Hormones Flashcards
Learn function, target tissues and pathologies
Growth Hormone
Secreted from the pituitary
Somatotrophins
Production increases at night and during exercise
Function: stimulate cell growth and division
Target: almost every tissue except bone
Why is GH not effective on bone?
Bone does not have GH receptors.
GH acts on liver inducing elevated production of IGF - 1
IGF-1
Not produced by all cells - especially bone
Involved in protien synthesis and growth
IGF-2
Same family as IGF- 1
Unlike IGF-1: is produced in the fetus
Produced by the liver.
- can also be produced in ther CNS after birth - adult
Once born liver switches from producing IGF-2 to IGF 1
Types of Neurotrophins
1) Nerve Growth Factor
2) Brain Derived Neurotrophic Factor
NGF
Nerve Growth Factor
•utilizes tyrosine kinase system
•helps with nerve growth
• produced by muscle
Target = nerve cells
- anti apoptotic
- in cases of damage increased production allows for repair/ re-innervation of tissues
- NGF can also come from other Nerve cells and impact DNA
- required for initial growth and development of fetus
BDNF
• Produced in the brain the brain
• development of CNS in fetus
• similar fnxn as NGF
• Anti apoptotic
• involved in making new dendritic & axon connections
•production stimulated by aerobic activity
- i.e. exercise
Erythropoietin
Epo Tyrosine kinase system Synthesized in kidney Release is simulated by: 1) drop in red blood cell count 2) decrease in oxygen carrying capacity Function: - increase red blood cell synthesis - helps erythroblast maturation into erythrocytes Target: - bone marrow
Hormones involved in wound healing
PDF - platelet derived growth factor
EGF - epidermal growth factor
FGF - fibroblast growth factor
Angiogenin
Thyroid Hormone (TH)
• precurser:
- Thyronglobulin
TH = utilized by almost every cell in the body
- has 2 b modefied to T3 to be active
TRH from hypothalamus → Anterior Pituitary → TSH → Thyroid gland
↳ T4 & T3 released
• TH =modefied AA
• same Mechanism as steriod hormone
• TH does not create metabolism. It only increases or decreases metabolic function
• negative feedback loop
• TH also goes to mitochondria = increases ATP Synthesis
Effects of TH on other hormones
• GH
- allows for GH production
• N G F
- direct effect on NGFsynthesis
- effecton growth & synthesis of CNS during Week 1
- initial growth= dependent on maternal TH
- TH Synthesis = Iodine dependent
- prolactin
TH release
1) Circadian rhythm ↳ release of TH decreases at night & increases during the day 2) Ambient Temp. a)warm/hot= decreases TH release b) cold= increases TH release 3) Exercise : = increases ATP ⇒ increases TH release 4) Diet • big meal = increases TH release ↳ allows for utilization of nutrients - diet/fasting = decrease in BMR ↳ conserve energy ↳ think starving fish exp.
Pathophysiology of TH
Hypo secretion :
1) Hashimotos:
- developement of antibodies to thyroid cells
= Thyroid cell distruction
= most common in women age 20-40
Symptoms:
- lethargy
- constantly cold
- fluid pouches under eyes
• Treatment :
- Levothyroxin (T4)
↳ start dose low, increase slowly until feeling normal
Pathophysiology of TH
__ _ _ _ deficiency
- Lethargy
- weak
- tired
No negative feedback
> increase in TSH & TG
⇒ accumulation goiter
Iodine deficiency
Hyper thyroidism
Graves Disease = long Acting Thyroid Stimulation (LAT) ↳ Prevalent in women ↳ AB binds 2 TSH receptors = increase in TH secretion - increase in BMR ↳ Hot all the time/sweaty - usually very thin -exopthalmus = fat deposit Behind the eyes= eye bulging Treatment= Radio Active Iodine (RAI) ↳ accumulates in thyroid gland ↳ degredation of RAI = death of colloid follicles too much= thyroid gland distruction ⇒ use levethyroxin to rebuild/replace Thyroid Gland
Thyroid Cancer
Primarily in women ↳early to mid 30's - tumors accumulate Ca Treatment: thyroid gland removal -P laced on Levethyroxin 2 compensate 4 Lack of Thyroid Gland
Calcitonin
decreases blood Ca by putting it into bone
- Stimulates osteoblasts
- Can also stim (progenitors) clast → blast
- Source= thyroid - Clear cells
↳release= Stim when blood Ca increases
Calcium
- One of the MOST important minerals in the body
1) maintain membrain potential
↳ important in Nerve impulse ability
2) Blood Clotting cofactor
↳ cofactor for many enzymes
3) essential for membrane Structure & fusion
Osteoprogenitors
1) osteoblasts
2) osteoclasts
Osteoblasts
build Ca
- increase Ca deposition in the bone
- Can beconverted to osteoclasts
↳ osteoclasts cannot be converted back to osteoblast
Osteoclast
Cleave
- pull Ca out of bone & put it into blood
> increase blood Ca levels
Bone Remodeling
moving Ca from one part of bone to another - or into blood
- prevents bone from growing out (width)
↳ ensure bone grows length wise
Calcitonin Targets
1) Parathyroid
↳ decreases PTH
2) Thyroid - negative feedback
3) Bone: Osteoblasts = deposition of Ca into bone
4) Kidney → dumps Ca
5) inhibits clast ⇒ activate blast = decreases blood Ca
↳ needs Testosterone or Estrodiol 2 effectively work w/ osteoblasts
PTH
Parathyroid hormone - Released when blood Ca increases - PKC system - Source: Parathyroid gland (on back of thyroid gland) - Targets : 1) decreases calcitonin in thyroid 2) decreases Bone formation ↳stimulates osteoclasts ↳ stimulates blast→clast 3) reabsorption of Ca in kidney - no significant effect in GI
Vitamin D
1) Cholesterol prod by liver ↳ bld 2 Skin ↳ UV+ chol. ⇒ 7 Dehydroxychol ↳ Skin 2 bld + body temp ⇒ vit D ⇒ Liver ⇒ 25 hydroxy Vit. D (Vit D precursor) - 25 hydroxy Vit D+ PTH = active Vit. D • Main fnxn= increase Ca absorption in Gut • source= kidney • P TH triggers rIs . Target= GI
What Cells monitor blood Ca levels ?
1) Clear Cells in thyroid gland
2) Cheif Cells in PTH
Pathophysiology of PTH
Hyperproduction
• Caused by tumor = increased Ca - bones become brittle ⇒ easily break - decrease in nerve signaling function - develop Kidney stones Treatment: - removal of tumor
Pathophysiology of PTH
Hyposecretion
Not enough PTH
- autoimmunity to cheifcells
↳ no cheif cells = no PTH ⇒ bood Ca decreases
- indirect = musculotetany & die
Osteomalaysia
Decrease in bone Ca 1) Young - decrease in Vit. D = rickets ↳ bones not properly mineralized ↳ no Ca absorbed from food ↳ bones bend & deform mostly gone in U. S however more recent have popped up in US
Why have rickets made areoccurence in US ?
kids spend less time outside ⇒ less sunlight (UV rays)
Milk has vit D in it however, kids drink less milk ⇒ less Vit D intake
Osteomalaysia
- Old
Osteoporosis = more prominent in women - loss of bone density ↳ taking Ca out w/o putting it back in - Lack of T or E - bones start to break more easily - load bearing bones break 1st ↳ i.e. Hip bone - men loose hormone more slowly
Treatments for Osteomalaysia
1- Start taking Ca Supplements early 2- Hormone Replacement Therapy 3- inhibit osteoclasts ↳ Fosemax, Boneva, Actinel = prevent removal of Ca from bone 4 - Evista ↳ Binds 2 Estrogen receptors = acts like estrogen 5- Miracalcin → IV = Calcitonin ↳ not effective w/o Sex hormones (T& E)
Gastrin
released from:
- G calls in the stomach
Target:
- Parietal cells = increase HCI production
- Stomach epithelium = increase mucous production
- GI smooth muscle = increase contractions
- Gl blood vessels = increase blood flow
CCK
Cholecystokinin
released from the I cells of the intestinal epithelium
stimulated by fats
Targets =
• Pancreatic Acini= increase exocrine enzyme production
• GI smooth muscle = increase contraction
• GI bhood vessels = increased blood flow
Pathophysiology for Gastirin
Zollinger Ellis Syndrome
• Pancreatic Tumor
- increases acid production
can cause diarrhea, heartburn,stomach & duodenal ulcers
Parietal Cells
- produce acid (HCI)
- Stimulated by Gastrin
- PKC system
Cheif Cells
• Produce Pepsinogen = pepsin precursor HCI converts pepsinogen to pepsin ↳ Breaks proteins down 2 amino acids • Targets: - cells in the epithelium ↳ increase mucous production _ Stimulates GI motility → moving Chyme to SI
Secretin
•Released from S cells of intestinal epithelium by acid
•Targets
a) pancreatic duct epithelium = increases bicarbonate production
b) G cells & parietal cells = decrease gastrin & HCI
c) GI smooth muscles = decrease contractions
VIP
Released by VIP cells in Stomach epithelium
↳ Caused by stomach distention
Targets
a) GI Blood Vessels = increase blood flow
b) GI smooth muscle = decrease Contractions
C) G cells = decrease gastrin production
GIP
Released from intestinal epithelium
Stimulated by Carbs
Targets:
a) Pancreatic beta cells = increase insulin production
b) G cells= decrease gastrin
c) GI smooth muscle = decrease contractions
Substance P
• Secreted from the hypothalamus
• increases hunger= want to eat
• stimulated by Ghrelin as well as Orexin release
. Tissues involved = empty stomach
Prater Willie Syndrome
• Defect on paternal chromosome 15
= always hungry ⇒ morbidly obese
• Ghrelin is 3-3.5 x higher than normal
• SNORED 116 = in hibits negative fb on ghrelin
Obestatin
- Produced when stomach is full
- inhibits substance P
- from hypothalamus
- decrease eating
- short term
- decreases NPY
Ghrelin
• Stimulated by empty stomach ↳ source= stomach • Stimulates release of Substance P increases eating / hunger target= hypothalamus • increases NPY
Orexin
- stimulated by Stress & being awake
- source= hypothalamus
- Target= hypothalamus
- increases NPY
- increases eating /hunger
Adiponectin
- Produced by Adipose Tissue
- Short Term
- decreases Substance P to stop eating
- decreases NPY
- Target= hypothalamus
Leptin
- Produced when adipose tissues are full
- Long term
- decreases substance P to stop eating
- decreases NPY
People w/ Anorrhexia
• increased ghrelin • decreased obestation • decreased leptin levels • decreased adiponectin = mental obssession w/ seeing themselves as fat ↳ overrides Physiological Signals to eat
Insulin
- decreases blood glc. levels
- moves glucose into cells
- produced by beta cells in the pancreas
Glucagon
- increases blood glc
- . moves glucose out of cell
- stimulated by decrease in blood glc levels
- produced by alpha cells in the pancrease
Type 1 diabetes
•Juvenile • autoimmune distraction of beta cells ⇒ no insulin production Treatment = a) insulin injection b) exercise c) low glycemic index diet
Type 2 Diabetes
- Typically known as adult onset diabetes bc would appear in 30'5-40's ↳ now starting to appear in younger pp l as well - non insulin dependent • Symptomes a) vision issues ↳ diabetic retinopathy ↳ Cateracs = glc. moving into aqueous humor b) tingling in feet c) elevated glc. levels • Treatments 1) Exercise 2) Low glycemic index diet ↳ prevents spikes in blood glc 3) Medications ↳ Ex: Metformin
Types of Glucose transporters
GLUT 1 = Brain Vasculature & RBC’s
GLUT2 = Liver, pancreatic b cells, & the serosal surface of the gut & kidney
GLUT 4 = Muscle & fat cells → requires insulin 2 b effective
GLUT 3 & 5 = work in the absence of insulin
A1C
corresponds to average blood sugar levels
Desired A1 C= ~ 5
Epinephrine
•Release= Stress induced • Targets: - different targets have different receptor types - alpha & beta receptors - Binds more strongly to beta receptors
Cortisol
•Source: Adrenal Cortex • released in a circadian rhythm • permissive effects • Anti inflammatory ↳ inhibits phospholipase A2 = no prostaglandin ⇒ no inflammatory response ↳ decreases swelling ↳ stabilizes Lysosomes involved in histamine release • Cortisol decreases TH levels - stimulates synthesis of surfactant ↳ prevents lungs from sticking together ↳ in fetus produced just before parturition