water to the brain in Dialysis Disequilibrium Syndrome

A

water intoxication and inappropriate secretion of ADH

NOT because of reverse urea syndrome

53
Q

EEG findings in Dialysis Encephalopathy (Dialysis Dementia)

A

invariably abnormal
paroxysmal and sometimes periodic sharp-wave or spike-and-wave activity (up to 500 mV and lasting 1 to 20 s) intermixed with abundant theta and delta activity.

54
Q

The heavy metal culprit in Dialysis Dementia

A

Aluminum

55
Q

The more severe area of microcavitation of the superficial layers of the cerebral cortex in Dialysis Dementia is found where?

A

left frontotemporal operculum

– explains the speech and language disturbance

56
Q

True or False. Paratonia, as well as polyneuropathy, is common in Septic Encephalopathy

A

TRUE

57
Q

Proposed pathogenesis of cerebral dysfunction in Septic Encephalopathy

A

altered phenylalanine metabolism and circulating cytokines

58
Q

the type of hyponatremic state induced by mannitol

A

HYPERTONIC

59
Q

SIADH causes what tyoe of hyponatremic state?

A

HYPOTONIC ISOVOLEMIC

60
Q

the type of hyponatremic state induced by hyperglycemia

A

HYPERTONIC

61
Q

the type of hyponatremic state induced by hyperlipidemia or hyperproteinemia

A

ISOTONIC

62
Q

Define hyponatremia

A

serum Na of

63
Q

Na concentration of normal saline solution

A

154 mEq/L

64
Q

Na concentration of 3% hypertonic saline solution

A

513 meq/L

65
Q

How to manage SIADH?

A

Fluid restriction per day:

if Na

66
Q

Formula for Na infusion for hyponatremia

A

(target Na - starting Na)x0.6 x weight *kg

67
Q

The brain retains its volume effectively in hypernatremia with hyperosmolarity because of the production of _____

A

idiogenic osmoles

possibly glucose metabolites and amino acids

68
Q

How to correct hypokalemia

A

IV infusion of K no more than 4-6 mEq/h

69
Q

Define hypercalcemia

A

serum Ca > 10.5mg/dL

70
Q

If the serum protein content is normal, Ca levels

greater than ______ are required to produce neurologic symptoms.

A

12 mg/ dL

71
Q

In young persons, the most common cause of hypercalcemia is

A

hyperparathyroidism

72
Q

in older persons, the most common cause of hypercalcemia is

A

osteolytic bone tumors, particularly metastatic carcinoma and multiple myeloma

73
Q

CPM histopathologic picture

A

dissolution of the sheaths of myelinated fibers and the sparing of axons

a grayish discoloration and fine granularity in
the center of the base of the pons

74
Q

Extrapontine myelinolysis structures involved

A

internal capsule, deep cerebral white matter and corpus callosum

75
Q

MRI finding of batwing lesion in the pons

A

CPM

76
Q

How to correct hyponatremia?

A

no more than 10 mEq/L in the initial 24 h

and by no more than about 21 mEq/L in the initial 48 h

77
Q

swollen and chromatolyzed nerve cells found in the cortical and subcortical regions (basal ganglia and thalamus) of the brains of people with Wilson disease and acquired hepatolenticular degeneration

A

Opalski cells

78
Q

histopathologic finding in the cerebellum of hyperthermic patients

A

loss, pyknosis, and disintegration of Purkinje cells

gliosis throughout the cerebellar cortex

degeneration of the dentate nuclei

79
Q

Vitamin deficiency that causes ataxia

A

E

80
Q

differentiate neurologic endemic cretinism from myxedematous endemic cretinism

A

neurologic deafness, dysarthria, proximal limb and truncal rigid-spastic motor disorder involving mainly the legs, and mental deficiency

myxedematous - no deafness or spastic rigidity of the limbs

81
Q

True or False. Thyroid hormone appears to be essential, not for neuronal formation and migration but
for dendritic-axonal development and organization

A

TRUE

82
Q

Osmolarity of Normal saline solution

A

314 mOsm/L

83
Q

Osmolarity of lactated ringers solution

A

289 mOsm/L

84
Q

Blood alcohol level where in you see: Euphoria or dysphoria, shy or expansive, friendly or argumentative. Impaired concentration, judgement and sexual inhibitions

A

50-150mg/dL

85
Q

Blood alcohol level where in you see: Slurred speech and ataxic gait, diplopia, nausea, tachycardia, drowsiness, or labile mood with sudden bursts of anger or antisocial acts

A

150-250 mg/dL

86
Q

Blood alcohol level where in you see: Stupor alternating with combativeness or incoherent speech, heavy breathing, vomiting

A

300 mg/dL

87
Q

Blood alcohol level where in you see: coma

A

400 mg/dL

88
Q

Blood alcohol level where in you see: Respiratory paralysis, death

A

500 mg/dL

89
Q

Chemicals associated with Parkinsonism

A 
Carbon monoxide
Carbon disulfide
Manganese
Other heavy metals
Cyanide

Res Quizzes (18 decks)

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