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4MB Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is type 1 diabetes?

A

Autoimmune destruction of pancreatic beta-cells causes reduced insulin production, resulting in hyperglycaemia

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2
Q

List aetiology/risk factors for type 1 diabetes

A

Autoimmunity
Genetics (HLA DR3/4)
Latent autoimmune diabetes of adulthood

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3
Q

List clinical features of type 1 diabetes

A 
Polyuria
Polydipsia
Weight loss
Fatigue
Malaise
Blurred vision (retinopathy)
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4
Q

What investigations would you do for type 1 diabetes?

A

Bloods: FBC, U+E, LFT’s, eGFR
Antibodies: anti- islet cell, GAD
Screening for retinopathy/nephropathy/neuropathy

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5
Q

What are the parameters for impaired glucose tolerance testing in diabetes?

A

Fasting: less than 7 mmol/l

2h oral glucose level: greater than 7.8, less than 11.1 mmol/l

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6
Q

What are the parameters for impaired fasting glucose testing in diabetes?

A

Fasting: greater than 6.1, less than 7 mmol/l

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7
Q

What are the WHO diagnostic criteria for diabetes?

A

Fasting glucose greater than 7 mmol/l
Random glucose greater than 11.1 mmol/l
HbA1C greater than 48
Either symptomatic + 1 positive lab test or asymptomatic + 2 positive lab tests

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8
Q

List two rapid-acting insulins

A

Humalog

Novorapid

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9
Q

List two short-acting insulins

A

Actrapid

Humulin S

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10
Q

List two intermediate-acting insulins

A

Insulatard

Humulin I

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11
Q

List two long-acting insulins

A

Lantus

Levemir

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12
Q

Novomix 30 insulin has how much short and how much long -acting insulin?

A

30% short-acting

70% long-acting

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13
Q

List the main insulin regimens that patients may be on

A

Once-daily: long-acting before bed
Twice-daily: short-acting pre-breakfast and pre-dinner
Basal-bolus: long-acting before bed, short-acting before meal

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14
Q

What is type 2 diabetes?

A

Relative insulin deficiency caused by insulin resistance/reduced sensitivity, resulting in hyperglycaemia

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15
Q

List aetiology/risk factors for type 2 diabetes

A 
Asians
Obesity
Low level of exercise
Cardiovascular disease
Monogenic twins
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16
Q

List clinical features of type 2 diabetes

A 
Polyuria
Polydipsia
Obesity
Fatigue
Malaise
Blurred vision
Recurrent infections
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17
Q

List the main drug classes (and examples) used in type 2 diabetes

A 
Biguanides (metformin)
Sulfonylureas (gliclazide, glibenclamide)
TZD's (pioglitazone)
DPP-IV inhibitors (sitagliptin)
GLP-1 analogue (exenatide)
Alpha-glucosidase inhibitors (acarbose)
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18
Q

What does metformin do? List side effects

A

Reduces hepatic gluconeogenesis, increases insulin sensitivity
No weight gain or hypo risk
SE: lactic acidosis, GI upset, avoid if eGFR less than 35

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19
Q

What does gliclazide do? List side effects

A

Increases insulin secretion from pancreatic B-cell

SE: weight gain, hypoglycaemia

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20
Q

What does pioglitazone do? List side effects

A

Enhances PPAR-alpha to increase insulin gene transcription, also reduces hepatic gluconeogenesis
SE: fluid overload, weight gain, osteoporosis

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21
Q

What does sitagliptin do?

A

Increases incretin effect of GLP-1 and GDP (delays gastric emptying, reduces appetite)

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22
Q

What are the components of metabolic syndrome?

A

Central obesity
Hypertension
Hyperglycaemia
Dyslipidaemia

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23
Q

Outline management of metabolic syndrome

A

Exercise (Tai Chi)
Weight reduction, orlistat
Statin, anti-hypertensive, metformin +/- pioglitazone

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24
Q

What is the pathophysiology of diabetic ketoacidosis?

A

Reduced insulin results in reduced cellular uptake of glucose, causing less pyruvate and more acetyl-coA
Acetyl-coA is converted to ketone bodies and acetate

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25
Q

List aetiology/risk factors for diabetic ketoacidosis

A 
Non-compliance
Missed dose, missed meal
Infection (esp UTI)
MI
Steroid use
Pancreatitis
Surgery
Alcohol-induced
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26
Q

List clinical features of diabetic ketoacidosis

A 
Drowsiness
Vomiting
Dehydration
Polyuria, polydipsia
Ketotic "pear-drop" breath
Kussmaul (deep) breathing
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27
Q

What investigations would you do for diabetic ketoacidosis?

A

Glucose usually greater than 11
Bloods: FBC, U+E, osmolarity, ABG
CXR
Urinary ketones, culture

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28
Q

Outline management of diabetic ketoacidosis

A

NG tube if vomiting/unconscious
IV insulin 6u per hour, increase if poor response
IM insulin 20u if no infusion pump
Monitor U+E ever hour, aim for glucose to drop by 5mmol/l
IV fluids

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29
Q

What is hyperosmolar hyperglycaemic state (HHS)?

A

Hyperosmolar state caused by uncontrolled hyperglycaemia, usually in type 2 diabetics

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30
Q

List clinical features of HHS

A

Dehydration
Stupor, coma
Impaired consciousness

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31
Q

Outline management of HHS

A

9L saline over 48h (slower rate than DKA)
Replace K
May or may not need insulin

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32
Q

List aetiology/risk factors of hypoglycaemia

A 
Insulin/sulfonylurea use
Increased activity 
Missed meal
Alcohol binge
Drugs (aspirin, ACEi, B-blocker, quinine)
Pituitary insufficiency
Liver failure
Addison's disease
Islet cell tumour
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33
Q

List clinical features of hypoglycaemia

A 
Sweaty
Anxious
Tremor
Confusion, coma
Dizziness
Vision trouble
Seizure
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34
Q

What investigations would you do for hypoglycaemia?

A

Blood glucose
Prolonged OGTT, fasting tests
Blood insulin/c-peptide/ketones if symptomatic

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35
Q

Outline management of hypoglycaemia

A

Oral sugar + long-acting starch

IV dextrose/IM glucagon

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36
Q

List aetiology/risk factors for hyperthyroidism

A 
Autoimmunity (Grave's disease, associated conditions such as vitiligo, T1DM, Addison's)
Toxic multinodular goitre (elderly, iodine-deficient)
TSH-secreting tumour
Acute thyroiditis (De Quervain's)
Amiodarone, lithium
Ectopic thyroid tissue
Iodine excess
Radiation exposure
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37
Q

List clinical features of hyperthyroidism

A 
Irritability, anxiety
Heat intolerance
Sweating, warm skin
Tremor
Increased sympathetic drive
Weight loss, diarrhoea
Labile emotions
Oligomenorrhoea
Thin hair
Goitre/nodule, bruit
Eye disease
Pretibial myxoedema in Grave's
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38
Q

List typical eye signs seen in Grave’s disease

A 
Lid lag
Lid retraction
Exophthalmus
Ophthalmoplegia
Proptosis
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39
Q

What investigations would you do for hyperthyroidism?

A 
TSH (low), T4 (high), T3 (high)
Anti-TPO antibody
Anti-TSH receptor antibody
IgG
Isotope scan for nodule/goitre shows smooth symmetrical butterfly-shape
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40
Q

Outline management of hyperthyroidism

A

Carbimazole, propylthiouracil in pregnancy
B-blocker for symptoms
Radioiodine
Thyroidectomy

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41
Q

What is thyroid storm?

A

Rapid deterioration of hyperthyroidism

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42
Q

List clinical features of thyroid storm

A 
Hyperthyroid signs and symptoms
Fever
Confusion, coma
Diarrhoea and vomiting
Goitre
AF/tachycardia
Heart failure
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43
Q

Outline management of thyroid storm

A 
Counteract peripheral effects and treat complications
Propranolol, osmolol in asthmatic
Carbimazole
Steroid
Digoxin if heart is fast
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44
Q

List aetiology/risk factors for hypothyroidism

A 
Autoimmunity (Hashimoto's)
Primary atrophy (diffuse lymphocytic infiltration)
Thyroidectomy
Radioiodine
Postpartum
Amiodarone, lithium, iodine
Turner's, Down's syndrome
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45
Q

List clinical features of hypothyroidism

A 
Tired, slow, sleepy
Low mood
Cold intolerance
Bradycardia
Sparse hair, dry skin, cold hands
Constipation
Menorrhagia
Weakness
Goitre
Weight gain, puffy face
Memory change/loss
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46
Q

What investigations would you do for hypothyroidism?

A

TSH (high), T4 (low), T3 (low)
Anti-TPO antibody
Anti-TBG antibody
FBC for anaemia

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47
Q

Outline management of hypothyroidism

A

Levothyroxine (T4)

Restore and monitor metabolic rate

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48
Q

What is myxoedema coma?

A

Severe hypothyroid state

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49
Q

List clinical features of myxoedema coma

A 
Hypothyroidism signs and symptoms
Often over 65yo
Hypothermia
Hyper-reflexia
Coma, seizures
Goitre
Hypotension
Cyanosis
50
Q

Outline management of myxoedema coma

A

Liothyronine (T3) intravenously
Hydrocortisone
IV fluids
Treat complications and heart failure

51
Q

List aetiology/risk factors for goitre

A 
Pregnancy
Puberty
Autoimmunity
Thyroiditis
Iodine deficiency
Radiation exposure
Malignancy, cysts
Tuberculosis
52
Q

What are the typical types of goitre?

A

Smooth non-toxic
Toxic (Grave’s, De Quervain’s)
Multinodular non-toxic
Toxic multinodular

53
Q

List clinical features of thyroid cancer

A 
Palpable nodule in neck, goitre
Dysphagia
Hoarseness
Weight loss
Signs of hyper/hypo thyroidism
54
Q

What investigations would you do for thyroid cancer?

A

USS-guided FNA
LN biopsy
Iodine scan

55
Q

What are the different subtypes of thyroid cancer?

A

Papillary
Follicular
Medullary
Anaplastic

56
Q

What is the most common subtype of thyroid cancer and how does it spread?

A

Papillary

Lymphatic spread to nodes, lung

57
Q

How does follicular thyroid cancer spread?

A

Haematogenous spread to bone, lung

58
Q

Which thyroid cancer may be part of MEN2 syndrome? From which cells does it arise and what does it produce?

A

Medullary
Derived from para-follicular C cells
Produces calcitonin

59
Q

Which thyroid cancer has the poorest prognosis?

A

Anaplastic

60
Q

List causes/pathophysiology of primary, secondary and tertiary hyperparathyroidism

A

Primary: adenoma, gland hyperplasia, cancer
Secondary: low vit D, chronic renal failure
Tertiary: prolonged secondary causes autonomous gland hyperplasia, causing unchecked PTH release

61
Q

Which lung cancer may produce PTH?

A

Squamous cell lung cancer

62
Q

List clinical features of hyperparathyroidism

A 
Weakness
Fatigue
Low mood
Thirst, dehydration
Polyuria
Renal stones
Abdo pain
Pancreatitis
Ulcers
Osteopenia/porosis, fractures
63
Q

Describe PTH and Ca levels in primary, secondary and tertiary hyperparathyroidism

A

Primary: increased PTH, increased Ca
Secondary: increased PTH, decreased Ca
Tertiary: very increased PTH, increased Ca

64
Q

Which scan would be used to detect PTH-related adenoma?

A

Sestamibi scan

65
Q

List causes/pathophysiology of primary, secondary, pseudo and pseudopseudo hypoparathyroidism

A

Primary: gland failure, autoimmunity, DiGeorge syndrome
Secondary: radiation, surgery, hypomagnesium
Pseudo: end-organ resistance to PTH due to GNAS1 mutation
Pseudopseudo: pseudo with normal biochemistry

66
Q

List clinical features of hypoparathyroidism

A 
Cramps
Numbness
Parasthesiae
Spasms
Trousseau sign
Rovstek sign
67
Q

Outline management of hypoparathyroidism

A

Ca supplements
Calcitriol
Synthetic PTH

68
Q

What are multiple endocrine neoplasia syndromes?

A

Inherited autosomal dominant disorders involving functioning hormone-producing tumours in multiple organs

69
Q

MEN1 syndrome involves altered tumour-suppressor/ret proco-oncogene gene (delete as appropriate)

A

MEN1 syndrome involves altered tumour-suppressor gene

70
Q

MEN2 syndrome involves altered tumour-suppressor/ret proco-oncogene gene (delete as appropriate)

A

MEN1 syndrome involves altered ret proco-oncogene

71
Q

Which tumours typically occur as part of MEN1 syndrome?

A 
Parathyroid hyperplasia/adenoma (95%)
Pancreatic tumours (gastrinoma, insulinoma, glucagonoma)
Pituitary adenoma
Adrenal tumour
Carcinoid tumour
72
Q

Which tumours typically occur as part of MEN2 syndrome?

A

Thyroid (medullary) carcinoma
Adrenal (phaeochromocytoma)
Parathyroid adenoma
Mucosal neuroma

73
Q

What is Von-Hippel Lindau syndrome?

A

Germ-line mutation of tumour suppressor on c3p

74
Q

Which tumours typically occur as part of Von-Hippel Lindau syndrome?

A

Bilateral renal cell cancer
Retinal and cerebellar hemangioblastoma
Phaeochromocytoma

75
Q

What is Addison’s disease?

A

Primary adrenal insufficiency

Destruction of adrenal cortex results in reduced aldosterone, cortisol and androgen release

76
Q

List aetiology/risk factors for Addison’s disease

A 
Autoimmunity
Tuberculosis
Adrenal mets (lung, breast, kidney)
Lymphoma
Opportunistic infections in HIV
Adrenal haemorrhage, adrenalectomy
77
Q

List clinical features of Addison’s disease

A 
Pigmented skin/palmar creases
Amenorrhoea
Tiredness
Weakness
Dizziness
Weight loss
Abdo pain
Vomiting
Postural hypotension
78
Q

What would you find on investigations for Addison’s disease?

A 
Bloods: hyponatraemia, hypokalaemia
Low glucose
Raised 9am ACTH
Short synACTHen test fails to increase cortisol
Plasma renin + aldosterone
79
Q

Outline management of Addison’s disease

A

Hydrocortisone
Fludricortisone if reduced aldosterone
Double dose in illness/injury

80
Q

List aetiology/risk factors for secondary adrenal insufficiency

A

Long-term steroid use

HP axis disease (reduced ACTH production)

81
Q

Skin pigmentation occurs in secondary adrenal insufficiency. True/False?

A

False

No ACTH produced so would not cross-react

82
Q

What are the 2 main causes of hyperaldosteronism?

A

Conn’s syndrome (adenoma)

Bilateral adrenal hyperplasia

83
Q

List clinical features of hyperaldosteronism

A

Asymptomatic
Hypertension
Hypokalaemia (weakness, tetany, cramps, numbness)

84
Q

What would you find on investigations for hyperaldosteronism?

A

Aldosterone : renin ratio (raised aldosterone, reduced renin)
Saline suppression test if APR increased (would fail to suppress aldosterone)
CT/MRI adrenals
Adrenal vein sampling

85
Q

Outline management of hyperaldosteronism

A

Adrenalectomy if unilateral adenoma

Spironolactone/amiloride if bilateral adrenal hyperplasia

86
Q

What is phaeochromocytoma?

A

Rare catecholamine-producing tumour arising from chromaffin cells in adrenal medulla (sympathetic ganglion cells)

87
Q

List aetiology/risk factors for phaeochromocytoma

A 
10% malignant
10% bilateral
10% extra-adrenal
10% familial
MEN2
Neurofibromatosis
Von-Hippel Lindau syndrome
88
Q

List clinical features of phaeochromocytoma

A

Episodic headache
Sweating
Tachycardia
Hypertension

89
Q

What investigations would you do for phaeochromocytoma?

A

Urinary catecholamines
Clonidine suppression test if borderline
Abdo CT/MRI, PET scan
MIBG scan

90
Q

Outline management of phaeochromocytoma

A

Alpha-blocker (phenoxybenzamine) then beta-blocker (propranolol)
Surgical excision

91
Q

What is Cushing’s syndrome?

A

Chronic glucocorticoid (cortisol) excess

92
Q

List ACTH-dependent causes of Cushing’s syndrome

A

Cushing’s disease (bilateral adrenal hyperplasia, ACTH-producing pituitary adenoma)
Ectopic ACTH production (small cell lung cancer)
Ectopic CRF (thyroid, medullary, prostate cancers)

93
Q

List ACTH-independent causes of Cushing’s syndrome

A

Adrenal adenoma
Steroid use
Adrenal nodular hyperplasia

94
Q

List clinical features of Cushing’s syndrome

A 
Weight gain
Mood change
Proximal weakness
Gonadal dysfunction
Central obesity
Moon-face
Achilles tendon rupture
Buffalo neck lump
Abdominal striae
95
Q

What would you find on investigations for Cushing’s syndrome?

A

Dexametasone suppression test in ACTH-dependent causes fails to suppress cortisol

96
Q

Outline management of Cushing’s syndrome

A

Trans-sphenoidal excision of adenoma
Adrenalectomy
Ectopic ACTH (metyrapone)

97
Q

List hypothalamic causes of hypopituitarism

A 
Kallman's syndrome
Tumour
Inflammation
Infection (meningitis, TB)
Ischaemia
98
Q

List pituitary causes of hypopituitarism

A 
Trauma
Surgery
Irradiation
Inflammation
Autoimmunity
Ischaemia (apoplexy, DIC, Sheehan syndrome)
99
Q

List clinical features of hypopituitarism (split up into hormone deficient features)

A

GH: central obesity, dry wrinkly skin, reduced strength and balance
FSH/LH: oligo/amenorrhoea, reduced fertility, low libido, hypogonadism (reduced pubic hair, small testes, low volume ejaculate)
TSH: hypothyroidism features
ACTH: adrenal insufficiency features
Alabaster skin in panhypopituitarism

100
Q

What investigations would you do for hypopituitarism?

A

Basal tests (hormone levels)
Dynamic tests (stress tests)
Insulin stress test for GH/ACTH (would induce hypoglycaemia to raise GH and cortisol normally)
Prolonged glucagon test if insulin test contraindicated
Water deprivation test for ADH (would induce ADH release normally)
SynACTHen test for ACTH (would induce cortisol release normally)

101
Q

List the common pituitary adenomas

A 
Usually benign adenomas
Prolactinoma
GH-secreting
PRL + GH -secreting
ACTH-secreting
LH/FSH/TSH - secreting
102
Q

List clinical features of pituitary tumours

A 
Headaches
Bitemporal hemianopia
Altered appetite
Precocious puberty
CN III, IV, VI palsy
CSF rhinorrhoea
Effect of hormone release
103
Q

Outline management of pituitary tumours

A

Hormone replacement
Trans-sphenoidal surgery for macroadenomas
Radiotherapy if resistant/recurrent
Dopamine agonist for prolactinoma (cabergoline)

104
Q

Where do craniopharyngiomas develop?

A

Arise from Rathke’s pouch, located between pituitary and floor of 3rd ventricle

105
Q

How does hyperprolactinaemia typically arise?

A

Loss of tonic inhibition of prolactin release by dopamine

106
Q

List aetiology/risk factors for hyperprolactinaemia

A 
Prolactinoma
Disinhibition by compression of pituitary stalk
Dopamine antagonists (metoclopramide)
Oestrogen therapy (OCP)
Antipsychotics
Alpha-methyldopa
Pregnancy
Breastfeeding
Stress
107
Q

List clinical features of hyperprolactinaemia

A 
Oligo/amenorrhoea
Infertility
Galactorrhoea
Weight loss
Dry vagina
Sexual dysfunction
Reduced pubic/facial hair
Osteoporosis
108
Q

Outline management of hyperprolactinaemia

A 
Dopamine agonist (cabergoline)
Trans-sphenoidal surgery for adenoma
109
Q

List clinical features of acromegaly

A 
Thickened skin and soft tissues
Change in appearance
Headache, vision disturbance
Big hands/feet
Coarse face, wide nose, big supraorbital ridge, big tongue
Weight gain
Amenorrhoea
Impotence, low libido
Acanthosis nigricans
Goitre
Proximal weakness
Carpal tunnel syndrome
110
Q

What investigations would you do for acromegaly?

A 
Glucose tolerance test (normally would suppress GH)
IGF-1 levels
MRI pituitary
Visual fields
Lipids, glucose
111
Q

Outline management of acromegaly

A 
Trans-sphenoidal surgery for adenoma
Somatostatin analogue (octreotide)
Dopamine agonist (cabergoline)
GH antagonist (pegvisomant)
112
Q

What is diabetes insipidus?

A

Deficiency (cranial) or insensitivity (nephrogenic) to ADH

113
Q

List aetiology/risk factors for cranial diabetes insipidus

A 
Idiopathic
Congenital defect
Tumour, craniopharyngioma, mets
Trauma
Hypophysectomy
Histiocytosis
Sarcoidosis
Haemorrhae
Encephalitis
114
Q

List aetiology/risk factors for nephrogenic diabetes insipidus

A

Inherited
Metabolic (hypokalaemia hypercalcaemia)
Chronic kidney disease
Drugs (lithoum, demeclocycline)

115
Q

List clinical features of diabetes insipidus

A 
Polyuria
Polydipsia
Dehydration
Nocturia
"tasteless" urine
116
Q

What would you find on investigations for diabetes insipidus?

A

Increased plasma osmolality
Decreased urine osmolality
Dilute urine
Water deprivation test would fail to concentrate urine

117
Q

Outline management of diabetes insipidus

A

Desmopressin for cranial DI

Thiazide for nephrogenic DI

118
Q

What is SIADH?

A

Inappropriately high ADH levels

119
Q

List aetiology/risk factors for SIADH

A 
Malignancy (SCLC, pancreas, prostate, thymus, lymphoma)
Pneumonia, TB
Meningitis
Vasculitis
Hypothyroidism
Alcohol withdrawal
Drugs (opiates, SSRI, psychotropics)
Trauma
120
Q

List clinical features of SIADH

A 
Confusion
Irritability
Fits
Coma
Nausea
121
Q

What would you find on investigations for SIADH?

A

Hyponatraemia (urine hypernatraemia)

Decreased plasma osmolality

122
Q

Outline management of SIADH

A 
Treat cause
Fluid restrict
Salt +/- loop diuretic if severe
Demeclocycline (ADH inhibitor)
Vaptans may be trialled

4MB Medicine (19 decks)

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