DM I Flashcards
What is the minimum rec. amount of times should monitor BMs in DMT1? [1]
In type 1 diabetics, recommend monitoring blood glucose at least 4 times a day, including before each meal and before bed
How can PDR lead to blindness? [4]
- 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
Which pathology is depicted? [1]
Diabetic maculopathy: hard exudates near to the macula
What is the management of diabetic retinopathy? [5]
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
Describe the treatment regime for diabetic peripheral neuropathy [4]
What are two additonal therapies if these don’t work? [2]
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
Describe the effects of diabetic autonomic neuropathy on genito-urinary [2]; GI [3] & CV [1] systems
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
What is the clinical presentation triad of diabetic nephropathy? [3]
Hypertension
Albuminuria
Decline renal function
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)
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
Name this sign [1] and disease [1] that is a complication of diabetes
Prayer sign; diabetic cheiroarthropathy
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
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.
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
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)
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
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
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`
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
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
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
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).
Which other electrolytes are common to have a deficiency in HHS? [2]
Hypophosphataemia and hypomagnesaemia are common in HHS.
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)
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 intraretinal microvascular abnormalities (IRMA) in 1 or more quadrant (1).
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 haemorrhage, or neovascularization elsewhere (NVE) greater than or equal to 1/2 disc area with vitreous or preretinal haemorrhage.
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
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
Label the treatment choices for the DM patients with multi-morbidities for patients already on metformin management and HbA1c remains above 53
CVD:
A: SGLT-inhibitor
B: GLP-1
Heart Failure:
C: SGLT-inhibitor
D: GLP-1
CKD
E: SGLT-inhibitor
F: GLP-1
High CV Risk:
G: SGLT-inhibitor
H: GLP-1
Frail / elderly:
I DPP-inhibitor (low hypoglycaemia risk)
Obesity
A: SGLT-inhibitor
B: GLP-1
Which drugs are contraindicated for patients with DMT2 who might also be suffering from:
Heart Failure [2]
CKD [1]
Frail / elderly [3]
Obesity [2]
Heart Failure:
- Pioglitazone: causes oedema as an AE
- Saxagliptin: increase risk of HF
CKD [2]
- Caution with SUs
Frail / elderly [3]
- SGLT2i (hypoglycaemia risk)
- GLPs (hypoglycaemia risk)
- Caution with SUs (hypoglycaemia risk)
Obesity
- SUs (weight gain)
- Pioglitzaone (weight gain)
Describe an overview of the drug pathway for glycaemic management of DMT2
- HbA1c above 48 at diet and lifestyle alone: condiser Ptx CV risk or CV disease
- If Ptx has low CV risk: metformin first line
- If Ptx has high CV risk or CV disease: metformin AND gliflozin
- If HbA1c continued not to be controlled: dual oral therapy
- If HbA1c continued not to be controlled: triple oral therapy
Describe basal bolus therapy regime for insulin
3 injections of rapid acting, 1 injection of long acting: mimics normal physiology
Name three anti-VEGF medications used to treat diabetic retinopathy [3]
ranibizumab, bevacizumab & Aflibercept
Describe in detail the different types of diabetic retinopathy [3]
What is the arrow pointing to? [1]
Cotton wool spot
Cotton wool spots appear as grayish/whitish spots with soft, fuzzy edges, giving them a resemblance to a ball of cotton wool. They do not usually appear in clusters like hard exudate.
Name this complication of diabetic retinopathy [1]
Diabetic retinopathy is one of several causes of neovascular glaucoma: a type of secondary glaucoma.
Neovascularization can occur within the iris and its trabecular meshwork (rubeosis) causing a narrowing and closure of the drainage angle and therefore increased intraocular pressure.
