Diabetes Flashcards
Diabetes Mellitus
In metabolic disease resulting from the breakdown in the ability of the body to either produce and or utilize insulin, resulting in inappropriate hyperglycemia
DM1
Pathology
Strongly associated with the presence of human leukocyte antigens (HLA-DR3 or HLA-DR4; antibodies against **glutamic acid decarboxylase are found in 80% patients with type 1)
Islet cell antibodies
** Ketone development usually occurs
Believed to be the result of an infectious or toxic environmental insult to pancreatic B cells genetically predisposed persons
DM1 signs and symptoms
Polyuria Polydipsia Polyphagia Nocturnal enuresis Weight loss Weakness
Lab diagnostics for DM 1 and 2
** Serum fasting BG >= 126 on more than one occasion
Random plasma BG >= 200 with signs of hyperglycemia
Plasma glucose >= 200 measured two hours after a glucose load
A1C >=6.5%
DM1 Managment
Analyze baseline studies
Optimal insulin regimen: basal insulin + mealtime blouses of rapid acting or short acting insulin
Somogyi Effect
Nocturnal hypoglycemia develop stimulating a surge of counter regulatory hormones which raise blood sugar. Note that the patient is hypoglycemic at 3 AM but rebounds with an elevated blood glucose at 7 AM
Tx: Reduce or omit the at bedtime dose of insulin
Dawn Phenomenon
Results when the tissue becomes desensitized to insulin nocturnally. Note that the blood glucose become progressively elevated throughout the night resulting in elevated glucose levels at 7 AM
Tx: add or increase the bedtime dose of insulin
DM2 Pathology
Circulating insulin exists enough to prevent ketoacidosis but is inadequate to meet the patient’s insulin needs
Is caused by either tissue in sensitivity to insulin or an insulin secretory defect resulting in resistance and or impaired insulin production
Associated with obesity and syndrome X
Syndrome X
Obesity
HTN
Abnormal lipid panel ( low HDL, High Triglycerides)
Metabolic Syndrome
Waist Circumference: Men >= 40, Women >= 35 inches BP>= 130/85 Triglycerides >= 150 FBG >= 100 HDL: men < 40 women <50
DM2 signs and symptoms
Insidious onset Polyuria Polydipsia Recurrent vaginitis Peripheral neuropathies Blurred vision Chronic skin infections
DM2 Management
Obtain baseline data
Therapy should begin with weight control for obese patients
Dietary treatment with guidelines
Exercise
Common drugs:
Metformin “starter”
Metformin
Lowers basal and posprandial glucose levels by affective glucose absorption and hepatic gluconeogenesis
May cause weight loss and refuses LDLs;
Black box warning: may cause lactic acidosis “muscle pain”
Trulicity
Mimic endogenous incretin glucagon-like-peptide (GLP-1); stimulate glucose dependent insulin release, reduce glucagon, and slow gastric emptying
Use with metformin may cause modest weight loss
Exenatide
Stabilizes both fasting plasma glucose and A1C in patients with fewer GI side effects; administered SQ inj
Liraglutide
dosed once a day without regard to meals
Dulaglutide and semaglutide
Dosed once weekly
All drugs may causes GI disturbances and slight risk for pancreatitis
DKA Pathology
A state of intracellular dehydration as a result of elevated blood glucose levels
Often, it is an acute complication of type one diabetes
Maybe the presenting sign of diabetes
DKA Signs and Symptoms
Polyuria Polydipsia Weakness N/V Kussmaul’s breathing LOC Fruity breath Orthostatic hypotension with Tachycardia Poor skin turgor
DKA Lab and Diagnostics
Hyperglycemia >250 *** Ketonemia and/or ketonuria Marked Glysuria Acidosis pH <7.30 Low bicarbonate Elevated HCT, BUN/Creatinine Hyperkalemia Leukocytosis Hyper osmolality
Osmarilarity formula
2[Na + K +glucose /18]
DKA Management
Protect airway
Administer O2
Isotonic fluids NS at least 1L in the first hour; Then 500ml/hr. If glucose > 500, use 1/2 NS after first hour (as water deficit exceeds sodium loss). When glucose falls <250 change to D51/2NS
0.1units/kg insulin IV bolus follow by 0.1 U/kg/hr. If glucose does not fall by at least 10% after the first hour, repeat bolus
Correct acidosis with bicarbonate gtt if <7.1
Do not treat initial hyperkalemia
Hourly urinary output monitoring
Supportive care
HHNK Pathology
State of greatly elevated serum glucose, hyperosmolality, and severe intracellular dehydration without ketone production
Usually occurs as a complication of type two diabetes
Patients cannot produce enough insulin to prevent severe hyperglycemia, osmotic diuresis an extra cellular fluid depletion
Mortality rate 30-50%
HHNK Signs and Symptoms
Polyuria Weakness Changes in LOC Hypotension Tachycardia Poor skin turgor Other signs of dehydration
HHNK Labs and Diagnostics
Greatly elevated serum glucose >= 600 commonly >1000
Hyper osmolality >310
Elevated BUN/Cr
Elevated A1C
Relatively normal pH
Normal anion gap
HHNK Management
Protect airway
Administer O2
Isotonic fluids at least 1 L in the first hour; then 500 mL per hour. If glucose greater than 500 use half normal sailing after first hour. When glucose levels fall less than 250 change to D5 half normal saline to prevent hypoglycemia
0.1U/kg bolus followed by 0.1u/kg/hr if glucose does not fall by at least 10% in the first hour repeat bolus
