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Diabetes (Diagnosis (Fasting serum BGL (DM > 7, Normal < 6,…
Diabetes
Management
Pharmacological
Sulfonylureas (e.g. gliclazide)
: MOA- increases insulin secretion; SE: hypoglycaemia, weight gain
Acarbose
: MOA- alpha glucosidase inhibitor which reduces breakdown of complex carbs in the gut --> less carb absorption; SE: diarrhoea, flatulence
Metformin
(biguanide): MOA- decreases hepatic gluconeogenesis; SE: N/V, lactic acidosis
Increntins
GLP1 agonist (e.g. exanatide)
: MOA- increases insulin secretion, decreases glucagon secretion, decrease appetite; SE: N&V, pancreatitis, weightloss
DPP4 inhibitor (e.g. sitagliptin)
: MOA- stops GLP1 & GIP from being broken down --> inhibit incretin degradation --> increase incretin conc.; SE: pancreatitis
Insulin-
standard of Rx for T1 w/ basal [e.g. Lantus] (40-50%) bolus [e.g. actrapid (short) or novorapid (very short)] (60%) OR mixed preparations OR insulin pump. New pts may begin with 0.3-0.4U/kg/day on basal/bolus regimen and titrate.
Thiazolidinediones (glitazones)
: MOA- reduce peripheral insulin resistance, decreases hepatic gluconeogensis and decrease lipolysis; SE: weight gain, fracture risk, macular oedema, fluid retention; CI: CCF
SGLT2:
MOA- reduce glucose reabsorption in the kidneys; SE: UTIs, risk of DKA, hypoglycaemia
T2DM: (1st) Metformin, (2nd) + sulfonlyurea/basal insulin/incretin
Glycaemic targets
T1DM: HbA1c < 7.1%, fasting BGL 4-7, post-prandial BGL 5-10
T2DM: HbA1c < 7%, fasting 4-8, postprandial < 10
Other
Self-monitoring
T1: BGL 4-6 times a day e.g. before/after meals, before driving. Check ketones if unwell, BGL continuously > 15, symptoms of DKA
T2: used if on insulin; if not on insulin- consider if unwell or pt preference or lifestyle changes
Lifestyle e.g. diet & exercise; If pre-diabetic this is mainstay of Mx
Risk factor monitoring in T2: LDL < 2, HDL > 1, total cholesterol < 4, TGL < 2, BP < 130/80
Check ups
: 3-6 mo- Sx control, self-monitoring, HbA1c, BP, weight, abdo circumference, foot checks; Yearly- lipids, eyes, microalbuminurea, GFR, SNAP, meds, immunisations, education
Complications
Macrovascular
Peripheral Vascular Disease
PVD + neuropathy --> increased risk of ulcers --> Mx: pressure offloading, debridement and Abx if needed
Cerebrovascular
Cardiovascular
Acute
Hyperosmolar non-ketotic state/HHS
Characterised by high BSL, raised urea and dehydration. Occurs in T2DM when plasma osmolality > 320.
Fluids 0.9% NaCl: 1L in 3 hours then slow to 150ml/hr
Insulin (actrapid): 0.5U/kg/hr, only begin when BGL plateaus after rehydration and K > 3.5
To avoid cerebral oedema, decrease BGL at a rate of < 5.5 per hour. BGL should still be > 15 at 24 hour mark. Once BGL < 15 commence IV glucose infusion until pt is able to eat
Subcut clexane
DKA
Diagnostic: Arterial pH < 7.3 (or bicarb < 16) + ketones in blood/urine +/- hyperglycaemia
Fluids 0.9% NaCl: 1L in 30 min, 1L in 1 hour, 1L in 2-4 hours
Short acting insulin (e.g. actrapid) at 0.1U/kg/hr- ensure K > 3.5.
BGL decline of 3-6mmol/hr. When BGL < 15 add 10% glucose at 150ml/hr
K+ replacement is added when serum K < 5.5 (usually during 2nd hour). Goal of 3.5 - 4.5. Measure every 2 hours until acidosis resolves
Monitoring: pH, BGL hourly
Change to s/c insulin when pH > 7.3, HCO3 > 18, ketones < 0.3 and able to eat
Hypoglycaemia
(BGL < 4)
If severe hypo: IM/SC glucagon or (2nd) IV Dextrose 50% in 20mls
If awake: jellybeans, check in 10-15 min and if hypo persists, repeat Rx. If resolved use long acting carb (e.g. sandwich)
Monitor more regularly for first 4 hours and find cause
Microvascular
Nephropathy
4 major histologic changes in the glomeruli in diabetic nephropathy include mesangial expansion, glomerular basement membrane thickening, podocyte injury, and glomerular sclerosis
Pathogenetic processes that contribute to diabetic nephropathy in susceptible individuals include glomerular hyperfiltration; hyperglycemia and the increased production of advanced glycation end products; hypoxia-inflammation and the activation of cytokines (e.g. VEGF, TGF-beta)
Retinopathy
2 types: proliferative (neoangiogenesis growing into vitreous --> bleeding, scarring, retinal detachment, blindness) and non-proliferative (small blood vessels of retina become damaged --> bleeding --> blurred vision)
Neuropathy
Includes distal sensory and motor neuropathies, asymmetric syndromes and autonomic neuropathy
Distal sensory polyneuropathy: glove and stocking distribution of loss of pain, temperature and vibration
Autonomic neuropathy: gastroparesis, erectile dysfunction, hypoglycaemic unawareness, orthostatic hypotension & loss of bladder tone
Charcot: condition affecting the bones, joints and soft tissue of foot and ankle, characterised by inflammation in early stages.Later stages are characterised by bony deformity with the hallmark deformity being midfoot collapse; pain or discomfort may be a feature in active stage.
Definitions
Latent Autoimmune Diabetes in Adults (LADA): slowly progressive form of T1DM. Present similar to T2 but lack other cardiometabolic features. Early on patients may have adequate beta cells reserve but quickly become insulin-dependent
T2DM: Relative insulin deficiency in relation to the degree of insulin resistance. Risk factors: HTN, dyslipidaemia, abdo obesity
T1DM: Absolute insulin deficiency caused by immune mediated destruction of insulin producing pancreatic beta cells. Antibodies found: anti-GAD, anti-insulin
Diagnosis
Impaired fasting glucose: fasting 6.1-6.9 BUT normal postprandial reading (< 7.8)
Impaired glucose tolerance: normal fasting (< 7) BUT postprandial reading 7.8-11.1
Any of the below tests can be used for diagnosis, however in an asymptomatic patient a second test should be done to confirm it
Fasting serum BGL
DM > 7
Normal < 6
Intermediate hyperglycaemia: 6.1 - 6.9 (Excess macro- but not micro-vascular risk)
Random serum BGL
DM > 11.1
Normal < 6
Symptoms of DM + 1 reading > 11.1 = diagnosis
OGTT
Normal < 7.7
Intermediate hyperglycaemia 7.8 - 11 (Excess macro- but not micro-vascular risk)
DM > 11.1
HbA1c
DM > 6.5% (single reading can be used to diagnose)