Exam 1 Flashcards
(296 cards)
1
Q
Most abundant hormones
A
proteins
2
Q
Least abundant hormones
A
Amines
3
Q
3 types of hormones
A
Proteins
Amines
Steroids
4
Q
Endorcrine organs (ones she said to worry about) (7)
A
Hypothalamus Pituitary Thyroid Parathyroid Pancreas Adrenal Testis/Ovary
5
Q
If a hormone has “releasing” or “inhibiting” in the name, it is from the:
A
Hypothalamus
6
Q
Rule of thumb:
Hormones ending in -Ole, -One, -Ene are a:
Hormones ending in -ine are a:
The rest are:
A
Steroid
Amine
Protein/peptide
7
Q
Proteins are ____ soluble. This means:
A
Water solube
they can bind to cell surface (membrane) receptors
8
Q
Proteins are ____ into the plasma through the ____. This is because:
A
Dissolved
Receptors
Because they can’t pass the lipid bilayer
9
Q
Protein synthesis occurs in the:
This forms a:
A
Occurs in the ER
Forms a Preprohormone
10
Q
In protein modification, what is removed? What is formed here?
A
Signal sequence is removed
forms Prohormone
11
Q
After protein modification, the prohormone is transported to the:
A
golgi network
12
Q
What happens to the protein during the formation of secretory vesicles in the golgi?
A
Prohormone is cleaved into the active hormone
13
Q
How is the protein secreted from the cell into the blood?
A
It is exocytosed. The cell is signaled to release the hormone and and of its fragments.
14
Q
Steroid hormones are derived from:
A
Cholesterol
15
Q
Steroid hormones are _____-soluble. This means:
A
Lipid soluble
This means they cannot typically be stored, so are made on demand
16
Q
How are steroids released into the blood stream?
A
They can diffuse through the cell membrane
17
Q
Steroids bind to:
A
Intracellular receptors
18
Q
What part of steroids can be stored or obtained from the blood?
A
Steroid precursors, such as cholesterol esters
19
Q
What is the 1st rate limiting reaction in the production of VARIOUS steroid hormones?
A
Conversion of cholesterol to pregnenolone
20
Q
What is required to convert cholesterol to pregnenolone?
A
P450scc/Desmolase
21
Q
Amines are derived from:
A
Tyrosine
22
Q
2 groups of amines:
A
Thyroid hormones
Catecholamines
23
Q
Thyroid hormones include:
A
T3 and T4
24
Q
T3:
A
Triiodothyromine
25
T4:
Thyroxine
26
How are thyroid hormones stored?
As large polhmers called Thyroglobulin
27
How are thyroid hormones secreted
Thyroglobulin is split off then secreted into the blood
28
Catecholamine hormones include:
Epinephrine
Norepinephrine
Dopamine
29
Dopamine is a:
Neurotransmitter
30
How are catacholamines stored and secreted?
They are transported into the vesicles for storage
| Secreted via exocytosis (similar to proteins)
31
enzymes that are used to synthesize amines are located where?
The tyroid, adrenal medulla, and the brain
32
where are catacholamines made?
in the cytoplasm
33
Concentration of hormones needed to be in the blood stream:
1 picogram/mL to a few micrograms/mL of fluid
34
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?)
35
Types of endocrine stimuli (3)
Humoral
Neural
Hormonal
36
Stimulus that is something resolved in the body, but is NOT a hormone (Ex.- calcium, sodium)
Humoral Stimulus
37
What stimulates the adrenal medulla?
Neural stimulus
38
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.
39
Negative feedback prevents
over activity of glands
40
negative feedback is usually due to:
rising hormone levels itself, or one of its products.
41
When does positive feedback occur?
Only in special circumstances, such as pregnancy
42
Mechanisms of Clearance (4)
Metabolic destruction
Binding with tissues
Excretion by liver into the bile
Excretion by kidneys into the urine
43
Plasma-protein bound hormones are cleared from the blood at a much _____ (FASTER/SLOWER) rate
slower
44
Cells cannot respond to a hormone unless it has:
a hormone receptor
45
Are receptors large or small proteins?
large
46
how many receptors does a cell have?
thousands
47
Are receptors always highly specific to what it will bind to?
No- but usually are.
48
Possible receptor locations:
Cell membrane
In the cytoplasm
In the nucleus
49
What will bind to receptors in the cytoplasm?
steroids
50
What will bind to receptors on the cell membrane?
Proteins/peptides and catecholamines
51
What will bind to receptors in the nucleus?
Thyroid hoirmones
52
3 types of cell membrane receptors
Ion Channel-Linked Receptors
Enzyme-Linked receptors
G-Protein-Linked receptors
53
What type of cell membrane receptor uses neurotransmitters to bind to a receptor/channel, causing it to open?
Ion Channel Linked Receptor
54
What type of cell membrane receptor includes binding of a single molecule directly activating an enzyme?
Enzyme-Linked receptor
55
Best studied enzyme-linked receptor?
Tyrosine Kinase Receptor
56
A complex of 3 subunits- alpha, beta and gamma
G-Protein
57
How is GProtein activated?
when a signal molecule binds to a receptor
58
In G Protein linked receptors, where does the alpha subunit activate multiple targets?
When GDP is exchanged for GTP
59
How are G Protein Linked receptors deactivated?
The G Protein hydrolyses the GTP and reassmbles its subunits
60
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
61
Fed state lasts how long?
2-4 hours after eating
62
Type of metabolism favored in the Fed state?
Anabolic
63
What is stored in the Fed state?
Carbohydrates and for for later use
64
In the Fed state, energy is stored as:
fat and glucogen, as well as ATP, Phosphocreatine, and protein
65
The Fasting state beings:
| If ends:
Starts after food is digested and absorbed.
| Continues until more food is ingested
66
Type of metabolism favored in the Fasting state:
Catabolic
67
what happens if protein is increasingly used for energy?
cellular function becomes compromised
68
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
69
Process of generating ATP from Fats
Fats -> digested fatty acids -> beta oxidation -> Acetyl CoA-> Citric Acid Cycle -> NADH and FADH2 ->Electron transport chain -> ATP
70
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
71
3 major stages of glycolysis
Early Glycolysis
Intermediate glycolysis
Late glycolysis
72
Step of glycolysis where there is an energy investment of 2 ATP. Goes from Glucose to Fructose 1,6 bisphosphate
Early glycolysis
73
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
74
Step of glycolysis where there is energy generation of 4 ATP
| Goes from glyceraldehyde 3-phosphate to pyruvate
Late glycolysis
75
Where is pyruvate converted into Acetyl-CoA>
In the mitochondria
76
What is lost when Pyruvate is converted into acetyl CoA?
CO2
77
Where does the Citric Acid Cycle take place?
in the mitochondria
78
In KREB cycle, how many carbon are lost? And in what form?
2 carbons are lost in the form of CO2
79
Products of KREB cycle (3)
3 NADH
1 FADH2
1 GTP
80
Oxygen's role in the body:
It combines with e- and H+ to form water.
| it is the "final e- acceptor"
81
Approx amount of ATP generated for 1 NADH
| For 1 FADH2?
2. 5 ATP for NADH
| 1. 5 ATP for 1 FADH2
82
total oxidation of 1 glucose produces approx how many ATP?
30
83
Lipolysis:
Free fatty acids
84
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)
85
An important enzyme involved in the hormonally regulated release of fatty acids and glycerol from adipocyte lipid stores
Hormone sensitive lipase
86
Beta oxidation can lead to:
ketogenesis
87
When a group of substances collectively known as ketone bodies are formed by the breakdown of fatty acids and ketogenic amino acids
ketogenesis
88
When will acetyl coa metabolize into ketone bodies?
when there is a low availability of carbohydrates and a high rate of beta oxidation
89
where does kitogenesis occur?
In the liver
90
When there are very high levels of ketones. The pH of the blood shifts to be more acidic.
Ketoacidosis
91
What happens once proteins are broken down into amino acids?
they are deanimated to remove NH4+.
92
NH4+ enters the _______ ______ to be eliminated by the:
urea cylce
| kidneys
93
what is converted into an intermediate of metabolism to form ATP?
Carbon skeleton
94
NH3+ + C Skeleton =
Amino acid
95
glucose is stored in the body as:
Glucogen
96
Glucogen is mostly stored where?
in the liver and skeletal muscle
97
Glucogen synthase:
Glycogenesis
98
Glucogen phosphoylase:
Glycogenlysis
99
gluconeogenesis is what type of metabolism?
anabolic
100
the body gets rid of what during fasting?
glucose and glycogen
101
raw materials needed for gluconeogenesis:
glycerol
lactate
several amino acids
102
Fatty acid synthesis
Lipogenesis
103
what starts lipogenesis?
Acetyl CoA is built up by added 2 carbon units
104
where does lipogenesis occur
in the cytoplasm
105
major enzyme used for lipogenesis:
Fatty Acid Synthase
106
Major sites for lipogenesis:
Adipose tissue and the liver
107
DNL:
De Novo Lipogenesis
108
the liver receives blood from:
GI tract and pancreas
109
The liver takes in:
Carbs
Lipids
Amino acids
110
What does carb metabolism in the liver increase?
Phosphorylation of glucose
Glycogen synthesis
Glycolysis
first 2 influenced by insulin
111
What does carb metabolism decrease?In liver
Gluconeogenesis
Glycogenolysis
both influenced by insulin
112
What does fat metabolism increase? In liver
de novo fatty acid synthesis
Triacylglycerol (TAG) synthese
Both influenced by insulin
113
What does amino acid metabolism increase? In liver
Amino acid degradation
| Protein synthesis
114
What is the purpose of amino acid degradation?
For it to be used for fath synthesis or for energy
115
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)
116
what does adipose fat metabolism increase? In liver
```
synthesis of fatty acids
TAG synthesis (insulin influenced)
```
117
adipocytes get most of their fatty acids from what 2 sources?
Chylomicrons
| VLDL
118
Droplets of cholesterol and TAGS from digestive tract
Chlomicrons
119
What does adipose fat metabolism decrease? In liver
TAG Degradation
120
What does carb metabolism in the skeletal muscle increase
glucose transport
glycogen synthesis
(both influenced by insulin)
121
In skeletal muscle, during fed state, what are the primary and secondary fuel sources?
primary: glucose
secondary: fatty acids
122
In skeletal muscle, during fasting state, what are the primary and secondary fuel sources?
primary: fatty acids
secondary: glucose
123
what increases in amino acid synthesis in the skeletal muscle?
protein synthesis (influenced by insulin)
124
purpose of protein synthesis in the skeletal muscle
to replace funcitonal protein that may have been lost during the last fasting period
125
what is the primary fuel for the brain and RBC?
Glucose
126
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
127
Why does the liver have glucose 6-phosphate?
so that it can release free glucose into the blood
128
glycogen degredation is influenced by:
glucagon and NE
129
Gluconeogenesis is influenced by:
glucagon
130
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
131
Fasting state- Adipose Carb metabolism- what decreases?
glucose transport into adipocytes due to low insulin
132
fasting state- adipose fat metabolism- what increases?
Degredation of TAG (activation of hormone-sensitive lipase)
Release of fatty acids
133
Degredation of TAG is influenced by:
glucagon and NE
134
fasting state- adipose fat metabolism- what decreases?
uptake of fatty acids from VLDL or chilomicrons
135
fasting state- skeletal muscle- Carb metabolism- what decreases?
rate of glucose update (due to low levels of insulin)
136
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
137
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)
138
Fasting state- skeletal muscle- Protein metabolism::
| what happens after several weeks?
proteolysis declines as more ketone bodies are produces and used (to spare protein)
139
skeletal muscle has no _____ receptors
glucagon
140
Fasting state- Brain- metabolism: what happens in the first few days?
Brain still uses glucose exclusively (supplied by gluconeogenesis and glycogenolysis from the liver)
141
Fasting state- Brain- metabolism: what happens in prolonged fasting?
Ketone bodies replace glucose as primary fuel (helps reduce dependancy on protein catabolism)
142
Fuel sources used bu the brain to meet energy needs after 5-6 weeks fasting:
Glucose
3-Hydroxybutyrate
Acetoacetate
Amino Acids
143
Fasting state- what happens in the kidney?
Gluconeogensis (prolonged fasting)
Compensation for the acidosis due to ketogenesis
144
Hypophysis, AKA:
Pituitary anatomy
145
Where is the pituitary gland located?
at the base of the brain
| connected to the hypothalamus via the pituitary stalk or infundibulum
146
bony cavity where the pituitary lies
Sella turcica
147
2 lobes of the pituitary
anterior (adenohypophysis)
| posterior (neurohypophysis)
148
anterior pitutary includes:
Pars tuberalis
Pars intermedia
Pars distalis
149
Posterior pituitary includes:
infundibular stalk
| pars nervosa
150
Hyopophydeal pouch, AKA
Rathke's Pouch
151
The anterior pituitary appears more:
While the posterior looks more like:
Gland-like
Neural tissue
152
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)
153
Hormones of the hypothalamus that either stimulate of inhibit the release of anterior pituitary hormones
Parvocellular cells of the paraventricular nucleus
154
Hypothalamic-Hypophyseal portal system: (6)
```
Hypothalamic neuroendocrine cells
Superior hypophyseal artery
Median eminence
Primary capillary plexus
Hypophyseal portal veins
Secondary capillary plexus
```
155
When appropriately stimulated, hypothalamic neurons secrete releasing and inhibiting hormones into the:
primary capillary plexus
156
Hypothalamic hormones travel where?
thorugh the portal veins
| to the anterior pituitary (where they stimulate or inhibit release of hormones)
157
anterior pituitary hormones are secreted into the:
secondary capillary plexus
158
Hormones produced in the posterior pituitary
none
159
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
160
magnocellular cells of the hypothalamus
supraoptic nucleus
| paraventricular nucleus
161
post. pituitary cells secrete:
oxytocin and vasopressin (ADH)
162
Where are hormones stored in the post. pituitary?
Herring bodies
163
blood supply to the post. pituitary:
inferior hypophyseal artery
164
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)
165
IGF-1 binds to:
a receptor that resembles the insulin receptor- has different effects
or a carrier protein (IGFBP) prolonging its half-life
166
Growth hormone causes:
Growth of almost all tissues capable of growing
167
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
168
increase rate of protein synthesis causes:
increased amino acid transport through membranes
increased mRNA transcription into protein
Decreased catabolis of existing protein
169
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
170
Decreased carbohydrate utilization causes:
decreased glucose uptake
increased glucose production by the liver
increased insuling secretion
171
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
172
Growth hormone effects on fat cells
stimulated lipolysis (bu stimulating hormone sensitive lipase)
stimulates the release of free fatty acids into the blood
173
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
174
Special growth hormone effects on the liver
Stimulates liver to produce IGF-1
stimulates gluconeogenesis and reduces glucose uptake by hepatocytes
175
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)
```
176
Inhibitors of the GH (7)
```
Increased blood glucose
Increased blood fatty acids
Obesity
Somatostatin (GHIH)
Growth Hormone (negative feedback)
Somatomedins (negative feedback)
Aging
```
177
GH is produced and stored where?
in the anterior pituitary
178
The production of GH is done when?
it is pulsatile (mostly at night)
179
GH stimulates:
Lypolysis
Protein synthesis
Production of IGF-1 (resposible for many effects of GH)
180
GH has anti_______ effects, and is said to be:
anti-insuling
diabetogenic
181
Somatotropin:
A growth hormone secreted by the ant .pituitary gland
182
Somatomedin
A hormone that acts as an intermediate in the stimulation of tissue growth by GH
183
Somatostatin:
GH Inhibining hormone
184
Somatotrophs
variouis cells of the ant. pituitary gland that secrete somatotropes.
185
Disease with protein deficiency on plasma concentration of growth hormone
Kwashiokor
186
2 types of bone development
endochondral
| intramembranous
187
2 types of bone growth
Epiphyseal- growth in length
Appositional- growth in diameter
188
Endochondral bones start as _______ which grow _____
chondrocytes
cartilage
189
Intramembranous ossification occurs in:
flat bones
190
Long bones grow in length at the:
epiphyseal plates
191
What happens in epiphyseal growth?
Chondrocytes proliferate and make cartilage to thicken the plate.
This is eventually replaced by bone.
192
What happens in appositional growth?
Osteoblasts lay down more laters on the surface
Resorption and remodeling hollow out the center.
193
GH Hyposecretion abnomalities
Panhypopituitarism
dwarfism
194
Deficiency in more then 1 anterior pituitary hormone
Panhypopituitarism
195
GH Deficiency only
Dwarfism
196
GW Abnormality symptoms do not typically manifest until:
75% of the ant. pituitary is damages
197
GH Hypersecretion abnormalites
gigantism
acromegaly
198
cause of childhood onset panhypopituiarism:
Usually due to a tumor that destroys the pituitary- especially the somatotrophs
199
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
200
What is childhood onset panhypopituitarism treated with?
hormone replacement
201
another type of dwarfism is due to:
Hereditary inability to form somatomedin
202
cause of adult onset Panhypopituitarism
pituitary is damaged by thrombosis of the pituitary blood vessels, or a tumor
203
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)
204
symptoms of adult onset panhypopituitarism
```
muscle atrophy
weight gain
feeling unwell
anxiety
loss of motivation
```
205
Overproduction of GH before plates close
Gigantism
206
____% of people with gigantism have diabetes
10%
207
Gigantistm is usually caused by:
A GH Secreting tumor (may eventually destroy itself, leading to hypopituitarism)
208
Hyposecretion of GH after growth plates close
Acromegaly
209
Bones that are most affected for people with acromegaly
Intramembranous bones- they are the most capable of continues appostitional growth
210
features of acromegaly
enlargement of hands and feet
enlarges cranium, jaw bone, vertebrae (kyphosis)
Enlarged internal organs
Osteoarthritis
211
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)
212
posterior pituitary is composed mainly of:
pituicytes
213
Pituicytes are ____-like cells that (DO/DO NOT) secrete hormones
Glial
do not
214
Pituicytes suppport:
the terminal nerve endings of neurosecretory cells from the hypothalamus
215
Neurosecretory cells are found in the
Post. Pituitary
216
Neurosecretory cells origin and pathway
Originate in the hypothalamus
Pass through the pituitary stalk
Terminate in the posterior pituitary
217
What does the neurosecretory cells secrete?
Oxytocin or ADH
218
ADH/Vasopressin is formed mostly in the:
supraoptic nuclei
219
Oxytocin is formed mostly in the:
Paraventricular nuclei
220
Oxytocin and ADH are carried to the post. pituitary bound to:
How long does this take?
neurophysins
Trip takes several days
221
Target tissues of ADH
Kidneys
Sweat glands
Arterioles
222
ADH function in kidneys
increase reabsorption of water
223
ADH function in sweat glands
Reduce water loss through sweat
224
ADH function in arterioles
vasoconstriction increases peripheral resistance, therefore pressure (hence other name- vasopressin)
225
What happens when ADH is secreted to the kidneys?
water is conserved and urine is more concentrated
226
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
227
What stimulates ADH secretion?
Increased extracellular osmolarity
Low blood volume
Low blood pressure
228
What detects increased extracellular fluid osmolarity?
Osmoreceptors in the hypothalamus
229
What detects low blood volume?
Lack of stretch receptor activation in the right atrium (ADH secretion is inhibited when they ARE stretched)
230
What detects low blood pressure?
Baroreceptors in the carotid sinus and aortic artery
231
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)
232
Roles of oxytocin in lactation
Suckling stimulus by the infant promotes smooth muscle contraction to move milk towards the nipple
233
Psycholgical effects of oxytocin
Any kind of bonding- the "love hormone".
234
The thyroid has how many lobes
2
235
Some people have a _____ lobe in the hypothalamus
pyramidal
236
where is the thyroid located
anterior to the cricoid and upper trachea
237
The thyroid contains:
| How large?
Thyroid follicles
| 100-300 microns in diameter
238
Thyroid is lined with what epithelium?
cuboidal
239
the thyroid is filled with a secretory substance called:
colloid
240
major component of colloid:
Thyroglobulin
241
One of the largest proteins in the body.
| A storehouse of Iodine and inactive thyroid hormones
Thyroglobulin
242
Each molecure of TG (thyroglobulin) contains:
about 70 tyrosine amino acids
243
93% of active thyroid hormone
Thyroxine (T4)
244
Almost all T4 is converted to ____ in the tissues
T3
245
Percentage of T3 secreted as an active thyroid hormone
7%
246
T3 is about _____ times (MORE/LESS) potent than T4
4 times more
247
Between T3 and T4, what metabolizes faster?
T3
248
What is necessary for thyroid hormone synthesis
Iodine
249
Iodine is classified as:
a micronutrient and dietary mineral
250
How much iodine is required in the diet?
50mgs per year (1mg per week)
251
Iodine is transported into _____ _____ ____ via the:
thyroid follicle cells
| via the NIS (sodium/iodide symporter)- a secondary active transport system
252
Iodine diffuses into the _____ ____ via:
follicle lumen via pendrin
253
The NIS pump is _____ dependent
TSH
| -required for iodide trapping
254
After pendrin pumps iodine into the follicle, what happens next?
Iodide is oxydized by peroxidase, which facilitates thyroglobulin sythesis
255
Thyroglobulin precursor is a protein synthesized in the:
| it is then secreted into :
ER
Follicle lumen
256
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
257
Iondination of the tyrosines within the thyroglobulin is also called
organification and coupling
258
thyroid can store a hormone for how long? How is it mostly stored?
2-3 months
stored mostly as T4
259
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
260
How are MIT and DIT recycled?
by deioninase
261
Thyroid hormones bind to ____ ____ via ___
plasma proteins
via TBG (thyroxine binding globulin)
262
Which thyroid hormone acts faster than the other?
T3
263
Half life of T3?
| T4?
T3- 3 days
| T4- 7 days
264
Thyroxine is converted to T3 in the tissues by:
Iodinase
265
Where is the thyroid receptor located?
in the nucleus
266
Thyroid receptors have a high affinity for:
T3
267
Thyroid receptors require another protein called"
Retinoid X
268
The thyroid receptor/Retinoid X is a:
Gene transcription factor
269
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
270
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
271
Most metabolic process increase with:
Thyroid hormones, especially protein synthesis
272
production of catabolic enzymes can also lead to
protein degredation
273
Growth is faster with elevated:
thyroid hormone levels (though it also causes growth plates to close earlier)
274
Increased production of enzymes for carbohydrate metabolism leads to:
Increased insulin and uptake of glucose by cells
Enhanced glycolysis
Enhanced gluconeogenesis
Increased glucose absorption
275
Lipids are metabolized how?
from fat stores increasing FFA in the blood
276
Thyroid hormones cause the liver to:
increase LDL uptake and secretion of cholesterol in the bile
277
Increased blood flow and cardiac output may be secondary to:
the consequences of increased BMR
278
Thyroid hormones affects CVP and GI by:
increasing blood flow and cardiac output
increasing heart rate
Increasing respiratory rate
Increasing GI motility
279
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
280
TRH increases:
TSH secretion
281
TRH release in increased by:
| Decreased by:
increased by cold
| decreased by anxiety and stress, and high cortisol activity
282
TRH and TSH are inhibited by
T3 and T4 via negative feedback
283
autoimmune disease where antibodies bind to TSH receptors and mimic TSH causing hypersecretion of T4/T3
Grave's Disease
284
Thyroid cell tumor in which thyroid hormones are overproduces
Thyroid adenoma
285
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
```
286
Endemic goiters
Iodide deficiency
287
Where is endemic goiters usually occuring?
in regions where there is a lack of iodine in the soil
288
goiter is caused by
resulting increase in TSH production; casuing gland hypertrophy
289
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)
290
Hypothyroidism symptoms
Myxedema (excess tissue gel matric deposited- causing non-pitting edema)
Atherosclerosis (accelerated plaque formation in arteries due to sluggish LDL uptake
291
Lack of thyroxine from or before birth
Cretinism
292
Potential causes of cretinism
could be from lack of thyroid gland or lack of iodine in mother
293
effects of cretinism
Severe and irreparable mental defects
stunted growth
reducted growth and function of many organs
294
Enlarged thyroid
goiter
295
Causes of goiter
```
iodine deficiency
selenium deficiency
autoimmune inflammation
nodules within the thyroid
tumors
Pregnancy/pubery
```
296
Goiters can compress:
the trachea or esophagus making breathing and swallowing difficult
