test #5 Flashcards
what is insomnia
the inability to fall asleep or remain asleep
what classifies chronic insomnia
insomnia lasting longer than 30 days
usually related to depression, manic disorders or chronic pain
how much sleep on average should a person get per day
7-8 hours of sleep to recouperate from the day
what are some causes of insomnia
- 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
what can sleeplessness chronically be a contributing factor to
the development of type II diabetes
what are non-pharmacological interventions to promote sleep
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
what should benzodiazepines not be taken with
alcohol
because it increases the risk for CNS depression
when should pharmacotherapy be used for insomnia
if the activities of daily living are being interrupted d/t lack of sleep
what classifies anxiety
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.
what does anxiety do physiologically
activates the SNS and triggers the flight or fight
what can anxiety cause
an affected quality of life
increased risk of GI and CV issues
Why aren’t symptoms of liver disease in the beginning of liver damage
Because the liver regenerates itself quickly.
What are the liver functions
Endocrine function- secreting angiotensinogen and glucagon
Metabolism Synthesizes vit k and clotting factors 27910 Detoxifying meds Bile Vitamin and mineral storage
What type of metabolism does the liver perform
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
symptoms one may have if they are experiencing anxiety
increased HR increased BP SOB pounding in ears excessive sweating dry mouth
possibly nausea
GI disorders
what are the 5 major categories of anxiety disorders
OCD PTSD GAD Panic disorder social anxiety disorder
what is OCD
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
what is PTSD
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
what can PTSD cause mentally
nightmares
hallucinations
flash backs
what can PTSD cause physiologically
CV issues: tachycardia
SOB
increased sweating
what is general anxiety disorder
excessive anxiety that persists for 6 months or longer.
these pts live with excessive worry and fear about things from everyday events, activities, etc.
what may patients be feeling with GAD
restless nervousness muscle tension inability to focus or concentrate overwhelming sense of dread
what are the 5 classes of anxiety related to
insomnia/ sleep disturbances
what is panic disorder
intense feelings of apprehension of terror or impending doom
how often does Panic disorder occur
as frequent as once a month
what is the goal of treating someone with panic disorder
getting to the core of what is causing them this panic
what is social anxiety disorder
unreasonable persistent feeling of being judged or embarrassed by others.
what are some sxs a pt will experience with social phobia
tachy
sweaty
trembling
GI issues- diarrhea/ cramping
what are non pharmacological interventions for anxiety
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
when is pharmacotherapy needed with anxiety
when the anxiety interferes with ADLs
what can long term use of sleep aids or anti anxiety meds do
worsen the insomnia because they cause physical and psychological dependence
what is the goal of sleep aids or anti anxiety meds
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.
what are the categories of CNS depressents
benzodiazepines and non benzodiazepines
when a CNS depressant is given at a higher dose what do they do?
at lower doses?
they cause sleep
at lower doses they are sedatives - calming
what does a sedative do
taken during the day
promotes relaxation, calmness
reduce anxiety
doesn’t interfere with the persons day
what do hypnotics do
taken at night.
used for sleep
how does physical dependance occur with CNS depressants
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
what are withdrawal symptoms
opposite of the drug. opposite CNS depressants: insomnia restlessness irritability headache anxiety
what is psychological dependence
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
what does it take for psychological dependance to occur
high doses of drugs are taken for a long period of time
what are the benzodiazepines
the drugs ending in “PAM”
prototypical drug is lorazepam
what is lorazepam used for
general anxiety disorder (anxiolytic)
routes for lorazepam
PO and IV
what are the off label uses for lorazepam
insomnia
pts going through alcohol withdrawal
given IV to treat seizures
is lorazepam a sedative or a hypnotic
its both because at higher doses it can induce sleep and maintain sleep
but is also used for short term tx of anxiety
how does lorazepam work
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
what is GABA
gamma aminobutyric acid
a natural inhibitory neurotransmitter in the brain
gives us our calming effect
what are the side effects of lorazepam
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
what is the hangover effect
tired/lethargy
ataxia(off balance)
what is paradoxical excitation
the opposite of what you want the drug to do
why do pts need to be tapered off benzodiazepines
to avoid the withdrawal symptoms
what is the antedote for benzodiazepines
flumazenil
it competes with the gabs receptors so benzos cannot attach to them
what is the onset and duration of fluazenil
onset 1-2 minutes
duration 1-2 hours
so the pt may need more than one dose
what is the indication for taking temazepam
for short term therapy of insomnia of <4wks
what is a concern for long term use of temazepam?
why?
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
is temazepam a sedative or a hypnotic
its a hypnotic because it produces sleep
when should temazepam be taken
at night
what are the adverse effects of temazempam
sleep related behaviors:
sleep driving
sleep walking
as well as (same as lorazepam):
dizzy, drowsy, confusion, hangover effect and paradoxical effect
what is dangerous about temazepam r/t its half life
its half is 10-20 hours which increases the risk of being in a sedated state when you wake up.
especially in the elderly
what are the non benzodiazepines
zolpidem (ambient)
lunesta
what is zolpidem used for
insomnia
to decrease sleep onset and the number of awakenings at night
what is the recommendation for taking zolpidem
to have 7-8 hours of planned sleep
how does zolpidem work
binds to the GABA receptors enhancing the effects of GABA
what are adverse effects of zolpidem
drowsy dizzy hallucination HA behavioral changes such as sleep driving
what is a risk of taking zolpidem
rebound insomnia if the med is d/c’d abruptly
how long should zolpidem be taken
the recommendation is 7-10 days of use and no longer d/t the risk of physical or psychological dependence.
what is a barbiturate
a sedative hypnotic and anti-seizure med
what is the barbiturate med and what does it do at low and moderate doses
phenobarbitol
low doses- reduce anxiety and cause drowsiness
moderate - inhibit seizure activity and promote sleep
why is phenobarbital not used for sleep or anxiety
because of the high risk of physical and psychological dependence
what is the action of phenobarbital
binds to GABA receptors and enhances their effects.
it also can decrease motor activity
what do you need to monitor when someone is given phenobarbital
monitor the phenobarbital levels
Range- 10-40mcg/mL
it becomes toxic if levels are higher than 40
what are adverse effects of phenobarbital
hangover effect, drowsy, hallucination, reps. depression
what can abrupt d/c of phenobarbital cause
seizures
what are the functions of the liver
endocrine- secreting angiotensin and glucagon
metabolism
hematologic- formation of clotting factors
excretory- bile
detoxifies
vitamin and mineral storage
what does the liver metabolize
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.
what clotting factors does the liver synthesize
1(fibrinogen) 2(prothrombin) 7 9 10
what will happen r/t clotting factors in a diseased liver
increased risk for bleeding/ increased PT time
GI bleed epistaxis gum bleeding petechiae hemataemesis
what are bile salts needed for
digestion of fat.
how does bile move out of the liver
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)
what does bile contain
cholesterol bile salts bilirubin water Na+ K+
what will happen with in liver disease r/t bile
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
why do we need fat
the storage of fat soluble vitamins (ADEK)
why might someone with liver disease have pruritus
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
what are proteins broken down to
breaks down proteins into ammonia (a nitrogenous by product of amino acids)
what happens to protein metabolism in liver disease
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
what are the functions of vitamin and mineral storage in the liver
stores iron as ferritin stores fat soluble vitamins stores B12 and folate stores vit K Converts vit D to intermediate metabolite
what is the livers role in calcium absorbtion
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)
what happens in liver disease r/t vit D
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
what are sinusoids
channels in the liver where the blood flows through he liver
what are the cells that line the sinusoids and what do they do
kupffer cells
responsible for breaking down and removing old red blood cells
bacteria
other debris that the liver doesn’t need/want
why do liver diseased pts have jaundice
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
what is a s/s of hyperbilirubinemia
- yellowing of the sclera
- yellowing of the skin
- dark urine
what are the 2 ways to prevent liver disease
limit alcohol
- 2 or less for women/day
- 3 or less for men/day
avoid acquiring hepatitis C by avoiding infected blood
what are the tests in a liver function panel
- 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
how is bilirubin formed
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
what is indirect bilirubin lab test and reference range
the measurement of UNCONJUGATED bilirubin
range: 0.1-1.1mg/dL
what are the causes of increased indirect bilirubin
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)
what is direct bilirubin
and the ref range
the measurement of conjugated bilirubin
range: 0.1-0.3mg/dL
what would cause an elevation in direct bilirubin
obstructive jaundice
inflammation
or tumors blocking excretion
what is alanine aminotransferase effective in identifying
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
what is the reference range for ALT
10-35U/L
during end stage liver disease the levels may appear normal because there are less hepatocytes able to secrete this enzyme
where is aspirate aminotransferase found
in the liver
heart
skeletal muscle
blood
what might increase AST levels
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
what is the range of AST
8-35 U/L
- in liver disease it raises 10x
- AST will remain elevated for a long period of time
where is alkaline phosphatase found
primarily in liver
also in the bone and kidneys
why would an ALP level be higher in teens
because ALP is found in bone, the elevated level is d/t bone growth and teens are growing. thus the elevation
what is the referance range of ALP
42-136U/L
what is ammonia and why would the dr want to order n ammonia level
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
why is ammonia levels a concern
because the ammonia can cross the blood brain barrier and the rising levels put the patient at great risk for hepatic encephalopathy
what is the reference range for ammonia
15-60mcg/dL
what is cirrhosis
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.
what are the early sxs related to cirrhosis
fatigue
this is why it is hard to diagnose liver disease early on. its very hard to recognize.
what are later manifestations of cirrhosis
jaundice weakness itching (bile salts) loss of appetite nausea edema/ascites bleeding issues.
how does portal hypertension come about
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
what is the problem with varices
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
what may occur with portal hypertension
coffee ground emesis- blood mixed with gastric contents
what are varices and where do they occur
swollen distended vessels caused from portal hypertension.
they occur in the esophagus, around and in stomach and rectum.
what is ascites
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
what causes ascites
- 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
what coincides with ascites
hypovolemia d/t the decreased colloidal pressure and portal hypertension
what are manifestations of ascites
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
what are s/s of hepatic encephalopathy
lethargy confusion inability to concentrate restlessness asterixis disorientation
what is hepatic encephalopathy caused from
the build up of ammonia that crosses the blood brain barrier causing neurologic toxic manifestations which cause hepatic encephalopathy
what are nursing considerations for hepatic encephalopathy
concerned with falls
put bed alarm up
may need 4x bed rales
sitter
what are the 2 meds to help with hepatic encephalopathy
neomycin and lactulose
what type of drug is neomycin
an aminoglycocide abx
what is the job of neomycin
decrease the amount of ammonia producing bacteria in the gut
where is neomycin metabolized
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
what are adverse effects of neomycin
Nephrotoxicity
ototoxicity
nausea
vomiting
ataxia
what labs do you need to look at when giving neomycin
BUN and Creatinine
and ammonia
what is the goal for neomycin therapy
improved neurological status and decreased ammonia levels
what routes does lactulose come in
oral and rectal
what does lactulose do
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
what are adverse effects of lactulose
belching cramps distention flatulence diarrhea (lactulose contains glucose which acts as an osmotic and thus softens stools therefore is also used for constipation) hyperglycemia
what are implementations for lactulose
can mix with fruit juice or water
because it is very sweet
who would you be cautious with when giving lactulose
diabetics because the high glucose content of lactulose
what is the outcome of lactulose
improved mental status so the ammonia is excreted in the stool and the pt improves
what are lifestyle modifications of a person with liver disease
- 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
if a pt has liver disease what should you want them to be on if they have to take warfarin
a proton pump inhibitor to decrease the risk of bleeding
what is the sodium recommendation for a person with liver disease
1500-2000/day
what are nursing considerations for a pt with liver disease
assess jaundice itching bruising bleeding abd girth edema urine stool color I&O appetite weight respiratory effort skin Liver related labs PT time meds
implement fall risks
