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Medicine Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define endocrinology

A

The study of hormones (and their gland of origin), their receptors, the intracellular signalling pathways, and their associated diseases

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2
Q

Describe functions of endocrine system

A

Rapid adaptive changes
Integration of whole body physiology
Chronic maintenance of metabolic environment
Communication for multi-cellular organisms

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3
Q

Define endocrine gland

A

These glands release secretions directly into the blood stream, without ducts

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4
Q

Give example of endocrine glands

A

Thyroid
Adrenal cells
Beta cells of pancreas

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5
Q

Define exocrine gland

A

These glands ‘pour’ secretions through a duct to site of action

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6
Q

Give example of exocrine glands

A

Submandibular
Parotid
Pancreas
(Amylase and lipase)

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7
Q

Where do endocrine hormones act?

A

Blood-borne, acting at distant sites

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8
Q

Where do paracrine hormones act?

A

Acting on nearby adjacent cells

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9
Q

Where do autocrine hormones acts?

A

Feedback on same cell that secreted hormone (acts on itself)

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10
Q

Describe differences between water-soluble and fat-soluble hormones

A 
Water-soluble:
Transported unbound
Bind to surface receptor on cells
Have a short half-life
Are cleared fast
Fat-soluble:
Transported bound to protein
Diffuse into cells
Have a long half-life
Are cleared slowly
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11
Q

Give example of water soluble hormone

A

Peptides and monoamines - both stored in vesicles before secretion

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12
Q

Give example of fat soluble hormone

A

Thyroid hormones
Steroids
*Synthesised on demand

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13
Q

Give examples of hormone classes

A

Peptides e.g. insulin
Amines e.g. dopamine, adrenaline, noradrenaline
Iodothyronines
Cholesterol derivatives and steroids

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14
Q

Describe how insulin works on insulin receptors

A 
Binds to insulin receptors.
Results in the phosphorylation of the receptor and activation of secondary messenger - TYROSINE KINASE.
Phosphorylation of signal molecules.
Cascade of effect.
Glucose uptake.
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15
Q

Give example of a peptide hormone

A

Insulin

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16
Q

Describe features of peptide hormones

A

Hydrophilic
Water soluble
Released in pulses or bursts
Cleared by tissue or circulating enzymes

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17
Q

Give product and reactant in synthesis, packaging of peptide hormones. Also give form in storage and secretion

A

Synthesis: Preprohormone -> Prohormone
Packaging: Prohormone -> Hormone
Storage: Hormone
Secretion: Hormone

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18
Q

Give example of amines

A

Dopamine
Adrenaline
Noradrenaline

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19
Q

Give order of chemicals that lead to formation of adrenaline

A 
Phenylalanine
L-Tyrosine
L-Dopa
Dopamine
Noradrenaline
Adrenaline
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20
Q

What breaks Noradrenaline down into Normetanephrine?

A

Catechol-O-methyl transferase (COMT)

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21
Q

What also breaks down Adrenaline into Metanephrine?

A

COMT

Catechol-O-methyl transferase

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22
Q

What can measurements of Normetanephrine and Metanephrine in serum be used for?

A

Act as indicators of noradrenaline or adrenaline activity

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23
Q

What is result of Adrenaline/Noradrenaline binding to alpha receptors?

A

Vasoconstriction
Bowel muscle contraction
Sweating
Anxiety

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24
Q

What is result of Adrenaline/Noradrenaline binding to beta receptors?

A

Vasodilation
Increased Heart Rate
Increased force of contractility
Relaxation of bronchial smooth muscles

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25
Q

What do iodothyronines bind to in blood?

A

Most is bound to THYROID-BINDING GLOBULIN (TBG)

Not soluble in water

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26
Q

What is T3 also known as?

A

Triiodothyronine

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27
Q

What is T4 also known as?

A

Thyroxine (less active than T3 but more produced)

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28
Q

What makes up iodothyrosines?

A

Incorporation of iodine on tyrosine molecule on thyroglobulin

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29
Q

What is made from conjugation of iodotyrosines and where are these products stored?

A

Gives rise to T3 and T4

Stored in Colloid bound to thryoglobulin

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30
Q

What is effect of TSH on thyroid?

A

Stimulates the movement of colloid into secretory cell

T3 and T4 cleaved from thyroglobulin

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31
Q

True or False:

Most T3 is made from breakdown of T4 to T3, which is converted OUTSIDE the thyroid gland

A

True

T4 can be thought of as a Reservoir for additional T3

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32
Q

How is Vitamin D transported and where on the cell does it act

A

Transported by vitamin D binding protein

Fat soluble and enters cell directly to bind to nucleus and stimulate mRNA production

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33
Q

Give example of steroid hormones/cholesterol derivates

A 
Vitamin D
Adrenocortical and Gonadal steroids e.g. Cortisol
Aldosterone
Testosterone
Oestrogen
Progesterone
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34
Q

What % of adrenocortical and gonadal steroids are protein bound?

A

95%

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35
Q

How does steroid hormone bind to cell receptor and what is effect?

A

Diffuses through plasma membrane and binds to cytoplasm receptor.
Receptor-hormone complex then enters nucleus, where it binds to Glucocoticoid Response Element (GRE).
Binding initiates transcription of gene to mRNA.
mRNA directs protein synthesis.

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36
Q

What hormone receptors are found on cell surface?

A

Peptides e.g. insulin

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37
Q

What hormone receptors are found in cytoplasm

A 
Steroids, e.g.:
Glucocorticoids e.g. cortisol
Mineralocorticoids e.g. aldosterone
Androgens e.g. testosterone
Progesterone
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38
Q

What hormone receptors are found at nucleus?

A

Thyroid hormones
Oestrogen
Vitamin

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39
Q

**What are different hormone secretion patterns?

A

Continuous release e.g. prolactin (inhibited by dopamine)
Pulsatile (multiple pulses throughout the day) e.g. insulin

Circadian rhythm e.g. ACTH, prolactin, GH, TSH and cortisol

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40
Q

Give example of continuous hormone secretion

A

Prolactin (inhibited by dopamine)

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41
Q

Give example of pulsatile hormone secretion

A

Insulin

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42
Q

What is effect of Somatostatin on growth hormone

A

Inhibits growth hormone, along with GHRH

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43
Q

What hormone helps regulate circadian rhythms

A

Melatonin

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44
Q

Where is melatonin secreted from?

A

Pineal gland

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45
Q

What parts of brain regulates your Circadian Rhythm?

A

Hypothalamus

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46
Q

What is your Circadian Rhythm

A

24-hour internal clock that is running in the background of your brain and cycles between sleepiness and alertness at regular intervals

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47
Q

What is meant by hormone receptor down regulation?

A

Hormone secreted in large quantities causes down regulation of its target receptor

(Down regulation = decrease in cellular component)
Up regulation is opposite

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48
Q

What is synergism?

Give example

A

Combined effects of two hormone amplified

e.g. glucagon with adrenaline - both released when hypoglycaemic to increase sugar levels

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49
Q

What is antagonism?

Give example

A

One hormone opposes other hormone

e.g. glucagon (raises glucose levels) antagonises insulin (reduces glucose levels)

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50
Q

Pituitary Anatomy: What is found lateral and next to the pituitary gland

A

Cavernous sinuses

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51
Q

Pituitary Anatomy: What is found in the cavernous sinus

A 
(Intracavernous) Carotid artery
Cranial nerves:
Oculomotor III
Trochlear IV
Abducent VI
Ophthalmic V1
Maxillary V2
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52
Q

Pituitary Anatomy: What sinus is found directly inferior to pituitary gland?

A

Sphenoid sinus

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53
Q

Pituitary Anatomy: What part of optic pathway is found directly superior to pituitary gland?

A

Optic chiasm

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54
Q

Pituitary Anatomy: Describe the location of pituitary gland

A

Lies in a pocket of sphenoid bone called the pituitary fossa at the base of the brain, just below the hypothalamus and inferior to the optic chiasm

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55
Q

Why can a pituitary tumour (e.g. acromegaly) lead to vision problems?

A

Causes pressure on optic chiasm

Can result in a hemianopia

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56
Q

What visual field defect can result from a pituitary tumour

A

Bitemporal Hemianopsia

pressure on optic chiasm

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57
Q

What visual fields are defective in bitemporal hemianopsia?

A

Both outer halves of the visual field

Medial halves of retina are defective so outer halves of visual field are not seen

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58
Q

Pituitary Anatomy: What connects the hypothalamus to the pituitary gland?

A

Infundibulum (or pituitary stalk)

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59
Q

What are the 2 pituitary glands?

A

Anterior pituitary gland (aka Adenophysis)

Posterior pituitary gland (aka Neurohypophysis)

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60
Q

What is contained in the infundibulum?

A

Axons from neurones in hypothalamus

Small blood vessels

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61
Q

What type of hormones are secreted by hypothalamus to act on anterior pituitary gland?

A

Hypophysiotropic hormones

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62
Q

**What nuclei in the hypothalamus send axons to the posterior pituitary gland?

A

Supraoptic

Paraventricular (more posterior)

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63
Q

How do hypophysiotropic hormones from the hypothalamus reach the anterior pituitary gland?

A

Hypothalamo-Hypophyseal Portal Vessels/Veins

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64
Q

Name hypophysiotropic hormones released from the hypothalamus that act on the anterior pituitary gland

A 
Corticotropin-Releasing Hormone CRH
Growth Hormone Releasing Hormone GHRH
Thyrotropin-Releasing Hormone TRH
Gonadatropin-Releasing Hormone GnRH
Dopamine DA
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65
Q

What hormones are released by the anterior pituitary

A

Adrenocorticotropic hormone ACTH (aka corticotrophin)
Growth hormone GH (aka somatotropin)
Thyroid Stimulating Hormone TSH (aka thyrotropin)
Luteinising hormone LH
Follicle Stimulating Hormone FSH
Prolactin

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66
Q

What is effect of Corticotropin-releasing hormone (CRH) on anterior pituitary?

A

Stimulates the release of Adrenocorticotropic hormone (ACTH)

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67
Q

What is effect of Growth Hormone Releasing Hormone (GHRH) on anterior pituitary?

A

Stimulates the release of growth hormone (GH)

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68
Q

What is effect of Thyrotropin-releasing hormone (TRH) on anterior pituitary?

A

Stimulates the release of thyroid stimulating hormone (TSH)

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69
Q

What is effect of Gonadatropin-releasing hormone (GnRH) on anterior pituitary?

A

Stimulates the release of Luteinising hormone (LH) and Follicle-stimulating hormone (FSH)

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70
Q

What is effect of Dopamine (DA) on anterior pituitary?

A

INHIBITS the release of prolactin

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71
Q

What would be the effect on prolactin levels if the infundibulum was damaged or destroyed?

A

Prolactin is under negative control by dopamine thus if the pituitary connecting stalk/infundibulum was destroyed then that would result in an
increase in the secretion of prolactin as its negative
pressure (dopamine) would not be able to reach it

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72
Q

True or False:

The anterior pituitary gland has an arterial blood supply

A

False

Anterior pituitary gland has no arterial blood supply

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73
Q

Where does the anterior pituitary gland receive its blood supply?

A

Through a portal venous circulation from the hypothalamus:

Hypothalamo-hypophyseal portal vessels/veins

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74
Q

What is a benefit of the Hypothalamo-hypophyseal portal vessels/veins supplying blood from the hypothalamus to anterior pituitary gland?

A

This local blood system provides a mechanism for hormones of the hypothalamus to directly alter the activity of the cells of the anterior pituitary
gland -
*Bypassing the general circulation and thus efficiently regulating hormone release from that gland

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75
Q

How many types of hormone producing cells are there in anterior pituitary?

A 
5 types
(produces 6 hormones in total)
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76
Q

What type of hormones are produced by anterior pituitary?

A

Peptide hormones

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77
Q

Name the 5 types of hormone producing cells of anterior pituitary

A 
Gonadotrophs
Corticotrophs
Thyrotrophs
Lactotrophs
Somatotrophs
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78
Q

What cells of the pituitary gland produce Growth Hormone?

A

Somatotrophs

of anterior pituitary

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79
Q

What cells of the pituitary gland produce Prolactin?

A

Lactotrophs

of anterior pituitary

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80
Q

What cells of the pituitary gland produce Thyroid-stimulating hormone (TSH)?

A

Thyrotrophs

of anterior pituitary

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81
Q

What hormone is produced by Corticotrophs of anterior pituitary gland?

A

Adrenocorticotropic hormone (ACTH)

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82
Q

What hormones are produced by Gonadotrophs of anterior pituitary gland?

A 
Follicle-stimulating hormone (FSH)
Lutenizing hormone (LH)
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83
Q

What is effect of FSH and LH in female?

A

Targets the gonads and stimulates gonad cell development (females = ovum; males = sperm)
FSH stimulates oestrogen release
Oestorgen also causes a positive feedback effect to stimulate release of more FSH and LH
LH stimulates the release of the egg which in turn stimulates progesterone release
Progesterone release results in increased thickening of uterine wall

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84
Q

What is effect of FSH and LH in male?

A

LH stimulates testosterone production from Leydig cells (interstitial cells of testes)
FSH stimulates testicular growth and enhances the production of an androgen-binding protein by the Sertoli cells, which are a component of the testicular tubule necessary for sustaining the maturing sperm cell.

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85
Q

What can be measured to reflect levels of GH in the body?

A

IGF-1

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86
Q

What is effect of GH on the body?

A

Stimulates growth and protein synthesis
(Effects the whole body)
Stimulates gluconeogenesis and inhibits insulin resulting in increased glucose
Works on adipose tissue to break down fat
Acts on liver to increase protein synthesis and stimulate IGF-1 which acts on skeleton to increase cartilage proliferation

87
Q

Where is IGF-1 produced/released?

A

Liver

GH acts here to stimulate IGF-1 release

88
Q

What region of the adrenal cortex secretes Cortisol?

A

Zona Fasiculata

produces glucocorticoids

89
Q

What are the 3 layers of the adrenal cortex from most superficial to deep

A

Zona Glomerulosa
Zona Fasciculata
Zona Reticularis
(Then adrenal medulla)

90
Q

What hormones are released by the Zona Glomerulosa

A

Mineralcorticoids e.g. Aldosterone

regulate mineral balance

91
Q

What hormones are released by the Zona Fasciculata?

A

Glucocorticoids e.g. Cortisol, Cortisone, Corticosterone

regulate glucose metabolism

92
Q

What hormones are released by the Zona Reticularis?

A

Androgens e.g. dehydroepiandrosterone

Stimulate masculinisation/sex hormones

93
Q

What do 3 layers of adrenal cortex produce?

A

Zona Glomerulosa - Mineralcorticoids - mineral balance
Zona Fasciculata - Glucocorticoids - glucose metabolism
Zona Reticularis - Androgens - sex hormone
(the deeper you go the sweeter it gets)
GFR

94
Q

What hormones are released by the adrenal medulla?

A

Stress hormones e.g. Adrenaline, Noradrenaline
(stimulate sympathetic ANS)
(Adrenaline is a major metabolic and stress hormone)

95
Q

What is the effect of ACTH?

A

Stimulates zona fasciculata (adrenal cortex) to secrete cortisol
Stimulates zona reticularis (adrenal cortex) to release androgens
Stimulates Adrenaline release from adrenal medulla

96
Q

ACTH causes the release of cortisol: What is the effect of cortisol?

A

Regulates and breaks down proteins, fats and carbohydrates
Anti-inflammatory effect (lowered immune response -bad if prolonged)
*Helps body overcome stress (therefore absence of it in case of Addisons disease can be severe)

97
Q

**TSH acts on thyroid to stimulate release of thyroid hormone: What is the effect of thyroid hormone?

A 
Controls rate of metabolic reactions
Accelerates food metabolism
Increases protein synthesis
Stimulates carbohydrate metabolism
Enhances fat metabolism
Increases ventilation rate
Increases cardiac output and heart rate
Brain development during foetal life and postnatal development
Accelerates growth rate
98
Q

What is half-life of T3?

A

1 day

99
Q

What is half-life of Thyroxine/T4?

A

5-7 days

100
Q

What is the effect of prolactin?

A

Stimulates the breasts to produce milk and helps with breast development

101
Q

What is effect of dopamine on milk production and breast development

A

Inhibits prolactin release

Inhibits milk production and breast development

102
Q

Describe the pituitary thyroid axis

A

Hypothalamus releases TRH
TRH acts on Anterior Pituitary gland to release TSH
TSH acts on Thyroid to release T3 and T4
T3 and T4 have a negative feedback effect on hypothalamus and pituitary gland

103
Q

Describe the pituitary gonadal (HPA) axis in woman

draw out

A

Hypothalamus releases GnRH
GnRH acts on anterior pituitary gland to release FSH and LH
FSH and LH targets gonads to increase oestrogen, progesterone and testosterone production

Testosterone has a negative feedback effect on hypothalamus and pituitary.

FSH causes oestrogen release from ovaries and also leads to Inhibin production that has a negative feedback effect on FSH production from anterior pituitary.
Oestrogen causes proliferation of endometrium.
Low concentrations of oestrogen have a negative feedback effect on hypothalamus and (FSH production from) anterior pituitary.
High concentrations of oestrogen have positive feedback effect on hypothalamus and LH production from anterior pituitary (LH surge).
LH surge causes ovulation.
Corpus luteum then produces progesterone (and oestrogen).
Progesterone has a negative feedback effect on hypothalamus

104
Q

Describe the HPA axis

A

Hypothalamus releases CRH
CRH acts on anterior pituitary gland to release ACTH
ACTH acts on adrenal glands to release cortisol (and other chemicals)
Cortisol has negative feedback effect on hypothalamus and pituitary gland

105
Q

Describe the GH / IGF-1 axis

A

Hypothalamus releases GHRH
GHRH acts on anterior pituitary gland to release GH
GH acts on liver to release IGF-1
IGF-1 has a negative feedback effect on hypothalamus

Hypothalamus can also release Somatostatin (SMS) which inhibits release of GH from pituitary gland

106
Q

Describe ovulation

A

LH surge (due to high oestrogen levels) caused ovulation

Dominant follicle undergoes meiosis I
36 hours later it ruptures and releases the secondary oocyte

107
Q

What is effect of somatostatin on growth and protein synthesis

A

Inhibits GH

Inhibits growth and protein synthesis

108
Q

What is a benefit of negative feedback?

A

Effective in dampening hormonal responses thereby limiting the extremes of hormone secretory rates.

109
Q

Describe negative feedback mechanism of the HPA axis and its benefit

A

When a stressful stimulus elicits increased secretion of CRH and in turn ACTH and then cortisol, the resulting elevation in plasma cortisol concentration feeds back to inhibit the CRH secreting neurones of the hypothalamus AS WELL AS the ACTH-secreting cells of the anterior
pituitary.

This means that cortisol does not increase as much as it would have done without negative feedback - this is important due to the damaging effects of excess cortisol on immune function & metabolic reactions.

110
Q

Which hormone released from the anterior pituitary does not have major control over another endocrine gland?

A

Prolactin

111
Q

Give a difference between the hormone production and storage of anterior and posterior pituitary gland

A

Hormone production for Posterior Pituitary gland happens ONLY in hypothalamus and is then stored in posterior pituitary gland.
Anterior pituitary gland produces the hormones it releases

112
Q

True or False:
The Posterior Pituitary gland is an extension of the hypothalamus and originates from neuronal tissue, with large numbers of glial-type cells present

A

True

113
Q

What 2 peptide hormones are released by the posterior pituitary gland?

A

ADH/Vasopressin

Oxytocin

114
Q

What nuclei in the hypothalamus is ADH produced in?

A

Supraoptic nucleus (cell body)

115
Q

What nuclei in the hypothalamus is Oxytocin produced in?

A

Paraventricular nucleus (cell body)

116
Q

True or False:

ADH and Oxytocin have a very long half-life so they are not regulated frequently once released (min-to-min basis)

A

False

ADH and Oxytocin have a very SHORT half-life so they ARE regulated frequently once released (min-to-min basis)

117
Q

What do the axons of the supraoptic and paraventricular nuclei pass down before terminating in posterior pituitary

A

Infundibulum

hormones enclosed in vesicles move down the axons to accumulate at the axon terminal in posterior pituitary

118
Q

What stimulates the release of ADH/Vasopressin?

A 
Decreased Blood Volume
Trauma
Stress
Increased Blood CO2
Decreased blood O2
Increased osmotic pressure of blood
119
Q

What are effects of ADH/Vasopressin?

A

Acts on collecting ducts to increase water reabsorption, thus decreasing water secretion in urine and retaining fluid in body.
Acts on smooth muscle cells around blood vessels to cause their constriction resulting in vasoconstriction thereby increasing blood pressure - this may occur in response to a decrease in blood pressure that resulted
from blood loss due to an injury.
Stimulates ACTH release from the anterior pituitary to increase ALDOSTERONE release to further increase fluid retention.

120
Q

Draw diagram of RAAS

A

Angiotensinogen from liver.
Decreased renal perfusion of Juxtaglomerular Apparatus increases Renin secretion.
Angiotensinogen is converted to Angiotensin I in kidney by Renin.
ACE in lungs converts Angiotensin I to Angiotensin II.

Angiotensin II:

  • acts on adrenal cortex to release aldosterone
  • increased sympathetic activity
  • increased ADH secretion from posterior pituitary (acts on collecting ducts to increase H2O reabsorption)
  • Arteriolar vasoconstriction (increases BP)
  • Aldosterone and Angiotensin II cause increased reabsorption of Na+ and Cl-, increased retention of H2O and excretion of K+

Angiotensin II ultimately increases water and salt retention. When this returns to normal, the perfusion of JGA increases - NEGATIVE FEEDBACK effect on Renin release from kidney.

121
Q

How does ADH increase water reabsorption in collecting duct?

A

ADH binds to ADH receptor (coupled to G protein) on basolateral membrane of collecting duct principal cell.
G protein activates Adenylate cyclase, which converts ATP into cyclic AMP.
cAMP then causes Protein Kinase A to stimulate Aquaporin-2 channels to fuse with apical membrane of principal cell.
This then increases reabsorption of water from tubular fluid into principal cell and into peritubular fluid and capillary.

(osmoreceptors detect osmolarity to decide on ADH secretion)

122
Q

What aquaporin molecule is found on apical membrane of principal cells and which is found on basolateral membrane?

A

Aquaporin-2 on apical membrane

Aquaporin-3 on basolateral membrane

123
Q

What are the 2 functions of Oxytocin?

A

Important for EJECTION of milk during breast feeding:
- The stimulation of mammary glands stimulates the release of oxytocin and that stimulates the release of milk

Pregnancy:

  • Stimulates the contraction of uterine smooth muscles until the baby is born
  • Promotes the onset of labour - important for contractions
124
Q

What type of receptor do ALL pituitary and hypothalamic hormones act on?

A

G-protein coupled receptors

125
Q

Other than GH, what other anterior pituitary hormone’s production is inhibited by SMS?

A

TSH

126
Q 
Which of the following is not under the control of the pituitary gland?
A. Thyroid
B. Adrenal cortex 
C. Adrenal medulla 
D. Testis
E. Ovary
A

C. Adrenal Medulla

Cells in the adrenal medulla secrete catecholamines in response to stimulation by sympathetic preganglionic neurons

127
Q

Which of the following statements is false?
A. The pituitary gland lies in the sella turcica
B. The weight of the pituitary gland is around 0.5g
C. ACTH is secreted from the pituitary during stress
D. The pituitary regulates calcium metabolism
E. The anterior and posterior pituitary are distinct on an MRI scan

A

D. The pituitary regulates calcium metabolism

Calcium metabolism is regulated by i) the parathyroids through secretion of PTH and ii) vitamin D

128
Q 
In men all the following are mainly
produced in the adrenal cortex
except?
A. DHEAS
B. Testosterone
C. Aldosterone
D. 17-OH progesterone E. Androstenedione
A

B. Testosterone

Testosterone mainly secreted by testis

129
Q

Which of the following regarding AVP (vasopressin) is false?
A. AVP levels have a linear relationship with serum osmolality
B. is produced in the pituitary gland
C. stimulates reabsorption of water in the collecting duct of the nephron
D. in hypotension baroreceptors predominantly activate ADH production and secretion
E. Further AVP production is no longer effective once urine osmolality has reached a plateau

A

B. is produced in the pituitary gland

AVP is produced in the hypothalamus and stored in the pituitary from which it is released

130
Q 
Secretion of the following hormones is stimulated by hypothalamic hormones except?
A. ACTH
B. Growth hormone 
C. TSH
D. Prolactin
E. LH
A

D. Prolactin

The predominant effect is for dopamine to inhibit prolactin release; there is some stimulatory effect from TRH and prolactin releasing factor

131
Q

What does IGF-1 stand for?

A

Insulin-like Growth Factor - 1

132
Q 
Where is growth hormone’s main site of action to stimulate IGF1 release?
A. Bone
B. Liver
C. Adrenal cortex 
D. Muscle
E. Pancreas
A

B. Liver

133
Q 
The following are typical features of excess growth hormone secretion except?
A. Polyuria
B. Joint pains 
C. Sweating
D. Hypotension 
E. Headaches
A

D. Hypotension

Excess growth hormone causes hypertension

134
Q 
The following hormones all have a circadian rhythm except?
A. Cortisol
B. Testosterone
C. DHEA
D. 17OH progesterone
E. Thyroxine (T4)
A

E. Thyroxine (T4)

Most hormones produced by the adrenal cortex have a circadian rhythm similar to cortisol

135
Q 
Typical features of cortisol deficiency include the following except?
A. Hypotension
B. Muscle aches
C. Weight loss
D. Hyperglycaemia 
E. Lethargy
A

D. Hyperglycaemia

Cortisol deficiency may result in hypoglycaemia; cortisol, GH, adrenaline and glucagon are the 4 main stress hormones secreted to couteract hypoglycaemia in normal physiology

136
Q 
A 38 year old lady presented with weight gain, menorrhagia and constipation. She is most likely to be suffering from?
A. Cushing’s syndrome
B. Addison’s disease
C. Primary hypothyroidism
D. Graves disease
E. Acromegaly
A

C. Primary hypothyroidism

137
Q 
Which test would you likely want to perform in
a patient with proximal muscle weakness,
purple striae and thin skin?
A. Synacthen test
B. Overnight dexamethasone suppression test
C. Insulin tolerance test
D. Glucagon test
E. Skin allergy tests
A

B. Overnight dexamethasone suppression test

The ONDST is a screening test for Cushing’s syndrome, synacthen test for adrenal insufficiency, insulin tolerance test for adrenal insufficiency and GH deficiency, glucagon test for growth hormone deficiency

138
Q 
A 24 year old girl presented with hirsutism, oligomenorrhoea and acne. What test would you likely carry out from the ones below?
A. Ultra sound adrenals
B. Ultra sound ovaries
C. MRI ovaries
D. CT scan adrenals
E. Prolactin
A

B. Ultra sound ovaries

The girl is suffering from PCOS; the diagnosis besides clinical features and radiological findings includes hormonal changes such as high testosterone and/or an increased LH:FSH ratio

139
Q 
The following may cause nephrogenic diabetes insipidus except?
A. Lithium
B. Myeloma
C. Amyloidosis
D. Hyperkalaemia 
E. Hypercalcaemia
A

D. Hyperkalaemia

Hypokalemia causes nephrogenic DI

140
Q 
A 54 year old gentleman presented with hyponatraemia. All the following conditions need excluding before confirming SIADH except?
A. Hypothyroidism
B. Hypervolaemia
C. Euvolaemia
D. Adrenal insufficiency
E. Diuretic use
A

C. Euvolaemia

141
Q

A 66 year old gentleman had a serum sodium of 124 mmol/l, serum osmolality 265 mmol/l and a urine sodium of 52 mmol/l. What would you like to perform first?
A. Chest X-ray
B. CT brain
C. Skin turgor and jugular venous pressure test
D. Thyroid function tests
E. Synacthentest

A

C. Skin turgor and jugular venous pressure test

142
Q

Describe essential criteria for diagnosis of SIADH

A
  • Hyponatraemia < 135 mmol/L
  • Plasma hypo-osmolality < 275 mOsm/Kg
  • Urine osmolality > 100 mOsm/Kg
  • Clinical euvolaemia
  • No clinical signs of hypovolaemia (orthostatic decreases in blood pressure, tachycardia, decreased skin turgor, dry mucous membranes)
  • No clinical signs of hypervolaemia (oedema, ascites)
  • Increased urinary sodium excretion > 30 mmol/L with normal salt and water intake
  • Exclude recent diuretic use, renal disease, hypothyroidism, and hypocortisolism
143
Q 
The following are most likely causes of SIADH except?
A. Multiple sclerosis
B. Lung abscess
C. Subdural haemorrhage
D. Lymphoma
E. Cerebrovascular accident
A

A. Multiple sclerosis

144
Q

**What is SIADH

A

Syndrome of inappropriate antidiuretic hormone secretion

body makes too much ADH

145
Q

Causes of SIADH

A

Central Nervous system disorders
Tumours
Respiratory causes
Drugs

146
Q

What CNS disorders can cause SIADH

A 
Headinjury
Meningitis
Encephalitis
Brain tumour
Brain abscess
Cerebral haemorrhage/thrombosis 
Guillain-Barre syndrome
Acute intermittent porphyria
147
Q

What tumours can cause SIADH

A 
Carcinoma(especiallylung) 
Lymphoma
Leukaemia
Thymoma
Sarcoma 
Mesothelioma
148
Q

Give examples of respiratory causes of SIADH

A 
Pneumonia
Tuberculosis
Emphysema
Severe Asthma 
Pneumothorax 
Positive-pressure ventilation
149
Q

What drugs can cause SIADH

A 
carbamazapine, 
clofibrate, 
chlorpropramide thiazides, 
phenothiazines, 
MAO inhibitors, 
Selective serotonin reuptake inhibitors, 
cytotoxics, 
desmopressin, 
vasopressin, 
oxytocin
150
Q 
A 28 year old presented with a microprolactinoma? What is the most unlikely symptom?
A. Galactorrhoea
B. Oligomenorrhoea
C. Decreasedsexual appetite
D. Headaches
E. Visualfielddefects
A

E. Visual field defects

Macroprolactinoma causes visual field defects due to optic chiasm compression

151
Q 
The following suppress appetite except:
A. Peptide YY 
B. Ghrelin
C. CCK
D. GLP1
E. Glucose
A

B. Ghrelin

Ghrelin stimulates eating during hunger; high when fasting and fall on refeeding

152
Q 
The main adipose signal to the brain is
A. CCK
B. Neuropeptide y
C. Leptin
D. Agouti-related peptide
E. Adiponectin
A

C. Leptin

153
Q

What does Leptin regulate

A

Leptin regulates levels of satiety according to size of fat stores

154
Q

A 65 year old lady is diagnosed with SIADH.
Her sodium is 123mmol/l. What is your first
line of management?
A. If she is symptomatic I will treat with fluid restriction
B. If she is asymptomatic I will treat with hypertonic saline
C. If she is asymptomatic I will treat with fluid restriction
D. If she is asymptomatic I will repeat the sodium level the next day
E. If she is asymptomatic I will give normal saline

A

C. If she is asymptomatic I will treat with fluid restriction

155
Q

A patient with Addison’s disease presents with a chest infection. What
do you do?

A. Omit his steroids to avoid immunosuppression
B. Stop his steroids as they have precipitated a chest infection
C. Double his steroid dose whilst unwell
D. Keep him on his usual steroid dose
E. Not of the above

A

C. Double his steroid dose whilst unwell

In normals during infection the HPA axis is
stimulated to release more cortisol to overcome the stressful episode; this is not possible in patients with adrenal insufficiency or in patients on chronic steroid treatment and therefore steroid doses need to be increased to compensate for this

156
Q 
The following tests are typical of secondary hypogonadism
A. Low LH; High testosterone
B. Low LH; Low testosterone
C. High prolactin; high testosterone
D. Low FSH; Low prolactin
E. None of the above
A

B. Low LH; Low testosterone

157
Q 
Typical features of hypogonadism in a male include the following except:
A. Decreased sweating
B. Joint and muscular aches
C. Decreased sexual appetite
D. Decreased hair growth
E. Asymptomatic
A

A. Decreased sweating

Hypogonadism causes increased sweating and flushes

158
Q

A patient has a noon testosterone level below the normal range. What will you do?
A. Treatwith testosterone gel
B. Repeat the test at 0900h and check for symptoms
C. Repeat the test at noon to keep things equal
D. Referto endocrinology
E. Ignore it

A

B. Repeat the test at 0900h and check for symptoms

Testosterone has a circadian rhythm with a peak in the morning and therefore should be tested between 0800 and 0900h; two positive tests on separate days are essential for diagnosis

159
Q 
Osmoreceptors are found in the:
A. Subfornical organ
B. Organum vasculosum of the lamina terminalis
C. Hypothalamus
D. All of the above
E. None of these
A

D. All of the above

160
Q 
The first line treatment for a patient with a symptomatic prolactinoma is usually:
A. Radiotherapy
B. Transphenoidal surgery
C. Dopamine agonists
D. Transfrontal surgery
E. Somatostatin analogues
A

C. Dopamine agonists

161
Q 
Typical visual field defect of a patient with a large pituitary mass is
A. Unilateral quadrantanopia
B. Bitemporal hemianopia
C. Complete unilateral visual field loss
D. Complete bilateral visual field loss
E. None of the above
A

B. Bitemporal hemianopia

162
Q

Satiety is
A. The physiological feeling of no hunger
B. Inhibitedby activation of POMC neurons
C. The physiological feeling of hunger
D. Induced by ghrelin release
E. Enhanced by Agouti- related peptide

A

A. The physiological feeling of no hunger

163
Q 
The centres of appetite regulation in the brain are mainly found in the:
A. Pituitary
B. Cerebellum
C. Hypothalamus
D. Basal ganglia
E. Brain cortex
A

C. Hypothalamus

164
Q 
Which of the following is not a sign of hyperthyroidism?
A. Palpitations
B. Tachycardia
C. Tremor
D. Goitre
E. Proximalmuscle weakness
A

A. Palpitations
not a SIGN
Palpitation is a typical SYMPTOM of hyperthroidism!!

165
Q

How many parathyroid glands are there?

A

4

166
Q

Actions of PTH

A

Increased bone resorption by osteoclasts
Increased intestinal calcium absorption
Actives 1,25-dihydroxyVD (calcitriol) in kidney
Increased calcium reabsorption and phosphate excretion in the kidney

167
Q

What % of calcium is stored in bone

A

99% as calcium phosphate

168
Q

What hormone control calcium balance and where are they found?

A

Parathyroid: PTH
Thyroid: Calcitonin

169
Q

What is calcitriol and how do levels of it change with PTH

A

Active vitamin D from kidneys

Increased by PTH and cause increased GI absorption and kidney (PCT) reabsorption of calcium

170
Q

What is function of calcitonin

A

When Ca2+ levels too high, thyroid stimulated to release calcitonin:
Inhibits GI absorption
Increases osteoBlast activity
Reduces Ca2+ levels

171
Q

Difference between Cushings Disease and Cushings Syndrome

A

Cushing’s syndrome refers to the condition caused by excess cortisol in the body, regardless of the cause. When Cushing’s syndrome is caused by a pituitary tumour, it is called Cushing’s disease.

172
Q

**What is amyloidosis

A

Build up of amyloid protetin in organs and tissues throughout the body

173
Q

Signs and symptoms of amyloidosis

A

Kidney failure
Heart failure - heart muscles become stiffer so harder to pump blood round the body
Build up in other organs e.g. liver, spleen, nerves or digestive system resulting in:
-feeling lightheaded or fainting, particularly after standing or sitting up
-numbness or a tingling feeling in the hands and feet (peripheral neuropathy)
-nausea, diarrhoea or constipation
-numbness, tingling and pain in the wrist, hand and fingers (carpal tunnel syndrome)
-an enlarged tongue
(Multiple myeloma in rare cases - link)

174
Q

Symptoms of kidney failure

A

Swelling, often in the legs, caused by fluid retention (oedema)
Tiredness
Weakness
Loss of appetite

175
Q

Symptoms of heart failure from amyloidosis

A

SoB
Oedema
Abnormal heartbeat (arrhythmia)

176
Q

Cause of amyloidosis

A

Abnormality of plasma cells in bone marrow
Plasma cells form a light chain of proteins which enter the bloodstream and form amyloid deposits
These chains can clump together into thread-like strings called Amyloid Fibrils that the body cant easily clear
Over time amyloid fibrils build up as deposits in tissues and organs. This gradually stops them functioning properly causing many symptoms

177
Q

What is purpose of light chain of amyloid in blood of normal person

A

Light chain proteins in their blood are part of their natural antibody proteins, which help protect the body from illness and infection.

178
Q

Diagnosis of amyloidosis

A

Symptoms are vague and not specific
Biopsy of affected part of body
Symptoms from around 30 years old

179
Q

Treatment of amyloidosis

A

No cure
Aim to stop more abnormal proteins being produced.
Chemotherapy - damages abnormal bone marrow cells and stops them producing abnormal proteins that form amyloid deposits.
Steroids (alongside chemo)
Stem cell transplant
Dialysis for kidney failure and other meds for heart issues etc

180
Q

What causes hereditary ATTR amyloidosis

A

Mutations in TTR gene

Cause amyloid deposits from abnormal versions of a blood protein called transthyretin (TTR)

181
Q

Other types of amyloidosis

A

Wild type TTR amyloidosis - mainly affects heart and can cause carpal tunnel syndrome (only appears usually in >65)
Hereditary TTR amyloidosis

182
Q

Diagnosis of ATTR amyloidosis

A
  • taking a sample of the affected tissues (tissue biopsy)
  • genetic testing
  • heart scans – such as an echocardiogram, a cardiac MRI or a special type of scan called a DPD
183
Q

Symptoms of Hypothyroidism

A 
Tiredness
Sleepy
Lethargic
Low mood
Cold-disliking
Increased weight
Constipation
Menorrhagia
Hoarse voice
Worse memory/cognition
Dementia
Myalgia
Cramps
Weakness
184
Q

Signs of hypothyoidism

A 
BRADYCARDIC
Bradycardia
Reflexes relax slowly
Ataxia (cerebellar)
Dry thin hair/skin
Yawning (drowsy)
Cold hands (low temp)
Ascites (and possible non-pitting oedema - lids, hands feet
Defeated demeanour
Immobile with or without ileus
CCF

Also Neuropathy, myopathy and goitre

185
Q

Most common hormonal disturbance of pituitary gland

A

Hyperprolactinaemia

especially for women

186
Q

What is amiodarone

A

Iodine-rich drug structurally like T4
Need to check TFTs every 6 months
2% of people on this develop significant thyroid problems from it

187
Q

Tests of hypopotuitarism

A

Basal tests (of hormones like LH, TSH etc)
Dynamic tests assessing each axis:
Short Synacthen test - adrenal axis
Insulin Tolerance Test - adrenal and GH axis
Arginine and GH-releasing hormone test
Glucagon stimulation test
MRI to investigate cause (hypothalamus or pituitary lesion)

188
Q

Treatment of hypopituitarism

A

Hydrocortisone for secondary adrenal failure (before hormones)
Thyroxine if hypothyroid
Other hormone replacements

189
Q

Describe TFTs

A

pg 216 of handbook

190
Q

Conditions that are Risk factors of obesity

A 
Type 2 diabetes
CHD
Some cancers e.g. bowel or breast cancer
Stroke
(Obesity can lead to depression)
191
Q

Obesity-related issues (not including fatness)

A 
breathlessness
increased sweating
snoring
difficulty doing physical activity
often feeling very tired
joint and back pain
low confidence and self-esteem
feeling isolated
192
Q

Treating obesity

A

Diet management - balanced, calorie-controlled as recommended by professional
Join weight loss group
Exercise
Eat slowly and avoid situations in which could overeat
Also:
psychological support could help
Orlistat if lifestyle changes not really working - reduces amount of fat absorb in digestion

193
Q

Primary
Secondary
Tertiary
hyperthyroid disease

A

-

194
Q

How can we reduce the impact of type 2 diabetes

A

Identifying people at risk of diabetes
Preventing diabetes (“Primary” prevention)
Diagnosing diabetes earlier (“Secondary” prevention)
Effective management and supporting self-management (“Tertiary” prevention)

195
Q

People at risk of diabetes

A

Sedentary job, sedentary leisure activities
Diet high in calorie dense foods/low in fruit and vegetables, pulses and wholegrain
“Obesogenic” environment

196
Q

Describe the obesogenic environment

A

Physical environment: eg TV remote controls, lifts, “car culture”
Economic environment: eg cheap TV watching, expensive fruit and veg
Sociocultural environment: eg safety fears, family eating patterns

197
Q

Mechanisms that maintain obesity

A

Physical/physiological - more weight = more difficult to exercise (arthritis, stress incontinence) and dieting -> metabolic response
Psychological - low self-esteem and guilt, comfort eating
Socioeconomic - reduced opportunities employment, relationships, social mobility

198
Q

Risk factors of diabetes - identifying who is at risk

A 
Age, sex, ethnicity, family history
Weight, BMI, waist circumference
History of gestational diabetes
Hypertension or vascular disease
Impaired Glucose Tolerance (IGT) or Impaired Fasting Glucose (IFG)
199
Q

True or False:

Screening tests are the same for pre-diabetes and diabetes

A

True

200
Q

**Screening tests available for Impaired GT and IFG

A 
HbA1c
Random capillary blood glucose
Random venous blood glucose
Fasting venous blood glucose
Oral glucose tolerance test (venous blood glucose 2 hours after oral glucose load)
201
Q

**Example of Primary prevention of diabetes - ‘Preventing diabetes’

A

Sustained increase in physical activity
Sustained change in diet
Sustained weight loss

202
Q

Which patients should you prioritise interventions for

A

Those with HbA1c = 44–47 mmol/mol OR fasting plasma glucose 6.5–6.9 mmol/l

(Added recommendation to use metformin if BMI >35 + HbA1c increasing OR lifestyle intervention not possible + HbA1c increasing)

203
Q

Example of Secondary prevention of diabetes - ‘Earlier diagnosis of diabetes’

A

Raising awareness of diabetes and possible symptoms in the community
Raising awareness of diabetes and possible symptoms in health professionals
Using clinical records to identify those at risk and/or using blood tests to screen before symptoms develop
Screening

204
Q

Example of Tertiary prevention of diabetes - ‘Supporting self-care for diabetes’

A

Self monitoring – helpful for some, particularly if on insulin, but not all
Diet - Support for changing eating patterns
Exercise - Support for increasing physical activity
Drugs - Support for taking medication
Education – professionals/expert patients
Peer support – Health Champions/ Health Trainers

205
Q

**Define obesity

A

Abnormal or excessive fat accumulation that may impair health
BMI > 30

206
Q

Costs of obesity

A

COST TO NHS = £5.1bn

Obesity medication £13.3m
Social care cost £352m
Sick days as result of obesity £16m

Cost to wider economy £27bm

207
Q

Tiers of obesity care

A

Tier 1 - Universal prevention (prevent future occurrences through information giving) e.g. environmental health promotion
Tier 2 - Lifestyle intervention (Encourage people with overweight and obesity to have healthier lifestyles) e.g. Multicomponent weight management
Tier 3 - Specialist services (management of severe obesity or obesity with complex other needs) e.g. Multidisciplinary intervention
Tier 4 - Surgery e.g. Bariatric surgery

208
Q

When would you give surgery like bariatric surgery for obesity care

A

Only considered for people with severe morbid obesity and a serious health condition

209
Q

Give examples of national action to reduce obesity

A

Labelling
Sugar reduction (sugar tax, ban on sale of energy drinks to children and
Retail - ban the promotion of HFSS food and drink
Marketing - 9pm watershed for advertising HFSS products in broadcast media and similar action online
Schools - encouraging exercise
Local communities - strengthen government buying standards for food and catering services

210
Q

Give examples of local action to reduce obesity

A

Planning – exclusion zones
Transport – active travel
Housing – quality and requirements for new developments
Open spaces – access and upkeep
Sport & Leisure – about more than just sport
Voluntary sector – huge reservoir of skills
Community-led action – lots of lived experience we can’t replicate

211
Q

Diagnosis of Primary Hypothyroidism

A

Low T3/T4
High TSH
(issue with thyroid)

212
Q

Diagnosis of Secondary Hypothyroidism

A

Low T3/T4
Low TSH
Normal/High TRH
(issue with pituitary)

213
Q

Diagnosis of Tertiary Hypothyroidism

A

(Low T3/T4
Low TSH)
Low TRH
(issue with hypothalamus)

214
Q

What other chemicals could be typical of hypothyroidism (not in thyroid axis)

A

High cholesterol is typical

Medicine Phase 2a (22 decks)

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