Conditions of the Male Reproductive System and musculoskeletal system
PROSTATITIS
It is inflammation of the prostate gland.
It is often associated with lower urinary tract manifestations and symptoms of sexual discomfort and dysfunction.
INCIDENCE
The condition affects 5% -10% of men
It is the most common urologic diagnosis in men younger than 50years and the third most common such diagnosis in men older than 50 years.
RISK FACTORS
Stress
Neuromuscular factors
CAUSES
Infection
Bacterial – E. coli ( commonly caused bacteria, Klebsiella and Proteus species)
Fungi
Urethral stricture
BPH
Urethritis
Reflux of infected urine into the ejaculatory and prostatic duct
During cystoscopy
Catheterization
Infrequent or excessive sexual intercourse
TYPES
There are four types of prostatitis
Acute bacterial prostatitis or type I
Chronic bacterial prostatitis or type II
Chronic prostatitis/ chronic pelvic pain syndrome (CP/CPPS) or type III. It presents in more than 90% of cases.
Asymptomatic inflammatory prostatitis or type IV
CLINICAL MANIFESTATIONS
Asymptomatic in type II
Fever
Chills
Perineal prostatic pain
Suprapubic pain
Dysuria
Foul- smelling urine
Urinary frequency
Urinary hesitancy
Urinary urgency
Nocturia
Prostate tenderness
Low back or pelvic floor pain
Haematuria
Haemospermia ( usually in type II)
DIAGNOSIS
Physical (rectal) examination to reveal tender, painful and swollen prostate which is warm to touch
Prostatic fluid and urethral fluid for culture and sensitivity
Tissue biopsy for histology
Protein – specific antigen (PSA) - serum analysis and will show increased values- greater than 4.0 ng/Ml. However PSA values may increase after ejaculation.
Ultrasonography to detect any abnormality
Clinical history
MEDICAL EXAMINATION
The aim of treatment is to eradicate the causative organism and specific treatment is based on the type of prostatitis and on the results of culture and sensitivity testing of the urine.
Antibiotics for bacterial prostatitis. Eg. Ciprofloxacin and Trimethoprim-sulfamethoxazole
If patient is afebrile and has normal urinalysis:
Anti-inflammatory agents
Alpha- adrenergic blockers eg tamsulosin to promote bladder and prostate muscle relaxation
Analgesics
Supportive therapies include
Pelvic floor training
Physical therapy
Reduction of prostatic fluid retention by ejaculation through sexual intercourse or masturbation
Sitz baths to relief the pain associated with prostatitis
Stool softeners to prevent straining at stool and pressure on the prostate
Evaluation of sexual partners to reduce the possibility of cross infection
NURSING MANAGEMENT
Provide adequate rest to relieve perineal and prostatic pain
Reassurance and psychological support
Monitor vital signs regularly
Monitor intake and output
Regular weight monitoring
Assess level of pain and effective ways to manage them
Serve balance diet
Ensure adequate hydration at least 8 glasses of water a day to prevent straining at stools and to promote flushing of the urinary tract system
Administer prescribed medications and observe for side effects
Serve stool softeners and encourage hot sitz bath as prescribed
Personal hygiene
Exercise
Elimination
Health education
Instruct patient to complete prescribed antibiotic regimen
Encourage hot sitz baths 10-20 minutes several times in a day
Liberal fluid intake
Foods and fluids that increase prostatic secretions such as alcohol, coffee, cola, spices and tea must be avoided
During periods of acute inflammation, sexual intercourse must be avoided
Patient should avoid sitting for too long
Encourage use of stool softeners
Regular medical checkups at least 6 months to 1 year.
COMPLICATIONS
Septicaemia
Urinary retention
Epididymitis
BPH
Orchitis
Recurrent urinary tract infections
Prostate cancer
ORCHITIS
It is a rare, acute inflammatory response of one or both testes.
It may occur as a complication of systemic infection or as an extension of an associated epididymitis.
INCIDENCE
It occurs in approximately 30% of postpubertal men
AETIOLOGY
Idiopathic
Viral infection- mumps ( very common in children)
Bacterial- Neisseria gonorrhea, Chlamydia trachomatis etc
Epididymitis
Trauma
Chemical
Parasites
SIGNS AND SYMPTOMS
Fever
Chills
Nausea and vomiting
Mild to severe pain
Unilateral or bilateral testicular swelling
Unilateral or bilateral testicular tenderness
Penile discharge
Blood in semen
Elevated WBCs
DIAGNOSIS
Physical examination
Urinalysis
FBC to show leukocytosis
Urethral culture
CT scan
MEDICAL MANAGEMENT
Treatment is based on the causative organism whether bacteria or virus.
Antibiotics for bacterial orchitis
Anti- inflammatory agents
Analgesics
Supportive treatment for viral orchitis
Adequate rest
Elevation of the scrotum to promote lymphatic drainage
Ice packs to reduce scrotal oedema
Analgesic
Mumps vaccination for those who have not had mumps or received immunization
NURSING MANAGEMENT
Bed rest and comfort
Reassurance
Elevate scrotum to reduce oedema and promote lymphatic drainage
Check vital signs and record
Assess pain level and swelling
Serve balance diet
Administer prescribed medication
Personal hygiene
Health education
Apply ice packs to reduce scrotal swelling
Provide scrotal support (truss, strapping or testes roll)
Compliance and completion of medication
Regular checkup on sterility
Inform patient to avoid strenuous activities until symptoms subsides ( sexual activities, lifting etc)
Vaccination against mumps
COMPLICATIONS
Hydrocele
Sterility or infertility
Testicular ischaemia
EPIDIDYMITIS
It is an infection of the epididymis which usually spreads from an infected urethra, bladder or prostate
INCIDENCE
The incidence is less than 1 in 1000 males per year.
Prevalence is greatest in men 19 to 35 years of age
Acute epididymitis occurs bilaterally in 5% to 10% of affected patients
RISK FACTORS
Recent surgery or procedure involving the urinary tract
Involvement in high risk sexual practices
History of sexual transmitted diseases
History of urinary tract infections
History of prostate infection or enlarged prostate
Lack of circumcision
Presence of chronic indwelling urinary catheter
CAUSES
Trauma
Infections ( organisms can be isolated in 80% of cases) by E. coli, C. trachomatis and N. gonorrhea) eg
Gonorrheoa
Syphilis
Urethritis
Prostatitis
Urinary obstruction
Surgery eg prostatectomy
In rare cases, it may be secondary to distant infections such as pharyngitis or tuberculosis
PATHOPHYSIOLOGY
The organism/ infection moves in an upward direction through the urethra and the ejaculatory duct. It is then transported along the vas deferens to the epididymis causing the inflammation and the subsequent manifestations.
SIGNS AND SYMPTOMS
Low-grade fever
Chills
Nausea and vomiting
Heaviness in the affected testicle
Testicular tenderness
Patient complains of unilateral pain and soreness in the inguinal canal along the course of the vas deferens
Pain and swelling in the scrotum and the groin
Pyuria
Bacteriuria
Pain during intercourse and ejaculation
Blood in semen
Urinary frequency
Urinary urgency
Dysuria
Patient shows characteristics of waddle
DIAGNOSIS
Patient history
Physical examination
Urinalysis- pyuria and bacteruria
FBC – elevated white blood cell
Gram stain of urethral discharge ( series of gram stain is applied to the specimen and stained smear is examined under a microscope to isolate a bacteria- its size, colour and shape to identify bacteria type
HIV and syphilis testing in sexually active men
Urethral culture and sensitivity
CT scan
Ultrasonography
MEDICAL MANAGEMENT
Infiltration of the spermatic cord with a local anaesthetic agent to relieve pain within the 24 hours after onset of pain
Antibiotics eg Doxycycline and tetracycline
Analgesic
Steroids to stop the inflammatory action
Supportive treatment
Reduction in physical activity
Scrotal support and elevation
Application of ice packs
Sitz bath
NB – Urethral instrumentation is avoided. Eg catheter insertion
SURGICAL MANAGEMENT
Epididymectomy- excision of the epididymis from the testis. This is performed for patients with recurrent, refractory and incapacitating series of infection.
NURSING MANAGEMENT
Ensure adequate rest for patient
Reassurance and psychological support
Ensure scrotal elevation with folded towel or scrotal bridge to prevent traction on the scrotum, promote venous drainage and to relieve pain
Vital signs
Assess the level and the nature of pain
Observe for scrotal abscess formation( localized hot, reddened and tender area)
Balance diet
Copious fluid intake
Administer prescribed medications
Apply ice packs to the area to reduce swelling and pain
Personal hygiene
Elimination
Health education
Instruct patient to avoid straining, lifting and sexual stimulation until infection is under control
Treatment compliance
Early reporting and treatment of urinary tract infections
Application of ice packs to relieve pain
Use of safer sex methods like condom use and abstinence to prevent further infection associated with sexual activity
COMPLICATIONS
Infertility
Epididymo-orchitis
Scrotal abscess
Testicular atrophy
INFERTILITY AND STERILITY
Infertility is defined as a couple’s inability to achieve pregnancy after at least one year or regular unprotected sexual intercourse or coitus. It should be at least twice or three times in a week
TYPES OF INFERTILITY
Primary infertility
Secondary infertility
PRIMARY INFERTILITY
This type of infertility refers to a couple who has never had a child or conceived.
SECONDARY INFERTILITY
This is a type of infertility where at least the couple has had one had conception but currently the couple cannot achieve a pregnancy despite having unprotected sexual intercourse.
CAUSES
MALE FACTORS
Azoospermia or oligospermia
Impaired spermatogenesis: it may be due to
Testicular hyperplasia
Testicular malformation
Undescended testes
Testicular atrophy
Obstruction of the seminal tract may result from congenital anomalies such as urethral strictures
Infections such as orchitis, epididymitis, prostatitis, mumps, gonorrhea and urethritis
Defective delivery of sperm into the vagina may result from surgery of the bladder neck in conditions like hypospadias ( the urethra open is under the side of the pens) epispadia,(urethral open on the dorsal surface of the penis)
Physical factors and life style such as:
Excessive heat due to wearing of synthetic tight underwear increases scrotal temperature which results in decrease sperm production
Exposure to environment hazards and toxins such as glues volatile organic solvents e.g. pain, pesticides, chemical dust, etc.
Driving long distance
Staying in separate homes
Cigarette smoking decrease sperm count and sperm cell motility
Too much sex
Working for a long period near hot oven
Chronic alcohol abuse
Bathing too hot water
It may also be affected by varicoceles, varicose veins, around the testicle which decrease semen quality by increasing testicular temperature.
Exposure to excessive radiation
Inadequate vitamin C and Zinc in the diet
Autoimmunity
Priapism
Drugs such as antihypertensive, marijuana and antidepressant.
Systemic diseases such as diabetes mellitus, high blood pressure, stress thyroid disorders and adrenal disorders
Erectile dysfunction: it is the persistent inability of a man to achieve an erection which is adequate in terms of hardness and duration for satisfactory sexual intercourse so long as a man can achieve a hard enough erection to permit vaginal penetration with a long enough staying power to perform the sexual act till ejaculation is attained, he is judged to be potent. The number of rounds per session is irrelevant.
Ejaculation problems:
Premature ejaculation: - is an inability to control the ejaculatory response for at least thirty seconds following penetration.
Premature ejaculations becomes a fertility problem when ejaculation occurs before a man is able to fully insert his penis into his partner’s vagina
Retrograde ejaculation: - where semen is ejaculated into your bladder.
For a woman to conceive, intercourse must take place around the time when an egg is released from her ovary.
FEMALE FACTORS
Failure to ovulate (anovulation)
Pelvic factors such as:
Tubal diseases like salpingitis
Strictures in the fallopian tube
Blockage of the fallopian tube
Uterine factors such as fibroids and polyps
Pelvic inflammatory diseases
Uterine displacement or malformation
Endometriosis
Other factors like malnutrition, severe anaemia and anxiety
High vaginal PH (alkaline) or low vagina PH (acid).
Antibodies in the vagina which destroys the sperms.
Diseases like diabetes mellitus, uncontrolled with complications
Over- weight or underweight.
DIAGNOSTIC INVESTIGATIONS
Hysterosalpingography: to rule out uterine or tubal abnormalities
Laparoscopy :- to determine the patency of the tubes and other pelvic structures (ovaries, uterus)
Semen analysis: provide information about the number of sperm (density) percentage of moving forms, quality of forward movement and morphology( shape and form)
From 2 to 6mls of watery alkaline semen is normal, a normal count has 8 million sperm/ml.
Impregnation is lessened only when the count decrease to less than 2 million sperm/ml.
Ultrasound of the ovaries.
TREATMENT
Counseling for both couples
Couples are taught how to identify the most fertile phase in the woman’s cycle when intercourse is most likely to result in pregnancy.
Ovulation signs - temperature increase
Lower abdominal pain
Discharge of fluid ( which is sticky – like)
Failure to ovulate is treated by stimulation of ovulation using drugs; they are given from the 5th day of the menstrual cycle such as tablet clomiphene citrate 50mg daily x 5 days. Follicle stimulating hormone.
Tubal anastomosis is done in cases of blockage
Invitro fertilization (IVF) – this involves ovarian stimulation, egg retrieval, fertilization and embryo transfer
Artificial insemination – it is the deposit of semen into the female genital tract by artificial means.
Intracytoplasmic sperm injection (ICSI) – an ovum is taken out and a single sperm is injected through the zona pellucida through the egg membrane and into the cytoplasm of the oocyte. The fertilized egg is then transferred back to the donor.
Eating iron rich foods.
STERILITY
Is inability of a man to produce potent spermatozoa or inability to make a woman become pregnant (absence of living sperms in the semen)
IMPOTENCY: inability to sexually gratify a woman
CAUSES
MALE FACTORS
Impotency of long standing
Short curved penis
Undescended or atrophied testes
Defective seminal discharge
Semen is thin and odourless
On attempting intercourse penis relaxes
Spasms during intercourse.
FEMALE FACTORS
Acidic secretions especially lactic acid in the vagina -when semen is discharged all the sperms are destroyed as they cannot live in acidic medium
Depth of the vaginal cavity: the depth is equal to the length of her fingers, thus females with long middle finger requires long organ( a male organ 1 to 2 inches longer than her middle finger is quite sufficient
Having intercourse when both the partners are not willing
The correct posture during intercourse is also imperative
Intercourse taking place just after meals or taking plenty of water
Sexual meetings should never by arranged during menses
Taking diet which is sour or rich in acids
New growth such as fibroids, or cancers
Hypertrophy of the cervix
Too frequent intercourse
Dysmenorrhea
Hard work (less of sexual passion)
Imperforated hymen
Mental worries, grief, anxiety etc.
TREATMENT
SAME AS INFERTILITY
DISEASES OF THE MUSCLO-SKELETAL SYSTEM
METABOLIC DISODERS
GOUT
DEFINITION
It is a metabolic disorder characterized by increased serum uric acid concentration and deposition of urate crystals in synovial fluids and surrounding joint tissues OR
It is a disorder of purine metabolism characterized by elevated uric acid levels and deposition of urate (usually in the form of crystals) in the joints and other tissues.
The increased level of uric acid in the blood is referred to as hyperuricaemia. The uric acid combines with sodium to form a complete monosodium or uric crystals.
Historically the condition was associated with royalty and the rich people but has not been shown to be entirely true.
INCIDENCE
It affects more men than women
The incidence increases with age and body mass index turns to affect people 40 years and above
TYPES OF HYPERURICAEMIA
Primary hyperuricaemia
Secondary hyperuricaemia
CAUSES
PRIMARY HYPERURICAEMIA
In primary hyperuricemia, the elevated serum urate levels or the manifestations of urate deposition results from defective purine metabolism. It accounts for 90% of all cases of gout
AETIOLOGY
Hereditary
Excessive intake of purine foods eg shell fish, beef, herring, organ meats (liver, brain, kidney), beer from yeast, bean, vegetables, oat meal etc
Severe dieting or starvation
SECONDARY HYPERURICAEMIA
This occurs following another condition or treatment which results in either promotion of uric acid production (10% of cases) or uric acid underexcretion (90% of cases).
Polycythemia
Haemolytic anaemia
Leukaemia
Chronic renal disease
Diabetic ketoacidosis
Diabetes insipidus
Drugs example, diuretics, pyrazinamide, cyclosporine, ethambutol etc – cause uric acid under excretion
Alcoholism
PATHOPHYSIOLOGY
Hyperuricaemia that is above 7.0mg/dl leads to the deposition of monosodium urate crystals in the joints and tissues. This initiates an inflammatory response marking the beginning of gout attacks.
Following repeated attacks, there is accumulation of sodium urate crystals called tophi and they are deposited in peripheral areas of the body such as the great toe, the hands, kidneys and ears. The recovered crystals are coated with immunoglobin G leading to phagocytosis which shows as immunologic activity.
STAGES OF GOUT
There are in four stages.
Stage I – Asymptomatic hyperuricaemia
Stage II -Acute gouty arthritis
It occurs within 3-10 days. It is triggered by trauma, alcohol, dieting, medications, illness or surgical procedures.
There is sudden onset of redness, swelling and warmth over the affected joint. Its presentations turn to occur in the night and awakens patient from sleep because of the nature of the pain
Stage III- Intercritical gout
This stage presents with no symptoms from months to years
Chronic tophaceous gout.
It is first observed after 10 years. Tophi are palpable or visible in joints. Most common areas affected are the Achilles tendon, synovium, olecranium bursa, soft tissues, intra patella, aortic walls, heart valves, nasal and ear cartilages, eyelids, cornea and sclera. Urolithiasis and renal impairment may occur.
SIGNS AND SYMPTOMS
Severe joint pain
Redden joint
Swollen joint
Tenderness of the joint
Loss of joint function
Fever
Chills
Malaise
Hyperuricemia
Joint stiffness
Elevated WBC
Joint deformity
Inflamed metatarsophalangeal joint of the big toe ( 90% of cases)
Tophi evident on joints and cartilages
Ulceration of tophi with chalky discharge
PRECIPITATING FACTORS FOR ACUTE GOUTY ATTACK
Alcohol ingestion – increase pain and inflammation
Medications
Surgical stress
Illness
Trauma
Dieting
DIAGNOSIS
Clinical history
X-ray of the affected part
24 hour urine collection to reveal uric acid under excretion
Serum uric acid estimation to reveal hyperuricaemia
Polarized light microscopy of synovial fluid – uric acid crystals will be seen within the polymorphonuclear leukocytes in the fluid – definitive diagnosis of gouty arthritis
Synovial fluid for culture and sensitivity
Synovial fluid aspiration to find out deposition of monosodium urate crystals and elevated WBCs
MEDICAL MANAGEMENT
The aims of the management are to:
Reduce inflammation
Decrease the production of uric acid and
Promote the excretion of uric acid
Uricosuric agents to promote the excretion of uric acid and dissolve deposited urate . Eg Probenecid and Sulfiripyrazone
Allopurinol to correct hyperuricaemia and prevent renal calculi.
Administration of Colchicines or NSAIDS such as Indomethacin to reduce inflammation to relieve acute gouty attacks
Corticosteroids therapy
Copious fluid intake and adequate rest
NURSING MANGEMENT
Rest and comfort because of the joint pains
Provide bed cradles to lift the bed covers off the sensitive and painful inflamed joints.
Reassurance and psychological support
Relaxation and distraction techniques
Put patient in a comfortable position
Assess for the level of pain and pain relief pattern
Assess for swelling, redness, warmth and effusion at the joint
Observe for the appearance of tophi over the pinna and at joints
Monitor urine for uric acid levels
Monitor vital signs four hourly
Monitor intake and out -put and record
Daily weighing of patient
Explain to patient on the need for dietary restrictions
Encourage patient to avoid intake of high purine foods like organ meat, sardines and sweet breads
Encourage patient to avoid alcohol intake
Encourage patient to take in copious fluid to prevent formation of kidney stones
Administer prescribed medication following the rights of medication
Personal hygiene
Elimination
Exercise – ROM, alternate exercise with rest and passive and active exercises
Health education
Avoidance of obesity and fluctuations in weight
Avoidance of alcohol intake – it precipitates gout attacks through over production and decreased excretion of the urate
Intake of low purine diet like sardines, shellfish and organ meats
Avoid medications that increase uric acid levels such as aspirin and diuretics
Avoidance of stress and trauma that increases pain and inflammatory process
COMPLICATIONS
Urate nephropathy
Uric acid renal calculus
Deformity
OSTEOPOROSIS
DEFINITION
It is a metabolic bone disorder in which there is total reduction in bone mass. There is increased bone reabsorption (osteoclastic activity) than turnover of bones formation. It literally means “porous bones”.
INCIDENCE
It occurs more in women than men because of decrease in oestrogen with age.
It is projected that one of every two Caucasian women and one of every five men will have an osteoporosis-related fracture at some point in their lives.
It is the most prevalent bone disease in the world and most age-related metabolic bone disorder
CLASSIFICATION
Primary oesteoporosis
Secondary oestoeporosis
CAUSES
Primary osteoporosis- the cause is unknown but the following are considered predisposing factors
Genetics – family history or Caucasian or Asian
Age – advancing age and postmenopause
Sex- being female
Sedentary lifestyles – lack of exposure to sunlight , smoking
Diet – low calcium intake, low vitamin D intake
Secondary osteoporosis – results from medications or other conditions / diseases
Prolong corticosteroid therapy
Malnutrition
Liver disease
Alcoholism
Rheumatoid arthritis
Malabsorption syndrome
Hypothyroidism
Hyperparathyroidism
Cushing syndrome
Renal failure
Total immobilization
PATHOPHYSIOLOGY
In osteoporosis, normal homeostatic bone turnover is altered. The rate of bone resorption that is maintained by osteoclasts is greater than the rate of bone formation that is maintained by osteoblasts resulting in reduced total bone mass.
The bones then become progressively porous, brittle and fragile and fracture easily under stresses that would not cause the bone to break under normal circumstance. This causes compression fractures to commonly occur in the thoracic and lumbar spine, hip fractures and Colles’ fractures of the wrist
Age related loss begins after achievement of peak bone mass. Calcitonin which inhibits bone resorption and promotes bone formation decreases, oestrogen which inhibits bone breakdown decreases with aging
On the other hand parathyroid hormone increases with aging increasing bone turnover and resorption. These changes eventually lead to net loss of bone mass over time
CLINICAL MANIFESTATIONS
Asymptomatic until later stages
Fracture following minor trauma
Low back pains
Loss of height (widow’s stoop)
Stiffness
Weakness
Muscle spasms
Porous , brittle and fragile bones
Progressive curvature of the spine (kyphosis) or Dowager’s lump
DIAGNOSIS
X-ray of the bone to detect abnormality after there has been 25 % - 40% demineralization
Dual – energy x-ray absorptiometry (DXA) when thoracic vertebrae become wedge shape and lumbar vertebrae become biconcave – shows decreased bone mineral density
CT scan of the bone
Serum calcium, phosphorus and alkaline phosphate will be within normal limits but parathyroid hormone may be elevated
Bone biopsy – thin and porous bone
MEDICAL MANAGEMENT
Management is primarily on preventive basis
Analgesics for pain
Calcium ( caltrate, citracal) and vitamin D supplementation – first line medications for treatment and prevention along with Vitamin C to promote absorption
Hormone replacement therapy eg oestrogen and testosterone
Bisphosphonates – eg Alendronate (Fosamax) and Calcitonin to inhibit osteoclast activities
Calcitonin administration by nasal spray or subcutaneous or intramuscular
Nutritional therapy eg skim or whole vitamin D –enriched milk or foods high in calcium
SURGERY
Surgical intervention of hip fractures by joint replacement or closed or open reduction with internal fixation.
Percutaneous vertebroplasty or kyphoplasty ( injection of polymethylmethacrylate bone cement into the fractured vertebra, followed by inflation of a pressurized balloon to restore the shape of the affected vertebra)
NURSING MANAGEMENT
Ensure comfortable bed rest
Encourage patient to use firm mattress to prevent sagging and to relieve the patient of pain
Provide side rails to reduce the incidence of falling and fractures
Provide back braces to support the back
Provide walking sticks or walkers for patient
Assess pain level and means to manage it for patient
Monitor vital signs
Daily weighing of patient
Encourage diet rich in calcium and vitamin D and vitamin C
High fiber diet to prevent constipation associated with immobility and medications
Serve copious water due to calcium supplementation
Personal hygiene
Elimination
Exercise – to strengthen trunk muscle and improve balance
Walking, good body mechanics and good posture
Educate on attending physiotherapy sessions
Daily weight-bearing exercise ( walking) to promote bone formation
Avoid heavy lifting and carrying of heavy objects
Advice to prevent sudden bending and encourage gentle movements
Avoid alcohol and smoking
Exposure to sunlight
Prevention of falls in the elderly to prevent fractures
COMPLICATIONS
Fractures
Kyphosis
Chronic back pain from compression fractures
RHEUMATOID ARTHRITIS
DEFINITION
It is a chronic, systemic inflammatory condition of the synovial joint at the hyaline cartilage and synovial membrane characterized by pains, stiffness and decreased mobility.
It is an autoimmune disease where the reaction starts in the synovial tissue.
INCIDENCE
It occurs worldwide in 0.5% - 1% of the population and 3x common in females than males
It is common between the ages of 30 and 50
CAUSE
The actual cause is unknown
PREDISPOSING FACTORS
Advancing age
Hereditary- they inherit the rheumatoid factor
Environmental factors- Estein-Barr virus is believed to initiate an autoimmune response
PATHOPHYSIOLOGY
In rheumatoid arthritis, immune response starts in the synovial tissues then antigen stimulus activates monocytes and T-lymphocytes which produce immunoglobulin antibodies to form immune complexes.
Phagocytosis of the immune complexes lead to inflammation and production of leukotriene and prostaglandins which cause the transportation of white blood cells to produce collagenase to breakdown collagen in normal joints
This in turn leads to oedema, increased synovial tissue production and pannus (granular tissue), destruction of cartilages and the erosion of bones.
This further leads to loss of articular surface and joint motion. The muscles degenerate with loss of elasticity and contractility of the tendons and ligaments.
STAGES OF RHEUMATOID ARTHRITIS
STAGE ONE- There is synovitis which develops from congestion and oedema of the synovial membrane and joint capsule
STAGE TWO- There is the formation of pannus, a thickened layer of granulation tissue. Pannus invade cartilage and destroys joint capsule and bone
STAGE THREE- Fibrous ankylosis. It deals with invasion of pannus by fibrous tissue, scar tissue occluding joint space and eventually joint deformity.
STAGE FOUR- Fibrous tissue calcifies resulting in bony ankylosis and total immobility
CLINICAL FEATURES
Severe joint pains, swelling, warmth, erythema of joints
Loss of function of the joint
Joint stiffness in the mornings
It starts from small joints to larger joints
Difficult movement
The onset is bilateral and symmetrical
Hands and feet are deformed
Spongy or boggy joint
“Swan’s neck deformity”
Enlargement of lymph nodes
Rheumatoid nodules
Weight loss
Fatigue
Anaemia
Weakness
Anorexia
Fever
DIAGNOSIS
X-ray of the affected part – shows bony erosions and narrowed joint spaces
Synovial fluid analysis- to rule out increased volume and WBC and decreased viscosity
Synovial biopsy
MRI
ESR – elevated levels
FBC – decreased red blood cells
Rheumatoid factor (RF) positive in 70% -80% cases – it is a test to measure rheumatoid factor antibodies in the blood in response to the autoimmune reaction
Arthrocentesis –a procedure where syringe is used to draw synovial fluid from joint capsule- reveals synovial fluid that is cloudy, milky or dark yellow
Bone scan
Physical examination – rheumatoid nodules, swollen joint and stiffness of the joint
MEDICAL MANAGEMENT
NSAIDS eg cyclo-oxygenase 2 enzyme blockers to stop the action of cyclo-oxygenase involved in the inflammatory process
Methotrexate (Rheumatrex) – standard treatment for RA because of its ability to preventing joint destruction and long term disability
Corticosteroids injection
Analgesics
Antidepressants for depression and sleep deprivation eg amitriptyline and sertraline
Heat and cold application
Antibiotics for secondary bacterial infection
SURGICAL MANAGEMENT
Reconstructive surgery is done for persistent, erosive and painful rheumatoid arthritis
Synovectomy – excision of the synovial membrane
Tenorrhaphy – suturing of a tendon
Arthrodesis - surgical fusion of the joint
Arthroplasty – surgical repair and replacement of a joint
NURSING MANAGEMENT
Ensure bed rest and comfort to relieve the pain associated with the condition
Reassurance and psychological support
Monitor vital signs four hourly
Assess the level of pain, sleep disturbances, fatigue, altered mood and impaired mobility
Daily weight monitoring as there is weight loss associate with the condition
Apply cold or heat compresses to the affected joints
Serve normal diet but high in protein and iron for tissue build up and repair
Administer prescribed medications eg NSAIDS and methotrexate
Observe side effects of medications such as anaemia, rashes and GI disturbances
Vitamin supplementation
Maintain personal hygiene
Care for pressure areas especially the joint areas
Educate patient to avoid prolong standing
Teach patient to change positions in bed
Encourage patient to alternate rest with exercise- range of motion exercise to prevent the development of complications
Educate on use of splints
Educate on application of cold and heat
Encourage patient and family to get assistive devices such as raised toilet seat, zipper pulls and walker
Advise patient to see an occupational therapist or physiotherapist
COMPLICATIONS
Pericarditis
Contractures
Joint deformities
Anaemia
Felty’s syndrome( neutropenia, splenomegaly and deformity)
OSTEOMALACIA
It is a metabolic bone disease characterized by inadequate mineralization of bone leading to softened and fragile bones
CAUSES
Malabsorption syndrome
Deficiency of vitamin D (calcitriol) –primary defect
Excessive loss of calcium from the body
Gastrointestinal disorders eg. Celiac disease
Renal failure
Liver failure
Medications eg anticonvulsants-phenytoin
Malnutrition
CLINICAL MANIFESTATIONS
Brittle, soft and fragile bones
Pain
Tenderness
Change in the shape of the pelvic bone
Muscle weakness ( from decreased calcium)
Waddling or limping gait
High risk of fractures ( distal radius and proximal femur)
Kyphosis
Impaired growth
Bowed legs in later stages
DIAGNOSIS
X-ray – to locate generalized demineralization
Serum calcium estimation to show low levels of calcium and phosphorus
Urinalysis and levels of calcium will be low
Bone biopsy to show increased amount of osteoid – a demineralized , cartilaginous bone matrix which is sometimes referred to as “prebone”
MEDICAL MANAGEMENT
Treat the underlying medical condition
Analgesics for pain
Administration of vitamin D
Supplementation of calcium
Nutritional therapy – diet rich in vitamin D and calcium
SURGERY
Osteotomy to correct long bone deformity
Braces application
NURSING MANAGEMENT
Bed rest and comfort
Ensure good lightening system
Monitor levels of serum calcium regularly
Expose patient to early morning sunlight as a cholesterol substance present in the skin is transformed to vitamin D by the ultraviolet radiations
Provide a walker or walking stick to patient to prevent possible falls
Encourage patient to eat food rich in calcium and vitamin D eg. Fortified milk, eggs, cereals and chicken livers
Encourage passive exercise
Other routine and general nursing care
PREVENTION
Good nutrition
Adequate exposure to sunlight
Early reporting and treating of infections eg intestinal infections
Calcium supplementation
COMPLICATIONS
Kyphosis
Rickets
Hypercalcaemia
Fractures
It is inflammation of the prostate gland.
It is often associated with lower urinary tract manifestations and symptoms of sexual discomfort and dysfunction.
INCIDENCE
The condition affects 5% -10% of men
It is the most common urologic diagnosis in men younger than 50years and the third most common such diagnosis in men older than 50 years.
RISK FACTORS
Stress
Neuromuscular factors
CAUSES
Infection
Bacterial – E. coli ( commonly caused bacteria, Klebsiella and Proteus species)
Fungi
Urethral stricture
BPH
Urethritis
Reflux of infected urine into the ejaculatory and prostatic duct
During cystoscopy
Catheterization
Infrequent or excessive sexual intercourse
TYPES
There are four types of prostatitis
Acute bacterial prostatitis or type I
Chronic bacterial prostatitis or type II
Chronic prostatitis/ chronic pelvic pain syndrome (CP/CPPS) or type III. It presents in more than 90% of cases.
Asymptomatic inflammatory prostatitis or type IV
CLINICAL MANIFESTATIONS
Asymptomatic in type II
Fever
Chills
Perineal prostatic pain
Suprapubic pain
Dysuria
Foul- smelling urine
Urinary frequency
Urinary hesitancy
Urinary urgency
Nocturia
Prostate tenderness
Low back or pelvic floor pain
Haematuria
Haemospermia ( usually in type II)
DIAGNOSIS
Physical (rectal) examination to reveal tender, painful and swollen prostate which is warm to touch
Prostatic fluid and urethral fluid for culture and sensitivity
Tissue biopsy for histology
Protein – specific antigen (PSA) - serum analysis and will show increased values- greater than 4.0 ng/Ml. However PSA values may increase after ejaculation.
Ultrasonography to detect any abnormality
Clinical history
MEDICAL EXAMINATION
The aim of treatment is to eradicate the causative organism and specific treatment is based on the type of prostatitis and on the results of culture and sensitivity testing of the urine.
Antibiotics for bacterial prostatitis. Eg. Ciprofloxacin and Trimethoprim-sulfamethoxazole
If patient is afebrile and has normal urinalysis:
Anti-inflammatory agents
Alpha- adrenergic blockers eg tamsulosin to promote bladder and prostate muscle relaxation
Analgesics
Supportive therapies include
Pelvic floor training
Physical therapy
Reduction of prostatic fluid retention by ejaculation through sexual intercourse or masturbation
Sitz baths to relief the pain associated with prostatitis
Stool softeners to prevent straining at stool and pressure on the prostate
Evaluation of sexual partners to reduce the possibility of cross infection
NURSING MANAGEMENT
Provide adequate rest to relieve perineal and prostatic pain
Reassurance and psychological support
Monitor vital signs regularly
Monitor intake and output
Regular weight monitoring
Assess level of pain and effective ways to manage them
Serve balance diet
Ensure adequate hydration at least 8 glasses of water a day to prevent straining at stools and to promote flushing of the urinary tract system
Administer prescribed medications and observe for side effects
Serve stool softeners and encourage hot sitz bath as prescribed
Personal hygiene
Exercise
Elimination
Health education
Instruct patient to complete prescribed antibiotic regimen
Encourage hot sitz baths 10-20 minutes several times in a day
Liberal fluid intake
Foods and fluids that increase prostatic secretions such as alcohol, coffee, cola, spices and tea must be avoided
During periods of acute inflammation, sexual intercourse must be avoided
Patient should avoid sitting for too long
Encourage use of stool softeners
Regular medical checkups at least 6 months to 1 year.
COMPLICATIONS
Septicaemia
Urinary retention
Epididymitis
BPH
Orchitis
Recurrent urinary tract infections
Prostate cancer
ORCHITIS
It is a rare, acute inflammatory response of one or both testes.
It may occur as a complication of systemic infection or as an extension of an associated epididymitis.
INCIDENCE
It occurs in approximately 30% of postpubertal men
AETIOLOGY
Idiopathic
Viral infection- mumps ( very common in children)
Bacterial- Neisseria gonorrhea, Chlamydia trachomatis etc
Epididymitis
Trauma
Chemical
Parasites
SIGNS AND SYMPTOMS
Fever
Chills
Nausea and vomiting
Mild to severe pain
Unilateral or bilateral testicular swelling
Unilateral or bilateral testicular tenderness
Penile discharge
Blood in semen
Elevated WBCs
DIAGNOSIS
Physical examination
Urinalysis
FBC to show leukocytosis
Urethral culture
CT scan
MEDICAL MANAGEMENT
Treatment is based on the causative organism whether bacteria or virus.
Antibiotics for bacterial orchitis
Anti- inflammatory agents
Analgesics
Supportive treatment for viral orchitis
Adequate rest
Elevation of the scrotum to promote lymphatic drainage
Ice packs to reduce scrotal oedema
Analgesic
Mumps vaccination for those who have not had mumps or received immunization
NURSING MANAGEMENT
Bed rest and comfort
Reassurance
Elevate scrotum to reduce oedema and promote lymphatic drainage
Check vital signs and record
Assess pain level and swelling
Serve balance diet
Administer prescribed medication
Personal hygiene
Health education
Apply ice packs to reduce scrotal swelling
Provide scrotal support (truss, strapping or testes roll)
Compliance and completion of medication
Regular checkup on sterility
Inform patient to avoid strenuous activities until symptoms subsides ( sexual activities, lifting etc)
Vaccination against mumps
COMPLICATIONS
Hydrocele
Sterility or infertility
Testicular ischaemia
EPIDIDYMITIS
It is an infection of the epididymis which usually spreads from an infected urethra, bladder or prostate
INCIDENCE
The incidence is less than 1 in 1000 males per year.
Prevalence is greatest in men 19 to 35 years of age
Acute epididymitis occurs bilaterally in 5% to 10% of affected patients
RISK FACTORS
Recent surgery or procedure involving the urinary tract
Involvement in high risk sexual practices
History of sexual transmitted diseases
History of urinary tract infections
History of prostate infection or enlarged prostate
Lack of circumcision
Presence of chronic indwelling urinary catheter
CAUSES
Trauma
Infections ( organisms can be isolated in 80% of cases) by E. coli, C. trachomatis and N. gonorrhea) eg
Gonorrheoa
Syphilis
Urethritis
Prostatitis
Urinary obstruction
Surgery eg prostatectomy
In rare cases, it may be secondary to distant infections such as pharyngitis or tuberculosis
PATHOPHYSIOLOGY
The organism/ infection moves in an upward direction through the urethra and the ejaculatory duct. It is then transported along the vas deferens to the epididymis causing the inflammation and the subsequent manifestations.
SIGNS AND SYMPTOMS
Low-grade fever
Chills
Nausea and vomiting
Heaviness in the affected testicle
Testicular tenderness
Patient complains of unilateral pain and soreness in the inguinal canal along the course of the vas deferens
Pain and swelling in the scrotum and the groin
Pyuria
Bacteriuria
Pain during intercourse and ejaculation
Blood in semen
Urinary frequency
Urinary urgency
Dysuria
Patient shows characteristics of waddle
DIAGNOSIS
Patient history
Physical examination
Urinalysis- pyuria and bacteruria
FBC – elevated white blood cell
Gram stain of urethral discharge ( series of gram stain is applied to the specimen and stained smear is examined under a microscope to isolate a bacteria- its size, colour and shape to identify bacteria type
HIV and syphilis testing in sexually active men
Urethral culture and sensitivity
CT scan
Ultrasonography
MEDICAL MANAGEMENT
Infiltration of the spermatic cord with a local anaesthetic agent to relieve pain within the 24 hours after onset of pain
Antibiotics eg Doxycycline and tetracycline
Analgesic
Steroids to stop the inflammatory action
Supportive treatment
Reduction in physical activity
Scrotal support and elevation
Application of ice packs
Sitz bath
NB – Urethral instrumentation is avoided. Eg catheter insertion
SURGICAL MANAGEMENT
Epididymectomy- excision of the epididymis from the testis. This is performed for patients with recurrent, refractory and incapacitating series of infection.
NURSING MANAGEMENT
Ensure adequate rest for patient
Reassurance and psychological support
Ensure scrotal elevation with folded towel or scrotal bridge to prevent traction on the scrotum, promote venous drainage and to relieve pain
Vital signs
Assess the level and the nature of pain
Observe for scrotal abscess formation( localized hot, reddened and tender area)
Balance diet
Copious fluid intake
Administer prescribed medications
Apply ice packs to the area to reduce swelling and pain
Personal hygiene
Elimination
Health education
Instruct patient to avoid straining, lifting and sexual stimulation until infection is under control
Treatment compliance
Early reporting and treatment of urinary tract infections
Application of ice packs to relieve pain
Use of safer sex methods like condom use and abstinence to prevent further infection associated with sexual activity
COMPLICATIONS
Infertility
Epididymo-orchitis
Scrotal abscess
Testicular atrophy
INFERTILITY AND STERILITY
Infertility is defined as a couple’s inability to achieve pregnancy after at least one year or regular unprotected sexual intercourse or coitus. It should be at least twice or three times in a week
TYPES OF INFERTILITY
Primary infertility
Secondary infertility
PRIMARY INFERTILITY
This type of infertility refers to a couple who has never had a child or conceived.
SECONDARY INFERTILITY
This is a type of infertility where at least the couple has had one had conception but currently the couple cannot achieve a pregnancy despite having unprotected sexual intercourse.
CAUSES
MALE FACTORS
Azoospermia or oligospermia
Impaired spermatogenesis: it may be due to
Testicular hyperplasia
Testicular malformation
Undescended testes
Testicular atrophy
Obstruction of the seminal tract may result from congenital anomalies such as urethral strictures
Infections such as orchitis, epididymitis, prostatitis, mumps, gonorrhea and urethritis
Defective delivery of sperm into the vagina may result from surgery of the bladder neck in conditions like hypospadias ( the urethra open is under the side of the pens) epispadia,(urethral open on the dorsal surface of the penis)
Physical factors and life style such as:
Excessive heat due to wearing of synthetic tight underwear increases scrotal temperature which results in decrease sperm production
Exposure to environment hazards and toxins such as glues volatile organic solvents e.g. pain, pesticides, chemical dust, etc.
Driving long distance
Staying in separate homes
Cigarette smoking decrease sperm count and sperm cell motility
Too much sex
Working for a long period near hot oven
Chronic alcohol abuse
Bathing too hot water
It may also be affected by varicoceles, varicose veins, around the testicle which decrease semen quality by increasing testicular temperature.
Exposure to excessive radiation
Inadequate vitamin C and Zinc in the diet
Autoimmunity
Priapism
Drugs such as antihypertensive, marijuana and antidepressant.
Systemic diseases such as diabetes mellitus, high blood pressure, stress thyroid disorders and adrenal disorders
Erectile dysfunction: it is the persistent inability of a man to achieve an erection which is adequate in terms of hardness and duration for satisfactory sexual intercourse so long as a man can achieve a hard enough erection to permit vaginal penetration with a long enough staying power to perform the sexual act till ejaculation is attained, he is judged to be potent. The number of rounds per session is irrelevant.
Ejaculation problems:
Premature ejaculation: - is an inability to control the ejaculatory response for at least thirty seconds following penetration.
Premature ejaculations becomes a fertility problem when ejaculation occurs before a man is able to fully insert his penis into his partner’s vagina
Retrograde ejaculation: - where semen is ejaculated into your bladder.
For a woman to conceive, intercourse must take place around the time when an egg is released from her ovary.
FEMALE FACTORS
Failure to ovulate (anovulation)
Pelvic factors such as:
Tubal diseases like salpingitis
Strictures in the fallopian tube
Blockage of the fallopian tube
Uterine factors such as fibroids and polyps
Pelvic inflammatory diseases
Uterine displacement or malformation
Endometriosis
Other factors like malnutrition, severe anaemia and anxiety
High vaginal PH (alkaline) or low vagina PH (acid).
Antibodies in the vagina which destroys the sperms.
Diseases like diabetes mellitus, uncontrolled with complications
Over- weight or underweight.
DIAGNOSTIC INVESTIGATIONS
Hysterosalpingography: to rule out uterine or tubal abnormalities
Laparoscopy :- to determine the patency of the tubes and other pelvic structures (ovaries, uterus)
Semen analysis: provide information about the number of sperm (density) percentage of moving forms, quality of forward movement and morphology( shape and form)
From 2 to 6mls of watery alkaline semen is normal, a normal count has 8 million sperm/ml.
Impregnation is lessened only when the count decrease to less than 2 million sperm/ml.
Ultrasound of the ovaries.
TREATMENT
Counseling for both couples
Couples are taught how to identify the most fertile phase in the woman’s cycle when intercourse is most likely to result in pregnancy.
Ovulation signs - temperature increase
Lower abdominal pain
Discharge of fluid ( which is sticky – like)
Failure to ovulate is treated by stimulation of ovulation using drugs; they are given from the 5th day of the menstrual cycle such as tablet clomiphene citrate 50mg daily x 5 days. Follicle stimulating hormone.
Tubal anastomosis is done in cases of blockage
Invitro fertilization (IVF) – this involves ovarian stimulation, egg retrieval, fertilization and embryo transfer
Artificial insemination – it is the deposit of semen into the female genital tract by artificial means.
Intracytoplasmic sperm injection (ICSI) – an ovum is taken out and a single sperm is injected through the zona pellucida through the egg membrane and into the cytoplasm of the oocyte. The fertilized egg is then transferred back to the donor.
Eating iron rich foods.
STERILITY
Is inability of a man to produce potent spermatozoa or inability to make a woman become pregnant (absence of living sperms in the semen)
IMPOTENCY: inability to sexually gratify a woman
CAUSES
MALE FACTORS
Impotency of long standing
Short curved penis
Undescended or atrophied testes
Defective seminal discharge
Semen is thin and odourless
On attempting intercourse penis relaxes
Spasms during intercourse.
FEMALE FACTORS
Acidic secretions especially lactic acid in the vagina -when semen is discharged all the sperms are destroyed as they cannot live in acidic medium
Depth of the vaginal cavity: the depth is equal to the length of her fingers, thus females with long middle finger requires long organ( a male organ 1 to 2 inches longer than her middle finger is quite sufficient
Having intercourse when both the partners are not willing
The correct posture during intercourse is also imperative
Intercourse taking place just after meals or taking plenty of water
Sexual meetings should never by arranged during menses
Taking diet which is sour or rich in acids
New growth such as fibroids, or cancers
Hypertrophy of the cervix
Too frequent intercourse
Dysmenorrhea
Hard work (less of sexual passion)
Imperforated hymen
Mental worries, grief, anxiety etc.
TREATMENT
SAME AS INFERTILITY
DISEASES OF THE MUSCLO-SKELETAL SYSTEM
METABOLIC DISODERS
GOUT
DEFINITION
It is a metabolic disorder characterized by increased serum uric acid concentration and deposition of urate crystals in synovial fluids and surrounding joint tissues OR
It is a disorder of purine metabolism characterized by elevated uric acid levels and deposition of urate (usually in the form of crystals) in the joints and other tissues.
The increased level of uric acid in the blood is referred to as hyperuricaemia. The uric acid combines with sodium to form a complete monosodium or uric crystals.
Historically the condition was associated with royalty and the rich people but has not been shown to be entirely true.
INCIDENCE
It affects more men than women
The incidence increases with age and body mass index turns to affect people 40 years and above
TYPES OF HYPERURICAEMIA
Primary hyperuricaemia
Secondary hyperuricaemia
CAUSES
PRIMARY HYPERURICAEMIA
In primary hyperuricemia, the elevated serum urate levels or the manifestations of urate deposition results from defective purine metabolism. It accounts for 90% of all cases of gout
AETIOLOGY
Hereditary
Excessive intake of purine foods eg shell fish, beef, herring, organ meats (liver, brain, kidney), beer from yeast, bean, vegetables, oat meal etc
Severe dieting or starvation
SECONDARY HYPERURICAEMIA
This occurs following another condition or treatment which results in either promotion of uric acid production (10% of cases) or uric acid underexcretion (90% of cases).
Polycythemia
Haemolytic anaemia
Leukaemia
Chronic renal disease
Diabetic ketoacidosis
Diabetes insipidus
Drugs example, diuretics, pyrazinamide, cyclosporine, ethambutol etc – cause uric acid under excretion
Alcoholism
PATHOPHYSIOLOGY
Hyperuricaemia that is above 7.0mg/dl leads to the deposition of monosodium urate crystals in the joints and tissues. This initiates an inflammatory response marking the beginning of gout attacks.
Following repeated attacks, there is accumulation of sodium urate crystals called tophi and they are deposited in peripheral areas of the body such as the great toe, the hands, kidneys and ears. The recovered crystals are coated with immunoglobin G leading to phagocytosis which shows as immunologic activity.
STAGES OF GOUT
There are in four stages.
Stage I – Asymptomatic hyperuricaemia
Stage II -Acute gouty arthritis
It occurs within 3-10 days. It is triggered by trauma, alcohol, dieting, medications, illness or surgical procedures.
There is sudden onset of redness, swelling and warmth over the affected joint. Its presentations turn to occur in the night and awakens patient from sleep because of the nature of the pain
Stage III- Intercritical gout
This stage presents with no symptoms from months to years
Chronic tophaceous gout.
It is first observed after 10 years. Tophi are palpable or visible in joints. Most common areas affected are the Achilles tendon, synovium, olecranium bursa, soft tissues, intra patella, aortic walls, heart valves, nasal and ear cartilages, eyelids, cornea and sclera. Urolithiasis and renal impairment may occur.
SIGNS AND SYMPTOMS
Severe joint pain
Redden joint
Swollen joint
Tenderness of the joint
Loss of joint function
Fever
Chills
Malaise
Hyperuricemia
Joint stiffness
Elevated WBC
Joint deformity
Inflamed metatarsophalangeal joint of the big toe ( 90% of cases)
Tophi evident on joints and cartilages
Ulceration of tophi with chalky discharge
PRECIPITATING FACTORS FOR ACUTE GOUTY ATTACK
Alcohol ingestion – increase pain and inflammation
Medications
Surgical stress
Illness
Trauma
Dieting
DIAGNOSIS
Clinical history
X-ray of the affected part
24 hour urine collection to reveal uric acid under excretion
Serum uric acid estimation to reveal hyperuricaemia
Polarized light microscopy of synovial fluid – uric acid crystals will be seen within the polymorphonuclear leukocytes in the fluid – definitive diagnosis of gouty arthritis
Synovial fluid for culture and sensitivity
Synovial fluid aspiration to find out deposition of monosodium urate crystals and elevated WBCs
MEDICAL MANAGEMENT
The aims of the management are to:
Reduce inflammation
Decrease the production of uric acid and
Promote the excretion of uric acid
Uricosuric agents to promote the excretion of uric acid and dissolve deposited urate . Eg Probenecid and Sulfiripyrazone
Allopurinol to correct hyperuricaemia and prevent renal calculi.
Administration of Colchicines or NSAIDS such as Indomethacin to reduce inflammation to relieve acute gouty attacks
Corticosteroids therapy
Copious fluid intake and adequate rest
NURSING MANGEMENT
Rest and comfort because of the joint pains
Provide bed cradles to lift the bed covers off the sensitive and painful inflamed joints.
Reassurance and psychological support
Relaxation and distraction techniques
Put patient in a comfortable position
Assess for the level of pain and pain relief pattern
Assess for swelling, redness, warmth and effusion at the joint
Observe for the appearance of tophi over the pinna and at joints
Monitor urine for uric acid levels
Monitor vital signs four hourly
Monitor intake and out -put and record
Daily weighing of patient
Explain to patient on the need for dietary restrictions
Encourage patient to avoid intake of high purine foods like organ meat, sardines and sweet breads
Encourage patient to avoid alcohol intake
Encourage patient to take in copious fluid to prevent formation of kidney stones
Administer prescribed medication following the rights of medication
Personal hygiene
Elimination
Exercise – ROM, alternate exercise with rest and passive and active exercises
Health education
Avoidance of obesity and fluctuations in weight
Avoidance of alcohol intake – it precipitates gout attacks through over production and decreased excretion of the urate
Intake of low purine diet like sardines, shellfish and organ meats
Avoid medications that increase uric acid levels such as aspirin and diuretics
Avoidance of stress and trauma that increases pain and inflammatory process
COMPLICATIONS
Urate nephropathy
Uric acid renal calculus
Deformity
OSTEOPOROSIS
DEFINITION
It is a metabolic bone disorder in which there is total reduction in bone mass. There is increased bone reabsorption (osteoclastic activity) than turnover of bones formation. It literally means “porous bones”.
INCIDENCE
It occurs more in women than men because of decrease in oestrogen with age.
It is projected that one of every two Caucasian women and one of every five men will have an osteoporosis-related fracture at some point in their lives.
It is the most prevalent bone disease in the world and most age-related metabolic bone disorder
CLASSIFICATION
Primary oesteoporosis
Secondary oestoeporosis
CAUSES
Primary osteoporosis- the cause is unknown but the following are considered predisposing factors
Genetics – family history or Caucasian or Asian
Age – advancing age and postmenopause
Sex- being female
Sedentary lifestyles – lack of exposure to sunlight , smoking
Diet – low calcium intake, low vitamin D intake
Secondary osteoporosis – results from medications or other conditions / diseases
Prolong corticosteroid therapy
Malnutrition
Liver disease
Alcoholism
Rheumatoid arthritis
Malabsorption syndrome
Hypothyroidism
Hyperparathyroidism
Cushing syndrome
Renal failure
Total immobilization
PATHOPHYSIOLOGY
In osteoporosis, normal homeostatic bone turnover is altered. The rate of bone resorption that is maintained by osteoclasts is greater than the rate of bone formation that is maintained by osteoblasts resulting in reduced total bone mass.
The bones then become progressively porous, brittle and fragile and fracture easily under stresses that would not cause the bone to break under normal circumstance. This causes compression fractures to commonly occur in the thoracic and lumbar spine, hip fractures and Colles’ fractures of the wrist
Age related loss begins after achievement of peak bone mass. Calcitonin which inhibits bone resorption and promotes bone formation decreases, oestrogen which inhibits bone breakdown decreases with aging
On the other hand parathyroid hormone increases with aging increasing bone turnover and resorption. These changes eventually lead to net loss of bone mass over time
CLINICAL MANIFESTATIONS
Asymptomatic until later stages
Fracture following minor trauma
Low back pains
Loss of height (widow’s stoop)
Stiffness
Weakness
Muscle spasms
Porous , brittle and fragile bones
Progressive curvature of the spine (kyphosis) or Dowager’s lump
DIAGNOSIS
X-ray of the bone to detect abnormality after there has been 25 % - 40% demineralization
Dual – energy x-ray absorptiometry (DXA) when thoracic vertebrae become wedge shape and lumbar vertebrae become biconcave – shows decreased bone mineral density
CT scan of the bone
Serum calcium, phosphorus and alkaline phosphate will be within normal limits but parathyroid hormone may be elevated
Bone biopsy – thin and porous bone
MEDICAL MANAGEMENT
Management is primarily on preventive basis
Analgesics for pain
Calcium ( caltrate, citracal) and vitamin D supplementation – first line medications for treatment and prevention along with Vitamin C to promote absorption
Hormone replacement therapy eg oestrogen and testosterone
Bisphosphonates – eg Alendronate (Fosamax) and Calcitonin to inhibit osteoclast activities
Calcitonin administration by nasal spray or subcutaneous or intramuscular
Nutritional therapy eg skim or whole vitamin D –enriched milk or foods high in calcium
SURGERY
Surgical intervention of hip fractures by joint replacement or closed or open reduction with internal fixation.
Percutaneous vertebroplasty or kyphoplasty ( injection of polymethylmethacrylate bone cement into the fractured vertebra, followed by inflation of a pressurized balloon to restore the shape of the affected vertebra)
NURSING MANAGEMENT
Ensure comfortable bed rest
Encourage patient to use firm mattress to prevent sagging and to relieve the patient of pain
Provide side rails to reduce the incidence of falling and fractures
Provide back braces to support the back
Provide walking sticks or walkers for patient
Assess pain level and means to manage it for patient
Monitor vital signs
Daily weighing of patient
Encourage diet rich in calcium and vitamin D and vitamin C
High fiber diet to prevent constipation associated with immobility and medications
Serve copious water due to calcium supplementation
Personal hygiene
Elimination
Exercise – to strengthen trunk muscle and improve balance
Walking, good body mechanics and good posture
Educate on attending physiotherapy sessions
Daily weight-bearing exercise ( walking) to promote bone formation
Avoid heavy lifting and carrying of heavy objects
Advice to prevent sudden bending and encourage gentle movements
Avoid alcohol and smoking
Exposure to sunlight
Prevention of falls in the elderly to prevent fractures
COMPLICATIONS
Fractures
Kyphosis
Chronic back pain from compression fractures
RHEUMATOID ARTHRITIS
DEFINITION
It is a chronic, systemic inflammatory condition of the synovial joint at the hyaline cartilage and synovial membrane characterized by pains, stiffness and decreased mobility.
It is an autoimmune disease where the reaction starts in the synovial tissue.
INCIDENCE
It occurs worldwide in 0.5% - 1% of the population and 3x common in females than males
It is common between the ages of 30 and 50
CAUSE
The actual cause is unknown
PREDISPOSING FACTORS
Advancing age
Hereditary- they inherit the rheumatoid factor
Environmental factors- Estein-Barr virus is believed to initiate an autoimmune response
PATHOPHYSIOLOGY
In rheumatoid arthritis, immune response starts in the synovial tissues then antigen stimulus activates monocytes and T-lymphocytes which produce immunoglobulin antibodies to form immune complexes.
Phagocytosis of the immune complexes lead to inflammation and production of leukotriene and prostaglandins which cause the transportation of white blood cells to produce collagenase to breakdown collagen in normal joints
This in turn leads to oedema, increased synovial tissue production and pannus (granular tissue), destruction of cartilages and the erosion of bones.
This further leads to loss of articular surface and joint motion. The muscles degenerate with loss of elasticity and contractility of the tendons and ligaments.
STAGES OF RHEUMATOID ARTHRITIS
STAGE ONE- There is synovitis which develops from congestion and oedema of the synovial membrane and joint capsule
STAGE TWO- There is the formation of pannus, a thickened layer of granulation tissue. Pannus invade cartilage and destroys joint capsule and bone
STAGE THREE- Fibrous ankylosis. It deals with invasion of pannus by fibrous tissue, scar tissue occluding joint space and eventually joint deformity.
STAGE FOUR- Fibrous tissue calcifies resulting in bony ankylosis and total immobility
CLINICAL FEATURES
Severe joint pains, swelling, warmth, erythema of joints
Loss of function of the joint
Joint stiffness in the mornings
It starts from small joints to larger joints
Difficult movement
The onset is bilateral and symmetrical
Hands and feet are deformed
Spongy or boggy joint
“Swan’s neck deformity”
Enlargement of lymph nodes
Rheumatoid nodules
Weight loss
Fatigue
Anaemia
Weakness
Anorexia
Fever
DIAGNOSIS
X-ray of the affected part – shows bony erosions and narrowed joint spaces
Synovial fluid analysis- to rule out increased volume and WBC and decreased viscosity
Synovial biopsy
MRI
ESR – elevated levels
FBC – decreased red blood cells
Rheumatoid factor (RF) positive in 70% -80% cases – it is a test to measure rheumatoid factor antibodies in the blood in response to the autoimmune reaction
Arthrocentesis –a procedure where syringe is used to draw synovial fluid from joint capsule- reveals synovial fluid that is cloudy, milky or dark yellow
Bone scan
Physical examination – rheumatoid nodules, swollen joint and stiffness of the joint
MEDICAL MANAGEMENT
NSAIDS eg cyclo-oxygenase 2 enzyme blockers to stop the action of cyclo-oxygenase involved in the inflammatory process
Methotrexate (Rheumatrex) – standard treatment for RA because of its ability to preventing joint destruction and long term disability
Corticosteroids injection
Analgesics
Antidepressants for depression and sleep deprivation eg amitriptyline and sertraline
Heat and cold application
Antibiotics for secondary bacterial infection
SURGICAL MANAGEMENT
Reconstructive surgery is done for persistent, erosive and painful rheumatoid arthritis
Synovectomy – excision of the synovial membrane
Tenorrhaphy – suturing of a tendon
Arthrodesis - surgical fusion of the joint
Arthroplasty – surgical repair and replacement of a joint
NURSING MANAGEMENT
Ensure bed rest and comfort to relieve the pain associated with the condition
Reassurance and psychological support
Monitor vital signs four hourly
Assess the level of pain, sleep disturbances, fatigue, altered mood and impaired mobility
Daily weight monitoring as there is weight loss associate with the condition
Apply cold or heat compresses to the affected joints
Serve normal diet but high in protein and iron for tissue build up and repair
Administer prescribed medications eg NSAIDS and methotrexate
Observe side effects of medications such as anaemia, rashes and GI disturbances
Vitamin supplementation
Maintain personal hygiene
Care for pressure areas especially the joint areas
Educate patient to avoid prolong standing
Teach patient to change positions in bed
Encourage patient to alternate rest with exercise- range of motion exercise to prevent the development of complications
Educate on use of splints
Educate on application of cold and heat
Encourage patient and family to get assistive devices such as raised toilet seat, zipper pulls and walker
Advise patient to see an occupational therapist or physiotherapist
COMPLICATIONS
Pericarditis
Contractures
Joint deformities
Anaemia
Felty’s syndrome( neutropenia, splenomegaly and deformity)
OSTEOMALACIA
It is a metabolic bone disease characterized by inadequate mineralization of bone leading to softened and fragile bones
CAUSES
Malabsorption syndrome
Deficiency of vitamin D (calcitriol) –primary defect
Excessive loss of calcium from the body
Gastrointestinal disorders eg. Celiac disease
Renal failure
Liver failure
Medications eg anticonvulsants-phenytoin
Malnutrition
CLINICAL MANIFESTATIONS
Brittle, soft and fragile bones
Pain
Tenderness
Change in the shape of the pelvic bone
Muscle weakness ( from decreased calcium)
Waddling or limping gait
High risk of fractures ( distal radius and proximal femur)
Kyphosis
Impaired growth
Bowed legs in later stages
DIAGNOSIS
X-ray – to locate generalized demineralization
Serum calcium estimation to show low levels of calcium and phosphorus
Urinalysis and levels of calcium will be low
Bone biopsy to show increased amount of osteoid – a demineralized , cartilaginous bone matrix which is sometimes referred to as “prebone”
MEDICAL MANAGEMENT
Treat the underlying medical condition
Analgesics for pain
Administration of vitamin D
Supplementation of calcium
Nutritional therapy – diet rich in vitamin D and calcium
SURGERY
Osteotomy to correct long bone deformity
Braces application
NURSING MANAGEMENT
Bed rest and comfort
Ensure good lightening system
Monitor levels of serum calcium regularly
Expose patient to early morning sunlight as a cholesterol substance present in the skin is transformed to vitamin D by the ultraviolet radiations
Provide a walker or walking stick to patient to prevent possible falls
Encourage patient to eat food rich in calcium and vitamin D eg. Fortified milk, eggs, cereals and chicken livers
Encourage passive exercise
Other routine and general nursing care
PREVENTION
Good nutrition
Adequate exposure to sunlight
Early reporting and treating of infections eg intestinal infections
Calcium supplementation
COMPLICATIONS
Kyphosis
Rickets
Hypercalcaemia
Fractures
About Health Delivery
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