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Phase 3 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Describe the pathophysiology, investigation and management of thyroid eye disease

A

Typically associated with Grave’s, but patients can be euthyroid, hypothyroid or hyperthyroid at presentation

Can be worsened by treatment, particularly radioiodine

Retro-orbital inflammation and lymphocyte infiltration results in swelling of the orbit

Eye discomfort, diplopia, exophthalmos, proptosis, lid retraction

Diagnose clinically

Treat hyper or hypothyroidism, avoid smoking, artificial tears, treat other symptoms

In later disease, high dose steroid may be used and surgery may be required

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2
Q

Describe symptoms of diabetes

A
  • Glycosuria - Depletion of Energy Stores
    • Tiredness, Weakness, Weight Loss, Difficulty Concentrating, Irritability
  • Glycosuria - Osmotic Diuresis
    • Polyuria, Polydipsia, Dry Mucous Membranes, Reduced Skin Turgor, Postural Hypotension
  • Glucose Shifts - Swollen Ocular Lenses
    • Blurred Vision
  • Ketone Production
    • Nausea, Vomiting, Abdominal Pain, Heavy/Rapid Breathing, Acetone Breath, Drowsiness, Coma
  • Depletion of Energy Stores
    • Weakness, Polyphagia, Weight Loss, Growth Retardation in Young
  • Complications
    • Macrovascular, Microvascular, Neuropathy, Infection
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3
Q

Define diabetes

A

“a metabolic disorder of multiple aetiology characterized by chronic hyperglycaemia with disturbances of carbohydrate, protein and fat metabolism resulting from defects in insulin secretion, insulin action, or both”

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4
Q

Describe the clinical effects of vitamin D deficiency

A

Can be due to poor sunlight exposure, malabsorption, gastrectomy, renal disease or enzyme-inducing drugs

Can result in osteomalacia in adulthood

Failure to ossify bones in adulthood as a result of Vit D deficiency

Presents insidiously with bone pain, proximal myopathy and hypocalcaemia

Characterised by low calcium, low phosphate, high ALP, low Vit D, elevated PTH

Treat with vitamin D replacement (cholecalciferol or alfacalcidol)

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5
Q

Describe Latent Autoimmune Diabetes of Adulthood

A

Age of onset >25yrs

Obesity is rare

Insulin usually required within months or years of diagnosis

Polygenic inheritance

GAD antibodies

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6
Q

Describe the pathophysiology, investigation and management of hyperprolactinaemia

A

Can be caused by prolactin-releasing pituitary tumours

Clinical features include galactorrhoea, headaches, mass effect, visual field defects, amenorrhoea, erectile dysfunction

Diagnose with serum prolactin (usually >6000) and pituitary MRI

Remaining pituitary function should also be tested (gonadal and thyroid hormones)

Treat with dopamine agonists (e.g. cabergoline, bromocriptine) as dopamine has a negative feedback mechanism on prolactin secretion

Surgery only indicated if medical therapy fails

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7
Q

Describe Whipple’s triad

A

collection of three criteria that suggest a patient’s symptoms result from hypoglycemia that may indicate insulinoma

  1. Low Plasma Glucose
  2. Symptoms Consistent with Hypoglycaemia
  3. Relief of Symptoms when Glucose is Raised to Normal
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8
Q

Describe the treatment of hypoglycaemia

A
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9
Q

Describe the pathophysiology, investigation and management of hyperthyroidism

A

Most commonly due to an autoimmune disease (Grave’s)

Symptoms include diarrhoea, weight loss, sweats, heat intolerance, palpitations, tremor

Signs include tachycardia, AF, lid lag, lid retraction, goitre, bruit, thyroid eye disease, pretibial myxoedema, thyroid acropachy

Investigate with TSH (suppressed) and Free T4 (elevated)

May also consider thyroid auto-antibodies and iodine uptake scan

Manage with beta-blockers and ‘block and replace’ with carbimazole and levothyroxine simultaneously

May require radio-iodine or thyroidectomy

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10
Q

Describe the normal physiological role and regulation of calcium

A

Functions include muscle contraction, membrane stabilisation, bone growth and remodelling, enzyme co-factor, secondary signalling messenger, hormone secretion

Most calcium is found in the skeleton, some intracellularly and some extracellularly (free or albumin-bound)

Regulated chiefly by parathyroid hormone, which raises blood calcium by increasing reabsorption at the renal distal tubule; increasing osteoclast activity; and increasing Vit D synthesis which increases calcium absorption from the gut

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11
Q

Describe the pathophysiology, investigation and management of Kallmann’s syndrome

A

A cause of primary hypogonadotropic hypogonadism

Most common form of isolated gonadotropin-releasing hormone deficiency

Due to a failure of cell migration of GnRH cells to the hypothalamus from the olfactory placode

Associated with anosmia and colour blindness

May have micropenis and cryptorchidism

Familial with variable penetration (X-Linked, Autosomal Dominant or Autosomal Recessive)

Diagnosed with clinical exam (usually due to delayed puberty) and hormone profile (LH, FSH, GnRH)

Treat with testosterone

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12
Q

Describe the pathophysiology, investigation and management of hypothyroidism

A

Common primary autoimmune causes include Hashimoto’s Thyroiditis (destruction of lymphocytic and plasma cell infiltration)

Other primary causes include iodine deficiency or post-thyroidectomy

Secondary hypothyroidism arises due to hypopituitarism (low TSH)

Causes fatigue, cold intolerance, weight gain, constipation, menorrhagia, bradycardia, dry skin/hair, goitre

Diagnosed with high TSH and low T4

Manage with levothyroxine replacement

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13
Q

Define gestational diabetes

A

Carbohydrate intolerance with onset, or diagnosis, during pregnancy

Risk factors include high body mass index, previous macrosomic baby or gestational diabetes, or family history of, or ethnic prevalence of, diabetes

All women with risk factors should have an OGTT at 24 to 28 weeks

Internationally agreed criteria for gestational diabetes using 75 g OGTT:

Fasting venous plasma glucose ≥ 5.1 mmol/l, or

One hour value ≥ 10 mmol/l, or

Two hours after OGTT ≥ 8.5 mmol/l

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14
Q

State causes of amenorrhoea

A
  • Primary
    • Chromosomal or Genetic Abnormalities (e.g. Turners)
    • Problems with Hypothalamus or Pituitary
  • Secondary
    • Pregnancy
    • Menopause
    • Chemotherapy
    • Certain Medications
    • PCOS
    • Thyroid Problems
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15
Q

Describe the pathophysiology and management of Diabetic Ketoacidosis

A

Absolute insulin deficiency results in activation of the ketone pathway, used in starvation states

This results in acetone (ketone) production, which along with profound hyperglycaemia can be life-threatening

Presents with osmotic symptoms, weight loss, breathlessness, abdominal pain, leg cramps, N&V, confusion

Characterised by a Metabolic Acidosis, Hyperglycaemia and Urinary/Plasma Ketones

Manage with IV fluids, insulin and assess need for potassium

Follow national DKA pathway

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16
Q

Describe the pathophysiology and management of Hyperglycemic Hyperosmolar State

A

Occurs in a relative insulin deficiency

No ketoacidosis

More insidious onset

Marked dehydration and hyperglycaemia

Rehydrate with saline and give insulin if glucose does not fall with fluids alone

LMWH prophylaxis and consider K+

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17
Q

Describe insulinoma

A

A rare neuroendocrine tumour, often benign

Presents as fasting hypoglycaemia with Whipple’s triad

Test with IV insulin and measure c-peptide (should normally be suppressed but this will not happen in insulinoma)

Image with CT/MRI and endoscopic USS

Manage with excision

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18
Q

Describe the pharmacology of SGLT-2 inhibitors

A

e.g. Empagliflozin, Canagliflozin

Inhibits sodium-glucose co-transporter in the renal tubules

Blocks glucose reabsorption and promotes loss of glucose in the urine

19
Q

Describe the pharmacology of Pioglitazone

A

Acts on PPAR receptors to increase peripheral insulin sensitivity

SE include hypoglycaemia, fractures, oedema

20
Q

Describe the pathophysiology, investigation and management of Phaeochromocytoma

A

Rare catecholamine-producing tumours arising from sympathetic paraganglia cells (collections of chromaffin cells) in the adrenal medulla

Often associated with hard to control hypertension

Episodes of headache, palpitations, pallor and sweating

Also associated with tremor, anxiety, nausea, vomiting, chest and abdominal pain

Diagnose with at least two 24 hour urinary catecholamines, CT abdomen and MIGB scan (chromaffin seeking analogue)

Medical management with alpha-blockade (phenoxybenzamine) first, then with beta blocker (bisoprolol) if tachycardic

Followed by surgical resection

21
Q

Compare and contrast type 1 and type 2 diabetes

A

Type 1 - Immune pathogenesis with severe insulin deficiency

Type 2 - Combination of insulin resistance and insulin deficiency

22
Q

State important causes of hypercalcaemia

A
  • PTH-Mediated (i.e. Elevated/Normal PTH)
    • Primary Hyperparathyroidism
    • Familial Syndromes (MEN-1, MEN-2)
    • Familial Hypocalciuric Hypercalcaemia
  • PTH-Independent (i.e. Undetectable PTH)
    • Malignancy
    • Granulomatous Disorders
    • Drugs (thiazides, lithium, calcium supplements)
    • Adrenal Insufficiency
    • Milk-Alkali Syndrome
    • Immobilisation
23
Q

State signs and symptoms of hypercalcaemia

A

May be asymptomatic if mild

Symptoms more common when calcium >3mmol/L

Muscle Weakness, Bone Pain, Osteoporosis

Anorexia, Nausea, Constipation, Pancreatitis

Confusion, Depression, Fatigue, Coma

Shortened QTc, Bradycardia, Hypertension

Polyuria, Nephrogenic DI, Stones

24
Q

Describe testosterone replacement therapy, its advantages and disadvantages

A

Can be given orally, IM or topically

Best option for androgen replacement in deficiency

Side effects include mood issues (aggression/behaviour changes), libido issues, increased haematocrit, acne, sweating, gynaecomastia

Testosterone is a drug of abuse in sports

25
Q

List causes of Secondary Diabetes

A

Genetic defects of beta-cell function

Genetic defects in insulin action

Disease of exocrine pancreas (pancreatitis, carcinoma, CF, haemochromatosis)

Endocrinopathies (acromegaly, cushings)

Immunosuppressive Agents (glucocorticoids, tacrolimus, ciclosporin)

Anti-Psychotics (clozapine)

Genetic Syndromes Associated with DM (Down’s, Turner’s, Kleinfelter’s)

26
Q

Define hypoglycaemia and describe symptoms

A

Insulin-Treated DM - <4mmol/L

Normal People - <2.8mmol/L

Autonomic - Sweating, Palpitations, Shaking, Hunger

Neuroglycopenic - Confusion, Drowsiness, Visual Disturbance

Nausea + Headache

27
Q

Describe causes of hirsutism

A

Male pattern hair growth in women

Causes are familial, idiopathic or due to increased androgen secretion by the ovary (e.g. PCOS, ovarian cancer), adrenal (e.g. CAH, Cushing’s, cancer) or drugs (e.g. Steroids)

Manage with oestrogens (combine contraceptive pill), metformin

Clomifene can be used for infertility

28
Q

State differential diagnoses for non-diabetes hypoglycaemia

A

Drugs

Critical Illness (hepatic/renal/cardiac failure, sepsis)

Hormone Deficiency (e.g. Cortisol)

Non-Islet Cell Tumour

Endogenous Hyperinsulinism (Insulinoma, Functional Islet Cell Disorders, Insullin Autoimmune Hypoglycaemia)

Accidental, Surreptitious, Malicious Hypoglycaemia

29
Q

Describe the rationale for Continuous Subcutaneous Insulin Infusion treatment

A

Can potentially provide significant improvement in glycaemic control and quality of life for some people with T1DM

Potentially make it easier to achieve glucose control with less danger of severe and incapacitating hypoglycaemia

Complications include reactions, infections at cannula site, tube blockage, pump malfunction

30
Q

Describe the different insulin regimens available

A

Insulin is a peptide, so cannot be given orally

Can be given as a once-daily basal, twice daily mix or basal-bolus therapy

Insulin pens are more convenient, accurate, discrete and less painful than conventional vial and syringes

31
Q

Describe the pathophysiology, investigation and management of Primary Gondal Disease

A

PGD is due to testicular failure

Causes include chromosomal defects (e.g. Kleinfelters), cryptorchidism or adult leydig cell/seminiferous tubule failure (due to trauma, chemotherapy, radiotherapy or multi-system disorders)

Characterised by low testosterone, high/normal LH and FSH and normal prolactin

Manage with testosterone replacement

32
Q

State the WHO diagnostic criteria for diabetes

A

Fasting Plasma Glucose >/= 7mmol/L

Random Plasma Glucose >/= 11.1mmol/L

One Abnormal Value if Symptomatic

Two Abnormal Values if Asymptomatic

Should not be diagnosed on the basis of HbA1c or glycosuria alone

33
Q

Describe the pathogenesis of type 1 and type 2 diabetes mellitus

A
  • Type 1 DM
    • Chronic, progressive metabolic disorder characterised by hyperglycaemia and the absence of insulin secretion
    • Type 1 diabetes results from autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans
    • Occurs in genetically susceptible subjects and is probably by one or more environmental agents
  • Type 2 DM
    • Chronic, progressive metabolic disorder characterised by hyperglycaemia, insulin resistance and relative impairment of insulin deficiency
    • Common with a prevalence that rises markedly with increasing levels of obesity
    • Most likely arises through a complex interaction among many genes and environmental factors
34
Q

Describe the pathophysiology, clinical features, investigation and management of Polycystic Ovarian Syndrome

A

See figure for Pathophysiology

Presents with hirsutism, acne, male-pattern hair loss, acanthosis nigricans, obesity

Lifestyle modification - diet, exercise, weight loss

Oestrogen (combined oral contraceptive)

Metformin (reduces glucose intolerance and hyperinsulinaemia)

Clomifene (selective oestrogen receptor modulator)

Gonadotropin therapy

35
Q

Describe the pathophysiology, investigation and management of acromegaly

A

Hypersecretion of growth hormone, most commonly due to a pituitary tumour

GH stimulates bone and soft tissue growth through increased secretion of insulin-like growth factor

Features include sweats and headaches, altered facial features (coarse features, macroglossia, frontal bossing, protruding jaw), spade-like hands, increased foot size, visual impairment, cardiomyopathy, increased inter-dental spaces

Diagnose with GH measurements with OGTT (glucose should suppress GH)

Measure IGF-1 and then Pituitary MRI

First line treatment is surgery

May require medical therapy such as somatostatin analogues, dopamine agonists or GH receptor antagonists

Radiotherapy may be used for residual tumour or if ongoing symptoms

36
Q

Describe MODY

A

Maturity Onset Diabetes of the Young

1-2% of all DM

Caused by a change in a single gene (monogenic)

Autosomal dominant

Main features include <25yrs onset, runs in families from one generation to next, managed by diet, OHAs and insulin

37
Q

Describe the pathophysiology, investigation and management of Primary Hyperaldosteronism

A

Excess production of aldosterone, independent of the RAS system, causing sodium and water retention and reduced renin release

Mostly caused by a solitary aldosterone-producing adenoma (Conn’s syndrome)

Other causes include bilateral adrenocortical hyperplasia or adrenal carcinoma

Often asymptomatic, may have hypokalaemia, weakness, cramps, paresthesia, polyuria, polydipsia, hypertension

Investigations include a raised aldosterone and aldosterone:renin ratio and suppressed renin

Confirm with a saline suppression test (2L saline over 4 hours followed by a 4h aldosterone >270pmol/L is highly suspicious)

Manage with MR antagonists or amiloride

Surgical management with unilateral laparoscopic adrenalectomy (only if adrenal adenoma)

38
Q

Describe the pathophysiology, investigation and management of Congenital Adrenal Hyperplasia

A

Autosomal recessive disorder

Deficiency in 21-alpha-hydroxylase

Results in steroidogenic defects including aldosterone and cortisol deficiency

This means more pregnenolone is converted to the androgen DHEA

Can result in ambiguous genitalia (female) and adrenal crisis and early virilisation (males)

Managed with mineralocorticoid and glucocorticoid replacement

39
Q

Describe the pathophysiology, investigation and management of Kleinfelters

A

Most common genetic cause of male hypogonadism

XXY

Manifests clinically at puberty

High LH and FSH, but seminiferous tubules regress and Leydig cells do not function normally

Wide clinical variation, including delayed puberty, suboptimal genital development, reduced secondary sexual characteristics, gynaecomastia, azoospermia and behavioural issues

Manage with androgen replacement, psychological support and fertility counselling

40
Q

Describe the pharmacology of DPP4 inhibitors

A

e.g. Sitagliptin

Blocks the action of DPP4, which destroys the enzyme incretin

Increased incretin levels inhibit glucagon, which increases insulin secretion

41
Q

Describe the pathophysiology, investigation and treatment of Cushing’s Syndrome/Disease

A

Cushing’s syndrome is the clinical state produced by chronic glucocorticoid excess and loss of the normal feedback mechanisms

Causes include exogenous steroid use, and a pituitary adenoma (specifically known as Cushing’s disease)

Symptoms include weight gain, mood change (depression, lethargy, irritability), proximal myopathy, gonadal dysfunction, acne

Signs include central obesity, moon face, buffalo hump, skin/muscle atrophy, bruises, abdominal striae, hypertension, hyperglycaemia

Investigate with MRI for pituitary mass, raised plasma cortisol, 24hr urinary free cortisol and dexamethasone suppression test (give dexamethasone at night and measure cortisol in the morning, should normally be suppressed but will not be in Cushing’s)

Manage by stopping offending medication, surgical removal of pituitary adenoma or adrenalectomy

42
Q

Describe the pathophysiology, investigation and management of adrenal insufficiency

A

Primary adrenal insufficiency (Addison’s disease) is rare and characterised by destruction of the adrenal cortex leads to glucocorticoid and mineralocorticoid deficiency

Causes include autoimmunity, adrenal TB, lymphoma, opportunistic infection

Symptoms include anorexia, weight loss, fatigue, lethargy, dizziness, hypotension, hyperkalaemia, abdominal pain, vomiting, diarrhoea, skin and mucous membrane pigmentation

Investigations include;

Biochemistry - hyponatraemia, hyperkalaemia and hypoglycaemia

High ACTH levels

Adrenal auto-antibodies

Renin (high) and aldosterone (low) levels

Short Synacthen Test - Measure plasma cortisol before and 30 minutes after IV ACTH injection. In normal situations, ACTH should increase cortisol levels. A normal result is a baseline of >250nmol/L and post-ACTH of >480. In Addison’s, there would be minimal cortisol response after ACTH injection

43
Q

Describe the pathophysiology and management of thyroid carcinoma

A

Papillary, Follicular, Medullary, Lymphoma or Anaplastic

Manage with thyroidectomy with or without radiotherapy

Phase 3 (14 decks)

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