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PHA 332 > thyroid and parathyroid glands > Flashcards

thyroid and parathyroid glands Flashcards

1
Q

what makes up the thyroid and parathyroid glands?

A 
epiglottis 
hyoid bone
larynx
superior parathyroid gland
thyroid gland
inferior parathyroid gland
trachea
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2
Q

what are the lobes of the thyroid gland linked by?

A

isthmus of thyroid gland

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3
Q

what cells make up the thyroid gland??

A

follicles- follicle cells surrounding colloid

parafollicular cells- c cels which secrete calcitonin

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4
Q

what regulate thyroid hormone secretion?

A

thyrotropin-releasing hormone and thyroid simulating hormone

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5
Q

what are the thyroid hormones present in the thyroid gland?

A

–90% T4and 10% T3–Bound to thyroxine-binding globulin, thyroxine-binding prealbumin, or albumin

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6
Q

what do the thyroid hormone affect?

A

Affect growth and maturation of tissues, cell metabolism, heat production, and oxygen consumption

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7
Q

what is the role of the parathyroid gland?

A

–Small glands located behind the upper and lower poles of the thyroid gland–Produce parathyroid hormone
•Regulator of serum calcium
•Antagonist of calcitonin

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8
Q

why is calcium regulation important? what regulates it?

A

Calcium important in conduction of electrical impulses in nervous and muscular systems
•Calcium is the ONLY element / mineral that has its own regulatory system->the parathyroid glands

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9
Q

what causes regulation of calcium in the parathyroid gland?

A

substances that lower cAMP levels
slight decrease in serum calcium
substances that raise the cAMP levels

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10
Q

what does calcitonin stimulate?

A

calcium salt deposit in bone

calcium homeostasis of blood 9-11mg/100ml

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11
Q

what are the alterations of parathyroid function?

A

hyperparathyroidism

hypoparathyroidism

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12
Q

what is hyperparathyroidism?

A

–Primary hyperparathyroidism
•Excess secretion of PTH from one or more parathyroid glands–Secondary hyperparathyroidism
•Increase in PTH secondary to a chronic disease

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13
Q

what is hypoparathyroidism?

A

–Abnormally low PTH levels

–Usually caused by parathyroid damage inthyroid surgery

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14
Q

what causes hyperparathyroidism?

A
  • Increase in the production of PTH–Usually due to a benign growth of 1:4parathyroid glands
  • Induces abnormally high serum Ca++levels
  • Bone decalcification
  • Development of kidney stones
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15
Q

what are the symptoms of hyperparathyroidism?

A
  • Fatigue
  • Apathy
  • Muscle weakness
  • Vomiting
  • Hypertension
  • Demineralization of bones
  • Development of kidney stones
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16
Q

what are the symptoms of hyperalcemic crisis?

A
  • Acute hypercalcemic crisis can occur with calcium levels over 15 mg/dl (3.75mmol/L)
  • Neurological, cardiovascular, and renal symptoms
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17
Q

what is the treatment aimed at decreasing serum calcium?

A

–IV fluids
–Phosphate therapy
–Calcitonin
–Dialysis

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18
Q

what causes hypoparathyroidism?

A

•Usually due to accidental removal of parathyroid glands during thyroid surgery
•Symptoms are due to hypocalcemia and hyperphosphatemia–Neuromuscular irritability
–Tetany
•Numbness, tingling, cramps
•Bronchospasm, laryngeal spasm, carpopedal spasm

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19
Q

how is the thyroid hormone synthesised?

A

uptake of iodine
iodination and coupling
endocytosis and secretion

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20
Q

how doe t4 get converted to t3?

A

remove an iodine

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21
Q

what are the 3 major thyroid-binding proteins?

A
  • Thyroid hormone-binding globulin (TBG)–Carries approximately 70% of T4and T3
  • Thyroxine-binding pre albumin (TBPA)–Binds approximately 10% of circulating T4and lesser amounts of T3
  • Albumin–Binds approximately 15% of circulating T4and T
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22
Q

what can t4 be converted into?

A

t3 and rT3

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23
Q

what can suppress TSH secretion?

A

At pharmacologic doses, dopamine, somatostatin, or glucocorticoids can also suppress TSH secretion.

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24
Q

what is the MOA of thyroid disease?

A
  • Dissociate of T3and T4from thyroxine-binding plasma proteins prior to entry into cells, either by diffusion or by active transport.
  • In the cell, T4is enzymatically deiodinated toT3, which enters the nucleus and attaches tospecific receptors.
  • The activation of these receptors promotesthe formation of RNA and subsequent protein synthesis, which is responsible for the effects of T4.
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25
Q

what are the major functions of thyroid hormone?

A
  • Increases metabolism and protein synthesis

* Influences growth and development in children–Mental development and attainment of sexual maturity

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26
Q

what occurs in hypothyroidism?

A

–Decreased metabolic rate
–Accumulation of hydrophilic mucopolysaccharide substance(myxedema) in the connective tissues
–Elevated serum cholesterol

27
Q

what happens in hyperthyroidism?

A

–Increased metabolic rate and oxygen consumption
–Increased use of metabolic fuels
–Increased sympathetic nervous system responsiveness

28
Q

what are the diseases caused by hyperthroidism?

A

–Thyrotoxicosis–Graves disease
•Pretibial myxedema–Hyperthyroidism resulting from nodular thyroid disease
•Goiter–Thyrotoxic crisis

29
Q

what is graves disease?

A

State of hyperthyroidism, goiter and ophthalmopathy (less commonly, dermopathy)
•An autoimmune disorder characterized by abnormal stimulation of the thyroid gland by thyroid-stimulating antibodies (thyroid-stimulating immunoglobulins [TSI]) that act through the normal TSH receptors
•Associated with human leukocyte antigen(HLA)-DR3 and HLA-B8
•Familial tendency is evident

30
Q

what are the manifestations of thyroid storm?

A
  • Very high fever
  • Extreme cardiovascular effects–Tachycardia, congestive failure, and angina
  • Severe CNS effects–Agitation, restlessness, and delirium
  • High mortality rate
31
Q

what causes primary hypothyroidism?

A
  • Subacute thyroiditis*
  • Autoimmune thyroiditis (Hashimotodisease)**
  • Painless thyroiditis
  • Postpartum thyroiditis
  • Myxedema coma–Congenital hypothyroidism–Thyroid carcinoma
32
Q

whay are the manifestations of hypothyroidism?

A 
Mental and physical sluggishness•
Myxedema
•Somnolence(drowsiness or sleepiness, in excess)
•Decreased cardiac output, bradycardia
•Constipation
•Decreased appetite
•Hypoventilation
•Cold intolerance
•Coarse, dry skin and hair
•Weight gain
33
Q

what are the manifestations of hyperthyroidism?

A
  • Thyroid storm
  • Restlessness, irritability, anxiety
  • Wakefulness
  • Increased cardiac output
  • Tachycardia and palpitations
  • Diarrhea, increased appetite
  • Dyspnea
  • Heat intolerance, increased sweating
  • Thin and silky skin and hair
  • Weight loss
34
Q

what is the difference between thyrotoxicosis and hypothyroidism in skin and appendages

A

T-Warm, moist skin; sweating; heat intolerance; fine, thin hair; Plummer’s nails; pretibial dermopathy(Graves’ disease)
H-Pale, cool, puffy skin; dry and brittle hair; brittle nails

35
Q

what is the difference between thyro and hypo in eyes and face?

A

t-Retraction of upper lidwith wide stare;periorbital edema;exophthalmos; diplopia(Graves’ disease)
h-Drooping of eyelids;periorbital edema; loss oftemporal aspects ofeyebrows; puffy, nonpittingface; large tongue

36
Q

what are the symptoms of exopthalmina?

A
  • Bilateral in Graves Disease

* Unilateral in orbital tumour

37
Q

what is the difference between t and h in CVS?

A

T-eripheral vascular resistance; ↑heart rate, stroke volume, cardiacoutput, pulse pressure;high-output heartfailure; ↑inotropic and chronotropic effects;arrhythmias; angina
h-peripheral vascular resistance; ↓heart rate, stroke volume, cardiacoutput, pulse pressure; low-output heart failure; ECG:bradycardia, prolonged PRinterval, flat T wave, lowvoltage; pericardial effusion

38
Q

what is the difference between t ad g in RS?

A

t-Dyspnea; ↓vital capacity

H-pleural effusions; hypoventilation and CO2retention

39
Q

what is the difference between t and H with GIT system?

A

t-of bowel movements ;hypoproteinemia

h- dec appeitite and freq of bowel movements; ascites

40
Q

what is the differece between t and H in CNS?

A

t-Nervousness ;hyperkinesia; emotionallability

h-Lethargy; general slowing of mental processes; neuropathies

41
Q

what is the difference between t and h with musculoskeletal system?

A

t-Weakness and muscle fatigue; increased deeptendon reflexes; hypercalcemia; osteoporosis
h-Stiffness and muscle fatigue;↓deep tendon reflexes; ↑alkaline phosphatase, LDH, AST

42
Q

what are the differences n t and h with the renal system?

A

t-Mild polyuria; ↑renal blood flow;↑glomerular filtration rate
h-Impaired water excretion;↓renal blood flow;

43
Q

what is the differnece between t and in the hematopoetic system?

A

t-↑erythropoiesis; anemia

h-erythropoiesis; anemia

44
Q

what is the difference between t and in the reporoductive system?

A

t-Menstrual irregularities; increased gonadal decreased ferlitysteroid metabolism
h-Hypermenorrhea ;infertility; decreased libido; impotence; oligospermia;↓gonadal steroid metabolism

45
Q

what is the difference between t and h in the metabolic system?

A

t-↑basal metabolic rate; negative nitrogenbalance; hyperglycemia↓cholesterol and triglycerides; ↑hormone ј requirements for fat- and water-soluble vitamins;↑drug metabolism; ↓warfarin requirement
h-↓basal metabolic rate; slight positive nitrogen balance; delayed degradation ofј ↑cholesterol and triglycerides; ↓hormone for fat- and water-soluble vitamins; ↓drug metabolism; ↑warfarin requirement

46
Q

what causes hashimoto’s thyroiditis? is there a goitre?

A
  • autoimmune destruction of thyroid
  • goitre present early, absent later
  • mild to severe
47
Q

how is a drug induced thyroid disease caused? is there a goiter present?

A

blocked hormone formation

goitre present

48
Q

how is dyshormono-genesis caused? is there a goitre present?

A
  • impaired synthesis of t4 due to enzyme deficiency
    goitre present
    mild to severe
49
Q

how is radiation , thyroidectomy caused?

A

destruction or removal of gland
goitre absent
severe degree of hypothyroidism

50
Q

how is congenital thyroid disease caused?

A

athyreosis or ectipic thyroid, iodine deficiency, tsh receptor blocking antibodies
goitre absent or present
severe

51
Q

how is secondary thyroid diseases caused?

A

due to pituitary or hypothalamic disease
goitre absent
mild

52
Q

what is used to disagnose thyroid disorders?

A 
tfts
resin uptake test
assessment of thyroid antibodies
radioiodine uptake test
thyroid scans
ultrasonography
CT and MRI
fine-needle aspiration biopsy of a thyroid nodule
53
Q

how would you asses thyroid function by lab?

A

sample- about 5ml o venous blood
blood plamsa- blood collected into tube containing anticoagulant
blood: collected into plain tube
request card info- drug and preexisting non-thyroid disease can affect interpretation
test also used to monitor the effectiveness of the therapy

54
Q

what is the normal value for total thyroxine t4?

A

4-11ug/dl

55
Q

what is the normal value for t3?

A

60-175ug/dl

56
Q

what is the normal value for ft4?

A

0.7-1.4ng/dl

57
Q

what is the normal result for ft3?

A

0.16-0.4ng/dl

58
Q

what is the normal value for tsh?

A

0.4-4.5ulU/ml

59
Q

what are the typical values for thyroid function tests?for subclinical primary hyperthyroidism

A
  • Plasma /serum TSH reduced
  • Plasma/serum FT4and FT3normal( often high normal)
  • Greater than normal risk of developing hyperthyroidism(usually Graves disease in long term )
  • Thyroid testing every 6-12 months
  • Subclinical Primary hyperthyroidism increase risk of
  • Atrial fibrillation in elderly
  • Reduced bone density (osteoporosis) in post menopausalwomen
60
Q

what are the clinical values for subclinical primary hypothyroidism?

A
  • Serum TSH raised
  • Serum FT4particularly high (>10mlU/L)
  • Offered annual thyroid testing
61
Q

what are the 3 treatments used in hyperthyroidism?

A

1- antithyroid agents
surgery
RAI

62
Q

how can stress affect the hypothalamus?

A

decrease TRH- this decreasing levels of t3 an t4

63
Q

what drugs treat hypothyroidism?

A

levothyroxine t4

and liothyronine t3- iv in emergency

PHA 332 (42 decks)

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