Endocrinology Flashcards

Question

What are the side effects of metformin?

Answer 1

Common: Abdominal pain; appetite decreased; diarrhoea; gastrointestinal disorder; nausea; taste altered; vitamin B12 deficiency; vomiting Rare or very rare: hepatitis; lactic acidosis (discontinue); skin reactions

Answer 2

Excreted unaltered by the kidneys Therefore contraindicated in patients with severe renal impairment. Dose reduction needed in patients with moderate renal impairment

Answer 3

1) Type 2 diabetes mellitus 2) SGLT2 inhibitors reduce the amount of glucose being reabsorbed in the kidneys so that it is passed out in the urine 3) UTI

Answer 4

1) Type 2 diabetes mellitus 2) GLP-1 receptor agonists stimulate the release of insulin and suppress glucagon secretion only when blood glucose concentrations are elevated; thus, the risk of hypoglycaemia is low 3) GI: decreased appetite, N + V, headache, renal impairment

Answer 5

Same as T1DM - HbA1c tests - 3 to 6 monthly - Capillary blood glucose (finger prick) - immediate glucose reading. Patients with T1DM and T2DM use these to self-monitor - Flash glucose monitoring (e.g. Freestyle Libre) - sensor placed in patient's arm allows reader to measure glucose levels of interstitial fluid. Reading lags 5 mins behind blood glucose levels. Need to change every 2 weeks.

Answer 6

In type 1 DM, cells cannot use glucose as fuel and think they are starving. They undergo ketogenesis so that they have usable fuel. - Over time the patient gets higher and higher glucose and ketones levels. - Initially, the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH. - Over time the ketone acids use up the bicarbonate and the blood becomes acidic > metabolic acidosis (pH < 7.3). This is called ketoacidosis.

Answer 7

Symptoms - Polyuria - Polydipsia - Nausea and vomiting Signs - Acetone smell to their breath - Dehydration and subsequent hypotension - Altered Consciousness - They may have symptoms of an underlying trigger (i.e. sepsis)

Answer 8

DEATH! The most dangerous aspects are dehydration, potassium imbalance and acidosis which can kill the patient

Answer 9

Hyperglycaemia (i.e. blood glucose > 11 mmol/l) Ketosis (i.e. blood ketones > 3 mmol/l) Acidosis (i.e. pH < 7.3)

Answer 10

FIG-PICK - follow local protocols carefully - F – Fluids – IV saline - I – Insulin – IV insulin - G – Glucose – monitor and add a dextrose infusion if too low (e.g. 14 mmol/l) - P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required - I – Infection – Treat underlying triggers such as infection - C – Chart fluid balance - K – Ketones – Monitor blood ketones/bicarbonate Establish the patient's normal subcutaneous insulin regime before stopping the insulin and fluid infusion.

Answer 11

DKA is a complete lack of insulin that results in high ketone production Medical emergency! Results from untreated T1DM or infections/illness

Answer 12

A disease characterised by marked hyperglycemia, hyperosmolality and mild/no ketosis Results from untreated T2DM usually

Answer 13

Low blood insulin means cells think the body is starving, increased gluconeogenesis which leads to hyperglycaemia, but enough insulin to inhibit ketogenesis Hyperglycemia -> osmotic diuresis (presence of increased glucose leads to increased urination) -> dehydration

Answer 14

Extreme diabetes symptoms and: - Confusion and reduced mental state - Lethargy - Severe dehydration

Answer 15

Replace fluid - 0.9% saline IV Insulin - at low rate of infusion! Restore electrolytes - e.g. K+ Low-moecular weight heparin (anti-coagulant)

Answer 16

Hyperthyroidism is a disease characterised by the over-production of thyroid hormones T3 and T4 by the thyroid gland.

Answer 17

- Graves disease - 65-75%, Autoimmune - Toxic multi-nodular goitre - Toxic adenoma - Metastatic follicular thyroid cancer - Iodine excess (e.g. IV contrast) - Secondary causes - TSH secreting pituitary tumour

Answer 18

An autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism (thyroid dysfunction) These TSH receptor antibodies are abnormal antibodies that mimic TSH and stimulate the TSH receptors on the thyroid.

Answer 19

Mainly young women 20 - 40 Ratio F to M 9:1

Answer 20

- Smoking - Stress - HLA-DR3 (susceptibility gene) - Other autoimmune diseases e.g. T1DM, Addisons, Vitiligo

Answer 21

Excess blood levels of T3 increases metabolic rate, cardiac output, bone resorption and stimulates the sympathetic nervous system

Answer 22

Everything goes faster than it should :( Symptoms: - Hot + sweaty - Diarrhoea - Hyperphagia (excessive eating) - Weight loss - Palpitations - Tremor - Irritability - Anxiety/restlessness Signs - Oligomenorrhoea (infrequent mensuration) - Goitre

Answer 23

- Beta-blockers - rapid relief from adrenaline related symptoms - 1st line Carbimazole - bocks synthesis of T4 (TETRAOGENIC!) - 2nd line Propylthiouracil - prevents T4->T3 conversion - Radioactive iodine is first-line definitive treatment in more-than-mild Graves’ - destroys part of thyroid - Thyroidectomy - hemi or total

Answer 24

Swelling of the thyroid glands due to viral infection, patient will present with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism. Hyperthyroid phase followed by a hypothyroid phase as the TSH level falls due to negative feedback. - Self-limiting condition - Treat with NSAIDs for pain and inflammation - Beta-blockers for symptom relief of hyperthyroidism

Answer 25

- Lithium (mood stabiliser) - Amiodarone (cardiac arrhythmia)

Answer 26

Post-partum women (around 8%) can develop lymphocytic thyroiditis, which causes transient primary hypothyroidism

Answer 27

- Hyperthyroidism symptoms plus: - Thyroid eye disease (25-50%) - Eyelid retraction - Periorbital swelling (swollen eyes) - Proptosis/Exophthalmos (bulging eyes) - Pretibial myxoedema (skin disorder associated with Graves disease) - Thyroid acropachy (signs associated with autoimmune thyroid disease)

Answer 28

Cardiovascular: heart failure, atrial fibrillation Musculoskeletal: osteoporosis Thyrotoxic crisis (thyroid storm): - Life-threatening, more severe form of hyperthyroidism, medical emergency! - Often occurs secondary to infection or trauma in patients with known hyperthyroidism

Answer 29

- Admission for monitoring - Supportive care with: - Fluid resuscitation - Antithyroid drugs: propylthiouracil - Corticosteroid: IV hydrocortisone - Beta-blockers: propanolol

Answer 30

Hypothyroidism is a pathological state reflecting a reduction in circulating T3 and T4. - Primary - abnormal decreased thyroid function resulting in failure to produce thyroid hormones - Secondary - abnormal decreased TSH production by the pituitary gland

Answer 31

Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes. Antibodies bind and block TSH receptors -> inadequate thyroid hormone production and secretion

Answer 32

4/1,000 per year Mainly >40 years old Ratio of affected female: male - 6:1

Answer 33

- Hashimoto's (inflammation and goitre) - Autoimmune disease where immune system attacks thyroid cells - More common in females 60-70 years old Primary atrophic hypothyroidism (atrophy -> no goitre)

Answer 34

Everything goes slower than it should! Fatigue Weight gain Loss of appetite Cold Lethargy Constipation Low mood/depression Menorrhagia (heavy periods) Goitre

Answer 35

- Bradycardia - Reduced Reflexes (deep tendon) - Dermatological: hair loss, loss of lateral eyebrows, dry and cold skin, coarse hair - Goitre - Carpal tunnel syndrome - Hoarse voice: rare

Answer 36

1st line: thyroid function tests - increased T4/T3, but: Primary hyperthyroidism (e.g. Graves): lower TSH than normal Secondary hyperthyroidism: higher TSH than normal Thyroid autoantibodies (anti-TSH receptor) Ultrasound and CT of the head (if serology cannot confirm_

Answer 37

TFTs - ↓T4 ↓T3 Primary: ↑TSH Secondary ↓TSH TPO (thyroid peroxidase) antibodies - associated with Hashimoto's

Answer 38

Levothyroxine (T4 analogue)

Answer 39

The clinical manifestation of pathological hypercortisolism from any cause

Answer 40

Adrenocorticotropic hormone (ACTH) dependent: - Cushing’s Disease - ACTH secreting from pituitary adenoma - Ectopic ACTH production from small-cell lung cancer ACTH independent: - Iatrogenic- steroid use (most common) - Adrenal adenoma

Answer 41

- Moon face - Central obesity - Buffalo hump - Acne - Hypertension - Abdominal striae (stretch marks) - Hirsutism (excessive hair growth in women) - weight gain

Answer 42

- Exogenous corticosteroid use (e.g. steroids) - Pituitary adenoma - Adrenal adenoma - Adrenal adenocarcinoma

Answer 43

- Random plasma cortisol- raised - Overnight dexamethasone suppression test- most sensitive - Low-dose dexamethasone suppression (1mg), normal/high cortisol with high-dose (8mg) dexamethasone - low cortisol > Cushing's syndrome - Urinary free cortisol (24 hr) (most commonly performed) - elevated - Plasma ACTH

Answer 44

An ACTH-dependent cause > high dose dexamethasone suppression test (8mg) If high-dose dexamethasone suppresses cortisol levels, then the diagnosis is Cushing's disease.

Answer 45

Suggests an ACTH-independent cause and warrants CT adrenals to look for adrenal pathology

Answer 46

Given at night (10pm), measured in the morning (9am) 8mg dexamethasone administered to patient, suppression of cortisol occurs in Cushing’s disease (pituitary adenoma), but not in an ectopic ACTH source

Answer 47

Pseudo-Cushing’s syndrome - caused by excess alcohol, resolves after 1-3 weeks of alcohol abstinence

Answer 48

Depending on the underlying cause: ACTH-dependent causes: - Cushing’s disease (pituitary adenoma): 1st line treatment is with trans-sphenoidal resection of the pituitary tumour. - Medical therapy (e.g. glucocorticoid antagonists) or radiotherapy if surgery fails - Ectopic ACTH source: treatment of underlying cancer ACTH-independent causes: - Iatrogenic: review the need for medication and try weaning if possible - Adrenal tumour: tumour resection or adrenalectomy

Answer 49

Release of excess growth hormone(GH)causing overgrowth of all systems

Answer 50

- Rare (3 per million/year) - Equal prevalence between males and females - Incidence is highest in people 40 +

Answer 51

- Most commonly caused by benign GH-producing pituitary tumours - Rare case caused by cancers that secrete ectopic GH release

Answer 52

5% are associated with the inherited disorder MEN-1 (multiple endocrine neoplasia-1)

Answer 53

- Prominent forehead and brow - Increased jaw size - Large hands, nose, tongue, feet - Visual field defect (bitemporal hemianopia) - Polyuria and polydipsia: due to T2DM - Profuse sweating - Lower pitch of voice - Obstructive sleep apnoea

Answer 54

- Increased GH either secreted by pituitary tumour or ectopic carcinoid tumour travels to tissues such as the liver and results in an increase in insulin-like Growth Factor-1 - This stimulates skeletal and soft tissue growth giving rise to ‘giant-like’ appearance and symptoms

Answer 55

1st line: Insulin-like Growth Factor 1 test = raised Gold standard: Oral glucose tolerance test while measuring GH levels (high glucose suppresses GH)

Answer 56

- 1st line: Transsphenoidal resection surgery (if cause is adenoma) - 2nd line: Somatostatin analogue eg. Octreotide

Answer 57

Benign adenoma of anterior pituitary gland producing excess prolactin.

Answer 58

- Most common hormonal disturbance of the pituitary - More common in females than males - Presents earlier in women ( with menstrual disturbance) but later in men (with erectile dysfunction)

Answer 59

- Micro tumour (less than 10mm diameter on MRI - 90%) - Macro tumour (more than 10mm diameter on MRI- 10%) - Non-functional tumour that compresses the pituitary gland, inhibiting dopamine release > disinhibition of prolactin release - Antidopaminergic drugs

Answer 60

Increased release of prolactin from the benign tumour in anterior pituitary gland can cause galactorrhoea (breast milk production not associated with pregnancy or breast-feeding) by stimulating milk production from the mammary gland and inhibiting FSH (follicle-stimulating hormone) and LH (luteinizing hormone)

Answer 61

- Visual field defect - Headache - Menstrual irregularity - Infertility - Galactorrhoea (milky discharge from nipples)

Answer 62

The baseline level of prolactin is measured and will be very high

Answer 63

Gold standard - Transsphenoidal resection surgery of pituitary gland 1st line - Dopamine agonists: Bromocriptine/cabergoline (Dopamine has an inhibitory effect on prolactin)

Answer 64

Primary hyperaldosteronism due to an aldosterone producing adrenal adenoma

Answer 65

Hypertension in patients: - Under 35 yrs with no family history of hypertension - With accelerated (malignant) hypertension - With hypokalaemia before diuretic therapy (helps rid the body of sodium and water) - Resistant to conventional antihypertensive therapy e.g. more than 3 drugs - With unusual symptoms e.g. sweating attacks or weakness

Answer 66

Excess production of aldosterone from the adrenal cortex, independent of the renin-angiotensin system leads to: - High Sodium and water retention - Increased potassium excretion in kidneys - Low renin release

Answer 67

Symptoms: - Lethargy - Mood disturbance - Paresthesia and muscle cramps (due to hypokalemia) Signs: - Hypokalaemia (< 3.5mmol/l) - Refractory hypertension

Answer 68

1) 1st line screening test: - Plasma aldosterone: renin ratio (ARR) > increased aldosterone, low renin > CT High-resolution CT abdomen: useful to exclude carcinoma

Answer 69

1st line: - Spironolactone - a potassium sparing diuretic for pre-op controls of BP and K+ levels Gold standard: - Laparoscopic Adrenalectomy The aim is to lower BP, decrease aldosterone levels and resolve electrolyte imbalance

Answer 70

Primary adrenal insufficency

Answer 71

- Very rare - 0.8 per 100,000 - Can be fatal - Marked female preponderance

Answer 72

- Autoimmune adrenalitis - most common 80% of cases in the UK - TB (most common cause worldwide) - Adrenal metastases

Answer 73

Destruction of the entire adrenal cortex resulting in mineralocorticoid (aldosterone, zona glomerulosa), glucocorticoid (cortisol, zona fasciculata) and androgens (precursors of sex hormones, zona reticularis) deficiency. Corticosteroids (glucocorticoids and mineralocorticoids) are involved in renal excretion of potassium and acid as well as sodium reabsorption. Hence, adrenal insufficiency results in a metabolic acidosis coupled with hyperkalaemia and hyponatraemia.

Answer 74

Autoimmune adrenalitis is associated with other autoimmune diseases including DMT1, pernicious anaemia and hypothyroidism If the patient has one of the above and present with symptoms of Addison's, it is worth considering

Answer 75

- Tanned skin - Lean - Fatigue - Pigmentation especially of palmar creases (increased ACTH cross-reacts with melanin receptors) - Postural Hypotension - Vomiting and nausea

Answer 76

1st line: - Morning serum cortisol (8 - 9am sample as peak cortisol levels) - abnormally low at <100 nanomols/L - 100 - 500nmol/L = refer to ACTH stimulation test - > 500nmol/L = normal Gold standard: - ACTH stimulation test: - Measure plasma cortisol before and 30 mins after IM TETRACOSACTIDE (Synacthen - ACTH analogue) - Addison’s is excluded if 30 min cortisol > 550nmol/L (diagnostic if below 550nmol/L) 8am plasma adrenocorticotrophic hormone (ACTH): increased due to loss of negative feedback from cortisol Serum electrolytes: hyponatraemia & hyperkalaemia due to a decrease in aldosterone

Answer 77

- Adrenal suppression due to the use of glucocorticoid - Central (secondary or tertiary) adrenal insufficiency (pituitary or hypothalamic lesions)

Answer 78

Replace steroids depending on signs, and symptoms: - Hydrocortisone (glucocorticoid) - replaces cortisol - Fludrocortisone (mineralocorticoid) - replaces aldosterone - Treat the underlying cause and warn against abruptly stopping steroids - Double hydrocortisone dose if intercurrent illness

Answer 79

Adrenal crisis or Addisonian crisis, is a state of acute insufficiency of adrenocortical hormones. Most often occurs in patients with established Addison's disease due to poor medication compliance, infection, trauma, surgery, or myocardial infarction.

Answer 80

Symptoms - Nausea and vomiting - Abdominal pain - Trigger e.g. infection or MI Signs - Hypotension - Hypovolemic shock - Reduced GCS

Answer 81

- Corticosteroid: hydrocortisone 100 mg IV STAT! - IV saline and dextrose if hypoglycemic

Answer 82

Syndrome of inappropriate ADH: abnormally increased ADH secretion from the posterior pituitary or an ectopic source, causing water retention and hypernatremia

Answer 83

- Tumours (SCLC, prostate, pancreatic) - Post-operative from major surgery - Infection (TB and pneumonia which causes lung abscess) - Head injury - Medications (thiazide diuretics) are the most common cause

Answer 84

Excess release of ADH will result in the increased aquaporin 2 channels in the collecting duct Excess water retention > dilute plasma > hyponatraemia < 135 mmol/L (more water so lower concentration of sodium) There is a loss of an effective feedback mechanism > continuous ADH production irrespective of serum osmolality > a low serum sodium and relatively high urinary sodium with concentrated urine.

Answer 85

Symptoms are a result of hyponatraemia: - Headache - Nausea - Fatigue - Muscle cramps - Confusion If severe > seizures and coma Fluid status: - Euvolaemic: no features of hypervolaemia or hypovolaemia as water reabsorbed is distributed evenly across the extra and intravascular compartment

Answer 86

SIADH is a diagnosis of exclusion as we do not have a reliable test to measure ADH activity directly. Clinical examination will show - Euvolaemia. - U+Es will show hyponatraemia (< 135mmol/L) - Urine sodium and osmolality will be high. Other causes of hyponatraemia need to be excluded: - Negative short synacthen (ACTH analogue) test to exclude adrenal insufficiency - No history of diuretic use - No diarrhoea, vomiting, burns, fistula or excessive sweating - No excessive water intake - No chronic kidney disease or acute kidney injury

Answer 87

- Stop causative medication - Fluid restriction to 500mls – 1litre. This may be enough to correct hyponatraemia without medications. - Tolvaptan. “Vaptans” are ADH receptor blockers. Causes a rapid increase in sodium. So initiated by a specialist endocrinologist and require close monitoring.

Answer 88

2 types: cranial and nephrogenic The passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption in the kidney either because of: - Reduced ADH secretion from the posterior pituitary - cranial AVD/DI - Impaired response of the kidney to ADH - nephrogenic AVD/DI

Answer 89

- Idiopathic (unknown cause) - Congenital - Tumour - Trauma - Infection

Answer 90

- Inherited - Metabolic (low potassium, high calcium) - Drugs (lithium) - Chronic renal disease

Answer 91

Symptoms Polyuria (excessive urine production) Polydipsia (excessive thirst) Signs Dehydration Postural hypotension Hypernatraemia

Answer 92

Polyuria and polydipsia can also be indicative of diabetes mellitus

Answer 93

GOLD STANDARD! Water deprivation test to determine if it is DI and desmopressin stimulation test to determine if cranial or nephrogenic - Patient goes without fluids for 8 hours - Urine osmolarity measured If cranial - urine osmolarity: - After water deprivation - low (still dilute) - After ADH analogue - high (back to normal) as kidneys can still respond to ADH If nephrogenic - urine osmolarity: - After water deprivation - low (still dilute) - After ADH analogue - low (still dilute) as kidneys cannot respond to ADH

Answer 94

- Treat underlying cause. Mild cases can be managed conservatively without any intervention. - Desmopressin (synthetic ADH) can be used in: - Cranial diabetes insipidus to replace ADH - Nephrogenic diabetes insipidus in higher doses under close monitoring

Answer 95

Family history

Answer 96

Parathyroid hormone (PTH) elicits several functions that increase plasma Ca2+ levels Hyperparathyroidism is the excessive secretion of PTH and can be primary, secondary or tertiary Primary hyperparathyroidism - excessive PTH secretion from the parathyroid glands Secondary hyperparathyroidism - hypertrophy of parathyroid glands to compensate for hypocalcemia Tertiary hyperparathyroidism - autonomous secretion of PTH from parathyroid glands due to hyperplasia.

Answer 97

Primary hyperparathyroidism - tumour of the parathyroid glands causing excessive secretion of PTH Secondary hyperparathyroidism - chronic kidney disease, and vitamin D deficiency due to diet or GI diseases (e.g. Crohn's) > hypocalcaemia Tertiary hyperparathyroidism - occurs after persistent parathyroid hyperplasia (as in secondary HPT) after correction of underlying cause, often seen in chronic renal failure

Answer 98

- Female sex: 3:1 female to male ratio in primary hyperparathyroidism - Radiation therapy to the neck - Severe vitamin D or calcium deficiencies - Familial rare conditions: MEN1 and 2A

Answer 99

Primary hyperparathyroidism - caused by uncontrolled parathyroid hormone produced by a parathyroid tumour which leads to hypercalcemia. - Serum calcium = high, PTH = high Secondary hyperparathyroidism - insufficient vitamin D or chronic renal failure leads to low calcium absorption from the intestines, kidneys and bones > hypocalcemia Parathyroid glands respond by releasing more PTH, and this leads to hyperplasia over time. - Serum calcium = low/normal, PTH = high Tertiary hyperparathyroidism is as a result of secondary hyperparathyroidism > hyperplasia of parathyroid gland > baseline PTH level inappropriately high even after the cause of SHP treated > high absorption of calcium in the intestines, reabsorption from kidneys and release from bones > hypercalcaemia. - serum calcium = high, PTH = high

Answer 100

Stones, bones, groans and moans! Renal stones Painful bones Abdominal groans - constipation, nausea and vomiting Psychiatric moans - fatigue, depression and psychosis

Answer 101

Measuring serum calcium and PTH levels Primary: serum calcium = high, PTH = high Secondary: serum calcium = low/normal, PTH = high Tertiary: serum calcium = high, PTH = high

Answer 102

Primary: surgical removal of the causative tumour Secondary: correcting the vitamin D deficiency or performing a renal transplant to treat renal failure. Tertiary: surgical removal of part of the parathyroid tissue to return the parathyroid hormone to an appropriate level or removal of whole gland

Answer 103

Primary hypoparathyroidism: low PTH due to parathyroid gland failure, autoimmune destruction or congenital DiGeorge syndrome (22q11 del) Secondary hypoparathyroidism: low PTH after parathyroidectomy or thyroidectomy surgery. This is the most common form of hypoparathyroidism

Answer 104

Low PTH results in: - Hypocalcaemia - Hyperphosphatemia (as PTH usually inhibits phosphate resorption at the kidneys)

Answer 105

It causes increased excitability of muscles and nerves so many symptoms are a result of this: Symptoms (experienced by patient): CATS Go Numb - Convulsions - Arrhythmia - Tetany (intermittent muscle spasms) - Spasm - Numbness Signs (found through examination/investigation): Chvostek’s sign - tapping on the facial nerve in the parotid gland (salivary gland below ears) causes ipsilateral twitching of facial muscles Trousseau’s sign - spasm of the wrist/hand caused by inflating the blood pressure cuff at the brachial artery above systolic pressure. Causes wrist flexion and fingers to pull together

Answer 106

- Thyroid surgery - Parathyroid surgery - Hyper- and hypomagnesaemia (magnesium needed for PTH production, but high levels can suppress process) - Moderate and chronic maternal hypercalcaemia (neonatal hypocalcaemia)

Answer 107

Bloods - Bone profile - Decreased Ca2+ - Decreased PTH - Increased/normal phosphate - Vitamin D - confirm/exclude deficiency as a cause for hypoparathyroidism ECG - Prolonged QT interval (time taken for ventricular depolarisation and repolarisation)

Answer 108

- Vitamin D deficiency - Hypomagnesaemia (low serum magnesium) - Hypoalbuminemia (low serum albumin)

Answer 109

- Severe symptomatic hypocalcemia: IV calcium - Vitamin D deficiency: calcitriol - Hypoparathyroidism: oral calcium + calcitriol - Synthetic PTH if required

Answer 110

Adrenaline is a catecholamine produced by the “chromaffin cells” in the adrenal medulla of the adrenal glands. A phaeochromocytoma is a tumour of the chromaffin cells that secrete unregulated and excessive amounts of adrenaline.

Answer 111

Rare condition Annual incidence: ~0.6 per 100,000 person-years

Answer 112

- Most sporadic - 25% familial and associated with multiple endocrine neoplasia type 2 (MEN 2) syndrome. There is a 10% rule to describe the patterns of tumours: - 10% bilateral - 10% cancerous - 10% outside the adrenal gland

Answer 113

Usually, adrenaline stimulates the sympathetic nervous system and is responsible for the “fight or flight” response. In patients with pheochromocytoma, the adrenaline is secreted in bursts giving periods of worse symptoms followed by more settled periods.

Answer 114

Signs and symptoms tend to fluctuate with periods when the tumour is secreting adrenaline: - Anxiety - Sweating - Headache - Hypertension - Palpitations, tachycardia and paroxysmal atrial fibrillation (irregular heartbeat that returns to normal within 7 days)

Answer 115

1) 1st line: - 24 hr urinary metanephrine (a breakdown product of catecholamines) collection - Plasma-free metanephrines: first-line along with urine metanephrines Results = elevated 2) CT abdomen and pelvis: if there is biochemical evidence of a phaeochromocytoma, then CT imaging can be performed to look at the adrenals

Answer 116

Alpha blockers (i.e. phenoxybenzamine) - to lower blood pressure Beta blockers once established on alpha blockers - to slow down the heart Adrenalectomy to remove tumour is the definitive management Patients should have symptoms controlled medically before surgery to reduce the risk of the anaesthetic and surgery.

Answer 117

Abnormally high serum calcium Normal serum calcium range is 2.13 to 2.63mmo/l and ionised calcium range is 1.15 to 1.27mmol/l Hypercalcemia = 2 standard deviations above normal range

Answer 118

- Mild asymptomatic hypercalcaemia occurs in 1 in 1000 of the population - Occurs especially in elderly women - Hypercalcaemia occurs in 20% to 30% of patients with cancer.

Answer 119

- Primary hyperparathyroidism and malignancy are the most common causes and account for 90% of cases - Secondary hyperparathyroidism - Tertiary hyperparathyroidism

Answer 120

Pathophysiology of primary, secondary and tertiary hyperparathyroidism is covered in the "hyperparathyroidism" flashcards Malignancies cause hypercalcaemia by: - Bony involvement by the tumour: may lead to massive osteoclastic activity (osteolytic lesions) Common malignancies leading to hypercalcaemia include multiple myeloma, leukaemia, lung cancer, and breast cancer. When malignancies cause hypercalcaemia, the tumour = advanced.

Answer 121

Hyperparathyroidism Stones, bones, groans and moans! - Renal stones - Painful bones - Abdominal groans - constipation, nausea and vomiting - Psychiatric moans - fatigue, depression and psychosis Malignancy Hypercalcemia usually occurs in advanced cancers

Answer 122

- Familial Multiple endocrine neoplasia (MEN) type 1 and MEN type 2a (Sipple) or isolated familial hyperparathyroidism. - There is an association of primary hyperparathyroidism with neurofibromatosis (syndrome where multiple tumours affect brain and spinal cord) and von Hippel-Lindau disease (condition that causes tumous to grow in parts of the body).

Answer 123

PTH/bone profile: - Low/undetectable PTH since tumour may be secreting parathyroid-like protein > hypercalcaemia but PTH levels will not increase - Low albumin (some serum calcium is bound to albumin) - Increased alkaline phosphatase - Protein electrophoresis to look for myeloma - B2-microglobulin will be present

Answer 124

Mild hypercalcaemia or asymptotic: treatment of underlying malignancy + supportive measures + monitoring Moderate/severe hypercalcaemia or symptom without advanced kidney disease: IV saline and IV biphosphonate/denosumab (prevents cancer related bone fractures and problems) Moderate/severe hypercalcaemia or symptom with advanced kidney disease: renal dialysis +- denosumab

Answer 125

Serum calcium will fall to its lowest within 7 days following bisphosphonate administration. Responses last 1 to 4 weeks, so constant calcium monitoring calcium is important.

Answer 126

- Acute kidney injury - Coma

Answer 127

Hypocalcaemia is a state of electrolyte imbalance in which the circulating serum calcium level is low (please note that hypocalcaemia usually has an underlying cause which should be investigated)

Answer 128

Chronic kidney disease is the most common cause of hypocalcaemia Severe vitamin D deficiency from: - Reduced UV exposure - Malabsorption - Anti-epileptic drugs - induce enzymes that increase vitamin D metabolism Primary or secondary hypoparathyroidism (see hypoparathyroidism flashcards)

Answer 129

It causes increased excitability of muscles and nerves because the threshold needed for neuron activation is decreased. Symptoms related to this. Symptoms (experienced by patient): CATS Go Numb Convulsions Arrhythmia Tetany Spasm Numbness Signs (found through examination/investigation): Chvostek’s sign - tapping on the facial nerve in the parotid gland causes ipsilateral twitching of facial muscles Trousseau’s sign - Carpopedal spasm caused by inflating BP cuff above systolic BP, causes wrist flexion and fingers to pull together

Answer 130

- ECG: prolongation of QT intervals (hypocalcaemia) - Decreased calcium and increased phosphate levels - LFTs: Alkaline phosphate raised in vitamin D deficiency and bone metastases - PTH - Vitamin D - U&Es: chronic kidney disease

Answer 131

- Aggressive IV fluids - Consider IV bisphosphonates if no response to fluids - Treat the underlying cause

Answer 132

3.5 – 5.3mmol/l

Answer 133

Hyperkalaemia is high serum potassium >5.5mmol/L Serum K+ > 6.5mmol/L = MEDICAL EMERGENCY!

Answer 134

Conditions: - Acute kidney injury (common) - Chronic kidney disease - Rhabdomyolysis (muscle cell (myocyte) lysis) - Adrenal insufficiency - Tumour lysis syndrome Medications: - Aldosterone antagonists aka potassium sparing diuretics) (spironolactone and eplerenone) (common) - ACE inhibitors (common) - Angiotensin II receptor blockers - NSAIDs (common) - Potassium supplements

Answer 135

The amount K+ in the blood determines the excitability of nerve and muscle cells, including the heart muscle or myocardium - Raised K+ levels in the blood reduces the difference in electrical potential between cardiac myocytes and outside of the cells - Threshold for action potential is significantly decreased - Increased abnormal action potentials - Thus abnormal heart rhythms that can result in ventricular fibrillation and cardiac arrest

Answer 136

Symptoms: - Muscle weakness - Muscle cramps - Paresthesia - Palpitations Signs: - Tachycardia associated with arrhythmias (Potential cardiac arrest)

Answer 137

- ECG - Bloods - full blood count & U and E (diagnostic) - Urine osmolality and electrolytes ECG: - Go - absent P wave - Go long - Prolonged PR interval (conduction through AV node >200ms)) - Go tall - Tall tented T waves - Go under - wide QRS interval (>120ms) Abnormal creatinine, urea and eGFR = hyperkalemia caused by acute or chronic renal failure

Answer 138

Medical emergency: >= 6.5mmol/L - IV 10ml 10% calcium gluconate - stabilises the cardiac muscle cells and reduces the risk of arrhythmias ≥ 6 mmol/L and ECG changes need urgent treatment ≤ 6 mmol/L with stable renal function = a change in diet and medications (i.e. stopping their spironolactone or ACE inhibitor). If non-urgent, then insulin and dextrose infusion. Insulin and dextrose drives carbohydrates into cells and takes potassium with it, reducing the blood potassium.

Answer 139

Low serum potassium of <3.5mmol/L Serum K+ < 2.5 mmol/L = MEDICAL EMERGENCY!

Answer 140

1) Increased secretion - Most common cause = diuretic treatment: thiazide diuretics e.g. bendroflumethiazide, loop diuretics e.g. furosemide - Renal disease - Conn's syndrome (excess aldosterone) 2) Decreased intake: - Dietary deficiency or fasting 3) Redistribution to intracellular: - Metabolic alkalosis - Drug effect (Insulin, B2 agonists) 4) GI losses: - Vomiting, severe diarrhoea and laxative abuse

Answer 141

Symptoms: - Usually asymptomatic - Fatigue and light-headedness - Weakness - Cramps - Palpitations - Constipation Signs: - Arrhythmias (especially AF) - Hypotonia - Hyporeflexia

Answer 142

- Serum K+ < 3.5mmol/L = hypokalaemia - Serum K+ < 2.5mmol/L = URGENT TREATMENT! ECG: - Small or inverted T waves - Depressed ST segments - Prominent U waves (after T waves) - Long PR interval

Answer 143

- K+ replacement (oral or IV) - Aldosterone antagonist (K+ sparing diuretics) - Identify and treat the underlying cause - Acute can resolve on own, majority just need withdrawal from diuretics or laxatives

Answer 144

Cancer of the thyroid glands: 4 types account for 98% of cases: - Papillary - Follicular - Anaplastic (worst prognosis :( ) - Medullary Papillary most common ~80% of cases

Answer 145

Symptoms Asymptomatic neck lump - most common presentation Hoarseness - suggests local invasion and recurrent laryngeal nerve involvement Signs: Dyspnoea: due to pressure on the trachea Cervical lymphadenopathy (abnormal enlargement of lymph nodes in head and neck - indicates lymphatic metastasis. Tracheal deviation: due to pressure effect

Answer 146

Thyroid function tests: usually normal - most cancers do not affect thyroid function Neck ultrasound: first-line imaging to visualise the thyroid and can be highly specific for certain subtypes e.g. papillary Fine needle biopsy: key procedure to confirm/exclude malignancy and performed under ultrasound guidance

Answer 147

Papillary, follicular and medullary: - Total thyroidectomy - Radioiodine ablation (I-131) - papillary and follicular subtypes - Lifelong levothyroxine (synthetic thyroxine T4) - Tyrosine kinase inhibitors in aggressive/metastatic disease Anaplastic: - Resection (if possible) - Palliative: isthmusectomy and radiotherapy

Answer 148

- Lung (50%) - Bone (30%) - Liver (10%) - Brain (5%)

Answer 149

Serum sodium concentration > 145 mmol/L Normal range is 135 - 145 mmol/l

Answer 150

Serum sodium concentration < 135 mmol/L

Answer 151

Carcinoid syndrome occurs due to release of serotonin (5-hydroxytryptamine) and other vasoactive peptides into the systemic circulation from a carcinoid tumour (type of neuroendocrine tumour that grows from neuroendocrine cells - cells in the body that release hormones).

Answer 152

Most commonly arise from GI tract followed by lungs, liver, ovaries thymus - Small intestine malignancy (Most common) - Appendix most common GI tract site - Liver most common site for metastasis from ileal tumours

Answer 153

- Neuroendocrine tumours normally secrete serotonin into the circulation. - With GI tract tumours, hormones secreted> enters enterohepatic circulation> liver inactivates hormones> No symptoms. - However, when liver metastases are present (liver tumour) > hormone secretion> released into circulation + liver dysfunction> symptoms.

Answer 154

Symptoms - Flushing of the skin (particularly face), - Diarrhoea - Abdominal cramps - Breathlessness and wheezing - Palpitations Signs Fibrosis (heart valve dysfunction)

Answer 155

1st line: Urinary 5-hydroxyindoleacetic acid test - elevated levels Chest X-ray + Chest/pelvic MRI/CT- helps locate primary tumours

Answer 156

- Surgery- Resection of tumour is the only cure for carcinoid tumours - Somatostatin analogues- Octreotide, blocks release of tumour mediators and counters peripheral effects - Debulking, embolization, or radiofrequency ablation for hepatic masses/metastases can decrease symptoms

Answer 157

- IBS - Crohn's - Menopause

Answer 158

- Non-diabetic hyperglycaemia (pre-diabetes) - Diabtes mellitus type 1 - Gestational diabetes

Answer 159

MODY describes a group of conditions characterised by an autosomal dominant mutation in a single gene, which leads to impaired beta-cell function. This is in contrast to T1DM and T2DM, which are polygenetic conditions. MODY does not involve autoimmune pathology or insulin resistance. Rather, the mutations involved lead to impaired glucose sensing and insulin secretion.

Answer 160

Type 3 (50-65%) Due to mutations in Hepatocyte nuclear factor-1-alpha Very responsive to Sulfonylurea (80% response)

Answer 161

- Presentation < 25 years of age - Strong family history - Normal BMI - Lack autoantibodies - No ketosis - Insulin not usually required

Answer 162

Often misdiagnosed as DM type 1 or young onset type 2. So genetic testing may be indicated in the following situations: - Young patient - Autosomal dominant mode of inheritance - Non-acute presentation - Lack of evidence of autoimmunity, e.g. autoantibody negative - Lack of evidence of insulin resistance, e.g. normal BMI

Answer 163

- Toxic nodular goitre - Painless, postnatal thyroiditis

Answer 164

- Painless thyroiditis - variant presentation of Hashimoto's thyroiditis - Graves disease

Answer 165

- Prolactinoma - Acromegaly - Cushing's syndrome

Answer 166

- Obesity - Metabolic syndrome

Answer 167

Essential hypertension

Answer 168

- Hypovolaemia - Pseudohyponatraemia

Answer 169

- Secondary hyperparathyroidism (DDx for this is primary hyperparathyroidism) - Hypercalacaemia of malignancy

Answer 170

- Iatrogenic post-surgery hypoparathyroidism - Vitamin D deficiency

Answer 171

Diabetes mellitus

Answer 172

- CKD - Diabetic ketoacidosis/hyperosmolar hyperglycaemic state (potassium shifts from the intracellular to the extracellular space due to a lack of insulin, resulting in hyperkalemia.)

Endocrinology Flashcards

(196 cards)