Final Exam Flashcards
meningitis
infection of the meninges contacted through blood stream; crosses through blood stream
manifestations of meningitis
nuchal rigidity, positive kernigs signs, brodzinskis sign
diagnosing meningitis
CT scan/MRI, lumbar puncture for bacterial culture and gram staining of CSF
CSF aspiration during meningitis
cloudy, low glucose, high protein, high WBC
preventative treatment of meningitis
meningococcal vaccine during high school and college, prophylaxis treatment when in contact with rifampin or ciprofloxacin w/in 24 hours
management of meningitis
antibiotics like vancomycin and cephalosporin, steroids, fluids, seizure precautions with phenytoin
nursing management of meningitis
neuro checks, VS, IOs, labs, daily weights, electrolytes, infection prevention, seizure precautions, pressure ulcer precautions, pneumonia, pt/family education
brain abscess
collection of infectious material within brain tissue; want to prevent otitis media and rhinosinusitis from progressing
findings of brain abscess
headache that is worse in the morning, fever, vomiting, signs of increased ICP
diagnosing brain abscess
MRI and CT scan
nursing management of brain abscess
neuro assessment, meds like antibiotics and steroids, supportive care
3 types of traumatic brain injry
concussion- mild; contusion- moderate to severe; diffuse axonal injury- severe
concussion
mild TBI; sudden trauma induced alteration at alert state; may or may not lose consciousness; small fx, bleed, or swelling may or may not occur
contusion
moderate to severe TBI; bruising of the brain; LOC with stupor and confusion; injury may be present at site of injury or at opposite side; damage to cortex; larger contusions may need to be surgically removed
diffuse axonal injury
severe TBI; deceleration injury with differential movement of brain and skull causing axonal shearing; high mortality rate; immediate onset with no lucid interval; posturing
decorticate posturing
damage to corticospinal tract (cortex lesion); interrupts pathway between brain and spinal cord; rigid extended legs, pointed and turned in toes, arms bent toward center of body, curled wrists and balled hands against chest
decerebrate posturing
severe injury to the brain at the level of brain stem; poor prognosis; rigid extended legs, pointed and turned in toes, flexed wrists, curled fingers, straight tense arms parallel to body
brain death
absence of brainstem reflexes and apnea; irreversible condition; coma is different due to distinguishable presence of brain stem response such as spontaneous breathing and reflexes
spinal shock
occurs immediately after injury (24hrs-6 weeks following); complete but temporary loss of motor function, sensation, and autonomic activity; brain unable to transmit signals to muscle and organs
treatment of spinal shock
spinal stabilization, maintain ABCs, PT, OT
clinical manifestations of spinal shock
flaccid paralysis, clonus is fist sign, no DTR, low visceral and somatic sensations, anhidrosis, paralytic ileus
cushings triad
HTN/widened pulse pressures, bradycardia, irregular breathing pattern; sign of brain injury
neurogenic shock
acute injury to brain, cervical, or thoracic spine; causes distributive shock d/t loss of autonomic nervous system and control of blood vessel
patho of neurogenic shock
loss of SNS tone, massive vasodilation and venous pooling, hypotension, low perfusion, cell death; occurs 30 minutes up to 6 weeks after injury
clinical manifestations of neurogenic shock
hypotension, bradycardia, poikilothermia (irregular temp), anhidrosis
treatment of neurogenic shock
spinal stabilization, vasopressors, atropine, pacemaker
mitral and aortic valve stenosis
valves do not completely open reducing blood flow through valve; thickened and stenotic valve leaflets
mitral and aortic valve regurgitation
valves do not completely close causing backflow of blood through valve
effects of mitral valve stenosis
reduced cardiac output; rising pressure in left atrium; left atrium hypertrophy and pulmonary congestion
effects of aortic valve stenosis
left ventricle hypertrophys
effects of mitral valve regurgitation
allows blood from left ventricle to left atria; reduced cardiac output; hypertrophy of left ventricle d/t pumping harder
mitral valve prolapse
part of one or both valve leaflets collapse back into the left atrium
symptoms of mitral valve prolapse
palpitations, chest pain, fatigue, dizziness, shortness of breath
types of valve repairs
valvuloplasty- valve repair and reconstruction done minimally invasive; commissurotomy- repair to stenosed mitral valve, fused commissures are incised
types of valve replacements
prosthetics consist of mechanical- long term disability, risk for thrombi/emboli, risk for infection, require lifelong antibx; biologic- durability <10yrs; homograft- human but limited availability; all procedures done if valvuloplasty cannot be done
cardiac tamponade
compression on the heart due to excessive fluid in pericardium; auscultate at PMI; treat with pericardiocentesis
assessment of valve disorders
decreased cardiac output and decreased cerebral perfusion; syncope with exertion; pulmonary edema; dyspnea; tachypnea; tachycardia; chest pain
diagnosing valvular disorders
TEE, echocardiogram, murmur auscultated d/t turbulent blood flow
treatment of valvular disorders
want NSR and avoid AFib; control HR with BB and CCB; valve repair
treatment of Afib
amiodarone and cardioversion
treatment of HF
diuretics and sodium restriction
heart failure
aka dilated cardiomyopathy; prone to dysrhythmias, valve dysfunction; causes sns stimulation to increase BP and narrow arteries and increase workload
signs and symptoms of dilated/HF
SOB on exertion, fatigue, weakness, cough while lying, orthopnea, chest pain, cardiomegaly, fluid retention, nausea. palpitations, syncope with exertion, S3 heart sound
diagnosing HF
echo to visualize and calculate ejection fraction, EKG, stress test, CXR, MRI, CT scan, cardiac cath lab, B natriuretic peptide (BNP)
treating HF
diet- sodium restriction; telemetry- monitor rhythms; meds like anticoagulants and antiplatelets; biventricular pacing; surgery
anticoagulants used for cardiac treatments
apixaban (eliquis), warfarin, rivaroxaban (xarelto)
antiplatelets used for cardiac treatments
aspirin, clopidogrel (plavix)
order of electrodes
salt pepper meat lettuce tomato; white pt top right, black pt top left, brown in middle sternum, green pt bottom right, red pt bottom left
electrical conduction system within heart
SA node is primary pacemaker and initiates atrial contraction, travels to AV node which is backup pacemaker and acts to depolarize atria and slow impulse, then atrial contraction begins and conduction travels to heart apex, then travels to bundle of his and bundle branches, then travels to purkinje fibers and through ventricular myocardium, causing ventricular contraction
moving from negative to positive (top to bottom)
causes positive deflections on 12 lead
P wave
atrial contraction (depolarization)
PR interval
from beginning of P wave to beginning of QRS; should be 0.12-0.2 sec
PR segment
from end of P wave to beginning of QRS complex; movement of electrical activity from atria to ventricles; impulse is held in AV node leading to isoelectric line
QRS complex
ventricular contraction (depolarization); should be 0.06-0.12 sec
ST segment
end of S wave to beginning of T; time between ventricular depolarization and repolarization
T wave
ventricular relaxation (repolarization)
QT interval
from beginning of QRS to end of T wave; time from beginning of ventricular contraction until ventricular repolarization; should be <0.4 sec
TP interval
end of t wave to beginning of P wave; ventricles are relaxing and filling
absolute refractory period
time where tissue cannot conduct any electrical impulse; QRS to T
EKG measurements
each box is 0.04s, each big box is 0.2 s, 5 large boxes is 1s, each strip is 6s
method of interpreting EKG
- measure the rate; 2. examine R-R interval to see if regular or irregular; 3. examine the p wave (constant, one for every QRS, upright); 4. measure PR interval; 5. is P wave followed by QRS; 6. Examine and measure QRS complex (wide or short); 7. measure QT interval; 8. identify the rhythm
sinus bradycardia
less than 60 bpm, regular R-R, upright regular and matching P wave; P wave precedes QRS
treatment for sinus bradycardia
speed up heart; atropine 0.5mg, dopamine, pacemaker
types of pacemakers
temporary- transcutaneous, transvenous, epicardial; permanent- pacemaker, implantable cardioverter defribrillator, biventricular pacemaker
atrial pacemaker spikes and ventricle pacemaker spike
atrial PM pacer spike occurs before P wave; ventricle pacer spike occurs before QRS (QRS will be wider if paced and that is normal)
sinus tachycardia
rate > 100 and <140; R-R interval is regular; P wave is regular upright and matching; P wave precedes QRS
treating sinus tachycardia
fluids, O2, fever, pain, rest; meds like beta blockers (metoprolol)
atrial fibrillation
irregular R-R interval; P wave is undistinguishable; unable to calculate PR interval; cannot identify if P wave precedes each QRS; QT interval cannot be determined
concern/problem with atrial fibrillation
loss of atrial kick which causes hypotension and blood stasis
atrial fibrillation RVR
rate greater than 110
treating atrial fibrillation
beta blockers, calcium channel blockers, digoxin, amiodarone (not as commonly used); all used to slow conduction from SA to AV node
atrial flutter
regular R-R interval; P wave cannot be distinguished but can see flutter “sawtooth”; cannot calculate PR interval; cannot identify if P wave precedes each QRS; QT interval cannot be determined
concern with atrial flutter
loss of atrial kick and blood stasis; not as bad as Afib; one spot of atria is misfiring
supraventricular tachycardia
rate is > 140; regular R-R interval; unable to identify P wave; cannot calculate PR interval; cannot identify if P wave precedes each QRS; unable to identify QT interval; fast and skinny; cannot distinguish between P and T waves
treating SVT
want to convert and slow; vagal maneuver, carotid massage, medications or cardioversion; adenosine
adenosine
1st line therapy for SVT when vagal does not work; given rapidly over 1-2 sec; temporarily inhibits AV node conduction and blocks to reset HR
ventricular tachycardia
extremely widened QRS; R-R interval is regular; P wave is undistinguishable; no PR interval; P wave does not precede each QRS; unmeasurable QT interval
cardiac tamponade on EKG
crescendo then decrescendo then crescendo; types of Vtach; treat with magnesium and peridcardial centesis
treating Vtach
stable with pulse- O2 therapy, antiarrhythmics like amiodarone, synchronized cardioversion; unstable without pulse- CPR, ACLS protocol for defib., possible intervention, drug therapy like epi vaso and amiodarone
ventricular fibrillation
complete loss of contraction; R-R interval is undeterminable; no p wave; PR interval is not calculable; P wave does not precede each QRS; no QT interval;
treating ventricular fibrillation
defibrillate; meds like epi and amiodarone
asystole
complete cessation of hear electrical impulses in heart; pt is pulseless and unconscious; treat with CPR and meds (no defib)
pulseless electrical activity
electrical activity shown on EKG but no pulse present; need to reverse underlying cause; treat with CPR and epinephrine
etiology of PEA
H’s and T’s; hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypoglycemia, toxins, tamponade, tension pneumo, thrombosis, trauma
premature ventricular contraction
can be completely normal; 3 in a row is considered Vtach; can be electrical or actual contraction; does not add to cardiac output; treat by monitoring and if frequent notify physician
elective cardioversion
admin electrical current synchronized with patients heart rhythm; ised to treat SVT, AF, Aflutter, Vtach with pulse that is med resistant; 50-150 joules x3
R on T phenomenon
administering cardioversion on T wave tat can cause and lead to lethal arrhythmias
digoxin
+ inotropic effect to increase squeeze; - dromotropic effect that slows impulses in AV node; - chronotropic effect causing to beat slower
mechanical circulatory support for HF
ventricular assist device, intra-aortic balloon pump
acute respiratory distress syndrome
severe form of respiratory failure; rapidly progressive hypoxemia; alveolar capillary injury; damage to endothelia lining of alveolar membrane increasing permeability; plasma and proteins leak from capillaries into interstitial spaces and alveoli that causes damage, reduces lung compliance, lung volume, and normal gas exchange; most fatal within 24-48 hrs
common etiology of ARDS
aspiration of gastric contents, pneumonia, covid, shock of any etiology, sepsis
manifestations of acute respiratory distress syndrome
hypoxia that does not improve with O2 (hallmark), tachypnea, increasing dyspnea, hyperventilation, resp. distress, no adventitious lung sounds, tachycardia, HTN, restlessness/anxiety, chest Xray resemble pulmonary edema, BNP to distinguish from pulmonary edema, visible bilateral infiltrates
why prone positioning/rotoprone for ARDS
improve oxygenation, increase end-expiratory lung volume, improve bronchial drainage, improve functional residual capacity, improve gas exchange
obstructive sleep apnea
upper airway obstruction causing decreased ventilation and gas exchange, intermittent breathing
clinical manifestations of OSA
snoring/snorting, apneic events, gasping, recurrent waking and sleep disruption, choking, excessive daytime sleepiness, workplace or car accidents, decreased cognitive functioning, retention and performance compromise; partners identify signs and symptoms
risk factors for OSA
obesity, DMII, HF, pulmonary HTN, large neck circumeference
diagnosing OSA
health history with sleep study
treating OSA
lifestyle modifications, CPAP, surgery as needed
pulmonary embolism
clot in pulmonary artery or branch; embolism can be fat, air, thrombus, amniotic, or septic; size determines severity; causes increased vascular resistance and increased pulmonary arterial pressure
risk factor for developing PE
vrichows triad- venous stasis, hypercoagulative state (pregnant or COPD), endothelial damage (HTN or DM); DVT
saddle PE
form clot at biforkation of lungs blocking blood flow
clot busting drug
alteplase
clot preventing drug
warfarin
manifestations of PE
sudden dyspnea, pleuritic chest pain, anxiety, tachycardia, cough, diaphoresis, hemoptysis, syncope, impending doom, petechiae
diagnosing PE
elevated D-dimer, EKG, chest xray, ABG, spiral CT or VQ scan, pulmonary arteriogram
Prevention of PE
active leg exercises, mobility with pt, early ambulation, anticoag therapy, SCDs
treatment of PE
measures to improve respiratory and vascular status like O2 therapy, ECG monitoring, IV access; anticoag therapy like heparin or warfarin, thrombolytic therapy like streptokinase and alteplase; surgical intervention like embolectomy
pulmonary HTN
mean pressure >25mmHg and pulmonary capillary wedge pressure > 5mmHG; can be idiopathic or d/t existing cardiac/pulmonary disease; more frequent in women; often fatal within 5 yrs
manifestations of pulmonary HTN
dyspnea, substernal chest pain (non cardiac), weakness, fatigue, syncope, signs of right sided HF
diagnostic testing for pulmonary HTN
chest xray, pulmonary function tests, ECG and echo, cardiac cath with measurement of right heart pressures
manag,ent of pulmonary HTN
supplemental O2 therapy, central venous access for prostanoids; meds like CB, phosphodiesterase inhibitor, prostanoids, lung transplant
prostanoids use for pulmonary HTN
active lipid mediators thar regulate inflammatory response
phosphodiesterase inhibitor use for pulmonary HTN
cause blood vessels to relax and widen, improve circulation, lower BP
pneumothorax
partial or complete collapse of lung due to positive pressure in pleural space; can be hemothorax, tension pneumo, or pneumo
hemothorax
blood in pleural space that collapses lung, d/t trauma or post op
tension pneumothorax
emergency situation with increasing positive pressure in pleural space that can displace lungs and heart; can be open or closed; will see TD d/t shifting mediastinum; can put pressure on vena cava and decrease blood return
treatment of pneumothorax
chest tube or dart in 2nd intercostal space to open up lung opening lung to intubate
diagnosing pneumothorax
presentation and assessment; related history, chest xray, ABG, respiratory acidosis due to decrease in PaO2 and increase in PaCO2
chest tube
breath changes aka tidaling is normal; should be no bubbling in water-seal chamber and if there is there could be an air leak
chest tube removal
suction is discontinued and set to water seal for 6-24 hours prior, cxr prior, lungs re-expanded and pleural drainage is complete, pre medicate and educate, remove sutures, have pt exhale and then remove, occlusive dressing over wound, pleura self heals, offer NSAIDs
chest tube occlusive dressing around tube
do not remove, if disconnected then place end in sterile water for seal; subcutaneous emphysema/crepitus aka air into subcutaneous tissue- inspect and palate at insertion site, report immediately to HCP
PaCO2
35-45; regulated by the lungs
HCO3
22-26; regulated by the kidneys
PaO2
80-100; regulated by the lungs
method of evaluating ABGs
- check pH for acidotic or alkalotic; 2. evaluate PaCO2; 3. Assess HCO3; 4. check PaO2 and O2 for hypoxemia and impaired oxygenation
normal ABG values
pH- 7.35-7.45; CO2- 35-45; HCO3- 22-26
ROME Method for ABG
Respiratory opposite- pH and CO2; Metabolic equal- pH and HCO3
uncompensated ABG values
pH is out of range but CO2 or HCO23 is in range
partially compensated ABG values
CO2, HCO3, and pH all out of range
fully compensated ABG values
pH is in range
respiratory compensation
body can partially compensate for metabolic imbalances by adjusting ventilation
metabolic compensation
respiratory imbalances can be compensated through changes in bicarbonate levels
respiratory acidosis
pH < 7.35 and CO2 > 45; lungs retaining too much CO2 and kidneys excrete hydrogen and retain bicarb; pt unable to breath out CO2 and require intubation
signs and symptoms of respiratory acidosis
increased respiratory rate, restlessness, confusion, headache, sleepy/coma
interventions for respiratory acidosis
administer O2, semi-fowlers, turn cough deep breath, pneumonia requiring increase in fluids; intubate if CO2 > 50
respiratory alkalosis
pH > 7.45 and CO2 < 35; lungs are losing too much CO2; kidneys excrete excess bicarb and retain hyhdrogen
signs and symptoms of respiratory alkalosis
increase heart rate, confused and tired, tetany, EKG changes, + chvosteks sign
pre-renal AKI
due to reduction in blood flow to the kidney; hypoperfusion and decreased O2
causes of prerenal AKI
hypovolemia from bleeding, hypotension, vasoconstriction, renal artery stenosis, inadequate cardiac output
intra-renal AKI
intrarenal failure is due to damage to the filtering structures in the kidney; aka acute tubular necrosis
causes of intra-renal AKI
acute tubular necrosis, nephrotic medications like NSAIDs, CT contrast, antibx ending in -mysin; diagnosed with creatinine >1.3; treat by removing underlying cause
acute tubular necrosis
destroyed tubular segment of the nephron causing uremia and renal failure; blood flow to kidney is disrupted
causes of acute tubular necrosis
ischemic injury, nephrotoxic injury, blood transfusion reaction, rhabdomyolysis, hypotension, major surgery, septic shock
post-renal AKI
renal blockage after the kidneys blocking outflow of urine causing increased pressure in kidneys that limit filtration ability
causes of obstruction to urine outflow
upper- renal calculi, tumors; lower- BPH, urethral strictures, occluded catheter; functional- neurogenic, spinal cord disease
diagnosing post renal AKI
xray to look for calculi/hydronephrosis, ultrasound to look for obstruction, CT without dye to check for obstruction and view renal perfusion
treating post renal AKI
remove underlying cause if possible, IV hydration, supportive measures
indications for temporary dialysis
volume overload that is unresponsive to diuretics, hyperkalemia, metabolic acidosis, progressive azotemia (BUN > 100); options are intermittent dialysis, continuous renal replacement therapy, peritoneal dialysis
end stage renal disease
GFR < 15; stage 5 CKD
risk factors for CKD
diabetes; HTN- nephrosclerosis, ACE/ARBs, glomerulonephritis
etiology of CKD
metabolic disorders, renal vascular disorders, immunologic disorders like lupus, infection like UTI or pyelonephritis, primary tubular disorders, urinary tract obstruction, congenital disorders like PKD, most frequently caused by DM and HTN
signs and symptoms of ESRD
decreased UOP, proteinuria and hematuria, lethargy, altered LOC/confusion, seizures, HTN, fluid volume excess, HF, anorexia, N/V, uremic fetor, metallic taste, impaired immune and inflammatory respone, uremic frost, pruritus, anemia, increased bleeding, prolonged bleeding, amenorrhea, ED, decreased libido
lab vales for ESRD
increased BUN, increased creatinine, increased K, increased Mg, decreased calcium, increased phosphate
indications for dialysis
ESRD- GFR < 5-10, BUN > 80-100, creatinine > 8; metabolic acidosis, poisonings to clear drugs/toxins, fluid volume excess in anuric pt; hyperkalemia unresponsive to therapy; AKI
central venous line access for dialysis
acute but temporary, use subclavian, internal jugular, or femoreal; cons- thrombosis, hematoma, not enough blood flow
AV fistula vascular access for hemodialysis
rapid flow that is surgically created, 2-3 months to mature and last 3 years; pros- last long, not prone to infection, excellent blood flow, can shower, less likely to have clots; cons- need to mature, need direct needles into skin
AV graft vascular access
inadequate blood vessel, 2-5 weeks to mature; pros- excellent blood flow, take shower after healing; cons- less time than fistula, more prone to infection, 2 weeks before use, clotting
pt education for fistula care
do- lanolin for dry skin, check bruit frequently, report bleeding/oozing of patch, medic alert bracelet, hold pressure for 20 min after removal of access; dont- no blood draws IVs or BP, no tight clothing or jewelry, do not lift heavy items, do not bump, do not itch/pick at scabs
hemodialysis
remove blood from patient and filter through dialysis membrane and return filtered blood to patient; outpatient 2-3 times per week at home; may clot,risk for infection; requires anticoag and BP sufficient to tolerate approx 1 pint of blood out of circulation at one time; hypotension and blood loss may occur; most efficient form of dialysis; dialysate formulated to pt specific need
contraindications to hemodialysis
inability to be anticoagulated, severe cardiac disease, hemodynamic instability
peritoneal dialysis
dialysate solution warmed to body temperature and infused into peritoneum; equilibration occurs across peritoneal membrane then solution is drained; heparin may be added to dialysate to prevent clot formation; want light yellow drainage; need bag to below insertion
complications
infection like peritonitis, bowel or bladder perforation, bleeding
methods of peritoneal dialysis
intermittent- dialysis is 3-5 weeks for 8-12 hours via automatic cycler machine; continuous; continuous- dialysate infused into peritoneum, dwells for 4-5 hours then drained; cyclic continuous- combines intermittent night time cycling with day time ambulatory dialysis
contraindications to peritoneal dialysis
severe obesity, COPD, less efficient, catheter can clog and be displaced
continuous renal replacement therapy
hemodynamically unstable patients; slow continuous microfiltration; need A line for accurate readings of pressure prior to CRRT
types of UTI
pyelonephritis (kidney infection), uretitis, cystitis, urethritis, prostatitis
signs and symptoms of UTI
frequent urination, painful urgent, burning; dark red milky or cloudy urine; foul smelling urine; pain in flank region; pressure in pelvic area; fever, fatigue, altered mental status; confusion in older adult
interventions for UTI
simple- trimethoprim/sulfamethazine, nitrofurantoin; complex- ciprofloxacin (can cause tendon rupture); pyridium analgesic for pain and spasms
renal calculi
can occur in renal tract (renal pelvic or calices), risk for development when increased stone component; predisposed if dehydrated, infection obesity, exercise
four types of kidney stones
calcium (oxalate and phosphate)- associated with increased calcium levels; magnesium ammonium phosphate (struvite)- associated with UTI; uric acid stones- related to uric acid levels; cystine stones- seen in cysturia
signs and symptoms
N/V; flank pain that may radiate to groin, testicles, abdominal pain; sharp sudden severe pain; hematuria, dysuria, urinary frequency
diagnosing kidney stone
US, IVP, renal stone analysis, KUB scan, serum calcium oxalate and uric acid
etiology of renal calculi
infection, urinary stasis/retention, immobility, dehydration, increased uric acid, increased urinary oxalate
treatment of renal calculi
calculi <4mm have 80% chance of passing with vigorous hydration, removal of stone via lithotripsy or nephrolithotomy, determine composition of stone, dietary consult, med treatment with analgesics diuretics and thiazides
thiazide effects on renal calculi
decrease calcium excretion in urine
leukemia
cancer of blood and blood forming organs; usually leukocytes; immature blast stage where cells cant mature and divide rapidly; drains the resources in bone marrow
signs and symptoms of leukemia
low RBC, low Hgb, low Hct, low platelets, bruising, bone pain, intermittent fever with no other findings
complications with leukemia
neutropenia, anemia, bleeding, DIC, fungal infections, tumor lysis syndrome
treatment of leukemia
chemotherapy, hematopoietic stem cell transplant, supportive care
goals for pt with leukemia
absence of complications and pain, attainment and maintenance of adequate nutrition, ability to proved self care and cope with diagnosis; understanding of disease
multiple myeloma
plasma cell cancer (b lymphocyte); bone marrow and skeleton tumors; malignant plasma cells penetrate BM forming tumors
signs and symptoms of multiple myeloma
bone pain in spine and chest; pain and numbness in legs; fatigue; weight loss; osteoporosis; bone fractures; renal impairment
complications with multiple myeloma
infection, brittle bones, enamia, kidney failure, hypercalcemia
treatment for multiple myeloma
HSCT, chemo, bisphosphonates, radiation; rarely cured but can manage pain
lymphoma
neoplasm of lymphoid origin; hodgkins and non-hodgkins
hodgkins lymphoma
single node; reed sternberg cells; epstein barr virus; genetic (20-30s); environmental
non hodgkins lymphoma
lymph tissue infiltrated with malignant cells; lymphadenopathy; chromosomal translocation; infections; environmental; AIDS; chemotherapy; radiation
clinical manifestations of lymphoma
swollen lymph nodes in axilla, neck, groin; weight loss; fever; night sweats
treatment of lymphoma
chemo, radiation, HSCT, NHL: immunotherapy
polycythemia vera
bone marrow is hypercellular; increased blood cell mass and viscocity;
manifestations of polycythemia vera
initially asymptomatic; CNS- headache, dizziness, TIA; CV- angina, claudication, SOB, HTN; fatigue, night sweats; ABD- early satiety, abdominal pain
complications with polycythemia vera
CVA, MI, bleeding risk from dysfunctional platelets
diagnosing polycythemia vera
elevated erythrocytes, leukocytes, platelets, HGB and HCT
CML
philadelphia cells; mutation in myeloid stem cells causing uncontrolled proliferation; failure of B cell
AML
defect in stem cell that differentiates into myeloid cells like monocytes, granulocytes, erythrocytes, platelets; peak incidence in 60s
ALL
uncontrolled proliferation of lymphoid cells from stem cell; young children mostly affected; peak incidence is 4 yrs; boys affected more often
prior to blood transfusion
type and cross match; explain procedure; informed consent; atleast 20 gauge IV; hospital policy and procedure with IV pump; label and compare to order; double nurse witness
sickle cell anemia
shortened red blood cell life due to hemolysis; sickled shape; blocks arteries; geneticcompl
complications with sickle cell anemia
stroke, hypoxia/ischemia; dehydration; MI; kidney disease; substance abuse; HF
bleeding disorders
thrombocytopenia, immune thrombocytopenic purpura, platelet defects, hemophilia, von willebrand
thrombocytopenia
deficient # of platelets causing bleeding into tissues; all coagulation factors are present and normal
signs and symptoms of thrombocytopenia
bleeding, petechiae, ecchymosis, epistaxis, bleeding gums
HIT
heparin induced thrombocytopenia; fall in platelet count; risk for clots; need to stop heparin and switch to another anticoag
disseminated intravascular coagulation
altered hemostasis mechanism; massive clotting in microcirculation; all clotting factors are consumed and causes profuse bleeding
signs and symptoms of DIC
petechiae, hematuria, melena, epistaxis
anemia
lower than normal Hgb and fewer circulating erythrocytes; microcytic, normocytic,, macrocytic, sickle cell
microcytic anemia
decrease RBC production, MCV <80; iron deficiency; smaller pale RBCs
normocytic anemia
MCV- 80-100; increased reticulocyte count- hemolytic anemia/hemorrhage/sickle cell; decreased reticulocyte count- bone marrow suppression, chronic disease
macrocytic anemia
MCV >100; megaloblastic- Vit B12 deficiency, folate deficiency; non-megaloblastic- alcohol
classic signs of anemia
pallor, fatigue, dyspnea on exertion, dizziness
interventions for anemia
balance physical activity and rest, adequate nutrition and hydration, med compliance, monitor VS, supportive therapy, complication management of HF parasthesia and confusion
do not take iron with…
calcium; take with vit c and fruit juice on empty stomach
acute hemolytic reaction
fever, chills, jaundice, flank pain, chest pain, heat feeling along vein, impending doom; fatal reaction risk increases if >100mL transfused
preoperative phase
decision is made and ends with pt on OR bed
intraoperative phase
patient OR bed and ends with admission to PACU
postoperative phase
begins with admission of pt to PACU and ends with follow up
intervention for thermal burns
remove charred clothing, saline or water to cool tissues, fluffed gauze in between fingers and toes individually
chemical brun intervention
remove by brushing or flushing with water, remove any clothing, neutralizing agents not recommended, tissue destruction for up to 72 hrs
acid vs alkaline burns
acid- protein denaturation and necrosis, short-lived and local; alkaline burns are far worse and cause progressive liquefaction necrosis with deeper tissue penetration and prolonged effect
electrical burn intervention
remove electrical current before touching, cell rupture, iceberg effects, bone fracture, identify entrance and exit, compartment syndrome
rule of 9s
entire head/neck is 9% (4.5 front and back); entire torso is 36* (18 front and back), entire right arm is 9% (4.5 front and back), entire left arm is 9% (4.5 front and back), entire right leg is 18% (9 front and back), entire left leg is 18% (9 front and back), groin is 1%
systemic burns
20% TBSA in adults and >10% in children
inhalation injury
damage to respiratory system due to breathing in smoke, thermal or chemical; deterioration in severely burned pt; need to be intubate
signs and symptoms of inhalation injury
charred burned or bright red lips, burn to head neck or face, wheezing, change in voice, difficulty breathing, singed nose hairs or eye brows, dark mucus
fluid resuscitation formula
weight in kg x %TBSA x 4mL; first half given over 8 hours, second half given over 16 hours; only for TBSA >20%
green triage
able to walk; victim with relatively minor injuries; status unlikely to deteriorate over days; may be able to assist in own care; “walking wounded”
yellow triage
unable to walk, spontaneous breathing, RR <30, radial pulse present or capillary refill <2, mental status able to obey commands; transport can be delayed; serious and potentially life-threatening injuries but status not expected to deteriorate significantly over several hours
red triage
unable to walk, spontaneous airway absent but recurs with airway repositioning, respiratory rate >30, radial pulse absent or capillary refill >2 sec, mental status does not obey commands; victim can be helped by immediate intervention and transport; requires medical attention within 60 minutes for survival; compromise to ABCs
black triage
unable to walk, no spontaneous breathing even with airway adjustment; victim unlikely to survive given severity of injuries or level of available care, palliative care and pain relief should be provided
