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)
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
What endocrine condition?
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
How many tests
2 thyroid function tests between 12 weeks to confirm diagnosis
↑TSH + ↓T4
What disease?
autoimmune chronic lymphocytic thyroiditis
(Hashimoto’s)
most common cause of multinodular goitre
Hashimoto’s
Multinodular goiter is a condition where the thyroid gland becomes enlarged and develops multiple growths or nodules. Hashimoto’s thyroiditis is one of the most common causes of multinodular goiter. Here’s why, explained simply:
-
Hashimoto’s Thyroiditis:
- In Hashimoto’s thyroiditis, the body’s immune system mistakenly attacks the thyroid gland.
- Over time, this inflammation can lead to thyroid enlargement, resulting in a goiter.
- As the thyroid tries to compensate for the damage, it may develop multiple nodules, causing the gland to become multinodular.
In summary, Hashimoto’s thyroiditis can lead to multinodular goiter because the immune system attack causes inflammation and enlargement of the thyroid gland, resulting in the formation of multiple nodules.
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
GTTT
- 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
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are medications used to treat type 2 diabetes and sometimes obesity. Here’s a simple explanation:
GLP-1 RAs mimic a natural hormone in your body called GLP-1. This hormone helps manage your blood sugar and appetite in several ways:
1. Increase Insulin: They help your pancreas release more insulin when your blood sugar is high, which lowers your blood sugar.
2. Reduce Glucagon: They lower the amount of glucagon, a hormone that raises blood sugar.
3. Slow Digestion: They slow down how quickly food leaves your stomach, which helps prevent blood sugar spikes after meals.
4. Reduce Appetite: They make you feel full, so you eat less and may lose weight.
Some examples of GLP-1 RAs include:
- Exenatide (Byetta, Bydureon): Injected either twice daily or once weekly.
- Liraglutide (Victoza, Saxenda): Injected once daily, with Saxenda also used for weight loss.
- Dulaglutide (Trulicity): Injected once weekly.
- Semaglutide (Ozempic, Rybelsus, Wegovy): Injected once weekly (Ozempic, Wegovy) or taken as a daily pill (Rybelsus).
- Lower Blood Sugar: They help keep your blood sugar levels in check.
- Weight Loss: They can help you lose weight, which is good for overall health.
- Heart Health: Some GLP-1 RAs also reduce the risk of heart problems in people with diabetes.
- Nausea: This is common, especially at first.
- Stomach Issues: You might experience vomiting, diarrhea, or constipation.
- Injection Site Reactions: If you’re using an injectable form, the injection site might get sore.
GLP-1 RAs are usually prescribed for people with type 2 diabetes, especially if other medications haven’t worked well enough. They can also be used for weight loss in some cases.
In summary, GLP-1 RAs help manage diabetes by improving blood sugar control and promoting weight loss, with additional benefits for heart health.
common causes of hypercalcemia
Primary hyperparathyroidism and malignancy
- 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
Hyperparathyroidism is a condition characterized by excessive production of parathyroid hormone (PTH) by the parathyroid glands. There are four parathyroid glands located in the neck behind the thyroid gland. These glands regulate calcium levels in the blood through the release of PTH, which increases blood calcium by stimulating the release of calcium from bones, absorption of calcium in the intestines, and reabsorption of calcium in the kidneys.
Hyperparathyroidism can be classified into three main types:
- Primary Hyperparathyroidism: This occurs when one or more of the parathyroid glands become overactive, often due to a benign tumor (adenoma), hyperplasia (increase in the number of cells), or rarely, cancer. This results in elevated PTH levels and hypercalcemia (high blood calcium levels).
- Secondary Hyperparathyroidism: This is a result of another condition causing low calcium levels, such as chronic kidney disease or vitamin D deficiency. The parathyroid glands become overactive in response to low calcium levels, producing more PTH in an attempt to normalize calcium levels.
- Tertiary Hyperparathyroidism: This occurs when secondary hyperparathyroidism becomes prolonged, and the parathyroid glands become irreversibly overactive, continuing to secrete excessive PTH even after the initial cause of low calcium levels is resolved.
Symptoms of hyperparathyroidism can include:
- Bone pain and fragility
- Kidney stones
- Excessive urination
- Abdominal pain
- Fatigue
- Depression or anxiety
- Muscle weakness
Diagnosis typically involves blood tests to measure calcium and PTH levels, and imaging studies to evaluate the parathyroid glands. Treatment options depend on the type and severity of the condition and may include surgical removal of the overactive glands, medications to manage symptoms, or addressing the underlying cause in secondary hyperparathyroidism.
Klinefelter syndrome complications
-Breast tumours.
-Thromboembolic disease.
-Obesity.
-Type II diabetes mellitus.
-Varicose veins
-Learning disabilities
