Ibs Iii Final

Front 1

What are the ovaries supported by?

Back 1

Supported by
mesovarium & a pair
of supporting
ligaments; ovarian &
suspensory ligaments.

Front 2

What are the ovaries attached to the uterus by?

Back 2

The ovarian ligament.

Front 3

What do the suspensory ligaments contain?

Back 3

Major blood
vessels connected to
ovary at ovarian hilum.

Front 4

What does the ovarian cortex contain?

Back 4

– primordial follicles
– developing follicles
– corpus luteum
– stromal cells

Front 5

What does the ovarian medulla contain?

Back 5

– vascular elements
(branches of uterine &
ovarian arteries)

Front 6

What are the steps in the process of oogenesis?

Back 6

-Oogonia complete their mitotic divisions before birth.
-Primary oocytes prepare to undergo meiosis; proceed as far as prophase of meiosis I, then remain suspended until individual reaches puberty.
-Not all primary oocytes survive until puberty.
-Ovaries contain 2 million primordial follicles at birth.
-By puberty drops to 400.000.
-Atresia
-Primary oocyte cytoplasm unevenly distributed during 2 meiotic divisions.
-Ovary releases a secondary oocyte, suspended in metaphase of meiosis II until fertilization.

Front 7

What is the first step in the maturation of follicles?

Back 7

-Primordial follicle: Basic reproduction unit of ovary
–Primary oocytes are surround by granulosa cells.
-Primordial follicle becomes a primary follicle when oocyte enlarges and cells change and zona pellucida forms.
-Zona pellucida is a membrane that will eventually surround the oocyte.

Front 8

What is the second step in the maturation of follicles?

Back 8

– Only a few proceed to this step.
– Begins with proliferation of granulosa cells and forming multilayer.
– Granulosa secrets follicular fluids, accumulates in small pockets.

Front 9

What is the third step in the maturation of follicles?

Back 9

--Tertiary (mature/ graafian follicle
– Formation of a follicular cavity or antrum.
– As granulosa cells enlarge and multiply, adjacent cells form a layer of theca cells.
– Until this time, primary oocyte suspended in prophase of meiosis I.
– LH level begins rising & it promotes primary oocyte to complete meiosis I.

Front 10

What is the fourth step in the maturation of follicles?

Back 10

– Tertiary follicle reaches 2 - 2.5 cm.
– Follicle swells and wall ruptures.
– Ovary releases secondary oocytes.
--Usually only one is ovulated.
– Second meiotic division completed when secondary oocyte unites with sperm cell to form zygote.

Front 11

What happens after the follicle matures?

Back 11

-Mature follicle become corpus luteum
– Granulosa cells become luteinized & in conjunction
with stromal cell form corpus luteum (under LH).
– Produce progesterone & small amount of estrogen.
– If fertilization occurs, corpus luteum persists.

Front 12

What happens to the corpus luteum if fertilization does not occur?

Back 12

In absence of fertilization: corpus luteum is replaced by fibrous tissues, producing a scar tissue “corpus albicans”

Front 13

What are the non-steriod ovarian hormones and where are they produced?

Back 13

– Granulosa cells → Inhibin (decr. FSH)
– Granulosa cells → Activin (incr. FSH)
– Corpus luteum → Relaxin (softening of uterine cervix & relaxation of pelvic ligaments).

Front 14

How is estrogen transported?

Back 14

– Bind with high affinity to Sex Hormone Binding Globulin (SHBG) (38%), Albumin (60%), 2% Free.
– SHBG increased by estrogens, decreased by androgens .
-Female [SHBG] = 2x male [SHBG].
– May play a role in estrogen transport across cell membrane.

Front 15

How is progesterone transported?

Back 15

– Binds strongly to Corticosteroid Binding Globulin (CBG, 18%).
– Albumin (80%), 2% Free.

Front 16

How is estradiol metabolized?

Back 16

– Rapidly converted to estrone in liver.
– Most of estrone is further metabolized to 16 α-OH-estrone → estriol → conjugated to glucuronic acid and sulfate.
– Mostly is excreted in urine & 1/5 is excreted in
bile.

Front 17

How is progesterone metabolized?

Back 17

– Rapidly cleared from circulation (t1/2 = 5 min).
– Metabolized in liver & conjugated to glucuronic
acid and excreted in urine.

Front 18

What physiological effects does estrogen have on the female reproductive system?

Back 18

- Stimulate maturation of female reproductive system
– vagina, uterus and uterine tubes at puberty, increase uterine and genital size.
– increase endometrial proliferation, decrease
cervical mucus viscosity.
– a role in closing of the epiphyses of long bones occurs at puberty.

Front 19

What physiological effects does estrogen have on secondary sex characteristics?

Back 19

-breast/ pelvic development, alter the body fat distribution to hip & breasts.

Front 20

What physiological effects does estrogen have on bone and muscle growth?

Back 20

– increase osteoblastic activity.
– decrease the rate of resorption of bone.
(antagonize PTH on bone)

Front 21

What physiological effect does estrogen have on CNS activity?

Back 21

– in hypothalamus increase sexual activity (libido).

Front 22

What physiological effects does estrogen have on the blood?

Back 22

– increase coagulability factors.
– decrease anti-thrombin activity.

Front 23

What is thrombin and anti-thrombin?

Back 23

-Anti-thrombin: It inhibits blood clotting by inactivating thrombin.
-Thrombin: An enzyme that is formed from prothrombin
and facilitates the clotting of blood by catalyzing
conversion of fibrinogen to fibrin.

Front 24

What are the physiological effects of estrogen on the cardiovascular system?

Back 24

– increase HDL, decrease LDL.
– decrease platelet aggregation.

Front 25

What is the mechanism of genomic action of estrogen?

Back 25

- Plasma estrogen in blood are bound to SHBG & albumin, from which they dissociate to enter the cell (by passive diffusion).
- Upon entering cell, hormone binds to estrogen receptor (ER).
- In the absence of ligand, ER is present in the cytoplasm and nucleus in an inactive monomeric state.
- Binding of hormone to its receptor alters its conformation and results in dimmerization. This increase the affinity of its binding to DNA binding site (ERE).
- The ER/DNA complex recruits one or more coactivator proteins to the promoter region.
- Coactivators recruit other proteins to the complex and initiate the formation of transcription complex leading to the gene transcription.

Front 26

How does progesterone aid in the preparation for pregnancy?

Back 26

– Stimulates secretory activity of uterine glands.
– Prepares uterus for implantation of fertilized ovum.
– Decreases the frequency and intensity of uterine contractions.
– Increases viscosity of cervical mucus.

Front 27

What are the effects of progesterone in the (female) body?

Back 27

-preparation for pregnancy
-Breast development (high conc.).
-Increases basal body temperature.
-Increases insulin level leading to insulin resistance.
-Decreases in Na+ re-absorption (compete with aldosterone).

Front 28

What are the effects of androgens in women?

Back 28

-Ovary secrets potent androgens:
--Testosterone (<300 μg/day) &
--Dihydrotestosterone
– Hair growth at puberty.
– Some metabolic effects → acne

Front 29

What occurs in the early follicular phase of the menstrual cycle?

Back 29

– Low E2 & PG →GnRH → FSH & LH → development of follicle → follicles secrete E2.
– Negative feedback: Rising E2 → inhibits FSH & LH secretion.

Front 30

What happens to the later part of the follicular phase in the menstrual cycle?

Back 30

– At mid-cycle: sustain high level of E2 exert a positive feed back on pituitary.
– Initiates preovulatory surge of LH.
– LH Surge → initiate midcycle surge of FSH
– LH stimulates follicle rupture → corpus luteum → PG & E2
– In absence of pregnancy menstruation occurs.

Front 31

What occurs during menopause?

Back 31

– At 40-50, cycles become irregular & ovulation fails to occur during many
cycles. A few months later the cycles stops.
– The cause is “burning out” of the ovaries.
– During reproductive life, ~400 primordial follicles grow & ovulate.
– At 45, only a few remain to be stimulated by FSH/LH → E2 decreases.

Front 32

What are the characteristics of hypogonadism in women?

Back 32

– Lack of ovaries, abnormal ovaries, poorly formed ovaries
– Prolonged growth of long bones (E2 in epiphyses)
– Smaller uterus and vagina, breast atrophy
– Amenorrhea: Absence or suppression of menses

Front 33

What are the characteristics of hyper-secretion of the ovaries?

Back 33

– Occurs in rare granulosa cell tumor in ovary (esp..after menopause)
-bleeding
-hypertrophy of uterine endometrium

Front 34

What concentration of sperm in the semen is considered to be sterile?

Back 34

– <20 million sperms/ml: Sterile

Front 35

Of all of the sperm that is released into the vagina, how many make it to the ampulla?

Back 35

– From 200 million sperms, only 200 reach ampulla.

Front 36

What structures promote the movement of sperm in the uterine tube?

Back 36

Uterine myometrium and ciliary current in uterine tube help sperm transport.

Front 37

What are the steps of fertilization?

Back 37

1. Ovulation releases a secondary oocyte and a first polar body; both are surrounded by corona radiata. At first, many sperms attach to the corona radiata.
2. Sperm cells bind to ZP3 receptors on the zona pellucida.
3. Acrosomal enzymes digest zona pellucida and helps sperm penetration. Fusion of secondary oocyte with sperm
causes zona pellucida to prevent second fertilization.
4. In response to sperm head entry, oocyte nucleus moves to one side of oocyte where it completes the second
meiotic division and gives off a second polar body. The oocyte nucleus now called female pronucleus.
5. Sperm head enlarges and becomes male pronucleus.
6. Two pronuclei fuse to form a single nucleus. Fertilization is complete and zygote results.

Front 38

What are the characteristics of implantation?

Back 38

-Implantation does not occur until 8-10 days after
fertilization.
-The date of ovulation and implantation are not known.
-Gestational weeks calculated from onset of last
menses.

Front 39

What are the four general processes that occur in the first trimester of pregnancy?

Back 39

-Cleavage
-Implantation
-Placentation
-Embryogenesis

Front 40

What are the characteristics of cleavage?

Back 40

-Occurs in the 1st trimester
-A series of cell division which subdivides the cytoplasm of zygote.
-First cleavage produces 2 identical cells “ balstomer”.
-It finally develops to multicellular complex known as blastocyst.

Front 41

What is a morula?

Back 41

Morula: A globular solid mass of blastomers (12 or more cells).

Front 42

What does the trophoblast become?

Back 42

becomes placenta, chorion & amnion

Front 43

What are the characteristics of implantation?

Back 43

-Attachment of the blastocyst to endometrium.
-Trophoblast invades maternal tissue.
-Syncytial trophoblasts erode a path through endometrium.
-Inner cell mass separated from trophoblasts by amniotic cavity.
-Trophoblast separated from
amniotic cavity by a layer named amnion.
-Developing villi helps to form placenta.
-Takes places in the fundus or in the body of uterus.
-In ectopic pregnancy, gestation occurs somewhere other than within uterus (e.g. fallopian tubes).

Front 44

When is an embryo considered a fetus?

Back 44

after 60 days

Front 45

What is languo?

Back 45

-fine soft hair covering the fetus

Front 46

What is the vernix caseosa?

Back 46

Waxy coat of epithelial cells protects fetus from
toxic nature of amniotic fluids formed by accumulation of waste products from the fetus.

Front 47

What are the characteristics of the fetal-placental unit?

Back 47

-By the end of first trimester, fetal endocrine
system is developed to influence placenta function.
– A source secretion of protein & steroid hormones
into maternal circulation.
– Controls the fetal endocrine function/growth and
development.
– Works as a selective barrier between fetus & mother.

Front 48

What are the placental protiens?

Back 48

- Human chorionic gonadotropin (hCG)
- Human placental lactogen (hPL)
-Other chorionic peptide hormones:
–Similar to TSH, FGF, EGF, PDGF, IGF

Front 49

What are the characteristics of hCG?

Back 49

-First measurable product of placenta, synthesized by trophoblast.
-hCG is detectable in maternal serum within 1
day after implantation or 3 gestational weeks.
-Glycoprotein with 237 aa, two subunits (α & β).
• α subunit is identical to TSH, LH, FSH.
• β subunit is similar to LH (67%), +24 aa.
-Long half-life (24 - 30 h); relative ease of obtaining → used therapeutically.

Front 50

What is the action of hCG?

Back 50

-Maintain corpus luteum until placenta can secrete progesterone; under hCG, corpus luteum secretes progesterone.
-In early pregnancy, hCG concentration doubles every 2 days; pregnancy diagnose.

Front 51

What are the characteristics of hPL?

Back 51

-human placental lactogen
-Second placental hormone; synthesized by trophoblasts and later by placenta.
-Reaches to detectable serum conc. in 4-5 gestational weeks.
-Protein with 190 aa, similar in structure to GH, PRL.
-An indicator of health of placenta.

Front 52

What is the action of hPL?

Back 52

-Weak growth-promoting and lactogenic activity.
-Insulin resistance of pregnancy can be induced by hPL:
–-contributes to altered maternal glucose metabolism.
–-causes hyperinsulinemic response to glucose load.
–-directly stimulates β cells in pancreatic islets.

Front 53

What is the relationship between the placenta and the corpus luteum?

Back 53

-Corpus luteum can be removed after 7th gestational
wks, placenta becomes source of PG.
-Placenta doesn’t produce 17-OH-PG; a marker of corpus luteum function.

Front 54

What are the basic hormone changes during pregnancy?

Back 54

- HCG reaches a max near the end of 1st trimester and then decr.
- PG continues to incr. until its level off near the end of pregnancy
- E2 incr. slowly throughout pregnancy, but they incr. rapidly as the end of pregnancy approaches.

Front 55

What are the changes in site of secretion of progesterone and estrogen through pregnancy?

Back 55

-Early in pregnancy, E2 & PG are secreted by ovary.
-During midpregnancy, there is a shift toward secretion by placenta.
-Late in pregnanacy, they are secreted by placenta.

Front 56

What are the changes in the blood during pregnancy?

Back 56

-volume: 50% increase by 2nd trimester
-hematocrit: decreases slightly
-fibrinogen: increases
-electrolytes: no change

Front 57

What are the physiological changes in the cardiovascular system during pregnancy?

Back 57

-heart rate: gradually increases by 20%
-blood pressure: gradually decreases 10% by 34 weeks, then increases to prepregnancy values
-cardiac output: rises rapidly by 20%, then gradually increases 10% by 28 weeks.

Front 58

How does the pituitary gland change during pregnancy?

Back 58

– Pituitary enlarges (by 1/3)
– Lactotrophs hyperplasia: PRL is increased (peaks at delivery).

Front 59

How does the thyroid gland change during pregnancy?

Back 59

– Thyroid enlarges.
– Iodide renal clearance is increased.
– Maternal total serum thyroxin (T4) and TBG are elevated.

Front 60

How does the parathyroid gland change during pregnancy?

Back 60

– The fetus Ca2+ need (≈ 30 g/term) is met by maternal parathyroid hyperplasia & maternal bone reserve.
– Maternal serum PTH is elevated.
– Maternal serum Ca2+ is decreased.

Front 61

How does the pancreas change during pregnancy?

Back 61

– Size of pancreatic islet is increased, β cell hyperplasia.
– Basal insulin is increased in the second trimester (elevated insulin secretion).
– Altered glucose tolerance test.
– Pregnancy is a hyperinsulinemic state with peripheral resistance to insulin.

Front 62

How do glucocorticoids change in pregnancy?

Back 62

Maternal plasma cortisol and CBG is increased in third trimester (high production and low catabolism in liver leads to increase in half life).

Front 63

How do mineralocorticoids change in pregnancy?

Back 63

-Maternal serum aldosterone is elevated (high production), reaches to peak by mid pregnancy and maintained until delivery.
-Renin and renin substrate are increased.

Front 64

How does the cervix change near the end of pregnancy?

Back 64

– Softening of cervix; lower uterine segment & cervix become softer and thinner.
– Relaxin produced by corpus luteum & placenta

Front 65

What does relaxin do?

Back 65

-ripens the cervix
-act with progesterone to inhibit uterine contraction.

Front 66

In the fetus, what gland is enlarged prior to parturition?

Back 66

Adrenal glands.

Front 67

What is the role of progesterone in maintaining pregnancy?

Back 67

– PG hyperpolarizes myometrium → decreases Ca2+
entry →prevents contraction.
– PG decreases α receptors.
– PG inhibits estrogen receptor synthesis.

Front 68

How does the estrogen/progesterone ratio change immediately prior to labor?

Back 68

– Estrogen antagonizes PG → ripening of uterine cervix.
– Increases maternal oxytocin release at posterior
pituitary gland.

Front 69

What are some factors used to induce labor?

Back 69

-Oxytocin infusion; increases the force of uterine contraction; Caution must be taken.
-PGF2α
-Catecholamine
-Nitric oxide synthase (NOS) inhibitors
-Fetal growth/ size: activate myometrium/neuroendocrine reflex

Front 70

What stimulates the neuroendocrine reflex?

Back 70

Fetus size.

Front 71

What are the characteristics of preeclampsia?

Back 71

A toxic condition developing in late pregnancy:
-Sudden rise in blood pressure, weight gain, edema, albuminuria, headache, and visual disturbances

Front 72

What causes hyperthyroidism during pregnancy?

Back 72

– Thyroid enlargement, increased cardiac output, peripheral vasodilation.

Front 73

When in pregnancy does gestational diabetes mellitus typically occur?

Back 73

-Usually occurs in the second or third trimester (by week 24 to 28) (4%).

Front 74

What are the contents of breast milk?

Back 74

-Breast milk: water, protein, amino acids, lipids, sugar, salt, and enzymes with antibiotic properties.

Front 75

What is the sequence of the initiation of lactation?

Back 75

-there is a decrease in the levels of progesterone and estrogen
-prolactin inhibitory factor (PIF) is inhibited
-prolactin release from the anterior pituitary leads to lactation

Front 76

What are the characteristics of A cells in the pancreas?

Back 76

-Make up 10% of the pancreas mass
-produce glucagon and proglucagon

Front 77

What are the characteristics of B cells in the pancreas?

Back 77

-Make up 75% of pancreas mass
-produce C-peptide/ proinsulin/islet amyloid polypeptide (IAPP)
-insulin

Front 78

What are the characteristics of D cells in the pancreas?

Back 78

-Make up 3-5% of the pancreas mass
-produce somatostatin

Front 79

What are the characteristics of F cells in the pancreas?

Back 79

-Make up less than 2% of pancreas cells
-produce pancreatic polypeptide

Front 80

What are the characteristics of basal insulin secretion?

Back 80

Basal insulin secretion:
– Insulin secreted in fasting state (in the absence of exogenous stimuli) (5-15 μu/ml; 30-90 Pmol/l).
- Insulin is released from pancreas at a rate of 1-2
U/h.
- Human pancreas secrets ≈ 40-50 U of insulin /day.
- Unit: Hypoglycemic activity of insulin in rabbits; on the basis of weight (28 unit = 1 mg).
– The entire pancreas contains up to 8 mg (about
200 units).

Front 81

What are the actions of insulin on the liver?

Back 81

--Promotes storage of glucose as glycogen.
- Inhibits glycogenolysis.
- Inhibits conversion of fatty acids (FA) to ketoacids (ketogenesis).
- Inhibits conversion of amino acids (AA) to glucose (gluconeogenesis).
- Reduces FA influx to the liver.
– An indirect effect to decrease hepatic ketogenesis and gluconeogenesis.

Front 82

What are the actions of insulin on muscle?

Back 82

-- Increased protein synthesis.
– increases amino acid (AA) transport.
– promotes incorporation of AA to protein.
– increases ribosomal protein synthesis.
– decreases protein catabolism.
-- Increased glycogen synthesis.
– increases glucose transporter (GLUT-4) in
membranes of muscle.

Front 83

What are the actions of insulin on adipose tissue?

Back 83

-- Reduced circulating FA.
-- Increased triglyceride (TG) storage or fat synthesis.
- by inducing lipoprotein lipase, hydrolyzes TG from lipoproteins.
- by inhibiting intracellular lipase, decreases lipolysis of stored TG.
- by increasing Glut-4 in membrane of adipose, increases G transport into cell provides glycerol phosphate to permit esterification of FA to TG.

Front 84

What are the characteristics of glucagon?

Back 84

-A large polypeptide contains 29 aa arranged in 1 chain.
--Human proglucagon
- Produced by alpha cells of islet of Langerhans from pro-glucagon.
- Other peptides within proglucagon: glicentin-related peptide, glucagon-like peptides (GLP)
- Short half-life (3-6 min); mainly removed by liver & kidney.

Front 85

What is truncated GLP-1?

Back 85

- an endogenous truncated derivative of GLP-1, with the first 6 of its 37 aa absent.
- extremely potent stimulator of pancreatic B cells.
- a major gut factor that potentiates glucose-induced insulin secretion after meals.
- released by small intestine.

Front 86

What is the action of glucagon?

Back 86

- Glucagon makes energy available to the tissues & induces hyperglycemic effects within minutes.
- Stimulates breakdown of glycogen in liver, glycogenolysis.
- Increases hepatic glucose output from amino acids, gluconeogenesis.
- Promotes hepatic ketone bodies output, ketogenesis.
- Increases protein catabolism & conversion to ketone bodies. Glucagon infusion for 4 h causes intensive liver glycogenolysis.
--Continued infusion causes continued hyperglycemia:
–by increasing the rate of amino acid uptake by liver and then conversion to glucose (gluconeogenesis).
-Increases lipolysis.
-Inhibits TG storage in liver.
-It works primarily on liver.
-In very high concentration has (+) inotropic effects on heart.

Front 87

What is the secretion of glucagon activated by?

Back 87

– Amino acids (arginine, alanine, leucine)
– Exercise
– Catecholamines, glucocorticoids
– GI Hormones (gastrin, CCK, gastric inhibitory polypeptide)

Front 88

What is the secretion of glucagon inhibited by?

Back 88

– Blood glucose concentration
– Insulin
– Somatostatin
– High levels of free fatty acids

Front 89

What are the characteristics of somatostatin?

Back 89

-In pancreas, produced by Delta cells of islet of Langerhans from preprosomatostatin.
-Single chain polypeptide with 14 AA.
-Some circulating hormone is 28-AA peptide; somatostatin-28 is more potent in inhibiting growth hormone & insulin.
-Very short half-life (< 3 min).

Front 90

What activates the secretion of somatostatin?

Back 90

– Increased blood glucose
– Increased amino acids
– Increased fatty acids
– Increased GI hormones in response to food intake.

Front 91

What are the inhibitory effects of somatostatin?

Back 91

– Acts locally within islets to depress insulin & glucagon secretion.
– Decreases the motility of stomach, duodenum and bladder.
– Decreases gastric emptying, gastric acid production.
– Reduces nutrient absorption in GI tract.
– Inhibits GH and TSH secretion from ant. pituitary.

Front 92

What calorie distribution should come from carbohydrates, protein, and fats based on a 2500 cal/day diet?

Back 92

-1400 carbs
-750 fat
-250 protein

Front 93

What are the effects of short-term fasting (3-7 days)?

Back 93

– Gluconeogenesis, lipolysis, ketogenesis all stimulated.
– Increased protein catabolism.

Front 94

What are the effects of long-term fasting (more than 7 days)?

Back 94

– Protein catabolism ↓
– Blood ketone ↑
– Brain utilization of ketones ↑ (reduces
dependence on glucose).

Front 95

What are the classifications of weight and bmi?

Back 95

Underweight: <18.5
Normal: 18.5-24.9
Overweight: 25.0-29.9
Obesity-
Class I: 30.0-34.9
Class II: 35-39.9
Class III: >40

Front 96

What are some of the diseases associated with obesity?

Back 96

– Type 2 Diabetes
– Hypertension
– Atherosclerotic Heart Disease & Stroke
– Hyperlipidemia & dyslipidemia
– Gallbladder Disease
– Osteoarthritis
– Cancer (e.g. endometrial, breast, prostate, and colon cancer)

Front 97

What is ascites?

Back 97

-Def: abdominal swelling created by accumulation of fluid in peritoneal cavity
-Increase rate of fluid movement into the peritoneal cavity
-Causes:
--Liver disease
--Kidney disease
--Heart failure

Front 98

What is peritonitis?

Back 98

-Def: inflammation of the peritoneal membrane
-Causes:
--Physical damage
--Chemical irritation
--Bacterial invasion
--Untreated appendicitis
-Complication of surgery when peritoneal cavity is opened

Front 99

What is mesentery?

Back 99

-A double layer of peritoneum that provides:
--Vascular and nerve supplies to the viscera
--A means to hold digestive organs in place and store fat

Front 100

What organs are retroperitoneal?

Back 100

pancreas, duodenum, ascending and descending colons, rectum, urinary bladder, aorta, inferior vena cava, kidneys, suprarenal glands

Front 101

What are some peritoneal organs?

Back 101

stomach, small intestine (jejunum and ileum), transverse colon, liver and gallbladder

Front 102

What are the 4 tunics of the walls of the GI tract?

Back 102

From the lumen outward they are the mucosa, submucosa, muscularis externa, and serosa.

Front 103

What are the characteristics of the mucosa of the GI tract?

Back 103

Mucosa – innermost layer of GI tract
-Def: moist epithelial layer that lines the lumen of the alimentary canal
--**epithelium (mucous membrane) – varies from one part of the tract to the next, provides important protective and absorptive functions
-stratified squamous epithelium
--lamina propria – contains mucous glands, lymph nodules,
and capillaries, helps with nourishment
--muscularis mucosa – innermost layer of smooth muscle, produce local movement of mucosa.

Front 104

What are the characteristics of the submucosa of the GI tract?

Back 104

Submucosa – consists of connective tissue (collagen, elastin) and also contains nerves and blood vessels
-areolar connective tissue

Front 105

What are the characteristics of the muscularis externa of the GI tract?

Back 105

-Muscularis externa – contractions of these
muscles mix and propel contents of intestinal
lumen
-- circular, longitudinal muscle
-- Segmentation, peristalsis

Front 106

What are the characteristics of the enteric plexus?

Back 106

-myenteric (located between circular and longitudinal
muscle)
--major nerve supply that controls GI tract motility
--parasympathetic ganglionic neurons
--sympathetic postganglionic fibers
-submucosal (located in submucosa)
--regulates glands and smooth muscle in the mucosa and submucosa
--parasympathetic ganglionic neurons
--sympathetic postganglionic fibers

Front 107

What are some parts of the GI tract that have adventitia?

Back 107

oral cavity, pharynx, esophagus, rectum

Front 108

What are the differences in cell types within the mucosa?

Back 108

-simple (stomach, small intestine, most of large
intestine)
-or stratified (areas with mechanical stress) columnar
epithelium and mucus-secreting cells

Front 109

What do the stomach and small intestine mucosa contain?

Back 109

-Enzyme-secreting cells
-Hormone-secreting cells (making them endocrine and
digestive organs) – enteroendocrine cells

Front 110

What is the general life span of GI mucosal epithelium?

Back 110

-Life span 2-3 days (esophagus) or 6 days (large
intestine)
-Related to rate of cell destruction and loss

Front 111

What protects the GI mucosal epithelium from precancerous lesions?

Back 111

Phytochemicals such as: Vit. C, Vit. E, carotenoids, retinoids, isothiocyanates,
polyphenols

Front 112

What are the 3 pairs of extrinsic salivary glands?

Back 112

-parotid: parotid duct opens into the vestibule next to the second upper molar
-Submandibular: Its ducts open at the base of the lingual frenulum
-sublingual: It opens via 10-12 ducts into the floor of the mouth

Front 113

What are the characteristics of the esophagus?

Back 113

-Esophageal mucosa – nonkeratinized stratified squamous epithelium
-The empty esophagus is folded longitudinally and flattens when food is present
-Glands secrete mucus as a bolus moves through the esophagus
-Muscularis changes from skeletal (superiorly) to smooth muscle (inferiorly)

Front 114

What is Esophageal Varices?

Back 114

-Def: dilated blood vessels within the wall of the esophagus
-Cause: portal hypertension –venous pressure in the hepatic portal vein becomes abnormally high
-blood flow through liver diminished
-venous drainage of esophagus
-hepatic portal vein to liver
-cirrhosis & other liver diseases
--Problem:
-distended veins in esophagus may bulge and constrict esophageal passageway
-veins susceptible to rupture- emergency situation

Front 115

What are the components of gastric juice?

Back 115

-Hydrogen ions (acid)
-intrinsic factor (required to absorb B12)
-Pepsin
-Mucin

Front 116

What are the muscles of the stomach?

Back 116

-Muscularis mucosa
--Innermost layer of smooth muscle
-Muscularis externa
--Circular and longitudinal muscle
-Oblique muscle layer (unique to stomach)
--deep to muscularis externa layer
--overlies mucosa
--Enhances gastric motility and mixing of food
-Rugae (temporary folds)
-Pyloric sphincter

Front 117

What are the types of glands in the stomach?

Back 117

-Oxyntic gland – fundus and body
-Pyloric gland – antrum
-Cardiac gland – cardia

Front 118

What is the location and product of surface mucus cells in the stomach?

Back 118

-all glands and mucosa
-produce mucins, bicarbonate

Front 119

What is the location and product of neck mucus cells in the stomach?

Back 119

-all glands
-produce mucins

Front 120

What is the location and product of parietal cells in the stomach?

Back 120

-Oxyntic glands
-produce HCl, intrinsic factor

Front 121

What is the location and product of chief cells in the stomach?

Back 121

-oxyntic glands
-produce pepsinogen

Front 122

What is the location and product of G cells in the stomach?

Back 122

-Antrum
-Gastrin
-Histamine

Front 123

What is the location and product of D cells in the stomach?

Back 123

-Antrum
-Somatostatin

Front 124

What are the actions of parietal cells in the stomach?

Back 124

-Secrete intrinsic factor (B12 absorption)
-Create acid environment within stomach
--kills microorganisms
--denature proteins
--destroys plant cell walls
--breaks down animal connective tissues
--activates pepsinogen (pepsin)

Front 125

What are the actions of chief cells in the stomach?

Back 125

-Secrete pepsinogen (proenzyme)
-Acidic environment activates pepsinogen
--pepsin activated within stomach
--proteolytic enzyme
--begins digestion of proteins

Front 126

What does gastrin stimulate in the stomach?

Back 126

-parietal cells secretion of acid
-chief cells secretion of pepsinogen
-gastric contractions

Front 127

What does histamine stimulate in the stomach?

Back 127

-parietal cell secretion of acid
--H2 (histamine receptor)

Front 128

What are the basic characteristics of the small intestine?

Back 128

- primary site for digestion
- primary site for absorption
--90% of absorption
- ~20 feet in length (6m)
-3 sections
-- Duodenum
-- Jejunum
-- Ileum

Front 129

What are the characteristics of the duodenum?

Back 129

-first section after stomach
-~10 inches in length (25cm)
-“mixing bowl” function
--chyme from the stomach
--bile from the liver
--pancreatic exocrine secretion
-alkaline pH (7-8)

Front 130

What are the characteristics of the jejunum?

Back 130

- middle section of Small Intestine
- ~8 feet in length (2.5m)
- supported by mesentery
- bulk of digestion
- majority of absorption

Front 131

What are the characteristics of the ileum?

Back 131

- last section of Small Intestine
- ~12 feet in length (3.5m)
- supported by mesentery
- ends at ileocecal valve (sphincter)
- controls entry into large intestine
- cecum contains vermiform appendix
- lower right quadrant

Front 132

What are plicae? (small intestine)

Back 132

- permanent transverse folds
- increased surface area
- Each plica is covered with millions of villi

Front 133

What are the functions of villi in the small intestine?

Back 133

- finger-like projections
- columnar epithelium covering
- Goblet cells – produce mucus
- Absorptive cells
-- microvilli (brush border)

Front 134

What are the cell types that make up the histology of the small intestine?

Back 134

1) absorptive cells
- brush border enzymes
- integral membrane proteins
- digestion of materials contacting brush border
2) goblet cells (mucus)
3) enteroendocrine cells
- secrete several hormones
4) grandular cells (Paneth’s cells)
- may help protect the intestinal epithelium from bacteria

Front 135

What are the regional variations in histology among the duodenum, jejunum, and ileum?

Back 135

-Duodenum
--few plicae
--many submucosal glands
-Jejunum
--many plicae, villi & microvilli
--diminish in size & number as approach ileum
-Ileum
--lacks plicae & few villi/microvilli

Front 136

What makes up the lamina propria of the small intestine?

Back 136

-extensive capillary network
--blood vessels originate in
submucosa
--transports gases, nutrients, etc. (water soluble)
-“Lacteal”
--lymph channel
--transports lipid soluble
materials
--chylomicrons
-Muscularis mucosa (wiggling)

Front 137

How long is the large intestine?

Back 137

About 5 feet (1.5 m)

Front 138

What are the characteristics of the cecum?

Back 138

-expanded pouch with ileocecal valve
-lower right abdominal quadrant
-vermiform appendix
-begins process of compaction

Front 139

What are the distinctive features of the colon?

Back 139

-Haustra (pouches)
-Taenia coli (longitudinal muscle)
-Epiploic appendages (fatty sacs)

Front 140

What are the major characteristics of the large intestine?

Back 140

- lack of villi
- abundance of goblet cells
-- mucus secretion
-- lubrication
- glands
-- no enzyme secretion

Front 141

How many deciduous teeth do humans usually have?

Back 141

20, they usually erupt at intervals between 6 and 24 months

Front 142

What are the characteristics of H. Pylori?

Back 142

-Helicobacter pylori
-Resides primarily in the mucin layer of the antrum
-Thick layer of mucus protects stomach lining
-H. pylori takes advantage of
this protection by living in the mucus lining.
- Protects itself by producing urease NH4+ and HCO3- which neutralizes acid
- Inflammatory response to the infection leads to gastritis and then an ulcer

Front 143

What are the characteristics of GI smooth muscle?

Back 143

-Capable of stretch
-Capable of prolonged contraction without fatigue
-Capable of tonic contraction or tone
--Sphincters remain tonically constricted
---Sphincter – thickening of the smooth muscle
-Low energy requirements

Front 144

How is smooth muscle innervated?

Back 144

- Smooth muscle lacks neuromuscular junctions
- Innervating nerves have bulbous swellings called varicosities
- Varicosities release neurotransmitters into wide synaptic clefts called diffuse junctions

Front 145

What are the microscopic anatomical characteristics of smooth muscle?

Back 145

- SR is less developed than in skeletal muscle and lacks a specific pattern
- T tubules are absent
- Plasma membranes have pouchlike infoldings called caveoli
- Ca2+ is sequestered in the extracellular space near
the caveoli, allowing rapid influx when channels are opened
- There are no visible striations and no sarcomeres
- Thin and thick filaments are present

Front 146

What is the involvement of actin and myosin in smooth muscle?

Back 146

- Actin and myosin contractile elements are not arranged in sarcomeres
- Loosely arranged in long bundles extending obliquely as lattice across the periphery of the cell
- Myosin filaments (thick filaments) have numerous heads along their length
- Myofilaments are longer than in skeletal muscles allowing them to be stretched further and still maintain tension

Front 147

How does stimulus-contraction coupling work in smooth muscle?

Back 147

Stimulus-contraction coupling:
- Stimulus
- → inc. cytoplasmic [Ca2+]
- → Ca2+ binds calmodulin
- → activates MLCK
- → myosin light chain (MLC) phosphorylation
- → cross-bridge formation between actin and myosin
- → contraction

Front 148

What is the role of calcium in the contraction of smooth muscle?

Back 148

- Ca2+ binds to calmodulin and activates it
- Activated calmodulin activates the kinase enzyme
- Activated kinase transfers phosphate from ATP to myosin cross bridges
- Phosphorylated cross bridges interact with actin to produce shortening
- Smooth muscle relaxes when intracellular Ca2+ levels drop

Front 149

What are the characteristics of myofilaments in smooth muscle?

Back 149

- Ratio of thick to thin filaments is much lower
than in skeletal muscle
- Thick filaments have heads along their entire length
- There is no troponin complex
- Thick and thin filaments are arranged diagonally, causing smooth muscle to contract in a corkscrew manner
- Noncontractile intermediate filament bundles
attach to dense bodies (analogous to Z discs) at
regular intervals

Front 150

What are the interstitial cells of Cajal?

Back 150

Interstitial cells of Cajal (myenteric plexus) are
the pacemaker cells that:
- Generate slow waves
- Oscillations of RMP in visceral smooth muscle
- Communicate with smooth muscle cells via gap junctions
- The slow wave provides intrinsic control over the timing and pattern
of smooth muscle contractions in the GI tract
- Resting membrane potential varies in time
- Low frequency oscillations vary from 3/min – stomach to 12/min duodenum

Front 151

What are the control systems of smooth muscle?

Back 151

1. Intrinsic activity of the pacemaker cells
2. Neurally released transmitters
3. Circulating hormones

Front 152

What are the different gastrointestinal peptides?

Back 152

- Neurotransmitters (or “neurocrines”)(ANS or ENS)
-- released by action potentials and act on cells at the synapse.
- Endocrine hormones (or “endocrines”)
-- released from mucosal endocrine cells and are transported by the blood back to the GI tract
-Local factors (“paracrines”) – short distance
-- mucosal endocrine cells act on other cells near their sites of release
- Have many different actions depending on which cells contain receptors or are in proximity to the sites of release.
- May inhibit or augment the effects of each other.

Front 153

What is the regulation of the digestive system from the ANS?

Back 153

-Sympathetic
-- Motor neuron cell bodies are in ganglia organized in
vertical chains near the spinal cord and in ganglia within the abdomen
-- Norepinephrine is the major NT
- Parasympathetic
-- Motor neuron cell bodies are located in ganglia that lie close to target organs
-- Acetycholine is the major NT

Front 154

What are the roles of the neural plexuses in digestive system regulation?

Back 154

-Myenteric plexus
-- Lies in between the circular and longitudinal layers of smooth muscle
-- primarily regulates motility
- Submucosal plexus
-- Located in the submucosa
-- primarily controls secretion, blood flow, and absorption

Front 155

What is the action of acetylcholine in the digestive system?

Back 155

Stimulates contractions of smooth muscle; stimulates
secretion of salivary glands (the watery secreted fluid), stomach, and pancreas

Front 156

What is the action of norepinephrine in the digestive system?

Back 156

Inhibits contractions of smooth muscle, stimulates
contractions of some sphincters, stimulates secretion of salivary glands (low volume & protein-rich) (only transient)

Front 157

What is the action of Vasoactive intestinal peptide
(VIP) in the digestive system?

Back 157

Inhibits contractions of smooth muscle, stimulates
intestinal and pancreatic secretion.

Front 158

What is the action of gastrin-releasing peptide in the digestive system?

Back 158

Stimulates secretion of gastrin.

Front 159

What is the action of enkephalins in the digestive system?

Back 159

Inhibit smooth muscle contraction, inhibit intestinal secretion

Front 160

What is the action of neuropeptide Y in the digestive system?

Back 160

Inhibits intestinal secretion of water and electrolytes, inhibits smooth muscle contraction

Front 161

What is the action of Substance P in the digestive system?

Back 161

Stimulates the contraction of smooth muscle.

Front 162

What is the action of nitric oxide in the digestive system?

Back 162

Inhibits smooth muscle contraction, vasodilator.

Front 163

What is the action of seratonin (5-HT) in the digestive system?

Back 163

Excitatory in neuroneuronal transmission.

Front 164

What is the action of GABA in the digestive system?

Back 164

Receptors modulate release of ACh, gastrin, somatostatin, histamine, and prostaglandins.

Front 165

What are the characteristics of gastrin?

Back 165

-From the stomach mucosa
-Stimulated by gastric distension, amino acids
-Stimulates gastric acid and motility

Front 166

What are the characteristics of Cholecystokinin (CCK)?

Back 166

-From the duodenal mucosa
-Stimulated by fatty chyme, partially digested proteins
-Inhibits gastric emptying, stimulates gallbladder and pancreatic functions

Front 167

What are the characteristics of secretin?

Back 167

-From the duodenal mucosa
-Stimulated by a pH of lower than 4.5 in the duodenum
-Stimulates pancreatic and liver bicarbonate secretion, inhibits gastric acid secretion and motility

Front 168

What are the characteristics of gastric inhibitory peptide (GIP)?

Back 168

-From the duodenum and jejunum
-Stimulated by Fatty acids,
amino acids, glucose
-Stimulates secretion of insulin, inhibits gastric emptying and gastric secretion of HCl

Front 169

What are the characteristics of motilin?

Back 169

-from the duodenum and jejunum
-stimulated by fasting
-Stimulates motility of the stomach and small intestines

Front 170

What are the characteristics of the lower esophageal sphincter (LES)?

Back 170

- Important barrier between the esophagus and the stomach
- A tonically constricted 3 – 4 cm ring of smooth muscle
- Not fully developed in infants - regurgitations or “spit-ups”
- During pregnancy, hormones (i.e. progesterone) reduce LES tension
-- Excessive reflux of gastric acid (about 0.1N HCl) lead to burning sensation, pyrosis (heartburn)

Front 171

What are the steps of the pharyngeal phase of swallowing?

Back 171

- Pressure by food in the back of the mouth activates sensory receptors that send impulses to a swallowing center in the medulla
- Programmed sequence of events in swallowing center
- Reflex: Upper esophageal sphincter (UES) relaxes, elevated pharynx opens the esophagus, food pushed into esophagus
- Events prevent bolus from entering respiratory passages
- During this period, the respiratory centers are inhibited and breathing stops
- UES pressure > atmospheric between swallows
- UES relaxes during swallows
- Swallowing initiates esophageal peristalsis

Front 172

What are the steps of the esophageal phase of swallowing?

Back 172

- Reflex: Epiglottis is tipped posteriorly, larynx
elevated to prevent food from passing into larynx
- Traveling pressure wave moves downward (primary peristalsis)
- Contraction initiated by the swallowing center and
mediated by the vagus nerve
- Begins at UES and moves until reaching LES
- The lower esophageal sphincter (LES) relaxes well in advance of the traveling bolus

Front 173

What are some factors that decrease pressure of the LES?

Back 173

- High fat meals
- Alcohol
- Chocolate
- Peppermint, spearmint
- Cigarette smoking
- Caffeine (coffee, cola, tea, citrus juices)

Front 174

What is the secondary peristaltic wave?

Back 174

- Distension of esophagus by large particles that remain in esophagus after the primary wave
- Do not involve swallowing center
- Involve local reflex centers

Front 175

What role do the pacemaker cells have in gastric motor activity?

Back 175

- basic electrical rhythm (BER) – determines the rate of slow wave
- Spike potentials – trigger contractions and occur at the peak of the depolarization phase
- After a meal, larger sustained contractions are superimposed on the BER

Front 176

What is the role of gastrin in gastric motor activity?

Back 176

Increases frequency and velocity of the gastric slow wave, stimulates antrum motility, constricts the pyloric sphincter, raises LES pressure

Front 177

What are the effects of the sympathetic and parasympathetic nervous systems on motility?

Back 177

- Motility stimulated by parasympathetic
- Motility inhibited by sympathetic

Front 178

What are the major factors that contribute to greater gastric emptying and motility?

Back 178

- Volume and chemical composition of chyme in the duodenum
-- Enterogastric reflex – inhibits gastric motility
-- Hormonal response
--- Enterogastrones (secretin, CCK, GIP) – inhibit gastric contractions
--- Fatty acids in the duodenum stimulate release of CCK stimulating constriction of the pyloric sphincter
--- CCK is the dominant regulator of gastric emptying
- Volume → distention mechanoreceptors stimulated → inhibition of gastric motility via intrinsic nerves
- Emptying:
-- pH (lower slower)
-- osmolality (isotonic faster)
-- particle size (larger slower)
-- caloric load of contents (high slower)

Front 179

What are the problems associated with accelerated and delayed emptying of the stomach?

Back 179

- Accelerated – delivery to duodenum may exceed the capability of the intestine to digest it
- Delayed – can lead to loss of appetite, nausea, and vomiting

Front 180

What is the mechanical sequence of emesis?

Front 181

What inhibits bacterial overgrowth in the small intestine in periods of fasting?

Back 181

Migrating motor complexes (MMCs).

Front 182

What are the movements of the colon?

Back 182

1. haustral churning – segmentation movements to
mix contents of adjacent haustra
2. mass movements – powerful peristaltic contractions
3. distension of rectum reflexively causes
evacuation of bowel

Front 183

What makes up saliva?

Back 183

- ~ 99.5% water
- Electrolytes – Na+, K+, Cl-, PO4 2–, HCO3–
- Digestive enzyme – salivary amylase
- Proteins – most protect against microorganisms
-Mucin – lubrication
-Lactoferrin, lysozyme, muramidase – inhibits bacterial growth in the mouth, tooth decay
- Defensins – local antibiotic, call defensive cells into mouth
- IgA antibodies
- Buffers – keep pH near 7.0

Front 184

What do acinar cells in salavary glands do?

Back 184

- Secrete primary saliva, iso-osmotic with plasma
- Secretions are mediated by second messengers (cAMP and
Ca2+)
- Secrete all proteins in saliva
-- Packaged in zymogen granules
-- Released into sac by exocytosis
- Secrete ions
-- Cl- - major secreted ion
-- Other ions: HCO3- and K+
- Secrete all of the water in saliva

Front 185

What do ductal cells in salavary glands do?

Back 185

- Modify saliva via ion transport systems
-- Na+ reabsorbed, HCO3- secreted (buffers for caries & reflux)
-- Cl- reabsorbed, K+ secreted
- pH and HCO3- increase with flow rate

Front 186

What are the autonomic controls on salavation?

Back 186

- Parasympathetic stimulation, saliva is secreted continuously at a basal rate
- Parasympathetic inhibition inhibits salivation and results in dry mouth

Front 187

What is the gastric mucosal barrier?

Back 187

- Maintains protective buffered layer of pH 7 mucus
along surface of epithelial cells
- Function: prevents damage to the gastric mucosa from
corrosive HCl and pepsin

Front 188

What do mucosal neck and surface epithelial cells secrete?

Back 188

Secrete specific products such as mucins (glycoproteins form protective flexible gel) and
bicarbonate

Front 189

What damages the gastric mucosal barrier?

Back 189

bile salts, ethanol, corticosteroids, and NSAIDS

Front 190

What are the detrimental effects of NSAIDs involving drug-induced gastric disease?

Back 190

- Cause breaks in gastric mucosal barrier
- H+ ion leaks into mucosa → epithelial cell injury & death
- Overwhelms mucosa ability to protect itself
- Local capillaries are also damaged → bleeding
- Inhibit activity of cyclo-oxygenase – enzyme important in synthesis of gastroprotective prostaglandins

Front 191

What does H. Pylori do?

Back 191

Bacteria protects itself by producing large amounts of urease → hydrolyzes the urea → ammonia → damage to mucous layer and epithelial cells

Front 192

What is used to treat H. Pylori infections?

Back 192

- Two antibiotics (i.e. metronidazole and tetracycline)
- Bismuth-containing compound (i.e. Pepto-Bismol)
- H2-receptor blocker (i.e. cimetidine or ranitidine) or PPI

Front 193

What do parietal cells do in relation to GI secretion?

Back 193

- Possess ion transport mechanisms, proton pumps
- Produce HCl– causes pH of stomach lumen to average 1-3
- CO2 from bloodstream (interstitial space) results in H+ and HCO3- via carbonic anhydrase (parietal cell)
- HCO3- is transported to the blood side (interstitial space) of the cell
- H+ is actively transported to stomach lumen, exchanged
for K+
- Acid activates pepsinogen
- Acid kills most bacteria and inactivates salivary
amylase

Front 194

How is HCl secretion in parietal cells inhibited?

Back 194

-HCl secretion is regulated through membrane receptors
- Parietal cell agonists
-- ACh – from vagal parasympathetic/enteric synaptic pathway bind with M3-muscarinic receptors → IP3 increase →
Ca2+ release → protein kinases → H+/K+ ATPase
-- Gastrin – from G cells after parasympathetic
stimulation bind with gastrin/CCK-B receptors → IP3
increase → Ca2+ release → protein kinases → H+/K+ ATPase
--Histamine- paracrine from enterochromaffin-like (ECL) mast cells in gastric mucosa bind with H2 receptors to increase cAMP → activates protein kinases → H+/K+ ATPase

Front 195

How is HCl secretion in parietal cells stimulated?

Back 195

- Parietal cell antagonists
-- Prostaglandins
-- EGF
-- SST

Front 196

How do proton pump inhibitors work?

Back 196

-Treat ulcers and GERD
- Act on H+/K+- ATPase on parietal cells
- Cause permanent inhibition of enzyme activity, leads to inhibition of H+ ions into the lumen of the stomach
- Secretion of acid only resumes after new molecules of H+/K+- ATPase are inserted into the gastric mucosa

Front 197

What are a few of the anticholinergic drugs used to decrease HCl production?

Back 197

•atropine
•dicyclomine (Bentyl)

Front 198

What is intrinsic factor?

Back 198

-produced by parietal cells
- *only indispensable constituent of gastric fluid
- Within the stomach, intrinsic factor combines with B12 to form complex necessary for absorption of B12 in the ileum of the small intestine
- Vitamin B12 – essential factor in formation of RBCs
-- Deficiency in bone marrow - Pernicious anemia

Front 199

What is pepsinogen?

Back 199

-Chief cells produce pepsinogen (stored and secreted form) in response to the presence of gastric acid
- Optimally active at pH=2
- Activated by H+, gives pepsin (active form)
- Activated pepsin begins the process of protein digestion

Front 200

What is gastric lipase?

Back 200

-Chief cells secrete gastric lipase (active at pH=3)
- Digest triglycerides

Front 201

What do pyloric glands -enteroendocrine cells- secrete?

Back 201

-Gastrin (G-cells)
-SST (D-cells)

Front 202

What does gastrin do?

Back 202

- Stimulates acid release by parietal cells
- Stimulates pepsinogen release by chief cells
- Stimulates stomach mucosal growth
- Stimulates contractions of the gastric wall that mix and stir the gastric contents

Front 203

What does SST do?

Back 203

- secreted by D-cells
- Inhibits gastrin release (G cells)
- Inhibits histamine release (mast cells)
- Inhibits acid secretion (parietal cells)

Front 204

What are the functions of the cephalic phase of gastric secretion?

Back 204

- **20-30% of gastric secretory response to a meal
- Proceeds food entering stomach
- Thoughts of food (smell, sight, or taste)
- Chewing or swallowing
- Mediated by vagus nerve and gastrin
- Promote HCl and pepsinogen secretion
-duration: minutes

Front 205

What are the functions of the gastric phase of gastric secretion?

Back 205

- **60-70% of gastric secretory response to a meal
- Elicited by the presence of food in the stomach
-- Distension → stretch receptors
-- Elevated pH → chemoreceptors
-- Protein
-- Caffeine
-- Alcohol
- Mediated by the intrinsic nerves, the vagus nerve, gastrin
-- Promote HCl and pepsinogen secretion
-duration: 3-4 hours

Front 206

What are the functions of the intestinal phase of gastric secretion?

Back 206

- About 10% of gastric secretory response to a meal
- Excitatory component
-- release of intestinal gastrin in response to the products of protein digestion in the duodenum
→ HCl and pepsinogen secretion
- Inhibitory component
-- Distension, lipids, acids, hyperosmotic chyme at duodenum inhibits gastric secretion by
--- Enterogastric reflex
--- Release of enterogastrones
----Secretin, CCK, GIP (all inhibit gastric secretion)
-duration: hours

Front 207

What is the general funciton of the pancreas?

Back 207

-Exocrine glands account for 98% of its mass
- Function:
1. Provide essential enzymes required for digestion
2. Neutralize stomach acid in the duodenum

Front 208

Where is pancreatic juice transported from the pancreas to the duodenum?

Back 208

The pancreatic duct.

Front 209

What does pancreatic juice do?

Back 209

-Alkaline and contains a high concentration of bicarbonate ion
-- Neutralizes the acidic chyme entering the duodenum
from stomach

Front 210

What do epithelial duct cells do in the pancreas?

Back 210

- sites of electrolyte and water secretion
- **secrete bicarbonate that will neutralize excess stomach acid in the duodenum

Front 211

What regulates release of pancreatic secretions?

Back 211

- CCK (acinar cell activity)
- Secretin (bicarbonate secretion by epithelial duct cells)

Front 212

What are acinar cells?

Back 212

-They produce enzymes in the pancreas.
-The enzymes are stored as zymogen granules.

Front 213

How are starch and disaccharides broken down?

Back 213

1. by salivary amylase
2. by pancreatic amylase
-broken into ogliosaccharides and disaccharides- lactose, maltose, sucrose
3. brush border enzymes in small intestine (dextrinase, glucoamylase, lactase, maltase, sucrase) break down to galactose, glucose, and fructose
4. galactose and glucose are involved in Na+ cotransport, fructose in facilitated diffusion
5. Enter the blood through villi and are transported to the liver by the hepatic portal vein

Front 214

How are unemulsified fats broken down?

Back 214

1. unelmusified fats are emulsified by detergent action of bile salts ducted in from the liver
2. pancreatic lipase action to give monoglycerides, glycerol, and fatty acids
3. diffusion into intestinal cells + protein = chylomicrons
4. Enter the lacteals (lymphatic capillaries of small intestine)through villi and are transported to systemic circulation via the lymph

Front 215

Where does blood flow to the liver come from?

Back 215

- About 1350 ml/min (27% of CO)
-Hepatic artery
-- Brings 300 ml/min of oxygenated blood from aorta
- Hepatic portal vein
-- Brings about 1050 ml/min of blood from digestive tract
-- Low in oxygen
-- High in nutrients absorbed from the intestines

Front 216

What are the different cell types in the liver?

Back 216

- Hepatocytes
-- liver cells
-- predominant cell type
- Endothelial cells
-- line passage ways (sinusoids)
- Kupffer cells
-- phagocytes

Front 217

What are sinusoids in the liver and where do they drain?

Back 217

sinusoids:
- spaces between plates
- empty into central vein

Front 218

What are the portal areas (triads) of liver lobules?

Back 218

- hepatic artery branch
-- delivers oxygenated blood
- portal vein branch
-- delivers absorbed & secreted materials
- bile duct branch
-- removes bile

Front 219

How does the liver act as a blood reservoir?

Back 219

-Liver is a large distensible organ
- 10% of blood volume
- As needed, blood may be mobilized to increase VR then increase CO

Front 220

How, in general, does the liver filter blood?

Back 220

- Protective function
- Kupffer cells, large phagocytic macrophages, line
hepatic venous sinuses
-- Take in and digest bacteria
-- Efficiently removes 99% of the bacteria from hepatic
portal blood

Front 221

What are IGFs?

Back 221

-Synthesis of IGFs (somatomedins) done by the liver
- Responsible for many of GH’s growth-promoting
effects

Front 222

What vitamins does the liver store?

Back 222

- Vitamin A – up to 10 months
- Vitamin D – 3-4 months
- Vitamin B12 – at least 1 year
- Iron (in form of ferritin) is released when circulating iron blood levels low

Front 223

What blood clotting factors does the liver produce?

Back 223

- Blood clotting factors (II, VII, IX, X)

Front 224

What hormones does the liver metabolize?

Back 224

- Thyroid hormone
- All steroid hormones (estrogen, cortisol, aldosterone…)

Front 225

What is bile?

Back 225

- Def: aqueous, yellow-green, alkaline fluid
consisting of a complex mixture
- Bile salts, bile pigments, cholesterol, neutral fats,
phospholipids, variety of electrolytes
- Bile salts are synthesized from cholesterol
- Bile salts are amphipathic (hydrophilic and hydrophobic regions) and arrange themselves around lipid droplets

Front 226

What are the functions of the gallbladder?

Back 226

-bile storage
-- 1 liter of bile produced/day
-- bile made continuously
-- enters gallbladder if sphincter closed
- bile modification
-- water reabsorbed
-- increased concentration (up to 20X)

Front 227

What stimulates the gallbladder to empty?

Back 227

The presence of dietary fat and protein.

Front 228

What are the hepatic and gallbladder ducts?

Back 228

- Cystic duct
-- leads in/out of gallbladder
- Common hepatic duct
-- Common drainage for all the lobes
- Bile duct
-- union of cystic and common hepatic ducts
-- joins pancreatic duct
-- opens into duodenum

Front 229

How do bile acids regulate bile release?

Back 229

-Target: hepatocytes
-Action: increases bile flow, inhibits bile acid synthesis

Front 230

How does secretin regulate bile release?

Back 230

-Target: bile ducts in the liver
-Action: stimulates secretion of water and bicarbonate into the bile

Front 231

How does CCK regulate bile release?

Back 231

Targets: gallbladder, Oddi's sphincter
Action: Stimulates contractions of the gallbladder and relaxes Oddi's sphincter

Front 232

How does the vagus nerve regulate bile release?

Back 232

Targets: gallbladder
Action: stimulates contractions (minor effect)

Front 233

What are the steps in the regulation of bile release?

Back 233

1. Acidic, fatty chyme entering duodenum causes release of CCK and secretin from duodenal wall enteroendocrine cells
2. CCK and secretin enter bloodstream.
3. Bile salts and secretin transported via bloodstream stimulate liver to produce bile more rapidly.
4. Vagal stimulation causes weak contractions of gallbladder
5. CCK (via bloodstream) causes gallbladder to contract and hepatopancreatic sphincter to relax, bile enters duodenum
6. Bile salts reabsorbed into blood

Front 234

What are the cell types in the small intestine?

Back 234

1) absorptive cells
- brush border enzymes
- integral membrane proteins
- digestion of materials contacting brush border
2) goblet cells (mucus)
3) enteroendocrine cells
- secrete enterogastrones (gastrin, secretin, CCK)

Front 235

What stimulates mucus stimulation of the goblet cells in the lg. intestine?

Back 235

- tactile stimuli and irritation
- parasympathetic stimulation

Front 236

What does the liver do to proteins?

Back 236

- Deamination of amino acids
- Formation of urea (for removal of ammonia from body fluids)
- Formation of plasma proteins (albumins, fibrinogen, globulins)
- Conversion of amino acids into other compounds

Front 237

What does the liver do to lipids?

Back 237

- Oxidation of fatty acids to supply energy for other functions
- Synthesis of cholesterol, phopholipids, and lipoproteins
- Synthesis of fat from proteins and carbohydrates

Front 238

What are the steps in the regulation of bile release?

Back 238

1. Acidic, fatty chyme entering duodenum causes release of CCK and secretin from duodenal wall enteroendocrine cells
2. CCK and secretin enter bloodstream.
3. Bile salts and secretin transported via bloodstream stimulate liver to produce bile more rapidly.
4. Vagal stimulation causes weak contractions of gallbladder
5. CCK (via bloodstream) causes gallbladder to contract and hepatopancreatic sphincter to relax, bile enters duodenum
6. Bile salts reabsorbed into blood

Front 239

What are the cell types in the small intestine?

Back 239

1) absorptive cells
- brush border enzymes
- integral membrane proteins
- digestion of materials contacting brush border
2) goblet cells (mucus)
3) enteroendocrine cells
- secrete enterogastrones (gastrin, secretin, CCK)

Front 240

What stimulates mucus stimulation of the goblet cells in the lg. intestine?

Back 240

- tactile stimuli and irritation
- parasympathetic stimulation

Front 241

What does the liver do to proteins?

Back 241

- Deamination of amino acids
- Formation of urea (for removal of ammonia from body fluids)
- Formation of plasma proteins (albumins, fibrinogen, globulins)
- Conversion of amino acids into other compounds

Front 242

What does the liver do to lipids?

Back 242

- Oxidation of fatty acids to supply energy for other functions
- Synthesis of cholesterol, phopholipids, and lipoproteins
- Synthesis of fat from proteins and carbohydrates

Front 243

What are the steps of protein digestion?

Back 243

1) Proteins are broken down by pepsin (in the presence of HCl) in the stomach leading to
2) Lg. polypeptides, broken down by pancreatic enzymes (trypsin, chymotrypsin, carboxypeptidase) in the small intestine
3) makes sm. polypeptides and peptides that are broken down by brush border enzymes (carboxypeptidase, aminopeptidases, dipeptidase) in the sm. intestine.
4) Leads to amino acids (and some di-and tri-peptides) that pair with cotransport Na+ to enter the blood through villi and are transported to the liver by the hepatic portal vein

Front 244

How are nucleic acids digested?

Back 244

1) nucleic acids are broken down in the sm. intestine by deoxyribonuclease and ribonuclease
2) Then broken down by brush border enzymes (nucleosidases and phosphatases) in sm. intestine
3) gives pentose sugars, N-containing bases, phosphate ions which enter the blood through villi and are transported to the liver by the hepatic portal vein

Front 245

What do bile salts do?

Back 245

They facilitate the action of pancreatic lipase and formation of micelles (small lipid-bile salt complexes).

Front 246

What is the relationship between water and the colon?

Back 246

- About 1.5 L of fluid passes the ileocecal valve each day
- Only 150 mL of water is lost in stools
- Maximum absorptive capacity is about 4.5 L and
when this is exceeded, diarrhea will occur
- Water moves by transcellular (through cell) and paracellular (between cell) mechanisms

Front 247

What are the relative volumes of fluids in the different body compartments?

Back 247

- 2/3 – intracellular fluid (ICF)
-- fluid within cells or cytosol
-- ICF = 0.4 x (body weight) = 28 L
- 1/3 – extracellular (ECF)
-- fluid found outside of cells
-- ECF = 0.2 x (body weight) = 14 L
-- 3/4 – interstitial fluid (0.15 x body weight = 10.5 L)
-- 1/4 – blood plasma (0.05 x body weight = 3.5 L)

Front 248

What are the concentrations of solutes in the ICF?

Back 248

- low sodium, chloride & bicarbonate
- high potassium & protein
- 50% of osmolality due to potassium

Front 249

What are the concentrations of solutes in the ECF?

Back 249

- high sodium, chloride & bicarbonate
- 50% of osmolality due to sodium & chloride
- low potassium

Front 250

In general, what are the different excretory systems of the body?

Back 250

-Respiratory system removes the metabolic waste product
-- CO2
- Digestive system removes:
-- Undigested materials
-- Bacteria
- Urinary System removes:
--Waste products
--- Urea, uric acid, creatinine, ammonia salts
-- Water
-- Toxic molecules
-- Excess ions

Front 251

What do renal functions regulate in the body?

Back 251

1. Homeostasis
a) water balance
b) electrolyte balance
c) acid/base balance
2. Arterial blood pressure
3. Erythrocyte production
4. Vitamin D metabolism
5. Metabolic waste & chemical excretion
6. Gluconeogenesis

Front 252

How is water balance regulated by the kidneys?

Back 252

- role in regulating blood volume
- water not actively pumped
-- “water follows salt”

Front 253

How is electrolyte balance regulated by the kidneys?

Back 253

- maintained at ~280-300 mosm/l
- large variations in intake & excretion
- intake = excretion over time

Front 254

How is acid/base balance regulated by the kidneys?

Back 254

- excretion of H+ is regulated
- reabsorption of HCO3- is regulated
- coordinated with ventilation
- H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3-

Front 255

How does renin help regulate arterial pressure on a short term basis?

Back 255

- Secreted by granular cells (kidney)
- Enzyme that acts on angiotensinogen
-- made by hepatocytes
-- serum protein
-- converted to Angiotensin I (AI) no biological activity - which is then converted to AII

Front 256

How does Angiotensin I lead to regulation of arterial pressure on a short term basis, as it in itself has no biological activity?

Back 256

- Angiotensin I converted to Angiotensin II
- Angiotensin Converting Enzyme
-- ACE (lungs)
-- ACE inhibitors
- Angiotensin II causes vasoconstriction
-- acutely raises blood pressure

Front 257

What are the renal functions that contribute to long term arterial pressure regulation?

Back 257

-Angiotensin II acts on:
-- adrenal cortex stimulating:
--- aldosterone secretion
--- increased renal reabsorption of electrolytes
--- “water follows the salt”
--- reabsorption expands blood volume
--- B.P. = C.O. x T.P.R.
-- brain
--- posterior pituitary – ADH release
--- thirst

Front 258

What are the characteristics of the erythrocytes that are produced in the kidneys?

Back 258

- erythrocyte production leads to secretion of erythropoeitin
- secreted by the macula densa
- secretion stimulated by tissue hypoxia
- stimulates the production of RBCs in bone marrow stem cells

Front 259

What are the functions of the kidney in vitamin D metabolism?

Back 259

- kidneys activate vitamin D
-- forms 1, 25 di-hydroxy vitamin D
- active form required for Ca2+ absorption
-- GI tract
- bone resorption & deposition
-- effects calcium & phosphate levels in blood

Front 260

What are the renal functions related to metabolic wastes and chemical secretion?

Back 260

- urea (amino acids → NH3 → urea)
- creatinine (creatine: muscle)
- uric acid (nucleic acids)
- bilirubin (hemoglobin)
- hormone breakdown products
- foreign chemicals & drugs
-- i.e. drugs: aspirin, penicillin, atropine

Front 261

What are the renal functions of gluconeogenesis?

Back 261

- “making new glucose”
- occurs in kidneys during fasting
- substrates:
-- amino acids
-- lactic acid
- liver is the major site of GNG

Front 262

Where are nocioceptors located in the urinary system?

Back 262

- no nocioceptors in renal tissue
- capsule and ureter have nocioceptors

Front 263

How much of the cardiac output and renal plasma flow does the urinary system recieve?

Back 263

- Receive 25% of the cardiac output
- Filter 20% of the renal plasma flow (RPF)

Front 264

What are the characteristics of the renal cortex?

Back 264

- outermost layer
- contains about 1 x 106 nephrons per kidney
-- Nephrons - filtering units that form urine

Front 265

What are the types of nephrons?

Back 265

- Cortical nephrons (80-85%) - lie completely within the cortex
- Juxtamedullary nephrons (15-20%) - lie in both the cortex and medulla

Front 266

What structures does the renal medulla contain?

Back 266

- triangular renal pyramids
- renal columns

Front 267

What are the triangular renal pyramids?

Back 267

- Contain parallel bundles of ducts carrying urine from the nephrons.

Front 268

What are the renal columns?

Back 268

- areas between pyramids
- extensions of the cortex
- provide a route for the passage of blood vessels
and nerves to and from the outer cortex

Front 269

What is the renal pelvis?

Back 269

- is funnel-shaped
- lies within the renal sinus
- collects urine from the pyramids and conveys it into the ureter for passage to the urinary bladder

Front 270

What are the general characteristics of urine?

Back 270

- portion of our blood that contains undesirable metabolic waste
- kidneys do not add anything to urine that was
not already in blood
- Peristaltic waves move urine down ureters
- When peristaltic contractions produce enough
pressure to overcome the resistance of sphincters, then urine enters the bladder
-- Involuntary internal sphincter
-- Voluntary external sphincter

Front 271

What are the ureters?

Back 271

- smooth muscle tube (passage)
- from each kidney
- to urinary bladder
- peristalsis pushes urine to bladder
- nocioceptors present
- pain with passage of kidney stone

Front 272

What are the characteristics of the urinary bladder?

Back 272

- smooth muscle sac
- receives urine from two ureters
- stretch receptors
- passes urine into one urethra
- ANS innervation

Front 273

What is the urethra?

Back 273

- tube from bladder to exterior
-- prostate gland
- internal sphincter:
-- neck of bladder (exit)
-- smooth muscle
--- tonically contracted (closed)
--- PNS innervation
--- spinal reflex
- external sphincter:
-- just distal to neck of bladder
-- skeletal muscle
-- somatic innervation (sacral nerves)
-- voluntary control
-- contraction blocks voiding

Front 274

About what percent of the blood profuses the renal cortex?

Back 274

- more than 90%

Front 275

What is the pattern of blood flow through the kidneys into the glomerulus?

Back 275

- aorta
- renal artery
- segmental artery
- lobar artery
- interlobar artery
- arcuate artery
- interlobular artery
- afferent arteriole
- glomerulus (capillaries)

Front 276

What is the pattern of blood flow from the kidneys to the inferior vena cava?

Back 276

- glomerulus (capillaries)
- efferent arteriole
- peritubular capillaries and vasa recta
- interlobular vein
- arcuate vein
- interlobar vein
- renal vein
- inferior vena cava

Front 277

What is the 1st capillary bed?

Back 277

The glomerulus.

Front 278

What is the peritubular capillary bed?

Back 278

- 2nd capillary bed
- located in renal pyramids
- after efferent arteriole
- surrounds tubular elements
- located in renal pyramids
- flows into renal veins
- role in renal secretion/reabsorption

Front 279

What are the vasa recta?

Back 279

- found only juxtamedullary nephrons
- series of vascular loops
- form 3rd capillary network
- located in renal medulla
- after efferent arteriole and peritubular capillaries
- surround Loop of Henle & collecting duct
- blood returns to cortex via ascending vasa recta
- bring O2 and nutrients to tubule
- role in concentrating & diluting urine

Front 280

What are the components of the renal corpuscle?

Back 280

- Glomerulus
-- capillary network
- Bowman’s capsule
-- surrounds the glomerulus
- Bowman’s space
-- space between capsule & glomerulus
- Epithelial layers
-- visceral & parietal layer

Front 281

What are the components of the nephron?

Back 281

* Renal Corpuscle
* Tubule
- Proximal convoluted tubule (PCT)
- Loop of Henle
-- Descending limb
-- Ascending limb
- Distal convoluted tubule (DCT)
- Collecting duct

Front 282

What are the major steps that occur from the glomerulus to the collecting duct?

Back 282

* Glomerulus and Bowman’s capsule
- Glomerular filtration apparatus
- Provides filtrate that is processed by the renal tubule
* Proximal tubule
- Reabsorption of nutrients and minerals
- Secretion of selected waste products (NH4+, nitrogenous wastes)
* Loop of Henle
- Formation of high concentration of NaCl and
urea in the medulla
- Formation of a dilute filtrate
* Distal tubule & collecting duct
- Final control of plasma ion concentrations
- Regulation of body osmolality
- Regulation of extracellular volume

Front 283

What cell types make up Bowman's capsule and tubule?

Back 283

- Bowman’s capsule and the tubule are formed from a single layer of epithelial segments
- Cells forming the visceral layer of Bowman's capsule are called podocytes.

Front 284

What cell types make up the proximal convoluted tubule?

Back 284

The proximal convoluted tubule is composed of brush border cuboidal epithelial cells with highly folded basolateral membrane

Front 285

What cell types are present in the loop of Henle and DCT?

Back 285

- Descending loop of Henle is composed of flattened cells with few microvilli and transport proteins. Cells are permeable to water but not NaCl.
- Ascending Loop of Henle and Early DCT cells have a glycoprotein covering of the
luminal membrane.
- cells are permeable to NaCl but not water
-- DCT – specialized for selective secretion and
reabsorption, more secretion

Front 286

What cell types are present in the juxtaglomerular apparatus?

Back 286

Juxtaglomerular apparatus is a junction between: DCT and afferent & efferent arterioles
* components:
- macula densa cells
-- osmoreceptors
- juxtaglomerular cells
-- mechanoreceptors

Front 287

What monitors are present in the juxtaglomerular apparatus?

Back 287

1. sodium concentration of filtrate
- renin
2. volume of filtrate
- renin
3. tissue hypoxia
- erythropoietin

Front 288

What are the cell types in the late DCT and collecting duct?

Back 288

- Composed of prinicipal (lack microvilli) and intercalated (abundant microvilli) cells

Front 289

What regulates sodium and water absorbtion in the late DCT and collecting duct?

Back 289

-Sodium and water reabsorption in this area is hormonally regulated
- Aldosterone (principal cells)
→ reabsorb Na + and secrete K+ and water follows → ↓ H2O loss
- ADH → increase H2O channels of principal cells → ↓ H20 loss

Front 290

What are the general characteristics of glomeruli filtration?

Back 290

- Def: movement of large quantities of water and
solutes through the filtration membrane from the
glomeruli into Bowman’s capsule
- Passive process involving bulk flow
- Driven by the hydrostatic pressure of the blood
- Electrolyte concentrations are equal (blood)
- Osmolality is “essentially” equal (blood)

Front 291

What are the characteristics of the glomerular filtrate?

Back 291

* Glomerular filtrate – fluid collecting in the capsular space is composed of
- water
- ions (Na, K, Cl)
- nitrogenous waste (urea, uric acid, creatinine)
- organic molecules (glucose, aa)
- Plasma minus blood cells and most proteins
- Little protein is found in the urine of healthy people
- Most (99%) reabsorbed

Front 292

What is the filtration barrier?

Back 292

Def: Fenestrated endothelium, basement membrane and pores formed by podocytes

Front 293

What are the layers of the filtration barrier?

Back 293

1. capillary endothelium
- found in all capillaries
2. basement membrane
- found in all capillaries
- The primary barrier to filtration
3. epithelial layer (podocytes)
- not normally found in capillaries

Front 294

What are the characteristics of the capillary endothelium layer of the filtration barrier?

Back 294

* fenestrated (holes)
- large in number & size
- allow most things to pass
- plasma proteins pass
- RBCs excluded
- similar to liver sinusoids

Front 295

What are the characteristics of the basement membrane layer of the filtration barrier?

Back 295

- surrounds endothelial layer
- thicker & denser than typical capillary
- collagen & proteoglycans
- excess negative charges
- primary barrier to filtration
- holes allow solutes to pass
- holes exclude large proteins & cells
- negatively charged
- negative charges repel small proteins

Front 296

What are the characteristics of the epithelial layer of the filtration barrier?

Back 296

- not normally found in capillaries
- podocytes (foot-like)
- discontinuous layer
-- “slit pores” (pedicles)
- minimal barrier to filtration

Front 297

What does hydrostatic blood pressure do in the filtration process?

Back 297

- Blood pressure drives water and small solutes OUT
(passive)
- 55 mmHg

Front 298

What does capsular hydrostatic pressure do in the filtration process?

Back 298

- Opposes filtration (IN)
- Force exerted by fluids of Bowman’s capsule
- 15 mmHg

Front 299

What does osmotic or plasma oncotic pressure do in the filtration process?

Back 299

- Opposes filtration (IN)
- Due to large proteins in blood that cannot filter
through
- 30 mmHg

Front 300

What is the net filtration pressure (NFP)?

Back 300

= 55 – (15 + 30) = 10 mm Hg
OUT

Front 301

What happens when there is no modification of solute in filtrate?

Back 301

- solute freely filtered
- no reabsorption
- no secretion
- filtration = excretion
- waste products
-- creatinine
-- inulin

Front 302

What happens when there is partial reabsorbtion of solute in filtrate?

Back 302

- solute is freely filtered
- portion of solute reabsorbed
- from tubules into peritubular capillaries
- excretion = filtration - reabsorption
- handling of most electrolytes
- sodium/chloride/bicarbonate
- control rate/amount of reabsorption

Front 303

What happens when there is complete reabsorbtion of solute in filtrate?

Back 303

- solute is freely filtered
- solute completely reabsorbed
- from tubules into peritubular capillaries
- filtration = reabsorption
- handling of most nutritional substances
- amino acids/glucose
- saturation characteristics
- carrier protein required
- energy source required
-- ATP or cotransport
- if amount in filtrate > reabsorption rate
-- “spill-over” into urine
-- Tmax is exceeded

Front 304

What happens to the filtrate when hyperglycemia occurs? (glucose > 200 mg%)

Back 304

- carrier protein saturated
- incomplete reabsorption
- glucose excreted
- diuretic effect

Front 305

What happens when solute is secreted?

Back 305

- solute usually freely filtered
- solute added to filtrate (secreted)
-- potassium & hydrogen ion
- from peritubular capillaries into tubules
- excretion = filtration + secretion
- increases rate of excretion (clearance)
- often regulated (aldosterone)

Front 306

What kinds of compounds does passive transport move?

Back 306

Passive transport moves water, urea, lipid-soluble,
nonpolar compounds.

Front 307

What are the steps of urine production?

Back 307

* In Proximal tubules
- Na+ and other substances removed
- Water follows passively
- Filtrate volume reduced
* In descending limb of loop of Henle
- Water exits passively, solute enters
- Filtrate volume reduced 15%
* In ascending limb of loop of Henle
- Na+, Cl-, K+ transported out of filtrate
- Water remains
* In distal tubules and collecting ducts
- Water movement out regulated by ADH
- If absent, water not reabsorbed and dilute urine produced
- If ADH present, water moves out, concentrated urine produced

Front 308

What is the osmolality in the glomerulus and Bowman's capsule?

Back 308

Filtrate = plasma osmolality (Isotonic)

Front 309

What is the osmolality in the proximal tubule?

Back 309

- Reabsorption and selected secretion
- Filtrate volume reduced by 65%
- Isotonic

Front 310

What is the osmolality in the loop of Henle?

Back 310

*Descending (hypERtonic)
- Formation of high concentration of NaCl and urea in the medulla (from 300 to 1200)
*Ascending (hypOtonic)
- Formation of a dilute filtrate (from 1200 to 100)

Front 311

What is the osmolality in the distal tubule and collecting duct?

Back 311

- Final control of plasma ion concentrations
- Regulation of body osmolality
- Regulation of extracellular volume
- Urea secretion in lower collecting duct
- Dilute filtrate (100 mOsm)

Front 312

What is the countercurrent multiplier?

Back 312

- Loop of Henle functions as a countercurrent multipier to establish the osmotic gradient
- Two limbs of the Loop of Henle establish the osmotic gradient in the medullary interstitial fluid
- Descending limb produces salty filtrate
- Ascending limb uses this high salt to maintain the
osmolality of the interstitial fluid in the medulla
-- Thin – passive transport
-- Thick – active transport
- Diffusion of urea from the lower portion of the collecting duct also contributes to high medullary
osmolality

Front 313

What is the countercurrent exchanger?

Back 313

*Vasa recta - countercurrent exchanger
- Blood leaving/reentering the cortex via the vasa recta
have the same solute concentration
*Why?
- Highly porous – act to cycle salt
- Sluggish blood flow – receive only 10% RBF
- -> Continuously equilibrates with the interstitial fluid
*Function?
- Protect the medullary gradient so acts countercurrent exchange
*How?
- By preventing rapid removal of salt from the medullary interstitial space

Front 314

What does ADH do?

Back 314

- Secreted by posterior
pituitary
- Increases water permeability in distal tubules and collecting ducts

Front 315

What does aldosterone do?

Back 315

- Produced in adrenal cortex
- Affects Na+ and Cl- transport in nephron and
collecting ducts

Front 316

What does renin do?

Back 316

- Produced by kidneys, causes production of angiotensin II

Front 317

What is atrial natriuretic
hormone?

Back 317

- Produced by heart when blood pressure increases
- Inhibits ADH production
- Reduces ability of kidney to concentrate urine

Front 318

What causes urine to flow through the nephron and the ureters?

Back 318

- Hydrostatic pressure forces urine through nephron
- Peristalsis moves urine through ureters

Front 319

What is the micturition reflex?

Back 319

- Stretch of urinary bladder stimulates reflex causing bladder to contract, inhibiting urinary sphincters
- Higher brain centers can stimulate or inhibit reflex

Front 320

What is GFR?

Back 320

- Def: the total filtrate formed by both kidneys per minute (ml/min)
- Normal systemic pressure: 120 mmHg → GFR 125 ml/min (180 L/day)
- Note: Greater than total body water (42 L)

Front 321

What is the GFR determined by?

Back 321

- Hydrostatic blood pressure (out) PHb
- Capsular hydrostatic pressure (in) PHc
- Osmotic or plasma oncotic pressure (in) PO

Front 322

How is GFR calculated?

Back 322

GFR = [PHb – (PO + PHc)] x Fc

Front 323

What is Fc?

Back 323

- Filtration coefficient (Fc or Kf)
- Def: Intrinsic permeability of the glomerular capillary and the glomerular surface area
available for filtration
- Fc = capillary permeability x filtration surface area
- Fc = 12.5 ml/min/mmHg

Front 324

What affects the filtration surface area (contributing to the Fc)?

Back 324

- decreases with age &/or pathology
- loss of nephrons
- loss of glomeruli
- size of filtration holes decrease

Front 325

What affects do some drugs and hormones have on Fc?

Back 325

- Vasodilate the glomerular arteries increase Fc
- Vasoconstrict the glomerular arteries decrease Fc

Front 326

What are the intra-renal (autoregulatory) controls of GFR?

Back 326

1. Myogenic control
2. Tubuloglomerular feedback
3. Prostaglandin controls
- During pathophysiological conditions
- PG produced locally act locally as vasodilators
- Prevents severe renal ischemia

Front 327

What is the kidney's response to high systemic BP?

Back 327

- High systemic pressure could lead to possible dehydration
- If BP = 140 mmHg then GFR 146 ml/min thus need renal autoregulation
- Kidney response:
-- constricted afferent arteriole gives dec. blood flow
-- GFR 125 ml/min
-- Once return back to BP = 120 mmHg
- Kidney response:
--dilated afferent arteriole
-- GFR 125 ml/min

Front 328

What is the kidney's response to low systemic BP?

Back 328

- Low systemic pressure means possible poor filtering
- If BP = 100 mmHg then GFR 104 ml/min then need renal autoregulation
- Kidney response:
-- Dilate afferent arteriole
-- inc. blood flow to GFR 125 ml/min
-- Once return back to BP = 120 mmHg
- Kidney response:
-- Constrict afferent arteriole -> GFR 125 ml/min

Front 329

What are the intra-renal tubuloglomerular controls of GFR?

Back 329

- Macula densa cells are sensitive to
-- filtrate osmolarity (NaCl)
-- rate of filtrate flow
- actions
-- initiate release of vasoconstrictor (adenosine, a paracrine)
---high adenosine gives vasoconstriction
---afferent low adenosine gives vasodilation efferent
-- send paracrine to JG cells which secrete renin

Front 330

What are the extra-renal controls of GFR?

Back 330

- Renin angiotensin system
- Atrial natriuretic factor (ANF)
- Sympathetic nerves and circulating Epi

Front 331

How does angiotensin II act as an extra-renal control of GFR?

Back 331

↓ efferent arteriole diameter → ↑ R
↓ blood flow out of glomerulus
↑ glomerular hydrostatic pressure
↑ GFR

Front 332

How does atrial natriuretic factor (ANF) act as an extra-renal control of GFR?

Back 332

- Released in response to high BP
- Results in decreased BV leading to decreased BP

Front 333

How does the sympathetic nervous system act as an extra-renal control of GFR?

Back 333

*Sympathetic control overrides renal autoregulation in cases of extreme stress or blood loss
*Intense vasoconstriction of renal blood vessels
- Purpose: allows blood is shunted to other vital organs
- Problem: can lead to kidney failure
*By reducing GFR → reduced fluid loss
- Problem: poor filtering at kidney

Front 334

What are the functions of the PCT?

Back 334

1. Reabsorb organic nutrients
- >99% glucose, aa, other organic nutrients
- Facilitated transport and cotransport
2. Reabsorb ions
- Active – Na+, K+, Mg2+, HCO3-, PO4 3-, SO4 2-
- Passive – other solutes
3. Reabsorb H2O
- Along PCT, 108 L/day
- Follows solute reabsorption
4. Secretion
- H+, organic anions, organic cations
- Exogenous organic compounds, including drugs

Front 335

What are the functions of the loop of Henle?

Back 335

- filtrate enters Loop at ~300 mosm/l
-- concentration ultrafiltrate = blood
- filtrate at ~1200 mosm/l at “turn-around”
-- water leaves as filtrate descends
- filtrate at ~100 as re-enters cortex
-- solutes leave as filtrate ascends
-- filtrate is more dilute than blood

Front 336

What are the functions of the late DCT and collecting tube (under regulation)?

Back 336

- Na+ reabsorbed
- Cl- reabsorbed
- K+ secreted
- H+ secreted
- HCO3- secreted

Front 337

What are the functions of the collecting system?

Back 337

1) convey tubular fluid to calyces
2) finalize urine composition
- solute concentration
-- sodium, bicarbonate, urea
- water volume
- pH
-- hydrogen ion
-- bicarbonate ion

Front 338

What are the characteristics of urea in the collecting system?

Back 338

- blood urea nitrogen (BUN normal up to 30 mg/dL)
- freely filtered
- segments impermeable to urea:
-- thick ascending limb (Loop of Henle)
-- DCT
-- cortical collecting ducts
- segments permeable to urea
-- urea diffuses out of medullary collecting ducts

Front 339

How much H20 does the normal human body contain?

Back 339

40 L

Front 340

What is the typical daily water intake?

Back 340

*Water Daily Intake – 2500 mL
- Food and drink – 2300 mL
- Cell metabolism – 200 mL

Front 341

What is the water daily output?

Back 341

*Water Daily Output - 2500 mL
- Kidneys – 1500 mL
- Skin – 600 mL
- Lungs – 300 mL
- GI Tract – 300 mL

Front 342

What are the target tissues of ADH in regulation of fluid homeostasis?

Back 342

- Target tissue – late DCT and collecting duct
- Cells become permeable to water only in the presence of
ADH

Front 343

How does the thirst mechanism work in regulation of fluid homeostasis?

Back 343

- Thirst mechanism – regulates water intake
- Dry mouth stimulates hypothalamic thirst center
- Hypothalamic osmoreceptors sensing an inc. in
osmolarity/conc. of solutes in the plasma → stim. thirst center
- Dec. BV → Dec. BP → stim. renin release → inc.
angiotensin II → stim. thirst center

Front 344

How does aldosterone function in regulation of fluid homeostasis?

Back 344

- Without aldosterone, cells of the late DCT and collecting duct don’t allow Na+ and K+ ions to pass
- Aldosterone inserts additional channels
- allows more Na+ to move from filtrate to blood
- allows more K+ to move from blood to filtrate
- If ADH is present, H2O will follow Na+
- Inc. H2O and Na+ moving to blood leads to Inc. BP

Front 345

How does the sympathetic nervous system function in regulation of fluid homeostasis?

Back 345

- Low BP → baroreceptors in heart, aortic arch, and
carotid arteries → medulla – inc. SNS
- Inc. SNS → NT release from the sympathetic nerves in the kidney → vasoconstriction → dec.
fluid loss → inc. BV and BP

Front 346

What are the required concentrations of electrolytes in the body?

Back 346

- Na+ : 136 –145 mEq/L
- K+: 3.5 – 5.1 mEq/L
- Ca2+: 9 – 11 mg/dL

Front 347

What are the functions of electrolytes in transport between cell membranes and interstitial fluid?

Back 347

- Na+/K+ ion pump – actively transports
-- 3 Na+ out, 2 K+ in
- Na+ ion channel – passive
- K+ ion channel – passive
- H2O movement via osmosis to area with higher solutes

Front 348

In general how are electrolytes transported between blood plasma and interstitial fluid?

Back 348

- Ions, other small solutes, and H2O move freely through gaps between endothelial cells
- Proteins too large to leave blood capillaries
- Protein conc. in IF is lower than plasma

Front 349

What are some causes of edema?

Back 349

- Edema is accumulation of fluid in the interstitial compartment
*Dec. colloid osmotic pressure (PO)
- ie. liver disease
*Inc. hydrostatic pressure (PHB)
- ie. hypertension
*Inc. capillary permeability
- ie. inflammation or injury
*Lymphatic obstruction
- ie. removal of lymph nodes

Front 350

What is hypernatremia?

Back 350

- > 145 mEq/L Na+
- Too much water lost from blood without Na+ loss
-- ie. sweating
- Too much Na+ added without H2O
-- ie. excessive salt intake
- cell shrinkage, inc. thirst, dec., inc. BV/BP

Front 351

What is hyponatremia?

Back 351

- < 136 mEq/L Na+
- cell swell, nerve impulse conduction, muscle contraction

Front 352

What are roles of potassium in the body?

Back 352

- Major intracellular positive ion
- Resting membrane potential
- Nerve impulse contraction
- Muscle contraction
- Maintenance of normal cardiac rhythm
- Acid/base balance (K+/H+ antiporter)

Front 353

How does aldosterone affect K+ concentration?

Back 353

Inc. Na+ reabsorption at expense of K+ loss

Front 354

How do diuretics affect K+ concentration in the body?

Back 354

- By promoting urine formation, some (loop) diuretics will cause hypokalemia.
- Na+ , K+, Cl- symporters
- No mechanism for compensating renal losses of K+
- To correct, must ingest additional K+

Front 355

What is hyperkalemia?

Back 355

> 5.1 mEq/L K+
- Excessive K+ intake
-- ie. overuse of salt substitutes
- Dec. K+ excretion
-- ie. renal failure
- Inc. K+ leaving cells
-- acidosis
- leads to muscle weakness, intestinal & cardiac problems
-- Death by cardiac arrest

Front 356

What is hypokalemia?

Back 356

< 3.5 mEq/L K+
- Decreased K+ intake
-- ie. unbalanced diet
- Inc. K+ excretion
-- ie. diuretics
- Dec. K+ leaving cells
-- alkalosis
- leads to muscle weakness, intestinal & cardiac problems
-- death by respiratory arrest

Front 357

What is the role of calcitonin on Ca 2+ concentration in the body?

Back 357

- Inhibits action of osteoclasts, which breakdown bone
- Stimulates action of osteoblasts, which cause bone
formation
- leads to dec. blood Ca2+ and PO4-

Front 358

What is the role of PTH on Ca2+ concentration in the body?

Back 358

- Increases number and action of osteoclasts, which
breakdown bone
- Inc. Ca2+ and Mg2+ reabsorption at kidney
- Inc. Vitamin D → calcitriol at kidney
- → inc. blood Ca2+

Front 359

What is the role of calcitriol?

Back 359

- Inc. Ca2+ and PO4- absorption from the GI tract

Front 360

What are the symptoms of hyper- and hypo- calcemia?

Back 360

*Hypercalcemia
- Heart dysrhythmias
- Fatigue
- Confusion
- Nausea
- Coma
- Cardiac arrest
- Calcification of the soft tissues
*Hypocalcemia
- Muscle spasms
- Tetanus b/c no Ca2+ for NT release
- Respiratory arrest

Front 361

How does chemical regulation work to control [H+] in the body?

Back 361

- Buffers resist changes in pH and are most effective at their pKa
- Phosphate buffer system – intracellular and in urine
H2PO4- + OH- ↔ HPO4 2- + H+
- Protein buffers – bind or release H+
NH2-X-COOH + H+ ↔ NH3+-X-COOH
NH2-X-COOH + OH- ↔ NH2 -X-COO-
- Carbonic acid/bicarbonate buffer system
H2CO3 ↔ H+ + HCO3-
*Carbonic anhydrase catalyzes this equation

Front 362

How does the respiratory system regulate [H+] in the body?

Back 362

- ↑ PaCO2 → ↑ [H+] → ↓ pH
- Chemoreceptors respond to changes in PaCO2, [H+], and pH
- Hyperventilation → ↓ PaCO2 and ↑ ECF pH
→ Hypoventilation → ↑ PaCO2 and ↓ ECF pH

Front 363

How do the kidneys function to regulate [H+] in the body?

Back 363

- Filtered HCO3- is reabsorbed
-- Excretion of HCO3- occurs when HCO3- ions are in
greater amounts than H+
- New HCO3- is formed by kidney tubule cells
- Secretion of H+
-- Tubular cells secrete H+ by primary and secondary active transport
-- H+ is titrated with Na2HPO4 and NH3 to yield
excretable acidic products

Front 364

What is the normal base to acid ratio in the body?

Back 364

base to acid ratio- 20:1

Front 365

What is respiratory acidosis and alkalosis?

Back 365

* Acidosis: inc. PaCO2 caused by hypoventilation
- ↑ CO2 + H2O ↔ ↑ H2CO3 ↔ H+ + HCO3-
- Compensation: renal H+ excretion
*Alkalosis: dec. PaCo2 caused by hyperventilation opposite of acidosis eqn.
- Compensation: renal HCO3- excretion

Front 366

What is metabolic acidosis?

Back 366

-Excess of nonvolatile acids or loss of HCO3-
- Causes:
-- Excess acid production
--- Diabetic ketoacidosis, starvation ketosis, lactic ketosis, kidney disease, hyperkalemia
-- Loss of base (found in intestines)
--- Diarrhea, excessive vomiting
- Compensation:
-- Inc. ventilation
-- Inc. excretion of H+ (titrated with NH3)

Front 367

What is metabolic alkalosis?

Back 367

- Excess base or loss of H+
- Causes:
-- Loss of acid
--- Vomiting, hypokalemia
-- Excess base
--- Ingesting too much HCO3-
- Compensation:
-- Dec. ventilation
-- Inc. excretion of HCO3-