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medicine phase 2 a > endocrine > Flashcards

endocrine Flashcards

1
Q

Causes of T1DM

A

HLA-DR/DQ polymorphism, environmental

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2
Q

which hypersensitivity is T1DM?

A

type IV

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3
Q

What are the effects of a lack of insulin?

A

-lipolysis/muscle breakdown
-Increased hepatic glucose output
-reduced peripheral glucose uptake
-reduces glucagon secretion inhibition

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4
Q

What are the key presentations of T1DM

A

days/week of polyuria, polydipisia, weight loss, weakness

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5
Q

What are the investigations for T1DM

A

HbA1C (gold standard), serum glucose, U&Es and blood cultures (DKA)

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6
Q

what is considered a normal random plasma glucose?

A

<11.1

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7
Q

what is considered a normal fasting plasma glucose?

A

<6.1 (>7 in diabetes)

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8
Q

what is considered a normal 2hr plasma glucose?

A

<7.8 (>11.1 in diabetes)

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9
Q

What is a normal HbA1C?

A

<42 (5.7%)

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10
Q

What are the diagnostic criteria for an asymptomatic patient suspected to have T1DM?

A

raised glucose on two separate occasions

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11
Q

what is a diabetic HbA1c?

A

> 47 (>6.5%)

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12
Q

What is 1st line treatment for T1DM

A

basal-bolus insulin (glargine), amylin analogue (pramlintide or metfromin)

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13
Q

What is the 2nd line treatment for T1DM

A

fixed insulin dose

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14
Q

What are the complications of T1DM

A

-DKA
-microvascular
-macrovascular
-CVD
-depression

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15
Q

What is DKA?

A

hyperglycaemia, ketonaemia, metabolic acidosis

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16
Q

Causes of DKA

A

T1DM, infection

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17
Q

Risk factors DKA

A

innappropriate insulin therapy, infection etc.

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18
Q

pathophysiology of DKA

A

insulin deficiency -> lipolysis/muscle breakdown
lipolysis= FFAs + glycerol
FFAs->ketones
reduced circulating volume

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19
Q

presentations of DKA

A

-gradual drowsiness
-vomiting
-dehydration (T1DM)

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20
Q

investigations for DKA

A

VBG, acidosis <7.35 or bicarbonate <15mmol/L
blood ketones > 1.6-2.9
blood glucose >11

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21
Q

What can insulin treatment for DKA lead to?

A

hypokalaemia due to movement into cells - can cause arrhythmias

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22
Q

What is the management of DKA

A

FIG-PICK
Fluids - 0.9% saline
Insulin - actrapid
Glucose - dextrose
Potassium - monitor
Infection - treat underlying cause
Chart - fluids
Ketones - monitor ketones

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23
Q

What are the complications of DKA?

A

cerebral oedema

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24
Q

What are key presentations of T2DM?

A

Glycosuria, obesity

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25
Q

What are the signs of T2DM?

A

polydipsia
polyuria
polyphagia
glycosuria

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26
Q

What is the 2nd line treatment for T2DM?

A

metformin - if newly diagnosed patients have an HbA1C over 48mmol/L

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27
Q

What is the 1st line management of T2DM?

A

lifestyle modification, weight loss, dietary modifications etc

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28
Q

What is the 3rd line management for T2DM?

A

metformin + 1 of: sulfonylurea, thiazalodinediones, DPP-4 inhibitor or SGLT-2

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29
Q

What is the 4th line treatment for T2DM?

A

insulin

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30
Q

how do you monitor T2DM

A

yearly diabetes reveiw
HbA1c 3-6 months
ACR annually

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31
Q

What are the microvascular complications of DM?

A

neuropathy, retinopathy, nephropathy

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32
Q

What are the macrovascular complications of DM?

A

stroke, hypertension, CAD, peripheral artery disease

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33
Q

What are the side effects of insulin treatment?

A

hypoglycaemia, weight gain, lipodystrophy

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34
Q

What are the side effects of metformin?

A

gastrointestinal upset, lactic acidosis
(nephrotoxic, cannot be used in pts with eGR <30)

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35
Q

What is the action of sulfonyureas?

A

stimulates beta cells to secrete insulin

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36
Q

Give an example of a sulfonylurea

A

gliclazide, glimepiride

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37
Q

What are the side effects of sulfonylureas?

A

hypoglycaemia
weight gain
hyponatraemia

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38
Q

What do thiazolidinediones (pioglitazone) do?

A

they promote adipogenesis and fatty acid uptake

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39
Q

What are the side effects of thiazolidinediones?

A

weight gain and fluid retention

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40
Q

What do DPP-4 inhibitors (-gliptins) do?

A

increase incretin which inhibits glucagon secretion

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41
Q

What are the side effects of DPP-4 inhibitors?

A

tolerated well but can cause pancreatitis

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42
Q

Give an example of a DPP4 inhibitor?

A

sitagliptin

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43
Q

What do SGLT-2 inhibs do?

A

inhibits reabsorption of glucose in the kidney

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44
Q

What are the side effects of SGLT-2 inhibs?

A

UTIs and weight loss

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45
Q

Give an example of an SGLT2 inhibitor

A

dapagliflozin

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46
Q

Give an example of a GLP-1 inhibitors

A

exenatide

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47
Q

Explain the pathophysiology of HHS

A

insulin insufficiency - enough insulin to stop ketogenesis but not enough to stop hepatic glucose production

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48
Q

How does hyperglycaemia effect osmolality?

A

it results in osmotic diuresis with a loss of sodium and potassium

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49
Q

What are the causes of Hyperosmolar Hyperglycaemic state

A

diabetes + infection

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50
Q

What are the key presentations of HHS?

A

acute cognitive impairment - psychosis, coma, seizures

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51
Q

What are the physiological characteristics of HHS?

A

severe hyperglycaemia >30
hypotension
hyperosmolality >320

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52
Q

1st line investigation for HHS

A

blood glucose >30
blood ketones -ve
VBG - mild acidosis
serum osmolality >320
U&Es, abnormal K

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53
Q

management of HHS

A

rehydrate - 0.9% saline over 48 hrs
replace K+ when urine flows
use insulin if blood sugar not falling
LMWH for VTE prophylaxis

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54
Q

What are the complications of HHS

A

stroke, MI, PE
treatment related hypokalcaemia/glycaemia

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55
Q

What are the symptoms of hypoglycaemia?

A

hypotension, tachycardia, sweating, anxiety, hunger, dizziness

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56
Q

How does decreased blood glucose effect adrenaline, GH and cortisol?

A

all of these hormones are produced in order to increase blood glucose rapidly

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57
Q

Below what glucose level do autonomic symptoms show?

A

<3.3mmol/L

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58
Q

Below what glucose level do neuroglycopenic symptoms show?

A

<2.8mmol/L

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59
Q

What are the symptoms of neurocytopenic hypoglycaemia?

A

weakness, vision changes, confusion, dizziness

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60
Q

management for hypoglycaemia

A

food- carbs
OR
IV 10% glucose 200ml/h (conscious)
IV 10% glucose 200ml/15mins (inconscious)

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61
Q

complications of hypoglycaemia

A

siezure
coma
brain damage

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62
Q

what is cushings syndrome

A

hypercorticolism

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63
Q

What are the causes of ACTH independent cushings?

A

iatrogenic - steroids e.g. prednisolone (glucocorticoid)
adrenal adenoma

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64
Q

What are the causes of ACTH dependent cushings?

A

anterior pituitary adenoma
ectopic ACTH
ACTH dependent are more rare

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65
Q

What are the risk factors for cushings?

A

female
20-50 yrs
pituitary/adrenal adenoma, carcinoma, neuroendocrine tumours

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66
Q

What are the effects of hypercorticolism?

A

increases gluconeogenesis/glycogenesis, reduced insulin secretion, increased proteolysis/lipolysis/bone resporption, Na+ reabsorption, K+ excretion, anti-inflammatory/immunosuppressive

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67
Q

What are the key presentation of cushings?

A

round “moon” face
central obesity
abdominal striae
buffalo hump
proximal limb muscle wasting
supraclavicular fat distribution

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68
Q

What is the first line investigation for cushings?

A

plasma cortisol - elevated

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69
Q

gold standard investigations for cushings

A

dexamethasone supression test
(48hr_
low dose 1mg: low cortisol->normal, high/normal cortisol->cushings

high dose 8mg: low cortisol->cushings, High/normal cortisol->ACTH low->adrenal cushings
->ACTH high->ectopic ACTH

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70
Q

What is the management of cushings?

A

depends on cause
iatrogenic -> stop medication
surgical removal of adenoma/tumour
removal of adrenal glands + replacement hormones

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71
Q

What are the complications of cushings?

A

CVD, hypertension, DM

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72
Q

What is Addisons disease?

A

failure of adrenal cortex to secrete cortisol and aldosterone (primary adrenal insufficiency)

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73
Q

What are the causes of primary adrenal insufficiency (Addisons)?

A

autoimmune adrenalitis - most common in developed countries
TB - most common worldwide

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74
Q

What are causes of secondary adrenal insufficiency?

A

inadequate ACTH production due to damage/loss of pituitary

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75
Q

What are the causes of tertiary adrenal insufficiency?

A

inadequate CRH from the hypothalamus, often due to long term (>3 weeks) oral steroids

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76
Q

What are the key presentations of addisons?

A

weight loss
hyperpigmentation (bronzing of hands)
fatigue
anorexia
salt cravings

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77
Q

What is the gold standard investigation for addisons?

A

short synacthen test (ACTH stimulation test)

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78
Q

How does the short synacthen test work?

A

synacthen (synthetic ACTH) given in the morning, cortisol measured at baseline, 30 and 60 mins, in healthy pt, cortisol should double

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79
Q

What is the management of Addisons?

A

hydrocortisone (glucocorticoid) to replace cortisol
fludrocortisone (mineralcorticoid) to replace aldosterone

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80
Q

What is the management of an addisonian crisis?

A

parenteral steroids - hydrocortisone 100mg
fluid resus
correct hypoglycaemia
monitor electrolytes

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81
Q

what is Conns syndrome?

A

hyperaldosteronism

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82
Q

What is primary hyperaldosteronism and what is it caused by?

A

the adrenal glands are responsible for producing too much aldosterone (renin will be low) - adrenal adenoma e.g. bilateral adrenal hyperplasia

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83
Q

What is secondary hyperaldosteronism?

A

high levels of aldosterone due to and increase in renin secretion

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84
Q

What are the key presentations of conns?

A

hypertension

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85
Q

What are the symptoms of conns?

A

muscle cramps

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86
Q

What are the investigations for conns?

A

aldosterone renin ratio - high in primary (gold standard)
plasma K+ will be low

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87
Q

What confirmatory investigation can be done for Conns?

A

MRI/CT to locate adrenal lesions
elective adrenal venous sampling

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88
Q

What medications can help manage Conns?

A

aldosterone antagonists
eplerenone
spironolactone

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89
Q

What surgical/interventional remedies are there for Conns?

A

adrenalectomy
percutaneous renal artery angioplasty

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90
Q

What are the Causes of hypokalaemia?

A

INCREASED EXCRETION:
drugs(thiazide/loops)
renal disease
GI loss
REDUCED INTAKE:
dietary deficiency
SHIFT TO INTRACELLULAR:
insulin/salbutamol

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91
Q

What does K+ do in the body

A

heart function, muscle contraction, water balance, nervous impulses

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92
Q

What are the signs of hypokalaemia?

A

arrhythmias, muscle paralysis, hypotonia. hyporeflexia, tetany

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93
Q

Gold standard investigations for hypokalaemia

A

ECG-> inverted T waves, ST depression, prominent U wave
U&Es <3.5 (<2.5 is severe)

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94
Q

What is the management of mild hypokalaemia?

A

oral potassium replacement

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95
Q

What is the management of severe hypokalaemia?

A

IV potassium chloride 40mmol in 1L 0.9% NaCl

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96
Q

Causes of hyperkalaemia

A

IMPAIRED EXCRETION:
AKI/CKD
drugs
renal tubular acidosis
INCREASED INTAKE:
IV therapy
increased dietary intake
SHIFT FROM INTRACELLULAR:
metabolic acidosis

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97
Q

key presentations of hyperkalaemia

A

arrhythmias, reduced power/reflexes, palpitations, chest pain

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98
Q

What are the gold standard Investigations for hyperkalaemia?

A

ECG-> peaked T waves, P wave flattening, PR prolongation, wide QRS complex
U&Es

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99
Q

How should you manage hyperkalaemia with ECG changes?

A

IV calcium gluconate/chloride - stabilised cardiac membrane
insulin + dextrose

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100
Q

How should you manage hyperkalaemia with NO ECG changes?

A

shift potassium into cells with IV insulin/dextrose or with nebulised salbutamol

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101
Q

What medications/procedures can remove potassium from the body?

A

calcium resonium, loop diuretics, dialysis

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102
Q

what are phaechromocytomas?

A

tumours arising from catecholamine-producing chromaffin cells of the adrenal medulla

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103
Q

causes of phaechromocytomas

A

MEN 2
neurofibromatosis
bilateral/malignant/extra-adrenal in 10%

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104
Q

pathophysiology of phaechromocytomas

A

tumour secreted catecholamines: adrenaline, noradrenaline and sometimes dopamine (metanephrines/normetanephrines)

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105
Q

key presentations of phaechromocytomas

A

episodic, hypertension, headaches, palpitations, sweating, pallor

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106
Q

gold standard investigation for phaechromocytomas

A

24hr urine collection for catecholamines, metaneprhines, normetanephrines plus same metabolites in blood

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107
Q

Management of phaechromocytomas

A

non emergency: alpha(phenoxybenzamine)/beta blockers, surgical excision (curative in 85%)
HTN crisis: antihypertensive agents (phentolamine)

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108
Q

what is Carcinoid syndrome?

A

symptoms due to release of vasoactive peptides (serotonin) into the blood stream, namely serotonin

109
Q

What causes carcinoid syndrome?

A

most commonly arise from the gut followed by lungs, liver, ovaries and thymus

110
Q

What is the pathophysiology of carcinoid syndrome?

A

neuroendocrine tumours secrete serotonin in to bloodstream
Gi tumours secrete hormones which are inactivated by the liver (enterohepatic system) unless there are liver metastases which cause liver dysfunction

111
Q

What are the key presentations of carcinoid syndrome?

A

diarrhoea, flushing, wheeze, abdominal cramps/masses

112
Q

gold standard investigations for carcinoid syndrome

A

high 5-hydroxyindoleacetic acid (breakdown product of serotonin, will be high)
liver ultrasound ( will show metastasis)

113
Q

Management of localised carcinoid syndrome

A

1st line - surgical recision
AND perioperative octreotide infusion

114
Q

Management of metastatic carcinoid syndrome

A

1st line - surgical recision AND perioperative octreotide infusion
adjunct - radiofrequency ablation
(somatostatin analogue or interferon alfa if not suitable for resection)

115
Q

complications of carcinoid syndrome

A

carcinoid heart disease
bowel obstruction/intestinal bleeding
pellagra
carcinoid crisis

116
Q

What is serotonin syndrome?

A

An excess of synaptic serotonin in the CNS

117
Q

What are the causes of serotonin syndrome?

A

SSRI, SNRIS, antidepressants, opioids, lithium

118
Q

What are the key presentations of serotonin syndrome?

A

Clonus
hyper-reflexia

119
Q

Symptoms of serotonin syndrome

A

anxiety, agitation, confusion, tremor, sweating, seizure

120
Q

investigations for serotonin syndrome

A

signs of serotonin toxicity

121
Q

Management of severe serotonin toxicity

A

Cessation of medications
adjuncts
- activated charcoal
- chlorpromazine

122
Q

Management of serotonin syndrome with rhabdomyolysis

A

cessation of medications
adjuncts
- activated charcoal
- chlorpromazine
AND
muscle paralysis and cooling

123
Q

What serum Na+ level constitutes hyponatraemia?

A

<135mmol/L

124
Q

What is a severely low Na+ serum level?

A

<125mmol/L

125
Q

What are the causes of hypovolaemic hyponatraemia?

A

volume depletion - third spacing of fluids (interstitial)

126
Q

What are the causes of euvolemic hyponatraemia?

A
  • hypothyroidism
  • adrenal insufficiency
  • polydipsia or potomania
  • medications
127
Q

What are the causes of hypervolemic hyponatraemia?

A

decreased arterial volume
- congestive heart failure
- cirrhosis
- nephrotic syndrome

128
Q

key presentations of hyponatraemia?

A

anorexia, nausea, lethargy

129
Q

symptoms of hyponatraemia?

A

headache, irritability, confusion, seizures, decreased GCS

130
Q

Management of asymptomatic chronic hyponatraemia

A

fluid restriction or demeclocycline (ADH antagonist)

131
Q

Management of acute or symptomatic hyponatraemia

A

cautious rehydration w/ 0.9% saline (do not correct rapidly -> central pontine myelinolysis)
consider using furosemide when not hypovolaemic to avoid fluid overload

132
Q

What medication is used to treat hyponatraemia to promote water excretion?

A

Vasopressor receptor antagonists (vaptans) e.g. tolvaptan, effective in treating hyper and euvolemic

133
Q

In emergency, what should be given to a hyponatraemic patient

A

hypertonic saline (1.8%) at 70mmol Na+/hr

134
Q

What are the complications of hyponatraemia?

A

cerebral oedema, osteoporosis, osmotic demyelination syndrome, increased risk of falls

135
Q

What serum Na+ concentration is considered hypernatraemic?

A

> 145 mmol/L

136
Q

What serum Na+ concentration is considered severe hypernatraemia

A

> 160mmol/L

137
Q

What are the 3 causes of hypernatraemia?

A

free water loss, pure free water intake deficit, sodium overload

138
Q

Give an example of free water loss hypernatraemia

A

renal concentrating defect, osmotic diuresis, diabetes insipidus

139
Q

give an example of sodium overload hypernatraemia

A

mineralcorticoid excess, ingestion of too much salt, administration of hypertonic fluids

140
Q

key presentations of hypernatraemia

A

lethargy, thirst, weakness

141
Q

symptoms of hypernatraemia

A

mood changes, coma/fits, decreased JVP

142
Q

Management of hypernatraemia

A

oral rehydration, IV glucose 5% 1L/hr
if hypovolaemic - use 0.9% saline

143
Q

complications of hypernatraemia

A

treatment related brain oedema
low chance of:
- myelinolysis
- rhabdomyolysis
- cardiac toxicity
- metabolic effects

144
Q

What is the difference between primary and secondary hypothyroidism?

A

secondary results from pituitary failure, primary is a due to thyroid dysfunction

145
Q

What is the most common form of hypothyroidism in the developed world?

A

hashimotos thyroiditis

146
Q

What antibodies is hashimoto’s thyroiditis associated with?

A

antithyroid peroxidase (anti-TPO)
and antithyroglobulin antibodies

147
Q

other than autoimmune, what are the other causes of hyothyroidism?

A

iodine deficeincy
hyperthyroid meds/treatment (carbimazole etc)

148
Q

What medications can cause hypothyroidism?

A

lithium, amiodarone

149
Q

What are some secondary causes of hypothyroidism?

A

tumours

150
Q

What is the gold standard investigation for hashimoto’s hypothyroidism?

A

antithryoid peroxidase antibodies positive

151
Q

How does hypothyroidism present?

A

weight gain, lethargy, dry skin, coarse hair/hair loss (lateral aspect of eyebrow), menorrhagia, constipation

152
Q

How does Graves cause hyperthyroidism?

A

circulating IgG antibodies target G coupled TSH receptors causing hypertrophy and hyperplasia of the thryoid gland

153
Q

What do thyroid hormones effect?

A

metabolic rate, thermogenesis, HR, cardiac contractility, CO, vasodilation

154
Q

What are the key presentations of hyperthyroidism

A

unintentional weight loss, heat intolerance, tremor, palpitations, diffuse goitre
Graves - exophthalmos and pretibial myxedema

155
Q

What are the symptoms of hyperthyroidism?

A

diarrhoea, menstrual irregularity, alopecia, fatigue, sexual dysfunction, hyperphagia (excessive appetite)

156
Q

What are the first line Investigations for hyperthyroidism?

A

TFTs
elevated T3/4, low TSH in primary, high in secondary

157
Q

What is the 1st line management of hyperthyroidism?

A

anti-thyroid drugs carbimazole (propylthiouracil, 2nd line) PLUS beta blockers

158
Q

What medication is used to treat thyrotoxic symptoms in hyperthyroidism?

A

propranolol

159
Q

What is used to treat de quervains hyperthryoidism?

A

NSAIDS

160
Q

Other managements for hyperthyroidism

A

radioactive iodine therapy
surgery to remove nodules/thyroid
anticoag if in AF

161
Q

complications of hyperthyroidism

A

hypothyroidsim (iatrogenic)
thyroid storm
HF
angina
osteoporosis

162
Q

What type of antibodies attack the thyroid in Graves disease?

A

IgG autoantibodies attack thyrotropin (TSH) receptor

163
Q

What are the key presentations of Graves disease?

A

exophthalmos, pretibial myxoedema, thyroid acropachy

164
Q

What is thyroid acropachy?

A

a triad of clubbing, soft tissue swelling of hands and feet and periosteal new bone formation

165
Q

What is de quervains thyroiditis?

A

inflammation of the thyroid gland resulting in pain and discomfort

166
Q

What are the key presentations of de quervains thyroiditis?

A

neck pain, thyroid enlargement, fever, palpitations

167
Q

What with TFTs and CRP show in de quervains thryoiditis?

A

T3/4 and CRP will be raised

168
Q

What is the management for de quervains thyroiditis in the hyperthyroid stage?

A

NSAIDs or corticosteroids

169
Q

What is a thyroid storm?

A

the severe end of thryotoxicosis, a

170
Q

What are the key presentations of a thyroid storm?

A

agitation, confusion, coma

171
Q

What are the symptoms of thyroid storm?

A

diarrhoea, goitre, acute abdomen (abdominal pain)

172
Q

Investigation for thyroid storm?

A

TFTs, high T3/4, low TSH primary, high in secondary

173
Q

What is the first line management for thyroid storm?

A

carbimazole - antithyroid treatment

174
Q

Why is hydrocortisone given in a thryoid storm?

A

it treats relative adrenal insufficiency and prevents conversion of T4 to T3

175
Q

what other treatments may be given in a thyroid storm?

A

supportive care, fluid resus, anti-arrhythmetics, beta blockers

176
Q

What are the complications of thyroid storm

A

thromboembolism, coma, heart failure, arryhthmia, death

177
Q

What is the prognosis of thyroid storm?

A

75% mortality without treatment

178
Q

What is the relationship between thyroid hormone levels and cholesterol and triglyceride levels?

A

They are inversely proportional

179
Q

What are the symptoms of hypothyroidism?

A

weight gain
coarse hair/hair loss
goitre
eyelid oedema

180
Q

What are the investigations for hypothyroidism?

A

TFTs low T3/4, high TSH in primary, low in secondary

181
Q

How do you manage hypothyroidism?

A

1st line levothyroxine (T4)
if over 65 with CAD -> low dose levothyroxine

182
Q

What are the 4 types of thyroid cancer?

A

papillary, follicular, anaplastic and medullary

183
Q

What do medullary thyroid cancers secrete? this can be tested in the blood to screen for recurrence

A

calcitonin

184
Q

What are the investigations for thyroid cancer?

A

TFTs, fine needle biopsy

185
Q

How do you treat a papillary or follicular thyroid cancer?

A

surgery + radioactive iodine ablation + TSH suppression
if recurrent/metastatic - chemo - sorafenib/lenvatinib

186
Q

How do you treat medullary thyroid cancer?

A

1st line - surgery + thyroid replacement
2nd line - vandentanib + thyroid replacement

187
Q

how do you treat anaplastic thyroid cancer?

A

palliative surgery + chemoradiation + thyroid replacement

188
Q

How do you treat lymphoma (thyroid cancer)?

A

chemo, external radiation - TSH suppression
(TSH suppression bc thyroid needs TSH to grow)

189
Q

Which of the thyroid cancers has the best prognosis

A

papillary>follicular>medullary>lymphoma>anaplastic

190
Q

What is the most common cause of acromegaly?

A

pituitary somatotroph adenoma ( benign anterior pituitary adenoma)

191
Q

What are the effects of growth hormone?

A

lipolysis
gluconeogenesis
glycogenolysis
decreased peripheral glucose uptake
protein synthesis
osteoblast stimulation
cell resistance to insulin increases

192
Q

What are the Symptoms of acromegaly?

A

excessive sweating
headache
tiredness
weight gains
deep voice
amenorrhea
change in appearance

193
Q

How can acromegaly effect vision?

A

pituitary adenoma -> bitemporal hemianopia

194
Q

What inhibits the release of GH?

A

somatostatin, high glucose levels and dopamine

195
Q

What are the investigations for acromegaly?

A

insulin like growth factor-1 (IGF-1) blood test
OGTT- GH nadir >1microgram/L

196
Q

Why is the OGTT used to diagnose acromegaly?

A

glucose should inhibits GH production but does not in acromegaly

197
Q

what is the 1st line treatment for acromegaly

A

transsphenoidal surgery

198
Q

what is the 2nd line treatment for acromegaly?

A

2nd line - octreotide (somatostatin analogue)

199
Q

What is the third line treatment for acromegaly?

A

GH receptor antagonist - pegvisomant OR
dopamine agonists - bromocriptine

200
Q

What are the complications of acromegaly?

A

carpal tunnel syndrome
T2DM
sleep apnea
hypertension
cardiac complications

201
Q

what are prolactinomas?

A

benign lactotroph adenomas (pituitary) expressing and secreting prolactin

202
Q

What does prolactin do?

A

it causes breasts to grow and make milk during pregnancy

203
Q

Risk factors for prolactinoma?

A

female
20-50yrs old
FH
oestrogen therapy

204
Q

What is the pathophysiology of prolactinomas?

A

hypersecretion of prolactin -> secondary hypogonadism (breast milk production)
dopamine has -ve feedback on prolactin, disruption of transport/ secretion = hyerprolactinaemia

205
Q

key presentations of prolactinomas?

A

women present with amenorrhea and galactorrhea
men present with sexual dysfunction, hypogonadism and gynaecomastia

206
Q

What are the investigations for preolactinomas?

A

serum prolactin - 1st line
MRI of pituitary - 2nd line

207
Q

What is the 1st line of management for prolactinomas?

A

dopamine agonists - bromocriptine/cabergoline

208
Q

What are the other treatments for prolactinomas?

A

2nd line - hormone therapy
3rd line surgery (medical treatments more effeicient)

209
Q

What are the complications of prolactinomas?

A

infertility, sight loss, anterior pituitary failure

210
Q

What is SIADH?

A

euvolemic, hypotonic, hyponatraemia - impaired water excretion due to ADH release

211
Q

What can cause SIADH?

A

many causes:
drugs- SSRIs amiodarone, NSAIDs
malignancy - lung
head injury
infection

212
Q

what is the pathophysiology of SIADH?

A

more ADH means more water retention, diluting electrolytes

213
Q

What are the key presentations of SIADH?

A

Mainly due to hyponatraemia:
headache
lethargy
muscle cramps
weakness
confusion

214
Q

What are the investigations for SIADH?

A

U&Es (low Na+), serum osmolality (low)
high urine osmolality and Na+

215
Q

How do you manage SIADH?

A

fluid restriction, 500mls-1L
vasopressor receptor antagonist - tolvaptan

216
Q

How do you manage severe SIADH?

A

IV hypertonic saline + fluid restriction + vasopressin receptor antagonist
+
furosemide

217
Q

What can happen as a result of rapid treatment of hyponatraemia?

A

central pontine myelinolysis

218
Q

What are the complications of SIADH?

A

cerebral oedema, seizure, coma, death, central pontine myelinolysis

219
Q

What is diabetes insipidus?

A

a disease characterised by decreased secretion of ADH (cranial) from posterior pituitary or an insensitivity to ADH (nephrogenic)

220
Q

What are the two causes of diabetes inspidus?

A

cranial, nephrogenic

221
Q

give examples of cranial causes of diabetes insipidus

A

idiopathic -50%
tumour
trauma
haemorrhage

222
Q

give an example of a nephrogenic cause of diabetes insipidus

A

hereditary
drugs- lithium, demeclocycline
chronic renal disease

223
Q

What is the pathophysiology of cranial diabetes insipidus

A

lack of ADH secretion post pituitary
reduced water reabsorption
high serum osmolality

224
Q

What is the pathophysiology of nephrogenic diabetes insipidus?

A

resistance to action of ADH

225
Q

What are the key presentations of diabetes inspidus?

A

polyuria
polydipsia

226
Q

What are the symptoms of diabetes insipidus?

A

nocturia, dry mucosa, sunken eyes, changes to skin turgor

227
Q

What are the gold standard investigations for diabetes insipidus?

A

water deprivation test, urine osmolality tested before and after synthetic ADH (desmopressin) given

228
Q

What is the difference in urine osmolality between cranial and nephrogenic DI in the water deprivation test?

A

urine osmolality remain lows in nephrogenic
urine osmolality will rise after desmopressin given in cranial (kidneys still respond to ADH)

229
Q

What is the treatment for cranial DI?

A

desmopressin

230
Q

What is the treatment for nephrogenic DI?

A

thiazide diuretics e.g bendroflumethiazide

231
Q

What can cause hypocalcaemia?

A

hypoparathyroidism
vit D deficiency
drugs
malignancy

232
Q

What is calcium used for in the body?

A

neurotransmission and muscle contraction, bone mineralisation, regulator of ion transport and membrane integrity

233
Q

What are the key presentations of hypocalcaemia?

A

CATs go numb
convulsions
arrhythmias
tetany
numbness in hands and feet

234
Q

What are the investigations of hypocalcaemia?

A
  • bone profile
  • corrected calcium
  • ECG - prolonged QT
  • parathyroid function
235
Q

What is the management of hypocalcaemia?

A

10ml calcium gluconate/chloride 10% slow IV
oral calcium
vit D

236
Q

What are the complications of hypocalcaemia?

A

seizure, cardiac arrest, convulsions, osteoporosis

237
Q

How can you treat acute hypocalcaemia?

A

IV calcium gluconate, 10%, 10ml, 10 mins

238
Q

How can you treat persistent hypocalcaemia?

A

vit D 50000 IU orally once a week for 8 weeks

239
Q

What can cause hypercalcaemia?

A

hyperparathyroidism, malignancy, sarcoidosis

240
Q

What are the key presentations for hypercalcaemia?

A

kidney stones, psychic groans (confusion), abdominal moans (constipation, acute pancreatitis)

241
Q

What is the gold standard investigation for hypercalcaemia?

A

PTH, bone profile
elevated PTH, high calcium, low/normal phosphates

242
Q

What are the main managements of hypercalcaemia?

A

rehydration with 0.9% saline, bisphosphonates, sometimes use loop diuretics e.g. furosemide

243
Q

What are the complications of hypercalcaemia?

A

pancreatitis, confusion, coma, death

244
Q

What is the most common cause of primary hyperparathyroidism?

A

parathyroid adenomas

245
Q

What else can cause primary hyperparathyroidism?

A

hyperplasia
congenital
lithium therapy

246
Q

What causes secondary hyperparathyroidism?

A

insufficient vit D or chronic renal failure resulting in low serum calcium

247
Q

What causes tertiary hyperparathyroidism?

A

occurs after prolonged secondary hyperparathyroidism, parathyroid becomes autonomous and secreted PTH without stimulation

248
Q

What is the pathophysiology of hyperparathyroidism?

A

PTH increase->increased renal Ca absorption, phosphate excretion, renal vit D synthesis, calcium intestinal absorption and bone remodelling

249
Q

What are the key presentations of hyperparathyroidism?

A

bones (osteoporosis)
kidney stones
psychic groans - fatigue/depression
abdominal moans - nausea/constipation

250
Q

What are the best investigations for hyperparathyroidism?

A

PTH/bone profile - high PTH, high calcium - low phosphates (depending on type of hyperparathyroidism)

251
Q

What is the treatment for primary hyperparathryoidism?

A

parathyroidectomy

252
Q

What is the treatment for secondary hyperparathyroidism?

A

vit D supplements or renal transplant in CKD

253
Q

What is the treatment for tertiary hyperparathyroidism?

A

surgical removal of part of the parathyroid to bring PTH to the right level

254
Q

What is cinacalet and what does it do?

A

its a calcimimetic, it increases the sensitivity of parathyroid to calcium causing less PTH secretion

255
Q

What are the key presentations of secondary/tertiary hyperparathyroidism?

A

CATs go numb
convulsions, arrhythmias, tetany and numbness in the hands and feet and around mouth

256
Q

What are the key presentations of hypoparathyroidism?

A

CATs go numb
convulsions, arrhythmias, tetany and numbness of extremities

257
Q

What is the gold standard investigation for hypoparathyroidism?

A

bone profile- low calcium, high phosphate, low PTH

258
Q

How do you manage hypoparathyroidism?

A

IV calcium and Vit D
magnesium supplement (if hypomagnesemic)
Ca supplements and calcitriol

259
Q

What are the side effects of SGLT-2 inhibs?

A

UTIs and weight loss

260
Q

What with TFTs and CRP show in de quervains thryoiditis?

A

T3/4 and CRP will be raised

261
Q

What with TFTs and CRP show in de quervains thryoiditis?

A

T3/4 and CRP will be raised

262
Q

What with TFTs and CRP show in de quervains thryoiditis?

A

T3/4 and CRP will be raised

263
Q

What with TFTs and CRP show in de quervains thryoiditis?

A

T3/4 and CRP will be raised

264
Q

What with TFTs and CRP show in de quervains thryoiditis?

A

T3/4 and CRP will be raised

265
Q

What with TFTs and CRP show in de quervains thryoiditis?

A

T3/4 and CRP will be raised

266
Q

What with TFTs and CRP show in de quervains thryoiditis?

A

T3/4 and CRP will be raised

267
Q

What with TFTs and CRP show in de quervains thryoiditis?

A

T3/4 and CRP will be raised

268
Q

Why is hydrocortisone given in a thryoid storm?

A

it treats relative adrenal insufficiency and prevents conversion of T4 to T3

269
Q

How can you treat persistent hypocalcaemia?

A

vit D 50000 IU orally once a week for 8 weeks

medicine phase 2 a (10 decks)

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