The Endocrine System Flashcards
(126 cards)
1
Q
Endocrine System
A
communication system where cells release messenger substances into blood stream that have actions on specific target tissues
2
Q
Messagers of the Endocrine System
A
Hormones
Neurohormones
Prostaglandins(Arachadonic Acid Cascade)
3
Q
Classes of Hormones
A
- Protein(peptide) hormones
- Amines (neurohormones + thyroxine)
- Steroid hormones
4
Q
Peptide + Amine Hormone Action
cAMP Mechanism
A
- Peptide/Amine hormone binds to membrane receptor
- activates G protein
- activates adenylate cyclase
- activates cAMP
- activates cAMP dependent Protein Kinases
5
Q
Peptide + Amine Hormone Action
IP3/DAG Mechanism
A
- membrane receptor recieves signalfrom Peptide/Amine hormone
- G protein activation
- Phospholipase C cleaves PIP2 into IP3 and DAG
- Calcium release
- cell membrane ion channel alteration
6
Q
Peptide + Amine Hormone Action
A
- cAMP Mechnanism
- IP3/DAG Mechanism
- Direct membrane Calcium Channel activation
7
Q
Steroid Hormone action
A
activates cycoplasmic and nucleus receptors, activates genes (transcription, translation), triggers protein synthesis
can activate membrane receptors
8
Q
Pituitary Gland
Anterior
A
synthesis of releasing factors and growth factors
derived from Rathke’s Pouch(mouth lining), contains blood portal system
9
Q
Pituitary Gland
Posterior
A
secretes hormones that are stored in the posterior pituitary(ADH, Oxytocin)
derived from brain tissue
10
Q
ADH
A
anti diuretic hormone,
small peptide (9AA)
11
Q
ADH Modes of Action
A
- water reabsorbtion by DCT, collecting duct of nephron, and action on sweat glands and GI tract
- binding to receptors on smooth muscle, stimulating calcium entry and contraction, vasocontriction
12
Q
Causes for ADH Release
A
- Changes is body osmolality (osmoreceptors shrinking-low bp)
- Drop in plasma volume (hemorrhage) detects 7-15% change
13
Q
Diabetes Insipidis
A
not sugar diabetes, large amount of dilute urine produced,
14
Q
Diabetes Insipidis
Neurogenic cause
A
no ADH release
15
Q
Diabetes Insipidis
Nephrogenic cause
A
failure of tubules to respond to ADH,
similar to results when consuming alcohol
16
Q
Oxytocin in Females
A
stimulates uterine contraction, released by milk ejection by mammary glands
does not induce labor naturally, but will trigger contractions if administered
17
Q
Oxytocin
Function in Males
A
uncertain, but oxytocin levels are high in people who have longtime partners
18
Q
Anterior Pituitary Cells
A
true endocrine cells, each cell produces their own hormones,
each cell can produce more that one hormone
19
Q
Anterior Pituitary Regulation
A
Anterior Pituitary hormone release is regulated by hypothalmus regulatory hormones
CRH, GnRH
20
Q
Anterior Pituitary Hormone
FSH, LH
A
stimulate gonads, Tropic Hormone
Follicle Stimulating hormone and Luteinizing hormone
Tropic Hormone - stimulates other glands
21
Q
Anterior Pituitary Hormone
TSH
A
stimulates thyroid, Tropic Hormone
Thyroid Stimulating hormone
Tropic Hormone - stimulates other glands
22
Q
Anterior Pituitary Hormone
ACTH
A
stimulates adrenal cortex, Tropic Hormone
Adrenocorticotropic Hormone
Tropic Hormone - stimulates other glands
23
Q
Growth Hormone
A
growth of body tissues, shifts body metabolism to anabolic paths, main target is liver,
triggers somatomedin(IGF-1, IGF-2) release from liver
24
Q
Prolactin
A
induces milk production in mature mammary glands
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# Growth Hormone
Insulin-like Actions
Muscle: increase AA uptake, protein synthesis (increases muscle mass)
Liver: increase protein synthesis
## Footnote
storage, increased protein synthesis
26
# Growth Homrone
Anti-insulin Actions
Muscle: decrease glucose uptake
Liver: increase gluconeogenisis
Adipose: increase lipolysis, decrease glucose uptake
## Footnote
increases plasma glucose
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Bone Somatomedins
increase protein and collagen synthesis, increase cell proliferation
## Footnote
linear increase (growth)
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Tissue Somatomedins
increase cell proliferation, increase DNA, RNA, and protein synthesis
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Acromegaly
too much growth hormone
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Growth Hormone System
Hypothalamus
1. increase GHRH
2. Decrease Somatostatin
Anterior Pituitary
3. GH release
Liver
4. GH stimulates somatomedins
5. inhibit Anterior Pituitary GH release
6. Stimulates somatostatin release by hypothalmus
7. further inhibits GH release
31
MSH
no function in humans, secreted by the Intermediate Lobe of Pituitary
| melanocyte stimulating hormone
## Footnote
oversecretion causes skin bronzing
32
Thyroid Gland
metabolic rate regulator, calcium homeostasis, bilobed gland, below larynx, linked at center by isthmus
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Thyroxine
growth, development, and metabolism regulator, causes increased oxygen consumption,
## Footnote
causes brown fat thermogenesis
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Glycogenolysis
glycogen breakdown
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Gluconeogenesis
glucose synthesis from fat
36
Lypolysis
mobilizes free fatty acids
## Footnote
mobilizes stored energy
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Follicular Cells
control the release of Thryoxine Hormone (TH)
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Colloid
Thyroglobulin, protein storage complex for Iodine, T3, T4 synthesis
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Parafollicular Cells
synthesizes Calcitonin, lowers plasma Ca++
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Parathyroid Gland
synthesizes Parathyroid Hormone, increases plasma Ca++, essential for life
## Footnote
4 pea sized glands on the Thyroid surface
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Hormonal Regulation Process
1. TRH from hypothalamus stimlates TSH from ant. pit.
2. active transport of Iodine into follicular cells
3. thyroglobulin synthesis
4. increased production of Thyroxine by colloid
5. increased pinocytosis of T3, T4
6. increased release of T3, T4 by follicular cell into blood
## Footnote
is a loop somehow
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# *
TH assembly
T4 = DIT + DIT
T3 = MIT + DIT
| tyrosine iodination
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DIT
diiodotyrosine
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MIT
monoiodotyrosine
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T4
4 iodines, high production, high plamsa concentration, prehormone
## Footnote
deiodinated to form T3
46
T3
3 iodines, low plasma concentration, biologically active,
## Footnote
product of deiodination of T4
47
RT3
biologically inactive, product of deiodination
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T3 and T4 in Plasma
they are bound to carrier proteins, inactive when bound
## Footnote
Thyroxine Bindng Globulin and Albumin, unbound is active, but there is less unbound so there is always a large reserve for a contant supply if needed
49
Hypothyroidism
underactive thyroid state
## Footnote
In children: Cretinism
In adults: Myxedema
50
# Hypothyroidism
Causes
1. Iodine Deficiency
2. Hypothalamus problem (decrease TRH)
3. Ant. Pit. problem (decrease in TSH or no response to TRH)
4. Hashimoto's Disease
51
Hashimoto's Disease
autoimmune disease, antibodies attack thyroid gland and diminish its output
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# Hypothyroidism
Symptoms
1. decreased metabolsm (weight and water gain)
2. decreased HR, SV, CO
3. cold, clammy, lethargic, decreased mental capability
4. depressed nail, bone, and hear growth
5. raspy voice (mucopolysaccharide accumilation in larynx)
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# Hyperthyroidism
Symptoms
1. increased metabolism (weight loss, water loss)
2. increased HR, SV, CO
3. increased temp
4. exopthalmos
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# Hyperthyroidism
Graves Disease
autoimmune disease whos antibodies resemble TSH and stimulate the thyroid
## Footnote
basically no TRH, but high T3 and T4 levels
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# Hyperthyroidism
Exopthalmos
swelling of eye muscles and fat, protruding eyes, autoimmune attack
## Footnote
common in Graves disease
56
# Hyperthyroidism
Treatment
drugs that block iodine uptake by follicular cells, drugs that block iodination, destruction of the thyroid gland
57
Destruction of the Thyroid Gland
done using surgery or radiation, treatment for hyperthyroidism
## Footnote
TH replacement is required after Thyroid removal
58
Goiters
enlarged thyroid glands, caused by hyperthyroidism(overstimulation), and hypothyroidism
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Hypothyroid Goiters
due to iodine deficiency, little T3, T4 for inhibition, high TSH stimulates glands
60
Where is Calcium located?
99% of body calcium is found in bones(calcium hydroxyapatite), 1% is in plasma
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Plasma Calcium
narrow range of 10mg/dl, 45% is bound to albumin, 10% in phosphate/citrate complexes, 45% free and subject to hormonal control
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Osteoblasts
Calcium deposition on bone(calcitonin)
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Osteoclasts
bone reabsorbtion (Ca++ uptake)(PTH)
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Major Regulators of Body Ca++
1. Parathyroid Homrone (PTH)
2. Calcitonin (calcium regulating)
3. Vitamin D3 (allows calcium to be absorbed in diet)
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Parathyroid Hormone (PTH)
release caused by low plasma Ca++, increases bone reabsorbtion, increased plasma Ca++, increases Ca++ reabsorbtion in PCT, stimulates Vit D3 production
66
Body Without PTH
1. low plasma Ca++ increases Na+ permeability
2. causes hyperexcitable nerves
3. leads to hypocalcemic tetany, Trousseau's sign
67
Trousseau's Sign
praying mantis arms, thumbs under pointer and middle fingers
68
# PTH
Estrogen Effects
1. Estrogen decreases PTH release
2. Menopause decreases estrogen and therefore increases PTH
3. Bone reabsorbtion increases
4. Osteoporosis can result
## Footnote
treatable with estrogen replacement therapy
69
Calcitonin
from Parafollicular "C" cells of thyroid, decreases plasma Ca++, decreases bone reabsorbtion, decreases kidney reabsorbion of Ca++
70
Vitamin D
allows Ca++ uptake by intestines, stimulate Ca++ reabsorbtion in kidneys, shuts down PTH release
| 1,25 dihydroxycholecalciferol
71
Vitamin D3 Synthesis
1. Synthesized with sunlight from dehydrocholesterol
2. in the liver, Vit D converted to 25 hydroxycholecalciferol
3. in the kidney, converted to 1,25 dihydroxycholecalciferol
72
Body without Vitamin D3
poor intestinal Ca++ reabsorbtion, rickets or osteomalacia
73
Osteomalacia
softening of bones due to lack of vitmain D
74
Islets of Langerhans
endocrine Pancreas cells, A, B, D, F cells
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# Islets of Langerhans
Alpha cells
glucagon, increases plasma glucose, catabolic
## Footnote
body tissue breakdown
76
# Islets of Langerhans
Beta cells
insulin, decrease in plasma glucose, anabolic
## Footnote
body tissue buildup
77
# Islets of Langerhans
Delta cells
somatostatin, inhibits A, B, and F cells
78
F cell
amylin, slows gastric emptying, slows nutrient absorbtion, slows post-prandial glucose spike
## Footnote
promotes satiety in concert with insulin
79
# Liver
Endocrine Functions
stores glucose, generates glucose through action of glucose 6 phosphate
80
Insulin structure
produced by B cells, short arm of chromosome 11, 5 minute half life, broken down by insulin protease in liver or kidney
## Footnote
proinsulin C chain is used to assay B cell funciton when exogenous insulin is administered
81
Insulin Function
1. increased transport of glucose, AA, and K+ into insulin sensitive tissues,
2. synthesis of glycogen synthase
3. stimulation of protein synthesis
4. increases lipogenic enzymes
5. inhibits protein breakdown
6. inhibits gluconeogenic enzymes
82
Insulin Sensitive Tissues
muscle, fat, liver
83
Insulin Modes of Action
1. Tyrosine Kinase Receptor signal pathway
2. Adds GLUT transporters to cell membrane
84
GLUT receptors
7 different types, allow for glucose to enter a cell
85
GLUT 4
most important for insulin action, found in muscle, heart and adipose tissue
86
GLUT 1, 3
found in brain, not insulin dependent
87
GLUT 2
found in liver, not insulin dependent
88
Diabetes Mellitus
sweet urine, lack of or inneffective use of insulin,
| "sugar diabetes"
89
Diabetes Mellitus Symptoms
Polyurea
Polydipsea
Polyphagia
90
Experimental Causes of Diabetes Mellitus
1. Pancreatectomy (removal of part of or entire pancreas)
2. Streptozocin (B cell toxin, kills B cells)
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Normal Blood Glucose
resting at 80 mg/dl
peak between 150-180 mg/dl
92
Diabetic Blood Glucose
resting above 120 mg/dl
peak above 200 mg/dl
93
Type 1 Diabetes
body does not produce insulin, observed in young ages, no strong genetic link, 10% of diabetics, caused by antibodies destroying B cells, triggered by viral infections
## Footnote
treated with insulin
94
Untreated Type 1 Diabetes
high BG, body burns fats and proteins, ketoacidosis,
## Footnote
acid + dehydration leads to coma and death
95
Hyperglycemic Coma
acid + dehydration leading to coma, caused by high BG
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Insulin Shock
patient administed insulin without eating, results in Hypoglycemic Coma, glucose cures
97
Type 2 Diabetes
usually ages 35+, obesity component, genetic component, peripheral tissues (muscle, liver, fat) becomes insulin resistant, reduced insulin output by B cells
98
Type 2 Diabetes Treatment
low cal + low fat diet, exercise, Sulfonylurea drugs
99
Sulfonylurea Drugs
1. depolarize B cells,
2. elevate intracellular Ca++,
3. enhance insulin release by B cells
100
HbA1C or A1C test
tests for glycated hemoglobin, long term average for blood sugar levels
## Footnote
Normal Person - 5%
Diabetic Target - 7%
Diabetic Uncontrolled - 25%
101
Metformins
enhances insulin sensitivity in peripheral tissues(muscles, liver, fat), suppresses gluconeogenesis by liver
102
GLP-1
| Glucagon Like Peptide
enhances insulin output by Beta cells when used with sulfonylurea drugs, suppresses glucagon release and slows gastric emptying
103
GLP -1 + GIP
enhance insulin secretion, reduce glucagon levels, delay gastic emptying, decrease food intake, discourages alchohol use
| gives a greater feeling of satiety
## Footnote
marketed as a weight loss drug
104
SLGT2 Inhibitors
blocks glucose reabsorbion in the PCT, excretes more glucose in urine
## Footnote
lowers HbA1C, can lead to UTIs, Type 2 Diabetics Only
105
Insulin Pumps
deliver various forms of insulin with a computer programmable pump
## Footnote
pump can change insulin levels with regards to diet, exercise, and time of day
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Artificial Pancreas
pump delivery of insulin and glucagon, manages blood glucose in real time
107
Stem Cell Treatments for Diabetes
pancreatic stem cells injected or transplanted to make a new pancreas
## Footnote
not approved in the US
108
BMI Formula's
mass in Kg/height in m squared
703 x weight in lbs/height in inches squared
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Potentially Underweight BMI
18-19
110
Healthy BMI
20-24
111
Overweight BMI
25-29
| 55% of Americans
## Footnote
increased risk of diabetes, stroke, heart disease, and cancer when over 27
112
Clinically Obese BMI
30+
## Footnote
even greater risk for medical conditions
113
Orexins
compounds released by Hypothalmus in response to low BG, increases appetite
114
Adrenal Gland
made of the cortex and medulla
115
Adrenal Gland Cortex
produces mineralocorticoids, glucocortoroids,
and sex steroid hormones
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Adrenal Gland Medulla
extension of sympathetic nervous system
## Footnote
epinephrine and norepinephrine production/release
117
Regulation and Secretory Control of Adrenal Cortex
1. CRH release from hypothalmus
2. stimulates ACTH release from pituitary
3. stimulates secretion of hormones from adrenal cortex (cortisols and androgens)
4. adrenal hormones provide negative feedback to hypothalmus and anterior pituitary to shut down ACTH production
118
3 Zones of the Adrenal Cortex
1. Zona Glomerulosa
2. Zona Fasiculata
3. Zona Reticularis
119
# Adrenal Cortex
Zona Glomerulosa
produces aldosterone, a mineralocorticoid
## Footnote
causes body to retain water
120
# Adrenal Cortex
Zona Fasiculata
produces glucocorticoids and cortisol compounds
121
cortisol effects
1. immune system inhibition
2. decrease in muscle, bone, and connective tissue mass
3. glycogenolysis, gluconeogenesis, FFA release
4. increase BP
5. increase GFR
## Footnote
useful as anti-inflammatory and anti-rejection drugs
122
Zona Reticularis
produces androgens and sex hormone precursors
123
Cushing's Syndrome
Excessive Cortisol Production leading to:
1. muscle atrophy
2. osteoporosis
3. thin skin w/visible blood vessels
4. accumulation of fat in the abdomen
5. capillary rupture and striae
124
Addisons Disease
Lack of Adrenocortical Function leading to:
1. anorexia, fatigue, hypoglycemia
2. poor stress tolerance
3. lack of negative feedback from adrenal hormones on pituitary
4. 3 causes hypersecretion of ACTH
5. 4 stimulates melanocytes causes localized dark pigmentation on the body
125
Conn's Syndrome
| Primary Hyperaldosteronism
adrenal tumor or hypersecretion of aldosterone from Zona Glomerulosa results in elevated BP and K+ depletion and muscle weakness
126
Androgenital Syndrome
excessive output of androgens causes masulization of the female body, can cause ambiguous genital development in infants
