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Physiology > ENDO 3 > Flashcards

ENDO 3 Flashcards

1
Q

About 93 % of the active hormones

secreted by the thyroid gland is — while on 7 % is —

A

Thyroxine (T4)

Triiodothyronine (T3)

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2
Q

is T3 or T4 more potent?

A

T3

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3
Q

Thyroid hormones impact (2). They also
have permission action on
—

A

metabolism and growth/development

catecholamines

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4
Q

Calcitonin

decreases

A

plasma

calcium

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5
Q

— is Required for Thyroid
Hormone Synthesis so Thyroid Follicular
Cells Actively Transport —
obtained from the diet.

A

Iodine (I2)

Iodide (I-)

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6
Q 
Na+/I– 
symporter (NIS)  
is capable of 
producing 
intracellular I– 
concentrations 
that are ---
times as great 
as the 
concentration 
in plasma.
A

20–40

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7
Q 
Iodide must also exit 
the thyrocyte across 
the apical membrane 
to access the colloid, 
where the initial 
steps of thyroid 
hormone synthesis 
occur. --- is a Cl
–/I– exchanger.
A

Pendrin

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8
Q

T3 and T4 Secretion into Blood (4 steps)

A
  1. Colloid is internalized by endocytosis.
  2. The vesicles fuse with lysosomes in the cell.
  3. Proteases cleave T3 and T4 from TG.
  4. T3 and T4 diffuse out of the cell and into
    capillaries.
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9
Q

Colloid is a reservoir

of

A 
thyroid hormones. 
“Humans can ingest a 
diet completely 
devoid of iodide (I-)for 
up to 2 months before 
a decline in circulating 
thyroid hormone 
levels is seen"
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10
Q

~99% of T3 and T4 bind with plasma proteins for transport: (3)

A
  • Thyroxine-Binding Globulin (TBG), Transthyretin (TTR), Albumin
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11
Q

Due to the strength of its binding to the transport protein, – has a long
half-life (6-7 days).

A

T4

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12
Q

– doesn’t bind as tightly so its half-life is only 2-3 days.

A

T3

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13
Q

Target cells make active T3 by using enzymes called — that remove an iodine from T4.

A

Deiodinases/Iodinases

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14
Q

Individual target cells can alter their exposure to T3 by regulating their

A

tissue Deiodinase

synthesis.

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15
Q

There are three different Deiodinases (D1, D2, D3). All contain the
rare amino acid —, with — in place of sulfur,
which is essential for their enzymatic activity.

A

selenocysteine

selenium (Se)

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16
Q

SKIPPED:

Various conditions inhibit Deiodinase activity:

A

selenium deficiency,
burns, trauma, advanced cancer, cirrhosis, chronic kidney disease,
MI and febrile states, fasting, stress. Could show signs of
hypothyroidism.

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17
Q

T3 actions occur sooner
(than T4) with the
maximum activity

A

~2-3

days.

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18
Q

Negative feedback: mainly at the

level of

A

anterior pituitary gland

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19
Q

– is the main circulating form;
responsible for most of the (-)
feedback

A

T4

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20
Q

TSH secretion is

A

pulsatile (note the stars
below that show pulses). Output starts to rise
at about 9:00 PM, peaks at midnight, and then
declines during the day.

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21
Q

Effects of Thyroid Hormone on Metabolism (5)

A
  • Stimulates oxygen consumption by most metabolically active tissues.
  • Increased Basal Metabolic Rate (BMR)
  • Stimulates carbohydrate metabolism tract
  • Stimulates protein catabolism & synthesis
  • Stimulates fat metabolism
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22
Q

Stimulates carbohydrate metabolism (3)

A

– Causes uptake of glucose by cells
– Enhances glycolysis & gluconeogenesis
– Increases rate of CHO absorption from G.I.
tract

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23
Q

Stimulates fat metabolism (3)

A

– Increases lipid mobilization & oxidation of fatty acids by cells
– Required to convert beta carotene to vitamin A (Hypothyroid patients have yellowish skin)
– Decreases circulating cholesterol levels (Hypothyroidism associated with hyperlipidemia)

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24
Q

Other Effects of Thyroid Hormones

NS: (5)

A 
• Needed for normal development 
of the NS 
• Impacts reflex time (i.e. 
hypothyroidism can cause 
prolonged reflex times)
• Muscle tremors due to increased 
reactivity of neuronal synapses
• Feeling of tiredness but difficulty 
sleeping
• Anxiety, worry and paranoia
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25
Q

Other Effects of Thyroid Hormones

ES: (3)

A 
• Increased glucose consumption 
results in increased insulin 
secretion being needed to 
maintain blood glucose levels
• Activation of bone formation 
causes a need for increased 
PTH secretion
• Causes increased inactivation of 
glucocorticoids which leads to 
more ACTH release
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26
Q 
Other Effects of Thyroid Hormones
Cardiovascular System (2)
A

• Increased expression of β-
adrenergic receptors
• Increased blood flow, heart
rate, and heart contractility.

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27
Q

Other Effects of Thyroid Hormones

GI: (2)

A 
• Increased appetite and food intake
• Increased rate of secretion and 
motility of the GI tract (i.e. 
hypothyroidism can produce 
constipation)
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28
Q

Goiter is

A

an enlarged thyroid that does not indicate

functional status.

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29
Q

Goiter is seen in (3)

A

Hypothyroidism, Hyperthyroidism, Euthyroidism

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30
Q

Goiter caused by excessive amounts of – secretion.

A

TSH

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31
Q

High TSH stimulates thyroid to secrete large amounts of

thyroglobulin colloid into follicles, resulting in

A

gland

enlargement

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32
Q

—is the most common form

of hyperthyroidism

A

Graves’ Disease

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33
Q

Hyperthyroidism can also occur due to a

A

thyroid

adenoma.

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34
Q

Graves’ Disease

A

An autoimmune disease where antibodies
to TSH receptor called thyroid-
stimulating immunoglobulins (TSIs)
stimulate the thyroid gland to excess

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35
Q

TSI antibodies have prolonged stimulating

effect on thyroid gland, lasting as much as

A

12 hours, in contrast to TSH of ~1 hour

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36
Q 
High levels of thyroid hormone secretion 
caused by (2)
A 
TSI suppress anterior pituitary 
TSH secretion (negative feedback)
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37
Q

Treatment of Hyperthyroidism (3)

A 
• Radioactive I 131 thyroid 
ablation, or Antithyroid Drugs 
(propylthiouracil or 
methimazole).          
– Surgery rarely indicated.
• Propanolol (b blocker) given 
for adrenergic symptoms while 
awaiting resolution. 
• L-thyroxine administered to 
prevent hypothyroidism in 
patients who have undergone 
ablation or surgery
38
Q

Hyperthyroidism Oral Symptoms (5)

A
  • Burning Mouth Syndrome
  • Gum disease
  • Excessive salivation
  • Weakening of mandible
  • Increased caries risk
39
Q

Burning Mouth Syndrome is more common in

A

women ?50

40
Q

Thyroid Storm (Thyrotoxicosis)

A

Elevated Thyroid Hormone with stressful events (trauma, surgery,
severe emotional distress) or serious illness (DKA, MI, etc.).

41
Q 
Thyroid Storm (Thyrotoxicosis)
symptoms:
A

fever, tachycardia, elevated BP, nausea, vomiting,

diarrhea, breathing problems, etc.

42
Q

In patients with hyperthyroidism or those that exhibit
signs/symptoms of it, administration of – is
contraindicated and elective dental care should be deferred.

A

epinephrine

43
Q

Hashimoto’s Thyroiditis

A

• Autoimmune reaction against thyroid gland destroys

gland rather than stimulating it.

44
Q

Most common cause of hypothyroidism

A

Hashimoto’s Thyroiditis

45
Q

Hashimoto’s Thyroiditis

Most patients first exhibit autoimmune

A

“thyroiditis,”

thyroid inflammation

46
Q

Hashimoto’s Thyroiditis

Inflammation leads to fibrosis of thyroid resulting in

A

decreased secretion of thyroid hormone.

47
Q

Hypothyroidism due to low —

A

iodine

48
Q

In hypothyroid states:
Goiter: — deficiency
No goiter: — deficiency

A

iodine

TSH

49
Q

Myxedema

• Seen in severely

A

hypothyroid patients

50
Q

Myxedema

A 
Increased quantities of 
hyaluronic acid and 
chondroitin sulfate bound 
with protein plus water 
accumulate in skin.
51
Q

Other characteristics of

hypothyroidism:

A 
low BMR, 
mental capacity, body 
temp., appetite, HR, RR, 
BP; anemia, weakness, 
lethargy, wt. gain; increased 
cholesterol and blood lipids
52
Q

Myxedema tx

A

thyroxine (T4)

53
Q

SKIPPED

Early symptoms of myxedema are

A 
fatigue, lethargy, cold intolerance, 
constipation, stiffness and 
cramping of muscles, carpal tunnel 
syndrome, menorrhagia, slowing of 
intellectual and motor activity, 
decline in appetite, increase in 
weight, and deepening of voice.
There is a dull, expressionless 
facies, with puffiness of eyelids. 
Skin appears swollen, cool, waxy, 
dry, coarse, and pale with 
increased skin creases.
54
Q

Cretinism

A

• Thyroid hormones required for

postnatal brain maturation.

55
Q

Cretinism

Results from: (2)

A 
– Congenital absence of thyroid gland 
(congenital cretinism)
– Iodine deficient diet (endemic 
cretinism): most common cause 
worldwide
56
Q

Cretinism causes

A

physical and mental

retardation of neonates

57
Q

in Cretinism, skeletal growth is more inhibited than

A

soft tissue growth (obese,
stocky and short with large
protruding tongue)

58
Q

Hypothyroidism Oral Manifestations (6)

A

• Macroglossia
• Dysgeusia
• Delayed tooth eruption
• Poor wound healing and increased risk of infection
(due to decreased activity of fibroblasts)
• Increased periodontal disease
• Salivary gland enlargement

59
Q

Patients with hypothyroidism are sensitive to (2), so these medications should be
used sparingly

A

central nervous

system depressants and barbiturates

60
Q

phosphate storage
85%
14-15%
1%

A

85% bones,
14-15% in cells
less than 1% in the EC fluid (HPO42- and H2PO4-)

61
Q

Changes in the phosphate level of the EC fluid to –X normal does not
cause major immediate effects.

A

2-3

62
Q

Only 0.1% of total body — is in the
EC fluid. 1% is in cells and organelles and the
rest is stored in bones. Free calcium is tightly
regulated (5%)

A

CALCIUM

63
Q

Calcium:
– Too low =
– Too high =

A

– Too low = neuronal hyper-excitability (tetany)

– Too high = neuronal depression

64
Q

Control points for calcium and phosphate (3)

A
  1. Absorption – via intestines
  2. Excretion – via urine (calcium and phosphate) and feces (calcium only)
  3. Temporary storage – via bones (hydroxyapatite) Ca10 (PO4)6 (OH)2
65
Q

Parathyroid Hormone (PTH) (4)

A

• increase Plasma Calcium and decrease Phosphate
– Mobilizes calcium from bone
– Enhances renal reabsorption of calcium
– Increases intestinal absorption of calcium (indirectly)

66
Q

Calcitriol (1,25-dihydroxycholecalciferol or vitamin D3) (2)

A

• increase Plasma Calcium and increase Phosphate
– Calcitriol is the primary hormone that enhances intestinal absorption of
calcium and it also causes absorption of phosphate.

67
Q

Calcitonin (from the Parafollicular cells of the thyroid

gland) (2)

A

• decrease Plasma Calcium and decrease Phosphate 21
Bone formation is stimulated by Calcitonin, Insulin, GH,
IGF-1, Estrogen and Testosterone

68
Q

Vitamin D3 & Parathyroid Hormone

Stimulate

A

Bone Matrix Resorption increase plasma calcium

69
Q

Calcitonin Stimulates

A

Bone Matrix Deposition & Inhibits Osteoclasts

decreases plasma calcium

70
Q

— affects almost 10 million individuals in the US, though only a small
proportion are diagnosed and treated. It occurs when there is an imbalance between
bone formation and resorption.

A

Osteoporosis

71
Q

Osteoporosis risk factors

A

vitamin D deficiency (secondary hyperparathyroidism),
inadequate calcium intake (secondary hyperPTH),
glucocorticoid medications,
reduced physical activity,
estrogen deficiency (post-menopausal),
cigarette smoking, alcohol, etc.

72
Q

Treatments for Osteoporosis (6)

A 
• Exercise (walking and weight-
bearing 3X per week)
• Physical Therapy (postural 
exercises, muscle strengthening)
• Estrogen (replacement or 
receptor agonists)
• Calcium (carbonate or citrate)
• Vitamin D
• Bisphosphonates
73
Q

Parathyroid Glands

A

Four pea-sized glands on the posterior

surface of the thyroid gland.

74
Q 
Parathyroid Hormone (PTH)
• Secreted by the
A

Chief Cells

75
Q

PTH:
• increase plasma calcium by (3)
• decrease plasma phosphate by (1)

A

(1) increase Intestinal Absorption,
(2) decrease Renal Excretion and
(3) increase Bone resorption.

(1) increase Renal Excretion

76
Q

↓ ECF Ca2+ concentration

A 
increase rate of PTH secretion
hypertrophy of 
parathyroid gland
o Pregnancy
o Rickets
o Lactation
77
Q

increase ECF Ca2+ concentration

A

↓ activity of parathyroid gland
↓ size of parathyroid gland
o increased vitamin D intake
o excess quantities of calcium in the diet
o bone resorption caused by factors other than PTH

78
Q

Increases Plasma Calcium (3)

A
  1. Bone Resorption
  2. Reabsorption of Calcium
    by Renal Tubules which
    reduces excretion
  3. Converts 25-
    hydroxycholecalciferol to
    1,25-
    dihydroxycholecalciferol
    (Vitamin D/Calcitriol),
    which causes intestinal
    calcium absorption.
79
Q

Decrease Plasma Phosphate (1)

A
  1. Decreased reabsorption
    by renal tubules leading
    to increased urinary
    excretion
80
Q

Calcitonin

A 
Peptide hormone 
secreted by  
parafollicular cells   
(C cells) of the 
thyroid gland
81
Q

Calcitonin is released in response to

A

elevated

free plasma Ca2+

82
Q

Calcitonin lowers

A 
plasma Ca2+ 
by decreasing 
activity of 
osteoclasts, thus 
decreasing bone 
resorption
83
Q

Calcitonin: not a major controller of – in humans

A

calcium

84
Q

Primary Hyperparathyroidism

A

Excess PTH secretion due
to a parathyroid gland
tumor

85
Q

Extreme osteoclastic
activity in bones causes
cystic bone disease
(osteitis fibrosa cystica) (4)

A 
– Hypercalcemia leads to 
polyuria and calcuria
– Low phosphate due to 
increased renal excretion
– Muscle weakness and 
easy fatigability
– Osteoblastic activity also 
increased leading to high 
secretion of alkaline 
phosphatase (ALP).
86
Q

Secondary Hyperparathyroidism

A

• High PTH levels occur as compensation for hypocalcemia

not due to primary abnormality of parathyroid glands

87
Q

Causes of hypocalcemia: (2)

A

– Vitamin D deficiency

– Chronic renal disease-cannot synthesize Vit D3

88
Q

Vitamin D deficiency leads to — in children,
— in adults [inadequate mineralization of
bones] and high PTH, which causes bone resorption. High
PTH is a risk factor for osteoporosis and fractures.

A

rickets

osteomalacia

89
Q

Primary Hypoparathyroidism:

Less common-often results from accidental

A

surgical

parathyroid gland removal

90
Q

Parathyroid gland removal decreases plasma Ca++

levels from – to –

A

10 mg/dL to 6-7 mg/dL

91
Q

Hypocalcemia increases membrane Na+

permeability leading to (3)

A

neuromuscular excitability &

muscle spasms & tetany

92
Q

Spasm of laryngeal muscles obstructs respiration

causing — unless appropriate treatment applied

A

death

Physiology (53 decks)

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