Endocrine Flashcards
Hypothalamus
Gland: hypothalamus
Function: regulates pituitary gland secretion, produces hormones of posterior gland - influencing thyroid (metabolism), adrenal gland (stress), and gonads (reproduction )
Hormones:
Hypophysiotropic hormones
TRH - thyrotropin-releasing hormone - stimulate production of thyroid-stimulating hormone (TSH)
CRH - corticotropin releasing hormone - stimulate production of ACTH - adenocorticotropin hormone
GnRH - gonadotropin releasing hormone
GHRH - GH releasing hormone
GHIH - GH inhibiting hormone - inhibits GH and TSH
PRH - Prolactin releasing hormone
PIH - Prolactin inhibiting hormone
Disease:
Excess hypothalamic secretion of any of the above hormones leads to excess of that hormone and the corresponding effects
Vice versa
Pituitary
Gland:
Anterior pituitary (Adenohypophysis)
Glandular epithelial tissue, connected to hypothalamus via vasculature, by which hypophysiotropic hormones are delivered to it
Posterior pituitary (Neurohypophysis)
Neural tissue
Stores hormones made in the hypothalamus - ADH and oxytocin
Function: regulate activity of thyroid (metabolism), adrenal gland (stress), gonads (reproduction)
Hormones:
AP produces :
TSH - aka thyrotropin
ACTH
GH
FSH
LH
Prolactin
PP stores:
ADH/Vasopressin
Promotes Na/H2O reabsorption in the kidneys’ distal tubules to elevate blood pressure
Oxytocin
Promote uterine contraction during birthing process
Disease:
Dysfunction of Hypothalamic ADH production/PP storage - (Central) Diabetes insipidus - kidneys can’t retain sodium and water → excessive urination
Nephrogenic diabetes insipidus - kidneys can’t respond to ADH → more ADH is secreted (in vain ofc)
Hyperpituitarism
(I guess excess growth hormone–)
Pronounced supra-orbital ridges and mandible
Spaces between teeth
Hypopituitarism
Adrenal
Gland:
Adrenal gland - adrenal cortex + adrenal medulla (inside)
Located on two sides just above each kidney
Function: stress - sympathetic nervous system response
General Adaptation System (GAS)
ALARM - FIGHT OR FLIGHT: Hypothalamic activation of SNS
Sends signals to adrenal medulla - secrete catecholamines - 5x Ad than nAd
Resistance - cortisol resists the stress
Exhaustion - allostatic overload
Hormones:
Adrenal medulla: catecholamines - nAd and Ad
Increase sympathetic nervous activity
Increase cardiac output by increasing heart rate and stroke volume
Bind to membrane-bound GPCRs
Adrenal cortex
Zona glomerulosa: mineralocorticoids - aldosterone
Zona fasciculata: glucocorticoids - cortisol
—> anti-inflammatory: lowers immune response, stress mediators - key role in resistance stage of GAS.
—> increases fuel metabolism — increase blood glucose at expense of lipids and proteins
—> increases bone resorption - to gain more amino acids for metabolism
—> increase sensitivity of CVS to catecholamines + angiotensin II to elevate blood pressure
—> increase RBC level
—> Stimulate gastric acid secretion
Zona reticularis: androgens - DHEA
Used to make androgens and estrogens
Disease:
Hyper adrenal secretion
Phaeochromocytoma - Adrenal medulla tumour - excess Ad and nAd secreted
Hyperglycemia, tachycardia, hypertension
Conn’s syndrome - tumour of Zona glomerulosa –> aldosterone excess
Hypertension from modest hypervolemia, hypernatremia, hypokalemia
Cushing’s syndrome
–> Cortisol and DHEA excess
–> Hyperglycemia, protein loss from muscles and bone leading to weakness and osteoporosis, lowered immune function
Hypo adrenal secretion
Addison’s disease –> damaged adrenal glands
Cortisol deficiency
Hypoglycemia → weight loss and weakness, hyperpigmentation (lack of negative feedback to hypothalamus and AP)
aldosterone deficiency leads to hypotension → circulatory shock, hyponatremia, hypokalemia
Thyroid
Gland: Thyroid gland - two sides of the trachea
Function: Regulate fuel metabolism
Hormones: T4 - thyroxine and T3- tri-iodothyronine
Synthesised by iodine
Increase basal rate of metabolism - increase size and number of mitochondria
Increase glucose uptake from GI
Upregulate B-adrenergic receptors → increases glycolysis+lipolysis, and HR/SV/CO.
Disease:
Hyperthyroidism
Graves’ disease - autoimmune disease where thyroid gland is attacked - ANTIBODIES LOOK LIKE TSH, causing excess secretion of thyroid from thyroid gland
Excess hypothalamic/anterior pituitary secretion of TRH or TSH respectively
Thyroid gland tumour
Hyperglycemia → increased susceptibility to caries/perio disease
Accelerated dental eruption
Osteoporosis
Burning mouth syndrome
Anxiety
Stress can cause thryotoxic crisis
Avoid giving Ad and NSAIDs (aspirin, ibuprofen)
Take HR and BP before appt
Shorter appts to minimise stress
Watch out for signs of thyrotoxic storm - admit to hospital immediately
Hypothyroidism
Failure of thyroid gland to secrete thyroid
Failure of hypothalamus/anterior pituitary secretion
Delayed dental eruption
Macroglossia, glossitis
Dysgeusia
Salivary gland enlargement
Compromised periodontal health - delayed bone resorption
Calcium
Gland: Parathyroid gland
Function: Regulate plasma calcium levels
Hormones:
1) Parathyroid hormone
Increase plasma calcium levels by:
Enhance bone dissolution
Binds to osteoblasts, increasing RANKL expression, which decreases the osteoclast-inhibiting osteoprogerin
Thereby increasing osteoclast action
Increase movement of Ca from labile pool to plasma
Increase Ca uptake from intestines
Decrease Ca excretion from kidneys
Activate vitD
2) Calcitonin
Works against PTH
Inhibit osteoclasts
Decrease mvmt of Ca from labile pool
Decrease Ca reabsoprtion from kidneys and intestines
3) Activated Vitamin D (Calcitriol)
Assists PTH
Increase Ca absorption from intestines
Increase sensitivity of bone tissues to PTH
Disease:
Hyperparathyroidism
Hypercalcemia - Slowed reactions
Bone disease, kidney disease
Osteoporosis
Hypoparathyroidism
Hypocalcemia - Tetany, muscle spasms
Also osteoporosis
Growth
Gland: Anterior pituitary - somatotrophs
Function: Regulate growth, fuel metabolism
Hormones:
Growth hormone
Promotes proliferation of epiphyseal cartilage → extension of long bones - bone remodelling
Proliferation of periosteal osteoblasts → bone thickening
Inhibited by somatomedins eg IGF (insulin-like growth factor) from liver, which stimulates release of somatostatin (GHIH)
GH is stimulated by GHRH which is produced when there is low BGL, low fatty acids… it promotes protein synth
Disease:
Hypersecretion of GH
In childhood → gigantism
Hyperglycemia, diabetes in 10%
Proportionate enlargement of body parts
In adulthood → acromegaly
Diabetes
Accelerated dental eruption - gaps between teeth
Macroglossia
Larger maxillary sinuses
Mandibular growth → Class 3 occlusion
Treatment: somatostatin analogs, surgery
Hyposecretion of GH
Pituitary dwarfism
Delayed dental eruption
Treatment: human GH +- cortisol, thyroxine
Insulin
Gland: B cells in the pancreas
Function: Regulate blood glucose levels
Hormones:
Insulin
Increases glycogenesis → conversion of glucose to glycogen for storage
Decrease gluconeogenesis → decrease the production of glucose from proteins/lipids
Increase uptake of glucose in cells - by increasing number of GLUT-4 transporters on cell surface membrane - thus decreasing BGL.
Increase rate of glucose metabolism
Brain + liver take up glucose regardless of insulin.
Disease:
Diabetes mellitus
Type 1
Failure of pancreatic B cells to produce adequate insulin
Without insulin, blood glucose levels remain high → hyperglycemia
Uncontrolled: Leads to osmotic diuresis/polyuria (ie excess urination), muscle wastage (decrease AA transport & protein synthesis)
No insulin to oppose glucagon actions → ketoacidosis occurs - beta-oxidation of fatty acids to form ketones → sweet breath
Type 2
Decreased sensitivity of tissues to insulin, lack of adequate response to insulin
Effector organs do not respond, BGL is not lowered, BGL remains high → hyperglycemia
HbA1c
5.7-6.4% pre-diabetic, >6.5% = diabetic
Pregnancy
When fertilisation of zygote occurs, hCG (human chorionic gonadotropin) produced by zygote to ‘rescue’ corpus luteum and keep corpus luteum producing progesterone, allowing for maintenance of endometrium so that zygote can implant on the uterine lining.
Hypothalamic-Gonadal Axis (HPG axis)
During pregnancy, levels of oestrogen and progesterone increase.
Levels of cortisol and aldosterone increase.
Increased aldosterone and cortisol –> Increased water retention from kidneys → increase in plasma & ECF –> Oedema
Sensitivity to insulin decreases (bc of cortisol)
1st trimester - hypotension - from peripheral vasodilation
Skin darkening - Hyperpigmentation from pituitary secretion of melanocyte stimulating hormone
Breathlessness (dyspnoea) from increased respiratory centre sensitivity to pCO2
Insomnia - sleep disturbances by fetal mvmt, feeling hot from peripheral vasodilation
Gastric reflux → tooth erosion
Increase in snacking - food cravings, tiredness - poor oral hygiene…
Pregnancy diabetes - tendency for hyperglycemia
Pregnancy gingivitis - pyogenic granuloma - benign tumours may form, usually resolve after birth - increase in progesterone result in exaggerated response to plaque
Periodontitis is linked with preterm labour
Avoid radiographs until 2nd trimester - wear lead apron
No NSAIDs, tetracyclines, codeine, NO, avoid GA
Semi-supine position, elevate right hip - to avoid supine hypotensive syndrome
Avoid amalgams - risk of mercury crossing placenta
Postpone non-urgent dental care
Advise monitor Vit A, C,D, Ca and PO4 levels
Aging
+ what are the effects of GH supplementation?
Oral effects:
Decrease in mucins in saliva
Masticatory muscles: loss in muscle fibre integrity and atrophy
Functions of oestrogen
Decrease bone resorption
Increase HDL, decrease LDL
Blood clotting
Support cardiomyocyte contractility
Decrease in oestrogen
Sarcopenia
Osteoporosis
Increase in LDL, decrease in HDL
Decrease in testosterone
Sarcopenia
Osteoporosis
Insulin resistance
Central adiposity
HRT linked to risk of breast/uterine cancer and prostate cancer respectively.
Slight Increase in cortisol - increase in stress
Decrease in growth hormone
GH supplementation can increase lean body mass and decrease adiposity, but it can cause oedema, hyperglycemia, and joint pain (arthralgia)
Hypertension
Diastolic/systolic
normal = 120/80
high = 140/90
low = 90/60 mmHg
Medications:
Captopril, Ramipril - ACE inhibitor - inhibits conversion of angiotensin I to angiotensin II → decreases aldosterone levels → decreased water reabsorption in kidneys → decreases BP.
Amlodipine, Nifedipine, Verapamil - Calcium channel blocker - blocks Ca entry into vascular smooth muscle cells, decreasing vasoconstriction
Ca channel blockers also relax afferent arterioles in kidneys, causing increase in renal blood flow → increase in GFR
Increase in afferent arteriolar pressure causes increase in Ca influx into glomerulus→ Ca is a secondary messenger inhibitor of renin secretion → Ca channel blockers inhibit renin, inhibiting RAAS → BP drop.
Frusemide - loop diuretic - increases Na excretion from ascending loop of Henle → decreases blood volume
Metoprolol - beta-blocker - blocks B-1 adrenergic receptors, reducing vasoconstriction
