Diabetes Flashcards
FML
Pancreas Components
exocrine (80) acini glands
endocrine (20) islets of langerhans
Islets of Langerhans components/secretions
alpha cells: glucagon
beta cells: insulin
delta cells: somastatin
f cells: pancreatic polypeptide
Insulin primary FX
synthesis of glycogen/protein in liver/muscle
suppression of gluconeogenesis/glycogenlysis/lipolysis
glycolysis/glucose transport
Insulin Release Process
BG increases –> insulin released –> BG lowers
Glucagon Release Process
BG decreases –> glucagon released –> BG raises
Endocrine Hormones Fueling Metabolism
Glucagon cortisol growth hormone epinephrine norepinephrine
Post-absorptive (fasting) State
provides glucose for brain/nervous tissue
higher ratio of glucagon to insulin
hepatic glycogenolysis/gluconeogenesis
muscle oxidizes ffa
Absorptive State
insulin levels rise
stimulates glucose uptake into tissues
excess glucose stored as glycogen
Starvation State
glucagon levels elevated
hepatic gluconeogenesis
brain oxidizes ketones for energy
Type 1 Diabetes DKA
increased mobilization of free fatty acids –> increased hepatic synthesis of ketones
diabetic ketoacidosis
Type 2 Diabetes DKA
ketone bodies not sufficient for DKA
Type 2 Diabetes
can’t produce/respond to insulin
can’t use energy in food as well
Type 1 Diabetes
lack of insulin secretion (total or partial)
auto-immune (pancreatic beta cells destroyed)
no oral meds
Hyperglycemia acute symptoms
increased thirst/urination
weight loss
Monogenic DM
neonatal diabetes
maturity-onset diabetes of oung
Gestation DM onset/TX
during pregnancy
dietary TX, oral meds, exogenous insulin
hyperglycemia can lead to fetal/maternal complications
Prediabetes DX
impaired fasting glucose (100-125)
impaired glucose intolerance (144-199)
increased hemoglobine
Diabetes (nonpregnant) DX
Hemoglobin >6.5% increase
random serum glucose >200
FAsting serum glucose >126
Most common Type 1 DM
T-cell mediated autoimmune against beta cells
Type 1 DM etiology
childhood disease
genetic predisposition
viruses
cow’s milk proteins
Type 1 DM pathogeneisis
environmental triggers immune response
autobodies develop (honeymoon period)
insulin production ceases
Type 1 DM s/s
hyperglycemia (fasting BG >126 x2) polyuria polyphagia (hunger) polydipsia glucosuria weight loss fatigue n/v
Insulin aspart
onset/peak/lasts/admin
rapid acting
(15 min onset) (1-3 hr peak) (lasts 3-5 hrs)
SQ 5-10 min AC
must eat within onset
Insulin regular
onset/peak/lasts/admin
short-acting
(30-60 min onset)(2-5 hr peak)(lasts 5-8 hr)
SQ 30-60 min AC
Iv for DKA (only IVP)
Insulin isophane (NPH) onset/peak/lasts/admin
intermediate acting
(onset 1-2 hr)(peak 4-12 hrs)(lasts 12-18 h)
SQ 30 min before 1st/last meals
NEVER IVP
insulin detemir
onset/lasts/admin
long-acting
gradual onset over 24 hr (lasts 24 hrs)
SQ HS
Insulin glargine
onset/lasts
long acting
gradual over 24 begining at 1 H
lasts 24 hrs
Use of combination insulin
long-acting+short-acting
use body’s natural levels to enhance control
should not cause hypoglycemia
Insulin that can’t be mixed
glargine
Hyperglycemia Med Induced
corticosteroids
NSAIDS
diuretics
Hyperglycemia ICU PT Targets
140-180
Hyperglycemia non-ICU PT Targets
<140 fasting
<180 random
Metabolic Syndrome
adipose tissue is an endocrine organ that produces hormones insulin resistance ab obesity increased LDL/BP/artery disease Waste circumference >35/40 Lifestyle changes
Type 2 DM insulin resistance physiology
unresponsive to insulin (b/c of receptors) –> blood glucose ^ –> pancrease secretes more insulin (hypersecretion) = beta cell exhaustion/death
Type 2 DM TX
lifestyle change antidiabetic drugs (lower BG) insulin
Type 2 TX goals
pre-prandial BG <110
HBA1C <6.5
Biguanides action/pro
decreases hepatic production of glucose/reduces insulin resistance
does not cause hypoglycemia
1st line med
METFORMIN
Biguanides Side effects
minor, GI-related
lactic acidosis
increased risk for renal disease/liver disease/severe infection/shoc/hypoxemia
Sulfonylureas MOA/ex/SE
glyburide/glipizide/glimepiride
stimulate release of insulin from pancreatic islet cells/increase receptors
hypoglycemia
Alpha-Glucosidase Inhibitors (ex/MoA/SE)
ACARBOSE/MIGLITOL
block enzymes in small intestines from breaking down CHO (delayed digestion)
GI SE most common
No hypoglycemia (unless w/ Insulin/sulfonylurea)
Meglitinides (ex/MoA/Duration/SE/Cont)
NATEGLINIDE/REPAGLINIDE) stimulates insulin from pancreatic islet cells short duration (2-4 hrs) well-tolerated hypoglycemia hepatic/renal disease
Thiazolidinediones (ex/MoA/optimal BG)
PIOGLITAZONE, ROSIGLITAZONE
decrease insulin resistance/inhibit hepatic gluconeogenesis
3-4 months
Thiazolidineiones SE/Contra
Fluid Retention/headache/weight gain
CHF, pulmonary edema, bladder cancer
NO hypoglycemia
Incretin Enhancers (MoA)
mimic hormones released in response to food (signal insulin secretion/stop glucagon production)
reduce food intake (feeling of fullness)
protect beta cells from injury
Incretin Enhancers (agonists/inhibitors)
(-glutides, -enatide)
-gliptins
Hypoglycemia Medical Emergency Levels
<60
Hypoglycemia s/s
hunger, sweating, palpitations, tremors, anxious, difficulty speaking, visual disturbances, atypical behavior, confusion, ,seizures
Hypoglycemia TX
glucose fast-acting simple CHO (juice,) glucagon (to convert glycogen to glucose) (5% Dextrose) (50% Dextrose if unconscious)
Somogyi Phenomenon
Hypoglycemia @ night (undetected)
Hyperglycemia in the morning
Somogyi Phenomenon s/s
night sweats, headaches, nightmares
Somogyi Phenomenon DX
BG 0200, 0200, 0600
Somogyi PHenomenon TX
complex carbs @ bedtime
may need to change insulin
Dawn Phenomenon and DX
Hyperglycemia in AM
Most common in Adolescents/YA
Testing @ HS, 0200, 0400, fasting
Dawn Phenomenon TX
based on testing if below 60 = reduce insulin
if above 120 increase insulin
snack @ bedtime
DKA patho
can be first sign of DM
absolute/relative insulin deficiency (most common with Type1)
not enough insulin = hyperglycemia = polyuruia, polydipsia, polyphagia = acidosis (fat breakdown)
DKA causes
infection skipping insulin new onset T1DM surgery trauma pregnancy
DKA TX
supportive, IV insulin, IV fluids, IV electrolyte replacements
DKA progression
hyperglycemia > dehydration > hemoconcentration > peripheral circulation failure > shock > hypotension > anuria > coma/death
Hyperglycemia Hyperosmolar Syndrome Patho
severe hperglycemia and coma
DKA - ketosis/acidosis/Kussmaul’s breathing
just enough insulin
Hyperglycemia Hyperosmolar Syndrome Etiology
T2 DM
excessive unreplaced fluid losses w/hyperglycemia
Hyperglycemia Hyperosmolar Syndrome s/s
r/t hyperglycemia, dehydration, hyperosmolality
neuro
vascular thromobosis
Hyperglycemic Hyperosmolar Syndrome DX
glucose >600 osmolality >320 profound dehydration alteration in consciousness Bicarbonate >18 pH >7.3
Hyperglycemic Hyperosmolar Syndrome TX
Support
IV Insulin
IV Fluids
IV Electrolytes
DKA DX
usually younger
BG >250
Serum Ketones
Bicarbonate <18
Diabetic Neuropathy Pathogenesis
incrreased polyol pathway –> NA retention > edema > myelin swelling > nerve degneration
Diabetic Neuropathy s/s
GI disturbances Nerve disturbances diarrhea neurogenic bladder impotence distal polyneuropathy
Diabetic Neuropathy TX
depends
Gabapentin can help
