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.
