Venue: Parklane Hotel corner Archibishop Reyes and Escario St, Cebu City

The Association of Nursing Service Administrators of the Philippines (ANSAP) Cebu Chapter Inc. will observe its 19th founding anniversary simultaneously with its Annual Regional Convention.

Theme:
“Nurse Administrators: The Driving Force in the Health Care System”

Keynote Speaker:
Dr. Carmelita T. Villanobos, governor, PNA REgion VII will address the assembly with a a message focusing on the theme.

Registration fee is P800.

Foe more details, you may Dr. Alma B. Ungab, ANSAP Cebu Chapter president at tel 2532592 or cell no. 0917-4588853 Mrs. Leila Toledanes, over-all chairman at 2612100 or Lyrma S. Soledad, Board of Director at 2557141 local 123 and cell no. 0916-4829323

:)One of my classmates, before, asked me in YM the type of situation which somehow happened not only in the hospital — where I am working — but definitely occurred no matter how you mastered to monitor your patient. The question is, “If your patient got 50ng/dl after getting the patient’s blood glucose level. At that moment, happened to be the scheduled time for the next insulin dose or oral hypoglycemic agent (any of the two). Will you give the next dose?

The answer would be NO.

Your independent nursing action in this situation would be to let the patient eat simple carbohydrates: in the form of candies or orange juices.  You are not going to give OHA or insulin for the time being since they are compelled to make your blood glucose run to normal level or at least make your blood sugar be lowered. Record and report the findings should you omit the next dose to the attending physician.

I strongly admit there’s no other website which provides the accurate information about CFGNS than itself. CGFNS International (formerly the Commission on Graduates of  Foreign Nursing Schools) is an internationally recognized authority  on credentials evaluation and verification pertaining to the education, registration and licensure of nurses and health care professionals worldwide.

Source? hhmmm www.cgfns.org

About Credentials Evaluation Services? Follow these simple steps:

• Create your account
• Verify your account
• Login
• Click on the services at the sidebars
• Fill out  an account for CES form then request.  

Note: It’ll take a month for you to have your CES form. Goodluck Guys!

Musculoskeletal - Upload a Document to Scribd

Patient X presents with extensive destruction of knees, subcutaneous nodules, and exquisite pain in the metatarsophalangeal joint? Biopsy shows needle-like crystals. What is the diagnosis? gouty arthritis.

Assessment Findings

1. Severe pain in the involved joints, initially the big toe.

2. Swelling and inflammation of the joint

3. TOPHI - yellowish-whitish irregular deposits in the skin that break open and reveal a gritty appearance.

4. PODAGRA - big toe

5. Fever, malaise

6. Body weakness and headache

7. Renal stones

LABORATORY DIAGNOSIS

Even if the clinical appearance strongly suggests gout, the diagnosis should be confirmed by needle aspiration of acutely or chronically inflamed joints or tophaceous deposits. During acute gouty attacks, strongly birefringent needle- shaped MSU (Monosodium Urate) crystals with negative elongation are largely intracellular. Synovial fluid cell counts are elevated from 2000 to 60,000/µL. Effusions appear cloudy due to leukocytes, and large amounts of crystals occasionally produce a thick pasty or chalky joint fluid. Bacterial infection can coexist with urate crystals in synovial fluid; if there is any suspicion of septic arthritis, joint fluid must also be cultured. MSU crystals can often be demonstrated in the first metatarsophalangeal joint and in knees not acutely involved with gout. Arthrocentesis of these joints is a useful technique to establish the diagnosis of gout between attacks. Serum uric acid levels can be normal or low at the time of the acute attack, since lowering of uric acid with hypouricemic therapy or other medications limits the value of serum uric acid determinations for the diagnosis of gout. Despite these limitations, serum uric acid is almost always elevated at some time and can be used to follow the course of hypouricemic therapy. A 24-h urine collection for uric acid is valuable in assessing the risk of stones, in elucidating overproduction or underexcretion of uric acid, and in deciding which hypouricemic regimen to use. Excretion of 800 mg of uric acid per 24 h on a regular diet suggests that causes of overproduction of purine should be considered. Urinalysis, blood urea nitrogen, serum creatinine, white blood cell (WBC) count, and serum lipids should be obtained because of possible pathologic sequelae of gout and other associated diseases requiring treatment.

® Elevated levels of uric acid in the blood

• Uric acid stones in the kidney
• (+) urate crystals in the synovial fluid

As a summary:

• Elevated levels of uric acid in the blood
• Uric acid stones in the kidney
• (+) urate crystals in the synovial fluid

RADIOGRAPHIC FEATURES:

Cystic changes, well-defined erosions described as punched-out lytic lesions with overhanging bony edges [Martel’s sign, or G sign (G for gout)], associated with soft tissue calcified masses are characteristic radiographic features of chronic tophaceous gout. However, similar radiographic signs can also be observed in erosive osteoarthritis, destructive apatite arthropathies, and rheumatoid arthritis.

Medical management

1. Allupurinol- take it WITH FOOD : Rash signifies allergic reaction

2. Colchicine: For acute attack

3. Probenecid: For uric acid excretion in the kidney
TREATMENT

Acute Gouty Arthritis The mainstay of treatment during an acute attack is the administration of an anti-inflammatory drug such as colchicine, nonsteroidal anti-inflammatory drugs (NSAIDs), or glucocorticoids depending on the age of the patient and comorbid conditions. Both colchicine and NSAIDs may be quite toxic in the elderly, particularly in the presence of renal insufficiency and gastrointestinal disorders. In elderly patients, one may favor the use of intraarticular glucocorticoid injections for attacks involving one or two larger joints or ice pack applications along with lower oral doses of colchicine for gouty synovitis affecting small joints. Colchicine given orally is a traditional and effective treatment, if used early in the attack, in at least 85% of patients. One tablet (0.6 mg) is given every hour until relief of symptoms or gastrointestinal toxicity occurs, or a total of four to eight tablets may be given in accordance with the age of the patient. The drug must be stopped promptly at the first sign of loose stools, and symptomatic treatment must be given for the diarrhea. Intravenous colchicine is sometimes used and can reduce, though not eliminated, the gastrointestinal side effects. Intravenous colchicine is most reliable for pre- or postoperative prophylaxis in 1- to 2-mg doses when patients cannot take medications orally. Life-threatening colchicines toxicity and sudden death have been described with the administration of 4 mg/d intravenously. The intravenous dose for acute gouty arthritis is 1 to 2 mg given slowly through an established venous line over 10 min in a soluset, and two additional doses of 1 mg each may be given at 6-h intervals, but the total dose should never exceed 4 mg. NSAIDs are affective in 90% of patients, and the resolution of signs and symptoms usually occurs in 5 to 7 days. The most effective drugs are those with a short half-life and include indomethacin, 25 to 50 mg tid, ibuprofen, 800 mg tid, or diclofenac, 50 mg tid. Cyclooxigenase-2 highly selective inhibitors are probably equally effective but with less short-term gastrointestinal toxicity. Oral glucocorticoids such as prednisone, 30 to 50 mg/d as the initial dose and tapered over 5 to 7 days, a single intravenous dose of methylprednisolone, 7 mg of betametasone, or 20 to 40 mg of intraarticular triamcinolone acetonide have been equally effective. ACTH as an intramuscular injection of 40 to 80 IU in a single dose or every 12 h for 1 to 2 days is effective in patients with acute polyarticular refractory gout or with a contraindication for using colchicine or NSAIDs.

Hypouricemic Therapy Attempts to normalize serum uric acid to <300µmol/L (5.0 mg/dL) to prevent recurrent gouty attacks and eliminate tophaceous deposits entail a commitment to long-term hypouricemic regimens and medications that generally are required for life. Hypouricemic therapy should be considered when the hyperuricemia cannot be corrected by simple means (control of body weight, low-purine diet, increase in liquid ingestion, limitation of ethanol intake, and avoidance of diuretic use). The decision to initiate hypouricemic therapy is usually made taking into consideration the number of acute attacks, family history of gout, presence of MSU tophaceous deposits, uric acid excretion >800 mg per 24 hours, presence of uric acid stones, and risk for acute uric acid nephropathy during chemotherapy for myeloproliferative disorders. Uricosuric agents, such as probenecid, can be used in patients with good renal function who underexcrete uric acid, with 600 mg in a 24-hour urine sample. Urine volume must be maintained by ingestion of 1500 mL of water every day. Probenecid can be started at a dosage of 200 mg twice daily and increased gradually as needed up to 2 g in order to maintain a serum uric acid level 300µmol/L (5 mg/dL). Probenecid is the drug of choice to treat elderly patients with hypertension and thiazide dependence; however, probenecid is not effective with a renal creatinine clearance _1 mL/s. These patients may require allopurinol or benzbromarone, which is another uricosuric drug that is effective in patients with renal failure and who are receiving diuretics. Allopurinol is the best drug to lower serum urate in overproducers, stone formers, and patients with advanced renal failure. It can be given in a single morning dose, 300 mg initially and increasing up to 800 mg if needed. In most patients, it is not necessary to start at a lower dose; however, in patients with renal failure, the dosage should be adjusted depending on the serum creatinine concentration in order to minimize side effects. Patients with frequent acute attacks may require lower initial doses to prevent exacerbations. Toxicity of allopurinol has been recognized increasingly in patients with renal failure who use thiazide diuretics and in those patients allergic to penicillin and ampicillin. The most serious side effects include skin rash with progression to life-threatening toxic epidermal necrolysis, systemic vasculitis, bone marrow suppression, granulomatous hepatitis, and renal failure. Urate-lowering drugs should not be initiated during acute attacks. This is especially important in patients who have refractory acute arthritis or who had a flare-up previously with hypouricemic drugs. Colchicine prophylaxis in doses of 0.6 mg one to two times daily is usually continued, along with hypouricemic therapy, until the patient is normouricemic and without gouty attacks for 3 months. However, prophylactic colchicine treatment may be necessary as long as tophi are present. Recombinant urate oxidase uricase can be used in the short-term prophylaxis and treatment of chemotherapy-associated hyperuricemia in patients with lymphoproliferative and myeloproliferative disorders.

Drug-Induced Gouty Arthritis

Diuretics, aspirin, cytotoxics, cyclosporine, alcohol, ethambutol

Nursing Intervention

1. Provide a diet with LOW purine

Avoid Organ meats, aged and processed foods

STRICT dietary restriction is NOT necessary

2. Encourage an increased fluid intake (2-3L/day) to prevent stone formation

3. Instruct the patient to avoid alcohol

4. Provide alkaline ash diet to increase urinary pH

5. Provide bed rest during early attack of gout

6. Position the affected extremity in mild flexion

7. Administer anti-gout medication and analgesics

Incision and Drainage of an Abscess

Surgical release of septic fluid from a confined tissue space (compartment) in the body.

An abscess is a collection of fluid and inflamed or necrotic tissue, usually related to a bacterial infection in a confined tissue space. The fluid is comprised of leukocytes, serum, and local tissue exudates that cannot be locally absorbed, accumulating under pressure and spreading towards the tissue planes of least resistance. In superficial or even those presentations of deeper origin, the abscess “points” to the skin producing the classical signs of inflammation, swelling, heat, redness, and tenderness. Once an abscess develops, prompt drainage is required. This may occur spontaneously when pressure necrosis destroys the overlying skin, releasing the septic fluid, to relieve the symptoms and avoid dissection of additional areas. On occasion, the abscess contents are “sterile.” Any abscess, whether from a deep (e.g., ruptured viscus) or a superficial (e.g., puncture wound) source,must be drained. Rarely will antibiotics alone reverse the process without accompanying drainage. Abscesses affecting certain structures must be treated according to special anatomical considerations (e.g., acute tenosynovitis).

Procedure

After skin preparation, choice of anesthetic is influenced by the local consideration and the patient’s tolerance to pain. The prominence of the inflammatory swelling is incised, obviously necrotic tissue is excised, and, often, an ellipse of skin about the incision is excised to prevent premature closure of the wound. The depth of the wound is cleansed (may be irrigated with antibiotic agent of choice), and the wound is packed loosely with gauze stripping to facilitate drainage. If the origin of the abscess is deep, a drain may be inserted. These wounds are not closed; dressings or a fluid-collecting pouch is applied.

 Digoxin

Digitalis Glycosides exert positive inotropic effects through improved availability of calcium to myocardial contractile elements, thereby increasing cardiac output in CHF. In CHF, digoxin improves the symptoms of CHF but does not alter long-term mortality. Antiarrhythmic actions of digoxin are caused by an increase in AV nodal refractory period via vagal tone, sympathetic withdrawal, and direct mechanisms. Digoxin also exerts a moderate, direct vasoconstrictor action on arterial venous smooth muscle.

Missed Doses: Take this drug at regular intervals. If you miss a dose and is has been less than 12 hours since your dose was due, take it as soon as you remember. If it is about time for the next dose, take the dose only. Do not double dose or take extra.

Serum Levels: Therapeutic: 0.5 – 2.0 µg/L

Adverse Reactions: Arrhythmic, listed by decreasing prevalence, are premature ventricular beats, second- and third-degree heart blocks, AV junctional tachycardia, atrial tachycardia with block, ventricular tachycardia, and SA nodal block. Visual disturbances are related to serum level and occur in up to 25% of patients with digoxin intoxication. They include blurred vision, yellow or green tinting, flickering light or halos, or red-green color blindness. GI symptoms occur frequently and include abdominal discomfort, anorexia, nausea, and vomiting. CNS side effects occur frequently but are nonspecific, such as weakness, lethargy, disorientations, agitation, and nervousness. Hallucinations and psychosis have been reported. Rare reactions include gynecomastia, hypersensitivity, and thrombocytopenia.

Contraindications: hypertrophic obstructive cardiomyopathy; suspected digitalis intoxication; second- or third-degree heart block in the absence of mechanical pacing; atrial fibrillation with accessory AV pathway; ventricular fibrillation.

Drug Interactions: Beta-blockers can worsen CHF or digoxin-induced bradycardia. Potassium loss caused by amphotericin B or diuretic can contribute to digoxin toxicity. Spironolactone can decrease digoxin renal elimination. ACE inhibitors, amiodarone, bepridil, diltiazem, nitredipine, quinidine, and verapamin can increase digoxin levels. Oral antacids, kaolin-pectin, oral neomycin, and sulfasalazine can reduce digoxin absorption.

Paremeters to Monitor: Obtain serum levels only when compliance, effectiveness, or systemic availability is questioned or toxicity is suspected. Monitor HR, ECG for digoxin-induced arrhythmias, subjective complaints of toxicity, and renal function. Monitor serum electrolytes (especially potassium) frequently initially and then q 1-2 months when stabilized.

Toxicity: Treatment of severe or life-threatening digoxin toxicity should include IV Digoxin Immune Fab (Digibind). About 40 mg (one vial) of digoxin-specific Fab fragments binds 0.6 mg of the glycoside. Exact dosage can be calculated based on estimated total body stores.

TUBERCULOSIS

Agent:

• Mycobacterium Tuberculosis (human)
• Mycobacterium Africanum (human)
• Mycobacterium bovis (animal, cattle)

Transmission:

• Airborne, droplet
• Direct invasion through mucous membrane (rare)
• Ingestion of contaminated unpasturized milk

Communicability: As long as bacilli are present in the sputum

Susceptibility: 6-12 months after exposure

• Common among children below 3 y.o., adolescents, young adults and old age
• HIV infected patient, under weight, diabetics and substance abusers

Signs and Symptoms:

• Cough more than 2 weeks
• Loss of appetite and loss of weight
• Afternoon fever and night sweats
• Chest and back pain
• Hemoptysis

Diagnostic Exam:

• Sputum Exam (early morning sputum, 3x negative result = rule out)
• Chest X-ray
• Sputum, gastric culture
• Physical exam - TB symptomatics
• Mantoux Test - read after 48-72 hours: 10 mm or more = (+)

30mm or higher = suggestive of secondary infection

Treatment:

Category I:

• New pulmonary TB cases with (+) sputum exam
• Sputum (-) with chest x-ray of moderate to far advance TB
• Extra pulmonary TB (e.g. TB meningitis, intestinal TB, etc.)

A.      Intensive Phase (2 months)

• Rifampicin 450 mg
• Isoniazid (INH) 300 mg
• Pyrazinamide (PZA) 500 mg (2 tabs)
• Ethambutol 400 mg (2 tabs)

* Sputum exam if (+) add 1 month intensive treatment

B.      Maintenance Phase (4 months)

• Rifampicin
• Isoniazid

Category II:

• Relapses
• Failures
• Others (Resistant Cases)

A.      Intensive Phase (2 months)

• Rifampicin 450 mg
• Isoniazid 300 mg
• Pyrazinamide 500 mg (2 tabs)
• Ethambutol 400 mg (2 tabs)
• Streptomycin SO₄ 1gm (IM)

B.      Intensive Phase (1 month)

• Rifampicin
• INH
• PZA
• Ethambutol

* Sputum Exam: if (+) add 1 month of RIPE

C.      Maintenance Phase (5 months)

• Rifampicin
• Isoniazid
• Ethambutol

Category III:

• New TB cases who are sputum (-)
• New serious extrapulmonary TB cases

A.      Intensive Phase (2 months)

• Rifampicin 450 mg
• Isoniazid 300 mg
• Pyrazinamide 500 mg

B.      Maintenance Phase (2 months)

• Rifampicin
• Isoniazid

Contraindications/Complications:

• PZA (Pyrazinamide) - gouty arthritis
• Streptomycin Sulfate - pregnant women, can cause deafness and ringing of ears
• INH (Isoniazid) - cause peripheral neuritis
• Rifampicin - not indicated to patient with liver and renal damage; can cause red-orange urine

Other treatment programs:

• SR: Standard Regimen

(INH and Streptomycin)

• SCC: Short Course Chemotherapy

(Rifampicin, INH, PZA)

• DOTS: Direct Observed Treatment Short Course

(taking anti TB drugs under direct supervision of health worker)

Prevention:

1.       BCG vaccination

2.       IEC (Public Education)

3.       Improve social conditions

4.       Active, passive case finding and treatment

Being A Nurse
You will never be bored
You will always be frustrated
You will be surrounded by challenges.
So much to do and so little time
You will carry immense responsibility
And limited authority.
You will step into people’s lives
And you will make a difference.
Some will bless you,
Some will curse you.
You will see people at their worst
And at their best.
You will never cease to be amazed
At people’s capacity for
Love, courage, and endurance.
You will experience resounding triumphs
And devastating failures.
You will cry a lot.
You will laugh a lot.
You will know what it is to be human
And to be humane.

CLEFT LIP AND CLEFT PALATE

Incomplete closure of the lip and palate or root of the mouth.

Etiology: The exact cause of the lip and palatal clefting is not known, but most experts feel that it is due to both genetic and environmental factors.

Related Causes: Genetic; Folic acid deficiency; steroid, exposure to TORCH.

Common problems:

• feeding difficulty

• infections - upper respiratory and ear

• speech defect (cleft palate)

• dental defect (nasal twang)

• altered normal body image

• respiratory distress

Treatment: Surgery

1. Cleft Lip: CHEILOPLASTY

2. Cleft palate: PALATOPLASTY - done before speech development.

Preoperative care:

• proper positioning especially during and after feeding - upright positioned

• burp or bubble the newborn more often

• feed the baby with the use cross cut large holed nipple or Breck feeder technique

• observe for signs of complication: Otitis Media

• For dental defects: Orthodontic exercise and surgery

• speech therapy

Postoperative care:

• Proper positioning: CL- supine or side lying; CP: prone

• Apply elbow restraint and release every 2 hours

• Give feeding with rubber tipped medicine dropper for cleft lip and paper cups and soup spoons for cleft palate

• Cleanse the wound with hydrogen peroxide

• Give post operative medications which include analgesic and antibiotic

• Avoid sucking, suctioning, blowing, pointed and sharp objects (spoon, fork, and straw)

• Make sure baby does not suck the LOGAN’S BAR OR BOW

Feeding an Infant with a Cleft:

Feeding an infant is important not only in providing nourishment, it also provides an intimacy and closeness for both the parent and the child. Infants with a cleft lip seldom have problems either by bottle or breast.

In babies with clefts of the hard palate, the opening in the roof of the mouth often causes difficulty in creating adequate pressure on the nipple, thus creating an inability to suck well enough to get adequate nourishment. Feeding the infant takes patience and practice.

During my school days, we recommended the use of soft squeezable plastic bottle like Mead Johnson with an orthodontic nipple such as Nuk. You can increase the flow by gently squeezing or putting pressure on the bottle. It is important to feed the infant before he/she becomes too hungry. Position the infant in an upright position with the head tilted back slightly. This position allows the milk to flow down into the throat and less into the nose. Infants with clefts do swallow more air and need to be burped frequently. At first, it may take extra time, but this will steadily decrease. Feeding time of the newborn varies from 20-30 minutes. When feeding takes longer than 45 minutes, the infant may be burning up calories necessary to gain weight.

Breast feeding the newborn with a cleft palate is often unsuccessful. Generally the infant cannot produce enough negative pressure to obtain ample breast milk to provide adequate nourishment. Using a breast pump to extract the milk and feeding the infant breast milk from squeezable bottle is recommended.