1
Q
1. Where is oxytocin synthesized?
A
Oxytocin is synthesized by the paraventricular nucleus (PVN).
2
Q
- How is oxytocin transported after synthesis?
A
Oxytocin is transported down the axons in synaptic vesicles by specific motor proteins.
3
Q
- What are the stimuli for oxytocin release?
A
Oxytocin is released in response to specific stimuli, including:<br></br>- Birthing process<br></br>- Suckling by the baby on the mother’s mammary glands<br></br>- Male ejaculation
4
Q
- What initiates the release of oxytocin during the birthing process?
A
The stretching of the cervix of the uterus by the baby during the birthing process activates specific stretch receptors within certain layers of the uterus. These receptors send signals to the hypothalamus, which then signals the paraventricular nucleus (PVN) to secrete already synthesized oxytocin.
5
Q
- Describe the signaling pathway leading to uterine contractions during the birthing process.
A
- Oxytocin travels through circulation and binds to specific receptors in the myometrium (second layer of the uterus composed of smooth muscle cells).<br></br>- Binding to the receptor activates a Gq protein.<br></br>- The activated Gq protein goes to an effector enzyme, Phospholipase C, on the cell membrane.<br></br>- Phospholipase C, acting as a GTPase-activating protein (GAP), produces energy used to cut Phosphatidylinositol Biphosphate (PIP2) into diacylglycerol (DAG) and inositol trisphosphate (IP3).<br></br>- DAG activates protein kinase C (pkC), leading to the phosphorylation of different proteins.<br></br>- IP3 increases intracellular Ca++ volume, activating Calmodulin and enhancing contractions, aiding in pushing the baby out.
6
Q
- What activates mechanoreceptors during suckling?
A
The baby’s suckling on the nipple activates specific mechanoreceptors, picking up tactile stimuli.
7
Q
- How does oxytocin release occur during suckling?
A
NAME?
8
Q
- What is the Milk Letdown Reflex?
A
The Milk Letdown Reflex is the enhanced contractile process in myoepithelial cells next to alveolar glands in the breasts, triggered by released oxytocin during suckling. This process helps eject the already produced milk.
9
Q
- What activates mechanoreceptors during suckling?
A
The baby’s suckling on the nipple activates specific mechanoreceptors, picking up tactile stimuli.
10
Q
- How does oxytocin release occur during suckling?
A
NAME?
11
Q
- What is the Milk Letdown Reflex?
A
The Milk Letdown Reflex is the enhanced contractile process in myoepithelial cells next to alveolar glands in the breasts, triggered by released oxytocin during suckling. This process helps eject the already produced milk.
12
Q
- What effect does oxytocin have on the vas deferens during male ejaculation?
A
Oxytocin, during the sexual orgasmic response before ejaculation, causes the contraction of the vas deferens. This contraction facilitates the movement of sperm up through the entire male reproductive tract.
13
Q
- How is oxytocin associated with love and compassion?
A
Oxytocin is associated with love and compassion, and it is sometimes referred to as the ‘cuddle hormone.’ Elevated oxytocin levels may lead to increased feelings of love and compassion.
14
Q
- Why might a woman be given synthetic oxytocin (pitocin) during the birthing process?
A
In the birthing process, if a woman needs assistance, she may be given synthetic oxytocin, known as pitocin.
15
Q
- What is uterine inertia, and how can it be related to hyposecretion of oxytocin?
A
Uterine inertia is a condition where contractions during labor are not strong enough to push the fetus out. Hyposecretion of oxytocin, where the body does not produce enough oxytocin, can lead to uterine inertia. This condition is uncommon and may be associated with postpartum hemorrhaging affecting the vessels between the hypothalamus and the neurohypophysis, known as Sheehan’s syndrome. It is more common in the anterior pituitary than in the posterior.
16
Q
What non-immunomodulatory measures are recommended in the management of SLE?
A
NAME?
17
Q
What is the recommended management for mild-moderate SLE, including skin disease and arthralgia?
A
- Hydroxychloroquine<br></br>- Short course of NSAIDs for symptomatic control<br></br>- Steroids (intra-articular for arthritis, topical for cutaneous manifestations)<br></br> - Topical steroids may be sufficient for skin-only disease.
18
Q
How is moderate-severe SLE managed, especially in cases of inflammatory arthritis or organ involvement?
A
NAME?
19
Q
What is the recommended treatment for severe organ involvement in SLE, such as lupus nephritis or CNS lupus?
A
Treatment often involves IV steroids and cyclophosphamide.
20
Q
In cases of unresponsive SLE, what additional therapies might be considered?
A
Other therapies such as IV immunoglobulin and rituximab may be necessary in unresponsive cases.
21
Q
How should SLE be monitored during treatment?
A
NAME?
22
Q
What complications are associated with long-term SLE and its management?
A
Increased prevalence of avascular necrosis, usually of the femoral head, which may be related to steroid use.
23
Q
- Where is antidiuretic hormone (ADH) produced?
A
ADH, also known as Vasopressin, is produced in the Supraoptic nucleus (SON) in the hypothalamus and secreted by the neurohypophysis.
24
Q
- What is the transportation method of ADH after synthesis?
A
After synthesis, ADH is transported down the axons in synaptic vesicles by specific motor proteins.
25
3. What stimuli are required for the release of ADH?
Certain stimuli are required for the release of ADH:
- Decreased blood volume and blood pressure
- Increased plasma osmolality
- Decreased blood volume and blood pressure
- Increased plasma osmolality
26
4. What hormone is secreted in response to low blood pressure?
Angiotensin II is secreted in response to low blood pressure.
27
5. What triggers the release of ADH in response to low blood pressure?
Angiotensin II binding to certain receptors signals the hypothalamus to release ADH in response to low blood pressure.
28
6. How is osmolality defined, and what are its high and low states?
Osmolality refers to the concentration of solutes and water inside the plasma. High plasma osmolality means decreased water and increased solutes, while low plasma osmolality means increased water and decreased solutes.
29
7. Name factors that inhibit the release of ADH.
Inhibitors of ADH release include:
- Increased blood volume
- Decreased plasma osmolality
- Alcohol consumption
- Increased blood volume
- Decreased plasma osmolality
- Alcohol consumption
30
8. What does the nephron consist of?
The nephron consists of:
- Renal corpuscles (Glomerulus, Bowman’s capsule)
- Kidney tubules (Proximal convoluted tubule, Loop of Henle, Distal convoluted tubule)
- Many nephrons empty their filtrate into one collecting duct.
- Renal corpuscles (Glomerulus, Bowman’s capsule)
- Kidney tubules (Proximal convoluted tubule, Loop of Henle, Distal convoluted tubule)
- Many nephrons empty their filtrate into one collecting duct.
31
9. What is the main target of ADH in the kidneys?
The collecting duct, made of principal cells, is the main target of ADH in the kidneys.
32
10. What type of receptors trigger an intracellular cascade in principal cells?
Vasopressin type 2 receptors on the cell membrane of principal cells trigger an intracellular cascade when activated by ADH.
33
11. What happens when ADH activates a G stimulatory protein?
The activated G stimulatory protein goes to an effector enzyme on the cell membrane called Adenylate cyclase, making it very active.
34
12. What enzyme does Adenylate cyclase possess, and what does it do?
Adenylate cyclase has a specific enzyme called GTPase. GTPase cuts GTP, turning it into GDP, which turns off the G protein. Energy produced is used to convert ATP to cAMP, activating protein kinase A (pkA).
35
13. What does the activated pkA do in the cell nucleus?
The activated pkA goes to the cell nucleus, stimulating specific genes that undergo transcription and translation, producing specific proteins.
36
14. What are the specific proteins produced, and where do they go?
The specific proteins produced go to the endoplasmic reticulum, then to the Golgi apparatus, and are packed into vesicles. The proteins, called aquaporin type 2, aquaporin type 3, and aquaporin type 4, have different locations and functions.
37
15. What is the role of protein kinase A (pkA) in aquaporin 2 activation?
pkA phosphorylates Aquaporin 2, leading to vesicle merging with the cell membrane.
38
16. What happens when Aquaporin 2 is phosphorylated?
When Aquaporin 2 is phosphorylated, water in the collecting duct goes into the principal cell and then into the blood.
39
17. What are the effects of increased intracellular Ca++ volume and water movement into the blood?
- Increased plasma volume
- Increased blood pressure
- Decreased plasma osmolality, making the plasma isotonic (about 300 milliosmoles per liter).
- Increased blood pressure
- Decreased plasma osmolality, making the plasma isotonic (about 300 milliosmoles per liter).
40
1. Where are ADH receptors (type V1) located?
ADH receptors (type V1) are located on the smooth muscle cells in any systemic blood vessel.
41
2. What is the mechanism activated when ADH binds to these receptors?
ADH binding to receptors activates a Gq protein mechanism, leading to an increase in intracellular Ca++ levels in the smooth muscle cells.
42
3. What is the result of increased Ca++ levels in smooth muscle cells?
Increased Ca++ levels lead to the contraction of smooth muscle cells, causing vasoconstriction. This results in an increased peripheral resistance and blood pressure.
43
4. How does ADH affect the perimeter of blood vessels?
ADH causes vasoconstriction by decreasing the perimeter of blood vessels.
44
5. What are the consequences of vasoconstriction induced by ADH?
The consequences of vasoconstriction include an increase in peripheral resistance and blood pressure.
45
6. What are the causes of Syndrome of Inappropriate ADH Secretion (SIADH)?
SIADH can be caused by tumors in the hypothalamus or posterior pituitary, bacterial infections that destroy tissues leading to a rise in ADH levels (e.g., meningitis).
46
7. What is the consequence of increased ADH in SIADH?
Increased ADH levels result in excessive water retention. If water levels surpass solutes (especially sodium and chlorine), water may leak out of blood vessels. If it leaks into the brain, it can cause cerebral edema, which is dangerous and may be treated with mannitol to pull the water out.
47
8. What causes Diabetes Insipidus?
Diabetes Insipidus can be caused by severe head trauma, which damages the hypothalamus or posterior pituitary, preventing ADH secretion.
48
9. What are the symptoms of Diabetes Insipidus?
Symptoms of Diabetes Insipidus include a decrease in ADH, leading to significant water losses through polyuria (excessive urine production) and a persistent feeling of thirst (polydipsia).
49
10. How was diabetes insipidus historically diagnosed?
Historically, diabetes insipidus was diagnosed by tasting urine. Sweet urine indicated diabetes mellitus, while bitter and watery urine indicated diabetes insipidus.
50
1. Which nucleus in the hypothalamus secretes Growth Hormone Releasing Hormone (GHRH)?
The arcuate nucleus in the hypothalamus secretes Growth Hormone Releasing Hormone (GHRH).
51
2. What are the secondary triggers for GHRH release?
Secondary triggers for GHRH release include increased amino acid levels, decreased glucose levels (hypoglycemia), decreased fatty acid levels, exercise, and healthy stressors.
52
3. What is the vascular connection between the hypothalamus and the anterior pituitary?
GHRH travels in the hypophyseal portal system, the vascular connection between the hypothalamus and the anterior pituitary (adenohypophysis).
53
4. Which cells in the adenohypophysis does GHRH stimulate?
GHRH stimulates somatotropes in the adenohypophysis to secrete growth hormone (GH) into the bloodstream.
54
5. What happens when a certain percentage of GH binds to specific receptors in the liver?
When a certain percentage of GH binds to specific receptors in the liver, it activates a tyrosine kinase-like receptor, leading to the phosphorylation of specific amino acids.
55
6. Which enzyme is activated in the liver when GH binds to its receptors?
The enzyme Janus kinase (JAK) is activated in the liver when GH binds to its receptors.
56
7. What is the role of Janus kinase (JAK) in GH action?
Janus kinase (JAK) phosphorylates the signal transducer activator of transcription (STAT).
57
8. What happens when activated STAT goes to the nucleus?
When activated STAT goes to the nucleus, it binds to a specific gene sequence of DNA, initiating transcription. The mRNA produced is translated into protein (Insulin-like growth factor (IGF) type 1).
58
9. What is the effect of GH on gluconeogenesis in the liver?
GH stimulates gluconeogenesis in the liver, increasing blood glucose levels by producing glucose from non-carbohydrate sources such as glycerol and odd-chain fatty acids.
59
10. What happens when GH binds to receptors in adipose tissue?
GH binding to receptors in adipose tissue activates hormone-sensitive lipase (HSL), initiating lipolysis, the breakdown of triglycerides into glycerol and fatty acids. Glycerol and odd-chain fatty acids are used for gluconeogenesis.
60
11. What is the effect of GH binding to receptors on skeletal muscle cells?
GH binding to receptors on the surface of skeletal muscle cells activates specific signaling pathways and genes, leading to the production of proteins that enhance amino acid uptake by increasing specific channels on the cell membrane.
61
1. What happens when IGF1 binds to receptors on the surface of skeletal muscle cells?
IGF1 binding to receptors on the surface of skeletal muscle cells activates specific signaling pathways, leading to gene activation, protein production, and increased amino acid uptake through specific channels on the cell membrane.
62
2. How does IGF1 contribute to muscle hypertrophy?
Inside the cell, another pathway stimulated by IGF1 promotes amino acids linking together to produce proteins, such as myofibrils (actin and myosin), leading to muscle hypertrophy and an overall increase in muscle size.
63
(1) IGF1 Regulation of Osteoblasts and Osteoclasts
IGF1 regulates osteoblasts and osteoclasts inside the bones, activating and regulating both. This results in increased bone deposition by osteoblasts and increased bone resorption by osteoclasts, leading to overall bone growth and thickness through appositional growth.
64
2. How does IGF1 affect bone density?
IGF1 stimulates protein synthesis, increasing bone density by promoting the production of collagen type 1 and proteoglycans in the bones.
65
1. What type of glands are mammary glands?
Mammary glands are essentially modified apocrine glands (sweat glands).
66
2. What is the main function of mammary glands?
The main function of mammary glands is to produce milk.
67
3. What are alveolar cells in mammary glands?
Alveolar cells in mammary glands produce milk and are affected by prolactin, which stimulates milk production.
68
4. What is the main part of the mammary gland?
The main part of the mammary gland is the lobules, which are tube-like structures made up of alveolar cells.
69
5. What is the function of the lobar connective tissue?
The lobar connective tissue is between and around the lobules, providing structural support to the gland.
70
6. What do Cooper's ligaments do?
Cooper's ligaments, found in the lobar connective tissue, anchor the breast mainly to the posterior wall.
71
7. What is the role of lactiferous ducts?
Lactiferous ducts are little tubes that drain the lobules in the mammary gland.
72
8. Where are lactiferous sinuses located?
Lactiferous sinuses are dilations of the lactiferous ducts, located just behind the nipple.
73
9. What is the function of the nipple?
The nipple is on the surface end of the ducts in the mammary gland.
74
10. What surrounds the nipple?
The areola surrounds the nipple.
75
11. Where is prolactin synthesized?
Prolactin is synthesized in specific cells called lactotropes in the anterior pituitary gland (adenohypophysis).
76
12. What is the main purpose of prolactin?
Prolactin is designed to promote lactation, which is the production of milk.
77
13. What is the role of Prolactin Inhibiting Hormone (PIH) or Dopamine?
PIH/Dopamine, secreted by the arcuate nucleus, inhibits lactotropes in the anterior pituitary, preventing prolactin secretion by binding to D2 receptors.
78
14. How does Thyrotropin-Releasing Hormone (TRH) affect prolactin?
TRH, secreted by the paraventricular nucleus, stimulates lactotropes in the anterior pituitary, leading to the secretion of prolactin by binding to specific receptors.
79
15. What is the direct stimulus on prolactin during breastfeeding?
The suckling of the baby during breastfeeding directly stimulates mechanoreceptors, triggering the production of oxytocin and stimulating prolactin production.
80
16. What role does high levels of Estrogen play in prolactin secretion?
High levels of Estrogen, especially during pregnancy, directly stimulate prolactin production in lactotropes and indirectly inhibit PIH secretion from the arcuate nucleus.
81
17. How do extremely high levels of Estrogen during pregnancy affect prolactin?
Extremely high levels of Estrogen during pregnancy stimulate the production of prolactin but inhibit its effect on alveolar cells. After birth, as Estrogen levels decrease, prolactin starts affecting alveolar cells.
82
18. What cells in the anterior pituitary produce prolactin?
Lactotropes in the anterior pituitary gland (adenohypophysis) produce prolactin.
83
19. What is the main function of prolactin?
The main function of prolactin is to promote lactation, which involves the production of milk.
84
20. How does Prolactin Inhibiting Hormone (PIH) prevent prolactin secretion?
PIH/Dopamine secreted by the arcuate nucleus inhibits lactotropes, preventing prolactin secretion by binding to D2 receptors.
85
1. How does prolactin reach alveolar cells?
Prolactin reaches alveolar cells by binding to specific receptors on the cell membrane through the blood circulation.
86
2. What is the role of Janus kinase (JAK) in prolactin action?
JAK is activated by prolactin and, in turn, activates STAT to initiate gene transcription.
87
3. What proteins are produced by gene transcription stimulated by prolactin?
Milk proteins such as casein and lactoferrin are produced, along with kinases that phosphorylate channels on the cell membrane.
88
4. Where are the proteins and substances produced by alveolar cells excreted?
These proteins and substances are directly excreted into the lumen of the lactiferous ducts.
89
5. What type of gland is the mammary gland?
b. Apocrine
90
6. What is the main part of the mammary gland?
b. Gland lobules
91
7. Where is prolactin synthesized?
c. Adenohypophysis
92
8. What is the effect of Dopamine?
a. Inhibits prolactin production
93
9. What is the effect of thyrotropin-releasing hormone (TRH)?
b. Stimulates prolactin production
94
10. What does suckling stimulate along with prolactin?
d. Oxytocin
95
11. In what way does Estrogen affect prolactin production?
c. Stimulates directly and indirectly
96
12. When do Estrogen levels inhibit prolactin's effect?
d. After the birthing process
97
13. Which substance is not part of the prolactin cascade?
c. Adenylate Cyclase
98
14. Which substance is not a milk ingredient?
d. Prolactin
99
1. What defines ligand-gated ion channels?
1. Ligand-gated ion channels are defined as ion channels that open in response to the binding of a ligand.
100
2. Why is only a small number of ligand-gated ion channels sufficient to elicit a response in a cell?
2. A small number of ligand-gated ion channels are sufficient due to the significant influx of ions through each channel.
101
3. Describe the structure of ligand-gated ion channels and their interaction with the lipid bilayer.
3. Ligand-gated ion channels have a membrane-spanning region with a hydrophilic channel. The channel allows ions to cross the membrane without interacting with the hydrophobic core of the phospholipid bilayer.
102
4. What is the mechanism of action when a ligand binds to the extracellular region of a ligand-gated ion channel?
4. When a ligand binds, the protein's structure changes, allowing specific ions to pass through, inducing depolarization or hyperpolarization.
103
5. How does the cellular response to ligand-gated ion channels differ from G-protein coupled receptors in terms of time?
5. The cellular response to ligand-gated ion channels occurs in milliseconds, contrasting with the seconds-long response of G-protein coupled receptors.
104
1. Describe the structure of G-protein coupled receptors, including their transmembrane region and coupling with G-proteins.
1. G-protein coupled receptors have a transmembrane region crossing the lipid bilayer seven times, coupled with a G-protein. They lack integral enzyme activity or ion channels.
105
2. What is the mechanism of action for GPCRs, from ligand binding to downstream effects?
2. Ligands binding to the extracellular portion induces a conformational change, allowing G-protein subunit binding. GTP replaces GDP, activating the G-protein. Downstream effects, such as ion channel opening or enzyme activity, occur.
106
3. How is the activity of G-proteins terminated after activation?
3. GTPase catalyzes the hydrolysis of GTP on the α-subunit, reassociating the G-protein complex.
107
4. Provide an example of GPCRs and their role in the fight or flight response.
4. Adrenoceptors, involved in the fight or flight response, are examples of GPCRs.
108
5. Explain the concept of signal amplification in GPCR signaling.
5. Despite one GPCR having one α-subunit, it can interact with several secondary messengers, leading to signal amplification by activating multiple enzymes and catalyzing numerous reactions.
109
1. What class of receptors do kinase-linked receptors belong to?
1. Kinase-linked receptors belong to the class of enzyme-linked receptors.
110
2. What is a kinase, and what is the role of receptor tyrosine kinase?
2. A kinase is an enzyme that transfers phosphate groups. Receptor tyrosine kinase specifically transfers phosphate groups to the amino acid tyrosine.
111
3. Describe the mechanism of action for kinase-linked receptors.
3. The mechanism involves ligand binding to extracellular domains, receptor dimerization, autophosphorylation, and relay proteins facilitating varied cellular responses.
112
4. What is the typical timeframe for the cellular response of kinase-linked receptors?
4. The cellular response for kinase-linked receptors occurs in minutes to hours.
113
5. Provide examples of molecules that act as kinase-linked receptors.
5. Insulin and growth hormone are examples of molecules that act as kinase-linked receptors.
114
1. What is autocrine regulation in cellular communication?
1. Autocrine regulation involves chemicals released from cells binding to receptors on the same cell that released them.
115
2. Define paracrine regulation in cellular communication.
2. Paracrine regulation is when chemicals released from cells bind to receptors on adjacent cells.
116
3. Explain endocrine regulation in cellular communication.
3. Endocrine regulation involves chemicals, usually hormones, released from secretory cells and transported via the circulatory system to target cells.
Endocrine system
flashcards
Decks in class (12)
# Cards
-
adrenal gland physilogy150
-
Reproductive physiology137
-
Ejaculation and Erection39
-
Hormones116
-
Endocrine physiology28
-
pituitary gland physiology54
-
physiology of pancrease104
-
DIABETES MELLITUS Type I&II DKA, HHS99
-
DIABETES MELLITUS part 2117
-
thyroid pgysiology138
-
HYPOTHYROIDISM100
-
Hyperthrodisum115
