Endocrinology Flashcards

1
Q

State 9 types of endocrine glands.

A
  1. simple tubule
  2. simple branched tubular
  3. simple coiled tubular
  4. simple acinar
  5. simple branched acinar
  6. compound tubular
  7. compound acinar
  8. compound tubuloacinar
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2
Q

How does endocrine gland secrete their secretory products?

A
  • No duct system
  • usually fenestrated capilary
  • release their secretory products (hormones) into the spaces between secretory cells (extracellular space) from where it enters the blood stream
  • close association with blood vessels
  • sparse supporting tissue
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3
Q

Is the following statement True or False?
One hormone can only triggers one cell.

A

False.
One hormone can triggers many cells with different reactions

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4
Q

state 5 endocrine organs (purely)

A
  1. pituitary gland
  2. pineal gland
  3. thyroid gland
  4. parathyroid gland
  5. adrenal gland
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5
Q

describe pituitary gland.

A
  • also called hypophysis
  • hangs inferior to hypothalamus (connected by infundibulum)
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6
Q

describe the microanatomy of posterior pituitary.

A
  • not glandular
  • connected with hyphothalamus via nerve bundle which run through the infundibulum
  • extension of the brain with nerve bundles
  • tract arises from neurons in the supraoptic and paraventricular nuclei of hypothalamus
  • neuroendocrine cell
    (i) receive neuronal input (neurotransmitter)
    (ii) release hormone (message molecules)
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7
Q

Describe anterior pituitary (adenohypophesis).

A
  • no neural connection, vascular
  • primary capillary plexus communicates with secondary capillary plexus via hypophyseal portal veins (within infundibulum)
  • Hypophyseal portal system
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8
Q

what does posterior pituitary?

A
  1. oxytocin
  2. ADH
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9
Q

What does anterior pituitary release?

A

Tropic hormone (act on another endocrine gland):
1. TSH
2. ACTH
3. FSH and LH

  1. GH
  2. PRL
  3. endorphins
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10
Q

describe the thyroid gland.

A
  • attatched to cranial portion of trachea
  • largest ductless gland
  • surrounded by thin capsule (dense irregular connective tissue)
  • septa extent into parenchyma (subdividing into lobes and lobules)
  • structural and functional units:
    (i) thyroid follicles
    (ii) follicular cells
    (iii) parafollicular cells
    (iV) connective tissue
    (v) capillaries
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11
Q

how many parathyroid glands des animal have?

A
  • 4 small glandular bodies
  • 2 on surface, 2 embedded.
  • thin CT capsule
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12
Q

What is the subdivision of adrenal gland?

A
  1. superficial adrenal cortex
    - stores lipids, cholesterol and fatty acid
    - produced steroid hormone (corticosteroids)
  2. inner adrenal medulla
    - secretory activity controlled by sympathetic division of sutonomic NS
    - produces epinephrine (adrenaline) and norepinephrine
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13
Q

What is the 3 regions of cortex?

A
  1. Zona arcuate/ glomerulosa (outer)
    - produce aldosterone
    - electrolyte and water homeaostasis (promote reabsorption of sodium in kidney)
  2. Zona fasciculata
    - glucocorticoids (stimulated by ATCH pituitary)
  3. Zona reticularis (inner)
    - androgen (sex hormone)
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14
Q

what does adrenal medulla produce?

A
  • adrenal medulla: fight or flight response (part of autonomic nervous system)
  • modified postganglion sympathetic neurons (direct synaptic control of chromaffin cells)
  • 2 types of secretory cells:
    (i) epinepgrine secreting cells (adrenaline)
    (ii) norepinephrine secreting cells (noradrenalin)
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15
Q

example of neuro-endocrine control

A

enterogastric reflex
- autonomic nervous system
- hormones from GIT

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16
Q

What are the types of hormones?

A
  1. Protein hormones
    - synthesized from chain of amino acids varying greatly in length forming peptides/ proteins that target specific receptors in the tissues
    - stored in secretory granules > secret out into the plasma usually
    - hydrophilic and are transported in blood in the dissolved form
  2. Steroid hormones
    - synthesized from cholesterol
    - production of dependent on presence of specific enzymes. No storage
    - lipophilic and are transported in blood specific (globulin) and nonspecific (albumin) binding protein.
  3. Amine hormones
    - derived from tyrosine
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17
Q

How do hormone interacts with each other?

A
  • target cells contain receptors for specific hormones (lock and key mechanism)
  • protein/ peptide hormone receptors are found on plasma membrane of the cell
  • steroid and amine hormones receptors are located in the cytoplasm or nucleus of the cells (access due to lipophilic nature/ slow to act due to influence on mRNA and protein synthesis)
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18
Q

Describe HPA- hypothalamus-pituitary-axis.

A
  • major regulatory structure for integrated feedback control and homeostasis
  • growth hormone is a good example
  • the pituitary is intimately connected to the central nervous system via the hypothalamus
  • hypothalamus is like a middle man.
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19
Q

Where is growth hormone produced?

A
  • produced by somatotrope cells in anterior pituitary
  • also called by somatotropin
  • regulates body growth and intermediary metabolism
  • negative feedback to inhibit the released of GH
  • positive feedback to release inhibin that also decrease the released of GH
    > negative and positive feedback inhibit the release of GH
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20
Q

What is growth hormone?

A
  • protein hormone
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21
Q

what does growth hormone do?

A

it is responsible for:

  1. protein synthesis
    - turning amino acid into new tissues > increase cell number
    - genetics plays a role
  2. hyperplasia (increase in number), hypertrophy (increase in size) of tissue
  3. bone growth (length and thickness)
  4. increase in fat breakdown
  5. stimulate fat breakdown. muscle use fatty acid rather than glucose as energy source
  6. GH decrease glucose uptake into muscle
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22
Q

What influence the release of GH?

A
  • GH (released in anterior pituitary) release a balance between GHIH and GHRH from hypothalamus
  • low blood glucose is the major stimuli for increasing GH
  • GH levels also increased by stress, exercise, high protein diet, diurnal rythms and ghrelin
  • GH has a major feedback on anything other on GHRH
  • GH: positive feedback to GHIH
  • GH: negative feedback to GHRH
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23
Q

What is IGF-1?

A
  • one of many somatomedins that control growth
  • produced in the liver and released into circulation
  • produced in other tissues but not released, e.g. gonads
  • contributes to growth and development: cell division/ bon (skeletal) growth/ protein synthesis
  • inhibit GH release form pituitary, reduces GHRH and increases GHIH
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24
Q

what is the effects of GH/ IGF-1 on bones?

A
  • GH stimulates bone growth in length and which via the somatomedin IGF-1
  • stimulate cartilage proliferation and osteoblast activity
  • lengthening only occurs while the growth plate is ‘open’
  • sex hormones influence closing of plates and cessation of lengthening at maturity
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25
Q

what is acromegaly?

A

abnormal growth, especially bone (thickness) due to high GH after maturity.

26
Q

What is the 3 sources of circulating glucose?

A
  1. intestinal absorption during digestion
  2. glycogenolysis (the breakdown of glycogen)
  3. gluconeogenesis (formation of glucose primarily from lactate and amino acid) in liver
27
Q

where is insulin and glucagon produced in?

A

insulin and glucagon are produced by pancreas

28
Q

Why is blood glucose important?

A
  • low blood glucose (hypoglycaemia) will fail to provide adequate energy to tissue > brain and red blood cells requires constant supply of glucose (life threatening if the brain stop)
  • high blood glucose levels (hyperglycaemia) may arise due to an inability of cells to take glucose from the plasma.
29
Q

describe the pancreas

A
  • has endocrine and exocrine functions
  • exocrine functions concerned with digestion
  • only 2% pancreatic weight concerned with endocrine function (glucose homeostasis)
  • islet of langerhans contains 3 types of cells:
    (i) α - glucaogon
    (ii) β - insulin
    (iii) δ - somatostatin
30
Q

Describe the structure of insulin

A
  • insulin is a protein made up of α and β chain joined by 2 disulfide bridges
  • once it is secreted into plasma, there’s 2 things with insulin (the important one) and the c-peptide.
31
Q

what is the effect of insulin?

A

insulin controls carbohydrates, fat and protein:

  1. Carbohydrate:
    - insulin stimulates glycolysis for fuel storage
    - liver, adipose tissue and muscle = glycogen
  2. Lipid:
    - insulin inhibits lipases = reduce lipolysis
    - FFA produced go to adipose tissue and more fat layed down
  3. Protein:
    - insulin promotes amino acid uptake into all cells
    - protein synthesis stimulated
  4. Other actions
    - promotes K+ uptake by cells thus inducing hypokalemia
32
Q

what is glucagon?

A
  • single chain peptide prodcued by a cells in the cell of langerhans
  • increase glucose level in blood when level have fallen
  • acts primarily on liver:
    (i) decrease glycogen synthesis
    (ii) increase glyconeogenesis (glucose is generated from pyruvate and/or LAC)
    (iii) increase gluconeogenesis (produce glucose)
  • fasting depletes liver of glycogen, glucagon then has no effect
  • prevent overshoot of glucose levels due to insulin

regulation: increased by hypoglycaemia (low blood glucose) / decreased by hyperglycaemia, insulin and somatostatin

33
Q

reason for the disruption of glycaemia control.

A
  1. sue to endocrine pancreas cell destruction (inflammation or auto-immune disease/ pancreatitis)
  2. due to altered insulin sensitivity in cells (insulin resistance)
34
Q

what happens when blood glucose levels increase? (that results in diabetes mellitus)

A
  • decrease glucose uptake into body tissue
  • increased protein catabolism resulting in increased hepatic gluconeogenesis
  • increased glycogenolysis
  • increased lipolysis
35
Q

what are the clinical signs of diabetes?`

A
  1. Polyuria: loss of glucose and water in urine
  2. Polydipsia: increase blood osmolarity and thirst
  3. Polyphagia: low energy signals hunger
  4. weight loss: increased catabolism of muscle and fat
    5.infection: damaged to blood vessels inhibits white cell function
36
Q

Describe the physiology anatomy of adrenal gland.

A
  • medulla: catecholamine = adrenaline (epinephrine) and nor-adrenaline (non-epinephrine) and dopamine
  • cortex: mineralcorticoids (aldosterone) and glucocorticoids (cortisol)

*Zona glomerulosa: mineralcorticoids = aldosterone
*Zona fasciculata: glucocorticoids
*Zona reticularis: adrenal androgens

37
Q
  1. What is the function of catecholamine (= adrenaline)?
  2. What is the secretion stimulated by?
  3. What is the change in metabolic energy?
A
  1. Function: flight or fight
  2. secretion is stimulated by hypoglycaemia and haemorrhage
  3. increased blood glucose & glycogeneolysis & lipolysis
38
Q

state the route of stress response that stimulate the release of epinephrine (adrenaline).

A
  1. stressor > hypothalamus >sympathetic nervous system > adrenal medulla > increase epinephrine (adrenaline)
  2. stressor > hypothalamus > posterior pituitary > increase vasopressin = ADH
  3. stressor > hypothalamus > increase CRH > anterior pituitary > increase ATCH > adrenal cortex > increase cortisol
39
Q

state the 2 major groups of hormone produced in the adrenal cortex.

A
  1. Glucocorticoids: cortisol (man/pig/horse/sheep/dog/cat) or corticosterone (rabbit/rodent/reptiles/birds)
  2. Mineralocortioids: aldosterone
40
Q

what is the action of glucocorticoid?

A

metabolic- increased energy availability:

  1. Carbohydrates:
    - stimnulate hepatic gluconeogenesis and inhibit glucose uptake extrahepatically leading to hyperglycaemia
  2. Protein:
    - stimulates reduction in extrahepatic anabolism and stimulation of catabolism leading to negative nitrogen balance
  3. Lipid:
    - stimulates lipolysis and decrease glucose uptake in fat tissue. metabolisation of fat occurs and can lead to pendulous abdomen.
41
Q

state the anti-inflammatory response of glucocorticoids.

A
  • GCS are antagonistic to many inflammatory responses
  • inhibit the formation of prostaglandins
  • down regulate fibroblast proliferation and collagen formation
  • reduce endothelial cell permeability
  • alter immune response
42
Q

Action of glucocorticoid in:
1. Nervous system
2. blood pressure
3. Fetal maturation
4. Water excretion

A
  1. High cortisol leads to euphoria/ Low. concentration leads to fear, irritability, increased sensitivity to olfactory stimulation
  2. unknown action
  3. stimulate surfactant production in lungs, hepatic enzymes and involved in initiation of parturition
  4. cortisol inhibits ADH causing polyuria
43
Q

What is the therapeutic actions of glucocorticoids?

A
  1. Lymphoid tissues:
    - high conc of cortisol receptors
    - see lysis of lymphoid tissue (spleen, thymus)
    - decreased levels of circulating lymphocytes and eosinophils so decreased cell and humoral mediated immunity
  2. Anti-inflammatory
    - Inhibit PLA2 which produces inflammatory causing substances (e.g. prostaglandins, thromboxanes, leukotrienes)
    - Capillary permeability increased when glucocorticoid levels decreased. therefore give cortisol in circulatory shock to reduce capilary permeability.
44
Q

what is the major mineralcorticoids produced in adrenal cortex?

A
  • Aldosterone

function: relates of electrolytes balance (Na and K) and blood pressure (body water) homeostasis
- control Na+ retention and water at the kidney, sweat and salivary gland and intestine (exchange for K and H)
- minor action: promote K+ entry into cells
- low level of aldosterone leads to the fall in extracellular Na and Cl, rise in K

45
Q

how to diagnose adrenal issue?

A
  1. ACTH stimulation test
    - cortisol levels are measured before and after injection of a synthetic form of ACTH
    - After injection of ACTH > will have a spike of cortisol
  2. Dexamethasone suppression test
    - cortisol level measure before and following injection of dexamethasone (suppress ACTH)
46
Q

what stimulate thyroid gland?

A

thyroid gland receive sympathetic stimulation

47
Q

describe the synthesis of hormones.

A
  • formed from tyrosine and iodine
  • iodine absorbed from intestine, actively trapped in follicle cells
  • iodination of thyroglobulin catalysed by thyroperoxidase
  • hormone stores in colloid
48
Q

Describe the release of thyroid hormone.

A
  • thyroglobulin re-enters follicular cells
  • T3 (triiodothyronine), T4 (thyroxine), MIT (monoiodotyrosine), DIT (diiodotyrosine) cleaved from TBG (thyroxine binding globulin) by lysosomal enzyme
  • MIT and DIT deiodinated
  • T4 and T3 released
49
Q

What is the action of thyroid hormones?

A
  1. Metabolic
    - increase basal metabolic rate and heat production
    - affects rate of synthesis and degeneration of fats, carbohydrates and protein
    - affects blood glucose (e.g. increase absorption from GIT)
  2. Growth and development
    - T4 and growth hormone are necessary for normal growth
  3. Reproduction
    - essential for reproduction
  4. skin and hair
    - low T4 leads to slow growth or loss
  5. skeletal muscle
    - efficiency and work capacity affected
  6. central nervous system
    - reduction in myelin and fewer cortical neurons
50
Q

state the route of thyroid secretion

A

hypothalamus release TRH (thyroid releasing hormone) > stimulate anterior pituitary to release TSH (thyroid stimulating hormone) > stimulate thyroid gland to increase T3 and T4 synthesis and release > release is regulated by negative feedback of T4 on anterior pituitary and hypothalamus

51
Q

what are the clinical signs of hyperthyroidism?

A
  • weight loss
  • increase appetite
  • increased HR and pulse pressure
  • increased metabolic rate and heat production
  • low tolerance to temperature change
52
Q

What does hypothyroidism lead to?
And what are the clinical signs?

A
  1. in young leads to developmental neurological defects, in adult - myxoedema
  2. Clinical signs:
    - oedema (especially face)
    - possible obesity
    - dry/ brittle hair/ fur
    - lethargy
    - CNS dysfunction
53
Q

whats is the physiological role of Ca2+?

A
  • muscle contraction
  • nerve cell activity
  • cell sound messenger
  • release of hormones by exocytosis
  • enzyme activity
  • blood coagulation bones and teeth
  • stability of cell membrane
54
Q

what hormones are involved in the regulation of Ca2+?

A
  1. parathyroid hormone (PTH)
  2. calcitonin
  3. vitamin D
55
Q

describe parathyroid hormone.

A
  • produced by parathyroid gland
  • peptide hormone
  • little storage but immediately synthesised and release when Ca2+ levels in plasma fall
  • metabolised by liver and kidney
56
Q

state the route of PTH responds to plasma calcium.

A

low plasma Ca > simulate parathyroid glands > increase PTH > increase Plasma Ca2+

high plasma Ca > stimulate thyroid c cells > increase calcitonin > decrease plasma Ca

57
Q

what is the actions of PTH?

A
  1. PTH increase Ca2+ and decrease PO4 (in plasma in ECF)
  2. Ca2+ + PO4 2- > CaPO4
  3. PTH acts on bone (increase bone reabsorption) / kidney (increase absorption of Ca2+ in renal tubular and stimulate production of vitamin D) / GI tract (increase absorption through action of vitamin D)
58
Q

what is the function of calcitonin?

A
  • counterbalance effects of PTH- induces hypocalcaemia and hypophosphatemia
59
Q

What is the action of calcitonin?

A
  1. Bone- prevent osteoclasts from reabsorbing Ca from bone and increases PO4 deposition in bone and ECF inducing hypophosphatemia
  2. Kidney- increase excretion of both Ca and PO4 are seen due to decreased reabsorption of both Ca and PO4 in the ascending limb of loop of henle and distal convoluted tubule
  3. Intestine- inhibits gastrin and gastric acid secretion and reducing Ca uptake
60
Q
A