Fluid & Electrolyte Balance: Module 2 PDF

Document Details

ValiantOrbit

Uploaded by ValiantOrbit

Grand Canyon University

Dr. O. Clarkson

Tags

fluid balance electrolyte imbalance medical physiology human biology

Summary

This document provides a detailed overview of fluid and electrolyte imbalances. It examines topics such as fluid balance, hormone regulation, and edema. The information is presented through a series of slides or pages and includes figures and images.

Full Transcript

Lymphedema is a build-up of lymph fluid in the body in the fatty tissue of your skin. It can cause swelling and discomfort, usually in t...

Lymphedema is a build-up of lymph fluid in the body in the fatty tissue of your skin. It can cause swelling and discomfort, usually in the arms or legs, Module 2 although it can occur in other parts of the body. Fluid & Image Source: Bob Tapper / Medical Images Electrolyte Imbalances Presented by Dr. O. Clarkson Fluid Balance Hyponatremia Objectives Edema Hypernatremia Hormones regulating fluid Hypokalemia balance Hyperkalemia to muchADH Syndrome of Inappropriate Hypercalcemia ADH Secretion (SIADH) to littleproduction ofADH 788 Hypocalcemia Diabetes Insipidus (DI) or kidneys are notesponding (a) Severe lymphedema, extending into the feet and toes. (b) Mild lymphedema, also extending into the toes with creases at the base of the toes. (c) The characteristic sparing of the feet seen in lipedema, which is typically bilateral and symmetric (Ratchford & Evans, 2017) 1 Corinthians 6:19-20 u “Do you not know that your bodies are temples of the Holy Spirit, who is in you, whom you have received from God? You are not your own; you were bought at a price. Therefore honor God with your bodies.” “Psychic Energy System” by Alex Grey, 1980 Total Body Water Interstitial fluid = interstitial space = 3 rd space TBW ICF ECF Lymph Plasma 20% of ECF Negligible, but still important What else? Interstitial Fluid water Body fluids compose 60% of total body weight. 80% of ECF 2/3rd of the body H2O is in the ICF. is ttInkYn 1/3rd of the body H2O is in the ECF. ECF is distributed between plasma (20% of ECF) and interstitial fluid (80% of ECF). Plasma Interstitial Intracellular fluid fluid u Interstitial Fluid & Plasma are nearly (skeletal muscle) identical because they are constantly 200 mixing. Na+ No Albumin Plasma membrane Capillary wall u Plasma proteins are too large to pass 150 HCO3– Milliequivalents per liter of H2O through the capillaries. HCO3– PO43– K+ 100 Na+ Cl– Na+ Cl– 50 Protein anions Protein K+ anions Other Other Other K+ Other Other 0 Cations Anions Cations Anions Cations Anions Diffusion vs. Osmosis W Follows solute a 0 Edema Excessive Accumulation Of Fluid In The Interstitial Spaces u Localized - due to trauma or around an organ u i.e. sprained ankle, pulmonary edema u Negative Pitting Edema u o Generalized - uniform distribution of fluid heart failure u Ex: Right sided CHF congestive u Positive Pitting Edema Hydrostatic ~ Push Osmotic ~ Pull IFOP IFHP Interstitial Space/ Extracellular Fluid/ 3rd Space CHP COP capillary CHP: Capillary Hydrostatic Pressure by Outward Pressures determined – Pushes fluid out of capillary (Blood Pressure) a CHP & IFOP Inward Pressures COP: Capillary Osmotic Pressure Capp venue sickof COP & IFHP – Pulls fluid into capillary (Albumin) IFHP: Interstitial Fluid Hydrostatic Pressure If Outward P > Inward P – Pushes fluid into capillary Filtration IFOP: Interstitial Fluid Osmotic Pressure If Inward P > Outward P Reabsorption – Pulls fluid into interstitial space (no albumin, 0 pressure) If Outward P > Inward P Hydrostatic ~ Push Filtration Osmotic ~ Pull If Inward P > Outward P IFOP IFHP Reabsorption Interstitial Space/ Extracellular Fluid CHP COP capillary Causes of Edema ↑Capillary Filtration ↑CHP (↑BV, ↑BP) CHF, fluid retention, venous obstruction ↓Capillary Reabsorption ↓COP (Hypoproteinemia) Cirrhosis, burns, lack of dietary protein, kidney disease ↑Capillary Permeability Histamine - (anaphylaxis, inflammation) Lymphatic Obstruction Why do we tell patient’s w/ heart failure to restrict their salt intake? Edema e edema auing to Ekin a u Net filtration = (CHP + IFOP) – (IFHP + COP) u ↑ CHP  EDEMA u HTN, CHF u Venous Obstruction u ↓ COP  EDEMA u ↓Albumin (liver failure or kidney disease) u ↑ in Capillary Permeability  EDEMA u Histamine (inflammation, anaphylaxis) CHP: Capillary Hydrostatic Pressure Pushes fluid out of capillary (Blood Pressure) COP: Capillary Osmotic Pressure Pulls fluid into capillary (albumin) Consequences Of Edema Swelling can lead to compression of surrounding tissue and circulatory structures u Tissue necrosis u Results in oxygen delivery and waste removal impaired u Pulmonary edema u Results in hypoxia u Cerebral edema u Results in headaches, nausea, seizures, coma, death u Circulatory shock u Results in excess fluid in tissue spaces causes low blood volume and low BP Left Sided CHF Right Sided CHF Congestion in the lungs Congestion in the Body Pulmonary Edema Pitting Edema, Ascites HEYKatinas Fife Orthopnea Ascites in u Accumulation of fluid in peritoneal space u MCC: Liver cirrhosis  Portal HTN u Pathophysiology - ↓Albumin ↓COP Edema u Dx: Ꚛ Fluid Wave Test Ascites Fluid Wave Test https://www.youtub e.com/watch?v=Dy mVKae1nsg Pair and Share. I’ll give you 3 minutes. Would capillary filtration ↑ or ↓ in these situations? Protein Deficiency Hypoalbuminemia in plasma LVP Histamine it ii ii closer to i hemisia ↑capillary permeability fluid in intersition space Hypernatremia Fluid would increase in the interstitial space Hormones Regulating Fluid Balance u ↓ Water Loss  ↑Blood Volume (BV) RB.P u ADH – Anti-Diuretic Hormone (Vasopressin) – H2O reabsorption in kidney u Aldosterone – Renal Reabsorption of Na+ (H2O follows Na+), excretes K+ u Effect on plasma: ↑H2O, ↑Na, ↓K hYPU in.mn ↑ Water loss  ↓BV ↓BP vacanre Tentniial u u ANP - Atrial Natriuretic Peptide u BNP - B-type Natriuretic Peptide u ↑ Renal secretion of Na+ (H2O follows Na+) anti on kidneys to reduce b P u Changes in blood volume affect blood pressure ANP & BNP What triggers their release? ↑BV / BP Effect ↓Na, ↓BV, ↓BP to finish Infinite FYI: Hypovolemia = ↓BV Hypervolemia = ↑BV RAAS ACEinhibitors Kidney releases Renin when it detects: ↓ BV ↓ BP ↓ Na+ need pis Effect we ↑ADH (vasopressin) ↑Thirst Sympathetic Nervous System EIGHTH Vasoconstriction ↑Aldosterone ↑BV  ↑BP ↑Na+, ↓K+ feel ↓Urine Output Infra What effect does Aldosterone have on the following? 0 Na+: K +: Blood Volume: Blood Pressure: Urine Output: ADH / Vasopressin What Triggers The Release Made in hypothalamus Of ADH? relate ADH dfyke.tk fHkeed ↑ osmolarity Stored in posterior pituitary Osmoreceptors in hypothalamus Targets DCT and CD in the kidney ↓BV/↓BP Reabsorbs H2O back into circulation Stretch receptors in atrium of heart. Well Hydrated? ↓ Little ADH Released Dehydrated? ↓ ADH Released From Posterior Pituitary going to be mtg p What channels allow for H2O reabsorption? collectingducts Alcohol Effects Alcohol suppresses ADH production by the pituitary Without ADH, higher amounts of water stay in the urine Large Volume Urine w/ low Osmolarity What Affect Do The Following Hormones Have On Blood Pressure? u Aldosterone: ↑/↓ BP u ANP: ↑/↓ BP u ADH: ↑/↓ BP u BNP: ↑/↓ BP I What Affect Do The Following Hormones Have On Sodium Levels In The Blood? u Aldosterone: ↑/↓ Na+ Hypernatremia = ↑ Na+ u ANP/BNP: ↑/↓ Na+ Hyponatremia = ↓ Na+ u ADH: ↑/↓ Na+ u Why? conservin more water chutes 7 hyperkalemia Problems with ADH u SIADH 7 DI u Syndrome of Inappropriate ADH Secretion Diabetes Insipidus u Too much ADH Too little ADH u↓Urine Output ↑Urine Output with salt osmarity goesup Urine Osmolarity ____ uUrine Osmolarity ____ Serum Osmolarity ____ dehydrated uSerum Osmolarity____ water intox SIADH DI Syndrome Of Inappropriate ADH Secretion Diabetes Insipidus u ↑ADH Isthmus Taste ↓ADH u Causes: Idiopathic, brain trauma, paraneoplastic Causes: Pituitary tumor, kidney damage, syndrome, Medication SE (e.g. thiazide diuretics, Medication SE chlorpropamide, carbamazepine, antipsychotics, S/S: antidepressants) Chan (1997) Excessive Thirst & Urination u S/S: u Fatigue, confusion, lethargy Pathophysiology: u Pathophysiology: ↑H2O Secretion  ↑[Na+] (concentrated) u ↑H2O Reabsorption  ↓[Na+] (diluted) ↑Serum osmolarity u ↓Serum osmolarity ↓Urine osmolarity u ↑Urine osmolarity ↑Urine Volume u ↓Urine Volume Tx: Synthetic ADH analogue (Desmopressin) u Tx: ADH receptor antagonists (Conivaptan) 12 to 20 liter a day “Water Intoxication” “Dehydration” Drugs & SIADH Paraneoplastic Syndrome A syndrome (a set of signs and symptoms) that is the consequence of cancer in the body, but unlike mass effect, is not due to the local presence of cancer cells. The two most common types of paraneoplastic syndrome associated with lung cancer are: 1. humoral hypercalcemia of malignancy in squamous cell carcinoma 2. syndrome of inappropriate antidiuretic hormone in small cell lung cancer u Causes Diabetes Insipidus u Neurogenic - absence of ADH u Pituitary problem such as brain tumor, hypophysectomy, aneurysm, thrombus, infection u Nephrogenic - inadequate response of renal tubules to ADH u Pyelonephritis, PKD, amyloidosis u Meds – Lithium, Colchicine (for gout), Amphotericin B, loop diuretics, general anesthetics u Signs and Symptoms u Excessive urination and thirst u Polyuria and polydipsia u Excretion of large volume dilute urine  dehydration u 8-12 L/day vs 1-2 L/day (normal) u Testing u ↑Serum osmolarity vs. ↓Urine osmolarity u Plasma ADH levels u CT scan Diabetes Insipidus vs. SIADH Tests SIADH DI u UrineOsmolarity u Serum Osmolarity ADH u ADH levels u Serum Na+ Urine u Urine Na+ Osmolarity u CT scan Serum Osmolarity Dehydration u S/S 22 1 u Hypotension & Tachycardia u Dx: u Decreased skin turgor u Urine: u Decreased urine output u Increased urine osmolarity ionsentration is u Blood: him is a 90 1 compared u increased Hct. Why? elevated redbloodcellsinblood 187 9 9 jow u increased serum osmolarity Treatment: u Increased BUN:Cr ratio ingym9419 to get PO rehydration u High BUN-to-creatinine ratiosoccur with sudden (acute) kidney problems, which may be IV rehydration caused by shock or severe dehydration. Quizizz Module 2 Part 1 https://quizizz.com/ad min/quiz/64fa4016edd 14b1cc1cc3d1d?source =quiz_share Sodium (Na+) u 135-145 mEq/L u Major cation outside of the cell u Maintains ECF osmotic balance u H2O follows Na+ u Function uMaintain tonicity of ECF uFacilitate nerve conduction and glandular secretions u Organs and Hormones involved controled uKidney: Renin-Angiotensin-Aldosterone uANP/BNP heart u says its to high Most often goes hand in hand with chloride ↑[Na+] = Hypernatremia ↓ [Na+] = Hyponatremia Iv with pure water [OSM]ICF = [OSM]ECF swell ↑H2O [OSM]ICF < [OSM]ECF or salt water ↓Na+ ShrievalUP ↑Na+ 1498841 or [OSM]ICF > [OSM]ECF ↓H2O Normal Osmolarity ↓[Na+] ↑[Na+] Na+ Na+ H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O Na+ Na+ Na+ Na+ Na+ Na+ H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O Na+ Na+ Na+ Na+ Na+ Na+ H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O Na+ Na+ Na+ Na+ hypotonic hypertonic Osmolarity: ↑|↓ 0 Osmolarity: ↑|↓ am Hypernatremia | Hyponatremia Hypernatremia | Hyponatremia Normal Osmolarity ↑H2O ↓H2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O Na+ Na+ Na+ Na+ Na+ Na+ H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O H 2O Na+ Na+ Na+ Na+ Na+ Na+ H 2O H 2O H 2O H 2O H 2O H 2O Na+ Na+ Na+ Na+ Na+ Na+ H 2O H 2O H 2O am Osmolarity: ↑|↓ 0 Osmolarity: ↑|↓ Hypernatremia | Hyponatremia Hypernatremia | Hyponatremia Osmolality, Sodium & Blood Volume u Osmolality – concentration of stuff in the blood u Na+:H2O ratio is in homeostasis u Hypertonic solution a osmolarity u Na+:H2O ratio is high u Hypernatremia u Decreased Water intake or Increased Water loss u DI – Diabetes Insipidus u Hypotonic solution – Dilute Blood u Na+:H2O ratio is low u Hyponatremia u Increased Water intake or Decreased water loss u SIADH – Syndrome of Inappropriate ADH Hyponatremia Hypernatremia u [Na+] 145 mEq/L (some books use 150) u Causes u ↓Na+ intake Causes u ↑Na+ loss ↑Na+ intake ↓ H2O intake uDiuretics, vomiting, diarrhea ↑ H2O loss u Na+ loss > H2O loss Sweating, Dehydration u ↑H2O intake Diuretics, vomiting, diarrhea u Total body water (TBW )increases more than Na+ H2O loss > Na+ loss uExercising withH2O intake Diabetes insipidus (↓ADH) and no Na+ intake Hypersecretion of aldosterone uWater intoxication Na+ Reabsorption / K+ Secretion Haugen u SIADH (↑ADH) Would also cause hypokalemia u Kidney, Heart, Liver dysfunction exam Hyponatremia Hypernatremia neurons are hyperactive S/S: S/S: u CNS symptoms CNS symptoms u Headache, Lethargy Headache, Restlessness u N/V N/V, THIRSTY, Tachycardia u Confusion, Disorientation, coma Confusion, Disorientation, u Seizures (less likely than w/ Seizures, coma hypernatremia) Muscle symptoms u Muscle symptoms Muscle twitching, spasms u Muscle weakness, cramps Hyperreflexia u Hyporeflexia Presence and severity of the symptoms are related to the severity of the imbalance and the speed at which the imbalance occurred. Fast drops in sodium  seizure vs Slow drop (may be asymptomatic) Hypokalemia Hyperkalemia u Reduced intake of K+ Ht Increased intake of K+ H u Elderly, alcoholism, anorexia Increased exit of K from cells + u Increased entry of K+ into cells Acidosis u Alkalosis Trauma Crush injuries, major burns u Too much insulin Insulin deficiency u Increased loss of body K+ Insulin moves K+ into ICF u Diarrhea, Vomiting Decreased renal excretion of K+ u ↓BV  ↑aldosterone  Renal failure Na+ reabsorption/K+ excretion Addison’s disease (↓Aldosterone) u K+ wasting diuretics K+ sparing diuretics No dumping u Lasix (Furosemide) MC Aldactone (Spironolactone) Works by stimulating Na+ excretion and K+ reabsorption in the DCT – water follows Na+ EKG and Ventricular Myocyte Action Potential Vendipolar cadt 1 2 NA 0 3 Kt ven repular a den 4 4 A ton run an P Wave PR Segment ST Segment T Wave Felted by k QRS Complex Hypokalemia Hyperkalemia S/S: S/S: u Muscle weakness, cramps Muscle weakness, spasticity u EKG: EKG: u Depressed/flattened T Waves Wide QRS w/ Tall peaked T Waves u Prominent U wave u 'U' waves are thought to represent repolarization of the Purkinje fibers. flattened Twavespike y wave K+ imbalance EKG’s are complicated Muscle Cramps In Hypokalemia? Muscle weakness is a more common presentation But muscle cramps can occur u Potassium helps move Calcium out of the cell u ↓ [K]EC  ↑ [Ca2+]IC u Larger K+ Gradient  as more K+ leaves  more Na+ & Ca2+ enters u ↑ [Ca2+]IC  ↑ Muscle Contractions Tx: Eat a banana It will help move the Ca2+ out of the cells, allowing the muscles to relax Hypo- Vs. Hyper-kalemia summary An Important Note About Calcium u Extracellular calcium exists in 3 states: floating free 1. Ionized Ca2+ (50%) = Free Ca2+ u Physiologically active form 2. Complexed Calcium (9%) uE.g. Ca(HCO₃)₂ or Calcium bicarbonate 3. Protein Bound Calcium (41%) u Mostly Albumin effected by PH levels u Some globulin Vitamin D activated by kidney Calcitriol (1,25-dihydroxycholecalciferol) [active form of VitD3] u Calcitriol u Activated in the Kidney u ↑Ca2+ Absorption in GI u ↑Ca2+ Reabsorption in Kidney u Enhanced bone mineralization  Strong bones restoclasts Astimulates u Kidney Failure? PTH hyper parathuroidis u Can’t activate Vit D3 secondary u ↓Ca2+ Absorption in GI setopenia then u ↓ Ca2+ Reabsorption in Kidney Osetophosis  Hypocalcemia Review Ca2+ Homeostasis ↑Ca2+  ↓PTH ↓Ca2+  ↑PTH PTH & Calcitonin ↓Calcitriol ↑PTH u Hypocalcemia u PTH - Parathyroid Hormone u@Kidney u ↑Ca2+ reabsorption  ↑Ca2+ u ↑Vitamin D activation  ↑Ca2+ u@Bone u ↑ Osteoclast activity  ↑Ca2+ u Hypercalcemia releases this thyroid u Calcitonin  ↓Ca2+ u Think “Maintain the TONE of Calcium” Calcium-Sodium Relationship u Hypercalcemia u Decreases Na+ entry into cell u Decreased excitability weakness in muscles u Pseudohyponatremia  Hyporeflexia u Hypocalcemia Na isn't able to enterbell u Easier for Na+ to enter the cell u Increased excitability u Pseudohypernatremia  Hyperreflexia u Imagine this cell is a neuron u Imagine this cell as a myocyte u Skeletal, cardiac & smooth Hypocalcemia hyper St sea gets shortened hypo STgets u S/S: lunner u Hyperreflexia (hyperactive reflexes) u Tetany u Paresthesias (tingling) of lips, tongue, fingers, feet u Intermittent muscle spasms (especially carpopedal spasms and facial spasms) u Convulsions/seizures the u EKG: Long QT interval hand the flexing u Trousseau Sign (hand) salt morme u Chvostek’s sign (face) tap on check Low ionized calcium levels in the extracellular fluid increases the permeability of neuronal membranes to sodium ion, which increases the possibility of action potentials [this is called pseudohypernatremia] Hypocalcemia Hypercalcemia QT Interval ST Segment Long QT Interval Short ST Segment Hypercalcemia S/S exam effects u Painful bones u Renal stones (kidney stones) ca MC u Abdominal groans (abdominal pain, N/V) u Thrones (polyuria  Dehydration) u Psychiatric Overtones (depression, anxiety, confusion, AMS, psychosis) u Other S/S that don’t rhyme, but just as important u Arrhythmias u Hyporeflexia u Muscle weakness Hypocalcemia Hypercalcemia u Causes: Causes: u Hypoparathyroidism Hyperparathyroidism u Vitamin D Deficiency Calcium antacid abuse u Malabsorption Bone Metastasis u Nutritional deficiencies PTH producing tumors u Pancreatitis Paraneoplastic syndrome u EKG Changes: EKG Changes: u Long QT Interval Short ST Segment EKG High Yield u Flattened T Wave u Tall, Peaked T Wave u Long QT interval u Short ST Segment EKG High Yield Flattened T Wave Tall, Peaked T Wave Long QT interval Short ST Segment ↑[H+] / ↓pH / Acidosis ↓[H+] / ↑pH / Alkalosis Signs and Symptoms Signs and Symptoms u Decreased excitability of Over excitability of the the CNS albuin to bindto an CNS effects Restlessness, confusion, uHeadache, lethargy,released convulsions, coma confusion, coma ca when to high Hypokalemia S/S u Hyperkalemia S/S Hypocalcemia S/S u Hypercalcemia S/S Quizizz Module 2 Part 2 https://quizizz.com/ad min/quiz/64fa9229edd 14b0300cc747d?sourc e=quiz_share References Chan T. Y. (1997). Drug-induced syndrome of inappropriate antidiuretic hormone secretion. Causes, diagnosis and management. Drugs & aging, 11(1), 27–44. https://doi.org/10.2165/00002512-199711010-00004 Huether, S. E., & McCance, K. L. (2020). Understanding pathophysiology (7th ed.). St. Louis, MO: Mosby/Elsevier. ISBN-13: 9780323639088 Ratchford, E. V., & Evans, N. S. (2017). Approach to Lower Extremity Edema. Current Treatment Options in Cardiovascular Medicine, 19(3). https://doi.org/10.1007/s11936-017-0518-6 Rockson, S. G. (2018). Lymphedema after Breast Cancer Treatment. New England Journal of Medicine, 379(20), 1937–1944. https://doi.org/10.1056/nejmcp1803290 Saladin, K. S. (2020). Anatomy & Physiology: the unity of form and function. (9th ed.). Mcgraw Hill.

Use Quizgecko on...
Browser
Browser