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CP1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Type 1 DM pathophysiology

A

Autoimmune
Autoantibodies targeted against the insulin-secreting beta cells of the Islets of Langerhans in the pancreas –> cell death + inadequate insulin secretion
May be triggered by viral infection

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2
Q

Type 1 DM clinical presentation

A

Childhood/adolescence, 2-6w history of…
Polyuria: high sugar content in urine –> osmotic diuresis
Polydipsia
Weight loss: fluid depletion, fat/muscle breakdown
Diabetic ketoacidosis a common 1st presentation

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3
Q

Type 2 DM pathophysiology

A

Insulin resistance associated with: aging, genetic factors, obesity, high fat diets, sedentary life
Beta cells decompensate, and can no longer produce excess insulin, leading to hyperglycaemia

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4
Q

Type 2 DM clinical presentation

A

Onset over months/years, classic triad (may be less obvious than T1DM)
Lack of energy
Visual blurring: glucose-induced refractive changes
Pruritis vulvae/balatitis: candida infection
Older patients: retinopathy, polyneuropathy, erectile dysfunction, arterial disease

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5
Q

Components of metabolic syndrome

A

T2DM
Central obesity
Dyslipidaemia: low HDL, hypertriglyceridaemia

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6
Q

Causes of secondary DM

A

Pancreatic disease: CF, chronic pancreatitis, pancreatic carcinoma
Endocrine: Cushing’s, acromegaly, thyroroxicosis, pheochromocytoma, glucagonoma
Drug induced: thiazide diuretics, corticosteroids, antipsychotics, antiretrovirals
Congenital disease: insulin receptor abnormalities, myotonic dystrophy, Friedreich’s ataxia

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7
Q

DM diagnostic criteria

A

HbA1c >48mmol/mol + symptoms
42-47mmol/mol = pre-diabetes
Plasma glucose >7mmol/L

Diagnose T1DM if symptomatic with random blood glucose >11mmol/L

Asymptomatic: 2x abnormal results

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8
Q

In which populations is the use of HbA1c inappropriate to diagnose diabetes?

A 
<18yo
Acutely unwell
Those taking medication that could raise blood sugars
Those with end-stage CKD
Those with HIV
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9
Q

Investigations for T2DM complications

A

Fundoscopy
Nephropathy screen: 1st pass urine for albumin:creatinine + serum creatinine for eGFR
Foot check: neuropathy, ischaemia, ankle-brachial pressure index, ulcers, deformity
Cardiovascular: BP<140/80 (<130/80 if kidney/eye/cerebrovascular damage), assess Qrisk2 (atorvostatin for those with a 10y risk >10%)

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10
Q

Lifestyle advice for T2DM management

A

Diet: low-GI carbs, limit sugar & saturated fats
Weight loss: if overweight, target 5-10% weight loss
Physical activity: 20-30m exercise/day
Smoking cessation
Alcohol: my exacerbate effect of hypoglycaemic drugs, have a carb-containing snack before + after consuming alcohol

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11
Q

What is the target HbA1c for those with DM

A

48mmol/mol (6.5%)

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12
Q

Pathogenesis of diabetic ketoacidosis

A

Insulin absense –> increased hepatic glucose production (gluconeogenesis) & reduced uptake of glucose peripherally
Rising plasma glucose –> osmotic diuresis + dehydration
Lipolysis occurs in glucose-starved tissues –> elevated free fatty acids
In liver: free fatty acids –> fatty acetyl-CoA
In mitochondria to generate energy: fatty acetyl CoA –> ketone bodies
Accumulation of ketone bodies = metabolic acidosis
Respiratory compensation = hyperventilation
Acidosis: vomiting (fluid/electrolyte loss)
Renal perfusion falls: impaired excretion of raised H+ and ketones
Increased secretion of Na+ & K+

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13
Q

Reasons for DKA development

A

Undiagnosed diabetes
Interruption of insulin therapy
Stress of intercurrent illness/surgery

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14
Q

DKA clinical presentation

A 
Prostration
Kussmaul respiration
Nausea &amp; vomiting
Abdominal pain
Confusion/stupor
O/E: evidence of marked dehydration, smell of ketones on the breath, history of marked polyuria
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15
Q

DKA diagnosis

A

Blood glucose: >11mmol/L
Capillary ketones: >3mmol/L (or ketones>2+ in urine)
Venous pH<7.35 (or venous HCO3- <15mmol/L)

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16
Q

DKA investigations

A

Bloods: U&Es, creatinine, blood glucose (raised WCC & amylase common)
VBG: metabolic acidosis with a raised anion gap
ECG
CXR
Cultures
Pregnancy test

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17
Q

Hyperosmolar hyperglycaemic state aetiology

A

Characteristic of T2DM
Severe hyperglycaemia –> hyperosmolar state with absence of severe ketosis
Typically elderly, undiagnosed T2DM
Precipitating factors: glucose-rich foods, thiazide-diuretics, steroids, beta-blockers, infection, MI

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18
Q

Hyperosmolar hyperglycaemic state presentation

A

Dehydration
Stupor/coma/seizures
Evidence of an underlying illness
No raised ketones, can be mild lactic acidosis

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19
Q

Hyperosmolar hyperglycaemic state diagnosis

A

Osmolality = 2(Na+) + urea + glucose
Normal: 280-295
HHG > 320

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20
Q

Hypoglycaemia symptoms

A

Autonomic: sweating, anxiety, hunger, tremor, palpitations
Neuroglycopenic: confusion, drowsiness/coma, seizures

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21
Q

Diabetic hypoglycaemia pathology & aetiology

A

Alpha-cells release glucagon to increase glycogenolysis & gluconeogenesis & inhibit glycogen synthesis

In T1DM, alpha-cells become insensitive to glucose falls

Aetiology:
Excess insulin (exogenous/insulinoma) inhibits hepatic gluconeogenesis & glycogenolysis
Depletion of hepatic glycogen: malnutrition, fasting, exercise, alcohol, liver failure
Other: pituitary/adrenal insufficiency, non-pancreatic neoplasms

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22
Q

Hypoglycaemia treatment

A

If able to swallow: 10-20g fast acting carbohydrate (liquid), avoid fatty foods which may delay stomach emptying, eat long-acting carb when symptoms improve

If unable to swallow: IM glucagon (<8y=500mg, >8y=1g), glucagon not effective if alcohol consumed, vomiting likely & may precipitate further hypo’s, take long-acting carb when possible

In hospital: IV dextrose (100ml of 20%) up to 3x

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23
Q

Non-proliferative diabetic retinopathy presentation

A

Asymptomatic, occurs 8-10y into DM

Fundoscopy: micro-aneurysms, exudates, haemorrhages (dot, blot, flamed-shaped), cotton wool spots (>5=pre-proliferative)

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24
Q

Proliferative diabetic retinopathy pathology & presentation

A

More common in T2DM
Development of new vessels on optic disc/retina in response to retinal ischaemia (VEGF production)
New vessels: fragile & likely to bleed = pre-retinal/vitreous haemorrhage
Untreated –> fibrosis & tractional retinal detachment, rubeosis iridis
Presentation: sudden deterioration of acuity

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25
Q

Risk factors for diabetic retinopathy

A

Poor diabetic control, smoking, hypertension, pregnancy

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26
Q

Diabetic maculopathy pathology

A

More common in T2DM
Presents as blurred vision
Types: focal/diffuse/ischaemic

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27
Q

Types of diabetic eye disease

A 
Non-proliferative diabetic retinopathy
Proliferative diabetic retinopathy
Diabetic maculopathy
Cataract formation
Progressive open-angle glaucoma
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28
Q

Types of diabetic neuropathy

A 
Symmetrical polyneuropathy
Acute painful neuropathy
Mononeuropathy
Diabetic amyotrophy
Autonomic neuropathy
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29
Q

Symmetrical polyneuropathy presentation

A

Glove-and-stocking sensory loss
Vibration, deep-pain, temperature lost first & reduced propriception (dorsal/posterior columns)
Interosseous wasting of small muscles of the feet
Abnormal pressure areas/unrecognised trauma: ulcers
Neuropathic arteropathy (Charcot’s foot)

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30
Q

Acute painful neuropathy presentation

A

Painful burning in feet, shins, anterior thighs
Associated with poor glycaemic control
Worse at night

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31
Q

Mononeuropathy presentation

A

Cranial nerve lesions: CN III, IV, VI, ocular palsies
Any nerve compression syndrome more common on DM: e.g. carpal tunnel/foot drop (sciatic nerve)
>1 nerve = mononeuritis multiplex

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32
Q

Diabetic amyotrophy presentation

A

Progressive wasting of muscle tissues
Middle aged men, rare
Painful wasting of quadriceps
Variable course, gradual but incomplete improvement

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33
Q

Autonomic neuropathy

A

Sympathetic dysfunction: postural hypotension, ejaculatory failure, reduced sweating, Horner’s syndrome
Parasympathetic: erectile dysfunction, constipation, urinary retention, Holmes-Adie pupil

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34
Q

Macrovascular complications of diabetes

A

2x increased risk of stroke
4x increased risk of MI
50x increased risk of amputation for gangrene

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35
Q

Goitre morphology

A

Diffuse/nodular
Simple/toxic (actively secreting thyroid hormone)
Benign/malignant

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36
Q

Diffuse goitre differentials

A

Physiological: puberty, pregnancy (increased iodine requirements)
Autoimmune: Grave’s, Hashimoto’s
Thyroiditis: sub-acute (De Quervain’s), Riedel’s
Endemic: iodine deficiency
Drugs: anti-thyroid drugs, lithium, iodine excess, amiodarone

37
Q

Nodular goitre differentials

A

Multinodular: toxic multinodular goitre, subacute thyroiditis
Solitary nodule: follicular adenoma, benign nodule, malignancy, lymphoma, mets, one prominant nodule from a multinodular goitre
Infiltration (rare): TB, sarcoid

38
Q

Goitre investigations

A

FBC: related anaemia?
ESR: thyroiditis/autoimmune?
TFTs: TSH, free T4
Thyroid autoantibodies: autoimmune?
CT neck & thorax: if pressure symptoms
USS: solid/cystic mass
Fine-needle aspiration: cytology: malignancy?

39
Q

Thyrotoxicosis aetiology

A

Disorder resulting from raised circulating levels of thyroid hormone
1% of population
5:1 women:men

40
Q

Thyrotoxicosis causes

A

Grave’s: IgG autoantibodies stimulate thyroid follicular cells (out of control of normal pituitary feedback)
Toxic multinodular goitre: Older women, hyperactive nodules develop outside of TSH control
Solitary toxic adenoma: Plummer’s disease
Thyroiditis
Drug-induced: amiodarone, excess levothyroxine
Excess iodine intake
Hashitotoxicosis: hyperthyroid phase of Hashimoto’s
Secondary causes: TSH secreting pituitary tumour, resistance to thyroid hormone

41
Q

Thyrotoxicosis symptoms & signs

A 
Anxiety/irritability
Heat intolerance/sweating
Increased appetite
Palpitations
Weight loss
Tremor
Loose motions
Fatigue/weakness
Eyelid retraction
Graves opthalmopathy
Goitre/bruit
Systolic hypertension
Tachycardia/AF
Tremor
Hyper-reflexia
Warm peripheries
Acropachy
Proximal weakness
Pre-tibial myxoedema
42
Q

Thyrotoxicosis symptoms & signs specific to Grave’s

A

Grave’s opthalmopathy
Thyroid bruit
Acropachy: soft-tissue swelling of the hands and clubbing of the fingers
Pre-tibial myxoedema

43
Q

Features of Grave’s opthalmopathy

A

Lagopthalmos: inability to close eyes completely
Exopthalmos/proptosis: bulging eyes
Opthalmoplegia: affecting upward and lateral gaze (superior (CNIII) and lateral (CNVI) rectus)
Periorbital oedema

More common in smokers

44
Q

Thyroid crisis/storm presentation

A 
Occurs in periods of stress (infection/surgery/childbirth) in those with uncontrolled hyperthyroidism
Hyperpyrexia
Severe tachycardia
Profuse sweating
Confusion/psychosis
Coma/death
45
Q

Hyperthyroidism investigations

A

TSH: suppressed
Free T3/4: both elevated (rare= T3-toxicosis)
TSH receptor antibody (TRAb): sensitive + specific for Grave’s
Technetium uptake scan: if TRAb not present: diffuse = Grave’s, one or more hot nodules = toxic nodular goitre, reduced/absent uptake = thyroiditis
CT/MRI of orbit: extent of eye disease in Grave’s

46
Q

Causes of hypothyroidism

A

Autoimmune: Hashimoto’s thyroiditis (goitre, T cell gland destruction, B cell secretion of inhibitory TSH-receptor antibodies), atrophic thyroiditis (no goitre)
Hyperthyroidism treatment
Drugs: amiodarone, iodine excess, lithium
Iodine deficiency: most common
Thyroiditis: often transient
Secondary causes: hypothalamic/pituitary disorders
Congenital agenesis
Neoplastic infiltration

47
Q

Hypothyroidism symptoms & signs

A 
Fatigue
Depression/psychosis
Cold intolerance
Weight gain
Constipation
Menorrhagia
Myxoedema coma (rare)
Hair loss
Loss outer third of eyebrow
Anaemia
Hoarse voice
Goitre
Bradycardia
Dry skin
Hyporeflexia
48
Q

Hypothyroidism investigations

A

FBC: anaemia? macrocytic = co-morbid pernicious anaemia, microcytic = menorrhagia
TFTs: raised TSH, reduced free T4 in primary causes
Low TSH in pituitary/hypothalamic disease
TPO antibodies: raised in Hashimoto’s
Cholesterol: raised due to hepatic hypothyroidism
CK: raised due to muscle hypothyroidism

49
Q

Acute thyroiditis presentation

A

May follow URTI
Fever/malaise, thyroid swelling & tenderness
Thyrotoxic features initially as stored hormone is released
Then hypothyroidism
Classically low/absent uptake on technetium scanning

50
Q

Papillary carcinoma aetiology

A

Most common malignant carcinoma
40-50y
Risk factor: neck irradiation
Spreads locally, mets: local nodes, bone/lung

51
Q

Follicular carcinoma aetiology

A

20% of malignant carcinoma

Mets: via bloodstream to bone

52
Q

Medullary carcinoma aetiology

A

5% of malignant carcinoma
Affects older adults
Affects children/young adults as part of multiple endocrine neoplasia syndromes (exclude pheochromocytomas prior to surgery)
Arises from parafollicular ‘C’ cells that secrete calcitonin

53
Q

Anaplastic carcinoma

A

<5% malignant carcinoma
Occurs in elderly populations
Locally aggressive: complications = tracheal/SVC obstruction

54
Q

Thyroid carcinoma presentation

A

Asymptomatic thyroid nodules/lymph nodes
Hoarseness/dysphagia
Thyroid dysfunction is rare

55
Q

Solitary thyroid nodule investigations

A

USS
Technetium scans: ‘hot’ = adenoma, ‘cold’ = malignancy
Fine needle aspiration & cytology

56
Q

What does the adenohypophysis synthesise and secrete?

A 
GH
Prolactin
Adrenocorticotropic hormone
TSH
Gonadotrophin luteinizing hormone (LH)
Follicle stimulating hormone (FSH)
57
Q

What does the neurohypophysis store and secrete

A

Hormones produced by the hypothalamus
ADH
Oxytocin

58
Q

Pituitary adenoma classification

A

Benign tumours of glandular tissue
<1cm = microadenoma
>1cm = macroadenoma
Functioning/non-functioning

59
Q

Non-functioning adenoma presentation

A

Bitemporal hemianopia
Ocular palsies: compression of CN III, IV, VI
Hypopituitarism: destroys normal functioning tissue
Signs of raised ICP: headache
Hypothalamic compression: altered appetite, thirst, sleep/wake cycle

60
Q

Functioning adenoma presentation

A

Acromegaly: excessive GH production
Hyperprolactinaemia
Cushing’s syndrome: excessive ACTH

61
Q

Hyperprolactinaemia clinical features

A 
Galactorrhoea
Oligo/amorrhoea
Decreased libido
Subfertility in males
Arrested puberty
Long-term: osteoporosis due to androgen/oestrogen deficiency
62
Q

Acromegaly diagnosis

A

Raised IGF-1 level (correlated with GH levels over the past 24h
Glucose tolerance test: >2mcg/ml at 2h = acromegaly

63
Q

Acromegaly symptoms & signs

A 
Change in appearance
Increased hand/foot size
Tiredness
Excessive sweating
Poor libido
Symptoms of diabetes
Headaches
Visual deterioration
Symptoms of hypopituitarism
Protruding mandible
Prominent supraorbital ridge
Interdental seperation
Large tongue
Spade-like hands/feet
Visual field defects
Hypertension
64
Q

Cushing’s syndrome causes

A

Exogenous administration of steroids
ACTH dependent causes: Cushing’s disease, ectopic ACTH (e.g. small cell lung cancer)
ACTH independent causes: excess adrenal cortisol production (adrenal tumour/nodular hyperplasia)

65
Q

Cushing’s syndrome symptoms and signs

A 
Central weight gain
Change of appearance
Depression &amp; insomnia
Poor libido
Thin skin/easy bruising
Excess hair growth/acne
Diabetes symptoms
Moon face
Frontal balding
Striae
Hypertension
Pathological fractures
Dorsal fat pad
Proximal myopathy
Hypokalaemia: mineralcorticoid activity of cortisol
66
Q

Cushing’s syndrome diagnosis

A

Raised cortisol
Overnight dexamathasone suppression test: Normal = cortisol level <50mmol/L at 8am, Cushing’s = unsuppressed
48h dexamethasone suppression test
24h urinary free cortisol
Midnight cortisol level
Plasma ACTH: if undetectable = adrenal cause likely
High dose dexamethasone suppression test: ectopic (no suppression) or Cushing’s disease (complete/partial suppression)
Corticotrophic releasing hormone test: cortisol raised with pituitary but not ectopic sources

67
Q

Pheochromocytoma aetiology

A

Catecholamine secreting tumours arising from sympathetic paraganglial cells (Chromaffin cells)
Usually in adrenal medulla
10% extra-adrenal
10% bilateral
10% familial (MEN 2a/b, neurofibromatosis, Von Hippel-Lindau syndrome)

68
Q

Pheochromocytoma presentation

A

Severe/episodic hypertension unresponsive to medical treatment
General: sweating, heat intolerance, pallor, flushing
Neurological: headaches, visual disturbances, seizures
CV: palpitations, chest tightness, dyspnoea, postural hypertension
GI: abdominal pain, nausea, constipation
Symptoms worstened by stress/exercise/drugs

69
Q

Pheochromocytoma diagnosis

A

3x24h urine collections for raised free metadrenaline & normadrenaline
MRI/CT/functional imaging to locate tumour

70
Q

Addison’s disease pathophysiology

A

Primary adrenal insufficiency
Destruction of adrenal cortex leading to glucocorticoid (cortisol), mineralcorticoid (aldosterone), sex-steroid deficiencies

71
Q

Addison’s disease aetiology

A 
Autoimmune: most common in UK
TB: common cause worldwide
Overwhelming sepsis
Metastatic cancer: lung/breast
Lymphoma
Adrenal haemorrhage: Waterhouse-Friderichsen syndrome
72
Q

Addison’s disease symptoms & signs

A 
Weight loss, malaise, weakness, myalgia
Syncope
Depression
Pigmentation, especially of new scars &amp; palmar creases
Postural hypotension
Signs of dehydration
Loss of body hair: axillary/pubic
73
Q

Addison’s disease investigations

A

FBC: anaemia
U&Es: low sodium, high potassium, uraemia, raised calcium
Glucose: low
Short ACTH stimulation test/Synacthen test
9am ACTH/cortisol
21-hydroxylase adrenal autoantibodies
CXR: TB
Adrenal CT: TB/mets disease if antibodies -ve

74
Q

Conn’s syndrome pathophysiology

A

Young females
Adrenal adenoma –> primary hyperaldosteronism
Leads to sodium and water retention

75
Q

Conn’s syndrome presentation

A

Most asymptomatic
Hypertension: resistant to treatment, headaches
Hypokalaemia: cramps, weakness, tetany, polyuria (urinary loss of K+)
Elevated plasma aldosterone:renin ratio
Plasma aldosterone not suppressed by fludrocortisone administration

76
Q

Conn’s syndrome investigations

A

Confirm primary hyperaldosteronism
Adrenal CT to differentiate Conn’s from adrenal hyperplasia
Adrenal scintography

77
Q

blood pH effects on ionised calcium

A

Acidotic: increase ionised by decreasing albumin binding
Alkalotic: decrease ionized calcium by increasing albumin binding

78
Q

Action of parathyroid hormone

A

Secreted by chief cells in the 4 parathyroid glands
Secreted when: Ca2+ low, low vitD, high phosphate
PTH increases plasma calcium by…
Stimulating calcium reabsorption from bone
Increasing renal tubular calcium reabsorption
Increasing vitD activation in the kidney –> stimulates increased GI calcium absorption
PTH increases renal phosphate secretion

79
Q

Action of vitamin D

A

Sustains plasma Ca2+ and phosphate levels by increasing flow from GI tract
Required for normal bone formation

80
Q

How is active vitamin D obtained

A

Endogenously synthesised in skin: D3, cholecalciferol
Exogenously ingested: D2, ergocalciferol
Hydroxylated in liver
2nd hydroxylation in kidney

81
Q

Causes of vitamin D deficiency

A

Inadequate sunlight exposure
Malabsorptive conditions
Liver/kidney disease

82
Q

Action of calcitonin

A

Secreted by thyroid ‘c’ cells in response to increased plasma calcium levels
Antagonises affect of PTH on bone

83
Q

Causes of raised serum calcium

A

Primary hyperparathyroidism
Tertiary hyperparathyroidism
Ectopic PTH secretion
Malignancy: myeloma, bony mets, paraneoplastic (PTHrp/production of osteoclastic factors)
Excess vitamin D: exogenous excess, granulomatous disease (TB/sarcoid), lymphoma
Excess calcium intake: ‘milk-alkali’ syndrome
Thyrotoxicosis
Addison’s
Severe AKI
Drugs: thiazide diuretics, lithium
Hereditary: familial hypocalciuric hypercalcaemia

84
Q

Primary hyperparathyroidism presentation

A

Bones: pain, pathological fractures, muscle weakness
Stones: renal, polyuria, AKI/CKD
Abdominal groans: pain, vomiting, constipation, pancreatitis, GI ulcers
Psychic moans: depression, confusion, tiredness, hypotonicity

ECG: reduced QT interval

85
Q

Causes of hypocalcaemia with low PTH

A 
Idiopathic
Primary hypoparathyroidism (autoimmune)
Post thyroid/parathyroid surgery
Post neck irradiation
Infiltration: sarcoid/malignancy
DiGeorge syndrome
Severe hypomagnesia
86
Q

Causes of hypocalcaemia with high PTH

A 
Vitamin D deficiency
Acute pancreatitis
Alkalosis
Acute hyperphosphataemia (renal failure)
Rhabdomyolysis
Tumour lysis
Drugs: bisphosphonates, calcitonin
87
Q

Hypocalcaemia symptoms

A 
Peripheral irritability: tetany/cramps, carpo-pedal spasm (+ve Trosseau's sign &amp; +ve Chvostek's sign)
Central irritability: seizures
Depression/anxiety
Perioral parasthesia
Cataracts
88
Q

Hypocalcaemia investigations

A

Serum calcium: low
Serum PTH: high/low (if low check PTH)
Serum vitD: deficiency?
ECG: prolonged QT

CP1 (12 decks)

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