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NRSG265 Exam Complete Questions and Correct Detailed Answers (Verified Answers)

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NRSG265 Exam Complete Questions and Correct Detailed Answers (Verified Answers)

Institution
Nrsg265
Course
Nrsg265

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March 25


NRSG265 Exam Complete Questions and Correct Detailed
Answers (Verified Answers)
Cause of T1DM


Ans: results from beta cell destruction leading to severe or absolute insulin
deficiency and chronic hyperglycaemia

2 types:

Idiopathic -beta cell destruction in the absence of autoimmune response

Non-immune mediated diabetes -secondary to other conditions -pancreatitis



Pathophysiology T1DM


Ans: Destruction of beta cells leads to very little/ no insulin production



GLUT-4s are not activated and glucose cannot be taken up by cells



Glucose continues to be released by liver - insulin is not available to regulate this
release. Increased production of glucagon --> continued glucose not being taken up
by the cells --> hyperglycaemia



T1DM Clinical Manifestations


Ans: The 3 P's (polydipsia, polyuria, and polyphagia), fatigue, weight loss, N & V
abdominal pain, confusion, weakness, tachycardia, ketonic breath, tachycardia,
tachypnoea, metabolic acidosis, seizures, coma



T1DM acute complications

pg. 1

, March 25
Ans: hypoglycaemia, DKA



T1DM management


Ans: Insulin, BGL monitoring, meal planning, annual health checks, exercise plan



T2DM causes


Ans: caused by insulin resistance at target tissues and a relative insulin deficiency



T2DM risk factors


Ans: genetic factors and family history, overweight and obese, hx of gestational
diabetes



T2DM pathophysiology


Ans: Decreased beta cell responsiveness to increased glucose levels, decreased
insulin production, increased insulin resistance at the cell (reduction in number of
binding sites, decreased in the amount of insulin biding to the receptors)



T2DM signs and symptoms


Ans: 3 P's (polyphagia, polyuria, polydipsia), fatigues, hyperglycaemia, repeated
infections, poor wound healing, blurred vision, weight changes



T2DM acute complications




pg. 2

, March 25
Ans: Hyperglycaemia, HHS



T2DM management


Ans: Healthy diet, Exercise, close BGL monitoring, possible need for oral
hypoglycaemic agents, insulin



Biguanides (Metformin)


Ans: Decreased hepatic release of glucose, decreases intestinal absorption of
glucose, improves insulin sensitivity by increasing peripheral uptake of glucose -->
reduced BGL



Sulphonylureas (gliceride)


Ans: stimulates insulin secretion from the beta cells --> hypoglycaemia



T1DM pathophysiology


Ans: genetic predisposition

immune response against beta cells

beta cell destructions

lack of insulin

GLUT-4s are not activated

glucose unable to be taken up

Hyperglycaemia




pg. 3

, March 25
interventions for DKA and HHS


Ans: Fluid resus, reverse hyperglycaemia, correct acid base & electrolyte balance,
cardiac monitoring, 1/24 obs



Recurrent infections with diabetes causes


Ans: Neuropathy, impaired vision, high glucose environment



HbA1C


Ans: assess long term control of diabetes, forms irreversibly from glucose and
haemoglobin

measures the average blood glucose throughout the life span



Coronary heart disease/coronary artery disease (CAD)


Ans: Blood vessel disorder that is included in the general category of atherosclerosis

can be asymptomatic or develop as chronic/stable angina



Myocardial Ischaemia


Ans: imbalance between oxygen supply and demand. Vasoconstriction
(atherosclerosis is a common cause) --> anaerobic respiration forms lactic acid -->
cells viable for 20mins --> cell death --> inflammation, granulation tissue formation
and scarring --> Thrombus



Manifestations of MI


pg. 4

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