Diabetes Flashcards

0
Q

Ketoacidosis clinical features

A
  • Dehydration (high-glucose-osmotic diuresis); tachycardia and hypotension
  • Air hunger (Kassmaul respiration-acidosis)
  • Smell of ketones
  • Vomiting and abdominal pain
  • Signs of precipitating cause – infection, myocardial infarct etc
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1
Q

Ketoacidosis - diagnostic triad

A
  • Hyperglycaemia
  • Ketonuria
  • Acidosis: medical cause of ileus, enteroparesis
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2
Q

Hypoglyceamia clinical features

A

Pale, cold, sweating, GCS, unconscious, tachycardiac, normotensive, normopnoeic, seizure, Todd’s paresis, hemiparesis, total body myoclonic jerk, hyperflexive, upgoing plantar responses, neuroglycopenia (note enough blood getting to brain), sympathetic overdrive

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3
Q

Ketoacidosis and potassium

A
  • Osmotic diuresis takes potassium
  • Dehydration: renin…angio…aldosterone – further potassium loss
  • Total body K+ always low eg. 200mmol deficit
  • Acidosis – H+ in cells forces K+ out (to maintain intracellular “cation balance”)
  • No insulin – no K+ intake until insulin replaced; then sudden fall
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4
Q

Ketoacidosis txt

A
  • Gastric aspiration (if vomiting or reduced conscious level)
  • Rehydration
  • Insulin replacement
  • Potassium replacement
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5
Q

Ketoacidosis - txt 1st hr

A

P​: Potassium – 20mmol if no peaked t wave
A​: Acidosis: if pH low (less than 7.30) get urgent advice
N: ​Normal saine; 1litre in first hour
I: ​Insulin by infusion
C​: Cathether and cultures; urine, blood etc
S​: Stomach aspiration; endotracheal tube first if no gag reflex

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6
Q

Medications - insulin

A
Basal: 
Glarine (Lantus) od
​Detamir (Levemir) od/bd
Bolus: 
Aspart (Novorapid) w/meals
​Glulisine (Apidra) w/meals
​Humalog lispro w/ meals
Mixed: 
Novomix 30 (30% SA, 70% LA)
​Humalin M3
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7
Q

Medications - other

A

Metformin: increases insulin sensitivity, promotes weight loss, S.E. GI-nausea, diarrhea, lactic acidosis, Contra: decreased eGFR, contrast, AKI

Sulphonylurea (Gliclarcide, Diamicron): Increases insulin release, promotes weight gain, S.E. Hypoglycaemia

DPP4 Inhibitors (Sitagliptin, Linagliptin): Increases insulin secretion, Increatin In-Creat-In (Insulin Creating Insulin), GLP-1 (glucagon like peptide), DPP4 normally breaks down GLP-1, Delays gastric emptying, nausea, increases fullness, S.E. well tolerated, no hypos, weight neutral

GLP-1 analogues (Exenatide, lira glutude): Increases insulin secretion, promotes weight loss, not likely to cause hypos, expensive, sub-cut injection

SGLT2 Inhibitors (dapagliflozin, canagliflozin, empagliflozin): Work in the kidneys, Sodium-Glucose-Loop-Transporter, promote weight loss (fluid loss), less effective in decreased eGFR, no risk of hypos, oral route, more expensive, S.E. increased risk of thrush, UTI, ~polyuria, Contra. Avoid in loop diuretics, gastroenteritis, N/V in elderly.

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8
Q

Targets of HbA1c

A

DM1: 48-53mmol/mol
* Diabetes control & complications trial research showing average vs. strict control*

DM2: Individualised, ~48-58 mmol/mol
Factors influencing targets for HbA1c
-Age, complications, duration of DM2, CV risk, co-morbidites, risk of hypos/awareness
UKPDS, UK prospective diabetes study showing intensive vs average control in newly diagnosed DM2 was benefical for microvascular vascular complications

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9
Q

Complications:

A
  • Microvascular: Retinopathy, Nephropathy (increased ACR, give ACEI or ARB), Neuropathy (Autonomic, peripheral)
  • Macrovascular: CVD, Cerebrovascular disease, Peripheral Vascular disease (txt statin, aspirin)
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10
Q

The diabetic foot

A
*Loss of protective sensation*
• Inspect – including heels
• Palpate – capillary refill and pulses
• Light touch – finger, cotton wool or monofilament
• Avoid pin prick testing
• Vibration sense
• Ankle jerks
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11
Q

Retinopathy

A
  1. Background – microaneurysms (dot haemorrhages), hard exudates (lipid leaked from microaneurysms), blot haemorrhages (up to 3”thumb prints” on retina)
  2. Maculopathy – based in location rather than severity, macula oedema usually looks normal through ophthaloscope, check for fall in corrected visual acuity, pinhole corrects for refractive errors
  3. Pre-proliferative – cotton wool spots (infarcts of unmyelinated nerve cell-layer in front of retina), more than 3 blot hemorrhages, venous beading and looping, IRMA (intra-retinal microvascular abnormalities)
  4. Proliferative – new vessel formation, hemorrhages
  5. End-stage – vitreous haemorrhage from fragile vessels, scarring, traction retinal detachment, blindness
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12
Q

Indications for eye referral

A
  • Fall in corrected visual acuity (cataracts or maculopathy)
  • Single cotton wool spot
  • 3 blot haemorrhages
  • Anything at macula
  • New vessels (emergency)
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13
Q

Laser treatment

A
  • Focal laser – small, mild burns in a grid for maculopathy
  • Pan-retinal photocoagulation (eg 1000 burns) for new vessel formation and severe pre-proliferative retinopathy
  • Avoid vessels and macula, aiming to create multiple peripheral laser burns
  • Reduces local growth factors by converting ischaemic retina into infarcts
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14
Q

Implications of microalbuminuria

A
  • Nephropathy is associated with increased risk of microvascular disease
  • And with increased mortality (related to macrovascular disease)
  • Can be detected early by screening for microalbuminuria
  • Usually tested for as the urinary albumin: creatinine ratio (ACR)
  • Extra attention to risk factors is then indicated (smoking, lipids, hypertension)
  • Angiotension converting enzyme inhibitor slow progression of renal impairment
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15
Q

Causes of peripheral neuropathy

A

A​: alcohol
B​: B12 deficiency (as well as causing subacute combined degeneration of cord)
C​: chronic renal failure and carcinoma (para-neoplastic)
D​: diabetes and drugs eg nitrofurantoin, metronidazole, ethambutol, isoniazid
E​: every vasculitis (RA, polyarthritis, sarcoid, scleroderma, Wegner’s)