{"id":110951,"date":"2023-07-28T16:55:05","date_gmt":"2023-07-28T16:55:05","guid":{"rendered":"https:\/\/learnexams.com\/blog\/?p=110951"},"modified":"2023-07-28T16:55:09","modified_gmt":"2023-07-28T16:55:09","slug":"nrnp-6560-final-exam-latest-2023-2024-version-2-exam-100-questions-and-correct-answers-verified-answerswalden-university","status":"publish","type":"post","link":"https:\/\/www.learnexams.com\/blog\/2023\/07\/28\/nrnp-6560-final-exam-latest-2023-2024-version-2-exam-100-questions-and-correct-answers-verified-answerswalden-university\/","title":{"rendered":"NRNP 6560 FINAL EXAM LATEST 2023-2024 VERSION 2 EXAM 100 QUESTIONS AND CORRECT ANSWERS (VERIFIED ANSWERS)WALDEN UNIVERSITY"},"content":{"rendered":"\n

EPAP<\/a><\/p>\n\n\n\n

expiratory positive airway pressure<\/a><\/p>\n\n\n\n

CPAP<\/a><\/p>\n\n\n\n

continuous positive airway pressure

a treatment for apnea involving keeping a patient’s airways open using air pressure delivered via a face mask

IPAP=EPAP<\/a><\/p>\n\n\n\n

ABCDE<\/a><\/p>\n\n\n\n

asymmetry, border, color, diameter >6mm, evolving<\/a><\/p>\n\n\n\n

skin eruptions or exanthema 3 groups<\/a><\/p>\n\n\n\n

1. Macular and maculopapular lesions
2. vesicular or bullous lesions
3. pustular, petechial, or purpuric lesions<\/a><\/p>\n\n\n\n

secondary changes of skin lesions<\/a><\/p>\n\n\n\n

comedones, crusting, excoriation, lichenification, scales, scarring, telangiectasia<\/a><\/p>\n\n\n\n

acne<\/a><\/p>\n\n\n\n

inflammatory disease of the skin involving the sebaceous glands and hair follicles

causes: corticosteriods, isoniazid<\/a><\/p>\n\n\n\n

bullous lesions<\/a><\/p>\n\n\n\n

Caused by exfoliative toxins A and B
Have the appearance of wrinkled tissue paper
Lead to widespread desquamation of the skin
Patients are left vulnerable to secondary bacterial infections

causes: barbiturate overdose, penicillamine, sulfonamides<\/a><\/p>\n\n\n\n

eczematous dermatitis<\/a><\/p>\n\n\n\n

most common inflammatory skin disorder, several forms including irritant contact dermatitis allergic contact dermatitis and atopic dermatitis

causes: abx, methyldopa, phenylbutazone, sulfonamides<\/a><\/p>\n\n\n\n

erythemia multiforme<\/a><\/p>\n\n\n\n

Hypersensitivity reaction characterized by targetoid rash and bullae; *HSV and mycoplasma infections; EM with oral mucosa and fever is steven-johnson syndrome

causes: barbiturates, hydantois, penicillin, salicylates, sulfonamides, sulfonylureas<\/a><\/p>\n\n\n\n

erythema nodosum<\/a><\/p>\n\n\n\n

inflammation of subcutaneous tissues resulting in tender, erythematous nodules; may be an abnormal immune response to a systemic disease, an infection, or a drug

causes: contraceptives, sulfonamides<\/a><\/p>\n\n\n\n

exfoliative dermatitis<\/a><\/p>\n\n\n\n

a condition in which there is widespread scaling of the skin, often with pruritus, erythroderma, and hair loss

causes: allopurinal, gold, indomethacin, phenylbutazone<\/a><\/p>\n\n\n\n

lichenoid eruption<\/a><\/p>\n\n\n\n

violaceous to purple, polygonal lesions that resemble those seen in lichen planus

Causes: cholorquine, chlorpropamide, mepacrine, quinidine, quinine, thiazides<\/a><\/p>\n\n\n\n

photosensitivity<\/a><\/p>\n\n\n\n

increased reaction of the skin to exposure to sunlight

causes: amiodarone, nalidixic acid, sulfonamides, tetracycline<\/a><\/p>\n\n\n\n

pigmentation<\/a><\/p>\n\n\n\n

coloration caused by deposit, or lack, of colored material in the tissues

causes: chloroquine, heavy metals, mepacrine<\/a><\/p>\n\n\n\n

Psoriasiform rash<\/a><\/p>\n\n\n\n

causes: gold, methyldopa<\/a><\/p>\n\n\n\n

purpura<\/a><\/p>\n\n\n\n

multiple pinpoint hemorrhages and accumulation of blood under the skin

causes: cytotoxic drugs, meprobamate, quinidine, quinine<\/a><\/p>\n\n\n\n

systemic lupus erythematosus (SLE)<\/a><\/p>\n\n\n\n

chronic autoimmune inflammatory disease of collagen in skin, joints, and internal organs

causes: hydralazine, isoniazid, penicillamine, procainamide<\/a><\/p>\n\n\n\n

urticaria<\/a><\/p>\n\n\n\n

allergic reaction of the skin characterized by the eruption of pale red, elevated patches called wheals or hives

causes: aspirin, imipramine, penicillin, serum, toxoid, vaccines<\/a><\/p>\n\n\n\n

Bulla<\/a><\/p>\n\n\n\n

a large blister that is usually more than 0.5 cm in diameter<\/a><\/p>\n\n\n\n

Comedones<\/a><\/p>\n\n\n\n

plug of keratin and sebum wedged in a dilated pilosebaceous<\/a><\/p>\n\n\n\n

crust<\/a><\/p>\n\n\n\n

accumulated dried exudate<\/a><\/p>\n\n\n\n

Excoriation<\/a><\/p>\n\n\n\n

a superficial loss of skin, e.g., by scratching<\/a><\/p>\n\n\n\n

lichenification<\/a><\/p>\n\n\n\n

area of increased epidermal thickening with exaggerated skin markings, caused by constant rubbing (atopic eczema)<\/a><\/p>\n\n\n\n

keloid<\/a><\/p>\n\n\n\n

a sharply elevated, irregularly shaped, progressively enlarging scar due to excessive collagen formation in the dermis during connective tissue<\/a><\/p>\n\n\n\n

macule<\/a><\/p>\n\n\n\n

flat, colored spot on the skin<\/a><\/p>\n\n\n\n

nodule<\/a><\/p>\n\n\n\n

circumscribed, palpable area of the skin that is >0.5 cm in diameter and appears in part or wholly within the dermis<\/a><\/p>\n\n\n\n

papule<\/a><\/p>\n\n\n\n

A circumscribed, solid elevation of skin < 1cm in diameter, with no visible fluid<\/a><\/p>\n\n\n\n

patch<\/a><\/p>\n\n\n\n

large macule, >2cm in diameter<\/a><\/p>\n\n\n\n

plaque<\/a><\/p>\n\n\n\n

circumscribed, disk-shaped elevated area of the skin >1cm diameter<\/a><\/p>\n\n\n\n

purpura<\/a><\/p>\n\n\n\n

multiple pinpoint hemorrhages and accumulation of blood under the skin<\/a><\/p>\n\n\n\n

pustule<\/a><\/p>\n\n\n\n

raised spot on the skin containing pus<\/a><\/p>\n\n\n\n

scales<\/a><\/p>\n\n\n\n

flakes or dry patches made up of excess dead epidermal cells<\/a><\/p>\n\n\n\n

scar<\/a><\/p>\n\n\n\n

area of fibrous tissue that replaces the lost epidermis<\/a><\/p>\n\n\n\n

stria<\/a><\/p>\n\n\n\n

streak-like, linear, atrophic, pink, purple, or white lesion caused by stretching of the skin<\/a><\/p>\n\n\n\n

Telangiectasia<\/a><\/p>\n\n\n\n

skin lesion due to permanently enlarged and dilated blood vessels that are visible<\/a><\/p>\n\n\n\n

ulcer<\/a><\/p>\n\n\n\n

loss of epidermis and part or whole of the dermis<\/a><\/p>\n\n\n\n

vesicle<\/a><\/p>\n\n\n\n

visible accumulation of fluid beneath the epidermis (<0.5 cm in diameter)<\/a><\/p>\n\n\n\n

weal<\/a><\/p>\n\n\n\n

circumscribed, elevated area of cutaneous edema<\/a><\/p>\n\n\n\n

Dermatitis Medicamentosa<\/a><\/p>\n\n\n\n

Hypersensitivity reaction to a drug.

onset is abrupt, widespread, and symmetric erythematous eruption<\/a><\/p>\n\n\n\n

type 1: immediate-type immunologic reaction<\/a><\/p>\n\n\n\n

IgE mediated
manifested by urticaria and angioedema of skin or mucosa, edema of other organ, and fall in BP (anaphylatic shock)<\/a><\/p>\n\n\n\n

Type 2: Cytotoxic reaction<\/a><\/p>\n\n\n\n

drug or causative agent causes lysis of cells, such as platelets or leukocytes, or may, by combo with another drug, produce antibodies (immune complexes) that causes lysis or phagocytosis<\/a><\/p>\n\n\n\n

type 3: serum sickness, drug-induced vasculitis<\/a><\/p>\n\n\n\n

IgG and IgM antibodies are formed against a drug
manifested by vasculitis, urticaria-like lesions, arthritis, nephritis, alveolitis, hemolytic anemia, thrombocytopenia, and agranulocytosis<\/a><\/p>\n\n\n\n

type 4: morbilliform (exanthematous) reaction<\/a><\/p>\n\n\n\n

cell-mediated immune reaction
sensitized lymphocytes react with the drug, releasing cytokines, resulting in cutaneous inflammatory response
Drug rash with eosinophilia syndrome (DRESS)
– present as hepatits, eosinophilia, pneumonia, lymphadenopathy, and nephritis
-symptoms may last 2-6 weeks after beginning the medication, most commonly associated with anticonvulsants, sulfonamines, beta blockers, antimicrobials, antidepressants, and allopurinal medication<\/p>\n\n\n\n

m\/c cause of urticaria and maculopapular allergic skin reaction<\/a><\/p>\n\n\n\n

penicillin-based medicaiton and trimethoprim-sulfamethoxazole<\/a><\/p>\n\n\n\n

penicillin-sensitive patients<\/a><\/p>\n\n\n\n

cephalosporins are assocaited with reaction in 5-15%
carbapenems 15-30%<\/a><\/p>\n\n\n\n

red man syndrome<\/a><\/p>\n\n\n\n

not an allergic reaction, associated with vanc often responds to slowing of infusion rate and administration of antihistamine<\/a><\/p>\n\n\n\n

ACE-I<\/a><\/p>\n\n\n\n

chronic cough and angioedema<\/a><\/p>\n\n\n\n

Beta Blockers<\/a><\/p>\n\n\n\n

precipitate asthma and should not be given to patients at high risk of anaphylaxis, BB may block the action of epi<\/a><\/p>\n\n\n\n

anticonvulsants and sulfonamines<\/a><\/p>\n\n\n\n

m\/c cause of toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS)<\/a><\/p>\n\n\n\n

radiocontrast media and opiois<\/a><\/p>\n\n\n\n

stimulate mast cell histamine release through a non-IgE-mediated mechanism<\/a><\/p>\n\n\n\n

lab and diagnostic for drug eruption<\/a><\/p>\n\n\n\n

LFT as a baseline
skin bx
allergy skin test
patch and photo test
challenge dosing<\/a><\/p>\n\n\n\n

Management of drug eruption<\/a><\/p>\n\n\n\n

withdrawal of drug
epi
antihistamines<\/a><\/p>\n\n\n\n

when does SJS or TEN usually occur<\/a><\/p>\n\n\n\n

during first 8 weeks of starting a new medicaiton<\/a><\/p>\n\n\n\n

m\/c medications to cause SJS or TEN<\/a><\/p>\n\n\n\n

allopurinol, lamotrigine, sulfonamines, sulfasalazine, nevirapine, and oxicams<\/a><\/p>\n\n\n\n

SCORTEN score<\/a><\/p>\n\n\n\n

prognosis of SJS\/TEN
seven variables with max score of 7
age 40 or greater = 1 pt
malignancy = 1 pt
body surface area detached greater than or equal to 10% = 1 pt
tachycardia greater or equal to 120 = 1 pt
serum urea >10 = 1 pt
serum glucose >14 = 1 pt
serum bicarb <20 = 1 pt<\/a><\/p>\n\n\n\n

Treatment of SJS\/TEN<\/a><\/p>\n\n\n\n

discontinue agent asap
treat them as a burn patient – thermoregulation and electrolyte management
immunomodulation: cyclosporine, ATN agent, IVIG, plasmapheresis<\/a><\/p>\n\n\n\n

long term affects of SJS\/TEN<\/a><\/p>\n\n\n\n

eye disorders
vulvovaginal and urinary sequelae<\/a><\/p>\n\n\n\n

causative agent of cellulitis<\/a><\/p>\n\n\n\n

gram + cocci
group A B-hemolytic streptococci and staphylcococcus aureus<\/a><\/p>\n\n\n\n

risk factors for cellulitis<\/a><\/p>\n\n\n\n

prior trauma, underlying skin lesion, DM, pedal edema, venous and lymphatic compromise, IV drug use<\/a><\/p>\n\n\n\n

cellulitis of the L.E. of the elderly is often complicated by?<\/a><\/p>\n\n\n\n

DVT<\/a><\/p>\n\n\n\n

Gram negative rods causing cellulitis<\/a><\/p>\n\n\n\n

e. coli<\/a><\/p>\n\n\n\n

gram negative bacilli causing cellulitis in neutropenic and immunosuppressed patient<\/a><\/p>\n\n\n\n

serratia, proteus, enterobacter, and fungi (cryptococcus neoformans)<\/a><\/p>\n\n\n\n

Facial or upper extremity cellulitis<\/a><\/p>\n\n\n\n

H. influenzae<\/a><\/p>\n\n\n\n

patient with DM, cellulitis pathogens<\/a><\/p>\n\n\n\n

streptococci and staphylococci<\/a><\/p>\n\n\n\n

Erysipelothrix rhusiopathiae<\/a><\/p>\n\n\n\n

A cause of disease in swine, turkeys, and marine mammals, including diamond skin disease.<\/a><\/p>\n\n\n\n

Aeromonas<\/a><\/p>\n\n\n\n

gram negative bacillus; freshwater exposure<\/a><\/p>\n\n\n\n

vibrio<\/a><\/p>\n\n\n\n

salt water exposure<\/a><\/p>\n\n\n\n

confirm the diagnosis of cellulitis<\/a><\/p>\n\n\n\n

lymph node enlargement and lymphatic streaking (lymphangitis)<\/a><\/p>\n\n\n\n

differential diagnosis of cellulitis<\/a><\/p>\n\n\n\n

DVT and necrotizing fasciitis<\/a><\/p>\n\n\n\n

necrotizing fasciitis<\/a><\/p>\n\n\n\n

very toxic appearing, bullae, crepitus, anesthesia of the involed skin, overlying skin necrosis, evidence of rhabdomyolysis (elevated creatinine phosphokinase), disseminated intravascular coagulation<\/a><\/p>\n\n\n\n

management of cellulitis<\/a><\/p>\n\n\n\n

abx coverage for both streptococci and staphylococci
outpatient duration 5 days
Mild cellulitis (nonpurulent)
– penicillin V-K
– cephalexin
– Dicloxacillin
– allergy to penicillin: clindamycin or doxy<\/a><\/p>\n\n\n\n

CA-MRSA Cellulitis Treatment<\/a><\/p>\n\n\n\n

Doxy
TMP-SMX
Clindamycin
linezolid<\/a><\/p>\n\n\n\n

MSSA cellulitis treatment<\/a><\/p>\n\n\n\n

Dicloxacillin
cephalexin
TMP-SMX DS<\/a><\/p>\n\n\n\n

inpatient therapy for cellulitis<\/a><\/p>\n\n\n\n

nafcillin or oxacillin
cefazolin<\/a><\/p>\n\n\n\n

MRSA cellulitis inpatient therapy<\/a><\/p>\n\n\n\n

Vanc
linezolid
deptomycin
ceftaroline
treat till afebrile then outpatient treatment
– linezolid
– clindamycin
– TMP-SMX DS<\/a><\/p>\n\n\n\n

Immunocompromised Cellulitis treatment<\/a><\/p>\n\n\n\n

hospitalization and empiric abx
Vanc + antipseidomonal abx

– cefepime
– zosyn
– imipenem-cilastatin
– meropenem<\/a><\/p>\n\n\n\n

Erysipelothrix cellulitis treatment<\/a><\/p>\n\n\n\n

penicillin, cephalexin, clindamycin<\/a><\/p>\n\n\n\n

Vibrio species cellulitis treatment<\/a><\/p>\n\n\n\n

doxy + ceftriaxone<\/a><\/p>\n\n\n\n

aeromonas hydrophila cellulitis treatment<\/a><\/p>\n\n\n\n

doxy + ceftriaxone or cipro<\/a><\/p>\n\n\n\n

Tinea (skin infection) treatment<\/a><\/p>\n\n\n\n

terbinafine hydrochloride 1%
butenafine 1%<\/a><\/p>\n\n\n\n

recurrence cellulitis caused by MSSA treatment<\/a><\/p>\n\n\n\n

long-term low dose Penicillin G<\/a><\/p>\n\n\n\n

recurrence cellulitis caused by MRSA treatment<\/a><\/p>\n\n\n\n

long-term low dose clindamycin<\/a><\/p>\n\n\n\n

herpes zoster (shingles)<\/a><\/p>\n\n\n\n

a disease that involves a painful, blistering rash accompanied by headache, fever, and a general feeling of unwellness<\/a><\/p>\n\n\n\n

herpes zoster lab\/diagnostics<\/a><\/p>\n\n\n\n

polymerase chain reaction testing, Tzanck smear<\/a><\/p>\n\n\n\n

ophthalmic zoster<\/a><\/p>\n\n\n\n

5th cranial nerve involvement: tip of the nose<\/strong> (emergency)<\/a><\/p>\n\n\n\n

50-50-50 rule<\/a><\/p>\n\n\n\n

guide for antiviral therapy
< 50 hrs since onset of lesions
> 50 years
> 50 lesions<\/a><\/p>\n\n\n\n

antiviral for herpes zoster treatment<\/a><\/p>\n\n\n\n

acyclovir
valacyclovir<\/a><\/p>\n\n\n\n

acyclovir-resistance varicella-zoster virus treatment<\/a><\/p>\n\n\n\n

foscarnet<\/a><\/p>\n\n\n\n

adjunct therapy for Herpes Zoster treatment<\/a><\/p>\n\n\n\n

tylenol, cold compress, tramadol, opioids, oral corticosteriods, hydroxyzine (pruritus)<\/a><\/p>\n\n\n\n

PHN treatment<\/a><\/p>\n\n\n\n

Lidocaine or capsaicin skin patch
Gabapentin (Gralise, Horizant, Neurontin) and pregabalin (Lyrica)
Antidepressants \u2014 such as nortriptyline (Pamelor), amitriptyline, duloxetine (Cymbalta) and venlafaxine (Effexor XR) can be effective<\/a><\/p>\n\n\n\n

Prevention of herpes zoster<\/a><\/p>\n\n\n\n

Zoster vaccine indicated in all patients above 60
-Zoster vaccine live
-recombinant zoster vaccine

should not be administered to immunocompromised patient or pregnant women<\/a><\/p>\n\n\n\n

m\/c type of Skin cancer in the US<\/a><\/p>\n\n\n\n

basal cell carcinoma<\/a><\/p>\n\n\n\n

basal cell carcinoma (BCC)<\/a><\/p>\n\n\n\n

malignant tumor of the basal layer of the epidermis;
papule or nodule with a central scab or eroded area. Nodule has a waxy “pearly” appearance<\/a><\/p>\n\n\n\n

squamous cell carcinoma<\/a><\/p>\n\n\n\n

nonhealing ulcer or wart-like nodule
found on skin-exposed areas in fair-skin people
may develop from actinic keratosis
malignant tumor or epithelial keratinocytes
– capacity to metastize
– usually the result of exogenous carcinogens<\/a><\/p>\n\n\n\n

BCC predisposing factors<\/a><\/p>\n\n\n\n

sun exposure
arsenic exposure
m\/c on face and neck<\/a><\/p>\n\n\n\n

SCC predisposing factors<\/a><\/p>\n\n\n\n

M-F ration 2:1
SCC of lip, temple, ear, oral cavity, tongue, and genitalia have a higher rate of metastasis
smokers have increased risk for lip involvement
legs of females
HPV<\/a><\/p>\n\n\n\n

BCC characteristics<\/a><\/p>\n\n\n\n

noldules, papules, non-healing ulcers, or scabbed lesions
waxy, pearly nodules with telangiectatic vessels, or as visual or scaly plaques
borders are translucent, elevated, and shiny with fine telangiectasia<\/a><\/p>\n\n\n\n

SCC characteristics<\/a><\/p>\n\n\n\n

scaly, red, hard nodular, crusty, does not heal
usually asymptomatic
firm, skin-colored to reddish-brown nodules on damaged skin
may arise out of actinic keratosis
central ulceration
scaling and crusting
heaped-up edges of lesions appear fleshy rather than clear
lesion on the lower lip appear as firm, whitish macules<\/p>\n\n\n\n

lab\/diagnostics for BCC and SCC<\/a><\/p>\n\n\n\n

bx, shaved or punch bx<\/a><\/p>\n\n\n\n

BCC and SCC management<\/a><\/p>\n\n\n\n

dermatologist referral
bx
curettage and electrodesiccation of BCC lesion <1cm in diameter and in nonfacial area

BCC follow up – annually for 5 years
SCC – every 3 months with close exam of lymph nodes for 1 year then twice a year after that<\/a><\/p>\n\n\n\n

Melanoma<\/a><\/p>\n\n\n\n

dark, pigmentation; may be flat or raised irregular borders; may be red, black, or bluish in color; size >6 mm
develop from benign melanocytic cells<\/a><\/p>\n\n\n\n

Melanoma predisposing factors<\/a><\/p>\n\n\n\n

leading cause of death from skin cancer
preventative measure – avoidance of blistering solar radiation and use of sunscreen
fair skin, freckles, blonde, blue eyes<\/a><\/p>\n\n\n\n

melanoma characterisics<\/a><\/p>\n\n\n\n

bleeding and ulceration are ominous signs
scaling
texture change and irregular border
size change >6mm
development of inflammation
color change
itching<\/a><\/p>\n\n\n\n

Six Signs of Malignant Melanoma (ABCDEEF<\/a><\/p>\n\n\n\n

Assymetry, Border, Color, Diameter, Elevation, Enlargement, Friend<\/a><\/p>\n\n\n\n

primary malignant melanomas<\/a><\/p>\n\n\n\n

superficial spreading – m\/c, caucasians
lentigo maligna
nodular malignant
acral lentiginous – palms, soles, and nail beds, more common in darkly pigmented people
malignant melanoma on mucous membrane
amelanotic (nonpigmented)
arising from blue nevi
congenital and giant nevocytic nevi<\/a><\/p>\n\n\n\n

labs\/diagnostics for melanoma<\/a><\/p>\n\n\n\n

surgical bx
should never be curetted, electrodesiccated, or shaved
sentinel lymph node bx for staging<\/a><\/p>\n\n\n\n

Staging of melanoma<\/a><\/p>\n\n\n\n

Stage I-II = Tumor (depth)
Stage III = Node involvement
Stage IV = Metastases<\/a><\/p>\n\n\n\n

management of melanomas<\/a><\/p>\n\n\n\n

dermatologist referral
follow up 3-6 months with skin exam
self exam skin weekly<\/a><\/p>\n\n\n\n

FAST<\/a><\/p>\n\n\n\n

face drooping, arm weakness, speech difficulty, Time to call 911<\/a><\/p>\n\n\n\n

LAPSS<\/a><\/p>\n\n\n\n

Los Angeles Prehospital Stroke Screen<\/a><\/p>\n\n\n\n

VAN assessment<\/a><\/p>\n\n\n\n

Vision, aphasia, neglect<\/a><\/p>\n\n\n\n

RACE<\/a><\/p>\n\n\n\n

Rapid arterial oCclusion Evaluation<\/a><\/p>\n\n\n\n

Lacunar stroke<\/a><\/p>\n\n\n\n

small subcortical infarcts <15mm diameter
basal ganglia, internal capsule, thalamus, corona radiata, and pons<\/a><\/p>\n\n\n\n

sxs of lacunar stroke<\/a><\/p>\n\n\n\n

hemiparesis or heiplegia
dysarthria and dysphagia<\/a><\/p>\n\n\n\n

Ataxic hemiparesis<\/a><\/p>\n\n\n\n

lacunar stroke of the anterior limb of internal capsule or PONS base

weakness and ataxia on ipsi side of body, usually leg weakness more than arm<\/a><\/p>\n\n\n\n

Stoke BP control<\/a><\/p>\n\n\n\n

lowering BP initially by 15% during first 24 hr<\/a><\/p>\n\n\n\n

tPA BP limits<\/a><\/p>\n\n\n\n

prior SBP <185 DBP <110
during and after <180 and DBP <105<\/a><\/p>\n\n\n\n

Cryptogenic stroke<\/a><\/p>\n\n\n\n

an ischemic stroke whose cause cannot be attributed to a specific source of embolism, thrombosis, or small artery disease even with extensive medical testing<\/a><\/p>\n\n\n\n

hemorrhagic stroke<\/a><\/p>\n\n\n\n

occurs when a blood vessel in the brain leaks or ruptures; also known as a bleed<\/a><\/p>\n\n\n\n

hemorrhagic stroke symptoms<\/a><\/p>\n\n\n\n

Impaired LOC, headache, nausea\/vomiting, mobility, speech patterns, one sided weakness, blood pressure, respiratory status, pulse rate<\/a><\/p>\n\n\n\n

risk factors for hemorrhagic stroke<\/a><\/p>\n\n\n\n

HTN, cerebral amyloid angiopathy, anticoag or thrombolytic use, street drugs, heavy alcohol use, hematologic disorders, OTC stimulants\/energy drinks<\/a><\/p>\n\n\n\n

leading cause of ICH in >60 y.o.<\/a><\/p>\n\n\n\n

cerebral amyloid angiopathy<\/a><\/p>\n\n\n\n

subarachnoid hemorrhage<\/a><\/p>\n\n\n\n

“Worst headache of my life”<\/a><\/p>\n\n\n\n

Hunt and Hess Scale<\/a><\/p>\n\n\n\n

predictor of mortality presenting with subarachnoid hemorrhage

1- no symptoms
2- CN palsy, HA, nuchal rigidity
3- mild focal deficit, lethargy, confusion
4- stupor, moderate\/severe hemiparesis
5- deep coma<\/a><\/p>\n\n\n\n

Fisher Grade<\/a><\/p>\n\n\n\n

Predicts vasospasm risk d\/t SAH based on CT scan
1 – no hemorrhage
4 – SAH with IPH and IVH<\/a><\/p>\n\n\n\n

intracerebral hemorrhage<\/a><\/p>\n\n\n\n

AIS and ICH<\/a><\/p>\n\n\n\n

basal ganglia hemorrhage<\/a><\/p>\n\n\n\n

Contralateral hemiparesis and hemisensory loss
ipsilateral Homonymous hemianopsia
ipsilateral Gaze palsy
decreased LOC<\/a><\/p>\n\n\n\n

Thalamic hemorrhage<\/a><\/p>\n\n\n\n

downward deviation of the eyes
pupils pinpoint with positive reaction
coma
flaccid quadriplegia<\/a><\/p>\n\n\n\n

Cerebellar hemorrhage<\/a><\/p>\n\n\n\n

NO HEMIPARESIS
facial weakness, ataxia, nystagmus, occipital headache, neck stiffness
ipsilateral horizontal conjugate gaze paresis
pupils PERRLA
inability to walk
vertigo and dysarthria<\/a><\/p>\n\n\n\n

formula for estimating ICH hematoma volume<\/a><\/p>\n\n\n\n

ABC\/2
(AxBxC)\/2
A=longest axis
B=longest axis perpendicular to A
C=# of slices x slice thickness<\/a><\/p>\n\n\n\n

management of ICH\/SAH<\/a><\/p>\n\n\n\n

avoid ketamine
succinylcholine can cause transient ICP increase
rocuronium is a neuromuscular blocking agent
BP control SBP <140
Cerebral perfusion pressure (MAP-ICP)
correction of coagulopathy (if INR >4)
check INR q 3-6 hr for first 24 hr
External ventricular drain placement (GCS <9)
goal ICP <20 and a CPP >60
strict bed rest
cardiac monitoring
no straining
seizures
cerebral edema (mannitol)
check serum osmolality and Na+ q8hr<\/p>\n\n\n\n

management of aneurysm<\/a><\/p>\n\n\n\n

surgical clipping or endovascular coiling ASAP<\/a><\/p>\n\n\n\n

cerebral vasospasm<\/a><\/p>\n\n\n\n

can occur before or after aneurism clipping and coiling; administer calcium channel blocker nimodipine (Nimotop);<\/a><\/p>\n\n\n\n

re-bleeding<\/a><\/p>\n\n\n\n

occurs between 2-19 days after initial rupture
repeat CT scan and occasionally repeat LP is needed to confirm re-bleed<\/a><\/p>\n\n\n\n

Cerebral salt wasting<\/a><\/p>\n\n\n\n

hyponatremia, excessive secretion of natriuretic peptides
crystalloid fluid replacement
3% saline solution to correct hyponatremia 30-60 ml\/hr
q8 hr serum osmolality and Na+
fludrocortisone<\/a><\/p>\n\n\n\n

m\/c medical complication in aneurysmal SAH<\/a><\/p>\n\n\n\n

fever<\/a><\/p>\n\n\n\n

blast injury<\/a><\/p>\n\n\n\n

hippocampus and brain stem<\/a><\/p>\n\n\n\n

prehospital\/emergancy department treatment for TBI<\/a><\/p>\n\n\n\n

ACLS
spinal immobilization
GCS <8 intubation
avoid hypoxemia o2 sat >90 PaO2 >60
avoid hyperventilation: goal ETCO2 or PaCO2 35-45<\/a><\/p>\n\n\n\n

avoid hyperventilation in TBI unless:<\/a><\/p>\n\n\n\n

herniation symptoms are present of if measured ICP is severely high<\/a><\/p>\n\n\n\n

AVPU<\/a><\/p>\n\n\n\n

Awake, responsive to voice, responsive to pain, unresponsive<\/a><\/p>\n\n\n\n

Decorticate posturing<\/a><\/p>\n\n\n\n

characterized by upper extremities flexed at the elbows and held closely to the body and lower extremities that are externally rotated and extended. occurs when the brainstem is not inhibited by the motor function of the cerebral cortex.<\/a><\/p>\n\n\n\n

Decerebrate posturing<\/a><\/p>\n\n\n\n

posturing in which the neck is extended with jaw clenched; arms are pronated, extended, and close to the sides; legs are extended straight out; more ominous sign of brain stem damage. Most Severe.<\/a><\/p>\n\n\n\n

lab studies for TBI<\/a><\/p>\n\n\n\n

toxicology drug and alcohol, CBC, chemistry, coagulation<\/a><\/p>\n\n\n\n

primary head injury<\/a><\/p>\n\n\n\n

involves features that occur at the time of trauma, including fractured skull, contusions, intracranial hematoma, and diffuse injury. Secondary complications include hypoxic brain damage, increased ICP, infection, cerebral edema, and posttraumatic syndromes.<\/a><\/p>\n\n\n\n

basilar fracture signs<\/a><\/p>\n\n\n\n

anterior or posterior skull base<\/a><\/p>\n\n\n\n

Sx’s of basilar skull fracture<\/a><\/p>\n\n\n\n

CN dysfunction
hemotympanum
battle sign – mastoid ecchymosis
raccoon eyes – periorbital ecchymosis
CSF leaking from ear or nose – + dextrostix, halo sign, salty taste in mouth, beta-2 transferrin
hearing loss<\/a><\/p>\n\n\n\n

brain injury<\/a><\/p>\n\n\n\n

concussion, contusion, hematoma, subdural hematoma, traumatic subarachnoid hemorrhage, diffuse axonal injury<\/a><\/p>\n\n\n\n

concussion<\/a><\/p>\n\n\n\n

coup-contrcoup injuries; m\/c found in the temporal lobe<\/a><\/p>\n\n\n\n

contusion<\/a><\/p>\n\n\n\n

m\/c seen lesions are in the orbitofrontal or anterior temporal regions<\/a><\/p>\n\n\n\n

Hematoma<\/a><\/p>\n\n\n\n

epidural: m\/c in the temporal\/parietal region
Subdural hematoma: m\/c caused by tearing of the bridging veins<\/a><\/p>\n\n\n\n

acute subdural hematoma sxs<\/a><\/p>\n\n\n\n

drowsiness, agitation, and confusion
HA
unilateral or bilateral pupil dilatation
hemiparesis
noncontrast CT
sx indications: >10mm thickness with >5mm midline shift regardless of GCS<\/a><\/p>\n\n\n\n

chronic subdural hematoma sxs<\/a><\/p>\n\n\n\n

HA
memory loss
personality changes
incontinence
ataxia
obtain CT scan
sx usually required, burr holes or craniotomy<\/a><\/p>\n\n\n\n

traumatic subarachnoid hemorrhage<\/a><\/p>\n\n\n\n

HA
reduced LOC
nuchal rigidity
hemiplegia
ipsilateral pupillary abnormalities
delayed vasospasm<\/a><\/p>\n\n\n\n

diffuse axonal injury<\/a><\/p>\n\n\n\n

type of brain injury characterized by shearing, stretching, or tearing of nerve fibers with subsequent axonal damage.<\/a><\/p>\n\n\n\n

penetrating head trauma abx<\/a><\/p>\n\n\n\n

ceftriaxone, metronidazole, and vanc immediately for minimum of 6 weeks<\/a><\/p>\n\n\n\n

management of TBI<\/a><\/p>\n\n\n\n

limit secondary injury
cerebral\/elevated ICP\/herniation<\/a><\/p>\n\n\n\n

herniation<\/a><\/p>\n\n\n\n

indicated by pupillary dilation
cushing triad: HTN, decreased RR, bradycardia, late finding of elevated ICP<\/a><\/p>\n\n\n\n

barbiturate coma<\/a><\/p>\n\n\n\n

may be used to treat ICP after admit; Reduces Metabolic Demand
Pentobarbital<\/a><\/p>\n\n\n\n

hyperosmolar therapy<\/a><\/p>\n\n\n\n

mannitol
serum osmolarity: maintain <320
hypertonic saline (2%,3%, or 23% NaCl)<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"

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