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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
Long term management of T1DM
- Insulin via basal bolus (1 long acting and then short-acting before meals0 - Monitor blood sugar and complications
26
Hypoglycaemia
- Hunger - Tremors - Sweating - Irritability - Dizziness - Pallor - Tx with rapid acting glucose followed by slower acting carbohydrates
27
T2DM
- Fasting glucose >7 - Random glucose >11.1 - HBA1c > 48
28
T2DM Treatment
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
29
Metformin pharmacology
1. increases insulin sensitivity/decreases glucose production 2. Does not cause weight gain/hypoglycaemia 3. S/E include GI symptoms and lactic acidosis
30
SGLT-2 Inhibitors pharmacology
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
31
Sulphonylurea pharmacology
1. Stimulate insulin release from pancreas 2. S/E include weight gain and hypoglycaemia
32
DPP-4 inhibitor pharmacology
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
Hyperglycaemic Hyperosmolar state
- Hyperosmolality: concentrated blood - Hyperglycaemia - Absence of ketone - Tx with IV fluids and monitoring
34
Diabetic Neuropathy
- Glove and stocking distribution - Management of AMT, Duloxetine, Gabapentin, Pregabalin - Topical capsaicin may be used for localised pain
35
What is Conn syndrome?
High levels of aldosterone caused by an adrenal adenoma producing too much aldosterone
36
RAAS Cycle
- 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
How does aldosterone increase BP?
- Increased sodium reabsorption in DT - Increase potassium secretion from DT - Increase hydrogen secretion from ducts
38
Causes of primary and secondary hyperaldosteronism?
Primary 1. Bilateral adrenal hyperplasia 2. Conns Secondary 1. Renal artery stenosis 2. Heart failure
39
Management of Conns
- Ald:Renin ratio (high Ald and low renin) - CT/MRI to look for andenoma - Tx includes spironolactone/surgery to remove adenoma
40
Hypothyroidism
Primary: Pathology at thyroid: High TSH, low T3/T4 Secondary: Pathology at pituitary: Low TSH, low T3/T4
41
Most common causes of hypothyroidism
Primary: Hashimotos in developed, Iodine deficiency in developing Secondary: Tumours, Surgery, Sheehans
42
Presentation of Hypothyroidism
- Weight gain - Fatigue - Dry skin - Cold intolerance - Coarse hair/loss - Constipation - Heavy/irregular periods - Goitre
43
Hashimotos
- Anti TPO antibodies and anti-TG antibodies
44
Hyperthyroidism
Primary: thyroid pathology: high T3, T4, low TSH Secondary: pituitary/hypothalamus pathology: high T3/T4, high TSH
45
Causes of hyperthyroidism
Graves Inflammation Solitary toxic thyroid nodule Toxic multinodular goitre
46
Presentation of hyperthyroidism
- Anxiety and irritability - Sweating and heat intolerance - Tachycardia - Weight loss - Fatigue - Diarrhoea - Sexual dysfunction
47
Graves specific features
- Diffuse goitre - Graves eye disease: proptosis - Pretibial myoxedema: waxy, appearance often on shins
48
Graves
- TSH receptor antibodies
49
De Quervains thyroiditis
1. Thyrotoxicosis 2. Hypothyroidism 3. Return to normal - Self limiting conditions, which requires supportive management
50
Thyroid Storm
- Rare presentation of hyperthyroidism with fever, tachycardia and delirium - Can be life threatening - Requires fluid resus, anti-arrhythmic
51
Tx of Hyperthyroidism
- 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
S/E of Carbimazole/Propylthiouracil
Carbimazole: Risk of acute pancreatitis, agranulocytosis Propylthiouracil: agranulocytosis, liver reactions
53
Parathyroid physiology
- 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
Symptoms of hypercalcaemia
- Kidney stones - Painful bones - Abdominal groans (constipation, N+V) - Psych moans (fatigue, depression and psychosis)
55
Hyperparathyroidism
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
Hypoparathyroidism
Primary: decreased PTH, low calcium and phosphate, tx with alfacalcidol
57
Presentation of hypoparathyroidism
- 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
SIADH
- Increased release of ADH from posterior pituitary which increases water reabsorption and causes euvolemic hyponatraemia - High urine osmolality and high urine sodium
59
Causes of SIADH
- Post op - Pneumonia/Lung abscess - Brain pathology - Iatrogenic e.g SSRI/Carbamazepine - Malignancy - small cell lung cancer
60
Presentation of SIADH
- Headaches - Fatigue - Muscle aches and cramps - Confusion - Seizures if severe
61
Management of SIADH
- 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
Complication of severe hyponatraemia
- Central pontine myelinolysis/osmotic demyelination syndrome
63
What is diabetes insipidus?
- Lack of ADH (cranial) - Lack of response to ADH (nephrogenic) - Causes polyuria, polydipsia, postural hypotension
64
Nephrogenic Causes
- Idiopathic - Medications e.g lithium - Genetic mutations - High calcium/low potassium - Renal disease
65
Cranial causes
- Idiopathic - Brain tumours/injury/surgery/infection - Genetic mutations
66
Investigations for DI
- 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
Tx of DI
Cranial: Desmopressin Nephrogenic: Fluids, high dose desmopressin, diuretics, NSAIDs
68
Phaeochromocytoma
- Tumour of chromaffin cells which secretes excessibe adrenaline - Common with MEN2, NF1 and von Hippel-lindau
69
Presentation of phaeochromocytoma
- Anxiety - Sweating - Headache - Tremor - Palpitations - HTN
70
Management of phaeochromocytoma
- Plasma free metanephrine/24 hoururine catecholamines - CT/MRI to confirm tumour - Tx includes alpha blockers e.g doxazosin, beta blocks and surgical removal
71
Thyroid eye disease
- 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
Thyroid nodules
- 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
Which diabetes medication causes weight loss?
SGLT-2 inhibitors e.g. empaglioflozin GLP-1 agonists e.g semaglutide
74
Electrolyte abnormality found in Addisons?
hyperkalaemia, hyponatraemia, hypoglycaemia
75

Phase 3A (10 decks)

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