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Year 4 Final > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Drugs that cause raised prolactin?

A

metoclopramide, domperidone
phenothiazines
haloperidol
very rare: SSRIs, opioids

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2
Q

Blood glucose target before meals at other times of the day?

A

4-7 mmol/L

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3
Q

Adverse effects of thiazolidineinones?

A

weight gain
liver impairment: monitor LFTs
fluid retention - therefore contraindicated in heart failure. The risk of fluid retention is increased if the patient also takes insulin
recent studies have indicated an increased risk of fractures
bladder cancer: recent studies have shown an increased risk of bladder cancer in patients taking pioglitazone

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4
Q

What levels are the C-peptide in a person with T1DM

A

C-peptide is made in the pancreas along with insulin; therefore, in patients with deficient insulin production (T1DM), it is low

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5
Q

DKA insulin management?

A

an intravenous infusion should be started at 0.1 unit/kg/hour
once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime

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6
Q

Why does praimry adrenal failure cause skin hyperpigementation?

A

ACTH is derived from a larger precursor called pro-opiomelanocortin (POMC), which also happens to be a precursor for beta-endorphin (which isn’t important in this case) and melanocyte stimulating hormone (MST). MST, as the name suggests, stimulates melanocytes giving the hyperpigmentation that can be seen in primary adrenal failure.

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7
Q

Thyrotoxicosis cardiac features?

A

palpitations, tachycardia
high-output cardiac failure may occur in elderly patients, a reversible cardiomyopathy can rarely develop

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8
Q

Symptoms of gastroparesis in T1DM?

A

erratic blood glucose control, bloating and vomiting

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9
Q

If patient is symptomatic
What fasting gluocse and random glucose levels are needed to diagnose diabetes?

A

fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

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10
Q

What can levothyroxine interact with?

A

iron, calcium carbonate

absorption of levothyroxine reduced, give at least 4 hours apart

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11
Q

Side effects of sulfonylureas?

A

hypoglycaemic episodes (more common with long acting preparations such as chlorpropamide)
weight gain
syndrome of inappropriate ADH secretion
bone marrow suppression
liver damage (cholestatic)
peripheral neuropathy

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12
Q

What is the management of bilateral adrenocortical hyperplasia

A

aldosterone antagonist e.g. spironolactone

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13
Q

What is the main drug that can’t be taken with lithium?

A

NSAIDs

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14
Q

What should be started for T2DM if high risk of CVD, established CVD or chronic HF?

A

Metformin and SGLT-2 inhibitor

q

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15
Q

Mneumonic for thyroid cancers. Most to least common

A

Please Feel My Awkward Lump
Papillary>Follicular>Medullary>Anaplastic>Lymphoma

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16
Q

Mechniasm of orlistat

A

inhibiting gastric and pancreatic lipase to reduce the digestion of fat

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17
Q

§What are the phases of De Quervian’s thyroiditis?

A

phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
phase 2 (1-3 weeks): euthyroid
phase 3 (weeks - months): hypothyroidism
phase 4: thyroid structure and function goes back to normal

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18
Q

Features of addison’s disease?

A

lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia

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19
Q

What is the TSH, thyroxine and T3 levels in sick euthyroid syndrome?

A

Low TSH, thyroxine and T3

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20
Q

Suppressed ACTH and not suppressed cortisol cause?

A

Cushing’s syndrome due to other causes (adrenal adenoma)

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21
Q

What is thyroid eye disease specific to?

A

Graves disease

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22
Q

Acromegaly second line if transpehonidal surgery doesn’t work?

A

Somatostatin analogue (octerotide)

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23
Q

Management in DKA?

A
  • fluid replacement
    • most patients with DKA are deplete around 5-8 litres
    • isotonic salineis used initially, even if the patient is severely acidotic
    • please see an example fluid regime below.
  • insulin
    • an intravenous infusion should be started at0.1 unit/kg/hour
    • once blood glucoseis < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hrin additionto the 0.9% sodium chloride regime
  • correction of electrolyte disturbance
    • serum potassium is often high on admission despite total body potassium being low
    • this often falls quickly following treatment with insulin resulting in hypokalaemia
    • potassium may therefore need to be added to the replacement fluids
    • if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required
  • long-acting insulin should be continued, short-acting insulin should be stopped
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24
Q

How much does thyorxine dose change during pregnancy?

A

Increased dose of thyroxine during pregnancy

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25
Q

Drug causes of gynaecomastia?

A
  • spironolactone (most common drug cause)
  • cimetidine
  • digoxin
  • cannabis
  • finasteride
  • GnRH agonists e.g.goserelin, buserelin
  • oestrogens, anabolic steroids
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26
Q

SGLT-2 inhibitors should also be given if any of the following apply?

A
  • the patient has a high risk of developing cardiovascular disease (CVD, e.g. QRISK ≥ 10%)
  • the patient has established CVD
  • the patient has chronic heart failure
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27
Q

What is phaeochromocytoma?

A

Rare catecholamine secreting tumour

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28
Q

Features in primary hyperaldosteronism?

A

Hypertension, hypokalaemia, metabolic acidosis

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29
Q

What is tertiary hyperparathyroidism?

A

Prologned secondary hyperpatathyroidism leading to tertiary hyperparathyroidism

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30
Q

First line for phaeochoromocytoma?

A

Give phenoxybenzamine before beta blockers

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31
Q

What is myxoedema coma?

A

Potentially fatal complication of longstanding undertreated hypothyroidism. It may be precipitated by illness, stress, and certain drugs. Apart from confusion and hypothermia, patients may have non-pitting periorbital and leg oedema, reduced respiratory drive, pericardial effusions, anaemia, seizures, and other symptoms of hypothyroidism.

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32
Q

First line treatment for diabetic neuropathy?

A

Amtitriptyline, duloxetine, gabapentin or pregabalin

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33
Q

First line for black patient with T2DM?

A

ARB like Losartan

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34
Q

Management of thyroid storm?

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

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35
Q

Management of gastroparesis in diabetic neuropathy?

A

metoclopramide, domperidone or erythromycin (prokinetic agents)

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36
Q

Adverse effects of SGLT-2 inhibitors

A

urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored

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37
Q

Drug causes of raised prolactin?

A

metoclopramide, domperidone
phenothiazines
haloperidol
very rare: SSRIs, opioids

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38
Q

Adverse effects of sulfonylureas?

A

hypoglycaemic episodes (more common with long-acting preparations such as chlorpropamide)
weight gain
hyponatraemia secondary to syndrome of inappropriate ADH secretion
bone marrow suppression
hepatotoxicity (typically cholestatic)
peripheral neuropath

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39
Q

How do sulfonylureas work?

A

Increase pancreatic insulin secretion

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40
Q

GLP-1 mimetics action?

A

drugs increase insulin secretion and inhibit glucagon secretion.

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41
Q

Major advance of GLP-1 mimetics?

A

Result in weight loss

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42
Q

most common cause of primary hyperaldosteronism

A

Bilateral idiopathic adrenal hyperplasia

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43
Q

What is aldosterone?

A

hormone that helps regulate your blood pressure by managing the levels of sodium (salt) and potassium in your blood and impacting blood volume.

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44
Q

Management of primary hyperaldosteronism?

A

adrenal adenoma: surgery (laparoscopic adrenalectomy)
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolacton

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45
Q

TD2M already on 2 drugs - if HbA1c > 58 mmol/mol then one of the following should be offered:

A

metformin + DPP-4 inhibitor + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT-2 if certain NICE criteria are met
insulin-based treatment

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46
Q

SGLT 2 inhibitors should be given in addition to metformin if the following apply?

A

the patient has a high risk of developing cardiovascular disease (CVD, e.g. QRISK ≥ 10%)
the patient has established CVD
the patient has chronic heart failure

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47
Q

What to do if metformin contraindicated?

A

If metformin is contraindicated
if the patient has a risk of CVD, established CVD or chronic heart failure:
SGLT-2 monotherapy
if the patient doesn’t have a risk of CVD, established CVD or chronic heart failure:
DPP‑4 inhibitor or pioglitazone or a sulfonylurea
SGLT-2 may be used if certain NICE criteria are met

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48
Q

Second line therapy for T2DM?

A

metformin + DPP-4 inhibitor
metformin + pioglitazone
metformin + sulfonylurea
metformin + SGLT-2 inhibitor (if NICE criteria met)

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49
Q

If triple therapy is not effective or tolerated consider what?

A

switching one of the drugs for a GLP-1 mimetic:
BMI ≥ 35 kg/m² and specific psychological or other medical problems associated with obesity or
BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months

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50
Q

Adverse effects of metofrmin?

A

Commonly GI effects
Lactic acidosis- Metformin increases lactate production and reducers lactate removal by the liver
Be careful in patients with renal impairment as worse at getting rid of lactate

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51
Q

Where does metformin act?

A

Actives ANPK. Increases insulin sensitivity

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52
Q

Action of insulin?

A

Insulin receptor agonist

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53
Q

Side effect of insulin?

A

Weight gain
Hypoglycaemia

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54
Q

Action of sulfonylureas (glybruride, glipizide)

A

Inhibit potassium ATP channels

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55
Q

Side effects of sulfonylureas (glybruride, glipizide)

A

Hypoglycaemia
Weight gain
Caution in patients with renal and hepatic disease. Metabolised in lvier and excreted by the kidneys

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56
Q

Action of GLP-1 agonists (tides)

A

Acitvates GLP-1 receptors

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57
Q

Side effects of GLP-1 agonists (tides)

A

Hypoglycaemia risk low
Weight loss
GI effects- Nausea and vomiting
Pancreatitis
Contraindicated in patients with thyroid c cell tumours (due to thyroid c cells go hyperplasia)
Decrease in cardiovascular risk- Use in cardiovascular disease with T2DM

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58
Q

Action of TZD (Glitazones)

A

PPAR gamma receptor.

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59
Q

Sie effects of TZD (Glitazones)

A

Weight gain
Oedema
Bone loss
Hepatotoxic
Increased risk for bladder cancer
Contraindicated in HF as lead to oedema
Imrpve lipid profile

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60
Q

Mechanism of action of SGLT2 inhibitors (gliflozins)

A

Inhibit SGLT-2

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61
Q

Side effects of SGLT2 inhibitors (gliflozins)

A

Weight loss
UTI
DKA
Dehydration
Hypotension
Decreased CV risk
Contraindicated in severe renal impairment

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62
Q

Mechanism of action of DPP-4 inhinbitos (gliptins)

A

Inhinbit DDP-4

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63
Q

Side effects of DPP-4 (gliptins)

A

Increased risk of infections (respiratory infection)
Rash
Angioedema

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64
Q

Mechanism of action of alpha glucosidase inhibitors (Acarbose, Miglifol)

A

Inhibit alpha glucosidase

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65
Q

Side effects of alpha glucosidase inhibitors (Acarbose, Miglifol)

A

GI effects

66
Q

Mechanism of non-sulfonylureas (glinides)

A

Inhibit potasssium ATP channel
Side effects is hypoglycaemia

67
Q

How does C-peptide differ in individuals with T1DM and T2DM?

A

C-peptide will be low in individuals with type 1 diabetes mellitus (as the pancreas is not making enough insulin precursor, which breaks down to form C-peptide and insulin) , and normal or high in individuals with type 2 mellitus.

68
Q

Hyponatraemia and hyperkalaemia in a patient with lethargy is highly suggestive of WHAT?

A

Addisons

69
Q

Definitive investigation for Addisons?

A

ACTH stimulation test (short Synacthen test)

70
Q

Adverse effects of SGLT2 inhibitors?

A

urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored

71
Q

The definitive management of primary hyperparathyroidism is what?

A

Total parathyroidectomy

72
Q

DKA resolution is defined as what?

A

pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L

73
Q

How quickly should ketonaemia and acidosis resolve in DKA?

A

Within 24 hours

74
Q

What is. along synacthen test used for?

A

used to differentiate adrenal from pituitary causes of Addison’s disease.

75
Q

Features of primary hyperaldosteronism?

A

hypertension
increasingly recognised but still underdiagnosed cause of hypertension
hypokalaemia
e.g. muscle weakness
this is a classical feature in exams but studies suggest this is seen in only 10-40% of patients, and is more common with adrenal adenomas
metabolic alkalosis

76
Q

Acromegaly investigations?

A

Serum IGF-1 levels have now overtaken the oral glucose tolerance test (OGTT) with serial GH measurements as the first-line test. The OGTT test is recommended to confirm the diagnosis if IGF-1 levels are raised.

77
Q

Possible causes of cushing’s?

A

iatrogenic: corticosteroid therapy
ACTH-dependent causes
Cushing’s disease (a pituitary adenoma → ACTH secretion)
ectopic ACTH secretion secondary to a malignancy
ACTH-independent causes
adrenal adenoma

78
Q

Tests for cushings?

A

overnight dexamethasone suppression test
this is the most sensitive test and is now used first-line to test for Cushing’s syndrome
patients with Cushing’s syndrome do not have their morning cortisol spike suppressed
24 hr urinary free cortisol

79
Q

Features seen in Graves’ but not in other causes of thyrotoxicosis

A

eye signs (30% of patients): exophthalmos and ophthalmoplegia
pretibial myxoedema
thyroid acropachy, a triad of:
digital clubbing
soft tissue swelling of the hands and feet
periosteal new bone formation

80
Q

Autoantibodies in graves?

A

TSH receptor stimulating antibodies (90%)
anti-thyroid peroxidase antibodies (75%)

81
Q

Bloods in primary hyperparathyroidism?

A

raised calcium, low phosphate
PTH may be raised or (inappropriately, given the raised calcium) normal

82
Q

Best prognosis for thyroid cancer?

A

Papillary

83
Q

Features of prolactinomas?

A

excess prolactin in women
amenorrhoea
infertility
galactorrhoea
osteoporosis

excess prolactin in men
impotence
loss of libido
galactorrhoea

other symptoms may be seen with macroadenomas
headache.
visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia)
symptoms and signs of hypopituitarism

84
Q

Management of a prolactonoma?

A

Dopamine agonists
Cabergoline

85
Q

What does Nuclear scintigraphy reveals patchy uptake suggest?

A

Toxic multinodular goitre

86
Q

Features of Kallman syndrome?

A

‘delayed puberty’
hypogonadism, cryptorchidism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above-average height

87
Q

Good side effect of SGLT-2s?

A

Lose weigjht

88
Q

Examples of SLGT-2 inhibitors?

A

canagliflozin, dapagliflozin and empagliflozin

89
Q

Adverse effects of thiazolidediones?

A

weight gain
liver impairment: monitor LFTs
fluid retention - therefore contraindicated in heart failure. The risk of fluid retention is increased if the patient also takes insulin
recent studies have indicated an increased risk of fractures
bladder cancer: recent studies have shown an increased risk of bladder cancer in patients taking pioglitazone (hazard ratio 2.64)

90
Q

Drugs causing gynaecomastia?

A

spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids

91
Q

Bad side effect of DKA especially oin young patients?

A

Cerebral oedema

92
Q

Non-functioning pituitary tumours present with what?

A

hypopituitarism and pressure effects

93
Q

DM diagnosis?

A

fasting > 7.0, random > 11.1 - if asymptomatic need two readings

94
Q

Management of a thyroi storm?

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

95
Q

Complications of hyperosmolar hyperglycaemic state?

A

vascular complications may occur due to hyperviscosity:
such as myocardial infarction
stroke

96
Q

How much can metformin be titrated up to?

A

500mg TDS

97
Q

HHS is characterised by what?

A

1.) Severe hyperglycaemia
2.) Dehydration and renal failure
3.) Mild/absent ketonuria

98
Q

Management of HHS?

A

fluid replacement
fluid losses in HHS are estimated to be between 100 - 220 ml/kg
IV 0.9% sodium chloride solution
typically given at 0.5 - 1 L/hour depending on clinical assessment
potassium levels should be monitored and added to fluids depending on the level

insulin
should not be given unless blood glucose stops falling while giving IV fluids

venous thromboembolism prophylaxis
patients are at risk of thrombosis due to hyperviscosity

99
Q

Gliptins memory aid?

A

GLiPtINs = keep the GLPs-IN

100
Q

What is Sick euthyroid syndrome

A

most commonly seen in chronically ill patients or those with starvation. The thyroid function tests are often low and the patient clinically euthyroid.

101
Q

What is adison’s disease?

A

Autoimmune destruction of the adrenal glands is the commonest cause of primary hypoadrenalism in the UK, accounting for 80% of cases. This is termed Addison’s disease and results in reduced cortisol and aldosterone being produced.

102
Q

Features of addisons disease?

A

lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia

103
Q

What is a phaeochromocytoma?

A

rare catecholamine secreting tumour. About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome

104
Q

Tests for phaeochromocytoma?

A

24 hr urinary collection of metanephrines (sensitivity 97%*)
this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)

105
Q

Management of phaechromocytoma?

A

Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)

106
Q

Insulin treatment in DKA?

A

an intravenous infusion should be started at 0.1 unit/kg/hour
once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime

107
Q

Autoantibodies in graves disease

A

TSH receptor stimulating antibodies (90%)
anti-thyroid peroxidase antibodies (75%)

108
Q

TSH and T3 and T4 levels in sick euthyroid syndrome?

A

In the majority of cases however the TSH level is within the >normal range (inappropriately normal given the low thyroxine and T3).

109
Q

High dose dexamaethasone suppresssion test possible results

A
110
Q

What to do if diarrhoea from metformin?

A

Start metformin modified release

111
Q

MEN1 features

A

Peptic ulceration, galactorrhoea, hypercalcaemia
3Ps

112
Q

What thyroid cancer is part of MEN2?

A

Medullary

113
Q

What PTH does?

A

Increased gut absorption of calcium
Increased reabsorption of calcium in kidney
Increased osteoclast activity. Increased absorption calcium
Basically raises calcium level

114
Q

Causes of secondary hyperparathyroidism

A

Decreased vit D or chronic renal failure

115
Q

Why does tertiary hyperparathyroidism occur?

A

Caused by long term secondary hyperparathyroidism
Hyperplasia of parathyroid gland

116
Q

Finger features in graves

A

thyroid acropachy, a triad of:
digital clubbing
soft tissue swelling of the hands and feet
periosteal new bone formation

117
Q

normal fT3 and fT4 levels suggest what?

A

Normal thyroid function

118
Q

What is sick euthyroid syndrome?

A

is often said that everything (TSH, thyroxine and T3) is low. In the majority of cases however the TSH level is within the >normal range (inappropriately normal given the low thyroxine and T3).

Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed.

119
Q

First line for peripheral neuropathy?

A

amitriptyline, duloxetine, gabapentin or pregabalin

120
Q

DKA insulin infusion rate

A

01 unit/kg/hr

121
Q

Management of primary hyperparathyrodisim?

A

the definitive management is total parathyroidectomy
conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage
patients not suitable for surgery may be treated with cinacalcet, a calcimimetic
a calcimimetic ‘mimics’ the action of calcium on tissues by allosteric activation of the calcium-sensing receptor

122
Q

Mmeory aid for diabetes medications that cause weight gain?

A

‘the fat flows with the tides’
SGLT2- flozins
GLP-1 - tides

123
Q

Thryoid storm management?

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

124
Q

best test to diagnosis Cushing’s syndrome

A

The low-dose (overnight) dexamethasone suppressio

125
Q

Features of insulinoma?

A

of hypoglycaemia: typically early in morning or just before meal, e.g. diplopia, weakness etc
rapid weight gain may be seen
high insulin, raised proinsulin:insulin ratio
high C-peptide

126
Q

Side-effects of thyroxine therapy

A

hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation

127
Q

Causes of primary hyperparathyroidism

A

85%: solitary adenoma
10%: hyperplasia
4%: multiple adenoma
1%: carcinoma

128
Q

Myxoedemic coma is treated with what?

A

thyroxine and hydrocortisone

129
Q

Features of myxoedema coma?

A

severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs

130
Q

Medullary thyroid cancers often secrete what?

A

Calcitonin

131
Q

What drug is used In pregnant woman who develop hyperthyroidism in the first trimester?

A

Propylthiouracil

132
Q

First line test for acromegaly?

A

Serum IGF-1

133
Q

Optimal treatment in HNF1A-MODY?

A

Sulfonylureas

134
Q

Glucocorticoid side-effects

A

endocrine: impaired glucose regulation, increased appetite/weight gain, hirsutism, hyperlipidaemia
Cushing’s syndrome: moon face, buffalo hump, striae
musculoskeletal: osteoporosis, proximal myopathy, avascular necrosis of the femoral head
immunosuppression: increased susceptibility to severe infection, reactivation of tuberculosis
psychiatric: insomnia, mania, depression, psychosis
gastrointestinal: peptic ulceration, acute pancreatitis
ophthalmic: glaucoma, cataracts
dermatological: acne
suppression of growth in children
intracranial hypertension
neutrophilia

135
Q

first-line investigation in suspected primary hyperaldosteronism

A

plasma aldosterone/renin ratio

136
Q

What to monitor in hypothyroidism?

A

TSH

137
Q

Causes of pseudo cushings?

A

often due to alcohol excess or severe depression

138
Q

Hashimoto’s thyroiditis is associated with what?

A

Thyroid lymphoma

139
Q

The Hba1c target for patients on a drug which may cause hypoglycaemia (eg sulfonylurea) is what?

A

53

140
Q

What do low levels of C peptide indicate?

A

result of the cleavage of proinsulin into insulin. Very low levels indicate the absolute absence of insulin, indicating type 1 diabetes mellitus.

141
Q

Adverse effects of carbimazole?

A

Agranulocytosis

142
Q

What is used to confirm the diagnosis of acromegaly if IGF-1 levels are raised.

A

OGTT

143
Q

Blood tests useful to distinguish between type 1 and type 2 diabetes

A

C-peptide levels and diabetes-specific autoantibodies

144
Q

Sulfonyeureas (tides) adverse effects?

A

hypoglycaemic episodes (more common with long-acting preparations such as chlorpropamide)
weight gain
Think about the rising tide being weight gain

145
Q

Features f hyperosmolar hyperglycaemic state

A

hypovolaemia
marked hyperglycaemia (>30 mmol/L)
significantly raised serum osmolarity (> 320 mosmol/kg)
can be calculated by: 2 * Na+ + glucose + urea
no significant hyperketonaemia (<3 mmol/L)
no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 – acidosis can occur due to lactic acidosis or renal impairment)

146
Q

In primary polydypsia results in a water deprivation test?

A

water deprivation will cause urine osmolality to be high. Desmopressin does not need to be given. A high urine osmolality after water deprivation rules out diabetes insipidus.

147
Q

In cranial DI results in a water deprivation test?

A

Patient lacks ADH. The kidneys are still capable of responding to ADH. Initially, the urine osmolality remains low as it continues to be diluted by the excessive water lost in the urine. After desmopressin is given, the kidneys respond by reabsorbing water and concentrating the urine. The urine osmolality will be high.

148
Q

In neprhogenic DI results in a water deprivation test?

A

Patient is unable to respond to ADH. The urine osmolality will be low both before and after the desmopressin is given.

149
Q

First line for prolactonomas?

A

Dopamine agonists (e.g. cabergoline, bromocriptine)

150
Q

DKA resolution is defined as:

A

pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L

151
Q

Features of Kallman’s syndrome?

A

‘delayed puberty’
hypogonadism, cryptorchidism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above-average height

152
Q

Management of phaechromocytoma?

A

Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)

153
Q

Investigations for phaechromocytoma?

A

24 hr urinary collection of metanephrines (sensitivity 97%*)
this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)

154
Q

A 55-year-old man presents to the GP for a review. It is found that his fasting glucose is elevated at 8.3 mmol/L. He feels well and has no polyuria or polydipsia.

He has a past medical history of a myocardial infarction and smokes 10 cigarettes a day and drinks 12 units of alcohol a week. His BMI is 34 kg/m².

What is the most appropriate next step for the GP to take?

A

Remeasure the blood glucose

155
Q

Endocrine parameters reduced in stress response:

A

Insulin
Testosterone
Oestrogen

156
Q

In T2DM if a triple combination of drugs has failed to reduce HbA1c then switching one of the drugs for what is recommended?

A

GLP-1 mimetic is recommended, particularly if the BMI > 35

157
Q

Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than what?

A

7

158
Q

Impaired glucose tolerance (IGT) is defined as an OGTT of what?

A

2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

159
Q

What is Nelson’s syndrome?

A

Rapid enlargement of a pituitary corticotroph adenoma (ACTH producing adenoma) that occurs after the removal of both adrenal glands (bilateral adrenalectomy) which is an operation used for Cushing’s syndrome. Removal of both adrenal glands eliminates the production of cortisol, and the lack of cortisol’s negative feedback can allow any pre-existing pituitary adenoma to grow unchecked. Continued growth can cause mass effects due to physical compression of brain tissue. Increased production of adrenocorticotrophic hormone (ACTH) can result in increased melanocyte stimulating hormone (MSH) which can result in hyperpigmentation

160
Q

The osteoporosis guidelines state if a postmenopausal woman has a fracture what should. be done?

A

Give bisphosphonates

161
Q

first-line for black TD2M patients who are diagnosed with hypertension

A

ARB

162
Q

What is the main drug that can’t be taken with lithium?

A

NSAIDs

Year 4 Final (39 decks)

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