diabetes Flashcards
Type 1 diabetes
Primary β-cell defect or failure results in severe insulin deficiency or no insulin secretion
2 types of Type 1 diabetes
immune mediated
idiopathic
type 2 diabetes
Insulin resistance with inadequate insulin secretion. Insulin resistance is universal and multifactorial. Insulin secretion declines over time
diagnostic criteria of diabetes
FPG ≥ 7
or A1C ≥ 6.5
or 2hPG in a 75 g OCGTT ≥11.1
or random PG ≥ 11.1
If asymptomatic, need repeat confirmatory testing
Hg A1C not commended for diagnosis in (special population
children & adolescents (as the sole diagnostic test)
pregnant individuals as part of routine screening for gestational diabetes
cystic fibrosis
suspected Type 1 diabetes
factors affecting HgA1C accuracy
erythroproiesis (B12/Fe deficiency, chronic liver disease)
altered hemoglobin
altered glycation (CKD)
Erythrocyte destruction (splenectomy)
Assays (Hyperbilirubinemia, Etoh, chornic opiates)
- increase with Age
may vary among ethic groups
prediabetes criteria
fast glucose 6.1-6.9
2h PG in a 75g OGTT 7.8-11
A1C 6.0-6.4
IFG (impaired fasting glucose)
due to increased hepatic glucose output caused by hepatic insulin resistance and increased glucagon levels
IGT (impaired glucose tolerance)
due to decreased insulin secretion, primarily resulting from peripheral (muscle) insulin resistance
LADA
latent autoimmune diabetes
antibodies targeting beta cells
HgA1C is a better predictor to ____ than FPG or 2hPG
cardiovascular event
To achieve A1C ≤7 aim for
FPG or preprandial PG target 4-7
2 hour post prandial 5-10
Type1 goal A1C target
≤7.5
signs and symptoms of type 1 diabetes
polyuria
polydipsia
polyphagia
fatigue
weight loss
poor wound healing
recurrent infections
genital pruritis
vision changes
paresthesias
CV symptoms
diabetic ketoacidosis (DKA)
typically seen in Type 1
Absolute insulin deficiency and increased glucagon (must use insulin)
Risk Factors: new diagnosis of DM, insulin omission, infection, MI, abdominal crisis, trauma, possibly continuous subcutaneous insulin infusion therapy, thyrotoxicosis, cocaine, atypical antipsychotics, possibly interferon
HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS)
Extracellular fluid volume (ECFV) depletion and hyperosmolarity are predominant; typically seen in Type 2
Relative insulin deficiency; may need insulin (fluids are first priority)
Risk Factors: same as DKA plus cardiac surgery, CVD/renal disease, drugs (diuretics, glucocorticoids, lithium, atypical antipsychotics), infections in 40-60% of cases
avoid SAD MANS to prevent dehydration
Sulfonylureas
ACE inhibitors
Diuretics
Metformin
Angiotensin receptor blocker
NSAID
SGLT2 inhibitors
hypoglycemia
glucose < 3.9
Development of adrenergic (autonomic) symptoms typically progressing to neuroglycopenic symptoms
potential complications of hypoglycemia
Neurologic:
short-term → impaired cognition, coma, death;
long-term → mild intellectual impairment, rare hemiparesis or pontine dysfunction
CV: ↑ mortality in T2DM + CVD MSK: falls, fractures Psychosocial: ↓ QoL, fear of hypoglycemia, burden/stress on support persons
Nocturnal Hypoglycaemia
which insulin is used to reduce the risk
A long-acting insulin analogue (i.e. degludec and glargine) may be used in place of NPH (i.e. Humulin N) to reduce the risk of hypoglycemia, including nocturnal hypoglycemia
Dawn phenomenon
An early morning rise in blood glucose level related to the physiologic release of GH, cortisol, and catecholamines without preceding hypoglycemia
Potential Causes:
The evening dose of intermediate-acting insulin is too low
Too much food before bed
Effect: Morning hyperglycemia WITHOUT overnight hypoglycemia
SOMOGYI EFFECT
(Rebound hyperglycemia following nocturnal hypoglycemia)
Overnight hypoglycemia that results in a compensatory morning rise in blood glucose level
Hormones of adrenaline, glucagon, GH, and corticosteroids are released in response to the hypoglycemia
Potential Causes:
Dose of evening intermediate or long-acting insulin is too high
Not having enough food before bed
Increased exercise
Effect: Morning hyperglycemia CAUSED BY overnight hypoglycemia
microvascular complications of diabetes
diabetic retinopathy
diabetic neuropathy
diabetic nephropathy
macrovascular complications of diabetes
cardiovascular
cerebrovascular
peripheral vascular
ABCDESSS for diabetes management
A1C targets
BP targets (130/80)
Cholesterol targets (LDL <2 or > 50% reduction)
Drugs for CV and /or cardiorenal protection
Exercise and healthy eating
Screening for complications
Smoking cessation
Self-management, stress
cardiovascular protection drugs
patients with cardiovascular disease (statin +ACEi/ARB+ASA)
patient with microvascular disease (statin +ACEi/ARB)
Patient age ≥55 with CV risk factors; age ≥40; age ≥ 30 and diabetes > 15 years (statin)
- NO ACEi/ARB or statin for pregnancy
complications of gestational diabetes
Neonatal hypoglycemia
Preeclampsia
Macrosomia: Increased placental transport of glucose, amino acids, and fatty acids stimulate the fetus’s endogenous production of insulin and insulin-like growth factor 1 (IGF-1) that result in fetal overgrowth
Stillbirth
glycemic targets for pregnancy
fasting and preprandial BG < 5.3
1h postprandial BG < 7.8
2h postprandial BG < 6.7
pre-existing diabetes in pregnancy
Aim for A1C ≤6.5% during pregnancy (≤6.1% if possible), if can be achieved safely, to lower the risk of late stillbirth & infant death
Screening for retinopathy & nephropathy
Good BP control
Start ASA 81mg at 12-16wks to ↓ risk of pre-eclampsia
management of diabetes in pregnancy
Insulin (preferred)
Metformin
Glyburide (if insulin refusal or uncontrolled on metformin)
screening for gestational diabetes
24-28 weeks
postpartum management of diabetes
Encourage immediate breastfeeding to avoid neonatal hypoglycemia and continue at least 3-4 months to prevent childhood obesity
Perform a 75g OGTT between 6 weeks to 6 months postpartum to screen for prediabetes and T2DM
If pre-existing diabetes: should have frequent blood glucose monitoring in the first days postpartum, due to ↑ risk of hypoglycemia; Insulin doses should be decreased immediately after delivery to below pre-pregnant doses and titrated as needed to achieve good glycemic control
If history of T1DM: screen for postpartum thyroiditis at 2-4 months postpartum with a TSH test
management of diabetes during delivery
Induction of labour offered at 38-40 wks for GDM, and 38-39 weeks if pre-existing diabetes (earlier if poor glycemic control/complications)
Maternal blood glucose levels should be kept between 4.0-7.0 mmol/L during L&D
Pregnancy screening of diabetes
Early screening (< 20 weeks) if high risk of undiagnosed T2DM
Consider increased fetal assessment in GDM that is poorly controlled +/- co-morbid conditions
If pre-existing diabetes, initate fetal well-being assessment at 30 – 32 weeks, and continue weekly starting at 34-36 wks
