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neuro > A9. Unconsciousness due to metabolic origin > Flashcards

A9. Unconsciousness due to metabolic origin Flashcards

1
Q

Unconsciousness due to metabolic origin is usually a disorder of

A

disorder of awareness

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2
Q

Unconsciousness due to metabolic origin can manifest as

A

persistent vegetative state (PVS),
also called unresponsive wakefulness syndrome (from lecture).

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3
Q

General symptoms of Unconsciousness due to metabolic origin

A
  • pupils are normal in size and reactive to light
  • eye movements are usually full and conjugate
  • depressed mental state
  • confusion with impairment of consciousness
  • depressed respiratory rate
  • limb movements are symmetrically reduced and associated with hypotonicity.
  • Hemiparesis can occur in:
    *non-ketotic hyperosmolar coma, *hepatic encephalopathy.
    *hyperglycemic encephalopathy.
    *uremic encephalopathy.
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4
Q

Causes of Unconsciousness due to metabolic origin

A

● Deficiency of essential substrates (glucose, oxygen, vitamin B12)

● Exogenous toxins
(eg. drugs, heavy metals, solvents)

● Endogenous toxins/systemic metabolic diseases
(eg. uremia, hepatic encephalopathy, electrolyte imbalances, thyroid storm

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5
Q

Deficiency of essential substrates that can cause Unconsciousness due to metabolic origin

A
  • glucose
  • oxygen
  • vitamin B12
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6
Q

Exogenous toxins that can cause Unconsciousness due to metabolic origin

A
  • drugs,
  • heavy metals,
  • solvents)
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7
Q

example of Endogenous toxins/systemic metabolic diseases which cause Unconsciousness due to metabolic origin

A
  • uremia,
  • hepatic encephalopathy,
  • electrolyte imbalances,
  • thyroid storm
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8
Q

causes of Disorder of glucose metabolism (prolonged hypoglycemia)

A

Can be due to
* insulin overdose,
* fasting,
* alcohol intoxication and
* rarely insulinomas

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9
Q

how to differentiate between comatose state due to hypoglycemia
and a structural cause.

A

In hypoglycemia, pupillary light reactions may be intact, while in structural damage they
are usually absent

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10
Q

does hypoglycemia lead to focal necrosis in brain, brainstem or spinal cord?

A

Hypoglycemia does NOT cause focal necrosis in brain, brainstem or spinal cord.
They remain intact even in long-standing, severe hypoglycemia

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11
Q

In Disorder of glucose metabolism (prolonged hypoglycemia) what is damaged

A

The superficial layers of the cortex are damaged,
but laminar necrosis (as in global ischemia) is NOT seen

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12
Q

Disorder of glucose metabolism (prolonged hypoglycemia - where does necrosis occur

A

Necrosis also develops in the
* superficial layers of the cortex
* hippocampus,
* caudate nucleus and
* granular cells of dentate gyrus

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13
Q

what blood glucose level can cause coma?

A

Blood glucose levels <0,6 mmol/l can cause coma

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14
Q

Hyperosmolar hyperglycemia results from

A

hyperosmolar effect of severe hyperglycemia

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15
Q

Hyperosmolar hyperglycemia can cause patient to have

A

involuntary movements,
seizures and
hemiparesis

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16
Q

is vascular thrombosis common in Hyperosmolar hyperglycemia

A

not uncommon

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17
Q

does ketoacidosis occur in Hyperosmolar hyperglycemia

A

Ketoacidosis is mild or does not occur

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18
Q

Diabetic ketoacidosis occurs in patient with

A

known diabetes, but can also be the first manifestation

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19
Q

Diabetic ketoacidosis is often precipitated by

A

infection
or
poor medical compliance

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20
Q

Diabetic ketoacidosis - what metabolites are accumulated

A

accumulation of acetone and ketone bodies

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21
Q

patients with Diabetic ketoacidosis present with

A
  • progressive neurological impairment
  • with lethargy, and
  • ultimately coma
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22
Q

Symptoms of diabetic ketoacidosis

A
  • dehydration (due to osmotic diuresis),
  • fatigue,
  • weakness,
  • headache,
  • abdominal pain,
  • Kussmal breathing,
  • confusion,
  • coma
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23
Q

causes of Hypoxia

A
  • May also occur at high altitudes (low O 2 tension of the atmosphere and in drowning

○ Reduced arterial oxygen pressure: e.g. lung disease or PE
■ Hypoxia due to PE causes confusion and lethargy before loss of consciousness

○ Reduced hemoglobin to carry oxygen: anemia or blood loss
19
■ pO 2 does not drop, but substrate availability is decreased or O 2 fails to bind to
hemoglobin

○ Reduced flow of blood containing O 2 (ischemic hypoxia): due to reduced cardiac output
→ reduced cerebral blood flow

○ Biochemical block of cerebral utilization of O 2 : e.g. cyanide poisoning (rare), also called
histotoxic hypoxia

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24
Q

causes of Reduced arterial oxygen pressure:

A
  1. lung disease
  2. or PE
    ■ Hypoxia due to PE causes confusion and lethargy before loss of consciousness
25
Q

causes of Reduced hemoglobin to carry oxygen:

A
  1. anemia or
  2. blood loss

■ pO2 does NOT drop, but substrate availability is decreased or O2 fails to bind to hemoglobin

26
Q

cause of Reduced flow of blood containing O 2 (ischemic hypoxia):

A

due to reduced cardiac output
→ reduced cerebral blood flow

27
Q

causes of Biochemical block of cerebral utilization of O 2

A
  • cyanide poisoning (rare), also called
    histotoxic hypoxia
28
Q

Hypoxia due to PE causes confusion and lethargy before what?

A

loss of consciousness

29
Q

if pO 2 drops under 40 mmHg

A

Consciousness is lost in some seconds

30
Q

how long can Hypoxic hypoxia (without ischemia) be tolerated without permanent damage

A

can be tolerated for 10-40 minutes without permanent damage to the brain,
even if pO 2 is below 20 mmHg

31
Q

CO intoxication leads to

A

bilateral necrosis of globus pallidus

32
Q

is grey matter or white more vulnerable to hypoxia

list structure most vulnerable

A

grey matter is more vulnerable than white
Vulnerability to hypoxia (most to least),
○ Frontal cortex (most)
○ Hippocampus, parietal/occipital cortex
○ Basal ganglia/cerebellum
○ Brain stem

33
Q

Symptoms of hypoxia - pupil and eye

A

Pupils: large-reactive

Eye movements: no movement – conjugate (if severe)

34
Q

Hypercapnia symptoms

A
  • headache,
  • confusion,
  • disorientation,
  • involuntary movements,
  • papilledema,
  • depressed limb reflexes,
  • extensor plantar response
35
Q

if PCO2 > 50 mmhg in
COPD
or
obesity-ventilation syndrome

A

CO2 narcosis may occur

36
Q

when does co2 narcosis occur in COPD or obesity-ventilation syndrome?

A

if pco2 over 50 mmhg

37
Q

Hypothermia
Common in

A
  • alcoholics with Wernicke encephalopathy (deficiency of B1)
38
Q

Renal/uremic encephalopathy is a sign of

A

acute renal failure

39
Q

what happens in Renal/uremic encephalopathy

A
  • Brain amino acid metabolism is also impaired, and
  • causes an imbalance between excitatory and inhibitory neurotransmitters
    or
  • accumulation of false neurotransmitters
40
Q

Renal/uremic encephalopathy EEG shows

A

Slow waves are found on the EEG

41
Q

can Renal/uremic encephalopathy be reversed?

A

condition is reversed with dialysis,
but may take 1-2 days before it is totally reversed

42
Q

Hepatic encephalopathy onset can be

A

Can have acute or chronic onset

43
Q

causes of hepatic encephalopathy

A
  • increased ammonia,
  • false neurotransmitters,
  • endogenous benzodiazepine-like structures,
  • abnormal fatty acid metabolism,
  • free radical damage,
  • cerebral edema and
  • increased mercaptans
44
Q

Symptoms of
Hepatic encephalopathy

A

○ Pupils: small-reactive

○ Eye movements: no movement – dysconjugate (if severe)

○ Increased respiratory rate

○ Asterixis, myoclonus, dysarthria, ataxia, hyperreflexia, hemiparesis

45
Q

how does patient with hepatic encephalopathy appear in early phase vs late

A
  • At earlier phases the patient is in an
    agitated confusional state
  • Unconsciousness and coma are the most severe stages.
46
Q

Hepatic encephalopathy- Neurological signs in comatose patients include

A
  • hemiparesis,
  • ocular bobbing,
  • dysconjugate eye movements and
  • tonic downward deviation of the eyes
47
Q

In deep coma what can be present

hepatic encephalopathy

A
  • decerebrate posture and
  • agonal respiration can be present
48
Q

Hepatic encephalopathy EEG shows

A

The EEG is always abnormal (shows triphasic slow waves)

49
Q

Electrolyte disturbances

A

● Hypernatremia
● Hyponatremia

● Hypercalcemia,
● hypocalcemia,

● hyperkalemia
● hypokalemia

● hypomagnesemia,

50
Q

Hypernatremia present as

A

Hyperosmolar diabetic hypernatremia:

mostly in elderly diabetic patients

51
Q

what does hypernatremia cause to the brain

A

○ Leads to osmotic dehydration of the brain

52
Q

Hyponatremia
range

A

Na <126 mmol/l

53
Q

Hyponatremia causes

A
  • primary renal disease,
  • osmotic diuresis,
  • adrenal insufficiency,
  • vomiting,
  • diarrhea,
  • burns,
  • ascites,
  • peritonitis,
  • edema,
  • dilution,
  • sickle cell syndrome,
  • hyperglycemia,
  • SIADH
54
Q

Hyponatremia treatment

A

slow correction of the sodium, over several days

○ Too fast correction can cause central pontine myelinolysis (symptoms can be vertical
gaze palsy, tetraplegia)

55
Q

○ Too fast correction of hyponatremia can cause

A

central pontine myelinolysis (symptoms can be:
vertical gaze palsy,
tetraplegia)

56
Q

central pontine myelinolysis symptoms

A
  • vertical gaze palsy,
  • tetraplegia)
57
Q

which electrolyte disturbances Can cause coma in severe cases

A
  • Hypercalcemia,
  • hypocalcemia,
  • hypomagnesemia,
  • hypokalemia,
  • hyperkalemia
  • hypernatremia
  • hyponatremia
58
Q

Other causes of Unconsciousness due to metabolic origin

A

● Hypothyroidism
● Lactic acidosis
● Addison’s disease

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