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PBL SEM 4 > CASE 9 > Flashcards

CASE 9 Flashcards

1
Q

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 _________
A
  • inferiorly
  • anteriorly
  • cuboidal
  • thyroglobulin
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2
Q

what does the thyroid secrete?

A

thyroxine (T4), triiodothyronine (T3), and calcitonin

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3
Q

what is thyroid secretion controlled by?

A

thyroid secreting hormone (TSH) from the anterior pituitary gland

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4
Q

what is iodide trapping?

A

the basal membrane of the thyroid actively pumps the iodide into the follicular cells of the thyroid gland through Na+/I= symporter

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5
Q

what stimulates iodide trapping?

A

TSH

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6
Q

what is the effect on iodide trapping when the thyroid gland becomes more active?

A

more iodide is actively transported into the follicle cell

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7
Q

what catalysed the oxidation of iodide ions?

A

peroxidase enzyme

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8
Q

what is iodide oxidised to?

A

iodine

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9
Q

where is peroxidase enzyme located?

A

either located in the apical membrane of the follicle cells or attached to it

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10
Q

what is the organification of thyroglobulin

A

the binding of iodine with the thyroglobulin molecule

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11
Q

what is tyrosine iodised to and then converted to?

A
  1. tyrosine is first iodised to monoiodotyrosine (MIT)
  2. MIT is then converted to diiodotyrosine (DIT)
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12
Q

what forms T3 and T4?

A

thyroxine = 2 coupled DIT molecules — T4. thyroxine remains part of the thyroglobulin molecule

triodothyronine (T3) = coupling of one MIT + one DIT — T3

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13
Q

effects of thyroid hormone on mitochondria

A

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

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14
Q

what effect does TH have on ion active transport?

A

increases ion active transport — increases NaK ATPase activity

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15
Q

what growth does TH promote?

A
  • promote growth in growing children
  • promotes growth of brain during foetal development and first few years of life
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16
Q

what effect does TH have on cholesterol, phospholipids and triglycerides levels? effect of hypothyroidism?

A

lowers levels (even though TH increases FFAs)

not enough TH —> excess deposition of fat in the liver

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17
Q

vitamins and TH

A

increases need for vitamins (therefore vitamin def can occur when there is excess TH)

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18
Q

effect of TH on heart and blood flow

A

increases blood flow, cardiac output, HR, heart strength (arterial pressure remains normal) (SBP elevates in hyperthyroidism and diastolic pressure decreases)

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19
Q

hyper vs hypo thyroidism on GI motility

A

TH increases GI motility therefore:

hypothyroidism - constipation
hyperthyroidism - diarrhoea

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20
Q

where is thyrotropin releasing hormone (TRH) released from? where does it then go?

A
  • 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
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21
Q

what does calcitonin do?

A

decreases plasma Ca conc

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22
Q

where is calcitonin made and secreted from?

A

C cells, lying in the interstital fluid between the follicles of the thyroid gland

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23
Q

what effect does increased plasma Ca conc have on calcitonin secretion?

A

increases calcitonin secretion

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24
Q

parathyroid hormone secretion is stimulated by what?

A

low Ca conc

25
Q

how does calcitonin decrease blood Ca ion conc?

A
  1. immediate effect — decrease the absorptive activities of osteoclasts thus shifting the balance in favour of deposition of calcium in the exchangeable bone calcium salts
  2. prolonged effect — decrease the formation of new osteoclasts
26
Q

how does parathyroid hormone (PTH) control extracellular calcium and phosphate concs?

A

by regulating:

  • intestinal reabsorption
  • renal excretion
  • exchange of these ions between the ECF and bone
27
Q

what does excess action of the parathyroid gland cause?

A

excess PTH release

  • rapid absorption of Ca slats form the bones — hypercalcaemia in ECF
28
Q

how does PTH increase Ca and phosphate absorption from the bone?

A
  1. rapid phase — results from activation of osteocytes to promote calcium and phosphate absorption
  2. slow phase — results from proliferation of the osteoclasts, followed by greatly increased osteoclast reabsorption of the bone itself
29
Q

what is the most common cause of endogenous hyperthyroidism?

A

Grave’s dosease

30
Q

Grave’s disease is characterised by what triad of clinical findings?

A
  1. hyperthyroidism due to diffuse, hyper functional enlargement of the thyroid
  2. infiltrative ophthalmopathy with resultant exophthalmos (protrusion f eyeball)
  3. pretibial myxoedema
31
Q

what antibodies are present in Grave’s disease?

A

TSH receptor

32
Q

what is the most common cause of hypothyroidism in areas of the world where iodine levels are sufficient?

A

Hashimoto thyroiditis — THIS DISEASE DESCRIEBS PATIETNS WITH GOITRE AND INTENSE LYMPHOCYTIC INFILTRATION OF THE THYROID

33
Q

what disease is characterised by the gradual thyroid failure due to autoimmune destruction of the thyroid?

A

hashimoto thyroiditis

34
Q

what antibodies are present in hashimoto thyroiditis?

A

antibodies against thyroid peroxidase, thyroglobulin and TSH receptors

35
Q

how does a goitre develop?

A
  • 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)
36
Q

where are the different types of B-receptors located?

A

B1 = mainly in heart and kidneys

B2 = lungs, GIT, liver, uterus, vascular smooth muscle, skeletal muscle

B3 = adipocytes

37
Q

what does B1 stimulation by adrenaline/noradrenaline result in?

A

heart — increases cardiac conduction velocity and automaticity

kidneys — renin release d

38
Q

what does stimulation of B2 receptors cause?

A

smooth muscle relaxation/bronchodilation

induces tremor in skeletal muscle

increases glycogenolysis in liver and skeletal muscle

39
Q

what does B3 stimulation cause?

A

lipolysis

40
Q

what is an adverse effect of blockade by beta blockers at B1, especially at macula densa?

A

inhibits renin release — decreases release of aldosterone, causing hyponatraemia and hyperkalaemia

41
Q

what are the effects on glucose levels by blockade of B2 receptors?

A

hypoglycaemia

because B2 adrenoreceptors normally stimulate glycogenolysis (hepatic glycogen breakdown) and pancreatic release of glucagon

42
Q

what is pronanolol?

A

non-selective B blocker

43
Q

in the zona glomerulosa, early action of what enzyme steers away from sex steroid precursors to aldosterone or cortisol?

A

HSD3B2

44
Q

what enzyme does the zona fasciculata contain for the production of cortisol?

A

CYP11B2

45
Q

describe CYP17A1 enzyme

A
  • in zona reticulosa
  • allows for the production of sex steroid precursors (androstenedione)
46
Q
A
47
Q

what is the ratio of production of T3:T4 ?

A

1:20 — lots more thyroxine

48
Q

half life of T3 vs T4?

A

longer for T4 - 4 days
T3 - a day

49
Q

what is more of a long term measure?

A

TSH (similar to HbA1c)

50
Q

subclinical hypothyroidism

A

TSH high and T4 normal

51
Q

subclinical hyperthyroidism

A

TSH low and T4 normal

52
Q

what would be seen if someone takes a load of thyroxine in one go?

A

high T4/3 and a normal TSH (takes longer)

53
Q

what is sick euthyroid syndrome?

A

low TSH and T4 — common in hospital inpatient . abnormal thyroid levels in patients with non-thyroid related illnesses

54
Q

what long term health effects can you get from hyperthyroidism?

A

atrial fibrillation, osteoporosis

55
Q

another name for primary adrenal insufficiency

A

addisons disease

56
Q

when does secondary adrenal insufficiency occur?

A

occurs when the pituitary gland doesn’t make enough of the hormone ACTH

57
Q

gad65 antibodies

A

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.

58
Q

primary vs secondary hypoadrenalism

A

primary = lack of cortisol AND aldosterone

secondary = normal aldosterone but deficient in cortisol (because don’t have any ACTH coming from pituitary gland)

PBL SEM 4 (50 decks)

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