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ENDOCRINE Flashcards

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1
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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2
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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3
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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4
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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5
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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6
Q

HYPOCALCAEMIA
Name 3 causes of hypocalcaemia

A

Hypoparathyroidism
Vitamin D deficiency
Hyperventilation
Drugs
Malignancy
Toxic shock

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7
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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8
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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9
Q

T2DM
What class of drugs can cause diabetes?

A

Steroids
Thiazides
Anti-psychotics

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10
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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11
Q

T2DM
what are the side effects of Sulfonylurea?

A

Hypoglycaemia
weight gain
hyponatraemia

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12
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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13
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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14
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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15
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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16
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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17
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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18
Q

PROLACTINOMA
What is the treatment for prolactinoma?

A

Dopamine agonists - cabergoline - inhibits prolactin release

Occasionally transsphenoidal pituitary resection

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19
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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20
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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21
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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22
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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23
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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24
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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25
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)
26
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)
27
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
28
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
29
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
30
THYROID GOITRE Name 4 types of sporadic non toxic goitre
1. Diffuse --> physiological --> Graves 2. Multi nodular 3. Solitary nodule 4. Dominant nodule
31
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
32
HYPERTHYROIDISM What are the thyroid function test results in primary hyperthyroidism?
high T4 high T3 low TSH
33
HYPERTHYROIDISM What are the thyroid function rests in secondary hyperthyroidism?
high T4 high T3 high TSH
34
HYPERTHYROIDISM What is a complication of hyperthyroidism?
- Thyroid crisis/storm - osteoporosis - proximal myopathy - thyrotoxic crisis - iatrogenic (agranulocytosis from carbimazole, congenital malformations, foetal goitre)
35
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
36
HYPOTHYROIDISM Briefly describe the pathophysiology of secondary hypothyroidism
Reduced release or production of TSH so reduced thyroid hormone release
37
HYPOTHYROIDISM Briefly describe the pathophysiology of tertiary hypothyroidism
Thyroid gland overcompensates until it can reestablish correct concentration fo thyroid hormone
38
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)
39
HYPOTHYROIDISM Name 3 causes of secondary hypothyroidism
- compression from a pituitary tumour - hypothalamic tumours - drugs (cocaine, steroids + dopamine)
40
HYPOTHYROIDISM What are the TFT results for primary hypothyroidism?
- High TSH - low T4
41
HYPOTHYROIDISM What are the TFT results for secondary hypothyroidism?
- normal/low TSH - low T4
42
HYPOTHYROIDISM what are the complications of hypothyroidism?
- hypercholesterolaemia - carpal tunnel - peripheral neuropathy - myoxedema coma - thyroid lymphoma
43
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)
44
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)
45
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
46
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
47
DIABETES INSIPIDUS What is the treatment for nephrogenic DI?
- manage fluid balance - treat underlying cause - sodium restriction - thiazide diuretics (BENDROFLUMETHIAZIDE)
48
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)
49
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
50
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
51
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
52
SIADH How do you treat very symptomatic SIADH?
Give 3% saline (hypertonic) demeclocycline or tolvaptan
53
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
54
DIABETES MELLITUS Name 3 exocrine causes of Diabetes
1. Inflammatory - actue/chronic pancreatitis 2. Hereditary haemochromatosis 3. Pancreatic neoplasia 4. Cystic fibrosis
55
PHEOCHROMOCYTOMA What is Pheochromocytoma?
A rare catecholamine secreting tumour in the adrenal medulla (chromatin cells)
56
PHEOCHROMOCYTOMA what are the clinical features of pheochromocytoma?
SYMPTOMS Headache Profuse Sweating Palpitations Tremor SIGNS Hypertension Postural hypotension Tremor hypertensive retinopathy Pallor
57
PHEOCHROMOCYTOMA What are the investigations for pheochromocytoma?
- Plasma metanephrines and normetanephrines - 24 hour urinary total catecholamines - CT – look for tumour
58
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)
59
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
60
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
61
CONNS SYNDROME What are the clinical features of Conn's syndrome?
SYMPTOMS - lethargy - mood disturbance - paraesthesia + muscle cramps SIGNS - refractory hypertension - metabolic alkalosis
62
CONNS SYNDROME A deficiency in which electrolyte causes the symptoms of Conn's syndrome?
HYPOKALAEMIA causes: 1. Muscle weakness 2. Tiredness 3. Polyuria
63
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
64
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
65
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
66
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
67
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
68
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
69
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 U have no Pot (potassium), no T, but a long PR and a long QT
70
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
71
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
72
THYROID CANCER What types of thyroid cancers are usually asymptomatic thyroid nodule (usually hard and fixed)?
Papillary Follicular Anaplastic
73
THYROID CANCER What is the most common form of thyroid cancer?
Papillary - 70%, young people, 3x more common in women | Follicular - 20%
74
DE QUERVAINS THYROIDITIS what is the treatment for de quervain's thyroiditis?
Treat with aspirin and only give prednisolone for severely symptomatic cases
75
DIABETES PHARMACOLOGY what is the mechanism of action for SGLT-2 inhibitors?
inhibits resorption of glucose in the kidney causing urinary glucose excretion
76
DIABETES PHARMACOLOGY what is the mechanism of action for pioglitazone?
PPAR gamma agoinsts reduce peripheral resistance
77
DIABETES PHARMACOLOGY what are the side effects of pioglitazones?
Weight gain Fluid retention Hepatotoxicity Bladder cancer
78
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
79
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 -
80
HYPERTHYROIDISM what is the mechanism of action for carbimazole?
prevents thyroid peroxidase from producing T3 and T4
81
ACROMEGALY what are the side effects of GH receptor antagonists e.g. pegvisomant?
- reactions at injection site - GI disturbance - hypoglycaemia - chest pain - hepatitis
82
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+
83
PHARMACOLOGY what are the side effect of vasopressin antagonists e.g. tolvaptan?
- GI disturbance - headache - increased thirst - insomnia
84
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
85
PHARMACOLOGY what are the side effects of vasopressin analogies e.g. desmopressin?
- headache - facial flushing - nausea - seizures
86
PHARMACOLOGY what is the mechanism of action for metyrapone?
- blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide enzyme
87
PHARMACOLOGY what are the side effects of metyrapone?
- GI disturbance - headache - dizziness - drowsiness - hirsutism
88
ADRENAL INSUFFICIENCY how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?
short ACTH = no change | long ACTH = increase
89
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
90
HYPERNATRAEMIA what is the management?
- fluid replacement = IV 5% dextrose - treat causes - suspend medications
91
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
92
HYPONATRAEMIA what are the complications?
- central pontine myelinolysis
93
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
94
DIABETES PHARMACOLOGY what is the mechanism of action for DPP-4 inhibitors?
prevent degradation of incretins _ promote insulin secretion
95
DIABETES PHARMACOLOGY what are the side effects of DPP-4 inhibitors e.g. linagliptin?
pancreatitis
96
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
97
DIABETIC KETOACIDOSIS what are the complications?
- venous thrromboembolism - arrhythmias - ARDS - AKI - cerebral oedema - hypokalaemia - gastric stasis
98
HYPERNATRAEMIA what are the complications?
- cerebral oedema - coma - death
99
HYPOTHYROIDISM what is the management for mxyoedema coma?
- ITU/HDU admission - IV thyroid replacement (levothyroxine) - antibiotics - IV hydrocortisone (100mg)
100
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)
101
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
102
DIABETES INSIPIDUS when is the desmopressin suppression test contraindicated?
- hypernatremia - uncontrolled diabetes mellitus - kidney insufficiency - pregnancy
103
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
104
PRIMARY HYPERALDOSTERONISM what are the causes?
- bilateral idiopathic adrenal hyperplasia (most common) - adrenal adenoma = Conn's syndrome - unilateral hyperplasia - familial hyperaldosteronism - adrenal carcinoma
105
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)
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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
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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
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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
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CARCINOID TUMOURS what are the investigations?
- urinary hormone levels = 5-HIAA - plasma chromogranin A y - CT or MRI - tissue biopsy
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CARCINOID TUMOURS what is the management?
- somatostatin analogues = octreotide - surgery - cyproheptadine can help with diarrhoea
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HYPERTHYROIDISM what antibody is raised in Grave's disease?
TSH receptor antibody
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HYPERTHYROIDISM what are the 2 methods of medical management?
1. suppress with carbimazole until euthyroid 2. block with carbimazole and replace with levothyroxine
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HYPERTHYROID what is the most serious side effect of carbimazole?
agranulocytosis

MY REVISION - ALL TO DO 2 (24 decks)

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