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Endocrine Flashcards

1
Q

Causes of hypoglycaemia?

A 
Too much insulin, too much exercise, too little carbohydrates or combination. 
Alcohol 
Sulphonylureas 
Adrenal failure
Liver failure 
Hypopituitarism 
Infection

Patients with DM secondary to total pancreatectomy more susceptible

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2
Q

What is C-peptide?

A

Low C-peptide = exogenous insulin

High C-peptide = endogenous insulin

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3
Q

Treatment of hypo if able to swallow?

A

Glucotabs/Glucogel, lucozade

Rpt CBG in 10-15 mins - repeat up to x3 if low

If no improvement –> IV glucose/IM glucagon

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4
Q

Management of hypo if unconscious?

A

75-100ml 20% glucose OR
150-200 ml 10% glucose over 15 mins

or IM glucagon 1mg

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5
Q

What to give after a hypo?

A

Continuous infusion of 10% glucose for 8hrs if due to insulin/sulphonylurea

Once CBG >4, long acting carbs/normal meal

CONTINUE NORMAL INSULIN DOSES

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6
Q

How long no driving after hypo?

A

45 mins

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7
Q

Diagnostic criteria for DKA?

A

Hyperglycaemia (>11mmol/L)

Acidosis (venous pH <7.3 or bicarb <15mmol/L)

Blood ketones >3mmol/L or ketonuria (>++)

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8
Q

When to give K+ in DKA?

A

Add potassium supplementation (40mmol/L after 1st bag) – max 2L.

Still give if K+ normal - only withhold K+ if >5.5 – if <3.5, GET HELP – need a central line.

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9
Q

Rate of infusion in DKA?

A

Fixed rate insulin IV infusion - 0.1 unit/kg/hr IV over a sliding scale.

50 units human soluble insulin e.g. Actrapid in 50ml 0.9% saline)

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10
Q

When to monitor ketones, K+ and pH in DKA?

A

Monitor glucose and ketones hourly, and venous HCO3-, K+ and pH at 60 min and 2 hourly thereafter; K+ will fall unless replaced.

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11
Q

When to stop insulin infusion in DKA?

A

Continue insulin infusion until ketones<0.3mmol/L and pH >7.3.

At this point convert to regular SC insulin if eating and drinking normally, otherwise using a sliding scale

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12
Q

Continue long acting insulin in DKA?

A

YES

Prevents rebound hyperglycaemia when IV stopped. Short-acting insulin stopped until about to discontinue IV

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13
Q

Diagnosis of T1DM?

A

Symptoms plus…

Random venous blood glucose >11.1
OR
Fasting venous blood glucose >7.0
OR
OGTT

If asymptomatic, need 2 separate results

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14
Q

Symptoms of diabetes?

A

Thirst, toilet, thinner, tired

Infections - skin, UTI, candida genital infections

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15
Q

HbA1c to diganose TIIDM?

A

48 mmol/mol

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16
Q

HbA1c targets in TIIDM?

A

Lifestyle/monotherapy - 48 mmol/mol

Hypo-associated drug - 53 mmol/mol

Dual therapy/triple therapy/insuline - 53 mmo/mol

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17
Q

Name, mechanism, benefits/disadvantages of biguanides?

A

Metformin

Decreases glucose production by liver and increases insulin sensitivity of body tissues.

Doesn’t put on weight or cause hypos, but causes bowel problems.
Not indicated if eGFR <35.

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18
Q

Name, mechanism, benefits/disadvantages of Sulfonylureas?

A

Gliclazide, glimepiride

Depolarises pancreatic beta cells, which opens voltage gated Ca2+ channels, leading to increased secretion of insulin.

Causes weight gain. Better than metformin at reducing blood glucose quickly – good if patient experiencing symptoms.

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19
Q

Name, mechanism, benefits/disadvantages of DDP-4 inhibitors?

A

Sitagliptin, alogliptin, linaliptin

Inhibits enzyme which breaks down incretin, which is released in response to oral glucose - ↓incretin –> ↓glucagon –> ↑insulin.

Linagliptin safe in renal impairment.

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20
Q

Name, mechanism, benefits/disadvantages of Thiazolidinediones?

A

Pioglitazone

Reduces insulin resistance in the liver and peripheral tissues, decreases gluconeogenesis in the liver –> reduces blood glucose.

Contraindicated in heart failure, hepatic impairment, DKA, history of bladder cancer, uninvestigated macroscopic haematuria.

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21
Q

Name, mechanism, benefits/disadvantages of SGLT2 Inhibitor?

A

Dapagliflozin, canagliflozin, empagliflozin

Inhibits reabsorption of glucose in the kidney –> lower blood sugar because peeing out glucose.

Can cause weight loss because of lost calories, but can cause UTI/thrush.

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22
Q

Name, mechanism of GLP-1 agonist?

A

Liraglutide, exendatide

Works on same pathway as DPP-4 inhibitors but are more potent.

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23
Q

Screening in TIIDM?

A

Retinopathy – screening programme

Foot problems – annual foot check

Nephropathy – annual screening (Urine ACR and eGFR)

Cardiovascular Risk Factors
Age, albuminuria, smoking status, blood glucose control, blood pressure, full lipid profile

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24
Q

What causes Grave’s disease?

A

IgG against TSH receptor

Process also directed towards soft tissues in the orbit –> inflammation and swelling

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25
Q

What is Grave’s associated with?

A

T1DM, Addison’s, Coeliac etc

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26
Q

Signs specific to Grave’s disease?

A
  1. Eye disease – exophthalmos, opthalmoplegia, swelling around the eyes (congestive opthalm-something)
  2. Pretibial myxoedema – odematous swellings above lateral malleoli.
  3. Thyroid acropachy – extreme manifestation, with clubbing, painful finger and toe swelling and periosteal reaction in limb bones
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27
Q

Complications of Grave’s disease?

A

Heart failure (thyrotoxic cardiomyopathy), angina, AF, osteoporosis, opthalmopathy, gynaecomastia.

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28
Q

Blood results in Grave’s disease? Other investigations?

A

TSH↓ (suppressed), T3 and T4↑

May be mild normocytic anaemia, mild neutropenia (Grave’s), ESR↑, Ca2+↑, LFT↑

Thyroid receptor antibody (TRAB), USS (if nodule –> possible Ca)

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29
Q

Drug management of Grave’s disease?

A

Symptomatic treatment = Beta-blockers
Long-term treatment = Antithyroid drugs

Carbimazole – for short-term control or to achieve remission. 18 months treatment usually recommended

Giving carbimazole and levothyroxine together reduces the risk of iatrogenic hypoT.

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30
Q

Surgical management of Grave’s disease?

A

Thyroidectomy

Risk of damage to recurrent laryngeal nerve/ hypoparathyroidism

Most become hypothyroid

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31
Q

Radioiodine management of Grave’s disease?

A

Increasingly 1st line - most become hypoT after treatment

Contraindicated in pregnancy and lactation

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32
Q

Causes of hypothyroidism?

A

Primary atrophic - no goitre

Hashimoto’s thyroiditis - goitre

Iodine deficiency, post thyroidectomy or iodine, drug induced, subacute thyroiditiis (temporary hypo after hyper phase)

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33
Q

Signs of hypothyroidism?

A

BRADYCARDIC

Bradycardia
Reflexes relax slowly
Ataxia (cerebellar)
Dry thin hair/skin Yawning/drowsy/coma
Cold hands
Ascites
Round puffy face/double chin/obese
Defeated demeanour, Immobile + ileus
CCF

Peaches and cream complexion

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34
Q

Management of hypothyroidism?

A

Levothyroixine

If IHD, start low and titrate dose upwards.

Treatment usually lifelong.

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35
Q

What does Addison’s result in the deficiency of?

A

Mineralocorticoids (aldosterone)

Glucocorticoids (cortisol)

Androgens (testosterone, DEHA)

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36
Q

Symptoms of Addison’s?

A

GENERAL = Fatigue, muscle weakness/pain

CVS = Hypotension (postural) –> dizziness and headache

GI = Anorexia, weight loss, N+V, intermittent abdo pain, salt craving

Decrease in pubic/axillary hair, depression, impotence/ amenorrhoea, hypoglycaemia, depression

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37
Q

Signs of Addison’s?

A

Skin pigmentation (due to high ACTH)

Dull, grey-brown colouration - exposed skin, pressure areas, palmar creases, knuckles, buccal mucosa, recent scars

May be associated with vitiligo –> patchy appearance

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38
Q

Triggers of Addisonian crisis?

A

Trauma
Severe hypotension
Sepsis

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39
Q

Presentation of addisonian crisis?

A 
Intensification of pre-existing symptoms, especially nausea, vomiting, epigastric pain
Fever
Lethargy
Hypotension
Hypovolaemic vascular shock
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40
Q

Management of Addisonian crisis?

A

Management = rapid elevation of circulating glucocorticoid and replacement of salt and glucose loss

GP – hydrocortisone 100mg IM –> hospital
IV fluids
Oral replacement once stable

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41
Q

Blood results in Addisons?

A

↓Na+, ↑K+/H+ - due to low aldosterone

↑Urea/albumin – due to dehydration

↑Serum renin – due to sodium depletion

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42
Q

Diagnosis of Addison’s?

A

Serum Cortisol levels - (8-9am)

If between 100-400 nanomol/L –> refer to specialist for short synacthen test

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43
Q

Management of Addison’s long term?

A

Treat cause + replace glucocorticoid and mineralocorticoid + education.

  • MedicAlert bracelet and steroid card
  • Hydrocortisone (10mg/M2 per day), fludrocortisone (0.1-0.3 mg/day) and dehydropiandrosterone (DHEA) daily
  • Screen for other autoimmune diseases (thyroid)

Requires lifelong treatment.

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44
Q

Features of diabetic foot disease?

A

Microangiopathy –> peripheral neuropathy

Sensory = decreased awareness of injury

Motor = distortion of weight bearing characteristics of foot

Autonomic = disruption of control of vascular supply/sweating

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45
Q

Actions of PTH?

A

2 ACTIONS ON KIDNEY, 1 ON BONE (high calcium, low phosphate)

Increases reabsorption of Ca2+ by kidney
Increases renal-1-hydroxlyase –> produces calcitirol (active form of vitamin D) –> more absorption from gut

Stimulates osteoclast activity –> release calcium from bone

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46
Q

What is primary hyperparathyroidism?

A

One or more parathyroid glands produce excess PTH – 80% = solitary adenoma.

47
Q

What is secondary hyperparathyroidism? (most common)

A

PTH secreted excessively in response to prolonged ↓Ca2+ and phosphate levels (due to kidney, liver or bowel disease) – chronic renal failure/malabsorption/vitamin D deficiency.

48
Q

What is tertiary hyperparathyroidism?

A

Autonomous secretion of PTH as a result of longstanding CKD (hyperplastic change of glands).

49
Q

Biochemistry of primary/ secondary/tertirary hyperparathyroidism?

A

Primary = ↑PTH, ↑Ca2+

Secondary = ↑PTH, ↓Ca2+

Tertiary = ↑↑PTH, ↑Ca2+ + Renal Failure

50
Q

Management of primary hyperparathyroidism?

A

Increase fluid intake to prevent stones and avoid thiazides/high Ca2+ and phosphate intake

Excision of adenoma if complications

Cinacalet - increases sensitivity of PT glands to Ca2+

51
Q

Management of secondary hyperparathyroidism?

A

Phosphate binders/vit D

Cinacalcet/parathyroidectomy

52
Q

Cancers that cause hypercalcaemia?

A 
NSCLC (squamous cell)
Breast
Renal cell
Multiple myeloma and lymphoma
H+N cancers
53
Q

How do cancers cause hypercalcaemia?

A

Transforming growth factor alpha - stimulates bone resorption

PTH related peptides - mimics PTH

54
Q

Features of hypercalcaemia?

A

Cats go numb with a short QT

Confusion, arrhythmia, tetany, numbness, long QT

(Bones, stones, moans, groans)

55
Q

Classification of hyperlipidaemia?

A

Primary - high LDL only

Familial - LDL receptor defects

Secondary - cushing’s, hypoT, nephrotic syndrome, cholestasis

Mixed - high LDL and triglycerides, caused by T2DM, metabolic syndrome, alcohol abuse and CKD

56
Q

Target for reducing cholesterol?

A

40% reduction in non-HDL cholesterol after 3 months

57
Q

Most common cause of hypoparathyroidism?

A

Destruction during surgery

Others = primary (idiopathic/congenital), DiGeorge syndrome, infiltration by iron (haemochromatosis, mets)

Hypomagnasaemia (Mg is necessary for PTH secretion)

Vitamin D excess

58
Q

What is pseudohypoparathyroidism?

A

Failure of target cells to respond to PTH (autosomal dominant - rare)

59
Q

Results in hypoparathyroidism?

A

Low calcium, high phosphate

Normal alk phos, low PTH

60
Q

Risk factors for thyroid cancer?

A 
Radiation to neck area 
Radioiodine treatment
Deficiency and excess dietary iodine
Prolonged stimulation with TSH (can be due to iodine deficiency)
Chronic lymphocytic thyroiditis
61
Q

Types of thyroid cancer?

A

Papillary adenocarcinoma (80%), follicular adenocarcinoma (10%), medullary adenocarcinoma (5%), anaplastic carcinoma (3%), thyroid lymphoma (1%)

62
Q

Presentation of thyroid cancer?

A

Rapidly growing hard thyroid mass

Lymphadenoapthy

Indicators of extrathyroidal invasion (hoarseness, dysphagia)

History of ionising radiation/family history of thyroid cancer

63
Q

What is a multinodular (toxic) goitre?

A

2nd most common cause of hyperT after Grave’s

Functionally autonomous thyroid nodules produce T3/T4

64
Q

Cause of multinodular goitre?

A

Iodine deficiency –> reduced T4 production –> thyroid cell hyperplasia

Predisposes to mutation in TSH receptor

If receptor is constitutively active, becomes toxic and produces excess T3/T4.

65
Q

What is a toxic nodule?

A

Benign tumour of thyroid gland - usually follicular adneoma.

Neoplasm resulting from a single cell

66
Q

Toxic nodule on examination?

A

Solitary, spherical, encapsulated lesion that is well demarcated from surrounding parenchyma. 3cm diameter on average.

67
Q

Complications of a simple (non toxic) goitre?

A

Dysphagia
Vocal changes
Dyspnoea
Facial congestion

68
Q

Types of thyroiditis?

A

Hashimoto’s (autoimmune) thyroiditis

De Quervains (subacute granulomatous thyroiditis)

Subacute lymphocytic/ painless thyroiditis

Riedel’s thyroiditis

69
Q

What is autoimmune thyroiditis?

A

Most common cause of hypothyroidism in non-iodine deficient areas.

Autoimmune –> extensive infiltration of the thyroid parenchyma by lymphocytes and plasma cells, with the formation of germinal centres.

70
Q

Examination findings in thyroiditis?

A

GOITRE + HYPOTHYROIDISM

Thyroid firm, well defined with enlarged pyramidal lobe and palpable neighbouring lymph nodes.

Enlargement slow and painless, but rarely may be more rapid and painful

71
Q

Progression of visual field defects in pituitary adenoma?

A

Superior bi-temporal quadrantanopia progressing to bi-temporal hemianopia

72
Q

What is Pheochromocytoma?

A

Functional neuroendocrine tumour that arises from chromaffin cells in adrenal medulla – secretes a high amount of catecholamines

Usually adrenaline/noradrenaline - can also secrete dopamine and ACTH

73
Q

Symptoms of Pheochromocytoma?

A

Hypertension –> hypertensive crisis (can be triggered by any stressor)

Headache, palpitations, tachycardia, sweating, anxiety, panic attacks, tremor, N+V, fever

Prolonged –> CCF + Pulmonary oedema

74
Q

Diagnosis of Pheochromocytoma?

A

24 hour collection of urinary catecholamines

Imaging to localise tumour (CT/MRI)

75
Q

Management of Pheochromocytoma?

A

Alpha blockers until definitive surgery

76
Q

Situations to consider Pheochromocytoma?

A

Hypertensive with orthostatic hypotension and tachycardia

Hypertensive whose symptoms respond poorly to anti-hypertensive treatment

Patient whose blood pressure fluctuates widel

Hypertensive with cafe au lait spots

77
Q

What is Cushing’s syndrome?

A

Clinical state produced by chronic glucocorticoid excess and loss of the normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis and loss of circadian rhythm of cortisol secretion

78
Q

ATCH dependent causes of Cushing’s syndrome?

A

CUSHING’S DISEASE
Bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma. Does not respond to dexamethasone suppression test.

ECTOPIC ACTH PRODUCTION
SCLC/carcinoid tumours pigmentation (due to ↑↑ACTH), hypokalaemic metabolic alkalosis (↑↑cortisol leads to mineralocorticoid activity), weight loss, hyperglycaemia

79
Q

ACTH-independent causes of Cushing’s syndrome?

A

IATROGENIC (most common)
Long term steroids

ADRENAL ADENOMA, ADRENAL NODULAR HYPERPLASIA
No suppression with dexamethasone because tumours/nodules are autonomous

80
Q

Symptoms of Cushing’s syndrome?

A

Weight gain

Mood change (depression, lethargy, irritability, psychosis)

Proximal weakness

Gonadal dysfunction (irregular menses, hirsutism, erectile dysfunction)

Acne

Recurrent Achilles tendon rupture

Occasionally virilisation if female

81
Q

Signs of Cushing’s syndrome?

A

Central obesity

Plethoric moon face

Buffalo neck hump

Supraclavicular fat distribution

Skin and muscle atrophy, bruises, purple abdominal striae

Osteoporosis, ↑BP, ↑glucose, infection-prone, poor healing

82
Q

How is congenital adrenal hyperplasia (adrenogenital syndrome) inherited?

A

Autosomal recessive inheritance

83
Q

Pathophysiology of congenital adrenal hyperplasia?

A

Enzyme deficiency leading to…

  1. Deficient cortisol/ aldosterone production
  2. Excess precursor steroids
84
Q

Features of congenital adrenal hyperplasia?

A

Virilisation (females)

Hyperpigmentation (males - scrotum)

Tall stature/precocious puberty (males)

Adrenal crisis (in first days of life)

85
Q

What happens if you have to much aldosterone secretion?

A

Hypokalaemia (excretion of K+)

Metabolic alkalosis (excretion of H+)

HTN (retention of Na+ and H2O)

86
Q

Primary cause of Hyperaldosteronism?

A

CONN’S SYNDROME

High aldosterone levels in absence of activation of RAAS

Can be caused by adrenal adenoma (majority), bilateral adrenal nodular hyperplasia and adrenal carcinoma

87
Q

Secondary causes of Hyperaldosteronism?

A

High levels of aldosterone are present as a result of activation of the RAAS

Causes = diuretic therapy, accelerated HTN, CCF, nephrotic syndrome, liver cirrhosis with ascites, renal artery stenosis, bronchial carcinoma (rare)

88
Q

Presentation of Hyperaldosteronism?

A

Asymptomatic

Mild HTN, lethargy, muscular weakness, polyuria/polydipsia, persistent hypokalaemia, intermittent paraesthesiae, tetany and occasionally paralysis.

Sodium usually mildly elevated or normal.

89
Q

Main cause of hirsutism?

A

PCOS

90
Q

Pathophysiology of PCOS?

A

Disordered LH production and peripheral insulin resistance with compensatory raised insulin levels –> raised ovarian androgen production.

↑Insulin –> ↑adrenal androgen production

Increased intraovarian androgens –> excess follicles and absent/irregular ovulation

↑Peripheral androgens –> hirsutism

91
Q

Consequences of PCOS?

A

At risk of TIIDM, endometrial cancer (unopposed oestrogen due to amenorrhoea), but normal oestrogen levels so not at risk of osteoporosis

92
Q

Why does obesity worsen PCOS?

A

Increasing body weight –> increased insulin –> increased androgen levels

93
Q

Investigations in hirsutism?

A

Measure early morning plasma total testosterone

Pelvic USS (is suspicion of PCOS)

Pregnancy test (if amenorrhoea)

LH/FSH, prolactin, TFTs etc.

94
Q

Treatment of hirsuitism?

A

Physical hair removal

Weight loss

Anti-androgens (cyproterone acetate/ spironolactone), oestrogen, GnRH analogues, glucocorticoids, metformin (in PCOS)

Topical eflornithine

95
Q

Features of HHS?

A

Hypovolaemia

Marked hyperglycaemia (30 mmol/L or more) without significant hyperketonaemia (pH 7.3, bicarbonate >15 mmol/L)

Osmolality usually 320 mosmol/kg or more

96
Q

When is ADH released?

A

In response to…

  1. Decrease in plasma volume
  2. Increase in serum osmolality

Opens aquaporins in DCT –> water flows back into circulation

97
Q

What is diabetes insipidus?

A

Passage of large volumes of dilute urine due to…

  1. Deficiency of ADH (cranial)
  2. Renal resistance to ADH (nephrogenic)
98
Q

Causes of cranial diabetes insipidus?

A

RARE

Alcohol (lol)

idiopathic, congenital, pituitary tumour, trauma

Infiltration (histiocytosis, sarcoidosis)

Vascular (haemorrhage – sheehan’s syndrome),

Infection

99
Q

Causes of nephrogenic diabetes insipidus?

A

Inherited

Metabolic (↓K+, ↑Ca2+ - hypercalcaemia causes polyuria and polydipsia),

Drugs (lithium, demeclocycline)

CKD

Post-obstructive uropathy

100
Q

Symptoms of diabetes insipidus?

A

Polydipsia, polyuria, nocturia

Confusion/coma if hypernatraemia (esp in cranial DI)

101
Q

Investigations in diabetes insipidus?

A

↑Na+

Plasma osmolality rasied
Urine osmolality low

102
Q

Definitive diagnosis in diabetes insipidus?

A

Fluid deprivation test - give desmopressin, measure urine osmolality over 12 hours

Cranial - will be able to concentrate urine

Nephrogenic - won’t be able to concentrate urine

103
Q

Investigations if TOO MUCH hormone

A

Measure at nadir
Try to suppress
Evaluate their 24 hour secretion
Measure preceding hormone (elevated T4, measure TSH)

104
Q

Investigations if TOO LITTLE hormone

A

Measure at peak
Try to stimulate
Measure preceding hormone (Elevated free T4, measure TSH)

105
Q

Determining aetiology of endocrine problems

A

Supplementary hormone tests
Immunology
Radiology/nuclear medicine

106
Q

Hyperpigmentation in Addison’s?

A

Melanocyte-stimulating hormone (MSH) and ACTH share the same precursor molecule, pro-opiomelanocortin (POMC).

After production in the anterior pituitary gland, POMC gets cleaved into gamma-MSH, ACTH, and beta-lipotropin. The subunit ACTH undergoes further cleavage to produce alpha-MSH, the most important MSH for skin pigmentation. In secondary and tertiary forms of adrenal insufficiency, skin darkening does not occur, as ACTH is not overproduced.

107
Q

Criteria for treating hypothyroid?

A

TSH >4, TPO +ve or TSH >10 TPO -ve

108
Q

Side effects of carbimazole?

A

Rash
Itch
GI upset
Agranuloctyosis (one to worry about)

109
Q

MEN1?

A

Parathyroid, pancreas, pituitary

110
Q

MEN2?

A

Phaeochromocytoma
Papillary cell carcinomas
Paratyhroid

111
Q

What does Mg deficiency do?

A

Inhibits PTH secretion –> hypocalcaemia

Magnesium deficiency caused by PPIs

112
Q

Causes of hypercalcaemia?

A

Hyperparathyroidism
Malignancy
Granulomatous disease (TB and Sarcoidosis)

Familial Hypocalciuric Hypercalcaemia
Drugs (thiazides, lithium, vit D excess)
Thyrotoxicosis/Addison’s

113
Q

Features of acute hypoadrenalism diagnostic features?

A 
Hyperpigmentation (primary)/Hypopigmentation (secondary)
Hypovolaemic collapse
Typical electrolyte changes
Other hormone abnormalities
Physical examination
114
Q

Features of secondary adrenal failure?

A

Bitemporal hemianopia

Hypopigmentation

- FINALS (24 decks)

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