final exam review summer 2010 chapters 16, 25, and 26

Final Exam Review

Summer 2010Chapters 16, 25, and 26

Kidney Functions

• Removal of toxins, metabolic wastes, and excess ions from the blood

• Regulation of blood volume, chemical composition, and pH

Kidney Functions

• Gluconeogenesis during prolonged fasting• Endocrine functions– Renin: regulation of blood pressure and kidney

function– Erythropoietin: regulation of RBC production

• Activation of vitamin D

Urine Movement1. glomerulus 2. proximal convoluted tubule 3. loop of Henle4. distal convoluted tubule 5. collecting duct6. minor calyx7. major calyx8. pelvis9. ureter10. bladder urethra

Figure 25.5

Nephron

• Functional unit of kidney• Units of nephron– Renal corpuscle• Bowman’s (glomerular) capsule• Glomerulus

– Tubules• PCT• Loop of Henle• DCT• Collecting duct

Figure 25.3

Renal cortex

Renal medulla

Major calyx

Papilla ofpyramidRenal pelvis

Ureter

Minor calyx

Renal column

Renal pyramid in renal medulla

Fibrous capsule

Renalhilum

(a) Photograph of right kidney, frontal section (b) Diagrammatic view

Filtration Membrane

• Porous membrane between the blood and the capsular space

• Consists of1. Fenestrated endothelium of the glomerular capillaries2. Visceral membrane of the glomerular capsule (podocytes

with foot processes and filtration slits)3. Gel-like basement membrane (fused basal laminae of the

two other layers)

Figure 25.9a

Glomerular capillarycovered by podocyte-containing visceral layer of glomerular capsule

Glomerular capillaryendothelium (podocyte covering and basement membrane removed)

Proximal convolutedtubule

Parietal layerof glomerular capsule

Afferentarteriole

Glomerular capsular space

Fenestrations(pores)

Efferentarteriole

Podocytecell body

Foot processesof podocyte

Filtration slits

Cytoplasmic extensionsof podocytes

(a) Glomerular capillaries and the visceral layer of the glomerular capsule

Figure 25.5

Fenestratedendotheliumof the glomerulus

Podocyte

Basementmembrane

Glomerular capsule: visceral layer

Filtration Membrane

• Allows passage of water and solutes smaller than most plasma proteins– Fenestrations prevent filtration of blood cells– Negatively charged basement membrane repels

large anions such as plasma proteins– Slit diaphragms also help to repel

macromolecules

Figure 25.9c

(c) Three parts of the filtration membrane

Fenestration(pore)

Filtrate incapsularspace

Foot processesof podocyte

Filtration slit

Slit diaphragm

Capillary

Filtration membrane• Capillary endothelium• Basement membrane• Foot processes of podocyte of glomerular capsule

Plasma

Kidney Physiology: Mechanisms of Urine Formation

• Filtrate– Blood plasma minus proteins

• Urine– <1% of total filtrate– Contains metabolic wastes and unneeded

substances

Juxtaglomerular Apparatus (JGA)

• One per nephron• Important in regulation of filtrate formation

and blood pressure• Involves modified portions of the– Distal portion of the ascending limb of the loop of

Henle– Afferent (sometimes efferent) arteriole


• Granular cells (juxtaglomerular, or JG cells)– Enlarged, smooth muscle cells of arteriole– Secretory granules contain renin– Act as mechanoreceptors that sense blood

pressure– decrease in BP stimulates renin secretion– Renin activates angiotensinogen then converted

to angiotensin II– Angiotensin II stimulates aldosterone secretion

and vasoconstriction


• Macula densa– Tall, closely packed cells of the ascending limb– Act as chemoreceptors that sense NaCl content

of filtrate

Figure 25.12

Stretch of smoothmuscle in walls of afferent arterioles

Blood pressure inafferent arterioles; GFR

Vasodilation ofafferent arterioles

GFR

Myogenic mechanismof autoregulation

Release of vasoactive chemical inhibited

Intrinsic mechanisms directly regulate GFR despitemoderate changes in blood pressure (between 80 and 180 mm Hg mean arterial pressure).

Extrinsic mechanisms indirectly regulate GFRby maintaining systemic blood pressure, whichdrives filtration in the kidneys.

Tubuloglomerularmechanism ofautoregulation

Hormonal (renin-angiotensin)mechanism Neural controls

SYSTEMIC BLOOD PRESSURE

GFR

Macula densa cellsof JG apparatus of kidney

Filtrate flow andNaCl in ascendinglimb of Henle’s loop

Targets

Granular cells ofjuxtaglomerularapparatus of kidney

Angiotensinogen Angiotensin II

Adrenal cortex Systemic arterioles

(+) Renin

Release

Catalyzes cascaderesulting in conversion

(+)

(+)

(+)

Kidney tubules

Aldosterone

Releases

Targets

Vasoconstriction;peripheral resistance

Blood volume

Na+ reabsorption;water follows

Systemicblood pressure

(+)

(+) (–)

IncreaseDecrease

StimulatesInhibits

Baroreceptors inblood vessels ofsystemic circulation

Sympatheticnervous system

(+)

(–)

Vasodilation ofafferent arterioles

Mechanisms of Urine Formation

1. Glomerular filtration2. Tubular reabsorption– Returns all glucose and amino acids, 99% of

water, salt, and other components to the blood

3. Tubular secretion– Reverse of reabsorption: selective addition to

urine

Glomerular Filtration

• Passive mechanical process driven by hydrostatic pressure

• The glomerulus is a very efficient filter because– Its filtration membrane is very permeable and it has a

large surface area– Glomerular blood pressure is higher (55 mm Hg) than

other capillaries• Molecules >5 nm are not filtered (e.g., plasma proteins)

and function to maintain colloid osmotic pressure of the blood

Sodium Reabsorption

• Na+ (most abundant cation in filtrate)– Primary active transport out of the tubule cell by– Na+-K+ ATPase

Sodium Reabsorption

• Low hydrostatic pressure and high osmotic pressure in the peritubular capillaries

• Promotes bulk flow of water and solutes (including Na+)

Reabsorption of Nutrients, Water, and Ions

• Na+ reabsorption provides the energy and the means for reabsorbing most other substances

• Organic nutrients are reabsorbed by secondary active transport

Reabsorption of Nutrients, Water, and Ions

• Water is reabsorbed by osmosis (obligatory water reabsorption)

• Cations and fat-soluble substances follow by diffusion

Formation of Dilute Urine

• Filtrate is diluted in the ascending loop of Henle

• In the absence of ADH, dilute filtrate continues into the renal pelvis as dilute urine

• Alcohol inhibits secretion of ADH• Na+ and other ions may be selectively

removed in the DCT and collecting duct, decreasing osmolality to as low as 50 mOsm

Formation of Concentrated Urine

• Depends on the medullary osmotic gradient and ADH

• ADH triggers reabsorption of H2O in the collecting ducts

• Facultative water reabsorption occurs in the presence of ADH so that 99% of H2O in filtrate is reabsorbed

Regulation of Water Output: Influence of ADH

• Water reabsorption in collecting ducts is proportional to ADH release

• ADH dilute urine and volume of body fluids

• ADH concentrated urine

Tubular Secretion

• Reabsorption in reverse – K+, H+, NH4

+, creatinine, and organic acids move from peritubular capillaries or tubule cells into filtrate

• Disposes of substances that are bound to plasma proteins

Tubular Secretion

• Eliminates undesirable substances that have been passively reabsorbed (e.g., urea and uric acid)

• Rids the body of excess K+

• Controls blood pH by altering amounts of H+ or HCO3

– in urine

Regulation of Water Output: Influence of ADH

• Hypothalamic osmoreceptors trigger or inhibit ADH release

• Other factors may trigger ADH release via large changes in blood volume or pressure, e.g., fever, sweating, vomiting, or diarrhea; blood loss; and traumatic burns

Figure 26.6

OsmolalityNa+ concentration

in plasma

Stimulates

Releases

Osmoreceptorsin hypothalamus

Negativefeedbackinhibits

Posterior pituitary

ADH

Inhibits

Stimulates

Baroreceptorsin atrium andlarge vessels

Stimulates Plasma volumeBP (10–15%)

Antidiuretichormone (ADH)

Targets

Effects

Results in

Collecting ductsof kidneys

OsmolalityPlasma volume

Water reabsorption

Scant urine

Disorders of Water Balance: Hypotonic Hydration

• Cellular over hydration or water intoxication• Occurs with renal insufficiency or rapid

excess water ingestion or SIADH • ECF is diluted hyponatremia net osmosis

into tissue cells swelling of cells severe metabolic disturbances (nausea, vomiting, muscular cramping, cerebral edema) possible death

Homeostatic Imbalances of ADH

• ADH deficiency — diabetes insipidus; huge output of urine and intense thirst

• ADH hypersecretion (after neurosurgery, trauma, or secreted by cancer cells)—syndrome of inappropriate ADH secretion (SIADH)

Disorders of Water Balance: Edema

• Atypical accumulation of IF fluid tissue swelling• Due to anything that increases flow of fluid out of

the blood or hinders its return• Blood pressure• Capillary permeability (usually due to inflammatory

chemicals) • Incompetent venous valves, localized blood vessel

blockage • Congestive heart failure, hypertension, blood

volume• Loss or decrease production of plasma proteins, liver

disease, urine loss of proteins

Edema

• Hindered fluid return occurs with an imbalance in colloid osmotic pressures, e.g., hypoproteinemia ( plasma proteins)– Fluids fail to return at the venous ends of capillary

beds– Results from protein malnutrition, liver disease, or

glomerulonephritis

Edema

• Blocked (or surgically removed) lymph vessels– Cause leaked proteins to accumulate in IF– Colloid osmotic pressure of IF draws fluid from

the blood– Results in low blood pressure and severely

impaired circulation

Composition of Body Fluids

• Electrolytes– Dissociate into ions in water; e.g., inorganic salts,

all acids and bases, and some proteins – The most abundant (most numerous) solutes– Have greater osmotic power than nonelectrolytes,

so may contribute to fluid shifts– Determine the chemical and physical reactions of

fluids

Composition of Body Fluids

• Water: the universal solvent • Solutes: nonelectrolytes and electrolytes– Nonelectrolytes: most are organic• Do not dissociate in water: e.g., glucose, lipids,

creatinine, and urea

Extracellular and Intracellular Fluids

• Each fluid compartment has a distinctive pattern of electrolytes

• ECF– All similar, except higher protein content of

plasma• Major cation: Na+ • Major anion: Cl–

Extracellular and Intracellular Fluids

• ICF:– Low Na+ and Cl–

– Major cation: K+

– Major anion HPO42–

Central Role of Sodium

• Most abundant cation in the ECF• The body’s water volume is closely tied to the

level of sodium in its respective space • Sodium salts in the ECF contribute 280 mOsm of

the total 300 mOsm ECF solute concentration• Na+ leaks into cells and is pumped out against its

electrochemical gradient• Na+ content may change but ECF Na+

concentration remains stable due to osmosis

Fluid Movement Among Compartments

• Regulated by osmotic and hydrostatic pressures

• Water moves freely by osmosis; osmolalities of all body fluids are almost always equal

• Two-way osmotic flow is substantial• Ion fluxes require active transport or channels• Change in solute concentration of any

compartment leads to net water flow

Electrolyte Balance

• Importance of salts– Controlling fluid movements– Excitability– Secretory activity– Membrane permeability

Regulation of Sodium Balance: Aldosterone

• Na+ reabsorption– 65% is reabsorbed in the proximal tubules – 25% is reclaimed in the loops of Henle

• Aldosterone active reabsorption of remaining Na+

• Water follows Na+ if ADH is present


• Renin-angiotensin mechanism is the main trigger for aldosterone release– Granular cells of JGA secrete renin in response to• Sympathetic nervous system stimulation• Filtrate osmolality• Stretch (due to blood pressure)


• Renin catalyzes the production of angiotensin II, which prompts aldosterone release from the adrenal cortex

• Aldosterone release is also triggered by elevated K+ levels in the ECF

• Aldosterone brings about its effects slowly (hours to days)

Figure 26.8

K+ (or Na+) concentrationin blood plasma*

Stimulates

Releases

Targets

Renin-angiotensinmechanism

Negativefeedbackinhibits

Adrenal cortex

Kidney tubules

Aldosterone

Effects

Restores

Homeostatic plasmalevels of Na+ and K+

Na+ reabsorption K+ secretion

Regulation of Potassium Balance

• Influence of aldosterone– Stimulates K+ secretion (and Na+ reabsorption) by

principal cells– Increased K+ in the adrenal cortex causes• Release of aldosterone• Potassium secretion

Regulation of Sodium Balance: ANP

• Released by atrial cells in response to stretch ( blood pressure)

• Effects• Decreases blood pressure and blood volume:– ADH, renin and aldosterone production– Excretion of Na+ and water– Promotes vasodilation directly and also by

decreasing production of angiotensin II

Figure 26.9

Stretch of atriaof heart due to BP

Atrial natriuretic peptide (ANP)

Adrenal cortexHypothalamusand posterior

pituitary

Collecting ductsof kidneys

JG apparatusof the kidney

ADH release Aldosterone release

Na+ and H2O reabsorption

Blood volume

Vasodilation

Renin release*

Blood pressure

Releases

Negativefeedback

Targets

Effects

Effects

Inhibits

Effects

Inhibits

Results in

Results in

Angiotensin II

Acid-Base Balance

• pH affects all functional proteins and biochemical reactions

• Normal pH of body fluids– Arterial blood: pH 7.4– Venous blood and IF fluid: pH 7.35– ICF: pH 7.0

• Alkalosis or alkalemia: arterial blood pH >7.45• Acidosis or acidemia: arterial pH < 7.35

Acid-Base Balance

• Most H+ is produced by metabolism– Phosphoric acid from breakdown of phosphorus-

containing proteins in ECF– Lactic acid from anaerobic respiration of glucose – Fatty acids and ketone bodies (strong organic

acids) or from fat metabolism – H+ liberated when CO2 is converted to HCO3

– in blood

Acid-Base Balance

• Concentration of hydrogen ions is regulated sequentially by– Chemical buffer systems: rapid; first line of

defense– Brain stem respiratory centers: act within 1–3 min– Renal mechanisms: most potent, but require

hours to days to effect pH changes

Chemical Buffer Systems

• Chemical buffer: system of one or more compounds that act to resist pH changes when strong acid or base is added

1. Bicarbonate buffer system2. Phosphate buffer system3. Protein buffer system

Bicarbonate Buffer System

• Mixture of H2CO3 (weak acid) and salts of HCO3

– (e.g., NaHCO3, a weak base)

• Buffers ICF and ECF• The only important ECF buffer


• If strong acid is added:– HCO3

– ties up H+ and forms H2CO3 • HCl + NaHCO3 H2CO3 + NaCl

– pH decreases only slightly, unless all available HCO3

– (alkaline reserve) is used up

– HCO3– concentration is closely regulated by the

kidneys


• If strong base is added– It causes H2CO3 to dissociate and donate H+

– H+ ties up the base (e.g. OH–)• NaOH + H2CO3 NaHCO3 + H2O

– pH rises only slightly– H2CO3 supply is almost limitless (from CO2 released

by respiration) and is subject to respiratory controls

Physiological Buffer Systems

• Respiratory and renal systems– Act more slowly than chemical buffer systems– Have more capacity than chemical buffer systems

Respiratory Regulation of H+

• Respiratory system eliminates CO2

• A reversible equilibrium exists in the blood:– CO2 + H2O H2CO3 H+ + HCO3

–

• During CO2 unloading the reaction shifts to the left (and H+ is incorporated into H2O)

• During CO2 loading the reaction shifts to the right (and H+ is buffered by proteins)


• Hypercapnia activates medullary chemoreceptors

• Rising plasma H+ activates peripheral chemoreceptors– More CO2 is removed from the blood

– H+ concentration is reduced


• Alkalosis depresses the respiratory center– Respiratory rate and depth decrease– H+ concentration increases

• Respiratory system impairment causes acid-base imbalances– Hypoventilation respiratory acidosis– Hyperventilation respiratory alkalosis

Acid-Base Balance

• Chemical buffers cannot eliminate excess acids or bases from the body– Lungs eliminate volatile carbonic acid by

eliminating CO2

– Kidneys eliminate other fixed metabolic acids (phosphoric, uric, lactic acids and ketones) and prevent metabolic acidosis

Renal Mechanisms of Acid-Base Balance

• Most important renal mechanisms– Conserving (reabsorbing) or generating new HCO3

–

– Excreting HCO3–

• Generating or reabsorbing one HCO3– is the

same as losing one H+ • Excreting one HCO3

– is the same as gaining one H+

Renal Mechanisms of Acid-Base Balance

• Renal regulation of acid-base balance depends on secretion of H+

• H+ secretion occurs in the PCT and in collecting duct type A intercalated cells:– The H+ comes from H2CO3 produced in reactions

catalyzed by carbonic anhydrase inside the cells

Reabsorption of Bicarbonate• Tubule cell luminal membranes are impermeable to

HCO3–

– CO2 combines with water in PCT cells, forming H2CO3

– H2CO3 dissociates– H+ is secreted, and HCO3

– is reabsorbed into capillary blood– Secreted H+ unites with HCO3

– to form H2CO3 in filtrate, which generates CO2 and H2O

• HCO3– disappears from filtrate at the same rate that it

enters the peritubular capillary blood

Generating New Bicarbonate Ions

• Two mechanisms in PCT and type A intercalated cells– Generate new HCO3

– to be added to the alkaline reserve

• Both involve renal excretion of acid via secretion and excretion of H+ or NH4

+

Excretion of Buffered H+

• Dietary H+ must be balanced by generating new HCO3

–

• Most filtered HCO3– is used up before filtrate

reaches the collecting duct

Excretion of Buffered H+

• Intercalated cells actively secrete H+ into urine, which is buffered by phosphates and excreted

• Generated “new” HCO3– moves into the

interstitial space via a cotransport system and then moves passively into peritubular capillary blood

Abnormalities of Acid-Base Balance

• Respiratory acidosis and alkalosis• Metabolic acidosis and alkalosis

Respiratory Acidosis and Alkalosis

• The most important indicator of adequacy of respiratory function is PCO2

level (normally 35–45 mm

Hg) – PCO2

above 45 mm Hg respiratory acidosis

• Most common cause of acid-base imbalances• Due to decrease in ventilation or gas exchange

• Characterized by falling blood pH and rising PCO2

Respiratory Acidosis and Alkalosis

• PCO2 below 35 mm Hg respiratory alkalosis

– A common result of hyperventilation due to stress or pain

Metabolic Acidosis and Alkalosis

• Any pH imbalance not caused by abnormal blood CO2 levels

• Indicated by abnormal HCO3– levels


• Causes of metabolic acidosis– Ingestion of too much alcohol ( acetic acid)– Excessive loss of HCO3

– (e.g., persistent diarrhea)

– Accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure


• Metabolic alkalosis is much less common than metabolic acidosis– Indicated by rising blood pH and HCO3

–

– Caused by vomiting of the acid contents of the stomach or by intake of excess base (e.g., antacids)

Respiratory and Renal Compensations

• If acid-base imbalance is due to malfunction of a physiological buffer system, the other one compensates– Respiratory system attempts to correct metabolic

acid-base imbalances– Kidneys attempt to correct respiratory acid-base

imbalances

Respiratory Compensation

• In metabolic acidosis– High H+ levels stimulate the respiratory centers– Rate and depth of breathing are elevated – Blood pH is below 7.35 and HCO3

– level is low

– As CO2 is eliminated by the respiratory system, PCO2

falls below normal

Respiratory Compensation

• Respiratory compensation for metabolic alkalosis is revealed by:– Slow, shallow breathing, allowing CO2

accumulation in the blood– High pH (over 7.45) and elevated HCO3

– levels

Renal Compensation

• Hypoventilation causes elevated PCO2

• (respiratory acidosis)– Renal compensation is indicated by high HCO3

– levels

• Respiratory alkalosis exhibits low PCO2 and high

pH– Renal compensation is indicated by decreasing

HCO3– levels

Mechanisms of Hormone Action

• Hormone action on target cells1. Alter plasma membrane permeability of

membrane potential by opening or closing ion channels

2. Stimulate synthesis of proteins or regulatory molecules

3. Activate or deactivate enzyme systems4. Induce secretory activity5. Stimulate mitosis


• Two mechanisms, depending on their chemical nature1. Water-soluble hormones (all amino acid–based hormones

except thyroid hormone)• Cannot enter the target cells• Act on plasma membrane receptors• Coupled by G proteins to intracellular second

messengers that mediate the target cell’s response


2. Lipid-soluble hormones (steroid and thyroid hormones)• Act on intracellular receptors that directly activate

genes

Target Cell Specificity

• Target cells must have specific receptors to which the hormone binds– ACTH receptors are only found on certain cells of

the adrenal cortex– Thyroxin receptors are found on nearly all cells of

the body

Target Cell Activation

• Target cell activation depends on three factors1. Blood levels of the hormone2. Relative number of receptors on or in the target

cell3. Affinity of binding between receptor and

hormone

The Posterior Pituitary

• Contains axons of hypothalamic neurons• Stores antidiuretic hormone (ADH) and

oxytocin• ADH and oxytocin are released in response to

nerve impulses• Both use PIP-calcium second-messenger

mechanism at their targets

Oxytocin

• Stimulates uterine contractions during childbirth by mobilizing Ca2+ through a PIP2-Ca2+ second-messenger system

• Also triggers milk ejection (“letdown” reflex) in women producing milk

• Plays a role in sexual arousal and orgasm in males and females

Antidiuretic Hormone (ADH)

• Hypothalamic osmoreceptors respond to changes in the solute concentration of the blood

• If solute concentration is high– Osmoreceptors depolarize and transmit impulses

to hypothalamic neurons– ADH is synthesized and released, inhibiting urine

formation

Antidiuretic Hormone (ADH)

• If solute concentration is low– ADH is not released, allowing water loss

• Alcohol inhibits ADH release and causes copious urine output

Growth Hormone (GH)

• Produced by somatotrophs • Stimulates most cells, but targets bone and

skeletal muscle• Promotes protein synthesis and encourages

use of fats for fuel• Most effects are mediated indirectly by

insulin-like growth factors (IGFs)

Adrenocorticotropic Hormone (Corticotropin)

• Regulation of ACTH release– Triggered by hypothalamic corticotropin-releasing

hormone (CRH) in a daily rhythm– Internal and external factors such as fever,

hypoglycemia, and stressors can alter the release of CRH

Glucocorticoids (Cortisol)

• Cortisol is the most significant glucocorticoid– Released in response to ACTH, patterns of eating

and activity, and stress– Prime metabolic effect is gluconeogenesis—

formation of glucose from fats and proteins– Promotes rises in blood glucose, fatty acids, and

amino acids

Mineralocorticoids

• Regulate electrolytes (primarily Na+ and K+) in ECF– Importance of Na+: affects ECF volume, blood

volume, blood pressure, levels of other ions– Importance of K+: sets RMP of cells

• Aldosterone is the most potent mineralocorticoid – Stimulates Na+ reabsorption and water retention

by the kidneys

Mechanisms of Aldosterone Secretion

1. Renin-angiotensin mechanism: decreased blood pressure stimulates kidneys to release renin, triggers formation of angiotensin II, a potent stimulator of aldosterone release

2. Plasma concentration of K+: Increased K+ directly influences the zona glomerulosa cells to release aldosterone

3. ACTH: causes small increases of aldosterone during stress

4. Atrial natriuretic peptide (ANP): blocks renin and aldosterone secretion, to decrease blood pressure

Adrenal Medulla

• Chromaffin cells secrete epinephrine (80%) and norepinephrine (20%)

• These hormones cause– Blood glucose levels to rise– Blood vessels to constrict– The heart to beat faster– Blood to be diverted to the brain, heart, and

skeletal muscle

Adrenal Medulla

• Epinephrine stimulates metabolic activities, bronchial dilation, and blood flow to skeletal muscles and the heart

• Norepinephrine influences peripheral vasoconstriction and blood pressure

Figure 16.16

Short-term stress More prolonged stress

Stress

Hypothalamus

CRH (corticotropin-releasing hormone)

Corticotroph cellsof anterior pituitary

To target in blood

Adrenal cortex(secretes steroidhormones)

GlucocorticoidsMineralocorticoids

ACTH

Catecholamines(epinephrine andnorepinephrine)

Short-term stress response

1. Increased heart rate2. Increased blood pressure3. Liver converts glycogen to glucose and releases glucose to blood4. Dilation of bronchioles5. Changes in blood flow patterns leading to decreased digestive system activity and reduced urine output6. Increased metabolic rate

Long-term stress response

1. Retention of sodium and water by kidneys2. Increased blood volume and blood pressure

1. Proteins and fats converted to glucose or broken down for energy2. Increased blood glucose3. Suppression of immune system

Adrenal medulla(secretes amino acid-based hormones)

Preganglionicsympatheticfibers

Spinal cord

Nerve impulses

Parathyroid Hormone

• PTH—most important hormone in Ca2+ homeostasis

• Functions– Stimulates osteoclasts to digest bone matrix – Enhances reabsorption of Ca2+ and secretion of

phosphate by the kidneys– Promotes activation of vitamin D (by the kidneys);

increases absorption of Ca2+ by intestinal mucosa• Negative feedback control: rising Ca2+ in the

blood inhibits PTH release

Figure 16.12

Intestine

Kidney

Bloodstream

Hypocalcemia (low blood Ca2+) stimulatesparathyroid glands to release PTH.

Rising Ca2+ inblood inhibitsPTH release.

1 PTH activatesosteoclasts: Ca2+

and PO43S released

into blood.

2 PTH increasesCa2+ reabsorptionin kidneytubules.

3 PTH promoteskidney’s activation of vitamin D,which increases Ca2+ absorptionfrom food.

Bone

Ca2+ ions

PTH Molecules

Glucagon

• Major target is the liver, where it promotes– Glycogenolysis—breakdown of glycogen to

glucose– Gluconeogenesis—synthesis of glucose from lactic

acid and noncarbohydrates– Release of glucose to the blood

Insulin

• Effects of insulin– Lowers blood glucose levels– Enhances membrane transport of glucose into fat

and muscle cells– Participates in neuronal development and learning

and memory– Inhibits glycogenolysis and gluconeogenesis

Homeostatic Imbalances of Insulin• Diabetes mellitus (DM)– Due to hyposecretion or hypoactivity of insulin– Three cardinal signs of DM• Polyuria—huge urine output• Polydipsia—excessive thirst• Polyphagia—excessive hunger and food consumption

• Hyperinsulinism:– Excessive insulin secretion; results in hypoglycemia,

disorientation, unconsciousness

Table 16.4

Gonadotropins

• Follicle-stimulating hormone (FSH) and luteinizing hormone (LH)

• Secreted by gonadotrophs of the anterior pituitary

• FSH stimulates gamete (egg or sperm) production

• LH promotes production of gonadal hormones• Absent from the blood in prepubertal boys

and girls

Homeostatic Imbalances of Growth Hormone

• Hypersecretion– In children results in gigantism– In adults results in acromegaly

• Hyposecretion– In children results in pituitary dwarfism

Homeostatic Imbalances of Glucocorticoids

• Hypersecretion—Cushing’s syndrome– Depresses cartilage and bone formation– Inhibits inflammation– Depresses the immune system– Promotes changes in cardiovascular, neural, and

gastrointestinal function• Hyposecretion—Addison’s disease– Also involves deficits in mineralocorticoids• Decrease in glucose and Na+ levels• Weight loss, severe dehydration, and hypotension

Homeostatic Imbalances of TH

• Hyposecretion in adults—myxedema; endemic goiter if due to lack of iodine

• Hyposecretion in infants—cretinism• Hypersecretion—Graves’ disease

final exam review summer 2010 chapters 16, 25, and 26

Documents

glomerular capsulefigure

glomerular capsule podocytes

regulation of blood

blood pressureinvolves

packed cells

kidney functionerythropoietin

filtration slitsgel

plasma proteinsfenestrations