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module 104 - theme 2 > hypoglycaemia > Flashcards

hypoglycaemia Flashcards

1
Q

what is hypoglycaemia?

A

when blood glucose falls below 4mM

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2
Q

why does a rapid fall in blood glucose cause sweating, tachycardia and agitation?

A

due to activation of the sympathetic nervous system and release of adrenaline and glucagon

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3
Q

what are the symptoms of hypoglycaemia?

A
  • moodiness
  • faintness
  • numbness in arms and hands
  • blurred vision
  • confusion
  • memory loss
  • dizziness
  • lethargy
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4
Q

what are the serious consequences of hypoglycaemia?

A

relate to the brain:

  • loss of cognitive function
  • seizures
  • coma
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5
Q

when does loss of conciseness occur with hypoglycaemia?

A

when blood glucose reaches 2.5mM

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6
Q

what are the causes of hypoglycaemia?

A
  • fasting or exercise
  • hypernatraemia
  • hypovolaemia from vomiting, dehydration…
  • pathologies such as adrenal insufficiency
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7
Q

when does alcohol-induced hypoglycaemia occur?

A
  • several hours after alcohol ingestion

- occurs on depletion of glycogen stores when blood glucose is reliant on hepatic gluconeogenesis

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8
Q

what happens in the short term with alcohol-induced hypoglycaemia?

A

consumption of alcohol places additional stresses on gluconeogenesis as alcohol is metabolised primarily in the liver by an unregulated process

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9
Q

what happens in the long term with alcohol-induced hypoglycaemia?

A

gluconeogenesis may also be decreased by liver damage and reduces muscle mass

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10
Q

what metabolises ethanol in the liver?

A

alcohol dehydrogenase

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11
Q

what is required for metabolism of ethanol in the liver?

A

NAD+ as a co-enzyme

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12
Q

what is the end result of ethanol metabolism in the liver?

A

a high NADH:NAD+ ratio in the cytosol

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13
Q

where is acetaldehyde transported to?

A

the mitochondria

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14
Q

what is acetaldehyde oxidises to and by?

A

oxidised to: acetate

oxidised by: acetaldehyde dehydrogenase

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15
Q

what does the oxidation of acetaldehyde result in?

A

high NADH:NAD+ ratio in the mitochondria

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16
Q

what is the metabolic consequence of alcohol metabolism?

A

reduces the availability of substrates for entry into gluconeogenesis to maintain plasma glucose levels

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17
Q

when do symptoms of alcohol-induced hypoglycaemia show?

A

occurs as a result of ethanol ingestion when blood glucose levels are reliant on gluconeogenesis

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18
Q

what are the symptoms of alcohol-induced hypoglycaemia?

A
  • fall in blood glucose leads to stress response, in an effort to enhance the stimulation of gluconeogenesis by combined action of glucagon and adrenaline
  • rapid breathing is a physiological response to metabolic acidosis resulting from excess lactic acid
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19
Q

what is the effect on lipid metabolism of long term alcohol consumption?

A
  • high levels of NADH inhibit fatty acid oxidation: instead the excess NADH signals that conditions are right for fatty acid synthesis
  • TGs accumulate in the liver causing a condition known as ‘fatty liver’ - also exported as VLDL
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20
Q

what are the 3 stages of fatty liver disease progression?

A

1) the liver becomes inflamed causing damage to the liver tissue (steatohepatits)
2) scar tissue forms at site of damage (fibrosis)
3) extensive scar tissue replaces healthy tissue (cirrhosis_

21
Q

what is acetate produced from EtOH converted to?

A

acetyl-CoA

22
Q

what is the effect on efficiency of ethanol metabolism with long term alcohol consumption?

A

further processing of acetyl-CoA in TCA cycle prevented because high levels of NADH inhibits both citrate synthase and alpha-ketoglutarate dehydrogenase

23
Q

what are the 2 consequences of accumulation of acetyl-CoA?

A

1) production of ketone bodies which are released into the blood and exacerbates the already acidic conditions resulting from high lactate levels
2) processing of acetate in the liver becomes inefficient, leading to a build up of acetaldehyde, which is highly toxic

24
Q

how does alcohol incited hepatomegaly occur?

A
  • alcohol consumption decreases the activity of the proteosome
  • leads to accumulation of protein, which causes enlargement of the liver
  • decreased proteasome activity also increases oxidative stress
25
Q

what deficiency do 50% of alcoholics with liver disease suffer with?

A

thiamine deficiency (B1)

26
Q

what are the symptoms of thiamine deficiency?

A
  • anorexia
  • irritability
  • difficulties with short term memory
27
Q

what are the causes of thiamine deficiency?

A
  • malnourishment
  • ethanol interferes with GI absorption
  • hepatic dysfunction which hinders storage and activation to thiamine pyrophosphate
28
Q

what is the half life of thiamine?

A

10-20 days

29
Q

what are glycogen storage diseases?

A
  • inherited disease in which the stores of glycogen are affected by defects in either the enzymes of synthesis or degradation of glycogen
30
Q

what type of disease are most glycogen storage diseases?

A

autosomal recessive

31
Q

what type of disease is glycogen storage IX disease?

A

sex-linked

32
Q

what do glycogen storage diseases result in??

A

production of abnormal amount or abnormal type of glycogen

33
Q

what is type 1 Von Gierke’s disease?

A

deficiency of glucose-6-phosphate in liver, kidneys and intestine

34
Q

what is type II Pompe’s disease?

A

deficiency of alpha-1,4 glucosidase activity in the lysosomes

35
Q

how does type II Pompe’s disease cause death?

A

by cardio respiratory failure

36
Q

what is type III Cori’s disease?

A

the amylo 1,6 glucosidase is deficient

37
Q

how does type III Cori’s disease work?

A

unable to break down glycogen resulting in hypoglycaemia

38
Q

what is type IV Andersen’s disease?

A

liver glycogen is in normal amounts but compromises long unbranched chains that have low solubility

39
Q

what is type V McArdle’s syndrome?

A
  • affects muscle glycogen phosphorylase

- muscle cannot breakdown glycogen

40
Q

what to patients who have type V McArdle’s syndrome suffer with?

A

sufferers have a low tolerance to exercise and fatigue easily, with painful muscle cramps after exercise

41
Q

what is the equation for the breakdown of glucose-6-phosphate?

A

G-6-P ——-> glucose + Pi

42
Q

what is the most common GSD?

A

Von Gierke’s disease (25%)

43
Q

what happens with Von Gierke’s disease?

A
  • catalyses the terminal reaction of glycogenolysis and gluconeogenesis
  • results in impaired export of glucose from liver from 2 pathways between meals
  • causes hypoglycaemia that doesn’t response to glucagon
44
Q

when do symptoms appear with Von Gierke’s disease?

A

when intervals between feeds increases and infants sleep through the night, or when illness prevents normal feeing routine

45
Q

what are the results of Von Gierke’s disease?

A
  • abnormal levels of glycogen accumulation in the liver and kidney: causing enlargement of the liver and kidneys
  • increased glycolysis leading to lactic acidosis
  • increased fatty acid, TG and VLDL synthesis and excretion
46
Q

what happens with the metabolism in Von Gierke’s disease?

A
  • body attempts to compensate for hypoglycaemia by releasing glucagon and adrenaline resulting in mobilisation of fat stores and release of fatty acids
  • conversion of fatty acids to TGs and VLDL in the liver resulting in accumulation of fat in liver and hyperlipidaemia
47
Q

what are the signs and symptoms of Von Gierke’s disease?

A
  • hepatomas
  • accumulation of fat in cheeks and buttocks
  • enlarged livers and/or kidneys
  • stunted growth
  • severe tendencies to hyperglycaemia, hyperlactaemia and hyperlipidaemia
  • hyperuricaemia
48
Q

how does hyperuricaemia occur in Von Gierke’s disease?

A

as a result of hyperlactaemia as lactic acid in the blood competes for the kidney transport mechanisms

49
Q

what are the management strategies and treatment of Von Gierke’s disease?

A
  • try to correct hypoglycaemia and maintain normoglycaemia
  • young infants can be fed glucose through nasogastric tubes whilst older children are fed glucose drinks at 2-3 hour intervals night and day to prevent fall in blood glucose and cerebral damage
  • uncooked cornstarch may be used to prolong period between feeds
  • restrict dietary lipids
  • liver transplant

module 104 - theme 2 (18 decks)

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