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
Q

Vitamin D

A
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
Q

What Cells monitor blood Ca levels ?

A

1) Clear Cells in thyroid gland

2) Cheif Cells in PTH

27
Q

Pathophysiology of PTH

Hyperproduction

A
• Caused by tumor
= increased Ca
- bones become brittle ⇒ easily break
- decrease in nerve signaling function
- develop Kidney stones
Treatment:
- removal of tumor
28
Q

Pathophysiology of PTH

Hyposecretion

A

Not enough PTH
- autoimmunity to cheifcells
↳ no cheif cells = no PTH ⇒ bood Ca decreases
- indirect = musculotetany & die

29
Q

Osteomalaysia

A
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
Q

Why have rickets made areoccurence in US ?

A

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
Q

Osteomalaysia

- Old

A
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
Q

Treatments for Osteomalaysia

A
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
Q

Gastrin

A

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
Q

CCK

A

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
Q

Pathophysiology for Gastirin

A

Zollinger Ellis Syndrome
• Pancreatic Tumor
- increases acid production
can cause diarrhea, heartburn,stomach & duodenal ulcers

36
Q

Parietal Cells

A
  • produce acid (HCI)
  • Stimulated by Gastrin
  • PKC system
37
Q

Cheif Cells

A
• 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
Q

Secretin

A

•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
Q

VIP

A

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
Q

GIP

A

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
Q

Substance P

A

• Secreted from the hypothalamus
• increases hunger= want to eat
• stimulated by Ghrelin as well as Orexin release
. Tissues involved = empty stomach

42
Q

Prater Willie Syndrome

A

• 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
Q

Obestatin

A
  • Produced when stomach is full
  • inhibits substance P
  • from hypothalamus
  • decrease eating
  • short term
  • decreases NPY
44
Q

Ghrelin

A
• Stimulated by empty stomach
↳ source= stomach
• Stimulates release  of Substance P
increases eating / hunger
target= hypothalamus
• increases NPY
45
Q

Orexin

A
  • stimulated by Stress & being awake
  • source= hypothalamus
  • Target= hypothalamus
  • increases NPY
  • increases eating /hunger
46
Q

Adiponectin

A
  • Produced by Adipose Tissue
  • Short Term
  • decreases Substance P to stop eating
  • decreases NPY
  • Target= hypothalamus
47
Q

Leptin

A
  • Produced when adipose tissues are full
  • Long term
  • decreases substance P to stop eating
  • decreases NPY
48
Q

People w/ Anorrhexia

A
• increased ghrelin
• decreased obestation
• decreased leptin levels
• decreased adiponectin
= mental obssession w/ seeing themselves as fat
↳ overrides Physiological Signals to eat
49
Q

Insulin

A
  • decreases blood glc. levels
  • moves glucose into cells
  • produced by beta cells in the pancreas
50
Q

Glucagon

A
  • increases blood glc
  • . moves glucose out of cell
  • stimulated by decrease in blood glc levels
  • produced by alpha cells in the pancrease
51
Q

Type 1 diabetes

A
•Juvenile
• autoimmune distraction of beta cells
⇒ no insulin production
Treatment = 
a) insulin injection
b) exercise
c) low glycemic index diet
52
Q

Type 2 Diabetes

A
- 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
Q

Types of Glucose transporters

A

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
Q

A1C

A

corresponds to average blood sugar levels

Desired A1 C= ~ 5

55
Q

Epinephrine

A
•Release= Stress induced
• Targets:
- different targets have different receptor types
- alpha & beta receptors
- Binds more strongly to beta receptors
56
Q

Cortisol

A
•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