Metabolism And Temperature Regulation Flashcards
1
Q
Classes of nutrients
A
Carbohydrates
Proteins
Fats
Water
Vitamins
Minerals
2
Q
BMI formula
A
Weight (kg) / height (m) ^2
3
Q
Normal bmi
Obese and severely obese?
A
20 - 24
>30 obese
>40 severely obese
4
Q
Average male calorie intake
A
BMR 2000 kcal/day
+500-2500 kcal more depending on activities
5
Q
Balanced diet percentages of nutrients for energy
A
55% carbs
15% protein
30% fat
6
Q
What is the role of salivary amylase
A
Breakdown of complex carbohydrates producing oligosaccerides
7
Q
Enzymes in intestine that brake oligosaccharides down to hexoses?
A
Maltase, lactase, sucrase
8
Q
Daily requirement of carbs for an adult
A
5-10g/kg
9
Q
Classifications of proteins in diet
A
Class I - contain all essential amino acids
Class II - lacking one or more essential amino acid
10
Q
Enzymes that break down proteins
A
Pepsin
Trypsin
Chemotrypsin
Peptidases (for short peptides)
11
Q
Average daily requirement of proteins for an adult
For a neonate
A
0.5-1g/kg
5g/kg
12
Q
What occurs to surpluses amino acids in the body
A
Excreted in urine
13
Q
What is a triglyceride
A
Three fatty acids and a glycerol
14
Q
Types of dietary lipids
A
Triglycerides
Cholesterol
Phospholipids
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
16
Q
Average intake of fat in diet
A
1-2g/kg
17
Q
Examples of essential fatty acids
A
Linoleic
Linolenic
Arachidonic acids
18
Q
What are vitamins
A
Organic molecules essential to life but which cannot be synthesised
19
Q
Water soluble vitamins
A
B and C
20
Q
Fat soluble vitamins
A
A,D,E,K
21
Q
What is needed for lipid soluble vitamin absorbtion
A
Bile and pancreatic lilase
22
Q
What proportion of energy from catabolism is available for work? What happens to rest
A
40%
Rest lost as heat
23
Q
What are subcatagories of energy expenditure
A
External work (eg muscles)
Internal work (eg cardiac contraction or cellular processes)
Energy stored
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
25
What influences basal metabolic rate?
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
26
Effect of emotional state on basal metabolic rate
Anxiety raises
Depression lowers
27
Effect of eating on Metabolic rate
Increases post injestion of food
28
What increase in BMR is seen with an increase of 1oC body temp?
10%
29
Basal metabolic rate in average young male in kcal and watts
2000kcal/24o
96watts/24hrs
30
Effect of thiamine deficiency
Beri beri and heart failure
31
Effect of flavine deficiency
Angular stomatitis
32
Effect of niacin deficiency
Pellagra dermatosis, mental disorders
33
Effect of folate deficiency
Macrocytic anaemia, stomatitis, diarrhoea
34
Result of cyanocobalamin deficiency
Macrocytic anaemia, optic neuritis
35
Effect of Vit a deficiency
Night blindness
36
Effect of Vit d deficiency
Rickets, osteomalacia
37
Effect of Vit e deficiency
Anaemia
38
Effect of zinc deficiency
Growth restriction
Hypogonadism.
39
How can BMR be meauresed
Whole body calorimeter
Place in chamber and measure temperature rise in a steady flow of water passed through the chamber.
40
How can BMR be estimated
Measuring oxygen consumption
Oxygen consuption per hour multiplied by 4.8kcal of heat produced per litre oxygen consumed
41
What is the respiratory quotient
What principle does it use
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
42
What are the respiratory quotient for food groups
Glucose 1
Fat 0.7
Protein 0.8-0.9
Ethyl alcohol 0.66
43
What can cause issues with RQ calculations
Co2 expired can vary with non metabolic states eg hyperventilation in anxiety
44
What is metabolism
Biochemical reactions with brakdown, synthesis, and dextoxification
45
What weight of atp does an adult at rest use every day
40kg (by continued recycling)
46
What is NADH
How does it carry energy
Nicotinamide adenine dinucleotide
Carries donated electron
47
Other than atp what other energy I carrying moleculese does the body use
NADH
Nadph
Coenzyme A
Creatine phosphate
Thiamine pyrophoshate
Flavine adenine dinucleatide (fadh2)
48
Mechanisms of metabolic control
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
49
What stimulates insulin secretion
Glucose and amino acid uptake
Parasympathetic innervation
50
Actions of insulin
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
51
What is Co-secreted with insulin?
What does it do
Amylin
Promotes lactate transfer back to liver and generation of fat stores.
52
Stimulation for glucagon secretion
Hypoglycaemia
53
Actions of glucagon
Inhibits glycogen synthesis
Stimulates glycogen breakdown and gluconeogenesis
Activates lipases in adipose tissue
54
Actions of adrenaline and NA on glucose
Promote glycogenolysis especially in muscles
Mobilise fatty acids.
55
Sources of glucose in the body
Dietary intake
Breakdown of complex carbs
Synthesis from precursors
56
Net gain of moles of atp from metabolism of one mole glucose under aerobic conditions
Energy from this
38 moles
288kcal per mole of glucose
57
What accessory carbohydrate pathway is there
Pentose phosphate pathway (Hexose monophosphate shunt)
58
What is glycolysis. What are the number of carbon atoms in starting and finishing molecules
Net gain of energy carriers
Breakdown of glucose (C6) to pyruvate (C3)
Net gain 2 ATP, 2 NADH,
59
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
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
Body reserve weight of glycogen
Where is it found
325g
3/4 in muscle
1/4 in liver
61
How is glucoses added to glycogen?
How is it separated
Added by phosphorylation and branching enzyme to create new branches
Phosphorylase enzyme and de branching enzyme to remove branches
62
How can muscle mass be converted into usable energy
Where does this occurs
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
What is the pentose phosphate pathway?
Where is it important
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
What happens to pyruvate before entering citric acid cycle
Oxidation to acetyl-coA creating one NADH and co2
65
What are the feeds into the citric acid cycle?
Carbs and lipids feed in via acetylCoA
Protein feeds in via oxaloacetate, alpha ketogultarate and fumarate
66
Energy production of the citric acid cycle
Three NADH
One gtp
One fadh2
67
Brief overview of oxidative phosphorylation
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
What is von gierkes disease
Effect
Glucokinase deficiency
Large liver and kidneys, stunted growth, lactic acidosis, dolls face
69
What groups are found on an amino acid carbon atom?
Amine, carboxyl, hydrogen atom, R group.
70
Uses of amino acid pool
Protein production
Purines and pyramidines
Hormones
Neurotransmitters
Creatine
Gluconeogenesis
Fatty acid synthesis
Citric acid cycle
71
How are amino acids broken down
Amino group removed and excreted as urea
Residue enters other pathways (eg citric acid cycle)
72
What is transamination
Transfer of amino (nh2) group to another molecule
73
What is demaination
Removal of amino group leaving a carbon skeleton that can be metabolised
eg. Serine to pyruvate and nh4
74
How is balance of amino acids considered?
What results in pos or neg balance
Nitrogen balance
Positive - growth, anabolic steroids, convalescence, decreased excretion (eg renal failure)
Negative hypermetabolic state (starvation, sepsis), burns,
75
How is nh4+ removed
Kidneys - converted to nh3 and h and excreted in urine
Liver - converted to carbamyl phosphate contributing to urea formation
76
What supplies the energy for first few seconds of muscle contraction
Atp generated from Creatine
77
What is creatinine
Anhydride of creatine formed as a metabolite for excretion in urine
78
Functions of purines and pyramidines
Dna and rna
Energy store (atp gtp etc)
Cofactors
79
Structure of a purine
Examples
Metabolism
Double ring - 6 and 5 membered nitrogenated ring
Adenine, guanine
Metabolised to uric acid
80
Structure of a pyramidine
Examples
Metabolism
Single six membered nitrogenated ring
Cytosine, thymine, uracil
Broken down in liver
81
Types of lipids in the body
Fatty acids
Triglycerides
Plasma lipoproteins
Phospholipids and glycolipids
Cholesterol
82
How are lipids transported in plasma
Lipoproteins 95%
Free fatty acids 5%
83
Energy gained from metabolism of fatty acid oxydation
9kcal/g
84
Why are fatty acids by weight of tissue so much more energy rich than glycogen
More energy per g of fatty acids
Hydrophobic so anhydrous thus no wasted weight with water
85
What is the process of fatty acid breakdown?
Where does it occur
Beta oxidation
In mitochondria matrix
86
Process of beta oxidation of fatty acid
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
Where does fatty acid synthesis occur
Cytoplasm
88
How does fatty acid synthesis occur
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
Function of cholesterol
In cell membranes produces fluidity
Precursor to steroid hormones
90
How do cells obtain cholesterol
From LDL
91
What does HDL do
Removes cholesterol from dying cells and membranes for recycling
92
Main function of ldl
Delivery Of cholesterol to cells
93
Main function of vldl
Carries excess triglycerides from liver
94
Function of chylomicrons
Carries dietary lipids to tissues for metabolism
95
What are the eicosanoids
Derivation?
Examples
C20 unsaturated fatty acids with a five carbon ring
Derived from arachidonic acid
Examples - prostaglandins, leukotriens, thromboxanes, prostacyclin
96
What is arachidonic acid formed from
Linoleic acid
97
Characteristics of eicosanoid effects
Highly localised
Short lived
98
What are the ketone bodies?
When are they formed?
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
What proportion of glucose does the brain utilise at rest? What accounts for most of the rest?
Brain 70-80%
Erythrocytes most if the rest
100
What do resting muscles use for metabolism
Fatty acids
101
What occurs over first 12-24 hours of starvation
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
What happens 24hrs to 4 days of starvation
Gluconeogenesis increases with breakdown of muscle proteins and lipolysis
Acetyl CoA accumulates leading to ketone formation
103
What happens after 4 days of starvation
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
How does exercise cause glucose to enter muscle cells
How else are muscle cell energy requirements met?
Glut4 - insulin independent (expression stimulated by insulin and exercise)
Glycogenolysis in the muscle
Gluconeogenesis as exercise prolongs
105
Effects of insulin in starvation
Decreased gluconeogenesis, glycogenolysis, proteins breakdown and lipolysis.
Increased peripheral glucose utilisation
106
Effect of glucagon in starvation
Increases gluconeogenesis, glycogenolysis, protein breakdown, lipolysis, and peripheral glucose utilisation
107
What hormones does glucagon stimulate the release of
Insulin
Growth hormone
Somatostatin
108
Effect of cortisol during starvation
Increased gluconeogenesis
Decreased glycogenolysis
Increased protein breakdown
Increased lipolysis
Decreased peripheral glucose utilisation
109
Effect of catecholamines during starvation
Increase hepatic gluconeogenesis, increased glycogenolysis, increased lipolysis, decreased peripheral glucose utilisation
110
Effects of growth hormone in starvation
Increased hepatic glycogenolysis
Decreased protein breakdown
Increased lipolysis s
111
Effect of progesterone and oestrogen during starvation ( and clinical squale commonly seen)
Decreased peripheral glucose utilisation
Gestational diabetes
112
Effects of thyroxine during starvation
Increased gluconeogenesis, glycogenolysis, proteins breakdown, lipolysis and increased glucose uptake from gut
113
Overall weight of liver
Largest lobe of the liver
1.5 to 2 kg
Right
114
Functional unit of the liver
Rough structure
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
What cell types line the hepatic lobule sinusoids and function
Hepatocytes - metabolism
Kupffer cells - macrophages - reticuloendothelial
116
Metabolic functions of the liver
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
How much albumin does the liver synthesise per day?
Half-life of albumin and implication clinically
Functions of albumin
200mg/kg/day
20 days - poor indicator of acute liver injury
Colloid oncotic pressure, transport of drugs bilirubin and some hormones
118
Important globulins synthesised in the liver
Ferritin
Caeruloplasmin
Haptoglobin
119
Role of haptoglobin
Binding and conservation of free haemoglobin
120
Vitamin k dependant clotting factors
II, VII, IX, X
121
Half life of factor 7
Half life of prothrombin
4o
28 days
122
Overall process of phase one and two drug metabolism
Phase 1 - modification to more polar and hydrophilic
Phase 2 - conjugation to increase solubility and increase renal excretion
123
Description of phase 1 metabolism
Mainly oxidative
Mediated by cyp enzymes mainly p450
Can involve hydolysis, hydration, reduction, n-oxidation, isomerisation
124
Overview of phase 2 drug metabolism
Conjugation on relative end groups left by phase 1 metabolism with hydrophilic substance such as glucuronic acid, acetate, sulphate or glutathione
125
What is the cercadian rhythm of core temperature
Lowest just before waking, highest in evening (0.7oC difference)
126
What is the typical rise in temp during ovulation
1oC
127
What forms most of the afferent sensation for thermoregulation
Core sensors, hypothalamus, spine, deep vicera - more important than peripheral sensation!
128
Where in the hypothalamus senses temp
What part sets temp
Senses at Preoptic area of anterior hypothalamus
Sets temp at posterior hypothalamus
129
Heat loss responses if warm threshold exceeded
Behavioural - eg removal of cloths
Cutaneous vasodilation
Sweating
Hairs lie flat to skin
130
Themogenic response if cold threshold exceeded
Behavioural - more cloths, seeking warm environment
Exercise to increase BMR and thus heat production
Cutaneous vasoconstriction
Shivering
Non shivering thermogenesis
Piloerection
131
How much does shivering raise BMR by
What tempers this response in raising temperature
600%
Causes increased blood flow to peripheral tissues resulting in heat loss
132
What is non shivering thermogenesis
Where is it most relevant
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
What drives fever?
Endogenous pyrogens including interleukins, interferons and TNF
These cause local release of prostaglandins in hypothalamus
134
What is malignant hyperpyrexia
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
Pathological causes of hyperpyrexia
Infection
Malignant hyperpyrexia
Drugs eg ecstasy
Pontine strokes
136
Neurological effects of hypothermia.
Decreased level of consciousness
Impaired cerebral auto regulation
Neuroprotective?
137
Cardiovascular effects of hypothermia
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
Respiratory effects of hypothermia
Reduced oxygen demand and delivery
Shift of odc to left
Gases more soluble
Increased tidal volumes
Apnea at 24o
139
Haematological effects of hypothermia
Increased blood viscosity
Thrombocytopenia (due to sequestration)
Leukopenia
Impaired coagulation (as impaired enzymes)
Poor wound healing and thrombogenic
140
Immune response to hypothermia
Immune suppression
141
Metabolic response to hypothermia
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
Renal effects of hypothermia
Reduced renal blood flow and oligourea
143
Causes of hypothermia
Exposure
Water/drowning
Old age
Hypothyroid
Prolonged surgery
144
What neurone type do cold and warm signals travel down
Cold a delta
Wam c
145
Why is surgery a major risk for hypothermia
Behavioural regulation abolished
Suppresses hypothermic threshold by 3-4o up to 12o post op
Vasodiation from anaesthetics
146
Sources and percentatages of heat loss during surgery
Radiation - 40%
Convection - 30%
Evaporation 8-15%
Respiratory - 8-10%
Conduction - 5%
