Other Hormones Of Physiologic Importance Flashcards
What are eicosanoids?
Biologically active substances derived from ARA i.e. PG, TX, PC, LT
Prostaglandins 1. Derived from what pathway/s? 2. Effect on: A. BVs B. Platelets C. Labor D. Pain sensitivity E. Temperature F. Secretions? Which of these are housekeeping?
Derived from Cyclooxygenase pathway (COX)
COX-1 (constitutive, responsible for HK fxn of PG) vs. COX-2 (inducible, pag may injury lang napproduce)
Diverse effects:
Housekeeping functions:
Prevent unwanted platelet aggregation, Increase mucus and bicarbonate secretion in the stomach
COX-2: Induce labor (so contraction of uterine smooth muscles), Sensitize pain receptors (Kaya masakit whenever you have an injury thus, take NSAIDs because it blocks COX so you dec synthesis of PGs especially COX-2 yung gusto natin iprevent), *Acts on thermoregulation
Thromboxanes
- Derived from what pathway?
- As discussed what is TXA2?
-From COX pathway
-Among the TXs, naaalala namin would be TXA2 (hemostasis)
-TXA2
>activator of platelets
>secreted by activated platelets as well
>This is why we give aspirin - we block TXA2 synthesis if we want to stop platelet aggregation
Leukotrienes
- Derived from what pathway?
- Effects?
-From LOX pathway
-Primarily for the immune response/inflammation
-LTB4: Potent chemotactic factor
-LTs also responsible for contraction of airway (bronchoconstriction)
-vasodilation and inc vascular permeability (so sa inflammation)
Feeding behavior
>Specific regions on the hypothalamus?
>Hormones affecting these centers
- a. Ventromedial nucleus (Satiety center): When activated leads to decreased appetite
b. Lateral hypothalamic area (Hunger/feeding center): - Hormones affecting these centersL
Leptin, Insulin, Ghrelin
Leptin
- Type of hormone
- Secreted by?
- Receptor?
- Purpose of leptin?
- T or F. Eating a lot of food will immediately stimulate leptin?
- Peptide Hormone
- Secreted by adipocytes
- LEP-R: a TKAR involving JAK/STAT
- Leptin sends anorexigenic signals for the hypothalamus (+ insulin)
>Decrease feeding (anorexia) together with insulin dec feeding behavior/feeding - Plasma lvl is not affected by food intake so this is a long-term regulator of feeding behavior compared to insulin na when you eat will inc then after sometime bababa
How does leptin and insulin affect feeding behavior?
CART: cocaine/amphetamine regulated transcript
AgRP: agouti related peptide
-
This is how leptin and insulin affect feeding behavior
-Would affect 2 neurons
Inc Leptin and Insulin:
-Activate anorexigenix neurons: POMC/CART (Proopiomelanocortin/Cart: Cocaine amphetamine related transcript neuron)
>When this site is activated, you’ll inc alpha-MSH -> alpha-MSH would bind to melanocortin receptors -> activation of this will dec food intake
-Inhibit Orexigenic (meaning kakain) neurons: AgRP/NPY
—> Dec NPY/AGRP (Neuropeptide Y/Agauti related peptide) expression
*AGRP when inc in mice, kakain ng kakain
-> so what happens, when this is inhibited, you have a dec in NPY and AGRP which eventually results to a dec in food intake so you’ll have anorexia
Ghrelin
- Type of hormone?
- Secreted by? Highest conc at?
- Receptor
- When is it secreted?
- What does it activate?
- Peptide Hormone
- Secreted by the GIT mucosa
(Highest conc at the fundus) - GH-secretagogue receptor 1a
-Opposite to leptin and insulin
-PH produced by the GIT mucosa
-Some books would say that the Ghrelin is primarily prod sa stomach bc they found out that the ghrelin secretion is highest in the fundus
>But kay Boron, all throughout the GIT may ghrelin secretion
-Receptor: GH-secretagogue receptor 1a (GHSR1a)
>GH secretagogue bc they previously thought that ghrelin is responsible for GH secretion
>But actually, it is a hunger hormone involved in your feeding hormone
-Actually activates Orexigenic neurons -> so more of NPY and AGRP resulting to an inc food intake and at the same time an inc lvl of AGRP would exert a negative effect on anorexigenic pathway (so kakain ka bc of Ghrelin)
What are vasoactive hormones?
These hormones are produced by the endothelial lining for the regulation of blood flow. (To regulate the diameter of your BVs)
>NO, Endothelin
Endothelin
1. What pathway does this hormone utilize?
- Pathway
- PLC pathway
- PLC pathway would lead to an inc in intracellular Ca2+ -> Ca2+-calmodulin complex -> activate MLCK -> ℗ myosin -> actin-myosin interaction -> contraction
Nitric Oxide
- Aka
- Effects
- Produced by?
- Mechanism of #3 in the endothelium?
- Endothelial-derived realxing factor (EDRF)
- Vasodilation of BVs; minor: antiplatelet aggregation/adhesion
- NO synthase (Isoenzymes: Neuronal NOS, Inducible NOS, Endothelial NOS, etc.)
- Endothelial NOS is activated when you have an increasing P (Pressure changes) -> produce NO from Arg (precursor of NO) -> NO will diffuse into the cells (gas) -> Once inside the smooth ms cells, it activated guanylyl cyclase ->inc cGMP -> activate MLCPhosphatase (remove ℗ from myosin) -> Prevent myosin-actin interaction -> Relaxation -> Vasodilation
Serotonin
- aka
- Produced from
- As a NT (Associated with)? As a hormone (Secreted by? Activates?)
- Aka 5-HT (5-hydroxytryptamine)
- Produced from decarboxylation of tryptophan
- As a neurotransmitter in CNS: Associated with emotions, cognition, learning, and memory
- As a hormone,
>activates the 5-HT3 receptors on the chemoreceptor trigger zone (involved in vomiting)
>secreted by activated platelets (so powerful vasoconstrictor ang serotonin)
Melatonin
- Produced by?
- Synthesis is activated by? Inhibited by?
- Effect?
- Produced by the pineal gland from serotonin
- Synthesis is:
Activated by darkness
Inhibited by light - Transmits outside signal that nighttime has arrived -> convert it to physiologic effects (sleeping, etc) so involved in the sleep wake cycle
Histamine 1. Derived from? 2. Effects as a hormone A. On smooth ms B. On GIT C. On the immune system
- Decarboxylation of Histidine
Acts as a NT too
- As a hormone:
A. Vasodilator because it induces NO release so -> smooth ms relaxation -> vasodilation
B. Sa GI will cause gastric acid release -> activation of proton pump -> so more HCl released
C. Histamine is secreted by mast cells and basophils whenever they are activated so involved in the inflammatory response/IgE sensitization
Erythropoietin
- What is EPO? Secreted by?
- Fetal source?
- Binds to?
- Secreted in response to?
- Effects
- Mechanism of synthesis?
- Glycoprotein secreted by fibroblast type I interstitial cells in the renal cortex and outer medulla (SO KIDNEYS)
- Fetal source: Liver
- Receptor: Tyrosine Kinase-Associated Receptor (JAK/STAT pathway)
- Secreted in response to hypoxia (main stimulus)
- Proerythroblast formation
- Under normoxia (normal oxygen levels), HIF-alpha (Hypoxia inducible factor) will be hydroxylated so it can’t enter the nucleus so it stays in the cytoplasm and eventually broken down
But at low levels, HIF will NOT be hydroxylated so it enters the nucleus -> inc transcription of EPO gene -> more EPO release