Endocrine 1 to 10
Outline the physiological effects of thyroid hormones.
- Heart: chronotropic; inotropic (increased number of B-adrenergic receptors; increased response to catecholamines; increased proportion of a-myosin heavy chain);
- Adipose tissue: catabolic (stimulated lipolysis);
- Muscle: catabolic (increased protein breakdown);
- Bone: developmental (promote normal growth(Cretin) and skeletal development);
- Nervous system: promote normal brain development;
- Gut: metabolic (increased CHO absorption);
- Lipoprotein: metabolic (formation of LDL receptors);
- other – calorigenic (increased metabolic rate, increased stimulation O2 consumption)
- 3 to pass including heart
Describe the mechanism regulating thyroid hormone.
- Negative feedback effect of T4 and T3 on hypothalamus and pituitary to inhibit TRH and TSH secretion respectively.
- Cold stimulates thyroid hormone secretion, stress and glucocorticoids inhibit
What metabolic effects does insulin have on the liver?
- decreased ketogenesis;
- increased protein synthesis;
- increased lipid synthesis;
- decreased glucose output due to decreased gluconeogenesis, increased glycogen synthesis, increased glycolysis
What are the effects of insulin deficiency on the body over?
- Decreased cellular glucose uptake
- Total body dehydration and acidosis.
What is the physiological role of aldosterone?
- Aldosterone causes Na+ and water retention, expanded ECF volume and shutting off the stimulus to increased renin secretion
What conditions increase aldosterone secretion?
- Primary: – Stress hormone, low pressure/volume states
- Secondary: Hyperaldosteronism: (eg. CCF, cirrhosis & nephrosis).
What factors affect Antidiuretic Hormone (ADH) secretion?
Prompt: ADH is also known as vasopressin. What stimulates vasopressin secretion?
- Plasma osmotic pressure – increase POP leads to increase ADH secretion. Sensitive to changes around 285mosm/kn\g
- Extracellular fluid volume – inverse relationship between ADH secretion and ECF volume. Primary mediators are the low pressure receptors in great veins, atria and pulmonary vessels
- Pain, emotion, stress, nausea vomiting– all increase ADH
- Drugs – eg, carbamazepine, clofibrate increase, alcohol decreases
- Angiotensin II – increases
What physiological factors affect renin secretion?
- Afferent arteriolar pressure – increased pressure at the level of JG cells in kidney causes decrease in renin secretion & vice versa
- Na & K transport across macula densa – increased reabsorption leads to decreased renin secretion & vice versa
- Angiotensin II – inhibitory feedback to JG cells
- Circulating catecholamines – increased SNS activity increases renin
- Other – Prostaglandins – increases renin; vasopressin – decreases renin
- 3 out of 5 bold to pass
What are the main regulatory factors for aldosterone secretion?
- Renin-angiotensin system
- Rise in plasma K concentration (via the adrenal cortex)
- Bold to pass
What happens to the insulin secretion when a person is injected with 50ml of 50% Dextrose?
- It would go up
Describe the mechanism of insulin secretion.
- The insulin is dumped from the beta cells of the Islets of Langerhans within 3-5 minutes followed by a plateau at 2-3 hrs by activation of the enzyme system
- Glucose is metabolised by the glucokinase and this involve ATP, decrease potassium efflux and increase calcium entry into cells that cause release of insulin by exocytosis
What are the physiologic actions of glucagon?
- Glycogenolysis in liver – not muscle
- Gluconeogenesis from amino acids
Only at very high levels.
- Lipolysis –
- +ve inotropic effect on heart
- Inc blood flow to kidneys
- Stimulates secretion of GH, insulin and somatostatin
What factors affect glucagon secretion?
- Beta adrenergic stimulants Cortisol, protein meal,vagal stimulation
- Starvation,stress, exercise, CCK, gastrin, theophylline
- Glucose —-most important insulin
- alpha Adrenergic stimulators.
Describe the biosynthesis and storage of norepinephrine at the synaptic junction?
- Dietary tyrosine mostly (some formed from phenylalanine)
- Tyrosine transported into catecholamine-secreting neurones by concentrating mechanism tyrosine -> dopa by tyrosine hydroxylase -> dopamine by dopa decarboxylase in cytoplasm
- Rate-limiting step [tyrosine -> dopa] is subject to feedback inhibition by dopamine and norepinephrine]
- Dopamine enters granulated vesicles à norepinephrine by dopamine beta-hydroxylase (DBH)
- Norepinephrine stored bound to ATP, with protein chromogranin A
- At least 4 in correct order
How is Norepinephrine removed from the synaptic junction?
- Norepinephrine is removed from the synaptic junction by:
- binding to postsynaptic receptors
- binding to presynaptic receptors
- reuptake into presynaptic neurons
- catabolism (MAO)
- Catabolism at noradrenergic nerve endings is catalysed by MAO (monoamine oxidase) and COMT
- (COMT mainly in liver, also at postsynaptic noradrenergic nerve endings
- Norepinephrine -> DOMA (3,4-dihydroxymandelic acid) & DHPG (3,4-dihydroxymandelic aldehyde)
- -> VMA (vanillylmandelic acid) & MHPG (3-methoxy-4- hydroxyphenylglycol) by systemic COMT
- These deaminated derivatives are physiologically inactive
What are the effects of thyroid hormones?
- Widespread actions
- Metabolically active tissues
- Heart – increased rate
- Brain – development
- Brain – reticular Act. System
- Gut – increased carbohydrate absorbtion
- Muskuloskeletal growth
- Adipose – lipolysis
- 4 out of 7
What is the mechanism of action?
- At the nuclear level
- O2 consumption regulator.
- T3 binds better than T4 to receptor
- Hormone/receptor binds to DNA
- Affects gene expression
- Two genesites
- Alpha Chromosome 17
- Beta Chromosome 3
- 4 out of 8