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Endocrinology Flashcards

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USMLE® Step 1 flashcards
1
Q

Cushing’s syndrome from excess ACTH

  1. Causes
  2. Disease definition
  3. Disease specific clinical feature
  4. Management
A
  1. Cushing’s disease, or non-pituitary ectopic ACTH producer (e.g. Small cell lung cancer)
  2. Raised cortisol level specifically due to raised ACTH from a pituitary tumour
  3. Hyperpigmentation as ACTH activates melanocytes
  4. Resection / radio / chemo
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2
Q

Cushing’s syndrome

  1. Causes
  2. Symptoms (‘CUSHING’ mnemonic)
  3. Pseudocushing’s - cause
  4. Screening test
  5. Complications (3)
  6. Test to determine whether disease or not
A
  1. Excess cortisol, or excess ACTH causing raised cortisol
  2. Central obesity/comedones, urinary free cortisol, striae, hirsuitism, immunodeficiency, neoplasms, glucose (raised)
  3. Alcohol excess
  4. 24 hour urinary free cortisol
  5. Cardiac problems, diabetes, osteoporosis
  6. Overnight dexamethasone suppression test
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3
Q

Cushing’s syndrome from raised cortisol

  1. Causes (2)
  2. Management
A
  1. Steroids, adrenal carcinoma / adenoma

2. Gradually reduce steroids, or resection/radio/chemo

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4
Q

Dexamethasone suppression test results

  1. Cortisol down from low or high dose
  2. No change after low dose, down after high dose
  3. No change even after high dose
  4. Causes of false positives (3)
A
  1. No pathology - dexamethasone suppresses cortisol
  2. Cushing’s disease - high levels able to suppress excess ACTH from pituitary
  3. Cushing’s syndrome high cortisol independent of ACTH, or ectopic ACTH e.g. SCLC
  4. Obesity, alcoholism, chronic renal failure
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5
Q

Aldosterone

  1. Secreted from
  2. Action
  3. High - symptoms
  4. High - signs (2)
A
  1. Adrenal gland
  2. Increased Na+ / water reabsorption and K+ secretion
  3. From low K+ poor vision, confusion, headaches, renal pain, muscle ache / weakness / spasm/ tingling, numbness, polydipsia
  4. Fluid overload, HTN
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6
Q

Primary hyperaldosteronism

  1. Commonest cause
  2. Other causes (2)
  3. 1st line investigation
  4. Blood results
  5. Management (2)
A
  1. Conn syndrome (aldosterone producing adenoma)
  2. Adrenal carcinoma, adrenal hyperplasia
  3. Renin:aldosterone ratio
  4. High Na+, low K+, metabolic alkalosis, LOW renin
  5. Aldosterone antagonist (e.g. spironolactone), calcium channel blockers
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7
Q

Secondary hyperaldosteronism

  1. Pathophysiology
  2. Causes (5)
  3. Blood results

Bartter’s syndrome

  1. Inheritance pattern
  2. Pathophysiology
  3. Presentation
  4. Bloods
  5. Urine test results
  6. Management
A
  1. Increased renin causing increased aldosterone levels
  2. Renal artery stenosis, chronic oedema, cardiac failure, liver failure, hypertension
  3. High Na+, low K+, metabolic alkalosis
    Metabolic alkalosis, HIGH renin
  4. Autosomal recessive
  5. Salt wasting via sodium and chloride leak in LoH due to transporter mutation
  6. Children - failure to thrive, polyuria, polydipsia, normal BP
  7. Low K+, metabolic alkalosis
  8. High urinary K+ and Cl-
  9. K+ replacement, NSAIDs, ACE-i
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8
Q

Primary adrenal insufficiency

  1. AKA
  2. Pathophysiology
  3. Symptoms
  4. Bloods
  5. Key diagnostic test
  6. Test result
  7. General management

Addisonian crisis

  1. Symptoms
  2. Precipitating factors
  3. Management
A
  1. Addison’s disease
  2. Autoimmune adrenal cortex destruction
  3. Hyperpigmentation, collapse, unexplained abdominal pain/vomiting
  4. Low Na+/ glucose/Hb, high K+/Ca2+/urate/eosinophils
  5. ACTH stimulation - Synacthen tests
  6. Cortisol remains low in long and short tests (high in both normally)
  7. Replace steroids via hydrocortisone 2-3x daily, mineralocorticoid (to treat postural hypotension)
  8. Abdominal pain, vomiting, hypotension, tachycardia, collapse, hypoglycaemia, hypovolaemic shock
  9. Infection, trauma, surgery, missed medication
  10. Bloods (cortisol + ACTH), hydrocortisone 100mg IV stat, IV saline bolus, monitor BM for hypos, investigate/treat infection
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9
Q

Hypoadrenalism signs

  1. Low cortisol
  2. Low aldosterone
  3. Low androgen
A
  1. Hyperpigmentation, hypoglycaemia
  2. Low Na+, high K+, low BP (fluid and Na+ loss)
  3. Lack of pubic hair (females), generalised malaise
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10
Q

SE of steroids

B
E
C
L
O
M
E
T
H
A
S
O
N
E
A 
Buffalo hump
Easy bruising
Cateracts
Large appetite
Obesity
Moon face
Euphoria
Thin arms / legs / skin
Hypertension / hyperglycaemia
Avascular necrosis of femoral head
Skin thinning
Osteoporosis
Negative nitrogen balance
Emotional liability
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11
Q

Secondary adrenal insuffiency

  1. Pathophysiology
  2. Causes (2)
  3. Important questions to ask
  4. Test results
  5. Signs to distinguish from Addison’s
A
  1. Dysfunction of hypothalamus, pituitary axis
  2. Iatrogenic (long term steroids), pituitary/hypothalamic problem (tumour/infection/infarct)
  3. Steroid use
  4. Low cortisol in short synacthen, cortisol rises in long synacthen test
  5. No hyperpigmentation (ACTH low), no electrolyte imbalance (aldosterone not low)
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12
Q

ACTH levels in

1) Primary hypoadrenalism
2) Secondary hypoadrenalism

A

1) High

2) Low

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13
Q

Type 2 DM

  1. Pathophysiology
  2. Diagnostic criteria
  3. C peptide
  4. 1st line management
  5. When to add 2nd line drug
  6. 2nd line drug if obese
A
  1. Long term high circulating blood glucose - loss of sensitivity to insulin
  2. Fasting glucose 7.0+ mmol/l and random glucose/OGTT 11.1+ mmol/l. If asymptomatic must meet criteria on 2 separate occasions
  3. High
  4. Lifestyle +/ metformin if 48+ mmol/mol
  5. HbA1c >58 mmol/mol (new target HbA1C is 53)
  6. DPP-4 inhibitors (e.g. sitagliptin)
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14
Q

Hypercalcaemia

  1. Causes (4)
  2. Features (6 key)
  3. ECG finding
  4. Main therapy
A
  1. Metastases, hyperparathyroidism (primary/tertiary), myeloid, sarcoidosis
  2. Renal stones, abdominal groans (pain), polydipsia, bone pain, psychiatric overtones (depression)
  3. Shortened QT
  4. Fluid rehydration
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15
Q

Hyperparathyroidism

Primary

  1. Commonest cause
  2. Other causes (2)
  3. Blood results
  4. Imaging - what does it show
  5. Management
  6. Associated neoplasm

Secondary

  1. Causes (3)
  2. Blood results
  3. Management

Tertiary

  1. Pathophysiology
  2. Blood results (serum Ca2+, vit D, PTH)
  3. Treatment
A
  1. Single parathyroid adenoma, then hyperplasia
  2. Diffuse parathyroid gland hyperplasia, carcinoma
  3. Serum Ca2+/ALP high, PTH high/normal, phosphate low, vit D normal
  4. USS, FNA, SESTANIBI (radionuclear scan) - bones have osteitis fibrosa cystica from severe resorption (phalange erosion/cyst/brown tumour), pepper pot skull
  5. Ressection, cinacalcet (increases sensitivity of parathyroid cells to Ca2+)
  6. MEN-1
  7. Renal failure (Vit D not activated), low vitamin D (osteomalacia), other osteomalacia
  8. PTH/phosphate/ALP high, serum Ca2+/ vit D low
  9. Alpha calcidol (replace vitamin D)
  10. Prolonged secondary so PTH becomes so high, calcium produced at very high level
  11. All high
  12. Correct vitamin D, should improve in a year or remove
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16
Q

Hypocalcaemia

  1. Causes
  2. Clinical signs
  3. Blood tests
  4. Monitoring requirements
  5. Management
A
  1. Vit D deficiency, CKD, hypoparathyroidism, magnesium deficiency, blood transfusion
  2. Pins and needles, myalgia, tetany, arrhythmias, chvostek’s sign - (facial muscles twitch when facial nerve tapped)
  3. Ca2+, PTH, vit D, phosphate, magnesium, U+E
  4. ECG
  5. IV calcium glucose 10% 10ml 10 mins
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17
Q

Hypoparathyroidism

  1. Commonest cause (secondary)
  2. Primary cause (gland failure)
  3. Blood results
  4. Pseudo cause
  5. Pseudo bloods
  6. Pseudo associates features
  7. Pseudopseudo features
A
  1. Iatrogenic - removal during thyroidecomy / post radiation
  2. Auto-immune, congenital e.g. Di George
  3. Low calcium, high phosphate, low PTH
  4. PTH resistance (genetic)
  5. Low calcium, high phosphate/PTH/ALP
  6. Low IQ, stature, shortened 4th + 5th metacarpals
  7. Similar phenotype to pseudo but normal biochemistry (genetic)
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18
Q

Impaired glucose tolerance

  1. Fasting glucose -
  2. 2 hours post glucose load -
A
  1. 7+

2. 11.1

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19
Q

Type 1 DM

  1. Presentation
  2. Diagnostic tests
  3. C peptide
  4. Management
  5. Blood glucose targets
  6. Other organs to monitor
  7. Genetics
  8. Daily monitoring requirements
A
  1. Age 12, polydipsia, polyuria, weight loss, +/- ketoacidosis
  2. FBC, BM, HbA1C, U+E, urine dip (ketones/glucose)
  3. Low
  4. Insulin
  5. 5-7 mmol/l on waking, 4-7 mmol/l before meals
  6. Eyes, renal, vascular
  7. HLA D3/D4 linked (Addison’s disease)
  8. At least 4x/day, including before meals + before bed
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20
Q

DKA

  1. Presentation
  2. Precipitants
  3. Insulin infusion rate
  4. Blood result
  5. Product to add into rehyration fluid
  6. Complications
A
  1. Young person with abdominal pain, reduced GCS, confusion, N+V, diarrhoea, lethargy, tachypnoea ‘Kussmaul breathing’, dehydration
  2. Sepsis, not taking insulin, MI
  3. Fixed rate of 0.1 units/kg/hour w/ 0.9% NaCl
  4. High BM, high ketones, low pH, low potassium
  5. Potassium
  6. Cerebral oedema (if lower BM too quickly - look for headache, drowsiness, irritability, papilloedema, bradycardia, HTN)
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21
Q

HbA1c target

  1. Managed by diet and lifestyle (+/- drug not causing hypoglycaemia)
  2. Taking a drug associated with hypoglycaemia (such as a sulphonylurea)
A
  1. 48 mmol/mol (6.5%) (this is level at which DM is diagnosed)
  2. 53 mmol/mol (7.0%)
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22
Q

Diabetes insipidus

  1. Definition
  2. Cranial causes (2)
  3. Nephrogenic causes (3)
  4. Symptoms
  5. Investigations
  6. Cranial DI result
  7. Nephrogenic DI result
  8. Cranial DI management
  9. Nephrogenic DI management
A
  1. Inability of kidneys to preserve water from either vasopressin deficiency (posterior pituitary) or insensitivity (kidney)
  2. Brain tumour / trauma
  3. Hypercalcaemia, hypokalaemia, CKD
  4. Polyuria, polydipsia
  5. Urine osmolality (low) + plasma osmolality (high), water deprivation test (give desmopressin and see response)
  6. Osmolality increases after desmopressin (water retained)
  7. Osmolality still low after desmopressin
  8. Desmopressin
  9. Thiazides, low salt/protein diet
23
Q

SIADH

  1. Cranial causes (4)
  2. Respiratory causes (3)
  3. Drug causes (2)
  4. Malignancy causes (3)
  5. Hyponatraemia type
  6. Diagnostic criteria
A
  1. Tumour, meningitis, encephalitis, SAH
  2. TB, COPD, cancer
  3. Diuretics, antidepressants
  4. Lung, lymph, pancreas
  5. Euvolaemic
  6. Concentrated urine (Na >20, osmolality >100) with hyponatraemia + low plasma osmolality
24
Q

Testes - 2 functions

A

Testosterone production

Spermatogenesis

25
Q

Hypogonadism in men

  1. Presentation
  2. Primary cause and associated phenotype
  3. Blood results
  4. Malignancy more at risk of

Secondary hypogonadism

  1. Pathophysiology
  2. Commonest cause
  3. Other causes

Gynaecomastia

  1. Hormone imbalance
  2. Causes
  3. Management
A
  1. Decreased libido, ED, gynaecomastia, fatigue, delayed puberty, tall, small/firm testes
  2. Testicular failure (Klinefelter syndrome, 47, XXY), others e.g. trauma, torsion, chemo/radiotherapy, post-orchitis
  3. LH high, testosterone low
  4. Breast cancer
  5. Low gonadotrophins (LH/FSH)
  6. Prolactinoma
  7. Kallman’s syndrome (isolated gonadotrophin deficiency, with anosmia and colour blindness), hypopituitarism
  8. Increased oestrogen:androgen ratio
  9. Hypogonadism, oestrogen-producing tumour, cirrhosis, drugs
  10. Testosterone if hypogonadism, +/- anti-oestrogen (e.g. tamoxifen)
26
Q

T2DM - medication

Action

  1. Metformin
  2. Gliclazide (sulphonylurea)
  3. Pioglitazone (thiazolidinedones)
  4. Alpha glucose inhibitors
  5. DPP4 inhibitor/gliptins

Side effects

  1. Metformin
  2. Sulfonylureas e.g gliclazide
  3. Glitazones
A
  1. Improves insulin sensitivity
  2. Stimulates pancreas to secrete insulin
  3. Improves insulin sensitivity
  4. Prevents intestinal sugar absorption
  5. Blocks DPP4 (usually destroys incretin)
  6. GI, lactic acidosis
  7. Hypos, increased appetite/weight, SIADH, cholestatic liver dysfunction
  8. Weight gain, fluid retention, liver dysfunction, fractures, hypos - DO NOT GIVE IN HEART FAILURE
27
Q

Gland products

  1. Anterior pituitary
  2. Posterior pituitary
  3. Adrenal zona glomerulosa (outer)
  4. Adrenal zona fasciculata (middle)
  5. Adrenal zona reticularis (inner)
A
  1. ACTH, TSH, LH, FSH, GH, prolactin
  2. ADH (vasopressin), oxytocin
  3. Aldosterone (in response to high angiotensin II)
  4. Glucocorticoids e.g. cortisol
  5. Androgens (e.g. testosterone precursor)
28
Q

Hyperprolactinaemia

  1. Prolactin function
  2. Causes (4 main)
  3. Presentation
  4. Bloods
  5. Urine test
  6. If benign causes excluded, do
  7. Management
A
  1. Stimulates mammary glands to lactate
  2. Pregnancy, drugs (metoclopramide, haloperidol, methyldopa), prolactinoma, PCOS
  3. Amenorrhoea, infertility, galactorrhoea, erectile dysfunction (give PDE5 inhibitor), osteoporosis, optic chiasm pressure symptoms
  4. Prolactin level (PRL) main test. Also low LH/FSH/ testosterone/oestrogen (inhibits GRH secretion). Also do TFT, U+E.
  5. Pregnancy test
  6. MRI pituitary
  7. Bromocriptine (dopamine agonist), surgery considered if visual symptoms/symptoms resistant to medical management
29
Q

Hypothyroidism

  1. Causes
  2. Associated diseases
  3. Problems in pregnancy

Features

  1. General
  2. Skin
  3. Psychological / neurological
  4. Cardiovascular
  5. Reproductive
  6. Management
  7. Start slower in which populations, and why
  8. Monitor response how
A
  1. Hashimoto’s (most common, has goitre), idiopathic (common, no goitre), drugs (amiodarone, lithium), iatrogenic, iodine deficiency, congenital
  2. Autoimmune (T1DM, Addison’s), Down’s/Turner’s, cystic fibrosis, primary biliary cholangitis
  3. Eclampsia, anaemia, prematurity, low birthweight, stillbirth, PPH
  4. Cold intolerance, lethargy, weight gain, low hoarse voice
  5. Dry skin and hair, loss of outer 1/3 of eyebrow
  6. Depression, slow reflexes, carpal tunnel syndrome
  7. Bradycardia, angina, non-pitting oedema
  8. Menorrhagia, infertility
  9. Levothyroxine
  10. Elderly/IHD, may precipitate angina/MI
  11. TSH levels
30
Q

Thyrotoxicosis

  1. Blood tests

Thyrotoxic storm

  1. Definition
  2. Clinical findings
  3. Management (4)
A
  1. TSH low, T3/4 high, normocytic anaemia
  2. Thyrotoxicosis causes acutely increased metabolism
  3. Life threatening tachycardia, HTN, fever
  4. Carbimazole/propylthiouracil
    IV propranolol (diltiazem if asthma)
    Lugol’s solution (aqueous iodine) after 4 hours
    Hydrocortisone
31
Q

Primary hyperthyroidism

  1. Causes (4)
  2. TFT results
  3. Test to do if anti-TSH is negative
  4. Result in GD
  5. Result in nodule
  6. Results in thyroiditis
A
  1. Graves disease, toxic multi-nodular goitre, toxic adenoma, hypothyrodism overtreatment
  2. TSH low, T4 high
  3. Radionucleotide scan
  4. Diffuse increased uptake
  5. ‘Hot’ areas of increased uptake
  6. Diffuse decreased uptake
32
Q

Secondary hyperthyroidism

  1. Cause
  2. TFT results
A
  1. Pituitary adenoma

2. TSH high, T4 high

33
Q

Hyperthyroidism - features

  1. General
  2. Skin
  3. Psychological
  4. Muscular
  5. Cardiovascular
  6. Menstrual features
A
  1. Tremor, heat intolerance, weight loss/muscle wasting, diarrhoea, sweating
  2. Dry skin
  3. Psychosis, emotional liability, restlessness
  4. Myopathy
  5. AF, tachycardia, palpitations
  6. Oligomenorrhoea
34
Q

Hyperthyroidism - treatment

  1. Medical - to achieve euthyroidism (+ time it takes)
  2. When to use propylthiouracil to achieve euthyroidism
  3. Medical - maintaining euthyroidism (2 regimes)
  4. Blood result to monitor
  5. Interventional
  6. Lifestyle advice following radioiodine treatment
  7. Surgical (+ indications)
  8. Complications of surgery
A
  1. Carbimazole for 4-8 weeks (with thyroxine if done quickly), Beta blocker (for rapid symptom control)
  2. 1st trimester of pregnancy, thyroid storm
  3. Titration block (titrate carbimazole levels), vs block and replace (high dose carbimazole and use alongside levothyroxine)
  4. T4
  5. Radioiodine (if Grave’s, but not if orbitopathy)
  6. Avoid close contact with children/pregnancy women for 3 weeks
  7. Thyroidectomy (prevent recurrence, malignancy, compression symptoms in large multinodular goitre, if thionamide treatment not possible)
  8. Recurrent laryngeal nerve palsy (hoarseness), hypoparathyroidism
35
Q

Features ONLY found in Graves disease

A 
Proptosis
Lid retraction
Preorbital oedema
Diplopia
Limited eye movements
Pretibial myxoedema
Thyroid acropachy
36
Q

Thyroid cancer

  1. Main benign cause (+ spread)
  2. Main malignant cause (+ spread)
  3. Other carcinoma types (2)
  4. One presenting with MEN syndrome
  5. Other malignancy (+ presentation)
  6. Suspected - questions to ask
  7. Suspected - investigations
  8. Management - 1st, 2nd, 3rd line
  9. Monitoring
A
  1. Follicular adenoma (blood to bone/lungs)
  2. Papillary (lungs/lymph nodes)
  3. Medullary, follicular
  4. Medullary (secretes CALCITONIN)
  5. Lymphoma (present with stridor/dysphagia)
  6. Mass, usually painless, dysphagia, dysphonia, hoarseness, weight loss, B symptoms
  7. CXR, USS, FNA, radioisotope
  8. 1st Line: thyroidectomy
    2nd Line: post-op radioactive iodine therapy
    3rd Line: radio/immunotherapy - incurable disease
  9. Thyroglobulin antibodies
37
Q

Phaeochromocytoma

  1. Cause
  2. Usual location
  3. Classic triad of symptoms
  4. Other symptoms
  5. Associations
  6. Specific test
  7. Management
A
  1. Catecholamine-producing tumour (chromaffin cells)
  2. Adrenal medulla
  3. Episodic headache, sweating, tachycardia
  4. Change in BP (think if HTN unusual or associated with low K+), GI upset, psychological/CNS disturbance
  5. Thyroid cancer, MEN 2a/2b, neurofibromatosis, von-Hippel Lindau
  6. 24 hr urinary metanephrine collection, high WCC
  7. Surgery; do alpha blockage pre-op (phenoxybenzamine), beta blockade if heart disease or tachycardic
38
Q

Which patients who take insulin DON’T need to inform the DVLA

A

Those on temporary treatment for < 3m

Gestational diabetes that are taking insulin for < 3m post delivery

39
Q

Endocrine facies

  1. Thyrotoxicosis
  2. Hypothyroidism
  3. Cushing’s syndrome
  4. Addison’s disease
  5. Acromegaly
  6. Hyperandrogenism (female)
  7. Hypopituitarism
  8. Hypoparathyroidism
  9. Pseudohypoparathyroidism
A
  1. Hair loss, pretibial myxoedema, onycholysis (nail separation from nailbed), bulging eyes (exophthalmos/proptosis)
  2. Hair loss, eyebrow loss, cold/pale skin, ‘toad-like’ face
  3. Central obesity, wasted limbs, moon face, buffalo hump, supraclavicular fat pads, striaie
  4. Hyperpigmentation (face, neck, palmar creases)
  5. Acral (distal) and soft tissue overgrowth, big jaw (macrognathia)/hands/feet, thick skin, coarse face
  6. Hirsuitism, temporal balding, acne
  7. Pale/yellow tinged skin, fine wrinkling around eyes/mouth, making patient look older
  8. Dry, scaly, puffy skin, brittle nails, coarse hair
  9. Short stature, short neck, short 4/5th metacarpals
40
Q

Hypothalamic pituitary axis - goes where, produces what

Anterior pituitary

  1. LH/FSH
  2. GH
  3. TSH
  4. Prolactin
  5. ACTH

Posterior pituitary

  1. Vasopressin
  2. Oxytocin
A
  1. Ovaries and testes; forms testosterone/oestrogen
  2. Many tissues
  3. Thyroid gland; forms thyroxine
  4. Breasts/gonads; promotes lactation
  5. Adrenal glands; forms steroids
  6. Renal tubules, retains H20 + increases BP
41
Q

DM - complications/management

Vascular disease

  1. Medical management
  2. Blood pressure targets

Diabetic nephropathy
3. Management - indication and drug

Diabetic retinopathy

  1. Screening frequency
  2. Background retinopathy - features/management
  3. Pre-proliferative retinopathy - features/management
  4. Proliferative retinopathy - features/management
  5. Maculopathy - symptoms/management
  6. Cataracts - types (2)
  7. Rubeosis iridis - what is this and what it leads to
A
  1. Statin, aspirin 75mg
  2. 135/85 in T1, 140/80 in T2, or 130/80 if end-organ damage
  3. A:CR >3, give ACE-i or CCB (sartan)
  4. Annually
  5. Microaneurysms (dots), haemorrhages (blots), hard exudates (lipid deposits); refer if near macula for IV triamcinolone
  6. Cotton-wool spots (infarcts), haemorrhages, venous beading; refer
  7. New vessels forming; urgently refer
  8. Reduced acuity; aspirin 2mg/kg/day, laser, intravitreal steroids, anti-angiogenics
  9. Juvenile ‘snowflake’, or senile
  10. New vessels on iris; glaucoma
42
Q

Diabetic neuropathy

  1. Signs

Management

  1. Educate
  2. Conservative
  3. Charcot joint
  4. Cellulitis - common organisms (3)
  5. Cellulitis - management
  6. Neuropathic pain ladder
  7. Mononeuritis multiplex e.g. CN II/III
  8. Autonomic neuropathy - signs and management
A
  1. Reduced sensation in stocking distribution, tingling, pain, absent ankle jerks, neuropathic deformity (e.g. Charcot joint), pes cavus, claw toes, loss of transverse arch, rocker bottom sole
  2. Daily foot inspection (mirror for sole), chiropody
  3. Bed rest, therapeutic shoes
  4. Bisphosphonates, 8 weeks bed rest/cast etc until oedema and local warmth reduce and bony repair complete
  5. Staph, strep, anaerobes
  6. Admit, IV benzylpenicillin + flucloxacillin +/- metronidazole
  7. Paracetamol, then amitriptyline, then duloxetine/ gabapentin/ pregabalin, then opiates
  8. Immunosuppression (steroids, IVIG, ciclosporin)
  9. Postural BP drop (fludrocortisone), gastroparesis (anti-emetics, erythromycin, gastric pacing), urine retention, gustatory sweating, diarrhoea (give codeine), ED
43
Q

Hypoglycaemia

  1. Definition
  2. Fasting hypoglycaemia - causes (‘EXPLAIN’)
  3. When to investigate
  4. Low insulin, high ketones (3)
  5. Low insulin, no ketones

Insulinoma

  1. Screening test
  2. Suppressive test
  3. Imaging
  4. Management
A
  1. Plasma glucose <4 mmol/l
  2. Exogenous drugs (e.g. insulin, sulphonylurea, glitazones), Pituitary insufficiency, Liver failure, Addison’s, Islet cell tumour (insulinoma), Non-pancreatic neoplasm (fibrosarcoma, haemangiopericytoma)
  3. Whipple’s triad - hypo symptoms, low BM, symptom resolution when glucose rises
  4. Alcohol, pituitary insufficiency, Addison’s
  5. Non-pancreatic neoplasm, anti-insulin receptor antibodies
  6. Hypoglycaemia + plasma insulin rise during fast
  7. Give IV insulin, measure C peptide (C-peptide not suppressed by exogenous insulin like expected)
  8. CT pancreas
  9. Surgery, or diazoxide + somatostatin
44
Q

Thyroid function tests (TFTs)

  1. T4 formed where
  2. T3 formed where
  3. When to do TFTs
  4. Hypothyroidism
  5. Treated/subclinical hypothyroidism
  6. TSH secreting tumour/thyroid hormone resistance
  7. Hyperthyroidism
  8. Subclinical hyperthyroidism
  9. Central hypothyroidism (hypothalamic/pituitary disorder)
  10. Sick euthyroidism/pituitary disease
  11. Antithyroid peroxidase (TPO) - found in
  12. TSH receptor antibody - found in
  13. Thyroglobulin
A
  1. Thyroid gland following TSH release from AP
  2. Peripherally
  3. AF, hyperlipidaemia, DM, pregnant T1DM, amiodarone or lithium (every 6 months), Down’s/Turner’s/Addison’s (yearly)
  4. TSH high, T4 low
  5. TSH high, T4 normal
  6. TSH high, T4 high
  7. TSH low, T3/4 high
  8. TSH low, T3/4 normal
  9. TSH low, T4 low
  10. TSH low, T3/4 low
  11. Hashimoto’s, Graves’
  12. Graves’
  13. Low if self-medicated hyperthyroidism, monitoring for carcinoma
45
Q

Goitre - causes

  1. Diffuse (4)
  2. Nodular (3)
  3. Nodule considered ‘functioning’ if
  4. Commonest benign causes of solitary nodule
  5. Investigations - first line
  6. Investigations - further
  7. Associated red flags
A
  1. Physiological, Graves’, Hashimoto’s thyroiditis, subacute de Quervain’s thyroiditis (painful, post-viral, hyper then hypo, may only need propanolol for hyper)
  2. Toxic multinodular (commonest, elderly, iodine deficient), toxic adenoma (hot nodule), carcinoma
  3. Associated with hyperthyroidism
  4. Follicular adenoma, hyperplastic nodules, thyroid cysts
  5. TSH, USS
  6. T4, CXR, FNA
  7. Rapidly growing, painless, stridor, in child, lymphadenopathy, dysphonia (larynx/recurrent laryngeal nerve invasion)
46
Q

Parathyroid gland and hormones

  1. Gland number and location
  2. PTH secreted in response to
  3. PTH secretion - effect on bones
  4. PTH secretion - effect on kidneys
  5. PTH secretion - effect on vitamin D
  6. PTH secretion - overall result
A
  1. 4, behind thyroid gland
  2. Low serum Ca2+ levels
  3. Increasing osteoclast activity, so releasing Ca2+ and phosphate from bones
  4. Increased Ca2+ and decreased phosphate resorption in the kidney
  5. Active vitamin D3 production increases
  6. Higher serum Ca2+, lower phosphate
47
Q

Multiple endocrine neoplasia (MEN) syndromes

  1. Type of gene
  2. MEN-1
  3. MEN-2a
  4. MEN-2b
  5. Von-Hippel Lindau
  6. Peutz-Jeghers
A
  1. Tumour suppressor
  2. Parathyroid hyperplasia, pancreas endocrine tumours, pituitary prolactinoma/GH secreting
  3. Thyroid medullary carcinoma, phaeochromocytoma, parathyroid hyperplasia
  4. Thyroid medullary carcinoma, phaeochromocytoma, mucosal neuromas, marfanoid appearance
  5. Familial, multisystem, bilateral RCC/cysts in 40s, retinal blastoma, phaeochromocytoma (cerebellar/visual signs)
  6. Multiple hamartomatous polyps in GI tract (AD), pigmented lesions, obstruction, bleeding
48
Q

Acromegaly

  1. Cause
  2. Pathophysiology
  3. Symptoms
  4. Signs
  5. Complications
  6. Blood tests
  7. 1st Diagnostic test
  8. Confirmative diagnostic test
  9. Further imaging
  10. Management
A
  1. Increased GH secretion from pituitary tumour or hyperplasia
  2. GH stimulates bone/soft tissue growth via increased secretion of insulin-like growth factor-1 (IGF-1)
  3. Acroparaesthesia, amenorrhoea, low libido, headache, sweating, snoring, arthralgia, back ache
  4. Hand/foot growth, coarse facial features, supraorbital ridges, macroglossia, widely spaced teeth, puffy lips/eyelids, scalp folds, skin darkening, acanthosis nigricans, laryngeal dyspnoea (fixed cords), obstructive sleep apnoea, goitre, carpal tunnel
  5. Impaired glucose tolerance, HTN, LVH, colon cancer
  6. High glucose, Ca2+, phosphate
  7. Serum IGF-1 levels
  8. OGTT - GH fails to suppress
  9. MRI scan of pituitary fossa
  10. Ressection
49
Q

Polycystic ovarian syndrome

  1. Symptoms
  2. Bloods
  3. USS
  4. Management - conservative
  5. Management - medical
  6. Other causes of hirsuitism
  7. Virilism - symptoms
  8. Virilism - cause
A
  1. Secondary oligo/amenorrhoea, infertility, obesity, acne, hirsuitism
  2. High testosterone, LH/FSH ratio, TSH, lipids; low sex hormone binding globulin
  3. Bilateral polycystic ovaries
  4. Healthy eating, optimise weight, hair removal if desired
  5. COCP (Yasmin/co-cyprindiol), metformin (insulin resistance), clomifene (infertility)
  6. Familial, idiopathic, increased androgen secretion from ovaries (ovarian cancer, OHCS), adrenal gland (Cushing’s syndrome, adrenal cancer), or drugs (steroids), virilism
  7. Amenorrhoea, clitoromegaly, deep voice, temporal hair recession, hirsuitism
  8. Androgen-secreting tumour (ovarian or adrenal)
50
Q

Hypopituitarism

  1. What is it
  2. Order in which effected
  3. Causes from 3 locations
  4. Hormone lack symptoms
  5. Hormonal management to give first
A
  1. Less secretion of anterior pituitary hormones
  2. GH, gonadotrophins (FSH/LH), TSH, ACTH, PRL
  3. Hypothalamus (e.g. Kallman’s), pituitary stalk, pituitary
  4. GH (central obesity, atherosclerosis, weaker), FSH/LH (reproductive symptoms), hypothyroid, adrenal insufficiency (but no skin pigmentation)
  5. Hydrocortisone for secondary adrenal failure
51
Q

Pituitary tumours

  1. Types and effects (3)

Pituitary apoplexy

  1. What it is, causes
  2. When to suspect
  3. Management
A
  1. Chromophobe (commonest, pressure effects/prolactin), acidophil (GH/PRL), basophil (ACTH)
  2. Rapid pituitary enlargement from bleed into tumour, causing cardiovascular collapse from acute hypopituitarism
  3. Acute onset headache, meningism, reduce GCS, visual field defect when known tumour
  4. Urgent hydrocortisone 100mg IV, fluid balance, cabergoline (if prolactinoma) and surgery
52
Q

Hyperosmolar hyperglycaemic state (HHS/HONK)

  1. Related DM
  2. Typical patient
  3. Pathophysiology
  4. Consequent electrolyte loss
  5. Presentation
  6. Diagnosis
  7. Serum osmolarity considered ‘significantly raised’
  8. Management
  9. Complications of hyperosmolar state
  10. Other neurological complications
  11. CPM - cause
A
  1. Type 2
  2. Elderly
  3. Hyperglycaemia leads to osmotic diuresis, increasing serum osmolarity and blood viscosity, so severe dehydration
  4. Sodium, potassium
  5. Lethargy, N+V, headache, papilloedema, weakness, hypotension, tachycardia
  6. Hypovolaemia, marked hyperglycaemia (>30) without significant ketonaemia/acidosis, + significantly raised serum osmolarity
  7. > 320 mosmol/kg
  8. Gradually rehydrate + normalise osmolarity (0.9% NaCl), replace electrolytes
  9. Increased plasma viscosity - stroke, VTE, MI
  10. Seizures, cerebral oedema. central pontine myelinolysis
  11. Too rapid correction of hyponatraemia
53
Q

Refeeding syndrome

  1. Risk factors
  2. Pathophysiology
  3. When it occurs
  4. Signs
  5. Prevention
  6. Management
A
  1. Artificial feeding post-starvation, malignancy, anorexia, alcoholism
  2. Fat/protein metabolism leads to low circulating insulin and depletes intracellular phosphate stores. When refeeding, high insulin and low phosphate
  3. Within 4 days
  4. Rhabdomyolysis, red and white cell dysfunction, respiratory insufficiency, arrhythmias, cardiogenic shock, seizures
  5. High dose pabrinex in first 4 days
  6. Parenteral and oral phosphate; manage signs

Medical School (28 decks)

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