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PHAR 123 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the purpose of the Endocrine System? How does it control this?

A

Maintain homeostasis using hormones

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2
Q

What are the lipid soluble hormones?

A

Steroids

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3
Q

What are the water soluble hormones?

A

Amines, Peptides, Proteins

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4
Q

What 3 factors determine circulation levels of hormones?

A

Synthesis, secretion, and transport

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5
Q

What do water soluble hormones need to get into the cell (usually)

A

Receptors

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6
Q

How is peptide hormone syntehsis controlled?

A

Modulating transcription

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7
Q

How is amine hormone synthesis controlled?

A

REgulation of enymes and substrate availability

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8
Q

Are precursor hormones active?

A

Usually not

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9
Q

How can Hormone Secretion be controlled?

A

Exocytosis via signaling
diffusion
pulsatile manner using gradients

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10
Q

How are hormones transported

A

In the Blood

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11
Q

What are the dependant factors of hormones reaching their target site in free-form?

A

Affinity of hormone for plasma protein carriers
hormone degradation
availabilty or receptors
receptor binding
hormone uptake

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12
Q

What functions do protein binding hormones have?

A

protect hormone from degradation or uptake
Allows for fine control of circulating levels
prevents hormone from binding to unintended sites
Allows transport of lipid soluble hormones

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13
Q

T or F, are plasma protein carriers regulated?

A

True

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14
Q

What influences the availability of receptors?

A

Up-regulation
Down-regulation

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15
Q

What is the difference in uptake of water soluble hormones and Lipid-soluble hormones?

A

Water soluble need an active uptake whereas lipid soluble use passive uptake

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16
Q

What do hormones regulate to maintain homeostasis

A

Extracellular fluid
Metabolism
Biological clock
Contraction of cardiac and smooth muscle
Glandular secretion
immune functions
growth and development
reprodcution

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17
Q

What can hormone binding cause a cell to do?

A

Synthesize a new molecule
Change permeability of the membrane
alter rate of reaction

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18
Q

what is a permissive hormone action?

A

bind to a target cellallowing different hormone to have its full effect

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19
Q

What is a synergistic hormone action?

A

2 hormones act together to achieve a greater effect

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20
Q

What is an antagonistic hormone action?

A

2 hormones produce an opposite effect

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21
Q

What is a negatve feedback loop?

A

High levels of hormone signal to reduce secretion/ production of itself
Low levels of hormone signl to increase secretion/ production

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22
Q

What is a positive feedback loop?

A

Action of the hormone causes more of the hormone to be released

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23
Q

Where is the pineal gland located?

A

Epithalamus

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24
Q

What is the function of the pineal gland?

A

Production of melatonin

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25
Q

What can stimulate/ inhibit melatonin?

A

Darkness/ Light

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26
Q

What can high levels of melatonin inhibit in children?

A

Puberty

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27
Q

What does the Pituitary gland do?

A

Control hormones sent from hypothalamus that cause secretion of various hormones

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28
Q

What are some hormones controled by the pituitary gland?

A

HGH
Thyroid stimulating hormone (TSH)
Folicle-stimulating and lutenizing hormone
Adrenocorticoiphic hormone
Melanocyte-stimulating hormone
Prolactin (inhbited by dopamine)

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29
Q

What does HGH do?

A

Promotes synthesis of a protein insulin-like growth factors. Increase cell growth and ATP use

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30
Q

How is HGH released?

A

Pulsatile secretion peaks in puberty, declines afterwards

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31
Q

Where does HGH normally bind?

A

Lier, Skeletal muscle, cartilage, and bone

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32
Q

How does Low blood sugar stimulate HGH?

A

LBS stimulates the release of growth hormone rleasing hormone; increases secretion of HGH from the pituitary gland

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33
Q

How does High blood sugar stimulate HGH?

A

HBS stimulates the release of growth hormone inhibiting hormone fro hypothalmus; reduces secretion of HGH

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34
Q

What is the consequence of excess HGH? How would it be treated?

A

Excess uncontorolled growth leading to extra stress on organs. Administration of somatostatin to lower HGH levels

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35
Q

How do you treat HGH defeciency?

A

Administration of an HGH analogue

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36
Q

What are the hypothalmus - Pituitary Gland interactions?

A

Growth hormone releasing hormone –> HGH
Thyrotropin releasing hormone –> thyroid stimulating hormone
Gonadotropin releasing hormone –> follicle stimulating and luteinizing hormone
Corticotropin releasing hormone –> adrenocorticotrophic hormone
Dopamine –> (inhib) prolactin
Somatostatin –> (inhib) HGH and thyroid stimulating hormone

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37
Q

What is the thyroid responsible for?

A

Synthesis, storage, and release of T3 and T4 thyroid hormones

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38
Q

What do T3 and T4 do?

A

Produce various physiological effects, crutial in homeostasis maintenance
Heart, adipose tissue, muscle, bone, nervouse system, gut, etc.

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39
Q

What is the colloid’s job?

A

Factory for T3 and T4 production; stores the building blocks as well as T3 and T4

40
Q

What are the follicular cells function?

A

Responsible for producing thyroglobulin, pumping in iodine, and pumping out T3 and T4

41
Q

What hormone controls the synthesis and secretion of T3 and T4?

A

Thyroid stimulating hormone (TSH) which is controlled bythyroglobulin releasing hormone

42
Q

What are the building blocks for the creation of T3/T4?

A

Iodide, thyroglobulin, and tyrosine

43
Q

How is T3/T4 created?

A

Iodine bindss with tyrosine that is attached to thyroglobulin (1I = MIT 2I - DIT). MIT+DIT = T3, DIT +DIT = T4

44
Q

Which is more potent T3or T4? What is the split in production of each enzyme? (%)

A

T3 is much more potent, 10% T3 vs 90% T4. T4 resevoirs because it can be easily converted to T3

45
Q

6 Steps to Thyroid hormone creation?

A

Thyroglobulin syntheisis
Iodide trapping
Oxidation of Iodide
Iodination of tyrosine
Coupling of MIT and DIT
Secretion of hormones

46
Q

How is T3 and T4 secretion controlled?

A

Negative feedback loop

47
Q

What can Excess iodide cause? Defeciency?

A

Excess causes intial decrease in production but, if excess is sustained the negative feedback loop can be ovecome.
DEfeciecny intially is a stimulant and mass produce T3 and T4 but with eventually be inhibitory as it will “run out”

48
Q

T or F, Most T3 and T4 exist as free form molecules.

A

Flase, most exist in protein bound form

49
Q

What does he parathyroid gland produce? what does it regulate?

A

Parathyroid hormone (PTH). REgulates calcium and phosphate

50
Q

How does PTH increase calcium?

A

Stimulation of activity of osteoclasts
Increase calium and magnesium reabsorption from urine
Increase synthesis of calcitriol, which increases calcium and magnesium absoprtion

51
Q

How does PTH decrease phosphate?

A

Increasing excretion from kidneys.

52
Q

What hormone opposes PTH?

A

Calcitonin

53
Q

What does the thymus do?

A

T-cell development, various hormones to stimulate T-cell development

54
Q

What is the treatment for hyperthyrodisim?

A

Radioactive iodine or surgery,
No curative pharmacotherapy available.

55
Q

What are the common causes of hyperthyroidism?

A

Toxic diffiuse goiter
Toxic multi-nodular goiter
Acute phase thyroiditis
Toxic adenoma

56
Q

Which disorder is:
more common in younger females, most common cause of hyperthyroidism, autoimmune disorder, creation of anibiodies against TSH receptor, and can result in hyperplasia of thyroid gland; enlargment.

A

Toxic Diffuse Goiter (Graves disease)

57
Q

Which disorder is: most common in older females (>50), second most common hyperthyroidism cause, iodide defeciecny most common trigger for growth, slowly develops over years.
Trigger causes receptors to mutate rather than be targeted.

A

Toxic multi-nodular goiter (Plummers disease)

58
Q

Which disorder is: benign tumours growing on thyroid gland, become active and act just like thyroid cells secreting T3/T4 and do not respond to negative feedback.

A

Toxic adenoma

59
Q

Which disorder is: causes inflammation and damage to thyroid gland, damage causes excess hormone release, eventually leads to hypothyroidism

A

Acute phase thyroiditis

60
Q

What are symptoms of hyperthyroidism?

A

anxiety, hyperreflexia, atrial fibrilation, hyperactivity, papitations, hair loss, insomnia, etc. (excess stimulation symptoms)

61
Q

What are clincial presentations/ symptoms of Toxic diffuse goiter disorder?

A

Exophthalmos (conective tissue around eye cosntantly stimualted)
Per-orbital edema
Diplopia (double vision)
Pretibial myxedema (waxy discoloration of skin usually on shins)

62
Q

What are the specific Treatments of Hyperthyroidism?

A
  1. PHarmacotherapy: thioamides, beta-blockers
  2. radioactive iodine
  3. surgery
63
Q

What are the thioamide drugs?

A

Propylthiouracil
Methimazole

64
Q

What is the usage of thioamides?

A

Used to reduce severity of hyperthyroidism, prepare patient for curative therapy.
About 1-20% have effectiveness over 20-30 years.

65
Q

What is the MOA of thioamides?

A

Inhibit T3 and T4 by preventing iodine from incorparating with tyrosine residue of thyroglobulin
Inbits coupling of MIT and DIT
This is done by inhibiton of thyroid peroxidase

66
Q

What differs between Propylthiouracil and methimazole?

A

Propylthiouracil additionally inhibits the conversion of T4 to T3 through inhibition of 5` deiodinase

67
Q

What are the thioamide treatment dosing for Mild? Moderate? Severe?

A

Methimazole:
Mild - Intial 10-15 mg OD, Maintanence 5-15mg OD
Moderate: Initial 20-30mg OD, Maintanence 5-15mg OD
Severe: intial 30-40mg OD, maintanence 5-15mg OD
Propylthiouracil:
Mild, Moderate, and Severe: Intial 300mg divided BID or TID, Maintanence 100-150mg BID -TID

68
Q

How long in thioamide treatment does it take to maintain a new steady state

A

4-6 weeks

69
Q

What are side effects of Thioamides?

A

GI upset
Rash
Arthralgia

70
Q

What are some potentially serious side effects of THioamides?

A

Agranulocytosis (0.3-0.4%)
- occurs in first 90 days
- WBC falls < 0.5 x 10^9
- abrupt onset
- Fever, malaise, sore throat
Neutropenia:
- immunosupression
- can be life threatening with a fever or illness
Hepatotoxicity and cholestatic jaundice (0.1-0.2%)
Vasculitis
- most common
- auto-immune process
- can lead to acute renal dysfunction, arthritis, skin ulcers/rashes, and respiratory problems
Polyarthritis: (1-2%)
- involves many joints

71
Q

What are the concerns with thioamides and pregnancy?

A

Propylthiouracil: low tetratogenacity but higher hepatotoxicity
Methimazole: some teratogenic cocnerns in 1st trimester but, less hepatotoxicity

72
Q

How do beta-blockers treat hyperthyroidism?

A

No direct influence on thyroid hormones but reduce symptoms related to cardiac over-stimulation like
- palpations
-tachycardia
- tremors
- anxiety
- heat intolerance

73
Q

What beta-blockers are not used in hyperthyroidism?

A

ISA beta blockers; acebutolol, pindolol

74
Q

How does surgery “cure” hyperthyroidism?

A

Thyroidectomy removes the thyroid and leads to permanent hypothyroidism (Can be treated pharmacologically)

75
Q

How does radioactive iodine “cure” hyperthyroidism?

A

Radioactive iodine taken up by thyroid causing ablation, causes temporary thyroiditis and worsening of hyperthyroidism followed by hypothroidism

76
Q

What is Thyroid Storm?

A

rare life-threatening condition
Severe manifestation of hyperthyroidism
Causes liver damage, cardiovascular collapse and shock

77
Q

How can thyroid storm occur?

A

Can occur in untreated hyperthyroidism
Often triggered by acute event such as:
- thyroid surgery or radioactive iodine
- trauma
- infection
- giving birth

78
Q

How do you treat thyroid storm?

A

supportive care (oxygen, ventilator, IV fluids), correct electrolyte imbalance, treat cardiac arrhythmias, control hyperthermia, administer beta-blockers to reduce symptoms, adminsiter anti-thyroid meds, adminsiter iodine 1 hour after throid meds, steroids to block T4 to T3, treat underlying conditions

79
Q

What is the most common cause of hypothyroidism?

A

Chronic autoimmune thyroiditis(Hashimoto’s disease)
antibodies form and bind to TSH receptors which directly destroy thyroid cells, other antibodies may form and interfere with production of T3 and T4

80
Q

What are early clinical presentations of hypothyroidism?

A

Weight gain
fatigue
sluggishness
bradycardia
constipation
brittle hair/hairloss
dry flaky skin
Opposite of excess stimulation

81
Q

What are advanced symptoms of hypothyroidism?

A

myxedema
hypothermia
confusion
stupor, coma
CO2 retention
hypoglycemia
hyponatremia

82
Q

How is hypothyroidism treated?

A

Replacement therapy of thyroid hormone
- desicated thyroid
- liothyronine
- levothyroxine
- combined T3/T4

83
Q

What are some characteristics of desicated thyroid?

A

Prepared from thyroid glands of animals
Contains both T3 and T4 and causes high T3 peaks
not well standardized from batch to batch
Normally 13:1 T4:T3 but with treatment ratio is 4:1

84
Q

What is the discontinuation rate of desiccated thyroid?

A

20%

85
Q

What are some characteristics of Liothyronine?

A

Contains T3 but no effect on T4
costly
fluctuations in serum levels
no routinely used but, is seen wehn T3 levels are still low while on levothyroxine

86
Q

Why would T3 be less desirable than T4?

A

T4 can be converted to T3, T4 is the less potent but more stored hormone, rest hormone

87
Q

What are some characteristics of levothyroxine?

A

Analogue of T4
standard first line therapy
half life of 7 days
conversion to T3 is regulated by body

88
Q

What is the dosing for levothyroxine?

A

average dose is 1.6mcg/kg/d
starting dose range from 12.5mcg/kg/d to max wt based
average replacement dose is 100mcg OD

89
Q

What facors can change levothyroxine dosing?

A

Age, weight, cardiac status, severity and duration of hypothyroidism, higher baseline TSH usually predicts higher T4 dose

90
Q

When do you titrate up dosing? How so?

A

Any CVD, rhythm disturbances, >50, sever, long-standing hypothyroidism.
Start at 12.5-50mcg, titrate up 12.5-25mcg q4-6 weeks.
ADminister on empty stomach, 30 minutes before meals or 1 hur after

91
Q

What are side effects of levothyroxine?

A

Minimal if dosed properly
hyperthyroidism symptoms
cardiac risk increase
aggrevate existing CVD
BMD reduction

92
Q

What are drug interactions of levothyroxine?

A

Antacids, H2 blockers, PPIs, Iron, Calcium/mineral supplements, cholestyramine, raloxifene
Chelate as it is a large molecule reducing overally absorption

93
Q

What monitoring parameters are taken for levothyroxine?

A

TSH levels
Free T3/T4 levels.

94
Q

What would need to be done if TSH levels were high?

A

Increased dose, high levels TSH means low levels of T4/T3

95
Q

What are some risks of subclincal hypothyroidism? Do patients need treatment?

A

increase risk of
atherosclerosis
heart failure
MI
depression
Low BMD
metabolic syndrome
Uncertain whether treatment is required; treat if pregnant, sever symptoms, heart failure, young.

PHAR 123 (18 decks)

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