Ch 21 & Ch 22

Front 1

What is homeostasis of body fluids maintained by?

Back 1

hypothalamus via osmoreceptors & thirst mechanisms (osmoreceptors)

kidneys via renin-angiotensin-aldosterone system

hormones via aldosterone

pH regulators such as electrolytes and buffers

Front 2

osmoreceptors

Back 2

specialized neurons in the hypothalamus that monitor the osmotic pressure of the blood

i.e. detect any changes in blood solute concentration

mainly Na+ concentration

Front 3

The Importance of water

Back 3

Universal solvent

Transport medium

necessary for metabolic reactions

% of body water decreases as the amount of fat and age increases - highest in the young, thin, & muscular

body routes for water loss include: kidneys, skin, lungs, & intestines

Front 4

Characteristics of electrolytes

Back 4

Compounds that separate in solution into +ve (cations) and -ve ions (anions)

conduct electric current in solution

important constituents of body fluid

exist in the blood as acids, bases, and salts

i.e. Na+, K, Ca, PO4-3, Cl-

non-electrolytes i.e. glucose, urea, and creatinine are found in body fluids in very small amounts

kidneys are main regulators of electrolyte balance

Front 5

Electrolyte functions

Back 5

Homeostasis of body fluids: blood conc. of electrolytes determines the direction of water movement between compartments (via osmosis)
 Maintain acid/base balance
 Some are cofactors needed for enzyme activity
 Carry electric current: necessary for the propagation of action potential, and for the secretion of neurotransmitters in the synaptic clefts

Front 6

Cations

Back 6

Sodium Na+, major + ve ion in ECF

Potassium K+, major +ve ion in ICF

Calcium Ca++, most abundant mineral in body

Front 7

Sodium Na+ cation

Back 7

major +ve ion in ECF

responsible for maintaining osmotic balance & fluid volume
• required for action potentials in nerve & muscle cells
• important in maintaining acid-base balance

Front 8

Potassium K+

Back 8

major +ve ion in ICF

required for membrane potential & repolarization
• involved in cellular enzymes activities

Front 9

Calcium Ca++

Back 9

most abundant mineral in body

required for bone formation, blood clotting, muscle contraction and nerve impulses

Front 10

Anions

Back 10

Chloride Cl-, most abundant anion in ECF

-essential for HCL formation

-regulates fluid balance & pH

Phosphate PO4-3

-in plasma membranes, nucleic acids & ATP

-essential in carbohydrate metabolism, bone formation, and acid-base balance

Front 11

hypernatremia

Back 11

increase Na+ in body fluids

due to decrease ADH, i.e. diabetes insipidus

renal failure, dehydration, severe vomiting

Front 12

hyponatremia

Back 12

decrease Na+ in body fluids

due to decrease aldosterone i.e. addison's disease

water intoxication, heart or kidney failure, liver cirrhosis, pH imbalance

Front 13

hyperkalemia

Back 13

increase of K+ in body fluid

due to acidosis, addison's disease, kidney failure or dehydration

Front 14

hypokalemia

Back 14

decrease of K+ in body fluid

due to alkalosis

increase aldosterone

diuretics

or acid/base imbalance

Front 15

Buffers

Back 15

maintain normal pH values by absorbing or releasing H+

i.e. controlling H+ ion concentration controls the pH balance

Front 16

acidosis

Back 16

decrease in body fluids pH

may result from: lung disease or kidney failure, prolonged diarrhea, inadequate carbohydrate metabolism i.e. DM type I or a low carb diet

Front 17

alkalosis

Back 17

increase in body fluids pH

may result from: hyperventilation, prolonged vomiting, excess antacids

Front 18

ketone bodies

Back 18

Acidic chemicals released from the catabolism of fats instead of glucose, for energy
--e.g. acetone, acetoacetate & beta-hydroxybutyrate
• Produced by the liver when insulin level is low
• Eliminated in urine; acetone may be eliminated via the lungs
 Ketosis: presence of ketone bodies in the blood
 Ketonuria: presence of ketone bodies in the urine
 Ketoacidosis: acidosis due to  blood levels of ketone bodies, as in DM type I

Front 19

effusion

Back 19

escape of fluid into a cavity or a space

Front 20

pleural effusion

Back 20

fluid in the pleural space

Front 21

pericardial effusion

Back 21

fluid in the pericardial space

Front 22

ascites

Back 22

fluid in the peritoneal cavity

Front 23

edema

Back 23

increase in interstitial/ECF fluid

due to:

injury > inc. capillary permeability > inc fluid loss into interstitial spaces

dec venous return

renal failure > dec urine volume

liver disease > dec plasma albumin > dec osmotic pressure> inc fluid in interstitial spaces

Front 24

water intoxication

Back 24

increase in both ICF and ECF

as in excessive:

drinking, normal saline from IV drip, ADH secretion

Front 25

isotonic solution

Back 25

a solution that has the same salt (solute)
concentration as those in the cells and blood
• has no effect on the RBCs
• e.g. normal saline (0.9% NaCl)
• the first fluid administered in an emergency

Front 26

hypotonic solution

Back 26

a solution that has a lower conc. of solute outside a cell, creating an environment with lower osmotic
pressure than what is contained within the cell >water flows into cells/tissues to equalize osmotic pressure
• e.g. sports drinks with salts & electrolytes; 0.45% NaCl (halfnormal saline solution)
• administered for dehydration cases

Front 27

Hypertonic solution

Back 27

a solution that has a higher conc. of solute
outside the cells, i.e., solute conc. inside the cell is lower
• e.g. serum albumin 25%, administered in cases of edema to pull out the excess interstitial fluid by osmosis
What happens to the RBCs if the osmotic pressure difference is too high?
Crenation of RBCs

Front 28

Kidney functions

Back 28

Excretion of metabolic waste
 Maintenance of water balance
 Regulation of acid-base balance
 Regulation of BP
 Regulation of RBC production

Front 29

Renal cortex

Back 29

extends into the medulla through renal columns

renal capsule, PCT, and DCT are in renal cortex

Front 30

renal medulla

Back 30

renal pyramids - cone-shaped masses of nephrons and collecting ducts

papilla - pointed end of a pyramid

loop of henle & collecting ducts extend into medulla

Front 31

renal pelvis

Back 31

funnel-shaped expansion at the upper end of the ureter

extends into 2-3 major calyces > minor calyces

each minor calyx surrounds a papilla & receives urine from it

Front 32

Nephron

Back 32

Functional unit of the kidney
• renal tubule + glomerulus
 Renal tubule: tiny coiled tube with a bulb at one end, the glomerular/Bowman’s capsule surrounding a tuft of capillaries, the glomerulus
 Renal corpuscle:
• glomerulus + its Bowman's capsule
 Renal Tubule:
• Proximal Convoluted Tubule (PCT)
• Loop of Henle (LOH)
• Distal Convoluted Tubule (DCT)
• Collecting duct

Front 33

Types of nephrons

Back 33

cortical nephrons (85%)

-renal corpuscle in the renal cortex

-function: excretory & regulatory

Juxtamedullary nephrons (15%)

-renal corpuscle closer to the renal medulla

-longer renal tubule

-function: concentration & dilution of urine

Front 34

Glomerulus

Back 34

The main filter of the nephron
 Afferent & efferent arterioles
 Only place in the body where capillaries drain into arterioles
 Glomerular capillaries are impermeable to blood cells & medium to large proteins (e.g. albumin & gamma globulins)

Front 35

Renal Capillaries

Back 35

Peritubular capillaries: arise from the glomerular efferent arteriole,
and travel alongside the nephron allowing reabsorption & secretion
between the blood & the nephron’s inner lumen
• Vasa recta: a second capillary bed arises from the efferent arteriole of
the juxtamedullary nephrons only & extend parallel to the LOH

Front 36

Renal tubule

Back 36

PCT: site of most tubular reabsorption
• by diffusion, osmosis, and active transport
 DCT: site for the regulation of Na+, K+ , Ca ++, H+
• pH regulation via the absorption of bicarbonate & secretion of H+ ions into the filtrate
• Na+ & K+ levels controlled by secreting K+ & absorbing Na+
• Ca++ regulation by absorbing Ca++ in response to the PTH
 Collecting duct: site of urine concentration
• participates in electrolyte & fluid balance

Front 37

principal cells

Back 37

respond to ADH & aldosterone

Front 38

intercalated cells

Back 38

secrete H+ (regulates pH)

Front 39

juxtaglomerular apparatus

Back 39

2 specialized cells at the point of contact of the DCT with the afferent arteriole control the rate of filtrate formation & BP

macula densa cells in the DCT

juxtaglomerular cells in the afferent arteriole

Front 40

formation of urine

Back 40

glomerular filtration

tubular reabsorption

tubular secretion

urine concentration

Front 41

glomerular filtrate

Back 41

water and soluble materials, i.e. electrolytes and small molecules such as nutrients, vitamins and drugs

fluid that enters bowman's capsule

~160-180 L/day

urine output is between 1-1.5L/day (i.e. most of the filtrate is reabsorbed)

Front 42

glomerular filtration

Back 42

movement of materials under BP from glomerulus to bowman's capsular space

Front 43

GFR

Back 43

glomerular filtration rate

amount of filtrate formed in both kidneys per minute

125 ml/minute

Front 44

tubular reabsorption

Back 44

Water, ions, glucose & amino acids are reabsorbed (via diffusion, osmosis & active transport ) into interstitial fluids > peritubular
capillaries /vasa recta > blood circulation
 Most of the urea & nitrogenous wastes (e.g. creatinine) are kept within the tubule to be eliminated in the urine

Front 45

obligatory reabsorption

Back 45

occurs all the time and is consistent

reabsorption of water and nutrients needed by the body

occurs in PCT

Front 46

facultative reabsorption

Back 46

variable reabsorption

depends on the body's needs

occurs in the DCT and the collecting ducts

controlled by ADH, ANP (atrial natriuretic Peptide) and RAAS

Front 47

Tm

Back 47

transport maximum

maximum amount of substance (mg/min) that can be reabsorbed per unit time

Front 48

renal threshold

Back 48

plasma concentration for a substance at which it exceeds the Tm & begins to spill into the urine

i.e. renal threshold for glucose is 180 mg/dl

in DM, blood glucose levels exceed amt and glucose begins to spill in urine

Front 49

tubular secretion

Back 49

Occurs at the DCT
 Secretions of ammonia, uric acid, some vitamins & drugs (e.g. penicillin) for elimination
 Active secretion of K+ & H+
• Secretion of K+ regulates electrolyte balance
• Secretion of H+ regulates the acid-base (pH) balance

Front 50

Urine Concentration

Back 50

Occurs at the DCT & collecting duct
 An intricate exchange of H2O & Na+ in LOH
 Main function of LOH is to create a hyperosmotic medullary tissue to reabsorb water & ions from the urine, using a counter-current mechanism in the medulla > leads to urine concentration & volume reduction

Front 51

descending limb of LOH

Back 51

low permeability to ions & urea

highly permeable to water

Front 52

thin ascending limb of LOH

Back 52

permeable to ions

not permeable to water

Front 53

medullary thick ascending lim of LOH

Back 53

Na, K, Cl ions are reabsorbed from urine by active transport

Front 54

cortical thick ascending limb of LOH

Back 54

drains urine into DCT

Front 55

Source and function of aldosterone

Back 55

Adrenal Cortex, stimulated by angiotensin

promotes reabsorption of Na and H2O from kidneys to conserve water and increase BP

Front 56

source and function of ANP

Back 56

atrial natriuretic peptide

from atrial myocardial cells

released when BP is too high

causes kidneys to excrete Na+ and H2O > dec blood volume and dec bP

Front 57

how does ADH affect renal function?

Back 57

Stimulates the walls of DCT & collecting ducts to be more permeable to water
• In the presence of ADH: water is drawn out of filtrate in the DCT & collecting ducts via the medulla osmotic gradient > urine is
concentrated
• In the absence or  of ADH (as in diabetes insipidus): DCT & collecting ducts are less permeable to water; water remains in the
tubules > dilute urine

Front 58

how does the body respond to dehydration

Back 58

hypothalamus > posterior pituitary > release of ADH > collecting ducts & DCT become more permeable to water > water is reabsorbed by osmosis > into peritubular capillaries > into blood circulation > inc blood volume

Front 59

Urinary bladder

Back 59

When empty, lies below the parietal peritoneum & posterior to the pubic joint; when full, may extend into the abdominal cavity
 An incomplete coat of peritoneum covers the upper portion only, the rest is fibrous connective tissue
 Mucosa: transitional epithelium & rugae
 Submucosa
 Detrusor muscle: 3 layers capable of great stretching

Front 60

trigone

Back 60

anatomical region in the floor of the bladder,
marked by the 2 ureter openings & the internal urethra
• believed to prevent urine backflow into the ureters, when thebladder is full & the muscles contract

Front 61

urinary meatus

Back 61

external urethral opening

Front 62

micturition

Back 62

urination, controlled by:

an internal involuntary urethral sphincter

external voluntary urethral sphincter

Front 63

enuresis

Back 63

involuntary urination usually at night

Front 64

characteristics of urine

Back 64

By volume, odor, acidity, color & density
• ~ 95% water & 5% dissolved solids, such as:
• salts & minerals, urea from protein digestion, uric acid, creatinine from
muscle breakdown, hormone waste & toxins, & urochrome
• Typical volume: 1-2 liters /24 hr/day (for a normal adult)
• Odor of fresh urine is mild; old urine smells like ammonia
• pH of freshly collected urine ~ 6.0 (ranges 4.5-8.0)
• Specific gravity: 1.002 (very dilute) to1.04 (very conc.)
• Normal urine color ranges from pale yellow to deep amber, due to urochrome (a yellow pigment that comes from the processing of dead blood cells in the liver)

Front 65

normal urine constituents

Back 65

Nitrogenous waste:
 e.g. urea; uric acid; ammonia ; creatinine
 Electrolytes:
 e.g. Na+, Cl-, K+, Ca++, Mg++, bicarbonates, sulfates, phosphates,
 Urochrome

Front 66

abnormal urine constituents

Back 66

urinary casts

glucose > glucosuria

albumin > albumminuria

blood > hematuria

ketone bodies > ketonuria

WBCs (pus) > pyuria

Front 67

abnormal urine colors

Back 67

dark yellow - liver problems/dehydration

orange- too many carrots/vit. C

brown- liver disease, hepatitis, melanoma, copper poisoning

greenish- UTI, bile problems, certain drugs

blue - high levels Ca++ or pseudomonas infec

reddish- RBCs, some foods, candy or red dye, lead or mercury poisoning`

Front 68

acute glomerulonephritis/acute poststreptococcal glomerulonephritis

Back 68

most common kidney disease
• usually occurs in children after a strep throat infection
• streptococcal Abs attach to the glomerular membrane injuring it> becomes permeable to RBCs & albumin >spill into urine >hematuria & albuminuria
• if chronic > permanent damage >kidney failure

Front 69

pyelonephritis

Back 69

inflammation of renal pelvis and renal tissues

Front 70

acute pyelonephritis

Back 70

commonly associated with bacterial UTI
 may be due to urinary stasis (partial obstruction of urine flow with stagnation)
 responds well to antibiotics, fluid replacement & fever control

Front 71

chronic pyelonephritis

Back 71

inc BP, albuminuria & dilute urine

may be due to urinary stasis, urinary backflow, or recurrent bacterial UTIs
 May lead to progressive kidney damage

Front 72

hydronephrosis

Back 72

distention of the renal pelvis & calyces with accumulated fluid due to a urinary tract obstruction
• Common causes include:
 pregnancy
 enlarged prostate
 kidney stone that dropped into the ureter
 tumor that presses on the ureter
 scars due to inflammation
• Prompt removal of obstruction > complete recovery

Front 73

polycystic kidney

Back 73

fluid-containing sacs in the renal active tissue destroy the nephrons (gradually via pressure)
• may be a hereditary
• Treatment: dialysis or transplantation

Front 74

kidney tumors

Back 74

most are slow growing
• Symptoms include hematuria & dull pain in kidney region
• do NOT respond to chemo or radiotherapy
• surgical removal is the best option for cure

Front 75

calculi

Back 75

kidney stones

calcium salts or uric acid precipitate out of urine
• Usually form in the renal pelvis or bladder
• May be due to dehydration, urinary stasis and/or UTI

Front 76

staghorn calculi

Back 76

masses of stones that fill renal pelvis and calyces

Front 77

lithotriptor

Back 77

stone cracker

uses external shock waves to shatter kidney stones

lithotripsy - procedure using lithotriptor

Front 78

acute renal failure

Back 78

a sudden, severe > kidney function > electrolyte & acid-base imbalances
• may be due to medical or surgical complications
• may be fatal

Front 79

chronic renal failure

Back 79

gradual loss of nephrons > renal insufficiency (a small dec renal function with fewer symptoms)
• Progression > inc blood levels of nitrogenous wastes > uremia

Front 80

symptoms of chronic renal failure

Back 80

dehydration in early stages

edema in late stages

electrolyte imbalance

hypertension

anemia

uremia

Front 81

treatment of renal failure

Back 81

dialysis - separation of solutes by selective diffusion through semipermeable membrane

Front 82

hemodialysis

Back 82

a semipermeable membrane & a dialysate
 the dialysate is adjusted to have lower solute conc. than in the patient’s blood > excess solutes are pulled out of the blood by
diffusion

Front 83

peritoneal dialysis

Back 83

dialysate in the peritoneal cavity
 the peritoneum acts as the semi-permeable membrane
 waste products & extra fluid pass from the blood into the dialysate, which is then thrown out

Front 84

strictures

Back 84

constricted or abnormally narrow ureters
• may be due to tumors or kidney stones

Front 85

renal ptosis

Back 85

kidneys drop or moving around
• may kink the ureter
• may be due to loss of renal fascia or adipose tissue
• e.g. in starvation, aging, or anorexia nervosa

Front 86

renal colic

Back 86

passage of a small stone along the ureter
• causes excruciating pain which may require morphine

Front 87

cystitis

Back 87

inflammation of the bladder
• a bacterial infection
• 10 x more common in women than men
• bacteria ascend through the urethra to the bladder > causing pain, urgency to urinate, & inc frequency of urination

Front 88

interstitial cystitis

Back 88

inflammation of tissue below the mucosa
• not a bacterial infection
• can only be diagnosed by a cystoscope
• dec bladder capacity & in rare cases ulcers in the bladder lining
• etiology unknown
• no effective treatment

Front 89

hypospadias

Back 89

in males

urethra opens on under surface of penis instead of at end

Front 90

urehtritis

Back 90

inflammation of urethral mucosal membrane and glands

more common in males and females

often due to STDs

Front 91

bladder tumor

Back 91

Most prevalent in men > 50
 90% arise from epithelial lining of the bladder
 Early symptoms: hematuria, frequent urination, absence ofpain or fever

Front 92

risk factors for bladder tumor

Back 92

Heavy cigarette smoking (50% of bladder cancers)
• Industrial chemicals, such as dyes, metals, leather, textiles, & organic chemicals (20-25% of bladder cancers)
• Chronic infestation
• Chronic bladder infections

Front 93

urinary incontinence

Back 93

Occurs twice as often among women as men, but affects both sexes as they age
 May result from:
• a neurological disorder
• trauma to the spinal cord
• weakness of the pelvic muscle
• impaired bladder function
• some medications

Front 94

forms of urinary incontinence

Back 94

Stress incontinence
• due to urethral incompetence
• small amount of urine is released during coughing, sneezing, laughing, lifting or exercising
• Urge incontinence (an overactive bladder)
• due to the inability to control bladder contractions once bladder fullness is sensed
• Overflow incontinence:
• involuntary loss of small amounts of urine resulting from mechanical forces on an over-distended bladder or from other effects of urinary retention on bladder and sphincter function

Front 95

treatment of urinary incontinence

Back 95

Lifestyle modifications: for all forms of incontinence
• modifying diet, reducing liquids before bedtime, eliminating or adding medications
 Kegel (pelvic floor muscle) exercises: for stress incontinence
• strengthen the muscles around the urethra so that urine is less likely to leak even under pressure
 Biofeedback: for stress & urge incontinence
• self-regulation of physiological processes
 Surgery: for stress & overflow incontinence