med surg final Flashcards
myocardium
heart muscle
perdcardium
protective covering of the heart
septum
muscualr wall that divided the heart
blood
superior vena cavaright atriumtricuspid valveright ventrclepulmonic semilunar valavelungs (oxygen)pulmonary veinsleft atriummitral valveleft ventricleaortic semiluar valveaorta body
MAP
to maintain adequate blood flow through the coronary arteries the mean arterial pressure must be at 60-70-to maintain perfusion at major body organs
diatole
filling
systole
contracing
CO
CO=HRxSVblood flow to systemic circulation is measured by CO (which is the amount of blood pumped from each ventricle each minture)-cardiact index is measured to adjust the differeces in people with different body sizes ( by dividing the CO by total body area)
SV
amount of blood ejected by the left ventricle during each contraction
preload
the degree of myocardial strech at the end of diastole just before contraction-determined by the amount of blood reurining to the heart from both the venous system and pulmonary system
afterload
pressure that the ventricles must overcome to eject blood
impedance
pressure heart must overcome to open aortic valve
arterial system
blood movies from larger arteirs to smaller blood vessles called arterioles-to deliver oxygen and nutrients to tissues
venours system
blood travels from capilaries to venules and to the larfer system of veins eventually returning to the vena cava-returns blood back to heart
BP
force of blood against the vessel wallsBP=COxperipheral vascular resistance
BP mechanisms
ANS- excited/inhibits SNS in response to the chemoreceptroskidneys- sence change in blood volume and activate the renin angiotenisn mechanismendocrine- relase hormones
systolic bp
amount of froce generated by left ventricle to take blood to aorta
diastolic bp
amount of force against arterial wall during relaxation phase of the heart
peripheral chemoreceptros
sensitive to hypoxemia- decrease in arterial oxygen. when stimulated they vasoconstrict and increase BP
hypercapnia
increase in partial pressure of arterial carbon dioxide
kidneys
when blood flow deacreases the kidneyes retain water and sodium and BP rises.
BMI
overweight 25-30obese >30
MI
increases in woemn older than 35 who smoke and take contrecaptives
CVD
chest pain dyspneafatiguepalpitationsweight gainsyncope
MI in wemen
dont experince chest pain but:indigestions, abdominal fullness, fatigue, inability to catch breath
ppl with advanced heart disease may experince
orthopnea- SOB when lying down the severeity is measured by the amount of pillows they sleep with
PND paroxysmal nocturnal dyspnea
develops after pt has been lying down for several hours. in this position blood from lower extremities is redristributed to venous system which increases venous return to the heart. a desases heart can not compensate for the increased fluid and pulmonary congestion occurs. pt wakes up with feeling of suffovation-sit up dange feel at side of bed
intermittent claudation
cramping in legs or butt when walking. caused by decared arterial tissue perfusion-relieved by resting or elevating he effected extremity to enhance arterial blood flow
signs of heart diesease
cacexic, confused, memory loss, malnourished, late sign- anascare- generalized edema as results of prolonged congestion of the livercyanosis- feom increased amount of deoxygenated bloodrubor- from arterial insufeincenydeacresed blood flow results into decreased temp
pulse pressure
difference between systolic and diastolic
ancle brachial index ABI
used to asses vasculat status of lower extremities. -cuff ppalced on lower eztremitiesthis is then divieded by brachial plusenormal values are 1.0 or higher0.8 moderate vasular disease0.5 severe vascular disease
JVP
normal 3-10 cm
s1 caused by closure of mitral valve and tricuspid valve
s2 caused by closure of aortic and pulmonary valvehigher pitched and heard at base of heart at end of ventricualr systole
s3 ventricular gllop
normal in those younger than 30
s4 atrial gallop
may be heart in pts with anemia hypertrophy MI plulmonary embloi may be heart with advancing age because of stifening ventricles
MI cardiact markers
troponincreatine kinase MBmyoglobin
tropnin
myocardial muscle protein realeased into blood with injury to heart muscle -have a wide diagnostit time range making them useful to pts who present several hours after the onset of chest pain Troponin levels increase about 3 hours after the onset of MI.BEST Troponin I levels rise rapidly and are detectable within 1 hour of myocardial injury.
creatine kinase ck
enzyme in heart brain skeletal muscle CK in blood indicated tissue necrosis of injury early diagnosit cmarket for MISince it has a short duration, it cannot be used for late diagnosis of acute Mrfalls after 3 days
myoglobin
is not cardiact specific thats why its not used a lot. one of the earliest markers detected first to elevate
homocystine
amino acid produced when protein breaks down CAD
c reactive protein
for inflamation
hypomagensemia
prolonged QT intervaldysrythmias
angiography arteriography
invasieve with flouroscopy and dye when there is an arterial obstruction, narrowing or anneurism
cardiact cath
most invasive but most definitiveekeep pt at bedrst 2-6 hrs
IVUS intravascullar ulrasonography
sound waves, for indicating plaque
EPS electrophysiologic study
invasive where electrical conduction of heart is done to cause and evaluate dysrythmias
excerisece test ir stress test
determines functional capaccity of heart and screesna for CAD
echocardiography
ultrasound waves to asses cardicat structures and mobility of the valves
TEE transesophageal echo
to view posterior cardiact structuresunltrousound placed behind heart from esophagus to stomach
MRI
noninvasive image of heart and vessles is produced by magnetic fields and radio waves, to detemine wall thickness and chamber dialation
iodine
before dye imaging
CO
cardiac output would be 5.6 L/min for a human male and 4.9 ..
CAD
Coronary heart disease (CHD) is a narrowing of the small blood vessels that supply blood and oxygen to the heart. CHD is also called coronary artery disease.
left sided HF (congestive HF)
caused by hypertension, CAD, vale disease, decreased tissue perfusion from pulmonary congestionleads to fatigue-as it becomes severe pt may have pink frothy sputums a life threrening pulmonary edema orthopneasystolic HF- heart cant contract fullydiastolic HF- heart cant relax adequalty signs- fatiue, pulmonary congestion, diziness, confusion, SOB, oliguria OLIGURIA
right sided HF
from MI, left HF, hypertensionsedema in lower legs, rings shoes are tight signs- a krexia, ascetis, edfema, JVD, enlarged liver , decresased urine
compensatory mechanisms for HF
sympathetic nervous systemrenin angiotenin activationventricular remodelingBtype nauretic peptideendothelin
SNS
increasen cathecolamines and exciting the SNS. this increases HR
renin angiotensin
reduced blood flow to kidneys activates this and kidneys cause water and sodium retention
b nauretic peptide
promote vasodialation thought diureseis-used to diagnose HF in pts with dyspnea
endothelin
secreated by endothelial cells when they are streched
HF
more african americansreduce sodium in nutrition to 3-2g dailtwater 2L daily
microalbuminuria
earl indicator of decreaed compliance
echocargiography
for HF
ace inhibotors
first line drugs for hfcause coughwatch potassium levels 3.5-5.
loop diuretics such as lasic
removie fluid but also removie it after edema is gone
thiazide diuretics
good for older aldus to remove edema because they deacrese after emdema is gone, so no dehydration problems primary signs of hypokalmua- weakness,, slow reflexes, irregular HR
potassoim
3.5-5
ventricual assist device
placed in heart in end stage HF
sight sitting position
with legs down to decrease venous return to heart
reynauds disease
vasospasm of arteries usually unilaterely, more common in women and in ppl older than 30’-vessles constricted and blanched or cause cyanosis-may be aggrevated by coldteach pt to wear gloves socks and keep warmNo smokingAvoid exposure to coldMedicationsVasodilatorsCalcium antagonistsMuscle relaxantsSurgery: sympathectomyAmputation for gangrene
thrompophlebitis
thrombus associcated with innflamationBedrestMoist heatElevate extremityNSAIDsMotrinAspirin
phlebothrmobiss
thrmbus without inflammation
phlebitis
vein inflamation may cause DVT
signs of DVT
tenderness, edema, pain, calf dorsiflextionlocalized edema rest and elevate extremity
varicose veins
distended protruding veinsprolonged stanidng after surgery ROM hourly Elastic stockingsRestElevate legsSclerotherapy
arthrosclerosis
herdening of arterial wall and plaque formation may have weak pulse from poor circulationbruits
peripheral vascular disease
alters blood flow through arteries and veins of peripheral circulation PAD- o2 and nutrients (cells starve)PVD- pooling edema, elevate leg
PAD peripheral arterial disease
reult of systemic artherosclerosisocclusion deprives lower extremitings with o2 and nutirentscells starvestage1- asymptomatic-decreased pedal pulses, bruits, stage2- intemitent caludation- pain when walking stage3- rest pain stage 4- necrosis gangrene check for pulses and pitting edemahair loss in extremities, dry skin, thick nails, protect skin so you dont get ulcers bcuz skin is already impared wear socks and keep warm , less coffe, smoking,
colateral circulation
new vessels form to help out to perfuse blood
surgical for PAD
arterial revascularization
PVD peripheral venous disease
when veins not opening properly blood pooling, edema more chance of dvt no oral contrecaptives , exercise legs, minerals and fat from bones from surgery may leak into blood and give more change for thrombus formation diagnosed by mri, venous duplex untrsonography- how blood flows throught veins, d dimer- give heapin coumadin, elevate leg
CAD
when arteries that supply blood to the myocardium become diseased
ischemia
insufficient oxygen
NSTEMI
in womenhave st and t wave changesstemi- have st elevation
when all three laywers are involved in an MI
trasnmiral MI
fibrinolytic therapy
Fibrinolytic therapy should be started within 6 hours of the onset of the MI, so the time at which the chest pain started is a major determinant of the appropriateness of this treatmentThe change in level of consciousness indicates that the patient may be experiencing intracranial bleeding, a possible complication of fibrinolytic therapy.
soidum
Milk and yogurt naturally contain a significant amount of sodium, and intake of these should be limited for patients on a diet that limits sodium to 2000 mg daily.
reducing preload
Rationale: Positioning the patient in a high-Fowler’s position with the legs dependent will reduce preload by decreasing venous return to the right atrium.
digoxin
Hypokalemia potentiates the actions of digoxin and increases the risk for digoxin toxicity, which can cause life-threatening dysrhythmias3.5-5
pulmonary embolism
pink frothy sputum
PTT
Normal PTT range 22-30Normal PTT for pt on Coumadin? multiply normal range by 1.5-2.5; so it is 45-70
HF
heart cant act as a pumpgoal is to increase cardiact output fluid restriction, bedrest, HOB elevated, low sodium
give morphine in MI
Morphine is administered because it decreases myocardial oxygen demand. first intervention in MI- give o2
electrocargiogram
he ECG is the quickest, most accurate, and most widely used tool to determine the location of myocardial infarction. Cardiac enzymes are used to diagnose MI but can’t determine the location. An echocardiogram is used most widely to view myocardial wall function after an MI has been diagnosed. Cardiac catheterization is an invasive study for determining coronary artery disease and may also indicate the location of myocardial damage, but the study may not be performed immediately.
kidneys do:
regulate BP and acid based balanceproduce erythropoetin for RBC synthesisconvert vitamin D into active formproduce prostaglandins
renin
hormone that regulates blood flow and GFR.renin is secreated when DCT cells sense changes in volume is low. renin then converts into angiotension 1 which then produces aldosterone.aldosterone then increases reabsorbtion of water and sodium into blood and promotes excretion of potassium.
GFR
electrolytes and other small particles are filtered in GFR.180 L each day125 ml each minutes
when afferent arteriole is constricted or the efferent arteriole is dialated
pressure in the GFR falls and filtration decreases
when the afferent arteriole is dialated or the efferent arteriole is constricted
pressure in the GFR rises and filtration increases
when mean BP drops below 70mm
GFR can not compensate and GFR stops
antidiuretic homrone ADH or casopressin
alows for reabsorbtion of water and sodiumalso causes arteriole constrictionaldosterone is an antidiuretic hormone
pts at risk for calculi if they ingest too much
protein or have poor fluid intake
contraindicated medications in kidey pts
antibiotics-may cause kideny injurycontrast dyes- may cause kidney injurydietary supplements or steroids for muslce building with synthetic creatine damages kidneysNSAIDS & tylenol long term can damage kidneys
uremia
buildup of nitrogenous waste in the blood as a result of kidney failure. s/s - anorexia, nausea, vomiting, muscle cramps, pruriturs, fatigue
kidney damage causes edema in
pedal or pretibial (shin), sacral area and around the eyes
normal urine output per day
1-3 L1500-2000ml
serum creatinine
produced when protein in the muslce breaks down levels higher in men because they have more muslce mass-createnine levels do not increase until 50% of kidnets have lost their function 0.5-1.1 mg.dl
BUN
measures the kidney excreation of urea nitrogen which is a byproduct of protein breakdown in the liver. -rapid cell distruction, infection, streoid therapy may increase BUN levelsincrase may indicate reanal disease, dehydration, high potassium diet, stressdecrease may indicate fluid excess or severe hepatic damage10-20 mmol.L
blood osmolarity
indicator of hydration when blood osmolarity is decreased ADH is inhibited and as a result water is excreated not retained which then increases blood osmolarity water reabsorbed- osmolarity decreaseswater secreated- osmolarity increases
increase in ADH
happends in times of stress, surgery, anesthesia, or drugs such as morphoine body retains water
gravity
increase gravity- dehydration and too much ADHas a result water is retained and the urine that is produced is more concentrateddecrease gravity- increased fluid intake, diabetes insipidus and increased in diuretic drugs that make urine less concentrated 1.005-1.030
pH
7 alkaloticurine specimes becaomse more acidic if left unrefrigerated for more than one hours4.6-8
glucose
filtered by glomerulus and reabsorbed in the nephron, when BG rises above 220, some glucose is present in urine
ketone bodies
incomplete metabolism of fatty acids, -produced when fat is used instead of glucose for celular energy
proteins
proteinurea doesnt indicate kidney disease, it may also be baceuse of infection
microalbinurea
presence of albumin in urine measured by dipstick between 2-20hihg levels may indicate early kidney disease especialy in pts with diabetes
leukoesterase
made of WBCindicated UTI
nitrates
indicates UTI
creatinine clerane
best indicator for kidney functionmeasures GFR rate-compares urine creatinine levles with blood createnine levels so both samples must be colected 80-125
kidney assesment
bruising in flank region near costovertebral angle; listen for bruit over each renal artery, palpate for kidney masses in flank region, left kidney deeper and cannot be palpated; CVA tenderness (kidney inflammation/infection)
kidney assesment
(uremic encephalopathy – lethargy to seizures to coma; sensory changes in pattern of glove and stocking pattern over hands and feet; weakness of upper and lower limbs (uremic neuropathy)CV manifestations- HTN, heart failure, pulm edema, extra heart sounds (S3)Resp manifestations – uremic halitosis- bad breath because of high urimic in breath , SOB; tachypnea, and hyperpnea (increased depth of breathing) occur with met acidosis, Kussmaul respiration; uremic lung (=pneumonitis – thick sputum, reduced coughing, tachypnea)Hemotologic – anemia (pallor, wekness, SOB, lethargy, fatigue, dizziness) bleeding; GI – foul breath, mouth ulceration, stool for OB; skeletal – osteodystrophy, fractures; urine manifestations – urine changes, protein or blood in urine; skin – yellowish coloration pigment in skin, uremic frost – urea crystals on face, eyebrows, axilla, groin of pts with advanced uremic syndrome
changes in kidney when agiing
Kidney changes in agingKidney loses cortical tissue (due to reduce blood flow) and gets smaller by 80 years of age; glomerular and tubular lining thicken, number of glomeruli and surface areas decrease; tubule length decrease; reduction in kidney mass and blood flow, decreased renin, aldosterone and activation of vitamin D – all these changes reduce ability to filter blood and excrete waste productsGFR decrease after 45 years of age, by age 65 it is half rate of young adult, this is more rapid in pts with diabetes, HTN, or heart failure; elderly greater risk for fluid overload, and reduced drug clearance, also more urgency and nocturnal polyuria (due to decreased ability to concentrate urine), also hypernatremia and increased risk of dehydration
KUB (kidney ureter bladder x ray)
no preparation, just xray -shows stones, strictures, calcifications,, shape and size
IVP intravenous pylepgraphy
bowel preparation- to ensure that urinary structures are not abstucted by feces- dye is IV injected, it circulates into kidneys to be fileted and excreated in urine, xrays are taken at times of injection -gives info aboutsize shape, filling rate,
if pt has alergy to contrast dye
drugs such as steroids or antihistamines can be given before procedures
pts taking metforming
are at risk for lactic acidosis when getting IV dye -it should be d.c 24 hrs before any procedurepts at risk for kidney injury from IV dye need to have excess fluid to wash out dye -diuretics may be given to increase dye excreation -pts with asthma have been shown to be at increased risk for IV dye alergy -ask pts for alergy to shellfish and eggs, milk and chocolate
computed tomography CT scan
3D info on kidneys, ureters, bladder-shows tumors, cysts, and other mases or obstructions
cystography or cystourethrpgraphy
a urinary cather is placed in pt and dye is instilled to show visibility of lower urinary tract. -dye injected in bladded by placing a catheter then xrays are taken, (xrays during voiding) -VCUG obtained obtained to determine if urine flows back into the ureter
renography (kidney scan)
to provide info about blood flow to kidneys -no danger from small amount of radiactive material present in agent. -radiactive agent is injected IV, then it is absorbed by the kidneys and gives of an radioactive emission which produce an image. -to PROVIDE INFO ABOUT BLOOD FLOW OR GFR-in some cases CAPOTEN (antihypertensive) is given to change blood flow to kidneys. asses for hypotensions
ultrasonography
test requires full bladder, ask pt to drink water to fill up bladder, sound waves produce images of the organs -to asses size, thickness, calices, obstruction, tumor, cystsin prone postions
renal arteriography angiography
dye enters renal blood vessels ang generates an image to determine blood vessle size and abnormalities,
cystoscopy or cystourethroscopy
operative procedures for diagnostic or treatment reasons -to identify bladder (cystoscopy) or urethral trauma (cystourethroscopy)may be used to remove bladder tumors or enlarged prostate gland, also for tumors, fistulas or diverticuli
retrograde procedures
going against normal flow of urine, instils dye into lower urinary tract,dye doesnt enter bloodstream therefor pt is not at risk for kidney injury or alergic response-placement of custoscope is placed in ureters and dye is instilled then xrays are takenretrograde with cystoscopy
CMG cystometrpgraphy
to determine how well bladder wall muslce functions and how well streches -for bladder capacity, baldder pressure, and voiding reflexes, -catheter placed, cystometer attaced to cather inserts fluid into bladder, then bladder pressure is recorded.-after pt asked to void and PVR recorded
urine stream testing
for pelvic muslcle strenth and incontinence
contrast-induced kidney failure
-greatest risk in older or dehydrated pt with renal insufficienc
respirations in kindey pts
Patients with kidney failure are anemic because they cannot produce the hormone erythropoietin. A high oxygen saturation in an anemic patient who is showing signs of respiratory distress may still be hypoxemic. Administering oxygen is necessary.
warning signals associated with lung cancer
hoarsnesscoughblood sputum (hemoptysis)dyspneachest painclubbing of fingerswheezing
CKD comonly caused by
hypertension and diabetes
for CKD% of nephrons
90-95% of nephrons must be lost before kidney dysfucton is obvousbecause the healthy nephrons become larger and work harder, the GFR is effective untill up to 90% is lost
for AKD % of nephrons
50% of nephrons must be lost before kidney dysfunction os obvious
AKD caused by
reduced blood flowtoxinsischemiainfectionsobstruction
when there is an reduction in blood flow to the kidneys (hypoperfusion) which happens in AKD
the kidneys compensate by constricting renal blood vessels, activating the renin pathways and secreating ADH. this increases blood vlume and increases kidney perfusion. -however the same response lowers urine output resulting in loiguria (less than 400/day) and azotemia (buildup of waste in body)
types of AKI
prerenal azotemiaintrarenal AKIpostrenal azotemia
prerenal azotemia
caused by poor blood flow to kidneys-cause hypovolemic shock and HFearly AKI often reversible by correcting blood volume, increasing BP and improving cardiac output(hypotension, tachycardia, HF, PE, shock, lethdary, oliguria) tachycardia, SOB, crackle)hyperkalemia and hypocalcemia
intrarenal AKI (AKA oliguric AKI)
caused by infection, drugs, tumors, inflamation
postrenal azotemia
caused by obstruction (uremia, anuria, lethargy,)trouble with urine stream
to promote healthy kidney function
urge pts to avoid dehydration, by drinking at leasr 2-3 L or 1-2 quarts ot fluid daily. this is especialy important for atheletes or ppl who do streneous excercise.
OLIGURIC phases of kidney injury
onset phase- gradual increase in nitrogen waste and BUN and createnineoliguirc phase- (low urine output of 100-400ml/day) electrolytes are increased because they are not excreated out, causes hypertension, hyperkalemia, hypermagnesemia, hyperphosphotemia BUT HYPOcalcemia, high BUN and creatinene diuretic phase- urine flow icnreases up to 10L/day, low electryoltes in the body because they are excreated out. causes hypotension, low BUN and createnine, recovery phase- pts gets to normal level
drugs for good kidney function
cardiact glycosides such as digoxin- used when HF induces kidney injury, improves contraction increaing blood flow to kidneys. vitamins and minerals and iron- when pt getting dialysis you have to supplement vit. that are removed from the blood. take frugs after dialysis, take iron with meals, iron causes constipation so take stool softners. eportin alfa- to increase RBC and prevent anemia
in pts with diabetes
IV fat imulsions can provide a nonproteins source of caories, in uremic pts fat emulsions are used in place of glucose to avoid problems with excessive sugars.
hemodyalisis for several weeks
usualy placed on subclavian or internal jugular vein
hemodyalysis for short term
placed in femoral vein
peritoneal dialysis
not applicable for those on ventilation because if increases the abdominal distention
diet in kidney pts
limit foods high in potassium, phosphorous, sodium and protein and may need to restrict fluid intake
uremia
Azotemia is another word that refers to high levels of urea, high urea BUN and createnine in blood s/s- metalic taste, anorexia, n/v, uremic frost, itching, fatigue, hiccups, crapms,
CKD
first stage- slightly normal GFR of >90, no obvious kidney damage but with reduced renal reserve but WITHOUT buildup of waste in body mild stage- GFR of 60-89, slight elevation of waste in body, increased output of urine may happen here which can cause dehydration, moderate stage- GFR of 30-59, restrict fluid, electrolytes and proteins as neededsevere stage- <15 GFR, excessive wastes in blood, Renal replacement therapy or transplant
as CKD porgresses
ability to produce dulute urine is reduced, resulting in isosthenuria (fixed osmolarity ) as kidney function declines BUN increases and urine output decreases putting pts in fluid overload
calculating GFR
serum createnine level, gender, age, race, body size
eary and late stages of CKD
early stage- pt is hyponatremia becuase there are few nephrones to reabsorb sodium, later stage-hypernatremia, excreation of sodium is reduced as urine production increases, (ANY INCREASE IN POTASIUM LOAD DURING THE LATER STAGE CAN LEAD TO HYPERKALEMIA)
Kussmaul respirations
as CKD worses acid retention increases and an increased respiration is needed to keep blood pH levels normal. rate and depth of breathing is increased called Kussmaul reespirations. -these pts need alkali replacement to conteract the acidosis in their bodyOxygen will not help his respirations and could make his acidosis worse.”
Renal osteodystrophy
is thought to be the result of hyperparathyroidism secondary to hyperphosphatemia combined with hypocalcaemia, both of which are due to decreased excretion of phosphate by the damaged kidney. Low activated vitamin D3 levels are a result of the damaged kidneys’ inability to convert vitamin D3 into its active form, calcitriol, and result in further hypocalcaemia.
hyperlipidemia
occur in CKD, this pts pts at risk for CAD
uremic cardiomyopathy
increased uremia effects the myocardium
stomatitis and halitosis
mouth contains urease which breaks down urea in ammonia, the amonia generated by this reaction causes stomatitis and halitosis
urge pts with diabetes
to have yearly testing for microalbuminurea
uremic encepalohathy
leathargy, seizures, coma,
uremic neurophathy
weakenss in upper and lower extremities
tachypnea and hyperpnea
increased respirations and increased depthy of breathing because of resp acidosis
uremic frost
layer of urea crystals from evaporated sweat may appear in face, eyebrows, froin or axilla.
use of furosemide with kidney damage
may cause ototoxticity so IV doeses give carefuly
calcium channel blockers
may improve GFR and blood flow with kidney
CKD early and hypocalcemia
Early CKD – reduced phosphate excretion, leading to hypocalcemia; parathyroid hormone then is released to get calcium from bones – leading to bone density loss ( extra calcium needed to balance plasma phosphate level); in severe CKD, even less calcitriol available leading to even less calcium level ( called renal osteodystrophy – low calcium and high phosphorus – cause bone pain, spinal sclerosis, fx, bone density loss, osteomalacia and tooth calcium loss)
Metastatic calcifications –
crystals from high plasma level of calcium-phosphate (if exceed 70 mg/dL) lodge in kidneys, heart, blood vessels, brain etc.; pt c/o increased skin itching with this
hemodylasiss
heparin most commonly used to prevent clots; vascular access – AV fistula (connect artery to vein in radial or brachial or cephalic vein, need to be matured before usage) or AV graft (when AV fistula doesn’t develop or its use is limited, commonly used in older adults) – assess for adequate circulation, check distal pulses and capillary refill, check for bruit and thrill, HD complication – thrombosis or clotting of AV access, infections, aneurysm in fistula, ischemia can occur range from cold and numb fingers to gangrene; dialysis disequilibrium syndrome may occur during or after HD, due to rapid decrease in fluid volume and BUN levels, can cause cerebral edema and increased intracranial pressure with neuro s/s – HA, N/V, restlessness, decreased level of consciousness, seizures, coma or death; infectious diseases – hep B and C may occur but the incidence has decreased due to increased use of erythropoietin ; HIV
mahurak - short term HD
perm cath- long term HD
peritoneal dialysis
Involves siliconized rubber catheter placed into abdominal cavity for infusion of dialysatePeritoneal PD complication – peritonitis s/s – cloudy or opaque effluent is earliest sign of peritonitis; pain; exit site and tunnel infections, poor dialysate flow usually related to constipation; dialysate leakage – occur more often with obese pts, DM, older adults and long term steroid therapy; bleeding, bowel perforation esp when catheter first placed
AV graft
A positive bruit and thrill indicate good blood flow through the graft. A dialysis access should only be used for dialysis. IVs should not be started, nor should blood pressure be taken in the same arm where the access is located. Elevation of the arm will not ensure function of the graft.
anithypertensive meds
Vasoactive drugs such as beta blockers like atenolol can cause hypotension during dialysis and are usually held until after treatment.
temp after dialysis
The patient’s temperature is elevated after dialysis because the dialysis machine warms the blood slightly. Weight and blood pressure should be decreased because excess fluid is removed during dialysis. Heparin is required during hemodialysis and increases clotting time. All invasive procedures should be avoided for 4 to 6 hours after dialysis.
restrictions in diet
Sodium is restricted because it causes retention of fluids. Potassium is restricted to prevent dangerous cardiac dysrhythmias. Vitamins must be supplemented, not restricted. There is an inverse relationship between phosphorus and calcium; when phosphorus is high, calcium is low and should not be restricted
diabetes in pts with CKD
Rationale: The patient with diabetes who has chronic kidney disease (CKD) often requires reduced doses of insulin and/or antidiabetic drugs because the failing kidneys do not excrete or metabolize these drugs well. Thus the drugs are effective longer, increasing the risk for hypoglycemia.
check function of fistula or graft
asses circulation in arm where AV is , check distal pulses and cap refil, DONT TAKE BP or IV IN THE ARMdont use AV or GRAFT to give iv fluids, only for dialysis
PD
cant be done if there is scaring in adominal area
The client with chronic kidney disease presents with bradycardia, prolonged PR interval, and diminished bowel sounds. For which of these should the nurse monitor?
Hyperkalemia may be present; electrocardiographic changes and paralytic ileus may develop.
Which teaching by the nurse will help the client prevent renal osteodystrophy?
Avoiding peas, nuts, and legumes CorrectCorrect: Kidney failure causes hyperphosphatemia; this client must restrict phosphorus-containing foods such as beans, peas, nuts (peanut butter), and legumes.
uremia and pericarditis
The client with uremia is prone to pericarditis; symptoms include inspiratory chest pain, low-grade fever, and ST segment elevation.
dyspenia and fluid
Dyspnea is a sign of fluid overload and possible pulmonary edema; the nurse assists the client in correlating symptoms of fluid overload with nonadherence to fluid restriction.
ACE INHIBITORS
(ACE) inhibitors appear to be the most effective drugs to slow the progression of kidney failure.
digoxin toxticity
Anorexia, nausea, and vomiting are symptoms of digoxin toxicity.
Which of the following represents a positive response to administration of erythropoietin
Treatment of anemia with erythropoietin will result in increased (H&H) and decreased shortness of breath (SOB) and fatigue.
for AV and fistuals
A bruit or swishing sound should be present, indicating patency of the fistula.Correct: A thrill or buzzing sensation upon palpation should be present, indicating patency of the fistula.Correct: No blood pressure, venipuncture, or compression such as lying on the fistula should occur.Incorrect Feedback:Incorrect: Distal pulses and capillary refill are checked; for a forearm fistula, the radial pulse is checked. The brachial pulse is proximal.Incorrect: Elevating the arm increases venous return, possibly collapsing the fistula.
immediately report what after pd
Temperature of 101.2 CorrectCorrect: Peritonitis is the major complication of PD caused by intra-abdominal catheter site contamination; use meticulous aseptic technique when caring for PD equipment.
NOT APPLICABLE FOR KIDNEY TRASNPLANT
Long-standing pulmonary disease and chronic infection typically exclude clients from transplantation; these conditions worsen with immune suppressants required to prevent rejection.
TRASNPLANT REJECTION
: Signs and symptoms of fluid retention are symptoms of transplant rejection.Correct: Increased blood pressure is a symptom of transplant rejection.Correct: Signs and symptoms of fluid retention are symptoms of transplant rejection.Incorrect Feedback:Incorrect: Increasing BUN and creatinine are symptoms of rejection; these reflect normal values.Incorrect: Fever, not normothermia, is symptomatic of transplant rejection.
INCREASED BUN
An increase in blood urea nitrogen can be an indication of dehydration, and an increase in fluids is needed.
dehydration
sodium is INCREASED
after kidney transplant
An abrupt decrease in urine output may indicate complications such as rejection, acute tubular necrosis (ATN), thrombosis, or obstruction.Blood-tinged urine is an expected finding after kidney transplantation.incisional pain is execcteedAn increase in urine output is initially expected after kidney transplantation.
invasive breast cancer
cancer penetrates the tissue sorrounding the duct
noninvasive breast cancer
the cancer remains within the duct
noninvasive breast cancers
ductal carcinoma in situ DCISlobular carcinoma in situ LCID
DCIS
non invasive breast cancer,althought it should be treated to prevent it from forming into invasive breast cancer, it doesnt metastesize at this stage
LCIS
noninvasive breast cancer is rare and its usually identified incidently from biopsy of another problem
invasive breast cancer (infiltrating duct carcinoma)
originates from mammary ducts then grows in the epithelial cells lining these ducts. at tumor continues to grow fibrosis (replacement of normal cells with connective tissue or collages) grows around the cancer. -the fibrosis may cause a shortening of the Coopers Ligaments which causes skin dimpling (inversion of nipple) in later stages of the disease-peaou de orange- thickening and putting of breast tissue seen in later stages of cancer
inflammatory breast cancer
is a invasive breast cancer, symptomas include swelling, redness, pain-its usually not presented as a lump thats why it is cought in later stages because even mamograms cant pick it up
chemotherapy in breast cancer
may cause infertility,
rist factors for breast cancer
having BRCA gencehigh doses of ionizing radiation to the thorax (especially before 20 years old)early menarche (12)late menopause (50)nulliparity (no giving birth)first birth after 30alchoholobesityHRT hormone replacement therapyolder age jewish heritage
breast examination
1 week after menstrual period, this time hormonal influence on the breast tissue is decreased so fluid retntion and tenderness are reduced
inframmamary ridge
the area of the breast where the skin folds under the breast, this thickeked area is usually mistaken for a lump
propholaxis treatment for breast cancer
prophoylactic mastectomy (removal of one ore both breasts)oophorectomy- removal of ovariesanti estrogen therapy
ask about drugs taken
for ppl with breat cancer such ashormone substances that stimulates hormones
memography
ability to reveal preclinical lesions (masses too small to be palpated)
ultrasonograghy
clarifies finding of the memmogram , is helpful from identiying a fluid filled cyst from a solid mass
MRI
to better examine suspicious areas found from memmogram
soy
not good for woman with breast cancer
neoadjuvant therapy
chemotherapy to shrink the tumpr before the removal of it. -an advantage is to remove the tumor by lumpectomy rather than mastectomy
simple mastectomy
breast removed but lymph nodes are intaact
radical mastectomy
brest and lymph nodes removed
lumpectomy
is a surgery to remove cancer from the breast. Unlike a mastectomy, a lumpectomy removes only the tumor and a small rim (area) of the normal tissue around it. So, the breast looks as close as possible to how it did before surgery. Most often, the general shape of the breast and the nipple area are kept.it is a breast conserving surgerymargins refer to the distance between the tumor and the edge of the tissue. the desired outcome of lumpectomy is to obtain negative margins in which no cancer cells extend to the edge of the tissue.
brest cancener side
aviod BP and taking blood from that arm
drainage amount from mastectomy
when pt returns to follow up visit drainage should 25ml/day or less
positioning pt with mastectomy
HOB 30 degrees with the affected arm on a pillow. keeping the arm elevated promotes lymphatic fluid return after removal of lymph nodes and channels.
sleeping
avioid sleeping in prone postion
brachytherapy (radioactive implants)
catheters are placed near the lumpectomy cavity and they emit radioactive Mx, more convenient and shorter treatments
chemotherapy CAF
cytoxan, adriomycin, 5-FU
targeted therapy
doesnt harm normal healthy cells therefore fewer side effects
hormonal therapy
to reduce estrogen -although supression of avarian function decreases the risk for breast cancer, the drastic drop in estrogen causes menopausal symptoms The purpose of hormonal therapy is to reduce the estrogen available to breast tumors to stop or prevent their growth.
selective estrogen receptor modulator SERMS
block effects of estrgoen but do not effect ovarian functionS/s hot flashes and weight gain
aaromatase inhibitors AI
reduce estrogen levels by inhibiting aromatase enzyme
bathes after mastectomy
may take sponge baths or tub baths making sute the area with the incision stays dry. may shower after stiches, and drains removed no deordorant, parfumes, lotions on that arm
if lymph node removal was done
instruct pt to rasie arm of efected area for about 30 min each day for 6 months
lymphedema
accumulation of protein fluid in the subq tissue of the affected limb after mastectoy.is a condition of localized fluid retention and tissue swelling caused by a compromised lymphatic system, which normally returns interstitial fluid to the thoracic duct and then the bloodstream. The condition can be inherited, though it is frequently caused by cancer treatments, and by parasitic infections. Though incurable and progressive, a number of treatments can ameliorate symptoms. Tissues with lymphedema are at risk of infection.
CKD
is a condition of localized fluid retention and tissue swelling caused by a compromised lymphatic system, which normally returns interstitial fluid to the thoracic duct and then the bloodstream. The condition can be inherited, though it is frequently caused by cancer treatments, and by parasitic infections. Though incurable and progressive, a number of treatments can ameliorate symptoms. Tissues with lymphedema are at risk of infection.
increased protein intake in PD
dietary protein guidelines for peritoneal dialysis (PD) differ from those for hemodialysis because of protein loss in the dialysate. During PD, protein intake must be high enough to compensate for the losses, so the nitrogen balance is maintained. The recommended protein intake is at least 1.2 g/kg of ideal body weight per day and is increased on the basis of individual needs of the patient.
BSE
The finger pads, which are more sensitive than the fingertips, are used when palpating the breasts.
MRI for breast cancer
he American Cancer Society recommends that high-risk women (greater than 20% lifetime risk) have an MRI and mammography every year beginning at age 30.
raadiation
Typically, radiation therapy follows surgery to kill residual tumor cells. Radiation therapy plays a critical role in the therapeutic regimen and is effective treatment for almost all sites where breast cancer can metastasize. The purpose of radiation therapy is to reduce the risk for local recurrence of breast cancer.
ginger
aliveates v/n
greatest risk for prostate cancer
those men higher than 65 years oldeating high in animal fat (red meat) and eatting complex carbshaving low fiber intkaevestectomyexposure to arsenic
screening for prostate cancer
starting at age of 50 men should get prostate screening
metastastis of prostate cancer
slowest growing cancer and it metastesises in a predictable patters, in nearby lymph nodes, lungs, bones and liver
s/s of prostate cancer
dificulty starting urinationhematurianocturia (urination at night)bone pain (s/s of advanced prostate cancer)pain during intercourse/ejaculationweight loss
dry climax
may occur if prostate is removed because it holds semen
PSA
glycoprotein produced by the prostate, it is used as a screening test for prostate cancernormal range should be <2.5, although in older adults it can go up to 6.5african americans have higher normal values of PSAincreased PSA after prostate surgery means the disease has reacurred
EPCA-2 early prostate cancer antigen
serum marker for prostate cancer, it can detect changes in the prostate gland early and its a very sensitive test. it may also eliminate the need to perform a biopsy of prostate tissue
TURS (trasnrectral ultrasound)
inserts a small probe in rectum and obtains a view of prostate, if cancer is suspected a biopsy is done
men with bone metastasis in prostate cancer
have elevated serum alkaline phosphatase levels
TURP
if obstruction occurs, turp is done
bilateral orchiectomy
removal of both testes, palliative surgery to slow the spread of cancer by removing the main source of testosterone.
LRP laproscopic radial prostatectomy
pts who quality for LRP need to have a PSA less than 10 and have had no abdominal surgery previouslyand no previous homrone therapy
open radial prostatectomy
surgeon removes entire prostate gland -the pt may expreience erectile dysfunction after the surgery and can be reversible but if not can take viagra
urge incontinece
with ipen radical prostatectomy, urinary sphinxters lie next to the prostate gland so they are often damaged during surgery, -teach pt kegal excercises such as tightening the perineal muscles for 3-5 sec like voiding then releaseing, brearing down like BM them realeasing.
EBRT external beam radiation therapy
intensity modulated radiation therapy- provides very hight dose to the prostate-can be used to relieve pain from bone metastasis -may cause ED after treamtnet is compleated-acute radiation cystitis-may occurs causing persistant pain and hematuria. avoid cafeine, drink plenty of fluids
radiation proctitis
rectal mucosa inflamation may develop from radiation, hematuria and cramping may occur limit spicy foods, caffeine, and dairy
low dose bradytherapy (internal radiation)
low dose radiation seeds directly at prosatate gland.
hormone therapy
because mose prostate tumors are hormone dependant, pts with tumors may be managed with androgen depravation,-Lutenizing hormone releasing hormone LH-RH and anti androgens are used.
anti androgen drugs
AKA androgen deprivation therapy blocks the bodys ability to use the available androgens-used to treat metastatic diseases/s- hot flasesh, low libido, gynocomastia
activity after prostate surgery
dont lift more than 15 lb for up to 6 weeksmaintain upright position, dont bend or flexno vigorous exercise dont strain to deficate, give stool softneser if taking opioids to avioid constipationshower not tub baths
The client with prostate cancer asks why he must have surgery instead of radiation, even if it is the least invasive type. What is the nurse’s best response?
“Surgery is the most common intervention to cure the disease.” CorrectCorrect: Because some localized prostate cancers are resistant to radiation, surgery is the most common intervention for a cure.
hich assessment finding causes the nurse to suspect that a client may have testicular cancer?
A painless lump or swelling in the testicles is the most common manifestation of testicular cancer
drugs after turp
antispasmodic drugs can be administered to decrease the bladder spasms that may occur after TURP.
After returning from transurethral resection of the prostate, the client’s urine in the continuous bladder irrigation system is burgundy. Which client need does the nurse anticipate after the surgeon sees the client?
The surgeon may apply traction on the catheter for a few hours to control the venous bleeding. Traction on the catheter is uncomfortable and increases the risk for bladder spasms. Analgesics or antispasmodics are usually prescribed.
Which method is a common complementary and alternative therapy for benign prostatic hyperplasia (BPH)?
Serona relens (Saw palmetto extract) (a natural herb) is often used by men with early to moderate BPH. They believe that this agent relieves their symptoms and prefer this treatment over prescription drugs or surgery. It should be noted that studies on its effectiveness of this herb have not shown that it is effective.
priapsim
This client has symptoms of priapism, which is considered a urologic emergency because the circulation to the penis may be compromised and the client may not be able to void with an erect penis.
BPH
Benign prostatic hyperplasia (BPH) is an enlarged prostate gland camera.gif. The prostate gland surrounds the urethra, the tube that carries urine from the bladder out of the body. As the prostate gets bigger, it may squeeze or partly block the urethra. This often causes problems with urinating.
low WBC in tumors
tumor cells enter the bone marrow and reduce the production of healthy WBC which is needed for normal immune function, -when tumor invades bone marrow it also causes anemia by decreasing RBC
diet in abdominal tumors
high in proteins and carms to maintain weight- tumorts in abdomen may reduce ability to absorb nutrients and elimiate waste
bone metastasis causes:
pain, fractures, spinal cord compression, hyprecalcemia
local radiation
radiation at only localised part of tumor, hair loss ONLY at the area being treated not alopecia
cells damaged by radiation
ether die or are unable to divide
gamma rays
mostly used for radiation therapy bcuz of their ability to deeply penetrate tissues
beta rays
weaker and must be placed very close
alpha rays
not used for cancer, very weak
radiation therapy two ways:
teletherapybrachytherapy
teletherapy
radiation delivered from a source outside the pt, bcuz source is external pt is not radioactive to others
brachytherapy
short or close therapy, pt is radioactive and hazerdous to others.
s/e of radiation therapy
fatigue and alterations in tastedry skin and break down -skin exposure risks up to 1 yr after radiation therapy
chemotherapy
treamtnet of cancer with chemical agents
alkalyting agents
make two DNA strands bing tightly which inhibits cell division
antimebolites
are fake metabolites that cannot function as proper metabolites, cells pick them up but their presence impairs cell division
antimitotic agents
interfere with action of microtubules that interefere with cell disivison
antitumor antibiotics
damage the cells DNA and inhibit DNA snythesis
intrathecal route drugs
delivers drugs into spinal canal
intraventricular route
delivers drugs into ventricels of brain
intraperitoneal route
delivers drugs within peritoneal cavity
intra-arterial route
for doses localy, used mostly for bone cancers
small amount of extravasation
such as <0.5mL can be resolved
s/e of chemotherapy
hemoragic cystitis, cardiact muscle damage, losss of bone density, anemia, neutropenia (low WBC leading to infectiion) alopecia, mucositis , thrombocytopenia (bleeding)
decreased RBC or erythrocytes causes
hypoxia, fatigue, high tendency to bleed
erythropoetin drugs
increase RBC in anemic cancer ptss/e of these drugs include hypertension, blood clots, stroke, heart attack
normal hematocrit
Adult males: 42% to 54%Adult women: 38% to 46%
ice cap
during or few hours after chemo reduces exposure of hair folicles to chemo resulting in less hair loss
chemotherapy induced neuropathy
loss of sensory and motor function of peripheral nerves -loss of sensation of hands and feet, neuropathic pain, orthostatic hypotension, taste discremination, constipation
s/e of hormonal manipulation
chest or facial hair may deveop in women, menstuations stop, FLUID retention, HYPERCALCEMIA, liver dysfunction, men become womanly with breasts, breast tenderness, testicular and penile atrophy, for men face and skin gets smoother
photodynamic therapy
laser light to destroy cancer cells-pt has sensitivity to light up to 12 weeks after radiation- drink water to avoid DEHYDRATION-SEVERE PHOTOSENSITIVITY
immunotherapy (biological response modifiers)
modify the pts bilogic response to tumor cells. the BRMs used as cancer therapy are cytokines which wre small protein hormones made by WBC. -some cytokines enhance immune function which plats an important role in cancer prevention
interlukins
BRMa group of 37 known substances the body makes to help regulate inflammation. -chanrge up the immune system and attack the cancer cellss/e severe inflamation, fluid SHIFT with widespread EDEMA, fever, chillds, flu like,
interferons
slow tumor cell divisionstimulate NK cellsmake cancer cells normals/e- peripheral neuropathyskin itching, dryness
THALOMID reduces TAGTAF tumor angiogenesis factor
taf IS NEEDED TO BRING BLOOD SUPPLY TO THE TUMOR. when it is reduced cancer cells die
cytoprotectats
protect healthy cells from extravasation
sepsis causes DIC (disseminated intravascular coagulation)
theres clotting and bleeding at the same time. -clots block blood flow to organs, dyspnea, tachycardia, bowel necrosisWATCH FOR SEPSIS AND ANTI INFECTIONwhen sepsis is present antibiotic therapy is initiated
SIADH (syndrome of innaporpriate ADH)
fluid overload because there is an increase in water retention , diluting the sodium levels HYPONATREMIA-muslce cramps, loss of appetitie, fatige -most comonly found in carcinoma of the lung (fluid restriction and give sodium) -DECLOMYCIN opposed ADH
SCC spinal cord conpression
when tumor directly enteers the spinal cord -causes back pain, leg or arm numbness, tingling in hands or feet, inablility to distingluish hot or cold, -treatment is often high dose of corticosteroids to reduce swelling around spinal cord to relieve symptoms
HYPERCALCEMIA
occurs often in bone metastasis, calcium from bones travels in the body-fatigue, loss of appetitie, n/v, increased urine, constipation,-paralytic ileus, dehydration, deep tendon reflexes-high change of fracture or bone pain-oral hydration to water down the high calcium
SVC superior vena cava syndrome
when SVC is compressed by tumor -s/s blockage of venous return from head, neck and upper trunk-when pt raises from nights sleep and tehre edema to face, around the eyes, tightness around shirt and colar-engorged blood vessles and erythema in upper body
tumos lysis syndrome
when tumor rapidly destroyed theres an increase in waste products and potassium and urea in the blood, urea may cause kindey damage
metastasis can be:
bloodborne or lymphatic
hematologic cancer
arise from blood cell-forming tissues (ie. Lymphomas and leukemias)
solid cancer
develop from specific tissues (ie. Breast, lung)
tumor grading
classifies cellular aspects of the cancer. Describes how aggressive a tumor is based on cellular characteristics.is a measure of the cell appearance in tumors and other neoplasms.
Staging—
classifies the exact location of the cancer and its degree of metastasis at diagnosis(degree of which cancer has spread) TNM (tumor, node,metastasis)
Ploidy
is the number of sets of chromosomes in the nucleus of a cell. Normally a gamete (sperm or egg) carries a full set of chromosomes that includes a single copy of each chromosome, as aneuploidy generally leads to severe genetic disease in the offspring.-calssifies tumor cells as normal of abnormal
dubling time
the amount of time it takes for the tumor to double in size
mitotic index
the percentage of dividing cells in the tumor , show haw fast tumor is growing
personal factors
immuneage genetic
chemical carcinogenis
exposure to hcemical such as tabacco, alchohol
viral carcinogenesis
HEP B
physical carcinogenesis
DNA danage from physical changes such as with radiation
primary- preventing
secondary - screeiningtertiary- delaing after crisis
radiation therapy s/e
taste changefatiguexerostomeia- dry mouth do not remove marking
bone marrow supression
Bone marrow suppression causes anemia, leukopenia, and thrombocytopenia
platelets
150,000 - 400,000
hemoglobin
Male: 13.8 - 17.2 g/dLFemale: 12 - 15.6 g/dL43 - 212 mg/dL
hematocrit
Male: 41 - 50 %Female: 35 - 46%
symptoms of neutropenea
Symptoms of neutropenia include low neutrophil count, fever, and signs and symptoms of infection; the student should be corrected.
stuporous
one is arousable only with vigorous or painful stimulation
remote or long term memory
ask Bday, school atended
immediate new memory
give pt two or three unrelated words and ask him to repeat
recall rescent memory
recent memory of hospital stay, diagnoses etc
attention
give a series of numbers
assesment of sensory functions
done for pts with problems affecting the spinal cord, pain and light touch are the most commonly assesed.
touch discrimination
pt closes eyes and nurse touches pt with a finger and asks the pt to point to the area touched
proprioception
position sense
cereblar motor or brainstem injury assesment
ask pt to close eyes and hold arms perpendicular to the body with palms up for 15-30 sec . if there is a cereblar injury the arms with the weak side will start to turp called pronator drift.
babinski sign
abnormal for anyone older than 2yrs old. and represents presence of a CNS disease. -abnormal relfex, can also occur with drug and alchohol intoxication, after a seizure or in MS or liver disease
hypocalcemia
hyperactive relfexes
hypercalcemia
hypoactive reflexes
clonus
sudden brief jerking muslce spasm seen is seizures
glasgow coma scale
good 15 bad 3 tests eye opening, motor responses, verbal resonse.
decortication
abnormal posturing seen in pts with lesions that interrupt the spinal pathway arms internal rotation (like holdning a teddy bear)feet plantar flextion
deccerebration
abnormal posturing with pronation of arms and plantation flextion of legs seen in brainstem dysfunction
cerebral angiography
to detect blocages in the arteries or beins in the brain and head and neck . with contrast medium
CT scan
scross sectional slices of pictures that give a 3D of brain and spinal cord. for bone, soft tissue, tumors, CT angiography- with dye to visualuze blocages or narrowing vessles.
xenon computed tomography
evaluates blood flow to brain and tissues
MRI
produces images that are better than a CT scan. to determine abnormal anatomy MRI angiography- with IV dye to visualize anurisms, blocages, not for ppl with tattos with lead
PET scan
provides info on the function of the brain (glucose, oxygenation and blood flow)
electromyography EMG
to identify nerve and muscle disorderes and spinal cord disease
electrocephalography EEG
for electrical activity of brain, with electrodes
lumbar puncture
inserting a needle into the spine to obtain CSF, for check for blocages or inject stuffpt stays in a fetal side lying positon
Parkinsons disease PD- progressive not autoimmune IN CNS
progressive neurodegenerative disease with RIGIDIDTY, BRADYKENISIA(slow movement) or AKENISIA (no movement)ACh transmits exitatory messages in basal ganglia, DOPAMINE inhibits messages in basal ganglia. -degeneration of substantia nigra leads to decrease in dopamine which controls voluntary movement. -also reduces sympathetic nervous system on the heart and blood vessles which results in orthostatic hypotension usually seen in PD.
rigidity in PD
cogwheel- interuptions in muslce movementplastic- mild restrictive movementlead pipe- total restriction to movement
in PD
masklike facies- eyes staring, dificulty chewing, slurred words, hesitancy speaking, slow motility causes difficulty urinating, CSF fluid may show decarese in dopamine leves, MRI shows degeneration of substantia nagra
S/S parskisons
pill rolling motion, rigidity, mask like face, no expresions, slurred speach, balance problems, freezing movements, tremors, shuffleling gaits. -as pts writes they writing gets progressively smaller, to diagnose parkinsons
what to do to help parkinsons
exercise- releases dopamineactive ROMantioxidants- slow progression of turning off dopamine
multiple sclerosis MS- IN CNS
AUTOIMMUNE DISEASE that attacts the mylein sheath and conduction pathway of CNS-inflammaation and patchy ares of plaque in white matter of the CNS, mylein sheath is demylenated. -CT scan shows plaque-Spinal tap shows immunoglobulins in CSF, body is making a immune response -doesnt get progressively worse, but it has remissions and exacerbationswoman 2X more than man, usually in young ppl
Mylein responsible for
inflammatory response that blocks transmission of impulses between brain and spinal cord
s/e of Multiple scleroses
diplopia (double vision)scotomas (changes in perpheral vision)nystagmus(inflountary eye movements)lose balancefelxor spasms may awaken pt from sleep fatigue, stifness+ BABINSKYnumbness tinglingchronic fatigue- watch for sexual dysfunction
multiple sclroses
autoimmune, mylein sheath
parkinsons
progressive, substantia nigra, low dopamine
ALS
loss of lower motor neurons found in spinal cord and brain stem
mysethenia gravis MG- PNS
autoimmue, body attacts autoimmuneACh receptors-ACh muscle waekness
ALS or leu gherigs disease
adult onset of upper and lower motor neuron disease, PROGRESSIVE WEAKNESS & MUSCLE WASTING
ALS-PNS
adult onset of upper and lower motor neuron disease, PROGRESSIVE WEAKNESS & MUSCLE WASTING, prgressive wakness and muslce wasting, death within 3 yrs of disease more common in men -neuron stiffness-paralysis,sensory intact- can feel pain, but cant move
s/e of ALS
Dysphagiadysarthia (slurred speach)droolingmuscle wasting-respiratory compromise, cant swallow, pt requires respiratory support faciculation(facial twiching)
MG myasthenia gravis- autoimmune PNS
autoimmue, body attacts autoimmuneACh receptors-low ACh causes muscle waeknessleads to respiratory failure, has remissions and exacerbations, -overgrowth of thymus may occur with MS- excessive thyroid hormone happens in most cases
s/e of MG
muscle weakness, droopy eyes, ASPIRATION PRECAUTIONS- watch nutritional intake
testing for MG
test the AChR antibodiestest bcuz pt may also have thymoma
tensilon testing MG
tensilon inhibits the breakdown of ACh. this is used to determine weather weakness is due to myesthenia or cholenergic crisis. -may cause ventricular fibiritations or cardiact arrest. can give atropine sulfate if this occurs. -In many patients with myasthenia gravis, the muscles will improve right after the Tensilon. -When there is an overdose of anticholinesterase (cholinergic crisis), Tensilon will make the person even weaker.
nephron
where urine is formed
GFR controlled by
blood pressure and blood flow. Glomerular filtration rate (GFR) is a test used to check how well the kidneys are working. Specifically, it estimates how much blood passes through the glomeruli each minute. Glomeruli are the tiny filters in the kidneys that filter waste from the blood.`
antibiotics may cause
ACUTE KIDNEY INJURY BECAUSE THEY ARE TOXIC TO THE KIDNEYS
creatine which is a muscle builder and NSAIDS and acetaminophen
can cause kidney toxticity
uremia
buildup of nutrogenous waste products in the blood as a result of kidney failure. s/e include n/v. muslce cramps, and pruritus itching
bruit in renal artery
swishing sound that may indicate narrowing of vessles
serum creatinine
produced when protein or muslce breaks down, levels slightly higher in men bcuz they have more muslce mass-creatine level doesnt increase until 50% of kidney function is lost, so if this happens it may require immediate intervention
BUN
tells if nitrogen products are being sectreated which is a byroduct of protein breakdown
urine gravity
increase in gravity shows dehydration or presence of ADH, a decrease in gravity shows increased fluid in body
nitrates
+ for UTI
CT scan of GU
shows 3d IMAGES OF URETERS, BLADDER AND TISSUES
KIDNEY SCAN, RENOGRAPHY
for blood flow to the kidneys
renal arteriography
blood flow to vessles
cytoscopy
Operative procedure for diagnoses after a trauma, or for toumors
retrograde procedures
instils dye into lower urinary tracts, dye doesnt cause kidney problems because it doesnt go into systemic circulation,identifies obstructions The flow of contrast (up from the bladder to the kidney) is opposite the usual flow of urine, hence the retrograde name.
AKI
trauma obstruction low blood volumeshock50% loss of nephrons
CKI
usually caused by hypertension and diabetes90% of nephrons must b destroied for this to be obvious
types of AKI
prerenal azotemia- caused by poor blood flow to kidneys, causes hypotension, tachycardia, oliguria, fatugueintrarenal AKI- caused by tumors, infections, antibiotics, NSAIDS, imflamation (hypertensions) SOBpostrenal azotemia- from OBSTRUCTION (anuria,
phases of kidney injury
oliguric phase- pt does not urinate, retains fluid which causes increased electrolytes in tehe body, watch for hyperkalemia, low sodium, low Ca, -PUSH FLUIDSdiuretic phase- pt urinates and causes decreased electrolyes, watch for hypokalemia
pts with AKI have high rate of
protein breakdown
diet for kidney failure
low protein high carb high cal
CKD
azotemia- buildup of nitrogen in blooduremia-metalic taste in mouthuremic syndrome-elevates BP acusing fluid and sodium overload -FLUID OVERLOAD, pulmonary edema, low CO,
uremic frost-
a pale frostlike deposit of white crystals on the skin caused by kidney failure and uremia. Urea compounds and other waste products of metabolism that cannot be excreted by the kidneys into the urine are excreted through the small superficial capillaries into the skin, where they collect on the surface.
liver
storafe protection metabolismdetoxifies-secretes bile in breakdown of fat-makes clotting factors AST and ALT
gallblader
stores bile
small intestine
digestion absorbtion
large intestine
movement elimination
air filled intestine
tympanic
increase in amylase and lipase
pancreatitis
barium enema or lowe GI serioes Xray
xray od large intestinestools chalky white for 1-3 days
PTC percutaneous trasnhepatic chlangiography
xray of bilary duct
endoscopy
to show bleeding or ulcerations
EGD
visual of esophagus stomach and duodenum -prevent aspiration
ERCP
examines liver, gallblader panceras and bile ducts to show any obstructions
colonoscopy
for large bowel
IBS irratable bowel syndrome
causes diareah, constipation, bloading and pain. effects women moreWATCH FOR NURTITION BECASUE OF MALABSORBTION-if there is bacteria give probiotics-AVIOD caffeine, alchohol, eggs, dairy, milk, wheat, give- calcium supplements and lactose fee foods. and FIBER INCREASE
CHRONS disease
inflamation of intestine or colon, causes thickening of bowel wall and puts pts at risk of developing fistulas.A fistula is an abnormal connection between an organ, vessel, or intestine and another structure. -SEVERE MALABSORBTION-tobacco users and jewish ppl
s/e of crohns
unintentional weight loss, guarding, rigidity, high pitched rushing sounds in narrowed bowel, pain, electrolyte imbalance, anemia from bleedingGIVE FOOD SUPPLEMENTS OR TPN to meet caloric intake needs 3000calories a day -xray shows narrowing, avoid milk, gluttem cafeine
cirrhosis
irreversible scaring of liver leading to necrosis -nodues that are formed block the blood flow throught liver
types of cirrhosis
postnectotic cirrhosis- caused by viral hepatitisleannes cirohsis- alchoholbilary cirosis- bilary obstruction
slenomegaly
blood flow backs up into the sleen and enlarges it, portal hypertensions occus causing ascites
s/e of cirohiss
fatigue, gi symptoms n.v, liver tenderness. abdominal pain, itching, jaundice,
low protein
cirosis
BBlumberg signlumberg’s
blumberg’s sign is a sign that is elicited during physical examination in medicine. It is indicative of peritonitis.The abdominal wall is compressed slowly and then rapidly released. A positive sign is indicated by presence of pain upon removal of pressure on the abdominal wall. It is very similar to rebound tenderness and might be regarded by some authors as the same thing, or at least a particular application of it.The name comes from German surgeon Jacob Moritz Blumberg.[1][2]Positive Blumberg sign or rebound tenderness is indicative of peritonitis. This method is specially useful in diagnosing appendicitis requiring urgent management.[3]
frontal lobe injury
The frontal lobes are considered our emotional control center and home to our personality. The frontal lobes are involved in motor function, problem solving, spontaneity, memory, language, initiation, judgement, impulse control, and social and sexual behavior Damage to the frontal lobe can cause increased irritability, which may include a change in mood and an inability to regulate behavior.[1] Particularly, an injury of the frontal lobe could lead to deficits in executive function, such as anticipation, goal selection, planning, initiation, sequencing, monitoring
temporal lobe
The temporal lobes are involved in the retention of visual memories, processing sensory input, comprehending language, storing new memories, emotion, and deriving meaning.[4]:21
buildup of bile salts and bilirubins
causes itching and jaundice in cihrossis
osteoblasts
bone forming cells
osteoclases
bone destroying cells
metastatic cancer to the bone; Paget’s disease
Hypercalcemia
oateoporosis
hypocalcemia
bone fx in healing stage, bone tumors
Hyperphosphatemi
osteomalacia
Hypophosphatemia
arthroscopy
tube inserted in the joint for direct visulation
systemic lupus
Autoimmune disease where bodys immune system attacks its own tissues and oegans causing inflammation. chronic, progressive, inflammatory, connective tissue disorder, can cause major body organs to fail . remissions and exacerbations
may cause kidney problems which is leading cause of death for this
w>m
20-40 yrs old
clinical manifestations of lupos
Butterfly rash—dry, red, scaly, raised rash on face; may increase in flare and disappear with remissioon
Polyarthritis—small joints and knees
osteonecrosis—hip most common; may result from chronic steroid therapy
Muscle atrophy—from skeletal muscle invasion or from chronic steroid; myalgias- muscle pain
Fever and fatigue—because of being inflammatory condition; fever sign of flare
manifestations of lupus in the organs
Renal—assess for urine output, hematuria, fluid retention
Lung—found in almost 50% of all SLE cases
Pericarditis—tachycardia, chest pain, myocardial ischemia; monitor VS q 4
Reynaud’s—exposure to cold, stress due to arteriolar vasospasm; severe pain
Neuro—psychoses, seizures, migraine headaches
Serositis—peritoneal involvement; abdominal pain
chronic fatigue,
SLE drug therapy
systematic lupus,
give topical cortizone drugs to reduce inflammation,
Plaquenil—decreases absorption of UV light and decreases risk for skin lesions; eye exams needed because of risk of retinal damage
Tylenol and NSAIDs for arthralgias and myalgias
Steroids—used to treat systemic disease process
Immunosuppressives—renal or CNS involvement
non-pharmacologic- mild soal, avoid parfume, use lotion, avoid drying sustances, monitor temps because rise in temp can mean flare up
systemic sclerosis (scleroderma)
chronic, inflammatory, autoimmune, connective tissue damage, not always progressive
Scleroderma—means hardening of the skin but is only one clinical manifestation
Inflamed tissue becomes fibrotic then sclerotic. Renal involvement is leading cause of death. Higher mortality rate than SLE.
,
Thickening of skin by buildup pf collagen
CREST syndrome (those who have scleroderma may have crest)
Calcinosis—calcium deposits Raynaud’s—1st symptom that occurs Esophageal dysmotility—dysphagia, reflux Sclerodactyly—scleroderma of digits Telangectasia—spider-like hemangiomas
manifistations of scleroderma
joints—pain but no inflammation
Skin–pitting edema in hands and fingers, skin taut and shiny
GI—dysphagia, reflux, malabsorption
Renal—organ failure
CV—Raynaud’s, digit necrosis, pain, autoamputation of digits, myocardial fibrosis
Lung—pulmonary HTN, fibrosis
Labs—similar to SLE
treatment for scleroderma
Steroids and immunosuppressants used but not as effective as in SLE
NSAIDs for arthralgias and myalgias
Treat early organ involvement
Skin—mild soap and lotions, treat ulcers
Comfort—room temp, gloves/socks for warmth, no smoking
GI—swallowing study, small frequent meals
Mobility—pain mgmt, safety
GOUT
urea crystals build up in the jounts and cause sharp pain and inflammation,
primary gout
uric acid that is being produced is larger than the amout that is excreated so it builds up in the body.
Asymptomatic—unaware unless uric acid drawn; no signs of disease; no treatment
Acute—starts with 1st attack of one or more small joints, usually MTP of the great toe; months or years may pass between attacks
Chronic—deposits of urate crystals develop under skin and within major organs (renal); kidney stones common
secondary gout
CKD, diuretics, diets, chemotherapy, CVD
manifestations of gout
acute gout- elevated uric acid, crystals in synovial fluid and inflammation
chronic gout- tophi- urate crystals in the ears, armas, fingers
treatment for gout
Colchicine and indocin for acute gout
Allopurinol and uloric for chronic gout—promote uric acid excretion
ASA and diuretics can cause attack
Alkaline—fruit juices, milk
Low purine—avoid organ meats, shellfish, oily fish with bones, give plenty of lfuids
lyme disease
caused by borrelia,
caused by infected deear tick bite
Systemic infectious disease
Stage I: bull’s eye rash, pain and stiffness in muscles and joints, symptoms occur 3-30 days after tick bite; oral abx
Stage II: 2-12 weeks after tick bite; IV abx for at least 30 days
Stage III: chronic complications
Prevention: avoid woods; use insect repellent; wear long sleeves and long pants; wear hat; bathe immediately; report rash or flu-like sx immediately and take antibiotics
bulls eye rash
psoriasis arthritis
skin condition chracterized by scaly itchy rash of knees, elbows and scalp. joint stiff especially in morning, effects 30% of people of people with psoriasis, neck and back pain
Thick scaly parts in skin
treatment of psoriasis
managing joint pain,
controlling skin leasion,
slowing disease progression
fibromyalgia
not an inflammatory dieasea, and it is a chronic pain syndrome.
pain stiffness and tenderness at neck, upper chest, trunk, low back and extremities
burning pain
GI—abd pain, diarrhea, constipation GU—dysuria, urinary frequency CV—dyspnea, chest pain Neuro—forgetfulness, concentration Vision—dry eyes, blurred vision
treamtnet for fibromyalgia
Drugs work to increase seratonin and norepinephrine
Limit caffeine, alcohol because they inhibit deep sleep
give lyrica and symbalata and
antidepressents - increase serotonin and norepinephrine in fibromyalgia they believe serotnin is low and substance P (pain) is high
chronic fatigue
severe fatigue for 6m ofr longer, usually following flu like symptoms 4 criteria must be met: sore throut impaired concentration myalgia multiple joint pain w/ redness or pain headach and unrefreshing sleep
fungal infections
Dermatophyte infection of the nails resulting in onycholysis(painless separation of nail from bed)
Fungal infections – when impaired skin in a susceptible host, most spread by direct contact with others, also objects (combs)
Tinea – used to describe dematophytoses, followed by location; tinea pedis – athlete’s foot; tinea manus – hands; tinea cruris – groin (jock itch); tinea capitis – head; tinea corporis – body (ringworm)
tinea corposes (ringworm)
These annular lesions are on the thigh.
tinea capitis
Tinea capitis, localized patch.
candida albican
Candida albicans fungal infection of the mouth (thrush).
Candida albicans – yeast infection; superficial skin infection and mucous membranes; high risk with immunosuppression, long-term antibiotic therapy, DM and obesity; s/s moist, red, irritated appearance, with itching and burning; perineum, vagina, axillae, under breasts and mouth (thrush); keep areas clean and dry
Promote – good personal hygiene
parasitic infections
Head louse infestation (pediculosis capitis). This close-up picture shows a single louse clearly enough to count its six legs, and a number of egg capsules (nits) attached to the hairs.
Parasitic infections
Pediculosis – infestation of human lice; Pediculosis capitis (head lice); Pediculosis corporis (body lice); Pediculosis pubis (pubic or crab lice); female louse lay hundreds of eggs (nits) and deposit in base of hair shafts
Common s/s – itching, excoriation from scratching, also secondary infection and carriers of other diseases (ex. typhus, recurrent fever)
Tx – chemical killing with Elimite, Kwell; also clothing, bed linens should be washed in hot water with detergent
scabies (parasitic disorder)
contagious skin disease with mite infestation, transmitted by close and prolonged contact with infested person/bedding; s/s curved or linear ridges in the skin (due to burrowing of organism under skin) with intense itching at night; examine skin between fingers and palms and inner aspects of wrists (common areas); hypersensitive reactions to mites (excoriated papules, pustules and crusted lesions may be noted on elbows, nipples, lower abdomen, buttocks, thighs, axillary folds, penis)
Dx – by scraping lesion and examining under microscope for mites and eggs
Tx – Kwell, Acticin, etc ; launder clothes and items with hot water and detergent
bedbugs(
Bedbugs – cimex lectularius – increasingly common due to global traveling and resistance to pesticides; do not live on humans but feeds on human blood for survival; do not carry disease; itchy discomfort; ‘hitch-hiking’ from infested hotel to home – telltale signs are presence of blood spots on bed linen or clothing from feeding; and bugs often found hiding around mattress
Tx – topical antihistamine; launder clothes and items, clean furniture, heat can kill insects and eggs
hepatitis
5 virus causing –
after exposure to causative agent – liver enlarged and congested with inflammatory cells, WBCs and fluid – resulting in right upper quad pain and discomfort – also inflammation and necrosis increase pressure within the portal circulation, interfering with blood flow and obstruction of bile channels (edema) lead to jaundice
Hep A –spread via fecal-oral route, contaminated water, food, person-person contact; incubation period of 15 to 50 days; non-life threatening, mild course (flu-like symptoms); but may be severe with older than 40 y o pts and also with other existing liver disease – may even require liver transplant and death may occur
Hep B – spread via blood ( sex, needle sharing, mother-fetus, etc.); s/s occur within 25 to 180 days of exposure – anorexia, N/V, fever, fatigue, right upper quad pain, dark urine and light stool, joint pain, jaundice; most recover and develop immunity but some become carriers (not sick themselves but infect others; have high-risk for liver cancer and cirrhosis later on)
Hep C - spread via blood, average incubation 7 weeks, most unaware of infection until abnormality detected; unlike Hep B, most do not recover and chronic infection develops; over years, liver cells scar leading to cirrhosis (Hep C induced cirrhosis is leading cause for liver transplantation in the US – often re-infected with Hep C after transplant); alcohol use increase progression and severity of cirrhosis
Hep D – Occurs only with Hep B (requires helper function of HBV); incubation is 14 to 56 days; transmitted by parenteral routes (IV drug, sexual contact, etc)
Hep E – similar to Hep A, fecal-oral route with incubation of 15 to 64 days, self-limiting and resolves on own
tests for hepatitis
Assess – abd pain, diarrhea/constipation, changes in color of urine or stool, skin or sclera, fever, lethargy, malaise, N/V, itching; palpate for liver tenderness, right upper quad pain, jaundice, clay-colored stool, dark urine (edema of bile channels causing intrahepatic obstruction)
Lab – Hep A, B, and C confirmed by liver enzyme elevations; and all Hep are found by its own specific antigen-antibodies are present (anti-HAV, anti-HEV, etc.)
During acute phase, tx – to rest inflamed liver to promote hepatic cell regeneration (rest to decrease metabolic demands and increase blood supply); diet – high carb and calories with mod amount of fat and protein after nausea and anorexia subside; small, freq meals, high-calorie snacks and supplemental vitamins often given; drugs given sparingly to rest liver, antiemetic for nausea; drugs (interferon – first line drug therapy for pt without cirrhosis; Baraclude – first line for those with cirrhosis but no co-infections; Hepsera – second line) most of these drugs cause muscle weakness
Health promotion – handwashing, avoid contaminated water/food, receive immunoglobulin within 14 days after exposure, vaccine before traveling,
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complications of hepatitis
Fulminant hepatitis – severe acute and fatal form; failure of liver cells to regenerate, progress to necrosis
Chronic hepatitis – when liver inflammation last longer than 6 months, as result of Hep B or C infection or Hep D with Hep B superimposed infection; lead to liver cancer and cirrhosis; many with multiple infection, Hep B, C, D or HIV.
hepatitis in US
: In the United States and worldwide, the incidence of liver cancer is increasing because there is an increase in cases of hepatitis C (HCV). Liver cancer tumors are most often seen in regions of Asia and the Mediterranean area. Worldwide the disease kills about 1 million people each year, and affects Vietnamese men more than any other group. Black and Hispanic populations have twice the rate of the disease as Euro-Americans, and older adults are affected more than other age-groups
HIV
Human immune deficiency virus – a parasite to enter and make copies of virus in new host cells; HIV virus has 2 enzymes (reverse transcriptase and integrase) to transfer its genetic material upon entering human cells; CD4 T cell (=helper/inducer T cells or also T4 cells) becomes ‘HIV factory’ – as HIV advances, number of HIV particles produced overwhelm the immune system with gradual CD4 T cell counts decrease with increase in viral load – and pts die of opportunistic infections or cancer
CD4 count
50-90% first infected with HIV develop acute infection within 4 weeks – fever, night sweats, chills, HA, muscle aches – over time CD 4 T cells drop below normal and those remaining do not function normally; poor CD4 T cell functions leads to immune abnormalities – lymphocytopenia (decreased # of lymphocytes), increased production of incomplete and nonfunctional antibodies; and abnormal functioning macrophages
500-1500 normal, under 200 AIDS
promotion and mantanace of HIV
education best prevention
perinatal, perental, and sexual transmition
opportunistic infections for AIDS
PCP, pneumocystis jiroveci pneumonia – assess for DOE, tachpnea, dry cough, persistent and low grade fever, fatigue, weight loss
Toxoplasmosis encephalitis –assess change in mental status, neuro deficits, HA, fever, seizures, lethargy, confusion
Cryptosporidiosis – intestinal infection, range from mild diarrhea to severe wasting
Fungal infections – overgrowth of normal flora; candida stomatitis or esophagitis – freq s/s of AIDS (mouth and back of throat – cottage cheese-like, yellowish white plaques and inflammation seen; esophagitis via endoscopic biopsy and culture); women have vaginal candidiasis with severe itching, perianal irritation, thick white vaginal discharge
Cryptococcosis – meningitis with s/s fever, HA, blurred vision, N/V, nuchal rigidity (stiffness of neck), confusion, mental status changes, seizures
Histoplasmosis – begin with resp infection and widespread – s/s dyspnea, fever, cough, weight loss, enlargement of lymph nodes, spleen or liver
Bacterial infections – Mycobacterium avium complex (MAC) most common, infect resp or GI tract and become systemic infection s/s fever, debility, weight loss, malaise, swollen lymph glands or organ
Tuberculosis, TB –s/s cough, chest pain, chill, dyspnea, night sweats, anorexia
Viral infection – cytomegalovirus (CMV) may infect eye, respiratory, GI and central nervous system – CMV can cause encephalitis, pneumonitis, adrenalitis, hepatitis, and disseminated infection; herpes simplex virus (HSV) in perrectal, oral and genital areas; varicella-zoster virus (VZV) – shingles, previous chicken pox present in nerve ganglia
Cancer – kaposi’s sarcoma (most common, highest risk when have co-infection with human herpes virus-8; small purplish brown, raised lesions on skin or mucous membranes); Hodgkin’s lymphoma, non-Hodgkin’s, etc.
Endocrine complications – gonadal dysfunction (men-low testosterone; women – irregular menses), adrenal insufficiency, DM, elevated triglycerides/cholesterol, body shape changes (fat redistribution =lipodystrophy - occur with antiretroviral therapies s/s buffalo humps or cervical neck fat, and large abd fat accumulation; other body areas, face, arm, legs have wasted appearance and how prominent vein patterns due to loss of SQ fat.)
clinical manifestations of AIDS
AIDS dementia complex (ADC) – occur in 70% of pts, infection of cells within CNS – cognitive, motor and behavioral impairments and changes
AIDS wasting syndrome
Skin changes – folliculitis, eczema, psoriasis
lab values for aids
Lymphocytes counts – low with WBC less than 3500 cells cubic mm (=leukopenic); less than 1500 lymphocytes/cubic mm (=lymphopenic)
Normal ratio of CD4 to CD8 T cells is 2:1 – in AIDS and HIV, low ratio
Normal CD4 T cells (500 to 1500) – may have fewer than 100 CD4 T cells while CD8 T cells are normal.
Antibody test for HIV measured by ELISA and Western blot Analysis (used to confirm when ELISA is +)
Viral load testing – such as quantitative RNA assays measure presence of HIV RNA genetic material in blood
elisa-tests for HIV antibodies, person can have low antibody if they get tested too soon,
-western blot- detects serum HIV antibodies
hiv and aids
when cd4 count drown to 200 or below you have aids
if you have aids you have HIV
but if you have HIV u dont necessaritly have aids
first manifestation of aids
When a person is infected with HIV, the first manifestations are fever, night sweats, chills, headache, and muscle aches. As time passes, CD4+ T-cells are infected and taken out of service. This cell count drops to below-normal levels, and those that remain may not function normally. Lymphocytopenia (decreased lymphocyte counts) occurs as a result. Also, as the CD4+ T-cell level drops, the patient is at risk for bacterial, fungal, and viral infections, as well as some opportunistic cancers.
purpose of inflammation
to protect by neutralizing, eliminating or destroying organisms invading internal env’t; actions only against non-self proteins and cells (infected body cells, cancer cells, etc.) recognizing self vs. non-self is called self-tolerance; unique proteins, human leukocyte antigens, HLA, found on surface of most cell – cellular fingerprint for that person; other people’s HLA are recognized as foreign
leukocytes WBC
protect body from effects of organisms
inflammation
Inflammation – immediate protection against tissue injury and invaders; part of innate immunity which include skin, mucosa, antimicrobial chemicals on skin, complement and natural killer cells; inflammation can occur without infection
Cell types involved in inflammation – neutrophils and macrophages (both use phagocytosis to destroy and eliminate invaders), eosinophils and basophils (both release chemicals to cause tissue-level responses to help neutrophils and macrophages)
purpose of inflammation
Purpose of inflammation and immunity – to protect by neutralizing, eliminating or destroying organisms invading internal env’t; actions only against non-self proteins and cells (infected body cells, cancer cells, etc.) recognizing self vs. non-self is called self-tolerance; unique proteins, human leukocyte antigens, HLA, found on surface of most cell – cellular fingerprint for that person; other people’s HLA are recognized as foreign
cell types in inflammation
Neutrophils – make up btwn 55-70% of WBC, also called granulocytes; mature neutrophils are called segmented neutrophils or polymorphonuclear cells; less mature are called band neutrophils; in healthy person, more than 100 billion fresh, mature neutrophils are released from bone marrow into circulation daily; large number is needed because life span is short – 12 to 18 hours; each can only take part in one episode of phagocytosis; protect from invaders, esp bacteria with phagocytosis and enzymatic digestion; absolute neutrophil count – number of mature circulating neutrophils (more number greater resistance to infection); bandemia or left shift – sepsis could cause having mostly less mature neutrophils (indicate pt’s bone marrow cannot produce enough mature neutrophils to keep pace with infection – immature neutrophils are unable to do phagocytosis)
Macrophages – monocytes mature into macrophages; liver, spleen and intestinal tract contain large number of macrophages; function – important in inflammatory responses and also AMI and CMI; phagocytosis, repair, antigen presenting/processing, and secretion of cytokines to control immune system; have long life span and take part in many phagocytic events
Basophils – make up only 1% of WBC; function – release chemicals (“vasoactive amines” – actions on blood vessels), include heparin, histamine, serotonin, kinins and leukotrienes
Eosinophils – 1 to 2% of WBC; function – very active against infestations of parasitic larvae and also limit inflammatory reaction; increased during allergic response
five cardinal signs of inflammation
warmth redness pain swelling decresed function
sequence of inlamation
Stage I (vascular) – Change in blood vessels: Phase I—constriction Phase II—hyperemia & edema Stage II (cellular exudate) – Neutrophilia, pus Stage III (tissue repair and replacement) – WBCs trigger new blood vessel and growth (angiogenesis) and scar tissue formation
immunity
adaptive internal protection; not automatic response, but a learned long-lasting specific response; Antibody-mediated immunity (AMI = humoral immunity) – involves antigen-antibody interaction to neutralize, eliminate, or destroy foreign proteins (antibody produced by B-lymphocytes (=B cells) – when it becomes sensitized to that specific protein) – macrophages and T-cells work with B-cells to start and complete antigen-antibody interactions
[B-cells – start as stem cells in bone marrow, the primary lymphoid tissue, then migrate to secondary lymphoid tissue such as spleen, lymph nodes, tonsils and mucosa of intestinal tract to mature]
immunity
Adaptive immunity - learned immunity
active immunity (when antigen enters body and actively make antibodies; 2 types – natural or artificial) Natural occur without human assistance and this type is most effective and longest lasting; artificial occur via vaccines (attenuated organisms) need booster to retain protection;
passive immunity (antibodies from another person transferred to a person, provide only immediate, short-term protection; 2 types- natural or artificial) – natural from mother to fetus via placenta, colostrums or milk; artificial injecting person with another person’s antibodies, lasting only days to weeks
cell mediated immunity
Also called cellular immunity
Involves many WBC actions and interactions
Another type of adaptive/acquired true immunity
For total immunocompetence, CMI must function optimally
AMI provide most effective long-lasting immunity but only if its actions are combined with cell-mediated immunity
CMI, cell-mediated immunity – provided by WBCs (T cells and natural killer cells); 3 T cell subsets – helper/inducer T cells (enhance activity of other WBCs, act as organizers and increase production of maturation of WBCs), suppressor T cells (prevent hypersensitivity or immune overreactions, and preventing antibodies against self cells such as autoimmune diseases; inhibit growth and activation of immune stem cells – opposite of helper T cells) and cytotoxic/cytolytic T cells (Tc-cells, a subset of suppressor T cells, destroy cells that contain HLAs, most effective against parasitic, virus or protozoa infections); natural killer cells (NK) not a true T cell also contribute to CMI with direct cytotoxic effects on non-self cells without being sensitized; destroys cancer cells and virally infected cells.
protection from CMI
Helps protect body through ability to differentiate self from non-self
Prevents development of cancer and metastasis after exposure to carcinogens
