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Year 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the major endocrine glands of the body?

A

Pituitary gland, thyroid gland, parathyroid gland, adrenal glands, pancreas, ovaries, testes

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2
Q

What are steroid hormones derived from?

A

Cholesterol

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3
Q

What is autocrine signalling?

A

When the cell produces signalling molecules which are released into the ECF and act on themselves to release more signalling molecules

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4
Q

What is paracrine signalling?

A

Cell produces signalling molecules which act on cells next to it

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5
Q

What is endocrine signalling?

A

signalling molecule is released into the ECF and enters the blood stream and travels a distance to the target cells

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6
Q

Which hormones act in a complementary way during exercise to prevent hypoglycaemia and hypokalaemia?

A

Glucagon, cortisol and Adrenaline

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7
Q

What is the role of Insulin?

A

Lowers plasma glucose levels by inhibiting hepatic glycogenolysis (breakdown of glycogen to glucose) and gluconeogenesis (formation of glucose) and stimulating glucose uptake into muscle and adipose tissue

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8
Q

What is the role of Glucagon?

A

Increases plasma glucose levels by stimulating hepatic glycogenolysis and gluconeogenesis.

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9
Q

Where does gluconeogenesis and glycogenolysis occur?

A

Liver

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10
Q

What is glucose stored as in the liver?

A

Glycogen

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11
Q

What type of hormone is adrenaline and how is it released into the body?

A

It is an amine hormone and is released into the ECF by a signal from calcium. It then enters the circulation and is hydrophillic in nature.

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12
Q

How does steroid storage differ from amine and polypeptide hormones storage?

A

Steroids are not stored- they are released right away and only synthesised when required. Amine and polypeptide are pre-made and stored waiting on a signal- this means they are faster at being released

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13
Q

Are steroid hormones hydrophillic or hydrophobic?

A

Hydrophobic- they must be bound to specialised transport proteins.

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14
Q

What are biologically active steroids?

A

The small percentage of steroid hormones that are not bound- they can cross capillary walls

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15
Q

Give examples of carrier proteins

A

Cortisol binding protein: binds cortisol in a selective manner (and some aldosterone)
Thyroxine binding globulin: binds thyroxine (T4) selectively and some T3
Sex steroid binding globulin: binds mainly testosterone and oestradiol

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16
Q

What is the role of Albumin?

A

It is a carrier protein that binds mainly steroids and thyroxine

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17
Q

Which carrier protein binds to hormones when there is a large surge, increasing plasma concentration?

A

Globulin

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18
Q

Where does corticotrophin releasing factor act on?

A

the anterior pituitary

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19
Q

Where does ACTH work on?

A

The adrenal cortex to secrete cortisol

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20
Q

What is the negative feedback of cortisol?

A

Cortisol can work on the anterior pituitary to stop producing ACTH and thus cortisol, or working on the hypothalamus to stop the release of corticotrophin releasing factor

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21
Q

What causes a positive effect on the hypothalamus to secrete more cortisol?

A

Physiological stress

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22
Q

Describe the pattern of production of cortisol

A

Diurnal variation- it peaks in the morning and steadily decreases until nighttime and then rises again

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23
Q

What is the half-life of Amine, protein/peptide and steroid hormones?

A

Amines: seconds
Proteins: minutes
Steroids: hours- due to extensive protein binding

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24
Q

How do amine hormones signal?

A

They act via G-protein coupled receptors

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25
Q

What hormones does the anterior pituitary produce?

A

ACTH, GH, FSH, LH, Prolactin, TSH

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26
Q

What hormones does the posterior pituitary produce?

A

ADH, Oxytocin

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27
Q

What hormone does the intermediate pituitary gland produce?

A

Melanotropic stimulating hormone

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28
Q

What hormones does the Parathyroid hormones produce?

A

Calcitonin and PTH

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29
Q

What hormones does the adrenal cortex produce?

A

Cortisol (glucocorticoids) and aldosterone

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30
Q

What hormones does the adrenal medulla produce?

A

Adrenaline and noradrenaline

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31
Q

Describe the processes leading to the secretion of T3 and T4

A

Thryotrophin releasing hormone is secreted in the hypothalamus and travels via the portal system to the anterior pituitary where it stimulates the thyroid stimulating hormone. TSH stimulates increased thyroidal iodine uptake by the thyroid and release of T3 and T4. T4 is converted to the biologically active T3 by TSH. T3 and T4 then enter cells and bind to nuclear receptors and promote increased metabolic and cellular activity.

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32
Q

What is the negative feedback of thyroid hormones?

A

The anterior pituitary and hypothalamus sense high levels of T3 and suppress TRH and TSH leading to reduced T3 and T4. If these levels get too low then TRH and TSH are secreted stimulating the thyroid to produce more T3 and T4.

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33
Q

What is primary hormone deficiency?

A

Due to a disease process in the endocrine end-organ which will lead to a loss of negative feedback and subsequent elevation in the corresponding anterior pituitary hormone

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34
Q

What is secondary gland failure?

A

There are low or inappropriately normal levels of the pituitary hormone in the face of a low end-organ hormone level e.g. Low T3 and T4 in the levels of a low TSH- pituitary disease should be suspected.

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35
Q

What does oversecretion and undersecretion of ADH cause?

A

Over: water retention and swelling
Under: dehydration

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36
Q

What does an oversecretion and undersecretion of growth hormone cause in children and adults?

A

Over: children- gigantism, adults- acromegaly
Under:dwarfism

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37
Q

What cells in the testes produce testosterone?

A

Leydig cells (in the presence of LH)

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38
Q

What is the role of LH in females?

A

it stimulates the release of the oocyte from the Graafian follicle and then develops it into the corpus luteum

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39
Q

What is the role of FSH in females?

A

stimulates the development of the follicle for ovulation

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40
Q

What is the role of FSH in men?

A

Spermatogenesis

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41
Q

What is the function of thyroxine?

A

regulates the basal metabolic rate of the cells in the body. it affects growth and functioning of the heart and nervous system, it stimulates growth and differentiation of tissue in a foetus and in children and it regulates body temperature

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42
Q

What is the role of aldosterone?

A

helps the uptake of sodium ions in the loop of henle in the kidneys and maintains salt balance

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43
Q

What does undersecretion of aldosterone cause?

A

Addisons disease

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44
Q

What does the beta, alpha and gamma cells secrete in the pancreas?

A

alpha- glucagon
Beta- insulin
Gamma- somatostatin

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45
Q

What happens in the sertoli cells?

A

Differentiation from germ cells into spermatazoa (caused by testosterone)

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46
Q

What is the role of progesterone?

A

prepares the endometrium for implantation once fertilisation of the egg cell has occurred. it is necessary for the production of the mucous plug to prevent sperm or other substances from entering the uterus during pregnancy.

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47
Q

What is the colloid?

A

it is a viscous fluid in the centre of the thyroid gland which contains thyroglobulin. When iodine binds to thyroglobulin, hormones are produced

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48
Q

What is T3 and T4 usually bound to?

A

Thyroxine binding globulus (TBG) or to albumin

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49
Q

Why type of thyroid hormone is biologically active?

A

T3

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50
Q

What causes a goitre?

A

When the T3 and T4 cannot be produced (may be due to iodine deficiency) then TSH is produced in increasing amounts. As a result of the hyperstimulation, thyroglobulin accumulates in the thyroid gland follicles increasing their deposits in the colloid which causes a goitre.

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51
Q

Why is iodine deficiency so important?

A

it is the primary cause of preventable mental retardation

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52
Q

What is neonatal hypothyroidism?

A

cognitive deficits, short stature, deafness and muteness in children and adults born to mothers who were iodine deficient during pregnancy

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53
Q

What is Calcitonin?

A

peptide hormone produced and secreted by the parafollicular cells of the thyroid gland that functions to decrease blood calcium levels. It is released in response to increased calcium levels.

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54
Q

How does Calcitonin function?

A

it decreases Calcium by:
inhibiting the activity of osteoclasts, increasing the activity of osteoblasts, decreasing Ca absorption in the intestines, increasing Ca loss in the urine

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55
Q

What are the 6 steps involved in the synthesis of iodine?

A
  1. Active transport: of iodide into follicular cells
  2. Thyroglobulin: large protein rich in tyrosine is placed in secretory vesicles
  3. Exocytosis: of thryoglobulin into follicular lumen where it is stored as colloid.
  4. Iodination: of thryoglobulin to form DIT and MIT.
  5. Coupling: of DIT with MIT to form T3 and DIT x2 to form T4
  6. Exocytosis: of iodinated thryoglobulin back into the follicular cell.
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56
Q

What is the treatment of hyperthyroidism?

A

Carbimazole

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57
Q

What is the treatment of hypothyroidism?

A

Thyroxine (T4)- it has a longer half life than T3

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58
Q

What is the infundibulum?

A

The stem that suspends the pituitary gland

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59
Q

What is the function of melanocyte stimulating hormone\?

A

Stimulates melanin formation in melanocytes

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60
Q

Does the posterior pituitary gland produce hormones?

A

No- it stores hormones that are made in the hypothalamus

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61
Q

Where is oxytocin produced?

A

The paraventricular nulcei in the hypothalamus

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62
Q

Where is ADH produced?

A

the supraoptic nucleus in the hypothalamus

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63
Q

What is the function of oxytocin?

A

When fetal development is complete, oxytocin stimulates uterine contractions and dilation of the cervix.

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64
Q

When is oxytocin released?

A

It is at high levels throughout pregnancy and increases during childbirth where it is continually released through a positive feedback system. It is also necessary for milk ejection.

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65
Q

How does oxytocin help with childbirth?

A

It promotes uterine contractions that push the foetal head to the cervix and in response, cervical stretching stimulates additional oxytocin to be stimulated by the hypothalamus which increases the intensity of the contractions and prompts additional dilation of the cervix.

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66
Q

What is the mechanism of action of ADH?

A

ADH causes reabsorption of water. in response to high blood osmolarity (which can be due to dehydration), the osmoreceptors signal the posterior pituitary to release ADH. Its effect is to increase epithelial permeability to water allowing increased water reabsorption

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67
Q

Explain negative feedback with ADH

A

As blood osmolarity decreases, the osmoreceptors sense the change and prompt a corresponding decrease in the secretion of ADH. As a result, less water is reabsorbed from the filtrate.

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68
Q

What is diabetes insipidus?

A

chronic underproduction of ADH that causes chronic dehydration. Symptoms are usually polydipsia and dysuria

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69
Q

What controls the release of growth hormone from the pituitary gland?

A

Somatostatin (GHIH) and GHRH

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70
Q

What is the glucose sparing effect?

A

It occurs when GH stimulates lipolysis or the breakdown of adipose tissue releasing fatty acids into the blood and so fatty acids is the main source of energy.

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71
Q

What is the Diabetogenic effect?

A

GH stimulates the liver to break down glycogen to glucose which is then deposited into the blood leading to a rise in blood glucose

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72
Q

How does growth hormone cause growth?

A

it triggers the liver and other tissues to produce IGF’s which enhance cellular proliferation and inhibit apoptosis or programmed cell death.

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73
Q

What acts on the anterior pituitary to produce growth hormone?

A

growth hormone releasing hormone

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74
Q

Explain the negative feedback of growth hormone

A

Growth hormone stimulates tissues to produce IGF’s but when there is too much, this is recognised by the hypothalamus which produces somatostatin (GHIH) to stop the production of GH.

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75
Q

What is the action of ACTH?

A

It stimulates the adrenal cortex to secrete corticosteroid and hormones such as cortisol

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76
Q

What regulates ACTH?

A

corticotrophin releasing hormone from the hypothalamus

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77
Q

What controls the secretion of ACTH?

A

hypothalamic-pituitary-adrenal axis

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78
Q

What happens when ACTH levels are low?

A

The hypothalamus releases CRH which acts on the anterior pituitary to release ACTH

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79
Q

How is Cortisol produced?

A

ACTH acts on the adrenal glands which stimulates the release of cortisol

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80
Q

What effect does increased cortisol have on ACTH?

A

Negative- increased cortisol it is noticed and the hypothalamus stops producing CRH which stops ACTH being released from the pituitary.

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81
Q

Which hormone initiates puberty?

A

gonadotrophin releasing hormone

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82
Q

GnRH stimulates the anterior pituitary to release which hormones?

A

FSH and LH

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83
Q

What is the function of FSH?

A

stimulates the production and maturation of sex cells including ova in women and sperm in men.

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84
Q

What is the function of LH?

A

triggers ovulation in women as well as the production of oestrogen and progesterone by the ovaries. LH stimulates the production of testosterone by the male testes.

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85
Q

What condition can cause too much ACTH?

A

Cushings disease- the most common cause of increased ACTH

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86
Q

How does FSH and LH contribute to the menstrual cycle?

A

At the end of the cycle, the hormones have both decreased and so the hypothalamus stimulates release of more FSH and LH which is released into the bloodstream. FSH will cause growth of the follicle in the ovary which produces oestradiol and inhibin. These are sensed by the hypothalamus and pituitary so less GnRH is released, and thus FSH and LH decrease

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87
Q

How does oestrogen manipulate the levels of LH and FSH

A

As the follicle in the ovary grows, more and more oestrogen is produced from the follicles, it stimulates a surge in LH and FSH which stimulates the release of an egg from a mature follicle e.g. ovulation

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88
Q

What happens after ovulation?

A

the ruptured follicle forms a corpus luteum that produces high levels of progesterone which inhibits FSH from being released. Towards the end of the cycle, the corpus luteum breaks down and progesterone stops and the next cycle begins as FSH starts to be produced again

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89
Q

What is hypergonadotropic hypogonadism?

A

When the gonads fail to create enough oestrogen, testosterone and/or inhibin which messes with FSH production and so FSH and LH rise

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90
Q

What are the effects of low FSH in women

A

leads to incomplete development at puberty and poor ovarian failure. in this situation, ovarian follicles do not form properly and do not release an egg causing infertility

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91
Q

What is Kallmann’s syndrome?

A

Delayed/absent puberty due to low FSH and impaired sense of smell

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92
Q

What is the role of LH in men?

A

stimulates leydig cells in the testes to produce testosterone

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93
Q

What is the role of LH in women?

A

in week 1-2 of mestruation, LH is required to stimulate oestradiol. Around day 14, there is a surge in LH levels which causes the ovarian follicle to tear and release a mature oocyte from the ovary e.g. ovulation. LH also stimulates the corpus luteum to produce progesterone (which supports fertilisation).

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94
Q

What hormone is responsible for ovulation?

A

LH (from oestradiol)

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95
Q

What can too much LH mean?

A

infertility (due to low levels of sex steroids)

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96
Q

What are the characteristics of PCOS?

A

high LH and reduced fertility

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97
Q

What is Klinefelters syndrome?

A

It is a male only disease when they have an extra X chromosome (XXY). They have small testes and so not secrete adequate levels of testosterone to support sperm production.

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98
Q

What is Turners syndrome?

A

It is a female only disorder caused by a partial or full deletion of an X chromosome. Ovarian function is impaired and LH may be high.

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99
Q

Where is Prolactin released from?

A

Lactroph cells in the pituitary gland

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100
Q

How does Dopamine influence prolactin release?

A

Dopamine restrains prolactin production so the more dopamine there is, the less prolactin is released

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101
Q

What is hyperprolactinaemia?

A

too much prolactin in the blood

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102
Q

Where does prolactin act on?

A

The mammary glands

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103
Q

What are the causes of hyperprolactinaemia?

A

Pregnancy, medications that reduce dopamine, thyroid underactivity and prolactinomas.

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104
Q

How are prolactinomas treated?

A

Most can be treated successfully with drugs that mimic the action of dopamine such as cabergoline

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105
Q

What is the primary cause of acromegaly?

A

too much growth hormone from a pituitary adenoma

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106
Q

What are the key diagnostic features of acromegaly?

A

coarsening of facial features, soft tissue and skin changes, carpal tunnel syndrome, joint pain and dysfunction, sleep apnoea and alterations in sexual functioning.

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107
Q

What is the diagnostic test for acromegaly?

A

OGTT (GH levels are measured after drinking sugar water. Normally, the pituitary would stop producing GH but a GH producing tumour won’t stop so levels will be unchanged)

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108
Q

A value of what confirms acromegaly?

A

If the lowest GH value during OGTT is above 1 microgram/L then acromegaly is confirmed.

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109
Q

Why can you not rely on GH levels for acromegaly?

A

because secretion of GH is pulsatile

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110
Q

What inhibits GH?

A

Glucose inhibits GH usually but not in acromegaly

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111
Q

What is the treatment of acromegaly?

A

Removal of the pituitary adenoma trans-sphenoidally

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112
Q

Is follow-up required for patients with acromegaly?

A

Yes- yearly GH, IGF-1, OGTT, visual fields and vascular assessment

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113
Q

What is Cushing’s syndrome?

A

When the body produces too much cortisol. it is usually caused by corticosteroid use

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114
Q

What is Cushing’s disease?

A

It is when there is too much ACTH producing too much cortisol from a pituitary adenoma

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115
Q

What are the features of cushings disease?

A

Abdominal/axillae striae, rapid and unexplained weight gain, skin changes such as bruising, acne, hair growth and red cheeks, memory loss, depression, mood and behaviour disorders, fatigue, muscle weakness, mensural cycle disorders, osteoporosis, high blood pressure, etc

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116
Q

What investigation is done in suspected Cushings disease?

A

a low dose dexamethasone test leads to no change in plasma cortisol

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117
Q

What is the treatment of Cushing’s Disease?

A

Selective removal of pituitary adenoma trans-sphenoidally

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118
Q

What does the Zona reticularis secrete?

A

Androgens

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119
Q

What does the Zona glomerulosa secrete?

A

Mineralcorticoids, mostly aldosterone

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120
Q

What does the Zona fasiculata secrete?

A

Glucocorticoids such as cortisol

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121
Q

What are the ACTH dependent causes of cushing syndrome?

A

Cushing’s disease and Ectopic ACTH production especially small cell lung cancer and carcinoid tumours

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122
Q

What are the ACTH independent causes of Cushing syndrome?

A

Adrenal adenoma/cancer, adrenal nodular hyperplasia, iatrogenic (steroids), McCune-Albright syndrome (rare)

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123
Q

What is diabetes inspidius?

A

metabolic disorder characterised by defective ability to concentrate urine in the kidneys result in the production of large quantities of urine.

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124
Q

What volume of urine would suggest diabetes insipidus?

A

> 3L/day

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125
Q

What is the cause of diabetes insipidus?

A

Usually due to low levels of ADH or resistance to its action in the collecting ducts

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126
Q

What are the clinical symptoms of Diabetes insipidus?

A

Polydipsia, polyuria and hypotonic urine

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127
Q

What investigations are carried out in diabetes insipidus?

A

Desmopressin test, urine osmolarity, serum osmolarity, water deprivation test

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128
Q

What is the treatment of diabetes insipidus?

A

1st line: desmopressin

2nd line: IV fluid management

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129
Q

What are the 4 types of diabetes insipidus?

A

Central- most common
nephrogenic
dipsogenic
pregnancy related

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130
Q

What is Desmopressin?

A

Synthetic ADH

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131
Q

What is the cause of central diabetes insipidus?

A

Damage to the pituitary gland or hypothalamus from head injury

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132
Q

What is nephorgenic diabetes insipidus?

A

the pituitary releases enough ADH into the body but the kidneys cannot respond to it. Can be caused by lithium, sickle cell disease or genetics.

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133
Q

What is the treatment for central diabetes insipidus?

A

desmopressin

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134
Q

What is the treatment for nephrogenic diabetes insipidus?

A

Anti-inflammatory medication such as indomethacin and bendorflumathiazide

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135
Q

What is dipsogenic diabetes insipidus?

A

excess fluid intake caused by a problem with the thirst mechanism or deliberately drinking too many fluids

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136
Q

How does hyperprolactinaemia present?

A

In women- missed periods

in men- erectile dysfunction

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137
Q

Where is prolactin secreted from?

A

The anterior pituitary

138
Q

What are the consequences of raised prolactin?

A

hypogonadism, infertility and osteoporosis by inhibiting secretion of gonadotrophin releasing hormone, hence decreased LH/FSH and decreased testosterone/oestrogen

139
Q

What are the causes of hyperprolactinaemia?

A

Excess production of prolactin from the pituitary adenoma,
Disinhibition by compression of the pituitary stalk which reduces dopamine levels,
use of dopamine antagonist

140
Q

Which drugs may cause hyperprolactinaemia?

A

metoclopramide, oestrogens, ectasy/MDMA, anti-psychotics

141
Q

What are the symptoms of hyperprolactinaemia?

A

amenorrhoea, oligiomenorrhoea, infertility, decreased libido, weight gain, dry vagina, ED, galactorrhoea

142
Q

What are the investigations carried out in suspected hyperprolactinaemia?

A

Basal prolactin, venepuncture, pregnancy test, MRI of the pituitary

143
Q

What is the treatment for hyperprolactinaemia?

A

Dopamine agonist such as cabergoline

144
Q

What is a microprolactinoma?

A

A tumour <10mm- treat with dopamine agonist or trans-sphenoid surgery if intolerant

145
Q

What is a macroprolactinoma?

A

a tumour >10mm. near the optic chiasm so may reduce visual acuity. Treat with dopamine agonists (bromocriptine) then consider surgery

146
Q

What is hypopituitarism?

A

Pituitary gland is completely deficient or partially deficient of hormones

147
Q

What lobe of the pituitary is affected in hypopituitarism? and in what order are they affected?

A

Anterior:

GH- FSH/LH- PRL- TSH- ACTH

148
Q

What are the causes of panhypopituitarism?

A

Hypothalamus: Kallmann’s syndrome, tumour inflammation, infection, ischaemia
Pituitary stalk: trauma, surgery, mass lesion, meningioma, carotid artery aneurysm
Pituitary: tumour, irradiation, inflammation, autoimmunity, infiltration (haemochromatosis, amyloid, metastases), ischaemia

149
Q

What are the features of panhypopituitarism?

A

GH lack: central obesity, atherosclerosis, dry wrinkly skin, reduced strength, reduced balance, exercise ability reduced, cardiac output decreased, osteoporosis, reduced glucose
FSH/LH lack: amenorrhoea, small testes, infertility, reduced libido
Thyroid: hypothyroidism
Cortisol: Addisons disease
Prolactin: no lactation

150
Q

What is the short synacthen test and what is it used for?

A

It measures the level of cortisol after an injection of ACTH. it is used in adrenal insufficiency

151
Q

What investigations are carried out in panhypopituitarism?

A

Basal levels for all the hormones, U & E’s, Hb, Short synacthen test, insulin tolerance test, 8am cortisol, Thyroid function, MRI of pituitary, oestradiol, IGF-1

152
Q

What is the treatment of panhypopituitarism?

A

hormone replacement and treatment for underlying cause:
Hydrocortisone- adrenal insufficiency
Thyroxine
oral corticosteroids- for ACTH deficiency
Oestrogen/progesterone/testosterone
Growth hormone
Desmopressin- ADH deficiency

153
Q

What are the types of pituitary tumours?

A

Chromophone- most common. Causes prolactin, ACTH or GH to be produced
Acidophil- secrete GH or prolactin
Basophil- secrete ACTH

154
Q

What is pituitary apoplexy?

A

bleeding into, or impaired blood flow to the pituitary gland. Leads to hypopituitarism which may cause CVS failure and death.

155
Q

What is the management of pituitary apoplexy?

A

Urgent steroids (hydrocortisone) and fluid balance, cabergoline and possible surgery

156
Q

What is a craniopharyngioma?

A

It is a tumour arising rathkes pouch and is the commonest childhood intracranial tumour

157
Q

What are the presenting symptoms?

A

acute visual loss and symptoms of intracranial hypertension. in adults they may present with diabetes and sexual dysfunction, growth failure

158
Q

Where are craniopharyngiomas found?

A

sellar/ suprasellar space

159
Q

What is Nelson’s syndrome?

A

Enlargement of an ACTH producing tumour in the pituitary gland following surgical removal of both adrenal glands in a patient with cushing’s disease. the tumour produces excess ACTH and in turn, cortisol.

160
Q

What are the symptoms of Nelsons syndrome?

A

Abnormal hormone secretion, enlargement of the pituitary gland, development of large adenomas, intense skin pigmentation, headaches, visual field defects, amenorrhoea

161
Q

What is Wolfram syndrome?

A

consists of diabetes insipidus, diabetes mellitus, optic atrophy and deafness

162
Q

What is empty sella syndrome?

A

When the pituitary looks flattened or shrunken within the sella turcica on MRI scan.

163
Q

What is the function of melanocyte stimulating hormone?

A

It causes melanocytes to produce melanin which absorbs UV radiation to protect cells from DNA damage. It also suppresses appetite

164
Q

What is the process behind hyperpigmentation in Addisons disease?

A

The adrenal glands don’t produce enough cortisol, therefore, the hypothalamus stimulates the production of ACTH to try to stimulate the adrenal glands. ACTH can be broken down to MSH because they are from the same precursor (pro-opiomelanocortin) leading to more pigment.

165
Q

What does a deficiency in melanocyte stimulating hormone cause?

A

lack of skin pigmentation and loss of protections from UV rays.

166
Q

What is the function of chief cells?

A

They secrete PTH in the absence of calcium

167
Q

How does parathyroid hormone increase levels of calcium?

A

Stimulates osteoclasts, inhibits osteoblasts, increased reabsorption of calcium in the kidney and it initiates the production of the steroid hormone calcitrol (1,25-dihydroxyvitamin D) which is an active form of vitamin D3. Calcitrol then causes increased absorption of dietary calcium by the intestines.

168
Q

What is the effects of calcitonin on bone?

A

stimulates osteoblasts, inhibits osteoclasts and therefore Calcium is removed from blood and used for bone

169
Q

What is hyperparathyroidism?

A

Abnormally high activity of the PTH gland to produce large volumes of PTH that results in excessive calcium reabsorption from the bone and gut/kidneys

170
Q

What effect does hyperparathyroidism have on the nervous system?

A

As blood calcium levels increase then the sodium is decreased and the responsiveness of the nervous system is reduced

171
Q

What is hypoparathyroidism?

A

When the PTH doesn’t produce much PTH leading to low Calcium levels in the blood. Might be due to surgery involving the thyroid gland.

172
Q

What effects does low calcium have on the levels of sodium?

A

Low calcium causes high sodium (by increasing membrane permeability) resulting in muscle twitching, cramping, spasms or convulsions

173
Q

What is produced when blood calcium is high?

A

Calcitonin (this further increases blood calcium)

174
Q

What is the most common cause of hyperparathyroidism?

A

a single parathyroid adenoma

175
Q

What are signs of hypercalcaemia?

A

weak, tired, depressed, thirsty, dehydrated but polyuric, renal stones, abdominal pain, pancreatitis and ulcers. Bone reabsorption can cause fractures and osteopenia/osteoporosis

176
Q

What are the phosphate levels in hyperparathyroidism?

A

Calcium is high, therefore phosphate is low (it is not getting reabsorbed from the kidney).

177
Q

What investigations are carried out in hyperparathyroidism?

A

Serum calcium, serum PTH, phosphate, Alk phos, 24 hour urinary calcium, imaging, DEXA bone scan

178
Q

What is the treatment for hyperparathyroidism?

A

advise increased fluid uptake to prevent stones, avoid thiazides, vitamin D supplement (colecalciferol). Reass after 6 months. Excision of adenoma or all 4 hyperplastic glands to prevent fractures and peptic ulcers.

179
Q

What are indications for surgery in hyperparathyroidism?

A

high serum or urinary Ca, bone disease, osteoporosis, renal calculi, decreased renal function, age below 50 years.

180
Q

What are the complications of removing the parathyroid glands?

A

hypoparathyroidism and recurrent laryngeal nerve damage

181
Q

What is secondary hyperparathyroidism?

A

Refers to excessive excretion of PTH by the parathyroid glands in response to hypocalcaemia and associated hyperplasia of the glands

182
Q

What is the most common cause of secondary hyperparathyroidism?

A

Chronic kidney failure. Failing kidneys do not convert enough Vitamin D to its active form and they do not adequately excrete phosphatase. When this happens, insoluble calcium phosphate forms in the body and removes calcium from the circulation

183
Q

What is the treatment for secondary hyperparathyroidism?

A

phosphate binders (used to reduce absorption of phosphate), colecalciferol (vit D), Cinacalet, parathyroidectomy if CKD stage 5.

184
Q

What is the mechanism of action of Cinacalet?

A

lowers PTH, calcium and phosphate

185
Q

What is tertiary hyperparathyroidism?

A

Excess production of parathyroid hormone that has escaped all normal body feedback controls and so persists even where the initial cause (low calcium) has been resolved.

186
Q

What is the cause of tertiary hyperparathyroidism?

A

Long term secondary hyperparathyroidism- the PTH glands have become overgrown and overactive. Or CKD (most common)

187
Q

What is the treatment of tertiary hyperparathyroidism?

A

Cinacalcet, parathyroidectomy, vitman D supplements

188
Q

What is malignant hyperparathyroidism?

A

Parathyroid related protein (PTHrP) is produced by some squamous cell lung caners, breast and renal cell carcinomas, This mimics PTH resulting in increased calcium.

189
Q

What are the chemical findings for primary, secondary, tertiary and malignant hyperparathyroidism?

A

Primary: high PTH, high Ca
Secondary: high PTH, low Ca
Tertiary: really high PTH, high Ca
Malignant: low PTH, high Ca

190
Q

What is primary hypoparathyroidism?

A

hypocalcaemia and hyperphosphataemia resulting from the primary absence or deficiency of parathyroid hormone or from the secretion of biologically inactive PTH

191
Q

What are the causes of primary hypoparathyroidism?

A

inadvertent surgical removal of all the parathyroid glands during thyroidectomy, destruction of the glands due to thyroiditis/radiotherapy/haemochromatosis/wilsons disease/amyloidosis or congential malformations.

192
Q

What are the signs of hypocalcaemia?

A 
Spasms- Trousseaus sign (BP cuff)
Perioral paraesthesiae
anxious, irritable, irrational
seizures
muscle tone increase in smooth muscle causing colic, wheeze and dysphagia
Orientation impaired
Dermatitis
Impetigo herpetiformis
Chvostek's sign (twitching of the facial muscles caused by tapping on the facial nerve)
193
Q

What is the treatment for hypoparathyroidism?

A

Calcium supplements, calcitrol

194
Q

What is secondary hypoparathyroidism?

A

Condition characterised by decreased PTH secretion which results from the inhibitory effect of PTH independent hypercalcaemia

195
Q

What type of thyroid cancer is associated with MEN 2A?

A

Medullary

196
Q

Which thyroid cancer affects young people and has a good prognosis?

A

Papillary

197
Q

Where does papillary cancer arise from?

A

Parafollicular C cells

198
Q

Which cancer causes raised calcitonin levels?

A

Papillary carcinoma

199
Q

What causes hypoparathyroidism?

A

Radiation, surgery and hypomagnesaemia

200
Q

What is the effect of the RAA system?

A

Increased sodium and water reabsorption and increased potassium

201
Q

When is Renin released?

A

in response to low sodium

202
Q

Where are catecholamines released from?

A

They are released from chromaffin cells in the adrenal medulla

203
Q

What is psuedohypoparathyroidism?

A

It results from resistance to the actions of PTH produced by a loss of G-protein mediated signalling. It is high PTH, low Ca and high phosphate

204
Q

What are the key diagnostic features of pseudohypoparathyroidism?

A

Family history of PHP, muscle cramp, paraethesia and muscle twitches

205
Q

What is the treatment for psuedohypoparathyroidism?

A

calcium supplements or calcitriol (vit D analogue)

206
Q

What is pseudopseudohypoparathyroidism?

A

It is the clinical features of psuedohypoparathyroidism but without the resistance to PTH

207
Q

What is Albright hereditary oestodystrophy?

A

It is the clinical manifestations seen in pseudohypoparathyroidism such as short stature, obesity, round face, brachymetacarpals and brachymetatarsals

208
Q

What is MEN1?

A

tumours of the pituitary (prolactinomas), parathyroid glands (primary hyperparathyroidism) and the pancreas (gastrinomas, insulinomas, glucagonoma, VIPoma).

209
Q

What is the mode of inheritance of MEN1

A

Autosomal dominant

210
Q

What is the effects of a gastrinoma?

A

excess secretion of gastrin by a gastrinoma causing the overproduction of acid in the stomach leading to stomach/duodenal ulcers

211
Q

How are prolactinomas managed?

A

Cabergoline or bromocriptine

212
Q

What is Men2A?

A

Medullary thyroid cancer, phaeochromocytoma, and hypreparathyroidism

213
Q

What gene is mutated in Men2A?

A

RET gene

214
Q

Where does medullary thyroid cancer arise from?

A

Parafollicular cells that release calcitonin.

215
Q

What is the triad of symptoms linked to phaeochromocytoma?

A

Sweating, palpitations and headaches

216
Q

What is the treatment of medullary thyroid cancer?

A

Total thyroidectomy

217
Q

What is the treatment of phaeochromocytoma?

A

Alpha blockers (phenoxybenzamine) What then beta blockers

218
Q

What is the treatment of primary hyperparathyroidism?

A

Surgical removal and lifelong activated vitamin D

219
Q

What is Men2B?

A

medullary thyroid cancer, phaeochromocytoma and mucosal neuromas of the lips, tongue and bowels

220
Q

When would you suspect MEN2B?

A

in babies with failure to thrive due to eating or growth problems and in those with features similar to marfans

221
Q

When is aldosterone released?

A

It is released from the zona glomerulosa when potassium is elevated, sodium is low, there is low blood pressure or low blood volume

222
Q

What is the function of aldosterone?

A

It increases the excretion of potassium and the retention of sodium which in turn increases blood pressure.

223
Q

How is aldosterone produced?

A

it is released from the adrenal glands when CRH acts on the anterior pituitary to release ACTH which then acts on the adrenal glands. It has the same pathways as corticosterone, until it is mediated by aldosterone synthase at the end.

224
Q

Where is Renin released from?

A

The kidney

225
Q

What is the role of Renin?

A

it converts into angiotensin 1 by angiotensinogen.

226
Q

What is the role of Angiotensin II?

A

it initiates vasoconstriction of the arterioles decreasing blood flow, it stimulates the kidneys to absorb NaCl and water increasing blood volume and it signals the adrenal cortex to secrete aldosterone

227
Q

How is RAAS activated?

A

The baroreceptors in the carotid sinus sense a loss in blood volume or a drop in BP. It can also be activated by a decrease in NaCl concentration that will stimulate the macula densa to signal the juxtaglomerular cells to release renin

228
Q

Does Angiotensin II cause vasodilation or vasoconstriciton?

A

Vasoconstriction

229
Q

What is the effect of constricting the afferent arterioles in the kidney?

A

increases the arteriolar resistance raising systemic arterial blood pressure and decreasing the blood flow. Angiotensin II then constricts efferent arterioles to force blood into the glomerulus to maintain GFR

230
Q

What is Conn’s syndrome?

A

It is primary hyperaldosteronism causing excess levels of Aldosterone to be produced causing low renin.

231
Q

What is the treatment of Conn’s?

A

Spironolactone- it is a mineralocorticoid antagonist

232
Q

21 hydroxylase deficiency causes what?

A

Congenital adrenal hyperplasia

233
Q

Why is there high testosterone is congenital adrenal hyperplasia?

A

because aldosterone and cortisol aren’t made because of the 21 hydroxylase deficiency causing a shunt towards testosterone production

234
Q

What causes Conn’s syndrome?

A

Adenoma or carcinoma of the adrenal gland

235
Q

What are the biochemistry results of phaeochromocytoma?

A

Hyperglycaemia and hypercalcaemia

236
Q

What are the causes of SIADH?

A

Hypovolaemia, hypotension, pain and N&V

237
Q

How do you treat congential adrenal hyperplasia?

A

Mineralcorticoids and glucocorticoids

238
Q

Where do neuroblastomas arise from?

A

The adrenal medulla

239
Q

What are the biochemistry results for Addisons?

A

Hyponatraemia, hyperkalaemia and hypoglycaemia

240
Q

What are the symptoms of congenital adrenal hyperplasia?

A

poor weight gain, hirsutism and acne, oligomenorrhoea and infertility

241
Q

Is cushings syndrome caused by an adrenal adenoma/carcinoma, ACTH independent or dependent?

A

Independent- the adrenal tumour is producing mass cortisol

242
Q

Is cushings disease caused by a pituitary adenoma, ACTH dependent or independent?

A

ACTH dependent- the adenoma is stimulating the pituitary to release ACTH

243
Q

What kind of inheritance is congenital adrenal hyperplasia?

A

Autosomal recessive

244
Q

What is the role of androgens during/after menopause?

A

It becomes the main source of oestrogen

245
Q

What causes the release of hormones from the adrenal medulla?

A

Sympathetic nervous system

246
Q

Which cells in the adrenal medulla secrete adrenaline and noradrenaline?

A

Chromaffin cells

247
Q

What is the effect of adrenaline and noradrenaline on blood glucose?

A

They convert glycogen into glucose

248
Q

What are the overall effects of catecholamines?

A

increase HR and BP, dilate airways raising blood oxygen levels and prompts vasodilation of airways. Causes vasoconstriction of the blood vessels

249
Q

What is the function of aldosterone?

A

Acts on the kidneys to increase BP by increasing sodium reabsorption. It has the opposite effect fro potassium

250
Q

What is the biochemistry of addisons disease?

A

Hyponatraemia (due to decrease in mineralcorticoids), hyperkalaemia and hypoglycaemia

251
Q

What is the results of the short synacthen test in Addisons?

A

30 minute cortisol should not be above 550. ACTH is given to trigger cortisol release but because the gland is fucked then its not going to release it

252
Q

What is the treatment of addisons?

A

Hydrocortisone and fludrocortisone

253
Q

What is Secondary adrenal insufficiency?

A

It is caused by long term steroid therapy leading to suppression of the pituitary-adrenal axis causing the pituitary to no longer produce ACTH.

254
Q

What is Addisons?

A

It is autoimmune destruction of the adrenal glands causing no release of cortisol, aldosterone or androgens regardless of high ACTH

255
Q

What is the dexamethasone suppression test and when is it used?

A

It is used in cushings and basically involves giving a load of dexamethasone and upon testing in the morning cortisol should be suppressed in normal people but in cushings it is not

256
Q

What is Hirsutism?

A

hair growth in women in the male pattern

257
Q

What biochemistry would be expected in PCOS?

A

increased testosterone (if >6 then look for an androgen secreting tumour), decreased sex binding globulin, high LH/FSH

258
Q

Which drugs can cause ED?

A

digoxin, B-blockers, diuretics, anti-psychotics, anti-depressants, oestrogens, narcotics

259
Q

What is primary hypogonadism?

A

It is failure of the gonads to produce testosterone due to testicular failure from local torsion, trauma, chemotherapy, post orchitis, renal failure, chromosomal abnormalities (Klinefelters)

260
Q

What is secondary hypogonadism?

A

low testosterone due to low gonadotrophins (LH & FSH) caused by hypopituitarism, prolactinoma or Kallmann syndrome (hypogonad with colour blindness)

261
Q

What is required to make a diagnosis of PCOS?

A

High androgen levels, no ovulation or ovarian cysts (2/3)

262
Q

What is the treatment for PCOS?

A

Lifestyle factors such as weight loss and exercise

263
Q

What is premature ovarian failure?

A

Loss of function of the ovaries before the age of 40

264
Q

What are the symptoms of premature ovarian failure?

A

Amenorrhoea, hypergonadotropism, hyperoestrogenism

265
Q

What is hypergonadotrophic hypogonadism?

A

condition characterised by hypogonadism due to an impaired response of the gonads to the gonadotrophins- high LH/FSH

266
Q

What are the genetic causes of premature ovarian failure?

A

Turner syndrome, XX gonadal agenesis, Fragile X

267
Q

Why is metformin sometimes used in PCOS?

A

it is a good induction tool for ovulation because it improves insulin resistance and thus causes a reduction in androgen production.

268
Q

What is endometriosis?

A

the presence of endometrial glands and stroma outside the endometrial cavity and uterine musculature

269
Q

What are the symptoms of endometriosis?

A

Chronic pelvic pain, dysmenorrhoea, dyspareuria (painful sex), menorrhagia, painful defaecation, chocolate cysts on ovary

270
Q

What is “salt crisis”?

A

adrenal glands release not enough aldosterone so too little salt is reabsorbed- it is lost in the urine

271
Q

What is the treatment of diabetes insipidus?

A

Central- desmopressin, Nephrogenic- thiazide diuretics

272
Q

What is Sheehan syndrome?

A

panhypopituitarism due to a postparum haemorrhage leading to ischaemia of the pituitary gland. This is seen in new mothers

273
Q

What is an Adrenal crisis?

A

When 90% of the adrenals have stopped working and the patient becomes very unwell. They have low blood sugar, low BP and dehydration

274
Q

How are steroids given when a patient is ill?

A

Double the dosage

275
Q

What is the most common cause of Conn’s syndrome?

A

Aldosterone producing adenoma

276
Q

What is secondary hyperaldosteronism?

A

It is due to a high renin from reduced renal perfusion e.g. in renal artery stenosis, hypertension, diuretics, CCF or hepatic failure

277
Q

What is Bartters syndrome?

A

it is a rare inherited disease in the thick ascending loop of Henle in which there is low potassium levels, increase blood pH and normal to low BP

278
Q

What antibody is present in Hashimotos?

A

TPO

279
Q

What is euthyroid sick syndrome?

A

State of adaptation or dysregulation of thyrotrophic feedback control wherein the levels of T3 or T4 is abnormal which occurs in the critically ill

280
Q

What biochemistry would you see in subclinical hypothyroidism?

A

High TSH, normal T3/T4

281
Q

What is pretibial myxoedema and in what condition would you see it?

A

oedematous swelling above the lateral malleolus seen in Graves disease

282
Q

What is toxic multinodular goitre?

A

nodules that secrete thyroid hormones usually seen in the elderly.

283
Q

What is a toxic adenoma of the thyroid gland?

A

It is a solitary nodule producing T3 and T4. On isotope scan the nodule is hot and the rest of the gland is suppressed.

284
Q

What is deQuervains thyroiditis?

A

self-limiting post viral with painful goitre. increased temp and ESR. Patients tend to cycle from hyper to hypo then back to normal

285
Q

What is the treatment for DeQuervains thyroditis?

A

NSAIDs

286
Q

How does Hashimotos look on thyroid isotope scan?

A

Diffuse painless goitre with decreased uptake

287
Q

How does Graves look on thyroid scan?

A

Increased uptake

288
Q

How does DeQuervains thyroiditis look on thyroid scan?

A

It is dependent on the disesase stage of the

289
Q

What kind of goitre is associated with Graves disease?

A

Large diffuse goitre, bruit may be present.

290
Q

How does Toxic multinodular goitre look on thyroid scan?

A

Hot and cold areas- hot where the nodules are

291
Q

What is the treatment for toxic multinodular goitre?

A

Radioactive iodine therapy

292
Q

How will a toxic thyroid adenoma look on thyroid scan?

A

Solitary, increased uptake hot spot

293
Q

How does thyroid cancer look on thyroid scan?

A

Cancers are usually cold

294
Q

Which thyroid cancer is the most common?

A

Papillary carcinoma

295
Q

Who are at risk of a follicular carcinoma of the thyroid gland?

A

Iodine deficiency, female predominance

296
Q

What is the treatment for medullary carcinoma?

A

Total thyroidectomy

297
Q

Which thyroid cancer has the worst prognosis?

A

Anaplastic

298
Q

Which thyroid cancer is associated with the orphaned annie nuclei?

A

Papillary

299
Q

How is a papillary carcinoma spread?

A

Spread by lymphatics

300
Q

How does PTH increase calcium levels?

A

increased osteoclast activity, increased absorption from the kidneys, activation of vitamin D

301
Q

Which cells produce vitamin d?

A

Keratinocytes

302
Q

What is the role of calcitonin?

A

Decreases the level of calcium

303
Q

What are the features of hypercalcaemia?

A

bones, stones, groans and psychiatric moans

304
Q

What are Chvosteks and Trousseaus sign indicative of?

A

Hypocalacaemia

305
Q

What is a solitary high alk phos indicative of?

A

Paget’s disease

306
Q

What is the biochemistry of osteomalacia?

A

low calcium, low phosphate, high PTH, high alk phos

307
Q

What is the diabetic range for HbA1c?

A

48 and over

308
Q

What is the diabetic range for fasting glucose?

A

7 mmol

309
Q

What is the diabetic range for random blood glucose?

A

11.1 mmol

310
Q

What antibodies may be associated with T1DM?

A

IA-2, IA-2B and ZnT8

311
Q

What is LADA?

A

Latent autoimmune diabetes in adults is a disorder in which the progression of autoimmune B-cell failure is slow

312
Q

Do you treat LADA with insulin?

A

No

313
Q

What is GAD testing?

A

A blood test which measures whether the body is producing a type of antibody which destroys its own GAD cells- presence of GAD indicates T1DM

314
Q

What is C-peptide?

A

It is released alongside insulin so can give a measure of how much natural insulin is being produced

315
Q

What does a low C-peptide show?

A

T1DM

316
Q

What are the microvascular complications of diabetes?

A

Retinopathy, nephropathy, neuropathy

317
Q

What are the macrovascular complications of diabetes?

A

Heart disease, stroke

318
Q

What is the difference between proliferative and pre-proliferative diabetic retinopathy?

A

the formation of new vessels is proliferative

319
Q

What is background retinopathy?

A

microaneurysms, haemorrhages and hard exudates

320
Q

What is symmetric sensory polyneuropathy?

A

Glove and stocking numbness, tingling and pain worse at night.

321
Q

What is autonomic neuropathy?

A

Postural BP drops, decrease in cerebrovascular autoregulation, loss of respiratory sinus arrhythmia, gastroparesis, urine retention, ED, sweating and diarrhoea

322
Q

What is the prehormone of insulin?

A

Preproinsulin

323
Q

How is insulin secreted?

A

glucose enters beta cells through the GLUT2 glucose transporter and is phosphorylated by glucokinase. A change in glucose concentration leads to a dramatic change in glucokinase activity leading to increased ATP concentration which then inhibits K+ channels depolarising the membrane. This opens Ca2+ channels leading to fusion of vesicles and release of insulin.

324
Q

Which 2 proteins are involved in KATP channels?

A

Kir6 and SUR1- both are required for functioning channel

325
Q

What is MODY?

A

monogenic diabetes with a genetic defect in Beta cell function

326
Q

Where is the mutation in MODY 2?

A

Glucokinase

327
Q

What is the treatment of MODY?

A

Sulfonylurea

328
Q

What are Ketone bodies?

A

They are formed in the liver mitochondria derived from acetyl-CoA which is from B-oxidation of fats

329
Q

What is DKA?

A

results from a shortage of insulin in response the body switches to burning fatty acids which produces acidic ketone bodies

330
Q

What is GAD?

A

It is an enzyme that converts glutamate to GABA which is an inhibitory neurotransmitter in the brain. They stop insulin being produced

331
Q

Does metformin cause weight loss?

A

Yes

332
Q

What is the side effect of metformin?

A

GI upset

333
Q

Do glitazones cause weight loss?

A

No, they cause weight gain

334
Q

What is the action of glitazones?

A

enhance action of insulin at target tissue- reduce insulin resistance

335
Q

Is there a risk of hypoglycaemia with SGLT-2 inhibitors?

A

Yes- they work by blocking the absorption of glucose in proximal tubule causing glucosuria

336
Q

What are examples of SGLT-2 inhibitors?

A

emipagliflozin, dapagliflozin, canagliflozin

337
Q

What is the function of DPP4 inhibitors/gliptins?

A

block DPP4 to allow incretin to work

338
Q

Do sulfonylureas cause weight gain?

A

yes

339
Q

What is the management of T2DM?

A
  1. metformin
  2. metformin + DPP4i/Sulfonylurea/Glitazone
  3. metformin + DPP4i + sulfonylurea
  4. insulin
340
Q

What biochemical parameters are required for diagnosis of DKA?

A

ketones >3
Blood glucose >11
Bicarbonate <15 or pH <7.3

341
Q

What is the treatment of DKA?

A

0.9% NaCl, insulin and potassium. When glucose falls past 15 then switch to dextrose

Year 2 (10 decks)

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