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M104 T2 > M104 T2 L13 > Flashcards

M104 T2 L13 Flashcards

1
Q

What are the symptoms of hypoglycaemia?

A

moodiness, faintness, numbness in arms and hands, blurred vision, confusion, memory loss, dizziness or lethargy that may progress to coma

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2
Q

What does hypoglycaemia have the same effects as?

A

cerebral anoxia

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3
Q

What are the serious consequences of hypoglycaemia?

A

loss of cognitive function, seizures and coma

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4
Q

At what blood glucose level is loss of consciousness achieved?

A

at 2.5 mM (45 mg/dL)

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5
Q

How is hypoglycaemia treated?

A

via the rapid restoration of blood glucose

by i.v. glucose or injection of glucagon

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6
Q

What is the effect of prolonged or repeated hypoglycaemia?

A

permanent brain damage

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7
Q

What is the criteria for hypoglycaemia?

A

having a blood glucose level of below 4 mM (72 mg/dL)

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8
Q

When might symptoms of hypoglycaemia develop?

A

at higher levels than 4 mM if there is rapid fall of previously elevated levels, although some individuals may show no effects even below 4 mM

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9
Q

What are the potential effects of a rapid fall in blood glucose levels?

A

sweating, tachycardia and agitation

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10
Q

What are the potential effects of a rapid fall in blood glucose levels caused by?

A

the activation of the sympathetic NS system and release of adrenaline & glucagon

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11
Q

How does hypoglycaemia present in healthy individuals and what might it be caused by?

A

presents as a mild case

cause - fasting or over exercise

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12
Q

What are the main causes of hypoglycaemia?

A

fasting or over exercise
excess of exogenous insulin / insulinoma
inhibition of endogenous glucose production

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13
Q

What is an example of a condition caused by Hypernatraemia?

A

diabetes insipidus

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14
Q

What are two examples of factors that can cause Hypovolaemia?

A

vomiting, dehydration

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15
Q

What’s an example of a pathology that can cause Hypovolaemia?

A

adrenal insufficiency

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16
Q

What are the lesser causes of hypoglycaemia?

A

Hypernatraemia
Hypovolaemia
certain pathologies

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17
Q

What might cause the inhibition of endogenous glucose production?

A

excess alcohol

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18
Q

How long does it take for alcohol-induced hypoglycaemia to occur after alcohol ingestion?

A

several hours

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19
Q

When does alcohol-induced hypoglycaemia occur?

A

on the depletion of glycogen stores, when the blood glucose levels are reliant on hepatic gluconeogenesis

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20
Q

What is the effect of alcohol-induced hypoglycaemia in the short term (24hrs)?

A

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

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21
Q

What is the effect of alcohol-induced hypoglycaemia in the long-term (years)?

A

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

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22
Q

What happens to ethanol in the liver?

A

it is rapidly metabolised by alcohol dehydrogenase (enzyme)

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23
Q

What is the structural formula of ethanol?

A

C2H2OH

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24
Q

What is the structural formula of acetaldehyde?

A

CH3CHO

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25
Q

What substance is involved in the conversion of ethanol to acetaldehyde?

A

the co-enzyme NAD+, which is reduced to NADH

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26
Q

What enzyme catalyses the conversion of ethanol to acetaldehyde?

A

alcohol dehydrogenase

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27
Q

What is the side-effect of the conversion reaction of ethanol to acetaldehyde?

A

there will be a high NADH:NAD+ ratio in cytosol

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28
Q

What happens to acetaldehyde produced from ethanol in the liver?

A

it is transported into the mitochondria where it is oxidised to acetate by acetaldehyde dehydrogenase

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29
Q

What is acetaldehyde converted into?

A

it is oxidised to acetate

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30
Q

What is the role of acetaldehyde dehydrogenase?

A

to catalyse the oxidation of acetaldehyde to acetate

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31
Q

What is acetate otherwise known as?

A

acetic acid

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32
Q

What is the structural formula of acetic acid?

A

CH3COOH

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33
Q

What are the metabolic consequences of ethanol metabolism in the liver?

A

it increases NADH + H+ and shifts the EQL of the reactions above
Reduces the availability of substrates for entry into gluconeogenesis to maintain plasma glucose levels

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34
Q

Why does alcohol-induced hypoglycaemia occur?

A

when ethanol is ingested when the bgc is reliant on gluconeogenesis

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35
Q

What are the effects of alcohol-induced hypoglycaemia?

A

rapid heartbeat, clammy skin

rapid breathing

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36
Q

What causes the effects of alcohol-induced hypoglycaemia?

A

a fall in blood glucose leads to a stress response in an effort to enhance the stimulation of gluconeogenesis by combined action of glucagon and adrenaline

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37
Q

Why is rapid breathing an effect of alcohol-induced hypoglycaemia?

A

bc it is a physiologic response to metabolic acidosis

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38
Q

What is rapid breathing in alcohol-induced hypoglycaemia caused by?

A

an excess of lactic acid

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39
Q

What are the effects of long-term alcohol consumption on lipid metabolism?

A

high levels of NADH inhibit FA oxidation; instead the excess NADH signals that conditions are right for FA synthesis
TGs accumulate in the liver causing ‘fatty liver’
TGs are exported as VLDL

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40
Q

What are the three stage of fatty liver disease? (SFC)

A

steatohepatitis
fibrosis
cirrhosis

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41
Q

What happens during the cirrhosis stage of fatty liver disease?

A

extensive scar tissue replaces healthy tissue

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42
Q

What happens during the fibrosis stage of fatty liver disease?

A

scar tissue forming at sites of damage

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43
Q

What happens during the steatohepatitis stage of fatty liver disease?

A

damage is caused to the liver by inflammation

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44
Q

What can acetate produced from EtOH be converted into?

A

acetyl-CoA

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45
Q

What happens to acetyl-CoA after it is produced from acetate?

A

its further processing in TCA cycle is prevented

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46
Q

Why is the further processing of acetyl-CoA in the TCA cycle prevented?

A

bc high levels of NADH inhibits both citrate synthase and α-ketoglutarate dehydrogenase

47
Q

What are the two effects of acetyl CoA accumulation?

A

ketone bodies are produced

acetaldehyde build-up

48
Q

What happens to ketone bodies produced

A

which are released into the blood and exacerbates the already acidic conditions resulting from high lactate levels

49
Q

What causes a build-up of acetaldehyde?

A

when the processing of acetate in the liver becomes inefficient

50
Q

Why is a build-up of acetaldehyde bad?

A

it is is highly toxic

51
Q

What is the effect of alcohol consumption on proteasomes?

A

it decreases their activity

52
Q

What happens when the activity of proteasomes is decreased?

A

protein accumulates, causing liver enlargement increases oxidative stress

53
Q

What is a feature of people with chronic alcoholism?

A

they frequently have deficient intakes of micronutrients and minerals

54
Q

What are examples of minerals that people with chronic alcoholism are often deficient in?

A

zinc and selenium

55
Q

What percentage of alcoholics with liver disease will have thiamine deficiency?

A

50%

56
Q

What are the symptoms of alcohol-induced thiamine deficiency?

A

anorexia, irritability, and difficulties with short-term memory

57
Q

What are the causes of alcohol-induced thiamine deficiency?

A

Malnourishment
Ethanol interferes with GI absorption
Hepatic dysfunction, which hinders storage and activation to thiamine pyrophosphate

58
Q

What is the half life of thiamine?

A

10-20 days

59
Q

What is the consequence of thiamine having a short half life?

A

deficiency can occur rapidly during depletion

60
Q

How do the types of Glycogen storage diseases differ?

A

they depend on which enzyme is affected

61
Q

What are the stores of glycogen are affected by in Glycogen storage diseases?

A

by defects in either the enzymes of synthesis or degradation of glycogen

62
Q

What are the genetics for all of the Glycogen storage diseases?

A

autosomal recessive

63
Q

What is the Glycogen storage disease that is genetically exceptional?

A

type IX which is sex-linked, not autosomal recessive

64
Q

What are the effects of Glycogen storage disease?

A

they all result in the production of an abnormal amount or abnormal type of glycogen

65
Q

What is the frequency of Glycogen storage disease?

A

1:20000-1:40000 births

66
Q

What are the effects of Glycogen storage disease??

A

May affect any of the enzymes involved in glycogen synthesis and breakdown

67
Q

What organs are mainly affected by Type I GSD?

A

liver and kidneys

68
Q

What is Type I GSD caused by?

A

a deficiency in G-6-Pase

69
Q

What is Type II GSD caused by?

A

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

70
Q

Which is one of the most devastating of the glycogen storage diseases?

A

Type II. Pompe’s disease

71
Q

What is the end result of severe Type II GSD?

A

death by cardiorespiratory failure

72
Q

What is Type III Cori’s disease caused by?

A

a deficiency of debranching enzyme

73
Q

What is de-branching enzyme otherwise known as?

A

amylo 1,6 glucosidase

74
Q

What is the effect of Type III GSD?

A

an inability to break down glycogen, resulting in hypoglycaemia

75
Q

What is the strange about the symptoms of Type III GSD?

A

the symptoms often disappear at puberty

76
Q

Which is one of the most severe of the glycogen storage diseases?

A

Type IV Andersen’s disease

77
Q

What is Type IV GSD caused by?

A

branching enzyme is affected

78
Q

What is the life expectancy for Type IV GSD?

A

five years

79
Q

What is Type V GSD caused by?

A

muscle (not liver) glycogen phosphorylase is damaged so that muscle cannot break down accumulating glycogen

80
Q

What is the effect of Type V GSD?

A

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

81
Q

What is the life span for Type V GSD?

A

normal

82
Q

What is the most common Glycogen storage disease and to what proportion?

A

Von Gierke’s Disease - 25%

83
Q

What is Von Gierke’s Disease caused by?

A

a deficiency of glucose-6-phosphatase in liver, kidneys and intestines

84
Q

What is Von Gierke’s Disease otherwise known as?

A

Type 1 Glycogen storage disease

85
Q

What reactions are catalysed by G-6-P?

A

the terminal reaction of glycogenolysis and gluconeogenesis

86
Q

What are the effects of Von Gierke’s Disease?

A

the impaired export of glucose from the liver from these two pathways between meals causes hypoglycaemia that does not respond to glucagon

87
Q

When do the symptoms of Von Gierke’s Disease appear?

A

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

88
Q

What is the effect of a lack of G-6-P in Von Gierke’s Disease?

A

means that glucose cannot be exported from the liver.
results in high levels of G-6-P in the liver & kidney
G-6 is metabolized to lactic acid or converted to glycogen or lipid

89
Q

What are the effects of high levels of G-6-P in the liver & kidney in 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 FA, TG and VLDL synthesis and excretion

90
Q

How does the body attempt to compensate for hypoglycaemia in Von Gierke’s Disease?

A

by releasing glucagon (hyperglucagonaemia) and adrenaline resulting in mobilisation of fat stores and release of FAs

91
Q

What is the effect of the conversion of FAs to TGs and VLDL in the liver in Von Gierke’s Disease?

A

accumulation of fat in liver and hyperlipidaemia
May lead to hepatoma
accumulation of fat in cheeks and buttocks.

92
Q

What are the effects of Von Gierke’s Disease on the patient?

A

enlarged livers and/or kidneys
stunted growth, severe tendencies to hypoglycaemia (convulsions)
hyperlactaemia and hyperlipidemia.
May also have hyperuricaemia as a result of hyperlactaemia as lactic acid in the blood competes for kidney transport mechanisms

93
Q

What is the aim of treatment in Von Gierke’s Disease?

A

to correct hypoglycaemia and maintain normoglycaemia

94
Q

What is the treatment in Von Gierke’s Disease for young infants?

A

they are fed glucose through nasogastric tubes

95
Q

What is the treatment in Von Gierke’s Disease for older children?

A

glucose drinks at 2-3 hour intervals night and day to prevent fall in blood glucose and cerebral damage.
Uncooked corn starch may be used to prolong period between feeds
Restrict dietary lipids
Liver transplant

96
Q

What are the products of the reversible reaction lactate + NAD+?

A

pyruvate + NADH + H+

97
Q

What are the products of the reversible reaction of malate + NAD+?

A

OAA + NADH + H+

98
Q

What are the products of the reversible reaction of G3P + NAD+?

A

DHAP + NADH + H+

99
Q

What three metabolic reactions are affected by alcohol metabolism in the liver?

A

pyruvate + NADH + H+ = lactate + NAD+
OAA + NADH + H+ = malate + NAD+
DHAP + NADH + H+ = G3P + NAD+

100
Q

How are the three metabolic reactions changed by alcohol metabolism in the liver?

A

it drives these reactions in the direction that alleviates the high NADH to NAD+ ratio

101
Q

What is the effect of high NADH levels caused by alcohol metabolism?

A

causes the three reactions to be driven in the direction by which NADH+ is produced from NADH + H+

102
Q

Why do high NADH levels result in increased NAD+ production in alcohol metabolism?

A

EQL - trying to redress that balance of the high NADH to NAD+ ratio by re oxidising NADH back to NAD+

103
Q

What are the effects of high NADH levels resulting in its conversion to NAD+ in alcohol metabolism?

A

shortage of pyruvate and OAA in the cell
these are substrates for gluconeogenesis.
so the cells are deprived of these raw materials for gluconeogenesis

104
Q

What is the biochemistry behind how ethanol in hepatocytes is converted to acetate?

A

via portal circulation, ethanol enters the hepatocyte < acetaldehyde via acetaldehyde dehydrogenase (NAD+ < NADH)
acetaldehyde enters the mitochondria < acetic acid (dissociates) < acetate and H+ (NAD+ < NADH)
increased ROS levels produced in the mitochondria, these can damage nucleic acids, proteins and lipids.

105
Q

What type of reaction is the conversion of NAD+ to NADH?

A

reduction

106
Q

What happens to the acetate produced in the mitochondria during the metabolism of alcohol?

A

some is exported from the liver for use by other tissues

most is converted to acetyl coenzyme A

107
Q

What happens to the acetyl coenzyme A produced from acetate during the metabolism of alcohol?

A

it is used to synthesise ketone bodies, which are secreted into the blood from the liver.

108
Q

What reaction occurs due to high levels of NADH and of acetyl-CoA?

A

FA synthesis which generates TGCs
some are stored and may generate fatty liver condition
some are packaged into VLDL and are exported into the blood = hyperlipidaemia

109
Q

What happens to the pyruvate generated by glucose and amacs during the metabolism of alcohol?

A

it’s converted to lactic acid, which is secreted into the blood where it can cause lactic acidaemia

110
Q

What is Type IV GSD caused by?

A

the presence of long unbranched chains of liver glycogen (in normal amounts) that have low solubility

111
Q

What is Type II GSD otherwise known as?

A

Pompe’s disease

112
Q

What is Type III GSD otherwise known as?

A

Cori’s disease

113
Q

What is Type IV GSD otherwise known as?

A

Andersen’s disease

114
Q

What is Type V GSD otherwise known as?

A

McArdle’s syndrome

M104 T2 (15 decks)

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