Nurs 265 Advanced Exam 1 review
Anatomy of the Kidney:
- The nephron is the functional unit of the kidney.
- Normal GFR is 120-125.
- If 75% of
... [Show More] 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. Bradykinins- vasodilation 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.
- 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)
Oliguria: 1-3 weeks. Begins one day after hypotensive event. Will NOT respond to a fluid challenge (Urine output is 100-400 mL/24hrs)
Diuresis: 2-6 weeks after. The start of kidney recovery, large amount of urine excreted. Volume loss of at least 3-4L/day. Loss of Na and K. BUN decreases and because normal kidney function is reestablished.
Recovery: 3-12 months. Continues until compete recovery up to 1 year. 30% do NOT recover GFR or tubular function.
- Diagnostics: Lab assessment (know #s), radiology to rule out mass, fluid collection, or obstructions, check structural formation. A significant increase in creatinine, especially when the increase occurs over hours or a few days, is a concern and must be reported urgently to the primary health care provider.
Chronic Kidney Disease: (pg. 1398 chart 68-2, 68-4, 68.6, 68.7)
- Pathophysiology: Slow loss of kidney function, progressive and irreversible, and kidney function does not recover. Defined as abnormalities in kidney structure or function that alter health and are present for longer than 3 months. There are no early s/sxs, may take months to years to occur, in the final stage kidneys are unable to remove excess waste and fluids.
- When kidney function and waste elimination are too poor to sustain life, CKD becomes end-stage kidney disease (ESKD). Terms used with CKD include azotemia (buildup of nitrogen-based wastes in the blood), uremia (azotemia with sxs), and uremic syndrome.
- Stages of CKD outlined on pg. 1399 table 68-6
- Weigh patient at the same time every day (1kg weight gain = 1L fluid retention), protect skin from breakdown (due to increased fluid in the body), prepare patient for hemodialysis (depending the stage of CKD they’re in) and promote frequent rest periods.
- Diet – high carbs, moderate fat. Restrict potassium, phosphorus, and magnesium
- Causes: Diabetes and hypertension. Autoimmune, polycystic kidney disease, glomerulonephritis, kidney stones, infections, trauma.
- Symptoms: loss of appetite, malaise, dark urine, HA, itching, weight loss, and N.
- Tests: LOOK AT THE URINE. 24-hr creatinine clearance = detects progression of kidney disease, renal ultrasound, and biopsy.
Treatment for AKI & CKD:
- AKI treat the underlying cause, support and improve renal function, and dialysis.
- CKD maintain body balance, and dialysis.
- Fluid Balance: Hypovolemia treat with volume & with transfusions if anemic. Hypervolemia diuresis, fluid restriction, and dialysis. Possible vasoactive meds to increase cardiac output EX. Dobutamine, norepinephrine, and dopamine- give in low doses to increase urine output.
- Metabolic Balance: Too much base, and they’re not secreting it (same with K).
- Hyperkalemia - diuretics, glucose, insulin, bicarb.
- Hyponatremia - fluid restriction and kayexalate.
- Hypomagnesemia - replace it.
- Hypocalcemia - replace it with vitamin D.
- Hyperphosphatemia – give slow, give with meals so you poop out phosphorus.
- Hematologic - if anemic, give iron/transfusions. Antacids and H2blockers to stop retaining acid and prevent GI bleed.
- Diet (pg. 1407 table 68-8): Protein, fluid, K (no orange juice), Na, and Phosphorus.
Hemodialysis:
- For advance CKD, does NOT cure or compensate. 3-4 hour treatments. A slight elevation in temperature is normal after dialysis.
Peritoneal Dialysis:
- Less restrictive, freedom from machine, control over daily activity. Assess the removed solution, and assess for infection. No peg tubers or abdominal injuries.
Pre-Treatment: Labs to dialysate that will be given, baseline vitals for comparison, graft size is changed with every treatment, hold BP meds. MINADRIN increases BP PO.
Post- Treatment: Expect a small increase in temperature, and a small decrease in BP. A drop in sugar is expected, give meds, and patient teaching about peritonitis and depression.
Hematologic System: Bone marrow makes RBS, WBS, and Platelets.
- Spleen: filters and cleans blood, assists in immune response, and blood reservoir.
- Homeostasis: Arrest of Bleeding: Injury, Platelet aggregation, fibrin clot, blood coagulation, then anticoagulation.
- Cascade/ Landslide: Intrinsic- effects the blood itself, Extrinsic- Conditions outside of the blood. Temperature Dependent!
(ITP) Autoimmune Thrombocytopenic Purpura:
- Makes antibodies against their own platelets destroying them.
- Females between 20-40
- S/S: Petichiae- 3mm. Purpura- 0.3-1cm. Bleeding and drop in platelet count.
- TX: Pallative treatment, steroids, cytotoxic medications, splenectomy.
(TTP) Thrombotic Thrombocytopenic Purpura:
- Platelets clump together occluding microcirculation. *Can be fatal in 90 days.
- Females at 30yrs.
- S/S: thrombocytopenia, anemia, and ischemic CNS symptoms.
- TX: prevent clumping. Aspirin, steroids, and plasma proteins with a 75% success rate.
(HIT) Heparin Induced Thrombocytopenia:
- Unexplained drop in platelet count after heparin treatment. 5- 10 days after.
- Risks: How long they’ve been on heparin, post-surg prophylaxis (heparin and SCD’s)
- S/S: DVT, PE, MI, or CVA
- TX: anticoagulation destroy the clot. (agratroban, refludan, angiomax) Pg. 897
(DIC) Disseminated Intravascular Coagulation:
- Causes: inflammation, infection, leukemia,
- Risks: transfusion reaction, cancer, pancreatitis, infection, pregnancy (placental fragments left behind), recent surgery, tissue injuries, and liver injuries.
- S/S: over clotting, microcirculation clots causing tissue hypoxia, abnormal bleeding from “used up” clotting proteins.
- Labs: Elevated D-Dimer- not normally present, but will be present after a clot formation. Increased FDP, decreased platelets, decrease fibrinogen, increased pt/ptt.
- TX: treat cause, transfusions, and blood thinners.
Hemophilia:
- S/S: 1st symptom at 1 year old from beginning to be on the move, hematomas with vaccinations, bruising, bleeding and hemarthritis.
- TX: prophylaxis with cryo and missing factor & PREVENTION.
Liver: Right upper quad. Storage, protection, and metabolism. Stores minerals and vitamins, protects, metabolizes amino acids and removes ammonia, synthesizes plasma proteins like albumin, metabolizes glycogen, and forms bile from fat breakdown.
-Assessment: Inspect, Auscultate, Percuss, and Palpate LAST. [Show Less]