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331 final exam Flashcards

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1
Q

types on seizures

A

focal or tonic/clonic

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2
Q

focal seizure

A

partial seizure (used to be called petite mal)– loss of awareness

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3
Q

tonic/clonic seizure

A

convulsion (used to be called gran mal) - tonic = contraction and associated with loss of conciseness and clonic = altering contraction and relaxation

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4
Q

seizures can be caused by

A

hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation, & sleep phases. increased ICP from brain tumor or injury, infection, drug withdrawal, vascular disease, metabolic problems, CNS degenerative diseases (such as Alzheimers or multiple sclerosis), and hypoxia

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5
Q

epilepsy

A

CNS disorder with multiple seizures of idiopathic cause. there is no cure but can be treated.

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6
Q

seizure vs epilepsy

A

seizure is a single occurrence (do not need to have epilepsy) while epilepsy is a medical condition that includes seizures

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7
Q

which vascular diseases can lead to seizure

A

CVA and aneurysm

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8
Q

how to diagnose of seizures

A

want to identify and eliminate the cause, EEG, CT, MRI, serum test for electrolytes and toxins

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9
Q

EEG

A

electroencephalogram is a test with sensors placed on a patients head used to find problems related to electrical activity of the brain.

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10
Q

what metabolic problems can cause a seizure

A

hepatic failure, electrolyte abnormalities, and hypoglycemia

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11
Q

things that decrease seizure threshold

A

stress, fatigue, hypoglycemia, fever, alcohol and antipsychotic drugs, hyperventilation, increased water ingestion, menses, light, and noise

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12
Q

if you increase the seizure threshold

A

you can reduce the occurrence of seizures

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13
Q

why does water intoxication increase the chances of seizures

A

it dilutes sodium

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14
Q

prodroma

A

early manifestations that appear a few days to hours before onset of seizure. can show as anxiety, depression, and inability to think clearly.

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15
Q

aura

A

partial seizure that manifests itself as dizziness, numbness, visual or auditory experience, or just a funny feeling

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16
Q

phases of seizures

A

preictal, ictal, postictal

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17
Q

what is included in the preictal phase

A

prodroma and aura

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18
Q

ictal phase includes

A

the seizure phase which includes tonic and clonic phases

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19
Q

what happens during the ictal phase

A

muscle contractions/relaxation and increase in metabolic demand which causes decreased level of conscious, increased O2 use, decreased glucose, and increased lactic acid

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20
Q

what needs to be done during the ictal phase

A

airway maintenance needs to be ensured and there may be relaxation of bowel and urinary sphincter which causes incontinence

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21
Q

postictal phase

A

period immediately following cessation of seizure activity

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22
Q

what happens during the postictal phase

A

decreased level of consciousness, dysphagia/dysphasia, confusion, memory loss, paralysis, and deep sleep

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23
Q

status epilepticus

A

severe seizure can be multiple lasting for 5 minutes, one longer than 30 minutes, or rapidly recurring seizures before a person has fully regained consciousness from preceding seizure

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24
Q

what do seizures do to metabolic demand

A

increases it

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25
Q

what does increased metabolic demand do?

A

uses up glucose and oxygen rapidly which leads to lactic acid accumulation in brain tissue because O2 and glucose are not available

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26
Q

hypotonia

A

decreased muscle tone

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27
Q

seizure treatment

A

correct or control cause if possible, anti-seizure medications, dietary, surgical interventions

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28
Q

goals for a patient going through seizure

A

pharmacology, oxygenation, and to prevent injury

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29
Q

dietary treatment for seizure patients

A

keto and adkins

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30
Q

status epileptics can cause

A

progressive and irreversible brain damage and can be life threatening

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31
Q

anti epileptic drug mechanism of action

A

not known but evidence has shown that it alters movement of Na, K, Mg, and Ca which stabilizes the hyper-excitable states and inhibits burst firing

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32
Q

anti epileptic drugs do what to nerve impulses

A

suppress transmission between nerve impulses which stabilizes cell membranes and decreases spread of impulses

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33
Q

anti epileptic drugs do what to nerve impulse conduction

A

decrease the speed of the nerve impulse conduction within a neuron

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34
Q

anti epileptic drugs do what to threshold

A

increase the threshold which decreases the neuronal response to stimuli

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35
Q

anti epileptic drug do what to GABA? which does what

A

enhance effects of GABA which helps regulate neuron excitability in the brain

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36
Q

besides seizures, anti epileptic drugs are also used for

A

psychiatric disorders, migraines, and neuropathic pain

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37
Q

GABA is a

A

inhibitory neurotransmitter

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38
Q

anti epileptic drug goal of therapy and how do you do that?

A

control seizure activity while avoiding adverse effects. you do this by titrating to the lowest sum drug level

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39
Q

indications of anti epileptic drugs

A

long term seizure maintenance and status epilepticus

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40
Q

adverse effects of anti epileptic drugs

A

decrease level of consciousness, SI, mood, GI upset, thrombocytopenia, and many induce hepatic metabolism

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41
Q

Carbamazepine (Tegretol) adverse effects

A

Stevens-johnson syndrome, toxic epidermal necrolysis, Nausea, headache, dizziness, unusual eye movements, visual change, behavioral changes, rash, abdominal pain, abnormal gait, GI upset

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42
Q

Phenytoin (Dilantin) adverse effects

A

Nystagmus, ataxia, drowsiness, rash, gingival hyperplasia, pancytopenia, agranulocytosis, hepatitis, GI upset

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43
Q

first line prototypical drug for both tonic/clonic and partial seizures

A

Phenytoin (Dilantin)

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44
Q

Phenytoin (Dilantin) routes

A

capsule and IV

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45
Q

Phenytoin (Dilantin) MOA

A

stabilize neurons (Na)

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46
Q

Phenytoin (Dilantin) therapeutic plasma level

A

10-20 mcg/mL

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47
Q

what if a patient has decreased albumin levels with phenytoin

A

Phenytoin (Dilantin) is highly protein bound and if a patient has low albumin = lots of active drug circulating = drug toxicity

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48
Q

what does phenytoin toxicity look like

A

nagstagmus, ataxia, encephalopathy (altered level of consciousness), dysarthria

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49
Q

nursing considerations with IV phenytoin

A

20 gage needle, dilute with NS and flush with Ns, filter must be used,

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50
Q

what is used to overcome chemical disadvantage of IV phenytoin?

A

IV fosphenytoin

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51
Q

Dose of IV phenytoin

A

10-15 mg/kg

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52
Q

risks of IV phenytoin and why

A

can cause extravagation because it is mixed with antifreeze at a ph of 12

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53
Q

BBW of IV phenytoin

A

IV infusion should not exceed 50 mg/min in adults. incr. risk severe hypotension and cardiac arrhythmias above recommended infusion rate

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54
Q

BBW of carbamazepine

A

bone marrow suppression which causes pancytopenia which causes decreased immunity, oxygen, and blood clotting

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55
Q

therapeutic levels of carbamazepine

A

4-12 mcg/mL

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56
Q

indication of carbamazepine

A

generalized tonic-clonic seizures and not for myoclonic or absent seizures

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57
Q

what can a patient not have if taking carbamazepine

A

grapefruit juice

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58
Q

stevens-johnson syndrom

A

peeling of the skin. adverse effect of carbamazepine. if not controlled leads to toxic epidermal necrolysis

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59
Q

levetiracetam brand name

A

Keppra

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60
Q

levetiracetam (Keppra) indication

A

adjunct therapy for partial seizures without secondary generalization

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61
Q

levetiracetam (Keppra) MOA

A

unknown however evidence shows it inhibits simultaneous neuronal firing

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62
Q

adverse effects of levetiracetam (Keppra)

A

excessive CNS depression when used in combination with other sedating drugs, leukopenia which puts you at risk for infection, dizziness, drowsiness, behavior changes

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63
Q

levetiracetam (Keppra) route

A

PO, IV, and IR (immediate release)

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64
Q

valproic acid MOA

A

facilitates inhibitory neurotransmitter GABA

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65
Q

valproic acid route, onset, and peak

A

PO and IV onset is 15-30 mins, and peaks in 1-4 hours

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66
Q

valproic acid indication

A

generalized seizures and can be used for bipolar disorder

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67
Q

valproic acid adverse effects

A

drowsiness, N/V, tremor, weight gain, transient hair loss

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68
Q

Capsules with long acting valproic acid granules are called

A

Depakote sprinkle

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69
Q

what does depakote do to hepatic metabolism

A

It does induce hepatic metabolism of other drugs due to it being a highly-protein bound drug. This is of significant consequence for any individual who has liver damage or disease, especially when you take into consideration that valproic acid can cause hepatotoxicity

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70
Q

therapeutic levels for Depakote

A

50-125 mcg/mL

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71
Q

adverse effects of Depakote

A

hepatotoxicity and pancreatitis

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72
Q

what Benzodiazepines did we learn

A

lorazepam and diazepam

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73
Q

Benzodiazepines indications

A

anxiolytic (decrease anxiety), ethanol withdrawal, acute seizures

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74
Q

therapeutic effect of Benzodiazepines? adverse effect of Benzodiazepines?

A

both are sedation

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75
Q

nursing considerations of Benzodiazepines

A

habit forming, can induce withdrawal seizures, risk for falls, monitor BP, assess for suicidal ideation

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76
Q

lorazepam trade name

A

Ativan

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77
Q

why are patients on Benzodiazepines a fall risk

A

because they are CNS depressants and have mind altering capabilities

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78
Q

Benzodiazepines reversal

A

flumazenil (romazicon)

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79
Q

flumazenil (romazicon) BBW

A

rebound seizures from stopping effects of benzo too fast

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80
Q

gabapentin (Neurontin) MOA

A

increases synthesis and synaptic accumulation of GABA between the neurons

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81
Q

gabapentin (Neurontin) indication

A

most commonly used for neuropathic pain

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82
Q

GABA does what to brain activity

A

inhibits it

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83
Q

pregabalin (Lyrica) MOA

A

affects calcium channels in the CNS tissue

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84
Q

pregabalin (Lyrica) indication

A

adjunct therapy for partial seizures. also commonly used for neuropathic pain, fibromyalgia, and postherpetic neuralgia

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85
Q

cerebrovascular disease

A

any abnormalities of the brain caused by a pathological process in the blood vessels

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86
Q

symptoms of cerebrovascular disease are

A

there are focal, unilateral, and global symptoms. slurred speech, difficulty swallowing, limb weakness, and paralysis

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87
Q

leading cause of disability

A

stroke, aka cerebrovascular disease

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88
Q

cerebrovascular disease can be

A

ischemic or hemorrhagic. can also be associated with hypoperfusion

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89
Q

severe effects of cerebrovascular disease

A

hemiplegia, coma, and death

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90
Q

risk factors to cerebrovascular disease

A

high total cholesterol or low HDL, smoking, HTN, A-fib, DM, thrombocythemia, increased blood viscosity, insulin resistance, heart disease, peripheral vascular disease

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91
Q

thrombocythemia

A

excess platelet production

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92
Q

polycythemia

A

over production of RBC

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93
Q

smoking increases risk of stroke by

A

50%

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94
Q

ischemic stroke

A

occurs when there is obstruction to arterial blood flow to the brain from thrombus formation, an embolus, or hypoperfusion

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95
Q

thrombus

A

chronic process that may take up to 20-30 years for obstruction to develop

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96
Q

cerebral thrombosis develops most often from

A

atherosclerosis/stenosis and inflammatory disease process that damage arterial wall

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97
Q

what adhere to a vessel wall that is damaged

A

platelets and fibrin to form a clot

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98
Q

embolic stroke

A

fragments that break from a thrombus formed outside the brain usually in the heart or carotids but can also be from blood, fat, air, or bacteria

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99
Q

risk factors for embolic stroke

A

A-fib, endocarditis, and MI

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100
Q

hypoperfusion

A

decreased cardiac output

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101
Q

hypoperfusion can be caused by

A

dehydration, low volume, HF, PE

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102
Q

conditions causing increased coagulation or inadequate cerebral perfusion can ________ the risk of thrombus

A

increase

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103
Q

TIA

A

neurological dysfunction lasting less than one hour resulting from focal cerebral ischemia

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104
Q

Focal brain ischemia

A

Focal brain ischemia occurs when a blood clot has occluded a cerebral vessel. Focal brain ischemia reduces blood flow to a specific brain region, increasing the risk of cell death to that particular area

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105
Q

what are you at risk for after a TIA

A

of having a stroke in the next 90 days

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106
Q

clinical manifestations of TIA

A

weakness, numbness, sudden confusion, loss of balance, sudden or severe headache

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107
Q

what should you watch with hypoperfusion stroke

A

hemodynamic monitoring

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108
Q

conditions that can cause increased coagulation or inadequate cerebral perfusion

A

dehydration, hypotension, prolonged vasoconstriction due to malignant HTN

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109
Q

bifurcation

A

vessel breaks into two smaller vessels which makes its lumen smaller

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110
Q

cerebral infarction

A

occurs when the brain loses its blood supply due to vascular occlusion

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111
Q

most common reasons for cerebral infarction and what are the dominant underlying processes

A

cerebral thrombi and emboli most commonly produce occlusion but atherosclerosis and hypertension are the dominant underlying processes

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112
Q

ischemic penumbra and central core

A

there is a central core of irreversible ischemia and necrosis with cerebral infarction. the central core is surrounded by a zone of borderline ischemic tissue called the ischemic penumbra

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113
Q

treatment for cerebral infarction

A

prompt restoration of perfusion in the penumbra by injection of thrombolytic agent, but the window of opportunity is 3 hours.

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114
Q

if patient with ischemic stroke is not able to be given a thrombolytic what treatment should you use?

A

arterial clot retrieval, anticoagulant therapy, anti platelet therapy, and control of risk factors

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115
Q

what happens to brain tissue after ischemic infarcts

A

affected area softens 6-12 hours after occlusion. 48-72 hours after infarction, necrosis and swelling occur, and there is an infiltration of macrophages and phagocytosis or necrotic tissue. necrosis resolves within 2 weeks and leaves a cavity surrounded by glial scarring

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116
Q

If unable to correct tissue death within the penumbra

A

all becomes a dark cavity

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117
Q

glial scarring

A

the scarring of the brain tissue after injury

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118
Q

primary causes of hemorrhagic stroke

A

hypertension/stimulants such as cocaine

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119
Q

goal of treatment of hemorrhagic stroke

A

stop or decrease bleeding, control ICP, and prevent rebleed

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120
Q

what can reduce the incidence of hemorrhagic stroke

A

prevention or control of hypertension

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121
Q

mass of blood

A

formed as bleeding continues into the brain tissue

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122
Q

what does the mass of blood do to other brain tissue

A

other brain tissue is compressed producing ischemia, edema, and increased intracranial pressure

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123
Q

clinical manifestation of hemorrhagic stroke

A

will either have excruciating headache with a lapse into unresponsive state, headache but with consciousness maintained, or overall sudden lapse into unconsciousness

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124
Q

why does cerebral edema occur during hemorrhagic stroke

A

neurons surrounding ischemic or infarcted area undergo changes that disrupt the plasma membrane which causes cerebral edema.

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125
Q

cerebral hemorrhage resolves through

A

reabsorption. macrophages and astrocytes clear blood from the area and a cavity surrounded by glial scarring is left

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126
Q

how do you know if a patient can receive tPA?

A

the stroke inclusion/exclusion criteria for tPA

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127
Q

FAST

A

facial droop, arm drift, slurred speech, time to call 911

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128
Q

stroke warning signs

A

sudden numbness or weakness of face, arm, or leg, confusion or trouble speaking, trouble walking, severe headache

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129
Q

RAS

A

reticular activating system

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130
Q

what is RAS

A

a large network of nuclei connecting the brain stem to the cortex. controls vital reflexes, sleep, focus, wakefulness, and attention

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131
Q

alterations in arousal can be caused by

A

structural, metabolic, or psychogenic disorders

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132
Q

AVPU

A

patient is awake, patient responds to verbal stimuli, patient responds to painful stimuli, and patient is completely unresponsive

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133
Q

most important function of RAS

A

control of consciousness

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134
Q

supratentorial disorders

A

produce changes in arousal by either diffuse or localized dysfunction caused by disease process that affect the cerebral cortex or underlying subcortical white matter

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135
Q

example of supratentorial disorders

A

encephalitis

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136
Q

extracerebral

A

disorders outside the brain but within the cranial vault

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137
Q

intracerebral

A

disorders within the brain substance

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138
Q

intracerebral disorders

A

hemorrhage, infarct, or emboli

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139
Q

extracerebral disorders

A

trauma with subdural bleeding, accumulation of pus in subdural space, and tumor

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140
Q

infratentorial disorders

A

produces a decline in arousal by direct destruction or compression of RAS or by destruction or obstruction of blood flow to the brain stem

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141
Q

examples of infratentorial disorders

A

stroke, infection with accumulation of pus, tumor, demyelination disorders

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142
Q

metabolic alterations in arousal

A

hypoxic, hypoglycemia, electrolyte imbalance, toxins

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143
Q

toxins the can alter arousal

A

urea, ammonia, or drugs

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144
Q

why would hypoglycemia cause alterations in arousal

A

glucose is the brains fuel

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145
Q

how can we get to toxic level of ammonia

A

liver and renal failure

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146
Q

psychogenic alterations in arousal

A

unresponsiveness and may signal psychiatric disorders

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147
Q

disorientation

A

beginning or ALOC usually presents as disoriented to time first

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148
Q

confusion

A

inability to think clearly

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149
Q

what happens with decreased level of consciousness

A

lower brainstem regulates breathing by responding to changes in PaCO2

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150
Q

how can we evaluate level of brain dysfunction?

A

through patterns of breathing, pupillary changes, and motor responses

151
Q

obtundation

A

mild to mederate reduction in arousal with limited response to environment and falls asleep unless stimulated

152
Q

stupor

A

condition of deep sleep or unresponsiveness. can be aroused only by vigorous stimulation

153
Q

light coma

A

associated with purposeful movement on stimulation

154
Q

coma

A

associated with non purposeful movement only on stimulation

155
Q

deep coma

A

associated with unresponsiveness or no response to any stimulus

156
Q

cheyne-stroke breathing

A

fast breathing with gradual decrease until apnea, then fast breathing

157
Q

what will pupils look like with hypoxia/ischemia

A

dilated and fixed

158
Q

what will pupils look like with hypothermia

A

fixed

159
Q

what will pupils look like with atropine

A

dilated and fixed

160
Q

what will pupils look like with sedatives and hallucinogens

A

fixed, unequal, mid-position or dilation

161
Q

what will pupils look like with opioids `

A

pinpoint

162
Q

Area of brain stem that controls arousal it right next

A

the area that controls pupillary response

163
Q

bilateral dilated and fixed pupils are a

A

ominous sign

164
Q

pinpoint pupils show

A

pons damage or drugs

165
Q

one dilated pupil can be a sign of

A

compressed cranial nerve 3

166
Q

decorticate

A

position in which the arms are drawn into the core

167
Q

decerebrate

A

position in which the arms are turned outward along the side

168
Q

responses to motor response assessment can be

A

purposeful, inappropriate, or not present

169
Q

assessment of motor response is used to determine

A

brainstem dysfunction and if there is unilateral damage

170
Q

if medulla oblongata is compressed or diseased what reflexes will be shown

A

vomiting, cough, swallowing, yawning, and hiccups

171
Q

breakdown of the blood brain barrier can contribute to

A

neuroinflammation and neurodegeneration

172
Q

substances that promote coagulation

A

platelets, Von Willebrand factor, activated clotting factors, and tissue thromboplastin

173
Q

hemophilia

A

a genetic disorder in which coagulation and hemostasis factors are limited or absent. the patient is a free bleeder

174
Q

Von Willebrand factor

A

primary function is binding to other proteins, in particular factor VIII, and it is important in platelet adhesion to wound sites

175
Q

substances inhibiting coagulation

A

prostacyclin, antithrombin 3, proteins C & S, tissue plasminogen activator

176
Q

prostacyclin

A

prostaglandin family. inhibits platelet activation. vasodilator

177
Q

tissue plasminogen activator

A

natural substance that dissolve already formed clots

178
Q

end result of both extrinsic and intrinsic clotting pathway is

A

fibrin

179
Q

heparin is _____ and the its for it is ______

A

intrinsic and use PTT

180
Q

Coumadin/warfarin is ______ and the test for it is _______

A

extrinsic and use pt/INR

181
Q

what activates thromboplastin? and what does it initiate

A

Thromboplastin, contained in vessel walls gets activated due to injury & then initiates the extrinsic pathway

182
Q

extrinsic pathway

A

outside penetration activates clotting factor 7 and 10. then enzymes (thrombin) and proteins (fibrinogen) work together to form a clot = fibrin

183
Q

intrinsic pathway

A

endothelial damage, factor 12, then enzymes (thrombin) and proteins (fibrinogen) work together to form a clot = fibrin

184
Q

reduced levels of fibrinogen will do what to PT/PTT times?

A

prolong them

185
Q

increased level of fibrinogen increases

A

risk for clot

186
Q

normal levels of fibrinogen in adults

A

200-400 mg/dL

187
Q

what needs to be present for fibrinolytic system to be activated

A

a clot and fibrin

188
Q

fibrinolysis

A

clot regulation and reverses the clotting process

189
Q

fibrin and plasminogen =

A

plasmin

190
Q

plasmin

A

protein that breaks down (lyses) thrombus

191
Q

tissue plasminogen activator

A

it dissolves already formed clots. we have it naturally and secreted by endothelial cells but it takes several days vs if we administer it (exogenous) it takes 30 minutes

192
Q

anticoagulants

A

prevents formation or progression of clot but does not bust up already present clot

193
Q

how do anticoagulants prevent thrombus

A

by decreasing blood coagulability

194
Q

Adverse effect of anticoagulants

A

bleeding

195
Q

indications for anticoagulants

A

CVA, MI, DVT, PE, A-fib, heart valves, PICC/central port

196
Q

indications for heparin

A

MI, unstable angina, a-fib, mechanical heart valves

197
Q

which clotting factor is most sensitive to heparin

A

thrombin

198
Q

MOA of heparin

A

deactivates thrombin, factor X and IX, which prevents conversion of fibrinogen to fibrin - overall turns off the coagulation pathway

199
Q

how is heparin dosed

A

weight based protocol. in Kg

200
Q

what do you need to do before administering heparin

A

PTT before and 2 RN check unless given prophylactically

201
Q

range of strengths of heparin

A

10 u/1mL to 40,000 u/1mL

202
Q

prophylactic dosing of heparin is given

A

subQ

203
Q

signs of heparin over dose

A

epistaxis, hematuria, melana, petechiae

204
Q

epistaxis

A

nose bleed

205
Q

what to do for a patient with heparin induced thrombocytopenia

A

stop heparin infusion, give protamine sulfate IV (antidote), and start on argatroban

206
Q

HIT type 2

A

heparin induced thrombocytopenia. immune mediated drug response that destroys platelets (platelets will fall by 50%).

207
Q

greatest risk of the patient with HIT

A

paradoxical occurrence of thrombosis. can be fatal if not treated quickly

208
Q

adverse effect of heparin

A

Bleeding, hematoma, anemia, thrombocytopenia

209
Q

argatroban

A

thrombin inhibitor can replace heparin if patient is effected by HIT

210
Q

PTT

A

evaluates overall ability to produce a clot in a reasonable amount of time

211
Q

higher than normal PTT

A

bleeding disorder

212
Q

enoxaparin brand name

A

lovenox

213
Q

advantage of lovenox

A

more predictable/stable response and fewer adverse effects

214
Q

how does lovenox come

A

in profiled syringes

215
Q

how is lovenox dosed

A

weight and indication

216
Q

how is lovenox given

A

subQ and need to rotate sites frequently

217
Q

what do you not want to do with lovenox

A

pirate or massage site, will have air bubble in syringe do not expel air bubble before injection

218
Q

are labs required for lovenox

A

no

219
Q

which has larger molecules heparin or lovenox

A

heparin. lovenox is just fragments

220
Q

BBW of lovernox

A

Spinal/Epidural Hematomas

221
Q

what can lovenox be used for?

A

bridge therapy

222
Q

what lab do you want to check with warfarin

A

INR

223
Q

what should a patients INR be when one warfarin

A

2-3.5

224
Q

geriatrics INR threshold

A

INR threshold decreases in older population

225
Q

Warfarin MOA

A

inhibits synthesis of vitamin And clotting factors that are produced in liver which prevents clot formation

226
Q

warfarin route

A

PO and IV. IV need to dilute with normal saline

227
Q

warfarin antidote

A

IV vitamin K. reverses effects in 6 hours

228
Q

warfarin drug interactions

A

amiodarone which increases INR by 50% so cut warfarin dose in half

229
Q

warfarin adverse effects

A

Bleeding, lethargy, muscle pain, purple toes

230
Q

warfarin brand name

A

coumadin

231
Q

what do patients prescribed warfarin need to be educated on

A

constant levels of vitamin K in diet. if they eat to much food with vitamin K in it the warfarin may not work

232
Q

how long does lovenox take to reach therapeutic therapy

A

2-3 days so it should be overlapped with lovenox for those days

233
Q

BBW of warfarin

A

fatal bleeding

234
Q

PT/INR

A

PT= prothrombin time, INR= international normalization ratio

235
Q

increased INR

A

blood clots too slowly - risk for bleed

236
Q

decreased INR

A

blood clots more quickly

237
Q

clopidogrel brand name

A

plavix

238
Q

Plavix

A

anti platelet, ADP inhibitor

239
Q

plavix MOA

A

prevents platelet adhesion before clotting cascade by altering platelet membrane

240
Q

indication for plavix

A

prevention of TIA, post MI, CAD

241
Q

side effects of plavix

A

fata intracranial bleeding, thrombotic thrombocytopenia, hepatotoxicity

242
Q

BBW plavix

A

genetic factors leading to higher risk of CV events - CYP450

243
Q

can plavix be given with aspirin?

A

yes - 81 mg for heart healthy dose. up to 325 mg

244
Q

ADP, TXA2

A

stimulators released from platelets – they increase the arrival of (recruit) more platelets to site and cause vasoconstriction

245
Q

clotting cascade

A

Blood vessel injury due to disruption in blood flow, trauma, or plaque rupture occurs. Collagen is exposed.
Platelets adhere and activate. Stimulators released from activated platelets. Platelets then aggregate at injury site.
Stimulators: ADP, TXA2
Call for aggregation
Vasoconstriction
fibrin plug

246
Q

alteplase brand name

A

activase

247
Q

alteplase

A

pharmaceutically available t-PA made through recumbent DNA techniques. is fibrin specific. is a clot buster

248
Q

alteplase MOA

A

degrades protein of fibrin and clotting factors

249
Q

how to give alteplase

A

within 3-4.5 hours of symptoms. with heparin to prevent reocclusion. as a bolus and followed by infusion

250
Q

side effect of alteplase

A

bleeding

251
Q

disadvantages of alteplase

A

no antidote and short half life

252
Q

what do you need to look out for when administering alteplase

A

repercussion injury which could lead to an acute ischemic stroke or acute MI

253
Q

nursing considerations with alteplase

A

neuro exam every 15 minutes, avoid invasive procedures after injection, watch for bleeding, and check PT/PTT and hemoglobin and hematocrit

254
Q

pharmacodynamics

A

what the drug does to the body

255
Q

pharmacokinetics

A

what our body does to the drug - absorption, distribution, metabolism, excretion

256
Q

bioavailability

A

amount of drug available for absorption - IV - 100%, sublingual - 100%

257
Q

inactive prodrugs

A

inactive until in your body

258
Q

pharmacogenomics

A

same drug but different response in different bodies

259
Q

GFR

A

gives us an idea of how fast a drug can be metabolized - BUN test

260
Q

cardinal signs of inflammation

A

(HEELP) heat (fever), erythema (redness), edema (swelling), loss of function, pain

261
Q

what happens when inflammation is present

A

vasodilation, increased vascular permeability, and white blood cell infiltration

262
Q

capillary hydrostatic pressure

A

pushing pressure inside the arterial part of the vessel where filtration is favored

263
Q

interstitial oncotic pressure

A

pulling pressure outside the vessel on the arterial side

264
Q

interstitial hydrostatic pressure

A

pushing pressure on venous side of vessel where reabsorption is favored

265
Q

plasma oncotic pressure

A

pulling pressure inside the vessel on the venous side

266
Q

Normal sodium levels

A

135-145 mEq/L

267
Q

extracellular electrolytes

A

sodium, chloride, bicarb

268
Q

intracellular electrolytes

A

potassium, magnesium, phosphate

269
Q

signs and symptoms of hyponatremia

A

ALOC, seizures, ICP, coma, cerebral adema, muscle weakness, twitching, or tremors

270
Q

Signs of hypernatremia

A

fever, flushed, increased fluid retention, edema, ALOC, coma, muscle twitching, hyperreflexion

271
Q

normal levels of potassium

A

3.5 -5

272
Q

hypokalemia signs and symptoms

A

irregular pulse, dysrhythmias, or arrest. everything is slow, can flatten T and U waves, muscle aches, paralysis, V/D

273
Q

hyperkalemia signs and symptoms

A

decreased cardiac contractibility, cramps, cause peaked Ts and widened QRS, Brady dysrhythmias or arrest, hyperactive smooth and skeletal muscle

274
Q

ph of less than 7.4

A

acidosis

275
Q

ph greater than 7.4

A

alkalosis

276
Q

regulations of ph

A

chemical buffers, intracellular phosphate and protein, lungs, kidneys

277
Q

chemical buffers

A

plasma: CO2, HCO3, and hemoglobin and intracellular: phosphate and protein

278
Q

uncompensated acidosis or alkalosis

A

CO2 or HCO3 normal

279
Q

fully compensated acidosis or alkalosis

A

ph is normal

280
Q

partially compensated acidosis or alkalosis

A

nothing normal

281
Q

respiratory acidosis vs metabolic acidosis

A

respiratory acidosis has a co2>44, metabolic acidosis has a HCO3<22

282
Q

respiratory alkalosis vs metabolic alkalosis

A

respiratory alkalosis has a CO2< 38, metabolic alkalosis has a HCO3 > 26

283
Q

acidosis symptoms

A

headache, SOB, coughing, arrhythmia, increased HR, seizures, weakness N/V/D

284
Q

alkalosis symptoms

A

light headedness, hand tremor, numbness or tingling, spasms N/V/D

285
Q

PaO2

A

O2 dissolved in blood 80-100 mmHg

286
Q

PaCO2

A

35-45 mmHg

287
Q

HCO3 levels

A

33-36 mEq/L

288
Q

acute therapy

A

short term

289
Q

maintenance therapy

A

ongoing

290
Q

palliative therapy

A

symptom relief

291
Q

prophylactic therapy

A

preventative

292
Q

supplemental therapy

A

replacement

293
Q

supportive therapy

A

recovery

294
Q

parasympathetic

A

rest and digest. cholinergic receptors

295
Q

sympathetic

A

fight or flight. adrenergic receptors with alpha and beta receptors

296
Q

what neurotransmitter is connected with parasympathetic

A

acetylcholine

297
Q

inotropic

A

contractibility of the heart

298
Q

chronotropic

A

effect heart rate

299
Q

dromotropic

A

electrical conduction of the heart

300
Q

sympathetic neurotransmitter

A

norepinephrine and epinephrine

301
Q

increase in RAAS leads to

A

decreased renal salt excretion so increase salt retention which can lead to HTN

302
Q

what can prolonged hypertension do to your body?

A

vascular remodeling, increase renin/angiotensin, renal sodium retention, and procoagulant

303
Q

primary hypertension

A

due to genetics and environment

304
Q

secondary hypertension

A

usually from disease process. Is reversible

305
Q

complicated hypertension

A

leads to target organ damage such as LVH, HF, CAD

306
Q

hypertensive crisis

A

BP 180/110+, rapid onset. can cause organ damage, CVA, or stroke

307
Q

what can cause a hypertensive crisis

A

alcohol withdrawal, stimulant drugs, or pregnancy

308
Q

High blood pressure guidelines

A

Normal: Less than 120/80 mm Hg;
Elevated: Systolic between 120-129 and diastolic less than 80;
Stage 1: Systolic between 130-139 or diastolic between 80-89;
Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg;
Hypertensive crisis: Systolic over 180 and/or diastolic over 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage

309
Q

adipokines

A

inflammatory mediators released by adipocytes

310
Q

adipokines release

A

leptin and adiponectin

311
Q

leptin control what in the body?

A

appetite suppression and increase metabolic rate

312
Q

what happens to leptin and adiponectin when you are obese?

A

increase in leptin and decrease in adiponectin

313
Q

what do adiponectins deal with

A

insulin

314
Q

what do increased levels of leptin do?

A

cause resistance by increases SNS, decreasing renal sodium excretion, and causing inflammation

315
Q

what does a decreased amount of adiponectin do to your body?

A

increases SNS, increases RAAS, and decreases nitric oxide

316
Q

what does higher levels of BNP mean? what is considered normal?

A

less than 100 = normal. higher than 100 = heart failure, increase in volume, or ventricle stretch

317
Q

vomiting and diarrhea may cause toxicity for which drug?

A

digoxin cause vomit and diarrhea can make you lose potassium and hypokalemia increases potential digoxin toxicity

318
Q

effects of decrease contractility

A

increase preload - stretching of myocardium and decrease of lumen coronary arteries - myocardial ischemia - leads right back to more decreased contractility

319
Q

effects of increased afterload

A

increases left ventricle workload - increase RAAS and SNS which causes hypertrophy causes increases demand for oxygen causes ventricular remolding which leads to decrease in contractility which increases RAAS and SNS and leads to more vascular resistance

320
Q

how does a patient present with left systolic heart failure

A

fatigue, pulmonary edema, dyspnea, orthopnea, cough with frothy sputum, S3 heart sound

321
Q

orthopnea

A

shortness of breath while laying down

322
Q

Ace inhibitors and ARBs

A

reduce preload and after load, decrease volume and PVR, are cardio and renal protective

323
Q

treatment for heart failure

A

beta blocker, anti platelet, salt restriction, diuretic, ACE inhibitor or ARB

324
Q

what is a first line treatment for HTN if no other comorbidities exist?

A

diuretic - decrease BP, CO, and preload

325
Q

Cardiac glycosides Mechanism of actions and what do they do to inotrope, chronotrpe, and dromotrope

A

increase sodium and calcium (positive inotrope), augments parasympathetic stimulation (negative chronotrope), prolongs conduction (negative dromotrope)

326
Q

what cardiac glycoside did we learn

A

Digoxin

327
Q

ROME

A

respiratory opposite, metabolic same

328
Q

what is a first line treatment for HTN if no other comorbidities exist?

A

diuretic - decrease BP, CO, and preload

329
Q

what do alpha receptors do

A

vasoconstrict cardiovascular, bladder constriction, promote glycogenolysis, mydriasis

330
Q

what do beta 1 receptors do

A

increase contractility in heart, increase HR, promote renin secretion

331
Q

what do beta 2 receptors do

A

bronchodilate, glycogenolysis, vasodilation

332
Q

adrenergic agonist (alpha and beta)

A

promote SNS. low dose beta, high dose alpha

333
Q

cor pulmonale

A

Right ventricular enlargement. can be hypertrophy, dilation, or both

334
Q

tests of high risk for diabetes

A

FPG of 100-125 mg/dL, 2 hr PG 140-199, hgbA1C- 5.7%-6.4%

335
Q

consequences of hyperglycemia

A

decreased cognition, neuropathy, cataracts, hypertension, stroke, heart disease, gastroparesis, nephropathy, chronic kidney disease, oxidative stress, infection, cancer, immunosuppression

336
Q

insulin counter regulator hormones

A

growth hormone, glucagon, epinephrine, cortisol

337
Q

characteristics to DKA

A

acidosis, ketonuria, ketonemia, hyperglycemia over 250 mg/dL, tachycardia, dehydrated

338
Q

laster signs of diabetic renal dysfunction

A

Hypoproteinemia, decrease oncotic pressure, fluid overload, anasarca, HTN

339
Q

as GFR decreases to less than 10 what type of signs occur

A

uremic signs - nausea, lethargy, acidosis, anemia, and HTN from having high levels of urea in the blood

340
Q

diabetic neuropathy sensory deficits

A

footdrop, amyotrophy, temp, and pain

341
Q

diabetic autonomic neuropathy deficits

A

delayed gastric emptying, altered bladder function, impotence, orthostatic hypotension, HR variability

342
Q

alpha cells release what?

A

glucagon

343
Q

first line drug for type 2 diabetes

A

metformin (Glucophage)

344
Q

insulin onset and duration times

A

rapid: 15 minutes onset of 3-5 hr duration
short: 30-60 minutes onset with 6-10 hr duration
long: 1-2 hour onset with 24 hr duration

345
Q

hypoglycemia blood glucose level

A

less than 70 mg/dL

346
Q

less sever signs on hypoglycemia

A

shaking, sweating, dizziness, hunger, fast HR, headache, weakness, irritable

347
Q

BUN

A

7-18 mg/dL

348
Q

Creatine

A

0.6-1.2 mg/dL

349
Q

albumin

A

3.5-6g/dL

350
Q

normal PTT

A

60-70 seconds

351
Q

normal aPTT

A

30-40 seconds

352
Q

PTT/aPTT on coagulants

A

will be 1.5-2.5 times longer than normal

353
Q

insulins

A

lispro - Humalog (rapid acting
regular - humbling R (short acting)
glargine - Lantus (long acting)

354
Q

adrenergic beta 2 agonist short acting

A

albuterol - inhaler for bronchospasm and asthma

355
Q

adrenergic beta 2 agonist long acting

A

salmeterol

356
Q

anticholinergic

A

ipatropium (Atrovent) for COPD

357
Q

corticosteroid

A

fluticasone (Flonase/Flovent)

358
Q

leukotriene receptor blocker

A

Montelukast (Singulair) - for allergic rhinitus and asthma

359
Q

Benzodiazepines

A

lorazepam (Ativan) and diazepam (Valium)

360
Q

antidiabetics

A

metormin (Glucopage) - decreases glucose production while increases insulin sensitivity

361
Q

sulfonylureas

A

glipizide (Glucotrol) stimulates pancreas to release insulin

362
Q

DPP 4 inhibitor

A

sitagliptine (Januvia) increase insulin release

363
Q

antiplatelets

A

clopidogrel (Plavix) and aspirin

364
Q

thrombolytic

A

alteplase (Activase)

365
Q

Anticonvulsant

A

phenytoin (Dilantin) - for tonic/clonic seizures

levetriacetam (Keppra) - partial seizures

366
Q

anti epileptic

A 
carbamazepine (Tegretol) 
Valpoirc acid (Depekote)
367
Q

nitrates

A

nitroglycerin

368
Q

cardiac glycoside

A

digoxin

369
Q

anticoagulants

A

Heparin
Enoxaparin (Lovenox)
Warfarin (Coumadin)

370
Q

Beta Blockers

A

metoprolol (Lopressor)

Carvedilol (Coreg)

371
Q

Calcium Channel Blockers

A

Diltiazem

Amlodipine (Norvasc)

372
Q

ACEs

A

Lisinopril

Enalopril (Vasotec)

373
Q

ARBS

A

Losartan (Cozzar)

NURSING School (17 decks)

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