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
