type 1 and 2 DM Flashcards
what causes T1D?
- autoimmune destruction of beta cells
- T cell mediated
- at time of dx 70-80% of beta cells are destroyed
risk factors for T1D
- family risk
- genetics- HLA mutations
- geography- further from equator
- must have genetic predisposition + trigger (most likely enterovirus)
si/sx of T1D
- polyuria
- polydipsia
- weight loss
- fatigue
- weakness
- blurred vision
- frequent infections
- abd pain
dx of diabetes
- random BS > 200 with sx*
- fasting BS > 126 on 2 separate occasions
- > 200 on GTT
- A1C > 6.5%
requirements for DKA dx
- hyperglycemia: > 250
- metabolic acidosis: pH < 7.3 or bicarb < 18
- moderate ketosis: blood or urine
si/sx of DKA
- vomiting
- tachypnea
- abd pain
- SOB
- mental status changes
- may mimic flu or gastroenteritis
DKA tx
- IV fluids
- insulin
- K- monitor levels, admin if low
- assess need for bicarb
workup once T1D is dx
- T1D antibodies: insulin, GAD, IA1
- thyroid ab
- initially TSH isnt helpful, can monitor once pts under control
- celiac anti-endomysial ab and tissue transglutamine ab
role of glucagon
- increase glucose levels in a hypoglycemic emergency
short acting insulins
- aka bolus insulin
- aspart
- glulisine
- lispro
- regular
long acting insulins
- aka basal insulins
- detemire
- glarginine
- NPH
what is the honeymoon phase
- phase where T1D are asymptomatic
- lasts months- years post dx
- when start insulin tx remaining beta cells function normally, eventually stop functioning
how often do T1D typically check BS
- 6-8 X day
routine diabetic care needed for T1D
- yearly eye check
- foot care
- renal bloodwork
- aggressive lipid control
- A1C q 3 mo
- dental check q6 mo
- psych if needed
complications of T1D
- diabetic retinopathy
- diabetic nephropathy
- peripheral neuropathy
non-proliferative retinopathy
- initial manifestation- asymptomatic
- due to increased vessel permeability
- see in first 15 yrs of dx- get laser tx to prevent blindness
- micro-aneurysms
- hemorrhages
- cotton wool spots
- lipid exudates
proliferative retinopathy
- late stage disease
- neovascularization
- worse visual prognosis- potential bilndness
- tighter glucose control needed
how does diabetic neuroapthy spread
- ascends
- starts in feet
- once it hits mid calf it spreads to hands
- “stocking glove pattern”
si/ sx of diabetic nephropathy
- albuminuria
- sometimes hematuria
dawn phenomenon
- surge of hormones daily around 4-5 AM
- causes high AM BS
- tx: increase overnight basal insulin
somogyi effect
- if pt has low BS in early Am hours hormones are released and overshoot the correction
- causes high AM BS
- tx: snack before bed or reduce overnight basal
how do you dx dawn vs somogyi
- have pt check BS at 2 AM
- if low BS = somogyi
si/sx of hypoglycemia
- shaky, teeth chattering
- dizzy
- tired, anxious
- sweaty
- brain function impairment at BS of 50
si/sx of hyperglycemia
- irritable
- tired
- thirsty
- frequent urination
- HA
- blurred vision
- “zoned out”
causes of DM2
- insulin resistance
- impaired insulin secretion
- increased glucose production
- some combo of the three
- all results in hyperglycemia
prediabetes
- aka impaired glucose tolerance
- body does not secrete enough insulin compared to the insulin insensitivity
dx of prediabeteis
- FPG 100-125
- plasma glucose 140-199 after GTT
- A1C 5.7-6.4%
risk factors for DM2
- family hx
- obesity- BMI > 25
- physical inactivity
- native american, AA
- impaired fasting glucose or impaired glucose tolerance
- hx of GDM or baby > 9 lbs
- PCOS
- A1C in prediabetes range
when does DM2 screening normally start
- adults > 45
- screen q 3 . years
when do you start DM2 screening early ( < 30)
- obese, sedentary
- 1st degree relative with DM
- high risk ethnic population
- baby > 9 lbs
- HTN
- HDL < 35 or TG > 250
- hx prediabetes
- hx CAD
clinical presentation of DM2
- insidious onset
- usually asymptomatic
- overweight or obese
- may present with weight loss
- chronic skin infections, esp fungal
- neuro or CV complications
- classic sx of DM1 less common
PE findings for DM2
- acanthosis nigricans
- candida infections
- decreased sensation
- loss of DTR in ankles
- dry feet
- foot ulcers
- muscle atrophy
CV risk factor management for DM2
- smoking cessation
- ASA
- BP and dyslipidemia control
- diet and exercise
routine health maintenance for DM2
- monitor A1C q 3 months
- check urine microalbumin yearly
- annual podiatry
- annual ophthalmology
- self monitor blood glucose
what is the target A1C goal
- < 7%
- higher for elderly, multiple comorbidities, limited life expectancy
non-pharm treatment for DM2
- weight reduction
- CHO controlled diet
- exercise
- bariatric surgery
when to initiate pharm tx for DM2
- A1C > 7.5 at dx, also implement lifestyle mod
- early pharm tx= better long term control and less complications
what is the first line tx for DM2
- metformin
sulfonylureas
- glyburide, glipizide, glimepiride
- glipizide safest in CKD
- relative C/I in hepatic or renal insufficiency
- risk of hypoglycemia, weight gain
glinides
- increase secretion of beta cells
- can cause hypoglycemia
- C/I in renal dysfunction
- consider in pts with allergy to SU as add on to metformin
alpha glucosidase inhibitors
- slows gut absorption of glucose
- drugs: acarbose, miglitol
- low risk hypoglycemia
- ADRs- flatulence, diarrhea
- c/i in renal insufficiency
TZDs
- sensitize peripheral tissues to insulin
- low risk hypoglycemia
- ADRs- HF, edema, osteoporosis, bladder ca, wt gain
- drugs “-glitazone”s
GLP-1
- sq injections
- low risk of hypoglycemia
- drugs: exenatide, liraglutide, semaglutide
- lira and sema have CV benefit
- C/I in hx of thyroid ca
SGLT2
- NOT used as initial therapy, not used often
- only slight hypoglycemia risk
- consider in CVD
- drugs “-flozin”s
DPP4
- used in combo
- low risk hypoglycemia
- consider as monotx if cant take metfrmin, SU, or TZDs
- drugs “-gliptin”s
intensifying DM2 regimen
- metformin first line
- add on second line agent if A1C not met within 3 mo
- if goal not met while on 2 PO agents add insulin
goal fasting plasma glucose levels
- 70-130
insulin regimens in DM2
- start with basal insulin
- check daily finger sticks and titrate insulin as needed
- assess A1C after 2-3 mo, if > 7% check meal time BS
- add one meal at a time
hyperglycemic hyperosmolar state (HHS)
- extreme hyperglycemia -> hypovolemia and electrolyte abnormalities
- “DKA” of DM2
precipitating factors for HHS
- major illnesses
- drugs: steroids, thiazides, atypical antipsychotics
- compliance issues
si/sx of HHS
- sx dev insidiously
- polyuria
- polydipsia
- weight loss
- lethargy
- decreased skin turgor
- dry membranes
- tachy
- hypotens
lab findings for HHS
- marked hypoglycemia > 1000
- hyperosmolality
- pre-renal azotemia
- acidosis and ketonemia absent/ mild
- low K, Mg, and phosphate
