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Pharmacy > Chapter 6 - Endocrine > Flashcards

Chapter 6 - Endocrine Flashcards

1
Q

Types of diabetes?

A

Type 1
Type 2
Gestational
Secondary (caused by pancreatic damage, hepatic cirrhosis, endocrine disease)

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2
Q

DVLA advice for diabetics?

A

Check BG < 2 hours of driving and every 2 hours whilst driving
Should be above 5mmol / L of below - snack (which should always be in the car)
If hypoglycaemia occurs; stop car in safe place, switch off engine/remove keys/move from drivers seat, eat sugar source, wait 45 mins after normal BG before driving again.

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3
Q

When would the target HbA1c concentration be 53mmol/mol (7%) instead of the usual 48mmol / mol (6.5%)?

A

When two or more anti diabetic drugs are used in combibation.

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4
Q

Why might HbA1c targets be relaxed?

A

If patient older, frail, if tight blood control not appropriate and may cause hypoglycaemia, poor life expectancy, if there are major comorbidities.

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5
Q

Why is metformin first line for anti diabetics?

A

It causes weight loss, has reduced risk of hypoglycaemia and cardiovascular benefits long term.

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6
Q

Why would you use Gliclazide or tolbutamide over other sulfonylureas in the elderly or renally impaired?

A

These are shorter acting sulfonylureas, consequently reducing the risk of hypoglycaemia in these two high risk groups

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7
Q

Why might you start a GLP1 receptor agonist with Metformin + sulfonylurea?

A

Triple therapy with metformin and two other oral anti diabetics have failed, contra indicated or not tolerated.

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8
Q

Why would a patient be taking a gliptin, pioglitazone or sulfonylurea first line?
*Gliflozins if the above not appropriate

A

If metformin not tolerated (severe gastrointestinal distress) or contraindicated (eGFR < 30mL/min/1.73m^2 or metabolic acidosis)

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9
Q

Why would a patient without hypertension be started on an ACEi or ARII antagonist?

A

Diabetic nephropathy initially detected with urinary protein and serum creatinine then microalbuminuria (confirmed with three positive tests) or nephropathy causing proteinuria is a sign of renal deterioration, ACEi will help prevent this.

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10
Q

When starting a diabetic patient on an ACEi why would you monitor the blood glucose?

A

These can increase the hypoglycaemic effect of insulin or oral anti diabetic drugs

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11
Q

Why do patients on Acarbose need to use glucose if hypoglycaemic and not sucrose?

A

Acarbose inhibits alpha glucosidases in the intestine thus preventing sucrose from being absorbed. Therefore patient should use 2 teaspoons of sugar, 3 sugar lumps, 55mL of Lucozade, 100mL of Coca Cola, 19mL of undiluted Ribena in a situations hypoglycaemia.

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12
Q

Why are Glucagon-like peptide receptor agonists injected subcutaneously?

A

Not absorbed by the gut

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13
Q

Why might you use Duraglutide over Exenatide?

A

Less frequent administration and less likely to cause hypoglycaemia.
Exenatide may cause over 1.5kg weight loss weekly and is cautioned in the elderly.

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14
Q

What are the symptoms of pancreatitis and what antidiabetics are associated with it?

A

Persistent, severe abdominal pain

GLP1 agonists e.g Liraglutide, Dulaglutide, Albiglutide, Lixisenatide, Exenatide

Gliptins e.g. Alogliptin, Liragliptin, Saxagliptin, Sitagliptin, Vildagliptin

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15
Q

Why do the gliptins augment insulin release?

A

Gliptins increase glucagon like peptide 1 and gastro inhibitory peptide by inhibiting their breakdown via dipeptidylpeptidase-4.
Increase insulin means increased glucose uptake / glycogen synthesis, and decreased glycogenolysis/ gluconeogenesis to ultimately reduce blood glucose.

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16
Q

Why would you use caution in giving Metformin to patients with renal/hepatic disease, with hypoxic pulmonary disease, chronic stable heart failure, acute renal impairing drugs, dehydration or shock.

A

Risk of lactic acidosis due to the above factors, pause treatment if dehydration occurs and avoid in conditions that worsen renal function or cause tissue hypoxia

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17
Q

Why would you avoid longer acting Sulfonylureas in the elderly or patients with renal impairment?

A

Increased risk of hypoglycaemia

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18
Q 
Why would you use sulfonylureas with caution in the following diabetic patient groups:
Elderly
Renal impairment 
Obese
Patient on Dapagliflozin
Patient on Linagliptin
A

Increased risk of hypoglycaemia for elderly and renal impairment

May cause weight gain so caution in those already obese

May need dose adjustment of sulfonylurea as the new drugs will increase their effectiveness

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19
Q

Why might you be concerned if a diabetic patient with gastrectomy / present a Rx for Metformin?

A

Metformin can (rarely) cause decreased B12 absorption especially with long term use, a gastrectomy can cause malabsorption even if patient eating good B12 sources such as eggs, meat, fish and dairy.

Together this could result in B12 deficiency leading to neurological problems and pernicious/ neurological anaemia.

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20
Q

What are the signs of lactic acidosis?

A 
Dyspnoea
Muscle cramps
Abdominal pain
Hypothermia
Asthenia
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21
Q

Why might you avoid Glibenclamide in children and instead opt for Metformin?

A

Due to being a long acting Sulfonylurea it can cause pronounced hypoglycaemia. Sulfonylureas tend to be avoided

Metformin is licensed in for children over 10 however (unlicensed 8-10)

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22
Q

What might you counsel patients to look out for when starting a Sulfonylurea?

A

Skin issues- Skin reactions, erythema multiform, exfoliative dermatitis - could occur in first 6-8 weeks.

Fever, hypersensitivity reactions, jaundice could occur in first 6-8 weeks

Hypoglycaemia symptoms - Headache, shaking / sweating, pins and needles, hunger, palpitation, double vision, difficulty concentrating, slurred speech, confusion, convulsions, behaviour change, truculence

Manage with 10-20g of glucose

Hypoglycaemia and driving

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23
Q

Why might you avoid Sulfonylureas in a patient with porphyrias?

A

It is a contraindication due to the potential to cause bone marrow toxicity (albeit rare)

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24
Q

Why might you be concerned about a diabetic presenting with dehydration?

A

Dehydration is one of the risk factors for diabetic ketoacidosis alongside low beta cell reserve, restricted food and sudden insulin reduction (which itself can arise from illness, surgery or alcohol abuse)

25
Q

What are the symptoms of diabetic ketoacidosis?

A 
Rapid weight loss
Abdominal pain
Sweet smelling breath
Unusual odour to urine or sweat
Tasting sweetness or metal
Polyuria
Thirst
Nausea and vomiting
26
Q

Why might you change a patient from long acting sulfonylurea like Glibenclamide onto Tolbutamide or Gliclazide?

A 
Patient could be at increased risk of hypoglycaemia - potentially through renal impairment this can result in the following symptoms:
Shaking
Trembling
Sweating 
Pin and needles in lips / tongue
Hunger
Palpitation
Headache
Double vision 
Slurred speech
Confusion 
Convulsions
Pallor
Concentration difficulties
Feeling cold
Loss of consciousnous
Coma
27
Q

The most appropriate insulin in pregnancy?

A

Isophane, an intermediate created by combination with protamine.

28
Q

How does blood glucose range change in children ?

A

Children fasting should range from 4-8 and under 10 after meals whereas adults should be 4-7 and under 9 respectively.

29
Q

Why might you need insulin adjustments in renal and liver disease?

A

Renal and liver impairment will REDUCE insulin requirements.

30
Q

Why advise site rotation in subcutaneous insulin injection?

A

To reduce lipohypertrophy site rotation of buttocks, thigh (inner and outer), abdomen and upper arm is recommended

Before subcutaneous injection site should be checked and free of bruising, swelling and infection to reduce erratic absorption (which can potentially affect glycaemic control.

31
Q

Why would you not recommend Metformin and Sulfonylureas in type 1 DM?

A

These both require endogenous insulin present in order to benefit patient.

32
Q

Why might you be concerned if a patient Linagliptin reports severe abdominal pain radiating to the back?

A

The gliptins, or DPP4 inhibitors can be associated with pancreatitis and severe abdominal pain is a sign and requires referral for investigation.

*Note Vildagliptin can also cause liver toxicity which could also present as abdominal pain.

33
Q

Why would you be concerned if a patient on Metformin showed signs of dehydration? (Sunken eyes, less skin turgor)?

A

This (with renal failure, tissue hypoxia and HF) is a risk factor for ketoacidosis

34
Q

Why would you counsel a patient on Pioglitazone on the following:
Haematuria, dysuria, urinary urgency

Liver issues

Hypertension

A

Pioglitazone is associated with increased bladder cancer risk and haematuria, dysuria and increased urinary frequency can be signs of it and require investigation, this risk increases with age.

Can cause liver dysfunction so patient should be aware of signs of jaundice, abdominal pain, pruritus, nausea and vomiting, fatigue.

The risk of HF is increased in those with predisposing factors such as hypertension, AF, and MI.

35
Q

Major counselling points of Meglitinides?

A

Can cause hypoglycaemia so should be give at meal times to stop hyperglycaemic peaking

During illness a Meglitinide should be substituted for insulin

36
Q

Why is Desmopressin more appropriate than Vasopressin in CVD?

A

As it is selective for the V2 receptors it means no V1 vasoconstriction or v3 platelet aggregation.

It is also longer acting allowing a simple dosing schedule.

37
Q

Why avoid nasal Desmopressin in nocturnal enuresis?

A

Increased side effects.

38
Q

Why would you use caution with ADH agonists in the elderly and renally impaired?

A

Elderly are at increased risk of hyponatraemia and hyponatraemic convulsions (aswell as risk of renal disease, CVD and HF) so cautionis needed and counselling direct in nocturnal diuresis (fluid restriction 1 hour before and for 8 hours after, stop medication in cases of vomiting and diarrhoea)

39
Q

Why would you counsel a Desmopressin patient on reporting signs of drowsiness, confusion and potentially convulsions?

A

These are signs of hyponatraemia.

40
Q

Why would careful renal and electrolyte monitoring be required when combining Desmopressin / Vasopressin with Diuretics, NSAIDs, k sparing diuretics, Chlorpromazine , SSRIs, SNRIs, MAOI, TCAs?

A

All these drugs increase the risk of hyponatraemia, recognisable with signs of drowsiness, confusion, convulsions and plasma sodium concentration under 142mmol /L

41
Q

Why advise patient to take care combining Desmopressin with Loperamide?

A

Loperamide increases the absorption of Desmopressin so could increase side effects including fluid retention, vomiting, abdominal pain and nausea.

42
Q

How does the MOA of V2 antagonists, Talvaptan and Demelocycline relate to side effects and cautions?

A

V2 antagonism causes reduced aquaporin rate formation and increase sodium levels in blood (decreased salt loss in blood), this would increase sodium so should not be used in hypernatraemia, anuria, impaired thirst perception. So salt and hydration to be monitored.

Gives rise to thirst, increased urination, dehydration.

43
Q

Why be wary of hyponatraemic signs in DM?

A

DM can be associated with PSEUDOhyponatraemia and would not need treatment of V2 antagonists.

44
Q

What would monitor in V2 antagonists?

A

Sodium concentration
Hydration
LFT

45
Q

How does corticosteroid use results in adrenal suppression? How to minimise and deal with this?

A

Increased steroid medications activate the negative feedback mechanism to decrease ACRF release from hypothalamus which decreases Corticotrophin release from anterior pituitary and reduce endogenous hormones from adrenal cortex in long term therapy.

This can be reduce with morning dosing (larger suppression occurs from nighttime dosing) and by gradual withdrawal to allow natural production to start (prevents adrenal insufficiency, hypotension and death).

46
Q

Under what circumstances would you recommend gradual steroid withdrawal?

A

If 40mg Pred or equivalent every day for one week
If course over 3 weeks
Course in patients who have used prolonged course within the last year
Causes of adrenal suppression (Addison’s)
Repeated courses recently
Repeated night time dosing

47
Q

Why use glucocorticoids with caution in DM?

A

MOA involves reduced glucose update and increase gluconeogenesis leading to hyperglycaemia do patients with diabetes or pre diabetes will have disturbed control, and could effect CVD and patients who are obese too.

48
Q

Why use glucocorticoids in caution for patients taking biphosphonates?

A

Can cause osteoporosis due to reduced calcium absorption (and increased excretion) so increasing risk of fractures (biphosphonates already increase hip fractures and jaw necrosis) as well as a vascular necrosis of femoral head.

49
Q

Why use glucocorticoids with caution in patients with DHx of steroid myopathy ?

A

Decreased protein anabolism and increased catabolism leads to muscle weakness

50
Q

Why is glucocorticoid use associated with moon face, increased abdominal fat and distension?

A

Causes lipase activation and fat redistribution

51
Q

Why does glucocorticoid use lead to decrease wound healing, increasing peptic ulceration, infections, candiasis, TB reactivation.

A

Immunosuppressive and anti-inflammatory actions via reduced neutrophils, macrophages T helpers, reduced complement factors, cytokines, NO, basophils.

Increases anti inflammatory via IL10 and 1 upregulation

This increases risk of infection from chickenpox and measles so patient should carry steroid cards.

52
Q

Why use Liothyronine in hypothyroid comas?

A

As T4 (levothyroxine) is converted to liothyronine in target cells it is skipping a step so acts faster within a few hours.

53
Q

Why check if a person receiving hypothyroid treatment is diabetic?

A

T3 and T4 can increase insulin requirements so patient may need higher doses to achieve normoglycaemia and blood glucose between 4-9mmol / L

54
Q

Why use the lowest dose possible for Propylthiouracil in pregnancy? (First trimester)

A

High doses are associated with foetal goitre and hypothyyoidism

55
Q

Counselling for Propylthiouracil and Carbimazole in thyrotoxicosis?

A

Be wary of neutropenia and agranulocytosis signs (fever, sore throat, mouth ulcers), referral to doctor needed

Liver toxicity possible

Rashes / itching can be treated with antihistamines.

May take time for effects due to T4 stores in body (Propylthiouracil quicker due to preventing T4 to T3 conversion in target cells.

56
Q

What is the rationale for high dose iodine in thyrotoxicosis?

A

A low iodine intake / level results in increase TRH release from the hypothalamus which stimulates the anterior pituitary to release thyrotrophin which causes T4 release and T3 (less T3) ultimately increase thyroid gland size and vascularity. High iodine treatment reduces the gland size and vascularity .

57
Q

Why increase thyroxine dose SLOWLY in CVD?

A

As excessive dosages can cause angina, restlessness, arrhythmias, diarrhoea, tremor, insomnia, palpitations, vomiting and tachycardia so an ECG before to determine baseline is recommended. Due to the cardiovascular side effects we would use caution in DM, CVD, HT and MI.

58
Q

Symptoms of hypothyroidism?

A 
Fatigue
Cold intolerance
Weight gain
Weakness
Constipation
Menstruated irregularities
Depression
Mental fog
Dry skin
Goitre
Oedema
Vocal deepening
Bradycardia
Slow speech 
Myxoedema

Pharmacy (17 decks)

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