Exam 1 review
Anatomy of the Kidney:
- The nephron is the functional unit of the kidney.
- Normal GFR is 120-125.
- If 75% of nephrons quit = renal insufficiency.
- Kidneys are sensitive to changes in cardiac output. VOLUME DEPENDENT. A decrease in
urine output indicates a decrease in cardiac output. - If the SBP is below 70 for over 40 minutes, the kidney will become hypo then ischemic.
- If the SBP drops, the arterioles dilate. If the SBP elevate, arterioles constrict.
Normal Functions of the Kidney: - Regulation of Water: Thirst regulates body fluid. Aldosterone- excretes K and reabsorbed
NA. ADH- reabsorbs water, is water conserving. ANP- inhibits NA and reabsorbs water. A
decrease in volume causes as increase in aldosterone.
When encouraging the patient to drink, provide a GOAL. - Excretion of Metabolic Waste: Reabsorbed = water and electrolytes. NOT reabsorbed =
creatinine, urea, lactic acid, and ketones. Check creatinine and BUN to assess kidney
function
Lactic acid is a byproduct of metabolism. When the lactic acid is high in decrease
kidney function, these patients have soreness everywhere. *give them water. - Regulation of Acid-Base Balance: The kidneys are 2nd place after the lungs. They excrete
hydrogen and reabsorb bicarb. - Regulation of Blood Pressure: Maintain VOLUME. Renin-Angiotensin- vasoconstricts then
releases aldosterone. Aldosterone. Prostaglandins- vasodilatation. Bradykininsvasodilation and vascular permeability. - RBC Synthesis: Renal Erythropoietin Factor stimulates bone marrow to make RBCs.
A dialysis patient is often anemic. - Regulation of Electrolytes: effecting neuro, cardiac, mental, and GI.
Electrolytes: - Sodium NA: 135-145. Hypo = change in LOC, seizures, and vascular collapse. Hyper =
dehydration. Treat hyper with diuretics, D5W because glucose pulls NA out. Correct the
problem slowly to avoid cerebral edema. 48 hours or more. - Potassium K: 3.5-5.2. Hyper = MI, chemo, autotransfusion (we did it), crushing injuries.
Hypo = diuretics, diarrhea, and GI suctioning. CARDIAC DYSRHYTHMIAS
No K to renal patients, if the kidney is not working correctly, they’re not regulating
levels causing build up. Monitor closely, and give slowly. Pt should be on monitor.
Cardiac patients should have an increase K to support cardiac functioning. NO PUSH.
NUR 265 Advanced Exam 1 - Calcium Ca: 8.5-10.2. Needed for nerve impulses, cardiac contraction, blood clotting,
and bones and teeth growth. Hypo = laryngospasm (AIRWAY), and respiratory collapse.
Transfusions decrease Ca. Basic Metabolic Panel is not accurate. A decrease in Ca
indicates a decrease in albumin.
Chovskeys-
Trouvosels- - Magnesium Mg: 1.8-2.4. Hyper = decease reflexes, hypertension, and cardiac
dysrhythmias. Hypo = increase in muscular and CNS activity.
K needs Mg. Give Mg first so K can be transported into the cells. - Phosphorus: 2.5- 4.9. Where Ca is… Phos is NOT! Opposite s/s as Ca.
Ask our Patient: current problem, what’s their normal, how much fluid do you drink daily, what
meds do you take, other health issues, and family history.
Nephrotic Syndrome: (pg. 1379 chart 67-3 sudden onset of sxs) - Pathophysiology – immunologic kidney disorder where the glomerular permeability
increases so larger molecules pass through the membrane into the urine and are then
excreted. This causes a massive loss of protein into the urine, edema formation, and
decreased plasma albumin levels. Many agents and disorders are possible causes of NS.
All glomerulonephritis diseases have features of nephrosis. - Causes – most common is glomerular membrane changes is altered immunity with
inflammation. Defects in glomerular filtration can also occur as a result of genetic
defects of the filtering system, like Fabry disease. glomerulonephritis, glomerular injury,
neoplastic disease, diabetes, and altered liver function (can also occur with NS, resulting
in increased lipid production and hyperlipidemia). - Symptoms – Severe proteinuria, hypoalbuminemia causing EDEMA, weight gain,
dyspnea, HTN, orthostatic, ascites, decrease output. - ACUTE = related to medications. CHRONIC = related to processes of disorders over time.
- Interventions – Tx of the underlining cause related to meds. 24-hour urine catch daily
weights, abdominal girths, I&O, monitor electrolytes. ORDERS – diuretics, steroids, low
NA and protein diet, replace albumin. - Management varies, depending on which process is causing the disorder (identified by a
kidney biopsy). Excess immunity can improve with suppressive therapy using steroids
and cytotoxic or immunosuppressive agents. Angiotensin-converting enzyme inhibitors
(ACEIs) can decrease protein loss in the urine and cholesterol-lowering drugs can
improve blood lipid levels. Heparin may reduce vascular defects and improve kidney
function. Diet changes are also prescribed – if glomerular filtration rate (GFR) is normal,
dietary intake of proteins is needed. If GFR is decreased, protein intake needs to be
decreased. Mild diuretics and sodium restriction may be needed to control the edema
and hypertension. Assess the patient’s hydration status because vascular dehydration is
common. If plasma volume is depleted, kidney problems worsen. Acute kidney injury
(AKI) may be avoided if adequate blood flow to the kidney is maintained.
Acute Kidney Injury: (pg. 1391 table 68-1, 68-2, 68-3, 68-4)
- Pathophysiology – rapid reduction in kidney function resulting in a failure to maintain
waste elimination, fluid & electrolyte imbalance, and acid-base balance. Occurs over a
few hours or days. Reversible if diagnosed and treated early. Retaining waste, and causes
a rise in creatinine by more than 0.3 mg/dl or more within 48 hours; or an increase in
serum creatinine to 1.5 times or more from baseline, which is known or presumed to
have occurred in the previous 7 days; or a urine volume of less than 0.5 ml/kg/hr for 6
hours (pg. 1391) - Although GFR is accepted as the best overall indicator of kidney function, it’s not
accurate during an acute or critical illness. - AKI also causes systemic effects and complications and can increase discomfort and risk
for death. - AKI causes an increase in magnesium, phosphorus and potassium. Patient needs to
decrease this in their diet and increase protein. - Classification:
- Prerenal failure: #1 cause of AKI in acute care. Impaired renal perfusion with a
sustained mean arterial pressure (MAP) of less than 65 mm Hg. Causes =
Hypovolemia – SHOCK, blood loss, diabetes, and misuse of diuretics. - Hypotension/Perfusion – CHF, decreased cardiac output, or clamping of renal
artery (during abdominal aneurysm surgery) - Intrarenal or intrinsic renal failure: damage to kidney tissue and reflects injury
to glomeruli, nephrons, or tubules. Causes = SEPSIS, trauma, inflammation,
glomerulonephritis, and vascular disease.
–>amikacin for sepsis patients.
–>Going to CT? Are you on dialysis? Contrast - Postrenal failure: RARE! Obstruction of urine flow. Clots, stones, crystals,
malignancy, endometriosis, prostate disease, bladder mass, and urethral
stricture. - Symptoms: findings aren’t bad until renal dysfunction gets severe. Malaise, n/v, weakness,
altered LOC, dyspnea, chest pain, oliguria, metallic taste, HA, weight gain, itchy dry skin. - Phases of AKI:
Onset: Onset to develop of oliguria (hours-days)