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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
ACROMEGALY What is the gold standard diagnostic test for acromegaly?
Oral glucose tolerance test - failure of glucose to suppress serum GH
26
ACROMEGALY what is the management for acromegaly?
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
27
ACROMEGALY What types of medical therapy can be used to treat acromegaly?
somatostatin analogue = octreotide dopamine agonist = cabergoline GH receptor antagonist = pegvisomant
28
ACROMEGALY Give 3 advantages of using dopamine agonists in the treatment of acromegaly
1. No hypopituitarism 2. Oral administration 3. Rapid onset
29
ACROMEGALY Name a dopamine agonist that can be used as a treatment for acromegaly
Cabergoline
30
ACROMEGALY Why can somatostatin analogues be used in the treatment of acromegaly?
They inhibit GH release
31
PROLACTINOMA what are the causes of prolactinoma?
1. Pituitary adenoma 2. Anti-dopaminergic drugs 3. Head injury - compression of the pituitary stalk
32
PROLACTINOMA what are the clinical features of prolactinoma
SYMPTOMS: amenorrhea, galactorrhoea, gynaecomastia, low libido, erectile dysfunction SIGNS: low testosterone, infertility visual field defects headache
33
PROLACTINOMA What is the treatment for prolactinoma?
Dopamine agonists - cabergoline - inhibits prolactin release | Occasionally transsphenoidal pituitary resection
34
CUSHINGS what are the causes of excess cortisol? And are they ACTH dependent or independent?
ACTH dependent (ACTH raised): - Cushing’s disease - Ectopic ACTH production - ACTH treatment ACTH independent (ACTH not raised) - adrenal adenoma - iatrogenic
35
CUSHINGS what are the investigations for Cushing's syndrome?
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
36
CUSHINGS What is the treatment for Cushing's syndrome?
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
37
ADDISONS DISEASE what are the causes of Addison's disease?
- 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
38
ADDISONS DISEASE what are the clinical features of Addison's disease?
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
39
ADDISONS DISEASE What is the pathophysiology of Addison's disease?
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
40
ADDISONS DISEASE What are the investigations for Addison's disease?
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)
41
ADDISONS DISEASE What investigations would you do to determine whether Adrenal insufficiency is primary or secondary?
Primary = adrenal antibodies, very long chain fatty acids, imaging and genetics Secondary = any steroids?, imaging and genetics
42
ADDISONIAN CRISIS What is the management of adrenal crisis (addisonian crisis)?
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)
43
ADDISONS DISEASE What would sodium and potassium levels be in someone with adrenal insufficiency?
Hyponatraemia = low sodium Hyperkalaemia = high potassium Lack of aldosterone and so less sodium reabsorbed and less potassium excreted
44
GRAVES DISEASE what is the clinical presentation of Grave's opthlmopathy?
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
45
GRAVES DISEASE what is the treatment for Grave's ophthalmology?
Conservative treatment – smoking cessation and sunglasses Anti-thyroid medication e.g. carbimazole IV METHYLPREDNISOLONE a surgical decompression/eyelid surgery
46
GRAVES DISEASE Name 5 risk factors for Graves disease
1. Female 2. Genetic association 3. E.coli 4. Smoking 5. Stress 6. High iodine intake 7. Autoimmune diseases
47
GRAVES DISEASE Name 5 autoimmune diseases associated with thyroid autoimmunity
1. T1DM 2. Addison's disease 3. Pernicious anaemia 4. Vitiligo 5. Alopecia areata 6. Rheumatoid arthritis
48
THYROID GOITRE Name 4 types of sporadic non toxic goitre
1. Diffuse --> physiological --> Graves 2. Multi nodular 3. Solitary nodule 4. Dominant nodule
49
HYPERTHYROIDISM what are the causes of hyperthyroidism?
PRIMARY - graves disease - toxic multinodular goitre (iodine deficiency) - toxic adenoma - subclinical hyperthyroidism - drugs (amiodarone) SECONDARY - pituitary adenoma - ectopic tumour - hypothalamic tumour
50
HYPERTHYROIDISM Name 4 drugs which can induce hyperthyroidism
1. Iodine 2. Amiodarone 3. Lithium 4. Radioconstrast agents
51
HYPERTHYROIDISM What are the thyroid function test results in primary hyperthyroidism?
high T4 high T3 low TSH
52
HYPERTHYROIDISM What are the thyroid function rests in secondary hyperthyroidism?
high T4 high T3 high TSH
53
HYPERTHYROIDISM Give 5 side effects of anti-thyroid drugs
1. Rash 2. Arthralgia 3. Hepatitis 4. Neuritis 5. Vasculitis 6. Agranulocytosis - very serious
54
HYPERTHYROIDISM What is a complication of hyperthyroidism?
- Thyroid crisis/storm - osteoporosis - proximal myopathy - thyrotoxic crisis - iatrogenic (agranulocytosis from carbimazole, congenital malformations, foetal goitre)
55
HYPERTHYROIDISM What is the treatment for a thyroid crisis?
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
56
HYPOTHYROIDISM Briefly describe the pathophysiology of secondary hypothyroidism
Reduced release or production of TSH so reduced thyroid hormone release
57
HYPOTHYROIDISM Briefly describe the pathophysiology of tertiary hypothyroidism
Thyroid gland overcompensates until it can reestablish correct concentration fo thyroid hormone
58
HYPOTHYROIDISM what are the causes of primary hypothyroidism
- 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)
59
HYPOTHYROIDISM Name 4 drugs that can cause hypothyroidism
1. Carbimazole (used to treat hyperthyroidism) 2. Amiodarone 3. Lithium 4. Iodine
60
HYPOTHYROIDISM Name 3 causes of secondary hypothyroidism
- compression from a pituitary tumour - hypothalamic tumours - drugs (cocaine, steroids + dopamine)
61
HYPOTHYROIDISM What are the TFT results for primary hypothyroidism?
- High TSH - low T4
62
HYPOTHYROIDISM What are the TFT results for secondary hypothyroidism?
- normal/low TSH - low T4
63
HYPOTHYROIDISM Name 3 antibodies that may be present in the serum in someone with autoimmune thyroiditis
1. TPO (thyroid peroxidase) 2. Thyroglobulin 3. TSH receptor
64
HYPOTHYROIDISM what are the complications of hypothyroidism?
- hypercholesterolaemia - carpal tunnel - peripheral neuropathy - myoxedema coma - thyroid lymphoma
65
HASHIMOTOS THYROIDITIS Give 3 symptoms of Hashimoto's thyroiditis
1. Rapid formation of Goitre 2. Dyspnoea or dysphagia 3. General hypothyroidism symptoms
66
HASHIMOTOS THYROIDITIS Name 3 triggers of Hashimoto's thyroiditis
1. Iodine 2. Infections 3. Smoking 4. Stress
67
HASHIMOTOS THYROIDITIS what are the complications of Hashimoto's thyroiditis?
Hashimoto's encephalopathy
68
DIABETES INSIPIDUS Define diabetes insipidus
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
69
DIABETES INSIPIDUS Name the 2 types of DI
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)
70
DIABETES INSIPIDUS what are the clinical features of DI?
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)
71
DIABETES INSIPIDUS what are the causes of cranial(central) DI?
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)
72
DIABETES INSIPIDUS what are the causes of nephrogenic DI?
CONGENITAL - mutations in vasopressin or aquaporin receptors ACQUIRED - drugs (lithium, gentamicin, cisplatin) - renal disease (renal amyloid, obstructive uropathy) - electrolyte disturbance (hypokalaemia, hypercalcaemia)
73
DIABETES INSIPIDUS Give 3 possible differential diagnosis's of DI
1. DM 2. Hypokalaemia 3. Hypercalcaemia
74
DIABETES INSIPIDUS what are the investigations for diabetes insipidus?
- 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
DIABETES INSIPIDUS What is the treatment for cranial DI?
- 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
DIABETES INSIPIDUS What is the treatment for nephrogenic DI?
- manage fluid balance - treat underlying cause - sodium restriction - thiazide diuretics (BENDROFLUMETHIAZIDE)
77
DIABETES INSIPIDUS Do you have hyponatraemia or hypernatraemia in diabetes insipidus?
Hypernatraemia
78
SIADH what are the clinical features of SIADH?
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
SIADH what are the causes of SIADH?
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
SIADH what are the investigations for SIADH?
- 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
SIADH Describe the treatment for SIADH
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
SIADH How do you treat asymptomatic SIADH?
Fluid restriction
83
SIADH How do you treat very symptomatic SIADH?
Give 3% saline (hypertonic) demeclocycline or tolvaptan
84
SIADH Would you expect a patient with SIADH to be hypovolaemic, euvolaemic or hypervolaemic?
Euvolaemic
85
SIADH Would you associate SIADH with hyponatraemia or hypernatraemia?
Hyponatraemia - <135 mmol/L
86
SIADH Would you associate SIADH with plasma hypo-osmolality or hyper-osmolality?
Plasma hypo-osmolality - <275 mOsmol/Kg
87
SIADH Would you associate SIADH with a high to low urine osmolality?
High urine osmolality
88
PITUITARY ADENOMA Give 4 local effects a pituitary adenoma
1. Headaches 2. Visual field defects - bitemporal hemianopia 3. Cranial nerve palsy and temporal lobe epilepsy 4. CSF rhinorrhoea
89
PROLACTINOMA What can lead to elevated levels of prolactin?
1. Stress 2. Drugs 3. Pressure on pituitary stalk 4. Prolactinoma
90
DIABETES PHARMACOLOGY Give an example of a sulfonylurea
gliclazide
91
DIABETES MELLITUS Name 3 exocrine causes of Diabetes
1. Inflammatory - actue/chronic pancreatitis 2. Hereditary haemochromatosis 3. Pancreatic neoplasia 4. Cystic fibrosis
92
PHEOCHROMOCYTOMA What is Pheochromocytoma?
A rare catecholamine secreting tumour in the adrenal medulla (chromatin cells)
93
PHEOCHROMOCYTOMA what are the different types of pheochromocytoma?
1. Familial type - more NAd | 2. Sporadic - more Ad
94
PHEOCHROMOCYTOMA what are the clinical features of pheochromocytoma?
SYMPTOMS Headache Profuse Sweating Palpitations Tremor SIGNS Hypertension Postural hypotension Tremor hypertensive retinopathy Pallor
95
PHEOCHROMOCYTOMA What are the investigations for pheochromocytoma?
- Plasma metanephrines and normetanephrines - 24 hour urinary total catecholamines - CT – look for tumour
96
PHEOCHROMOCYTOMA What is the treatment for pheochromocytoma?
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
PHEOCHROMOCYTOMA What is the management of a phaeochromocytoma crisis?
Non-competitive alpha-blocker e.g. phenoxybenzamine Excision of paraganglioma Biochemistry: measure plasma and serum metanephrines
98
DIABETIC NEPHROPATHY Describe the treatment for diabetic nephropathy
1. Glycaemic and BP control 2. Angiotensin receptor blockers/ACE inhibitors - RAMIPRIL or CANDESARTAN 3. Proteinuria and cholesterol control
99
DIABETIC NEUROPATHY Give 5 signs of autonomic neuropathy in diabetic neuropathy
1. Hypotension 2. HR affected 3. Diarrhoea/constipation 4. Incontinence 5. Erectile dysfunction 6. Dry skin
100
DIABETIC NEUROPATHY What are the 4 main threats to skin and subcutaneous tissues in someone with diabetic neuropathy
1. Infections 2. Ischaemia 3. Abnormal pressure 4. Wound environments
101
DIABETES MELLITUS what infections can poorly controlled diabetes lead to?
1. UTIs 2. Staphylococcal infection of skin 3. Mucocutaneous candidiasis 4. Pyelonephritis 5. TB 6. Pneumonia 7. rectal abscess
102
CONNS SYNDROME What is Conn's syndrome?
Primary hyperaldosteronism caused by an adrenal adenoma High aldosterone levels independent of RAAS activation - H20 and sodium retention and potassium excretion
103
CONNS SYNDROME What are the clinical features of Conn's syndrome?
SYMPTOMS - lethargy - mood disturbance - paraesthesia + muscle cramps SIGNS - refractory hypertension - metabolic alkalosis
104
CONNS SYNDROME A deficiency in which electrolyte causes the symptoms of Conn's syndrome?
HYPOKALAEMIA causes: 1. Muscle weakness 2. Tiredness 3. Polyuria
105
CONNS SYNDROME What hormone is raised in Conn's syndrome and what hormone is reduced? Where are these hormones synthesised?
1. Aldosterone is raised - synthesised in the zone glomerulosa 2. Renin is reduced - synthesised in the juxta-glomerular cells
106
CONNS SYNDROME What investigations might you do in someone to confirm a diagnosis of Conn's syndrome?
1st line = aldosterone renin ratio (high aldosterone + low renin) serum U&Es = hypokalaemia + hypernatraemia high resolution CT abdomen adrenal venous sampling
107
CONNS SYNDROME Give 4 ECG changes you might see in someone with Conn's syndrome
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
CONNS SYNDROME What is the treatment for Conn's syndrome?
1st line - laparoscopic adrenalectomy for unilateral - spironolactone for bilateral 2nd line - spironolactone if surgery is inappropriate in unilateral disease
109
HYPERKALAEMIA what are the clinical features of hyperkalaemia?
SYMPTOMS Fatigue Palpitations Muscle weakness Muscle cramps Paresthesia SIGNS Arrhythmias Reduced power Reduced reflexes Signs of underlying cause
110
HYPERKALAEMIA what are the causes of hyperkalaemia
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
HYPERKALAEMIA What ECG changes might you see in someone with hyperkalaemia?
GO - absent/flat P waves GO LONG - prolonged PR GO TALL - Tall T waves GO WIDE - Wide QRS
112
HYPERKALAEMIA What is the treatment for hyperkalaemia?
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
HYPOKALAEMIA what are the clinical features of hypokalaemia?
SYMPTOMS: - fatigue - muscle weakness - palpitations - constipation (from diminished peristalsis) SIGNS: - hypotonia - diminished deep tendon reflexes
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HYPOKALAEMIA Give 3 causes of hypokalaemia
- poor intake - excessive loss (vomiting, diarrhoea, high-stoma output, dialysis) - diuretic use (loop + thiazide) - insulin or salbutamol use - metabolic alkalosis
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HYPOKALAEMIA What ECG changes might you see in someone with hypokalaemia?
1. Increased amplitude and width of P waves 2. ST depression 3. Flat T waves 4. U waves 5. QT prolongation
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HYPOKALAEMIA What is the treatment for hypokalaemia?
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
THYROID CANCER Name 5 types of thyroid cancer
1. Papillary - thyroid epithelium 2. Follicular - thyroid epithelium 3. Anaplastic - thyroid epithelium 4. Lymphoma 5. Medullary - calcitonin C cells
118
THYROID CANCER What types of thyroid cancers are usually asymptomatic thyroid nodule (usually hard and fixed)?
Papillary Follicular Anaplastic
119
THYROID CANCER What is the most common form of thyroid cancer?
Papillary - 70%, young people, 3x more common in women | Follicular - 20%
120
DE QUERVAINS THYROIDITIS what is the clinical presentation of de quervain's thyroiditis?
Usually accompanied by fever, malaise and pain in the neck
121
DE QUERVAINS THYROIDITIS what is the treatment for de quervain's thyroiditis?
Treat with aspirin and only give prednisolone for severely symptomatic cases
122
DIABETES PHARMACOLOGY what are the side effects of metformin?
GI upset AKI N+V lactic acidosis
123
DIABETES PHARMACOLOGY what is the mechanism of action for SGLT-2 inhibitors?
inhibits resorption of glucose in the kidney causing urinary glucose excretion
124
DIABETES PHARMACOLOGY what are the side effects of SGLT-2 inhibitors?
UTI
125
DIABETES PHARMACOLOGY what is the mechanism of action for pioglitazone?
PPAR gamma agoinsts reduce peripheral resistance
126
DIABETES PHARMACOLOGY what are the side effects of pioglitazones?
Weight gain Fluid retention Hepatotoxicity Bladder cancer
127
HYPEROSMOLAR HYPERGLYCAEMIC STATE what are the risk factors for hyperosmolar hyperglycaemic state?
- infection - consumption of glucose rich fluids - concurrent medication (thiazides or steroids) - MI - poor medication compliance
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HYPEROSMOLAR HYPERGLYCAEMIC STATE what is the pathophysiology of hyperosmolar hyperglycaemic state?
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
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HYPEROSMOLAR HYPERGLYCAEMIC STATE what is the clinical presentation of hyperosmolar hyperglycaemic state?
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
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HYPEROSMOLAR HYPERGLYCAEMIC STATE what is the treatment for hyperosmolar hyperglycaemic state?
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
HYPERTHYROIDISM what is the mechanism of action for carbimazole?
prevents thyroid peroxidase from producing T3 and T4
132
ACROMEGALY what are the side effects of GH receptor antagonists e.g. pegvisomant?
- reactions at injection site - GI disturbance - hypoglycaemia - chest pain - hepatitis
133
PHARMACOLOGY what is the mechanism of action for vasopressin antagonists e.g. tolvaptan?
- inhibits vasopressin-2 receptor -> increases fluid excretion - causes aquaresis (excretion of H2O with no electrolyte loss) -> increased Na+
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PHARMACOLOGY what are the side effect of vasopressin antagonists e.g. tolvaptan?
- GI disturbance - headache - increased thirst - insomnia
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PHARMACOLOGY what is the mechanism of action for vasopressin analogues e.g. desmopressin?
binds to V2 receptors -> aquaporin 2 inserted in collecting duct which increases water reabsorption
136
PHARMACOLOGY what are the side effects of vasopressin analogies e.g. desmopressin?
- headache - facial flushing - nausea - seizures
137
PHARMACOLOGY what is the mechanism of action for metyrapone?
- blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide enzyme
138
PHARMACOLOGY what are the side effects of metyrapone?
- GI disturbance - headache - dizziness - drowsiness - hirsutism
139
ADRENAL INSUFFICIENCY how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?
short ACTH = no change | long ACTH = increase
140
CARCINOID TUMOURS where is the most common site for carcinoid tumours?
appendix and small intestine patients with GI carcinoid tumours will only experience symptoms if they have liver mets
141
CUSHINGS what investigation can be used to differentiate between cushing's syndrome and cushing's disease?
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
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HYPERNATRAEMIA what are the causes?
six Ds - diarrhoea - dehydration - diuresis (secondary to diuretic use) - diabetes insipidus - doctors (iatrogenic - over administration of IV hypertonic NaCl or steroid use) - disease (renal)
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HYPERNATRAEMIA what are the risk factors?
- increasing age - diabetes insipidus - severe burns or trauma
144
HYPERNATRAEMIA what are the clinical features?
- thirst - confusion - irritability - weakness - oliguria - dry mucous membranes - tachycardia - reduced skin turgor - weight loss
145
HYPERNATRAEMIA what is the management?
- fluid replacement = IV 5% dextrose - treat causes - suspend medications
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HYPONATRAEMIA what are the causes?
HYPOVOLAEMIC - D+V - sweat - burns - diuretics - 3rd space - addisons EUVOLAEMIC - SIADH - hypothyroidism HYPERVOLAEMIC - HF - renal failure - liver failure
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HYPONATRAEMIA what are the clinical features
MILD - N+V - headache - lethargy MODERATE - weakness - muscle aches - confusion - ataxia SEVERE - reduced consciousness - seizures - respiratory arrest
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HYPONATRAEMIA what is the management?
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
HYPONATRAEMIA what are the complications?
- cerebral oedema - central pontine myelinolysis
150
ADDISONIAN CRISIS what are the investigations?
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
DIABETES INSIPIDUS What are the test results for serum osmolality, urine osmolality + post desmopressin urine osmolality in cranial + nephrogenic DI?
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
DIABETES PHARMACOLOGY what are the side effects of sulfonylureas?
- weight gain - hypoglycaemia
153
DIABETES PHARMACOLOGY Give an example of DPP-4 inhibitors
linagliptin sitagliptin
154
DIABETES PHARMACOLOGY what is the mechanism of action for DPP-4 inhibitors?
prevent degradation of incretins _ promote insulin secretion
155
DIABETES PHARMACOLOGY what are the side effects of DPP-4 inhibitors e.g. linagliptin?
pancreatitis
156
DIABETIC KETOACIDOSIS what are the causes?
- infection - inadequate insulin or non-adhederence to insulin therapy - MI - physiological stress (trauma or surgery) - co-morbidities (hypothyroidism, pancreatitis) - drugs (corticosteroids, diuretics, salbutamol)
157
DIABETIC KETOACIDOSIS what is the management?
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
DIABETIC KETOACIDOSIS what are the complications?
- venous thrromboembolism - arrhythmias - ARDS - AKI - cerebral oedema - hypokalaemia - gastric stasis
159
HYPOPARATHYROIDISM what are the complications?
- calcifications - renal stones - renal failure - cataracts - life-threatening hypocalcaemia
160
HYPERNATRAEMIA what are the complications?
- cerebral oedema - coma - death
161
HYPOTHYROIDISM what are the side effects of levothyroxine?
- hyperthyroidism - AF - osteoporosis - angina
162
HYPOTHYROIDISM what is the management for mxyoedema coma?
- ITU/HDU admission - IV thyroid replacement (levothyroxine) - antibiotics - IV hydrocortisone (100mg)
163
SIADH what are the diagnostic criteria?
- Low plasma osmolality <275mOsm/kg - High urine osmolality >100mOsm/kg - High urine sodium >30mmol/L - Clinical euvolaemia - Exclusion of glucocorticoid deficiency or hypothyroidism
164
HYPERLIPIDAEMIA what is the management?
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
DIABETES INSIPIDUS how do you differentiate between cranial and nephrogenic DI?
DESMOPRESSIN SUPPRESSION TEST - cranial DI = decreased urine volume + increased urine osmolality - nephrogenic DI = no response
166
DIABETES INSIPIDUS when is the desmopressin suppression test contraindicated?
- hypernatremia - uncontrolled diabetes mellitus - kidney insufficiency - pregnancy
167
CUSHINGS what are the results for high dose dexamethasone suppression test for cushings syndrome, disease and ectopic ACTH syndrome?
CUSHINGS SYNDROME - cortisol = not suppressed - ACTH = suppressed CUSHINGS DISEASE - cortisol = supressed - ACTH = suppressed ECTOPIC ACTH SYNDROME - cortisol = not suppressed - ACTH = not suppressed
168
PRIMARY HYPERALDOSTERONISM what are the causes?
- bilateral idiopathic adrenal hyperplasia (most common) - adrenal adenoma = Conn's syndrome - unilateral hyperplasia - familial hyperaldosteronism - adrenal carcinoma
169
HYPERCALCAEMIA OF MALIGNANCY what is the pathophysiology?
three main mechanisms: - secretion of PTH-related protein (PTHrP) = most common - osteolytic metastases - secretion of 1,25-dihydroxyvitamin D (calcitriol)
170
HYPERCALCAEMIA OF MALIGNANCY what types of cancer is PTHrP secretion associated with?
- renal cancer - ovarian cancer - endometrial cancer - squamous cell carcinoma
171
HYPERCALCAEMIA OF MALIGNANCY what is the mechanism of action of PTHrP?
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
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HYPERCALCAEMIA OF MALIGNANCY what types of cancer are associated with calcitriol secretion?
lymphomas
173
HYPERCALCAEMIA OF MALIGNANCY what are the risk factors?
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
HYPERCALCAEMIA OF MALIGNANCY what is the management?
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
CARCINOID TUMOURS what are they?
a type of neuroendocrine tumour are typically slow growing and can potentially become malignant can secrete serotonin
176
CARCINOID TUMOURS what is the difference between carcinoid tumours and carcinoid syndrome?
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
CARCINOID TUMOURS what are the clinical features?
SYMPTOMS - abdominal pain - diarrhoea - flushing - wheezing - pulmonary stenosis patients with GI carcinoid tumours will only experience symptoms if they have liver mets
178
CARCINOID TUMOURS what are the investigations?
- urinary hormone levels = 5-HIAA - plasma chromogranin A y - CT or MRI - tissue biopsy
179
CARCINOID TUMOURS what is the management?
- somatostatin analogues = octreotide - surgery - cyproheptadine can help with diarrhoea

MY REVISION - ALL TO DO (21 decks)

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