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Endocrinology Flashcards

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1
Q
A

Direct communication

  • Transportation via gap junctions or connexins
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2
Q
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Contact communication

  • Information processing via molecules integrated into the membrane
  • Typical in cells of the immune system
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3
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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
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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
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Classical endocrine effect

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

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16
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Pituitary gland

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17
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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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Hypothalamus ## Footnote *TRH*
26
Hypophysis ## Footnote *TSH*
27
Thyroid gland ## Footnote *Thyroxine synthesis increases*
28
Blood vessel: Thyroxine level increases
29
30
31
Give examples of IC "second messengers"
* cAMP * cGMP * Ca2+ * Diaglycerol (DAG) * Inositol triphosphate (IP3)
32
Which processes occur between: * Signals being received * The appearance of biological effects
Signal transduction processes
33
What are the reasons that a hormone-like substance could have varying effects on different cells?
* There are separate receptors in the different tissues * The receptor is the same but a different signalling pathway is initiated
34
Title the figure
Scatchard analysis
35
Bmax (No. of binding sites) given by the point of intersection
36
What is a Scatchard analysis used for?
Used for measuring the properties of receptor-ligand interaction
37
Which parameters can be estimated from a Scatchard analysis?
* The total number of binding sites * Strength (affinity) of binding between the receptor and the ligand
38
Title the figure
Regulation of receptor number
39
* Either: * Long lasting hormone treatment * The decrease of cellular metabolic needs
40
"Down-regulation" Inhibition of receptor expression
41
Either: * Removal of the endocrine gland * Increase of cellular metabolic needs
42
"Up-regulation" Facilitation of receptor expression
43
How do _lipophilic_ hormones have an effect on cells?
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
44
How do _water-soluble/hydrophilic_ peptides and glycoprotein hormones have an effect on cells?
Exert actions by binding to membrane surface receptors
45
G-protein _dependent_ transduction outcomes
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
46
Describe the receptor of G-protein _independent_ transduction
The receptor is a transmembrane protein: * EC ligand binding part * Central part * IC part which exhibits _phosphorylase_ activity
47
Describe G-protein independent transduction
1. Ligand bond formation 2. IC polypeptide chain phosphorylates 3. Receptor activates 4. Biological action
48
Describe cell activation when the _receptor is in the cytoplasm_
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
49
Title the figure
Fine structure of the nuclear receptor
50
Lypophilic hormone
51
LBD ## Footnote *Ligand binding domain*
52
DNA-BD *DNA binding domain*
53
HRE ## Footnote *Hormone-responsive element*
54
BPE ## Footnote *Basal promoter element*
55
VD ## Footnote *Variable domain*
56
The function of the VD
Locating of the base-pair segment of the DNA ## Footnote *Specific to the particular hormone*
57
The function of HRE
Binds the DBD
58
DBD
DNA binding domain *Amino* *acid segment of the hormone-receptor complex*
59
The function of the BPE
1. Activated by receptor-DNA complex 2. Expression of the structural gene begins
60
Title the figure
The receptor in the form of an ion channel
61
Describe the structure of a receptor which is acting as an ion channel
* 5 membrane-integrated domains * Ligand binding site on the EC side * 2x alpha subunits * 2x beta subunits * 1x delta subunit
62
Give examples of receptors which are ion channels
* n-ACh-R *(Nicotinic acetylcholine receptor)* * Glutamate receptors * Anion receptors
63
Nicotinic acetylcholine receptors can be inhibited by...
d-tubocurarine
64
n-ACh-R can be stimulated/inhibited by substances affecting the...
Receptor's 5 subunits
65
What are the states n-ACh-R can be in?
* Closed (before ACh binding) * Open (After ACh binding)
66
Describe the processes after ACh binds to the receptor
1. Conformational change 2. Cation channel opens *("open state")* 3. Flow of cations 4. Local excitatory potential formed 5. AP is triggered
67
Describe the closing of n-ACh-R
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
68
Give the main groups of glutamate-sensitive receptors
* NMDA receptor * AMPA receptor * Kainate-receptor
69
NMDA receptor * Function
**N-****metil****-D-aspartate** * Binding Mg2+ keeps receptor closed * Mg2+ dissociated after receptor activation * Ca2+ influx maintains a lasting effect
70
Opening of anion-receptors causes
Hyperpolarisation of CNS inhibitory synapses
71
What can cause hyperpolarisation of anion receptors
Nonspecific anions * Cl- * HCO3-
72
Give the main mediators of anion-receptors
* GABA * Glycine
73
The function of GABA in the anion-receptor
* Either GABA-A / GABA-B * GABA-B activation: * Decrease IC cAMP * Affects K+ channels
74
G-protein structure
* 3 subunits form a complex: * Alpha subunit + GDP * Beta subunit * Gamma subunit
75
G-protein mechanism of action
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
76
Describe the return of G-protein to its resting state
1. GTP → GDP 2. Alpha subunit binds to gamma + beta again 3. G protein → Resting state
77
Describe Gs effect
* Activated G-protein migrates to a remote ion channel protein * Activates the channel
78
Describe Gi effect
* Activated G-protein migrates to a remote ion channel protein * Inactivates the channel
79
1. M2 ACh-R 2. K+ channel opens
80
1. alfa2 type R 2. K+ channel opens
81
1. D2 type R 2. K+ channel opens
82
1. GABA type R 2. K+ channel opens
83
1. S2 type R 2. K+ / Ca2+ channel opens
84
1. OP type R 2. Ca2+ channel opens
85
Title this figure
Adenylate cyclase mechanism
86
Summarise the adenylate cyclase mechanism
* Influenced by G-proteins * Gs: adenylate cyclase activity ↑ * Gi: adenylate cyclase activity ↓
87
Describe the steps of the Gs mechanism
1. Glucagon mobilises Gs G-protein 2. Liberates hepatic glycogen stores
88
Describe the steps of the Gi mechanism
* _alpha2-adrenergic_ receptor activated * IC cAMP levels ↓
89
List receptors of the Gs pathway
* Prostacyclin * Dopamine D1 * Catecholamine beta * Anterior pituitary * Histamine H2 * 2-type ADH
90
List receptors of the Gi pathway
* Dopamine D2 * Alpha1 catecholamine * Some glutamate * Some opioid
91
Title the figure
Phospholipase C mechanism (PLC)
92
Give the steps of the phospholipase C (PLC) mechanism
1. Activation of G-protein 2. Stimulates Phospholipase C 3. Converts membrane phospholipids → _IP3/DAG_
93
IP3
* 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
94
DAG
* Similar behaviour to cAMP * Activates type-C protein kinases * Triggers several phosphorylation pathways * Biological effects
95
Give examples of ligands in the PLC mechanism
* ACh * Histamine * Purin * PGE * TXA2 * ADH * Oxytocin All of which release Ca2+
96
Give the steps of the Phospholipase A2 (PLA2) mechanism
1. G-protein activation 2. Converts phospholipids → _arachidonic acid_ *(substrate)* 3. Arachidonic acid → Several products
97
Besides active G-proteins, what else can activate the PLA2 mechanism?
Ca2+
98
Arachidonic acid can pass through which further pathways?
* Lipoxygenase pathway * Cyclooxygenase pathway * Epoxygenase pathway
99
List the products of the lipoxygenase pathway
* Leukotrienes (LT) * Lipoxins (LX)
100
List the products of the cyclooxygenase pathway
* Prostacyclins (PGIs) * Prostaglandins (PGs) * Thromboxanes (TXs)
101
Describe the mechanism when a receptor is also an IC enzyme
1. Ligand bond formed on the outer surface 2. IC polypeptide chain phosphorylates 3. Activation of the receptor 4. Biological action
102
Give an example of direct enzyme stimulation
Insulin receptor ## Footnote *The receptor is able to phosphorylate itself and other proteins on the IC part of the cell*
103
Auto-phosphorylation
1. Self phosphorylating enzyme phosphorylates tyrosine residues of the IC receptor sequence 2. Phosphorylated tyrosine residues bind intracellular proteins 3. Specific IC responses elicited
104
Describe the processes after autophosphorylation
1. *Autophosphorylation* 2. Receptor-enzyme complex is taken up by the cell 3. Inactivation
105
Describe the figure
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
106
The hypothalamus is divided into which parts?
* Magnocellular area (with large cells) * Parvocellular area (with small cells)
107
Describe the movement of hormones from the hypothalamus
1. Hormones produced in the parvocellular area → Adenohypophysis 2. Hormones produced in the magnocellular area → Neurohypophysis
108
Which nuclei are found in the magnocellular area?
* Supraoptic nucleus (Oxytocin production) * Paraventricular nucleus (ADH production)
109
Which nuclei are found in the parvocellular area?
* Ventromedial nucleus * Dorsomedial nucleus * Infundibular nucleus ## Footnote *Inhibit/release substances which can reach the adenohypophysis*
110
Describe the transport of neurosecretions from the _parvocellular area_
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
111
Describe the transport of neurosecretions from the _magnocellular area_
1. Magnocellular area 2. From the site of production (Neurone) 3. The site of release (Neurohypophysis)
112
Title the figure
Axonal transport
113
Describe the steps of axonal transport
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
114
Basal membrane
115
Axonal transport, neurosecretion
116
First capillarisation (Median eminence)
117
Portal circulation
118
Second capillarisation (anterior pituitary)
119
Which portal vessel do peptides travel down in axonal transport?
Pituitary stalk
120
Give the proteins of axonal transport
* Kinesin (Transport from soma to synapse) * Dynein (Returning of residues to the soma)
121
In axonal transport, what determines the direction of transport of proteins?
Polarity
122
Parvocellular areas synthesise releasing and inhibitory substances which influence...
Tropic-hormone production of the adenohypophysis
123
Hypophyseotrop hormones
Hypothalamic substances that influence production + release of the pituitary gland
124
Give the parvocellular hormone systematic names
* RH/RF (Releasing hormone/ Releasing factor) * IH/IF (Inhibiting hormone/ Inhibiting factor) * '+' (Facilitates synthesis + secretion hormones) * '-' (Inhibits hormone synthesis and release) ## Footnote *E.g TSH-RH = Thyrotropin hormone releasing hormone*
125
In adenohypophyseal systematic naming, what do the following abbreviations mean *(Prior to 'RH' or 'RF')*? * T * C * Gn * G * P * M
* T = Thyrotropin, TSH * C = Corticotropin, ACTH * Gn = Gonadotropin, FSH/LH * G = Growth hormone, STH * P = Prolactin, PRL * M = Melanocyte stimulating hormone, MSH
126
1. TSH+ 2. Thyroliberin
127
1. ACTH+ 2. Corticoliberin
128
1. FSH+, LH+ 2. Gonadoliberin
129
1. GH+ 2. Somatoliberin
130
1. PRL+ 2. VIP, TRH
131
1. MSH+ 2. MSH-RH
132
List the releasing factors (short name)
* TRH * CRF * GnRH * GRF * PRF * MRF
133
Function: Thyrotropin-releasing hormone
* Stimulates thyroid gland * Stimulates hormone release
134
Function: Corticotropin-Releasing Factor
* Adrenocorticotropin (ACTH) stimulating hormone * Facilitates synthesis + release of: * ACTH * MSH * Endogenous opiates * Stimulating + splitting + synthesis of POMC
135
Function: Gonadotropin-releasing hormone
* Facilitates synthesis + release of: * FSH (Follicle stimulating hormone) * LH (Luteinising hormone) * In males + females
136
Function: Growth hormone releasing factor (GRF)
Synthesis + release of growth hormone
137
Function: Prolactin-releasing hormone (PFR)
* Prolactin synthesis + release * Lactation * Ovulation in the rat
138
What are the main parvocellular inhibiting factors?
* Dopamine * Somatostatin * GABA * VIP
139
In adenohypophyseal systematic naming, what do the following abbreviations mean (Prior to 'IH' or 'IF')? * G * P * M
* G = Growth hormone, somatotropin, STH * P = Prolactin, PRL * M = Melanocyte-stimulating hormone, MSH
140
1. TRH-, PRL- 2. TSH-IH, PRL-IH
141
1. GH- 2. GH-IH, somatostatin
142
1. PRL- 2. PRL-IH
143
1. GH+ 2. MSH-IH, Melatostatin
144
1. General, an indirect inhibitor 2. Norepinephrine
145
1. General, an indirect inhibitor
146
Function: GIF
* Systematic name for Somatostatin * GIF = Growth hormone inhibiting factor * Somatotropin inhibiting hormone
147
Function: PIF
* Systematic name for inhibiting factor of prolactin release + production * Regulated by dopamine * Hypothalamic peptide is known to decrease prolactin production
148
1. PRL+, GIF 2. GIF+ In the pancreas
149
1. PRL+ 2. Substance-P antagonist
150
1. GH, PRL+ 2. MSH-IH, melanostatin
151
1. General facilitator 2. Peptide family actin on gastrin
152
1. PRL+, GH+, TSH+ 2. Paracrine action of tachykinins in HP
153
1. PRL+
154
The function of: Vasoactive intestinal peptide (VIP)
* PL+ * Somatostatin-
155
The function of: Angiotensin-II
* Synthesis + release of somatotropin + prolactin * MSH-inhibiting effect
156
1. Stimulation of water reabsorption 2. Increase BP, V1 receptor, IP3
157
1. Preparation of uterine contractions for estrogen response, basket cell contraction 2. Classical neuroendocrine reflex
158
Give an example of neuroendocrine reflexes
Oxytocin-mechanisms
159
What are the essential characteristics of a neuroendocrine reflex?
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
160
Describe the reflexes for milk ejection
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)*
161
Give the hormonal profile of a cow in stress
* Plasma glucocorticoid level increases, causing: * Oxytocin fall * Prolactin fall * Milk ejection decrease to minimum
162
What are glandotropic hormones? Give examples
Those acting exclusively on endocrine glands * TSH * ACTH * FSH * LH
163
What are histiotropic hormones? Give examples
Those acting on certain organs * STH * PRL
164
The adenohypophysis develops in which structure?
Rathke's pouch
165
The adenohypophysis is formed by...tissue
Entodermal glandular
166
The neurohypophysis is formed by...tissue
Ectodermal nervous
167
Give the cell types of the hypophysis
* A = Acidophils * B = Basophils * C = Chromophobes
168
Somatotropin (GH) producing cells
169
Adrenocorticotropin (ACTH) producing cells
170
Thyrotropin (TSH) producing cells
171
Prepubertal hypopituitarism/Removal of the pituitary gland
* Results in proportional dwarfism * In adults: * Smaller organs * Thin hairs * Decreased sexual function * Decreased protein/glycogen stores * Decreased BMR
172
Congenital hyperpituitarism
* Gigantism * In adult life: * Acromegaly: Increase in the size of enlargeable extremities and other parts. *E.g limbs*
173
Metabotropic hormones of the hypophysis
* GH * ACTH * TSH
174
Gonadotropic hormones of the hypophysis
* PRL * FSH * LH
175
STH/GH receptor mechanism of action
1. Hormone binds to the receptor 2. IC conformational change 3. Activation of the second messenger system 4. = G-protein activated cAMP
176
What direct biological effect does GH have on the body?
* Stimulates somatomedins (further hormones) in the liver * GH is therefore considered to be glandotropic + histiotropic
177
Increased growth hormone secretion in young age results in...
Gigantism
178
Increased growth hormone secretion in adults results in...
Asymmetrical growth of: * Limbs * Jaw * Certain flat bones
179
Give the episodic release of GH
180
The effect of growth hormone on protein metabolism
* Increases amino acid uptake * Increases intracellular protein synthesis * Positive nitrogen balance
181
The effect of growth hormone on lipid metabolism
* 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
182
The effect of growth hormone on carbohydrate metabolism
* Antiinsuline effects: * Decrease insulin-dependent glucose uptake in adipose * Diabetogenic effects: * Increase plasma glucose level * Glucogenesis * Glucagon production * Houssay's experiment
183
Houssay's experiment
Adenohypophysectomy improved the status of a diabetic dog
184
GH stimulates...in the liver
* Activation of thyroid hormones * Synthesis of somatomedins
185
Function of somatomedins
* Influence bone, cartilage and connective tissue * Circulate in plasma, bound by carrier proteins
186
Somatomedins have a similar structure to...
Insulin * They are therefore known as IGFs (Insulin-like growth factors)* * They cannot exert any effect on insulin receptors*
187
Somatomedins are also known as...
Sulphating factors
188
IGF =
Somatomedins (Sm)
189
IGF-I
Sm-C
190
IGF-II =
MSA ## Footnote *Multiplication stimulating activity*
191
Give the effects of IGF-I
Stimulation of: * Chondrocyte sulphate intake * Chondrocyte + osteoblast bone forming activity * Longitudinal bone growth * Transversal + periosteal bone growth * Acromegaly
192
Rat tibia test
* 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
193
Describe the regulation of GH secretion
* Plasma levels of: * Glucose * Arginine * Thyroid hormone * Hypothalamic factors
194
Peripheral feedback of GH regulation consists of which compounds?
* Plasma metabolites * IGF * IGF-BP (Binding protien)
195
Title the figure
Regulation of GH secretion
196
Regulators of GH secretion
* Plasma glucose + amino acid levels * Sex * Stress * Age
197
Regulators of GH secretion
Neurosecretion: * GH-RH * GH-IH
198
Regulators of GH secretion
Trop. hormone: * GH
199
Regulators of GH secretion
* Metabolites of peripheral tissues + IGF levels * GH receptors * IGF binding proteins
200
Practical approaches of GH
* Increase productivity * Milk * Genetic engineering * rpGH = recombinant-porcine growth hormone
201
Show the GH effects in cow (Graph)
202
Biochemical function of ACTH
In the adrenal fasciculate + reticular zones: 1. ACTH increases cAMP pathway 2. Stimulating glucocorticoid synthesis
203
What is the primary regulator of aldosterone?
Plasma [K+] ## Footnote *Not ACTH*
204
Many hormones produced in the pituitary gland are synthesised from a common precursor hormone called...
PRE-POMC * (PRE-PROOPIOMELANOCORTIN)* * The name is derived from the most important hormones derived from it*
205
List the hormones derived from Pre-POMC
* Opioid peptides * MSH * ACTH
206
Hormones derived from Pre-POMC are involved in which processes?
Adaptive processes of the body
207
ACTH is released in the incidence of...
Stress: * Mobilises energy reserves * Decreases sensation of pain
208
Which substance stimulates all the shown cleaving processes? Where is this substance produced?
CRF (Corticotropin-releasing factor) Produced in the hypothalamus
209
LPH =
Lipotropic hormone
210
CLIP =
Corticotropin like intermediate peptide
211
Endorphin =
Endogenous morphine
212
Enkephalin=
Endogenous opioid / Signal peptide
213
Give the steps of ACTH production
1. Pre-POMC 2. POMC 3. ACTH
214
Give the effect of ACTH in the glomerulosa layer
Increases cholesterol-pregnenolone conversion → Increasing mineralocorticoid synthesis
215
Synthesis of ACTH is regulated according to the...
Classical feedback principle
216
Long feedback
Involvement of glucocorticoid concentration in ACTH feedback
217
Ultra-short feedback
The inhibiting effect of ACTH on CRF
218
Give the steps of neural impulses causing ACTH secretion
1. Nerve impulses → Hypothalamus 2. Impulses are integrated by CRF synthesising cells 3. Circadian fluctuation of CRF 4. Determination of ACTH release
219
Title the figure
Regulation of ACTH synthesis
220
Exogenous/endogenous effects
221
* Serotonin * ACh
222
CRF
223
ACTH
224
Neurosecretion
225
Tropic
226
Steroids
227
* Norepinephrine * GABA
228
Circadian rhythm of ACTH
* 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)
229
Annotate the figure
* ACTH levels increase in early morning hours
230
TSH
* Gonadotropic peptide hormone * Alpha chain: Species specificity * Beta chain: Biological specificity
231
What increases TSH levels
* Thyroid hormones * Hypothalmic TRH
232
What decreases TSH levels?
* Cortisol * Dopamine * Somatostatin
233
Role of TSH
Stimulation of thyroxine
234
Plasma TSH concentration is increased by...
TRH
235
FSH
* Increase oestrogen synthesis in the follicle * Maturation of the follicle * Increased testicular spermatogenesis
236
FSH expression is directed by...
* GnRH * Steroids * Inhibin
237
LH
* Luteinising hormone * Located: Leydig cell → Testis / Granulosa cell → Ovary * Increases synthesis of androgens in both organs * Primary factor initiating ovulation
238
PRL
Prolactin * Stimulate mammary gland differentiation * Stimulate + maintain milk production * Metabolic hormone
239
How is PRL stimulated
* Hypothalamic neuronal activity 1. Oestrogen inhibits dopamine synthesis 2. Stimulating PRL production during ovulation
240
Give the effects of PRL
* Facilitation of lactogenesis * Facilitation of galactopoiesis * Support of suckling * Ovulation in the rat
241
Describe the steps toward spontaneous inhibition of PRL
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
242
List the stimuli of PRL production
* Pregnancy * Suckling * Stress * Sleep * Hypoglycaemia * Dopamine
243
List the inhibitors of PRL production
* Dopamine * GABA * GAP * Drug: Bromocryptine
244
Positive physiological stimuli and negative effects
245
Serotonin opioids
246
Neurosecretion + Peripheral blood-derived signals
247
PRL
248
Trophormone
249
Udder: * Suckling * Maternal behaviour Other: Increase of metabolism
250
'Tonic' central inhibition
251
* Dopamine * GABA * GAP
252
PRL regulation by neurosecretion involves which hormones?
* TRH * GnRH * VIP * Galanin
253
PRL regulation by peripheral blood involves which hormones?
* Serotonin * Angiotensin-II * Oestrogens
254
MSH
* Formed from ACTH * Stimulation of pigment granule production * Transport along the microtubule system → Decoloration of cells
255
Effect of MSH on pigment cells
* Microtubule system from the nucleus * MSH causes: * Granules to migrate along microtubules * Even distribution of granules, darkening cell
256
Function of melatonin
Hormone: * Stimulates migration of scattered pigment granules * Back to the vicinity of the nucleus
257
Pineal gland produces
Produces serotonin + melatonin
258
Melatonin secretion
* 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
259
Describe the innervation of the pineal gland
* Not directly connected to the CNS * Innervated by postganglionic sympathetic fibres
260
Describe the effect of decreased light intensity on the pineal gland
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)*
261
Title the figure
Innervation of the pineal gland
262
Norepinephrine
263
Beta-receptor + Adenylate cyclase
264
AMP → cAMP
265
Give the steps of Melatonin production
266
Give the degradation of melatonin
267
How does melatonin have a counter-effect on MSH?
1. It inducts concentration of pigment granules 2. Skin becomes pale
268
Give the three effects of melatonin in mammals
* Sexual function * Psychic effects * Defence against free radicals
269
(Mammals) Influence of melatonin on the sexual cycle
* Termination of the production of: * GnRH * FSH * LH * Sheep - Initiates oestrous cycle * Horse - Inhibits estrous cycle ## Footnote *Relevance to seasonality*
270
Describe melatonin levels at different human sexual maturation stages
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
Melatonin levels during ovulation (Human)
272
During and before ovulation, the night time peak of melatonin is...
Significantly decreased * *Inhibition of LH production decreased* * *Ovulation is stimulated*
273
Describe sexual cycle activity in the cat and horse
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
Describe sexual cycle activity in the sheep and goat
* A decrease of daylight: * Oestrous activity * Fertilisation in autumn → 5-month pregnancy → Progeny born in spring * Melatonin is _g__onado__-stimulative_
275
Summarise photo-gonado stimulation in birds (graph)
276
Psychic effects of melatonin
Maintenance of cyclic processes Determined by: * Day/night * Seasonal changes
277
Explain jet-lag
* High diurnal melatonin * Adaptation requires 1 day for each time zone
278
Seasonal emotional fluctuations
* Short diurnal periods - Irregular periods of depression * Lethargy/sleepiness/hunger * Assigned to melatonin overproduction * Symptoms eliminated with physiotherapy
279
Effect of melatonin on free radicals
* Melatonin has a defence role against free radicals * Thought to be the cause of melatonin's high plasma content
280
Scavenger substances
Compounds suitable for binding and neutralisation of free radicals → Melatonin is an example
281
List some reactive radicals
* Superoxide O2- * Hydrogen peroxide H2O2 * Hydroxyl OH-
282
HRE
* Hormone-responsive elements * Control gene expression of: * Metabolic enzymes * Structural proteins
283
HRE presence is controlled by...
Thyroid hormone
284
The function of the thyroid hormone in reptiles
* Growth * Not thermoregulation
285
Thyroid gland secretes...
* Thyroxine (T4) * Triiodothyronine (T3) * Reverse triiodothyronine (rT3) * Calcitonin
286
T4 is converted to...
T3
287
How can thyroid hormones production be stopped
By removal of the thyroid * Surgical removal * Thyroid destruction by radioactive iodine
288
Symptoms of thyroid hormone deficiency in _young_ animals
* Dwarfism * Neural symptoms * Sexual development retarded
289
Symptoms of thyroid hormone deficiency in _adult_ animals
* Dermal symptoms - Myxoedema * Neural functions * Sexual functions * Metabolic effects
290
A neural symptom of thyroid deficiency in young animals
Cretinism * Bad grasp * Poor learning * Constant apathy
291
Dermal symptoms of adult thyroid deficiency
* Shaggy fur/Hair loss * Subcut. CT becomes swollen
292
Symptoms of thyroid hormone overproduction
* Emphasised catabolic processes * Hypoxia sensitivity increases * Increased fat burning * Decreased lipid + protein storage * Decreased body weight * Tachycardia * Left ventricle hypertrophy * Increased irritability
293
Basedow's syndrome
* Form of hyperthyroidism * Enlarged thyroid gland + overproduction * Eyes protrude from their sockets (Exophthalmus)
294
TRH synthesis is affected by which feedback loop
Long
295
Production of TRH/TSH is inhibited by
* Feedback loops Long/short * An increase of IC T3 level in hypothalamic cells
296
Give the exogenous effects of T4 concentration
* Photoperiod * Feeding * Temperature * Stress
297
Give the endogenous effects of T4
* Genetic determination * Physiological state * Changes of hormone receptor * Activation ability of peripheral cells
298
Title the figure
General regulation of thyroid hormone
299
Exogenous effects ## Footnote *e.g cold*
300
Which thyroid hormones influence metabolism
T4 + T3
301
Title the figure
Thyroid hormone synthesis
302
1
Iodine enters gland by _active pump_ mechanism
303
2
Iodine ion → Atomic iodine ## Footnote *Lysosomal peroxidase enzyme*
304
3
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
MIT + DIT =
T3
306
DIT + DIT =
T4
307
4
* Epithelial cells synthesise colloid * TG with thyroid hormones enter the follicle by endocytosis
308
5
Start of hormone release: * Endocytosis of TG
309
6
Protein molecules degraded intracellularly * Residual iodine-containing amino acids are recycled
310
7
Hormones leave on the basal side of the cells by passive diffusion
311
What stimulates almost every step of Thyroid hormone synthesis?
TSH
312
Thyroid hormones are built on a...frame
Thyronine ## Footnote *Formed by 2 tyrosine frames*
313
What is needed in order to keep thyroid hormones dissolved in water?
Binding proteins
314
Name the binding proteins of thyroid hormones
* Thyroid-binding globulin (TBG) * Thyroid-binding prealbumin (TBPA) * T4
315
Liver thyroid hormone transit time
5 Seconds
316
Brain thyroid hormone transit time
1 second
317
90% of thyroid gland secretum is...
Inactive T4
318
5' deiodinase (5'D) function
T4 → active T3
319
5 deiodinase (5D) function
* T4 → Inactive rT3 * T3 → Inactive T2 ## Footnote *Inactivation pathway*
320
Give some deiodinases
* D1 ORD * IRD * D2 ORD * D3 IRD
321
Type I Deiodinase function
Produce T3
322
Type II Deiodinase function
* Provide 5' deiodination * Regulatory role
323
Type III Deiodinase function
5 deiodination (inactivation)
324
BAT
Brown adipose tissue
325
IRD
Inner-ring deiodinase
326
ORD
Outer ring deiodinase
327
List the metabolic effects of thyroid hormone
* Thermogenesis * Regulates the Intermediary metabolism * Facilitates the carbohydrate metabolism * Lipid metabolism * Protein metabolism
328
How to thyroid hormones increase BMR?
* Increased number of mitochondria * Na+/K+ ATPase activity increases
329
Effect of thyroid hormone on carbohydrate metabolism
* Intestinal absorption of glucose increases * Rates of gluconeogenesis + glycogenolysis increase * Insulin secretion increases
330
Effect of thyroid hormone on lipid metabolism
* Increase anabolism * Increase mobilisation * Increase catabolism * FFA increases in plasma
331
Effect of thyroid hormone on protein metabolism
* Increase in protein synthesis + breakdown * In the case of no hormone: * No protein-anabolism * In the case of overdose: * Catabolism becomes dominant
332
Effect of thyroid hormone on the nervous system
* Development of myelinisation * Widespread synaptic connectivity develops between neurons
333
Effect of thyroid hormone on the cardiovascular system
* Permissive effect: * Effect of catecholamines is potentiated * Increased cardiac function + O2 consumption
334
Goitre
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
List the goitre inducing substances
* SCN- * *Brassica* sp. * Thiourea-derivates * Lithium * High iodine intake
336
How does SCN- cause goitre?
Inhibits iodine uptake
337
How does *Brassica* cause goitre?
Inhibitors iodine incorporation
338
How do thiourea derivates cause goitre?
Inhibits the reduction of ionic iodine
339
How does lithium cause goitre?
Inhibits release of hormones
340
How does a high amount of iodine cause goitre?
Inhibits hormone synthesis and secretion
341
Which locations do not have a lot of iodine in the diet?
Locations far from the sea
342
Give the processes leading to endemic goitre
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
Give the most important reserve of iodine in the body
The thyroid gland 5-7mg
344
Goitre by excessive iodine intake
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
Canine hypothyroidism Symptoms + treatment
* Un-rare * Symmetrical hair loss * Administration of thyroid hormones * Replacement of T4 + T3
346
Feline hyperthyroidism Symptoms
* Disease of cardiac muscle (Cardiomyopathy) * Cardiac hypertrophy develops
347
Adrenal cortex
* Produces steroid hormones * Mineralocorticoids * Glucocorticoids * Mineral + water metabolism * Mobilisation of energy stores
348
List the zones of the adrenal cortex
* *z. glomerulosa(ruminants) /z. arcuata* * *z. fasciculata* * *z. reticularis*
349
Which species don't have separate zones of the adrenal medulla
Birds
350
Is the adrenal cortex innervated?
No
351
*z.* *glomerulosa* produces...
Mineralocorticoids
352
*z. fasciculata* produces
Glucocorticoids
353
*z. reticularis* produces...
* Androgens * Estrogens
354
Title the figure
Long feedback loop of ACTH on the adrenal cortex
355
The basis of all adrenal hormone production originates from...
Cholesterol (+de novo)
356
What are the three groups of adrenal cortex hormone frames?
* Pregnane (21-carbon) * Androstane (19-carbon) * Estrane (18 carbon)
357
Examples of pregnanes
* Mineralocorticoids * Glucocorticoids
358
Androstane
Male sexual hormones
359
Enzyme 1
20,22-demolase
360
Enzyme 2
3-beta-hydroxysteroid dehydrogenase-4-5-isomerase
361
Enzyme 3
17-alpha-hydroxylase
362
Enzyme 4
C21 hydroxylase
363
Enzyme 5
18-aldolase
364
Enzyme 6
17-20 desmolase
365
Enzyme 7
Aromatase
366
20, 22 demolase function
* Key enzyme of steroid synthesis * Belong to P450 enzyme family
367
3-beta-hydroxysteroid dehydrogenase-4-5-isomerase function
* Lack of this enzyme = fatal * Needed for mineralocorticoid + glucocorticoid synthesis
368
17-alpha-hydroxylase function
* Determines glucocorticoid direction * If it is lacking: * Overproduction of aldosterone + corticosterone * No synthesis of: * Glucocorticoids * Androgens * Estrogens
369
C21 hydroxylase enzyme function
* 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
18-aldolase function
Precondition of aldosterone synthesis
371
17-20-desmolase function
Determines sexual steroid direction
372
Aromatase enzyme function
Determines sexual hormone synthesis
373
Give the main mineralocorticoid hormone
Aldosterone
374
Overdose of mineralocortiocoids
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
Water reabsorption
376
|soosmotic hypervolemia
377
Compensatory effect of the kidney in 'renal escape'
378
Only 10% (instead of 20%)
379
* Muscular weakness * Paralysis * Alkalosis (Aciduria)
380
Title the figure
Mineralocorticoid deficiency
381
* Loss of Na+ and water * K+ + H+ retention
382
Acidosis
383
Isoosmotic extracellular hypovolemia
384
Hyposmotic extracellular hypovolemia (25%)
385
Paradox intracellular hypervolemia
386
* Decrease blood volume + BP * A decrease of renal blood flow * Azotemia * Death
387
Give the factors regulating mineralocorticoids in order of importance
1. The increase of plasma K+ conc. 2. Renin-angiotensin system 3. The decrease of Na+ content in the body 4. ACTH
388
How does an increase of plasma K+ regulate mineralocorticoids?
Increases aldosterone synthesis
389
How does the renin-angiotensin system regulate mineralocorticoids?
1. System activated 2. JGA detects Na+ deficiency 3. Angiotensin II synthesised 4. Aldosterone synthesised
390
Give the most prominent glucocorticoids
* Cortisol * Corticosterone
391
The physiological effect of glucocorticoids
* Long-lasting mobilisation of the energy reserves of the body * Carbohydrate metabolism * Protein metabolism * Lipid metabolism
392
Effects of glucocorticoids on the carbohydrate metabolism
* Glyconeogenesis (GNG) * Amino acids → Liver * Amino acid mobilisation * Excessive GNG → Metasteroid diabetes develops
393
Effect of glucocorticoids on protein metabolism
* Decrease protein synthesis * Increase protein cleaving * Nitrogen balance decreases
394
Effect of glucocorticoids on lipid metabolism
* Increase lipolysis * Increase plasma FFA levels * Increased extent of fat burning * Redistribution of fat: * Fat moves from periphery → liver
395
Circulatory effects of glucocorticoid insufficiency
* Na+ loss, oligemia * K+ increase → Cardiac weakness * Increased capillary permeability → oedema
396
Blood cell effects of glucocorticoid insufficiency
AC overproduction: * A decrease of: Eosinophils + basophils * Lymphoid tissue degrades AC extirpation: * Lymphoid hyperplasia
397
Neural effects of glucocorticoid insufficiency
* AC hyperfunction - Convulsive susceptibility increase * AC extirpation - Depression, psychic disorders
398
Pharmacological effects of glucocorticoids
* Anti-inflammatory effect
399
Effect of continuous high level of glucocorticoids (Such as stress/ drugs)
* Inhibition of mesenchymal cell proliferation * Antiphlogistic effect * Antiallergic effect
400
Inhibition of mesenchymal cell proliferation
* Fibroblast + collagen formation is inhibited * Cicatrisation is prolonged * Granulation + healing of wounds is inhibited * Osteolysis → osteoporosis
401
Anti-inflammatory effect of glucocorticoids
* PLA2 blocking effect * The decrease of inflammatory colour, dolor and tumor * Decrease basophil degranulation (decrease allergic reactions) * Masking effect
402
Antiallergenic effects of glucocorticoids
* Inhibit histamine release * No direct influence on the antigen-antibody reaction
403
Give the responses to stress
* Specific response * Aspecific response
404
Stress is elicited by...
Stressors
405
List some physical stressors
* Mechanical stimuli * Surgical intervention * Limitation of motion * Temperature
406
List some pathogenic stressors
* Virus * Bacterium * Parasite
407
List some stressors related to feeding
* Deficiencies: * Vitamins * Microelements * Intoxications
408
Give some examples of emotional stressors
* Psychic stress * Pain * Lack of stimuli
409
1
**Initial stage** * Release of ACTH * Often accompanied by _Cannon's alarm reaction_ * Effect of catecholamines declines * ACTH remains high
410
2
**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
3
**Exhaustion stage** * Energy reserves of organism expire * Stage of collapse * Animal dies
412
4
Adaptive disorders stage * Arthritis * Chronic hypertension * Ulcer * Hepatic failure
413
The adrenal medulla is part of the...nervous system
Sympathetic
414
The adrenal medulla produces...
Epinephrine
415
Which cell type is found in the adrenal medulla
Chromaffin cells
416
Chromaffin cells: Large, few granules indicates
Noradrenaline
417
Chromaffin cells: many, small granules indicates
Adrenaline
418
Body condition after removal of the adrenal medulla
* 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
The process of removal of the adrenal medulla
Demedullation (AMX)
420
How can demedullation be executed surgically?
By keeping the adrenal cortex intact ## Footnote *Lack of medulla is compensated by the sympathetic nervous system*
421
Epinephrine
422
Norepinephrine
423
Dopamine
424
Adrenal medullar hormones are collectively called...
Catecholamines
425
Tyrosine
426
DOPA
427
Dopamine
428
Norepinephrine
429
Title the figure
Adrenaline synthesis + Peptidergic co-transmission
430
Amine precursor
431
H+
432
DBH → NE ## Footnote *DBH = Dopamine-beta-hydroxylase enzyme*
433
H+ ## Footnote *Via ATPase pump*
434
NE
435
PNMT ## Footnote *Enzyme*
436
E | (Epinephrine)
437
Chromogranin
438
Degradation of hormones allows...
Suspension of hormonal effects
439
Give the methods of hormone inactivation
* Reuptake * Enzymatic cleavage
440
Give the two enzymes involves in enzymatic cleavage of hormones
* MAO (Monoamine oxidase) * COMT (Catecholamine-O-methyltransferase)
441
Catecholamines exert their effects through...and...receptors
* Alpha * Beta
442
Hormonal actions are divided into...
* Effects on circulation * Effects on particular organs
443
Norepinephrine stimulates...receptors
* Alpha 1 * Beta 1
444
Epinephrine stimulates...receptors
* Alpha 1 * Beta 2
445
* Agonist: Phenylephrine * Antagonist: Phenoxybenzamine
446
* Agonist: Phenylephrine * Antagonist: Prazosin
447
* Agonist: Clonidine * Antagonist: Yohimbine
448
* Agonist: Isoproterenol * Antagonist: Propranolol
449
* Agonist: Prenalterol * Antagonist: Methoprolol
450
* Agonist: Metaproterenol * Antagonist: Butoxamine
451
Catecholamine receptors exert their effects mostly by...
G-protein dependent cAMP system
452
Title the figure
Alpha receptor signaling
453
ATP → cAMP ## Footnote *AC*
454
Inactive PK
455
Active PK
456
DAG
457
Active PK-C
458
IP3
459
Ca2+
460
Title the figure
Beta receptor signaling
461
ATP
462
cAMP
463
Active PK
464
Alpha-1 receptor effects
* Smooth muscle contraction * Glycogenolysis * Sympathetic synaptic transduction
465
Alpha-2 receptor effects
Regulation of transmitter release in the CNS
466
Beta-1 receptor effects
* Stimulation of the heart * Stimulation of adipose cells
467
Beta-2 receptor effects
* Smooth muscle relaxation * Increase metabolism
468
Where do catecholamines effect?
* Circulation * Smooth muscles * Intermediary metabolism * Different organs
469
Effects of catecholamines on circulation
* Similar to sympathetic nervous system effects
470
Norepinephrine (NE) \> Epinephrine (E)
471
Smooth muscles
472
Smooth muscle contraction
473
Isoproterenol \> E \> NE
474
Cardiac, coronary
475
Enhancing, dilation
476
Epinephrine
477
* Bronchi * Smooth muscles of skeletal muscle vessels
478
Dilation
479
The receptor-type used is dependent on...
Plasma concentration
480
* α1: Vasoconstriction * β1: Increase of cardiac output * Σ: Increase of blood pressure
481
* β1: Increase of cardiac output * β2: Vasodilation in skeletal muscles * Σ: Redistribution of circulation
482
* Differences are observed * Σ: redistribution of circulation, increase of blood pressure
483
β1: Increase in cardiac output: Positive effects
* Chronotrop * Inotrop * Dromotrop * Bathmotrop
484
Receptors in the _arteriole wall_ in _intestinal_ _tract_
* Too many alpha receptors * Very few beta receptors
485
Receptors in the _arteriole wall_ in _skeletal muscle_
* Too many beta 2 receptors * Very few alpha receptors
486
Receptors in the smooth muscle internal to the intestinal tract
* Many alpha receptors * Many beta2 receptors
487
Describe the hormonal sympathetic activation of smooth muscles ## Footnote *Blood distribution*
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
Effect on the smooth muscle of high epinephrine
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
Effect on the smooth muscle of high norepinephrine
Similar to epinephrine 1. Norepinephrine has very low Beta 2 effects 2. Contraction of smooth muscle internal to intestines is stronger
490
Effects of catecholamines on the intermediary metabolism
* Increase BMR * Increase O2 consumption * Cardiac output increases * Respiration increases * The calorigenic effect is significant + rapid
491
Effects of catecholamines on the carbohydrate metabolism
* 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
Effects of catecholamines on the lipid metabolism
* The utilisation of fat increases * FFA levels increase * Beta receptor effects dominate in adipose tissue
493
* Glycogenolysis * Lipolysis * Glyconeogenesis
494
Lipolysis
495
Glycogenolysis
496
* β2: Insulin secretion increases * α2: Insulin secretion decreases
497
* β1: Increase contractility, condition, frequency * α1: vasoconstriction * β2: Vasodilation
498
Dilation
499
* α1 : M. radialis contraction * β2: M. ciliaris relaxation
500
Increase of renin secretion
501
* α1: Contraction * β2: Relaxation
502
Alarm reaction
* 'Fight or flight' * Body enabled for rapid utilisation of a high amount of energy * Enhancement of efficiency of physical abilities
503
Give the effects of the alarm reaction
* Pupils dilate * CO increases * Dilation of blood vessels * Contraction of spleen * O2 + Heat production increases * Inhibited GI + glandular function * Plasma glucose level increases
504
What regulates the adrenal cortex?
* Sympathetic nervous system * Hypoglycemia * Alarm reaction * Receptor-regulation
505
Hypoglycaemia regulation of adrenal cortex
Direct stimulus
506
Alarm reaction regulation of adrenal cortex
Organism able to focus on releasing energy by secretion of catecholamines
507
Receptor-regulation of the adrenal cortex
Complex regulation: Up and down regulation
508
Summarise epinephrine effects
* Hormone of fighting * Produced by the effects of: * Muscle activity * Cold * Drop of blood pressure
509
Summarise norepinephrine effects
* Aggressive behaviour * Produced by the effects of: * Hypoxia * Pain * Emotional anxiety
510
Give the main hormones of the pancreas
* Insulin * Glucagon
511
Pancreas acts as what kind of gland
* Endocrine * Exocrine
512
Insulin is produced by which cells?
B cells / Beta cells
513
Isletas of Langerhans are composed of which cells?
* B cells * D cells * A cells * F cells
514
B-cells
* Insulin production * Synthesised as pre-pro-insulin * Role: Stimulation of anabolic + storage processes
515
Insulin is made up of
* A chain * B chain * Zinc
516
A-cells
* Glucagon production * Acts only in the liver * Roles: * Increase plasma glucose * Decrease glycogen synthesis * Stimulate GNG
517
D-cells
* Somatostatin production * Roles: * Inhibition of insulin + glucagon overproduction * Inhibit A + B cell activity * Inhibition of every phase of digestion * Motility decrease * Secretion decrease
518
F-cells
* Pancreatic polypeptide (PP) production * Roles: * Biliary secretion + secretion of pancreatic enzymes * Gastric secretion + motility increase ## Footnote *Protein intake enhances its secretion*
519
Which mechanisms regulate hormone synthesis of islets of Langerhans?
* The regulatory system based on paracrine activity * Glucose + amino acid levels of the plasma * Neural regulatory effects
520
Give the steps of regulation of islets of Langerhans by paracrine activity
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
Describe the regulation of plasma glucose
* 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
Without GIP + enteroglucagon...
Glucose loss
523
In the presence of GIP + enteroglucagon
Glucose saving
524
Give the two-stage process of insulin release
* Stored insulin is released * Newly synthesised insulin released
525
In the case of food consumption with high _glucose_ content...
B-cells informed about the energy sources before the increase of plasma glucose level
526
In the case of food consumption with high carbohydrate content...
GIP + Enteroglucagon are liberated * This causes the secretion of insulin in advance ('feed forward')
527
Title the figure
Stimulation of B cells
528
AC
529
ATP → cAMP
530
GLUT2
531
* ATP increase: K+ channel closes → Depolarisation * Glucose-6-P → Insulin synthesis, late release
532
Immediate release
533
De novo synthesis
534
Insulin
535
Title the figure
Neural effects on the B- and A-cell
536
Autonomic nervous system affect insulin production via...
* Sympathetic: Alpha and beta receptors * Parasympathetic: Acetylcholine receptors
537
Blocking of insulin release via the sympathetic system
* Blocking through alpha-2 receptors * Insurance of high plasma glucose levels * Blocking of insulin release
538
Alpha2: Insulin glucagon block
539
N. vagus: Insulin glucagon transient release
540
Beta2: Insulin glucagon transient release
541
Glucose gets through the membrane via...
GLUT transporters ## Footnote *Insulin dependent tissues*
542
In some tissues glucose tranpsorters are regulated by...
Insulin
543
How many subtypes of GLUT transporters are there?
7
544
GLUT-1 transporter * Affinity * Location
* Intermediate affinity * In several tissues
545
GLUT-2 transporter * Affinity * Location
* Low affinity * Pancreas cells
546
GLUT-3 transporter * Affinity * Location
* High affinity * Neurons
547
GLUT-4 transporter * Affinity * Location
* High affinity * Muscle, adipose tissue
548
GLUT-5 transporter * Location
* Intestines, testis
549
Describe insulin-receptor interaction
1. Two insulin molecules bind to these subunits 2. Conformational change in the (IC) beta subunit 3. IC protein kinase enzymes activated
550
The effects of insulin can be divided into which groups?
* Glucose uptake * Metabolic effects
551
Effect of insulin on metabolic processes
Increases storing and anabolic processes
552
List the insulin-_independent_ tissues
* Brain cells * RBC/WBC * Brain capillaries * Liver * Uptake in muscle + adipose
553
List the insulin-_dependent_ tissues
* Muscle * Adipose tissue
554
Insulin-independent tissues
Tissues metabolising glucose that can only take up glucose without the presence of insulin
555
Which GLUT receptor is found in the islets of Langerhans?
GLUT2
556
Insulin increases the synthesis of...
* Glycogen * Protein * Fat ## Footnote *By inhibiting their respective enzymes*
557
The effects of insulin on carbohydrate metabolism
* Incorporates amino acids into proteins: GNG * Decrease glucose level
558
The effects of insulin on lipid metabolism
* Triglyceride synthesis increase * Degradation of lipid decrease * Stimulate fatty acid synthesis from AcCoA
559
The effects of insulin on protein metabolism
* Stimulate amino acid uptake of all cells øhepatocytes * Enhance protein synthesis * The decrease in protein degradation * Positive nitrogen balance
560
Amino acid
561
Glucose
562
FFA
563
Every action of insulin is antagonised by...
Glucagon ## Footnote *However, only in the liver*
564
Effect of insulin on: Dependent tissues
Facilitates glucose entry
565
Effect of insulin on: Adipocytes
* Glucose entry increases * Triglyceride synthesis increases * Lipase activity decreases
566
Effect of insulin on: Muscle cell
* Glucose entry + storing increases * Glucose → energy conversion increases * Amino acid entry, protein synthesis increases
567
Effect of insulin on: Liver
* Glucose entry not regulated * Glycogen synthesis increases * Glucose release decreases * Ketogenesis and GNG decreases
568
Effect of insulin on: Neuron
* Enhances K+ entry * Hyperpolarisation effects
569
Title the figure
Glucose metabolism
570
Foodstuff glucose
571
Plasma glucose
572
Lactic Acid
573
* H2O * CO2
574
Adipocyte
575
FFA
576
Liver glucose
577
During glucose metabolism, if there are too high AcCoA concentrations...
Ketone bodies appear * Citric acid cycle activity decreases
578
What are the two outcomes of insulin deficiency on _protein_ metabolism?
* Dehydration * Negative N balance
579
Utilisation of glucose decreases
580
Protein catabolism
581
K+ loss
582
Tissue K+ decreases
583
Polyuria + polydypsia
584
Amino acid levels decrease
585
GNG increases
586
Urinary N-secretion increases
587
What are the two outcomes of insulin deficiency on _fat_ metabolism?
* Na+ loss * Acidosis
588
Glucose utilisation decreases
589
Lipogenesis (storage) decreases
590
Mobilisation of adipose deposits increase: Lipemia
591
Production of ketone substances in the liver: Ketonemia
592
Ketonuria
593
Utilisation of glucose decreases
594
* Liver glycogenolysis * Muscle glycogenolysis
595
Hyperglycemia
596
* Glycosuria (Excess sugar in urine) * Osmotic diuresis (Increased urine production)
597
H2O + electrolyte loss
598
* Dehydration * Hemoconcentration
599
Breakdown of circulation
600
Production of ketone substances increases
601
* Vomiting * Diarrhoea
602
* Na+ loss * K+ loss
603
* Fall of blood pressure * RBF decrease * Anuria (Failure of urine production) * Coma
604
Exitus
605
Parallel to metabolic acidosis, what else occurs?
Protein degredation
606
List the types of diabetes
* Type-1 (Human) * Type-2 (Human) * Type-3 (Canine)
607
Type-1 diabetes
* Appears in juvenile age * Effects of the disease are through insulin deficiency * Excess of glucagon * Rapid * Hereditary * Insulin-dependent diabetes mellitus (IDDM)
608
IDDB
* Insulin-dependent diabetes mellitus * Caused by insufficient insulin production
609
Type-II diabetes
* 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
Type-III diabetes
* Adults, 5-15 years * Insulin-sensitive * Late-onset, nutritive
611
What are autacoids?
* Biological factors which act as local hormones * Brief duration * Act near the site of synthesis
612
What are the two groups of Autacoid?
* Peptides * Eicosanoids (Fatty acid-like substances)
613
Where are eicosanoids produced?
All cells in the body
614
Characteristics of Eicosanoids
* 20-carbon fatty acids * The product of enzymatic reactions of phospholipids * Mediated by G-protein → Activating PLA2 enzyme
615
Title the figure
Eicosanoid synthesis
616
MPL stands for...
Membrane phospholipids
617
Phospholipase-A2
618
Lipoxygenase
619
List the effects of eicosanoids of veterinary importance
* Increase inflammation * Insulin release * Bone resorption * Reproduction * Thrombocyte aggregation * Renal effects
620
Effect of eicosanoids on inflammation
* Initiate inflammation * Example: Through PMN cells * Cause: * Vasodilation * Chemotaxis * IL-1 fever
621
Effect of eicosanoids on insulin release
* HPETE stimulates PGE2 pathway * Inhibition of insulin release
622
Effect of eicosanoids on​ bone resorption
* PGE2 produced by osteoblast cellular membrane * Parathyroid hormone-like effect on Ca2+ mobilisation * Allows Ca2+ entry into the plasma
623
Effect of eicosanoids on reproduction
* 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
Effect of eicosanoids on thrombocyte aggregation
* 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
Effect of eicosanoids on the kidney
* Prostacyclin synthesis in renal tubule enhances renin secretion * Increase RPF * Antagonises effect of ADH
626
Regulation of eicosanoid production
* 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
Peptide autacoids are part of which system?
Diffuse Neuro-endocrine system (DNES)
628
* K + PNE Cells * BLP, SN, Enkephalin
629
* C-cell * CT
630
* G-cell + D-cell * Gastrin, enkephalin
631
* Brush cells * Secretin, SP, SK, glucagon, gastrin, CCK
632
* A, B, D, G, PP * Glucagon, insulin, SN, gastrin
633
* Chromaffin * NPY, enkephalin, endorphin, BLP
634
* Merkel * CT, BLP, VIP
635
Abbreviation: BLP
Bombesin-like peptide
636
Abbreviation: CCK
Cholecystokinin
637
Abbreviation: CRH
Corticotropin-releasing hormone
638
Abbreviation: CT
Calcitonin
639
Abbreviation: NPY
Neuropeptide Y
640
Abbreviation: NT
Neurotensin
641
Abbreviation: PP
Pancreatic polypeptide
642
Abbreviation: PYY
Peptide YY
643
Abbreviation: SK
Substance K
644
Abbreviation: SN
Somatostatin
645
Abbreviation: SP
Substance P
646
Abbreviation: VIP
Vasoactive intestinal peptide
647
List the classifications of peptide hormones
* Bombesin * Kinins * Somatostatin * Neurotensin * Endogen opioid * Tachykinin
648
Bombesin peptides
* GRP * Neuromedins * Ranatensins
649
Kinin peptides
* Kininogens * Bradykinin * Kallikreins
650
Neurotensin peptides
* Angiotensin * Xenopsin
651
Endogen opioids
* Enkephalin * Dynorphins * Exorphins
652
Tachykinin hormones
* Substance-P * Neurokinin A, B, K * VIP
653
Major effects of bobmesins
* Hypothermia * Hypoglycemia * Gastric juice secretion
654
Major effects of kinins
* Vasodilation * PH-synthesis
655
Major effects of somatostatins
* Hyperkinesis * Excitation * Periphery: * All metabolic processes are blocked
656
Major effects of neurotensins
* Most potent analgesic * Opioid independent
657
Major effects of endogen opioids
* CNS: * Analgesic * GI tract * Synchronisation of motility
658
Major effects of tachykinins
* Control of exocrine pancreas * Modulates AC steroid secretion
659

Physiology (18 decks)

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