Vasopressin

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Tarang Patel
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Outline

Overview

  1. Indications
    1. Diabetes Insipidus
    2. Lack of ADH
      1. Resection of posterior pituitary gland
    3. Low blood pressure
  2. Patho background
    1. Anti-diuretic hormone (ADH) = Vasopressin
    2. Vasopressin is secreted from the posterior pituitary gland.
    3. Factors that cause the release of vasopressin in the body
      1. Hypovolemia
      2. Blood loss
      3. Low blood pressure
      4. Low kidney perfusion
  3. Mechanism of action
    1. Causes kidneys to reabsorp water which will increase blood volume and blood pressure
    2. Causes vasoconstriction which increases blood pressure

Nursing Care

Overview

  1. Vasopressin – given IV drip
  2. Desmopressin- tablet form

Assessment

  1. Assess for side effects
    1. Headache
    2. Nausea
    3. Bronchoconstriction
    4. Abdominal cramps
    5. Water intoxication
    6. Hyponatremia
      1. CNS changes
      2. Decreased LOC
      3. Dizziness
      4. Confusion
    7. Hypokalemia
      1. Cardiac arrhythmias

Therapeutic Management

  1. Monitor blood pressure closely
  2. Monitor electrolytes closely
  3. Monitor for water intoxication

Nursing Concepts

  1. Fluid and Electrolyte Balance
    1. Patients taking Vasopression should have their fluid status and electrolytes monitored closely.
  2. Perfusion
    1. Vasopressin my be prescribed to treat hypotension.
  3. Pharmacology

Patient Education

  1. Educate patient on the signs of hyponatreamia and instruct them to contact their provider if they experience any neurological changes.

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Transcript

Vasopressin. So, we gonna learn today the factor that increases the production of vasopressin in our body, what is the mechanism of action of vasopressin, what are the indication and the side effects. So, first of all, the mechanism of action. In that one, we’ll look like what are the factors that actually releases the vasopressin. And before that, what is vasopressin? So, if you have heard the name of anti-diuretic hormone, Anti-Diuretic Hormone, ADH, that is vasopressin. Now, what factors that increases the release of ADH in the body is Hypovolemia. So, if you have a fluid loss, blood loss, basically low volume of fluid in your body, that’s gonna increase the release of vasopressin or ADH. If you have a decrease in blood pressure, that would definitely increases the release of vasopressin. Low perfusion to kidneys, basically the RAA system. So, if you have watched the video of RAA system, you’d know that the decrease in kidney perfusion will initiate the RAA system and that would increase the secretion of ADH. And also, the increase in blood osmolarity. Now, that’s basically concentrated blood. And what concentrated blood means, there is a loss of water that would trigger this secretion of vasopressin.

Where is vasopressin gets secreted from? So, in our brain, there’s a called Hypothalamus, and in that one, we have a pituitary gland. And there are two parts of pituitary gland, I mean, 2 section. There is a anterior pituitary gland and posterior pituitary gland. And from the posterior pituitary gland, the vasopressin gets secreted depending on all the signals that body sensed to the hypothalamus which is in the brain. Okay, like the signals, like a hypovolemia, decrease in arterial pressure, low perfusion to kidneys and increase in blood osmolarity.

So, what is the mechanism of action of vasopressin? There are two main mechanism of action of the vasopressin. Let’s look at the first one that works on vasopressin, the mechanism of action of vasopressin on kidneys. So, the main functional unit of kidney is nephron. And I’m not really great at drawing but this is bonus capsule, and then you have a, this is proximal convoluted tubules, that’s loop of Henle, and you have a distal convoluted tubules and you have here the collecting ducts. Now this is kinda divided into part. This part is cortex, this part is medulla. Like a renal cortex and a renal medulla. So, let’s say this is proximal convoluted tubule, this whole part is loop of Henle, this is distal convoluted tubules, now, we are interested in this portion which is collecting ducts. Now, whenever there is a decrease in perfusion of kidney, decrease in arterial pressure or there’s a low volume in the blood, I’m sorry, low volume in body vessels, what it does, it sends signal to the hypothalamus and say, “Hey, we have a problem here.” Like a decrease in blood pressure, or there’s something wrong. We need more fluid in our body. Then, hypothalamus send signals to the pituitary glands especially to the posterior pituitary gland and tells it to release the ADH. Now, when it gets secreted in our body, it comes to the collecting ducts, and what it does, it increases reabsorption of water in collecting ducts. So, here, you have a urine going through and it’s gonna go through the bladder and gonna get excreted. What happens, ADH comes here and works on these collecting ducts and makes it more permeable to water. So, this is mostly all the thing right here in medulla, it’s all salty, like there’s a high concentration of sodium. So, this whole part is salty right here. Now, when the ADH makes this whole thing permeable to water, which usually it is not. If there is no ADH here, then it’s not really permeable to the water. So water can’t pass through this collecting ducts outside. So, it just gets excreted through the urine. But when ADH makes it permeable, the water moves from here, from urine to out in here. Because this part is salty, so, the water’s gonna move from low concentration to the high concentration. And, that’s how the water gets reabsorbed, and this, and goes back to get reabsorbed because you have like a whole network of arteries and veins and everything right here. This water gets reabsorbed back to the blood and increases the fluid volume. And that will increases the blood pressure, will take care of the, well, also, increases the fluid volume and will increase… So, if you go back to the slide, they will take care of the hypovolemia. By increasing the fluid volume, it’s gonna take care of the hypovolemia, it’s gonna increase the arterial pressure, it’s gonna increase perfusion to the kidneys because it’s gonna increase the blood pressure and fluid volume’s gonna get, kidneys gonna get more perfused. And so the, and also, it’s gonna decrease in blood osmolarity. That means, blood was concentrated, now, more water is getting absorbed, it’s gonna dilute the blood and it’s gonna make it less concentrated. So, that’s how it works in the kidneys. And those are the effects that vasopressin has on our body through the kidney.

Now, there’s another effect it has on arterial blood vessel. So, there are vasopressin receptors on blood vessels, especially the arteries. So, when vasopressin gets secreted from our hypothalamus, especially the posterior pituitary gland, it goes and binds to this vasopressin receptor on our blood vessels, arteries. And it causes the vasoconstriction. Vasoconstriction. And that’s gonna increase blood pressure as well. Now, here’s the main point, in our body, we have anti diuretic hormone present all the time. However, the physiological concentration of ADH or vasopressin, it’s so low that it does not causes the vasoconstriction. So, normally, we all have vasopressin or anti-diuretic hormone present in our body but the level is not that high that it will cause vasoconstriction. But let’s say if someone having a low blood pressure then you would put them on vasopressin drips. That concentration is really high than you found normally in the body. That will cause the vasoconstriction. So, to cause the vasoconstriction, it requires higher concentration than normal physiological concentration of vasopressin. So, that’s the one of the mechanism of action, it increases the blood pressure as well. And also works in kidney as we talked in the previous slide. And usually, you see these vasopressin drugs in critical care. If someone having hypotension and they will put them on vasopressin IV drips. So, that’s the main use.

Let’s say, what are the indication? So, if you have heard about the Diabetes Insipidus, in Diabetes Insipidus, what happens is basically there’s a decrease in ADH in our body. Okay. Now, when there’s a decrease in ADH in our body, kidney will excrete more water. ‘Cause if you saw in the previous slide, this works in collecting ducts by increasing the reabsorption of water. While if it is, there are two types of Diabetes Insipidus. We’ll talk in a bit about that too. So, when there’s a problem in ADH, let’s say, then kidney won’t be able to reabsorb more water and it will excrete through the urine. And basically, that causes the DIabetes Insipidus. Now, there are two types of Diabetes Insipidus. One is neurogenic, and another one is nephrogenic. Now, as we all know now that the ADH gets secreted from the posterior pituitary gland. So, if someone has a problem in posterior pituitary gland, let’s say, if they have a resection of posterior pituitary gland, then ADH doesn’t get secreted from the brain. That’s why it’s called the neurogenic. And if your body doesn’t have enough ADH, kidneys are not gonna be able to reabsorb more water from the collecting ducts. And that’s how our body gonna lose more and more water. That’s basically Diabetes Insipidus. And also, since I work in the neurocritical care and we see those patients a lot, that they have a neurogenic Diabetes Insipidus, since they have like a tumor of the pituitary gland and they get that resection of pituitary gland. Their body won’t produce anymore ADH because there is no pituitary gland left. Now, another one is called nephrogenic. Now, their nervous system is in tacked, their posterior pituitary gland is in tacked, it’s secreting enough anti-diuretic hormone, ADH, means, vasopressin as well. However, their kidneys are not responding well to the ADH. So, even though they have enough ADH in their body, the kidney won’t be reacting to the ADH because of a certain reason, could be like a damage / trauma to kidneys, change in structure, changes in kidneys as well. So, because of that as well, kidneys gonna lose more and more water. And won’t be able to reabsorb that water from the collecting ducts. So, now, since we talked about the Diabetes Insipidus, we can say what are the symptoms of Diabetes Insipidus. Like, they are losing more water through the urine. So, they will have a frequent urination, their urine will be dilute, because they’re gonna, you’re losing more water in urine, so there’s like pretty much water. And I have seen patient with the Diabetes Insipidus that their urine is pretty much like clear water. Concentrated Blood. So, what will happen, if this one happens, concentrated blood, they are all the electrolyte like sodium, potassium, calcium, their values will go up. And that can cause, like if sodium is going up, it can cause the neurological change, confusion, level of consciousness change. Potassium can cause cardiac arrhythmia. And, calcium and magnesium will go up as well and they’ll cause like a problem in muscle contraction and so forth. So, that was a little bit overview about the Diabetes Insipidus. So, since you understood what happens in Diabetes Insipidus, basically, either their brain is not producing enough ADH or their kidneys are not reacting to ADH. So, we have to give this vasopressin from outside in order to prevent body losing more water.

Now, we also give this one for low blood pressure and you will often see this vasopressin given for low blood pressure in critical care and as a drip, not as a pill or other tablet. And this is a, kinda like a temporary fix for the blood pressure until we find the real cause. So, we use this for Diabetes Insipidus and low blood pressure mainly.

Alright. So, what are the side effects of vasopressin? So, the main side effects are headache, nausea, nausea is pretty much for all the medication. But, the headache, bronchoconstriction, abdominal cramps, now water intoxication and hyponatremia. Those are the main ones to understand. So, let’s talk about that a little bit. Now, if you’re giving vasopressin, it’s gonna work on kidneys, and now, kidney gonna retain more water. Now, what happens if kidney retains more water? You can have water intoxication or like hypervolemia. Now, since this one is reabsorbing only water, remember this, this is the main difference, only reabsorbs the water. Now, it’s only reabsorbing water while it’s not reabsorbing extra sodium, potassium, so it’s gonna pretty much stay the same in body while the body is, while the kidneys are reabsorbing more water. So, the blood is gonna get dilute. Diluted Blood. And, from that, it’s gonna cause decrease in sodium, decrease in potassium, decrease in calcium. All electrolytes is gonna decrease, in all the electrolytes. And one of the main one can do is sodium. I mean, all the electrolytes while this gonna go down, so, let’s say for instance, if we talk about the sodium, it can cause a hyponatremia. Now, what are the symptoms of hyponatremia? Mostly, the nervous system changes, like the level of consciousness changes, dizziness, confusion, so forth. If they have a hypokalemia, it can cause the hypokalemia. They’ll have the cardiac changes, cardiac arrhythmias. So, those are the main symptoms that usually asked in NCLEX, like, so patient is on vasopressin, and if they’re having a change in level of consciousness, now, patient is not awake, they cannot, they don’t respond to the stimuli, what would you do? And then, the main reason those symptoms are caused by vasopressin. Or they may ask you, like, these are the symptoms, what do you think the patient is on what medication? And they’ll give you the list of medication. Mostly because of the vasopressin.

And what are the examples of this vasopressin? First of all, you will see the vasopressin used as a IV drips in critical care. So, that’s IV drips. Now, here is a desmopressin. That is a tablet form. And whenever, as I talked to you in the previous slide, that I’ve seen many patient with the Diabetes Insipidus. Now, because if they have a pituitary gland tumor, they get their pituitary removed. Now, that’s a permanent problem. Their pituitary is not there anymore. What will happen? Especailly the posterior pituitary. They don’t have any pituitary gland in their body to make the ADH. So, usually, they put them on the desmopressin. Sometime, body gets a chance to not having a pituitary gland but what if it doesn’t, then they have to put them on desmopressin when they go home and that comes in a tablet form. And when they are on desmopressin, they have to do frequent labs as well, frequent labs when they are on the desmopressin to make sure they’re not getting more intoxication and all the electrolytes are staying within the range.

So, that was it about the vasopressin, if you have any question, you can contact us or e-mail us. Thanks for watching.

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Concepts Covered:

  • Upper GI Disorders
  • Anxiety Disorders
  • Depressive Disorders
  • Medication Administration
  • Disorders of the Posterior Pituitary Gland
  • Respiratory Disorders
  • Female Reproductive Disorders
  • Neurologic and Cognitive Disorders
  • Shock
  • Cardiac Disorders
  • Cardiovascular Disorders
  • Urinary Disorders
  • Pregnancy Risks
  • Disorders of Pancreas
  • Liver & Gallbladder Disorders
  • Hematologic Disorders
  • Nervous System
  • Substance Abuse Disorders
  • Personality Disorders
  • Dosage Calculations
  • Urinary System
  • Learning Pharmacology
  • Immunological Disorders
  • Test Taking Strategies
  • Prefixes
  • Suffixes
  • Bipolar Disorders
  • Concepts of Population Health
  • Factors Influencing Community Health
  • Community Health Overview
  • Trauma-Stress Disorders
  • Cognitive Disorders
  • Psychotic Disorders
  • Somatoform Disorders
  • EENT Disorders
  • Musculoskeletal Trauma
  • Integumentary Important Points
  • Musculoskeletal Disorders
  • Integumentary Disorders
  • Disorders of the Thyroid & Parathyroid Glands
  • Disorders of the Adrenal Gland
  • Oncology Disorders
  • Labor Complications
  • Lower GI Disorders
  • Central Nervous System Disorders – Brain
  • Emergency Care of the Neurological Patient
  • Neurological Emergencies
  • Central Nervous System Disorders – Spinal Cord
  • Noninfectious Respiratory Disorder
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  • Infectious Respiratory Disorder
  • Vascular Disorders
  • Emergency Care of the Cardiac Patient
  • Circulatory System
  • Postoperative Nursing
  • Intraoperative Nursing
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  • Eating Disorders
  • Renal Disorders
  • Infectious Disease Disorders
  • Musculoskeletal Disorders
  • Renal and Urinary Disorders
  • EENT Disorders
  • Gastrointestinal Disorders
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  • Digestive System
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  • Concepts of Mental Health
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  • Prioritization
  • Basics of NCLEX
  • Communication
  • Emotions and Motivation
  • Delegation
  • Legal and Ethical Issues
  • Basic
  • Note Taking
  • Studying

Study Plan Lessons

Proton Pump Inhibitors
SSRIs
TCAs
Vasopressin
Anti-Infective – Penicillins and Cephalosporins
Metronidazole (Flagyl) Nursing Considerations
Ciprofloxacin (Cipro) Nursing Considerations
Vancomycin (Vancocin) Nursing Considerations
Nitro Compounds
NSAIDs
Parasympatholytics (Anticholinergics) Nursing Considerations
Hydralazine (Apresoline) Nursing Considerations
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Diuretics (Loop, Potassium Sparing, Thiazide, Furosemide/Lasix)
Epoetin Alfa
Parasympathomimetics (Cholinergics) Nursing Considerations
Benzodiazepines
Calcium Channel Blockers
Cardiac Glycosides
Autonomic Nervous System (ANS)
Sympathomimetics (Alpha (Clonodine) & Beta (Albuterol) Agonists)
Sympathomimetics (Alpha (Clonodine) & Beta (Albuterol) Agonists)
ACE (angiotensin-converting enzyme) Inhibitors
Angiotensin Receptor Blockers
Atypical Antipsychotics
Atypical Antipsychotics
Injectable Medications
Injectable Medications
IV Infusions (Solutions)
Complex Calculations (Dosage Calculations/Med Math)
Renin Angiotensin Aldosterone System
Basics of Calculations
Dimensional Analysis Nursing (Dosage Calculations/Med Math)
Oral Medications
The SOCK Method – S
The SOCK Method – O
The SOCK Method – C
The SOCK Method – K
Essential NCLEX Meds by Class
6 Rights of Medication Administration
The SOCK Method – Overview
12 Points to Answering Pharmacology Questions
12 Points to Answering Pharmacology Questions
54 Common Medication Prefixes and Suffixes
Therapeutic Drug Levels (Digoxin, Lithium, Theophylline, Phenytoin)
Communicable Diseases
Disasters & Bioterrorism
Disasters & Bioterrorism
Cultural Care
Environmental Health
Technology & Informatics
Epidemiology
Health Promotion & Disease Prevention
Alcohol Withdrawal (Addiction)
Grief and Loss
Paranoid Disorders
Personality Disorders
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Depression
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Somatoform
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Integumentary (Skin) Important Points
Nursing Care and Pathophysiology of Osteoarthritis (OA)
Nursing Care and Pathophysiology of Osteoporosis
Burn Injuries
Pressure Ulcers/Pressure injuries (Braden scale)
Nursing Care and Pathophysiology for Herpes Zoster – Shingles
Diabetes Management
Nursing Care and Pathophysiology of Diabetic Ketoacidosis (DKA)
Hyperglycaemic Hyperosmolar Non-ketotic syndrome (HHNS)
Nursing Care and Pathophysiology for Hyperthyroidism
Nursing Care and Pathophysiology for Hypothyroidism
Nursing Care and Pathophysiology of Diabetes Mellitus (DM)
Nursing Care and Pathophysiology for Cushings Syndrome
Nursing Care and Pathophysiology for Diabetes Insipidus (DI)
Nursing Care and Pathophysiology for SIADH (Syndrome of Inappropriate antidiuretic Hormone Secretion)
Oncology Important Points
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Levels of Consciousness (LOC)
Nursing Care and Pathophysiology for Hemorrhagic Stroke (CVA)
Chest Tube Management
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Nursing Care and Pathophysiology of Coronary Artery Disease (CAD)
Nursing Care and Pathophysiology for Heart Failure (CHF)
Premature Ventricular Contraction (PVC)
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Hemodynamics
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Normal Sinus Rhythm
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Echocardiogram (Cardiac Echo)
X-Ray (Xray)
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Glucose Lab Values
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Blood Urea Nitrogen (BUN) Lab Values
Creatinine (Cr) Lab Values
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Coagulation Studies (PT, PTT, INR)
Albumin Lab Values
Cholesterol (Chol) Lab Values
Cholesterol (Chol) Lab Values
Ammonia (NH3) Lab Values
Hematocrit (Hct) Lab Values
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Platelets (PLT) Lab Values
Red Blood Cell (RBC) Lab Values
Hemoglobin (Hbg) Lab Values
Chloride-Cl (Hyperchloremia, Hypochloremia)
Hypotonic Solutions (IV solutions)
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Potassium-K (Hyperkalemia, Hypokalemia)
Sodium-Na (Hypernatremia, Hyponatremia)
Metabolic Alkalosis
Base Excess & Deficit
Isotonic Solutions (IV solutions)
ABG (Arterial Blood Gas) Interpretation-The Basics
Respiratory Acidosis (interpretation and nursing interventions)
Respiratory Alkalosis
Metabolic Acidosis (interpretation and nursing diagnosis)
ABGs Nursing Normal Lab Values
Varicella – Chickenpox
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Scoliosis
Rubeola – Measles
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Autism Spectrum Disorders
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Enuresis
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Defects of Increased Pulmonary Blood Flow
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Obstructive Heart (Cardiac) Defects
Mixed (Cardiac) Heart Defects
Asthma
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Congenital Heart Defects (CHD)
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Dehydration
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Growth & Development – School Age- Adolescent
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Fundal Height Assessment for Nurses
Gravidity and Parity (G&Ps, GTPAL)
Gestation & Nägele’s Rule: Estimating Due Dates
Family Planning & Contraception
Antepartum Testing
Discomforts of Pregnancy
Physiological Changes
Maternal Risk Factors
Gestational Diabetes (GDM)
Chorioamnionitis
Nutrition in Pregnancy
Gestational HTN (Hypertension)
Hydatidiform Mole (Molar pregnancy)
Ectopic Pregnancy
Disseminated Intravascular Coagulation (DIC)
Fetal Development
Infections in Pregnancy
Mechanisms of Labor
Process of Labor
Fetal Circulation
Fetal Environment
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Fetal Heart Monitoring (FHM)
Leopold Maneuvers
Precipitous Labor
Preterm Labor
Abruptio Placentae (Placental abruption)
Breastfeeding
Postpartum Discomforts
Postpartum Physiological Maternal Changes
Dystocia
Initial Care of the Newborn (APGAR)
Mastitis
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Newborn Reflexes
Body System Assessments
Newborn Physical Exam
Transient Tachypnea of Newborn
Meconium Aspiration
Babies by Term
Newborn of HIV+ Mother
Hyperbilirubinemia (Jaundice)
Head to Toe Nursing Assessment (Physical Exam)
Blood Glucose Monitoring
Specialty Diets (Nutrition)
Enteral & Parenteral Nutrition (Diet, TPN)
Bowel Elimination
Pain and Nonpharmacological Comfort Measures
Hygiene
Intake and Output (I&O)
Patient Positioning
Complications of Immobility
Urinary Elimination
Defense Mechanisms
Abuse
Overview of Developmental Theories
Overview of Developmental Theories
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Overview of the Nursing Process
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Isolation Precaution Types (PPE)
Maslow’s Hierarchy of Needs in Nursing
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