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AKT revision > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Describe pathophysiology of T2DM?

A

In T2DM, the response to insulin is diminished, and this is defined as insulin resistance. During this state, insulin is ineffective and is initially countered by an increase in insulin production to maintain glucose homeostasis, but over time, insulin production decreases, resulting in T2DM.

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2
Q

What criteria is used to diagnose T2DM?

A

HbA1c > 48mmol
Fasting glucose > 7mmol
Random glucose > 11.1mmol

Usually these are monitored over several repeat readings, to ensure the diagnosis is correct.

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3
Q

In which patient groups is HbA1c not reliable to use?

A

Under 18 years
Pregnancy or 2 months post-partum
Recent pancreatic injury or surgery
On certain medications causing hyperglycaemia (i.e. steroids)
ESRD
T2DM patients who have had acute illness

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4
Q

What lifestyle advice should be given for T2DM?

A

Diet - high fibre, low-glycaemic-index sources of carbohydrate (such as fruit, vegetables, wholegrains, and pulses), low-fat dairy products, and oily fish. Low sugar intake, regular meal times.
Weight loss - if obese, aim for 5-10% body weight loss.
Regular exercise
Alcohol advice - risk of hypoglycaemia due to interaction with medications
Smoking cessation
Risk of periodontitis - regular review

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5
Q

How often should HbA1c be measured in T2DM?

A

3–6 monthly intervals initially until stable on unchanging antidiabetic treatment, and then every 6 months to ensure adequate blood glucose control.

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6
Q

What is the first line medication for T2DM?

A

Metformin monotherapy

OR

Metformin with SGLT-2 inhibitor if high risk for CVD

When starting an adult with type 2 diabetes on dual therapy with metformin and an SGLT-2 inhibitor as first-line therapy, introduce the drugs sequentially, starting with metformin and checking tolerability. Start the SGLT-2 inhibitor as soon as metformin tolerability is confirmed.

ALSO

ensure you calculate Qrisk - if risk > 10% over 10 years, start statin

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7
Q

What is the MOA of metformin?

A

Inhibiting hepatic gluconeogenesis and opposing the action of glucagon (released from the alpha cells of islets of langerhans in pancreas in response to hypoglycaemia, in order to stimulate glucose production) - overall lowering the levels of glucose in the bloodstream.

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8
Q

What are some contraindications to metformin?

A

Renal dysfunction (eGFR < 30mmol)
Congestive cardiac failure needing drug treatment.
Hypersensitivity to metformin.
Acute or chronic metabolic acidosis.
Impaired hepatic function.

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9
Q

What are some side effects of metformin?

A

Abdominal pain; appetite decreased; diarrhoea; gastrointestinal disorder; nausea; taste altered; vitamin B12 deficiency; vomiting - the GI effects are common, and usually improve with length of treatment

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10
Q

When would you consider first line metformin PLUS SGLT-2 inhibitor for T2DM?

A

If the patient already has chronic heart failure,
established atherosclerotic cardiovascular disease, or
at high risk of developing cardiovascular disease.

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11
Q

How does an SGLT-2 inhibitor work?

A

Blocking SGLT2 protein located in the proximal convoluted tubule of the nephron.

The SGLT2 protein is responsible for the resorption of approximately 90% of filtered glucose while the remainder is reabsorbed by SGLT1 proteins found on the distal part of the proximal convoluted tubule.

SGLT2 inhibition results in glycosuria (and natriuresis as the protein is a co-transporter), thereby lowering plasma glucose concentrations.

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12
Q

How does pioglitazone work for T2DM?

A

Thiazolidinediones, such as pioglitazone, activate peroxisome proliferator-activated receptor gamma (PPAR gamma) to improve insulin sensitivity. However, they also cause increased sodium and fluid retention, thereby leading to a 42% increased risk of incident heart failure.

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13
Q

What is the second line management of T2DM (also what should be offered if metformin is not tolerated or contraindicated)?

A

Offer an SGLT-2 inhibitor to people with chronic heart failure or established atherosclerotic cardiovascular disease, and consider offering an SGLT-2 inhibitor to people at high risk of developing cardiovascular disease.

For other people, consider one of the following as first-line treatment:

A dipeptidyl peptidase-4 inhibitor (DPP-4 inhibitor).
Pioglitazone.
A sulfonylurea.
A sodium-glucose cotransporter-2 inhibitor (SGLT-2 inhibitor) — this may be considered instead of a DPP-4 inhibitor if a sulfonylurea or pioglitazone is not appropriate.

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14
Q

How does a DPP-4 inhibitor work?

A

DDP-4 inhibitors work by blocking the action of the enzyme DPP-4, which destroys incretins – hormones - that the body makes. Incretins are naturally produced by the stomach when we eat. They help the body produce more insulin when it’s needed and lowers blood sugar levels

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15
Q

What are some examples of SGLT-2 inhibitors?

A

Dapagliflozin
Canagliflozin
Empagliflozin

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16
Q

What are some examples of DPP-4 inhibitors?

A

Sitagliptin
Vildagliptin

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17
Q

What are contraindications to SGLT-2 inhibitors?

A

CKD - eGFR < 60
liver disease
increasing age - avoid in over 85 years (risk of volume depletion)
active foot disease

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18
Q

What are contrainidications to DDP-4 inhibitors?

A

Ketoacidosis.
Hepatic impairment — avoid vildagliptin; avoid saxagliptin and alogliptin if severe hepatic impairment.
Heart failure — avoid vildagliptin if severe heart failure; avoid alogliptin if moderate-to-severe heart failure.

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19
Q

what are the different treatment steps for T2DM?

A

first line - metformin / metformin + SGLT-2 inhibitor if indicated

second line - dual agent therapy - usually metformin + one of the other medications

third line - triple agent therapy

fourth line - insulin

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20
Q

what are some complications of T2DM?

A

Macrovascular -
Atherosclerotic cardiovascular disease (CVD)

Microvascular -
chronic kidney disease
diabetic retinopathy
peripheral neuropathy
foot complications

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21
Q

what is the role of urine albumin:creatinine ratio?

A

Performed first thing in the morning
Indicative of level of kidney disease in the context of HTN or T2DM - if urine albumin: creatinine ratio high, this indicates worsening renal disease

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22
Q

what screening is associated with T2DM management?

A

Diabetic eye screening will be offered at diagnosis and:
Every 2 years for people at low risk of sight loss (no identified diabetic retinopathy on two successive screening tests).
At least annually for all other people with diabetes.

Yearly diabetic foot review

Yearly diabetes review
Yearly screening for diabetic nephropathy - U+E monitoring, urine albumin:creatinine ratio

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23
Q

what are some side effects of SGLT-1 inhibitors?

A

Urinary and genital infections

Fournier’s gangrene

Normoglycaemic ketoacidosis

Increased risk of lower limb amputation so need to monitor feet carefully

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24
Q

what type of drug is gliclazide?

A

SULFONYLUREA

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25
Q

examples of sulfonylureas?

A

Gliclazide

Tolbutamide

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26
Q

Effect of SGLT-2 inhibitors on weight

A

weight loss

27
Q

Mechanism of action of sulfonylureas

A

Increased pancreatic excretion of insulin

28
Q

Where in the pancreas do sulfonylureas work?

A

ATP dependent K+ channels on the cell membrane of pancreatic beta cells

to increase pancreatic insulin secretion

29
Q

Side effects of sulfonylureas

A

Hypoglycaemia

Weight gain

SIADH

Bone marrow suppression

Cholestatic liver damage

Peripheral neuropathy

30
Q

Effect of sulfonylureas on weight

A

weight gain

31
Q

Which T2DM medication can cause liver damage?

A

Sulfonylureas cause cholestatic liver damage

Pioglitazone causes liver impairment, need to monitor LFTs

32
Q

Example of thiazolidinediones

A

Pioglitazone

33
Q

Mechanism of action of pioglitazone

A

Reduces peripheral insulin resistance

by agonising the PPAR-gamma receptor

34
Q

Which T2DM medication reduces peripheral insulin resistance?

A

Pioglitazone

35
Q

Side effects of pioglitazone

A

Weight gain

Liver impairment

Fluid retention so C/I in heart failure

Increased risk of fractures

Increased risk of bladder ca

36
Q

Effect of pioglitazone on weight

A

weight gain

37
Q

what are the causes of hypothyroidism?

A

primary:
- hashimotos
- iodine deficiency
- thyroidectomy
- radiation damage to the thyroid
- subacute thyroiditis (de quervains)
- medications (such as amiodarone)

secondary:
- hypopituitrisim
- i.e. tumours
- Sheehans syndrome

38
Q

what is the pathophysiology of hashimotos hypothyroidism?

A

autoimmune condition where anti-TPO antibodies and anti-thyroglobulin antibodies are produce which attack the thyroid gland.

39
Q

what are the symptoms of hypothyroidism?

A

weight gain
fatigue
cool peripheries
hair loss
goitre
dry skin
oedema
constipation
menorrhagia
decreased reflexes
carpal tunnel syndrome

40
Q

what are the clinical features of hashimotos?

A

signs of hypothyroidism + painless goitre

41
Q

what is de quervains thyroiditis?

A

Although the precise cause is not known, De Quervain’s thyroiditis is believed to be caused by a viral infection and the inflammatory process associated with such infections.

42
Q

what are the clinical features of de quervains thyroiditis

A

signs of hypothyroidism + associated with a painful goitre and raised ESR

43
Q

what is the de quervains thyroiditis characterised by?

A

Triphasic course of transient thyrotoxicosis, followed by hypothyroidism, followed by a return to euthyroidism.

44
Q

what is riedel thyroiditis?

A

Fibrous tissue replacing the normal thyroid parenchyma

45
Q

what are the clinical symptoms of riddle thyroiditis?

A

hypothyroidism symptoms + painless goitre

46
Q

what drugs cause hypothyroidism?

A

amiodarone
lithium

47
Q

TFT in primary hypothyroidism?

A

TSH high
T3 and T4 low

48
Q

TFT in secondary hypothyroidism?

A

T3 and T4 low
TSH low

49
Q

management of primary hypothyroidism?

A

commence levothyroxine

50
Q

how should levothyroxine be commenced in the elderly or those with ischaemic heart disease?

A

initial starting dose of levothyroxine should be lower in elderly patients and those with ischaemic heart disease.

The BNF recommends that for patients with cardiac disease, severe hypothyroidism or patients over 50 years the initial starting dose should be 25mcg od with dose slowly titrated. Other patients should be started on a dose of 50-100mcg od

51
Q

how often should TFT be checked when commencing levothyroxine?

A

8- 12 weeks after a dose change

once TSH stable (2 readings, 3 months apart) then check annually

52
Q

how should levothyroxine be taken?

A

Advise the person to take LT4 medication on an empty stomach in the morning before other food or medication.

53
Q

what are some side effects of levothyroxine therapy?

A

hyperthyroidism: due to over treatment

reduced bone mineral density

worsening of angina
atrial fibrillation

54
Q

what dose change should occur for women who have become pregnant and are taking levothyroxine?

A

women with established hypothyroidism who become pregnant should have their dose increased ‘by at least 25-50 micrograms levothyroxine’* due to the increased demands of pregnancy. The TSH should be monitored carefully, aiming for a low-normal value

55
Q

what is subclinical hypothyroidism?

A

TSH raised but T3, T4 normal
no obvious symptoms

56
Q

management of subclinical hypothyroidism if TSH > 10?

A

consider offering levothyroxine if the TSH level is > 10 mU/L on 2 separate occasions 3 months apart

57
Q

management of subclinical hypothyroidism if TSH < 10, and patient is symptomatic?

A

consider 6 month trial of levothyroxine

58
Q

management of subclinical hypothyroidism if asymptomatic or elderly?

A

watch and wait
repeat TFT in 6 months

59
Q

causes of hyperthyroidism?

A

graves disease
toxic nodular goitre

60
Q

TFT in hyperthyroidism?

A

T3 and T4 high
TSH low

61
Q

what are signs of thyrotoxicosis?

A

weight loss with a normal or increased appetite
heat intolerance with increased sweating
palpitations
tremor
anxiety
proximal muscle weakness
alopecia
increased fatigability

62
Q

what are specific signs of graves disease?

A

eye signs (30% of patients)
- exophthalmos
- ophthalmoplegia
- pretibial myxoedema
thyroid acropachy, a triad of:
- digital clubbing
- soft tissue swelling of the hands and feet
periosteal new bone formation

63
Q

what is the pathophysiology of graves disease?

A

autoimmune condition where antibodies TSH receptor stimulating antibodies and anti-thyroid peroxidase antibodies are produced which stimulates TSH production

64
Q

Management of hyperthyroid in primary care?

A

consider commencing beta blocker such as propranolol for symptom control

consider commencing carbimazole under specialist guidance

AKT revision (10 decks)

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