Part 2 HENRYS

Question 1

1. there’s usually is autoimmune destruction of insulin-producing beta cells
2. Genetic Susceptibility to Develop Type 1 Diabetes is associated with ____ on chromosome ___
3. develop from untreated Type 1 Diabetes
   - ____ therapy is required
4. Autoantibody assays are available for the following:
   - found on the surface membrane of pancreatic islet beta cell secretory granules (2)
   - older assays measures
   - has the highest sensitivity (91%) ; more common in adults
   - more common in young children who develop type 1 diabetes

Answer 1

1. Islets of the Pancreas
2. HLA-DR/DQ on chromosome 6
3. Diabetic Ketoacidosis
   - Insulin therapy
   4.
   - ZINC TRANSPORTER 8 & INSULINOMA ASSOCIATION PROTEIN 2
   - islet cell antigen 512 autoantibodies
   - GLUTAMIC ACID DECARBOXYLASE65
   - INSULIN (IAA)

Question 2

1. Enhanced prediction for the development of type 1 diabetes
2. established a proficiency testing service
3. Islet Autoantibody Standardization Program is previously called
4. began as collab between ____ & _____

Answer 2

1. Diabetes Prevention Trial- Type 1 risk score
2. Islet Autoantibody Standardization Program
3. Diabetes Antibody Standardization Program
4. Immunology of Diabetes Society & Centers for Disease
   Control and Prevention

Question 3

1. recommends screening for type 2 diabetes in any overweight or obese adult if one or more risk factors are
   present
2. preferred test
3. if random plasma glucose level is _____ or higher, a fasting plasma
   glucose, HbA1c, or 2- hour 75- g OGTT should be performed
4. HOME BLOOD GLUCOSE MONITORING: If an individual does have a capillary glucose test on one of these instruments that reads _______ individual should be rescreened with a fasting plasma glucose, HbA1c, or
   OGTT, using venous samples

Answer 3

1. American Diabetes Association
2. Fasting plasma glucose
3. 160 mg/dL (8.9 mmol/L)
4. ≥140mg/dL (7.8 mmol/L)

Question 4

1. reduction in cardiovascular disease was also found in the groups that had been intensively treated
2. reduction in microvascular complications in type 2 diabetes was reported
   - micro vascular complications were decreased by ______
   - by lowering the HbA1C from ___ to ____
3. formed non enzymatically by the two- step reaction
   - produces ______ (aka _____)
   - undergoes _______
   - then converted to a ______ (______ hgb)

Answer 4

1. Epidemiology of Diabetes Interventions and Complications
2. United Kingdom Prospective Diabetes Study
   - 25%
   - 7.9 to 7.0%
3. Glycosylated hemoglobin (
   - labile aldimine (aka Schiff base)
   - Amadori rearrangement
   - stable ketoamine(glycosylated hgb)

Question 5

1. Defined HbA1c as the hemoglobin A that is irreversibly glycosylated at one or both N- terminal valines of
   the β- chains of the tetrameric hemoglobin molecule
2. provides an index of average blood glucose levels over the past 2 to 4 months
3. life span of RBCs approx
4. HbA1C levels represent ____ of glucose levels
5. ___% of the HbA1c level is determined by plasma glucose levels over the previous month

Answer 5

1. International Federation of Clinical Chemistry Working Group
2. HbA1c testing
3. 90-120 days
4. Weighted average
5. 50%

Question 6

1. HbA1c assays should be calibrated using the reference measurement system developed by the ______
2. point- of- care device that has superior accuracy and precision, has been approved by the FDA for use in the diagnosis of diabetes
3. Interferes with uremia in some older method
4. cause interference by acetylated species
5. can adversely affect accuracy in certain assays
6. can falsely lower levels by inhibiting glycosylation (2)

Answer 6

1. International Federation of Clinical Chemistry
2. Afinion
3. Carbamylated hemoglobin
4. Salicylates
5. Hemoglobinopathies
6. Vitamins C and E

Question 7

1. trait that have abnormal hemoglobin but normal red cell turnover
2. can be useful when setting glycemic goals for specific individuals to help avoid overtreatment and
   hypoglycemia
3. not well standardized and are sensitive to variations in temperature
   - should not be performed if the serum albumin level is
4. better standardized, more precise, and inexpensive
   - results can be reported as a ____
5. dietary monosaccharide, is filtered in the glomerulus and competes with glucose for reabsorption in the
   renal tubules.p

Answer 7

1. SICKLE CELL TRAIT
2. GLUCOSE MANAGEMENT INDICATOR
3. FRUCTOSAMINE ASSAYS
   - ≤3.0 g/dL (0.45 mmol/L)
4. GLYCATED ALBUMIJ ASSAYS
   - PERCENT OF TOTAL ALBUMIN
5. 1,5-anhydroglucitol

Question 8

1. 3 MAIN KETONE BODIES
2. _____ & _____ are greatly increased in DKA as a result of the altered redox state and elevated levels of NADH in hepatic mitochondria
   - ratio
   - concentrations of ____ to ___ mmol/L
3. Ketone testing is to detect ______
4. turn purple in the presence of elevated levels of acetoacetic acid
5. detected in the presence of glycine
   - FALSE NEGATIVE = occur w/ _____
   - FALSE POSITIVE = use of ______ such as _____

Answer 8

1. β- hydroxybutyric acid, acetoacetic acid, and acetone
2. β- Hydroxybutyric acid and acetoacetic acid
   - 1:1
   - 0.5 to 1.0
3. KETOSIS
4. Sodium nitroprusside
5. Acetone
   - OLD STRIPS
   - sulfhydryl- containing medications such as captopril

Question 9

1. not detected as the acid levels fall and acetoacetic acid and acetone levels rise during the treatment of DKA
2. reference range
   - healthy individuals who have fasted overnight
   - meet biochemical criteria for diagnosis of DKA
3. triggered by ANS
   - catecholamine mediated (3)
   - acetylcholine release (3)
4. triggered by CNS

Answer 9

1. β- Hydroxybutyric acid
2. reference range
   - >0.5mmol/L
   - >2mmol/L
3. Neurogenic symptoms
   - Tremulousness, palpitations, and anxiety
   - diaphoresis, hunger, and
   paresthesias
4. Neuroglycopenic symptoms

Question 10

1. refers to symptoms consistent with hypoglycemia associated with a documented low plasma glucose level and relief of symptoms with correction of hypoglycemia
2. directly damages pancreatic beta cells
3. associated with increased insulin and C- peptide levels in susceptible individuals
4. due to increased peripheral glucose utilization
5. cause hypoglycemia by antagonizing catecholamine- mediated glycogenolysis

Answer 10

1. Whipple’s triad
2. Pentamidine
3. Sulfonamide- induced hypoglycemia
4. Salicylate- induced hypoglycemia
5. Propranolol

Question 11

1. decrease in glycogen reserves coupled with failure of gluconeogenesis and enhanced
   glucose utilization
2. risk for hypoglycemia during prolonged fasting, presumably related to poor availability of the gluconeogenic substrate alanine (2)
3. defective gluconeogenesis; reduced insulin clearance
4. Patient with ESRD on peritoneal dialysis

Answer 11

1. severe sepsis
2. spinal muscular atrophy and congenital myopathy
3. end- stage renal disease
4. Gabapentin

Question 12

HORMONE DEFICIENCIES
1. initially stimulates glycogenolysis and later gluconeogenesis to increase plasma glucose levels
2. increase glycogenolysis, gluconeogenesis, and lipolysis
3. mediate glycogenolysis and gluconeogenesis
4. Poor glucagon and _____ responses to hypoglycemia are common in patients with long- standing
diabetes mellitus
5. deficiency to infants & children that can develop hypoglycemia
6. deficiency to adults that can develop hypoglycemia

Answer 12

1. Glucagon
2. Catecholamines
3. Growth hormone and cortisol
4. epinephrine
5. cortisol
6. glucocorticoid

Question 13

1. originates from non–beta cell tumors, which cause hypoglycemia without producing insulin.
2. tumors of mesenchymal origin (3)
3. tumors of epithelial origin (2)

Answer 13

1. Non–islet cell tumor hypoglycemia
2. • mesothelioma,
   • hemangiopericytoma
   • solitary fibrous tumors
3. • hepatocellular
   • gastrointestinal stromal tumor

Question 14

1. Produced by the liver and is relatively independent of growth hormone
2. Primary transcription product
3. frequently associated with hypoglycemia due to insulin- like activity of big IGF- II
4. gold standard method for detecting big IGF- II
5. rapid, reproducible, and sensitive method for the determination of big IGF- II

Answer 14

1. Insulin- like growth factor- II
2. Pre- proIGF- II
3. Hypokalemia
4. Size- exclusion acid chromatography
5. Immunoblot analysis