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
0.45% NaCl-1/2 saline solution
high particles, low water content
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?
Syndrome of Inappropriate ADH (SIADH)
excessive ADH secretion=excessive water retention
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
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?
loop of henle
distal convoulted tubule
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?
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)
obstruction and 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?
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
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?
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
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)
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
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
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