ENDOCRINE Flashcards

1
Q

2 major regulatory/ control systems

A

endocrine
nervous system

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2
Q

endocrine system
(messenger, speed, purpose)

A

Slow acting
Long term slow response
Hormone messengers

Regulates activities of longer duration than speed
(growth, development, reproduction)

Maintains homeostasis
Long term slow response

Hormonal signaling (reach all body cells by affects target cells)

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2
Q

endocrine system
(messenger, speed, purpose)

A

Slow acting
Long term slow response
Hormone messengers

Regulates activities of longer duration than speed
(growth, development, reproduction)

Maintains homeostasis
Long term slow response

Hormonal signaling (reach all body cells by affects target cells)

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3
Q

nervouvs syste, (messenger, speed, function)

A

Fast acting
Short term quick response
Neurotransmitters

Regulates activity of muscles and glands

Quick responses

Local signaling
(paracrine – nearby, synaptic

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4
Q

hormones definition

A

substances released by endocrine glands, transported throughout bloodstream to target tissues where they act to regulate specific functions

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5
Q

hormones activity

A

1) Exerts effect in low conc
2) Bind to target cell receptors to initiate biochemical reaction
3) Each hormone act on specific receptor on target tissue
□ SELECTIVITY: hormone-specific receptors in (target cell’s cell mem. Cytoplasm/ nucleus)

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6
Q

classification of hormones

A

1) endocrine gland (ductless vs exocrine)
2) chemical nature (peptide, steroids,amines)

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7
Q

endocrine definition

A

ductless, produce hormones into surrounding tissue fluid

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8
Q

central endocrine glands

A

pineal, hypothalamus, pituitary

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9
Q

peripheral endocrine gland

A

thyroid, thymus, adrenal, pancreas, ovary, testis

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10
Q

secondary endocrine glands definition and eg

A

hormones secreted by organs which also have other major functions

kidney, heart, stomach, SI, skeleton, skin, adipose tissue, placenta

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11
Q

exocrine glands

A

nonhormonal substance, ducts that carry substances to mem surface

eg: Sweat, saliva glands

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12
Q

hypothalamus hormones

A

Releasing & inhibiting hormones
TRH, CRH, GnRH, GHRH, PRH

GHIH, PIH

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13
Q

pituitary anterior lobe hormones

A

Luteinising hormone (LH)
Follicle-stimulating hormone (FSH)
Prolactin (PRL)
growth hormone (GH)
adrenocorticotropin (ACTH)
Thyroid-stimulating hormone (TSH)

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14
Q

posterior lobe pituitary hormones

A

ADH/ vasopressin
Oxytocin

(produced by hypo, secreted by pituitary)

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15
Q

Thyroid gland hormones

A

Thyroxine (T4)
3,5,3’ - triiodothyronine (T3)
Calcitonin

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16
Q

parathyroid gland hormones

A

PTH -parathyroid hormone

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17
Q

adrenal gland hormones

A

CORTEX = Cortisol, aldosterone, androgens (puberty)

MEDULLA = Epinephrine, norepinephrine

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18
Q

gonads - testis hormones

A

Testosterone
estradiol
inhibin
Mullerian-inhibiting hormone (MIH)

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19
Q

gonads - overy hormones

A

Estradiol
progesterone
inhibin

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20
Q

placenta hormones

A

Human chorionic gonadotropin (hCG)
Progesterone
estrogen

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21
Q

pancreas hormones

A

Insulin, glucagon, somatostatin

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22
Q

pineal hormone

A

Melatonin (regulates body clock)

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23
Q

hormone disrupters effect
- mimic hormone action

A

F: incr breast tumours

M: fall sperm count, cryptorchidism (testes undescended)

Animal: gender bending (hermaphrodites both F, M)

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24
Q

hydrophilic hormones activity

A

Hydrophilic hormones: dissolved & transported free in blood

binds to cell surface proteins

Cell mem receptor/ plasma protein: 50% catecholamines, protein hormones

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25
Q

hydrophilic hormones 2 types

A

proteins/ peptide hormone

amines

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26
Q

lipophilic hormones group

A

steroids

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27
Q

hydrophobic hormone
activity

A

Hydrophobic hormones: bound to plasma proteins (binds to intracellular proteins)

Cross plasma mem, act on receptors inside cell

Steroid hormones, thyroid hormones
(hydrophobic

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28
Q

protein/ peptide hormone eg

A

Follicle-stimulating hormone (FSH)
Prolactin, growth hormone, adrenocorticotropin
Thyroid-stimulating hormone (TSH)

ADH/ vasopressim. oxytocin

Calcitonin

Parathyroid hormone (PTH)

inhibin

Human chorionic gonadotropin (hCG)

Insulin, glucagon,

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29
Q

steroid hormone eg

A

(adrenal cortex) Cortisol, aldosterone

(gonads)
Testosterone,
Estradiol, progesterone

(kidney) Calcitriol (vit D)

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30
Q

amines hormone eg

A

Thyroxine (T4)
3,5,3’ - triiodothyronine (T3)

Melatonin

(adrenal medulla) Catecholamines (Epinephrine, norepinephrine )

31
Q

mechanism after hormone binds to receptor

A

1) signal amplification (2nd messenger, PK cascade)
2) hormone activate genes, alter proteins synthesised
3) alter channel permeability (insulin GLUT4)

32
Q

hormone imablance caused by

A

result in excess or deficiency target-cell responsiveness

33
Q

hormones test

Blood (plasma)
Urine (hormone excreted via kidney)
Saliva
Other biologic sample (tissue - hormone internalized by target cells)

A

1) Radioimmunoassay (RIA)
2) Enzyme-linked immunosorbent assay (ELISA)

  • Pregnancy test kits (for hCG hormone – sandwiched between 2 AB)
34
Q

negative feedback

A

inhibit initial stimulus, restore body to balanced state

35
Q

thyroid gland location

A

neck, anterior surface of trachea, below larynx

36
Q

thyroid gland structure

A

○ 2 lobes connected by isthmus

○ Extensive blood supply: hormone released directly into bloodstream
(Deep red colour)

37
Q

thyroid gland cell types

A

1) Follicle cells
□ Synthesis thyroglobulin (globular proteins)
□ Secreted into colloid of thyroid follicles

2) Thyroid follicles
□ Functional unit for Thyroid hormone production

3) Colloid
□ Extracellular space where thyroglobulin with attached iodine atoms are stored (T3, T4)

4) C cells/ parafollicular
□ (in between follicles)
□ Secrete calcitonin (regulate Ca levels in blood)

38
Q

thyroid hormone synthesis requires which 2 basic ingredients

A

1) Tyrosine – an aa synthesised in suff amts by body

2) Iodine – from dietary intake
□ To be reduced to I- (iodide) before absorption by SI

occurs on Thyroglobulin – produced by thyroid follicular cells

39
Q

thyroid production step 1 (TG secretion, exocytosis)

A

TG produced by ER/ GA of thyroid follicular cells

Tyrosine + TG molecules = Tyrosine-containing TG: backbone

Exported in vesicles from follicular cells into colloid by exocytosis

40
Q

thyroid hormone synthesis step 2

  • iodide trapping (iodine oxidation)
A

Thyroid gland capture I- from blood, transfer to colloid (iodide pump Na+ K+ pump)

      Follicular cell --> colloid  (iodide pump)
 transport Na into follicular cell down conc gradient
Transport I- into cell against con gradient

I- oxidised ——> active iodide (mem bound enzyme: Thyroperoxidase TPO)

Active iodide exists through channel into colloid

41
Q

step 3 (iodination)

A

In colloid, TPO attach iodide to tyrosine (of TG mole)

1 I = MIT (mono-iodotyrosine)
   2 I = DIT (di-iodotyrosine))
42
Q

step 4 (coupling, conjugation)

A

MIT + DIT = T3 (1+2)
DIT + DIT = T4 (2+2)

Attached to TG by peptide bonds
within colloids

43
Q

step 5 (colloid resorption, endocytosis)

A

Stimulus for thyroid hormone

follicular cells internalise portion of Tg-hormone complex (phagocytosis piece of colloid)

44
Q

step 6 (Thyroglobin proteolysis, break from TG backbone)

A

Lysosome attack engulfed vesicle, split iodinated products from TG

T3, T4 diffuse freely follicular cells –> blood/ plasma protein/ transport// storage – bound to TG store in follicular lumen

Iodinase enzyme: remove iodide from MIT/ DIT (NOT T3, T4)

Freed I- recycled for synthesis of more hormones

45
Q

thyroid hormone metabolism, excretion

A
  • high conc plasma (90% released from thyroid)
  • 80% of T3 <—- T4
  • metabolic inactivation (T4>3): conjugation w/ glucuronic acid in liver.
    -conjugate secreted into bile, faeces (Elim)
    - small amt in urine
46
Q

thyroid hormone negative feedback controlled by

A

HPT (hypothalamus, piuitary, thyroid axis) axis

hypo hormones (TRH)
ant pitui hormone (TSH/ thyrotrropin)
thyroid hormone (T3,4)

47
Q

thyroid hormone (stimulating pathway)

A

1) TH low, stimulate pitui and hypotha
2) TSH from anterior pituitary gland

3) stimulate (2nd messenger, incr cAMP, PKA, PLC = Ca2+ release)

4) incr synthesis and secretion of TH (iodine trapping, iodination, coupling, colloid resorption, TG proteolysis)

48
Q

T3, T4 physiologic effects

A

1) basal metabolic rate
2) sympathomimetic effect
3) CVS effect
4) bone growth, maturation
5) nervous system development
6) incr metabolism of proteins, lipis, carbs

49
Q

BMR levels

A

euthyroid, normal = 150ml/min
hyperthyroid = 400ml/min

50
Q

why incr BMR

A

□ Incr size, number of mitochondria

□ Incr enzymes that regulate oxidative phosphorylation

□ Incr oxygen consumption, energy use at rest condition
-Incr metabolic activity, more heat prodn (calorigenic effect)

51
Q

Sympathomimetic effect

A

-Mimics activation of SNS
-TH increase proliferation of catecholamines (epinephrine, norepinephrine) target cell receptors
□ Incr target-cell responsiveness to catecholamines

Ventilate, sweat,

52
Q

Cardiovascular effect

A
  • Incr heart responsiveness to catecholamines (E, NE by adrenal medulla)
  • Increase HR, force of contraction
  • Incr CO

Meets demand of O2 consumption

53
Q

Normal bone growth and maturation

A

-TH stimulates GF secretion, incr IGF-1 production by liver

Promote effect of GH, IGF-1 on synthesis of new structural proteins + skeletal growth

54
Q

Role in normal development of nervous system (brain)

A

§ Esp in brain during childhood
□ Hypothyroid: growth stunted in children

§ For normal CNS activity in adults
□ Hyperthyroid: hyperactive, unable to process info

55
Q

Increase metabolism of proteins, lipids, carbohydrates

A

Synthesis but degradation (metabolism)
- mobilisation of endogenous proteins, carb, fat

Hyperthyroid: prevents weight gain due to high metabolism

56
Q

hypothyroid causes

A

1) Primary failure of thyroid gland itself
2) 2nd to deficiency of TRH, TSH, both
3) Inadequate dietary supply of iodine

57
Q

hypothyroid symptoms

LOW METABOLIC ACTIVITY

A

Cold
Hair loss, brittle nails, dry skin
Constipation
Muscle ache, weak
Slow speech
Menstrual disturbances
Dull-blank expression
Extreme fatigue
Weight gain
Cardiac complications
- bradycardia

58
Q

hyperthyroidism causes

A

1) autoimmune Graves disease (prodn TSI - stimulating immunoglobulins)

2) 2nd to excess of TRH, TSH, both
3) Hypersecreting thyroid tumour

59
Q

diffuse goiter

A
  • enlarged thyroid
  • from incr production of TSH
          (by pituitary gland --> which acts on thyroid gland)
60
Q

hyperthyroidism symptoms

A

Tremor
HR incr, BP
Yawn, fatigue
Restless
Amenorrhea
Heat
Diarrhea
Irritability
Sweat
Muscle waste, weight loss
Amenorrhea (no period)
exophthalmos

61
Q

BULGING EYES (Exophthalmos) cause

A
  • fluid retention behind eyeballs, bulge forward. Cytokines promote inflamm, oedema
62
Q

hyperthyroid treatment

A
  1. Anti-thyroid drugs
    a. Interfere with TH synthesis
    b. Block uptake of I- (step2)
    c. Drug inhibit TPO (iodination 2)
  2. Prevent iodine coupling to thyroglobulin (MIT) (step 3)
  3. Surgical removal of portion of over-secreting thyroid gland
    a. Risk hypothyroidism
    b. Thyroid replacement surgery
  4. Administer radioactive iodine
    a. Destroy thyroid cells
    b. Reduce amt of thyroxine (T4)
    c. Reduce size of gland
63
Q

treat hypothyroidism

A
  1. Thyroid replacement therapy
  2. Iodine diet
64
Q

pancreas exocrine

A

Acinar and duct cells
NaHCO3- solution, digestive enzymes

65
Q

pancreas endocrine
□ Hormones into bloodstream

A

□ β Cell –> insulin, amylin
□ α Cell –> glucagon
□ D Cell –> somatostatin
High capillary network!

66
Q

insulin glucose control pathway

A

1) Glucose enter by passive facilitated diffusion (GLUT2)
2) Convert to glucose-6-phosphate (GLYCOLYSIS)
3) Krebs cycle (mitochondria)
4) ATP act on ATP-sensitive K+ channel, closing it
5) K+ in cell, depolarization
6) Acts on voltage gated Ca2+ channel
7) Excitation-secretion coupling
8) Release Ca2+
9) Stimulate insulin vesicles to be secreted out of β Cell
10) Reduce BGL to normal 4-6nM

67
Q

GLUT uses

A

• GLUT 4: muscle, adipose tissue
• GLUT2: kidney, liver, pancreatic b cell
• GLUT3: neurons

68
Q

insulin functions

A

Increase uptake of glucose, translocate GLUT 4
Glycogenesis (glucose –> glycogen store liver, muscles)
lipogenesis (FFA–> TG in adipose tissue)
Proteogenesis (aa –> proteins in muscle)

69
Q

glucagon MOA

A

1) Stimulate α Cell
2) Mobilise energy-rich molecules from stores
3) Incr BGL

70
Q

glucagon functions

A

• Glycogenolysis
• Glycogen –> glucose
• Lipolysis
• TGL –> FFA –> glycerol + ketones
• Proteolysis
• Protein –> aa
• Gluconeogenesis
• Aa –> glucose
• Glycerol –> glucose

71
Q

type 1 DM cause

Insulin-dependent diabetes
Childhood-onset/ juvenile
5-10%

A

Autoimmune process (β Cell no longer makes insulin)
• Genetics
• Environmental factors

72
Q

type II causes

Non-insulin dependent
Adult-onset
90-95%

A

Insulin resistance
• Makes insulin, but not used well

• Lifestyle (obesity)
• Genetics (obesity)
    • Environmental factors
73
Q

ACUTE consequences of DM

A

1) polyuria, polydipsia (thirst) –> renal failure
2) polyphagia (appetite)
3) ketosis (rapid breathing) –> metabolic acidosis –> diabetic coma
4) weight loss (muscle waste, worsen hypergly)

5) DEATH

74
Q

CHRONIC conseq of DM

A

§ Degenerative blood vessels
□ Microvascular: retinopathy, nerve damage, kidney failure

  □ Macrovascular: stroke, heart attack, reduce blood circ