Diabetes Flashcards
Key difference: Type 1 vs Type 2 diabetes
T1DM: total insulin deficiency
T2DM: reduced insulin production and/or insulin resistance
Impact of diabetes to KIDNEYS
=> glucose infiltrate
=> saturation of glucose transporters
=> glucose remains in urine
=> increased osmotic gradient
=> more water retained in urine
=> increased water loss
=> increased plasma osmolarity
s/s:
- glycosuria
- polyuria
- polydipsia
Impact of diabetes to BLOOD VESSELS and NERVES
Too much glucose in blood = GLYCOSYLATION in:
BLOOD VESSELS
=> reduced gas and nutrient exchange
=> ischemia/hypoxia
=> tissue damage
=> interrupted inflammatory response
=> poor wound healing
NERVES
=> disrupts A.P. conduction
=> neuropathies
complications from both:
- neuropathy
- nephropathy
- retinopathy
Impact of diabetes to CELLS:
Not enough glucose in cells:
=> increased gluconeogenesis (increased breakdown of fats/proteins)
=> increased lipolysis
1-> fatty acid use by cells for ATP generation
1 -> increased production of ketone bodies
1-> s/s ketoacidosis
OR/AND
2-> hyperlipidemia and hypercholesterol
2-> atherosclerosis and associated complications
Diabetes risk factors:
- obesity
- old age
- glucose intolerance
- pancreatitis or pancreatic cancer
- family history
- GDM
- sedentary lifestyle
Diabetes management
initial:
- glycemic control
- insulin management
- hbA1c test
Metformin
- reducing glucose production in the liver and enhancing insulin sensitivity in peripheral tissues. It inhibits liver enzymes, decreasing excessive glucose release, and improves cellular uptake of glucose, leading to lower blood sugar levels and improved glycemic control in patients with diabetes.
- Effects: abdominal discomfort, Cough, Shaking/chills
Insulin- mechanism of action
- the beta cells have K+ channels that are regulated by intracellular ATP
- when blood glucose increases more glucose enters the beta cells which increases the intracellular ATP which closes the ATP channel
- this depolarisation of beta cells initiates an influx of Ca2+ ions triggering insulin release
- the insulin receptors are membrane-spanning glycoproteins
Humulin NPH (isophane insulin)
- is an intermediate-acting insulin with an onset of action within 1-2 hours, peak effect in 4-12 hours, and duration of up to 24 hours. It works by lowering BGL through promoting cellular uptake of glucose, inhibiting glucose production by the liver, and facilitating its storage as glycogen in tissues.
- Effects: allergic reaction to site, hunger, thickened skin
Humalog (insulin lispro)
- is a rapid onset, short acting insulin that can be taken before or shortly after meals to lower blood sugar levels. Taken to support Humulin PRN.
- Effects: weight gain, nausea, fast heart rate
Short-acting regular insulins
- soluble insulins that may be human or animal
- only forms suitable for IV administration
- onset of action: 30-60mins (subcut)
- peak action: 2-4hrs
- duration: up to 8hrs
- can be given IV in emergencies but half life of about 5mins when given via this route and effect disappears in about 30mins
examples:
- HUMALOG, NOVORAPID, human actrapid, humalis S, human velosulin, insuman rapid, pork velosulin,
Longer acting-cloudy insulins
- absorption can be slowed by precipitating the insulin into crystals or particles of no uniform shape and “suspending” these particles in solution
- the insulin crystals or amorphous particles are formed by complexing the insulin with suitable zinc salts or with protamine
- suitable for SC only
examples: HUMULIN isophane (NPH), insuman basal, human insultard, human ultratard
Biphasic insulin
- some combination of soluble and suspended insulins
examples: humulin M3, human mixtard 20/80
Long-acting insulins
- LANTUS
- action up to 24hours with less peaked profile than other long acting insulins
- T2DM: combined with short-acting oral hypoglycemic; T1DM: combined with short-acting insulin
issue of diabetes in children
Compliance, self-management, exercise, alcohol
