Endocrinology Flashcards
Causes of secondary diabetes
Pancreatic disorders:
*Chronic pancreatitis
Endocrine disorders:
*Cushing syndrome
*Acromegaly *Phaeochromocytoma
*Polycystic ovarian syndrome
*Haemochromatosis
Drug-induced diabetes (transient):
*Thiazide diuretics
*Corticosteroids
*Oestrogen therapy (high dose—not with low-dose HRT)
Other transient causes
*Gestational diabetes
*Medical or Surgical stress
neonate blood glucose level of <2.6 mmol/L
childhood hypoglycaemia
childhood hypoglycaemia treatment
IV dextrose 10%, 2.5 to 5 mL/Kg followed by 0.03 to 0.05 mL/Kg/minute
Adult hypoglycaemia treatment
IV dextrose 50%
hypoglycaemia risk factors
– Alcohol abuse-suppression of gluconeogenesis.
– Liver failure.
– Cognitive impairment.
– Increasing age
– Previous history of hypoglycaemia.
– Vigorous and prolonged exercise.
DM (type 2) Screening
*People with known impaired fasting glucose/glucose tolerance (‘prediabetes’)
(FBS yearly for this scenario)
*Age >40 years
*>30 years: 1st degree relative with T2D), BMI >30), high-prevalence ethnic groups
*Age >18 years in Aboriginal and Torres Strait Islanders
*Previous GDM
*People on long-term steroids or antipsychotics
*PCOS, especially if overweight
*Previous cardiovascular event
The optimal frequency is every 3 years from age 40 years using AUSDRISK
If the score is ≥12, do fasting blood glucose or HbA1c.
Screen annually in very high-risk groups:
*Aboriginal and Torres Strait Islander people
*Prediabetes pacients
Diagnosis DM in Symptomatic
At least two of: Polydipsia, polyuria, frequent skin infections or frequent genital thrush
Skin signs of diabetes:
a) Recurrent staphylococcus folliculitis
b) Candida albicans erosio interdigitalis
c) Candida albicans balanitis.
Fasting venous blood glucose (VBG) ≥7.0 mmol/L
or
Random VBG (at least 2 hours after last eating) ≥11.1 mmol/L
or
HbAIc >6.5% (>48 mmol/mol)
Diagnosis DM in Asymptomatic
At least two separate elevated values: Either fasting (≥7.0 mmol/L), 2 or more hours postprandial (≥11.1 mmol/L)
or
Two altered values from an oral glucose tolerance test (OGTT)
OGTT
The 2-hour blood sugar on an OGTT is still the gold standard for the diagnosis of uncertain diabetes >11.1 mmol/L.
If random or fasting VBG lies in an uncertain range (5.5–11.0 mmol/L) in either a symptomatic patient or a patient with risk factors (over 50 years, overweight, first-degree relative with T2D), perform an OGTT. The cut-off point for further testing is 5.5 mmol/L.
The OGTT should be reserved for true borderline cases and for diagnosing gestational diabetes, where a 75 mg OGTT is recommended at 24–28 weeks gestation.
CV risk assessment
every 2 yrs after 45yrs
>35yrs for aboriginals
Diabetic ketoacidosis: Clinical features
Develops over a few days, but may occur in a few hours in ‘brittle’ diabetics
Hyperglycaemia (often >20 mmol/L, lower or normal if on SGLT2 inhibitor)
Preceded by polyuria, polydipsia, drowsiness
Vomiting and abdominal pain, dehydration
Hyperventilation—severe acidosis (acidotic breathing): ↓BP, ↑pulse, ↑resp. rate
Ketosis (blood and urine)
Diabetic retinopathy ophthalmic referral
low risk: 2 yearly
high risk: yearly
Diabetic ketoacidosis: Management
Early IV fluids—normal saline fast first litre, then caution
IV insulin—slow, e.g. 10 U in first hour
ECG—arrhythmia in electrolyte disturbances
Diabetic ketoacidosis with coma: Fluids, sodium (3 L N saline), potassium (KCl) and insulin.
Hyperosmolar hyperglycaemia: Clinical features
Marked hyperglycaemia and dehydration without ketoacidosis.
Altered conscious state varying from stupor to coma and with marked dehydration.
The onset may be insidious over a period of weeks, with fatigue, polyuria and polydipsia.
Typically in uncontrolled type 2 diabetes, especially in elderly patients.
There may be evidence of an underlying disorder such as pneumonia or a urinary infection.
Extreme hyperglycaemia and high plasma osmolarity.
The condition has a high mortality—even higher than ketoacidosis.
Hyperosmolar hyperglycaemia: Treatment
IV fluids, e.g. normal to 1⁄2 normal saline, given slowly
Insulin—relatively lower doses than acidosis
Lactic acidosis: Clinical features
Marked hyperventilation ‘air hunger’ and confusion.
Must be considered in the very ill person taking metformin, especially if kidney function is impaired.
High mortality rate.
Lactic acidosis: Investigations
blood acidosis (low pH)
low bicarbonate
high serum lactate
absent serum ketones
large anion gap
Lactic acidosis: Treatment
Removal of the cause
Rehydration
Alkalinisation with IV sodium bicarbonate.
Other diabetes complicactions
- Erectile dysfunction
Treatment: Appropriate counselling and (if not taking nitrates) one of the phosphodiesterase inhibitors (Sildenafil), starting with a low dose - Reduced vaginal lubrication with arousal. Tratmement: Lubricants
- Postural hypotension
The usual strict blood pressure targets may need to be relaxed, particularly in the elderly.
Treatment: Graduated compression stockings & Fludrocortisone. - Gastroparesis
Treatment options include medication with domperidone, cisapride or erythromycin.
Injections of botulinum toxin type A into the pylorus via gastroscopy.
Practice tips DM
Hyperglycaemia is a common cause of tiredness. If elderly people with type 2 diabetes are very tired, think of hyperglycaemia and consider giving insulin to improve their symptoms.
If a person with diabetes (particularly type 1) is very drowsy and looks sick, consider first the diagnosis of ketoacidosis.
Treat associated hypertension with ACE inhibitors or a calcium-channel blocker (also good in combination).
‘Never let the sun go down on pus in a diabetic foot’—admit to hospital.
If a foot ulcer hasn’t healed in 6 weeks, exclude osteomyelitis. Arrange for an MRI and investigate the vasculature (Dolppler).
ABC of diabetes care
A: HbA1c <7%
B: BP <140/90
C: Cholesterol <4 mmol/L
Smoking Quit
Hypoglycaemia
Blood glucose falling below 4.0 mmol/L, although symptoms usually start at <3.5 and become serious at <3.0
Treatment:
In alert patients able to swallow
Give refined carbohydrate orally
Repeat BGL every 15 minutes. If <4, repeat above. If >4, give complex carbohydrate snack or meal (minimum 15 g, e.g. tub of yoghurt, slice of bread, piece of fruit)
Reduced conscious state or unconscious
30 mL 50% glucose slow IV push (instil rectally using the nozzle of the syringe if IV access difficult).
Usually 10 mL in children.
or
1 mL (= 1 ampoule) glucagon IM or SC (0.5 mL in child <25 kg)
Hormone changes during a critical illness?
Increase cortisol, decrease in TSH
Muscle weakness and proximal myopathy (shoulder pain)
Hyperthyroidism
absence of headache + anxiety + palpitation + diaphoresis
Hyperthyroidism
Sinus tachycardia + shortening of the PR interval on ECG
Hyperthyroidism
AF on ECG
Hyperthyroidism
Common symptoms among both hyperthyroidism and hypothyroidism
Decreased libido
Psychosis
Hyperthyroidism/Hypothyroidism initial follow up
6-8 weeks
Hyperthyroidism/Hypothyroidism dose adjustment follow up
4-6 weeks
subnormal TSH + normal T3 and T4
Subclinical hyperthyroidism (Graves)
auto-antibodies is 90% specific to the diagnosis of Graves disease
Anti-TSH receptor antibodies
↑TSH + ↓T3 and T4
Hypothyroidism
↑TSH + normal T3 and T4
Subclinical hypothyroidism
Subclinical hypothyroidism
2 thyroid function tests between 12 weeks to confirm diagnosis
↑TSH + ↓T4
autoimmune chronic lymphocytic thyroiditis
(Hashimoto’s)
most common cause of multinodular goitre
Hashimoto’s
unilateral neck swelling without any symptoms
Multinodular goitre
Thyroid goitre causes
Hashimoto thyroiditis
- Graves’ disease
- Familial or sporadic multinodular goitre
- Iodine deficiency
- Follicular adenoma
- Colloid nodule or cyst
- Thyroid cancer
Thyroid goitre features
- ↑ TSH
Thyroid goitre surgical indications
- Pemberton sign (Puffiness of face on raising arms above the shoulder)
- fail to respond to medical therapy
Thyroid nodule disease Investigaton approach
- thorough clinical evaluation,
- TFT
- an US of thyroid gland and FNAC
biopsy if nodule > 1 cm
Thyrotoxicosis causes
- Graves 70%
- Toxic multinodular goitre 15%
- Toxic adenoma 5%
- Thyroiditis 5%
Thyrotoxicosis symptoms
Weight loss (weight gain in 10%)
- Heat intolerance
- Palpitations
- Breathlessness
- irritability/insomnia
- Tiredness/lethargy
- Diarrhoea
- fine tremor
- sweating, tachycardia
- alopecia
- pretibial myxoedema
- wide pulse pressure
- eye changes
Glucagon-like-peptide receptors agonists
– Stimulate glucose-mediated insulin secretion
– Suppress glucagon secretion
– Delay gastric emptying
– Decreased appetite
Treatment depends on Ca 2+
Rehydration
Bisphophonate
Calcitonin
Steroid
common causes of hypercalcemia
Primary hyperparathyroidism and malignancy ( not Secondary)
- Sarcoidosis/Tb
– Malignancies like lymphoma, leukaemia. – Hyperthyroidism.
– Vitamin D overdose.
- Men
- Lithium therapy
rare causes of hypercalcemia
- familial benign hypercalceriuc Hypercalcaemia ( low 24 h urinary calcium excretion)
- SCC lung ( ectopicproduction of PTHrP)
- Thyrotoxicosis( Osteoclast high)
- Sarcoidosis
Primary hyperparathyroidism should undergo parathyroidectomy
- age < 50 years
- markedly elevated urine calcium excretion
- kidney stones on radiography
- decreased creatinine clearance,
- markedly elevated calcium or one episode of life-threatening hypercalcemia,
- substantially decreased bone mass
hypercalcemia in malignancy
- symptomatic for hypercalcaemia (Fatigue.
Bone pain.
Headaches.
Nausea and vomiting.
Constipation etc) - usually higher calcium concentrations
hypercalcemia in primary hyperparathyroidism
- undetectable or very low PTH
MEN Syndrome 1
- Pituitary adenoma
- Parathyroid hyperplasia
- Pancreatic tumours
MEN Syndrome 2A
- Parathyroid hyperplasia
- Pheochromocytoma
- Medullary thyroid carcinoma
MEN Syndrome 2B
- Mucosal neuromas
- Marfanoid body habitus
- Medullary thyroid carcinoma
- Pheochromocytoma
headache + palpitation + diaphoresis + elevated serum metanephrines
Pheochromocytoma
Pheochromocytoma
-
episodes
-Anxiety like (ddx) - adrenal gland tumour
- sympathetic stimulation
- hypertension
- ↑ serum epinephrine/metanephrine
- hypercalcaemia
- hyperglycaemia
- erythrocytosis
physiological gynecomastia
- Neonatal gynecomastia= resolves by 1 year of life
- pubertal = at 10years age , peak btwn 13-14yrs, disapperas by 17yrs of age
- Adults btwn 50-80yrs age
Pathologic causes of gynecomastia
Rule out:
- Steroid abuse
- Hypogonadism
- Chronic liver or renal disease
- Hyperthyroidism
- Testicular and adrenal tumours
- malnutrition
- Hyperprolactaemia
25% cases are idiopathic gynecomastia
Persistent pubertal gynecomastia
- present beyond 17yrs of age
- not resolving after 2 years
Drugs causing gynecomastia
Methyldopa
Flutamide, Finasteride
Ketoconazole
Digoxin
Isoniazid
**Spironolactone*
Cimetidine, cyproterene acetate
Omeprazole, Oestrogen
Anabolic steroids
B/L parotid enlargement + gynecomastia+ alcohol intake
suspect alcoholic liver disease
Asymptomatic Pubertal gynecomastia
Dont require evaluation
follow up in 6months
Gynecomastia >5cm
Macromastia
Gynecomastia for futher evaluation
- Macromastia
- Tender, recent onset, progressive/ unknown malignancy
- concerned Ca testis or non breast malignancies
-lump irregular, stony hard, fixed, wt loss, loss appetite, nipple chages
4 features of gynecomastia
symmetrical shape, tender on palpation, central, B/L
H/o Non proliferative breast lesions in a female (FIbrocystic diseases)
No risk of Ca breast
Foot ulcers
Peripheral neuropathy
Pph vascular disease
Infections
diabetic foot ulcers step-wise approach
1-Debridement
2-Wound swabs
3- Antibiotics
4- Imaging (X-ray for osteomyelitis)
Foot ulcers treatment
uninfected: daily wet dressing, no abs required
Mild infection:
-Oral Amoxicillin + clavulanate
- Cephalexin + metronidazole (penicillin
allergy)
- Ciprofloxacin + clindamycin or lincomycin
Moderate:
- dicloxacillin/flucloxacillin
- + Metronidazole if discharge odorous
Severe:
- Piperacillin + Tazobactam
- Ticarcillin + clavulanate or (if penicillin allergic)
- Ciprofloxacin + either clindamycin or lincomycin
Autonomic diabetic neuropathy
Dry skin
bright lights sensitivity
urine incontinence
constipation
diarrhea
Erectile dysfunction
Orthostatic hypotension, tachy, brady
fainting
Personal history of benign thyroid diseases
increased Risk of thyroid cancer
Family risk history of benign thyroid diseases
No Risk of thyroid cancer
Pt on adequate doses of bisphosphonates + 2 minimal trauma #
change drug
- Teriparatide
BMD T-score <-1.5 + minimal risk fractures
osteoporosis
T-scores between -1 to -2.5
osteopenia
AT score of -1
normal
Osteoporosis treatment
- Alendronate, risedronate and zoledronic acid: first-line therapy in **postmenopausal osteoporosis **
and prevent vertebral, Non-vertebral and hip fractures. - bisphosphonates: primary prevention of fractures in px who never had minimal trauma fracture, secondary prevention of fractures
- Strontium ranelate: primary prevention of osteoporosis in women
- bisphosphonates and raloxifene: secondary prevention of fractures in women who have had minimal trauma fractures
- Strontium ranelate for severe osteoporosis or those with minimal trauma fractures while on adequate dose of bisphosphonates.
Osteoporosis treatment not going to plan, what to do
- BMD T-score of =<-2.5
- > 1 symptomatic new
fracture after at least 12-months of
continuous therapy - > 2 minimal trauma fractures despite being on sufficient doses of bisphosphonates.
switch to teriparatide for 18 months
Males fracture post-op management
- routine biochemical tests for renal or hepatic disease, a full blood count (FBC), serum testosterone,
calcium, alkaline phosphatase, 25-
hydroxyvitamin D, and 24-hour urine cortisol. - Supplement deficiency related to above results
most common cause of pathologic fractures
Osteoporosis
- start bisphosphonates
hip fracture surgery are in the highest risk for
venous thromboembolism (VTE)
Anticoagulation for post-surgery
1st line: LMWH 12 hours after the surgery up to 35 days
- Warfarin id px desires
persistent hypotension + hyperpigmentation + hyponatremia + hyperkalaemia
Aldosterone/adrenal insufficiency (Addison’s)
Aldosterone/adrenal insufficiency management
Known dx: parenteral administration of corticosteroids (Hydrocortisone)
Previous dx:
dexamethasone
Weight gain + menstrual irregularities + Hypertension + Hyperglycaemia + Proximal muscle weakness
Cushing syndrome
Cushing syndrome causes
exogenous steroids (rheumatic diseases, SLE, RA)
Cushing syndrome investigation
24-hour urine cortisol level
Cushing syndrome treatment
surgery
thyroidectomy consequence
hypocalcaemia
Prolactin < 5000 mU/L
Hyperprolactinemia due to antipsychotic (risperidone)
Prolactin > 5000 mU/L
Prolactinoma
tall stature + small testes + small penis + gynecomastia + decreased facial and axillary hair growth + decreased libido
Klinefelter syndrome (chromosome 47 XXY
abnormality)
Klinefelter syndrome complications
-Breast tumours.
-Thromboembolic disease.
-Obesity.
-Type II diabetes mellitus.
-Varicose veins
-Learning disabilities
most common cause of the pubertal delay
constitutional delay of growth and
puberty (CDGP).
Severe hypertension resistant to 3 antihypertensive drugs + Hypokalaemia + Adrenal mass/A family history of early onset hypertension or cerebrovascular events less than 40 years
Primary aldosteronism (Conn’s)
Primary aldosteronism (Conn’s) investigation
aldosterone-renin ratio
How to differentiate Conn’s from RAS
CHECK Renin
Conn’s: low
RAS: high
Unilateral RAS treatment
ACEi
Bilateral RAS treatment
Ca Blocker
Adult + frontal bossing + increased hand and foot size + mandibular
enlargement + widened space between the lower incisor teeth +
characteristic coarse facial features, + large fleshy nose
acromegaly
acromegaly investigation
Insulin-like growth factor supressed
Perform OGTT
SLE screening
ANA
SLE confirmation
dsDNA
Endocrinal drugs that are teratogenic
1st sem:
- carbimazole
- methimazole
*switch to PTU
2nd sem:
- propylthiouracil
*switch to carbimazole
Post op fever on 1st day
Pulmonary atelectasis
Post op hyponatremia
SIADH
thyroid tumours are most commonly associated with
autoimmune thyroiditis?
Thyroid lymphoma
Pituitary disorders
- Pituitary tumor
- Hyperprolactaemia
- Acromegaly
- Diabetes insipidus and SIADH
- Hypopituitarism
Pituitary Adenomas - Presentation
- Benign adenomas (Prolactinoma- most common)
- Hormon deficiency
- Hypersecretory Syndromes (Prolactin, GH, ACTH)
- Local tumor mass symptoms (headache, visual field loss, raised ICP)
Pituitary Adenomas - Microadenoma (< 1cm)
- Review (MRI)
Pituitary Adenomas - Macroadenoma (> 1cm)
- without symptoms
review: MRI - +neurological Symptoms or visual field defects
Neurosurgery ( transphenoidal), Radiation, Hormonal Replacement
Hyperprolactaemia - Cause
- Pituitary adenoma (micro/macro)
- Pituitary stalk damage
(1. compressing- Mass/Tumor- Infitration - Sarcoidosis
- Stalk section - Head injury, surgery)
- Drugs (antipsychotics, antidepressant, Metoclorpamide, cimetidine, oestrogen, opiats, Marijuana)
Pysiological (pregnancy/breastfeeding)
Hyperprolacataemia - Presentation
- general: headache, bitemporal hemianopia, reduced libido
- Female : galactorrhoe, amenorrhoe/oligomenorrhoe
- Male: hypogonadism, reduced facial hair, erectile dysfunction
Hyperprolacataemia- Investigation
- Prolactin level
norm <400 mU/L
Prolactinoma >5000 mU/L
DD think of other cause < 5000mU/L
- MRI (best investigation)
Hyperprolacataemia- Management & complication
- Dopamin agonist (Bromocriptin, Cabergoline)
- Surgery (transphenoidal)
- Complication of Surgery DI or Hypopituitarism
Acromegaly - Association
- Diabetes
- Sleep apnoe
- Carpal tunnel syndrome
- Arthritis
- Increased risk for colon cancer
- Hypertrophic cardiomyopathy
Acromegaly - Presentation
- thickened sof tissue (plams,foot)
- sweating, frontal blossing, thick greasy skin
- large bones, deep voice
- Hypertension
- Osteoarthritis
Nehlson Syndrom
development of an ACTH-producing pituitary tumour after the surgical removal of both adrenal glands due to a lack of cortisol and negative feedback.
- skin pigmentation (high ACTH)
- bitemporal hemianopia
- lack of other pituitary hormones
Acromegaly test
IGF 1
Best oral glucose tolerance test (OGTT) with serial GH
gynaecomastia
myxedoma Coma
- High mortality
- Emergency
- decreased mental status
- hypothermia
- slowing down functions
myxedoma Coma cause
- severe longstanding Hypotension
infection
myocardial infarction
cold exposure
sedetative drugs (opioids)
myxedoma Coma treatment
t4 intravenous
corticosteroid
supportive care
oral T4 if stable
NG tube
