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Endocrinology Flashcards

1
Q

Define hormone

A

Any substance found in very small along in one specialised organ or group of cells carried to another organ upon which it has a specific physiological effect

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2
Q

Name 7 key endocrine organs

A 
Hypothalamus 
Pituitary 
Thyroid
Parathyroid
Adrenal 
Pancreas
Gonads
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3
Q

What are the 3 broad ways hormones act on the body

A

To enable and promote development of physical, sexual and mental characteristics

To keep certain physiological parameters constant

To enable and promote the adjustment of physiological adaptations

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4
Q

2 ways to class a hormone based on how it acts

A

Effector

Tropic

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5
Q

What are the 4 main structural types of hormone

A

Peptide hormone
Steroid hormones
Amino hormones
Arachidonic acid derived

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6
Q

What are steroids

A

Lipid hormones derived from cholesterol

Not water soluble

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7
Q

How are steroid hormones transported

A

In the blood bound to plasma proteins

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8
Q

What are amine hormones derived from

A

Tyrosine or tryptophan

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9
Q

What kind of hormone is dopamine

A

Amine

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10
Q

What are are arachidonic acid derived hormones synthesised from

What response are they important in

A

Linoleic acid

Inflammatory responses

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11
Q

What do NSAIDs do

A

They are Non Steroidal Anti Inflammatory Drugs

They inhibit arachidonic acid derived hormones

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12
Q

What is 5-HPETE

A

Arachidonic acid 5-hydroxyperoxidase

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13
Q

What is 5-LO

A

5-lipoxygenase

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14
Q

What directs peptide hormones to the secretory pathway in the cell

What happens when it reaches the ER

A

The N terminal sequence

This sequence is cleaved from the protein hormone, activating the hormone

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15
Q

What must happen for a pre hormone to become a hormone

A

The signal peptide sequence must be removed from the pre hormone leaving only the active hormone

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16
Q

How is a hormone formed from a preprohormone

A

The signal peptide must be removed, then the pro sequence must be removed, leaving only the hormone

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17
Q

What is the RF-amide family

A

Peptide hormones that require addition of an amide group at the carboxyl terminus to become active

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18
Q

Where is kisspeptide secreted

What does it do

A

In the arcuate and anteroventral periventricular regions of the hypothalamus

Stimulates secretion of gonadotrophin releasing protein (GnRH)

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19
Q

What is GnRH

A

Gonadotrophin releasing hormone

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20
Q

What is GnIH

A

Gonadotrophin inhibitory hormone

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21
Q

Where is GnIH produced

What action does it have

A

Paraventricular and dorsomedial regions of the hypothalamus

Inhibits release of gonadotrophin hormones from the pituitary

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22
Q

How do hormones signal via the GPCR pathway

A

Hormones bind to GPCR to activate G proteins which stimulate/ inhibit intracellular adenylyl cyclase

Stimulating adenylyl cyclase increases [cAMP] which activates PKA which alters cellular activities by phosphorylation

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23
Q

Describe hormone signalling via the DAG/IP3 pathway

A

Hormones bind to GPCR which activate G proteins to stimulate phospholipase C.
Phospholipase C converts PIP2 to IP3 and DAG

IP3 stimulates Ca2+ release from internal stores which binds to calmodulin, activating Calmodulin Activated Protein Kinase

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24
Q

What is the common domain structure of nuclear receptors

A

3 domains:
AF1 (an activation domain)

Zn2+ finger (a DNA binding domain)

Ligand binding/ dimerisation domain

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25
Q

How do lipid soluble hormones act on cells

A

They pass freely through the PM and bind to receptors in the cytoplasm
Ligand binding allows the receptor to dissociate from the heat shock receptor and to enter the nucleus, bringing about changes to gene transcription

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26
Q

Can hormone/ receptor complexes stimulate responses at the cell membrane

Eg?

A

Yes

T3

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27
Q

What links the hypothalamus and pituitary

A

A portal system links the hypothalamus to the anterior pituitary

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28
Q

What is the neural connection from the anterior pituitary to the hypothalamus

What about for the posterior pituitary

A

There is no direct neural between the anterior pituitary and the hypothalamus

The nerve fibres from the paraventricular and supraoptic nuclei pass directly to the posterior pituitary where they secrete the hormones the contain into the blood stream

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29
Q

Which parts of the hypothalamus contain oxytocin and vasopressin

What else does this part contain

A

The paraventricular nucleus ( to be secreted from posterior pituitary)

Neurons that regulate ACTH and TSH secretion

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30
Q

True or false

The hypothalamus helps regulate our rhythms

A

True it helps regulate many seasonal and circadian rhythms

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31
Q

What is the neurohypophysis

A

Posterior pituitary

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32
Q

What is the other name for the anterior pituitary

A

Adenohypophysis

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33
Q

Is the posterior pituitary part of the brain

A

Yes

Embryologically it is a down growth from the brain

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34
Q

What hypothalamic nerves doe the neurohypophysis contain

A

Paraventricular and supraoptic

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35
Q

What is the arrangement of the supraoptic and paraventricular nerves

Where are the hormones made

A

The cell bodies are in the hypothalamus and the nerve endings are in the posterior pituitary

Hormones are made in cell body and transported to nerve endings for storage in vesicles. They are released from here directly into the bloodstream

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36
Q

What are the hormones released from the neurohypophysis

A

ADH

oxytocin

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37
Q

Is the anterior pituitary part of the brain

A

No - there are no nerve fibres travelling from the hypothalamus

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38
Q

How does the hypothalamus communicate with the anterior pituitary

A

Via the hypophyseal portal vessels

Neurosecretory cells in the hypothalamus secrete releasing hormones into the primary capillary plexus which are delivered to the anterior pituitary

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39
Q

Is the release of hormones from the hypothalamus to the anterior pituitary constant

A

No it is pulsatile

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40
Q

Give 5 evidence for the control of anterior pituitary secretions by hypothalamic releasing hormones

A

1) lesions in the hypothalamus produce atrophy of some endocrine glands, similar to that when the anterior pituitary
2) electrical stimulation of hypothalamus evokes secretion of anterior pituitary hormones
3) transaction of the pituitary stalk results in atrophy of some endocrine glands
4) transplantation of the anterior pituitary to another site does not give endocrine function but if a blood supply connects to the hypothalamus, function is restored
5) addition of purified hypothalamic releasing hormones to pituitary explants in culture results in secretion of anterior pituitary hormones

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41
Q

How long is a circadian rhythm cycle

A

24 hours

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42
Q

What is the periodicity of a pulsatile

A

30 mins to 2 hours

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43
Q

How does the release of sex hormones vary

A

According to breeding seasons not the oestrous cycle

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44
Q

What are the 2 general methods for hormone production regulation

A

Negative feedback

Positive feedback

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45
Q

How are hormones usually measured

A

Immunoassays

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46
Q

1 immunoassay that uses colour change

1 that used a radio scope

A

Enzyme immunoassays
ELISA
EIA

RIA

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47
Q

What is the competitive ELISA method

A

The sample containing the hormone to be measured is mixed with a fixed amount of the same hormone labelled with an enzyme

The greater the amount of unknown hormone in the sample, the greater the competition with the labellled hormone for binding to the well

The higher the hormone concentration in the original sample the lower the visual signal

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48
Q

What happens for both types of ELISA in data collection

A

Standard curve is generated using pure hormone at known concentration

Comparison with unknown samples must be in the linear range of the standard curve

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49
Q

Give the method for a general ELISA

A

The sample with an unknown amount of hormone is immobilised in the wells of a microtiter plate via an antibody

A detection antibody covalently linked to an enzyme (eg peroxidase) is added forming a complex with the hormone

Between each step the plate is washed to remove any proteins that are not specifically bound

The antibody/ hormone complex is detected by adding an enzymatic substrate to produce a visible signal

The higher the hormone concentration in the original sample, the higher the visual signal

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50
Q

True or false

The adrenal gland is structurally and functionally 3 endocrine organs

A

False - it is functionally 2 endocrine organs

The outer cortex secretes glucocorticoids, mineralcorticoids and sex steroids

The inner medulla secreted the catecholamines adrenaline and noradrenaline

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51
Q

What are adrenal steroids derived from

A

Cholesterol

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52
Q

What is the principal glucocorticoid

What is the principal mineralocorticoid

A

Cortisol

Aldosterone

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53
Q

Describe regulation of adrenal gland secretions

A

Hypothalamic neurons released corticotrophin releasing hormone (CRH) into the portal system to stimulate pituitary corticotrophs to release ACTH into the circulation

ACTH stimulates glucocorticoid and sex hormone production from the adrenal cortex

ACTH DOES NOT regulate mineralocorticoid or catecholamine secretion

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54
Q

What is ACTH

A

Adrenocorticotrophic hormone

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55
Q

Which hormone causes skin pigmentation

A

ACTH

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56
Q

What is a primary adrenal insufficiency

What does this mean for hormone production

A

When there is a problem with the adrenal gland directly

Increased ACTH
Decreased glucocorticoids, androgens and mineralocorticoids

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57
Q

Why does ACTH production increase in primary adrenal insufficiency

A

Less glucocorticoids are produced as the actual adrenal gland is abnormal but the pituitary is normal so ACTH won’t drop

But usually there is a negative feedback loop, whereby glucocorticoids inhibit ACTH production
With reduced glucocorticoids, the negative feedback is lost and ACTH production increases

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58
Q

What is secondary adrenal insufficiency

What happens to hormone production

A

When there is a problem with the hypothalamus/ pituitary

Decreased ACTH, therefore decreased glucocorticoids and androgen
Mineralocorticoids remain normal
This is because ACTH does not affect mineralocorticoid production

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59
Q

What is ACTH derived from

A

Proteolytic processing of POMC

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60
Q

What is POMC

A

Pro-opiomelanocortin

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61
Q

What regulates aldosterone

What is the main action of aldosterone

A

Regulated by renin-angiotensin system and by plasma levels of Na and K

Conservation of body sodium by stimulating reabsorption game sodium in the kidney in exchange for potassium

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62
Q

What is the main glucocorticoid in humans and in other animals

A

Humans- cortisol

Animals- corticosterone

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63
Q

Discuss the circadian rhythms of plasma cortisol

A

Cortisol levels are highest in the morning and decline during the day
This reflects the patterns of ACTH secretion by the anterior pituitary

This probably reflects the body’s response to low blood glucose after overnight fasting

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64
Q

Why is it important to understand the circadian rhythms of cortisol

A

Cortisol replacement therapy in clinical treatment

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65
Q

6 key physiological actions associated with cortisol

A 
Starvation
Inflammation 
Immune system
Pregnancy 
The CNS
the cardiovascular system
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66
Q

Tell me about cortisol and starvation

A

Cortisol is a glucocorticoid and as the name suggests it is associated with glucose levels:

It raises blood glucose during fasting/ starvation and protects liver glycogen reserves

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67
Q

What’s up with cortisol and inflammation?🤷🏿‍♀️

A

Cortisol inhibits the synthesis of inflammatory substances (eg NO and prostaglandins)
Cortisol derivatives are used medically to reduce inflammations and swellings in joints

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68
Q

Is inflammation normal?

What causes inflammation?

A

It is a normal response at the site of infection

Caused by NO, prostaglandins and leukotrienes secreted from immune cells

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69
Q

What are cellular immune responses mediated by

A

interleukin production

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70
Q

What do interleukins promote secretion of

A

CRH
ACTH
cortisol

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71
Q

How does cortisol interact with interleukins

A

Inhibits secretion of interleukins by immune cells, this creating a negative feedback loop

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72
Q

How does cortisol affect the foetus (not in detail)

A

Late in gestation cortisol is secreted by the fetal adrenal gland in preparation for birth

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73
Q

Give the 7 effects of cortisol on the foetus to prepare it for birth

A
  • Production of lung surfactant
  • Disposition of glycogen in the liver
  • Allows The intestinal tract to secrete digestive enzymes and absorb nutrients
  • acid secretion by the stomach
  • increased filtration rate in kidney
  • T4 converted to T3
  • in sheep, it stimulates steroid secretions from the placenta into the mother to initiate birth
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74
Q

How do cortisol and the CNS interact

A

As cortisol can easily cross the blood brain barrier it can alter mood

Jet lag is also caused by circadian production of cortisol being out of synch with real time

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75
Q

How does cortisol interact with the cardiovascular system

A

Permissive for vasoconstriction actions of catecholamines

Important in maintaining blood pressure

Stimulates erythropoietin synthesis to increase RBC production

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76
Q

What kind of responses are associated with the adrenal medulla

A

It is part of the SNS - fight or flight
secretes catecholamines in response to stress
Short lived responses

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77
Q

Give 9 actions of catecholamines

A 
Stimulate heart rate
Increased heart contractility
Increased cardiac output
Increased systolic pressure
Reduced diastolic pressure
Piloerection
Reduced gut motility
Increased breakdown of glycogen to glucose in the liver
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78
Q

What causes the release of catecholamines

A

SNS stimulation of chromaffin cells

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79
Q

What can cause hyperadrenocorticism

A

Adrenal gland tumour
Increased ACTH
Increased CRH
Exogenous corticosteroid treatment

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80
Q

What are symptoms of hyperadrenocorticism (7)

A

Weight gain
Rosy cheeks
Skin pigmentation (if ACTH is increased eg in Cushing’s syndrome)
Purple abdominal striations
Capillary fragility
Immunosuppression
Glucose intolerance, hyperglycaemia and insulin resistance

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81
Q

How can Cushing’s be treated

A

Removal of adrenal gland

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82
Q

What is the most common endocrine disorder in dogs

In which dogs is it particularly common

What is the usual cause

A

Canine Cushing’s syndrome

Poodles
Boxers
Dachshunds

80% caused by pituitary tumour

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83
Q

What are the symptoms of canine Cushing’s

A

Pot belly due to hepatomegaly and abdominal muscle weakness

Polyuria and polydipsia and polyphagia

General muscle wasting

84
Q

Discuss equine Cushing syndrome (4)

A

Less common than in dogs

Excessive hairy coat

Polyuria/ polydipsia

Muscle wasting

Sweating

85
Q

What is Addison’s Disease

A

Primary hypoadrenocorticism

Which results in deficiency of both glucocorticoids and mineralocorticoids

86
Q

What causes Addison’s syndrome

A

Destruction of adrenals
Autoimmune reaction or inflammatory disease
Haemorrhage

87
Q

What causes secondary hypoadrenocorticism

what does it result in

A

Lack of ACTH

Deficiency of glucocorticoids only

88
Q

What are the symptoms of Secondary hypoadrenocorticism

What do they depend on

What if ACTH production isn’t impaired

A

It depends on whether aldosterone is lacking

If both aldosterone and cortisol is lacking it leads to hypotension and eventual death.
Tiredness and weakness
Vomiting
Skin pigmentation

No pigmentation; loss of body hair in females, in males get sex hormones from their testes

89
Q

What causes congenital adrenal hyperplasia

How does the body try to compensate

A

Lack of enzyme involved in cortisol production (21-hydroxylase or 11-β-hydroxylase)

Increase CRH-ACTH levels

90
Q

What does congenital adrenal hyperplasia lead to if caused by 21-hydroxylase deficiency

A

Excessive production of sex steroids
Masculinisation of female foetus
Decreased production of mineralocorticoids which could mean life threatening salt loss

91
Q

How much of congenital adrenal hyperplasia is caused by each enzyme deficiency

A

21-hydroxylase : 95%

11-β hydroxylase : 5%

92
Q

What does congenital adrenal hyperplasia caused by 11-β hyroxylase deficiency

A

Excessive deoxycorticosterone which has mineralocorticoid activity

This leads to life threatening hypertension

93
Q

How does congenital adrenal hyperplasia affect males vs females

A

Females: in uterus there is clitoral hypertrophy, fusion of labia and urogenital opening at the base of pseudo-phallus

Treaty by surgical reconstruction of genitalia

Males: precocious puberty

94
Q

Where is the thyroid

A

Attached to the trachea just below the larynx

95
Q

True or false

The blood supply to the thyroid has a poor, tortuous blood supply

A

False

It has a rich blood and autonomic never supply

96
Q

What are the 3 hormones secreted by the thyroid

A

Thyroxine (T4)
Tri- iodothryonine (T3)
Calcitonin

97
Q

What are the iodine containing thyroid hormones attached to

Where are they stored

A

Thyroglobulin

In the colloid material

98
Q

What are C cells

What is their function

A

Parafollicular cells in the thyroid

Secrete calcitonin

99
Q

What does calcitonin do

A

Regulates plasma Ca2+ levels

100
Q

What controls blood supply to the thyroid

A

Nerves

101
Q

What regulates thyroid secretions

A

The hypothalamic pituitary axis

102
Q

Describe the hypothalamic - pituitary axis regulation of the thyroid

A

TRH from the hypothalamus stimulates the anterior pituitary to release TSH

TSH acts on the thyroid to increase T4/T3

103
Q

What is TRH

A

Thyrotrophin releasing hormone

104
Q

What is TSH

A

Thyroid stimulating hormone

105
Q

Which is the most potent thyroid hormone

A

T3

106
Q

what is DI

what is its function

where is it found

A

Deiodinase enzyme

Converts T4 to T3

It is found in target tissue and also in the pituitary to facilitate negative feedback (

107
Q

How is T4 formed

A

Iodine is attached to tyrosine to produce MIT and then again to produce DIT

DIT is coupled with another DIT to produce T4

108
Q

How is T3 made

A

Iodine is added to tyrosine to form MIT and then again to form DIT

DIT is coupled with MIT to form T3

109
Q

How is T3 formed from T4

A

Monodeiodination

(Removal of an iodine)

Depending on which iodine this can form either active T3 or reverse T3

110
Q

How is iodide taken into the thyroid epithelial cells from the blood

A

By SLC5A5 (a sodium-iodide symporter)

TAKEN UP AS IODIDE NOT IODINE

111
Q

How is iodide turned into iodine in the thyroid epithelial cells

A

By a peroxidase

112
Q

What happens to iodine that has just entered the thyroid colloid

A

It is added onto exposed Tyrosine residues on thyroglobulin

113
Q

What happens to thyroglobulin after iodine bonding to tyrosine residues

A

It is taken into the epithelial cells via endocytosis

114
Q

What happens to thyroglobulin once it emerges into the epithelial cells

A

Broken down by lysosomes to release T3 and T4 into the circulation

115
Q

How does TSH increase T3 and T4 release

A

It stimulates iodide uptake via the SLC5A5,
increases iodide oxidation to iodine,
increases endocytosis of thyroglobulin
and stimulates secretion of T3/T4

116
Q

How does T3 act

A

Binds to specific nuclear receptors to alter transcription

117
Q

3 things thyroid hormones affect

What is the overall function

A

Whole body growth

Basal metabolic rate

Cardiac output

Overall: increase substrates for oxidative respiration in cells

118
Q

What is the mechanism of T3 on peripheral thermogenesis

A

Stimulates Na/K pump, glycerol phosphate dehydrogenase (GPDH), uncoupling protein 3 (UCP3), and SERCA

To generate heat

119
Q

Why does T3 stimulate UCP3

A

Uncoupling the electron transport chain produces heat instead of ATP

120
Q

What is SERCA

A

Smooth endoplasmic reticulum Ca2+ ATPase

121
Q

What are the mechanisms of thyroid hormones in central thermogenesis

A

T3 acts on ventromedial hypothalamus (VMH) to inhibit AMPK and increase SNS signals to brown adipose to generate heat via UCP1

122
Q

Why is brown adipose so high in babies

A

For thermogenesis

Muscular thermogenesis is not fully developed yet so T3 must act on brown adipose

123
Q

What used to be called cretinism

A

Lack of thyroid hormone during late fetal life and early post natal development that resulted in severe mental retardation

124
Q

Why can hypothyroidism be caused by

A

Iodine deficiency
Thyroid disease (eg autoimmunity (Hashimoto’s Disease)) - primary hypothyroidism
Lack of TSH - secondary hypothyroidism
congenital absence of thyroid

125
Q

Give 6 symptoms of hypothyroidism

A 
Weight gain
Goitre
Cold extremities
Lethargy
Muscle weakness
Reduced cardiac output and slow pulse
126
Q

How might you treat hypothyroidism

A

Administer Levothyoxine (T4 stereoisomer)

127
Q

What can hyperthyroidism be caused by

A

Overactive thyroid

Autoimmune - anti bodies bind to TSH receptor and activate it (Graves’ disease)

128
Q

True or false:

Hyperthyroidism is more common in men

A

False

It is 10x more common in women

129
Q

Give 9 symptoms of hyperthyroidism

A 
Weight loss
Sweating
Goitre
Agitated/ nervous
Fast heart rate and atrial fibrillation 
Muscle weakness
Rapid growth/ bone maturation in children
Opthalmopathy (bulging/staring eyes)
Infertility/ lack of periods
130
Q

Treatment for hyperthyroidism

A

Administer anti thyroid drugs then Levothyroxine to replace the hormones at the correct levels

Surgery

Destruction of thyroid by radio-iodine treatment

131
Q

What is the most common endocrine condition in cats (especially older cats)

What is it often caused by

What are symptoms

A

Hyperthyroidism

Benign thyroid adenoma

Weight loss
Rapid heart loss
Vomiting/ diarrhoea
Increased water constipation

132
Q

How do you treat feline hyperthyroidism

A

Block/ replacement therapy to block hormone production and give oral thyroxine

Surgery

Destruction of thyroid by radiotherapy

133
Q

When is Human fetal growth greatest

A

Between 16-20 weeks of gestation

134
Q

Describe how rates of growth vary throughout human life

A

Increases steadily in gestation, reaching a peak at 20 weeks then decreases until birth

After birth, growth velocity declines after birth until pubertal growth spurts

135
Q

True or false

The earlier the growth spurt at puberty the shorter the final height

A

True

136
Q

3 factors involved in growth

A

Genetic
Environmental
Physiological

137
Q

What is the structure of growth hormone

A

191 amino acid polypeptide

2 disulphide bridges

138
Q

What is another name for growth hormone

A

somatotropin

139
Q

What 2 proteins is somatotropin closely associated with

A

Prolactin

Placental lactogens

140
Q

6 factors that influence growth hormone

A 
GHRH 
Arginine
Ghrelin 
Hypoglycaemia 
Sleep
Exercise
141
Q

What is GHRH

A

A 44 amino acid peptide from arcuate neurons in the hypothalamus

142
Q

What is the relevance of arginine stimulating GH release

A

It is used to clinically diagnose GH deficiency

143
Q

What is the release of GH decreased by

Which of these is used to diagnose GH deficiency

A 
Somatostatin 
GH via negative feedback 
IGF1 (via negative feedback)
Lipids
Age
Thyroid deficiency 
Hyperglycaemia (used to diagnose GH deficiency)
144
Q

What is somatostatin

A

A 14 amino acid peptide released from periventricular neurons in hypothalamus

145
Q

How many amino acids in GHRH

A

44

146
Q

Where is GHRH produced

Where is it released into and what is its effect

A

By arcuate hypothalamic neurons

Released into portal system to stimulate somatotropins in the anterior pituitary to produce GH

147
Q

What kind of receptor is the GHRH receptor

What is the cascade

A

A GPCR

G proteins increase cAMP in somatotrophs

148
Q

Are GH effects always direct

A

No

GH has direct effects in muscle, bone and adipose
But has indirect effects via IGF1 (a somatomedin)

149
Q

What is the effect of GH on bones

A

Promotes bone growth in long bones by stimulating chondrocytes at the epiphyseal growth plate

150
Q

What are the metabolic effects of growth hormone

A

Inhibition of glucose uptake by muscle and fat cells

Increased lipolysis

Increased sodium and fluid retention through increased GFR

increased BMR

hepatic gluconeogenesis

Reduced sensitivity to insulin

151
Q

7 types of growth factor

A 
Nerve growth factor
Epidermal growth factor
Transforming growth factor
Fibroblast growth factor 
Platelet derived growth factor
Erythropoietin 
Interleukin
152
Q

Other than GH what are other hormones involved

A 
Growth factors 
Thyroid hormones
Gonadal steroids
Glucocorticoids
Insulin
153
Q

How are thyroid hormones involved in growth

What happens if the thyroid is under active

A

They are permissive for growth and helps with maturation of the CNS

154
Q

How do gonadal steroids affect growth

A

Systemic effect- stimulate HH release to bring about pubertal growth spurts

Increased rate of long bone growth

Local effects: sex steroids eventually trigger epiphyseal fusion to limit long bone growth

155
Q

How are glucocorticoids involved in growth

A

Growth inhibition when present in excess

156
Q

How is Insulin involved in growth

A

Essential for normal growth especially in utero

157
Q

Give 2 growth hormone disorders

What’s the difference

A

Gigantism: hyper secretion of GH before puberty

Acromegaly: hyper secretion of GH in adulthood

158
Q

How common is acromegaly

What is a common cause

A

60 per million

Pituitary tumour

159
Q

What is the clinical appearance of acromegaly

A

Increased cartilaginous growth resulting in enlarged ears and loss, growth of jaw, enlargement of hands and feet and enlargement of tongue

160
Q

What is the clinical appearance of gigantism

A

Normal proportions just very tall

161
Q

What are pituitary dwarves

How is it treated

A

GH deficiency during childhood causes reduced growth with normal body proportions

Caused by a problem with the pituitary

Treated with GH injections but must use species specific GH

162
Q

How is achondroplasia different from pituitary dwarfism

A

Achondroplasia presents with reduced growth with abnormal body proportions

Achondroplasia is caused by mutation in FGFR3

163
Q

What is a joule

A

The work done when 1N moves 1m

164
Q

What is power

1W=?

A

Rate of work

1W= 1J/s

165
Q

How many joules in a kilocalorie

A

1Kcal= 4184 joules

166
Q

What is BMR

A

Basal metabolic rate

The energy required to keep a resting awake individual alive in a thermoneutral environment

167
Q

What is required for BMR (ie how many calories)

A

1800kcal/day

168
Q

Why is the recommended guideline daily amount of calories higher than needed for BMR

A

To account for movement and environment temperature

169
Q

What is the GDA for men, women and children

A

Men: 2500
Women: 2000
Children (5-10yrs): 1800

170
Q

How can metabolic rate be measured

A

By indirect calorimetry

171
Q

What is indirect calorimetry

A

Measuring the amount of heat generated in an oxidative reaction by determining the intake of O2 or by measuring the amount of CO2 released and translating these quantities into a heat equivalent

172
Q

Describe the action of insulin and glucagon

A

Regulation of blood glucose

They act antagonistically: insulin promotes energy storage and glucagon decreases energy storage

173
Q

What are incretins

A

GLP-1 and GIP

they are peptides released by the digestive tract in response to a meal and act on the islets of Langerhans To help modulate blood glucose levels

They stimulate insulin release and inhibit glucagon production

174
Q

How is ATP used up in the body

A 
25% Na/K pump
30% RNA/DNA synthesis
25% protein synthesis
10% gluconeogenesis
5% Ca2+ pump
5% muscle contraction
175
Q

Where is GLP-1 released from

A

L cells in the GI tract

176
Q

What secretes GIP

A

K cells in duodenum

177
Q

What is the importance of incretins?

A

They cause insulin release before blood glucose changes as incretin release is stimulated by glucose in the GI tract not in the blood

178
Q

What does anoretic mean

A

Appetite suppression

179
Q

What does oretic mean

A

Appetite stimulation

180
Q

What has ablation taught us about appetite

A

Destruction of the lateral hypothalamus (LH) in rats reduced food intake

Destruction of the ventromedial nucleus (VMN) induced hyperphagia and obesity

181
Q

Who discovered leptin

What experiments did he do

A

Hervey (1956)

Parabiosis

182
Q

Describe Hervey’s parabiosis experiments

A

An obese rat (with a VMN lesion) was connected to a normal rat

The normal rat stopped eating and died of starvation

Blood born satiety factor was produced in obese rat but didn’t affect it and passed into normal rat, decreasing appetite

183
Q

How big is leptin

What produces if

A

16 kDa

White and brown adipose tissue

184
Q

The level of leptin in the blood is directly proportional to what?

A

The amount of adipose tissue in the body

185
Q

Which mice have a mutation in the leptin gene and which had a mutation in the receptor

What symptoms are common between them

A

Gene: (ob/ob) (obese=ob)

Receptor (db/db) (diabetes=db)

Symptoms: hyperphagia, obese, and increased risk of T2 diabetes

186
Q

Can leptin cross the blood brain barrier

A

Yes

The ObRa (shorter leptin receptor) binds leptin and allows leptin to cross the barrier to have an effect on the hypothalamus 
The ObRb receptor initiates a signalling cascade
187
Q

Briefly explain the parabiosis experiments with db/db and ob/ob nice

A

db/db mice have high leptin levels that act on normal and ob/ob mice to suppress feeding (usually ending with them dying of starvation)

Ob/ob mice do not make leptin so cannot influence feeding behaviour of normal mice

188
Q

How many amino acids in Ghrelin

What is it produced by

A

28

P/D1 cells and ε cells

189
Q

Where are P/D1 cells

Where are ε cells

What do they produce

A

P/D1 : fundus of the stomach

ε cells: islets of Langerhans

Produce Ghrelin

190
Q

What happens to Ghrelin levels after a meal

A

Levels fall

191
Q

How does Ghrelin act as an orectic peptide

A

Stimulates NPY/AgRP neurons in the hypothalamus

192
Q

How does Ghrelin affect GH

A

Increases GH secretion from the pituitary

193
Q

Which neurons in the arcuate nucleus are satiety neurons

A

POMC/CART

194
Q

What is the key receptor in the VMH satiety centre

A

MC3/4R

195
Q

What is the key receptor in the LH feeding centre

A

Y1/Y5 receptor

196
Q

What does α MSH do

A

Acts through MC3/4 receptor to suppress feeding

197
Q

What does a defective MC4 receptor lead to

A

Obesity

198
Q

What does NPY

A

Acts through Y1/5 receptor to stimulate feeding

199
Q

How does AgRP interact with the Mc3/5 receptor

A

AgRP is an antagonist if MC3/4 R

200
Q

How does leptin interact with NPY/ AgRP and POMC/CART

A

Leptin inhibits NPY/ AgRP neurons

Leptin stimulates POMC/ CART neurons

201
Q

What is the relationship between Ghrelin and insulin levels

A

Inverse

202
Q

How do neuronal pathways affect appetite regulation

A

Provide information about stomach distension and food digestion via vagus nerve to the dorsal Vagal complex

203
Q

What gut hormones stimulate satiety

Where are they released from

A

CCK (via vagus nerve)
Oxyntomodulin (OXM)
Peptide YY (PYY)
Glucagon-like peptide 1 (GLP-1)

Lower GI tract

204
Q

Where is pancreatic polypeptide secreted from

What is its role

A

Islets of Langerhans

Stimulate satiety

205
Q

4 treatments for obesity

A

Eat less (both in life style and via bariatric surgery)
Exercise
Restrict food absorption
Liposuction (THIS IS ONLY COSMETIC)

206
Q

By How much does bariatric surgery reduce stomach volume

A

From 1000ml to 30ml

207
Q

How is iodide pumped into follicular cells

A

SLC5A5 (sodium iodide symporter)

HOM (11 decks)

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