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Physiology > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q
A

Direct communication

  • Transportation via gap junctions or connexins
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2
Q
A

Contact communication

  • Information processing via molecules integrated into the membrane
  • Typical in cells of the immune system
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3
Q
A

Communication by secretion

  • Cells are located relatively far away
  • Molecules are secreted and received
  • Typical of the immune and nervous system
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4
Q
A

Cytoskeletal communication

  • Metabolism of a cell is influenced
  • This is relayed by the cytoskeletal system
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5
Q

Give the types of cell communication

A
  • Direct communication
  • Contact communication
  • Communication by secretion
  • Cytoskeletal communication
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6
Q
A

Classical endocrine effect

  • Cells secrete hormones
  • Hormones reach recipient cells via blood stream
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7
Q
A

Paracrine effect

  • Signals do not enter the blood
  • Acting on cells of the same tissue adjacent to the original cell
  • Signals are called local chemical mediators
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8
Q

Give the fate of local chemical mediators in the paracrine system

A

They can be either:

  • Broken down
  • Immobilised
  • Taken up by cells
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9
Q
A

Autocrine effect

  • A special form of paracrine effect
  • Signal-producing cell sends and receives its own signals
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10
Q

List the types of information processing in the endocrine system

A
  • Classical endocrine effect
  • Paracrine effect
  • Autocrine effect
  • Neurotransmitters
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11
Q

Which part of the CNS is the integrator of the endocrine system?

A

The hypothalamus

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12
Q

The function of the hypothalamus in the endocrine system depends on…

A
  • The levels of hormones
  • Information arriving from:
    • Nervous system
    • Immune system
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13
Q

Title this figure

A

Feedback within the endocrine system

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14
Q

What is the function of the feedback mechanism in the endocrine system?

A

It allows fine-tuning in the regulation of signals

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15
Q
A

Hypothalamus

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16
Q
A

Pituitary gland

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17
Q
A

Target organ

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18
Q
A

“Smart” end-users: Peripheral cells

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19
Q

Give the classifications of endocrine feedback mechanisms

A
  • Long feedback
  • Short feedback
  • Ultra-short feedback
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20
Q

Give an example of where long feedback occurs

A

Between:

  • A peripheral gland
  • Hypothalamus
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21
Q

Give an example of where short feedback occurs

A

Between:

  • A peripheral gland
  • Pituitary gland
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22
Q

Give an example of where ultra-short feedback occurs

A

Between:

  • Hypothalamus
  • Pituitary gland
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23
Q

Which hormones are used to demonstrate the classical regulatory pathway?

A

Thyroid hormones

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24
Q

Title this figure

A

Thyroid feedback

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25
Q
A

Hypothalamus

TRH

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26
Q
A

Hypophysis

TSH

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27
Q
A

Thyroid gland

Thyroxine synthesis increases

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28
Q
A

Blood vessel:

Thyroxine level increases

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29
Q
A
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30
Q
A
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31
Q

Give examples of IC “second messengers”

A
  • cAMP
  • cGMP
  • Ca2+
  • Diaglycerol (DAG)
  • Inositol triphosphate (IP3)
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32
Q

Which processes occur between:

  • Signals being received
  • The appearance of biological effects
A

Signal transduction processes

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33
Q

What are the reasons that a hormone-like substance could have varying effects on different cells?

A
  • There are separate receptors in the different tissues
  • The receptor is the same but a different signalling pathway is initiated
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34
Q

Title the figure

A

Scatchard analysis

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35
Q
A

Bmax (No. of binding sites) given by the point of intersection

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36
Q

What is a Scatchard analysis used for?

A

Used for measuring the properties of receptor-ligand interaction

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37
Q

Which parameters can be estimated from a Scatchard analysis?

A
  • The total number of binding sites
  • Strength (affinity) of binding between the receptor and the ligand
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38
Q

Title the figure

A

Regulation of receptor number

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39
Q
A
  • Either:
    • Long lasting hormone treatment
    • The decrease of cellular metabolic needs
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40
Q
A

“Down-regulation”

Inhibition of receptor expression

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41
Q
A

Either:

  • Removal of the endocrine gland
  • Increase of cellular metabolic needs
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42
Q
A

“Up-regulation”

Facilitation of receptor expression

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43
Q

How do lipophilic hormones have an effect on cells?

A
  1. They easily pass the cell membrane
  2. Binding to cytoplasmic proteins
  3. They then reach the nucleus
  4. Modification of genetic expression of proteins
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44
Q

How do water-soluble/hydrophilic peptides and glycoprotein hormones have an effect on cells?

A

Exert actions by binding to membrane surface receptors

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45
Q

G-protein dependent transduction outcomes

A
  1. ​Migration of G-protein to ion channel protein, activating/inactivating it
  2. Activate enzymes bound to the IC side of the membrane
  3. Influence adenylate cyclase activity → IC cAMP conc.
  4. Control phospholipase C activity → Produces messengers
  5. Control PLA2 enzyme → Arachidonic acid
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46
Q

Describe the receptor of G-protein independent transduction

A

The receptor is a transmembrane protein:

  • EC ligand binding part
  • Central part
  • IC part which exhibits phosphorylase activity
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47
Q

Describe G-protein independent transduction

A
  1. Ligand bond formation
  2. IC polypeptide chain phosphorylates
  3. Receptor activates
  4. Biological action
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48
Q

Describe cell activation when the receptor is in the cytoplasm

A
  1. Lipophilic hormones pass the cell membrane
  2. Hormones bind to cytoplasmic proteins (receptors)
  3. Receptor-ligand complex formation
  4. DNA-binding domain of the receptor protein ‘finds’ HRE
  5. Biological response initiated through transcription of a protein
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49
Q

Title the figure

A

Fine structure of the nuclear receptor

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50
Q
A

Lypophilic hormone

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51
Q
A

LBD

Ligand binding domain

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52
Q
A

DNA-BD

DNA binding domain

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53
Q
A

HRE

Hormone-responsive element

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54
Q
A

BPE

Basal promoter element

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55
Q
A

VD

Variable domain

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56
Q

The function of the VD

A

Locating of the base-pair segment of the DNA

Specific to the particular hormone

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57
Q

The function of HRE

A

Binds the DBD

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58
Q

DBD

A

DNA binding domain

Amino acid segment of the hormone-receptor complex

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59
Q

The function of the BPE

A
  1. Activated by receptor-DNA complex
  2. Expression of the structural gene begins
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60
Q

Title the figure

A

The receptor in the form of an ion channel

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61
Q

Describe the structure of a receptor which is acting as an ion channel

A
  • 5 membrane-integrated domains
  • Ligand binding site on the EC side
  • 2x alpha subunits
  • 2x beta subunits
  • 1x delta subunit
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62
Q

Give examples of receptors which are ion channels

A
  • n-ACh-R (Nicotinic acetylcholine receptor)
  • Glutamate receptors
  • Anion receptors
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63
Q

Nicotinic acetylcholine receptors can be inhibited by…

A

d-tubocurarine

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64
Q

n-ACh-R can be stimulated/inhibited by substances affecting the…

A

Receptor’s 5 subunits

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65
Q

What are the states n-ACh-R can be in?

A
  • Closed (before ACh binding)
  • Open (After ACh binding)
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66
Q

Describe the processes after ACh binds to the receptor

A
  1. Conformational change
  2. Cation channel opens (“open state”)
  3. Flow of cations
  4. Local excitatory potential formed
  5. AP is triggered
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67
Q

Describe the closing of n-ACh-R

A
  1. The open channel becomes inactivated
  2. Ligand bond still exists
  3. Change of conformation doesn’t allow cation flow
  4. Channel is “inactive”
  5. Dissociation of the ligand
  6. Channel closes
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68
Q

Give the main groups of glutamate-sensitive receptors

A
  • NMDA receptor
  • AMPA receptor
  • Kainate-receptor
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69
Q

NMDA receptor

  • Function
A

N-metil-D-aspartate

  • Binding Mg2+ keeps receptor closed
  • Mg2+ dissociated after receptor activation
  • Ca2+ influx maintains a lasting effect
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70
Q

Opening of anion-receptors causes

A

Hyperpolarisation of CNS inhibitory synapses

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71
Q

What can cause hyperpolarisation of anion receptors

A

Nonspecific anions

  • Cl-
  • HCO3-
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72
Q

Give the main mediators of anion-receptors

A
  • GABA
  • Glycine
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73
Q

The function of GABA in the anion-receptor

A
  • Either GABA-A / GABA-B
  • GABA-B activation:
    • Decrease IC cAMP
    • Affects K+ channels
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74
Q

G-protein structure

A
  • 3 subunits form a complex:
    • Alpha subunit + GDP
    • Beta subunit
    • Gamma subunit
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75
Q

G-protein mechanism of action

A
  1. The ligand binds to the EC receptor
  2. Conformational change in the 7-M protein
  3. Beta + gamma subunits bind to the IC side of the receptor
  4. Alpha subunit conformational change
  5. Alpha subunit binds GTP
  6. Alpha subunit-GTP complex liberated
  7. Stimulates/inhibits ion channel/enzyme
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76
Q

Describe the return of G-protein to its resting state

A
  1. GTP → GDP
  2. Alpha subunit binds to gamma + beta again
  3. G protein → Resting state
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77
Q

Describe Gs effect

A
  • Activated G-protein migrates to a remote ion channel protein
  • Activates the channel
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78
Q

Describe Gi effect

A
  • Activated G-protein migrates to a remote ion channel protein
  • Inactivates the channel
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79
Q
A
  1. M2 ACh-R
  2. K+ channel opens
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80
Q
A
  1. alfa2 type R
  2. K+ channel opens
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81
Q
A
  1. D2 type R
  2. K+ channel opens
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82
Q
A
  1. GABA type R
  2. K+ channel opens
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83
Q
A
  1. S2 type R
  2. K+ / Ca2+ channel opens
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84
Q
A
  1. OP type R
  2. Ca2+ channel opens
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85
Q

Title this figure

A

Adenylate cyclase mechanism

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86
Q

Summarise the adenylate cyclase mechanism

A
  • Influenced by G-proteins
  • Gs: adenylate cyclase activity ↑
  • Gi: adenylate cyclase activity ↓
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87
Q

Describe the steps of the Gs mechanism

A
  1. Glucagon mobilises Gs G-protein
  2. Liberates hepatic glycogen stores
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88
Q

Describe the steps of the Gi mechanism

A
  • alpha2-adrenergic receptor activated
  • IC cAMP levels ↓
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89
Q

List receptors of the Gs pathway

A
  • Prostacyclin
  • Dopamine D1
  • Catecholamine beta
  • Anterior pituitary
  • Histamine H2
  • 2-type ADH
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90
Q

List receptors of the Gi pathway

A
  • Dopamine D2
  • Alpha1 catecholamine
  • Some glutamate
  • Some opioid
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91
Q

Title the figure

A

Phospholipase C mechanism (PLC)

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92
Q

Give the steps of the phospholipase C (PLC) mechanism

A
  1. Activation of G-protein
  2. Stimulates Phospholipase C
  3. Converts membrane phospholipids → IP3/DAG
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93
Q

IP3

A
  • Binds to IP3 receptor (on the surface of Ca2+ sequesters)
  • The receptor is an ion channel
    • IP3 opens the channel
    • Increasing IC Ca2+
    • Cellular effects
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94
Q

DAG

A
  • Similar behaviour to cAMP
    • Activates type-C protein kinases
    • Triggers several phosphorylation pathways
    • Biological effects
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95
Q

Give examples of ligands in the PLC mechanism

A
  • ACh
  • Histamine
  • Purin
  • PGE
  • TXA2
  • ADH
  • Oxytocin

All of which release Ca2+

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96
Q

Give the steps of the Phospholipase A2 (PLA2) mechanism

A
  1. G-protein activation
  2. Converts phospholipids → arachidonic acid (substrate)
  3. Arachidonic acid → Several products
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97
Q

Besides active G-proteins, what else can activate the PLA2 mechanism?

A

Ca2+

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98
Q

Arachidonic acid can pass through which further pathways?

A
  • Lipoxygenase pathway
  • Cyclooxygenase pathway
  • Epoxygenase pathway
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99
Q

List the products of the lipoxygenase pathway

A
  • Leukotrienes (LT)
  • Lipoxins (LX)
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100
Q

List the products of the cyclooxygenase pathway

A
  • Prostacyclins (PGIs)
  • Prostaglandins (PGs)
  • Thromboxanes (TXs)
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101
Q

Describe the mechanism when a receptor is also an IC enzyme

A
  1. Ligand bond formed on the outer surface
  2. IC polypeptide chain phosphorylates
  3. Activation of the receptor
  4. Biological action
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102
Q

Give an example of direct enzyme stimulation

A

Insulin receptor

The receptor is able to phosphorylate itself and other proteins on the IC part of the cell

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103
Q

Auto-phosphorylation

A
  1. Self phosphorylating enzyme phosphorylates tyrosine residues of the IC receptor sequence
  2. Phosphorylated tyrosine residues bind intracellular proteins
  3. Specific IC responses elicited
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104
Q

Describe the processes after autophosphorylation

A
  1. Autophosphorylation
  2. Receptor-enzyme complex is taken up by the cell
  3. Inactivation
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105
Q

Describe the figure

A
  1. Tyrosine residues are present in the enzyme’s IC domain
  2. Ligand binding
  3. Phosphorylation of IC regulatory proteins (RP1+RP2)
  4. Biological effects
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106
Q

The hypothalamus is divided into which parts?

A
  • Magnocellular area (with large cells)
  • Parvocellular area (with small cells)
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107
Q

Describe the movement of hormones from the hypothalamus

A
  1. Hormones produced in the parvocellular area → Adenohypophysis
  2. Hormones produced in the magnocellular area → Neurohypophysis
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108
Q

Which nuclei are found in the magnocellular area?

A
  • Supraoptic nucleus (Oxytocin production)
  • Paraventricular nucleus (ADH production)
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109
Q

Which nuclei are found in the parvocellular area?

A
  • Ventromedial nucleus
  • Dorsomedial nucleus
  • Infundibular nucleus

Inhibit/release substances which can reach the adenohypophysis

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110
Q

Describe the transport of neurosecretions from the parvocellular area

A
  1. Parvocellular area
  2. Portal circulation of pituitary stalk via axons
  3. Arrive at the adenohypophysis
  4. Influence production + release of hormones into the blood
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111
Q

Describe the transport of neurosecretions from the magnocellular area

A
  1. Magnocellular area
  2. From the site of production (Neurone)
  3. The site of release (Neurohypophysis)
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112
Q

Title the figure

A

Axonal transport

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113
Q

Describe the steps of axonal transport

A
  1. Peptide travels from hypothalamic cell → axon
  2. First capillarisation (Median eminence)
  3. Portal circulation
  4. Second capilarisation (anterior pituitary)
  5. Cells of anterior pituitary
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114
Q
A

Basal membrane

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115
Q
A

Axonal transport, neurosecretion

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116
Q
A

First capillarisation (Median eminence)

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117
Q
A

Portal circulation

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118
Q
A

Second capillarisation (anterior pituitary)

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119
Q

Which portal vessel do peptides travel down in axonal transport?

A

Pituitary stalk

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120
Q

Give the proteins of axonal transport

A
  • Kinesin (Transport from soma to synapse)
  • Dynein (Returning of residues to the soma)
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121
Q

In axonal transport, what determines the direction of transport of proteins?

A

Polarity

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122
Q

Parvocellular areas synthesise releasing and inhibitory substances which influence…

A

Tropic-hormone production of the adenohypophysis

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123
Q

Hypophyseotrop hormones

A

Hypothalamic substances that influence production + release of the pituitary gland

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124
Q

Give the parvocellular hormone systematic names

A
  • RH/RF (Releasing hormone/ Releasing factor)
  • IH/IF (Inhibiting hormone/ Inhibiting factor)
  • ’+’ (Facilitates synthesis + secretion hormones)
  • ’-‘ (Inhibits hormone synthesis and release)

E.g TSH-RH = Thyrotropin hormone releasing hormone

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125
Q

In adenohypophyseal systematic naming, what do the following abbreviations mean (Prior to ‘RH’ or ‘RF’)?

  • T
  • C
  • Gn
  • G
  • P
  • M
A
  • T = Thyrotropin, TSH
  • C = Corticotropin, ACTH
  • Gn = Gonadotropin, FSH/LH
  • G = Growth hormone, STH
  • P = Prolactin, PRL
  • M = Melanocyte stimulating hormone, MSH
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126
Q
A
  1. TSH+
  2. Thyroliberin
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127
Q
A
  1. ACTH+
  2. Corticoliberin
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128
Q
A
  1. FSH+, LH+
  2. Gonadoliberin
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129
Q
A
  1. GH+
  2. Somatoliberin
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130
Q
A
  1. PRL+
  2. VIP, TRH
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131
Q
A
  1. MSH+
  2. MSH-RH
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132
Q

List the releasing factors (short name)

A
  • TRH
  • CRF
  • GnRH
  • GRF
  • PRF
  • MRF
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133
Q

Function: Thyrotropin-releasing hormone

A
  • Stimulates thyroid gland
  • Stimulates hormone release
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134
Q

Function: Corticotropin-Releasing Factor

A
  • Adrenocorticotropin (ACTH) stimulating hormone
  • Facilitates synthesis + release of:
    • ACTH
    • MSH
    • Endogenous opiates
  • Stimulating + splitting + synthesis of POMC
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135
Q

Function: Gonadotropin-releasing hormone

A
  • Facilitates synthesis + release of:
    • FSH (Follicle stimulating hormone)
    • LH (Luteinising hormone)
  • In males + females
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136
Q

Function: Growth hormone releasing factor (GRF)

A

Synthesis + release of growth hormone

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137
Q

Function: Prolactin-releasing hormone (PFR)

A
  • Prolactin synthesis + release
  • Lactation
  • Ovulation in the rat
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138
Q

What are the main parvocellular inhibiting factors?

A
  • Dopamine
  • Somatostatin
  • GABA
  • VIP
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139
Q

In adenohypophyseal systematic naming, what do the following abbreviations mean (Prior to ‘IH’ or ‘IF’)?

  • G
  • P
  • M
A
  • G = Growth hormone, somatotropin, STH
  • P = Prolactin, PRL
  • M = Melanocyte-stimulating hormone, MSH
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140
Q
A
  1. TRH-, PRL-
  2. TSH-IH, PRL-IH
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141
Q
A
  1. GH-
  2. GH-IH, somatostatin
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142
Q
A
  1. PRL-
  2. PRL-IH
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143
Q
A
  1. GH+
  2. MSH-IH, Melatostatin
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144
Q
A
  1. General, an indirect inhibitor
  2. Norepinephrine
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145
Q
A
  1. General, an indirect inhibitor
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146
Q

Function: GIF

A
  • Systematic name for Somatostatin
  • GIF = Growth hormone inhibiting factor
  • Somatotropin inhibiting hormone
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147
Q

Function: PIF

A
  • Systematic name for inhibiting factor of prolactin release + production
  • Regulated by dopamine
  • Hypothalamic peptide is known to decrease prolactin production
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148
Q
A
  1. PRL+, GIF
  2. GIF+ In the pancreas
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149
Q
A
  1. PRL+
  2. Substance-P antagonist
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150
Q
A
  1. GH, PRL+
  2. MSH-IH, melanostatin
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151
Q
A
  1. General facilitator
  2. Peptide family actin on gastrin
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152
Q
A
  1. PRL+, GH+, TSH+
  2. Paracrine action of tachykinins in HP
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153
Q
A
  1. PRL+
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154
Q

The function of: Vasoactive intestinal peptide (VIP)

A
  • PL+
  • Somatostatin-
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155
Q

The function of: Angiotensin-II

A
  • Synthesis + release of somatotropin + prolactin
  • MSH-inhibiting effect
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156
Q
A
  1. Stimulation of water reabsorption
  2. Increase BP, V1 receptor, IP3
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157
Q
A
  1. Preparation of uterine contractions for estrogen response, basket cell contraction
  2. Classical neuroendocrine reflex
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158
Q

Give an example of neuroendocrine reflexes

A

Oxytocin-mechanisms

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159
Q

What are the essential characteristics of a neuroendocrine reflex?

A
  1. Translation of neural information from sensory nerve to the language of the endocrine system (using the hypothalamus)
  2. Effect/response is not neural but hormonal
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160
Q

Describe the reflexes for milk ejection

A
  1. Excitation from udder sensory fibres → Spinal cord
  2. Excitation → Hypothalamus
  3. Enhanced oxytocin synthesis evoked
  4. Oxytocin release increases from the neurohypophysis
  5. Oxytocin reaches the mammary gland via blood
  6. Contraction of myoepithelial cells (For milk ejection)
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161
Q

Give the hormonal profile of a cow in stress

A
  • Plasma glucocorticoid level increases, causing:
    • Oxytocin fall
    • Prolactin fall
    • Milk ejection decrease to minimum
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162
Q

What are glandotropic hormones?

Give examples

A

Those acting exclusively on endocrine glands

  • TSH
  • ACTH
  • FSH
  • LH
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163
Q

What are histiotropic hormones?

Give examples

A

Those acting on certain organs

  • STH
  • PRL
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164
Q

The adenohypophysis develops in which structure?

A

Rathke’s pouch

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165
Q

The adenohypophysis is formed by…tissue

A

Entodermal glandular

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166
Q

The neurohypophysis is formed by…tissue

A

Ectodermal nervous

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167
Q

Give the cell types of the hypophysis

A
  • A = Acidophils
  • B = Basophils
  • C = Chromophobes
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168
Q
A

Somatotropin (GH) producing cells

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169
Q
A

Adrenocorticotropin (ACTH) producing cells

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170
Q
A

Thyrotropin (TSH) producing cells

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171
Q

Prepubertal hypopituitarism/Removal of the pituitary gland

A
  • Results in proportional dwarfism
  • In adults:
    • Smaller organs
    • Thin hairs
    • Decreased sexual function
    • Decreased protein/glycogen stores
    • Decreased BMR
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172
Q

Congenital hyperpituitarism

A
  • Gigantism
  • In adult life:
    • Acromegaly: Increase in the size of enlargeable extremities and other parts. E.g limbs
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173
Q

Metabotropic hormones of the hypophysis

A
  • GH
  • ACTH
  • TSH
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174
Q

Gonadotropic hormones of the hypophysis

A
  • PRL
  • FSH
  • LH
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175
Q

STH/GH receptor mechanism of action

A
  1. Hormone binds to the receptor
  2. IC conformational change
  3. Activation of the second messenger system
  4. = G-protein activated cAMP
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176
Q

What direct biological effect does GH have on the body?

A
  • Stimulates somatomedins (further hormones) in the liver
  • GH is therefore considered to be glandotropic + histiotropic
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177
Q

Increased growth hormone secretion in young age results in…

A

Gigantism

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178
Q

Increased growth hormone secretion in adults results in…

A

Asymmetrical growth of:

  • Limbs
  • Jaw
  • Certain flat bones
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179
Q

Give the episodic release of GH

A
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180
Q

The effect of growth hormone on protein metabolism

A
  • Increases amino acid uptake
  • Increases intracellular protein synthesis
  • Positive nitrogen balance
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181
Q

The effect of growth hormone on lipid metabolism

A
  • Increases catabolic processes:
    • FFA + plasma triglyceride increase
    • Fatty deposits are mobilised
  • Glucose oxidation decreases
  • Gluconeogenesis increases
  • Increased plasma acetoacetic acid levels
  • Increased plasma beta-OH-butyrate levels
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182
Q

The effect of growth hormone on carbohydrate metabolism

A
  • Antiinsuline effects:
    • Decrease insulin-dependent glucose uptake in adipose
  • Diabetogenic effects:
    • Increase plasma glucose level
      • Glucogenesis
      • Glucagon production
  • Houssay’s experiment
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183
Q

Houssay’s experiment

A

Adenohypophysectomy improved the status of a diabetic dog

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184
Q

GH stimulates…in the liver

A
  • Activation of thyroid hormones
  • Synthesis of somatomedins
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185
Q

Function of somatomedins

A
  • Influence bone, cartilage and connective tissue
  • Circulate in plasma, bound by carrier proteins
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186
Q

Somatomedins have a similar structure to…

A

Insulin

  • They are therefore known as IGFs (Insulin-like growth factors)*
  • They cannot exert any effect on insulin receptors*
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187
Q

Somatomedins are also known as…

A

Sulphating factors

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188
Q

IGF =

A

Somatomedins (Sm)

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189
Q

IGF-I

A

Sm-C

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190
Q

IGF-II =

A

MSA

Multiplication stimulating activity

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191
Q

Give the effects of IGF-I

A

Stimulation of:

  • Chondrocyte sulphate intake
  • Chondrocyte + osteoblast bone forming activity
  • Longitudinal bone growth
  • Transversal + periosteal bone growth
  • Acromegaly
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192
Q

Rat tibia test

A
  • A biological hormone identification method
  • Rat epiphysis’ do not close: always ready to grow
  1. Unknown substance is administered
  2. The thickness of the tibial disk is compared with its previous normal size
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193
Q

Describe the regulation of GH secretion

A
  • Plasma levels of:
    • Glucose
    • Arginine
    • Thyroid hormone
    • Hypothalamic factors
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194
Q

Peripheral feedback of GH regulation consists of which compounds?

A
  • Plasma metabolites
  • IGF
  • IGF-BP (Binding protien)
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195
Q

Title the figure

A

Regulation of GH secretion

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196
Q

Regulators of GH secretion

A
  • Plasma glucose + amino acid levels
  • Sex
  • Stress
  • Age
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197
Q

Regulators of GH secretion

A

Neurosecretion:

  • GH-RH
  • GH-IH
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198
Q

Regulators of GH secretion

A

Trop. hormone:

  • GH
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199
Q

Regulators of GH secretion

A
  • Metabolites of peripheral tissues + IGF levels
  • GH receptors
  • IGF binding proteins
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200
Q

Practical approaches of GH

A
  • Increase productivity
    • Milk
  • Genetic engineering
    • rpGH = recombinant-porcine growth hormone
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201
Q

Show the GH effects in cow (Graph)

A
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202
Q

Biochemical function of ACTH

A

In the adrenal fasciculate + reticular zones:

  1. ACTH increases cAMP pathway
  2. Stimulating glucocorticoid synthesis
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203
Q

What is the primary regulator of aldosterone?

A

Plasma [K+]

Not ACTH

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204
Q

Many hormones produced in the pituitary gland are synthesised from a common precursor hormone called…

A

PRE-POMC

  • (PRE-PROOPIOMELANOCORTIN)*
  • The name is derived from the most important hormones derived from it*
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205
Q

List the hormones derived from Pre-POMC

A
  • Opioid peptides
  • MSH
  • ACTH
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206
Q

Hormones derived from Pre-POMC are involved in which processes?

A

Adaptive processes of the body

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207
Q

ACTH is released in the incidence of…

A

Stress:

  • Mobilises energy reserves
  • Decreases sensation of pain
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208
Q

Which substance stimulates all the shown cleaving processes?

Where is this substance produced?

A

CRF (Corticotropin-releasing factor)

Produced in the hypothalamus

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209
Q

LPH =

A

Lipotropic hormone

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210
Q

CLIP =

A

Corticotropin like intermediate peptide

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211
Q

Endorphin =

A

Endogenous morphine

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212
Q

Enkephalin=

A

Endogenous opioid / Signal peptide

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213
Q

Give the steps of ACTH production

A
  1. Pre-POMC
  2. POMC
  3. ACTH
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214
Q

Give the effect of ACTH in the glomerulosa layer

A

Increases cholesterol-pregnenolone conversion →

Increasing mineralocorticoid synthesis

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215
Q

Synthesis of ACTH is regulated according to the…

A

Classical feedback principle

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216
Q

Long feedback

A

Involvement of glucocorticoid concentration in ACTH feedback

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217
Q

Ultra-short feedback

A

The inhibiting effect of ACTH on CRF

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218
Q

Give the steps of neural impulses causing ACTH secretion

A
  1. Nerve impulses → Hypothalamus
  2. Impulses are integrated by CRF synthesising cells
  3. Circadian fluctuation of CRF
  4. Determination of ACTH release
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219
Q

Title the figure

A

Regulation of ACTH synthesis

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220
Q
A

Exogenous/endogenous effects

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221
Q
A
  • Serotonin
  • ACh
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222
Q
A

CRF

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223
Q
A

ACTH

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224
Q
A

Neurosecretion

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225
Q
A

Tropic

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226
Q
A

Steroids

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227
Q
A
  • Norepinephrine
  • GABA
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228
Q

Circadian rhythm of ACTH

A
  • Short half-life
  • Conc. is higher in the early morning
  • Lowest at midnight

This is the cause of the fluctuation of glucocorticoid conc. (diurnal rhythm)

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229
Q

Annotate the figure

A
  • ACTH levels increase in early morning hours
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230
Q

TSH

A
  • Gonadotropic peptide hormone
  • Alpha chain: Species specificity
  • Beta chain: Biological specificity
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231
Q

What increases TSH levels

A
  • Thyroid hormones
  • Hypothalmic TRH
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232
Q

What decreases TSH levels?

A
  • Cortisol
  • Dopamine
  • Somatostatin
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233
Q

Role of TSH

A

Stimulation of thyroxine

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234
Q

Plasma TSH concentration is increased by…

A

TRH

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235
Q

FSH

A
  • Increase oestrogen synthesis in the follicle
  • Maturation of the follicle
  • Increased testicular spermatogenesis
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236
Q

FSH expression is directed by…

A
  • GnRH
  • Steroids
  • Inhibin
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237
Q

LH

A
  • Luteinising hormone
  • Located: Leydig cell → Testis / Granulosa cell → Ovary
  • Increases synthesis of androgens in both organs
  • Primary factor initiating ovulation
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238
Q

PRL

A

Prolactin

  • Stimulate mammary gland differentiation
  • Stimulate + maintain milk production
  • Metabolic hormone
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239
Q

How is PRL stimulated

A
  • Hypothalamic neuronal activity
  1. Oestrogen inhibits dopamine synthesis
  2. Stimulating PRL production during ovulation
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240
Q

Give the effects of PRL

A
  • Facilitation of lactogenesis
  • Facilitation of galactopoiesis
  • Support of suckling
  • Ovulation in the rat
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241
Q

Describe the steps toward spontaneous inhibition of PRL

A
  1. Spontaneous production of Ca2+ signal in the hypothalamus
  2. Dopamine synthesis in hypothalamus changes
  3. Levels of dopamine alter according to a tonic pattern
  4. Stimulation + suppression of adenohypophyseal PRL production + release
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242
Q

List the stimuli of PRL production

A
  • Pregnancy
  • Suckling
  • Stress
  • Sleep
  • Hypoglycaemia
  • Dopamine
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243
Q

List the inhibitors of PRL production

A
  • Dopamine
  • GABA
  • GAP
  • Drug: Bromocryptine
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244
Q
A

Positive physiological stimuli and negative effects

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245
Q
A

Serotonin opioids

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246
Q
A

Neurosecretion + Peripheral blood-derived signals

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247
Q
A

PRL

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248
Q
A

Trophormone

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249
Q
A

Udder:

  • Suckling
  • Maternal behaviour

Other: Increase of metabolism

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250
Q
A

‘Tonic’ central inhibition

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251
Q
A
  • Dopamine
  • GABA
  • GAP
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252
Q

PRL regulation by neurosecretion involves which hormones?

A
  • TRH
  • GnRH
  • VIP
  • Galanin
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253
Q

PRL regulation by peripheral blood involves which hormones?

A
  • Serotonin
  • Angiotensin-II
  • Oestrogens
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254
Q

MSH

A
  • Formed from ACTH
  • Stimulation of pigment granule production
  • Transport along the microtubule system → Decoloration of cells
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255
Q

Effect of MSH on pigment cells

A
  • Microtubule system from the nucleus
  • MSH causes:
    • Granules to migrate along microtubules
    • Even distribution of granules, darkening cell
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256
Q

Function of melatonin

A

Hormone:

  • Stimulates migration of scattered pigment granules
  • Back to the vicinity of the nucleus
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257
Q

Pineal gland produces

A

Produces serotonin + melatonin

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258
Q

Melatonin secretion

A
  • Circadian rhythm, affected by light
  • Decreased illumination acts positively
  • Increased daylight acts negatively

Some species:

  • Melatonin production positively influences sexual activity
  • In other species, it may have a negative influence
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259
Q

Describe the innervation of the pineal gland

A
  • Not directly connected to the CNS
  • Innervated by postganglionic sympathetic fibres
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260
Q

Describe the effect of decreased light intensity on the pineal gland

A
  1. Decreased illumination to retina → Sympathetic activity
  2. Suprachiasmatic nucleus (SCN) connection
  3. Excitation from cervical ganglion → CP
  4. Norepinephrine released here → NAT synthesis (used in melatonin synthesis)
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261
Q

Title the figure

A

Innervation of the pineal gland

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262
Q
A

Norepinephrine

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263
Q
A

Beta-receptor + Adenylate cyclase

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264
Q
A

AMP → cAMP

265
Q

Give the steps of Melatonin production

A
266
Q

Give the degradation of melatonin

A
267
Q

How does melatonin have a counter-effect on MSH?

A
  1. It inducts concentration of pigment granules
  2. Skin becomes pale
268
Q

Give the three effects of melatonin in mammals

A
  • Sexual function
  • Psychic effects
  • Defence against free radicals
269
Q

(Mammals) Influence of melatonin on the sexual cycle

A
  • Termination of the production of:
    • GnRH
    • FSH
    • LH
  • Sheep - Initiates oestrous cycle
  • Horse - Inhibits estrous cycle

Relevance to seasonality

270
Q

Describe melatonin levels at different human sexual maturation stages

A

Melatonin inhibits sexual maturation in humans

  • High in children between 1-6 years old
  • Decreases later during puberty: GnRH synthesis occurs
  • Decrease with age
271
Q

Melatonin levels during ovulation (Human)

A
272
Q

During and before ovulation, the night time peak of melatonin is…

A

Significantly decreased

  • Inhibition of LH production decreased
  • Ovulation is stimulated
273
Q

Describe sexual cycle activity in the cat and horse

A

Increased light exposure → Increased sexual activity

  • Cat: 15-minute increase of light exposure decreases melatonin
  • Horse: Increased daylight cycle in February:
    • Early spring estrus cycles
274
Q

Describe sexual cycle activity in the sheep and goat

A
  • A decrease of daylight:
    • Oestrous activity
  • Fertilisation in autumn → 5-month pregnancy → Progeny born in spring
  • Melatonin is g__onado__-stimulative
275
Q

Summarise photo-gonado stimulation in birds (graph)

A
276
Q

Psychic effects of melatonin

A

Maintenance of cyclic processes

Determined by:

  • Day/night
  • Seasonal changes
277
Q

Explain jet-lag

A
  • High diurnal melatonin
  • Adaptation requires 1 day for each time zone
278
Q

Seasonal emotional fluctuations

A
  • Short diurnal periods - Irregular periods of depression
  • Lethargy/sleepiness/hunger
  • Assigned to melatonin overproduction
  • Symptoms eliminated with physiotherapy
279
Q

Effect of melatonin on free radicals

A
  • Melatonin has a defence role against free radicals
  • Thought to be the cause of melatonin’s high plasma content
280
Q

Scavenger substances

A

Compounds suitable for binding and neutralisation of free radicals

→ Melatonin is an example

281
Q

List some reactive radicals

A
  • Superoxide O2-
  • Hydrogen peroxide H2O2
  • Hydroxyl OH-
282
Q

HRE

A
  • Hormone-responsive elements
  • Control gene expression of:
    • Metabolic enzymes
    • Structural proteins
283
Q

HRE presence is controlled by…

A

Thyroid hormone

284
Q

The function of the thyroid hormone in reptiles

A
  • Growth
  • Not thermoregulation
285
Q

Thyroid gland secretes…

A
  • Thyroxine (T4)
  • Triiodothyronine (T3)
  • Reverse triiodothyronine (rT3)
  • Calcitonin
286
Q

T4 is converted to…

A

T3

287
Q

How can thyroid hormones production be stopped

A

By removal of the thyroid

  • Surgical removal
  • Thyroid destruction by radioactive iodine
288
Q

Symptoms of thyroid hormone deficiency in young animals

A
  • Dwarfism
  • Neural symptoms
  • Sexual development retarded
289
Q

Symptoms of thyroid hormone deficiency in adult animals

A
  • Dermal symptoms - Myxoedema
  • Neural functions
  • Sexual functions
  • Metabolic effects
290
Q

A neural symptom of thyroid deficiency in young animals

A

Cretinism

  • Bad grasp
  • Poor learning
  • Constant apathy
291
Q

Dermal symptoms of adult thyroid deficiency

A
  • Shaggy fur/Hair loss
  • Subcut. CT becomes swollen
292
Q

Symptoms of thyroid hormone overproduction

A
  • Emphasised catabolic processes
  • Hypoxia sensitivity increases
  • Increased fat burning
  • Decreased lipid + protein storage
  • Decreased body weight
  • Tachycardia
  • Left ventricle hypertrophy
  • Increased irritability
293
Q

Basedow’s syndrome

A
  • Form of hyperthyroidism
  • Enlarged thyroid gland + overproduction
  • Eyes protrude from their sockets (Exophthalmus)
294
Q

TRH synthesis is affected by which feedback loop

A

Long

295
Q

Production of TRH/TSH is inhibited by

A
  • Feedback loops Long/short
  • An increase of IC T3 level in hypothalamic cells
296
Q

Give the exogenous effects of T4 concentration

A
  • Photoperiod
  • Feeding
  • Temperature
  • Stress
297
Q

Give the endogenous effects of T4

A
  • Genetic determination
  • Physiological state
  • Changes of hormone receptor
  • Activation ability of peripheral cells
298
Q

Title the figure

A

General regulation of thyroid hormone

299
Q
A

Exogenous effects

e.g cold

300
Q

Which thyroid hormones influence metabolism

A

T4 + T3

301
Q

Title the figure

A

Thyroid hormone synthesis

302
Q

1

A

Iodine enters gland by active pump mechanism

303
Q

2

A

Iodine ion → Atomic iodine

Lysosomal peroxidase enzyme

304
Q

3

A

Iodine → Organic bonds of thyroglobulin (TG)

  • Binding to tyrosine residues of the protein
    • 1 iodine = Monoiodotyrosine (MIT)
    • 2 iodine = Diiodotyrosine (DIT)

Thyronines are created by condensation of MIT + DIT

305
Q

MIT + DIT =

A

T3

306
Q

DIT + DIT =

A

T4

307
Q

4

A
  • Epithelial cells synthesise colloid
  • TG with thyroid hormones enter the follicle by endocytosis
308
Q

5

A

Start of hormone release:

  • Endocytosis of TG
309
Q

6

A

Protein molecules degraded intracellularly

  • Residual iodine-containing amino acids are recycled
310
Q

7

A

Hormones leave on the basal side of the cells by passive diffusion

311
Q

What stimulates almost every step of Thyroid hormone synthesis?

A

TSH

312
Q

Thyroid hormones are built on a…frame

A

Thyronine

Formed by 2 tyrosine frames

313
Q

What is needed in order to keep thyroid hormones dissolved in water?

A

Binding proteins

314
Q

Name the binding proteins of thyroid hormones

A
  • Thyroid-binding globulin (TBG)
  • Thyroid-binding prealbumin (TBPA)
  • T4
315
Q

Liver thyroid hormone transit time

A

5 Seconds

316
Q

Brain thyroid hormone transit time

A

1 second

317
Q

90% of thyroid gland secretum is…

A

Inactive T4

318
Q

5’ deiodinase (5’D) function

A

T4 → active T3

319
Q

5 deiodinase (5D) function

A
  • T4 → Inactive rT3
  • T3 → Inactive T2

Inactivation pathway

320
Q

Give some deiodinases

A
  • D1 ORD
  • IRD
  • D2 ORD
  • D3 IRD
321
Q

Type I Deiodinase function

A

Produce T3

322
Q

Type II Deiodinase function

A
  • Provide 5’ deiodination
  • Regulatory role
323
Q

Type III Deiodinase function

A

5 deiodination (inactivation)

324
Q

BAT

A

Brown adipose tissue

325
Q

IRD

A

Inner-ring deiodinase

326
Q

ORD

A

Outer ring deiodinase

327
Q

List the metabolic effects of thyroid hormone

A
  • Thermogenesis
  • Regulates the Intermediary metabolism
  • Facilitates the carbohydrate metabolism
  • Lipid metabolism
  • Protein metabolism
328
Q

How to thyroid hormones increase BMR?

A
  • Increased number of mitochondria
  • Na+/K+ ATPase activity increases
329
Q

Effect of thyroid hormone on carbohydrate metabolism

A
  • Intestinal absorption of glucose increases
  • Rates of gluconeogenesis + glycogenolysis increase
  • Insulin secretion increases
330
Q

Effect of thyroid hormone on lipid metabolism

A
  • Increase anabolism
  • Increase mobilisation
  • Increase catabolism
  • FFA increases in plasma
331
Q

Effect of thyroid hormone on protein metabolism

A
  • Increase in protein synthesis + breakdown
  • In the case of no hormone:
    • No protein-anabolism
  • In the case of overdose:
    • Catabolism becomes dominant
332
Q

Effect of thyroid hormone on the nervous system

A
  • Development of myelinisation
  • Widespread synaptic connectivity develops between neurons
333
Q

Effect of thyroid hormone on the cardiovascular system

A
  • Permissive effect:
    • Effect of catecholamines is potentiated
    • Increased cardiac function + O2 consumption
334
Q

Goitre

A

Enlargement of the thyroid gland

  • Can be accompanied by hyper- or hypothyroidism
  • Developed when no hormones are secreted into the blood
  • Can be caused by a lack of iodine
335
Q

List the goitre inducing substances

A
  • SCN-
  • Brassica sp.
  • Thiourea-derivates
  • Lithium
  • High iodine intake
336
Q

How does SCN- cause goitre?

A

Inhibits iodine uptake

337
Q

How does Brassica cause goitre?

A

Inhibitors iodine incorporation

338
Q

How do thiourea derivates cause goitre?

A

Inhibits the reduction of ionic iodine

339
Q

How does lithium cause goitre?

A

Inhibits release of hormones

340
Q

How does a high amount of iodine cause goitre?

A

Inhibits hormone synthesis and secretion

341
Q

Which locations do not have a lot of iodine in the diet?

A

Locations far from the sea

342
Q

Give the processes leading to endemic goitre

A
  1. Low iodine
  2. Disturbed synthesis of thyroid hormones
  3. Synthesis of TRH + TSH
  4. Higher BMR of thyroid
  5. More iodine extracted from the blood
  6. The growth of the gland
343
Q

Give the most important reserve of iodine in the body

A

The thyroid gland

5-7mg

344
Q

Goitre by excessive iodine intake

A

Decreased hormone production

  1. Acts as physiological feedback inside the gland
  2. Inhibits unnecessarily high rates of hormone production
  3. Can result in sustained high TSH levels
  4. Thyroid grows, unable to produce hormones
345
Q

Canine hypothyroidism

Symptoms + treatment

A
  • Un-rare
  • Symmetrical hair loss
  • Administration of thyroid hormones
  • Replacement of T4 + T3
346
Q

Feline hyperthyroidism

Symptoms

A
  • Disease of cardiac muscle (Cardiomyopathy)
  • Cardiac hypertrophy develops
347
Q

Adrenal cortex

A
  • Produces steroid hormones
    • Mineralocorticoids
    • Glucocorticoids
  • Mineral + water metabolism
  • Mobilisation of energy stores
348
Q

List the zones of the adrenal cortex

A
  • z. glomerulosa(ruminants) /z. arcuata
  • z. fasciculata
  • z. reticularis
349
Q

Which species don’t have separate zones of the adrenal medulla

A

Birds

350
Q

Is the adrenal cortex innervated?

A

No

351
Q

z. glomerulosa produces…

A

Mineralocorticoids

352
Q

z. fasciculata produces

A

Glucocorticoids

353
Q

z. reticularis produces…

A
  • Androgens
  • Estrogens
354
Q

Title the figure

A

Long feedback loop of ACTH on the adrenal cortex

355
Q

The basis of all adrenal hormone production originates from…

A

Cholesterol (+de novo)

356
Q

What are the three groups of adrenal cortex hormone frames?

A
  • Pregnane (21-carbon)
  • Androstane (19-carbon)
  • Estrane (18 carbon)
357
Q

Examples of pregnanes

A
  • Mineralocorticoids
  • Glucocorticoids
358
Q

Androstane

A

Male sexual hormones

359
Q

Enzyme 1

A

20,22-demolase

360
Q

Enzyme 2

A

3-beta-hydroxysteroid dehydrogenase-4-5-isomerase

361
Q

Enzyme 3

A

17-alpha-hydroxylase

362
Q

Enzyme 4

A

C21 hydroxylase

363
Q

Enzyme 5

A

18-aldolase

364
Q

Enzyme 6

A

17-20 desmolase

365
Q

Enzyme 7

A

Aromatase

366
Q

20, 22 demolase function

A
  • Key enzyme of steroid synthesis
  • Belong to P450 enzyme family
367
Q

3-beta-hydroxysteroid dehydrogenase-4-5-isomerase function

A
  • Lack of this enzyme = fatal
  • Needed for mineralocorticoid + glucocorticoid synthesis
368
Q

17-alpha-hydroxylase function

A
  • Determines glucocorticoid direction
  • If it is lacking:
    • Overproduction of aldosterone + corticosterone
    • No synthesis of:
      • Glucocorticoids
      • Androgens
      • Estrogens
369
Q

C21 hydroxylase enzyme function

A
  • Lack of this enzyme:
    • Lack of aldosterone → loss of minerals
  • ACTH prevalence → synthesis of only androgens/estrogens
  • May stimulate male secondary sexual attributes in females
370
Q

18-aldolase function

A

Precondition of aldosterone synthesis

371
Q

17-20-desmolase function

A

Determines sexual steroid direction

372
Q

Aromatase enzyme function

A

Determines sexual hormone synthesis

373
Q

Give the main mineralocorticoid hormone

A

Aldosterone

374
Q

Overdose of mineralocortiocoids

A
  1. Na+ increase
  2. Water reabsorbed with Na+
  3. Results in isoosmotic hypervolemia
  4. Increased urinary excretion (renal escape)
  5. Decreased K+ in the body
  • Muscular weakness
  • Paradox alkalosis
375
Q
A

Water reabsorption

376
Q
A

|soosmotic hypervolemia

377
Q
A

Compensatory effect of the kidney in ‘renal escape’

378
Q
A

Only 10% (instead of 20%)

379
Q
A
  • Muscular weakness
  • Paralysis
  • Alkalosis (Aciduria)
380
Q

Title the figure

A

Mineralocorticoid deficiency

381
Q
A
  • Loss of Na+ and water
  • K+ + H+ retention
382
Q
A

Acidosis

383
Q
A

Isoosmotic extracellular hypovolemia

384
Q
A

Hyposmotic extracellular hypovolemia (25%)

385
Q
A

Paradox intracellular hypervolemia

386
Q
A
  • Decrease blood volume + BP
  • A decrease of renal blood flow
  • Azotemia
  • Death
387
Q

Give the factors regulating mineralocorticoids in order of importance

A
  1. The increase of plasma K+ conc.
  2. Renin-angiotensin system
  3. The decrease of Na+ content in the body
  4. ACTH
388
Q

How does an increase of plasma K+ regulate mineralocorticoids?

A

Increases aldosterone synthesis

389
Q

How does the renin-angiotensin system regulate mineralocorticoids?

A
  1. System activated
  2. JGA detects Na+ deficiency
  3. Angiotensin II synthesised
  4. Aldosterone synthesised
390
Q

Give the most prominent glucocorticoids

A
  • Cortisol
  • Corticosterone
391
Q

The physiological effect of glucocorticoids

A
  • Long-lasting mobilisation of the energy reserves of the body
  • Carbohydrate metabolism
  • Protein metabolism
  • Lipid metabolism
392
Q

Effects of glucocorticoids on the carbohydrate metabolism

A
  • Glyconeogenesis (GNG)
  • Amino acids → Liver
  • Amino acid mobilisation
  • Excessive GNG → Metasteroid diabetes develops
393
Q

Effect of glucocorticoids on protein metabolism

A
  • Decrease protein synthesis
  • Increase protein cleaving
  • Nitrogen balance decreases
394
Q

Effect of glucocorticoids on lipid metabolism

A
  • Increase lipolysis
  • Increase plasma FFA levels
  • Increased extent of fat burning
  • Redistribution of fat:
    • Fat moves from periphery → liver
395
Q

Circulatory effects of glucocorticoid insufficiency

A
  • Na+ loss, oligemia
  • K+ increase → Cardiac weakness
  • Increased capillary permeability → oedema
396
Q

Blood cell effects of glucocorticoid insufficiency

A

AC overproduction:

  • A decrease of: Eosinophils + basophils
  • Lymphoid tissue degrades

AC extirpation:

  • Lymphoid hyperplasia
397
Q

Neural effects of glucocorticoid insufficiency

A
  • AC hyperfunction - Convulsive susceptibility increase
  • AC extirpation - Depression, psychic disorders
398
Q

Pharmacological effects of glucocorticoids

A
  • Anti-inflammatory effect
399
Q

Effect of continuous high level of glucocorticoids (Such as stress/ drugs)

A
  • Inhibition of mesenchymal cell proliferation
  • Antiphlogistic effect
  • Antiallergic effect
400
Q

Inhibition of mesenchymal cell proliferation

A
  • Fibroblast + collagen formation is inhibited
  • Cicatrisation is prolonged
  • Granulation + healing of wounds is inhibited
  • Osteolysis → osteoporosis
401
Q

Anti-inflammatory effect of glucocorticoids

A
  • PLA2 blocking effect
    • The decrease of inflammatory colour, dolor and tumor
    • Decrease basophil degranulation (decrease allergic reactions)
  • Masking effect
402
Q

Antiallergenic effects of glucocorticoids

A
  • Inhibit histamine release
  • No direct influence on the antigen-antibody reaction
403
Q

Give the responses to stress

A
  • Specific response
  • Aspecific response
404
Q

Stress is elicited by…

A

Stressors

405
Q

List some physical stressors

A
  • Mechanical stimuli
  • Surgical intervention
  • Limitation of motion
  • Temperature
406
Q

List some pathogenic stressors

A
  • Virus
  • Bacterium
  • Parasite
407
Q

List some stressors related to feeding

A
  • Deficiencies:
    • Vitamins
  • Microelements
  • Intoxications
408
Q

Give some examples of emotional stressors

A
  • Psychic stress
  • Pain
  • Lack of stimuli
409
Q

1

A

Initial stage

  • Release of ACTH
  • Often accompanied by Cannon’s alarm reaction
  • Effect of catecholamines declines
  • ACTH remains high
410
Q

2

A

Resistive stage

  • High production of glucocorticoids
    • Unnecessary effects reduced to a minimum
    • The immune system becomes inhibited
    • Storing processes inhibited
  • Energy needs:
    • Burning fat
    • Burning protein stores
    • Muscles decomposed
411
Q

3

A

Exhaustion stage

  • Energy reserves of organism expire
  • Stage of collapse
  • Animal dies
412
Q

4

A

Adaptive disorders stage

  • Arthritis
  • Chronic hypertension
  • Ulcer
  • Hepatic failure
413
Q

The adrenal medulla is part of the…nervous system

A

Sympathetic

414
Q

The adrenal medulla produces…

A

Epinephrine

415
Q

Which cell type is found in the adrenal medulla

A

Chromaffin cells

416
Q

Chromaffin cells: Large, few granules indicates

A

Noradrenaline

417
Q

Chromaffin cells: many, small granules indicates

A

Adrenaline

418
Q

Body condition after removal of the adrenal medulla

A
  • Activity at a general state
  • Reproductive functions don’t change
  • Animal reacts appropriately in case of emergency
  • Blood glucose stable
  • Catecholamine plasma levels show characteristic changes
419
Q

The process of removal of the adrenal medulla

A

Demedullation (AMX)

420
Q

How can demedullation be executed surgically?

A

By keeping the adrenal cortex intact

Lack of medulla is compensated by the sympathetic nervous system

421
Q
A

Epinephrine

422
Q
A

Norepinephrine

423
Q
A

Dopamine

424
Q

Adrenal medullar hormones are collectively called…

A

Catecholamines

425
Q
A

Tyrosine

426
Q
A

DOPA

427
Q
A

Dopamine

428
Q
A

Norepinephrine

429
Q

Title the figure

A

Adrenaline synthesis + Peptidergic co-transmission

430
Q
A

Amine precursor

431
Q
A

H+

432
Q
A

DBH → NE

DBH = Dopamine-beta-hydroxylase enzyme

433
Q
A

H+

Via ATPase pump

434
Q
A

NE

435
Q
A

PNMT

Enzyme

436
Q
A

E

(Epinephrine)

437
Q
A

Chromogranin

438
Q

Degradation of hormones allows…

A

Suspension of hormonal effects

439
Q

Give the methods of hormone inactivation

A
  • Reuptake
  • Enzymatic cleavage
440
Q

Give the two enzymes involves in enzymatic cleavage of hormones

A
  • MAO (Monoamine oxidase)
  • COMT (Catecholamine-O-methyltransferase)
441
Q

Catecholamines exert their effects through…and…receptors

A
  • Alpha
  • Beta
442
Q

Hormonal actions are divided into…

A
  • Effects on circulation
  • Effects on particular organs
443
Q

Norepinephrine stimulates…receptors

A
  • Alpha 1
  • Beta 1
444
Q

Epinephrine stimulates…receptors

A
  • Alpha 1
  • Beta 2
445
Q
A
  • Agonist: Phenylephrine
  • Antagonist: Phenoxybenzamine
446
Q
A
  • Agonist: Phenylephrine
  • Antagonist: Prazosin
447
Q
A
  • Agonist: Clonidine
  • Antagonist: Yohimbine
448
Q
A
  • Agonist: Isoproterenol
  • Antagonist: Propranolol
449
Q
A
  • Agonist: Prenalterol
  • Antagonist: Methoprolol
450
Q
A
  • Agonist: Metaproterenol
  • Antagonist: Butoxamine
451
Q

Catecholamine receptors exert their effects mostly by…

A

G-protein dependent cAMP system

452
Q

Title the figure

A

Alpha receptor signaling

453
Q
A

ATP → cAMP

AC

454
Q
A

Inactive PK

455
Q
A

Active PK

456
Q
A

DAG

457
Q
A

Active PK-C

458
Q
A

IP3

459
Q
A

Ca2+

460
Q

Title the figure

A

Beta receptor signaling

461
Q
A

ATP

462
Q
A

cAMP

463
Q
A

Active PK

464
Q

Alpha-1 receptor effects

A
  • Smooth muscle contraction
  • Glycogenolysis
  • Sympathetic synaptic transduction
465
Q

Alpha-2 receptor effects

A

Regulation of transmitter release in the CNS

466
Q

Beta-1 receptor effects

A
  • Stimulation of the heart
  • Stimulation of adipose cells
467
Q

Beta-2 receptor effects

A
  • Smooth muscle relaxation
  • Increase metabolism
468
Q

Where do catecholamines effect?

A
  • Circulation
  • Smooth muscles
  • Intermediary metabolism
  • Different organs
469
Q

Effects of catecholamines on circulation

A
  • Similar to sympathetic nervous system effects
470
Q
A

Norepinephrine (NE) > Epinephrine (E)

471
Q
A

Smooth muscles

472
Q
A

Smooth muscle contraction

473
Q
A

Isoproterenol > E > NE

474
Q
A

Cardiac, coronary

475
Q
A

Enhancing, dilation

476
Q
A

Epinephrine

477
Q
A
  • Bronchi
  • Smooth muscles of skeletal muscle vessels
478
Q
A

Dilation

479
Q

The receptor-type used is dependent on…

A

Plasma concentration

480
Q
A
  • α1: Vasoconstriction
  • β1: Increase of cardiac output
  • Σ: Increase of blood pressure
481
Q
A
  • β1: Increase of cardiac output
  • β2: Vasodilation in skeletal muscles
  • Σ: Redistribution of circulation
482
Q
A
  • Differences are observed
  • Σ: redistribution of circulation, increase of blood pressure
483
Q

β1: Increase in cardiac output: Positive effects

A
  • Chronotrop
  • Inotrop
  • Dromotrop
  • Bathmotrop
484
Q

Receptors in the arteriole wall in intestinal tract

A
  • Too many alpha receptors
  • Very few beta receptors
485
Q

Receptors in the arteriole wall in skeletal muscle

A
  • Too many beta 2 receptors
  • Very few alpha receptors
486
Q

Receptors in the smooth muscle internal to the intestinal tract

A
  • Many alpha receptors
  • Many beta2 receptors
487
Q

Describe the hormonal sympathetic activation of smooth muscles

Blood distribution

A
  1. Low epinephrine → Beta effect dominates
  2. Vessels of skeletal muscles dilate (Beta 2 effect)
  3. Vasoconstriction in areas of low beta receptors (Alpha 1 effect)
  4. Blood translocated to muscles from intestines
  5. Intestinal tract relaxes (Beta2 effect)
488
Q

Effect on the smooth muscle of high epinephrine

A
  1. Alpha effect becomes dominant
  2. Vessels contract all over the body (Alpha 1 effect)
  3. Cardiac output increases
  4. BP increases
  5. Beta2 + Alpha1 effects reach equilibrium - lumen doesn’t change
489
Q

Effect on the smooth muscle of high norepinephrine

A

Similar to epinephrine

  1. Norepinephrine has very low Beta 2 effects
  2. Contraction of smooth muscle internal to intestines is stronger
490
Q

Effects of catecholamines on the intermediary metabolism

A
  • Increase BMR
  • Increase O2 consumption
  • Cardiac output increases
  • Respiration increases
  • The calorigenic effect is significant + rapid
491
Q

Effects of catecholamines on the carbohydrate metabolism

A
  • Liver glycogen utilisation increase
  • Plasma glucose level increase
  • Glucose uptake in the muscle increases
  • Glycolysis → Lactic acid synthesis increases
  • Cori-cycle → Carbohydrate stores shifted from periphery to the centre
492
Q

Effects of catecholamines on the lipid metabolism

A
  • The utilisation of fat increases
  • FFA levels increase
  • Beta receptor effects dominate in adipose tissue
493
Q
A
  • Glycogenolysis
  • Lipolysis
  • Glyconeogenesis
494
Q
A

Lipolysis

495
Q
A

Glycogenolysis

496
Q
A
  • β2: Insulin secretion increases
  • α2: Insulin secretion decreases
497
Q
A
  • β1: Increase contractility, condition, frequency
  • α1: vasoconstriction
  • β2: Vasodilation
498
Q
A

Dilation

499
Q
A
  • α1 : M. radialis contraction
  • β2: M. ciliaris relaxation
500
Q
A

Increase of renin secretion

501
Q
A
  • α1: Contraction
  • β2: Relaxation
502
Q

Alarm reaction

A
  • ‘Fight or flight’
  • Body enabled for rapid utilisation of a high amount of energy
  • Enhancement of efficiency of physical abilities
503
Q

Give the effects of the alarm reaction

A
  • Pupils dilate
  • CO increases
  • Dilation of blood vessels
  • Contraction of spleen
  • O2 + Heat production increases
  • Inhibited GI + glandular function
  • Plasma glucose level increases
504
Q

What regulates the adrenal cortex?

A
  • Sympathetic nervous system
  • Hypoglycemia
  • Alarm reaction
  • Receptor-regulation
505
Q

Hypoglycaemia regulation of adrenal cortex

A

Direct stimulus

506
Q

Alarm reaction regulation of adrenal cortex

A

Organism able to focus on releasing energy by secretion of catecholamines

507
Q

Receptor-regulation of the adrenal cortex

A

Complex regulation: Up and down regulation

508
Q

Summarise epinephrine effects

A
  • Hormone of fighting
  • Produced by the effects of:
    • Muscle activity
    • Cold
    • Drop of blood pressure
509
Q

Summarise norepinephrine effects

A
  • Aggressive behaviour
  • Produced by the effects of:
    • Hypoxia
    • Pain
    • Emotional anxiety
510
Q

Give the main hormones of the pancreas

A
  • Insulin
  • Glucagon
511
Q

Pancreas acts as what kind of gland

A
  • Endocrine
  • Exocrine
512
Q

Insulin is produced by which cells?

A

B cells / Beta cells

513
Q

Isletas of Langerhans are composed of which cells?

A
  • B cells
  • D cells
  • A cells
  • F cells
514
Q

B-cells

A
  • Insulin production
  • Synthesised as pre-pro-insulin
  • Role: Stimulation of anabolic + storage processes
515
Q

Insulin is made up of

A
  • A chain
  • B chain
  • Zinc
516
Q

A-cells

A
  • Glucagon production
  • Acts only in the liver
  • Roles:
    • Increase plasma glucose
    • Decrease glycogen synthesis
    • Stimulate GNG
517
Q

D-cells

A
  • Somatostatin production
  • Roles:
    • Inhibition of insulin + glucagon overproduction
      • Inhibit A + B cell activity
    • Inhibition of every phase of digestion
      • Motility decrease
      • Secretion decrease
518
Q

F-cells

A
  • Pancreatic polypeptide (PP) production
  • Roles:
    • Biliary secretion + secretion of pancreatic enzymes
    • Gastric secretion + motility increase

Protein intake enhances its secretion

519
Q

Which mechanisms regulate hormone synthesis of islets of Langerhans?

A
  • The regulatory system based on paracrine activity
  • Glucose + amino acid levels of the plasma
  • Neural regulatory effects
520
Q

Give the steps of regulation of islets of Langerhans by paracrine activity

A
  1. B-cells exert reduce glucagon synthesis + A-cell activity
  2. Glucagon stimulates insulin secretion, the glucose level is limited (prevented from being lost in the urine)
  3. Glucagon stimulates somatostatin
  4. Somatostatin has a negative effect on A- and B-cells
521
Q

Describe the regulation of plasma glucose

A
  • High plasma glucose stimulates insulin secretion
  • Low plasma glucose stimulates glucagon secretion
  • Glucagon stimulates insulin synthesis of B-cells
    • Plays role in ‘feed-forward’ mechanism
522
Q

Without GIP + enteroglucagon…

A

Glucose loss

523
Q

In the presence of GIP + enteroglucagon

A

Glucose saving

524
Q

Give the two-stage process of insulin release

A
  • Stored insulin is released
  • Newly synthesised insulin released
525
Q

In the case of food consumption with high glucose content…

A

B-cells informed about the energy sources before the increase of plasma glucose level

526
Q

In the case of food consumption with high carbohydrate content…

A

GIP + Enteroglucagon are liberated

  • This causes the secretion of insulin in advance (‘feed forward’)
527
Q

Title the figure

A

Stimulation of B cells

528
Q
A

AC

529
Q
A

ATP → cAMP

530
Q
A

GLUT2

531
Q
A
  • ATP increase: K+ channel closes → Depolarisation
  • Glucose-6-P → Insulin synthesis, late release
532
Q
A

Immediate release

533
Q
A

De novo synthesis

534
Q
A

Insulin

535
Q

Title the figure

A

Neural effects on the B- and A-cell

536
Q

Autonomic nervous system affect insulin production via…

A
  • Sympathetic: Alpha and beta receptors
  • Parasympathetic: Acetylcholine receptors
537
Q

Blocking of insulin release via the sympathetic system

A
  • Blocking through alpha-2 receptors
  • Insurance of high plasma glucose levels
    • Blocking of insulin release
538
Q
A

Alpha2: Insulin glucagon block

539
Q
A

N. vagus: Insulin glucagon transient release

540
Q
A

Beta2: Insulin glucagon transient release

541
Q

Glucose gets through the membrane via…

A

GLUT transporters

Insulin dependent tissues

542
Q

In some tissues glucose tranpsorters are regulated by…

A

Insulin

543
Q

How many subtypes of GLUT transporters are there?

A

7

544
Q

GLUT-1 transporter

  • Affinity
  • Location
A
  • Intermediate affinity
  • In several tissues
545
Q

GLUT-2 transporter

  • Affinity
  • Location
A
  • Low affinity
  • Pancreas cells
546
Q

GLUT-3 transporter

  • Affinity
  • Location
A
  • High affinity
  • Neurons
547
Q

GLUT-4 transporter

  • Affinity
  • Location
A
  • High affinity
  • Muscle, adipose tissue
548
Q

GLUT-5 transporter

  • Location
A
  • Intestines, testis
549
Q

Describe insulin-receptor interaction

A
  1. Two insulin molecules bind to these subunits
  2. Conformational change in the (IC) beta subunit
  3. IC protein kinase enzymes activated
550
Q

The effects of insulin can be divided into which groups?

A
  • Glucose uptake
  • Metabolic effects
551
Q

Effect of insulin on metabolic processes

A

Increases storing and anabolic processes

552
Q

List the insulin-_independent_ tissues

A
  • Brain cells
  • RBC/WBC
  • Brain capillaries
  • Liver
  • Uptake in muscle + adipose
553
Q

List the insulin-_dependent_ tissues

A
  • Muscle
  • Adipose tissue
554
Q

Insulin-independent tissues

A

Tissues metabolising glucose that can only take up glucose without the presence of insulin

555
Q

Which GLUT receptor is found in the islets of Langerhans?

A

GLUT2

556
Q

Insulin increases the synthesis of…

A
  • Glycogen
  • Protein
  • Fat

By inhibiting their respective enzymes

557
Q

The effects of insulin on carbohydrate metabolism

A
  • Incorporates amino acids into proteins: GNG
  • Decrease glucose level
558
Q

The effects of insulin on lipid metabolism

A
  • Triglyceride synthesis increase
  • Degradation of lipid decrease
  • Stimulate fatty acid synthesis from AcCoA
559
Q

The effects of insulin on protein metabolism

A
  • Stimulate amino acid uptake of all cells øhepatocytes
  • Enhance protein synthesis
  • The decrease in protein degradation
  • Positive nitrogen balance
560
Q
A

Amino acid

561
Q
A

Glucose

562
Q
A

FFA

563
Q

Every action of insulin is antagonised by…

A

Glucagon

However, only in the liver

564
Q

Effect of insulin on: Dependent tissues

A

Facilitates glucose entry

565
Q

Effect of insulin on: Adipocytes

A
  • Glucose entry increases
  • Triglyceride synthesis increases
  • Lipase activity decreases
566
Q

Effect of insulin on: Muscle cell

A
  • Glucose entry + storing increases
  • Glucose → energy conversion increases
  • Amino acid entry, protein synthesis increases
567
Q

Effect of insulin on: Liver

A
  • Glucose entry not regulated
  • Glycogen synthesis increases
  • Glucose release decreases
  • Ketogenesis and GNG decreases
568
Q

Effect of insulin on: Neuron

A
  • Enhances K+ entry
  • Hyperpolarisation effects
569
Q

Title the figure

A

Glucose metabolism

570
Q
A

Foodstuff glucose

571
Q
A

Plasma glucose

572
Q
A

Lactic Acid

573
Q
A
  • H2O
  • CO2
574
Q
A

Adipocyte

575
Q
A

FFA

576
Q
A

Liver glucose

577
Q

During glucose metabolism, if there are too high AcCoA concentrations…

A

Ketone bodies appear

  • Citric acid cycle activity decreases
578
Q

What are the two outcomes of insulin deficiency on protein metabolism?

A
  • Dehydration
  • Negative N balance
579
Q
A

Utilisation of glucose decreases

580
Q
A

Protein catabolism

581
Q
A

K+ loss

582
Q
A

Tissue K+ decreases

583
Q
A

Polyuria + polydypsia

584
Q
A

Amino acid levels decrease

585
Q
A

GNG increases

586
Q
A

Urinary N-secretion increases

587
Q

What are the two outcomes of insulin deficiency on fat metabolism?

A
  • Na+ loss
  • Acidosis
588
Q
A

Glucose utilisation decreases

589
Q
A

Lipogenesis (storage) decreases

590
Q
A

Mobilisation of adipose deposits increase: Lipemia

591
Q
A

Production of ketone substances in the liver: Ketonemia

592
Q
A

Ketonuria

593
Q
A

Utilisation of glucose decreases

594
Q
A
  • Liver glycogenolysis
  • Muscle glycogenolysis
595
Q
A

Hyperglycemia

596
Q
A
  • Glycosuria (Excess sugar in urine)
  • Osmotic diuresis (Increased urine production)
597
Q
A

H2O + electrolyte loss

598
Q
A
  • Dehydration
  • Hemoconcentration
599
Q
A

Breakdown of circulation

600
Q
A

Production of ketone substances increases

601
Q
A
  • Vomiting
  • Diarrhoea
602
Q
A
  • Na+ loss
  • K+ loss
603
Q
A
  • Fall of blood pressure
  • RBF decrease
  • Anuria (Failure of urine production)
  • Coma
604
Q
A

Exitus

605
Q

Parallel to metabolic acidosis, what else occurs?

A

Protein degredation

606
Q

List the types of diabetes

A
  • Type-1 (Human)
  • Type-2 (Human)
  • Type-3 (Canine)
607
Q

Type-1 diabetes

A
  • Appears in juvenile age
  • Effects of the disease are through insulin deficiency
  • Excess of glucagon
  • Rapid
  • Hereditary
  • Insulin-dependent diabetes mellitus (IDDM)
608
Q

IDDB

A
  • Insulin-dependent diabetes mellitus
  • Caused by insufficient insulin production
609
Q

Type-II diabetes

A
  • Adults/elderly
  • The insufficient response of B-cells to carbohydrates
  • Though that GLUT2 isn’t functioning properly
  • Insulin production still regulated
  • Can be normalised with a controlled diet
  • Non-insulin-dependent diabetes mellitus (NIDDM)
610
Q

Type-III diabetes

A
  • Adults, 5-15 years
  • Insulin-sensitive
  • Late-onset, nutritive
611
Q

What are autacoids?

A
  • Biological factors which act as local hormones
  • Brief duration
  • Act near the site of synthesis
612
Q

What are the two groups of Autacoid?

A
  • Peptides
  • Eicosanoids (Fatty acid-like substances)
613
Q

Where are eicosanoids produced?

A

All cells in the body

614
Q

Characteristics of Eicosanoids

A
  • 20-carbon fatty acids
  • The product of enzymatic reactions of phospholipids
  • Mediated by G-protein → Activating PLA2 enzyme
615
Q

Title the figure

A

Eicosanoid synthesis

616
Q

MPL stands for…

A

Membrane phospholipids

617
Q
A

Phospholipase-A2

618
Q
A

Lipoxygenase

619
Q

List the effects of eicosanoids of veterinary importance

A
  • Increase inflammation
  • Insulin release
  • Bone resorption
  • Reproduction
  • Thrombocyte aggregation
  • Renal effects
620
Q

Effect of eicosanoids on inflammation

A
  • Initiate inflammation
  • Example: Through PMN cells
  • Cause:
    • Vasodilation
    • Chemotaxis
    • IL-1 fever
621
Q

Effect of eicosanoids on insulin release

A
  • HPETE stimulates PGE2 pathway
  • Inhibition of insulin release
622
Q

Effect of eicosanoids on​ bone resorption

A
  • PGE2 produced by osteoblast cellular membrane
  • Parathyroid hormone-like effect on Ca2+ mobilisation
  • Allows Ca2+ entry into the plasma
623
Q

Effect of eicosanoids on reproduction

A
  • In large animals
  • PGF2-alpha production of the uterus
  • The twisted part of a. ovarica + v. uterina allows diffusion of PGF2-alpha
  • Leutolytic effect
624
Q

Effect of eicosanoids on thrombocyte aggregation

A
  • Endothelial cells release PGI continuously
  • This binds to membrane receptors of platelets
  • cAMP increase in platelets
  • Inhibited activity of PLA2
  • Platelets don’t aggregate

During injury

  • This mechanism is stopped
  • TXA2 synthesis begins → Aggregation + thrombus
625
Q

Effect of eicosanoids on the kidney

A
  • Prostacyclin synthesis in renal tubule enhances renin secretion
  • Increase RPF
  • Antagonises effect of ADH
626
Q

Regulation of eicosanoid production

A
  • Corticosteroids + mepacrine inhibit eicosanoid synthesis
  • Salicylic acid, indomethacin and ibuprofen inhibit cyclooxygenase enzyme
  • Benzydamine and imidazole inhibit thromboxane synthase enzyme
    • Normal production of prostaglandins
    • Decreased synthesis of thromboxane
627
Q

Peptide autacoids are part of which system?

A

Diffuse Neuro-endocrine system (DNES)

628
Q
A
  • K + PNE Cells
  • BLP, SN, Enkephalin
629
Q
A
  • C-cell
  • CT
630
Q
A
  • G-cell + D-cell
  • Gastrin, enkephalin
631
Q
A
  • Brush cells
  • Secretin, SP, SK, glucagon, gastrin, CCK
632
Q
A
  • A, B, D, G, PP
  • Glucagon, insulin, SN, gastrin
633
Q
A
  • Chromaffin
  • NPY, enkephalin, endorphin, BLP
634
Q
A
  • Merkel
  • CT, BLP, VIP
635
Q

Abbreviation: BLP

A

Bombesin-like peptide

636
Q

Abbreviation: CCK

A

Cholecystokinin

637
Q

Abbreviation: CRH

A

Corticotropin-releasing hormone

638
Q

Abbreviation: CT

A

Calcitonin

639
Q

Abbreviation: NPY

A

Neuropeptide Y

640
Q

Abbreviation: NT

A

Neurotensin

641
Q

Abbreviation: PP

A

Pancreatic polypeptide

642
Q

Abbreviation: PYY

A

Peptide YY

643
Q

Abbreviation: SK

A

Substance K

644
Q

Abbreviation: SN

A

Somatostatin

645
Q

Abbreviation: SP

A

Substance P

646
Q

Abbreviation: VIP

A

Vasoactive intestinal peptide

647
Q

List the classifications of peptide hormones

A
  • Bombesin
  • Kinins
  • Somatostatin
  • Neurotensin
  • Endogen opioid
  • Tachykinin
648
Q

Bombesin peptides

A
  • GRP
  • Neuromedins
  • Ranatensins
649
Q

Kinin peptides

A
  • Kininogens
  • Bradykinin
  • Kallikreins
650
Q

Neurotensin peptides

A
  • Angiotensin
  • Xenopsin
651
Q

Endogen opioids

A
  • Enkephalin
  • Dynorphins
  • Exorphins
652
Q

Tachykinin hormones

A
  • Substance-P
  • Neurokinin A, B, K
  • VIP
653
Q

Major effects of bobmesins

A
  • Hypothermia
  • Hypoglycemia
  • Gastric juice secretion
654
Q

Major effects of kinins

A
  • Vasodilation
  • PH-synthesis
655
Q

Major effects of somatostatins

A
  • Hyperkinesis
  • Excitation
  • Periphery:
    • All metabolic processes are blocked
656
Q

Major effects of neurotensins

A
  • Most potent analgesic
  • Opioid independent
657
Q

Major effects of endogen opioids

A
  • CNS:
    • Analgesic
  • GI tract
    • Synchronisation of motility
658
Q

Major effects of tachykinins

A
  • Control of exocrine pancreas
  • Modulates AC steroid secretion
659
Q
A

Physiology (18 decks)

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