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Flashcards in Endocrine System Deck (57)
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1
Q

What is cushings syndrome? How is it diagnosed and treated?

A

It is excessive cortisol secretion in the body often caused by benign tumours.

Overnight dexamethasone suppression test is how it is diagnosed. Usually, when dexamethasone is given, it supresses cortisol production for the next 24 hours but in patients with cushings, this doesn’t happen.

Treated by surgery, oral ketoconazole (hepatotoxic) or metyrapone.

2
Q

What is the MHRA advice regarding corticosteroids (all routes) ?

A

Rare risk of central serious chorioretinopathy. Report any blurred vision or visual disturbances.

3
Q

Which are the mineralocorticoids and which side effects are associated with them?

A

Fludrocortisone, hydrocortisone,

Remember mineral side effects: hypertension, hypernatraemia, water retention, hypokalaemia, hypocalcaemia.

4
Q

Which are the glucocorticoids and which side effects are associated with them?

A

Prednisolone, hydrocortisone

diabetes, osteoporosis, muscle wasting peptic ulcers, psychiatric reactions.

5
Q

How is corticosteroid deficiency managed?

A

Adrenal cortex normally secretes cortisol (hydrocortisone) which has glucocorticoid activity and the mineralcorticoid aldosterone.

In deficiency states e.g Addison’s/ post adrenalectomy, give hydrocortisone + fludrocortisone
In hypopituitarism, only glucocorticoid replacement is needed.

6
Q

Which glucocorticoid doses are equivalent to prednisolone 5mg?

A

Hydrocortisone 20mg
Dexamethasone 750 micrograms
deflazacort 6mg
Methylpred 4mg

7
Q

What are the notable side effects of systemic corticosteroids?

A
  • Adrenal suppression
  • Infections- increased susceptibility. Possibility of severe chickenpox and measles - get immunised
  • Psychiatric disorders- depression, suicidal thoughts
  • Serious GI effects
  • musculoskeletal
  • ophthalmic
  • hiccups - pred, dex, bethametasone
8
Q

When should steroids be tapered?

A
  • 40mg pred (or equivalent for ≥ 1 week)
  • been on steroids for OVER 3 weeks
  • repeated doses at night
  • repeated courses
  • short course within 1 year of stopping long-term therapy

Dose can be reduced rapidly to physiological doses (pred 7.5mg) then reduced more gradually.

9
Q

What is diabetes insipidus and how is it managed?

A

Can be caused by insufficient ADH (cranial/prituitary) caused by trauma or surgery. Can also be caused by the kidneys not registering the ADH (nephrogenic). This leads to excessive thirst and polyuria.

Treated with vasopressin (ADH) or desmopressin.
If nephrogenic, thiazides or carbamazepine may help.

NOTE: limit fluids while on desmopressin inc. if swimming. Can cause hyponatraemia/ overload.
Avoid in HF.

10
Q

How can SIADH and hyponatraemia be managed.

A

Tolvaptan is used for hyponatraemia secondary to SIADH. Rapid correction of hyponatraemia can lead to neuropathy (due to dehydration)

Discontinue tolvaptan if jaundice/ signs of hepatotoxicity. STOP if rapid rise in Na+ (>12mmol in 24 hours or >18mmol in 48 hours).
Monitor serum Na and for dehydration every 6 hours in first 2 days.

11
Q

When must a person with diabetes notify DVLA?

What must they do whilst driving?

A

If on insulin for over 3 months or if they have had any hypos.

Check BMs 2 hours before driving and every 2 hours whilst driving. Must be above 5mmol/L. If BMs drop below 4mmol/L stop and don’t restart driving until 45 minutes after BMs are normal.

12
Q

What do you know about HBA1c?

What are the targets?

A

It reflects glycemic control over the past 2-3 months
Can be used to diagnose type 2 diabetes (symptoms >2 months)
It is invalid in patients with anaemia/ abnormal haemoglobin.

Targets
Type 1 diabetes = 48mmol/mol
Type 2 diabetes = 48mmol/mol
Type 2 diabetes = 53mmol/mol if taking 2 or more antidiabetic drugs or pt on a single drug associated with hypos (e.g sulfonylureas)

**Targets should be relaxed in old/frail patients to prevent hypoglycemia.

13
Q

What are the main complications of diabetes?

How are they managed?

A
  • Nephropathy- ACEi (can cause hypos with unsulin)
  • cardiovascular disease,
  • retinopathy,
  • neuropathy - paracetamol, nsaids, neuropathic pain drugs, capsaicin, opioids (e.g tramadol)
  • peripheral artery disease.
  • DKA
14
Q

Which patients with type 1 diabetes may also benefit from metformin?

A

Those with BMI >25 (>23 in south asians)

15
Q

What insulin regimes can a patient be on?

A
  1. Basal- bolus multiple daily injections.
    Basal insulin: ins. detemir (levemir) ins. glargine (lantus)
    Recommended bolus : insulin aspart (novorapid)
  2. Bixed (biphasic) regimen
    Intermediate acting: Humulin I + rapidacting: Humalog
    OR just biphasic (e.g novomix 30, humalog mix 30)

3.Continuous subcutaneous insulin infusion.
Rapid/short acting via insulin pump. Specialist only.

16
Q

What drugs can mask awareness of hypoglycaemia?

A

Beta blockers

17
Q

What can be caused by repeatedly injecting insulin at the same site?

A

Lipohypertrophy which can lead to erratic insulin absorption which can lead to poor glycaemic control.

18
Q

What range should blood glucose lie in?

A

4-9mmol/L (4-10mmol/L in children)
4-7mmol/L before meals,
<9mmol/Lafter meals
>5mmol/L when driving

19
Q

What is the onset and duration of rapid acting insulin?

Are there any special directions?

A

Rapid acting

  • Onset- within 15 minutes
  • duration 2-5 hours
  • Inject BEFORE meals. Routine post meal injections lead to increased risk of high postprandial glucose and hypos.
20
Q

What is the onset and duration of short acting insulin?

Can it be given via another route?

A

Short acting

  • Onset 30-60 minutes
  • duration up to 9 hours
  • Can be given IV for emergencies e.g diabetic ketoacidosis. Onset= instantaneous but short duration.
21
Q

What is the onset and duration of intermediate acting insulin?

A

Intermediate acting

  • onset 1-2 hours
  • duration 11-24 hours

Biphasic insulin is intermediate +short/rapid acting - to be administered before meals

22
Q

What is the onset and duration of long acting insulin?

A

Duration up to 36 hours.

Reaches steady state after 2-4 days.

23
Q

When should therapy for type 2 diabetes be intensified?

A

If HBA1c is constantly above 58mmol/L

24
Q

What is the treatment pathway for type 2 diabetes?

Assume metformin is tolerated.

A

First line:
metformin ( ifHBA1c>48 despite lifestyle change)

Second line: dual therapy
metformin +
sulphonylurea (e.g gliclazide) OR pioglitazone OR DPP4 inhibitor (gliptin) OR SGLT-2 inhibitor (gliflozin)

Third line : triple therapy
metformin + sulphonylurea + DPP4i
metformin + sulphonylurea + pioglitazone
metformin + sulphonylurea + SGLT-2 inhibitor
metformin + pioglitazone + SGLT-2 inhibitor (NOT dapagliflozin as you cant use it with pioglitazone)
alternatively insulin can be started

4th line: triple therapy
metformin + sulphonylurea + GLP-1 agonist (e.g exetanide/ liraglutide)

25
Q

Which SGLT-2 inhibitor can’t be used with pioglitazone?

What is a specific caution during hospitalisation?

A

dapagliflozin

Manufacturer recommends switching to insulin when hospitalised for acute serious illness due to the risk of DKA.

26
Q

What are the conditions for using GLP-1 agonists?

A

BMI > 35kg/m2 OR
cant use insulin OR
weight loss would benefit the patient

After 6 months, review and only continue if:
reduction of at least 11mmol/L in HBA1c or
weight loss of at least 3% initial weight

27
Q

What is the treatment pathway for type 2 diabetes if the patient cannot tolerate metformin?

A

First line:
sulphonylurea OR DPP4 inhibitor OR pioglitazine

Second line
dual therapy with 2 of the above 3.
If insufficient control, you can add in insulin.

28
Q

What is diabetic ketoacidosis (DKA)?

What are the symptoms and how is it managed?

A

The body runs out of insulin and starts breaking down fat to produce energy leading to build up of ketones.

Symptoms: strong sweet smell to breath: pear drops/ nail varnish, N+V, weight loss.

Treated by giving fluids + electrolytes and insulin.
Continue insulin until blood ketones <0.3mmol/L, pH7.3 and the patient can eat and drink.

29
Q

How are diabetic drugs and insulin managed during surgery?

A
  • If HBA1c < 69mmol/L - Give normal long acting insulin at 80% of usual dose on the day of surgery.
  • If major surgery or poor glycaemic control- put on VRII
  • If patient is having insulin, stop all oral antidiabetic drugs only GLP-1 agonists can be continued.
  • If no insulin, only omit sulphonylurea on the day of surgery until patient is eating and drinking again.
  • metformin should only be stoped if the patient wil miss more than one meal or at risk of AKI.
30
Q

Which antidiabetic drugs are safe during pregnancy and breastfeeding?

A

Only metformin and insulin should be used during pregnancy. Glibenclamide can be considered from 11 weeks for women who cant have metformin or insulin.
Isophane insulin (Humulin I) is first choice in pregnancy.
Reduce insulin immediately after birth- risk of hypos

Metformin and glibenclamide can be used in breastfeeding.

31
Q

What do you know about metformin?

MOA and max dose.

A

MOA- decreases gluconeogenesis, increases peripheral glucose utilisation. Only active if endogenous insulin is present. Doesnt stimulate insulin production so doesn’t cause hypos.

Risk of lactic acidosis- report dyspnoea, muscle aches, abdo pain, asthenia (STOP metformin)
Max dose 2g daily.

32
Q

What do you know about sulphonylureas?

MOA, contraindications, side effects.

A

MOA- increase insulin secretion so can cause hypos. Residual beta cell activity is needed.

AVOID in acute porphyrias
Associated with weight gain and hypos.
Examples: glimepiride, glimbeclamide
gliclazide max dose 320mg OD/ MR 120mg OD

33
Q

What do you know about DPP4- inhibitors

A

MOA-increase insulin secretion and lower glucagon by increasing incretins.

Examples: sitagliptin, linagliptin, saxagliptin.

STOP if signs of pancreatitis (severe abdo pain)
No weight gain, causes less hypos than sulphonylureas

34
Q

What do you know about SGLT-2 inhibitors?

A

MOA- reduce glucose reabsorption by increasing urinary excretion.

Increased risk of UTIs
Can cause volume depletion- correct hypovolemia before initiating.
Risk of DKA

Examples: canagliflozin, dapagliflozin

35
Q

What is the MHRA alert regarding SGLT-2 inhibitors?

A

Risk of fatal DKA- pt aware of warning signs and STOP if DKA suspected

MHRA: RISK of Fournier’s gangrene (necrotising fascitis of genitalia or perineum)

36
Q

What do you know about pioglitazone?

What are the MHRA alerts regarding this drug?

A

MOA- reduces peripheral insulin resistance

MHRA warnings

  1. increased risk of heart failure when given with insulin. STOP if heart function deteriorates. Contraindicated in patients with history of HF
  2. increased risk of bladder cancer . STOP in haematouria. C/I in patients with history of bladder Ca.

Rare reports of liver problems. STOP if jaundiced.

37
Q

What is the MHRA alert regarding canagliflozin?

A

RISK of lower limb amputation (mainly toes)- foot care

38
Q

What do you know about acarbose?

A

MOA- delays digestion of starch and sucrose.
Smaller effect than other antidiabetic drugs. To be taken with food.
Hypos on this treatable with GLUCOSE not sucrose.
Can cause GI side effects but antacids are ineffective.

Contraindicated in IBS or previous abdo surgery.

39
Q

How is hypoglycaemia (BMs <4mmol/L) managed?

A
  • Glucose 10-20g (lucozade/coca cola)
  • If unconscious IM glucagon 1mg. If that is not effective, IV glucose 20%.
  • Long acting carbohydrate snack/meal after

Chronic hypos: diazoxide (not for acute hypos)

40
Q

What is the treatment pathway for osteoporosis?

A
Ensure adequate intake of calcium and vitamin D first.
1st line: 
oral bisphosphonates (alendronic)

2nd line:
IV bisphosphonates (ibandronic/ zolendronic acid)
denosumab (if osteoporosis is not caused by steropids)
teriparatide (max 24 months treatment)

Review bisphosphonate use after 5 years (3 years for zolendronic acid)

41
Q

What are the MHRA alerts regarding bisphosphonates AND denosumab?

A

RISK of atypical fermoral fractures (report hip/groin pain)

RISK of osteonecrosis of the jaw- higher risk in IV opptions. dental hygeine key. report moth pain.

RISK of osteonecrosis of the auditiory canal (report any ear pains)

42
Q

What is the MHRA alert regarding denosumab?

A

RISK of hypocalcaemia.

& same 3 as bisphosphonates- jaw, ear, hip.

43
Q

What are the counselling points when starting a patient on oral bisphosphonates?

A
  • Take first thing in the morning 30 mins before other medicines, food and drinks
  • Take with full glass of water only
  • Stay upright at least 30 minutes after taking it
  • Report any hip, mouth or ear pain. Oral hygiene is key.

Patient should STOP taking if oesophagitis occurs- new dysphagia, heartburn, pain on swallowing.

44
Q

What medicines can be used to suppress lactation?

A

cabergolide, bromocriptine.

45
Q

What is endometriosis and how is it treated?

A

-The lining of the uterus grows outside of the uterus.
-Leading to pelvic pain, painful periods, subfertility
-Treatments mostly supress oestrogen and are contraceptive such as the pill (combined, PO) danazol. Can also be treated with surgery- hysterectomy.
Can also use gonadotrophin releasing hormone analogues (leuprorelin)

46
Q

When do you need to give progestogens alongside oestrogen therapy when used in HRT?

A

Women with a uterus.
A progestogen should be added to reduce the risk of cystic hyperplasia of the endometrium and possible transformation to cancer.

47
Q

When are the early menopause and menopause ages?

A

Early menopause= 45 years

Menopause age= 50 years

48
Q

What are the risks of HRT (inc. tibolone)?

A
  • Breast cancer- ALL HRT- excess risk disappears 5 years after stopping.
  • Stroke ALL HRT- risk increases with age
  • Coronary heart disease- in women who started combined HRT more than 10 years after menopause.
49
Q

What are the risks of OESTROGEN only or combined HRT (due to the oestrogen aspect)?

A
  • Endometrial cancer- OESTROGEN only. Adding progesterone only removes risk but causes other issues.
  • Ovarian cancer- with long term COMBINED or OESTROGEN only HRT use.
  • VTE + PE- COMBINED or OESTROGEN only HRT use.
50
Q

How is HRT managed before surgery?

A

STOP HRT 4-6 weeks before any surgery (VTE risk)

Only restart after full mobilisation

51
Q

What reasons would you STOP HRT?

A
  • hepatitis, jaundice, liver enlargement
  • BP systolic >160mmHg or diastolic >95mmHg
  • sudden breathlessness/ chest pain (cardiac issues/PE)
  • unexplained swelling in leg (DVT)
  • serious neurological effects- severe headache, seizures, severe vision and auditory changes (stroke)
52
Q

How can heavy menstrual bleeding be managed?

A

Tranexamic acid/ mefenamic acid.
Oral progestogens
Ulipristal- a progestogen (heavy bleeding associated with fibroids- up to four courses)

53
Q

What do you know about cyproterone?

A

Anti-androgen used for hypersexuality and sexual deviation in men.
Also used for prostate cancer in men & acne in women.

STOP if it caues hepatotoxicity.
Can also cause depressed mood and temp infertility.

54
Q

How is hyperthyroidism managed?

What about in pregnancy?

A

1st line- carbimazole STOP if sore throat bone marrow suppression

2nd line- propylthiouracil (STOP if hepatotoxicity occurs. can also cause bone marrow suppression.

In pregnancy, use propylthiouracil first line in first trimester as carbimazole associated with congenital defects. But switch to low dose carbimazole in second trimester due to hepatotoxicity risk.

55
Q

How is thyrotoxicosis managed?

What are the symptoms?

A

Excess hyperthyroidism

Symptoms: weight loss, diarrhoea, palpitations, insomnia

IV fluids, propanolol (for palpitations), hydrocortisone , (carbimazole or propylthiouracil)
Radioactive iodide can also be used to treat this.

56
Q

What medicine decreases absorption of levothyroxine and what must be done?

A

Calcium supplements. Separate them by a minimum of 4 hours.

57
Q

What is the relation with TSH and T4 and thyroid?

A

High T4- hyPERthyroidism

High TSH- hypOthyroidism.

Think TSH is longer than T4 so you will need EXTRA supplementation (levothyroxine) if TSH is high.