endocrine system

what are hormones ?

chemical messengers secreted by ductless glands that travel in blood to target cells

what brain region controls the pituitary gland ?

hypothalamus

the pineal gland secretes

melatonin

the hypothalamus secretes

TRH, GnRH, CRH

the pituitary secretes

hormones that act on other glands - master gland

ATCH, TSH, FSH, prolactin, ADH

the thyroid secretes

thyroxine

the thymus secretes

thymosin

role of thymosin

essential for development and maturation of T cells

the pancreas secretes

insulin and glucagon

the adrenal glands secrete

adrenaline, cortisol, aldosterone

the gonads secrete

sex hormones - androgens (testosterone), progesterone and oestrogen

endocrine glands control what major processes ?

• osmolarity of blood

• cellular metabolism

• reproduction

why are endocrine glands referred to as “regulators” ?

alter magnitude of existing system - no de novo production

what are the 3 hormone classes

amino acid based

steroids

eicosanoids

most hormones are what class ?

amino acid based

insulin and glucagon are what hormone class

amino acid based - peptide

eicosanoids

not technically hormones

active lipids that illicit response

hormone-like activity

leukotrienes, prostaglandins

3 mechanisms of hormone action

• direct

• paracrine - autocrine

• endocrine

direct signalling can be

juxtacrine

through gap junctions or plasmodesmata

autocrine signalling

specialised type of paracrine signalling where cell releases chemicals that act on same cell

specialised types of paracrine signalling

autocrine

neuronal

the vast majority of cell signalling is

endocrine

hormones alter target cell activity via what 2 mechanisms ?

secondary messengers

direct gene activation

secondary messengers are what hormone class

amino acid based

how do secondary messenger systems work

hormone = first messenger

binds to receptor

activates G protein

cAMP cascade (2nd messenger)

activates PK - leads to response

direct gene activators are what hormone class

steroid hormones

how do steroid hormones illicit change in target cell ?

lipid soluble

bind to intracellular receptor

binds to dna of nucleus

transcriptional change - increase or decrease transcription of certain protein

3 mechanisms of hormone release

hormonal, humoral and neural

hormonal hormone release

secretion of one hormone stimulates release of another

humoral hormone release

triggered by changes in the levels of non-hormone chemicals in bodily fluids, like blood eg. ions or nutrients

neuronal hormone release

direct nervous stimuli signals to gland

calcium homeostasis mechanism

high calcium levels causes calcitonin release

increased deposition into bones

decreased uptake in intestines and reabsorption from urine

returns levels to normal

role of ADH

regulates water reabsorption in kidneys

excess salt in the body triggers

brain to increase fluid intake

ADH secreted posterior pituitary

epinephrine can bind to how many receptors and illicit how many effects ?

2 receptors 3 effects

acromegaly

too much growth hormone later in life

Cushing’s Syndrome

prolonged exposure to high levels of cortisol

often caused by steroid use

Diabetes Insipidus

excess ADH

increased thirst and production of large amounts of dilute urine

Hashimoto’s Thyroiditis

autoimmune disease that attacks thyroid

effects metabolism

hypogonadism

reduction of reproductive hormones

hypothalamic pituitary axis

neuroendocrine system that regulates the body's response to stress and stress-related functions (fight or flight)

communicates hypothalamus, pituitary and adrenal glands

oxytocin and ADH are transported from hypothalamus to posterior pituitary via

hypothalamic-hypophseal tract

anterior vs posterior pituitary

anterior is larger and produces and secretes own hormones

posterior - produced by hypothalamus

what 3 hormones do the adrenal glands secrete

adrenaline

aldosterone

cortisol

adrenal cortex produces

steroid hormones - androgens, glucocorticoids, mineral corticoids

adrenal medulla produces

catecholamines and peptides

cortisol is a

glucocorticoid

aldosterone is a

mineralcorticoid

epinephrine and norepinephrine are

catecholamines

stress is regulated short term by what system

neural - sympathetic NS

fight or flight

how does the sympathetic NS respond to stress ?

adrenal medulla releases epinephrine and norepinephrine

cause glycogen to break down into glucose, increased BP etc.

(chronic) stress is regulated long term by what system ?

HPA axis

HPA axis

neuroendocrine system

regulates the body's response to stress

hypothalamus, pituitary, adrenals

how does the HPA axis respond to stress ?

ATCH released from anterior pituitary into blood

adrenal cortex releases:

• mineralcorticoids - retention of Na+ and water by kidneys

• glucocorticoids - protein and fats broken down and converted into glucose

expected values for normal fasting BG

3.5 - 6.5 mmol/L

high blood sugar promotes

insulin release from pancreas

formation of glycogen from glucose in liver (glycogenesis)

stimulates uptake of glucose from blood

low blood sugar promotes

glucagon release from pancreas

formation of glucose from glycogen (glycogenolysis)

raises BG

gluconeogenesis

metabolic process of producing glucose from non-carbohydrate sources like amino acids, glycerol, and lactate

how does insulin allows for the uptake of glucose ?

signals to cell to insert GLUT4 transporters into mem allowing glucose into cell

what is diabetes ?

chronic disease characterised by raised BG levels - hyperglycaemia

pancreas unable to produce or respond to insulin

results in abnormal metabolism of carbohydrates

symptoms of diabetes

polyuria, polydipsia and fatigue

sign vs symptom

sign = measurable

signs of diabetes

hyper-glycemia and diabetic ketoacidosis

diabetic ketoacidosis

break down of fats and proteins as alternative source (to glucose)

build up of ketones in blood lowering pH - acidosis

what 4 tests can be used for diabetes ?

fasting BG, random BG, oral glucose tolerance, HbA1c

oral glucose tolerance test

pt given 75g of liquid glucose and test 2hrs later for reaction

HbA1c (glycosylated haemoglobin)

measure of glucose control over past 2-3 months

quantity of glucose that has been glycosylated - attached to haemoglobin

higher HbAC1 = higher BG level

type I diabetes

beta cells do not produce enough insulin

autoimmune disease

selective destruction of B-cells of pancreas by T cells

peak incidence in childhood

treatment of diabetes I

exogenous insulin via pump or injection

short acting insulin is given

before meals

intermediate long acting insulin is given

once daily - acts as background insulin

hybrid closed loop systems (HCL)

link continuous glucose monitoring (CGM) with insulin pump technology to manage blood sugar levels in people with type 1 diabetes

“artificial pancreas”

type II diabetes

insulin deficiency and resistance (desensitisation)

similar osmotic symptoms to type 1 - frequent urination etc.

but no weight loss as some insulin present

who is at risk of type II diabetes and why ?

individuals with metabolic syndrome

• increased BMI, LDLs and triglycerides

• decreased HDLs

• hypertension

• disrupted BG levels

what glucose lowering drugs are used to treat diabetes II

• SGLT2

• sulphanyle ureas (SU)

• glitazones (TZD)

• GLP-1 - analogues

• DPP-4 - inhibitors

• basal inhibitors

what are 5 diabetes associated complications

microvascular - retinopathy, nephropathy, neuropathy

macro - cardiovascular and cerebrovascular disease

how is retinopathy treated ?

anti-VEGF injections into eye or laser treatment

neuropathy

damage to blood vessels that supply nerves

stop nutrients reaching them

nerve fibres become damaged

cardiovascular disease

blood vessels of heart

glucose sticks to RBCs causing blockage and damage

risk factors - high HbA1c, smoking and obesity

artherosclerosis

buildup of fats, cholesterol and other substances in and on the artery walls

how many pregnancies result in gestational diabetes ?

5 - 10%

macrosomia

baby has significantly higher birth rate

(high BG of mother during pregnancy so more glucose to baby)

gestational diabetes treatment

metformin or insulin injections

hyperthyroidism

over active

thyroid produces increased amount of thyroid hormone

but lower levels of TSH

under active thyroid

decreased thyroid hormone production

high TSH

diseases of the thyroid

Hashitmoto’s, cancer, nodules

where is the thyroid gland located ?

saddles trachea just below larynx

anatomy of thyroid gland

butterfly shape

right and left lobes joined by isthmus

which lobe of the thyroid is larger ?

right lobe

what is the functional unit of the thyroid gland ?

spherical thyroid follicles - lined with follicle cells

how many parathyroid glands are there ?

4 - lie between 2 layers of capsule at base of lobes

function of thyroid

produces hormones that aid in regulating metabolism

thyroid hormones

• thyroxine (T4)

• triiodothyronine (T3)

• calcitonin - peptide hormone

thyroid hormones contain what elements

iodine and tyrosine

what is the biologically active thyroid hormone

T3 - triiodothyronine

metabolic effects of thyroid hormone

increase basal metabolic rate and gut absorption

stimulates lipolysis

decrease cholesterol levels - promotes its conversion and excretion into bile.

cardiovascular effects of thyroid hormone

increases HR, respiration, oxygen use, mitochondrial activity and blood flow

developmental effects of thyroid hormones

increase growth rate

role in brain maturation during foetal development

role of thyroid in cognitive function

regulates sleep and thought patterns

increased levels of thyroid hormones associated with faster speed of thought but decreased focus - adhd

how does high iodine affect the thyroid ?

can inhibit activity (Wolff-Chaikoff effect)