Endocrine Flashcards
In type 1 diabetes mellitus, excessive lipolysis can lead to an uncontrolled increase in ketone bodies, which cause _______.
diabetic ketoacidosis
Type 1 diabetes is usually diagnosed (before/after) the age 30.
before
Diabetic ketoacidosis causes increased production of ketones such as ________.
beta-hydroxybutyrate and acetoacetate
A ______ state is much more common in type 2 diabetes than in type 1 diabetes, and it causes increased plasma osmolarity due to extreme dehydration and concentration of the blood.
hyperosmolar hyperglycemic
Volume repletion in patients with diabetic ketoacidosis is achieved using (isotonic/hypertonic) saline.
isotonic
Insulin sensitivity is (high/low) in diabetes mellitus type 1.
high
Type 1 diabetes mellitus is caused by type (III/IV) hypersensitivity
IV
_______ is a type of acid-base imbalance seen in diabetic ketoacidosis due to a loss of bicarbonate.
High anion gap metabolic acidosis
The mainstay of the treatment of diabetes mellitus type 1 is (insulin/oral hypoglycemics).
Insulin
The treatment regimen for type 2 diabetes mellitus should be adjusted to keep the fasting blood sugar below _____.
130
Diabetes mellitus type 2 has a relatively (strong/weak) genetic predisposition.
strong
Histology shows islet leukocytic infiltrate in diabetes mellitus type (1/2).
1
The most common initial manifestation of type 1 diabetes mellitus is elevated blood glucose (with/without) ketonemia.
with
Diabetes mellitus type 1 has association with HLA-DR3 and ________.
HLA-DR4
Patients with diabetes mellitus type 2 have (high/low) insulin sensitivity.
low
Diabetes mellitus type (1/2) is caused by a type IV hypersensitivity reaction.
1
In type 2 DM, _______ causes the pancreas to increase insulin production.
insulin resistance
DM type (1/2) is primarily associated with hyperosmolar non-ketotic hyperglycemia.
2
Polyphagia, glycosuria, polyuria, and polydipsia are all symptoms of _______.
uncontrolled diabetes mellitus
Anti-glutamic acid decarboxylase and islet cell cytoplasmic antibodies are associated with diabetes mellitus type (1/2).
1
DM type 2 (is/is not) associated with the human leukocyte antigen system.
is not
Patients with type 1 DM have (high/low) levels of serum c-peptide.
low
The blood glucose level of patients with DKA is usually above _______ mg/dl.
250
Insulin deficiency is (mild to moderate/severe) in DM type 1.
severe
Patients with diabetes mellitus type 2 show (mild to moderate/severe) glucose intolerance.
mild to moderate
________ is a severe life-threatening complication of diabetes mellitus characterized by severe hyperglycemia and accelerated ketogenesis.
Diabetic ketoacidosis
__________ in the pancreas produce insulin
Beta cells
Two-hour postprandial blood glucose greater than _______ mg/dl is an essential criterion for the diagnosis of diabetes mellitus.
200
DM type 1 has association with _______ and HLA-DR4
HLA-DR3
Insulin treatment is (always/sometimes) necessary in DM type 2.
sometimes
_______ is described as deep, labored breathing commonly associated with DKA.
Kussmaul breathing
In DKA, serum sodium is falsely (high/low) due to the osmotic load of glucose.
low
Fasting blood glucose of more than ______ mg/dl on two separate occasions is an essential criterion for diagnosing DM.
126
Type (1/2) DM is more commonly associated with DKA.
1
DKA occurs more often in DM type (1/2)
1
Ketoacidosis is (common/rare) in DM type 2.
rare
DM type 1 is caused by a type (I/II/III/IV) hypersensitivity reaction.
IV
_________ is a compound that gives patients with DKA a fruity odor to their breath.
Acetone
DM type (1/2) results from autoimmune destruction of beta cells in the pancreatic islets.
1
The beta-cell in the pancreatic islets of a patient with DM type 2 have ______ deposits.
amyloid
Cells that produce glucagon and insulin are located in the cluster of cells called the _______ in the pancreas.
Islet of Langerhans
Patients with DKA may have (prerenal/intrarenal/postrenal) azotemia due to volume depletion caused by osmotic diuresis.
prerenal
The primary defect of DM type 2 is increased insulin (resistance/deficiency).
resistance
The primary defect in DM type 1 is autoimmune destruction of the _____ of the pancreas.
beta-cells
Treatment of DKA includes hydration, management of electrolyte abnormalities, and ___________.
insulin
_________ is the most common non-inherited risk factor for developing DM type 2.
Obesity
IV bicarbonate should be given if the blood pH is lower than ___.
6.9
_______ is rare in DM type 2 as endogenous insulin usually prevent lipolysis.
DKA
The pathophysiology of type 1 DM is insulin (resistance/deficiency).
deficiency
______ is the biochemical pathway that is initially upregulated in DKA causing the increase in ketones.
Lipolysis
The total K+ level during DKA is (increased/decreased) while the serum level might be increased.
decreased
Type 2 DM is associated with (high/low) serum insulin.
high
DM type 1 (is/is not) associated with obesity.
is not
Blood sugar levels in patients with DLA are usually (higher/lower) than that of hyperosmolar hyperglycemic state.
lower
_____ is the best initial pharmacologic therapy for type 2 DM.
Metformin
The age for patients with DM type 2 usually is (more/less) than 40 years.
more
_______ breathing presents as rapid, deep breathing and is seen in DKA.
Kussmaul
Fasting serum glucose levels greater than or equal to ______ on two separate occasions are diagnostic of DM in an asymptomatic patient
126
The treatment regimen for type 2 DM should be adjusted to keep the glycosylated hemoglobin below _____ percent.
7
Serum insulin level is low in DM type (1/2).
1
In DKA, total body stores of potassium are (high/low).
low
DKA causes a(n) (increase/decrease) in epinephrine production.
increase
DM type 1 has a relatively (strong/weak) genetic predisposition.
weak
When starting the treatment of DKA, insulin bolus (is/is not) recommended before confirming the serum potassium is > or = 3.3 mEq/L.
is not
A 60-year-old male comes to the clinic complaining of numbness in his toes. He cannot quite pinpoint exactly when it started, but for the past three months, the patient has been unable to feel his big toes in his shoes. The patient can walk without any weakness in the legs, and he does not have any symptoms in the arms or fingers. The patient’s diet consists mainly of processed food and contains very few raw fruits or vegetables. Medical history includes obesity, chronic lower back pain, and type 2 DM. Medications include Tylenol and Metformin. The patient’s temp is 37, P 80, R 20, and BP 135/85. Physical examination reveals the patient to be comfortable, and the extremity exam demonstrates bilaterally diminished ankle reflexes and loss of monofilament sensation over the forefront of both plantar surfaces. Labs show a normal CBC and a Hgb A1c of 10.5%. Which of the following mechanisms is most likely contributing to this patient’s symptoms?
Protein kinase C deactivation
Sorbitol dehydrogenase deficiency
Fructose excess
NADPH excess
Aldose reductase deficiency
Sorbitol dehydrogenase deficiency