CASE 9 Flashcards
THYROID
- located _________ to the larynx on each side of and _________ to the trachea
- composed of lots of follicles — follicles are lined with _______ epithelial cells that secrete into the interior of the follicles
- the secretory fluid in the follicles is called colloid
- the main component of colloid is _________
- inferiorly
- anteriorly
- cuboidal
- thyroglobulin
what does the thyroid secrete?
thyroxine (T4), triiodothyronine (T3), and calcitonin
what is thyroid secretion controlled by?
thyroid secreting hormone (TSH) from the anterior pituitary gland
what is iodide trapping?
the basal membrane of the thyroid actively pumps the iodide into the follicular cells of the thyroid gland through Na+/I= symporter
what stimulates iodide trapping?
TSH
what is the effect on iodide trapping when the thyroid gland becomes more active?
more iodide is actively transported into the follicle cell
what catalysed the oxidation of iodide ions?
peroxidase enzyme
what is iodide oxidised to?
iodine
where is peroxidase enzyme located?
either located in the apical membrane of the follicle cells or attached to it
what is the organification of thyroglobulin
the binding of iodine with the thyroglobulin molecule
what is tyrosine iodised to and then converted to?
- tyrosine is first iodised to monoiodotyrosine (MIT)
- MIT is then converted to diiodotyrosine (DIT)
what forms T3 and T4?
thyroxine = 2 coupled DIT molecules — T4. thyroxine remains part of the thyroglobulin molecule
triodothyronine (T3) = coupling of one MIT + one DIT — T3
effects of thyroid hormone on mitochondria
increase mitochondrial activity — increases the size and number of mitochondria. the total membrane SA of the mitochondria also increase in proportion to the increased metabolic rate — more ATP production and cellular function
what effect does TH have on ion active transport?
increases ion active transport — increases NaK ATPase activity
what growth does TH promote?
- promote growth in growing children
- promotes growth of brain during foetal development and first few years of life
what effect does TH have on cholesterol, phospholipids and triglycerides levels? effect of hypothyroidism?
lowers levels (even though TH increases FFAs)
not enough TH —> excess deposition of fat in the liver
vitamins and TH
increases need for vitamins (therefore vitamin def can occur when there is excess TH)
effect of TH on heart and blood flow
increases blood flow, cardiac output, HR, heart strength (arterial pressure remains normal) (SBP elevates in hyperthyroidism and diastolic pressure decreases)
hyper vs hypo thyroidism on GI motility
TH increases GI motility therefore:
hypothyroidism - constipation
hyperthyroidism - diarrhoea
where is thyrotropin releasing hormone (TRH) released from? where does it then go?
- secreted by nerve endings in the median eminence of the hypothalamus
- from the median eminence, the TRH is then transported to the anterior pituitary by the way of the hypothalamic-hypophysial portal blood
what does calcitonin do?
decreases plasma Ca conc
where is calcitonin made and secreted from?
C cells, lying in the interstital fluid between the follicles of the thyroid gland
what effect does increased plasma Ca conc have on calcitonin secretion?
increases calcitonin secretion
parathyroid hormone secretion is stimulated by what?
low Ca conc
how does calcitonin decrease blood Ca ion conc?
- immediate effect — decrease the absorptive activities of osteoclasts thus shifting the balance in favour of deposition of calcium in the exchangeable bone calcium salts
- prolonged effect — decrease the formation of new osteoclasts
how does parathyroid hormone (PTH) control extracellular calcium and phosphate concs?
by regulating:
- intestinal reabsorption
- renal excretion
- exchange of these ions between the ECF and bone
what does excess action of the parathyroid gland cause?
excess PTH release
- rapid absorption of Ca slats form the bones — hypercalcaemia in ECF
how does PTH increase Ca and phosphate absorption from the bone?
- rapid phase — results from activation of osteocytes to promote calcium and phosphate absorption
- slow phase — results from proliferation of the osteoclasts, followed by greatly increased osteoclast reabsorption of the bone itself
what is the most common cause of endogenous hyperthyroidism?
Grave’s dosease
Grave’s disease is characterised by what triad of clinical findings?
- hyperthyroidism due to diffuse, hyper functional enlargement of the thyroid
- infiltrative ophthalmopathy with resultant exophthalmos (protrusion f eyeball)
- pretibial myxoedema
what antibodies are present in Grave’s disease?
TSH receptor
what is the most common cause of hypothyroidism in areas of the world where iodine levels are sufficient?
Hashimoto thyroiditis — THIS DISEASE DESCRIEBS PATIETNS WITH GOITRE AND INTENSE LYMPHOCYTIC INFILTRATION OF THE THYROID
what disease is characterised by the gradual thyroid failure due to autoimmune destruction of the thyroid?
hashimoto thyroiditis
what antibodies are present in hashimoto thyroiditis?
antibodies against thyroid peroxidase, thyroglobulin and TSH receptors
how does a goitre develop?
- low iodine levels
- decreased synthesis and secretion of TH
- compensatory increase in TSH
- follicular cell hypertrophy and hyperplasia
- growth and enlargement of thryoid gland (goitre)
where are the different types of B-receptors located?
B1 = mainly in heart and kidneys
B2 = lungs, GIT, liver, uterus, vascular smooth muscle, skeletal muscle
B3 = adipocytes
what does B1 stimulation by adrenaline/noradrenaline result in?
heart — increases cardiac conduction velocity and automaticity
kidneys — renin release d
what does stimulation of B2 receptors cause?
smooth muscle relaxation/bronchodilation
induces tremor in skeletal muscle
increases glycogenolysis in liver and skeletal muscle
what does B3 stimulation cause?
lipolysis
what is an adverse effect of blockade by beta blockers at B1, especially at macula densa?
inhibits renin release — decreases release of aldosterone, causing hyponatraemia and hyperkalaemia
what are the effects on glucose levels by blockade of B2 receptors?
hypoglycaemia
because B2 adrenoreceptors normally stimulate glycogenolysis (hepatic glycogen breakdown) and pancreatic release of glucagon
what is pronanolol?
non-selective B blocker
in the zona glomerulosa, early action of what enzyme steers away from sex steroid precursors to aldosterone or cortisol?
HSD3B2
what enzyme does the zona fasciculata contain for the production of cortisol?
CYP11B2
describe CYP17A1 enzyme
- in zona reticulosa
- allows for the production of sex steroid precursors (androstenedione)
what is the ratio of production of T3:T4 ?
1:20 — lots more thyroxine
half life of T3 vs T4?
longer for T4 - 4 days
T3 - a day
what is more of a long term measure?
TSH (similar to HbA1c)
subclinical hypothyroidism
TSH high and T4 normal
subclinical hyperthyroidism
TSH low and T4 normal
what would be seen if someone takes a load of thyroxine in one go?
high T4/3 and a normal TSH (takes longer)
what is sick euthyroid syndrome?
low TSH and T4 — common in hospital inpatient . abnormal thyroid levels in patients with non-thyroid related illnesses
what long term health effects can you get from hyperthyroidism?
atrial fibrillation, osteoporosis
another name for primary adrenal insufficiency
addisons disease
when does secondary adrenal insufficiency occur?
occurs when the pituitary gland doesn’t make enough of the hormone ACTH
gad65 antibodies
The glutamic acid decarboxylase 65-kilodalton isoform (GAD65) antibody is a biomarker of autoimmune central nervous system (CNS) disorders and, more commonly, nonneurological autoimmune diseases. Type 1 diabetes, autoimmune thyroid disease, and pernicious anemia are the most frequent GAD65 autoimmune associations.
primary vs secondary hypoadrenalism
primary = lack of cortisol AND aldosterone
secondary = normal aldosterone but deficient in cortisol (because don’t have any ACTH coming from pituitary gland)
