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
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
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
4
Q
Pancreas
A
Controls glucose/insulin
Exocrine: secrete directly into ducts (NOT BLOODSTREAM)
Endocrine: secrete insulin directly into bloodstream
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
6
Q
What lowers blood glucose levels?
A
Insulin
7
Q
What raises blood glucose levels?
A
- Glucagon
- Epinephrine
- Glucocorticoids
- Growth hormone
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
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
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
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)
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
13
Q
Insulin deficiency and Glycosuria
A
- Excretion of sugar in the urine
- Increases acetones in urine
14
Q
What are the 3 Ps of s/s with diabetes?
A
Polyphagia
Polydipsia
Polyuria
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
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
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
Diabetic Retinopathy
- Leading cause of blindness
| - Hypoxemia, damage to retinal blood vessels, RBC aggregation, and HTN
26
Diabetic Nephropathy
- 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
4 types of insulin
```
Rapid acting (lispro - humaLOG)
Short acting (human regular - Humulin R)
Intermediate (NPH - Humulin N)
Long acting (Glargine - Lantus)
```
28
Where do you inject insulin shots?
SQ in the back of arms, stomach, and thighs
29
Rapid acting - insulin lispro
Onset: 15 min
Peak: 1 hour
Duration: 2-4 hours
* Administered w/ meals
* Must be used in combo w/ intermediate or long-acting
30
Short acting - insulin regular
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
Intermediate acting insulin - NPH
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
Long acting insulin: Glargine (Lantus)
Onset: 70 min
Peak: None
Duration: 24 hours
* QD dosing
* Often given at night
* Never mix w/ other insulins
33
Insulin complications
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
DM teaching points
- 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
Sulfonylureas
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
Biguanides
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
DPP4 Inhibitors
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
GLP-1 Receptor Agonist
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
Sodium-Glucose Cotransporter 2 inhibitor (SGLT2)
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
Glucagon
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
What do you caution when someone is diabetic but changing lifestyle?
At risk for hypoglycemia because exercise can lower BG levels
