T1DM

Question 1

Features of DKA

Answer 1

abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
acetone-smelling breath (‘pear drops’ smell)

Question 2

Use of HbA1c in diagnosis of T1DM

Answer 2

HbA1c is not as useful for patients with a possible or suspected diagnosis of T1DM as it may not accurately reflect a recent rapid rise in serum glucose

Question 3

Which protein levels are typically low in patients with T1DM

Answer 3

C-peptide levels

Question 4

Antibodies present in t1dm

Answer 4

Anti-GAD
Islet cell antibodies(ICA)
Insulin autoantibodies(IAA)

Question 5

Diagnostic criteria for T1DM

Answer 5

If the patient is symptomatic:
fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.

Question 6

How often should HbA1c be monitored in type 1 diabetics and what should their target be

Answer 6

should be monitored every 3-6 months

adults should have a target of HbA1c level of 48 mmol/mol (6.5%) or lower. NICE do however recommend taking into account factors such as the person’s daily activities, aspirations, likelihood of complications, comorbidities, occupation and history of hypoglycaemia

Question 7

NICE advice on self-monitoring of blood glucose

Answer 7

recommend testing at least 4 times a day, including before each meal and before bed
more frequent monitoring is recommended if frequency of hypoglycaemic episodes increases; during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding

Question 8

Blood glucose targets in T1DM

Answer 8

5-7 mmol/l on waking and

4-7 mmol/l before meals at other times of the day

Question 9

When do NICE recommend metformin in type 1 diabetes management

Answer 9

NICE recommend considering adding metformin if the BMI >= 25 kg/m²

Question 10

Why is coeliac disease more common in those with T1DM

Answer 10

The HLA-DQ2 genotype sometimes seen in T1DM is also associated with coeliac disease, and therefore coeliac disease is more common in those with T1DM

Question 11

What type of hypersensitivity reaction is involved in T1DM

Answer 11

T1DM is most commonly a type IV hypersensitivity autoimmune reaction, in which CD4+ T helper cells and CD8+ cytotoxic T cells attack pancreatic beta cells, eventually eliminating any insulin production

Question 12

Why is there blurred vision in hyperglycaemia

Answer 12

Hyperglycaemia can cause an acute, reversible swelling of the lens.

This is a different mechanism to that seen in the chronic complication of diabetic retinopathy.

Question 13

When is HbA1c unreliable

Answer 13

HbA1c can be unreliable if a patient has any concurrent condition affecting red blood cell survival.

Question 14

What causes DKA

Answer 14

DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

Question 15

Most common precipitating factors of DKA

Answer 15

The most common precipitating factors of DKA are infection, missed insulin doses and myocardial infarction.

Question 16

Diagnosis of DKA

Answer 16

glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick

Question 17

Mx of DKA

Answer 17

fluid replacement: most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially.
insulin: an intravenous infusion should be started at 0.1 unit/kg/hour. Once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started
correction of hypokalaemia
long-acting insulin should be continued, short-acting insulin should be stopped

Question 18

Complications of DKA

Answer 18

gastric stasis
thromboembolism
arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
acute respiratory distress syndrome
acute kidney injury

Question 19

Pathophys of diabetic retinopathy

Answer 19

Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes

Question 20

What does damage to endothelial cells and pericytes in the retinal vessel walls from hyperglycaemia result in

Answer 20

Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy.

Pericyte dysfunction predisposes to the formation of microaneurysms.

Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia

Question 21

Classification of diabetic retinopathy

Answer 21

Patients are typically classified into those with non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR) and maculopathy.

Question 22

Features of non-proliferative diabetic retinopathy

Answer 22

microaneurysms
blot haemorrhages
hard exudates
cotton wool spots (‘soft exudates’ - represent areas of retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

Question 23

Key features of proliferative diabetic retinopathy

Answer 23

retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years

Question 24

Key features of diabetic maculopathy

Answer 24

based on location rather than severity, anything is potentially serious
hard exudates and other ‘background’ changes on macula
check visual acuity
more common in Type II DM

Question 25

General management of diabetic retinopathy

Answer 25

optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology

Question 26

Management of diabetic maculopathy

Answer 26

if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors

Question 27

Management of non-proliferative retinopathy

Answer 27

regular observation

if severe/very severe consider panretinal laser photocoagulation

Question 28

Management of proliferative retinopathy

Answer 28

laser photocoagulation
intravitreal VEGF inhibitors
if severe or vitreous haemorrhage: vitreoretinal surgery

Question 29

What causes diabetic foot disease

Answer 29

It occurs secondary to two main factors:
neuropathy: resulting in loss of protective sensation (e.g. not noticing a stone in the shoe), Charcot’s arthropathy, dry skin

peripheral arterial disease: diabetes is a risk factor for both macro and microvascular ischaemia

Question 30

Presentation of diabetic foot disease

Answer 30

neuropathy: loss of sensation
ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication
complications: calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene

Question 31

how should diabetics be screened for diabetic foot disease

Answer 31

All patients with diabetes should be screened for diabetic foot disease on at least an annual basis

screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse

screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot

Question 32

DM sick day rules

Answer 32

Increase frequency of blood glucose monitoring to four hourly or more frequently
Encourage fluid intake aiming for at least 3 litres in 24hrs
If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake
It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell
Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis

Question 33

Diabetic nephropathy screening

Answer 33

all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria

Question 34

BP control target if diabetic nephropathy

Answer 34

BP control: aim for < 130/80 mmHg

Question 35

Management of diabetic nephropathy

Answer 35

dietary protein restriction
tight glycaemic control
benefits independent of blood pressure control have been demonstrated for ACE inhibitors (ACE-i) and angiotensin II receptor blockers (A2RB)
control dyslipidaemia(statins)

Question 36

Use of C peptide test in diabetes

Answer 36

can be used to distinguish between type 1 and type 2 diabetes, as it can determine how much of their own insulin a person is producing, regardless of exogenous insulin

Question 37

What is alopecia areata?

Answer 37

One or more round bald patches that appear suddenly, most often on the scalp - associated with diabetes

Question 38

Risk factors for alopecia areata

Answer 38

FHx
FHx of autoimmune disease
Down syndrome
Drug induced(biologics)

Question 39

Mx of alopecia areata

Answer 39

Treatment not always required because spontaneous regrowth common

Topical steroids
Minoxidil
Counselling
Camouflaging hair loss