Signs and Symptoms of Tonsillitis

• Persistent or recurrent sore throat
• Swollen, bright red tonsils that may be covered with white exudate
• Dysphagia
• Mouth breathing and an unpleasant mouth odor
• Fever
• Coughing
• Weakness
• Snoring

Medical Management for Tonsillitis

1. NSAIDs, Paracetamol/Acetaminophen, Ibuprofen
2. Salt water gargle, Lozenges, and Warm liquids
3. If tonsillitis is caused by Group A Beta-Hemolytic Streptococci, antibiotics like penicillin, amoxicillin, erythromycin, or clindamycin.

Surgical Management for Tonsillitis

Chronic tonsillitis, tonsillitis that occurs 5-6 times a year, calls for a Tonsillectomy the surgical removal of the tonsils on both sides of the throat. Tonsillectomy is also performed in response to cases of repeated occurrence of acute tonsillitis or adenoiditis, obstructive sleep apnea, nasal airway obstruction, snoring, or peritonsillar abscess.

Nursing Interventions Preoperatively

• Assess for signs of active infection.
• Assess bleeding and clotting studies because the throat is vascular.
• Prepare the client for a sore throat post-operatively, and instruct the client that he or she will need to drink liquids.
• Assess for any loose teeth to decrease the risk of aspiration during surgery.

Nursing Interventions Postoperatively

• Position the client prone or side-lying to facilitate drainage.
• Elevate the bed to 45 degrees when client is fully awake to decrease surgical edema and increase lung expansion.
• Have an emesis basin ready at beside to catch drainage or vomiting.
• Have suction equipment available, but do not suction unless airway obstruction occurs.
• Monitor for signs of hemorrhage (frequent swallowing); if hemorrhage is suspected turn the client to his side and notify the physician.
• Discourage coughing or clearing the throat.
• Provide clear, cool, non-citrus, and non-carbonated fluids.
• Avoid milk products initially because they coat the throat.
• Avoid red liquids, which stimulate the appearance of blood if the client vomits.
• Do not give the client any straws, forks, or sharp objects that can be put in the mouth.
• Instruct parents or relatives to notify the physician if bleeding, persistent earache, or fever occurs.
• Instruct the parents to keep the client away from crowds until healing has occurred.
• Administer ice collar as ordered.

If the pulmonary vascular resistance is higher than the systemic resistance, the shunt is from right to left; likewise is the systemic resistance is higher than the pulmonary resistance, the shunt is left to right.

Tetralogy of Fallot in Infants

Infants may be acutely cyanotic at birth or may have mild cyanosis that may progress over the first year of life as the pulmonic stenosis worsens.

• Characteristic murmur
• Episodes of cyanosis and hypoxia (hypercyanotic spells) also called as blue spells or tet spells
• Syncope
• Polycythemia

Tetralogy of Fallot in Children

With increasing cyanosis, squatting, clubbing of fingers, and poor growth may occur.

Management

Knee-Chest Position

Surgical Management

Blalock-Taussig Procedure

It is a pallative shunt where it increases pulmonary blood flow and increases oxygen saturation in infants who cannot undergo primary repair. The shunt will provide blood flow to the pulmonary arteries from the left or right subclavian artery.

Post-Operative Nursing Considerations: No blood pressure monitoring and no venipunctures in the affected extremity.

Brock Procedure

It is a complete repair usually performed in the first year of life. It includes the closure of the Ventricular Septal Defect and the resection of the stenosis, with a pericardial patch to enlarge the right ventricular outflow tract. This repair requires a median sternotomy and cardiopulmonary bypass.

Pathophysiology of Liver Cirrhosis

With underlying causes, an increase in triglyceride or fatty acid production occurs. This can lead to fatty liver and the development of fibrosis and nodulation of the liver. With the formation of fibrosis and nodulations, cirrhosis occurs.

Signs and Symptoms of Liver Cirrhosis

1. Gastritis – Due to the engorged vein in the gastrointestinal tract. It impairs the bile synthesis and fat metabolism.
2. Anemia, Leukopenia – Destruction of the blood cells by the enlarged spleen.
3. Asterixis or Hepatic Encephalopathy – Asterixis is the flapping or tremors of the hand when the arm is extended. It is due to the increase in ammonia absorption and increased in neurotoxins in the blood.
4. Malnutrition or Muscle-wasting – It is due to the impaired fat or nutrient metabolism.
5. Bleeding or Bruising – Impaired vitamin K synthesis. There is decreased platelets due to the destruction by the enlarged spleen.
6. Jaundice – Due to impaired bilirubin metabolism and excretion.
7. Edema, Ascites
8. Esophageal varices
9. Gynecomastia, Impotence, and Infertility – It is due to altered sex hormone metabolism.

Complications of Cirrhosis

Hepatic Encephalopathy

An increase in proteins would increase ammonia in the blood and is neurotoxic.

1. Asterixis
2. Changes in personality and mentation
3. Agitation, Confusion, Drowsiness
4. Slurred speech
5. Deep coma (Last stage)

• Low protein diet to decrease ammonia formation.
• Medications like lactulose and neomycin.
• Administer enema.
• Increase acidity of colonic contents.
• Decrease ammonia formation.

Esophageal Varices

Engorgement of esophageal veins can lead to rupture and hemorrhage.

1. Lavage with normal saline solution
2. Endoscopy for ligation
3. Medications like Somatostatin, Octreotide, and Vasopressin
4. Inject vitamin K
5. Balloon tamponade

Hepatorenal Syndrome

Acute Renal Failure, Oliguria, and Hypotension may occur.

Same with management for Acute Renal Failure.

Hemorrhoids

Vasodilation of rectal veins.

1. Pain
2. Rectal bleeding
3. Feeling of rectal fullness

1. Liver Function Test
   • Alanine Amino Transferase (ALT)
   • Aspartate Amino Transferase (AST)
   • Alkaline Phosphatase
   • Gamma Glutamic Transferase
2. Prolonged Prothrombin Time
3. Increased Serum Biliburin
4. Abdominal Ultrasound
5. CT Scan
6. Esophagoscopy
7. Liver Biopsy (Confirmatory)

1. Diuretics like Spironolactone
2. Lactulose and Neomycin
3. Nadolol
4. Oxazepam
5. Ferrous Sulfate
6. Vitamin K

Nursing Diagnosis for Liver Cirrhosis

Excess Fluid Volume

1. Assess weight, abdominal girth, central venous pressure, and input/output.
2. Decrease fluid intake

Disturbed Thought Process

1. Assess levels of consciousness and neurologic status
2. Decrease protein diet

Ineffective Protection related to Decreased Coagulation Factor, Vitamin K, and Platelets

1. Monitor for signs of bleeding
2. Inject vitamin K when needed

Imbalanced Nutrition: Less Than Body Requirements

1. Increase caloric intake: Increase Carbohydrate and fiber/roughage. Decrease Protein and Sodium.

Causes of Anemia

• Blood loss
• Increase in red blood cell destruction (hemolysis)
• Defective or insufficient hemoglobin
• Decrease in red blood cell production

Signs and Symptoms of Anemia

• Pallor in the mucous membrane
• Difficulty on exertion
• Fatigue
• Poor concentration
• Dizziness

Pathophysiology of Anemia

Iron Deficiency Anemia (IDA)

Signs and Symptoms:

1. Cheilosis – a fissure in the corners of the lips.
2. Spoon-shaped nails
3. Diarrhea

Management for Iron Deficiency Anemia

• Iron supplement
• Administration of Dextran, intramuscularly with z track technique or deep subcutaneous. (To prevent skin discoloration)

Folic Acid Deficiency Anemia

Also called as Megaloblastic anemia.

Signs and Symptoms:

Neurologic manifestation: Paresthesia and proprioception

Management for Folic Acid Deficiency Anemia:

Oral supplements

Vitamin B12 Deficiency Anemia (Cyanocobalamin)

It is a macrocytic or megaloblastic anemia because of a decrease vitamin B12 diet.

Aplastic Anemia

Causes:

Use of Chloramphenicol, chemotherapeutic drugs, radiation, and substances like benzene and arsenic.

Pathophysiology of Aplastic Anemia

With the intake of the causes destruction of the bone marrow and are replaced by fats. This leads to fancytopenia that can lead to the decrease of red blood cells, white blood cells, and platelets.

Management:

• Remove the cause
• Immunosuppressants – Cyclosporine
• Blood transfusion

Thalassemia

Hemoglobin is genetically tranmitted. A defective hemoglobin chain can cause Beta Thalassemia Minor, Beta Thalassemia Major and Intrauterine Fetal Death.

Anemia due to Blood Loss

Acute blood loss leads to decrease circulating blood volume and decrease in normocytic, hormochromic anemia. Chronic blood loss leads to microcytic, hypochromic anemia.

Diagnostic Exam for Anemia

1. Complete Blood Count – Findings indicate a decrease hemoglobin, red blood cell, and hematocrit.
2. Schilling’s test – To assess for pernicious anemia versus megaloblastic anemia.
3. Peripheral blood smear
4. Serum Ferritin Level – decreased; Serum Total Iron Binding Capacity – increased

Cerebrovascular accident is considered a medical emergency and can cause permanent neurological damage and even death. Risk factors can include: age, hypertension, diabetes, high cholesterol, cigarette smoking, previous stroke or transient ischemic attack, and atrial fibrillation.

Classification of Cerebrovascular Accidents

Causes of Cerebrovascular Accidents

Cause of Acute Renal Failure

The causes for acute renal failure can be classified into three. Pre-Renal, Intra-Renal, and Post-Renal. Pre-Renal causes are cardiogenic shock, hemorrhage, excessive gastrointestinal fluid loss, dehydration, sepsis, anaphylaxis, and burns. Intra-Renal causes are acute glomerulonephritis, vasculitis, disseminated intravascular coagulation, rhabdomyolysis, metabolic imbalances, pyelonephritis, infections, toxin (aminoglycosides), NSAIDs, contrast medium, and dye. Post-Renal causes are calculi, stricture, cancer, and prostatic enlargement.

Types of Chronic Renal Failure

1. Decreased Renal Reserve – Glomerular Filtration Rate 50%. It is asymptomatic and azotemia.
2. Renal Insufficiency – Glomerular filtration Rate 20-50%.
3. End-Stage Renal Disease – Glomerular Filtration Rate <5%. Uremia is present. Signs of End-Stage Renal Disease
   • Uremic fetur
   • Uremic frost – skin is yellowish due to accumulation of metabolic wastes.
   • Anemia – decreased erythopoietin
   • Decreased platelets
4. Renal Failure – Glomerular Filtration Rate 10-20%, with positive signs.

Pathophysiology of Acute Renal Failure

Stages of Acute Renal Failure

1. Oliguric or Initiation = 1-3 weeks
   • Urine output less than 400mL per day.
   • Increased BUN, Creatinine
   • Hyperkalemia, Phosphatemia, Magnesemia
   • Hyponatremia
   • Edema
   • Hypertension
   • Metabolic acidosis = 4-6 weeks
2. Diuretic or Maintenance
   • Normal blood pressure, creatinine, BUN
   • Negative for edema
   • Hypokalemia
3. Recovery = 3-12 months

Management for Acute Renal Failure

1. Treat hyperkalemia
   • Sodium bicarbonate
   • Glucose
   • Insulin
   • Calcium chloride
   • Sodium Polysterene Sulfonate (Kayexalate): For the exchange of Sodium and Potassium in the gastrointestinal tract.
2. Treat hyperphosphatemia: Aluminum hydroxide (Amphojel)
3. Diuretics: Furosemide, Mannitol
4. Dopamine
5. ACE inhibitor: Captopril
6. Diet: Decreased Protein, increased Calcium
7. Fluids
8. Dialysis

Nursing Care Management for Acute Renal Failure

1. Excess Fluid Volume
   Nursing Care Management:
   • Weight, hourly check the urine output
   • BUN, creatinine
   • Restrict fluids and sodium
   • Offer hard candies and ice chips
2. Imbalanced Nutrition: Less Than Body Requirements
   Nursing Care Management:
   • Frequent small feedings
   • Ask the family members to join the patient in eating
   • Provide a high caloric or carbohydrate diet

Diagnostic Exam for Acute Renal Failure and Chronic Renal Failure

1. Urinalysis – Increased white blood cell, red blood cell, casts (cellular debris), and epithelial cells.
2. BUN, creatinine
3. Kidney, Ureter, Bladder Ultrasound
4. Intravenous Pyelogram
5. Complete Blood Count – Decreased hemoglobin, hematocrit, and red blood cells.
6. Blood Chemistry – Increased potassium, phosphorus, magnesium; decreased sodium and proteins

Management for Chronic Renal Failure

Dialysis

1. Severe fluid volume
2. Hyperkalemia
3. Uremia
4. Metabolic acidosis

• Hemo-connection: A-V Fistula is the preferred site. Nurses should watch out for disequilibrium syndrome due to increased intracranial pressure. Signs and symptoms for disequilibrium syndrome are headache and levels of consciousness changes. Nurses should also monitor for signs of infection at the site of insertion, hypotension, and chills.
• Peritoneal dialysis – dialysing surface

Pathophysiology of Pyelonephritis

Pyelonephritis most often occur in children with vesicoureteral reflux, pregnant women, and people who experience lower urinary tract infection. The infection then ascend causing the inflammation of the renal pelvis. It in turn produces edema of renal pelvis.

Signs and Symptoms of Pyelonephritis

• Flank pain
• High fever with chills
• Positive kidney punch (Costovertebral angle tenderness)
• Frequency in urination
• Urgency
• Dysuria
• Hematuria

Diagnostic Exam for Pyelonephritis

• Urinalysis presents with an increase in white blood cell count
• Urine culture
• Kidney, Ureter, Bladder Ultrasound

Management for Pyelonephritis

1. Urinary antibiotics
   • Nitrofurantoin – Given with meals, Rinse mouth to prevent from staining.
   • Trimethoprim-Sulfamethoxazole, Co-trimoxazole (Bactrim) – Given with meals.
2. Administer sulfonamides as ordered.
3. Administer urinary analgesic, Phenazopyridine (Pyridium). Medication discolors the urine into orange or red.
4. Increase oral fluid intake.
5. Decrease protein diet.
6. Acid ASH Diet.

Nursing Diagnosis for Pyelonephritis

Acute Pain

1. Apply warm moist packs.
2. Provide a warm Sitz bath.
3. Balance rest and activity.
4. Administer analgesic as ordered.

Pathophysiology of Appendicitis

Signs and Symptoms of Appendicitis

1. Anorexia
2. Epigastric pain (Periumbilical)
3. Right lower quadrant pain (McBurney’s area)
4. Nausea and vomiting
5. Diarrhea
6. Body malaise
7. Low grade fever
8. Sudden relief of pain (Signifies rupture of the appendix)

Findings on Physical Examination for Appendicitis

1. Direct tenderness
2. Rebound tenderness
3. When hyperextension of the right thigh is performed, there is positive right lower quadrant pain (Psoas’ Sign)
4. Internal examination reveal that there is positive cervical tenderness

Diagnostic Exams for Appendicitis

1. Ultrasound – confirmatory diagnostic exam for appendicitis
2. Chest X-Ray – to rule out right lobar pneumonia
3. CBC – look for increased white blood cell count

Management for Appendicitis

• Administer IV Antibiotics.
• Appendectomy.
• For ruptured appendix, an emergency explore laparotomy is performed. Peritoneal lavage is done with normal saline solution.

Nursing Diagnosis for Appendicitis

Acute Pain

1. Assess the severity and location of pain. If client presents with board-like rigidity and severe pain, suspect for peritonitis.
2. Administer analgesics after a diagnosis is made.
3. Assess the effectiveness of the analgesic given.
4. Position client in a supine position with thighs slightly flexed.

Risk for Infection

1. Administer antibiotics as ordered.
2. Practice aseptic technique.
3. Position client in right lateral semi-Fowler’s position post-operation for ruptured appendix to localize infectious process.

Blood pressure can be obtained by the formula BP= Cardiac output (CO) x Peripheral resistance (PR).

The determinants for cardiac output are blood volume and cardiac contractility. The determinants for peripheral resistance are:

1. Sympathetic Nervous System (SNS) – Baroreceptors affect the aortic arch and carotid sinus. Decreased blood pressure stimulation, increase in heart rate and cardiac output, leads to increased blood pressure.
2. Adrenal – Cathecholamines affect the medulla. Epinephrine and Norepinephrine increases the temperature, pulse, and respiration which then increases the blood pressure.
3. Renin Angiotensin Aldosterone System (RAAS) – The stimulation of the kidneys produces aldosterone and converts angiotensinogen. The release of aldosterone would then increase sodium retention and potassium excretion. this would then increase the blood pressure. Angiotensinogen is converted to angiotensin I which is then converted to angiotensin II which increases the temperature, pulse, and respiration, and would increase the blood pressure.
4. Anti Diuretic Hormone-Posterior Pituitary Gland – The stimulus, like hypovolemia, causes a decrease in the blood volume which then increases the ADH, that cause the re-absorption of water.

Pathophysiology of Hypertension

Risk Factors for the Development of Hypertension

1. Family history
2. Aging
3. Diet (increased saturated fats or low-density lipoprotein (LDL)
4. Central obesity
5. Smoking
6. Chronic alcoholism
7. Race

Medical Management for Hypertension

1. ACE Inhibitors – Captopril, Penindopril, Lisinopril. Mode of Action: Blocks the conversion of Angiotensin I to Angiotensin II, Decreases temperature, pulse, and respiration.
   Nursing Considerations:
   • Take orally before meals.
   • Adverse effects: Cough, first dose hypotension, and hyperkalemia.
   • Change position gradually.
2. Beta Adrenergic Blockers – Metoprolol, Propranolol. Mode of Action: Inhibits beta 1 receptors in the heart and decreases SNS.
   Nursing Considerations:
   • Watch out for bradycardia.
3. Calcium Channel Blocker – Diltiazem, Verapamil, Nifedipine, Nimodipine. Mode of Action: Blocks the influx of calcium ions across the cell membrane of the vascular tissue.
   Nursing Considerations:
   • Increase oral fluid intake.
   • Increase fiber intake.
4. Vasodilators – Hydralazine, Minoxidil. Mode of Action: Relaxation of the vascular smooth muscles.
   Nursing Considerations:
   • Systemic lupus erythematosus like symptoms.
   • Excessive growth of hair.
5. Centrally Acting Symphatolytics – Clonidine, Quanabenz, Quantacine, Methyldopa. Mode of Action: Stimulates the Angiotensin II receptors in the CNS, which decreases the SNS and then the blood pressure.
   Nursing Considerations:
   • Do not stop the medication suddenly.
6. Diuretics – Thiazides. Mode of Action: Prevents tubular re-absorption of Sodium and fluids.
   Nursing Considerations:
   • Take in the morning.
   • watch out for dehydration.
7. Angiotensin II Receptor Blockers – Losartan, Landesartan. Mode of Action: Blocks the effect of Angiotensin II on the receptors.
8. Alpha Adrenergic Blockers – Prazosim, Terazosim. Mode of Action: blocks Alpha Adrenergic effects to the heart.

Prevention of Hypertension and Nursing Care Management for Hypertension

Lifestyle Modifications

1. Diet – Low sodium, Low fat diet.
2. Physical Activity – Aerobic (walking, jogging, swimming)
3. Avoid sedentary lifestyles.
4. Reduce weight and stress.
5. Stop smoking and limit alcohol intake to less than 15 mL per day.

Pathophysiology of Burns

Seen below is the pathophysiology of burns in flowchart form. It starts with a direct damage to the skin which stimulates several different reactions. It eventually leads to cell necrosis, acute renal failure, decreased urine output, no bowel sounds on the ileus, and Curling’s ulcer.

3 Zones:

• Zone of Coagulation – Area of direct damage. Site of the burned tissue. With coagulated skin.
• Zone of Stasis – Edematous tissues are found. There is an impairment of blood supply.
• Zone of Hyperemia – Outermost zone.

Types of Burns

1. First Degree Burns – Affects the epidermis only. It is erythematous, dry, and painful
2. Second Degree Burns – Affects the epidermis and a part of the dermis. It is moist, pinkish in color, is more painful than the first degree burn, and has vesicles or blisters.
3. Third Degree Burns – Affects the epidermis, dermis, and subcutaneous tissue. It is pearly white in color, with eschar, and in painless.
4. Fourth Degree Burn – Affects the epidermis, dermis, subcutaneous tissue, muscle and bone. It is charred and painless.

Stages of Burns

1. Shock (Emergent Phase) – First 48 hours. Features: Fluid shift (intravascular to interstitial spaces), Hypovolemia, Hemoconcentration (increased Hematocrit), Hyponatremia, Hyperkalemia, Generalized dehydration, Oliguria, and Metabolic Acidosis.
2. Diuretic (Acute Phase) – Occurs on the third to fourth day. Features: Fluid shift (interstitial to intravascular), Hypervolemia, Hemodilution (decreased Hematocrit), Hyponatremia, Hypokalemia, Diuresis (polyuria), and Metabolic acidosis.
3. Recovery Phase – Occurs on the fifth day onwards. Features: Hypocalcemia (used up for tissue regeneration), Negative nitrogen balance (increased protein break down), and Hypokalemia.

Management for Burns

Assess the Severity of Burns

1. Rule of Nines – Total Body Surface Area
   • 9% for the head
   • 9% for the right arm
   • 9% for the left arm
   • 18% for the anterior trunk
   • 18% for the posterior trunk
   • 1% for the groin
   • 18% for the right thigh and leg
   • 18% for the left thigh and leg
2. Age-Specific Burn Chart

1. Burn depth – 3rd to 4th degree: Full thickness burns, Severe; 1st to 2nd degree: Partial thickness burns
2. Location of Burns
3. Health condition
4. Age

Treat Minor Burns

TBSA <15% for <40 year old; TBSA <10% for >40 year old.

1. Initial Wound Care
   • Submerge the affected part in cool water.
   • Remove the clothes and cover or wrap affected area.
   • Flush with water every 20 minutes.
   • Irrigate the affected eye from inner to outer eye.
   • Do not apply neutralizing agents.
2. Tetanus Prophylaxis
3. Pain Management
4. Active Range of Motion exercises

Treat Major Burns

1. Maintain a patent airway and breathing
   • Administer 100% oxygen via face mask.
   • Place in Fowler’s position
   • Assess for difficulty of breathing. Check for sooty sputum, erythema, blisters, and singed hair; this indicates inhalation injury.
2. Prevent burn shock
   • Infuse Intravenous fluid (isotonic), Proximal to the burned site with 2 large bore intravenous needles.
3. Prevent Aspiration
   • Place in Fowler’s Position
   • Use Nasogastric Tube for decompression.
4. Wound Care
   • Do daily cleaning and dressing.
   • Irrigate with Normal Saline Solution.
   • Clean with sterile water and mild soap.
   • Apply Silver Sulfadiazine or Mafenide Acetate.
   • Cover with sterile gauze.
   • Debridement – removal of loose non-viable tissue.
5. Prevent Tissue Ischemia
   • Elevate the affected part above the heart level to decrease edema.
   • Active and Passive Range of Motion exercises.
   • Escharotomy – Opening of the eschar.
   • Fasciotomy – to expand edematous layer.

Nursing Care Plan for Burns

1. Impaired Gas Exchange
   • Assess respiratory status every 2 to 4 hours
   • Deep breathing exercises
   • Fowler’s position
2. Ineffective Airway Clearance
   • Suction the secretion
   • Monitor Oxygen Saturation, Arterial Blood Gases
   • Assess for signs of Respiratory Distress (Crackles, difficulty of breathing, chest retraction)
3. Deficient Fluid Volume
   • Administer intravenous fluid as ordered
   • Monitor input and output
4. Ineffective Tissue Perfusion: Renal or Peripheral
   • Monitor the characteristics and amount of urine; Dark colored urine: Hemochromogens (Hemoglobin, Myoglobin)
   • Assess for CRT, peripheral pulses
5. Risk for Infection