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3rd Year Drugs > Endocrine drugs > Flashcards

Endocrine drugs Flashcards

1
Q

What is fludrocortisone

A

A synthetic mineralcorticoid

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2
Q

Uses of fludrocortisone

A

1) Replace aldosterone in forms of adrenal insufficiency
2) Orthostatic intoleance and postual orthostatic tachycardia syndrome (POTS) –> 1st line to increase Na+ levels
3) Hypotension treatment (if severe)
4) Confirms Conn’s syndrome

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3
Q

What is Conns syndrome

A

An aldosterone producing adenoma

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4
Q

What usually secretes aldosterone

A

The zona glomerulosa of the adrenal cortex

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5
Q

Action of fludrocortisone

A

Binds to mineralcorticoid receptors and mimics the action of aldosteroine
Acts on the distal nephron, promotes Na/K exchange
Sodium retention and urinary loss of K and H+
CL- is absorbed in conjuction with Na –> water follows

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6
Q

Adverse effects of fludrocortisone

A 
FEATURES OF CONNS
Sodium/water retention --> nocturia
Hypokalaemia
Hypertension
Weakness
Nocturia
Tetany
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7
Q

Warnings of fludrocortisone

A

Contraindicated in patients with systemic fungal infections

Steroids can cause immunosuppression

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8
Q

Interactions of fludrocortisone

A

1) Amphotericin B/K+ Depleteing diruiteics –> enhance hypokalaemia
2) oral anticoagulants –> decrease prothrombin time
3) Aspirin –> Increased ulcerogenic effect
4) Antidiabetic drugs –> diminished antidiabetic effect
5) Oestrogen –> oestrogen increases the amoutn of corticosteroid binding globulin (inactivates the drug) BUT balanced by decreased metabolism of corticosteroid hence may need a reduced drug dose.

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9
Q

Name a biguanide

A

Metformin

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10
Q

Metformin indications

A

1) Type 2 DM –> First choice to control it –> use alone or in combo with other oral hypoglycaemiacs or insulin

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11
Q

Action of biguanides

A

NOT A REPLACEMENT FOR LIFESTYLE CHANGES
Increases the response (sensitivity) to glucose
Suppresses hepatic gluconeogenesis and glycogenolysis
Also increases glucose uptae and utilization by skeletal muscle
Suppresses intestinal glucose absoprtion

Overall decreaes blood glucose

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12
Q

What effect do biguanides have on insulin secretion

A

NO EFFECT –> as it doesnt stimulate pancreas insulin secretions, it only makes cells more sensitive to insulin
Hence there is no risk of hypoglycaemic episodes

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13
Q

What effect do biguanides have on weight

A

It reduces weight gain and can induce weight loss (as it doesnt increase insulin secretion)
This prevenet the worsening of insulin resistance and the slow deteorioration of diabetes

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14
Q

Adverse effects of metformin

A

1) GI Upset - common
2) Lactic acidosis - can be fatal. Onlyl occurs if precipitated by illness that causes metformin accumulation (e.g. renal function decreased), or lactate production increased (sepsis, hypoxia, cardiac failure), or decreased lactate metabolism (liver failure)

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15
Q

Contraindications of metformin

A

1) severe renal impairment –> need to significnalty reduce

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16
Q

When should we acutely withhold metformin

A

AKI e.g. sepsis, shock, dehydration
Severe tissue hypoxia e.g. MI, cardiac/resp failure

Withhold in actue alcohol intoxictaion –> may precipiate lactic acidosis

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17
Q

Caution of metformin in

A

1) Hepatic impairment –> decreased lactate clearance

2) Chronic Alcohol overuse –> risk of hypoglycaemia

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18
Q

Interactions of metformin

A

1) IV contrast media –> increased risk of renal impairment
2) Drugs affecting renal function e.g. NSAIDs, ACEi, diuretics
3) Prednisolone, thiazide and loop diuretics –> these elevate blood glucose hence oppose the action and reduce its efficacy

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19
Q

HbA1c target with metformin

A

<58

Also test renal function before and annually

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20
Q

How is metformin excreted

A

Unchanged by the kidneys

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21
Q

Symtpoms of lactic acidosis

A 
Vomiting
Stomach ache/pain
Muscle cramps
Difficutly breathing
Severe tiredness
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22
Q

Link between insulin and weight gain

A

Insulin is an anabolic hormone

This means drugs that increase insulin secretion cause WEIGHT GAIN hence worsening DM over time

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23
Q

Name a sulphnoylurea

A

Glicazide

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24
Q

Indications for sulphonylureas

A

1) Type 2 DM –> a signel agent where metformin CI or not tolerated
2) DM –> in combo with metformin or other agents if BM not adequately controlled

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25
Q

How should you take sulphonylureas

A

Orally with meals, start low dose and increase gradually

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26
Q

How do sulphonylureas work

A

Stimulate pancreatic insulin secretion
They block ATP dependent K+ channels in pancreatic B cell membranes –> this causes depolarisation and opening of voltage gated Ca2+ channels –> the rise in intracellular calcrium causes insulin secretion

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27
Q

Adverse effects of sulphonylureas

A

Weight gain –> as insulin is anabolic
GI Upset
Hypogylcaemia –> more likely with increased doses
Rare hyperesensetitivity reactions e.g.
a) Haematological abnormalities (agranulocytosis)
b) Hepatic toxicity (cholestatic jaundice)
c) Drug hypersensitivity syndrome (rash, fever, internal organ involvement)

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28
Q

What happens to insulin resistance in acute illness

A

Increased insulin resistace
Also impairs hepatic and renal function
Oral hypoglycaemic become less effective
Insulin may be needed temporarily

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29
Q

Warnings of using sulphonylureas

A

1) Hepatic and renal impairment
2) High risk of hypoglycaemia e.g. those with hepatic impairment (reduced gluconeogenesis), malnutrition, adrenal or pituitary insufficiency (lack of counter regulatory hormones) and the elderly

30
Q

Interactions of Sulphonylureas

A

1) Antidiabetic drugs –> risk of hypoglycaemia

2) efficacy reduced by drugs that increase blood glucose e.g. steroids, loop and thiazide diuretics

31
Q

What are the syptoms of hypoglycaemia

A

Dizziness, nausea, sweating, confusoin

Take something sugary and then something starchy

32
Q

How are sulphonylureas excreted

A

Excreted unchanged in the urine

33
Q

Name thyroid hormone repolacement

A

Levothyroxine

Liothyroxine

34
Q

Indications for thyroid hormones

A

Hypothyroidism

35
Q

Action of thyroid homrones

A

Thyroid hormones regulate emtabolism and growth

36
Q

What is levothyroxine

A

Synthetic T4 - the inactive from –> most common for long term replacement

37
Q

What is liothyroxine

A

Synthetic T3 –> shorter half life, quicker onset and offset, hence usually reserved for emergency treatment of severe or acute hypothyroidism

38
Q

Adverse affects of thyroid homrones

A

Usually related to overdose –> GI upset, neurological (tremors, restlessness, insomnia), Cardiac (palpitations, angina, arryhythmia)

39
Q

Warnings of thyroid hormones

A

1) Coronary artery disease –> can increase heart rate and metabolism
2) Hypopituatism –> must start corticosteroids before thyoird homrones, otherwise may precipitate an addisonian crisis

40
Q

Interactions of thyroid hormones

A

1) Antacids, Ca2+ or Fe2+ salts reduce the GI absorption of levothyroxine
2) CP450 inducers (phenytoin, carbamazepine) increase speed of elimination
3) DM –> can increase insulin or oral hypoglycaemic requirement due to changes in metabolism
4) Enhances warfarins effect

41
Q

Name calcium and vitamin D replacements

A

Calcium carbonate, calcium gluconate, colecalciferol, alfacalcidol

42
Q

Indications for calcium and vitamin D

A

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

43
Q

Symptoms of hypocalcaemia

A

Paraesthesia

Tetany Seizures

44
Q

Action of calcium and vitamin D

A

Need Ca for normal muscle/bone/nerve function –> controlled by Vit D and PTH
Calciutonin decreases serum Ca levels

45
Q

Why do we need calcium and vitamin D in CKD

A

Impaired phosphate excretion and decreased activation of itamin D cause high phosphate and low potassium –> this stimulates secondary hyperparathyroidism –> leads to osteodystrophy

Give oral calcium supplements to bind phopshate in the gut
Give alfacalcidol to provide vitamin D that doesn’t require renal activation

46
Q

How does calcium treat hyperkalemia

A

Increaes the myocardial threshold potential, reducing the risk of arryhtmias

It has no effect on serum K+ levels

47
Q

Adverse effects of Calcium

A

Oral - dypspesia and constipation

IV - if given for hyperkalaemia can cause CV collapse or local tissue damage if given too quickly

48
Q

Interactions of calcum

A

1) Oral Ca –> decreases absorption of many drugs e.g. iron, bisphosphonates, tetracyclines, levothyroxine
2) IV –> MUST MIX WITH SODIUM BICARBONATE –> risk of precipitations

49
Q

What foods should you wait 2 hours with after taking calcium

A

Spinach
Banana
Whole cereals

50
Q

Name some bisphosphonates

A

Alendronic Acids
Disodium pamidronate
Zoledronix acid

51
Q

Indicatinos of bisphosphonates

A

1) Osteoporotis fragility fractures risk
2) Severe hypoermcalcaemi of maligancy
3) MYeloma and breast cancer with bone metastases
4) Pagets disease - first line treatment to reduce bone turnover and pain

52
Q

Action of bisphosphonates

A

Inhibit action of osteoclasts –> decreses bone turnover
Similar sturcture to natural pyrophosphate hence incorporated into bone, when bone is resorbed they accumulate in osteoclasts –> inhibit their activity and promote apoptosis

NET EFFECT IS REDUCTION IN ONE LESS AND IMPROVEMENT IN BONE MASS

53
Q

Adverse effect of bisphosphonates

A

1) Osteophagitis - if taken orally
2) hypophosphataemia
3) Jaw osteonecrosis (rare, more likley if high-dose IV)
4) atypical femoral fracture

54
Q

Contraindications of bisphophantes

A

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

55
Q

Caution of bisphosphonates in

A

Smokers
Major Dental disease

This is because of the higher risk of jaw osteonecrosis

56
Q

Interactinos of bisphosphonates

A

1) Calcium salts, antacids and FE –> bind calcium and reduce its absorption

57
Q

How should you take bisphosphonates

A

Take 30 mins before breakfast –> take with plenty of water –> sit upright for 30 mins after taking it to reduce the risk of oesophagitis

58
Q

Indications of insulin use

A

1) Type 1 - DM insulin replacement, Type 2 DM –> if oral hypoglycaemics not working/tolerated
2) Diabetic emergencies –> give IV e.g. diabetic ketoacidosis, hyperglycaemic hyperosmolar syndrome and peri-operative hyperglycaemic control
3) Hyperkalaemia –> give with glucose

59
Q

Action of insulin

A

Stimulates glucose uptake from circulation into tissues
Stimulates glycogen, lipid and protein synthesis
Inhitis gluconeogenesis and ketogenesis

Also drives K+ into cells –> only for short term though

60
Q

Rapid insulin

A

Insulin apart e.g. novarapid

61
Q

Short insulin

A

Actrapid

62
Q

Adverse effects of insulin

A

Hypoglycaemia –> can lead to coma/death

Lipohypertrophy –> if given SC repeatedly at the same site

63
Q

Warning of insulin

A

Renal impairment –> insulin clearance is reduced hence increased risk of hypo

64
Q

Interactions of insulin

A

1) other hypoglycaemics

2) Systemic corticosteroids –> icnreases insulin requirements and steroids increase glcuose

65
Q

When to use carbimazole

A

Treats hyperthyroidism

66
Q

How does carbimazole work

A

Acts via its active metabolist methimazole

Substrate inhibitor of peroxidase –> which itself is iodinated and degraded within the thyroid –> this diverst oxidized iodine from thyroglobulin hence decreasing thyroid hormone biosynthesis

It also has an mmunosuppressant action within the thyroid and interferes with generation of oxygen free radicals in macrophages (and hence antigen presentation)

67
Q

Adverse effects of carbimazole

A

Usually well tolerated BUT;

1) Pruritis and rashes
2) Neutropenia –> rare
3) Nausea, hair loss, fever, leukopneia, arthralgia

68
Q

Use of carbimazole in pregnancy

A

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

69
Q

Contraindicatinos of carbimazole

A

1) hypersensitivity

2) Severe hepatic insufficiency

70
Q

Warnings of carbimazole

A

Stop during whil undergoing radio-iodine treatment to acoid a thyroid crisis

71
Q

Interactions of carbimazole

A

1) Warfarin –> carbimazole is a vitmain K antagonist hence increases anticoagulation
2) Theophylline toxicity –> serum levels can increse if concurrent use without decreases dose of theophylline
3) Prednisolone –> concurrent therapy increases prednisolone clearance
4) Beta-adrenergic blockers –> increases their clearance

3rd Year Drugs (10 decks)

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