Med Surge 1 PDF

NUR 340  Describe current state of CV disease in U.S.  Review basic pathophysiology  Review assessment related to CV disease  Discuss treatment of angina and myocardial infarction  1 of every 4 deaths caused by heart disease  More than half of these deaths were men  Wom...

NUR 340  Describe current state of CV disease in U.S.  Review basic pathophysiology  Review assessment related to CV disease  Discuss treatment of angina and myocardial infarction  1 of every 4 deaths caused by heart disease  More than half of these deaths were men  Women: 2 of 3 women who died suddenly had no previous symptoms  Total cost: 207 billion! CDC- Heart Disease Fact Sheet  ↳ set by the government goals  Decrease coronary heart disease deaths  Increase cardiovascular health in U.S. population  Increase dietary adherence in at-risk individuals  Increase number of adults who are aware of and can respond to symptoms of heart attack Healthy People 2030 Dissecte se a  Arteriosclerosis: abnormal thickening and hardening of arteries ↳ stiffening Y due gets worse as we age to losing flexibility  Atherosclerosis: deposit of plaque in inner layers of arteries -Build up of fats Chloesterol  Zu Embolism VS Thrombis ↳ blood slows leading to coagulation ↳ platelets stick to the plaque breaks ↳ If plaque to off it can travel, , other vessels ? Can obstruct  Coronary arteries ↳ around the heart  Peripheral arteries (PAD-Honan pp. 530-538) ↳ Clotacation & discomfort claudication s define & Intermittent  Subclavian arteries  Blood vessels reroute 2 Body will create a new route & Vessels are smaller  Due to arterial occlusion  Adjust gradually  Increases mortality and morbidity  Leads to critical limb ischemia  Symptoms? ↓pulses  Treatment  Vasodilator  anticoagulant Refresh  surgical intervention  Cardiac output  Blood pumped by ventricles  SV x HR = CO  Stroke volume  Amount ejected per heartbeat  Heart Rate  Determined by ANS (symp & parasymp)  Preload 7 a How well B Filling  Afterload  Contractility it contract ↳ how well Channel blockers e calcium  Ejection Fraction ↳ Left Ventricle is the most important 6 % pumped out & Test : echocardigram   What do they supply? Highest of >  Left – anterior wall and lateral wall (circumflex) rate  Right – inferior wall, posterior wall mortality & Cardiac Cauterization looks at both  Where do they come from?  Just above aortic valve & Widow malen Harder the heart Works , the more OG needs  Increased oxygen demands ↳ Heart says "Can't breathe  Decreased oxygen supply EITHER CAN LEAD TO CARDIOVASCULAR EVENT!  Health History  Clinical Manifestations  Lab Values/Diagnostics  Nonmodifiable: ↳ age ↳ genetics / family history ↳ genden ↳ ethincity  Modifiable: ↳ Diet (Una EdFats)& is smoking ↳ Hypertension us Hyperlipidemia ↳ Obesity ↳ Sedentary lifestyle alcono use ↳ obsessive  ↳ Issues thept areadas  Insulin resistance  Abdominal obesity  Dyslipidemia  Hypertension  Elevated C-reactive protein (CRP) > - Somewhere in the body there is inflammationee s what  Elevated fibrinogen &Fibrinogen becomes fibrin which creates clots · Always assume Cardiac until proven Otherwise ↳ heartburn's ingestion  Angina & Chest discomfort  Pericarditis Inflammation r of the pericardial a  PE/Pneumonia & pulmonaryne givehear as  Gastric reflux  Anxiety/panic disorders  Costochondritis reInflammation bronchitis > happens - of the with or intercostal pneumonis spaces  Dissecting aneurysm - tear carsing in the a artery pocket for blood to pool  Ischemia: An inadequate blood supply that deprives the cardiac muscle cells of oxygen needed for their survival  Angina pectoris: Chest pain that is brought about by myocardial ischemia  Classic signs and symptoms of myocardial ischemia  Almost always associated with a significant obstruction of a major coronary artery  Anginal pain can have widely varying characteristics  Diagnosis is usually by history, ECG, and cardiac biomarker analysis  Stable Ghave the Chest discomfort away with With activity then goes rest  Unstable ↳Takes to longer with rest away go  Intractable/refractory ↳ so bad you can not be relieved  Variant/Prinzmetal’s Guasospasms cause the ↓is comfort  Silent ischemia Guo symptoms  Always assume cardiac in nature until ruled out! Iwill always Check the Cardiac system First  Lipid Profile- evaluate risk for atherosclerosis  Cholesterol n Tc less than 200  Triglycerides - less 150 than  Lipoproteins  HDL  LDL ↳ - less than Bad one 100  CRP  Think inflammation   Cardiac Biomarkers or Cardiac Enzymes- released when myocardial cells are injured See of &  CK/CK-MB ↳ any ↳ Creatine Kinase these On  Enzyme within heart muscle blood test Myoglobin highis ab   Similar to hemoglobin - Earliest indicator of heart disease heart ·curing  Troponin ~ should be in the not blood stream  Protein found in heart muscle  Level >0.3ng/mL indicates elevated troponin - if troponin does this = MI  Electrocardiogram Delectrical activity of the heart are for an ST elevation (called a stemi ↳ For MI its we  Echocardiogram/Transesophageal Echocardiogram · TTE : Thoracic ↳ ultrasound of the Chest ↳ Less risk factors · TEE : Esophageal ↳ Invasive UNPO ! Put pt to sleep  Stress Testing ↳ make pt exercise with leads and watch how the heart responds to do it L Cardiac pts will have Frequently  Cardiac catheterization ↳ Femoral or radial ↳ release air from the pressure dressings to flat For 24hrs ↳ Femoral its have lay  Control cholesterol levels  Manage hypertension  Manage diabetes  Morphine -help with pain  Oxygen administration  Nitrates- vasodilates  Aspirin-antiplatelet medication - platelets aggregation  Beta blockers ↓ His &BP  Calcium channel blockers  Anticoagulants  Surgical intervention  Medications include aspirin, nitroglycerin, morphine, beta blockers, ACE inhibitors, and statins  Thrombolytics ↳ break up clots  Analgesics  Reperfusion therapy  Cardiac rehabilitation  Nursing care focuses on relieving pain, promoting respiratory function, promoting tissue perfusion, reducing anxiety, and monitoring for - complications   The nurse caring for a patient with an MI knows that the top priority in the care of this patient is what? A. Balancing intake and output B. Decreasing energy expenditure of the myocardium C. Balancing myocardial oxygen supply with demand D. Decreasing nutritional need of myocardial muscle  · ADH holds on to the fluid to BP fluids Diabetes Insipidus of we ↓ADH , the body can't hold on to the ◦ A deficiency of ______________________ DH is characterized by - excessive thirst (polydipsia) and large volumes of dilute urine. ◦ Three types: ◦ Neurogenic (central): Something going on in the brains damage to the pituitary gland related Pituitary to tumor or brain trauma ◦ Nephrogenic: Something Kidneys in the ◦ Psychogenic: ◦ Who’s at Risk? G can not sneeze with mouth closed around the G Cerebral Spinal Flood red ring mucus ↳ can blow nose  Diabetes insipidus-Clinical Findings ◦ R/T decrease of ADH G test lab Work ◦ Polyuria, nocturia, polydipsia - 400 mL of voided per Ihr for 2hrs. 4 ◦ Low urine specific gravity and low urine osmolality ↳ how dense urine isverydilute cas is ◦ High plasma (blood) osmolality (300 mOsm or more) the urine is compared to water ↳allthe substances a b i a ◦ Plasma sodium: elevated G Body is flushing out too muchtoa ◦ Dehydration!! Diabetes Insipidus: Treatment ◦ Treatment goals: · give vasopressin · keep ◦ Nursing management includes: ◦ Maintaining adequate fluid volume ◦ Monitoring patient’s weight ◦ Administering vasopressin ◦ Monitoring VS ↓ BP, 4 HR ◦ Monitoring patient’s I/O DI-Medical Management ◦ FLUID REPLACEMENT ◦ Replace ADH ◦ DDAVP (desmopressin) – nasal spray or IV & form adh of ◦ Vasopressin tannate in oil- IM ◦ Other: ◦ Thiazide diuretics - Works > counteracts - with disease ◦ Prostaglandin inhibitors: e.g. ibuprofen more for ↳ nephry ↳ Promote blood flow' mucus Secretions Syndrome of Inappropriate Antidiuretic Hormone (SIADH) ◦ Cannot excrete diluted urine ◦ Develop dilutional hyponatremia & dilutes Na So much it drops it & Confusion, Comatose ⑧ Too much Fluid build ·4 urine specific gravity , plasma osmolarity , 4 ◦ Medical management: ↳ Fluid restriction with Ana intake  SIADH ◦ Excess of ADH ◦ Water retention and dilutional hyponatremia ◦ Plasma sodium: decreased secondary to fluid retention ◦ Normal Na = Ganything 135-145 less than 120 = hypona Symptoms ◦ Decreased serum osmolality L - SIADH-Clinical Findings ◦ Symptoms primarily r/t hyponatremia: confusion lethargy weakness depressed reflexes myoclonus ~ Seizure activity coma SIADH-Medical and Nursing Management ◦ Medical management ◦ Diuretics ◦ Fluid restriction ◦ 3% normal saline infusion ◦ What type of solution is this? Ghypertonic in the bloods Causes blood to be pulled from the Cells ◦ Nursing management monitor for · Cushing's reflex G Shows Pt Cushing triad you a has a 4ICP ↳ Can cause Uncle herniation into the brain Stem Hyperthyroidism ◦ Overproduction of T3 and/or T4 - low TSH ◦ Graves’ disease is a common cause ◦ Treated with radioactive iodine, antithyroid agents, and surgery ↓ Slows the Stimulation & production Hyperthyroid/Grave’s Disease Patient with Grave’s Disease Exophthalmos & eye bulge Pushing eyes outwards outward due to particles “Thyroid Storm” > - & hyperthyroidism high tempg crisis HR, dehydration Hyperthyroidism-Nursing Management ◦ Assessment focuses on symptoms related to accelerated or exaggerated metabolism ◦ Goals and interventions focus on: ◦ Improved nutritional status due to malnourishment ◦ Improved coping ability and self-esteem ◦ Maintenance of normal body temperature - cooling blankets ◦ Absence of complications  Thyroid Tumor and Cancer ◦ Often accompanied by a goiter ◦ Presentation depends on the etiology of the growth ◦ Treatments include medications and surgery ◦ Nursing priorities after thyroidectomy include: ◦ Airway maintenance & Monitor for resp distress due toa inflammation related to Surgery ◦ Pain management ◦ Fluid balance ◦ Monitoring for complications, especially hemorrhage, hematoma formation, edema of the glottis, and hypoparathyroidism want a Calm environment  Hyperparathyroidism ◦ Excess of PTH ◦ Increase serum calcium ◦ Can be life-threatening ◦ Actions of PTH elevated due to presence of Vitamin D ◦ Ionized Ca regulates PTH ◦ Increased Ca  decreased secretion of PTH ◦ Elevated serum Ca and phosphorus become calcified Hyperparathyroidism-Medical and Nursing Management ◦ Nursing management ◦ Provide hydration ◦ Encourage mobility ◦ Dietary changes ◦ Provide emotional support ◦ Monitor for hypercalcemic crisis due Okidney stones delevop to ↑ calcium they block the Flow of Haw in the body &4 Hao helps Flush 4C9 out offractures due to ↑PTH Pulling Ca From bones & Talk ◦ Medical management about Fall prevention ◦ Surgical removal of abnormal parathyroid tissue Hypoproliferative Anemia Iron Deficiency Anemia Most common type worldwide Leads to fatigue d/t ↓ cellular oxygen not RBCs enough hemoglobin · or Diagnosis: Microcytic anemia Transferrin Sat women Occurs in a single node Causes enlargement of node Reed-Sternberg cells – malignant, large tumor cell Presence aid in diagnosis know they diagnosis Cause unknown, relation to EBV GM : Chemotherapy & radiation Non-Hodgkin Lymphoma ↳ most aggressive s harder to treat it can ↳ due to aggressive chemo x cause myelosuppression Involve malignant B lymphocytes Largely infiltrate lymphoid tissue Low grade: Ex: CLL and follicular lymphoma Longer survival rate Delayed treatment High grade: Ex: B-cell & T-cell lymphomas, Burkitt’s lymphoma Require aggressive chemotherapy Blood Transfusions Common blood product transfusions RBCs, platelets, FFPs Table 20-6, p. 612 (blood transfusion therapy) Follow the process for transfusions Monitor for adverse effects or reaction Usually occurs within first 15 minutes Pts can refuse transfusion – Jehovah’s Witness · have to know what pts blood type Compatability Transfusion Reactions Transfusion-Related Acute Lung Injury (TRALI) New lung injury within 6 hours of transfusion S/s: dyspnea, fever, chills, hypoxia, cyanosis, hypotension Transfusion-Associated Circulatory Overload (TACO) > too much - little blood time in too Hypervolemia – blood infused too quickly 4hrs ↳ give over S/s: tachycardia, JVD, crackles, HTN, dyspnea ↓ assess before & after Allergic Reaction Rash, pruritis, wheezing Benadryl/steroids given prophylactically  Pyelonephritis “Infection and inflammation of kidney pelvis, calyces, and medulla” Usually begins in lower urinary tract and ascends into kidney: often caused by E. coli Acute: active bacterial infection ◦ Interstitial inflammation with enlarged kidney ◦ Tubular cell necrosis ◦ Abscess formation ◦ Temporarily altered kidney function Chronic: Repeated infections that cause progressive inflammation and scarring ◦ Kidneys become contracted and non-functional ◦ Progressive kidney injury can lead to renal failure  Pyelonephritis Acute: ◦ Clinical manifestations: acutely ill with chills, fever, elevated WBCs, abdominal/low back pain, N/V, fatigue and symptoms of UTI ◦ Treatment: po antibioticlevaquin (cipro or Chronic: ◦ Clinical manifestations: occur with acute exacerbation-fatigue, headache, poor L appetite, polyuria, thirst, and weight loss body can build up resistance ◦ Treatment: Prophylatis antibiotics to antibiotic ◦ ◦ Surgery if needed: pyelolithotomy, nephrectomy, ureteroplasty ◦ Complications: septic shock; hypertension; chronic kidney disease  Renal Calculi-aka “Kidney Stones” Renal calculi: most common cause of urinary obstruction ◦ Nephrolithiasis: Formation of stones in the Kidney ◦ Urolithiasis: formation of stones in the bladder or Urinary tract Theories of stone formation ◦ Supersaturation: What substances? hyperparathyroidism ↳ , 4 calcium ◦ Deficiency of substances that prevent crystallization in urine ◦ Patient volume status keep pts hydrated - ◦ Acidity/alkalinity of urine Risk factors ◦ 30-50 year olds ◦ Men ◦ Metabolic defects: hyperparathyroidism and gout ◦ Genetic predisposition ◦ Spring and summer  Renal Calculi Clinical Manifestations ◦ Severe flank pain- “Renal colic” ◦ Fever ◦ Urinary frequency ◦ Diaphoresis, pallor, N/V ◦ Hematuria ◦ Oliguria/anuria: stone completely obstructing urinary flow-medical emergency Medical Management ◦ “Force fluids” and strain urine to see if stone has passed ◦ Medications: analgesics, anti-spasmodics, antibiotics ◦ Extracorporeal shock wave lithotripsy (ESWL) ◦ Surgical intervention ↳ Bust up the stone  11/6/2024 LIVER, DISEASES Med-Surg I Fall 2024 LIVER RUQ 2 main lobes ↳ 100 of lobules 2 sources of blood supply ↳ hepaticartery carries Oxygenatedboa Holds ~1 pint of blood Lots of jobs Removes Functions Fights Toxins(mes · Infections · of byFilterino a the Liver · Prevents nutrient deficiency Produces · Liver disease Issues with coagulation · Billirubin Metabolizes Bloodproducta tion onutrients · Albumin coagulation · 6 stores glucose as glycogen 1  11/6/2024 DIAGNOSTICS Labs Liver Function Tests (LFTs) - Nevers = liver damage , Infection, or obstruction ALT- > 7 55 Units/L - AST- 8 48 units/ - ALP - > 40-129 Units Bilirubin0 1-1 2 myld - lowbilirubin is.. issue an Total Protein 6 3-7 9 d malnutrition occuring.. = (12 malnourism Albumin above 5 (2 5-Sis range) 5.. = Ammonia 14-40 for adults ; 180 for children US/Transient elastography y size liver is , masses , elastography shows how squishy the Isquisher the better CT/MRI - obstruction > do we have an MRI Biopsy LIVER DISEASES/DISORDERS Non-Alcoholic vs Alcoholic e can berevise Factor Non-alcoholic- > not fa Infection Cancer Obesity Alcoholic HEPATITIS - Inflammation of the liver Viral cuteFomFodorwater contaminatin is A, B, C · A = - B · C Causes Alcoholic Toxin/Drug-Induced : tylenol , chemo , antivirals Autoimmune Immunesystem isattackingis - e systemic lupus 2  11/6/2024 goesnahan 7 NAFLD NASH Non-alcoholic Fatty fatty liver Non-alcoholic steatohepatitis Liver disease Diseases lipid first stage of accumulation liver damage Associated with central adiposity, insulin resistance, can be DM2, takes meds at night progressive hyperlipidemia, - CV disease ↑ has started G If it be ↳ damage managed , can slowedstop a damage RISK FACTORS to4ETSpe · se reverin a ↳ inflammation 3  11/6/2024 CIRRHOSIS non- advanced scar tissue tissue injury tissue repair functioning liver disease development liver tissue Not a disease; a process A sign/symptom of advanced liver disease Does not always correlate with LFT values 3-stages -Full recovery 1) prodromal (pre-icteric) symptoms - fu like , ↓ appetite 2) Icteric - Seeing jaundice might be , able to half the damage 3)Recovery (post-icteric) Slow process - damage Interic - > tissue scarring Permanet We are SYMPTOMS & TREATMENT Skin t could hand his tamina blocker  Symptoms - Ekhy  Fatigue, jaundice, enlarged spleen, pruritis, slow healing, dark urine (bilirubin in urine), ascites ↳ can't 4infection  Treatment ↳  Depends on cause  Antivirals ~ hepatotoxic  Immunological  Risk factor management  Diet - ↓ fat 4 exercise , , liver toxi is  Transplant & have to  Symptom management alcohodrug be Free Canttake any  Rest to give body time to heal the number I drug statins are lipids for controlling I can cause muscle pain COMPLICATIONS Portal hypertension Lactulose absorbs excessive amonic s Causes diarrhea caput medusae Compression of portal circulation Venous congestion - back this up blood causes of Hepatic encephalopathy- > monitor LFTS amonia levels ↓ a nervous system disorder brought on varices get a gues by severe liver disease Toxin build up- meds or amonia build up · Hepatorenal syndrome Kidney injury r/t advanced liver disease RAAS system over-activation caused ascites by portal hypertension ↳ mismatch in Vital signs 4  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