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taz- year 3 med > diabetes > Flashcards

diabetes Flashcards

1
Q

How can diabetes be diagnosed? (3 ways)

A
  1. random blood glucose test over 11.1 with symptoms
  2. fasting glucose >7, if theyre asymptomatic you need two >7
  3. Hba1c> 6.5%
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2
Q

Give 5 symptoms of diabetes mellitus?

A
  • tiredness
  • frequent UTIs
  • Weightloss (T1 only)
  • Polyurea
  • Polydipsia
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3
Q

Describe the presentation of decompensated ketoacidosis?

A
  • 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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4
Q

What may precipitate DKA? (4)

A
  • 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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5
Q

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

A
  • 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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6
Q

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

A
  • 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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7
Q

Describe the management of DKA in detail

A
  • 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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8
Q

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

A

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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9
Q

What could cause HHS?

A
  • infections
  • inability to take medications
  • hypo/hyperthermia
  • MI
  • Medications
  • undiagnosed/ first presentation of diabetes
  • Many others
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10
Q

How is HHS present?

A

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

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11
Q

How is HHS treated?

A
  • 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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12
Q

Describe 3 early and 3 late signs of hypoglycaemia

A 
early= hungry, sweats, tremor, palpitations, shaking 
late= confused, headache, drowsy, slurred speech, coma
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13
Q

Describe treatment of hypoglycaemia if theyre conscious and orientated

A

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

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14
Q

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

A
  • Iv dextrose (120-200ml 20% solution)

- or IM glucagon often given in community

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15
Q

Describe the diagnosis criteria for DKA and HHS

A

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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16
Q

What is Diabetes Insipidus?

A

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

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17
Q

Give 3 symptoms of Diabetes Insipidus

A

Polyuria
Polydipsia
Dehydration

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18
Q

Give 3 causes of Cranial DI

A

Congenital (ADH genetic defects)
Tumour
Trauma

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19
Q

GIve 3 causes of Nephrogenic DI

A

Inherited
Chronic Renal Disease
Drugs (Lithium, Demeclocycline)

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20
Q

What 4 investigations could you do if you suspected DI?

A

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

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21
Q

How would you treat Cranial DI?

A

Desmopressin

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22
Q

How would you treat Nephrogenic DI?

A

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

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23
Q

Describe the pathophysiology of Type 1 DM

A

Onset in childhood
Autoimmune destruction of pancreatic B cells
HLA association

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24
Q

Describe the pathophysiology of Type 2 DM

A

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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25
Q

Give 4 other causes of DM

A

Steroids
Pancreatitis
Cushings Disease
Glycogen Storage Disease

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26
Q

What is the triad of DM symptoms

A

Polyuria
Polydipsia
Weight Loss

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27
Q

What are the parameters for diagnosing DM in terms of Venous Glucose?

A

Fasting >7mmol/l

Random >11.1mmol/l

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28
Q

What is the parameter for diagnosing DM using the OGTT?

A

> 11.1mmol/l

29
Q

What is the parameter for diagnosing DM using HbA1c?

A

> 48mmol/l

>6.5%

30
Q

What are the parameters for ‘Pre-Diabetes’?

A

Fasting glucose of 5.5-6.9mmol/l

HbA1c of 42-47mmol/l (6-6.4%)

31
Q

What is required for a Diabetes diagnosis?

A

Either
Symptoms and ONE positive blood result
Or
Positive bloods on two separate occasions

32
Q

What advice would you give patients who are diagnosed with Type 1 DM? Give 4 points.

A

Review and research diet
Try to limit other things contributing to CVS risk
Ensure foot care
Avoid binge drinking (delayed hypoglycaemia)

33
Q

Name one ultrafast, one medium and one long acting insulin

A

Ultrafast - Novorapid
Medium - Isophane Insulin
Long - Insulin Glargine

34
Q

Name a premixed insulin

A

Novomix (30% short, 70%long)

35
Q

Describe 2 different regimens to manage T1DM

A

BD - Twice Novomix daily

QDS - Ultrafast at meals, long acting at night (more flexible)

36
Q

What could you give patients if they struggle with the insulin regime?

A

Insulin Pump

37
Q

Give three important pieces of advice for T1DM regarding insulin

A

Vary injection site
Change needles
Continue insulin if ill (and replace lost calories with milk)

38
Q

Describe the 4 step (up) therapy for T2DM

A

1) Lifestyle and Diet
2) Metformin
3) Dual Therapy (Metformin + another)
4) Triple Therapy or Insulin Therapy

39
Q

What is Metformin’s action?

A

Biguanide that increases insulin sensitivity

40
Q

Give 3 SE of Metformin

A

Nausea, Abdo Pain, Lactic Acidosis (in renal impairment)

hypoglycaemia and weight gain are NOT SE

41
Q

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

A

Sitagliptin

DPP4 destroys incretins which enhance insulin release

42
Q

Name a Glitazone. What is it’s action?

A

Pioglitazone

Increases insulin sensitivity

43
Q

When are Glitazones contraindicated? What are their side effects?

A

CI - Osteoporosis, CCF

SE - Hypoglycaemia, Fractures

44
Q

Name a Sulphonylurea? What is it’s action?

A

Gliclazide

Increases insulin secretion by binding to ATP sensitive potassium channels, closing them

45
Q

Name an SGLT2 inhibitor. What is it’s action?

A

Dapaglifozin

Blocks glucose reabsorption in the PCT

46
Q

Name a GLP1 analogue. What is it’s action?

A

Exenatide

Incretin mimics

47
Q

Name four complications of Diabetes

A

Vascular disease
Nephropathy
Retinopathy
Neuropathy

48
Q

Give two eye diseases associated with Diabetes

A

Diabetic Retinopathy

Cataracts

49
Q

Describe the pathophysiology of Diabetic Retinopathy

A

Microvascular occlusion causes retinal ischaemia

Leads to AV shunts, Neovascularisation and Oedema

50
Q

Describe 3 characteristic features of Diabetic Retinopathy

A

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

51
Q

How would Diabetic Retinopathy present?

A

Often gradual painless visual deterioration

If haemorrhages - sudden onset of dark, painless floaters which may resolve over several days.

52
Q

Most Diabetic Retinopathies are not treated, however if they are, give 2 treatment options

A

Laser Treatment - aim is to induce regression of new blood vessels and reduce central macular thickening

Intravitreal Steroids

53
Q

Give 4 possible features of foot neuropathy

A

Reduced sensation in stocking distribution
Absent ankle jerks
Charcot Joint
Claw Toes

54
Q

How would a diabetic ulcer present?

A

Punched out ulcer in area of thick callus

55
Q

Describe 3 non surgical managements of ‘Diabetic Foot’

A

Regular Chiropody
Bisphophonates
Antibiotics

56
Q

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.

A 
Exogenous Drugs (ACEI, B Blockers)
Pituitary Insufficiency 
Liver Failure 
Addisons 
Insulinoma 
Non pancreatic Neoplasms
57
Q

Give 3 autonomic and 3 neuroglycopenic symptoms of Hypoglycaemia.

A

Autonomic - Sweating, Anxiety, Hunger

Neuroglycopenic - Confusion, Drowsiness, Coma

58
Q

What is Whipple’s Triad?

A

symptoms + Hypoglycaemia + Resolution as plasma glucose rises

59
Q

Describe two features you are looking for on an X-Ray of a diabetic foot

A

Osteomyelitis

Gas Gangrene

60
Q

Why is ABPI generally done on right arm?

A

Steal Syndrome is more common on the left

You generally stand to the right of the patient

61
Q

Explain the ABPI value indicating Diabetic Foot

A

> 1.2
Due to calcification of the peripheral arteries increasing the pressure (NOT because they have superior blood flow to PAD)

62
Q

what is gestational diabetes

A

increased glucose during pregnancy

important as untreated can lead to problems in. other and baby

63
Q

what is MODY

A

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

64
Q

what gene is affected for MODY 2 and MODY 3

A

MODY 2- glucokinase gene

MODY 3- HNFalpha

65
Q

what is LADA

A

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.

66
Q

what is the first line medication for T2D

A

metformin

67
Q

below what eGFR should you avoid metformin

A

<36

68
Q

what are some side effects of SGLT2 inhibitors

A

increases the risk of UTIs and causes polyuria

69
Q

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

A

• 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

taz- year 3 med (10 decks)

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