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Primary Physiology > Metabolism And Temperature Regulation > Flashcards

Metabolism And Temperature Regulation Flashcards

1
Q

Classes of nutrients

A

Carbohydrates
Proteins
Fats
Water
Vitamins
Minerals

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2
Q

BMI formula

A

Weight (kg) / height (m) ^2

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3
Q

Normal bmi
Obese and severely obese?

A

20 - 24
>30 obese
>40 severely obese

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4
Q

Average male calorie intake

A

BMR 2000 kcal/day
+500-2500 kcal more depending on activities

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5
Q

Balanced diet percentages of nutrients for energy

A

55% carbs
15% protein
30% fat

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6
Q

What is the role of salivary amylase

A

Breakdown of complex carbohydrates producing oligosaccerides

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7
Q

Enzymes in intestine that brake oligosaccharides down to hexoses?

A

Maltase, lactase, sucrase

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8
Q

Daily requirement of carbs for an adult

A

5-10g/kg

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9
Q

Classifications of proteins in diet

A

Class I - contain all essential amino acids
Class II - lacking one or more essential amino acid

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10
Q

Enzymes that break down proteins

A

Pepsin
Trypsin
Chemotrypsin
Peptidases (for short peptides)

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11
Q

Average daily requirement of proteins for an adult
For a neonate

A

0.5-1g/kg
5g/kg

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12
Q

What occurs to surpluses amino acids in the body

A

Excreted in urine

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13
Q

What is a triglyceride

A

Three fatty acids and a glycerol

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14
Q

Types of dietary lipids

A

Triglycerides
Cholesterol
Phospholipids

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15
Q

How are triglycerides absorbed in the intestine
How are they transported

A

Simple diffusion post breakdown to free fatty acids by lipase or as micelles
Reformed in cell to form triglycerides then transported with phospholipids, cholesterol and carrier proteins as chylomicrons

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16
Q

Average intake of fat in diet

A

1-2g/kg

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17
Q

Examples of essential fatty acids

A

Linoleic
Linolenic
Arachidonic acids

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18
Q

What are vitamins

A

Organic molecules essential to life but which cannot be synthesised

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19
Q

Water soluble vitamins

A

B and C

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20
Q

Fat soluble vitamins

A

A,D,E,K

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21
Q

What is needed for lipid soluble vitamin absorbtion

A

Bile and pancreatic lilase

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22
Q

What proportion of energy from catabolism is available for work? What happens to rest

A

40%
Rest lost as heat

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23
Q

What are subcatagories of energy expenditure

A

External work (eg muscles)
Internal work (eg cardiac contraction or cellular processes)
Energy stored

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24
Q

What is basal metabolic rate

A

Total energy expanded over 24 hours by a subject under standard conditions at mental and physical rest in comfortable environmental temperature and fasted for 12 hours

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25
Q

What influences basal metabolic rate?

A

Age (increases in childhood, decreases in elderly)
Sex (higher in men)
Height, weight and BSA (core body temp better maintained in obesity thus lower bmr)
Pregnancy, menstruation and lactation
Hormones (eg thyroxine, adrenaline)
Conscious level
Temp
Eating
Emotional state
Activity
Presence of sepsis or disease
Malnutrition

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26
Q

Effect of emotional state on basal metabolic rate

A

Anxiety raises
Depression lowers

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27
Q

Effect of eating on Metabolic rate

A

Increases post injestion of food

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28
Q

What increase in BMR is seen with an increase of 1oC body temp?

A

10%

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29
Q

Basal metabolic rate in average young male in kcal and watts

A

2000kcal/24o
96watts/24hrs

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30
Q

Effect of thiamine deficiency

A

Beri beri and heart failure

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31
Q

Effect of flavine deficiency

A

Angular stomatitis

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32
Q

Effect of niacin deficiency

A

Pellagra dermatosis, mental disorders

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33
Q

Effect of folate deficiency

A

Macrocytic anaemia, stomatitis, diarrhoea

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34
Q

Result of cyanocobalamin deficiency

A

Macrocytic anaemia, optic neuritis

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35
Q

Effect of Vit a deficiency

A

Night blindness

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36
Q

Effect of Vit d deficiency

A

Rickets, osteomalacia

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37
Q

Effect of Vit e deficiency

A

Anaemia

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38
Q

Effect of zinc deficiency

A

Growth restriction
Hypogonadism.

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39
Q

How can BMR be meauresed

A

Whole body calorimeter
Place in chamber and measure temperature rise in a steady flow of water passed through the chamber.

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40
Q

How can BMR be estimated

A

Measuring oxygen consumption
Oxygen consuption per hour multiplied by 4.8kcal of heat produced per litre oxygen consumed

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41
Q

What is the respiratory quotient
What principle does it use

A

Dimensionless number used in calculation of BMR
Ratio at steady state of co2 expired to o2 consumed
That the amount of energy released from food is proportional to o2 used

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42
Q

What are the respiratory quotient for food groups

A

Glucose 1
Fat 0.7
Protein 0.8-0.9
Ethyl alcohol 0.66

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43
Q

What can cause issues with RQ calculations

A

Co2 expired can vary with non metabolic states eg hyperventilation in anxiety

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44
Q

What is metabolism

A

Biochemical reactions with brakdown, synthesis, and dextoxification

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45
Q

What weight of atp does an adult at rest use every day

A

40kg (by continued recycling)

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46
Q

What is NADH
How does it carry energy

A

Nicotinamide adenine dinucleotide

Carries donated electron

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47
Q

Other than atp what other energy I carrying moleculese does the body use

A

NADH
Nadph
Coenzyme A
Creatine phosphate
Thiamine pyrophoshate
Flavine adenine dinucleatide (fadh2)

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48
Q

Mechanisms of metabolic control

A

Substrate availability - control of transport of substrate into cells (e.g insulin promoting glucose entry into cell)
Allosteric enzyme control - binding of modulator away from active site (eg 2.3-DPG)
Hormonal control - wide ranging hormones create wideranging systemic effects

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49
Q

What stimulates insulin secretion

A

Glucose and amino acid uptake
Parasympathetic innervation

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50
Q

Actions of insulin

A

Glucose uptake to cells
Hepatic glycogen synthesis
Inhibition of gluconeogenesis
Stimulation of fatty acid precursor formation
Increased uptake of branched amino acid from gut
Stimulates protein formation

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51
Q

What is Co-secreted with insulin?
What does it do

A

Amylin
Promotes lactate transfer back to liver and generation of fat stores.

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52
Q

Stimulation for glucagon secretion

A

Hypoglycaemia

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53
Q

Actions of glucagon

A

Inhibits glycogen synthesis
Stimulates glycogen breakdown and gluconeogenesis
Activates lipases in adipose tissue

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54
Q

Actions of adrenaline and NA on glucose

A

Promote glycogenolysis especially in muscles
Mobilise fatty acids.

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55
Q

Sources of glucose in the body

A

Dietary intake
Breakdown of complex carbs
Synthesis from precursors

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56
Q

Net gain of moles of atp from metabolism of one mole glucose under aerobic conditions
Energy from this

A

38 moles
288kcal per mole of glucose

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57
Q

What accessory carbohydrate pathway is there

A

Pentose phosphate pathway (Hexose monophosphate shunt)

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58
Q

What is glycolysis. What are the number of carbon atoms in starting and finishing molecules

Net gain of energy carriers

A

Breakdown of glucose (C6) to pyruvate (C3)

Net gain 2 ATP, 2 NADH,

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59
Q

How is 2.3 DPG produced, how does it work to produce right shift of the ODC
What is the concentration of 2.3 DPG in stored blood

A

Produced from 1.3 DPG (a step in glycolysis)
Binds allosterically between the two beta chains of Hb reducing affinity for oxygen
In stored blood there is low concentrations, thus can be hard to offload o2

60
Q

Body reserve weight of glycogen
Where is it found

A

325g
3/4 in muscle
1/4 in liver

61
Q

How is glucoses added to glycogen?
How is it separated

A

Added by phosphorylation and branching enzyme to create new branches
Phosphorylase enzyme and de branching enzyme to remove branches

62
Q

How can muscle mass be converted into usable energy
Where does this occurs

A

De-amination of amino acids into pyruvate and lactate then conversion of these to glucose by gluconeogenesis via oxaloacetate intermediatery
Liver, some in renal cortex

63
Q

What is the pentose phosphate pathway?
Where is it important

A

Conversion of glucose-6-phosphate into ribose-5-phosphate, co2 and nadph

Important where reductive power of nadph is needed such as cell memebrane repair, amino acid synthesis, steroid synthesis, fatty acid synthesis and production of nucleus acids (found in liver, fat, erythrocytes and testes)

64
Q

What happens to pyruvate before entering citric acid cycle

A

Oxidation to acetyl-coA creating one NADH and co2

65
Q

What are the feeds into the citric acid cycle?

A

Carbs and lipids feed in via acetylCoA
Protein feeds in via oxaloacetate, alpha ketogultarate and fumarate

66
Q

Energy production of the citric acid cycle

A

Three NADH
One gtp
One fadh2

67
Q

Brief overview of oxidative phosphorylation

A

Atp generation using the high potential electrons in NADH and fadh2 passed down through carrier proteins on inner mitochondrial membrane
Transfer of electron from carrier to protein activates proton pump pumping H+ out, creating a H+ gradient
As h+ flows back in through atp synthase generates ATP

68
Q

What is von gierkes disease
Effect

A

Glucokinase deficiency
Large liver and kidneys, stunted growth, lactic acidosis, dolls face

69
Q

What groups are found on an amino acid carbon atom?

A

Amine, carboxyl, hydrogen atom, R group.

70
Q

Uses of amino acid pool

A

Protein production
Purines and pyramidines
Hormones
Neurotransmitters
Creatine
Gluconeogenesis
Fatty acid synthesis
Citric acid cycle

71
Q

How are amino acids broken down

A

Amino group removed and excreted as urea
Residue enters other pathways (eg citric acid cycle)

72
Q

What is transamination

A

Transfer of amino (nh2) group to another molecule

73
Q

What is demaination

A

Removal of amino group leaving a carbon skeleton that can be metabolised
eg. Serine to pyruvate and nh4

74
Q

How is balance of amino acids considered?
What results in pos or neg balance

A

Nitrogen balance
Positive - growth, anabolic steroids, convalescence, decreased excretion (eg renal failure)
Negative hypermetabolic state (starvation, sepsis), burns,

75
Q

How is nh4+ removed

A

Kidneys - converted to nh3 and h and excreted in urine
Liver - converted to carbamyl phosphate contributing to urea formation

76
Q

What supplies the energy for first few seconds of muscle contraction

A

Atp generated from Creatine

77
Q

What is creatinine

A

Anhydride of creatine formed as a metabolite for excretion in urine

78
Q

Functions of purines and pyramidines

A

Dna and rna
Energy store (atp gtp etc)
Cofactors

79
Q

Structure of a purine
Examples
Metabolism

A

Double ring - 6 and 5 membered nitrogenated ring
Adenine, guanine
Metabolised to uric acid

80
Q

Structure of a pyramidine
Examples
Metabolism

A

Single six membered nitrogenated ring
Cytosine, thymine, uracil
Broken down in liver

81
Q

Types of lipids in the body

A

Fatty acids
Triglycerides
Plasma lipoproteins
Phospholipids and glycolipids
Cholesterol

82
Q

How are lipids transported in plasma

A

Lipoproteins 95%
Free fatty acids 5%

83
Q

Energy gained from metabolism of fatty acid oxydation

A

9kcal/g

84
Q

Why are fatty acids by weight of tissue so much more energy rich than glycogen

A

More energy per g of fatty acids
Hydrophobic so anhydrous thus no wasted weight with water

85
Q

What is the process of fatty acid breakdown?
Where does it occur

A

Beta oxidation
In mitochondria matrix

86
Q

Process of beta oxidation of fatty acid

A

Combined with acetyl CoA in cytoplasm
Carried on carrier protein carnitine into mitochondria
Dissociates from carnitine which then returns to cytoplasm (carnitine shuttle)
C2 fragments then broken off fatty acid producing acetly CoA

87
Q

Where does fatty acid synthesis occur

A

Cytoplasm

88
Q

How does fatty acid synthesis occur

A

Adding successive acetyl CoA molecules transferred out of mitochondria on citrate carriers
Citrate dissociates in cytoplasm converted to pyruvate which is transported back into mitochondira to reform citrate
Acetyl CoA molecules joined by reducing power of nadph

89
Q

Function of cholesterol

A

In cell membranes produces fluidity
Precursor to steroid hormones

90
Q

How do cells obtain cholesterol

A

From LDL

91
Q

What does HDL do

A

Removes cholesterol from dying cells and membranes for recycling

92
Q

Main function of ldl

A

Delivery Of cholesterol to cells

93
Q

Main function of vldl

A

Carries excess triglycerides from liver

94
Q

Function of chylomicrons

A

Carries dietary lipids to tissues for metabolism

95
Q

What are the eicosanoids
Derivation?
Examples

A

C20 unsaturated fatty acids with a five carbon ring
Derived from arachidonic acid
Examples - prostaglandins, leukotriens, thromboxanes, prostacyclin

96
Q

What is arachidonic acid formed from

A

Linoleic acid

97
Q

Characteristics of eicosanoid effects

A

Highly localised
Short lived

98
Q

What are the ketone bodies?
When are they formed?

A

Acetoacetate and gamma hydroxybuteyric acid

When excess acetyl CoA is present diverted to form ketones
When uncontrolled diabetes or starvation acetyl CoA formed from fatty acids. When insulin very low, increased glucagon levels (stimulating beta oxidation) or decreased oxaloacetate due to high gluconeogenesis then acetyl CoA can become excessive.

99
Q

What proportion of glucose does the brain utilise at rest? What accounts for most of the rest?

A

Brain 70-80%
Erythrocytes most if the rest

100
Q

What do resting muscles use for metabolism

A

Fatty acids

101
Q

What occurs over first 12-24 hours of starvation

A

Glycogen increases triggering glycogenolysis to maintain glucose for the brain
Glycogen reserves then become depleted in 12-24 hrs and blood glucose falls to subnormal levels.
Noradrenaline, cortisol, growth hormone, thyroxine and oestrogen then increase.

102
Q

What happens 24hrs to 4 days of starvation

A

Gluconeogenesis increases with breakdown of muscle proteins and lipolysis
Acetyl CoA accumulates leading to ketone formation

103
Q

What happens after 4 days of starvation

A

As ketones increase then protein metabolism decreases - does slowly continue to break down however to provide glucose for certain tissues such as erythrocytes and some of CNS.
Half of the brains energy now derived from ketones
Once fat stores depleted death follows as result of protein malnutrition

104
Q

How does exercise cause glucose to enter muscle cells
How else are muscle cell energy requirements met?

A

Glut4 - insulin independent (expression stimulated by insulin and exercise)
Glycogenolysis in the muscle
Gluconeogenesis as exercise prolongs

105
Q

Effects of insulin in starvation

A

Decreased gluconeogenesis, glycogenolysis, proteins breakdown and lipolysis.
Increased peripheral glucose utilisation

106
Q

Effect of glucagon in starvation

A

Increases gluconeogenesis, glycogenolysis, protein breakdown, lipolysis, and peripheral glucose utilisation

107
Q

What hormones does glucagon stimulate the release of

A

Insulin
Growth hormone
Somatostatin

108
Q

Effect of cortisol during starvation

A

Increased gluconeogenesis
Decreased glycogenolysis
Increased protein breakdown
Increased lipolysis
Decreased peripheral glucose utilisation

109
Q

Effect of catecholamines during starvation

A

Increase hepatic gluconeogenesis, increased glycogenolysis, increased lipolysis, decreased peripheral glucose utilisation

110
Q

Effects of growth hormone in starvation

A

Increased hepatic glycogenolysis
Decreased protein breakdown
Increased lipolysis s

111
Q

Effect of progesterone and oestrogen during starvation ( and clinical squale commonly seen)

A

Decreased peripheral glucose utilisation
Gestational diabetes

112
Q

Effects of thyroxine during starvation

A

Increased gluconeogenesis, glycogenolysis, proteins breakdown, lipolysis and increased glucose uptake from gut

113
Q

Overall weight of liver
Largest lobe of the liver

A

1.5 to 2 kg
Right

114
Q

Functional unit of the liver
Rough structure

A

Hepatic lobule
Hexagonal shape
Central vein which drains to hepatic vein
At angles branch of portal vein, hepatic artery and bile ducts run.
Portal venous and hepatic arterial blood runs through sinusoids back to central vein.

115
Q

What cell types line the hepatic lobule sinusoids and function

A

Hepatocytes - metabolism
Kupffer cells - macrophages - reticuloendothelial

116
Q

Metabolic functions of the liver

A

Storage (iron, copper, glycogen, protein, bile, vitamins)
Metabolism (fat, carbs, proteins, bile, hormones, coagulation factors)
Excretion and detoxification
Innumological (Ig production, phagocytosis by kupffer cells)

117
Q

How much albumin does the liver synthesise per day?
Half-life of albumin and implication clinically
Functions of albumin

A

200mg/kg/day
20 days - poor indicator of acute liver injury
Colloid oncotic pressure, transport of drugs bilirubin and some hormones

118
Q

Important globulins synthesised in the liver

A

Ferritin
Caeruloplasmin
Haptoglobin

119
Q

Role of haptoglobin

A

Binding and conservation of free haemoglobin

120
Q

Vitamin k dependant clotting factors

A

II, VII, IX, X

121
Q

Half life of factor 7
Half life of prothrombin

A

4o
28 days

122
Q

Overall process of phase one and two drug metabolism

A

Phase 1 - modification to more polar and hydrophilic
Phase 2 - conjugation to increase solubility and increase renal excretion

123
Q

Description of phase 1 metabolism

A

Mainly oxidative
Mediated by cyp enzymes mainly p450
Can involve hydolysis, hydration, reduction, n-oxidation, isomerisation

124
Q

Overview of phase 2 drug metabolism

A

Conjugation on relative end groups left by phase 1 metabolism with hydrophilic substance such as glucuronic acid, acetate, sulphate or glutathione

125
Q

What is the cercadian rhythm of core temperature

A

Lowest just before waking, highest in evening (0.7oC difference)

126
Q

What is the typical rise in temp during ovulation

A

1oC

127
Q

What forms most of the afferent sensation for thermoregulation

A

Core sensors, hypothalamus, spine, deep vicera - more important than peripheral sensation!

128
Q

Where in the hypothalamus senses temp
What part sets temp

A

Senses at Preoptic area of anterior hypothalamus
Sets temp at posterior hypothalamus

129
Q

Heat loss responses if warm threshold exceeded

A

Behavioural - eg removal of cloths
Cutaneous vasodilation
Sweating
Hairs lie flat to skin

130
Q

Themogenic response if cold threshold exceeded

A

Behavioural - more cloths, seeking warm environment
Exercise to increase BMR and thus heat production
Cutaneous vasoconstriction
Shivering
Non shivering thermogenesis
Piloerection

131
Q

How much does shivering raise BMR by
What tempers this response in raising temperature

A

600%
Causes increased blood flow to peripheral tissues resulting in heat loss

132
Q

What is non shivering thermogenesis
Where is it most relevant

A

Adrenaline and na uncouple oxidative phosphorylation so it produces heat instead of atp
Increases heat production 10-15% in adults but most relevant in brown fat in neonates

133
Q

What drives fever?

A

Endogenous pyrogens including interleukins, interferons and TNF
These cause local release of prostaglandins in hypothalamus

134
Q

What is malignant hyperpyrexia

A

Widespread persistent muscle contraction triggered by stress or specific anaesthetic agents. Causes massive heat production, metabolic acidosis and myoglobinurea.
Underlying issue is defective ryanodine receptors resulting in excessive ca release

135
Q

Pathological causes of hyperpyrexia

A

Infection
Malignant hyperpyrexia
Drugs eg ecstasy
Pontine strokes

136
Q

Neurological effects of hypothermia.

A

Decreased level of consciousness
Impaired cerebral auto regulation
Neuroprotective?

137
Q

Cardiovascular effects of hypothermia

A

Depressed myocardial contractility, reduced myocardial o2 demand
Reduced inotropic effects of catecholamines
Enhanced negative effects of voletiles
Vasoconstriction
Bradycardia and j waves
Decreased cardiac output
Arrhythmias below 32, vf below 28

138
Q

Respiratory effects of hypothermia

A

Reduced oxygen demand and delivery
Shift of odc to left
Gases more soluble
Increased tidal volumes
Apnea at 24o

139
Q

Haematological effects of hypothermia

A

Increased blood viscosity
Thrombocytopenia (due to sequestration)
Leukopenia
Impaired coagulation (as impaired enzymes)
Poor wound healing and thrombogenic

140
Q

Immune response to hypothermia

A

Immune suppression

141
Q

Metabolic response to hypothermia

A

Decreased BMR
Increased oxygen uptake due to shivering
Reduced tissue perfusion and metabolic acidosis
Hyperglycaemia
Reduced drug metabolism
Reduced hepatic blood flow
Increased protein catabolism and decreased protein synthesis

142
Q

Renal effects of hypothermia

A

Reduced renal blood flow and oligourea

143
Q

Causes of hypothermia

A

Exposure
Water/drowning
Old age
Hypothyroid
Prolonged surgery

144
Q

What neurone type do cold and warm signals travel down

A

Cold a delta
Wam c

145
Q

Why is surgery a major risk for hypothermia

A

Behavioural regulation abolished
Suppresses hypothermic threshold by 3-4o up to 12o post op
Vasodiation from anaesthetics

146
Q

Sources and percentatages of heat loss during surgery

A

Radiation - 40%
Convection - 30%
Evaporation 8-15%
Respiratory - 8-10%
Conduction - 5%

Primary Physiology (15 decks)

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