- Fluid resus: 0.9% normal saline, can use hypotonic (0.45%) if serum osmolality not going down, however this is rare. You dont want osmolality to decrease too fast (>10mmol/l/hr) - Fixed rate iv infusion of insulin- 0.05 units per kg per hr - monitor closely (blood biochemistry as well as neuro function)

diabetes Flashcards by Tarun Zachariah

How can diabetes be diagnosed? (3 ways)

random blood glucose test over 11.1 with symptoms
fasting glucose >7, if theyre asymptomatic you need two >7
Hba1c> 6.5%

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Give 5 symptoms of diabetes mellitus?

tiredness
frequent UTIs
Weightloss (T1 only)
Polyurea
Polydipsia

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Describe the presentation of decompensated ketoacidosis?

onset over 24 hrs
PMH T1 diabetes, recent precipitating factor
polyurea and poly dipsia
N+ V
Altered mental state
weakness
lethargy
hyperventilation
pear drop smell on breath
dehydrated and volume deplete on examination

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What may precipitate DKA? (4)

Infection.
Discontinuation of insulin (unintentional or deliberate).
Inadequate insulin.
Cardiovascular disease - eg, stroke or myocardial infarction.
Drug treatments - eg, steroids, thiazides or sodium-glucose co-transporter 2 (SGLT2) inhibitors.

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How should DKA be investigated? (group into diagnosis, finding cause and assessment of severity/ complications)

To diagnose: Blood glucose, blood ketones, urine dip for ketones, ABG showing low bicarbonate (metabolic acidosis)
To asses severity: U&E- for dehydration and hyperkalaemia, also urea and creatine raised if AKI, 12 lead ECG, CT/ MRI of head, anion gap raised
to find cause: blood cultures, urine dip, CXR to look for infection

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Describe and explain serum osmolality, K+ and Na+ changes in DKA?

K+ usually high due to acidosis meaning H+ going into cells and K+ coming out, however may be low due to osmotic diuresis
Osmolality is low due to glucose and ketones causing osmotic diuresis, which is also why Na+ conc seems high or normal. Can be low as body compensates by letting sodium go

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Describe the management of DKA in detail

Fixed rate IV infusion of insulin dose of 0.1 units/ Kg bodywieght every hour
IV fluids to rehydrate: 1st bag= 1L normal saline over an hour, then 1L normal saline with K= over 2 hrs, then same then 1L NS w/ K+ over 4 hrs then same again, then 1L NS w/ k+ over 6 hrs. Reason for this is the insulin will cause cells to uptake K+ and cause hypokalaemia.
Monitor closely (every hour) and if targets in HCO3- increases and ketone decreases are not met then increase the insulin
When blood glucose is over 14mmol/l add 5% dextrose solution infusion to prevent hypo, continue until eating and drinking normally
treat complications

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When does hyperosmolar hyperglycaemic state/ syndrome (HSS) occur?

It occurs in T2 diabetes when blood glucose levels are allowed to be very high for a sustained period of time, causing an osmotic diuresis and so loss of water meaning high serum osmolality. There is no ketoacidosis as there is still a basal level of insulin they respond to sufficient to prevent ketoacidosis but too low to prevent hyperglycemia.

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What could cause HHS?

infections
inability to take medications
hypo/hyperthermia
MI
Medications
undiagnosed/ first presentation of diabetes
Many others

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How is HHS present?

With severe dehydration, fast deterioration, focal or global neurological dysfunction, often PMH of diabetes, N+V, lethargy, seizures

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How is HHS treated?

Fluid resus: 0.9% normal saline, can use hypotonic (0.45%) if serum osmolality not going down, however this is rare. You dont want osmolality to decrease too fast (>10mmol/l/hr)
Fixed rate iv infusion of insulin- 0.05 units per kg per hr
monitor closely (blood biochemistry as well as neuro function)

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Describe 3 early and 3 late signs of hypoglycaemia

early= hungry, sweats, tremor, palpitations, shaking 
late= confused, headache, drowsy, slurred speech, coma

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Describe treatment of hypoglycaemia if theyre conscious and orientated

Oral glucose (dextrose tablets, 150-200ml fruit juice/ original lucozade/ glucojuice) with complex carbs later (bread etc)

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Describe treatment of severe hypoglycaemia (unconscious or unable to swallow)

Iv dextrose (120-200ml 20% solution)

- or IM glucagon often given in community

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Describe the diagnosis criteria for DKA and HHS

DKA: acidaemia (ph<7.3 or hco3 <15) and hyperglycaemia (>11.1) and ketonuria (++) or ketonaemia (>3)
HHS: hyperglycaemia >30, no acidosis, no ketosis, serum osmolality >320

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What is Diabetes Insipidus?

Reduced ADH secretion/kidney response to ADH causes passage of large volumes of dilute urine

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Give 3 symptoms of Diabetes Insipidus

Polyuria
Polydipsia
Dehydration

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Give 3 causes of Cranial DI

Congenital (ADH genetic defects)
Tumour
Trauma

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GIve 3 causes of Nephrogenic DI

Inherited
Chronic Renal Disease
Drugs (Lithium, Demeclocycline)

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What 4 investigations could you do if you suspected DI?

U&Es
Glucose (rule out DM)
Urine Osmolality (rule out primary polydipsia)
8hr Deprivation Test

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How would you treat Cranial DI?

Desmopressin

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How would you treat Nephrogenic DI?

Treat underlying causes
NSAIDs (Prostaglandins locally inhibit ADH)
Bendroflumethiazide (inducing hypovolaemia may kickstart RAAS)

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Describe the pathophysiology of Type 1 DM

Onset in childhood
Autoimmune destruction of pancreatic B cells
HLA association

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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

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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 - Twice Novomix daily | QDS - Ultrafast at meals, long acting at night (more flexible)

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 that increases insulin sensitivity

Give 3 SE of Metformin

Nausea, Abdo Pain, Lactic Acidosis (in renal impairment) hypoglycaemia and weight gain are NOT SE

Name a DPP4 Inhibitor. What is it's action?

Sitagliptin | DPP4 destroys incretins which enhance insulin release

Name a Glitazone. What is it's action?

Pioglitazone | Increases insulin sensitivity

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

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

Microvascular occlusion causes retinal ischaemia | Leads to AV shunts, Neovascularisation and 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 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)

what is gestational diabetes

increased glucose during pregnancy important as untreated can lead to problems in. other and baby

what is MODY

Mature onset diabetes of the young MODY is a rare form of diabetes which is different from both Type 1 and Type 2 diabetes, and runs strongly in families. MODY is caused by a mutation (or change) in a single gene. If a parent has this gene mutation, any child they have, has a 50% chance of inheriting it from them. may progress to have comps such as DKA

what gene is affected for MODY 2 and MODY 3

MODY 2- glucokinase gene MODY 3- HNFalpha

what is LADA

Latent autoimmune diabetes in adults (LADA) is a slow-progressing form of autoimmune diabetes. Like the autoimmune disease type 1 diabetes, LADA occurs because your pancreas stops producing adequate insulin, most likely from some "insult" that slowly damages the insulin-producing cells in the pancreas.

what is the first line medication for T2D

metformin

below what eGFR should you avoid metformin

<36

what are some side effects of SGLT2 inhibitors

increases the risk of UTIs and causes polyuria

what are some risk factor modification measures that could be taken in a diabetic patient

• Blood Pressure: target <140/80 (<130/80 if end-organ damage) ◦ If microalbuminuria, target becomes <125/75 ◦ 1st line = ACE-inhibitors • Lipids: NICE 2014 = only if QRISK2 >10% ◦ 1st line/1º prevention = atorvastatin 20mg ON ◦ 2º prevention (i.e. known IHD, CVA, PAD) = atorvastatin 80mg ON • Antiplatelets: should NOT be offered unless existing CVD