NUR 239 Final Exam
Study online at https://quizlet.com/_6ksdez
1. What is -Beta cell destruction usually leading to absolute insulin deficiency.
the pathophysi- -Type IA: immune system destroys beta cells
ology of type 1 di- -Type IB: genetic cause
abetes?
2. What are the -Polyuria: increased urination
signs and symp- -Polydipsia: increased thirst
toms of type 1 di- -Polyphagia: increase hunger
abetes? -Weight loss
-Fatigue
-Increased frequency of infections
-Rapid onset
-Insulin dependent
-Familial tendency
-Peak incidence from 10-15 years
3. What is -May range from predominantly insulin resistance with relative insulin deficiency
the pathophysi- to a predominantly secretory defect with insulin resistance.
ology of type 2 di- -Result of beta-cell exhaustion due to long-standing insulin resistance.
abetes? -Genetics and family history put you at an increased risk
1. Stomach converts food to glucose
2. Glucose enters bloodstream
3. Pancreas produces sufficient insulin but it is resistant to effective use
4. Glucose unable to enter body effectively
5. Glucose levels increase
4. What are risks -Sedentary lifestyle
factors for type 2 -Familial tendency
diabetes? -Average age 50 years
-Hx of increased BP
-Fatigue and decreased energy
-Obese
, NUR 239 Final Exam
Study online at https://quizlet.com/_6ksdez
-Recurrent infections
-Polyuria
-Polydipsia
-FBS > 126 mg/dl
5. What are the -Insulin resistance -failure of target cells to respond to insulin. Often predated by
metabolic abnor- compensatory beta cell hyperfunction and hyperinsulinemia
malities? -Increased glucose production in liver - overproduction of glucose despite fasting
hyperinsulinemia
-Impaired secretion of insulin by pancreatic beta cells - may be result of decrease
in beta cell mass, increased apoptosis, decrease regeneration of beta cells, beta
cell exhaustion due to long standing insulin resistance
6. What are -BG > 600 mg/dL
the characteris- -High plasma osmolarity (pulls fluid out of cells and into extracellular fluid)
tics of hyper- -Severe dehydration, thirst
glycemia hyper- -Absence of ketoacidosis (suppressed by insulin available)
osmolar state? -Many neurological symptoms
-Insidious onset
-More common is Type 2 DM
-May also occur with MI, acute pancreatitis, severe infections, oral or parenteral
nutrition solutions
-Treatment similar to DKA, but with larger amounts of IV fluid replacement
7. What are the -Hyperglycemia: BG>250mg/dL
characteristics of -Begins with polyuria, polydipsia, N, V, fatigue, stupor
diabetic ketoaci- -Onset: over 4-10 hours
dosis and what -Causes: lack of insulin, GI upset, febrile illness
do they need to -Symptoms:
treat it? ^Breath smells like juicy fruit gum
^Kussmaul respirations
^Thirsty, dehydration, dry mouth
, NUR 239 Final Exam
Study online at https://quizlet.com/_6ksdez
^Stomach pain
^Sleepiness
^Increased pulse
^Vomiting
^Flushed face
^Tachycardia
^Hypotension
^Acidosis
^High Blood Sugar (>240mg/dl)
^Hyperkalemia
^Polyuria
-Patient will need hydration, insulin, and electrolyte replacement.
^Regular Insulin IV push and infusion
^K+ replacement
^IV fluids (NS at first, then add Dextrose as BG lowers)
^Frequent BS checks, labs
8. What diabetes 140-180mg/dL
patients are criti-
cal care?
9. What are -BG < 70
the character- -Low blood sugar symptoms
istics of hy- -Symptoms:
poglycemia and ^Headache
what do they ^Shaking
need? ^Hunger
^Weakness
^Feeling tired
^Sweating
^*T*achycardia
^*I*rritability
, NUR 239 Final Exam
Study online at https://quizlet.com/_6ksdez
^*R*estless
^*E*xcessive hunger
^*D*iaphoresis
^*D*epression
^Anxious
^Confusion
^Blurred/Double vision
^Cool, clammy skin
-Onset: Rapid. 1-3 hours.
-Causes: Insufficient food, excess exercise, excess insulin
-Patients need their blood sugar increased with glucose, glucagon, or dextrose
(IV)
10. What is the som- -Rebound hyperglycemia
ogyi effect? -Cycle of insulin induced post-hypoglycemic episodes
-Insulin induced hypoglycemia produces compensatory increase in blood levels
of catecholamines, glucagon, cortisol, growth hormone
-Causes blood glucose to become elevated
-Produces some degree of insulin resistance
-Hypoglycemic episode may occur at night
-Requires change in diet and dose or time of insulin
11. What is the blood -Hot and dry: sugar high
sugar mnemon- -Cold and clammy: need some candy
ic?
12. What are the -Angiopathy
chronic compli- -Peripheral vascular disease
cations of dia- -Retinopathy
betes? -Nephropathy
-Neuropathy
Study online at https://quizlet.com/_6ksdez
1. What is -Beta cell destruction usually leading to absolute insulin deficiency.
the pathophysi- -Type IA: immune system destroys beta cells
ology of type 1 di- -Type IB: genetic cause
abetes?
2. What are the -Polyuria: increased urination
signs and symp- -Polydipsia: increased thirst
toms of type 1 di- -Polyphagia: increase hunger
abetes? -Weight loss
-Fatigue
-Increased frequency of infections
-Rapid onset
-Insulin dependent
-Familial tendency
-Peak incidence from 10-15 years
3. What is -May range from predominantly insulin resistance with relative insulin deficiency
the pathophysi- to a predominantly secretory defect with insulin resistance.
ology of type 2 di- -Result of beta-cell exhaustion due to long-standing insulin resistance.
abetes? -Genetics and family history put you at an increased risk
1. Stomach converts food to glucose
2. Glucose enters bloodstream
3. Pancreas produces sufficient insulin but it is resistant to effective use
4. Glucose unable to enter body effectively
5. Glucose levels increase
4. What are risks -Sedentary lifestyle
factors for type 2 -Familial tendency
diabetes? -Average age 50 years
-Hx of increased BP
-Fatigue and decreased energy
-Obese
, NUR 239 Final Exam
Study online at https://quizlet.com/_6ksdez
-Recurrent infections
-Polyuria
-Polydipsia
-FBS > 126 mg/dl
5. What are the -Insulin resistance -failure of target cells to respond to insulin. Often predated by
metabolic abnor- compensatory beta cell hyperfunction and hyperinsulinemia
malities? -Increased glucose production in liver - overproduction of glucose despite fasting
hyperinsulinemia
-Impaired secretion of insulin by pancreatic beta cells - may be result of decrease
in beta cell mass, increased apoptosis, decrease regeneration of beta cells, beta
cell exhaustion due to long standing insulin resistance
6. What are -BG > 600 mg/dL
the characteris- -High plasma osmolarity (pulls fluid out of cells and into extracellular fluid)
tics of hyper- -Severe dehydration, thirst
glycemia hyper- -Absence of ketoacidosis (suppressed by insulin available)
osmolar state? -Many neurological symptoms
-Insidious onset
-More common is Type 2 DM
-May also occur with MI, acute pancreatitis, severe infections, oral or parenteral
nutrition solutions
-Treatment similar to DKA, but with larger amounts of IV fluid replacement
7. What are the -Hyperglycemia: BG>250mg/dL
characteristics of -Begins with polyuria, polydipsia, N, V, fatigue, stupor
diabetic ketoaci- -Onset: over 4-10 hours
dosis and what -Causes: lack of insulin, GI upset, febrile illness
do they need to -Symptoms:
treat it? ^Breath smells like juicy fruit gum
^Kussmaul respirations
^Thirsty, dehydration, dry mouth
, NUR 239 Final Exam
Study online at https://quizlet.com/_6ksdez
^Stomach pain
^Sleepiness
^Increased pulse
^Vomiting
^Flushed face
^Tachycardia
^Hypotension
^Acidosis
^High Blood Sugar (>240mg/dl)
^Hyperkalemia
^Polyuria
-Patient will need hydration, insulin, and electrolyte replacement.
^Regular Insulin IV push and infusion
^K+ replacement
^IV fluids (NS at first, then add Dextrose as BG lowers)
^Frequent BS checks, labs
8. What diabetes 140-180mg/dL
patients are criti-
cal care?
9. What are -BG < 70
the character- -Low blood sugar symptoms
istics of hy- -Symptoms:
poglycemia and ^Headache
what do they ^Shaking
need? ^Hunger
^Weakness
^Feeling tired
^Sweating
^*T*achycardia
^*I*rritability
, NUR 239 Final Exam
Study online at https://quizlet.com/_6ksdez
^*R*estless
^*E*xcessive hunger
^*D*iaphoresis
^*D*epression
^Anxious
^Confusion
^Blurred/Double vision
^Cool, clammy skin
-Onset: Rapid. 1-3 hours.
-Causes: Insufficient food, excess exercise, excess insulin
-Patients need their blood sugar increased with glucose, glucagon, or dextrose
(IV)
10. What is the som- -Rebound hyperglycemia
ogyi effect? -Cycle of insulin induced post-hypoglycemic episodes
-Insulin induced hypoglycemia produces compensatory increase in blood levels
of catecholamines, glucagon, cortisol, growth hormone
-Causes blood glucose to become elevated
-Produces some degree of insulin resistance
-Hypoglycemic episode may occur at night
-Requires change in diet and dose or time of insulin
11. What is the blood -Hot and dry: sugar high
sugar mnemon- -Cold and clammy: need some candy
ic?
12. What are the -Angiopathy
chronic compli- -Peripheral vascular disease
cations of dia- -Retinopathy
betes? -Nephropathy
-Neuropathy
