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HORMONE REGULATION OF TUBULAR REABSORPTION/SECRETION
Hormone
What triggers it
Angiotensin ↓ blood volume
II
↓ BP
(stims rennin-induced
production of ango II.
What/Where it happens
Stimulates activity of Na/H+ antiporters
Prosximal tubule cells
Effects
↑ reabsorption of Na+, other solutes, and
water, which ↑ blood volume.
Aldosterone ↑ angiotensin II level and
↑ increased level of plasma K+
promote release of aldosterone
by adrenal cortex.
Enhances activity of Na/K+ pump in
basolateral membrane and Na+ channels in
apical membrane of principal cells in
collecting duct.
↑ secretion of K+ and reabsoption of Na+,
Cl↑ reabsorption of water which
↑ bld volume.
ADH/
↑Increased osmolarity of
Stimulates insertion of water channel
Vasopressin extracellular fluid or
proteins (aquaporin-2) into the apical
↓ bld volume promote release of membranes of principal cells.
ADH from the posterior pituitary
gland.
↑ facultative reabsorption of water which ↓
osmolarity of body fluids.
Atrial
natriuretic
peptide
(ANP)
↑ excretion of Na+ in urine (natriuresis)
↑ urine output (diuresis)
↓ blood volume.
Streching of atria of heart
stimulates secretion of ANP
Suppresses reabsorption of Na+ and water
in proximal tubule and collecting duct
Inhibits secretion of aldosterone and ADH
RENAL CORPUSCLE
GLOMERULAR FILTRATION RATE
FILTERED SUBSTANCES
PROXIMAL CONVOLUTED TUBULE
REABSORPTION into blood of filtered
Water
Na+
K+
Glucose
Amino acids
ClHCO3Urea
Ca+, Mg2+
105-125 mL/min or fluid that is isotonic to blood
Water and all solutes present in blood (except proteins) including ions, glucose,
amio acids, creatinine, uric acid
65% (osmosis)
65% (Na/K pump)
65% (diffusion)
100% (symporters and facilitated diffusion)
100% (symporters and facilitated diffusion)
50% (diffusion)
80-90% (facilitated diffusion)
50% (diffusion)
Variable (diffusion)
SECRETION into urine of:
H+
NH4+
Urea
Creatinine
Variable –antiporters
Variable, increases in acidosis- antiporters
Variable- diffusion
Small amount
****At end of PC Tubule, tubular fluid is still isotonic to blood (300 mOsm/liter)****
LOOP OF HENLE
REABSORPTION into blood of:
Water
15% - osmosis in descending limb
Na+
K+
ClHCO3Ca2+, Mg2+
20-30% -symporters in ascending limb
20-30% -symporters in ascending limb
35% -symporters in ascending limb
10-20% -facilitated diffusion
Variable –diffusion
SECRETION into urine of:
Urea
Variable –recycling from collecting duct
****At end of loop of Henle, tubular fluid is hypotonic (100-150 mOsm/liter)****
DISTAL CONVOLUTED TUBULE
REABSORPTION into blood of:
Water
Na+
ClCa+
10-15% -osmosis
5% -symporters
5% -symporters
Variable- stimulated by parathyroid hormone
PRINCIPLE CELLS IN LATE DISTAL TUBULE AND COLLECTING DUCT
REABSORPTION into bood of:
Water
5-9% -insertion of water channels stimulated
by ADH
Na+
1-4% - Na/K+ pump
Urea
Variable –recycling to loop of Henle
SECRETION into urine of:
K+
Variable amount to adjust for dietary intakeleakage channels
****Tubular fluid leaving the collecting duct is dilute when ADH level is low and concentrated when ADH level is high.****
INTERCALATED CELLS IN LATE DISTAL TUBULE AND COLLECTING DUCT
REABSORPTION into blood of:
HCO3Variable amount, depends on H+ secretion –
antiporters
Urea
Variable – recycling to loop of Henle
SECRETION into urine of:
H+
Variable amounts to maintain acid-base
homeostasis – H+ pumps
REGULATION OF GLOMERULAR FILTERATION RATE (GFR)
Type of Regulation
Major stimulus
Mechanism and site of action
Effect on
GFR
RENAL
AUTOREGULATION
Myogenic
↑ stretching of smooth muscle Streched smooth muscle fibers contract, thereby narrowing the ↓
mechanism
fibers in afferent arteriole walls lumen of the afferent arterioles
due to ↑ BP
Tubuloglomerular
feedback
↓ release of nitric oxide (NO) by the juxtaglomerular
Rapid delivery of Na+ and Cl- to apparatus causes constriction of afferent arterioles.
the macula densa due to ↑ BP
↓
NEURAL
REGULATION
↑ in level of activity of renal
sympathetic nerves releases
norepinephrine
Constriction of afferent arterioles though activation of alpha1 ↓
receptors and ↑ release of renin
HORMONE
REGULATION
↓ blood volume or BP stimulates Constriction of both afferent and efferent arterioles.
production of angiotensin II.
↓
Angiotensin II
Atrial natriuretic
peptide (ANP)
Streching of the atria of the heart Relaxation of mesangial cells in glomerulus increases
stimulates secretion of ANP
capillary surface area available for filtration
↑
CHARACTERISTICS OF NORMAL URINE
CHARACTERISTIC DESCRIPTION
Volume
Color
Turbidity
Odor
pH
Specific gravity
(density)
1-2 L in 24 hrs but varies considerably
Yellow or amber but varies with urine concentration and diet. Color is due to urochrome and urobilin.
Concentrated urine is darker in color. Diet, medication, and certain diseases affect color. Kidney stones may
produce blood in urine.
Transparent when freshly voided but becomes turbid (cloudy) upon standing.
Mildly aromatic but becomes ammonia-like upon standing.
Some people inherit the ability to form methylmercaptan from digested asparagus that gives urine a
characteristic odor.
Urine of diabetics has a fruity odor due to presence of ketone bodies.
4.6-8.0 with an avg of 6.0.
Will vary with diet; high protein increases acidity and vergitarian increases alkalinity
1.001-1.035
Ration of the weight of a volume of a substance to the weight of an equal volume of distilled water. The higher
the concentration of solutes = higher the specific gravity.
FACTORS THAT MAINTAIN BODY WATER BALANCE
FACTOR
MECHANISM
Thirst center in
Stimulates desire to drink fluids
Hypothalamus
Angiotensin II
Stimulates secretion of aldosterone
Aldosterone
By promoting urinary reabsorption of Na+ and Cl-, increases water reabsorption
via osmosis
EFFECT
Water gain if thirst is
quenched.
↓ loss of water in urine
↓ loss of water in
urine.
Strial Natriuretic Peptide
(ANP)
Promotes natriureses, elevated urinary excretion of Na+ and Cl-, accompanied by ↑ loss of water in urine
water
Antidiuretic hormone
(ADH)/ vasopressin
Promotes insertion of water-channel proteins (aquaporin-2) into the apical
membranes of principal cells in the collecting ducts of the kidneys.
As a result, the water permeability of these cells increases and more water is
reabsorbed
↓ loss of water in
urine.
ABNORMAL CONSTITUENTS IN URINE
ABNORMAL SO…?
CONSTITUEN
T
Albumin
∙Is normal in plasma.
∙Usually appears in only very sm amts in urine because it is too large to pass through capillary fenestration.
∙ALBUMINURIA- increase in permeability of filtration membrane due to injury or disease, increased BP, or
irritation of kidney cells by substances such as bacterial toxins, ether, or heavy metals.
Glucose
∙GLUCOSURIA- usually indicated diabetes mellitus.
∙May be caused by stress which can cause excessive amnts of epinephrine to be secreted. Epinph-stimulates the
breakdown of glycogen and liberation of glucose from the liver.
RBCs
Ketone bodies
∙HEMATURIA-indicates a pathological condition d/t acute inflammation of the urinary organs as a result of disease
of irritation from kidney stones, or tumors, trauma, and kidney disease.
∙Ketonuria- may indicate diabetes mellitus, anorexia, starvation, or too little carbs in the diet.
Bilirubin
∙When RBCs are destroyed by macrophages, the globin portion of hemoglobin is split off and the heme is converted
to biliverdin. Most of the biliverdin is converted to bilirubin, which fives bile its major pigmentation.
∙ An above normal level of bilirubin in urine is called BILIRUBINURIA.
Urobilinogen
∙(a breakdown product of hemoglobin)
∙UROBILINOGENURIA-trace amounts are normal, but elevated urobilinogen may be due to hemolytic or
pernicious anemia, infectious hepatitis, biliary obstruction, jaundice, cirrhosis, CHF, or infectious mononucleosis.
Casts
∙(tiny masses of material that have hardened and assumed the shape of the lumen of the tubule in which they
formed.)
∙Are named after the cells or substances that compose them or based on their appearance. Ex: WBC casts, RBC casts.
Microbes
∙Most common: E. coli, Candida albicans, Trichomonas vaginalis.
FACTORS THAT MAINTAIN BODY WATER BALANCE
FACTOR
MECHANISM
Thirst center in
Stimulates desire to drink fluids
Hypothalamus
Angiotensin II
Stimulates secretion of aldosterone
EFFECT
Water gain if thirst is
quenched.
↓ loss of water in urine
↓ loss of water in
urine.
Aldosterone
By promoting urinary reabsorption of Na+ and Cl-, increases water reabsorption
via osmosis
Strial Natriuretic Peptide
(ANP)
Promotes natriureses, elevated urinary excretion of Na+ and Cl-, accompanied by ↑ loss of water in urine
water
Antidiuretic hormone
(ADH)/ vasopressin
↓ loss of water in
urine.
Promotes insertion of water-channel proteins (aquaporin-2) into the apical
membranes of principal cells in the collecting ducts of the kidneys.
As a result, the water permeability of these cells increases and more water is
reabsorbed
WHAT MAINTAINS pH OF BODY FLUIDS
MECHANISM
COMMENTS
BUFFER SYSTEMS
∙Most consist of a weak acid and the salt of that acid, which functions as a weak base.
∙They prevent drastic changes in body fluid pH
Proteins
∙The most abundant buffers in body cells and blood
∙Hemoglobin inside RBCs in a good buffer
Carbonic acid-bicarbonate
∙Important regulator of blood pH.
∙Most abundant buffers in ECF
Phosphates
∙Important buffers in intracellular fluid and in urine
Exhalation of CO2
Kidneys
∙↑ exhalation = of CO2, pH rises
∙↓ exhalation of CO2 = pH falls
∙Renal tubules secrete H+ into the urine and reabsorb HCO3- so it is not lost in the urine.
BLOOD ELECTROLYTE IMBALANCES
Deficiency
ELECTROLYTE
NAME/CAUSE
S/S
Excess
NAME/CAUSE
S/S
Sodium
HYPONATREMIA d/t
Muscle wkness, dizziness, HA, HYPERNATREMIA
Intense thirst, hypertension,
136-148 mEq/liter ↓ Na+ intake
Hypotension, tachycardia, shock, Dehydration, water deprivation, edema, agitation, and
↑ Na+ loss through vomiting, diarrhea, mental confusion, coma
excessive Na+ in diet or IV
convulsions.
↓ aldosterone, diuretics, and excessive
fluids
water intake
Causes hypertonicity of ECF,
which pulls water out of body
cells into ECF, causing cellular
dehydration.
Chloride
HYPOCHLOREMIA d/t
Muscle spasms, metabolic
HYPERCHLOREMIA
Lethargy, wknss, metabolic
95-105
excessive vomiting, over hydration, alkalosis, shallow respiration,
d/t water loss, excessive chloride acidosis, and rapid deep
↓aldosterone CHF, and therapy with hypotension, and tetany
intake, severe renal failure,
breathing
diuretics
hyperaldosteronism, acidosis and
certain drugs
Potassium
HYPOKALEMIA d/t
m. fatigue, flaccid paralysis,
HYPERKALEMIA
Irritability, nausea, vomiting,
3.5-5.0
vomiting or diarrhea, ↓K+ intake,
mental confusion,↑ urine output, d/t excessive intake, renal failure, diarrhea, m. wkness
hyperaldosteronism, kidney disease, shallow respiration, and changes ↓aldosterone , crushing injuries Can cause death by inducting
and diuretics
in the electrocardiogram, flatting to body tissues, or transfusion of ventricular fibrillation.
of T waves
hemolyzed blood
Calcium
HYPOCALCEMIA
N-T of fingers, hyperactive
HYPERCALCEMIA
Lethargy, wkness, anorexia,
5.9-10.5
d/t ↑ ca+ loss, reduced ca+ intake,
reflexes, m. cramps, tetany, and d/t hyperparathyroidism, CA,
nausea, vomiting, polyuria,
↑elevated levels of phosphate
convulsions. Bone fx, spasms of excessive intake of vit. D and
itching, bone pain, depression,
hypoparathyroidism
laryngeal muscles that cause
Paget’s disease of bone.
confusion, paresthesia, stupor,
death by asphyxiation
and coma.
Phosphate
HYPOPHOSPHATEMIA d/t
Confusion, seizures, coma, chest, HYPERPOSPHATEMIA
Anorexia, nausea,vomiting,
1.7-2.6
↑ urinary losses,
and muscle pain, numbness and d/t kidneys fail to excrete excess muscular weakness, hyperactive
↓ intestinal absorption, or ↑ utilization tingling or the fingers, ↓
phosphate (in renal failure,), also reflexes, tetany, and tachycardia.
coordination, memory loss and d/t ↑ intake of phosphates or
lethargy
destruction of body cells which
releases phosphates into the
blood.
Magnesium
HYPOMAGNESEMIA d/t
Wknss, irritability, tetany,
HYPERMAGNESEMIA
Hypotension, muscular
1.3-2.1
inadequate intake or excessive loss in deliruium, convulsions,
d/t renal failure, ↑ intake of Mg weakness, or paralysis, nausea,
urine or feces, alcoholism,
confusion, anorexia, nausea,
as in antacids; ↓aldosterone
vomiting, and altered mental
malnutrition, DM, and diuretic therapy vomiting, paresthesia, and
deficiency and hypothyroidism. functioning.
cardiac arrhythmias
ACIDOSIS AND ALKALOSIS
CONDITION DEFINITION
COMMON CAUSES
COMPENSATORY MECH.
Respiratory ∙↑ Pco2 and
Acidosis
∙↓ pH if there is no
compensation
Hypoventilation d/t emphysema,
Renal:↑ excretion of H+
pulmonary edema, trauma to respiratory ↑ reabsorption of HCO3-.
center, airway obstructions or dysfunction If compensation is complete, pH will be within
of muscles of respiration
the normal range but Pco2 will be high
Respiratory ∙↓ HCO3- and
Alkalosis
∙↓ pH if there is no
compensation
Hyperventilation d/t O2 defiiciency,
pulmonalry disease, CVA or severe
anxiety
Renal: ↓ excretion of H+
↓ reabsorption of HCO3If compensation is complete, pH will be within
the normal range but Pco2 will be low.
Metabolic
Acidosis
∙↓ HCO3- and
∙↓ pH if there is no
compensation
Loss of bicarbonate ions d/t diarrhea,
accumulation of acid (ketosis), renal
dysfunction.
Respiratory: Hyperventilation, which increases
loss of CO2.
If compensation is complete, pH will be within
the normal range but HCO3- will be low.
Metabolic
Alkalosis
∙↑ HCO3- and
∙↑ pH if there is no
compensation
Loss of acid d/t vomiting, gastric
suctioning, or use of certain diuretics;
excessive intake of alkaline drugs.
Respiratory: Hypoventilation, which slows loss
of CO2. If compensation is complete, pH will
be within the normal range but HCO3- will be
high.