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Phase 3A > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is acromegaly?

A
  • Excess growth hormone, normally secondary to pituitary adenoma
  • Spade like hands and feet, large tongue, excessive sweating, raised prolactin, protruding jaw
  • Sometimes features of pituitary tumour: headaches, bitemporal haemianopia
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2
Q

Investigations of acromegaly?

A
  • IGF1 levels initially then OGTT as gold standard (GH will not be suppressed)
  • Pituitary MRI
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3
Q

Management of acromegaly?

A
  • Trans-sphenoidal surgery
  • Somatostatin analogues which inhibit GH release e.g Octreotide
  • Pegvisomant which is GH receptor antagonist
  • Dopamine agonists e.g. bromocriptine
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4
Q

What is Addisons disease?

A
  • Autoimmune destruction of darnel glands causing primary hypoadrenalism
  • Reduced cortisol and aldosterone
  • Lethargy, anorexia, weight loss, hyperpigmentation, ‘salt craving’
  • Hyponatraemia and Hyperkalaemia
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5
Q

Other causes of hypoadrenalism?

A
  • TB
  • Metastases
  • HIV
  • Antiphospholipid
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6
Q

How to tell difference between primary Addisons and secondary adrenal insufficiency?

A
  • Hyperpigmentation is only in primary Addisons
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7
Q

Investigations for Addisons

A
  • 9am serum cortisol
  • Synacthen test (gold standard): cortisol levels will not increase adequately
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8
Q

Management of Addisons

A
  • Replacement glucocorticoid (cortisol): hydrocortisone
  • Replacement mineralocorticoid (aldosterone): fludrocorticoid
  • Doses given to mirror cycle of release in body
  • Patient education around illness and symptoms of adrenal crisis
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9
Q

Addisonian crisis

A
  • Causes by sepsis, surgery, haemorrhage or steroid withdrawal
  • Hypotension, shock, delirium, abdo pain, vomiting, headaches, fever
  • Managed with IM/IV Hydrocortisone, IV fluids
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10
Q

What is Bartter’s syndrome?

A
  • Inherited cause of severe hypokalaemia due to defective chloride absorption at the loop of Henle
  • Presents with failure to thrive in childhood/diabetes like symptoms
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11
Q

Corticosteroid Groups

A
  • Mineralocorticoid: Fludrocortisone
  • Glucocorticoid: Hydrocortisone, Dexamethasone, Betamethasone
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12
Q

Steroids side effects

A
  • Impaired glucose regulation
  • Increased appetitie/weight gain
  • Hirsutism
  • Hyperlipidaemia
  • Cushings syndrome (moon face, buffalo hump)
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13
Q

Steroids management

A
  • Doses should be doubled in intercurrent illness for those on long-term steroids
  • Should not be withdrawn abruptly: Addisionian crisis
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14
Q

Cushings disease

A
  • Pituitary adenoma secreting excessive ACTH which stimulates excessive cortisol from the adrenals
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15
Q

Causes of Cushings syndrome (high levels of glucocorticoids in the body)

A
  • Cushings disease
  • Adrenal adenoma (excess cortisol)
  • Paraneoplastic syndrome
  • Exogenous steroid use
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16
Q

Cushings syndrome presentation

A
  • Moon face
  • Central obesity
  • Abdominal striae
  • Buffalo hump
  • Hirsutism
  • Hyperpigmentation of skin in Cushings disease
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17
Q

Conditions associated with Cushings

A
  • HTN
  • T2DM
  • Osteoporosis
  • Dyslipidaemia
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18
Q

What sign helps to distinguish cushings diseases as a cause compared to steroids/adrenal adenoma?

A

Hyperpigmentation of skin (ACTH stimulates melanin production)

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19
Q

Management of Cushings

A
  • High dose dexamethasone supression test
  • Removal of pituitary/adrenal tumour
  • Adrenalectomy plus lifelong steroid replacement
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20
Q

T1DM

A
  • Pancreas stops producing adequate insulin
  • Hyperglycaemia: polyuria, polydipsia, weight loss
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21
Q

Insulin production

A
  • Beta cells in islets of langerhans in pancreas -> causes absorption of glucose by cells and promotes glycogenesis where glucose is stored as glycogen in liver
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22
Q

DKA Triad

A
  • Ketoacidosis
  • Dehydration
  • Potassium imbalance
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23
Q

Presentation of DKA

A
  • Polyuria
  • Polydipsia
  • N+V
  • Sweet smelling breath
  • Dehydration
  • Weight loss
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24
Q

Treatment of DKA

A
  • IV Fluids
  • Insulin
  • Glucose
  • Potassium
  • Infection
  • Chart fluids
  • Ketone monitoring
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25
Q

Long term management of T1DM

A
  • Insulin via basal bolus (1 long acting and then short-acting before meals0
  • Monitor blood sugar and complications
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26
Q

Hypoglycaemia

A
  • Hunger
  • Tremors
  • Sweating
  • Irritability
  • Dizziness
  • Pallor
  • Tx with rapid acting glucose followed by slower acting carbohydrates
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27
Q

T2DM

A
  • Fasting glucose >7
  • Random glucose >11.1
  • HBA1c > 48
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28
Q

T2DM Treatment

A
  1. Metformin
  2. SGLT-2 inhibitor e.g empagliflozin for patients with high risk of CVD
  3. DPP-4 inhibitor e.g. Sitagliptin
  4. Sulfonylurea e.g. Gliclazide
  5. Insulin
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29
Q

Metformin pharmacology

A
  1. increases insulin sensitivity/decreases glucose production
  2. Does not cause weight gain/hypoglycaemia
  3. S/E include GI symptoms and lactic acidosis
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30
Q

SGLT-2 Inhibitors pharmacology

A
  1. Blocks reabsorption of glucose from urine into blood causing it to be excreted
  2. Cause cause hypoglycaemia when used with sulfonylurea/insulin
  3. S/E include urinary frequency/urgency, thrush, weight loss, DKA
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31
Q

Sulphonylurea pharmacology

A
  1. Stimulate insulin release from pancreas
  2. S/E include weight gain and hypoglycaemia
32
Q

DPP-4 inhibitor pharmacology

A
  1. Block action of DPP enzyme allowing increased incretin activity which increase insulin secretion, inhibit glucagon production
  2. S/E include headaches and low risk of acute pancreatitis
33
Q

Hyperglycaemic Hyperosmolar state

A
  • Hyperosmolality: concentrated blood
  • Hyperglycaemia
  • Absence of ketone
  • Tx with IV fluids and monitoring
34
Q

Diabetic Neuropathy

A
  • Glove and stocking distribution
  • Management of AMT, Duloxetine, Gabapentin, Pregabalin
  • Topical capsaicin may be used for localised pain
35
Q

What is Conn syndrome?

A

High levels of aldosterone caused by an adrenal adenoma producing too much aldosterone

36
Q

RAAS Cycle

A
  • Renin produced in afferent arterioles in kidney and is secreted from BP is low
  • Renin converts angiotensiongen into angiotensin I
  • ACE convers AG I into AG2 which stimulates release of aldosterone from adrenals
37
Q

How does aldosterone increase BP?

A
  • Increased sodium reabsorption in DT
  • Increase potassium secretion from DT
  • Increase hydrogen secretion from ducts
38
Q

Causes of primary and secondary hyperaldosteronism?

A

Primary
1. Bilateral adrenal hyperplasia
2. Conns
Secondary
1. Renal artery stenosis
2. Heart failure

39
Q

Management of Conns

A
  • Ald:Renin ratio (high Ald and low renin)
  • CT/MRI to look for andenoma
  • Tx includes spironolactone/surgery to remove adenoma
40
Q

Hypothyroidism

A

Primary: Pathology at thyroid: High TSH, low T3/T4
Secondary: Pathology at pituitary: Low TSH, low T3/T4

41
Q

Most common causes of hypothyroidism

A

Primary: Hashimotos in developed, Iodine deficiency in developing
Secondary: Tumours, Surgery, Sheehans

42
Q

Presentation of Hypothyroidism

A
  • Weight gain
  • Fatigue
  • Dry skin
  • Cold intolerance
  • Coarse hair/loss
  • Constipation
  • Heavy/irregular periods
  • Goitre
43
Q

Hashimotos

A
  • Anti TPO antibodies and anti-TG antibodies
44
Q

Hyperthyroidism

A

Primary: thyroid pathology: high T3, T4, low TSH
Secondary: pituitary/hypothalamus pathology: high T3/T4, high TSH

45
Q

Causes of hyperthyroidism

A

Graves
Inflammation
Solitary toxic thyroid nodule
Toxic multinodular goitre

46
Q

Presentation of hyperthyroidism

A
  • Anxiety and irritability
  • Sweating and heat intolerance
  • Tachycardia
  • Weight loss
  • Fatigue
  • Diarrhoea
  • Sexual dysfunction
47
Q

Graves specific features

A
  • Diffuse goitre
  • Graves eye disease: proptosis
  • Pretibial myoxedema: waxy, appearance often on shins
48
Q

Graves

A
  • TSH receptor antibodies
49
Q

De Quervains thyroiditis

A
  1. Thyrotoxicosis
  2. Hypothyroidism
  3. Return to normal
    - Self limiting conditions, which requires supportive management
50
Q

Thyroid Storm

A
  • Rare presentation of hyperthyroidism with fever, tachycardia and delirium
  • Can be life threatening
  • Requires fluid resus, anti-arrhythmic
51
Q

Tx of Hyperthyroidism

A
  • Referral to secondary care if Graves
  • Carbimazole for 12-18 months with either maintenance for life or block and replace with levothyroxine
  • Propylthiouracil
  • Radioactive iodine to block and replace
  • Propranolol
  • Surgery to remove then replace
52
Q

S/E of Carbimazole/Propylthiouracil

A

Carbimazole: Risk of acute pancreatitis, agranulocytosis
Propylthiouracil: agranulocytosis, liver reactions

53
Q

Parathyroid physiology

A
  • PTH glands produce PTH in response to hypocalcaemia
  • PTH increases osteoclast activity (calcium reabsorption via bones), increases reabsorption in kidneys and increases vit D which increases calcium absorption in intestines
54
Q

Symptoms of hypercalcaemia

A
  • Kidney stones
  • Painful bones
  • Abdominal groans (constipation, N+V)
  • Psych moans (fatigue, depression and psychosis)
55
Q

Hyperparathyroidism

A

Primary: uncontrolled PTH production by PTH tumour causing hypercalcaemia, treated with removal
Secondary: insufficient vit D/CKD causes hypocalcaemia and so excess PTH, treated with treat cause
Tertiary: secondary HPT of occurs for long time causes hyperplasia and high PTH and hypercalcaemia, treated with removal of some parathyroid

56
Q

Hypoparathyroidism

A

Primary: decreased PTH, low calcium and phosphate, tx with alfacalcidol

57
Q

Presentation of hypoparathyroidism

A
  • Muscle twitching, cramps and spasms
  • Prolonged QT interval
  • Perioral paraesthesia
  • Chvostek sign: tapping over parotid causes facial twitch
  • Trousseau sign: carpal spams when brachial artery occleded
58
Q

SIADH

A
  • Increased release of ADH from posterior pituitary which increases water reabsorption and causes euvolemic hyponatraemia
  • High urine osmolality and high urine sodium
59
Q

Causes of SIADH

A
  • Post op
  • Pneumonia/Lung abscess
  • Brain pathology
  • Iatrogenic e.g SSRI/Carbamazepine
  • Malignancy - small cell lung cancer
60
Q

Presentation of SIADH

A
  • Headaches
  • Fatigue
  • Muscle aches and cramps
  • Confusion
  • Seizures if severe
61
Q

Management of SIADH

A
  • Clinical features from bloods/urine dip
  • Exclude other causes
  • CTTAP if suspect cancer
  • Tx includes treat cause, fluid restriction and tolvaptan (blocks ADH receptors but works very quickly so needs close monitoring)
62
Q

Complication of severe hyponatraemia

A
  • Central pontine myelinolysis/osmotic demyelination syndrome
63
Q

What is diabetes insipidus?

A
  • Lack of ADH (cranial)
  • Lack of response to ADH (nephrogenic)
  • Causes polyuria, polydipsia, postural hypotension
64
Q

Nephrogenic Causes

A
  • Idiopathic
  • Medications e.g lithium
  • Genetic mutations
  • High calcium/low potassium
  • Renal disease
65
Q

Cranial causes

A
  • Idiopathic
  • Brain tumours/injury/surgery/infection
  • Genetic mutations
66
Q

Investigations for DI

A
  • Low urine osmolality, high/normal serum osmolality
  • Water deprivation test:
    Cranial: Low UO after water deprivation, high after desmopression
  • Nephrogenic: Low UO after both
67
Q

Tx of DI

A

Cranial: Desmopressin
Nephrogenic: Fluids, high dose desmopressin, diuretics, NSAIDs

68
Q

Phaeochromocytoma

A
  • Tumour of chromaffin cells which secretes excessibe adrenaline
  • Common with MEN2, NF1 and von Hippel-lindau
69
Q

Presentation of phaeochromocytoma

A
  • Anxiety
  • Sweating
  • Headache
  • Tremor
  • Palpitations
  • HTN
70
Q

Management of phaeochromocytoma

A
  • Plasma free metanephrine/24 hoururine catecholamines
  • CT/MRI to confirm tumour
  • Tx includes alpha blockers e.g doxazosin, beta blocks and surgical removal
71
Q

Thyroid eye disease

A
  • Smoking is the most important risk factor
  • Can be with hypo/hyper
  • Proptosis, optic disc swelling, conjunctival oedema
  • Tx with topical lubricants, steroids, radiotherapy
72
Q

Thyroid nodules

A
  • Requires exclusion of thyroid cancer
  • Benign include: Goitre, thyroid adenoma, cysts
  • Malignant include: Papillary carcinoma, follicular carcinoma
  • US is imaging of choice
  • Malignancy treated with thyroidectomy, radioiodine and yearly thyroglobulin levels
73
Q

Which diabetes medication causes weight loss?

A

SGLT-2 inhibitors e.g. empaglioflozin
GLP-1 agonists e.g semaglutide

74
Q

Electrolyte abnormality found in Addisons?

A

hyperkalaemia, hyponatraemia, hypoglycaemia

75
Q
A

Phase 3A (10 decks)

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