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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
Risk factors for diabetic retinopathy
Poor diabetic control, smoking, hypertension, pregnancy
26
Diabetic maculopathy pathology
More common in T2DM Presents as blurred vision Types: focal/diffuse/ischaemic
27
Types of diabetic eye disease
``` Non-proliferative diabetic retinopathy Proliferative diabetic retinopathy Diabetic maculopathy Cataract formation Progressive open-angle glaucoma ```
28
Types of diabetic neuropathy
``` Symmetrical polyneuropathy Acute painful neuropathy Mononeuropathy Diabetic amyotrophy Autonomic neuropathy ```
29
Symmetrical polyneuropathy presentation
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)
30
Acute painful neuropathy presentation
Painful burning in feet, shins, anterior thighs Associated with poor glycaemic control Worse at night
31
Mononeuropathy presentation
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
32
Diabetic amyotrophy presentation
Progressive wasting of muscle tissues Middle aged men, rare Painful wasting of quadriceps Variable course, gradual but incomplete improvement
33
Autonomic neuropathy
Sympathetic dysfunction: postural hypotension, ejaculatory failure, reduced sweating, Horner's syndrome Parasympathetic: erectile dysfunction, constipation, urinary retention, Holmes-Adie pupil
34
Macrovascular complications of diabetes
2x increased risk of stroke 4x increased risk of MI 50x increased risk of amputation for gangrene
35
Goitre morphology
Diffuse/nodular Simple/toxic (actively secreting thyroid hormone) Benign/malignant
36
Diffuse goitre differentials
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
Nodular goitre differentials
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
Goitre investigations
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
Thyrotoxicosis aetiology
Disorder resulting from raised circulating levels of thyroid hormone 1% of population 5:1 women:men
40
Thyrotoxicosis causes
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
Thyrotoxicosis symptoms & signs
``` 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
Thyrotoxicosis symptoms & signs specific to Grave's
Grave's opthalmopathy Thyroid bruit Acropachy: soft-tissue swelling of the hands and clubbing of the fingers Pre-tibial myxoedema
43
Features of Grave's opthalmopathy
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
Thyroid crisis/storm presentation
``` Occurs in periods of stress (infection/surgery/childbirth) in those with uncontrolled hyperthyroidism Hyperpyrexia Severe tachycardia Profuse sweating Confusion/psychosis Coma/death ```
45
Hyperthyroidism investigations
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
Causes of hypothyroidism
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
Hypothyroidism symptoms & signs
``` 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
Hypothyroidism investigations
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
Acute thyroiditis presentation
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
Papillary carcinoma aetiology
Most common malignant carcinoma 40-50y Risk factor: neck irradiation Spreads locally, mets: local nodes, bone/lung
51
Follicular carcinoma aetiology
20% of malignant carcinoma | Mets: via bloodstream to bone
52
Medullary carcinoma aetiology
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
Anaplastic carcinoma
<5% malignant carcinoma Occurs in elderly populations Locally aggressive: complications = tracheal/SVC obstruction
54
Thyroid carcinoma presentation
Asymptomatic thyroid nodules/lymph nodes Hoarseness/dysphagia Thyroid dysfunction is rare
55
Solitary thyroid nodule investigations
USS Technetium scans: 'hot' = adenoma, 'cold' = malignancy Fine needle aspiration & cytology
56
What does the adenohypophysis synthesise and secrete?
``` GH Prolactin Adrenocorticotropic hormone TSH Gonadotrophin luteinizing hormone (LH) Follicle stimulating hormone (FSH) ```
57
What does the neurohypophysis store and secrete
Hormones produced by the hypothalamus ADH Oxytocin
58
Pituitary adenoma classification
Benign tumours of glandular tissue <1cm = microadenoma >1cm = macroadenoma Functioning/non-functioning
59
Non-functioning adenoma presentation
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
Functioning adenoma presentation
Acromegaly: excessive GH production Hyperprolactinaemia Cushing's syndrome: excessive ACTH
61
Hyperprolactinaemia clinical features
``` Galactorrhoea Oligo/amorrhoea Decreased libido Subfertility in males Arrested puberty Long-term: osteoporosis due to androgen/oestrogen deficiency ```
62
Acromegaly diagnosis
Raised IGF-1 level (correlated with GH levels over the past 24h Glucose tolerance test: >2mcg/ml at 2h = acromegaly
63
Acromegaly symptoms & signs
``` 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
Cushing's syndrome causes
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
Cushing's syndrome symptoms and signs
``` Central weight gain Change of appearance Depression & 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
Cushing's syndrome diagnosis
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
Pheochromocytoma aetiology
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
Pheochromocytoma presentation
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
Pheochromocytoma diagnosis
3x24h urine collections for raised free metadrenaline & normadrenaline MRI/CT/functional imaging to locate tumour
70
Addison's disease pathophysiology
Primary adrenal insufficiency Destruction of adrenal cortex leading to glucocorticoid (cortisol), mineralcorticoid (aldosterone), sex-steroid deficiencies
71
Addison's disease aetiology
``` Autoimmune: most common in UK TB: common cause worldwide Overwhelming sepsis Metastatic cancer: lung/breast Lymphoma Adrenal haemorrhage: Waterhouse-Friderichsen syndrome ```
72
Addison's disease symptoms & signs
``` Weight loss, malaise, weakness, myalgia Syncope Depression Pigmentation, especially of new scars & palmar creases Postural hypotension Signs of dehydration Loss of body hair: axillary/pubic ```
73
Addison's disease investigations
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
Conn's syndrome pathophysiology
Young females Adrenal adenoma --> primary hyperaldosteronism Leads to sodium and water retention
75
Conn's syndrome presentation
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
Conn's syndrome investigations
Confirm primary hyperaldosteronism Adrenal CT to differentiate Conn's from adrenal hyperplasia Adrenal scintography
77
blood pH effects on ionised calcium
Acidotic: increase ionised by decreasing albumin binding Alkalotic: decrease ionized calcium by increasing albumin binding
78
Action of parathyroid hormone
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
Action of vitamin D
Sustains plasma Ca2+ and phosphate levels by increasing flow from GI tract Required for normal bone formation
80
How is active vitamin D obtained
Endogenously synthesised in skin: D3, cholecalciferol Exogenously ingested: D2, ergocalciferol Hydroxylated in liver 2nd hydroxylation in kidney
81
Causes of vitamin D deficiency
Inadequate sunlight exposure Malabsorptive conditions Liver/kidney disease
82
Action of calcitonin
Secreted by thyroid 'c' cells in response to increased plasma calcium levels Antagonises affect of PTH on bone
83
Causes of raised serum calcium
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
Primary hyperparathyroidism presentation
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
Causes of hypocalcaemia with low PTH
``` Idiopathic Primary hypoparathyroidism (autoimmune) Post thyroid/parathyroid surgery Post neck irradiation Infiltration: sarcoid/malignancy DiGeorge syndrome Severe hypomagnesia ```
86
Causes of hypocalcaemia with high PTH
``` Vitamin D deficiency Acute pancreatitis Alkalosis Acute hyperphosphataemia (renal failure) Rhabdomyolysis Tumour lysis Drugs: bisphosphonates, calcitonin ```
87
Hypocalcaemia symptoms
``` Peripheral irritability: tetany/cramps, carpo-pedal spasm (+ve Trosseau's sign & +ve Chvostek's sign) Central irritability: seizures Depression/anxiety Perioral parasthesia Cataracts ```
88
Hypocalcaemia investigations
Serum calcium: low Serum PTH: high/low (if low check PTH) Serum vitD: deficiency? ECG: prolonged QT

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