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Endo/Repro > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Most abundant hormones

A

proteins

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2
Q

Least abundant hormones

A

Amines

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3
Q

3 types of hormones

A

Proteins
Amines
Steroids

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4
Q

Endorcrine organs (ones she said to worry about) (7)

A 
Hypothalamus
Pituitary
Thyroid
Parathyroid
Pancreas
Adrenal
Testis/Ovary
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5
Q

If a hormone has “releasing” or “inhibiting” in the name, it is from the:

A

Hypothalamus

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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

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7
Q

Proteins are ____ soluble. This means:

A

Water solube

they can bind to cell surface (membrane) receptors

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8
Q

Proteins are ____ into the plasma through the ____. This is because:

A

Dissolved
Receptors

Because they can’t pass the lipid bilayer

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9
Q

Protein synthesis occurs in the:

This forms a:

A

Occurs in the ER

Forms a Preprohormone

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10
Q

In protein modification, what is removed? What is formed here?

A

Signal sequence is removed

forms Prohormone

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11
Q

After protein modification, the prohormone is transported to the:

A

golgi network

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12
Q

What happens to the protein during the formation of secretory vesicles in the golgi?

A

Prohormone is cleaved into the active hormone

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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.

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14
Q

Steroid hormones are derived from:

A

Cholesterol

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15
Q

Steroid hormones are _____-soluble. This means:

A

Lipid soluble

This means they cannot typically be stored, so are made on demand

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16
Q

How are steroids released into the blood stream?

A

They can diffuse through the cell membrane

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17
Q

Steroids bind to:

A

Intracellular receptors

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18
Q

What part of steroids can be stored or obtained from the blood?

A

Steroid precursors, such as cholesterol esters

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19
Q

What is the 1st rate limiting reaction in the production of VARIOUS steroid hormones?

A

Conversion of cholesterol to pregnenolone

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20
Q

What is required to convert cholesterol to pregnenolone?

A

P450scc/Desmolase

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21
Q

Amines are derived from:

A

Tyrosine

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22
Q

2 groups of amines:

A

Thyroid hormones

Catecholamines

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23
Q

Thyroid hormones include:

A

T3 and T4

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24
Q

T3:

A

Triiodothyromine

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25
Q

T4:

A

Thyroxine

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26
Q

How are thyroid hormones stored?

A

As large polhmers called Thyroglobulin

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27
Q

How are thyroid hormones secreted

A

Thyroglobulin is split off then secreted into the blood

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28
Q

Catecholamine hormones include:

A

Epinephrine
Norepinephrine
Dopamine

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29
Q

Dopamine is a:

A

Neurotransmitter

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30
Q

How are catacholamines stored and secreted?

A

They are transported into the vesicles for storage

Secreted via exocytosis (similar to proteins)

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31
Q

enzymes that are used to synthesize amines are located where?

A

The tyroid, adrenal medulla, and the brain

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32
Q

where are catacholamines made?

A

in the cytoplasm

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33
Q

Concentration of hormones needed to be in the blood stream:

A

1 picogram/mL to a few micrograms/mL of fluid

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34
Q

2 factors that can increase/decrease the concentration of a hormone in the blood:

A

1- Rate of hormone secretion (how much is made?)

2- Rate of Removal/Clearace (how fast can it be metabolized?)

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35
Q

Types of endocrine stimuli (3)

A

Humoral
Neural
Hormonal

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36
Q

Stimulus that is something resolved in the body, but is NOT a hormone (Ex.- calcium, sodium)

A

Humoral Stimulus

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37
Q

What stimulates the adrenal medulla?

A

Neural stimulus

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38
Q

Process of a hormonal stiulus

A

The hypothalamus secretes hormones to stimulate the pituitary gland.
The pituitary gland secretes hormones to stimulate other endocrine organs to secrete hormones.

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39
Q

Negative feedback prevents

A

over activity of glands

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40
Q

negative feedback is usually due to:

A

rising hormone levels itself, or one of its products.

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41
Q

When does positive feedback occur?

A

Only in special circumstances, such as pregnancy

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42
Q

Mechanisms of Clearance (4)

A

Metabolic destruction
Binding with tissues
Excretion by liver into the bile
Excretion by kidneys into the urine

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43
Q

Plasma-protein bound hormones are cleared from the blood at a much _____ (FASTER/SLOWER) rate

A

slower

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44
Q

Cells cannot respond to a hormone unless it has:

A

a hormone receptor

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45
Q

Are receptors large or small proteins?

A

large

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46
Q

how many receptors does a cell have?

A

thousands

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47
Q

Are receptors always highly specific to what it will bind to?

A

No- but usually are.

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48
Q

Possible receptor locations:

A

Cell membrane
In the cytoplasm
In the nucleus

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49
Q

What will bind to receptors in the cytoplasm?

A

steroids

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50
Q

What will bind to receptors on the cell membrane?

A

Proteins/peptides and catecholamines

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51
Q

What will bind to receptors in the nucleus?

A

Thyroid hoirmones

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52
Q

3 types of cell membrane receptors

A

Ion Channel-Linked Receptors
Enzyme-Linked receptors
G-Protein-Linked receptors

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53
Q

What type of cell membrane receptor uses neurotransmitters to bind to a receptor/channel, causing it to open?

A

Ion Channel Linked Receptor

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54
Q

What type of cell membrane receptor includes binding of a single molecule directly activating an enzyme?

A

Enzyme-Linked receptor

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55
Q

Best studied enzyme-linked receptor?

A

Tyrosine Kinase Receptor

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56
Q

A complex of 3 subunits- alpha, beta and gamma

A

G-Protein

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57
Q

How is GProtein activated?

A

when a signal molecule binds to a receptor

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58
Q

In G Protein linked receptors, where does the alpha subunit activate multiple targets?

A

When GDP is exchanged for GTP

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59
Q

How are G Protein Linked receptors deactivated?

A

The G Protein hydrolyses the GTP and reassmbles its subunits

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60
Q

Things we need energy for: (5)

A

Maintain blood glucose- especially in the brain
Provide energy for other cells in the body
Thermoregulation
Food digestion
Physical Activity

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61
Q

Fed state lasts how long?

A

2-4 hours after eating

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62
Q

Type of metabolism favored in the Fed state?

A

Anabolic

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63
Q

What is stored in the Fed state?

A

Carbohydrates and for for later use

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64
Q

In the Fed state, energy is stored as:

A

fat and glucogen, as well as ATP, Phosphocreatine, and protein

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65
Q

The Fasting state beings:

If ends:

A

Starts after food is digested and absorbed.

Continues until more food is ingested

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66
Q

Type of metabolism favored in the Fasting state:

A

Catabolic

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67
Q

what happens if protein is increasingly used for energy?

A

cellular function becomes compromised

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68
Q

Process of generating ATP from Carbohydrates

A

Carbohydrates -> digested simple sugars ->conversion into glucose ->phosphorylated glucose ->Acetyl CoA-> Citric Acid Cycle -> NADH and FADH2 ->Electron transport chain -> ATP

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69
Q

Process of generating ATP from Fats

A

Fats -> digested fatty acids -> beta oxidation -> Acetyl CoA-> Citric Acid Cycle -> NADH and FADH2 ->Electron transport chain -> ATP

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70
Q

Process of generating ATP from proteins

A

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

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71
Q

3 major stages of glycolysis

A

Early Glycolysis
Intermediate glycolysis
Late glycolysis

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72
Q

Step of glycolysis where there is an energy investment of 2 ATP. Goes from Glucose to Fructose 1,6 bisphosphate

A

Early glycolysis

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73
Q

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

A

Intermediate glycolysis

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74
Q

Step of glycolysis where there is energy generation of 4 ATP

Goes from glyceraldehyde 3-phosphate to pyruvate

A

Late glycolysis

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75
Q

Where is pyruvate converted into Acetyl-CoA>

A

In the mitochondria

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76
Q

What is lost when Pyruvate is converted into acetyl CoA?

A

CO2

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77
Q

Where does the Citric Acid Cycle take place?

A

in the mitochondria

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78
Q

In KREB cycle, how many carbon are lost? And in what form?

A

2 carbons are lost in the form of CO2

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79
Q

Products of KREB cycle (3)

A

3 NADH
1 FADH2
1 GTP

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80
Q

Oxygen’s role in the body:

A

It combines with e- and H+ to form water.

it is the “final e- acceptor”

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81
Q

Approx amount of ATP generated for 1 NADH

For 1 FADH2?

A
  1. 5 ATP for NADH

1. 5 ATP for 1 FADH2

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82
Q

total oxidation of 1 glucose produces approx how many ATP?

A

30

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83
Q

Lipolysis:

A

Free fatty acids

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84
Q

during catabolism of fatty acids, the fatty acids are converted into what?
what metabolism is used?

A

converted into several Acetyl CoA molecules

Done by Beta Oxidation (catabolism)

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85
Q

An important enzyme involved in the hormonally regulated release of fatty acids and glycerol from adipocyte lipid stores

A

Hormone sensitive lipase

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86
Q

Beta oxidation can lead to:

A

ketogenesis

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87
Q

When a group of substances collectively known as ketone bodies are formed by the breakdown of fatty acids and ketogenic amino acids

A

ketogenesis

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88
Q

When will acetyl coa metabolize into ketone bodies?

A

when there is a low availability of carbohydrates and a high rate of beta oxidation

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89
Q

where does kitogenesis occur?

A

In the liver

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90
Q

When there are very high levels of ketones. The pH of the blood shifts to be more acidic.

A

Ketoacidosis

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91
Q

What happens once proteins are broken down into amino acids?

A

they are deanimated to remove NH4+.

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92
Q

NH4+ enters the _______ ______ to be eliminated by the:

A

urea cylce

kidneys

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93
Q

what is converted into an intermediate of metabolism to form ATP?

A

Carbon skeleton

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94
Q

NH3+ + C Skeleton =

A

Amino acid

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95
Q

glucose is stored in the body as:

A

Glucogen

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96
Q

Glucogen is mostly stored where?

A

in the liver and skeletal muscle

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97
Q

Glucogen synthase:

A

Glycogenesis

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98
Q

Glucogen phosphoylase:

A

Glycogenlysis

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99
Q

gluconeogenesis is what type of metabolism?

A

anabolic

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100
Q

the body gets rid of what during fasting?

A

glucose and glycogen

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101
Q

raw materials needed for gluconeogenesis:

A

glycerol
lactate
several amino acids

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102
Q

Fatty acid synthesis

A

Lipogenesis

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103
Q

what starts lipogenesis?

A

Acetyl CoA is built up by added 2 carbon units

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104
Q

where does lipogenesis occur

A

in the cytoplasm

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105
Q

major enzyme used for lipogenesis:

A

Fatty Acid Synthase

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106
Q

Major sites for lipogenesis:

A

Adipose tissue and the liver

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107
Q

DNL:

A

De Novo Lipogenesis

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108
Q

the liver receives blood from:

A

GI tract and pancreas

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109
Q

The liver takes in:

A

Carbs
Lipids
Amino acids

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110
Q

What does carb metabolism in the liver increase?

A

Phosphorylation of glucose
Glycogen synthesis
Glycolysis

first 2 influenced by insulin

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111
Q

What does carb metabolism decrease?In liver

A

Gluconeogenesis
Glycogenolysis

both influenced by insulin

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112
Q

What does fat metabolism increase? In liver

A

de novo fatty acid synthesis
Triacylglycerol (TAG) synthese

Both influenced by insulin

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113
Q

What does amino acid metabolism increase? In liver

A

Amino acid degradation

Protein synthesis

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114
Q

What is the purpose of amino acid degradation?

A

For it to be used for fath synthesis or for energy

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115
Q

what does adipose carb metabolism increase? In liver

A

Glucose transport into adipocytes (insulin influenced)- glucose can then be used in fatty acid synthesis

Glycolysis (supplies sustrates for glycerol in TAG synthesis)

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116
Q

what does adipose fat metabolism increase? In liver

A 
synthesis of fatty acids
TAG synthesis (insulin influenced)
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117
Q

adipocytes get most of their fatty acids from what 2 sources?

A

Chylomicrons

VLDL

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118
Q

Droplets of cholesterol and TAGS from digestive tract

A

Chlomicrons

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119
Q

What does adipose fat metabolism decrease? In liver

A

TAG Degradation

120
Q

What does carb metabolism in the skeletal muscle increase

A

glucose transport
glycogen synthesis
(both influenced by insulin)

121
Q

In skeletal muscle, during fed state, what are the primary and secondary fuel sources?

A

primary: glucose
secondary: fatty acids

122
Q

In skeletal muscle, during fasting state, what are the primary and secondary fuel sources?

A

primary: fatty acids
secondary: glucose

123
Q

what increases in amino acid synthesis in the skeletal muscle?

A

protein synthesis (influenced by insulin)

124
Q

purpose of protein synthesis in the skeletal muscle

A

to replace funcitonal protein that may have been lost during the last fasting period

125
Q

what is the primary fuel for the brain and RBC?

A

Glucose

126
Q

for carb metabolism in the liver during the fasting state, ____ _____ is first used, followed by:

Why?

A

Glycogen degredation

gluconeogenesis

to maintain blood glucose for glucose requiring tissues

127
Q

Why does the liver have glucose 6-phosphate?

A

so that it can release free glucose into the blood

128
Q

glycogen degredation is influenced by:

A

glucagon and NE

129
Q

Gluconeogenesis is influenced by:

A

glucagon

130
Q

What is increased in the liver during the fasting state- Fat metabolism

A

Fatty acid oxidation (fats obtained from TAG hydrolysis in adipose)

Synthesis of ketone bodies

131
Q

Fasting state- Adipose Carb metabolism- what decreases?

A

glucose transport into adipocytes due to low insulin

132
Q

fasting state- adipose fat metabolism- what increases?

A

Degredation of TAG (activation of hormone-sensitive lipase)

Release of fatty acids

133
Q

Degredation of TAG is influenced by:

A

glucagon and NE

134
Q

fasting state- adipose fat metabolism- what decreases?

A

uptake of fatty acids from VLDL or chilomicrons

135
Q

fasting state- skeletal muscle- Carb metabolism- what decreases?

A

rate of glucose update (due to low levels of insulin)

136
Q

fasting state-0 skeletal muscle- fat metabolism- what increases?

A

the use of fatty acids from adipose tissue and ketone bodies from the liver as primary fuels

137
Q

Fasting state- skeletal muscle- Protein metabolism:

what happens in the first few days?

A

Rapid breakdown of muscle protein (influenced by cortisol) (to be used by the liver for gluconeogenesis)

138
Q

Fasting state- skeletal muscle- Protein metabolism::

what happens after several weeks?

A

proteolysis declines as more ketone bodies are produces and used (to spare protein)

139
Q

skeletal muscle has no _____ receptors

A

glucagon

140
Q

Fasting state- Brain- metabolism: what happens in the first few days?

A

Brain still uses glucose exclusively (supplied by gluconeogenesis and glycogenolysis from the liver)

141
Q

Fasting state- Brain- metabolism: what happens in prolonged fasting?

A

Ketone bodies replace glucose as primary fuel (helps reduce dependancy on protein catabolism)

142
Q

Fuel sources used bu the brain to meet energy needs after 5-6 weeks fasting:

A

Glucose
3-Hydroxybutyrate
Acetoacetate
Amino Acids

143
Q

Fasting state- what happens in the kidney?

A

Gluconeogensis (prolonged fasting)

Compensation for the acidosis due to ketogenesis

144
Q

Hypophysis, AKA:

A

Pituitary anatomy

145
Q

Where is the pituitary gland located?

A

at the base of the brain

connected to the hypothalamus via the pituitary stalk or infundibulum

146
Q

bony cavity where the pituitary lies

A

Sella turcica

147
Q

2 lobes of the pituitary

A

anterior (adenohypophysis)

posterior (neurohypophysis)

148
Q

anterior pitutary includes:

A

Pars tuberalis
Pars intermedia
Pars distalis

149
Q

Posterior pituitary includes:

A

infundibular stalk

pars nervosa

150
Q

Hyopophydeal pouch, AKA

A

Rathke’s Pouch

151
Q

The anterior pituitary appears more:

While the posterior looks more like:

A

Gland-like

Neural tissue

152
Q

Adenohypophydeal cells and their hormones (5)

A

Corticotropes- Adrenocorticotropic hormone

Thyrotropes- Thyroid stimulating hormone

Gonadotropes- Follicle stimulating and lutenizing hormone

Mammotropes/lactotropes- prolactin

Somatotropes- Growth hormone (somatotropin)

153
Q

Hormones of the hypothalamus that either stimulate of inhibit the release of anterior pituitary hormones

A

Parvocellular cells of the paraventricular nucleus

154
Q

Hypothalamic-Hypophyseal portal system: (6)

A 
Hypothalamic neuroendocrine cells
Superior hypophyseal artery
Median eminence
Primary capillary plexus
Hypophyseal portal veins
Secondary capillary plexus
155
Q

When appropriately stimulated, hypothalamic neurons secrete releasing and inhibiting hormones into the:

A

primary capillary plexus

156
Q

Hypothalamic hormones travel where?

A

thorugh the portal veins

to the anterior pituitary (where they stimulate or inhibit release of hormones)

157
Q

anterior pituitary hormones are secreted into the:

A

secondary capillary plexus

158
Q

Hormones produced in the posterior pituitary

A

none

159
Q

Hormones in the posterior pituitary are made where?

A

In the hypothalamus by neurosecretory cells

then are transported to the neurohypophysis to be stored and secreted

160
Q

magnocellular cells of the hypothalamus

A

supraoptic nucleus

paraventricular nucleus

161
Q

post. pituitary cells secrete:

A

oxytocin and vasopressin (ADH)

162
Q

Where are hormones stored in the post. pituitary?

A

Herring bodies

163
Q

blood supply to the post. pituitary:

A

inferior hypophyseal artery

164
Q

Growth hormone can affect the tissues how?

A

Either directly or

by stimulating the liver to produce somatomedin C (AKA insulin-like growth factor 1 - IGF1)

165
Q

IGF-1 binds to:

A

a receptor that resembles the insulin receptor- has different effects

or a carrier protein (IGFBP) prolonging its half-life

166
Q

Growth hormone causes:

A

Growth of almost all tissues capable of growing

167
Q

metabolic effects of growth hormones

A

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
Q

increase rate of protein synthesis causes:

A

increased amino acid transport through membranes

increased mRNA transcription into protein

Decreased catabolis of existing protein

169
Q

increased fatty acid mobilization can cause a ____ effect.

A

Ketogenic effect- large quantities of acetoacetic acid are formed by the liver and released into the body causing ketosis

170
Q

Decreased carbohydrate utilization causes:

A

decreased glucose uptake

increased glucose production by the liver

increased insuling secretion

171
Q

growth hormone effects on bone

A

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
Q

Growth hormone effects on fat cells

A

stimulated lipolysis (bu stimulating hormone sensitive lipase)

stimulates the release of free fatty acids into the blood

173
Q

special growth hormone effects on skeletal muscle

A

Stimulates amino acid uptake and incorporation into protein (hypertrophy of sarcomeres)

suppresses breakdown of proteins

GH and IGF-1 both effect skeletal muscle

174
Q

Special growth hormone effects on the liver

A

Stimulates liver to produce IGF-1

stimulates gluconeogenesis and reduces glucose uptake by hepatocytes

175
Q

stimulators of growth hormone (10)

A 
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
Q

Inhibitors of the GH (7)

A 
Increased blood glucose
Increased blood fatty acids
Obesity
Somatostatin (GHIH)
Growth Hormone (negative feedback)
Somatomedins (negative feedback)
Aging
177
Q

GH is produced and stored where?

A

in the anterior pituitary

178
Q

The production of GH is done when?

A

it is pulsatile (mostly at night)

179
Q

GH stimulates:

A

Lypolysis
Protein synthesis
Production of IGF-1 (resposible for many effects of GH)

180
Q

GH has anti_______ effects, and is said to be:

A

anti-insuling

diabetogenic

181
Q

Somatotropin:

A

A growth hormone secreted by the ant .pituitary gland

182
Q

Somatomedin

A

A hormone that acts as an intermediate in the stimulation of tissue growth by GH

183
Q

Somatostatin:

A

GH Inhibining hormone

184
Q

Somatotrophs

A

variouis cells of the ant. pituitary gland that secrete somatotropes.

185
Q

Disease with protein deficiency on plasma concentration of growth hormone

A

Kwashiokor

186
Q

2 types of bone development

A

endochondral

intramembranous

187
Q

2 types of bone growth

A

Epiphyseal- growth in length

Appositional- growth in diameter

188
Q

Endochondral bones start as _______ which grow _____

A

chondrocytes

cartilage

189
Q

Intramembranous ossification occurs in:

A

flat bones

190
Q

Long bones grow in length at the:

A

epiphyseal plates

191
Q

What happens in epiphyseal growth?

A

Chondrocytes proliferate and make cartilage to thicken the plate.
This is eventually replaced by bone.

192
Q

What happens in appositional growth?

A

Osteoblasts lay down more laters on the surface

Resorption and remodeling hollow out the center.

193
Q

GH Hyposecretion abnomalities

A

Panhypopituitarism

dwarfism

194
Q

Deficiency in more then 1 anterior pituitary hormone

A

Panhypopituitarism

195
Q

GH Deficiency only

A

Dwarfism

196
Q

GW Abnormality symptoms do not typically manifest until:

A

75% of the ant. pituitary is damages

197
Q

GH Hypersecretion abnormalites

A

gigantism

acromegaly

198
Q

cause of childhood onset panhypopituiarism:

A

Usually due to a tumor that destroys the pituitary- especially the somatotrophs

199
Q

Effects of child onset panhypopituitarism:

A

Development rate is greately reduces, though body parts are developed proportionally

They fail to produce gonadotropins, so do not go through puberty

200
Q

What is childhood onset panhypopituitarism treated with?

A

hormone replacement

201
Q

another type of dwarfism is due to:

A

Hereditary inability to form somatomedin

202
Q

cause of adult onset Panhypopituitarism

A

pituitary is damaged by thrombosis of the pituitary blood vessels, or a tumor

203
Q

Effects of adult onself panhypopituitarism

A

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
Q

symptoms of adult onset panhypopituitarism

A 
muscle atrophy
weight gain
feeling unwell
anxiety
loss of motivation
205
Q

Overproduction of GH before plates close

A

Gigantism

206
Q

____% of people with gigantism have diabetes

A

10%

207
Q

Gigantistm is usually caused by:

A

A GH Secreting tumor (may eventually destroy itself, leading to hypopituitarism)

208
Q

Hyposecretion of GH after growth plates close

A

Acromegaly

209
Q

Bones that are most affected for people with acromegaly

A

Intramembranous bones- they are the most capable of continues appostitional growth

210
Q

features of acromegaly

A

enlargement of hands and feet

enlarges cranium, jaw bone, vertebrae (kyphosis)

Enlarged internal organs

Osteoarthritis

211
Q

Other anterior pituitary hormones:

A

PO (related to pregnancy and lactation)
LH and FSH (female reproductive physiology)
TSH-(related to thyroid gland)
ACTH (related to the adrenal gland)

212
Q

posterior pituitary is composed mainly of:

A

pituicytes

213
Q

Pituicytes are ____-like cells that (DO/DO NOT) secrete hormones

A

Glial

do not

214
Q

Pituicytes suppport:

A

the terminal nerve endings of neurosecretory cells from the hypothalamus

215
Q

Neurosecretory cells are found in the

A

Post. Pituitary

216
Q

Neurosecretory cells origin and pathway

A

Originate in the hypothalamus
Pass through the pituitary stalk
Terminate in the posterior pituitary

217
Q

What does the neurosecretory cells secrete?

A

Oxytocin or ADH

218
Q

ADH/Vasopressin is formed mostly in the:

A

supraoptic nuclei

219
Q

Oxytocin is formed mostly in the:

A

Paraventricular nuclei

220
Q

Oxytocin and ADH are carried to the post. pituitary bound to:

How long does this take?

A

neurophysins

Trip takes several days

221
Q

Target tissues of ADH

A

Kidneys
Sweat glands
Arterioles

222
Q

ADH function in kidneys

A

increase reabsorption of water

223
Q

ADH function in sweat glands

A

Reduce water loss through sweat

224
Q

ADH function in arterioles

A

vasoconstriction increases peripheral resistance, therefore pressure (hence other name- vasopressin)

225
Q

What happens when ADH is secreted to the kidneys?

A

water is conserved and urine is more concentrated

226
Q

what happns when ADH is absent/inhibited in the kidneys?

A

Water reabsorption is prevented by collecting tubules and ducts to cause more water loss- leads to more diluted urine

227
Q

What stimulates ADH secretion?

A

Increased extracellular osmolarity

Low blood volume

Low blood pressure

228
Q

What detects increased extracellular fluid osmolarity?

A

Osmoreceptors in the hypothalamus

229
Q

What detects low blood volume?

A

Lack of stretch receptor activation in the right atrium (ADH secretion is inhibited when they ARE stretched)

230
Q

What detects low blood pressure?

A

Baroreceptors in the carotid sinus and aortic artery

231
Q

Roles of Oxytocin in labor:

A

Causes a positive feedback loop to increase uterine contractions
(detected by stretching of the uterus/cervix feeding back to the hypothalamus)

232
Q

Roles of oxytocin in lactation

A

Suckling stimulus by the infant promotes smooth muscle contraction to move milk towards the nipple

233
Q

Psycholgical effects of oxytocin

A

Any kind of bonding- the “love hormone”.

234
Q

The thyroid has how many lobes

A

2

235
Q

Some people have a _____ lobe in the hypothalamus

A

pyramidal

236
Q

where is the thyroid located

A

anterior to the cricoid and upper trachea

237
Q

The thyroid contains:

How large?

A

Thyroid follicles

100-300 microns in diameter

238
Q

Thyroid is lined with what epithelium?

A

cuboidal

239
Q

the thyroid is filled with a secretory substance called:

A

colloid

240
Q

major component of colloid:

A

Thyroglobulin

241
Q

One of the largest proteins in the body.

A storehouse of Iodine and inactive thyroid hormones

A

Thyroglobulin

242
Q

Each molecure of TG (thyroglobulin) contains:

A

about 70 tyrosine amino acids

243
Q

93% of active thyroid hormone

A

Thyroxine (T4)

244
Q

Almost all T4 is converted to ____ in the tissues

A

T3

245
Q

Percentage of T3 secreted as an active thyroid hormone

A

7%

246
Q

T3 is about _____ times (MORE/LESS) potent than T4

A

4 times more

247
Q

Between T3 and T4, what metabolizes faster?

A

T3

248
Q

What is necessary for thyroid hormone synthesis

A

Iodine

249
Q

Iodine is classified as:

A

a micronutrient and dietary mineral

250
Q

How much iodine is required in the diet?

A

50mgs per year (1mg per week)

251
Q

Iodine is transported into _____ _____ ____ via the:

A

thyroid follicle cells

via the NIS (sodium/iodide symporter)- a secondary active transport system

252
Q

Iodine diffuses into the _____ ____ via:

A

follicle lumen via pendrin

253
Q

The NIS pump is _____ dependent

A

TSH

-required for iodide trapping

254
Q

After pendrin pumps iodine into the follicle, what happens next?

A

Iodide is oxydized by peroxidase, which facilitates thyroglobulin sythesis

255
Q

Thyroglobulin precursor is a protein synthesized in the:

it is then secreted into :

A

ER

Follicle lumen

256
Q

What happens to the tyrosines in the thyroglobulin?

A

they become iodinated by 1-2 oxidized iodides.

then they are coupled to form T3 and T4

257
Q

Iondination of the tyrosines within the thyroglobulin is also called

A

organification and coupling

258
Q

thyroid can store a hormone for how long? How is it mostly stored?

A

2-3 months

stored mostly as T4

259
Q

To release thyroid hormones, what happens

A

small amounts of thyroglobulin is pinocytosed into vesicles

fused to lysosomes which break down the thyroglobulin into T3 and T4 and then secreted

260
Q

How are MIT and DIT recycled?

A

by deioninase

261
Q

Thyroid hormones bind to ____ ____ via ___

A

plasma proteins

via TBG (thyroxine binding globulin)

262
Q

Which thyroid hormone acts faster than the other?

A

T3

263
Q

Half life of T3?

T4?

A

T3- 3 days

T4- 7 days

264
Q

Thyroxine is converted to T3 in the tissues by:

A

Iodinase

265
Q

Where is the thyroid receptor located?

A

in the nucleus

266
Q

Thyroid receptors have a high affinity for:

A

T3

267
Q

Thyroid receptors require another protein called”

A

Retinoid X

268
Q

The thyroid receptor/Retinoid X is a:

A

Gene transcription factor

269
Q

New mitochondrial activation may be a direct affect of:

A

Thyroid hormone binding to it or

increase in protein synthesis and their functions increase need for mitochondrial activity

270
Q

Gene transcription/protein synthesis and activity of mitochondria effects:

A

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
Q

Most metabolic process increase with:

A

Thyroid hormones, especially protein synthesis

272
Q

production of catabolic enzymes can also lead to

A

protein degredation

273
Q

Growth is faster with elevated:

A

thyroid hormone levels (though it also causes growth plates to close earlier)

274
Q

Increased production of enzymes for carbohydrate metabolism leads to:

A

Increased insulin and uptake of glucose by cells
Enhanced glycolysis
Enhanced gluconeogenesis
Increased glucose absorption

275
Q

Lipids are metabolized how?

A

from fat stores increasing FFA in the blood

276
Q

Thyroid hormones cause the liver to:

A

increase LDL uptake and secretion of cholesterol in the bile

277
Q

Increased blood flow and cardiac output may be secondary to:

A

the consequences of increased BMR

278
Q

Thyroid hormones affects CVP and GI by:

A

increasing blood flow and cardiac output

increasing heart rate

Increasing respiratory rate

Increasing GI motility

279
Q

Effects of the thyroid stimulating hormone

A

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
Q

TRH increases:

A

TSH secretion

281
Q

TRH release in increased by:

Decreased by:

A

increased by cold

decreased by anxiety and stress, and high cortisol activity

282
Q

TRH and TSH are inhibited by

A

T3 and T4 via negative feedback

283
Q

autoimmune disease where antibodies bind to TSH receptors and mimic TSH causing hypersecretion of T4/T3

A

Grave’s Disease

284
Q

Thyroid cell tumor in which thyroid hormones are overproduces

A

Thyroid adenoma

285
Q

Symptoms of hyperthyroid

A 
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
Q

Endemic goiters

A

Iodide deficiency

287
Q

Where is endemic goiters usually occuring?

A

in regions where there is a lack of iodine in the soil

288
Q

goiter is caused by

A

resulting increase in TSH production; casuing gland hypertrophy

289
Q

Autoimmune destruction of thyroid cells.

antibodies attach to something other than the receptors, causing the thyroid cells to be destroyed

A

Hashimoto thyroiditis (Type of hypothyroidism)

290
Q

Hypothyroidism symptoms

A

Myxedema (excess tissue gel matric deposited- causing non-pitting edema)

Atherosclerosis (accelerated plaque formation in arteries due to sluggish LDL uptake

291
Q

Lack of thyroxine from or before birth

A

Cretinism

292
Q

Potential causes of cretinism

A

could be from lack of thyroid gland or lack of iodine in mother

293
Q

effects of cretinism

A

Severe and irreparable mental defects
stunted growth
reducted growth and function of many organs

294
Q

Enlarged thyroid

A

goiter

295
Q

Causes of goiter

A 
iodine deficiency
selenium deficiency 
autoimmune inflammation
nodules within the thyroid
tumors
Pregnancy/pubery
296
Q

Goiters can compress:

A

the trachea or esophagus making breathing and swallowing difficult

Endo/Repro (4 decks)

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