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Year 2 > Endocrine Week 3 > Flashcards

Endocrine Week 3 Flashcards

1
Q

Describe the anatomy of the pituitary gland and its relationship to the hypothalamus and the blood supply between them:

A

AP - endocrine
PP - extension of neuronal tissue from the hypothalamus
- At infundibulum, capillaries of hypothalamus and pituitary fuse forming hypophyseal system
- These vessels provide direct blood supply between hypothalamus and AP therefore hormones are needed in lower quantity and have rapid effect
- Axons of nuclei in the hypothalamus extend down into PP and their nerve endings terminate onto blood vessels

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2
Q

Name 5 hormones produced by the anterior pituitary gland:

A 
ACTH (adrenocorticotrophic hormone)
TSH (thyroid stimulating hormone)
Prolactin
FSH/LH
GH
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3
Q

Name 5 hormones produced by the hypothalamus and what they trigger from the AP:

A

“Girl, girl, come to daddy’

GHRH (growth hormone releasing hormone) -> GH
GnRH (Gonadotrophin releasing hormone) -> FSH/LH
CRH (corticotrophin releasing hormone) -> ACTH
TRH (thyroid releasing hormone) -> TSH
Dopamine -> LESS prolactin

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4
Q 
What cells in the anterior pituitary produce:
- GH
- FSH/LH
- ACTH
- TSH
- prolactin
and what are their relative proportions?
A 
GH produced by somatotrophs (50%)
FSH/LH produced by GONADOTROPHS (10%)
ACTH produced by corticotrophs (10%)
TSH produced by thyrotrophs (5%)
Prolactin produced by LACTOTROPHS (20%)
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5
Q

What is the somatotroph axis?

A

HYPO releases GHRH
AP releases GH
GH triggers liver to release IGF1 and has other effects on the body and on metabolism
(Negative feedback occurs by end products on AP and HYPO)

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6
Q

What is the gonadotroph axis?

A

HYPO releases GnRH
AP releases FSH/LH
In males:
- LH triggers leydig cells to release testosterone
- FSH triggers sertoli cells to release inhibin
- Testosterone also triggers sertoli cells to release inhibin

In females:

  • LH triggers ovaries to produce oestrogen and progesterone
  • FSH triggers ovaries to produce inhibin

(Negative feedback occurs by end products on AP and HYPO)

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7
Q

What is the corticotroph axis?

A

HYPO releases CRH
AP releases ACTH
Adrenals release cortisol and androgens
(Negative feedback occurs by end products on AP and HYPO)

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8
Q

What is the thyrotroph axis?

A

HYPO releases TRH
AP releases TSH
Thyroid releases T3/4
(Negative feedback occurs by end products on AP and HYPO)

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9
Q

What is the lactotroph axis?

A

HYPO releases dopamine
AP REDUCES its release of prolactin
Prolactin stimulates lactation and is involved in mammary gland development

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10
Q

What hormones are stored by the posterior pituitary (produced by the hypothalamus) and what are their functions?

A

Oxytocin and ADH
Oxytocin:
- Important in labour for uterine contraction and cervix dilation
- Called ‘love hormone’
- Involved in let down reflex in breast feeding, as prolactin from AP stimulates milk production and nipple stimulation causes oxytocin release which causes smooth muscle cells of alveolar cells in breast to contract allowing milk to be expelled

ADH: (vasopressin)

  • released in response to low plasma volume and high plasma osmolarity
  • causes water retention by triggering insertion of AQP channels on basolateral membrane of collecting duct (the side facing the interstitium or blood)
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11
Q

What is diabetes insipidus?

How is it diagnosed and treated?

A
  • When there is a lack of production or responsiveness to ADH leading to osmotic diuresis (more than 3L/day)
  • Cranial cause: when AP fails to produce ADH, can be idiopathic, due to genetic mutation or trauma
  • Can be nephrogenic: kidney fails to respond to ADH, can be due to drugs, renal disease or genetic mutation (e.g. of AVPR2 receptor)
  • Diagnose using water deprivation test followed by desmopressin (synthetic ADH) testing
  • Treat cranial form with desmopressin
  • Treat nephrogenic form by treating the underlying cause e.g. lithium containing drugs (this form is more difficult to treat due to possible genetic cause)
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12
Q

What can pituitary tumours cause?

A

XS production of inappropriate hormones, commonly prolactinomas

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13
Q

What is acromegaly?

A

XS GH production after growth plates have fused.
Causes sweats, headaches, palpations, increased ring and shoe size, coarse facial appearance, hypertension, HF and high BP.

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14
Q

What 3 methods are used to diagnose acromegaly?

How is acromegaly treated?

A
  • Glucose tolerance test (normally glucose will suppress GH release)
  • Measure IGF-1 levels (as GH causes IGF-1 release)
  • Take MRI of pituitary to look for swelling/tumour
  • Treat with pituitary surgery, radiotherapy or medications (somatostatin analogues to lower GH secretion)
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15
Q

What is goitre?

A

Enlargement of the thyroid gland causing swelling of the neck
Can occur in hypo and hyperthyroidism

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16
Q

What is the embryological origin and brief anatomy of the thyroid gland?

A
  • Develops as endodermal downgrowth called the thyroglossal duct from the developing pharynx
  • Remnant in adult at back of tongue called foramen caecum
  • In anterior neck weighing 15-20g
  • 2 lobes connected by isthmus
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17
Q

Describe brief anatomy and histology of the parathyroid glands:

A

Contains 3 cell types: (COW)

  • chief cells -> make PTH
  • oxyphil cells -> function unknown
  • water-clear cells -> like chief cells with pools of glycogen
  • We have 4 parathyroid glands separated from thyroid gland by thick connective tissue
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18
Q

What is embryological development of the pituitary gland?

A

AP - dorsal outgrowth of embryonic pharynx
PP - ventral downgrowth of diencephalon
Surrounded by thin fibroelastic capsule that originates from pia mater

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19
Q

What cell populations make up the anterior pituitary gland?

A

Contains chromophobes and chromophils.
Chromophobes - exhausted secretory cells (pale staining)
Chromophils - active secretory cells (darker staining)
Chromophils can be divided into

Basophils (bind to basic stains like H staining blue)
- thyrotrophs, gonadotrophs and corticotrophs

Acidophils (bind to acidic dyes like E staining red)
- somatotrophs and lactotrophs

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20
Q

What if parents disagree over a child’s medical care?

A

Only one parent needs to give consent, other disagreeing parent can go to court if they wish.

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21
Q

What if parents disagree with a treatment doctors propose for their child?

A

Doctor cannot over-ride parents wishes and must seek authority from court and go through ‘Children Scotland Act 1995)

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22
Q

What age does a child gain legal capacity in Scotland/England/Wales?

A

Scotland - 16yrs

England/Wales - 18yrs

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23
Q

What are the Fraser guidelines?

A

Doctor can give contraceptive advice and treatment to a girl under 16yrs without parents if: BUSC - P
1 - In the Best interests of the patient
2 - The patient Understands the advice
3 - The patient will Suffer mental/physical harm without treatment
4 - Patient will Continue/start having sexual intercourse without the treatment
5 - Doctor cannot Persuade girl to tell parents

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24
Q

What are the GMC guidelines of confidentiality around sex?

A

The medical professional can tell the police or relevant services (e.g. social services) if they have concerns that:

  • young person is too young to consent to sex
  • sexual partner has a position of trust
  • there are large differences in age and power between sexual partners
25
Q 
What is the parental responsibility of a childs:
1 - mother
2 - father (married or unmarried)
3 - step parents
4 - adoption parents
5 - permanent foster carers
A

1 - have automatic parental responsibility
2 - have automatic parental responsibility if name is on birth certificate
3 - must get court application for parental responsibility
4 - gain PR after application and natural parents then lose PR
5 - SHARE PR by court application

26
Q

What do you do in medical care if an adult lacks capacity?

A

Get power of attorney before adult loses capacity.
If no welfare attorney (the person who has applied for the power of attorney) is in place, then doctor can follow treatment plan as specified in the certificate of incapacity.

27
Q

What are the three main mechanisms by which water is regulated in the body?

A

ADH - aquaporin insertion
AT2 - vasoconstriction and Na reabsorption and K excretion
Aldosterone - ENaC channel insertion so more Na reabsorbed
* Water and Na always move together

28
Q

What is hyponatraemia, how is it caused and what are its clinical features?

A

Lack of Na
Cause 1 - inappropriate ADH expression and too much water retention
Cause 2 - Hypovolaemia -> loss of Na via GI tract (in vomiting or diarrhoea)
Cause 3 - Hypervolaemia -> dilutes Na content of the body
Features: often asymptomatic, drowsy, gait instability, confusion, seizures
Can cause brain oedema as plasma osmolality is low so water moves out of blood (to increase osmolality) and into cells.

29
Q

How is

  • acute
  • chronic hyponatraemia used?
A

Acute -> give hypertonic saline to quickly bring Na back up

Chronic -> use AVPR2 receptor antagonists to block the action of ADH

30
Q

What is hypernatraemia, how is it caused and managed?

A

XS Na, usually due to insufficient H2O
Main causes: insensible losses (sweating, burns), GI losses, diabetes insipidus
Management - slow fluid replacement to avoid cerebral oedema

31
Q

What are the causes, signs/symptoms and treatment for hypercalcaemia?

A

Main causes: hyperparathyroidism or malignancy (PTH secreting tumour)

Signs: ‘Bones, stones, moans and abdominal groans.’

  • > osteoporosis
  • > kidney stones
  • > depression
  • > constipation
  • > peptic ulcer disease

Treatment: rehydration, bisphosphonate therapy (zolendronic acid inhibits OC activity), calcitonin (inhibits OC activity), glucocorticoids (inhibit vit D production), parathyroidectomy

32
Q

What are causes, symptoms and management of hypocalcaemia?

A

Low PTH (very rare usually iatrogenic after surgery)
High PTH (if there is chronic renal failure or vitamin D deficiency)
Drugs (chronic bisphosphonates)
Hypomagnesaemia

Symptoms: numbness, ramps, tingling hands, dysrhythmias, hypotension

Treat: Mg infusion, IV Ca replacement, treat the cause e.g. vitamin D replacement

33
Q

How do bisphosphonates work?

A

Inhibit osteoclast activity reducing bone resorption e.g. alendronate, zolendronate

34
Q

How do anti-thyroid drugs work?

A

Inhibit iodide oxidation and iodotyrosine coupling e.g. carbimazole

35
Q

What preparations of corticosteroids are used for clinical practice?

A

Hydrocortisone (a glucocorticoid to mimic cortisol)

Fludrocortisone (a mineralocorticoid to mimic aldosterone)

36
Q

What medicines can be used to treat prolactinoma?

A

Dopamine agonists e.g. cabergoline, quinagolide

37
Q

What pharmacological preparations of ADH are available and when are they used?

A

To treat diabetes insipidus
Desmopressin -> ADH anologue without vasoconstrictor effect
Terlipressin -> ADH analogue with vasoconstrictor effect so used in management of low BP

38
Q

Describe anatomy and cell structure of the thyroid gland:

A
  • spans C5-T1
  • endocrine, inferior to thyroid cartilage of larynx
  • arteries: superior (from common carotid) and inferior thyroid arteries (from subclavian artery) and possibly also a thyroid ima artery in 10% people from the brachiocephalic trunk.
  • veins: superior/middle (from internal jugular) and inferior thyroid vein (from subclavian)
  • highly vascularised organ with sacs of cells called follicles
  • enveloped in fibrous capsule with septa dividing into lobules
  • AP controls secretions
  • vasomotor control from superior/middle/inferior sympathetic ganglions
  • Follicles: single layer of epithelial cells on a basement membrane, central lumen filled with colloid
  • > colloid contains thyroglobulin (storage form of T3/4)
  • parafollicular C cells scattered throughout thyroid gland and secrete calcitonin
39
Q

What is thyroglobulin?

A

= a glycoprotein-tyrosine complex with 140 tyrosines (storage form of T3/4)

40
Q

What is the histology of the thyroid gland when it is stimulated?

A

Cells are columnar and lumen depleted of colloid

41
Q

What is the histology of the thyroid gland when it is suppressed/unactive?

A

Cells are flat and colloid accumulates in the lumen

42
Q

What is the daily requirement of iodine and why is it essential?

A
  • 150-300ug
  • found in seawater, fruit and veg
  • essential for thyroid hormone synthesis
  • deficiency rare due to salt supplementation with iodine
43
Q

How is T3/T4 synthesised?

A
  • Iodine is absorbed in the GI tract into the blood
  • Iodine transported using a Na/I symporter (NIS) across the PM of follicular cells and into the cell cytoplasm
  • Once inside the iodine molecule is too bulky to leave but Na is removed and recycled by Na/K ATPase
  • Iodine moves down concentration gradient to the luminal edge of the follicular cells and transport molecule called pendrin moves it into the colloid filled follicle lumen
  • In the lumen, the enzyme thyroid peroxidase converts iodine into iodide free radicals (Io)
  • Thyroglobulin is present in the colloid and has tyrosines
  • Tyrosines have 2 possible binding sites for iodide
  • If one iodide binds to thyroglobulin - MIT (monoiodotyrosine)
  • If two iodide bind to thyroglobulin - DIT (di-iodotyrosine)
  • The follicular cells synthesise thyroglobulin and thyroid peroxidase
  • T3 is formed by MIT + DIT
  • T4 is formed by DIT + DIT
44
Q

How are T3/4 released?

A
  • when thyroid hormones are required, cytoplasmic extensions of the follicular cells project into the colloid lumen and engulf portions of the colloid containing thyroglobulin and T3/T4
  • in the cytoplasm of the follicular cells there are lysosomes which digest the thyroglobulin breaking it down into individual amino acids, and then T3 and T4 are then free and can be released into the bloodstream
  • Of the TH released, 90% = T4 and 10% = T3
  • T3 is more metabolically active and can be produced in the periphery by removing an iodotyrosine unit from T4
45
Q

How are thyroid hormones transported?

A
  • 0.5% TH are free, 99.5% are bound
  • only free TH can enter cells and exert their effect
  • TH are bound to plasma proteins e.g. globulin, albumin, thyroxine-binding globulin
  • the bound proportion of TH is a reservoir that is drawn on when required
46
Q

How to TH bind to target tissues and cause their effect?

A
  • free T3 binds to nuclear receptor of target cell
  • depending on the tissue the receptor is wither an alpha or beta receptor
  • gene transcription is then induced causing protein synthesis
47
Q

What effects do thyroid hormones have?

A

Metabolic:

  • increase FA release from adipocytes
  • increase CHO absorption from GI
  • increase Na/K ATPase activity
  • increase B-adrenergic receptors all over the body

Growth:

  • Th needed for GH production
  • needed for formation of myelin, nerve terminals and synapses
  • Essential that maternal iodine is sufficient so that foetal thyroid hormones can be made sufficiently to prevent cretinism (a form of mental retardation)

GI:

  • enhances GI function
  • increases metabolic rate and appetite

Neuromuscular:

  • high TH levels cause rapid skeletal muscle movements and reactions
  • low TH levels cause sluggish movements
  • TH essential for normal brain development and cognitive function
48
Q

What are the consequences/causes of hyperthyroidism (thyrotoxicosis)?

A

Grave’s disease -> autoantibodies that stimulate NIS transporter and stimulate XS TH production

Drug induced -> amiodarone (an antiarrhythmic drug that can affect follicular cells causing XS release of T3/4)

Thyroid storm -> rare form due to stress/infection/trauma

Post-partum -> hormone inbalances can cause hyper or hypothyroidism

49
Q

What are TH and TSH levels like in primary hyperthyroidism?

A

Low TSH and high TH

50
Q

Describe causes of Grave’s disease and clinical features:

A
  • patient has autoimmunity, auto-antibodies are present that bind to TSH receptors and stimulate the NIS transporter
  • multinodular goitre
  • autoantibodies
  • hormone secreting tumours
  • XS thyroxine administration
  • common in females 20-40yrs
  • results in eye disease/sore watery eyes, lid retraction, proptosis (due to immune attack of posterior eye structures not due to the XS TH hormone)
51
Q

What is proptosis?

A

Bulging of eyes, characteristic of Grave’s disease

52
Q

What are signs/symptoms of hyperthyroidism and how would you diagnose it?

A

Heat intolerance, sweating, weight loss, diarrhoea, tremor, increased HR, increased appetite

Blood tests (high TH, low TSH, high thyroid peroxidase enzyme)
Autoantibodies present
Fine needle biopsy - malignancy?
US/MRI
Radio-iodine uptake test
53
Q

What are the consequences/causes of hypothyroidism (thyrotoxicosis)?

A

Hashimoto’s disease -> autoimmune, autoantibodies present against thyroid peroxidase enzyme

Iodine deficiency -> compromises TH synthesis

Genetic defect -> dyshormonogenesis (Pendred’s syndrome causing decreased thyroid gland function)

54
Q

What are signs and clinical features of hypothyroidism?

A

Weight gain, cold intolerance, constipation, bradycardia, anaemia, slow reflexes, menorrhagia (abnormally long heavy periods)
Myxedema = overexpression of GAG’s causing water retention and puffiness (normally TH stop XS GAG presentation)
Goitre

55
Q

How would you diagnose/test for hypothyroidism?

A

High TSH and low T4 (primary) - underactive thyroid
Low TSH and low T4 (secondary) - reduced pituitary function
- test for autoantobodies
- increased creatinine kinase levels

56
Q

How would you treat hyperthyroidism?

A

1) Use anti-thyroid drugs to inhibit TH synthesis
- carbimazole (inhibits thyroid peroxidase enzyme)
- thiamazole (active metabolite of carbimazole)
- propylthiouracil (also inhibits peroxidase enzyme)
All can have side effects of rash and take time to show effect as T4 has half life of 10-20 days

2) Radioactive iodine
- thyroid takes up most iodine in the body to ingested to destroy a portion of the thyroid gland
- long term -> patient may need to take thyroxine replacement medication if XS thyroid destroyed and become hypo
- short term -> risk to the public as they are radioactive

3) Surgery
- if patient is not responding to 1) or 2)
- may be complications like haemorrhage or recurrent laryngeal nerve damage depending on the surgeon

57
Q

How would you treat hypothyroidism?

A

1) Replacement therapy
- levothyroxine (T4) given for life
- although biochemically resolved, patients may get symptoms of hyperthyroidism

2) Monitoring
- change levothyroxine doses as required
- thyroid registers are kept to see annually how patient are coping and if replacement therapy is effective

58
Q

Why should you avoid aspirin usage in hyperthyroidism?

A

It displaces TH from its globulin carriers like albumin and increases the % of free TH in the body

59
Q

What is sick euthyroid?

A

Low TSH and T4
Unrelated to abnormal thyroid but caused by another illness that reduces these hormone levels e.g. pneumonia, anorexia, trauma

Year 2 (22 decks)

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