IMMUNULOGIC

AUTOIMMUNE DISEASES
MULTIPLE SCLEROSIS
 scattered patches of demyelination within the spinal
cord and brain

 Incidence: affects women more than men, usually

occurs from 20-40 years of age,
 more frequent in cool or temperate climates

 Cause is unknown; virus or an auto immune origin

 Characterized by remission and exacerbations

 sensitized T cells
 Blood brain barrier- ( in
normal condition it check
CNS for antigen ang then
leave)
 Remain in CNS
 Immune system attacks
 Inflammation that destroy
myelin sheet
 Plaques of sclerotic tissue
appear
 Interrupting transmission
of impulse
 Variety of manifestation
depending which nerve is
affected
Process of Demyelination
CAUSES  More women than men are
 Unknown affected=30-40y/o
 Genetics  Characterized with
 Environmental factors
REMISSIONS and
EXACERBATIONS
 Viral infections
 Exacerbation- new symptoms
 Autoimmune
appear and existing worsen
 Remission- symptoms decrease
or disappear
 Relapse- emotional and physical
stress
Symptoms- varied depend on the
lesion or combination of lesions
1. visual disturbance: blurred
vision, scotomas ( blind
spots), diplopia
2. Scanning speech,
dysphagia, impaired
speech
3. Respiratory paralysis
4. impaired sensation: touch,
pain, temperature, or
position sense; paresthesia
such as numbness ,
tingling
5. impaired motor function:
weakness, paralysis,
spasticity
6. impaired cerebellar function:
ataxic gait, intention
tremor,
7. bladder/ bowel: retention or
incontinence/ constipation
8. sexual impotence in the
male
9. euphoria
 CHARCOAT’S
TRIAD
 SCANNING SPEECH
 INTENTION
TREMORS
 NYSTAGMUS

Lhermmitte’s Sign- sudden

electric shock sensation
experienced in passive
flexion of the neck
Diagnostics
 MRI
 Visualized plaques
 Evaluate the effect of
the treatment
CSF analysis- increased
CHON; increased IgG
 MEDICAL
MANAGEMENT

 No cure existing problems

 To delay progression
 Manage chronic symptoms
 Treat acute exacerbation
MEDICINES
 ABC + R
 Beta 1a- (avorex)- decrease the appearance of
lesion (once a week- IM)
 Beta 1b-(betaseron) decrease frequency of relapse
(q other day- SQ)
 Glatiramen acetate (copaxone) decrease number
of lesion and relapse rate (q day SQ)
 Refib – to treat relapsing MS (3x a week SQ)
MEDICINES
 Antidepressants, opiates – seizures and pain
 Anticholinergic- mgt. of bowel control
 Alpha -Adrenergic bloclers
 Baclofen (lioresal) to treat spasm
 Valium- to treat spasm
 Vit C- to acidify urine- bacterial growth less
likely
NURSING DIAGNOSIS
 Impaired physical mobility related to
weakness, muscle paresis, spasticity
 \risk for injury and visual impairment
 Impaired urinary and bowel elimination
 Impaired speech and swallowing related to
cranial nerve involvement
NURSING DIAGNOSIS
 Disturbed thought process related to cerebral
dysfunction
 Ineffective coping related to uncertainty of course of
MS
 Impaired home maintenance management related
physical, psychological and social limits imposed by
MS
 Potential for sexual dysfunction related to spinal
cord involvement or psychological reactions to
conditions
NURSING INTERVENTION
 Weakness:
 muscle stretching and strengthening exercise
 assistive devices such as cane, walkers, rails, wheelchairs as
necessary
 Administer medication as ordered
 corticosteroids and prednisone
 for spasticity: diazepam or valium
 interferon:
 institute bowel / bladder program
 maintain urinary elimination
 administer urecholine
 perform intermittent catheterization as ordered
 force fluids to 3 l/day
 promote use of acid-ash foods
NURSING INTERVENTION
 prevent injury related to sensory problems:
 test bath water with thermometer
 avoid heating pads, hot water bottles
 inspect body parts frequently for injury
 make frequent position change
 avoiding the use of scatter rugs
 eat a balance diet including low-fat, high-fiber foods and
foods high in potassium
 discharge teaching includes:
 balance between activity and rest
 well balance diet
 fresh air and sunshine
 avoid fatigue, overheating or chilling, stress and infection
A client with multiple sclerosis lose control of bowel
and requires regular bowel
training. Which of the following measures would be
least likely helpful :

 a. eating a diet high in roughage

 b. setting a regular time for elimination
 c. raising toilet seat for easy access by wheelchair
 d. Ensuring fluid intake is equivalent to 1 liter per
day
GUILAN BARRE- SYNDROME
GRAVE’S DISEASE =parry’s do/
basedow’s do /toxic diffuse goiter
 Graves' disease is thought
to be an autoimmune
disorder of the thyroid
which causes over-
production of thyroid
hormones. Hallmarks of
the condition are bulging
eyes (exophthalmos), heat
intolerance, increased
energy, difficulty sleeping,
diarrhea and anxiety.
Grave’s Disease
Thyroid gland
 STIMULATED BY
THYROID STIMULATING
HORMONE (TSH)
 NEEDS IODINE TO
SYNTHESIZE HORMONE
 SECRETES:
 THYROXINE (T4)
 TRIIODOTHYRONIN
E (T3)
ENDOCRINE HORMONE FUNCTION
GLAND
Regulate metabolic rate
THYROID T3 & T4’
P,C,F metabolism

Regulate physical & mental

growth & development
Decrease serum Ca by
THYRO-
increasing bone deposition
CALCITONIN
Increaseserum calcium by
PARA- PTH
promoting bone decalcification
THYROID
THYROID DISTURBANCES
DIAGNOSTIC TESTS:
 B.M.R.- AMT OF O2 USED BY A PERSON @ A GIVEN TIME
 PBI – MEASURE IODINE LIBERATED IN THE BLOOD WITH
THYROID DAMAGE
 SERUM THYROXINE (T4), SERUM
TRIIODOTHYRONINE (T3), SERUM TSH
 BLOOD SERUM CHOLESTEROL
 RADIOACTIVE IODINE TESTS:
 T3 RED CELL UPTAKE
 RADIOACTIVE IODINE UPTAKE (I131
 THYROID SCAN
 Most common form of
hyperthyroidism or thyrotoxicosis
OTHER FORMS OF HYPERTHYROIDISM
 Toxic adenoma- small benign nodule in thyroid
gland
 Thyrotoxicosis factitia-results from ingestion of
thyroid hormone for thyrotropin suppression
 Functioning metastatic thyroid carcinoma- excess
production of thyroid hormone
 Subacute thyroiditis- granulomatous inflammation of
the thyroid producing transient hyperthyroidism
 Silent thyroiditis- transient form of hyperthyroidism
with no inflammatory symptoms
Causes…
 Graves disease is caused
by an abnormal immune
system response that
attacks the thyroid gland,
and causes too much
production of thyroid
hormones. Risk factors are
being a woman over 20
years old, although the
disorder may occur at any
age and may affect men as
well
Causes….
 Immunulogic
 Genetic
 DM type1
 Defect in T-lymphocyte function
 precipitated by excessive dietary intake of
iodine or possibly stress
Signs and Symptoms
 Enlarged thyroid resulting from increased stimulation or a
response to increased metabolic demand
 Nervousness
 Heat intolerance and sweating
 Weight loss despite increased appetite
 Frequent bowel movements
 Tremor and palpitations
 Exopthalmos-due to abnormal connective tissue deposition in
the orbit and extraocular muscles which can be visualized by
CT or MRI.
 EXOPHTHALMOS – ACCUMULATION OF FLUID IN THE
FAT PADS BEHIND HE EYEBAL

 LID LAG – PROMINENT PALPEBRAL FISSURE WHEN THE

PATIENT LOOKS DOWN

 THYROID STARE - (DARYMPLE’S SIGN)

– INFREQUENT EYE BLINKING

 JEFFREY’S SIGN
-FOREHEAD REMAINS SMOOTH WHEN ONE LOOKS UP
Other Signs and Symptoms

 Difficulty concentrating
 Moist, smooth warm flushed skin
 Increased RR, dyspnea on exertion and at rest
 Excessive oral intake with weight loss
 Amenorrhea
 AF, dysrhythmia – caused by excessive
amount of thyroid hormone
 oesteoporosis
 Thyrotoxicosis can lead to thyroid
storm ,
A life threatening emergency that can have
cardiac, hepatic and renal consequences.
Signs and Symptoms of thyroid storm..
 Extreme irritability, hypertension
 High fever (up to 41.1 C)
 Tachycardia, pulmonary edema, shock
 Tremors, emotional lability, confusion,
delirium, psychosis, apathy, stupor, coma
 Diarrhea, abdominal pain nausea and
vomiting ,jaundice, hyperglycemia
Complications….
 Muscle wasting, atrophy and paralysis
 Visual loss or diplopia
 Heart failure, arrhythmias
 Hypoparathyroidism after surgical removal of
thyroid
 Hypothyroidism after radioiodine treatment
Diagnosis….
 Depends on careful clinical history and
physical examination, a high index of
suspicion and routine hormone
determinations.
 Confirmatory test includes:
1. Radioimmunoassay showing increased
serum T4 and T3 levels
3.Thyroid scan showing increased uptake of
radioactive iodine
4. Ultrasonography
Treatment
 Antithyroid drugs
 Single –oral dose of radioactive iodine –
treatment of choice for patients not planning
to have children (Concentrates on the gonads,
informed consent is needed)
 Surgery
ANTITHYROID DRUGS
 LUGOL’S SOLUTION
(POTASSIUM IODIDE)
 DECREASE THYROID VASCULARITY
 INHIBIT IODINE RELEASE
 DILUTED IN MILK / JUICE
 STAINS THE TEETH- USE STRAW
 THIOUREA & DERIVATIVES
(PTU,METHIMAZOLE)
 BLOCK THYROID HORMONE RELEASE
 TOXIC SIGNS: FEVER, SORETHROAT, LEUKOPENIA
 RADIOACTIVE IODINE
 PATIENT IS ISOLATED FOR 3 DAYS
 BETA BLOCKERS
 PROPANOLOL
NURSING DIAGNOSIS
 Imbalance nutrition; less than body requirements
related to exaggerated metabolic rate, excessive
appetite, and increased gastrointestinal activity
 Ineffective coping related to irritability,
hyperexcitability, apprehension and emotional
instability
 Low self esteem related to changes in appearance,
excessive appetite and weight loss
 Altered body temperature
NURSING INTERVENTIONS
 Improve nutritional status
 Enhancing coping measures
 Improving self esteem
 Maintaining body temperature
 Monitoring and managing complication
 Promoting home and Community-based care
EVALUATION
 Improves nutritional status
 Demonstrates effective coping method in
dealing with family, friends and co-workers
 Achieves increased self esteem
 Maintain normal body temperature
 Absence of complication
THYROID DISTURBANCES
HYPOTHYROIDISM HYPERTHYROIDISM

CRETINISM- infants, GRAVE’S DSE or

young children Exophthalmic goiter
HYPOTHYROIDISM
WITHOUT MYXEDEMA-
atrophy/ destruction of
thyroid gland
MYXEDEMA –adults
HYPOTHYROIDISM HYPERTHYROIDISM
Reduction in HEAT Increase heat
PRODUCTION
Failure of MENTAL &
PHYSICAL GROWTH
increased storage of C, P
Deranged C metabolism,
&F glycosuria
Abnormal collection of
Increase use of F & P as
WATER fuel
HYPOTHYROIDISM HYPERTHYROIDISM

SERUM
CHOLESTEROL:
INCREASED DECREASED

BMR:
DECREASED INCREASED

SKIN:
WARM, MOIST, FLUSHED
THICK, PUFFY, DRY
HAIR:
SOFT, SILKY
DRY, BRITTLE
HYPOTHYROIDISM HYPERTHYROIDISM
NERVOUS SYSTEM:
APATHETIC HYPERACTIVE

LETHARGIC LABILEMOOD
MAYBE HYPERSENSITIVE
HYPERIRRITABLE TENSED
SLOW CEREBRATION

WEIGHT:
INCREASED DECREASED

APPETITE:
DECREASED INCREASED
HYPOTHYROIDISM HYPERTHYROIDISM
MEDICAL: MEDICAL:
HORMONE REST
REPLACEMENT ANTITHYROID
DESSICATED THYROID DRUGS:
THYROGLOBULIN LUGOL’SSOLUTION
Na LEVOTHYROXINE THIOUREA DERIVATIVES
Na LYOTHYRONINE RADIOACTIVE IODINE

BETA-BLOCKERS

SURGICAL:
SUBTOTAL
THYROIDECTOMY
Myasthenia gravis
 is a neuromuscular
disorder characterized
by variable weakness
of voluntary muscles,
which often improves
with rest and worsens
with activity. The
condition is caused by
an abnormal
immune response
Causes, incidence, and risk factors
 weakness occurs when the
nerve impulse to initiate or
sustain movement does not
adequately reach the muscle
cells. This is caused when
immune cells target and
attack the body's own cells
(an autoimmune response).
This immune response
produces antibodies that
attach to affected areas,
preventing muscle cells from
receiving chemical messages
(neurotransmitters) from the
nerve cell.
ACETYLCHOLINE
 acetylcholine, often
abbreviated as ACh,
was the first
neurotransmitter to be
identified. It is a
chemical transmitter in
both the
peripheral nervous syst
em
(PNS) and
central nervous system
(CNS)
Causes…
 unknown.
 may be associated with
tumors of the thymus
 myasthenia gravis have a
higher risk of having
other autoimmune
disorders like
thyrotoxicosis ,
rheumatoid arthritis , and
systemic lupus
erythematosus
Symptoms new
 Vision changes:  Drooping head
 Double vision  Difficulty climbing stairs
 Difficulty maintaining steady  Difficulty lifting objects
gaze  Need to use hands to rise from
 Eyelid drooping sitting positions
 Patients with generalized disease  Difficulty talking
may also have:  Difficulty chewing
 Swallowing difficulty , frequent
gagging or choking  Additional symptoms that may
 Weakness or paralysis (may be associated with this disease:
worsen with exertion later in  Hoarseness or changing voice
the day)
 Muscles that function best after
 Fatigue
rest  Facial paralysis
 Drooling
 Breathing difficulty
DIAGNOSTICS
 Standard EMG results are
usually normal.
 Repetitive stimulation (type
of nerve conduction study )
is more sensitive.
 Single-fiber EMG is even
more sensitive.
 Acetylcholine receptor anti
bodies
may be present in the
blood. The
chemical compound
 A Tensilon test
TREATMENT
 There is no known cure
for myasthenia gravis.
However, treatment
may result in
prolonged periods of
remission.
TREATMENT
 Some medications, such as neostigmine or
pyridostigmine, improve the communication
between the nerve and the muscle. Prednisone
and other medications that suppress the
immune response (such as azathioprine,
cyclosporine, or mycophenolate mofetil) may
be used if symptoms are severe and there is
inadequate response to other medications
TREATMENT
 Plasmapheresis, a technique in which blood
plasma containing antibodies against the body
is removed from the body and replaced with
fluids (donated antibody-free plasma or other
intravenous fluids), may reduce symptoms
temporarily and is often used to optimize
conditions before surgery
TREATMENT
 Surgical removal of the
thymus (thymectomy)
may result in
permanent remission or
less need for medicines
Expectations (prognosis):
 There is no cure, but long-term remission is possible.
There may be minimal restriction on activity in
many cases. Patients that only have eye symptoms
(ocular myasthenia gravis), may progress to have
generalized myasthenia over time.
 Pregnancy is possible for a woman with myasthenia
gravis but should be closely supervised. The baby
may be temporarily weak and require medications
for a few weeks after birth but usually does not
develop the disorder.
COMPLICATION
 Restrictions on lifestyle (possible)
 Side effects of medications (see the specific
medication)
 Complications of surgery
 Myasthenic crisis (breathing difficulty), may
be life threatening
ANTICHOLINESTERASE
MEDICATIONS
 ACTION: Increase levels of acethycholine at
the myoneyral junction
 Medications
 Neostigmine bromide {Prostigmin}
 Pyridostigmine bromide {Mestinon, regonol}
 Edrophoniumchloride (tensilon}
 Side effects
 Sweating, salivation, nausea, diarrhea and
abdominal cramps, Bradycardia, hypertension.
INTERVENTION
 Administer medications on time
 Administer medications 30 minutes before
meals with milk and crackers to reduce
gastroinstinal upset
 Monitor and record muscle strength
 Note that excessive dose lead to cholinergic
crisis
 Have antidote (atropine sulfate) available
MYASTHENIA CRISIS
 Acute exacerbation of the disease
 Caused by rapid, unrecognized progression of the
disease, Inadequate amount of medication, infection,
fatigue or stress
 Increase RR,PR, Bp,, anorexia, cyanosis, bowel and
bladder incontinence, decrease urine output, absent cough
and swallow reflex
 Assess for myasthenia crisis
 Increase anticholinesterase medications
Cholinergic crisis
 Results in depolarization of the motor ends
plates
 Cause by overmedication of anti-
cholinesterase
 flaccid muscle paralysis
Cholinergic crisis
 Assessment
 Abdominal cramps, nausea, vomiting, diarrhea, blurred
vision,pallor, facial muscle twitching, hypotension,
pupillary miosis
 Interventions
 Hold anticholinesterase
 Prepare to administer antidote (atropine sulfate)
Tensilon test (Edrophonium)
 Test to diagnose
myasthenia gravis and
to differentiate
myasthnia crisis and
cholinergic crisis
 (+) - ↑ muscle strength
 (-) – no improvement
can even deteriorate
To differentiate….
 Myasthenia crisis  Cholinergic crisis
 Tensilon is  Tensilon is
administered and if administered and if
strength improves the weakness is more
client needs more severe, the client is
medication overmedicated,
administer atropine
sulfate, the antidote is
prescribed
NURSING MANAGEMENT
 Monitor respiratory status
 Monitor respiratory failure
 Maintain suctioning and emergency equipment
 Monitor vital signs
 Monitor speech and swallowing abilities to prevent
aspiration
 Encourage to sit up when eating
 Assess muscle status
Nursing management
 Instruct to conserve strength
 Monitor for myasthenic and cholinergic crisis]
 Administer anticholinesterase medications as
prescribed
 Instruct to avoid infection, stress, fatigue and
over the counter medication
 Instruct to wear Medic-Alert bracelet
ADDISON’S DISEASE
 disorder involving
disrupted functioning of
the part of the adrenal
gland called the cortex.
 This results in decreased
production of two
important chemicals
(hormones) normally
released by the adrenal
cortex: cortisol and
aldosterone
Description
 The adrenals are two
glands, each perched on
the upper part of the two
kidneys. The outer part of
the gland is known as the
cortex; the inner part is
known as the medulla.
Each of these parts of the
adrenal gland is
responsible for producing
different types of
hormones
Cortisol
 is a very potent hormone
produced by the adrenal
cortex. It is involved in
regulating the functioning
of nearly every type of
organ and tissue
throughout the body, and is
considered to be one of the
few hormones absolutely
necessary for life.
Cortisol is involved

 the very complex processing and

utilization of many nutrients,
including sugars (carbohydrates),
fats, and proteins
 the normal functioning of the
circulatory system and the heart
 the functioning of muscles
 normal kidney function
 production of blood cells
 the normal processes involved in
maintaining the skeletal system
 proper functioning of the brain and
nerves
 the normal responses of the immune
system
Aldosterone,
 produced by the adrenal
cortex, plays a central role
in maintaining the
appropriate proportions of
water and salts in the body.
 When this balance is
upset, the volume of blood
circulating throughout the
body will fall dangerously
low, accompanied by a
drop in blood pressure.
CAUSES:
 the destruction and/or shrinking (atrophy) of
the adrenal cortex.
 autoimmune disorder.
 PTB
 FUNGAL INFECIONS
 INVASION OF ADRENAL GLANDS BY
CANCERS
PATHOPHYSIO
 Adrenal gland under active
 Produce inadequate amounts of adrenal hormone
 Kidney unable to concentrate urine
 Excrete excessive urine , K retain, Na excrete
 Low serum Na and high serum K
 Dehydration
 Decrease blood volume
 SHOCK
PATHO
 Less corticosteroid
 Leads to sensitivity to insulin
 Blood sugar fall
 Prevents body from manufacturing CHO to CHON
 poor wound healing
 Weak mucles
 Hear unable to pump blood adequately
 Low BP
 SHOCK
PATHO- SKIN PIGMENTATION
 ADDISON’S DISEASE
 Pituitary gland produce more corticotropin in
attempt to stimulate adrenal glands
 Corticotropin also stimulates melanin
production
 Dark pigmentation of the skin and lining of
the mouth often develop
SYMPTOMS
 fatigue and loss of energy,
 decreased appetite,
 nausea, vomiting, diarrhea,
abdominal pain, weight
loss, muscle weakness,
dizziness when standing,
dehydration,
 unusual areas of darkened
(pigmented) skin, and dark
freckling. (areas un
exposed to sun)
Progression…
 very tanned, or bronzed skin,
with darkening of the lining of
the mouth, vagina, and rectum,
and dark pigmentation of the
area around the nipples (aereola)
 As dehydration becomes more
severe, the blood pressure will
continue to drop and the patient
will feel increasingly weak and
light-headed.
 Some may have psychiatric
symptoms, including depression
and irritability.
 Women lose pubic and underarm
hair, and stop having normal
menstrual periods.
DIAGNOSTICS
 Blood glucose and sodium
 K+
 WBC
 Plasma cortisol and urinaly 17
hydroxycorticosteroids
MEDICAL MANGEMENT
 Combat circulatory shock
 Hydrocortisone IV w/NSS
 Vasopressor
 Supplementary therapy during stress
 Supplementary intake with salt
 S
NURSING MANAGEMENT
 Prepare to administer glucocorticoids,
Hydrocortisone sodium succinate IV as prescribed
 Following resolution of the crisis, administer
glucocorticoid and mineralocorticoid orally as
prescribed
 Monitor VS/esp. BP
 Monitor nerological status noting irritability and
confusion
 Monitor laboratory values (Na, K+, BG)
NURSING MANAGEMENT
 Monitor intake and output
 Administer IV as prescribed
 Protect client for infection
 Maintain bed rest and provide quiet
environment
ULCERATIVE COLITIS
 is a disease that causes
inflammation and sores,
called ulcers, in the lining
of the rectum and colon.
 Ulcers form where
inflammation has killed the
cells that usually line the
colon, then bleed and
produce pus.
 Inflammation in the colon
also causes the colon to
empty frequently, causing
diarrhea.
 When the inflammation
occurs in the rectum and
lower part of the colon it is
called ulcerative proctitis.
If the entire colon is
affected it is called
pancolitis. If only the left
side of the colon is affected
it is called limited or distal
colitis.
 an inflammatory bowel disease (IBD), the general
name for diseases that cause inflammation in the
small intestine and colon. It can be difficult to
diagnose because its symptoms are similar to other
intestinal disorders and to another type of IBD called
Crohn’s disease. Crohn’s disease differs because it
causes inflammation deeper within the intestinal wall
and can occur in other parts of the digestive system
including the small intestine, mouth, esophagus, and
stomach.
 Ulcerative colitis can occur in people of any age, but
it usually starts between the ages of 15 and 30, and
less frequently between 50 and 70 years of age. It
affects men and women equally and appears to run
in families, with reports of up to 20 percent of
people with ulcerative colitis having a family
member or relative with ulcerative colitis or Crohn’s
disease. A higher incidence of ulcerative colitis is
seen in Whites and people of Jewish descent.
 2 types
 Acute
Glomerulonephritis-
occurs 2-3 weeks after
streptococcal infection
 Chronic
Glomerulonephritis-
occur after acute phase
Complications:
 Heart failure
 Hypertensive encephalophaty
 Pulmonary edema
 Renal failure
symptoms
 abdominal pain and
bloody diarrhea
 Gross hematuria
 Dark, smoky cola
colored or red brown
urine
 Protienuria
 High specific gravity
Symptoms:
 Low urinary Ph
 Oliguria or anuria
 Headache
 Pallor
 Edema in face, periorbital area, feet or generalized
 Shortness of breath, ascities, pleural effusion
 And CHF
Other manifestations
 anemia
 fatigue
 weight loss
 loss of appetite
 rectal bleeding
 loss of body fluids and
nutrients
 skin lesions
 joint pain
 growth failure (specifically
in children)
 About half of the people
diagnosed with ulcerative colitis
have mild symptoms.
 Others suffer frequent fevers,
bloody diarrhea, nausea, and
severe abdominal cramps.
 Ulcerative colitis may also cause
problems such as arthritis,
inflammation of the eye, liver
disease, and osteoporosis.
 It is not known why these
problems occur outside the
colon.
 Scientists think these
complications may be the result
of inflammation triggered by the
immune system. Some of these
problems go away when the
colitis is treated
 Many theories exist about what causes
ulcerative colitis. People with ulcerative
colitis have abnormalities of the immune
system, but doctors do not know whether
these abnormalities are a cause or a result of
the disease. The body’s immune system is
believed to react abnormally to the bacteria in
the digestive tract
DIAGNOSTICS
 Physical exam
 Blood exam-check for
anemia
 Colonoscopy or
sigmoidoscopy
 Barium Enema
 CT Scan
Medical Management
 Treatment for
ulcerative colitis
depends on the severity
of the disease.
 Each person
experiences ulcerative
colitis differently, so
treatment is adjusted
for each individual
Drug therapy
 The goal of drug therapy is to induce and
maintain remission, and to improve the
quality of life for people with ulcerative
colitis. Several types of drugs are available
 Aminosalicylates,
 Corticosteroids
 Immunomodulators
 Aminosalicylates, drugs that contain 5-
aminosalicyclic acid (5-ASA), help control
inflammation. Most people with mild or
moderate ulcerative colitis are treated with
this group of drugs first. This class of drugs is
also used in cases of relapse
 Corticosteroids such as prednisone,
methylprednisone, and hydrocortisone also
reduce inflammation.
 Immunomodulators such as azathioprine and 6-
mercapto-purine (6-MP) reduce inflammation by
affecting the immune system. These drugs are used
for patients who have not responded to 5-ASAs or
corticosteroids or who are dependent on
corticosteroids. Cyclosporine A may be used with 6-
MP or azathioprine to treat active, severe ulcerative
colitis in people who do not respond to intravenous
corticosteroids
 Other drugs may be given to relax the patient
or to relieve pain, diarrhea, or infection.
 Some people have remissions—periods when
the symptoms go away—that last for months
or even years. However, most patients’
symptoms eventually return
Medical Management
 Restoration of fluid and electrolytes
 Control of diarrhea
 TPN
 Surgery
 Eleostomy
 Elioanal anastomosis
 Ileostomy, in which the surgeon creates a small
opening in the abdomen, called a stoma, and attaches
the end of the small intestine, called the ileum, to it.
Waste will travel through the small intestine and exit
the body through the stoma. The stoma is about the
size of a quarter and is usually located in the lower
right part of the abdomen near the beltline. A pouch
is worn over the opening to collect waste, and the
patient empties the pouch as needed.
 Ileoanal anastomosis is  .
a surgical procedure in
which the large
intestine is bypassed
and the lower portion
of the small intestine is
directly attached to the
anal canal. It is also
called an ileal pouch-
anal anastomosis
 Not every operation is appropriate for every
person. Which surgery to have depends on the
severity of the disease and the patient’s needs,
expectations, and lifestyle. People faced with
this decision should get as much information as
possible by talking to their doctors, to nurses
who work with colon surgery patients
(enterostomal therapists), and to other colon
surgery patients. Patient advocacy organizations
can direct people to support groups and other
information resources.
 Nursing management

 Acute phase: maintain NPO and administer

fluids and
 Restrict the client’s activity to reduce
intestinal activity
 Monitor bowel sounds and for abdominal
tenderness and cramping
 Nursing
Nursing Management
Management
 Monitor stools, noting color, consistency and
the presence or absence of blood
 Monitor for perforation, peritonitis and
hemorrhage
Glumerulonephritis
 Necrotizing
glomerulonephritis;
 Glomerulonephritis -
crescentic;
 Crescentic
glomerulonephritis
 Glomerulonephritis is a
type of kidney disease
caused by
inflammation of the
internal kidney
structures (glomeruli).
 The glomeruli are
small structures inside
the kidneys. They are
the area where blood
flows through very
small capillaries and is
filtered through
membranes to form
urine.
 glomerular nephritis and abbreviated GN', is a primary or
secondary immune-mediated renal disease
 characterized by inflammation of the glomeruli, or small
blood vessels in the kidneys.
 It may present with isolated hematuria and/or proteinuria
(blood resp. protein in the urine); or as a nephrotic syndrome,
a nephritic syndrome, acute renal failure, or chronic renal
failure.
 Primary causes are one which are intrinsic to the kidney,
whilst secondary causes are associated with certain infections
(bacterial, viral or parasitic pathogens), drugs, systemic
disorders (SLE, vasculitis) or cancers.
Common causes
 Impetigo
 URTI
 Mumps
 Varicella
 Epstein Barr virus
 Hepa B
 Medications
 Foreign serum
PATHOPHYSIOLOGY
ANTIGEN (GROUP A BETA-HEMOLYTIC STREPTOCICCUS

ANTIGEN-ANTIBODY PRODUCT

DEPOSITION OF ANTIGEN-ANTIBODY COMPLEX IN GLOMERULOS

INCREASED PRODUCTION OF EPITHELIAL CELLS LINING THE

GLOMERULUS
PATHOPHYSIOLOGY
LEUKOCYTES INFILTRATE THE GLOMERULOS

THICKENING THE GLOMERULAR FILTRATION MEMBRANE

SCARRING AND LOSS OF GLOMERULAR FILTRATION

MEMBRANE

DECREASED GLOMERULAR FILTRATION RATE

CLINICAL MANIFESTATIONS
 Hematuria
 Oliguria
 Protienuria
 Edema
 HPN
 Dsypnea
 Engorge neck veins
 Elevated serum creatinine
(0.7-1.4 mg/dl and BUN
CLINICAL MANIFESTATIONS
 Cardiomegaly
 Pulmonary edema
 Confusion seizures
Treatment
 Treating symptoms
 Preserve kidney function
 Medicines
 Streptococcal infection- penicillin
 Corticosteroids
 Immunosuppresive
 Protein is restricted if with renal insufficiency and
nitrogen retention
 Sodium is restricted
 •Monitor vital signs
 Nursing •Monitor intake and output
Manage •Monitor daily weight
-ment
•Monitor for edema
•Monitor for fluid overload, ascites,
pulmonary edema and CHF
•Restrict fluid intake as prescribed
•Provide a high calorie and low protein
diet
•Restrict sodium intake as prescribed if
edema is present
 Nursing
Manage-
ment • Provide bed rest and limited activity
•Instruct the client to obtain treatment for
infections specially sorethroats and URTI
•Administer diuretics, antihypetensives
and antibiotics as prescribes
•Monitor for signs of renal failure,
cardiac failure and hypertensive
encephalopathy
•Instruct the client to report signs of
bloody urine, headache and Edema
 Pernicious anemia is
caused by a lack of
intrinsic factor, a substance
needed to absorb
vitamin B12 from the
gastrointestinal tract.
Vitamin B12 is necessary
for the formation of red
blood cells.
 1) the progressive
destruction of parietal cells
from the gastric mucosa
leading to intrinsic factor
destruction and
 2) the binding of blocking
autoantibodies to the
vitamin B12-binding site of
intrinsic factor, preventing
the formation of the
vitamin B12-intrinsic
factor complex
 [3]. If confirmation of
malabsorption due to
intrinsic factor deficiency
is needed, the Schilling test
can be performed
OTHER NAMES
 Macrocytic achylic anemia; Congenital
pernicious anemia; Juvenile pernicious
anemia; Vitamin B12 deficiency
(malabsorption
SYMPTOMS
 Shortness of breath
 Fatigue
 Pallor
 Rapid heart rate
 Loss of appetite
 Diarrhea
 Tingling and numbness of hands and feet
 Sore mouth
 Unsteady gait , especially in the dark
 Tongue problems
 Impaired sense of smell
 Bleeding gums
 Positive Babinski's reflex
 Loss of deep tendon reflexes
 Personality changes, "megaloblastic madness
DIAGNOSTIC TEST
 Tests that may indicate pernicious anemia include:
 CBC results that show low hematocrit and hemoglobin with elevated MCV (low
red blood cell count with large-sized red blood cells)
 CBC showing low white blood count and low platelets
 Low reticulocyte count
 Bone marrow examination (only needed if diagnosis is unclear)
 Serum LDH
 Below normal serum vitamin B12 level
 Schilling test
 Measurement of serum holotranscobalamin II
 Measurement of methylmalonic acid (MMA
NURSING INTERVENTIONS

 Administer Vit B12 injection as prescribed

weekly initially and then monthly for
maintenance (lifelong)