Hormones Flashcards
1. Where is oxytocin synthesized?
Oxytocin is synthesized by the paraventricular nucleus (PVN).
- How is oxytocin transported after synthesis?
Oxytocin is transported down the axons in synaptic vesicles by specific motor proteins.
- What are the stimuli for oxytocin release?
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
- What initiates the release of oxytocin during the birthing process?
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.
- Describe the signaling pathway leading to uterine contractions during the birthing process.
- 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.
- What activates mechanoreceptors during suckling?
The baby’s suckling on the nipple activates specific mechanoreceptors, picking up tactile stimuli.
- How does oxytocin release occur during suckling?
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- What is the Milk Letdown Reflex?
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.
- What activates mechanoreceptors during suckling?
The baby’s suckling on the nipple activates specific mechanoreceptors, picking up tactile stimuli.
- How does oxytocin release occur during suckling?
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- What is the Milk Letdown Reflex?
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.
- What effect does oxytocin have on the vas deferens during male ejaculation?
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.
- How is oxytocin associated with love and compassion?
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.
- Why might a woman be given synthetic oxytocin (pitocin) during the birthing process?
In the birthing process, if a woman needs assistance, she may be given synthetic oxytocin, known as pitocin.
- What is uterine inertia, and how can it be related to hyposecretion of oxytocin?
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.
What non-immunomodulatory measures are recommended in the management of SLE?
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What is the recommended management for mild-moderate SLE, including skin disease and arthralgia?
- 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.
How is moderate-severe SLE managed, especially in cases of inflammatory arthritis or organ involvement?
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What is the recommended treatment for severe organ involvement in SLE, such as lupus nephritis or CNS lupus?
Treatment often involves IV steroids and cyclophosphamide.
In cases of unresponsive SLE, what additional therapies might be considered?
Other therapies such as IV immunoglobulin and rituximab may be necessary in unresponsive cases.
How should SLE be monitored during treatment?
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What complications are associated with long-term SLE and its management?
Increased prevalence of avascular necrosis, usually of the femoral head, which may be related to steroid use.
- Where is antidiuretic hormone (ADH) produced?
ADH, also known as Vasopressin, is produced in the Supraoptic nucleus (SON) in the hypothalamus and secreted by the neurohypophysis.
- What is the transportation method of ADH after synthesis?
After synthesis, ADH is transported down the axons in synaptic vesicles by specific motor proteins.
- What stimuli are required for the release of ADH?
Certain stimuli are required for the release of ADH:<br></br>- Decreased blood volume and blood pressure<br></br>- Increased plasma osmolality
- What hormone is secreted in response to low blood pressure?
Angiotensin II is secreted in response to low blood pressure.
- 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.
- 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.
- Name factors that inhibit the release of ADH.
Inhibitors of ADH release include:<br></br>- Increased blood volume<br></br>- Decreased plasma osmolality<br></br>- Alcohol consumption
- What does the nephron consist of?
The nephron consists of:<br></br>- Renal corpuscles (Glomerulus, Bowman’s capsule)<br></br>- Kidney tubules (Proximal convoluted tubule, Loop of Henle, Distal convoluted tubule)<br></br>- Many nephrons empty their filtrate into one collecting duct.
- 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.
- 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.
- 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.
- 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).
- 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.
- 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.
- 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.
- 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.
- What are the effects of increased intracellular Ca++ volume and water movement into the blood?
- Increased plasma volume<br></br>- Increased blood pressure<br></br>- Decreased plasma osmolality, making the plasma isotonic (about 300 milliosmoles per liter).
- Where are ADH receptors (type V1) located?
ADH receptors (type V1) are located on the smooth muscle cells in any systemic blood vessel.
- 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.
- 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.
- How does ADH affect the perimeter of blood vessels?
ADH causes vasoconstriction by decreasing the perimeter of blood vessels.
- What are the consequences of vasoconstriction induced by ADH?
The consequences of vasoconstriction include an increase in peripheral resistance and blood pressure.
- 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).
- 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.
