Glucose Flashcards
Pancreatic acini
Secretes digestive juices from the pancreas into the dudodenum
Islet of Langerhans
Responsible for secreting hormones that affect blood sugar levels
Alpha cells
Secrete glucagon
Beta cells
Secrete insulin
Delta cells
Secrete somatostatin
Somatostatin
Inhibit release of insulin and glucagon and decreases release of pituitary gland hormones
What slows down GI activity after ingesting food?
Somatostatin
What is required by the cells for the uptake of glucose?
Insulin
Functions of Inuslin
- -Binds to receptors to trigger series of events that transport glucose into the cell
- Promotes protein synthesis and formation
- Lipid storage
- Facilitates transport of potassium, phosphate, and magnesium into the cells
- Increases glycogen synthesis, decreases gluconeogenesis
Function of Glucagon
Promotes glycogen breakdown
Increases gluconeogenesis
(Increases blood sugar)
When is Glucagon secreted?
Between meals when there is no take (b/c blood sugar is getting lower) to prevent hypoglycemic state
Insulin secretion increases when there is an increase in…
Blood glucose, amino acids, glucagon, gastrin
Insulin secretion decreases when there is…
Low blood glucose, high insulin levels
Insulin works on positive or negative feedback?
Negative
Catecholamines
Help maintain blood glucose levels during periods of stress
Two types of catecholamines
Epinephrine and norepinephrine
Growth Hormone
Increases protein synthesis in all cells of the body, mobilizes fatty acids from adipose tissue, and antagonizes effects of insulin
Glucocorticoids
Stimulate gluconeogenesis by the liver
DM
Inability to regulate glucose leading to the inadequate metabolism of macronutrients
How much insulin is there in Type 1?
None
How does Type 1 occur?
Usually occurs due to cell-mediated immunodestruction of beta cells in the pancreas (manifests after 90% of beta cells are destroyed)
Type IV hypersensitivity reaction
Type 1a
Immune mediated DM
Type 1b
Idiopahic diabetes (no evidence of autoimmune destruction of beta cells)
Type 1 leads to (2)
Hyperglycemia and Hyperketonemia
Type 1 Clinical Manifestations
3 P's Hyperglycemia symptoms (weight loss, fatigue, blurred vision, paresthesia, dry skin, skin infections, slow wound healing)
Diagnostic Criteria for Type 1
History and physical exam Blood glucose levels (fasting, random) Oral glucose test Glycosylated Hemoglobin (HbA1c) Insulin levels Positive urine microalbumin
Treatment for Type 1
Insulin replacement therapy
Count CHO intake with insulin
Exercise
How is insulin in Type 2?
Insulin resistance leads to a reduction in adequate insulin secretion
What is the greatest risk factor for type 2?
Obesity
Which type is the most common type in those with diabetes?
Type 2
How does reduced insulin secretion occur?
Insulin resistance –> beta cell atrophy due to consistently high levels –> reduction in adequate insulin secretion
Clinical Manifestations of type 2
-Often asymptomatic and vague in comparison to type 1
-BUT chronic damage can occur throughout the body
Neuropathy (damage of nerves)
Recurrent infections
Coronary artery disease
PVD
Diabetic retinopathy (visual changes)
Nephropathy (kidneys)
Fatigue
Diagnostic criteria of Type 2
History and physical exam
Blood glucose level
Test for presence of long-term complications (eye exam, heart and kidney function, sensation)
What diagnostic criteria differentiates type 1 and type 2?
Insulin level
What is the first and main treatment of type 2?
Weight control through diet and exercise
How does exercise influence insulin?
Exercise increases insulin sensitivity of cells
Treatment for type 2
Weight control
Oral glycemic agents
What is the goal in type 2 treatment?
maintain optimal blood glucose levels
Normal range of glucose
70-100
Normal HbA1c range
6.5-7%
Prediabetes
Impaired fasting plasma glucose or impaired glucose tolerance
Hemoglobin A1C
Normal -
Prediabetes -
DM
Normal - about 5%
Pre - 5.7-6.4
DM - 6.5 or greater
Fasting plasma glucose
Normal -
Prediabetes -
DM
Normal - 99 mg/dL or lower
Pre - 100-125 mg/dL
DM - 126 or greater
Oral Glucose Tolerance test
Normal -
Prediabetes -
DM
Normal - 139 or lower
Pre - 140-199
DM - 200 or greater
Acute complications
Hypoglcemia
Hyperglycemia (DKA, HHS)
Somogyi effect
Dawn phenomenon
Hypoglycemia - level at which clinical manifestation starts
45-60 mg/dL
Causes of Hypoglycemia
Overproduction/overadministration of insulin
Excessive exercise
Infection (body requires more blood sugar)
Inadequate food intake
Several anti-hyperglycemic meds for type 2
Clinical manifestations of Hypoglycemia
Pallor Flushing Diaphoresis Tremor Tachycardia Palpitations Blurred vision Headache, confusion, poor judgment, anxiety, irritability
Complications of Hypoglycemia
Seizures, coma, death
Treatment for Hypoglycemia
IV
Glucose
Orange juice, candy at first, then carbs (more substantial)
Two types of hyperglycemia
DKA and HHS
DKA occurs in which type?
Type 1
HHS occurs in which type?
Type 2
Blood sugar level in DKA
Greater than 250 mg/dL
Patho of DKA
No insulin, thus breakdown of fat and ketogenesis, leads to ketoacidosis
Clinical manifestations of DKA
- Kussmaul’s respiration (rapid, deep breathing, compensation for acidosis)
- Fruity breath (acetone in body blown off with breath)
- Tachycardia to compensate for low BP
- Altered level of consciousness
- Nausea, vomiting, abdominal pain
- Polyuria
- Dehydration
Treatment of DKA
Insulin !
Check potassium to avoid hypokalemia
Manage acidosis (administer bicarbonate)
May not need a lot of fluids because blood sugar is not as high like in HHS
Clinical manifestations of HHS
Severe hyperglycemia Low blood volume secondary to severe dehydration -CNS manifestations -Dry, warm skin -Dry rough oral mucosa -Decreased BP -Tachycardia -Decreased O2 and glucose to the brain leads to lethargy, weakness, confusion Increased plasma osmolarity
Is there ketoacidosis in HHS?
No ketoacidosis
Treatment for HHS
Fluid resuscitation to maintain blood volume
Potentially insulin
Somogyi effect
Rebound hyperglycemia as a result of insulin-induced hypoglycemia
In Somogyi, when does hypoglycemia occur?
During the night
In Somogyi, do you wake up with hypo or hyperglycemia? Why?
Rebound hyperglycemia because the body tries to compensate for the hypoglycemia at night by releasing catecholamines, glucagon, cortisol, and growth hormone
What is a common mistake patients make to fix somogyi?
Over-administration of evening insulin - people think they need to administer more insulin before sleep to prevent hyperglycemia in the morning
-But actually they are exacerbating the situation
Treatment for Somogyi Effect
Decrease bedtime insulin
Oral glycemics
Dawn Phenomenon
Hormone release leads to steady rise of blood glucose throughout the night
With Dawn do you wake up with hypo or hyperglycemia? Why?
Hyperglycemia due to early AM release of hormones
Treatment for Dawn Phenomenon
Limit evening snacks, increase evening inuslin
How do you distinguish between Dawn and Somogyi
Check blood glucose in the middle of the night for hypoglycemic state
Between Dawn and Somogyi, which one experiences hypoglycemia?
Somogyi
What are the chronic macrovascular complications of DM (typically type 2)?
Coronary artery disease
Stroke
PVD
Characteristics of macrovascular complications
Damage to blood vessels, plaque buildup (atherosclerosis), poor blood flow
What are the microvascular complications of DM?
Diabetic retinopathy
Diabetic nephropathy
Other chronic complications
Diabetic neuropathies Slow wound healing Reduced response Increased risk of infection (UTI, Candida, yeast infection) Dental caries, gingivitis, periodontitis Cataracts
Pregnancy complications in DM
- Blood sugar can damage vasculature of placenta
- Increased incidence of spontaneous abortions
- Infants increase size and weight for date, may experience rebound hypoglycemia in first hours postnatal
