Nurs 1873 UPDATED ACTUAL Questions and CORRECT
Answers
Type 2 diabetes sedentary life style, familial tendency, avg age 50 year, hx of high bp, obese
recurrent infections, polyuria, polydipsia, fbs > 126 mg/dl
DKA Tachycardic, hypotensive, acidosis, high BS > 240 mg/dl, hyperkalemia,
polyuria, breath smells like juicy fruit, kussmal respirs, dehydration, thirsty,
, History of DKA -Lack of Insulin, GI upset, and Febrile illness
Onset of DKA 4-10 hrs
Physiology of High glucose in the blood Insulin is released and pushes glucose into the cells to provide energy, glucose
is received by the insulin receptor thereby decreasing blood glucose
Physiology of low glucose in the blood Glucagon is released which turns to glycogen which breaks down glucose
thereby increasing the blood sugar
Type 1 diabetes disorder in which the body cannot produce enough insulin (immune d/o)
-insulin dependent
-prevalence is 5-10%
-Autoimmune in origin, genetics
-Ketosis-related
-3 P's
Type 2 diabetes progressive disorder in which body cells become less responsive to insulin
-formerly know as adult-onset db or non-insulin dependent
-most prevalent type 90-95%
-Many risk factors: obesity, advanced age, family history,
-Greater prevalence in ethnic groups
-Pancreas continue to produce some endogenous insulin but not enough
-Some modifiable risk factors (obesity, diet)
-3 P's
Basal-bolus intensive therapy It consists of multiple daily insulin injections or an insulin pump together with
frequent BGM or CGM. Injections include rapid- or short-acting (bolus) insulin
before meals and intermediate- or long-acting (basal) background insulin once
or twice a day.
counterregulatory hormones Work against the effects of insulin (glucagon, epinephrine, growth hormone
[GH], cortisol)
1.) Increase glucose levels by stimulating glucose and release by the liver and
2.) decreasing movement of glucose into cells
Dawn phenomenon Hyperglycemia present on awakening (hormones responsible are cortisol and
GM)
Somogyi effect early-morning hyperglycemia that occurs as a result of nighttime hypoglycemic
episodes from night-time insulin so then the counterregulatory hormones work
to produce more insulin (glucagon, epinephrine, growth hormone [GH],
cortisol)
Answers
Type 2 diabetes sedentary life style, familial tendency, avg age 50 year, hx of high bp, obese
recurrent infections, polyuria, polydipsia, fbs > 126 mg/dl
DKA Tachycardic, hypotensive, acidosis, high BS > 240 mg/dl, hyperkalemia,
polyuria, breath smells like juicy fruit, kussmal respirs, dehydration, thirsty,
, History of DKA -Lack of Insulin, GI upset, and Febrile illness
Onset of DKA 4-10 hrs
Physiology of High glucose in the blood Insulin is released and pushes glucose into the cells to provide energy, glucose
is received by the insulin receptor thereby decreasing blood glucose
Physiology of low glucose in the blood Glucagon is released which turns to glycogen which breaks down glucose
thereby increasing the blood sugar
Type 1 diabetes disorder in which the body cannot produce enough insulin (immune d/o)
-insulin dependent
-prevalence is 5-10%
-Autoimmune in origin, genetics
-Ketosis-related
-3 P's
Type 2 diabetes progressive disorder in which body cells become less responsive to insulin
-formerly know as adult-onset db or non-insulin dependent
-most prevalent type 90-95%
-Many risk factors: obesity, advanced age, family history,
-Greater prevalence in ethnic groups
-Pancreas continue to produce some endogenous insulin but not enough
-Some modifiable risk factors (obesity, diet)
-3 P's
Basal-bolus intensive therapy It consists of multiple daily insulin injections or an insulin pump together with
frequent BGM or CGM. Injections include rapid- or short-acting (bolus) insulin
before meals and intermediate- or long-acting (basal) background insulin once
or twice a day.
counterregulatory hormones Work against the effects of insulin (glucagon, epinephrine, growth hormone
[GH], cortisol)
1.) Increase glucose levels by stimulating glucose and release by the liver and
2.) decreasing movement of glucose into cells
Dawn phenomenon Hyperglycemia present on awakening (hormones responsible are cortisol and
GM)
Somogyi effect early-morning hyperglycemia that occurs as a result of nighttime hypoglycemic
episodes from night-time insulin so then the counterregulatory hormones work
to produce more insulin (glucagon, epinephrine, growth hormone [GH],
cortisol)
