Clinical Diabetes Flashcards
What is the diagnostic criteria for diabetes in terms of:
Fasting Blood Glucose (or FBS-fasting blood sugar)
Symptoms with Random Blood sugar
HbA1c
2hr. oral glucose tolerance test
FBS: greater than 126mg/dL on 2 occasions
or
Diabetes symptoms with random blood sugar over 200mg/dL
or
HbA1c greater than 6.5%
or
2 hour oral glucose tolerance test greater than 200mg/dL
What is impaired fasting glucose?
Range between normal fasting glucose (less than 100mg/dL) and diagnosed DM (greater than 126mg/dL)
Name the 3 types of insulin treatment for Type 1 DM.
Short Acting: Lispro
Intermediate: NPH
Long Acting: Glargine
What is the honeymoon phase of Type 1 DM?
Patient usually presents with emergent diabetic ketoacidosis (DKA). Upon insulin therapy they magically regain the ability to secrete their own insulin. Lasts only a few weeks and they still require moderate exogenous insulin therapy
What is the Dawn Phenomenon?
Early morning diurnal hormones (GH, cortisol, catecholamines) cause the liver to release glucose. In Type 1 DM the lack of insulin leads to hyperglycemia
What is the Somogyi Effect?
Night time hypoglycemia causes a nocturnal glucose release by the liver
Hallmark of Type 2 DM.
Insulin Resistance
Best initial treatment for Type 2 DM.
Weight loss, diet, exercise
Name the 3 sulfonylurea drugs.
Glyburide
Glipizide
Glimeperide
Name the two Meglitinides and when they are taken.
Repaglinide
Nateglinide
Taken only pre-prandial
Biggest side effects of Metformine.
Lactic Acidosis, diarrhea, abdominal discomfort
MOA of alpha glucosidase inhibitors.
Slows carbohydrate uptake by the GI tract.
-leads to excessive flatulence leading to poor compliance
Name the 2 Alpha Glucosidase Inhibitors
- Acarbose
2. Miglitol
Name the 2 Thiazolidinediones.
- Rosiglitazone
2. Pioglitazone
Effect of Thiazolidinediones in Type 2 DM.
Insulin sensitization
Decrease TGs
Increases HDL and LDL
Name the two Incretin Mimetics and the MOA.
Exenatide
Liraglutide
MOA: GLP-1 analog that mimics endogenous insulin
What are the goals for DM treatment regarding
FBS
HS
HbA1c
FBS: 80-120mg/dL
HS: 100-140 mg/dL
HbA1c: less than 7%
What are the microvascular and macrovascular complications of DM 1 and 2?
Micro: retinopathy, neuropathy, nephropathy
Macro: coronary artery disease, peripheral vascular disease, stroke
Treatment of orthostasis seen in DM.
Midodrine
Main two sequelae from Peripheral Sensory neuropathy caused by DM.
Foot Ulcers
Carcot Deformity
(check feet every visit)
Tx for gastroparesis caused by DM.
Erythromycin
Best two targets for treatment of Nephropathy in DM.
Glycemic Control: lifestyle changes
HTN control: ACE-Is and ARBs
What are the targets to reduce risk of CAD in DM patients and the respective goal levels?
Total Cholesterol: less than 200 LDL: less than 100 HDL: greater than 60 TGs: less than 150 BP less than 120/80
What 4 things should be included in every check up in a patient w/ DM?
- Eye exam
- Foot Exam
- Lipid Panel
- Microalbumin
Flu Vaccine annually
Describe how to diagnose Gestational DM.
Oral Glucose Tolerance Test (OGTT)
Administration of 100g of Glucose
If two are (+) then positive diagnosis
- Fasting Glucose greater than 95 mg/dL
- 1hr post prandial greater than 180mg/dL
- 2hr post prandial greater than 155
- 3hr post prandial greater than 140
Tx for GDM.
Insulin Therapy
Sulfonylureas
Metformin
Pathology of MODY.
Impaired glucokinase function in pancreatic beta cells. Inability to trap glucose.
(other mutations do occur but this is most common)
Major fuel source leading to diabetic ketoacidosis (DKA).
Fatty Acids (FA)
What is the biochemical definition of DKA?
Blood Sugar: greater than 250
pH: less than 7.3
Bicarb: less than 18
Ketonuria or ketonemia
Name the major Ketone Bodies that accumulate and the one that exacerbates nausea and vomiting.
Acetone
Acetoacetic Acid
Beta-hydroxyl butyric acid (N/V)
Body’s attempt to correct the metabolic acidosis of DKA.
Kussmaul Breathing
Describe the general mechanism of DKA.
- Lack of insulin causes accumulation of glucose in blood
- Counter regulator hormones think the body is starving and influence the liver to make more glucose and induce lipolysis.
- Ketones are made from the fat and used as energy causing acidosis
- Glucose is filtered by the kidneys and they use water to remove the excess glucose causing dehydration
Main cause of DKA.
It is the first presentation of undiagnosed diabetes patients
Primary infectious organism that causes DKA.
Klebsiella pneumonia
Biggest component of DKA treatment.
Fluid replacement
isotonic saline
Describe Hyperosmolar Nonketotic State.
State of hyperglycemia (greater than 600) with no rise in ketone bodies.
Altered mental status, dehydration, basic pH
More common in Type 2 DM, often preceded by some illness (MI, CVA, infection)
Tx for Hyperosmolar Nonketotic State.
Fluid replacement
Correct hyperglycemia with insulin
Treat the underlying cause
What is Whipple’s Triad
Seen in hypoglycemia
- Documented low blood sugar
- signs and symptoms of hypoglycemia
- Reversal of symptoms with glucose administration
