endocrinology Flashcards

Question

What is the effect of different nutrients on satiety

Answer 1

Highly refined sugar – quick and short satiety Low glycaemic index foods – better High protein – prolonged satiety High fat – stimulate and entice people to eat more

Answer 2

Hypothalamus

Answer 3

36 amino acids Structurally similar to NPY Binds NPY receptors Secreted by neuroendocrine cells in ileum, pancreas and colon in response to food Inhibits gastric motility Reduces appetite

Answer 4

Neuropeptide Y It stimulates food intake, preferably carbohydrates

Answer 5

Receptors in pyloric sphincter Delays gastric emptying Gall bladder contraction Insulin release And via vagus – satiety

Answer 6

Olfactory, gustatory, cognitive and visual stimuli

Answer 7

increase satiety

Answer 8

CCK, Glucagon like peptide-1 (GLP), insulin and Peptide YY

Answer 9

A disease in which the body’s ability to produce or respond to the insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated levels of glucose in the blood.

Answer 10

Type 1 Type 2 – includes gestational and medication induced diabetes Maturity-onset diabetes of the young (MODY) Pancreatic diabetes Endocrine diabetes – Cushing’s/ acromegaly Malnutrition related diabetes

Answer 11

Chronic hyperglycaemia due to insulin dysfunction – can’t move glucose from blood into cells. Leads to low glucose in cells with starve of energy.

Answer 12

an insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction.

Answer 13

inappropriately low insulin secretion and peripheral insulin resistance

Answer 14

Lack of insulin drives the mobilisation of energy stores from muscles, fat and the liver Glucose accumulates in the blood, causing hyperglycaemia In the kidneys, the glucose reabsorption mechanism becomes saturated and glucose appears in the urine Glucose within renal tubules draws water in by osmosis, leading to osmotic diuresis The raised plasma osmolality stimulates the thirst centre Over time, diabetes damages capillaries and markedly accelerates atherosclerosis

Answer 15

excessive secretion of growth hormone. Insulin resistance rises.

Answer 16

increased insulin resistance, reduced glucose uptake into peripheral tissues.

Answer 17

glucocorticoids increase insulin resistance

Answer 18

initiated by genetic susceptibility and environmental triggers

Answer 19

combination of genetic predisposition and environmental factors (obesity and lack of physical activity)

Answer 20

single gene defect altering beta cell function

Answer 21

Thirst (osmotic activation of hypothalamus) Polyuria (osmotic diuresis) Weight loss and fatigue (lipid muscle loss due to unrestrained gluconeogenesis) Hunger (lack of useable energy source) Pruritis vulvae and balanitis Blurred vision (due to uptake of glucose/ water into lens)

Answer 22

Onset in childhood/ adolescence Lean body habitus Acute onset of osmotic symptoms Prone to ketoacidosis High levels of islet autoantibodies

Answer 23

Usually presents in over 30s Onset is gradual Diet, exercise and oral medication can often control hyperglycaemia

Answer 24

Parents affected with diabetes Absence of islet autoantibodies Evidence of non-insulin dependence Sensitive to sulphonyl urea

Answer 25

Fasting >7mmol/L plasma glucose Random plasma glucose >11mmol/L HbA1c 6.5%/ 48mmol/mol

Answer 26

sensation (10mg monofilament), vibration perception (tuning fork), ankle reflexes.

Answer 27

It can lead to fat metabolism and the formation of ketone bodies.

Answer 28

reduced insulin leads to fat breakdown, forming free fatty acids, which: Impair glucose uptake Are transported to the liver, providing energy for gluconeogenesis Are oxidised to form ketone bodies (acetone, beta-hydroxybutyrate) Ketone bodies dissolve in the blood and release H+, causing acidosis.

Answer 29

Absence of insulin and rising counterregulatory hormones leads to increasing hyperglycaemia and rising ketones. Glucose and ketones escape in the urine but lead to an osmotic diuresis and falling circulating blood volume Ketones cause anorexia and vomiting

Answer 30

hyperglycaemia, raised plasma ketones and metabolic acidosis

Answer 31

Polyuria and polydipsia Nausea and vomiting Weight loss Abdominal pain

Answer 32

Hyperventilation Dehydration ‘Fruity breath’ Hypotension Tachycardia Coma

Answer 33

Rehydration Insulin Replacement of electrolytes (K+) Treat underlying cause

Answer 34

Leading cause of blindness in working age adults – diabetic retinopathy Diabetic nephropathy – leading cause of end-stage renal disease Peripheral vascular disease Stroke Cardiovascular disease – leading cause of mortality Diabetic Peripheral Neuropathy – leading cause of non-traumatic lower extremity amputations

Answer 35

Acute hyperglycaemia- metabolic emergencies, DKA, HHS Hyperglycaemic hyperosmolar state Chronic hyperglycemia- tissue complications side effects of treatment- hypoglycemia

Answer 36

Pain – burning, paraesthesia Autonomic – orthostatic hypotension, constipation, ED Insensitivity – foot ulceration, Charcot foot, amputation Peripheral neuropathy – glove and stocking sensory loss

Answer 37

hypertension, smoking, changes in HbA1c, diabetes duration

Answer 38

good glycaemic control, anticonvulsants, opioids.

Answer 39

Micro-aneurysms: pericyte and smooth muscle loss Leakage: basement membrane thickening reduced junctional contact with endothelial cells Ischaemia: pericyte loss

Answer 40

laser therapy to stabilise changes, not improve sight.

Answer 41

Restore the physiology of the beta cell

Answer 42

Insulin treatment (twice daily with meals) Awareness of blood glucose lowering effect of exercise Ability to judge CHO intake DAFNE: dose adjustment for normal eating (reduces DKA and severe hypos)

Answer 43

Weight loss and exercise are substantial and will reverse hyperglycaemia

Answer 44

Patients with type 2 diabetes don’t tend to respond to these lifestyle changes, due to their lifestyle choices.

Answer 45

Medication to control BP, blood glucose and lipids. Metformin = weight loss Metformin + sulphonyl urea but side effect of weight gain + chance of hypo Insulin

Answer 46

A complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. unwell patients with type 2 DM

Answer 47

Weakness Leg cramps Vision problems An altered level of consciousness marked dehydration glucose >30mmol/L.

Answer 48

There is no switch to ketone metabolism, so ketonemia stays <3MMOL/L AND PH >7.3.

Answer 49

>320mosmol/kg.

Answer 50

focal CNS signs, chorea, Disseminated intravascular coagulation (DIC), leg ischaemia

Answer 51

Give LMWH prophylaxis to all unless contraindication Rehydrate slowly with 0.9% saline IVI over 48h Replace K+ when urine starts to flow

Answer 52

Overproduction of thyroid hormone Leakage of preformed hormone from thyroid Ingestion of excess thyroid hormone

Answer 53

Grave’s disease Toxic multinodular goitre Toxic adenoma Congenital hyperthyroidism Thyroiditis

Answer 54

Weight loss Tachycardia Anxiety Heat intolerance Sweating Diarrhoea Menstrual disturbance

Answer 55

Diffuse goitre Thyroid eye disease Acropachy

Answer 56

Solitary nodule

Answer 57

Euthyroid hyperthyroxinemia is defined as a condition in which the serum total T4 and T3 concentrations are increased, but the thyroid-stimulating hormone (TSH) concentration is normal and there are no clinical signs or symptoms of thyroid dysfunction.

Answer 58

Thyroid function tests to confirm biochemical hyperthyroidism Clinical history, physical signs usually sufficient for diagnosis Supporting investigations – thyroid antibodies

Answer 59

Antithyroid drugs e.g. thionamides (carbimazole) Beta blockers Radioiodine Surgery (partial/ subtotal thyroidectomy)

Answer 60

An autoimmune disease affecting the thyroid that causes hyperthyroidism and results in an enlarged thyroid.

Answer 61

The immune system is tricked into targeting receptors on the thyroid gland, causing it to become overactive - hyperthyroidism. Increased levels of TSH receptor stimulating antibody (TRAb) which causes excess thyroid hormone secretion (low TSH in the blood stream, but high thyroid hormone levels (T3 and T4) due to the TRAb having the same effects as TSH on the thyroid).

Answer 62

Anxiety and irritability A fine tremor of your hands or finger Heat sensitivity and an increase in perspiration or warm, moist skin Weight loss, despite normal eating habits Enlargement of thyroid gland (goiter) Bulging eyes – Graves’ ophthalmopathy Thick, red skin usually on the shins or tops of the feet - Graves’ dermopathy

Answer 63

Inhibition of the production of thyroid hormones and to block the effect of the hormones on the body.

Answer 64

Radioactive iodine therapy – oral radioactive iodine. This destroys the overactive thyroid cells over time, causing the gland to shrink and to lessen symptoms gradually Anti-thyroid medications – interfere with the thyroid’s use of iodine to produce hormones e.g. carbimazole Beta blockers e.g. propranolol – provide rapid relief of irregular heartbeats, tremors, heat intolerance and muscle weakness Ophthalmopathy – corticosteroids/ orbital decompression surgery Thyroidectomy

Answer 65

Subnormal activity of the thyroid gland due to intrinsic underactivity of the thyroid gland.

Answer 66

Subnormal activity of the thyroid gland due to reduced stimulation of the gland caused by a deficiency of TSH due to disease of the pituitary gland

Answer 67

Subnormal activity of thyroidgland due to low TRH caused by hypothalamic disease

Answer 68

Primary >99% Most cases due to Hashimoto’s thyroiditis (autoimmune hypothyroidism)

Answer 69

Hashimoto’s thyroiditis Thyroidectomy Iodine deficiency

Answer 70

Pituitary tumour

Answer 71

Neonatal hypothyroidism Resistance to thyroid hormone Isolated TSH deficiency

Answer 72

Fatigue, loss of energy, lethargy Weight gain Decreased appetite Cold intolerance Dry skin Muscle pain, joint pain, weakness in the extremities Depression Emotional lability, mental impairment Forgetfulness, impaired memory, inability to concentrate Constipation Menstrual disturbances, impaired fertility Decreased perspiration Paraesthesia and nerve entrapment syndromes Blurred vision

Answer 73

Weight gain Slowed speech and movements Dry skin Jaundice Pallor Coarse, brittle, straw-like hair Loss of scalp hair, axillary hair, pubic hair, or a combination Hoarseness Bradycardia Pericardial effusion

Answer 74

Addison disease Goiter Chronic fatigue syndrome Hypopituitarism Iodine deficiency

Answer 75

Sinus bradycardia, low pulse pressure, pericardial effusion, coronary artery disease TSH and thyroxine tests

Answer 76

Increased TSH, usually decreased free T4, decreased T3 T4/T3 may be below normal in positive titre of TPO antibodies in Hashimoto’s

Answer 77

TSH inappropriately low for reduced T4/T3 levels

Answer 78

Full replacement of 100 µg thyroid hormone (Levothyroxine) – titre according to TSH Requirements vary according to cause e.g. higher disease in thyroid ablation Monitoring treatment

Answer 79

Dose titrated until TSH normalises T4 half-life is long – check levels 6-8 weeks after dose adjustment In secondary/ tertiary hypothyroidism TSH will always be low, T4 is monitored

Answer 80

Hypothyroidism due to aggressive autoimmune destruction of thyroid cells. An autoimmune thyroid disease characterised by diffuse enlargement of the thyroid and high titres of thyroid autoantibodies.

Answer 81

Sex – women more likely Age – most commonly during middle age Heredity – family history of Hashimoto’s disease Other autoimmune disease Radiation exposure – (more common in Japan)

Answer 82

Inflammation from Hashimoto’s disease, chronic lymphocytic thyroiditis, often leads to an underactive thyroid gland – hypothyroidism. Activated CD4+ helper T-cells recruit CD8+ cytotoxic T-cells which destroy thyroid follicular epithelial cells Anti-thyroid autoantibodies produced by activated B-cells may also contribute

Answer 83

Iodine Infection Smoking

Answer 84

Fatigue and sluggishness Increased sensitivity to cold Constipation Pale, dry skin A puffy face Brittle nails Hair loss Muscle weakness Joint pain and stiffness Unexplained weight gain

Answer 85

Diagnosis is based on signs and symptoms Blood tests – thyroid hormone and TSH levels produced in the pituitary gland Hormone test – underactive thyroid – level of thyroid hormone is low but TSH is elevated Antibody test – Hashimoto’s disease involved the production of abnormal antibodies. Blood test confirm presence of antibodies against thyroid peroxidase (TPO antibodies).

Answer 86

Synthetic hormones – synthetic thyroid hormone levothyroxine Resection of obstructive goitre

Answer 87

papillary (most common 60%), follicular (≤25%), medullary (5%), lymphoma (5%) and anaplastic (rare).

Answer 88

Radiation exposure is a well-documented risk factor for thyroid carcinoma, most notably papillary carcinoma. Iodine deficiency, particularly for follicular carcinomas

Answer 89

Epithelial tumours that originate from thyroid follicular cells.

Answer 90

Thyroid carcinoma most commonly manifests as a painless, palpable, solitary thyroid nodule. Increased rate of malignancy in males Nodular growth Rapid growth: ominous sign Usually painless; sudden onset of pain more strongly associated with benign disease Hard and fixed nodules

Answer 91

Thorough head and neck examination, including thyroid gland and cervical soft tissues Fine-needle aspiration biopsy (FNAB) Indirect laryngoscopy Lab tests – serum calcitonin – elevated levels suggest medullary thyroid carcinoma

Answer 92

Malignancies require surgical intervention

Answer 93

Younger patients Spread – lymph nodes and lung

Answer 94

total thyroidectomy to remove non-obvious tumour. Consider node excision/ radioiodine to ablate residual cells Give levothyroxine to suppress TSH

Answer 95

Middle age Spreads early via blood (bone, lungs) Treatment – total thyroidectomy + T4 suppression + radioiodine ablation

Answer 96

Sporadic (scattered) or part of MEN syndrome (multiple endocrine neoplasia) May produce calcitonin which can be used a cancer marker Do not concentrate iodine Treatment – thyroidectomy + node clearance External beam radiotherapy may prevent regional recurrence

Answer 97

Female: male = 3:1 May present with stridor/ dysphagia Do full staging pre-treatment (chemotherapy) Assess histology for mucosa-associated lymphoid tissue (MALT)

Answer 98

Female: male = 3:1 Elderly Poor response to any treatment Excision + radiotherapy may be tried

Answer 99

a tumour on the pituitary gland that causes the gland to produce too much ACTH, leading to high levels of cortisol production.

Answer 100

an abnormal condition caused by chronic excess levels of corticosteroids (particularly cortisol) in the body due to hyperfunction of the adrenal gland (often due to the use of corticosteroid medication).

Answer 101

Iatrogenic – pharmacological use of steroids leads to increased cortisol in circulation Cushing’s disease

Answer 102

Weight gain Mood change – depression, lethargy, irritability Proximal weakness Gonadal dysfunction – irregular menstruation, erectile dysfunction Acne

Answer 103

Central obesity - round face, supraclavicular fat distribution Skin and muscle atrophy Purple abdominal striae Osteoporosis

Answer 104

Alcoholism Anorexia nervosa Bulimia nervosa Depression Obesity Pseudo-Cushing syndrome

Answer 105

Overnight dexamethasone suppression test If this test is positive, test for plasma ACTH

Answer 106

Tumour adenoma of the adrenal glands

Answer 107

1mg dexamethasone at midnight, the take serum cortisol at 8am Normally cortisol suppresses to <50nmol/L – NO suppression in Cushing’s syndrome

Answer 108

Iatrogenic – stop medications if possible Cushing’s disease – selective removal of pituitary adenoma

Answer 109

The abnormal growth of hands, feet and face due to overproduction of growth hormone.

Answer 110

growth hormone stimulates growth of bone and soft tissue, through secretion of Insulin-like growth factor-1.

Answer 111

Acral enlargement (peripheries – hands and feet) Arthralgias (joint pain) Maxillofacial changes Excessive sweating Headache Backache Hypogonadal symptoms Acroparaesthesia (burning, tingling sensations in the extremities) Amenorrhoea (absence of menstruation) Decreased libido

Answer 112

Growth of hands Coarsening face; wide nose Macroglossia (big tongue) Puffy lips, eyelids and skin Obstructive sleep apnoea Goitre

Answer 113

Marfan syndrome Precocious puberty Prolactinoma Gigantism

Answer 114

IGF-1 test, GH test, glucose tolerance test

Answer 115

GH cannot be relied on alone as the secretions are pulsatile and at peaks acromegalic and normal levels overlap. GH also increases during pregnancy, stress, and sleep.

Answer 116

1st line: Pituitary surgery (trans-sphenoidal surgery) – size of the tumour and the surgeon will determine the success of the surgery Medical therapy – dopamine agonists e.g. cabergoline Radiotherapy

Answer 117

Primary hyperaldosteronism: a disease of the adrenal glands involving excess production of aldosterone (independent of the renin-angiotensin system). It can cause high blood pressure.

Answer 118

Conn’s syndrome causes excess aldosterone production due to a solitary aldosterone-producing adenoma (linked to mutations in K+ channels). Aldosterone causes an exchange of transport of sodium and potassium in the distal renal tubule. Therefore, hyperaldosteronism causes increased reabsorption of sodium and excretion of potassium.

Answer 119

Often asymptomatic Signs of hypokalaemia Weakness Cramps Paraesthesia Polyuria (excessive urine production) Polydipsia (excessive thirst)

Answer 120

High blood pressure May cause headaches, blurred vision, dizziness Low potassium levels (not reliable as some patients will have normal levels) This may cause fatigue, numbness, increased urination, increased thirst

Answer 121

Congenital adrenal hyperplasia (autosomal recessive disorder) Secondary hyperaldosteronism Exogenous mineralocorticoid excess Liddle syndrome

Answer 122

Investigate for suppressed renin and increased aldosterone Adrenal vein sampling U&E – potassium may be low or normal

Answer 123

Laparoscopic adrenalectomy Spironolactone (25-100)mg for 4 weeks pre-op controls BP and K+.

Answer 124

excess aldosterone production due to a high renin from decreased renin perfusion e.g. in renal artery stenosis, accelerated hypertension, diuretics, CCF or hepatic failure.

Answer 125

A condition in which the adrenal glands do not produce adequate amounts of steroid hormone (mainly cortisol). (and aldosterone)

Answer 126

Autoimmune destruction of the entire adrenal cortex. Loss of cortex leads to reduction in ability to produce cortisol and/or aldosterone. Excess ACTH stimulates melanocytes, resulting in the pigmentation.

Answer 127

Addison’s disease Destruction of the adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency.

Answer 128

Hypopituitarism/ long-term steroid therapy leading to suppression of the pituitary-adrenal axis.

Answer 129

Fatigue Weight loss Dizzy Faints Poor recovery from illness Adrenal crisis Headache Abdominal pain Diarrhoea/ constipation

Answer 130

Hypotension and cardiovascular collapse Fatigue Fever Hypoglycaemia Hyponatraemia and hyperkalaemia

Answer 131

Pigmentation and pallor Primary – Hyperpigmentation Secondary – no pigmentation Hypotension

Answer 132

Adrenal crisis Eosinophilia Hyperkalaemia Sarcoidosis Tuberculosis

Answer 133

Short ACTH stimulation test – give ACTH, if cortisol remains low then it diagnoses AI.

Answer 134

Past history TB Post partum bleed Cancer Family history Autoimmunity – most common Congenital disease Any previous use of steroids

Answer 135

Replace the aldosterone with fludrocortisone (for primary AI) Hydrocortisone 2/3 times daily to replace the cortisol Mineralocorticoids to correct postural hypertension

Answer 136

A rare metabolic disorder in which the patient produces large quantities of dilute urine and is constantly thirsty. also known as argenine vasopressin insufficiency/resistance

Answer 137

It is due to a deficiency of the pituitary hormone vasopressin (ADH), which regulates reabsorption of water in the kidneys. This means that the body can’t make enough concentrated urine and too much water is passed

Answer 138

Most common type of diabetes insipidus Not enough AVP in the body to regulate urine production Caused by damage to the hypothalamus/pituitary gland e.g. after infection, operation, brain tumour or brain injury.

Answer 139

There’s enough AVP in the body, but the kidneys fail to respond to it. It can be caused by kidney damage, or sometimes inherited as a problem Congenital Acquired - lithium (used to treat bipolar disorder) can cause nephrogenic diabetes insipidus by damaging the cells of the kidney

Answer 140

Polydipsia (extreme thirst) Polyuria (excessive urine) – up to 20litres per day in severe cases Tiredness (having to pass urine at night) Irritability Difficulty concentrating

Answer 141

Histiocytosis Hypercalcaemia Hypokalaemia Medullary cystic disease Type 1 diabetes mellitus

Answer 142

Water deprivation test Vasopressin test MRI scan

Answer 143

not drinking any liquid for 8 hours – in diabetes insipidus the body will still pass large amounts of dilute urine instead of small amount of concentrated urine.

Answer 144

inject small dose AVP. If it stops urine production = cranial DI (shortage of AVP). If urine production continues = nephrogenic DI (no response to AVP)

Answer 145

view images of the brain to see if there is damage to the hypothalamus or pituitary gland.

Answer 146

Treatment not always necessary – fluid intake must be increased to compensate for excess fluid lost through urine. Medication called desmopressin can be used to replicate the functions of AVP (cranial DI) Nephrogenic DI often treated with thiazide diuretics, which reduce the amount of urine the kidneys produce

Answer 147

The hyponatraemia and hypo-osmolality resulting from inappropriate, continued secretion or action of the ADH arginine vasopressin (AVP) despite normal or increased plasma volume, which results in impaired water excretion.

Answer 148

Malignancy – lung small-cell, pancreas, prostate, thymus, or lymphoma CNS disorders – meningoencephalitis, abscess, stroke, subarachnoid/ subdural haemorrhage Chest disease – TB. Pneumonia, abscess Drugs – opiates, cytotoxics Other – trauma, major abdominal surgery, symptomatic HIV

Answer 149

Disordered hypothalamic -pituitary secretion or ectopic production of ADH.

Answer 150

Decreased Na+ with decreased or normal urea and creatinine Decreased plasma osmolality Increased urine osmolality Increased urine Na+

Answer 151

Nausea Irritability and headache with mild dilutional hyponatraemia Fits and coma with severe hyponatraemia

Answer 152

CSW (cerebral salt-wasting syndrome) – excessive ADH secretion caused by stimulation of the hypothalamus after trauma or ischaemia.

Answer 153

Full blood count Diagnose by serum concentrations of sodium, potassium, chloride and bicarbonate Hyponatraemia with corresponding hypo-osmolality Concentrated urine (Na+>20mmol/L) and osmolality (>100mOsmol/Kg)

Answer 154

Treat the cause and restrict the fluid Consider salt +/- loop diuretic if severe. Vasopressin receptor antagonists - Vaptan

Answer 155

Excessive secretion of parathyroid hormone, usually due to a small tumour in one of the parathyroid glands. Results in hypercalcaemia. Primary is most common.

Answer 156

Primary – caused by a solitary adenoma, or occasionally hyperplasia of all glands. Secondary – caused by decreased vitamin D intake or chronic renal failure Tertiary – occurs after prolonged secondary hyperparathyroidism, causing glands to act autonomously after undergoing hyperplastic or adenomatous change.

Answer 157

Parathyroid hormone (PTH) is normally secreted in response to low ionized Ca2+ levels, by 4 parathyroid glands situated posterior to the thyroid. The glands are controlled by negative feedback via Ca2+ levels.

Answer 158

Primary – adenoma or hyperplasia provides additional secretive tissue to provide excess PTH Secondary – parathyroid gland becomes hyperplastic in response to chronic hypocalcaemia Tertiary – glands become autonomous, producing excess of PTH even after the correction of calcium deficiency

Answer 159

Often asymptomatic, occasionally bones, stones, groans, moans

Answer 160

kidney disease, with skeletal or cardiovascular complications

Answer 161

bones, stones, groans, moans

Answer 162

Bones – osteitis fibrosa cystica, osteoporosis Kidney stones Psychic groans – confusion Abdominal moans – constipation, acute pancreatitis

Answer 163

Adverse drug reaction to lithium/ thiazide diuretics Cancers producing parathyroid hormone Leprosy Exogenous calcium intake Multiple endocrine neoplasms

Answer 164

Increased Ca2+ and PTH Increased Alkaline phosphatase (ALP) – from bone resorption

Answer 165

Low serum calcium Raised PTH

Answer 166

Raised calcium Raised PTH

Answer 167

surgical removal of adenoma.

Answer 168

calcium correction; treat underlying cause

Answer 169

Calcium mimetic, total or subtotal parathyroidectomy

Answer 170

Subnormal activity of the parathyroid glands, causing a fall in the blood concentration of calcium and muscular spasms.

Answer 171

genetics, autoimmune (polyglandular type 1), infiltration of the parathyroid glands by iron overload (haemochromatosis), surgery (parathyroidectomy)

Answer 172

PTH stimulates the activation of vitamin D, which facilitates intestinal calcium absorption, renal reabsorption of calcium as well as calcium release from bone.

Answer 173

increased excitability of muscles and nerves. Numbness around the mouth/ extremities, cramps, tetany, convulsions. Chvostek sign- facial twitch of touching Trousseau sign- hand and foot spasm under ischaemia

Answer 174

A genetic defect that causes lack of response to parathyroid hormone.

Answer 175

short stature, obesity, round faces, mild learning difficulties, short fourth metacarpals

Answer 176

calcium and vitamin D can reverse most of the features.

Answer 177

a condition in which all the symptoms of pseudohypoparathyroidism are present, but the patient’s response to parathyroid hormone is normal.

Answer 178

A higher-than-normal level of calcium in the blood due to a malignancy secreting parathyroid hormone-related protein.

Answer 179

Malignancies of the lung, oesophagus, skin, cervix, breast and kidney can be a cause. The tumour secretes parathyroid hormone-related protein which results in increased calcium levels. Another cause is local osteolysis. Main cause is primary hyperparathyroidism.

Answer 180

Bones – osteitis fibrosa cystica, osteoporosis Kidney stones Psychic groans – confusion Abdominal moans – constipation, acute pancreatitis Weight loss Anorexia Nausea Polydipsia Polyuria Constipation Abdominal pain Dehydration Weakness Confusion Seizure – short QT interval on ECG Coma

Answer 181

Hyperparathyroidism Hypernatremia

Answer 182

Raised Ca2+ Decreased albumin Decreased Cl- Alkalosis Decreased K+ Increased PO43-

Answer 183

Aggressive rehydration Bisphosphonates e.g. zoledronic acid IV, usually normalize calcium within 3 days and can be given as a repeated infusion Long term – control of underlying malignancy

Answer 184

An abnormally low calcium concentration in the blood.

Answer 185

HAVOC hypoparathyroidism, acute pancreatitis, vit D deficiency, Osteomalacia, CKD

Answer 186

SPASMODIC spasms, paraesthesiae, anxious, seizures, muscle tone increase, orientation impaired, dermatitis, impetigo herpetiformis, cardiomyopathy

Answer 187

Hypoparathyroidism Hypoalbuminemia Metabolic alkalosis Acute kidney injury Acute pancreatitis

Answer 188

Dysphagia Wheezing; bronchospasm Syncope Congestive heart failure Angina

Answer 189

Measure serum albumin levels to rule out hypoalbuminemia Chvostek’s sign – tap over facial nerve and look for spasm of facial muscles Trousseau’s sign – compression of brachial artery causes carpopedal spasm (wrist and fingers flex) eGFR to look for chronic kidney disease PTH and vitamin D levels

Answer 190

Family history Lack of sun exposure Low-calcium diet Drugs – antibiotics, loop diuretics, oestrogen

Answer 191

Mild symptoms Give calcium 5mmol/6 hours, with daily plasma Ca2+ levels Severe symptoms 10ml of 10% calcium gluconate IV over 30min. Hypoparathyroidism – alfacalcidol correct resp. alkalosis if thats the cause

Answer 192

An abnormally high concentration of potassium in the blood, usually due to failure of the kidneys to secrete it.

Answer 193

Mild: 5.5-6.0mEq/L Moderate: 6.1-7.0mEq/L Severe: ≥7.0mEq/L

Answer 194

Renal impairment Rhabdomyolysis (muscle injury – death of muscle fibres that release their contents into the bloodstream) Metabolic acidosis Addison’s disease (primary adrenal insufficiency) Drugs interfering with potassium excretion e.g. ACEi Burns

Answer 195

A fast, irregular pulse Chest pain Weakness Palpitations Light-headedness Dyspnoea Paraesthesia Frank muscle paralysis

Answer 196

Metabolic acidosis Rhabdomyolysis Acute tubular necrosis

Answer 197

Plasma potassium >6.5mmol/L – emergency, needs urgent assessment Bloods: check potassium, recheck unexpected result ECG: tall tented T waves, small P waves, wide QRS complex and ventricular fibrillation Urine potassium, sodium and osmolality

Answer 198

Calcium gluconate – protects heart (prevents ventricular fib) Insulin + dextrose (drives potassium into cells) Salbutamol nebulised Calcium resonium

Answer 199

Treat underlying causes, review medications Polystyrene sulfonate resin, binds K+ in the gut, preventing absorption and bringing K+ levels down over a few days. If vomiting – 30g enema, followed by a 9 hour colonic irrigation Dietary potassium and loop diuretic

Answer 200

Abnormally low levels of potassium in the blood: occurs in dehydration.

Answer 201

Diuretics - hyperaldosteronism Vomiting and diarrhoea Pyloric stenosis Intestinal fistula Cushing’s syndrome/ steroids/ ACTH Conn’s syndrome Alkalosis

Answer 202

Muscle weakness Hypotonia Hyporeflexia Cramps Tetany (intermittent muscular spasms) Palpitations Light-headedness (arrhythmias) Constipation

Answer 203

Bartter syndrome (inherited defect that causes low potassium levels) Hyperthyroidism and thyrotoxicosis Metabolic alkalosis

Answer 204

If potassium <2.5mmol/L, urgent treatment is required. ECG: T wave inversion, prominent U wave Urine potassium, sodium and osmolality

Answer 205

Mild (>2.5mmol/L) Oral K+ supplement Review after 3 days

Answer 206

Severe (<2.5mmol/L) IV potassium (no more than 20mmol/h and 40mmol/L) Do not give K+ if oliguric.

Answer 207

Tumours that form from cells that release hormones into the blood in response to a signal from the nervous system.

Answer 208

Pressure on local structure e.g. optic nerves – bitemporal hemianopia Pressure on normal pituitary – hypopituitarism Functioning tumour – prolactinoma, acromegaly, Cushing’s disease

Answer 209

Lactotroph cell tumour of the pituitary

Answer 210

tumour >1cm

Answer 211

macroadenoma Headache Visual field defect (bi-temporal hemianopia) CSF leak (rare)

Answer 212

Menstrual irregularity/ amenorrhoea Galactorrhoea Infertility Loss of libido Low testosterone in men

Answer 213

Ultrasound CT MRI PET

Answer 214

Management is medical rather than surgery – use dopamine agonists such as cabergoline. Remarkable shrinkage usual with macroadenoma – sight saving Microadenoma – usually respond to small doses of cabergoline just once or twice a week

Answer 215

Catecholamine (adrenaline) secreting tumour.

Answer 216

Tumours of the chromaffin cells of the medulla that produce catecholamine

Answer 217

Episodic Headaches Palpitations Sweating Tremor Anxiety and nausea Hypertension Tachycardia Pallor

Answer 218

24 hour urine collection for urinary catecholamines and metabolites Plasma catecholamines

Answer 219

Surgery – this must be preceded by alpha and beta blocker to stagger adrenaline loss

Answer 220

Neuroendocrine tumours that particularly affect the small bowel, large bowel or appendix.

Answer 221

Carcinoid tumours are a group of tumours of enterochromaffin cell origin, capable of producing 5HT. They secrete bioactive compounds e.g. serotonin and Kallikrein which cause carcinoid syndrome. GI carcinoid tumours only cause this if they metastasise to liver.

Answer 222

Initially, few GI tumours can cause appendicitis, intussusception or obstruction. Hepatic metastases may cause RUQ pain. then clinically present as expected based on location

Answer 223

the collection of symptoms some people get when a neuroendocrine tumour (usually hepatic involvement) releases hormone such as serotonin into the blood stream.

Answer 224

Bronchoconstriction Diarrhoea Skin flushing Carcinoid crisis – when a tumour outgrows its blood supply, mediators flood out. Life-threatening vasodilation, hypotension, tachycardia, bronchoconstriction and hyperglycaemia occur.

Answer 225

Increased 24h urine 5-hydroxyindoleacetic acid (5HIAA) CXR + chest/pelvis MRI/CT to help locate primary tumours Echocardiography can be used to investigate carcinoid heart disease Liver ultrasound – confirm metastases

Answer 226

Octreotide; blocks release of tumour mediators and counters peripheral effects.

Answer 227

Loperamide for diarrhoea Tumour resection is only cure for carcinoid tumours – vital to find primary site. Debulking, embolisation or radiofrequency ablation of hepatic metastases can decrease symptoms