CH39: Acquired Metabolic Disorders

Question 1

What is the formula for OSM?(p. 1157)

Answer 1

OSM= 2x Na + glucose/18 +bun/3

mOSM/L

Question 2

In the physiology of hypoxic and ischemic damage, what level of mmHg will additional compensation in the form of increased oxygen extraction allows normal energy metabolism to continue? (p. 1157)

Answer 2

below 60 to 70mmHg

Question 3

With predominant anoxia, neurons in portions of these areas are particularly vulnerable (p. 1158)

Answer 3

hippocampus

deep folia of the cerebellum

Question 4

Mild degrees of hypoxia without los of consciousness symptoms (p. 1158)

Answer 4

inattentiveness, poor judgment, inoccordination

Question 5

Beyond how many minutes, there will be permanent injury in hypoxia? (p. 1158)

Answer 5

5 mins

Question 6

Hypoperfusion dominantes. There are two syndromes (p. 1160)

Answer 6

1. Visual agnosia including Balint and cortical blindness

2. Man in the barrel syndrome

Question 7

In carbon monixide poisoning, headache, nausea, dyspnea, confusion, dizzines and clumsiness happens when carboxyhemoglobin level reaches (p. 1162)

Answer 7

20-30% of total hemoglobin

Question 8

Treatment for carbon monoxide poisoning (p. 1162)

Answer 8

Inspired oxygen, hyperbaric at 2-3 atm

Question 9

For high altitude sickness, at this level, headache, anorexia, nauea and vomiting, weaknes and insomnia appear (p. 1163)

Answer 9

8,000ft

Question 10

For high altitude sickness, at this level, ataxia, tremor, drowsines, mild confusion and hallucinations appear(p. 1163)

Answer 10

> 8,000ft

Question 11

At this level, 50% of individuals develop asymptomatic retinal hemorrhages (p. 163)

Answer 11

16,000ft

Question 12

For hypercapnic pulmonary disease, this is the most effective therapeutic measure (p. 1163)

Answer 12

positive pressure ventilation

Question 13

When this drug is admnistered for the treatmetn of underlying pulmonary disease, it may produce high levels and a tendency to produce seizures (p. 1163)

Answer 13

aminophylline

Question 14

In hypoglycemic encephalopathy, with glucose at about this level, this cerebral disorder takes form of a conusional state (p. 1163)

Answer 14

30mg/dL

Question 15

In hypoglycemic encephalopathy, with glucose at about this level, coma ensues (p. 1163)

Answer 15

10mg/dL

Question 16

Glucose is metabolized by the bran at arate of (p. 1164)

Answer 16

60-80mg/min and can sustain cerebral activity for 30mins or less once blood sugar is no longer avilable

Question 17

How many percent of glucose is oxidized? (p. 1164)

Answer 17

85 to 90 percent. The remainder is used in the formation of proteins and other substances

Question 18

EEG finding in hepatic stupor or coma (p. 1166)

Answer 18

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

Question 19

Acute vs chronic portal-systemic encephalopathy MRI findings (p. 1168)

Answer 19

Chronic: high signal intensity on T1 weighted sequences in the globus pallidus
Acute: abnormal T2 hyperintensity throughout the cerebral hemispheres in insula, thalamus and cingulate

Question 20

Pathologic findings of hepatic coma (p. 1167)

Answer 20

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

Question 21

Treatment of hepatic encephalopathy (p. 1168)

Answer 21

Restriction of dietary protein
neomycin or kanamycin
lactulose

Question 22

Mechanism of action of lactulose (p. 1168)

Answer 22

produces hydrogen ions and shifts ammonia to ammonium

Question 23

This syndrome is characterized by acute brain swelling in association with fatty infiltration of the viscera, particularly the liver (p. 1168)

Answer 23

Reye syndrome

Question 24

EEG finding in uremic encephalopathy (p. 1169)

Answer 24

diffusely and irregularly slow and may remain so for several weeks after the institution of dialysis

Question 25

70% of patients experience this symptom in dialysis disequilibrium syndrome (p. 1170)

Answer 25

headache

Question 26

A characteristic of dialysis encephalopathy is the transient improvement in speech with the administration of ___ (p. 1170)

Answer 26

Intravenous diazepam

Question 27

EEG in dialysis encephalopathy (p. 1170)

Answer 27

invariably abnormal, taking the form of paroxysmal and sometimes periodic sharp-wave or spike and wave activity, intermixed with abundant theta and delta activity

Question 28

Dialysis is represented a form of this drug intoxication (p. 1171)

Answer 28

Aluminum

Question 29

Hypotonic isovolemic hypernatremia is most often a result of __ (p. 1171)

Answer 29

SIADH

Question 30

Restriction of fluids in SIADH (p. 1172)

Answer 30

500ml/24hrs if Na < 120

1,000ml/24hrs if Na < 130

Question 31

formula for infused Na load (p. 1172)

Answer 31

([target Na- starting Na] x 0.6) x weight kg= infused Na load (meq)

Question 32

300 to 500ml of 3% saline, infused rapidly IV will increase he serum Na concenration by about ___ (p. 1172)

Answer 32

1meq/L/h for 4 hours

Question 33

Level of Ca to produce neurologic symptoms (p. 1173)

Answer 33

12mg/dL

Question 34

Usual manifestations of hypocalcemia (p. 1173)

Answer 34

paresthesias, tetany and seizures

Question 35

Pathologic attribute of CPM (p. 1173)

Answer 35

remarkable dissolution of the sheaths of myelinated fibers and the sparing of the neurons

Question 36

First symptom of chronic acquired hepatocerebral degeneration (p. 1175)

Answer 36

tremor of the outstretched arms, fleeing arrhythmic twitches of the face and limbs or a mild unsteadiness of gait with action tremor

Question 37

Ammonia levels when neurologic correlates in hepatocerebral degeneration (p. 1176)

Answer 37

> = 200mg/dL

Question 38

Pathologic findings in chronic acquired hepatocerebral degeneration (p. 1176)

Answer 38

more cortical than Wilson disease
resemble hypoxic ones concentrated in the vascular border zones
myelinated and fibers and nerve cells are destroyed with marginal fibrous gliosis

Question 39

Calcifications in chronic hypocalcemia (p. 1176)

Answer 39

basal ganglia, dentate nuclei, cerebellar cortex

Question 40

Pathologic finding in this disease is scattered unusual glycogen-containing bodies (p. 1177)

Answer 40

Cerebellar ataxia with myxedema (the bodies are called myxedema bodies)

Question 41

The changes in hyperthermia is disproportionaely severe in this structure (p. 1177)

Answer 41

cerebellum

Question 42

Neuro findings associated with gluten- sensitive eneropathy (p. 1177)

Answer 42

progressive cerebellar ataxia of gait and limbs

sometimes with polymyoclonus in association with a gluten - sensitive enteropathy

Question 43

In association with sprue in more than 90% of patients with the ___ (p. 1177)

Answer 43

HLA DQ2, DQ8 genotypes

Question 44

not autoantibodies but are directed against gluten, the offending agent (p. 1178)

Answer 44

antigliadin antibodies

Question 45

Attributes that usually allow an encephalopathic confusional state to be distinguished from dementia (p. 1178)

Answer 45

drowsiness and inattentiveness

Question 46

EEG findings in Cushing syndrome and corticosteroid psychosis (p. 1178)

Answer 46

less well-modulated and slower frequencies appear

Question 47

Neurologic findings in hyperthyroidism (p. 1179)

Answer 47

Action tremor; chorea occasionally w combinations of proximal muscular weakness

Question 48

Treatment for Hashimoto Encephalopathy (p. 1179)

Answer 48

High tighters of antithyroid antibodies respond well to steroid therapy