Endocrinology Flashcards
الحقني يادكتور والله مابقدر عاينته وانا عيان وممنوع من السكر
What hormones does the anterior pituitary gland release (6)
Theanterior pituitary glandreleases:
Thyroid-stimulating hormone(TSH)
Adrenocorticotropic hormone(ACTH)
Follicle-stimulating hormone(FSH) andluteinising hormone(LH)
Growth hormone(GH)
Prolactin
What hormones does the posterior pituitary gland release? (2)
Oxytocin
Antidiuretic hormone(ADH)
Explain the thyroid axis
Hypothalamus 💦 thyrotropin releasing hormone (TRH)
TRH 💥 anterior pituitary => 💦 thyroid stimulating hormone (TSH)
TSH 💥 thyroid => 💦 T3 (triiodothyronine) + T4 (thyroxine)
How does the thyroid axis self regulate
Negative feedback loop
T3 + T4 💥 hypothalamus + anterior pituitary => 🚫✋ TSH + TRH
What organ releases cortisol? How is cortisol released throughout the day?
secreted by adrenals
released in pulses and in response to stressful stimuli
peaks in early morning and lowest in late evening
Explain the adrenal axis
Hypothalamus 💦 CRH (corticotropin-releasing hormone)
CRH💥anterior pituitary => 💦ACTH (adrenocorticotropic hormone)
ACTH💥adrenal glands => 💦cortisol
How does the adrenal axis self-regulate?
Negative feedback loop
Cortisol 💥hypothalamus + anterior pituitary => 🚫✋CRH +ACTH
5 actions of cortisol within the body:
- increases alertness
- inhibits the immune system
- inhibits bone formation
- raises blood glucose
- increases metabolism
Explain the Growth Hormone Axis
Hypothalamus 💦 GHRH (growth hormone-releasing hormone)
GHRH 💥anterior pituitary => 💦 growth hormone
Growth hormone 💥 liver => 💦IGF-1 (insulin-like growth factor 1)
Name 4 functions of growth hormone:
- stimulates muscle growth
- increases bone density and strength
- stimulates cell regeneration and reproduction
- stimulates growth of internal organs
Explain the Parathyroid axis:
(low serum calcium) 💥 4 parathyroid glands 💦 PTH (parathyroid hormone)
What is the role of parathyroid hormone?
increase serum Ca concentration
How does PTH increase serum Ca levels?
- increases activity of osteoclasts in bone => reabsorption of calcium from bone into blood
- stimulates calcium reabsorption in the kidneys (less Ca excreted in urine)
- stimulates kidneys to convert Vit D3 into calcitriol (active vit D, which promotes Ca absorption from food)
How does the parathyroid axis regulate itself?
Negative feedback
When the serum calcium level is high, it suppresses the release of PTH
What is renin? Which cells/location is it released from?
Renin is an enzyme
Secreted by juxtaglomerular cells
in the afferent arterioles of the kidney
Explain the Renin-Angiotensin-Aldosterone System:
Low BP 💥 (juxtaglomerular cells) afferent arterioles in the kidney 💦 renin
Liver 💦 angiotensinogen
Angiotensinogen (+renin) => angiotensin I
(in lungs) angiotensin I + ACE (angiotensin-converting enzyme) => angiotensin II
Angiotensin II causes vasoconstriction
Angiotensin II 💥 adrenal glands 💦 aldosterone => hypertrophy of cardiac myocytes (cardiac remodelling)
Aldosterone 💥nephrons =>
- inc Na reabsorption from distal tubule (osmosis => inc intravascular volume)
- inc K secretion from distal tubule
- inc H secretion from collecting ducts
How does aldosterone work?
Aldosterone is a mineralocorticoid steroid hormone. It acts on the nephrons in the kidneys to:
- Increase sodium reabsorption from the distal tubule
- Increase potassium secretion from the distal tubule
- Increase hydrogen secretion from the collecting ducts
When sodium is reabsorbed in the kidneys, water follows it by osmosis. This leads to increased intravascular volume and, subsequently, blood pressure.
What is the difference between primary and secondary hyperthyroidism? What lab results would correspond to each?
Primary - thyroid issue, produces excess T3/T4, suppressing TSH
⬆️ T3 ⬆️T4 ⬇️TSH
Secondary - pituitary issue, produces excess TSH
⬆️T3 ⬆️T4 ⬆️TSH
What is the difference between primary and secondary hypothyroidism? What lab results would correspond to each?
Primary - thyroid issue, produces inadequate T3/T4, leads to inc TSH
⬇️T3/T4 ⬆️TSH
Secondary - pituitary problem, produces inadequate TSH, so less T3/T4
⬇️T3/T4 ⬇️TSH
Name 3 thyroid antibodies. What diseases are they present in?
Anti-TPO (anti-thyroid peroxidase antibodies) - work against the thyroid gland
:: against autoimmune thyroid diseases e.g. Grave’s, Hashimoto’s
Anti-Tg (anti-thyroglobulin antibodies) - against thyroglobulin (protein produced by thyroid)
:: Grave’s :: Hashimoto’s :: thyroid ca
TSH receptor Ab’s - mimic TSH, bind to receptor, stimulate T3/T4 release
:: Grave’s disease
What imaging can be used in investigating thyroid pathology?
USS - diagnose thyroid nodules, distinguishes cystic and solid nodules, guides biopsies of a thyroid lesion
Radioisotope scans - investigate hyperthyroidism and thyroid cancer
:: radioactive iodine given IV or PO
:: gamma camera detects gamma rays emitted by I
How to interpret radioisotope thyroid scan results?
Diffuse high uptake = Grave’s disease
Focal high uptake = toxic multinodular goitre and adenoma
“Cold” areas (low uptake) = thyroid cancer
What is subclinical hyperthyroidism?
thyroid hormones (T3 and T4) are normal and thyroid-stimulating hormone (TSH) is suppressed (low). There may be absent or mild symptoms.
What is Grave’s disease?
autoimmune condition
TSH receptor Ab’s cause 1° hyperthyroidism
most common cause of hyperthyroidism
What is toxic multinodular goitre?
nodules on thyroid
unregulated by thyroid axis
continuously produce excess thyroid hormones
most common in >50 y/o
What is exophthalmos?
aka proptosis
bulging of eyes
caused by Grave’s disease
due to inflammation, swelling and hypertrophy of tissue behind eyeballs
What is pretibial myxoedema?
skin condition caused by deposits of glycosaminoglycans on pre-tibial area
discoloured, waxy, oedematous appearance
specific to Grave’s disease
reaction to TSH receptor Ab’s
Give 4 causes of hyperthyroidism (mnemonic)
GIST
Graves
Inflammation (thyroiditis)
Solitary toxic thyroid nodule
Toxic multinodular goitre
What are some causes of thyroiditis?
Thyroiditis can cause initial hyperthyroidism followed by hypothyroidism
Caused by:
- De Quervain’s thyroiditis
- Hashimoto’s thyroiditis
- Postpartum thyroiditis
- Drug-induced thyroiditis
Signs and symptoms of hyperthyroidism. Give 4 Grave’s specific features.
Symptoms:
:: anxiety/irritability :: sweating/heat intolerance :: weight loss :: fatigue :: insomnia :: loose stool :: sexual dysfunction ::
Signs:
:: tachycardia :: weight loss :: brisk reflexes
Grave’s specific:
:: diffuse goitre (not nodular) :: Grave’s eye disease :: peritbial myxoedema :: thyroid acropachy (hand swelling, finger clubbing)
What is solitary toxic thyroid nodule?
single abnormal thyroid nodule
release excessive thyroid hormone
usually benign adenoma
Tx: surgical removal
What is De Quervain’s thyroiditis? What are the treatment options? What is the prognosis?
aka subacute thyroiditis
temporary inflammation of thyroid, self-limiting
There are typically 4 phases;
- phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
- phase 2 (1-3 weeks): euthyroid
- phase 3 (weeks - months): hypothyroidism
- phase 4: thyroid structure and function goes back to normal
Tx:
1) supportive: NSAIDs, Beta-blockers, levothyroxine
10% remain hypothyroid long-term
What is a thyroid storm? What is the management?
rare, severe, life-threatening presentation of hyperthyroidism
Presentation:
- fever
- tachycardia
- delirium
Tx:
- admit
- supportive treatment: IVI, beta-blockers
What are the pharmacological options for managing hyperthyroidism? (contraindications) Other management options?
1st) carbimazole (12-18m)
:: once euthyroid (4-6w) continue maintenance of carbimazole and either:
- titration-block of carbimazole
- higher dose block all thyroid production + levothyroxine (block and replace)
:::::::C/I in pancreatitis::::::::::
:::::::risk of agranulocytosis (low WCC) => severe infections (look out for sore throat):::::::::
2nd) propylthiouracil
::::::::risk of severe liver reaction inc death :::::
:::::::risk of agranulocytosis (low WCC) => severe infections (look out for sore throat):::::::::
3rd) radioactive iodine
drink single-dose of radioactive iodine. usually needs long-term levothyroxine
:::::::C/I: pregnancy or breastfeeding within 6 months of treatment, men must not father children within 4 months of treatment, limit contact with people (esp children and pregnant ::::::::
Adjunct: beta-blockers e.g. propranolol
Definitive: thyroidectomy + life-long levothyroxine
What is the difference between primary and secondary hypothyroidism? What labs markers (TFT) would correlate with either condition?
Primary = problem in thyroid.
⬇️T3/4 ⬆️TSH
Secondary = problem in pituitary
⬇️TSH ⬇️T3/4
What is the most common cause of primary hypothyroidism?
Hashimoto’s thyroiditis
autoimmune condition
assoc. w/ anti-thyroid peroxidase (anti-TPO) + anti-thyroglobulin (anti-Tg) ab’s
What is Cushing’s syndrome? What is Cushing’s disease?
Syndrome: Features of prolonged high levels of glucocorticoids in the body e.g. cortisol
Disease: a pituitary adenoma secreting excessive adrenocorticotropic hormone (ACTH), stimulating excessive cortisol release from the adrenal glands.
::::::high ACTH => hyperpigmentation
What are some physical features of Cushing’s?
- Round face (known as a “moon face”)
- Central obesity
- Abdominal striae (stretch marks)
- Enlarged fat pad on the upper back (known as a “buffalo hump”)
- Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
- Male pattern facial hair in women (hirsutism)
- Easy bruising and poor skin healing
- Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)
What are some metabolic effects of Cushing’s?
- Hypertension
- Cardiac hypertrophy
- Type 2 diabetes
- Dyslipidaemia (raised cholesterol and triglycerides)
- Osteoporosis
Causes of Cushing’s syndrome? (mnemonic)
CAPE
C – Cushing’s disease (a pituitary adenoma releasing excessive ACTH)
A – Adrenal adenoma (an adrenal tumour secreting excess cortisol)
P – Paraneoplastic syndrome e.g. SCLC
E – Exogenous steroids (patients taking long-term corticosteroids)
What is the 1st line investigation for Cushing’s?
Dexamethasone suppression test
Normal response : dex causes negative feedback on hypothalamus => less CRH => pituitary less ACTH => low cortisol
There are three types of dexamethasone suppression test:
- Low-dose overnight test (used as a screening test to exclude Cushing’s syndrome)
- Low-dose 48-hour test (used in suspected Cushing’s syndrome)
- High-dose 48-hour test (used to determine the cause in patients with confirmed Cushing’s syndrome)
What is the difference between low-dose and high-dose dexamethasone suppression tests?
Low overnight: 1mg ON. if cortisol is not suppressed => ?Cushing’s syndrome (needs further investigation)
Low 48-hr: 0.5mg QDS (8 doses). cortisol checked at 9am on day 1 and day 3.
:::::: no cortisol suppression => ?Cushing’s syndrome (needs further Inv)
High 48-hr: 2mg QDS (8 doses)
::::::suppression => Cushing’s disease (pituitary adenoma)
::::::no suppression => adrenal adenoma, ectopic ACTH
Dex suppression tests::::
low dose = ⬆️ cortisol,
high dose = ⬆️ cortisol,
low ACTH
Diagnosis?
adrenal adenoma
Dex suppression tests::::
low dose = ⬆️ cortisol,
high dose = ⬇️ cortisol,
high ACTH
Diagnosis?
pituitary adenoma
Dex suppression tests::::
low dose = ⬆️ cortisol,
high dose = ⬆️ cortisol,
high ACTH
Diagnosis?
Ectopic ACTH e.g. SCLC
What are some other investigations for Cushing’s disease (not dex)
24-hr urinary free cortisol
What are the treatments of Cushing’s syndrome?
Treat the underlying cause
- surgically remove the tumour
- surgically remove both adrenals and give life-long steroid replacement therapy
- metyrapone
How do cardiac symptoms present in acute hypokalaemia?
Patients may experience palpitations, angina-like chest pain, or syncopal episodes due to arrhythmias like ventricular tachycardia or fibrillation. On examination, signs of heart failure such as peripheral oedema and pulmonary crackles may be noted.
What muscular manifestations occur in acute hypokalaemia?
Muscle weakness, often affecting proximal muscles more than distal ones, is common. In severe cases, it can progress to flaccid paralysis. Deep tendon reflexes may also be diminished.
What are the cardiac effects in chronic hypokalaemia?
Chronic hypokalaemia can lead to left ventricular hypertrophy and interstitial fibrosis, increasing the risk of arrhythmias. While patients might report palpitations, physical examination findings are often unremarkable.
How does chronic hypokalaemia affect muscles?
Muscle weakness is milder compared to acute hypokalaemia. Patients may complain of fatigue, myalgia, or cramps, but muscle strength is generally preserved on examination.
What renal manifestations are seen in chronic hypokalaemia?
Chronic hypokalaemia may lead to renal tubular acidosis (type I or II), nephrogenic diabetes insipidus, and chronic kidney disease. Patients may present with polyuria and nocturia, though these symptoms are often non-specific.
What is the diagnostic serum potassium level for hypokalaemia?
Below 3.5 mmol/L.
Which electrolyte disturbance is commonly associated with hypokalaemia and may exacerbate it?
Hypomagnesaemia
What does a metabolic alkalosis on an ABG test suggest in the context of hypokalaemia?
Renal loss of potassium.
What are the typical ECG changes seen in hypokalaemia?
ST depression, T wave flattening or inversion, prominent U waves, and prolonged QT interval.
What medications can cause hypokalaemia? (3)
Loop and thiazide diuretics
Corticosteroids
Beta-2-agonists
What are common symptoms of acute hyperkalaemia?
Malaise, muscle weakness, and palpitations.
What might be found during the physical examination of a patient with acute hyperkalaemia?
Reduced muscle power, reflexes, and in severe cases, flaccid paralysis or respiratory failure.
What ECG changes occur as hyperkalaemia becomes more severe?
PR interval prolongation, QRS complex widening, and possibly a sine wave pattern.
How can Addison’s disease lead to hyperkalaemia?
Due to decreased aldosterone production, causing potassium retention.
Which medications can induce hyperkalaemia?
Potassium-sparing diuretics, ACE inhibitors, ARBs, and NSAIDs.
How does insulin/dextrose infusion help in managing hyperkalaemia?
It causes a short-term shift of potassium from the extracellular to the intracellular compartment.
What is the role of IV calcium gluconate in hyperkalaemia management?
It stabilizes the cardiac membrane but does not lower serum potassium levels.
What potassium level is considered mild, moderate, and severe hyperkalaemia according to the European Resuscitation Council?
Mild: 5.5-5.9 mmol/L, Moderate: 6.0-6.4 mmol/L, Severe: ≥ 6.5 mmol/L.
How is hyponatraemia categorized?
It can be categorized based on the patient’s volume status into hypovolaemic, euvolaemic, or hypervolaemic hyponatraemia.
What are the potential severe neurological symptoms of hyponatraemia?
Seizures and coma due to cerebral oedema.
How is acute symptomatic hyponatraemia managed?
With urgent treatment using hypertonic saline.
What is the risk of overly rapid correction of sodium in hyponatraemia?
Osmotic demyelination syndrome, , which can result in dysarthria, quadriparesis, seizures, and locked-in syndrome.
What are common medications that can cause hyponatraemia? (2)
Thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs).
What is the clinical presentation of severe hyponatraemia?
Severe cases can present with cerebral oedema, causing seizures, respiratory arrest, coma, or death.
What is pseudohyponatraemia?
A false low sodium level due to hyperlipidaemia or hyperproteinaemia.
What condition is associated with euvolaemic hyponatraemia?
Syndrome of inappropriate antidiuretic hormone secretion (SIADH).
How can you differentiate renal from non-renal causes of hyponatraemia?
By measuring urine sodium concentration: low levels indicate non-renal causes, while high levels suggest renal causes.
What fluids are typically used for treating hypernatraemia?
Hypotonic fluids or dextrose solutions are used, with close monitoring of serum electrolytes.
What are rare causes of hypernatraemia?
Hyperosmolar hyperglycaemic state and diabetes insipidus.
What does a urine osmolality >600 mOsm/kg suggest in hypernatraemia?
It suggests an appropriate renal response to the hyperosmolar state.
What does a urinary sodium concentration >20 mmol/L indicate?
It implies renal salt wasting.
What conditions may contribute to hypovolaemic hypernatraemia?
Gastrointestinal losses (e.g., diarrhoea, vomiting), renal losses (e.g., diabetes insipidus), and cutaneous losses (e.g., sweating, burns).
What conditions are associated with euvolaemic hypernatraemia?
Inadequate water intake and hypodipsia/adipsia (impaired thirst mechanism).
What conditions can cause hypervolaemic hypernatraemia?
Sodium overload (e.g., excessive hypertonic saline) and mineralocorticoid excess (e.g., Conn’s syndrome, Cushing’s syndrome).
What is the recommended rate of correction for hypernatraemia?
Serum sodium levels should be reduced gradually, not exceeding 10 mmol/L in a 24-hour period.
What should be done for hypovolaemic hypernatraemia in terms of fluid management?
Immediate fluid resuscitation with isotonic saline is recommended.
What are the most frequent causes of hypercalcaemia?
Primary hyperparathyroidism, malignancies such as lung and breast cancer, and multiple myeloma.
What are common non-specific symptoms of hypercalcaemia?
Polyuria, polydipsia, constipation, nausea, fatigue, and cognitive impairment.
What severe symptoms may occur in cases of hypercalcaemia?
Cardiac arrhythmias and coma.
What can be seen on ECG in hypercalcaemia?
- short QT interval
- in severe hypercalcaemia, Osborn waves (J waves)
How does hypervitaminosis D contribute to hypercalcaemia?
It leads to increased intestinal absorption and renal reabsorption of calcium.
Which medications can contribute to hypercalcaemia?
Thiazide diuretics and lithium.
What are the initial steps in managing hypercalcaemia?
Immediate stabilisation, rehydration with intravenous saline, and inhibition of bone resorption using bisphosphonates or corticosteroids.
What is the mechanism of action of sulfonylureas?
increasing pancreatic insulin secretion and hence are only effective if functional B-cells are present. On a molecular level they bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells.
What diabetic medication is recommended in patients with CVD risk (in addition to metformin or instead of metformin if C/I)?
SGLT-2 inhibitors e.g. dapagliflozin
What is the most common cause of Cushing’s syndrome?
Prolonged use of exogenous corticosteroids (e.g., prednisolone or dexamethasone).
What would ACTH levels show in different causes of Cushing’s syndrome?
Low ACTH: Adrenal adenoma or exogenous steroids
High ACTH: Pituitary adenoma (Cushing’s disease) or ectopic ACTH production
What imaging techniques are used to investigate the causes of Cushing’s syndrome?
MRI of the brain for pituitary adenoma
CT of the chest for small cell lung cancer
CT of the abdomen for adrenal tumours
What is Nelson’s syndrome, and what are its key features?
Nelson’s syndrome occurs after adrenalectomy when there is no cortisol feedback, leading to an ACTH-producing pituitary tumour. Symptoms include skin pigmentation, bitemporal hemianopia, and lack of other pituitary hormones.
What is Addison’s disease?
Addison’s disease is primary adrenal insufficiency, where the adrenal glands are damaged, reducing cortisol and aldosterone secretion, most commonly due to autoimmune causes.
What causes secondary adrenal insufficiency?
Inadequate ACTH from the pituitary gland due to pituitary tumours, surgery, radiotherapy, Sheehan’s syndrome, or trauma, leading to low cortisol production.
What is tertiary adrenal insufficiency, and how is it caused?
Tertiary adrenal insufficiency results from inadequate CRH release by the hypothalamus, often caused by long-term steroid use that suppresses the hypothalamus. Sudden withdrawal of steroids can cause the condition.
What are the symptoms of adrenal insufficiency?
Fatigue
Muscle weakness and cramps
Dizziness and fainting
Salt craving
Weight loss
Abdominal pain
Depression
Reduced libido
What are the key signs of adrenal insufficiency on physical examination?
Bronze hyperpigmentation of the skin (especially in creases, scars, lips, buccal mucosa)
Hypotension (particularly postural hypotension)
What are the key biochemical findings in adrenal insufficiency?
Hyponatraemia (low sodium)
Hyperkalaemia (high potassium)
Hypoglycaemia (low glucose)
Raised urea and creatinine (due to dehydration)
Hypercalcaemia (high calcium)
What test is used to diagnose adrenal insufficiency?
The short Synacthen test (ACTH stimulation test), where synthetic ACTH is given, and cortisol levels are measured before and after to assess adrenal function.
How does the short Synacthen test distinguish between primary and secondary adrenal insufficiency?
In primary adrenal insufficiency, cortisol fails to rise after Synacthen. In secondary insufficiency, cortisol may rise but still inadequately due to adrenal atrophy from low ACTH.
What is the role of ACTH levels in diagnosing adrenal insufficiency?
High ACTH indicates primary adrenal insufficiency (e.g., Addison’s disease), while low ACTH suggests secondary adrenal insufficiency (due to pituitary pathology).
How is adrenal insufficiency managed?
Replacement steroids: hydrocortisone for cortisol and fludrocortisone for aldosterone if necessary. Hydrocortisone doses are doubled during illness, and patients receive steroid cards, ID tags, and emergency instructions.
What is an adrenal crisis (Addisonian crisis), and what are the symptoms?
An adrenal crisis is a life-threatening emergency where steroid hormones are critically low, leading to:
- Reduced consciousness
- Severe hypotension
- Hypoglycaemia
- Hyponatraemia and hyperkalaemia
What is the emergency management of adrenal crisis?
- ABCDE approach
- Intramuscular or intravenous hydrocortisone (100mg initially)
- IV fluids for dehydration
- Correct hypoglycaemia (e.g., IV dextrose)
- Monitor electrolytes and fluid balance
What is Conn’s syndrome?
Conn’s syndrome is a form of primary hyperaldosteronism where an adrenal adenoma produces too much aldosterone.
What is the key presenting feature of hyperaldosteronism?
Hypertension is the key presenting feature, though many patients are asymptomatic. Symptoms, when present, include headaches, muscle weakness, and fatigue.
What are the actions of aldosterone in the kidneys?
Aldosterone increases:
Sodium reabsorption from the distal tubule
Potassium secretion from the distal tubule
Hydrogen secretion from the collecting ducts
What is primary hyperaldosteronism, and what are its causes?
Primary hyperaldosteronism occurs when the adrenal glands themselves overproduce aldosterone, typically due to:
- Bilateral adrenal hyperplasia (most common)
- An adrenal adenoma (Conn’s syndrome)
- Familial hyperaldosteronism (rare)
What is secondary hyperaldosteronism, and what causes it?
Secondary hyperaldosteronism results from excessive renin production, stimulating aldosterone release. Causes include:
- Renal artery stenosis
- Heart failure
- Liver cirrhosis and ascites
How is renal artery stenosis related to hyperaldosteronism, and how is it diagnosed?
Renal artery stenosis reduces blood flow to the kidney, leading to increased renin release and secondary hyperaldosteronism. It is diagnosed using:
- Doppler ultrasound
- CT angiogram
- Magnetic resonance angiography (MRA)
What does a high aldosterone-to-renin ratio (ARR) indicate?
High aldosterone and low renin suggest primary hyperaldosteronism.
High aldosterone and high renin suggest secondary hyperaldosteronism.
What are the effects of hyperaldosteronism on blood tests?
- Hypertension (raised blood pressure)
- Hypokalaemia (low potassium)
- Alkalosis (from increased hydrogen secretion)
What imaging tests are used to investigate the cause of hyperaldosteronism?
- CT or MRI for adrenal tumours or hyperplasia
- Renal artery imaging (Doppler, CT angiogram, or MRA) for renal artery stenosis
- Adrenal vein sampling to determine which adrenal gland is producing more aldosterone
How is hyperaldosteronism medically managed
Aldosterone antagonists are used, including:
- Eplerenone
- Spironolactone
What are the surgical treatments for hyperaldosteronism?
- Surgical removal of the adrenal adenoma (for Conn’s syndrome)
- Percutaneous renal artery angioplasty to treat renal artery stenosis
How can C-peptide levels distinguish type 1 and type 2 diabetes?
Low in type 1, high in type 2
What is the primary hormonal imbalance that causes gynecomastia?
An imbalance between estrogen and androgens (e.g., testosterone), typically with higher estrogen and lower androgen levels.
What are some conditions that can increase estrogen levels and cause gynecomastia?
Obesity, testicular cancer, liver cirrhosis, hyperthyroidism, and hCG-secreting tumors.
What are conditions that can reduce testosterone levels, contributing to gynecomastia?
Testosterone deficiency, hypothalamic or pituitary disorders, Klinefelter syndrome, orchitis, and testicular damage.
List some medications and drugs that can cause gynecomastia.
Anabolic steroids, antipsychotics, digoxin, spironolactone, GnRH agonists, opiates, marijuana, and alcohol.
How can you differentiate between gynecomastia and pseudogynecomastia?
In gynecomastia, there is firm tissue behind the areolas, whereas pseudogynecomastia involves soft, evenly distributed adipose tissue.
What initial investigations might be performed for gynecomastia?
Blood tests including renal profile, liver function tests, thyroid function tests, testosterone, SHBG, estrogen, prolactin, LH, FSH, and cancer markers.
What imaging studies may be indicated for suspected gynecomastia?
Breast ultrasound, mammogram, biopsy, testicular ultrasound, and chest X-ray if lung cancer is suspected.
How is gynecomastia typically managed in adolescents?
Gynecomastia in adolescents often resolves with time and may be managed with watchful waiting.
What treatments are available for problematic gynecomastia?
Treatment options include stopping causative drugs, tamoxifen, or surgical intervention if there is pain or psychological distress.
What is the main problem in Type 1 Diabetes?
The pancreas stops producing adequate insulin, causing high blood glucose (hyperglycemia).
What are the possible triggers for Type 1 Diabetes?
Genetic predisposition and certain viruses, like Coxsackie B and enterovirus.
List three key features of Diabetic Ketoacidosis (DKA).
Ketoacidosis, dehydration, and potassium imbalance
What are the three criteria to diagnose DKA?
- Hyperglycemia (e.g., blood glucose > 11 mmol/L)
- Ketosis (blood ketones > 3 mmol/L)
- Acidosis (pH < 7.3).
What is the FIG-PICK mnemonic in DKA treatment?
F – Fluids – IV fluid resuscitation with normal saline (e.g., 1 litre in the first hour, followed by 1 litre every 2 hours)
I – Insulin – fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)
G – Glucose – closely monitor blood glucose and add a glucose infusion when it is less than 14 mmol/L
P – Potassium – add potassium to IV fluids and monitor closely (e.g., every hour initially)
I – Infection – treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – monitor blood ketones, pH and bicarbonate
What is the criteria for stopping DKA treatment (fixed-rate insulin)?
- Ketosis and acidosis should have resolved
- They should be eating and drinking
- They should have started their regular subcutaneous insulin
What is ketogenesis, and when does it normally occur?
Ketogenesis is the liver’s process of converting fatty acids into ketones for fuel. It typically occurs during prolonged fasting or low-carbohydrate diets when glucose is insufficient.
How does dehydration occur in DKA?
High blood glucose overwhelms the kidneys, causing glucose to spill into the urine, drawing water out through osmotic diuresis, leading to polyuria and severe dehydration.
What causes potassium imbalance in DKA?
Insulin usually drives potassium into cells, but without insulin, potassium remains outside cells, leading to a total body potassium deficiency. Insulin treatment can quickly cause hypokalemia.
Why is cerebral edema a risk in children with DKA?
Rapid correction of dehydration and hyperglycemia causes water to shift from the extracellular to the intracellular space in brain cells, leading to swelling and potential brain injury.
What symptoms indicate cerebral edema during DKA treatment?
Symptoms include headache, altered behavior, bradycardia, and changes in consciousness.
What are the management options for cerebral edema in DKA?
Slowing IV fluids, administering IV mannitol, or giving IV hypertonic saline, under the guidance of an experienced pediatrician.
Why should fluid boluses generally be avoided in pediatric DKA?
To minimize the risk of cerebral oedema
When should IV dextrose be added during DKA treatment?
when blood glucose falls below 14 mmol/L
What are the common symptoms of DKA?
Symptoms include polyuria, polydipsia, nausea, vomiting, weight loss, acetone breath, dehydration, hypotension, altered consciousness, and possibly signs of an underlying infection.
How should potassium be managed during DKA treatment?
Add potassium to IV fluids and monitor serum potassium closely to avoid imbalances, especially after insulin administration via VBG/CBG.
What key lab markers should be monitored to assess DKA progress?
VBG/CBG: Blood glucose, ketone levels, and pH
What is Type 2 diabetes?
A condition where insulin resistance and reduced insulin production cause persistently high blood sugar levels.
What causes insulin resistance in Type 2 diabetes?
Repeated exposure to glucose and insulin makes cells resistant, leading to higher insulin needs; over time, this fatigues the pancreas, reducing insulin output.
What is acanthosis nigricans and how is it related to Type 2 diabetes?
A skin condition with darkened, velvety patches, often seen on the neck, axilla, and groin, associated with insulin resistance.
What is pre-diabetes, and what HbA1c level indicates it?
Pre-diabetes signals progression towards diabetes, with an HbA1c of 42–47 mmol/mol.
At what HbA1c level is Type 2 diabetes diagnosed?
HbA1c of 48 mmol/mol or above.
What are the HbA1c treatment targets for Type 2 diabetes according to NICE guidelines?
48 mmol/mol for new diabetics, 53 mmol/mol for patients on more than one medication
How often should HbA1c be measured once it is stable?
every 3-6m
What is the mechanism of action of SGLT-2 inhibitors?
e.g. dapagliflozin
They block glucose reabsorption in the kidneys, causing glucose to be excreted in urine, lowering HbA1c, and reducing blood pressure.
What are some side effects of metformin?
Gastrointestinal symptoms (nausea, pain, diarrhea) and, rarely, lactic acidosis.
Which patients might benefit from adding an SGLT-2 inhibitor to their Type 2 diabetes treatment?
e.g. dapagliflozin
Patients with cardiovascular disease, heart failure, or a QRISK score over 10%
What is a common side effect of SGLT-2 inhibitors that patients should be aware of?
e.g. dapagliflozin
Increased frequency of urinary tract infections and genital infections inc Fournier’s gangrene
can cause DKA!!
What are the notable side effects of pioglitazone?
Weight gain, heart failure, risk of bone fractures, and slight increase in bladder cancer risk.
What is the 1st, 2nd, 3rd and 4th line pharmacological managements of T2DM?
1st: metformin
then add SGLT-2 inhibitor (e.g., dapagliflozin), if pt has CVD or HF or QRISK >10%
2nd: sulfonylurea, pioglitazone, DPP-4 inhibitor (e.g. sitagliptin) or SGLT-2 inhibitor.
3rd:
- Triple therapy with metformin and two of the second-line drugs
- Insulin therapy (initiated by the specialist diabetic nurses)
4th + BMI >35: switch a drug for GLP-1 mimetic (e.g. semaglutide aka ozempic)
What treatment might be considered for patients who fail triple therapy and have a BMI over 35 kg/m²?
A GLP-1 mimetic can replace one of the drugs in triple therapy
e.g dulaglutide (trulicity) or semaglutide (ozempic)
What types of insulin are used in managing diabetes, and how do they vary in duration?
Rapid-acting (4 hrs), short-acting (8 hrs), intermediate-acting (16 hrs), and long-acting (24+ hrs).
What is the main difference between DKA and HHS (Hyperosmolar Hyperglycemic State)?
HHS has hyperosmolality and high glucose without ketones, while DKA has ketones and acidosis.
What is the preferred first-line medication for hypertension in patients with Type 2 diabetes?
ACE inhibitors.
How is chronic kidney disease managed in Type 2 diabetes?
With ACE inhibitors if ACR >3 mg/mmol, and SGLT-2 inhibitors if ACR >30 mg/mmol.
What suffix do SGLT-2 inhibitors typically end with?
-gliflozin.
Besides lowering HbA1c, what other effects do SGLT-2 inhibitors have?
-gliflozin
They reduce blood pressure, lead to weight loss, and improve heart failure outcomes.
Why should SGLT-2 inhibitors be used cautiously with insulin or sulfonylureas?
They can cause hypoglycemia when used with insulin or sulfonylureas.
Which SGLT-2 inhibitors are specifically licensed for treating heart failure?
Empagliflozin and dapagliflozin.
Which condition, aside from diabetes and heart failure, is dapagliflozin licensed to treat?
CKD
What class of drug is pioglitazone?
Thiazolidinedione.
How does pioglitazone help manage blood sugar in diabetes?
It increases insulin sensitivity and decreases glucose production by the liver.
Does pioglitazone typically cause hypoglycemia?
No
What are notable side effects of pioglitazone?
Weight gain, heart failure, increased risk of bone fractures, and a small increase in bladder cancer risk.
What is the most common sulfonylurea?
Gliclazide
How do sulfonylureas work in the body?
They stimulate insulin release from the pancreas.
What are notable side effects of sulfonylureas?
Weight gain and hypoglycemia.
What is the role of incretin hormones in blood sugar regulation?
They increase insulin secretion, inhibit glucagon production, and slow gastrointestinal absorption.
The main incretin is glucagon-like peptide-1 (GLP-1). Incretins are inhibited by an enzyme called dipeptidyl peptidase-4 (DPP-4).
Name two examples of DPP-4 inhibitors.
Sitagliptin and alogliptin.
Do DPP-4 inhibitors typically cause hypoglycemia?
No
What are notable side effects of DPP-4 inhibitors?
Headaches and a low risk of acute pancreatitis.
How are GLP-1 mimetics administered?
SC
Name two examples of GLP-1 mimetics
Exenatide and liraglutide and semaglutide (ozempic)
What are notable side effects of GLP-1 mimetics?
Reduced appetite, weight loss, and gastrointestinal symptoms like nausea and diarrhea.
What is the first-line treatment for acromegaly in most patients?
Trans-sphenoidal surgery.
Which medication class is used to directly inhibit the release of growth hormone in acromegaly?
Somatostatin analogues e.g. octreotide
Effective in 50-70% of patients.
What medications can be used in acromegaly if the pituitary tumour is inoperable or surgery is unsuccessful?
- 1st - Somatostatin analgue e.g. octreotide
- Pegvisomant (GH receptor antagonist)
- dopamine agonist (e.g. bromocriptine)
What is the mechanism of action of pegvisomant in treating acromegaly?
It is a GH receptor antagonist that prevents dimerization of the GH receptor.
It is very effective, achieving normal IGF-1 levels in 90% of patients.
Pegvisomant does not reduce tumour volume, so surgery may be needed if there is a mass effect
What dopamine agonist was the first effective medical treatment for acromegaly?
Bromocriptine
only effective in minority of pts
When might external irradiation be considered in acromegaly management?
For older patients or after failed surgical and medical treatment.
What electrolyte imbalance is associated with Cushing’s syndrome?
HYPOkalaemic metabolic alkalosis
cortisol stimulates aldosterone which inc K excretion => hypokal
+ bicarb resorption => alkalosis
What can be seen on thyroid scintigaphy in De Quervain’s/Subacute thyroiditis?
globally reduced uptake of iodine-131
