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Endocrinology Flashcards

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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
Most common cause of hypothyroidism in UK
Hashimoto's thyroiditis
26
Most common cause of hypothyroidism in consanguin relationships
Congenital hypothyroidism
27
Wolff-Chaikoff effect
Iodine excess causing hypothyroidism Inhibits thyroid hormone synthesis
28
Causes of hypothyroidism
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
29
Hypothyroidism manifestations
Fatigue Weight gain Loss of appetite Cold Lethargy Constipation Low mood/depression Menorrhagia Goitre
30
Hypothyroidism investigations + results
TFTs ↓T4 ↓T3 Primary: ↑TSH Secondary ↓TSH Autoantibodies (anti-TPO)
31
Cushing's syndrome causes
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
32
Cushing's syndrome features
Moon face Central obesity Buffalo hump Acne Hypertension Striae Hirsutism Weight gain
33
Cushing's syndrome investigations + results
Random plasma cortisol- raised Overnight dexamethasone suppression test- cortisol will not be suppressed in Cushing’s Disease Urinary free cortisol (24 hr) Plasma ACTH
34
Cushing's syndrome treatment
Iatrogenic: stop medications if possible Cushing’s disease: removal of pituitary adenoma= transsphenoidal surgery Adrenal adenoma: adrenalectomy Cortisol synthesis inhibition: Metyrapone, Ketoconazole
35
Acromegaly causes
Pituitary Adenoma= most common(99%) Secondary to a malignancy that secretes ectopic GH eg. lung cancer
36
Acromegaly pathophysiology
GH acts directly on tissues such as liver, muscle bone or fat, as well as indirectly through induction of insulin like growth factor
37
Acromegaly features
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
Acromegaly investigations + results
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
Acromegaly management
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
Prolactinoma types
Micro(tumour less than 10mm diameter on MRI; most common-90%) Macro(tumour more than 10mm diameter on MRI)
41
Prolactinoma manifestations
Visual field defect Headache Menstrual irregularity Infertility Galactorrhoea
42
Prolactinoma investigations
Prolactin levels CT head
43
Prolactinoma treatment
Gold standard: Transsphenoidal resection surgery of pituitary gland 1st line: Dopamine agonists: Bromocriptine/cabergoline (Dopamine has an inhibitory effect on prolactin)
44
Conn's syndrome pathophysiology
Excess production of aldosterone, independent of renin-angiotensin system Causing: High Na and water retention Increased K excretion in kidneys Low renin release
45
Conn's syndrome aetiology
Primary hyperaldosteronism due to an aldosterone producing adenoma
46
Conn's syndrome features
Hypertension Hypokalaemia Nocturia Polyuria Mood Disturbance Difficulty concentrating
47
Conn’s syndrome investigations + results
Aldosterone-Renin Ratio blood test: Increased Plasma potassium: reduced U+E
48
Conn’s syndrome treatment
1st line: Spironolactone (pre-op controls BP and K+ levels) - if hyperplasia Gold standard: Laparoscopic adrenalectomy - if Adenoma
49
Addison's disease pathophysiology
Destruction of adrenal cortex leads to decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)
50
Causes of Addison's disease
Autoimmune destruction (80% in UK and developed countries) TB(most common cause worldwide) Adrenal metastases
51
Addison's disease manifestations
Tanned Lean Fatigue Pigmented palmar creases Postural Hypotension
52
Addison's disease investigations + results
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
Addison's disease management
Replace steroids depending on signs,symptoms: Hydrocortisone- replaces cortisol Fludrocortisone- replaces aldosterone -Treat underlying cause and warn against abruptly stopping steroids
54
SIADH causes
Post-operative from major surgery Infection (atypical pneumonia+lung abscess) Head injury Medications (thiazide diuretics) is most common cause
55
SIADH manifestations
Headache Nausea Fatigue Muscle cramps confusion Severe hyponatraemia
56
SIADH investigations
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
SIADH volume and electrolytes
Euvolaemic hyponatraemia K+ normal
58
SIADH management
Stop causative medication Fluid restriction Tolvaptan (ADH receptor blocker)
59
Hyperkalaemia manifestations
Fatigue and light-headedness Weakness Chest pain Palpitations Arrhythmias (Potential cardiac arrest) Reduced power + reflexes Flaccid paralysis
60
Hyperkalaemia causes
Impaired excretion AKI/CKD Medication Renal tubular acidosis Addison's disease Shift to extracellular Metabolic acidosis Rhabdomyolysis Decreased insulin Tumour lysis syndrome
61
Hyperkalaemia ECG changes
Tall T Long PR Wide QRS Small P
62
Hyperkalaemia management
Calcium gluconate - protect myocardium Insulin+dextrose or nebulised salbutamol - Drive K+ intracellularly Treat underlying cause
63
Hypokalaemia ECG changes
U waves Small T wave Long PR Long QT
64
Hypokalaemia management
Potassium replacement
65
Diabetes insipidus manifestation
Polyuria Polydipsia Dehydration
66
Diabetes insipidus pathophysiology
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
Causes of diabetes insipidus
Cranial: Idiopathic Congenital Tumour Trauma Infection Nephrogenic: Inherited Metabolic (low potassium, high calcium) Drugs (lithium) Chronic renal disease
68
Diabetes insipidus investigations + results
Gold standard: 8 hour water deprivation test to diagnose Then Desmopressin test=establish cranial or nephrogenic Other Investigations: cranial MRI
69
Diabetes insipidus management
Conservatively if mild - rehydration Cranial: Desmopressin Nephrogenic: Bendroflumethiazide
70
Hypocalcaemia ECG findings
Small T Long QR
71
Hypocalcaemia manifestations
Chevotek's sign - facial spasm when facial nerve is tapped Trousseau's sign - wrist flexion + fingers pull together Convulsions Parasthesia Arrhythmias
72
Hypercalcaemia ECG findings
Tall T Short QT
73
Hypoparathyroidism PTH, calcium + phosphate results
Low PTH Low calcium High phosphate
74
Primary causes of hypoparathyroidism
Autoimmune destruction DiGeorge syndrome
75
Pseudohypoparathyroidism PTH, calcium + phosphate results
Hypocalcaemia - PTH resistance High PTH Low calcium High phosphate
76
Primary hyperparathyroidism: PTH, calcium + phosphate results
High PTH High calcium Low phosphate
77
Secondary hyperparathyroidism PTH, calcium + phosphate results
Vitamin D deficiency High PTH Low calcium Low phosphate
78
Tertiary hyperparathyroidism PTH, calcium + phosphate results
High PTH High calcium Phosphate varies depending on kidney function
79
Multiple endocrine neoplasia type 1 tumours
Parathyroid Pituitary Pancreas Adrenal + thyroid
80
Multiple endocrine neoplasia type 2a tumours
Medullary thyroid cancer Parathyroid cancer Phaeochromocytoma
81
Multiple endocrine neoplasia type 2b manifestations
Medullary thyroid cancer Phaeochromocytoma Marfanoid body Neuromas
82
Genes causing multiple endocrine neoplasia + mode of inheritance
Type 1 - MEN 1 tumour suppresor gene Type 2 - RET proto oncogene Autosomal dominant
83
Phaeochromocytoma associated familial syndromes
Multiple endocrine neoplasia Neurofibromatosis Von-Hippel Lindau disease
84
Which cells are affected in phaechromocytoma?
Chromaffin cells secrete catecholamines
85
Phaeochromocytoma presentation
Headache Sweating Tachycardia & palpitations Postural hypotension
86
Phaeochromocytoma investigations
Raised metadrenaline and noradrenaline Raised WCC CT
87
Phaeochromocytoma management
Non-competitive alpha blocker e.g. phenoxybenzamine Excision of paraganglioma
88
VIPoma presentation
Watery diarrhoea Pancreatic cholera Hypokalaemia Absent abdo pain
89
VIPoma pathophysiology
Neuroendocrine tumour within pancreas Release of VIP (vasoactive intestinal peptide)
90
What is released from tumours causing carcinoid syndrome?
Serotonin Bradykinin
91
Carcinoid syndrome investigations
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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