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Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Treatment algorithm for T2DM

A

Duodenal jejunal bypass if BMI >41

Otherwise:

1) Metformin If HbA1c >58:
2) + DPP4 inhibitor/ pioglitazone/ sulfonylurea
3) Metformin + DPP4 + SU
4) Metformin + pioglitzaone + SU
5) GLP-1 agonist (liraglutide) or SGLT2 inhibitors (-flozins)
6) + insulin

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2
Q

What should the Hba1c target be?

A

<48mmol

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3
Q

What should the target be if there is a hypo risk + how is this achieved?

A

Monotherapy to keep Hba1c at 53mmol

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4
Q

When to add a 2nd + 3rd drug?

A

Hba1c >53, 58mmol

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5
Q

When to diagnose T1DM?

A

Fasting glucose >7

Glucose tolerance >11.1

Urine dip ++ glucose

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6
Q

What is the mechanism behind DKA?

A

Metabolic acidosis, hyperglycaemia, ketonamia

Lack of insulin = reduced production of pyruvate

Acetyl coA increases so ketones increase

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7
Q

Genetic link with diabetes

A

T1DM - HLA D4/3 lniked

T2DM - stronger family link but no HLA association

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8
Q

T2DM RF

A

CVD risk factors - HTN, high cholesterol

Age >45

Obesity Fam Hx

Ethnicity - Asian + Hispanic

Gestational DM or baby >4.5kg

PCOS - leads to insulin resistance

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9
Q

Diagnosis of T2DM

A

Symptomatic + 1 positive test result

Asymptomatic + 2 positive test results

Positive tests: fasting >7, random >11.1, OGTT >11.1

HbA1c >48 = diagnostic

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10
Q

Microvascular complications of DM

A

Retinopathy Nephropathy Neuropathy

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11
Q

Macrovascular complications of DM

A

IHD Stroke PVD

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12
Q

General complications of DM

A

Immunocompromised - due to bacteria thriving in hyperglycaemic environment

Poor healing

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13
Q

Annual monitoring for DM

A

ABCDEFG

Advice

BP

Cholesterol

Diabetic control - HbA1c, albumin:creatinine ratio

Eyes - fundoscopy

Feet - diabetic foot exam

Glycaemic control (drugs)

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14
Q

What is ACR?

A

Albumin: creatinine ratio/ PCR first wee in the morning

Should be low <30 - high result indicates nephropathy

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15
Q

What are the stages of diabetic retinopathy?

A

Background = dot+blot haemorrhages, microaneurysms, hard exudates

Maculopathy = decreasing visual acuity, haemorrhages around macular

Pre-proliferative = cotton wool spots

Proliferative = new vessel formation

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16
Q

Difference between microaneurysms + haemorrhages

A

Microaneurysms = along the line of blood vessels Haemorrhages = random bleeds (flame + splinter)

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17
Q

What are cotton wool spots + hard exudates?

A

Soft exudate = ischaemia of retina

Hard exudates = lipid deposition

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18
Q

Types of insulin

A

Short, medium + long acting

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19
Q

Types of insulin regime

A

BD biphasic: premixed insulins BD

QDS regimen (basal bolus): before meals short acting insulin + long acting at bedtime

ON regime: OD long acting before bed

DAFNE regime: calculate carbs + adjust insulin

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20
Q

What is the sick day rule?

A

Don’t stop, maintain calorie intake, check BM QDS

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21
Q

Mechanism of metformin + CI

A

Biguanide

Increases sensitivity to insulin

Doesn’t increase amount of insulin therefore no hypos

Helps with weight loss

CI with high creatinine

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22
Q

SE of metformin

A

Nausea + diarrhoea - less so with modified release

Doesn’t cause hypos

23
Q

Mechanism + SE of SU, name of SU

A

eg Gliclazide, Glimeparide

Increases insulin secretion

Causes weight gain

Can get hypos

Need to monitor BM + inform DVLA

24
Q

Mechanism, names of + SE of DPP4 inhibitors

A

eg Sitagliptin

Blocks action of DPP4 - augments insulin + lowers blood glucose

25
Q

Mechanism, names of + SE of Glitazone

A

eg Pioglitazone

Increases insulin sensitivity

CI in HF - due to fluid retention

Can get hypos

SE: deranged LFTs, fluid retention

26
Q

Mechanism, names of + SE of SLGT-1

A

eg Gliflozins

Blocks reabsorption of glucose in kidneys

27
Q

What are the diabetic emergencies?

A

DKA HHS Hypo

28
Q

S+S of DKA

A

Drowsiness, vomiting, dehydration

Abdo pain Polyuria/ dipsia

Kussmaul hyperventilation = trying to blow off CO2 (trying to get a respiratory alkalosis to compensate)

29
Q

ABG results for DKA

A

high O2, low CO2 (due to hyperventilation - normal if not)

pH = acidotic, base excess will be low, bicarb low <18

30
Q

Causes of DKA

A

Infection, surgery, MI, pancreatitis, non-compliance (diabolemia)

31
Q

Management of DKA

A

ABCDE approach

If hypotensive = fluid challenge (1L over an hour, then 1L over 2 hours, then 1L over 4 hrs)

Fixed rate insulin infusion 0.1 units/ kg/ hour (70kg = 7 units per hour)

Check VBG at 1h, 2h + 2hrly afterwards

When glucose <14, start 10% glucose fluids

32
Q

Caution of hypokalaemia in DKA

A

Insulin pushes K+ into cells causing hypokalaemia

Check VBGs regularly, and give K+ if hypokalaemic

33
Q

When do you stop insulin infusion in DKA?

A

When ketones <0.3, venous pH <7.3, HCO3 >18

34
Q

What is a hypo?

A

BM <4 GCS <15

35
Q

What is bronze diabetes?

A

Caused by haemochromatosis

likely to get liver cancer

36
Q

How often are diabetics checked up?

A

Diet controlled - once a year

Tablet controlled - twice a year

Unstable/ symptomatic - 4 times a year (HbA1c takes 3 months to change)

37
Q

What is HHS caused by?

A

Hyperglycaemia >40

High serum osmolality >320

Absence of significant acidosis

38
Q

S+S of HHS

A

Confusion

Dehydration

Neuro dysfunction

Weakness

Seizures

Coma

39
Q

Management of HHS

A

IV 0.9% NaCl

Aim for fall in glucose no more than 5mmol/ hr

Start IV insulin when blood glucose no longer falling with fluids

Treat underlying cause

40
Q

Complications of HHS

A

Vascular complications eg MI, stroke, PAD can cause:

Seizures, cerebral oedema + central pontine myelinosis

41
Q

Describe the pathology of central + nephrotic diabetes insipidus, how it is diagnosed + treated

A

Central diabetes insipidus = due to ADH deficiency
Nephrogenic diabetes insipidus = due to ADH insensitivity
DI – diagnose with water deprivation test – if plasma osmolarity increases + urine remains dilute = DI. Then give desmopressin – if urine becomes concentrated = CDI. If not, NDI
Treat CDI with desmopressin, NDI with thiazide diuretics

42
Q

What investigation is used for chacot’s arthropathy + foot infection in diabetics?

A

Charcots = x ray, MRI if inconclusive

Infection = send soft tissue sample to microbio, consider x ray for osteomyelitis

43
Q

What is the initial management of a diabetic foot ulcer?

A

Use SINBAD or Uni of Texas system to classify ulcer

Offer: offloading, control of foot infection + ischemia, wound debridement + dressings

44
Q

What is the SINBAD classification?

A

Site

Ischemia

Neuropathy

Bacterial infection

Area

Depth

45
Q

Management of charcot’s arthropathy

A

Non-removable offloading device

Take serial x rays until it resolves

Likely to resolve with sustained temperature difference of less than 2 degrees

46
Q

Management of diabetic foot infection

A

?osteomyelitis - get an x ray

Take cultures + start abx

Osteomyelitis = abx for 6 weeks

47
Q

What clinical factors suggest osteomyelitis?

A

Grossly visible bone

Ulcer larger than 2cm

Ulcer duration longer than 2 weeks

ESR >70

48
Q

What bacteria cause diabetic foot infections?

A

Superficial = aerobic gram positive cocci

Deep/ chronic = polymicrobial

49
Q

Smart goals for DM (ABCDES)

A

A1C <7%

BP – optimise

Cholesterol <2 (LDL)

Drugs: ACEi, statin + aspirin

Exercise + eating

Smoking cessation

50
Q

Total insulin requirements for T1/2DM

A

T1 = 0.5 units/kg/day

T2 = 0.3 units/kg/day

51
Q

Which DM med is best for CV disease?

A

SGLT2 inhibitor

52
Q

Which DM meds are the most effective at lowering A1c?

A

GLP-1 + SGLT2

53
Q

When to prescribe BP meds, statins + aspirin in DM?

A

ACEi if:

  • Microvascular disease present
  • Age >55

Statin if:

  • Microvascular disease
  • Age >40
  • Age <40 AND diabetes >15 years or CV RF

Aspirin if:

  • Pts with established CVD

Endocrine (6 decks)

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