Exam 6 review Flashcards
BUN/creatinine: normal value- what does increased/ decreased mean
BUN (6-24) / creatinine(0.7-1.3)- if both increased indicated kidney damage
if only BUN is increased indicated Dehydration
s/s of increased BUN/ Cretinine
Fatigue, confusion, nausea
Normal Potassium Level
3.5-5.2
s/s of hyperkalemia
Muscle weakness, cardiac arrhythmias, peaked T wave
Normal Sodium lab value
135-145
S/s of hyponatremia
Confusion, headache, lethargy
S/s of Metabolic Acidosis
Kussmaula respirations, confusion, fatigue
Treatment for Pericarditis (complication of ARF)
Dialysis/ anti-inflammatory meds
Treatment for Anemia (complication of ARF)
Erythropoietin injections and iron supplements- kidneys play a large part of filtration and production of blood/ RBC- when it is damaged your RBC is impacted
Treatment for Fluid/ electrolyte imbalance (complication of ARF)
Restrict fluid/ salt- dialysis in severe cases
How do you figure out weight loss/ gain on a dialysis patient
1kg= 1000cc (1L) of fluid; helps assess fluid gain/loss
Prerenal injury s/s- who is at the greatest risk
Happens d/t decreased blood flow to the kidneys (typicaly hypovolemia)
s/s: Vomiting, thirst, bleeding hypotension, tachycardia, decreased skin turgor
Greatest risk: dehydration, sepsis, HF
Intrarenal injury s/s- who is at the greatest risk
d/t structural damage within the kidneys ie nephrotoxic drugs or glumerulonephritis
s/s: Puriritic rash, SQ nodules
greatest risk: glumerulonephritis, antibiotics
Postrenal injury s/s- who is at the greatest risk
Caused by blockage in the Urinary tract preventing urine from draining
S/S: flank pain, nocturia, frequency and hesitency\
Greastest Risk: neurogenic bladded, narrowing of urethra, kidney stones, bladded cancer
Initiation phase of Acute renal failure
Injury to kidney occurs- happens over a period of hours to days
Causes
Prevention
Treatment
Oliguric phase of Acute renal failure
Urine output decreased d/t damage to renal tubules- daily output: 50-500mL/day
Causes
Prevention
Treatment
Recovery phase of ARF
Kidney function improves- tubular edema resolves- takes weeks to months to filly recover
Causes
Prevention
Treatment
Diuretic phase of ARF
Urine output increased- tubural scaring and damage may occur
Causes
Prevention
Treatment
Vascular access cares
o Assess for infection
o Listen for Bruit
o Avoid taking BP on access arms or any blood draws, tight clothes etc.
o Feel for the thrill
Peritoneal dialysis advantages
Done at home, less restrictive diet;
put it in- let it set for a bit- then do outflow.
The outflow should be more than in flow
Peritoneal dialysis disadvantages
r/4 peritonitis hemorrhage, improper placement of caterer, poor return(blockage), hyperglycemia(sugar is in some of the solutions) , fluid and electrolyte imbalance
Hemodialysis advantages
More effective waste removal, stricter diet
Hemodialysis disadvantages
risk of infection and access complications.
Hypotension, muscle cramps, infection
Prorites of peritoneal dialysis
PREVENT INFECTION (aseptic technique) monitor fluid balance and electrolytes
CRRT why used
for critically ill patients needing slow, continuous fluid removal. Watch for hypotension, electrolyte imbalances.
CRRT potential complication
clots, hypotension, pink tingled urine(anything other than yellow, really), dysrhythmias, confusion, not enough fluid coming off
Nursing responsibilites for CRRT
Hourly output checks, watch BP, watch for clots
whats to prevent contract dye injury
Pre-hydrate, avoid nephrotoxins, use low-osmolar contrast
how to prevent renal failure with use of nephrotoxic drugs
adjust the doses, monitor kidney functon, avoid NSAIDs and some antibiotics(-mycin’s)
med administration with hemodialysis
generally do not give meds via dialysis post- however right after water-soluable meds can be given
What meds are given before disalysis
Fat soluable
what meds are withheld until after dialysis
water soluable and blood pressure meds- Dialysis will excrete water soluable meds. pt bp may change during dialysis therefore you dont want to give until after- as we take fluid off their blood pressure will decrease
Time and schedule of med admin
give long acting meds during non dialysis days when possible (dialysis will excrete them)
Drug clearence by dialysis
Any medication that are easily dialyzable should be held till after to ensure they reach therapeutic levels
what is dialysis diseequilibrum syndrome
Rapid removal of urea causes CNS symptoms; headache, confusion N/V, hypertension, seizure— reduction of urea from the vascular system- cells are pulling fluid in, causing brain cells to swell, resulting in symptoms of ICP
how do you fix/ prevent Dialysis disequilibrium syndrome
Slow dialysis or reduce flow rates.- most common for first-time dialysis and or 1-2 hrs of starting dialysis
how is organ retrival/ transplant done?
Obtain consent, match done/ recipient, access compatibility- nurses don’t talk to family; doctor does
What is the first requirement in looking at organ transplats?
ABO and HLA compatability
Generalized rejection signs and symptoms
Fever and decreased organ function- generalized discomfort, pain/ swelling
Hyperacute rejection
within min of transplant- when antigens are incompatable
Acute rejection
occurs within the first 6 months- immune system attacks the new organ
chronic rejection
months to years post transplant
What are potential complications for patients who are donating organs and how can they be treated
-Surgical Complications: Bleeding, infection, clots, organ injury → Treat with antibiotics, anticoagulants, surgical repair.
-Pain/Discomfort: Post-op pain → Manage with analgesics, ice packs, and physical therapy.
-Psychological Impact: Anxiety, depression → Support groups, counseling, medications if needed.
-Organ Function Changes: Reduced organ reserve → Monitor function, lifestyle changes, dietary modifications.
-Long-term Health Risks: Hypertension, proteinuria → Manage with antihypertensives, ACE inhibitors/ARBs.
What are the transplant rejection meds- why are they given
Cyclosporine: Prevents organ rejection by inhibiting T-cell activation.
Side effects: Nephrotoxicity, hypertension, infection risk.
Requires regular blood level monitoring.
Tacrolimus:More potent calcineurin inhibitor; prevents T-cell activation.
Side effects: Nephrotoxicity, hyperglycemia, neurotoxicity, infection risk.
Requires therapeutic level monitoring.
Purpose: Suppress the immune system to prevent rejection of transplanted organs.
Often combined with other immunosuppressive drugs for better efficacy.
DIC symptoms, labs, treatment complications
Symptoms:
Bleeding: Petechiae, ecchymoses, Pain/swelling in extremities, organ ischemia
General: Hypotension, tachycardia, fatigue, altered mental status.
Labs:
Prolonged PT/aPTT
Low fibrinogen & platelets
Elevated D-dimer
Treatment: Treat Cause ( infection/ trauma)
Complications:
Severe bleeding →Hypovolemic shock, Organ failure from ischemia.
HIT- what is it- lab values
Increased platlets
An immune response to heparin causing increased clot risk
Liver failure – causes, s/s, treatment, patho, complications
Causes: Viral hepatitis, drug toxicity, ischemia, Alcohol abuse, non-alcoholic fatty liver disease, hepatitis B/C.
Signs/Symptoms:
Jaundice, ascites, coagulopathy, hepatic encephalopathy, fatigue.
Elevated liver enzymes, hypo/hyperalbuminemia,
Treatment: Acetylcysteine for acetaminophen toxicity, lactulose for encephalopathy.
Liver dysfunction → Impaired detoxification, protein synthesis, and bile excretion → Accumulation of toxins (ammonia) → Organ failure and encephalopathy.
Complications:
Hepatic encephalopathy, bleeding, infection, renal failure, sepsis, multi-organ failure.
Ascites- causes, treatment, s/s
Causes Portal hypertension.
S/S: Abdominal distention, SOB.
Treatment: Diuretics, paracentesis.
Hepatic encephalopathy (portal-systemic encephalopathy) - potential causes, treatment (why done)
Causes: Ammonia buildup.
Treatment: Lactulose to reduce ammonia.
Pancreatitis- identifying prognosis, treatment
Prognosis Factors: High WBC, amylase, lipase.
Treatment: NPO, IV fluids, pain management.
Acetylcysteine: why used, how does it work
Why: Prevents contrast-induced nephrotoxicity.
How: Replenishes glutathione, neutralizing free radicals.
Aminoglycosides: why used, how does it work
Why: Antibiotic for severe infections.
How: Inhibits bacterial protein synthesis; monitor renal function (nephrotoxic).
Azithromycin: why used, how does it work
Why: Broad-spectrum antibiotic.
How: Inhibits bacterial protein synthesis.
Cyclosporine: why used, how does it work
Why: Prevents organ rejection.
How: Inhibits calcineurin, suppressing T-cell activation.
Kayexalate: why used, how does it work
Why: Treats hyperkalemia.
How: Exchanges potassium for sodium in the intestines, excreting potassium.
Lactulose: why used, how does it work
Why: Treats hepatic encephalopathy.
How: Lowers ammonia by converting it to ammonium and increasing excretion.
Methylprednisolone: why used, how does it work
Why: Anti-inflammatory for organ rejection or severe inflammation.
How: Suppresses immune response.
Neomycin: why used, how does it work
Why: Reduces gut bacteria in liver disease.
How: Decreases ammonia production by gut flora.
Sodium Bicarbonate: why used, how does it work
Why: Treats metabolic acidosis.
How: Neutralizes excess acid, restoring pH balance.
