interactive lecture diabetes Flashcards
what are diabetes the leading cause of
end-stage renal disease
adult blindness
lower limb amputations
theories for causation of diabetes mellitus
genetic
autoimmune
environmental: viral, obesity
normal insulin level
70-130 mg/dL
purpose of insulin
allows transport of glucose from blood stream into the cells cytoplasm
where are insulin released from in the pancreas
beta cells
which 4 regulatory hormones increase blood glucose levels to maintain normal bg lvls
glucagon
epinephrine
growth hormone
cortisol
what is gestational diabetes
develops during pregnancy detected around 24 - 28wks of gestation;
will return to normal 6 weeks postpartum
the high bg of mother will bring extra glucose to the baby -> causing the baby to gain weight
what is secondary diabetes and what can cause it
treatment of a medical condition that in turn cause increased bg
corticosteroids - prednisone
thiazides
Total parental nutrition (TPN)
pancreatic dx
3 requirements for diagnosis of prediabetes
- IGT: 2 hr plasma glucose 140 -199
- IFG: fasting glucose lvls >100 but <126
- A1c lvls: 5.7-6.4%
what are the A1c levels for normal, prediabetes, and diabetes
normal: <= 5.6
prediabetes: 5.7-6.4
diabetes: 6.5+
what are the fasting blood sugar test (FPG) levels for normal, prediabetes, and diabetes
normal: <=100
prediabetes: 100-125
diabetes: >=126
what are the oral glucose tolerance test (OGTT) levels for normal, prediabetes, and diabetes
normal: <=140
prediabetes: 140-199
diabetes: >=200
Type 1 diabetes peak onset, and most often occurs in people how old
happens to people <30yrs old
peak onset 11-13 yrs old
autoimmune disease
classic symptoms of diabetes type 1
polyuria - frequent urination
polydipsia - extreme thirst
polyphagia - excessive hunger
ketoacidosis
weight loss
weakness/fatigue/blurred vision
etiology and pathophysiology of diabetes
pancreas produces insulin but either not enough or poorly used
can be prevented or delayed with weight loss & physical activity
4 major metabolic abnormalities of diabetes type 2
- insulin resistance
- pancreas decreased ability to produce insulin
- not enough insulin produced
- alteration in hormones and adipokines
clinical manifestations of diabetes type 2
gradual onset with nonspecific symptoms
fatigue
recurrent infections/prolonged wound healing
visual changes
4 diagnostic studies for diabetes
- fasting plasma glucose lvl >126
- random plasma glucose >=200 mg/dL w/ symptoms
- 2hr OGTT >=200 mg/dl using glucose load 75G
- A1c>6.5% on 2 separate occasions
what does A1c measure
the amount of glucose that gets attached to Hgb over the RBC lifespan 90-120 days
what is the ambulatory glucose profile (AGP)
summary of a pt’s daily glucose and insulin patterns over time
why use AGP or A1c
AGP is great for those prone to glycemic swings vs. A1c only show one snapshot
target range of bg for diabetics
70-180 at least 70% of the time with minimal hypo or hyperglycemia
who is exogenous insulin prescribed for
type 1 diabetes
type 2 who can’t control bg by other means
fastest absorption rate of insulin injection locations
abdomen, back of arm, thigh, butt
name 3 meds in class sulfonylureas
glipizide (Glucotrol), glimepiride (Amaryl), glyburide
purpose of sulfonylureas
help pancreas make and secrete insulin for DM2
decreases A1C by 1-2%
patient considerations for sulfonylureas
hypoglycemia - severe
GI: N&V, constipation
drug in class biguanides
metformin
purpose of metformin
Increases glucose tolerance by:
decrease glucose absorption in intestines
decrease hepatic glucose production
increase glucose uptake and usage
-> decrease A1c by 1.5-1.8% in DM2
contraindications for metformin
renal failure,
liver dx,
severe infection
considerations for metformin
hold 48hrs before invasive procedure such at cath lab
GI issues
what 2 drugs go in the thiazolidinediones (TZDs) class
pioglitazone (Actos)
rosiglitazone (Avandia)
purpose of thiazolidinediones
insulin ensitizers that decrease insulin resistance by inhibiting hepatic gluconeogenesis
reduce A1c 1.5%
considerations for taking TZDs
- fluid retention -> don’t use in CHF [may cause weight gain, edema]
- weeks to months to work
- start low dose, titrate q2-4wks
- reduce effectiveness of oral contraceptives
- liver function tests (LFTs)
list the drug under DPP-4 inhibitors
sitagliptin (Januvia)
how does sitagliptin work
increase incretins and increase GLP-1 levels (released in response to food and regulates insulin), thus increasing insulin secretion
lowers A1c 0.5-1%
few side effects
what are the 2 incretin mimetics inj meds
exenatide (Byetta)
liraglutide (Victoza)
how do incretin mimetics work
binds to GLP-1 receptors and slow down digestion of food -> glucose absorbed slower
can reduce appetite -> weight loss
causes of DKA
hyperglycemia
dehydration
infection
mostly in DMtype1
DKA signs and symptoms
- 3Ps - polyurea, polydipsia, polyphagia
- dehydration - -poor skin turgor, dry mucosa, tachycardia
- orthostatic hypotension
- Kussmaul’s respirations
- acetone breath, fruity breath
DKA labs - 4
bg >240-300
arterial blood pH <7.3
serum bicarbonate <15mEq/L
ketones in blood and urine
DKA treatment
- ensure airway/O2
- IV NS 1/L until stable BP & urine output >30/hr
- insulin bolus Regular IV 5-10units
- then cont. insulin drip until bg around 250 1-2U/hr 0.5U/kg/hr, add D5W to prevent hypoglycemia
- monitor bg q1-2hr
- potassium (K) replacement
what is hyperosmolar hyperglycemic syndrome (HHS) and treatment
occurs mostly in elderly >60yrs with DMtype2 - prolonged hyperglycemia >400 but no ketoacidosis because there is enough insulin
treat is similar to DKA
what is considered hyperglycemia and symptoms
bg>200
3P’s
weight loss, visual changes
or asymptomatic
causes of hyperglycemia
- not enough basal insulin (overnight insulin)
- dawn phenomenon & Somogyi effect
- poor food choices
- incorrect timing of insulin given
- insulin resistance
- illness/stress
dawn phenomenon vs. Somogyi effect
how to tell difference
dawn phenomenon (our body produces cortisol and growth hormone to wake up but also effects bg)
Somogyi effect (hypoglycemia at night but hormones overcompensate to hyperglycemia)
check if bg is low around 2-3AM, if it’s low it’s Somogyi
if normal or high it’s dawn phenomenon
how to avoid dawn phenomenon and Somogyi effect
- avoid carbs at bedtime
- have a low fat, high fiber dinner
- use insulin pump at night, take insulin before bedtime instead of late afternoon
what range of bg should diabetics be kept in
140-180 bg maintained
premeal bg <140
no higher than 180 after therapy
common causes of hypoglycemia
- meal delayed
- insulin timing
- excessive exercise
- alcohol
signs and symptoms of hypoglycemia
- confusion/irritability
- diaphoresis, tremors
- hunger
- weakness
- visual disturbances
hypoglycemia treatment
if ALERT and can swallow:
- 15-20g simple carbs, 4-6oz fruit juice, regular soft drink
avoid foods with fat: decrease absorption of sugar
recheck bg 15mins after until bg>70
if NOT awake:
- 1mg of glucagon IM/subQ (may cause rebound hypoglycemia)
- ingest complex carbs after recovery
- 20-50mls of D50W IVP
factors that worsen and exacerbate chronic diabetes issues
obesity
smoking
hypertension
high fat intake
sedentary lifestyle
areas mostly effected by chronic diabetes
eyes: retinopathy
kidneys: nephropathy
skin
erectile dysfunction
typically 10-20 yrs of diabetes
most common cause of diabetic retinopathy
hyperglycemia leading to microvascular damage to the retina
what to screen to prevent nephropathy
yearly screening of albumin in urine, serum creatinine
what happens in nephropathy
damage to small blood vessels that supply the glomeruli, Main cause of end-stage renal disease
how does diabetes effect the immune system
- defect in mobilization of inflammatory cells
- impairment of phagocytosis by neutrophils & monocytes
—> more likely to get infections
