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ESA 2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Which pathway comes first efferent or afferent

A

Afferent->efferent

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2
Q

What is the biological rhythm set by?

A

Cicardiam rhythm

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3
Q

Where are the collection of neurones responsible for the cicardian rhythm

A

Suprachiasmatic nucleus

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4
Q

What hormone is involve in setting the biological clock?

A

Melatonin

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5
Q

Where is melatonin released from to control the biological clock?

A

Pineal gland

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6
Q

What type of feedback is the most common?

A

Negative

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7
Q

When would we want positive feedback?

A

When we want a rapid response, blood clotting, ovulation

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8
Q

What is body osmotic pressure monitored by?

A

Osmoreceptors in the hypothalamus

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9
Q

What happens if osmolality is low (hypotonic)

A

Osmoreceptors send signal to posterior pituatry to secrete less ADH

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10
Q

Is less ADH is secreted due to low osmolality what is the result?

A

Decreased reabsorbtion of H20 in collecting ducts leading to large amount of dilute urine

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11
Q

If osmolality is detected and it is high, what signals do the osmoreceptors send?

A
  1. Stimulate thirst

2. Signal to post pituatry to secrete more ADH- increasing H20 reabsorbtion in collecting ducts of kidney

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12
Q

What does insulin stimulate?

A

Uptake of glucose and glycogenesis to decrease plasma glucose levels

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13
Q

What does glucagon stimulate?

A

Glycogenolysis to increase plasma glucose levels

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14
Q

What are the 4 hormone classifications

A

Peptide
Amino acid derivative
Glycoproteins
Steroids

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15
Q

Are peptide hormones water soluble?

A

Yes

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16
Q

Are amino acid derivatives water soluble?

A

Adrenal medulla hormones are

Thyroid hormones are lipid soluble

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17
Q

Are glycoproteins hormones water soluble?

A

Yes

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18
Q

Are steroid hormones water soluble?

A

No, lipid soluble

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19
Q

Name some peptide hormones

A

Insulin,
Glucagon
Growth hormone

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20
Q

What types of amino acids are amino acid derivative hormones synthesised from?

A

Aromatic

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21
Q

Name some amino acid derivative hormones and there precursor

A

Adrenaline, noradrenaline, thyroid hormones (tyrosine), melatonin (tryptophan)

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22
Q

Are glycoprotein hormones small or large generally?

A

Large made of sub units

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23
Q

What are some examples of glycoproteins hormones?

A

TSH, FSH

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24
Q

What are steroid hormones derived from?

A

Cholesterol

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25
Q

What are some examples of steroid hormones?

A

Cortisol, aldosterone, testosterone

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26
Q

The fact that many hormones need carrier proteins gives what kind of equilibrium? Why?

A

Dynamic because the hormones bound are inactive

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27
Q

What effect do carrier proteins have on hormones?

A

Increase solubility, increase half life, create a readily available reserve

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28
Q

What 3 main factors determine the level a hormone will be in the blood?

A

Rate of production (synth and secreion)
Rate of delivery (blood flow to organ)
Rate of degradation

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29
Q

Hormones circulate at what kind of concentration?

A

Picomolar

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30
Q

What kind of receptors do water soluble hormones need? Why?

A

G coupled or tyrosine kinase because they cant cross the plasma membrane

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31
Q

Binding of adrenaline to a G protein receptor does what?

A 
Causes dissociated of alpha sub unit
Activates adenyl cyclase
CAMP activated
Activate protein kinase
Phosphorylate target
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32
Q

What happens when something like insulin binds to a tyrosine kinase receptor ?

A

Initial dimerisation
Autophosphorlyation of specific tyrosines
Recruitment of adapter proteins and protein kinase
Phosphorylation of target proteins

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33
Q

How does a type 1 lipid soluble hormones work?

A

Bind to a cytoplasmic receptor making a complex that enters the nucleus binding to dna

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34
Q

How does a type 2 lipid soluble hormone work?

A

Enters the nucleus ad binds to a pre bound receptor on the dna

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35
Q

What produces a slower response a water soluble hormone or lipid soluble

A

Lipid- has to await the transcription and translation of its target gene

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36
Q

What nucleus plays a key role in apeitite/satiety control?

A

Arcuate nucleus

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37
Q

What two types of neurones are in the arcuate nucleus?

A

Stimulators (of apetite)

Inhibitors promote satiety

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38
Q

What to the stimulators in the arcuate nucleus contain?

A

Neuropeptide Y (NPY)
Agouti-related peptide (AgRP)
Promote hunger

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39
Q

What do the inhibitory neurones in the Arcuate nucleus contain?

A

Pro-opiomelanocortin (POMC)- with alpha MSH and beta-Endorphin neurotransmitters
Promote satiety

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40
Q

What’s ghrelin? When is it released? What does it stimulate?

A

Peptide hormone
Stomach empty
The arcuate nucleus promoting hunger

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41
Q

What does leptin tell the brain?

A

Fat store levels

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42
Q

What kind of hormone is leptin? Where is it release from? What does it stimulate? What other hormone can do this?

A

It’s a peptide hormone
Released by adipocytes
Stimulates POMC in accurate to suppress apetite
Insulin

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43
Q

What is amylin? What does it do?

A

Peptide hormone from pancreas

Suppresses apetite

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44
Q

What do some obese people (very rare) have?

A

Loss of functioning leptin gene

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45
Q

Where is the thyroid gland located?

A

Below thyroid cartilage (Adams apple)

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46
Q

How many lobes does the thyroid gland have? What’s it joined by?

A

2

Isthmus

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47
Q

Where is the isthmus?

A

From the 2-3rd ring of trachea

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48
Q

What is the first endocrine to develop? When does this occur?

A

Thyroid gland

3-4 weeks gestation

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49
Q

What does the thyroid gland appear as in development?

A

Epithelial proliferation in floor of pharynx at the base of the tongue, migrating after several weeks

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50
Q

The thyroid gland migrates in development but remains connected to the tongue, how?

A

Via thyroglossal duct

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51
Q

Histilogically what can be seen in the thyroid?

A

Follicular cells in spheres called thyroid follicles

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52
Q

What are thyroid follicles filled with? What is it?

A

Colloid

A deposit of thyroglobulin

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53
Q

Despite being in the cell, what is colloid?

A

Extracellular

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54
Q

How does the parathyroid differ histilogically from the thyroid?

A

Smaller follicles

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55
Q

What do thyroid parafollicular cells produce?

A

Calcitonin

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56
Q

What cells of the parathyroid produce parathyroid hormone?

A

Chief cells

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57
Q

The parathyroid hormone is key in what

A

Calcium control

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58
Q

What’s the difference between T3 and T4 thyroid hormone

A

An extra iodine

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59
Q

What is T3 formed from

A

Monoiodotyrosine and diiodotyrosine

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60
Q

How many aromatic rings does t3/t4 have?

A

2

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61
Q

What is t4 formed form?

A

X2 diiodotyrosine

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62
Q

What is thyroglobulin?

A

The scaffold that thyroid hormone forms on

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63
Q

Thyroglobulin (134 tyrosines) - what happens to its residues?

A

They become iodinated

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64
Q

What happens to iodinated residues of thyroglobulin?

A

They undergo coupling reactions to make t3/t4, these stay attached until they need to be released

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65
Q

What 3 reactions does the enzyme thyroid peroxidase regulate?

A

Oxidation- idodide to iodine (needs H2O2)
Addition of iodine- to the tyrosine receptor residues of thyroglobulin
Coupling- MIT or DIT-> t3/4

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66
Q

Dietary iodine needs what to happen to be absorbed?

A

Reduced to iodide in small intestine

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67
Q

What are the only molecules in the body that contain iodine

A

Thyroid hormones and its precursors

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68
Q

Where is 95% of the bodies iodine

A

Thyroid gland

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69
Q

How does the thyroid get all the iodine?

A

Epithelial cells have sodium iodide symporter (iodide trap)

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70
Q

What is more active in the body t3 or t4

A

T3 4x more likely

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71
Q

What happens to 90% of t4?

A

Converted to t3 in the liver and kidneys

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72
Q

What is 80% of t3 derived from?

A

T4

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73
Q

How do t3 and t4 travel?

A

Bound to thyroxine binding globulin

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74
Q

What is the pathway of t3/4 secretion

A

Hypothalamus-> TRH-> ant pit-> TSH-> thyroid gland-> T3/4

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75
Q

What are the 2 main principal effects of thyroid hormones?

A

Metabolic pathway effects

Cellular differentiation and development

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76
Q

What type of hormone is TSH? What’s it composed of?

A

Glycoproteins

2 non covalently bonded subunits

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77
Q

What is the alpha subunit of TSH? What is the beta?

A

Alpha-FSH and LH

Beta-unique

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78
Q

How does TSH hormone cause T3/4 release?

A 
Stimulates:
Iodide uptake
Iodide oxidation
Thyroglobulin synthesis
Thyroglobulin iodisation
Colloid Pinocytosis
Proteolysis of thyroglobulin
Cell growth
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79
Q

How does TSH have such a wide range of effect?

A

Can couple Gs and Gq inducing cAMP and DAG/IP3

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80
Q

Thyroid hormones increase basal metabolic rate and heat production everywhere except?

A

Brain
Spleen
Testis

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81
Q

How does thyroid hormone increase base metabolic rate

A

By increasing mitochondria size and stimulating synthesis of enzymes in resp chain

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82
Q

What metabolic pathways does thyroid hormone predominantly stimulate

A

Catabolic-
Lipolysis + beta oxidation
Gluconeogenesis
Glycogenolysis

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83
Q

What is the so called sympathomimetics effect of thyroid hormone?

A

Increases target cells response to catecholamines by increasing number of receptors

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84
Q

What is the CVS specific effect of thyroid hormone

A

Increase cardiac output

Increase peripheral vasodilation

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85
Q

What is the nervous system specific effect of thyroid hormones

A

Increase myelination of nerves and development of neurons

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86
Q

Where are thyroid hormone receptors?

A

Nucleus

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87
Q

What modulates the gene expression that thyroid hormone has? What happens in the abscence of thyroid hormone

A

Transcription factors on specific genes (conformation change)
In abscence there is transcription repression

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88
Q

What’s goitre

A

Enlargement of thyroid gland

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89
Q

When does goitre occur?

A

When thyroid gland is overstimulated, this can be hypo or hyper thryroid is

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90
Q

What are some causes of hypothyroidism

A 
autoimmune (hashimotos)
Inadequate dietary iodine
TSH/TRH defficent
Surgical removal
Anti-thyroid drugs
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91
Q

How do you treat hypothyroidism

A

Oral thyroid hormone

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92
Q

What are symptoms of hypothyroidism

A 
Obesity
Lethargy
Cold intolerance
Bradycardia
Dry skin
Slowed reflexes
Constipation
Menorhagia
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93
Q

What would serum levels show in hypothyroidism

A

Low t3/4, high tsh

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94
Q

What are some causes of hyperthyroidism?

A

Autoimmune (graves)
Toxic multinodular thyroid
Excessive t4 therapy
Thyroid carcinoma

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95
Q

What are some symtoms of hyperthyroidism

A 
Weight loss
Irritable
Heat intolerance
Tachy
Fatigue
Increased bowel movements
Hyper-reflexia
Loss of libido
Breathless
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96
Q

What’s an anti-thyroid drug, what does it do?

A

Carbimazole
Blocks formation of thyroid hormone by preventing thyroid peroxidase
Pro drug

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97
Q

What is used in thyroid scans looking at uptake

A

Technetium 99

Short half life

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98
Q

What’s myxedema?

A

Thick puffy skin, slow speech, muscle weakness, mental deterioration seen in hypothyroid

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99
Q

What can hypothyroid cause in infant?

A

Cretinism

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100
Q

When can you feel a normal thyroid gland?

A

You can’t, if its felt its pathological

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101
Q

Why does the thyroid move with swallow?

A

Attached to tranches and larynx by pre teaches fascia

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102
Q

How can the thyroid be imagined?

A

US

Uptake scan

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103
Q

Where does thyroid development start in development

A

Foramen caecum

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104
Q

What’s a thyroglobulin duct cyst?

A

Remantents of the epithelium from development

Swelling on the midline within body of hyoid

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105
Q

Why is TSH a good screening tool for thyroid issues?

A

98% of metabolic thyroid disease is thyroid primary
Pituatry adenoma could produce excess TSH rare
Pituatry failure with just TSH change very very rare

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106
Q

What is the TSH level an indicator of?

A

What the brain thinks the thyroid function is like

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107
Q

What’s normal TSH range

A

0.505ml IU/L

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108
Q

What does the endocrine system seem to be particulary succeptible to ?

A

Autoimmune diseases

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109
Q

How can goitres be described?

A

Diffuse
Single nodule
Multinodular

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110
Q

When can normal thyroid function with goitre occur?

A

Pregnancy, menopause, menarche (1st menstruation)

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111
Q

What’s the most common GLOBAL form of goitre?

What’s the most common in the uk?

A

Iodine defficency globally

Multinodular in uk (thyroid function ok unless toxic)

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112
Q

What are symptoms of cretinism

A

Mental retardation, deaf retardation, deaf mute, short, goitre, hypothyroidism

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113
Q

What can multinodular goitres do to the trachea?

A

Enlarge inferiorly compressing trachea

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114
Q

What symptom doesn’t really fit with hypotyroidims?

A

Mennorhagia

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115
Q

What symptom doesn’t really fit with hyperthyroidism

A

Amernorhagia

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116
Q

What’s thyrotoxicosis?

A

Overproduction of thyroxine leading to anxiety, heat intolerance, shaking, palpitation, bounding pulse, lid lag and staring eyes

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117
Q

Why do you get lid lag in thyrotoxicosis

A

10% of lid control is smooth muscle,

Increase thyroxine and you get sympathomimetics

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118
Q

What’s can a toxic adenoma of the thyroid do?

A

Produce thyroxine autonomously

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119
Q

If you have a thyroid nodule but no metabolic disturbance, what should be investigated?

A

Thyroid cancer

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120
Q

The hypothalamic pituatry axis is the major linn between what 2 systems?

A

Endocrine and nervous

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121
Q

Where is the pituatry gland?

A

Beneath the hypothalamus in socket called sella turcica

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122
Q

What are some of the key functions covered by the hypothalamic pituatry axis?

A 
Body growth
Thyroid function
Adrenal gland function
Water homeostasis
Lactation
Reproduction
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123
Q

What hormones does the posterior pituatry synthesise?

A

It doesnt synthesise any hormones

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124
Q

Where does the ant pituatry arise from embryologically

A

Oral ectoderm (primary gut tissue)

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125
Q

Where does the post pituatry originate from embryologically

A

Neuroectoderm (primitive brain tissue)

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126
Q

Which part of the pituatry is connected to the hypothalamus?what connects them?

A

Post

Infundibulum

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127
Q

Where are the hormones of the posterior pituatry synthesised?

A

Oxytocin and ADH are produced in the supraoptic and paraventricular nuclei of the hypothalamus

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128
Q

Hormones from the hypothalamus to the anterior pituatry go where before being released into the hypophyseal portal system?

A

Down axons and stored in median eminence

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129
Q

The hormones secreted from the ant pituatry exert effects in what way?

A

Endocrine
Autocrine
Paracrine

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130
Q

The hypophyseal portal system affects the endocrine cells of where?

A

Ant pituatry

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131
Q

The pathway between the hypothalamus and post pituatry is considered what?

A

Direct

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132
Q

The hypo-post pituatry system has what hormones, with what effects?

A

oxytocin- uterus contraction and milk

ADH/Vasopressin- regulate body water volume

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133
Q

What are tropic hormones

A

Hormones that affect the release of other hormones

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134
Q

What are the hormones released by the hypothalamus to the ant pit

A 
TRH
PRH
PIH
CRH
GnRH
GHRH
GHIH
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135
Q

What’s TRH what does it modulate?

A

Thyrotropin releasing hormone

Modulates release of TSH

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136
Q

What’s PRH what does it regulate?

A

Prolactin releasing hormone

Positive control of prolactin release

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137
Q

What’s PIH what does it modulate? What else is it called

A

Prolactin release inhibition hormone.
Negative control of prolactin
Dopamine

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138
Q

What’s CRH, what does it regulate

A

Corticotropin releasing hormone

Regulates release of ACTH

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139
Q

What GnRH, what does it regulate

A

Gonadotropin releasing hormone

Regulates leutanising hormone and follicle stimulating hormone

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140
Q

What GHRH

A

Growth hormone releasing hormone

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141
Q

What’s GHIH

A

Growth hormone inhibiting hormone

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142
Q

What hormones are produced in the anterior pituatry?

A 
TSH
ACTH 
LH
FSH
Prolactin 
Growth hormone
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143
Q

What does TSH stand for?

A

Thyroid stimulating hormone

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144
Q

What does ACTH stand for?

A

Adrenocorticotropic hormone

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145
Q

What does LH stand for

A

Leutinising hormone

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146
Q

What is the affect of ACTH release?

A

Secretion of hormones from adrenal cortex

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147
Q

What does LH release stimulate

A

Ovulation and secretion of sex hormones

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148
Q

What does FSH stimulate

A

Egg and sperm developement

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149
Q

What does prolactin stimulate

A

Mammary gland development and milk secretion

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150
Q

What does growth hormone stimulate

A

Growth and energy metabolism and IGFs

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151
Q

What must happen for proper folding of growth hormone

A

Signal peptide cleavage

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152
Q

What is secreted from where in response to GH

A

Insulin like growth factors from liver and skeletal muscle

153
Q

What does growth hormone stimulate in childhood?

A

Long bone growth (length and pre-epiphyseal closure)

Cartilage growth

154
Q

In adults what does GH do?

A

Maintains muscle and bone mass and promotes healing and repair

155
Q

How is growth hormone mainly controlled?

A

Growth hormone releasing hormone and somatostatin (GHIH)

156
Q

What can alter the release of GHRH/somatostatin explaining why we get variations in levels

A 
CNS regulation
Surge with deep sleep
Decrease with R.E.M. Sleep
Increase with stress
Increase with exercise
Low glucose or fatty acids increase it
High glucose or fatty acids decrease it
157
Q

How is GHRH regulated?

A

IGFs inhibit release of GHRH and stimulate soomatostatin

GH itself stimulates somatostatin release

158
Q

What does low GH in childhood result in

A

Dwarfism (proportionate)

159
Q

Growth hormone excess in children results in what?

A

Gigantism

160
Q

Growth hormone excess In adults results in what?

A

Acromegaly

161
Q

At a cellular level what does GH cartilage to stimulate IGF production?

A

Janus Kinases

162
Q

What’s the major growth factor in adults?

A

IGF1

163
Q

What’s the major growth factor in fetal growth

A

IGF2

164
Q

What do IGF receptors modulate?

A

Hypertrophy, hyperplasia, protein synthesis rate, lipolysis rate

165
Q

What happens with GH and hybrid receptors?

A

Cross over receptors respond to insulin and IGf1

Result in mitogenic and metabolic effects

166
Q

What other hormones, asides from GH influence growth

’

A 
Insulin
Throid hormones
Androgens
Estrogens
Glucocorticosteroids
167
Q

What hormones influence somatic growth?

A

Insulin increases

Estrogen and glucocorticosteroids inhibit

168
Q

How do thyroid hormones influence growth

A

Enhance GH secretion

169
Q

What effect do androgens have on growth?

A

Accelerate pubertal growth
Close epiphyseal plates
Increase muscle mass

170
Q

How do pituatry tumours present as a result of…

A

Mass effect or

Abnormal pituatry function

171
Q

What important structures surround the pituatry gland?

A

Optic chiasm
Occulomotor nerve
Trochlear nerve
Internal carotid artery

172
Q

A pituatry tumour with superior growth would impede on what? What would this cause?

A

Optic chiasm

Bitempora hemianopia

173
Q

A pituatry tumour exerting lateral mass effect will cause what?

A

Pressure on trochlear and occulomotor nerve causing double vision

174
Q

Hypopituatrism results in down regulation of what and up regulation of what?

A

Down regulation of those under positive control

(GH, LF/FSH, TSH, ACTH) up regulation of negative controlled prolactin

175
Q

An early pituatry tumour is likely to manifest in what?

A 
Ganadotropin defficeny
(GH, FSH, LH)
176
Q

A early pituatry tumour has what characteristic features?

A

Loss of secondary sexual characteristic, loss of periods in women

177
Q

An early pituatry hormone affects GH, LH, FSH, what would the next likely deficit be as the tumour develops?

A

TSH deficency

178
Q

What would the blood serum look like in someone with TSH defficency due to a pituatry tumour?

A

Low TSH, low T3/4

179
Q

What is a dangerous complication of a pituatry tumour?

A

If it progresses to ACTH deficency- low cortisol- life threatening

180
Q

Tumours that cause hyperpituatry functions- what are common manifestations?

A

High prolactin, Gh or ACTH

181
Q

What are rare elevations due to hyperpituatry functions/

A

TSH, LH/FSH

182
Q

When testing the pituatry axis, when are basal blood tests sufficient?

A

When lookin at the thyroid axis, gonadal acids and prolactin axis

183
Q

When are dynamic blood tests needed in the pituatry axis tests

A

Adrenal axis and GH axis

184
Q

How do you look for a defficency in the adrenal or GH axis?

A

You stimulate the release of the hormone and measure response

185
Q

How do you test for the excess of hormone from adrenal axis or Gh axis?

A

You suppress them and see the outcome

186
Q

How do you test for adrenal deficency ?

A

Either by ACTH stimulation or a hypoglycaemic stress test, both should induce adrenal work

187
Q

How do you test for excess adrenal stimulation?

A

You suppress them with steroids. If there axis is normal they will feel rotten

188
Q

How do you test for a deficency in GH

A

Insulin stress test

189
Q

How do you test for GH axis excess

A

Suppress GH axis with glucose, test levels

190
Q

Why do you get bitemporal heminopia?

A

Chiasmal lesion affecting the right and left TEMPORAl fields only

191
Q

How do you treat a prolactinoma?

A

Dopamine agonist (dopamine inhibits prolactin)

192
Q

Who presents late with a prolactinoma?

A

Men as they have no menstrual disturbance

193
Q

What are some symptoms of prolactinoma

A

Menstrual disturbance
Fertility issues
Galactorhoeas

194
Q

If the prolactin is over 5000 what is it very likely to be

A

Prolactinoma

195
Q

If the prolactin is less than 5000, what might it be instead of prolactinoma

A

Stalk effect

196
Q

What is stalk effect in relation to raised prolactin

A

Prolactin is under tonic inhibitory control by dopamine

If you block the stalk prolactin will raise

197
Q

What can cause high prolactin that isn’t a prolactinoma and isn’t stalk effect/

A 
Pregnancy
Dopamine agonists (anti psychotics)
198
Q

How does a non functioning pituatry adenoma present?

A

Symptoms of mass effect or low pituatry hormones (other than prolactin)

199
Q

What does a GH secreting pituatry tumour cause?

A

Acromegaly

200
Q

What are some long term complications of a GH secreting pituatry tumour?

A

CV death, colonic tumours, disfiguring body changes, HTN, diabetes

201
Q

How would you test for a GH secreting pituatry tumour?

A

Oral glucose tolerance test

GH day curve

202
Q

What’s the treatment for a GH secreting tumour?

A

Surgical removal
Dopamine agonist (decrease GH secretion)
Somatostatin analogues
GH receptor blockers

203
Q

Cushing disease (not syndrome) is a result of what

A

ACTH secreting pituatry tumour

204
Q

What symptoms come wth Cushing disease

A 
Round pink face
Round abdomen
Skinny weak arms
Thin skin
Striae of abdomen
HTN
Diabetes
Osteoporosis
205
Q

What can Cushing syndrome be a result of?

A

Adrenal tumour, actopic ACTH, steroids

206
Q

What’s diabetes insipidus

A

Large quantities of pale urine and extreme thirst.

Inhibition of ADH

207
Q

Pituatry disease resulting in defficency of vasopressin is termed what

A

Cranial diabetes insipidus

208
Q

Vasopressin resistance due to kidney disease is termed what?

A

Nephrogenic diabetes insipidus

209
Q

What does untreated diabetes insipidus result in?

A

Very high sodium levels, severe dehydration, coma, death

210
Q

What is a pituatry apoplexy

A

Acute stroke/vascular event in pituatry tumour

211
Q

What symptoms come with pituatry apoplexy?

A

Headache, double vision, visual field loss, cranial nerve palsy
Hypopituatrism with cortisol deficency being the main danger

212
Q

In the peripheral nervous system where do afferent branches go?

A

Towards the brain

213
Q

In the peripheral nervous system where do efferent branches go?

A

Away from the brain

214
Q

Where is the hypothalamus located?

A

Diencephalon

215
Q

Where is the medulla oblongata located?

A

Brain stem

216
Q

What are regions of the medulla involved in controlling?

A

Ventilation and cardiovascular system

217
Q

What is ‘hunting behaviour’ in relation to negative feedback?

A

The tendency to overshoot the normal value, indicative of a dynamic equilibrium

218
Q

How is ovulation an example of positive feedback

A

Build up of FSH causes release of oocyte from follicle in ovary

219
Q

What should always be noted when testing cortisol levels?

A

The time

220
Q

How long is a humansdiurnal cycle?

A

24 hours 11 minutes

221
Q

What are zetigebers

A

Environmental ques that keep us on a 24 h cycle

222
Q

What happens if there is a mismatch between zeitgebers and the diurnal cycle

A

Jet lag

223
Q

What % of lean body weight is
Intracellular fluid
Extracellular fluid
Blood plasma

A

35%
12%
5%

224
Q

What hormones are normally stored within the cell?

A

Polypetide

Catecholamines

225
Q

Steroid hormones arent stored in cells that produce them, but what is?

A

Cholesterol

226
Q

What hormone concentration matters?

A

Free hormone

227
Q

What do trophic hormones do?

A

Stimulate growth in target tissue

228
Q

How are steroid hormones excreted?

A

Small chemical structure change making them water soluble-excreted in urine and bile

229
Q

How are protein hormones excreted?

A

Undergo extensive chemical changes and are degraded to amino acids that are reused for protein synthesis

230
Q

What POMC

A

Pro-opiomelanocortin

231
Q

What is POMC cleaved into?

A

Beta endorphin
ACTH
Alpha melanocytes stimulating hormone

232
Q

What does alpha melanocytes stimulating hormone (from POMC) do?

A

Acts on mealocortin 4 receptors to suppress apetite

233
Q

What is beta endorphins action?

A

Prince euphoric, tired feeling after a meal

234
Q

What does stretch of the stomach wall inhibit?

A

Ghrelin release

235
Q

How does leptin produce heat?

A

Induces expression of uncoupling proteins in mitochondria

236
Q

What two nerves are in close proximity to the thyroid gland?

A

Recurrent laryngeal

External branch of superior laryngeal

237
Q

What cells are present in the thyroid gland?

A

Follicular and parafollicular

238
Q

When are higher levels of TSH released?

A

Night

239
Q

What trophic effects does TSH have

A

Increase vascularity, size and number of follicle cells

240
Q

In hashimotos disease what is happening?

A

Destruction of thyroid follicles or production of antibody that blocks TSH receptors

241
Q

In Graves’ disease what is happening?

A

Antibodies produced that stimulate TSH receptors on follicle cells

242
Q

What is the hypothalamus-> post pituatry a classic example of?

A

Neurocrine signalling

243
Q

What is the release of hormone from post pituatry into systemic circulation regulated by?

A

Neuronal inputs into hypothalamus

244
Q

What does ADH induce to allow more reabsorbtion of water?

A

Translocation of aquaporin channels in the duct cells

245
Q

What hormone is particulary important in resorting BP in hypoboelemic shock?

A

ADH

246
Q

What cells produce growth hormone?

A

Somatotrope cells

247
Q

What loops does GH secretion have to control its release?

A

Long and short

248
Q

What is the long loop in growth hormones release?

A

IGF mediated inhibition of GHRH release and stimulated release of somatostatin.

249
Q

What is the short loop of GH release?

A

GH itself stimulating somatostatin

250
Q

What’s the most common cause of pituatry malfunction?

A

Benign tumour (adenoma)

251
Q

What are the anatomical divisions of the adrenal gland?

A
  1. Capsule
  2. Cortex- GFS, glomerulosa, fasciculata, reticularis
  3. Medulla- chromaffin cells
252
Q

What hormones are produced by the adrenal gland and from where?

A 
Salt, sugar, sex, excitement (deeper=better)
G- mineralcorticoids (aldosterone)
F- glucocorticoids (cortisol)
R- androgens 
Medulla- Arenaline and noradrenaline
253
Q

Describe the structure of steroid hormones?

A

Cholesterol basis. Lipid soluble

254
Q

How do steroid hormones affect target tissue?

A

Modulate gene transcription via nuclear receptors

255
Q

How do glucocorticoids affect target tissue

A
  1. Bind to receptor causing dissociation of chaperones
  2. translocate into nucleus
  3. Bind to glucocorticoid response element (GRE) or transcription factors
256
Q

How is cortisol secretion controlled?

A

Hypothalamus-> CRH-> ant pit-> ACTH-> adrenal cortex-> cortisol (negative feedback on CRH and ACTH)

257
Q

How does increased ACTH lead to hyperpigmentation?

A

Low cortisol causes increased production of ACTH
ACTH is made from POMC peptide. Other fragment of peptide is MSH (melanin stimulating hormone) also high ACTH directly stimulates melanin synthesis

258
Q

What are the main physiological actions of cortisol?

A 
Proteolysis
Increased gluconeogensis
Increased lipolysis
Inhibition of glut 4 receptors 
Increase sensitivity to vasoconstrictors
Anti Inflam (inhibit macrophage and mast cell degranulation)
Immune suppression
259
Q

What is the structure and function of adrenaline

A

It’s a dopamine based structure involved in fight or flight responses

260
Q

What is made in the zone reticularis

A

Androgens
Androstenedione- becomes oestrogen and testosterone
Dehydropiandrosteone

261
Q

What is made in the zona fasculata

A

Glucocorticoids

Cortisol, corticosterone, cortisone

262
Q

What is made in the zona glomerulosa?

A

Aldosterone

263
Q

What are glucocorticoids, mineralcorticoids, androgens, oestrogen, progestin?

A

Steroids

264
Q

How is alodesterone transported in the blood?

A

Bound to albumin and to a lesser extent transcortin (mainly takes cortisol)

265
Q

What does aldosterone do?

A

Promotes expression of Na/K pump in distal tubule and collecting duct of nephron

266
Q

What is the cause of high aldosterone with low renin?

A

Primary- bilateral idiopathic adrenal hyperplasia or conns syndrome ( adrenal adenoma)

267
Q

What’s the cause of high aldosterone with high renin?

A

Secondary- renal artery stenosis or a renin producing tumour

268
Q

How can you differentiate between primary and secondary hyperaldosterone?

A

Renin levels. Low if it’s primary. High in secondary

269
Q

What are signs of hyperaldosterone?

A 
High bp
LVH
High Na
Low K
Stroke
270
Q

What is the treatment for hyperaldosterone?

A

Adenoma surgery if that is the cause

Sprironalactone- mineralcorticoids antagonist

271
Q

How does cortisol travel in the blood?

A

Bound to transcortin

272
Q

Why are corticosteroids useful as medication?

A
  1. Anti-inflam- inhibit macrophages and mast cell degranulation
  2. Immune suppression
273
Q

Chronic high levels of cortisol has what effect on fat?

A

Redistribution to stomach, buffalo hump and moon face

274
Q

What is Cushing? What are the overarching sources/causes?

A

Chronic high cortisol

External (glucocorticoid) endogenous

275
Q

What are some endogenous causes of Cushing?

A

Cushing disease- pituatry tumour secreting ACTH
Adrenal Cushing- adrenal adenoma secreting cortisol
Ectopic- somewhere else making cortisol like lung SMC

276
Q

What’s the most common cause of Cushing?

A

Corticosteroid use

277
Q

What is Addison’s disease? What is the most common cause?

A

Chronic adrenal insufficency

Autoimmune

278
Q

What are some symptoms of Addison’s disease?

A

Lethargy, anorexia, weight loss skin pigmentation, hypoglycaemia, hypotension

279
Q

What is an Addison’s crisis? Why does it happen? What are symptoms?

A

Life threatening adrenal insufficency-
Extremely low cortisol and high acth. Could be due to Addison’s or coming off steroids quickly (adrenal suppressed)
Vomiting, hypotension, nausea, pyrexia

280
Q

What is the timeline of adrenaline synthesis?

A

Tyrosine-> LDOPA-> Dopamine-> noradrenaline-> adrenaline

281
Q

What enzyme converts noradrenaline to adrenaline?

A

N methyl transferase

282
Q

What does an alpha 1 GPCR do?

A

Activate phospholipsae C
Cleave pip to ip3 and dag
Activating PKC and calcium via Ip3

283
Q

What do beta 1 and beta 2 receptors do?

A

Positive effect on adenyl cyclase-> Camp-> PKA

284
Q

What does an alpha 2 GPCR do

A

Negative effect on adenyl cyclase

285
Q

What receptors in lung and heart

A

We have 1 heart and 2 lungs
Beta 1 heart
Beta 2 lungs

286
Q

What receptors are on skin and gut? What happens when noradrenaline stim?

A

Alpha 1- vasoconstriction

287
Q

What receptors for adrenaline on skeletal muscle vessels?

A

Beta 2- dilation

288
Q

How does adrenaline increase HR

A 
Stimulates beta 1 receptor
Increase ardenyl cyclase therfore activate cAMP and PKA
CAMP-  HCN activation
PKA- HCN and L type calcium channel 
Speeds up funny current
289
Q

What’s a pheochromocytoma

A

Chromaffin tumour secreting adrenaline

290
Q

What are symptoms of pheochromocytoma

A

Extreme HTN, Palpitation, headache, anxiety, sweating

291
Q

Secretions from islets of langerhann enter what blood vessel?
What is the pancreas anterior to?
What is the pancreas superior to?

A

Portal vein for endocrine excretion
Aorta
Duodenum

292
Q

What are the 2 functions of the pancreas?

A

Exocrine- digestive enzymes to duodenum

Endocrine from islets of langerhann (1% of tissue)

293
Q

The endocrine hormones are what type of hormone??

What are the 7 and there corresponding cells?

A

Polypeptide hormones

  1. Insulin- beta cells
  2. Glucagon- Alpha cells
  3. somatostatin- delta cells
  4. Pancreatic polypeptides- PP cells
  5. Ghrelin- E cells
  6. Gastrin- G cells
  7. Vasoactive intestinal peptide-VIP cells
294
Q

In apetite control what do AgRP and NPY do?

What does alpha MSH do? Where is it from

A

AgRP and NPY promote hunger

Alpha MSH promotes satiety (from POMC)

295
Q

What hormones in particular affect hunger? What are they?

A

Insulin and leptin inhibit hunger

Ghrelin and PYY (SI) promote hunger

296
Q

What tissues does insulin target?

What about glucagon

A

Insulin- liver, skeletal muscle and adipose

Glucagon- liver and adipose

297
Q 
What are plasma glucose levels?
What are they after a meal?
What's the renal threshold?
What fasting level is indicative of DM?
What random level is indicative of DM/
A 
3-3.6 normal level
Up to 7-8 after a meal
10 is the renal threshold
Fasting above 7
Random above 11.1
298
Q

What are some key features of both insulin and glucagon?

A

Water soluble
Half lives of 5 mins
Cell surface receptors
Receptors become internalised cone activated

299
Q

What properties does insulin have?

What is its structure?

A

It’s anti lipolytic and anti ketogenic

A chain and B chain with 2 disulphide bonds and a 3rd within the A chain

300
Q

How is insulin synthesised?

A

Preproinsulin enters the ER, leaves as proinsulin where it goes to the Golgi, cleaved into proinsulin and c peptide, in vesicles near cell surface membrane

301
Q

How is insulin secreted?

A

Glucose enters cell via glut 2, ATP rises which inhibits the potassium channel (keeping cell hyperpolarised), cell depolarises, calcium influx leading to vesicle release

302
Q

Describe the insulin receptor?what action does it have?

A

Dimer of 2 sub-units made of alpha and beta
When activated it caused insertion of glut 4 receptor to cell. Glycogenesis stim, fatty acid synthesis and affects pyruvate

303
Q

What’s the effect of insulin in the liver, muscle and adipose?

A

Liver- increase glycogen, inhibit AA breakdown
Muscle- increase uptake of AA for protein synthesis
Adipose- increase storage of triglycerides

304
Q

What are the effects of glucogen?

What cells

A

Alpha cells

Glyconeolytic, glucogenic, lipolytic and ketogenic

305
Q

What are the rapid effects of GLu/Ins?

A

Glucose uptake and glycolyis

306
Q

What are the intermediate effects of INS/GLU?

A

Glucogenesis, glycogenesis, glycogenolysis

307
Q

What are the slow effects of INS/GLU

A

Lipogenesis, lipolysis, ketogenesis

308
Q

Increased insulin results in what?
Decreased insulin results in what?
Increase glucagon?
Decrease glucagon?

A

Increase INS hypoglycaemia, decrease INS- hyperglycaemia

Increase GLU worsens DM decrease GLU Hypoglycaemia

309
Q

T1DM is usually due to what? When can you get relative B cell destruction?

A

Autoimmune destruction of B cell

Relative due to abnormal K pump

310
Q

What is the issue in T2DM

A

Normal insulin but a decrease in sensitivity peripherally, or an excessive release of glucagon

311
Q

What are some common complications of DM

A 
Kidney disease
Amputation
CVD-stroke, CAD
Retinopathy
Neuropathy
Nephropathy
312
Q

What is metabolic syndrome?

A 
Cluster of increased waist size + 2 or more:
Increase triglycerides
Decreased HDL
Increased BP
Increased fasting glucose/ diabetes
313
Q

What are symptoms of hyperglycaemia?

A

Polyuria
Polydipsia
Blurring of vision
UTI

314
Q

What are some symptoms of inadequate energy utilisation seen in T1DM

A

Tiredness, weakness, lethargy, weight loss

315
Q

HBA1c test for what?

A

DM

6.5% and above

316
Q

Type 1 onset is characterised by what?

A

Rapid onset
Weight loss, polyuria, polydipsia
If doesnt present then could be vomiting due to ketoacidosis

Patient is usually young with raised plasma glucose and ketones

317
Q

Type2 DM onset is characteristed by what?

A

90% overweight
Often asymptomatic and picked up on general health check
May have symptoms of polyuria, polydipsia and weight loss

No urinary ketones but raised plasma glucose

318
Q

How do the management of type 1 and 2 DM differ?

A

Type 1- insulin injection

Type 2- begin with exercise and diet change, progress to metformin tablets, progress to insulin

319
Q

Hyperglycaemia results in what for T1DM and what for T2DM

A

T1- ketoacidosis

T2- hyperosmolar non ketotic syndrome

320
Q

Hypoglycaemia results in what?

A

Coma

321
Q

What are 4 key components of a control system?

A

Communication
Control centre
Receptor
Effector

322
Q

What hormones are lipophillic and require specialist transport proteins

A

Steroid and thyroid

323
Q

How does a hydrophilic hormone elicit a repsonse

A

Via a 2nd messenger from cell surface receptors

324
Q

What hormones are hydrophilic?

A

Proteins and catecholamines

325
Q

What is cytoplasmic NADPH production used for?

A

Biosynthesis
Detoxification
Recycling of oxidised glutathione
C5 production for nucleotides

326
Q

What does an enzyme activity of 1.3 U/g haemoglobin mean?

A

1 unit of enzyme activity is the amount of enzyme that will catalyse the transformation of 1 µmol of substrate per min at optimal conditions

So for haemoglobin it means that for every gram of haemoglobin there will be enough G6PDH to catalyse the oxidative decarboxylation of 1.3µmol of glucose 6 phosphate per min

327
Q 
e normal activities of glucose 6-phosphate dehydrogenase in
different tissues (U/g) are:
Red blood cells 13
Liver 1
Adipose tissue 1.5
Skeletal muscle 0.01
Brain 0.2
How do you account for these differences?
A

Red blood cells - maintenance of protein –SH groups. Liver - lipid synthesis and detoxification reactions. Adipose tissue – lipid synthesis. Brain – synthesis of lipids. Skeletal muscle - no major requirement

328
Q

What drugs can have a serious effect on individuals with G6PDH defficency? Why?

A

Primaquine, aspirin, sulphonamides

They oxidise celllular glutathione which under normal conditions would be recycled back by glutathione reductase, which requires NADPH from PPP

329
Q

Why does GSPDH cause Heinz bodies

A

Haemoglobin and other proteins become cross linked by disulphide bonds resulting in insoluble aggregates.
Disulphide bonds due to oxidative damage as glutathione not reduced by NADPH and glutathione reductase

330
Q

Other than red blood cells where else is likely to get damaged in G6PDH defficency?

A

Lens of eye as requires adequate NADPH to protect against oxidative damage. This can cause damage to the lens (cataracts) caused by denatured crystalline protein

331
Q

What stimulates increased t3.4 release?

A

Stress and fall in temp

332
Q

TSH affects what cells?

A

Follicular cells of thyroid

333
Q

How is TSH released?(pattern)

A

Low amplitude pulses following diurnal rhythm

Higher levels durin night and low in early hours

334
Q

What effect does TSH have to cause goitre

A

Trophic

335
Q

What does t3/4 travel bound to?

A

Thyroxine binding globulin, pre albumin and albumin

336
Q

How do thyroid hormones increase heat?

A

The increased rate of protein synthesis stimulates oxidative energy metabolism in the target cells to provide the extra energy required for protein synthesis. In addition, protein synthesis produces increased amounts of specific functional proteins leading to increased cell activity and an increased demand for energy.

337
Q

How do t3 and 4 increase metabolic rate?

A

T3 and T4 increase the metabolic rate of most tissues, stimulate glucose uptake and metabolism, stimulate mobilisation and oxidation of fatty acids and stimulate protein metabolism. Their metabolic effects are generally catabolic and lead to an increase in BMR, heat production and increased oxygen consumption.

338
Q

What specific effects does t3/4 have on
Bone
Heart muscle
CNS

A

Bone- directly affect bone mineralisation
Heart- increase protein synthesis of heart muscle protein
CNS- development of cellular processes of nerve cells, hyperplasia of cortical neurone and myelination of fibres

339
Q

Hypothyroidism symptoms? And why

A

Weight gain due to reduced BMR.
Cold intolerance due to reduced BMR.
Lethargy/tiredness due to reduced uptake of nutrients by
muscle.
Bradycardia – slow heart rate due to reduced responsiveness
to catecholamines and reduced heart muscle protein
synthesis.
Dry skin and hair loss due to reduced synthesis of proteins.
Slow reflexes and clumsiness due to reduced sensitivity to
catecholamines.
Constipation due to reduced responsiveness of GI tract
Hoarse voice.

340
Q

Symptoms of hyperthyroidism?

A 
Weight loss
Heat intolerance
Irritability
Tachy
Fatigue
Increased bowel movement
Menstrual disturbance
Hyper reflexive
Possible tremor
341
Q 
Weight loss
Heat intolerance
Irritability
Tachy
Fatigue
Increased bowel movement
Menstrual disturbance
Hyper reflexive
Possible tremor
Why do these occur in hyperthyroidism
A

Catabolic effects of T3 on tissue metabolism increasing metabolic rate
Effect of catecholamine sensitivity
Bone and nervous system specific effects

342
Q

What does somatostatin inhibit

A

Release of GH

343
Q

When is CRH secreteed?

A

Response to physical (temp and pain)
Chemcical (hypo)
Emotional stressors

344
Q

Why can cortisol have androgen like effects at high concentrations?

A

Binding domains have 60% sequence homology- therefore can bind to have limited activation

345
Q

What is steroid diabetes?

A

Due to the increased proteolysis and gluconeogensis in high coricosteroid doses hyperglycaemia can develop

346
Q

Why do you get purple striae in Cushing

A

Reflects the catabolic nature- catabolic effect on protein structure

347
Q

Why do you get HTN in Cushing

A

Mineralcorticoids effects may produce sodium retention

348
Q

Why do you get postural hypotension in Addison’s?

A

Fluid depletion due to lack of aldosterone

349
Q

What is the onset of addisons normally like?

A

Insidious non specific symptoms of tiredness, muscle weakness, anorexia, weight loss, dizziness

350
Q

How would an addisonian diseased person react to stress?

A

May not be appropriate as adrenal steroids likely not working properly
May lead to addisonian crisis

351
Q

What’s the treatment of addisonian crisis

A

Fluid replacement 5% dectose in saline

Cortisol

352
Q

Signs and symptoms of type 1 diabetes

A 
Hyperglycaemia
Glycosuria
Polyuria
Polydipsia
Weight loss
Ketoacidosis
353
Q

What does ketoacidosis occur in T1DM

A

Increase rate of lipolysis therefore large amounts of fatty acids
Activation of ketogenic enzymes

354
Q

What are some of the long term consequences of persistent hyperglycaemia

A

Macrovascular: increased risk of stroke and mi, poor circulation

Microvascular:
Eye disease-glaucoma, retinopathy, cataracts
Nephropathy
PVD
Diabetic foot
355
Q

How much calcium in the body roughly? How much in bone? As what?

A

1000g, 99% in bone as hydroxyapatite

356
Q

What’s our dietary intake, how much is lost in the GI, how much is entreated in the day through urine

A

1000mg, 825 lost in the GI 175 lost in urine

357
Q

What 3 hormones control calcium regulation?
Add a + if they increase plasma levels
And a - if they decrease plasma levels

A

PTH +
Calcitrol +
Calcitonin -

358
Q

What is PTH action?

A

Releases calcium into circulation (encourage osteoclast activity)
Increases calcium reabsorbtion in the kidney
Causes hydroxylation of D3 to calcitrol

359
Q

What does calcitrol do? What stimulates it

A

Increases intestinal absorbtion and renal reabsorbtion, stimulated by PTH

360
Q

What’s calcitonins action? Where is it produced

A 
Counteracts PTH (pretty minimal) 
Made in C cells/ parafollicular cells of the THYMUS
361
Q

Where is PTH secreted form?
How does it travel in the blood?
What is its half life?

A

Chief cells of parathryroid
No serum binding protein
4.5 minutes

362
Q

How is PTH regulation controlled?

A

Controlled by calcium levels. Low levels increase gene transcription and prolong the survival of the mRNA
High levels- Calcium binds to GPCR and Q subunit caused IP3 to increase intracellular calcium that inhibits PTH secretion

363
Q

Where does PTH exert its effects? What does it do at each site?

A

Bone- increases resorption
Gut- activated vit D to increase GI uptake
Kidney- decreases loss of calcium

364
Q

What are the 2 functions of bone?

A

Structure and maintaining calcium concentration in the plasma

365
Q

How does PTH increase plasma calcium in regards to bone?>

A

Stimulates osteolysis

Induces cytokine release from osteoclasts

366
Q

What is a key effect the PTH hormone has on the kidney? Both to increase calcium levels but decrease risk of kidney stones

A

Increase calcium reabsorbtion and inhibit phosphate reabsorbtion

367
Q

How do we get calcitrol?

A

Conversion of cholesterol with sunlight
Diet d3 (yeast and dairy)
Diet D4 (fungi)
Conversion via PTH

368
Q

How doe calcitrol travle in the blood, whats its half life?

A

Bound to CBP

.25 days

369
Q

What symptoms are assocaited with hypocalcaemia? What is a key principle to do with low calcium

A

Decreased calcium brings nerve tissue closer to threshold

Pins and needles, tettany, paralysis, convulsions

370
Q

What is hyperthyroidism associated with

A

Stones, moans and groans

371
Q

In the blood, what is calciums role?

A

Clotting factor IV

372
Q

What is used in blood for blood transfusions to stop the blood clotting? What’s the relevance of that?

A

Citrate

If a patient recieves many blood transfusions they also need calcium

373
Q

What are some key clinical causes of hypercalcaemia

A

Malignant osteolytic bone met
Multiple myeloma
Adenoma

374
Q

What are 5 cancers that mainly cause bone mets?

Which are osteolytic and which are osteoblastic

A 
Prostate- blastic
Breast- lytic 
Lungs
Renal
Thyroid
375
Q

Where are the main site of bone mets?

A

Femur, vertabrae, pelvis, humerus, skill

376
Q

What’s a primary hyperparathyroidism? What would the serum show?

A

Primary adenoma of the parathyroid
Raised serum calcium (pth action)
Low serum phosphate (pth action)
High alkaline phosphotase (osteolytic

377
Q

What’s secondary hyperparathyoidism? What’s the cause? What would serology show

A

Low vitamin D
Low serum calcium
High PTH
Bone pain due to osteolysis ++

378
Q

What are 2 signs of hypocalcaemia? Tests

A

Carpopedal spasm

Chvostek Sign

379
Q

What’s the difference between osteomalacia and osteoporosis

A

Porosis the proportion of mineral to matrix is normal, there’s just less of it and therefore brittle
Malaria, there is not enough mineral , and therefore bendy

ESA 2 (10 decks)

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