Exam 1 Flashcards
Most abundant hormones
proteins
Least abundant hormones
Amines
3 types of hormones
Proteins
Amines
Steroids
Endorcrine organs (ones she said to worry about) (7)
Hypothalamus Pituitary Thyroid Parathyroid Pancreas Adrenal Testis/Ovary
If a hormone has “releasing” or “inhibiting” in the name, it is from the:
Hypothalamus
Rule of thumb:
Hormones ending in -Ole, -One, -Ene are a:
Hormones ending in -ine are a:
The rest are:
Steroid
Amine
Protein/peptide
Proteins are ____ soluble. This means:
Water solube
they can bind to cell surface (membrane) receptors
Proteins are ____ into the plasma through the ____. This is because:
Dissolved
Receptors
Because they can’t pass the lipid bilayer
Protein synthesis occurs in the:
This forms a:
Occurs in the ER
Forms a Preprohormone
In protein modification, what is removed? What is formed here?
Signal sequence is removed
forms Prohormone
After protein modification, the prohormone is transported to the:
golgi network
What happens to the protein during the formation of secretory vesicles in the golgi?
Prohormone is cleaved into the active hormone
How is the protein secreted from the cell into the blood?
It is exocytosed. The cell is signaled to release the hormone and and of its fragments.
Steroid hormones are derived from:
Cholesterol
Steroid hormones are _____-soluble. This means:
Lipid soluble
This means they cannot typically be stored, so are made on demand
How are steroids released into the blood stream?
They can diffuse through the cell membrane
Steroids bind to:
Intracellular receptors
What part of steroids can be stored or obtained from the blood?
Steroid precursors, such as cholesterol esters
What is the 1st rate limiting reaction in the production of VARIOUS steroid hormones?
Conversion of cholesterol to pregnenolone
What is required to convert cholesterol to pregnenolone?
P450scc/Desmolase
Amines are derived from:
Tyrosine
2 groups of amines:
Thyroid hormones
Catecholamines
Thyroid hormones include:
T3 and T4
T3:
Triiodothyromine
T4:
Thyroxine
How are thyroid hormones stored?
As large polhmers called Thyroglobulin
How are thyroid hormones secreted
Thyroglobulin is split off then secreted into the blood
Catecholamine hormones include:
Epinephrine
Norepinephrine
Dopamine
Dopamine is a:
Neurotransmitter
How are catacholamines stored and secreted?
They are transported into the vesicles for storage
Secreted via exocytosis (similar to proteins)
enzymes that are used to synthesize amines are located where?
The tyroid, adrenal medulla, and the brain
where are catacholamines made?
in the cytoplasm
Concentration of hormones needed to be in the blood stream:
1 picogram/mL to a few micrograms/mL of fluid
2 factors that can increase/decrease the concentration of a hormone in the blood:
1- Rate of hormone secretion (how much is made?)
2- Rate of Removal/Clearace (how fast can it be metabolized?)
Types of endocrine stimuli (3)
Humoral
Neural
Hormonal
Stimulus that is something resolved in the body, but is NOT a hormone (Ex.- calcium, sodium)
Humoral Stimulus
What stimulates the adrenal medulla?
Neural stimulus
Process of a hormonal stiulus
The hypothalamus secretes hormones to stimulate the pituitary gland.
The pituitary gland secretes hormones to stimulate other endocrine organs to secrete hormones.
Negative feedback prevents
over activity of glands
negative feedback is usually due to:
rising hormone levels itself, or one of its products.
When does positive feedback occur?
Only in special circumstances, such as pregnancy
Mechanisms of Clearance (4)
Metabolic destruction
Binding with tissues
Excretion by liver into the bile
Excretion by kidneys into the urine
Plasma-protein bound hormones are cleared from the blood at a much _____ (FASTER/SLOWER) rate
slower
Cells cannot respond to a hormone unless it has:
a hormone receptor
Are receptors large or small proteins?
large
how many receptors does a cell have?
thousands
Are receptors always highly specific to what it will bind to?
No- but usually are.
Possible receptor locations:
Cell membrane
In the cytoplasm
In the nucleus
What will bind to receptors in the cytoplasm?
steroids
What will bind to receptors on the cell membrane?
Proteins/peptides and catecholamines
What will bind to receptors in the nucleus?
Thyroid hoirmones
3 types of cell membrane receptors
Ion Channel-Linked Receptors
Enzyme-Linked receptors
G-Protein-Linked receptors
What type of cell membrane receptor uses neurotransmitters to bind to a receptor/channel, causing it to open?
Ion Channel Linked Receptor
What type of cell membrane receptor includes binding of a single molecule directly activating an enzyme?
Enzyme-Linked receptor
Best studied enzyme-linked receptor?
Tyrosine Kinase Receptor
A complex of 3 subunits- alpha, beta and gamma
G-Protein
How is GProtein activated?
when a signal molecule binds to a receptor
In G Protein linked receptors, where does the alpha subunit activate multiple targets?
When GDP is exchanged for GTP
How are G Protein Linked receptors deactivated?
The G Protein hydrolyses the GTP and reassmbles its subunits
Things we need energy for: (5)
Maintain blood glucose- especially in the brain
Provide energy for other cells in the body
Thermoregulation
Food digestion
Physical Activity
Fed state lasts how long?
2-4 hours after eating
Type of metabolism favored in the Fed state?
Anabolic
What is stored in the Fed state?
Carbohydrates and for for later use
In the Fed state, energy is stored as:
fat and glucogen, as well as ATP, Phosphocreatine, and protein
The Fasting state beings:
If ends:
Starts after food is digested and absorbed.
Continues until more food is ingested
Type of metabolism favored in the Fasting state:
Catabolic
what happens if protein is increasingly used for energy?
cellular function becomes compromised
Process of generating ATP from Carbohydrates
Carbohydrates -> digested simple sugars ->conversion into glucose ->phosphorylated glucose ->Acetyl CoA-> Citric Acid Cycle -> NADH and FADH2 ->Electron transport chain -> ATP
Process of generating ATP from Fats
Fats -> digested fatty acids -> beta oxidation -> Acetyl CoA-> Citric Acid Cycle -> NADH and FADH2 ->Electron transport chain -> ATP
Process of generating ATP from proteins
Proteins -> Digested into amino acids -> converted to either pyruvate, acetyl CoA, or intermediate KREB cycle -> Citric Acid Cycle -> NADH and FADH2 ->Electron transport chain -> ATP
3 major stages of glycolysis
Early Glycolysis
Intermediate glycolysis
Late glycolysis
Step of glycolysis where there is an energy investment of 2 ATP. Goes from Glucose to Fructose 1,6 bisphosphate
Early glycolysis
Step of glycolysis where there is a cleavage of 6 carbon sugar into two 3 carbon sugars.
goes from fructose 1,6 bisphosphate to glyceraldehyde 3-phosphate
Intermediate glycolysis
Step of glycolysis where there is energy generation of 4 ATP
Goes from glyceraldehyde 3-phosphate to pyruvate
Late glycolysis
Where is pyruvate converted into Acetyl-CoA>
In the mitochondria
What is lost when Pyruvate is converted into acetyl CoA?
CO2
Where does the Citric Acid Cycle take place?
in the mitochondria
In KREB cycle, how many carbon are lost? And in what form?
2 carbons are lost in the form of CO2
Products of KREB cycle (3)
3 NADH
1 FADH2
1 GTP
Oxygen’s role in the body:
It combines with e- and H+ to form water.
it is the “final e- acceptor”
Approx amount of ATP generated for 1 NADH
For 1 FADH2?
- 5 ATP for NADH
1. 5 ATP for 1 FADH2
total oxidation of 1 glucose produces approx how many ATP?
30
Lipolysis:
Free fatty acids
during catabolism of fatty acids, the fatty acids are converted into what?
what metabolism is used?
converted into several Acetyl CoA molecules
Done by Beta Oxidation (catabolism)
An important enzyme involved in the hormonally regulated release of fatty acids and glycerol from adipocyte lipid stores
Hormone sensitive lipase
Beta oxidation can lead to:
ketogenesis
When a group of substances collectively known as ketone bodies are formed by the breakdown of fatty acids and ketogenic amino acids
ketogenesis
When will acetyl coa metabolize into ketone bodies?
when there is a low availability of carbohydrates and a high rate of beta oxidation
where does kitogenesis occur?
In the liver
When there are very high levels of ketones. The pH of the blood shifts to be more acidic.
Ketoacidosis
What happens once proteins are broken down into amino acids?
they are deanimated to remove NH4+.
NH4+ enters the _______ ______ to be eliminated by the:
urea cylce
kidneys
what is converted into an intermediate of metabolism to form ATP?
Carbon skeleton
NH3+ + C Skeleton =
Amino acid
glucose is stored in the body as:
Glucogen
Glucogen is mostly stored where?
in the liver and skeletal muscle
Glucogen synthase:
Glycogenesis
Glucogen phosphoylase:
Glycogenlysis
gluconeogenesis is what type of metabolism?
anabolic
the body gets rid of what during fasting?
glucose and glycogen
raw materials needed for gluconeogenesis:
glycerol
lactate
several amino acids
Fatty acid synthesis
Lipogenesis
what starts lipogenesis?
Acetyl CoA is built up by added 2 carbon units
where does lipogenesis occur
in the cytoplasm
major enzyme used for lipogenesis:
Fatty Acid Synthase
Major sites for lipogenesis:
Adipose tissue and the liver
DNL:
De Novo Lipogenesis
the liver receives blood from:
GI tract and pancreas
The liver takes in:
Carbs
Lipids
Amino acids
What does carb metabolism in the liver increase?
Phosphorylation of glucose
Glycogen synthesis
Glycolysis
first 2 influenced by insulin
What does carb metabolism decrease?In liver
Gluconeogenesis
Glycogenolysis
both influenced by insulin
What does fat metabolism increase? In liver
de novo fatty acid synthesis
Triacylglycerol (TAG) synthese
Both influenced by insulin
What does amino acid metabolism increase? In liver
Amino acid degradation
Protein synthesis
What is the purpose of amino acid degradation?
For it to be used for fath synthesis or for energy
what does adipose carb metabolism increase? In liver
Glucose transport into adipocytes (insulin influenced)- glucose can then be used in fatty acid synthesis
Glycolysis (supplies sustrates for glycerol in TAG synthesis)
what does adipose fat metabolism increase? In liver
synthesis of fatty acids TAG synthesis (insulin influenced)
adipocytes get most of their fatty acids from what 2 sources?
Chylomicrons
VLDL
Droplets of cholesterol and TAGS from digestive tract
Chlomicrons
What does adipose fat metabolism decrease? In liver
TAG Degradation
What does carb metabolism in the skeletal muscle increase
glucose transport
glycogen synthesis
(both influenced by insulin)
In skeletal muscle, during fed state, what are the primary and secondary fuel sources?
primary: glucose
secondary: fatty acids
In skeletal muscle, during fasting state, what are the primary and secondary fuel sources?
primary: fatty acids
secondary: glucose
what increases in amino acid synthesis in the skeletal muscle?
protein synthesis (influenced by insulin)
purpose of protein synthesis in the skeletal muscle
to replace funcitonal protein that may have been lost during the last fasting period
what is the primary fuel for the brain and RBC?
Glucose
for carb metabolism in the liver during the fasting state, ____ _____ is first used, followed by:
Why?
Glycogen degredation
gluconeogenesis
to maintain blood glucose for glucose requiring tissues
Why does the liver have glucose 6-phosphate?
so that it can release free glucose into the blood
glycogen degredation is influenced by:
glucagon and NE
Gluconeogenesis is influenced by:
glucagon
What is increased in the liver during the fasting state- Fat metabolism
Fatty acid oxidation (fats obtained from TAG hydrolysis in adipose)
Synthesis of ketone bodies
Fasting state- Adipose Carb metabolism- what decreases?
glucose transport into adipocytes due to low insulin
fasting state- adipose fat metabolism- what increases?
Degredation of TAG (activation of hormone-sensitive lipase)
Release of fatty acids
Degredation of TAG is influenced by:
glucagon and NE
fasting state- adipose fat metabolism- what decreases?
uptake of fatty acids from VLDL or chilomicrons
fasting state- skeletal muscle- Carb metabolism- what decreases?
rate of glucose update (due to low levels of insulin)
fasting state-0 skeletal muscle- fat metabolism- what increases?
the use of fatty acids from adipose tissue and ketone bodies from the liver as primary fuels
Fasting state- skeletal muscle- Protein metabolism:
what happens in the first few days?
Rapid breakdown of muscle protein (influenced by cortisol) (to be used by the liver for gluconeogenesis)
Fasting state- skeletal muscle- Protein metabolism::
what happens after several weeks?
proteolysis declines as more ketone bodies are produces and used (to spare protein)
skeletal muscle has no _____ receptors
glucagon
Fasting state- Brain- metabolism: what happens in the first few days?
Brain still uses glucose exclusively (supplied by gluconeogenesis and glycogenolysis from the liver)
Fasting state- Brain- metabolism: what happens in prolonged fasting?
Ketone bodies replace glucose as primary fuel (helps reduce dependancy on protein catabolism)
Fuel sources used bu the brain to meet energy needs after 5-6 weeks fasting:
Glucose
3-Hydroxybutyrate
Acetoacetate
Amino Acids
Fasting state- what happens in the kidney?
Gluconeogensis (prolonged fasting)
Compensation for the acidosis due to ketogenesis
Hypophysis, AKA:
Pituitary anatomy
Where is the pituitary gland located?
at the base of the brain
connected to the hypothalamus via the pituitary stalk or infundibulum
bony cavity where the pituitary lies
Sella turcica
2 lobes of the pituitary
anterior (adenohypophysis)
posterior (neurohypophysis)
anterior pitutary includes:
Pars tuberalis
Pars intermedia
Pars distalis
Posterior pituitary includes:
infundibular stalk
pars nervosa
Hyopophydeal pouch, AKA
Rathke’s Pouch
The anterior pituitary appears more:
While the posterior looks more like:
Gland-like
Neural tissue
Adenohypophydeal cells and their hormones (5)
Corticotropes- Adrenocorticotropic hormone
Thyrotropes- Thyroid stimulating hormone
Gonadotropes- Follicle stimulating and lutenizing hormone
Mammotropes/lactotropes- prolactin
Somatotropes- Growth hormone (somatotropin)
Hormones of the hypothalamus that either stimulate of inhibit the release of anterior pituitary hormones
Parvocellular cells of the paraventricular nucleus
Hypothalamic-Hypophyseal portal system: (6)
Hypothalamic neuroendocrine cells Superior hypophyseal artery Median eminence Primary capillary plexus Hypophyseal portal veins Secondary capillary plexus
When appropriately stimulated, hypothalamic neurons secrete releasing and inhibiting hormones into the:
primary capillary plexus
Hypothalamic hormones travel where?
thorugh the portal veins
to the anterior pituitary (where they stimulate or inhibit release of hormones)
anterior pituitary hormones are secreted into the:
secondary capillary plexus
Hormones produced in the posterior pituitary
none
Hormones in the posterior pituitary are made where?
In the hypothalamus by neurosecretory cells
then are transported to the neurohypophysis to be stored and secreted
magnocellular cells of the hypothalamus
supraoptic nucleus
paraventricular nucleus
post. pituitary cells secrete:
oxytocin and vasopressin (ADH)
Where are hormones stored in the post. pituitary?
Herring bodies
blood supply to the post. pituitary:
inferior hypophyseal artery
Growth hormone can affect the tissues how?
Either directly or
by stimulating the liver to produce somatomedin C (AKA insulin-like growth factor 1 - IGF1)
IGF-1 binds to:
a receptor that resembles the insulin receptor- has different effects
or a carrier protein (IGFBP) prolonging its half-life
Growth hormone causes:
Growth of almost all tissues capable of growing
metabolic effects of growth hormones
Increased rate of protein synthesis in most cells
Increase mobilization of fatty acids from adipose tissue into the blood
Increased use of fatty acids for energy
decreased rate of carbs utilization throughout the body
increase rate of protein synthesis causes:
increased amino acid transport through membranes
increased mRNA transcription into protein
Decreased catabolis of existing protein
increased fatty acid mobilization can cause a ____ effect.
Ketogenic effect- large quantities of acetoacetic acid are formed by the liver and released into the body causing ketosis
Decreased carbohydrate utilization causes:
decreased glucose uptake
increased glucose production by the liver
increased insuling secretion
growth hormone effects on bone
directly and indirectly effected by IGF-1
Increases formation of new bone and cartilage
Epiphyseal plates widen to lengthen long bones
helps maintain normal bone remodeling in adults
Growth hormone effects on fat cells
stimulated lipolysis (bu stimulating hormone sensitive lipase)
stimulates the release of free fatty acids into the blood
special growth hormone effects on skeletal muscle
Stimulates amino acid uptake and incorporation into protein (hypertrophy of sarcomeres)
suppresses breakdown of proteins
GH and IGF-1 both effect skeletal muscle
Special growth hormone effects on the liver
Stimulates liver to produce IGF-1
stimulates gluconeogenesis and reduces glucose uptake by hepatocytes
stimulators of growth hormone (10)
Decreased blood glucose Decreased blood fatty acids Trauma, stress, excitement Exercise Starvation/fasting/Protein deficiency Certain Amino Acids (arginine) Testosterone/Estrogen Deep Sleep Growth Hormone Releasing Hormone Ghrelin (appetite stimulator, from the stomach)
Inhibitors of the GH (7)
Increased blood glucose Increased blood fatty acids Obesity Somatostatin (GHIH) Growth Hormone (negative feedback) Somatomedins (negative feedback) Aging
GH is produced and stored where?
in the anterior pituitary
The production of GH is done when?
it is pulsatile (mostly at night)
GH stimulates:
Lypolysis
Protein synthesis
Production of IGF-1 (resposible for many effects of GH)
GH has anti_______ effects, and is said to be:
anti-insuling
diabetogenic
Somatotropin:
A growth hormone secreted by the ant .pituitary gland
Somatomedin
A hormone that acts as an intermediate in the stimulation of tissue growth by GH
Somatostatin:
GH Inhibining hormone
Somatotrophs
variouis cells of the ant. pituitary gland that secrete somatotropes.
Disease with protein deficiency on plasma concentration of growth hormone
Kwashiokor
2 types of bone development
endochondral
intramembranous
2 types of bone growth
Epiphyseal- growth in length
Appositional- growth in diameter
Endochondral bones start as _______ which grow _____
chondrocytes
cartilage
Intramembranous ossification occurs in:
flat bones
Long bones grow in length at the:
epiphyseal plates
What happens in epiphyseal growth?
Chondrocytes proliferate and make cartilage to thicken the plate.
This is eventually replaced by bone.
What happens in appositional growth?
Osteoblasts lay down more laters on the surface
Resorption and remodeling hollow out the center.
GH Hyposecretion abnomalities
Panhypopituitarism
dwarfism
Deficiency in more then 1 anterior pituitary hormone
Panhypopituitarism
GH Deficiency only
Dwarfism
GW Abnormality symptoms do not typically manifest until:
75% of the ant. pituitary is damages
GH Hypersecretion abnormalites
gigantism
acromegaly
cause of childhood onset panhypopituiarism:
Usually due to a tumor that destroys the pituitary- especially the somatotrophs
Effects of child onset panhypopituitarism:
Development rate is greately reduces, though body parts are developed proportionally
They fail to produce gonadotropins, so do not go through puberty
What is childhood onset panhypopituitarism treated with?
hormone replacement
another type of dwarfism is due to:
Hereditary inability to form somatomedin
cause of adult onset Panhypopituitarism
pituitary is damaged by thrombosis of the pituitary blood vessels, or a tumor
Effects of adult onself panhypopituitarism
Hypothyroidism (decreased TSH)
Lack of cortisol (decreased ACTH)
Impotence, infertility, atrophy of sex organs (decreased FSH and LH)
Prolactin deficiency in women (causes failure of lactation)
symptoms of adult onset panhypopituitarism
muscle atrophy weight gain feeling unwell anxiety loss of motivation
Overproduction of GH before plates close
Gigantism
____% of people with gigantism have diabetes
10%
Gigantistm is usually caused by:
A GH Secreting tumor (may eventually destroy itself, leading to hypopituitarism)
Hyposecretion of GH after growth plates close
Acromegaly
Bones that are most affected for people with acromegaly
Intramembranous bones- they are the most capable of continues appostitional growth
features of acromegaly
enlargement of hands and feet
enlarges cranium, jaw bone, vertebrae (kyphosis)
Enlarged internal organs
Osteoarthritis
Other anterior pituitary hormones:
PO (related to pregnancy and lactation)
LH and FSH (female reproductive physiology)
TSH-(related to thyroid gland)
ACTH (related to the adrenal gland)
posterior pituitary is composed mainly of:
pituicytes
Pituicytes are ____-like cells that (DO/DO NOT) secrete hormones
Glial
do not
Pituicytes suppport:
the terminal nerve endings of neurosecretory cells from the hypothalamus
Neurosecretory cells are found in the
Post. Pituitary
Neurosecretory cells origin and pathway
Originate in the hypothalamus
Pass through the pituitary stalk
Terminate in the posterior pituitary
What does the neurosecretory cells secrete?
Oxytocin or ADH
ADH/Vasopressin is formed mostly in the:
supraoptic nuclei
Oxytocin is formed mostly in the:
Paraventricular nuclei
Oxytocin and ADH are carried to the post. pituitary bound to:
How long does this take?
neurophysins
Trip takes several days
Target tissues of ADH
Kidneys
Sweat glands
Arterioles
ADH function in kidneys
increase reabsorption of water
ADH function in sweat glands
Reduce water loss through sweat
ADH function in arterioles
vasoconstriction increases peripheral resistance, therefore pressure (hence other name- vasopressin)
What happens when ADH is secreted to the kidneys?
water is conserved and urine is more concentrated
what happns when ADH is absent/inhibited in the kidneys?
Water reabsorption is prevented by collecting tubules and ducts to cause more water loss- leads to more diluted urine
What stimulates ADH secretion?
Increased extracellular osmolarity
Low blood volume
Low blood pressure
What detects increased extracellular fluid osmolarity?
Osmoreceptors in the hypothalamus
What detects low blood volume?
Lack of stretch receptor activation in the right atrium (ADH secretion is inhibited when they ARE stretched)
What detects low blood pressure?
Baroreceptors in the carotid sinus and aortic artery
Roles of Oxytocin in labor:
Causes a positive feedback loop to increase uterine contractions
(detected by stretching of the uterus/cervix feeding back to the hypothalamus)
Roles of oxytocin in lactation
Suckling stimulus by the infant promotes smooth muscle contraction to move milk towards the nipple
Psycholgical effects of oxytocin
Any kind of bonding- the “love hormone”.
The thyroid has how many lobes
2
Some people have a _____ lobe in the hypothalamus
pyramidal
where is the thyroid located
anterior to the cricoid and upper trachea
The thyroid contains:
How large?
Thyroid follicles
100-300 microns in diameter
Thyroid is lined with what epithelium?
cuboidal
the thyroid is filled with a secretory substance called:
colloid
major component of colloid:
Thyroglobulin
One of the largest proteins in the body.
A storehouse of Iodine and inactive thyroid hormones
Thyroglobulin
Each molecure of TG (thyroglobulin) contains:
about 70 tyrosine amino acids
93% of active thyroid hormone
Thyroxine (T4)
Almost all T4 is converted to ____ in the tissues
T3
Percentage of T3 secreted as an active thyroid hormone
7%
T3 is about _____ times (MORE/LESS) potent than T4
4 times more
Between T3 and T4, what metabolizes faster?
T3
What is necessary for thyroid hormone synthesis
Iodine
Iodine is classified as:
a micronutrient and dietary mineral
How much iodine is required in the diet?
50mgs per year (1mg per week)
Iodine is transported into _____ _____ ____ via the:
thyroid follicle cells
via the NIS (sodium/iodide symporter)- a secondary active transport system
Iodine diffuses into the _____ ____ via:
follicle lumen via pendrin
The NIS pump is _____ dependent
TSH
-required for iodide trapping
After pendrin pumps iodine into the follicle, what happens next?
Iodide is oxydized by peroxidase, which facilitates thyroglobulin sythesis
Thyroglobulin precursor is a protein synthesized in the:
it is then secreted into :
ER
Follicle lumen
What happens to the tyrosines in the thyroglobulin?
they become iodinated by 1-2 oxidized iodides.
then they are coupled to form T3 and T4
Iondination of the tyrosines within the thyroglobulin is also called
organification and coupling
thyroid can store a hormone for how long? How is it mostly stored?
2-3 months
stored mostly as T4
To release thyroid hormones, what happens
small amounts of thyroglobulin is pinocytosed into vesicles
fused to lysosomes which break down the thyroglobulin into T3 and T4 and then secreted
How are MIT and DIT recycled?
by deioninase
Thyroid hormones bind to ____ ____ via ___
plasma proteins
via TBG (thyroxine binding globulin)
Which thyroid hormone acts faster than the other?
T3
Half life of T3?
T4?
T3- 3 days
T4- 7 days
Thyroxine is converted to T3 in the tissues by:
Iodinase
Where is the thyroid receptor located?
in the nucleus
Thyroid receptors have a high affinity for:
T3
Thyroid receptors require another protein called”
Retinoid X
The thyroid receptor/Retinoid X is a:
Gene transcription factor
New mitochondrial activation may be a direct affect of:
Thyroid hormone binding to it or
increase in protein synthesis and their functions increase need for mitochondrial activity
Gene transcription/protein synthesis and activity of mitochondria effects:
Increase basal metabolic rate
Increase active transport of Na+/K+ pump
Growth effects
Stimulation of carbohydrate and fat metabolism
Increase cardiac and respiratory activity
Most metabolic process increase with:
Thyroid hormones, especially protein synthesis
production of catabolic enzymes can also lead to
protein degredation
Growth is faster with elevated:
thyroid hormone levels (though it also causes growth plates to close earlier)
Increased production of enzymes for carbohydrate metabolism leads to:
Increased insulin and uptake of glucose by cells
Enhanced glycolysis
Enhanced gluconeogenesis
Increased glucose absorption
Lipids are metabolized how?
from fat stores increasing FFA in the blood
Thyroid hormones cause the liver to:
increase LDL uptake and secretion of cholesterol in the bile
Increased blood flow and cardiac output may be secondary to:
the consequences of increased BMR
Thyroid hormones affects CVP and GI by:
increasing blood flow and cardiac output
increasing heart rate
Increasing respiratory rate
Increasing GI motility
Effects of the thyroid stimulating hormone
Increases proteolysis of the thyroglobulin
Increases activity of iodide pump
Increases iodination of tyrosine
Increases secretory activity of thyroid cells
Hypertrophy and hyperplasiam of thyroid cells
mechanism -> cAMP and protein kinase
TRH increases:
TSH secretion
TRH release in increased by:
Decreased by:
increased by cold
decreased by anxiety and stress, and high cortisol activity
TRH and TSH are inhibited by
T3 and T4 via negative feedback
autoimmune disease where antibodies bind to TSH receptors and mimic TSH causing hypersecretion of T4/T3
Grave’s Disease
Thyroid cell tumor in which thyroid hormones are overproduces
Thyroid adenoma
Symptoms of hyperthyroid
Excessive sweating Heat intolerance Increased bowel movements Tremor Nervousness rapid heart rate weight loss fatigue decreased concentraion irregular and scant menstural flow bulging eyes
Endemic goiters
Iodide deficiency
Where is endemic goiters usually occuring?
in regions where there is a lack of iodine in the soil
goiter is caused by
resulting increase in TSH production; casuing gland hypertrophy
Autoimmune destruction of thyroid cells.
antibodies attach to something other than the receptors, causing the thyroid cells to be destroyed
Hashimoto thyroiditis (Type of hypothyroidism)
Hypothyroidism symptoms
Myxedema (excess tissue gel matric deposited- causing non-pitting edema)
Atherosclerosis (accelerated plaque formation in arteries due to sluggish LDL uptake
Lack of thyroxine from or before birth
Cretinism
Potential causes of cretinism
could be from lack of thyroid gland or lack of iodine in mother
effects of cretinism
Severe and irreparable mental defects
stunted growth
reducted growth and function of many organs
Enlarged thyroid
goiter
Causes of goiter
iodine deficiency selenium deficiency autoimmune inflammation nodules within the thyroid tumors Pregnancy/pubery
Goiters can compress:
the trachea or esophagus making breathing and swallowing difficult
