3D Endo - Pharmacology Flashcards

(57 cards)

1
Q

What does the ‘25’ mean in Humalog Mix 25?

A

It means the insulin is a mix: 25% short-acting insulin lispro and 75% intermediate-acting insulin lispro protamine.

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2
Q

What is a basal-bolus insulin regimen?

A

A regimen where patients take long-acting (basal) insulin daily with short-acting (bolus) insulin at mealtimes.

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2
Q

How does a mixed (biphasic) insulin regimen differ from basal-bolus?

A

Mixed regimens involve 1–3 daily injections of a fixed combination of short- and intermediate-acting insulin, unlike basal-bolus where insulin is adjusted with meals.

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3
Q

What is carbohydrate counting and how does it affect insulin prescribing?

A

Patients calculate insulin bolus doses based on the grams of carbohydrate they eat.
→ This makes prescribing difficult as bolus doses vary and cannot be easily written as fixed prescriptions.

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4
Q

What advice can be given for difficult-to-treat morning hypoglycaemia?

A

Advise a late-night snack to help prevent early morning hypos.

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5
Q

How should you treat severe hypoglycaemia in a drowsy, nil-by-mouth patient like Julie (BM 3.4 mmol/L)?

A
  • IV glucose (10% or 20% dextrose) over 15 minutes
  • IM glucagon if no IV access (note: less effective in malnourished patients)
    (as glycogen is mobilised from the liver and stores need replenishing)
  • Avoid oral glucose gel (e.g., Glucogel) as patient cannot swallow safely and is nil by mouth for surgery
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6
Q

What is a fixed rate insulin infusion?

A

A constant rate of 0.1 units/kg/hr, regardless of glucose levels.
→ IV dextrose is added if the patient becomes hypoglycaemic

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7
Q

What is a variable rate insulin infusion?

A

The insulin dose varies depending on capillary blood glucose
→ titrated accordingly every hour

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8
Q

What is the top priority in early DKA management?

A

Fluid resuscitation is the priority—IV access and fluids before insulin

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8
Q

Should you continue long-acting insulin during DKA treatment?

A

Yes – continue the patient’s long-acting insulin alongside the fixed rate infusion

  • continue long-acting insulin, stop short-acting
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9
Q

When can the fixed rate insulin be stopped in DKA?

A

Only when ketonaemia and acidosis have resolved, even if blood glucose is normal.

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10
Q

What should you do if a patient becomes hypoglycaemic during fixed rate insulin?

A

Give IV dextrose while continuing the insulin infusion.

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11
Q

What should be prescribed as the first 3 fluid bags in DKA?

A
  • First bag: No potassium
  • Monitor potassium and prescribe based on VBG results at 60 mins, 1 hour, and 2-hourly thereafter
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12
Q

What is the likely explanation for Jack’s abnormal TFTs during hospitalisation for urosepsis?

A

Likely sick euthyroid syndrome – TFTs can be altered by acute illness. Repeat them when he’s recovered unless symptomatic.

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13
Q

What is the best approach to mild hypothyroidism picked up during acute illness?

A

Recheck thyroid function once recovered unless there are overt signs/symptoms of thyroid dysfunction.

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14
Q

What advice should you give patients about taking levothyroxine?

A
  • Take 30–60 minutes before breakfast, caffeine, or other medicines.
  • Absorption is reduced with calcium, iron, and some foods/drugs.
  • Requires regular blood monitoring.
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15
Q

What are the possible side effects of levothyroxine?

A

Mostly due to over-treatment (iatrogenic hyperthyroidism).
→ Watch for palpitations, tremor, weight loss, insomnia.

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16
Q

Who needs a lower levothyroxine dose?

A

Elderly patients and those with cardiac disease.

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17
Q

A patient on steroids presents with confusion, hypotension, and abdominal pain. What are your top differentials?

A

Suspect adrenal crisis (likely due to steroid withdrawal, infection, or stress without adequate steroid cover).

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18
Q

What is your first step in managing suspected adrenal crisis?

A
  • Give IV hydrocortisone 100 mg STAT
  • Do not wait for blood tests (life-saving bolus dose of glucocorticoid needs to be given)
  • Consider giving a fluid bolus
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19
Q

Why are 3 daily doses of hydrocortisone used in adrenal insufficiency?

A

Mimics the natural cycle of corticosteroid release – high in morning, lower/stable throughout the day

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20
Q

What must patients be told when starting lifelong steroid therapy?

A
  • They will need lifelong replacement
  • How to recognize symptoms of adrenal crisis
  • How to use IM hydrocortisone
  • Sick day rules
  • To carry a steroid card
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21
Q

A patient has weight loss, palpitations, and labs show low TSH, high T4, positive TPO and TSH-receptor antibodies. Diagnosis?

A

Graves’ disease (autoimmune hyperthyroidism)

22
Q

What symptomatic treatment can be offered before specialist input in Graves’ disease?

A

Propranolol can help with the adrenergic symptoms → palpitations, tremor, tachycardia, anxiety

23
What is missing from this prescription on the FP10?
- Patient’s DOB - No. days treatment/amount of tablets - Blank space not crossed out - Registration number of prescriber - Contact number for prescriber
24
A 55-year old female presents with a 3-month week history of progressive hot flushes, palpitations and sweating occurring up to 10 times per day and often making uninterrupted sleep difficult. . Investigations: - serum oestradiol 23 pmol/L (> 100) - serum follicle-stimulating hormone U/L 87 (<30) - serum luteinising hormone U/L 110 (<30) . Which drug treatment is most likely to help these symptoms? - A - aprepitant - B - clonidine - C - levetiracetam - D - propranolol - E - verapamil
B - clonidine - this 55yo woman presents with vasomotor symptoms (hot flushes, palpitations, sweating, sleep disturbance) - her hormonal profile shows: low oestrogen & pituitary trying to compensate by increasing FSH and LH → 1st-line treatment is HRT (oestrogen alleviates hot flushes, palpitations, and night sweats) (But, in this case Clonidine (centrally acting alpha-2 adrenergic agonist) is the correct option for non-hormonal treatment) . The symptoms and biochemistry are consistent with menopausal state. Clonidine is effective in reducing the vasomotor symptoms.
25
What is the mechanism of action of metformin in T2DM & what class of drug is it?
increases insulin sensitivity and decreases glucose production by the liver - It is a biguanide
26
What are common side effects of metformin?
- GI upset → pain, nausea and diarrhoea (depending on the dose) - Lactic acidosis (eg. secondary to AKI)
27
What is an alternative if standard-release metformin causes GI side effects?
Switch to modified-release metformin (released more gradually)
27
What are examples of SGLT-2 inhibitors?
canagliflozin, dapagliflozin and empagliflozin (-flozin)
27
What is the mechanism of action of SGLT-2 inhibitors?
Block glucose reabsorption in the renal proximal tubule → increase urinary glucose excretion - The SGLT 2 protein is found in theproximal convoluted tubules of the kidneys --> it acts to reabsorb glucose from the urine back into the blood
28
What are key benefits of SGLT-2 inhibitors?
- ↓ HbA1c - ↓ BP - weight loss - improved heart failure and CVD outcomes
29
Name 2 important adverse effects of SGLT-2 inhibitors.
- Increased frequnecy of UTIs and genital thrush → the glucose in the urine provides a nutrient-rich environment for bacteria to thrive, making them more likely to multiply and cause infection - normoglycaemic DKA
30
What is the mechanism of action of pioglitazone (thiazolidinedione)?
Increases insulin sensitivity and decreases hepatic glucose production
31
What is the mechanism of action of sulfonylureas (e.g. gliclazide)?
Stimulate insulin release from pancreatic beta cells - note: require pancreatic beta-cells to be functional
32
What are the main side effects of sulfonylureas?
- Weight gain - Hypoglycaemia
33
What is the mechanism of GLP-1 mimetics (e.g. exenatide, liraglutide)?
The main incretin is glucagon-like peptide-1 (GLP-1) -> incretins are secreted in response to large meals and act to reduce blood sugar by: - Increasing insulin secretion - Inhibiting glucagon production - Slowing absorption by the GI tract
33
Why should sulfonylureas be avoided in breastfeeding and pregnancy?
due to the risk of neonatal hypoglycaemia (low blood sugar) in the infant
33
What are the key side effects of GLP-1 mimetics?
- Nausea, vomiting - risk of pancreatitis.
34
What is a major benefit of GLP-1 mimetics (aswell as lowering blood glcuose levels)?
Weight loss
35
When should GLP-1 mimetics be considered according to NICE?
If BMI ≥ 35 with weight-related issues or BMI < 35 and insulin is unsuitable
35
How does propylthiouracil differ from carbimazole in its action?
as well as central mechanism of inhibiting thyroid peroxidase, it also has a peripheral action by inhibiting 5'-deiodinase which reduces peripheral conversion of T4 to T3
35
How is carbimazole typically dosed initially?
High dose for 6 weeks until euthyroid, then reduced
36
What is the mechanism of DPP-4 inhibitors (e.g. sitagliptin)?
Inhibit DPP-4 enzyme → increase endogenous GLP-1 and GIP levels (by decreasing their peripheral breakdown) . - Incretins are inhibited by an enzyme called dipeptidyl peptidase-4 (DPP-4). - DPP-4 inhibitors block the action of DPP-4, allowing increased incretin activity
37
What is the mechanism of action of carbimazole?
Inhibits thyroid peroxidase → blocks iodination and coupling of tyrosine residues on thyroglobulin → ↓ thyroid hormone synthesis
38
What is a serious haematological adverse effect of carbimazole?
Agranulocytosis (severe lack of neutrophils in blood)
39
Can carbimazole be used in pregnancy?
Yes, at low doses, although it crosses the placenta.
40
What endocrine side effects are associated with glucocorticoid use?
Impaired glucose regulation and increased appetite/weight gain.
41
What features of Cushing’s syndrome can result from glucocorticoid use?
Moon face, buffalo hump, and striae.
42
What musculoskeletal side effects are associated with glucocorticoids?
Osteoporosis, proximal myopathy, and avascular necrosis of the femoral head.
43
How do glucocorticoids affect the immune system?
They cause immunosuppression, increasing susceptibility to severe infections
44
What psychiatric side effects may occur with glucocorticoid use?
Insomnia, mania, and psychosis
45
Why can glucocorticoids cause neutrophilia?
Due to demargination of neutrophils
46
What are the main side effects of mineralocorticoids?
Fluid retention and hypertension.
47
What should be done to corticosteroid doses during intercurrent illness in long-term users?
The dose should be doubled
48
Why should long-term corticosteroids not be stopped abruptly?
They suppress endogenous steroid production → risk of Addisonian crisis if stopped suddenly
49
How do corticosteroids affect diabetic control?
Use of corticosteroids can worsen diabetic control due to their anti-insulin effects → corticosteroids oppose the action of insulin and stimulate hepatic gluconeogenesis