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NUR 325 Funds of Pathopharm > Week 3 Diabetes > Flashcards

Week 3 Diabetes Flashcards

1
Q

Diabetes

A

Metabolic disorder characterized by hyperglycemia that results from defects in insulin secretion, insulin action, or both

Extensive long-term damage when uncontrolled

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2
Q

What are carbs? Where are they broken down?

A

Simple and complex sugar

Duodenum and proximal jejunum

Blood glucose levels temp rise then lower back to baseline

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3
Q

Where does glucose break down?

A

Liver

  • Extracts glucose
  • Synthesizes it into glycogen (energy storage)
  • Glycogenolysis ( breakdown glycogen)

Muscle and fat cells
- Extract the glucose for their energy need

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4
Q

Pancreas

A

Controls glucose/insulin

Exocrine: secrete directly into ducts (NOT BLOODSTREAM)

Endocrine: secrete insulin directly into bloodstream

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5
Q

Islet of langerhans

A

Small islands of cells within the pancreas that make up the endocrine function

Alpha cells: secrete glucagon in response to low blood sugar
Beta cells: produce insulin, lowering glucose levels

Glucagon: stimulates the liver to release stored glucose into the blood

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6
Q

What lowers blood glucose levels?

A

Insulin

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7
Q

What raises blood glucose levels?

A
  • Glucagon
  • Epinephrine
  • Glucocorticoids
  • Growth hormone
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8
Q

What is insulin?

A
  • A hormone secreted by the pancreas (beta cells)
  • Stimulates uptake, utilization, and storage of glucose
  • Stimulates the liver to store glucose (glycogen)
  • Insulin decreases plasma concentrations of glucose
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9
Q

Insulin and lipid metabolism

A
  • Insulin promotes fatty acid synthesis in the liver
  • Insulin inhibits the breakdown of fat in adipose tissue
  • Insulin drives cells to use CHO instead of fat or energy
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10
Q

What happens when you don’t have enough insulin?

A
  • Cannot breakdown CHO efficiently
  • Decreased glucose use by cells

LEADING TO…

  • Rapid build up of glucose in blood = hyperglycemia
  • Cells use alternate sources for energy which is bad
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11
Q

What does insulin deficiency do to FFAs?

A
  • Increase lipolysis (fat breakdown)
  • Causing more FFAs in blood leading to higher cholesterol (long term)
  • FFAs can also break down to acetyl-CoA
  • Create ketone bodies causing metabolic acidosis (short term)
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12
Q

How does insulin deficiency affect protein metabolism?

A
  • Body unable to store protein effectively
  • Increased protein catabolism = muscle wasting
  • Cessation of protein synthesis = use alternate energy source
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13
Q

Insulin deficiency and Glycosuria

A
  • Excretion of sugar in the urine

- Increases acetones in urine

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14
Q

What are the 3 Ps of s/s with diabetes?

A

Polyphagia

Polydipsia

Polyuria

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15
Q

T1D

A
  • Most common pediatric chronic disease
  • Usually diagnosed around 12 yo
  • Can be idiopathic
  • Usually an autoimmune process; genetic predisposition, slowly progressive t-cell mediated disease that destroys beta cells
  • Complete lack of endogenous insulin
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16
Q

T1D clinical manifestations

A
  • Diagnosed 11-13 years old
  • Hyperglycemia
  • Same diagnostic criteria as T2
  • S/S: 3 Ps, weight loss, fatigue, recurrent infections, prolonged wound healing, general pruritis, visual changes, parathesias, cardiovascular symptoms
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17
Q

T2D risk factors

A
  • Genetic/environmental aspect usually responsible
  • Age, obesity, HTN, physical inactivity, family hx
  • INSULIN RESISTANCE
18
Q

T2D clinical manifestations

A
  • Symptoms are not as evident in T2D
  • Usually vague manifestations of hyperglycemia
    • Fatigue, recurrent infections, visual changes, prolonged wound healing
  • Drs usually test those at high risk - overweight, dyslipidemic, HTN
19
Q

Metabolic complications w/ T2D

A
  • Impaired insulin secretion -> B cell exhaustion due to overuse
  • Peripheral insulin resistance -> increased visceral fat
  • Increased hepatic glucose production -> impaired suppression of gluconeogenesis within the liver
  • Altered production of hormones and cytokines by adipose tissue
20
Q

Diabetic ketoacidosis (DKA)

A
  • More common in T1D
  • Serious complication r/t insulin deficiency
  • Hyperglycemia, acidosis, and ketonuria
21
Q

Hyperosmolar hyperglycemic syndrome. (HHNS)

A
  • T2D complication
  • High hyperglycemia and osmolality, normal pH
  • Less profound insulin deficiency than DKA but more significant fluid deficiency
22
Q

Acute complications of diabetes: Hypoglycemia

A
  • Happens in both T1 and T2
  • Rapid onset
  • Blood sugar <55-60
  • Usually r/t meds
23
Q

Symptoms of hypoglycemia

A
  • Pallor, sweating, tachycardia, palpitations, hunger, restlessness, anxiety, tremors, convulsion, coma
24
Q

Diabetic neuropathy

A
  • Most common complication of diabetes
  • Loss of pain, temp, and vibration sensations
  • Can lead to ulcers, infection, and amputation
25
Q

Diabetic Retinopathy

A
  • Leading cause of blindness

- Hypoxemia, damage to retinal blood vessels, RBC aggregation, and HTN

26
Q

Diabetic Nephropathy

A
  • Most common cause of chronic kidney disease and end stage kidney disease
  • Check feet and monitor kidneys
  • 50% of DM pts will get this
27
Q

4 types of insulin

A 
Rapid acting (lispro - humaLOG)
Short acting (human regular - Humulin R) 
Intermediate (NPH - Humulin N)
Long acting (Glargine - Lantus)
28
Q

Where do you inject insulin shots?

A

SQ in the back of arms, stomach, and thighs

29
Q

Rapid acting - insulin lispro

A

Onset: 15 min
Peak: 1 hour
Duration: 2-4 hours

  • Administered w/ meals
  • Must be used in combo w/ intermediate or long-acting
30
Q

Short acting - insulin regular

A

Onset: 30 - 60 min
Peak: 2 - 6 hours
Duration: 3 - 8 hours

  • Given before meals
  • Can be given for longer acting glycemic control
  • Hospital - tube feeding
  • Insulin infusions (IV)
31
Q

Intermediate acting insulin - NPH

A

Onset: 2 - 4 hours
Peak: 4 - 10 hours
Duration: 10 - 20 hours

  • Cloudy - need to shake before admin
  • BID to help w/ meals and throughout night
  • Combo w/ rapid and short acting
32
Q

Long acting insulin: Glargine (Lantus)

A

Onset: 70 min
Peak: None
Duration: 24 hours

  • QD dosing
  • Often given at night
  • Never mix w/ other insulins
33
Q

Insulin complications

A

Hypoglycemia

  • s/s: tachy, sweating, nervous, headache, drowsy, fatigue, decreased LOC
  • Tx: oral CHO, parenteral glucagon, IV dextrose

Lipodystrophies
- Feels hard at injection sites

Somogyi effect

  • OD insulin causing hypoglycemia
  • From poor DM management

Dawn phenomenon
- Hyperglycemia in the morning due to natural hormone release

34
Q

DM teaching points

A
  • Monitor glucose levels
  • Carry source of CHO for hypoglycemia (NOT CANDY)
  • Rotate insulin sites
  • Insulin vials are good for 30 days at room temp
35
Q

Sulfonylureas

A

glipizIDE, glyburIDE

MOA: Binding and closing the K-ATP channels in the pancreatic beta cells thereby stimulating secretion of insulin

Indication: Diabetes

Side Effect: Hypoglycemia, more likely from liver/kidney dysfunction

Nursing considerations: Do not take during pregnancy, ETOH, NSAIDs, Tagamet (heartburn), sulfa-based ATB potentiates SEs

36
Q

Biguanides

A

Metformin

MOA: lowers BG by decreasing production of glucose in the liver, enhances glucose uptake and utilization by muscle, does not promote insulin release from pancreas, no hypoglycemia

Indication: Diabetes, prevent T2D, PCOS

Side Effect: abdominal bloating, N/V/D, acidosis risk w/ elevated creatinine, NOT for elevated ALT levels

Nursing considerations: onset several days, peak 2-4 weeks, monitor serum glucose levels, give 30 min before meals, held 48 hours post IV contrast, do not use w/ HF, kidney failure, liver disease, or excessive ETOH intake

37
Q

DPP4 Inhibitors

A

linagLIPTIN, sazaGLIPTIN, sitaGLIPTON

MOA: inhibits DPP4 (enzyme that inactivates the incretin hormone), increases insulin release, reduces glucagon release, decreases hepatic glucose production, slows down digestion and decreases appetite

Indication: Diabetes

Side Effect: GI probs, flu-like symptoms, skin reactions, increased risk of pancreatitis

Nursing considerations: Use in combo w/ other lifestyle mod and diet, used alone or w/ other meds, no hypoglycemia

38
Q

GLP-1 Receptor Agonist

A

dulagluTIDE, exenaTIDE, semagluTiDE

MOA: enhances glucose dependent secretion, stimulates glucose-dependent release of insulin, inhibits postprandial release of glucagon, and suppresses appetite, slowed gastric emptying

Indication: Diabetes

Side Effect: N/V/D, injection site reactions, headache, upper respiratory infections, weight loss

Nursing considerations: Usually combo med, peak 2 hours, half life 2.5 hours (take often daily), BBW: thyroid c-cell tumors, not recommended for pt w/ ESRD or pancreatitis

**GILA MONSTER

39
Q

Sodium-Glucose Cotransporter 2 inhibitor (SGLT2)

A

dapagliFLOZIN

MOA: Prevents kidneys from reabsorbing glucose back into the blood (urine), block sodium-glucose transport proteins so that less glucose gets reabsorbed

Indication: Diabetes, increase use in HF and stop progression of kidney disease

Side Effect: UTIs, genital mycotic infections, HoTN, fainting, dizziness, fatigue

Nursing considerations: Not for ESRD or T1D pts, combo w/ other meds

40
Q

Glucagon

A

Hypoglycemia antidote

MOA: activates hepatic glucagon receptors, stimulates glycogenolysis and release of glucose

Indication: Diabetes

Side Effect: Dizziness, HoTN, nausea, headache

Nursing considerations: Short duration, may need multiple doses, check FSBG every 15 min post admin

41
Q

What do you caution when someone is diabetic but changing lifestyle?

A

At risk for hypoglycemia because exercise can lower BG levels

NUR 325 Funds of Pathopharm (10 decks)

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