Anesthesia Pharmacology: Diabetes Management
Practice Questions
Secretory product associated with pancreatic alpha cells:
insulin
proglucagon
somatostatin
pancreatic polypeptide
A & C
Major manifestations of diabetes mellitus:
inappropriate hyperglycemia
disordered metabolism
both
neither
Type I diabetes:
most often presents in adults
anabolic metabolic disorder
circulating insulin is virtually absent
glucagon levels are low
ketoacidosis is rarely seen
Extrinsic factors which may affect pancreatic B cell function:
mumps virus
toxic chemicals
coxsackievirus
A & B
A, B & C
Consistent with the idea that autoimmune processes are a major factor in pathogenesis of Type I diabetes is the observation that of this/these drug(s) may diminish pancreatic B cell damage:
metaproterenol
azathioprine
propranolol
A & C
A, B & C
Ketoacidosis really occurs in this Type I diabetes because of adequate circulating endogenous insulin:
Type I diabetes
Type II diabetes
Characteristic(s) of Type II diabetes
absence of endogenous insulin
tissue supersensitivity to insulin
most patients are obese
hyper-responsiveness of pancreatic B cell-response to insulin
ketoacidosis
Somatostatin -- secreted from this pancreatic islets cell type:
alpha cells
beta cells
delta cells
F cells
Drugs used to correct hyperglycemia associated with Type II diabetes:
insulin
sulfonylureas
both
neither
Stimulants of insulin release from pancreatic B cells:
leucine
vagal activity
mannose
B & C
A, B & C
Ion influx mow strictly associated with insulin secretion:
potassium
sodium
calcium
magnesium
chloride
The two main organs that remove insulin from circulation:
liver and GI tract
kidney and pancreas
pancreas and liver
liver and kidney
GI tract and kidney
Most of ENDOGENOUSLY secreted insulin is cleared from the blood by:
liver
kidney
pancreas
GI tract
lung
Most of EXOGENOUSLY administered insulin is cleared from the blood by:
liver
kidney
GI tract
pancreas
lung
Glucose transporter is most important to in terms of lowering blood glucose:
GLUT-1
GLUT-2
GLUT-3
GLUT 4
GLUT-5
Postprandial insulin release induces phosphorylations which activate:
pyruvate carboxylase
glucose 6-phosphatase
glucokinase
fructose bisphosphatase
phosphoenolpyruvate carboxykinase
Insulin endocrine effect(s):
anabolic action: promotes glucose storage as glycogen
anabolic action: increases triglyceride synthesis
muscle effect: increases protein synthesis
adipose tissue: increases triglyceride storage
all of the above
Mechanism(s) by which insulin reduces circulating free fatty acids and promotes adipocytes triglyceride storage: