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Urogenital, Reproductive, Genetics, Endocrine > Thyroid & hormones > Flashcards

Thyroid & hormones Flashcards

1
Q

Name the 2 hormones released by the posterior pituitary gland

A
  • Anti Diuretic Hormone (ADH) / Vasopressin
  • Oxytocin
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2
Q

Name the 6 Hormones released by the anterior pituitary gland

A

FLAT PeG

  • Follicle Stimulating Hormone (FSH)
  • Luteinising Hormone (LH)
  • Adrenocorticotrophin Hormone (ACTH)
  • Thyroid Stimulating Hormone (TSH)
  • Prolactin
  • endorphins
  • Growth Hormone (GH)
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3
Q

Describe the thyroid hormone axis

A
  • Hypothalamus makes thyrotropin releasing hormone (TRH)
  • Anterior pituitary makes thyrotropin/ thyroid stimulating hormone (TSH)
  • Thyroid gland makes (T3) Triiodothyronine / (T4) Thyroxine
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4
Q

Describe the difference between T3/T4

A
  • T4 = Thyroxine / Tetraiodothyronine
  • T3 = Triiodothyronine
  • Secretion T4 > T3
  • T3 more biologically active
  • T4 converted to T3 by deiodinase enzymes
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5
Q

Name some implications of hyperthyroid disease

A

↑ GIT glucose absorption
↑ GIT motility
↑ gluconeogenesis & glycogenolysis
↑ proteolysis & lipolysis
↑ metabolic enzymes
↑ protein synthesis
↑ BMR & Calorigenesis
- Vitamin deficiencies

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6
Q

Name some implications of Hypothyroidism

A
  • *↓ protein synth**
  • *↓ O2 consumption**
  • *↓ BMR, Calorigenesis**
  • *↓ proteolysis, lipolysis**
  • *↓ LDL receptors → ↑ cholesterol**

Children - ↓ GH, ↓ bone growth

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7
Q

What is the pathophysiology of Hashimoto’s Thyroiditis?

A

Autoimmune disease involving the production of:

  • Thyroid peroxidase antibodies (TPO Ab)
  • Thyroglobulin antibodies (Tg Ab)
  • TSH receptor-blocking antibody

Most people with Hashimoto’s have high levels of these

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8
Q

What are the effects of cortisol in the body?

A
  • Promotes catabolism of proteins & fats
  • Helps body adapt to stress
  • Can function as anti inflammatory drug & immunosuppressive
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9
Q

What are some locations of thyroid hormone receptors?

A
  • DNA/Ribosomes → Nuclear receptors that act as transcription factors, affecting regulation of gene transcription & translation
  • Mitochondria/Na-K pump → 2nd messenger activation & cellular response
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10
Q

What are peripheral effects of thyroid hormones?

A

↑ Protein synthesis

↑ O2 consumption

↑ energy production and use

This increases activity of BMR via anabolic and catabolic pathways

Ie- in hyperthyroidism, an over creation and breakdown of structures and metabolites, leading to ↑↑ BMR increase and inefficiency

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11
Q

Name some signs & symptoms of Hyperthyroidism

A
  • Exophthalmos
  • Goitre
  • Muscle weakness
  • Weight loss
  • Increased appetite
  • Vitamin deficiencies
  • Hyper-reflexia
  • Restlessness, Anxiety
  • Irritability, Insomnia
  • Fine tremor
  • Heat intolerance, sweating, superficial vasodilation
  • Warm, soft skin
  • Diarrhoea
  • Pre-tibial myxedema
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12
Q

Name some signs and symptoms of Hypothyroidism

A
  • Goiter
  • Loss of appetite
  • Weight gain
  • Hypo-reflexia
  • Poor concentration
  • Impaired memory
  • Cognitive dysfunction
  • Constipation
  • Cold intolerance
  • Depression
  • Coarse hair, dry skin
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13
Q

What are some causes of secondary Thyroid disease

A
  • UNCOMMON
  • Hyperthyroidism
    • TSH overproduction - eg due to pituitary adenoma/ hypothalamic disease
    • Elevated serum T4, T3 & elevated TSH levels
  • Hypothyroidism
    • Disease of Pituitary or Hypothalamus
    • Reduced TSH secretion
    • Reduced serum levels of T3, T4 & TSH
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14
Q

4 things potentially involved in treatment of Hyperthyroidism

A
  • Beta-blockers - symptom reliever only
  • Anti thyroid drugs - Carbimazole, Propylthiouracil (PTU)
  • Radioiodine (I131)
  • Thyroidectomy
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15
Q

Treatment of Hypothyroidism

A
  • Replace thyroid hormone - levothyroxine (T4)
  • About 80% of oral absorbed from GIT
  • Repeat in 3-4 weeks, adjust dose every 4-8 weeks
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16
Q

Describe the steps of Thyroid hormone synthesis

A
  1. Iodide actively transported from blood into follicle cell (I- / Na+co-transporter). Moved to colloid space and oxidised (thyroid peroxidase).
  2. Thyroglobulin is synthesised and secreted (exocytosis) into colloid space
  3. Iodine added to tyrosines of Thyroglobulin
  4. Thyroglobulin returns (endocytosis) into follicle cell.
    Lysosomal proteases then hydrolyse this polymer into many T3/T4 monomers
  5. T3 & T4 diffuse into capillaries, and taken mostly (~70%) by transport proteins
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17
Q

Describe pathophysiology of goitre development in Grave’s disease

A
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18
Q

Describe the pathophysiology of goitre development in iodine deficient hypothyroidism

A
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19
Q

What are the 2 types of secreting cells in the Thyroid gland, and their secretions?

A
  • Follicular cells - T3/T4
  • Paracollicular C-cells - Calcitonin
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20
Q

How many parathyroid glands are there?

A

4

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21
Q

Parathyroid → cells, receptors, hormones

A
  • Mostly chief cells
  • Have calcium sensing receptors
  • Produce parathyroid hormone when plasma calcium concentration falls
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22
Q

What is the “big picture” function of the Adrenal glands?

A
  • Maintain homeostasis via affecting:
    • glucose
    • salt
    • water
    • BP
    • stress response
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23
Q

What are the 4 adrenal zones/layers?

A

From outermost to innermost:

  • 3x cortex regions
    • Zona glomerulosa - mineralocorticoids
    • zona faciculata - glucocorticoids
    • zona reticularis - androgens
  • Medulla
    • epinephrine
    • norepinephrine
    • tiny amounts dopa & dopamine
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24
Q

Describe adrenal hormones in general

A
  • Steroids - synth from cholesterol
  • Lipid soluble - not stored in vesicles
  • Diffuse into cell of target tissue - activate intracellular receptors
  • Transported in blood by binding proteins
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25
Q

Name the 3 pathways of Aldosterone secretion

A
  • Hypotension (RAAS)
  • Hyperkalemia
  • ACTH secretion
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26
Q

Aldosterone secretion leads to retention of which ion in particular?

A

Na+

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27
Q

Actions of Angiotensin II include:

A
  • Generalised vasoconstriction
  • ↑ Norepinephrine release from sympathetic nerves (↑ SV & HR)
  • Stimulation of Na+ reabsorption kidneys (prox tubules)
  • Stimulation of ADH secretion via hypothalamus receptors
  • Stimulates thirst. ↑ fluid intake, thus ↑ ECF & ↑ BP
  • Aldosterone secretion → adrenal cortex - Na+ reabsorption (dist tubules)
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28
Q

What does decreased renal perfusion pressure trigger?

A
  • Release of Renin from juxtaglomerular cells (JGC’s)
  • This converts already circulating Angiotensinogen (made in liver) to Angiotensin-I
  • ACE (angiotensin-converting-enzyme - circulating and in pulmo-vasculature) then converts this to Angiotensin-II
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29
Q

Angiotensin II effects

A

↑ Thirst
↑ TPR
↑ Na+ - H+ exchange → ↑Na+ reabsorption
↑ Aldosterone - ↑Na+ reabsorption

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30
Q

How is non-pathological, genetic short stature determined?

A

Low levels of Growth Hormone Binding Protein (GHBP) is genetically predetermined

This affects circulating levels of growth hormone

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31
Q

How does pregnancy affect levels of triiodothyronine (T3) & thyroxine (T4)?

A

Elevated oestrogen stimulates production of Thyroxin Binding Globulin

This lowers free circulating levels of T3/T4

→ reduces negative feedback inhibition of TRH, TSH

thus more T3/T4 is created

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32
Q

Insufficient thyroid hormone in childhood leads to:

A

Inadequate stimulation of Growth Hormone production, which leads to

  • poor bone growth
  • mental retardation

with thyroxine Rx, bone growth can be largely restored but mental function cannot

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33
Q

What causes T1DM

A

An auto-immune disease caused by immune mediated destruction of insulin-producing β-cells in the pancreas

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34
Q

Name some theories behind development of T1DM

A
  • Genetic susceptibility → Higher concordance rates in identical twins.
    Recent genome studies have identified multiple succeptible loci for type 1 diabetes
  • Environmental factors → Evidence that factors such as viral infections may be involved in triggering islet cell destruction
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35
Q

Describe timeframe of insulin-producing β-cells destruction in T1DM

A

Typically after onset of symptomatic disease, β-cell destruction continues and leads to absolute insulin deficiency within 5 years

“Honeymoon phase” initial total daily requirements <0.3 units insulin/kg/day

Lifelong disease, lifelong insulin requirement

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36
Q

What does metabolic syndrome include?

A

Insulin resistance

Hypertension

Cholesterol abnormalities

Increased risk of clotting

Often overweight or obese, but uncommonly symptoms may occur in patients with normal body weight

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37
Q

Signs and symptoms of metabolic syndrome include:

A
  • Fasting hyperglycaemia
  • Hypertension
  • Elevated triglycerides
  • Decreased HDL cholesterol
  • Central obesity → waist circ > 102cm men, 88cm women
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38
Q

Risk factors metabolic syndrome

A

Central obesity

Physical inactivity

Over 50y

Prolonged stress → HPA (hypothalamic-pituitary-adrenal) axis imbalance leading to high blood cortisol, and thus high blood glucose and insulin

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39
Q

How to diagnose T2DM

A

Random blood glucose >11mmol/L

Fasting blood glucose > 7 mmol/L

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40
Q

Causes of type 2 diabetes (think micro)

A
  • Decreased sensitivity to insulin - decreased response of insulin sensitive tissues
  • Dysfunctional insulin secretion - Insulin secretion is impaired, and unable to compensate for resistance in peripheral tissues
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41
Q

Insulin resistance is defined as:

A

The failure of target tissues to respond normally to insulin

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42
Q

“Incretins” are:

A

Gut hormones that stimulate insulin release -

Eg: glucagon like peptide (GLP-1)

Responsible for increased insulin release that occurs post meal - vs IV glucose inj

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43
Q

Other professionals to refer to for management of diabetes

A

Dietitian

Exercise Physiologist

Opthamologist or optometrist

Podiatrist

Dentist

44
Q

Rx algorithm for T2 diabetes

A

Begin at the top, if not working, add the next

  1. Lifestyle modification - diet, weight, physical activity
  2. Metformin (1st line Rx)
  3. Add one of →

SGLT-2 inhibitors - (Dr Jack Big Fan - other extraglycaemic benefits renal, cardiac) OR
GLP-1 Therapies (Dr Jack Big Fan - other extraglycaemic benefits weight loss)OR

  1. Sulphonylurea - (DR Jack not a fan - oldschool, high hypo risk)
    Acarbose OR
    Glitazone OR
  2. Insulin → last resort really
45
Q

Give an example of a Biguanide, its MOA and some side effects

A

Metformin:

MOA:

  • Decreases hepatic gluconeogenesis
  • Increases peripheral insulin sensitivity

Side effects:

  • Lactic acidosis
  • GIT discomfort or diarrhoea
46
Q

What hormones are secreted by pancreatic islets?

A
47
Q

Describe composition of pancreatic islets - (endocrine cells or islets of langerhans)

A
48
Q

What prompts glucagon release

A

Decreased blood glucose (major)

Increased intake of amino acids (minor - think keto)

Cortisol, exercise, infections (stressors - minor)

CCK, Gastrin (enteric endocrin)

49
Q

GLUT 2 transporters are low affinity, which means:

A

They only transport glucose into the cell when concentrations are high

50
Q

Primary targets of glucagon are:

A

Liver and adipose tissue

51
Q

In liver, glucagons actions are

A

Gluconeogenesis (prodn of glucose)

Glycogenolysis (breakdown of glycogen)

52
Q

In adipose tissue, glucagon:

A

Activates hormone sensitive lipase → fat catabolism

Release of FFAs

Activation of ketogenesis → metabolism of FFAs

53
Q

2 major sites for insulin action

A

Hepatocytes - remember, it passes through portal circulation to here first!

Skeletal muscle

54
Q

Describe metabolic effects of insulin

A
55
Q

Describe the main effects of glucagon

A
56
Q

Glucagon’s primary targets are:

A

Liver (major)

Adipose tissue - tiny bit

57
Q

Insulin receptor down regulation occurs with:

A

Chronically high insulin levels

Obesity

Excess growth hormone

(decreased insulin sensitivity)

58
Q

Insulin receptor up regulation occurs with:

A

Exercise

Starvation

(increased insulin sensitivity)

59
Q

Early, Intermediate and Late effects of Insulin:

A

Early:

  • Absorption of glucose from blood

Intermediate:

  • Modulation of enzymes (phosporylation) → metabolic processes

Late:

  • Proliferation, growth, differentiation
60
Q

Describe Insulin effects on blood levels of key metabolites

A

↓Glucose
↓Fatty acids
↓Keto acids
↓Amino acids

61
Q

Describe glucagon effects on blood levels of key metabolites

A

↑Glucose
↑Fatty acids
↑Keto acids
No effect amino acids

62
Q

How do insulin and glucagon effect Glycogenolysis?

(Think hormones)

A
63
Q

How do insulin and glucagon effect Gluconeogenesis?

A
64
Q

How do insulin and glucagon effect Glycolysis?

A
65
Q

Define Gestational Diabetes Mellitus (GDM)

A

Inability to compensate for pregnancy metabolic needs

Insulin resistance in pregnancy

66
Q

Glucose transporters and their location

A

GLUT 1 - RBCs → work without insulin

GLUT 2 - Liver, Kidneys (2 way) → Phosphorylation of glucose in hepatocyte by hexokinease maintains glucose gradient as more glucose enters cell

GLUT 3 - Neurones - in brain, work without insulin

GLUT 4 - Skeletal muscles, Adipose tissue (1 way) → Insulin dependent

67
Q

Diabetes type 2 pathophysiology leads to both:

A

Decrease in responsiveness of peripheral cells to insulin

Inadequate responsiveness of B-cells to glucose

68
Q

In type 2 diabetes, what causes hyperglycaemia?

A
  • In response to a glucose load, ~70% less glucose is secreted than nondiabetic patients
  • Pattern of insulin affected - no post intake spike (smaller, slower, erratic)
  • ALSO → excessive hepatic glucose production, compounding higher levels of fasting glucose
  • Sustained hyperglycaemia impedes insulin signalling and β cell function
69
Q

Risk factors for GDM (Gestational Diabetes Mellitus)

A
  • Genetic predisposition (ethnic groups)
  • History of macrosomia (birth weight >4500 g or >90th centile)
  • Polycystic ovary syndrome
  • Essential or pregnancy-related hypertension
  • History of spontaneous abortions/unexplained still births
  • Family history of diabetes/history of GDM
  • Obesity (pre pregnancy BMI >30)
  • Medications - corticosteroids, antipsychotics
70
Q

Complications of GDM (Gestational Diabetes Mellitus) - Mother & Foetus

A

Maternal risks:

  • Increased risk of UTIs
  • Preeclampsia
  • Caesarean delivery/delivery of large baby

Foetal Risks

  • Hypoglycaemia
  • Macrosomia (birth weight >4000g)
  • Shoulder dystocia/brachial plexus injury
  • Stillbirth
71
Q

Explain HbA1c - Glycated Haemoglobin

A

Haemoglobin with a glucose molecule attached

Indicated excessive blood glucose

Measurement is a general indicator of a 3 month average of blood glucose (remember 120 day average RBC lifespan)

Higher amounts of HbA1c in patients indicates poorer glucose control

72
Q

Describe the production of insulin.

Also, what is it and where does the magic happen?

A

Insulin is a protein, made in pancreatic β cells:

  • mRNA encodes Proinsulin
  • Proinsulin enters ER, packaged to Golgi
  • In the golgi, proteases break down proinsulin to make:
    • Insulin and C-peptide
  • Both are secreted via exocytosis
73
Q

Explain C-peptide - a byproduct of insulin creation - and advantages of measuring it

A
  • No known physiological functions

But, it can be measured as an indicator of β cell function because:

  • Created in equal amounts with insulin
  • Longer plasma half life than insulin
  • Excreted unchanged in urine
74
Q

Steps in the secretion of insulin

A

Pancreatic β cells have GLUT-2 transporters, which have low glucose affinity

Ie, a significant increase in blood glucose leads to an increase in Insulin secretion

  1. Glucose enters β cell via GLUT-2 transporter,
  2. Glucose phosphorylated by glucokinase to glucose-6-phosphate (remember glycolysis)
  3. G-6-P metabolised to produce ATP
  4. ↑ ATP inhibits ATP sensitive K+ channels
  5. → β cell depolarises
  6. Depolarisation opens voltage sensitive Ca2+ channels
  7. → Influx of Ca2+
  8. High intracellular Ca2+ leads to exocytosis of vesicles w insulin & c-peptide
75
Q

How do increased plasma levels of amino acids lead to secretion of insulin?

A
  • Amino acids are absorbed by pancreatic β cell
  • Converted to energy in Kreb cycle via pyruvate & Acetyl CoA
  • ⇑ Cellular ATP → closure of ATP sensitive K+ channels
  • Cell depol, opening of voltage sensitive Ca2+ channels → Ca2+ influx
  • High intracellular Ca 2+ leads to exocytosis of insulin & c-peptide vesicles
76
Q

Describe ANS (Autonomic nervous system) impact on insulin release

A

Parasympathetic (feeding) → Ach → ⇡ Insulin release

Sympathetic (fight or flight) → NE → ⇣ Insulin release

77
Q

Describe the actions of Glucagon

A
  • Promote Gluconeogenesis
  • Promote Glycogenolysis
  • Promote release of FFAs from adipose tissue (activates hormone sensitive lipase)
  • Promote Ketogenesis - metabolism of FFAs
78
Q

Describe the actions of Insulin

A
  • Triggers GLUT-4 translocation to cell surface of SKM - ⇡ glucose absorption
  • Triggers GLUT-2 translocation to cell surface of Hepatocytes - ⇡ glucose absorption
  • Promotes glycogenesis
  • Inhibits proteolysis
  • Promotes fat synthesis
  • Inhibits hormone sensitive lipase
79
Q

Number of available insulin receptors is affected by

A
  • Exercise
  • Diet
  • Insulin and other hormones (pancreatic polypeptide)
80
Q

Insulin receptor up regulation occurs with

A
  • Exercise
  • Starvation
81
Q

Insulin receptor down regulation occurs with

A
  • Chronically high insulin levels
  • Obesity
  • Excess growth hormone
82
Q

Glucagon-like-peptide 1 (GLP-1) is a potent stimulant for?

A

Insulin release from pancreatic B cells

83
Q

Describe Ghrelin - Where it comes from, triggers for release and what it does

A
  • Ghrelin comes from pancreatic E cells (ε) and the stomach
  • It is secreted in response to negative energy balance - important regulator of hunger
  • Secretion of Ghrelin has an inhibitory effect on:
    • Insulin
    • Leptin (stimulates satiety)
    • CCK
    • GLP-1 (glucagon-like peptide1)
84
Q

Describe Pancreatic Polypeptide (PP) -

Where it comes from, what it does

A
  • Secreted from F cells in pancreatic islets
  • Thought to slow absorption of food by inhibiting:
    • bile secretion
    • gall bladder contraction
    • secretion by exocrine pancreas
  • Also reduces expression of GLUT-2 receptors in liver ⇢ more glucose passes liver and is available in peripheries
85
Q

Common distribution of diabetic ulcers

A

Glove and stocking

86
Q

Microvascular complications of diabetes

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
87
Q

Macrovascular complications of diabetes

A
  • IHD (ischaemic heart disease)
  • Stroke - Cerebrovascular Disease
  • PVD (Peripheral vascular disease)
88
Q

What immunosensitivity reaction causes T1DM

A

Type 4 - T cell mediated

89
Q

Name the 3 antibodies involved in T1DM

A
  • Anti - B cell antibodies
  • Anti insulin antibodies
  • Anti GAD antibodies (Glucuronic Acid Decarboxylase) → enzyme involved in B cell Glycolysis
90
Q

Dx of diabetes

A

Fasting BGL > 7mmol/L

Incidental BGL > 11.1 mmol/L

HbA1c > 6.5% or >48mmol/L

Antibody testing (B cell, anti insulin, anti GAD antibodies) - T1

Glucose sensitivity test

Biometric testing for metabolic syndrome

91
Q

Describe mechanisms of hyperglycaemia

A
  • Glucose can deposit on cell walls causing thickening
  • Glucose has osmotic drive causing fluid extravasation (oedema)
  • ⇡ Glucose metabolised by different pathway to normal glycolysis → produces sorbitol
    • Sorbitol has higher osmotic deposition preference → deposits around vessels which supply neurones → neuropathy
  • ⇡ Fatty acids → ⇡ Atherosclerosis

LOOK THESE BADBOIS UP

  • ⇡ Hyalin deposits (glucose breakdown product) → hyalinsclerosis?
  • ⇡ Amyloid → coats cells and thickens membranes → amyloidosis?
92
Q

6 I’s of DKA (diabetic ketoacidosis) and HHS (hyperglycaemic hyperosmolar syndrome)

A
  • Insulin → insufficient - either undiagnosed or poorly managed
  • Infections → ⇡ metabolic demand
  • Inflammation → ⇡ metabolic demand
  • Intoxication → alcohol, cocaine, amphetamines
  • Infarction → AMI, CVA
  • Iatrogenic → corticosteroids, surgery (wound healing)
93
Q

How do norepinephrine, cortisol, glucagon and insulin affect free fatty acid (FFA) release?

A
  • Norepinephrine, cortisol and glucagon all activate Hormone Sensitive Lipase (HSL) - which promotes FFA release
  • Insulin inhibits Hormone Sensitive Lipase (HSL) - which decreases FFA release
94
Q
A

Ca2+ released from sarcoplasmic reticulum (SR) causes translocation of Glut-4 receptors (as well as facilitating actin & myosin interaction)

95
Q

How does diabetes mess shite up?

A

Non enzymatic glycosylation of proteins → damages proteins

In eyes, kidneys and neural tissue there is a lack of Sorbitol Dehydrogenase which is a 2ndary metabolism pathway.

Lack of this enzyme particularly in these cells increases intracellular osmotic gradient, which can cause lysis or damage of surrounding structures

96
Q

Compare and contrast the half-lives and temporal effects of ADH and cortisol

A

ADH

  • Short ½ life (15-30 minutes) → soluble in plasma, exposed to degrading enzymes
  • Rapid effects - seconds -minutes → receptor binding affects existing proteins in collecting duct

CORTISOL

  • Longer ½ life → protein bound in plasma (steroid hormone), protected from enzymatic destruction
  • Nuclear or cytosolic (intracellular) receptors - take longer to work as promote protein production
97
Q

Describe the nervous system components of the stress response

A

Sympathetic NS

Postganglionic neurons release norepinephrine

Some preganglionic neurons synapse at adrenal medulla, release epinephrine

Both act at adrenoreceptors

98
Q

Describe endocrine component of stress response

A
  • Hypothalamus releases CRH (corticotrophin-releasing hormone)
  • Pituitary releases ACTH (adreno corticotrophic hormone)
  • Adrenal zona faciculata releases cortisol (a glucocorticoid)
  • Cortisol increases production of adrenaline - increasing adrenal medulla response
  • Major role of cortisol is to
    • make glucose available in the blood
    • conversion of amino acids to glucose
    • muscle catabolism
99
Q

How does the stress response affect immune function?

A

Cortisol → inhibits release Arachadonic acid →

Reduction of prostaglandins and leukotrienes that are important inflammatory mediators

Further, inhibits release of Histamine and serotonin

100
Q

Describe “growth hormone binding protien”

A

Circulating levels are genetically determined → influences attained adult height

It extends ½ life of GH by keeping it from being excreted

101
Q

Describe key hormones in puberty

Where they come from, and how pattern changes at puberty?

A

GnRH from Hypothalamus

LH & FSH from anterior pituitary

In puberty, increase in amplitude and frequency of release pulses, which normally start during sleep

102
Q

Describe sex hormone binding globulin

A

Glycoprotein that binds to androgens and oestrogens

Created in sertoli cells in seminiferous tubules of testes

AKA androgen binding protein in this case

103
Q

Describe the HPA axis
3 key centres
3 key hormones

A

Hypothalamus (Paraventricular nucleus @ median eminence spec.) - CRH

Anterior Pituitary - ACTH

Zona Faciculata - Cortisol (Has a negative feedback cycle on first 2)

  • CRH = Corticotrophin Releasing Hormone
  • ACTH = AdrenoCorticoTrophic Hormone
104
Q

Main release triggers of cortisol (via HPA axis)

A

CRH->ACTH->Cortisol

  • Diurnal cycle
  • Stress
  • Hypoglycaemia
105
Q

Main effects of Cortisol

A

Think - energy, immune, bone

  • Stimulates Gluconeogenesis (liver)
  • Decrease peripheral tissue insulin sensitivity
  • Works indirectly with adrenaline to promote glycogenolysis
  • Promotes lypolysis
  • Prolonged high levels can lead to proteolysis (to provide glucogenic amino acids for gluconeogenesis)
  • Reduces B-cell mediated antibody response (save energy for fighting/fleeing)
  • Reduces bone formation (a/a)
  • Raises free serum amino-acids - inhibiting collagen formation and reducing muscle amino acid uptake
106
Q

What is the mechanism that cortisol and adrenaline affect glycogenolysis

A

Activation of glycogen phosporylase (which is a rate limiting step in glycogenolysis)

107
Q

Pathophysiology of Graves Disease

A
  • Auto-immune response
  • Creation of Thyroid Stimulating Immunoglobulins - mainly IgG
  • These act like TSH - but to an excessive amount, and chronically stimulate follicular cells to create T3 & T4 - However, as it is not truely TSH stimulating the follicular cells, the normal TPA axis negative feedback loop does not work

Urogenital, Reproductive, Genetics, Endocrine (3 decks)

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