neuro alterations, cardiac alterations) Questions With
Complete Solutions
kidney rejection: hyperacute vs accelerated vs acute
1. hyperacute (mins to hours) d/t humoral or antibody rxn
S&S: shock
2. accelerated (24 hrs-5 days) d/t pre-sensitization from prior
exposure to one or more antigen
S&S: fever, edema, gross hematuria, pain, high BUN/creat,
weight gain, HTN, oliguria
3. acute (days to 3mo) d/t cell-mediated response
S&S: fever, edema, gross hematuria, pain, high BUN/creat,
weight gain, HTN, oliguria
tx for all:
-high dose corticos and optimizing immunosupp mgmt
-close monitoring of drug levels (-limus can cx nephrotoxicity)
!! classic manifestations of accelerated and acute kidney
transplant rejection
1. gross hematuria
2. high BUN/creat
3. weight gain
4. HTN
5. oliguria
,liver transplant
chronic liver disease (cirrhosis, carcinoma) or fulminant liver
failure (acute - ex. acetaminophen OD, trauma, infection)
-can be whole organ, left lobe, or split liver (btwn adult and
child)
fulminant LF
acute - ex. acetaminophen OD, trauma, infection
MELD score
criteria for qualifying liver transplant pts
-look at:
1. serum creat (check for hepatorenal syndrome)
2. bilirubin (fxn of liver)
3. INR (liver stim prod of platelets, proteins for clotting factors)
have high risk of bleeding, thrombocytopenia
disqualifying criteria
-active malignancies (unless it is non-metastasized
hepatocellular carcinoma)
-active smoker, alcoholic, illicit drug user
-advanced cardiopulm dx
-uncontrolled or untx HIV
post-liver transplant: NI
med mgmt: triple anti-rejection therapy
1. Tacrolimus (Prograf) or cyclosporine
2. corticosteroid
3. CellCeft or Imuran
,monitor incision site, I&Os, rejection
-monitor for signs of bleeding
-biliary leaks (pancreatic enzyme leakage can cx auto-digestion
of tissue) - bad
-biliary obstructions/strictures
severe abdominal pain and abdominal girth in a post-liver
transplant pt
think potential biliary leak (pancreatic enzymes can leak and cx
auto-digestion of tissue)
hyperacute rxn in post-liver transplant pt
humoral or antibody mediated rejection (mins to hrs)
S&S: shock
tx: high dose corticosteroids and optimizing immunosuppression
mgmt
-close monitoring of drug lvls
!! acute rxn in post-liver transplant pt
T-cell mediated rejection (days to 3 mo)
1. !! S&S: elevated AST/ALT (transamititis)
2. abd discomfort
3. ascites
4. jaundice
5. dark urine (bilirubinemia) - liver not breaking things down or
hemolysis of RBCs (in relation to meds pt is on) watch I&Os
tx: high dose corticosteroids and optimizing immunosuppression
, mgmt
-close monitoring of drug lvls
!! transamititis
elevated in liver enzymes ALT/AST (> 35 units/L)!!
!! classic sign in acute rejection post-liver transplant
!! classic signs of acute rejection in post-liver transplant pts
1. transamititis (elevated ALT/AST)
2. abd discomfort
3. ascites
4. jaundice
5. dark urine (bilirubinemia) d/t liver not breaking down
products properly or hemolysis of RBCs
what other conditions can immunosuppressants put pt at risk for
besides infection?
-hyperglycemia r/t steroid use
-nephrotoxicity, neurotoxicity (-limus)
-cushing's (high lvls of cortisol)
-higher risk for cancer
-gastritis, stomach ulcers, GI bleeding
key points with neurologic alterations
-brain does not have O2 stores...a brief interruption in blood
supply can cx significant ischemic damage (lactic acid buildup)
-without adequate BF. cell membrane integrity is lost → ECF
flows into cell → cellular edema
what happens to cerebral arteries when PaO2 is < 50 mmHg