Lab Values:
Hematology:
ABC- 4-6 million
Platelet-150,000-400,000
Hgb- 12-18
Hematocrit- 37-52
APTT- 30-40 seconds
WBC- 5,000-10,000
PT-11-12.5
INR- 0.8-1.1 (Warfarin should be 2-3)
Electrolytes:
Sodium- 135-145
Calcium- 8-10
Potassium- 3.2-5
Magnesium- 1.8-2.2
qR
ABGs:
pH: 7.35-7.45
HCO3: 22-26
02: 93%-100%
ROME
CO2: 35-45
PaO2: 80-100
_pH
PaCO2
HCO3
Respiratory acidosis
Decreases
Increases
normal.
Respiratory alkalosis
Increases
Decreases
normal
Metabolic acidosis
Decreases
normal
Decreases
Metabolic alkalosls
Increases
normal
Increases
*A1c- <5.7%, 6.5% shows diabetes
Plasma glucose concentration equal to or greater than 200 mg/dL
Fasting plasma glucose great than or equal to 126 mg/dL
Two-hour post-load equal to or greater than 200 mg/dL
Lipid Profile:
Total Cholesterol- less than 200 mg/dL
LDL Cholesterol- less than 100 mg/dL
HDL Cholesterol- 60mg/dl and higher
Renal:
BUN: 7-20 mg/dL
Urine specific gravity is 1.005 to 1.030.
Upper GI:
Albumin: 3.5-5.0
ALT: 29-33 (males) and 19-25 for females
AST: 8-48
Bilirubin: ~
t) . "J
\.O
tr'u,.~f'\\~ :' \
Exam4
I':>
(:,~9..-:.
Ch 26 Nursing assessment: Renal and Unnar:y Tract Function
Review the anatomy and pathophysiology of kidney function on the regulation of fluid balance,
filtration, electrolyte balance, regulation of acid-base balance, and b/p; pg. 790-796.
1. Fitter. Every day, the kidneys filter gallons of fluid from the bloodstream.
2. Waste processing. The kidneys then process this filtrate, allowing wastes and
excess ions to leave the body in urine while returning needed substances to the
blood in just the right proportions.
3. Elimination. Although the lungs and the skin also play roles in excretion, the kidneys
bear the major responsibility for eliminating nitrogenous wastes, toxins, and
drugs from the body.
4. Regulation. The kidneys also regulate the blood's volume and chemical makeup so
that the proper balance between water and salts and between acids and bases is
maintained.
s. Other regulatory functions. By producing the enzyme renin, they help regulate
blood pressure, and their hormone erythropoietin stimulates red blood cell
production in the bone marrow.
6. Conversion. Kidney cells also convert vitamin D to its active form.
~6r ~ \ ·•t'\C.C1n\.~l'\(j. ,~
l.)n~~~
~t.~"
Ch 21 Nursing management: Patients w;th renal disorders (l c: 2a: 3be: 4b: 5d}
Review the etiology, manifestations, stages, management and complications of AKI; pg.
816-821.
Etiology:
.-~ \.-)f~i6
·hlQ~-~I'\
- C..\'<y;
()r\lJ~O. ..
lolcic.4 , ~ jl"
1) Prerenal azotemia is caused by hypoperfusion of the kidneys which decreases urine
output and GFR. Examples:.¢aehydration, hemorrhage or GI losses, decreased cardiac
output suctws Ml, HF, or cardiogenic shock, and vasodilated states such as sepsis and
anaphylaxis "\f>~' , 1"1fO'tn"l~,ICMl,
,41<~,
2) lntrarerial is caused by the renal parenchyma or nephron being damaged. Ex: ATN (MAP
below 65 mmg), renal ischemia, nephrotoxic agents such as aminoglycosides and
radiocontrast agents, bums, crush injuries, myoglobin and hemoglobin are liberated,
myoglobinuria, rhabdomyolysis, NSAIDS, ACE or ARBS,
,'i· W.) , 14.fW'"' \
3) Postrenal is when the outflow of urine is obstructed. El: Renal calculi, tumors, benign
prostatic hyperplasia, strictures, and blood clots.
*
~-,c.
*Look at box 27-3*
Manifestations: Oliguria less than 400 ml, urine has a low specific gravity, hematuria,
decreased sodium levels and urinary casts, and other cellular debris. Increased BUN, NN,
lethargy, headache, muscle twitching, and seizures, increased creatinine, hyperkalemia;l
oliguria and anuria, weakness, dysrhythmias, and cardiac arrest, metabolic acidosis, increased
phosphate and decreased calcium, anemia
Phases:
-~"'"~~
- ,.~~,.......,
Initiation/onset: Triggering event and ends when cellular injury and oliguria develop. Significant
fluid or blood loss, bums, or diabetes insipidus. Some can develop nonoliguric renal failure
associated with nephrotoxic agents. It can occur with bums, traumatic injury, and use of
halogenated anesthetic agents.
Oliguric: Fluid overload and an increase in the serum concentration of wastes, such as urea,
creatinine, organic acids, and the electrolytes potassium, phosphorus, and magnesium. 8-14
day period. Dialysis is usually needed until kidney function returns to normal.
Diuretic: ARF is corrected. This phase is marked by a gradual increase in urine output which
signals glomerular filtration has started to recover. The pt needs to be monitored for
dehydration and hypokalemia.
Recovery: Improvement of kidney function and energy level and may take 6-12 months. If the
residual damage to the glomerular basement membrane occurs, residual renal impairment may
result.
Complications:
Metabolic acidosis. Waste products could not be eliminated by the kidneys and they can
contribute to metabolic acidosis and Fluid and electrolyte imbalances. Imbalances may
occur due to hemorrhage, renal losses, and gastrointestinal losses.
\.\~~~.x:,..a.~,CA -"') h'\~C"M'AO\
\:fl
r
Review the etiology, manifestations, stages, management and complications of CKD & ESRD;
pg. 821-827
Etiology: Diabetes, hypertension, proteinuria, family history, increasing age, chronic
glomerulonephritis, pyelonephritis, obstruction of the urinary tract, hereditary lesions such as
polycystic kidney disease, vascular and autoimmune disorder such as SLE, infections,
medications, or toxic agents, being a man, lead, cadmium, mercury, and chromium.
Stages:
stage 1: GFR greater than or equal to 90
S_tage 2: GFR= 60-89 mUmin, hematuria, proteinuria or abnormal renal anatomy, hephrons
highly susceptible to failure (Mild CKD)
Stage 3a: 45-59 m:/min (moderate CKD)
Stage 3b: 30-44 (moderate CKD)
, Ma'iW
~-c,.~,
~I,,.
nt\ttS
Stage 4: 15-29 (severe CKD)
nu-\~
6 'C. cw-<.
L.)1\tl "\'lf\~w-& ,.~i\aM-w\,c...- 1' ,
«'~~Of\ , · tN
Stage 5: (End-stage CKD) GFR less than 15 or dial~is dependent
I ci.t. 'l t.r- W'CW".
or'
L½\~..<)
=, ~ : "'"' \)r".rt. ~?'-' ..,.
~""'~~
Management: Phosphate-binding agents, calcium supplements, antihypertensive and cardiac
medications, anticonvulsants, and erythropoietin~inders for hypocalcemia and
hyperphosphatemia, protein restriction, restriction on fluids, sodium, potassium, and
phosphorus, patient should adhere to a daily fluid allowance of 500-800 ml
-Potassium foods-+ citrus, tomatoes, melons, green leafy vegetables, and potatoes I Cc.n¾\a>~ , ~
-Phosphorus foods-+ dairy, peas, beans, nut, and cola products
-Sodium-+ contained in many canned and processed foods and in smoked foods lunch meats
as well as MSG
Complications: Hyperkalemia, pericarditis, pericardia! effusion, and pericardia! tamponade,
hypertension, anemia, bone disease and metastatic and vascular calcifications
Review renal replacement therapies, (hemodialysis, CART, PD and kidney transplant);
indications, complications and management; pg. 827-842.
Hemodialysis: Eliminates fluids, electrolytes, and waste products from the body 3x a week.
Before the procedure, check for vascular access such as checking patency of the AV shunt.
We listen for a bru!Je and feel the thrill and distal pulses. Assess patient vital signs, lab
values and weight.
o\\l "'-
~"'°"~ ,-.,,.'\
,a"
Complications: Hypotension, cramping, n/v, and bleeding due to heparin. Give protamine
sulfate for antidote, low lab values. Compare weight before and after dialysis. 1L-,
-fdisequilibrium syndrome (LOC, seizures due to ICP), slow exchange rate, and lower head of the
bed
Management: Increase protein intake, advice to avoid carrying things with access sites and
sleeping on it also, when they get their fistula ... do hand exercises
c,."' ,
,
\C,. 'l""O.~
~-c--•"'
Peritoneal Dialysis: If older patients have issues with anticoagulants such as heparin or
vascular access difficulties, then we would use this. Instil and dwell hypertonic peritoneal cavity
for waste products
-(.c,A,1Mf\
o.\o
t ,rvf-t,w,
L=, .tilf\\~ .f.c.. :w
d~ \\ , d.ro.CY' ~
,<.~c~, ~,, .~,
cvo"''
Car'l\f'io,.'it.M t),l. 4i\)rt.\\tS : c,'.c)'ttlc'\c.~~'t , f\~,
<Y•IW\,e'I.,!,
\X)\\)we
ck~Ge '-
lte11ei,
,&_"~'
"'~~•q''f~
wl 6\•'at"' ~_..
1~
O.•~~~.
\
,\~nt ~
s
-Get_ weight, wann the dialysate solution, use sterile technique, during the procedure closely
monitor the inflow and outflow of the dialysate, keep the outflow lower than the patient's
abdomen, monitor the color of outflow.. needs to be clear and no red or cloudy,
r
-Complications: peritonitis- fever, purulent drainage, erythema, swelling, and discolored
dialysate, pro~ein loss (increase protein), hyperglycemic, poor inflow and outflow (make sure
1,,...there are no kmks, address any constipation, reposition pt, and melt tubing to break up cl~ts- ')o..-',,.,
•
f' tt'.\t.c." ... Eol-¥', l,,ll,\.t ..;.. , ..... . ,l,..-1 .... 11.. •1'1" ,wi,~• /oil,\:~ Kidney Transplant Give immunosuppressants and after monitoring urine output . It should be
over 30 ml and is the standard monitor for fever, hypertension, pain, and provides pt teaching
such as high fiber and prowJn, low sodium, and low-fat diet. Avoid contact sports
... ~""'"
.
.
CRRT: Used on patients demonstrating hemodynamic instability such as hypotensron, or rn
those who cannot tolerate the rapid fluid shifts that may occur in hemodialysis. -~-~
-lc:11'~~
"· ,, 00,~
us
(.if t.
"°
Review assessment and teaching of vascular access pg. 828-830.
Fistula: Joins artery to a vein. The patient is encouraged to perform exercises such as
squeezing ~;ubber ball, to help the access mature and to increase the size of these vessels.
(4-6 week~ - c:.\a. ¥\0'< +u1&& ~f CV' '4'ta. (6.i-< 0 ~
'1 \o\,,)-fl'O~:" 'lltt.\
- I:) C.~"' C.. \I- lh•~•r,
,JI
Graft: Synthetic graft material between an artery and vein. Not suitable for diabetes. Look out
for infection and thrombosis. Pt should be given information about the access and about
potential changes in body image. (2-3 months)
• -'0 !'(,\:,~ W\~'-. (~-~,S I q•1"- c;c..\lye_
)I
Chapter 21: Nursing Assessment: Digestive, Gastrointestinal. and Metabolic function Od: 2acd:
3b: 4d: 5dl.
Review the anatomy and pathophysiology of the major organs of the digestive system; pg.
626-637.
Liver: considered chemical factor that manufactures, stores, alters, and excretes a large
number of substances involved in metabolism: importance of glucose, protein, and
blood-clotting factors, conversion o~mmonia to urea) protein ~ d fat metabolism, vitamin and
iron storage, drug metabolism, bile (absorbs fat) fonnation, and'f>ilirubin excretion (substance
that makes urine makes it yellow, if not excreted sclera looks yellowajaundice)~
Bile: manufactured by the liver and plays a major role in the digestion and absorption of fats in
the GI tract, stored in the gallbladder until it is needed for digestion at which time the
gallbladder empties and bile enters the intestine Of you live without a gallbladder, you lower
your fat content). Even NPO, bile formation happens
-'uver cannot be palpated under nonnal conditions but if you are an alcoholic or have growth,
you can palpate the liver for the disorder
~\\ , "vc."'l't., • ob~"""'° ~n,..
i
V\\J"""t i-4- d
e.k_
I'.I ½c.r
c.
fl"
;f
Gallbladder: storage for b'I1 W
.
so that the ·
. .
e. ater in the bile is absorbed through the walls for the gallbladder
r
gall. Bile is five to ten times more concentrated than the originally secreted by the
iver. when the food enter the duodenum, the gallbladder contracts the sphincter of oddi
relaxed, which allows the biles to ender the Intestine
-I Pancreas: exocrine(secretion of pane. Enzymes into the gl tract through the pancreatic
(amylase, trypsin, and lipase) and endocrine include secretion of insulin, glucagon, and
somatostatin directing in the bloodstream ... (insulin)
,~~,O\\~\>\.o.'o~., ~<.~\, ~,~.._,
. Ph.
/
ys1cal assessment
and diagnostic tests of the digestive system; pg. 634-657. (Stool,
Rev1ew
breath tests, endoscopy, colonoscopy, ERCP, LFT, liver biopsy, paracentesis)•
,r-•Pylori. The b~ic
Sto~I: Fecal ~ccult blood testing is the most common which detects
version examines the stoom for consistency, color, and occult blood. Red meats, turnips,
1
vitamin C, and fish can give a false positive~
"vo"~o~~~cr,.\ tM, 1\1+-GC,.,., tO, ft <'- , lfuLt•t,rJ
~tl'C-) \-' ....ll>J, ~~"'\
Breath tests: The pt ingests a Tsule of carbon-labled urea, and a breath sample i~ obtained
10-20 minutes later. Because H. pylori metabolizes urea rapidly, the labeled carbon 1s
absorbed quickly, then it can be measured as carbon dioxide in the expired breath to
determine whether H.pylori is present.
\!>~ t\\, S
(.~~
Endoscopy: Detects ulceration in the stomach. It determines function of esophageal lining and
~~extent of inflammatory, scarring, and strictures
::)
~~rt.
• -'
\ Colonoscopy: If not clear, then call the provider. '
~u
L") ~~"'
Cdc:,,,(O~
$
ERCP: For biliary tract such as stones, strictures, obstruction and caution with acute
Ji( pancreatitis
c1 ~~""'
\otJ¥t, ,<llt6tk- ,bi\°"'f
qc.t\l
-l,.c.~ 1, ,.. l",..._...
JJ( J-FT: ALT (specific to liver injury like hepatitis or cirrhosis) and AST (due to other clotting
~
actors.. )
1
~""""-.,~ \v'\'\:Y)
"\' bH.'-'C.t e\'\~
'2 •-\L tw ~~'""' " s'-""
Liver biopsy: Watch for bleeding when leaning forward.
..s'i(.'\\ •
Q..
.) ,_
.J
Paracentesis: Ora.in fluid. The liquid news to be clear•
..-K.LIII 1,c,iu..,c;_,1t'J ~vt'.S'&'j
ltl'1&,,\\ ~~\tl
Review health promotion guidelines for colon and rectal cancer screening; pg. 649.
At the age of 50, both men and woman should follow one of these testing schedules:
-Anual high-sensitivity FOBT
-sDNA test every three years
-Flexible sigmoidoscopy every five years
&.) tJ90 cl~ ~;dr\,'91,yt-
.,..
t.. ..
(lc,M'II\ 1 I \
'(.I-lull~
-Colonoscopy every 10 years
-Double-contrast barium enema every 5 years
- fw
tt,..
juAckl\\\~ I U'1,..,r
(.~..,_
.t•n-,
~,')Y'f'O\ci. ..."')U\'\~-
-CT colonoscopy every 5 years. All tests with positive results should be followed up with a
colonoscopy..
t
Risk factors: personal history of colorectal cancer or adenomatous polyps, strong family hiS ory
of colorectal cancer or colorectal adenomas found in first-degree relatives, history of chronic
inflammatory bowel disease, hx of hereditary colorectal cancer syndrome, and patient who
have curative-intent resection of colorectal cancer
2 3
Chapter 25: Nursing management; Patients with Hepatic and Biliary rnsn[ders ll c: b; b: 4d.:.
~-1,H,~~c;.,CI'
u ~', t,J..\U' k> ~tv"OrhD-1tc., ~cl-Review the etiology and POC of patients with common GI disorders (Hepatitis, acute
pancreatitis, liver failure/cirrhosis); (pg. 748-772; pg. 780-783)
Hepatitis: Alcohol, immune, Type ABC
A=Transmitted fecal oral route
L1"'
-=,
~r.~
\c.,
~'dr.t
. -~•"
G,= bodily flui&¾i :)::;,~ ") (;¼:) ~t
Band
L")
z-.i;.;at. i
&U
fol~·
<.\.\_GU),•~
.
W° Co..'->\'- l,'-t.,..-""-"
0 "'""~
\\ \,(_, o..u-tt'Y'~ r -
Risk factors: IV drug use, body piecing, unprotected sex, underdeveloped countries,
·
Flu-like symptoms, jaundice, clay-colored stools, dark-colored urine
-1'
Elevated ALT and AST and b i l ~
-\c,
~,\,f\foir
Treatment for A: self-limiting and bed rest
B & C=antiviral
Acute pancreatitis:
..,...,c;,..,dc:hl"\
(9'-?_"1Ji
I~ e\C<\',0
4t _. q t s \ \ ~
JI
e>lt
"'°
Minimal (mild or acute) edema and inflammation, within 6 months with pr~r~ssion. You are at
risk for hypovolemic shock, fluid and electrolyte disturbances, and sepsis-'{
-patient may develop systemic complications with organ failure such as pulmonary
insufficiency with hypoxia, shock, kidney failure, and GI bleeding
Patho- self-digestion of pancreas by its own proteolytic enzymes. Activation can lead to
inflammation,J1ecrosis, erosion, and hemorrhage. Another cause is due to contraceptives
T' 1.-, liCc.. ~ ~ · , . - ,
.
S/S: severe ABD pain, pain is acute in onset, occurring 24e48 h~ rs after a very heavy meal or
alcohol ing,~tion, Nt.).tcchymosis in the flank (Grey-Turner sign'; or around the umbilicus
(Cullen signT, hypovolemia , e.9iq~c;~,l.. ~'" Y-~•O.+I~
'4.+t ~~\1\-or
~ -Dx: serum amylase and lipase (elevate three times), can use US or CT/MRI and look for c t
and abscesses
oJr, u\
YS s
I'
't
f',4,\..
q,o.>Ul',,L \t_\l(.lr
.=, ~,c,'O~tc.
-~,t.
\ti~
' - - - - - - - - - - - · "'-' Ct)
c_\..l \.X, ~\\ll"'- t- e,~
O".'j6t°' ~\'-"<-1
~n-..? • vii
f-_,1.j'{,
...,
~' '4-ita\~
1 ~ ~{\U
\C'\f\lffrt1l...C:., \loll
~,~'<•~.,
~V"\C)~/
The overall mortality is severe due to the sh
.
.
and electrolyte imbalance give them
. ock of the hypoxia, anox1a, hypotension, or fluid
syndrome), withhold oral i~take
IV fluids, watch for fluid overload (compartment .fNursing management: pain man
.
are lower than oral f d"
agement (morphine pump, no oral medication), when enzymes
88 mgs but other than that no, maintain electrolytes NG suction have
altered ment a I status due t
·
·
'
'
_ ~-.M \\i,_'t)
Cl~ai~~~;fety measures, maintenance of bed rest
·
Assess breath"mg pattern due to pain and pressure on diaphragm lie on side knees on
t h e .chest .to all evia
· t e pain
· and breathing, we need good urinary output,' maintaining
' equilibrium,
having fluid out of the lungs,
·
. NI f~ings or J tube to prevent malnutrition and prevents pancreatic enzyme secretion,
mom~or weight and lab test, monitor serum glucose levels every 4-6 hours, as symptoms
subside and labs are normal, then introduce oral feedings, low in fats and proteins and high in
carbohydrates •\~ ,~iu. ~'tJi ,qi\lU: b\
,"-,..,c..""- "-"' ~L,o -~e11 ~!.~
~~-:.
-\\,C\~·
........
-F&E: monitor NN, do it IV ,
~c.
lob'-'-
bU.\tU ,f"''"
weftcc
- ~ \,Jf>C,
-Shock: due to hypovolemia and sequestering of fluid in the peritoneal cavity, hemorrhagic~~
shock, septic shock,
OtClfJr'c:f.\S :
,
\ (Vlfit"~
..,
,
-• ,.~"'-11\
- 6't0(\\,,C. ~v-ou,.\\~
- 6,\11(,o.lt-iCf' o\-~''"""'J
L ' ) ~ ,.....
....., - ,._. . ""
- h~\4. "()~ ~(.\
- ~..' " ' ~ (.C,,\,e.f.~~,
-
Liver failure/Cirrhosis:
.
<W;)\c,- ~ "
-~.,.,....
Etiology: Excessive alcohol consumption, injury, hepatitis, hemochromatosis, right-sided heart
POC: high-calorie and medium to high protein diet, sodium restriction to 2g, fluid restriction / CA\ a:N)J
1-1.5 liters/day, activity, paracentesis to alleviate ascites, and Senstaken-Blackmore or
- 'jr,,,.\l
Minnesota tube to control hemorrhaging.Octreotide, diuretics, lactulose, and antibioti<,S
...-.,u
ft
CJ '\' ~-ouW}, ~l111t-a.V,J'\"7 d- ½¼t\<:h..':J
-Check for bleeding, fluid retention by weight and measuring abdominal girth, and assessing
- Z..- °?
patient's level of consciousness ,~d, c.o.~c), ~-"1 'Qrto.-"\...
-¥ ~¾ct s
04
Chapter 24: Nursing management- patjents with lntestjnal and Rectal Disorders {1c: 2b· 3b: 4c:
~-
Review the etiology and POC of patients with lower GI disorders (IBD-Crohns and Ulcerative
Colitis pg. 728-733).
.
.,,. .\"'\ (.,'1,.\/\, rc.i
• r n,.{l.~
\),ll\\ ,
(~'&.l~~~ ~«> ~ Ii~
( ~\,<;\.<>\.
'--
·,\.11..~"'<'0
C.'«f:\•°'":c~ IBD-Crohns:lnflammation and ulceration of the small intestine as oppo;ed
to th~ colon and
1
o~"' results in sporadic lesions. Carries a risk of fistula. ru.~ \o.lq~ V'°,c, • \c:,a.)
~~Y'(),..4 vn~c.t:,<;,(I" kv-,C¼.i') \j.tJ.,v- '> '-»I \-e<:i,.\-\-h:, -\\ s<;.~
.
sis_ ri~ht lower quadrant 1P.aiQ,. pain, fever, 5 loose stools, sterrorhea, ab distention , h-Jfo~' ':,
~
(
~ (\)\\\~<;".),
n-o,\ I'(,~ °''.,
<J,t-0~--c.-, lt_O..,)n~
n H~ <;
1
r ~q\-\-\ L Q t ~ •n
\..~~~
$
POC: Decreased Hgb and hct, decreased albumin,increased ESR and CRP, elevated WBC
1'e'I~
"° .,,.,.,.
tu~
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