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Fall 22 > Patho exam 2 > Flashcards

Patho exam 2 Flashcards

1
Q

Which cranial nerve forms the optic nerve?

A

Carnial nerve 2

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2
Q

what are medications that dilate pupils?

A

mydratics

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3
Q

What color is the optic disk normally?

A

yellow, circular, clearly defined

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4
Q

What is responsible for central vision?

A

macula

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5
Q

what is responsible for sharp vision?

A

fovea

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6
Q

what visual reflex is a direction of eye towards an object attracting a persons attention?

A

fixation

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7
Q

what impairs fixation?

A

drugs, alcohol, fatigue, inattention

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8
Q

what rare condition does the pupil accommodate but does not react to light?

A

Argy II robertson pupil

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9
Q

What 3 things occur with accommodation?

A

-pupil changes in size when object is brought closer to nose
-eyes should converge
-size of pupils decrease in response to object coming closer

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10
Q

Which system decreases pupil size?

A

PNS

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11
Q

which system increases pupil size?

A

SNS

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12
Q

what is another term for increasing pupil size?

A

mydriasis

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13
Q

what is another term for decreasing pupil size?

A

miosis

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14
Q

what is the function of the lens?

A

bends light rays to fall onto retina

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15
Q

what is the function of the ciliary body?

A

-changes shape of lens
-secretes aqueous humor

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16
Q

what disease process is known as visual field loss secondary to optic nerve damage?

A

glaucoma

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17
Q

what is the leading cause of preventable blindness?

A

glaucoma

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18
Q

what are the two types of glaucoma?

A

-primary open angle glaucoma
-acute angle closure glaucoma

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19
Q

what structures are affected by glaucoma?

A

-ciliary muscle
-trabecular meshwork
-canal of schlemn

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20
Q

If ciliary muscle if relaxed what occurs?

A

Obstruction of the canal

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21
Q

where is aqeuous humor produced?

A

ciliary muscle

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22
Q

ciliary muscle is controlled by which system?

A

ANS

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23
Q

what type of stimulation causes the ciliary muscle to relax which will block drainage?

A

SNS stimulation

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24
Q

which system causes the ciliary muscle to contract to allow drainage of aqeuous humor?

A

PNS

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25
Q

what type of glaucoma is the most common form in the US?

A

primary open angle glaucoma

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26
Q

which type of glaucoma has progressive optic nerve damage, with eventual impairment of vision, and increased IOP?

A

primary open angle glaucoma

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27
Q

Does primary open angle glaucoma have symptoms?

A

not until significant and irreversible optic nerve damage occurs

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28
Q

what are the risk factors for primary open angle glaucoma?

A

-elevated IOP
-family history
-old age
-african and south american ancestry

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29
Q

how do you treat primary open angle glaucoma?

A

-reducing elevated IOP
-chronic therapy with drugs

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30
Q

how do drugs lower IOP for glaucoma?

A

assist with aqeuous humor outflow and decrease aqeuous humor production

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31
Q

what is the preferred route of drug therapy for glaucoma?

A

topical

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32
Q

if drug therapy for glaucoma are ineffective, what other interventions can be done?

A

surgical intervention

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33
Q

what are two surgical procedures for glaucoma?

A

-laser trabeculoplasty
-trabeculectomy

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34
Q

what cholinergic drugs can be given for glaucoma?

A

-acetylcholine
-echothiophate

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35
Q

what beta adrenergic blocking agents can be given for glaucoma?

A

timolol

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36
Q

what do cholingerics mimic

A

PNS actions of acetylcholine

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37
Q

what actions do cholinergics do?

A

-pupil constriction
-ciliary muscle contraction
-enhancing aqeuous humor drainage
-reducing IOP

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38
Q

what do beta blockers do for glaucoma?

A

block SNS nerve endings in ciliary epithelium to cause a decrease in aqeuous humor production

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39
Q

what is the MOA for direct acting miotic Acetylcholine?

A

constricts pupils

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40
Q

What is an example of a direct acting miotic?

A

acetylcholine

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41
Q

11What is the onset and peak of acetylcholine?

A

instant

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42
Q

iwhat is the duraction of action of acetylcholine?

A

10 minutes

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43
Q

what is another term for pupils constriciting?

A

miotics

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44
Q

what is an example of an indirect acting miotic?

A

echothiophate

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45
Q

what is the MOA for echothiophate?

A

inhibits cholinesterase enzymes which allows for pupils to constrict because acetylcholine is not broken down

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46
Q

what is the onset for echothiphate?

A

10-30 minutes

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47
Q

what is the duration of action for echothiophate?

A

7-28 days

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48
Q

why are indirect acting drugs not commonly used for long term use?

A

can cause cataracts

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49
Q

What are cholinergic drug adverse effects?

A

-abdominal cramps
-asthma attacks
-diarrhea
hypotension
-headache
-nausea
-vomiting

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50
Q

what is the drug class for timolol?

A

opthalmic beta adrenergic blocker

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51
Q

what are the indications for opthalmic beta adrenergic blockers?

A

acts on beta 1 and beta 2 receptors

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52
Q

what is the onset of timolol?

A

15-30 minutes

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53
Q

what is the peak for timolol?

A

1-2 hours

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54
Q

what is the duration of action for timolol?

A

12-24 hours

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55
Q

what are the side effects of timolol?

A

arrthymia, bradycardia, bronchospams, heartblock

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56
Q

what are adverse effects of beta adrenergic blocking agents LOCALLY?

A

minimal effects

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57
Q

what are adverse effects of beta adrenergic blocking agents SYSTEMICALLY?

A

heart and lungs are affected which can lead to bradycardia and bronchospasms

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58
Q

for beta adrenergic blocking agents, what type of agents are recommended or patients with asthma?

A

cardioselective

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59
Q

after instilling timolol through eye drops, what is the next step?

A

apply light pressure on lacrimal sac for 1 minute after instilling drug

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60
Q

why do you have to put pressure on the lacrimal sac after administering timolol?

A

to minimize systemic absoprtion

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61
Q

what are nursing implications for timolol?

A

-assess patient history
-med history
-baseline vitals
-visual acuity
-physical assessment of they eye
-contrainidcaitons
-avoid touching eye with the tip of the dropper

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62
Q

what are the steps to administering eye drops?

A

–remove any lenses prior
-clean debris
-have patient look at the ceiling
-place drops in conjuctival sac
-gently close eye
-apply pressure on inner canthus

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63
Q

which type of glaucoma is known as precipitated by displacement of iris which prevents aqeuous humor from exiting?

A

angle closure glaucoma

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64
Q

Another name for angle closure glaucoma is?

A

narrow angle glaucoma

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65
Q

how do you treat angle closure glaucoma?

A

Cannot treat and irrevesible vision loss within 1-2 days

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66
Q

what type of corrective surgery can be done for angle closure glaucoma?

A

-laser iridotomy
-iridectomy

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67
Q

how does angle closure glaucoma present itself?

A

-sudden onset
-painful

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68
Q

what drugs dilate pupils?

A

mydriatics

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69
Q

when do you use mydriatics?

A

-measure refraction
-intraocular exams
-introcular surgery

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70
Q

what drug loosens cerumen?

A

carbamide peroxide

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71
Q

what are 3 structures bridge sound to middle ear?

A

malleus, incus, stapes

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72
Q

what is the function of the middle ear?

A

-conducts sound vibrations from outer to inner central hearing
-protects inner ear by reducing amplitude of sounds
-eustachian tube allows for equalization of pressure

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73
Q

what does cerumen protect against?

A

fungus and bacteria

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74
Q

what is the function of the eustachian tube?

A

allows for passage of air and connects middle ear with nasopharynx

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75
Q

what parts of the ear does conductive hearing loss affect?

A

outer and middle ear

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76
Q

what happens in conductive hearing loss?

A

sound transmission is impaired to middle ear

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77
Q

what type of environments do patients prefer with conductive hearing loss?

A

noisy environments

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78
Q

how do you treat conductive hearing loss?

A

treat cause or recommend a hearing aid

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79
Q

what occurs in sensorineural hearing loss?

A

ability to hear sound but inability to understand speech

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80
Q

what can be done to help sensorineural hearing loss?

A

hearing aids make sounds louder but not clearer

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81
Q

what are clinical manifestations for hearing loss and deafness?

A

-early signs are often unnoticed by patients
-pressure from others is a big factor to get help
-understanding should be validated
-ineffective communication and interaction can be frustrtaing for both parents and cargivers

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82
Q

what is known as the perception of noise without actual source of noise?

A

tinnitus

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83
Q

what is known as the first sign of hearing loss?

A

tinnitus

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84
Q

What things may cause tinnitus?

A

-noise
-more than 200 drugs

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85
Q

What test can assess a patients hearing ability?

A

whisper test

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86
Q

how do you perform a whisper test?

A

-be out of patients line of sight
-whisper a sentence or series of words 1-2 feet away
-ask patient to repeat

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87
Q

what can cause conductive hearing loss?

A

cerumen buildup

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88
Q

what is the MOA for carbamide peroxide?

A

softens, loosens, and removes cerumen

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89
Q

what is the recommended dose for carbamide peroxide?

A

BID for 4 days and then reevaluate

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90
Q

what are the side effects for carbamide peroxide?

A

no known side effects

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91
Q

how do you assess the ear an adult?

A

pull pinna up and back

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92
Q

how do you assess the ear in a child?

A

pull pinna down and back

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93
Q

what are the contraindications for carbamide peroxide?

A

-ear drainage
-tympanic membrane rupture
-significant pain or irritation

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94
Q

what may be given for ear infections?

A

-antibiotics for infection
-steroids for reducing inflammation and itchiness

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95
Q

what are nursing and collaborative care management techniques for hearing loss?

A

environmental noise control

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96
Q

Otoxic is also known as?

A

renal toxic

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97
Q

What are 4 examples of ototoxic drugs?

A

-salicylates
-loop diuretics
-chemotherapy drugs
-antibiotics

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98
Q

what are 3 ototoxic substances?

A

-toulene
-carbon disulfide
-mercury

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99
Q

what are assistive devices and techniques for hearing loss?

A

hearing aids

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100
Q

what do hearing aids do?

A

-provide amplification
-sound lateralization
-speech discrimination

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101
Q

what is the known as the body’s ability to resist disease?

A

immunity

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102
Q

what are the immune response functions?

A

-defend
-homeostasis
-surveillance

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103
Q

What do antibodies connect with to start the immune response?

A

antigen

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104
Q

what are the two types of immunity?

A

innate and adaptive

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105
Q

which type of immunity is present at birth, is the first line of defense, has a nonspecific response?

A

innate

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106
Q

innate immunity contains primarily which WBC?

A

neutrophils and monocytes

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107
Q

which type of immunity is cell mediated and specific?

A

adaptive

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108
Q

which type of adaptive immunity does NOT produce antibodies, goes through cell destruction through T lymphocytes, and destroys pathogens inside the cell?

A

cell mediated immunity

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109
Q

which type of adaptive immunity produces antigen specific antibodies, destroys cells through B cells, and destroys pathogens outside the cell?

A

humoral immunity

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110
Q

what is the patho of the immune response?

A

-pathogen invades (outside to inside)
-innate immunity kicks in and try to phagocytize pathogen
- if innate immunity fails, adaptive immunity kicks in
-macrophages and dendritic cells present antigen of pathogen to T cell
-T cell then differentiates into T helper or T killer
-T helper activates B cells and T killer destroys pathogen
-B cells secrete antibodies that help destroy pathogen and then create memory cells

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111
Q

what is known as the function to defend against pathogens?

A

immune response

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112
Q

what activates the immune response?

A

inflammation

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113
Q

inflammation is part of the immune response but may not always indicate what?

A

infection

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114
Q

what is known as when the defense system fails & pathogens takes over?

A

infections

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115
Q

what is a sequential reaction to cell injury?

A

inflammation

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116
Q

what response removes necrotic material?

A

inflammatory response

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117
Q

what response establishes environment suitable for healing and repair?

A

inflammatory response

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118
Q

what are the 3 phases of the inflammation?

A

-vascular response
-cellular response
-formation of exudate

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119
Q

what are examples of acute inflammation?

A

allergic reactions, chemical irritants, infection, trauma injury, burns

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120
Q

what are examples of chronic inflammation?

A

cardiovascular disease, neurological disease, arthritis, lupus

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121
Q

What occurs in the vascular response of the inflammatory reaction?

A

-after injury -> arterioles vasoconstrict
-histamine and other chemicals are released to dilate vessels
-chemical mediators cause increased capillary permeability
-serous exudate followed by exudate with plasma proteins such as albumin
-oncotic pressure draws fluid from blood vessels
-vasodilation and increased capillary permeability

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122
Q

what are the signs of vascular response?

A

redness, heat, swelling

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123
Q

In the vascular phase, what occurs with fibrinogen?

A

-fibrinogen leaves blood and is activated into fibrin
-fibrin strengthens blood clot formed by platelets

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124
Q

what do platelets release in vascular phase?

A

growth factors and start healing process

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125
Q

what are the functions of blood clots in vascular phase?

A

-trap bacteria
-prevent further spread
-framework for healing

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126
Q

what is chemotaxis?

A

neutrophils and monocytes move to site of injury

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127
Q

which inflammatory response accumlates WBCs at site of injury?

A

cellular response

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128
Q

which WBC move to site of injury during cellular response?

A

-neutrophils
-monocytes
-lymphocytes

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129
Q

What is the final phase of the inflammatory response?

A

exudate formation

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130
Q

what occurs in exudate formation?

A

-fluid and WBCs move from circulation to site of injury
-hemorrage may occur: rupture of blood vessels

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131
Q

what are local clinical manifestations of inflammation?

A

-redness
-heat
-swelling
-loss of function

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132
Q

what are systemic clinical manifestations of inflammation?

A

-leukocytes shift to left
-malaise
-nausea/anorexia
-fever
- increased heart rate and respiratory rate

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133
Q

what is the patho for fever?

A

-WBC release cytokines
-cytokines trigger onset of fever
-metabolic changes in hypothalamus
-synthesize prostaglandins which increase thermostatic point
-hypothalamus activates ANS
-ANS increases temp
-epinephrine is released
=fever

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134
Q

what are the 3 types of inflammation?

A

-acute
-subacute
-chronic

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135
Q

which type of inflammation has a healing process of 2-3 weeks, has no residual damage. and is predominately neutrophils?

A

acute inflammation

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136
Q

which type of inflammation has same features as acute inflammation but healing will last longer (weeks to months)?

A

subacute inflammation

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137
Q

which type of inflammation lasts weeks, months, or years, agent persists or repeatedly injures tissues, includes lymphocytes and macrophages?

A

chronic inflammation

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138
Q

where are corticosteroids secreted?

A

adrenal cortex

139
Q

what are the two types of corticosteroids?

A

-glucocorticoids
-mineralcorticoids

140
Q

What is the MOA for corticosteroids?

A

-inhibits inflammatory and immune response

141
Q

why are corticosteroids not good for someone in an active immune response (active infection)?

A

surpresses immune response to fight

142
Q

How do corticosteroids affect the body?

A

-increase BG levels
-increased breakdown of proteins to amino acids
-stimulates bone demineralization & stabilizes mast cells

143
Q

What is an example of a glucocorticoid?

A

prednisone

144
Q

what are the broad indications for prednisone?

A

-anti-inflammatory
-immunosurpressant

145
Q

how do you administer prednisone?

A

oral

146
Q

what are 3 contraindiactions for prednisone?

A

-allergy
-serious infections
-Diabetes mellitus

147
Q

What do you avoid with prednisone?

A

-long term administration
-if patient presents with serious infection
-breastfeeding because it can be secreted in breastmilk

148
Q

What is important about corticosteroids taper dosing?

A

should not be stopped abruptly

149
Q

What does taper dosing allow for with corticosteroids?

A

-allows pituitary time to recover
-starts stimulating the normal production of endogenous hormones

150
Q

what may a patient risk if they abruptly stop taking corticosteroids?

A

-causes endogenous production of hormones to stop
-causes impaired stress respone -> risk for crisis

151
Q

long term steroid therapy may require what?

A

stress dose

152
Q

what are potential adverse affects with prednisone?

A

-moon face
-hyperglycemia
-psychosis
-adrenal surpression
-insomnia
-nervousness
-impaired wound healing
-many drug reactions

153
Q

what are nursing considerations with prednisone?

A

-monitor administration in patients with DM
-monitor for cardiac, renal, liver diagonosis due to alterations in elimination
-caution in patients with gastritis, reflux disease, or ulcer diagnosis because of potential for GI perforation

154
Q

what keeps our gut in balance?

A

normal flora

155
Q

which type of bacteria is easier to kill?

A

gram positive

156
Q

what happens during infection?

A

-normal defense is compromised
-microorganisms take control
-body is overwhelmed and symptoms appear

157
Q

what are signs and symptoms of infection?

A

-fever
-chills
-sweats
-redness
-pain
-swelling
-fatigue
-increased WBC

158
Q

what is the normal lab values for WBC?

A

5,000 - 10,000 WBC

159
Q

What is known as a microorganism that causes disease?

A

pathogen

160
Q

what can assist the body to combat infection?

A

antibiotics

161
Q

How are antibiotics most effective?

A

if combined with functional defense mechanisms

162
Q

what is known as bacteria are present but not with over signs/symptoms?

A

colonization

163
Q

if you treat colonization, what may happen?

A

can lead to drug resistance

164
Q

what are the two types of infections?

A

-community associated infection
-health care associated infection

165
Q

which type of infection is acquired by a person who has not been hospitalized or had a recent exposure?

A

community associated infection

166
Q

a health care associated infection is also known as?

A

nosocomial infection

167
Q

which type of infection is acquired while getting health care treament or in a hospital?

A

health care associated infection

168
Q

which type of health care associated infection is difficult to treat, can be drug resistant, highly virulent, and is the top 10 leading cause of death in the US?

A

health care associate infections

169
Q

what are the 3 types of antibiotic therapy?

A

-empiric
-definitive
-prophylactic (preventative)

170
Q

which type of therapy requires immediate antibiotics and given antibiotics that can kill most organisms?

A

empiric therapy

171
Q

When do you obtain a culture with empiric therapy?

A

prior to adminstation of antibiotics

172
Q

which type of therapy does the lab identify microorganism and tests susceptibility to various antibiotics? based on the results, you will adjust the therapy

A

definitive therapy

173
Q

which type of antibiotic will you use with definitive therapy?

A

narrow spectrum and least toxic drug

174
Q

overuse of broad spectrum antibiotics can lead to?

A

resistance

175
Q

Which type of therapy is used to prevent an infection in situations with high contamination, usually prior to surgury?

A

prophylactic therapy

176
Q

when do you give antibiotics before surgery for prophylactic antibiotic therapy?

A

30 min prior

177
Q

How will we know if antibiotics were therapeutic?

A

decreased signs and symptoms

178
Q

how will we know if antibiotics were subtherapeutic?

A

signs anf symptoms do not improve

179
Q

what are adverse effects of antiobiotcs?

A

-toxic levels such as serum levels are too high
-allergic or adverse reaction
-chills, joint pain, difficulty breathing, wheezing

180
Q

what occurs in superinfections?

A

when antibiotics reduce or eliminate normal flora and other bacteria/fungi take over

181
Q

what are 3 examples of a superinfection?

A

vaginal yeast infection, ABX associated diarrhea, C. Diff (serious superinfection)

182
Q

what are signs and symptoms of C.Diff?

A

-watery diarrhea
-abdominal pain
-fever

183
Q

what should be avoided with C. Diff

A

avoid taking probiotics

184
Q

what is a patient at risk for with C. Diff?

A

dehydration or fluid imbalance

185
Q

what are 4 categories/classes of antibiotics?

A

-penicillins
-cephalosporins
-macrolides
-tetracyclines

186
Q

what is the MOA of antibiotics?

A

-interfere with bacterial cell wall synthesis
-interfere with protein synthesis
-interfere with replication of DNA and RNA
-antimetabolite action

187
Q

what are the two type of antibiotics?

A

bacteriostatic and bactericidal

188
Q

which type of antibiotic does not actually destroy bacterial just inhibits growth?

A

bacteriostatic

189
Q

which type of antibiotic kills a wide variety of gram + and some gram - bacteria?

A

bactericidal

190
Q

what should you do prior to administering antibiotics?

A

-review history of hypersensitivity or allergic reactions
-review WHAT the reaction was
-review current meds
-lab tests
-obtain cultures if possible
-full head to toe assessment (any rashes)

191
Q

what occurs in bacterial resistant infections?

A

bacterial infections no longer respond to ABX treatment

192
Q

bacterial resistant infections are due to what?

A

-overprescribing ABX
-lack of ABX completion
-education

193
Q

what occurs with ABX resistance?

A

-bacteria survived
-adapt to surroundings
-mutate over time so that it can survive attack by bacteria

194
Q

What are characteristics of beta lactamase antibiotics?

A

-will kill bacteria that contains beta lactam rings
-contributes to bacterial resistance
-stronger against bacterial strains

195
Q

what is an example of a penicillin?

A

amoxicillin

196
Q

what type of antibiotic are penicillins?

A

bactericidal

197
Q

what are penicillins derived from?

A

mold on bread/fruit

198
Q

what inhibitors do pencillins bind with?

A

beta lactamase inhibitors

199
Q

what beta lactamase enzyme targets penicillin?

A

penicillinases

200
Q

what is penicillins MOA?

A

-binds to penicillin building protein
-inhibits peptidoglycan which interefers with cell wall synthesis
-results in defective cell wall that is easily broken down
-bacterial death due to lysis

201
Q

what are contraindications for penicillin?

A

-drug allergy
-increased risk for allergy to other beta lactam ABX
-cephalosporins

202
Q

what are adverse effects of pencillins?

A
  • GI system is most common
    -may need to adjust doses for renal dysfunction
    -unpredictable reactions -> stevens Johnson syndrome (unique rash on whole body)
203
Q

What are penicillin specific nursing interventions?

A

-high rate of hypersensitivity/allergies
-assess for asthma, aspirin allergy, & sensitivity to cephalosporins
-monitor serum levels (potassium and sodium)
-take with water NOT juices
-take with food to avoid upset stomach
-epinephrine for anaphylactic reactions
-not all end in “cillin”

204
Q

what is an example of a semisythetic antibiotic that is related to penicillin and has almost all the same characteristics?

A

cephalosporins

205
Q

how can you administer cephalosporins?

A

IV and PO

206
Q

what are the adverse effects of cephalosporins?

A

GI and skin

207
Q

Cephalosporin has a high cross sensitivity with ?q

A

penicillin

208
Q

what is the MOA for cephalosporins? (same as penicillin)

A

-binds to penicillin building protein
-inhibits peptidoglycan which interefers with cell wall synthesis
-results in defective cell wall that is easily broken down
-bacterial death due to lysis

209
Q

what is an example of a 1st generation cephalosporin?

A

cefazolin

210
Q

what kind of bacteria is cefazolin used for?

A

great for gram positive bacteria but limited with gram negative

211
Q

how can you administer cefazolin?

A

parenteral use only

212
Q

what are the indications for cefazolin?

A

-surgical prophylaxis
-susceptibility to staph infections

213
Q

What are 3 specific nursing interventions for cephalosporins?

A

-thorough assessment of allergies
-note specific generation
-avoid alcohol or alcohol containing products

214
Q

what is an example of a macrolide?

A

erythromycin

215
Q

what is erythromycins MOA?

A

inhibit protein synthesis and is bacteriostatic

216
Q

in high enough doses what is erythromycin?

A

Bactericidal

217
Q

how can you administer erythromycin?

A

oral, IV, topic, opthalmic

218
Q

what are 3 additional therapeutic effects of erythromycin?

A

-Irritates GI tract
-stimulates smooth msucle and GI motility
-beneficial to patients with delayed gastric emptying

219
Q

what are 3 adverse affects of erythromycin?

A

-Nausea/vomiting/stomach irritation
-cardiac & liver related issues
-tinnitus & hearing loss

220
Q

what are 4 macrolide specific nursing interventions

A

-reduce effectiveness of oral contraceptives
-not to be given with fruit juices
-assess cardiac and liver function
-baseline hearing status

221
Q

what is an example of a tetracycline?

A

Doxycycline

222
Q

what is MOA for doxycycline?

A

inhibit bacterial protein synthesis and is bacteriostatic

223
Q

what does doxycycline bind to?

A

-magnesium
-calcium
-metallic ions

224
Q

What will happen if you coadministrate doxycycline with milk, antacids, or iron salts?

A

reduces oral absorption of tetracycline (doxycyline)

225
Q

what are 2 indications for tetracyclines?

A

-variety of gram - and gram + bacteria
-lyme disease, chlamydia, & adolescent/adult acne

226
Q

what are 3 contraindications for tetracyclines?

A

-allergy
-pregnancy or lactating mothers
-children < 8 years old

227
Q

what are 7 adverse effects of tetracyclines?

A

-teeth discoloration
-effects on fetal development
-photosensitivity
-alteration of intestinal and vaginal flora
-thrombocytopenia
-upset stomach
-reduction of oral contraceptives

228
Q

what are 6 tetracycline nursing interventions?

A

-interacts with dairy products, antidiarrheals, calcium, magnesium, iron
-may potentiate effects of oral anticoagulants
-decrease effectiveness of oral contraceptives
-sun exposure
-fluids with oral doses
-monitor skin for IV administration

229
Q

what are 2 examples of topical antimicrobials?

A

neomycin and polymyxin B

230
Q

How are antibiotics different from topical antimicrobials?

A

differ in absorption, distribution, toxicities, and adverse effects

231
Q

what type of antibiotic is neomycin and polymyxin B?

A

broad spectrum

232
Q

over use of neomycin and polymyxin B can result in?

A

increased likelihood of future allergic reactions of the skin

233
Q

what are 6 nursing considerations for antibiotics?

A

-administer within recommended time frames
-give with fluids/foods as indicated
-administer around the clock
-do not omit or double up doses
-check herbal supplements interactions
-monitor for hypersensitivty reactions

234
Q

what 5 things should be assessed with antibiotics?

A

-full assessment, lab values, current meds, vitals signs
-previous reaction to antibiotics?
-obtain cultures if you can prior to starting abx
-most common side effect of abx = n/v/d
-monitor for allergic or hypersensitivity reactions

235
Q

what is the 1st thing you do for hypersensitivity reactions?

A

stop medication, contact provider, monitor patient

236
Q

when do hypersensitivity reactions happen?

A

-30 min or up to days later
-delayed responses can occur after 72 hours

237
Q

what are symptoms of hypersensitivity?

A

-rash
-itching
-swelling of face, tongue or hands
-SOB
-wheezing
-if anaphylaxis -> epinephrine

238
Q

what is another term for stroke?

A

cerebral vascular accident

239
Q

infarcation results in?

A

cell death

240
Q

what are the two types of strokes?

A

ischemic and hemorrhagic

241
Q

what does the brain require?

A

oxygen and glucose to neurones

242
Q

if bloodflow is interrupted, what happens?

A

-neurologic metabolism is altered - 30 secs
-metabolism stops - 2 min
-cell death - 5 minutes

243
Q

what does the brain have to regulate blood flow?

A

cerebral autoregulation
-cerebral blood vessels change diameter in response to BP so blood flow is constant

244
Q

during ischemia, what is impaired?

A

autoregulation of blood flow

245
Q

if cerebral autoregulation is impaired, how is this a problem?

A

brain is dependent on systemic BP

246
Q

what are 4 nonmodifiable risk factors?

A

-gender
-age
-ethnicity or race
-family history

247
Q

what are 10 modifiable risk factors for strokes?

A

-hypertension
-heart disease
-diabetes
-smoking
-obesity
-sleep apnea
-metabolic syndrome
-lack of exercise
-diet
-drug/alcohol use

248
Q

what is the cause for 90% of strokes?

A

smoking

249
Q

what is known as a mini stoke, is a brief episode of neurologic dysfunction, without infarction but can progress to stroke?

A

transient ischemic attack

250
Q

how long do transient ischemic attacks last?

A

< 1 hour

251
Q

why do transient ischemic attacks happen?

A

microemboli or temporary clot that blocks blood flow

252
Q

what is ischemia?

A

temporary periods of hypoxia due to decreased blood flow

253
Q

what is infarction?

A

blood flow is cut off which leads to necrosis (cell death)

254
Q

what is known as inadequate blood flow to brain due to a blockage of a cerebral artery by a blood clot?

A

ischemic stroke

255
Q

what are the two types of ischemic strokes?

A

-thrombotic (blood clot stays put)
-embolic (blood clot travels)

256
Q

which type of ischemic stroke is the most common, is normally preceded by a Transient Ischemic Attack, and the narrow vessel becomes occluded which results in infarction?

A

thrombotic

257
Q

what are 3 risk factors for thrombotic stroke?

A

-hypertension
-DM
-atherosclerosis

258
Q

what is the second most common ischemic stroke where an embolus lodges and occludes cerebral artery?

A

embolic stroke

259
Q

how do most embolic strokes occur?

A

starts as plaque, breaks off, enters circulation, and lodges in narrow vessel

260
Q

what are 4 common causes of embolic ischemic strokes?

A

-atrial fibrilation
-MI
-infective endocarditis
-rheumatic heart disease

261
Q

what are 2 less common ways to have an embolic ischemic stroke?

A

air and fat emboli

262
Q

what are characteristics of embolic ischemic strokes?

A

-severe manifestations
-develops suddenly
-no warning signs
-conscious with headaches
-neurological deficits (can be temporary if clot breaks up)
-recurrence is common

263
Q

what is the patho for hemorrhagic strokes?

A

weakened blood vessels ruptures and bleeding into brain

264
Q

what are the most common causes of hemorrhagic strokes?

A

aneurysms and AVMs

265
Q

during hemorrhagic strokes where does the bleeding occur?

A

inracerebral (brain tissue) and into the subarachnoid space or ventricles

266
Q

what is known as ballooing or bulging of a blood vessel that can leak or rupture?

A

aneurysm

267
Q

what is known as an abnormal tangle of blood vessels, connection of arteries and veins, disrupts normal blood flow and oxygen, can weaken & rupture and lead to hemorrhage?

A

arteriovenous malformation (AVM)

268
Q

what are clinical manifestations of strokes?

A

-neurological symptoms that are similar for ischemic and hemorrhagic because they both cause lack of blood flow to the brain
-related to location of stroke
-functions affected are related to artery involved

269
Q

what are possible outcomes that strokes are related to?

A

-motor function and communication
-affect and intellectual function
-spatial perceptual problems (unaware of what is going on with you)
-elimination (dont know what it feels like if bladder is full so you dont pee)

270
Q

what motor function abilities are affected with strokes?

A

-mobility
-respiratory function
-swallowing & speech
-gag reflex
-self care abilities

271
Q

If a patient has a left sided stroke, which side of the body is affected?

A

right side (contralateral)

272
Q

what is another term for difficulty communicating?

A

aphasia

273
Q

what are the three types of aphasia?

A

receptive, expressive, and global aphasia

274
Q

what type of aphasia is unable to comprehend what is being said?

A

receptive aphasia

275
Q

what type of aphasia has the inability to produce speech?

A

expressive aphasia

276
Q

what type of aphasia is the inability to communicate?

A

global aphasia

277
Q

What are the AFFECT clinical manifestations for strokes?

A

patient is
-emtional, unpredictable
-frustrated
-outburts (inappropriate reactions to things and do not realize its wrong)

278
Q

what are the INTELLECTUAL FUNCTION clinical manifestations for strokes?

A

patient will have
-memory issues
-left brain -> slow and cautious
-right brain -> impulsive

279
Q

what are the SPATIAL - PERCEPTUAL clinical manifestations for strokes?

A

patient will:
-deny illness
-perception of self is off

280
Q

which disease process results in half of your visual field is lost from each eye? (sensory perceptual problem)

A

homonymous hemianopsia

281
Q

what do you monitor for in homonymous hemianopsia?

A

monitor for
-diplopia
-prosis
-loss of corneal refex

282
Q

what is super important when it comes to strokes?

A

TIME

283
Q

What is golden hour routine for strokes?

A

-get a CT scan within 20 min of arrival (to assess ischemic or hemorrhagic stroke)
-check glucose levels (any deviation from norm is DEADLY for strokes)
-assess using NIHSS scale (high score = worse stroke is)
-give fibrinolytic therapy if ischemic stroke
-surgical intervention if indicated to remove clots)
- 12 lead EKG & labs
-Door to needle time is typically 1 hour

284
Q

How do you treat a stroke?

A

-multi drug approach
-supportive therapy
-pharmacological and surgical interventions

285
Q

how do you diagnose a stroke?

A

CT scan w/o contrast bc it takes longer with contrast and will need an IV

**hemorrhagic will have a massive white blob on screen indicating bleeding while an ischemic will not show that

286
Q

what acute care should be done for an ischemic stroke?

A

-prevent further damage and reduce disabilities
-gather history (onset and symptoms)
-go to stroke center if possible
-treat hypertension (SBP > 220 and DBP > 120)
** Increased BP constricts vesels bc brain is not getting blood flow** autoregulation which is not good for this time
-glycemic control

287
Q

What surgical interventions can be done for ischemic stroke?

A

surgical/endovascular therapy such as an angioplasty

288
Q

What acute care can be done for a hemorrhagic stroke?

A

-drug therapy
-NO anticoagulants or platelet inhibitor because there are no clots!
-main drug: antihypertensives
-normal - high BP (SBP less < 160)
-seizure precautions in acute phase

289
Q

what term means any process that stops bleeding?

A

hemostasis

290
Q

what is an example of mechanical hemostasis?

A

compression at bleeding site

291
Q

what is an example of surgical hemostasis?

A

clamping or cauterization

292
Q

what term refers to hemostasis occurs due to physiologic clotting of blood?

A

coagulation

293
Q

What is the process of hemostasis?

A

-initial injury
-vasospasm (spasming to control blood loss)
-platelet plug formation
-coagulation

294
Q

A tear in blood vessel is referred to as?

A

an injury

295
Q

if there is an a leakage in a blood vessel, what is the hemostatic response?

A

vasoconstrict

296
Q

what is the technical term for blood clot?

A

thrombus

297
Q

if platelet plug is not enough, what steps in to strengthen the plug?

A

coagulation

298
Q

what is the result of the coagulation pathway?

A

large clot forming substance fibrin

299
Q

what are the two pathways for coagulation cascade?

A

extrinsic and intrinsic

300
Q

What type of pathway are blood vessels damaged by penetration from the outside, thromboplastin is released and activates factor X?

A

extrinsic pathway

301
Q

which pahway is a clotting response to trauma/internal damage inside the blood vessels, components in blood are present in inactive forms, and are activated when clotting factors come in contact with collage on inside of damaged blood vessels?

A

intrinsic pathway

302
Q

what does thrombin do?

A

converts fibrinogen to fibrin

303
Q

What are the functions for clot retraction and dissolution?

A

-counter mechanism to blood clotting
-keeps blood in fluid state
-antithrombin activity
-vessel and platelet activity
-fibrinolysis

304
Q

What does antithrombin do?

A

antagonizes thrombin (prevents clotting)

305
Q

what reverses the clotting process?

A

fibrinolysis

306
Q

What starts the fibrinolytic system?

A

-activation of plasminogen
-fibrin binds to plasminogen and converts it to plasmin

307
Q

what activates the fibrinolytic system?

A

-tissue plasminogen activator or thrombin

308
Q

what is plamsin?

A

an enzymatic protein that breaks down thrombus

309
Q

what is the pharmacological treatment for a stroke?

A

Anticoagulants

310
Q

How can anticoagulants be used?

A

-as a preventative (TIA, thrombus, embolus)
-used to reverse or maintain hemostasis

311
Q

what are characteristics of anticoagulants?

A

-all work in clotting cascade
-prevent formation of a clot by inhibiting clotting factors
-no directeffect on clot already formed
-prevents further thrombosis by lowering blood coagulability
-prevents extension of established blood clot

312
Q

what are 4 contraindications for anticoagulants?

A

-drug allergy
-active bleeding
-high risk for bleeding
-risk vs benefit

313
Q

what is an example of an anticoagulant?

A

heparin

314
Q

What are characteristics of heparin?

A

-administered through IV or SQ
-weight based
-inds to antuthrombin III
-turns off 3 major clotting factors
-turns off coagulation pathway
-cannot lyse clots
Two types: LMWH or unfractioned

315
Q

which type of heparin is a large molecule, will require frequent lab monitoring, is activated through partial thromboplatin time, is continuous IV, and weight based?

A

unfractioned heparin

316
Q

which type of heparin is a small structure, synthetic, has a more predictable outcome, no lab monitoring is required, is bridge therapy, can only administer as injections and is known as enoxaprin?

A

LMWH

317
Q

How is warfarin administered?

A

orally

318
Q

what is warfarins MOA?

A

-inhibits vtiamin K synthesis
-inhibits production of certain clotting factors

319
Q

what do you monitor on warfarin?

A

lab values only and drug interactions!

320
Q

what can you educate a patient about on warfarin?

A

-foods high in vitamin K can decrease ability to prevent clot
-be consistent in diet
-herbal products

321
Q

what are 4 adverse effects of anticoagulants?

A

-bleeding
-heparin induced thrombocytopenia**
-localized or systemic adverse effects
-depends on underlying illness

322
Q

all toxic effects of anticoagulants result in what?

A

hemorrhagic in nature

323
Q

what are signs and symptoms of anticoagulant toxicity and overdose?

A

-hematuria
-melena
-petechia
-ecchmyoses
-gum/mucus membrane bleeding (stop drug immediately

324
Q

what are toxicity managements for heparin?

A

-stopping drug may be enough
-if overdose is significant -> protamine sulfate is an antidote

325
Q

what is toxicity management for warfarin?

A

-discontinue medication FIRST
-toxicity inactivates vitamin K dependent clotting factors
-may take 36 hours to resynthesize clotting factors to reverse warfarin
-may need tranfusions of plasma, platelets
-administer antidote if needed (vitamin K orally or IV)

326
Q

What to measure with anticoagulants?

A

-measure clotting time (high number indicates long time to clot)

HEPARIN -> measure activated partial thromboplastin time

COUMADIN-> prothrombin time and international normalized ratio

327
Q

what is normal aPTT/PTT values? Heparin

A

normal 25-35 seconds
target on heparin: 60-88 seconds for heparin

328
Q

what are normal PT values? Coumadin

A

normal 11-13 seconds
target on coumadin: 18 seconds

329
Q

what are normal INR values?

A

normal 2-3
target level on warfarin: 2.5-3.5

330
Q

What are functions of antiplatelets?

A

-prevents clot formation
-prevents platelet adhesion at site of blood vessel injury
-occurs BEFORE clotting cascade

331
Q

what is a stimulator for platelet adhesion?

A

collagen

332
Q

what is MOA for antiplatelets?

A

-affects cyclooxygenase pathways
-final enzymatic pathway that operates within platelets & on cell walls

333
Q

what are the indications for antiplatelets?

A

-depends on drug
-aspirin -> stroke prevention
-clopidogrel -> reduces risk of thrombotic stroke & TIA

334
Q

What does aspirin inhibit?

A

-inhibits clooxygenase in platelet
-inhibits enzyme so cannot regenerate which prevents formation of thromboxane (thromboxane causes vessels to constrict and platelets to clot

335
Q

what are indications for aspirin?

A

stroke pervention

336
Q

what are doses and route for aspirin?

A

dose: 81-325 mg
Route: oral and rectal

337
Q

what are contraindications for aspirin?

A

-thrombocytopenia
-bleeding
-GI bleeding

338
Q

What are characteristics of clopidogrel?

A

inhibits activation of fibrinogen attaching to platelet receptor

339
Q

what are the indications for clopidogrel?

A

-reduces risk of thrombotic stroke
-TIA prophylaxis
-prevention of thrombosis

340
Q

what are contraindications for clopidogrel?

A

-thrombocytopenia
-bleeding
-GI bleeding

341
Q

what are adverse effects of clopidogrel?

A

-chest pain
-edema
-flu-like symptoms
-abdominal pain
-epistaxis
-rash
-pruritis

342
Q

how can you administer clopidogrel?

A

oral only

343
Q

What are nursing considerations for anticoagulants & antiplatelets?

A

During/after administration:
-assess skin, oral mucous membranes, gums, urine, stool
assess for bleeding after brushing, nosebleeds, shaving

Monitor labs:
-CBC
-Platelet count
-Clotting studies
-liver function tests

assess LMWH injection site

344
Q

what is a deadly combo?

A

heparin with LMWH

Fall 22 (2 decks)

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