Diabetes Flashcards
What is Diabetes Insipidus?
Reduced ADH secretion/kidney response to ADH causes passage of large volumes of dilute urine
Give 3 symptoms of Diabetes Insipidus
Polyuria
Polydipsia
Dehydration
Give 3 causes of Cranial DI
Congenital (ADH genetic defects)
Tumour
Trauma
Give 3 causes of Nephrogenic DI
Inherited
Chronic Renal Disease
Drugs (Lithium, Demeclocycline)
What 4 investigations could you do if you suspected DI?
Us and Es
Glucose (rule out DM)
Urine Osmolality (rule out primary polydipsia)
8hr Deprivation Test
How would you treat Cranial DI?
Desmopressin
How would you treat Nephrogenic DI?
Treat underlying causes
NSAIDs (Prostaglandins locally inhibit ADH)
Bendroflumethiazide (inducing hypovolaemia may kickstart RAAS)
Describe the pathophysiology of Type 1 DM
Onset in childhood
Autoimmune destruction of pancreatic B cells
HLA association
Describe the pathophysiology of Type 2 DM
Decreased insulin secretion/increased insulin resistance
Associated with obesity/sedentary lifestyle
No HLA association
There is an autosomal dominant form affecting young people
Give 4 other causes of DM
Steroids
Pancreatitis
Cushings Disease
Glycogen Storage Disease
What is the triad of DM symptoms
Polyuria
Polydipsia
Weight Loss
What are the parameters for diagnosing DM in terms of Venous Glucose?
Fasting >7mmol/l
Random >11.1mmol/l
What is the parameter for diagnosing DM using the OGTT?
> 11.1mmol/l
What is the parameter for diagnosing DM using HbA1c?
> 48mmol/l
>6.5%
What are the parameters for ‘Pre-Diabetes’?
Fasting glucose of 5.5-6.9mmol/l
HbA1c of 42-47mmol/l (6-6.4%)
What is required for a Diabetes diagnosis?
Either
Symptoms and ONE positive blood result
Or
Positive bloods on two separate occasions
What advice would you give patients who are diagnosed with Type 1 DM? Give 4 points.
Review and research diet
Try to limit other things contributing to CVS risk
Ensure foot care
Avoid binge drinking (delayed hypoglycaemia)
Name one ultrafast, one medium and one long acting insulin
Ultrafast - Novorapid
Medium - Isophane Insulin
Long - Insulin Glargine
Name a premixed insulin
Novomix (30% short, 70%long)
Describe 2 different regimens to manage T1DM
- BD biphasic regimen - Twice Novomix daily
- QDS - Ultrafast at meals, long acting at night (more flexible - can adjust dose with meal size and exercise)
What could you give patients if they struggle with the insulin regime?
Insulin Pump
Give three important pieces of advice for T1DM regarding insulin
Vary injection site
Change needles
Continue insulin if ill (and replace lost calories with milk)
Describe the 4 step (up) therapy for T2DM
1) Lifestyle and Diet
2) Metformin
3) Dual Therapy (Metformin + another)
4) Triple Therapy or Insulin Therapy
What is Metformin’s action?
Biguanide reduce hepatic glucose output and increases insulin sensitivity
do not stimulate insulin = do not cause hypoglycaemia
Give 4 SE of Metformin
Nausea
Abdo Pain
Lactic Acidosis (in renal impairment)
modest weight loss
Name a DPP4 Inhibitor. What is it’s action?
Sitagliptin
DPP4 destroys incretins which enhance insulin release so by inhibiting this = lower blood glucose by preventing incretin degradation
incretin action is glucose dependent so do not stimulate inuslin secretion at normal glucose concentrations = unlikely to cause hypoglycaemia
Name a Glitazone (thiazolidinediones). What is it’s action?
Pioglitazone
Increases insulin sensitivity in muscle and adipose tissue
decrease insulin resistance and decrease hepatic glucose
When are Glitazones contraindicated? What are their side effects?
CI - Osteoporosis, CCF
SE - Hypoglycaemia, Fractures
Name a Sulphonylurea? What is it’s action?
Gliclazide
Increases insulin secretion by binding to ATP sensitive potassium channels, closing them
Name an SGLT2 inhibitor. What is it’s action?
Dapaglifozin
Blocks glucose reabsorption in the PCT = decrease blood glucose by passing urine
Name a GLP1 analogue. What is it’s action?
Exenatide
Incretin mimics
Name four complications of Diabetes
Vascular disease
Nephropathy
Retinopathy
Neuropathy
Give two eye diseases associated with Diabetes
Diabetic Retinopathy
Cataracts
Describe the pathophysiology of Diabetic Retinopathy
capillary basement membrane thickening leading to leaky vessels, occluded vessels and macular oedema
Describe 3 characteristic features of Diabetic Retinopathy
Microaneurysms - physical weakening of vascular walls
Haemorrhages - when weakened vessels rupture, can be small or large (AKA Flame - track along nerve-fibre bundles in superficial retinal layers)
Cotton Wool Spots - Build up of axonal debris
How would Diabetic Retinopathy present?
Often gradual painless visual deterioration
If haemorrhages - sudden onset of dark, painless floaters which may resolve over several days.
Most Diabetic Retinopathies are not treated, however if they are, give 2 treatment options
Laser Treatment - aim is to induce regression of new blood vessels and reduce central macular thickening
Intravitreal Steroids
Give 4 possible features of foot neuropathy
Reduced sensation in stocking distribution
Absent ankle jerks
Charcot Joint
Claw Toes
How would a diabetic ulcer present?
Punched out ulcer in area of thick callus
Describe 3 non surgical managements of ‘Diabetic Foot’
Regular Chiropody
Bisphophonates
Antibiotics
Hypoglycaemia is classified as <3mmol/l glucose. Majority of times it’s a diabetic cause, but using the mnemonic EXPLAIN, state 7 non diabetic causes.
Exogenous Drugs (ACEI, B Blockers) Pituitary Insufficiency Liver Failure Addisons Insulinoma Non pancreatic Neoplasms
Give 3 autonomic and 3 neuroglycopenic symptoms of Hypoglycaemia.
Autonomic - Sweating, Anxiety, Hunger
Neuroglycopenic - Confusion, Drowsiness, Coma
What is Whipple’s Triad?
Symptoms + Hypoglycaemia + Resolution as plasma glucose rises
Describe the pathophyiology of DKA
Without insulin to drive glucose into the cells, the body is forced into starvation state, using ketones for energy and causing acidosis
Name causes/ triggers of DKA
Infection Non Compliance Surgery/trauma undiagnosed T1D drugs affecting carbohydrate metabolism Chemo
Name 5 symptoms of DKA
Drowsiness
Abdo Pain, N&V
Dehydration
Polydipsia, Polyuria
Describe 3 diagnostic classifications of DKA
Acidaemia - pH<7.3
hyperglycaemia - >11.1mmol/l
Ketonaemia (>3mmol/l) or Ketonuria (>2+)
Describe a four step initial management plan of DKA
A-E and IV access - 2 large bore
1. 1L 0.9% saline bolus
2. 50 units act rapid in 50ml fluid at 0.1 unit/kg/hr (fixed rate insulin infusion)
3. add potassium to second bag
4. once glucose <14 mmol/L start dextrose infusion
Ref ITU input
Give 3 complications of DKA
Cerebral Oedema
Hypokalaemia
Aspirational Pneumonia
Describe the different between Dry and Wet Gangrene
Dry Gangrene - Black ‘mummified’ toes that often autoamputate
Wet Gangrene - indicates infection
Describe four features indicating Necrotising Fasciitis from Diabetic Foot
Spreading Cellulitis
Black Spots
Dishwater Fluid Appearance
Crepitus (tissue paper sound when pressing - gas gangrene)
Describe two features you are looking for on an X-Ray of a diabetic foot
Osteomyelitis
Gas Gangrene
Why is ABPI generally done on right arm?
Steal Syndrome is more common on the left
You generally stand to the right of the patient
Explain the ABPI value indicating Diabetic Foot
> 1.2
Due to calcification of the peripheral arteries increasing the pressure (NOT because they have superior blood flow to PAD)
Describe the Doppler Sounds of vessels
Monophasic
Biphasic
Triphasic
Monophasic is diseased, and triphasic is healthy (you can hear the elastic recoil in competent vessels)
Using the mnemonic SWOMPD, how would you manage a diabetic foot?
Sepsis Wound Management Offloading (Orthotics) Mechanical (Orthopaedics input) Perfusion (Lifestyle, Meds, Surgical) Diabetic Control
What antimicrobials would you use for MILD Diabetic Foot?
Flucloxacillin
What antimicrobials would you use for MODERATE Diabetic Foot?
Flucloxacillin, Ciprofloxacin and Metronidazole
What antimicrobials would you use for SEVERE Diabetic Foot?
Piperacillin, Tazobactam and Vancomycin
name 4 short acting insulins - Rapid acting and soluble
rapid acting - novorapid & humalog
soluble - humulin S & actrapid
name 4 intermediate acting insulins
Isophane
Insulatard
Humulin 1
Insuman basal
name 4 long acting insulins
insulin glargine - lantus
insulin detemir - levemir
insulin degludec - tresiba
name 4 symptoms of hyperglycaemia
polyuria
polydipsia
blurring of vision
urogenital infections - thrush
name 4 symptoms of inadequate energy utilisation
tiredness
weakness
lethargy
weight loss
what insulin regimen is good to use when switching from tablets to insulin in T2DM?
once-daily before-bed long-acting
why is insulin given SC?
insulin is inactivated by GI enzymes
where is best to inject insulin and why?
plenty of SC fat - abdomen
quick absorption
why is it important to rotate injection sites?
prevent lipohypertrophy
which causes erratic absorption leading to poor glycaemic control
what do you have to check injection sites for?
swelling
bruising
infection
lipohypertrophy
what advice should you give someone taking insulin regarding sickness?
do not stop taking insulin
maintain calorie intake with milk
check blood glucose at least 4 times a day
monitor for ketonuria
increase insulin if blood glucose increases
what are some dangers of taking insulin
hypoglycaemia allergy hypokalaemia painful injections heart failure lipohypertrophy
what are the 2 functions of insulin?
Cause cells to absorb glucose from blood and use it as fuel
Cause muscle and liver cells to absorb glucose and store it as glycogen
side effects of DPP4 inhibitor - sitagliptin
GI upset
headache
side effects of sulphonylureas - glicazide
hypoglycaemia - stimulation of insulin secretion
weight gain
gi upset
side effects of SGLT2 inhibitors - dapagliflozin
increased risk of UTI and genital tract infections
what are the microvascular complications of diabetes?
diabetic retinopathy
nephropathy
neuropathy
what are the macrovascular complications of diabetes?
PVD, stroke, MI, intermittent claudication
how does diabetic neuropathy come about?
multiple mechanisms - including damage to small blood vessels nourishing the peripheral nerves and abnormal sugar metabolism
what are the manifestations of diabetic neuropathy?
peripheral sensory neuropathy - progresses from loss of vibration to glove and stocking sensory loss
mononeuropathies
amyotrophy - painful wasting of thigh muscle
autonomic neuropathy
what is autonomic neuropathy
damage to the autonomic nerves from high levels of blood glucose leading to postural hypotension, bladder dysfunction, sweating, temperature regulation issues, and other orthostatic symptoms like nausea, palpitations, light-headedness, tinnitus, SOB
what is nephropathy?
hypoglycaemia leads to increased glomerular capillary pressure, podocyte damage.
albuminuria is first sign
how is nephropathy diagnosed?
microalbuminuria = A:Cr 3-30mg/mmol
not detected on urine dip stick at this stage
how is nephropathy treated?
good DM control BP <130/80 ACEi - reduce proteinuria sodium restriction statin
what medications should be used with caution in CKD?
sulfonylureas
Biguanides
SGLT2i
Exenatide
signs of DKA
volume depletion - dry mucous membranes - poor skin turgor - sunken eyes - tachycardia - hypotension kussmaul respiration - rapid and deep respiration due to acidosis acetone breath
further management of DKA - not initial steps
monitor blood ketone levels and blood glucose levels
consider catheter
check VBG at 2 4 8 12 and 24 hours
What is a Hyperosmolar Hyperglycaemic State?
Seen in unwell patients with T2DM
Hx of a weeks dehydration with glucose>30mmol/l
NO KETONE METABOLISM as insulin levels are sufficient to prevent this
How would you manage Hyperglycaemic Hyperosmolar State?
A-E + access
Rehydrate slowly - 0.9% NaCl
Replace K+ when urine starts to flow
Only use insulin if glucose is falling at rate < 5 mmol/L/hr despite adequate fluid replacement - start low 0.05units/kg/hr
what causes HHS?
poor diabetic control
infection - sepsis
dehydration
features of HHS
hypovolaemia - volume depletion
hyperglycaemia - >30mmol/L without ++ ketones
hyperosmolarity - >320mosmol/kg
much longer hx than DKA
