Final (Combining Decks) Flashcards

(726 cards)

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

Low-density lipoproteins

LDL

A

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

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4
Q

High- Density Lipoproteins

HDL

A

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

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5
Q

Desired Total cholesterol level

A

<200

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6
Q

Desired Total LDL level

A

<130
For diabetics or increased risks <70

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7
Q

Desired Total triglyceride level

A

<200

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8
Q

Desired Total HDL level

A

> 50

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9
Q

Lipid lowering drugs: HMG CoA Reductase inhibitors (Statins)

DRUGS (5)

A

Lovastatin
Pravastatin
Simvastatin
Atorvastatin
Rosuvastatin (Most potent)

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10
Q

Lipid lowering drugs: Fibrates
(3)

DRUGS

A
  • Gemfibrozil
  • Fenofibrate
  • Fenofibric acid
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11
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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12
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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13
Q

Lipid lowering drugs: Bile acid sequestrants

DRUGS (3)

CCC | start with “chole” = gallbladder = bile

A

Colesevelam
Cholestyramine
Colestipol

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14
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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15
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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16
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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17
Q

Nursing Considerations (Labs/vital sings): Statin

caution combining with what med?

A
  • Common to experience muscle pain, fatigue, & mild digestive issues
  • Assess for muscle pain & monitor for side effects
  • LFTs and liver enzymes (manage by reducing the dose or stopping until levels return to normal)
  • Lipid panel - check 4-6 weeks after starting
  • start with lower dose and increase as needed
  • caution with combining statins with fibrates
  • pregnancy category X
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18
Q

Side Effects: CAI

CAI work on small intestines…

A
  • Abdominal pain and Diarrhea (most common)
  • Upper airway infections
  • Arthralgias (joint pain)
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19
Q

Pt Education: CAI

Can be given with? Who should not take?

A

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

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20
Q

Nursing Considerations (Labs/vital sings): CAI

Contraindications? Can take with?

A

Contraindications
* Allergy
* Pregnancy or lactation
* Severe liver disease

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

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21
Q

Nursing Considerations: B.A.S

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

A
  • Can inhibit absorption of Vit: A, D, E, K
  • Can be used together with fibrates
  • Will decrease LDL but may also increase triglycerides/HDL
  • Can be used with pregnant women/pt with acute liver disease (monitor liver enzymes)
  • when mixing: give the medication right away because it will turn solid if it sits
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22
Q

Side Effects: PCSK9 Inhibitors

Administered SUBQ

A
  • Itching
  • Swelling
  • Pain or bruising at injection site
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23
Q

Side Effects: Bile Acid Sequestrants (5)

A
  • Constipation
  • Abdominal Pain
  • Diarrhea
  • Heartburn
  • Gallstones
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24
Q

Nursing considerations: PCSK9 Inhibitors

Admin how often? Can be given with? Reserve for who?

A

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

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25
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
26
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
27
What does 'euthyroid' refer to?
Normal thyroid gland function
28
What is a goiter?
Visible enlargement of the thyroid gland
29
What is Graves Disease?
Antibody mediated autoimmune disease resulting in hyperthyroidism
30
What is Hashimoto’s Thyroiditis?
Autoimmune disease often resulting in hypothyroidism
31
What are the normal thyroid levels for TSH?
0.4 to 4.5
32
What TSH level indicates hyperthyroidism?
Less than 0.4
33
What TSH level indicates hypothyroidism?
Above 4.5 ## Footnote Can be primary or autoimmune (Hasimotos, thyroiditis)
34
List some symptoms of hypothyroidism. (9)
* Fatigue * Depression * Dry Skin * Constipation * Bradycardia * Altered menstrual cycles * Weight gain * Changes in hair * Cold intolerance
35
What is myxedema?
Severe hypothyroidism online: "a condition, often associated with severe hypothyroidism, characterized by a buildup of mucin in the skin and other tissues, leading to swelling and thickening."
36
What medication is commonly used for hypothyroidism?
Levothyroxine
37
What is the brand name for synthetic T4?
Synthroid, Levoxyl
38
What is the half-life of Levothyroxine?
6-7 days
39
What should be avoided when taking Levothyroxine/ Armour Thyroid
Calcium containing medications, antacids, or iron supplements
40
What is hyperthyroidism?
Increased in circulating T3 and T4 from overactive thyroid or excessive thyroid hormone production ## Footnote Graves disease is hyper-functioning thyroid
41
What is the main treatment for Graves Disease?
Beta blockers (e.g., Propranolol or Atenolol)
42
What are the symptoms of hyperthyroidism? (10)
* Anxiety * Restlessness * Diaphoresis * Diarrhea, N/V * Tachycardia / AFib * Weight loss * Heat intolerance * Exophthalmos * Changes in menstrual cycle * Insomnia
43
What is Lugol’s Solution used for? | IODINE
* Inhibits release of T3 and T4 * short-term use * can cause iodinism
44
What are the side effects of Iodine Solutions?
* Metallic taste * Stomatitis * Sore throat * Hypersensitivity
45
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
46
What is the drug of choice for hyperthyroidism?
Methimazole
47
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
48
What is the treatment goal for hyperthyroidism?
Decreasing thyroid hyperactivity and preventing complications
49
What must be monitored when using PTU?
* LFTs * CBC
50
What is the usual duration for checking TSH after starting thyroid medication?
6-8 weeks after starting and after dose changes
51
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
52
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
53
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
54
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
55
Most frequent side effects of metformin?
* GI side effects (common) * Bloating * Diarrhea * Abdominal pain * Nausea * Metallic taste | Increased risk for B12 deficiency
56
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
57
What lab test other than the BS should the nurse be aware when administering metformin?
Renal/hepatic? B12 b/c increased risk of B12 deficiency
58
How do the sulfonylureas reduce blood sugar?
Stimulates Beta cells to secrete insulin Decrease glucose production by the liver | *Glipizide and glyburide*
59
Why do sulfonylureas cause weight gain?
online: the increased insulin levels promote the storage of excess glucose as fat
60
What are the nursing interventions for Sulfonylureas? Onset?
* Monitor for hypoglycemia * Onset at 90 minutes and peak in 2-3 hours
61
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
62
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
63
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)
64
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.
65
-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
66
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
67
# 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?
68
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
69
Major nursing considerations for DPP-4?
Hypoglycemia
70
How do sodium glucose co transport inhibitors work?
Inhibit reabsorption of glucose in the proximal renal tubules; promote glucose excretion in urine
71
Side effects of sodium glucose co transport inhibitors?
Increase risk : Yeast infections, UTIs, and Amputation?
72
Glycemic Targets (ADA) A1C FPG PPG
* A1C < 7% * FPG 80-130 * PPG <140
73
What is the goal of insulin therapy?
To mimic the physiological control of blood glucose levels
74
What are the two physiological blood glucose levels of insulin secretion?
* Basal insulin levels – during fasting * Postprandial levels – after eating
75
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
76
What is the recommended method of insulin administration?
Only use an insulin syringe and administer subcutaneously
77
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
78
What should be the distance between insulin injection sites?
About 1.5 inches away from each other
79
What are the methods of insulin administration?
* Insulin pumps * Insulin pen injectors * Insulin syringes
80
Name the types of insulin.
* Rapid-Acting * Short-Acting (Regular) * Intermediate * Long-Acting
81
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
82
What is the onset time for Aspart, Glulisine, and Lispro?
5-15 minutes ## Footnote Inhaled insulin onsent within ONE minute
83
What is the peak time for rapid-acting insulin?
30-90 minutes ## Footnote inhaled insulin within 12-15 min
84
True or False: Food must be present when administering rapid-acting insulin.
True
85
What is the duration of action for rapid-acting insulin?
3-5 hours
86
What is the primary use for short-acting insulin? | AKA REGULAR INSULIN
To cover the glucose rise after eating a meal
87
When should short-acting insulin be administered?
30 minutes before meals
88
What happens if regular insulin is cloudy?
Throw it out
89
What is intermediate-acting insulin also known as?
Isophane or NPH (Neutral Protamine Hagedorn)
90
How often is intermediate-acting insulin usually given?
Twice a day
91
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
92
What is the onset of action for long-acting insulin?
Up to 1.5 – 2 hours
93
What is the duration of action for long-acting insulin?
24+ hours
94
What is a notable characteristic of long-acting insulin absorption?
Even absorption with no peaks and valleys | Frequently used in Type 2 DM
95
What is the dosing range for insulin?
0.6-0.8 units/kg/day
96
What is sliding-scale insulin?
Adjusted doses dependent on individual blood glucose, usually reserved for inpatient use
97
How should unopened vials of insulin be stored?
Refrigerated until needed
98
How long can opened insulin vials be stored at room temperature?
1 month
99
What is the antidote for hypoglycemia?
Sugar
100
What should patients with Type 1 DM do even if NPO?
Will need insulin
101
What should diabetic patients wear as a precaution?
A medical alert tag
102
Nursing considerations for Rapid- Acting Insulin
* Must be given with food * Usually given in conjunction with intermediate acting insulin * Always monitor for hyPOglycemia
103
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
104
Hypothyroid medications (2)
Levothyroxine Armour Thyroid (desiccated)
105
Hyperthyroid medications
Methimazole Propylthiouracil (PTU) Iodine Solutions
106
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)
107
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 Used for hyperthyroidism
108
Medication given for Thioamides | Both have THI?
Methimazole Propylthiouracil (PTU)
109
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)
110
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
111
I-131
* Iodine (Radioactive) * Use for thyroid cancer, thyrotoxicosis/special cases * Not for pregnancy * Increase fluid intake * Radiation precautions
112
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
113
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.
114
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.
115
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
116
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.
117
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.
118
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.
119
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.
120
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.
121
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.
122
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.
123
Define hypoglycemia.
Blood glucose level < 70 mg/dL with or without symptoms. ## Footnote Most commonly occurs in patients treated with insulin.
124
What are common electrolyte issues in DKA?
* Hyponatremia * Hyperkalemia ## Footnote These imbalances need to be monitored during treatment.
125
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
126
What is ketosis?
A metabolic state where the body uses free fatty acids for energy instead of glucose
127
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
128
Polyphagia
Increased appetite with weight loss -Insulin deficiency-cells not receiving glucose- sets into effect compensatory processes to increase blood glucose levels.
129
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
130
What causes blurred vision in diabetes?
Accumulation of glucose in aqueous fluid in the cornea alters refraction of light entering the eye
131
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).
132
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 * medications
133
What is the role of glucagon in hypoglycemia?
Triggers the release of glycogen from the liver
134
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.
135
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.
136
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 ## Footnote Metabolic syndrome 5 criteria: abdominal obesity, high blood pressure, high triglyceride levels, low HDL cholesterol, and elevated blood sugar
137
What are the glucose-regulating hormones?
Amylin, somatostatin, glucagon, and incretins ## Footnote Amylin slows glucose absorption, while glucagon promotes glucose production.
138
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.
139
When are insulin levels their highest?
After a meal ## Footnote Insulin levels decrease during fasting.
140
What are the symptoms of hypoglycemia? (13) | FSHDRAISBCLSC
* 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.
141
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.**
142
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.
143
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
144
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.
145
Fill in the blank: The body responds to increased blood sugar levels by stimulating the pancreas to release _______.
[insulin]
146
True or False: Type 2 diabetes accounts for 90-95% of all diabetes cases. | Why
True
147
Insulin stimulates the uptake, use, and storage of _____
glucose
148
Which hormone is required to initiate active transport of glucose into the cell?
Insulin
149
Different ways to regulate glucose: | Increased: what cells release what? Decreased: what cells release what?
Increased blood glucose: - Beta cells --> Insulin & Amylin Vs Hypoglycemia: - Alpha cells --> Glucagon
150
What is the normal glucose levels?
70-100
151
What glucose levels are considered prediabetic?
101-125
152
What glucose level is considered to be diabetic?
>126
153
Physical Symptoms of metabolic syndrome
Increased waist circumference or belly fat (Apple Shape) High triglycerides Elevated BP High BS Low HDL Ancanthosis Nigricans
154
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
155
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 | Can be given with? Decrease what?
- 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 | Don't take with, will need what, not recommended for who
- 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: 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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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)
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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? | if my birth control fails, ill want to kms
- 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 (7)
- 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 (6)
- chronic neuropathic pain - anxiety - hot flashes/night sweats - headaches - hiccups - alcohol withdrawal
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Gabapentin (Neurontin): side effects | FML WEET GS
- 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
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Role of Thrombin and the development of the clot
online: Thrombin plays a central role in clot development by converting fibrinogen into fibrin, the main structural component of a blood clot, and activating other factors that contribute to clot stabilization. It also helps activate platelets, which further contribute to clot formation
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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 (monitored with heparin) PT- Extrinsic (PT/INR monitored with warfarin)
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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? Level up RN: “a horse CLOPping on platelets so they don’t combine”
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 aspirin
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Nursing considerations for pt on anti-platelets - how long to stop before surgery? take how often? who can stop med? Who should not be on anti-platelets (6)
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 slowly compared to heparin online: After being stopped, warfarin takes 5–7 days to clear the body.
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How do Factor Xa inhibitors work? (DOAC)
-Prevent factor Xa from changing prothrombin to thrombin. They bind directly to factor Xa ## Footnote Common factor Xa inhibitors include rivaroxaban (Xarelto), apixaban (Eliquis), and edoxaban (Savaysa). BANS Xa
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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 online: Factor Xa inhibitors are different from warfarin primarily because they act on a specific enzyme in the clotting cascade, while warfarin affects a broader range of clotting factors.
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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
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How does heparin work?
Anti-thrombin inhibitor- interferes with conversion of thrombin to prothrombin
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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.
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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
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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 receive one over the other?
Unfractionated heparin: * 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
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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
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why would tPA be administerd? What are the criteria or contraindications which must be met before administration? | what specific nursing actions to do - are obvious
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
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Common cause of hospital acquired infection?
Accounts for about 50% of all hospital acquired infections Catheter Acquired UTI (CAUTI)
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UTI Classifications
Lower - Bladder and structures below the bladder Upper -Kidneys -Ureters
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Example of Lower Urinary tracts infection
Cystitis
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Example of Upper Urinary tracts infection
Pyelonephritis
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Most uncomplicated Lower UTI are caused by which bacteria? Where does it usually enter through?
E. Coli? Urethra
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Washout phenomenon
occurs when urine washes out the bacteria in the urethra during urination
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Complicated UTI bacteria
Staphylococcus saprophyticus Klebsiella pneumoniae Proteus mirablis Pseudomonas species
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Causes of UTI: Obstruction | Anatomic vs Functional
Anatomic: - Stones, BPH, Pregnancy Functional: - Infrequent voiding etc.
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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 symptoms of UTI:
Symptoms can vary: * Incontinence * Foul smelling concentrated urine * Fatigue * Confusion * Dementia * Hallucinations
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UTI In Children: | More prevalent in what gender after what age? What type of UTI?
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
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Urinary Testing: Nitrites
What: Enzyme released by Enterobacteriaceae Normal: Negative *Can be negative 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: Negative 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 therapy 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 | 6 specific antibiotics listed
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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Glomerular Filtration | how much /day
GFR: average adult 125mL/minute or 180L/day
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How does the kidney concentrate urine (3 factors)
* Osmolarity of interstitial fluids * Anti diuretic hormone * Action of ADH on the cells in the collecting tubules of the kidney
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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) | What is it? Causes of ATN? What type of renal disorder?
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
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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 | Retains what (CUPS)?
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) | What is it? Criteria?
**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(2)/Medications(4)/Diet modifications(2)/Complication(3)
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 | Effects of DM and HTN on the renal system/damages
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
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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
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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 (7)
* 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
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Uses of loop diuretics | Decreases what?
Decrease blood volume, which decreases venous return and blood pressure
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Key side effects of loop diuretics? Any black box warnings?
- hyponatremia - **hypokalemia** - hypovolemia - hypomagnesemia - hyperglycemia - ototoxicity
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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
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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 spironolactone and eplerenone
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Mechanism of action of spironolactone and eplerenone
blocks the exchange of sodium for potassium in the distal tubules - potassium sparing
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Uses of spironolactone and eplerenone
Indications: hypertension and heart failure - used when one drug is not enough to treat symptoms
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Key side effects of spironolactone and eplerenone? Any black box warnings?
- can cause gynecomastia
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What specific actions does nurse need to take with spironolactone and eplerenone? Labs, vitals, nursing considerations?
- monitor potassium (can cause hyperkalemia) - monitor LFTs - monitor BUN/Cr - do not give in renal insufficiency
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Patient education with spironolactone and eplerenone? Any specific or key instructions?
- take with meals - avoid taking with: -- ACE inhibitors/ARBs -- heparin -- NSAIDs
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Meds in class with digoxin
Class name: digitalis glycosides - digoxin - deslanoside - mitildigoxin
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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)
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Uses for digoxin
indications: heart failure and atrial fibrillation not first-line treatment
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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
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Therapeutic margin for digoxin?
Normal level: 0.5-2.0 Desired level: 0.8
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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
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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)
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Stages of heart failure (image)
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Classification of heart failure (image)
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What is the normal ejection fraction for the left ventricle?
between 50-70%
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Ejection fractions and heart failure: HFrEF, HFmrEF, HFpEF
- HFrEF: heart failure with reduced ejection fraction - HFmrEF: heart failure w/ mid-range ejection fraction - HFpEF: heart failure w/ preserved ejection fraction
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Heart failure and activation of the sympathetic nervous system (SNS is fight or flight)
- increases HR and contractility; tachycardia - vasoconstriction - activates the RAS system - direct cardiotoxicity - increases myocardial O2 demand - increases wall stress - decreased preload and increased afterload
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Right-sided heart failure
Not as common as left-sided HF - have deoxygenated blood coming from body, but right side not pumping as well as should be - leads to a "back up" of blood in body **peripheral swelling** Symptoms: - weakness, fatigue - leg/feet edema - vein distension - weight gain - increased urination - hepatomegaly - increased abdominal girth Ascites, edema
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Right-sided heart failure: Symptoms
Symptoms: - weakness, fatigue - leg/feet edema - vein distension - weight gain - increased urination - hepatomegaly - increased abdominal girth
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Left-sided heart failure
Left ventricle is unable to pump re-oxygenated blood from lungs to the heart's left atrium - ventricles too stiff - not contracting properly Leads to: - decreased cardiac output - **pulmonary congestion** Common cause of right-sided heart failure Types of left-sided heart failure: - systolic heart failure - diastolic heart failure Crackles in lungs, expect SOB
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The cycle of left ventricle (left-sided) heart failure
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Left-sided heart failure: systolic heart failure
LV cannot contract forcefully enough to keep blood circulating normally throughout the body - deals with contraction of the heart - low ejection fraction (<40%) Symptoms: - tiredness/fatigue - decreased urine production - increased HR, may be irregular - elevated BP - enlarged heart - pulmonary "congestion" = SOB - coughing (often worse at night) - weight gain - decreased blood flow to extremities
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Left-sided heart failure: Diastolic heart failure
LV has grown stiff or thick; is unable to fill the heart properly, which reduces the amount of blood pumped out to the body - issue with ventricle being too stiff to properly fill heart and being able to contract: ventricular hypertrophy - ejection fraction is typically normal (EF >50%) - often resulting from HTN no medications available to fix diastolic dysfunction
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Left-sided heart failure: Symptoms/Image
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Meds in class of ACE inhibitors (A-pril)
end in -pril - lisinopril - enalapril (can be given IV) - ramipril - captopril
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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
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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
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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
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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
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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
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Meds in class of thiazide diuretics
- hydrochlorothiazide (HCTZ) - chlorthalidone
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Mechanism of action of thiazide diuretics | Inhibits what? Decreases what? Better for who?
- 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
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Uses of thiazide diuretics
treat hypertension; first-line medication
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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
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What specific actions does the nurse need to take with thiazide diuretics? Labs, vitals, nursing considerations? | who should not have? any drug toxicitys? Give when
- 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
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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
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Meds in ARBs class (angiotensin II receptor blockers)
end in -sartan - losartan - irbesartan - valsartan
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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
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Uses of ARBs
first-line treatment of hypertension; when ACE inhibitor cannot be used
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Key side effects of ARBs? Any black box warnings? (7) | angiotensin receptor blocker
- cough (less than an ACEI) - hyperkalemia (less than ACEI) - headaches - dizziness and syncope - GI complaints - xerostomia (dry mouth) - alopecia
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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
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Patient education with ARBs? Any specific or key instructions?
- avoid during pregnancy - do not take with ACE inhibitor - can take with or without food
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Meds in class of calcium channel blockers: dihydropyridines | FAN of "pine" trees
- felodipine - amlodipine - nifedipine
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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
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Uses of calcium channel blockers: dihydropyridines | What do they treat (5)
- hypertension - angina - rate control in AFib - SVT - Raynaud's phenomenon
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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
403
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
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Patient education with calcium channel blockers: dihydropyridines? Any specific or key instructions? | Diet alterations? Check..?
- do not drink grapefruit juice - increase fiber in diet - always check HR prior to taking and make sure not less than 60
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Meds in class of calcium channel blockers: non-dihydropyridines
- verapamil - diltiazem both can be given IV
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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
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Uses of calcium channel blockers: non-dihydropyridines | What do they treat (4)
- hypertension - angina - arrhythmias (AFib, SVT) - migraines (verapamil)
408
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 | verapamil, diltiazem
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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
410
Patient education with calcium channel blockers: non-dihydropyridines? Any specific or key instructions? | Diet alterations? Check...?
- increase fiber in diet - always check heart rate before taking and make sure not less than 60 - do not drink grapefruit juice
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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
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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 Helps to improve symptoms, reduce hospitalizations, and enhance survival in patients with heart failure with reduced ejection fraction (HFrREF) **blocks SNS responses** - decrease HR - decrease BP - decrease muscle contraction - increase blood flow to the kidneys - decrease renin release
413
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
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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
415
What specific actions does the nurse need to take with Beta Blockers? Labs, vitals, nursing considerations? | Caution in what patients? Check what? Starting dose 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)
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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
417
Meds in class: Entresto (Sacubitril plus Valsartan)
Class: angiotensin receptor-neprilysin inhibitor (ARNI) Entresto (sacubitril + valsartan) is the only ARNI
418
Mechanism of action of Entresto (Sacubitril plus Valsartan) | Increases 3 things
Increase: - naturetic peptides (like BNP) - bradykinin (vasodilation) - other mediators which increase vasodilation
419
Uses of Entresto (Sacubitril plus Valsartan)
Used for systolic heart failure to improve symptoms and reduce remodeling
420
Key side effects of Entresto (Sacubitril plus Valsartan)? Any black box warnings? | Combo med
- angioedema - hypotension - hyperkalemia - renal failure - cough
421
What specific actions does the nurse need to take with Entresto (Sacubitril plus Valsartan)? Labs, vitals, nursing considerations?
monitor potassium, BUN, Cr, BP
422
Patient education with Entresto (Sacubitril plus Valsartan)? Any specific or key instructions?
- contraindicated in pregnancy - DO NOT TAKE WITH NSAIDs (NSAIDs vasoconstrict so counteracts)
423
Meds in Nitrates class
nitroglycerin isosorbide hydralazine and nitrates (combined)
424
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)
425
Uses of nitrates?
prevention and treatment of attacks of angina pectoris and heart failure
426
Key side effects of nitrates? Any black box warnings?
- when taking: tingles or burns under tongue - headache - dizziness
427
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
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Nitrates: Isosorbide
- oral nitrate - has a drug free period in the delivery system (works for about 18 hours) - can be short acting or sustained-release - side effects similar to NTG (nitroglycerin)
429
Hydralazine & Nitrates
- first drug regimen shown to improve symptoms of heart failure - combined use of hydralazine and nitrate (isosorbide) to: -- decrease preload & afterload by achieving both venous and arterial vasodilation -- decrease systemic & pulmonic vascular resistance -- **positive ionotropic effect on heart** Used in patients who: - have symptoms despite ACEI, BB, diuretic therapy - those who can not tolerate routine therapy
430
Patient education with nitrates? Any specific or key instructions? | Absolutely do not take with...?
- 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
431
Meds in Alpha Blockers class
- doxazosin (cardura) - prazosin (minipress)
432
Mechanism of Action of Alpha Blockers
- inhibit alpha synapse at the alpha adrenergic receptors (blocks SNS) - prevent feedback of norepinephrine
433
Uses of Alpha Blockers
not really used in blood pressure control; considered 3rd or 4th line treatment - "almost work too well"
434
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
435
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
436
Patient education with Alpha Blockers? Any specific or key instructions?
- let them know about first dose effect and that adverse effects are significant
437
What are the characteristics of metabolic syndrome?
- hypertension - obesity (especially apple shape; abdominal fat) - abnormal cholesterol levels (hyperlipidemia) - chronic inflammation - insulin resistance
438
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
439
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
440
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
441
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.
442
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.
443
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
444
Meds to check for apical HR
Beta blockers: Carvedilol, metoprolol, bisopropolol DIGOXIN Calcium channel blockers
445
How do meds work for Heart failure? Vasodilators, loop diuretics, Beta blocks
Vasodilators- decrease workload of overworked cardiac muscle Loop diuretics- Decrease blood volume which decreases venous return and blood pressure Beta blockers (beta-adrenergic antagonists) - decrease contractions and workload b/c decrease calcium flow into myocardial cells
446
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
447
What type of cells in the epithelial lining produce mucus?
Goblet cells ## Footnote These cells play a crucial role in trapping particles and pathogens.
448
What is perfusion?
The movement of blood through the pulmonary circulation ## Footnote Perfusion is necessary for delivering oxygen to the tissues.
449
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.
450
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.
451
What is hemoptysis?
Coughing up blood ## Footnote Hemoptysis can be associated with conditions such as tuberculosis, lung cancer, or infection.
452
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.
453
What are the common causes of atelectasis?
* Post-operative complications * Compression by a mass
454
What is hypoxia?
Oxygen level in blood inadequate to meet needs of the tissue
455
What is hypoxemia?
Insufficient amount of oxygen in blood
456
Rhinitis | *Rhinosinusitis- Path. of both are similar but affects diff structures
Inflammation and congestion of the nasal mucosa - Seasonal (hay fever) Inflammatory response to a specific allergen -Symptoms: Nasal congestion, sneezing, stuffiness, watery eyes
457
Sinusitis | *Rhinosinusitis- Path. of both are similar but affects diff structures ## Footnote Timing, causes, symptoms
Inflammation of the mucus membranes lining the para sinuses Can be acute, subacute, or chronic -Viral (7-10days) - Allergies -Bacterial (up to 4 weeks) -Symptoms: Headache, pain over sinus area, pressure, nasal congestion, purulent discharge
458
Common Clinical manifestations- Rhinosinusitis
Nasal Congestion Cough Bronchial Secretions
459
Pharmacological management of Rhinosinusitis
Treatment of nasal congestion and cough -May be OTC/prescriptions -Analgesics (acetaminophen/ibuprofen)
460
Rhinosinusitis Med classes: | Treatmeant for nasal congestions/cough ## Footnote NAAME
Nasal decongestants Antitussives Antihistamines Expectorants Mucolytics
461
Nasal Decongestants: General info | Used for? Adverse effects? Pt education?
Used to relieve nasal obstruction and discharge -decreases inflammation of nasal membranes Adverse effects: local stinging and burning Rebound congestion SNS symptoms: increased HR and BP, Urinary retention Pt education: dont use for more than 5 days unless instructed otherwise ## Footnote All drugs are category C pregnancy
462
Nasal Decongestants: Drugs in class
Pseudoephedrine (Sudafed) Oxymetazoline (Afrin) Phenylephrine (Vazculep; Neo-synephrine) Fluticasone (Flonase) Triamcinolone (Nasacort)
463
Rhinosinusitis: Antitussives | Used for? Drugs in class? Adverse effects of one of meds and all?
Used to suppress non-purposeful cough - Depresses the cough receptors in brain, throat, trachea, or lungs Drugs in Class: - Benzonate (Tessalon Perles) - Dextromethorphan (Delsym) -Adverse effects: nausea, drowsiness, rash, and difficulty breathing - Codeine - Hydrocodone bitartrate Adverse effects: Drying of mucus membranes, headache, drowsiness, dizziness ## Footnote All Drugs are Pregnancy Category C(D during labor)
464
How do antitussives work?
Used to suppress non-purposeful cough -Depresses the cough receptors in brain, throat, trachea, or lungs
465
Side effects of antitussives?
Adverse effects: Drying of mucus membranes, headache, drowsiness, dizziness Dextromethorphan – nausea, drowsiness, rash, and difficulty breathing
466
Nursing considerations for antitussives? | contraindications
Contraindications: History of allergy to drugs, those with a head injury, or could be impaired by CNS depression Caution in those with asthma and COPD Caution in children with atopic syndrome Dextromethorphan – Avoid use with alcohol and several psych drugs ## Footnote Dont use for more than 5 days unless specified
467
Medications in antihistamines class ## Footnote ONLY THE BOLD ONES ON POWER POINT
First Gen: Diphenhydramine(Benadryl)** Hydroxyzine (Vistaril Second Gen: Certirizine (Zyrtec)** Loratadine (alavert, claritin) Third Gen: Fezofenadine (allegra)
468
Indications for antihistamines?
Used for the relief of symptoms associated with allergic responses (i.e. seasonal allergies, angioedema, motion sickness, allergic reactions)
469
How do antihistamines work?
Block the release or action of histamine at the histamine-1 receptor sites Also have anticholinergic and antipruritic effects
470
Side effects of antihistamines?
May cause dryness of mucus membranes and thickening of secretions drink plenty of fluids ## Footnote first generation also have more drowsiness effects - have gotten better w/ later generations
471
Nursing considerations for antihistamines?
* May cause drowsiness, dizziness, or impaired mental alertness * Do not smoke * Do not drive or operate heavy equipment after taking * Avoid other medications that also cause sedation * Do not take more than one antihistamine at a time * Many otc cold and “nighttime” or “PM” sinus and allergy medications contain an antihistamine * Also otc sleep aids contain Diphenhydramine (Benadryl) * Avoid prolonged exposure to sunlight **Take with meals to avoid GI upset
472
Medications in expectorants class | Onset? Duration?
Guaifenesin (Mucinex) Onset: 30 minutes Duration: 4-6 hours
473
How do the expectorants work?
Increase productive cough to clear the airway by: * Liquify lower respiratory tract secretions * Decrease the viscosity of secretions
474
Side effects of expectorants?
rash, headache, nausea/vomiting, dizziness
475
Nursing considerations of expectorants?
* History of allergy to drugs * Persistent cough due to smoking, asthma, emphysema * Productive cough lasting more than 1 week
476
Medications in mucolytics class?
Acetylcysteine (Acetadote, parvolex) Fast onset via nebulizer Dornase alfa (Pulmozyme
477
Indications for mucolytics?
Used to treat cystic fibrosis, asthma, bronchiectasis, COPD, and chronic bronchitis
478
How do mucolytics work?
Breakdown and liquefy of respiratory tract secretions
479
Side effects of mucolytics? (7)
* GI upset * stomatitis * rhinorrhea * Bronchoconstriction * bronchospasm * urticaria * rash
480
Nursing considerations for mucolytics?
History of allergy to drugs Presence of acute bronchospasm - Can be given in nebulizer form- pt should know how to use one
481
Respiratory: herbal meds | Cold remedies
* Echinacea different preparations no better that a placebo * Vitamin C decrease incidence and severity of colds and influenza Regular used appears to play a role in the defense mechanisms of the respiratory system * Zinc Sulfate decrease incidence and severity of cold symptoms in adults Can lead to loss of smell with nasal zinc *
482
Role of histamine r/t the respiratory system?
First chemical mediator releases in immune and inflammatory responses
483
Asthma (pathophy)
There are 3 major components: Bronchoconstriction – in response to a trigger Airway inflammation – due to t-helper cells and ige-mediated pathways Bronchial hyperresponsiveness –due to activated mast cells which lead to the release of inflammatory mediators (Histamine, prostaglandins, and leukotrienes) ## Footnote Overtime, Airway thickening and hyperplasia of the smooth muscle may lead to remodeling of lung tissue
484
Asthma- Clinical Manifestations
Dyspnea, wheezing, cough, prolonged expiration Chest tightness Accessory muscle use
485
Exercise-induced asthma: Treatment
*Short-acting beta-agonists (SABAs) -**take before exercising.** - include albuterol (ProAir HFA, Proventil-HFA, Ventolin HFA) and levalbuterol (Xopenex HFA). are inhaled medicines that help open airways. Should not be used every day As it can make them less effective. *Ipratropium, a SAMA, (Atrovent HFA) is an inhaled medicine that relaxes the airways 
486
Nocturnal asthma | Wouldn't go to the MALL at night ## Footnote W
symptoms: wheezing, chest tightness, difficulty breathing at night Treatment: * Montelukast (Singulair) * Albuterol * Long-Acting-beta agonists * Leukotrienes ## Footnote Worse at night and may disrupt sleep
487
Status asthmaticus
**Acute, Severe asthma that is refractory to treatment. Can be life threatening** Patient may have no wheezing or cough
488
Types of Bronchodilators | BMLM: Better Maximization of Lung Movement?? idfk
* Beta 2 adrenergic agonists (short/Long) * Muscarinic antagonists * Leukotriene Receptor Antagonists * Methylxanthines
489
Adrenergic meds: Short-acting Beta-Agonists (SABA) | Known as? Med? Administration?
**Known as "rescue drug" Always used first to treat an acute attack** Meds: Albuterol (proair, ventolin, proventil) Administration * Shake the inhaler before use * 2-4 puffs every 20 minutes, up to 3 doses * No relief, call the physician
490
Short acting- Albuterol | Administration (exercise-ind., inhaled), contraindications, side effects ## Footnote Provent Provent
Aka: Proair, Ventolin, Proventil Administration: - Exercise-induced – 2 puffs 15 to 30 minutes before exercising - Bronchospasm/Constriction -- Inhaler solution – 3 to 4 times a day -- Inhaled powder – 3-4 times a day Contraindications: CAD, HTN, Diabetes, Seizure disorder Side Effects: - Muscle tremors - Cardiac: Angina, tachy, palpitations - CNS: agitations, anxiety, insomnia, seizures
491
How do adrenergic medications work
Causes: - Smooth muscle relaxation in the lungs, muscles, and liver - vasodilation of the bronchial passage - release of insulin
492
Side effects of adrenergics? | Adrenergics make you Anxious
Side effects: Tachycardia, tremors/shakiness, palpitations, anxiety, sweating, and arrhythmias, and insomnia
493
Nursing considerations for adrenergic medications | Avoid use with what 2 types of meds?
Avoid use with Beta-blockers and Nsaids
494
Adrenergics- Long-acting Beta Agonists ## Footnote LABA
Maintenance Drug- allows airway to stay open -Seen as inhaler-metered dose or dry powder -**used in combination with steroid** Meds: Salmeterol (serevent)
495
Long- acting Beta Agonist: Black-box warning and information
**salmeterol (Serevent) and formoterol (Foradil) should not be used without a steroid in asthma for all ages Need to weigh the risk vs benefits** NEVER USE AS A RESCUE INHALER - SHOULD NOT BE USED IN CHILDREN LESS THAN AGE 4 and NEVER WITHOUT A STEROID ## Footnote USE WITH A STEROID!!
496
How do anticholinergics work? | Used after what? ## Footnote aka- anticholinergic
Blocks muscarinic cholinergic receptors by antagonizing the neurotransmitter acetylcholine in smooth muscle ## Footnote USED AFTER SABA
497
Side effects of anticholinergics? | Local and systemic
Local: dry mouth, hoarseness Systemic: * dizziness * headache * fatigue * palpitations * urinary retention
498
Medications in muscarinic receptors class ## Footnote Short/Long
-Ipratropium Bromide (Atrovent):*Short acting* -Tiotropium Bromide (Spiriva):*Long acting*
499
Muscarinic Antagonists: Ipratropium (Atrovent) | What is it? Can cause? Not for? Can not use if...?
Short-acting (SAMA) Can cause anticholinergic side effects NOT FOR ACUTE BRONCHOSPASM Can not use if allergic to peanuts or SOY products
500
Muscarinic Antagonists: Tiotropium Bromide (Spiriva) | Inhibits what? Can cause? Not for what?
Long-Acting (LAMA) Inhibits the muscarinic M3 receptors in the lungs Can cause a cough/dry mouth Not for acute bronchospasm
501
Methylxanthines: General info | Bronchodilator
Bronchodilator **Current asthma guidelines do not support it's use** May be used at second-line treatment Several drug interations **DO not use if breastfeeding or pregnant**
502
Side effects/Nursing considerations of Methylxanthines?
Side effects: N/v, irritability, tremors, insomnia, tachyarrhythmias Requires drug monitoring due to **very narrow therapeutic range** Avoid caffeine Avoid smoking
503
Corticosteroids: Meds | Respiratory
~sone~ Beclomethasone (Qvar) Fluticasone (Flovent)
504
Indications/ how do they work: corticosteroids? | respiratory
Mainstay of asthma treatment and advanced COPD * Suppress airway inflammation * Decrease mucus secretions * Suppress the release of histamines by mast cells * Increase sensitivity of beta-2 adrenergic receptors **only about 10-30% make it into the lungs**
505
Corticosteroids: Flovent
May be used alone or in combination with other bronchodilators - Caution with hepait patients
506
Side effects of corticosteroids (flovent)?
Side effects: * headache * dry mouth * cough * hoarseness * candida infection (rinse mouth) * adrenal insufficiency * hyperglycemia Also QVAR - rinse mouth after use (thrush) - caution in hepatic patients - not for emergencies
507
Nursing considerations for corticosteroids (flovent)?
Teach patient to rinse mouth after use Inhaled steroids are not for emergency use
508
Leukotriene modifiers: singulair - when is it taken
Taken at night | Montelukast
509
Indications for Leukotriene modifiers (singulair)?
Asthma (rarely used) Exercise-Induced Bronchoconstriction Allergic rhinitis
510
Side effects of Leukotriene modifiers (singulair)?
Headache, GI symptoms, liver dysfunction Generally, well tolerated BLACK BOX WARNING: Neuropsychiatric: agitation, aggression, depression, sleep disturbances, suicidal thoughts & behavior
511
Nursing considerations for Leukotriene modifiers (singulair)? | Age? Reduced effect w/?
Age limitations (Exercise-induced) - 1 tablet at least 2 hours before exercise for patients 6 years and older. Seasonal allergic rhinitis: Daily, age 2 and older Asthma – age 12 months and older ## Footnote Reduced effect if taken with phenytoin
512
Any black box warnings for Leukotriene modifiers (singulair)? | singulair can make you psycho?
black box warning: psychiatric side effects such as aggression, depression, agitation, sleep disturbances, suicidal thoughts, and suicide.
513
Immunosuppressant monoclonal antibodies: Xolair | Used as what
Adjunctive therapy for moderate to severe asthma | omalizumab
514
Indications for immunosuppressant monoclonal antibodies (xolair)?
Used in children 6+ years
515
Side effects of immunosuppressant monoclonal antibodies (xolair)?
pain at injection site, headache, nausea, fatigue
516
Any black box warnings for immunosuppressant monoclonal antibodies (xolair)?
<0.1% anaphylaxis
517
Mast cell stabilizers: Cromolyn
Prevent bronchoconstriction by preventing the release of chemical mediators from mast cells - Effective long-term therapy - - Not for treatment of asthma attacksd
518
Side effects of mast cell stabilizers (cromolyn)?
Side effects: * hypotension * sore throat * taste changes * bronchospasm * chest pain * restlessness * nausea * dizziness
519
How to use an inhaler?
* Shake canister before each use * Breath out steadily * Place mouthpiece between lips * Tilt head back slightly * Depress the inhaler while taking a slow, deep breath in * Hold breathe for about 10 seconds then exhale slowly * Repeat after 5 minutes, if needed * Clean mouthpiece ## Footnote Rinse mouth after
520
Assessment of the GI tract should look at:
- swallowing - eructation (burping) - thrush - abdominal pain - emesis
521
What meds work on parietal cells?
has proton-pump so PPIs has H2 receptors so H2-receptor agonists
522
Why are prostaglandins important in gastric acid secretion?
There are high concentrations in the gastric mucosa and secretions - inhibit acid secretion - stimulate mucus and bicarbonate secretion
523
Function of goblet cells in the stomach?
secrete mucus
524
Function of parietal cells in the stomach?
- secrete HCl: sterilizes and breaks down food (mainly protein and carbs) - secrete intrinsic factor: needed to absorb B12 in small intestines - acid synthesis controlled by proton pump: pump triggers acetylcholine, histamine, gastrin
525
Abdominal pain: types, mediators
Three types: - parietal (localized, knife-like, sharp) - visceral: distention, inflammation (colicky, crampy) - referred Biochemical mediators of inflammatory response (histamine, bradykinin, serotonin) stimulate organic nerve endings producing abdominal pain - abd. organs are sensitive to stretching and distention
526
What is GERD?
A backward movement of gastric contents into the esophagus - lower esophageal sphincter relaxes spontaneously 1-2hr after eating, allowing regurgitate into esophagus Causes Esophageal mucosal damage: - erosive esophagitis - Barrett esophagus (repeated injury causes metaplasia, change to columnar epithelium, precancerous) Many people self medicate Diagnosis: endoscopy and manometry
527
What are causes of GERD?
Certain conditions, substances, foods, and medications can weaken or hinder closure of the lower esophageal sphincter - alcohol - acidic foods - fatty foods - chocolate - coffee - nicotine - obesity - pregnancy - hiatal hernia - medications: anticholinergics, beta agonists, CCBs, nitrates, progesterone
528
Clinical manifestations of GERD?
- **dysphagia** - **heartburn** - **regurgitation** - bitter taste - upper abd. pain w/in hour of eating - increases w/ lying or increased intra-abdominal pressures - can have symptoms w/ no acid - cough, increasing asthma symptoms - may seem like angina also increases risk of aspiration, especially with chronic GERD
529
Treatment for GERD | Lifestyle/diet and pharm?
**Lifestyle and diet changes**: - decrease dietary fats - eat small meals - stop smoking - avoid lying down for 3hr following a meal - avoid alcohol - weight loss - elevate HOB **Pharmacology** - antacids - H2 blockers - PPIs - prokinetic agents
530
What is celiac disease? Clinical manifestations, labs, and treatment?
An autoimmune disorder triggered by gluten Clinical manifestations: - abd. pain - bloating - diarrhea - weight loss - steatorrhea (fat in stool; oily, gray) - weakness - flatus - fatigue Labs: H/H, CMP, genetic testing, IgA, antibody testing Treatment: - remove gluten from diet - vitamin replacement - corticosteroids
531
What is H. Pylori? Spread how? Commonly causes?
Gram-negative rods that colonize in the mucus-secreting epithelial cells of the stomach - increased incidence in those of Hispanic and African American ethnicity Spread person-person through saliva, feces, vomiting Commonly causes: - peptic ulcers - gastritis - gastric cancer Most are asymptomatic
532
H. Pylori gastritis caused by
- small curved gram-negative rods **secretes urease (enzyme) that converts urea to ammonia, which neutralizes acidity of the stomach for bacteria to survive** - burrows into mucosal layer leading to erosion and inflammation - produces enzymes and toxins: -- impacts protection of mucosa to acidic environment -- intense inflammatory response -- creates immune response w/ T and B cells
533
Symptoms vary with H. pylori but include...? (7)
- many asymptomatic - dull burning pain in abdomen - increase pain w/ empty stomach - N/V - dyspepsia - bloating - weight loss
534
How is h. pylori diagnosed?
- urea breath test - serologic tests - stool antigen test - endoscopic biopsy
535
Treatment for h. pylori?
- antibiotics - Bismuth (has antibacterial effect) - PPI (raises the pH) - H2 blockers
536
What is peptic ulcer disease? Causes?
- inflammatory erosion in stomach (gastric ulcer) or duodenal lining (duodenal ulcer) - occur in upper portion of the GI tract Patho: - hypersecretion of HCl - ineffective mucus production - poor cellular repair Has periods of exacerbation and remissions - commonly seen in middle aged individuals Causes: - **h. pylori infection** - **use of ASA or NSAIDs** - stress - alcohol
537
Patho of h. pylori PUD (image)
538
PUD: Gastric Ulcer - where, occurs when, causes what, symptoms, and patho?
- occur in the stomach -- tends to develop in antral region of stomach adj. to acid-secreting mucosa in body -- ages 55-65 male and female - epigastric pain 1-2 hours after eating - can cause hematemesis or melena - heartburn, chest discomfort, and early satiety are common - can cause gastric carcinoma Patho: - primary defect is increased mucosal permeability to hydrogen ions - frequent H. pylori - gastric secretion normal or less than normal
539
PUD: Duodenal ulcer - where, occurs when, causes what, caused by, symptoms?
**most common type of PUD** - occurs in the duodenum - epigastric pain 2-3 hours after eating: -- increased gastrin levels stay high after eating and continue to stimulate secretion of acid -- impaired duodenal bicarb secretion -- failure of feedback where acid in antrum inhibits gastrin release -- rapid gastric emptying overwhelms buffering - can cause melena or hematochezia - heartburn, chest discomfort are less common but may be seen - pain may waken patient during the night Causes: H. pylori, smoking, NSAIDs, stress, genetic predisposition
540
Clinical manifestations of duodenal ulcer
- chronic intermittent pain in epigastric area - pain increases about 30 mins-2 hours after eating - night time pain between 11p-2a - spasm and acid - RELIEVED w/ food, antacids Treat h. pylori, help acids, relieve pain can cause melena or hematemesis can lead to hemorrhage, perforation, gastric outlet obstruction
541
Clinical manifestations of gastric ulcer
- pain tends to INCREASE with eating - belching - early satiety - anorexia - N/V - weight loss - tends to be chronic can cause melena or hematemesis can lead to hemorrhage, perforation, gastric outlet obstruction
542
Goals of treatment for both gastric and duodenal ulcers
- promote healing - relieve pain - decrease acid levels - prevent recurrence Treat with: - lifestyle changes (avoid caffeine, alcohol, tobacco, spicy high fat foods, ASA, NSAIDs) - antibiotics - PPIs - H2 inhibitors
543
What is borborygmus?
rushing of fluids and gurgling sounds as gas moves
544
What is constipation?
Infrequent, incomplete, or difficult passage of stool - most common GI complain - treatment directed toward relieving cause
545
Diagnosis for chronic constipation is based on what for 6 months or more? Rome IV Criteria (Need 2):
- fewer than 3 spontaneous BMs/week - passage of hard/lumpy stool with >25% of defecations - straining >25% of defecations - incomplete evacuation or obstruction >25% of time - manual maneuvers to remove stool >25% of time
546
Causes of constipation (primary and secondary)
Primary: idiopathic Secondary: r/t medical conditions, medications, structural abnormalities, lifestyle: - primary disorder of GI motility - disease processes (DM, MS, spinal cord injury, obstruction, etc) - certain medication s(like opioids) - post surgery - diet; poor fluid intake
547
Diet concerns with constipation
- high carb/low fiber diet want high fiber diet and fluids
548
Constipation: soluble fiber
attracts water and turns to gel during digestion; slows digestion - found in oat bran, barley, nuts, seeds, beans, lentils, peas, some fruits and veggies; also psyllium
549
Constipation: Insoluble fiber
Adds bulk to the stool and helps food pass faster through the intestines - found in wheat bran, lentils, whole grains, bran cereal, shredded wheat
550
Contraindications for laxatives?
- severe abdominal pain, nausea, cramps - appendicitis, enteritis, diverticulitis - ulcerative colitis - acute surgical abdomen - fecal impaction - habitual use (abuse)
551
Types of laxatives include...?
- chemical/stimulants - bulk forming/stimulants - osmotic stimulants - surfactant laxatives - lubricants - emollients - saline cathartics - GI opioid receptor antagonists
552
Constipation: chemical/stimulant laxatives work how
Stimulant improve defecation by increasing motility through **irritating the mucosa and increasing water in the stool** - **releases prostaglandins and cAMP** - increases smooth muscle contractions and electrolyte which stimulates peristalsis Also increase water in intestines Should only be used periodically Can be given oral (work in 6-12hr) or rectal (work in 15-20mins)
553
Constipation: chemical/stimulant laxatives - medications
- **bisacodyl (dulcolax)** - cascara - castor oil - **senna (sennokot)** Note: sennokot S is the stool softener
554
Constipation: chemical/stimulant laxatives side effects
- diarrhea - abdominal cramping - nausea - fluid and electrolyte imbalance
555
Constipation: Bulk stimulants laxatives - work how? | Best given when and with what? Drug of choice for who?
Increase GI motility by **increasing size of fecal matter** - used for short-term constipation - need to be taken with plenty of water - best given at night b/c slow-acting Drug of choice for elderly, during post-partum, and with poor diets - safe in pregnancy
556
Constipation: Bulk stimulants laxatives - medications
- methycellulose (citrucel) - polycarbophil (FiberCon) - **psyllium (metamucil)**
557
Constipation: Bulk stimulants laxatives - side effects
- diarrhea - abdominal cramping - nausea - fluid and electrolyte imbalances
558
Constipation: osmotic stimulant laxatives - work how?
Work by having solutes that increase osmotic "pull of fluid" INTO the GI tract - will increase the pressure in GI tract and stimulate more intestinal motility
559
Constipation: osmotic stimulant laxatives - caution with?
- those with renal impairment - abuse concerns
560
Constipation: osmotic stimulant laxatives - medications
- magnesium sulfate (epsom salts) - magnesium citrate - magnesium hydroxide (milk of mag) - lactulose - polyethylene glycol (miralax) - polyethylene glycol electrolyte solution (GoLytely)
561
Constipation: osmotic stimulant laxatives - side effects
- diarrhea - abdominal cramping - nausea - fluid and electrolyte imbalances
562
Constipation: lubricants - work how?
Used to make defecation easier WITHOUT stimulating the movement of the GI tract
563
Constipation: lubricants - medications
- mineral oil - glycerin - docusate (colace)
564
Constipation: surfactant laxatives (emollients) - work how?
Aka: stool softener - makes defecation easier WITHOUT stimulating movement of GI tract - given when straining to have a BM is harmful Do not rely on medication to provide relief or prevent constipation
565
Constipation: GI Opioid Receptor Antagonist: Methylnaltrexone (Relistor) | Used for? Acts where? Doesn't cross what?
- used for opioid-induced and/or refractory constipation - is a selective antagonists to opioid binding at the mu-receptor - do not cross BBB and acts specifically at **peripheral opioid receptor sties** like GI tract, but does **not affect the analgesic effects of opioids in CNS**
566
Constipation: GI Opioid Receptor Antagonist: Naldemedine (Symproic) | Approved for treatment of what?
Opioid antagonist approved for treatment of opioid-induced constipation in adults with chronic noncancer pain
567
What are consequences of constipation?
- abdominal or rectal discomfort - painful defecation - N/V - anorexia - impaction - ileus - hemorrhoids - ruptured bowel - anal fissure
568
Patient education with constipation
- dietary fiber: need 20-35 grams/day; higher amounts may cause bloating and gas pains - need to find balance -- go slow -- fiber 1 cereal or bars are good -- metamucil, citrucel -- fruit (apples, peaches, pears, raisins, grapes, cherries) - increase fluids especially with fiber - exercise - bathroom hygiene (footstool), leave enough time, schedule time periods - stool diary with Bristol chart
569
What is diarrhea?
loose or watery stools (>3/day)
570
Causes and other factors of diarrhea
Causes: - infection - drug-induced - emotional stress - colitis - DM - liver disease, etc Other factors: - water content - presence of unabsorbed food - bacteria content - intestinal secretions/mucus - children vs. adult
571
Clinical manifestations of diarrhea (systemic and local)
Systemic: - dehydration - electrolyte imbalances - metabolic acidosis or alkalosis - weight loss - signs of infection Local: - cramps - abdominal pain - steatorrhea - hematochezia
572
What is osmotic diarrhea?
- injury to gut, dietary factors, or problem with digestion - associated with large stool volumes Example: lactose intolerance
573
What is secretory diarrhea?
- intestines secrete more fluids and electrolytes that can be absorbed - associated w/ large stool volumes Ex: infection and inflammation
574
What is exudative diarrhea?
- alterations in mucosal integrity, epithelial loss, enzyme destruction - associated w/ more than 6 stools a day Ex: inflammatory diseases, cancer, cancer treatments
575
Treatments for diarrhea
- remove cause - fluid and electrolyte replacement - opioids (paregoric, deodorized tincture of opium (DTO)) - **diphenoxylate Hcl/atropine (Lomotil)** - **loperamide (imodium)** - yogurt - kaolin/pectin (kaopectate) - bismuth subsalicylate (pepto bismol) - bulk forming agents - probiotics
576
Diarrhea: Diphenoxylate HCl/atropine (Lomotil): how does it work? | route? how many times can it be given in a day?
- decreases peristalsis - promotes reabsorption of water from GI tract - increases transit time oral medication can be given up to 4x/day
577
Diarrhea: Diphenoxylate HCl/atropine (Lomotil): side effects | Do Dry RUNS
- nausea - dry mouth - urinary retention - dizziness - sedation - restlessness
578
Diarrhea: Diphenoxylate HCl/atropine (Lomotil): contraindications
- do not use in children under 4 y/o - hepatic impairment
579
Diarrhea: Diphenoxylate HCl/atropine (Lomotil): drug interactions | DAt BAT
- barbiturates - alcohol - tranquilizers
580
Diarrhea: Loperamide (Imodium): how does it work?
- slows intestinal motility and by affecting water and electrolyte movement through bowel - decreases peristalsis oral medication
581
Diarrhea: Loperamide (Imodium): side effects
- constipation - dizziness - nausea - abdominal cramping - urinary retention
582
Diarrhea: Loperamide (Imodium): contraindications
- children under 2 y/o - patients w/ bloody stools and high fever - pt w/ acute UC - basically intestinal infections: -- bacterial enterocolitis caused by invasive organisms -- pseudomembranous colitis
583
What are the consequences of diarrhea?
- dehydration - orthostasis - electrolyte imbalances (hyperkalemia, seizures) - malnutrition - CV or renal compromise - impaired immune function - perianal skin breakdown - reduced absorption of oral meds - pain - anxiety - exhaustion - decreased quality of life
584
What is irritable bowel syndrome (IBS)? | Characterized by? More common in? Avoid?
Characterized by a variable combination of chronic and recurrent intestinal symptoms - increased motility and abnormal intestinal contractions associated w/ stressful situations - women > men - no special diet Avoid fatty and/or gas producing foods, alcohol, caffeine
585
Symptoms of IBS
- **abdominal pain** - altered bowel function - flatulence - bloating - nausea - anorexia - constipation or diarrhea
586
Drugs for IBS
- alostron - eluxadoline - lubiprostone - lyoscyamine anti-spasmotics, anticholinergics
587
What is Crohn's Disease?
A recurrent, granulomatous type of inflammatory response affecting the GI tract - **cobblestone appearance** - most common site is terminal ileum or cecum - periods of exacerbations and remissions **slow but progressive; involving ALL layers of GI**
588
Symptoms of Crohn's disease? | DAW FML
- diarrhea - abdominal pain - weight loss - fluid and electrolyte imbalances - malaise - low-grade fever
589
Complications of Crohn's disease?
- fistula formation - abdominal abscess - intestinal obstruction
590
What is ulcerative colitis (UC)?
Non-specific inflammatory condition of the colon - often begins gradually and can become worse over time - cause is unknown Commonly occurs: - between ages 15030 - older than 60 - have family member w/ IBD - is Ashkenazi Jewish descent Treatment depends on severity Increases risk of colon cancer - can have megacolon or perforation **only impacts mucosal and submucosal layers**
591
Symptoms of ulcerative colitis (UC)?
- diarrhea w/ blood or pus - abdominal discomfort - urgent need to have BM - fatigue - nausea - loss of appetite -> malnutrition - weight loss - fever - anemia
592
Chron vs UC Image - this is not the right image my bad, will fix tomorrow (Sunday) on my laptop
593
Diverticular disease: Diverticulosis | Commonly where - associated w/ what type of pain?
A condition of having diverticula (outpouching) in the colon - commonly in the descending or sigmoid colon (LLQ pain) - affects about 40% of US pop. by age 60 can be asymptomatic until inflamed
594
Diverticular disease: diverticulitis
Is an inflammation of the diverticulum Causes: - pain - N/V - fever - elevated WBCs
595
Complications of diverticular disease
- perforation w/ peritonitis - abscesses - hemorrhage - fistula - bowel obstruction
596
Histamine 2 (H2) blockers: work how?
Block histamine 2 receptors on parietal cells leading to **decreased gastric acid secretions** - also decrease HCl production by about 70%
597
Histamine 2 (H2) blockers: indications
GERD and PUD
598
Histamine 2 (H2) blockers: medications
End in **"tidine"** - ranitidine (zantac) - famotidine (pepcid) - cimetidine (tagamet) can get OTC Cross the placenta and breast milk
599
Histamine 2 (H2) blockers: side effects 2D 2H
- diarrhea/constipation - drowsiness - headache - hypotension
600
Histamine 2 (H2) blockers: patient education
- smoking can decrease effectiveness; no smoking - should be taken 30 mins before meals - avoid overeating - **no NSAIDs**
601
Proton pump inhibitors (PPIs): work how
Suppresses gastric acid production - more effective than H2 blockers
602
Proton pump inhibitors (PPIs): indications (4)
- PUD - H. pylori - GERD - dyspepsia (indigestion)
603
Proton pump inhibitors (PPIs): side effects
- nausea - diarrhea - abdominal pain - fatigue - headache are well tolerated
604
Proton pump inhibitors (PPIs): increase risk of...
- fractures - dementia - infection - gastric cancer - cardiovascular events - kidney disease Also pernicious anemia bc can affect B12 absorption
605
Proton pump inhibitors (PPIs): labs to monitor
B12, calcium, magnesium, iron - can cause pernicious anemia - increase risk of osteoporosis esp if on long-term
606
Proton pump inhibitors (PPIs): drug interaction
Clopidogrel (which is a platelet inhibitor)
607
Proton pump inhibitors (PPIs): drugs in class
End in **"prazole"** - omeprazole (prilosec) - lansoprazole (prevacid) - rabeprazole (aciphex) - pantoprazole (protonix) - esomeprazole (nexium)
608
Antacids: work how?
Neutralize stomach acid by direct contact - may stimulate prostaglandins Should take 1-2hr after a meal because digestion occurs then and increases level of acid Have multiple drug interactions
609
Antacids: indications
- gastritis - GERD - PUD
610
Antacids: types
- sodium bicarbonate (baking soda) - calcium carbonate (tums) - aluminum hydroxide (can cause constipation) - magnesium hydroxide (can cause diarrhea)
611
Antacids: side effects
- depends on type - constipation/diarrhea - sodium loading
612
Antacids: Patient education
- **take all medications at least 1 hour before or after taking the antacid b/c multiple interactions** - chew tablets and drink at least 8oz of fluid after - shake liquid before pouring dose
613
Mucosal protectants: sucralfate: work how?
A polymer of sucrose with aluminum hydroxide - forms a protective coating on the mucosal lining, particularly in ulcerated areas - adheres to epithelial cells, ulcer craters, or eroded areas - can prevent mucositis Can cause constipation b/c of aluminum hydroxide
614
Mucosal protectants: medication
Sucralfate (carafate) Misoprostol (cytotec)
615
Mucosal protectants: sucralfate: administration
given QID on an empty stomach, one hour before meals and at bedtime - can dissolve in 20oz of water and drink Caution in patients with renal impairment
616
Mucosal protectants: sucralfate: drug interactions
- antacids - warfarin - phenytoin - fluoroquinolones
617
Mucosal Protectants: Misoprostol (cytotec): works how?
A prostaglandin analog - binds to prostaglandin receptors in parietal cells - decreases gastric acid secretion - increased GI blood flow - stimulates mucus production administer 2-4 times/day
618
Mucosal Protectants: Misoprostol (cytotec): indications
- PUD - not effective for GERD
619
Mucosal Protectants: Misoprostol (cytotec): side effects | would've HAD a baby w/out this if taken too early in preg
- diarrhea - abdominal pain - headache
620
Mucosal Protectants: Misoprostol (cytotec): contraindications
- pregnancy and lactation (used for abortion and inducing labor) - IBD
621
What is nausea?
- the conscious recognition of the imminent need to vomit - may or may not result in vomiting - mediated by the ANS
622
What is retching/dry heaves?
- rhythmic and spasmodic movement involving diaphragm and abdominal muscles - controlled by the respiratory center in the brainstem
623
Neuroreceptors influencing chemoreceptor trigger zone, vomiting center, vestibular centers and GI tract
- **dopamine-2** (CTZ) - **serotonin** (CTZ, GI tract) - neurokinin-1 (CTZ) - corticosteroid - acetylcholine - histamine - opioid - muscarinic - cannabinoid
624
Consequences of un/undertreated N/V
- decreased quality of life - non-compliance - dehydration - electrolyte imbalances - decreased self-care - decreased function - nutritional deficits - taste changes - decreased performance status - esophageal tears - weight loss - anorexia
625
Chemotherapy-induced nausea and vomiting (CINV): acute | risk factors too
- occurs within mins-hrs after chemo - depends on type, dose, route, schedule risk factors: - gender (women>men) - age - stage of disease - alcohol use - comorbidities
626
Chemotherapy-induced nausea and vomiting (CINV): anticipatory
think they will get sick so they do
627
Chemotherapy-induced nausea and vomiting (CINV): delayed
- occurs at least 24hr following chemo - acute n/v increase risk other risk factors: - high-dose chemo - certain agents - poorly controlled n/v
628
Chemotherapy-induced nausea and vomiting (CINV): breakthrough
- occurs despite standard treatment - requires further intervention
629
Chemotherapy-induced nausea and vomiting (CINV): refractory
- unrelieved n/v despite standard and breakthrough treatment
630
Types of anti-emetics
- anticholinergics (scopolamine, dicyclomine (bentyl)) - antihistamines - neurolytics (chlorpromazine, haldol) - prokinetics (metoclopramide, cisaprine) - serotonin (ondanestron) - adjunct medications: corticosteroids, benzodiazepines, cannabinoids Can be administered PO, SL, rectal, IV, IM, SQ, transdermal
631
Anti-emetics: anticholinergics - work how?
Block acetylcholine at the muscarinic receptors - also used to treat motion sickness - must be removed before an MRI b/c contains aluminum **scopolamine (transderm scop)**
632
Anti-emetics: anticholinergics - side effects (5) | Cant see can't pee cant spit
- dry mouth - urinary retention - blurred vision - exacerbation of narrow-angle glaucoma - skin irritation
633
Anti-emetics: 5-HT3 (serotonin) antagonist - works how?
Need to be given before N/V experienced Serotonin receptors are present both peripherally and centrally - given for chemo, radiation, therapy, or post-op N/V - metabolized in the liver and excreted in the urine
634
Anti-emetics: 5-HT3 (serotonin) antagonist - drugs in class
Drugs end in **"setron"** - **ondansetron (zofran)** - granisetron (kytril) - dolasetron (anzemet) - palonosetron (aloxi)
635
Anti-emetics: 5-HT3 (serotonin) antagonist - side effects
- **headache** (usually r/t spread of infusion IV) - diarrhea - fever - hypotension - QT prolongation
636
Anti-emetics: 5-HT3 (serotonin) antagonist - Ondansetron (Zofran): works how
Blocks serotonin in the CTZ - routes: PO, SL, IV, IM - dose: 4mg or 8mg Pregnancy category B
637
Anti-emetics: 5-HT3 (serotonin) antagonist - Ondansetron (Zofran): Contraindications
- patients taking anticonvulsants b/c can decrease seizure threshold Use lowest dose in hepatic and renal impairment
638
Anti-emetics: 5-HT3 (serotonin) antagonist - Ondansetron (Zofran): side effects
- headache - constipation - diarrhea - fatigue Serotonin syndrome from too much in body; can be mild or life-threatening
639
Anti-emetics: Dopamine 2 Antagonist - three subtypes?
- piperaze phenotiazine/antipsychotics (prochlorperazine) - metoclopramide (reglan) - butyrophenon derivate/antipsychotics (droperidol and haloperidol)
640
Anti-emetics: Dopamine 2 Antagonist - indications
- motion sickness - chemo-induced N/V - post-op N/V Considered second-line therapy Have antihistamine and anticholinergic properties
641
Anti-emetics: Dopamine 2 Antagonist - work how
- block dopamine receptors in CTZ and acetylcholine - are not to be give in Parkinson's b/c can make it worse
642
Anti-emetics: Dopamine 2 Antagonist - other drugs in class
- promethazine (phenergan) - trimethobenazamide (tigan)
643
Anti-emetics: Dopamine 2 Receptor Antagonist: Metoclopramide (reglan): routes/admin
Also classified as a non-phenothiazine - routes: oral, IV, IM Pregnancy Category B
644
Anti-emetics: Dopamine 2 Receptor Antagonist: Metoclopramide (reglan): indications
- GERD - diabetic gastroparesis - N/V
645
Anti-emetics: Dopamine 2 Receptor Antagonist: Metoclopramide (reglan): any black box warnings?
May cause tardive dyskinesia
646
Anti-emetics: Dopamine 2 Receptor Antagonist: Metoclopramide (reglan): contraindications
- bowel obstruction - GI bleeding - pheochromocytoma - epileptics
647
Anti-emetics: Dopamine 2 Receptor Antagonist: Metoclopramide (reglan): side effects | NERDS
- restlessness - drowsiness - extrapyramidal symptoms (EPS) - neuroleptic malignant syndrome (NMS): hypernatremia, change in LOC, rigidity - suicidal ideations
648
Anti-emetics: Dopamine 2 Receptor Antagonist: Haloperidol (Haldol): routes/admin | Pregnancy category?
Butyrophenone derivative Routes: PO, IV, IM Pregnancy Category C - cleft palate
649
Anti-emetics: Dopamine 2 Receptor Antagonist: Haloperidol (Haldol): indications
- schizophrenia - control of tics and vocal utterances of Tourette's disorder - N/V
650
Anti-emetics: Dopamine 2 Receptor Antagonist: Haloperidol (Haldol): any black box warnings?
elderly patients with dementia-related psychosis
651
Anti-emetics: Dopamine 2 Receptor Antagonist: Haloperidol (Haldol): contraindications
- patients with severe toxic CNS depression or comatose states from any cause - hypersensitivity to drug - Parkinson's disease - dementia
652
Anti-emetics: Dopamine 2 Receptor Antagonist: Haloperidol (Haldol): side effects SET DDQ
- sedation - EPS - tardive dyskinesia - dystonia - dizziness - QT prolongation
653
Anti-emetics: phenothiazines - work how?
Are centrally acting Routes: oral, suppositories, IM, IV
654
Anti-emetics: phenothiazines - indications
Used for N/V related to: - anesthesia - severe vomiting - intractable hiccoughs
655
Anti-emetics: phenothiazines - contraindications (4)
- patients in comas or severe CNS suppression - severe hypo/hypertension - liver dysfunction - severe renal impairment
656
Anti-emetics: phenothiazines - drugs in class
- **prochlorperazone (compazine)** - chlorpromazine (thorazine) - perphenazine (trilafon) - thiethylperazine maleate (torecan (IM) or norazine (PO or PR))
657
Anti-emetics: phenothiazines - adverse effects include | DU PEACH
- decreased CNS stimulation - hypotension - cardiac arrhythmias - autonomic effects - urine may become pink to red-brown in color - endocrine effects - photosensitivity
658
Anti-emetics: phenothiazines: Prochlorperazine (compazine) - routes, indications
Piperaze Phenothiazine Routes: PO, IV, IM, PR Metabolized by the liver, excreted in urine Indications: - N/V - schizophrenia - non-psychotic anxiety - morning sickness
659
Anti-emetics: phenothiazines: Prochlorperazine (compazine) - side effects | prochlorperazine is also a dopamine 2 antagonist
- drowsiness - hypotension - EPS - **tardive dyskinesia** - NMS - dystonia - photophobia - blurred vision
660
Anti-emetics: phenothiazines: Prochlorperazine (compazine) - any black box warnings?
is a vesicant
661
Anti-emetics: phenothiazines: Prochlorperazine (compazine) - contraindications? | prochlorperazine is also a dopamine 2 antagonist
- patients taking antipsychotic drugs - children - older adults -> psychosis
662
Anti-emetics: H1 Receptor Antagonist - work how? indications?
AKA: antihistamines - also have anticholinergic properties - block muscarinic receptors Indications: - motion sickness - morning sickness - allergies
663
Anti-emetics: H1 Receptor Antagonist - drugs in class?
- **diphenhydramine (benadryl)** - meclizine - promethazine - doxylamine succinate
664
Anti-emetics: H1 Receptor Antagonist - side effects? (5) | can't see can't pee can't spit
- drowsiness - blurred vision - dry mouth - hypo/hypertension - urinary retention
665
Anti-emetics: Corticosteroids - work how? admin? | remember Shelby's story w these
Precise mechanism of action is not known - suppresses prostaglandin release from hypothalamus - may inhibit the process of N/V - anti-inflammatory Cochrane report: low-degree of evidence for N/V Administer slowly: if you go too fast, weird sensations in the lower region are felt
666
Anti-emetics: Corticosteroids - indication
used as an adjunct to treat CINV
667
Anti-emetics: Corticosteroids - drugs in class
- dexamethasone (decadron): is compatible with zofran - prednisone (deltasone)
668
Anti-emetics: Corticosteroids - side effects?
- insomnia - anxiety - acne - hyperactivity
669
Anti-emetics: Cannabinoids - use, types, efficacy?
Have been used for a variety of ailments Types: - CB-1 receptors: GI tract - CB-2 receptors: inflammatory & epithelial cells Equal in efficacy to ondansetron
670
Anti-emetics: Cannabinoids - drugs in class
- **drobabinol (marinol)** - nabilone (cesamet)
671
Anti-emetics: Cannabinoids - side effects? (6) | what ppl feel like when high
- sedation - vertigo - euphoria - dry mouth - tachycardia - paranoid reactions
672
Anti-emetics: Cannabinoids: Dronabinol (marinol) - Route, admin
- oral route - dosage: 2.5mg, 5mg, 10mg - pregnancy category C - **highly protein bound - increases interactions**
673
Anti-emetics: Cannabinoids: Dronabinol (marinol) - indications?
- anorexia - CINV that has failed standard treatment - appetite stimulant
674
Anti-emetics: Cannabinoids: Dronabinol (marinol) - caution with?
- elderly patients due to increased risk of neuro-psychoactive effects - patients with a history of alcohol and/or substance abuse - patient with underlying psychiatric disorders (mania, depression, schizophrenia)
675
Anti-emetics: Cannabinoids: Dronabinol (marinol) - side effects?
- mood changes - euphoria - depression - insomnia - psychosis (in extreme cases)
676
Anti-emetics: Olanzapine (zyprexa) - what is it? route?
Thienobenzodiazepine - also an antipsychotic Routes: PO, IM Pregnancy Category C
677
Anti-emetics: Olanzapine (zyprexa) - indications?
- depressive episodes r/t bipolar I - treatment resistant depression - acute agitation r/t schizophrenia and bipolar I mania - N/V
678
Anti-emetics: Olanzapine (zyprexa) - any black box warnings?
elderly patients with dementia-related psychosis
679
Anti-emetics: Olanzapine (zyprexa) - contraindications? People and what three meds
- elderly patients with dementia-related psychosis - fluoxetine in combination - in combination with lithium or valproate
680
Anti-emetics: Olanzapine (zyprexa) - labs to monitor?
CBC, glucose, lipid profile
681
Anti-emetics: Olanzapine (zyprexa) - side effects? (5)
- hypotension - weight gain - suicidal ideations - NMS - sedation
682
Anti-emetics: Anxiolytics/benzodiazepines - how do they work?
Affects GABA neurotransmitter - CNS depressant; interferes with afferent nerves
683
Anti-emetics: Anxiolytics/benzodiazepines - drugs in class
- alprazolam (xanax) -- dose/route: 0.5-2mg PO - lorazepam (ativan) -- dose/routes: 0.5-2mg PO, SL, IV
684
Anti-emetics: Anxiolytics/benzodiazepines - indications?
- typically used as an adjunct agent for acute or delayed N/V - anticipatory N/V
685
Anti-emetics: Anxiolytics/benzodiazepines - side effects?
- drowsiness - sedation - confusion - agitation - dependence and withdrawal symptoms - hallucinations
686
Anti-emetics: Neurokinin-1 Antagonist (NK-1) - how do they work
Inducer of the CYP450 system - also inhibits substance P Routes: PO and IV Given in combination with other anti-emetics
687
Anti-emetics: Neurokinin-1 Antagonist (NK-1) - indications?
to prevent and treat acute and delayed nausea associated with **highly emetogenic chemotherapy**
688
Anti-emetics: Neurokinin-1 Antagonist (NK-1) - drugs in class
**Ends in "pitant"** - **arepitant (emend)** - fosaprepitant dimeglumine (emend) - rolapitant (varubi)
689
Anti-emetics: Neurokinin-1 Antagonist (NK-1) - side effects
- diarrhea - constipation - gastritis - anorexia - headache - fatigue
690
Anti-emetics: Neurokinin-1 Antagonist (NK-1): Arepitant (Emend) - route, dosage, patho info
Route: IV Dosage: 150mg Can cross the BBB - metabolized in liver and excreted in the urine and feces
691
Anti-emetics: Neurokinin-1 Antagonist (NK-1): Arepitant (Emend) - drug interactions
- pimozide - warfarin - oral contraceptives - corticosteroids
692
Anti-emetics: Neurokinin-1 Antagonist (NK-1): Arepitant (Emend) - side effects
- liver enzyme elevation - dehydration - hiccups - Steven-Johnson syndrome
693
Anti-Emetic Miscellaneous Medications: other drugs, herbal and vitamin supplements, medications used to augment anti-emetics
Other drugs to control N/V: - scopolamine (anticholinergic) Herbal and vitamin supplements: - ginger - pyridoxine (vitamin B6) Medications used to augment anti-emetics: - diphenhydramine (benadryl) - lorazepam - megestrol acetate (megace)
694
Anti-emetic use across the lifespan: pediatrics
- should be used with caution - increased risk for adverse effects
695
Anti-emetic use across the lifespan: adults
- frequently used for surgery and chemo - pregnancy and lactation: -- has not been studied -- many drugs can enter breast milk
696
Anti-emetic use across the lifespan: older adults
- more likely to experience an adverse effect from drug(s) - issue of hepatic and/or renal impairment
697
Lab studies for anti-emetics
- weight - hydration status - serum electrolytes - creatinine - LFTs - intake and output
698
What are extrapyramidal symptoms (EPS)?
Manifested primarily as acute dystonic reactions Dystonic reactions may include: - sudden onset of muscular spasms esp in head, neck, or opisthotonos - laryngospasm, dysphagia, oculogyric crisis - involuntary spasms of the tongue and mouth: difficultly speaking and swallowing - akathisia, restlessness, akinesia, other Parkinsonian-like symptoms (tremor)
699
Treatment of extrapyramidal symptoms (EPS)?
- depends on severity of symptoms - reduce or discontinue drug - anticholinergic drugs can be used to treat acute dystonic reactions
700
When are emetics given?
- may be given in cases of overdosing or poisoning - used to induce vomiting - no longer recommended for home use
701
What is an example of an emetic?
ipecac
702
Emetics: Ipecac
- standard of practice prior to 2003 - standard of practice now -- dispose of any ipecac in home -- if needed: call poison control center
703
Anti-emetics: nursing considerations
- assess/identify factors contributing to symptoms of N/V - administer antiemetic as prescribed - if patient receiving anticholinergic, monitor for side effects Focused assessment: - skin - cardiac - intake and output - lab studies - s/s of dehydration Evaluation: - did symptoms improve - good urine output - able to tolerate food
704
Anti-emetics: General patient education
- drink plenty of fluids - small frequent meals - avoid strong smells
705
When planning administration of antiemetic medications to a client, the nurse is aware that combination therapy is preferred because of which drug effect?
Different vomiting pathways are blocked - combining antiemetic drugs from various categories allows the blocking of the vomiting center and CTZ through different pathways, enhancing antiemetic effect
706
A patient is receiving an anticholinergic drug to treat their N/V. The nurse should instruct the patient to expect which adverse effect?
Dry mouth - anticholinergic drugs block the PNS -> causes the body to "rest and digest" - blocking of these effects leads to constipation, urinary retention, and decreased secretions (dry mouth)
707
Which drug works by blocking serotonin receptors in the GI tract, vomiting center, and CTZ?
Ondansetron (Zofran) - is a serotonin blocker
708
What are counter-regulatory hormones r/t insulin?
Hormones that counteract the effects of insulin: glucagon, epinephrine, cortisol, and growth hormones ## Footnote They help increase blood glucose levels when they drop.
709
Insulin types/ peaks and trough and onset tables
710
What is the function of T4 and T3?
Needed for metabolism
711
What are the functions of thyroid hormones? | Important b/c relates to hypo and hyperthyroidism when effected
* 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
712
What happens to TSH levels when thyroid hormone levels are high?
Inhibition of TSH
713
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.
714
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
715
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.
716
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
717
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
718
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
719
Cardiac output
Stroke Volume X HR Normally, 4-8L /min
720
What are the types of cells found in the stomach?
- gastric goblet cells (mucus secretion) - parietal cells: HCl and intrinsic factor - chief cells -- pepsinogen: converts to pepsin; protein breakdown - G cells: gastrin
721
Why are prostaglandins important in gastric acid secretion?
There are high concentrations in the gastric mucosa and secretions - inhibit acid secretion - stimulate mucus and bicarbonate secretion
722
Function of chief cells in the stomach?
secrete pepsinogen which converts to pepsin, the enzyme for protein digestion
723
What is the function of gastric mucosal cells?
Prostaglandin E2 (PGE2) - protective - stimulates gastric mucus production and pancreatic bicarb secretion
724
GI disorders by location - image
725
Pathways of N/V (image)
726
Mechanics of Emesis (image)