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Year 2 Endocrine > Physiology > Flashcards

Physiology Flashcards

1
Q

What are the four types of receptors?

A

Ligand Gated
G protein coupled
Tyrosine-kinase
Nuclear

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2
Q

What agonists work on ligand gated ion channels/

A

Neurotransmitter

Hormones

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3
Q

What is the difference between a neurotransmitter and a hormone?

A

They can be the same substance, neurotransmitters are released across synapse from a nerve.

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4
Q

What occurs after agonist binds to the ion channel?

A

Conformational change in structure.

Ions allowed to pass through membrane.

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5
Q

How quick is the response in ligand gated ion channels?

A

Milliseconds

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6
Q

How quick is the response in G protein coupled receptors?

A

Seconds

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7
Q

In a G protein coupled receptor describe the structure of the G proteins?

A

Alpha subunit attached to a GDP

Beta and Gamma subunits bound in a dimer

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8
Q

In B2 adrenoreceptor what. type of G protein is present?

A

Gs alpha

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9
Q

Upon binding of adrenaline to B2 adrenoreceptor what occurs?

A

Conformational change of the receptor.
GDP is swapped for charged GTP on the alpha subunit.
Alpha subunit breaks away and binds to adenyl cyclase

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10
Q

What does adenyl cyclase do?

A

Converts ATP to cAMP

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11
Q

What is cAMP?

A

A cell signalling molecule?

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12
Q

In B2 adrenoreceptors what does an increase intracellular cAMP do?

A

PKA is activated
Inhibits MLCK activity
Bronchodilation

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13
Q

In G coupled protein receptors why does the reaction stop?

A

Weak bond between agonist and receptor.

GTP is hydrolysed breaking bond between alpha submit and adenyl cyclase

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14
Q

In A2 adrenoreceptors what is the difference in adenyl cyclase?

A

Adenyl Cyclase is active before activation

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15
Q

What G protein alpha subunit is present in A2 adrenoreceptors?

A

Gi (Inhibits)

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16
Q

What occurs after agonistic binding to receptor in A2 adrenoreceptors?
Alpha subunit only

A

Alpha subunit is activated by GTP.
B
Alpha subunit binds to adenyl cyclase inhibiting it.

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17
Q

What occurs after agonistic binding to receptor in A2 adrenoreceptors?
Beta and Gamma subunits only

A

The dimer binds to K+ channels

Cell membrane becomes hyperpolarized

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18
Q

What is the resultant action upon A2 adrenoreceptor activation?

A

Smooth muscle relaxation especially in GI tract

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19
Q

In alpha 1 adrenoreceptors what G subunit is present

A

Gq

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20
Q

What does the activated alpha subunit do in A1 adrenoreceptors?

A

Activates phospholipase C

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21
Q

What is the function of phospholipase C in regards to A1 adrenoreceptors?

A

Converts PIP2 into DAG and IP3

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22
Q

What does an increase in intracellular DAG and IP3 result in?

A

Increase in intracellular Ca2+

Vasoconstriction

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23
Q

Where are A1 adrenorecpetors commonly present?

A

Within the vasculature

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24
Q

In regards to G coupled reactions what kind of response do they evoke?

A

Amplification a large reaction from smaller stimuli

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25
Q

In regards to Tyrosine Kinase what kind of response do they evoke?

A

Divergent reaction, lots of different responses from the same stimuli.

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26
Q

What are the agonists of tyrosine kinase receptors?

A

Hormones e.g. insulin

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27
Q

What is the structure of a tyrosine kinase receptor?

A

They are a dimer

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28
Q

Upon binding of the agonist to the tyrosine kinase receptor what occurs?

A

It undergoes a conformational change bringing the two pieces together.
Intracellular tyrosine molecules are activated by ATP (phosphorylated)
Relay proteins bind to tyrosine triggering different cellular responses.

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29
Q

What are relay proteins?

A

These are individual proteins which bind to the tyrosine molecules present on the intracellular extension of the receptor, each one triggers a different response within the cell.

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30
Q

How long is the response in tyrosine kinase receptors?

A

Up to a few hours

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31
Q

How many folds pass across the membrane in a G protein coupled receptor?

A

7 times

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32
Q

Autocrine regulation

A

Self limiting

Chemical released by the cell bind to receptors on the same cell

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33
Q

Example of autocrine regulation

A

Somatostatin released from D cells

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34
Q

Paracrine regulation

A

Chemicals released by cell bind to receptors on cells located proximally

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35
Q

Example of paracrine regulation

A

Somatostatin released by D cells binds to parietal cells to inhibit release of HCL
Both located in stomach

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36
Q

How is endocrine regulation divided?

A

Negative and positive feedback

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37
Q

Endocrine Regulation

A

Chemicals released by cells into the circulatory system where they travel and bind to receptors on target cells.

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38
Q

Example of endocrine regulation

A

Insulin released by B cell in pancreas and target cells in liver.

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39
Q

Negative feedback

A

Primary Mechanism of maintaining homeostasis by resisting fluctuations away from physiological set point.

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40
Q

Positive feedback

A

Initial stimuli initiates a response which exaggerates the initial change

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41
Q

Examples of positive feedback

A

Oxytocin in childbirth

Blood clot cascade

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42
Q

What makes up intrinsic regulation?

A

Autocrine and Paracrine

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43
Q

What makes up extrinsic regulation?

A

Nervous system and endocrine

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44
Q

Example of negative feedback ?

A

Cortisol stress cycle

Cortisol is the final product but high levels of cortisol inhibits ACTH and CRh production all of which are precursors.

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45
Q

What is the function of GLUT2 receptors?

A

Censorship of blood glucose levels

Allows diffusion of glucose into the B cells in the pancrease.

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46
Q

What enzyme is responsible for monitoring blood glucose and how does it complete its function?

A

Glucokinase
An enzyme responsible for glycolysis
Increased glucose increases ATP conc

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47
Q

As a result of high ATP levels in the B cells due to high glucose levels what happens?

A

ATP sensitive K+ channels close
Voltage Gated Ca 2+ channels open
Excretion of insulin via exocytosis

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48
Q

What is the structure of insulin?

A

Polypeptide dimer held together by disulphide bridges

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49
Q

How is insulin produced then activated

A

Produced in RER of B cell

Cleaved to form active form

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50
Q

What can be used to monitor inulin production?

A

C protein

A by product of the cleaving of insulin to form active enzyme

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51
Q

Describe insulin release

A

Its biphasic
1st phase is dependant on dose larger dose = larger spike
2nd phase smaller as vesicles need to be prepared

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52
Q

What is the 1st phase of insulin release called?

A

Readily Released Pool

Insulin already packaged in active vesicles so quick response

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53
Q

In type II diabetes what happens to the phases?

A

They weaken and flatten

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54
Q

Why in type II diabetes does the pattern of release change?

A

As glucokinase activity is downregulated

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55
Q

Why in type II if enough weight is lost can they symptoms of diabetes disappear?

A

As B cells still producing insulin however, Blood glucose concentration is higher than the KM of glucokinase so its working at capacity basically.
By loosing weight glucose conc can be brought below KM of glucokinase.

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56
Q

What kind of receptor are the ATP sensitive K+ channels?

A

Inward rectifier - ion channel
Contain a sulphonylurea receptor - regulatory unit
Octomeric structure - 8 subunits

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57
Q

What is the function of K+ ATP channels and what stimulates them?

A

They inhibit insulin release by preventing Ca2+ entry

Diazoxide

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58
Q

What are the two main thyroid hormones?

A

T4 and T3

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59
Q

What is T3

A

Tri-iodothyronine

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60
Q

What is T4

A

Thyroxine

61
Q

What is the basic functional unit of the thyroid?

A

Follicle

62
Q

What makes up a follicle?

A

Colloid surrounded by cuboidal follicular cells

63
Q

What is dispersed between follicles?

A

Parafollicular cells or C-cells

Neuroendocrine cells

64
Q

What do C - cells excrete?

A

Calcitonin

65
Q

What is the function of calcitonin?

A

Reduces blood calcium by opposing the action of parathyroid hormone

66
Q

What do follicular cells produce?

A

Thyroglobulin

67
Q

What is thyroglobulin?

A

Tyrosine packed full of proteins

68
Q

What occurs within the follicular cells before formation of MIT and DIT?

A

Uptake and concentration of Iodide I-
Oxidation of Iodide I- to iodine I
Iodination of Thyroglobulin

69
Q

What is MIT

A

Mono-iodotyrosine unit

Tyrosine bound to 1 unit of iodine

70
Q

What is DIT

A

Di-iodotyrosine unit

Tyrosine bound to 2 units of iodine

71
Q

How is T3 formed?

A

MIT + DIT
Mono + Di
1 iodine units + 2 iodine units = Tri-iodotyronine

72
Q

How is T4 formed?

A

DIT + DIT
Di + Di
2 iodine units + 2 iodine units = Thyroxine

73
Q

When synthesised where are T3 and T4 stored?

A

They are stored within the colloid thyroglobulin

74
Q

What percentage of thyroid hormone produced T4?

A

90%

75
Q

Which is the most potent thyroid hormone?

A

T3 is 4x more potent than T4

76
Q

Where is T4 converted into T3?

A

Liver and the kidney

77
Q

What is cycle leading to T3 and T4 secretion?

A

Hypothalamus stimulates pituitary gland
Anterior pituitary gland secretes Thyroid stimulating hormone
TSH causes stored T3 and T4 to be secreted

78
Q

What does excess free T3 and T4 trigger?

A

Negative feedback

Inhibits at the hypothalamus and pituitary

79
Q

What hormones are secreted by the anterior pituitary?

A 
Growth Hormone GH
Thyroid stimulating Hormone TSH
Adrenocorticotropic Hormone ACTH
Follicle Stimulating Hormone FSH
Prolactin PRL
Luteinizing Hormone LH
80
Q

Where do the majority of thyroid hormones find themselves bound to in transport?

A

Serum proteins

81
Q

What serum proteins are relevant in thyroid hormone transport?

A

Thyroxine binding globulin. TBG 70%
Thyroxine binding pre albumin TBPA 20%
Albumin 8%

82
Q

How else can thyroid hormones be transported?

A

Free within the blood

83
Q

In what form can thyroid hormones enter the cells?

A

Only when free and unbound

84
Q

What % of T3 is unbound?

A

0.33%

85
Q

What percentage of T4 id unbound?

A

0.015%

86
Q

Why does T3 have a more rapid onset of action?

A

As it is less avidly bound by TBG and TBPA than T4

87
Q

What are some affects of thyroid hormones

A

Increased Metabolic rate and glucose uptake
Increased Glycogenolysis and Gluconeogenesis
Increased lipolysis
Decreased Gylcogenesis and lipogenesis
Increase breathing, heart rate and force of contraction

88
Q

What is the metabolic affect of hyperthyroidism?

A

Increased number and size of mitochondria
Increased oxygen use and ATP hydrolysis
Increased synthesis of respiratory chain enzymes

89
Q

What percentage of patients with hyperthyroidism have heat intolerance?

A

30%

90
Q

What is the affect of hypothyroidism on growth?

A

Stunted growth

91
Q

Why does hypothyroidism result in stunted growth?

A

As thyroid hormones required for growth hormone releasing hormone production and secretion

92
Q

What are the three types of thyroid hormone degrading enzymes?

A

D1
D2
D3

93
Q

Where is D1 found?

A

Found within the liver and kidneys

94
Q

Where is D2 found?

A 
Found in : Heart
                 Skeletal Muscle
                 CNS
                 Thyroid
                  Pituitary
95
Q

Where is D3 found?

A

Foetal placenta and brain

96
Q

What is the main function of thyroid hormone degrading enzymes?

A

Conversion of T4 into the more metabolically active T3

97
Q

What does the thyroid usually weigh?

A

15-25g

98
Q

Where does the thyroid hormone originate from?

A

Foramen caecum

99
Q

From what week does the thyroid develop

A

4th week

100
Q

Where does the thyroid descend down?

A

Thyroglossal duct

Descends past the larynx

101
Q

Where do the c cells originate from?

A

Originate around area where thyroid descends to

102
Q

Where should thyroid be found?

A

C5 level of thyroid cartilage

T1 Fifth tracheal ring

103
Q

What hormones are produced in the anterior pituitary?

A 
ACTH
TSH
GH
Prolactin
FSH
LH
104
Q

What hormones are stored in the posterior pituitary?

A

ADH

Oxytocin

105
Q

Where are hormones stored in the posterior pituitary produced?

A

Hypothalamus

106
Q

What are the precursor hormones for Cortisol?

A

CRH (hypothalamus)
ACTH (Pituitary)
Cortisol (Adrenal glands)

107
Q

What are the precursor hormones for testosterone?

A

GnRH (Hypothalamus)
LH FSH (Pituitary)
Testosterone (Testes)

108
Q

What are the precursor hormones for growth hormone?

A

GHRH (Hypothalamus)

GH (Pituitary)

109
Q

What is different about Prolactin?

A

Dopamine inhibits Prolactin

110
Q

What are the precursor enzymes for thyroxine?

A

Thyrotropin Releasing Hormone (Hypothalamus)
Thyrotropin TSH (Pituitary)
Thyroxine (Thyroid)

111
Q

How does the hypothalamus communicate with the anterior pituitary?

A

Portal system hormones travel within the blood

112
Q

How does the hypothalamus communicate with the posterior system?

A

Hormones travel down nerves within axoplasm

113
Q

What is the paired hormone of ACTH?

A

Cortisol

114
Q

What is the paired hormone of TSH?

A

Thyroxine

115
Q

What is the paired hormone of LH/FSH?

A

Testosterone or Estradiol

116
Q

What is the paired hormone of GH?

A

IGF-1

Insulin like Growth Factor 1

117
Q

Which nerves run close to the pituitary that control eye movement?

A

3
4
6

118
Q

Which branches of which nerve run close to the pituitary?

A

5 Facial Nerve
Ophthalmic division
Maxillary division

119
Q

What nerve makes up the optic chiasm?

A

2 Optic

120
Q

What are the two types of dynamic test?

A

Too much - test suppresses hormone

Too little - test stimulates hormone

121
Q

In a normal patient how should they react to a dynamic test for too much hormone?

A

levels of the hormone should drop

122
Q

In a normal patient how should they react to a dynamic test for too little hormone?

A

Levels of hormone should rise

123
Q

Give an example of a too little test used in measuring cortisol level ?

A

Insulin stress test
IV insulin given to induce a hypoglycaemic event
Cortisol and GH levels should rise

124
Q

Give an example of a too much test used in measuring cortisol level test?

A

SynACTHen test
IV synthetic ACTH
Cortisol levels measured at 0, 30, 60 mins

125
Q

In the synACTHen test how should the cortisol levels change?

A

Should rise by 150 and reach around 500 in a healthy patient.

126
Q

Where is the anterior pituitary derived from?

A

Rathkes pouch

127
Q

What is the posterior pituitary?

A

Extension of neuronal tissue formed from modified glial cells and axonal bodies.

128
Q

What cells secrete GH?

A

Somatotroph

129
Q

What cells secrete PRL?

A

Mammotrophs

130
Q

What cells secrete ACTH?

A

Corticotrophs

131
Q

What cells secrete TSH?

A

Thyrotrophs

132
Q

What cells secrete FSH and LSH?

A

Gonadotrophs

133
Q

What three zones make up the adrenal cortex?

A

Glomerulose
Fasciculata
Reticularis

134
Q

What is produced in the glomerulose layer?

A

Mineralocrticoids

135
Q

What is produced in the fasciculata?

A

Glucocorticoids

136
Q

What is produced in the Reticularis?

A

Adrenal androgens

137
Q

What makes up the medullary zone?

A

Chromaffin cells
Medullary veins
Splanchnic nerves

138
Q

What does the medullary zone produce?

A

Catelcholamines

139
Q

What is th starting point for all steroid synthesis?

A

Cholesterol

140
Q

Under what control is aldosterone under?

A

Renin-angiotensin system

141
Q

What is released when a low blood pressure is detected in the kidneys?

A

Renin

142
Q

What is the function of renin?

A

Fist step in the cycle

Converts Angiotensinogen to Angiotensin 1

143
Q

What enzyme is responsible for the second step in the renin angiotensin system?

A

ACE

Converts Angiotensin I in II

144
Q

What is the third and final step in the Renin angiotensin cycle?

A

Angiotensin II causes aldosterone to be released by the adrenal glands

145
Q

What is the function of aldosterone ?

A

Causes Reabsorption of Sodium and water.

Increases blood volume and in turn BP.

146
Q

As well as acting as a triggering the release of Aldosterone what other affect does Angiotensin II have?

A

Causes vasoconstriction
Increases systemic resistance
Increasing BP

147
Q

Where are mineralocorticoid receptors mainly located?

A

Kidney
Salivary Gland
Gut
Sweat Glands

148
Q

What is the main role of mineralocorticoids?

A

Regulates BP extracellular volume and Na+ retention

Year 2 Endocrine (21 decks)

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