Exam #2 Watkins PDF

Exam #2 Watkins 1.Metabolic Acidosis - signs and symptoms Perry Book: Metabolic acidosis occurs from an increase of metabolic acid or a decrease of base (bicarbonate). The kidneys are unable to excrete enough metabolic acids, which accumulate in the blood, or bicarbonate is removed from the body d...

Exam #2 Watkins 1.Metabolic Acidosis - signs and symptoms Perry Book: Metabolic acidosis occurs from an increase of metabolic acid or a decrease of base (bicarbonate). The kidneys are unable to excrete enough metabolic acids, which accumulate in the blood, or bicarbonate is removed from the body directly as with diarrhea. In either case the blood HCO3− decreases, and the pH falls. With an increase of metabolic acids, blood HCO3− decreases because it buffers metabolic acids. Similarly, when patients have conditions that cause the removal of HCO3−, the amount of HCO3− in the blood decreases. SHerpath: Metabolic acidosis is characterized by a pH level less than 7.35 and a bicarbonate (HCO3–) level less than 22 mEq/L. Metabolic acidosis: is caused by increased acid produced as a by-product of a metabolic process or a loss of bicarbonate (HCO3–) ions. The lungs compensate for metabolic acidosis by increasing the rate and depth of ventilation, known as Kussmaul respiration. This respiratory pattern removes excess carbon dioxide, thereby lowering the carbonic acid in the system. Underlying Cause of Metabolic Acidosis: -Starvation ketoacidosis *Inadequate caloric intake *Prolonged fasting -What Happens: In the absence of glucose, fat stores are used for energy and keto-acids accumulate in the blood. -Diabetic ketoacidosis *Type I diabetes mellitus -What Happens: Glucose is not transported into cells because of the lack of insulin. Fat is used for energy, and keto-acids accumulate in the blood. -Lactic acidosis *Sepsis *Cardiac arrest *Trauma *Seizures -What Happens: Lack of oxygen results in anaerobic metabolism in cells and lactic acid accumulation. -Renal tubular acidosis *Renal failure -What Happens: The kidneys are unable to remove acids through urine acidification. -Hyperchloremic acidosis *Diarrhea *Laxative abuse -What Happens: Gastrointestinal loss of bicarbonate (HCO3–) occurs. Signs and Symptoms of metabolic acidosis: -decreases a person’s level of consciousness -Decreased LOC (lethargy, confusion, coma) -Increased RR & INcreased respiratory depth (compensatory hyperventilation) -Abdominal pain -Dyrythmias Laboratory findings: Arterial blood gas alterations: pH below 7.35, PaCO2 normal if uncompensated or below 35 mm Hg (4.7 kPa) if compensated, HCO3− level below 21 mEq/L Imbalance andd Related Causes- Increase of Metabolic Acids (High Anion Gap): -Ketoacidosis (diabetes, starvation, alcoholism) -Hypermetabolic state (severe hyperthyroidism, burns, severe infection) -Oliguric renal disease (acute kidney injury, end-stage renal disease) -Circulatory shock (lactic acidosis) -Ingestion of acid or acid precursors (e.g., methanol, ethylene glycol, boric acid) Loss of Bicarbonate (Normal Anion Gap): -Diarrhea -Pancreatic fistula or intestinal decompression -Renal tubular acidosis The anion gap is a calculation used to help identify the cause of metabolic acidosis. It represents the difference between the positively charged ions (cations) and negatively charged ions (anions) in the blood. The formula is: Anion gap = (Na⁺) - (Cl⁻ + HCO₃⁻) Where: Na⁺ = sodium (positively charged ion) Cl⁻ = chloride (negatively charged ion) HCO₃⁻ = bicarbonate (negatively charged ion) In simple terms, the anion gap helps doctors assess whether there are extra acids in the blood that aren't accounted for by the usual measurements of sodium, chloride, and bicarbonate. Anion Gap- Normal range 4-12 mEq/L Metabolic acidosis- >12mEq/L Treatment: bicarbonate infusions, ACE inhibitors are used to lower K+ levels, Insulin IV for DKA, starvation, restoration of tissue O2 in lactic acidosis, drugs to counteract methanol poisoning or salicylate poisoning 2.Be able to identify metabolic acidosis, respiratory acidosis, metabolic acidosis alkalosis and respiratory alkalosis. What are the causes and signs and symptoms of each. Which kind of conditions is each associated with? Conditions that can lead to metabolic acidosis, respiratory acidosis, metabolic acidosis alkalosis and respiratory alkalosis. - need to redo these on my flash cards Normal cellular functioning requires the pH of body fluids to be between 7.35 and 7.45. Death can occur if the pH falls below 6.9 or rises higher than 7.8. Two compensatory mechanisms, the respiratory (carbon dioxide) and renal (metabolic) systems, maintain homeostasis. To maintain homeostasis, the kidneys compensate for respiratory acid-base imbalances, and the respiratory system compensates for metabolic acid-base imbalances. These compensatory mechanisms do not correct the problem but assist the body to adapt. People develop acid-base imbalances when their normal homeostatic mechanisms are dysfunctional or overwhelmed. Four types of acid-base imbalances can occur: -Respiratory acidosis -Respiratory alkalosis -Metabolic acidosis -Metabolic alkalosis ROME stands for: Respiratory -Opposite Metabolic- Equal *Tip: When applying the method for ABG interpretation, remember to keep the R and O together and the M and E. What does Respiratory Opposite mean? The CO2 (remember carbon dioxide represents the respiratory system) and pH will be OPPOSITE of each other…one will be elevated while the other will be decreased…this means it’s a respiratory disorder. CO2 ⬆, pH ⬇: Respiratory acidosis CO2 ⬇, pH ⬆: Respiratory alkalosis What does Metabolic Equal mean? The HCO3 (remember bicarb represents the metabolic system) and pH will be EQUAL…either both will be elevated or decreased….this means it’s a metabolic disorder. HCO3 ⬇, pH ⬇: Metabolic acidosis HCO3 ⬆, pH ⬆: Metabolic alkalosis Lab Normal Range in Adult ABG: (on flashcards already) pH 7.35-7.45 PaCO2-35-45 mmHg (4.7-6 kPa) HCO3- 21-28 mEq/L (21-28 mmol/L) PaO2- 80-100 mmHg (10.7-13.3 kPa) SaO2 95% - 100% Base Excess -2 to +2 mEq/L (mmol/L) Simply: Acid-base imbalances occur when the body’s pH goes out of its normal range (7.35–7.45). There are four main types: Respiratory Acidosis: Happens when the lungs can’t remove enough oxygen (CO₂), causing acid buildup and lowering pH. This may occur with breathing problems like COPD or asthma. Respiratory Alkalosis: Happens when the lungs remove too much CO₂, raising pH and making the blood too basic. This can occur with hyperventilation (breathing too fast). Metabolic Acidosis: Caused by excess acid or loss of bicarbonate in the body, often due to kidney issues, severe diarrhea, or diabetes. This lowers pH, making the blood more acidic. Metabolic Alkalosis: Caused by too much bicarbonate or a loss of acid, often due to vomiting or overuse of antacids, raising pH and making the blood too basic. Another simple version: (on flashcards already) -Respiratory Acidosis: occurs when the lungs cannot remove enough CO2, leading to an increase in hydrogen ions and a decrease in pH -Respiratory Alkalosis: occurs when the lungs remove too much CO2, leading to a decrease in hydrogen ions and an increase in pH -Metabolic Acidosis: occurs when the body produces too much acid or cannot remove enough acid, leading to an increase in hydrogen ions and a decrease in pH -Metabolic Alkalosis: occurs when the body loses too much acid or produces too much base, leading to a decrease in hydrogen ions and an increase in pH Respiratory acidosis: (from perry book) Perry Book:Arises from alveolar hypoventilation; the lungs are unable to excrete enough CO2. The PaCO2 rises, creating an excess of carbonic acid in the blood, which decreases pH. The kidneys compensate by increasing excretion of metabolic acids in the urine, which increases blood bicarbonate. This compensatory process is slow, often taking 24 hours to show clinical effect and 3 to 5 days to reach steady state. Decreased cerebrospinal fluid (CSF) pH and intracellular pH of brain cells cause decreased level of consciousness. Respiratory acidosis: (from ssherpath Is caused by decreased gas exchange in the lungs caused by changes in ventilation, perfusion, or diffusion. During the expiratory phase of the respiratory cycle, the lungs expel carbon dioxide (CO2). CO2 that is not exhaled combines with water to form carbonic acid. Carbonic acid in the body leads to hypercapnia or increased levels of CO2 in the blood and a decrease in pH. Acute respiratory acidosis is characterized by a pH less than 7.35 and a PaCO2 greater than 45 mm Hg. Signs And Symptoms: Headache, light-headedness, decreased level of consciousness (confusion, lethargy, coma), dysrhythmias Laboratory findings: Arterial blood gas alterations: pH below 7.35, PaCO2 above 45 mm Hg (6 kPa), HCO3− level normal if uncompensated or above 28 mEq/L (28 mmol/L) if compensated Conditions associated with respiratory acidosis include: (from sherrpath) -Chronic obstructive pulmonary disease (COPD) or asthma exacerbations -Pulmonary edema -Medications (specifically anesthetics, opioids, and sedatives) -Obstructive sleep apnea -Chest injury or trauma (rib injury) -Brainstem injury -Neuromuscular disorders (e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic lateral sclerosis) -COPD is associated with an elevated PaCO2 value with a normal pH level. Chronic damage to the lungs limits gas exchange, resulting in an elevated PaCO2 level. Elevated PaCO2 levels trigger compensatory excretion of excess metabolic acids and conservation of bicarbonate by the kidneys. The result of this compensation mechanism is chronic respiratory acidosis. Imbalance and related causes: (from perry book) -Impaired Gas Exchange: -Type B COPD (chronic bronchitis) or end-stage type A COPD (emphysema) -Bacterial pneumonia -Airway obstruction -Extensive atelectasis (collapsed alveoli) -Severe acute asthma episode -Impaired Neuromuscular Function: -Respiratory muscle weakness or paralysis from hypokalemia or neurological dysfunction Respiratory muscle fatigue, respiratory failure Chest wall injury or surgery causing pain with respiration Dysfunction of Brainstem Respiratory Control: Drug overdose with a respiratory depressant Some types of head injury -Respiratory acidosis: Decreased PH, Increased PaCO2, Increased HCO3 (on flashcards already) -Respiratory Alkalosis: (from perry book) Respiratory alkalosis arises from alveolar hyperventilation; the lungs excrete too much carbonic acid (CO2 and water). The PaCO2 falls, creating a deficit of carbonic acid in the blood, which increases pH. Respiratory alkalosis usually is short lived; therefore the kidneys do not have time to compensate. When the pH of blood, CSF, and ICF increases acutely, cell membrane excitability also increases, which can cause neurological symptoms such as excitement, confusion, and paresthesia. If the pH rises high enough, central nervous system (CNS) depression can occur. -Respiratory Alkalosis: (from Sherpath) Respiratory alkalosis is caused by hyperventilation. Excess CO2 is exhaled when respiration is excessively deep and rapid (tachypnea), resulting in hypocapnia. Respiratory alkalosis is characterized by a pH greater than 7.45 and a PaCO2 less than 35 mm Hg. Conditions associated with respiratory alkalosis include: (from sherpath) -Pain -Anxiety or fear -Salicylate overdose -Nicotine overdose -Increased metabolic states (fever, high altitudes) -Abnormal brainstem stimulation Hypoxemia from any cause (e.g., initial part of asthma episode, pneumonia) Imbalance and related causes: (from perry book) Acute pain Anxiety, psychological distress, sobbing Inappropriate mechanical ventilator settings Stimulation of brainstem respiratory control (e.g., meningitis, gram-negative sepsis, head injury, aspirin overdose) The kidneys compensate for respiratory alkalosis by preserving metabolic acids and decreasing the amount of available bicarbonate. This results in a decrease in pH and bicarbonate levels. Signs and Symptoms: Light-headedness, numbness and tingling of fingers, toes, and circumoral region, increased rate and depth of respirations, excitement and confusion possibly followed by decreased level of consciousness, dysrhythmias Laboratory findings: Arterial blood gas alterations: pH above 7.45, PaCO2 below 35 mm Hg (4.7 kPa), HCO3− level normal if short lived or uncompensated or below 21 mEq/L (21 mmol/L) if compensated -Respiratory Alkalosis - Increased PH- Ddecreased PaCO2 - Decreased HCO3 (on flashcards already) Metabolic Acidosis: Perry Book: Metabolic acidosis occurs from an increase of metabolic acid or a decrease of base (bicarbonate). The kidneys are unable to excrete enough metabolic acids, which accumulate in the blood, or bicarbonate is removed from the body directly as with diarrhea. In either case the blood HCO3− decreases, and the pH falls. With an increase of metabolic acids, blood HCO3− decreases because it buffers metabolic acids. Similarly, when patients have conditions that cause the removal of HCO3−, the amount of HCO3− in the blood decreases. Metabolic acidosis (Sherpath): is caused by increased acid produced as a by-product of a metabolic process or a loss of bicarbonate (HCO3–) ions. The lungs compensate for metabolic acidosis by increasing the rate and depth of ventilation, known as Kussmaul respiration. This respiratory pattern removes excess carbon dioxide, thereby lowering the carbonic acid in the system. Metabolic acidosis is characterized by a pH level less than 7.35 and a bicarbonate (HCO3–) level less than 22 mEq/L. Underlying Cause of Metabolic Acidosis: -Starvation ketoacidosis *Inadequate caloric intake *Prolonged fasting -What Happens: In the absence of glucose, fat stores are used for energy and keto-acids accumulate in the blood. -Diabetic ketoacidosis *Type I diabetes mellitus -What Happens: Glucose is not transported into cells because of the lack of insulin. Fat is used for energy, and keto-acids accumulate in the blood. -Lactic acidosis *Sepsis *Cardiac arrest *Trauma *Seizures -What Happens: Lack of oxygen results in anaerobic metabolism in cells and lactic acid accumulation. -Renal tubular acidosis *Renal failure -What Happens: The kidneys are unable to remove acids through urine acidification. -Hyperchloremic acidosis *Diarrhea *Laxative abuse -What Happens: Gastrointestinal loss of bicarbonate (HCO3–) occurs. Signs and Symptoms of metabolic acidosis: -decreases a person’s level of consciousness -Decreased LOC (lethargy, confusion, coma) -Increased RR & INcreased respiratory depth (compensatory hyperventilation) -Abdominal pain -Dyrythmias Laboratory findings: Arterial blood gas alterations: pH below 7.35, PaCO2 normal if uncompensated or below 35 mm Hg (4.7 kPa) if compensated, HCO3− level below 21 mEq/L Imbalance andd Related Causes- Increase of Metabolic Acids (High Anion Gap): -Ketoacidosis (diabetes, starvation, alcoholism) -Hypermetabolic state (severe hyperthyroidism, burns, severe infection) -Oliguric renal disease (acute kidney injury, end-stage renal disease) -Circulatory shock (lactic acidosis) -Ingestion of acid or acid precursors (e.g., methanol, ethylene glycol, boric acid) Loss of Bicarbonate (Normal Anion Gap): -Diarrhea -Pancreatic fistula or intestinal decompression -Renal tubular acidosis Metabolic Acidosis: Decreased Ph - Decreased PaCO2 - DDecreased HCO3 Metabolic Alkalosis Metabolic alkalosis (Sherpath): is caused by an increase in serum bicarbonate (HCO3–) concentration. The increased HCO3– is a consequence of the loss of hydrogen (H+) ions or a direct gain of HCO3–. Metabolic alkalosis is characterized by a pH greater than 7.45 and an HCO3– greater than 26 mEq/L. The following table lists the underlying conditions for metabolic alkalosis. Metabolic alkalosis (Perry Books): occurs from a direct increase of base HCO3− or a decrease of metabolic acid, which increases blood HCO3− by releasing it from its buffering function. Common causes include vomiting and gastric suction. The respiratory compensation for metabolic alkalosis is hypoventilation. The decreased rate and depth of respiration allow carbonic acid to increase in the blood, as seen by an increased PaCO2. The need for oxygen may limit the degree of respiratory compensation for metabolic alkalosis. Because HCO3− crosses the blood-brain barrier with difficulty, neurological signs and symptoms are less severe or even absent with metabolic alkalosis Underlying Cause of Metabolic Alkalosis: -Emesis -Gastric suction -What Happens:An active loss of stomach acid occurs. Extracellular fluid deficit Dehydration Circulatory shock What happens: Increased renal excretion of acid and retention of HCO3– occurs in response to the contracted vascular space. Loop or thiazide diuretic therapy What happens:Diuretics facilitate increased excretion of hydrogen ions. Hypokalemia What happens:Hydrogen ions shift into cells, causing increased renal excretion of acid and decreased concentration of hydrogen ions in circulating blood. Ingestion of baking soda or bicarbonate products (i.e., antacids) What Happens:Bicarbonate is absorbed by the gastrointestinal tract and increases blood HCO3– concentration. Imbalance andd Relatedd Causes: Increase of Bicarbonate: Excessive administration of sodium bicarbonate Massive blood transfusion (liver converts citrate to HCO3−) Mild or moderate ECV deficit (contraction alkalosis) Loss of Metabolic Acid: Excessive vomiting or gastric suctioning Hypokalemia Excess aldosterone Signs and Symptoms: Light-headedness, numbness and tingling of fingers, toes, and circumoral region; muscle cramps; possible excitement and confusion followed by decreased level of consciousness, dysrhythmias (may be caused by concurrent hypokalemia) Laboratory findings: Arterial blood gas alterations: pH above 7.45, PaCO2 normal if uncompensated or above 45 mm Hg (6.0 kPa) if compensated, HCO3− above 28 mEq/L (28 mmol/L) Metabolic Alkalosis: Increased pH - Increasedd PaCO2 - Increased HCO3 Respiratory acidosis - Change in PH Value: Decreased: pH < 7.35 - Other lab Value Changes: PaCO2 > 45 mm Hg Respiratory alkalosis- Changes in Ph Value: Increased: pH > 7.45 - Other lab Value Changes: PaCO2 < 35 mm Hg Metabolic acidosis- Changes in Ph Value: Decreased pH < 7.35 - Other lab Value Changes: HCO3– < 22 mEq/L Metabolic alkalosis - Changes in Ph Value: Increased: pH > 7.45 Other lab Value Changes: HCO3– > 26 mEq/L 3.Normal values of arterial blood gas (PH, Partial pressure of oxygen (PaO2) , Partial pressure of carbon dioxide (PaCO2) Lab Normal Range in Adult ABG: (on flashcards already) -pH: 7.35-7.45 -PaCO2:-35-45 mmHg (4.7-6 kPa) -HCO3: 21-28 mEq/L (21-28 mmol/L) -PaO2: 80-100 mmHg (10.7-13.3 kPa) -SaO2: 95% - 100% -Base Excess: -2 to +2 mEq/L (mmol/L) These values help assess lung and kidney function and determine if there are any acid-base imbalances in the body. 4.Phlebitis vs infiltration and treatment for both Infiltration: occurs when an IV catheter becomes dislodged or a vein ruptures and IV fluids inadvertently enter subcutaneous tissue around the venipuncture site. When the IV fluid contains additives that damage tissue, extravasation occurs. Infiltration and extravasation cause coolness, paleness, and swelling of the area. When infiltration occurs, immediately assess for any additives in the infiltrated fluid to determine the type of action necessary to prevent local tissue damage and sloughing. Vasoconstrictors, high-dose potassium, and other IV additives in subcutaneous tissue need different treatments from those needed for an infiltrated additive-free IV. Although the INS does not include an infiltration scale for adults in its 2021 standards, the society does recommend using a standardized scale for documentation V.S. Phlebitis :(i.e., inflammation of a vein) results from chemical, transient mechanical, infectious, or postinfusion causes. Risk factors for phlebitis include acidic or hypertonic IV solutions; rapid IV rate; IV drugs such as KCl, vancomycin, and penicillin; VAD inserted in area of flexion; poorly secured catheter; poor hand hygiene; and lack of aseptic technique. The typical signs of inflammation (i.e., heat, erythema [redness], tenderness) occur along the course of a vein. When a patient has dark skin, these signs may be less obvious; assess carefully for subtle color changes at the VAD site that might indicate phlebitis. Phlebitis Scale: Grade/Clinical Criteria 0: No symptoms 1: Erythema at access site with or without pain 2: Pain at access site with erythema and/or edema 3: Pain at access site with erythema; streak formation; palpable venous cord 4 : Pain at access site with erythema; streak formation; palpable venous cord >2.54 cm (1 inch) in length; purulent drainage Score/Observation: Score 0: IV site appears healthy Score 1: Observation- One of the following signs is evident: Slight pain near IV site or slight redness near IV site Score 2: Observation- Two of the following signs are evident: Pain at IV site Erythema Swelling Score 3: Observation- All of the following signs are evident: Pain along the path of cannula Induration Score 4:Observation- All of the following signs are evident and extensive: Pain along the path of cannula Erythema Induration Palpable venous cord Score 5: Observation- All of the following signs are evident and extensive: Pain along the path of cannula Erythema Induration Palpable venous cord Pyrexia -Phlebitis is dangerous because the inflammation of the vein wall can lead to associated blood clots (thrombophlebitis). Clots form along the vein and in some cases cause emboli, which can break off and enter the circulation. This may permanently damage veins. Frequent changes of peripheral IV catheters to reduce infection are not recommended. -In the absence of phlebitis, local infection at the venipuncture site is usually caused by poor aseptic technique during catheter insertion, daily monitoring, or catheter removal. Early recognition of local infection and treatment is important to prevent bacteria from entering the bloodstream. Bloodstream infections may arise from short peripheral IV catheter sites. -Air embolism occurs when air is present inside syringes, IV tubing is not primed with fluid, or connectors are not removed before use and cause air to enter a patient’s vein. It also can occur if the VAD is not clamped before changing the tubing or if the IV tubing is punctured inadvertently -Bleeding can occur around the venipuncture site during the infusion or through the catheter or tubing if these become disconnected inadvertently. Bleeding is more common in patients who receive heparin or other anticoagulants or who have a bleeding disorder (e.g., hemophilia or thrombocytopenia). Complication: Infiltration and extravasation Description:Infiltration- IV fluid entering subcutaneous tissue around venipuncture site. Extravasation- technical term used when a vesicant (tissue-damaging) drug (e.g., chemotherapy) enters tissues Asssessment Findings: Skin around catheter site taut, blanched, cool to touch, edematous; may be painful as infiltration or extravasation increases; infusion may slow or stop Nursing Interventions (treatment):Use standard scale for assessing and documenting infiltrationStop infusion. Discontinue IV infusion if no vesicant drug. If vesicant drug, disconnect IV tubing and aspirate drug from catheter. Agency policy and procedures may require delivery of antidote through catheter before removal.Elevate affected extremity. Avoid applying pressure over site; can force solution into contact with more tissue. Contact health care provider if solution contained KCl, a vasoconstrictor, or other potential vesicant. Apply warm, moist, or cold compress according to procedure for type of solution infiltrated. Start new IV line in other extremity. V.S. Complication: Phlebitis Description: Inflammation of inner layer of a vein Assesment Findings: Redness, tenderness, pain, warmth along course of vein starting at access site; possible red streak and/or palpable cord along vein Nursing Interventions (treatment): Use standard scale for assessing and documenting phlebitis. Stop infusion and discontinue IV line. Start new IV line in other extremity or proximal to previous insertion site if continued IV therapy is necessary. Apply warm, moist compress or contact IV therapy team or health care provider if area needs additional treatment. Elevate affected extremity. Document phlebitis using a standardized scale, including nursing interventions per agency policy and procedure. The other most common complications of IV therapy involve phlebitis and infiltration. Prevention of these complications requires frequent assessment of the peripheral VAD site to see if replacement of a VAD is clinically indicated. Standards recommend the following: 1. Assess a VAD site, an entire infusion system, and a patient for signs of complications at a frequency dependent on patient factors, such as age, clinical condition, and cognition; type/frequency of infusion solution; and health care setting. 2. Palpate and inspect the VAD site, including catheter pathway in vein, for integrity of skin, dressing, and securement device. 3. In acute care and nursing facilities, assess the VAD site at least daily. 4. In outpatient or home care settings, assess the VAD site at every visit. Teach the patient or caregiver to check the VAD site with each infusion or at least daily or, for continuous PICC infusions, every 4 hours during waking hours. Discontinue IV access after infusion of the prescribed amount of fluid; when infiltration, phlebitis, or local infection occurs; or if the IV infusion slows or stops, indicating the catheter has developed a thrombus at its tip. presents the steps for discontinuing peripheral IV access. Help patients and families understand that moving from IV infusion to oral fluid intake is a sign of progress toward recovery. 5. Normal lab value of potassium and treatment for hyperkalemia. Signs and symptoms of hyperkalemia (on flashcards already) Normal Lab Value Potassium: 3.5–5.0 mEq/L (3.5–5 mmol/L) Hyperkalemia: (high potassium) is the term used when the serum potassium concentration is above 5.0 mEq/L. General Causes: Hyperkalemia is most often a result of impaired renal excretion in renal failure and can be a life-threatening problem for patients. Additional causes include: -Excessive intake of potassium -Certain medications -Cushing syndrome -Extensive tissue damage caused by trauma or burns -Severe infections causing the release of intracellular potassium Clinical Factors: In the clinical setting, excessive or rapid infusion of IV fluids with potassium, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor antagonists may cause a rise in the potassium level. Other medications such as potassium-sparing diuretics can also cause hyperkalemia. A common example of a potassium-sparing diuretic is spironolactone, which blocks aldosterone, causing retention of potassium and loss of sodium. Signs And Symptoms: Neuro anxiety, confusion, drowsiness, irritability lethargy, thready pulse, ↓ BP, initial tachycardia followed by bradycardia, ECG peaked, T waves, widened QRS complex, PR prolongation, terminal, sine-wave pattern, ↓intestinal motility, N/V/D, Ilieus, abdominal cramping, MS skeletal muscle weakness (legs);weak or paralyzed skeletal muscles; cramping leg pain; tremors, twitching,vague muscle weakness, flaccid, paralysis, paresthesia, ABG: ↓arterial pH level OR "MURDER" is a mnemonic to remember the symptoms of hyperkalemia (high potassium levels). It stands for: M – Muscle weakness U – Urine abnormalities (like reduced urine output) R – Respiratory distress D – Decreased cardiac contractility (weakened heart contractions) E – ECG changes (like peaked T waves) R – Reflexes (hyperreflexia or flaccid paralysis) Treatments: Monitor EKG Eliminate potassium from the body Eliminate oral intake Remove potassium from IVs Dialysis peritoneal, hemodialysis, continuous renal replacement therapy (CRRT) -Meds sodium bicarbonate if acidotic, calcium, diuretics, kayexalate, insulin/glucose -initiate potassium restricated diet -potassium excreting diuretics -administartion of IV calcium gluconate & IV sodium bicarbonate -avoid the use of salt ssubsttitutes or other potassium containing substances -Force K+ from ECF to ICF by IV Insulin and a ß-adrenergic agonist such as albuterol (stimulate the action of sodium-potassium pump) 6.Intravascular fluid vs extravascular fluid vs transcellular fluid, give examples Body fluids are located in two distinct compartments: extracellular fluid (ECF): outside the cells and intracellular fluid (ICF): inside the cells In adults,intracellular fluid (ICF) comprises approximately two-thirds of total body water.extracellular fluid (ECF) makes up approximately one-third of total body water.extracellular fluid (ECF) has two major divisions (intravascular fluid and interstitial fluid) and a minor division (transcellular fluids). Intravascular fluid is the liquid part of the blood (i.e., the plasma). Interstitial fluid is located between the cells and outside the blood vessels. Transcellular fluids such as cerebrospinal, pleural, peritoneal, and synovial fluids are secreted by epithelial cells Imbalances of sodium (Na+), potassium (K+), calcium (Ca2+), magnesium (Mg2+), or phosphate (PO43-) can cause significant morbidity and mortality in patients. The most common reasons for electrolyte imbalance result from alterations in intake or absorption, alterations in excretion, shifts between intracellular and extracellular fluid, and fluid volume abnormalities within the body. Diagram is divided into three sections is marked from top to bottom as intravascular plasma (3L); interstitial fluid (11L); and intracellular fluid (28L), with two adjacent layers separated by cell membrane. Intravascular plasma, cell membrane, and interstitial fluid is collectively labeled as extracellular fluid (1L), with curve on right from intravascular plasma to interstitial marks lymphatics. An intake and output(kidneys, lungs, feces, sweat, and skin) is connected at the top. ,intracellular fluid (ICF):comprises approximately two-thirds of total body water, Intravascular fluid is the liquid part of the blood (i.e., the plasma),Percentage of fluid in body 64-67% & ⅔ & makes up 28 L worth.extracellular fluid (ECF) : makes up approximately one-third of total body water, has two major divisions (intravascular fluid and interstitial fluid) and a minor division (transcellular fluids). Percentage of fluid in body ⅓ and makes up 14 L worthVolume imbalances are disturbances of the amount of fluid in the extracellular compartment. Transcellular fluids: is plassama andd in cerebrospinal, pleural, peritoneal, and synovial fluids are secreted by epithelial cells(cerebrospinal fluid, intraocular, pericardial fluid, pleural fluid,GI track fluids, peritoneal fluids, jointspaces)“Third spacing” loss of ECF into space that does not contribute to equilibrium (ascites). Percentage of fluid in body 4-8% Sherpath AI: Intravascular fluid refers to the fluid contained within the blood vessels, specifically the plasma portion of blood. Examples include blood plasma and lymph fluid. Extravascular fluid is the fluid outside of blood vessels, divided into: - Interstitial fluid: The fluid between cells and surrounding tissues. Examples include fluid in the skin, muscles, and organs. - Transcellular fluids: Specialized bodily fluids contained in cavities. Transcellular fluids are examples of extravascular fluids found in specific compartments, such as: - Cerebrospinal fluid in the brain and spinal cord - Synovial fluid in joint cavities - Pleural fluid between the lungs and chest wall - Peritoneal fluid in the abdominal cavity - Pericardial fluid around the heart Osmosis Fluid Video First, fluid is found in two major compartments in the body: inside the cells, called intracellular fluid, and outside the cells, called extracellular fluid. The extracellular fluid compartment is further divided into the intravascular space, which is inside the blood vessels; the interstitial space, which is found between cells; and the transcellular space, where fluid, like pericardial, cerebrospinal, and synovial fluid, is contained in epithelial-lined spaces. Now, the fluid in these compartments is mostly made up of water. In fact, over half of an adult's body weight and volume is water, which is called total body water. In addition, fluid is also made up of small and large solutes. Small solutes can easily cross cell membranes and are found in both intracellular and extracellular spaces. They include gases like oxygen and carbon dioxide, glucose, and electrolytes. On the other hand, large solutes can't easily cross cell membranes and are typically found in the extracellular space. These solutes include plasma proteins and blood components like red blood cells, platelets, and white blood cells. Chat Gpt: In the body, fluids are distributed among different compartments, each serving specific functions. Here’s a breakdown of the three types of fluids: 1. Intravascular Fluid:This is the fluid within the blood vessels and is part of the extracellular fluid. Examples: Blood plasma and the fluid in the vascular system. It’s primarily involved in transporting nutrients, hormones, and waste products throughout the body. 2. Extravascular Fluid:This refers to the fluid outside of the blood vessels, making up the rest of the extracellular fluid. It’s further divided into interstitial fluid and transcellular fluid. Examples: Interstitial Fluid: The fluid surrounding the cells in tissues, helping with nutrient exchange between blood and cells. Lymph Fluid: Found in the lymphatic system, which helps with immune responses and fluid balance. 3. Transcellular Fluidss: This is a specialized portion of the extracellular fluid that is separated by cellular barriers and found in specific compartments. Examples: Cerebrospinal fluid (CSF) around the brain and spinal cord, synovial fluid in joints, pleural fluid in the pleural cavity around the lungs, peritoneal fluid in the abdominal cavity, and aqueous humor in the eye. Each of these fluid types plays a unique role in maintaining homeostasis and supporting physiological processes in the body. Volume imbalances are disturbances of the amount of fluid in the extracellular compartment. Extracellular Volume Deficit: -Body fluids have ↓ volume but normal Osmolality -Na+ & H2O intake < than output => isotonic loss -Severely ↓ oral intake of water & salt -↑GI output: vomiting, diarrhea, laxative overuse, drainage from fistulas or tubes -↑renal output: diuretics, adrenal insufficiency (deficit of cortisol & aldosterone) -Loss of blood or plasma: hemorrhage or burns -Massive sweating without water & salt intake. -PE: sudden weight loss (overnight), postural hypotension, tachycardia, thready pulse, dry mucous membranes, poor skin turgor, slow vein filling, flat neck veins when supine, dark yellow urine -If severe: ↓LOC (confusion,restlessness), thirst, hypotension, oliguria (UO < 30 mL/hr); cold, clammy skin; hypovolemic shock -Labs: ↑Hct, ↑BUN > 20 mg/dL (7.1 mmol/L) (hemoconcentration); urine specific gravity > 1.030, unless renal cause Extracellular Water Excess: -Na+ & H2O intake > output => isotonic gain -Excessive administration of Na+- containing isotonic IVF or oral intake of salty foods & water -Renal retention of Na+ & H2O: heart failure, cirrhosis, aldosterone or glucocorticoid excess, acute or chronic oliguric renal disease -PE: sudden weight gain (overnight), edema (especially in dependent areas), full neck veins when upright or semi-upright, crackles in lungs -If severe: confusion, pulmonary edema - Labs: ↓Hct, ↓ BUN < 10 mg/dL (3.6mmol/L) (hemodilution) Hyptertonic fluid deficit -Fluid loss is made up of more water than solute (sodium). *Decreased intracellular fluid: Increased serum osmolality causes water to shift out of the cells via osmosis. This causes the cells to shrink and become dysfunctional. -Increased serum osmolality: Greater water loss than sodium, which increases the serum concentration of sodium. *Decreased extracellular (intravascular and interstitial) fluid volume: The same feature as occurs with isotonic FVD. Random Fact she said we need to know in class: Food High in calcium : BANANAS & POTATOES 7. Nursing interventions for blood transfusion reactions Blood transfusion, or blood component therapy, is the IV administration of whole blood (RBCs, WBCs, platelets) OR a blood component (packed red blood cells [RBCs], platelets, or plasma. Objectives: (1) ↑ circulating blood volume after hemorrhage, trauma , surgery (2) ↑ #RBCs & maintain hemoglobin levels in pts with severe anemia. (3) Replacement therapy for albumin, clotting factors, platelets Blood transfusion is a high-risk nursing intervention. RN Responsibility: (1) thorough pt assessment (2) Check blood product against MD’s orders (3) Check against pt identifiers (4) monitor for adverse reaction Caring for patients receiving blood or blood-product transfusion is a nursing responsibility. You must be thorough in patient assessment, checking the blood product against prescriber’s orders, checking it against patient identifiers, and monitoring for any adverse reactions. Blood transfusions are never regarded as routine; overlooking any minor detail can have dangerous and life-threatening events for a patient Vargas powerpoint how to start blood transsfusion: Verify the order Consent Explain the procedure to the patient Access V/S and temperature prior to the transfusion Remain with the patient during the initial 15 minutes 18 to 20 gauge for standard transfusion 2 RNs needed Priming / flushing : normal saline Initiate transfusion immediately upon receiving blood Administer blood over 2-4 hours (sherpath AI) If a blood transfusion reaction occurs, the key nursing interventions are: - Stop the transfusion immediately and keep the IV line open with normal saline - Notify the physician or provider right away - Monitor and document the patient's vital signs frequently - Provide supplemental oxygen if needed - Administer medications as ordered (e.g. diphenhydramine, acetaminophen, corticosteroids) - Keep all transfusion supplies including tubing and blood bag for investigation - Monitor for signs of acute kidney injury and disseminated intravascular coagulation - Provide supportive care such as keeping the patient warm and comfortable - Document the reaction details thoroughly per institutional policy Prompt recognition and management of transfusion reactions is crucial to prevent life-threatening complications. Careful monitoring, stopping the transfusion, notifying the provider, and providing supportive care are essential nursing actions. Anaphylactic Reaction interventions: -Stop transfusion. -Have epinephrine ready for injection** -Support BP. Initiate CPR PRN. Do Not restart transfusion. Febrile Nonhemolytic reaction (most common) Interventions (her pp): -Stop transfusion. -Give antipyretics. No aspirin in thrombocytopenic pts. -Do Not restart transfusion. Perry Book: -Stop the transfusion. -Change administration set and administer 0.9% sodium chloride at rate to maintain patent IV access. - Institute transfusion reaction protocol. Administer antipyretics as ordered to treat fever. -Document clinical symptoms, when transfusion was stopped, notification of health care provider and blood bank, nursing interventions and response to interventions, and patient teaching. Mild Allergic Reaction Interventions for blood transfusions (her pp): -Stop transfusion temporarily. -Administer antihistamine. Perry Book: Stop the transfusion. -Change administration set and administer 0.9% sodium chloride at rate to maintain patent IV access. -Notify health care provider and blood bank -Administer antihistamines as ordered. -Monitor and document vital signs every 15 min. -Transfusion may be restarted if fever, dyspnea, and wheezing are not present. Acute intravascular hemolytic reaction (worst reaction) intervention(her pp): Stop transfusion & save blood bag & tubing for f/u. Keep IV site open w/ NS infused via new tubing. Maintain BP & treat shock as ordered. Obtain blood samples slowly to avoid hemolysis send to lab. Send urine specimen to lab. Give diuretics to maintain urine flow. Insert FC; strict I&O. Dialysis may be required. Perry Book: -Stop the transfusion. -Get help immediately. -Change administration set and administer 0.9% sodium chloride at rate to maintain patent IV access. -Notify health care provider and blood bank. Treat shock. Maintain blood pressure and renal perfusion. - Insert Foley catheter. Monitor intake and output hourly. -Dialysis may be required. -Obtain blood and urine samples and send to laboratory with unused part of unit of blood. -Document reaction according to agency policy. Severe allergic reaction (anaphylaxis)Interventionss (perry book): -Stop the transfusion. -Change administration set and administer 0.9% sodium chloride at rate to maintain patent IV access. -Notify health care provider and blood bank. -Administer antihistamines, corticosteroids, epinephrine, and antipyretics as ordered. -Monitor and document vital signs until stable. -Initiate cardiopulmonary resuscitation if necessary. Transfusion-related acute lung injury (TRALI) (perry book) interventions: Stop the transfusion. -Provide respiratory support, -administer oxygen; -frequently mechanical ventilation is required; - administer vasopressor agents. Transfusion Associated circulatory overload (TACO) Cause: Blood administered faster than circulation can accommodate Prevention: Adjust transfusion volume & flow rate based on pt size & clinical status. Have blood bank divide unit into smaller aliquots for better spacing of fluid input Cues:Dyspnea, cough, crackles, or rales in dependent lobes of lungs; distendedneck veins when upright INterventions: Adjust transfusion volume & flow rate based on pt size & clinical status. Have blood bank ssplit unit Perry book: Stop the transfusion. Place patient in high-Fowler position, -notify health care provider - administer oxygen and diuretics. Iron overload transfusion reaction interventions (perry book) -No effective therapy. -Iron chelation therapy. -Monitor patient for heart failure, cardiac disorder, liver disorder, serum transferrin. Bacterial contamination infusion reaction interventionss (perry book): -Stop the transfusion. -Treat shock, and administer ordered steroids and antibiotics. -Culture patient’s blood, blood component, and all intravenous solutions. Sepsis blood transfusion interventions: -Stop transfusion. -Obtain culture of pt’s blood & send bag with remaining blood to blood bank fur further study. -Treat as ordered: antibx, IVFs, Vasopressors, glucocorticoids. Hemolysis (the breaking down or destruction of red bloodd cells release hemoglobin into the blood stream,life threatning) Intervention: Stop the transfusion immediately! Keep the IV line open. Disconnect the Y tubing at the hub closest to the insertion site. Attach new tubing with 0.9% NS at a slow rate. You must change out all the tubing. Notify the MD &/or RRT stat! Stay with the pt, obtain VS q5min, monitor s/s Administer emergency drugs PRN (antihistamines, vasopressors, fluids, & corticosteroids per MD/protocol). Perform CPR PRN Save the blood bag, Y tubing, attached labels & transfusion record for return to Blood Bank. Obtain blood & urine specimens per MD order/protocol. Perry Book:A transfusion reaction is an adverse event that occurs from transfusion of a blood product. Many transfusion reactions involve immune system reaction to the transfusion that ranges from a mild response to severe anaphylactic shock or acute intravascular hemolysis, both of which can be fatal. Table 42.15 presents the causes, manifestations, management, and prevention of the most common acute transfusion reactions. Prompt intervention when a transfusion reaction occurs maintains or restores a patient’s physiological stability. When you suspect acute intravascular hemolysis, do the following (DeLisle, 2018): Stop the transfusion immediately. Keep the IV line open by replacing the IV tubing down to the catheter hub with new tubing and running 0.9% sodium chloride (normal saline) at a slow rate. Do not turn off the blood and simply turn on the 0.9% sodium chloride (normal saline) that is connected to the Y-tubing infusion set. This would cause blood remaining in the IV tubing to infuse into the patient. Even a small amount of additional blood can make the situation worse. You must change out all the IV tubing. Immediately notify the health care provider or emergency response team. Remain with the patient, observing signs and symptoms and monitoring vital signs as often as every 5 minutes. Prepare to administer emergency drugs such as antihistamines, vasopressors, fluids, and corticosteroids per health care provider order or protocol. Prepare to perform cardiopulmonary resuscitation. Save the blood container, tubing, attached labels, and transfusion record for return to the blood bank. Obtain blood and urine specimens per health care provider order or protocol. 8.Conditions associate with chronic diarrhea Hypocalcemia & Hypokalemia - one of the primary causes is chronic diarrhea (including laxative abuse) The homeostatic maintenance of phosphates is tightly regulated. A serum phosphate concentration below 1.7 mEq/L is hypophosphatemia. Hypophosphatemia is caused by factors that decrease phosphate intake or shift phosphate from extracellular fluid to cells. Decreased Absorption of Phosphate from the GI Tract: Chronic Diarrhea Electrolyte: Potassium (K+) Output/Losss of it creates: Aldosterone, black licorice, hypomagnesemia, and polyuria increase renal excretion; oliguria decreases renal excretion.Acute or chronic diarrhea increases fecal excretion. -Imbalance andd related Causes: Hypokalemia—Low Potassium (K+) Concentration: Increased K+ Output: Acute or chronic diarrhea Electrolyte:Calcium (Ca2+) Output/Los of it createss: Thiazide diuretics decrease renal excretion. Chronic diarrhea and undigested fat increase fecal excretion -Imbalance andd related Causes: Hypocalcemia—Low Serum Calcium (Ca2+) Concentration: Decreased Ca2+ Intake and Absorption: Calcium-deficient diet; vitamin D deficiency (includes end-stage renal disease); chronic diarrhea; laxative misuse; steatorrhea Increased Ca2+ Output: Chronic diarrhea; Electrolyte:Magnesium (Mg2+) Output/Losss of it creates: Rising blood ethanol increases renal excretion; oliguria decreases renal excretion. Chronic diarrhea and undigested fat increase fecal excretion. -Imbalance andd related Causes: Hypomagnesemia—Low Magnesium (Mg2+) Concentration: Decreased Mg2+ Intake and Absorption: Malnutrition; chronic alcoholism; chronic diarrhea; laxative misuse; steatorrhea Increased Mg2+ Output: Chronic diarrhea; steatorrhea; other GI losses (e.g., vomiting, nasogastric or fistula drainage); use of thiazide or loop diuretics; aldosterone excess Gastrointestinal output: Increased output of fluid through the GI tract is a common and important cause of fluid, electrolyte, and acid-base imbalances and requires accurate measurement and assessment. Always note the volume and appearance of any output. Vomiting and diarrhea, either acute or chronic, can cause (extracellular volume)ECV deficit, hypernatremia, clinical dehydration, and hypokalemia by increasing the output of fluid, Na+, and K+. In addition, chronic diarrhea can cause hypocalcemia and hypomagnesemia by decreasing electrolyte absorption. Removal of gastric acid from the body through vomiting or nasogastric suction can cause metabolic alkalosis. In contrast, removal of the bicarbonate-rich intestinal or pancreatic fluids through diarrhea, intestinal suction, or fistula can cause metabolic acidosis Sherpath ai Sherpath AI answered: Chronic diarrhea can lead to several acid, fluid, and electrolyte imbalances: Metabolic acidosis: Loss of bicarbonate-rich intestinal fluids through chronic diarrhea can cause metabolic acidosis. Extracellular fluid volume (ECV) deficit: Excessive fluid loss from diarrhea can result in dehydration and ECV deficit. Hypokalemia: Increased potassium loss through diarrheal stools can deplete total body potassium, leading to hypokalemia. Which can lead to cardiac arrest Hyponatremia: Sodium depletion from diarrhea can cause hyponatremia. Hypocalcemia and hypomagnesemia: Chronic diarrhea decreases absorption of calcium and magnesium, potentially causing deficiencies. Proper fluid and electrolyte replacement, along with addressing the underlying cause of chronic diarrhea, is crucial to prevent and correct these imbalances Causes of vitamin B12 deficiency include vegan diets or other diets lacking proteins, small bowel resection, chronic diarrhea, 9. Febrile nonhemolytic reaction A febrile nonhemolytic transfusion reaction is a type of transfusion reaction characterized by fever and chills, but without evidence of hemolysis (breakdown of red blood cells). It typically occurs 1-6 hours after the start of the transfusion. Symptoms may include fever, chills, nausea, headache, and anxiety. The reaction is caused by cytokines or antibodies in the transfused blood product that trigger an inflammatory response in the recipient. Treatment involves stopping the transfusion, providing supportive care, and administering antipyretics as needed. Proper identification and reporting of the reaction are essential. Perry Book: Febrile, nonhemolytic reaction from blood tranfsuion is the Most common type of transfusion reaction; caused by WBC antigen-antibody reaction. It happens Acute& Immediate (1°C (2°F) or more above baseline, chills, headache, vomiting -Prevention/Medications: Premedicate as ordered with antipyretics if prior history of reaction. Use leukocyte-reduced blood products. -Interventions: -Stop the transfusion. -Change administration set and administer 0.9% sodium chloride at rate to maintain patent IV access. -Institute transfusion reaction protocol. -Administer antipyretics as ordered to treat fever. -Document clinical symptoms, when transfusion was stopped, notification of health care provider and blood bank, nursing interventions and response to interventions, and patient teaching. Her Powerpoint: Febrile Nonhemolytic reaction (most common) Interventions: -Stop transfusion. -Give antipyretics. No aspirin in thrombocytopenic pts. -Do Not restart transfusion. 10. Education regarding iron supplements Iron is a mineral that is required for proper body function. There are many dietary sources of iron; however, iron supplements are sometimes required to treat iron deficiency anemia. Ferrous sulfate is the prototype drug that will be reviewed. Ferrous sulfate is the treatment of choice for iron deficiency anemia and is known as a ferrous iron salt. Ferrous sulfate is also used for the prevention of iron deficiency anemia. Ferrous sulfate (FeSO4) is the most frequently used form of oral iron. It is dosed as 300 mg two to three times a day for most adult patients. Confusion arises with ferrous sulfate because the dose is 300 mg, but many commercially available products are 324 mg. The two doses are used interchangeably. Each tablet contains 65 mg of elemental iron. The adult dose of elemental iron is 50 to 100 mg given two to three times daily. Pediatric dosing is based on elemental iron. Mechanism of Action Iron carries oxygen in hemoglobin and myoglobin. In addition, iron is a component required for energy transfer. Ferrous sulfate replaces the iron found in hemoglobin and allows the transport of oxygen via hemoglobin. Administration considerations: -Although absorption of iron products is better on an empty stomach, most patients experience gastrointestinal upset when taking an iron supplement on an empty stomach. In these cases, it may be administered with a small nondairy snack. -Allow 2 hours before or after the administration of iron supplements to allow the patient to consume milk or administer an antacid. -Administer oral iron with 4 to 6 ounces of water (not milk). -Have the patient sit upright for at least 30 minutes after taking oral forms of iron to decrease the risk for esophageal irritation or corrosion. Patient Edducation: Teaching the patient about safe use and storage of iron preparations is a critical component of safe administration and part of the nursing role. Teach the patient taking iron supplementation to take the medication exactly as prescribed. Sometimes patients assume that this is a “simple” dietary supplement. However, it is important for patients to regard iron supplementation as they would any medication. Encourage the patient to follow-up with the health care provider for monitoring of the iron deficiency anemia. -Educate the patient that Iron supplements cannot be used interchangeably -teach the patient how to read the dose on commercially available iron products -Inform the patient that the iron supplementation will turn the stool to a tarry black color. -If the patient is taking a liquid form of iron, teach the patient to drink the solution through a straw to avoid staining of the teeth. -If the medication causes stomach upset, it can be taken with a small snack; however, milk should be avoided. -Take the iron with at least 4 to 6 oz of water to increase absorption and decrease gastrointestinal irritation. -Remind the patient to remain sitting upright for 30 minutes after taking the iron. -Teach the patient about the need to store the medication safely. Iron toxicity is the most common cause of pediatric death resulting from poisoning. To children, some iron supplements that are coated look like candy. -Toxicity can occur from excessive elemental iron as well as corrosion of the gastric mucosa. -Store the medication in a childproof bottle out of reach of children. -Be sure to educate the patient on nutritional intake of a diet high in iron. -Meats, certain vegetables such as dark leafy greens, and grains or fortified cereals are all good sources of dietary iron. Which teaching points would a nurse share with a patient who has been newly prescribed ferrous sulfate? -Take the ferrous sulfate with 4 to 6 oz of water. It is important for the patient to take ferrous sulfate with plenty of water (i.e., 4 to 6 oz) because it can help increase absorption and reduce gastrointestinal irritation. -Take the medication on an empty stomach if possible. Ideally, iron is better absorbed on an empty stomach; however, most patients experience gastrointestinal upset. -Wait 2 hours before or after taking ferrous sulfate before taking an antacid. If a patient needs an antacid, he or she should wait 2 hours before or after taking ferrous sulfate to take an antacid. 11.What foods contain folate? ​Folic acid is a water-soluble B-complex vitamin. It is also referred to as folate, the name of its anionic form. The human body requires the oral intake of folic acid. Dietary sources of folic acid include dried beans, peas, oranges, and green vegetables. Be sure to educate the patient on nutritional intake of a diet high in iron. Meats, certain vegetables such as dark leafy greens, and grains or fortified cereals are all good sources of dietary iron. Foods that are good sources of folate (the natural form of folic acid) include: - Leafy green vegetables like spinach, romaine lettuce, and asparagus - Citrus fruits like oranges and grapefruits - Beans and lentils - Nuts and seeds - Whole grains like bread, pasta, and rice - Liver and other organ meats - Fortified cereals, breads, pastas, and other grain products Folate is water-soluble, so fresh, uncooked foods tend to be better sources than cooked or processed items. Adequate folate intake is especially crucial during pregnancy to prevent neural tube defects in the developing fetus. 12. Pernicious anemia vs Sickle cell anemia vs Megaloblastic anemia Anemia is a reduction in the number of RBCs, the amount of hemoglobin, or the hematocrit (percentage of packed RBCs per deciliter of blood). It is a clinical indicator, not a specific disease, and occurs with many health problems. For men a hemoglobin level of less than 14 g/dL (8.7 mmol/L) indicates anemia, and a level less than 12.0 g/dL (7.4 mmol/L) indicates anemia in women (Pagana et al., 2022). The many causes of anemia include dietary problems, genetic disorders, bone marrow disease, or excessive bleeding. GI bleeding is a common reason for anemia in adults. There are many types and causes of anemia (Table 34.1). Some are caused by a deficiency in one of the components needed to make fully functional RBCs. Others are caused by decreased RBC production, increased RBC destruction, or chronic RBC loss. Despite the many causes, the symptoms (Box 34.3) and the nursing interventions are similar for all types of anemia. Sherpath AI: Pernicious anemia is a type of megaloblastic anemia caused by vitamin B12 deficiency due to lack of intrinsic factor, leading to malabsorption. It is an autoimmune disorder. Sickle cell anemia is a hereditary disorder caused by a mutation in the hemoglobin gene, resulting in abnormally shaped red blood cells that can block blood vessels and cause painful episodes. Megaloblastic anemia is a broader term referring to anemias caused by impaired DNA synthesis, leading to larger than normal red blood cells. It can be due to vitamin B12 or folate deficiency, and pernicious anemia is one type. Med Surge Book pernicious anemia : Anemia resulting from failure to absorb vitamin B12, caused by a deficiency of intrinsic factor (a substance normally secreted by the gastric mucosa), which is needed for intestinal absorption of vitamin B12. A client with a hemoglobin level of 10.2 g/dL and pale skin has developed a fissure in the corner of the mouth. Which condition would the nurse anticipate? * Pernicious anemia Patients who have pernicious anemia are given vitamin B12 injections weekly at first and then monthly for the rest of their lives. Oral B12 preparations and nasal spray or sublingual cobalamin preparations may be used to maintain vitamin levels after the patient’s deficiency has first been corrected by the traditional injection method. Anemia resulting from failure to absorb vitamin B12 (pernicious anemia) is caused by a deficiency of intrinsic factor (a substance normally secreted by the gastric mucosa), which is needed for intestinal absorption of vitamin B12. Pernicious anemia is a type of autoimmune disorder. All autoimmune problems may have a genetic predisposition and may be present in other family members. Pernicious anemia is more common among older adults, who may have reduced gastric absorption of many nutrients Sickle cell anemia- Common Causes Autosomal recessive inheritance of two defective gene alleles for hemoglobin synthesis The CBC can measure other features of the RBCs, called the red blood cell indices. The mean corpuscular volume (MCV) measures the average size of individual RBCs and is useful for classifying anemias. When the MCV is elevated, the cell is larger than normal (macrocytic), as seen in megaloblastic anemias. When the MCV is decreased, the cell is smaller than normal (microcytic), as seen in iron deficiency anemia. Vitamin B12 deficiency anemia, also known as cobalamin deficiency, is caused by conditions that fail to activate enzymes needed to move folic acid into precursor RBCs for cell division and growth into functional RBCs. These precursor cells then undergo improper DNA synthesis and increase in size. This anemia is described as megaloblastic or macrocytic anemia because of the large size of the abnormal cells. Causes of vitamin B12 deficiency include vegan diets or other diets lacking proteins, small bowel resection, chronic diarrhea, diverticula, tapeworm, or overgrowth of intestinal bacteria. Anemia resulting from failure to absorb vitamin B12 (pernicious anemia) is caused by a deficiency of intrinsic factor (a substance normally secreted by the gastric mucosa), which is needed for intestinal absorption of vitamin B12. Pernicious anemia is a type of autoimmune disorder. All autoimmune problems may have a genetic predisposition and may be present in other family members. Pernicious anemia is more common among older adults, who may have reduced gastric absorption of many nutrients Lilly Book: Pernicious anemia : A type of megaloblastic anemia usually seen in older adults and caused by impaired intestinal absorption of vitamin B12 (cyanocobalamin) as a result of lack of availability of intrinsic factor anemias arising from nuclear maturation defects. These occur because of defects in deoxyribonucleic acid (DNA) or protein synthesis. Both DNA and protein synthesis require vitamin B12 and folic acid (B9) to be present in normal amounts for their proper production. If either of these two vitamins is absent or deficient, anemias secondary to nuclear maturation defects may develop. In such anemias, RBCs actually appear to be normochromic (normal in color) but are commonly macrocytic (larger than normal) on blood smear. One example is pernicious anemia. This type of anemia results from a deficiency of vitamin B12, which is used in the formation of new RBCs. The usual underlying cause is the failure of the stomach lining to produce intrinsic factor, a gastric glycoprotein that allows vitamin B12 to be absorbed in the intestine (see Chapter 53). Another example is the anemia caused by folic acid deficiency. Both pernicious anemia and folic acid deficiency anemia are also known as types of megaloblastic anemia because they are both characterized by large, immature RBCs. Megaloblastic anemias that are not the result of a lack of intrinsic factor are usually related to poor dietary intake and are most commonly seen in infancy, childhood, and pregnancy. Vitamin b12 deficiency or/and folic acid deficiency = Rbc nuclear maturation defects = megaloblastic anemia = pernicious anemia & folic acid deficieny anemia Intrinsic factors: sickle cell anemia Cyanocobalamin (vitamin B12) (Cyanocobalamin is a synthetic form of vitamin B12, used to prevent and treat vitamin B12 deficiencies), which is discussed in Chapter 53, is used to treat pernicious anemia and other megaloblastic anemias. It can be given orally or intranasally to treat vitamin B12 deficiency but is usually given by deep intramuscular injection to treat pernicious anemia. Once remission of the anemia is seen, cyanocobalamin can be dosed once a month. Cyanocobalamin is used to treat deficiency states that develop because of an insufficient intake of the vitamin. It is also included in multivitamin formulations that are used as dietary supplements. Deficiency states are most often the result of malabsorption or poor dietary intake, including gastric bypass surgery or consumption of a strict vegetarian diet, because the primary source of cyanocobalamin is foods of animal origin. The most common manifestation of untreated cyanocobalamin deficiency is pernicious anemia. The use of vitamin B12 to treat pernicious anemia and other megaloblastic anemias results in the rapid conversion of a megaloblastic bone marrow to a normoblastic bone marrow. The preferred route of administration of vitamin B12 in treating megaloblastic anemias is deep intramuscular injection. If not treated, deficiency states can lead to megaloblastic anemia and irreversible neurologic damage. Cyanocobalamin is also useful in the treatment of pernicious anemia caused by an endogenous lack of the intrinsic factor. The nurse is assessing a patient who is to receive folic acid supplements. It is important to rule out which condition before giving the folic acid? - Pernicious anemia Chat Gpt - Pernicious Anemia Definition: Pernicious anemia is an autoimmune disorder characterized by the inability to absorb vitamin B12, leading to a deficiency that affects red blood cell production. -Causes:Pernicious anemia occurs when the immune system attacks and destroys cells in the stomach lining that produce a protein called intrinsic factor. Intrinsic factor is essential for the absorption of vitamin B12 in the small intestine. Without sufficient vitamin B12, the body cannot produce healthy red blood cells, leading to anemia. -Symptoms:Fatigue, weakness, and pallor (paleness) Neurological symptoms like numbness, tingling in hands and feet, balance issues, and memory loss due to the role of B12 in nervous system function, Glossitis (swollen, red tongue) Loss of appetite and weight loss -Diagnosis:Blood tests showing large red blood cells (macrocytic anemia), low vitamin B12 levels, and high levels of methylmalonic acid and homocysteine. Presence of antibodies against intrinsic factor or parietal cells in the stomach. -Treatment: Vitamin B12 injections (usually cyanocobalamin) are often required, as oral B12 may not be absorbed effectively. Lifelong treatment is typically necessary. Prognosis:With regular B12 supplementation, symptoms can be managed, but untreated pernicious anemia can lead to severe neurological damage.  Sickle Cell Anemia Definition: Sickle cell anemia is a genetic disorder where red blood cells assume an abnormal crescent or “sickle” shape, leading to blockages in blood vessels, poor oxygen delivery, and red cell destruction. -Causes:Caused by a mutation in the HBB gene that produces abnormal hemoglobin (hemoglobin S). Hemoglobin S causes red blood cells to distort into a sickle shape under low oxygen conditions.Sickle cells are rigid, sticky, and can block blood flow in small vessels, leading to pain and tissue damage. -Symptoms:Episodes of severe pain, known as sickle cell crises, often triggered by dehydration, stress, or infection. Chronic anemia, as sickle cells have a shorter lifespan than normal red blood cells. Fatigue, paleness, and shortness of breath due to anemia. Jaundice from rapid breakdown of red blood cells. Complications like organ damage, infections, and stroke. -Diagnosis:Blood tests, including hemoglobin electrophoresis, confirm the presence of hemoglobin S. Newborn screening programs can detect sickle cell disease early. -Treatment:Pain management during sickle cell crises. Regular blood transfusions to prevent complications. Hydroxyurea, a medication that increases fetal hemoglobin and reduces sickling episodes. Stem cell or bone marrow transplant may be curative but is complex and has significant risks. -Prognosis: Sickle cell anemia is a chronic condition that requires lifelong management. Life expectancy can be reduced, but advances in treatment are improving quality of life and survival. Megaloblastic Anemia Definition: Megaloblastic anemia is characterized by the production of abnormally large red blood cells (megaloblasts) due to impaired DNA synthesis, often related to vitamin deficiencies. Causes:Most commonly caused by deficiencies in vitamin B12 or folate (vitamin B9), both of which are essential for DNA synthesis in red blood cell production. Other causes include certain medications, alcohol use, and diseases affecting nutrient absorption (e.g., celiac disease, Crohn’s disease). Symptoms:Fatigue, weakness, pallor, and shortness of breath due to anemia. Glossitis and mouth sores. Neurological symptoms if due to B12 deficiency, including numbness, tingling, memory problems, and depression. Diagnosis:Blood tests show large red blood cells with increased mean corpuscular volume (MCV).Low levels of vitamin B12 or folate, with increased levels of homocysteine. Bone marrow biopsy may show megaloblastic changes in severe cases. Treatment:Supplementation of the deficient vitamin (B12 or folate).Dietary adjustments to increase intake of B12- or folate-rich foods.Treating the underlying cause if absorption is impaired. Prognosis:With proper treatment, megaloblastic anemia is typically reversible. Untreated vitamin B12 deficiency, however, can lead to irreversible neurological damage. 13. NSAIDS and anemia, side effects of NSAIDS Some common causes of iron deficiency anemia are blood loss, surgery, childbirth, gastrointestinal (GI) bleeding (which can be caused by the ingestion of nonsteroidal antiinflammatory drugs [NSAIDs]; NSAIDs can cause GI disturbances and decrease platelet aggregation (clotting), which can result in bleeding. Therefore observe the patient for gastric discomfort or vomiting and for bleeding or bruising All NSAIDs can cause GI side effects, bleeding, and acute kidney injury if used long-term. Therefore, they are prescribed at the lowest effective dose. Remind patients to take celecoxib with food to decrease GI distress. Teach your patient about potential adverse effects and the need to report them to the primary health care provider. Examples include having dark, tarry stools; shortness of breath; edema; frequent dyspepsia; hematemesis (bloody vomitus); and changes in urinary output. Sherpath AI NSAIDs (nonsteroidal anti-inflammatory drugs) can contribute to anemia through several mechanisms: 1. Gastrointestinal bleeding: NSAIDs can cause erosions, ulcers, and inflammation in the stomach and intestines, leading to chronic blood loss and iron deficiency anemia. 2. Inhibition of erythropoietin production: Long-term NSAID use may suppress erythropoietin production by the kidneys, impairing red blood cell production and causing anemia. 3. Platelet dysfunction: NSAIDs can impair platelet function, increasing the risk of bleeding and exacerbating anemia. 4. Bone marrow suppression: In rare cases, NSAIDs may cause bone marrow suppression, reducing red blood cell production. 5. Interference with iron absorption: Some evidence suggests NSAIDs may interfere with iron absorption from the gut. The risk is higher in elderly patients, those with pre-existing kidney disease, and those on long-term or high-dose NSAID therapy. Regular monitoring of complete blood counts and iron studies is recommended. NSAIDs are contraindicated in patients with vitamin K deficiency, peptic ulcer disease, or conditions that increase bleeding risk. They should be used cautiously during pregnancy and lactation due to potential adverse effects. Chat Gpt- NSAIDS and ANemia: NSAIDs (Nonsteroidal Anti-Inflammatory Drugs), such as ibuprofen, aspirin, and naproxen, can contribute to anemia primarily through gastrointestinal (GI) bleeding, which can lead to blood loss and iron deficiency anemia. Here’s how NSAIDs can be linked to anemia: Gastrointestinal Bleeding: NSAIDs can irritate the stomach lining and increase the risk of stomach ulcers, which may lead to bleeding in the stomach or intestines. Chronic or unnoticed GI bleeding can result in significant blood loss over time, leading to iron deficiency anemia. Iron Deficiency Anemia: With long-term NSAID use, the risk of iron deficiency increases as iron stores are depleted to compensate for chronic blood loss, even if the bleeding is slow or not visibly apparent. Bone Marrow Suppression (Rare): Although uncommon, some NSAIDs can suppress bone marrow function, reducing the production of red blood cells and potentially leading to anemia. Symptoms of NSAID-Related Anemia: Patients may experience general symptoms of anemia, such as fatigue, weakness, shortness of breath, and pale skin, due to low red blood cell levels from blood loss or bone marrow suppression. Risk Factors: People with a history of GI ulcers, elderly individuals, those on high doses or long-term NSAID therapy, and patients taking corticosteroids or blood thinners are at higher risk for NSAID-related anemia. Sherpath AI Side Effects Of NSAIDS: Gastrointestinal effects: - Heartburn, nausea, vomiting, abdominal pain - Gastritis, peptic ulcers - Gastrointestinal bleeding and perforation - Acute kidney injury - Fluid and electrolyte abnormalities - Worsening of chronic kidney disease - Increased risk of heart attack and stroke - Elevated blood pressure - Heart failure exacerbation - Anemia due to bleeding or bone marrow suppression - Platelet dysfunction and bleeding risk - Dizziness, headache, rash - Liver toxicity - Asthma exacerbation - Hearing loss - Fetal risks during pregnancy Adverse Efftects: Noncardiogenic pulmonary edema, increased risk for myocardial infarction and stroke, Gastrointestinal, Dyspepsia, heartburn, epigastric distress, nausea, vomiting, anorexia, abdominal pain, gastrointestinal bleeding, mucosal lesions (erosions or ulcerations) Hematologic, Altered hemostasis through effects on platelet function Hepatic, Acute reversible hepatotoxicity, Renal Reduction in creatinine clearance, acute tubular necrosis with renal failure, Other Skin eruption, sensitivity reactions, tinnitus, hearing loss Chat Gpt: NSAIDs can cause side effects such as stomach pain, heartburn, nausea, vomiting, diarrhea, constipation, dizziness, headaches, high blood pressure, fluid retention, kidney damage, increased risk of heart attack or stroke, ulcers, bleeding in the stomach or intestines, liver damage, and, in rare cases, severe skin reactions or allergic reactions, 14. Side effects of anticoagulants Anticoagulant side effects: Bleeding, hematoma, anemia, thrombocytopenia,dizziness, shortness of breath, fever, urticaria,hematoma, dizziness, rash, gastrointestinal distress, anemia,lethargy, muscle pain, purple toes, Sherpath AI The main side effects of anticoagulants include bleeding episodes ranging from minor to life-threatening, hematoma formation, thrombocytopenia, osteoporosis with long-term heparin use, skin necrosis with warfarin, nausea, hair loss, rash, headache, and increased risk of stroke or systemic embolism if anticoagulation is subtherapeutic ChatGpt: Anticoagulants can cause side effects like easy bruising, nosebleeds, gum bleeding, heavier menstrual periods, blood in urine or stool, nausea, stomach upset, diarrhea, abdominal pain, skin reactions, fatigue, severe or uncontrollable bleeding, headaches, confusion, vision changes, allergic reactions (like rash and breathing issues), rare blood clots, liver damage (yellowing of skin or eyes, dark urine), bone loss with prolonged use, and occasionally hair loss, so monitoring for unusual bleeding or severe side effects is essential. 15. Excessive clotting vs Diminished clotting Sherpath The scope of clotting can range from increased or excessive clotting to an inability to adequately clot, either locally at the site of an injury or systemically. Decreased clotting can result in bleeding and threaten a person’s life. Increased clotting (hypercoagulability) due to an excess of platelets or excessive platelet stickiness can impair blood flow. Impaired clotting may result in either excessive or inadequate clotting. Risk factors for increased clotting include: -Immobility or decreased mobility:Slows venous blood flow to the heart and can result in venous stasis and venous thromboembolism (VTE). -Polycythemia:Excessive production of red blood cells can cause clot formation. -Diabetes mellitus: Associated with decreased blood flow. -Atrial fibrillation:Causes pooling of blood in the atria (stasis) and can lead to embolic stroke. -Smoking:Causes platelets to become stickier and more likely to aggregate. -Age: Platelets become stickier. -Venous valves that normally prevent the backflow of blood become weak and inadequate as adults age. The result is venous stasis and an increased risk for VTE. Decreased clotting most often occurs when there is an inadequate number of circulating platelets (thrombocytopenia) or clotting factors. -Chemotherapeutic drugs and corticosteroids cause bone marrow suppression where platelets and other blood cells are produced. -Cirrhosis of the liver causes decreased production of clotting factors, including prothrombin. Her powerpoint Increased clotting: Risk factors—increased or excessive clotting Immobility or decreased mobility Polycythemia Smoking Certain chronic health problems Physiologic Consequences: Increased clotting: Venous thrombosis Assessment: Increased risk for clotting Venous thrombosis (redness, pain, swelling, warmth) Arterial thrombosis (not observable, but marked by decreased perfusion to distal extremity or internal organ) Critical rescue Teach patients at risk for increased clotting to: Drink fluids Avoid crossing legs Ambulate frequently Stop smoking Report redness, pain, swelling, and warmth of lower extremity Decreased clotting: Risk factors—decreased clotting Chemotherapeutic agents and/or corticosteroids Cirrhosis of the liver Rare genetic diseases Physiologic Consequences: Decreased clotting: Prolonged internal or external bleeding Assessment: Decreased clotting Bruising Petechiae Occult or frank blood in urine and/or stool Frank bleeding from gums/nose Teach patients with decreased clotting ability to report unusual bleeding or bruising immediately Interventions Anticoagulants/antiplatelet drugs Direct thrombin inhibitors Newer anticoagulants called direct thrombin inhibitors may be given to decrease the risk of stroke in patients with atrial fibrillation. Monitor patients receiving any of these drugs for signs of bleeding, including bruising and blood in the urine or stool. From med surge book: Physiologic consequences: -For patients at risk for increased or excessive clotting, clots can occur in either venous or arterial blood vessels. *Venous thrombosis is a clot formation in either superficial or deep veins (most often), usually the leg. *If a thrombus becomes dislodged, it is known as an embolus. *Emboli most often travel to the brain (causing a stroke) or lung (pulmonary embolus). For patients with a decreased ability to clot, prolonged internal (systemic) or external (localized) bleeding may occur. -Internally: *Brain (hemorrhagic stroke) *Gastointestinal (GI) tract (frank or occult blood in the stool) *Urinary tract (hematuria) *Under the skin (purpura) -Externally: *Epistaxis (nosebleeds) *Prolonged bleeding at the site of soft tissue trauma Impaired clotting can lead to unusual bleeding or bruising. Assessment and interventions for impaired clotting are essential for patient safety. Assessments for clotting: -Observe patients for signs and symptoms of decreased clotting. -Purpuric (hemorrhagic) lesions: -Ecchymosis (bruising) -Petechiae (pinpoint purpura) -Prolonged bleeding as a result of injury or trauma -Occult or frank blood in urine or stool -Bleeding from the gums or nose For patients with increased risk for clotting or excessive clotting: -Observe for signs and symptoms of venous thrombosis. -Localized redness, pain, swelling, and warmth -A mesenteric artery thrombosis can cause small bowel ileus and gangrene if not treated quickly. -A renal artery thrombosis can cause acute kidney injury. Laboratory tests are available to measure clotting factor levels and bleeding time The most common tests are: -Prothrombin time (PT) -Activated partial thromboplastin time (aPTT) -International normalized ratio (INR): -Indicating a derived measure of prothrombin -Used to monitor the effectiveness of warfarin Health promotionss for pts with impaired clotting: Teach the patient with decreased clotting ability to report unusual bleeding or bruising immediately to the primary health care provider or nurse. Teach patients at risk for increased clotting to: -Drink adequate fluids to prevent dehydration. -Avoid crossing the legs. -Ambulate frequently and avoid prolonged sitting. -Explore smoking-cessation programs as needed. -Call the primary health care provider if redness, pain, swelling, and warmth occur in a lower extremity. How is impaired clotting assessed and treated? Impaired clotting can lead to unusual bleeding or bruising. Assessment and interventions for impaired clotting are essential for patient safety. Select each tab to learn more. Assessments for Clotting: Observe patients for signs and symptoms of decreased clotting. -Purpuric (hemorrhagic) lesions: -Ecchymosis (bruising) -Petechiae (pinpoint purpura) -Prolonged bleeding as a result of injury or trauma -Occult or frank blood in urine or stool -Bleeding from the gums or nose For patients with increased risk for clotting or excessive clotting: -Observe for signs and symptoms of venous thrombosis. -Localized redness, pain, swelling, and warmth -A mesenteric artery thrombosis can cause small bowel ileus and gangrene if not treated quickly. -A renal artery thrombosis can cause acute kidney injury. Laboratory tests are available to measure clotting factor levels and bleeding time. The most common tests are: Prothrombin time (PT) Activated partial thromboplastin time (aPTT) International normalized ratio (INR): Indicating a derived measure of prothrombin Used to monitor the effectiveness of warfarin Health Promotion for Patients With Impaired Clotting Teach the patient with decreased clotting ability to report unusual bleeding or bruising immediately to the primary health care provider or nurse. Teach patients at risk for increased clotting to: -Drink adequate fluids to prevent dehydration. -Avoid crossing the legs. -Ambulate frequently and avoid prolonged sitting. -Explore smoking-cessation programs as needed. -Call the primary health care provider if redness, pain, swelling, and warmth occur in a lower extremity. Interventions for Patients With Impaired Clotting For many adults at increased risk for clotting, anticoagulants or antiplatelet drugs (blood thinners) may be prescribed in either community or inpatient settings. Two medications that require frequent laboratory testing are: -Heparin -Warfarin Teach adults the importance of obtaining these laboratory tests to ensure that they are within the desired range Newer anticoagulants called direct thrombin inhibitors may be given to decrease the risk of stroke in patients with atrial fibrillation. Monitor patients receiving any of these drugs for signs of bleeding, including: Bruising , Blood in the urine or stool, Continued bleeding can lead to anemia or hemorrhage, depending on the location and severity of the bleeding. Perry Book: An inability to form adequate clots can result in bleeding and threaten a person’s life. In some cases an excess of platelets or excessive platelet stickiness can lead to hypercoagulability (increased clotting ability), which can impair blood flow. Therefore, the scope of clotting can range from increased or excessive clotting to an inability to adequately clot, either locally at the site of an injury or systemically. Common Risk Factors for Impaired Clotting When taking a patient and family history, be aware that impaired clotting may result in either excessive or inadequate clotting. Common risk factors for increased clotting include immobility or decreased mobility, health problems such as polycythemia, and smoking. Immobility slows venous blood flow to the heart and can result in venous stasis and venous thromboembolism (VTE), described later in this text. Certain chronic health problems such as diabetes mellitus are also associated with decreased blood flow, making patients more likely than healthy adults to develop VTE or arterial clots. Polycythemia causes an excessive production of red blood cells, which can lead to multiple clots. Atrial fibrillation causes pooling of blood in the atria (stasis) and often leads to embolic stroke. Physiologic Consequences of Impaired Clotting For patients at risk for increased or excessive clotting, recognize that clots can occur in either venous or arterial blood vessels. Venous thrombosis is a clot formation in either superficial or deep veins (most often), usually in the leg. If a thrombus becomes dislodged, it is known as an embolus. Emboli most often travel to the brain (causing a stroke) or lung (pulmonary embolus). For patients with a decreased ability to clot, prolonged internal (systemic) or external (localized) bleeding may occur. Internal bleeding may occur in the brain (hemorrhagic stroke), GI tract (frank or occult blood in the stool), and/or urinary tract (hematuria). It may also occur under the skin (purpura). External bleeding often manifests as epistaxis (nosebleeds) or prolonged bleeding at the site of soft tissue trauma. Assessment of Clotting Observe patients for signs and symptoms of decreased clotting, especially purpuric (hemorrhagic) lesions such as ecchymosis (bruising) and petechiae (pinpoint purpura). Notice if bleeding is prolonged as a result of injury or trauma. Check urine and stool for the presence of occult or frank blood. Observe for frank bleeding from the gums or nose. For patients with increased risk for clotting or excessive clotting, observe for signs and symptoms of venous thrombosis such as localized redness/hyperpigmentation, pain, swelling, and warmth. A mesenteric artery thrombosis can cause small bowel ileus and gangrene if not treated in a timely manner. A renal artery thrombosis can cause acute kidney injury. Health Promotion Strategies to Maintain Clotting and Prevent Impaired Clotting: Teach the patient with decreased clotting ability to report unusual bleeding or bruising immediately to the primary health care provider or nurse, depending on where the patient is. Be sure to teach patients at risk for increased clotting to: Drink adequate fluids to prevent dehydration. Avoid crossing the legs. Ambulate frequently and avoid prolonged sitting. Explore smoking-cessation programs as needed. Call your primary health care provider if redness/hyperpigmentation, pain, swelling, and warmth occur in a lower extremity. 16. Carbonic Acid Perry Book: An excessive buildup of carbon dioxide (CO2) combines with water (H2O) to produce carbonic acid. Body fluids contain different types of acids and bases. The most common base in human body fluid is bicarbonate (HCO3−); the most common acid is carbonic acid (H2CO3). In periods of health, the body keeps these substances at a constant ratio of 1 molecule of carbonic acid to 20 free bicarbonate ions (1:20).To maintain this ratio, both carbonic acid and bicarbonate must be carefully controlled. This constant ratio is related to balancing the production and elimination of carbon dioxide (CO2) and hydrogen ions (H+). Carbon dioxide (CO2) is a gas that forms carbonic acid when combined with water, making carbon dioxide a part of carbonic acid. Carbonic acid is not stable, and the body needs to keep a 1:20 ratio of carbonic acid to bicarbonate. When carbonic acid is formed from water and carbon dioxide, it begins to separate into free hydrogen ions and bicarbonate ions. Therefore the carbon dioxide content of a fluid is directly related to the amount of free hydrogen ions in that fluid. Whenever conditions cause carbon dioxide to increase, more free hydrogen ions are created. Likewise, whenever free hydrogen ion production increases, more carbon dioxide is produced. Bicarbonate is produced from carbonic acid primarily in the pancreas, kidneys, and inside red blood cells. It also can be reabsorbed from urine in the kidney and returned to the blood. Unlike free hydrogen ion production, no natural pathologic conditions lead to excessive production of bicarbonate. Buffers are the first line of defense against changes in free hydrogen ion levels. These buffers are always present in body fluids and act fast to reduce or raise the amount of free hydrogen ions to normal. By acting as hydrogen ion “sponges,” buffers can bind free hydrogen ions when too many are present or release them when not enough are present. Bicarbonate, a weak base, is the main buffer of the ECF. It comes from the GI absorption of ingested bicarbonate, pancreatic production of bicarbonate, movement of cellular bicarbonate into the ECF, kidney reabsorption of filtered bicarbonate, and the breakdown of carbonic acid. Normal ratio of carbonic acid to bicarbonate is 1:20. Sherpath: Respiratory acidosis is caused by decreased gas exchange in the lungs caused by changes in ventilation, perfusion, or diffusion. During the expiratory phase of the respiratory cycle, the lungs expel carbon dioxide (CO2). CO2 that is not exhaled combines with water to form carbonic acid. Carbonic acid in the body leads to hypercapnia or increased levels of CO2 in the blood and a decrease in pH. Chat Gpt: Carbonic acid (H₂CO₃) forms when carbon dioxide (CO₂) mixes with water. It’s a weak acid that helps keep the pH of blood stable. In the body, carbonic acid can break down into bicarbonate, which helps to balance acids and bases. It also plays a role in how CO₂ is carried in the blood and exhaled by the lungs. In oceans, carbonic acid forms from CO₂ in the air and can lower the pH, affecting marine life. IN CLASS SHE SAID: CARBONIC ACID -IS THE EXCESSSIVE BUILD UP OF CO2 AND H2O TO PRODUCE CARBONIC ACID AND A BUILD UP OF CO2 IN THE BLOOD(increased levels) AND A DECREASE IN PH AND IT HAPPENS IN RESPIRATORY ACIDOSIS 17. What is the nervous system responsible for Lilly Book: There are two divisions of the autonomic nervous system (ANS): the parasympathetic nervous system (PSNS) and sympathetic nervous system (SNS). Stimulation of the autonomic nervous system (ANS) is controlled by the neurotransmitters acetylcholine and norepinephrine. Receptors for both divisions of the autonomic nervous system (ANS) are located throughout the body in a variety of tissues. autonomic nervous system (ANS) physiology is reviewed in greater detail in Chapters 18 to 21. Receptors located between the postganglionic fiber and the effector cells (i.e., the postganglionic receptor) are called the muscarinic or cholinergic receptors in the the parasympathetic nervous system (PSNS). Receptors in the sympathetic nervous system (SNS) are called adrenergic or noradrenergic receptors (i.e., alpha or beta receptors). Physiologic activity at muscarinic receptors is stimulated by acetylcholine and cholinergic agonist drugs and is inhibited by cholinergic antagonists (anticholinergic drugs; see Chapter 21). Similarly, physiologic activity at adrenergic receptors is stimulated by norepinephrine, epinephrine, and adrenergic agonists and is inhibited by antiadrenergics (adrenergic blockers; i.e., alpha or beta receptor blockers). Fig. 22.2 shows how these various receptors are arranged in both the parasympathetic nervous system (PSNS) and sympathetic nervous system (SNS) and indicates their corresponding neurotransmitters The centrally acting adrenergic drugs clonidine and methyldopa work by stimulating the alpha2-adrenergic receptors in the brain. The alpha2-adrenergic receptors are unique in that receptor stimulation actually reduces sympathetic outflow, in this case from the central nervous system (CNS) Centrally acting adrenergic drugs: Drugs that modify the function of the sympathetic nervous system in the brain by stimulating alpha2 receptors. Alpha2 receptors are inhibitory in nature and thus have a reverse sympathetic effect and cause decreased blood pressure. Medical Surgical Book This ability depends primarily on the function of the central and peripheral nervous system and the musculoskeletal system and is sometimes referred to as functional ability. The primary interrelated concepts are pain and sensory perception. Pain can be categorized by duration as acute or persistent (chronic). Acute pain is short-lived, temporary, and typically confined to an injured area of the body (localized). It serves a biologic purpose to activate the sympathetic nervous system and other physiologic responses. Persistent (chronic) pain does not serve this purpose and tends to last more than 3 months. It is often described as diffuse and not confined to one area of the body. The two major types of persistent pain are persistent cancer pain and persistent noncancer pain. Pain can also be categorized by its underlying mechanism into nociceptive and neuropathic pain. Nociceptive pain results from skin or organ damage or inflammation. Neuropathic pain involves a set of mechanisms related to the nervous system with or without tissue damage. Patients experiencing acute pain usually have one or more sympathetic nervous system signs and symptoms including nausea, vomiting, diaphoresis (sweating), increased blood pressure, increased respiratory rate, increased pulse, and dilated pupils (Rogers, 2023). This “flight or fight” reaction does not occur in patients with persistent pain. Persistent pain can cause psychosocial issues, including anxiety and depression. Mobility is the ability of an individual to perform purposeful physical movement of the body. Mobility is needed to perform activities of daily living (ADLs) such as eating, dressing, and walking. This ability depends primarily on the function of the central and peripheral nervous system and the musculoskeletal system and is sometimes referred to as functional ability. The primary interrelated concepts are pain and sensory perception. Patients who have dysfunction of the musculoskeletal or nervous system are most at risk for decreased mobility or immobility neuropathic pain: The result of abnormal processing of stimuli believed to be associated with damage to or dysfunction of the parasympathetic nervous system (PNS) and/or central nervous system (CNS) Cholinergic Antagonist Causes bronchodilation by inhibiting the parasympathetic nervous system, allowing the sympathetic system to dominate, releasing norepinephrine that activates beta2 receptors. The purpose is to prevent asthma attacks or COPD bronchospasms and improve gas exchange, although some are considered reliever drugs. The autonomic nervous system (ANS) is composed of two parts: the sympathetic nervous system (SNS) and the parasympathetic nervous system. ANS functions are not usually under conscious control but may be altered in some people by using biofeedback and other methods. The SNS cells originate in the gray matter of the spinal cord from T1 through L2 or L3. This part of the ANS is considered thoracolumbar because of its anatomic location. The SNS stimulates the functions of the body needed for “fight or flight” (e.g., heart and respiratory rate). It also inhibits certain functions not needed in urgent and stressful situations. The parasympathetic cells originate in the gray matter of the sacral area of the spinal cord (from S2 through S4) plus portions of cranial nerves III, VII, IX, and X (craniosacral). The parasympathetic nervous system can slow body functions when needed and contribute to digestion and reproduction (“feed and breed”). Parasympathetic fibers to the organs have some sensory ability in addition to motor function. Sensory perceptions of irritation, stretching of an organ, or a decrease in tissue oxygen are transmitted to the thalamus through pathways not yet fully understood. Because pain from internal organs is often felt below the body wall innervated by the spinal nerve, it is presumed that there are connections between the viscera and body structure that relay pain sensation. Her powerpoint: Physiologic and Psychosocial Consequences One or more sympathetic nervous system signs and symptoms: -Acute -“Fight or flight” reaction -Nausea -Vomiting -Diaphoresis -Increased blood pressure, respirations, pulse -Dilated pupils -Persistent -No “fight or flight” reaction -Can lead to anxiety, depression Ssherpath AI: The parasympathetic nervous system is one division of the autonomic nervous system that helps conserve energy and regulate "rest and digest" functions like slowing the heart rate and aiding digestion. The autonomic nervous system controls involuntary bodily functions like heart rate, breathing, digestion, and glandular activity. It has two divisions - the sympathetic and parasympathetic systems that work in opposition to maintain homeostasis. The central nervous system consists of the brain and spinal cord. The peripheral nervous system includes the cranial and spinal nerves that connect the CNS to the rest of the body. The sympathetic nervous system is the other division of the autonomic nervous system. It activates the "fight or flight" response by increasing heart rate, blood pressure, breathing rate, and preparing the body to expend energy in stressful situations. The autonomic nervous system is responsible for regulating involuntary bodily functions like heart rate, breathing, digestion, blood pressure, and other visceral activities. The parasympathetic division is responsible for conserving energy and regulating "rest and digest" functions like slowing heart rate, increasing digestion, and allowing the body to recover. The sympathetic division activates the "fight or flight" response by increasing heart rate, blood pressure, breathing rate, and preparing the body for strenuous activity in stressful situations. The central nervous system (brain and spinal cord) is responsible for integrating sensory information, cognition, decision making, and controlling all bodily functions and behaviors. Sherrpath: Mobility is the ability of an individual to perform purposeful physical movement of the body and is needed to perform activities of daily living (ADLs) such as eating, dressing, and walking. This ability is also called functional ability, and it depends on the function of the: Central nervous system Peripheral nervous system Musculosskeletal system Patients who have dysfunction of the musculoskeletal or nervous system are most at risk for decreased mobility or immobility. Patients experiencing acute pain usually have one or more sympathetic nervous system sign or symptom. Nausea/vomiting Diaphoresis (sweating) Increased blood pressure Increased respiratory rate Increased pulse Dilated pupils Nociceptive Pain: Results from skin or organ damage or inflammation Neuropathic Pain: Involves a set of mechanisms related to the nervous system with or without tissue damage 18. Side Effects of Opiods Opioids do have concern related to abuse and addiction. Persistent cancer pain often requires opioids at the end of life to provide comfort and prepare for a “good death.” Remain alert to the potential side effects of opioid administration: constipation, nausea, sedation, respiratory depression, or myoclonus. Family members often worry about potential addiction to opioid medications. The most common side effects of opioids include nausea, vomiting, constipation, and memory and thought changes Common Opioid Side Effects Thought and memory impairment Drowsiness, sedation, and sleep disturbance Confusion Hallucinations, potential for diminished psychomotor performance Delirium Depression Dizziness and seizures Pupil constriction Bradypnea Hypoventilation Hypotension Bradycardia Peripheral edema Constipation Nausea and vomiting Delayed gastric emptying Urinary retention Hormonal and sexual dysfunction  Hypoglycemia—reported with tramadol and methadone Pruritus Immune system impairment possible with chronic use Muscle rigidity and contractions Osteoporosis Pregnancy and breastfeeding When at all possible, avoid opioid use during pregnancy to prevent fetal risks Tolerance Over time, increased doses needed to obtain analgesic effect Withdrawal syndrome Rapid or sudden cessation or marked dose reduction may cause rhinitis, chills, pupil dilation, diarrhea, “gooseflesh” 19. pain control for post op patients For postoperative pain control, basal continuous dose of patient-controlled analgesia. Pain and emotional stress are the most common sources of decreased comfort. To prevent these sensations, anticipate which patient may experience them and provide preplanned inter