Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 3 Week 6 > Thyroid Gland Driscoll > Flashcards

Thyroid Gland Driscoll Flashcards

1
Q

What is this:
Located immediately below the larynx
on each side of and anterior to the
trachea

Normally weighs 15-20g in adults

A

thyroid gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What make thryoid hormone?

A

foliicular eptihelial cells of the thyroid gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What line the capillaries and provide blood supply to the follicles.

A

endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

(blank) involved in the production of calcitonin, a hormone involved in calcium metabolism

A

parafollicular or C cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What all are in a thryoid gland?

A 
Follicular cells
endothelial cells
parafollicular cells or C cells
fibroblasts
lymphocytes
adipocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the morphology of the thyroid gland?

A

it is a bunch of closed follicle filled with colloid (thryoglobulin)
lined by epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Thyroid epithelial cells are morphologically and functionally (blank)

A

polarized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Apical surfaces of the thyroid epithelial cells face the (blank).

A

Follicular lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is colloid stored?

A

in the follicular lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The basolaterlal surface of the thyroid eptihelial cell faces the (blank) and is exposed to the bloodstream.

A

interstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

I accumulation and hormone biosynthesis is dependent on (blank)

A

cellular and tissue organization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is this:
93% of total secretion (~80 µg/day)
Most is converted to T3 in the tissues

A

T4 (thyroxine) Tetraiodothryonine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is this:
7% of total secretion (~5 µg/day)
Similar function as thyroxine but ~4x more potent
At lower levels in plasma than T4

A

triiodothyronine (T3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 5 factors involved in thyroid hormone synthesis?

A 
TSH
thryoglobulin
Iodine
Membrane Transporters
Enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

(blank) plays an important role in the synthesis and storage of thyroidhormone

A

Thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

(blank) is a large glycoprotein containing multiple tyrosine residues

A

thryoglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is thyroglobulin synthesized?
Where is it secreted?
Where is it stored?

A

Thyroid follicular epithelial cells
through apical membrane into follicular lumen
Colloids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

(blank) can be considered a scaffold upon which thryoid hormone synthesis take place

A

Thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is iodine important?

A

thryoid hormones need it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

(blank) is the worlds most prevalent, yet easily preventable cause of brain damage.

A

iodine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What takes place in both the collid and follicular epithelial cells?

A

biosyntehsis of thryoid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the first stage of thyroid hormone synthesis and what does it do?
What is it influenced by?

A

step 1: iodide trapping
transport of iodides from the blood into the thyroid cell and follicles (conc. iodide in cell)
TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the mechanism of iodide trapping?

A

Na/I symport (puts iodide into cell)
via Na/K Atpase
Transporters out of cell into follicle lumen via Pendrin (Cl/I countertransporter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Iodide transcellular transport relies on the functional and morphologic (blank) of the cell

A

polarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is iodide more concentrated, inside the thyroid cells or in the blood?

A

30X higher in thyroid cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is stage 2 of thryoid hormone synthesis and what does it do?

A

Formation and secretion of thryoglobulin

Synthesized thyroglobulin in ER and Golgi and putting it into follicular colloid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Thryoglobuin is made up of a bunch of what and does what?

A

tyrosine (140)

Makes thryoid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

(blank) form within the thryoglobin molecule.

A

thryoid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is stage 3 of thryoid hormone synthesis and what does it do?

A

Oxidation of iodide and coupling of iodine w/ thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does Stage 3 happen?

A

iodide gets oxidized by TPO (thyroperoxidase)

Oxidized iodide combines w tyrosine AAs from thyroglobulin molecule (organification of iodide).

20% of tyrosine is iodinated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

After you get to stage 3 of thyroid hormone synthesis you are left with iodinated tyrosine,then what happens?

A

iodination and coupling of iodotyrosine residues to form T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Explain the successive stages of iodination and coupling of iodotyrosine residues to form T3 and T4?

A

1) tyrosine iodized to monoiodotyrosine (MIT)
and then to DIT
2) DIT and DIT= T4
3) DIT and MIT= T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is Reverse T3 and is it important?

A

it is 3,3,5 triiodothyronine instead of T3 which is 3,5,3 triiodothyronine.
No it is not importnant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does TPO (thyroperoxidase) do?

A

oxidates iodide
iodination of tyrosines on thryoglobulin (organification)
synthesis of T4 or T3 from two DIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

If (blank) is blocked or hereditarily absent: rate of formation of thyroid hormones falls to zero

A

TPO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Is goiter present in hypothyroidism or hyperthyroidism?

A

both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

(blank) in the colloid acts as storage form of thyroid hormones

A

Thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Do thyroglobulins contain large amounts of T4 and T3?

A

no small amounts but enough to supply body for 2-3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Where are thyroid hormones located when in storage form?

A

in follicular colloid of thryoglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

If you dont have iodine for a few months are you screwed?

A

no, cuz of the storage of hormones in your follicular colloid of your thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the fourth stage of thyroid hormone synthesis?

A

endocytosis of thryoglobulin and release of thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Explain the mechanism of stage four

A

thryoglobulin enters follicular cell via endocytosis (pseudopodia)
lysosoe fuses with vesicle
thryoglobin is digested (by protease)
T3 and T4 are released into blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Is thyroglobulin released into the blood?

A

nope, just T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is stage five of thyroid hormone synthesis?

A

recycling of iodine for reuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does iodine get recycled?

A

75% of MIT and DIT are not turned into Thyroid hormones, instead the unused MIT and DIT get cleavedby deiodinase in cytosol to make iodine which is reused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

(blank) is an iodine deficiency due to failure of the recycling process

A

Congenital absence of deiodinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

(blank) provide a substantial reservoir of extrathyroidal hormone

A

Plasma Binding proteins

i.e they store thyroid hormones until they need to be used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

In the blood stream what happens to T3 and T4?

A

combine immediately w/ plasma proteins synthesized by the liver
TBG (major)
Transthyretin
Albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

If T3 and T4 doesnt bind to a plasma protein in the blood (1%) what happens?

A

it is free in the circ.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Are binding proteins saturated?

A

no and store 3X the amount secreted per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Do acute changes in hormone secretion have a large effect on free hormone concentrations?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

The binding capacity of plasma proteins for thyroid hormones is far from saturated, an even massive increase in secretion rate would have little effect on the conc. of hormone that is unbound.
T or F?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Changes in binding protein levels alters (Blank) concentrations.

A

thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How can you alter the binding-hormone capacity of an individual?

A

by disease or hormonal changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

If you have high estrogen levels (like in pregnancy), how will this effect your total thyroid hormone levels?

A

high estrogen-> high binding protein synthesis-> new equilibrium b/w free and bound hormone-> increased total thyroid hormones-> dynamic changes occur throughout life of individual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Does the plasma binding proteins for thyroid hormones have a high or low affinity?
What does this tell us?

A

high affinity

That thyroid hormones are released slowly to the tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Which has a longer half life, T3 or T4 and why?

A

T4 because binding proteins have a higher affinity for them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What does the thyroid hormone typically release and what happens to this when it gets to extrathryoidal tissues?

A

mostly is released as T4 but gets deiodinated via deiodinase to T3 in the extrathryoidal tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the most active hormone and the most used hormone by the tissues?

A

T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

The metabolism of T3 and T4 into active and inactive intermediates involves the action of 3 types of (blank)

A

deiodinases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

HOw can thyroid hormones be excreted into bile?

A

can be conjugated to glucuronic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Where do we find deiodinase type I?

A

in the liver, kidney and thyroid

63
Q

Where do we find deiodinase type II?

A

brain, pituitary, thryoid, skeletal and cardiac

64
Q

Where do we find deiodinase type III?

A

brain, placenta, and fetal tissues

65
Q

What deiodinase can catalyze both outer and inner ring deiodination?

A

deiodinase type I

66
Q

What deiodinase has only outer-ring deiodination activity?

A

deiodinase type II

67
Q

What deiodinase has only inner-ring deiodination activity?

A

deiodinase type III

68
Q

what does this:
-T4 ->T3 (major source of circulating T3)
-T4-> reverse T3 (rT3)
-T3 ->T2 (inactive)
(converts everything into a number lower)

A

deiodinase type I

69
Q

What does this:
- T4 ->T3 (and rT3 ->T2)
- major source for local production of T3in tissues
(makes T3)

A

deiodinase type II

70
Q

What does this:
inactivate T3 (so regulates intracellular T3 levels)
Protects placenta (decreases T3 to fetus)
Protects brain action thyroid conc.
i.e keeps T3 levels low

A

deiodinase type III

71
Q

Describe the duration and onset of T4 hormone

A

has a very slow onset like 2-3 days and last for a really long time (like 8 weeks)

72
Q

Describe the duration and onset of T3 hormone

A

has a quick onset (within half a day) and lasts for a few days

73
Q

What do thryotropes of the anterior pituitary gland secrete?

A

TSH (the principal regulator of thryoid synthesis and release)

74
Q

What is the principal regulator of thryoid hormone synthesis and release?

A

TSH

75
Q

Explain how TSH increase thryoid synthesis?

A

TSH binds to Gs receptors in thryoid cells which utilizes GTP to initiate second messenger cascade via cAMP. This increase secretory activity of thyroid glandular cells

76
Q

What are the genomic effects of TSH binding to Gs receptors of the thryoid cells?

A

increased synthesis of iodide pump, thyroglobulin, enzymes involved in T3/T4 synthesis like TPO, Nitric oxide synthase, and local growth factors.
I.e it just promotes the transcription of all things PRO thryoid hormone synthesis :)

77
Q

What does NO do?

A

Aids in vasodilation thus increasing blood flow

78
Q

What do local growth factors do?

A

increase size and number of thryoid cells

79
Q

What happens if you have too many local growth factors?

A

hyperplasia and hypertrophy of gland :(

80
Q

What are the non-genomic effects of TSH binding on thryoid cells?

A

increased proteolysis of thryoglobulinn (release of T3/T4)
increased iodide pump activity
increase iodination of tyrosine

81
Q

What does proteolysis of thryoglobin allow for?

A

they release of T3 and T4

82
Q

What does increase iodide pumping allow for?

A

increased iodide trapping (getting iodide into the cell so we can pump it into the colloid and get it oxidized)

83
Q

What does increased iodination of tyrosine do?

A

it allow for increased synthesis of T3 and T4

84
Q

Explain how in normal circumstances we do not get a build up of thyroid hormones

A

The hypothalamus gets stimulated to release TRH which stimulates anterior pituitary to release TSH which stimulates thryoid cells to secrete thryoid hormones which will inhibit the anterior pituitary and the hypothalamus (so negative feedback inhibition)

85
Q

What is the principal regulator of TSH secretion?

A

TRH :)

86
Q

Increased thyroid hormone in the body fluids (blank) secretion of TSH

A

decreases

87
Q

What does thyroid hormone do to the anterior pituitary?

A

inhibits TSH and TRH receptor synthesis in the pituitary and thus TSH release :)

88
Q

(blank ) receptors are able to bind to DNA and effect the transcription of genes.

A

nuclear

89
Q

What kind of receptors are TRs and how do they work?

A

They are nuclear receptors on tissues that bind T3 and T4 and the utilize these thyroid hormones to bind to response elements on DNA to transcribe new proteins.

90
Q

Upon activation, TRs initiate transcription and thus formation of (blank) which will cause actions on these tissues.

A

proteins

91
Q

What do thyroid hormones do to the CV?

A 
increase CO
increase BF
increase HR
increase heart strength
Increase respiration
92
Q

What will thryoid hormones do to metabolism?

A 
increase mito
increase Na/K atpase
Increase O2 consumption
Increase glucose absorp
increase gluconeogenesis
increase glycogenolysis
increase lipolysis
increase protein synthesis
increase BMR
93
Q

What are the genomic biological effects of thyroid hormones?

A

allows for transcriptional regulation of genes which increase proteins synthesis and increase activity in the body

94
Q

What are the non-genomic effects of thyroid hormones?

A

The regulation of ion channels and oxidative phosphorylation through secondary messengaers (cAMP) and protein kinase signaling cascade
(i.e through signal amplification)

95
Q

What is the site of nongenomic thyroid hormone action?

A

PM, cytoplasm, mito

96
Q

What is the main effect of thyroid hormones?

A

increase activity in the body

97
Q

Why does basal metabolic rate increase up 60-100% above normal and you get hot when large quantities of thyroid hormone is released?

A

because TH increase mitochondria and activate transport of ions (Na/K atpase) and increase synthesis of metabolic proteins which increases oxygen consumption, this will increase your basal metabolic rate and produce heat :)

98
Q

WHen you have increased levels of thyroid hormones what happens to your carbohydrate metabolism?

A

you increase your glucose levels in the blood, sooo increase glucose absorption, increased uptake of glucose from cells

99
Q

When you have increased levels of thyroid hormones what happens to your lipid metabolism?

A

mobilize lipids to FA in plasma and increasing FA oxidation and you need cholesterol to be broken down so you increase the uptake of it in LDL receptors thus lowering plasma levels of cholesterol
I.e increase FA levels in plasma, reduce cholesterol levels in plasma

100
Q

When you have increased levels of thryoid hormone what happens to your nitrogen metabolism?

A

Increased protein synthesis and degradation, degredation wins out

101
Q

What is the overall effect of thyroid hormone on metabolism?

A

increased mobilization of carbs, proteins, and fats and increased BMR and oxygen consumptions

102
Q

Plasma concentration of cholesterol is (blank) correlated with thryoid hormone levels. With this information how could you diagnosis hypothyroidism?

A

inversely

increased

103
Q

How come when you have increased TH you need more vitamins? So clinically, why is this significant?

A

TH increases synthesis of proteins which often requires vitamins, thus you need more.
Hyperthyroidism could lead to vitamin deficiency

104
Q

If you have increased thryoid hormone then you will usually have (blank) weight
If you have decreased thryoid hormone then you will usually have (blank) weight

A

low

high

105
Q

Sometimes when you have increased thyroid hormone you wont lose weight, why is that?

A

because increased thryoid hormone makes you hungry and can occasionally counterbalance the effects of increased basal metabolic rate

106
Q

When can growth retardation occur?

A

if you have thyroid hormone deficiency

107
Q

What is absolutely dependent on thyroid hormone in perinatal development?

A

CNS development

108
Q

What all does TH do for the CNS during development?

A

cerebral and cerebellar growth, myelinzation, vascularization, axonal and dendritic density, cell migration, and differentiation

109
Q

Fun fact, thyroid hormone controls the transformation of a (blank) into a frog

A

tad pole :))))))

110
Q

Explain why thyroid hormone increases blood flow and cardiac output?

A

TH causes increased oxygen consumption and metabolic end products and a need for heat elimination thus vasodilation occurs

111
Q

How does TH increase heart rate?

A

it directly increase b adrenergic receptors

112
Q

How does TH increase heart strength?

A

Cardiac contractility depends on the relative ratio of different types of myosin proteins in cardiac muscle. Transcription of some myosin genes is stimulated by thyroid hormones, while transcription of others in inhibited. The net effect is to alter the ratio toward increased contractility.

113
Q

What will T3 do to arterial pressure?

A

will increase HR, CO, SV and systolic BP

will decrease PVR, diastolic BP

114
Q

What happens to heart strength if there are extremely high levels of TH?

A

the heart strength becomes depressed because of increased protein catabolism

115
Q

Explain the effects of T3 on cardiovascular hemodynamics

A

T3 causes the need for heat elimation which will cause the systemic vascular resistance to decrease through the release of NO, this will cause the diastolic BP to drop and thus decreases the MAP, this decrease in MAP will be sensed by the JGcs of the kidney which will cause an increase in sodium reabsorption and thus an increase in ECF volume which will increase preload, meanwhile the decreased diastolic blood pressure has led to decreased afterload. With this increased preload and decreased afterload, T3 also stimulates increased contractility and HR which in the end increase CO.

116
Q

How does TH effect respiration?

A

increased rate of metabolism leads to increased rate and depth of breathing

117
Q

How does TH effect GI motility?

A

Increased TH leads to increased hunger and food intake which will increase digestive enzymes and thus motility and bowel movements

118
Q

If you have hypothyroidism how will your bowel movements be?

A

you will be constipated

119
Q

How does TH effect sleep?

A

Be super tired cause your metabolism exhausts your musculature and CNS

120
Q

If you have hyperthryoidism how will you be activity wise?

If you have hypothryoidism how will you be activity wise?

A 
Constant tiredness but have trouble sleeping
extreme somnolence (sleepiness)
121
Q

One of the most characteristic signs of hyperthyroidism is a (blank)

A

fine muscle tremor

122
Q

How does TH affect the CNS?
For hyperthyroidism?
For hypothyroidism?

A

excitatory effects
nervousness and psychoneurotic tendencies
lack of energy, slow speech, dulled mental capacity

123
Q

How does TH affect the ANS?

A

amplifies sympathetic stimulation via increase Beta adrenergic receptors and upregulation of Gs and down regulation of Gi

124
Q

How does Th Affect the pancreas?

A

Increased insulin secretion due to increased TH which leads to increased glucose concentration

125
Q

How does TH affect the pituitary?

A

regulates synthesis of pituitary hormones via stimulation of GH and inhibition of TSH

126
Q

What is primary hyperthyroidism?

A

it is where the thyroid gland (on its on) produces too much thyroid hormone

127
Q

How can you get primary hyperthyroidism?

A
  • **Via antibodies binding to Thyroid hormone receptors (graves disease, autoimminue)
  • **Via hyperfunctioning thyroid nodules (low TSH levels)
  • **Therapy induced hyperthyroidism
  • **Thyroiditis (thyroid hormone leaks into blood stream)
128
Q

How can you get secondary hyperthyroidism?

A 
Pituitary tumor (have high TSH, and T4 and T3)
*** Cant suppress TSH despite high levels of free thyroid hormone)
129
Q

What is a goiter?

A

an enlarged thyroid gland

130
Q

Explain the mechanism of Grave’s Disease. What will your thyroid hormone levels be and what will your TSH levels be?

A

There are antibodies that bind to thyroid hormone receptors and stimulates prolonged release of thyroid hormones.
Thyroid hormone levels will be high and your TSH levels will be low (cuz thyroid hormone inhibits the TSH but your thryoid gland doesnt care cuz it doesnt need TSH anyway to secrete TH cuz its got antibodies baby)

131
Q

What are these symptoms of:

goiter, pretibial myxedema, graves opthalmopathy

A

Graves disease

132
Q

If you have goiter, pretibial myxedema or graves opthalmopathy will you you have graves disease?

A

not necessarily

133
Q

Why do you get enlargement of thryoid gland when you have thryoid problems?

A

because of hypertrophy and hyperplasia and decreased colloid volume

134
Q

What is a specific form of cutaneous and dermal edema secondary to increase deposition of connective tissue components?

A

Myexdema

135
Q

is it common to see chronic pretibial myxedema (thyroid dermopathy) in graves diseaes?

A

no it is rare

136
Q

Why do people with graves disease have protruding eyeballs (exopthalmos)?

A

Cuz the antibodies in graves disease causes edema behind the eye and degrades the muscles in the eye

137
Q

What is the thryoid stare and why does it occur?

A

Cuz of graves disease and its antibodies making edema in the back of your eye and decaying the muscle there,
The stare is the inability to look where you want to and getting pressure behind the eye and double vision sometimes

138
Q

Why can you get irritation/ulceration of the cornea in graves disease?

A

inability to close your eyes completely

139
Q 
What are these signs and symptoms of?
high state of excitability
intolerance to heat
increased sweating
mild to extreme weight loss
increase frequency of bowel movements
muscle weakness
nervousness or other pyschic disorders
extreme fatigue but inability to sleep
tremor of the hands (due to increased sympathetic activity)
A

Hyperthyroidism

140
Q

What is ONLY found in graves disease and not other types of hyperthyroidism?

A

lid retraction
lid lag
pretibial myxoedema

141
Q

What are the 6 you can get primary hypothyroidism?

A 
Hashimotos disease (autoimmune)
Cretinism (congenital defect)
Edemic Colloid Goiter (dietary iodine deficiency)
Inherited defects of hormone synthesis
Treatments for hyperthyroidism
Thyroid surgery and radiation therapy
142
Q

What are some ways you can get secondary hypothyroidism?

A

Problems with anterior pituitary or hypothalamus

Lack of stimulation of TSH receptor due to impaired TSH release (low level of TSH, T4 and T3)

143
Q

Explain how hashimotos disease works

A

Body makes antibodies against thyroglobulin, thryoperoxidase and TSH receptors and blocks these and results in thyroidistis where the gland deterioriates.

144
Q

What are the levels of T4 and T3 and TSH in hashimotos disease?

A

Low T4 and T3 and high TSH

145
Q

How does someone get an endemic colloid goter?

A

dietary iodine deficiency

146
Q

What is congenital hypothyroidism called?

A

cretinism

147
Q

What are the levels of TSH, T4 and T3 in secondary hypothyroidism?

A

low TSH, T4 and T3

148
Q 
What are these symptoms of:
fatigue
muscle sluggishness
slow heart rate and decreased CO
weight gain
constipation
mental sluggishness
myxedema (generalized)
intolerance to cold
hoarseness
goiter (often nodular due to TSH stimulation of a healthy area)
hypercholesterolemia (due to decreased secretion of cholesterol by liver)
A

hypothyroidism

149
Q

How do thyrocytes get destroyed?

A

activation of cytotoxic T cells

150
Q

How do you get endemic colloid goiter?

A

iodide deficiency causes increased TSH stimulation and increased Thyroglobulin in colloid\
(i.e. high TSH causes goiter)

151
Q

What are some ways you can get goiter?

A

high TSH levels due to iodide deficiency:

  • deficient iodide trapping
  • deficient peroxidase system (iodide doesnt get oxidized)
  • deficient coupling of iodine to tyrosine
  • deficient deiodinase enzyme-> lack of iodine recovery
152
Q

Explain cretinism

A

congenital hypothyroidism due to lack of thryoid gland or dietary iodide insufficency

153
Q 
What is this:
neonate may have normal appearance and function (maternal thyroid hormones)
Symptoms appear a few weeks after birth:
sluggish movements, retarded physical 
and mental development
A

cretinism

154
Q

Why is it important to catch cretinism early?

How do you treat it?

A

if you wait too long, mental retardation can occur
(skeletal growth more inhibited than soft tissue)
Thryoxine or iodide replacement

Block 3 Week 6 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions