-
Acute Complications of Diabetes
Diabetic coma; DKA
-
Diabetic ketoacidosis =
Pronounced hyperglycemia with insulin deficiency
-
DKA: lab values
Hyperglycemia > 250 mg/dL or glycosuria 4+ ; Acidosis with blood pH < 7.3; Serum bicarb < 15 mEq/L; Serum positive for ketones
-
Screening for Chronic Complications of Diabetes
Ocular comps; Nephropathy; Peripheral neuropathy; CVD (Heart dz; PVD)
-
Pronounced hyperglycemia with insulin deficiency =
DKA
-
DM: Ocular Complications
Retinopathy; Cataracts; Glaucoma; pts w/ DM need an annual ophthalmologic exam
-
Diabetic Retinopathy: microaneurysms =
Small blow-out swellings of blood vessels
-
DM Retinopathy: Exudates =
Small leaks of fluid from damaged blood vessels
-
DM Retinopathy: hemorrhages
Small bleeds from damaged blood vessels
-
DM Retinopathy: Blood vessels:
may become blocked, causing reduced blood & oxygen supply to small sections of the retina; New abnml vessels may grow from damaged vessels (AKA proliferative retinopathy); new vessels are delicate & bleed easily
-
Test for DM Nephropathy:
urine microalbumin
-
Urine microalbumin: more sensitive than:
dipstick protein
-
Urine microalbumin: May use:
albumin:creatinine (A:C) ratio
-
Urine microalbumin: Correlates with:
nocturnal systolic blood pressure
-
Treatment of renal failure due to DM:
renal transplant more promising than dialysis (if patient eligible)
-
Most common complication of DM:
Neuropathy
-
Characterize DM Neuropathy
Distal symmetrical polyneuropathy with loss of motor & sensory function, esp. of long nerves
-
DM Neuropathy clinical features
Painful diabetic neuropathy with hypersensitivity to light touch; Diabetic gastroparesis; Erectile dysfunction
-
Diabetic Foot Ulcer
Painless due to peripheral neuropathy; pt unaware unless vigilant with & able to do self exams; Prone to infection & enlargement
-
Test for Diabetic Foot Ulcer with:
10g monofilament test ; Comprehensive foot exam
-
Screening for Complications of Diabetes: Eye
Funduscopic exam by optometrist or ophthalmologist for retinopathy
-
Diabetes Screening: USPSTF Guidelines (2008)
No need to screen asymptomatic adults with BP ≤135/80; Should screen adults with HTN (sustained BP >135/80)
-
T1DM ID’d by:
sero autoimmune markers of pancreatic islet dysfn and genetic markers
-
Major Metabolic Defects in T2DM
Peripheral insulin resistance in mx & fat; Decreased pancreatic insulin secretion; Increased hepatic glucose output
-
DM risk factors
FH; Age > 45; High-risk ethnic pop; Habitual physical inactivity; Meds (transplant, HIV, anti-psychotics); Obesity
-
Obesity & DM
fat cells = endocrine organs
-
Glycemic recommendations for non-PG adults w/ DM
A1C <7.0%; Preprandial capillary plasma glucose 70–130 mg/dL; Peak postprandial cap plasma glu <180 mg/dL; More or less stringent glycemic goals may be appropriate for individual patients.
-
HbA1c & DM dx
Dx s/b made if A1c <6.5; s/b confirmed w/ repeat test; not nec for sx pt w/plasma glu ≥200 mg/dL
-
Pts with A1c below DM threshold but ≥6.0 should:
receive demonstrably effective preventive interventions
-
DM clinical features
Polyuria; Polydipsia; Wt loss; Fatigue; Sometimes blurred vision; Susceptibility to infxn; May be asymptomatic, esp Type 2
-
DM: Polyuria occurs when:
serum glu >180 mg/dL (exceeds renal threshold for glu, which leads to increased urinary glu excretion)
-
DM: Glycosuria causes:
osmotic diuresis (ie, polyuria) and hypovolemia
-
DM: Polydipsia is due to:
enhanced thirst because of increased serum osmolality from hyperglycemia & hypovolemia
-
DM: Wt loss is a result of:
hypovolemia and increased catabolism
-
DM & wt loss
Insulin def in DM kids impairs glucose utilization in sk mx & increases fat / mx breakdown; initially, appetite is incd; over time, kids may become anorexic, contributing to wt loss
-
DM: Wt loss: Less common in:
Type 2 DM
-
Acute life threatening complications of DM:
DKA; Nonketotic hyperosmolar syndrome (high blood viscosity; pts w/this syndrome usu have extremely high blood glucose)
-
DM: Acute life threatening comps: incidence:
DKA ( 4.6-8 episodes per 1000 pts w/ DM); hyperglycemic hyperosmolar syndrome (HHS: < 1% of all primary DM admissions)
-
DKA: economics
DKA tx = 1 in 4 healthcare dollars for direct spend on T1DM pts; 100k hosps / yr for DKA; $13,000 / DKA pt; >1B dollars / yr
-
DKA: Dx
Hyperglycemia; Ketonemia; Acidemia
-
DKA: Presentation
“the worse I ever felt”; N/V; Weak; Lethargy; Fruity Breath; Abd Pain; Hyperventilation
-
Ketones: Why
Insulin def: Inc lipase activity increases breakdown of TGs to glycerol & free fatty acids (= precursors to ketone bodies)
-
DKA mgmt
continuous insulin drip (monitor) (MOST IMPORTANT); Fluids; Potassium; EKG;
-
T2DM PE findings
Acanthosis nigricans, skin tags
-
T2DM PE findings: PCOS
PCOS (polycystic ovarian syndrome): hirsutism
-
Major cause of mortality for DM pts:
CVD
-
Diabetic nephropathy: incidence
occurs in 20–40% of DM pts
-
Leading cause of ESRD:
Diabetic nephropathy
-
DM retinopathy: prevalence strongly related to:
the duration of diabetes
-
Most common cause of new blindness in pts 20–74 yo:
Diabetic retinopathy
-
DM neuropathy: tx
Specific tx for underlying nerve damage: not available; only improved glycemic ctrl (may slow progression but rarely reverses neuronal loss)
-
DM lifestyle mods: Months 1–6:
16 individual sessions with a registered dietitian (RD)
-
DM lifestyle mods: Months 7–36:
Minimum of 1 session every other month with RD; additional support as needed
-
DM lifestyle mods: Focus of sessions
Review food & activity records; Problem-solve difficulties; Praise participant's effort
-
Modest wt loss & DM
modest wt loss reduces incidence of new-onset DM in at-risk popn
-
DM & ABCs of CHD prevention: A =
Aspirin; ACEI; A1C control
-
DM & ABCs of CHD prevention: B =
Beta-blockade; BP control
-
DM & ABCs of CHD prevention: C =
Chol mgmt
-
DM & ABCs of CHD prevention: D =
Diet; do not smoke; decrease DM risk
-
DM & ABCs of CHD prevention: E =
Exercise
-
Glycemic control promotes:
WBC function & facilitates wound healing;
-
When to Start Insulin Tx for T1DM
multi dose insulin injxns (3–4 / day of basal & prandial insulin) or CSII tx ; matching prandial insulin to CHO intake, pre-meal blood glu, & anticipated activity; for many pts (esp if hypoglycemia is problem), use of insulin analogs
-
When to Start Insulin: T2DM: Insulin can:
(when used in adequate doses) decrease any level of elevated A1C to, or close to, the therapeutic goal
-
When to Start Insulin: T2DM: insulin max dose
Unlike other blood glucose–lowering medx, there is no max dose of insulin beyond which a tx effect will not occur
-
When to Start Insulin: T2DM: Large insulin doses
Relatively lg doses of insulin (1 unit/kg), cf w/ those required to tx T1DM, may be necessary to overcome the insulin resistance of T2DM and lower A1C to the target level
-
Rapid acting insulin:
Lispro; Aspart; Glulisine
-
Short acting insulin:
Regular
-
Intermediate acting insulin:
NPH
-
Basal insulin:
Glargine (Lantus); Detemir (Levemir)
-
Premixed insulin:
70/30 regular; 70/30 aspart; 75/25 lispro; 50/50
-
Action: Lispro, Aspart
Onset of Action 5-15 min; Peak 30-90 min; Duration of Action 4-6 h
-
Glulisine
Onset of Action 5-15 min; Peak 30-90 min; Duration of Action 6-8 h
-
Action: Regular
Onset of Action 30-60 min; Peak 2-4 h; Duration of Action 6-10 h
-
Action: NPH
Onset of Action 1-2 h; Peak 4-8 h; Duration of Action 10-20 h
-
Action: Glargine
Onset of Action 1-2 h; Peak: None; Duration of Action 24 h
-
Action: Detemir
Onset of Action 1-2 h; Peak 6-8 h; Duration of Action 12-24 h
-
Fx on insulin absorption: Exercise
Strenuous use of injected limb within one hour
-
Fx on insulin absorption: Massage of area
Do not rub site vigorously
-
Fx on insulin absorption: Temperature
Heat increases, cold decreases
-
Fx on insulin absorption: Site of Injection
Abdomen>arms>thigh (R & N only)
-
Fx on insulin absorption: Lipohypertrophy
Delays absorption
-
Fx on insulin absorption: Large doses (>80 units)
Delay onset and duration
-
Factors affecting insulin absorption in hospitalized pt
Severity of illness; Meds (g’corticoids, pressors); Diet: different, unpredictable; Type of diabetes; Previous glycemic ctrl; Setting: ICU vs ward
-
Fx on insulin absorption: Jet injectors
Increase absorption rate
-
Fx on insulin absorption: Certain insulin mixtures
Lente causes loss of rapid acting insulin action
-
Fx on insulin absorption: Large doses (>80 units)
Delay onset and duration
-
Fx on insulin absorption: Suspension form
Proper resuspension needed
-
MOA: Alpha-glucosidase inhibitors
decrease glucose absorption in intestines
-
MOA: Biguanides
Decrease hepatic glucose output; increase glucose uptake
-
MOA: TZDs
Mx & adipose tissue: decrease insulin resistance; increase glucose uptake
-
MOA: Sulfonylurea & Repaglinide
Pancreas: increase insulin secretion
-
GLP-1 is secreted from:
L-cells of the jejunum & ileum
-
GLP-1
stimulates glucose-dependent insulin secretion; suppresses glucagon secretion; slows gastric emptying; leads to reduction in food intake; increases insulin sensitivity
-
GLP-1: LT fx in animal models:
increase in beta cell mass; improved beta fn
-
Contraindications to continuing certain oral DM agents
Worsened hepatic fn; advanced CHF
-
Oral DM agents: If creatinine >1.5 (1.4):
stop metformin
-
Oral DM agents: Contrast dye load / cardiac catheterization:
hold metformin
-
Use of sliding scale insulin:
should NOT be used as monotherapy
-
Target/recommendations: HbA1c
target <7.0; <6.0 if poss w/o inducing hypoglycemia
-
Target/recommendations: BP
<130/80 (ACEI / ARB)
-
Target/recommendations: Lipids
LDL <100 (<70 optimal); HDL >40 M, >50 F; TG <150; statin for CV hx or >40 yo to lower LDL 30-40%
-
Target/recommendations: ASA
>40 yo or other risk factors; all w/ CV hx
-
Target/recommendations: ACEI
> 55 yo w/ other CV risk factor
-
Potential for hypoglycemia is increased in:
Acute illness; Erratic food intake; Poor coordination of insulin dosing with meals
-
Hypoglycemia Tx: D50
IV Dextrose (D50) Admin = most rapid method of alleviating hypoglycemia; appropriate for pts who are unconscious, severely symptomatic, or NPO
-
Hypoglycemia Tx: pts who are alert and able to eat should:
be given 15 gm CHO in a rapidly available form (ie, ½ cup of fruit juice, 4 oz nondiet soda, or 3 glucose tablets)
-
Hypoglycemia Tx: A common error:
to over-treat hypoglycemia with an excess of carbohydrate (this, plus counter-reg hormone response to hypoglycemia, facilitates subsequent hyperglycemia)
-
Troubleshooting low blood sugars
N/V (consider checking BG before meal & rapid insulin just after, if N/V consistent prob); sepsis? Renal/Liver prob? Too much insulin? Other endocrine prob (hypothyroid/ adrenal)
-
Troubleshooting high blood sugars
First find underlying cause (insufficient insulin dosing OR other)
-
high blood sugars: causes other than insuff insulin dose
Infxn; Dehydration; Cardiac; hormones (ie epinephrine); Stress / Surgery; Rebound from a prior episode of HYPOglycemia ; Medications (ie, steroids)
-
Metabolic syndrome (insulin resistance syn): Dx:
3 of 5: Waist circum >40 (M) / >35 (F); TG ≥150; HDL <40 (M) / <50 (F); BP ≥ 130/85; FPG ≥110
-
Metabolic syndrome: other major dx criteria
acanthosis nigricans, estd T2DM, central obesity
-
Metabolic syndrome: minor dx criteria
hypercoagulability , PCOS, vascular endothelial dysfunction, CAD, microalbuminuria
-
-
-
Levothyroxine
Synthroid, Unithroid, Levoxyl, Levothroid
-
-
Class: Liothyronine
Hypothyroid Agent
-
Class: Liotrix
Hypothyroid Agent
-
Class: Levothyroxine
Hypothyroid Agent
-
Class: Methimazole
Hyperthyroid Agent
-
Class: Propylthiouracil (PTU)
Hyperthyroid Agent
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
Class: Insulin Lispro
Rapid acting insulin
-
Class: Insulin Aspart
Rapid acting insulin
-
Class: Insulin Glulisine
Rapid acting insulin
-
Class: Insulin Glargine
Long acting insulin
-
Class: Insulin Detemir
Long acting insulin
-
Class: Glyburide
Sulfonylurea
-
Class: Glipizide
Sulfonylurea
-
Class: Glimepiride
Sulfonylurea
-
Class: Repaglinide
Meglitinide
-
Class: Nateglinide
Meglitinide
-
Class: Metformin
Biguanide
-
Class: Rosiglitazone
Thiazolidinedione
-
Class: Pioglitazone
Thiazolidinedione
-
Class: Acarbose
Alpha-glucosidase Inhibitor
-
Class: Miglitol
Alpha-glucosidase Inhibitor
-
Class: Sitagliptin
DPP-4 inhibitor
-
Class: Saxagliptin
DPP-4 inhibitor
-
Class: Exenatide
Incretin mimetic GLP-1 agonist
-
Class: Liraglutide
Incretin mimetic GLP-1 agonist
-
Class: Pramlintide
Amylin analog
|
|