Final (Combining Decks) Flashcards

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 triglyceride level

A

<200

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11
Q

Desired Total HDL level

A

> 50

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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

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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19
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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20
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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21
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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22
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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23
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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24
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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25
Nursing Considerations (Labs/vital sings): Statin | caution combining with what med?
- 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
26
Side Effects: CAI | CAI work on small intestines...
* Abdominal pain and Diarrhea (most common) * Upper airway infections * Arthralgias (joint pain)
27
Pt Education: CAI | Who should not take?
Can be given in combination with statins Do not take in pregnancy or breastfeeding
28
Nursing Considerations (Labs/vital sings): CAI | Contraindications? Can take with?
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
29
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
30
Side Effects: PCSK9 Inhibitors | Administered SUBQ
* Itching * Swelling * Pain or bruising at injection site
31
Side Effects: Bile Acid Sequestrants (5)
* Constipation * Abdominal Pain * Diarrhea * Heartburn * Gallstones
32
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
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
What is the brand name for synthetic T4?
Synthroid, Levoxyl
53
What is the half-life of Levothyroxine?
6-7 days
54
What should be avoided when taking Levothyroxine/ Armour Thyroid
Calcium containing medications, antacids, or iron supplements
55
What is hyperthyroidism?
Increased in circulating T3 and T4 from overactive thyroid or excessive thyroid hormone production ## Footnote Graves disease is hyper-functioning thyroid
56
What is the main treatment for Graves Disease?
Beta blockers (e.g., Propranolol or Atenolol)
57
What are the symptoms of hyperthyroidism?
* Anxiety * Restlessness * Diaphoresis * Diarrhea, N/V * Tachycardia / AFib * Weight loss * Heat intolerance * Exophthalmos * Changes in menstrual cycle * Insomnia
58
What is Lugol’s Solution used for? | IODINE
* Inhibits release of T3 and T4 * short-term use * can cause iodinism
59
What are the side effects of Iodine Solutions?
* Metallic taste * Stomatitis * Sore throat * Hypersensitivity
60
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
61
What is the drug of choice for hyperthyroidism?
Methimazole
62
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
63
What is the treatment goal for hyperthyroidism?
Decreasing thyroid hyperactivity and preventing complications
64
What must be monitored when using PTU?
* LFTs * CBC
65
What is the usual duration for checking TSH after starting thyroid medication?
6-8 weeks after starting and after dose changes
66
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
67
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
68
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
69
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
70
Most frequent side effects of metformin?
* GI side effects (common) * Bloating * Diarrhea * Abdominal pain * Nausea * Metallic taste | Increased risk for B12 deficiency
71
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
72
What lab test other than the BS should the nurse be aware when administering metformin?
Renal/hepatic?
73
How do the sulfonylureas reduce blood sugar?
Stimulates Beta cells to secrete insulin Decrease glucose production by the liver | *Glipizide and glyburide*
74
Why do sulfonylureas cause weight gain?
online: the increased insulin levels promote the storage of excess glucose as fat
75
What are the nursing interventions for Sulfonylureas? Onset?
* Monitor for hypoglycemia * Onset at 90 minutes and peak in 2-3 hours
76
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
77
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
78
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)
79
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.
80
-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
81
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
82
# 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?
83
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
84
Major nursing considerations for DPP-4?
Hypoglycemia
85
How do sodium glucose co transport inhibitors work?
Inhibit reabsorption of glucose in the proximal renal tubules; promote glucose excretion in urine
86
Side effects of sodium glucose co transport inhibitors?
Increase risk : Yeast infections, UTIs, and Amputation?
87
Glycemic Targets (ADA) A1C FPG PPG
* A1C < 7% * FPG 80-130 * PPG <140
88
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.
89
What does insulin stimulate in the liver?
Synthesis of glycogen
90
How does insulin affect protein and fat storage?
Promotes protein synthesis and helps store fat by preventing its breakdown for energy
91
From where is insulin released?
Beta cells of the Islet of Langerhans in response to increased blood sugar
92
What is the goal of insulin therapy?
To mimic the physiological control of blood glucose levels
93
What are the two physiological blood glucose levels of insulin secretion?
* Basal insulin levels – during fasting * Postprandial levels – after eating
94
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
95
What is the recommended method of insulin administration?
Only use an insulin syringe and administer subcutaneously
96
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
97
What should be the distance between insulin injection sites?
About 1.5 inches away from each other
98
What are the methods of insulin administration?
* Insulin pumps * Insulin pen injectors * Insulin syringes
99
Name the types of insulin.
* Rapid-Acting * Short-Acting (Regular) * Intermediate * Long-Acting
100
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
101
What is the onset time for Aspart, Glulisine, and Lispro?
5-15 minutes ## Footnote Inhaled insulin onsent within ONE minute
102
What is the peak time for rapid-acting insulin?
30-90 minutes ## Footnote inhaled insulin within 12-15 min
103
True or False: Food must be present when administering rapid-acting insulin.
True
104
What is the duration of action for rapid-acting insulin?
3-5 hours
105
What is the primary use for short-acting insulin? | AKA REGULAR INSULIN
To cover the glucose rise after eating a meal
106
When should short-acting insulin be administered?
30 minutes before meals
107
What happens if regular insulin is cloudy?
Throw it out
108
What is intermediate-acting insulin also known as?
Isophane or NPH (Neutral Protamine Hagedorn)
109
How often is intermediate-acting insulin usually given?
Twice a day
110
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
111
What is the onset of action for long-acting insulin?
Up to 1.5 – 2 hours
112
What is the duration of action for long-acting insulin?
24+ hours
113
What is a notable characteristic of long-acting insulin absorption?
Even absorption with no peaks and valleys | Frequently used in Type 2 DM
114
What is the dosing range for insulin?
0.6-0.8 units/kg/day
115
What is sliding-scale insulin?
Adjusted doses dependent on individual blood glucose, usually reserved for inpatient use
116
How should unopened vials of insulin be stored?
Refrigerated until needed
117
How long can opened insulin vials be stored at room temperature?
1 month
118
What is the antidote for hypoglycemia?
Sugar
119
What should patients with Type 1 DM do even if NPO?
Will need insulin
120
What should diabetic patients wear as a precaution?
A medical alert tag
121
Nursing considerations for Rapid- Acting Insulin
* Must be given with food * Usually given in conjunction with intermediate acting insulin * Always monitor for hyPOglycemia
122
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
123
Hypothroid medications (2)
Levothyroxine Armour Thyroid (desiccated)
124
Hyperthyroid medications
Methimazole Propylthiouracil (PTU) Iodine Solutions
125
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)
126
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
127
Medication given for Thioamides | Both have THI?
Methimazole Propylthiouracil (PTU)
128
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)
129
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
130
I-131
* Iodine (Radioactive) * Use for thyroid cancer, thyrotoxicosis/special cases * Not for pregnancy * Increase fluid intake * Radiation precautions
131
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
132
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.
133
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.
134
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
135
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.
136
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.
137
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.
138
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.
139
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.
140
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.
141
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.
142
Define hypoglycemia.
Blood glucose level < 70 mg/dL with or without symptoms. ## Footnote Most commonly occurs in patients treated with insulin.
143
What are common electrolyte issues in DKA?
* Hyponatremia * Hyperkalemia ## Footnote These imbalances need to be monitored during treatment.
144
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
145
What is ketosis?
A metabolic state where the body uses free fatty acids for energy instead of glucose
146
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
147
Polyphagia
Increased appetite with weight loss -Insulin deficiency-cells not receiving glucose- sets into effect compensatory processes to increase blood glucose levels.
148
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
149
What causes blurred vision in diabetes?
Accumulation of glucose in aqueous fluid in the cornea alters refraction of light entering the eye
150
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).
151
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
152
What is the role of glucagon in hypoglycemia?
Triggers the release of glycogen from the liver
153
What happens during gluconeogenesis?
The body creates glucose from non-carbohydrate sources instead of using the Krebs cycle
154
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.
155
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.
156
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.
157
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
158
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.
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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.
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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
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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
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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.
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What are the glucose-regulating hormones?
Amylin, somatostatin, glucagon, and incretins ## Footnote Amylin slows glucose absorption, while glucagon promotes glucose production.
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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.
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When are insulin levels their highest?
After a meal ## Footnote Insulin levels decrease during fasting.
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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.
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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.
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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.
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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
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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.
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Fill in the blank: The body responds to increased blood sugar levels by stimulating the pancreas to release _______.
[insulin]
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True or False: Type 2 diabetes accounts for 90-95% of all diabetes cases. | Why
True
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Insulin stimulates the uptake, use, and storage of _____
glucose
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Which hormone is required to initiate active transport of glucose into the cell?
Insulin
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Different ways to regulate glucose:
Increased blood glucose Beta cells Insulin & Amylin Vs Hypoglycemia Alpha cells Glucagon
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What is the normal glucose levels?
70-100
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What glucose levels are considered prediabetic?
101-125
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What glucose level is considered to be diabetic?
>126
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Physical Symptoms of metabolic syndrome
Increased waist circumference or belly fat High triglycerides Elevated BP High BS Low LDL Apple Shape Ancanthosis Nigricans
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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
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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)
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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.
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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
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Why is it necessary for a person to maintain blood glucose no lower than 70?
To maintain a continuous supply of glucose for energy
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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
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Patient education with PCSK9 Inhibitors
- are very expensive compared to other classes - can be given in conjunction with statins - decrease LDL, cholesterol, and triglycerides
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Patient education with fibrates
- do not take with warfarin or statins - will need periodic monitoring - not recommended for diabetics
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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
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Why are statins not just for cholesterol lowering?
they play some role in vasodilation
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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
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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
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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.
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What are the inhibitory neurotransmittors?
dopamine, serotonin, and GABA
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What are the excitatory neurotransmitters?
ACH (acetylcholine) and norepinephrine
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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
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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
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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
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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)
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Neurotransmitters: Norepinephrine
an excitatory neurotransmitter in the brain stress hormone within the endocrine system
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Neurotransmitters: Glutamate
- major mediator of excitatory signal - involved in cognition, memory, and learning
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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
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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
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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
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What are seizures?
a single episode of abnormal electrical discharge from cortical neurons that results in an abrupt and temporary altered state
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What is epilepsy
a group of syndromes characterized by unprovoked, recurrent seizures
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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
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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
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What are common causes of epilepsy?
- genetic causes (mutated genes) - head trauma - medical disorders (dementia, meningitis, encephalitis) - prenatal injury - developmental disorders (autism, Down syndrome)
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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
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Examples of generalized seizures?
- absence (petit mal) - tonic-clonic (grand mal) - atonic/akinetic (drop attacks) - status epilepticus
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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
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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
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Types of focal or partial seizure
- focal - retains awareness - focal - altered awareness - partial seizure
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Focal seizure - retaining awareness
- no impairment of consciousness - similar to partial seizures - may have movement of body parts - may experience an aura
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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)
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Partial seizure
- begins in one part of hemisphere (typically in the temporal or frontal lobe) - may be simple or complex
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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
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Tonic-clonic seizure
- begin with rigid violent contractions (tonic) - followed by repetitive clonic activity of all extremities - body stiffens and relaxes generalized
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Tonic seizure
generalized - muscle stiffness, dilation of pupils, altered respirations - usually lasts less than a minute
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Absence seizures
generalized - short episodes of staring and loss of consciousness for about 10 seconds
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Myoclonic seizures
generalized - bilateral jerking of muscles - no loss of consciousness
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Atonic seizure
generalized - sudden loss of muscle - "drop to the ground"
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What is needed for a diagnosis of seizure and/or epilepsy
- H&P - neurological exam - diagnostic procedures (chemistries, tox screen, CT, MRI, EEG)
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What are the phases of seizures?
Pre-ictal, ictal, and post-ictal
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What is the pre-ictal phase of a seizure?
may be started by a trigger and/or preceded by an aura
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What is the ictal phase of a seizure?
- actual seizure - increases in metabolic demand (uses a lot of energy)
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What is the post-ictal phase of a seizure?
- has decreased responsiveness - feels fatigue
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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
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What are broad-spectrum anticonvulsants used for
effective for treatment of focal and generalized seizures
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What are narrow-spectrum anticonvulsants used for
used primarily for focal-onset seizures (including focal which evolve to be convulsive seizures)
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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
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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"
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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)
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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
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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)
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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
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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
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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
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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
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Phenobarbital (Solfoton, Luminal): side effects
- sedation - diplopia - cognitive skill impairment - respiratory depression - hypotension - hyperactivity and inattention in children
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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
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What type of seizures is carbamazepine (tegretol) the drug of choice for?
partial and generalized tonic-clonic seizures
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What seizures does carbamazepine make worse?
absence and myoclonic seizures
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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
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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
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Oxycarbazepine (trileptal): How does it work? What class?
Sodium channel blocker - same efficacy as carbamazepine but is better tolerated
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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
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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
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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
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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)
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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
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Gabapentin (neurontin): off-label uses
- chronic neuropathic pain - anxiety - hot flashes/night sweats - headaches - hiccups - alcohol withdrawal
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Gabapentin (Neurontin): side effects
- fatigue: given at night often - **mental cloudiness** - leukopenia - weight gain - edema - emotional lability - tremors - GI side effects - suicidal thoughts
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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
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What is glycogenolysis
the breakdown of stored glycogen to glucose
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What is gluconeogenesis
the synthesis of glucose from non-carbohydrate sources - the opposite process of glycolysis
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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
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Role of Thrombin and the development of the clot
263
General diffference between intrinsic/extrinsic pathway
Online: The main difference between the intrinsic and extrinsic pathways in blood coagulation lies in their initiation: - the intrinsic pathway is activated by factors within the blood itself, - while the extrinsic pathway is activated by tissue factor released from damaged tissues outside the blood. Both pathways ultimately converge on the common pathway, where factor X is activated, leading to clot formation aPTT- intrinsic PT- Extrinsic
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How does ASA work as an anti-platelet?
-Decreases aggregation and formation of the platelet clot (Blocks Cox-1) -Inhibits prostaglandin production
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How is Clopidogrel a different type of medication? Who takes this medication?
Also an anti-platelet but it INHIBITS platelet aggregation via P2Y12 -It keeps platelets in your blood from attaching to each other and making blood clots -Used for post stent/Post MI/Post stroke patients Starts to work in 24-48 hours but not see full effect for 4-6 days *Used for patients who need the combined therapy of asparin
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Nursing considerations for pt on anti-platelets Who should not be on anti-platelets
Should be stopped at least 2-5 days before surgery Must take everyday unless told otherwise Only provider can stop medication DO NOT GIVE- * Known bleeding disorder * * Active bleeding * * Closed head injuries * * CVA until prove no bleed * * Pregnancy (risk benefit) * * Lactation
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Who can discontinue anti-platelet therapy?
A Qualified healthcare provider
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How does warfarin work?
Inhibits the production of Vit K
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Who might take warfarin?/ Why does warfarin have so many drug interactions?
Used in atrial fibrillation, Valvular heart disease, CVA, DVT and PE prevention, post joint replacement (People at risk of blood clot) - Due to the drug being highly protein-bound
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What is the lab test which monitors warfarin therapy and what is the desired level?
PT/INR Want INR at 2 to 3 For mechanical heart valve = 2.5 to 3.5
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When is Warfarin started and administered? How many days until therapeutic levels are achieved?
Takes 4-7 days for take effect
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What is the antidote for warfarin? List all potential options
Phytonadione (Vitamin K)
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Nursing considerations for warfarin? How long does it take to clear the body?
-Takes 4-7 days to take effect -Should be taken in the evening -Requires frequent lab monitoring (PT/INR) -Narrow therapeutic range -Works slowely compared to heparin
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How do Factor Xa inhibitors work? (DOAC)
-Prevent factor Xs from changing prothrombin to thrombin. They bind directly to factor Xa ## Footnote Common factor Xa inhibitors include rivaroxaban (Xarelto), apixaban (Eliquis), and edoxaban (Savaysa).
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Why is dabigatran (pradaxa) different from the others? What are special nursing considerations (patient teaching) for dabigatran?
it directly blocks thrombin, the enzyme responsible for clot formation, whereas the others are direct factor Xa inhibitors. | Twice daily dosing
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Dabigatran (pradaxa): Antidote? Which patient group should take with caution/have reduced dose?
-Praxbind -Must reduce in renal failure
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Common Coagulation tests
PTT (prothrombin time) International Normalized Ratio (INR) Activated partial thromboplastin time (aPTT)
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Why is this drug class (Factor Xa drugs) different than warfarin? Which patients should NOT receive this medication? ## Footnote Ex. Eliquis/Xarelto
-Do not take with Clopidogrel -Must reduce in renal failure
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What is the antidote for the DOAC class of medications? Which of these medications are once daily dosing and which are twice daily dosing?
Andexanet (For eliquis/xarelto) Praxbind (for pradaxa) Pradaxa-is twice daily
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Why might warfarin be a better choice for some patients than the DOAC class?
Less expensive
281
How does heparin work?
Anti-thrombin inhibitor- interferes with conversion of thrombin to prothrombin
282
How long does heparin take to work and how long does it take to clear the body after it is turned off?
online: Heparin works quickly, with IV heparin taking effect within minutes, and subcutaneous heparin within 1-2 hours. The anticoagulant effect of therapeutic doses of heparin is mostly eliminated within 3-4 hours after stopping continuous IV administration, with a half-life of about 60-90 minutes.
283
What lab value is used to monitor heparin therapy?
Monitored by aPTT usually 1.5-2.5 times baseline control Pt should normalize 2-6 hours after heparin is stopped
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How is heparin dosed? Antidote?
Starts by administering an IV bolus dose, followed by continuous dripL Bolus usually 5000units Followed by 1000-1300units/hour Or 80u/kg (can be less) bolus and then 18u/kg/hour Antidote: Protamine sulfate | ALWAYS CHECK DOSE WITH ANOTHER NURSE
285
A patients’ aPTT after 6 hour is 45 seconds. What action should the nurse take?
-Measures time is takes for plsma to clot when exposed to a reagent -30-45 seconds -Intrinsic pathway -A prolonged APTT can be an indicator of bleeding disorders like hemophilia or von Willebrand disease. -The APTT test is commonly used to monitor the effectiveness of heparin, a blood thinner, and ensure that the patient's blood clotting time is within the therapeutic range.
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What is the difference between unfractionated heparin and low molecular weight heparin? Why would someone receieve one over the other?
* Inhibit thrombus and clot formation by blocking factors Xa * Routes: SQ * Should not be mixed with other medications; multiple interactions * Safe to use during pregnancy, but is considered 2nd line therapy * Adverse Effects: Bleeding, Heparin-Induced Thrombocytopenia, Hypersensitivity Narrow therapeutic range : Requires lab monitoring Want PTT in therapeutic range= 46-70 If aPTT > 70, call the physician LOW MOLECULAR WEIGHT HEPARIN: Commonly used for DVT prophylaxis, MIs Drugs: Enoxaparin (Lovenox) Dalteparin (Fragmin) Route: SQ only Administer 2 inches from the umbilicus; No rubbing/No aspiration Okay to use during pregnancy, considered 1st line Does not require lab monitoring
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How long does it take for enoxaparin (lovanox) to reach a steady state?
Online - about 2 days
288
What are special considerations which need to be taken when administering enoxaparin?
inject into "love handles" Alternate between sites Do not inject air bubble prior to injection Do Not just injection site after
289
why would tPA be administerd? What are the criteria or contraindications which must be met before administration?
Stroke! Only given IF within 3-4 hours of onset of symptoms. Only give through a peripheral IV, not a central line (so you can compress the site) NO injections No SQ, or IM No ABGs (blood gas) Monitor vital signs and neurologic status If possible CVA, must do head CT before administering Place patient on bleeding precautions
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Urinary Tract Infections- general info
Second most common type of infection Occurs in Women more than males Accounts for About 50% of all hospital-acquired infections
291
Common cause of hospital acquired infection?
Accounts for about 50% of all hospital acquired infections Catheter Acquired UTI (CAUTI)
292
UTI Classifications
Lower - Bladder and structures below the bladder Upper -Kidneys -Ureters
293
Example of Lower Urinary tracts infection
Cystitis
294
Example of Upper Urinary tracts infection
Pyelonephritis
295
Most uncomplicated Lower UTI are caused by which bacteria? Where does it usually enter through?
E. Coli? Urethra
296
Washout phenomenon
occurs when urine washes out the bacteria in the urethra during urination
297
Complicated UTI bacteria
Staphylococcus saprophyticus Klebsiella pneumoniae Proteus mirablis Pseudomonas species
298
Causes of UTI: Obstruction
Anatomic: - Stones, BPH, Pregnancy Functional: - Infrequent voiding etc.
299
Causes of UTI: Reflux
Ureterovesical Reflux: -Cough or squatting can cause urine to move back from the bladder into the urethra and then back into the bladder Vesicoureteral Reflex: - Occurs at the level of the bladder and ureter
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Who is at risk of UTI
Sexually active women Post menopausal women Pregnancy Bladder cancer Renal stones (Calculi) Men with prostate abnormalities (no circumsicion) Anal intercourse Older adults Others at Risk Catherization Instrumentation Diabetes Use of antibiotics
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All UTI in men are considered..?
Complicated
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Clincal manifestations of Uncomplicated UTI: (5)
Dysuria Frequency Urgency Hematuria Suprapubic pain
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Clincal manifestations of complicated UTI:
May be asymptomatic or present with septic shock Fever, chills, nausea, vomiting Back pain/flank pain
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Urosepsis
spread of infection from urinary tract to bloodstream
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Older adult sympomts of UTI:
Symptoms can vary: Incontinence Foul smelling concentrated urine Fatigue Confusion Dementia Hallucinations
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UTI In Children:
After 3 months old, more prevalent in girls. -Frequently involved upper urinary tract
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Interstitial Cycstitis
* Pain (Pelvic/Perineal) * Urgency * Feeling of bladder fullness/pressure * Women>Men * Exact cause unknown Rule out: Infection Endometriosis Urodynamic Testing
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Urinary Testing: Specific Gravity
What: Amount of solutes in urine Normal: No true normal but approximately 1.010 Considerations: Extremes of either side can indicate pathology
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Urinary Testing: pH
What: Acid-base Normal: 6.5-7 in the AM 7.5-8 in the PM Considerations: Can be affected by food etc
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Urinary Testing: WBCS (leukocytes)
What: Enzyme given off by WBC Normal: Negative *Present in all patients with UTIS
311
Urinary Testing: Nitrites
What: Enzyme released by Enterobacteriaceae Normal: Negative *Can be neagtive and still have UTI
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Urinary Testing: Blood
What: Can be micro and macrocytic Normal: Negative *Can see in trauma, hemolysis, UTI, malignancy
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Urinary Testing: Protein
What: Measuring Albumin Normal: Netagive Considerations: Renal disease, Pregnancy, Inflammation
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Urinary Testing: Glucose
What: Renal threshold to eliminate excess glucose Normal: Negative
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Urinary Testing: Ketones
What: Measures metabolites of fat metabolism Normal: Negative *Insulin insufficiency, starvation, vomiting
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Urinary Testing: Biliruben
Normal: Negative *Liver disease obstruction
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Urinary Testing: Urobilinogen
Normal: Negative *Liver disease, hemolysis, mono, cirrhosis
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Urinary Testing: Casts
What: Coagulated protein by kidney cells Normal: Negative Hyaline (0-5) in healthy people ceullar not normal *Hyaline are clear. Can have cellular RBC or WBC
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Urinary Testing: Cystals
What: Wastes solutes. Based on pH and urine temp Normal: None but some are ok
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Management of UTIs: General
Pharmacologic thearpy Pt education Acute UTI: 3-7 day course of antibiotic, if uncomplicated Chronic or relapse UTI: Up to 2 week course of antibiotics
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Management of UTI's: Medications
Cephalexin Ciprofloxacin Levofloxacin Ampicillin Amoxicillin Bactrim
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UTI medications: Fluoroquinolones
(Ciprofloxacin or Levofloxacin) are not routinely recommended due to their side effects and increasing bacterial resistance
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Patient education: UTI
Drink plenty of fluids daily Void before and after sexual intercourse Avoid douching Take Antibiotics as prescribed Avoid tight/restrictive clothing Shower, don’t bath Personal Hygiene
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Normal renal functions (9)
* Excretion of waste prodcts and urine * Regulation of BP * RBC production- erythropoietin * Breakdown of drugs * Metabolism of hormones * Regulation of Electrolytes and acid-base balance * Synthesis of Vit D * Fluid Balance * Balance of pH of blood stream
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Nephrons
Adults tend to lose approximately 10% of their nephrons for each decade beginning at 40 ## Footnote by age 70- nephrons will be down 30mL/min=95mL/min
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Glomerular Filtration | how much /day
GFR: average adult 125mL/minute or 180L/day
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How does the kidney conccentrate urine (3 factors)
* Oslomarity of interstitial fluis * Anti diuretic hormone * Action of ADH on the cells in the collecting tubules of the kidney
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Elimination functions of the kidney
Removal of: - Water - waste products - excess electrolytes - unwanted substances
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Renal Disorder Categories (3)
Prerenal, Intrarenal, Post renal
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Prerenal disorders | What is it
Decrease in blood flow and perfusion
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Intrarenal disorders | what is it
Secondary to actual injuries to the kidney itself
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Post Renal disorders | what is it
Related to the obstruction of urine outflow from the kidneys
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Pre-renal disorders
* Hypotension * Shock * Diarrhea/Vomiting (severe) * Bleeding/hemorrhage * Diuretics * diabetes insipidis * Burns * Heart Failure/MI * Cirrhosis * Sepsis
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Intra-renal disorders
* Vasculitis * Venous Occlusion * Pre-eclampsia * Acute Tubular Necrosis * Multiple Myeloma * Hypercalcemia * IV contact dyes * Pyelonephritis * Certain meds: NSAIDS, ACE inhibitors, Heavy metals * Transfusion Reaction * Rhabdomyolysis
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Post-renal disorders
* Renal Calculi * Enlarged prostate * cancer * diabetes * Functinal obstruction due to drugs * blood clot * Trauma
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Acute Tubular Necrosis (ATN)
Most common cause of acute kidney injury Damage to renal tubes causing cells to slough into the tubular lumen and lumen becomes blocked -Decrased urine formation Causes: -Post-ischemia (all causes of severe pre-renal disease) -Nephrotoxic *Permanent injury if not reversed | INTRA renal disorder
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Acute Tubular Necrosis Labs: Creatinine
Creatinine clearance (100-150 cc/min): Less than 5-10cc/min
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Acute Tubular Necrosis Labs: Urine Sodium
Urine sodium (10-20 meQ/L): >20 med/L
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Acute Tubular Necrosis Labs: Specific Gravity
Normal: (1.005-1.025) ATN: 1.010 fixed
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Acute Tubular Necrosis Labs: Urine osmolality
Normal: (200-1200) ATN: Osmotic = 300mOM
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Acute Tubular Necrosis Labs: Serum BUN/creatinine
(10-20) 10:1 Fixed
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Acute Tubular Necrosis Labs: Urinalysis
Red/white cells, casts, epithelial cells
343
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Azotemia Labs: Creatinine
Normal: (100-150( Azo: 15-80cc
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Azotemia Labs: Urine sodium
>10 meq/L | normal: 10-20
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Azotemia Labs: Specific gravity
>1.015
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Azotemia Labs: Urine osmolality
Concentrated >450 | Normal: 200-1200
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Azotemia Labs: Serum BUN/Creatinine
> 15:1 | 10-20
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Azotemia Labs: Urinalysis
Normal
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Phases of Acute Kidney Injury (4)
Initial Oliguria Late Diuretic Recovery
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AKI: Initial Onset
0-2 days Initial Insult to point when BUN/Crt rise and/or Urine output drops
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AKI: Oliguria phase
1-2 days to 6-8 weeks Drop in GFR, retention of urea, Potassium, sulfate and creatinine. Decrease Urine output and edema
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AKI: Late Diuretic phase
2-8 days Begins with a slow, gradual increase in urine output, then high output
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AKI: Recovery phase
2-4 months Labs return to normal
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Clinical manifestation/Diagnosis of AKI
-Pt will have oliguria and fluid overload -Build up of nitrogenous waste --Uremia, metabolic acidosis, thrombocytopenia -Edema Labs: Urinalysis Serum electrolytes Bun/crt ABG CBC -Imaging -Renal Biopsy
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Treatment of AKI
- Return to normal chemical balance, prevent futher complications, restore renal function *Fluid administration diuretics Monitor electrolytes Cardiac monitoring Hemodialysis
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Indications for Dialysis
Volume overload K+ > 6 meQ/L Metabolic acidosis/serum HC03 >0.15 BUN > 120 mg/dL
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Chronic Kidney Disease (CKD)
An irreversible, progressive disease Often Asymptomatic initially until disease is far advanced * Kidney damage or a GFR < 60 mL/min/1.73 m2 for 3 months or longer. * Numerous Causes: * *Hypertension, *Diabetes, obesity, glomerulonephritis, SLE, polycystic kidney disease * Loss of functioning nephrons, progressive deterioration of glomerular filtration, ability of tubules to reabsorb, endocrine functions. * As nephrons are destroyed remaining hypertrophy to take on the work.
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Renal Dysfunction stages (1-5)
Stages 1/2: Often asymptomatic + crt normal -Compensation will occur GFR: normal >90 Stage 3: Decreased function <50% nephrons working. -Lab changes -No longer able to compensate GFR- 30-59 Stage 4: -Renal insufficiency is evident -nephrons dead -Diet restriction of proteins -GFR 15-29 Stage 5: Dialysis/transplant GFR: <15
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Clinical manifestations of CKD
-Buildup of nitrogenous waste: Encephalopathy/Anemia/Thrombocytopenia -Hyperkalemia - hyPOcalcemia (VitD not activated)....leads to hyperparathyroidism/Bone breakdown - Normochromic/normocytic anemia - low albumin - hyPERphostphatemia
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Treatment of CKD
Treat underlying cause Monitor labs Smoking cessation Manage hyperglycemia, if diabetic Manage anemia Exercise program Decrease sodium Avoid alcohol Dialysis Kidney transplant
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Glomerulonephritis | symptoms/complications
Inflammation of the glomerular capillaries Causes about 25-30% of all ESRD cases Can be acute or chronic Most common cause of acute is post-streptococcal glomerulonephritis *Symptoms:* Pink or cola-colored urine, proteinuria, hematuria, hypertension, fluid retention/edema, decrease urine, nausea and vomiting, muscle cramps, fatigue *Complications*: Accumulation of wastes or toxins in the bloodstream., Poor regulation of essential minerals and nutrients, Loss of red blood cells, Loss of blood proteins.
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Pathology of Glomerulonephritis
Begins with an antigen-antibody reaction Antigen-antibody complex damages structures of the glomeruli which causes nephron dysfunction: * Decreased filtration of blood * Decreased urine production * Hypervolemia * Hypertension
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Clinical manifestations of Glomerulonephritis
-Oliguria often the first symptom Followed by hematuria, proteinuria -Cola colored urine * Edema often of face and hands * HTN * Elevated anti-strep antibodies(ASO) * Increased Creatinine * Decreased serum albumin * Treat the cause and full recovery is expected.
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Treatment of Glomerulonephritis ## Footnote Goal of treatment/Medications/Diet modifications/Complication
Goal of treatment is to: Increase urine output Decrease urinary protein Medications: Corticosteroids Antibiotics, if needed Antihypertensives, if needed Antipyretics Diet modifications: Low sodium Low protein Monitor for complications: HTN encephalopathy Heart failure Pulmonary edema
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Nephrotic Syndrome
Damage to the glomerulus -The filter is damaged and things which should stay in are able to leak out through the pores which become bigger due to the damage -Leads to increased permeability of proteins and other substances in the blood -Diabetic nephropathy most common type but can be due to other causes such as: Lupus or amyloidosis ( top 3 causes account for 90% of all cases) --Also vasculitis, allergies, preeclampsia, HTN, and other infections
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Clinical manifestations/Diagnosis Nephrotic syndrome
Albuminuria/Proteinuria EDEMA Labs: -Urinalysis (proteinuria/hematuria) -Elevated BUN/CRT -Low serum albumin -Tests of lupus/hep B/C -24 hours urine *renal US and Renal Biopsy
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Treatment for nephrotic syndrome ## Footnote Diet/Vaccines/Complications
Monitor diet: Low sodium Protein Adequate fluid intake, but avoid fluid overload Vaccines – pneumococcal and influenza ACE inhibitor or ARB Monitor for complications: Hyperlipidemia Thromboembolism
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Nephritic Syndrome
Produces inflammatory response Related to: -immune complexes and antibody-antigen complexes lodge in capillary. --Immune response develops against the antigens -Inflammatory processes occlude glomerular capillary lumen & damage capillary wall. -Damage allows RBCs to escape into urine. -Alterations due to decrease in GFR, fluid retention and nitrogen waste accumulation. -Also proteinuria, oliguria.
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Post strep Glomerular Nephritis Vs Nephrotic syndrome
*Post strep G.NephRITIS* Typically seen ages 4-7 Onset: 10-14 days after strep infection Anti-strep titer + Urine- cola colored Heamturia-massive Proteinuria-minimal Hypertension Edema-moderate Hyperkalemia Elevated BUN *NephPHROTIC syndrome* Ages 2-3 years (males) Anti-strep titer NEG Urine- clear Hematuria - microscopic Pretineuria- Massive BP- normal or slightly decreased Hypoalbuminemia Edema-massive K+ normal BUN- normal Hyperlipidemia
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Diabetes and hypertension: Renal
Diabetes -Thickening of basement membrane -Dysfunction of glomerular podocytes -Remember they cover the urinary side of the glomerular basement membrane. -Inflammation (T cells and macrophages) into glomerulus Hypertension -Vascular changes -Glomerular changes -Damage to basement membrane (podocytes) - damaged -Allows plasma proteins to escape
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Impact NSAIDS on renal function
* NSAIDs work by inhibiting prostaglandins * Renal prostaglandins protect against decrease renal flow * Prostaglandin inhibition can depress already decreased renal blood flow * Leads to reduction in renal perfusion and decreased GFR
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Those at risk for NSAID issues: Renal
* Dehydration * Arterial volume depletion due to heart failure, nephrotic syndrome or cirrhosis * Chronic kidney disease (CKD), especially stage 3 or worse (estimated GFR <60 mL/min * Volume depletion from aggressive diuresis, vomiting, or diarrhea * Older age * Severe hypercalcemia with associated renal arteriolar vasoconstriction
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NSAIDS IN healthy people: renal
* In extreme exercise especially in heat the skin and muscle complete for blood flow * Takes away from the pancreas, GI, liver and kidneys * When exercising at max GRF can be reduced by 30-60% * Add dehydration, heat stress * Add chronic NSAID use * Avoid NSAID use outside of recommended doses * Avoid in those with HTN, HF, DM, and Metabolic syndrome * Avoid in states of dehydration * Increase fluids in athletes. * As anti-inflammatory use for shortest time and try to use acetaminophen as well
375
Asprin (ASA) Indications (who needs it)
CAD/CVA/PAD prevention * Maintains AV grafts * Post MI * Post Stent placement * Other vascular disease
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Aspirin Drug interactions
Oral anticoagulants, Heparin, Methotrexate, oral DM meds, and Insulin – can increase the risk of toxicity when taken with ASA * Steroids may decrease the ASA effect and cause ulcers * ACE and Beta Blockers * NSAIDS
377
anticoagulant Alternatives for Heparin-induced thrombocytopenia
Argatroban Lepirudin
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DOAC patient education
Patient Education: * Meds must stay in original bottle, don’t place in pill box * Pills should not be crushed * Don’t stop taking for GI issues, unless there is black, tarry stools * Hold before having surgery * Don’t take with Clopidogrel * Watch for drug interactions * Must reduce dose in renal failure * Caution in abrupt stopping * Antidote: Praxbind (idarucizumab) is for Dabigatran only
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Contraindication for tPA
Uncontrolled BP (185/110) * History of Hemorrhagic Stroke, aneurysm, or AV malformations * Heparin in the last 48 hours * Current oral anticoagulant * DOAC use * Surgery within 3 months * Platelet count <100,000
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WHAT SHOULD THE NURSE DO IF A PATIENT TAKES AN EXTRA DOSE OF ANY OF THE ANTI-COAGULANTS?
Check for signs of bleeding vital signs labs
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A patient is ordered a PT/INR blood test. As the nurse you know that this blood test assesses? A. Extrinsic pathway of coagulation and common pathways B. Intrinsic pathway of coagulation and common pathways C. Clotting factors XII, XI, IX, VIII D. Only clotting factor II (prothrombin)
A: Extrinsic pathway of coagulation and common pathways. The PT/INR assesses the extrinsic pathway of coagulation (which uses clotting factor VII) and common pathways (which uses factor I, II, V, X). The extrinsic pathway is activated when there is outside/external injury that results in blood loss from the vascular system.
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Your patient is being evaluated for a bleeding disorder. The physician orders an aPTT blood test. Which statement is TRUE about this coagulation test? A. The aPTT is an important result used to assess the effectiveness of Warfarin. B. The aPTT assesses the intrinsic pathway of coagulation and common pathways. C. The aPTT is measured in milliseconds. D. The aPTT only assesses clotting factor VII.
The aPTT assess the intrinsic pathway of coagulation and common pathways. The aPTT assesses the intrinsic pathway of coagulation and common pathways. Therefore, clotting factors I, II, V, X (which are part of common pathways) and clotting factors XII, XI, IX, VIII (which are part of intrinsic pathway) are assessed. The intrinsic pathway is activated when there is inside injury within the vascular system. The aPTT is an important result used to assess the effectiveness of Heparin (NOT Warfarin), and it's measured in SECONDS (not milliseconds).
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What is the approximate normal range for an aPTT result? A. 2-3 second B. 30-40 seconds C. 1.5-2.5 times the normal range D. 10-12 seconds
B: 35-45 seconds (This range varies among labs).
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A patient is receiving continuous IV Heparin. In order for this medication to have a therapeutic effect on the patient, the aPTT should be? A. 0.5-2.5 times the normal value range B. 2-3 times the normal value range C. 1.5-2.5 times the normal value range D. 1-3.5 times the normal value range
An aPTT should be 1.5-2 times the normal value range for Heparin to achieve a therapeutic effect in a patient to prevent blood clots. If the aPTT is too low, blood clots can form. If the aPTT is too high, bleeding can occur.
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A patient is prescribed Warfarin (Coumadin) for the treatment of a blood clot. What is the therapeutic INR range for this medication to be effective? A. 2-3 B. 1-3 C. 4-8 D. 0.5-2.5
The answer is A. The therapeutic INR range is 2-3. It may be slightly higher if a patient is at a high risk for clot formation….(ex: up to 4.5)
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What is an approximate normal range for a PT (prothrombin) level? A. 10-12 seconds B. 2-3 seconds C. 30-40 seconds D. 60-80 seconds
The answer is A: 10-12 second
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Your patient, who is prescribed Warfarin for blood clots, has an INR of 1. As the nurse you know that this means? A. The medication is therapeutic. B. The medication is not effective at preventing blood clots. C. The patient is at risk for bleeding. D. The patient is experiencing Warfarin toxicity.
The answer is B. A therapeutic INR for a patient taking Warfarin should be 2-3. Therefore, the patient’s medication is not effective at this time for preventing blood clots
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Fill in the blank: Prothrombin turns into _________ with the assistance of clotting factor V. A. fibrinogen B. fibrin C. thrombin D. vitamin K
The answer is C: Thrombin....Prothrombin turns into thrombin by clotting factor V. When thrombin is on board it is responsible for turning fibrinogen to fibrin. Fibrin is one of the main ingredients for clot formation.
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A patient’s PT result is 30 seconds. What conditions below could cause this result? Select all that apply: A. None, this is a normal PT range. B. Vitamin K deficiency C. Liver disease D. Warfarin
The answers are B, C, and D. All of these could increase the PT level (a normal range is approximately 10-12 seconds).
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Your patient's aPTT level is 32 seconds. The nurse would interpret this lab result as? A. Too high, the patient is at risk for bleeding. B. Too low C. Normal
The answer is C: Normal...an approximate normal range for an aPTT is about 35-45 seconds.
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Medications in loop diuretics class
- **furosemide (Lasix)** - bumetanide - torsemide
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Mechanism of action of loop diuretics
Inhibit reabsorption of sodium or chloride at the loop of Henle - decrease workload on heart (less water in body) - decrease pulmonary congestion - decrease preload, stroke volume, cardiac output
393
Uses of loop diuretics
Decrease blood volume, which decreases venous return and blood pressure
394
Key side effects of loop diuretics? Any black box warnings?
- hyponatremia - **hypokalemia** - hypovolemia - hypomagnesemia - hyperglycemia - ototoxicity
395
What specific actions does the nurse need to take for loop diuretics? Any labs, vitals, nursing considerations?
- monitor potassium level! -- monitor other electrolytes too, but potassium very important - monitor I&Os - monitor blood sugar
396
Patient education for loop diuretics? Any specific or key instructions?
- change position slowly due to potential orthostatic changes - report weight gain of more than three pounds in a day - enjoy potassium-rich foods especially because hypokalemia is a big risk (raisins are great source) (pulled this from online) MONITOR I & O MONITOR POTASSIUM level | Bumentanide furosemide Torsemide
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Meds in class of spironolactone
- spironolactone is a mineralcorticoid receptor antagonist -- AKA aldosterone receptor blocker
398
Mechanism of action of spironolactone
blocks the exchange of sodium for potassium in the distal tubules - potassium sparing
399
Uses of spironolactone
Indications: hypertension and heart failure - used when one drug is not enough to treat symptoms
400
Key side effects of spironolactone? Any black box warnings?
- can cause gynecomastia
401
What specific actions does nurse need to take with spironolactone? Labs, vitals, nursing considerations?
- monitor potassium (can cause hyperkalemia) - monitor LFTs - monitor BUN/Cr - do not give in renal insufficiency
402
Patient education with spironolactone? Any specific or key instructions?
- take with meals - avoid taking with: -- ACE inhibitors/ARBs -- heparin -- NSAIDs
403
Meds in class with digoxin
Class name: digitalis glycosides - digoxin - deslanoside - mitildigoxin
404
Mechanism of action of digoxin
- increases intracellular calcium - allows more calcium to enter myocardial cell during depolarization - **positive ionotropic effect (increase force of contraction)** - increased renal perfusion with a diuretic effect -- decrease in renin release - slowed conduction through AV node (decrease HR)
405
Uses for digoxin
indications: heart failure and atrial fibrillation not first-line treatment
406
Key side effects of digoxin? Any black box warnings?
Has very narrow therapeutic margin: - normal: 0.5-2.0 - desired level: 0.8 Digoxin toxicity: - vision changes, N/V, dizziness - increased risk of hypokalemia - can be life-threatening
407
What specific actions does the nurse need to take with digoxin? Labs, vitals, nursing considerations? Antidote? Check? Monitor? Caution in?
Antidote: digibind - **always check apical HR and call MD if less than 60** - monitor BUN/Cr and potassium - rapid onset and absorption - caution in: -- pregnancy and lactation -- pediatric and geriatric -- renal insufficiency
408
Patient education with digoxin? Any specific or key instructions?
- take at the same time every day - take 1 hour before or 2 hours after eating - take apical HR before taking: report to provider if less than 60 - learn signs of digoxin toxicity (Nausea, vomiting and vision changes) - cuz when a DIGit goes up your butt you’ll get nausea vomiting and vision changes.. (pulled this from online)
409
Meds in class of ACE inhibitors (A-pril)
end in -pril - lisinopril - enalapril (can be given IV) - ramipril - captopril
410
Mechanism of action of ACE inhibitors
Prevents the conversion of angiotensin 1 to angiotensin 2 - works by vasodilation and by blocking RAAS/aldosterone - helps prevent cardiovascular remodeling Pathophysiology: - decrease aldosterone production - inhibit angiotensin 2 production - decrease vasoconstriction - interfere with RAAS - keep vasodilation effects of bradykinin
411
Uses of ACE inhibitors
First-line treatment for heart failure and hypertension; decrease the workload of overworked cardiac muscle Indications: - HTN - HF - DM - post MI and PCI
412
Key side effects of ACE inhibitors? Any black box warnings?
- generally well tolerated and absorbed - hyperkalemia - dizziness - **cough** ("ACE cough") -- related to kinins and activation of arachidonic pathway and prostaglandin production -- begins 1-2 weeks of initiation; typically resolves within few days of stopping med - **angioedema** **BLACK BOX WARNING**: - **serious fatal abnormalities: not given in pregnancy and caution in childbearing-age women** - esp in 3rd trimester - contraception very important
413
What specific actions does the nurse need to take with ACE inhibitors? Labs, vitals, nursing considerations? Be aware of…
- be aware of renal function and potassium - assess orthostasis - awareness of administration to childbearing women - NO NSAID use - should be taken on empty stomach Labs: potassium, BUN, Cr Vitals: BP
414
Patient education with ACE inhibitors? Any specific or key instructions?
- do not give to pregnant women! do not take if pregnant, especially if in 3rd trimester - take on an empty stomach - no NSAID use
415
Meds in class of thiazide diuretics
- hydrochlorothiazide (HCTZ) - chlorthalidone
416
Mechanism of action of thiazide diuretics
- inhibit reabsorption of sodium and chloride from the distal tubules in the kidneys - decrease peripheral resistance - decrease preload - better for sodium sensitive HTN as in african americans and older adults
417
Uses of thiazide diuretics
treat hypertension; first-line medication
418
Key side effects of thiazide diuretics? Any black box warnings?
- anyone with sulfa allergy should not take - hypokalemia - hyperglycemia (watch w/ diabetics) - can cause exacerbation of gout -- increases uric acid - other electrolyte imbalances (calcium) - orthostasis
419
What specific actions does the nurse need to take with thiazide diuretics? Labs, vitals, nursing considerations?
- anyone with allergy to sulfa should not take - should not be given to patients with history of gout - avoid in renal failure - digoxin toxicity - may decrease effect of diabetic medications - lithium toxicity - give early in morning b/c urination Check potassium, glucose, BP, HR
420
Patient education with thiazide diuretics? Any specific or key instructions? (Lifestyle type of recommendations)
- adherence! - watch diet, exercise - decrease alcohol, stop smoking - avoid NSAIDs which increase BP
421
Meds in ARBs class (angiotensin II receptor blockers)
end in -sartan - losartan - irbesartan - valsartan
422
Mechanism of action of ARBs
- bind with AG-2 receptors in vascular smooth muscle and adrenal cortex to stop vasoconstriction and aldosterone production - blocks AG-2 from binding at receptor sites in brain, kidneys, heart, periphery, and adrenal tissue
423
Uses of ARBs
first-line treatment of hypertension; when ACE inhibitor cannot be used
424
Key side effects of ARBs? Any black box warnings? | angiotensin receptor blocker
- cough (less than an ACEI) - hyperkalemia (less than ACEI) - headaches - dizziness and syncope - GI complaints - xerostomia (dry mouth) - alopecia
425
What specific actions does the nurse need to take with ARBs? Labs, vitals, nursing considerations? Do not give with, monitor what
- do not give with an ACE inhibitor - drug interactions with diltiazem, oral anti-fungals - monitor renal function - some drug interactions related to the cytochrome P450 - can be given with or without foods Labs: creatinine; can increase due to possible decreased GFR; LFTs Vitals: I&Os, BP
426
Patient education with ARBs? Any specific or key instructions?
- avoid during pregnancy - do not take with ACE inhibitor - can take with or without food
427
Meds in class of calcium channel blockers: dihydropyridines
- amlodipine - felodipine - nifedipine
428
Mechanism of action of calcium channel blockers: dihydropyridines
- more vascular selection - more of a direct effect on vasodilation and less reduction of calcium - no effect on AV contraction; may increase HR due to vasodilation overall patho of CCBs: - decrease cardiac workload and myocardial O2 consumption - inhibits movement of calcium across membranes of myocardial/arterial muscle cells - alter action potential and block muscle cell contractions - decrease contractility and slows AV conduction - relax and dilate arteries
429
Uses of calcium channel blockers: dihydropyridines | What do they treat
- hypertension - angina - rate control in AFib - SVT - Raynaud's phenomenon
430
Key side effects of calcium channel blockers: dihydropyridines? Any black box warnings?
- peripheral edema (common) - headache - flushing - lightheadedness - dizziness - can have increased HR (double check. It should cause decrease) - GI side effects
431
What specific actions does the nurse need to take with calcium channel blockers: dihydropyridines? Labs, vitals, nursing considerations? What is important to consider with CCBs | CA-Pines (California pine trees)
- **always check HR prior to giving; call MD if less than 60** - be aware of conduction issues - avoid use in those with heart failure - avoid grapefruit juice - check orthostasis no lab monitoring vitals: HR | Amlodipine Felodipine Nifedipine
432
Patient education with calcium channel blockers: dihydropyridines? Any specific or key instructions?
- do not drink grapefruit juice - increase fiber in diet - always check HR prior to taking and make sure not less than 60
433
Meds in class of calcium channel blockers: non-dihydropyridines
- verapamil - diltiazem both can be given IV
434
Mechanism of action of calcium channel blockers: non-dihydropyridines
- **negative ionotropic effects (decrease force of contraction)** - slow AV conduction and rate of SA node overall patho of CCBs: - decrease cardiac workload and myocardial O2 consumption - inhibits movement of calcium across membranes of myocardial/arterial muscle cells - alter action potential and block muscle cell contractions - decrease contractility and slows AV conduction - relax and dilate arteries
435
Uses of calcium channel blockers: non-dihydropyridines | What do they treat
- hypertension - angina - arrhythmias (AFib, SVT) - migraines (verapamil)
436
Key side effects of calcium channel blockers: non-dihydropyridines? Any black box warnings?
- bradycardia (can really drop) - decreased cardiac output - GI side effects - should not be used in those with heart block
437
What specific actions does the nurse need to take with calcium channel blockers: non-dihydropyridines? Labs, vitals, nursing considerations?
- **always check HR prior to giving; call MD if less than 60** - be aware of conduction issues - avoid use in those with heart failure - avoid grapefruit juice (especially with diltiazem) - check orthostasis no lab monitoring vitals: HR
438
Patient education with calcium channel blockers: non-dihydropyridines? Any specific or key instructions?
- increase fiber in diet - always check heart rate before taking and make sure not less than 60 - do not drink grapefruit juice
439
Meds in Beta Blockers class?
"-lol ending" - carvedilol - metoprolol - bisoprolol - labetalol - atenolol Selective Beta 1: - metoprolol - atenolol - esmolol - bisoprolol Non selective: - propranolol - carvedilol - nasolol - sotalol
440
Mechanism of action of Beta Blockers
Block the beta-receptors in the sympathetic nervous system, decreasing calcium flow into the myocardial cells, and causing decreased contraction and workload - decreases catecholamine stimulation - decreases myocardial energy demands - reduces remodeling **blocks SNS responses** - decrease HR - decrease BP - decrease muscle contraction - increase blood flow to the kidneys - decrease renin release
441
Uses of Beta Blockers
Used in treatment for heart failure; cause decreased contraction and workload - hypertension but not first line - decrease risk of sudden death after MI - all patients after MI and PCI - HR reduction in AFib - palpitations - heart failure - migraines - performance anxiety - hyperthyroidism Special uses: - metoprolol: HR and post MI - propranolol: social anxiety, headaches
442
Key side effects of Beta Blockers? Any black box warnings?
- hypotension - **bradycardia** (why you check apical HR) - bronchospasm (don't want to give to COPD or asthma pt) - exacerbation of peripheral vascular disease - fatigue - depression - impotence - sleep issues adverse effects: - worsening of HF especially when first started; why you need to start at low dose
443
What specific actions does the nurse need to take with Beta Blockers? Labs, vitals, nursing considerations?
- always start at very low doses b/c can make HF worse - **always check apical heart rate** and call MD if less than 60 - caution use in chronic lung disease b/c may increase risk of asthma attacks (blocks B2 receptor) - may mask hypoglycemic episodes so monitor diabetics - caution in those with brady arrhythmias b/c will drop HR - check for orthostasis - make sure patient is given medication even when NPO - assess for side effects Labs: glucose level especially is patient is diabetic; no other major lab concerns Vitals: HR (check apical)
444
Patient education with Beta Blockers? Any specific or key instructions?
- ALWAYS check apical heart rate before taking - NEVER stop abruptly: need to taper off -- SNS will surge and go to an extreme if stopped abruptly
445
Meds in class: Entresto (Sacubitril plus Valsartan)
Class: angiotensin receptor-neprilysin inhibitor (ARNI) Entresto (sacubitril + valsartan) is the only ARNI
446
Mechanism of action of Entresto (Sacubitril plus Valsartan)
Increase: - naturetic peptides (like BNP) - bradykinin (vasodilation) - other mediators which increase vasodilation
447
Uses of Entresto (Sacubitril plus Valsartan)
Used for systolic heart failure to improve symptoms and reduce remodeling
448
Key side effects of Entresto (Sacubitril plus Valsartan)? Any black box warnings? | Comno med
- angioedema - hypotension - hyperkalemia - renal failure - cough
449
What specific actions does the nurse need to take with Entresto (Sacubitril plus Valsartan)? Labs, vitals, nursing considerations?
idk? monitor potassium, BUN, Cr, BP
450
Patient education with Entresto (Sacubitril plus Valsartan)? Any specific or key instructions?
- contraindicated in pregnancy - DO NOT TAKE WITH NSAIDs (NSAIDs vasoconstrict so counteracts)
451
Meds in Nitrates class
nitroglycerin isosorbide hydralazine and nitrates (combined)
452
Mechanism of action of nitrates
Actions: - arterial and venous dilator (potent vasodilator) - decreases preload and afterload - increases oxygen demand to heart; decrease myocardial oxygen demand Pharmacokinetics: - very rapidly absorbed - tolerance develops easily; need drug-free period - drug-drug interaction with Sildenafil (viagra)
453
Uses of nitrates?
prevention and treatment of attacks of angina pectoris and heart failure
454
Key side effects of nitrates? Any black box warnings?
- when taking: tingles or burns under tongue - headache - dizziness
455
What specific actions does the nurse need to take with nitroglycerine? Labs, vitals, nursing considerations?
- must stay in original bottle and be protected from light - watch BP before and after giving - always wear gloves when administering (absorbed rapidly) Routes (essentially every route): SL, translingual, transmucosal, OR, OR-SR, IV, topical, transdermal
456
Patient education with nitrates? Any specific or key instructions?
- can 1 every 5 minutes up to 3 taken - pain continues call 911 - DO NOT take with viagra (sildenafil) - must be sitting or lying when taking it - keep medication in original bottle to protect from light
457
Meds in Alpha Blockers class
- doxazosin (cardura) - prazosin (minipress)
458
Mechanism of Action of Alpha Blockers
- inhibit alpha synapse at the alpha adrenergic receptors (blocks SNS) - prevent feedback of norepinephrine
459
Uses of Alpha Blockers
not really used in blood pressure control; considered 3rd or 4th line treatment - "almost work too well"
460
Key side effects of Alpha Blockers? Any black box warnings?
adverse effects are significant - first dose effect! - orthostatic hypotension - vertigo, syncope, dizziness - tachycardia - sexual dysfunction
461
What specific actions does the nurse need to take with Alpha Blockers? Labs, vitals, nursing considerations?
- need to monitor patient very closely after giving first dose - avoid use in older adults due to increased sedation and confusion vitals: BP and HR
462
Patient education with Alpha Blockers? Any specific or key instructions?
- let them know about first dose effect and that adverse effects are significant
463
What are the characteristics of metabolic syndrome?
- hypertension - obesity (especially apple shape; abdominal fat) - abnormal cholesterol levels (hyperlipidemia) - chronic inflammation - insulin resistance
464
Explain how the "circle of death" plays into increasing blood pressure and blood sugar in metabolic syndrome
obesity and high-fat diet coupled with sedentary lifestyle cause buildup of adipose tissue, brought on by macrophages and lymphocytes, and produce low-grade chronic inflammatory state - from obesity and inflammation, cells fail to make effective use of insulin - blood sugar increases - beta cells in pancreas secrete insulin - insulin resistance: insulin is not able to reduce blood sugar -- compensatory insulin fails and person remains hyperglycemic insulin resistance causes: - increased catecholamines - **stimulates sodium reabsorption and increases BP** -- BP can decrease with meds that improve insulin sensitivity - endothelial dysfunction - RAAS and SNS dysfunction - smooth muscle proliferation -> hypertrophy and TOD
465
Explain how diet and exercise break the circle of death
modify factors to break the cycle - exercise and diet can break the obesity and insulin resistance portion of the circle of death
466
Explain how ACE inhibitors improve endothelial dysfunction
ACE inhibitors block the converting enzyme - stopping angiotensin 1 from becoming angiotensin 2 - which stops the stimulation of aldosterone secretion -- blocking the increased water and sodium retention -- blocking increased preload - stops constriction of vascular smooth muscle -- stops increased afterload inappropriate RAAS activation from increased angiotensin 2 causes endothelial dysfunction and vascular remodeling (and elevated BP & atherosclerosis) so inhibiting AG2 stops this
467
Explain how beta blockers improve endothelial dysfunction
Online: Beta-blockers, particularly newer "third-generation" ones like nebivolol and carvedilol, **can improve endothelial dysfunction by enhancing the production of nitric oxide (NO) from endothelial cells**, which helps relax blood vessels and improve blood flow, primarily through their antioxidant properties and by modulating the activity of the enzyme endothelial nitric oxide synthase (eNOS) - essentially promoting better vascular function beyond just lowering heart rate and blood pressure.
468
Explain how metformin improves endothelial dysfunction
Online: Metformin improves endothelial dysfunction **primarily by activating the AMP-activated protein kinase (AMPK) pathway, which leads to increased nitric oxide (NO) production**, reduced oxidative stress, decreased inflammation, and inhibition of endothelial cell apoptosis - thereby enhancing vascular function and protecting against damage to the endothelial lining of blood vessels.
469
Explain how HTN and metabolic syndrome lead to the development of coronary artery disease, cerebral vascular disease, and peripheral arterial disease
- LDL deposits cholesterol between layers in the artery wall - inflammatory cells (macrophages) engulf deposited cholesterol - inflammatory resp. -- macrophages become giant foam cells -- a fatty streak develops between layers of artery wall - foam cells continue to expand the core of the plaque -- a fibrous outer cap forms from converted smooth muscle cells and other elements - large unstable plaque within thin fibrous cap and can rupture - a blood clot (thrombus) forms at site of plaque rupture - can lead to blockage and blocked artery starts to die
470
Cardiac output
Stroke Volume X HR Normally, 4-8L /min
471
Stroke Volume
Cannot directly meausre so we measure cardiac output via: preload, afterload, and contractility
472
Preload
At the end of diastole, or when L ventricle is filled/ mitral valve closed. More stretching = more blood which is good. But excessive stretching can lead to heart failure | Preload = stretching
473
Normal ejection fraction
55-70% anything below 40% is abnormal
474
Meds to check for apical HR
Beta blockers: Carvedilol, metoprolol, bisopropolol DIGOXIN Calcium channel blockers
475
How do meds work for Heart failure? Vasodilators, loop diuretics, Beta blocks
Vasodilators- decrease workload Loop diuretics- Decreae blood volume Beta blocks- decrease contractions and workload
476
What specific actions does the nurse need to take with nitrates? Labs, vitals, nursing considerations?
Very rapidly absobed Tolerance developes easily Must have drug free periods **do not take with sildenafil
477
How many lobes are on the left side of the lungs?
Two lobes
478
How many lobes are on the right side of the lungs?
Three lobes
479
What does the trachea divide into?
Two main bronchi
480
What are the smaller branches of the bronchi called?
Bronchioles
481
What are the air sacs in the lungs called?
Alveoli
482
What are the two major components of the respiratory system?
* Conducting airway * Respiratory airway
483
What is included in the conducting airway?
* Nose * Mouth * Pharynx * Larynx * Trachea * Bronchi
484
What is the primary function of the respiratory airway?
Gas exchange
485
What components make up the lobules of the lungs?
* Bronchiole * Arteriole * Pulmonary capillaries * Veins
486
What does the process of ventilation change about atmospheric air?
Warms, moistens, and filters ## Footnote This process enhances the quality of air before it reaches the lungs.
487
What type of cells in the epithelial lining produce mucus?
Goblet cells ## Footnote These cells play a crucial role in trapping particles and pathogens.
488
What are the structures involved in the ventilation process?
Nose, sinuses, nasal cavity, pharynx, larynx, bronchi ## Footnote These structures work together to condition the air.
489
What are the main defense mechanisms for the lungs?
* Alveolar macrophages * Neutrophils * Mast cells * Cough reflex ## Footnote These mechanisms help protect the lungs from infection and damage.
490
What is the function of alveolar macrophages?
Phagocytosis of pathogens and debris ## Footnote They are essential for maintaining lung health.
491
What role do neutrophils play in lung defense?
Respond to infection and inflammation ## Footnote They are a type of white blood cell involved in the immune response.
492
What do mast cells release during an immune response?
Histamines and other mediators ## Footnote They are involved in allergic reactions and inflammation.
493
True or False: The cough reflex is a defense mechanism for the lungs.
True ## Footnote It helps expel irritants and pathogens from the airways.
494
What are the components of the respiratory tract?
Lobules and alveoli ## Footnote The respiratory tract is essential for gas exchange.
495
What are the functional units of the lungs where gas exchange occurs?
Alveoli ## Footnote Alveoli are also referred to as respiratory sacs.
496
Which cells produce surfactant in the alveoli?
Type II cells ## Footnote Surfactant helps reduce surface tension in the alveoli.
497
What structure separates the lungs?
Mediastinum ## Footnote The mediastinum contains the heart, esophagus, thymus gland, and other blood vessels and nerves.
498
From which part of the heart does the alveoli receive unoxygenated blood?
Right ventricle ## Footnote This blood is delivered via the pulmonary artery.
499
Fill in the blank: The alveoli are the functional units of the lungs where _______ occurs.
gas exchange
500
True or False: Surfactant is produced by type I cells in the alveoli.
False ## Footnote Surfactant is produced by type II cells.
501
What does the mediastinum contain?
* Heart * Esophagus * Thymus gland * Blood vessels * Nerves
502
What is the mucociliary apparatus?
A specialized cellular mechanism within the bronchioles ## Footnote It plays a crucial role in clearing mucus and pathogens from the respiratory tract.
503
What types of cells are found in the mucociliary apparatus?
* Ciliated pseudostratified columnar epithelial cells * Goblet cells ## Footnote These cells work together to produce and move mucus.
504
What is the function of the cilia in the mucociliary apparatus?
Moves mucus from the bronchioles to the throat ## Footnote The cilia beat in a wave-like motion to facilitate this movement.
505
What is the role of goblet cells in the mucociliary apparatus?
Produce mucus ## Footnote Mucus traps dust, pathogens, and other particles.
506
How does the mucociliary apparatus help in swallowing mucus?
Cilia move mucus upward to the throat ## Footnote This process helps keep the airways clear and allows for mucus to be swallowed.
507
What factors can affect the mucociliary apparatus?
* Smoking * Respiratory Infections ## Footnote These factors can impair the function of the mucociliary apparatus.
508
True or False: The mucociliary apparatus is only composed of ciliated epithelial cells.
False ## Footnote It also includes goblet cells which are essential for mucus production.
509
Fill in the blank: The wave-like movement of cilia enables the movement of mucus _______ to the throat.
[downward] ## Footnote This downward movement is essential for clearing mucus effectively.
510
Where does gas exchange occur?
In the alveoli ## Footnote Alveoli are tiny air sacs in the lungs where the exchange of oxygen and carbon dioxide takes place.
511
What happens to oxygen during gas exchange?
Oxygen enters the alveolus and moves across the alveolar membrane into the blood ## Footnote This process is crucial for supplying oxygen to the body's tissues.
512
What does oxygen combine with in the blood?
The heme portion of hemoglobin ## Footnote Hemoglobin is a protein in red blood cells responsible for transporting oxygen.
513
What is formed when oxygen combines with hemoglobin?
Oxyhemoglobin ## Footnote Oxyhemoglobin is the compound formed when oxygen binds to hemoglobin, facilitating oxygen transport in the bloodstream.
514
What is ventilation?
The process of inspiration and expiration of air ## Footnote Ventilation is essential for gas exchange in the lungs.
515
What controls ventilation?
The respiratory center in the brain ## Footnote It receives input from chemoreceptors and lung receptors (stretch and irritant receptors).
516
Which nerve stimulates diaphragm contraction?
Vagus nerve ## Footnote The vagus nerve plays a crucial role in regulating breathing.
517
What is perfusion?
The movement of blood through the pulmonary circulation ## Footnote Perfusion is necessary for delivering oxygen to the tissues.
518
What does the ventilation-perfusion ratio (V-Q Ratio) measure?
The ratio of the amount of oxygen reaching the alveoli to the amount of blood reaching the alveoli ## Footnote This ratio is critical for effective gas exchange.
519
What is the ideal state of the ventilation-perfusion ratio?
Both ventilation and perfusion should be equal ## Footnote An equal ratio facilitates optimal gas exchange.
520
What happens when there is an imbalance in ventilation-perfusion?
Leads to a decrease in gas exchange ## Footnote Imbalances can result from various conditions affecting either ventilation or perfusion.
521
What is dead space in the context of ventilation and perfusion?
An area where there is no perfusion ## Footnote Dead space can occur in certain lung conditions, reducing overall efficiency of gas exchange.
522
Pulmonary function Tests (PFT's)
523
What is the most common sign of a pulmonary problem?
Dyspnea (Shortness of breath) ## Footnote Dyspnea indicates difficulty in breathing and is a key clinical manifestation in respiratory issues.
524
What is a cough?
Involuntary response to mechanical or chemical stimulation of the bronchial tree ## Footnote A cough serves to eliminate stimulants from the respiratory tract.
525
What are the two types of cough?
Productive and non-productive ## Footnote A productive cough brings up mucus, while a non-productive cough does not.
526
What is hemoptysis?
Coughing up blood ## Footnote Hemoptysis can be associated with conditions such as tuberculosis, lung cancer, or infection.
527
True or False: Hemoptysis is only associated with lung cancer.
False ## Footnote Hemoptysis can also be associated with tuberculosis and various infections.
528
What is atelectasis?
Collapse of alveoli, resulting in decreased gas exchange ## Footnote Commonly occurs post-op and can also occur due to compression by a mass.
529
What are the common causes of atelectasis?
* Post-operative complications * Compression by a mass
530
What is hypoxia?
Oxygen level in blood inadequate to meet needs of the tissue
531
What is the PaO2 level indicative of hypoxia?
Less than 60 mm Hg
532
What is hypoxemia?
Insufficient amount of oxygen in blood
533
What is Erythropoietin?
A hormone secreted by the kidneys in response to low oxygen levels ## Footnote Erythropoietin plays a crucial role in regulating red blood cell production.
534
What stimulates the production of Erythropoietin?
Low oxygen levels ## Footnote This response is critical for maintaining adequate oxygen levels in the body.
535
What is the effect of Erythropoietin on the bone marrow?
Stimulates the bone marrow to increase the production of Red blood cells ## Footnote This process is essential for improving oxygen transport in the blood.
536
What types of disorders can stimulate the production of Erythropoietin?
Any disorder that causes hypoxia, such as: * COPD * High altitudes * Cardiac disease ## Footnote These conditions lead to reduced oxygen availability, triggering Erythropoietin secretion.
537
What causes the common cold?
Several viruses invade the upper respiratory tract leading to an inflammatory response.
538
What is the typical duration of a common cold?
About 5-7 days.
539
What happens to mucus membranes during a common cold?
Mucus membranes become engorged.
540
What is the effect on mucus production during a common cold?
There is an increase in mucus production.
541
What hygiene practice is important to prevent the common cold?
Hand hygiene.
542
True or False: Antibiotics are recommended for treating the common cold.
False.
543
Antitussives: Medications in class
544
Indications for antitussives
545
How do antitussives work?
546
Side effects of antitussives?
547
Nursing considerations for antitussives?
548
Any black box warnings for antitussives?
549
Medications in antihistamines class
550
Indications for antihistamines?
551
How do antihistamines work?
552
Side effects of antihistamines?
553
Nursing considerations for antihistamines?
554
Any black box warnings for antihistamines?
555
Medications in expectorants class
556
Indications for expectorants?
557
How do the expectorants work?
558
Side effects of expectorants?
559
Nursing considerations of expectorants?
560
Any black box warnings for expectorants?
561
Medications in mucolytics class?
562
Indications for mucolytics?
563
How do mucolytics work?
564
Side effects of mucolytics?
565
Nursing considerations for mucolytics?
566
Any black box warnings for mucolytics?
567
Respiratory: herbal meds
568
Respiratory: hypersensitivity reactions - types
569
Role of histamine r/t the respiratory system?
570
Asthma
571
Exercise-induced asthma
572
Nocturnal asthma
573
Status asthmaticus
574
Adrenergic meds: Short-acting vs Long-acting
575
Indications for adrenergic medications
576
How do adrenergic medications work
577
Side effects of adrenergics?
578
Nursing considerations for adrenergic medications
579
Any black box warnings for adrenergic medications
580
Adrenergic medications: Short acting and long acting
581
Anticholinergics: Atrovent
582
Anticholinergics: Spirva
583
Indications for anticholinergics?
584
How do anticholinergics work?
585
Side effects of anticholinergics?
586
Nursing considerations for anticholinergics?
587
Any black box warnings for anticholinergics?
588
Medications in muscarinic receptors class
589
Indications for muscarinic receptors?
590
How do muscarinic receptors work?
591
Side effects of muscarinic receptors?
592
Nursing considerations for muscarinic receptors?
593
Any black box warnings for muscarinic receptors?
594
Methylxanthines: Theophylline
595
Indications for Methylxanthines?
596
How do Methylxanthines work?
597
Side effects of Methylxanthines?
598
Nursing considerations of Methylxanthines?
599
Any black box warnings for Methylxanthines?
600
Corticosteroids: Flovent
601
Indications for corticosteroids (flovent)?
602
How do corticosteroids (flovent) work?
603
Side effects of corticosteroids (flovent)?
604
Nursing considerations for corticosteroids (flovent)?
605
Any black box warnings for corticosteroids (flovent)?
606
Leukotriene modifiers: singulair
607
Indications for Leukotriene modifiers (singulair)?
608
How do Leukotriene modifiers (singulair) work?
609
Side effects of Leukotriene modifiers (singulair)?
610
Nursing considerations for Leukotriene modifiers (singulair)?
611
Any black box warnings for Leukotriene modifiers (singulair)?
612
Immunosuppressant monoclonal antibodies: Xolair
613
Indications for immunosuppressant monoclonal antibodies (xolair)?
614
How do immunosuppressant monoclonal antibodies (xolair) work?
615
Side effects of immunosuppressant monoclonal antibodies (xolair)?
616
Nursing considerations for immunosuppressant monoclonal antibodies (xolair)?
617
Any black box warnings for immunosuppressant monoclonal antibodies (xolair)?
618
Mast cell stabilizers: Cromolyn
619
Indications for mast cell stabilizers (cromolyn)?
620
How do mast cell stabilizers (cromolyn) work?
621
Side effects of mast cell stabilizers (cromolyn)?
622
Nursing considerations for mast cell stabilizers (cromolyn)?
623
Any black box warnings for mast cell stabilizers (cromolyn)?
624
How to use an inhaler?
625