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Yr 3 - Pharmacology > Drugs - Endocrine > Flashcards

Drugs - Endocrine Flashcards

1
Q

In an unconscious patient with suspected severe hypoglycaemia, what is the 1st line pharmacological management?

A

IV glucose (e.g. 150-160 ml of 10% glucose)

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2
Q

If IV access is not able to be established rapidly in an unconscious patient with suspected hypoglycaemia, what can be administered instead?

A

administer glucagon 1mg via IM or SC route

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3
Q

In a conscious patient with suspected hypoglycaemia, what is the 1st line pharmacological management?

A

Administer glucose gel by mouth (e.g. GlucoGel)

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4
Q

How does glucagon treat hypoglycaemia?

A

This is a natural hormone that stimulates hepatic glycogenolysis and gluconeogenesis.

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5
Q

What are the 4 main indications for inuslin?

A
  • Insulin replacement in type 1 diabetes
  • Control of blood glucose in type 2 diabetes
  • Treatment of diabetic emergencies (e.g. DKA) → given IV
  • Alongside glucose to treat hyperkalaemia while are other measures (e.g. treatment of underlying cause) are initiated
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6
Q

In what conditions would insulin be prescribed in type 2 diabetes?

A

where oral hypoglycaemic treatment is inadequate or poorly tolerated

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7
Q

What should insulin be administered alongside in the treatment of hyperkalaemia?

A

Glucose (to prevent hypoglycaemia)

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8
Q

Mechanism of insulin in hyperkalaemia?

A
  • Insulin drives K+ into cells reducing serum K+ concentrations
  • This a short-term solution – when insulin is stopped, K+ leaks back out of the cells into the circulation
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9
Q

Mechanism of insulin in T1DM?

A

Mimics endogenous insulin produced by beta cells of the pancreas (T1D involves autoimmune destruction of beta cells of pancreas) by binding to insulin receptor:

  • Stimulates glucose uptake from circulation into tissues, including skeletal muscle and fat
  • Increases use of glucose as an energy source
  • Stimulates glycogen, lipid and protein synthesis and inhibits gluconeogenesis and ketogenesis
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10
Q

Why is insulin considered a high risk drug?

A
  • Risk of hypoglycaemia (overdose) → Can cause life threatening seizures and coma
  • Risk of hyperglycaemia (due to under-dose) → Can lead to life threatening DKA
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11
Q

Is blood glucose too high or low in DKA?

A

High

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12
Q

Give some symptoms of hypoglycaemia

A
  • Sweating, dizziness, shakiness, hunger, tachycardia, tingling in hands/feet/lips or tongue
  • Blurred vision, trouble concentration, confusion
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13
Q

Can insulin be taken in renal impairment?

A

Insulin is renally excreted - insulin clearance is reduced so increased risk of hypoglycaemia.

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14
Q

Indication for metformin?

A

Type 2 diabetes

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15
Q

What is the 1st choice medication for control of blood glucose in T2DM when lifestyle changes alone have not helped?

A

Metformin

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16
Q

What class of drug is metformin?

A

Biguanide

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17
Q

What is the main mechanism by which metformin reduces blood glucose?

A

By reducing hepatic glucose output

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18
Q

How does metformin reduce hepatic glucose output?

A

Inhibits glycogenolysis (breakdown of glycogen into glucose) and gluconeogenesis (production of glucose).

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19
Q

What is the minor mechanism by which metformin reduces blood glucose?

A

Increases glucose uptake and utilisation by skeletal muscle

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20
Q

Does metformin cause hypoglycaemia? Why?

A

No - Does NOT stimulate insulin secretion

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21
Q

Most common side effects of metformin?

A
  • GI upset – N&V, diarrhoea
  • Taste disturbance
  • Can sometimes lead to weight loss
  • Lactic acidosis
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22
Q

Contraindications of metformin?

A
  • Renal impairment – dosage reduction required if eGFR <45
  • AKI
  • Severe tissue hypoxia e.g. cardiac failure, sepsis
  • Acute alcohol intoxication
  • Chronic alcohol abuse  risk of hypoglycaemia
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23
Q

How is metformin eliminated?

A

Excreted unchanged in the urine (kidney function required)

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24
Q

What complication of metformin is more likely if metformin is taken in the context of renal impairment?

A

Lactic acidosis

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25
Q

Which diabetic drug should be stopped prior to imaging with contrast (e.g. CT scans, coronary angiography). Why?

A

Metformin → increased risk of renal impairment (contrast is nephrotoxic), metformin accumulation and lactic acidosis

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26
Q

Explanation of mechanism of metformin to patient:

A
  • Reduces amount of sugar produced by cells in the liver
  • Increases sensitivity of muscle cells to insulin – enabling cells to remove sugar from blood more effectively
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27
Q

What is initial treatment for T2DM?

A

A healthy diet with increased physical activity, promoting weight loss if applicable, and this should be tried for at least 3 months before commencing drug therapy

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28
Q

What is the HbA1c threshold for pharmacological therapy?

A

48 mmol/mol

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29
Q

Does metformin cause weight gain? Why?

A

No - has no effect on insulin

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30
Q

Why does insulin and drugs which cause insulin secretion (e.g. sulphonylureas) cause weight gain?

A

Insulin is an anabolic hormone

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31
Q

What class of drug is gliclazide?

A

Sulphonylurea

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32
Q

Indication for gliclazide?

A

T2DM:

  • In combination with metformin (and/or other hypoglycaemic agents) where blood glucose is not adequately controlled
  • As a single agent to control blood glucose and reduce complications where metformin is contraindicated
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33
Q

Mechanism of sulphonylureas?

A

Sulphonylureas lower blood glucose by stimulating pancreatic insulin secretion (through the beta cell sulphonylurea receptor):

  • They block ATP-dependent K+ channels in pancreatic B cell membranes, causing depolarisation of the cell membrane and opening of voltage-gated Ca2+ channels
  • This increases intracellular Ca2+ concentrations, stimulating insulin secretion
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34
Q

Does gliclazide cause weight gain? Why can this negatively affect diabetes?

A

Yes - insulin is an anabolic hormone so stimulation of insulin secretion by sulphonylureas is associated with weight gain

Weight gain can increase insulin resistance and worsen DM long-term.

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35
Q

Can gliclazide cause hypoglycaemia?

A

Yes

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36
Q

Metformin vs gliclazide in risk of developing CVS disease?

A

Metformin - no increased risk

Gliclazide - increased risk of CVS disease and MI when used as monotherapy (i.e. on its own (hence why not given 1st line)

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37
Q

Side effects of gliclazide?

A
  • Weight gain
  • GI upset – N&V, diarrhoea, constipation
  • Hypoglycaemia (Risk increased if drug metabolism is reduced (hepatic impairment) or other hypoglycaemics are prescribed)
  • Hypersensitivity reactions:
    • Hepatic toxicity – cholestatic jaundice
    • Drug hypersensitivity syndrome – rash, fever, internal organ involvement
  • Increased risk of CVS disease and MI when used as monotherapy (i.e. on its own)
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38
Q

Contraindications for gliclazide?

A
  • Hepatic impairment – gliclazide is metabolised in the liver
  • Renal impairment – gliclazide is excreted in the urine
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39
Q

What class of drug is pioglitazone?

A

Thiazolidinediones (Glitazones)

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40
Q

Indication of pioglitazone?

A

Type 2 diabetes mellitus (alone or in combination with metformin or a sulfonylurea)

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41
Q

Mechanism of pioglitazone?

A
  • Reduces insulin resistance and improves insulin sensitivity, allowing the insulin that the body produces to work more effectively
  • Helps protect cells in the pancreas, allowing them to produce insulin for longer
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42
Q

Main 2 indications of levothyroxine?

A
  • 1ary Hypothyroidism
  • Hypothyroidism 2ary to hypopituitarism
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43
Q

Is levothyroxine synthetic T4 or T3?

A

T4

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44
Q

Is T3 or T4 active?

A

Thyroid gland produces thyroxine (T4) which is converted to the more active triiodothyronine (T3) in target tissues

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45
Q

Where is T4 converted to T3?

A

In target tissues

46
Q

Another name for T4?

A

Thyroxine

47
Q

Side effects of levothyroxine?

A

Overtreatment:

  • GI (e.g. diarrhoea, vomiting, weight loss)
  • Cardiac (e.g. palpitations, arrhythmias, angina)
  • Neurological (e.g. tremor, restlessness, insomnia)
48
Q

2 main contraindications of levothyroxine?

A
  • Coronary artery disease
  • Hypopituitarism
49
Q

Why is levothyroxine contraindicated in coronary artery disease?

A
  • Thyroid hormones increase heart rate and metabolism
  • Can precipitate cardiac ischaemia
50
Q

Why is levothyroxine contraindicated in hypopituitarism?

A

Corticosteroid therapy must be initiated before thyroid hormone replacement to avoid precipitating an Addisonian crisis

51
Q

How can cytochrome P450 inducers (e.g. phenytoin, carbamazepine) affect levothyroxine?

A

may need a higher dose of levothyroxine

52
Q

How does levothyroxine interact with antacids, calcium and iron salts?

A

reduces GI absorption of levothyroxine

53
Q

How can levothyroxine affect warfarin?

A

levothyroxine can enhance effects of warfarin

54
Q

Is levothyroxine treatment for hypothyroidism for life?

A

Yes

55
Q

What is the 1st line pharmacological treatment in hyperthyroidism?

A

Carbimazole

56
Q

Mechanism of carbimazole?

A

Inhibits thyroid peroxidase (TPO) that catalyses the iodination of tyrosine residues in thyroglobulin and the oxidative coupling of iodinated tyrosine

57
Q

Side effects of carbimazole?

A
  • Bone marrow disorders
  • Haemolytic anaemia
  • Severe cutaneous adverse reactions (SCARs)
  • Thrombocytopenia
58
Q

What class of drug are Alendronic acid, disodium pamidronate, zoledronic acid?

A

Bisphosphonates

59
Q

What is the 1st line drug treatment option for patients at risk of osteoporotic fragility fractures?

A

Alendronic acid

60
Q

What are 3 other indications for bisphosphonates?

A
  • Used in treatment of severe hypercalcaemia of malignancy after appropriate IV rehydration
  • For patients with myeloma and breast cancer with bone metastases → reduces risk of pathological fractures, cord compression and the need for radiotherapy or surgery
  • 1st line treatment of metabolically active Paget’s disease with the aim of reducing bone turnover and pain
61
Q

What is the 1st line treatment of metabolically active Paget’s disease?

A

Bisphosphonates

62
Q

Mechanism of bisphosphates?

A
  • Bisphosphonates reduce bone turnover by inhibiting the action of osteoclasts (the cells responsible for bone resorption).
  • Bisphosphonates have a similar structure to naturally occurring pyrophosphate – hence they are readily incorporated into bone.
  • As bone is resorbed, bisphosphonates accumulate in osteoclasts, where they inhibit activity and promote apoptosis → net effect is reduction in bone loss and improvement in bone mass
63
Q

What cell does bisphosphonates inhibit the action of?

A

Osteoclasts

64
Q

What are osteoclasts responsible for?

A

bone resorption

65
Q

Why are bisphosphonates readily incorporated into bone?

A

have a similar structure to naturally occurring pyrophosphate

66
Q

What are 2 common side effects of bisphosohonates?

A
  • Oesophagitis (when taken orally)
  • Hyperphosphataemia
67
Q

What are 2 rare but serious side effects of bisphosohonates?

A
  1. Osteonecrosis of the jaw
  2. Atypical femoral fracture
68
Q

When is osteonecrosis of the jaw more likely?

A

WIth high dose IV therapy

69
Q

What is important in minimising the risk of osteonecrosis of the jaw?

A

Good dental hygiene

70
Q

Contraindications of bisphosphonates?

A
  • Severe renal impairment – are renally excreted
  • Hypocalcaemia
  • Upper GI disorders (oral)
  • Smokers & dental disease → due to risk of jaw osteonecrosis (prescribe with caution)
71
Q

effect of bisphosphonates on calcium levels?

A

By inhibiting bone resorption, bisphosphonates reduce calcium efflux from bone into the circulation, leading to the development of hypocalcemia.

72
Q

Main interaction of bisphosphonates?

A

Bisphosphonates bind calcium → their absorption is reduced if taken with calcium salts (including milk) as well as antacids and iron salts

73
Q

What should be checked before commencing bisphosphonates?

A

Vitamin D and calcium levels

74
Q

What scan is used to monitor efficacy of bisphosphonates?

A

DEXA scans

75
Q

In women aged >75 years who have had a fragility fracture, is a DEXA scan necessary?

A

No - can assume a diagnosis of osteoporosis and start treatment with a bisphosphonate without need for further investigation.

76
Q

What are alfacalcidol and colecaliferol?

A

Vitamin D analogues

77
Q

2 major indications for calcium AND vitamin D?

A
  • Osteoporosis
  • CKD
78
Q

Why is calcium & vitamin D indicated in osteoporosis?

A

To ensure positive calcium benefit when dietary intake and/or sunlight exposure are insufficient

Other treatments e.g. bisphosphonates may also be given

79
Q

How does vitamin D affect calcium?

A

Vitamin D is needed for the absorption of calcium from the gut

80
Q

Why is calcium & vitamin D indicated in CKD?

A

To treat and prevent 2ary hyperparathyroidism and renal osteodystrophy

81
Q

What is calcium gluconate indicated in?

A

severe hyperkalaemia to prevent life-threatening arrhythmias

82
Q

What other treatments can be given alonside calcium gluconate in severe hyperkalaemia?

A

Insulin with glucose are given to lower potassium concentration

83
Q

Indications for calcium?

A
  • Severe hyperkalaemia (calcium gluconate)
  • Hypocalcaemia that is symptomatic or severe
84
Q

Symptoms of hypocalcaemia?

A

paresthesia, tetany, seizures

85
Q

What is calcium essential for?

A

is essential for normal function of muscle, nerves, bone, and clotting

86
Q

What is calcium homeostasis controlled by?

A
  • Parathyroid hormone & vitamin D → increase serum calcium levels and bone mineralisation
  • Calcitonin → reduces serum calcium levels (released in hypercalcaemia)
87
Q

How does CKD affect vitamin D?

A

Impaired activation of vitamin by kidneys → reduced absorption of calcium from gut

88
Q

How does CKD affect phosphate and calcium levels?

A

impaired phosphate excretion and reduced vitamin D activation cause hyperphosphataemia and hypocalcaemia

89
Q

How does CKD affect PTH levels?

A

Hypocalcaemia triggers 2ary hyperparathyroidism

90
Q

What is the effect of 2ary hyperparathyroidism in severe CKD?

A

Leads to a range of bone changes called renal osteodystrophy

91
Q

How can oral calcium supplements manage hyperphosphataemia in CKD?

A

oral calcium supplements to bind phosphate in the gut

92
Q

How can alfacalcidol be useful in CKD?

A

alfacalcidol can provide vitamin D that does not depend on renal activation → treats hypocalcaemia

93
Q

Compare the mineralocorticoid vs glucocorticoid activity of fludrocortisone

A

very high mineralocorticoid activity and insignificant glucocorticoid activity

94
Q

Indications of fludrocortisone?

A
  • Used to help control the amount of sodium and fluids in your body
  • Neuropathic postural hypotension
  • Addison’s disease and syndromes where excessive amounts of sodium are lost in the urine (i.e. mineralocorticoid replacement in adrenocortical insufficiency)
95
Q

Mechanism of fludrocortisone?

A

Decreases amount of sodium lost in urine by increasing reabsorption by the kidney.

96
Q

A 55 y/o man attends the GP for a planned review. 3 months ago, he was found to have type 2 diabetes and has since made concerted efforts to follow lifestyle advice. You advise him to have a blood test to measure HbA1c concentration. What HbA1c threshold best describes the level at which pharmacological therapy should be offered?

  1. 28 mmol/mol
  2. 48
  3. 53
  4. 58
  5. 64
A

48 mmol/mol

97
Q

A 56 y/o woman was diagnosed with type 2 diabetes 3 months ago. She has a BMI of 27 and no known allergies. Despite lifestyle changes, her blood glucose control is poor and her HbA1c is below target. She has normal renal function. Her GP advises her to commence pharmacological therapy. What drug would be the most appropriate initial therapy?

  1. Acarbose
  2. Gliclazide
  3. Insulin
  4. Metformin
  5. Sitagliptin
A

Metformin

98
Q

Why is metformin preferred over sulphonylureas as the 1st choice for T2DM?

A
  • Metformin is 1st choice for T2DM as it lowers blood glucose without causing weight gain or hypoglycaemia. It is associated with a decreased risk of CVS mortality and is cheap.
  • Sulfonylureas (e.g. gliclazide) lowers blood glucose by stimulating pancreatic insulin secretion. This is associated with weight gain and increased risk of hypoglycaemia.
99
Q

A 45 y/o man with T2DM is taking metformin. What is the main means by which metformin lowers blood glucose concentrations?

  1. Increased pancreatic insulin secretion
  2. Increased peripheral insulin sensitivity
  3. Increased urinary glucose excretion
  4. Reduced hepatic glucose output
  5. Reduced intestinal glucose absorption
A

reduced hepatic glucose output

100
Q

An 84 y/o woman has started taking anastrozole, after being found to have advanced breast cancer. What best describes the mechanism of action of anastrozole?

  1. 5a-reductase inhibitor
  2. Aromatase inhibition
  3. Inhibition of ergosterol synthesis
  4. LH/FSH suppression
  5. Selective oestrogen receptor modulation
A

Aromatase inhibition

101
Q

A 78 y/o man is admitted to the ED with loss of consciousness and is found to have a blood glucose concentration of 1.2 mmol/L/. His usual medications are bendroflumethiazide, bisoprolol, gliclazide, metformin and prednisolone. What drug is most likely to have caused his hypoglycaemia?

  1. Bendroflumethiazide
  2. Bisoprolol
  3. Gliclazide
  4. Metformin
  5. Prednisolone
A

Gliclazide

102
Q

What class of drug can mask the symptoms of hypoglycaemia (sweating, shaking, tachycardia, anxiety)?

A

Beta blockers

103
Q

A 50 y/o man presents to review the results of recent blood tests. He has a PMH of T2DM and HTN. He takes metformin 1g 2x daily and ramipril 10mg daily. Investigations: creatinine 148 (60-110), eGFR 44 (>60). What complication is more likely if metformin is taken in the context of renal impairment?

  1. DKA
  2. Hypersensitivity reaction
  3. Lactic acidosis
  4. Megaloblastic anaemia
  5. Respiratory alkalosis
A

Lactic acidosis

104
Q

A 70 y/o woman presents with abdominal pain and shock. A surgical cause is suspected, and she is placed ‘nil by mouth’ while arrangements for an emergency laparotomy are made. She has a PMH of polymyalgia rheumatica. She has taken prednisolone 5mg daily for several years but none in the last 3 days because of nausea. What is the most appropriate option for immediate steroid replacement?

  1. Budesonide
  2. Fludrocortisone
  3. Fluticasone
  4. Hydrocortisone
  5. Prednisolone
A

Hydrocortisone

105
Q

Why can chronic use of systemic corticosteroids lead to adrenocortical atrophy?

A
  • Medically administered systemic corticosteroids suppress hypothalamic secretion of CRH and pituitary secretion of ACTH
  • When taken chronically, prolonged suppression of ACTH release leads to adrenocortical atrophy
106
Q

If long-term exogenous steroids are stopped abruptly, what can happen?

A

If the exogenous steroid is stopped abruptly, the atrophied adrenal glands may be unable to meet this need → acute adrenal insufficiency (Addisonian crisis) which may cause hypotension and various non-specific symptoms (e.g. confusion, weakness, nausea, abdominal pain)

107
Q

A 28 y/o woman is started on Tamoxifen for locally advanced oestrogen-receptor positive breast cancer. What is the most appropriate advice to give her regarding potential side effects?

  1. It can stimulate milk production from her breasts
  2. It causes infertility
  3. It is safe to take during pregnancy
  4. There is an increased risk of cancer of the lining of the womb
  5. There is an increased risk of ovarian cancer
A

There is an increased risk of cancer of the lining of the womb

108
Q

A 58 y/o man with T2DM is taking metformin and gliclazide. Despite this, his blood glucose is poorly controlled, and his GP advises him to commence saxagliptin, a DPP-4 inhibitor. His PMH includes COPD, CCF, fatty liver, gout and pancreatitis. Which medical condition is a relative contraindication to DPP-4 inhibitor?

  1. COPD
  2. CCF
  3. Fatty liver
  4. Gout
  5. Pancreatitis
A

Pancreatitis → A rare adverse effect of DPP-4 inhibitors is acute pancreatitis

109
Q

A 72 y/o woman is admitted with a suspected PE and requires a CT pulmonary angiogram with contrast. She is taking Alendronic acid, atorvastatin, diltiazem, metformin and ramipril. What drug should be withheld now and for 48 hours after the procedure?

  1. Alendronic acid
  2. Atorvastatin
  3. Diltiazem
  4. Metformin
  5. Ramipril
A

metformin → there is an increased risk of renal impairment due to contrast nephropathy – this can lead to metformin accumulation and lactic acidosis

110
Q

A 66 y/o woman with a new diagnosis of T2DM sees her GP to commence treatment with an oral hypoglycaemic drug. She has been researching options on the internet and asks what the difference is between metformin and a sulphonylurea. What statement about metformin compared with a sulphonylurea is most correct?

  1. It causes more weight gain
  2. It is associated with a lower risk of abdominal side effects
  3. It is associated with a lower risk of death from CVS complications
  4. It is associated with an increased risk of hypoglycaemia
  5. It is more expensive
A

It is associated with a lower risk of death from CVS complications

111
Q

Why do bisphosphonates lead to hyperphosphataemia?

A

Bisphosphonates lead to hypocalcaemia due to reduced osteoclast activity. Hypocalcaemia means there is less calcium to bind excess phosphate in the gut.

Yr 3 - Pharmacology (18 decks)

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