Diabetes II Flashcards

1
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

A patient with DMT2 is presenting with symptoms of gastroparesis.

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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]

A

Swtich to variable-rate intravenous insulin infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

Sulfonylureas (e.g. gliclazide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the pathophysiology of diabetic retinopathy [3]

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the three classifications of diabetic retinopathy? [2]

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Hard exudates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can PDR lead to blindness? [4]

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which pathology is depicted? [1]

A

Diabetic maculopathy: hard exudates near to the macula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the management of diabetic retinopathy? [5]

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the treatment regime for diabetic peripheral neuropathy [4]

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

A

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

21
Q

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

A

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

22
Q

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

A

Hypertension
Albuminuria
Decline renal function

23
Q

What does the green arrows point to? [1]

A

Kimmelstein-Wilson lesion

24
Q

Describe the pathophysiology of diabetic nephropathy [4]

A

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

25
Describe the treatment regime for nephropathy (have microalbuminuria) [7]
**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
26
When should you stop prescribing metformin a patient suffering from diabetic nephropathy? [1]
**Stop metformin when eGFR < 30 mls/min** Refer to specialist if eGFR < 45 mls/min
27
What are common skin presentations of diabetes? [6]
- **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)
28
What is the name of this skin complication of diabetes? [1]
Granuloma annulare
29
Describe the two rheumatological complications / manifestations of diabetes need to know?
**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
30
Name this sign [1] and disease [1] that is a complication of diabetes
**Prayer sign; diabetic cheiroarthropathy**
31
What is the most common cause of visual loss in patients with diabetes? [1] Describe this [1]
**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
32
DMO can be subcategorised into three categories. Describe them [3]
**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.
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]
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**
34
State 4 medical causes of hypoglycaemia [4]
 **Liver disease**  **Progressive renal impairment**  **Hypoadrenalism** (is associated with Type 1 diabetes)  **Hypothyroidism**  Hypopituitarism (rare)  Insulinoma (rare)
35
Neuroglycopenic symptoms occurs at a glucose level of ~ [] mmol/L [1] Name 5 symptoms
**Neuroglycopenic symptoms– Glucose ~ 2.7 mmol/L**  Confusion  Drowsiness  Slurred speech  Aggression  Visual disturbances
36
How can you reverse hypoglycaemic unawareness? [3]
May be improved by “hypo holiday”:  **Strict** **hypoglycaemia** **avoidance** by relaxing glycaemic control  Use of **analogue insulin**  **Continuous Subcutaneous Insulin Infusion** (insulin pump therapy)
37
Treatment of mild [2], moderate [2] and severe [4] hypoglycaemia?
**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
38
Diagnosis of DKA? Venous blood gases [2] CBG [1] Ketones? [1]
** 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
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]
**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`
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]
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**
41
What are the treatments for Hyperosmolar hyperglycemic state (HHS)? [2]
 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
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]
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**
43
What pathology is a risk of rapid shift of glucose in HHS patient treatment? [1] Why? [1]
 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).
44
How long do you not give insulin for HHS treatment? [1] Why? [1]
**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**
45
Which other electrolytes are common to have a deficiency in HHS? [2]
**Hypophosphataemia and hypomagnesaemia are common in HHS.**
46
All patients should receive **[]** for the **full duration** of HHS admission unless contraindicated Explain why [1]
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)
47
Describe the different severities of NPDR [3]
**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 i**ntraretinal microvascular abnormalities (IRMA) in 1 or more quadrant (1).**
48
Describe the difference between early and high risk PDR [2]
**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 haemorrhag**e, or **neovascularization elsewhere (NVE) greater than or equal to 1/2 disc area with vitreous or preretinal haemorrhage.**
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
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