module 13 DM Flashcards
Type 1
autoimmune destruction of Beta cells
type IV hypersensitivity
s/s do not arise until sufficient destruction has occurred, could be years after the initial trigger
type 2
insulin resistance
other types of diabetes
maturity onset diabetes of youth - genetic defect in insulin production or release Gestation DM - during preg Various endocrine disorders - cushings - acromegaly - pheochromocytoma
Type 1 clinical
onset < 20 normal weight dec. blood insulin anti-islet cell antibodies ketoacidosis is common
type 2 clinical
obese
inc. blood insulin
no antibodies
HHNK more common
Type 1 DM: 2 forms
1A: immune mediated - 3 subcategrories -- polygenic -- monogenic -- latent autoimmue 1B: idiopathic
polygenic 1A
2 or more genetic loci
monogenic 1A
rare assoc with IPEX syndrome
- immune dysfunction
- polyendocinopathy
- enteropathy
- X-linked
latent autoimmune 1A
development of T-cell reactivity in adulthood
Acute complications of DM
hypoglycemia: over tx
diabetic ketoacidosis
- no energy in cell, rely on fatty acid’s to work
Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
ketogenesis
ketone bodies: used to generate energy without glucose
- acetoacetate
- acetone
- B-hydroxybutyrate
HHNK vs DKA
Glucose: HHNK(900) > DKA(600) Na: HHNK: high, DKA: nml pH: HHNK: slightly low, DKA: very low Bicarb: HHNK: slightly low, DKA: very low anion gap: DKA elevated
Risk factors DM type 2
aging
sedentary lifestyle
obesity
- inc. abd. fat inc. risk
chronic complications of DM
hyperglycemia and nonenzymatic glycosylation microvascular disease - retinopathy - nephropathy - cardiomyopathy Macrovascular disease - coronary artery disease - stroke - peripheral arterial disease - accelerated atherosclerosis diabetic neuropathy
glycosylation
glycosylation end products (AGE’s)
- proteins that bind to glucose
inc. glucose -> inc. binding -> inflammation
AGE chemical properties
cross link polypeptides of same protein trap nonglycosylated proteins (LDL) confer resistance to proteolytic digestion induce lipid oxidation inactivate nitric oxide bind nucleic acids
AGE bind to receptors and induce
monocyte emigration cytokine and GF secretion inc. vascular permeability procoagulant activity enhanced cellular prolieferation enhanced ECM production proinflammatory
AGE/glycosylation adverse effects
microangiopathy, cerebravascular infarcts HTN retinopathy, cataracts, glaucoma MI gastoparesis Islet cell loss Atherosclerosis peripheral vascular disease -> infections, gangreen peripheral neuropathy nephroscerolsis - glomerulosclerosis - arteriosclerosis - pyelonephritis
retinopathy
background diabetic retinopathy: earliest phase
- arteriesi n retina become weakened and leak, forming small, dot-like hemorrhages
Proliferative retinopathy: later stage
- circulation problems cause ischemia -> neovascularization that leak
nephropathy
hyperglycemia-> inc. renal blood flow
-> inc. glomerular capillary pressure -> inc. protein excretion -> glomerular damage -> dec. GFR and renal failure, and HTN
glomerular damage DM
protein excretion -> glomerular damage
- loss of negative charge
- glomerulosclerosis
- thickening of basement membrane
- mesangial expansion
neuropathy
peripheral neuropathy causes either pain or loss of feeling in toes, feet, legs, hands, and arms
- pressure injury will go unnoticed
glucose-> neuron: H2O follows -> swelling and inflammation
Autonomic neuropathy
causes changes in digestion, bowel and bladder function, secual response, and perspiration
focal neuropathy
results in sudden weakness of one nerve, or a group of nerves -> weakness or pain
