NURS 5461 EXAM GUIDE ON DIABETES WITH COMPLETE
SOLUTIONS A+ 2023 UPDATE
What is Diabetes?
Person does not produce enough insulin. Inability to use insulin appropriately. Liver overproduces
glucose [from stored glycogen]. Insulin receptors &/or Insulin transporters. Insulin is a carrier protein
that gets glucose out of the bloodstream and into the cells where it is used for fuel. It also stores sugar
in the form of trigs, which can be turned into fat. It prevents the breakdown of fat.
Symptoms Fatigue Weakness Polyuria Polydipsia Polyphagia Infections Slowed healing Blurred vision
Diagnostic Criteria for Diabetes
Fasting glucose >126 mg/dl confirmed by a repeat test Casual glucose >200 mg/dl plus classic
signs/symptoms 2 hr. postprandial glucose >200mg/dl after 75 g glucose load A1C >/= 6.5% [do not use
with hemoglobinopathies]
Categories of Increased Risk Formerly called “borderline” DM Impaired Fasting Glucose [IFG] 100-125
mg/dL fasting Impaired Glucose Tolerance [IGT] 140-199 mg/dL 2 hours after a 75 gram glucose load
Both of these categories will demonstrate an A1C of 5.7- 6.4%
Who Do We Test? Those with: BMI of 25 or more
Additional Risk Factors Children >85% for weight Those that meet criteria for Metabolic Syndrome Those
that had diabetes during pregnancy If no risk factors—test at age 45 and if testing is unremarkable—
retest every 36 months Screen with A1C [depending on payor], FPG, 2° postprandial glucose or 2° oral
glucose tolerance test [not commonly needed
ADA Criteria for Gestational Diabetes Screen for undiagnosed Type II @ 1st visit for those at risk
Perform a 2 hour OGTT at 24-28 weeks gestation for ALL pregnancies [without diabetes] done in the AM
using 75 gram glucose load [after an 8 hour fast] Diagnosis can be made if ANY of the following are
found: Fasting glucose < 95 mg/dL 1 hour post glucose load < 140 mg/dL hour post glucose load < 120
mg/dL Screen women with GDM 6-12 weeks postpartum with OGTT and standard diagnostic criteria &
every 3 years thereafter with standard diagnostic criteria
Type I Diabetes 5-10% of all diabetics Insulin dependent Insulin level or C-peptide is low Antibody
markers usually seen—insulin autoantibodies, islet cell antibodies, glutamic acid decarboxylase
antibodies [GAD] Insulin sensitive Genetic predisposition Patient needs insulin even when NPO
Symptoms Rapid onset of symptoms Weight loss Ketones + in urine & blood Kussmaul respirations
Type II Diabetes 90-95% of all patients Primarily insulin resistant and with time eventual decline in
insulin production Insulin and C-peptide levels vary— could be very high, normal or low Strong family hx
No autoantibodies
,NURS 5461 EXAM GUIDE ON DIABETES WITH COMPLETE
SOLUTIONS A+ 2023 UPDATE
Associated with HTN, obesity & dyslipidemia Symptoms Gradual onset Weight gain Usually no ketones in
blood or urine May present with end organ damage— paresthesias, vision loss, etc.
Other Categories Latent Autoimmune Diabetes of Adulthood [LADA] Often diagnosed as Type II Some
have anti-GAD antibodies Insulin deficiency occurs more quickly than in Type II, but slower than in Type
I Maturity Onset Diabetes of the Young [MODY] Several genetic defects in ẞ cell function can cause
diabetes at early age This term is NOT used for the common
,NURS 5461 EXAM GUIDE ON DIABETES WITH COMPLETE
SOLUTIONS A+ 2023 UPDATE
Type II DM that is occurring more & more frequently in children & adolescents
Metabolic Syndrome Root cause is inability to use insulin [insulin resistance] More insulin needed to
keep patient euglycemia This syndrome is related to HTN, obesity, dyslipidemia This syndrome can
appear long before BG starts to elevate Genetic influence Some factors influence its progression—
sedentary lifestyle, obesity, smoking AND High fat diet Highly processed foods—high fructose corn
syrup, trans fats ?stress ?depression ?lack of sleep
How Do We Diagnose Metabolic Syndrome? When 3 or more of the following 5 criteria are present
— then patient has Metabolic Syndrome [CDC, 2018] Waist circumference—men >40 inches; women
>35 inches Triglycerides >150 mg/dL HDL cholesterol—men 130/85 FBS >100 mg/dL
What Else Can We Call It? Also known as: Insulin Resistance Syndrome Cardiovascular Dysmetabolic
Syndrome Deadly Quartet ICD-10 Code is E88.81
Definition/Epidemiology Metabolic syndrome [Syndrome X] is a cluster of disorders first discussed by
Reaven & colleagues in 1987 Elevated insulin levels lead to other abnormalities Hypertension
Dyslipidemia ? Atherosclerosis Microalbuminuria Abnormalities of fibrinolytic system Hyperuricemia
Pathophysiology Abdominal obesity contributes to IR: Adipose tissue in the abdomen enhances insulin
resistance Tissue sensitivity to insulin is decreased by 30-40% when a person is >35% over Ideal Body
Weight Fat cells found in abdominal obesity are larger and more insulin resistant Abdominal fat is also
more metabolically active→ releasing excess FFAs that interfere with hepatic insulin clearance, causing
↑ levels of circulating insulin IR is impaired insulinstimulated glucose uptake by skeletal muscles,
adipose tissue or liver Mechanisms Abnormal insulin molecules Decreased number of insulin receptors
Decreased glucose transporters Defective post receptor activity When cells get resistant to insulin, our
body compensates by making more insulin to overcome resistance and to maintain normoglycemia
Fasting ↑ insulin occurs in response to elevated fasting plasma glucose
Hypertension European Group for the Study of Insulin Resistance [1996], found that for each 10 unit
increase in insulin resistance SBP increases 1.7 mm Hg and DBP increased 2.3 mm Hg Insulin is a stimulus
for growth of vascular endothelial and smooth muscle cells Hyperinsulinemia can result in a thickening in
arterial blood vessel walls [end result of this effect is unclear]
Dyslipidemia High triglycerides Low HDL High small dense LDL Pattern B Atherogenic dyslipidemia The
higher the glucoses, the higher the fasting triglycerides Insulin impairs normal suppression of FFA
release from adipose tissue Increased FFA release and delivery to liver offers an efficient substrate for
increased synthesis of triglycerides When the liver content of lipids is elevated, gluconeogenesis is
, NURS 5461 EXAM GUIDE ON DIABETES WITH COMPLETE
SOLUTIONS A+ 2023 UPDATE
elevated
Microalbuminuria Insulin Resistance and Atherosclerosis Study [1996], found that acute
hyperinsulinemia causes renal vasodilatation, increased glomerular hydrostatic pressure and increased
GFR Localized elevated pressure in glomerular vessels is involved in elevated microalbumin secretion
Microalbuminuria Predictor of CV morbidity ++++++ Predictor of CV mortality ++++++
Hyperuricemia Uric acid is elevated in patients with elevated insulin levels, elevated triglycerides,
low HDL and hypertension
Microvascular Angina Syndrome X was used by H.G. Kemp [1973] to describe microvascular angina as
impaired perfusion of microvessels of the heart can occur in the absence of macrovascular
SOLUTIONS A+ 2023 UPDATE
What is Diabetes?
Person does not produce enough insulin. Inability to use insulin appropriately. Liver overproduces
glucose [from stored glycogen]. Insulin receptors &/or Insulin transporters. Insulin is a carrier protein
that gets glucose out of the bloodstream and into the cells where it is used for fuel. It also stores sugar
in the form of trigs, which can be turned into fat. It prevents the breakdown of fat.
Symptoms Fatigue Weakness Polyuria Polydipsia Polyphagia Infections Slowed healing Blurred vision
Diagnostic Criteria for Diabetes
Fasting glucose >126 mg/dl confirmed by a repeat test Casual glucose >200 mg/dl plus classic
signs/symptoms 2 hr. postprandial glucose >200mg/dl after 75 g glucose load A1C >/= 6.5% [do not use
with hemoglobinopathies]
Categories of Increased Risk Formerly called “borderline” DM Impaired Fasting Glucose [IFG] 100-125
mg/dL fasting Impaired Glucose Tolerance [IGT] 140-199 mg/dL 2 hours after a 75 gram glucose load
Both of these categories will demonstrate an A1C of 5.7- 6.4%
Who Do We Test? Those with: BMI of 25 or more
Additional Risk Factors Children >85% for weight Those that meet criteria for Metabolic Syndrome Those
that had diabetes during pregnancy If no risk factors—test at age 45 and if testing is unremarkable—
retest every 36 months Screen with A1C [depending on payor], FPG, 2° postprandial glucose or 2° oral
glucose tolerance test [not commonly needed
ADA Criteria for Gestational Diabetes Screen for undiagnosed Type II @ 1st visit for those at risk
Perform a 2 hour OGTT at 24-28 weeks gestation for ALL pregnancies [without diabetes] done in the AM
using 75 gram glucose load [after an 8 hour fast] Diagnosis can be made if ANY of the following are
found: Fasting glucose < 95 mg/dL 1 hour post glucose load < 140 mg/dL hour post glucose load < 120
mg/dL Screen women with GDM 6-12 weeks postpartum with OGTT and standard diagnostic criteria &
every 3 years thereafter with standard diagnostic criteria
Type I Diabetes 5-10% of all diabetics Insulin dependent Insulin level or C-peptide is low Antibody
markers usually seen—insulin autoantibodies, islet cell antibodies, glutamic acid decarboxylase
antibodies [GAD] Insulin sensitive Genetic predisposition Patient needs insulin even when NPO
Symptoms Rapid onset of symptoms Weight loss Ketones + in urine & blood Kussmaul respirations
Type II Diabetes 90-95% of all patients Primarily insulin resistant and with time eventual decline in
insulin production Insulin and C-peptide levels vary— could be very high, normal or low Strong family hx
No autoantibodies
,NURS 5461 EXAM GUIDE ON DIABETES WITH COMPLETE
SOLUTIONS A+ 2023 UPDATE
Associated with HTN, obesity & dyslipidemia Symptoms Gradual onset Weight gain Usually no ketones in
blood or urine May present with end organ damage— paresthesias, vision loss, etc.
Other Categories Latent Autoimmune Diabetes of Adulthood [LADA] Often diagnosed as Type II Some
have anti-GAD antibodies Insulin deficiency occurs more quickly than in Type II, but slower than in Type
I Maturity Onset Diabetes of the Young [MODY] Several genetic defects in ẞ cell function can cause
diabetes at early age This term is NOT used for the common
,NURS 5461 EXAM GUIDE ON DIABETES WITH COMPLETE
SOLUTIONS A+ 2023 UPDATE
Type II DM that is occurring more & more frequently in children & adolescents
Metabolic Syndrome Root cause is inability to use insulin [insulin resistance] More insulin needed to
keep patient euglycemia This syndrome is related to HTN, obesity, dyslipidemia This syndrome can
appear long before BG starts to elevate Genetic influence Some factors influence its progression—
sedentary lifestyle, obesity, smoking AND High fat diet Highly processed foods—high fructose corn
syrup, trans fats ?stress ?depression ?lack of sleep
How Do We Diagnose Metabolic Syndrome? When 3 or more of the following 5 criteria are present
— then patient has Metabolic Syndrome [CDC, 2018] Waist circumference—men >40 inches; women
>35 inches Triglycerides >150 mg/dL HDL cholesterol—men 130/85 FBS >100 mg/dL
What Else Can We Call It? Also known as: Insulin Resistance Syndrome Cardiovascular Dysmetabolic
Syndrome Deadly Quartet ICD-10 Code is E88.81
Definition/Epidemiology Metabolic syndrome [Syndrome X] is a cluster of disorders first discussed by
Reaven & colleagues in 1987 Elevated insulin levels lead to other abnormalities Hypertension
Dyslipidemia ? Atherosclerosis Microalbuminuria Abnormalities of fibrinolytic system Hyperuricemia
Pathophysiology Abdominal obesity contributes to IR: Adipose tissue in the abdomen enhances insulin
resistance Tissue sensitivity to insulin is decreased by 30-40% when a person is >35% over Ideal Body
Weight Fat cells found in abdominal obesity are larger and more insulin resistant Abdominal fat is also
more metabolically active→ releasing excess FFAs that interfere with hepatic insulin clearance, causing
↑ levels of circulating insulin IR is impaired insulinstimulated glucose uptake by skeletal muscles,
adipose tissue or liver Mechanisms Abnormal insulin molecules Decreased number of insulin receptors
Decreased glucose transporters Defective post receptor activity When cells get resistant to insulin, our
body compensates by making more insulin to overcome resistance and to maintain normoglycemia
Fasting ↑ insulin occurs in response to elevated fasting plasma glucose
Hypertension European Group for the Study of Insulin Resistance [1996], found that for each 10 unit
increase in insulin resistance SBP increases 1.7 mm Hg and DBP increased 2.3 mm Hg Insulin is a stimulus
for growth of vascular endothelial and smooth muscle cells Hyperinsulinemia can result in a thickening in
arterial blood vessel walls [end result of this effect is unclear]
Dyslipidemia High triglycerides Low HDL High small dense LDL Pattern B Atherogenic dyslipidemia The
higher the glucoses, the higher the fasting triglycerides Insulin impairs normal suppression of FFA
release from adipose tissue Increased FFA release and delivery to liver offers an efficient substrate for
increased synthesis of triglycerides When the liver content of lipids is elevated, gluconeogenesis is
, NURS 5461 EXAM GUIDE ON DIABETES WITH COMPLETE
SOLUTIONS A+ 2023 UPDATE
elevated
Microalbuminuria Insulin Resistance and Atherosclerosis Study [1996], found that acute
hyperinsulinemia causes renal vasodilatation, increased glomerular hydrostatic pressure and increased
GFR Localized elevated pressure in glomerular vessels is involved in elevated microalbumin secretion
Microalbuminuria Predictor of CV morbidity ++++++ Predictor of CV mortality ++++++
Hyperuricemia Uric acid is elevated in patients with elevated insulin levels, elevated triglycerides,
low HDL and hypertension
Microvascular Angina Syndrome X was used by H.G. Kemp [1973] to describe microvascular angina as
impaired perfusion of microvessels of the heart can occur in the absence of macrovascular
