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Adams 10th Ed > Chap 40 - Acquired Metabolic Disorders > Flashcards

Chap 40 - Acquired Metabolic Disorders Flashcards

1
Q

Main features of reversible metabolic encephalopathies:

A

Confusion, Asterexis, Myoclonus, Absent focal signs

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2
Q

Formula of serum osmolality

A

OSM = 2 x Na + Glu/18 +BUN/3

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3
Q

Normal serum osmolality

A

270-290 mOsm/L

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4
Q

Discrepancy of 10 mOsm/L of calculated & actual means:

A

additional circulating ions present

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5
Q

Medical conditions causing HIE

A

Global reduction of cerebral blood flow, Hypoxia from suffocation, Respiratory drive problem, Non-ischemic hypoxia

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6
Q

Oxygen saturation curve is

A

Not Linear

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7
Q

Compensatory dilation of resistant vessels in response to reduciton of cerebral perfusion then maintains blood flow at constant rate

A

Autoregulation

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8
Q

In total cerebral ischemia, tissue depletes sources of energy in how many minutes:

A

5 min

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9
Q

T/F. Pathologic effects of ischemia differs from pure anoxia

A

TRUE

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10
Q

Brain areas vulnerable for anoxia

A

Hippocampus & deep folia of cerebellum; brainstem & spinal cord resistant to anoxia & hypotension

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11
Q

“No reflow” phenomenon

A

irreversibilty of the ischemic lesion due to swelling of endothelium, blockage of circulation in to ischemic tissue

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12
Q

Mild degree of hypoxia w/o LOC

A

Inattentiveness, poor judgement, incoordination. Visual and verbal long term memory & mild aphasia

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13
Q

T/F. Degree of hypoxia that at no time abolishes conciousness rarely cause permanent damage

A

TRUE

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14
Q

Poor prognostic sign in HIE / Grave sign

A

Myoclonus

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15
Q

Most common early pathologic changes in anoxic encephalopathy

A

Loss of grey-white matter interface

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16
Q

Represents most severe degree of hypoxia, w/ comatose and isoelectric EEG

A

Brain Death Syndrome

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17
Q

Conditions that may look like Brain Death Syndrome

A

Anesthesia, Drug intoxication, Hypothermia

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18
Q

Freqent post-hypoxic syndromes

A

Persistent coma/stupor, Dementia, Extrapyramidal signs w/ cognitive impairment, Choreoathetosis, Cerebellar ataxia, Lance-Adams Syndrome, Amnesic state

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19
Q

Watershed syndromes between PCA & MCA

A

Balint syndrome & Anton Syndrome

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20
Q

Watershed syndrome between MCA & ACA

A

Man-in-the-barrel syndrome; w/ weakness of the hip

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21
Q

Initial improvement after anoxic event, then relapse. Imaging shows white matter disorder, where mitochondrial disorder suggested underlying mechanism

A

Delayed Postanoxic Leukoencephalopathy

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22
Q

5 clinical signs at 1 day after that may predict poor neurologic outcome /death

A

Absent corneal reflex & pupillar reaction, NO WTP, No motor response

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23
Q

Drug of choice for polymyoclonus post-anoxic

A

Clonazepam (8-10mg/day)

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24
Q

Affinity of CO for Hgb

A

200x of Oxygen

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25
Q

Level of carboxyHgb where headache, nausea, dyspnea, confusion, dizziness, clumsiness occurs

A

20-30%

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26
Q

Level of carboxyHgb where comatose occurs

A

50-60%

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27
Q

Clinical feature seen in delayed neurologic detoriation after chronic CO exposure

A

Parkinsonia gait & bradykinesia

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28
Q

Characteristic lesion of CO poisoning that produced coma

A

discrete lesions in bilateral globus pallidus & inner putamen

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29
Q

Half-life of CO

A

5 hours

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30
Q

Indication of administration of hyperbaric oxygen of 2-3 atm. Reduces cognitive sequelae from 45 to 25%. 3 hyperbaric sessions in the first 24 hrs.

A

carboxyHgb level 40% or if coma or w/ seizures

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31
Q

This is implicated as cause of cerebral edema in High-altitude sickness

A

Over-expression of VEGF

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32
Q

Most effective preventive measure for High-altitude sickness

A

Acclimatization of 2-4 days in intermediate altitudes

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33
Q

Drugs that may be used for High-altitude sickness

A

Dexamethasone & Acetozolamide

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34
Q

Chronic High Altitude Sickness seen among Peruvians is also known as

A

Monge Disease

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35
Q

Hypercapnic Pulmonary disease is described by Adams as:

A

headache, papilledema, mental dullness, drowsiness, confusion, stupor, coma, asterixis

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36
Q

T/F. In CO2 narcosis, Normally the CSF is basic compare to blood and PC02 is less than blood by 10mmHg

A

FALSE. CSF is acidic & has more pCO2

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37
Q

Important diagnostic features in Hypercapnic Pulmonary Disease

A

Papilledema, myoclonus, asterexis

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38
Q

Levels of blood glucose that will manifest the ff: 1) confusional state or seizures related to adrenal overacitvity 2) irreversible damage

A

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

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39
Q

Factor in both depression of conciousness & residual dementia

A

RATE of blood glucose decline; same goes for most metabolic encephalopathies

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40
Q

Normal glucose reseve in the brain is in the form of:

A

Glycogen

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41
Q

Glucose reserve may sustain brain activity for

A

30 min

42
Q

Convulsion in hypoglycemia is attributed to:

A

altered integrity of neuronal membrane, elevated NH3, & depressed GABA & lactate levels

43
Q

Most common causes of Hypoglycemic encephalopathy

A

Overdose of anti-diabetic meds, Islet cell insulin secreting tumor, Depletion of liver glycogen, glycogen storage disease of infancy, idiopathic hypoglycemia in neonatal, subacute & chronic hypoglkycemia islet cell dysfunction

44
Q

Sensitive and reliable indicator of impending coma in Hepatic encephalopathy

A

EEG

45
Q

Repeated attacks of hepatic coma resulting to irreversible dementia, & disorder or posture & movement

A

Chronic acquired hepatocerebral degeneration

46
Q

MRI in Portal-systemic encephalopathy____ / result to deposition of what mineral _____

A

High signal intensity of globus pallidus ; Manganese

47
Q

T/F. Concentration of NH3 levels in excess of 200mg/dL, parallels neurologic & EEG findings

A

TRUE

48
Q

In Hepatic Enecphalopathy: this cells are diffuse increase in number & size of protoplasmic astrocytes in deep layers of brain, w/ PAS staining of glycogen inclusions

A

Alzheimers type II astrocytes

49
Q

Chronic cases of Hep encephalopathy results to this neuropathologic changes

A

neuronal loss in deep layers of cerebral & cerebellar cortex, lenticular nuclei, & vacuolization of tissue

50
Q

More or less specific to Hep Enceph

A

EEG features, & astrocytic hyperplasia

51
Q

T/F. The brain has urea cycle enzymes to eliminate ammonia

A

FALSE. Absent, hence hypertrophy of astrocytes to compensate

52
Q

Removal of ammonia depends on the formation of _____, a reaction catalyzed by ATP -dependent enzyme _______, compartmentalized in astrocytes

A

glutamate, glutamate synthase

53
Q

in Hepatic enceph, this neurotransmitter increases in activity, as a result inhibits binding of endogenous benzodiazepines. Clinical effect is transient arousal.

A

GABA; GABA-benzodiazepine theory

54
Q

Concept that unifies hyperammonemia & neurotransmitters

A

Ammonia inhibits metabolism of GABA by the astrocytes & enhances GABAnergic transmission

55
Q

Treatment of hepatic encpehalopathy

A

Protein restriction, reduction of bowel flora, enemas

56
Q

Mainstay treatment for hepatic encephalopathy, that produces hydrogen ion and shift ammonia to ammonium, nontoxic product

A

Lactulose

57
Q

Drug that may have transient beneficial effect as well as diagnostic for hepatic encephalopathy

A

Flumazenil

58
Q

Prominent finding of fulminant hepatic failure & main cause of death in patients awaiting liver transplant

A

Cerebral edema

59
Q

Individuals w/ Hep C treated w/ ____ develops subtle cognitive impairment, worsening of headache, vomiting, altered conciousness

A

Interferon-alpha

60
Q

Occuring in children & adolescents, acute brain swelling w/ fatty infiltration of viscera esp liver, due to aspirin given during infection.

A

Reye Syndrome

61
Q

Improtant diagnostic clue as to the cause of the cerebral changes in Reye Syndrome

A

Liver englargement

62
Q

EEG characterized by arrhythmic delta, progressing to electrocerebral silence for patient who failed to survive

A

Reye syndrome

63
Q

Major pathologic findings of Reye syndrome

A

Cerebral edema w/ cerebellar herniation, & infiltration of hepatocytes w/ fine droplets of fats, mitochondrial dysfunction is implicated

64
Q

Initial symptoms of uremic encephalopathy

A

apathy, fatigue, inattentiveness & irritability

65
Q

Usually occur early in course of uremic enceph, where px begins to twitch & jerk & convulse, incessant during wakefulness & sleep

A

uremic twitch-convulsive syndrome

66
Q

Reason why in uremic px, low levels of AEDs may suppress seizures:

A

Serum albumin is depressed in uremia hence more unbound AEDs

67
Q

Shift of water into the brain is akin to water intoxication & results to inappropriate secretion of ADH; may present w/ headache resembling migraine, muscle cramps, agitation, drowsiness, seizures.

A

Dysequilibrium syndrome

68
Q

Symptoms of dysequilibrium syndrome occurs in ____ of dialysis and may reach up to ____ after dialysis

A

3rd-4th hr of dialysis; 48 hours

69
Q

Hepatic paraplegia is attributed to

A

loss of Betz cell in frontal cortex

70
Q

Neuropathologic changes of mild degree of microcavitation of superficial layer of cerebral cortex more severe in ____ hence distinctive of its disorder of speech & language

A

Dialysis Dementia

71
Q

Subacutely progressing syndrome w/ speech and language disorder, follwoed seizures, personality changes & intellectual changes in HD patients

A

Dialysis Dementia

72
Q

Plausible view of pathogenesis of dialysis encephalopathy

A

Aluminum intoxication

73
Q

Possible complications of Renal transplant patient.

A

Primary lymphoma, Progressive multifocal leukoencephalopathy, PRES, Fungal CNSi, CMV infection

74
Q

In how many percent do patients become disoriented within hours of onset of systemic infection

A

70%

75
Q

Hypotonic isovolemic hypernatremia, results to excretion of urine that is hypertonic relative to plasma

A

SIADH

76
Q

SIADH repsond to restriction fluid intake by how many in Na level 120meqs/L & 130meqs/L in 24 hrs

A

120 meqs/L: 500 mL; 130 meq/L 1000mL

77
Q

Formula for sodium correction

A

(target Na- actual Na) x 0.6 x weight in kg

78
Q

Administration of hypertonic solution should include this to decrease intravascular volume

A

Furosemide

79
Q

To avoid Osmotic demyelination correction of Na should not exceed

A

10mmol/L in first 24 hrs or 21 mmol/L in 48 hours

80
Q

Sodium loss is attributable to production of natriuretic polypeptide factor from heart & brain

A

Cerebral salt wasting

81
Q

Serum level for calcium to produce neurologic symptoms w/ normal albumin; & low albumin

A

12mg/dL; 10mg/dL

82
Q

Most common cause of hypercalcemia in young persons; older persons

A

hyperparathyroidism; osteolytic bone tunmors

83
Q

Usual manifestation of hypocalcemia

A

parasthesia, tetatny & convulsions

84
Q

Pathologic feature of pontine myelinosis

A

destruction of myelinated sheaths w/ sparing of axons & neurons

85
Q

ODS is commonly seen In half of this pateints w/

A

Chronic alcoholism

86
Q

In pontine lesions in ODS, MRI discloses a characteristic appearance

A

Batwing lesion

87
Q

Neurologic abnormalities observed in acute hepatic encephalopathy is similar in chronic hepatocerebral degeneration EXCEPT

A

Irreversible & progressive in chronic type

88
Q

Pathologic changes in myxedema patients that may distinguish from malnutrition & alcholoisms

A

loss of Purkinje celss & gliosis of molecular layer pronounced in vermis

89
Q

Damaging effects of hyperthermia is disproportionately seen in

A

Cerebellum

90
Q

Antibody that correspond to neurologic manifestation in celiac disease

A

antigliadin antibody

91
Q

Psychic effect seen among 10-15 % of patients taking steroids

A

High dose (60-100mg/d equivalent of prednisone)

92
Q

Encephalopathy consisting of confusion, altered conciousness, & prominent myoclonus, high titers of antibodies of _____ & ______, which is responsive to steroids

A

Hashimoto encephalopathy

93
Q

Most frequent & potentially & correctable metabolic mental defect in the world

A

Cretinism or Neonatal Myxedema

94
Q

Clinical manifestation usually seen in 6th -12th month of life, manifesting as

A

prolonged physiologic jaundice, widening of posterior fontanelle, mottling of skin, psychomotor retardation

95
Q

Two types of early life hypothyroidism:

A

Sporadic & endemic

96
Q

Sporadic type of cretenism is characterize by

A

Consequence of congenital metabolic or anatomic defect of thyroid gland, stunting of growth, delay in psychomotor devt, preventable by treatment of thyroid hormone

97
Q

Endemic cretenism is characterize by

A

occurrence is due to iodine deficiency; two types neurologic cretenism & myxedematous endemic cretenism

98
Q

Difference of neurologic & myxedematous endemic cretenism

A

Neurologic form: deaf-mutism, rigid spastic motor disorder & mental deficiency; lack of available iodine at 2nd or 3rd trimester; prevented by giving iodine in 1st trimester::::: Myxedematous form: short stature, microcephaly, coarse facial features, psyhomotor retardation

99
Q

T/F. Thyroid hormone is essential for neuronal formation & migration

A

FALSE. It is for dendritic-axonal development & organization

100
Q

Pathologic findings of cretenism

A

decrease interneuronal distances, packing density in increased in immature cortex, deficiency of neuropil; poverty of dendritic branching & synapses

Adams 10th Ed (8 decks)

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