Pathophysiology of Neuroendocrine system

I.
Diabeties Mellitus
A. Comparison of Type I and II

about

Characteristic

Type I
[IDDM]

Type II
[non-IDDM]

onset

<30 yrs

>30 yrs

incidence

10-15% of all DM cases

clinical picture

hyperglycemia & DKA

hyperglycemia
& insulin resistance
rarely DKA

antibody production leading

to destruction of islet cells

yes

no

Associated obesity

no

yes

Propensity to ketoacidosis
requiring Insulin Tx

yes

no

Endogenous Insulin secretion

low to undetectable

low levels of insulin

production

Islet pathology

selective loss of beta cells

smaller, normal
appearing islet cells

Hyperglycemia responds to
sulfonylureas

no

yes, initially in most pts

B. Signs and symptoms

1. Type I presents with symptomatic hyperglycemia or DKA, while Type II presents with
asymptomatic hyperglycemia picked up on routine exam
2. sypmptomatic hyperglycemia
a. polyuria, polydipsia and wt loss as a result of glucosuria and osmotic diuresis
leading to dehydration.
b. hyperglycemia may be accompanied by blurred vision, fatigue, nausea, and
various types of fungal and bacteria infections
3. late complications
a. atherosclerosis may lead to CAD, claudication, skin breakdown and infections
b. peripheral vascular disease and gangrene result in need for amputation
c. retinopathy does not affect vision initially, but may lead to macula edema with
retinal detachment and hemorrhage which can cause blindness
d. nephropathy occurs in 1/3 of Type I DMs
1) GFR initially increases in response to hyperglycemia, then after
5 years the pt develops albuminuria which signals a decrease in GFR,
leading to ESRD in 3 to 20 yrs
2) the development of HPB accelerates the onset of ESRD, ACE
Inhibitors may prevent or delay onset of ESRD
e. polyneuropathy causes numbness, tingling, and paresthesias in the extremities
f. autonomic neuropathy can cause postural hypotension, disordered sweating,
impotence impaired bladder function, delayed gastic emptying, esophageal
dysfunction, diarrhea or constipation,
g. foot ulcers and joint problems are important causes of morbidity in Dms
h. risk of infection caused by decreased cellular immunity caused by
hyperglycemia often manifest as peripheral and oral skin infections and vaginal

candida. Foot ulcers are often undetected until the advanced stage has
reached. Deep ulcers require immediate hospitalization and surgical
to prevent the development of systemic toxicity

been
debridement

C. Diagnosis
1. fasting serum glucose > 140mg/dL on two separate occasions
2. impaired glucose tolerance
D. Labs
1. treat elevated Chol and HBP
2. monitor glucose levels daily
3. periodically determine glycosylated hemoglobin (Hb A1c) to estimate plasma glucose
control over preceding 2 to 3 months. Elevated levels of glycosylated hbg occurs when the
glycohemoglobin bound to the RBC increases in the presence of hyperglycemia. In poorly
controlled DMs the Hb A1c increase to >12%
4. fructosamine levels reflect glucose control in the previous 1 to 3 weeks and will show a
change before differences will appear in Hb A1c levels.
5. urine ketone testing should be performed whenever the pt develops a cold, flu, or
symptoms of hyperglycemia
E. insulin
1. syringes - jets, pens, CSII (pumps), traditional insulin syringe
2. types
type
onset
peak
duration
regular
15-30 min
2 - 4 hr
6 - 8 hr
intermediate
1 - 3 hr
6 - 12 hr
18 - 26 hr
long-acting
4 - 8 hr
14 - 24 hr
28 - 36 hr
3. initial dosage

to

lactic

1) Type I usu 40 U/day, Type II may require more

2) divide dose to give 1/2 before breakfast, 1/4 at dinner, and 1/4 at HS
3) adjust the dose to maintain FBS 80 - 150mg/dL
4) increase dose 10% at a time and wait 3 days between adjustments
4. maintainence schedule
1) bedtime intermediate-acting insulin
2) before breakfast mixed insulin (70/30)
3) before lunch and dinner regular insulin
5 complications
a. hypoglycemia - result of excessive exogenous insulin, unplanned exercise,
missed meal. pt/cg should be instructed in how to administer glucagon
b. dawn phenomenon (increase in AM FBS secondary to midnight surge of
growth hormone) Treat with hs intermediate acting insulin
c. local allergic rx at site of injection usu spontaneously subside after several
weeks of therapy
d. generalized insulin allergy leading to bronchospasm and sometime circulatory
collapse. Treat with antihistamine and epi If the condition persists after
stabilization, use skin testing to determine sensitivity and have physician perform
desensitization measures
e. insulin resistance - pt requires >200 U/day. usu due to develop of antibodies
insulin. switch to porcine or human insulin to reduce requirement
F. Oral antidiabetic meds for use with Type IIs only
1. sulfonylureas - lower insulin levels by stimulating insulin secretion; may be given in
combination with insulin
2. antihyperglycemics
a. metformin- decreases hepatic glucose production, may be given with
sulfonylureas, promotes wt loss and dec lipid levels, contraindicated in
acidosis, liver or kidney disease

with

b. acarbose - inhibits the hydrolysis of monosaccacharides, delaying CHO

digestion and absorption in the small intestines; may be given in combination
other oral agents
c. troglitazone - improve insulin sensitivity in skeletal muscle and suppresses
hepatic glucose output; may be used with Type IIs who require insulin therapy,
but dose of insulin should be lowered during initiation of therapy.
G. Treatment of the hospitalized DM
1. Mgt of the IDDM medical client
a. consider use of sliding scale until condition stabilizes
b. give 50 to 70% of daily dose of insulin in divided doses
c. for those on TPN consider continuous IV infusion of regular insulin
2. Mgt of the IDDM surgical client
a. on morning of the operation, give 1/3 to 1/2 the usual insulin dose
b. start IV infusion of 5% dextrose to infuse 1L over 6 - 8 hrs
c. post-operatively closely monitor serum glucose/ketones q 2 - 4 hr
d. give regular insulin to keep serum glucose at 100- 200 mg/dL
or
a. hold all subcu insulin and add 6 to 10U of regular insulin to 1L of 5%
dextrose
solution and infuse at 150/ml per hr and adjust rate according to serum
glucose/ketones levels
3. Mgt of the NIDDM
a. insulin is not required for the client who is treated by diet alone or with
sulfonylureas
b. withhold the sulfonylureas 2 to 3 days prior to operation and monitor serum
glucose levels q 6 hr pre- and post-op (Beers & Berkow, 1999)

II.

lipid

III

Diabetic Ketoacidosis (DKA)

A. cause
1. result of grossly deficient insulin availability leading to a transition from glucose to
oxidation and metabolism.
2. In type I, DKA is due to lapse in insulin tx or infection, trauma, or infarction
3 Type II rarely have DKA, but may have mild ketone formation and acidosis due to
decreased food intake and decrease in insulin secretion. (Beers & Berkow, 1999)
Hyperglycemic Hyperosmolar Nonketotic Coma (HHNK)
A. Cause
1. any condition (infection, fever, etc) in the Type II DM which causes a period of
symptomatic hyperglycemia and inadequate fluid intake
2. drugs that impair glucose tolerance (glucocorticoids)
3. drugs that increase fluid loss (diuretics)
4. peritoneal dialysis or hemodialysis, tube feedings, TPN(Beers & Berkow, 1999)

IV

Syndrome of Inappropriate ADH (SIADH)

A. definition - less than maximally dilute urine in the presence of plasma hypo-osmolality and
hyponatremia due to sustained ADH release
B. etiology
1. SIADH is associated with variety of disorders
a. malignancies: pulmonary, duodenum, pancreas, lymphoma, CNS
b. pulmonary: pneumonia, lung abscess, TB, aspergillosis, positive pressure
breathing
c. CNS: encephalitis, meningitis, brain abscess, Guillain-Barre,
subdural/subarachnoid hemorrhage acute psychosis, stroke

C. signs and symptoms

1. when plasma osmolality drops below 240 mOsm/kg, symptoms of hyponatremia result
2. rate of drop in Na levels as well as the absolute blood level affect the onset of
symptoms
3. CNS changes: altered personality, lethargy, confusion
4 changes due to hyponatremia: volume depletion (extracellular fluid volume
contraction)
or overload (extracellular fluid volume expansion)
5. when Na drops below 115mEq/L stupor, neuromuscular hyperexcitability, convulsions,
coma and death can occur
6. anatomic changes: cerebral edema, cerebellar tonsil herniation, pontine demyelinating
lesions
D. Prognosis
1. mortality is greater in acute vs chronic hyponatremia
2. debilitating comorbid conditions (alcoholism, cirrhosis, heart failure malignancy)
reduce
survival rates
E. Treatment
1. for thiazide diuretic-induced hyponatremia - eliminate the diuretic and replace Na and
K
2. for parenteral infusions in the client with impaired water excretion - stop the infusion
3. the presence of hyponatremia, hyperkalemia and hypotension should suggest adrenal
insufficiency - treat with IV glucocorticoids
4 when adrenal function is normal but hyponatremia is associated with ECF volume
depletion and hypotension - give saline 0.9% and restict free water intake to 500 - 1000
ml/day
5. for dilutional hyponatremia associated with ECF volume expansion due to Na retention
(CHF, cirrhosis, nephrotic syndrome) - restrict water intake and treat underlying disease
a. ACE inhibitor and loop diuretic effectively treat ECF volume expansion states
due to increased activity of the renin-angiotensin-aldosterone mechanism
6. use extreme caution in correcting increasing Na levels (3% saline infusion)
a. raise the Na levels no more than 1mEq/L/hr and no more than 10mEq/L/day
(Beers & Berkow, 1999)
V.

Hyperthyroidism
A. causes
1. increased synthesis and secretion of T3 and T4 from the thyroid gland caused by
thyroid
gland stimulators in the blood or autnomous thyroid hyperfunction
2. may also be caused by excessive release of thyroid hormone from the thyroid gland into
the peripheral circulation without increased synthesis of the hormones, usually due to
destructive changes caused by thyroiditis.
3 conscious or accidental ingestion of excess quantities of thyroid hormone
B. Laboratory Classifications
1. high thyroid radioactive iodine uptake and circulating thyroid stimulators
a. Graves Disease - most common cause of hyperthyroidism, an autoimmune
disorder, caused by an antibody against the thyroid TSH receptor, resulting in
continuous stimulation of the gland and synthesis and secretion of excessive
quantitites of T4 and T3. characterized by the development of exophthalmia,
goiter
b. inappropriate TSH secretion - all clients with hyperthyroidism have
undetectable TSH levels except those with TSH secreting anterior pituitary tumor
or those with pituitary resistance to thyroid hormone. The TSH in this condition
is
biologically more active than normal TSH and serves as a marker for a TSH
secreting pituitary tumor
c. molar pregnancy, choriocarcinoma, hyperemesis gravidarum produce elevated
levels of human chorionic gonadotropin which is a thyroid stimulator
2. High radioactive iodine uptake without circulating thyroid stimulators
a. toxic solitary or multinodular goiter (Plummers disease) - most common in
the
elderly, causes mutation in the TSH receptor resulting in continuous thyroid
stimulation

receptor

b.nonautoimmune, autosomal dominant hyperthyroidism - genetically inherited

occurs during infancy caused by a mutation in the gene for the TSH
resulting in continuous stimulation of the thyroid gland
lithium-induced goiter - due to an inhibitory effect on the release of iodide from
the tyroid
3. low thyroid radioactive iodine uptake
a. inflammatory disease (thyroiditis) - causes hyperthyroidism secondary to
destructive changes in the gland and release of stored hormone
b. iodine induced - due to excessive iodine ingestion resulting in increased
synthesis and release of excess thryoid hormone

C. Signs and symptoms

1. goiter, tachycardia, widening pulse pressure, sweating, tremor, a-fib, nervousness,
hypersensitivity to heat, palpitations, fatigue, increased appetite, wt loss, insomnia,
weakness, diarrhea
2. eye signs: lid lag, stare, lid retraction, exophthalmia, photophobia, double vision,
weakness of the EOM
3 thyroid storm, a life-threatening emergency, characterized by fever, marked weakness,
extreme restlessness, wide emotional swings, confusion, psychosis, coma,
circulatory
collapse and shock. Results from inadequately treated hyperthyroidism
and may be
precipitated by infection, trauma, surgical procedure, embolism, diabetic
acidosis, toxemia
a. treatment
1) iodine (15 drops of K iodide soln or 1 gm Na iodide slow IV over 24
hours) inhibits the release of T3 and T4 and decreases the vascularity of
thyroid gland
2) propylthiouracil 900-1200 mg/day to dec uptake of iodide and inhibit
conversion of T4 to T3
3), propranolol (beta blocker) 160mg/day in 4 divided doses to reduce
symptoms due to adrenergic stimulation - tachycardia, tremor, heat
intolerance, diarrhea
4) IV glucose,
5) correct dehydration and electrolyte imbalance,
6) cooling blanket for hyperthermia,
7) dig if needed, treat underlying cause,
8) corticosteroids 100-300 mg hydrocortisone/day, and
9) ablation of thyroid gland with radioactive iodine or surgery.
D. Diagnosis
1. lab findings
a. condition

TSH

T4

T3

T3 Resin
Uptake

Radioiodine Uptake

hyperthyroidism low
high
high
high
high
hypothyroidism high
low
low
low
low(Beers & Berkow, 1999)
VI
Hypothyroidism
A. Etiology
1. primary hypothyroidism
a. most common, probably due to autoimmune disease occurring as a result of
Hashimotos thyroiditis, may have a firm goiter in early stages, and later
shrunken
thyroid gland with no function
b. may be result of treatment of hyperthyroidism (thyroidectomy, ablation therapy,
proplthiouracil)
c. iodine deficiency (rare in the US with use of iodized salt) causes decrease in
thyroid hormone production resulting in increase in TSH
2. secondary hypothyroidism
a. due to failure of the hypothalamic-pituitary mechanism caused by deficient
TRH
secretion from the hypothalamus or lack of TSH secretion from the pituitary

B. signs and symptoms

1. dull facial expression, hoarseness, slow speech, periorbital swelling, cold intolerance,
ptosis of eyelids, hair and skin are coarse, dry, scaly, wt gain, mental impairment,
bradycardia, cardiomegaly, pleural, pericardial and abdominal effusions due to
extravasation of high protein content fluids, paresthesias,
2. myexedema coma, a life-threatening complication of hypothyroidism, due to
longstanding hypythyroidism characterized by coma, hypothermia, areflexia, seizures,
CO2
retention, respiratory depression, May be precipitated by exposure to cold, illness,
infection, trauma, and CNS depressants
C. Treatment
1. primary hypothyroidism
a. T4 replacement with synthetic preparations usu 75 to 100 mcg/day po
T3 is generated from the T4 in peripheral tissues
b. T3 replacement should not be used for long-term therapy because it is rapidly
absorbed and will need to be given bid, also clients on T3 will become clinically
hyperthyroid for several hours per day and will be at risk for cardiac
complications
2. myxedema coma
a. give large initial doses of T4 or T3 IV until T4 can be given orally
b. do not rapidly rewarm the client because of danger of cardiac dysrhythmias
c. monitor administration of all medications which will be metabolized more
slowly in the hypothyroid client
d. consider mechanical ventilation in the client with a compromised respiratory
status(Beers & Berkow, 1999)

Mr T is a 24 yo nursing student. In addition to going to school full time he works as a security guard two
nights per week. He eats on the go and often is unable to plan nutritious meals. He has been a diabetic
since he was 12 years old. He currently takes a total of 32 units of insulin daily: 10U of NPH and 6 U of
regular each morning and evening. He monitors his blood glucose three times per week.
One day during clinical he notices that he is thirsty and begins to urinate frequently. He feels very tired and
has blurred vision but attributes that to only having 4 hours sleep the night before, studying late for a final
examination. He remembers that he forgot to take his AM insulin dose, but thinks that he will be alright
until lunch time. At noon he begins to develop abdominal pain, tachycardia, feels weak, vomits and
develops chest pain. His instructor sends him to the ER
ASSESSMENT FINDINGS
Mr. T presents to the ER with the following clinical data: BS 500 mg/dL. Urine large ketones, ABG: ph
7.1, pO2 88, pCO2 33, HCO3 18. T 99, P 135, R 44. BP 1102/2. Severe chest pain. Na 155, CO2 19, K5.8
Cl 111, BUN 30, Cr 1.2

VII

Seizure Disorders

A. kinds
1. isolated, nonrecurrent - e.g. after a febrile state or after head trauma
2. epilepsy - recurrent paroxysmal disorder of cerebral function characterized by sudden
brief attacks of altered consciousness, motor activity, sensory phenomena, or
inappropriate
behavior
B. Etiology
1. seizures result from a focal or generalized disturbance of cortical function which may
be
due to various cerebral or systemic disorders
2. may result from withdrawal of long term use ETOH, hypnotics, or tranquilizers
3. classification of epilepsy
a. symptomatic - due to a cause which is treatable
b. idiopathic - unknown cause
1) begins between 2 and 14 yrs of age
2) disorders before 2 yrs are due to developmental defects, birth injuries,
or metabolic disease
3) disorders occuring after 25 yrs may be due to cerebral trauma,
tumors,
CVA
C. Signs and symptoms
1. depend on type of seizure - partial (localized or focal region of the brain) or
generalized
(throughout the entire cortex)
2. auras - sensory or psychic manifestation immediately preceding a complex partial or
generalized seizure
3. postictal state - immediately follows a generalized seizure characterized by a deep sleep,
headache, confusion, and muscle soreness
D. Classification
1. simple, partial seizure
a. motor, sensory or psychomotor phenomena without loss of consciousness
2. jacksonian
a. begin in one hand and travel up the extremity, or may first affect the face and
move down the body, or may begin by raising an extremity and turning
the head to
the moving part
b. some jacksonian seizures progress to generalized convulsions
3. complex partial seizures
a. clt loses contact with surroundings for 1 to 2 min, may stare, perform
automatic
movements, utter unintelligible sounds and resist aid. Mental confusion
follows
for another 1 to 2 min after the motor activity subsides.
b. if restrained, the clt may lash out and become aggressive
c. clt with complex partial seizures have a higher incidence of psychiatric
disorder
(may be schizoid or depressive psychoses)
4. generalized seizures
a. are characterized by loss of consciousness and motor function at onset
b. usu have a genetic or metabolic cause
c. may be primarily generalized (entire cortex) or secondarily generalized (local
focus which spreads to entire cortex)
d. types
1)infantile spasms - generalize seizures occuring during the first 3yrs of
life and are replaced by other types of seizures as the child ages
2) absence seizures (formerly called petit mal) - brief generalized
seizures
with 10-30 sec loss of consciousness with eyelid fluttering; clt does not
fall or convulse, no postictal state and no knowledge that
seizure has
occurred; are genetic and occur predominantly in
children
3) generalized tonic-clonic seizures - begin with an outcry, continue with
loss of consciousness and falling, followed by tonic, then clonic
contractions of the muscles of the extremities, trunk and head, urinary
and fecal incontinence may occur; seizures last 1 -2 min
4) atonic seizures - occur in children and are brief generalized seizures
with loss of muscle tone and consciousness

or
loss

had

5) myoclonic seizures - brief, lightning-like jerks of limb, several limbs

trunk. may be repetitive leading to tonic-clonic seizures. there is no
of consciousness
6) febrile - associated with fever without evidence of intracranial
infection; usu occur in children usu benign but have a 2% incidence of
developing subsequent epilepsy
7) status epilepticus
a) generalized convulsive states may be fatal
b) complex partial or absence status epilepticus may only
manifest as confusion and will need an EEG to confirm
8) epilepsia partialis continua - rare focal motor seizure involving the
or face recurring for a few seconds or min for days or years, in the adult
usu follows a stroke

E. Diagnosis
1. attempt to distinguish between idiopathic and symptomatic
2. record duration, frequency and type of seizure
3. focal seizures suggest tumor, cerebrovascular disease, or residual traumatic abnormality
4. observe for stiff neck which may suggest menigitis, subarachnoid hemorrhage,
encephalitis
5. lab data
a. EEG
1) generalized tonic-clonic: symmetrical burst of sharp and slow activity
2) absence: spikes and slow waves
3) in 30% of cases EEG obtained during seizure-free period is normal
4) several EEGs may be needed to confirm dx
b. serum glucose, Na, Mg, Ca
c. MRI
d. lumbar puncture to rule out infection
F. Prognosis
1. 1/3 of cases drug therapy eliminates seizure activity, and is greatly reduced in another
1/3/; about 2/3 of clts with well controlled seizures can eventually discontinue
the drugs
w/o relapse
2. bet seizures most are neurologically normal, however anticonvulsants can dull senses
G. Treatment
1. encourage normal socializing activity; most drivers licenses can be restored after 1 yr
of
seizure free; ETOH, cocaine and other illicit drugs can provoke seizure activity
2 reserve institutionalization for the severely mentally retarded
3. during the seizure position clt on side, do not place anything in the mouth, loosen
clothing around the neck and protect the head
4. correct underlying physical disorders (fever, infection, endocrine abn
5 consider treating head injuries with skull fx, intracranial hemorrhages, focal deficits, or
amnesia with prophylactic drug therapy
6. anticonvulsants are given in combination and depend on type of seizure, after one yr of
seizure free the drugs may be gradually decreased ( chart pg 309 AACN text)
7. status epilepticus is a medical emergency
a. valium IV and dilantin IV to prevent recurrence
b. anesthetic IV doses of phenobarb, valium or pentobarbital may be needed in
refractory cases, at which time the clt will need to be intubated and mechanically
ventilated with oxygen(Beers & Berkow, 1999)
VIII

65yrs,

Parkinsons Disease
A. Definition
1. progressive degenerative CNS disorder characterized by slow decreased movement,
muscular rigidity, resting tremor, and postural instability
2 4th most common neurodegenerative disease of the elderly, affect 1% of those over
mean age at onset is 57 yrs, and may begin in childhood or adolescence
B. Etiology

1. primary Parkinsons - the pigmented neurons of dopaminergic cell groups are lost,
resulting in depletion of dopamine; unknown cause
2. secondary Parkinsons - due to loss or interference of with the action of dopamine in
the
basal ganglia due to other idiopathic degenerative diseases, drugs or exogenous toxins;
most common cause is ingestion of antipsychotic drugs or reserpine, which produce
parkinsons by blocking dopamine receptors, co-administration with anticholinergic drugs
may lessen symptoms. Less common causes are: carbon monoxide or manganese
poisoning, hydrocephalus, brain lesions, subdural hematoma. An illicit drug (n-methyltetrahydropyridine) synthesized from demerol causes irreversible Parkinsons in IV drug
abusers
C. Signs and Symptoms
1. begins with pill-rolling in one hand that is maximal at rest, diminishes during
movement,
and is absent during sleep. is enhanced during emotional upset or fatigue
2. affects the hands, arms, and legs in that order
3. jaw, and tongue may be affected, voice is undistrubed
4. in some clt only rigidity is evident
5. movement steadily decreases (hypokinesia) is slow (bradykinesia) and difficult to
initiate
(akinesia)
6. face becomes masklike, mouth remains open and eyes blink less frequently
7 posture stoops, gait shuffles, arms are held flexed at the side and do not swing with
stride
8. clt may break into a run to keep from falling (festination)
9 a loss of postural reflexes result in tendency to fall forward (propulsion) or backward
(retropulsion)
10. speech becomes monotonous and stuttering
11 dementia affects 50% of clts and depression is common
Treatment
1. levodopa - precursor to dopamine which crosses the blood-brain barrier into the basal
ganglia where it decaroboxylates to form dopamine. Drug reduces bradykinesia, rigidity
and tremors. levodopa may be in combination with carbidopa to reduce side
effects
(nausea, palpitations, flushing). Some MDs believe that levodopa hastens the
progression
of dyskinesia and will withhold the drug as long as possible
2. amantadine - mechanism of action is unclear but is given to treat a mild early form of
the
disease or as adjunct with levodopa
3. bromocriptine and pergolide are ergot alkaloids that activate dopamine receptors in the
basal ganglia
4. selegiline an MAO Type B inhibitor, inhibits one or two major enzymes that
breakdown
dopamine, prolongs the action of levodopa; if used as initial treatment can delay
need to
add levodopa for 1 yr
5. anticholinergics (artane and cogentin)
6. surgical intervention - usu the point at which the ACNP will treat Parkinsons
a. pallidotomy - ablation of posteroventral globus pallidus
b. thalamotomy - blockage of neurotransmitter receptors in the subthalamic
nucleus(Beers & Berkow, 1999)

XI

Myasthenia Gravis
A. Definition
1. autoimmune disorder that impairs acetylcholine receptors at the postsynaptic
neurotransmitter junction, interfering with neuromuscular transmission. What
causes the
development of the antibodies is unknown. More common in women
and occurs between
20 to 40 yrs of age.
B. Signs and Symptoms
1. ptosis, doplopia and muscle fatigue after exercise.
2, dysarthria, dysphagia, and limb weakness

crisis

nerve

3. the disease may fluctuate in severity over the course of hours or days
4 myasthenic crisis occurs in 10% of all cases leading to respiratory arrest
C. Diagnosis
1. Tensilon test - a short acting anticholinesterase drug used to determine myasthenic
(sudden improvement) or cholinergic crisis (sudden deterioration)
a. draw up 10mg and administer 2 mgIV, if no rx occurs in 30 sec administer the
rest of the drug
b. be prepared for cardiorespiratory depression, have atropine (antidote) and
mechanical ventilation ready.
2. CT or MRI may confirm a thymoma
3. positive serum acetylcholine-receptor antibodies in serum in 90% of the cases
4. electrophysiology studies show decrease in muscle action potential with repetitive
stimulation
D. Treatment
1. consult with specialist
2. anticholinesterases and plasmapheresis (removal of circulating antibodies) relieve
symptoms; corticosteroids, immunosuppressive drugs, and thymectomy interfere with
autoimmune pathogenesis
3. drugs
a. anticholinesterases (neostigmine, prostigmine) which must be given carefully
around the clock, and often the disease becomes refractory.(Beers &

Berkow,
XII

are

attacks

1999)
Transient Ischemic Attack (TIA)
A. Definition
1. focal neurological abnormality of sudden onset and brif duration that reflect dysfunction
in the distribution of the internal carotid-middle cerebral or vertebrobasilar arterial system
2. Most TIAs are due to cerebral emboli from ulcerated atherosclerotic plaques in the
carotid or vertebral arteries, or less often from mural thrombi in a diseased heart. Some
due to brief reduction in blood flow through stenosed arteries
3. HBP, arteriosclerosis, heart disease, a-fib, DM, polycythemia predispose the clt to TIAs
B. Signs and symptoms
1. begin suddenly last 2 to 30 min then abate w/o sequela; consciousness remains intact
2. symptoms are identical to a stroke but last only briefly
a. if the carotid artery is involved, symptoms are unilateral
b. aphasia indicates involvement of the dominant hemisphere
c. when the vertebrobasilar system is involved (which supplies brain stem,
cerebellum, and portions of the temporal and occipital lobes) symptoms reflect
brain stem dysfunction
3. may have several TIAs daily or two or three over several years
C. Diagnosis and Treatment
1. differentiate from convulsive seizures, neoplasms, migraine, Menieres , other forms of
vertigo, and hyperinsulinism
2. noninvasive ultrasonography, MRI or arteriography can confirm presence of stenosis.
3. subclavian artery occlusion will be indicated when BP on affected side is lower than
opposite arm
4 when occlusion is > 70% endarterctomy will improve outcome
5. when occlusion is < 30% treat medically
6. antiplatelet drugs or anticoagulants are used when the obstruction is intracranial,
vertebrobrasilar or involves the vertebral or carotid arteries
a. heparin may be used for recent daily attacks, coumadin for less frequent
b. for occasionally attacks use antiplatelet meds (ASA, ticlopidine, use of
persantine not well established) (Beers & Berkow, 1999)

XIII

Stroke (CVA)
A. types

10

1. evolving - an enlarging brain infarct manifested by neuro symptoms that worsen over
to 48 hours
2. completed - brain infarct characterized by neuro changes that indicate stable injury
B. Signs and symptoms
1. in evolving stroke - neuro dysfunction begins in one extremity and progresses over
serveral hours or day w/o producing headache or fever.
2. acute completed stroke is most common - symptoms are rapidly occurring and
maximize
w/in minutes. over next one to two days deficits worsen and consciousness
become
clouded. Unless infarct is large, symptoms usually improve immediately with
further
improvement over months
3. middle cerebral artery is most often affected - results in contralateral hemiplegia,
aphasia, and motor and sensory impairment
4. internal carotid has same symptoms as middle cerebral artery and includes ocular
symptoms
5. anterior cerebral - uncommon, if present results in contralateral hemiparesis, and
urinary
incontinence
6. posterior cerebral artery hemisensory loss, spontaneous thalamic pain
7. vertebrobasilar system - cranial nerve signs, visual disturbance, pupillary abnormalities,
changes in consciousness, death often results
C. Diagnosis
1. onset during sleep suggests infarction, onset during exercise suggest hemorrhage
2. concomitant signs of MI, a-fib suggest embolism
3. headache, coma stupor, convulsive seizures suggest hemorrhage
4 neck pain suggests dissection
5 perform labs to rule out polycythemia, hypercoagulopathy, infections; ESR to exclude
vasculitis; chest xray to identify lung tumor or cardiovascular disorder, ECG
6. LP - CSF is usu normal, WBCs transiently increased, glucose dec slightly, elevated
protein, color is clearafter infarct and bloody after hemorrhage.
7. MRI will detect evolving infarct
8 CT and MRI will differenctiate ischemia from hemorrhage
D. Prognosis
1. 20% will die in the hospital, mortality increases with age
2. extent of recovery depends on age, state of health, severity of injury
3. impaired consciousness, mental deterioration, brain stem signs indicate poor prognosis
4 immediate signs of improvement have better prognosis; 50% with moderate or severe
hemiparesis will have gradual return of deficits to enable performance of ADLs
E. Treatment
1. oxygenation - airway maintainence, oxygen
2. fluids to maintain nutritional status and hydration
3. maintain bowel/bladder function
4. prevent decubitus ulcer formation
5 PROM to all extremities
6. nipride for malignant HBP
7. recombinant tissue plasminogen activator (tPA) should be given w/in 3 hr of onset
0.9mg/kg IV, 10% by rapid IV injection and remainder by drip
8 heparin may be used in those who are not candidates for tPA
9 guidelines for anticoagulation
a. clt with nonhemorrhagic infacts of cardioembolic origin should be treated with
heparin the switched to coumadin to increase INR to 2.0 - 3.0 and should be
continued for 6 months
begin heparin and infuse to increase PTT 1.5 to 2 times control values
b. delay heparin for 5 to 7 days in those with large nonhemorrhagic infarcts and 2
to 4 weeks in those with cerebral bleed
c. use of antiplatelet drugs remains under investigation(Beers & Berkow, 1999)
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