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BMS 430 Endocrinology Exam 2 > Hormones > Flashcards

Hormones Flashcards

Learn function, target tissues and pathologies

1
Q

Growth Hormone

A

Secreted from the pituitary
Somatotrophins
Production increases at night and during exercise

Function: stimulate cell growth and division

Target: almost every tissue except bone

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2
Q

Why is GH not effective on bone?

A

Bone does not have GH receptors.

GH acts on liver inducing elevated production of IGF - 1

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3
Q

IGF-1

A

Not produced by all cells - especially bone

Involved in protien synthesis and growth

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4
Q

IGF-2

A

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

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5
Q

Types of Neurotrophins

A

1) Nerve Growth Factor

2) Brain Derived Neurotrophic Factor

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6
Q

NGF

A

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

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7
Q

BDNF

A

• 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

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8
Q

Erythropoietin

A 
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
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9
Q

Hormones involved in wound healing

A

PDF - platelet derived growth factor
EGF - epidermal growth factor
FGF - fibroblast growth factor
Angiogenin

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10
Q

Thyroid Hormone (TH)

A

• 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

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11
Q

Effects of TH on other hormones

A

• 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
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12
Q

TH release

A 
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.
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13
Q

Pathophysiology of TH

Hypo secretion :

A

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

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14
Q

Pathophysiology of TH
__ _ _ _ deficiency

  • Lethargy
  • weak
  • tired

No negative feedback
> increase in TSH & TG
⇒ accumulation goiter

A

Iodine deficiency

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15
Q

Hyper thyroidism

A 
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
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16
Q

Thyroid Cancer

A 
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
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17
Q

Calcitonin

A

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

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18
Q

Calcium

A
  • 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
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19
Q

Osteoprogenitors

A

1) osteoblasts

2) osteoclasts

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20
Q

Osteoblasts

A

build Ca
- increase Ca deposition in the bone
- Can beconverted to osteoclasts
↳ osteoclasts cannot be converted back to osteoblast

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21
Q

Osteoclast

A

Cleave
- pull Ca out of bone & put it into blood
> increase blood Ca levels

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22
Q

Bone Remodeling

A

moving Ca from one part of bone to another - or into blood
- prevents bone from growing out (width)
↳ ensure bone grows length wise

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23
Q

Calcitonin Targets

A

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

24
Q

PTH

A 
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
25
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 ```
26
What Cells monitor blood Ca levels ?
1) Clear Cells in thyroid gland | 2) Cheif Cells in PTH
27
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 ```
28
Pathophysiology of PTH | Hyposecretion
Not enough PTH - autoimmunity to cheifcells ↳ no cheif cells = no PTH ⇒ bood Ca decreases - indirect = musculotetany & die
29
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 ```
30
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
31
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 ```
32
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) ```
33
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
34
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
35
Pathophysiology for Gastirin
Zollinger Ellis Syndrome • Pancreatic Tumor - increases acid production can cause diarrhea, heartburn,stomach & duodenal ulcers
36
Parietal Cells
* produce acid (HCI) * Stimulated by Gastrin * PKC system
37
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 ```
38
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
39
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
40
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
41
Substance P
• Secreted from the hypothalamus • increases hunger= want to eat • stimulated by Ghrelin as well as Orexin release . Tissues involved = empty stomach
42
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
43
Obestatin
* Produced when stomach is full * inhibits substance P * from hypothalamus * decrease eating * short term * decreases NPY
44
Ghrelin
``` • Stimulated by empty stomach ↳ source= stomach • Stimulates release of Substance P increases eating / hunger target= hypothalamus • increases NPY ```
45
Orexin
* stimulated by Stress & being awake * source= hypothalamus * Target= hypothalamus * increases NPY * increases eating /hunger
46
Adiponectin
* Produced by Adipose Tissue * Short Term * decreases Substance P to stop eating * decreases NPY * Target= hypothalamus
47
Leptin
* Produced when adipose tissues are full * Long term * decreases substance P to stop eating * decreases NPY
48
People w/ Anorrhexia
``` • increased ghrelin • decreased obestation • decreased leptin levels • decreased adiponectin = mental obssession w/ seeing themselves as fat ↳ overrides Physiological Signals to eat ```
49
Insulin
* decreases blood glc. levels * moves glucose into cells * produced by beta cells in the pancreas
50
Glucagon
* increases blood glc * . moves glucose out of cell * stimulated by decrease in blood glc levels * produced by alpha cells in the pancrease
51
Type 1 diabetes
``` •Juvenile • autoimmune distraction of beta cells ⇒ no insulin production Treatment = a) insulin injection b) exercise c) low glycemic index diet ```
52
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 ```
53
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
54
A1C
corresponds to average blood sugar levels | Desired A1 C= ~ 5
55
Epinephrine
``` •Release= Stress induced • Targets: - different targets have different receptor types - alpha & beta receptors - Binds more strongly to beta receptors ```
56
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 ```

BMS 430 Endocrinology Exam 2 (1 decks)

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