NRSG 265 exam/ Questions with correct verified
answers/ 100% guaranteed pass/ 2025 EDITION!!/
RATED A+
Cause of T1DM - ANSWER 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 - ANSWER 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 - ANSWER 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 - ANSWER hypoglycaemia, DKA
T1DM management - ANSWER Insulin, BGL monitoring, meal planning, annual health checks,
exercise plan
,T2DM causes - ANSWER caused by insulin resistance at target tissues and a relative insulin
deficiency
T2DM risk factors - ANSWER genetic factors and family history, overweight and obese, hx of
gestational diabetes
T2DM pathophysiology - ANSWER 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 - ANSWER 3 P's (polyphagia, polyuria, polydipsia), fatigues,
hyperglycaemia, repeated infections, poor wound healing, blurred vision, weight changes
T2DM acute complications - ANSWER Hyperglycaemia, HHS
T2DM management - ANSWER Healthy diet, Exercise, close BGL monitoring, possible need for
oral hypoglycaemic agents, insulin
Biguanides (Metformin) - ANSWER Decreased hepatic release of glucose, decreases intestinal
absorption of glucose, improves insulin sensitivity by increasing peripheral uptake of glucose -->
reduced BGL
Sulphonylureas (gliceride) - ANSWER stimulates insulin secretion from the beta cells -->
hypoglycaemia
T1DM pathophysiology - ANSWER 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
interventions for DKA and HHS - ANSWER Fluid resus, reverse hyperglycaemia, correct acid base
& electrolyte balance, cardiac monitoring, 1/24 obs
Recurrent infections with diabetes causes - ANSWER Neuropathy, impaired vision, high glucose
environment
HbA1C - ANSWER 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) - ANSWER Blood vessel disorder that is
included in the general category of atherosclerosis
can be asymptomatic or develop as chronic/stable angina
Myocardial Ischaemia - ANSWER 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 - ANSWER pain (may radiate to neck, lower jaw, left arm, left shoulder
occasionally back or down right arm), pallor, diaphoresis, dyspnoea
Angina - ANSWER imbalance between myocardial oxygen demand and supply --> ischemia --
>insufficient oxygen to meet cardiac needs = decreased tissue perfusion = angina sectors (chest
pain)
, Angina clinical manifestions - ANSWER 3-5mins pain, chest discomfort (heaviness and pressure),
radiation of pain to L arm, pallor, dyspnoea
Angina management - ANSWER drugs reduce oxygen demands
nitrates (GTN, anginine)
adverse effects: hypotension, flushing, headache, fainting
Nitrates MOA - ANSWER Nitrates metabolised and converted to nitric oxide (NO) in vessel walls
--> No vasodilation of blood vessels --> decreased preload and after load --> decreased SV -->
decreased CO --> Decreased O2 demands --> reduced cardiac workload
acute myocardial infarction - ANSWER result of sustained ischaemia, causing irreversible
myocardial cell death (necrosis), loss of contractile function (STEMI or NSTEMI)
Atrial fibrillation - ANSWER rapid, random, ineffective contractions of the atrium. P waves
replaced by chaotic, fibrillary waves
causes a decrease in CO and an increased risk of stroke
atrial fibrillation management - ANSWER Drugs that control ventricular rate and/or convert to
sinus rhythm, electrical cardioversion, anticoagulation, radio frequency ablation
Heart Failure - ANSWER inadequate cardiac pumping/filling, insufficient blood supply/oxygen to
tissues
ACE inhibitors - ANSWER widen/dilate blood vessels that increases CO and lower BP, raise blood
flow that reduced the hearts workload
Inhibits the enzyme ACE -> no conversion to Ag II --> no vasoconstriction --> no release of
aldosterone --> no Na+ and water retention --> decreased BP
answers/ 100% guaranteed pass/ 2025 EDITION!!/
RATED A+
Cause of T1DM - ANSWER 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 - ANSWER 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 - ANSWER 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 - ANSWER hypoglycaemia, DKA
T1DM management - ANSWER Insulin, BGL monitoring, meal planning, annual health checks,
exercise plan
,T2DM causes - ANSWER caused by insulin resistance at target tissues and a relative insulin
deficiency
T2DM risk factors - ANSWER genetic factors and family history, overweight and obese, hx of
gestational diabetes
T2DM pathophysiology - ANSWER 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 - ANSWER 3 P's (polyphagia, polyuria, polydipsia), fatigues,
hyperglycaemia, repeated infections, poor wound healing, blurred vision, weight changes
T2DM acute complications - ANSWER Hyperglycaemia, HHS
T2DM management - ANSWER Healthy diet, Exercise, close BGL monitoring, possible need for
oral hypoglycaemic agents, insulin
Biguanides (Metformin) - ANSWER Decreased hepatic release of glucose, decreases intestinal
absorption of glucose, improves insulin sensitivity by increasing peripheral uptake of glucose -->
reduced BGL
Sulphonylureas (gliceride) - ANSWER stimulates insulin secretion from the beta cells -->
hypoglycaemia
T1DM pathophysiology - ANSWER 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
interventions for DKA and HHS - ANSWER Fluid resus, reverse hyperglycaemia, correct acid base
& electrolyte balance, cardiac monitoring, 1/24 obs
Recurrent infections with diabetes causes - ANSWER Neuropathy, impaired vision, high glucose
environment
HbA1C - ANSWER 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) - ANSWER Blood vessel disorder that is
included in the general category of atherosclerosis
can be asymptomatic or develop as chronic/stable angina
Myocardial Ischaemia - ANSWER 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 - ANSWER pain (may radiate to neck, lower jaw, left arm, left shoulder
occasionally back or down right arm), pallor, diaphoresis, dyspnoea
Angina - ANSWER imbalance between myocardial oxygen demand and supply --> ischemia --
>insufficient oxygen to meet cardiac needs = decreased tissue perfusion = angina sectors (chest
pain)
, Angina clinical manifestions - ANSWER 3-5mins pain, chest discomfort (heaviness and pressure),
radiation of pain to L arm, pallor, dyspnoea
Angina management - ANSWER drugs reduce oxygen demands
nitrates (GTN, anginine)
adverse effects: hypotension, flushing, headache, fainting
Nitrates MOA - ANSWER Nitrates metabolised and converted to nitric oxide (NO) in vessel walls
--> No vasodilation of blood vessels --> decreased preload and after load --> decreased SV -->
decreased CO --> Decreased O2 demands --> reduced cardiac workload
acute myocardial infarction - ANSWER result of sustained ischaemia, causing irreversible
myocardial cell death (necrosis), loss of contractile function (STEMI or NSTEMI)
Atrial fibrillation - ANSWER rapid, random, ineffective contractions of the atrium. P waves
replaced by chaotic, fibrillary waves
causes a decrease in CO and an increased risk of stroke
atrial fibrillation management - ANSWER Drugs that control ventricular rate and/or convert to
sinus rhythm, electrical cardioversion, anticoagulation, radio frequency ablation
Heart Failure - ANSWER inadequate cardiac pumping/filling, insufficient blood supply/oxygen to
tissues
ACE inhibitors - ANSWER widen/dilate blood vessels that increases CO and lower BP, raise blood
flow that reduced the hearts workload
Inhibits the enzyme ACE -> no conversion to Ag II --> no vasoconstriction --> no release of
aldosterone --> no Na+ and water retention --> decreased BP
