Term
| Exocrine: where is signal sent? example? |
|
Definition
duct -> outside of body
(sweat glands, mammary glands, stomach, liver, pancreas...) |
|
|
Term
| juxacrine: where is signal sent? example? |
|
Definition
cells in contact
(growth factor, cytokine, chemokine receptors) |
|
|
Term
| autocrine: where is signal sent? example? |
|
Definition
self
(IL-1: external stimuli->activate IL-1 on the same cell that produced it) |
|
|
Term
| paracrine: where is signal sent? example? |
|
Definition
nearby cell
(prostaglandings, histamines) |
|
|
Term
| endocrine: where is signal sent? example? |
|
Definition
into bloodstream
(hypothalamus, pineal, pituitary, adrenal, etc...) |
|
|
Term
| Steroid: Receptor Location Derived From? Response Rate Duration of Response Examples |
|
Definition
| Receptor Location: intracellular Derived From?: cholesterol Response Rate: slow Duration of Response: long Examples: estrogen, testasterone, cortisol |
|
|
Term
Nuclear
Receptor Location
Derived From?
Response Rate
Duration of Response
Examples |
|
Definition
can be located in nucleus with absense of H
Receptor Location: intracellular
Derived From?: tyrosine
Response Rate: slow
Duration of Response: long
Examples: T4, T3; estrogen; retinoic acid; vitD |
|
|
Term
Peptides
Receptor Location
Derived From?
Response Rate
Duration of Response
Examples |
|
Definition
Receptor Location: on membrane
Derived From?: a.a.
Response Rate: fast
Duration of Response: short
Examples: prolactin, ACTH, ADH, oxytocin |
|
|
Term
catecholamines
Receptor Location
Derived From?
Response Rate
Duration of Response
Examples |
|
Definition
Receptor Location: on membrane
Derived From?: tyrosine
Response Rate fast
Duration of Response short
Examples: dopamine, NE, epi |
|
|
Term
|
Definition
to activate GPCR:
H binds to R
->conf change
->beta and gamma dissociate
->alpha xchange GDP for GTP
->activates AC
->AC converts ATP to cAMP
-> inc. PKA |
|
|
Term
|
Definition
to activate GPCR:
H binds R
-> inc. PLC
-> PLC converts PIP2 to DAG+IP3
->DAG stays in membrane to phos other proteins
and IP3 binds receptor in ER and inc. Ca release |
|
|
Term
|
Definition
1. remove H
2. hydolyse GTP to GDP (GTPase)
3. cAMP->AMP (PDE)
4. de-phos DAG+PKA (phosphatase) |
|
|
Term
|
Definition
| keeps Galpha active->inc.cAMP-> inc. water, Cl, Na, and K secretion->dehydration and diarea |
|
|
Term
|
Definition
whooping cough
keeps Gi active->dec. cAMP->dec. PKA |
|
|
Term
| receptor tyrosine kinases (examples and mech) |
|
Definition
Insulin receptor, IGF, growth factors in general
Rec. dimerizes->phos tyrosine residues->SH2 domain associates with tyrosine residues->downstream phos |
|
|
Term
| What is the mechanism of action of a guanylyl cyclase receptor? (and examples) |
|
Definition
GC converts GTP to cGMP
->inc. PKG
(there are membrane bound guanylate cyclase receptors (BNP, ANP) and soluble guanylate cyclase receptors (NO)) |
|
|
Term
| How does Viagra use the guanylyl cyclase receptor mechanism to inrease blood flow to the penis? |
|
Definition
NO binds GC
->inc cGMP->smooth muscle relax->vasodilation->inc blood flow.
Viagra blocks PDE5 so that it can't inactivate cGMP to GMP |
|
|
Term
| How do arrestins work to G-protein coupled receptors? |
|
Definition
2 ways:
1. blocks binding site so G-protein cant be activated
2. link rec. to clathrin allows internalization |
|
|
Term
| How does BARK serve as a negative feedback enzyme to prevent over-stimulation of the β2- adrenergic receptor? |
|
Definition
| PKA phos BARK-> phosphorylates serine/threonine kinases on its own receptor->activates beta arrestins->BARK acts as neg feedback preventing overstimulation of the beta adrenergic rec. |
|
|
Term
| mechanism of activation for steroid rec. |
|
Definition
| intracellular rec. diffuses into the nucleus and alters gene txn |
|
|
Term
|
Definition
NH2-TAD-DBD-LBD-COOH
TAD: tans-activation domain
DBD: DNA-binding domain (zinc fingers)
LBD: Ligand binding domain (HSP) |
|
|
Term
|
Definition
bound by steriod rec.
inc. when exposed to temp or stress
act as chaperones to prevent unwanted aggregation |
|
|
Term
| What is the difference in the relationship of the anterior and posterior pituitary with the hypothalamus? |
|
Definition
Anterior pituitary: Forms a portal system with the hypothalamus
Posterior pituitary: No portal system, |
|
|
Term
| outline the pathway of 5 hypothalamic hormones |
|
Definition
TRH→TSH→T3,T4 from thyroid gland
CRH→ACTH→cortisol from adrenal cortex
GnRH→ FSH, LH→ estrogen, androgens from gonads
GHRH→GH→liver→IGF-1
- somatostatin inhibits GH.
Dopamine→inhibits PRL→ decrease milk production |
|
|
Term
| Women with PRL secreting tumors may have difficulties conceiving. Why do you think this is? |
|
Definition
| PRL inhibits GnRH, so secreting excess PRL→ decrease GnRH→ decrease FSH, LH→ no ovulation |
|
|
Term
| anterior pituitary hormones |
|
Definition
| GH, TSH, ACTH, FSH, LH, PRL |
|
|
Term
|
Definition
dimers as rest, no intrinsic tyr activity.
H binds->Jack phos tyr residues->STAT->nucleus altered gene expression
cells of the immune systme, autocrine or paracrine |
|
|
Term
| How is growth hormone regulated by the hypothalamus? At what point during the day are growth hormone levels highest? |
|
Definition
| Circadian clock→ GH has circadian rhythm. Highest GH during night. |
|
|
Term
| What are the metabolic effects of GH? |
|
Definition
| -increased protein synthesis, decreased glucose utilization, decreased insulin sensitivity, increased fat breakdown in adipocytes |
|
|
Term
| what are the symptoms of abnormal GH levels in children and adults? |
|
Definition
Deficiency:
Adults: Obesity (b/c increase glucose metabolism instead of fat metabolism)
Children: dwarfism, b/c long bones are not stimulated to grow. Males may not have thick vocal chords→ high pitched voice.
Excess:
Adults: Thick skin. Acromegaly→ enlargement of the extremities. Diabetes b/c interacts with IGF-1, hypertension, enlarged heart
Children: Gigantism. All organs increase in size |
|
|
Term
| When is CRH secretion highest? |
|
Definition
| Early morning b/c circadian activity of hypothalamus. Another peak in late evening |
|
|
Term
| ACTH is synthesized from what precursor? How does ACTH affect melanin synthesis? |
|
Definition
| POMC→ ACTH, gamma-MSH, beta lipotropin. ACTH is further broken down to alpha-MSH and CLIP. Alpha-MSH makes melanin. |
|
|
Term
|
Definition
| Decreased cortisol/glucocorticoids, increased CRH and ACTH. Patients will have fatigue, nausea, hyperpigmentation. Low BP |
|
|
Term
|
Definition
| moon face, Increased cortisol, decrease ACTH, CRH. Increased fat in face, abdomen, and at top of back behind neck. Skin will get stretched and break. |
|
|
Term
| When is ADH released? What does it do upon release? |
|
Definition
| ADH is released if blood osmolarity increases→ increase ADH which acts on Gs to increase cAMP. Acts on collecting duct in kidney to increase Aq-2 channels. Aq-2 channels allow water to be reabsorbed by kidney therefore making the urine more concentrated. |
|
|
Term
| How does alcohol affect ADH? |
|
Definition
| Alcohol blocks ADH, thus there are no Aq-2 channels secreted into the collecting duct and water is excreted in the urine making the urine more dilute and eventually resulting in dehydration. |
|
|
Term
| What signal transduction mechanism does oxytocin utilize? |
|
Definition
| Gq. Leads to an increase in calcium and PLC. |
|
|
Term
|
Definition
uterine contractions from stretch cervix, and
Mechanoreceptors in the breasts are activated when the baby suckles→ oxytocin release from hypothalamus→ milk let down. |
|
|
Term
|
Definition
-myxedema: inc synth of mucus polysacc->draws fluid to thick and swollen skin
-exopthalamus: eyes popping out with hyperthyroidism
-Hashimoto's thyroiditis: hypo autoimmune
-Graves': hyper antibodies target TSH Rec and stimulate it
-Cretinism: A decrease in thyroid hormone during development. This is typically due to maternal iodine deficiency. Cretinism is characterized by mental retardation and stunted growth. |
|
|
Term
| primary, secondary, and teritary effects of hypothyroidism |
|
Definition
primary: I definiciency-> dec.T3T4-> inc. TRH incTSH
secondary: dec. T3T4, dec TSH, incTRH
tertiary: dec T3T4, decTSH decTRH |
|
|
Term
| primary, secondary, and tertiary hormone effects hyperthyroidism |
|
Definition
primary: incT4T3, decTSH, decTRH
secondary: incT4T3, incTSH, decTRH
tertiary: inc T4T3, inc TSH, Inc TRH |
|
|
Term
| drugs to treat thyroid disorders |
|
Definition
hypo: Thyroxin
hyper: PTU blocks TPO→ decrease iodine uptake
or radioactive I131 |
|
|
Term
| List the steps of thyroid hormone synthesis. |
|
Definition
1. Iodide trapping: active transport of iodide across the basement membrane:
- On basolateral membrane: Na+/K+ pump and Na+/I- symport. The driving force of sodium helps bring I- into the cell.
- I- is transported across the apical membrane by pendrin.
2. Synthesis of thyroglobulin (TGB). Made in the rough ER.
3. Secretion of thyroglobulin into follicle.
4. Organification: Iodine is oxidized and the tyrosine residues in thyroglobulin are iodinated to give MIT + DIT residues. This is catalyzed by TPO. Occurs at the apical-colloid border. Two DIT fuse to form T4 and one MIT+one DIT fuse to form T3.
5. Pinocytosis of iodinated thyroglobulin.
6. Proteolysis of thyroglobulin. This releases T3, T4. |
|
|
Term
| What three things must be functional in order for thyroid hormone synthesis to occur? |
|
Definition
1. Sodium/Iodide symport: without this, iodide would never enter the follicle lumen
2. Thyroglobulin (TGB): Made in the RER→ transported to Golgi→ put into exocytic vesicles→ vesicles fuse with cell’s apical basement membrane→ released into follicular lumen.
3. Thyroid peroxidase (TPO): this catalyzes the conversion of thyroglobulin to MIT + DIT. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| neg feedback inc hypothal production and incTRH,TSH and TSH stimulated thyroid gland to grow |
|
|
Term
| What will a deficit in pendrin result in? |
|
Definition
| Pendrin transports iodide across the basement membrane, without it, iodide will not be transported across the basement membrane and thyroid hormones will not be synthesized. There will be a decrease in T3, T4 and then an increase in TRH and TSH leading to a goiter. |
|
|
Term
| What specific processes does thyroid stimulating hormone stimulate |
|
Definition
| Iodide trapping, synthesis of thyroglobulin, and organification. |
|
|
Term
| What are the metabolic effects of thyroid hormone |
|
Definition
| Increase oxygen consumption, increase uncoupling of proteins, increase glycogenolysis. General increase in metabolic rate. |
|
|
Term
| What are the affects of thyroid hormone on the heart? |
|
Definition
| Increase heart rate, contractility, synthesis of sodium/potassium pump in heart. |
|
|
Term
| Outline the hormonal control of the androgens for males |
|
Definition
Hypothalamus→ GnRH→ acts on anterior pituitary to secrete FSH and LH.
FSH→ acts on the sertoli cells to secrete anti-mullerian hormone, androgen binding protein, and inhibin. Inhibin inhibits FSH. LH acts on the leydig cells to secrete testosterone. Testosterone is converted to DHT by 5-alpha reductase and to estradiol by aromatase. |
|
|
Term
| What are the precursors to testosterone |
|
Definition
| cholesterol in mito->(via STAR)->chol in cytoplasm-(via P40scc)->pregnenolone->progesterone->antrostenedione->testosterone-(aromatase)->estradiol |
|
|
Term
| What changes the frequency and amplitude of GnRH pulses? |
|
Definition
estradiol dec amp
testosterone,DHT dec freq |
|
|
Term
| What are some effects of testosterone and DHT? |
|
Definition
inc: agressoveness, ABP, penis size, libido, hair, thicken vocal chords, LDL
dec: HDL |
|
|
Term
| tyr inhib dopamine how does this affect mother? |
|
Definition
normally dopamine inhib prolactin (PRL)
so an inc PRL with inc milk production |
|
|
Term
| what would be the affect on FSH and LH if you have a tumor blocking posterior pituitary? |
|
Definition
| nothing because FSH and LH are secreted by the anterior pituitary |
|
|
Term
| what would happen if you take exogenous prolactin on FSH, LH |
|
Definition
| normally prolactin inhib GnRH so taking more inhibits this more and therefore dec. FSH, LH |
|
|
Term
| when dehydrated what does ASH do |
|
Definition
| inc aquaporin-2 -> inc H2O reabsorption-> dec water loss and conc. urine |
|
|
Term
| what hormone is used to induce labor |
|
Definition
|
|
Term
| what happens to thyroid hormones with disfunctional Na/I symport |
|
Definition
| no I trapping-> no T4T3 -> hypothyroidism |
|
|
Term
| What would happen with a deficit of TGB? |
|
Definition
TGB-(TPO)-> MIT + DIT
so no T4T3 |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| : hyper antibodies target TSH Rec and stimulate it |
|
|
Term
|
Definition
| : A decrease in thyroid hormone during development. This is typically due to maternal iodine deficiency. Cretinism is characterized by mental retardation and stunted growth. |
|
|
Term
| enzymes that inhib catecholamines |
|
Definition
MAO (first antidepressants)
COMT |
|
|
Term
|
Definition
| steriod hormone in adrenal cortex inc Na reabsorption inc BV and K secretion |
|
|
Term
|
Definition
| act like NE for vasoconstriction (agonist) |
|
|
Term
| Menstrual (Estrous) Cycle |
|
Definition
| Consists of the ovarian cycle and the uterine cycle |
|
|
Term
|
Definition
| consists of the early and late follicular phase and the early and late luteal phase |
|
|
Term
|
Definition
| consists of the proliferative and the secretory phase |
|
|
Term
|
Definition
| developing follicle secreates estrogen and inhibin A -> dec FSH and Dec GnRH amp -> dec stim of follicles, moste with most FSH receptors stimulate estrogen production |
|
|
Term
|
Definition
| inc. estrogen -> stim of LH, a little FSH -> inc sensitivity GnRH and furthur inc LH -> estrogen inc positive feedback LH -> LH surge -> ovulation |
|
|
Term
|
Definition
| Graffian follicle bursts and releases oocyte |
|
|
Term
|
Definition
| ovulation -> dec estrogen and inhibin. hight LH -> develope corpus luteum, granulosa cells inc progesterone |
|
|
Term
|
Definition
| progesterone max inhib GnRH and FSH/LH -> dec FSH and LH -> dec estrogen progesterone -> cycle starts over (low FSH and LH and high basal temp at luteal phase) |
|
|
Term
|
Definition
| uterine cycle: at beginning endometrial tissue is dead. estrogen inc -> growth of endometrial cells and divide/thicken |
|
|
Term
|
Definition
inc progesterone -> exocrine secretion mucopolysacharides.
12 days after ovulation, low levels of estrogen and progesterone cause endometrium to slough off |
|
|
Term
|
Definition
Decreased proliferation by estrogen
increase secretory gland activity
increase spirality of arterioles
inhibits cell growth |
|
|
Term
|
Definition
inc cell division
inc myometrium cell growth
inc excitability of myometrium |
|
|
Term
| protaglandins during menstal cycle |
|
Definition
| inc contractility of endometrium during late luteal phase |
|
|
Term
| female secondary sexual characteristics after puberty |
|
Definition
- Growth and development of breasts
- Increased pubic and axillary hair
- Increased sebaceous gland activity (stimulated by androgens; estrogens contribute to making secretions more fluid)
- Increased body odor
- Increased HDL, decreased LDL
- Increased calcium in bone
- Increased growth spurt
- Increased ossification of epiphyseal plates
- Increased tendency of blood to clot
- Increased pigmentation of nipples |
|
|
Term
| treatments for estrogen-dependent breast cancer |
|
Definition
Tamoxifen, Raloxifen, Aromatase inhibitors
They are estrogen antagonists and act to decrease estrogen expression specifically on the breasts. |
|
|
Term
|
Definition
- abstinence
- barrier→ condom, diaphragm
- coitus interruptus
- progestin, ethinyl estradiol (effects similar to progesterone→progesterone can suppress ovulation)
- IUD: device placed in the uterus to prevent pregnancy.
- tubal ligation→ vasectomy
-inject prostaglandins into uterus
-emergency contraception: They contain high doses of estrogen, progestins, or both. This prevents ovulation and thickens the cervical mucus to prevent the entry of sperm |
|
|
Term
|
Definition
- During ovulation, the Graffian follicle bursts and release the oocyte. The oocyte is caught by fimbrae and moves through the fallopian tubes towards the uterus. Fertilization occurs in the fallopian tubes. Once the oocyte that was arrested in Metaphase II is fertilized it can complete its second meitotic division.
- A zygote now forms and eventually becomes a blastocyst. The inner cell mass of the blastocyst is what eventually gives rise to the fetus.
- The embryo is implanted into the endometrial lining of the woman’s uterus.
-The outermost layer of the embryo is known as the chorion, and the chorionic villi allow for the transfer of maternal blood to the fetus.
- The umbilical cord connects the fetus to the placenta. |
|
|
Term
|
Definition
- The placenta connects the fetus to the uterine wall and allows for nutrient uptake, waste elimination, and gas exchange. The placenta secretes HCG within one day after implantation of the blastocyst. HCG serves to ensure that the corpus luteum is maintained and continues to secrete estrogen and progesterone. If progesterone levels are not maintained the endometrium will slough off and pregnancy will be lost.
- The placenta also secretes hPL which promotes growth of the mammary gland and regulates maternal glucose and protein levels. It can also decrease oxytocin receptors until labor.
- Relaxin can be produced by the placenta and corpus luteum of the ovary and serves to decrease contractility of the myometrium, weaken the pubic symphysis and widen the birth canal for delivery |
|
|
Term
|
Definition
- The fetal adrenals begin to produce 17-hydroxyprogesterone which inhibits early contractility.
- Produce DHEA-sulfate which acts on androstenedione to produce testosterone, and eventually estradiol, estrone, and estriol. |
|
|
Term
|
Definition
| blastocyst implants in Fallopian Tube |
|
|
Term
| SRY gene present sexual development |
|
Definition
testes (Testosterone is converted to DHT by 5-alpha reductase which leads to development of the penis and prostate.)
->testosterone(wolffian ducts->epididymis, vas deferens, seminal vesicles, prostate)
->MIF (mullerian ducts dead) |
|
|
Term
| sexual development no SRY gene |
|
Definition
ovaries develop->
wolffian ducts dead
no MIF (mullerian duct lives->uteus, fallopian tubes, upper region of vagina)
estrogen (secondary sexual characteristics at puberty)
progesterone (maintain endometrium) |
|
|
Term
|
Definition
There is a mutation in the androgen receptor (testosterone) which leads to the inability of testosterone to signal to the wolffian ducts to survive, thus there are no wolffian ducts. MIS is still functional, so there are no Mullerian ducts. This person looks like a female externally, and a male internally (have testes).
These people typically have a 5 alpha reductase deficiency so they have testes, but external female genitalia. |
|
|
Term
|
Definition
What genitalia does a person who is genetically XY, has normal testosterone levels, but a 5 alpha reductase deficiency have before and after puberty?
This person appears to be female before puberty because there is no formation of male external genitalia due to the decrease in DHT. Then at puberty, there is an increase in testosterone which allows tissues to respond directly to it without needing DHT. This surge in testosterone results in the tests descending into the labia majora and the formation of a penis. |
|
|
Term
|
Definition
woman XO
She is typically short and mentally challenged, has webbed neck, and is not fertile due to dysfunctional ovaries |
|
|
Term
|
Definition
| women who have it are called “superwoman”. Women are typically normal because only one of the X chromosomes and the others are inactive and form Barr bodies |
|
|
Term
| What happens when someone is XX with an SRY gene on the X chromosome instead of Y |
|
Definition
|
|
Term
|
Definition
| They develop hypogonadism and infertility. They develop gynecomastia and have low levels of testosterone and high levels of FSH and LH. |
|
|
Term
|
Definition
| This is treated with GnRH analogs in order to down-regulate receptors in the pituitary. If GnRH is secreted all at once instead of in pulses, the receptors in the pituitary will de-sensitize and the anterior pituitary will not secrete FSH and LH. |
|
|
Term
|
Definition
| Ob/ob mice have mutations in the gene for leptin. These mice look obese but when they are given leptin they become thin! |
|
|
Term
|
Definition
| Leptin acts on receptors in the hypothalamus to decrease appetite. When leptin is not present there is no appetite leading to obesity. |
|
|
Term
|
Definition
| When there is a decrease in fat content, adipocytes release less leptin, and there is a decrease in GnRH leading to a halt in menstruation. As leptin increases, GnRH release also increases. |
|
|
Term
| alpha, beta, and delta cells |
|
Definition
alpha secrete glucagon
beta secrete inculin
delta secrete somatostain |
|
|
Term
| How does glucose stimulate insulin secretion? |
|
Definition
-Glucose enters the Beta cells in the pancreas through the GLUT2 transporter.
-Glucose binds hexokinase and is converted to G6P which undergoes glycolysis→ ATP generated
-ATP-dependent potassium channels close and the membrane depolarizes
-After depolarization→ voltage gated calcium channels open and calcium flows into the cell
-Increased calcium in the cell causes the exocytosis of insulin containing secretory vesicles |
|
|
Term
|
Definition
stimulate insulin secretion:
They block the potassium ATP channels→ membrane depolarization→ calcium entry and exocytosis of insulin containing vesicles |
|
|
Term
|
Definition
- Incretins cause an increase in insulin after eating before blood glucose levels increase.
- The main incretins are GLP-1 and GIP. GLP-1 increases insulin secretion and decreases glucagon secretion from the pancreas. GIP also increases insulin secretion. |
|
|
Term
|
Definition
-Increase glucose uptake because of insertion of GLUT4 transporter in adipose tissue and skeletal muscle
Increase glucose uptake from blood and store it as glycogen in the liver and muscle. Insulin activates hexokinase which phosphorylates glucose and inhibits glucose-6-phosphatase. This results in the increase in storage of glucose in the form of glycogen in the liver.
-Insulin increases synthesis of fatty acids in the liver.
-Insulin inhibits breakdown of fat in adipose tissue by inhibiting lipase which normally hydrolyzes triglycerides.
-Decreases gluconeogenesis.
-inc net protein synthesis and aa uptake |
|
|
Term
|
Definition
- Glucagon is a hormone of the fasted state. Its secretion is stimulated by decreased glucose and it is inhibited by increase glucose, insulin, somatostatin, and incretins.
- The effects of glucagon include increased glycogen breakdown, increased gluconeogenesis, and increased hormone sensitive lipase.
- Increases gluconeogenesis.
- Increases lipase to release glycerol and fatty acids into circulation. |
|
|
Term
|
Definition
- Due to decreased production of insulin because of auto-immune destruction of pancreatic beta cells.
- As blood glucose increases, there is an increase in plasma osmolarity.
-Polyuria, or increased urination
-Polydipsia, or increased thirst
- Can develop ketoacidosis because there is a shortage of insulin so the body burns fatty acids instead. |
|
|
Term
|
Definition
- Insulin resistance
-Polyuria, polydipsia
-To detect: glycated hemoglobin value less than 6%. As the average amount of plasma glucose increases, the glycated hemoglobin value increases because more hemoglobin is exposed to plasma glucose. |
|
|
Term
|
Definition
What Happens:
-The body can’t use glucose as fuel because there is no insulin. Instead there is an increased in the beta-oxidation of fatty acids. This results in an increase in the production of acetone which decreases pH and results in depression of the CNS which can lead to coma.
-The acidosis can also lead to hyperventilation
-Also, with an increase in glucose there is an increase in glucosuria which leads to dehydration which leads to a decrease in blood pressure, thus giving rise to tachycardia and resulting in circulatory shock and death.
Treatment: Need to correct the high blood glucose levels, so you can do this by giving insulin. |
|
|
Term
|
Definition
A. What Happens
-Glucose levels are too low.
-If one is a diabetic, this can occur when: take too much insulin, don’t eat enough, suddenly increase exercise without increasing food (this is because exercise consumes more glucose and makes insulin more efficient).
-If glucose is between 60-70 mg/dL: sleepy/irritated
-If glucose is between 30-40 mg/dL: strong sympathetic response, increase tachycardia and sweating, vasoconstriction, increase blood pressure, confusion, loss of consciousness
-If glucose is less than 30 mg/dL: seizures→ death
B. Treatment
-Eat something with sugar in it.
C. Can Be Caused by
-increase insulin caused by: incretins, sulfonylureas, dipeptidase |
|
|
Term
|
Definition
allow people to efficiently metabolize food to deposit fat. This would be most beneficial during times of famine. However, when there is an abundance of food, it simply results in people becoming obese.
-People with the “apple” body shape are at risk of: diabetes, hypertesnion, stroke, high LDL, and heart attack.
-Why might people with the “apple” body shape be at risk of diabetes
They are also at risk of heart attack because adipocytes increase and lead to an increased secretion of leptin and resistin and decreased secretion of adiponectin. |
|
|
Term
| treatment metabolic syndrome |
|
Definition
-PPARgamma agonist: stimulates lipid uptake and increases secretion of adiponectin and decreases secretion of resistin.
-Metformin: decrease gluconeogenesis, increase insulin sensitivity |
|
|
Term
|
Definition
-Bone is constantly being formed and resorbed, this process is known as remodeling.
-Osteoblasts are the cells that build bone and secrete osteoid. Osteoclasts are the cells that resorb bone.
-Osteoid is composed of collagen I and contributes to mineralization of bone.
-The diaphysis is the long part of the bone and the epihphysis is the ends of the bone. Growth cartilage is contained in the epiphyseal plates where there is a high concentration of osteoblasts.
-The main mineral part of bone is known as hydroxyapatite.
1. Hydroxyapatite molecules have the ability of forming crystals, what might happen if one has increased formation of hydroxyapatite crystals in the joints?
This will cause inflammation of the joints and their surrounding tissues. A possible treatment is to inject corticosteroids to reduce inflammation or mechanically break up the calcium deposits. |
|
|
Term
| teeth calcium homeostasis |
|
Definition
| Fluroapatite is present in the enamel of teeth and provides protection against cavities |
|
|
Term
|
Definition
-Calcium concentration is high outside the cell and low inside the cell.
-Chelating agents are able to bind calcium and reduce blood clotting.
1. What are some of the effects of calcium?
Calcium can trigger the exocytosis of vesicles containing neurotransmitters and hormones. It can also increase muscle contracion of both skeletal and smooth muscle. |
|
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Term
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Definition
| the extracellular calcium concentration decreases, this increases the excitability of cells. If it is extreme, it can lead to a sustained muscle contraction known as tetanus. |
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Term
| hormone regulation of calcium |
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Definition
| Parathyroid hormone (PTH) is the primary regulator of calcium. When there is low plasma calcium: increase PTH release→ Calcium is released from bone and taken up in kidney. |
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Term
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Definition
| Calcium sensors are located on parathyroid cells. They are GPCR (Gq) and sense extracellular calcium, thus, when calcium is low they are activated. When Gq is activated→ IP3 and DAG active→ increase extracellular calcium and decrease in intracellular calcium→ inhibits secretion of PTH. Calcium normally causes exocytosis of hormone-containing vesicles, but in parathyroid cells it does not because magnesium has this role |
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Term
| vit D and calcium homeostasis |
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Definition
Calcitriol is the biologically active form of vitamin D and acts to increase calcium absorption in the intestine. When there is low blood calcium→ PTH secreted→ stimulates calcium uptake in kidney→ activates vitamin D→ increases calcium uptake in intestines.
Vitamin D also promotes bone resorption (increase osteoclast). |
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Term
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Definition
| In children this is called rickets and in adults this is called osteomalacia. This results in muscle weakness, hypocalcemia, tetany, and increased tendency for bone fractures. |
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Term
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Definition
| Normal fasting glucose is considered to lie in the range of 70-110 mg/dL. Metabolic syndrome patients usually have normal fasting glucose levels, although they may lie in the upper limit of the normal range, 90-120 mg/dL. A fasting plasma glucose level equal to or higher than 126 mg/dL is diagnostic of diabetes. |
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Term
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Definition
build bone
PTH Calcitol receptors
M-CSF (inc div of macrophages), OPG, RANKL, release calcium from bone |
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Term
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Definition
increase Ca absorbtion from GI and kidney
inc osteoblast
inhib calcitonin
activated by PTH |
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Term
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Definition
decoy recpetor from osteoblast
inhib RANKL |
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Term
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Definition
membrane of osteoblast
inhib by OPG
activates osteoclasts
inc by IL-1, IL-6 |
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Term
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Definition
activated by PTH and RANKL
have calcitonin receptors |
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Term
| mechanism by which osteoclasts resorb bone |
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Definition
attach to bone surface
form adhesive ring
ruffled border above bone surface
releases H ions through border into resorptive area
bone acidified and mineralized |
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Term
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Definition
secreted from C cells of the thyroid gland
inhibits osteoclast activity -> reducing calcium levels
(opposes effects of PTH) |
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Term
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Definition
disease bone mineral reduced -> more fracture prone
treatments: bisphosphonates, vitD, Ca |
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Term
| adrenal cortex secretions |
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Definition
glucocorticoids (cortisol)
mineralocoricoids (aldosterone)
androgens (DHEA-S+DHEA, androstenedione) |
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Term
| adrenal medulla secretions |
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Definition
sympathetic ganglion
NE and Epi |
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Term
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Definition
| cholesterol -> mito -STAR-> mito. matrix -> pregenolone |
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Term
| cortisol metabolic effects |
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Definition
inc gluconeogenesis
inc lipotysis
inc proteolysis
inc glucose
inc insulin insensitivity |
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Term
| cortisol on immune system |
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Definition
dec inflammation
dec protaglandin and laukotriene synth
dec IL-1 |
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Term
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Definition
mood changes
dec concentration
short tem memory |
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Term
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Definition
hypercortisol
large abdomen
"moon face"
hypertension |
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Term
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Definition
hypocortisol
weakness
weight loss
loss of appetite
inc pigmentation due to high ACTH |
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Term
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Definition
| - Hormones with antagonistic effects: growth hormone, cortisol, epinephrine |
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Term
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Definition
is the third “P” of diabetes. This is because glucose is not metabolized signals hunger
chronic need to eat (absence of insulin, hypothalamic satiety center does not become activated) |
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Term
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Definition
| presence of glucose in urine (blood glucose higher than renal threshold 300mg/L SBLT in prox tubule) |
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Term
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Definition
| retention of glucose in the filatrate -> osmotic diuresis (excess glucose in filtrate draws water from circulatory into filtrate causing lorge volumes of water loss -> dehydration -> dec BV and BP) |
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Term
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Definition
chronic thirst (triggered by dehydration and dec BP)
ncreased blood glucose Increased osmolarity ADH, thirst (polydipsia)
Glucose above 300mg/dL (proximal tubule has SGLTs to reabsorp glucose) glucose lost in urine increases urine osmolarity increases H2O lost in urine polyuria/glusouria dehydration increased osmolarity of blood polydipsia |
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Term
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Definition
What allows for HbA1c levels to be a good measure of BGL over the course of the past few months?
Hb reacts/binds with glucose (high concen) --> measure HbA1C levels
Glycated Hb circulating for abt 130days - - - normal is less than 6% |
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Term
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Definition
| chondrocytes and osteoblasts are present |
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Term
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Definition
| A majority of Ca++ in the body is found in the bones/teeth. This Ca++ is in crystalline form and is called hydroxyapatite. This form of Ca++ dissolves when the pH decreases. |
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Term
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Definition
Blood clotting
Exocytosis of NTs, hormones and other secretions
Regulation of excitability
Muscle contraction (cardiac, skeletal, smooth) |
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Term
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Definition
if excitability is high and a patient is experiencing tingling/tetanus, what are his/her Ca++ levels?
Hypocalcemia
Mechanism: dec EC Ca++ fewer Ca++ ions neutralizing negative charges on proteins (EC side) of voltage-gated channels protein pulled outward even when membrane potential is at rest open channel increases excitability |
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Term
| Ca++ and Parathyroid glands |
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Definition
Ca++ usually increases secretion, but it dec PTH secretion by negative feedback
Endogenous precursors (sunlight on skin) or from diet --> vit D --> liver --> 25(OH)D3 --> kidney --> calcitriol --> bone, distal neph, intestine --> inc plasma Ca++ --> neg fdvck inhibit PTH relase
Dec plasma Ca++ --> PTH --> stimulate kidney
PTH --> bone
1,25 (OH)2-D --> intestine --> Ca++ absorption --> inc Ca++ transport; inc calbindin ; inc Ca++ pumps |
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Term
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Definition
inc Na+ resorption
inc Na/K ATPase
inc Na and K channels
inc K excretion |
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Term
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Definition
comes from kidney juxaglomerular apparatus and is secreted with dec BP
liver->angiotension-Renin->angiotension 1-ACE->angiotension2 |
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Term
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Definition
| synthesizes catecholamines from the amino acid tyrosine |
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Term
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Definition
catalyzes the conversion of norepinephrine to epinephrine
stimulated by cortisol |
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Term
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Definition
adjacent to zona fasciculata
high conc of cortisol results in amp of PNMT favoring epinephrine synthesis |
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Term
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Definition
Chromaffin cell tumors
they result in increased epinephrine and norepinephrine secretion. Symptoms of pheochromocytomas include chronic anxiety, the feeling of impending doom, tachycardia and palpitations (β1 adrenergic receptors), increased blood pressure due to vasoconstriction (α1 adrenergic receptors), sweating, paleness, and weightloss due to increased lipolysis (β3 adrenergic receptors) and glycogenolysis. Further, increased adrenergic input to the JGA results in the over-stimulation of the RAAS pathway. |
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Term
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Definition
2 main types alpha and beta
alpha more sensitive to NE,
beta linked to Gs pathway |
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Term
| alpha 1 receptors, sensitivity, selected action of agonist, mech |
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Definition
NE>Epi
smooth muscle contract, vaso constrict
Gq PLC activated->inc IP3+Ca |
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Term
| alpha 2 receptors, sensitivity, selected action of agonist, mech |
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Definition
Epi>_NE
smooth muscle constrict
neurotrans inhib
GI and pancreas target
Gi dec cAMP |
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Term
| beta 1 receptors, sensitivity, selected action of agonist, mech |
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Definition
epi=NE
inc heart rate and contractility
inc glomerular filtration
Gs inc cAMP |
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Term
| beta 2 receptors, sensitivity, selected action of agonist, mech |
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Definition
epi>>NE
smooth muscle relax
vasodil
bonchodil
inc glycogenolysis
Gs or Gi inc cAMP |
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Term
| beta 3 receptors, sensitivity, selected action of agonist, mech |
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Definition
NE>Epi
adipocytes inc lipolysis
Gs inc cAMP |
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Term
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Definition
| 2 main enzymes that will metabolize Epi and NE and dopamine into inactive products that are then excreted in the urine |
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