PATHOPYSIOLOGY|PHARMACOLOG
Y II (NURS 432) STUDY SHEET FOR
QUIZ 3 (a comprehensive and
thorough review of all the material
that will be tested on Quiz 3 in this
course) PACE UNIVERSITY.
,NURS 432 – Pathophysiology/Pharmacology II Exam 3 Study
Sheet
Endocrine System
(Patho Chapter 10)
Pancreas & Diabetes Mellitus: (Chapter 57)
Metabolic Consequences of Insulin Deficiency: insulin deficiency puts the body into catabolic
mode
➢ In the absence of insulin:
• Glycogen: converted into glucose
• Proteins: degraded into amino acids
• Fats: converted to glycerol & free fatty acids
➢ Insulin deficiency promotes hyperglycemia via:
• Increased glycogenolysis:
breakdown of glycogen into free
glucose
• Increased gluconeogenesis:
generation of glucose; due to amino
acids & fatty acids produced from
metabolic breakdown of proteins &
fats
• Reduced glucose utilization: due
to ↓ cellular uptake of glucose and
↓ conversion of glucose to glycogen
T1DM vs T2DM:
➢ Type-1 Diabetes Mellitus: aka Child-onset DM or Insulin-dependent DM
• Onset: typically develops during childhood or adolescence
• Patho: involves autoimmune destruction of pancreatic beta cells
• Treatment: insulin supplementation
• DKA:
➢ Type-2 Diabetes Mellitus: aka Adult-onset or Insulin-independent DM
• Onset: typically develops in adulthood
• Genetics: strong familial association/predisposition
• Patho: insulin is still produced, however, there’s reduced binding, # of receptors &
receptor responsiveness
• Treatment: initially may be managed w/ lifestyle modifications (i.e., diet)
o Drug Tx: PO meds progression to insulin
• HHNS: (hyperglycemic hyperosmolar nonketotic syndrome) involves very high
blood sugar levels and can be life threatening
o Prevalence: more common in older people who have T2DM, but can happen to
anyone
➢ Complications:
• Short term: hyperglycemia, hypoglycemia
• Long term: HTN, HD, nephropathy, retinopathy, neuropathy, amputation
Gestational DM:
• Placental hormones: antagonize the actions of insulin
• Fetal hyperinsulinemia: glucose passes freely from maternal to the fetal circulation
• Duration & resolution: considering re-dx
• DOC Agents: insulin, metformin (2 line)
nd
Diabetes Diagnostics:
• Normal glucose: 70-110 mg/dL
➢ Fasting plasma glucose: (FPG) at least 8hrs after eating
, • Normal: <100 mg/dL
• Pre-diabetes: 100-125 mg/dL
• DM: ≥ 126 mg/dL
• If >200: advance to OGTT
➢ Casual plasma glucose test: no fasting
• DM: ≥ 200 mg/dL plus symptoms of diabetes
• Concurrent s/s: polyuria, polydipsia, rapid weight loss
➢ Oral glucose tolerance test: (OGTT) used when others not definitive; measured 2h post 75g
PO glucose
• Normal: < 140 mg/dL
• DM: ≥ 200 mg/dL
1
, ➢ HgbA1c: control over 3m
• DM: ≥ 6.5
• Target: <7 for most
• Inaccuracies: may be caused by pregnancy, CKD, liver DX, recent blood
loss or transfusions, or blood dx (thalassemia, Fe deficiency anemia, B12
deficiency anemia)
Lifestyle Modifications: used for all, regardless of drug therapy; continued w/ drug TX; may be
initial for T2DM
• Weight control
➢ Diet: carbohydrates, fat, proteins
• No ideal %: instead, based on current eating patterns, preferences, and goals
• Counting: calories
• Approach: experienced-based approach
➢ Physical activity: ≥ 150 minutes of moderate-intensity aerobic activity weekly
• Strenuous exercise: hypoglycemia
• Establish a safe balance: activity, caloric intake, insulin
Insulin Products:
Insulin Combo Products:
Y II (NURS 432) STUDY SHEET FOR
QUIZ 3 (a comprehensive and
thorough review of all the material
that will be tested on Quiz 3 in this
course) PACE UNIVERSITY.
,NURS 432 – Pathophysiology/Pharmacology II Exam 3 Study
Sheet
Endocrine System
(Patho Chapter 10)
Pancreas & Diabetes Mellitus: (Chapter 57)
Metabolic Consequences of Insulin Deficiency: insulin deficiency puts the body into catabolic
mode
➢ In the absence of insulin:
• Glycogen: converted into glucose
• Proteins: degraded into amino acids
• Fats: converted to glycerol & free fatty acids
➢ Insulin deficiency promotes hyperglycemia via:
• Increased glycogenolysis:
breakdown of glycogen into free
glucose
• Increased gluconeogenesis:
generation of glucose; due to amino
acids & fatty acids produced from
metabolic breakdown of proteins &
fats
• Reduced glucose utilization: due
to ↓ cellular uptake of glucose and
↓ conversion of glucose to glycogen
T1DM vs T2DM:
➢ Type-1 Diabetes Mellitus: aka Child-onset DM or Insulin-dependent DM
• Onset: typically develops during childhood or adolescence
• Patho: involves autoimmune destruction of pancreatic beta cells
• Treatment: insulin supplementation
• DKA:
➢ Type-2 Diabetes Mellitus: aka Adult-onset or Insulin-independent DM
• Onset: typically develops in adulthood
• Genetics: strong familial association/predisposition
• Patho: insulin is still produced, however, there’s reduced binding, # of receptors &
receptor responsiveness
• Treatment: initially may be managed w/ lifestyle modifications (i.e., diet)
o Drug Tx: PO meds progression to insulin
• HHNS: (hyperglycemic hyperosmolar nonketotic syndrome) involves very high
blood sugar levels and can be life threatening
o Prevalence: more common in older people who have T2DM, but can happen to
anyone
➢ Complications:
• Short term: hyperglycemia, hypoglycemia
• Long term: HTN, HD, nephropathy, retinopathy, neuropathy, amputation
Gestational DM:
• Placental hormones: antagonize the actions of insulin
• Fetal hyperinsulinemia: glucose passes freely from maternal to the fetal circulation
• Duration & resolution: considering re-dx
• DOC Agents: insulin, metformin (2 line)
nd
Diabetes Diagnostics:
• Normal glucose: 70-110 mg/dL
➢ Fasting plasma glucose: (FPG) at least 8hrs after eating
, • Normal: <100 mg/dL
• Pre-diabetes: 100-125 mg/dL
• DM: ≥ 126 mg/dL
• If >200: advance to OGTT
➢ Casual plasma glucose test: no fasting
• DM: ≥ 200 mg/dL plus symptoms of diabetes
• Concurrent s/s: polyuria, polydipsia, rapid weight loss
➢ Oral glucose tolerance test: (OGTT) used when others not definitive; measured 2h post 75g
PO glucose
• Normal: < 140 mg/dL
• DM: ≥ 200 mg/dL
1
, ➢ HgbA1c: control over 3m
• DM: ≥ 6.5
• Target: <7 for most
• Inaccuracies: may be caused by pregnancy, CKD, liver DX, recent blood
loss or transfusions, or blood dx (thalassemia, Fe deficiency anemia, B12
deficiency anemia)
Lifestyle Modifications: used for all, regardless of drug therapy; continued w/ drug TX; may be
initial for T2DM
• Weight control
➢ Diet: carbohydrates, fat, proteins
• No ideal %: instead, based on current eating patterns, preferences, and goals
• Counting: calories
• Approach: experienced-based approach
➢ Physical activity: ≥ 150 minutes of moderate-intensity aerobic activity weekly
• Strenuous exercise: hypoglycemia
• Establish a safe balance: activity, caloric intake, insulin
Insulin Products:
Insulin Combo Products:
