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nrsg265 > NRSG exam > Flashcards

NRSG exam Flashcards

1
Q

How is BGL regulated?

A

Food consumed –> carbohydrate broken down into glucose –> increased BGL –> detected by pancreas –> beta cells release insulin
Low BGL –> alpha cells release glucagon

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2
Q

What does glucagon do?

A

Stimulates the liver to convert glycogen back into glucose
Stimulates the conversion of amino acids into glucose
Stimulates the liver to convert triglycerides and free fatty acids to glucose

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3
Q

What is DM?

A

Group of metabolic diseases characterised by chronic hyperglycemia due to issues with insulin secretion and/ or action

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4
Q

Define T1 DM

A

Beta cell destruction resulting in insulin deficiency (total lack of insulin production)

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5
Q

Define T2 DM

A

Impaired insulin action due to:

  • increased insulin resistance at target tissues due to reduced number of insulin binding sites and/ or decreased amount of insulin binding to receptors
  • decreased beta cell responsiveness to insulin
  • Decreased insulin production as disease progresses
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6
Q

What are the causes of T1 DM?

A

Autoimmune destruction of beta cells

Environmental and genetic factors trigger autoimmune response

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7
Q

What are the causes of T2 DM?

A 
Ethnicity
Age
Overweight
>35 years 
Genetics
Gestational DM
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8
Q

What are the acute complications of T1 DM?

A

DKA

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9
Q

What are the acute complications of T2 DM?

A

HHS

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10
Q

Describe the pathophysiology of T1 DM

A

Genetic factors + environmental factors –> immune response against beta cells –> beta cell destruction –> no insulin produced –> GLUT4 transporters are not activated –> glucose unable to be taken up by cells –> cell starvation –> compensatory release of glucagon by alpha cells + continued impaired glucose uptake –> hyperglycemia –> T1 DM

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11
Q

Describe the pathophysiology of T2 DM

A

Non-modifiable risk factors (age, genetics, ethnicity) + modifiable risk factors (lifestyle, diet, weight) –> increased adiposity –> increased free fatty acids (proinflammatory cytokines) –> chronic cell inflammation –> increased ROS –> oxidative stress –> liver and muscle cell damage –> decreased insulin production/ ineffective function –> increased BGL –> compensatory glucagon release from alpha cells + continued impaired glucose uptake –> hyperglycemia –> T2 DM

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12
Q

Explain how DM leads to the 3 Ps

A
  1. Polyphagia: impaired glucose uptake prevents cells from making ATP –> liver cells, muscle cells and adipose tissue break down glycogen and triglyceride stores to make glucose and ATP –> these stores eventually depleted –> cell starvation –> increased appetite
  2. Polyuria: excess glucose removed from blood by the kidneys –> glucose is a osmotic diuretic and draws water with it to the kidneys –> increased urine production
  3. Polydipsia: polyuria –> dehydration –> increased thirst sensation –> worsens polyuria –> worsens polydipsia
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13
Q

What is DKA?

A

Dangerously high blood ketones and metabolic acidosis related to hyperglycemia
Develops over hours - days

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14
Q

How does DKA occur?

A

Lack of insulin –> cells unable to take up and use glucose –> adipose tissue broken down to make ATP –> ketones produced as by-product and accumulate in blood –> ketoacidosis
Also: severe hyperglycemia –> osmotic diuresis –> fluid shifts from cells and loss of fluid through urine –> dehydration

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15
Q

What are the clinical manifestations of DKA?

A

Ketonic breath
Kussaml’s respirations
Polyuria
Polydipsia, sunken eyes, tachycardia, dry skin, headache, seizures, coma
Hypotension
Impaired cerebral functioning, lethargy, ALOC, seizures
BGL >11, ketones in urine

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15
Q

What are the clinical manifestations of DKA?

A

Ketonic breath
Kussaml’s respirations
Polyuria
Polydipsia, sunken eyes, tachycardia, dry skin, headache, seizures, coma
Hypotension
Impaired cerebral functioning, lethargy, ALOC, seizures
BGL >11, ketones in urine

16
Q

What is HHS?

A

Severe hyperglycemia, dehydration and high serum osmolality without ketoacidosis
Develops over days - weeks

17
Q

How does HHS occur?

A

Severe hyperglycemia –> excess glucose causing osmotic diuresis –> fluid shifts out of cells and into BVs –> excess glucose excreted in urine –> water follows –> dehydration –> increased osmotic solutes in blood –> hyperosmolality (high concentration of osmotically active solutes in blood) –> continued fluid loss –> hypotension, hypovolemia, dehydration, impaired perfusion –> ALOC, seizures, coma

18
Q

Why is there no ketone production in HHS?

A

HHS is a complication of T2DM; in T2DM insulin is still being produced (although it can’t be used) –> insulin inhibits ketogenesis (the breakdown of adipose tissue to make ATP), which is what produces the ketones

19
Q

What are the clinical manifestations of HHS?

A 
Polyuria
Polydipsia
Sunken eyes
Hypotension
Tachycardia
Headache
Fatigue
Seizures
ALOC
Coma
BGL >30mmol/L
No blood/ urine ketones
20
Q

What are the interventions for DKA and HHS in order of priority and the rationale for each?

A
  1. IV fluid resuscitation - 24 - 72 hours; increase intravascular volume so fluid moves back into cells
  2. Reverse hyperglycemia - IV insulin infusion +/- dextrose infusion; the underlying cause of the condition
  3. Correct acid-base and electrolyte imbalance - regular BGLs, monitor urine ketones, K+, Na+, urea, cardiac monitoring, fluid balance
  4. Regular vitals
21
Q

What causes hyoglycemia?

A

medication OD, not eating enough, exercise

22
Q

What are the clinical manifestations of hypoglycemia?

A 
Trembling 
Dizziness
Diaphoresis
Hunger
Headaches
Lack of coordination and concentration
Vision changes
seizures
ALOC
Coma
23
Q

What is the management of hypoglycemia?

A
  1. Check BGL
  2. Eat 15 - 20g fast acting carbohydrate
  3. Re-check BGL
  4. Eat 20g slow acting carbohydrate
    If unconscious:
  5. Position on side, ensure airway patency
  6. IV dextrose bolus or IM glucagon (if no IV access)
  7. One pt alert and stable eat 20g slow acting carbohydrate
24
Q

What does insulin do?

A

Enables glucose uptake into cells
Stores glucose as glycogen in muscle and liver cells
Inhibits the liver from producing glucose
Stimulates glucose to be stored as triglycerides in adipose tissue

25
Q

What is the role of OHAs?

A

Increase insulin action or encourage glucose uptake

26
Q

What happens to RBCs if DM is poorly managed?

A

Persistent hyperglycemia –> glucose irreversibly bound to RBCs –> AGEs produced (toxic metabolites)

27
Q

How does DM lead to retinopathy?

A

Hyperglycemia –> glucose bound to RBCs –> AGEs formed –> vasoconstriction –> hypertension –> increased pressure in retina and hemorrhage –> decreased perfusion –> ischaemia –> cell damage/ death

28
Q

How does DM lead to nephropathy?

A

Hyperglycemia –> glucose bound to RBCs –> AGE formation –> vasoconstriction –> hypertension –> increased glomerular blood flow –> increased GFR –> impaired filtration –> microalbuminuria –> kidney damage –> renal failure

29
Q

How does DM cause neuropathy

A

Hyperglycemia –> glucose bound to RBCs –> AGE formation –> vasoconstriction –> decreased nerve perfusion –> ischemia –> impaired nerve function and demyelination –> impaired nerve impulse transmission:

  • peripheral neuropathy: pins & needles, numbness in peripheries
  • autonomic neuropathy: incontinence, digestive issues
30
Q

How does DM lead to ATH

A

Hyperglycemia –> glucose binds to RBCs –> AGE formation –> decreased nitric oxide –> vasoconstriction –> hypertension –> endothelial injury
Also leads to increased vascular permeability –> monocytes and LDLs enter endothelium
AGE also promotes platelet aggregation

31
Q

How does hyperglycemia lead to peripheral vascular disease?

A

ATH formation due to AGE –> reduced peripheral perfusion –> ischemia -> pain, pallor, paresthesia, pulselessness –> necrosis

32
Q

How does hyperglycemia increase infection risk?

A
  1. Hyperglycemia impairs chemotaxis –> prevents WBCs migrating to site of inflammation –> prevents phagocytosis
  2. Hyperglycemia inhibits complement cascade activation –> complement cascade activation cause bacteria to become porous due to formation of protein channels –> fluid enters –> bacteria swell and burst
  3. AGE –> vasoconstriction –> impaired blood flow and delivery of WBCs, O2 etc required for healing
  4. High glucose environment good for bacterial growth
  5. Vision and sensation changes –> loss of early warning signs

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