Endocrine system

Danielle Richardson
Mind Map by Danielle Richardson, updated more than 1 year ago
Danielle Richardson
Created by Danielle Richardson almost 5 years ago
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Description

Degree Medicine (Physiology) Mind Map on Endocrine system, created by Danielle Richardson on 04/07/2015.
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Resource summary

Endocrine system
1 Autocrine
1.1 Released then acts on self
2 Paracrine
2.1 Acts on nearby cells
3 Endocrine
3.1 Released into blood- distant cells
4 Neuroendocrine
4.1 Released by neurone into blood stream- distant cells
5 Hormones
5.1 Steroids
5.1.1 Steroidogenesis
5.1.1.1 Cholesterol
5.1.1.1.1 Mineral corticoids
5.1.1.1.1.1 Glucocorticoids
5.1.1.1.1.1.1 Androgen
5.1.1.1.1.1.1.1 Oestrogen
5.1.1.1.1.1.1.2 Zona reticularis
5.1.1.1.1.1.1.2.1 Adrenal gland
5.1.1.1.1.1.1.2.1.1 Medulla
5.1.1.1.1.1.1.2.1.1.1 Epinephrine and norepinephrine

Annotations:

  • Catecholamines= epinephrine, norepinephrine and dopamine 
5.1.1.1.1.1.1.2.1.2 regulated by
5.1.1.1.1.1.1.2.1.2.1 hypothalamus
5.1.1.1.1.1.1.2.1.2.2 RAA system
5.1.1.1.1.1.1.2.1.3 arterial supply
5.1.1.1.1.1.1.2.1.3.1 Inferior phrenic
5.1.1.1.1.1.1.2.1.3.1.1 Abdominal aorta
5.1.1.1.1.1.1.2.1.3.2 Renal arteries
5.1.1.1.1.1.1.2.1.4 Venous drainage
5.1.1.1.1.1.1.2.1.4.1 Right suprarenal veins
5.1.1.1.1.1.1.2.1.4.1.1 Drains direct into IVC
5.1.1.1.1.1.1.2.1.4.2 Left suprarenal veins
5.1.1.1.1.1.1.2.1.4.2.1 Renal veins first
5.1.1.1.1.1.1.2.1.4.2.1.1 Then IVC
5.1.1.1.1.1.2 Cortisol

Annotations:

  • Breaks down protein into amino acids to make glucose, rises blood glucose levels. Also glycogenolysis 
5.1.1.1.1.1.2.1 Too much= cushings
5.1.1.1.1.1.2.1.1 Weight gain
5.1.1.1.1.1.2.1.2 Bruise easily
5.1.1.1.1.1.2.1.3 Muscle/bone aches
5.1.1.1.1.1.2.1.4 loss of labido
5.1.1.1.1.1.2.1.5 Causes
5.1.1.1.1.1.2.1.5.1 tumour in pituitary gland
5.1.1.1.1.1.2.1.5.1.1 lots of ACTH
5.1.1.1.1.1.2.1.5.1.2 uncommonly can develop in lungs and produce ACTH
5.1.1.1.1.1.2.1.5.2 Current corticosteroid medication
5.1.1.1.1.1.3 Zona fasciculata
5.1.1.1.1.1.3.1
5.1.1.1.1.2 Progesterone
5.1.1.1.1.3 Zona glomerulosa
5.1.1.1.1.3.1 Adrenal gland
5.1.1.1.1.4 aldosterone
5.1.2 Lipid soluble
5.1.2.1 Pass through plasma membrane to bind with receptor in cell
5.2 Peptide/ protein hormones
5.2.1 Bind to cell surface receptor
5.2.1.1 G protein coupled receptor

Annotations:

  • inhibitory Gi
5.2.1.1.1 Adenylyl cyclase
5.2.1.1.1.1 Increase in cAMP
5.2.1.1.1.1.1 phospholipases
5.2.1.1.1.1.1.1 Increase in Ca2+
5.2.2 Tyrosine kinase receptor for large peptides
5.2.2.1 Two binding sites, when both bound are a dimer
5.2.2.1.1 Phosphates bind to tyrosines
5.3 Amino acid derived
5.3.1 From tyrosin-> dopamine-> norepinephrine
5.3.2 Water soluble
5.3.2.1 Cell-surface receptor
5.3.2.1.1 Signal transduction
5.4 Secretion
5.4.1 Episodic
5.4.2 Response to stimulus
5.4.3 Circadian
5.4.3.1 24 hour cycle
5.5 Melatonin secreted from pineal gland
5.5.1 regulates circadian cycle
5.6 Growth hormone works by stimulating the liver to release IGF1

Annotations:

  • insulin like growth factor 1
5.7 Too much prolactin can be due to
5.7.1 adenoma of pituitary

Annotations:

  • adenoma= tumour of the gland Sarcoma= tumour of muscle
5.7.2 Dopamine receptor antagonist

Annotations:

  • Dopamine (released from hypothalamus) inhibits prolactin (released from ant. pituitary).  Somatostatin inhibits Growth hormone (same sites) 
5.7.3 Lesion blocking dopamine delievery
6 Corticotrophin releasing hormone CRH (hypothalamus)
6.1 Adrenocorticotrophic hormone ACTH (ant. pitutary)
6.1.1 Cortisol
6.1.2 Pituitary = hypophysis
7 Blood glucose
7.1 glycaemic index
7.1.1 how quickly a food triggers rise in blood sugar
7.1.2 50-100
7.2 Controlled in pancreas
7.2.1 acini
7.2.1.1 exocrine function
7.2.1.1.1 digestive enzymes for GI
7.2.1.1.1.1 Emptied into ampulla of vater
7.2.1.1.1.1.1 sphincter of oddi controls the release
7.2.2 islets of Langerhans
7.2.2.1 insulin
7.2.2.1.1 released when too high
7.2.2.1.2 beta cells
7.2.2.2 glucogon
7.2.2.2.1 released when too low
7.2.2.2.2 alpha cells
7.2.2.3 Somatostatin
7.2.2.3.1 delta cells
7.2.2.3.2 Stops both insulin and glucagon

Annotations:

  • by paracrine
7.2.3 Anatomy
7.2.3.1 Body
7.2.3.2 Head
7.2.3.2.1 Cancer most common here
7.2.3.2.1.1 Presents with jaundice or pancreatitis
7.2.3.3 Uncinate process
7.2.3.3.1 Bit that curves round
7.2.4 Hypoglycaemia
7.2.4.1 Treat with beta blockers
7.2.4.1.1 In type 2 diabetes
7.2.4.1.1.1 Decrease in insulin produced
7.3 Diabetes
7.3.1 Type 1
7.3.1.1 no insulin produced
7.3.1.2 Complication
7.3.1.2.1 Diabetic ketoacidosis
7.3.1.2.1.1 No insulin
7.3.1.2.1.1.1 So cells have no glucose
7.3.1.2.1.1.1.1 So break down fat instead
7.3.1.2.1.1.1.1.1 Producing ketones
7.3.2 Diabetic annual review
7.3.2.1 Purpose
7.3.2.1.1 Screen for complications
7.3.2.1.2 Check education
7.3.2.1.3 Identify risk factors
7.3.2.2 Before appointment
7.3.2.2.1 HbA1c

Annotations:

  • looking at glycated haemoglobin i.e. Hb with glucose attached, which is directly proportional to the amount of glucose in the blood
7.3.2.2.2 Cholesterol

Annotations:

  • HDL, LDL, ratio between them, total cholesterol, triglycerides
7.3.2.2.3 Creatine, U&Es
7.3.2.2.4 EMU for microalbumin/creatine ratio

Annotations:

  • EMU= early morning urine
7.3.2.2.5 BP
7.3.2.2.6 BMI
7.3.2.2.7 Waist/Hip ratio
7.3.2.2.8 Urinalyis

Annotations:

  • For blood, protein, ketones, glucose
7.3.2.2.9 Visual acuity
7.3.2.3 At appointment
7.3.2.3.1 Discuss results
7.3.2.3.2 General wellbeing
7.3.2.3.3 Examination

Annotations:

  • Feet- deformation, innervation, blood supply, ulcers BP
7.3.2.3.3.1 Foot examination
7.3.2.3.3.1.1 Use tuning fork
7.3.2.3.3.1.2 Inspection
7.3.2.3.3.1.2.1 between toes as well
7.3.2.3.3.1.3 Palpate
7.3.2.3.3.1.3.1 Foot pulses
7.3.2.3.3.1.4 Monofilament
7.3.2.3.3.1.4.1 pointy thing

Annotations:

  • start with big toe, then metatarsals
7.3.2.3.4 Identify risk factors

Annotations:

  • hypoglycaemia frequency and occurrence  Diet Weight Exercise
7.3.2.3.5 Assess educational needs

Annotations:

  • Diet, exercise, self-administering medicine, self-monitoring, understanding risk and tx targets 
7.3.2.3.6 Issues/questions from patient
7.3.2.3.7 Agree tx plan

Annotations:

  • Targets for next year Review if poor control Refer for educational needs
7.3.2.3.8 Complications screen
7.3.3 Insulin
7.3.3.1 Kept in a fridge
7.3.3.2 Inject SC

Annotations:

  • don't withdraw needle
7.3.3.3 Hold for 6 secs
7.4 hypoglycaemia

Annotations:

  • hungry, headache, sweating, tired, seizures, coma, nausea, palpitations, pallor
7.4.1 Blood glucose <3mmol/L
7.4.1.1 Pathological <2.5mmol/L
7.4.2 Diagnosis
7.4.2.1 Low blood glucose
7.4.2.2 Symptoms of hypoglycaemia
7.4.2.3 Symptoms resolve after tx
7.4.3 Causes
7.4.3.1 Diabetic
7.4.3.1.1 To much insulin
7.4.3.1.2 Alcohol, illness, injecting into scarred site, exercise
7.4.3.2 Not diabetic
7.4.3.2.1 Endocrine disorders

Annotations:

  • CAH, Addison's disease, 
7.4.3.2.2 liver/gut disease

Annotations:

  • Liver failure Alcohol abuse
7.4.3.2.3 Other

Annotations:

  • Malignancy, hypothermia, malaria
7.4.4 Treatment
7.4.4.1 Quick acting carb
7.4.4.1.1 10-20g glucose
7.4.4.1.1.1 2 teaspoons of sugar
7.4.4.1.1.1.1 Glucogel
7.4.4.1.1.1.1.1 20% glucose
7.4.4.1.1.1.1.1.1 1mg glucagon IM
7.4.4.2 Long acting carb
7.4.5 Hyperglycaemia
7.4.5.1 Diabeteic ketoacidosis
7.4.5.2 Hypoosmolic Hyperglycaemia State
7.5 Monitoring
7.5.1 Finger prick test
7.5.1.1 Clean with alcohol wipe
7.5.1.2 Patient wash hand with soap and water
7.5.1.3 Insert test strip
7.5.1.4 Use single use lancet device in side of patient's finger
7.5.1.5 Wait 10 seconds then put on test strip
7.6 Glucose control
7.6.1 Stays between 4-6mmol/L
7.6.2 Glycogenolysis
7.6.2.1 Glycogen broken down into glucose-6-phosphate
7.6.2.2 After meals peaks then drops quickly
7.6.3 Gluconeogenesis
7.6.3.1 Makes glucose from lactate and amino acids

Annotations:

  • Protein breaking down
7.6.3.2 Last thing at night
7.6.4 Diet
7.6.4.1 Food raises blood glucose
7.6.5 How to decrease blood glucose
7.6.5.1 Insulin
7.6.5.1.1 Anabolic

Annotations:

  • building things up using energy
7.6.5.1.2 Lipogenesis
7.6.5.1.2.1 triglyceride
7.6.5.1.3 Glycogenesis
7.6.5.1.3.1 Glycogen
7.6.5.1.4 Protein synthesis
7.6.5.1.4.1 Protein
7.6.6 How to increase blood glucose
7.6.6.1 Glucagon

Annotations:

  • From a cells in pancreas Increased between meals (i.e. when blood glucose is lower) Short half life
7.6.6.1.1 catabolic

Annotations:

  • breaking things down and producing energy
7.6.6.2 Cortisol

Annotations:

  • Twice a day Chronically elevated in stress
7.6.6.3 GH
7.6.6.4 Adrenaline

Annotations:

  • Acute stress Prolonged exercise
7.6.6.5 Lipolysis
7.6.6.5.1 Free fatty acids
7.6.6.5.1.1 Ketone bodies

Annotations:

  • Brain can use these
7.6.6.6 Glycogenolysis
7.6.6.7 Gluconeogenesis
7.7 postprandial= mild dip in blood glucose after a meal
8 Thyoid
8.1 Arterial supply
8.1.1 Superior
8.1.1.1 External carotid
8.1.2 Inferior
8.1.2.1 Thyrocervical
8.1.2.1.1 Subclavian
8.2 Venous supply
8.2.1 Inferior
8.2.1.1 Brachiocephalic
8.2.2 Middle and Superior
8.2.2.1 Internal jugular
8.3 Embryology
8.3.1 Foramen Cecum
8.3.1.1 Tongue base
8.3.1.2 Thyroglossal duct
8.3.1.2.1 Thyroid
8.3.1.2.2 Should close
8.3.1.2.2.1 if doesn't close in adulthood= abnormal
8.3.1.2.2.1.1 Midline swelling
8.4 Produces calcitonin
8.4.1 Reduces calcium levels

Annotations:

  • blood calcium
8.4.1.1 hypocalcaemia mostly caused by vitamin D
8.4.2 Opposite of parathyroid hormone
8.4.2.1 Hypercalcaemia in hyperparathyroidism

Annotations:

  • Abdo pain, polydipsia, polyuria, dehydration
8.5 Goitre
8.5.1 Swelling of thyroid
8.5.1.1 Hyperthyroidism

Annotations:

  • aka thyrotoxicosis 
8.5.1.1.1 Causes
8.5.1.1.1.1 Grave's disease

Annotations:

  • CD4 cells stimulate B cells to make TSI antibodies which stimulate thyoid
8.5.1.1.1.1.1 Autoimmune
8.5.1.1.1.1.2 thyroid stimulating immunoglobulins
8.5.1.1.2 Symptoms
8.5.1.1.2.1 Anxiety
8.5.1.1.2.2 Hyperactivity
8.5.1.1.2.3 Weight loss
8.5.1.1.2.4 Muscle weakness
8.5.1.1.2.5 Dry skin
8.5.1.1.3 Tx
8.5.1.1.3.1 thionamides
8.5.1.1.3.2 Anti-thyroid drugs

Annotations:

  • Carbimazole
8.5.1.1.4 decreased TSH, increased T4
8.5.1.1.5 Secondary
8.5.1.1.5.1 Increased TSH increased T4
8.5.1.1.6 Complication
8.5.1.1.6.1 thyrotoxic storm
8.5.1.1.6.1.1 tx: beta blocker
8.5.1.2 Hypothyroidism
8.5.1.2.1 reduced thyroxine
8.5.1.2.2 Causes
8.5.1.2.2.1 Iodine defiency
8.5.1.2.2.2 Hashimoto's disease

Annotations:

  • CD4 cells recruit B cells to make antibodies against thyroid and CD8 cells to destroy thyroid.
8.5.1.2.2.2.1 Auto-immune
8.5.1.2.2.2.2 Thyroid peroxidase antibodies present
8.5.1.2.2.2.2.1 in Graves as well
8.5.1.2.3 Symptoms
8.5.1.2.3.1 Cold
8.5.1.2.3.2 Weight gain
8.5.1.2.3.3 Tired
8.5.1.2.3.4 Brittle hair and nails
8.5.1.2.3.5 Depressed
8.5.1.2.3.6 Constipated
8.5.1.2.3.7 Slow reflexes
8.5.1.2.4 Increase TSH
8.5.1.2.5 Can lead to anaemia
8.5.1.2.6 Secondary= low TSH= low T4
8.5.1.3 Lack of iodine
8.6 Thyrotropin releasing hormone TRH
8.6.1 Thyrotropin (thyroid stimulating hormone) TSH

Annotations:

  • Normal levels: 0.4-3mlU/L. Also causes hyperproliferation of thyroid cells TSI= antibodies which mimic TSH
8.6.1.1 Thyroxine (T4)

Annotations:

  • normal levels: 0.8-2 T3 and T4 are formed from tyrosine -&gt; thyroglobin-&gt; thyroxineT4 converted to T3 (active) via iodinase
8.6.1.1.1 Thyroid hormone receptor

Annotations:

  • TRa1,2 TRb 1,2 TRa2 (T3 only) Receptors are in the nucleus
8.6.1.1.2 Bound to protein

Annotations:

  • Thyroxine binding globule TBG Transthyretin TTR Albumin 
8.6.1.2 T3 triiodothyronine

Annotations:

  • Normal free levels: 2.4-4.2
8.6.1.2.1 Active thyroxine

Annotations:

  • 20% released directly from thyroid. Rest is converted by kidneys and liver from thyroxine. 
8.6.1.3 Need iodine

Annotations:

  • Iodine is now in salt
8.7 Thyroid autoimmune disorders associated with type 1 diabetes
8.7.1 Lots of T3/4 promotes hyperlycaemia

Annotations:

  • Makes more glucose absorbed More glycogenolysis and gluconeogenesis Increases insulin clearance
9 Terms
9.1 permissiveness
9.1.1 one hormone influences another
9.1.2 not enough GF nother enough T3
9.1.3 T3 increases number of binding sites for epinephrine
9.2 Synergism
9.2.1 More hormones are better than one to create an affect
9.2.1.1 FSH and testosterone
9.3 Antagonism
9.3.1 one hormone prevents the other from working
9.3.1.1 Somatostatin prevents glucagon and insulin
9.4 Tropic gland
9.4.1 Gland which releases a hormone to affect another gland
9.5 Endocrine disorders
9.5.1 Primary
9.5.1.1 Peripheral gland
9.5.2 Secondary
9.5.2.1 Tropic gland
10 Investigations of pituitary disease
10.1 Urine and electrolyte sample
10.2 Blood sample
10.3 Renal function
10.4 MRI of pituitary/ hypothalamus
10.4.1 CT

Annotations:

  • calcium deposit in cancer
10.5 Lateral skull XR

Annotations:

  • enlarged pituitary fossa
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