Diabetes Mellitus and Metabolic Syndrome Flashcards
within the context of glucose, fat, and protein metabolism, explain glycogenolysis, gluconeogenesis, ketosis, and ketoacidosis.
glycogenolysis: the breakdown of glucose
gluconeogenesis: the creation of new glucose
ketosis: Ketosis refers to the metabolic state in which the body converts fat stores into energy, releasing ketones in the process.
Ketoacidosis: Diabetic ketoacidosis (DKA) is a life-threatening problem that affects people with diabetes. It occurs when the body starts breaking down fat at a rate that is much too fast. The liver processes the fat into a fuel called ketones, which causes the blood to become acidic.
Compare pancreatic alpha, beta, and delta cells regarding location and hormone produced
alpha: are located in the islets of Langerhans. The α-cells secrete glucagon as a response to low blood glucose. The major function of glucagon is to release glucose from the glycogen stores in the liver.
beta: are located in the islets of Langerhans. Beta cells (B cells) produce insulin and are the most abundant of the islet cells.
delta: are located in the islets are Langerhans
The somatostatin-secreting δ-cells comprise ~5% of the cells of the pancreatic islets. The δ-cells have complex morphology and might interact with many more islet cells than suggested by their low numbers. δ-Cells contain ATP-sensitive potassium channels, which open at low levels of glucose but close when glucose is elevated. This closure initiates membrane depolarization and electrical activity and increased somatostatin secretion.
explain the stimulus for release and roles of insulin and glucagon
stimulus for release of insulin: Insulin release is stimulated by GH, cortisol, PRL, and the gonadal steroids. It is decreased by PTH.
Physiologically, the main stimulus for glucagon release is hunger (hypoglycemia).
roles of insulin:
- promoting glucose uptake by target cells and storage of glucose as glycogen (in liver and muscles) or fat (in adipose tissue)
- inhibiting fat and glycogen breakdown
- inhibiting gluconeogenesis and increasing protein synthesis.
during stress and fasting, explain the roles of corticosteroids and catecholamines (epinephrine). Relate administration of steroids to the development of hyperglycemia.
what does epi do?
epinephrine helps to maintain blood glucose levels during periods of stress by stimulating glycogenolysis in the liver, thus causing large quantities of glucose to be released into the blood. The use of these internal energy stores by muscles conserves blood glucose for use by tissues such as the brain.
The fast effects are complemented by slower glucocorticoid receptor-mediated effects which facilitate suppression of temporary raised excitability, recovery from the stressful experience and storage of information for future use.
Steroid medications can raise blood glucose levels by reducing the action of insulin (causing insulin resistance) and making the liver release stored glucose into the bloodstream.
define diabetes type one. describe the incidence in age, race, and gender.
type one diabetes is characterized by destruction of the pancreatic beta cells. 5% of cases. most are immune mediated.
age: more commonly occurring in young people.
race: more likely in people with Asian or African ancestry.
gender: males get type one diabetes more
define diabetes type two. Describe the incidence in age, race, and gender along with risk factors and symptoms.
diabetes type two is a heterogenous condition that describes the presence of hyperglycemia in association with relative insulin deficiency.
age: adult onset
race: African American, Alaska Native, American Indian, Asian American, Hispanic/Latino, Native Hawaiian, or Pacific Islander.
gender: men are more likely to develop type two diabetes.
risk factors: genetics, being obese, having high blood pressure.
symptoms: increased thirst, frequent urination, hunger, fatigue, and blurred vision. In some cases, there may be no symptoms.
in diabetes type one, explain the etiology, pathogenesis, and development of initial symptoms.
etiology: autoimmune reaction
pathogenesis: autoimmune destruction of the beta (insulin producing) cells in the pancreas.
development of initial symptoms: the initial symptoms develop as the insulin stores deplete in the body. they usually develop very quickly in young people but can develop more slowly in adults.
Symptoms include increased thirst, frequent urination, hunger, fatigue, and blurred vision.
in diabetes type 2, explain the etiology, pathogenesis, and development of clinical manifestations.
etiology: Cells in muscle, fat and the liver become resistant to insulin
pathogenesis: the development of insulin resistance associated with compensatory hyperinsulinemia, followed by progressive beta-cell impairment that results in decreasing insulin secretion and hyperglycemia.
development of clinical manifestations: is gradual, usually subtle, often asymptomatic.
for metabolic syndrome, explain mechanisms of insulin resistance, describe the role of adipose tissue, list criteria for diagnosis, and list complications.
insulin resistance: caused by obesity, high levels of plasma triglycerides, low HDL, hypertension, systemic inflammation, abnormal fibrinolysis, abnormal function of the vascular endothelium, and macrovascular disease.
adipose tissue: the increased adipose tissue and/or dense distribution of central adiposity challenge the vascular perfusion of that tissue. Tissue macrophages respond to the hypoxic-ischemic cellular damage that induces a condition of chronic inflammation. inadequate response to insulin.
diagnosis of metabolic syndrome is based on: increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels.
complications of metabolic syndrome: hardening of the arteries (atherosclerosis),heart attack, kidney disease, stroke, nonalcoholic fatty liver disease, peripheral artery disease, cardiovascular disease
define gestational diabetes including risk factors and common outcomes.
risk factors: family history of diabetes
common outcomes: complicated pregnancy, mortality, and fetal abnormalities (macrosomia, hypoglycemia, hypocalcemia, polycythemia, and hyperbilirubinemia).
Women with GDM have an increased risk of developing type 2 DM, therefore, they should be followed after delivery to diagnose diabetes early in it’s course.
explain the role of free fatty acids and keto acids in type one diabetes.
free fatty acids: in the absence of insulin, ketosis develops when these fatty acids are released from fat cells and converted to ketones in the liver.
keto acids: the abundance of ketosis from the FFAs make people even more prone to ketoacidosis.
define Kussmaul respirations and explain the compensatory role in diabetic ketoacidosis.
Kussmaul respirations are respirations that have increased rate and depth (faster, shallower) as compared to normal respirations.
They are being like this to act as a compensatory mechanism to prevent further decrease in pH.
compare and contrast DKA and HHS (etiology/pathogenesis, clinical manifestations, basic treatment)
E/P for DKA: hyperglycemia, ketosis, and metabolic acidosis.
Clinical manifestations for DKA: a day or more of polyuria, polydipsia, vomiting and marked fatigue. breath can have a characteristic fruity smell on the breath. HR increased, Kussmaul respirations.
basic treatment for DKA: improve circulatory volume and tissue perfusion, decrease blood glucose, correct the metabolic acidosis, correctly electrolyte imbalances. These objectives are usually achieved through the administration of insulin along with IV fluids and electrolyte imbalances. Because insulin resistance accompanies severe acidosis, low dose insulin therapy may be used.
HHS: a partial or relative insulin deficiency may initiate HHS by reducing glucose utilization while increasing glucagon effects and hepatic glucose output. the hyperglycemia leads to large volume water loss through osmotic diuresis. renal function decreases and further elevates blood glucose levels.
clinical manifestations: weakness, dehydration, polyura, neurologic alterations and excessive thirst.
treatment: careful patient monitoring and correction of dehydration, hyperglycemia, and electrolyte imbalance. Be careful of cerebral edema.
describe common etiologies and clinical manifestations of hypoglycemia in people with diabetes.
which manifestations are related to neuroglycopenia vs. stimulation of the autonomic nervous system>
etiologies: error in insulin dose, increased exercise, failure to eat, decreased insulin need after removal of a stress situation, medication changes, and a change in insulin injection site.
clinical manifestations
neuroglycopenic: headache, difficulty in problem solving, disturbed/altered behavior, coma and seizures.
autonomic nervous system: anxiety, tachycardia, sweating, and constriction of the skin vessels (ie the skin is cool and clammy).
explain the complications of chronic hyperglycemia: macrovascular, microvascular, and increased risk for infections.
macrovascular: coronary artery disease, peripheral vascular disease, stroke, cerebrovascular disease.
microvascular: neuropathy, retinopathy, and disorders of gastrointestinal mobility.
neuropathy is where the person loses sensation in their extremities. This is especially risky for people who have diabetes and who get a sore or something on their foot–they often don’t know that it’s there, and by the time they know it’s there, it’s infected.
increased risk of infections: People who have had diabetes for a long time may have peripheral nerve damage and reduced blood flow to their extremities, which increases the chance for infection. The high sugar levels in your blood and tissues allow bacteria to grow and allow infections to develop more quickly.
