NUR 516 > Quiz 4 > Flashcards

Quiz 4 Flashcards

(Lipid meds, Thyroid, Diabetic Oral meds, Insulin done, Diabetes type 1/2) (261 cards)

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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
Pt Education: CAI | Who should not take?
Can be given in combination with statins Do not take in pregnancy or breastfeeding
26
Mechanism of Action/Pathophys: Bile Acid Sequestrants (B.A.S)
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 ## Footnote Not routinely used but strong record of efficacy and safety
27
Side Effects: Bile Acid Sequestrants (5)
* Constipation * Abdominal Pain * Diarrhea * Heartburn * Gallstones
28
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?
- 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
29
Side Effects: PCSK9 Inhibitors | Administered SUBQ
* Itching * Swelling * Pain or bruising at injection site
30
Mechanism of Action/Pathophys: PCSK9 Inhibitors | Reserved for which patients? Safe to use with?
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)
31
Nursing considerations: PCSK9 Inhibitors
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
32
Mechanism of Action/Pathophys: Fibrates
* Inhibition of cholesterol synthesis - decrease triglyceride synthesis * Inhibition of lipolysis in adipose tissue * lower total cholesterol, LDL - Increase HDL - helps remove from blood
33
Side Effects: Fibrates (Flushed…flush the urine)
* Flushed Face/Neck * Increased uric acid levels (be careful in those with gout) * Increase risk of rhabdomyolysis (rare) * GI tract issues * Headache
34
Nursing Considerations (Labs/vital sings): Fibrates Monitor when? Not recommended for who? Drug interactions?
* 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
35
What is the largest endocrine gland?
Thyroid gland ## Footnote The thyroid is responsible for producing key hormones that regulate metabolism.
36
Name the three hormones produced by the thyroid gland.
* Thyroxine (T4) * Triiodothyronine (T3) * Calcitonin
37
What is the function of T4 and T3?
Needed for metabolism
38
What does 'euthyroid' refer to?
Normal thyroid gland function
39
What is a goiter?
Visible enlargement of the thyroid gland
40
What is Graves Disease?
Antibody mediated autoimmune disease resulting in hyperthyroidism
41
What is Hashimoto’s Thyroiditis?
Autoimmune disease often resulting in hypothyroidism
42
What are the functions of thyroid hormones?
* 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
43
What controls the secretion of T3 and T4?
Thyroid Stimulating Hormone (TSH) from the anterior pituitary
44
How does TSH control the rate of thyroid hormone release?
Via a negative feedback mechanism
45
What happens to TSH levels when thyroid hormone levels are high?
Inhibition of TSH
46
What are the normal thyroid levels for TSH?
0.4 to 4.5
47
What TSH level indicates hyperthyroidism?
Less than 0.4
48
What TSH level indicates hypothyroidism?
Above 4.5 ## Footnote Can be primary or autoimmune (Hasimotos, thyroiditis)
49
List some symptoms of hypothyroidism.
* Fatigue * Depression * Dry Skin * Constipation * Bradycardia * Altered menstrual cycles * Weight gain * Changes in hair * Cold intolerance
50
What is myxedema?
Severe hypothyroidism
51
What medication is commonly used for hypothyroidism?
Levothyroxine
52
Hypothroid medications (2)
Levothyroxine Armour Thyroid (desiccated)
53
Hyperthyroid medications
Methimazole Propylthiouracil (PTU) Iodine Solutions
54
What is the brand name for synthetic T4?
Synthroid, Levoxyl
55
What is the half-life of Levothyroxine?
6-7 days
56
What should be avoided when taking Levothyroxine/ Armour Thyroid
Calcium containing medications, antacids, or iron supplements
57
What is hyperthyroidism?
Increased in circulating T3 and T4 from overactive thyroid or excessive thyroid hormone production ## Footnote Graves disease is hyper-functioning thyroid
58
What is the main treatment for Graves Disease?
Beta blockers (e.g., Propranolol or Atenolol)
59
What are the symptoms of hyperthyroidism?
* Anxiety * Restlessness * Diaphoresis * Diarrhea, N/V * Tachycardia / AFib * Weight loss * Heat intolerance * Exophthalmos * Changes in menstrual cycle * Insomnia
60
What is Lugol’s Solution used for? | IODINE
* Inhibits release of T3 and T4 * short-term use * can cause iodinism
61
I-131
* Iodine (Radioactive) * Use for thyroid cancer, thyrotoxicosis/special cases * Not for pregnancy * Increase fluid intake * Radiation precautions
62
What are the side effects of Iodine Solutions?
* Metallic taste * Stomatitis * Sore throat * Hypersensitivity
63
What is desiccated thyroid? | AMOUR THYROID
Thyroid extract from animal thyroid glands that have been dried and powdered -Contains both T3/T4 Side Effects: Change in appetite, chest pain, diarrhea
64
Nursing Considerations: Armour thyroid
Based on TSH results Life-long medications Safe in pregnancy Should have TSH checked regularly until stablized (6-8 weeks after then annually)
65
What is the drug of choice for hyperthyroidism?
Methimazole
66
What does Propylthiouracil (PTU) do?
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
67
What is the treatment goal for hyperthyroidism?
Decreasing thyroid hyperactivity and preventing complications
68
What must be monitored when using PTU?
* LFTs * CBC
69
What is the usual duration for checking TSH after starting thyroid medication?
6-8 weeks after starting and after dose changes
70
Can thyroid medications be used safely during pregnancy?
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
71
Thioamides Baseline labs? When to take? | Inhibits what? Methimazole/PTU
* 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
72
Medication given for Thioamides | Both have THI?
Methimazole Propylthiouracil (PTU)
73
Methimazole | THIOAMIDE
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)
74
PTU | THIOAMIDE
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
75
Adjuvant therapy-Beta blockers | hyperthyroidism
* Propanolol/Atenolol * To control symptoms * Used in Tachy/arrythmic/HTN adults * Used to control sxs while waiting for meds to take effect
76
Explain the process of insulin resistance and how it leads to the development of Type 2 DM
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
77
Glycemic Targets (ADA) A1C FPG PPG
* A1C < 7% * FPG 80-130 * PPG <140
78
Explain how the SNS, RAAS and the inflammatory response increase insulin resistance?
From her type 2 diabetes PP: Basically, RAAS/SNS leads to increased inflammation which leads to more insulin resistance
79
How does metformin reduce blood sugar in the Type 2 DM?
- Improves how insulin works in the body (Insulin sensitizer) - Decreases absorption of carbohydrates - Decreases glucose production in the liver - Decreases appetite
80
Most frequent side effects of metformin?
* GI side effects (common) * Bloating * Diarrhea * Abdominal pain * Nausea * Metallic taste | Increased risk for B12 deficiency
81
What are the significant nursing interventions needed for those patients who take Metformin?
- 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
82
What lab test other than the BS should the nurse be aware when administering metformin?
Renal/hepatic?
83
How do the sulfonylureas reduce blood sugar?
Stimulates Beta cells to secrete insulin Decrease glucose production by the liver | *Glipizide and glyburide*
84
Why do sulfonylureas cause weight gain?
online: the increased insulin levels promote the storage of excess glucose as fat
85
What are the nursing interventions for Sulfonylureas? Onset?
* Monitor for hypoglycemia * Onset at 90 minutes and peak in 2-3 hours
86
Patients allergic to what medications should take sulfonylureas with caution?
DO NOT GIVE IF ALLERGIC TO SULFA DRUGS ## Footnote ALso not for pregnant/lactating women/beta blockers
87
How are the Meglitinides the same as the sulfonlyureas? different from the sulfonylureas
online: They induce insulin secretion from pancreas, with a different mechanism of action from sulfonylureas
88
How will the nurse know if Meglintinides are working? | When should pt take it?
Check BS levels?? Onset at 90 minutes and peak in 2-3 hours ## Footnote Should be taken with first bite of food (CUZ IM MEGA HUNGRY)
89
How do alpha glucosidase inhibitors work to decrease blood sugar?/ When are these meds used most frequently?
"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.
90
-How do Thiazolidinediones work to reduce blood sugar? -Contraindicated for which group of patients? -Why do these patients gain weight?
-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
91
Explain the role of the incretins in glucose control? | GLP-1 Agonist
enhancing insulin release, suppressing glucagon, slowing digestion, and reducing appetite, ultimately improving blood sugar control and potentially leading to weight loss
92
# INCRETINS (GLP-1) -Why do these patietns often lose weight on these meds? -Who should NOT receive these meds?
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?
93
How do the DPP-4 inhibitors work to decrease blood sugar?
* 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
94
Major nursing considerations for DPP-4?
Hypoglycemia
95
How do sodium glucose co transport inhibitors work?
Inhibit reabsorption of glucose in the proximal renal tubules; promote glucose excretion in urine
96
Side effects of sodium glucose co transport inhibitors?
Increase risk : Yeast infections, UTIs, and Amputation?
97
What is the primary action of insulin?
Hormones that controls the storage and metabolism of carbohydrates, proteins, and fats ## Footnote This activity occurs primarily in the liver, in muscle, and in adipose tissues.
98
What does insulin stimulate in the liver?
Synthesis of glycogen
99
How does insulin affect protein and fat storage?
Promotes protein synthesis and helps store fat by preventing its breakdown for energy
100
From where is insulin released?
Beta cells of the Islet of Langerhans in response to increased blood sugar
101
What is the goal of insulin therapy?
To mimic the physiological control of blood glucose levels
102
What are the two physiological blood glucose levels of insulin secretion?
* Basal insulin levels – during fasting * Postprandial levels – after eating
103
What are the indications for insulin use?
* 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
104
What is the recommended method of insulin administration?
Only use an insulin syringe and administer subcutaneously
105
What is lipodystrophy?
A condition that can be prevented by rotating injection sites ## Footnote Keep injections about 1.5 in away from eachother and if BID use both L and R side
106
What should be the distance between insulin injection sites?
About 1.5 inches away from each other
107
What are the methods of insulin administration?
* Insulin pumps * Insulin pen injectors * Insulin syringes
108
Name the types of insulin.
* Rapid-Acting * Short-Acting (Regular) * Intermediate * Long-Acting
109
What are the names of rapid-acting insulin drugs? All, guys, like, Inside. Which is rapid…and deadly..
* Aspart * Glulisine * Lispro * Inhaled Insulin | most deadly type of insulin
110
Nursing considerations for Rapid- Acting Insulin
* Must be given with food * Usually given in conjunction with intermediate acting insulin * Always monitor for hyPOglycemia
111
What is the onset time for Aspart, Glulisine, and Lispro?
5-15 minutes ## Footnote Inhaled insulin onsent within ONE minute
112
What is the peak time for rapid-acting insulin?
30-90 minutes ## Footnote inhaled insulin within 12-15 min
113
True or False: Food must be present when administering rapid-acting insulin.
True
114
What is the duration of action for rapid-acting insulin?
3-5 hours
115
What is the primary use for short-acting insulin? | AKA REGULAR INSULIN
To cover the glucose rise after eating a meal
116
When should short-acting insulin be administered?
30 minutes before meals
117
What happens if regular insulin is cloudy?
Throw it out
118
Nursing considerations: Short acting (Normal) insulin
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
What is intermediate-acting insulin also known as?
Isophane or NPH (Neutral Protamine Hagedorn)
120
How often is intermediate-acting insulin usually given?
Twice a day
121
What is the typical dosing schedule for intermediate-acting insulin?
2/3 in the morning and 1/3 in the evening ## Footnote 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
What is the onset of action for long-acting insulin?
Up to 1.5 – 2 hours
123
What is the duration of action for long-acting insulin?
24+ hours
124
What is a notable characteristic of long-acting insulin absorption?
Even absorption with no peaks and valleys | Frequently used in Type 2 DM
125
What is the dosing range for insulin?
0.6-0.8 units/kg/day
126
What is sliding-scale insulin?
Adjusted doses dependent on individual blood glucose, usually reserved for inpatient use
127
How should unopened vials of insulin be stored?
Refrigerated until needed
128
How long can opened insulin vials be stored at room temperature?
1 month
129
What is the antidote for hypoglycemia?
Sugar
130
What should patients with Type 1 DM do even if NPO?
Will need insulin
131
What should diabetic patients wear as a precaution?
A medical alert tag
132
what is Type-1 Diabetes Mellitus | types?
-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
What is ketosis?
A metabolic state where the body uses free fatty acids for energy instead of glucose
134
What is polyuria?
Increased amount and frequency of urination due to renal threshold for glucose reabsorption being exceeded. | Glucose >180 ## Footnote Results in glucose remaining in renal tubule and an osmotic gradient that pulls water from tubule cells into urine.
135
What are the classic symptoms of Type 1 Diabetes Mellitus? 3 P’s
* Polyuria * Polydipsia * Polyphagia ## Footnote Other symptoms may include blurred vision, fatigue, and weakness.
136
What is diabetic ketoacidosis (DKA)? symptoms? (4) Occurs mainly in?
A hyperglycemic emergency characterized by hyperglycemia, metabolic acidosis, dehydration, and electrolyte loss. ## Footnote Often presents in Type 1 Diabetes but can occur in Type 2. -stored fatty acids can cause DKA
137
What triggers ketosis in diabetes?
Insulin deficiency leads to the breakdown of fat into free fatty acids and glycerol, converted into ketones by the liver. ## Footnote Ketones are strong acids that can lead to metabolic acidosis.
138
What is the dawn phenomenon?
Increase in fasting blood glucose and/or insulin requirements during early morning hours due to nocturnal elevation of growth hormone. ## Footnote Not triggered by nocturnal hypoglycemic events.
139
Difference between dawn phenomenon and somogyi effect
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
What is the Somogyi effect?
Nocturnal hypoglycemia followed by rebound hyperglycemia due to counter-regulatory hormone release. ## Footnote Occurs from too much or too little insulin at bedtime.
141
Clinical manifestations of Diabetes type-1
* 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
Polyphagia
Increased appetite with weight loss -Insulin deficiency-cells not receiving glucose- sets into effect compensatory processes to increase blood glucose levels.
143
What are the three main causes of DKA?
* Infection or illness * Lack of Insulin * Undiagnosed or undertreated diabetes ## Footnote These factors can precipitate DKA in patients.
144
What is the initial treatment for DKA?
Fluid replacement to restore intravascular volume and correct electrolyte imbalances. ## Footnote Insulin therapy is also initiated once fluids are administered.
145
What are the clinical manifestations of DKA?
* Extreme dehydration * Poor skin turgor * Dry mucous membranes * Tachycardia * Hypotension * Acetone breath * Kussmaul respirations * Changes in LOC ## Footnote Presenting symptoms also include the 3 P’s and weight loss.
146
What does hyperglycemia cause in relation to thirst?
Increased osmotic pressure in the extracellular compartment causes water to shift out of the intracellular space, leading to cellular dehydration and thirst sensation. ## Footnote This condition is known as polydipsia.
147
Define hypoglycemia.
Blood glucose level < 70 mg/dL with or without symptoms. ## Footnote Most commonly occurs in patients treated with insulin.
148
What is the normal glucose levels?
70-100
149
What glucose levels are considered prediabetic?
101-125
150
What glucose level is considered to be diabetic?
>126
151
What are common electrolyte issues in DKA?
* Hyponatremia * Hyperkalemia ## Footnote These imbalances need to be monitored during treatment.
152
What causes blurred vision in diabetes?
Accumulation of glucose in aqueous fluid in the cornea alters refraction of light entering the eye
153
What characterizes Type 1 Diabetes Mellitus?
Total destruction of the pancreatic beta cells due to autoimmune response ## Footnote Includes Type 1A (90-95%) and Type 1B (idiopathic, no autoimmune).
154
What is the glucose range for hypoglycemia? Common causes?
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
What is the role of glucagon in hypoglycemia?
Triggers the release of glycogen from the liver
156
What happens during gluconeogenesis?
The body creates glucose from non-carbohydrate sources instead of using the Krebs cycle
157
What are the functions of glucose, fat, and proteins in meeting the energy needs of the body?
Glucose provides energy for cells, fat is the most dense fuel storage, and proteins are building blocks for tissues ## Footnote Glucose is absorbed into the bloodstream at the intestines and is essential for normal cerebral function.
158
What are counter-regulatory hormones?
Hormones that counteract the effects of insulin: glucagon, epinephrine, cortisol, and growth hormones ## Footnote They help increase blood glucose levels when they drop.
159
What distinguishes Type 1 diabetes from Type 2 diabetes?
Type 1 is characterized by autoimmune destruction of pancreatic beta cells; Type 2 involves insulin resistance and deranged insulin secretion/gestational/drug induced ## Footnote Type 1A is autoimmune, while Type 1B is idiopathic.
160
Define metabolic syndrome and its association with Type 2 diabetes.
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
Physical Symptoms of metabolic syndrome
Increased waist circumference or belly fat High triglycerides Elevated BP High BS Low LDL Apple Shape Ancanthosis Nigricans
162
Clinical manifestations of Metabolic syndromes
* Hyperglycemia causes intracellular fluid shifts ------>polydipsia * Excessive diuresis causes polyuria * Cell starvation from lack of glucose ---------> polyphagia * Fatigue * Weakness * Weight loss * Visual disturbances
163
What happens to glucose in the presence of oxygen?
It breaks down to form CO2 and water ## Footnote This process is part of cellular respiration.
164
What happens to glucose after absorption?
It is used for energy, stored as glycogen in the liver, or converted into fat ## Footnote Excess glucose can also be excreted in urine.
165
What is glycogenolysis?
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
What is gluconeogenesis?
The synthesis of glucose by the liver from non-carbohydrate sources ## Footnote It primarily occurs from amino acids and fats. Can lead to development of ketones
167
What role does insulin play in glucose metabolism?
Insulin stimulates the uptake, use, and storage of glucose by promoting glycogen synthesis and inhibiting gluconeogenesis ## Footnote It is released by beta cells in the pancreas.
168
What are the glucose-regulating hormones?
Amylin, somatostatin, glucagon, and incretins ## Footnote Amylin slows glucose absorption, while glucagon promotes glucose production.
169
Different ways to regulate glucose:
Increased blood glucose Beta cells Insulin & Amylin Vs Hypoglycemia Alpha cells Glucagon
170
Insulin stimulates the uptake, use, and storage of _____
glucose
171
Which hormone is required to initiate active transport of glucose into the cell?
Insulin
172
What are the risk factors for Type 2 diabetes?
* Family history * Obesity * Ethnicity * Age * Gestational diabetes * Hypertension * Polycystic ovary syndrome (PCOS) * Smoking and alcohol ## Footnote These factors contribute to insulin resistance and deranged insulin secretion.
173
Why does obesity cause insulin resistance?
* 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
When are insulin levels their highest?
After a meal ## Footnote Insulin levels decrease during fasting.
175
What are the symptoms of hypoglycemia? (13)
* Fatigue * Sweating * Hunger * Dizziness * Rapid heart rate * Anxiety * Irritability * Shakiness * Blurred vision * Confusion * Loss of consciousness * Seizures * Coma ## Footnote Symptoms vary from mild to severe depending on blood sugar levels.
176
What is Hyperosmolar Hyperglycemic Syndrome (HHS)? Causes? How is it unlike DKA?
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 ## Footnote Unlike DKA, there is no ketone formation in HHS.
177
Symptoms/Treatment of HHS (hyperosmolar hyperglycemic state)
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
What is the diagnostic criteria for diabetes?
* 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) ## Footnote These criteria help in the accurate diagnosis of diabetes.
179
Glycated Hemoglobin A1c
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
What causes diabetic neuropathy? Types?
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
What lifestyle factors increase insulin resistance?
* Sedentary lifestyle * Poor diet (high glycemic carbohydrates) * Smoking ## Footnote These factors contribute to obesity and stress on pancreatic beta cells.
182
Fill in the blank: The body responds to increased blood sugar levels by stimulating the pancreas to release _______.
[insulin]
183
True or False: Type 2 diabetes accounts for 90-95% of all diabetes cases. | Why
True
184
Why is it necessary for a person to maintain blood glucose no lower than 70?
To maintain a continuous supply of glucose for energy
185
Patient education with bile acid sequestrants
- 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
Patient education with PCSK9 Inhibitors
- are very expensive compared to other classes - can be given in conjunction with statins - decrease LDL, cholesterol, and triglycerides
187
Patient education with fibrates
- do not take with warfarin or statins - will need periodic monitoring - not recommended for diabetics
188
What are the differences between the statins?
- 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
Why are statins not just for cholesterol lowering?
they play some role in vasodilation
190
What does it mean to stabilize the plaque? Why is that important?
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
What is included in a lipid profile? Where do we want the patient to be?
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
What does improve endothelial function mean? How do statins play a role?
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
What are the inhibitory neurotransmittors?
dopamine, serotonin, and GABA
194
What are the excitatory neurotransmitters?
ACH (acetylcholine) and norepinephrine
195
Neurotransmitters: Acetylcholine - where is it found, what type of action?
- 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
Neurotransmitters: Serotonin (5-hydroxytrptamine) - where is it found, what type of action?
- derived from tryptophan - found primarily in the GI tract, platelets, and brainstem - contributor to feeling of well being - inhibitory
197
Neurotransmitters: Dopamine - where is it found, what type of action?
- 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
Neurotransmitters: GABA (gamma amino butyric acid) - where is it found, what type of action?
- 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
Neurotransmitters: Norepinephrine
an excitatory neurotransmitter in the brain stress hormone within the endocrine system
200
Neurotransmitters: Glutamate
- major mediator of excitatory signal - involved in cognition, memory, and learning
201
How do neurons do conduction?
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
What are the three phases of an action potential?
- depolarization of the neuron: positively charged ion - repolarization of neuron: return of neuron to a negative value - resting period
203
What leads to seizures, regarding the action potential?
impulses that do not maintain a systematic order (excitatory, inhibitory, and resting phase) become irregular and chaotic and can lead to seizures
204
What are seizures?
a single episode of abnormal electrical discharge from cortical neurons that results in an abrupt and temporary altered state
205
What is epilepsy
a group of syndromes characterized by unprovoked, recurrent seizures
206
What is status epilepticus?
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
What are common causes of seizures?
- trauma - ETOH withdrawal - illicit drug use - brain tumor - congenital malformations - stroke - metabolic disorders (uremia, electrolyte imbalance) - alzheimer's disease - neurodegenerative disease - idiopathic
208
What are common causes of epilepsy?
- genetic causes (mutated genes) - head trauma - medical disorders (dementia, meningitis, encephalitis) - prenatal injury - developmental disorders (autism, Down syndrome)
209
Pathophysiology of seizures
- 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
Examples of generalized seizures?
- absence (petit mal) - tonic-clonic (grand mal) - atonic/akinetic (drop attacks) - status epilepticus
211
Pathophysiology of focal seizure
- **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
What are automatisms?
- 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
Types of focal or partial seizure
- focal - retains awareness - focal - altered awareness - partial seizure
214
Focal seizure - retaining awareness
- no impairment of consciousness - similar to partial seizures - may have movement of body parts - may experience an aura
215
Focal seizure - altered awareness
- impairment of consciousness - spreads to both hemispheres (this confuses me though because i thought it should start and remain in one hemisphere)
216
Partial seizure
- begins in one part of hemisphere (typically in the temporal or frontal lobe) - may be simple or complex
217
Pathophysiology of generalized seizures
- **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
Tonic-clonic seizure
- begin with rigid violent contractions (tonic) - followed by repetitive clonic activity of all extremities - body stiffens and relaxes generalized
219
Tonic seizure
generalized - muscle stiffness, dilation of pupils, altered respirations - usually lasts less than a minute
220
Absence seizures
generalized - short episodes of staring and loss of consciousness for about 10 seconds
221
Myoclonic seizures
generalized - bilateral jerking of muscles - no loss of consciousness
222
Atonic seizure
generalized - sudden loss of muscle - "drop to the ground"
223
What is needed for a diagnosis of seizure and/or epilepsy
- H&P - neurological exam - diagnostic procedures (chemistries, tox screen, CT, MRI, EEG)
224
What are the phases of seizures?
Pre-ictal, ictal, and post-ictal
225
What is the pre-ictal phase of a seizure?
may be started by a trigger and/or preceded by an aura
226
What is the ictal phase of a seizure?
- actual seizure - increases in metabolic demand (uses a lot of energy)
227
What is the post-ictal phase of a seizure?
- has decreased responsiveness - feels fatigue
228
What are anticonvulsants used for
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
What are broad-spectrum anticonvulsants used for
effective for treatment of focal and generalized seizures
230
What are narrow-spectrum anticonvulsants used for
used primarily for focal-onset seizures (including focal which evolve to be convulsive seizures)
231
Mechanism of actions by group - fit anticonvulsants (just an image in ppt that may be helpful)
232
Sodium channel blockers: what do they do with seizures
- prevent return of the channel to active state, stabilizes them to inactive state - prevents repetitive firing
233
Calcium channel blockers: what do they do with seizures
- 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
What do GABA enhancers do with seizures
- 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
What do glutamate blockers do with seizures?
- bind to glutamate, which is an excitatory neurotransmitter, therefore blocking it from binding and creating excitation - glutamate receptor has 5 potential binding sites
236
What does "pharmacologic management” mean regarding seizures
- 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
Phenytoin (Dilantin): what type of med? How does it work? Indications?
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
Phenytoin (Dilantin): Therapeutic range and administration?
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
Phenytoin (Dilantin): side effects? *”pheny” = funny smile *
- **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
Phenobarbital (Solfoton, Luminal): what does it do? what class? administration considerations?
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
Phenobarbital (Solfoton, Luminal): side effects
- sedation - diplopia - cognitive skill impairment - respiratory depression - hypotension - hyperactivity and inattention in children
242
Carbamazepine (Tegretol): What class? What does it do? When is it used? Storage?
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
What type of seizures is carbamazepine (tegretol) the drug of choice for?
partial and generalized tonic-clonic seizures
244
What seizures does carbamazepine make worse?
absence and myoclonic seizures
245
Carbamazepine: What needs to be monitored?
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
Carbamazepine: Side effects
- 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
Oxycarbazepine (trileptal): How does it work? What class?
Sodium channel blocker - same efficacy as carbamazepine but is better tolerated
248
Oxycarbazepine (trileptal): What seizures is it used for and NOT used for? Considerations?
- 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
Valproic Acid/Valproate (Depakote): How does it work? What class? Indications?
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
Valproic Acid/Valproate (Depakote): Administration and monitoring Can give with? Monitor what? Therapeutic range?
- 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
Valproic Acid/Valproate (Depakote): side effects
- N/V - sedation/dizziness - pancreatitis - increased ammonia levels - thrombocytopenia (monitor CBC) - suicidal thoughts - can cause liver toxicity (watch LFTs)
252
Gabapentin (Neurontin): Action? Seizure indications?
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
Gabapentin (neurontin): off-label uses
- chronic neuropathic pain - anxiety - hot flashes/night sweats - headaches - hiccups - alcohol withdrawal
254
Gabapentin (Neurontin): side effects
- fatigue: given at night often - **mental cloudiness** - leukopenia - weight gain - edema - emotional lability - tremors - GI side effects - suicidal thoughts
255
Gabapentin (Neurontin): Administration considerations
- 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
What is glycolysis?
the step by step process of breaking down of glucose into pyruvic acid, NADH, and ATP (energy)
257
What is glycogen?
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
What is gluconeogenesis
process of glucose formation from non-carbohydrate substances
259
What is glycogenolysis
the breakdown of stored glycogen to glucose
260
What is gluconeogenesis
the synthesis of glucose from non-carbohydrate sources - the opposite process of glycolysis
261
What is glucagon?
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
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