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Thompson- spring > Thyroid and and Parathyroid Function > Flashcards

Thyroid and and Parathyroid Function Flashcards

1
Q

What’s a Positive Feedback Loop?

A

Positive Feedback Loop – increase in one action triggers increase in target​

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2
Q

Example of a (+) Feedback Loop

A

Childbirth contractions trigger oxytocin, which in turn amplifies the contractions​

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3
Q

What’s a Negative Feedback Loop?

A

Negative Feedback Loop – response is opposite to the perturbation​
​

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4
Q

Example of a (-) Feedback Loop

A

Pituitary TSH and thyroid T4

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5
Q

What are the glands responsible for regulating the activity of the Thyroid?

A

Hypothalamus and pituitary regulate thyroid, as well as intrinsic regulation by the gland itself​

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6
Q

How does Hypothalamus and Pituitary regulate Thyroid activity?

A

Hypothalamus produces thyroid releasing hormone (TRH), which acts on anterior pituitary​

Thyroid stimulating hormone (TSH) released by anterior pituitary into blood stream​

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7
Q

What are the 3 thyroid hormones?

A

Triiodothyronine (T3)​
Thyroxine (T4)​
Calcitonin​ (Weak effect on calcium-phosphorus balance​)

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8
Q

Function of T3 and T4 (2)

A

T3 and T4

  • regulate metabolic rate of body
  • increase protein synthesis​
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9
Q

What is Calcitonin’s function?

A

Weak effect on calcium-phosphorus balance​

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10
Q

Name 2 routes that aid in Thyroid stimulation:

A

Vascular supply (iodine) and Sympathetic nervous system​

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11
Q

Trace the mechanism of Thyroid stimulation (negative loop) from the Iodine in the blood stream to the TRH from the hypothalamus.

A

Iodine traveling in blood (from diet) absorbed into thyroid follicle cell to combine with Thyroglobulin (TGB) to form T3 and T4 (thyroid hormones)​

Stimulated by TSH released by anterior pituitary into blood stream​

Stimulated initially by hypothalamus TRH​

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12
Q

What’s the best stimulus for TRH?

A

Exposure to cold

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13
Q

What’s the end result of the Thyroid negative feedback loop?

A

Negative feedback loop control​

T3 and T4 in circulation limit production​

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14
Q

Name 4 major actions of T3 and T4.

A
  1. Enter cell and bind with receptors in nucleus​
    DNA stimulated for gene expression​
    Altered protein synthesis within cells​
  2. Brain growth and development​
  3. Bone growth and development​
  4. Function of metabolism, cardiac system, heat production, glucose and fat metabolism​
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15
Q

What are the 3 main functions of the Thyroid?

A

Metabolism, growth, and development​

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16
Q

Explain how is Thyroid involved in metabolism?

A

Increase thermogenesis
Basal metabolic rate and heat production​

Metabolic effect- Energy substrate utilization​
Glucose absorption and enzyme enhancement​
Lipolysis and lipolytic hormone use​
​

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17
Q

Explain how is Thyroid involved in growth and development?

A

Growth and development

Stimulate GH release and enhanced effects​

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18
Q

What is the cardiovascular effect of Thyroid activity?

A

Cardiovascular effects:
Increase HR and contractility possibly by enhancing effect of epi and norepi​ (release by the medulla of adrenal glands)

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19
Q

What are some confounding variables when trying to diagnose Thyroid dysfunction at an older age?

A

After age 60, thyroid may be mistaken for dementia, depression, heart disease​

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20
Q

Name 3 risk factors for Thyroid dysfunction

A

family history
age (>50)
gender (female)​

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21
Q

Name a few effects of alterations in Thyroid functioning

A

Alterations in thyroid can produce changes in hair, nails, skin, eyes, GI, respiratory tract, cardiovascular, neuromuscular, musculoskeletal systems – virtually everything​

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22
Q

What test diagnoses thyroid dysfunction​?

A

TSH (thyroid stimulating hormone) test

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23
Q

What is the normal range of TSH?

A

0.5 - 4.70 µIU/mL​

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24
Q

Name 8 sets of characteristics specific to hypothyroidism

A

Fatigue, feeling run down or tired, difficulty concentrating, depression, slowed heart beats

Non tender swelling around the neck

Muscle cramps, muscle weakness

weight gain

dry, coarse itchy skin
dry, coarse thinning hair

intolerance to cold especially in the hands and feet

increased menstrual flow, irregular periods, infertility / miscarriage

constipation

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25
Q

Name 8 sets of characteristics specific to hyperthyroidism

A

Nervousness, irritability, restlessness, increased perspiration, palpitation, insomnia, heart racing, panic

Non tender swelling around the neck

Muscular weakness and tremor especially the upper arms and thighs. In later Grave’s disease eyes may bulge

weight loss

thinning skin
fine and brittle hair

intolerance to heat

less frequent periods with lighter flow

frequent bowel movements

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26
Q

Describe hormonal levels in hypothyroidism

A

High TSH, low T3, T4

Antibodies to TPO in Hashimoto’s thyroiditis

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27
Q

Describe hormonal levels in hyperthyroidism

A

Low TSH, High T3, T4

Antibodies to TSH receptors in Grave’s disease

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28
Q

Goiter ………..

A

Goiter, enlargement commonly due to lack of iodine in diet​

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29
Q

Describe the feedback loop present in goiter in relation to dietary lack of iodine

A

Inhibits normal thyroid hormone production, causing hypersecretion of TSH due to lack of negative feedback loop​
Almost eradicated in US due to iodized salt​

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30
Q

clinical presentation of goiter

A

Would see increased neck size, pressure on trachea and esophagus, dysphagia, hoarseness, difficulty breathing​

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31
Q

true/false “ Goiter is a hyperthyroidism​ condition or manifestation “

A

False

“goiter” term also applied to any enlargement, so can be hypo- or hyperthyroidism​

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32
Q

What’s thyroidits?

A

Thyroiditis – inflammation of thyroid gland​

​

33
Q

Clinical presentation of thyroiditis

A

Painless thyroid enlargement, dysphagia, “tightness,” non-mechanical upper quarter pain, swollen gland, symptoms of hypothyroidism​

34
Q

True/false “ Thyroiditis is an exclusively endocrine disorder”

A

May be from infection, autoimmune disorder

35
Q

some facts about Hashimoto’s thyroiditis

A

Hashimoto’s thyroiditis – seen more often in women in the 30-50 y.o. age group, can destroy the thyroid and result in hypothyroidism​

36
Q

Common name of Hyperthyroidism (thyrotoxicosis)

A

Graves’ disease – enlargement of the gland, protruding eyes, inflammation of ocular muscles​
May first be picked up by optometrist​

37
Q

Three common signs of Grave’s disease:

A

tachycardia, fatigue, weight loss​

38
Q

Other s/s of Grave’s disease

A

hyperactive reflexes, sweating, heat intolerance, tremor, nervousness, polydipsia, dyspnea​

39
Q

Associated clinical presentations with Grave’s disease

A

Chronic periarthritis and calcific arthritis, usually in shoulder​

Proximal muscle weakness, usually resolves with treatment​

May see myasthenia gravis as a complication (defect in neuromuscular junction, Ach transmission)​

40
Q

What’s the most common Hyperthyroid Treatment​?

A

Typically thyroidectomy​

41
Q

other 3 treatment for hyperthyroidism excepting thyroidectomy

+ one adjunct treatment

A

Antithyroid agents
Iodide
Radioactive Iodine
Beta-Adrenergic Blockers (adjunct)

42
Q

what are antithyroid agents?

A

Antithyroid agents –drugs to inhibit thyroid hormone synthesis​

43
Q

How does Iodide and Radioactive Iodine work in treatment of hyperthyroidism?

A

Iodide-inhibit thyroid hormone biosynthesis (short term, 2 weeks)​

Radioactive Iodine- selectively destroy thyroid tissue​
Cancer and Graves treatment, requires monitoring of parathyroid function​

44
Q

How are Beta-Adrenergic Blockers used in treatment of Hyperthyroidism?

A

Beta-Adrenergic Blockers for symptom suppression (tachycardia, restlessness, palpitations) - adjunct to primary treatment​

45
Q

What brings on a thyroid storm?

A

Usually seen in undiagnosed thyroid disease, or precipitated by trauma, surgery, infection​

46
Q

Clinical presentation of a thyroid storm:

A

Hypermetabolism, with severe tachycardia, heart failure, shock, hyperthermia (105° F)

47
Q

Do you do PT with a patient immediately after a thyroid Storm?

A

NO

48
Q

True/False

Hypothyroidism is more common than hyperthyroidism​

A

True

49
Q

General presentation of Hypothyroidism

A

Insufficient hormone production, generalized depression of metabolism​
If present in fetal development, usually results in cretinism​ - congenital birth defect

50
Q

Name the 2 types of Hypothyroidism and briefly describe the mechanism

A

Primary – reduced function of thyroid tissue or impaired hormonal synthesis​

Secondary (less common) – impaired due to pituitary dysfunction​

51
Q

Hypothyroidism- rate of occurrence (age, sex)

A

Women 10X more likely than men, increasing with age​

52
Q

Name one other cause of hypothyroidism ( not primarily hormonal)

A

May also be caused by medications (lithium, amiodarone)​

53
Q

One obvious clinical presentation of Hypothyroidism

A

Ichthyosis – dry, scaly skin​

more in table 11-5

54
Q

S/S of Myxedema (form of Hypothyroidism)

A

​connective tissue changes due to increased mucopolysaccharides and proteins, causing a boggy, pitting edema in eyes, hands, feet, supraclavicular area;

thickening of tongue and oropharyngeal complex, with slurred speech​

Dense, viscous synovial fluid – “bulge sign” at knee​

Calcium crystals, chondrocalcinosis​

55
Q

Clinical presentation of Myxedema / associated conditions:

A

Flexor tenosynovitis, CTS​

Pain and proximal muscle weakness​

May have a prolonged DTR due to slow muscle contraction​

TrPs, diffuse aches and cramps​

56
Q

Medical and therapeutic interventions for Myxedema

A

Proper treatment of thyroid and soft tissue work, strengthening​

57
Q

True/ False

Thyroid Neoplasm is relatively rare and slow-growing​

A

True

58
Q

Thyroid Neoplasm Prevalence

A

Caucasian females over 40​

59
Q

S/S of Thyroid Neoplasm

A 
Asymptomatic nodules in thyroid,
hoarseness, 
hemoptysis, 
dyspnea, 
elevated BP​
60
Q

Two type of treatments for Hypothyroidism

A

Increase iodine intake​

Thyroid hormone replacement- Synthroid or other drugs to mimic T3 or T4 or both​

61
Q

Parathyroid Function:

A

Calcium homeostasis​

62
Q

Short description of PTH activity and calcium secretion:

What type of feedback?

A

PTH released when there is a reduction in blood calcium levels- negative feedback loop​
Stimulates calcium production in bone, kidney and GI tract​

63
Q

Effect of PTH at high levels over bones, kidney and GI:

A

Bone- High PTH levels increases osteoclasts (breakdown bone)​

Kidney- High PTH increases reabsorption of Ca++ while eliminating phosphate
​
GI- PTH and vitamin D metabolism stimulating calcium absorption from intestines​

64
Q

What’s the normal balanced state of bone formation?

What;s determined by?

A

Bone function- balance between bone formation (osteoblasts) and mineral resorption (osteoclasts)​
Body framework​
Calcium pool​

65
Q

Effect of increased secretion of PTH over bone:

A

Prolonged and continuous release of Parathyroid Hormone​

Accelerates bone breakdown​

66
Q

Effect of normal secretion of PTH over bone:

A

Normal intermittent PTH​

Enhance bone formation​

67
Q

Role of Vitamin D in Bone Mineral Homeostasis

A

Consumed in diet or produced from UV light in skin​

Role is to enhance bone formation by increasing calcium and phosphate minerals necessary;
limits PTH release, thereby limiting catabolism​

68
Q

Role of Calcitonin in Bone Mineral Homeostasis

A

Calcitonin- thyroid hormone​
Physiologic antagonist of PTH​

Stimulates bone formation and therefore lowers Ca++ in blood​

Also enhances phosphate incorporation into bone formation​

69
Q

Role of different Glucocorticoids in Bone Mineral Homeostasis

A

Glucocorticoids (steroids discussed previously)- catabolic effect on bone​

Prostaglandins- stimulate bone resorption​

Estrogen, androgens, GH, insulin, and thyroid hormones enhance bone formation​

70
Q

Presentation of Hyperparathyroidism

A 
Hyper- postmenopausal women​
Excessive PTH​
Excessive bone demineralization​
Excessive calcium in blood​
Decreased bone density​
Kidney stones​
71
Q

Presentation of Hypoparathyroidism

A 
Hypo- injury or accidental removal or autoimmune​
Hypocalcemia​
Hypophosphatemia​
Neuromuscular irritability​
Cardiac irritability​
72
Q

Necessary daily intake of calcium and Vitamin D (supplements)

A

Hyper and hypocalcemia​

Calcium supplements, ~ 1000 units/day​

Vitamin D ~ 2000 units/day​

73
Q

What is the role of Calcitonin?

A

​
Calcitonin- decreases blood Ca++ ​
Treat hypercalcemia​

74
Q

Other mineral involved in osteoporosis and Paget’s disease:

A

Biophosphonates- osteoporosis, Paget’s disease, others​

Fosamax, Aredia, etc.

75
Q

Why is estrogen therapy used in postmenopausal women?

A

Estrogen therapy for post menopausal women and ovariectomy (also called oophorectomy) to preserve bone density​

76
Q

Short presentation of Osteoporosis

A

Age related bone remodeling and body type​
Breakdown is greater than build-up​
Bone growth and storage into the 20’s - diet and exercise puts bone in the bank!​

Systemic and bilateral​
Fracture and deformity risk systemically​

77
Q

Short Clinical Presentation of Paget’s:

A

Larger bone but weaker​ - Fracture risk, deformity​

Specific area not systemic​ - Pelvis, spine, skull, tibia (unilateral), etc.​

78
Q

True/False

Paget’s is a genetic or viral infection​

A

True

79
Q

Treatment for parathyroid dysfunctions (7)

A 
Exercise​ - Stretching, strengthening, balance​
Assistive device/bracing​
Sunlight​
Surgery​
Diet/Supplements​
Smoking- quit​
Alcohol consumption- moderation​

Thompson- spring (13 decks)

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