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heather watson

on 19 June 2016

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Transcript of DIABETES

the pancreas type 1 immune
insult Finished frank diabetes Risk Factors Last step autoimmunity (cc) image by nuonsolarteam on Flickr type 2 hypoinsulinemia Finished hepatic
prod Risk Factors frank diabetes insulin
resistance (cc) image by nuonsolarteam on Flickr complications acute chronic DKA outcomes insulin deficiency protein catabolism amino
acids nitrogen
loss gluconeogenesis glucose uptake hyperglycemia athrosclerotic effects renal effects gestational effects osmotic diuresis electrolyte depletion dehydration signs tx lipolysis glycerol free
acids ketogenesis ketoemia & ketouria pathology treatments pharmalogic non stain = insulin stain = glycagon beta alpha insulin gestational DX fetal risks maternal risks triglyceride
synthesis K+
glucagon direct indirect BG SNS
liver adipose glucose ketones cAMP IP3 PIP 2 gycogenolysis

triglyceride lysis

gluconeogenesis GH glycerol FFAs ketogenesis DX random > 11.1 | fast > 7 | OGTT 2hr > 11.1 __ __ __ 3 P's weightloss polyuria
polyphagia ketones
strength Familial: 40% mz twin condordant
higher heritability from father

b-cell degranulation Ag+ ICA
GAD islet cell anitgen insulin autoantibodies glutamic acid decarboxylase By the decomposition of glucose, ATP is produced in the beta cells. The increased [ATP]
closes the K+ channel, leading to a depolarisation which in consequence opens the Ca2+ channel. Ca2+ activates the insulin gene expression and by exocytosis, the produced insulin is set free in the blood. insulin agonists decrease insulin resistance

increase insulin production

decrease hepatic glucose production

decrease ingestion of CHO TZDs



a-1-glucosidase glyburide

meglinitide risk of hypoglycemic events can be used in setting of CRF rosiglitazone

activate PPARs
peroxisome proliferator-activated receptors associated w CVD, liver disease metformin

risk of hypoglycemic events
risk of LACTIC ACISOSIS canNOT be used in setting of CRF beano

competative binding at brush border
in small intestine thiazolidinediones ameliorates postperandrial hyperglycemia inhibitor starting doses
lean 5 U @ hs
obese 10 U @ hs BASAL BOLUS carb-counting
1 unit : 15 g BID TID QID TID 80% b-cell destruction honeymooning tx @ this stage can
allow remaining 20%
b-call population to
function as they expire caffiene can obscure results DX random > 11.1 | fast > 7 | OGTT 2hr > 11.1 __ __ __ caffiene can obscure results 95% of DM 6% of general population 3 P's blurred vision polyuria
polyphagia fat, calorie diet
sedentary lifestyle
family Hx overproduction of insulin
to compensate for resistance

exhausts islet capacity metabolic syndrome NO
PG-1 Vascular tone
leukocyte adhesion
free radicals DM2
polycystic ovary smoking
LDL acanthosis nigricans central obesity screening upon Dx HTn
Coagulation assay
Renal fxn study
EKG if > 35 yrs
dipstick urinalysis > 130/80
tx: ACEi, ARB | Diuretics, Ca2+-blockers | b-blockers LDL > 2.5
TG > 2
TC/HDL > 4 thrombotic risk assessment repeat @ preg
planning 10g S-W monofilament < 50% sensitile one-third of people with type 1 diabetes have thyroid disease albuminuria
24 hr urine & creatinine clearance
> 300 mg/24h NEPHROPATHY 25% 75% hyperglycemia protein
glycosylation polyol
pathway inactivation thickened
membranes cell
injury sorbitol osmotic
dyreg'd inhibit
pumps sorbitol
toxicity LDL impairs afinity
w/ LDL receptors remains in
circulation HDL upregulates
turnover decreases
circulation accumulates
on vessel wall Renal basement membrane impairs filtration;
hardening of glomeruli;
hyalinization of renal arteries impairs RBF glycosylation hyperosmotic
stress cellular
dehydration impaired
mobility decreased
gene expression ie: cellular fxn uncouple
Ca2+ from
in PCT BG > 14 AG pH vomiting, thirst, polyuria, weight loss, abdominal pain, weakness 5-10% mortality 25% new DM1 risks M.I.
pancreatitis Tx low pH
high BUN:Cr
high BG 35% recent
infection resolve acidosis
restore perfusion
correct lytes
treat cause IV insulin, bicarb normal saline potassium, calcium antibiotics insulin tx
initial <10 U bolus
ongoing 0.1 U/kg/hr
6 hr goal: BG > 12
supplement w glucose
overal goal: BG 4-6
insulin tx
initial <10 U bolus
ongoing 0.1 U/kg/hr
6 hr goal: BG > 12
supp't w glucose
overal goal: BG 4-6 if pH < 6.95 intial tx = 1 L bolus

ongoing = 500 ml/hr
for 2 hours [K+] usually elevated on presentation
admin of insulin drives K+ into cells
monitor closely, keep [K+] 4-5 mmol
hold insulin if [K+] < 3 mmol/L hypoglycemia non-ketotic hyperosmolarity BG < 4 mmol/L endogenous
insulin secretion
suppressed glucagon
GH ANS symptoms neuroglycopenia @ BG 3.7 @ BG 3.7 trembling
tingling @ BG 2.5 loss of consciousness poor concentration

confusion, drowsiness,
vision changes, speech
difficulty, headache @ BG 4.2 glucagon direct indirect BG SNS
Glucocorticoids liver adipose glucose ketones cAMP IP3 PIP 2 gycogenolysis

triglyceride lysis

gluconeogenesis GH glycerol FFAs ketogenesis counter-regulatory hormones >> insulin average fluid deficit is 10 L
pH often as high as 7.5 onset more insidious
than DKA, presentation
often later-stage severe moderate can self-treat mild risk factors advanced age
renal, liver, GI disease
alcohol, exercise, diet
hypoglyc' unawareness leukocyte formation fungal infxn, complication of infections vaccination retinopathy pathophysiology diagnostic features prevention treatment screening 2 4 5 neuropathy pathophysiology diagnostic features prevention treatment non-proliferative pre-proliferative proliferative 2 10 20 screening nephropathy pathophysiology diagnostic features prevention treatment 2 4 5 screening macrovasular pathophysiology diagnostic features prevention treatment 2 4 5 screening microaneurysms
neovascularization #1 cause of blindness under age 70 years from DM dx microaneurysms
dot + blot hemorrhage
hard exudates "cotton wool" soft exudate
cap drop-out ischemia -> inflammation neovascularization blindness 3% DM2
14% DM2 + insulin
23% DM1 40% DMs
test +ve 10% DM2s
+ve at Dx #1 cause of cateracts fundoscopy @ time of Dx
@ age 15 annually
@ 5 yrs post-dx annually
@ DM2 annually, biannually
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