LARYNGITIS

LARYNGITIS

An inflammation of the mucosa of the larynx

CAUSES

v  Voice abuse musicians

v  Public speakers

v  Pastors

v  Inhalation of irritating gases e.g carbon monoxide

v  Sudden temperature changes

v  Immunosuppressant

SIGNS AND SYMPTOMS

v  Hoarseness of voice

v  Severe dry cough

v  Fever

v  Pain in the larynx

MANAGEMENT

v  Bed rest in warm room

v  Restrict speaking

v  Encourage other means of communication e.g whispering, writing and the use of a bell

v  Avoid or stop smoking

v  Analgesics eg paracetamol

v  Expectorants for cough

v  Copious fluid intakes

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SINUSITIS

SINUSITIS

It is inflammation of the mucosa membrane of one or more paranasal sinuses.

TYPES

1.     Acute Sinusitis: occurs suddenly with severe onset of symptoms

2.      Chronic Sinusitis: is a severe persistent or recurrent attack of sinusitis. It may persist for the rest of the person’s life.

CAUSES

1.      Common cold

2.      Viral infections

3.      Bacteria (staphylococcus, Aureus, Streptococcus, Pneumonia, Haemophillis influenza)

4.      Allergens

5.      Air pollution

6.      Inhalation of toxins

 SIGNS AND SYMPTOMS

v  Pain and pressure in the sinuses

v  Purulent nasal secretions

v  Red edematous nasal mucosa

v  Frontal headache

v  Maxillary sinuses: pain is referred to the lateral side of the nose and the upper part of the teeth.

v  Nasal congestion

v  Resonance of speech

v  Occipital pain

v  Fever

v  Epistaxis (nose bleeding)

v  Anosmia (unable to smell)

MANAGEMENT

ü  Analgesic: paracetamol for pain

ü  Avoid allergens if allergic reaction is suspected

ü  Antibiotics for bacterial causes

ü  Postural drainage and antrum wash out

     Provide warmth

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LEUKEMIA (BLOOD CANCER)

LEUKEMIA (CANCER OF BLOOD)

It is a malignant disorder of  blood and blood forming tissues (bone marrow, lymph system and spleen) characterized by a proliferation of abnormal white blood cells in the body.

PATHOPHYSIOLOGY

Leukemia occurs  as a result of a malignant transformation of the stem cells or communited precursors of leukocytes (white blood cells) causing bone marrow production of immature WBCs (white blood cells) that cannot function normally. The abnormal leukocytes proliferate rapidly by cloning instead of normal mitosis. They spread into the circulating system where they steadily replace normally functioning WBCs.

As this occurs, the protective lymphocyte functions as well as cellular and humeral immunity are reduced leaving the body vulnerable to infections. Bone marrow production of normal blood cells such as RED BLOOD CELLS (RBCs), and PLATELETS is affected resulting in anaemia (less haemoglobin in blood), thrombocytopenia (reduction of number of platelets in blood),leucopaenia (reduction in the number of WBCs), neutropenia (reduction in the number of neutrophils in blood) and abnormal bleeding.

TYPES OF LEUKEMIA

types of leukemia

There are two main types of leukemia. They are:

v  Acute leukemia

v  Chronic leukemia

ACUTE LEUKEMIA

Acute leukemia refers to proliferation of immature haemapoietic (WBCs, RBCs and PLATELETS) cells by cloning. This results from a malignant transformation of a particular type of leukocyte which replicates and expands by cloning. It can be divided into the following subtypes;

v  Acute Lymphoblastic/lymphocytes Leukemia (ALL)

This accounts for 25% of all childhood cancer and 75% of leukemia in children. The peak age of onset of leukemia  is two years. It is common in boys and Caucasians.

v  Acute Myelogenous Leukemia (AML)

Incidence increases with aging. It is common in adults within 60 to 70 years of age. It affects all ethnic groups. It can affect children. It accounts for about 85% of acute leukemia in adults. It has a sudden onset with rapid proliferation of myeloblasts which infiltrates other organs.    

CHRONIC LEUKEMIA

In chronic leukemia more mature WBCs are affected and the condition develops more gradually. It is rare in children. The subtypes of chronic leukemia include;

v  Chronic Myelogenous Leukemia/Chronic Granulocytic Leukemia

It accounts for about 15% of leukemia cases. It affects people of ages 25 to 60 years. It is caused by excessive development of mature neoplastic granulocytes in the bone marrow which moves into circulation and eventually infiltrates the liver and the spleen. The condition develops very slowly over several years.

v  Chronic Lymphocytic Leukemia

This affects older adults 50 to 70 years and accounts for 25% of leukemia cases, but make up about 85% of chronic leukemia. It is characterized by quite mature but dysfunctional lymphocytes especially B cells. The abnormal cells infiltrate the bone marrow, spleen and liver causing generalized lymphadenopathy (disease of the lymph nodes).

v  Hairy Cell Leukemia

This accounts for about 2% of leukemia in adults. It usually affects males over 40 years of age. It is a chronic disease characterized by proliferation of B lymphocytes that infiltrate the bone marrow and the spleen. The cells have hair-like projections on microscopic examination.

CLINICAL FEATURES

COMMON SYMPTOMS

v  Recurrent fever

v  Headache

v  Fatigue and weakness

v  Pallor

v  Anaemia

v  Malaise

v  Anorexia

v  Joint and bone pain

v  Bleeding tendencies eg gum bleeding, rectal bleeding

v  Enlargement of liver and spleen

v  Swollen lymph nodes

v  Frequent and unusual infections

v  Pain and tenderness in long bones

 CAUSES

There is no known cause of leukemia, however it’s predisposing factors include:

v  Genetic factors

v  Chromosomal changes/defects such as Down Syndrome

v  Ionizing radiations

v  Chemical agents such as benzene

v  Chemotherapeutic agents eg. Alkylating agents

v  Children with immunodeficiency

v  Exposure to viruses before or after birth

v  Smoking and tobacco use

DIAGNOSTIC INVESTIGATIONS

v  Cell Blood Count (CBC) will reveal thrombocytopenia, neutropenia and anaemia

v  Bone marrow aspiration  (biopsy) will reveal immature and abnormal lymphoblast

v  Serum electrolytes – increased uric acid, calcium, potassium and phosphorus

v  CT scan

v  Lumbar puncture/cerebrospinal fluid (CSF) test for spread

v  MRI of the brain

v  Lymph node biopsy

BONE MARROW

MANAGEMENT/MEDICAL/RADIATION/RADIOTHERAPY

Chemotherapy: this is done according to the following stages:

·        Induction

·        Consolidation

·        Continuation

·        Treatment

During the INDUCTION phase, the patient receives an intense course of chemotherapy that that is meant to causes a complete remission of the disease. Complete remission occurs when the patient has less than 5% of the bone marrow cells as blast cells and the peripheral blood counts are normal.

Once remission has been sustained for one month, the patient enters the CONSOLIDATION phase, during which she or he receives a modified course of chemotherapy to eradicate any remaining disease.

The CONTINUATION OR MAINTENANCE phase may continue for more than a year during which time the patient receives small doses of chemotherapy every 3 to 4 weeks.

TREATMENT of CNS leukemia is an essential component of therapy that has replaced irradiation which leads to significant CNS complications with intensive intrathecal and systemic chemotherapy for most patients. Some patient also need transfusions with blood component therapy to control infection and prevent bleeding and anemias.

Chemotherapeutic agents;

1.      Anthracycline [ idarubicin or daunorbicin] or anthracenedione [ mitoxantrone] combined for induction and remission

2.       Vincristine prednisone

Surgery

Bone marrow transplantation [ BMT] is an option for some patients.

Early BMTS were allogenic transplants using stem cells that had been harvested from bone marrows

 Nursing Management

Observation/observe and document the following;

1.      Response to chemotherapy or radiation treatments

2.      Emotional response to the diagnosis of cancer or the use of reverse isolation

3.      Comprehension of treatment plan, including care; Purpose and potential side effects of radiation and chemotherapy; bone marrow transplant

4.      Presence of complications; Infection, bleeding, poor wound healing, ineffective coping by the patient or significant others

5.      Observation and physical assessment every 3 hours for effect of drugs and bruising

6.      Monitor renal function [intake and output and specific gravity]

7.      Monitor dietary intake, vomiting and constipation

8.      Level of consciousness

Protection  From Injury and Infection

1.      Protect the patient from injury and infection. To limit the risk of bleeding hold firm pressure on all puncture wounds for at least 10 minutes or until they stop oozing.

2.      Limit the use of intramuscular injections and intravenous catheter placement when the patient is pancytopenic.

3.      Avoid taking rectal temperatures, using rectal suppositories, or performing a rectal examination.

4.      Use soft tooth brushes and sponges to prevent  injury

5.      Treat  pressure areas to prevent bed sores

6.      Turn client 2 hourly to prevent  complication related to pneumonia

7.      Ensure strict asepsis during nursing procedures such as wound dressing, drug administration feeding bathing and mouth care.

Psychological Care

1.      If the patient does not respond to treatment be honest about the patient’s prognosis.

2.      Determine from parents and relatives how much information they want to share with the client about a terminal disease.

3.      Work with the patient, significant others, and chaplain to help the patient plan for a terminal illness and achieve a compassionate death.

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G6PD/GLUCOSE 6 PHOSPHATE DEHYDROGENASE DEFICIENCY

G6PD/GLUCOSE 6 PHOSPHATE DEHYDROGENASE DEFICIENCY

G6PD is a Red Blood Cell (RBC) enzyme that acts as an initial catalyst in glycolysis (breakdown of glucose). G6PD is an X linked enzymopathy that directly affects the erythrocytes’ (RBCs) ability to resist oxidative damage. Consequently, when G6PD is reduced, there is a disease in glucose use by the RBCs. If  RBCs are exposed to oxidative foods and drugs,the metabolic needs of RBCs increase with older RBCs being damaged leading to haemolysis (breakdown of RBCs).

G6PD is common among Africans, African Americans, Mediterraneans and Jews.

Haemolytic crisis is triggered by viral and bacterial infections.

 

IF ONE PARENT IS A CARRIER

SIGNS AND SYMPTOMS

·        When the RBCs can no longer transport oxygen effectively throughout the body; a condition called haemolytic anaemia arises

·        Neonatal jaundice

·        Abdominal and back pain

·        Dizziness

·        Headache

·        Dyspnoea and palpitation

·        Sudden rise of body temperature and yellow colouring of skin and mucous membrane

·        Dark yellow-orange urine

·        Pallor, fatigue

·        General deterioration of physical condition

·        Heavy, fast breathing

·        Weak rapid pulse

DRUGS TO AVOID

MEDICATIONS

·        Ascorbic acid, isobutyl nitrite, chloramphenicol, isoniazid, choloquine, sodium sulfate, ciprofloxacin, naphthalene

·        Dapsone, oxidase urate, dopamine

·        Pacetamol, procainamide, probenecid, phenylbutazone, quinine, phenytoin

FOODS TO AVOID

FOODS TO AVOID EATING

·        All legumes

·        Blue berries

·        Soya products

·        Red wine

·        Soda water

·        Farm beans

MANAGEMENT

In severe cases the following measures will be initiated in the hospital;

·        Nasal oxygen administration

·        Physiotherapy

·        Bed rest

·        Folic acid

·        Blood transfusion

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SICKEL CELL DISEASE

 SICKEL CELL DISEASE

sickled red cells

It is a genetic, autosomal recessive disorder that results in abnormalities of the globin gene of the hemoglobin molecule of the red blood cells (RBCs)

Ø  TYPES

Ø  Sickle cell anemia (S S) – heterozygous

Ø  Sickel cell trait (S A)

Ø  Sickle cell (S C)

SICKEL CELL TRAIT (S A)

This is the most common form of sickle cell disease. The patient has one normal hemoglobin gene and one abnormal hemoglobin gene. The patient is a carrier of sickle cell anemia and rarely has symptoms of the disease.

SICKEL CELL (Hgb C)

This is the second most frequent type of sickle cell disease. The affected cells assume a C –shape instead of an S – shape.

SICKEL CELL ANEMIA (S S) HOMOZYGOUS

Is a hereditary hemoglobinopathy characterized by the complete replacement of the normal hemoglobin with abnormal hemoglobin (S S). It is very common among Africans, Africa Americans and Mediteterranean

PATHOPHYSIOLOGY

 The red blood cells (RBCs) that contain more hemoglobin S than hemoglobin A are more prone to sickling when they are exposed to decreased oxygen tension (saturated) in the blood. The cells become more enlongated (sickled), rigid, fragile and rapidly destroyed. The sickled cells have a short survival life span of about 30 to 40 days as compared to 120 days for normal RBCs. They also have a decreased oxygen carrying capacity and low hemoglobin amount and obstruct capillary blood flow. This leads to engorgement tissue ischemia and necrosis. The resultant tissue hypoxia (lack of oxygen) causes further sickling and ultimately large infarction and pain.

PRECIPITATING FACTORS FOR SICKEL CELL CRISIS

·         Hypoxia or deoxygenated of the RBCs

·         Viral or bacterial infections – most common

·         High altitude

·         Emotion or physical stress;  excessive exercise

·         Surgery and blood loss

·         Dehydration – vomiting, diarrhoea, or diaphoresis (severe sweating)

·         Cold

·         Fever

·         Menstruation

SIGNS AND SYMPTOMS

v  Children are usually asymptomatic until 4 to 6 months due to high amount of fetal hemoglobin

v  Growth retardation/failure to thrive

v  Enuresis (bed wetting)

v  Delayed puberty

v  Bossing of the forehead

v  Anemia

v  Pallor

v  Jaundice

v  Hepatomegaly

v  Chronic led ulcers

v  Aching in the joints

v  Menstrual changes

v  Headache

v  Convulsions

v  Fatigue

v  Retinopathy (eye problems)

v  Retinal detachment

v  Osteoporosis

v  Osteomyelitis

v  Spinal deformities

v  Hematuria (urinating blood)

DIAGNOSIS

v  Electrophoresis – determines the type of hemoglobin

v  Hemoglobin

v  RBCs survival time

v  Skeletal x-rays demonstrates bone, joint deformities and flattering

v  MRI, this test usually reveals cerebrospinal accidents

v  Sickle turbidity test (sickled)

SICKEL CELL CRISIS

Is the acute exacerbation of sickling

TYPES

VASO OCCLUSIVE CRISIS

Is the most common type that occurs suddenly due to occlusion of the blood vessels from sickled cells. It causes tissue hypoxia (lack of oxygen) and pain. It affects various body parts especially chest, back, abdomen and extremitries.

SIGNS AND SYMPTOMS

v  Fever

v  Pain

v  Tissue engorgement

SPLENIC/SEQUESTRATION CRISIS

It is caused by pooling of blood in the spleen. It is life threatening and can cause death.

SIGNS AND SYMPTOMS

v  Profound anemia

v  Hypovolemia (decrease blood supply)

v  Shock

APLASTIC CRISIS

Reduced production and increased destruction of the RBCs usually due to viral infectious or depletion of folic acid

HAEMOLYTIC CRISIS

This is due to rapid haemolysis

SIGNS AND SYMPTOMS

v  Anemia

v  Pallor

MANAGEMENT OF SICKEL CELL ANEMIA

v  It has no cure

v  Immediate treatment of infections e.g malaria

v  Prophylactic antibiotic treatment e.g penincillin

v  Glucose

v  Avoidance of precipitating factors

v  Genetic counseling

v  Bone marrow transplant

TREATMENT OF CRISIS

v  Vigorous analgesic treatment

v  Administration of oxygen

v  Blood transfusion for anemia

v  Bed rest to conserve oxygen

v  Iv fluids

PAIN MANAGEMENT

ü  Analgesics

ü  Massaging

ü  Rehydration; encourage oral fluid intake and administer prescribed Iv fluids

ü  Monitor intake and output of fluids

ü  Ensure adequate nutrition

COMPLICATIONS

ü  CVA (stroke)

ü  Acute chest syndrome

ü  Pneumonia

ü  Priapism (prolong painful erect penis)

ü  Sickle cell crisis

ü  Pulmonary hypertension

ü  Renal failure

ü  Congestive heart failure

ü  Liver cirrhosis

ü  Retinopathy

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