Endocrinology Flashcards
Specific Cutaneous Signs of Endocrinology Disorders:
What are the Specific Cutaneous Signs of Hyperthyroidism?
- Hair loss
- Onycholysis (when your nail separates from the skin underneath it)
- Bulging eyes (stare)
- Pretibial Myxedema (orange peel on anterior leg)
Specific Cutaneous Signs of Endocrinology Disorders:
What are the Specific Cutaneous Signs of Hypothyroidism?
- Hair and eyebrow loss
- Cold, pale skin
- Characteristic ‘toad-like’ face
Specific Cutaneous Signs of Endocrinology Disorders:
What are the Specific Cutaneous Signs of Cushing’s Syndrome (hypercortisolism)?
- Central obesity and wasted limbs (lemon on sticks)
- Moon face
- Buffalo hump
- Supraclavicular fat pads
- Striae (red stretch marks)
Specific Cutaneous Signs of Endocrinology Disorders:
What are the Specific Cutaneous Signs of Addison’s Disease (adrenal insufficiency)?
- Hyperpigmentation (face, neck, palmar creases)
Specific Cutaneous Signs of Endocrinology Disorders:
What are the Specific Cutaneous Signs of Acromegaly?
- Distal + soft tissue overgrowth
- Large jaw, hands and feet
- Thick skin and coarse facial features
Specific Cutaneous Signs of Endocrinology Disorders:
What are the Specific Cutaneous Signs of Hypopituitarism?
- Pale/ yellow tinged thin skin
- Fine wrinkling round eyes and mouth (looks old)
Specific Cutaneous Signs of Endocrinology Disorders:
What are the Specific Cutaneous Signs of Hypoparathyroidism?
- Dry, scaly, puffy skin
- Brittle nails and coarse hair
DIABETES MELLITUS
What is the primary cause of DM?
DM results from a lack of or reduced effectiveness of endogenous insulin and chronic hyperglycaemia.
DIABETES MELLITUS
Hyperglycaemia cause microvascular and macrovascular problems.
Name examples of microvascular problems.
- Retinopathy
- Nephropathy
- Neuropathy
DIABETES MELLITUS
Hyperglycaemia cause microvascular and macrovascular problems.
Name examples of macrovascular problems.
- Stroke
- Heart disease
- Limb ischaemia
- Renovascular disease
DIABETES MELLITUS
Name some symptoms of hyperglycaemia.
- Polyuria (excessive urine)
- Polydipsia (excessive thirst)
- Weight loss
- Visual blur
- Genital thrush
- Lethargy
DIABETES MELLITUS
How is DM diagnosed
- Hyperglycaemia symptoms
- Fasting glucose of 7 mmol/L
- normal glucose of over 11 mmol/L
- HbA1c over 48 mmol/L (6.5%)
DIABETES MELLITUS
what is type 1 DM
it is insulin deficiency from autoimmune destruction of insulin-secreting pancreatic beta cells.
DIABETES MELLITUS
What is type 2 DM
it is decreased insulin secretion +- increased insulin resistance
DIABETES MELLITUS
Name some features that would suggest type 1 DM
- Weight loss
- Persistent hyperglycaemia despite diet/medication
- ICA and GAD antibodies
DIABETES MELLITUS
name the difference in causes between type 1 and type 2
Type 1 is autoimmune beta cell DESTRUCTION.
Type 2 is beta cell DYSFUNCTION/ insulin resistance.
DIABETES MELLITUS
Risk factors for type 2 diabetes
- obese
- Asian
- age >40
- family history
- gestation diabetes
- diet in high fat/sugar
- high cholesterol
DIABETES MELLITUS
Acute signs of DM
type 1- weight loss, polydipsia, polyuria
type 2- mainly asymptomatic but still complications
DIABETES MELLITUS
general treatment for DM
- Address risk factors (quit smoking, start statin, control BP)
- Inform DVLA
- foot care
- exercise
- low fat/ sugar diet
- Avoid alcohol
- educate on what to do if they hypo (sugar drinks)
DIABETES MELLITUS
Treatment for type 1
Insulins.
1) ultra fast at start of meal- Novorapid
2) Isophane insulin- peaks at 4-12hrs
3) mixture-Novomix
4) long acting- insulin determir (bedtime)
vary injection site between thigh/abdomen
DIABETES MELLITUS
Treatment for type 2
1) Lifestyle changes
2) metformin
3) add gliptin or sulfonylurea or pioglitazone
4) triple therapy of metformin plus 2 above
5) triple therapy of metformin, sulfonylurea and GLP-1 mimetic
DIABETES MELLITUS
How is diabetes monitored
- Fingerprick glucose
- HbA1c- mean glucose over past 8 weeks
Hypoglycaemia
symptoms?
plasma glucose reading?
treatment?
- sweating, hunger, dizzy, confusion, tired, visual issues
- < 3mmol/L
- oral/ IV glucose depending if they can swallow
DIABETEIC KETOACIDOSIS
symptoms?
- Drowsiness
- Pear drop breath (due to acetones)
- Kussmaul Breathing- trying to get rid of acid by respiratory compensation
- Dehydration and vomiting
DIABETEIC KETOACIDOSIS
what can trigger DK
- Infection, surgery, MI, wrong insulin dose
DIABETEIC KETOACIDOSIS
diagnosis?
- Acidaemia blood pH < 7.3
- Hyperglycaemia and Ketonaemia
DIABETEIC KETOACIDOSIS
Treatment?
-Fluids and IV insulin
Hyperglycaemic, hyperosmolar non- ketotic (HONK) coma
what is it?
Long history of dehydration and glucose is > 35mmol/L
what is the treatment for a HONK coma
- Rehydrate slowly with IV saline, replace K+ when urine starts to flow
THYROID
What does the thyroid gland secrete?
hormones T3 and T4. (thyroxine is T4, triiiodothyronin is T3)`
THYROID
How is T3 produced and what does it do
T3 is produced by the peripheral conversation of T4 and it acts to control metabolism/ increase BMR.
HYPERTHYROIDISM
signs and symptoms?
- Diarrhoea
- weight loss
- increased appetite
- irritability and over-active
- Fast irregular pulse
- warm, moist skin
- fine tremor
- Lid lag (eyelid lags behind eyes as it descends to follows finger)
HYPERTHYROIDISM
What tests would be done and what would they show?
- TSH low
- increased T3 and T4
- Mild anaemia
HYPERTHYROIDISM
how is it treated
- beta blockers (propranolol- rapid symptom relief)
- anti thyroid meds ( carbimazole)
- thyroidectomy if severe
GRAVE’S DISEASE
What is it?
Circulating IgG autoantibodies bind to and activate G-protein thyrotropin receptors, this causes thyroid enlargement and increased production of T3.
GRAVE’S DISEASE
what may trigger graves disease and what age/ gender is most likely to get it
triggers: stress, childbirth infection
age: 40-60 years
F:M 9:1
GRAVE’S DISEASE
Signs?
- eye disease
- pretibial myxoedema (swelling above lateral malleoli)
- thyroid acropachy
- clubbing and swlling of fingers/toes
GRAVE’S DISEASE
Tests?
test for the signs and also may have mild neutropaenia
GRAVE’S DISEASE
Treatment?
- propranolol
- Carbimazole +- thyrozine
- 50% will relapse and need radioiodine/ surgery
HYPOTHYROIDISM
Causes?
- Hashimotos Thyroiditis (goitre due to lymphocytic and plasma cell infiltration)
- F:M 6:1
- iodine deficiency
- post thyroidectomy
HYPOTHYROIDISM
associations?
pregnancy problems ( Eclampsia, anaemia, prematurity, low birth weight, postpartum haemorrhage)
HYPOTHYROIDISM
signs?
Bradycardic Reflexes relax slowly Ataxia (cerebellar) Dry skin/hair Yawn/drowsy Cold hands/ low temp Ascites Round face/obese Defeated demeanour Immobile CCF (congestive cardiac failure)
HYPOTHYROIDISM
Tests?
- high TSH
- low T4
- high cholesterol
HYPOTHYROIDISM
treatment?
- Levothyroxine (T4)
THYROID CANCERS
What are the types of thyroid cancer?
- Papillary 60%
- Follicular 25%
- Medullary 5%
Lymphoma 5%
-Anaplastic (rare)
THYROID CANCERS
what is the treatment for the cancers?
- thyroidectomy
- radiotherapy
- node clearance/excision
- thyroxine to suppress TSH in papillary
THYROID CANCERS
how many more women have this than men?
F:M 3:1
What is the function of the ADRENAL CORTEX?
Production of:
- Glucocorticoids (cortisol, carb,fat,protein metabolism)
- steroids
- Mineralocorticoids (aldosterone, Na+ and K+ balance)
- Androgens (sex hormones, e.g. convert to testosterone)
What does corticotrophin releasing factor (CRF) do?
CRF from the hypothalamus stimulates ACTH from pituitary, this initiates cortisol and androgen production.
CUSHING’S SYNDROME
What is it?
• Clinical state produced by chronic glucocorticoid excess + loss of normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis and loss of circadian rhythm of cortisol secretion
CUSHING’S SYNDROME
what is Cushing’s disease?
Bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma
CUSHING’S SYNDROME
What may cause Cushing’s syndrome?
it may be caused by: - oral steroids - Cushing's Disease - Ectopic ACTH production - Decreased ACTH due to –ve feedback • Adrenal adenoma/cancer
CUSHING’S SYNDROME
symptoms?
- weight gain
- acne
- Recurrent achilles rupture
- mood change
- ED
- irregular menstruation
CUSHING’S SYNDROME
signs?
- central obesity
- plethoric moonface
- skin/muscle atrophy
- osteoporosis
CUSHING’S SYNDROME
Tests?
- the overnight dexamethasone test (DST). Dexamethasone suppresses the production of cortisol, if there is no suppression then this patient has Cushing’s.
CUSHING’S SYNDROME
Treatment for Cushing’s is cause dependant. what are they?
Iatrogenic- stop meds
Cushing’s Disease- bilateral adrenalectomy
Ectopic ACTH production- surgery, metyrapone
Adrneal adenoma- adrenalectomy+ radiotherapy
ACROMEGALY
what is acromegaly caused by?
- increased GH from a pituitary tumour OR
- hyperplasia ectopic GH releasing hormone from a carcinoid tumour
ACROMEGALY
What does growth hormone do?
GH stimulates bone& tissue growth by the secretion of IGF-1
ACROMEGALY
how many people in the UK have acromegaly?
3 per million a year
ACROMEGALY
symptoms?
- paraesthesia ( pins and needles in extremities)
- amenorrhea
- low libido
- Arthralgia (joint pain)
ACROMEGALY
Signs?
- large hands, feet and jaw
- wide nose
- macroglossia (large tongue)
- Acantosis nigricans- hyperpigmentation in folds of skin
ACROMEGALY
complications?
- DM
- vascular (HTN,CCF,LVH, IHD, arrhythmias, cardiomyopathy)
- Neoplasia ( increased risk of colon cancer)
ACROMEGALY
Tests?
- MRI
- OGTT (high glucose suppresses GH so if GH still high then= acromegaly)
ACROMEGALY
treatment?
- excising lesion
- reduce GH and IGF-1 by: surgery, GH antagonist, somatostatin analogues
HYPERALDOSTERONISM
what is it?
excess aldosterone independent of RAAS, increased Na+ and water retention, decreased renin.
HYPERALDOSTERONISM
symptoms?
- signs of hypokalaemia ( weakness, polydipsia, polyuria, paraesthesia)
HYPERALDOSTERONISM
Causes?
2/3- Conn’s syndrome (solitary aldosterone producing adenoma)
1/3- bilateral adrenal hyperplasia
HYPERALDOSTERONISM
what tests would you carry out?
- U+E, renin, aldosterone
HYPERALDOSTERONISM
Treatments?
conn’s- laproscopic adrenalectomy, spironolactone pre-op
Hyperplasia- spironolactone, amiloride, eplerenone
ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)
What is it?
glucocorticoid and mineralocorticoid deficiency due to destruction of the adrenal cortex. Not enough cortisol or aldosterone.
ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)
What is it caused by?
- 80% due to autoimmunity.
- Worldwide TB is the most common cause.
- Adrenal metastases
- Lymphoma
ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)
Symptoms and signs?
- Depression/ low self esteem
- Tanned, tired, tearful, weak, faint, flu, myalgias, arthralgias
- GI, (nausea, diarrhoea/ constipated)
- postural hypotension
ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)
Tests?
Na+ low and K+ high due to less aldosterone
Low glucose due to less cortisol
ACTH stimulation test- measure plasma cortisol 30 mins before/after tetracosactide, Addison’s excluded if over 550nmol/L
21- hydroxylase autoantibodies positive in autoimmune disease
ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)
Treatment?
- replace steroids with oral hydrocortisone
- mineralocorticoids to correct postural hypotension (fludrocortisone oral)
ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)
Common differential diagnosis?
Commonly misdiagnosed with anorexia, viral infection.
however, in anorexia K+ DECREASES, in Addison’s, K+ INCREASES.
ADDISON’S DISEASE (ADRENAL INSUFFICIENCY)
What may occur after long term steroid therapy?
Suppression of pituitary- adrenal axis
DIABETES INSIPIDUS
What is it?
Passage of large volumes (>3L a day) of dilute urine due to impaired water retention of the kidneys
DIABETES INSIPIDUS
What are the two types of DI and what is the difference?
Too little ADH from posterior pituitary gland (cranial DI)
OR
Kidney not responding to ADH (nephrogenic DI)
DIABETES INSIPIDUS
What are the causes for each type of DI?`
Cranial DI: Head trauma, pituitary tumour
Nephrogenic DI: Drugs (eg: Lithium), CKD
DIABETES INSIPIDUS
What are the signs and symptoms?
- polyuria
- polydipsia
- dehydration
- hypernatremia symptoms (lethargy, weak, thirst, irritated and confusion)
DIABETES INSIPIDUS
How is it diagnosed and tested for?
Water Deprivation Test
1) deprive of fluids, measure osmolality and volume of urine every 2 hours
2) if still dilute, give DESMOPRESSIN (distinguish cranial or nephrogenic)
3) If there is a response and concentrated urine begins to be produced then it is CRANIAL DI
DIABETES INSIPIDUS
Treatment?
Cranial DI- Desmopressin (synthetic ADH analogue), MRI to find cause
Nephrogenic DI-
Bendroflumethiazide
(causes more Na+ excretion -increased water lost makes body responds by reducing GFR, so treat DI)
NSAIDS- inhibit prostaglandin synthase (inhibits ADH), so reduced GFR and decreased volume of urine
Syndrome of Inappropriate ADH Secretion (SIADH)
What is it?
Too much secretion of ADH despite hypertonicity and volume being normal.
Concentrated urine and hyponatraemia
Syndrome of Inappropriate ADH Secretion (SIADH)
Causes?
Any neoplastic process
Any pulmonary process (pneumonia, chronic obstructive pulmonary disease, pulmonary hypertension, pulmonary embolism, etc)
CNS disturbances due to stroke, hemorrhage, or trauma
Metabolic- alcohol withdrawal
Syndrome of Inappropriate ADH Secretion (SIADH)
Symptoms?
- Nausea
- Hyponatraemia ( anorexia, irritability, headache, confusion, weakness)
- Malaise (feeling of general discomfort)
Syndrome of Inappropriate ADH Secretion (SIADH)
Diagnosis and Tests?
- Measure urine and plasma osmolality, both low
- continued Na+ secretion
Syndrome of Inappropriate ADH Secretion (SIADH)
Treatment?
- Treat underlying cause
- Restrict fluids
- Vasopressin receptor antagonists (‘vaptans’, block the action of ADH)
PARATHYROID HORMONE
What is the action of PTH?
Increased bone resorption by osteoclasts
Increased intestinal calcium absorption
Actives 1,25-dihydroxyVD (calcitriol) in kidney
Increased calcium reabsorption and phosphate excretion in the kidney
OVERALL INCREASE CALCIUM AND DECREASE PHOSPHATE
HYPERPARATHYROIDISM
Causes?
80% = solitary adenoma 20% = parathyroid hyperplasia Rare = parathyroid cancer
HYPERPARATHYROIDISM
Presentation?
hypercalcaemia: weak, tired, depressed, thirsty, renal stones
Bone resorption causes pain, fracture, osteoporosis
Hypertension
HYPERPARATHYROIDISM
Investigation?`
Bloods:
Primary: ↑PTH, ↑Ca, ↓Phosph
Secondary: ↑PTH, ↓Ca, ↑Phosph
Tertiary: ↑everything (progression of secondary)
Increased 24hr urinary calcium excretion
DEXA bone scan for osteoporosis
HYPERPARATHYROIDISM
Treatment?
Fluids
surgically treat underlying cause
Bisphosphonates
HYPOPARATHYROIDISM
Aetiology: Autoimmune destruction of PT glands Congenital Surgical removal (secondary) Mg deficiency, VD deficiency
Clinical: Signs and symptoms of hypocalcaemia
Tx: Ca supplement, calcitriol, synthetic PTH
HYPERKALAEMIA
Investigations?
ECG-
Tall, tented T waves
Small/ no P wave
Wide QRS complex
HYPERKALAEMIA
Treatment?
Non-urgent-
Polystyrene sulphonate resin= Binds K+ in the gut decreasing uptake
Urgent-
Calcium gluconate= decreases VF risk in the heart
Insulin= drives K+ into the cells
HYPOKALAEMIA
Investigations?
ECG!
Rhyme- U have no Pot (K+) & no Tea but a Long PR & a long QT.
U waves
No T waves/ inversion
Long PR
Long QT
HYPOKALAEMIA
Hypokalaemia is when K+ is <3.5mmol/L, what will this cause?
Low K+ in the serum (ECF) causes a water concentration gradient out of the cell (ICF)
Increased leakage from the ICF causing hyperpolarisation of the myocyte membrane decreasing myocyte excitability.
HYPOKALAEMIA
Treatment? (easiest answer ever)
Mild- oral K+
Severe- IV K+
What is calcium levels controlled by?
Calcium balance controlled by:
Parathyroid: PTH
Thyroid: Calcitonin
What are the functions of PTH and Calcitriol?
Parathyroid hormone causes stimulation of kidneys and GI tract to increase absorption of calcium and causes stimulation of osteoclasts to break down bone and release calcium stored there.
Calcitriol (active vitamin D) levels are increased by PTH and cause increased GI and Kidney absorption of Calcium.
HYPOCALCAEMIA
Causes?
H- hypoparathyroidism A- Acute pancreatitis V- Vitamin D Deficiency O- Osteomalacia C- Chronic Kidney Disease
HYPOCALCAEMIA
Clinical Features?
S – spasms P - peripheral paraesthesia A - anxious S - seizures M – muscle tone increase in SM O- Orientation impaired D- Dermatitis I- Impetigo herpetiformis (severe pustular psoriasis) C- cataracts
HYPOCALCAEMIA
Ix?
ECG- long QT interval
HYPOCALCAEMIA
Treatment?
Mild= Adcal (oral calcium)
Severe= IV Calcium gluconate
In CKD- Alfacalcidol
HYPERCALCAEMIA
Causes?
90% is due to primary hyperparathyroidism or cancer.
HYPERCALCAEMIA
Symptoms?
Painful Bones
Renal Stones
Abdo Groans (nausea, constipation, indigestion)
Psychiatric Moans (lethargy, memory loss, depression)
HYPERCALCAEMIA
Investigations?
Investigations-
1) find cause:
Corrected calcium levels
PTH
2) identify damage:
U&E (Renal damage)
XRay
HYPERCALCAEMIA
Treatment?
rehydration
Saline (NaCl) (dilute blood of calcium)
Bisphosphonates (pamidronate) (encourage osteoclast apoptosis so bone resorption)
What is Hashimoto’s Thyroiditis?
goitre due to lymphocytic and plasma cell infiltration
When would you do the ACTH stimulation test and briefly describe it?
Addison’s- Adrenal Insufficiency
ACTH stimulation test- measure plasma cortisol 30 mins before/after tetracosactide (ACTH)
Addison’s excluded if over 550nmol/L (would mean its responsive to ACTH)
