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202D > test #5 > Flashcards

test #5 Flashcards

1
Q

what is insomnia

A

the inability to fall asleep or remain asleep

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2
Q

what classifies chronic insomnia

A

insomnia lasting longer than 30 days

usually related to depression, manic disorders or chronic pain

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3
Q

how much sleep on average should a person get per day

A

7-8 hours of sleep to recouperate from the day

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4
Q

what are some causes of insomnia

A
  • depression
  • manic disorders
  • chronic pain
  • foods/drinks containing substances
  • tobacco(can cause restlessness)
  • alcohol (produces vivid dreams causing frequent awakening)
  • large meals close to bedtime-increases metabolic rate
  • too much light
  • uncomfortable room temp
  • snoring
  • nightmares
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5
Q

what can sleeplessness chronically be a contributing factor to

A

the development of type II diabetes

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6
Q

what are non-pharmacological interventions to promote sleep

A 
lower or avoid caffeine
stop smoking
limit/no alcohol intake
increase exercise during the day
establish sleeping pattern
-alternative therapy- Kava, valerian root, chamomile, lavender
turn off smart phone
counseling if have nightmares
yoga
aromatherapy
massage
accupuncture
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7
Q

what should benzodiazepines not be taken with

A

alcohol

because it increases the risk for CNS depression

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8
Q

when should pharmacotherapy be used for insomnia

A

if the activities of daily living are being interrupted d/t lack of sleep

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9
Q

what classifies anxiety

A

an excessive or irrational response

worry, apprehension, fear or uneasiness over a perceived threat.

an excessive or irrational response that can last 6 months and can get worse if not treated.

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10
Q

what does anxiety do physiologically

A

activates the SNS and triggers the flight or fight

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11
Q

what can anxiety cause

A

an affected quality of life

increased risk of GI and CV issues

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12
Q

Why aren’t symptoms of liver disease in the beginning of liver damage

A

Because the liver regenerates itself quickly.

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13
Q

What are the liver functions

A

Endocrine function- secreting angiotensinogen and glucagon

Metabolism 
Synthesizes vit k and clotting factors 27910
Detoxifying meds
Bile
Vitamin and mineral storage
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14
Q

What type of metabolism does the liver perform

A

Protein: synthesize and breakdown protein / maintain colloidal pressure

Fat metabolism: breaks down fat into triglycerides-absorbed into the portal vein and further broke. Down into fatty acids and cholesterol

CHO: glycogenesis-storage of glycogen, glycogenolysis when storage is depleted, gluconeogenesis- when the body is starved of glucose

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15
Q

symptoms one may have if they are experiencing anxiety

A 
increased HR
increased BP
SOB
pounding in ears
excessive sweating
dry mouth

possibly nausea
GI disorders

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16
Q

what are the 5 major categories of anxiety disorders

A 
OCD
PTSD
GAD
Panic disorder
social anxiety disorder
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17
Q

what is OCD

A

obsessive compulsive disorder

it is 2 parts

  • obsessive- involves thoughts- obsesses over the same thoughts
  • compulsion is the action, have to act upon that thought
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18
Q

what is PTSD

A

situational anxiety that develops in response re-experiencing a previous life event

a person who witnesses or experiences traumatic life event and they feel a sense of helplessness

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19
Q

what can PTSD cause mentally

A

nightmares
hallucinations
flash backs

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20
Q

what can PTSD cause physiologically

A

CV issues: tachycardia
SOB
increased sweating

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21
Q

what is general anxiety disorder

A

excessive anxiety that persists for 6 months or longer.

these pts live with excessive worry and fear about things from everyday events, activities, etc.

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22
Q

what may patients be feeling with GAD

A 
restless 
nervousness
muscle tension
inability to focus or concentrate
overwhelming sense of dread
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23
Q

what are the 5 classes of anxiety related to

A

insomnia/ sleep disturbances

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24
Q

what is panic disorder

A

intense feelings of apprehension of terror or impending doom

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25
Q

how often does Panic disorder occur

A

as frequent as once a month

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26
Q

what is the goal of treating someone with panic disorder

A

getting to the core of what is causing them this panic

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27
Q

what is social anxiety disorder

A

unreasonable persistent feeling of being judged or embarrassed by others.

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28
Q

what are some sxs a pt will experience with social phobia

A

tachy
sweaty
trembling
GI issues- diarrhea/ cramping

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29
Q

what are non pharmacological interventions for anxiety

A

uncover the underlying condition for the anxiety and address those causes

  • work with counselors to discuss anxiety and to identify the situations that cause the anxiety – find ways to deal with stress
  • biofeedback- you get information on how your body response to anxiety- goal is to learn how to decrease those physiological changes
  • meditation
  • herbal products- valarian route
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30
Q

when is pharmacotherapy needed with anxiety

A

when the anxiety interferes with ADLs

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31
Q

what can long term use of sleep aids or anti anxiety meds do

A

worsen the insomnia because they cause physical and psychological dependence

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32
Q

what is the goal of sleep aids or anti anxiety meds

A

to use them to overcome the insomnia or lessen the anxiety
but in the process have the person learn how do deal with the anxiety and doing non pharmacological interventions to get off the meds.

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33
Q

what are the categories of CNS depressents

A

benzodiazepines and non benzodiazepines

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34
Q

when a CNS depressant is given at a higher dose what do they do?
at lower doses?

A

they cause sleep

at lower doses they are sedatives - calming

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35
Q

what does a sedative do

A

taken during the day

promotes relaxation, calmness
reduce anxiety

doesn’t interfere with the persons day

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36
Q

what do hypnotics do

A

taken at night.

used for sleep

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37
Q

how does physical dependance occur with CNS depressants

A

it is caused by the adaptation of the nervous system caused by repeated substance

over time the body becomes accustomed to the substance.
problem is when someone is physically dependent withdrawal symptoms may occur when the drug is discontinued

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38
Q

what are withdrawal symptoms

A 
opposite of the drug. 
opposite CNS depressants:
insomnia 
restlessness
irritability 
headache
anxiety
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39
Q

what is psychological dependence

A

no obvious physical signs of discomfort even after the med is discontinued
but the person has an overwhelming desire to continue the drug despite the consequences

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40
Q

what does it take for psychological dependance to occur

A

high doses of drugs are taken for a long period of time

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41
Q

what are the benzodiazepines

A

the drugs ending in “PAM”

prototypical drug is lorazepam

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42
Q

what is lorazepam used for

A

general anxiety disorder (anxiolytic)

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43
Q

routes for lorazepam

A

PO and IV

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44
Q

what are the off label uses for lorazepam

A

insomnia
pts going through alcohol withdrawal
given IV to treat seizures

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45
Q

is lorazepam a sedative or a hypnotic

A

its both because at higher doses it can induce sleep and maintain sleep
but is also used for short term tx of anxiety

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46
Q

how does lorazepam work

A

it binds to GABA receptors and intensifies the effect.
acts on the GABA sites and helps have calmness,
skeletal muscle relaxation
increase sleep
decrease anxiety

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47
Q

what is GABA

A

gamma aminobutyric acid
a natural inhibitory neurotransmitter in the brain
gives us our calming effect

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48
Q

what are the side effects of lorazepam

A 
dizzy 
daytime drowsyness
confusion
hangover effect
paradoxical excitation- causing manic, talkative, euphoria, nightmares
blurred vision

when given IV form- increases the risk for respiratory depression

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49
Q

what is the hangover effect

A

tired/lethargy

ataxia(off balance)

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50
Q

what is paradoxical excitation

A

the opposite of what you want the drug to do

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51
Q

why do pts need to be tapered off benzodiazepines

A

to avoid the withdrawal symptoms

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52
Q

what is the antedote for benzodiazepines

A

flumazenil

it competes with the gabs receptors so benzos cannot attach to them

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53
Q

what is the onset and duration of fluazenil

A

onset 1-2 minutes
duration 1-2 hours

so the pt may need more than one dose

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54
Q

what is the indication for taking temazepam

A

for short term therapy of insomnia of <4wks

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55
Q

what is a concern for long term use of temazepam?

why?

A

risk of physical or psychological dependence
because over time the patient becomes tolerant to the dose so an increase dose is needed to work.
over time this dependence develops

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56
Q

is temazepam a sedative or a hypnotic

A

its a hypnotic because it produces sleep

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57
Q

when should temazepam be taken

A

at night

58
Q

what are the adverse effects of temazempam

A

sleep related behaviors:
sleep driving
sleep walking

as well as (same as lorazepam):
dizzy, drowsy, confusion, hangover effect and paradoxical effect

59
Q

what is dangerous about temazepam r/t its half life

A

its half is 10-20 hours which increases the risk of being in a sedated state when you wake up.
especially in the elderly

60
Q

what are the non benzodiazepines

A

zolpidem (ambient)

lunesta

61
Q

what is zolpidem used for

A

insomnia

to decrease sleep onset and the number of awakenings at night

62
Q

what is the recommendation for taking zolpidem

A

to have 7-8 hours of planned sleep

63
Q

how does zolpidem work

A

binds to the GABA receptors enhancing the effects of GABA

64
Q

what are adverse effects of zolpidem

A 
drowsy
dizzy
hallucination
HA
behavioral changes such as sleep driving
65
Q

what is a risk of taking zolpidem

A

rebound insomnia if the med is d/c’d abruptly

66
Q

how long should zolpidem be taken

A

the recommendation is 7-10 days of use and no longer d/t the risk of physical or psychological dependence.

67
Q

what is a barbiturate

A

a sedative hypnotic and anti-seizure med

68
Q

what is the barbiturate med and what does it do at low and moderate doses

A

phenobarbitol

low doses- reduce anxiety and cause drowsiness
moderate - inhibit seizure activity and promote sleep

69
Q

why is phenobarbital not used for sleep or anxiety

A

because of the high risk of physical and psychological dependence

70
Q

what is the action of phenobarbital

A

binds to GABA receptors and enhances their effects.

it also can decrease motor activity

71
Q

what do you need to monitor when someone is given phenobarbital

A

monitor the phenobarbital levels
Range- 10-40mcg/mL
it becomes toxic if levels are higher than 40

72
Q

what are adverse effects of phenobarbital

A

hangover effect, drowsy, hallucination, reps. depression

73
Q

what can abrupt d/c of phenobarbital cause

A

seizures

74
Q

what are the functions of the liver

A

endocrine- secreting angiotensin and glucagon
metabolism
hematologic- formation of clotting factors
excretory- bile
detoxifies
vitamin and mineral storage

75
Q

what does the liver metabolize

A

protein- synthesizes and breaks down proteins into amino acids

fat- breaks down into triglycerides - absorbed into the portal vein and further broken down into fatty acids and cholesterol

CHO - liver stores glycogen through glycogenesis- body will stimulate glycogenolysis and gluconeogenesis when the body needs sugar.

76
Q

what clotting factors does the liver synthesize

A 
1(fibrinogen)
2(prothrombin) 
7
9
10
77
Q

what will happen r/t clotting factors in a diseased liver

A

increased risk for bleeding/ increased PT time

 GI bleed
epistaxis
gum bleeding
petechiae
hemataemesis
78
Q

what are bile salts needed for

A

digestion of fat.

79
Q

how does bile move out of the liver

A

the bile is formed by the hepatocytes and into the caniculi in the liver, the bile flows out of the liver to the common hepatic duct to the pancreatic duct to the duodenum
(some bile goes to the gallbladder for later use)

80
Q

what does bile contain

A 
cholesterol
bile salts
bilirubin
water
Na+
K+
81
Q

what will happen with in liver disease r/t bile

A

the bile is not flowing to the duodenum and the stool may result in a clay color because there is not the bile in there which gives it its brown color

also they may have steatorrhea (fat in stool)
because the fat is not being digested because there is no bile to break down that fat.

vitamin deficiencies of ADEK because these are fat soluble vitamins, therefore if the fat is being expelled the vitamins can’t be absorbed leading to deficiency

82
Q

why do we need fat

A

the storage of fat soluble vitamins (ADEK)

83
Q

why might someone with liver disease have pruritus

A

because if the bile is not flowing out of the liver, it begins to build up and overflows to the blood stream and the those bile acids cause itching

84
Q

what are proteins broken down to

A

breaks down proteins into ammonia (a nitrogenous by product of amino acids)

85
Q

what happens to protein metabolism in liver disease

A

the proteins are broken down but the liver is unable to convert the ammonia to urea so the ammonia builds up in the body leading to hepatic encephalopathy.
the ammonia crosses the blood brain barrier

86
Q

what are the functions of vitamin and mineral storage in the liver

A 
stores iron as ferritin
stores fat soluble vitamins
stores B12 and folate
stores vit K
Converts vit D to intermediate metabolite
87
Q

what is the livers role in calcium absorbtion

A

inactive vitamin D is sent to the liver where it is converted to the intermediate form of vitamin D which is CALCIFEDIOL

(from there it goes to the kidneys where PTH stimulates the kidneys to convert the calciferol to calcitriol which enhances calcium abosorption)

88
Q

what happens in liver disease r/t vit D

A

the liver is unable to convert vit d to Calcifediol
without calcifediol the kidneys cannot convert to calcitriol and therefore calcium cannot be absorbed

leading to Osteoporosis
- there is more bone breakdown (resorption) for the calcium and this is occurring faster than bone formation

89
Q

what are sinusoids

A

channels in the liver where the blood flows through he liver

90
Q

what are the cells that line the sinusoids and what do they do

A

kupffer cells
responsible for breaking down and removing old red blood cells
bacteria
other debris that the liver doesn’t need/want

91
Q

why do liver diseased pts have jaundice

A

because of the breakdown of RBCs, the liver has less kupffer cells in the sinusoid and the liver is unable to get rid of old RBCs resulting in the accumulation of bilirubin

92
Q

what is a s/s of hyperbilirubinemia

A
  • yellowing of the sclera
  • yellowing of the skin
  • dark urine
93
Q

what are the 2 ways to prevent liver disease

A

limit alcohol

  • 2 or less for women/day
  • 3 or less for men/day

avoid acquiring hepatitis C by avoiding infected blood

94
Q

what are the tests in a liver function panel

A
  • Alanine aminotransferase (ALT)
  • Asparate aminotransferase (AST)
  • Alkaline phosphatase (ALP)
  • Direct and indirect bilirubin
may be separate for LFT but MDs may ask for 
ammonia
albumin
total protein
PT time
95
Q

how is bilirubin formed

A

the heme portion of the hgb is released from the RBC
the heme is converted to
UNCONJUGATED bilirubin (unbound)

this bilirubin is carried by proteins to the liver
once in the liver the unconjugated bilirubin “marrys” glucarinic acid and is now CONJUGATED (bound)
this bilirubin enters the bile and is eventually excreted in our stool

96
Q

what is indirect bilirubin lab test and reference range

A

the measurement of UNCONJUGATED bilirubin

range: 0.1-1.1mg/dL

97
Q

what are the causes of increased indirect bilirubin

A

hemolytic anemia (the RBCs are being broken down faster than the liver can get rid of it)

or

a reaction of blood transfusions (the body creates antibodies and breaks down all the transfused RBCs)

98
Q

what is direct bilirubin

and the ref range

A

the measurement of conjugated bilirubin

range: 0.1-0.3mg/dL

99
Q

what would cause an elevation in direct bilirubin

A

obstructive jaundice
inflammation
or tumors blocking excretion

100
Q

what is alanine aminotransferase effective in identifying

A

an elevation in ALT will indicate liver dysfunction because it will tell us the severity of cellular injury to the hepatocytes
its primarily found in the liver

101
Q

what is the reference range for ALT

A

10-35U/L

during end stage liver disease the levels may appear normal because there are less hepatocytes able to secrete this enzyme

102
Q

where is aspirate aminotransferase found

A

in the liver
heart
skeletal muscle
blood

103
Q

what might increase AST levels

A

liver disease
strenuous exercise
musckuloskeletal trauma
heart conditions

because it is in multiple places in the body, AST is not definitive of liver conditions
it needs to be in combination with ALT

104
Q

what is the range of AST

A

8-35 U/L

  • in liver disease it raises 10x
  • AST will remain elevated for a long period of time
105
Q

where is alkaline phosphatase found

A

primarily in liver

also in the bone and kidneys

106
Q

why would an ALP level be higher in teens

A

because ALP is found in bone, the elevated level is d/t bone growth and teens are growing. thus the elevation

107
Q

what is the referance range of ALP

A

42-136U/L

108
Q

what is ammonia and why would the dr want to order n ammonia level

A

it is the end product of protein digestion
the liver breaks down protein to ammonia and then is converted to urea and excreted via urine.

the dr would order ammonia levels in suspicion of liver disease, the liver cannot convert ammonia to urea

109
Q

why is ammonia levels a concern

A

because the ammonia can cross the blood brain barrier and the rising levels put the patient at great risk for hepatic encephalopathy

110
Q

what is the reference range for ammonia

A

15-60mcg/dL

111
Q

what is cirrhosis

A

the liver cells attempt to regenerate but the process is disorganized resulting in the overgrowth of collagen and fibrinous connective tissue.
this leads to the distortion of the liver and the structure resulting in the liver being irregular size and shape.
as this evolves
it slows the blood flow through the liver

as the blood flow decreases, it leads to hypoxia and d/t the lack of O2 and nutrients the hepatocytes die.

112
Q

what are the early sxs related to cirrhosis

A

fatigue

this is why it is hard to diagnose liver disease early on. its very hard to recognize.

113
Q

what are later manifestations of cirrhosis

A 
jaundice
weakness
itching (bile salts)
loss of appetite
nausea
edema/ascites
bleeding issues.
114
Q

how does portal hypertension come about

A

when there is resistance in the liver caused by liver cirrhosis/damage there is a backflow of blood in the portal vein backing up towards the stomach, esophagus and spleen causing the veins to become tortuous and compressed

this causes the liver to create new routes of blood supply because it senses not enough perfusion but these new routes become clogged eventually as well

causing an increase in portal vein pressure causing varices

115
Q

what is the problem with varices

A

they are fragile and easily ruptured thus increased risk for bleeding
in addition pts with liver disease don’t have as many clotting factors to stop bleeding

116
Q

what may occur with portal hypertension

A

coffee ground emesis- blood mixed with gastric contents

117
Q

what are varices and where do they occur

A

swollen distended vessels caused from portal hypertension.

they occur in the esophagus, around and in stomach and rectum.

118
Q

what is ascites

A

a continual problem in end stage renal disease

the accumulation of fluid in the abdominal cavity d/t the decreased albumin production and total protein

119
Q

what causes ascites

A
  • hypoalbuminemia (liver not able to synthesize albumin)
  • decrease colloidal osmotic pressure
  • decreased protein d/t loss of appetite
  • portal hypertension- caused from protein shift pushing proteins to the interstitial space causing fluid to shift to the interstitial space
120
Q

what coincides with ascites

A

hypovolemia d/t the decreased colloidal pressure and portal hypertension

121
Q

what are manifestations of ascites

A

abd distention
anorexia (full abdomen- pressure, not feeling hungry)
gastric varices
dehydration
difficulty breathing d/t large abdomen pressing up on diaphragm
-muscle pain caused from muscle breakdown d/t the decreased protein intake

122
Q

what are s/s of hepatic encephalopathy

A 
lethargy
confusion
inability to concentrate
restlessness
asterixis
disorientation
123
Q

what is hepatic encephalopathy caused from

A

the build up of ammonia that crosses the blood brain barrier causing neurologic toxic manifestations which cause hepatic encephalopathy

124
Q

what are nursing considerations for hepatic encephalopathy

A

concerned with falls
put bed alarm up
may need 4x bed rales
sitter

125
Q

what are the 2 meds to help with hepatic encephalopathy

A

neomycin and lactulose

126
Q

what type of drug is neomycin

A

an aminoglycocide abx

127
Q

what is the job of neomycin

A

decrease the amount of ammonia producing bacteria in the gut

128
Q

where is neomycin metabolized

A

90% by the kidneys

can’t give a med that is metabolized by the liver because the liver is damaged and it won’t metabolize

129
Q

what are adverse effects of neomycin

A

Nephrotoxicity
ototoxicity

nausea
vomiting
ataxia

130
Q

what labs do you need to look at when giving neomycin

A

BUN and Creatinine

and ammonia

131
Q

what is the goal for neomycin therapy

A

improved neurological status and decreased ammonia levels

132
Q

what routes does lactulose come in

A

oral and rectal

133
Q

what does lactulose do

A

lowers the pH of the colon
by lowering the pH we can inhibit the ammonia from diffusing across the colon and into the blood stream thus the ammonia is excreted in the stool

134
Q

what are adverse effects of lactulose

A 
belching
cramps
distention 
flatulence
diarrhea (lactulose contains glucose which acts as an osmotic and thus softens stools therefore is also used for constipation)
hyperglycemia
135
Q

what are implementations for lactulose

A

can mix with fruit juice or water

because it is very sweet

136
Q

who would you be cautious with when giving lactulose

A

diabetics because the high glucose content of lactulose

137
Q

what is the outcome of lactulose

A

improved mental status so the ammonia is excreted in the stool and the pt improves

138
Q

what are lifestyle modifications of a person with liver disease

A
  • alcohol abstinence
  • seeking options to cease drinking
  • avoid hepatotoxic drugs
  • eat more plant based foods for nutritional substances- fruits and veggies for protein
  • eat small frequent balanced meals
  • eating soft foods b/c esophageal varices

-low sodium diet because they don’t have the colloidal osmotic pressure. salty foods make you thirsty- the more you drink the further you are increasing your third spacing

  • avoid straining d/t rectal varices
  • soft toothbrush d/t increased bleeding
  • avoid harsh blowing of nose d/t epistaxis
  • avoid aspirin, NSAIDS
139
Q

if a pt has liver disease what should you want them to be on if they have to take warfarin

A

a proton pump inhibitor to decrease the risk of bleeding

140
Q

what is the sodium recommendation for a person with liver disease

A

1500-2000/day

141
Q

what are nursing considerations for a pt with liver disease

A 
assess jaundice
itching
bruising
bleeding
abd girth
edema
urine
stool color
I&amp;O
appetite
weight
respiratory effort
skin
Liver related labs
PT time
meds

implement fall risks

202D (6 decks)

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