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Physiology B2 & B3 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the embryological derivation of the adrenal gland?

A
  1. Mesoderm – 90% -> cortex
  2. Ectoderm (neural crest) – 10% -> becomes renal medulla (part of SyNS)
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2
Q

What are the layers of the adrenal gland, from outside -> inside?

A
  1. Superficial: capsule of connective tissue
  2. Cortex (2-4) -> GFR MGS
      1. zona glomerulosa -> mineral corticoid
      1. zona fasciculate -> glucocorticoids
      1. zona reticularis -> sex hormones (DHEA, androstenedione)
  3. Medulla (5) ->adrenaline and noradrenaline
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3
Q

For reference, pathways of steroid synthesis

A
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4
Q

How is the release of cortisol regulated?

A
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5
Q

What are the biological actions of glucocorticoids?

A
  • Bound in plasma to corticosteroid binding protein. Targets all cells/organs and the response depends upon the organ.
  • Two primary effects:
    • Metabolic:
      • ↑ gluconeogenesis, ↓glucose utilisation by cells -> net ↑ in plasma glucose
      • ↑intra hepatic protein synthesis but ↓ in all other tissues, freeing of amino acids for gluconeogenesis
      • ↑fatty acid mobilisation from peripheral adipose stores
    • Anti-inflammatory:
      • ↓production of cytokines, ↓clonal amplification of lymphocytes
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6
Q

What are the main drivers of aldosterone secretion?

A

Angiotensin II (primary) , ↑[K+] (major), ACTH (minor)

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7
Q

Despite the similarity of structure between cortisol and aldosterone and the 1000x higher cortisol concentration, why does cortisol not activate the MC receptor?

A

MC receptor protected by 11-beta-hydoxysteroid dehydrogenase which converts cortisol to inactive cortisone. Unless the concentration is high.

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8
Q

What androgens are produced by the zona reticularis of the adrenal cortex?

A

DHEA, androstenedione (weak androgens) and estrogen (minute amounts)

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9
Q

What are the major hormones secreted by the adrenal medulla?

A

Adrenaline, noradrenaline and dopamine

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10
Q

Which receptors do adrenaline and nor-adrenaline act upon? What is there action upon activation?

A
  • Adrenaline – β1 & β2
  • Noradrenaline – α1 & β1
  • Actions of receptors:
    • α1 – vasoconstriction
    • β1 – positive inotrope/chronotrope
    • β2 – SMC relaxation
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11
Q

What are the metabolic actions of adrenaline ,noradrenaline and dopamine?

A
  • ↑gluconeogenesis, ↑amino acid uptake into muscle, ↑uptake of K+ and PO4-
  • ↑glucagon, ↑renin, ↑GH
  • ↑dopamine -> ↓ prolactin secretion
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12
Q

What is Cushing’s syndrome? What are the causes?

A

Cushing’s syndrome = excess glucocorticoid production

Causes:

  1. Iatrogenic (medications)
  2. ↑pituitary ACTH (cushing’s disease)
  3. Primary adrenal pathology
  4. Ectopic ACTH production (lung cx)
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13
Q

What is Addison’s disease? What changes might you notice to the pts skin?

A
  • Addisons = glucocorticoid defiency.
  • Can present as tiredness, fatigue, weightloss, but also as emergency in an addisonian crisis
    • -> hypotension, dehydration, hyperkalaemia and metabolic acidosis.
  • Skin pigmentation may be present dt excessive ACTH production.
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14
Q

What is Conn’s syndrome? What is the difference between primary and secondary causes?

A
  • Conn’s syndrome – hypokalaemic alkalosis associated with hypertension
  • Primary -> adrenal adenoma -> excess aldosterone
  • Secondary -> ↑renin dt renal artery stenosis
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15
Q

What is CAH? What can it result in? What is the most common deficiency? How do you test for it?

A
  • Cogenital adrenal hyperplasia, inborn error of steroid metabolism, most commonly a deficiency in C21 hydroxylase deficiency.
  • Diagnostic testing -> high 17-hydroxyprogesterone
  • Signs/symptoms: cortisol deficiency + adrenal virilisation +/- salt wasting tendancy. Most commonly presents in neonates
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16
Q

What is the basic structure and function of a lipoprotein?

A

Allows insoluble lipids to be transported around the body

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17
Q

What is a triglyceride and what are the components of a triglyceride? How are they absorbed from diet?

A
  • Ester derived from glycerol and three fatty acids.
  • Major source of fatty acid and glycerol in diet.
  • In triglyceride form, cannot be absorbed in duodenum.
  • Pancreatic lipase breaks TGs down to monoglycerides, fatty acids and glycerol to be absorbed and then reassembled into chylomicrons to be transported to tissue -> remnants then return (cholesterol) to liver via LDLr
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18
Q

What hormone is responsible for triglyceride mobilisation from adipose stores?

A
  • Hormone sensitive lipase mobilises TGs, which release free fatty acids to blood where they bind to albumin and are distributed in the tissue.
  • Undergo beta-oxidation in mitochondria & peroxisomes -> acetyl-CoA, NADH, FADH2 for citric acid cycle.
  • In muscle Acetyl CoA ->ATP, Liver acetyl-CoA -> ketone bodies
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19
Q

What is the difference between a short and long feedback loop?

A

Short feedback: pituitary hormones -> hypothalamus

Long feedback: target gland hormone -> hypothalamus

20
Q

What are the hormones released from the posterior pituitary and what are their affect?

A

ADH

  • produced in supra optic nuclei.
  • Action: Aquaporin insertion in CD, thirst
  • Deficiency: Diabetes insipidus – extreme thirst and polyuria, ↑Na+ and osmolality
  • Excess: Inappropriate ADH -> water intoxication

Oxytocin

  • milk let down
21
Q

What are the hormones of the anterior pituitary and what is their function?

A

TSH

  • Stimulates
    • Thyroxine synthesis & thyroid growth
  • Release triggered by
    • TRH (hypothalamus)
  • Inhibited by
    • inhibited by thyroid hormones

FSH

  • Stimulates
    • Males: sertoli cells -> development of spermatozoa
    • Females: granulose cell of ovarian follicle
  • Release triggered by
    • GnRH
  • Inhibited by
    • Inhibited by test. and estrogen

LH

  • Stimulates
    • Males; Leydig cells -> testosterone
    • Females: interstitial cells -> estrogen, androgens and progestins
  • Release triggered by
    • GnRH
  • Inhibited by
    • Inhibited by test. and estrogen

ACTH (adrenocorticotrophic hormone)

  • Stimulates
    • Cortisol primarily and other adrenocortical hormones (androgens)
  • Release triggered by
    • CRF
  • Inhibited by
    • Inhibited by cortisol release

Prolactin

  • Stimulates
    • Lactation and inhibits reproductive hormone secretion
  • Release triggered by
    • nil
  • Inhibited by
    • Inhibited by dopamine (prolactin inhibitory factor)

GH

  • Stimulates
    • Promotes growth: skeleton, muscle, viscera
    • Metabolic: anti-insulin, anabolic, positive nitrogen balance
  • Release triggered by
    • Stimulated by GHRH, stress and exercise
  • Inhibited by
    • Inhibited by somatostatin
22
Q

What hormone is most commonly associated with pituitary hyperfunction?

A
  • Prolactin -> infertility and galactorrhea
  • **Acromegaly **-> excess GH
  • **Cushings **-> dt ACTH, but can be adrenal cortex or ectopic source
23
Q

What hormones are NOT associated with pituitary hypofunction?

A

Prolactin and oxytocins – no clinically recognised syndrome associated with deficit.

24
Q

What are the common features of a pituitary tumour?

A

Headache, impingement on optic chiasm -> bitemporal hemianopia, hypopituitarism, hyperprolactinaemia, diabetes insipidus

25
Q

What are the clinical features of acromegaly?

A
  • Increase in ring size, shoe, glove or hat size
  • Increase in size of nose, lips, soft tissue of face, tongue or jaw (prognathism) -> coarsening of features
  • Deep cavernous voice
  • Fleshy enlarged hands and feet
  • ↑metabolic rate: sweating, warm skin
  • Skin tags
  • Joint problems
26
Q

What are the metabolic and visceral features of acromegaly?

A

Hypertension, glucose intolerance, cardiac enlargement and failure, enlarged liver, spleen, kidneys, thyroid and adrenal.

27
Q

What are the functions of the pancreas?

A
  • Exocrine – 97-98% of pancreatic mass -> digestive enzymes
  • Endocrine function – Islet cells of Langerhans
  • BADFuckers – insulin, glucagon, somatostatin, pancreatic polypeptide
28
Q

What are the triggers for glucagon secretion? What affect does it produce?

A
  • Low glucose and elevated amino acids
  • Glucagon -> activates hepatic glycogenolysis and gluconeogenesis, activates lypolysis in adipocytes
29
Q

What triggers somatostatin release from delta cells?

A

Secreted in response to elevated glucose, inhibiting both glucagon and insulin secretion. Role poorly understood.

30
Q

What factors augment glucose-stimulated insulin secretion?

A
  • Other nutrients – FFA, amino acids
  • Incretin hormones – glucagon-like peptide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)
  • Parasympathetic NS
31
Q

What factors suppress insulin secretion?

A
  • Sympathetic NS, adrenaline
  • Somatostatin
32
Q

What is the difference between glut 1 and glut 4 glucose transporters?

A

Glut-1 responsible for basal glucose uptake, insulin translocates GLUT4 from intracellular pool to plasma membrane in insulin sensitive tissue

33
Q

What are the metabolic actions of insulin?

A
  • **Glucose metabolism **-> stimulates uptake by muscle, heart and adipose tissue, suppresses hepatic production
  • Protein metabolism -> stimulates AA transport, promotes anabolism and inhibits protein degredation
  • Lipid metabolism -> inhibits lypolysis in adipocytes and promotes hepatic VLDL secretion, activates lipoprotein lipase (hydrolysis of chlymicrons and VLDL) allowing fat uptake into peripheral tissue
34
Q

What is the normal fasting and fed state levels of blood glucose. What signs might you expect in a hypoglycaemic patient?

A
  • Fasting 3.5 – 5 mmol/l
  • Fed 4.0 – 7.0 mmol/l
  • Hypoglycemia
    • SyNS activation -> sweating, palpatations, anxiety
    • Brain dysfunction -> parathesia, confusion, seizures, coma
35
Q

During embryological development, where does the thyroid begin growth? What is the clinical significance of this?

A
  • Begins development at root of tongue in a tubular invagination called the foramen cecum, grows downwards infront of trachea and the distal end degenerates usually by 5th -> 6th week of fetal development.
  • This is clinically significant as its possible to have a thyroid that has no descended enough (lingual thyroid) or a thyroid that has descended too far (substernal thyroid)
36
Q

What are the steps involved in T3 & T4 production?

A

(Thyroglobulin has already been produced by thyroid epithelial cells (from tyrosine) is in follicular cells)

  1. Dietary iodine converted to iodide in gut and absorbed
  2. Taken up into thyroid dt massive concentration gradient (stimulated by TSH)
  3. Via thyroperoxidase, iodine is convalently bound to tyrosine residues in the thyroglobulin molecule, forming monoiodotyrosine (MIT) and diiodotyrosine (DIT)
  4. T4 (thyroxine) produced by combining 2 DIT -> prohormone
  5. T3 (triiodothyronine) produced by combining MIT and DIT -> active version
  6. Under influence of TSH, thyroglobulin with T3/T4 take up into endosome, digested and released as either T3 or T4
37
Q

Is thyroid hormone heavily bound or unbound? What is the purpose of this?

A

Thyroid hormones are tightly bound to plasma proteins, giving a large pool of hormones to ensure even delivery of thyroid hormones to all the tissues of the body.

38
Q

What three proteins are thyroid hormones bound too?

A
  • Thyroxine binding globulin
  • transthyretin
  • albumin
39
Q

Is the majority of T3 produced in the thyroid or in the periphery?

A

Majority formed in periphery by tissue deiodinases (d1, d2, d3 specific for tissues). Also forms rT3 (inactive) and DIT

40
Q

What are the effects of thyroid hormone on the heart, adipose tissue, muscle, bone and nervous system?

A
  • Heart: chronotropic and inotropic
  • adipose tissue: catabolic
  • muscle: catabolic
  • bone: development
  • nervous system: developmental
41
Q

What are the basic steps in oogenesis?

A
  • No primary oocytes form after birth, primordial germ cells in fetal development replicate ~2.5 mil primary oocytes present at birth (arrested in prophase (4n, crossing over occurred, prior to ovulation)
  • 36-48 hrs before ovulation, first meiotic division occurs, now 2’ ooctye and degenerating polar body
  • At ovulation, 2nd meiotic division begins and stops at metaphase
  • At fertilization, second meiotic division completes and second polar body extruded

Summary: 1 primary oocyte -> 1 ovum

42
Q

What are the basic steps involved in spermatogenesis

A
  1. Primordial germ to base of seminiferous tubules where they are spermatogonia
  2. At puberty spermatogonia undergo mitotic divisions -> clonal expansion
  3. Entry into first meiotic division -> primary spermatocytes (4n)
  4. Each primary spermatocyte divides into 2 secondary spermatocytes (2n)
  5. Secondary spermatocytes enter into second meiotic division, producing 2 spermatids (1n)
  6. Further maturation of spermatid into mature sperm in epididymis

Summary: 1 primary spermatocyte -> 4 spermatozoa

43
Q

Summarise the steps involved in fertilization

A
  • Ovulated egg has jelly cumulus (sperm swin through) and tough zona pellucida
  • Acrosome on sperm head eats through zona pellucida
  • Contact with cell membrane and sperm fuse -> triggers electrical signal that causes mucus secretion and coating of egg to prevent any other sperm penetrating it
  • Sperm head disintegrates revealing chromosomes & egg completes 2nd meiotic division
  • Fusion of pronuclei
44
Q

Summarise the steps of blastocyst implantation into endometrium

A
  • During first 3-4 days, zygote still in ampula
  • During this time, mitosis occurs forming morula
  • Progesterone produced by corpus luteum builds up nutrients in endometrium (purpose of waiting 3-4 days) and leads to relaxation of oviduct
    • (After 3-4days) -> morula descent
  • Morula developes into blastocyst
  • Trophoblast makes contact with endometrium, secretion digestive enzymes
  • Digestive enzymes allow penetration of endometrium by finger like trophoblastic cells
  • Carves out hole for blastocyst and implanted completed in endometrium
45
Q

What are the key system changes that occur during pregnancy?

A
  • Cardiovascular: increased HR, lower BP and higher CO
  • Resp: lower TV and higher RR
  • Renal: increased total body water, increased gfr, increased renal blood flow
  • GIT: decreased gastric motility
  • Coagulation: reduced platelets and increased clotting factors
46
Q

What are the placental hormones and what is their function?

A
47
Q

What are the relative phases of the ovarian and uterine cycle? What happens to hormone levels throughout this period?

A

Physiology B2 & B3 (5 decks)

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