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67 Cards in this Set
- Front
- Back
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What is anxiety?
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When a person feels that the demands of a situation are greater than their ability to cope with it
Imbalance between stress and ability to cope with it. |
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What factors affect a response to stress?
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Natures of stress -- intensity, chronicity, unpredictability, situational factors (circumstances)
COPING RESOURCES personality, resilience, previous stressful experiences, social support |
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What are the 2 main components that lead to an anxiety response?
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Exaggerated perception of threat/danger
Propensity to respond with anxiety (Genetics) |
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Anxiety is always pathological. T/F
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False
it can be physiological |
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What characteristics determine whether anxiety is physiological or pathological?
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Intensity
Quality of experience (are they in control or overwhelmed) Duration Context and APPROPRIATENESS (true alarms - presence of real danger, false alarms - no real danger) NEGATIVE EFFECTS on behaviour and functioning |
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Anxiety is always an impairment to functioning.
T/F |
False
a small amount of anxiety may height performance - senses, awareness... Can become debilitating when the person has severe anxiety (such as in panic) |
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What are some classifications of Anxiety disorders?
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Panic disorder (+/- agoraphobia)
Generalised anxiety disorder - GAD Social anxiety disorder / social phobia - SAD Specific phobias (ie spiders, water, enclosed spaces) Obsessive-complulsive disorder OCD Post-traumatic stress disorder PTSD |
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What are the 3 main components of ANXIETY?
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SUBJECTIVE FEELING OF ANXIETY
(feeling of fear, impending doom, dread, excessive worry, anxious, increased alertness, vigilance, inability to relax, problems with concentration or insomnia) PHYSIOLOGICAL (bodily) CHANGES (Increased arousal, SNS, palpitaions, SOB, hyperventilation, sweating, tremor, dizzy, faint, dry mouth, churrning stomach, diarrhoea, polyuria, tension HA, muscle pain) ANXIETY ASSOCIATED BEHAVIOURS (avoidance, escape, safety-seeking, reassurance seeking) |
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What is the difference between anxiety and fear?
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Similarities: negative effect, accompanied by bodily sensations, elicited by threat or danger, may be future orientated (anticipation)
Differences: NATURE of threat (Fear - known; anxiety - unknown) RESPONSE (Fear- fight or flight; anxiety - vigiliance) ONSET: (Fear -clear cut; anxiety - vague) COURSE (fear - episodic/acute; anxiety - chronic/persistent) QUALITY OF EXPERIENCE: (Fear - rational; Anxiety: puzzling) |
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What is the lifetime risk of anxiety disorders?
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25%
Not very well recognised |
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What is the main difference in anxiety experienced between those with generalised anxiety disorder GAD and those with Phobic disorders?
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Phobic - anxiety only comes on with trigger --> ie spiders..
GAD - anxiety is ALWAYS present - may get worse but are generally always at a high level of anxiety - very debilitating |
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What are the treatment modalities for anxiety?
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Pharmacotherapy
Psychotherapy - CBT, marital, supportive, psychodynamic Symptom Control - relaxation techniques, breathing retraining |
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What are all the different Endocrine organs?
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testis, ovary, pancreas, duodenum, stomach, adrenal gland, thyroid, parathyroid, pituitary, pineal gland, hypothalamus, kidney, skin, adipose tissue, heart, thymus
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There are 2 types of endocrine gland systems. What are these and give an example.
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1) normal CNS input -- hypothalamus -- releasing hormone -- pituitary -- trophic hormone -- peripheral gland -- hormone -- target organ -- effect (ie thyroid hormone system)
2) varied input -- free-standing endocrine gland -- hormone -- target -- effect (stomach, duodenal, parathyroid functions) |
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What are some peptide hormones?
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GH, PT, insulin
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What are some Amine Hormones
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Thyroid, catecholamines
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What are some steroid hormones
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testosterone, oestrogen, prostaglandin, Vit D, glucocorticoids, retinoids
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Which hormones can be stored and which must have immediate release?
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can be stored: peptide and amine hormones
Steroid hormones are always released straight away! |
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How can hormones be transported in the blood?
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Protein bound (form of storage)
As free hormone (biologically active form) |
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What are the main mechanisms hormones can have their effects?
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Alter channel permeability of preexisting proteins
Second messenger to alter activity of preexisting proteins Activate/inactivate specific genes to cause formation of new proteins |
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Generally how do steroids elicit their effects?
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Via nuclear receptors
These receptors bind DNA promotor regions of target genes and modulate transcription of target genes |
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T/F
Hormones always act on only 1 type of receptor. |
False - may have more than 1 receptor type
Eg. Angiotension II --> AT1a, AT1b, AT2 |
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What does Adenylate Cyclase do?
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synthesises cAMP from ATP
phosphodiesterases break down cAMP |
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In terms of hormone actions what do the following mean?
Permissive: Synergistic: Antagonistic: |
Permissive: you need 1 hormone for another to have its effect (thyroid and catecholamines)
Synergistic: when 2 hormones are present - the effect is greater than each individual response together (very big response) - FSH and testosterone Antagonistic: hormones work against each other (glucagon and insulin) |
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How are hormone signals terminated?
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Hormone is metabolised
Intraceullar signals are metabolised (cAMP degraded) Receptor recycling/ degradation Negative feedback to endocrine organ |
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There are many diseases/syndromes associated with endocrine dysfunction. What can go wrong with an endocrine pathway?
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ENDOCRINE GLAND
Destruction, hyperplasia, tumour, Ab induced hypersecretion HORMONE Dysfunctional, ectopic production, antibody block / antagonism, TARGET ORGAN defective receptor, intracellular signalling pathways, response |
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What are the thyroid hormones and what are their relative activities and amounts?
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T3, T4, reverseT3 --> Also CALCITONIN
T3 (9%) > T4 (90%) > rT3 (1%) |
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What is necessary for thyroid hormone production?
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Iodine
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What are the steps involved in thyroid hormone production?
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Iodine (I-) is taken up by thyroid follicular cells
Thyroglobulin (TGB) is produced by Thyroid follicular cells I- and TGB --> are transported to the COLLOID where they are used to make MITs and DITs -- iodination of tyrosine residues on TGB. These are then combined to make T3 (MIT + DIT) and T4 (2x DIT) - via peroxidase These are then taken back up into the thyroid follicular cell and T3 and T4 are released into the circulation. MIT = monoiodotyrosine DIT = diiodotyrosine |
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How does TSH regulate thyroid hormone production?
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It regulates I- uptake, secretion of hormones and peroxidase activity
It also increases the size and number of thyroid follicular cells |
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How is iodine moved into the thyroid follicular cells and into the colloid?
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into follicular cells -- active transport
into colloid -- facilitated diffusion due to concentration gradient |
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Where does TSH come from?
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anterior pituitary
its release is stimulated by TRH - thyrotrophin releasing hormone Thyrotrophin = TSH |
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What is the active Thyroid hormone?
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T3
T4 is converted into T3 and rT3 in the kidney, liver and pituitary |
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What are some inhibitors of thyroid hormone T4 conversion to T3?
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propylthiouracil
propanolol (beta-blocker) glucocorticoids burns, trauma, renal failure, infarct, reduced food intake |
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What kind of receptor does T3 bind?
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intracellular receptors
Steroid like actions -- modulates RNA synthesis Slow on/off effects |
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What are the 2 main classes of Thyroid hormone effects?
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Calorigenic
(heat producing, metabolism, growth and development) Sympathomimetic (facilitate catecholamine functions, increased SNS) |
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Describe the Calorigenic Actions of Thyroid Hormone.
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HEAT PRODUCING
increased BMR, Heat production, energy use, O2 consumption, number and size of mitochondria METABOLISM Glucose: ↑ absorption rate, ↑ uptake into cells Fat: ↑ clearance of lipoproteins, ↑ turnover Protein: ↑ AA uptake, ↑ protein synthesis (if too high - protein catabolism) may affect vitamins |
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Describe the Sympathomimetic Effects of thyroid hormone.
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Facilitated action of catecholamines (NA, Adr)
Increased SNS activity ↑ beta Adr receptors - number and affinity Some of these effects can be treated with beta blockers |
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What are some characteristics of hyperthyroidism?
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Sympathomimetic:
jumpy, anxious, tremor, ↑ HR, bounding pulse, palpitations ↑S. BP, ↓ D. BP (due to ↓ TPR) -- Wide pulse pressure peripheral vasodilation head intolerance brisk reflexes Wt Loss Goiter - SOB, swallowing and breathing difficulties proximal myopathy pembertons sign, berry's sign Graves - exopthalmos, lid lag, periorbital puffiness, kymosis, dyplopia, impaired eye muscle function, clubbing, ...pretibial myxoedema |
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What are some characteristics of hypothyroidism?
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Fetus: impaired CNS development
Child: ↓ height, mental retardation, coarse hair, impaired mental function, intolerance, dry skin, husky voice, ↓ relfexes (hung up reflexes) inceased weight brain fog (memory) hair loss constipated lethargy bradycardia loss of outer 1/3 of eyebrow |
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T/F
The presence of a goitre is always associated with hyperthyroidism. |
FALSE
With reduced TH --> you would get an ↑ TSH which would cause hypertrophy of the thyroid gland, also non-functional nodules, ... may also be euthyroid |
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What are the mechanisms which maintain self Tolerance?
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CENTRAL TOLERANCE
Deletion of self reactive cells in the thymus AIRE gene PERIPHERAL TOLERANCE Need for costimulation --- Anergy Fas-FasL interactions Treg Cells |
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What environmental insults can lead to a breakdown of self tolerance?
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Infection - Viral, bacteria
Drugs - IFN for Hep C (Thyroid disease) Smoking - RA Transient auto-immune responses can occur after inflammation - but only persist in the presence of Genetic Susceptibility |
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T/F
The presence of one autoimmune disease predisposes to other autoimmune diseases. |
TRUE
Relatives of people with Hashimoto's - 50% have Ab for Hashimoto's Disease and 20% Pernicious Anaemia |
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There are 2 main clusters of autoimmune diseases.
What are these clusters called and examples of diseases. |
THYROGASTRIC Cluster
Pernicious Anaemia, Hypoparathyroidism, vitiligo, thyroiditis, myasthenia gravis, diabetes, mellitus, ovarin failure, adrenalitis LUPUS cluster RA, Sjogrens disease, dermatomyositis, scleroderma, myasthenia gravis, chronic active hepatitis, SLE |
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What are some genetic associations to Type 1 Diabetes?
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HLA class II
PTPN22 CTLA-4 IL2Ra IFN helicase protein insulin |
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T/F
Frequency of anti-thyroid and anti-nuclear auto-Ab increase with Age. |
TRUE
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What antibodies are associated with Hashimoto's Thyroiditis?
Clinical Significance? |
Thyroid Peroxidase (TPO)
Thyroglobulin (TG) Damage to thyroid -- loss of function... CLINICALLY --> Goitre + Hypothyroidism |
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What Ab's are associated Primary Myxoedema ?
Clinical Significance? |
TSH-R
Blocking Ab to TSH-R (TSH can not activate - antagonist effect) CLINICALLY: Hypothyroidism |
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What antibodies are associated with Grave's Disease?
Clinical Significance? |
TSH-R
Stimulating Ab to TSH-R --> Cross reactive T cells with Ag in extraocular muscles CLINICALLY: Hyperthyroidism (no neg. feeback), goitre, opthalmopathy |
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What antibodies are associated with T1DM?
Clinical Significance? |
Pancreatic Islet Cell Antigens (ICA)
Glutamic Acid Decarboxylase (GAD-65) Tyrosine phosphatase (IA-2) Insulin CLINICALLY: islet cell destruction - no insulin |
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What are the target Ag associated with Addison's Disease?
Clinical Significance? |
Adrenal cortex enzymes in steroid biosynthesis - 17alpha-hydroxylase, 21-hydroxylase
T cells CLINICAL: Hypoadrenalism (Reduced cortisol) |
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What are the target Ag associated with Hypogonadism?
Clinical significance? |
Leydig Cells (Testis), Granulosa, Theca (Ovary), Cytochrome p450, 17hydroxylase....
T cells Clinical: Infertility |
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What are the target Ag associated with Hypoparathyroidism?
Clinical significance? |
Parathyroid Calcium Sensing R
T cells Clinical: hypocalcaemia |
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What are the target Ag associated with Pernicious Anaemia?
Clinical Significance: |
Gastric Parietal Cell H/K ATPase (proton pump)
T cells (also detect anti-intrinsic factor Ab) Clinical: Gastritis + IF deficiency - B12 deficiency |
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What are the target Ag associated with Vitiligo?
Clinical Significance? |
melanocyte tyrosinase (T cells
T cells Clinical: Depigmented skin |
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Presence of Auto-antibodies indicates presence of disease.
T/F |
FALSE
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What are 3 types of treatment for auto-immune endocrine disease?
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1) Replacement Therapy
Thyroxin - hypothyroidism Insulin - T1D Vit B12 - Pernicious Anaemia 2) Suppression of inflammatory response (short term) Autoimmune thyroiditis 3) Suppression of Auto-immune response "immunosupression" - Progressive opthalmopathy in Grave's disease |
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How is heat produced?
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Arises from exothermic reactions
--- a by product of inefficiency energy transfer ATP breakdown without work, coupling opposed pathways (futile cycles), uncoupling of pathways... Mitochondria is a key site -- ATP or Heat out (uncoupling protein) |
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Thermogenesis can be generally divided into 2 categories. What are these.
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Obligatory - RMR - relaxed at 23 degrees C
Adaptive - increased Metabolic rate |
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Regulation of adaptive thermogenesis involve sensing and effector arms. What are the components of these?
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Sensing Arm: hypothalamus - Temp and nutrient receptors
Effector Arm: Thyroid hormone (important in obligatory and adaptive thermoregulation), SNS |
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Where does adaptive thermogenesis occur?
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Brown adipose tissue (non-shivering thermogenesis)
Skeletal muscle: Acute - shivering Prolonged - Change in muscle fibre type - impaired efficiency of energy transfer Futile Metabolic cylcles |
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What is an example of a futile cycle?
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Coupled glycolysis and gluconeogenesis
Leaky ion channels - activate ATPase channels (Ca channels - in skeletal muscle; Na channels in cells - membrane potential) Heat lost due to ATP breakdown |
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What is the role of mitochondria in Heat production?
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A series of proteins transfer electrons and drive protons (H+) into the intermembrane space.
These protons flow back via a ATP synthase (driven by the H+ gradient) and ATP is synthesised. Insertion of the UCP (uncoupling proton) provides an alternate route for protons without ATP synthesis. Heat arises from futile recycling of protons. |
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How is heat production regulated by thyroid hormone?
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Increased expression of uncouping proteins
Reduced efficiency of mitochondrial proton pumping promotion of SERCA expression (Ca uncoupling in Skeletal muscles) ↑ SNS effects |
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What hormones other than thyroid hormone affect heat production?
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ADRENALIN - ↑ gluconeogenesis, BV vasodilation in skeletal mm, promote T4 conversion to T3
LEPTIN - ↑ SNS INSULIN - cold exposure increases glucose uptake and metabolism GLUCAGON - ↑ gluconeogenesis |
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How can you measure Heat production?
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Direct - calorimetry
Indirect - indirect calorimetry (measure O2 consumption) |
