Diabetes Flashcards
S and S of Hypoglycemia
BG more then 4.0 mmol/L • Confusion – change in LOC • Sweating • Rapid pulse • Tremors
S and S of Hyperglycemia
• BG > 7.0 mmol/L (11 is VIHA) • Polyuria – excessive urination • Polyphagia – increased hunger • Polydipsia – increased thirst • Glucosuria – high levels of glucose in the urine • Weight loss • Fatigue 
Review…
Effects of Insulin
Normal response to High BG
Simulates glucose uptake into cells and storage of glucose as glycogen in the liver and muscles.
Also stimulates protein synthesis and free fatty acid storage in adipose tissue.
Inhibits gluconeogenesis and lypolysis
Review
Effects of Glucagon
Normal response to low BG. Stimulating Gluconeogenesis and breakdown of glycogen
Diabetes is…
And is a major risk factor for….
Characterized by disturbances in carbohydrate, protein and fat metabolism
Ineffective insulin production, poor insulin sensitivity.
A major risk factor for MI, stroke, renal failure, retinopathy, peripheral and autonomic neuropathy and peripheral vascular disease
Cause of type 1 vs type 2
Type I: autoimmune disease strongly associated with leukocyte antigens DR3 and DR4. May be associated with certain viral infections. Beta-cells destroyed
Type 2: may result from impaired insulin secretion, peripheral insulin resistance, increased basal hepatic glucose production obesity, hormonal contraceptives, pregnancy, insulin antagonists i.e. phenytoin over the counter regulatory hormones
Why is glucagon not inhibited when those with DKA or HHS.
Inhibition of glucagon requires insulin. Signal for more glucose (glucagon stim) is coming from cells, who are glucose starved. Insulin is required to get glucose into cell and stop the signalling.
How do DKA and HHS differ in the aspect of insulin levels?
DKA – no insulin therefore gluconeogenesis and lipolysis
Production ketone bodies (acetone breath) and ketoacidosis (can be severe)
HHS – insulin still present therefore gluconeogenesis and lipolysis mainly inhibited. Ketones mild/absent and pH normal/mild
Major problems of HHS and DKA
DKA- Hyperglycemia, Acidosis, Osmotic diuresis (dehydration)
HHS- Hyperglycemia, Osmotic Diuresis (Worse then DKA)
What sort of events might cause DKA or HHS and why
Reduced insulin admin (DKA) OR Stress events: Infection MI Diarrhea and vomiting Stroke Trauma Pancreatitis Unknown etiology
Acute Stress -> hormone releas glucagon, corticosteroids, catecholamines)
All attempt to increase glucose further to deal with the stress (fight or flight)
All worsen an already high blood glucose level
ANY trauma will bring stress response
S and S of DKA
Can develop quickly ( 13.9 mmol/L
Acetone breath, ketones in urine, acidosis, confusion/coma all from ketone production
Kussmaul breathing (deep rapid breathing) and abdominal pain from metabolic acidosis
Polyuria from high glucose (osmotic diuresis) glc in urine
Polydipsia and tachycardia from dehydration
Sodium may be increased/ decreased or normal
Hypotension from dehydration
AND… Blurred vision, Weakness, Headache, Orthostatic hypotension, frank hypotension (volume depletion), anorexia, nausea, vomiting, and pain (r/t acidosis), , mental status changes. Hyperkalemia (before Tx)
Main S and S of HHS
Develops more slowly than DKA (days to weeks)
Blood glucose > 33.3 mmol/L
No ketone breath and ketone in urine
Stupor/coma from hyperosmolar state
Profound Dehydration -> high sodium,
polyuria from high glucose (osmotic diuresis) glc in urine
Hypotension- Polydipsia and tachycardia from dehydration
Higher mortality then DKA 10-40%
COMPARE those at risk of DKA and HHS
DKA - Type 1 (Can be Type 2)
HHS- Occurs predominantly in type II diabetics (some cases of type 1)
Older people with no history of diabetes or mild T2DM
Key Requirements of Patient with DKA
Insulin
Hydration
Electrolytes replacement
Diagnostics common in DKA patient
Elevated bld Glucose – severity of DKA is not necessarily related to blood glucose
Low Bicarb levels
Accumulation of ketones (bld and urine)
Electrolyte levels (K+, Na+)
Elevated Creatinine, BUN (ARF)
(post rehydration continued elevation present in the pt with renal insufficiency