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Phase 2a > Endocrine Diseases > Flashcards

Endocrine Diseases Flashcards

1
Q

What is the aetiology of SIADH?

A
  • Tumours: Prostate, thymus, pancreas, small cell carcinoma of lung
  • Pulmonary lesions: pneumonia, TB
  • Metabolic causes: Alcohol withdrawal
  • CNS: Meningitis, tumours, head injury, subdural haematoma
  • Drugs: Chlorpromide, carbamezapine etc
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2
Q

Briefly explain the pathophysiology of SIADH?

A
  • Excess ADH release causes excess insertion of aquaporin 2 channels in apical membrane of collecting duct
  • Therefore excess water retention and hyponatraemia
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3
Q

How is SIADH diagnosed?

A
  • Low serum Na+, high urine Na+
  • Euvolaemia: normal blood vol
  • Low plasma osmolality, high urine osmolality
  • Test with saline - sodium depletion will respond but SIADH won’t
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4
Q

What are the clinical features of SIADH?

A
  • Symptoms due to hyponatraemia
  • Varied and genetic
  • Anorexia, nausea and malaise
  • Weakness and aches
  • Reduction in GCS and confusion with drowsiness
  • Fits and coma if severe
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5
Q

How is SIADH treated?

A
  • Treat underlying cause
  • Restrict fluids to 500-1000ml daily
  • Hypertonic saline if really symptomatic to prevent brain swelling
  • Oral demeclocycline daily (Inhibits ADH)
  • Vasopressin antagonist e.g. oral tovaptan daily
  • Salt and loop diuretic
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6
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism= Excess production of aldosterone, independent of the renin-angiotensin system. Resulting in increased sodium, and thus water retention (and increased blood pressure), and decreased renin release

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7
Q

What is the epidemiology of Conn’s syndrome?

A

Rare condition accounting for less than 1% of hypertension

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8
Q

What is the aetiology of Conn’s syndrome?

A
  • 2/3rds= Adrenal adenoma that secretes aldosterone

- 1/3rd= Bilateral adeno-cortical hyperplasia

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9
Q

What are the risk factors for Conn’s syndrome?

A
  • Hypertension under 35, with no family history
  • Hypokalaemia before diuretics
  • Conventional antihypertensives don’t work
  • Unusual symptoms e.g. sweating
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10
Q

Briefly explain the pathophysiology of Conn’s syndrome

A
  • Excess aldosterone production due to aldosterone producing carcinoma
  • Na+ and water retention, thus K+ loss (to balance charge
  • Thus hypokalemia and hypertension
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11
Q

What is the clinical presentation of Conn’s syndrome?

A
  • Often asymptomatic
  • Hypertension due to increased blood vol, associated with renal, cardiac and retinal damage
  • Hypokalaemia: Weakness, cramps, paraesthesia, polyuria
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12
Q

How is Conn’s syndrome diagnosed?

A
  • Hypokalaemic ECG= Flat T wave, ST depression, Long QT
  • Serum hypokalaemia
  • Plasma aldosterone:Renin (ARR)= If increased aldosterone levels that are not suppressed w 0.9% saline infusion= Diagnostic
  • CT or MRI on adrenal
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13
Q

How is Conn’s syndrome treated?

A
  • Laproscopic adrenalectomy

- Aldosterone antagonist e.g. oral sprinolactone for 4 weeks pre-op to control BP and K+

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14
Q

What is giantism?

A

Excessive GH production in children before fusion of epiphyses of long bones

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15
Q

What is acromegaly?

A

Excessive GH in adults

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16
Q

What is the aetiology of acromegaly?

A
  • Most cases are due to benign GH producing pituitary tumour, but can be due to hyperplasia
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17
Q

What is the epidemiology of acromegaly?

A

Rare, increased incidence in middle age

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18
Q

What are the risk factors for acromegaly?

A

5% associated with MEN-1

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19
Q

Briefly explain the pathophysiology of acromegaly

A
  • Increased GH due to pituitary tumour or ectopic carcinoid tumour
  • Binds to receptors, resulting in increased IGF-1
  • This stimulates skeletal muscle and soft tissue growth
  • Local tumour expansion can also cause compression of tissue and thus symptoms
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20
Q

List some symptoms of acromegaly

A
  • Headaches
  • Excessive sweating
  • Bitemporal hemianopia
  • Snoring
  • Wonky bite
  • Low weight
  • Low libido
  • Amenorrhea
  • Backache
  • Increased size of hands and feet
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21
Q

List some signs of acromegaly

A 
Skin darkening
Fatigue
Deep voice
Carpal tunnel syndrome
Macroglossia
Coarsening face with wide nose
Prognanthism and big supraorbital ridge
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22
Q

List some common co-morbidities with acromegaly

A
  • Low glucose tolerance
  • Diabetes
  • Sleep apnoea
  • CVS Problems
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23
Q

How is acromegaly diagnosed?

A
  • High glucose, Calcium, and phosphate
  • IGF1= Raised = Diagnostic
  • Plasma GH levels= Can rule out acromegaly if random GH is undetectable or is low
  • Pituitary function test
  • Glucose tolerance test= No suppression of glucose= Diagnostic
  • MRI of pituitary fossa
  • Old photos= See changes
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24
Q

How is acromegaly treated?

A
  • 1st line treatment= Trans-sphenoidal surgery to remove tumour and fix compression. If this fails, try somatostatin analogues e.g. IM octreotide
  • GH receptor antagonists if intolerant to SSA= Supresses IGF-1
  • Dopamine agonist e.g. Oral cabergoline
  • Stereotactic radiotherapy
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25
Q

What is the epidemiology of diabetes mellitus type 1?

A

Typically occurs in childhood
Increasing incidence
Common in Northern Europe

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26
Q

Briefly explain the pathophysiology of DMT1

A

Autoimmune destruction of auto anti-bodies of the pancreatic insulin secreting beta-cells in the islets of langerhans causing insulin deficiency and thus continued breakdown of liver glycogen leading to glycosuria and ketonuria as more glucose is in the blood.

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27
Q

What is the aetiology of DMT1?

A

Autoimmune against Beta cells
Idiopathic
Genetic susceptibility

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28
Q

What are the risk factors for DMT1?

A
  • Northern European
  • Family history
  • Associated with autoimmune disease: thyroidisms, coeliacs, Addison’s, perncious anaemia
  • Environment: Diet, Vit D deficiency, cleaner environment, enteroviruses
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29
Q

How is DMT1 treated?

A
  • Self adjusted doses using finger pricking glucose
  • Synthetic human insulin via a subcut injection into abdomen, thighs or upper arm (change site to avoid lipohypertrophy)
  • Can use short acting insulin, short acting insulin analogues or longer acting insulins
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30
Q

What are the complications of DMT1 treatments?

A

Hypoglycaemia
Lipohypertrophy
Insulin resistance
Weight gain

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31
Q

What is the aim of DMT1 treatment?

A

Aims to restore the physiology of the beta cell

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32
Q

What is the acute presentation of diabetes mellitus?

A 
Young people (usually DMT1) often present in first 2-6 weeks with polyuria and nocturia, polydipsia and weight loss 
Patients may have ketonuria and breath smelling of ketones (Pear drops)
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33
Q

What is the subacute presentation of diabetes mellitus?

A

Occurs during first months-years
Typical triad of polyuria, polydipsia and weight loss but all are less marked
Also lack of energy, visual blurring, infections

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34
Q

What are the complications that can be the presenting features for diabetes mellitus?

A
  • Staph. skin infection
  • Retinopathy
  • Polyneuropathy causing tingling and numbness in the feet
  • Erectile dysfunction
  • Arterial disease
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35
Q

What would be the only clinical feature of asymptomatic diabetes mellitus?

A

Glycosuria/hyperglycaemia

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36
Q

What is the plasma glucose concentration that is diagnostic for diabetes mellitus (DMT1 usually)?

A
  • Random plasma glucose >11.1 mmol/L
  • Fasting plasma glucose >7 mmol/L
    In symptomatic individuals, one result is diagnostic. If there is only one positive, perform a oral glucose tolerance test (again >7 for fasting, and >11.1 for random)
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37
Q

What test can be performed for diabetes mellitus risk?

A

IGT (Impaired glucose tolerance)

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38
Q

What is the main test for DMT2?

A

HbA1c > 48

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39
Q

What is the epidemiology of hyperosmolar, hyperglycaemic state?

A

Patients present in middle/later life often with previously undiagnosed diabetes

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40
Q

What are the risk factors for hyperosmolar, hyperglycaemic state?

A

Infection= Most common cause
Consumption of glucose rich food
Concurrent medications such as thiazide diuretics or steroids

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41
Q

Briefly explain the pathophysiology of hyperosmolar, hyperglycaemic state?

A

Endogenous insulin levels are reduced but are still sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production

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42
Q

What is the clinical presentation of hyperosmolar, hyperglycaemic state?

A
  • Severe dehydration
  • Decreased consciousness
  • Hyperglycaemia
  • Hyperosmolality
  • No ketones in blood/urine
  • Stupor or coma
  • Bicarbonate isn’t lowered
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43
Q

How is hyperosmolar, hyperglycaemic state diagnosed?

A
  • Hyperglycaemia= blood glocse >11mmol/L
  • Urine dipstick shows heavy glycosuria
  • Plasma osmolality is extremely high
  • Total body K+ is low, but serum K+ is often raised
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44
Q

How is hyperosmolar, hyperglycaemic state treated?

A

Lower rate of insulin infusion
Fluid replacement with 0.9% saline
Restore electrolyte loss
Low molecular weight heparin (SC Enoxaparin) to reduce risk of thromboembolism, MI, stroke, and arterial thrombosis

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45
Q

What are the types of hypoglycamia?

A
  • Plasma glucose <4 mmol/L
  • Serious= plasma glucose <3mmol/L
  • Severe= Impaired cognitive incidence
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46
Q

What is the aetiology of hypoglycamia?

A
  • In diabetes= due to insulin or sulphonylurea treatment
  • In non diabetes= Exogenous drugs, pituitary insufficiency, liver failure, Addison’s disease, Islet’s cell tumour, Non pancreatic neoplasm
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47
Q

What is the clinical presentation of hypoglycamia?

A
  • Autonomic= Sweating, anxiety, hunger, tremor, palpitations, dizziness
  • Neuroglycopenic= Confusion, drowsiness, visual trouble, seizures, coma
  • Rarely, focal symptoms= Personality change, transient hemiplegia, mutism etc
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48
Q

How is hypoglycamia diagnosed?

A

Fingerprick blood glucose= Shows hypoglycaemia, C peptide and ketones
Take drug history and exclude liver failure

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49
Q

How is hypoglycamia treated?

A

Oral sugar and long acting starch
If cannot swallow, give 50% glucose IV or IM
In diabetics, re-educate

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50
Q

What is the epidemiology of diabetic nephropathy?

A

Clinical nephropathy secondary to glomerular disease usually manifests 15-25yrs after diagnosis and affects 25-35% of patients diagnosed under age 30

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51
Q

What is the pathophysiology of diabetic nephropathy?

A

Thickening of the basement membrane in glomerulus due to poor glycaemic control, which leads to micro-albuminuria

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52
Q

What are the risk factors for diabetic nephropathy?

A

Poor blood pressure and blood glucose control

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53
Q

How is diabetic nephropathy diagnosed?

A
  • Urine albumin:creatinine ratio >3 will indicate micro albuminuria
  • This may progress to intermittent albuminuria followed by persistent proteinuria
  • Normochromic normocytic anaemia and raised ESR
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54
Q

How is diabetic nephropathy treated?

A
  • Aggressive treatment of BP
  • Reductions in insulin dosage as insulin sensitivities is increased
  • Avoid drugs excreted via kidney
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55
Q

What is the epidemiology of diabetic neuropathy?

A

Affects 30-35% of patients with diabetes

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56
Q

What is the aetiology of diabetic neuropathy?

A

Isolated mononeuropathies are thought to be as a result of occlusion of the vasa nervorum. More diffuse neuropathies may arise from the accumulation of the fructose and sorbitol which disrupts the structure and function of the nerve

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57
Q

What are the risk factors of diabetic neuropathy?

A

Hypertension, Smoking, HbA1c, BMI

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58
Q

What are the clinical features of diabetic neuropathy?

A
  • Pain: allodynia, burning etc
  • Autonomic: Postural hypotension, gastroparesis, diarrhoea, constipation
  • Insensitivities: Glove and stocking sensory loss
  • Mononeuritis multiplex
  • Diabetic amyotrophy
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59
Q

How is diabetic neuropathy treated?

A
  • Good glycaemic control
  • Treated with paracetamol
  • Tricyclic antidepressants
  • Anticonvulsants
  • Opiates
  • Transcutaneous nerve stimulation
  • Avoidance of weight bearing
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60
Q

What are the most common complications of diabetes?

A
  • Atherosclerosis= Stroke, MI, peripheral vascular disease
  • Microvascular complications= Diabetic retinopathy, nephropathy, neuropathy
  • Diabetic foot ulceration
  • Infection
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61
Q

What is the epidemiology of diabetic foot ulceration?

A

Foot ulceration occurs in 15% of people with DM

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62
Q

What is the pathophysiology of diabetic foot ulceration?

A

Neuropathy results in increased risk of silent trauma of the foot. Furthermore, neuropathy results in autonomic features that results in increased skin dryness of foot, which is thus more susceptible to cracking and ulceration.

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63
Q

What are some preventative methods for diabetic foot ulceration?

A
  • Diabetic foot screening and education
  • Check shoes for sharp bodies
  • Tie shoe laces loosly
  • Keep feet away from heat
64
Q

List some common infections in diabetes?

A
  • UTI
  • Skin infections such as cellulitis, boils, abscesses, staph. infections. Lipohypertrophy
  • Rectal abscess
  • Pyelonephritis
  • Pneumonia
65
Q

List some suggestive features of DMT1 over DMT2?

A
  • DMT1 tends to occur in childhood
  • Acute presentation
  • Tend to be leaner
  • More prone to ketoacidosis
  • High levels of autoantibodies
66
Q

List some suggestive features of DMT2 over DMT1?

A
  • Usually over 30s
  • Onset is gradual
  • Family history
  • Diet and exercise often helps
67
Q

What is the epidemiology of DMT2?

A
  • Very common (incidence increasing)
  • Older, usually over 30
  • More common in men
  • Ethnicity- middle Eastern, SE Asian, Western Pacific
68
Q

What are the causes of DMT2?

A
  • Obesity, lack of exercise, calorie and alcohol excess
  • No HLA disturbance but genetic link
  • Polygenic disorder
69
Q

What are the risk factors for DMT2?

A
  • Family history
  • Increasing age
  • Obesity and poor exercise
  • Ethnicity- middle Eastern, SE Asian, Western Pacific
  • Low birth weight
70
Q

Briefly explain the pathophysiology of DMT2

A

Polygenic. Environmental factors (central obesity) trigger onset in genetically susceptible. Beta cell mass reduced to 50% of normal. Inappropriately low insulin secretion and peripheral insulin resistance.

71
Q

How is DMT2 treated?

A
  1. Exercise, diet, weight loss, BP and lipid control
  2. Biguanide e.g. metformin (Reduces rate of gluconeogenesis and increases cell sensitivity to insulin)
  3. GLP analogues, SGL2 inhibitors, insulin, glitazones
72
Q

What is Cushing’s syndrome?

A

A general term which refers to chronic excessive and inappropriate elevated levels of circulating cortisol, whatever the cause

73
Q

What is Cushing’s disease?

A

Specifically refers to the excess of glucocorticoids resulting from inappropriate ACTH secretion from the pituitary due to a tumour

74
Q

What is the epidemiology of Cushing’s syndrome?

A
  • 10 per 100,000
  • Higher incidence in diabetics
  • 2/3rds are due to cushing’s disease
75
Q

What is the aetiology of Cushing’s syndrome?

A
  • ACTH dependent causes= Cushings disease, Ectopic ACTH production, ACTH treatments (e.g. for asthma)
  • ACTH independent causes= Adrenal adenoma, iatrogenic e.g. oral glucocorticoids
76
Q

Briefly explain the pathophysiology of Cushing’s syndrome?

A

Excess cortisol can either result from excess ACTH which stimulates cortisol, or from adrenal neoplasms which cause zona reticularis to release cortisol.

77
Q

What is pseudo-Cushings syndrome?

A

Alcohol excess mimicking Cushing’s syndrome

Will get better after 48 hrs without alcohol

78
Q

What is the clinical presentation of Cushing’s syndrome?

A
  • Proximal weakness and Osteoporosis
  • Plethoric complexion with moon face and acne
  • Mood= Depression, lethargy, irritability, psychosis
  • Obesity= Fat distribution is central (Buffalo hump) with purple striae
  • Muscle atrophy, thick skin that bruises easily
  • Failure for children to grow tall
  • Gonadal dysfunction
  • Infections
  • High BP
  • Hyperglycaemia
79
Q

How is Cushing’s disease diagnosed?

A
  • Drug history to exclude oral steroids
  • Overnight dexamethasone suppression test (No suppression in Cushings
  • Random plasma cortisol (but may be inaccurate)
  • Urine free cortisol over 24hrs
  • **
  • CT/MRI on adrenals
  • Corticotropin releasing hormone test= if cortisol responds, cushings is likely
  • Salivary cortisol
80
Q

How is Cushing’s syndrome treated?

A
  • Iatrogenic= Stop steroids
  • Cushings disease= Surgical selective removal of pituitary adenoma/ bilateral adrenalectomy if source is undetectable
  • Cortisol synthesis inhibition: Metyrapone, ketoconazole
81
Q

What is the clinical presentation of hyperthyroidism?

A
  • Palpitations, tremor and hyperkinesia
  • Diarrhoea, weight loss and increased appetite
  • Olgiomenorrhoea
  • Heat intolerance and sweating
  • Behavioural change= Anxiety and irritability
  • Lid lag and “stare”
  • Proxima myopathy and muscle wasting
  • Hands: Palmar erythma, fine tremor
  • Diffuse goitre
  • Lymphadenopathy and splenomegaly
82
Q

How is hyperthyroidism diagnosed?

A
  • Clinical
  • Thyroid function tests- low TSH, High T4/3
  • Will be raised TSH in secondary hyperthyroidism
  • TPO and thyroglobulin antibodies
  • Ultrasound of thyroid
  • TSH receptor stimulating antibodies are raised (Diagnostic of graves)
83
Q

How is hyperthyroidism treated?

A
  • Antithyroid drugs = Propylthiouracil (Stops conversion of T4 to T3) or Oral carbimazole (Blocks thyroid hormone biosynthesis and immunosuppressant)
  • This can be done via titration or block-replace therapy
  • Radioactive iodine
  • Surgery
84
Q

What are the causes of hyperthyroidism?

A
  • Graves’ (most common)
  • Toxic multinodular goitre
  • Solitary toxic adenoma
  • Drug induced hyperthyroidism
  • De Quervain’s thyroiditis
85
Q

What is the epidemiology of Hashimoto’s thyroiditis?

A
  • Much more common in women

- Most common cause of goitrous hypothyroidism

86
Q

What are the clinical features of Hashimoto’s thyroiditis?

A
  • Thyroid gland may enlarge rapidly, occasionally with dyspnoea or dysphagia from pressure on neck= nodular goitre
  • Hypothyroidism= Fatigue, cold intolerance, slowed movement, decreased sweating
87
Q

Briefly explain the pathophysiology of Hashimoto’s thyroiditis

A

Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes. Antibodies bind and block TSH receptors= Inadequate thyroid hormone production and secretion

88
Q

How is Hashimoto’s thyroiditis diagnosed?

A
  • TSH levels raised

- Thyroid antibodies

89
Q

How is Hashimoto’s thyroiditis treated?

A
  • Thyroid hormone replacement (levothyroxine)

- Resection of obstructive goitre

90
Q

What are the complications of Hashimoto’s thyroiditis?

A
  • Hyperlipidaemia and complications
91
Q

What is the aetiology of secondary hypoadrenalism ?

A
  • Commonest cause is iatrogenic: due to long term steroid therapy leading to suppression of the pituitary adrenal axis
  • Rarer cause is hypothalamic-pituitary disease resulting in decreased ACTH production
92
Q

Briefly explain the pathophysiology of secondary hypoadrenalism

A

Reduction in the release of ACTH results in decreased glucocorticoid (cortisol), mineralocorticoid production remains intact

93
Q

What is the clinical presentation of secondary hypoadrenalism?

A
  • Patient may have vague symptoms of feeling unwell

- No skin hyperpigmentation since ACTH is reduced

94
Q

How is secondary hypoadrenalism diagnosed?

A

ACTH levels are low

Mineralocorticoid production is intact

95
Q

How is secondary hypoadrenalism treated?

A
  • Adrenals will recover if long-term steroids are slowly weaned off- but long and difficult process
  • Oral hydrocortisone
96
Q

What are the risk factors for diabetic retinopathy?

A
  • Long duration DM
  • Poor glycaemic control
  • Hypertensive
  • On insulin treatment
  • Pregnancy
97
Q

How will proliferative retinopathy be seen?

A
  • New vessels on disc and elsewhere
  • Pre retinal or vitreous haemorrhage
  • Fibrous +/- tractional retinal detachment
98
Q

How is diabetic retinopathy treated?

A
  • Laser therapy = stabilises deterioration and prevents progression (doesn’t cure)
99
Q

How is diabetic retinopathy usually diagnosed?

A
  • National eye screening programme with retinal photography
100
Q

What is the epidemiology of diabetic ketoacidosis?

A
  • Hallmark of DMT1

- Usually can’t occur in DMT2 unless very advanced

101
Q

What are the clinical features of diabetic ketoacidosis?

A
  • The excess ketones are excreted in the urine and appear in the breath= pear drop scent
  • Profound dehydration and vomitting= eyes are sunken, tissue turgor is reduced and tongue is dry
  • Gradual drowsiness
  • May have severe abdominal pain
  • Kussmaul’s respiration (Deep and rapid)
  • Body temp is often subnormal
102
Q

What are the risk factors for diabetic ketoacidosis?

A
  • Stopping insulin therapy
  • Infection e.g. UTI
  • Surgery
  • MI
  • Pancreatitis
  • Undiagnosed diabetes
103
Q

How is diabetic ketoacidosis diagnosed?

A
  • Blood glucose>11mmol/l
  • Plasma ketones >3mmol/L
  • Acidaemia, blood pH <7.3
  • Bicarbonate <15mmol/L
  • Urine dipstick= Glycosuria and ketonuria
  • Total body K+ is low
  • Increased urea and creatinine due to dehydration
104
Q

How is diabetic ketoacidosis treated?

A
  • Immediate ABC
  • Replace fluid loss
  • Restore electrolytes
  • Restore acid-base balance
  • Monitor blood glucose
  • Replace deficient insulin
105
Q

Briefly explain the pathophysiology of diabetic ketoacidosis

A
  • High hepatic gluconeogenesis and peripheral uptake by tissues is reduced
  • High circulating glucose levels result in an osmotic diuresis by the kidneys and consequent dehydration and loss of electrolytes
  • Peripheral lipolysis leading to an increase in circulating FFAs, which are broken down into ketone bodys within the mitochondria
  • Metabolic acidosis then occurs
  • As pH falls, pH dependant enzyme systems can’t function
106
Q

What is the epidemiology of Addison’s disease?

A
  • Very rare= 0.8 per 100,000

- Marked female preponderance

107
Q

What are the common causes of Addison’s disease?

A
  • Autoimmune adrenalitis
  • TB
  • Adrenal metastases
  • Long term steroid use
  • Opportunistic infections in HIV
  • Adrenal infarction
108
Q

Briefly explain the pathophysiology of Addison’s disease

A
  • Destruction of the entire adrenal cortex
  • Reduced glucocorticoid, mineralocorticoid and androgen production
  • Increased CRH, and ACTH in response to low cortisol levels
109
Q

What is the clinical presentation of Addison’s disease?

A
  • Lethargy
  • Low mood, Low self esteem
  • Anorexia and weight loss
  • Vitiligo, tanned skin, pigmentation of skin
  • Vomitting and nausea
  • Diarrhoea, constipation and abdominal pain
  • Amenorrhoea
  • Postural hypotension, dizziness
  • Lean build
  • Dehydration, critical deterioration
110
Q

How is Addison’s disease diagnosed?

A
  • Blood tests: Hyponatraemia, hyperkalaemia, hypoglycaemia, hypoaldosteronism, low cortisol, uraemia, Raised Ca2+, FBC, Eosinophilia
  • Short ACTH stimulation test= Measure cortisol 30mins after IM tetracosactide. Exclude Addisons if cortisol >550nmol/L
  • Adrenal antibodies = Adrenalitis
  • 9am ACTH. If increased= Addison’s
111
Q

How is Addison’s disease treated?

A
  • If patient is seriously ill= IV hydrocortisone, IV 0.9% saline, glucose infusion if hypoglycaemia
  • Replace steroids x3 daily= Glucocorticoids (oral hydrocortisone) and mineralocorticoids (oral fludrocortisone)
  • Increase steroids in stress, illness, pregnancy
112
Q

What are the clinical features of an Adrenal crisis?

A
  • Vomitting and nausea
  • Abdominal pain
  • Muscle cramps
  • Confusion
113
Q

How is an Adrenal crisis treated?

A
  • IV hydrocortisone immediately
114
Q

What is the epidemiology of hypocalcaemia?

A
  • Very common in hospitalised patients

- Correlates with severity of illness

115
Q

What is the clinical presentation of hypoparathyroidism/hypocalcaemia?

A

SPASMODIC= Spasms (Tetany), Paresthesia, Anxiety, Seizures, Muscle tone increased (wheeze), Orientation impaired, Dermatitis and diarrhoea, Cataracts, Chvostek’s sign and cardiomyopathy

116
Q

What are the causes of hypocalcaemia?

A
  • Chronic kidney disease
  • Severe vitamin D deficiency
  • Reduced PTH function= hypoparathyroidism, pseudohypoparathyroidism, pseudopseudohypoparathyroidism
117
Q

What are the clinical features of pseudohypoparathyroidism?

A
  • Short stature
  • Short metacarpals (4th)
  • Subcutaneous calcification
  • May be intellectual impairment
118
Q

What are the results of a pseudohypoparathyroidism serum blood test?

A
  • High serum PTH
  • Low serum Ca2+
  • High serum phosphate
119
Q

How is hypocalcaemia diagnosed?

A
  • Blood tests= Ca2+, PTH, PO4
  • X ray of metacarpals for pseudohypoparathyroidism
  • Serum urea, creatinine and eGFR for renal function
  • Parathyroid antibodies in idiopathic hypoparathyroidism
  • Vit D and magnesium levels
  • ECG= QT elongation in hypocalcaemia
120
Q

What are the results of a hypoparathyroidism serum blood test?

A
  • Low serum Ca2+
  • Low serum PTH
  • High serum PO4
121
Q

What are the results of a pseudopseudohypoparathyroidism serum blood test?

A
  • Normal serum Ca2+
  • Normal serum PTH
  • Normal serum PO4
122
Q

How is hypocalcaemia/hypoparathyroidism treated?

A
  • IV calcium gluconate over 30 mins with ECG monitoring
  • If vit D defiency= Oral cholecalciferol or oral adcal
  • Hypoparathyroidism= Calcium supplements and calcitriol
123
Q

What is the epidemiology of Graves’ disease?

A
  • More common in females

- Most commonly presents at 40-60 yrs

124
Q

What are the risk factors for Graves’ disease?

A
  • Female
  • Genetic- HLA B8, DR3, DR2
  • E coli and other gram negative bacteria
  • Smoking
  • Stress
  • High iodine intake
  • Autoimmune disease= Vitiligo, DMT1, Addiso’s etc
125
Q

Briefly explain the pathophysiology of Graves’ disease

A
  • Thyroid stimulating immunoglobulins recognise and bind to immunoglobulins recognise and bind to the TSH receptor which stimulates T3/4
  • Thyroxine receptors in the pituitary are activated by excess hormone
  • Therefore reduced release of TSH in negative feedback loop, so high levels of T3/4 and low TSH
126
Q

What are the specific clinical features of Graves’ disease?

A
  • Graves ophthalmopathy= Presents in most Graves’ and some autoimmune hypothyroidism patients. Includes retro-orbital inflammation, eye discomfort, conjunctival oedema, photophobia, reduced acuity
  • Graves dermopathy= Pretibial myxoedema, and swollen clubbed fingers
127
Q

What is the epidemiology of thyroid carcinoma?

A
  • Not common

- More common in females

128
Q

What are the types of thyroid carcinoma?

A
  • Papillary (70%)
  • Follicular (20%)
  • Anaplastic (<5%)
  • Lymphoma (2%)
  • Medullary cell (5%)
129
Q

What is the most common type of thyroid carcinoma?

A

Papillary (70%)

130
Q

What are the clinical features of thyroid carcinoma?

A
  • Thyroid nodules
  • Thyroid may increase in size, and be hard and irregular
  • May have dysphagia or hoarseness of voice due to tumour compression
131
Q

How is thyroid carcinoma diagnosed?

A
  • Fine needle aspiration cytology biopsy and ultrasound: distinguish between benign and malignant
  • Blood tests (TFTs): To check if hyper or hypo thyroid
132
Q

How is thyroid carcinoma treated?

A
  • Radioactive iodine
  • Levothyroxine to keep TSH reduced
  • Chemotherapy to reduce risk of spread and treat micrometastases
  • Thyroidectomy
133
Q

What is the aetiology of nephrogenic diabetes insipidus?

A
  • Hypokalaemia
  • Hypercalcaemia
  • Drugs: Lithium chloride, glibenclamide
  • Renal tubular acidosis
  • Sickle cell disease
  • Prolonged polyuria of any cause
  • Familial
134
Q

What are the clinical features of diabetes insipidus?

A
  • Polyuria
  • Compensatory polydipsia
  • Hypernatraemia due to water loss in excess of Na+ loss: lethargy, thirst, weakness
  • Can lead to severe dehydration if the thirst mechanism or consciousness is impaired or patient is denied fluid
135
Q

How is diabetes insipidus diagnosed?

A
  • Urine vol to confirm polyuria
  • Check blood glucose to exclude DM
  • Water deprivation test
  • To differentiate between neurogenic or cranial- give IM desmopressin. Urine will not be concentrated in nephrogenic, but will in cranial
136
Q

How is nephrogenic diabetes insipidus treated?

A
  • Treat the cause- usually renal disease
  • Give thiazide diuretics
  • NSAIDs
137
Q

What is the aetiology of cranial diabetes insipidus?

A
  • Idiopathic
  • Congenital defects in ADH gene
  • Diseases of the hypothalamus
  • Tumour
  • Trauma
138
Q

How is cranial diabetes insipidus treated?

A
  • Find the cause- MRI of head and test ant. pituitary

- Give synthetic analogue of ADH e.g. oral desmopressin

139
Q

What is the aetiology of hypokalaemia?

A
  • Increased renal excretion= Diuretics (most common), increased aldosterone, renal disease, mineralocorticoids
  • Reduced dietary K+ intake
  • Redistribution into cells
  • GI losses
140
Q

What are the clinical features of hypokalaemia?

A
  • Usually asymptomatic
  • Muscle weakness
  • Cramps
  • Hypotonia
  • Hyporeflexia
  • Tetany
  • Palpitations
  • Light headedness
  • Constipation
141
Q

How is hypokalaemia diagnosed?

A
  • Serum K+ (less than 3.5= hypokalaemia, less than 2.5. is an emergency)
  • ECG= Small or inverted T waves, prominent U waves, a long PR interval, depressed ST segment
142
Q

How is hypokalaemia treated?

A
  • Medication review (withdrawal from diuretics)
  • Give oral K+ supprlements
  • Can give IV K+ but with extreme caution
143
Q

What is the aetiology of hyperkalaemia?

A
  • Decreased exertion= AKI or oliguric renal failure, Some medications, Addisons
  • Diabetic ketoacidosis
  • Metabolic acidosis
  • Tissue lysis/ necrosis
144
Q

What are the clinical features of hyperkalaemia?

A
  • Asymptomatic until K+ is high enough to cause cardiac arrest
  • Fast irregular pulse, chest pain, dizziness
  • Muscle weakness and fatigue
  • May be associated with metabolic acidosis = kussmauls respiration
145
Q

How is hyperkalaemia treated?

A
  • Medication review
  • Dietary K+ restriction
  • Polystyrene sulfonate resin
  • If urgent, calcium gluconate to stabilise cardiac membrane, and soluble insulin to drive K+ into cells
146
Q

How is hyperkalaemia diagnosed?

A
  • Serum K+. Over 5.5 is hyperkaelaemia, and over 6.5 is emergency
  • Progressive abnormalities on ECG= Tall tented T waves, small P waves, Wide QRS complex
147
Q

What are the clinical features of carcinoid syndrome?

A
  • Diarrhoea
  • Flushing
  • Palpitations
  • Abdominal cramps
  • Signs of right heart failure
  • Bronchospasm
148
Q

How is carcinoid syndrome diagnosed?

A
  • High vol of 5-hydroxyindolaecetic acid
  • Metabolic panel and LFTs
  • Liver ultrasound to confirm metastases
149
Q

How is carcinoid syndrome treated?

A
  • Local disease: Surgical resection and perioperative octreotide infusion
  • Metastases: above and additional radiotherapy ablation
150
Q

What is phaeochromocytoma?

A

A very rare adrenal medullary tumour that secretes catecholamines

151
Q

What are the clinical features of phaeochromocytoma?

A
  • Headache
  • Profuse sweating
  • Palpitations
  • Hypertension
  • Postural hypotension
  • Tremor
  • Hypertensive retinopathy
  • Pallor
152
Q

How is phaeochromocytoma diagnosed?

A
  • Plasma metanephrines and normatanephrines
  • 24 hr urinary total catecholamines
  • CT for tumour
153
Q

How is phaeochromocytoma treated?

A

Alpha blockers
Antihypertensive crisis
Tumour removal

154
Q

What would raised TSH receptor stimulating antibodies be indicative of?

A

Graves’ disease

155
Q

What would TPO and thyroglobulin antibodies be indicative of?

A

Graves or other causes of hyperthyroidism

156
Q

What are the clinical features of hypothyroidism?

A
  • Cold intolerance
  • Low mood
  • Fatigue
  • Constipation
  • Weight gain
  • Decreased sweating
  • Amenorrhea

Phase 2a (31 decks)

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