Diabetes Flashcards
Insulin
Stimulates synthesis of glycogen and helps glucose enter the cells of striated muscle and adipose tissue
Promotes protein synthesis and helps the body store fat by preventing its breakdown for energy.
Beta Cells in Pancreas
secrete 0.2-0.5 units/kg/day of insulin ex- someone weighing 150lbs will secrete on an average of 15-35 units per day
Lipodystrophy
when the body can’t maintain fat tissue and
why a diabetic should change injection sites
Rapid acting Insulin
-Names of Drugs: Aspart, Glulisine, Lispro, Inhaled
-Fast acting: 5-15mins
-Peak: 45-75 mins
-Duration: 2-4 hours
-Deadliest insulin
-Always monitor for hypoglycemia
Short acting Insulin
(regular)
given 30 mins before meals
Short Acting: 30-60min
Peak: 2-4 hours
Duration: 5-8 hours
If Regular insulin (clear) is mixed with NPH human insulin (cloudy), the Regular insulin should be drawn into the syringe first.
Intermediate-Acting Insulin
or NPH (neutral Protamine Hagedorn)
-also called ‘isophane’
-2X daily 70/30 mixture pen
room temp for 10 days
Acting: 1-2hours
Peak: 4-12
Duration: 18-24 hours
(Provide basal insulin overnight)
Long actin insulin
Onset - 2 hours
Peak-3-9 or none
Duration- 24 hours
Types: Glargine & Determir
-even absorption no peaks or valleys
-used in both Type 1 and 2 (common in 2)
Doses of Insulin
0.6-0.8ukg/day
2/3-AM and1/3-PM
-Start with 1 unit of insulin per 15 grams carbs, adjust while checking glucose levels
Keytones
Caused by high glucose
Altered process of aerobic and anaerobic metabolism
Breakdown of fat into free fatty acids and glycerol; for energy.
Converted into ketones by the liver
Are strong acids that accumulate in the blood and can lead to metabolic acidosis
Gluconeogenesis occurs instead of Krebs or citric acid cycle
Hypoglycemia
Blood glucose > 60
Symptoms: Sweating, clammy, confused, hungry, lightheaded, dizzy, blurred vision, seizures, coma
Common causes: Excessive exercise, alcohol, poor food intake, too much insulin, stress, surgery, and medications.
Epinephrine and Glucagon are released causing activation of the SNS which is responsible for most of the signs and symptoms
As hypoglycemia continues, epinephrine and glucagon promote glycogenolysis and gluconeogenesis in the liver
“I’m sweaty, cold, clammy, give me some candy”
Atherosclerotic
Glucose sticks to proteins in blood vessel’s making them hard and form plaque.
Leads to heart disease, stroke, hypertension, infections, poor eye sight
Diabetic ketoacidosis
(DKA)
Is a hyperglycemic emergency
-burning of ketones for energy (diabetes type 1)
- leads to acid in blood
Characterized by: Metabolic acidosis, dehydration, and electrolyte loss
Diagnosis:
Serum glucose >250mg/dl
Ketonemia and urine
Low pH
Low HCO3
Three main causes of DKA
-Infection or illness
-Lack of Insulin
-Undiagnosed or undertreated diabetes
Symptoms: thirsty, rapid breathing (getting rid of extra co2), fruity breath
Hyperglycemia hyperosmolar nonketotic syndrome
HHNS
Increase blood sugar without burning ketones. (Type 2 diabetes)
Symptoms: dehydration, thirsty, high BS, mental status changes
3 ps
Polyuria- increase urination
Polyphagia- increase in appetite
Polydipsia-increase in thirst
Clinical Manifestations of DKA
Presenting Symptoms:
The 3 P’s and weight loss
Abdominal pain
Severe nausea and vomiting, and fatigue
Extreme Dehydration
Poor skin turgor
Dry mucous membranes
Tachycardia
Hypotension
Acetone breath,
Kussmaul respirations (similar to hyperventilation) respirations
Changes in Level of consciousness
Treatment for DKA
Fluid replacement first!
-To restore intravascular volume
-To clear ketones
-To correct electrolyte imbalances
Insulin – regular-considered short acting
Need to monitor for cerebral edema as fluid shifts back to the cells
Hyponatremia and Hyperkalemia are most common electrolyte issues
Morning Hyperglycemia
(Dawn Phenomenon)
Increase in fasting blood glucose and/or insulin requirements during the early morning hours
Occurs naturally in everyone
Is the result of circadian variations in hormone secretion
Somogyi Effect
Nocturnal hypoglycemia followed by rebound hyperglycemia.
The hypoglycemia triggers the release of counter-regulatory hormones: releasing glycogen from the liver; epinephrine, cortisol and growth hormone
Occurs due to too much or too little insulin at bedtime or skipped nighttime snack
Treat by decreasing insulin dose or changing time of adm
Type 1
Autoimmune
Types:
Type 1A (90-95%)
Type B (idiopathic,no autoimmune)
Requires exogenous insulin to stop the catabolic process, lower the BS and prevent ketosis.
Has circulating autoantibodies (humoral immunity) to islet cells of the pancreas, insulin and other enzymes needed for insulin production
Macrophage & lymphocytic infiltration of the beta cells leads to cytokine production and ultimate apoptosis of the beta cells
Ketosis: When there is no insulin, no lipolysis, body uses Fat For Atp for energy
Other Blood Tests for Type 1
C-peptide
-Detects natural insulin secretion, C-peptide released when pancreas able to secrete insulin
Islet Cell Autoantibodies (ICA)
-Often detected in those with Type 1 DM
Insulin Autoantibodies (IAA)
-Looks for the antibodies targeting insulin.
Insulinoma-Associated-2 Autoantibodies (IA-2A)
-Looks for antibodies mounted against a specific enzyme in beta cells. Both the IA-2A and GADA tests are common T1D antibody tests.
Zinc Transporter 8 (ZnT8Ab)
-Looks at antibodies targeting an enzyme that is specific to beta cells.
Glutamic Acid Decarboxylase Autoantibodies (GADA or Anti-GAD)
-Looks for antibodies built against a specific enzyme in the insulin-producing pancreatic beta cells.
C-peptide Test
Detects natural insulin secretion, C-peptide released when pancreas able to secrete insulin
Islet Cell Autoantibodies (ICA) Test
Often detected in those with Type 1 DM
Insulin Autoantibodies (IAA) Test
Looks for the antibodies targeting insulin.
Insulinoma-Associated-2 Autoantibodies (IA-2A) Test
Looks for antibodies mounted against a specific enzyme in beta cells. Both the IA-2A and GADA tests are common T1D antibody tests.
Zinc Transporter 8 (ZnT8Ab) Test
Looks at antibodies targeting an enzyme that is specific to beta cells
Glutamic Acid Decarboxylase Autoantibodies (GADA or Anti-GAD)
Looks for antibodies built against a specific enzyme in the insulin-producing pancreatic beta cells.
Glycogenesis
Process of glycogen formation when glucose supplied excess need for ATP synthesis
Glucose is stored in cells to a saturation point for about 12-24 hours.
Stored mainly in the liver and muscle
Reverse process of glycolysis
Genesis=Formation
Glycogenolysis
Breakdown of stored glycogen to make glucose
Process occurs when the glucose levels become too low (i.e. prolonged starvation)
Process occurs in the liver and muscle tissue in response to hormonal and neural signals
-Epinephrine
-Glucagon
-Insulin
Process also inhibits glucogenesis
Gluconeogenesis
Synthesis of glucose by the liver from non-carbohydrate sources
Process primarily occurs in liver
Amino acids (protein) and fats are converted to glucose
From stored fat to fatty acids and/or glycerol
Amino acids to lactic acid
Can lead to the development of ketones
Happens when there is not enough glucose to meet the needs for the body
Also play a role in maintaining acid-base balance
Functions of the Pancreas
Exocrine acini -> digestive juices -> duct -> duodenum
Endocrine Islets of Langerhans -> hormones
-> blood
Beta cells—>Insulin, amylin
Alpha cells—> Glucagon
Delta cells —>Somatostatin (which is a growth hormone)
F/PP cells—> Pancreatic polypeptide
Insulin Hormone
Required by the body cells to initiate active transport of glucose into the cell
-Skeletal cells – store glucose as glycogen
-Adipose tissue – stops release of fatty acids
-Liver – stops gluconeogenesis, starts producing glycogen and fat
Brain does not require insulin for glucose uptake
Insulin stimulates the uptake, use, and storage of glucose
Ancanthosis Nigricans-
signs of insulin resistance:
Darkening and thickness of skin on armpits and neck
Why Does Obesity Cause Insulin Resistance?
Causes increases in adipose and free fatty acids
Induces inflammation and release of the associated inflammatory mediators
Increases stress on pancreatic B cells as insulin is increased
Results in liver increase glucose in the blood (impaired suppression)
Why Does A Sedentary Lifestyle Increase Insulin Resistance?
NO EXERCISE
- have decreased intracellular enzymes such as pyruvic acid
EXERCISE
-Increases mitochondrial enzymes,
-Increases insulin sensitivity
-TG get broken into FFA to use for fuel
-Decrease BS, decrease insulin
-Increase glucagon
-Causes uptake of glucose from circulation
Glycated Hemoglobin A1C
Used to diagnose or monitor diabetes
Glucose does not normally go into the RBC but the membrane is very permeable.
When the glucose level is chronically high, it will move into the RBC.
Once glucose is in the RBC, it can not leave
The HgbA1C measures the amount of glucose over 120 days (3 month period)
Somatic neuropathy
Diminished perception: vibration, pain, temperature
Hypersensitivity: light touch; occasionally severe “burning” pain
Autonomic neuropathy
Defects in vasomotor and cardiac responses
Urinary retention
Impaired motility of the gastrointestinal tract
Sexual dysfunction
Hyperosmolar Hyperglycemic Syndrome (HHS)
Only seen in type 2
Characterized by severe hyperglycemia (>600), hyperosmolality, and dehydration caused by insulin resistance
At same time, the cells are not absorbing glucose
Sets up the same hyperosmolarity as in DKA.
ECF increases and there is intracellular dehydration
Because there is some insulin there is
NO KETONE formation
Causes: Infection, non-compliance with diet or medications, undiagnosed, substance abuse, alcohol, etc.
Symptoms: extreme glucose level, rapid/thread pulse, hypotension, profound dehydration, polydipsia, polyuria, confusion, disorientation, possible seizure, or coma
Treatment:
Hydration (given first)
IV insulin- rehydrate the cells (GIVE before INSULIN)
Electrolyte replacement (Potassium, Intercellular)
Why is it necessary for a person to maintain blood glucose no lower than 70?
To improve insulin secretion
To allow beta cells to have periods of rest
To maintain a continuous supply of glucose for energy
To avoid too much glucagon from being broken down in the liver
Glucagon
Hormone secreted by alpha cells
Causes liver to breakdown stored glycogen
Activates gluconeogensis
