Prednisolone is four times more potent than hydrocortisone, and therefore, a dose of 12.5 mg would be equivalent to 50 mg of hydrocortisone.
The following table summarises the relative potency of the main corticosteroids compared with hydrocortisone:
Corticosteroid
Potency relative to hydrocortisone
Prednisolone
4 times more potent
Triamcinolone
5 times more potent
Methylprednisolone
5 times more potent
Dexamethasone
25 times more potent

Metformin is a biguanide used as the first-line to treat type 2 diabetes mellitus. It has a good reputation as it has an extremely low risk of causing hypoglycaemia compared to the other agents for diabetes. It does not affect the insulin secreted by the pancreas or increase insulin levels. Toxicity with metformin can, however, cause lactic acidosis with associated hypoglycaemia.

Insulin is used mainly in type 1 diabetes, where the pancreas makes no insulin and can sometimes be prescribed in type 1 diabetes. There are different types of insulin categorized by their onset of action:

1. Intermediate-acting insulins (isophane insulin NPH):
– intermediate duration of action, designed to mimic the effect of endogenous basal insulin
– starts their action in 1 to 4 hours
– peaks in 4 to 8 hours
– dosing is usually twice a day and helps maintain blood sugar throughout the day
– Isophane insulin is a suspension of insulin with protamine

2. Short-acting insulins (regular insulin)
– starts the action in 30 to 40 minutes
– peaks in 90 to 120 minutes
– duration of action is 6 to 8 hours
– taken before meals, and food is necessary within 30 minutes after its administration to avoid hypoglycaemia

3. Long-acting insulins (glargine, detemir, degludec)
– start action in 1 to 2 hours
– plateau effect over 12 to 24 hours
– Dosing is usually during the night-time after meals. Their long duration of action helps in reducing the frequency of dosing throughout the day.

4. Rapid-acting insulins (lispro, aspart, glulisine)
– start their action in 5 to 15 minutes
– peak in 30 minutes
– The duration of action is 3 to 5 hours
– generally used before meals and always used along with short-acting or long-acting insulins to control sugar levels throughout the day.

The DVLA sends a detailed information sheet about their licence and driving to all drivers with diabetes mellitus. The primary danger of driving while diabetic is hypoglycaemia.

The DVLA must be notified of the following diabetic patients:
All of the drivers are on insulin. (Licenses are being reviewed more frequently.)
Those who are at high risk of hypoglycaemia and have had more than one episode of severe hypoglycaemia in the previous year. (Severe hypoglycaemia is defined as requiring the assistance of another person to manage.)
Those who are unaware of their hypoglycaemia
Anyone who has ever been in a car accident due to hypoglycaemia
Anyone with diabetic retinopathy who needs laser treatment (to both eyes or to a second eye if sight only in one eye)
Patients with diabetes complications that impair their ability to drive.

To drive, drivers with insulin-treated diabetes must meet the following requirements:
They need to be aware of hypoglycaemia.
They must not have had more than one episode of hypoglycaemia in the previous 12 months that necessitated the assistance of another person.
They must check their blood glucose levels no later than 2 hours before the first journey.
While driving, they must check their blood glucose levels every two hours.
The visual acuity and visual field standards must be met.

Any significant changes in their condition must be reported to the DVLA. Furthermore, on days when they are not driving, group 2 licence holders must test their blood glucose twice daily using a metre that can store three months’ worth of readings.

In addition to this advice, the DVLA also offers the following advice to diabetic patients:
When taking tablets that have the potential to cause hypoglycaemia (such as sulfonylureas and glinides), monitoring may be necessary if there has been more than one episode of severe hypoglycaemia.
Drivers must show good control and be able to recognise hypoglycaemia.
Verify that your vision meets the required standard.

If a patient feels hypoglycaemic or has a blood glucose level of less than 4.0 mmol/L, they should not drive. Driving should not be resumed until blood glucose levels have returned to normal, which should take 45 minutes.

If there are any warning signs, patients should carry rapidly absorbed sugar in their vehicle and stop, turn off the ignition, and eat it.

If resuscitation is required, a card stating which medications they are taking should be carried.

If hypoglycaemia causes an accident, a diabetic driver may be charged with driving under the influence of drugs.

An overdose of levothyroxine can happen by accident or on purpose. Intentional overdosing is sometimes done to lose weight, but it can also happen in patients who are suicidal. The development of thyrotoxicosis, which can lead to excited sympathetic activity and high metabolism syndrome, is the main source of concern. The time between ingestion and the emergence of clinical features associated with an overdose is often quite long.

After a levothyroxine overdose, the majority of patients are asymptomatic. Symptoms and signs are usually only seen in patients who have taken more than 10 mg of levothyroxine in total.

The following are the most commonly seen clinical features in patients developing clinical features:
Tremor
Agitation
Sweating
Insomnia
Headache
Increased body temperature
Increased blood pressure
Diarrhoea and vomiting
Less common clinical features associated with levothyroxine overdose include:
Seizures
Acute psychosis
Thyroid storm
Tachycardia
Arrhythmias
Coma

The continued absorption of the ingested levothyroxine causes a progressive rise in both total serum T4 and total serum T3 levels in the first 24 hours after an overdose. However, in some cases, the biochemical picture is completely normal. Thyroid function tests are not always recommended after a thyroxine overdose. Although elevated thyroxine levels are common, they have little clinical significance and have no impact on treatment. Following a levothyroxine overdose, the following biochemical features are common:
T4 and T3 levels in the blood are elevated.
Free T4 and Free T3 levels are higher.
TSH levels in the blood are low.
If the patient is cooperative and more than 10 mg of levothyroxine has been consumed, activated charcoal can be given (i.e., likely to become symptomatic)
Within an hour of ingestion, the patient presents.

The treatment is mostly supportive and aimed at managing the sympathomimetic symptoms that come with levothyroxine overdose. If beta blockers aren’t an option, try propranolol 10-40 mg PO 6 hours or diltiazem 60-180 mg 8 hours.

Diabetes ketoacidosis is an acute complication of diabetes mellitus. Insulin is administered to achieve euglycemia, and crystalloids or colloidal solution is administered to achieve euvolemia and euelectrolytaemia.

Potassium levels severely fluctuate during the treatment of DKA, hypokalaemia being more common. Insulin promotes the cell to take up potassium from the extracellular space via increased sodium-potassium pump activity.

It is important to monitor potassium levels during the treatment of DKA regularly. It is widely suggested that the normal saline shall be used for initial resuscitation, and once the potassium level is retrieved, the patient can be started on potassium replacement should the serum potassium level be between 3.3 and 4.5 mmol/L
If potassium levels fall below 3.3 mmol/l, insulin administration may need to be interrupted to correct the hypokalaemia.

Prednisolone is four times more potent than hydrocortisone, and therefore, a dose of 25 mg would be equivalent to 100 mg of hydrocortisone.
The following table summarises the relative potency of the main corticosteroids compared with hydrocortisone:
Corticosteroid
Potency relative to hydrocortisone
Prednisolone
4 times more potent
Triamcinolone
5 times more potent
Methylprednisolone
5 times more potent
Dexamethasone
25 times more potent

Pioglitazone is used to treat type 2 diabetes mellitus. It selectively stimulates the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and to a lesser extent PPAR-α.

Of the medications mentioned in this question, only pioglitazone is a recognized cause of hypoglycaemia.