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.
hypercalcemia in malignancy
- symptomatic for hypercalcaemia (Fatigue.
Bone pain.
Headaches.
Nausea and vomiting.
Constipation etc) - usually higher calcium concentrations
hypercalcemia in primary hyperparathyroidism
PTH level
- undetectable or very low PTH
In primary hyperparathyroidism, hypercalcemia (high blood calcium levels) is usually caused by an overproduction of parathyroid hormone (PTH). However, if you have hypercalcemia with undetectable or very low PTH, it suggests a different cause for the high calcium levels.
In simple terms, here’s why this can happen:
- PTH-independent Hypercalcemia: When PTH levels are low or undetectable, it means the parathyroid glands are not the ones causing the high calcium. Instead, the high calcium is due to another condition.
-
Possible Causes:
- Cancer: Certain cancers can produce substances similar to PTH, called PTH-related protein (PTHrP), which can increase calcium levels without involving the parathyroid glands.
- Vitamin D Overdose: Excessive vitamin D can increase calcium absorption from the gut.
- Medications: Some medications, like thiazide diuretics, can increase blood calcium levels.
- Other Medical Conditions: Conditions like sarcoidosis or tuberculosis can cause increased calcium levels due to increased production of vitamin D by the immune system.
So, if your PTH is very low or undetectable, it means that something other than your parathyroid glands is causing your hypercalcemia.
MEN Syndrome 1
- Pituitary adenoma
- Parathyroid hyperplasia
- Pancreatic tumours
Multiple Endocrine Neoplasia type 1 (MEN 1) is a hereditary disorder that leads to the development of tumors in multiple endocrine glands. The condition is caused by mutations in the MEN1 gene, which provides instructions for producing a protein called menin that acts as a tumor suppressor.
MEN 1 is characterized by the following key features:
- Parathyroid Tumors: These tumors occur in nearly all individuals with MEN 1 and lead to primary hyperparathyroidism. This results in elevated levels of parathyroid hormone (PTH) and hypercalcemia (high blood calcium levels), which can cause symptoms like kidney stones, bone pain, fatigue, and muscle weakness.
-
Pancreatic Neuroendocrine Tumors (NETs): These tumors can develop in the pancreas and other parts of the gastrointestinal tract. They may produce hormones such as gastrin, insulin, glucagon, and vasoactive intestinal peptide (VIP), leading to various symptoms depending on the hormone involved:
- Gastrinomas: These produce excessive gastrin, leading to Zollinger-Ellison syndrome with peptic ulcers and diarrhea.
- Insulinomas: These produce excessive insulin, causing hypoglycemia.
- Glucagonomas: These produce excessive glucagon, leading to diabetes and skin rash.
- VIPomas: These produce excessive VIP, leading to severe diarrhea and electrolyte imbalance.
- Pituitary Tumors: These can produce excess hormones such as prolactin, growth hormone, or ACTH, leading to conditions like prolactinomas (with symptoms like galactorrhea and menstrual irregularities), acromegaly (with enlarged features and hands/feet), and Cushing’s disease (with symptoms like weight gain and hypertension).
Diagnosis:
- Family history and genetic testing for mutations in the MEN1 gene.
- Blood tests to measure hormone levels.
- Imaging studies (e.g., MRI, CT scans) to identify tumors.
Treatment:
- Regular monitoring and management of hormone levels.
- Surgical removal of tumors when necessary.
- Medications to control hormone production or address symptoms caused by excess hormones.
Individuals with MEN 1 require lifelong surveillance and management to address the various endocrine tumors and their associated symptoms.
MEN Syndrome 2A
- Parathyroid hyperplasia
- Pheochromocytoma
- Medullary thyroid carcinoma
Multiple Endocrine Neoplasia type 2A (MEN 2A) is a hereditary disorder that predisposes individuals to develop tumors in multiple endocrine glands. It is caused by mutations in the RET proto-oncogene, which plays a crucial role in cell growth and differentiation.
MEN 2A is characterized by three main types of tumors:
-
Medullary Thyroid Carcinoma (MTC):
- This is a common and often early manifestation of MEN 2A.
- MTC arises from the parafollicular C cells of the thyroid and produces calcitonin, a hormone involved in calcium regulation.
- Early detection and surgical removal of the thyroid gland are critical to prevent metastatic spread.
-
Pheochromocytoma:
- These are tumors of the adrenal medulla that produce excess catecholamines (epinephrine and norepinephrine).
- Symptoms can include high blood pressure, headaches, sweating, palpitations, and anxiety.
- Pheochromocytomas can be bilateral (affecting both adrenal glands) and may require surgical removal.
-
Parathyroid Hyperplasia:
- This involves an overgrowth of the parathyroid glands, leading to primary hyperparathyroidism.
- Symptoms are similar to those seen in primary hyperparathyroidism, including hypercalcemia, kidney stones, bone pain, and fatigue.
- Surgical removal of the affected parathyroid glands can be necessary to control symptoms.
- Genetic Testing: Identification of mutations in the RET gene confirms the diagnosis.
- Biochemical Tests: Measurement of serum calcitonin, catecholamines, and calcium levels.
- Imaging Studies: Ultrasound, CT, MRI, or nuclear scans to identify tumors.
- Prophylactic Thyroidectomy: For individuals with known RET mutations, early thyroidectomy is recommended to prevent MTC.
- Regular Monitoring: Lifelong surveillance for the development of pheochromocytoma and parathyroid hyperplasia.
- Surgical Intervention: Removal of pheochromocytomas and hyperplastic parathyroid glands as needed.
- Medications: Drugs to manage high blood pressure and other symptoms associated with pheochromocytoma.
- MEN 2A is inherited in an autosomal dominant pattern, meaning a 50% chance of passing the mutation to offspring.
- Genetic counseling and testing for at-risk family members are important for early diagnosis and management.
Individuals with MEN 2A require ongoing medical care to monitor for and manage the various
MEN Syndrome 2B
- Mucosal neuromas
- Marfanoid body habitus
- Medullary thyroid carcinoma
- Pheochromocytoma
M
Multiple Endocrine Neoplasia type 2B (MEN 2B) is a rare genetic disorder that leads to the development of tumors in multiple endocrine glands and other parts of the body. Like MEN 2A, it is caused by mutations in the RET proto-oncogene.
MEN 2B is characterized by the following:
-
Medullary Thyroid Carcinoma (MTC):
- MTC is often aggressive in MEN 2B and can develop at a young age.
- It arises from the parafollicular C cells of the thyroid, which produce calcitonin.
- Early thyroidectomy is recommended to prevent metastatic spread.
-
Pheochromocytoma:
- Tumors of the adrenal medulla that produce excess catecholamines (epinephrine and norepinephrine).
- Symptoms include high blood pressure, headaches, sweating, palpitations, and anxiety.
- They can be bilateral and may require surgical removal.
-
Mucosal Neuromas:
- These are benign growths on the mucous membranes, often found on the lips, tongue, and lining of the mouth.
- They can cause a characteristic appearance with swollen lips and a “blubbery” aspect to the mouth.
-
Marfanoid Habitus:
- Many individuals with MEN 2B have a Marfan-like appearance, including a tall, thin body with long limbs and fingers.
- This physical trait is called Marfanoid habitus.
-
Gastrointestinal Issues:
- Intestinal ganglioneuromatosis can cause issues like constipation, diarrhea, and abdominal pain.
- Genetic Testing: Identifying mutations in the RET gene confirms the diagnosis.
- Biochemical Tests: Measuring serum calcitonin, catecholamines, and calcium levels.
- Imaging Studies: Ultrasound, CT, MRI, or nuclear scans to identify tumors.
- Prophylactic Thyroidectomy: Early removal of the thyroid gland is crucial, often in infancy or early childhood, to prevent MTC.
- Regular Monitoring: Lifelong surveillance for the development of pheochromocytoma and gastrointestinal issues.
- Surgical Intervention: Removal of pheochromocytomas and management of any gastrointestinal complications as needed.
- Medications: Drugs to manage high blood pressure and other symptoms associated with pheochromocytoma.
- MEN 2B is inherited in an autosomal dominant pattern, meaning a 50% chance of passing the mutation to offspring.
- Genetic counseling and testing for at-risk family members are important for early diagnosis and management.
Individuals with MEN 2B require ongoing medical care to monitor for and manage the various endocrine and non-endocrine manifestations associated with the syndrome. Early intervention and regular follow-up can significantly improve outcomes and quality of life.
headache + palpitation + diaphoresis + elevated serum metanephrines
Pheochromocytoma
Pheochromocytoma
-
episodes
-Anxiety like (ddx) - adrenal gland tumour
- sympathetic stimulation
- hypertension
- ↑ serum epinephrine/metanephrine
- hypercalcaemia
- hyperglycaemia
- erythrocytosis
Pheochromocytoma is a rare type of tumor that forms in the adrenal glands, which are located on top of your kidneys. These tumors produce excessive amounts of adrenaline and noradrenaline, hormones that control your body’s fight-or-flight response.
-
What It Is:
- A tumor in the adrenal glands.
- Produces too much adrenaline and noradrenaline.
-
Symptoms:
- High blood pressure (often severe and sudden).
- Headaches.
- Sweating a lot.
- Rapid or irregular heartbeat (palpitations).
- Tremors.
- Feelings of anxiety or panic attacks.
- Pale skin.
-
Diagnosis:
- Blood and Urine Tests: Check for high levels of adrenaline and noradrenaline.
- Imaging: CT scans, MRI, or MIBG scintigraphy to locate the tumor.
-
Treatment:
- Surgery: Remove the tumor. This is the main treatment.
- Medications: Manage blood pressure and symptoms before surgery.
-
Important to Know:
- It’s a rare but serious condition.
- If untreated, it can lead to severe complications like heart problems or stroke.
- It can occur at any age but is most common in people between 30 and 50.
- Often the cause is unknown.
- Sometimes it is linked to genetic conditions like Multiple Endocrine Neoplasia (MEN) or von Hippel-Lindau disease.
- With proper treatment, most people recover well.
- Regular follow-up is necessary to monitor for recurrence.
In summary, pheochromocytoma is a rare adrenal gland tumor that causes high levels of stress hormones, leading to symptoms like high blood pressure and palpitations. Diagnosis involves blood tests and imaging, and treatment typically involves surgery.
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
After how many years not resolving?
Cut off point
- 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
A common mnemonic used to remember drugs that can cause steroid-like side effects is “MFFD SPOCA.” Here’s how it breaks down:
Methyldopa
Flutamide, Finasteride
Ketoconazole
Digoxin
Isoniazid
Spironolactone
Pimetidine, Pyproterone acetate
Omeprazole, Oestrogen
Corticosteroids
Anabolic steroids
This mnemonic can help recall these drugs when studying or when encountering patients who may be experiencing steroid-like side effects due to medication use.
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.
Sure, here is the breakdown in simpler terms:
-
Alendronate, Risedronate, and Zoledronic Acid:
- These medications are first-choice treatments for postmenopausal women with osteoporosis.
- They help prevent fractures in the spine, other bones (non-vertebral), and hips.
-
Bisphosphonates:
- These drugs can be used to prevent fractures in two scenarios:
- Primary prevention: For people who have never had a fracture from a minor injury.
- Secondary prevention: For people who have already had a fracture and need to prevent further ones.
- These drugs can be used to prevent fractures in two scenarios:
-
Strontium Ranelate:
- This is used for the primary prevention of osteoporosis in women, meaning it helps prevent the condition before it starts.
-
Bisphosphonates and Raloxifene:
- These medications are used for secondary prevention of fractures, meaning they are given to women who have already had fractures from minor injuries to prevent more fractures.
-
Strontium Ranelate for Severe Osteoporosis:
- This is prescribed for severe osteoporosis or for people who continue to have fractures from minor injuries even while taking the right dose of bisphosphonates.
Osteoporosis treatment not going to plan, what to do
Switch from biphosphonate - when ( 2 occasions)
- 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
Afterwards
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 occurs when there is too much cortisol, a hormone produced by the adrenal glands, in the body. One of the most common causes is taking exogenous steroids (steroids that are given as medication) over a long period. Here’s a simple explanation:
-
What Are Exogenous Steroids?
- Exogenous steroids are medications like prednisone, used to treat inflammatory and autoimmune conditions such as rheumatic diseases, systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA). These steroids help reduce inflammation and suppress the immune system.
-
How They Cause Cushing Syndrome:
- When you take these steroids for a long time, they can mimic the effects of cortisol, leading to an excess of this hormone in the body.
- Your body’s natural cortisol production decreases because the medication provides all that your body needs and more. Over time, the high levels of steroids cause the symptoms of Cushing syndrome.
-
Symptoms of Cushing Syndrome:
- Weight Gain: Especially around the face, neck, and abdomen.
- Round Face: Often called “moon face” due to fat accumulation.
- Buffalo Hump: A fatty hump between the shoulders.
- Thin Skin and Easy Bruising: Because of the effects on collagen.
- High Blood Pressure: Cortisol increases blood pressure.
- Muscle Weakness: Due to the breakdown of muscle tissue.
Taking exogenous steroids for conditions like rheumatic diseases, SLE, and RA can lead to Cushing syndrome because these medications increase cortisol levels in your body. Over time, the high levels of steroids cause symptoms like weight gain, a round face, and muscle weakness.
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, also known as Conn’s syndrome, is a condition where the adrenal glands produce too much aldosterone, a hormone that helps regulate blood pressure by controlling the balance of sodium and potassium in the blood. Here’s a straightforward explanation:
-
Cause:
- The adrenal glands, located above the kidneys, produce excessive amounts of aldosterone.
- This overproduction can be due to a benign tumor (aldosterone-producing adenoma) or hyperplasia (overactivity) of the adrenal glands.
-
Effects:
- Increased Sodium Retention: Aldosterone causes the kidneys to retain sodium, leading to increased water retention and higher blood pressure.
- Potassium Loss: It also causes the kidneys to excrete more potassium, which can lead to low potassium levels in the blood (hypokalemia).
-
Symptoms:
- High blood pressure (often resistant to treatment).
- Muscle weakness or cramps (due to low potassium).
- Fatigue.
- Headaches.
- Increased thirst and urination.
-
Diagnosis:
- Blood Tests: To measure levels of aldosterone and renin (another hormone involved in blood pressure regulation).
- Imaging: CT scans or MRIs to detect adrenal gland abnormalities.
- Aldosterone-Renin Ratio (ARR): A high ratio suggests primary aldosteronism.
-
Treatment:
- Surgery: Removal of the adrenal gland if a tumor is present (adrenalectomy).
- Medications: If surgery is not an option or if both adrenal glands are affected, medications like aldosterone antagonists (e.g., spironolactone or eplerenone) can block the effects of aldosterone.
- Lifestyle Changes: Low-sodium diet and other lifestyle modifications to manage blood pressure.
Treating primary aldosteronism is crucial because uncontrolled high blood pressure can lead to serious complications such as heart disease, stroke, and kidney damage. Additionally, correcting potassium levels can prevent muscle and heart problems associated with hypokalemia.
In summary, primary aldosteronism (Conn’s syndrome) is a condition where the adrenal glands produce too much aldosterone, leading to high blood pressure and low potassium levels. It can be treated with surgery or medications, and effective management is essential to prevent complications.
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
SLE screening
ANA
SLE confirmation
dsDNA
Endocrinal drugs that are teratogenic
1st sem:
- carbimazole
- methimazole
*switch to PTU
2nd sem:
- propylthiouracil
*switch to carbimazole
acromegaly investigation
Insulin-like growth factor supressed
Perform OGTT
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 of the surgery
- Dopamin agonist (Bromocriptin, Cabergoline)
- Surgery (transphenoidal)
- Complication of Surgery DI or Hypopituitarism
Dopamine agonists, such as bromocriptine and cabergoline, are medications that mimic the action of dopamine by stimulating dopamine receptors. They are commonly used to treat conditions where there is a deficiency of dopamine or where modulation of dopamine activity is beneficial. Here’s what they do:
-
Prolactin-Secreting Pituitary Adenomas (Prolactinomas):
- Mechanism: Bromocriptine and cabergoline bind to dopamine D2 receptors on pituitary lactotroph cells, inhibiting the secretion of prolactin.
- Effect: Reduction in prolactin levels, leading to the shrinkage of prolactinomas and relief from symptoms such as galactorrhea (milk production), amenorrhea (absence of menstrual periods), and infertility.
-
Parkinson’s Disease:
- Mechanism: These drugs stimulate dopamine receptors in the brain, compensating for the decreased dopamine levels seen in Parkinson’s disease.
- Effect: Improvement in motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and overall mobility.
-
Acromegaly:
- Mechanism: Dopamine agonists can reduce the secretion of growth hormone in patients with acromegaly, especially in those who have concomitant prolactin secretion.
- Effect: Lowering of growth hormone levels, leading to improvement in symptoms and reduction of complications associated with excessive growth hormone.
-
Restless Legs Syndrome (RLS):
- Mechanism: By stimulating dopamine receptors, these drugs can alleviate the uncomfortable sensations in the legs that lead to the urge to move them.
- Effect: Reduction in the frequency and severity of RLS symptoms, improving sleep and quality of life.
-
Bromocriptine:
- Has a shorter half-life, often requiring more frequent dosing.
- Used in the treatment of Parkinson’s disease, hyperprolactinemia, acromegaly, and type 2 diabetes (to improve glycemic control).
-
Cabergoline:
- Has a longer half-life, allowing for less frequent dosing (often once or twice a week).
- Preferred for hyperprolactinemia due to better tolerance and effectiveness in reducing prolactin levels with fewer side effects.
- Prolactinomas: Dopamine agonists are preferred over surgery and radiotherapy for initial treatment due to their effectiveness in shrinking tumors and normalizing prolactin levels with relatively fewer risks.
- Parkinson’s Disease: Dopamine agonists are often used in early stages or as an adjunct to levodopa therapy to manage symptoms and reduce the “off” periods associated with levodopa treatment.
In summary, dopamine agonists like bromocriptine and cabergoline are crucial in managing conditions related to prolactin secretion, dopamine deficiency, and excessive growth hormone, offering targeted treatment with effective outcomes.
Acromegaly - Association
- Diabetes
- Sleep apnoe
- Carpal tunnel syndrome
- Arthritis
- Increased risk for colon cancer
- Hypertrophic cardiomyopathy
Acromegaly is associated with several health conditions due to the excessive production of growth hormone. Here’s why:
- Diabetes: Excess growth hormone can cause insulin resistance, leading to higher blood sugar levels and diabetes.
- Sleep Apnea: Overgrowth of tissues in the upper airway can cause obstruction, leading to sleep apnea.
- Carpal Tunnel Syndrome: Tissue overgrowth can compress the median nerve in the wrist, causing carpal tunnel syndrome.
- Arthritis: Joint cartilage can be overgrown and worn down, leading to arthritis.
- Increased Risk for Colon Cancer: Growth hormone can stimulate cell growth, increasing the risk of developing colon polyps and cancer.
- Hypertrophic Cardiomyopathy: Excessive growth hormone can cause the heart muscle to thicken, leading to hypertrophic cardiomyopathy.
Acromegaly - Presentation
- thickened sof tissue (plams,foot)
- sweating, frontal blossing, thick greasy skin
- large bones, deep voice
- Hypertension
- Osteoarthritis
Post op fever on 1st day
Pulmonary atelectasis
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.
Key Points:
-
Gold Standard Test:
- The 2-hour blood sugar test during an OGTT is the best method for diagnosing uncertain diabetes if levels are over 11.1 mmol/L.
-
When to Perform an OGTT:
- Conduct an OGTT if random or fasting VBG is between 5.5 and 11.0 mmol/L in symptomatic patients or those with risk factors (age over 50, overweight, close relative with type 2 diabetes).
- Further testing is needed if blood sugar is 5.5 mmol/L or higher.
-
Special Cases:
- Use OGTT for true borderline cases.
- Use a 75 mg OGTT to diagnose gestational diabetes between 24–28 weeks of pregnancy.
