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NUR 516 > Quiz 4 > Flashcards

Quiz 4 Flashcards

(Lipid meds, Thyroid, Diabetic Oral meds, Insulin done, Diabetes type 1/2)

1
Q

Desired outcomes of lipid lowering meds

A

Lower serum levels of : cholesterol and LDLs
Prevention of CAD

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2
Q

How do meds prevent CAD?

protect what tissue?

A

Protection of endothelial tissue
Prevents plaque from rupturing
Slows down the progression of atherosclerosis

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3
Q

Cholesterol

precursor to..?

A
  1. A lipid that is an essential part of bile acid and cell membranes
  2. Insoluble in blood
  3. A precursor of the steroid hormone
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4
Q

Triglyceride

made from? Acquired how? Stored where? inversely related to?

A
  1. A lipid made from fatty acids and glycerol
  2. Aquired through diet
  3. Stored in adipose tissue
  4. Levels corrolate with LDL and are inverse to HDL
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5
Q

Lipoproteins

Produced by?

A

Carrier proteins that aid in the transportation of cholesterol and triglycerides in the blood
-produced by the liver

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6
Q

Low-density lipoproteins

LDL

A

-Tightly packed cholesterol, triglycerides, and lipids
-“BAD” cholesterol
-Primary transport for cholesterol

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7
Q

High- Density Lipoproteins

HDL

A

-loosely packed lipids
-Used for energy
-Brings fats/cholesterolds to liver for excretion

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8
Q

Desired Total cholesterol level

A

<200

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9
Q

Desired Total LDL level

A

<130
For diabetics or increased risks <70

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10
Q

Desired Total HDL level

A

> 50

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11
Q

Desired Total triglyceride level

A

<200

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12
Q

Lipid lowering drugs: HMG CoA Reductase inhibitors (Statins)

DRUGS (5)

A

Lovastatin
Pravastatin
Simvastatin
Atorvastatin
Rosuvastatin (Most potent)

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13
Q

Lipid lowering drugs: Fibrates
(3)

DRUGS

A
  • Gemfibrozil
  • Fenofibrate
  • Fenofibric acid
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14
Q

Lipid lowering drugs: Cholesterol Absorption inhibitor (1)

DRUGS

If TIMBER falls in the woods the sound is absorbed..? idk

A

Ezetimibe

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15
Q

Lipid lowering drugs: PCSK9 Inhibitor

DRUGS (2)

Cumab | “mab” - monoclonal antibody
Birds EVOlved in the AIR

A

Evolocumab (Repatha)
Alirocumab

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16
Q

Lipid lowering drugs: Bile acid sequestrants

DRUGS (3)

CCC | start with “chole” = gallbladder = bile

A

Colesevelam
Cholestyramine
Colestipol

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17
Q

Mechanism of Action/Pathophys: Statin

Decreaes LDLS by…? What does it inhibit?

A
  • Block synthesis of cholesterol in the liver by competitively inhibiting HMG-CoA reductase activity
  • Decreases levels of LDL by 25-65%
  • reduce smooth muscle changes, reduce inflammatory cells inside plaque, stabilizes the endothelium, reduces friction in blood flow and reduces proteins associated with inflammation
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18
Q

Who should be on a statin?

A
  • Hx of cardiovascular disease
  • LDL >190
  • Adults 40-75 with diabetes
  • adults with high LDL <190 who have a risk of developing CVD at (least 5%) over the next 10 years
  • Pregnancy Category X
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19
Q

Side Effects: Statin

CNS? GI? CONTRAINDICATED?

A
  • CNS- headaches, dizziness, insomnia, fatigue
  • GI effects- flatus, abdominal pain, nausea, vomiting, constipation (most common)
  • Myopathy (may cause rhabdomyolysis-muscle breakdown)
  • Increase in liver enzymes
  • Coenzyme Q10 deficiency
  • Contraindicated in pregnant women
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20
Q

Pt Education: Statin

Avoid? (2)
Dosing?
When to take it?
when is blood work?
Contra in?

A
  • Avoid grapefruit juice
  • Start w/ a lower dose & increase as needed
  • Take doses in the evening or before bedtime (except rosuvastatin & atorvastatin which can be in morning) as prescribed
  • Schedule follow up visit w/ provider 4-6 weeks after starting medication to check lab levels
  • Limit alcohol consumption
  • active liver disease is a contraindication
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21
Q

Nursing Considerations (Labs/vital sings): Statin

caution combining with what med?

A
  • Common to experience muscle pain, fatigue, & mild digestive issues
  • Assess for muscle pain & monitor for side effects
  • LFTs and liver enzymes (manage by reducing the dose or stopping until levels return to normal)
  • Lipid panel - check 4-6 weeks after starting
  • start with lower dose and increase as needed
  • caution with combining statins with fibrates
  • pregnancy category X
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22
Q

Mechanism of Action/Pathophys: Cholesterol Absoprtion Inhibitors (CAI)

EZETIMIBE (ZETIA)

Works on which organ? Lowers what? Good for which types of patients?

A

Works on the small intestine to inhibit the absorption of cholesterol
Helps lower LDL and triglycerides

-Indications
* Lower serum cholesterol levels
* Those who can not tolerate
statins

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23
Q

Side Effects: CAI

CAI work on small intestines…

A
  • Abdominal pain and Diarrhea (most common)
  • Upper airway infections
  • Arthralgias (joint pain)
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24
Q

Nursing Considerations (Labs/vital sings): CAI

Contraindications? Can take with?

A

Contraindications
* Allergy
* Pregnancy or lactation
* Severe liver disease

Can take with meals
Can be given in combinations with statins or to those who can’t tolerate statins

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25
Q

Pt Education: CAI

Who should not take?

A

Can be given in combination with statins
Do not take in pregnancy or breastfeeding

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26
Q

Mechanism of Action/Pathophys: Bile Acid Sequestrants (B.A.S)

A

Bind with the cholesterol in the intestine so it can not be absorbed and is excreted in stool
- promote an increase in bile acid excretion
- enhance the conversion of cholesterol to bile acids by the liver

Not routinely used but strong record of efficacy and safety

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27
Q

Side Effects: Bile Acid Sequestrants (5)

A
  • Constipation
  • Abdominal Pain
  • Diarrhea
  • Heartburn
  • Gallstones
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28
Q

Nursing Considerations: B.A.S

Inhibits what?
Can be used w/?
Which pt are ok to us?
What will happen to med when mixed
Will reduce but might increase?

A
  • Can inhibit absorption of Vit: A, D, E, K
  • Can be used together with fibrates
  • Will decrease LDL but may also increase triglycerides/HDL
  • Can be used with pregnant women/pt with acute liver disease (monitor liver enzymes)
  • when mixing: give the medication right away because it will turn solid if it sits
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29
Q

Side Effects: PCSK9 Inhibitors

Administered SUBQ

A
  • Itching
  • Swelling
  • Pain or bruising at injection site
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30
Q

Mechanism of Action/Pathophys: PCSK9 Inhibitors

Reserved for which patients?
Safe to use with?

A

A protein produced by the liver that plays a role in regulating LDL, decrease LDL, cholesterol, and triglycerides
- reserved for those with very high LDL, very high cholesterol, or those who cannot tolerate statins
- often given with statins (synergistic effect)

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31
Q

Nursing considerations: PCSK9 Inhibitors

A

Administered by SQ injection weekly or monthly
- Can be given with statins
- reserved for those w/ very high LDL or can’t tolerate statins
- are monoclonal antibodies

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32
Q

Mechanism of Action/Pathophys: Fibrates

A
  • Inhibition of cholesterol synthesis
  • decrease triglyceride synthesis
  • Inhibition of lipolysis in adipose tissue
  • lower total cholesterol, LDL
  • Increase HDL
  • helps remove from blood
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33
Q

Side Effects: Fibrates
(Flushed…flush the urine)

A
  • Flushed Face/Neck
  • Increased uric acid levels (be careful in those with gout)
  • Increase risk of rhabdomyolysis (rare)
  • GI tract issues
  • Headache
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34
Q

Nursing Considerations (Labs/vital sings): Fibrates
Monitor when? Not recommended for who? Drug interactions?

A
  • Monitor lipid levels in 4-6 weeks
  • Then every 3-4 months
  • because of increase in uric acid levels, may not want to give to patients with history of gout
  • not recommended for diabetics because it can cause hyperglycemia

Drug interactions: Warfarin and Statins

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35
Q

What is the largest endocrine gland?

A

Thyroid gland

The thyroid is responsible for producing key hormones that regulate metabolism.

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36
Q

Name the three hormones produced by the thyroid gland.

A
  • Thyroxine (T4)
  • Triiodothyronine (T3)
  • Calcitonin
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37
Q

What is the function of T4 and T3?

A

Needed for metabolism

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38
Q

What does ‘euthyroid’ refer to?

A

Normal thyroid gland function

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39
Q

What is a goiter?

A

Visible enlargement of the thyroid gland

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40
Q

What is Graves Disease?

A

Antibody mediated autoimmune disease resulting in hyperthyroidism

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41
Q

What is Hashimoto’s Thyroiditis?

A

Autoimmune disease often resulting in hypothyroidism

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42
Q

What are the functions of thyroid hormones?

A
  • Stimulates metabolic activity and oxygen consumption of cells
  • Produces heat and thermogenesis
  • Stimulates carbohydrate, fat and protein metabolism
  • Increases rate of glucose absorption
  • Increases erythropoiesis
  • Influences mood
  • Works with growth hormone, insulin, and sex steroids to promote growth
  • Required for normal respiratory response to hypoxia and hypercapnia
  • Critical for fetal neural and skeletal development
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43
Q

What controls the secretion of T3 and T4?

A

Thyroid Stimulating Hormone (TSH) from the anterior pituitary

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44
Q

How does TSH control the rate of thyroid hormone release?

A

Via a negative feedback mechanism

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45
Q

What happens to TSH levels when thyroid hormone levels are high?

A

Inhibition of TSH

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46
Q

What are the normal thyroid levels for TSH?

A

0.4 to 4.5

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47
Q

What TSH level indicates hyperthyroidism?

A

Less than 0.4

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48
Q

What TSH level indicates hypothyroidism?

A

Above 4.5

Can be primary or autoimmune (Hasimotos, thyroiditis)

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49
Q

List some symptoms of hypothyroidism.

A
  • Fatigue
  • Depression
  • Dry Skin
  • Constipation
  • Bradycardia
  • Altered menstrual cycles
  • Weight gain
  • Changes in hair
  • Cold intolerance
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50
Q

What is myxedema?

A

Severe hypothyroidism

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51
Q

What medication is commonly used for hypothyroidism?

A

Levothyroxine

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52
Q

Hypothroid medications (2)

A

Levothyroxine
Armour Thyroid (desiccated)

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53
Q

Hyperthyroid medications

A

Methimazole
Propylthiouracil (PTU)
Iodine Solutions

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54
Q

What is the brand name for synthetic T4?

A

Synthroid, Levoxyl

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55
Q

What is the half-life of Levothyroxine?

A

6-7 days

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56
Q

What should be avoided when taking Levothyroxine/ Armour Thyroid

A

Calcium containing medications, antacids, or iron supplements

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57
Q

What is hyperthyroidism?

A

Increased in circulating T3 and T4 from overactive thyroid or excessive thyroid hormone production

Graves disease is hyper-functioning thyroid

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58
Q

What is the main treatment for Graves Disease?

A

Beta blockers (e.g., Propranolol or Atenolol)

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59
Q

What are the symptoms of hyperthyroidism?

A
  • Anxiety
  • Restlessness
  • Diaphoresis
  • Diarrhea, N/V
  • Tachycardia / AFib
  • Weight loss
  • Heat intolerance
  • Exophthalmos
  • Changes in menstrual cycle
  • Insomnia
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60
Q

What is Lugol’s Solution used for?

IODINE

A
  • Inhibits release of T3 and T4
  • short-term use
  • can cause iodinism
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61
Q

I-131

A
  • Iodine (Radioactive)
  • Use for thyroid cancer, thyrotoxicosis/special cases
  • Not for pregnancy
  • Increase fluid intake
  • Radiation precautions
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62
Q

What are the side effects of Iodine Solutions?

A
  • Metallic taste
  • Stomatitis
  • Sore throat
  • Hypersensitivity
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63
Q

What is desiccated thyroid?

AMOUR THYROID

A

Thyroid extract from animal thyroid glands that have been dried and powdered
-Contains both T3/T4

Side Effects: Change in appetite, chest pain, diarrhea

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64
Q

Nursing Considerations: Armour thyroid

A

Based on TSH results
Life-long medications
Safe in pregnancy
Should have TSH checked regularly until stablized (6-8 weeks after then annually)

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65
Q

What is the drug of choice for hyperthyroidism?

A

Methimazole

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66
Q

What does Propylthiouracil (PTU) do?

A

Inhibits Conversion T4 to T3

Medscape: Inhibits synthesis of thyroid hormone by blocking oxidation of iodine in thyroid gland; blocks synthesis of T4 and T3

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67
Q

What is the treatment goal for hyperthyroidism?

A

Decreasing thyroid hyperactivity and preventing complications

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68
Q

What must be monitored when using PTU?

A
  • LFTs
  • CBC
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69
Q

What is the usual duration for checking TSH after starting thyroid medication?

A

6-8 weeks after starting and after dose changes

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70
Q

Can thyroid medications be used safely during pregnancy?

A

It depends on which ones. PTU can be used in first trimester. Desiccated thyroid can be. Methimazole shouldn’t be used, same with I-131

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71
Q

Thioamides

Baseline labs?
When to take?

Inhibits what? Methimazole/PTU

A
  • Inhibits formation of thyroid hormones in the cells
  • Inhibits conversion of T4 –> T3
  • Need baseline CBC/LFTs
  • Take on empty stomach/30 minutes before eating
  • Takes several weeks to see effect
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72
Q

Medication given for Thioamides

Both have THI?

A

Methimazole
Propylthiouracil (PTU)

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73
Q

Methimazole

THIOAMIDE

A

Thioamide-

  • Drug of choice unless pregnant
  • Side Effects: Less GI effects
  • Can cause bone marrow suppression

Pharmacology (Medscape):
- Inhibits synthesis of thyroid hormone by blocking oxidation of iodine in thyroid gland
- blocks synthesis of thyroxine (T4) and triiodothyronine (T3)

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74
Q

PTU

THIOAMIDE

A

Thioamide

  • inhibits Conversion of T4-T3
  • Can be used during first trimester of pregnancy only
  • Need to monitor LFT’s/CBC

Medscape:
- Inhibits synthesis of thyroid hormone by blocking oxidation of iodine in thyroid gland
- blocks synthesis of T4 and T3

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75
Q

Adjuvant therapy-Beta blockers

hyperthyroidism

A
  • Propanolol/Atenolol
  • To control symptoms
  • Used in Tachy/arrythmic/HTN adults
  • Used to control sxs while waiting for meds to take effect
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76
Q

Explain the process of insulin resistance and how it leads to the development of Type 2 DM

A

online: Initially, the body compensates by producing more insulin, but over time, the pancreas struggles to keep up, leading to elevated blood sugar levels and eventually, T2DM

From her slides in diff power point: Initially there is increased insulin secretion by the Beta cells to bring down the BS. Insulin not effective/cant bring down blood glucose/ then body needs to increase levels of glucose/beta cells become exhausted

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77
Q

Glycemic Targets (ADA)
A1C
FPG
PPG

A
  • A1C < 7%
  • FPG 80-130
  • PPG <140
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78
Q

Explain how the SNS, RAAS and the inflammatory response increase insulin resistance?

A

From her type 2 diabetes PP:
Basically, RAAS/SNS leads to increased inflammation which leads to more insulin resistance

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79
Q

How does metformin reduce blood sugar in the Type 2 DM?

A
  • Improves how insulin works in the body (Insulin sensitizer)
  • Decreases absorption of carbohydrates
  • Decreases glucose production in the liver
  • Decreases appetite
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80
Q

Most frequent side effects of metformin?

A
  • GI side effects (common)
  • Bloating
  • Diarrhea
  • Abdominal pain
  • Nausea
  • Metallic taste

Increased risk for B12 deficiency

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81
Q

What are the significant nursing interventions needed for those patients who take Metformin?

A
  • Hold 48 hours prior to contrast dyes
    (may lead to lactic acidosis or acute
    kidney injury)
  • Contraindicated in patients with renal
    or hepatic impairment, and heart
    failure
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82
Q

What lab test other than the BS should the nurse be aware when administering metformin?

A

Renal/hepatic?

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83
Q

How do the sulfonylureas reduce blood sugar?

A

Stimulates Beta cells to secrete insulin
Decrease glucose production by the liver

Glipizide and glyburide

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84
Q

Why do sulfonylureas cause weight gain?

A

online: the increased insulin levels promote the storage of excess glucose as fat

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85
Q

What are the nursing interventions for Sulfonylureas?
Onset?

A
  • Monitor for hypoglycemia
  • Onset at 90 minutes and peak in 2-3 hours
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86
Q

Patients allergic to what medications should take sulfonylureas with caution?

A

DO NOT GIVE IF ALLERGIC TO SULFA DRUGS

ALso not for pregnant/lactating women/beta blockers

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87
Q

How are the Meglitinides the same as the sulfonlyureas? different from the sulfonylureas

A

online: They induce insulin secretion from pancreas, with a different mechanism of action from sulfonylureas

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88
Q

How will the nurse know if Meglintinides are working?

When should pt take it?

A

Check BS levels??

Onset at 90 minutes and peak in 2-3 hours

Should be taken with first bite of food (CUZ IM MEGA HUNGRY)

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89
Q

How do alpha glucosidase inhibitors work to decrease blood sugar?/ When are these meds used most frequently?

A

“Starch Blocker”

Inhibit alpha-glucosidase, by delaying
the absorption of glucose in the small
intestines after a meal; does not
increase insulin secretion

Online: used to manage post-meal blood sugar spikes by slowing down carbohydrate absorption.

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90
Q

-How do Thiazolidinediones work to reduce blood sugar?

-Contraindicated for which group of patients?

-Why do these patients gain weight?

A

-Improve the effectiveness of insulin by decreasing insulin resistance in adipose and muscles cells

-Contraindicated in those patients with heart failure or hepatic impairment

-online: fluid retention, increased fat storage, and a shift in fat distribution towards subcutaneous fat can cause weight gain

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91
Q

Explain the role of the incretins in glucose control?

GLP-1 Agonist

A

enhancing insulin release, suppressing glucagon, slowing digestion, and reducing appetite, ultimately improving blood sugar control and potentially leading to weight loss

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92
Q

INCRETINS (GLP-1)

-Why do these patietns often lose weight on these meds?

-Who should NOT receive these meds?

A

online: because these medications mimic the effects of the natural hormone glucagon-like peptide-1 (GLP-1), which helps regulate appetite, slows down digestion, and increases feelings of fullness, leading to reduced food intake and weight loss.

online: Patients with hx of pancreatitis?

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93
Q

How do the DPP-4 inhibitors work to decrease blood sugar?

A
  • Inhibits dipeptidyl peptidase 4 (DDP-4) enzyme, which destroys the GI incretin hormones GLP-1 and GIP
  • Increase insulin secretion
  • Decrease glucagon secretion to decrease glucose production
  • Allows incretin hormones to remain in circulation longer
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94
Q

Major nursing considerations for DPP-4?

A

Hypoglycemia

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95
Q

How do sodium glucose co transport inhibitors work?

A

Inhibit reabsorption of glucose in the proximal renal tubules; promote glucose excretion in urine

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96
Q

Side effects of sodium glucose co transport inhibitors?

A

Increase risk :
Yeast infections, UTIs, and Amputation?

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97
Q

What is the primary action of insulin?

A

Hormones that controls the storage and metabolism of carbohydrates, proteins, and fats

This activity occurs primarily in the liver, in muscle, and in adipose tissues.

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98
Q

What does insulin stimulate in the liver?

A

Synthesis of glycogen

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99
Q

How does insulin affect protein and fat storage?

A

Promotes protein synthesis and helps store fat by preventing its breakdown for energy

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100
Q

From where is insulin released?

A

Beta cells of the Islet of Langerhans in response to increased blood sugar

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101
Q

What is the goal of insulin therapy?

A

To mimic the physiological control of blood glucose levels

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102
Q

What are the two physiological blood glucose levels of insulin secretion?

A
  • Basal insulin levels – during fasting
  • Postprandial levels – after eating
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103
Q

What are the indications for insulin use?

A
  • Diabetes Type 1
  • Diabetes Type 2
    • When not controlled with lifestyle and oral meds
  • Treat severe DKA or diabetic coma
  • Treat hyperkalemia in combination with glucose
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104
Q

What is the recommended method of insulin administration?

A

Only use an insulin syringe and administer subcutaneously

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105
Q

What is lipodystrophy?

A

A condition that can be prevented by rotating injection sites

Keep injections about 1.5 in away from eachother and if BID use both L and R side

106
Q

What should be the distance between insulin injection sites?

A

About 1.5 inches away from each other

107
Q

What are the methods of insulin administration?

A
  • Insulin pumps
  • Insulin pen injectors
  • Insulin syringes
108
Q

Name the types of insulin.

A
  • Rapid-Acting
  • Short-Acting (Regular)
  • Intermediate
  • Long-Acting
109
Q

What are the names of rapid-acting insulin drugs?
All, guys, like, Inside.
Which is rapid…and deadly..

A
  • Aspart
  • Glulisine
  • Lispro
  • Inhaled Insulin

most deadly type of insulin

110
Q

Nursing considerations for Rapid- Acting Insulin

A
  • Must be given with food
  • Usually given in conjunction with intermediate acting insulin
  • Always monitor for hyPOglycemia
111
Q

What is the onset time for Aspart, Glulisine, and Lispro?

A

5-15 minutes

Inhaled insulin onsent within ONE minute

112
Q

What is the peak time for rapid-acting insulin?

A

30-90 minutes

inhaled insulin within 12-15 min

113
Q

True or False: Food must be present when administering rapid-acting insulin.

114
Q

What is the duration of action for rapid-acting insulin?

115
Q

What is the primary use for short-acting insulin?

AKA REGULAR INSULIN

A

To cover the glucose rise after eating a meal

116
Q

When should short-acting insulin be administered?

A

30 minutes before meals

117
Q

What happens if regular insulin is cloudy?

A

Throw it out

118
Q

Nursing considerations: Short acting (Normal) insulin

A

If Regular insulin (clear) is mixed with NPH human insulin (cloudy), the Regular insulin should be drawn into the syringe first.

*May be given IV

119
Q

What is intermediate-acting insulin also known as?

A

Isophane or NPH (Neutral Protamine Hagedorn)

120
Q

How often is intermediate-acting insulin usually given?

A

Twice a day

121
Q

What is the typical dosing schedule for intermediate-acting insulin?

A

2/3 in the morning and 1/3 in the evening

Can be pre made in a 70/30 mixture of regular/NPH.
-Supplied as a pen which makes for very easy administration.
-Can be at room temp for 10 days

122
Q

What is the onset of action for long-acting insulin?

A

Up to 1.5 – 2 hours

123
Q

What is the duration of action for long-acting insulin?

124
Q

What is a notable characteristic of long-acting insulin absorption?

A

Even absorption with no peaks and valleys

Frequently used in Type 2 DM

125
Q

What is the dosing range for insulin?

A

0.6-0.8 units/kg/day

126
Q

What is sliding-scale insulin?

A

Adjusted doses dependent on individual blood glucose, usually reserved for inpatient use

127
Q

How should unopened vials of insulin be stored?

A

Refrigerated until needed

128
Q

How long can opened insulin vials be stored at room temperature?

129
Q

What is the antidote for hypoglycemia?

130
Q

What should patients with Type 1 DM do even if NPO?

A

Will need insulin

131
Q

What should diabetic patients wear as a precaution?

A

A medical alert tag

132
Q

what is Type-1 Diabetes Mellitus

types?

A

-Total destruction of the pancreatic beta cells
-autoimmune
-Types :
-1A (90-95%)
- Type B (idiopathic, no autoimmune)
- Rapid destruction in kids/Slower in adults

133
Q

What is ketosis?

A

A metabolic state where the body uses free fatty acids for energy instead of glucose

134
Q

What is polyuria?

A

Increased amount and frequency of urination due to renal threshold for glucose reabsorption being exceeded.

Glucose >180

Results in glucose remaining in renal tubule and an osmotic gradient that pulls water from tubule cells into urine.

135
Q

What are the classic symptoms of Type 1 Diabetes Mellitus?

3 P’s

A
  • Polyuria
  • Polydipsia
  • Polyphagia

Other symptoms may include blurred vision, fatigue, and weakness.

136
Q

What is diabetic ketoacidosis (DKA)?
symptoms? (4)
Occurs mainly in?

A

A hyperglycemic emergency characterized by hyperglycemia, metabolic acidosis, dehydration, and electrolyte loss.

Often presents in Type 1 Diabetes but can occur in Type 2.
-stored fatty acids can cause DKA

137
Q

What triggers ketosis in diabetes?

A

Insulin deficiency leads to the breakdown of fat into free fatty acids and glycerol, converted into ketones by the liver.

Ketones are strong acids that can lead to metabolic acidosis.

138
Q

What is the dawn phenomenon?

A

Increase in fasting blood glucose and/or insulin requirements during early morning hours due to nocturnal elevation of growth hormone.

Not triggered by nocturnal hypoglycemic events.

139
Q

Difference between dawn phenomenon and somogyi effect

A

Check glucose level in the middle of the night
A. Dawn = Normal/High Glucose at 3 AM
B. Somogyi = Low Glucose at 3 AM

140
Q

What is the Somogyi effect?

A

Nocturnal hypoglycemia followed by rebound hyperglycemia due to counter-regulatory hormone release.

Occurs from too much or too little insulin at bedtime.

141
Q

Clinical manifestations of Diabetes type-1

A
  • Three “P’s”:
    • Polydipsia
    • Polyuria
    • Polyphagia
  • Weight loss
  • Abdominal pain
  • Neuro symptoms
    • Blurred vision (accumulation of aqueous humor in the eye)
  • Other symptoms
    • Frequent Candida infections
  • Extremely elevated glucose
  • Ketones in urine
  • Metabolic acidosis
142
Q

Polyphagia

A

Increased appetite with weight loss
-Insulin deficiency-cells not receiving glucose- sets into effect compensatory processes to increase blood glucose levels.

143
Q

What are the three main causes of DKA?

A
  • Infection or illness
  • Lack of Insulin
  • Undiagnosed or undertreated diabetes

These factors can precipitate DKA in patients.

144
Q

What is the initial treatment for DKA?

A

Fluid replacement to restore intravascular volume and correct electrolyte imbalances.

Insulin therapy is also initiated once fluids are administered.

145
Q

What are the clinical manifestations of DKA?

A
  • Extreme dehydration
  • Poor skin turgor
  • Dry mucous membranes
  • Tachycardia
  • Hypotension
  • Acetone breath
  • Kussmaul respirations
  • Changes in LOC

Presenting symptoms also include the 3 P’s and weight loss.

146
Q

What does hyperglycemia cause in relation to thirst?

A

Increased osmotic pressure in the extracellular compartment causes water to shift out of the intracellular space, leading to cellular dehydration and thirst sensation.

This condition is known as polydipsia.

147
Q

Define hypoglycemia.

A

Blood glucose level < 70 mg/dL with or without symptoms.

Most commonly occurs in patients treated with insulin.

148
Q

What is the normal glucose levels?

149
Q

What glucose levels are considered prediabetic?

150
Q

What glucose level is considered to be diabetic?

151
Q

What are common electrolyte issues in DKA?

A
  • Hyponatremia
  • Hyperkalemia

These imbalances need to be monitored during treatment.

152
Q

What causes blurred vision in diabetes?

A

Accumulation of glucose in aqueous fluid in the cornea alters refraction of light entering the eye

153
Q

What characterizes Type 1 Diabetes Mellitus?

A

Total destruction of the pancreatic beta cells due to autoimmune response

Includes Type 1A (90-95%) and Type 1B (idiopathic, no autoimmune).

154
Q

What is the glucose range for hypoglycemia?
Common causes?

A

Defined as blood glucose < 70 mg/dL with or without symptoms
Common causes: Excessive exercise, alcohol, poor food intake, too much insulin, stress, surgery, and medications

155
Q

What is the role of glucagon in hypoglycemia?

A

Triggers the release of glycogen from the liver

156
Q

What happens during gluconeogenesis?

A

The body creates glucose from non-carbohydrate sources instead of using the Krebs cycle

157
Q

What are the functions of glucose, fat, and proteins in meeting the energy needs of the body?

A

Glucose provides energy for cells, fat is the most dense fuel storage, and proteins are building blocks for tissues

Glucose is absorbed into the bloodstream at the intestines and is essential for normal cerebral function.

158
Q

What are counter-regulatory hormones?

A

Hormones that counteract the effects of insulin:
glucagon, epinephrine, cortisol, and growth hormones

They help increase blood glucose levels when they drop.

159
Q

What distinguishes Type 1 diabetes from Type 2 diabetes?

A

Type 1 is characterized by autoimmune destruction of pancreatic beta cells; Type 2 involves insulin resistance and deranged insulin secretion/gestational/drug induced

Type 1A is autoimmune, while Type 1B is idiopathic.

160
Q

Define metabolic syndrome and its association with Type 2 diabetes.

A

Metabolic syndrome is a cluster of conditions that increase the risk of heart disease, stroke, and diabetes, often associated with obesity and insulin resistance

161
Q

Physical Symptoms of metabolic syndrome

A

Increased waist circumference or belly fat
High triglycerides
Elevated BP
High BS
Low LDL
Apple Shape
Ancanthosis Nigricans

162
Q

Clinical manifestations of Metabolic syndromes

A
  • Hyperglycemia causes intracellular fluid shifts ——>polydipsia
  • Excessive diuresis causes polyuria
  • Cell starvation from lack of glucose ———> polyphagia
  • Fatigue
  • Weakness
  • Weight loss
  • Visual disturbances
163
Q

What happens to glucose in the presence of oxygen?

A

It breaks down to form CO2 and water

This process is part of cellular respiration.

164
Q

What happens to glucose after absorption?

A

It is used for energy, stored as glycogen in the liver, or converted into fat

Excess glucose can also be excreted in urine.

165
Q

What is glycogenolysis?

A

The breakdown of stored glycogen to make glucose
-This process occurs in the liver and muscle tissue when glucose levels are low. (Prolonged starvation)
-In response to Epinrephrine, glucagon, insulin

166
Q

What is gluconeogenesis?

A

The synthesis of glucose by the liver from non-carbohydrate sources

It primarily occurs from amino acids and fats. Can lead to development of ketones

167
Q

What role does insulin play in glucose metabolism?

A

Insulin stimulates the uptake, use, and storage of glucose by promoting glycogen synthesis and inhibiting gluconeogenesis

It is released by beta cells in the pancreas.

168
Q

What are the glucose-regulating hormones?

A

Amylin, somatostatin, glucagon, and incretins

Amylin slows glucose absorption, while glucagon promotes glucose production.

169
Q

Different ways to regulate glucose:

A

Increased blood glucose
Beta cells
Insulin & Amylin

Vs

Hypoglycemia
Alpha cells
Glucagon

170
Q

Insulin stimulates the uptake, use, and storage of _____

171
Q

Which hormone is required to initiate active transport of glucose into the cell?

172
Q

What are the risk factors for Type 2 diabetes?

A
  • Family history
  • Obesity
  • Ethnicity
  • Age
  • Gestational diabetes
  • Hypertension
  • Polycystic ovary syndrome (PCOS)
  • Smoking and alcohol

These factors contribute to insulin resistance and deranged insulin secretion.

173
Q

Why does obesity cause insulin resistance?

A
  • Causes increases in adipose and free fatty acids
  • Induces inflammation and release of the associated inflammatory mediators
  • Increases stress on pancreatic B cells as insulin is increased
  • Results in liver increase glucose in the blood (impaired suppression)
174
Q

When are insulin levels their highest?

A

After a meal

Insulin levels decrease during fasting.

175
Q

What are the symptoms of hypoglycemia? (13)

A
  • Fatigue
  • Sweating
  • Hunger
  • Dizziness
  • Rapid heart rate
  • Anxiety
  • Irritability
  • Shakiness
  • Blurred vision
  • Confusion
  • Loss of consciousness
  • Seizures
  • Coma

Symptoms vary from mild to severe depending on blood sugar levels.

176
Q

What is Hyperosmolar Hyperglycemic Syndrome (HHS)? Causes? How is it unlike DKA?

A

A condition seen only in Type 2 diabetes characterized by severe hyperglycemia(>600), hyperosmolality (like DKA), and dehydration due to insulin resistance
- Can develop over several days to weeks
-Causes: INfection, non-complicance with diet/meds, substance abuse, alcohol

Unlike DKA, there is no ketone formation in HHS.

177
Q

Symptoms/Treatment of HHS (hyperosmolar hyperglycemic state)

A

Symptoms: extreme glucose level, rapid/thread pulse, hypotension, profound dehydration, polydipsia, polyuria, confusion, disorientation, possible seizure, or coma

Treatment:
Hydration (given first)
IV insulin
Electrolyte replacement

178
Q

What is the diagnostic criteria for diabetes?

A
  • Fasting blood glucose > 126 (2 readings)
  • 2-hour plasma glucose during OGTT > 200
  • Random blood glucose > 200 with hyperglycemic symptoms
  • Hgb A1C > 6.5% (2 readings)

These criteria help in the accurate diagnosis of diabetes.

179
Q

Glycated Hemoglobin A1c

A

HgbA1c measures the amount of glucose over 120 days.
Glucose doesnt normally move into RBCs but when glucose is chronically high it will—> once inside it cannot leave.

180
Q

What causes diabetic neuropathy? Types?

A

High blood sugar levels leading to nerve damage

Somatic neuropathy:
Diminished perception: Vibration, pain, temp. Hypersensitivity: Light touch, occasionally severe “Burning” pain

Autonomic neuropathy:
Defects in vasomotor and cardiac responses
Urinary retention
Impaired motility of the gastrointestinal tract
Sexual dysfunction

181
Q

What lifestyle factors increase insulin resistance?

A
  • Sedentary lifestyle
  • Poor diet (high glycemic carbohydrates)
  • Smoking

These factors contribute to obesity and stress on pancreatic beta cells.

182
Q

Fill in the blank: The body responds to increased blood sugar levels by stimulating the pancreas to release _______.

183
Q

True or False: Type 2 diabetes accounts for 90-95% of all diabetes cases.

Why

184
Q

Why is it necessary for a person to maintain blood glucose no lower than 70?

A

To maintain a continuous supply of glucose for energy

185
Q

Patient education with bile acid sequestrants

A
  • can be used with fibrates
  • can be used with pregnant women
  • this med has a strong record of efficacy and safety
  • take right away when mixed
186
Q

Patient education with PCSK9 Inhibitors

A
  • are very expensive compared to other classes
  • can be given in conjunction with statins
  • decrease LDL, cholesterol, and triglycerides
187
Q

Patient education with fibrates

A
  • do not take with warfarin or statins
  • will need periodic monitoring
  • not recommended for diabetics
188
Q

What are the differences between the statins?

A
  • rosuvastatin is the most potent; if there was trouble tolerating - you can change from one statin to another
  • should take them in the evening or at bedtime, but rosuvastatin and atorvastatin can be given in the morning
189
Q

Why are statins not just for cholesterol lowering?

A

they play some role in vasodilation

190
Q

What does it mean to stabilize the plaque? Why is that important?

A

inflammatory cells inside the plaque are reduced and the endothelium is stabilized, which in turn stabilizes the plaque. this is important because it reduces the risk of thromboembolic issues if a part of the plaque breaks off and travels through the bloodstream

191
Q

What is included in a lipid profile? Where do we want the patient to be?

A

Total Cholesterol: desired level is less than 200
LDL: desired level is less than 130
HDL: desired level is 50 or higher
Triglycerides: desired level is less than 200

In diabetics and those with increased risk: want LDL < 70

192
Q

What does improve endothelial function mean? How do statins play a role?

A

It means to reduce the progression of atherosclerosis and cardiovascular disease by helping increase nitric oxide availability. Endothelial dysfunction occurs from oxidative stress from dyslipidemia, diabetes, smoking, HTN, obesity, and aging. By controlling these factors that shred blood vessels, it reduces endothelial dysfunction. Statins play a role in reducing smooth muscle changes, stabilizing endothelium, reducing friction, and reducing proteins associated with inflammation.

193
Q

What are the inhibitory neurotransmittors?

A

dopamine, serotonin, and GABA

194
Q

What are the excitatory neurotransmitters?

A

ACH (acetylcholine) and norepinephrine

195
Q

Neurotransmitters: Acetylcholine - where is it found, what type of action?

A
  • found in the CNS, PNS, and ANS
  • can be either excitatory or inhibitory (depends on neurons secreting it)
    – PNS: excitatory at neuromuscular junctions
    – ANS: inhibitory and slows heart rate
196
Q

Neurotransmitters: Serotonin (5-hydroxytrptamine) - where is it found, what type of action?

A
  • derived from tryptophan
  • found primarily in the GI tract, platelets, and brainstem
  • contributor to feeling of well being
  • inhibitory
197
Q

Neurotransmitters: Dopamine - where is it found, what type of action?

A
  • located mainly in the substantia nigra of midbrain/basal ganglia region
  • numerous functions:
    – behavior and cognition
    – voluntary motor movement
    – motivation punishment and reward
    – attention
    – working memory
    – learning
  • involved in many neuropsychiatric and voluntary motor movement disorders:
    – social phobia, ADHD, drug and alcohol dependence
    – Parkinson’s disease
    – Tourette’s syndrome
198
Q

Neurotransmitters: GABA (gamma amino butyric acid) - where is it found, what type of action?

A
  • chief inhibitory transmitter in the CNS
  • has a relaxing, antianxiety, and anticonvulsant effect on the brain
  • has inhibitory effect on muscles (decreases muscle spasms and improved tone)
199
Q

Neurotransmitters: Norepinephrine

A

an excitatory neurotransmitter in the brain
stress hormone within the endocrine system

200
Q

Neurotransmitters: Glutamate

A
  • major mediator of excitatory signal
  • involved in cognition, memory, and learning
201
Q

How do neurons do conduction?

A

action potential (neuron conducts impulses)
- abrupt changes in the membrane potential permit nerve signals to be transmitted from the cell body down the axon
- stimulates sodium, potassium, and calcium ions to move across the axonal membrane

202
Q

What are the three phases of an action potential?

A
  • depolarization of the neuron: positively charged ion
  • repolarization of neuron: return of neuron to a negative value
  • resting period
203
Q

What leads to seizures, regarding the action potential?

A

impulses that do not maintain a systematic order (excitatory, inhibitory, and resting phase) become irregular and chaotic and can lead to seizures

204
Q

What are seizures?

A

a single episode of abnormal electrical discharge from cortical neurons that results in an abrupt and temporary altered state

205
Q

What is epilepsy

A

a group of syndromes characterized by unprovoked, recurrent seizures

206
Q

What is status epilepticus?

A

continuous seizure activity for more than 5 minutes
- OR 2 or more sequential seizures that occur WITHOUT full recovery of consciousness between attacks
- is a neurological emergency
- requires immediate intervention

207
Q

What are common causes of seizures?

A
  • trauma
  • ETOH withdrawal
  • illicit drug use
  • brain tumor
  • congenital malformations
  • stroke
  • metabolic disorders (uremia, electrolyte imbalance)
  • alzheimer’s disease
  • neurodegenerative disease
  • idiopathic
208
Q

What are common causes of epilepsy?

A
  • genetic causes (mutated genes)
  • head trauma
  • medical disorders (dementia, meningitis, encephalitis)
  • prenatal injury
  • developmental disorders (autism, Down syndrome)
209
Q

Pathophysiology of seizures

A
  • messages from the body are carried by the neurons of the brain through discharges of electrochemical energy; impulses occur in bursts
  • during periods of unwanted discharged, parts of body may act erratically
  • for an actual seizure to occur:
    – need excitable neurons
    – need increase in excitatory glutaminergic activity
    – need reduction in activity of normal inhibitory GABA projection
  • anyone can have a seizure
210
Q

Examples of generalized seizures?

A
  • absence (petit mal)
  • tonic-clonic (grand mal)
  • atonic/akinetic (drop attacks)
  • status epilepticus
211
Q

Pathophysiology of focal seizure

A
  • starts and remains in one hemisphere
  • high-frequency bursts of action potentials and hypersynchronization
  • may have motor, sensory, and autonomic symptoms and automatisms
    – autonomic: due to stimulation of ANS (pallor, sweating, pupillary dilation, epigastric sensation)
    – automatisms: often associated with temporal lobe seizures; patient is unaware
212
Q

What are automatisms?

A
  • may happen with focal seizures
  • coordinated involuntary movements happening during state of impaired consciousness either during or after seizure
  • patient is unaware
  • often associated with temporal lobe seizures
213
Q

Types of focal or partial seizure

A
  • focal - retains awareness
  • focal - altered awareness
  • partial seizure
214
Q

Focal seizure - retaining awareness

A
  • no impairment of consciousness
  • similar to partial seizures
  • may have movement of body parts
  • may experience an aura
215
Q

Focal seizure - altered awareness

A
  • impairment of consciousness
  • spreads to both hemispheres (this confuses me though because i thought it should start and remain in one hemisphere)
216
Q

Partial seizure

A
  • begins in one part of hemisphere (typically in the temporal or frontal lobe)
  • may be simple or complex
217
Q

Pathophysiology of generalized seizures

A
  • start in one hemisphere and spreads with involvement of both hemispheres
  • may have motor and/or nonmotor symptoms
  • affects both hemispheres of the brain
  • impairment of consciousness
218
Q

Tonic-clonic seizure

A
  • begin with rigid violent contractions (tonic)
  • followed by repetitive clonic activity of all extremities
  • body stiffens and relaxes

generalized

219
Q

Tonic seizure

A

generalized
- muscle stiffness, dilation of pupils, altered respirations
- usually lasts less than a minute

220
Q

Absence seizures

A

generalized
- short episodes of staring and loss of consciousness for about 10 seconds

221
Q

Myoclonic seizures

A

generalized
- bilateral jerking of muscles
- no loss of consciousness

222
Q

Atonic seizure

A

generalized
- sudden loss of muscle
- “drop to the ground”

223
Q

What is needed for a diagnosis of seizure and/or epilepsy

A
  • H&P
  • neurological exam
  • diagnostic procedures (chemistries, tox screen, CT, MRI, EEG)
224
Q

What are the phases of seizures?

A

Pre-ictal, ictal, and post-ictal

225
Q

What is the pre-ictal phase of a seizure?

A

may be started by a trigger and/or preceded by an aura

226
Q

What is the ictal phase of a seizure?

A
  • actual seizure
  • increases in metabolic demand (uses a lot of energy)
227
Q

What is the post-ictal phase of a seizure?

A
  • has decreased responsiveness
  • feels fatigue
228
Q

What are anticonvulsants used for

A

AKA antiepileptic drugs (AED)
- used for long-term management of chronic epilepsy
- management of seizures not caused by epilepsy
- off label use: anxiety, bipolar disorder, chronic pain, migraines

229
Q

What are broad-spectrum anticonvulsants used for

A

effective for treatment of focal and generalized seizures

230
Q

What are narrow-spectrum anticonvulsants used for

A

used primarily for focal-onset seizures (including focal which evolve to be convulsive seizures)

231
Q

Mechanism of actions by group - fit anticonvulsants (just an image in ppt that may be helpful)

232
Q

Sodium channel blockers: what do they do with seizures

A
  • prevent return of the channel to active state, stabilizes them to inactive state
  • prevents repetitive firing
233
Q

Calcium channel blockers: what do they do with seizures

A
  • calcium going in during cells’ resting state facilitates development of an action potential
  • CCBs slow depolarization which is needed for spike-wave bursts
  • CCBs help to “lock the channel”
234
Q

What do GABA enhancers do with seizures

A
  • may enhance Cl- influx which makes cells more negative and harder for the cell to generate an action potential
  • some decrease metabolism of GABA so that more GABA is available (GABA is inhibitory)
235
Q

What do glutamate blockers do with seizures?

A
  • bind to glutamate, which is an excitatory neurotransmitter, therefore blocking it from binding and creating excitation
  • glutamate receptor has 5 potential binding sites
236
Q

What does “pharmacologic management” mean regarding seizures

A
  • medications are to control seizures NOT cure
  • medication prescribed based on the type of seizure
  • many drugs require blood monitoring
  • patient education (take as prescribed, never stop taking on own, side effect management)
237
Q

Phenytoin (Dilantin): what type of med? How does it work? Indications?

A

Sodium channel blocker
- works to stabilize the neurons from becoming too excited
- stops the spread of seizure activity in the motor cortex
- highly (90%) protein-bound drug: increased risk of drug interactions

Indications:
- tonic-clonic seizures
- status epilepticus
- prophylaxis for surgery

238
Q

Phenytoin (Dilantin): Therapeutic range and administration?

A

Therapeutic range: 10-20mcg/mL
- very narrow therapeutic window
- need to monitor levels

Given PO, IM, or IV
- if administered IV, w/ NSS
- infuse over 30-60 minutes
- can be very irritating to veins

Tube feeds: need to stop feed for 2 hours before AND after

239
Q

Phenytoin (Dilantin): side effects?
*”pheny” = funny smile *

A
  • gingival hyperplasia
  • neurologic:
    – drowsiness
    – ataxia
    – irritability
    – visual problems
    – peripheral neuropathy
    – headache
  • N/V
  • Cardiovascular: hypotension, arrhythmias
  • can cause suicidal thoughts
  • skin rash including SJS can occur
240
Q

Phenobarbital (Solfoton, Luminal): what does it do? what class? administration considerations?

A

Classified as a barbiturate
- inactivates fast sodium channels leading to enhanced GABA effects and decreased glutamate release

Administration consideration: very long half-life
- habit forming and dependence

241
Q

Phenobarbital (Solfoton, Luminal): side effects

A
  • sedation
  • diplopia
  • cognitive skill impairment
  • respiratory depression
  • hypotension
  • hyperactivity and inattention in children
242
Q

Carbamazepine (Tegretol): What class? What does it do? When is it used? Storage?

A

Sodium channel blocker
- similar to Phenytoin (also an SCB) in mechanism of action
- inhibits spread of seizure activity

Used for several different types of seizures:
- drug of choice for partial and generalized tonic-clonic seizures
- also used for trigeminal neuralgia and bipolar disorder
- WILL MAKE ABSENCE AND MYOCLONIC SEIZURES WORSE

Needs to be in dry location

243
Q

What type of seizures is carbamazepine (tegretol) the drug of choice for?

A

partial and generalized tonic-clonic seizures

244
Q

What seizures does carbamazepine make worse?

A

absence and myoclonic seizures

245
Q

Carbamazepine: What needs to be monitored?

A

Labs:
- CBC: especially WBC
- Drug level: 4-12 mcg/mL

Monitor drug levels, sodium, CBC, LFTs, and BUN/Cr especially in those with renal impairment

246
Q

Carbamazepine: Side effects

A
  • Neuro: headache, diplopia, ataxia, drowsiness, sedation
  • N/V
  • hyponatremia
  • decreased blood counts (neutropenia and thrombocytopenia)
  • rashes can be common - watch for SJS
  • increases suicidal thoughts
  • take with food
  • cannot abruptly discontinue
247
Q

Oxycarbazepine (trileptal): How does it work? What class?

A

Sodium channel blocker
- same efficacy as carbamazepine but is better tolerated

248
Q

Oxycarbazepine (trileptal): What seizures is it used for and NOT used for? Considerations?

A
  • used as adjunctive therapy or monotherapy for partial seizures in children and adults
  • NOT used for absence and myoclonic - makes them worse

Considerations:
- increase risk of suicidal ideations
- decreases efficacy of oral contraceptives

249
Q

Valproic Acid/Valproate (Depakote): How does it work? What class? Indications?

A

GABA enhancer; inactivation of fast sodium channels

Indications: really any seizure activity
- absence, myoclonic, tonic-clonic, partial, neonatal seizures
- used to control symptoms of acute mania in bipolar disorder

250
Q

Valproic Acid/Valproate (Depakote): Administration and monitoring
Can give with? Monitor what? Therapeutic range?

A
  • can be given with phenytoin
  • take with food
  • can cause liver toxicity, need to monitor LFTs
  • narrow therapeutic range
    – need to check levels (50-100 mcg/mL)
  • must be diluted when given IV with at least 50mL NSS or D5W
    – give over an hour (no more than 20mg/min)
  • avoid sudden withdrawal
  • monitor CBC because can cause thrombocytopenia
251
Q

Valproic Acid/Valproate (Depakote): side effects

A
  • N/V
  • sedation/dizziness
  • pancreatitis
  • increased ammonia levels
  • thrombocytopenia (monitor CBC)
  • suicidal thoughts
  • can cause liver toxicity (watch LFTs)
252
Q

Gabapentin (Neurontin): Action? Seizure indications?

A

Thought to act on the calcium channels to decrease glutamate and increase GABA in the brain

Indications:
- partial seizures
- new onset epilepsy
- MAY MAKE MYOCLONIC SEIZURES WORSE

253
Q

Gabapentin (neurontin): off-label uses

A
  • chronic neuropathic pain
  • anxiety
  • hot flashes/night sweats
  • headaches
  • hiccups
  • alcohol withdrawal
254
Q

Gabapentin (Neurontin): side effects

A
  • fatigue: given at night often
  • mental cloudiness
  • leukopenia
  • weight gain
  • edema
  • emotional lability
  • tremors
  • GI side effects
  • suicidal thoughts
255
Q

Gabapentin (Neurontin): Administration considerations

A
  • reduced dose in renal patients: monitor BUN/Cr
  • caution in those with addiction history
  • no drug monitoring needing b/c wide therapeutic range
  • withdrawal slowly
  • doses will be very high for pain control
256
Q

What is glycolysis?

A

the step by step process of breaking down of glucose into pyruvic acid, NADH, and ATP (energy)

257
Q

What is glycogen?

A

when your body does not immediately need glucose from the food you eat for energy, it stores glucose primarily in muscle and the liver as glycogen for later use

258
Q

What is gluconeogenesis

A

process of glucose formation from non-carbohydrate substances

259
Q

What is glycogenolysis

A

the breakdown of stored glycogen to glucose

260
Q

What is gluconeogenesis

A

the synthesis of glucose from non-carbohydrate sources
- the opposite process of glycolysis

261
Q

What is glucagon?

A

a hormone produced by alpha cells in the pancreas
- it is released in response to a drop in blood sugar, prolonged fasting, exercise, and protein-rich meals

NUR 516 (22 decks)

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