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Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

T1DM risk factors

A

HLA DR3-DQ2 or HLA DR4-DQ8
Autoimmune diseases

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2
Q

T1DM pathophysiology

A

Autoantibodies attack Beta cells in the Islets of Langerhans -> Insulin deficiency -> hyperglycaemia

Continuous breakdown of glycogen from liver (gluconeogenesis) -> glycosuria

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3
Q

T1DM diagnosis

A

Random plasma glucose > 11mmol/L

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4
Q

T1DM management

A

Education
Insulin
Short-acting insulins and insulin analogues - 4-6 hours
Longer acting insulin - 12-24 hours

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5
Q

T2DM risk factors

A

Lifestyle factors: obesity, lack of exercise, calorie and alcohol excess
Higher prevalence in asian men
> 40 years old - later onset
Hypertension

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6
Q

T2DM investigation results

A

Fasting plasma glucose > 7 mmol/L
Random plasma glucose > 11 mmol/L
OGTT after 2 hours > 11 mmol/L
HbA1c > 48 mmol/L

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7
Q

Impaired glucose tolerance investigation results

A

Fasting plasma glucose > 6 mmol/L
OGTT after 2 hours > 7.8 mmol/L

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8
Q

T2DM lifestyle changes as 1st line management

A

Dietary advice: high in complex carbs, low in fat
Smoking cessation
Decrease alcohol intake
Encourage exercise
Regular blood glucose and HbA1c monitoring

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9
Q

T2DM pharmacological management

A

1st: Metformin
[+ SGLT-2 inhibitors if heart failure!]

2nd:
Dual therapy: + SGLT-2 inhibitor, sulphonylurea, pioglitazone, DPP4 inhibitors

3rd:
Triple therapy

4th:
Insulin

Injectables are last line

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10
Q

DKA pathophysiology

A

Absence of insulin -> uncontrolled catabolism -> unrestrained gluconeogenesis and decreased peripheral glucose uptake -> hyperglycaemia

Hyperglycemia -> osmotic diuresis -> dehydration

Peripheral lipolysis for energy -> increase in circulating free fatty acids -> oxidised to Acetyl CoA -> ketone bodies (acidic) = Acidosis

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11
Q

DKA general management

A

IV fluids - 0.9% saline
IV insulin
K+ replacement

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12
Q

Hyperosmolar hyperglycaemic state pathophysiology

A

Low insulin -> increased gluconeogenesis -> hyperglycaemia, but enough insulin to inhibit ketogenesis

Hyperglycemia -> osmotic diuresis -> dehydration

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13
Q

Hyperosmolar hyperglycaemic state investigation results

A

Random plasma glucose >11mmol/L
Urine dipstick: glucosuria
Plasma osmolality - high
U+E - ↓ total body K+, ↑ serum K+

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14
Q

Hyperosmolar hyperglycaemic state treatment

A

Replace fluid - 0.9% saline IV
Insulin - At low rate of infusion!
Restore electrolytes - e.g. K+
LMWH

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15
Q

Hyperosmolar hyperglycaemic state manifestations

A

Extreme diabetes symptoms

Plus:
Confusion and reduced mental state
Lethargy
Severe dehydration

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16
Q

Hyperthyroidism risk factors

A

Smoking
Stress
HLA-DR3
Other autoimmune diseases: T1DM, Addisons, Vitiligo

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17
Q

Causes of hyperthyroidism

A

Graves disease - 65-75%, Autoimmune, F>M - 9:1
Toxic multinodular goitre
Toxic adenoma
Metastatic follicular thyroid cancer
Iodine excess (e.g. IV contrast)
Secondary causes - TSH secreting pituitary tumour

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18
Q

Hyperthyroidism pathophysiology

A

↑T3 increases metabolic rate, cardiac output, bone resorption and activates sympathetic nervous system

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19
Q

Grave’s disease pathophysiology

A

IgG autoantibodies (anti-TSHR-Ab) bind to TSH receptors to increase T4/T3 production
They also react with orbital autoantigens

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20
Q

Hyperthyroidism presentation

A

Hot + sweaty
Diarrhoea
Hyperphagia
Weight loss
Palpitations
Tremor
Irritability
Anxiety/restlessness
Oligomenorrhoea
Goitre

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21
Q

Grave’s disease: eye symptoms + other

A

Thyroid eye disease (25-50%)
Eyelid retraction
Periorbital swelling
Proptosis/Exophthalmos

Pretibial myxoedema
Thyroid acropachy

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22
Q

Hyperthyroidism TFTs + antibodies + other investigations

A

TFTs - ↑T4/T3, Primary: ↓TSH, Secondary: ↑TSH
Thyroid autoantibodies (anti-TSHR)
US + CT Head

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23
Q

Hyperthyroidism management

A

Drug management
Beta-blockers - Rapid symptom relief
1st line Carbimazole - Blocks synthesis of T4
2nd line Propylthiouracil - Prevents T4->T3 conversion

Radioiodine
Thyroidectomy

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24
Q

Most common cause of hypothyroidism worldwide

A

Iodine deficiency

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25
Q

Most common cause of hypothyroidism in UK

A

Hashimoto’s thyroiditis

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26
Q

Most common cause of hypothyroidism in consanguin relationships

A

Congenital hypothyroidism

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27
Q

Wolff-Chaikoff effect

A

Iodine excess causing hypothyroidism
Inhibits thyroid hormone synthesis

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28
Q

Causes of hypothyroidism

A

Autoimmune causes
Hashimotos (inflammation -> goitre). More common F 60-70 years old
Primary atrophic hypothyroidism (atrophy -> no goitre)

Other primary
Iodine deficiency
Drugs (antithyroid drugs, iodine, lithium)
Post thyroidectomy/ radioiodine

Secondary - Hypopituitarism

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29
Q

Hypothyroidism manifestations

A

Fatigue
Weight gain
Loss of appetite
Cold
Lethargy
Constipation
Low mood/depression
Menorrhagia
Goitre

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30
Q

Hypothyroidism investigations + results

A

TFTs
↓T4 ↓T3
Primary: ↑TSH
Secondary ↓TSH

Autoantibodies (anti-TPO)

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31
Q

Cushing’s syndrome causes

A

ACTH dependent:
Cushing’s Disease-ACTH secreting from pituitary adenoma
Ectopic ACTH production from small cell lung cancer

ACTH independent:
Iatrogenic- Steroid use(most common)
Adrenal adenoma

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32
Q

Cushing’s syndrome features

A

Moon face
Central obesity
Buffalo hump
Acne
Hypertension
Striae
Hirsutism
Weight gain

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33
Q

Cushing’s syndrome investigations + results

A

Random plasma cortisol- raised
Overnight dexamethasone suppression test- cortisol will not be suppressed in Cushing’s Disease
Urinary free cortisol (24 hr)
Plasma ACTH

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34
Q

Cushing’s syndrome treatment

A

Iatrogenic: stop medications if possible
Cushing’s disease: removal of pituitary adenoma= transsphenoidal surgery
Adrenal adenoma: adrenalectomy

Cortisol synthesis inhibition:
Metyrapone, Ketoconazole

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35
Q

Acromegaly causes

A

Pituitary Adenoma= most common(99%)
Secondary to a malignancy that secretes ectopic GH eg. lung cancer

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36
Q

Acromegaly pathophysiology

A

GH acts directly on tissues such as liver, muscle bone or fat, as well as indirectly through induction of insulin like growth factor

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37
Q

Acromegaly features

A

Prominent forehead and brow
increased jaw size
Large hands, nose, tongue, feet
Visual field defect(bitemporal hemianopia)
Profuse sweating
Lower pitch of voice
Obstructive Sleep apnoea

38
Q

Acromegaly investigations + results

A

1st line: Insulin like Growth Factor 1 test= raised

Gold standard: Oral glucose tolerance test

Other tests: Random serum GH raised, MRI scan of pituitary fossa

GH cannot be measured reliably as its levels change throughout the day

39
Q

Acromegaly management

A

1st line: Transsphenoidal resection surgery(if cause is adenoma)
2nd line: Somatostatin analogue eg. Ocreotide
3rd line: GH receptor antagonist eg. Pegvisomant
4th line: Dopamine agonist eg. Cabergoline

40
Q

Prolactinoma types

A

Micro(tumour less than 10mm diameter on MRI; most common-90%)
Macro(tumour more than 10mm diameter on MRI)

41
Q

Prolactinoma manifestations

A

Visual field defect
Headache
Menstrual irregularity
Infertility
Galactorrhoea

42
Q

Prolactinoma investigations

A

Prolactin levels
CT head

43
Q

Prolactinoma treatment

A

Gold standard: Transsphenoidal resection surgery of pituitary gland
1st line: Dopamine agonists: Bromocriptine/cabergoline (Dopamine has an inhibitory effect on prolactin)

44
Q

Conn’s syndrome pathophysiology

A

Excess production of aldosterone, independent of renin-angiotensin system
Causing:
High Na and water retention
Increased K excretion in kidneys
Low renin release

45
Q

Conn’s syndrome aetiology

A

Primary hyperaldosteronism due to an aldosterone producing adenoma

46
Q

Conn’s syndrome features

A

Hypertension
Hypokalaemia
Nocturia
Polyuria
Mood Disturbance
Difficulty concentrating

47
Q

Conn’s syndrome investigations + results

A

Aldosterone-Renin Ratio blood test: Increased
Plasma potassium: reduced
U+E

48
Q

Conn’s syndrome treatment

A

1st line: Spironolactone (pre-op controls BP and K+ levels) - if hyperplasia
Gold standard: Laparoscopic adrenalectomy - if Adenoma

49
Q

Addison’s disease pathophysiology

A

Destruction of adrenal cortex leads to decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)

50
Q

Causes of Addison’s disease

A

Autoimmune destruction (80% in UK and developed countries)
TB(most common cause worldwide)
Adrenal metastases

51
Q

Addison’s disease manifestations

A

Tanned
Lean
Fatigue
Pigmented palmar creases
Postural Hypotension

52
Q

Addison’s disease investigations + results

A

1st line: U+E= Hyponatraemia, hyperkalaemia, blood glucose (hypoglycaemia)
Gold standard: Short SynACTHen test (ACTH stimulation test)
Presents with: Low cortisol, high ACTH
Plasma renin and aldosterone: High renin, low aldosterone

Other tests:
Adrenal CT or MRI
21-Hydroxylase adrenal autoantibodies- is positive in autoimmune diseases in more than 80%

53
Q

Addison’s disease management

A

Replace steroids depending on signs,symptoms:
Hydrocortisone- replaces cortisol
Fludrocortisone- replaces aldosterone

-Treat underlying cause and warn against abruptly stopping steroids

54
Q

SIADH causes

A

Post-operative from major surgery
Infection (atypical pneumonia+lung abscess)
Head injury
Medications (thiazide diuretics) is most common cause

55
Q

SIADH manifestations

A

Headache
Nausea
Fatigue
Muscle cramps
confusion
Severe hyponatraemia

56
Q

SIADH investigations

A

Diagnosis of exclusion
U+E= hyponatraemia
Urine sodium=high
Urine osmolality= high

Causes of Hyponatraemia need to be excluded:
-ve Short SynACTHen Test- exclude Adrenal insufficiency
No diarrhoea, vomiting
No history of diuretic use
No AKI/CKD

57
Q

SIADH volume and electrolytes

A

Euvolaemic hyponatraemia

K+ normal

58
Q

SIADH management

A

Stop causative medication
Fluid restriction
Tolvaptan (ADH receptor blocker)

59
Q

Hyperkalaemia manifestations

A

Fatigue and light-headedness
Weakness
Chest pain
Palpitations
Arrhythmias (Potential cardiac arrest)
Reduced power + reflexes
Flaccid paralysis

60
Q

Hyperkalaemia causes

A

Impaired excretion
AKI/CKD
Medication
Renal tubular acidosis
Addison’s disease

Shift to extracellular
Metabolic acidosis
Rhabdomyolysis
Decreased insulin
Tumour lysis syndrome

61
Q

Hyperkalaemia ECG changes

A

Tall T
Long PR
Wide QRS
Small P

62
Q

Hyperkalaemia management

A

Calcium gluconate - protect myocardium
Insulin+dextrose or nebulised salbutamol - Drive K+ intracellularly
Treat underlying cause

63
Q

Hypokalaemia ECG changes

A

U waves
Small T wave
Long PR
Long QT

64
Q

Hypokalaemia management

A

Potassium replacement

65
Q

Diabetes insipidus manifestation

A

Polyuria
Polydipsia
Dehydration

66
Q

Diabetes insipidus pathophysiology

A

Impaired water resorption from the kidneys:
large volumes of dilute urine
because of reduced ADH
secretion from the posterior pituitary(Cranial)
OR
Impaired response of the kidney to ADH(Nephrogenic)

67
Q

Causes of diabetes insipidus

A

Cranial:
Idiopathic
Congenital
Tumour
Trauma
Infection

Nephrogenic:
Inherited
Metabolic (low potassium, high calcium)
Drugs (lithium)
Chronic renal disease

68
Q

Diabetes insipidus investigations + results

A

Gold standard: 8 hour water deprivation test to diagnose
Then Desmopressin test=establish cranial or nephrogenic

Other Investigations: cranial MRI

69
Q

Diabetes insipidus management

A

Conservatively if mild - rehydration

Cranial: Desmopressin
Nephrogenic: Bendroflumethiazide

70
Q

Hypocalcaemia ECG findings

A

Small T
Long QR

71
Q

Hypocalcaemia manifestations

A

Chevotek’s sign - facial spasm when facial nerve is tapped
Trousseau’s sign - wrist flexion + fingers pull together

Convulsions
Parasthesia
Arrhythmias

72
Q

Hypercalcaemia ECG findings

A

Tall T
Short QT

73
Q

Hypoparathyroidism PTH, calcium + phosphate results

A

Low PTH
Low calcium
High phosphate

74
Q

Primary causes of hypoparathyroidism

A

Autoimmune destruction
DiGeorge syndrome

75
Q

Pseudohypoparathyroidism PTH, calcium + phosphate results

A

Hypocalcaemia - PTH resistance

High PTH
Low calcium
High phosphate

76
Q

Primary hyperparathyroidism: PTH, calcium + phosphate results

A

High PTH
High calcium
Low phosphate

77
Q

Secondary hyperparathyroidism PTH, calcium + phosphate results

A

Vitamin D deficiency

High PTH
Low calcium
Low phosphate

78
Q

Tertiary hyperparathyroidism PTH, calcium + phosphate results

A

High PTH
High calcium
Phosphate varies depending on kidney function

79
Q

Multiple endocrine neoplasia type 1 tumours

A

Parathyroid
Pituitary
Pancreas

Adrenal + thyroid

80
Q

Multiple endocrine neoplasia type 2a tumours

A

Medullary thyroid cancer
Parathyroid cancer
Phaeochromocytoma

81
Q

Multiple endocrine neoplasia type 2b manifestations

A

Medullary thyroid cancer
Phaeochromocytoma

Marfanoid body
Neuromas

82
Q

Genes causing multiple endocrine neoplasia + mode of inheritance

A

Type 1 - MEN 1 tumour suppresor gene
Type 2 - RET proto oncogene

Autosomal dominant

83
Q

Phaeochromocytoma associated familial syndromes

A

Multiple endocrine neoplasia
Neurofibromatosis
Von-Hippel Lindau disease

84
Q

Which cells are affected in phaechromocytoma?

A

Chromaffin cells secrete catecholamines

85
Q

Phaeochromocytoma presentation

A

Headache
Sweating
Tachycardia & palpitations
Postural hypotension

86
Q

Phaeochromocytoma investigations

A

Raised metadrenaline and noradrenaline
Raised WCC
CT

87
Q

Phaeochromocytoma management

A

Non-competitive alpha blocker e.g. phenoxybenzamine
Excision of paraganglioma

88
Q

VIPoma presentation

A

Watery diarrhoea
Pancreatic cholera
Hypokalaemia
Absent abdo pain

89
Q

VIPoma pathophysiology

A

Neuroendocrine tumour within pancreas
Release of VIP (vasoactive intestinal peptide)

90
Q

What is released from tumours causing carcinoid syndrome?

A

Serotonin
Bradykinin

91
Q

Carcinoid syndrome investigations

A

Urine: High volume of 5-hydroxyindoleacetic acid (breakdown product of serotonin)
Metabolic panel and LFTs
Liver ultrasound: confirm metastases

GOLD STANDARD:
Octreoscan: Radiolabelled octreotide (somatostatin analogue)

Medicine (13 decks)

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