Urinary Tract Infections & Other Urological Conditions PDF

URINARY TRACT INFECTIONS COMMON WITH CATHETER INSERTION PROPER TECHNIQUE LOWER UTI COMMONLY TRANSURETHRAL S/S: FREQUENCY, URGENCY, BURNING, HEMATURIA & Adults : ↑HR/NBP , burning orgen (y , G elderly : confusion Gypts...

URINARY TRACT INFECTIONS COMMON WITH CATHETER INSERTION PROPER TECHNIQUE LOWER UTI COMMONLY TRANSURETHRAL S/S: FREQUENCY, URGENCY, BURNING, HEMATURIA & Adults : ↑HR/NBP , burning orgen (y , G elderly : confusion Gypts I tab after with Frequent UTI can take a dose as needed a trigger DIAGNOSTICS: URINALYSIS, URINE CULTURE  URINARY TRACT INFECTIONS UPPER UTI PYELONEPHRITIS S/S: ENLARGED KIDNEYS, CVA TENDERNESS, FEVER, CHILLSSignificant Flank Pain DIAGNOSTICS: LEUKOCYTOSIS, CT SCAN, URINE CULTURE TX: ANTIBIOTICS, ANALGESIC PROMOTE HYDRATION ↳hydrationhelpso aeria CONSIDERATION FOR ELDERLY ↳ can become systemic  URINARY INCONTINENCE 17 MILLION AMERICANS ↑ PREVALENCE IN DIABETES ↳ risk higher REMAINS UNDERDIAGNOSED SUBTLE CUES COMMON AMONG THE ELDERLY ACUTE ONSET DUE TO OTHER ISSUES UTI CONSTIPATION & retention ↓ ESTROGEN LEVELS ↑ GLUCOSE LEVELS Treatment Ganticholinergics ↳ oxybutinin /Ditropan) ↓ QoAmental toll  URINARY INCONTINENCE TYPES OF INCONTINENCE STRESS – INVOLUNTARY FROM SNEEZING, COUGHING, MOVEMENT ~ Women > men URGE – INVOLUNTARY, STRONG URGE TO VOID REFLEX – INVOLUNTARY, ABSENCE OF NORMAL SENSATION - neurological/neve issue OVERFLOW – INVOLUNTARY, OVERDISTENTION related FUNCTIONAL – FUNCTION INTACT, BUT ↓ COGNITION +O Pt With in the > - hx of Cognition elderly IATROGENIC – INVOLUNTARY, DUE TO MEDS EX: ALPHA ADRENERGIC BLOCKERS  URINARY INCONTINENCE MANAGEMENT FOCUSES ON TYPE SEE BOX 28-6 FOR STRATEGIES legal ↳ exercises TREAT WITH: ANTICHOLINERGICS ANTISPASMODICS (I.E. OXYBUTYNIN [DITROPAN]) HORMONE THERAPY > if - they give estrogen they , won't give Po estrogen because it could make it worse SURGICAL CORRECTION  URINARY INCONTINENCE NURSING CONSIDERATIONS TOILETING SCHEDULE BENEFICIAL FOR CONFUSED OR ELDERLY USUALLY EVERY 2 HOURS CONDITION IS REVERSIBLE/TREATABLE ENCOURAGE EXERCISES, LOG OF FREQUENCY o promote circulation Prevent skin break down ,  PRIAPISM INVOLUNTARY PROLONGED, PAINFUL ERECTION BLOOD FLOW IMPAIRED UROLOGICAL EMERGENCY NOT RELATED TO SEXUAL STIMULATION TREATMENT INCLUDES: aspirated the the blood penis from : vasoconstricts Phenylephrine  PHIMOSIS/PARAPHIMOSIS COMMON AMONG UNCIRCUMCISED MALES PHIMOSIS – TIGHTENING THAT PREVENTS RETRACTION 9ofthe foresina aft of the penis ; usually TREATMENT: caused by lack hygiene of the Foreskin back retract PARAPHIMOSIS – CONSTRICTION THAT PREVENTS COVERING OF GLANS UROLOGIC EMERGENCY TREATMENT: Compress until it the glass underneath the until Foreskin the Foreskin  4/25/2023 NURSING MANAGEMENT OF PATIENTS WITH IMMUNODEFICIENCY, HIV INFECTION, AND AIDS NUR334 FALL 2022 Deborah Toddes Med-Surg I - Spring 2023 1 OBJECTIVE  Define immunodeficiency  Discuss patients who are susceptible to immunodeficient disease processes  Distinguish between HIV Infection and AIDS  Identify how to diagnose and treat.  Discuss nursing management and diagnoses related to caring for individuals with immunodeficient disease processes 2 IMMUNODEFICIENCY DISORDERS  Part of the immune system is missing or defective ~can'tdo wata  Reduces the ability to fight infection drugs  Primary or Secondary · either underactive or overactive immune system 3 1  4/25/2023 Primary Immune Deficiency G genetic , certain Cells uncommon , missing B-cell T-cell  Manifestations: PRIMARY ↳ willseeverya ou well being IMMUNODEFICIENCY Combination  Complications: Defective of B & T Usmallest thing could cause life-long complication S phagocytes deficiencies G eat the bacteria  Examples Complement halps of lymphocytes Idiopathic excessive level deficiencies themicalthatemere 4 Secondary Immune Deficiency Far morecommon outside cause a  Extrinsic causation  SECONDARY Manifestations: IMMUNODEFICIENCY  Treatment: resolve underlying process, if possible ↳ keep possible Chemo it as healthy as  Examples: Most well-known example: HIV/AIDSis Suppress the viral load G splenectomy immune response it Hiw Pts will always have 5 HIV & AIDS G the 80s emergent thing in  HIV - human immunodeficiency virus - actual virus that causes aids  1.2M in the US (2022) – holding steady  38.8M globally (2021) – growing  1.5M new cases a yr globally  650K HIV-related deaths  AIDS – acquired immune deficiency syndrome ↳ When HIV becomes the full blown disease  Bloodborne - any bodily fluids  Transmittable in pregnancy ↳ mother to baby 6 2  4/25/2023 HIV PATHOLOGY  Targets CD4 T-cell, ~ Portiaa  Retrovirus ↳ requir mostOnsita  New viral particles bud from the cell ↳ Becomes permanent part of the human a Cell 7 Problem identify it · Elisa it won't With that if it too most likely HIV DIAGNOSIS is is early , disease e Lyme ↳LooksFr thepa antibodies Y Looks For · monitoring I E 8 STAGES OF HIV INFECTION Primary infection: Stage 1 – Acute, Asymptomatic  By about 6 months, the rate of viral replication reaches a lower but relatively steady state edue cloak vari Stage 2 – Chronic/ symptomatic: e can without lasty G treatment &  The number of CD4+ T cells gradually falls I more infections , denergy Stage 3 - conversion to AIDS  The CD4+ T-cell level drops below 200 cells/mm3 infections Ano longer fighting · CD4 T-cell never Fully recovers HIV virus invades When the suppresthe goal with · is to 9 3  4/25/2023 MANIFESTATIONS OF HIV  Pulmonary Le pneumonia  GI to see loofapt  Immune l Pneumosistic premnat ↳cancer(apozi  Integumentary  Musculoskeletal 3 muscle pain due toNlactic acid  Psycholgical BNOTIS With 4 yeast infections 10 MANIFESTATIONS (CONT) ↳ treated withantivir as 11 IMMUNE RECONSTITUTION INFLAMMATORY SYNDROMES (IRIS) blate rxn  Over reaction to previous infection I seen in immunocompromised u waits to attacks something  Overwhelming  Paradoxical Gnothingshowinga  Treatment unknown - Support them immune responses overwhelming cascade of can be Fatal 12 4  4/25/2023 HIV TREATMENT  Based on number of factors E socioecon a ↳viralload n  At least 3 active drugs from at least 2 classes ↳ combinationto hitc s a  Strict adherence imperative & HIV is prolific  Treatment side effects can affect plan  PreP treatments ↳weighthePros o cons i s u superexpensiveassocial 13 TREATMENT OF OPPORTUNISTIC INFECTIONS ia These infections ↳takeadvantage asystem ↳ o  Pneumocystis Pneumonia - Bactrumdistress resp, ↳ can cause life threatening ↳ Bactrum G Fungal infections  Mycobacterium avium complex (MAC) ↳ respiratory Syndrome ↳ Erthry om your  Cytomegalovirus ↳ an tiviral for diseaseran a 4risk ↳ liver  Kaposi Sarcoma ↳ no treatment 14 NURSING CONSIDERATIONS FOR CARE OF PATIENTS WITH HIV/AIDS  Challenging ↳isnggbehin.  Assessment into ↳timeyouWam t pon s  Physical and psychosocial Fow stance 15 5  4/25/2023 POTENTIAL NURSING DIAGNOSES Physical Related Psych-Social Related  Imbalanced Nutrition: Less Than Body  Social Isolation Requirements  Powerlessness  Fatigue  Deficient Knowledge  Acute/Chronic Pain  Disturbed Thought Process  Impaired Skin Integrity  Anxiety/Fear  Impaired Oral Mucous Membrane  Impaired health maintenance (risk or  Risk for Injury actual)  Risk for Infection 16 NURSING INTERVENTIONS  Pain relief  Support nutritional status  Evaluate for infection  Education 17 6  11/19/2024 Vascular Disorders NUR334 – MED-SURG I FALL 2024 1 OBJECTIVES Identify factors that affecting peripheral blood flow & tissue oxygenation Identify clinical manifestations, management, and prevention of arterial & venous disorders Describe nursing management of lymphedema 2 Peripheral Vascular Disease (PVD) Progressive decrease in peripheral venous circulation Causes of elasticity spasm up/blockage loss , plaque · build , Risk factors · Diabetesaesterol ·insung from infection · clotS · genetics · Smokinggeny lifestyle Clinical Manifestations extremity , edema numbness fight Shiny Shin hair loss on , · Cool skin , deep reddish-blue discoloration , , pain , non-traumatic wounds Complications loss of limb · Infection , Gangrene , neuropathy death leads to loss of limb leads to tissue Infection Poor perfusion leading to open Slow healing wounds Stasis ulcers : blood pooling causing 3 Build up of deoxygenated blood 1  11/19/2024 Peripheral Artery Disease (PAD) painting Reduced peripheral arterial blood flow G reduced flow of of to body Causes Risk factors are similar to PVD Clinical Manifestations slow healing wounds m lackofounds Pdineationsa · Complications partisn'tgettingaen ocriticallimischemattotal ocuion ,thebody P+S 4 PVD/PAD Management Pharmacological manageunderlyingconditia · meas · - triptaline Non-pharmacological Sedation ↳ heavy ◦ Angioplasty (w/ or w/o stenting) a ◦ Endarterectomybuseantigsafterward sugi ◦ By-pass Surgery 2 ↳infectine Invasive · Education : Na, d process readings 5 ↳ diet : low carb , low the Foods better , a fat , label their heart Pumps Y Stay active : more they more Vascular Ulcers Arterial Where dorsal region footstoes of AreaPaharsiscemia Clinical manifestations a ↳ gr Management Venous Where on legs calf heels : , , Clinical manifestations matted dinage Very Slowtoheal,infestate ManagementWound, , Glong-term care · want a moist , red Wound bed 6 B 2  11/19/2024 Long Term, Recurrent, Complicated 7 Other Vascular Disorders Upper Extremity Arterial Occlusive Disease ◦ Atherosclerosis ◦ brachio-cephalic trunk, subclavian and axillary arteries G high risk for gangrene loss of limb ↳ happens quickly Raynaud’s Phenomenon autoimmune - ◦ Intermittent -blood Flow ◦ Occurs during cold exposure ◦ Fingers change colors ◦ Primary or Secondary ↳nocrea for frostbite 8 Venous Thrombosis - DVT know ! " Thrombus in deep vessel – typically LE or Lungs Causes Virchow's triad eovement >dehydratin - Risk Factors · virchow's triad · Lengthy inactivity ungentialthrombin define a se Clinical Manifestations · swelling Warmst symptom ; chest pain that feels like ana Complications 9 3  11/19/2024 DVT Management IV heparin Ip ++ every Ghrs ; weight based ◦ Bolus + infusion Oral anticoagulation ◦ warfarin, rivaroxaban (Xarelto), apixaban (Eliquis) e people with Atrial a high risk for Du T dyrhythmias are at Thrombectomy Preventative measures for at-risk individual -best treatment ◦ sub-Q heparin ◦ Enoxaparin (Lovenox) 10 Nursing Considerations for DVT ptt before heparin Monitor labs (draw CBC giving a Bleeding precautions & Education - bleeding precautions & Signs of internal bleeding Positioning - > elevate legs Compression Education Prevention 11 Varicose Veins Dilated, tortuous superficial veins Risk Factors of standing, venous disease obesity genetics , long · , periods Clinical Manifestations after sitting veins dark blue pain Heavy Feeling achy , bulging · , , , Complications Bleeding · , clotsukerst or below the varicose Management stripping , e a scheein Compression , · 12 * 4  11/19/2024 Lymphedema Risks node removal l a Inflammatory processes · Lymph Radiation o disorders circulatory · · Age Complications ·Miliyskinintegritto · infection Management ·Compressiona inage Nursing Considerations positioninga tion · un na boots 13 # Tight, Shinywith · hoirs and Lymphedema 14 5 NEUROMUSCULAR DISORDERS NUR 334  the Cranial nerves Remember CRANIAL NERVE REVIEW DIAGNOSTICS PET G Shows M the functionality E blood of the organs CT/MRI J ↳ done in nuclear medicine EEG EMG & looking impulses for by nerve LP/CSF analysis ↳ Cerebral Spinal Fluid analyzing BRAIN TUMORS Pituitary Tumor 12-19% of all tumors Slow growing Can lead to: Visual disturbances Increased ICP - causes an ICP Diabetes Insipidus Transsphenoidal surgery Can cause pressure on the back of the eye can't opt can't sneeze with mouth close I have to breath through mouth ; blow hose Glook for CSF (red-ring) BRAIN TUMORS Meningiomas Most common among adults Slow growing on meninges Acoustic neuromas ↳ deficutally with hearing Benign, affects CN VIII Larger tumors affect CN V BRAIN TUMORS Angiomas Consist of abnormal blood vessels Can cause seizures, HA I can have ancursyms Gliomas Glioblastoma multiforme (GBM) most common Uneven edges, infiltrate surrounding tissue Difficult to resect fully ↳ highest morbidity poor prognosis ↳ grow rapidly INCREASED ICP t know TYPES OF SEIZURES Partial (Focal) Seizures Simple – remains awake Complex – loss of consciousness Begin in one hemisphere Abnormal firing of neurons Cause can be idiopathic or acquired · Talk seizure to pts during the to figure out the type  TYPES OF SEIZURES Generalized – occurs in both hemispheres consciousness Tonic – muscle stiffening lose All Clonic – muscle jerking Tonic-clonic (gran mal) & Can be & Seizure Very pads violent on railing Atonic – “Drop attack” seizures - pt has to wear a helmet Myoclonic – jerking in one muscle group Absence – staring Status epilepticus – ongoing for >5 minutes ↳ worried about the brain getting enough Oxygen CARE OF THE SEIZURE PATIENT Goals of treatment: Stop seizure Oxygenation Patient safety Turn on side Nothing in mouth Support head CARE OF THE SEIZURE PATIENT DURING A SEIZURE AFTER A SEIZURE Length of event - time the from the length beginning Post-ichtal > really - tired after the seizures Patient LOC Assess VS Suctioning prn Check LOC/Reorient MENINGITIS Inflamed meninges Bacterial or Viral Viral Meningitis More common Not contagious Symptoms similar to bacterial LP to diagnose · Symptoms : nuchal ridgity for both ↳ wear precautions BACTERIAL MENINGITIS Caused by Strep or Neisseria bacteria Common within dense communities Symptoms include: Neck stiffness, photophobia, HA, fever, altered LOC, rash Positive Kernig sign e can pt extend their leg Fully Positive Brudzinski sign LP to diagnose Treat with antibiotics ↳ 3rd generation Cephalosporins MENINGITIS COMPARISON ENCEPHALITIS Acute inflammation Caused by virus, bacterial infection, fungal infection S/S: HA, fever, nuchal rigidity Dx with MRI/CT, CSF analysis ↳ not always to dx Treat underlying cause enough otherpes Simplex is the most common cause BELL’S PALSY CN VII inflammation Facial hemiplegia Difference from stroke? ↳ One-sided Get can't raise eyebrow May develop issues with speech or taste Facial pain on affected side Tx: Antivirals or corticosteriods think it it · Always stroke until is proven isn't  PARKINSON DISEASE Neurodegenerative disease Slow progression Irreversible, no cure Decreased dopamine and neuronal cell destruction Imbalanced signals to voluntary muscles lost fine motor first functioning, · motor , Drugs Increase dopamine · last to keep with the progression · The drugs do not long enough up · pill-rolling tremor  CHARACTERISTICS OF PD TRAP Tremor Rigidity Akinesia Posture on arrowed shuffled gait to feet to more ↳ Difficulty lift TREATMENT OF PD No Cure! On/Off affect of medications Levodopa Carbidopa-Levodopa MAO-B inhibitors Table 46-2 Med review Deep Brain Stimulation MULTIPLE SCLEROSIS Autoimmune ↳ body attacks the myelin Demyelination – destruction of myelin in CNS Commonly diagnosed among adults ages 20-40 Gnumbness ↳ tingling Women > Men Unknown etiology Yslow but shouldn't to progression treat pts wait ↳ ↓ muscle function all over MS DIAGNOSTICS MRI positive for plaque/lesions CSF with oligoclonal banding Electrophoresis monitors extent of disease  Need info on the types CHARACTERISTICS OF MS Symptoms vary Types (Figure 46-5): Relapsing-remitting Primary progressive esteady progression getting of worse Secondary progressive G Starts as R-R but progresses beyond baseline M Progressive-relapsing · Relapsing Remiting - MULTIPLE SCLEROSIS Psychological toll Treatment includes: Symptom management Slow progression Improve overall QOL  MYASTHENIA GRAVIS Autoimmune Disorder of neuromuscular junction Causes voluntary muscle weakness Young women at increased risk Decreases acetylcholine receptor sites Leads to diminished impulses o numbness , tingling , spasms but full M G Ocular - affects the eye only Progress to. · can. aworried about function respiratory CHARACTERISTICS OF MG Ocular muscle involvement Diplopia & ptosis Generalized muscle weakness Bulbar symptoms Weakness of face and throat muscles E might have difficulty swallowing Medication involvement Certain antibiotics cause muscles weakness - do not give these antibiotics Avoid in patients with autoimmune disorders MYASTHENIA GRAVIS Diagnostics: Acetylcholinesterase testing (Tensilon) Ice-pack test for ptosis Positive if ptosis improves after 2 minutes Enlarged thymus gland Presence of acetylcholine receptor antibodies Manage symptoms, improve functioning Prevent further injury, aspiration, corneal damage TREATMENT FOR MG Anticholinesterase meds Pyridostigmine bromide (Mestinon) IV Immunoglobulin > - decreases the attacks that occur Corticosteroids/Immunosuppressants Plasmapheresis Thymectomy GUILLAIN-BARRE SYNDROME Autoimmune Affects peripheral nerve myelin Schwann cells spared Causes · estarts ascending weakness · inthe toes risealongs Precipitated by viral infection CSF detects elevated protein MANAGEMENT OF GBS Rapid progression life-long Egoes away , not Concern for respiratory involvement Prevention of PE/DVTs Plasmapheresis – reduces antibodies IVIG – improves function AMYOTROPHIC LATERAL SCLEROSIS (ALS) Degenerative, loss of upper/lower motor neurons Leads to atrophic changes · loss of motor function 10% hereditary If it starts in the it is often o hands , a worse prognosis Prognosis based on area affected No specific diagnostic testing Based on symptoms present Electromyogram – measures muscle fiber electrical activity Military veterans at increased risk CHARACTERISTICS OF ALS Gradual onset, asymmetrical Fatigue Decreased dexterity Changes in gait Spasticity Dysphasia, Dysphagia Decreased respiratory effort CHARACTERISTICS OF ALS Gradual onset, asymmetrical Fatigue Decreased dexterity Changes in gait Spasticity Dysphasia, Dysphagia Decreased respiratory effort  Genetic Disorders NUR334 Med-Surg I Fall 2024  Genes Basic units of heredity Composed of DNA (except retroviruses) Genetics Passed from generation to generation & Genetics Genomics Study of genes and their role in trait inheritance Epigenetics How environmental and behavioral factors can affect gene expression without altering the DNA sequence Genomics The study of a person’s genetic makeup (genome) Includes how genes interact within a person and with the environment Looks for patterns in inheritance & mutations  Transcription Genetic Creation of RNA from DNA First step in gene expression replication and Translation Mutation “Reading” of the RNA to create a protein Second step in gene expression Mutation A permanent change in the DNA sequence of a gene -genetic change ; actual change Many causes – intrinsic and extrinsic G radiation , Pollution etc. Sometimes harmless, other times troublesome  Dominant vs Recessive Genotype vs Phenotype Inheritance Autosomal Patterns - Dominant = Only one copy of a mutated gene is needed for the trait to be expressed - Freckles , dimples knowpesone Affected by gene Recessive = Both copies of a gene need to be mutated for the trait to be expressed location, dominance vs ↳ attached ↳ ear Fibrosis lobes Cystic recessive, and gender X-linked - A mutated gene on the X chromosome GSeX-linked Gmost from likely Coming mom Complex - No clear Mendelian pattern of inheritance Mitochondrial - Genes located in the mitochondria are exclusively passed from the mother to all offspring.  Genetic Disorders Single Gene - caused by a mutation in a single gene ↳ Sickle-cell anemia a Fibrosis cystic ↳ hemophilia ↳ huntington's Multifactorial - caused by a combination of genes and other factors G environmental , Chromosomal GBRCA plus environment or other mutations breast Cancer gene = Chromosomal - arises due to an abnormality in the number or structure of chromosomes within a cell Y down Syndrome ↳ turner syndrome (missing an X Chromsome ↳ Klinefeiters ↳ partial deletion  Screening – the first level of detection General or targeted ~ amnio , triple-screen For at-risk individuals - PSA , BREA Interpretation: Genetic Testing – for a specific reason Screening Focused Family history & Unusual symptoms or presentation Testing Interpretation: Direct-to-Consumer buy- a lit on internet Common Relatively inexpensive Risks  Experimental & limited Ghoning in on meds that are appropriate Potential to supply a missing gene or enhance treatment Requires a vector Gene blive virus Promising for: Therapy Inherited diseases Some cancers Chronic viral diseases - HIV  Genetic Counseling Family - has had a genetic hx of a disorder Requires a referral May not be covered Pre-natal - triple screen , amnio & Pharmacogenetics Improved pharmacological disease management Nursing Ethics Considerations Genetically engineered babies “Playing God” Who can afford it Support Preparation Education  Anatomy CerebroVascular Accident Types of Stroke Symptoms Diagnostics N Left-Sided Stroke: right-sided symptoms CT: within first 5 minutes; used to look for Ischemic Stroke Hemorrhagic Stroke Right-Sided Stroke: left-sided symptoms blood/clot, blood looks white on image MRI: looks for blood/clot clot/occlusion vessel burst/bleed Sensory/Motor Loss (depending on what Angiogram 80% of strokes #1 cause = hypertension area of the brain is affected); stroke pts can Echocardiogram raise eyebrows, suspect Bell’s Palsy if pt Physical Assessment/Symptoms Transient Ischemic Attack can’t raise eyebrows predecessor; increases risk of recurrent stroke Speech Impairment Results of CT/MRI: if the pt is not bleeding Symptoms: depends on involved vessels Dysphagia; dysarthria (muscle movement (hemorrhagic stroke), they may be a candidate of swallowing) for thrombolytics Visual Disturbances Risk Factors Modifiable Non-Modifiable Treatment AntiCoagulants: prevent future blood clots Hypertension Statins: decrease cholesterol, prevent future blood clots & hypertension Family History Smoking AntiHypertensives: decrease blood pressure, htn = #1 cause of hemorrhagic strokes Gender Type II Diabetes Identification of Risk Factors: make changes to decrease modifiable risk factors Age Diet/Exercise Prevention of Recurrent Stroke Race/Ethnicity Obesity Angiogram: sometimes used to look, can be clot retrieval, Atrial Fibrillation Thrombectomy: surgical removal of blood clot to restore blood flow Anterior Cerebral Artery Broca’s vs Wernicke’s Complications Broca’s: located in parietal lobe; Internal Carotid Artery chronic disability Supplies: Frontal Lobe risk for infection Signs/Symptoms: greater function is broadcasting speech post-stroke depression pneumonia = #1 caused by vessel insufficiency mortality weakness in legs, gait apraxia (leg - Signs/Symptoms: expressive UTI (low blood can mimic an ICA Vessels function is okay, but difficulty aphasia rehabilitation needs sleep apnea stroke, but symptoms resolve walking) Wernicke’s: located in temporal lobe; when blood pressure increases) function is receiving language Middle Cerebral Artery - Signs/Symptoms: receptive Signs/Symptoms: greater Nursing Considerations weakness in arms, bodily aphasia early recognition of signs and symptoms neglect Supplies: Parietal Lobe, portion of Posterior Cerebral Artery Amaurosis Fugax: temporary BE FAST (balance, eyes, face, arms, speech, time) Frontal Lobe vision loss, r/t decreased blood frequent neurological assessments largest artery, most common for stroke Supplies: Occipital Lobe flow to the retina patient & family education Signs/Symptoms: greater weakness Signs/Symptoms: visual decrease complications in arms, bodily neglect changes; visual agnosia reduce recurrence of strokes