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Fluid & Electrolyte Balance
involves the composition and movement of body fluids
What are included in body solutions?
- solutes (electrolytes)
- solvents (water)
- substances that dissociate in a solution to form a charged particle or ion
- anions (-)-attracted to the anode
- cations (+)-attracted to the cathode of a wet electrical cell
- substances that do not dissociate in a solution or carry a charge
- glucose, urea
What is the major cation of ECF?
What is the major cation of ICF?
What is the major anion of ECF?
What do serum level measure?
- sodium should be higher and potassium should be low
What are the functions of body fluids?
- transport (nutrients to the cells, bring waste products for elimination, gas exchange)
- hydrolyze food (transform food into energy)
- medium for chemical reactions (regulation of body temperature, transport of oxygen, etc.)
What is the TBW in infants? adult males? adult females? who has a greater fat content?
- infants TBW=75-80%
- adult males=60%
- adult females=50%
- -females have greater % of body fat than men
premature infants have more or less TBW? obese individuals?
- premature infants have a large amount of TBW
- obese individuals have a low amount of TBW because adipose tissue with regards to fat is basically water free
With regards to body fluid, elderly persons have ____ fat & ____ water.
With regards to body fluid, newborns have ____ fat & ____ water.
What is TBW balance determined by?
intake and output
What is the daily water requirements for healthy adults and infants?
1500ml/m2 of body surface area
What are the sources of fluid gains?
- drinking (1000mL)
- foods (1300mL)
- oxidative metabolism (200mL)
Sensible water loss
- measurable loss, person aware
- urine, defecation, drainage from wounds, tubes
- urine b/t 1-2L/QD, 1ml/kg/hr
- feces 200 ml/day, 500ml/day diarrhea
Insensible water loss
- difficult to measure, unaware
- lung (air we exhale)-300ml
- skin (sweating)-500ml
What is the total amount of water loss per day?
What is the distribution of body fluids?
- intracellular fluids (within the cells)-2/3
- extracellular fluids-1/3
What is the ECF broken into?
plasma (vascular) compartmentsinterstitial spaces (fluid b/t cells and outside of the blood vessels)transcellular compartments (1% of our fluid, cerebral spinal fluid, pericardial sac, pleural fluid, etc.)
Is the ECF or ICF higher in babies?
ECF > ICF = high risk for volume deficit (dehydration)
The classification of osmotic activity of body fluids is based on...
concentration, osmolality, tonicity (interchangable terms)
What is the normal osmotic concentration in the body?
What determines serum osmolatity and how is it determined?
- determined by doubling serum sodium level (N=135-145)
- equal distribution of water and particles
- body fluids are normally isotonic
- 0.9% NaCl-normal saline
- low particles, high water content
- cell swells
- 0.45% NaCl-1/2 saline solution
- high particles, low water content
- cell shrinks
- 3% NaCl solution
Passive transport mechanisms
- movement across a semi-permeable membrane
- the movement of solvent (water) through a selectively permeable membrane from an area of lower concentration of solute (particles) and greater concentration of water to higher concentration of solute (particles) and lower concentration of water
- movement of particles along a concentration gradient
- process by which particles move from an area of higher particle concentration to an area of lower particle concentration
- may or may not be able to pass through semi-permeable membrane
- particles are moved from an area of lower concentration to an area of higher concentration
- requires energy from adenosine triphosphate or ATP
- ex. Na and K movement in and out of cells
- a.k.a. capillary filtration pressure
- the force of fluid pressing outward against the vessel wall
- arterial > venous
Colloid osmotic pressure
- the pulling force exerted by colloids (proteins) in a solution which are too large to pass through the walls
- plasma proteins typically do not leave the capillary
- proteins pull fluid back in
- excess fluids and osmotically active plasma proteins are picked up by vessels of the lymphatic system
- without the function of the lymph system, excessive amounts of fluid would accumulate in the interstital spaces
- if lymph system is working properly would pick up excess proteins and prevent edema
What are the 2 main physiologic mechanisms that assist in regulating body water?
- thirst-regulate water intake
- ADH-regulate water output
- occurs with 2% water loss/change in serum osmolality
- conscious desire for water-major factor that determines fluid intake
- osmoreceptors in hypothalamus stimulated by an increase in osmotic pressure of body fluids to initiate thirst
- thirst also stimulated by a decrease in ECF (from sweating, blood loss)
- key role-regulated by ADH
- regulation of ECF volume and osmolality
- increase ECF=increase urine excretion
- decrease ECF=decrease urine excretion
- regulates release of stored ADH
- "water retention hormone"
- increase secretion of ADH=increase water retention
- decrease secretion of ADH=decrease water retension
What regulates the release of ADH?
- plasma osmolality
- volume depletion
Syndrome of Inappropriate ADH (SIADH)
- excessive ADH secretion=excessive water retention
- -dilutional hypoatremia
Diabetes Insipidus (DI)
- caused by (1) decrease ADH secretion or (2) decrease response to ADH
- -causes excessive water excretion
- neurogenic: due to head injury or surgery
- nephrogenic: decrease responses by the kidneys to ADH due to medications, electrolyte imbalances, genetic trait
- secrete aldosterone-primary regulator of sodium
- acts on distal tubules to promote sodium reabsorption in exchange for potassium and hydrogen ions being excreted
- aldosterone cause sodium retention and expansion of ECF and causes excretion of K
What causes the release of aldosterone?
- decrease in Na, blood volume
- increase in K
- angiotension 2
- renin is secreted by glomerular cells in kidneys when there is a decrease in BP, decrease in blood volume, or decrease in Na
- renin is released->blood stream
- converts angiotensinogen to angitensin 1-> converted to angiotensin 2
- angiotensin 2 stimulates Na reabsorption by renal tubules and constricts renal blood vessels
- outcomes: decrease renal blood flow, decrease Na excretion or increase Na reabsorption, decrease urinary output and water reabsorption, increase secretion of aldosterone which further increases Na reabsorption at the distal tubule of the kidney
What activates ANP (atrial natriuretic peptide hormone)?
- prolonged aldosterone elevation
- chronic retention of fluid
- excessive secretion (adrenal tumor)
What is the mechanism involved in ANP activation?
- increase venous return which increases atrial distention which increases the stretch of receptors in the atria and blood vessels
- this action increases the release of the hormone ANP and tells the kidneys to increase excretion of Na and water
- result-decrease blood volume and BP
What does atrial muscle stretching do and what is the result?
- inhibits ADH, renin, and aldosterone in the kidney tubules
- results in-decrease Na reabsorption in tubules, Na and water excretion, and decreased blood volume and BP
What are the functions of the renal system?
- rids body of waste products (cellular metabolism)
- maintains fluid volume (regulates water excretion)
- regulates electrolyte concentration
- maintains normal pH of blood
- control RBC production (secretes erythropoietin hormone)
- maintains normal BP (secretes renin enzyme)
What is the primary organ of the urinary system and what does it do?
- form urine and perform urinary function
- filters blood, removes wastes, excretes the wastes
What are the accessory structures of the urinary system and what do they do?
- ureters-carry urine away from kidneys to bladder
- bladder-reservoir for urine
- urethra-carries urine from bladder to the outside
What are the 3 steps of urine formation?
- 1. glomerular filtration
- 2. tubular reabsorption
- 3. tubular secretion
What occurs during glomerular filtration?
- blood enters kidney through renal artery into afferent arteriole into glomerulus where blood is filtered
- the blood leaves through efferent arteriole and the filtrates enter the glomerular capsule (Bowman's)
- the rate of filtration is related to filtration pressure (the greater the pressure, the greater the filtration and the greater the production of urine)
- filtration is influenced by the blood pressure in the glomerulus, hydrostatic pressure of the fluid in the glomerular capsule, and oncotic pressure from plasma proteins
What occurs during tubular reabsorption?
- 65% of all reabsorption and secretory processes occurs in the proximal tubule: almost complete reabosprtion of nutritionally important substances such as glucose, amino acids, lactate and water soluble vitamins
- filtration of Na, K, Cl, and bicarbonate are 65-80% reabsorbed
- water and urea osmotic reabsorbed
- the PCT secretes H and other unneeded substances
What structure are involved in tubular reabsorption?
- proximal tubule
- loop of henle
- distal convoulted tubule
- collecting duct
What occurs in the Loop of Henle?
- waterm Ns, and Cl are reabsorbed in the descending limb
- only Na and Cl is reabsorbed in the ascending limb, water is impermeable
- the thick ascending loop is site that loop diruetics act
Where is the site that loop diuretics act?
thick ascending loop of henle
What occurs in the distal convoulted tubule and collecting duct?
- the DCT in the prescence of aldosterone reabsorbs Na and water
- Ca reabsorption in prescence of PTH
- the collecting duct in the prescence of ADH reabsorbd water
- distal tubule site of action thiazide diuretics
- 1% of filtrate are excreted in the urine
Where is the site of action for thiazide diuretics?
What occurs during tubular secretion?
- adds substances such as drugs, H, K, creatinine, and histamin to urine
- accumulation of substances in body become toxic
- H ion secretion regulates pH of the blood
- substances are absorbed into collecting duct from efferent arteriole
What are the functions of juxtaglomerular appartus?
- ascending limb comes in contact with afferent arteriole
- ascending limb contant (called the macula densa) it monitors Na and Cl in the urine and influences juxtaglomerular cells
- afferent arteriole produce renin (RAAs) which regulate BP through vasoconstriction
What is the functional unit of the kidney?
- 1.25 million nephrons in the kidneys
amount of filtrate formed each minute as blood moves through the glomerulus
volume of plasma cleared each minute
What is urine output an indicator of?
renal perfusion, NOT renal function
What does aldosterone cause?
Na reabsorption and K secretion
What does ADH cause?
- called vasopressin
- causes water reabsorption and results in the formation of concentrated urine
What causes a urinary tract infection?
- bacteria enter from blood or lower urinary tract
- most common cause-E. Coli bc of its location in G.I. to the rectum
- other causes: uncomplicated UTIs (staphylococcus saprophyticus), complicated UTIs (non E. coli gram neg. rods-proteus mirabilis, klebsilla species, enterobacter species, pseudomonas aeruginosa) and gram pos. cocci-staphy. aureus
What are the etiology factors of UTIs?
- host defense (washout phenomenon)
- pathogen virulence
- obstruction and reflux
- urethrovesical reflux
- vesicourethral reflux
- catheter induced infections
What organism causes and what are the symptoms of cystitis?
- inflammation of the bladder
- organism-most common: E. coli
- symptoms: asymptomatic or urine frequency, urgency, dysuria, suprapubic and low back pain
- severe: hematuria, cloudy urine, flank pain
- UA-bacteria present, 100,000 CFU or more per ml urine; gram stain to determine type of organism present
What are some practices to prevent cystitis?
- drink 8-10 glasses of fluid/day (not just straight water bc can have fluid volume overloas)
- women should wipe front to back
- avoid vaginal deodorants and bubble baths
- urinate after intercourse
What is the 2nd leading cause of kidney failure worldwide?
What are the causes, mainfestations and treatment of acute pyelonephritis?
- upper UTI
- infection of tubules, renal pelvis and interstitium
- causes: gram-neg. bacteria (e. coli, proteus, klebsiella, enterobacter and pseudomonas)
- uncommon: staphylococcus species and streptococcus faecalis
- manifestations: actue fever, chills, flank or groin pain, frequency, dysruia
- treatment: antibiotics for 10-14 days; if doesn't treat may need to be hospitalized
What are the routes of acute pyelonephritis?
- from lower urinary tract (ascending infection) outflow obstruction, catherterization, urinary instrumentationm vesicoureteral refluw, pregnancym neurogenic bladder
- bloodstream (hematogenous spread) less common, result from course of septicemia or infective endocarditis. most frequenctly debilitated chronically ill persons, those receiving immunosuppressive therapy. mestastatic staph or fungal infection may spread to kidney from distant foci in skin or bone
What is the pathology of acute pyelonephritis?
- infection causes WBC with renal inflammation, renal edema, and purulent urine
- abscesses form in the medulla and cortex
- followed by scar tissue and then atrophy of the kidney tubules
What are the causes, symptoms, and pathology of chronic pyelonephritis?
- upper UTI
- persistent or recurrent bacterial infection of kidney with inflammation and scarring of kidney, deformation of renal calyces and pelvis, atrophy and thinning of overlying cortex
- causes: most common reflux which results from superimposition of infection on congenital vesicoureteral reflux or intrarenal reflux. may be unilateral or bilateral, leading to scaring and atrophy of both kidneys
- patho: lesions in the interstitial spaces between tubules
- symptoms: HTN due to retention of Na and fluid, frequency, dysruis, flank pain, renal failur
Drug related Nephropathies
- involve functional and structural changes in kidney
- drugs/toxic substances: dec. renal blood flow, obstructing urine flow, directly damage tubulointerstitial structures or produce hypersensitivity reactions
- diuretic, radiocontrat media, immunosuppressive drugs, NSAIDs
- chronic analgesic nephritis
- illicit drug use
What are the causes of glomerular disorders?
- inflammation of the glomerulus
- caused by immunologic disorders, ischemia, free radicals, drugs and toxins, vascular disorders, and systemic diseases
- most cases of primary and many cases of secondary glomerular disease probably have immune origin
- nonimmunologic-metabolic (diabetes), hemodynamic (HTN), toxic (drugs, chemical)
- inflammation of the glomerulus causes a loff of negative and postive charges resulting in a loss of membrane permeability
- most common cause of chronic and end-stage renal failure
What are the clinical manifestations of glomerular disorders?
- 1. acute nephritic syndromes
- 2. rapidly progressive glomerulonephritis
- 3. nephrotic syndrome
- 4. asymptomatic disorders of urinary sediment (hematuria, proteinuria)
- 5. chronic glomerulonephritis
What is the difference between nephritic and nephrotic syndromes?
- nephritic syndromes produce a proliferative inflammatory response
- nephrotic syndrome produces increased permeability of the glomerulus
- most are mixed
Acute Nephritic syndrome
- clinical correlate of acute proliferative inflammation that occludes glomerular capillary lumen and damages capillary wall
- i.e. acute postinfectious glomerulonephritis
What are the causes, pathology, and symptoms of acute postinfectious glomerulonephritis?
- causes: streptococcal infections-throat and skin. occurs 7-12 days after infection
- pathology: immune complexes are deposited in the glomerulus causing cell proliferation and thickening of the glomerulus. most recover without loss of renal function or recurrence of the disease
- symptoms: oliguria, hematuria, proteinuria, cola-colored urine (bc of breakdown of RBC in urine), edema (face and hands), HTN, diminshed GFR, signs of impaired renal function
- primarily seen in children, esp. in 3rd world countries
Nephrotic Syndrome-path? Characteristics? Types?
- proteinuria> 3.5g/day
- not a specific disease but a constellation of clinical findings (related to symptoms)
- patho: loss of proteins due to glomerular injury, increased permeability
- characteristics: massive proteinuria (3.5g/day in adults), lipiduria (free fat, oval bodies, fatty casts), hypoalbuminemia (<3g/dL), edema (generalized), hyperlipidemia vit. D definciency
- types: membranous glomerulonephritis, focal segmental glomerulosclerosis
- most common primary in adults, 5-6 decades of life
- diffuse thickening of basement membrane due to deposition of immune complexes
Focal Segmental Glomerulsclerosis
- ch. by sclerosis (increased collagen deposition)
- common in hispanics and AA
- increased since 1980s, may be associated with reduced oxygen in blood (sickle cell disease, cyanotic congenital heart ds, HIV or IV drug use)
- in 5-10 years may progress to kidney failure
What are the symptoms associated with nephrotic syndrome?
- urine color: smoky brown-tinged urine (glomerular membrane hematuria), pink or red colored urine (lower site)
- UA: RBC casts, proteinuria (>3 to 5g/day)
- decreased GFR: fluid retention, Na and water reabsorption, fluid volume expansion, HTN
- if untreated: develop renal insufficiency, nephrotic syndrome or end-stage renal failure within 10-20 years
Chronic glomerulonephritis-causes? path?
- represents the chronic phase of a number of specific types of glomerulonephritis
- causes: primary (nephrotic and nephritic syndromes) or seconday (infections, DM, SLE, HTN)
- slow, progressive, with variable onset
- patho: antigen-antibody (IgG or IgA) are depostied in the glomerulus, activating inflammation mediators (complement, leukocytes, fibrin). the inflammatory mediators stimualte the release of neutrophils, monocytes, and lysosomal enzymes which damage the glomerular cell wall causing proliferation of the glomerulus which impedes glomerular blood flow. the loss of charges alters the membrane permeability allowing proteins to be filtered (proteinuria). the damage also leads to platelet aggregation (hematuria)
What is the most common cause of urinary obstruction?
renal calculi (nephrolithiasis)
What are the varies types of renal calculi or stones?
- calcium oxalate or phosphate
- struvite (magnesium ammonium phosphate)
- uric acid
Calcium oxalate or phosphate stones
70-80%, middle age men with family history, prolonged immobilization
Struvite (magnesium ammonium phosphate) stones
15%, form alkaline urine prescence of bacteria. bc phosphate levels are increased in alkaline urine and magnesium always is present in urine, struvite stones form. enlarge as bacteria count grow, can fill entire renal pelvis-staghorn stones. too large to pass lithotripsy or surgical removeal (more common in women)
Uric acid stones
7%, gout or high purine diets (organ meats, red meats, fish, fruits, spinach, lentils, mushrooms, peas, asparagus)
What are the signs/symptoms and treatment of renal calculi?
- signs: renal colic-intense, colicky pain, lasting up to 5 minutes, in flank area and upper outer quadrant of abdomen on affected side; nausea, vomitting, extremely anxious, skin cool and clammy
- treatment: pain meds (Toradol or Demerol), increased fluid intake, decrease dietary sources, strain all urine to catch stone to send for analysis
Renal Adenomas-symptoms? treatment?
- benign tumors near kidney cortex (rare)
- renal cell carcinoma (RCC): 90-95% of all tumors. common in men ages 55-84, 5 year survival rate. 90% if tumor not extended beyond renal capsule, drops 30% if metastasis has occurred
- 7th leading malignancy in men
- symptoms: early-asymptomatic, late-gross hematuria is the most common, flank pain, palpable flank mass, weight loss
- treatment: surgery treatment of choice
- loss of renal function
- it is associated with multiple systemic effects due to their vital regulatory roles, therefore it must be treated aggressively
- 2 types: acute and chronic renal failure
acute renal failure (ARF)
- sudden onset renal failure, usually reversible
- 3 classifications of causes which is determined by patient history: prerenal, intrarenal or intrinsic,postrenal
Prerenal cause of ARF
- hypoperfusion of kidneys resulting in azotemia without structural damage
- causes: hypovolemia-hemorrhage, dehydration, excessive loss of GI fluids, excessive loss due to burn injury; decreased vascular filling-anaphylatic shock, septic shock; heart failure and cardiogentic shock; decreased renal perfusion due to sepsis, vasoactive mediators, drugs, diagnostic agents
Intrarenal or Intrinsic cause of ARF
- structural damage to glomeruli or kidney tubules (acute tubular necrosis)
- causes: actue tubular necrosis (ATN)-prolonged renal ischemia, exposure to nephrotoxic drugs (aminoglycosides), heavy metals and organix solvents, intratubular obstruction resulting from hemoglobinuria, myglobinuria, myeloma light chains, or uric acid casts; acute renal disease-glomerulonephritis or pyelonephritis
Postrenal cause of ARF
- bilateral obstruction to urine flow out of the kidney
- causes: obstruction of outflow from kidenys
- bladder obstruction-tumors or neurogenic bladder rare unless one kidney is already damaged or person only have 1 kidney
- ureteral obstruction-calculi and strictures-both must be obstructed
- urethral obstruction-prostatic hyperplasia-most common underlying problem
What are the 3 phases of acute tubular neccrosis (ATN)?
- 1. onset or initiating phase
- 2. maintenance phase
- 3. recovery
What occurs during the onset or initiating phase of ATN?
onset of percipitating event (ischemia phase of prerenal failure or toxin exposure) until tubular injury occurs
What occurs during the maintenance phase of ATN?
- decreased GFR-sudden retention of endogenous metabolites (urea, K, sulfate, Cr) normally cleared by kidneys-urine output decreased
- fluid retention-edema, eater intoxication, pulmonary congestion
- oliguria prolonged-HTN develops with signs uremia which leads to neuromuscular irritability
What occurs during the recovery phase of ATN?
- repair of renal tissue takes place
- gradual increase in urine output
- fall in serum creatinine indicating nephrons have recovered to point urine excretion is possible
What are the symptoms of acute renal failure?
- urinary changes: output decreases to less than 400 ml/24hrs or 30ml/hr
- UA: hematuria, casts, RBC, WBC, specific gravity fixed at 1.010, urine osmolality 300 mOsm/kg, specific gravity and osmolality same as for plasma levels reflecting tubular damage with loss of concentrating ability of kidney
- fluid vol. excess: urine output dec., resulting in fluid retention. symptoms include JVD, bounding pulse, edema, HTN
- metabolic acidosis
- electrolyte imbalance: hyponatremia, hyperkalemia, hypocalcemia
- uremia: accumulation of nitrogenous products (elevated BUN and Cr levels)
- anemia: dec. erythropoietin production, dec. RBC life span, blood loss from GL tract from uremic gastric lesions
What is the treatment for acute renal failure?
- fluid challenge: 250ml NS over 15 min
- diuretics: osmotics, loop
- low dose dopamine: 5-10mcg/kg/min
- maintain electrolyte balance
Chronic renal failure/chronic kidney disease
- progressive loss of renal function over months to years
- nephron destruction is replaced by non-functional scar tissue
- it's defined by a GFR of less than 60ml/min/1.73m2 for 3 months or more
- advancement of the ds can sometimes be slowed, but is ultimately irreversible and terminates in end-stage renal ds (ESRD), the final stage of CKD
- without dialysis or kidney transplantation, the mortality assocaited with ESRD is 100%
- potential risk factors for susceptibility to and initiation of CKD-
- clinical factors: diabetes, HTN, autoimmune ds, systemic infections, UTI, urinary stones, neoplasia, family history of CKD, recovery from acture kidney failure, exposure to nephrotoxic drugs, low birth weight
- sociodemographic factors: AA, American Indian, Hispanic, Asian or Pacific Islander, elderly, low income, low education