Diabetes II

Question 1

[2] are first-line treatment for prolactinomas, even if there are significant neurological complications

Answer 1

Dopamine agonists (e.g. cabergoline, bromocriptine) are first-line treatment for prolactinomas, even if there are significant neurological complications

Question 2

Diagnosis of prediabetes involves specific criteria:

Impaired Fasting Glucose (IFG): Fasting blood glucose levels between [] mmol/L

Impaired Glucose Tolerance (IGT): Two-hour oral glucose tolerance test (OGTT) values between [] mmol/L

Answer 2

Diagnosis of prediabetes involves specific criteria:

Impaired Fasting Glucose (IFG): Fasting blood glucose levels between 6.1-6.9 mmol/L

Impaired Glucose Tolerance (IGT): Two-hour oral glucose tolerance test (OGTT) values between 7.8-11.1 mmol/L

Question 3

A patient with DMT2 is presenting with symptoms of gastroparesis.

What drug could you rec. to resolve this? [1]

Answer 3

First line treatment for this condition as recommended by NICE is with Domperidone, a dopamine receptor antagonist

Question 4

A 55 year old male who is acutely unwell is booked for emergency surgery to manage a bowel perforation. His is a known diabetic with poor control and his most recent HbA1c is 74 mmol2. It is likely the operation will go on for many hours and he will miss at least two meals.

How would you adapt is diabetic therapy for the procedure? [1]

Answer 4

Swtich to variable-rate intravenous insulin infusion

Question 5

What is the preferred treatment choice for MODY? [1]

Answer 5

Sulfonylureas (e.g. gliclazide)

Question 6

A 45-year-old woman is prediabetic (HbA1c 44 mmol/mol) and is enquiring about being prescribed liraglutide which she has heard about from a friend.

Given she is prediabetic, what other criteria must she meet to be considered for liraglutide under NICE guidance?

BMI > 25 kg/m2
BMI > 35 kg/m2
BMI >30 kg/m2
Being prediabetic is the only criteria
Hypertension

Answer 6

A 45-year-old woman is prediabetic (HbA1c 44 mmol/mol) and is enquiring about being prescribed liraglutide which she has heard about from a friend.

Given she is prediabetic, what other criteria must she meet to be considered for liraglutide under NICE guidance?

BMI > 25 kg/m2
BMI > 35 kg/m2
BMI >30 kg/m2
Being prediabetic is the only criteria
Hypertension

Question 7

After starting an ACE inhibitor, significant renal impairment may occur if the patient has undiagnosed []

Answer 7

After starting an ACE inhibitor, significant renal impairment may occur if the patient has undiagnosed bilateral renal artery stenosis

Question 8

A patient is end of life and you are trying to work out how to adapt their DMT2 treatment.

What should you do? [1] Explain x

Answer 8

Hypoglycaemic agents such as Insulin and sulfonylureas carry a significant risk of precipitating hypoglycaemia in patients at the end of their lives, due to their reduced oral intake.

UK therefore recommend stopping all oral hypoglycaemic agents in Type 2 diabetics.

As an insulin sensitizer, Metformin is safe to continue at the end of life, unless there is renal impairment with an estimated glomerular filtration rate (eGFR) of less than 30 ml/L/1.73m^2.

Question 9

Following an MI, how you alter DMT2 treatment? [1]

Answer 9

type 2 diabetics are converted to intravenous insulin in the immediate period following a myocardial infarction.

Question 10

Patient with diabetes who have had [] hypoglycaemic episodes requiring help needs to surrender their driving licence

Answer 10

Patient with diabetes who have had two hypoglycaemic episodes requiring help needs to surrender their driving licence

Question 11

Which is the strongest risk factor for diabetic complications? [1]
Name 3 others [3]

Answer 11

1st: Smoking
2nd: HTN
3rd: Dysplidaemia
4th: Hyperglycaemia

Question 12

Describe the pathophysiology of diabetic retinopathy [3]

Answer 12

Chronic hyperglycemia causes:
- basement membrane thickening
- loss of pericytes
- endothelial cell damage in retinal blood vessels (microaneurysms & venous beeding

Question 13

Describe the three classifications of diabetic retinopathy? [2]

Answer 13

non-proliferative diabetic retinopathy (NPDR) marked by:
- microaneurysms
- retinal haemorrhages (dot haemorrhages)
- hard exudates (yellowish deposits of lipid due to vessel leakage)

proliferative diabetic retinopathy (PDR) (more advanced and severe stage), is characterized by:
- the proliferation of new, fragile blood vessels that can bleed into the vitreous, leading to vision loss due to VEGF upregulation
- can be new vessels on disc (NVD) OR new vessels everywhere (NVE)

Diabetic maculopathy:
- Presence of any retinopathy within 1 disc diameter around macula:
Can be:
- Focal
- Diffuse
- Ischaemic

Question 14

What does this yellow arrow depict in non-proliferative diabetic retinopathy? [1]

Answer 14

Hard exudates

Question 15

Describe what the arrows & circle depict on this image of non proliferative diabetic retinopathy [3]

Answer 15

intraretinal microvascular abnormality (IRMA; green arrow)

venous beading and segmentation (blue arrow)

cluster haemorrhage (red circle)

featureless retina suggestive of capillary non-perfusion (white ellipse)

Question 16

How can PDR lead to blindness? [4]

Answer 16

• New blood vessels are very fragile; easily break and leak
• Retinal haemorrhage can lead to acute blindness
• If repeated; leads to fibrosis & scarring
• Can lead to: tractional retinal detachment: when scar tissue or other tissue grows on your retina and pulls it away from the layer underneath

Question 17

Which pathology is depicted? [1]

Answer 17

Diabetic maculopathy: hard exudates near to the macula

Question 18

What is the management of diabetic retinopathy? [5]

Answer 18

Laser photocoagulation

Anti-VEGF medications such as ranibizumab, bevacizumab & Aflibercept

Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease or a vitrectomy may be necessary to clear severe vitreous hemorrhage or to relieve tractional retinal detachment.

Corticosteroids: (triamcinolone, dexamethasone implant) can also be used, particularly in refractory DME.

Pan-retinal photocoagulation (PRP): laser used to make small burns evenly across the peripheral retina - should make blood vessels shrink and dissapear

Question 19

What are the different types of diabetic neuropathy? [5]

Answer 19

• Periperal sensory neuropathy
• Autonomic neuropathy
• Proximal motor neuropathy (amyotrophy; femoral nerve neuropathy - severe pain in anterior thigh & quadricep wasting)
• Cranial nerve palsies (CN III, VI & VII)
• Median nerve / Carpal tunnel syndrome

Question 20

Describe the treatment regime for diabetic peripheral neuropathy [4]

What are two additonal therapies if these don’t work? [2]

Answer 20

first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin

if the first-line drug treatment does not work try one of the other 3 drugs
tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain

topical capsaicin may be used for localised neuropathic pain

pain management clinics may be useful in patients with resistant problem

Question 21

Describe the effects of diabetic autonomic neuropathy on genito-urinary [2]; GI [3] & CV [1] systems

Answer 21

Genito-urinary
- ED
- Atonic bladder: difficulty voiding / urinary incontinence

Gastrointestinal [3]:
- Gastroparesis: stomach doesn’t empty properly, causing outflow problems: recurrent vomiting & early satiety
- Chronic constipation & diarrhoea
- Gustatory sweating: severe sweating on eating

CV [1]:
- Postural hypotension

Question 22

What is the clinical presentation triad of diabetic nephropathy? [3]

Answer 22

Hypertension
Albuminuria
Decline renal function

Question 23

What does the green arrows point to? [1]

Answer 23

Kimmelstein-Wilson lesion

Question 24

Describe the pathophysiology of diabetic nephropathy [4]

Answer 24

Oxidative stress consumes nitric oxide, which prevents flow-mediated dilation of blood vessels (endothelial dysfunction): subjecting the endothelium to injury

Leads to production of cytokines, acceleration of inflammation, worsening of blood vessel rigidity due to atherosclerosis, and further impairment of FMD and susceptibility to oxidative stress.

Platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) mediate mesangial expansion and fibrosis via the stimulation of matrix protein (collagen and fibronectin) synthesis and decreased matrix degradation

Angiotensin II (ATII), elevated in DKD, constricts the efferent arteriole in the glomerulus, causing high glomerular capillary pressures, and also stimulates fibrosis and glomerular inflammation

Question 25

Describe the treatment regime for nephropathy (have microalbuminuria) [7]

Answer 25

Control BP:
- ACE inhibitor: captopril; elanapril; lisinopril; ramipril
- ARB if ACE inhibitor not tolerated; losartan; valsartan
- Add calcium-channel blocker amlodopine; felopdipine; nifedipine and/or thiazide-like diuretic: hydrochlorothiazide; and/or beta-blocker carvedilol; metaprolol

Optomise blood glucose control

Manage CV risk factors aggressivey

Manage lipid levels: atorvostatin

Stop metformin when eGFR < 30 mls/min

Refer to specialist if eGFR < 45 mls/min

Renal transplant if giving pancreatic transplant

Question 26

When should you stop prescribing metformin a patient suffering from diabetic nephropathy? [1]

Answer 26

Stop metformin when eGFR < 30 mls/min

Refer to specialist if eGFR < 45 mls/min

Question 27

What are common skin presentations of diabetes? [6]

Answer 27

• Oral / genital candidiasis
• Skin abcesses
• Rhinocerebral mucormycosis infection
• Fungal nail infections
• Aconthosis nigricans (sign of insulin resistance)
• Bullosis Diabeticorum (blisterng)
• Granuloma annulare
• Necrobiosis Lipoidica Diabeticorum (pink skin lesion on lower legs)

Question 28

What is the name of this skin complication of diabetes? [1]

Answer 28

Granuloma annulare

Question 29

Describe the two rheumatological complications / manifestations of diabetes need to know?

Answer 29

Charcot neuroarthopathy: chronic, devastating, and destructive disease of the bone structure and joints in patients with neuropathy; it is characterized by painful or painless bone and joint destruction in limbs that have lost sensory innervation

Diabetic cheiroarthropathy: limited mobility of the joints of the hands

Question 30

Name this sign [1] and disease [1] that is a complication of diabetes

Answer 30

Prayer sign; diabetic cheiroarthropathy

Question 31

What is the most common cause of visual loss in patients with diabetes? [1]

Describe this [1]

Answer 31

Diabetic macular oedema (DMO)

DMO is the commonest cause of visual loss in patients with diabetes

DMO is characterised by oedematous changes in or around the macula. As the macula is responsible for central vision, affected patients tend to complain of blurred vision when reading or difficulty recognising faces in front of them. DMO is the commonest cause of visual loss in patients with diabetes.9

Question 32

DMO can be subcategorised into three categories. Describe them [3]

Answer 32

Focal/diffuse macular oedema:
* the fluid that escapes from damaged vessels can be well-circumscribed (focal) or more widespread and poorly demarcated in nature (diffuse).

Ischaemic maculopathy:
- patients will be symptomatic with defects in visual acuity due to ischaemia at the site of the macula. These areas are best visualised with fluorescein angiography.

Clinically significant macular oedema (CSMO):
- CSMO describes significant changes associated with retinopathy, such as hard exudates and retinal thickening, found within a certain distance to the fovea or greater than a certain size.

Question 33

Diabetic ketoacidosis: once blood glucose is < 14 mmol/l due to NaCl and fixed rate insulin has been given. What is the next appropriate step? [1]

Answer 33

Diabetic ketoacidosis: once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the saline regime

Question 34

State 4 medical causes of hypoglycaemia [4]

Answer 34

 Liver disease
 Progressive renal impairment
 Hypoadrenalism (is associated with Type 1 diabetes)
 Hypothyroidism
 Hypopituitarism (rare)
 Insulinoma (rare)

Question 35

Neuroglycopenic symptoms occurs at a glucose level of ~ [] mmol/L [1]
Name 5 symptoms

Answer 35

Neuroglycopenic symptoms– Glucose ~ 2.7 mmol/L
 Confusion
 Drowsiness
 Slurred speech
 Aggression
 Visual disturbances

Question 36

How can you reverse hypoglycaemic unawareness? [3]

Answer 36

May be improved by “hypo holiday”:
 Strict hypoglycaemia avoidance by relaxing glycaemic control
 Use of analogue insulin
 Continuous Subcutaneous Insulin Infusion (insulin pump therapy)

Question 37

Treatment of mild [2], moderate [2] and severe [4] hypoglycaemia?

Answer 37

Mild:
 Sugary drink, e.g. lucozade, ordinary coke, orange juice
 5-7 glucose tablets, or 3-4 heaped teaspoons of sugar in water

Moderate:
 Glucogel® – 1-2 tubes buccally (into cheek), or jam, honey, treacle massaged into the cheek.
 Intramuscular glucagon if needed

Severe (unconscious)
 Do not put anything in the mouth
 Place the person in the recovery position Administer 0.5-1mg glucagon IM
 If carer is unable to administer glucagon, call 999
 In hospital, administer iv glucose:
- Ideally 75mls of 20% glucose or 150mls 10% glucose over 15 mins
- 50mls 50% glucose can be given, but take care with veins – extravasation can cause chemical burns

Question 38

Diagnosis of DKA?
Venous blood gases [2]
CBG [1]
Ketones? [1]

Answer 38

 Venous blood gases:
- show acidosis (pH < 7.35, bicarb < 15)

 Capillary Blood Glucose (CBG)
- usually over 14 mmol/L, but can be lower (euglycaemic ketosis or alcoholic ketosis)

 Raised Urea and Creatinine
 Urine or plasma ketones
- elevated: above 3 mmol/L

Question 39

Describe fluid therapy provided for DKA patients:

Sodium chloride:
- What %? [1]
- How many litres, over what time period? [4]

Glucose:
- What %? [1]
- What level CBG mmol/L is required before giving? [1]
- How much ml/hr? [1]

Answer 39

Sodium chloride 0.9%
* 1 Litre stat
* 1 Litre in 1 hour
* 1 Litre over 2 hours (+20 mmol potassium chloride) 1 Litre over 4 hours (+potassium chloride)
* 1 Litre over 4 hours (+potassium chloride)

5% or 10% Glucose
* Start when the CBG is < 12 mmol/L and continue at 125ml/hr
* 10 % glucose may be necessary to increase insulin infusion Increase infusion rate if glucose falls below 6.0 mmol/L`

Question 40

When is potassium provided in DKA fluid therapy? [1]
What levels of K are provided for patients with serum K of:
* < 3.5 [1]
* 3.5-5.5 [1]
* > 5.5 [1]

Answer 40

For the first 1-2 bags fluid, give no potassium as fluid is given too rapidly

For every subsequent bag of NaCl 0.9% or glucose 5% use a bag of fluid containing KCl as follows according to serum K+:
- < 3.5: May need additional K+ and delay insulin
- 3.5-5.5: 20-40 mmol/l
- > 5.5: none

Question 41

What are the treatments for Hyperosmolar hyperglycemic state (HHS)? [2]

Answer 41

 Due to the significant fluid deficit, the initial management requires fluid resuscitation to restore circulating volume:
- 0.9% NaCl and at least 1 litre should be given over an hour (quicker in the presence of significant hypotension).
- Fluid replacement alone with 0.9% sodium chloride solution will result in falling blood glucose
- Further fluids can be given aiming for a positive fluid balance based on hourly measurement of urine output. A proposed target is 2-3 litres positive by 6 hours.

 Insulin:
- IVI as for DKA – but consider slower fluids if elderly / heart failure
- much lower dose insulin – (maybe) no insulin for 1st 12 hours, then very low doses : rate of 0.05 units/kg/hour if blood ketones (beta-hydroxybutyrate) are ≤3.0 mmol/L and the patient is not acidotic

Question 42

What K should be given for the following serum K levels when treating HHS & DKA?

Serum K+ > 5.5 mmol/L: [1]
Serum K+ 3.5-5.5 mmol/L: [1]
Serum K+ < 3.5 mmol/L: [1]

Answer 42

Serum K+ > 5.5 mmol/L: Nil potassium replacement
Serum K+ 3.5-5.5 mmol/L: 40 mmol potassium replacement
Serum K+ < 3.5 mmol/L: Senior review for more invasive potassium replacement

Question 43

What pathology is a risk of rapid shift of glucose in HHS patient treatment? [1]
Why? [1]

Answer 43

 Rapid shifts in glucose should be avoided due to risk of rapid fluid / sodium shifts, and risk of central pontine myelinolysis (CPM):
- destruction of the layer (myelin sheath) covering nerve cells in the middle of the brainstem (pons).

Question 44

How long do you not give insulin for HHS treatment? [1]

Why? [1]

Answer 44

12hrs

Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse
as water moves out of the intravascular space, with a resulting decline in intravascular volume

Question 45

Which other electrolytes are common to have a deficiency in HHS? [2]

Answer 45

Hypophosphataemia and hypomagnesaemia are common in HHS.

Question 46

All patients should receive [] for the full duration of HHS admission unless contraindicated

Explain why [1]

Answer 46

All patients should receive prophylactic low molecular weight heparin (LMWH) for the full duration of admission unless contraindicated

Higher risk of VTE: (DM is a risk factor; hospitilisation; hypovolaemia)

Question 47

Describe the different severities of NPDR [3]

Answer 47

Mild NPDR:
- Characterized by the presence of at least one microaneurysm. At this stage, the disease might not be apparent to the patient.

Moderate NPDR:
- More extensive microaneurysms are present, along with haemorrhages and hard exudates. The retina may also exhibit cotton-wool spots, which are areas of nerve fibre layer infarctions.

Severe NPDR:
- Defined by the ‘4:2:1 rule’. This means there are either more than 20 intraretinal haemorrhages in each of 4 quadrants (4), definite venous beading in 2 or more quadrants (2), or prominent intraretinal microvascular abnormalities (IRMA) in 1 or more quadrant (1).

Question 48

Describe the difference between early and high risk PDR [2]

Answer 48

Early PDR:
- New vessels less than 1/3 of the disc area, no vitreous haemorrhage, and no tractional retinal detachment.

High-risk PDR:
- Characterized by any of the following: neovascularization of the disc (NVD) greater than or equal to 1/3 of the disc area, any NVD associated with vitreous or preretinal haemorrhage, or neovascularization elsewhere (NVE) greater than or equal to 1/2 disc area with vitreous or preretinal haemorrhage.

Question 49

A 32 year-old woman with diabetes mellitus undergoes a retinal screen and is found to have maculopathy.

Which is the most characteristic of diabetic maculopathy?

A single cotton wool spot

Dot and blot haemorrhages at the fovea

Flame shaped haemorrhages

Hard exudates at the optic disc

Neovascularisation

Answer 49

A 32 year-old woman with diabetes mellitus undergoes a retinal screen and is found to have maculopathy.

Which is the most characteristic of diabetic maculopathy?

A single cotton wool spot

Dot and blot haemorrhages at the fovea

Flame shaped haemorrhages

Hard exudates at the optic disc

Neovascularisation