Endocrine Flashcards
Calcium is important in functioning of
Nerves and muscles (such as the heart)
Hypocalcaemia
Low serum albumin = low total serum calcium
Consequences of hypocalcaemia
Parasthesia (pins and needles) Muscle spasm - hands and feet Seizures Basal ganglia calcification Cataracts ECG abnormalities - Long QT interval (and vice versa for hypercalcaemia)
Key signs of hypocalcemia
Chvostecks sign - spasm of facial muscles after tapping over the facial nerve
Causes of hypocalcemia
VitD deficiency
Vitamin D deficiency
Secondary hyperparathyroidism
Raised PTH
Low Ca
Low phosphate
Hypoparathyroidism
Low PTH
Low Ca
Raised phosphate
Pseudohypoparathyroidism
Resistance to PTH
Classic sign - Short fourth metacarpals
Pseudohypoparathyroidism
Raised PTH
Low Ca
Raised phosphate
Pseudopseudohypoparathyroidism
Normal Ca metabolism (normal PTH, Ca, phosphate)
However, pseudo phenotype symptoms present
Hypercalcaemia symptoms
Thirst, polyuria Nausea Constipation Confusion (leads to coma) Renal stones ECG abnormalities - Short QT
Hypercalcaemia - Causes
Malignancy - bone mets, myeloma
Primary hyperparathyroidism
Hypercalcaemia
Low PTH
Raised Ca
Variable phosphate
Primary hyperparathyroidism - Consequences
Bones - osteoporosis
Stones - kidney
Groans - confusion
Moans - constipation
Primary hyperparathyroidism - Main cause
Single benign adenoma
Primary hyperparathyroidism
Raised PTH
Raised Ca
Low phosphate
Tertiary hyperparathyroidism
Renal failure - can’t activate VitD, leads to VitD deficiency
Tertiary hyperparathyroidism
Raised PTH
Raised Ca
Raised phosphate
Diabetes mellitus
Disorder of carb metabolism characterised by hyperglycaemia
Diabetes - Serious complications
Diabetic retinopathy Diabetic nephropathy Stroke CVD Diabetic neuropathy
Diabetes - Types
Type 1 Type 2 - includes gestational and medication-induced MODY Pancreatic diabetes Endocrine diabetes - acromegaly/cushings Malnutrition related diabetes
Cortisol - glucose relationship
Raised cortisol = raised glucose
Diabetes definition
Symptoms and random plasma glucose above a set threshold
Type 1 diabetes - pathogenesis
Insulin deficiency characterised by loss of beta cells due to autoimmune destruction
Beta cells express antigens of HLA histocompatibility system perhaps in response to an environmental event such as virus or initiated by genetic susceptibility
Activates a chronic cell-mediated immune process leading to chronic ‘insulitis’
Increased cortisol and adrenaline on top of this leads to ultimate progressive catabolic state and increasing levels of ketones
Type 2 diabetes - Aetiology
Impaired insulin secretion
Insulin resistance
Progressive hyperglycaemia and high free fatty acids
Fat (free fatty acids) deposits back into pancreatic beta cells which drives this cycle further
Lipid deposition in liver and pancreas leads to both insulin resistance and impaired insulin secretion
Type 2 diabetes - Treatment
Weight loss and exercise if substantial will reverse hyperglycaemia
Medication to control BP, blood glucose and lipids
Insulin types
Basal insulin
Meal-time insulin/prandial insulin (rapid-acting analogues)
T2DM
Earlier insulin initiation is needed
Human premixed 70/30 insulin
70% long acting
30% short-acting
Basal insulin - Pros and cons
Pros - less risk of hypoglycaemia at night
Cons - Doesn’t cover meals
Premixed insulin - Pros and cons
Pros - Both basal and prandial components in a single insulin preparation
Cons - Requires strict and consistent meal/exercise patterns
T1DM
Basal-bolus insulin therapy is the gold standard treatment (long and short-acting combo)
Hypoglycaemia
Low plasma glucose causing impaired brain function - neuroglycopenia
Hypoglycaemia - symptoms
Palpitations Sweating Confusion Dizziness Weakness Nausea Headache
Hypoglycaemia - Risk factors
Advancing age
Renal impairment
Hypoglycaemia - Consequences
Seizures
Cognitive dysfunction
CVD
Pituitary-thyroid axis
Hypothalamus - (TRH) - pituitary - (TSH) - thyroid - (T4+T3)
T4 is converted to T3 which is the activated form
T4 contains 4 iodine molecules whereas T3 only 3
Pituitary-gonadal axis
Hypothalamus - Pituitary - Testosterone - Sperm
Inactive pituitary in females results in lack of periods (amenorrhea)
HPA (Hypo-Pit-Adrenal) axis
Hypothalamus - Pituitary - ACTH - Adrenal - Cortisol
Growth hormone/IGF1 axis
Hypo - (GHRH + SMS) - Pit - (GH) - Liver - (IGF1)
Dopamine
Hypo - (Dopamine) - Pituitary
Prolactin raised if dopamine inhibited
Prolactin important in breast milk production
Hypothalamus hormones
GHRH and SMS GnRH CRH TRH Dopamine
Pituitary hormones
GH LH and FSH ACTH TSH Prolactin
Pituitary diseases
Benign pituitary adenoma Craniopharyngioma Trauma Apoplexy (pituitary bleed causing expansion and local compression)/sheehans Sarcoid/TB
Tumours cause
Pressure on local structure (optics nerves - bitemporal hemianopia (both outer visual fields are blocked, centre fields are fine))
Pressure on normal pituitary (hypopituitarism)
Functioning tumor - Too much hormone released (Cushing’s, prolactinoma, acromegaly/gigantism)
Hypopituitarism presentation
Pale
No body hair
Central obesity
Cushing’s syndrome
Raised cortisol (leads to immunosuppression and infections)
Raised glucocorticoid
Excess fat which leads to weight loss very strangely
Redistribution of fat and muscle wasting
In adults, can get bruising and recurrent ulcers/infections
Cushing’s syndrome
Fat - increased and redistributed (weight gain, central obesity, moon face, buffalo hump, fat pads)
Protein - catabolism (muscle wasting, weakness, thin skin, striae, bruising)
Androgenic effects - Acne
Cushing’s syndrome - Definition
Chronic, excessive and inappropriate elevated levels of circulating plasma glucocorticoids (cortisol)
Cushing’s syndrome - Causes
Tumour of the pituitary gland (ACTH-dependent)
Tumour of another organ (lungs) (ACTH-dependent)
Adrenal tumour (ACTH-independent)
Cushing’s syndrome - Female to male ratio
Female>Male
Cushing’s syndrome - Clinical features
Carb - diabetes Eelctrolyte - Hypertension Immune suppression Central - Malaise, depressioon Suppressed gonadal function - amenhorrea
Cushings - Diagnosis
1 - Cushing’s syndrome
2 - Cause (ACTH dependent or independent)
Cushing’s syndrome - Screening
Urinary free cortisol
Low dose dexamethasone suppression tests
Late night/midnight serum or salivary cortisol
Cushing’s syndrome vs disease
When the ACTH comes from the pituitary gland it is called Cushing’s disease
Confirming Cushing’s syndrome
Measure plasma ACTH
Low plasma ACTH - Adrenal CT - Lesion (adenoma)
Raised plasma ACTH - Pituitary MRI/ CT/MRI thorax/abdo
Cushing’s syndrome - Management
Surgery
Radiotherapy
Acromegaly - Pathogenesis
Growth hormone-secreting pituitary tumour
IGF1 released at liver
Body enlargement (increased height, tissues - hands, feet, jaw)
Acromegaly - Comorbidities
Hypertension/CVD Headache Arthritis Diabetes Sleep apnea
Acromegaly - Diagnosis
Clinical features
GH
IGF1
Acromegaly - Clinical features
Acral enlargement Arthralgias (aches and pains) Maxillofacial changes Excessive sweating Headache Hypogonadal symptoms
Acromegaly - Diagnostic test
Glucose tolerance test
Acromegaly - Treatment
Pituitary surgery (decompression) Radiotherapy
Microadenomas vs macroadenomas
Cure rate after surgery is higher for microadenomas
Pituitary surgery - Complications
Diabetes insipidus
Hypopituitarism
Stereotactic Radiotherapy
Single fraction
Less radiation to surrounding tissues
Medical therapy
Dopamine agonists - Cabergoline
Somatostatin analogues
GH receptor antagonist
Dopamine agonists
Cabergoline
Control GH and IGF1
Oral admin
Rapid onset
Somatostatin analogues
Octreotide
Injection once monthly
Controls GH and IGF1
Pegvisomant
GH analogue
SC admin
Prevents GH binding at liver (inhibits IGF1 production)
Prolactinoma - Female to male ratio
F>M
Prolactinoma - Pathogenesis
Lactotroph cell tumour of the pituitary
Prolactinoma - Clinical features
Galactorrhoea Headache Bitemporal hemianopia CSF leak Menstrual irregularity/amenorrhea Infertility Low testosterone in men
Prolactinoma - Management
Medical rather than surgical
Dopmaine agonists - Cabergoline
Prolactinoma - Summary
Cause of infertility and hypogonadism
Galactorrhea
Cortisol circadian rhythm
Cortisol secretion patterns
Rise at early morning
Peak during morning
Fall during afternoon
Metabolic problems arise when this rhythm is disrupted
Liver expects low levels at night times so if disrupted then liver presents metabolic problems
Higher cortisol levels keep you awake and vice versa
Body clock - The sleep/wake cycle
Superchisasmatic nuclei in eye
Central clock controls peripheral clocks
Glucocorticoids are the secondary messenger from central to peripheral clocks (organs)
Addison’s disease
Primary adrenal insufficiency - Low cortisol
Autoimmune adrenalitis
Vitiligo - autoimmune lack of melanin in the skin
Weight loss
Infection (TB)
Adrenal insufficiency
Primary - Addison’s disease
Secondary - Hypopituitarism (Cranio apoplexy, infection, mets, pituitary macroadenoma)
Tertiary - Suppression of HPA (Steroids, oral, inhaler, creams)
Adrenal insufficiency - Diagnosis
Symptoms - Weight loss, fatigue, headache, steroid history, TB, cancer, postpartum bleed, autoimmunity
Signs - Pigmentation and pallor, hypotension, Low Na
Adrenal insufficiency - Investigation
Biochemical - Cortisol and ACTH tests at 9am
Synacthen test
Adrenal insufficiency - Investigation causes
Primary - Adrenal antibodies
Secondary - Steroids
Adrenal insufficiency - Treatment
Hydrocortisone (synthetic cortisol) - replace cortisol levels
Fluids
Thyroid autoantibodies found in autoimmune hypothyroidism
Thyroglobulin Thyroid peroxidase (TPO)
Mechanism of thyroid cell destruction
Cytotoxic T cell-mediated
Thyroid autoantibodies may cause secondary damage
Graves disease - TSH receptor antibodies
Thyroid-stimulating antibodies cause Graves
Hyperthyroidism - Graves (stimulating TSH receptor)
Hypothyroidism - Myxoedema (blocking TSH receptor)
Thyroid autoimmunity - Risk factors
F>M (sex hormones - oestrogen)
Genetic
Environmental - stress, high iodine intake, smoking
Autoimmune diseases associated with thyroid autoimmunity
T1DM Addison's Pernicious anemia Vitiligo RA SLE Sjogren's syndrome Chronic active hepatitis
Thyroid associated ophthalmopathy
Present in most Graves and some autoimmune hypothyroidism Periorbital oedema (swelling in extraocular muscles) Glycosaminoglycans are released which trap water and cause oedema which results in swelling
Neonatal Graves
Graves disease is caused by thyroid stimulating antibodies that may cross the placenta and cause neonatal graves
GOITRE
Palpable and visible thyroid enlargement
endemic in iodine-deficient areas
Sporadic non-toxic GOITRE
Commonest endocrine disorder
Thyroid enlargement
Hyperthyroidism
Excess of thyroid hormones in the blood
Hyperthyroidism - 3 mechanisms of increased levels
Overproduction of thyroid hormone
Leakage of preformed hormone from the thyroid
Ingestion of excess thyroid hormone
Hyperthyroidism - Causes
Graves
Multinodular GOITRE
Toxic adenoma
All forms of thyroiditis increase levels of thyroid hormones by
Leakage
Drug-induced hyperthyroidism
Iodine
Amiodarone
Hyperthyroidism - Clinical features (everything goes up)
Wt loss Tachycardia Hyperphagia Tremor Sweating Diarrhoea Menstrual disturbance
Hyperthyroidism - Investigations
Thyroid function tests (Raised free T3 and T4, suppressed TSH) Clinical history Physical signs Thyroid antibodies Isotope uptake scan
Primary vs secondary hyperthyroidism
Primary hyperthyroidism - (Raised free T3 and T4, suppressed TSH)
Secondary hyperthyroidism - (Raised free T3 and T4, Raised TSH)
Hyperthyroidism - Treatment
Antithyroid drugs (Thionamides)- Carbimazole (decreases synthesis of thyroid hormone), PTU (inhibit the conversion of T4-T3)
Radioiodine
Surgery (partial, subtotal thyroidectomy)
Thionamides - Side effects
Rash
Arthralgia
Hepatitis
Thrombocytopenia
Iodine
Essential for thyroid hormone production
Actively transported by NA/I symporter into thyroid follicular cells
Surgery
Graves - whole
Adenoma - partial
Hypothyroidism
Primary - Absent from birth/dysfunction, Hashimoto’s thyroiditis
Secondary - Pituitary dysfunction
Tertiary - Hypothalamic dysfunction
Hypothyroidism - Drug causes
Iodine
Amiodarone
Neonatal hypothyroidism
Thyroid ectopia
Resistance to thyroid hormone
Hypothyroidism - Clinical features
Fatigue Wt gain Constipation Menstrual disturbance Oedema Muscle cramps
Hypothyroidism - Investigation
Thyroid function test
Hypothyroidism - Thyroid function test results
Primary - Raised TSH, normal T4, low T3
Secondary/Tertiary - Low TSH, reduced T4/T3
Hypothyroidism - Treatment
Synthetic L-Thyroxine (T4)
Pregnancy - Metabolic changes
Increased erythropoietin, cortisol and noradrenaline High cardiac output Plasma volume expansion High cholesterol Pro thrombotic and inflammatory state Insulin resistance
Pregnancy - Gestational syndromes
Gestational diabetes
Postpartum thyroiditis
Lipid disorders
Derbyshire neck
GOITRE
Glycoprotein hormones
TSH
LH
FSH
Beta HCG
Hypothyroidism in pregnancy
Gestational hypertension Placental abruption Low birth weight Neonatal GOITRE Neonatal resp distress Postpartum haemorrhage
Antithyroid drugs can cause in severe cases
Agranular cytosis
TSHR autoantibodies
TRAB/TBII
Drugs which disrupt thyroid function
Amiodarone
Interferon
Amiodarone
Iodine rich Treats arrhythmias (AF)
Interferon
Anti-cancer drug
Vasopressin
Aka ADH
Made in hypo, released from the posterior pituitary
Binds to G protein-coupled 7 transmembrane domain receptors
Aquaporin molecules are inserted which allow reabsorption of water
V1a - Vasculature
V2 - Renal collecting tubules
V1b - Pituitary
Release controlled by - Osmoreceptors in the hypothalamus - day to day, Baroreceptors in the brainstem and great vessels - emergency
Posterior pituitary diseases
Lack of vasopressin - Cranial diabetes insipidus
Resistance to action of vasopressin - Nephrogenic diabetes insipidus
Too much vasopressin release when it shouldn’t be released - Syndrome of anti-diuretic hormone secretion (SIADH)
Diabetes insipidus
Inappropriate dilute urine for plasma osmolality
Polyuria
Polydypsia
No glycosuria
Diagnosis - Measure urine volume, check renal function and serum calcium
Anterior pituitary tumours do not cause
Diabetes insipidus
Nephrogenic diabetes insipidus - Causes
Genetic
Chronic renal impairment
Meabolic - Hypercalcemia
Cranial diabetes insipidus - Causes
Tumours (mets) Trauma Infection (TB, encephalitis, meningitis) Infarction Genetic
Desmopressin
A synthetic analogue of vasopressin
Diabetes insipidus - Diagnostic tests
Water deprivation test
Copeptin
Cranial DI - Treatment
Desmopressin (Activates V2 receptor)
Nephrogenic DI - Treatment
V high dose of desmopressin
Otherwise difficult to treat
Hyponatraemia
Tends to be due to excess water rather than salt loss
Hyponatraemia - Signs and symptoms
Headache N&V Confusion Convulsions Unstable gait - falls
Hyponatraemia - Diagnostic tests and treatment
Urinary Na
TFT
Cortisol levels
Check whether dehydrated or not (then either give saline or restrict fluids to balance levels)
Liver cirrhosis causes
Fluid retention (overload)
SIADH
Syndrome of inappropriate antidiuretic hormone secretion
SIADH - Causes
CNS - Head trauma, meningitis, encephalitis, tumour, abscess
Drug effects
SIADH - Treatment
Fluid restriction
Vaptan - V2 receptor antagonist (oral)
Osmotic demyelination syndrome
Death of the pons (brainstem) leading to brain cell dysfunction
Destruction of the myelin sheath covering nerve cells in the pons of the brainstem
Pituitary mass lesions
Non-functioning pituitary adenomas Endocrine active pituitary adenomas Malignant pituitary tumours (functional and non-functional pituitary carcinoma) Mets in the pituitary (breast, lung, stomach, kidney) Pituitary cysts (Rathke's cleft cyst)
Anterior vs posterior pituitary tissue
Anterior pituitary - Glandular tissue
Posterior pituiatary - Nerve tissue
Craniopharyngioma
Arises from remnants of Rathke’s pouch
Can be calcified
Solid and cystic
Raised ICP, visual disturbances, pituitary hormone deficiency
Rathke’s cyst
Derived from remnants of rathke’s pouch
Mostly small
Headache, amenorrhea, hydrocephalus, hypopituitarism
Meningioma
Complication of radiotherapy
Visual disturbance and endocrine dysfunction
Lymphocytic hypophysitis
Inflammation of pituitary gland due to an autoimmune reaction
Common in women - pregnancy/postpartum
Stalk and pituitary enlargement
Non-functioning pituitary adenoma
Visual disturbances
Headaches
Trans-sphenoidal surgery if threatening eyesight or showing signs of aggression (increasing size)
Testing pituitary function
Hormones
Circadian rhythms
If peripheral target organ is working normally then pituitary is normal
Testing pituitary-thyroid axis
TSH and Ft4 (Free T4) levels are key determinants
Primary hypothyroid - Raised TSH, Low Ft4
Hypopituitary - Normal/Low TSH, Low Ft4
Graves disease - Suppressed TSH, HIigh Ft4
TSHoma - Normal/High TSH, High Ft4
Hormone resistance - Normal/High TSH, High Ft4
Testing gonadal axis in men
Testosterone (T) levels and LH/FSH
Primary hypogonadism - Low T, raised LH/FSH
Hypopituiary - Low T, Normal/Low LH/FSH
Anabolic use - Low T, Suppressed LH
Testing gonadal axis in women
Before puberty - Oestradiol low/undeetctable, Low LH/fsh
Puberty - Raised LH/Oestradiol
Post-menarche - Menstrual cycle with everything raised
Primary ovarian failure (menopause) - High LH/FSH, Low oestradiol
Hypopituitary - Low oestradiol, Normal/Low LH/FSH
Testing HPA axis
Circadian rhythm - Measure cortisol at 9am
Primary adrenal insufficiency - Low cortisol, high ACTH
Hypopituitarism - Low cortisol, Low/normal ACTH
Testing GH/IGF1 axis
GH is secreted in pulses with greatest pulse at night
GH levels fall with age and are low in obesity
Measure IGF1 and GH - Glucagon test, Insulin stress test
Measuring prolactin levels
Prolactin is a stress hormone
Prolactin may be raised because of stress, prolactinoma
Diabetes insipidus - Test
Water deprivation test
Key tests
Dexamethasone suppression testing – Cushing’s
Oral glucose GH suppression test - Acromegaly
CRH stimulation – Cushing’s
TRH stimulation – TSHoma
GnRH stimulation – gonadotrophin deficiency
Insulin-induced hypoglycemia – GH/ACTH deficiency
Glucagon test – GH deficiency
Treating pituitary hormone deficiencies
GH - Growth hormone LH/FSH - Testosterone (M) or Oestradiol+progesterone (F) TSH - Levothyroxine ACTH - Hydrocortisone ADH - Desmopressin
Radiological evaluation
MRI (Preferred for pituitary imaging) - Soft tissues/vasculature
CT - Bony/calcified structures
Testosterone replacement
Improves libido, energy levels and wellbeing
Oestrogen replacement
Oral or combined with progesterone
Improves vaginal atrophy
Diabetes - Presenting features
Thirst
Polyuria
Weight loss - due to gluconeogenesis
Fatigue
Hunger
Pruritus vulvae/Balanitis (vaginal candidiasis, chest infections)
Blurred vision (altered acuity due to uptake of glucose and water into lens)
Type 1 - Suggestive features
Childhood-onset
Lean body habitus
Prone to ketoacidosis
High levels of islet autoantibodies
Presentation depends on
Rate of Beta cell destruction
Type 1 diabetes - Clinical features of newly diagnosed
A short history of severe symptoms
Weight loss
Large urinary ketones
T2D - Suggestive features
Gradual onset
100% concordance in identical twins
Lifestyle often can control it, insulin may be required later in disease
T1 vs T2
T2 - Younger patients, weight loss+ketouria
T1 - Obese
If in doubt with diagnosing diabetes, treat with
Insulin
Ketoacidosis
Absence of insulin and rising counteregulatory homrones leads to increasing hyperlgycaemia and rising ketones
Glucose and ketones escape in the urine and lead to an omsotic diuresis and falling circulating blood volume
Ketones (weak organic acids) cause anorexia and vomiting
Vicous cycle of increasing dehhydration and hyperglycaemia
Diabetic ketoacidosis
Hyperglycaemia
Raised plasma ketones
Metabolic acidosis (Raised plasma bicarbonate)
Diabetic ketoacidosis - Triad of
Hyperglycamia
Ketones
Acidosis
DKA - Symptoms
Polyuria Polydipsia N&V Wt loss Abdo pain Confusion/drowsiness
DKA - Signs
Hyperventilation Dehydration Hypotension Tachycardia Coma
DKA - Management
Firstly, Rehydration - Fluids (dilutes acid and glucose)
Secondly, Insulin (Stops new ketone production and glucose production)
Thirdly, Electrolyte replacement (K)
DKA - Complications
Cerebral oedema Resp distress syndrome Thromboemolism - Venous and arterial Aspiration pneumonia Death
Aims of treatment in T1D
Prevent ketoacidosis
Prevent microvascular and macrovascular complications
Microvascular complications
Nephropathy
Retinopathy
Neuropathy
T1D - Treatment
Insulin - Twice daily mixture, Basal bolus
Glucose monitoring with insulin intake
Blood glucose meters and pens
T1 VS T2
T1 more difficult to control than T2
Hypoglycaemia - Symptoms
Shaking Fast heartbeat Sweating Dizziness Anxious Hunger Impaired vision Weakness Fatigue
Acute deprivation of glucose within the brain leads to
Cerebral dysfunction (loss of concentration, confusion, coma)
Physiological defences to hypoglycaemia
Release of adrenaline and glucagon
Symptoms - autonomic and neuro
Insulin pumps
T1D
Continuous infusion of insulin as opposed to carrying a pen or injection
Insulin and weight
Tend to gain weight
MODY - Maturity-onset diabetes of the young
Autosomal dom
Non-insulin dependent
Single gene defect altering beta-cell function
Tend to be non-obese
MODY is typically misdiagnosed as T1D or young-onset T2D
Permanent neonatal diabetes
Diagnosed less than 6 months old
Signs - small babies, epilepsy, muscle weakness
Treatment - Sulfonylureas
MIDD - Maternally inherited diabetes and deafness
Mutation in mitochondrial DNA
Loss of beta-cell mass
Similar presentation to T2D
Wide phenotype
Lipodystrophy
Selective loss of adipose tissue
Associated with insulin resistance
Exocrine pancreas - Diseases
Inflammatory - Acute (hyperglycaemia)
Chronic pancreatitis - Alcohol
Hereditary haemochromatosis - Auto rec (Triad of cirrhosis, diabetes and bronzed hyperpigmentation due to excess iron deposition)
Deposition - Amyloidosis, cystinosis
Pancreatic neoplasia - Loss of glucagon function means prone to hypo. Require SC insulin
Cystic fibrosis - CTFR (CF Transmembrane conductance regulator) regulates chloride secretion, viscous secretions lead to duct obstruction and fibrosis, Insulin treatment required
Insulin improves cystic fibrosis quality of life by
Improving bodyweight, reduces infections, lung function
Endocrine causes of diabetes
Acromegaly - Excess GH secretion, insulin resistance rises which impairs insulin action
Cushing’s syndrome - Excess glucocorticoids increase insulin resistance
Drug-induced diabetes
Thiazides
Antipsychotics
Protease inhibitors (HIV treatment)
Hyperthyroidism - Presentation
Head - Anxiety, heat intolerance (hot) Eyes - Bulging Mouth - Increased appetite Neck - GOITRE (Bulging) Chest - Tachycardia Hands - Tremor, clubbing, sweating Abdo - Weight loss, diarrhoea
Hypothyroidism - Presentation
Head - Cold intolerance (cold) Face - Blank expression Mouth - Decreased appetite Chest - Bradycardia Hands - Brittle nails Abdo - Weight gain
Cancer
Weight Loss
Hyperkalemia
Arrhythmias and death
TSH raised
High T4 - Pituitary problem
Low T4 - Thyroid problem
TSH low
High T4 - Thyroid problem
Low T4 - Pituitary problem
T4 and T3
T4 - Thyroxine
T3 - Triiodothyronine
Addison’s disease
Autoimmune attack of adrenal gland
Tanned
Tired
Tearful
Long term steroids can lead to
Adrenal insufficiency (Addison’s disease)
3 Functions of parathyroid hormone
To increase blood calcium from bone resorption
Kidney reabsorption of Ca
Increased gut absorption of Ca
Hypercalcaemia
Bones
Groans (Abdo)
Stones (Renal)
Moans (Pysch)
Bisphosphonates
Hypercalcemia
