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3rd Year Drugs > Endocrine Drugs > Flashcards

Endocrine Drugs Flashcards

1
Q

Indications of Insulin

A

1) Type 1 DM, or Type 2 DM when control of blood glucose is inadequate with oral hypoglycaemic treatment
2) Diabetic emergencies –> give IV
3) Hyperkalaemia –> give with glucose and calcium gluconate

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2
Q

How does insulin work

A

Functions similar to endogenous insulin
Stimulates glucose uptake from circulation into tissues
Increases use of glucose as an energy source

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3
Q

How does insulin treat hyperkalaemia

A

Drives potassium into cells (however only short term)

Once insulin is stopped potassium leaks back out hence need to start other treatment

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4
Q

What are the adverse effects of insulin

A

Hypoglycaemia –> can lead to coma/death

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5
Q

What are the warnings of using insulin

A

Renal impairment - insulin clearance is reduced hence higher risk of hypoglycaemia

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6
Q

Interactinos of insulin

A

1) Other hypoglycaemics

2) Systemic corticosteroids –> corticosteroids increase glucose in blood sugar

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7
Q

How often should you check HbA1c?

A

At least annually

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8
Q

Name bisphosphonates

A

Alendronic Acid
Disodium pamidronate
Zoledronic acid

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9
Q

What is disodium pamidronate

A

A bisphosphonate

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10
Q

Indications for bisphosphonates

A

1) Osteoporotic fragility fracture risk - 1st line
2) Severe hypercalcaemia of malignancy - use pamedronate and zoledronic
3) Myeloma + breast cancer with bone metastases
4) Paget’s disease - 1st line treatment if metabolically active

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11
Q

What should we treat severe hypercalcaemia of malginancy with

A

Pamedronate and coledronic acid

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12
Q

What should we treat myeloma and breast cancer with metastases with

A

Pamidronate and zoledronic acid

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13
Q

How do bisphosphonates work?

A

Inhibits the action of osteoclasts (osteoclasts break down bone) –> hence bone turnover is decreased

Bisphopshonates have a similar structure to natural pyrophosphate –> they are readily incorporated into bone –> when bone is resorbed the bisphosphonates accumulate in the osteoclasts –> these inhibit their activity and promote apoptosis

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14
Q

What is the net effect of bisphosphoantes

A

Reduction in bone loss

Improvement in bone mass

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15
Q

Adverse effects of bisphosphonates

A

1) Oesophagitis (if taken orally)
2) Hypophosphataemia
3) Jaw osteonecrosis (rare and mroe likely if given high dose IV)
4) Atypical femoral fracture - rare but important

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16
Q

Contraindications of bisphosphonates

A

1) Severe renal impairment - they are renally excreted
2) Hypocalcaemia
3) Oral administration in upper GI disorders

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17
Q

What is the effect of osteoclasts

A

They break down bone

Release calcium from bone to blood

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18
Q

Who should we take caution in using bisphosphonates in

A

1) Smokers
2) Major dental disease

BOTH OF THESE INCREASE JAW NECROSIS

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19
Q

Interactions of bisphosphoantes

A

Calcium salts, antacids and Iron

Bisphosphonates bind calcium so these all decrease its absorption

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20
Q

When do the calcium lowering effects of bisphosphonates become most apparent

A

3-4 days post administration their effect becomes apparent

Max effect at 7-10 days

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21
Q

How should you take alendronic acid

A

Take tablet whole 30 minutes before breakfast or other meals
Take with plenty of water
Sit upright for 30 minutes after to reduce the risk of oesophagitis

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22
Q

What monitoring should we do for bisphosphonates in osteoporosis

A

Check and replace calcium and vitamin D before starting treatment

Do a DEXA every 1-2 years

Monitor hypercalcaemia and sympytoms/bone complications in myeloma and Paget’s

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23
Q

Name some calcium and vitamin D supplements

A

Calcium carbonate
Calcium gluconate
Colecalciferol
Alfacalcidol

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24
Q

Indications of the use of calcium and vitamin D

A

1) Osteoporosis
2) CKD –> helps to treat and prevent secondary hyperparathyroidism and renal osteodystrophy
3) Hypocalcaemia that is symptomatic
4) Vitamin D deficiency –> treat and privent rickets and osteomalacia
5) Severe hyperkalaemia

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25
Q

What are the symptoms of hypocalcaemia

A

Paraesthesia
Tetany
Seizures

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26
Q

How do the kidneys influence calcium/vitamin D

A

Kidneys activate vitamin D

Vitamin D is needed to abrorb calcium

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27
Q

What goes wrong with calcium, vitamin D and phosphate in CKD

A

1) Kidneys dont activate vitamin D - calcium isnt absorbed
2) Kidneys dont filter out phosphate so phosphate levels rise
3) PTH is produced in large quantities –> this can cause renal osteodystrophy

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28
Q

What does calcitonin do

A

It decreases serum calcium levels

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29
Q

What happens in osteoporisis

A

Loss of bone mass - causing an increased risk of fragility fractures

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30
Q

What do bloods look like in CKD

A

Raised phosphate
Low calcium

This stimulates renal osteodystrophy

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31
Q

How should we treat CKD

A

Oral calcim supplements to bind phosphate in teh gut

Alfacalcidol to provide vitamin D that doesn’t need renal activation

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32
Q

How does hypercalcaemia affect the heart

A

High calcium raises the myocardial threshold potential

Makes arrhythmias more likely

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33
Q

Do calcium and vitamin D supplements have an effect if potassium levels

A

No

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34
Q

What are the adverse effects of oral calcium

A

Dyspepsia
Constipation

IV - if given for hyperkalaemia then can cause cardiovascular collapse if given too fast and local tissue damage if accidentally given into SC tissue

35
Q

Interactions of oral calcium

A

Oral calcium decreases the absorption of many other drugs: iron, bisphophonates, tetracyclines and levothyroxine

IV Calcium MUSTNT mix with sodium bicarbonate –> risk of precipitation

36
Q

How should we administer calcium gluconate

A

Slow IV injection over 5-10 minutes into a large vein

37
Q

How much should time should we seperate calcium gluconate and sodium bicarbonate by

A

4 hours

38
Q

What symptoms should we warn patients taking oral calcium or vitamin D to look out for

A

Abdominal or limb pain –> this may be a sign of hypercalcaemia

39
Q

How should we take oral calcium

A

Chewed then swallowed

40
Q

Indications of thyroid hormones

A

1) Primary hypothyroidism

2) Hypothyroidism secondary to hypopituitarism

41
Q

Action of thyroid hormones

A

T4 is normally produced by thyroid –> converted to T3 (the active form)

42
Q

What is levothyroxine

A

Synthetic T4 - most common for long term replacement

43
Q

What is liothyroxine

A

Synthetic T3 - shorter T-half life than levothyroxine, quicker onset (few hours) and offset (24-48 hours)

Often reserved for treatment of sever or acute hypothyroidism

44
Q

Adverse of effect of thyroid hormones

A

Usually due to excessive doses –> similar to hyperthyroid effects

DnV, Weight Loss
Palpitations, angina, arrhytmias
Tremor, restlessness, insomnia

45
Q

Warnings of using thyroid hormones

A

Coronary artery disease

Thyroid hormones can increase heart rate and metabolism –> this can precipitate cardiac ischaemia. Start cautiously at low dosease and monitor

2) Hypopituatarism –> MUST START CORTICOSTEROIDS BEFORE THYROID HORMONES –> otherwise may precipirate an addisonian crisis

46
Q

Interactions of thyroid hormones

A

1) Antacids, Iron, Calcium and Iron salts –> all decrease the GI absorption of levothyroxine
2) CP450 Inducers (phenytoin, carbamazepine) –> need to increase levothyroxine dose
3) Diabetes mellitus - can increase hypoglycaemic requirements due to changes in metabolism
4) Enhances warfarin effects

47
Q

Do we need to monitor thyroid hormones

A

Initially change dose according to symptoms

Do TFTs after 3 months

48
Q

What should you do if a patient experiences hyperthyroid symptoms after starting thyroid homrones

A

Lower dose and review in 1-2 weeks
Look for re-emergence of hypothyroidism

TFTs are unhelpful in this situation

49
Q

Name a sulphnyurea

A

Glicazide

50
Q

Indications for sulphonylureas

A

1) Type 2 DM - as single agent or a combination

51
Q

Action of sulphonylureas

A

Stimulates pancreatic insulin secretion
Blocks ATP dependednt K+ channels in pancreatic B-cell membranes –> causes depolarisation –> Calcium channels open –> increases intracellular calcium –> causes insulin secretino

52
Q

Is insulin anabolic or catabolic

A

Anabolic –> hence increased insulin causes weight gain

This weight gain can worsen DM over time

53
Q

Adverse effects of sulphonylureasa

A

GI Upset
Hypoglycaemia
Rare hypersensitivity reactoins

54
Q

What are the rare hypersensitivity reactions of sulphonylureas

A

1) Haeamatological abnormalities - agranulocytosis
2) Hepatic toxicity - cholestatic jaundice
3) Drug hypersensitivity syndrome (rash, fever, internal organ involvement)

55
Q

Warnings of using sulphonylureas

A

1) Hepatic impairment - dose reduction
2) Renal impairment - monitor carefully
3) Increased risk of hypoglycaemia –> e.g. those with hepatic impairment (reduced gluconeogenesis), adrenal or pituitary insufficiency (as there is a lack of counter-regulatory hormones)

56
Q

Interactions of sulphonyureas

A

1) Increased risk of hypoglycaemia with other antidiabetic drugs
2) Decreased efficacy by drugs that increase blood glucose e.g. steroids, thiazide and loop diuretics

57
Q

Symptoms of hypoglycaemic attacks

A

Dizziness, nausea, sweating and confusion

58
Q

HbA1c target for those on sulphonylureas

A

Less than 58

59
Q

Name a biguanide

A

Metformin

60
Q

Does metformin cause weight gain

A

NO - this is because it doesnt stimulate insulin secretion, it just increases the receptors sensitivity to insulin

61
Q

Indications of metformin

A

1) Type 2 DM

62
Q

Action of metformin

A

Increase the response (sensitivity) to insulin
Suppresses hepatic gluconeogenesis and glycogenolysis

It also increases glucose uptake and utilization by skeletal muscle
Suppresses intestinal glucose absorption

63
Q

Adverse efects of metformin

A

GI upset - common
Lactic acidosis - rare. This occurs if precipitated by a intercurrent illnesss that cause metformin accumulation e.g. decrease renal function or increased lactate production (sepsis, hypoxia, cardiac failure) or decrease lactate metaboism (e.g. liver failure)

64
Q

Symptoms of lactic acidosis

A 
Vominting
Stomach aches/cramps
Muscle cramps
Difficulty breathing
Severe tiredness
65
Q

Contraindications of metformin

A

Severe renal impairment (decreased dose if moderate impairment)

66
Q

When should we acutely withhold metformin

A

AKI e.g. sepsis, shock, dehydration
Severe tissue hypoxia e.g. cardiac/respiratory fialure, MI

Acute acohol intoxication - may precipitate lactate acidosis

67
Q

Caution of using metformin in

A

Hepatic impairment - lactate clearnce is impaired

Chronic alcohol overuse - risk of hypo

68
Q

Interactins of metformin

A

1) IV contrast media - withold metformin before and 48 hours after as increased risk of renal impairment and metformin accumulation
2) Drugs affecting renal function e.g. ACEi, NSAIDs and diuretics
3) Prednisolone, thiazide and loop diuretics –> these all elevate blood glucose hence oppose action and reduce efficacy of metformin

69
Q

Name a synthetic mineralcorticoid

A

Fludrocortisone

70
Q

Indications of fludrocortisone

A

1) Replace aldosterone in forms of adrenal insufficiency
2) Orthostatic intolerance and postural orthostatic tachycardiac syndrome
3) Treats severe hypotension
4) Confirms conns syndrome - as you do a fludrocortisone suppression test

71
Q

What is conns syndrome

A

An aldosterone producing adenoma

72
Q

Name some forms of adrenal insufficiency

A 
Addisons
Salt wasting (21-hydroxylase deficiency) a form of CAH
73
Q

Action of fludrocrotisone

A

Binds to mineraolcorticoid recepot and mimics the action of aldosterone

Acts on deistal nephron - promotes Na/K exchange
Sodium retention and urinary loss of K/H
Cl- is reabsorbed in conjunction with Na+
Water is alco reabsorbed

74
Q

Adverse effects of fludrocortisone

A

Causes features of Conn’s syndrome

Oedema
Nocturia
Hypokalaemia
Hypertension
Weakness
Tetany
75
Q

Contraindications of fludrocortisone

A

Systemic fungal infection

76
Q

Interactions of fludrocortisone

A

1) Amphotericin B/K+ depeleting diuretics –> enhances hypokalaemia
2) Oral anticoagulants - decreased prothrombin time
3) Aspirin - increaed ulcerogenic effect
4) Antidiabetic drugs –> diminished antidiabetic effect
5) Oestrogen –> oestrogen increases the amount of corticosteroid binding gloculin (inarivates the drug) but balanced by decreased metablism of corticosteroids hence may need a reduce drug dose

77
Q

Indications for carbimazole

A

1) Treates hyperthyroidism

78
Q

Action of carbimazole

A

Acts via its active metabolite METHIMAZOLE
Substrate inhibitor of peroxidase, which itself is iodinated and degraded within the thyroid
This divert oxidized iodine from thyroglocbulin hence decreasing hormone biosynthesis

ALSO HAS AN IMMUNOSUPPRESSANT ACTION WITHIN THE THYROID –> interferes with the generation fo oxygen free radicals in macrophages and hecne antigen presentation

79
Q

Adverse effects of carbimazole

A 
Pruritis and rashes
Neutropenia 
Nausea
Hair loss
Drug fever
Leukopenia
Arthralgia
80
Q

Use of carbimazole in pregnancy

A

Causes aplasia cutis in newborn (this is the absence of a portion of skin)

81
Q

Contraindications of carbimazole

A

Hypersentivit

Severe hepatic insufficiency

82
Q

Warnings of carbimazole

A

Stop whilst on radio-iodine treatment

83
Q

Interactions of carbimazole

A

1) Warfarin - as carbimazole is a vitamin K antagonist –> hence enhances anticoagulant effect
2) Theophylline toxicity - serum levels increae if concurrent use
3) Prednisolone –> concurrent therapy increases prednisolone clearnce
4) Increased clearance of beta-blockers

3rd Year Drugs (10 decks)

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