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1
Q

HYPERPARATHYROIDISM
what is the pathophysiology of tertiary hyperparathyroidism?

A
  • Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder,
  • hyperplasia of all 4 glands is usually the cause
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2
Q

HYPERPARATHYROIDISM
What blood results would you see in the 3 types of hyperparathyroidism?

A

PRIMARY =

  • PTH = high
  • calcium = high
  • phosphate = low
  • alk phos = high

SECONDARY =

  • PTH = high
  • calcium = low
  • phosphate = high
  • alk phos = high

TERTIARY -

  • PTH = high
  • calcium = high
  • phosphate = high
  • alk phos = high
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3
Q

HYPERPARATHYROIDISM
Describe the treatment for hyperparathyroidism

A

PRIMARY
- parathyroidectomy
- calcimimetics (cinacalet)
- bisphosphonates
- HRT

SECONDARY
- vitamin D supplementation
- renal transplant
- calcium supplementation
- phosphate binding agent

TERTIARY
- parathyroidectomy
- cinacalet

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4
Q

HYPERPARATHYROIDISM
How does a calcium mimetic work?

A

Increases sensitivity of parathyroid cells to calcium so less PTH secretion occurs

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5
Q

HYPOPARATHYROIDISM
what are the clinical features of hypoparathyroidism?

A

SYMPTOMS:CATs go numb

  1. convulsions / seizures
  2. arrhythmias / anxious
  3. tetany / muscle spasms
  4. numbness

SIGNS:

  • CHVOSTEK’S SIGN - tap over facial nerve and look for spasm of facial nerves
  • TROUSSEAU’S SIGN - inflate BP cuff 20 mmHg above systolic for 5 mins = hand spasm - hypocalcaemia
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6
Q

HYPOPARATHYROIDISM
what are the causes of hypoparathyroidism?

A
  • iatrogenic (neck surgery)
  • autoimmune (isolated autoimmune hypothyroidism)
  • metabolic (hyper/hypomagnesaemia)
  • congenital (DiGeorge syndrome)
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7
Q

HYPOPARATHYROIDISM
What is the treatment for hypoparathyroidism?

A

ACUTE
- IV 10% calcium gluconate

LONG TERM
- increased dietary calcium + vitamin D
- calcium supplements
- Vitamin D supplements
- thiazide diuretics

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8
Q

HYPERCALCAEMIA
what are the causes of Hypercalcaemia?

A

Hyperparathyroidism
Malignancy
Sarcoidosis
Thyrotoxicosis
Drugs

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9
Q

HYPERCALCAEMIA
What is the treatment for hypercalcaemia?

A
  • Treat underlying cause
  • increase circulation volume, increase excretion
    .- Bisphosphonates, glucocorticoids, gallium, dialysis
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10
Q

HYPERCALCAEMIA
Give 2 ECG changes that you might see in someone with hypercalcaemia

A
  1. Tall T waves
  2. Shortened QT interval
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11
Q

HYPOCALCAEMIA
Name 3 causes of hypocalcaemia

A

Hypoparathyroidism
Vitamin D deficiency
Hyperventilation
Drugs
Malignancy
Toxic shock

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12
Q

HYPOCALCAEMIA
what is the treatment for hypocalcaemia?

A

10ml calcium gluconate/chloride 10% slow IV,
oral calcium and Vit D

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13
Q

HYPOCALCAEMIA
Give 2 ECG changes that you might see in hypocalcaemia?

A
  1. Small T waves
  2. Long QT interval
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14
Q

T1DM
Give 4 potential complications of insulin therapy

A
  1. Hyperglycaemia
  2. Lipohypertrophy at injection site
  3. Insulin resistance
  4. Weight gain
  5. Interference with life style
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15
Q

DIABETIC KETOACIDOSIS
Describe the pathophysiology of diabetic ketoacidosis

A
  • net reduction in insulin + increase in other hormones (cortisol, glucagon, catecholamines + GH)
  • this leads to reduced glucose entry into cells
  • cells metabolise lipids as alternative energy source
  • uncontrolled lipolysis leads to elevated free fatty acids + ketone bodies
  • this leads to a state of ketoacidosis
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16
Q

T2DM
What class of drugs can cause diabetes?

A

Steroids
Thiazides
Anti-psychotics

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17
Q

T2DM
what are the risk factors for T2DM?

A
  • increasing with age (increasingly common in adolescents)
  • Asian + African ethnicities
  • Family history
  • Obesity
  • Gestational diabetes
  • PCOS
  • Drugs (corticosteroids, thiazides)
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18
Q

T2DM
Describe the treatment pathway for T2DM

A

MEDICATIONS
1st line = metformin
if patient has HF offer metformin + SGLT2i (-gliflozin)

if HbA1c >58, commence dual therapy
1. DPP4i (linagliptin, sitagliptin)
2. Sulfonylurea (gliclazide)
3. Pioglitazone
4. SGLT2i (dapagliflozin, empagliflozin)

if HbA1c > 58 despite dual therapy, commence intermediate acting insulin or triple therapy

triple therapy = metformin + sulfonylurea + GLP-1 mimetic (liraglutide)

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19
Q

T2DM
what are the side effects of Sulfonylurea?

A

Hypoglycaemia
weight gain
hyponatraemia

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20
Q

HYPOGLYCAEMIA
Why does hypoglycaemia continuously get worse?

A

Glucagon is not produced so rely only on adrenaline and the threshold for adrenaline release gradually lowers after time

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21
Q

HYPOGLYCAEMIA
Briefly describe the treatment of hypoglycaemia

A

CONSCIOUS + CAN SWALLOW:
- fast acting carbohydrate (glucose tablets, glucose 40% gels, glucose liquid, fruit juice), repeat blood glucose after 10-15 mins
- long acting carbohydrate once blood gluucose >4mmol/L (biscuit, bread)
- IM glucagon or IV glucose 10% if patient does not respond to fast acting carb

REDUCED CONSCIOUSNESS/EMERGENCY
- IM glucagon
- IV 10% glucose 150-200ml
- long acting carbohydrate, once blood glucose is >4mmol/L (biscuit, bread, milk or normal carb containing meal)

in malnourished/alcoholic patients, IV glucose should be given alonside thiamine to prevent wernicke’s encephalopathy

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22
Q

Name 5 possible diseases of the pituitary

A
  1. Benign pituitary adenoma
  2. Craniopharygioma
  3. Trauma
  4. Apoplexy/Sheehans
  5. Sarcoid/TB
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23
Q

ACROMEGALY
what are the clinical features of acromegaly?

A

SYMPTOMS:
visual disturbance
headaches
rings and shoes are tight
polyuria + polydipsia due to T2DM
tingling in hands
galactorrhoea
menstrual irregularity/erectile dysfunction

SIGNS:
hypertension,
bitemporal hemiopia
prominent jaw + supraorbital ridge
coarse facial appearance
Prognathism (protrusion of lower jaw)
Macroglossia (large tongue)
Spade-like hands
Sweaty palms + oily skin

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24
Q

ACROMEGALY
What are the investigations for acromegaly?

A

1st line = IGF-1 (high)
2nd line = oral glucose tolerance test (gold standard)
3rd line = pituitary function tests
4th line = MRI

also investigate for complications

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25
Q

ACROMEGALY
What is the gold standard diagnostic test for acromegaly?

A

Oral glucose tolerance test - failure of glucose to suppress serum GH

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26
Q

ACROMEGALY
what is the management for acromegaly?

A

1st line = trans sphenoidal surgery

2nd line
- medical = CABERGOLINE (dopamine agonist), bromocriptine is alternative
- OCTEOTIDE (somatostatin analogue) used in moderate/severe disease

3rd line = PEGVISOMANT (GH receptor antagonist)

4th line = radiotherapy

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27
Q

ACROMEGALY
What types of medical therapy can be used to treat acromegaly?

A

somatostatin analogue = octreotide

dopamine agonist = cabergoline

GH receptor antagonist = pegvisomant

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28
Q

ACROMEGALY
Give 3 advantages of using dopamine agonists in the treatment of acromegaly

A
  1. No hypopituitarism
  2. Oral administration
  3. Rapid onset
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29
Q

ACROMEGALY
Name a dopamine agonist that can be used as a treatment for acromegaly

A

Cabergoline

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30
Q

ACROMEGALY
Why can somatostatin analogues be used in the treatment of acromegaly?

A

They inhibit GH release

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31
Q

PROLACTINOMA
what are the causes of prolactinoma?

A
  1. Pituitary adenoma
  2. Anti-dopaminergic drugs
  3. Head injury - compression of the pituitary stalk
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32
Q

PROLACTINOMA
what are the clinical features of prolactinoma

A

SYMPTOMS:
amenorrhea,
galactorrhoea,
gynaecomastia,
low libido,
erectile dysfunction

SIGNS:
low testosterone,
infertility
visual field defects
headache

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33
Q

PROLACTINOMA
What is the treatment for prolactinoma?

A

Dopamine agonists - cabergoline - inhibits prolactin release

Occasionally transsphenoidal pituitary resection

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34
Q

CUSHINGS
what are the causes of excess cortisol? And are they ACTH dependent or independent?

A

ACTH dependent (ACTH raised):
- Cushing’s disease
- Ectopic ACTH production
- ACTH treatment

ACTH independent (ACTH not raised)
- adrenal adenoma
- iatrogenic

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35
Q

CUSHINGS
what are the investigations for Cushing’s syndrome?

A

CONFIRM HYPERCORTISOLISM
- 1st line = overnight dexamethasone suppression test (shows failure of cortisol suppression)
- 24hr urinary free cortisol (2 measurements required)

SOURCE LOCALISATION
- 9am ACTH (elevated = ACTH-dependant cause)
if positive then perform
- high dose dexamethasone suppression test

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36
Q

CUSHINGS
What is the treatment for Cushing’s syndrome?

A

ACTH-dependent
- cushings disease - 1st line = trans-sphenoidal resection
- ectopic ACTH source - treat underlying cause of cancer

ACTH-independent
- iatrogenic = review need for medication + try weaning
- adrenal tumour = tumour resection/adrenalectomy

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37
Q

ADDISONS DISEASE
what are the causes of Addison’s disease?

A
  • autoimmune destruction (21-hydroxylase present in 60-90%) - most common in developed countries
  • TB - most common in developing countries
  • adrenal metastases- long term steroid use
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38
Q

ADDISONS DISEASE
what are the clinical features of Addison’s disease?

A

SYMPTOMS
Lethargy + weakness
N+V
weight loss
‘salt cravings’
collapse + shock (addisonian crisis)

SIGNS
Hyperpigmentation (particularly in palmar creases)
loss of pubic hair
hypotension + postural drop

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39
Q

ADDISONS DISEASE
What is the pathophysiology of Addison’s disease?

A

Destruction of the adrenal cortex results in decreased production of the hormones
All steroids reduced
Reduced cortisol levels = increased CRH and ACTH production through feedback

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40
Q

ADDISONS DISEASE
What are the investigations for Addison’s disease?

A

1st line = 8-9am cortisol (<100nmol/L = highly suggestive, 100-500nmol/L = refer for ACTH stimulation test)

Gold standard = ACTH stimulation test (short syntacthen test) - failure of rise in cortisol = addisions

Other tests
- 8am ACTH
- adrenal antibodies (anti-21-hydroxylase)
- U&Es (hyponatraemia + hyperkalaemia)
- aldosterone/renin ratio (decreased)
- CT adrenal (atrophied glands)

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41
Q

ADDISONS DISEASE
What investigations would you do to determine whether Adrenal insufficiency is primary or secondary?

A

Primary = adrenal antibodies, very long chain fatty acids, imaging and genetics

Secondary = any steroids?, imaging and genetics

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42
Q

ADDISONIAN CRISIS
What is the management of adrenal crisis (addisonian crisis)?

A

ACUTE
- IV fluids - normal saline
- Corticosteroids = HYDROCORTISONE 100mg IV stat followed by 200mg over 24hrs. Oral replacement after 24 hrs with reduction to maintenance level over 3-4 days
- treat underlying cause

CHRONIC
- long term hydrocortisone + fludrocortisone

Fluid resuscitation - saline (IV)

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43
Q

ADDISONS DISEASE
What would sodium and potassium levels be in someone with adrenal insufficiency?

A

Hyponatraemia = low sodium
Hyperkalaemia = high potassium
Lack of aldosterone and so less sodium reabsorbed and less potassium excreted

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44
Q

GRAVES DISEASE
what is the clinical presentation of Grave’s opthlmopathy?

A

SYMPTOMS
Eye discomfort
Grittiness
increased tear production
Photophobia
Diplopia
reduced acuity

SIGNS
Exophthalmos – protruding eye
Proptosis – eye protrudes beyond orbit
Conjunctival oedema
Corneal ulceration
Ophthalmoplegia – paralysis of eye muscles

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45
Q

GRAVES DISEASE
what is the treatment for Grave’s ophthalmology?

A

Conservative treatment – smoking cessation and sunglasses
Anti-thyroid medication e.g. carbimazole
IV METHYLPREDNISOLONE a
surgical decompression/eyelid surgery

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46
Q

GRAVES DISEASE
Name 5 risk factors for Graves disease

A
  1. Female
  2. Genetic association
  3. E.coli
  4. Smoking
  5. Stress
  6. High iodine intake
  7. Autoimmune diseases
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47
Q

GRAVES DISEASE
Name 5 autoimmune diseases associated with thyroid autoimmunity

A
  1. T1DM
  2. Addison’s disease
  3. Pernicious anaemia
  4. Vitiligo
  5. Alopecia areata
  6. Rheumatoid arthritis
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48
Q

THYROID GOITRE
Name 4 types of sporadic non toxic goitre

A
  1. Diffuse –> physiological –> Graves
  2. Multi nodular
  3. Solitary nodule
  4. Dominant nodule
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49
Q

HYPERTHYROIDISM
what are the causes of hyperthyroidism?

A

PRIMARY
- graves disease
- toxic multinodular goitre (iodine deficiency)
- toxic adenoma
- subclinical hyperthyroidism
- drugs (amiodarone)

SECONDARY
- pituitary adenoma
- ectopic tumour
- hypothalamic tumour

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50
Q

HYPERTHYROIDISM
Name 4 drugs which can induce hyperthyroidism

A
  1. Iodine
  2. Amiodarone
  3. Lithium
  4. Radioconstrast agents
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51
Q

HYPERTHYROIDISM
What are the thyroid function test results in primary hyperthyroidism?

A

high T4
high T3
low TSH

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52
Q

HYPERTHYROIDISM
What are the thyroid function rests in secondary hyperthyroidism?

A

high T4
high T3
high TSH

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53
Q

HYPERTHYROIDISM
Give 5 side effects of anti-thyroid drugs

A
  1. Rash
  2. Arthralgia
  3. Hepatitis
  4. Neuritis
  5. Vasculitis
  6. Agranulocytosis - very serious
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54
Q

HYPERTHYROIDISM
What is a complication of hyperthyroidism?

A
  • Thyroid crisis/storm
  • osteoporosis
  • proximal myopathy
  • thyrotoxic crisis
  • iatrogenic (agranulocytosis from carbimazole, congenital malformations, foetal goitre)
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55
Q

HYPERTHYROIDISM
What is the treatment for a thyroid crisis?

A

symptomatic treatment e.g. paracetamol
treatment of precipitating event
beta blockers e.g. IV propranolol
anti-thyroid drugs - methimazole/propylthiouracil
lugols iodine
dexamethasone 4mg IV QDS to stop conversion of T4 to T3

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56
Q

HYPOTHYROIDISM
Briefly describe the pathophysiology of secondary hypothyroidism

A

Reduced release or production of TSH so reduced thyroid hormone release

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57
Q

HYPOTHYROIDISM
Briefly describe the pathophysiology of tertiary hypothyroidism

A

Thyroid gland overcompensates until it can reestablish correct concentration fo thyroid hormone

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58
Q

HYPOTHYROIDISM
what are the causes of primary hypothyroidism

A
  • autoimmune thyroiditis (hashimotos thyroiditis)
  • De Quervains thyroiditis (follows viral prodrome)
  • post-partum thyroiditis
  • iodine deficiency
  • post-thyroidectomy or post-radioiodine
  • drugs (amiodarone, lithium, anti-thyroid drugs e.g. carbimazole)
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59
Q

HYPOTHYROIDISM
Name 4 drugs that can cause hypothyroidism

A
  1. Carbimazole (used to treat hyperthyroidism)
  2. Amiodarone
  3. Lithium
  4. Iodine
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60
Q

HYPOTHYROIDISM
Name 3 causes of secondary hypothyroidism

A
  • compression from a pituitary tumour
  • hypothalamic tumours
  • drugs (cocaine, steroids + dopamine)
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61
Q

HYPOTHYROIDISM
What are the TFT results for primary hypothyroidism?

A
  • High TSH
  • low T4
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62
Q

HYPOTHYROIDISM
What are the TFT results for secondary hypothyroidism?

A
  • normal/low TSH
  • low T4
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63
Q

HYPOTHYROIDISM
Name 3 antibodies that may be present in the serum in someone with autoimmune thyroiditis

A
  1. TPO (thyroid peroxidase)
  2. Thyroglobulin
  3. TSH receptor
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64
Q

HYPOTHYROIDISM
what are the complications of hypothyroidism?

A
  • hypercholesterolaemia
  • carpal tunnel
  • peripheral neuropathy
  • myoxedema coma
  • thyroid lymphoma
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65
Q

HASHIMOTOS THYROIDITIS
Give 3 symptoms of Hashimoto’s thyroiditis

A
  1. Rapid formation of Goitre
  2. Dyspnoea or dysphagia
  3. General hypothyroidism symptoms
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66
Q

HASHIMOTOS THYROIDITIS
Name 3 triggers of Hashimoto’s thyroiditis

A
  1. Iodine
  2. Infections
  3. Smoking
  4. Stress
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67
Q

HASHIMOTOS THYROIDITIS
what are the complications of Hashimoto’s thyroiditis?

A

Hashimoto’s encephalopathy

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68
Q

DIABETES INSIPIDUS
Define diabetes insipidus

A

Diabetes insipidus (DI) is an inability of the body to concentrate urine.

Passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption in the kidney due to hypo secretion or insensitivity to ADH

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69
Q

DIABETES INSIPIDUS
Name the 2 types of DI

A
  1. Cranial (central) DI = reduced vasopressin (ADH) produced by hypothalamus and secreted by the posterior pituitary
  2. Nephrogenic DI = impaired response of the kidney to ADH (kidneys are resistant to ADH)
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70
Q

DIABETES INSIPIDUS
what are the clinical features of DI?

A

SYMPTOM

  • Polyuria + nocturia
  • Polydipsia
  • No glycosuria
  • fatigue

SIGNS
Volume depletion
- Dry mucosa
- Sunken eyes
- Changes in skin turgidity
- Can lead to dehydration
Hypernatremia
- irritability
- hyper-reflexia
- confusion

  • bitemporal hemianopia (when there is a craniopharyngioma)
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71
Q

DIABETES INSIPIDUS
what are the causes of cranial(central) DI?

A

CONGENITAL
- malformations of hypothalamus
- wolfram syndrome

ACQUIRED
- pituitary surgery
- tumours (craniopharyngiomas + metastasis, NOT pituitary adenomas)
- traumatic brain injury
- subarachnoid haemorrhage
- CNS infections (meningitis + encephalitis)
- pituitary stalk disease (sarcoidosis)
- drugs (phenytoin)

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2
3
4
5
Perfectly
72
Q

DIABETES INSIPIDUS
what are the causes of nephrogenic DI?

A

CONGENITAL
- mutations in vasopressin or aquaporin receptors

ACQUIRED
- drugs (lithium, gentamicin, cisplatin)
- renal disease (renal amyloid, obstructive uropathy)
- electrolyte disturbance (hypokalaemia, hypercalcaemia)

73
Q

DIABETES INSIPIDUS
Give 3 possible differential diagnosis’s of DI

A
  1. DM
  2. Hypokalaemia
  3. Hypercalcaemia
74
Q

DIABETES INSIPIDUS
what are the investigations for diabetes insipidus?

A
  • Urine + serum osmolality = low urine osmolality + high serum osmolality
  • U&Es = normal/raised Na
  • serum glucose (to rule out DM)
  • 24hr urine output (if <3L, DI is unlikely)
  • Water deprivation test = low urine + high serum osmolality
  • desmopressin suppression test = in cDI, urine volume decrease + osmolality increases, in nDI no response

To consider
- MRI pituitary
- anterior pituitary function tests
- genetic testing

75
Q

DIABETES INSIPIDUS
What is the treatment for cranial DI?

A
  • desmopressin
  • manage fluid balance (water readily available in patients able to manage own fluids, IV fluids for those not able to)
  • low sodium diet
76
Q

DIABETES INSIPIDUS
What is the treatment for nephrogenic DI?

A
  • manage fluid balance
  • treat underlying cause
  • sodium restriction
  • thiazide diuretics (BENDROFLUMETHIAZIDE)
77
Q

DIABETES INSIPIDUS
Do you have hyponatraemia or hypernatraemia in diabetes insipidus?

A

Hypernatraemia

78
Q

SIADH
what are the clinical features of SIADH?

A

MILD
- N+V
- headache
- lethargy

MODERATE
- weakness
- muscle aches
- confusion
- ataxia

SEVERE
- reduced consciousness
- seizures
- respiratory arrest

All patients are EUVOLAEMIC (no features of hyper/hypovolaemia)

79
Q

SIADH
what are the causes of SIADH?

A

NEURO
- meningitis
- encephalitis
- intracranial haemorrhage
- stroke

MALIGNANCY
- small cell lung cancer

INFFECTION
- pneumonia
- TB

ENDOCRINE
- hypothyroidism

DRUGS
- SSRIs + TCAs
- PPIs
- Carbamazepine
- Cyclophosphamide
- Sulfonylureas

OTHER
- porphyria
- PEEP

80
Q

SIADH
what are the investigations for SIADH?

A
  • urine osmolality = inappropriately high in relation to serum osmolality
  • urine sodium concentration = high
  • ADH levels
  • U and Es (low sodium normal potassium),
  • fluid status

distinguish SIADH from salt & water depletion - test with 1-2L of
0.9% saline:
* Sodium depletion will respond
* SIADH will NOT RESPOND

81
Q

SIADH
Describe the treatment for SIADH

A

ACUTE (<48hrs)
- hypertonic 3% NaCl

CHRONIC (>48hrs)
- Na correction maximum 10mmol/L per day
- mild-moderate asymptomatic cases = fluid restriction (750-1000ml per day)
- severe or symptomatic = demeclocycline or tolvaptan

82
Q

SIADH
How do you treat asymptomatic SIADH?

A

Fluid restriction

83
Q

SIADH
How do you treat very symptomatic SIADH?

A

Give 3% saline (hypertonic)
demeclocycline or tolvaptan

84
Q

SIADH
Would you expect a patient with SIADH to be hypovolaemic, euvolaemic or hypervolaemic?

A

Euvolaemic

85
Q

SIADH
Would you associate SIADH with hyponatraemia or hypernatraemia?

A

Hyponatraemia - <135 mmol/L

86
Q

SIADH
Would you associate SIADH with plasma hypo-osmolality or hyper-osmolality?

A

Plasma hypo-osmolality - <275 mOsmol/Kg

87
Q

SIADH
Would you associate SIADH with a high to low urine osmolality?

A

High urine osmolality

88
Q

PITUITARY ADENOMA
Give 4 local effects a pituitary adenoma

A
  1. Headaches
  2. Visual field defects - bitemporal hemianopia
  3. Cranial nerve palsy and temporal lobe epilepsy
  4. CSF rhinorrhoea
89
Q

PROLACTINOMA
What can lead to elevated levels of prolactin?

A
  1. Stress
  2. Drugs
  3. Pressure on pituitary stalk
  4. Prolactinoma
90
Q

DIABETES PHARMACOLOGY
Give an example of a sulfonylurea

A

gliclazide

91
Q

DIABETES MELLITUS
Name 3 exocrine causes of Diabetes

A
  1. Inflammatory - actue/chronic pancreatitis
  2. Hereditary haemochromatosis
  3. Pancreatic neoplasia
  4. Cystic fibrosis
92
Q

PHEOCHROMOCYTOMA
What is Pheochromocytoma?

A

A rare catecholamine secreting tumour in the adrenal medulla (chromatin cells)

93
Q

PHEOCHROMOCYTOMA
what are the different types of pheochromocytoma?

A
  1. Familial type - more NAd

2. Sporadic - more Ad

94
Q

PHEOCHROMOCYTOMA
what are the clinical features of pheochromocytoma?

A

SYMPTOMS
Headache
Profuse Sweating
Palpitations
Tremor

SIGNS
Hypertension
Postural hypotension
Tremor
hypertensive retinopathy
Pallor

95
Q

PHEOCHROMOCYTOMA
What are the investigations for pheochromocytoma?

A
  • Plasma metanephrines and normetanephrines
  • 24 hour urinary total catecholamines
  • CT – look for tumour
96
Q

PHEOCHROMOCYTOMA
What is the treatment for pheochromocytoma?

A

Without HTN crisis:
1st Line = Alpha blockers (PHENOXYBENZAMINE)
Most patients will eventually get the tumour removed and then managed medically.

With HTN crisis:
1st Line = Antihypertensive agents (PHENTOLAMINE)

97
Q

PHEOCHROMOCYTOMA
What is the management of a phaeochromocytoma crisis?

A

Non-competitive alpha-blocker e.g. phenoxybenzamine
Excision of paraganglioma
Biochemistry: measure plasma and serum metanephrines

98
Q

DIABETIC NEPHROPATHY
Describe the treatment for diabetic nephropathy

A
  1. Glycaemic and BP control
  2. Angiotensin receptor blockers/ACE inhibitors - RAMIPRIL or CANDESARTAN
  3. Proteinuria and cholesterol control
99
Q

DIABETIC NEUROPATHY
Give 5 signs of autonomic neuropathy in diabetic neuropathy

A
  1. Hypotension
  2. HR affected
  3. Diarrhoea/constipation
  4. Incontinence
  5. Erectile dysfunction
  6. Dry skin
100
Q

DIABETIC NEUROPATHY
What are the 4 main threats to skin and subcutaneous tissues in someone with diabetic neuropathy

A
  1. Infections
  2. Ischaemia
  3. Abnormal pressure
  4. Wound environments
101
Q

DIABETES MELLITUS
what infections can poorly controlled diabetes lead to?

A
  1. UTIs
  2. Staphylococcal infection of skin
  3. Mucocutaneous candidiasis
  4. Pyelonephritis
  5. TB
  6. Pneumonia
  7. rectal abscess
102
Q

CONNS SYNDROME
What is Conn’s syndrome?

A

Primary hyperaldosteronism caused by an adrenal adenoma

High aldosterone levels independent of RAAS activation - H20 and sodium retention and potassium excretion

103
Q

CONNS SYNDROME
What are the clinical features of Conn’s syndrome?

A

SYMPTOMS
- lethargy
- mood disturbance
- paraesthesia + muscle cramps

SIGNS
- refractory hypertension
- metabolic alkalosis

104
Q

CONNS SYNDROME
A deficiency in which electrolyte causes the symptoms of Conn’s syndrome?

A

HYPOKALAEMIA

causes:
1. Muscle weakness
2. Tiredness
3. Polyuria

105
Q

CONNS SYNDROME
What hormone is raised in Conn’s syndrome and what hormone is reduced? Where are these hormones synthesised?

A
  1. Aldosterone is raised - synthesised in the zone glomerulosa
  2. Renin is reduced - synthesised in the juxta-glomerular cells
106
Q

CONNS SYNDROME
What investigations might you do in someone to confirm a diagnosis of Conn’s syndrome?

A

1st line = aldosterone renin ratio (high aldosterone + low renin)

serum U&Es = hypokalaemia + hypernatraemia

high resolution CT abdomen

adrenal venous sampling

107
Q

CONNS SYNDROME
Give 4 ECG changes you might see in someone with Conn’s syndrome

A

HYPOKALAEMIC ECG
1. Increased amplitude and width of P waves
2. Flat T waves
3. ST depression
4. Prolonged QT interval
5. U waves

108
Q

CONNS SYNDROME
What is the treatment for Conn’s syndrome?

A

1st line
- laparoscopic adrenalectomy for unilateral
- spironolactone for bilateral

2nd line
- spironolactone if surgery is inappropriate in unilateral disease

109
Q

HYPERKALAEMIA
what are the clinical features of hyperkalaemia?

A

SYMPTOMS
Fatigue
Palpitations
Muscle weakness
Muscle cramps
Paresthesia

SIGNS
Arrhythmias
Reduced power
Reduced reflexes
Signs of underlying cause

110
Q

HYPERKALAEMIA
what are the causes of hyperkalaemia

A

IMPAIRED EXCRETION
- AKI and CKD
- drugs (spironolactone, ACEi, heparin)
- renal tubular acidosis (T4)
- Addisons disease

INCREASED INTAKE
- IV therapy
- increased dietary intake
- massive blood transfusion

SHIFT TO EXTRACELLULAR
- metabolic acidosis
- rhabdomyolysis
- DKA
- iatrogenic (digoxin, beta-antagonists)

111
Q

HYPERKALAEMIA
What ECG changes might you see in someone with hyperkalaemia?

A

GO - absent/flat P waves
GO LONG - prolonged PR
GO TALL - Tall T waves
GO WIDE - Wide QRS

112
Q

HYPERKALAEMIA
What is the treatment for hyperkalaemia?

A

CARDIAC MEMBRANE PROTECTION
- 10ml 10% IV calcium gluconate or calcium chloride given immediately

POTASSIUM REDUCTION
- insulin/dextrose infusion
- nebulised salbutamol
- potassium binders (sodium zirconium cyclosilicate or calcium resonium)
- sodium bicarbonate
- haemodialysis

113
Q

HYPOKALAEMIA
what are the clinical features of hypokalaemia?

A

SYMPTOMS:
- fatigue
- muscle weakness
- palpitations
- constipation (from diminished peristalsis)

SIGNS:
- hypotonia
- diminished deep tendon reflexes

114
Q

HYPOKALAEMIA
Give 3 causes of hypokalaemia

A
  • poor intake
  • excessive loss (vomiting, diarrhoea, high-stoma output, dialysis)
  • diuretic use (loop + thiazide)
  • insulin or salbutamol use
  • metabolic alkalosis
115
Q

HYPOKALAEMIA
What ECG changes might you see in someone with hypokalaemia?

A
  1. Increased amplitude and width of P waves
  2. ST depression
  3. Flat T waves
  4. U waves
  5. QT prolongation
116
Q

HYPOKALAEMIA
What is the treatment for hypokalaemia?

A

POTASSIUM REPLACEMENT
- mild to moderate = oral supplements (Sando-K)
- severe = 20-40mmol IV KCl in 0.9% saline.

  • the fastest rate of correction is 10mmol/hr so 1L bag with 40mmol KCl is run over 4hrs or more

TREAT UNDERLYING CAUSE

117
Q

THYROID CANCER
Name 5 types of thyroid cancer

A
  1. Papillary - thyroid epithelium
  2. Follicular - thyroid epithelium
  3. Anaplastic - thyroid epithelium
  4. Lymphoma
  5. Medullary - calcitonin C cells
118
Q

THYROID CANCER
What types of thyroid cancers are usually asymptomatic thyroid nodule (usually hard and fixed)?

A

Papillary
Follicular
Anaplastic

119
Q

THYROID CANCER
What is the most common form of thyroid cancer?

A

Papillary - 70%, young people, 3x more common in women

Follicular - 20%

120
Q

DE QUERVAINS THYROIDITIS
what is the clinical presentation of de quervain’s thyroiditis?

A

Usually accompanied by fever, malaise and pain in the neck

121
Q

DE QUERVAINS THYROIDITIS
what is the treatment for de quervain’s thyroiditis?

A

Treat with aspirin and only give prednisolone for severely symptomatic
cases

122
Q

DIABETES PHARMACOLOGY
what are the side effects of metformin?

A

GI upset
AKI
N+V
lactic acidosis

123
Q

DIABETES PHARMACOLOGY
what is the mechanism of action for SGLT-2 inhibitors?

A

inhibits resorption of glucose in the kidney causing urinary glucose excretion

124
Q

DIABETES PHARMACOLOGY
what are the side effects of SGLT-2 inhibitors?

125
Q

DIABETES PHARMACOLOGY
what is the mechanism of action for pioglitazone?

A

PPAR gamma agoinsts reduce peripheral resistance

126
Q

DIABETES PHARMACOLOGY
what are the side effects of pioglitazones?

A

Weight gain
Fluid retention
Hepatotoxicity
Bladder cancer

127
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE
what are the risk factors for hyperosmolar hyperglycaemic state?

A
  • infection
  • consumption of glucose rich fluids
  • concurrent medication (thiazides or steroids)
  • MI
  • poor medication compliance
128
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE
what is the pathophysiology of hyperosmolar hyperglycaemic state?

A

hyperglycaemia drives osmotic diuresis, resulting in fluid + electrolyte loss (hyperosmolality + hypovolaemia)

due to presence of small amounts of circulating insulin, lipolysis does not occur so ketoacidosis is not seen

129
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE
what is the clinical presentation of hyperosmolar hyperglycaemic state?

A

SYMPTOMS
- generalised weakness + leg cramps
- confusion, lethargy, hallucinations + headache
- visual disturbance
- polyuria
- polydipsia
- N+V
- abdominal pain

SIGNS
- reduced GCS
- dehydration (tachycardia, hypotension, dry mucous membranes, reduced skin turgor)
- seizures

130
Q

HYPEROSMOLAR HYPERGLYCAEMIC STATE
what is the treatment for hyperosmolar hyperglycaemic state?

A

FLUID REPLACEMENT
- IV 0.9% NaCl
- aim to replace 50% fluid loss in first 12 hrs

FIXED RATE INSULIN INFUSION
- do not use insulin initially due to risks of rapid correction
- IV insulin only used if there is ketonaemia or if blood glucose is not longer falling with IV fluids alone, otherwise do NOT start insulin

POTASSIUM REPLACEMENT
- if >5.5 in first 24hrs = no replacement required
- if 3.5-5.5 in first 24hrs = 20-40mmol/L KCl
- if <3.5 in first 24hrs = require senior review

ANTICOAGULATION
- LMWH unless contraindicated
-

131
Q

HYPERTHYROIDISM
what is the mechanism of action for carbimazole?

A

prevents thyroid peroxidase from producing T3 and T4

132
Q

ACROMEGALY
what are the side effects of GH receptor antagonists e.g. pegvisomant?

A
  • reactions at injection site
  • GI disturbance
  • hypoglycaemia
  • chest pain
  • hepatitis
133
Q

PHARMACOLOGY
what is the mechanism of action for vasopressin antagonists e.g. tolvaptan?

A
  • inhibits vasopressin-2 receptor -> increases fluid excretion
  • causes aquaresis (excretion of H2O with no electrolyte loss) -> increased Na+
134
Q

PHARMACOLOGY
what are the side effect of vasopressin antagonists e.g. tolvaptan?

A
  • GI disturbance
  • headache
  • increased thirst
  • insomnia
135
Q

PHARMACOLOGY
what is the mechanism of action for vasopressin analogues e.g. desmopressin?

A

binds to V2 receptors -> aquaporin 2 inserted in collecting duct which increases water reabsorption

136
Q

PHARMACOLOGY
what are the side effects of vasopressin analogies e.g. desmopressin?

A
  • headache
  • facial flushing
  • nausea
  • seizures
137
Q

PHARMACOLOGY
what is the mechanism of action for metyrapone?

A
  • blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide enzyme
138
Q

PHARMACOLOGY
what are the side effects of metyrapone?

A
  • GI disturbance
  • headache
  • dizziness
  • drowsiness
  • hirsutism
139
Q

ADRENAL INSUFFICIENCY
how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?

A

short ACTH = no change

long ACTH = increase

140
Q

CARCINOID TUMOURS
where is the most common site for carcinoid tumours?

A

appendix and small intestine

patients with GI carcinoid tumours will only experience symptoms if they have liver mets

141
Q

CUSHINGS
what investigation can be used to differentiate between cushing’s syndrome and cushing’s disease?

A

dexamethasone suppression test
- overnight = cushing’s syndrome (including disease) is confirmed when there is no suppression

  • 48 hours = cushing’s syndrome (not disease) = no suppression
142
Q

HYPERNATRAEMIA
what are the causes?

A

six Ds
- diarrhoea
- dehydration
- diuresis (secondary to diuretic use)
- diabetes insipidus
- doctors (iatrogenic - over administration of IV hypertonic NaCl or steroid use)
- disease (renal)

143
Q

HYPERNATRAEMIA
what are the risk factors?

A
  • increasing age
  • diabetes insipidus
  • severe burns or trauma
144
Q

HYPERNATRAEMIA
what are the clinical features?

A
  • thirst
  • confusion
  • irritability
  • weakness
  • oliguria
  • dry mucous membranes
  • tachycardia
  • reduced skin turgor
  • weight loss
145
Q

HYPERNATRAEMIA
what is the management?

A
  • fluid replacement = IV 5% dextrose
  • treat causes
  • suspend medications
146
Q

HYPONATRAEMIA
what are the causes?

A

HYPOVOLAEMIC
- D+V
- sweat
- burns
- diuretics
- 3rd space
- addisons

EUVOLAEMIC
- SIADH
- hypothyroidism

HYPERVOLAEMIC
- HF
- renal failure
- liver failure

147
Q

HYPONATRAEMIA
what are the clinical features

A

MILD
- N+V
- headache
- lethargy

MODERATE
- weakness
- muscle aches
- confusion
- ataxia

SEVERE
- reduced consciousness
- seizures
- respiratory arrest

148
Q

HYPONATRAEMIA
what is the management?

A

ACUTE (<48hrs)
- mild/no symptoms = stop non-essential fluids + meds that can provoke hyponatraemia + treat cause
- moderate/severe symptoms = hypertonic 3% NaCl

CHRONIC (>48hrs)
- maximum increase 10mmol/L per day
- if hypovolaemic = 0.9% NaCl
- if hypervolaemic = fluid restriction

149
Q

HYPONATRAEMIA
what are the complications?

A
  • cerebral oedema
  • central pontine myelinolysis
150
Q

ADDISONIAN CRISIS
what are the investigations?

A

12 lead ECG = hyperkalaemic changes (flat P waves, short QT, broad QRS, ST depression + tented T waves)

VBG = metabolic acidosis, hyponatraemia, hyperkalaemia

FBC + CRP
TFTs

once crisis is under control, if patient has not already been investigated for Addisons they should now undergo these tests.

151
Q

DIABETES INSIPIDUS
What are the test results for serum osmolality, urine osmolality + post desmopressin urine osmolality in cranial + nephrogenic DI?

A

CRANIAL
- high serum osmolality
- low urine osmolality
- high urine osmolality post desmopressin suppression

NEPHROGENIC
- high serum osmolality
- low urine osmolality
- no response post desmopressin suppression

152
Q

DIABETES PHARMACOLOGY
what are the side effects of sulfonylureas?

A
  • weight gain
  • hypoglycaemia
153
Q

DIABETES PHARMACOLOGY
Give an example of DPP-4 inhibitors

A

linagliptin
sitagliptin

154
Q

DIABETES PHARMACOLOGY
what is the mechanism of action for DPP-4 inhibitors?

A

prevent degradation of incretins _ promote insulin secretion

155
Q

DIABETES PHARMACOLOGY
what are the side effects of DPP-4 inhibitors e.g. linagliptin?

A

pancreatitis

156
Q

DIABETIC KETOACIDOSIS
what are the causes?

A
  • infection
  • inadequate insulin or non-adhederence to insulin therapy
  • MI
  • physiological stress (trauma or surgery)
  • co-morbidities (hypothyroidism, pancreatitis)
  • drugs (corticosteroids, diuretics, salbutamol)
157
Q

DIABETIC KETOACIDOSIS
what is the management?

A

IV FLUIDS
- if SBP<90 500ml bolus of 0.9% NaCl over 15 mins + call for senior help
- if SBP>90 1L 0.9% NaCl over 1 hour, 1 litre 0.9% NaCl with kCl over 2hrs, 2hrs, 4hrs, 4hrs and then 6hrs

INSULIN
- fixed rate insulin infusion
- 0.1U/kg/hr
- once glucose <14mmol/L add 10% glucose + consider reducing insulin
- do not stop long acting insulin

POTASSIUM REPLACEMENT
- >5.5 in first 24hrs = no replacement required
- 3.5-5.5 in first 24hrs = 40mmol/L KCl
- <3.5 in first 24hrs = consider HDU/ITU

158
Q

DIABETIC KETOACIDOSIS
what are the complications?

A
  • venous thrromboembolism
  • arrhythmias
  • ARDS
  • AKI
  • cerebral oedema
  • hypokalaemia
  • gastric stasis
159
Q

HYPOPARATHYROIDISM
what are the complications?

A
  • calcifications
  • renal stones
  • renal failure
  • cataracts
  • life-threatening hypocalcaemia
160
Q

HYPERNATRAEMIA
what are the complications?

A
  • cerebral oedema
  • coma
  • death
161
Q

HYPOTHYROIDISM
what are the side effects of levothyroxine?

A
  • hyperthyroidism
  • AF
  • osteoporosis
  • angina
162
Q

HYPOTHYROIDISM
what is the management for mxyoedema coma?

A
  • ITU/HDU admission
  • IV thyroid replacement (levothyroxine)
  • antibiotics
  • IV hydrocortisone (100mg)
163
Q

SIADH
what are the diagnostic criteria?

A
  • Low plasma osmolality <275mOsm/kg
  • High urine osmolality >100mOsm/kg
  • High urine sodium >30mmol/L
  • Clinical euvolaemia
  • Exclusion of glucocorticoid deficiency or hypothyroidism
164
Q

HYPERLIPIDAEMIA
what is the management?

A

1st line
- lifestyle modifications (dietary changes, increased physical activity, weight loss + smoking cessation)
- statins (atorvastatin or simvastatin)
- fibrates

2nd line
- ezetimibe
- PCSK9 inhibitors (evolocumab)

165
Q

DIABETES INSIPIDUS
how do you differentiate between cranial and nephrogenic DI?

A

DESMOPRESSIN SUPPRESSION TEST
- cranial DI = decreased urine volume + increased urine osmolality
- nephrogenic DI = no response

166
Q

DIABETES INSIPIDUS
when is the desmopressin suppression test contraindicated?

A
  • hypernatremia
  • uncontrolled diabetes mellitus
  • kidney insufficiency
  • pregnancy
167
Q

CUSHINGS
what are the results for high dose dexamethasone suppression test for cushings syndrome, disease and ectopic ACTH syndrome?

A

CUSHINGS SYNDROME
- cortisol = not suppressed
- ACTH = suppressed

CUSHINGS DISEASE
- cortisol = supressed
- ACTH = suppressed

ECTOPIC ACTH SYNDROME
- cortisol = not suppressed
- ACTH = not suppressed

168
Q

PRIMARY HYPERALDOSTERONISM
what are the causes?

A
  • bilateral idiopathic adrenal hyperplasia (most common)
  • adrenal adenoma = Conn’s syndrome
  • unilateral hyperplasia
  • familial hyperaldosteronism
  • adrenal carcinoma
169
Q

HYPERCALCAEMIA OF MALIGNANCY
what is the pathophysiology?

A

three main mechanisms:
- secretion of PTH-related protein (PTHrP) = most common
- osteolytic metastases
- secretion of 1,25-dihydroxyvitamin D (calcitriol)

170
Q

HYPERCALCAEMIA OF MALIGNANCY
what types of cancer is PTHrP secretion associated with?

A
  • renal cancer
  • ovarian cancer
  • endometrial cancer
  • squamous cell carcinoma
171
Q

HYPERCALCAEMIA OF MALIGNANCY
what is the mechanism of action of PTHrP?

A

stimulates osteoclastic resorption and inhibits osteoblast formation of the bone
this results in excessive calcium release from the skeleton

also acts on the kidneys to reduce calcium clearance, further increasing calcium levels in blood

172
Q

HYPERCALCAEMIA OF MALIGNANCY
what types of cancer are associated with calcitriol secretion?

173
Q

HYPERCALCAEMIA OF MALIGNANCY
what are the risk factors?

A

the type of cancer
- multiple myeloma
- breast cancer
- lung cancer (squamous)
- renal cancer
- thyroid cancer (squamous)
- lymphoma (all types)

medications
- thiazide diuretics
- lithium
- OTC supplements containing calcium or vitamin D

174
Q

HYPERCALCAEMIA OF MALIGNANCY
what is the management?

A

SUPPORTIVE
- stop medications that contribute to hypercalcaemia (thiazides, calcium supplements, vitamin D supplements, lithium)
- stop medications that can worsen renal function (NSAIDs, ACEis)
- medications for associated symptoms
= laxatives for constipation
= anti-emetics for nausea
= analgesia for bone pain

REHYDRATION
- IV fluids (3 litres in first 24hrs)

BISPHOSPHONATES
- 1st line = IV zoledronic acid 4mg
- 2nd line = disodium pamidronate 30-90mg

  • if hypercalcaemia lasts >7 days then further bisphosphonates may be considered or denosumab
175
Q

CARCINOID TUMOURS
what are they?

A

a type of neuroendocrine tumour
are typically slow growing and can potentially become malignant
can secrete serotonin

176
Q

CARCINOID TUMOURS
what is the difference between carcinoid tumours and carcinoid syndrome?

A

carcinoid tumours = type of neuroendocrine tumour which can secrete serotonin

carcinoid syndrome = liver mets impair hepatic excretion of serotonin during 1st pass metabolism, resulting in increased serotoninergic symptons

177
Q

CARCINOID TUMOURS
what are the clinical features?

A

SYMPTOMS
- abdominal pain
- diarrhoea
- flushing
- wheezing
- pulmonary stenosis

patients with GI carcinoid tumours will only experience symptoms if they have liver mets

178
Q

CARCINOID TUMOURS
what are the investigations?

A
  • urinary hormone levels = 5-HIAA
  • plasma chromogranin A y
  • CT or MRI
  • tissue biopsy
179
Q

CARCINOID TUMOURS
what is the management?

A
  • somatostatin analogues = octreotide
  • surgery
  • cyproheptadine can help with diarrhoea

MY REVISION - ALL TO DO (21 decks)

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