Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Med-Surg I > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Type 1 diabetes

A

pancreas not functioning
insulin dependent
destruction of beta cells
ONLY insulin used
before the age of 20-30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

type 2 diabetes

A

pancreas functioning
weight loss and diet –> oral hypoglycemics –> insulin
after age 30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what to treat gestational diabetes with

A

insulin
NOT oral hypoglycemics (harms the fetus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

risk for type 2 diabetes increases ___% each year following pregnancy

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what drugs give secondary diabetes

A

steroids like prednisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

prediabetes is high glucose after what age

A

40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

prediabetes blood glucose levels (fasting and post prandial)

A

100-126 fasting
140-200 post prandial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

A1c levels

A

<5.7% normal
5.7-6.5% prediabetes
6.5%+ diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

A1c and glucose level goals for diabetic pts

A

<7% and glucose <126

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

where is insulin produced and what does it do

A

beta cells of the pancreas
metabolizes glucose for energy
Insulin signals liver to stop releasing/breaking down glucose when we don’t need it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

where is glucagon made

A

alpha cells of the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

criteria for diagnosing diabetes (3)

A

fasting: 126+ on 2 occasions
HbA1c: 6.5%+ on 2 occasions
OGTT: glucose 200+ on 2 occasions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

triglycerides in type 2 diabetes

A

usually very high
>250 indicates high risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

metabolic syndrome (5)

A

increased serum creatinine
insulin resistance
dyslipidemia
BP >130/85
abdominal obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

high risk ethnic population for diabetes

A

african americans, native americans, hispanic ppl (minorities)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

considerations for hispanic ppl in diabetes

A

Hispanic ppl prioritize others, they may cook for the family but not properly for themselves
See diabetes as a punishment from god

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

babies in relation to diabetes

A

women who give birth to babies over 9 pounds are at risk for diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

complications of type 2 diabetes (6)

A

Cardiovascular disease
PVD
CVA
kidney disease
blindness
neuropathy (most common cause of nontraumatic amputation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

virus exposure in type 1 diabetes

A

Virus triggers autoimmune response against islet cells of pancreas causing destruction of beta cells (absolutely no insulin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

glycogenolysis when eating (when you have diabetes)

A

prevented
no conversion of stored glycogen into glucose for energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

gluconeogenesis

A

conversion of protein to glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

which type of DM is DKA seen in

A

type 1 bc no insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

RBG of hyperglycemia

A

> 250

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what 3 electrolytes get excreted in urine in diabetes

A

Na+
Cl-
K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

pH imbalance in ketosis

A

metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

blood glucose in ketonuria

A

> 300

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

which s&s are more common in type 1 diabetes (8)

A

kussmaul breathing
lethargy
stupor
weight loss
fruity breath
N/V
abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3 kinds of complications of hypoglycemia

A

macrovascular
microvascular
neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

macrovascular complications of DM

A

Cardiovascular and cerebrovascular disease (increase in RBC aggregation bc they become stiff and don’t flow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

microvascular complications of DM

A

damages small vessels of eyes and kidneys causing retinopathy/nephropathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

neuropathy

A

nerve cells become cirrhosed
not vascular!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

why are diabetics at risk of amputations

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

S&S of type 1 diabetes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

S&S of type 2 diabetes

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

mnemonic for glucose levels

A

hot and dry=sugar high
cool and clammy= need some candy
(confusion, lightheadedness, tremors, double vision)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

NPO how many hours before fasting blood glucose sample

A

8-12 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

oral glucose tolerance test

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

monofilament testing

A

Fine, threadlike material rubbed against extremities to test for feeling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

fats for diabetic diet

A

30% or less of total calories
10% saturated
combine starch with protein and fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

CHO (complex or simple) in diabetic diet

A

50-60%
whole grains good

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

protein in diabetic diet

A

10-20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

why should we decrease alcohol consumption in diabetes

A

impairs gluconeogenesis (glucose isn’t being created)
increases insulin secretion (HYPOglycemia)
if diabetes well controlled, MODERATE alcohol is fine with meals or slowly after

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

omega-3 fatty acids and fiber for diabetes

A

lowers cholesterol, sat fats, and LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

daily limit of cholesterol for diabetes

A

300 mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

cinnamon for diabetes

A

lowers blood glucose
1/4 tsp 2x daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

FIT acronym for diabetic fitness

A

f-frequency: 3x/week
i-intensity: 60-80% maximum HR
t-time: aerobic activity 20-30 min with 5-10 min warm up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

exercise and blood glucose

A

ELEVATES with hard core exercise
LOWERS with light exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what to eat before and after exercising w diabetes

A

15g of carbs or 1 complex carb with proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

rapid insulin onset and peak

A

onset: 5-15 min
peak: 30-60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

names of rapid acting insulin

A

Lispro (humalog), aspart (novolog), glulisine (apidra)
Inhaled insulin (exubera)
allergies to beef or pork insulins?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

onset and peak of short acting insulin

A

onset: 30-60 mins
peak: 2-3 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

names for regular insulin

A

Novolin R, humalog R, iletin regular
for insulin coverage
SQ or IV in emergencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

NPH insulin onset and peak

A

onset: 2-4 hours
peak: 4-12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

NPH names

A

Novolin L (lente)
Novolin N (NPH)
Humalog N
Taken AFTER food and at night
Regular insulin combined with a large protein, protamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

long acting insulin onset, duration

A

onset: 1-6 hours
continuous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

names for long acting insulin

A

levemir
lantus (insulin glargine)
DO NOT MIX
TAKE SAME TIME EVERY DAY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

rolling insulin (what types can/can’t be rolled)

A

DON’T roll rapid or short
ROLL intermediate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

degrees for injections of insulin

A

45 if loose skin or thin
otherwise 90 (abdomen always 90)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

lipoatrophy

A

loss of SQ fat with dimpling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

lipohypertrophy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what type of insulin is via pump

A

fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

who are oral antidiabetic drugs contraindicated in

A

type 1 DM
severe renal/liver disease
hypersensitivity to sulfa
pregnancy/lactation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

order for diabetic agents

A

diet and exercise
oral hypoglycemics (type 2)
insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

sulfonylureas and meglinitides

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

alpha-glucosidase inhibitors “starch blockers”

A

target GI tract
slow carb absorption
monitor liver function q3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

biguanides

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Thiazolidinediones TZD

A

Reduces production of glucose by liver
Target liver (tests done every 2 months)
Monitor for fluid retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

how much should a1c drop for every class of oral hypoglycemics added

A

1-1.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what to eat when hypoglycemic and what is blood glucose

A

juice, then starch and protein
concentrated CHO (cheese and crackers)

blood sugar <60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

signs of mild hypoglycemia

A

Headache
Hunger
Weakness
Stimulation of sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

signs of moderate hypoglycemia and what to give

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

signs of severe hypoglycemia

A

Disorientation
Seizures
Loss of consciousness
Diabetic coma
death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

at what blood glucose is a person still arousable

A

50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

reversal of hypoglycemia when sick

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

glucose in illness

A

increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what to eat when sick (diabetic)

A

juice, soda, jell-o, small portions of CHO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

how often to assess glucose and ketones when diabetic sick

A

q1-4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

when should you notify the provider about a sick diabetic patient

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

symptoms of DKA

A

dehydration
delirium
dizziness
onset slow: 4-10 hours
tachy
high blood sugar
hyperkalemia and hyponatremia
kussmaul breathing
fruity breath
abd pain
ketonuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Treatment of DKA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Precipitators of DKA (5 S’s)

A

sepsis
surgery
sugar high
stress
substance abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

when NOT to give K+ to a patient with DKA

A

low urine output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what solution is insulin compatible with

A

NS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

rule when mixing insulin and NS

A

discard first 50 ml of solution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

HHNS

A

SOME insulin produced, not like DKA
in type 2 DM
More serious than DKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

causes of HHNS

A

severe dehydration
infection
stress
medications
med conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

urine tests for HHNS

A

+ for glucose
- for ketones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

electrolyte imbalance in HHNS

A

hypernatremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

management of HHNS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

HHNS symptoms

A

hypotension
polyuria
glycosuria
polydipsia
decreased LOC from increased Na+
hyperthermia
seizures
paralysis
nephropathy with microalbuminuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

dawn phenomenon

A

early morning hyperglycemia (3-4AM)
decreased insulin
growth hormones secreted during the night
blood sugar assessed at night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

treatment of dawn phenomemon

A

Increase evening to intermediate or long acting dose of insulin
Change time of insulin administration from early evening to closer to bedtime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

somogyi effect

A

nocturnal hypoglycemia
Normal or elevated blood glucose at night
Hypoglycemia later
2-3AM
Hyperglycemia in the morning
3AM-breakfast
due to excessive insulin dosage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

treatment of the somogyi effect and 2 S&S

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

microvascular complications

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

neuropathic complications

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

macrovascular complications

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what is the thyroid gland regulated by

A

anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what increases cellular metabolism

A

thyroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

paro globulin in blood

A

breakdown of thyroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what do antithyroid meds cause

A

hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Med that increases thyroid hormone

A

dilantin (phenytoin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

is t3 or t4 more potent

A

t3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what are t3 and t4 made of

A

iodine
thyroid gland takes iodine and converts into t3 and t4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

what is negative feedback controlled by (2)

A

hypothalamus and anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

goiter and hyper/othyroidism

A

goiter doesn’t necessarily mean you have one or the other
but if you have hyperthyroidism you WILL have hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

best source of iodine

A

table salt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

special characteristic of thyroid gland

A

very vascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

TRI and TRAB

A

binds to TSH receptor sites, acts like TSH, makes the gland secrete t3 and t4, then anterior pituitary tells gland to stop producing TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

most common cause of hyperthyroidism

A

graves disease
more common in women 20-40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

iodine deficiency leads to what

A

toxic nodular goiter
decrease of t3 and t4, increase in TSH causing goiter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

SNS and hyperthyroidism

A

increased SNS activity
Diaphoresis, SOB, palpitations, weight loss, muscle weakness, blurred vision, decreased attention span

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

clinical manifestations of thyrotoxicosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

pretibial myxedema

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

exophthalmos

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

eyelid lag

A

Upper eyelids don’t descend when person gazes down slowly
Eyelid lags behind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

globe lag

A

Upper eyelids pull back faster than eyeball when looking upwards
Eyeball lags behind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

classifications of goiter

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

clinical manifestations of goiter (from progression)

A

AFIB
increased SBP and decreased DBP
cardiac decompression
osteoporosis
fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

cardiac effects of goiter

A

Sinus tachycardia
Dysrhythmias
Increased pulse pressure
Palpitations
Myocardial hypertrophy
Heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

clinical manifestations of hyperthyroidism in elderly

A

apathetic hyperthyroidism
only cardiovascular symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

diagnostics of hyperthyroidism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

antithyroid meds are for who and used for how long

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Thionamide: Propylthiouracil (PTU)

A

suppresses thyroid hormone
used for severely ill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

thionamide: methimazole

A

for hyperthyroid
blocks iodine
most common for pregnant and under 18
10x more potent than PTU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

contraindications of antithyroid meds

A

bleeding disorders
diabetes
lithium therapy
late pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

iodides

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

SE of antithyroid meds

A

Agranulocytosis
-Most serious
-Report fever, chills, sore throat
-Especially seen in elderly
Leukopenia
Thrombocytopenia
Pruritus
Dermatitis
Arthralgia (joint pains)
Mouth ulcers
Nausea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

what not to take with iodides

A

expectorants
bronchodilators
salt substitutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

signs of iodism

A

swelling of buccal mucosa
excessive salivation
coryza (inflammation of mucous membrane with a cold)
lesions in mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Radioactive iodine (1-131)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

thyroidectomy

A

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

133
Q

risk of thyroid surgery

A

damage of parathyroid and laryngeal nerves
HEMORRHAGE

134
Q

preop management of thyroid surgery

A

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

135
Q

postop management of thyroid surgery

A

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

136
Q

hypocalcemia teaching in thyroid post-op

A

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

137
Q

3 things to have available after thyroid surgery

A

sandbags
trach set
Ca+ gluconate ampoules (patent IV line)

138
Q

nutrition for preop thyroidectomy

A

increase calories, protein, and carbs bc they metabolize rapidly
avoid foods causing diarrhea
small, frequent meals
vits and minerals
monitor weight, I&Os

139
Q

environment for preop thyroidectomy

A

no stimulation
restrict visitors
CALM
comfortable temp and clothes

140
Q

3 complications of hyperthyroid treatment

A

relapse or recurrent hyperthyroidism
permanent hypothyroidism
thyroid storm

141
Q

thyroid storm

A

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)

142
Q

precipitating factors of thyroid storm

A

trauma
PE
MI
infection
stress
DKA

143
Q

manifestations of thyroid storm

A

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

144
Q

management of thyroid storm

A

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

145
Q

what to use to reduce temp in thyroid storm

A

tylenol, NOT aspirin

146
Q

SE of RAI

A

N/V

147
Q

SE of PTU and tapazole

A

Pruritus, rash, arthralgia, fever, sore throat, mouth ulcers, nausea, hepatitis, vasculitis, agranulocytosis

148
Q

nursing care for hyperthyroidism

A

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

149
Q

nursing care of exophthalmos

A

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!!

150
Q

nursing care of pretibial edema

A

hydrocortisone ointments
compression wraps

151
Q

pt education for hyperthyroidism

A

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

152
Q

nutrition for hyperthyroidism

A

High carb, high calories, high protein until meds take effect
Avoid stimulants such as caffeine
Small frequent meals

153
Q

primary hypothyroidism

A

glandular dysfunction
hashimoto’s disease (most common, immune system attacks thyroid gland)
decreased thyroid tissue or secretion of hormone

154
Q

secondary hypothyroidism

A

anterior pituitary insuffiency

155
Q

tertiary hypothyroidism

A

hypothalamic disorder
inadequate secretions of TSH

156
Q

hypothyroidism is accumulation of what in SQ and interstitial tissue

A

mucopolysaccharides

157
Q

incidence of hypothyroidism

A

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

158
Q

hypothyroidism in elderly

A

from atrophy of thyroid gland

159
Q

hypothyroidism in the US

A

from thyroid surgery or RAI treatments

160
Q

hypothyroidism worldwide

A

common in areas where soil and water have little iodine leading to endemic goiter

161
Q

untreated goiter for 5+ years leads to what

A

permanent damage of thyroid gland with stimulation of TSH

162
Q

risk factors of hypothyroidism

A

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)

163
Q

what substances produce thyroid hormones

A

iodide and tyrosine

164
Q

free thyroxine index

A

t4

165
Q

lab values in hypothyroidism

A

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

166
Q

hypothyroidism in the elderly

A

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

167
Q

symptoms of hypothyroid

A

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

168
Q

clinical manifestations of hypothyroid

A

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)

169
Q

clinical manifestations of advanced stage myxedema

A

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

170
Q

myxedema coma

A

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

171
Q

management of myxedema

A

hospitalization
fix symptoms:
hypothermia
hypoventilation
resp acidosis
hypotension
hyponatremia/glycemia
resp failure
coma

172
Q

triggers of myxedema coma

A

Illness, infection, trauma, anesthesia, surgery, hypothermia, chemotherapy, etc.
Older women during cold weather

173
Q

management of myxedema coma

A

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

174
Q

medical management of hypothyroidism

A

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

175
Q

dosage of thyroid HRT is based on what (4)

A

age
weight
cardiac status
severity

176
Q

nursing care of hypothyroidism

A

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

177
Q

patient education for hypothyroidism

A

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

178
Q

Muscles in parkinon’s

A

RIGID

179
Q

meds with meals for parkinson’s?

A

yes

180
Q

juvenile parkinsonism

A

pts <40

181
Q

primary idiopathic parkinsonism

A

genetics but not hereditary
atherosclerosis of brain
excessive oxygen free radicals or environmental

182
Q

secondary parkinsonism

A

known cause
damage to substantia nigra
seen in boxers

183
Q

iatrogenic parkinsonism

A

antipsychotic drugs
tranquilizers

184
Q

pseudoparkinsonism

A

some diseases mimic
progressive supranuclear palsy
corticobasal degeneration

185
Q

post encephalitic parkinsonism

A

levodopa given
pts with encephalitis as kids grow up and develop symptoms of parkinsonism

186
Q

where does parkinson’s start

A

basal ganglia, responsible for voluntary movement

187
Q

men or women are more affected by parkinson’s

A

men

188
Q

what med MIGHT help reduce risk of parkinson’s

A

2 aspirin a day

189
Q

Patho of parkinson’s

A

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

190
Q

signs of parkinson’s

A

resting tremors
micrographia
pill-rolling
hypomimia
supination-pronation of forearm
may be unilateral in the beginning
tongue tremors causing dysphagia (difficulty speaking)

191
Q

plastic rigidity

A

mild
makes simple movements hard
should have chairs with an arm and shoes with velcro/slip-on
rock back and forth in chair

192
Q

cogwheel/spastic rigidity

A

increasing rigidity with rhythmic interruption of muscle
prevents spontaneous movement and gives problems pivoting
lose their balance from postural rigidity

193
Q

lead-pipe/akinesia

A

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

194
Q

rigidity of throat muscles in parkinson’s causes what

A

raspy voice, then hard to talk, then can’t talk
pooling of food, choking, aspiration PNA
give semisolid foods and thick liquids

195
Q

rigidity of chest wall and intercostal muscles in parkinson’s leads to what

A

breathing difficulties

196
Q

bradykinesia

A

decreased arm swing when talking
decreased blinking
speaking slowly
walking slow and leans forward with trunk flexed
leads to akinesia

197
Q

TRAP parkinson’s

A

tremors
rigidity
akinesia
postural instability

198
Q

festination

A

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)

199
Q

propulsive gait

A

What keeps them from falling
Caused by shuffling movement, propelling them to walk faster
They keep the trunk forward to try and keep up

200
Q

stages of parkinsons

A

stage 1: initial unilateral mild
stage 2: mild bilateral
stage 3: moderate
stage 4: severe disability
stage 5: complete dependence (still intellectually intact though)

201
Q

diagnosis of parkinson’s

A

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)

202
Q

secondary symptoms of parkinson’s

A

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

203
Q

levodopa

A

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)

204
Q

levodopa-carbidopa (sinemet)

A

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

205
Q

non ergot derivatives

A

for parkinson’s
requip, mirapex
early stages
mimics dopamine
works slowly, SE wear off
effective in controlling symptoms before levodopa started

206
Q

dopamine agonists

A

parlodel, permex
given early until it loses effectiveness

207
Q

MAO inhibitors

A

for parkinson’s
selegiline
used with sinemet
inhibits dopamine breakdown
can cause HTN crisis

208
Q

antivirals for parkinson’s

A

amantadine (symmetrel)
used alone or with levodopa
used early to reduce cardinal signs
low SE

209
Q

COMT inhibitors

A

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)

210
Q

antidepressants and antihistamines

A

anticholinergic to decrease tremors

211
Q

are parkinson’s meds given with meals

A

yes

212
Q

parkinson’s medication side effects

A

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

213
Q

drug holiday

A

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

214
Q

stereotactic surgery for parkinson’s

A

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

215
Q

autologous tissue transplant for parkinson’s

A

adrenalectomy
small parts taken out with dopamine producing cells, then implanted into striatum where neurons are active (palliative)

216
Q

deep brain stimulation for parkinson’s

A

same effects of stereotactic
electrodes in thalamus connected to pacemaker interfering with tremor cells in thalamus

217
Q

neurotransplantation

A

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

218
Q

nursing management of parkinson’s

A

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

219
Q

patho of myasthenia gravis (MG)

A

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

220
Q

Clinical manifestations of MG

A

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)

221
Q

diagnosis of MG

A

history and physical
tensilon test
prostigmin
serum test
EMG
chest x-ray

222
Q

history and physical to diagnose MG

A

raise hands or look up, hold for 3 minutes, ptosis and falling arms occur, MG suspected if this is resolved with rest

223
Q

tensilon test to diagnose MG

A

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)

224
Q

prostigmin to diagnose MG

A

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

225
Q

SE of prostigmin (neostigmine bromide)

A

cardiac arrythmia
diaphoresis
increased secretions
cramping
bradycardia
N/V/D

226
Q

antidote for tensilon and prostigmin tests

A

ATROPINE SULFATE

227
Q

serum test to diagnose MG

A

antibodies to Ach
patients with MG have antibodies to Ach receptors circulating

228
Q

EMG to diagnose MG

A

muscle response to stimulation
single musce fibers stimulated by electrical impulse

229
Q

chest x-ray to diagnose MG

A

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)

230
Q

pharmacological management of MG (anticholinesterase)

A

First choice, enhances effects of Ach on muscle fibers

pyridostigmine bromide (mestinon, least SE)
neostigmine bromide (prostigmin, more severe SE)

231
Q

pharmacological management of MG (immunosuppressive)

A

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

232
Q

for MG, as corticosteroids increase in dose, acetylcholine

A

decreases

233
Q

plasmapheresis for MG

A

removes circulating antibodies to Ach receptors
done to stabilize a person in crisis
given pre-op for thymectomy, reduces symptoms of MG

234
Q

thymectomy for MG

A

very complex
high risk for complications of anesthesia

235
Q

Myasthenia crisis

A

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!!

236
Q

triggers of myasthenia crisis

A

INFECTION
surgery
emotional stress
failure to take meds on time
hyperkalemia
certain abx
corticosteroids tapered too quickly

237
Q

cholinergic crisis

A

overdose on anticholinesterase drugs (opposite of MG crisis)
decrease dose!
severe muscle weakness
affects resp muscles causing resp failure

238
Q

how to differentiate MG crisis vs cholinergic crisis

A

TENSILON TEST
in MG crisis: symptoms improve temporarily
in cholinergic crisis: symptoms WORSEN!! atropine is antidote

239
Q

pt teaching of meds for MG

A

take meds at exact time
alarm clock
peak action at meal time (meds 30-60 min prior)
TAKE MEDS BEFORE ADLs TO AVOID WEAKNESS

240
Q

pt teaching of airway for MG

A

postural drainage to clear secretions
insufficient air exchange and inability to speak causing them to panic

241
Q

pt teaching of nutrition for MG

A

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

242
Q

pt teaching about eyes in MG

A

wear sunglasses
med alert bracelet
artificial tears to prevent corneal damage
tape eyes closed for short periods

243
Q

patho of MS

A

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

244
Q

contributing factors of MS

A

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

245
Q

diagnosis of MS

A

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)

246
Q

relapsing-remitting MS

A

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**

247
Q

primary progressive MS

A

no acute exacerbations
symptoms gradually worsen
occasional minor and temporary recovery

248
Q

secondary progressive MS

A

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

249
Q

progressive relapsing MS

A

escalates very quickly to severe disability with very few periods of remission
in periods of remission, symptoms worsen

250
Q

exacerbation and remission in MS

A

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

251
Q

triggers of MS

A

heat, infection, trauma, pregnancy, fatigue, stress
numb legs during infection

252
Q

visual manifestations of MS

A

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)

253
Q

other manifestations of MS

A

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

254
Q

secondary/tertiary symptoms of MS

A

UTI
ulcers
constipation
pedal edema
contractures
PNA
depression
mood swings
vocational problems (job stuff)
personal issues (marriage)

255
Q

nursing goals for MS (mobility)

A

wide based gait like parkinson’s
PT for stretching
occupational therapist
activity but know limits
stop when fatigued

256
Q

fluid intake with MS

A

increase to 2000-3000 mL per day
400-500 with each meal
200 in morning and afternoon
decrease in evening bc decreased bladder control

257
Q

bladder nursing considerations MS

A

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

258
Q

diet for MS

A

high fiber and complex carbs, low fat
avoid laxatives

259
Q

spasticity in MS

A

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!!

260
Q

cortisone for MS

A

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

261
Q

what to report when taking cortisone for MS

A

anorexia, nausea, hypokalemia, muscle weakness
Can cause ulcers on empty stomach (gastric bleeding)
Watch stools for black, tarry stools (indicates bleeding)

262
Q

anticholinergics and antispasmodics for MS

A

for bladder dysfunction

263
Q

amantadine HCl for MS

A

for fatigue

264
Q

antidepressants for MS

A

prozac or zoloft
depression causes fatigue which is a trigger

265
Q

BB, diuretics, and antihistamines for MS

A

for tremors and ataxia

266
Q

anti seizure meds for MS

A

spastic pain
tegretol, depakote

267
Q

muscle relaxants for MS

A

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

268
Q

SE of muscle relaxants

A

dizziness, drowsiness, fatigue

269
Q

immunoregulatory meds for MS

A

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)

270
Q

SE of immunoregulatory meds for MS

A

depression, liver and thyroid gland can be affected, severe flu-like symptoms from interferons (treated with NSAIDS)

271
Q

guillain-barre syndrome etiology

A

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)

272
Q

patho of GBS

A

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

273
Q

general clinical manifestations of GBS

A

vision problems
loss of DTR
dyskinesia
dysphagia leading to aphasia (from glossopharyngeal nerves being affected)

274
Q

cardiac manifestations of GBS

A

palpitations and tachy/bradycardia
orthostatic hypo/hypertension from damage to vagus nerves

275
Q

bladder and bowel manifestations of GBS

A

difficulty urinating or not fully emptying bladder
incontinence
constipation
dizziness first 24-72 hours
cramps

276
Q

resp manifestations of GBS

A

SOB, cramps, entire body aches
vocal paralysis leading to resp paralysis and death
AIRWAY PATENCY IS IMPORTANT!!

277
Q

initial period of GBS

A

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

278
Q

secondary symptoms of GBS

A

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

279
Q

recovery of GBS

A

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)

280
Q

diagnosis of GBS

A

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

281
Q

medical management of GBS

A

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

282
Q

nursing management of GBS

A

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

283
Q

epilepsy

A

recurrent seizures

284
Q

what happens during a seizure

A

CNS depression, consciousness affected
pt may go into deep sleep or be fatigued/confused after episode
increased need for oxygen and glucose

285
Q

where do nonepileptic seizures originate

A

outside the CNS
fever
hypoxia
poisoning
drug intoxication
alcohol withdrawal

286
Q

precipitators of epileptic seizures

A

stress
lack of sleep
emotional upset
alcohol
missed meds
abnormally high level of excitatory neurotransmitters
abnormally low level of inhibitory neurotransmitters

287
Q

primary (idiopathic) seizures

A

recurrent
prior to ages 20-30
inherited threshold, not actual seizure disorder

288
Q

secondary (acquired) seizures

A

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

289
Q

how are seizures classified

A

by where they originate

290
Q

simple partial seizures

A

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

291
Q

temporal lobe seizure

A

sensory symptoms

292
Q

if frontal lobe/motor cortex affected in seizure

A

one side affected

293
Q

occipital region affected during seizure

A

vision affected (flashing lights)

294
Q

complex seizure

A

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

295
Q

generalized seizure

A

involves whole brain
not cured with meds but can be avoided with them

296
Q

preictal phase

A

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

297
Q

ictal phase

A

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

298
Q

postictal phase

A

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)

299
Q

what to document for grand mal seizure

A

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

300
Q

petit mal seizures (absence)

A

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

301
Q

myoclonic seizures

A

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

302
Q

Atonic seizure

A

Total loss of muscle tone
Falls to the floor
Briefly nods off
Confused post ictal
Must wear headgear at all times

303
Q

EEG

A

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

304
Q

CT and MRI for seizures

A

detect abnormalities (MRI includes those due to aging)

305
Q

telemetry for seizures

A

brain activity

306
Q

phenytoin for seizures

A

MONITOR BLOOD LEVELS
see how long it takes to metabolize so you can see how often they need to take the med

307
Q

toxicity with seizure meds

A

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

308
Q

rule with using more than 1 seizure med

A

start with one med
as one is added, the other is tapered

309
Q

dosage of seizure meds depend on what 3 things

A

age
type of seizures
frequency

310
Q

meds for seizures (6)

A

phenytoin (dilantin): prevents
carbamazepine (tegretol): prevents
valproate (dekapan)
clonazepam (klonopin): avoid in pregnancy, avoid ETOH
diazepam (valium): SEDATING
luminal (phenobarbital): SEDATING

311
Q

pt teaching of phenytoin for seizures

A

gingival hyperplasia
hirsutism
bone marrow suppression
VFIB
nausea
diplopia
nystagmus
hyperthermia
ataxia
slurred speech
sedation
confusion
coma

312
Q

pt teaching of phenobarbital

A

extreme sedation
depression
confusion
hallucinations
ataxia
falls!

313
Q

rule for driving when you have epilepsy

A

must be 2 years free

314
Q

when to call EMS for seizures

A

if it lasts >10 min
resp injury
pregnant
2nd seizure starts before 1st one ends

315
Q

vagal nerve stimulation for seizures

A

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

316
Q

temporal lobectomy for seizures

A

curative surgery
removal of where seizures start, without causing neuro deficit

317
Q

corpus callosum resection for seizures

A

palliative for tonic-clonic seizures
or for atonic to make them tolerable

318
Q

cortical resection for seizures

A

for complex partial seizures

319
Q

stereotactic surgery for seizures

A

specific area of brain targeted
monitor pre-op for location
avoid areas of brain that control memory and speech

320
Q

status epilepticus

A

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)

321
Q

nursing management of seizures

A

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

322
Q

dysphagia

A

swallowing difficulties

323
Q

dysphasia

A

trouble with language (can’t put words into a sentence)

324
Q

dysarthria

A

difficulty speaking from weak muscles

325
Q

sulfonyureas and meglinitides with or without food

A

15-30 min before meals

326
Q

biguanides with or without meals

A

with

327
Q

iodides with or without food

A

with water (SSKI) or milk (lugol’s)
with meals

328
Q

MG med time

A

30-60 min before meals

329
Q

cortisone for MS with or without food

A

with food or milk

Med-Surg I (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions