Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
304 Cards in this Set
- Front
- Back
|
when is ADH released ? |
dehydration when the ECF decreases or increase of solute concentration what hormone is released
|
|
|
What does ADH cause |
reabsorption of water in kidney which increases plasma volume and decrease osmolality |
|
|
When ADH is released what happens to the urine output |
decreases |
|
|
What hormone is released when there is an increase of serum calcium |
calcitonin |
|
|
which gland releases calcitonin |
thyroid |
|
|
What is the action of calcitonin? |
1. renal excretion of Ca 2.decreased loss of Ca from bones 3.opposite action of PTH |
|
|
What is the main goal of calcitonin? |
decrease serum calcium |
|
|
decreasing the loss of Ca from bones it makes the bones |
stronger |
|
|
What hormone is increases when the calcium serum is low? |
PTH- parathyroid hormone |
|
|
what does the Parathyroid hormone do? |
1. increase calcium absorption in intestines 2. increase calcium resorption from bones 3.increase calcium reabsorption in kidneys 4. decrease calcium excretion in kidneys |
|
|
What is the main goal for PTH |
increase calcium serum levels
|
|
|
impact of the stress hormone on the cardiovascular system |
increase vasoconstriction increase bp increase HR increase perfusion to core organs |
|
|
in a pt with increased blood sugar, what follows h20 ? |
glucose |
|
|
What happens when the bs are high? |
h20 follows glucose as it is exerted by kidneys cause polyuria |
|
|
cause can happen due to poly uria? |
dehydration |
|
|
stress and hypoglycmia causes what stress hormone to increase? |
cortisol |
|
|
what happens when there is an increase in cortisol? |
liver converts amino acids to glucose which increases blood sugars |
|
|
what does aldosterone do? |
regulates BP increases sodium decreases potassium |
|
|
What can cause aldosterone hormone to increase? |
decrease in bp decrease in na increase in K |
|
|
what happens when the aldosterone is increased? |
1.renal absorption Na (h2o follows na causing the bp to rise) 2.renal exertion of K |
|
|
3 fluid spaces of the body? |
1.intracellular (ICF) 2.Extracellular (ECF) 3.Transcellular - includes GI tract, CSF |
|
|
What are the divisions within the extracellular fluid? |
1. vascular (organs) 2.intersitial (cell) |
|
|
Fluid shift between ICF space and ECF? (Hypertonic) |
ICF to ECF |
|
|
Fluid shift between ICF space and ECF? (Hypotonic) |
ECF to ICF |
|
|
Fluid shift between ICF space and ECF? (Isotonic) |
no shift |
|
|
What is hydrostatic pressure? |
fluid pressure against a vessel/ organ wall. |
|
|
Omosis |
fluid travels through membrane |
|
|
oncotic |
more solute, the higher the pull
|
|
|
Fluid overload and decrease of plasma oncotic pull causes |
edema |
|
|
Why is edema caused during fluid overload and decreased plasma oncotic pull |
increase in hydrostatic pressure causes the fluid to be pushed into the tissues, causing edema |
|
|
H2O |
hypotonic |
|
|
NS |
Isotopic |
|
|
D5W |
isotopic but when dextrose is metabolized it becomes hypotonic |
|
|
What would happen if hypertonic solution was infused? |
it would move vascular to intercellular |
|
|
If NS and D5W was introduced in large amounts what would happen? |
no fluid overload |
|
|
What happens when the pt is vomiting and diarrhea? |
increases isotonic losses |
|
|
treatment for isotonic losses? |
IV NS (isotonic) |
|
|
What happens when the cells are swollen? |
there is a CNS alternation and hypertonic IV fluid to draw out ICF |
|
|
Severe dehydration causes |
ICF fluid drawn into hypertonic ECF region causing the cell to shrink |
|
|
What is the treatment for severe dehydration |
IV D5W or PO water (hypotonic) |
|
|
Why is PO water and IV D5W given to someone who severely dehydrated? |
fills vascular compartments and replaces ICF |
|
|
isotonic solution |
level 1 dehydration; replaces vascular fluid |
|
|
hypotonic |
fluids moves from ECF to ICF |
|
|
hypertonic |
fluid moves intracellular to vascular |
|
|
Where is Na found?
|
Extracellular |
|
|
3 major functions of lytes? |
1. ECF osmolity 2.Regulates Nerve Impulses 3. A role of Acid-Base Balance |
|
|
What is gastroenteritis? |
inflamed stomach and small intestine mucosa |
|
|
what causes gastroenteritis? |
virus, bacteria, parasite |
|
|
S&S of gastroenteritis? |
n&v diarrhea ( bloody mucous in stool) abd cramping and distension fever with increase WBC |
|
|
interventions for gastroenteritis? |
treat causative agent, treat of possible ( i.e. flatly for C-Diff) medical asepsis ( gloves, gowns) for fever - antipyretics, anti-invectives if indicated diarrhea- Imodium ( not for C-diff) n&v- anti emetic, lytes fluid replacement, NPO (IV fluid and glucose) and monitor I&O |
|
|
What is the difference between irritable bowel syndrome and inflammatory bowel disease? |
colitis- inflammation in the colon only; after surgery no more flare ups of colitis Crohns- inflammation is often in ileum and colon but many occur anywhere in the GI tract; difficulty to tx b/c it can pop up again anywhere |
|
|
Colisis causes |
thickening of tissues and narrowing of lumen secondary to inflammation and ulceration of mucusa |
|
|
inflammation over time |
causes fibrotic tissue formation (scarring, thickening of tissues) which causes an narrowing of the lumen. the intestine becomes ineffective and decrease of pertisalsis and it can caused by acute or chronic |
|
|
an obstruction of the colon is caused by |
the thickening and narrowing of the lumen |
|
|
symptoms of obstruction? |
1.absent of bowel sounds 2. ++ distention 3.++ N&V |
|
|
what causes perforation in colitis? |
obstruction and ulceration of mucosa |
|
|
perforation can cause |
sepsis or peritonitis and hemmhorage |
|
|
sepsis and hemorrhage can lead to |
shock |
|
|
how can thickening of the walls of the colon cause dehydration |
the thickening of the walls, decreases absorption |
|
|
inflammation which is over exaggerated can |
cause vasodilation and thinning of the the colon wall. which eventually leads to ulcers and damage to the walls. causing bloody stools and perforation. |
|
|
long term crohns and colitis can cause what in the future |
cancer |
|
|
peritonitis |
stool leak out which causes it to stick to the membrane of the peritoneal causing lots of pain and eventually cause death |
|
|
what is crohns |
inflammation is most often in ileum and colon but many occur anywhere in GI tract |
|
|
ulceration in mucusa s&s |
fever, malaise, anorexia, weight loss, pain and cramps |
|
|
What causes IBD |
virus bacteria autoimmune response allergies environemnt genetics stress |
|
|
What is the action of histamine 2 receptor blockers? |
blocks action of histamine on H2 reception which decreases HCI secretion (decreases the digestive enzymes) |
|
|
How to treat peptic ulcer disease |
give histamine 2 receptor blockers, proton pump inhibitors and antacids, and anticholinergic |
|
|
example of histamine 2 receptor blockers? |
ranitidine |
|
|
proton pump inhibitors? |
blocks adenosine triphosphatase (ATPase) enzyme which decreased hydrochloric acid |
|
|
what does decrease of hydrochloric acid do? |
decreases the conversation of pepsinogen to pepsin ( digestive enzyme) |
|
|
Antacids |
increase ph to neutralize acid and binds to bile salts |
|
|
when the antacid binds to bile what happens |
bile less harmful to mucosa |
|
|
how should an antacid be taken? |
duration 20-30 min with no good d/t fast evacuation, but with food it lasts 3-4 hrs. |
|
|
example of proton pump inhibitor? |
panteloc/pantoprazole |
|
|
anticholinergic drugs |
decrease cholinergic HCL secretion which decrease damage and increase healing |
|
|
risks of anticholinergic |
decrease motility -may increase acid stasis -increase ulcer development |
|
|
example of anticholinergic |
glycopyralate |
|
|
Cytoprotective drug therapy example |
sucralfate |
|
|
cytoprotective drug therapy |
protects mucosal cells |
|
|
when in cytoprotective drug therapy effective? |
in low Ph -30 min ac or pc antacide |
|
|
interventions for acute peptic ulcer |
pain meds anxiety- education and meds rest and relax ( decreases HCL secretions) |
|
|
nursing interventions for acute peptic ulcers |
vital signs q hr ( shock detotion) -blood transfusion due to bleeding (coffee grounds and old bloods) -NPO- IV fluids(pantoloc), TPN ( decrease HCl secretion) -n&V- ng tube, meds |
|
|
s&s pf appendicitis |
acute pain to RLQ nausea anorexia fever at times |
|
|
risk of appendicitis |
peritonitis |
|
|
Crohn's and colitis tx |
counselling for lifestyle changes opened ended (job loss, body image change) |
|
|
nursing treatment for crohn's colitis |
CBC, lytes, WBC increase -blood transfusion- due to loss of blood -analgesic- cramps -b12 injections- if decreased absorption) -bowel rest, IV fluids, lytes -TPN increase calorie,protein, low residue, diet -immunosuppressants and corticosteroids to decrease inflammation |
|
|
nursing interventions for chrons and colitis |
stool chart (amount, colour and consistency) stool occult blood test colonoscopy for visualization and biopsy- need bowel prep and NPO for 8 hrs bowel surgery |
|
|
4 example of mechanical bowel obstruction |
1.neoplasm-chemo, radiations, surgery 2.adhesions-surgery 3.hernia pressing on lumen-surgery 4.twisting of sigmoid-colonscopy and surgery |
|
|
4 examples of non mechanical bowel obstructions |
paralytic ileus- most common form abdominal surgery meds- anaesthetics and analgesic shock (decrease blood supply) inflammation of the colon thoracic increase lumbar fracture |
|
|
non mechanical bowel obstruction causes |
decrease or absent of persitalsis |
|
|
is surgery needed for non mechanical bowel obstructions |
no, usually not needed. often self bowel resolves with rest |
|
|
mechanical bowel obstruction causes |
fluid, gas and bowel contents to accumulate proximal to obstruction |
|
|
what happens because of the obstruction |
decrease fluid absorption- decreased bp, lyte disruption -risk of perforation causing peritonitis and sepsis. |
|
|
s&S of obstruction |
distention pain n&v - causes metabolic alkalosis |
|
|
treatment for mechanical bowel obstruction |
surgery if needed NG tube- solves symptoms to relief discomfort analgesic IV fluids bowel rest, TPN if needed to prevent if needed |
|
|
diagnostic blood work for bowel obstruction |
increase WBC- d/t inflammation increase HCT- fluid, dehydration decreased hub- bleeding na,k,cl - decreased - bowels not able to absorb increase BUN -dehydration and pre-renal failure |
|
|
s&S of bowel obstruction |
n&v ng tube bowel rest meds iv fluids with lights abd distention abd pain constipation no flatus high pitched sounds above obstruction |
|
|
should laxatives be given for an bowel obstruction |
no |
|
|
dx for bowel obstruction |
abd xray barium enema colonoscopy sigmoidoscopy |
|
|
mechanical obstruction often requires |
surgery- resection and anastomosis |
|
|
appendicitis |
-hyper growth of lymphoid tissue occludes lumen of appendix -fecalith occludes appendineal lumen |
|
|
interventions for appendicitis due to hyper growth of lymphoid tissue occludes lumen of appendix |
removal of appendix |
|
|
fecalith causes |
edema venous engorgement invasion of bacteria which causes gangrene and perforation |
|
|
edema,venous, invasion of bacteria s&s |
acute pain nausea anorexia fever at times |
|
|
gangrene and perforation s&s |
antibiotics normal of debris lavage of peritoneum |
|
|
where is the appendix located |
lies still with right leg flexes LQ palpation yields RLQ pain |
|
|
surgical therapy |
hemicolectomy -temp. ileostomy with anastemosis as goal -removed of ileum ileotransverse anastamosis left hemicolectoy |
|
|
hemicolectomy |
removal of a portion of the colon -immediate anastomosis or temp colostomy or ileo |
|
|
anterior resection |
sigmoid colon and rectum -immediate anastamosis or temp colostomy |
|
|
APR- abdominal perineal resection |
through and and perineum, lower portion of colon, rectum and entire anal sphincter removed -permanent colostomy (abd and perineal wounds) |
|
|
total proctolectomy |
removal of colon and rectum, anus is closed -permanent ileo (abd drsg and pad for closed anus) |
|
|
total proctolectomy and ill pouch |
removal of colon and rectum, distal ends of small intestine made into a pouch and sewn to working anus muscles -reversible ileostomy (ileal pouch: will pass 3-6 pasty BMs/day-"somewhat normal BM function" |
|
|
hartmann's pouch |
proximal bowel is a stoma, distal bowel sewn closed for possible future anastomosis |
|
|
Post up stoma healthy |
-pink, rose- to brick red (viable stoma mucosa) -mild to moderate edema- normal in the initial post op -small amount of bleeding- oozing from the stomal mucosa when touched or cleansed is normal because of its high vascularity |
|
|
not health post up stoma |
-pale pink- may indicate anemia -blanching, dark red to purple- indicates inadequate blood supply to the stoma, low flow state, excessive tension on the bowel mesentery at the time of construction, or venous congestion; usually occurs in the first 72hr after surgery -moderate to severe edema- obstruction proximal to the stoma -moderate to large amount- moderate to large amount of bleeding from the stomal mucosa could indicate coagulation factor defence trauma to the stoma; moderate to larger amount from intestinal stoma opening could indicate lower gastrointestinal bleeding |
|
|
what dressing are you assessing for an and perineal reception? |
abd |
|
|
output from ileum |
water stool |
|
|
output from colostomy |
formed stool |
|
|
sodium is regulated where? |
Gi tract and renal via aldosterone and ADH |
|
|
secondary to excessive Na intake |
increased serum osmolity |
|
|
if the serum becomes hypertonic where is fluid drawn out of |
ICF |
|
|
what happens when the fluid is drawn out of the ICF |
increase retention of vascular fluid |
|
|
what are the s&s of the retentions of vascular fluid |
increase bp and edema (secondary to hydrostatic pressure) |
|
|
what happens to the cell when fluid is drawn out of ICF |
cell shrinkage which alters CNS |
|
|
treatment for increase na intake |
restrict na iv dsw Po H20 diuretic for Na secretion |
|
|
hyponatremia secondary to sodium loss |
there is an increase in serum osmolality which causes a fluid shift from ICF to ECF- CNS alteration secondary cell shrinkage |
|
|
hyponatremia secondary to sodium loss- treatment |
decreased bp replenish with hypotonic fluids treat the cause |
|
|
decreased sodium due to decreased to na intake or renal losses |
the fluid shifts to interstitial space which causes edema |
|
|
decreased sodium due to decreased na intake or renal losses treatment |
cause hypertonic solution |
|
|
decreased sodium due to fluid over load treatment |
fluid restriction and diuretics |
|
|
how might excessive fluid intake lead to pulmonary edema
|
fluid overload increases hydrostatic pressure |
|
|
what does hydrostatic cause pulmonary edema |
fluid leak into through pulmonary vessels |
|
|
pulmonary edema |
crackles heard decreased air entry at bases |
|
|
highest concentration of K is found |
ICF |
|
|
4 major functions of K |
1. nerve impulses 2. cardiac rhythms 3. muscles contractions 4. acids base balance 5. ICF osmolality |
|
|
increase potassium is caused by |
potassium sparing diuretics increase potassium intake renal failure acidosis decreased aldosterone production |
|
|
increase serum k causes |
cardiac arrhythmias |
|
|
treatmen to of increased serum K |
decrease intake of K use non-k sparing diuretics dialysis resolve acidosis calcium gluconate |
|
|
kayexalate |
sodium- watch out for watery bowels |
|
|
how to resolve acidosis |
insulin for short term - moves K to ICF |
|
|
how does calcium gluconate decrease serum K |
decreased cardiac cell excitability (decreasing arrhythmias) |
|
|
decreased serum K is caused by |
vomiting diarrhea ng suction alkalosis renal losses lasix starvation decrease of K intake hyper-aldosterone |
|
|
decreased serum K causes |
cardiac arrhythmias |
|
|
treatment for serum K |
po or IV k increase K diet K sparing diuretic treat the underlying cause |
|
|
4 functions of calcium |
1.nerve impulses 2.muscle contractions 3.blood clotting 4.bone and tooth formation |
|
|
increase ca serum is caused by |
meds- some diuretics increase vit D increase PTH bone tumour decreased mobilization |
|
|
s&s of increased Ca |
confusion weakness dysrhythmias |
|
|
treatment of increased serum Ca |
-pomidronate ( decreased bone resorption) -Isotonic IV to flush Ca -Lasix -decreased ca in diet -synthetic calontonin -increased activity to decrease bone resorption of Ca |
|
|
decreased serum ca caused by |
decrease ca intake decrease PTH pancreatitis lasix |
|
|
decreased serum ca will use |
increase muscle contraction and cardiac arrhythmias |
|
|
tetany |
muscle contractions |
|
|
treatment for decrease serum Ca |
oral/ IV ca increase vit D change diuretics |
|
|
increase serum mg is caused by |
increase MG intake renal failure |
|
|
increase serum mg causes |
CNS/neuromusclular dysfunction decreased loc, rr, cardiac function |
|
|
if there is decreased cardiac function what is done |
iv calcium gluconate |
|
|
treatment of increase serum mg |
dialysis increase fluid mg restriction |
|
|
decreased mg is caused by |
-diuretic -starvation -alcoholism ( decrease Mg intake and increase diuresis) -GI fluid loss- decrease mg absorption -increase blood sugar= increase diuresis |
|
|
decrease mg serum causes |
neuro/muscle dysfunction cardiac arrhythmias |
|
|
treatment for mg serum |
CIWA- ativan po/iv mg |
|
|
DECREASED albumin is caused by |
liver dysfunction burns |
|
|
what happens when the serum albumin is low |
fluid shifts from vessels to tissues |
|
|
what is the treatment for low albumin levels |
increase carb/protein ( do not with hepatic failure) -albumin transfusion |
|
|
increased albumin serum is caused by |
dehydration |
|
|
treatment of increased serum protein |
rehydrate with PO/IV fluids |
|
|
Normal range for acid base balance |
7.35-7.45 |
|
|
range for impaired cellular function |
7.55 and below 7.25 and higher |
|
|
death occurs for acid base balance
|
6.8 and less 7.8 and more |
|
|
what happens when pt is experiencing respiratory acidosis |
-decrease ventilation which increases co2 buildup and increasing hydrogen in blood. This decreased ph levels causing resp acidosis. |
|
|
how long does it take for the kidneys to compensate for resp acidosis
|
kidneys start to compensate in 24hrs |
|
|
what does the kidney do to compensate for resp acidosis |
conserve bicarb increase hydrogen excretion |
|
|
treatment for resp acidosis |
restore ventilation and bicard (HCO3) IV |
|
|
respiratory alkalosis |
the pt starts to hyperventilat so the pt is breathing out excessive CO2 which increases the ph levels |
|
|
increased of ph is |
akalosis |
|
|
treatment for resp alkalosis |
restore ventilation resolve pt pain or anxiety |
|
|
what happens to the kidneys during resp akalosis |
renal compensation- takes time to start - HCO3 excretion and H retention |
|
|
What causes metabolic acidosis |
1.diabetic ketoacidosis- increase ketones = acidic 2.shock- anaerobic metabolism- increasing lactic acid 3.diarrhea- loss of alkolatic enzyme 4.renal disease- bicard loss and H retention |
|
|
decrease ph levels in metabolic acidosis causes |
resp compentation- increase in RR and excretes increase CO3 |
|
|
treatment for metabolic acidosis |
treat the cause dialysis sodium bi card |
|
|
what causes metabolic alkalosis |
ng suction or vomiting -decreased bicarb excretion which increases the serum bicard |
|
|
when the ph level is high what happens ? |
-renal compensation, if there is no renal failure the renal excretes HCO3 -RR compensation which decreases RR rate increasing CO2 retention |
|
|
ABG's include |
Ph PCO2 HCO3 PO2 |
|
|
what does the Na-K pump do? |
only able to control K and Na shifts in and out of the ICF |
|
|
Acidosis |
excess H in ECF |
|
|
due to the excess H in ECF where does the fluid flow? |
H flows freely into ICF |
|
|
why does Hydrogen flow to ICF |
to keep the electrical charge neutral the Na- K pump kicks K out of the cell which increases the serum K |
|
|
What happens during alkalosis |
abnormally low serum H |
|
|
where does H flow in alkalosis |
H flows from ICF into the ECF |
|
|
why does H flow from ICF into the ECF (alkalosis) |
to keep neutral, the pump draws K into the ICF to decrease the K |
|
|
what does calcinotin do? |
keeps the calcium from going into the blood |
|
|
what does aldosterone hold on to |
na |
|
|
Adh hold on to |
fluid |
|
|
what does alcohol decrease |
mg |
|
|
albumin is usually |
in the blood stream |
|
|
high hydrogen |
increased acidosis |
|
|
bicard is made where? |
in the kidney |
|
|
how does the body compensate if the bp drops? |
increasing HR and aldosterone |
|
|
what does compensate mean? |
bringing body to therapeutic range |
|
|
decrease nutrients and oxygen causes |
cells to go into anaerobic metabolism causing lactic acid |
|
|
anticholinergic can be used for |
stress ulcers NPO- empty stomach, greater chance of the HCL to damage the mucous and with any anti-inflammatory med to protect the mucous |
|
|
What are electrolytes? |
-potassium chloride bicarbonate sodium -essential for normal function of our cells and organs |
|
|
what is diffusion |
movement of particles from a region in which they are higher in concentration to region of lower concentration |
|
|
what is hypernatremia |
rise in serum sodium |
|
|
what is hyponatremia |
decrease in serum sodium
|
|
|
what are peptic ulcers |
lesion in the lining of the digestive tract, typically in the stomach or duodenum caused by the digestive action of pepsin and stomach |
|
|
what causes osteomyelitits |
infectious organism enters body and there is a infectious growth in bone |
|
|
what increases when there is an increase of growth of microorganism in bone |
increase pressure on vasculature |
|
|
necrosis of the bone is caused by |
increase pressure of the vasculature |
|
|
necrotic material can separate and enter the blood stream, where can it go |
-lung infection and possible PE -brain infection and possible stroke |
|
|
micro organism growth in bone causes what s&S |
bone pain fever chills swelling altered mobility increase risk of fracture with vertebrae |
|
|
lab tests when organisms enters the body |
WBW- increased ESR- increased |
|
|
ESR |
erythrocyte sedimentation rate |
|
|
erythrocyte sedimentation rate |
nonspecific test for inflammation, the rate at which red blood cels sediment in a period of one hour |
|
|
diagnostics for Osteomyetilitis |
bone and tissue biopsy -blood and wound C&S- for possible Sepsis -imaging (MRI, CT) |
|
|
vasculature |
distribution of blood vessels in an organ or body part |
|
|
what causes a bone tumor |
maybe a primary or result of metastases -mets may travel to other areas (lungs) |
|
|
diagnostics for bone tumor |
biopsy of the bone CT PET MRI |
|
|
treatment of the bone tumor |
analgesic chemo radiation surgery |
|
|
chemo |
kills all cells, good or bad especially WBC "neutrophils" causes nausea and pancytopenia |
|
|
S&S of bone tutor |
-pain -fever -swelling -increased WBC -decreased ROM -increased serum calcium- risk of fracture |
|
|
pancytopenia |
deficiency of all three cellular components of the blood (red cells, white cells, and platelets) |
|
|
what causes amputations |
peripheral vascular disease malignant turmor limb trauma diabetes atherosclerosis |
|
|
decreased pedal sensation combined with constrictive footwear causes |
decrease perfusion to lower portion of extremity |
|
|
decrease perfusion to the lower portion of extreity |
delays healing and or tissue death increasing the risk of sepsis |
|
|
s&s of decrease perfusion to lower portion of extremity |
pain loss of sensation pallor decrease CWMS decrease pedal pulses |
|
|
diagnostic testing of amputation |
arteriography venography doppler studies |
|
|
nursing considerations arteriography and venography |
do not want to sit up, lay flat and check vs and dressing |
|
|
treatment of decreased perfusion to limbs |
correct underlying problem, if possible revacsularization surgery |
|
|
amputation patient is risk of |
-disturbed body image -phantom limb pain -atelectasis due to decrease mobility post op -constipation -impaired mobility -decrease skin integrity due to bedrest and prosthesis fitting- use compressions and holding wraps -wound infection/dehiscence risk - |
|
|
treatment for phantom pain |
ambulation and time -anticonvulsants and antidepressants -narcotics -nerve stimulation -acupuncture |
|
|
treatment for impaired mobility |
ROM exercises- avoid contractors encouragement |
|
|
when/ who changes the lower extremity amputation dressing |
POD 5 surgeon |
|
|
Joint erosion/deformity/damage is caused by |
tumor trauma arthrittis |
|
|
s&s of Joint erosion/deformity/damage |
pain immobility- r/o contracture |
|
|
diagnostic for Joint erosion/deformity/damage |
physical exam imaging |
|
|
treatment for Joint erosion/deformity/damage |
anti-inflammation med analgesic immuni suppressants- if the cause is related to suppressing the immune system -joint replacement surgery |
|
|
Synovectomy |
removal of most of the synovial membrane (connective tissue that lines cavity of joints) with an arthroscope |
|
|
why remove synovial membrane? |
chronic inflammation of joint causing synovial membrane to thicken |
|
|
S&s of thicker synovial membrane |
pain decreased ROM |
|
|
S&S of synovectomy |
decrease pain decrease ROM |
|
|
over time after the surgery what happens to the synovial membrane |
regenerate and thickens |
|
|
what is the treatment when the synovial membrane regenerates and thickens |
repeat synovectomy or arthroplasty (if damage too diffuse or severe to joint) |
|
|
total arthroplasty |
femoral prosthesis (ball) and acetabular socket |
|
|
partial |
(ball) femoral prosthesis is replaced only |
|
|
extracapsular |
anything outside the socket joint -may need hip precautions for comfort |
|
|
intracapsular |
within the ball and acetabular socket -hip precautions very important |
|
|
cemented hip arthroplasties
|
older adults <25 yrs to live FWB (full wt bearing)- almost immediately doest last long |
|
|
cementless |
long to FBW, as it is bone growth that stabilized prothesis - as surrounding muscles and tendons heal, they provide stability to the ball and socket |
|
|
Hip precautions should be followed for how many months |
2 months |
|
|
what are some hip precautions |
>90 degrees ( no hip below the knee) no adduction past midline avoid leg rotation |
|
|
femoral neck fracture |
cannulated screw/nails for repair as joint socket not involbed, dislocation is not a risk: there for a decrease need for hip precations but may be used for comfort. ** hard ware may be removed at a later time depends on fracture |
|
|
partial knee replacement |
1.femur head 2.patella 3.tibia plate |
|
|
destruction/deterioration of knee causes |
pain and instability which leads to total/partial knee arthroplasty |
|
|
post op knee replacement |
compression drsg to imbolize joint in extended position removed in 24 hrs. with orderd- 4wks of physio, medicated flexion |
|
|
nursing considerations of total/partial knee arthroplasty |
-nausea give antiemetic -pain- give analgesic (OPIODs, NSAIDS) - pulmonary emboli- treat with heparin -pneumonia- mobilize, breathing excerises -constipation- fibre, water, laxatives, mobility - decreased circulating volume- monitor CBC, VS, fluids, IV, blood -urinary retention post op- bladder scan, i&o foley -Dvt -infection- monitor wounds, wbc, change dressing, antibiotics -nerve impairment- neuro checks -pneumatic stockings |
|
|
DVT assessment |
visual inspection INR, D-Dimer Doppler U/S |
|
|
DVT teaching |
foot exercises meds- warfarin, heparin, dalteparin |
|
|
pneumatic stockings |
like the action of walking <1 hr removal (protocol)- r/o creating blood clots and dislodging them take of 10 minutes at a time |
|
|
how long should warfarin be monitored for |
3 wrks post op PT and INR testing |
|
|
for long should dalteparin be monitored for |
2 weeks post op |
|
|
which anticoagulant to pick during post op |
depends on many factors including age and health of pt |
|
|
Post- op knee replacement |
compression drsg to immobilize joint in extended position remove in 24 hours with order |
|
|
transverse fracture |
line of the fracture extends across the bone shaft at a right angle to the longitudinal |
|
|
spiral |
line of the fracture extends in a spiral direction along the shaft of the bone |
|
|
greenstick |
incomplete fracture with one side splinter and other side bent |
|
|
comminuted |
fracrtue with more than 2 fragments; smaller fragments appear to be floating |
|
|
oblique |
fracture in which the line of fracture extends in an oblique direction |
|
|
pathological |
spontaneous fracture at site of a bone |
|
|
stress fracture |
in normal/abnormal bone that is subject to repeated stress ie. jogging, running |
|
|
S&S of a fracture |
edema and swelling muscle spasm deformity ecchymosis or contusion loss of function crepitation |
|
|
crepitation
|
grating and crushing together of bone fragment |
|
|
in the first 72 hours of a fracture |
bleeding occurs, and there is a fracture hematoma (semi solid clots) |
|
|
what does the hematoma convert to |
granulation tissue |
|
|
what is the basis for new bone substance called |
osteoid |
|
|
what minerals are deposited into the osteoid |
ca mg pho |
|
|
how does one receive the minerals |
diet |
|
|
how long is the time period of the hematoma to convert into granulation tissue |
3-14 days |
|
|
callus formation |
bone forming and women around the fracture |
|
|
after the bone is formed and woven what happens |
ossification = hardening |
|
|
time period of ossification
|
3-6 months |
|
|
PT progression during ossification |
progresses from traction to cast or cast may be removed to allow limited mobility |
|
|
consolidation |
radiological union |
|
|
remodelling takes how long |
up to year or longer |
|
|
what happens during the remodelling of the bone> |
excess bone tissue aborbed and union is complete -strength and shape return |
|
|
pt teaching regarding fracture |
-very important to stabilize limb during healing -increasing exercise- new bone is deposition into sites based on stress |
|
|
increase of myoglobin treatment |
bolus of fluid |
|
|
3 goals in fracture management? |
fracture reduction fracture immobilization restoration of function |
|
|
fracture reduction |
closed reduction ( healing or manipulation without surgery) -ORIF, OREF -tractions |
|
|
fracture immobilization |
-casting/ splinting -traction -external fixation -internal fixation\ |
|
|
restoration of function |
pt ot |
|
|
casts |
1 24 hr above heart and avoid dependant position to avoid edema and pressure under cast |
|
|
external fixation |
at risk for infection - NS cleanse pins |
|
|
drug therapy |
pain therefore muscle relaxants -open compound fractures- antibiotics and tetanus |
|
|
nutrition |
protein, vitamin b (red blood cells), C (immuno and healing) and D ( calcium - minerals (calc, phos, mg) |
|
|
neurovascular assessment |
CWMS PP- may need doppler neuro checks |
|
|
pallor or coolness and decrease pulse means |
arterial insuffiency |
|
|
cap refill less than 3 seconds |
good arterial perfusion |
|
|
hip fracture or dislocation s&s |
external rotation shortening of affected extreme. muscle spasm and pain |
|
|
prothesis of femoral, is at risk for what during post of |
dislocation |
|
|
post of management of fracture |
-anxiety/knowledge deficit -pain -ABC, vitals (decreased BP) and decreased hub -pneumonia - BD and C exercises -infection, compartment hemorrhage syndrome -nausea (diet) -constipation - myoglobin from muscle damage yields renal injury (jammed up in tables)- dark, reddish, brown urine -urinary retention -DVT- heparin -muscle wasting and pressure sores -fall risk |
|
|
use of ice |
check facility policy- usually 10 min on and off (avoid overuse, rebound inflammation) |
|
|
fat emboli |
-prevented by keeping fracture limb immobile before reduction -managed with supportive care- (corticosteroids, fluid and ph manage, o2 and intubation) -pulmonary embolism- heparin and supportive care |
|
|
compartment syndrome |
unrelenting pain with no relief from meds -use splint cast or fasciotomy |
|
|
s&s of compartment syndrome |
pain tingling coolness pallor paralysis pulselessness increase myoglobin release from muscle injury do not evaluate on ice, as will increase ischemia |
|
|
etiology of compartment syndrome |
pressure may be increasing due to bleeding or swelling within the confines of the surrounding muscle fascia (this is an internal cause). however, the problem may also arise externally, as in the swelling of a limb beneath a constrictive cast |
