Endocrinology Flashcards

Question 1

Q

Define acromegaly.

Answer

A

A rare, chronic disease caused by excessive secretion of growth hormone (GH), usually due to a pituitary somatotroph adenoma.

Question 2

Q

Explain the aetiology/risk factors of acromegaly.

Answer

A

Certain familial conditions can increase the risk of getting acromegaly.

Question 3

Q

Summarise the epidemiology of acromegaly.

Answer

A

The prevalence of acromegaly is 5 per million. It usually presents between the ages of 30-50 years old.

Question 4

Q

Recognise the presenting symptoms of acromegaly. Recognise the signs of acromegaly on physical examination.

Answer

A

Coarsening of facial features Soft-tissue and skin changes Carpal tunnel syndrome Joint pain and dysfunction Snoring Alterations in sexual functioning Fatigue Hypertension, arrhythmias Organomegaly Increased appetite, polyuria/polydipsia Headaches

Question 5

Q

Identify appropriate investigations for acromegaly and interpret the results.

Answer

A

Test for IGF-1 in blood

Oral glucose tolerance test (OGTT)

Random serum growth hormone (GH)

Question 6

Q

Generate a management plan for acromegaly.

Answer

A

Transsphenoidal surgery: Treatment of choice. This is really effective. After surgery, there will be yearly follow ups by an endocrine clinic.

External irradiation: This is usually done as a follow up to a failed surgery and is more common in older patients.

Somatostatin analogue e.g. Octreotide

Question 7

Q

Identify the possible complications of acromegaly and its management.

Answer

A

Organomegaly Increased risk of DM2 Hypertension Colon polyps Osteoarthritis Carpal tunnel syndrome Hypopituitarism

Question 8

Q

Summarise the prognosis for patients with acromegaly.

Answer

A

Acromegaly is associated with serious complications and premature death. Prior to recent years with the routine implementation of more effective treatment modalities, the mean mortality estimate for acromegaly was 2- to 3-fold the expected level in the general population.

Question 9

Q

Define adrenal insufficiency.

Answer

A

Addison's disease, or primary adrenal insufficiency, is a disorder that affects the adrenal glands, causing decreased production of adrenocortical hormones (cortisol, aldosterone, and dehydroepiandrosterone). Another condition which can manifest as adrenal insufficiency is congenital adrenal hyperplasia.

Question 10

Q

Explain the aetiology/risk factors of adrenal insufficiency.

Answer

A

The most common cause of Addison’s disease worldwide is TB, however, in the UK, the most common cause is autoimmune disease.

CAH is a congenital disorder and the most common cause is the loss of the 21-hydroxylase enzyme, meaning that there is lack of production of adrenocortical hormones.

Question 11

Q

Summarise the epidemiology of adrenal insufficiency.

Answer

A

An epidemiological study of Addison’s disease carried out in Norway in 1999 showed a prevalence of 140 patients per million and a recorded mean incidence in the past decade of 0.62 per 100,000. Screening studies indicate a worldwide incidence of classical 21-hydroxylase-deficient CAH as 1 in 13,000 to 1 in 54,000 live births.

Question 12

Q

Recognise the presenting symptoms of adrenal insufficiency. Recognise the signs of adrenal insufficiency on physical examination.

Answer

A

Babies with the salt-wasting form of CAH typically presents a week after birth with severe hypotension, weight loss and inability to feed. This is a medical emergency and if the child is not treated, then it will die. Addisons’s disease can be characterised by the following signs and symptoms: Fatigue Anorexia Weight loss Hyperpigmentation Hypotension

Question 13

Q

Identify appropriate investigations for adrenal insufficiency and interpret the results.

Answer

A

A short synACTHen test is the gold standard.

Question 14

Q

Generate a management plan for adrenal insufficiency.

Answer

A

Fludrocortisone

Prednisolone

Question 15

Q

Identify the possible complications of adrenal insufficiency and its management.

Answer

A

Secondary Cushing's syndrome

Osteopenia/osteoporosis

Treatment-related hypertension

Question 16

Q

Summarise the prognosis for patients with adrenal insufficiency.

Answer

A

Patients should receive replacement therapy for life. Adherence to treatment is high, since non-compliance results in uncomfortable symptoms. Furthermore, patients know that non-compliance is potentially life-threatening.

Question 17

Q

Define carcinoid syndrome.

Answer

A

Carcinoid syndrome occurs due to release of serotonin (5-hydroxytryptamine) and other vasoactive peptides into the systemic circulation from a carcinoid tumour. A carcinoid tumour is a neuroendocrine tumour.

Question 18

Q

Explain the aetiology/risk factors of carcinoid syndrome.

Answer

A

Genetic multiple endocrine neoplasia type 1 (MEN-1) syndrome

Question 19

Q

Summarise the epidemiology of carcinoid syndrome.

Answer

A

The incidence of carcinoid syndrome in a population in central Sweden was estimated as being approximately 0.5 per 100,000 population per year.

Question 20

Q

Recognise the presenting symptoms of carcinoid syndrome. Recognise the signs of carcinoid syndrome on physical examination.

Answer

A

Diarrhoea Flushing Palpitations Abdominal cramps Telangiectasia Signs of right heart failure Cardiac murmurs Hepatomegaly

Question 21

Q

Identify appropriate investigations for carcinoid syndrome and interpret the results.

Answer

A

Serum chromogranin A/B Urinary 5-hydroxyindoleacetic acid Metabolic panel Liver function tests Full blood count

Question 22

Q

Define Cushing’s syndrome.

Answer

A

Cushing’s syndrome is caused by excessive steroids in the body. This may be due to many different causes such as a pituitary adenoma secreting too much ACTH or exogenous steroids from medication.

Question 23

Q

Explain the aetiology/risk factors of Cushing’s syndrome.

Answer

A

Exogenous corticosteroid use Pituitary adenoma Adrenal adenoma Adrenal carcinoma

Question 24

Q

Summarise the epidemiology of Cushing’s syndrome.

Answer

A

Cushing syndrome is relatively uncommon in the general population. However, newer studies of high-risk groups report a significantly greater prevalence. Hypercortisolism has been reported in 0.5% to 1% of patients with hypertension, 2% to 3% of patients with uncontrolled diabetes, 6% to 9% of patients with adrenal masses, and 11% of patients with osteoporosis and vertebral fractures.

Question 25

Q

Recognise the presenting symptoms of Cushing’s syndrome. Recognise the signs of Cushing’s syndrome on physical examination.

Answer

A

“Moon” Round face Interscapular fat pad Centripetal obesity Striae Menstrual irregularities

Question 26

Q

Identify appropriate investigations for Cushing’s syndrome and interpret the results.

Answer

A

9am cortisol High dose dexamethasone suppression test Low dose dexamethasone suppression test 24 hour urinary free cortisol

Question 27

Q

Generate a management plan for Cushing’s syndrome.

Answer

A

Reduce exogenous steroids Transsphenoidal hypophysectomy Bilateral adrenalectomy

The treatment depends on the cause of the Cushing’s.

Question 28

Q

Identify the possible complications of Cushing’s syndrome and its management.

Answer

A

Adrenal insufficiency secondary to adrenal suppression Cardiovascular disease Hypertension Diabetes mellitus Osteoporosis Nephrolithiasis Hypopituitarism

Question 29

Q

Summarise the prognosis for patients with Cushing’s syndrome.

Answer

A

Untreated disease carries a dismal survival rate of 50% at 5 years.

Within the first year of effective therapy, many of the characteristic features will resolve or show marked improvement.

Despite improvement of complications in most patients, cardiovascular risk, hypertension, obesity, and decreased quality of life may persist in some patients even after biochemical cure.

Question 30

Q

Define diabetes insipidus.

Answer

A

Diabetes insipidus (DI) is a metabolic disorder characterised by defective ability to concentrate urine in the kidneys, resulting in the production of large quantities of dilute urine.

Question 31

Q

Explain the aetiology/risk factors of diabetes insipidus.

Answer

A

Iatrogenic Idiopathic Drug induced Pituitary surgery

Question 32

Q

Summarise the epidemiology of diabetes insipidus.

Answer

A

DI is uncommon, although the exact prevalence in the general population is difficult to estimate. For both central DI and nephrogenic DI, there are no clear differences in prevalence between genders or among ethnic groups.

Question 33

Q

Recognise the presenting symptoms of diabetes insipidus. Recognise the signs of diabetes insipidus on physical examination.

Answer

A

Polyuria Polydipsia Nocturia CNS symptoms of hyponatraemia

Question 34

Q

Identify appropriate investigations for diabetes insipidus and interpret the results.

Answer

A

BM Water deprivation test without ADH Water deprivation test with ADH Serum salts

Question 35

Q

Generate a management plan for diabetes insipidus.

Answer

A

Desmopressin: V2 agonist IV or oral fluids may be given in acute complications.

Question 36

Q

Identify the possible complications of diabetes insipidus and its management.

Answer

A

Hypernatraemia Thrombosis Bladder and renal dysfunction Iatrogenic hyponatraemia

Question 37

Q

Summarise the prognosis for patients with diabetes insipidus.

Answer

A

Diabetes insipidus is a life-long condition but most patients are well controlled on DDAVP.

Question 38

Q

Define diabetic ketoacidosis.

Answer

A

Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment. It is characterised by absolute insulin deficiency and is the most common acute hyperglycaemic complication of type 1 diabetes mellitus.

Question 39

Q

Explain the aetiology/risk factors of diabetic ketoacidosis.

Answer

A

Poor control of DM (particularly type I) Infection MI

Question 40

Q

Summarise the epidemiology of diabetic ketoacidosis.

Answer

A

In England, the incidence of hospital admissions for DKA among adults with type 2 diabetes increased 4.24% annually between 1998 and 2013; hospitalisations for DKA in adults with type 1 diabetes increased from 1998 to 2007, and remained static until 2013.

Question 41

Q

Recognise the presenting symptoms of diabetic ketoacidosis.

Answer

A

Polyuria Polyphagia Polydipsia Weight loss Weakness Nausea or vomiting Abdominal pain

Question 42

Q

Recognise the signs of diabetic ketoacidosis on physical examination.

Answer

A

Dry mucous membranes Poor skin turgor Sunken eyes Tachycardia Hypotension Acetone breath Altered mental status

Question 43

Q

Identify appropriate investigations for diabetic ketoacidosis and interpret the results.

Answer

A

U+Es BM Serum salts (sodium, potassium, magnesium) Urinalysis LFTs ABG Serum lactate Serum amylase Serum osmolality FBC

Question 44

Q

Generate a management plan for diabetic ketoacidosis.

Answer

A

Fluid replacement: IV or oral fluids until rehydrated. This replaces the fluid lost through excessive urination as well as dilutes the excess ketones in the blood.

Electrolyte replacement: The absence of insulin can decrease the level of several electrolytes in blood. IV electrolyte is usually given.

Insulin therapy: Insulin reverses the processes that cause diabetic ketoacidosis. Once BM falls to about 11.1 mmol/L, stop IV insulin and resume normal insulin therapy.

Question 45

Q

Identify the possible complications of diabetic ketoacidosis and its management.

Answer

A

Hypoglycaemia Hypokalaemia Arterial or venous thromboembolic events Non-anion gap hyperchloremic acidosis Cerebral oedema/brain injury Acute respiratory distress syndrome (ARDS)

Question 46

Q

Summarise the prognosis for patients with diabetic ketoacidosis.

Answer

A

The mortality rate is 5% in experienced centres. Death is rarely caused by the metabolic complications of hyperglycaemia or ketoacidosis but rather relates to the underlying illness. The prognosis is substantially worsened at the extremes of age and in the presence of coma and hypotension.

Question 47

Q

Define diabetes mellitus type 1.

Answer

A

Type 1 diabetes mellitus is a metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency. The condition develops due to destruction of pancreatic beta cells, mostly by immune-mediated mechanisms.

Question 48

Q

Explain the aetiology/risk factors of diabetes mellitus type 1.

Answer

A

Geographical region Genetic predisposition Infectious agents

Question 49

Q

Summarise the epidemiology of diabetes mellitus type 1.

Answer

A

Type 1 diabetes accounts for about 5% to 10% of all patients with diabetes. It is the most commonly diagnosed diabetes of youth (under 20 years of age) and causes ≥85% of all diabetes cases in this age group worldwide.

Question 50

Q

Recognise the presenting symptoms of diabetes mellitus type 1. Recognise the signs of diabetes mellitus type 1 on physical examination.

Answer

A

Polyuria Polydipsia Young age Weight loss Blurred vision Nausea and vomiting Abdominal pain Tachypnoea Lethargy

Question 51

Q

Identify appropriate investigations for diabetes mellitus type 1 and interpret the results.

Answer

A

Random plasma glucose Fasting plasma glucose 2-hour plasma glucose Plasma or urine ketones HbA1c

Question 52

Q

Generate a management plan for diabetes mellitus type 1.

Answer

A

1st line: Basal-bolus insulin

Adjunct: Pre-meal insulin correction dose Amylin analogue Fixed-dose insulin

Question 53

Q

Identify the possible complications of diabetes mellitus type 1 and its management.

Answer

A

Diabetic ketoacidosis (DKA) Hypoglycaemia Retinopathy Diabetic kidney disease Peripheral or autonomic neuropathy Cardiovascular disease

Question 54

Q

Summarise the prognosis for patients with diabetes mellitus type 1.

Answer

A

Untreated type 1 diabetes is a fatal condition due to diabetic ketoacidosis. Poorly controlled type 1 diabetes is a risk factor for chronic complications such as blindness, renal failure, foot amputations, and heart attacks.

Question 55

Q

Define diabetes mellitus type 2.

Answer

A

Type 2 diabetes mellitus is a progressive disorder defined by deficits in insulin secretion and action that lead to abnormal glucose metabolism and related metabolic derangements.

Question 56

Q

Explain the aetiology/risk factors of diabetes mellitus type 2.

Answer

A

Older age Overweight/obesity Gestational diabetes Pre-diabetes Family history of type 2 diabetes Non-white ancestry Physical inactivity Polycystic ovary syndrome Hypertension Dyslipidaemia Cardiovascular disease Stress

Question 57

Q

Summarise the epidemiology of diabetes mellitus type 2.

Answer

A

Diabetes prevalence is increasing worldwide, compounded by population growth and an ageing population. In 1980, the global age-standardised diabetes prevalence was 4.3%.

Question 58

Q

Recognise the presenting symptoms of diabetes mellitus type 2. Recognise the signs of diabetes mellitus type 2 on physical examination.

Answer

A

Asymptomatic Candidal infections Skin infections Urinary tract infections Fatigue Blurred vision Polydipsia Polyphagia Polyuria Paraesthesias Nocturia Unintentional weight loss Acanthosis nigricans

Question 59

Q

Identify appropriate investigations for diabetes mellitus type 2 and interpret the results.

Answer

A

HbA1c Fasting plasma glucose Random plasma glucose 2-hour post-load glucose after 75g oral glucose

Question 60

Q

Generate a management plan for diabetes mellitus type 2.

Answer

A

1. Lifestyle and metformin

2. Sulphonylureas + Insulin

3. Glitazones

SGLT2 inhibitors, GLP-1 agonists, DPP-4 inhibitors are used after this.

Question 61

Q

Summarise the prognosis for patients with diabetes mellitus type 2.

Answer

A

Diabetes increases the likelihood of major cardiovascular events and death, but the increased risk is variable across patients depending on age at diabetes onset, duration of diabetes, glucose control, blood pressure control, lipid control, tobacco control, renal function, microvascular complication status, and other factors.

Question 62

Q

Define Graves' disease.

Answer

A

Graves' disease is an autoimmune thyroid condition associated with hyperthyroidism.

Question 63

Q

Explain the aetiology/risk factors of Graves' disease.

Answer

A

Other autoimmune conditions Tobacco use

Question 64

Q

Summarise the epidemiology of Graves' disease.

Answer

A

In the UK the incidence of clinical hyperthyroidism was shown to be 0.8/1000 women a year, with a negligible incidence in men. Graves' disease is the most common form of hyperthyroidism in most areas of the world.

Answer 65

A

Irritability Wide pulse pressure Cardiac flow murmur Moist, velvety skin Scalp hair loss

Answer 66

A

TSH Serum free or total T4 Serum free or total T3 Calculation of total T3/T4 or FT3/FT4 ratio

Answer 67

A

Hypogonadism in males is a clinical syndrome that comprises symptoms and/or signs, along with biochemical evidence of testosterone deficiency.

Answer 68

A

Genetic anomaly Type 2 diabetes mellitus Use of alkylating agents, opioids, or glucocorticoids Use of exogenous sex hormones and GnRH analogues Hyperprolactinaemia Pituitary tumour or apoplexy Critical illness Testicular damage

Answer 69

A

The prevalence of hypogonadism increases with age. About a quarter of the US male population have total testosterone levels that are below 10.4 nanomol/L (<300 nanograms/dL) (considered by many experts to be the lower end of normal).

Answer 70

A

Decreased libido Loss of spontaneous morning erections Erectile dysfunction Gynaecomastia Infertility Decreased energy and fatigue Delayed puberty Decreased muscle mass and strength Loss of axillary and pubic hair Lack of facial hair Poor concentration and memory Depressed moo Sleep disturbance Hot flushes and sweats Increasing BMI Tall stature Fine wrinkling of facial skin

Answer 71

A

Serum total testosterone Serum sex hormone binding globulin (SHBG) Serum free testosterone Serum LH/FSH

Answer 72

A

Hypopituitarism refers to the partial or complete deficiency of one or more pituitary hormones. It may arise as a congenital defect during the development of the pituitary gland or as a result of acquired diseases of the pituitary gland, the parasellar structures, or the hypothalamus.

Answer 73

A

Pituitary tumour Pituitary apoplexy Pituitary surgery Cranial radiation Traumatic brain injury Genetic defects Hypothalamic disease

Answer 74

A

Hypopituitarism is relatively rare, with a prevalence of 45 cases per 100,000 and an incidence of about 4 cases per 100,000 per year in the normal population.

Answer 75

A

Presence of risk factors Headaches Failure to thrive or short stature Infertility Hypoglycaemia Amenorrhoea/oligomenorrhoea Galactorrhoea Delayed puberty Hypotension Visual field defects Ophthalmoplegia Cardiovascular events Cold intolerance Weight gain Erectile dysfunction and reduced libido Nausea/vomiting Fatigue Weakness Dizziness Constipation Dry skin Delayed relaxation of reflexes

Answer 76

A

Serum electrolytes Serum and urine osmolarity 8 a.m. cortisol and adrenocorticotrophic hormone Thyroid function tests 8 a.m. testosterone, follicle-stimulating hormone, and luteinising hormone in men Oestradiol, follicle-stimulating hormone, and luteinising hormone in women Prolactin Insulin-like growth factor-1 Cosyntropin/tetracosactide stimulation test

Answer 77

A

Treat underlying cause. Treat pituitary apoplexy with IV hydrocortisone.

Answer 78

A

Male infertility Female infertility Corticosteroid over-replacement Thyroxine over-replacement Desmopressin over-replacement Growth hormone over-replacement Testosterone over-replacement

Answer 79

A

Hypopituitarism has been associated with a 1.8-fold higher mortality compared with an age- and sex-matched population. Cardiovascular and cerebrovascular death rates are higher in patients with hypopituitarism compared with the normal population.

Answer 80

A

Hypothyroidism is a clinical state resulting from underproduction of the thyroid hormones thyroxine (T4) and triiodothyronine (T3). Most cases (95%) are due to primary hypothyroidism, a failure of the thyroid gland to produce thyroid hormones.

Answer 81

A

Iodine deficiency Family history of autoimmune thyroiditis Autoimmune disorders Graves' disease Post-partum thyroiditis Turner's and Down's syndromes Primary pulmonary hypertension Multiple sclerosis Radiotherapy Amiodarone use Lithium use

Answer 82

A

The incidence of primary hypothyroidism in the UK is estimated to be 0.41% per year for women and 0.06% per year in men. It is more common in middle aged women.

Answer 83

A

Weakness Lethargy Cold sensitivity Constipation Weight gain Depression Menstrual irregularity Myalgia Dry or coarse skin Eyelid oedema Thick tongue Bradycardia Deep voice Goitre

Answer 84

A

Serum thyroid-stimulating hormone (TSH) Free serum T4 Serum cholesterol FBC Fasting blood glucose

Answer 85

A

Levothyroxine

Answer 86

A

Angina Resistant hypothyroidism Atrial fibrillation Osteoporosis Myxoedema coma Complications in pregnancy

Answer 87

A

Prognosis is generally excellent with full recovery upon adequate replacement of thyroid hormones. The levothyroxine replacement dose may change over a period of years as the disease progresses or other conditions affecting thyroid hormone metabolism develop, but achieving excellent control of the disease is generally easily accomplished.

Answer 88

A

Multiple endocrine neoplasia (MEN) syndromes are hereditary tumour syndromes of variable neoplastic patterns and characterised by the development of multiple endocrine tumours.

Answer 89

A

Familial cases of MEN RET proto-oncogene mutation MEN1 (menin) mutation

Answer 90

A

MEN syndromes are relatively rare.

Answer 91

A

Young age (MEN1/2) Positive family history (MEN1/2) Episodic triad of sweating, palpitations, and headache (MEN2) Clinical features of kidney stones (MEN1/2) Facial angiofibromas or collagenomas (MEN1) Mucosal neuromas (MEN2B) Arm span and upper-to-lower-body-segment ratio (MEN2B) Palpable thyroid nodule (MEN2) Irregular menses (MEN1) Visual changes (MEN1) Unexplained flushing (MEN2) Infertility (MEN1) Clinical features of acromegaly (MEN1) Clinical features of thyrotoxicosis (MEN1)

Answer 92

A

Serum calcitonin (MEN2) Serum carcinoembryonic antigen (MEN2) Plasma metanephrines (MEN2) Serum parathyroid hormone and calcium (MEN1/2) Fasting serum gastrin (MEN1) Serum chromogranin A (MEN1) Serum prolactin (MEN1) Insulin-like growth factor-1 (MEN1) 24-hour urine metanephrines and catecholamines (MEN2) 24-hour urine calcium (MEN1/2) Thyroid biopsy (MEN2)

Answer 93

A

Pituitary adenomas are the third most common intracranial neoplasms in adults, accounting for about 10% of all intracranial tumours. They are diagnosed when patients present with hormone hypersecretion, plus visual and neurological deficits and hypopituitarism as a result of mass effect.

Answer 94

A

Multiple endocrine neoplasia type 1 (MEN-1) Familial isolated pituitary adenomas (FIPA) Carney complex (CNC)

Answer 95

A

Pituitary adenomas are the third most common intracranial neoplasms (behind meningiomas and astrocytomas), accounting for about 10% of all intracranial tumours in adults. There is no known sex or racial difference in prevalence. The prevalence of pituitary adenoma varies from 19 to 28 cases per 100,000, in the UK.

Answer 96

A

Headaches Erectile dysfunction Gynaecomastia Amenorrhoea Infertility Loss of libido Hot flushes Fatigue Nausea/vomiting Bitemporal hemianopia

Answer 97

A

Prolactin Insulin-like growth factor 1 LH, FSH Testosterone/oestradiol Thyroid-stimulating hormone, free thyroxine Morning cortisol ACTH stimulation test Insulin tolerance test for cortisol Basic metabolic panel FBC MRI pituitary with gadolinium enhancement Contrast enhanced CT pituitary

Answer 98

A

Obesity can be defined as a chronic adverse condition due to an excess amount of body fat. While there are many methods to determine the relative amount of body fat, the most widely used method to determine obesity is the BMI. BMI >30

Answer 99

A

Hypothyroidism Hypercortisolism Corticosteroid therapy

Answer 100

A

In 2008, 24% of men and 25% of women aged 16 years or over in England were classified as obese (BMI ≥30 kg/m^2).

Answer 101

A

Height Weight Waist circumference Hip circumference Comorbid conditions

Answer 102

A

Clinical exam

Answer 103

A

Osteomalacia is a metabolic bone disease characterised by incomplete mineralisation of the underlying mature organic bone matrix (osteoid) following growth plate closure in adults.

Answer 104

A

Dietary calcium and vitamin D deficiency Chronic kidney disease Limited sunlight exposure Inherited disorders of vitamin D and bone metabolism Hypophosphatasia Anticonvulsant therapy

Answer 105

A

In the US and Europe, more than 40% of the adult population older than age 50 years are vitamin D deficient, this being the most prominent cause of osteomalacia. In developing countries, such as Tibet and Mongolia, vitamin D deficiency leading to clinical rickets is reported in 60% of infants.

Answer 106

A

Old age Vitamin D and calcium deficient diets Lack of sunlight exposure Fractures Malabsorption syndromes Diffuse bone pain and tenderness Proximal muscle weakness Family history of osteomalacia Waddling gait

Answer 107

A

Serum calcium level Serum 25-hydroxyvitamin D level Serum phosphate level Serum urea and creatinine Intact PTH Serum alkaline phosphatase 24-hour urinary calcium

Answer 108

A

Osteoporosis is a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue, resulting in increased bone fragility and susceptibility to fracture.

Answer 109

A

Prior fragility fracture Female sex White ancestry Older age (>50 years for women and >65 years for men) Low BMI Postmenopause Secondary amenorrhoea Primary hypogonadism Smoking Excessive alcohol use Prolonged immobilisation Low calcium intake Vitamin D deficiency Glucocorticoid excess Corticosteroid use

Answer 110

A

In the UK and Europe, fractures caused by osteoporosis affect 1 in 2 women and 1 in 5 men aged >50 years.

Answer 111

A

Back pain Kyphosis Impaired vision Impaired gait, imbalance, and lower-extremity weakness Vertebral tenderness

Answer 112

A

DXA scan Serum alkaline phosphatase Serum calcium Serum 25-hydroxy vitamin D Serum parathyroid hormone Thyroid function tests

Answer 113

A

A chronic bone disorder that is characterised by focal areas of increased bone remodelling, resulting in overgrowth of poorly organised bone. This unbalanced process may lead to osseous deformities, altered joint biomechanics, nerve compressions, and pathological fractures.

Answer 114

A

Family history of Paget's disease Age >50 years Male sex (45- to 74-years age group) Infection Environmental factors

Answer 115

A

It is the second most common chronic bone-remodelling disorder after osteoporosis. The majority of cases are sporadic, but between 5% and 40% of patients report a first-degree relative with Paget's disease of bone.

Answer 116

A

Asymptomatic Femoral, pelvis, and/or skull involvement Long-bone or back pain Pathological fracture Bony deformities (e.g., frontal bossing, prognathism, bone bowing) Increased local temperature Hearing loss

Answer 117

A

Plain x-ray Bone scan Total serum alkaline phosphatase Bone-specific alkaline phosphatase Serum calcium Serum procollagen 1 N-terminal peptide (P1NP) Serum C-terminal propeptide of type 1 collagen (CTX) LFTs Serum 25-hydroxyvitamin D

Answer 118

A

A tumour arising from catecholamine-producing chromaffin cells of the adrenal medulla that classically presents with headaches, diaphoresis, and palpitations in the setting of paroxysmal hypertension.

Answer 119

A

Multiple endocrine neoplasia (MEN) syndrome type 2A and B Von Hippel-Lindau (VHL) disease Succinate dehydrogenase (SDH) subunits B, C, and D gene mutations

Answer 120

A

Phaeochromocytoma is a rare condition; the annual incidence in the general population is around 0.6 per 100,000 person-years.

Answer 121

A

Headache Palpitations Diaphoresis Hypertension Hypertensive retinopathy Pallor Impaired glucose tolerance/diabetes mellitus Tachyarrhythmias and myocardial infarction Panic attacks or a 'sense of doom' Orthostatic hypotension Hypercalcaemia Diarrhoea

Answer 122

A

24-hour urine collection for catecholamines, metanephrines, normetanephrines, and creatinine

Serum free metanephrines and normetanephrines

Plasma catecholamines

Genetic testing

Answer 123

A

Polycystic ovary syndrome (PCOS) includes symptoms of hyper-androgenism, irregular or absent periods, and polycystic ovaries on ultrasound. PCOS is a spectrum; some patients can exhibit symptoms of PCOS.

Answer 124

A

Family history of PCOS Premature adrenarche Low birth weight Fetal androgen exposure Obesity Environmental endocrine disruptors

Answer 125

A

PCOS affects 6% to 8% of women of reproductive age in the US (using the 1990 National Institutes of Health criteria); symptoms generally start at the time of puberty.

Answer 126

A

Acne Overweight or obesity Hypertension Scalp hair loss Oily skin or excessive sweating Acanthosis nigricans

Answer 127

A

USS Ovaries Serum androgens Serum testosterone and DHEAS Serum prolactin Serum TSH

Answer 128

A

In primary aldosteronism (PA), aldosterone production exceeds the body's requirements and is relatively autonomous with regard to its normal chronic regulator, the renin-angiotensin II system.

Answer 129

A

Family history of PA Family history of early onset of hypertension and/or stroke

Answer 130

A

For many years, PA was considered a rare (<1%) cause of hypertension and not worth seeking unless hypokalaemia was present. However, since 1992, evidence has accumulated that PA is much more common than was previously thought, and that most patients are normokalaemic.

Answer 131

A

Hypertension Age 20 to 70 years Nocturia, polyuria Lethargy Mood disturbance (irritability, anxiety, depression) Difficulty concentrating

Answer 132

A

Plasma potassium Aldosterone/renin ratio

Answer 133

A

Aldosterone antagonists Unilateral adrenalectomy

Answer 134

A

Perioperative complications Stroke Myocardial infarction Heart failure Atrial fibrillation Impaired renal function Aldosterone antagonist- or mineralocorticoid receptor antagonist-induced hyperkalaemia

Answer 135

A

Patients undergoing unilateral adrenalectomy for unilateral PA: This procedure leads to cure of hypertension in 50% to 60% of carefully selected patients and improvement in all of the remainder.

Answer 136

A

Primary hyperparathyroidism (PHPT) is an endocrine disorder in which autonomous overproduction of parathyroid hormone (PTH) results in derangement of calcium metabolism.

Answer 137

A

Female sex Age ≥50-60 years Family history of PHPT Multiple endocrine neoplasia (MEN) 1, 2A, or 4 Current or historical lithium treatment Hyperparathyroidism-jaw tumour syndrome

Answer 138

A

Primary hyperparathyroidism is a relatively common disorder affecting 1 in 500 women and 1 in 2000 men aged over 40 years. A population-based study suggested 2% of post-menopausal women have PHPT, with the disorder being the most common cause of hypercalcaemia in outpatients.

Answer 139

A

History of osteoporosis or osteopenia Bone pain Poor sleep Fatigue Anxiety Depression Memory loss Myalgias Paraesthesias Muscle cramps Constipation

Answer 140

A

Serum calcium Serum intact PTH with immunoradiometric or immunochemical assay

Answer 141

A

1st line: Parathyroidectomy Adjunct: Vitamin D supplementation

2nd line: Monitoring Adjunct: Bisphosphonate Cinacalcet Vitamin D supplementation

Answer 142

A

Neck haematoma following surgery Recurrent and superior laryngeal nerve injury following surgery Hypocalcaemia following surgery Pneumothorax following surgery Osteoporosis Bone fractures Nephrolithiasis

Answer 143

A

For asymptomatic patients who do not meet the criteria for surgical intervention, 75% have stable disease for up to 10 years. Twenty-five percent of patients progress to meeting criteria for parathyroidectomy. Parathyroidectomy has a cure rate of over 95% and as high as 99% in expert hands.

Answer 144

A

Prolactinomas are benign lactotroph adenomas expressing and secreting prolactin.

Answer 145

A

Female gender, 20 to 50 years of age Genetic predisposition Oestrogen therapy Male gender, 30 to 60 years of age

Answer 146

A

Prolactinomas are the most common type of pituitary adenoma, constituting about 40% of these tumours.

Answer 147

A

Amenorrhoea or oligomenorrhoea Infertility Galactorrhoea Loss of sexual desire (libido) Erectile dysfunction Visual deterioration (e.g., temporal hemianopia) Osteoporosis

Answer 148

A

Serum prolactin Pituitary MRI Computerised visual-field examination

Answer 149

A

Cabergoline/bromocriptine Octreotide Transsphenoidal hypophysectomy

Answer 150

A

Visual field impairment Anterior pituitary failure and/or diabetes insipidus Hypopituitarism associated with radiotherapy Cabergoline-associated valvular insufficiency Pituitary apoplexy Cerebrospinal fluid leakage

Answer 151

A

This benign disease follows a progressive improving course while medically treated. In some patients, dopamine agonist treatment may be withdrawn after several years without tumour recurrence.

Answer 152

A

Any disorder that results in hypocalcaemia will elevate parathyroid hormone levels and can serve as a cause of secondary hyperparathyroidism. The most frequent causes of the condition are chronic kidney disease (CKD), malabsorption syndromes, and chronic inadequate sunlight exposure, acting via alterations in vitamin D, phosphorus, and calcium.

Answer 153

A

Ageing Chronic renal failure Vitamin D deficiency: inadequate sunlight exposure Nutritional deficiency (especially absence of dairy products and fish) Vitamin D deficiency: malabsorption

Answer 154

A

Twenty-six million American adults have CKD and millions of others are at increased risk of vitamin D deficiency. Over 60% of these patients are at risk for the development of secondary hyperparathyroidism. Virtually all dialysis-dependent chronic renal failure patients develop secondary hyperparathyroidism.

Answer 155

A

Features of chronic renal failure Features of underlying malabsorption syndrome Muscle cramps and bone pain Perioral tingling or paresthesia in fingers or toes Chvostek's sign Trousseau's sign Bowed legs or knock knees Fractures

Answer 156

A

Serum calcium Serum intact parathyroid hormone (iPTH) Serum creatinine Serum urea nitrogen

Answer 157

A

Treat the cause. Apart from CKD, most causes can be treated with better nutrition and vitamin D supplementation.

Answer 158

A

Osteodystrophy Osteoporosis Uraemia Calciphylaxis

Answer 159

A

The patient outlook for secondary hyperparathyroidism mirrors the underlying disease. In patients with chronic kidney disease, aggressive electrolyte management will help optimise the situation; many patients will require calcimimetics, a treatment that has reduced the frequency of surgery for this condition.

Answer 160

A

The syndrome of inappropriate antidiuretic hormone (SIADH) is characterised by hypotonic hyponatraemia, concentrated urine, and a euvolemic state.

Answer 161

A

Age >50 years Pulmonary conditions (e.g., pneumonia) Nursing home residence Malignancy Medicine associated with SIADH induction Central nervous system (CNS) disorder

Answer 162

A

A report of 184 episodes of severe hyponatraemia (reported as ≤120 mmol/L [≤120 mEq/L]) in hospitals across the US and UK found that in 21% of people the condition was of acute duration and in 79% it was of chronic duration.

Answer 163

A

Absence of hypovolaemia Absence of hypervolaemia Absence of signs of adrenal insufficiency or hypothyroidism Nausea/vomiting Altered mental status Headache Seizure Coma

Answer 164

A

Serum sodium Serum osmolality Serum urea Urine osmolality Urine sodium

Answer 165

A

Fluid restriction Furosemide Vaptans

Answer 166

A

Central pontine myelinolysis (CPM or osmotic demyelination syndrome)

Answer 167

A

The brain adapts slowly to hyponatraemia by secretion of intracellular solutes such as sodium and potassium initially, followed by amino acids and myoinositol (organic osmolytes). Overcorrection of hyponatraemia can subject solute-poor cerebral cells to shrinkage and CPM.

Answer 168

A

If the underlying cause is found and treated successfully, SIADH typically resolves. If the underlying condition persists, SIADH is difficult to manage, secondary to difficulty complying with necessary fluid restriction or medicines.

Answer 169

A

Cancer of the thyroid gland. Four types account for more than 98% of thyroid malignancies: papillary, follicular, anaplastic, and medullary.

Answer 170

A

Head and neck irradiation Female sex

Answer 171

A

Thyroid cancer is the most common endocrinological malignancy and is more common in women than in men. Thyroid cancer is notable in that rates of new thyroid cancer cases have been rising over the past few decades.

Answer 172

A

Palpable thyroid nodule Early adulthood Hoarseness Dyspnoea Dysphagia Tracheal deviation Cervical lymphadenopathy Rapid neck enlargement

Answer 173

A

TSH Fine-needle biopsy Ultrasound, neck Laryngoscopy

Answer 174

A

Viral thyroiditis is a self-limited inflammation of the thyroid gland. It is associated with a triphasic clinical course that lasts for a few weeks to many months, characterised by transient thyrotoxicosis, hypothyroidism, and then a return to normal thyroid function in >90% of patients.

Answer 175

A

Viral infection

Answer 176

A

There does not seem to be any global difference in epidemiology. The overall age- and sex-adjusted annual incidence rate calculated for one state in the US was estimated to be 4.9 cases per 100,000.

Answer 177

A

Neck pain Tender, firm, enlarged thyroid Fever Palpitations Recent viral infection Myalgia Malaise Tremor Heat intolerance

Answer 178

A

Thyroid-stimulating hormone (TSH) Total T4, total T3, T3 resin uptake, free thyroxine index T3:T4 ratio Radioactive iodine uptake ESR CRP Antithyroid antibodies (thyroid peroxidase antibodies)

Answer 179

A

Thyroid pain and tenderness: Analgesic or corticosteroid Tachycardia or anxiety or tremor: Beta-blocker or calcium-channel blocker Severe thyrotoxicosis: Potassium iodide plus prednisolone

Answer 180

A

Thyroid storm Long-term hypothyroidism

Answer 181

A

In ≥90% of patients, there is a complete and spontaneous recovery and a return to normal thyroid function. However, the thyroid gland may exhibit irregular scarring between islands of residual functioning parenchyma. Up to 10% of patients may require permanent replacement with levothyroxine due to persistent hypothyroidism.

Brainscape's Knowledge GenomeTM

Endocrinology Flashcards

Brainscape's Knowledge Genome^TM