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NUR 146 Lecture > Week 1 & 2 - Diabetes > Flashcards

Week 1 & 2 - Diabetes Flashcards

1
Q

Describe Diabetus Mellitus

A

A group of metabolic diseases characterized by:

(Causes):
- Decreased insulin secretion / Insulin deficiency
- Insulin resistance

Which leads to hyperglycemia (high blood sugar levels)

Prolonged hyperglycemia affects nearly all body tissue, and it’s associated with various complications

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2
Q

LECTURE OBJECTIVE - Differentiate the (3) types of Diabetes

A

Type 1 Diabetes Mellitus (insulin dependent):
- Typically occurs in younger people
- Cause unknown; may result from autoimmune process

Type 2 Diabetes Mellitus (non-insulin dependent):
- Defects in insulin release and use + insulin resistance
- Common in diabetic patients

Gestational Diabetes Mellitus
- Glucose intolerance of any degree during pregnancy

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3
Q

LECTURE OBJECTIVE (Differentiating Types of Diabetes)

Type 1 Diabetes Mellitus Pathophysiology

Patho
Effect on Kidneys
Effect on Energy Production

A
  • Destruction of (Beta) islet cells in pancreas leads to insufficient insulin and excess glucagon
  • Hyperglycemia (high blood sugar) occurs

Kidneys:
- Hyperglycemic blood going to kidneys causes glycosuria (excess glucose in urine) and osmotic diuresis (excess urine production d/t excess glucose holding onto water)
Energy:
- Body can’t use carbs, instead uses fats and proteins for energy which = ketosis & weight loss
- Results in: polyphagia (insatiable hunger) and fatigue

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4
Q

LECTURE OBJECTIVE (Differentiating Types of Diabetes)

Pathophysiology: Type 2 Diabetes Mellitus

A
  • Normally, insulin binds to cell receptors and causes reaction for glucose metabolism
  • But in T2DM, these intracellular reactions are diminished which = insulin less effective at causing glucose uptake and regulating gluconeogenesis by liver
  • If beta cells cannot keep up, blood glucose rises and T2DM develops
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5
Q

LECTURE OBJECTIVE (Differentiating Types of Diabetes)

Pathophysiology: Gestational Diabetes Mellitus

A
  • Placental hormones cause insulin resistance which = development of hyperglycemia
  • Anti-insulin effects of Progesterone, cortisol and placenta lactogen increase amount of insulin needed to maintain glycemic control
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6
Q
A
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7
Q

What are the hormones and enzymes produced by the pancreas?

A

Hormones:
Beta cells - Insulin
Alpha cells - Glucagon
Somatostatin - Delta Cells

Enzymes:
Amylase
Lipase

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8
Q

Describe insulin action

A

Insulin = “Use the ‘free’ glucose, and hang on to all the stored energy”

Glucose

  • Increase Glycogenesis; insulin stimulates liver and muscles to store excess glucose as glycogen

Fats
- Increased lipogenesis; glucose transport into adipose cells for storage
- Inhibits lipolysis: breakdown of fat

Liver
- Inhibits glycogenolysis: conversion of stored glycogen to glucose
- Inhibits gluconeogenesis: production of new glucose

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9
Q

What is insulin release normally stimulated by?

A

Stimulated:
-Parasympathetic stimulation: ()
-Elevated serum glucose: (Glucose intake, then needs to be stored)
-Increased GI hormones:
-Increased serum potassium:

Inhibited:
- Sympathetic

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10
Q

Effects of insulin on:
Glucose
Fats
Liver
Protein
Potassium

A

Glucose - Mobilizes to be used as energy
- Increased glycogenesis - transport of glucose into cells, resulting in increased glycogen synthesis

Fats:
- Increases lipogenesis - glucose transport into adipose cells for storage
- Inhibits lipolysis - Breakdown of fat

Liver:
- Inhibits glycogenolysis - conversion of stored glycogen to glucose

Protein:
- Facilitates transport of amino acids into cells

Potassium:
- Facilitates intracellular transport of potassium

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11
Q

Glucagon:

Function
Stimulation for release/

A

Acts to keep blood glucose elevated
(antagonist to insulin)

Stimulated by:
- Sympathetic stimulation
- Decreased serum glucose
- Secretion of growth hormone

Decreased stimulation by:
- Increased glucose levels

Functions:
- Stimulates glycogenolysis (breakdown glycogen into glucose)
- Stimulates gluconeogenesis (make new glucose)
- Enhances lipolysis (breakdown fats)

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12
Q

Manifestations of Type 1 Diabetes

A

“The 3 P’s”
- Polyuria - Frequent urinating
- Polydipsia - Frequent drinking
- Polyphagia - Frequent eating

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13
Q

Identify diagnostic studies as it relates to diagnosis and management of diabetes mellitus

A
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14
Q

Explain the relationship between diet and glycemic control

A

How fast the blood sugar rises after eating something

Goal for diabetes patients:
- Prevent “rollercoaster” of blood sugar spikes

High GI may also lead to sugar crash, low GI helps provide steady energy

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15
Q

What is the relationship of Diabetes Patients and Alcohol Consumption?

A
  • Patients can have in moderation
  • BUT, liver gets busy breaking down alcohol
  • ## Liver then can’t produce glucose, which leads to hypoglycemia
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16
Q

Explain the relationship between exercise and glycemic control/diabetes

A

Patients should exercise at the same time, preferably whenever blood sugar is highest

  • Lowers blood glucose
  • Lower cardiovascular risk
  • Weight loss

Pt with diabetes lack physical sensation, make sure they have good shoes

17
Q

Exercise precautions for diabetes patients

A

Avoid exercise if:
- Blodo sugar >250 mg/dl
- Ketones in urine

If pt is on insulin:
- Eat 15g CHO prior to exercise
- Monitor for delayed hypogylcemia

  • Pt should inform others of thei diabetes
  • Pt should get cardiac clearance
18
Q

Describe pharmacologic modalities used to manage blood glucose, including insulin and oral antidiabetic agents

A
19
Q

Describe oral antidiabetic meds used to manage blood glucose, including insulin and oral antidiabetic agents:

Glucophage (metformin)

A

Only for pt with Type 2

Mechanism of action:
- Inhibits production of glucose by liver
- Increases tissue sensitivity to insulin + increases insulin uptake
- Decreases hepatic synthesis of cholesterol

Beneficial features:
- Improved glycemic control in most patients
- Effective as monotherapy

Major side effect of all is hypoglycemia (drug does their job too well)

20
Q

Dipeptidyl Peptidase-4

Januvia (sitagliptin)

A

Mechanism of Action:
- Prolongs the action of incretin
- Results in improved glucose control

Side effects:
- Frequent URIs
- Headache
-GI Side effects
- Hypoglycemia if combined with sulfonylurea

21
Q

Trulicity (dulaglutide)

A

Mechanism of action:
- Enhances glucose dependent insulin secretion
- Incretin mimetic

Side effects:
- Pancreatitis
- Weight loss
- GI effects

22
Q

Ozempic (semaglutide)

A
23
Q

Mounjaro (tirezepatide)

A

Incretin mimetic

Side effects:
- Pancreatitis
- GI symptoms
- Weight loss
- Hypoglycemia

24
Q
A
25
Q

Implement the nursing process as a framework for care of a patient with diabetes mellitus

A
26
Q

Understanding the importance of self-care and prevention of long-term complications

A
27
Q

What is Glycemic Index?

A

How fast the blood sugar rises after eating something

Goal for diabetes patients:
- Prevent “rollercoaster” of blood sugar spikes

High GI may also lead to sugar crash, low GI helps provide steady energy

28
Q

Describe potential complications of diabetes mellitus, including DKA, HHS and long-term complications

A
29
Q

Complications of diabetes:

Hypoglycemia

A

Causes:
- Too much insulin
- Result of oral hypoglycemic agents
- Excessive physical activity

Timing:
- Can occur day or night
- Often occurs just before meals or if meals are delayed
- Can occur when insulin levels are peaking

Mild s/s: sympathetic nervous stimulation; sweating, tremors, tachycardia, palpitations

Moderate s/s: CNS stimulation, brain deprived of energy; trouble concentrating, headache, memory lapses, confusion, slurred speech

30
Q

Diabetic KetoAcidosis (DKA)

A

More common in Type 1 Diabetes Mellitus; caused by insulin deficit

Patho:
- Insulin deficit
- Gluconeogenesis leads to hyperglycemia
- Kidneys attempt to eliminate glucose –> osmotic diuresis –> dehydration, electrolyte loss
- Lipolysis results in production of ketone bodies (which are acidic)

Clinical features aka “What to look for”:
- Hyperglycemia
- Dehydration, electrolyte losses
- Acidosis

s/s:
- Ketonemia, ketonuria
- Fruity ordor
- Dry mucus membranes
- Hypotension, tachycardia
- Blurred vision, weakness, headache
- Kussmaul respirations

DKA Diagnostic Findings:
- Blood Glucose levels 250 - 800 mg/dl
- Metabolic acidosis: low pH, low serum HCO3, low PCO2
- Ketone bodies in blood and urine
- Evidence of dehydration: elevated Hct, BUN, creatinine
- Sodium and potassium abnormalities 7

31
Q

Hyperglycemic Hyperosmolar Syndrome (HHS)

A

Usually in Type 2 Diabetes

Mortality rate: 5-16%

Causes:
- Relative insulin deficiency secondary to increased demands
- Physiologic stress
- Dialysis
- Medications

Pathophysiology
- Hyperglycemia –> hyperosmolarity –> osmotic diuresis –> dehydration, electrolyte imbalances –> intracellular to extracellular shifts

Clinical manifestations:
- Hypotension, tachycardia
- Profound dehydration
- Altered level of consciousness, seizures

Diagnostic findings:
- Blood Glucose >600mg/dl
- Osmolality >320 mOsm/kg
- Elevated BUN, creatinine
- Mental status changes secondary to cerebral dehydration
- No ketosis, normal pH

32
Q

Gestational Diabetes

A

Any degree of glucose intolerance with onset during pregnancy

  • Usually diagnosed in 2nd or 3rd trimesters; often resolves after birth of fetus

Treated with insulin

33
Q

Latent Autoimmune Diabetes of Adults

A
34
Q

Prediabetes

A

Impaired glucose tolerance or impaired fasting glucose

  • Blood glucose values higher than normal, but lower than classified diabetes
  • Often leads to diagnosis of diabetes
35
Q

Long Term Complications prevention:

Macrovascular Complications

A

Prevention:

  • Risk factor modification
  • Diet, exercise, smoking cessation
  • Glycemic control
36
Q

Long term complications prevention:

Microvascular

A

Retinopathy - Vessel damage of retinal vessels

Management:
- Glycemic control, smoking cessation, BP Control
- Laser surgery

Nephropathy - Kidney disease secondary to diabetic microvascular changes

Management:
- Glycemic control, BP Control, avoid neprhotoxic agents, low sodium, low protein diet
- ESRD: Dialysis or transplant

37
Q

Long Term Complications prevention:

Neuropathy

A

Peripheral neuropathy - Affects distal portion of nerves

Management:
- Glycemic control, pain meds prn

Autonomic neuropathy:
- Autonomic (fight or flight) nervous system

Management:
- Specific to symptoms

NUR 146 Lecture (5 decks)

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