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FRCA Physiology > Metabolic Physiology > Flashcards

Metabolic Physiology Flashcards

1
Q

Oxidative phosphorylation occurs in the nucleus of cells

A

False. Oxidative phosphorylation takes place in the inner membrane of the cells mitochondria.

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2
Q

Acetyl CoA is the only route into the Kreb’s cycle

A

False. Lactate (via oxygenation to pyruvate), ketoacids and amino acids gain access to the Kreb’s cycle via various intermediate molecules, not through the acetyl CoA route.

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3
Q

Fats undergo β-oxidation to produce glycerol and free fatty acids (FFA)

A

False. β-oxidation of fats produces only FFA, not glycerol.

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4
Q

Glycolysis of glucose produces a net yield of 2 ATP

A

True. 4 ATP molecules are produced but 2 ATP are required in the glycolytic process, leaving a net yield of 2 ATP.

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5
Q

The yield of ATP from FFA depends on the size of the FFA

A

True. In β-oxidation two-carbon units are sequentially cleaved from the FFA chain. From each of these two-carbon fragments an acetyl CoA molecule is formed. The longer the FFA chain the more acetyl CoA and hence more ATP is synthesized.

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6
Q

For every glucose molecule, a lactate molecule is produced

A

False. For every glucose molecule, 2 pyruvate and therefore 2 lactate molecules are produced.

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7
Q

There is a net yield of 2 ATP for every glucose molecule metabolized

A

True. 4 ATP are created, but the initial reaction requires 2 ATP therefore there is a net gain of only 2 ATP.

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8
Q

Lactate enters the Krebs Cycle

A

False. The Kreb’s cycle requires oxygen and is therefore isn’t part of anaerobic metabolism.

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9
Q

Anaerobic glycolysis produces the same net yield of ATP as glycolysis in aerobic metabolism

A

True. Glycolysis produces a net yield of 2 ATP regardless of whether it is aerobic or anaerobic.

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10
Q

Anaerobic metabolism takes place in the cytoplasm of muscle cells

A

True. Anaerobic metabolism occurs in the cytoplasm of all of the bodies cells.

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11
Q

Lactic acid

Is formed from pyruvate in the absence of oxygen

A

True. In anaerobic metabolism pyruvate is converted to lactate rather than acetyl CoA.

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12
Q

Lactic acid

Is converted to glucose by the Cori cycle

A

True. Lactate is transported to the liver to be converted back to glucose in the presence of oxygen in a process called the Cori cycle.

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13
Q

Lactic acid

Can be increased in the blood even if inhaling an FiO2 of 1.0

A

True. Hypoxia may still be present in cells even when breathing 100% oxygen.

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14
Q

Lactic acid

Is not formed in red blood cells

A

False. Anaerobic metabolism can occur in red blood cells.

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15
Q

Lactic acid

Can enter the Kreb’s cycle directly via the cycle’s intermediate molecules

A

False. Lactic acid cannot enter the Kreb’s cycle directly unless converted back to glucose first via the Cori cycle (the vast majority) or through conversion back to pyruvate.

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16
Q

The end products of full aerobic metabolism of glucose are ATP, H2O and CO2

A

True. The equation is: C6H12O6 + 6O2 → 6H2O + 6CO2 + 38ATP

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17
Q

Acetyl CoA combines with citric acid to enter the Kreb’s cycle

A

False. Acetyl CoA combines with oxaloacetate to produce citric acid in the first step of the Kreb’s cycle.

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18
Q

Amino acids only gain access to metabolic pathways via pyruvate

A

False. They can also gain acces via the Krebs cycle intermediate molecules (oxaloacetate, fumarate, succinate, α-ketoglutarate).

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19
Q

Glycolysis is anaerobic

A

True. Glycolysis occurs in the cytoplasm and requires no oxygen.

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20
Q

Proton pumps are essential in the aerobic generation of ATP

A

True. Proton pumps are essential in the electron transport chain to create a hydrogen ion gradient across the inner membrane of the mitochondrion. The hydrogen ions (protons) then flow through ATP synthetase channels, thus generating ATP.

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21
Q

Starvation causes:

Increased protein breakdown

A

True. Protein breakdown increases to maintain blood glucose levels though gluconeogenesis.

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22
Q

Starvation causes:

Increased glycogen synthesis

A

False. This synthetic reaction is decreased.

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23
Q

Starvation causes:

Decreased lipid metabolism

A

False. Lipid metabolism is increased to create energy.

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24
Q

Starvation causes:

Increased plasma glucose levels

A

False. Plasma glucose levels decrease over the first few days to about 3.5, but is then maintained at this new lower level by gluconeogenesis.

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25
Q

Starvation causes:

Increased cellular glucose uptake

A

False. Cells begin to use ketoacids rather than glucose for their energy needs.

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26
Q

In starvation:

The renal cortex converts to using ketoacids as its main substrate

A

True. However glucose remains the renal medulla’s primary substrate.

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27
Q

In starvation:

Death occurs due to protein malnutrition

A

True. Once the body’s fat stores are depleted, protein metabolism accelerates and death will follow.

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28
Q

In starvation:

Athletes tend to live longer than obese people

A

False. Once the body’s fat stores are depleted, protein metabolism accelerates and death will follow.

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29
Q

In starvation:

Glycogen stores only occur in the liver

A

False. Glycogen also occurs in muscle.

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30
Q

In starvation:

Glycogen is broken down to ketoacids

A

False. Glycogen is broken down to glucose.

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31
Q

Starvation causes:

Metabolic alkalosis

A

False. The pH status is kept within the normal range in the face of increased ketoacid load.

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32
Q

Starvation causes:

Rapid exhaustion of carbohydrate stores

A

True. Carbohydrate stores in the form of glycogen are exhausted within the first day of the last food intake.

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33
Q

Starvation causes:

Increase in urinary nitrogen excretion

A

True. Increase in protein breakdown for gluconeogenesis causes an increase in urinary nitrogen excretion.

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34
Q

Starvation causes:

Rapid neuroglycopaenia

A

False. Blood glucose levels are kept constant up towards the terminal phase of starvation and death although at a lower set level of 3.5 mmol/l.

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35
Q

Starvation causes:

Increased utilization of glucose by the brain

A

False. 50% of the CNS converts to ketoacid metabolism to conserve glucose stores.

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36
Q

In starvation:

Enterocytes convert to ketoacid metabolism

A

True. Enterocytes do convert to ketoacid metabolism (erythrocytes don’t).

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37
Q

In starvation:

Full ketoadaptation takes only a few days to implement

A

False. Full ketoadaptation takes up to two weeks to implement.

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38
Q

In starvation:

There is increased fat breakdown

A

True. This occurs to preserve the protein.

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39
Q

In starvation:

There is a negative nitrogen balance

A

True. This can be used in intensive care units to determine a patient’s nutritional status. If the amount of nitrogen in a patient’s feed is less than the amount of nitrogen being excreted in the patient’s urine, the patient is in negative nitrogen balance.

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40
Q

In starvation:

The renal medulla converts to ketoacid metabolism

A

False. The renal medulla remains unable to metabolise ketoacids, using only glucose as an energy substrate.

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41
Q

Consider the following statements regarding the regulation of blood glucose.
Blood glucose concentration is increased by cortisol

A

True. Cortisol stimulates gluconeogenesis and decreased glucose utilization by cells and therefore increases blood glucose concentration.

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42
Q

Consider the following statements regarding the regulation of blood glucose.
Hypoglycaemia may result from alpha-adrenergic stimulation

A

False. Alpha-adrenergic stimulation causes inhibition of insulin secretion. Beta-adrenergic stimulation causes glucagon secretion. Both cause an increase in blood glucose levels.

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43
Q

Consider the following statements regarding the regulation of blood glucose.
Insulin inhibits entry of potassium into cells

A

False. Insulin increases potassium entry into cells and is a common treatment for hyperkalaemia.

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44
Q

Consider the following statements regarding the regulation of blood glucose.
Insulin is anabolic

A

True. Insulin stimulates synthesis of glycogen, protein and fat (all anabolic processes).

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45
Q

Consider the following statements regarding the regulation of blood glucose.
Growth hormone and insulin have opposite effects on fat metabolism

A

True. Insulin causes fat synthesis, and growth hormone causes fat breakdown.

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46
Q

Consider the following statements regarding insulin secretion.
Occurs from the alpha cells of the pancreas

A

False. It occurs from the beta cells of the islets of Langerhan in the pancreas

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47
Q

Consider the following statements regarding insulin secretion.
Is increased during surgery

A

False. The stress response that occurs during surgery causes a decrease in insulin levels.

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48
Q

Consider the following statements regarding insulin secretion.
Is decreased by somatostatin

A

True. A paracrine effect. Somatostain is released by delta cells of the islets of Langerhan in the pancreas.

49
Q

Consider the following statements regarding insulin secretion.
Is decreased by glucagon

A

False. Glucagon stimulates the release of insulin, again a paracrine effect.

50
Q

Consider the following statements regarding insulin secretion.
Increases the number of glucose transporters in the plasma membrane

A

True. This is a mechanism by which glucose uptake in cells is increased. Specifically cell surface expression of GLUT-4 transporters on skeletal muscle and adipose tissue is increased by raised insulin levels.

51
Q

Consider the following statements regarding the regulation of glucose.
Glucagon is released in response to starvation

A

True. Glucagon is released in starvation.

52
Q

Consider the following statements regarding the regulation of glucose.
Growth hormone stimulates fat synthesis

A

False. Growth hormone stimulates lipolysis.

53
Q

Consider the following statements regarding the regulation of glucose.
Growth hormone stimulates muscle to increase carbohydrate uptake

A

False. Insulin stimulates carbohydrate uptake in muscle.

54
Q

Consider the following statements regarding the regulation of glucose.
Glucagon has a pharmacological use as an inotrope

A

True. Glucagon is used as an inotrope especially in heart failure due to β-blocker overdose.

55
Q

Consider the following statements regarding the regulation of glucose.
Glucagon causes hypoglycaemia

A

False. Glucagon release is stimulated by hypoglycaemia to raise blood sugar levels.

56
Q

Consider the following statements about adrenaline.

Increases plasma concentration of free fatty acids

A

True. Adrenaline causes lipolysis

57
Q

Consider the following statements about adrenaline.

Decreases blood sugar levels

A

False. It increases blood sugar levels.

58
Q

Consider the following statements about adrenaline.

Increases liver glycogenolysis

A

True. It does stimulate glycogenolysis.

59
Q

Consider the following statements about adrenaline.

Is needed by peripheral tissues to take up glucose

A

False. Insulin is required by peripheral tissues to take up glucose.

60
Q

Consider the following statements about adrenaline.

Stimulates glucagon secretion via α2 adrenergic receptors

A

False. Glucagon secretion is enhanced by β2-adrenergic stimulation not α2.

61
Q

Consider the following statements regarding glucose metabolism.
Gluconeogenesis can only occur in the liver

A

False. Gluconeogenesis also occurs in other tissues such as the kidney.

62
Q

Consider the following statements regarding glucose metabolism.
Glycogenolysis occurs in all cells

A

False. Glycogen is stored in the liver and muscle and therefore glycogenolysis does not occur in all cells.

63
Q

Consider the following statements regarding glucose metabolism.
Glycogen synthesis is inhibited by adrenaline

A

True. Adrenaline causes glycogenolysis.

64
Q

Consider the following statements regarding glucose metabolism.
Gluconeogenesis is the formation of glucose from glycogen

A

False. Gluconeogenesis is the formation of glucose from glycerol and amino acids not glycogen. The formation of glucose form glycogen is glycogenolysis.

65
Q

Consider the following statements regarding glucose metabolism.
Glycogen synthesis is inhibited by cortisol

A

False. Cortisol actually stimulates glycogen synthesis and maintains stores of glycogen which is contrary to other hyperglycaemic hormones.

66
Q

Hypoglycaemia may result from:

Excessive vagal stimulation

A

True. The vagus nerve stimulates insulin secretion and therefore could cause hypoglycaemia.

67
Q

Hypoglycaemia may result from:

Excessive noradrenaline secretion

A

False. Noradrenaline causes inhibition of insulin secretion and therefore hyperglycaemia.

68
Q

Hypoglycaemia may result from:

Steroid treatment

A

False. Steroids can cause secondary diabetes and therefore hyperglycaemia.

69
Q

Hypoglycaemia may result from:

α- adrenergic stimulation

A

False. α-adrenergic stimulation causes inhibition of insulin secretion and therefore hyperglycaemia.

70
Q

Hypoglycaemia may result from:

Hypothermia

A

False. Hypothermia causes an increase in glucose levels.

71
Q

Ingested lipids:

Are mainly triglycerides

A

True. Triglycerides make up to 90% of dietary lipids.

72
Q

Ingested lipids:

Are composed of essential and non-essential fatty acids

A

True. Alpha-linolenic acid and linoleic acid are examples of essential fatty acids. Humans do not possess the enzyme systems to synthesize them.

73
Q

Ingested lipids:

Are broken down primarily in the terminal ileum

A

False. 10-30% are broken down in the stomach, the rest is broken down in the duodenum and upper jejunum. Bile salts are absorbed in the terminal ileum.

74
Q

Ingested lipids:

Are used as a source of ATP

A

True. It is a relatively energy dense molecule, providing more than double that from glucose.

75
Q

Ingested lipids:

Increase in the faeces with a decrease in bile secretion

A

True. Bile salts are required solubilizing agents for fats and aid in their absorption.

76
Q

Regarding Basal Metabolic Rate (BMR):

It is the lowest possible rate

A

False. It can be lower when asleep.

77
Q

Regarding Basal Metabolic Rate (BMR):

BMR decreases with age

A

True. It is higher in children. There is also a gender difference with males having a higher BMR than females.

78
Q

Regarding Basal Metabolic Rate (BMR):

For every 1 degree centigrade rise in body temperature, the BMR increases by 8%

A

False. This is true for the cerebral metabolic rate not the body’s basal metabolic rate.

79
Q

Regarding Basal Metabolic Rate (BMR):

BMR is the energy output of an individual per unit time at rest, at room temperature

A

True. It must also be measured 12-14 hr after their last meal (a time when one is said to be thermoneutral).

80
Q

Regarding Basal Metabolic Rate (BMR):

May be measured using an ergometer

A

False. It may be measured indirectly using a Wet Spirometer not an ergometer. An ergometer is used to measure energy expenditure whilst active.

81
Q

Insulin:

Is antagonised by growth hormone

A

True. The 5 counter-regulatory hormones that antagonise insulin-induced hypoglycaemia are adrenaline, noradrenaline, glucagon, growth hormone and cortisol.

82
Q

Insulin:

Facilitates protein anabolism

A

True. Insulin is the only major anabolic hormone. Hence it stimulates synthesis of proteins, fat and glycogen.

83
Q

Insulin:

Promotes glycogen synthesis in the liver

A

True.

84
Q

Insulin:

Facilitates the deposition of fat

A

True.

85
Q

Insulin:

Inhibits the passage of potassium ions into cells

A

False. Insulin facilitates the passage of potassium ions into cells and is often used as a treatment for hyperkalaemia.

86
Q

Considering lactate metabolism:

One molecule of lactate is produced for every glucose molecule during anaerobic metabolism

A

False. Each glucose is converted to 2 pyruvate and these are converted to 2 molecules of lactate.

87
Q

Considering lactate metabolism:

Fitness training does not affect the rate of rise in plasma lactate

A

False. At a certain level of exercise the plasma lactate level rises sharply. This is at between 50-80% of maximal O2 consumption. In an untrained person plasma lactate will rise at a lower level of exercise than in the trained.

88
Q

Considering lactate metabolism:

Glucose metabolism to lactate releases ATP at the same rate as oxidation within the mitochondria

A

False. Glucose metabolism to lactate releases ATP at least twice as rapidly as mitochondrial metabolism and can optimally provide energy for 1.5 minutes of maximal muscle activity.

89
Q

Considering lactate metabolism:

After exercise lactate is largely reconverted into glucose

A

True. After exercise 80% of lactate present is reconverted to glucose in the liver via the Cori cycle.

90
Q

Considering lactate metabolism:

Lactate filtered in the kidney is actively reabsorbed

A

True. Filtered lactate is actively reabsorbed by the nephron to a transport maximum of 75 mg/min.

91
Q

Hyperglycaemia may result from the administration of:

Adrenaline

A

True. Adrenaline increases glucagon secretion and stimulates gluconeogenesis.

92
Q

Hyperglycaemia may result from the administration of:

Thyroid stimulating hormone

A

True. Thyroid hormone stimultaes: increased glucose absorption from the gut, glycogenolysis and gluconeogenesis.

93
Q

Hyperglycaemia may result from the administration of:

Beta blockers

A

False. Patients on beta blockers are at risk of hypoglycaemia under general anaesthesia.

94
Q

Hyperglycaemia may result from the administration of:

Thiazide diuretics

A

True. Thiazide diuretics commonly precipitate Type 2 diabetes.

95
Q

Hyperglycaemia may result from the administration of:

Glucagon

A

True.

96
Q

Glucagon release:

Stimulates gluconeogenesis

A

True. Glucagon is gluconeogenic, glycogenolytic, and lipolytic.

97
Q

Glucagon release:

Inhibits adenylate cyclase in liver cells

A

False. It acts via G-protein linked receptors.

98
Q

Glucagon release:

Stimulates secretion of growth hormone

A

True. Glucagon is formed in the pancreatic alpha-cells. Secretion is stimulated by beta-mediated sympathetic nerves to the pancreas, acetylcholine, amino acids, CCK and gastrin.

99
Q

Glucagon release:

Is inhibited by cortisol

A

False. Secretion is stimulated by cortisol and infection, but inhibited by alpha stimulation, insulin, glucose, ketones, phenytoin and somatostatin.

100
Q

Glucagon release:

Is stimulated by theophylline

A

True. Theophylline and other phosphodiesterase inhibitors also stimulate its release.

101
Q

In starvation:

Free fatty acid oxidation in the liver, muscle and heart is increased

A

True. In starvation, glycogenolysis occurs and the liver begins to use fatty acids as a source of energy.

102
Q

In starvation:

Muscle glycogen and brain glycogen are replenished by gluconeogenesis

A

False. As the glycogen is depleted, gluconeogenesis increases using amino acids from the breakdown of muscle protein. Glycogen is not replenished until the return of nutrients, this restorative process is under the control of cortisol.

103
Q

In starvation:

Ketone bodies produced in the liver from free fatty acids can be utilized by brain cells but glucose is still essential

A

True. Most tissues, including the brain, can ultimately adapt to the use of ketone bodies as a fuel source. However the brain cannot survive without glucose.

104
Q

In starvation:

The odour of the breath is due to ketosis

A

True.

105
Q

Insulin and growth hormone have directly opposing effects on:
Fat catabolism

A

True. Growth hormone causes fat breakdown.

106
Q

Insulin and growth hormone have directly opposing effects on:
Glucose utilisation

A

True. Growth hormone inhibits glucose utilization, whereas insulin stimulates glucose absorption.

107
Q

Insulin and growth hormone have directly opposing effects on:
Fat anabolism

A

True. Insulin stimulates fat deposition.

108
Q

Insulin and growth hormone have directly opposing effects on:
Protein anabolism

A

False. Both insulin and growth hormone promote protein synthesis.

109
Q

Insulin and growth hormone have directly opposing effects on:
Glycogen production

A

True. Insulin stimulates glycogen deposition, whereas growth hormone encourages glycogenolysis.

110
Q

Consequences of starvation include:

Increased brain uptake of glucose

A

False. Glucose supply to the brain is a priority in starvation as it is largely dependent on glucose as an energy substrate. The brain can however metabloise ketones.

111
Q

Consequences of starvation include:

Reduction of the respiratory quotient

A

True. As metabolism switches to the burning of fats the respiratory quotient drops towards 0.7.

112
Q

Consequences of starvation include:

Elevated blood glucagon levels

A

True. Glucagon levels go up as the body enters a catabolic phase with increased glycogenolysis.

113
Q

Consequences of starvation include:

Increased urinary nitrogen output

A

True. Increased protein breakdown leads to increased urinary nitrogen excretion.

114
Q

Consequences of starvation include:

Development of metabolic alkalosis

A

False. The accumulation of acetyl-CoA leads to ketoacidosis, not alkalosis.

115
Q

Considering ketone bodies:

The majority of amino acids can be converted into acetoacetate

A

True. The majority of amino acids after deaminationcan be converted into acetyl-CoA from which acetoacetate can be formed.

116
Q

Considering ketone bodies:

The liver converts fatty acids into acetoacetate for transport to other parts of the body

A

True. Fatty acid degradation occurs largely in the liver where aceyl-CoA is formed leading to acetoacetate production. This is transported at low levels but with efficient flux to the rest of the body.

117
Q

Considering ketone bodies:

Ketosis can arise from a diet composed almost entirely of fat

A

True. Ketosis, the presence of excessive levels of acetoacetate, beta-hydroxybutyrate or acetone in the blood can arise in starvation, diabetes mellitus or in a very high fat based diet.

118
Q

Considering ketone bodies:

Citrate availability limits entry of acetyl-CoA into the citric acid cycle

A

False. Sufficient oxaloacetate is needed to receive acetyl-CoA into the citric acid cycle.

119
Q

Considering ketone bodies:

Ketoacidosis causes hyponatraemia

A

True. Ketoacids are easily excreted by the kidney but being strong acids they are excreted combined with Na+ from the extracellular fluid. The resultant hyponatraemia leads to an increased acidosis beyond that occasioned by the direct rise in ketoacid levels.

FRCA Physiology (6 decks)

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