Exam 3 Flashcards
Type 1 diabetes
pancreas not functioning
insulin dependent
destruction of beta cells
ONLY insulin used
before the age of 20-30
type 2 diabetes
pancreas functioning
weight loss and diet –> oral hypoglycemics –> insulin
after age 30
what to treat gestational diabetes with
insulin
NOT oral hypoglycemics (harms the fetus)
risk for type 2 diabetes increases ___% each year following pregnancy
10%
what drugs give secondary diabetes
steroids like prednisone
prediabetes is high glucose after what age
40
prediabetes blood glucose levels (fasting and post prandial)
100-126 fasting
140-200 post prandial
A1c levels
<5.7% normal
5.7-6.5% prediabetes
6.5%+ diabetes
A1c and glucose level goals for diabetic pts
<7% and glucose <126
where is insulin produced and what does it do
beta cells of the pancreas
metabolizes glucose for energy
Insulin signals liver to stop releasing/breaking down glucose when we don’t need it
where is glucagon made
alpha cells of the pancreas
criteria for diagnosing diabetes (3)
fasting: 126+ on 2 occasions
HbA1c: 6.5%+ on 2 occasions
OGTT: glucose 200+ on 2 occasions
triglycerides in type 2 diabetes
usually very high
>250 indicates high risk
metabolic syndrome (5)
increased serum creatinine
insulin resistance
dyslipidemia
BP >130/85
abdominal obesity
high risk ethnic population for diabetes
african americans, native americans, hispanic ppl (minorities)
considerations for hispanic ppl in diabetes
Hispanic ppl prioritize others, they may cook for the family but not properly for themselves
See diabetes as a punishment from god
babies in relation to diabetes
women who give birth to babies over 9 pounds are at risk for diabetes
complications of type 2 diabetes (6)
Cardiovascular disease
PVD
CVA
kidney disease
blindness
neuropathy (most common cause of nontraumatic amputation)
virus exposure in type 1 diabetes
Virus triggers autoimmune response against islet cells of pancreas causing destruction of beta cells (absolutely no insulin)
glycogenolysis when eating (when you have diabetes)
prevented
no conversion of stored glycogen into glucose for energy
gluconeogenesis
conversion of protein to glucose
which type of DM is DKA seen in
type 1 bc no insulin
RBG of hyperglycemia
> 250
what 3 electrolytes get excreted in urine in diabetes
Na+
Cl-
K+
pH imbalance in ketosis
metabolic acidosis
blood glucose in ketonuria
> 300
which s&s are more common in type 1 diabetes (8)
kussmaul breathing
lethargy
stupor
weight loss
fruity breath
N/V
abdominal pain
3 kinds of complications of hypoglycemia
macrovascular
microvascular
neuropathy
macrovascular complications of DM
Cardiovascular and cerebrovascular disease (increase in RBC aggregation bc they become stiff and don’t flow)
microvascular complications of DM
damages small vessels of eyes and kidneys causing retinopathy/nephropathy)
neuropathy
nerve cells become cirrhosed
not vascular!!!
why are diabetics at risk of amputations
WBCs become unable to function and blood flow is bad
neuropathy and nonfunctioning WBCs cause decreased warning of injury
injury won’t heal and decreased blood supply to wound cause infection and possible amputation
S&S of type 1 diabetes
Abrupt onset
3 “P’s”, weight loss
Weakness
Mild fatigue
Dehydration
Muscular wasting
Muscle cramps
Abdominal pain
N/V
Ketosis: fruity “acetone” breath
Mental status changes
Increased frequency of infections
S&S of type 2 diabetes
Fatigue
Drowsiness
Irritability
Nocturia
Itchy skin
Especially vaginal
Poorly healing wounds
Muscle cramps
Proteinuria
Average age 50 years
History of HTN
Leg pain
Impotence from vascular damage
Recurrent infections
Blurring of vision (from chronic hyperglycemia)
mnemonic for glucose levels
hot and dry=sugar high
cool and clammy= need some candy
(confusion, lightheadedness, tremors, double vision)
NPO how many hours before fasting blood glucose sample
8-12 hrs
oral glucose tolerance test
for gestational diabetes
FBG taken, drink the stuff and take blood samples every few hours (usually 3)
can’t have nutrients besides water during the test
monofilament testing
Fine, threadlike material rubbed against extremities to test for feeling
fats for diabetic diet
30% or less of total calories
10% saturated
combine starch with protein and fat
CHO (complex or simple) in diabetic diet
50-60%
whole grains good
protein in diabetic diet
10-20%
why should we decrease alcohol consumption in diabetes
impairs gluconeogenesis (glucose isn’t being created)
increases insulin secretion (HYPOglycemia)
if diabetes well controlled, MODERATE alcohol is fine with meals or slowly after
omega-3 fatty acids and fiber for diabetes
lowers cholesterol, sat fats, and LDL
daily limit of cholesterol for diabetes
300 mg
cinnamon for diabetes
lowers blood glucose
1/4 tsp 2x daily
FIT acronym for diabetic fitness
f-frequency: 3x/week
i-intensity: 60-80% maximum HR
t-time: aerobic activity 20-30 min with 5-10 min warm up
exercise and blood glucose
ELEVATES with hard core exercise
LOWERS with light exercise
what to eat before and after exercising w diabetes
15g of carbs or 1 complex carb with proteins
rapid insulin onset and peak
onset: 5-15 min
peak: 30-60
names of rapid acting insulin
Lispro (humalog), aspart (novolog), glulisine (apidra)
Inhaled insulin (exubera)
allergies to beef or pork insulins?
onset and peak of short acting insulin
onset: 30-60 mins
peak: 2-3 hours
names for regular insulin
Novolin R, humalog R, iletin regular
for insulin coverage
SQ or IV in emergencies
NPH insulin onset and peak
onset: 2-4 hours
peak: 4-12 hours
NPH names
Novolin L (lente)
Novolin N (NPH)
Humalog N
Taken AFTER food and at night
Regular insulin combined with a large protein, protamine
long acting insulin onset, duration
onset: 1-6 hours
continuous
names for long acting insulin
levemir
lantus (insulin glargine)
DO NOT MIX
TAKE SAME TIME EVERY DAY
rolling insulin (what types can/can’t be rolled)
DON’T roll rapid or short
ROLL intermediate
degrees for injections of insulin
45 if loose skin or thin
otherwise 90 (abdomen always 90)
lipoatrophy
loss of SQ fat with dimpling
lipohypertrophy
fibro-fatty masses at the site with scarring
Disturbance of fat metabolism, interferes with absorption of insulin
Do not give insulin at these sites
At least ½ inch away
what type of insulin is via pump
fast
who are oral antidiabetic drugs contraindicated in
type 1 DM
severe renal/liver disease
hypersensitivity to sulfa
pregnancy/lactation
order for diabetic agents
diet and exercise
oral hypoglycemics (type 2)
insulin
sulfonylureas and meglinitides
Targets the pancreas
Stimulates beta cells to make insulin (must have working beta cells)
15-30 minutes before meals
Avoid alcohol
After diet, exercise, and monotherapy (metformin or glucophage) fail
alpha-glucosidase inhibitors “starch blockers”
target GI tract
slow carb absorption
monitor liver function q3 months
biguanides
Target the liver
D/C for 48h before radiographic test with iodine
Take with food to decrease GI upset
Need B12 and folic acid supplements
Metformin, glucophage
Thiazolidinediones TZD
Reduces production of glucose by liver
Target liver (tests done every 2 months)
Monitor for fluid retention
how much should a1c drop for every class of oral hypoglycemics added
1-1.5%
what to eat when hypoglycemic and what is blood glucose
juice, then starch and protein
concentrated CHO (cheese and crackers)
blood sugar <60
signs of mild hypoglycemia
Headache
Hunger
Weakness
Stimulation of sympathetic nervous system
signs of moderate hypoglycemia and what to give
Impaired functioning of CNS
Cerebral S/S
Inability to concentrate
Confusion
Lightheadedness
Headache becomes worse
Memory lapses
Lips and tongue go numb
slurred speech
Double vision
Emotional changes
Acting like they’re drunk
MEDICAL ALERT BRACELET!!
In mild and moderate, OJ, hard candy, or honey can be administered to reverse effects
signs of severe hypoglycemia
Disorientation
Seizures
Loss of consciousness
Diabetic coma
death
at what blood glucose is a person still arousable
50
reversal of hypoglycemia when sick
give simple carbs, have a snack, 4 oz of juice, then starch and protein (cheese and crackers)
Repeat in 10-15 minutes
Give glucagon IM 1mg or SQ
IV with 50% dextrose
Works in 1-2 hours
Slowly regains consciousness in 5-20 minutes
May be repeated if not eating or vomiting
glucose in illness
increased
what to eat when sick (diabetic)
juice, soda, jell-o, small portions of CHO
how often to assess glucose and ketones when diabetic sick
q1-4 hours
when should you notify the provider about a sick diabetic patient
illness lasts >1 day
Glucose >240 mg/dL
Unable to tolerate foods or fluids
ketones in urine for over 24 hours
temp over 101
Changes in mental status (sleepiness)
symptoms of DKA
dehydration
delirium
dizziness
onset slow: 4-10 hours
tachy
high blood sugar
hyperkalemia and hyponatremia
kussmaul breathing
fruity breath
abd pain
ketonuria
Treatment of DKA
reverse hyperkalemia, hypokalemia happens so give NS with K+ then regular insulin once glucose drops to 250-300
hydration
to correct dehydration: 1,000 ml NS first hour, 2,000-8,000 ml over next 24 hours
IV line needed (SQ tissue too dehydrated)
correct acidosis
Precipitators of DKA (5 S’s)
sepsis
surgery
sugar high
stress
substance abuse
when NOT to give K+ to a patient with DKA
low urine output
what solution is insulin compatible with
NS
rule when mixing insulin and NS
discard first 50 ml of solution
HHNS
SOME insulin produced, not like DKA
in type 2 DM
More serious than DKA
causes of HHNS
severe dehydration
infection
stress
medications
med conditions
urine tests for HHNS
+ for glucose
- for ketones
electrolyte imbalance in HHNS
hypernatremia
management of HHNS
Fluids, electrolytes, and insulin
Insulin is administered at a slow rate
Insulin administered at lower dosage via infusion pump
Remove triggering situation
2-3L of fluid rapidly
Difference is that insulin administered slow and little bc body has some insulin, DKA has no insulin
HHNS symptoms
hypotension
polyuria
glycosuria
polydipsia
decreased LOC from increased Na+
hyperthermia
seizures
paralysis
nephropathy with microalbuminuria
dawn phenomenon
early morning hyperglycemia (3-4AM)
decreased insulin
growth hormones secreted during the night
blood sugar assessed at night
treatment of dawn phenomemon
Increase evening to intermediate or long acting dose of insulin
Change time of insulin administration from early evening to closer to bedtime
somogyi effect
nocturnal hypoglycemia
Normal or elevated blood glucose at night
Hypoglycemia later
2-3AM
Hyperglycemia in the morning
3AM-breakfast
due to excessive insulin dosage
treatment of the somogyi effect and 2 S&S
Decrease evening insulin dose
Give bedtime snack
Or decrease in intermediate dose at supper and moving it to bedtime
Measure blood glucose level between 2-4AM and at 7AM
HA and lethargy
microvascular complications
diabetic retinopathy
-control blood glucose and BP
-eye exams every year
nephropathy
-small vessels damaged by high glucose and BP
-no early symptoms
-2-3L oral intake
neuropathic complications
Mononeuropathy
Polyneuropathy
Autonomic neuropathy
When glucose is very high, nerves become edematous, myelin sheath becomes damaged, nerve cells become damaged
Feet and lower legs become numb, burn, ache, or throb
Can cause impotence or decreased libido
High glucose decreases circulation to nerves, causing damage
do foot care
macrovascular complications
Macrovascular
CAD
CVD
HTN
PVD
Infections from immobilized WBC, usually in mouth, feet, bladder, female reproductive organs, causes gingivitis
High lipid levels when blood glucose is high
High cholesterol, LDL, triglycerides (increase risk of MI and blood vessel damage)
Dehydration of cells, causes stiffening
monitor cholesterol, triglycerides, BP
exercise
low fat diet, high fruits, veggies, and whole grains
what is the thyroid gland regulated by
anterior pituitary
what increases cellular metabolism
thyroid hormone
paro globulin in blood
breakdown of thyroid hormone
what do antithyroid meds cause
hyperglycemia
Med that increases thyroid hormone
dilantin (phenytoin)
is t3 or t4 more potent
t3
what are t3 and t4 made of
iodine
thyroid gland takes iodine and converts into t3 and t4
what is negative feedback controlled by (2)
hypothalamus and anterior pituitary
goiter and hyper/othyroidism
goiter doesn’t necessarily mean you have one or the other
but if you have hyperthyroidism you WILL have hyperthyroidism
best source of iodine
table salt
special characteristic of thyroid gland
very vascular
TRI and TRAB
binds to TSH receptor sites, acts like TSH, makes the gland secrete t3 and t4, then anterior pituitary tells gland to stop producing TSH
most common cause of hyperthyroidism
graves disease
more common in women 20-40
iodine deficiency leads to what
toxic nodular goiter
decrease of t3 and t4, increase in TSH causing goiter
SNS and hyperthyroidism
increased SNS activity
Diaphoresis, SOB, palpitations, weight loss, muscle weakness, blurred vision, decreased attention span
clinical manifestations of thyrotoxicosis
Fine tremors
Heat intolerance
Many loose stools daily
Warm moist skin
Skin salmon color
Rapid pulse at rest and with exertion (ECG changes, 90-160 BPM)
Hyperactive DTR (deep tendon reflexes)
Increased appetite
Weakness
Menstrual abnormalities (decreased flow and increase in time between periods)
Insomnia
Nervousness
Restlessness
Emotional hyperexcitability
Irritable
Apprehensive
Rapid speech
Fine, soft, silky hair
SNS increased
May be mild with remission or exacerbations, may progress relentlessly, may be transient, or permanent
pretibial myxedema
skin becomes thin, dark, and dry
accumulation of hyaluronic acid and mucin in SQ and interstitial tissue
Causes dry, waxy, velvety, smooth swelling in front surfaces in lower legs
Looks like lumpy reddish thickening of skin in front of the shin
Usually painless and nonpitting
May be caused by immune reaction exacerbated by trauma in hyperthyroidism
exophthalmos
earliest sign of graves disease
edema in extraocular muscles and increase in fatty tissue behind the eye
bloodshot appearance with tearing and photophobia
focusing problems
corneal osserations and infection from dryness
tape eyelids shut when sleeping
eyelid lag
Upper eyelids don’t descend when person gazes down slowly
Eyelid lags behind
globe lag
Upper eyelids pull back faster than eyeball when looking upwards
Eyeball lags behind
classifications of goiter
0=no palpable or visible goiter
1=mass is not visible with the neck in normal position. Goiter can be palpated and moves up with swallowing
2=mass is visible as swelling of the neck in normal position. Goiter is easy to palpate; usually asymmetrical
Bruits: turbulence from increased blood flow
clinical manifestations of goiter (from progression)
AFIB
increased SBP and decreased DBP
cardiac decompression
osteoporosis
fractures
cardiac effects of goiter
Sinus tachycardia
Dysrhythmias
Increased pulse pressure
Palpitations
Myocardial hypertrophy
Heart failure
clinical manifestations of hyperthyroidism in elderly
apathetic hyperthyroidism
only cardiovascular symptoms
diagnostics of hyperthyroidism
TRH stimulation test
Serum TSH (low)
Free t3 and t4 (high)
radioactive iodine uptake with thyroid scan (signs of enlarged thyroid gland, bruits)
Ultrasound of thyroid gland
Clinical manifestations
Medical and surgical history
antithyroid meds are for who and used for how long
Patients with small goiters as first line treatment
Initial control of thyrotoxicosis
Pregnant and under 18
Patients not wanting to take 1-131 or surgical removal
used for 1-3 years
Thionamide: Propylthiouracil (PTU)
suppresses thyroid hormone
used for severely ill
thionamide: methimazole
for hyperthyroid
blocks iodine
most common for pregnant and under 18
10x more potent than PTU
contraindications of antithyroid meds
bleeding disorders
diabetes
lithium therapy
late pregnancy
iodides
block thyroid hormones
short term use
can stain teeth
SSKI (take with water)
or lugol’s solution with milk
lugols + SSKI, use a straw
take with meals and at regular intervals
SE of antithyroid meds
Agranulocytosis
-Most serious
-Report fever, chills, sore throat
-Especially seen in elderly
Leukopenia
Thrombocytopenia
Pruritus
Dermatitis
Arthralgia (joint pains)
Mouth ulcers
Nausea
what not to take with iodides
expectorants
bronchodilators
salt substitutes
signs of iodism
swelling of buccal mucosa
excessive salivation
coryza (inflammation of mucous membrane with a cold)
lesions in mouth
Radioactive iodine (1-131)
radiation precautions not needed
most become euthyroid after 3-6 months
eye related symptoms, take glucocorticoids
contraindicated in under 18, pregnancy and breastfeeding
destroys thyroid cells (may become hypothyroid)
can take 2-3 weeks to start, effects not seen until 3-6 weeks
TAKE WITH A STRAW
CAN ALSO BE USED FOR THYROID CANCER
thyroidectomy
5/6 of the gland is removed leading to prolonged remission
remaining gland sutured to the trachea
total thyroidectomy only done for cancer, requires life long HRT
for pts with such a large goiter it causes compression or who don’t want/respond to PTU or radioactive iodine
risk of thyroid surgery
damage of parathyroid and laryngeal nerves
HEMORRHAGE
preop management of thyroid surgery
takes 2-3 months
must be euthyroid with no S&S
PTU to decrease size
SSKI or lugol’s for 10-14 days to decrease blood flow
BB to decrease HR
iodide
high protein, high carb diet
postop management of thyroid surgery
coughing/deep breathing
support neck when coughing or moving by putting hands at size of the neck or keep pillows/sandbags at side of the neck
2 pillows
hoarse voice for a few days bc endotracheal tube placement
discourage talking
life-long HRT taken on empty stomach 30+ min before meals
monitor VS every 15-30 min until stable
monitor pain or discomfort
monitor laryngeal damage (resp obstruction or stridor which is an EMERGENCY CALL PHYSICIAN)
Monitor hypocalecmia
-calcium gluconate 1-7 days post op MEDICAL EMERGENCY CALL PHYSICIAN
pain
edema (trach set)
high fowlers
avoid hyperextension of neck
airway humidification to thin secretions
patent IV
suction
check dressing BEHIND neck
dyspnea, obstruction or pressure behind suture line (bleeding normal 24 hours postop)
have pt speak q2h
sutures removed 2-3 days postop
inspect for redness, tenderness, drainage, or swelling
hypocalcemia teaching in thyroid post-op
most common complication
chvostek and trousseau’s signs
report paresthesia at hands and feet
numbness around mouth
weak pulse
increased GI motility
hyperactive DTR
twitching
3 things to have available after thyroid surgery
sandbags
trach set
Ca+ gluconate ampoules (patent IV line)
nutrition for preop thyroidectomy
increase calories, protein, and carbs bc they metabolize rapidly
avoid foods causing diarrhea
small, frequent meals
vits and minerals
monitor weight, I&Os
environment for preop thyroidectomy
no stimulation
restrict visitors
CALM
comfortable temp and clothes
3 complications of hyperthyroid treatment
relapse or recurrent hyperthyroidism
permanent hypothyroidism
thyroid storm
thyroid storm
sudden surge of large amounts of thyroid hormone in blood stream
after surgery of thyroid gland (if meds are not taken or d/c abruptly)
precipitating factors of thyroid storm
trauma
PE
MI
infection
stress
DKA
manifestations of thyroid storm
High fever (hyperpyrexia, 106F)
Severe agitation
Dehydration
Abdominal pain
N/V/D
Confusion
Malignant exophthalmos
Edema
Tachycardia (>160 BPM)
Systolic HTN
Chest pain
Dyspnea
Palpitations
Cardiovascular collapse
Coma
Psychosis
Delirium
Rapid weight loss
CHF with pulmonary edema
management of thyroid storm
Manage airway patency/adequate ventilation
Reduce body temp
Stabilize hemodynamic status
Administer meds to reduce HR and rehydrate with IV fluids
Treat respiratory failure
Antithyroid medications
-Firstline treatment (PTU)
-Sodium iodide IV (to block release of hormones already in the body)
Hydrocortisone
-Treats shock and adrenal insufficiency
Antiarrhythmics
-Propranolol and digoxin
what to use to reduce temp in thyroid storm
tylenol, NOT aspirin
SE of RAI
N/V
SE of PTU and tapazole
Pruritus, rash, arthralgia, fever, sore throat, mouth ulcers, nausea, hepatitis, vasculitis, agranulocytosis
nursing care for hyperthyroidism
monitor SE
monitor thyroid crisis
private room (and monitor temp bc heat intolerance)
VS
sleep meds to help pt calm down bc hypermetabolism
avoid stimulus
modify daily routine
nursing care of exophthalmos
corticosteroids
for dry eyes:
-methylcellulose eye drops during the day or gel at night
-restrict salt intake to reduce edema
-elevate head of the bed
apply cool compress
eyeglasses with prisms for double vision
protect eyes from bright light and UV
relieve pressure at night by elevating head of bed
tape eyelids shut at night
avoid smoking
orbital decompression or eye muscle surgery
treating hyperthyroidism doesn’t fix the eyes!!
nursing care of pretibial edema
hydrocortisone ointments
compression wraps
pt education for hyperthyroidism
rationale for treatment
dosage and SE of meds
meds need to be taken for about 2 years (or life if thyroidectomy/uncontrolled)
do not abruptly d/c
notify physician of fever
effects not evident for about 3 weeks
no decongestants!
symptoms of thyroid storm
periodic examinations
symptoms of hypothyroidism
nutrition for hyperthyroidism
High carb, high calories, high protein until meds take effect
Avoid stimulants such as caffeine
Small frequent meals
primary hypothyroidism
glandular dysfunction
hashimoto’s disease (most common, immune system attacks thyroid gland)
decreased thyroid tissue or secretion of hormone
secondary hypothyroidism
anterior pituitary insuffiency
tertiary hypothyroidism
hypothalamic disorder
inadequate secretions of TSH
hypothyroidism is accumulation of what in SQ and interstitial tissue
mucopolysaccharides
incidence of hypothyroidism
more prevalent in women 30-60
history of autoimmune thyroiditis
treatment for hyperthyroidism
treated with lithium or para-aminosalicylic acid
coexistent with autoimmune disorders
occurs in all ages
hypothyroidism in elderly
from atrophy of thyroid gland
hypothyroidism in the US
from thyroid surgery or RAI treatments
hypothyroidism worldwide
common in areas where soil and water have little iodine leading to endemic goiter
untreated goiter for 5+ years leads to what
permanent damage of thyroid gland with stimulation of TSH
risk factors of hypothyroidism
hashimoto’s disease
DM type 1
RA
atrophy of thyroid gland from aging
therapy for hyperthyroidism (RAI, thyroidectomy, lithium, iodine, antithyroid meds)
radiation to head and neck
scleroderma (hardening of skin with scarring from excess collagen)
what substances produce thyroid hormones
iodide and tyrosine
free thyroxine index
t4
lab values in hypothyroidism
normal t4 and elevated TSH (if mild)
increased cholesterol and triglycerides (CAD and atherosclerosis)
CHOLESTEROL IMPORTANT BC SLOW METABOLISM SO IT CAN’T BE CLEARED FROM THE BLOOD
hypothyroidism in the elderly
more in women
asymptomatic
fatigue and muscle aches
mental confusion
atypical: depression, apathy, decreased mobility, weight loss, constipation
annual TSH screening should be done over 60
cardiac: mild or diastolic HTN
symptoms of hypothyroid
lethargy
-sleep for 14-16 hours a day
edema of eyelids, hands, and face
hoarse voice
menstrual disorder
-heavy, irregular menstruation
-menorrhagia (pain)
-amenorrhea
loss of libido
clinical manifestations of hypothyroid
Subnormal temperature
Intolerance to cold
Skin dry, coarse, thick, cool, pale, carotene, yellowish (HYPER is moist and salmon, the opposite)
No eyebrows
Thick, brittle nails
Hair thins/falls out
Cardiovascular
-Bradycardia
-Hypotension
Pulmonary
-pleural effusion
-dyspnea
Face expressionless
constipation/flatulence
Weight gain
Paresthesia of fingers
Muscle ache
Dull mental processes
depression/paranoia
Apathy
Slow speech
Tongue enlarges
Drooling
Deafness
Massive goiter
Anemia
Activity intolerance
Anorexia
Abdominal distension
Lethargy
Confusion
Decreased BMR (metabolic rate)
clinical manifestations of advanced stage myxedema
Personality and cognitive changes
Inadequate ventilation
Sleep apnea
pleural effusion
Pericardial effusion
Respiratory muscle weakness
Subnormal temperature
Increased cholesterol
Atherosclerosis
Coronary artery disease
Poor ventricular function
Abnormal sensitivity to sedatives, opioids, anesthetic agents (can’t be excreted bc slow metabolism)
cardiac enlargement from pericardial effusion
ascites
decreased bowel sounds
slowed DTR
cerebellar ataxia
dementia-myxedema madness (hallucinations, paranoid ideation, hyperactive delirium)
pseudomyotonia (muscle stiffness)
carpal tunnel syndrome
myxedema coma
occurs in pts on levothyroxine therapy who abruptly d/c meds
HYPOTHERMIA
progressive mental deterioration
decreased metabolism in cardiac tissues
decreased perfusion leading to multiple organ failure
alveolar hypoventilation
narcosis from CO2 retention
nonpitting edema everywhere
puffy face and tongue
altered LOC
management of myxedema
hospitalization
fix symptoms:
hypothermia
hypoventilation
resp acidosis
hypotension
hyponatremia/glycemia
resp failure
coma
triggers of myxedema coma
Illness, infection, trauma, anesthesia, surgery, hypothermia, chemotherapy, etc.
Older women during cold weather
management of myxedema coma
maintain VS
IV glucose
thyroid HRT PO (levothyroxine, IV bolus then PO)
corticosteroids
blankets
maintain patent airway
continuous ECG
check temp frequently
rehydrate
monitor BP and mental status
hypercapnia
monitor for S&S of infection
medical management of hypothyroidism
thyroid HRT
synthetic t4 (levothyroxine synthroid or levothroid)
dose titrated slowly for elderly and CVD
effects not seen for 2 weeks (initially decrease in facial edema and increase in urination)
stick to same brand of meds
monitor for SE (tachy, dyspnea, hyperactivity, insomnia, dizziness, GI upset)
serum FTI and TSH monitored
dosage of thyroid HRT is based on what (4)
age
weight
cardiac status
severity
nursing care of hypothyroidism
HRT with low dose and increase gradually
monitor cardio and neuro SE:
-angina
-HF
-dementia
-confusion
-agitation
-dyspnea
-orthopnea
-palpitations (notify provider if HR >100)
-nervousness
-insomnia
pt not able to excrete meds, can accumulate
be alert of opioids or barbs while taking thyroid meds
may be sensitive to agents if taking insulin or digitalis
increase dose once euthyroid
patient education for hypothyroidism
S&S
meds:
-take same time every morning and don’t change brand
-1-2 hours after breakfast
-avoid laxatives (decrease absorption)
-follow-ups to measure TSH
-don’t abruptly d/c
-take on empty stomach
signs of hypo/hyperthyroidism
manage symptoms:
-fatigue
-dry skin (moisturize and drink water)
-constipation (fiber and fluids 2000 ml daily)
-cold intolerance (blankets ONLY)
-activity intolerance and mental functioning improve
watch for complications:
-angina, HF, myxedema coma
Muscles in parkinon’s
RIGID
meds with meals for parkinson’s?
yes
juvenile parkinsonism
pts <40
primary idiopathic parkinsonism
genetics but not hereditary
atherosclerosis of brain
excessive oxygen free radicals or environmental
secondary parkinsonism
known cause
damage to substantia nigra
seen in boxers
iatrogenic parkinsonism
antipsychotic drugs
tranquilizers
pseudoparkinsonism
some diseases mimic
progressive supranuclear palsy
corticobasal degeneration
post encephalitic parkinsonism
levodopa given
pts with encephalitis as kids grow up and develop symptoms of parkinsonism
where does parkinson’s start
basal ganglia, responsible for voluntary movement
men or women are more affected by parkinson’s
men
what med MIGHT help reduce risk of parkinson’s
2 aspirin a day
Patho of parkinson’s
low dopamine
Ach normal but look high in comparison
destruction of cells in substantia nigra
loss of control, coordination, and initiation of voluntary movement
Muscle contractions
dopamine-producing neurons diminish as we age, causing less stimulation
tremors due to high excitatory signals but not enough dopamine to balance it out
signs of parkinson’s
resting tremors
micrographia
pill-rolling
hypomimia
supination-pronation of forearm
may be unilateral in the beginning
tongue tremors causing dysphagia (difficulty speaking)
plastic rigidity
mild
makes simple movements hard
should have chairs with an arm and shoes with velcro/slip-on
rock back and forth in chair
cogwheel/spastic rigidity
increasing rigidity with rhythmic interruption of muscle
prevents spontaneous movement and gives problems pivoting
lose their balance from postural rigidity
lead-pipe/akinesia
total resistance to movement
freezing phenomena
truncal rigidity (trunk won’t move)
need to move as a unit
can’t pivot, very stiff
stiffness of neck and back causing “old man posture”
stooped, trunk is flexed, bent at waist and elbows, shoulders abducted
rigidity of throat muscles in parkinson’s causes what
raspy voice, then hard to talk, then can’t talk
pooling of food, choking, aspiration PNA
give semisolid foods and thick liquids
rigidity of chest wall and intercostal muscles in parkinson’s leads to what
breathing difficulties
bradykinesia
decreased arm swing when talking
decreased blinking
speaking slowly
walking slow and leans forward with trunk flexed
leads to akinesia
TRAP parkinson’s
tremors
rigidity
akinesia
postural instability
festination
Short shuffling accelerating steps as the body tries to keep the feet directly under the trunk
May look drunk
Person unable to move (especially if multitasking)
High risk of falls because they can trip on rugs (don’t keep rugs)
propulsive gait
What keeps them from falling
Caused by shuffling movement, propelling them to walk faster
They keep the trunk forward to try and keep up
stages of parkinsons
stage 1: initial unilateral mild
stage 2: mild bilateral
stage 3: moderate
stage 4: severe disability
stage 5: complete dependence (still intellectually intact though)
diagnosis of parkinson’s
2/3 cardinal symptoms (tremors, rigidity, bradykinesia)
trial dose of levodopa
Consistent response rules out parkinson’s-like diseases
Person asked to walk across the room and will be observed for rigidity or resting tremors
If positive, placed on medication (main goal is to control symptoms)
secondary symptoms of parkinson’s
aspiration: sialorrhea and dysphagia
weight loss
constipation
UTI
breathing
skin breakdown
insomnia
LE edema
hypotension
dizziness
blepharospasm: total eyelid closure or stuck in one direction
depression
levodopa
hallmark med for parkinson’s
not effective on it’s own because 90% doesn’t cross BBB
SE of large amounts are twitching and hallucinations
benefits wear off in 5-10 years (last resort)
levodopa-carbidopa (sinemet)
replaces dopamine into a form the brain can use
reduces SE
competes with proteins to reach the BBB, so protein should be evenly distributed during the day
avoid B6 in whole grain cereals and pyridoxine
could cause agitation and hallucinations
orthostatic hypotension is common
monitor VS at first for orthostatic HTN, palp, and lightheadedness
can cause suicidal or paranoic ideation
can damage liver and kidneys
non ergot derivatives
for parkinson’s
requip, mirapex
early stages
mimics dopamine
works slowly, SE wear off
effective in controlling symptoms before levodopa started
dopamine agonists
parlodel, permex
given early until it loses effectiveness
MAO inhibitors
for parkinson’s
selegiline
used with sinemet
inhibits dopamine breakdown
can cause HTN crisis
antivirals for parkinson’s
amantadine (symmetrel)
used alone or with levodopa
used early to reduce cardinal signs
low SE
COMT inhibitors
for parkinson’s
comtam
blocks essential enzyme that breaks down levodopa before it reaches brain
good for end of dose wearing off
used in combination with levodopa (increases duration)
antidepressants and antihistamines
anticholinergic to decrease tremors
are parkinson’s meds given with meals
yes
parkinson’s medication side effects
orthostatic HTN
dyskinesia (wild, involuntary movements when meds like sinemet reach their peak)
on-off phenomena (sinemet wears off and causes effects to come and go, higher helps but can cause twitching, hallucinations, and dyskinesia)
end of dose wearing off
hallucinations
agitation
drug holiday
drug holiday
causes parkinson’s crisis
needs to be in a non-stimulating environment with subdue lighting
severe exacerbation of tremors, rigidity, bradykinesia, anxiety, extreme diaphoresis, and tachy
stereotactic surgery for parkinson’s
Targets brain cells to quiet tremors and restore mobility
-pallidotomy: targets internal globus pallidus to improve functional ability
-thalamotomy: targets thalamus
complications are ataxia and hemiparesis
for idiopathic parkinson’s and highest dose of meds
autologous tissue transplant for parkinson’s
adrenalectomy
small parts taken out with dopamine producing cells, then implanted into striatum where neurons are active (palliative)
deep brain stimulation for parkinson’s
same effects of stereotactic
electrodes in thalamus connected to pacemaker interfering with tremor cells in thalamus
neurotransplantation
fetal cell transplantation
cells of substantia nigra from aborted fetuses are transplanted in the caudate nucleus of brain
these cells appear within 6-8 weeks of gestation
awake for procedure
done after drug treatments lose effects
nursing management of parkinson’s
meds (drug peak=time of most demanding task)
drug holiday (quiet, dim room)
diet (don’t take pyridoxine, ETOH, limit protein)
edema
mental
movement (wide gait, tai-chi or yoga)
immobility
swallowing
aspiration
referral
safe environment
speech therapy for dysphasia/phagia
muscle strengthening activity for breathing
PT to stay mobile and maintain flexibility
raised toilet
social worker
support groups
patho of myasthenia gravis (MG)
syndrome of fatigue and exhaustion of muscles
autoimmune neuromuscular progressive disease
VOLUNTARY muscles
Ach receptor sites depleted
antibodies prevent change or destroy receptor sites
prevents excitatory messages to muscles
weakness in sustained contraction (symptoms depend on muscle)
relieved with rest
progresses over 5-7 years
younger women and older men
infection and stress are triggers
Clinical manifestations of MG
ocular: diplopia and ptosis
facial: dysphasia (trouble speaking), dysphonia (nasal voice), mastication (chewing becomes tiring)
larynx: dysarthria (trouble speaking from muscle weakness), aspiration, dysphagia
limbs: unsteady gait, mostly seen in arms, hands, fingers, and neck. not LE
head
diaphragm and intercostal (resp distress)
diagnosis of MG
history and physical
tensilon test
prostigmin
serum test
EMG
chest x-ray
history and physical to diagnose MG
raise hands or look up, hold for 3 minutes, ptosis and falling arms occur, MG suspected if this is resolved with rest
tensilon test to diagnose MG
2 mg edrophonium chloride (anticholinesterase) is given IV. If muscle tone increases, 8 mg more given. Strength improves in 30 seconds and lasts 5-10 minutes in a positive test (since tensilon is short acting)
prostigmin to diagnose MG
neostigmine bromide used if pt doesn’t respond to tensilon but MG still suspected
injected IM and lasts longer
better analysis of muscle tone but more serious SE
SE of prostigmin (neostigmine bromide)
cardiac arrythmia
diaphoresis
increased secretions
cramping
bradycardia
N/V/D
antidote for tensilon and prostigmin tests
ATROPINE SULFATE
serum test to diagnose MG
antibodies to Ach
patients with MG have antibodies to Ach receptors circulating
EMG to diagnose MG
muscle response to stimulation
single musce fibers stimulated by electrical impulse
chest x-ray to diagnose MG
Enlarged thymus behind the breast bone
Usually large in infancy but it can recede by puberty and be replaced by fat as we age in normal circumstances
In MG, it stays or even enlarges
Thymus plays important part in development of immune system in early life
In MG, it’s thought to be responsible to cause symptoms (since it’s an immune reaction)
pharmacological management of MG (anticholinesterase)
First choice, enhances effects of Ach on muscle fibers
pyridostigmine bromide (mestinon, least SE)
neostigmine bromide (prostigmin, more severe SE)
pharmacological management of MG (immunosuppressive)
prednisone:
-drug of choice
-careful with dose
-too much=decreased ability to fight infection WE WANNA AVOID INFECTION IT’S A TRIGGER
-taken every other day
-monitor swallowing and respirations
imuran:
-for more severe MG, severe SE
-suppresses production of abnormal antibodies and improves muscle strength
-given bc it may be immune reaction where antibodies are destroying receptor sites
for MG, as corticosteroids increase in dose, acetylcholine
decreases
plasmapheresis for MG
removes circulating antibodies to Ach receptors
done to stabilize a person in crisis
given pre-op for thymectomy, reduces symptoms of MG
thymectomy for MG
very complex
high risk for complications of anesthesia
Myasthenia crisis
under-dose of meds
increase anticholinesterase drugs or place on ventilator until strength comes back (48 hours)
resp muscles affected
too weak to swallow meds
take meds on time to prevent!
LT weakness causing resp failure
take tensilon to improve symptoms
have suctioning available!!
triggers of myasthenia crisis
INFECTION
surgery
emotional stress
failure to take meds on time
hyperkalemia
certain abx
corticosteroids tapered too quickly
cholinergic crisis
overdose on anticholinesterase drugs (opposite of MG crisis)
decrease dose!
severe muscle weakness
affects resp muscles causing resp failure
how to differentiate MG crisis vs cholinergic crisis
TENSILON TEST
in MG crisis: symptoms improve temporarily
in cholinergic crisis: symptoms WORSEN!! atropine is antidote
pt teaching of meds for MG
take meds at exact time
alarm clock
peak action at meal time (meds 30-60 min prior)
TAKE MEDS BEFORE ADLs TO AVOID WEAKNESS
pt teaching of airway for MG
postural drainage to clear secretions
insufficient air exchange and inability to speak causing them to panic
pt teaching of nutrition for MG
Cutting foods in small bites
Avoid clear liquids that can cause choking (thicken liquids)
Sit up while eating
May need PEG tubing
Closely monitor meals and swallowing
Main meals should be when pt is less fatigued (AM>PM)
Avoid ETOH bc it interferes with normal absorption of meds
Also avoid tonic water bc it contains quinine which can lead to weakness
Novacaine, abx, cardiovascular and psychotropic drugs can also trigger crisis
pt teaching about eyes in MG
wear sunglasses
med alert bracelet
artificial tears to prevent corneal damage
tape eyes closed for short periods
patho of MS
CENTRAL nervous system (not ANS or PNS)
inflamed nerves
loss of myelin
increase in oligodendrocyte:
-cells that produce myelin
-increases to repair myelin, but not fast enough
-presence of oligoclonal bands in CNS (diagnosis, immune system malfunction)
involves NERVES, not muscles like parkinson’s and MG
patches of plaque in white matter of CNS
schwann cells destroyed (irreversable)
immune system attacks myelin leaving scars
nerves become inflamed and edematous
sheath damage causes flow of nerve impulses to slow down
symptoms depend on area of demyelination
optic nerves affected
contributing factors of MS
20-40 year old women
viral
-something triggers dormant virus from before 15 years old (rubeola, herpes, and mono)
familial or genetic (higher incidence in siblings and twins)
environmental (high incidence north of equator)
high suicide rate
lifespan unaffected but indirect complications can kill
diagnosis of MS
no lab tests
history of random symptoms, family background, evidence of remission (come and go)
mcdonald criteria (2 episodes of neuro symptoms one month apart, MRI of several damaged areas of CNS [lesions])
evoked potential (how long it takes for stimulus to reach the brain)
relapsing-remitting MS
Most people usually start with this
Exacerbations (relapse) and periods of remission
Relapse can last for days, weeks, or months
Recovery can be slow and gradual or instantaneously
No disease progression during remission**
primary progressive MS
no acute exacerbations
symptoms gradually worsen
occasional minor and temporary recovery
secondary progressive MS
progression of relapsing-remitting MS
occurs within 10-25 years after
gradual worsening of symptoms, no recovery
usually seen in older people
seen in those who don’t respond to meds when they have RRMS
progressive relapsing MS
escalates very quickly to severe disability with very few periods of remission
in periods of remission, symptoms worsen
exacerbation and remission in MS
Exacerbations and remissions in all types
Can occur at unpredictable times depending on area of CNS damage
During exacerbation, new symptoms appear and old ones may get worse
During remission, symptoms may decrease or go away altogether
Exacerbations become longer as disease gets worse
Remission gets shorter as exacerbations become longer
triggers of MS
heat, infection, trauma, pregnancy, fatigue, stress
numb legs during infection
visual manifestations of MS
Blurring (first symptom from optic neuritis from damage and inflammation of optic nerve)
Diplopia
Blindness
Nystagmus (repetitive, uncontrolled movements)
Oscillopsia (objects that jump in field of vision)
other manifestations of MS
intentional tremors unlike parkinson’s
loss of coordination
numbness
spasms (warm bath relieves them NOT HOT)
heat sensitivity
fatigue (fall to the ground)
lassitude (extreme fatigue)
forgetful and short attention span but cognition is intact
impaired judgment and reasoning
weakness
paresthesia
pain around trunk from spasm of spinal cord
secondary/tertiary symptoms of MS
UTI
ulcers
constipation
pedal edema
contractures
PNA
depression
mood swings
vocational problems (job stuff)
personal issues (marriage)
nursing goals for MS (mobility)
wide based gait like parkinson’s
PT for stretching
occupational therapist
activity but know limits
stop when fatigued
fluid intake with MS
increase to 2000-3000 mL per day
400-500 with each meal
200 in morning and afternoon
decrease in evening bc decreased bladder control
bladder nursing considerations MS
void q2h
don’t ignore sensation to void (bedpan closeby)
voiding schedule (30 min after drinking fluids, then increase time)
kegel exercises for older population
DON’T use diapers
NO retention catheters
intermittent instead
diet for MS
high fiber and complex carbs, low fat
avoid laxatives
spasticity in MS
MAJOR problem bc it affects movement and can lead to disability
ROM exercises at least 2x daily
need a PT
don’t cause fatigue bc exacerbation!!
cortisone for MS
prednisone (IV) useful for the eye
methylprednisolone
ACTH
anti inflammatory
shortens episodes of exacerbation
take in the morning
monitor glucose
weight gain and peripheral edema
BP
take with food or milk
avoid aspirin
what to report when taking cortisone for MS
anorexia, nausea, hypokalemia, muscle weakness
Can cause ulcers on empty stomach (gastric bleeding)
Watch stools for black, tarry stools (indicates bleeding)
anticholinergics and antispasmodics for MS
for bladder dysfunction
amantadine HCl for MS
for fatigue
antidepressants for MS
prozac or zoloft
depression causes fatigue which is a trigger
BB, diuretics, and antihistamines for MS
for tremors and ataxia
anti seizure meds for MS
spastic pain
tegretol, depakote
muscle relaxants for MS
Baclofen, dantrium, valium, klonopin
Baclofen pump surgically implanted for severe symptoms (gives minute doses directly to spinal cord)
Baclofen is especially effective to decrease muscle spasms in the lower extremities
SE of muscle relaxants
dizziness, drowsiness, fatigue
immunoregulatory meds for MS
avonex
beta-interferon (betaseron/feron)
copaxone
rebif (reduces rate of MS and damage)
novantrone (decreases frequency of exacerbations, toxic effects, used for =<3 years)
imuran
cytoxan
ABCs and Rs are best, others cause liver damage?
tysabri (was canceled and brought back, reduces flareups, no new lesions and slowed progression)
SE of immunoregulatory meds for MS
depression, liver and thyroid gland can be affected, severe flu-like symptoms from interferons (treated with NSAIDS)
guillain-barre syndrome etiology
no high incidence in any specific gender or ethnic background
high incidence in pts with lupus, HIV, and hodgkin’s
occurs in the ages 15-36 and 50-75
1-2 weeks after mild viral infection (gastroenteritis, bronchitis, or flu)
8 weeks after vaccination
pregnancy (CRAWLING SENSATION IN LEGS, ascends rapidly, vent and trach needed)
patho of GBS
schwann cells spared (unlike MS) which is why recovery is possible
antibodies in plasma
inflammation and destruction of myelin sheath
slowed communication between brain and peripherals leading to paralysis (unlike MS which is CNS)
doesn’t affect cognition
doesn’t recur
general clinical manifestations of GBS
vision problems
loss of DTR
dyskinesia
dysphagia leading to aphasia (from glossopharyngeal nerves being affected)
cardiac manifestations of GBS
palpitations and tachy/bradycardia
orthostatic hypo/hypertension from damage to vagus nerves
bladder and bowel manifestations of GBS
difficulty urinating or not fully emptying bladder
incontinence
constipation
dizziness first 24-72 hours
cramps
resp manifestations of GBS
SOB, cramps, entire body aches
vocal paralysis leading to resp paralysis and death
AIRWAY PATENCY IS IMPORTANT!!
initial period of GBS
Weakness in varying degrees in legs and arms
Numbness, tingling, dyskinesia, hyporeflexia/loss of DTR
Sensitivity of hot and cold due to paresthesia
Difficulty distinguishing textures due to paresthesia
Cranial nerves become affected, leading to blurred vision and blindness from optic nerve demyelination
secondary symptoms of GBS
Aspiration
PNA
DVT from immobility
Contractures from immobility
Risk for infections
Although mostly ascending, can sometimes be descending
Starting at jaw, then tongue, pharynx, larynx, sternocleidomastoid and downward
Respiratory involvement is quick and fatality is high
recovery of GBS
Within 2-4 weeks from start, progression stops but symptoms continue
Plateau period, pt may be taken off the ventilator
2-4 weeks later, recovery
Recovery is slow bc injured nerves take a long time to recover
Most function comes back within a year or two (recovery phase)
diagnosis of GBS
Symptoms
History of viral infections and physical exam
Rapid onset of ascending weakness
Loss of DTR
Lumbar puncture (shows elevated fluid protein in CSF)
EPS
Crawling sensation of legs and arms
medical management of GBS
No prevention and no cure
ICU to monitor breathing and cardiac status
Mechanical ventilation
Heart monitor
Anticoagulant
SCD
Plasmapheresis (whole blood removed, cells separated, then returned)
Immunoglobulin (large doses IV to block receptors where antibodies attach and do damage, few side effects)
Assess respiratory status, intake and output, VS, and BP
nursing management of GBS
ventilator (ween off later)
incentive spirometer
chest PT
aspiration risk
turn head to side
suction
HOB 15-30 degrees
positioning
P-ROM
padding bony areas
thigh high embolic stockings
SCD
bowel sounds
gag reflex
I&Os
IV fluids
TPN
G-tube
explain stuff
pictures
speech therapist
epilepsy
recurrent seizures
what happens during a seizure
CNS depression, consciousness affected
pt may go into deep sleep or be fatigued/confused after episode
increased need for oxygen and glucose
where do nonepileptic seizures originate
outside the CNS
fever
hypoxia
poisoning
drug intoxication
alcohol withdrawal
precipitators of epileptic seizures
stress
lack of sleep
emotional upset
alcohol
missed meds
abnormally high level of excitatory neurotransmitters
abnormally low level of inhibitory neurotransmitters
primary (idiopathic) seizures
recurrent
prior to ages 20-30
inherited threshold, not actual seizure disorder
secondary (acquired) seizures
brain pathology
trauma, brain tumor, meningitis, childhood fevers from childhood problems, CVA, hypoxia, vascular disease, aneurysm, infections from AIDS
metabolic disorder
electrolyte imbalance
drugs/alcohol
kidney/liver failure
cerebral hypoxia
risk increases with age bc of degenerative process of brain
how are seizures classified
by where they originate
simple partial seizures
no LOC
changes in senses
aware of surroundings but can’t control
lasts 30 seconds
very specific signs
emotional symptoms
can progress to generalized seizures
temporal lobe seizure
sensory symptoms
if frontal lobe/motor cortex affected in seizure
one side affected
occipital region affected during seizure
vision affected (flashing lights)
complex seizure
LOC
automatism (purposeless repetitive symptoms)
blacks out
bizarre behavior
looks dazed
confusion or psychosis when they recover (may do WILD things, THIS IS PART OF THE SEIZURE)
recovery when they don’t remember what happened
longer than simple, 1-3 min but can be up to 15
generalized seizure
involves whole brain
not cured with meds but can be avoided with them
preictal phase
first phase of grand mal seizure
They feel an aura, like a smell, emotional swing, dizziness, etc
pt may recognize the aura and lay down to prepare for seizure
NOT convulsive
ictal phase
tonic-clonic
2nd phase of grand mal seizure
tonic:
30-60 seconds long
stiffness and rigidity
eyes open, pupils fixed
epileptic cry from forced expiration of air
cyanosis
administer oxygen
clonic:
2-5 mins
jerking of extremities
rhythmic shaking, muscle contractions and relaxation
incontinence
person may bite tongue or lips
foaming at mouth (turn to side)
suctioning and oxygen kept at bedside
postictal phase
final phase of grand mal seizure
deep sleep for 1/2-4 hours
flaccid muscles
stridor with excessive salivations, keep head turned to side
no memory of seizure
confused, headache
need to be reoriented (priority intervention)
what to document for grand mal seizure
Document movement of eyes, what went on with head, muscle rigidity especially once seizure began (gives clue of location of brain where it started)
Progression and duration of seizure
Respiratory status
LOC
Pupillary reaction
Incontinence
Can’t check HR and BP during ictal phase, so take vitals continuously during postictal phase
when person becomes conscious
events preceding seizure
timing
body parts affected
descriptions of each phase
sequence of involvement
eye deviation
patient condition
postictal behavior
petit mal seizures (absence)
brief LOC
vacant facial expression
rapid blinking or lip smacking
“daydreaming”
5-30 seconds
they DON’T fall
back to normal activity
can be due to hx of childhood fevers or birth injury
in children, diminish after puberty
occurs during the day
may not be diagnosed until it progresses to tonic-clonic
school nurses work w families to avoid triggers
myoclonic seizures
generalized
Brief jerking of muscles
Brief LOC
Can last from a few seconds to a minute
Brief episode of involuntary, jerky movements of one single muscle or multiple
Pt may lose consciousness for a moment and are confused postictally
Triggered by fatigue
Atonic seizure
Total loss of muscle tone
Falls to the floor
Briefly nods off
Confused post ictal
Must wear headgear at all times
EEG
most common and definitive diagnosis for seizures
detects abnormalities in electrical activity (location and type)
difficult to diagnose bc normal activity between episodes
best if done 24h after seizure
if it begins deep in brain, EEG may not detect it
withhold caffeine but don’t fast
CT and MRI for seizures
detect abnormalities (MRI includes those due to aging)
telemetry for seizures
brain activity
phenytoin for seizures
MONITOR BLOOD LEVELS
see how long it takes to metabolize so you can see how often they need to take the med
toxicity with seizure meds
can go into allergic shock (life threatening)
drug toxicity may occur in the beginning bc we try to titrate the dose
chronic toxicity if prolonged use
rule with using more than 1 seizure med
start with one med
as one is added, the other is tapered
dosage of seizure meds depend on what 3 things
age
type of seizures
frequency
meds for seizures (6)
phenytoin (dilantin): prevents
carbamazepine (tegretol): prevents
valproate (dekapan)
clonazepam (klonopin): avoid in pregnancy, avoid ETOH
diazepam (valium): SEDATING
luminal (phenobarbital): SEDATING
pt teaching of phenytoin for seizures
gingival hyperplasia
hirsutism
bone marrow suppression
VFIB
nausea
diplopia
nystagmus
hyperthermia
ataxia
slurred speech
sedation
confusion
coma
pt teaching of phenobarbital
extreme sedation
depression
confusion
hallucinations
ataxia
falls!
rule for driving when you have epilepsy
must be 2 years free
when to call EMS for seizures
if it lasts >10 min
resp injury
pregnant
2nd seizure starts before 1st one ends
vagal nerve stimulation for seizures
implantable device used with meds
in cervical area under clavicle, connected to vagus nerve
short burst of elec stimulation to the brain, controlling and reducing seizure activity
temporal lobectomy for seizures
curative surgery
removal of where seizures start, without causing neuro deficit
corpus callosum resection for seizures
palliative for tonic-clonic seizures
or for atonic to make them tolerable
cortical resection for seizures
for complex partial seizures
stereotactic surgery for seizures
specific area of brain targeted
monitor pre-op for location
avoid areas of brain that control memory and speech
status epilepticus
when pts abruptly stop taking meds
continuous or one long seizure
LOC
lasting at least 30 min
oxygen and glucose depletion
resp arrest
brain damage!
cardiac dysrhythmias, lactic acidosis and renal failure (muscle breakdown, myoglobin accumulates in kidneys)
nursing management of seizures
assess for aura, triggers
establish airway
administer oxygen and glucose
move objects away
position on side
resp status
NG tube and continuous VS unless tonic-clonic
dia/lorazepam IV
dysphagia
swallowing difficulties
dysphasia
trouble with language (can’t put words into a sentence)
dysarthria
difficulty speaking from weak muscles
sulfonyureas and meglinitides with or without food
15-30 min before meals
biguanides with or without meals
with
iodides with or without food
with water (SSKI) or milk (lugol’s)
with meals
MG med time
30-60 min before meals
cortisone for MS with or without food
with food or milk
