Homeostasis Management and the Kidney's Role

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Homeostasis Management and the Kidney's Role by Mind Map: Homeostasis Management and the Kidney's Role

1. Blood Pressure Regulation

1.1. MECHANISM: Completed through the renin-angiotensin pathway, starting with the release of hormone renin through the macula densa from the distal tubule wall when it makes contact with the endothelium of the arterioles. These are called the juxtaglomerular apparatus or complex, cells that are responsible for maintaining constant blood flow through the glomerulus via a tubule feedback mechanism

1.1.1. HIGH VALUES: If blood pressure is high, cells in the juxtaglomerular apparatus sends a signal to reduce the release of renin. This creates a negative feedback system to stop the renin-angiotenin system. Risk: Sustained high blood pressure will damage blood vessel walls which may impair blood flow and further release renin which worsens the existing hypertension.

1.1.1.1. RISK FACTORS: Lifestyle improvements can be made to prevent HTN, such as smoking ccessation, reducing alcohol intake, exercise and health diet.

1.1.2. LOW VALUES: When blood pressure is low (IE due to dehydration), the justaglomeruluar apparatus releases renin to initiate the renin angiotenin system to vasoconstrict the efferent arteriole in the glomerulus. This increases GFR which similarly increases bloof pressure. Risk: If there is low hydrostatic pressure - reduced ability to excrete nitrogenous waste, leading to the inability to regulate water/electrolytes.

1.1.2.1. RENIN-ANGIOTENSIN PATHWAY: dehydration, detected sodium deficiency or hemorrhage leads to a decrease in blood volume/pressure triggering the kidney’s release of renin. Renin causes release of angiotensin I which is converted to angiotensin II via the angiotensin converting enzyme which stimulates the adrenal cortex to release aldosterone. Aldosterone reabsorbs sodium and water into plasma and causes excretion of potassium in the urine which increases blood volume and blood pressure.

1.2. Nursing Diagnosis: Risk for hypertension in relation to impaired excretion of urine and renal insufficiency.

1.2.1. Objective S+S: shortness of breath, nausea, systolic >130mmHg or diastolic >80mmHg, confusion, behavioural changes, trouble speaking or understanding words

1.2.2. Subjective S+S: headache, dizziness, vision disturbances, chest pain, fatigue or confusion, anxiety, tingling sensation

1.2.3. NSG Intervention: monitor intake and output, elevated BUN, serum creatinine, potassium, phosphorus, decreased creatinne clearance, edema, blood pressure, changes in mental status, daily weight, GFR, urine sodium, specific gravity, provide support for anxiety, administer anti-hypertensive medications as prescribed.

2. Electrolyte Balance

2.1. Potassium (3.5-5mmol/L)- aids in excitability of nerve and muscle cells through maintenance of membrane potential. Reabsorption occurs in the proximal tubule. Aldosterone is the only hormone that affects potassium levels. Through a negative feedback system, rises in potassium causes aldosterone to be secreted which causes secretion of potassium via the distal tubule of the nephron into urine. When aldosterone levels decrease, less potassium is secreted.

2.1.1. HIGH VALUES: Hyperkalemia can result in abnormal nerve and muscle function.

2.1.2. LOW VALUES: Hypokalemia is linked to excess losses such as diarrhea, vomiting, and excessive intake of diuretics. Insulin can be used to promote cellular uptake of potassium.

2.2. Calcium (1.03-1.23 mmol/L) - aids in controlling muscle and nerve electrical conduction, and constitutes bone; reabsorption is in relation to circulating parathyroid hormone levels. Mostly reabsorbed passively in the proximal tubule

2.2.1. HIGH VALUES: Hypercalcemia can lead to pruritus, extra-skeletal calcification, renal calculi, peptic ulceration, changes in mental function such as depression and memory loss.

2.2.2. LOW VALUES: Low calcium will lead to tetany, muscle cramps, convulsions.

2.3. Phosphate (0.8-1.5mmol/L)- aids in maintaining plasma pH and is in equilibrium with calcium. It is a main constituent in bone alongside calcium.

2.3.1. HIGH VALUES: it is excreted through urine via the distal tubule

2.3.2. LOW VALUES: filtered phosphate is reabsorbed into the proximal tubule.

2.4. Magnesium (1.5-2mEq/L) - needed for energy production and storage. Normally found in bones. Actively absorbed through the proximal tubule

2.4.1. HIGH VALUES: neuromuscular depression, muscle weakness, lethargy, respiratory depression, bradycardia, nausea/vomiting

2.4.1.1. Diuretics and alcohol increase renal excretion of magnesium

2.4.2. LOW VALUES: muscle tremors, weakness, athetoid movement, hyperactive deep tendon reflexes, tetany, possible seizure

2.4.2.1. PTH increases tubular reabsorption of magnesium.

2.5. Nursing Diagnosis: Risk for complications of arrhythmias in relation to anemia and electrolyte imbalance (calcium, potassium magnesium and phosphorus)

2.5.1. Objective: abnormal rate and rhythm, decreased SaO2, hypotension, change in LOC

2.5.2. Subjective: palpitations, chest pain, fatigue, syncope

2.5.3. NSG intervention: monitor ECG patterns and changes, monitor oxygen saturation and application of O2 as needed, electrolyte replacement as ordered by MD, monitoring electrolyte levels and ABGs as necessary

3. Drug & Metabolite Excretion

3.1. PURPOSE: The kidneys maintain electrolyte and water balances in the blood to provide the body with the necessary nutrients for survival. Additionally, it filters toxins and medications not needed via the formation of urine.

3.1.1. Urine is normally clear, with varying colour which is dependent on concentration. There is no unpleasant odour, and the pH is normally slightly acidic at pH 6.

3.1.1.1. Rate of excretion dependent on molecular size & charge

3.2. MECHANISM: Excretion of excess ions, metabolic wastes, metabolites of hormones and drugs.

3.2.1. EXCESS IONS outside of the following values are excreted - sodium(135-145mmol/L), potassium (3.5-5mmol/L), magnesium (1.5-2mEq/L), ammonium (15-50mmol/L), calcium (1.03-1.23mmol/L), bicarbonate (18-22mmol/L), phosphate (0.8-1.5mmol/L) Metabolic waste - urea (1.2-3 mmol/L), creatinine (0.8-1.3mg/dL), uric acid (0.18-0.48mmol/L), nitrogenous waste

3.2.2. METABOLIC WASTES: Urea, creatinine, uric acid, nitrogenous waste

3.2.3. METABOLITES OF HORMONES: IE Human chorionic honadotropin in urine (used for detection of early signs of pregnancy)

3.2.4. DRUG METABOLITES: detoxified in the liver and excreted through the kidney

3.3. Nursing Diagnosis: Risk for impaired urinary elimination in relation to impaired kidney function and decreased GFR.

3.3.1. Objective S&S:oliguria, anuria, hesitancy, urinary retention, nocturia, vomiting

3.3.2. Subjective S&S: lethargy, itching, nausea

3.3.3. NSG Intervention: Monitor BUN, Creatinine, uric acid levels, intake and output, assess pain, elimination patterns, skin turgor and mucous membranes, monitor blood pressure

4. Regulation of Acid-Base Balance

4.1. PURPOSE: pH is a system utilized to measure the concentration of free hydrogen ions (H+) in a fluid. The kidneys regulate the concentration of H+ in the body to maintain a target pH level of 7.35 to 7.45, a healthy environment for cell growth and proliferation. Bicarbonate ions are directly linked to hydrogen ion concentrations as well.

4.1.1. If filtered bicarbonate levels are normal, it is reabsorbed in the proximal tubule (90%) and the distal tubule (10%)

4.1.1.1. Kidneys are responsible for bicarbonate ion concentrations whereas the lungs control PCO2 in the bicarbonate reaction sequence

4.2. MECHANISM: Target pH level in the human body are achieved via the bicarbonate buffering system

4.2.1. CO2 +H2O <-->H2CO3<--> HCO3- + H+

4.2.2. The following values are measured and assessed in regulating the acid/base system: Bicarbonate 18-22mmol/L PCO2 35-45mmHg PO2 75-100mmhG H+ 36-44mmol/L

4.2.2.1. HIGH VALUES: If bicarbonate levels are high (Acidosis), Initial response from the body is to create CO2 to be blown off through the respiratory system. This is a temporary compensatory mechanism

4.2.2.1.1. To correct, Bicarbonate trapping occurs, in which bicarbonate ions are preserved in plasma and excess hydrogen ions are excreted through binding with ammonia ions.

4.2.2.1.2. Nursing Diagnosis: Risk for metabolic acidosis in relation to impaired ability to excrete hydrogen ions and bicarbonate loss from decreased renal reabsorption.

4.2.2.2. LOW VALUES: If bicarbonate concentration is low, body decreases amount of hydrogen ions secrete into urine, decreasing bicarbonate plasma levels and reducing ventilation rate of the lungs. This will increase bicarbonate ions.

4.2.2.2.1. Nursing Diagnosis: Risk for metabolic alkalosis in relation to excess acid loss due to reduced glomerular filtration rate, hyperaldosteronism or hypovolemia.

5. Body Fluid Osmolality

5.1. MECHANISM: manipulation of sodium which is influenced by three hormones: ADH, aldosterone, and atrial natriuretic peptide. Increased sodium will lead to Hypertension and edema; decreased sodium will lead to hypotension and dehydration

5.1.1. ADH - secreted by posterior pituitary gland based on the osmoreceptors of the hypothalamus. It detects a rise in plasma osmolality and sends signals to the pituitary gland to secrete ADH. ADH receptors in the collecting ducts open water channels and move the water into the circulatory system which reduces osmolality to normal and dilutes the plasma.

5.1.1.1. A fall in plasma osmolality reduces the secretion of ADH through negative feedback which reduces the reabsorption of water into the blood.

5.1.1.1.1. Renin-angiotensin system

5.1.2. Aldosterone is secreted from the adrenal cortex. It influences the distal tubule of the nephrons, stimulating production of aldosterone which increases the amount of sodium and water reabsorbed

5.1.2.1. It is regulated by peptide angiotensin II in the renin-angiotensin pathway

5.1.3. Atrial natriuretic peptide - secreted by cardiac atrial cells in response to a stretch in the atria

5.1.3.1. ANP inhibits aldosterone secretion by the adrenal cortex, reduces renin release in the kidney, reduces the ADH released from the posterior pituitary, causes vasodilation and natriuresis and diuresis which causes excretion of sodium and water, reducing extracellular fluid volume.

5.2. Nursing Diagnosis: Risk for excess fluid volume in relation to acute or chronic renal failure in relation to decrease in glomerular filtration rate and sodium retention.

5.2.1. Objective S+S: edema, taut/shiny skin, hypertension, weight, oliguria, changes in mental status, distended jugular vein, coarse crackles audible in the lungs

5.2.1.1. fluid excess

5.2.2. Subjective S+S: restlessness, anxiety, difficulty breathing

5.2.3. NSG Intervention: monitor ins and outs, daily weights, sodium (80-100mmol/day) and fluid restrictions,, monitor blood pressure, heart rate, and use of ACE inhibitors, lipid levels, HbA1C, CBC and electrolytes (calcium, glucose, and phosphate, hemoglobin/RBC), elevation of head of bed and extremities as needed, administration of diuretics as prescribed.

6. Erythropoietin Production

6.1. PURPOSE: Erythropoietin is a hormone promotes proliferation and differentiation of erythrocyte precursors in bone marrow. Prevents anemia and maintains an adequate RBC count, promoting proper oxygenation of cells.

6.2. MECHANISM: Peritubular cells (most likely cortical fibroblasts, AKA REPOS cells) are stimulated by hypoxia, which releases Erythropoietin. This stimulates the stem cells in bone marrow to produce erythrocytes which produces RBCs. RBCs carry oxygen to kidneys and stimulate reduction of erythropoietin release, leading to a negative feedback response.

6.3. Nursing Diagnosis: Risk for anemia in relation to decreased RBC production and survival rate of erythropoietin due to elevated uremic toxins.

6.3.1. Objective S+S: Dyspnea, Tachycardia, easy bruising, low HGB and hematocrit

6.3.2. Subjective S+S: Fatigue, Palpitation, generalized weakness

6.3.3. NSG Intervention: Minimize risk for bleeding through use of soft bristle toothbrushes, monitor CBC, apply oxygen as needed, assess temperature and respiratory changes, administer erythropoietin therapy and blood products as ordered. Chronic renal failure related anemia can be corrected with the use of recombinant erythropoietin.