Npb 101 Exam 3 Flashcards

Front 1

4 layers of dig. syst

Back 1

Mucosa, submucosa, muscularis externa, serosa

Front 2

layers of the mucosa

Back 2

mucous membrane - epithelial layer

Front 3

Four functions of dig syst

Back 3

Motility – Secretion – Digestion – Absorption

Front 4

Motility

Back 4

Two types propulsive and mixing

Front 5

Fat Digestion Yields

Back 5

Fatty acids and monoglycerides

Front 6

absorption

Back 6

Small units resulRng from digesRon, along with water, vitamins, and electrolytes are transferred from digesRve tract lumen into blood or lymph

Front 7

Bilary system

Back 7

Liver and gallbladder

Front 8

Mucosa

Back 8

Endocrine, exocrine, has GALT, and thin layer of sm muscle the muscularis mucosa
• Lines lumen of digestive tract • Highly folded surface greatly increases absorptive area • Three layers • Modified for secreRon and absorption • Contains – Exocrine gland cells – secrete digestive juices – Endocrine gland cells – secrete blood‐borne gastrointestinal hormones – Epithelial cells – specialized for absorbing digestive nutrients – Lamina propria • Houses gut‐associated lymphoid Rssue (GALT) – Important in defense against disease‐causing intesRnal bacteria – Muscularis mucosa • Sparse layer of smooth muscle

Front 9

Submucosa

Back 9

allows stretch, has submucosal plexus (nerves), has big lymph and BV.
• Thick layer of connective tissue • Provides digestive tract with distensibility and elasticity • Contains larger blood and lymph vessels • Contains nerve network known as submucosal plexus

Front 10

Muscularis Externa

Back 10

• Major smooth muscle coat of digesRve tube • In most areas consists of two layers – Circular layer • Inner layer • ContracRon decreases diameter of lumen – Longitudinal layer • Outer layer • ContracRon shortens the tube • ContracRle acRvity produces propulsive and mixing movements • Myenteric plexus – Lies between the two muscle layers

Front 11

serosa

Back 11

• Secretes serous fluid – Lubricates and prevents fricRon between digesRve organs and surrounding viscera • ConRnuous with mesentery throughout much of the tract – Acachment provides relaRve fixaRon – Supports digesRve organs in proper place while allowing them freedom for mixing and propulsive movements

Front 12

Digestive motility and secretion are regulated by

Back 12

Autonomous smooth muscle function – Intrinsic nerve plexuses – Extrinsic nerves – Gastrointestinal hormones

Front 13

short reflex pathway

Back 13

receptors in dig. tract - intrinsic nerve plexuses - sm. muscle, exocrine, endocrine

Front 14

long relex pathway of dig tract.

Back 14

external influences - extrinsic autonomic nerves - sm. muscle, exocrine, endocrine

Front 15

swallowing center in the brain

Back 15

Swallowing center inhabits respiratory center in brain stem

Front 16

gastric emptying process

Back 16

1) peristalsis starts in upper fundus and goes down 2) becomes stronger as it goes to thick antrum which pushes chyme forward 3) few mL pushed into duodenum (stronger pushes = more out) 4) when peristalsis reaches pyloric sphincter it closes tight and the chyme moving forward bounces off and tosed backwards mixing

Front 17

factors that control gastric emptying

Back 17

Amount of chyme in stomach is main factor in strength, in duodenum fat, acid and hypertonicity, and distension inhibit stomach emptying

Front 18

Three types of gastric exocrine secretory cells

Back 18

Mucous cells - Line gastric pits and entrance of glands Chief cells • Secrete pepsinogen – Parietal (oxyntic) cells secrete HCl and intrinsic factor

Front 19

Two distinct areas of gastric mucosa that secrete gastric juice

Back 19

Oxyntic mucosa • Lines body and fundus – Pyloric gland area (PGA) • Lines the antrum

Front 20

diagram stomach and the gastric pits and cell found in each area

Back 20

PGA - only G and D cells Oxyntic mucosa: surface epi., mucosa cells, chief cells, parietal cells, Enterochrmaffin-like cells

Front 21

Parietal Cell

Back 21

HCl Secretion activates pepsinogen to pepsin, breakdown of connective tissue and muscle fibers – Denatures protein – Along with salivary lysozyme, kills most of the microorganisms ingested with food

Front 22

Chief cells

Back 22

pepsinogin which is activated by H+ and can autocatayze

Front 23

Phases of Gastric Secretion

Back 23

cephalic, gastric and intestinal Cephalic phase – increased HCl and pepsinogen in response to stimuli in the head before food reaches stomach • Gastric phase – Begins when food actually reaches the stomach – protein increases gastric secretions • Intesnal phase – Inhibitory phase – Helps shut off flow of gastric juices as chyme begins to empty into small intestine

Front 24

Gastric Mucosal Barrier

Back 24

Enables stomach to contain acid without

Front 25

What digestion occurs in the stomach

Back 25

Carbs continue in the body, and protein dig, begins in antrum.

Front 26

Stomach absorption

Back 26

No food or water, but alcohol and asprin.

Front 27

Small IntesJne

Back 27

• Site where most digesJon and absorpJon take place • Three segments – Duodenum – Jejunum – Ileum • MoJlity includes – SegmentaJon – MigraJng moJlity complex

Front 28

segmentation

Back 28

– Primary method of moJlity in small intesJne

Front 29

What initiates segmentation of the sm int. and what is the rate

Back 29

pacemaker cells which produce BER. Look up the rate

Front 30

Migrating motility complex

Back 30

sweeps intestines clean between meals

Front 31

Control of ileocecal valve/sphincter

Back 31

gastrin relaxes it.

Front 32

Secretion by the sm int.

Back 32

Juice secreted do not contain any digestive enzymes – Synthesized enzymes act within brush‐border membrane of epithelial cells • Enterokinase • Disaccharidases • aminopeptidases

Front 33

What is happening in general with digestion in the small intestine?

Back 33

Pancreatic enzymes continue carbohydrate and protein – Brush‐border enzymes complete digestion of carbohydrates and protein – Fat is digested entirely within small intestine lumen by pancreatic lipase

Front 34

how much does the surface area increase due to folds and villi in the sm int

Back 34

600X

Front 35

general info about absorption in the small intestine

Back 35

absorbs almost everything presented to it – Most occurs in duodenum and jejunum – Adaptations that increase small intestine’s surface area • Inner surface has permanent circular folds • Microscopic finger‐like projections called villi • Brush border (microvilli) arise from luminal surface of epithelial cells – Lining is replaced about every three days – Products of fat digestion undergo transformations that enable them to be passively absorbed • Eventually enter lymph

Front 36

Where does fat digestion take place

Back 36

exclusively in the small intestine

Front 37

where are the villi

Back 37

on the surface of the rings in the sm int.

Front 38

what forms the brush border

Back 38

the microvilli on the epithelial cells of the sm int.

Front 39

Makeup of the villus

Back 39

epi cells, mucus cells, capillaries, and a central lacteal, provided blood by an arteriole and drained by and drains to a venule.

Front 40

lacteal

Back 40

lymphatic capillary that absorbs dietary fats in the villi of the small intestine.

Front 41

Pancreas

Back 41

Elongated gland located behind and below the

Front 42

Exocrine secretion by pancreas controlled by

Back 42

secretin and CCK.

Front 43

Proteolytic enzymes from the pancreas

Back 43

Trypinogen, Chymotrypsinogen, procarboxypeptidase

Front 44

carbolytic enzymes

Back 44

Pancreatic and salivary amylases – Converts polysaccharides into the disaccharide

Front 45

Cells of pancreas

Back 45

Duct cells - secrete aqueous NaHCO3, Acinar cells - secrete digestive enzymes Islets of Langerhans - make insulin, and glucagon

Front 46

Response to acid in duodenum

Back 46

duodenal mucosa (s cells in crypts) releases secretin into blood which stims pancreatic duct cells to secrete bicarb.

Front 47

Hormonal response to fat and protein in duodenum

Back 47

CCK released from mucosal epi. pancreatic acinar cells to secrete dig. enzymes

Front 48

Crypts of Lieberkuhn

Back 48

also house antimicrobial stuff like lysozyme.

Front 50

production and recycling of bicarb and H+

Back 50

Cl-, CO2 and water come in from blood into stomach parietal cells. CO2 and water with and Carbonic anhydrase makes bicarb and H+, bicarb leaves parietal cells to go back to the blood and ends up in pancreatic duct cell and is secreted with a Na+ into duodenum. They all react in the duodenum and NaCl and CO2 and H2O are made which are taken back up by the intestinal epithelial cells to be recycled

Front 51

Liver

Back 51

• Largest and most important metabolic organ in the body • Body’s major biochemical factory • Importance to digesMve system – secreMon of bile salts

Front 52

diagram liver blood flow

Back 52

Hepatic portal vein forms from small venules coming from dig syst. which then drains into the liver before going into primary circulation where it is purified. It also mixes with arterial blood that comes from hepatic artery. Reforms hepatic vein to go to the inferior vena cava.

Front 53

production of bile salts are done by what cells

Back 53

Hepatocytes produce the salts from cholesterol or recycled from salts in hepatic circulation. Builds up and is stored in gall bladder.

Front 54

Bile made up of

Back 54

• Bile salts • Cholesterol • Lecithin • Bilirubin

Front 55

Ways to break up fat globules for digestion

Back 55

Bile salts have negatively charged hydrophobic portion (carboxyl at end of glycine or taurine chain) and a lipid soluble part made from cholesterol. They adsorb on the exterior and segmentation breaks up droplets into smaller portions which the salts keep from sticking back together. End up about 1mm which is still too small for digestion. Micelle formation

Front 56

micelle formation

Back 56

Cholesterol and lecithin adds to droplet with bilesalts. Becomes about 10nm

Front 58

Digestion and absorption of carbs

Back 58

Amylase makes disaccharides, which are broken down into single monosaccharides through diff pathways done on brush border which also bring them into the cell. Galactose and glucose have a Na+ cotransport (sodium and energy dependent secondary active tranport). Fructose comes into cell through passive facilitated diffusion.

Front 59

protein and small peptide absorption and digestion

Back 59

pepsin in stomach then pancreatic enzymes in sm int. break down the protein. AAs absorbed by Na+and energy dependent absorption. AA transport out on the basal side due to high concentration inside into lumen of the villus which then diffuses into the capillary. Small peptides broken down by aminopeptidases on brush border or intracellular aminopeptidases

Front 60

Fat absorption and digestion

Back 60

large globs - bile salts chelest. and emulsify to micelles. - lipase turns triglyc. to monoglyc. and fatty acids on interior of micelles. Micelle hits epi surface, dumps monoglyc. and FFAs into cell. Then makes triglyc. from mono and FFAs. aggregagte and coated with lipoprotein to make chylomicron. - basal memb. exocyt. chylomicrons - go to lacteals and lymph.

Front 61

longitudinal fibers in L.int.

Back 61

tinae coli

Front 62

gastrocolic reflex - definition and what hormone causes it

Back 62

– Mediated from stomach to colon by gastrin and by autonomic nerves – Most evident after first meal of the day – Often followed by urge to defecate

Front 63

Mass movements

Back 63

massive movements that move stuff to end of L.int.

Front 64

Defecation reflex

Back 64

rectal stretch receptors stimmed by distension, internal anal sphincter relaxes, rectum and sigmoid colon to contract more. If external anal sphincter relaxed defecation occurs.

Front 65

Gastrointestinal Hormones

Back 65

Gastrin, CCK, GIP,

Front 66

Gastrin

Back 66

stimulated by protein in stomach, inhibited by acid in stomach. Increases HCl and pepsinogen secr. Ups gastric and ileal motility, relaxes ileocecal sphincter, induces mass movements in colon, • Helps maintain well‐developed, functionally viable digestive tract lining (mucosal lining of stomach and small intestine)

Front 67

Secretin

Back 67

Stims bicarb release by pan. duct cells, inhibits gastric emptying, stims bicarb rich bile release, Along with CCK, is trophic to exocrine pancreas

Front 68

CCK (Cholecystokinin)

Back 68

motility, panc enz. secretion, contract gallbladder, relax sphincter of Oddi,

– Functions • Inhibits gastric motility and secretion • Stimulates pancreatic acinar cells to increase secretion of pancreatic enzymes • Causes contraction of gallbladder and relaxation of sphincter of Oddi (sphincter for gallbladder duct) • Along with secretin, is trophic to exocrine pancreas • Implicated in long‐term adaptive changes in proportion of pancreatic enzymes in response to prolonged diet changes • Important regulator of food intake

Front 69

GIP

Back 69

Glucose dependent insulinotrophic peptide – Made in duodenum Stimulates insulin release by pancreas

Front 70

External work

Back 70

Energy expended when skeletal muscles are contracted to move external objects or to move body in relaNon to the environment

Front 71

Internal work

Back 71

All other forms of biological energy expenditure that do not accomplish mechanical work outside the body – Skeletal muscle acNvity used for purposes other than external work (postural maintenance contracNons, shivering) – All the energy‐expending acNviNes that go on conNnuously just to sustain life

Front 72

eating control centers in brain and effect of leptin on these centers

Back 72

2 regions in the hypothalamus in the arcuate nucleus: one for satiety which secretes melanocortins, one for appetite secretes neuropeptide Y to increase food intake. Leptin inhibits NP-Y and stims melanocortins

Front 73

ghrelin

Back 73

hunger hormone produced in the stomach regulated by feeding status stims NP-Y neurons

Front 74

Peptide YY3‐36

Back 74

signals satiety – Produced by small and large intestines – important mealtime terminator

Front 75

Lateral hypothalamus area (LHA)

Back 75

secretes orexins • Strong stimulators of food intake

Front 76

Hypothalamic Paraventricular nucleus (PVN) and eating

Back 76

Releases neuropepNdes that decrease food intake

Front 77

Parathyroid Hormone

Back 77

increases in plasma calcium through action at bone, GI Tract & kidney. • Requires Active Vitamin D for optimal affects.

Front 78

calcitonin

Back 78

no known effects from deficiencies Some of Parathyroid Hormone effects, less potent.

Front 79

Distribution Calcium in Body

Back 79

• Plasma – 8.6 – 10.6 mg/dl. 1000 mg total content in plasma. • If plasma concentration falls below 7 mg/dl  increase membrane excitability. Loss of selective permeability, and tetany in skeletal muscles • Bone - 1 x 10^6 mg or 1 kg 1. Soluble, rapidly mobilized Ca pool 2. Stable, slowly mobilized Ca pool

Front 80

Bone

Back 80

Collagen and Protein Matrix in which Calcium, Phosphate, and Hydroxide (Hydroxyapatite Crystals) deposited.

Front 81

Osteocyte

Back 81

osteoblast that is surrounded by formed bone. Cells no longer have the ability to lay down new bone.

Front 82

Osteoclast

Back 82

Bone Dismantling. Cells, which differentiate from macrophages, responsible for bone breakdown – release of Calcium and Phosphate from bone into blood.

Front 83

Balance between Osteoblast and Osteoclast activity

Back 83

determines if there is net bone Accresion or net Bone Dismantling,

Front 84

Greater Osteoblast Activity

Back 84

Decrease Plasma Ca & PO4 & Bone Formation (Accresion)

Front 85

Greater Osteoclast Activity (Dismantling)
cause and effect

Back 85

stimmed by PTH stimming OPGL and RANKL production by osteoblasts.
OPG inhibits.
Increase Plasma Ca & PO4.

Front 86

Sources of Vitamin D

Back 86

• Sunlight acting on Dihydrocholesterol  Precursor to Vit D  Inactive Vit D • Diet – fortified milk, cereals, etc.

Front 87

Formation of either Inactive or Active Vitamin D determined by hydroxylation where, and done where

Back 87

• Inactive Vitamin D – precursor hydoxylated at #1 & #24 positions • Active Vitamin D (Calcitriol) – precursor hydroxylated at #1 & #25 positions. • Conversion of Inactive Vit D to Calcitriol occurs in Kidney

Front 88

Calcitriol formed when

Back 88

• Ca and P04 plasma levels are low. • Parathyroid Hormone levels increase • Low levels of Calcitriol, stimulate conversion of Inactive Vit D to Calcitriol

Front 89

Actions of Active Vitamin D

Back 89

Net Effects: Increase both Plasma Ca and P04 from Bone, Increase Ca and PO4

Front 90

osteoblast signaling

Back 90

1. Bone Dismantling through Osteoprotegerin Ligand (OPGL) –directly binds to receptors on osteoclasts stimulating bone dismantling (increases alkaline phosphatase activity  stimulates breakdown of bone mineral) 2. Inhibition of Bone Dismantling by Osteoprotegerin (OPG) – binds to OPGL & prevents OPGL preventing OPGL stimulation of osteoclast activity. (Sex steriods, estrogen and testosterone, increase the synthesis and secretion of OPG by osteoblasts, reducing OPGL stimulation of osteoclasts. Therefore, sex steriods, shift balance in favor of bone accresion.)

Front 91

Ca homeostasis requires

Back 91

both Calcitriol and Parathyroid Hormone.

Front 92

Stimulus for PTH secretion

Back 92

decreasing Ca++ levels

Front 93

Effect in the drop of phosphate on PTH secretion

Back 93

does nothing

Front 94

Sites of Action: PTH

Back 94

Kidney, Intestine & Bone
• Kidney Inactive Vit D to Calcitriol, reabsorb Ca and decrease reabsorb PO4 • (Note: Mass action of decrease in plasma PO4 on soluble fraction of bone release of Ca and PO4 from bone.)
Intestine - absorb Ca & PO4 (Maximal absorption of ingested Ca and PO4 requires active Vit D)
Bone • Stimulates synthesize & release of RANKL (Receptor Activator of NF-kB ligand) & Osteoprotegrin (OPG) when • Ca low  increase RANKL over OPG. • Increase RANKL stimulate conversion of Macrophages  osteoclasts  bone dismantling over accresion  increase both plasma Ca and plasma PO4.

Front 95

Net Effect: PTH

Back 95

Increases Ca and PO4.Ca increases more than PO4 because of kidney

Front 96

Regulation of Plasma Phosphate

Back 96

• Parathyroid Hormone does not directly regulate Plasma PO4 • Plasma PO4 regulated through action of Calcitriol. • Stimulus: Decreases Plasma PO4  stimulate conversion of Inactive Vit D  Calcitriol. • Action Calcitriol on PO4: • Increases absorption of PO4 from GI Tract • Increases reabsorption of PO4 from Kidney • Stimulates Osteoclast activity  increase rate of bone dismantling  increase plasma PO4.

Front 97

Link between Neural & Endocrine Regulation

Back 97

link between Hypothalamus and Posterior Pituitary is Direct Neural. Posterior Pituitary contains nerve terminals of neurons originating in Hypothalamus

Front 98

Vascular Link between Hypothalamus and Anterior Pituitary

Back 98

via Hypothalamic Hypophyseal Portal System (HHPS)

Front 99

List pit hormones their effects and what stimulates them from the hypothalamus

Back 99

Growth Hormone (GH) or Somatotropin

Front 100

(ADH) or Vasopressin
cells and cause for stimulus
receptor types and each of their effects

Back 100

Stim for ADH secretion increase in osmol. by Receptors in supraoptic nucleus. 2. Decrease in circulating blood volume leads increase ADH secretion. inhibitory afferent input from volume (stretch) receptors at the junction of the pulmonary veins and left atrium to the supraoptic neurons (disinhibition by decreasing circulating blood volume). • Action – Stims insertion of (Aquaporins). Constricts afferent and efferent arterioles. Reduction vasa recta blood flow which conserves medullary gradient by reducing vascular removal of the kidney medullary osmotic gradient.

Front 101

Overview of Feedback Control of Hypothalamic Neurosecretion and Anterior Pituitary Hormone Secretion

Front 102

What causes the death of the corpus luteum

Back 102

PGF2alpha

Front 103

Gigantism

Back 103

Proportional Growth of Skeletal and Muscle Tissue

Front 104

Excess Growth Hormone Post Puberty

Back 104

Acromegaly – Growth of Soft Cartilaginous Tissue – Enlarged, Protruding Cheek Bones; Enlarged, Protruding Sternum and Ribs; Enlarged hands and Feet

Front 105

glycerol absorption

Back 105

too big to get through cell membranes

Front 106

Deficiency Growth Hormone Prior to Puberty

Back 106

Dwarfism – small body, poor muscle dev., subcut. fat because deficiency of Growth Hormone, or normal Growth Hormone but lack of Growth Hormone receptors, or normal Growth Hormone but low levels of IGF-1 (liver hormone that stims cell growth and inhibits apoptosis).

Front 107

African Pigmy

Back 107

Normal GH levels but lower than normal IGF-1 levels

Front 108

Thyroid Gland & Thyroid Hormones

Back 108

Permissive, regulates metabolism, enzymes and (oxid. phosphor.) PRL and GH need normal levels. Thyroxine ( T3 – Active Form; T4 – Inactive or Prohormone) 5/27/08 4 Broad Range of General Metabolic Effects • Permissive Action – Establishes metabolic conditions for synthesis and action other hormones. • Regulates Metabolism • Stimulates mitochondrial oxidative phosphorylation. Required for normal energy production. • Stimulates normal synthesis of enzymes and proteins. • Required Normal Growth and Development • Prolactin and Growth Hormone both require normal levels of T3. • Pre and postnatal neural development requires normal levels of T3. • Bone Growth

Front 109

T4

Back 109

Tetraiodothyronine – Inactive or Prohormone. 80% hormone produced & secreted by Thyroid Follicles is T4.

Front 110

T3

Back 110

Triiodothyronine – Active Hormone. 20% hormone produced & secreted by Thyroid Follicles is T3. • Inactive T4 converted to Active T3 in the Liver.

Front 111

Three Steps in the Synthesis of Thyroid Hormones

Back 111

1. Uptake of Iodine from the Blood by the Follicle Cells & conversion to iodine to iodide by peroxidase enzyme within Follicle Cells. 2. Iodination of tyrosine within thyroglobulin molecule - occurs within the Lumen of the Follicle. Iodination produces two products: • Monoiodotyrosine (MIT) & Diiodotyrosine (DIT). 3. Coupling within the Lumen of the Follicle of MIT + DIT  T3, and DIT + DIT T4

Front 112

Long Loop Negative Feedback of T3

Back 112

• T3 inhibits TSHRH by Neurosecretory Neurons in Hypothalamus • T3 inhibits the Synthesis and Secretion of TSH by Thyrotrophs in Anterior Pituitary

Front 113

Hypothyroidism

Back 113

lack of or low levels of T3.

Front 114

cretinism

Back 114

poor neurological development if low levels of T3 before and in first few years of life.

Front 115

adult hypothyroidism

Back 115

Myxedema in Adult + decrease contractility, decrease responsiveness to sympathetic activity , decrease ability to mobilize lipid stores + other effects

Front 116

Causes of Hypothyroidism

Back 116

no Iodine, inability to synthesize T3 & T4, no Negative Feedback on TSHRH & TSH secretions. TSH stimulates follicle hypertrophy get Goiter (Grossly enlarged Thyroid Gland producing mass in the front of the neck. Or no Receptors in the Follicles of the gland so won't respond to TSH. No negative feedback to Hyp. and Ant. Pit. by T3 High Levels of TSHRH & TSH but no Goiter. Also may lack TSHRH receptors in Ant, Pit. Thyrotrophs.

Front 117

How would you expect circulating levels of TSHRH and TSH to change in absence of TSHRH receptors?

Front 118

Hypersecretion of TSHRH, TSH or T3 –T4 Secreting Tumors

Back 118

Excess T3 – T4 is an emergency – increase sensitivity of norepi. and epi. leads to cardiac arrhythmias, very high BP, stroke.

Front 119

Hyperthyroidism

Back 119

Graves Disease - Immune system synth. of (TSI) Same affects as TSH but nofeedback which leads to const. stim. of T3 and T4 production. Question: What would you expect to happen to the levels of TSHRH and TSH in the presence of TSI? Would you expect a goiter?

Front 120

Exophthalmos

Back 120

protruding eyeballs (Fig. 19-5 textbook) as a consequence of high levels of TSI because of accumulation of mucopolysaccharide behind the eye. Edema around eyes. Lid retraction  drying of the cornea.

Front 121

Adrenal Cortex & Adrenal Steroid Hormones

Back 121

Mineralocorticoid is Aldosterone Glucocorticoid is Cortisol and Sex Steroids – Estrogen and Testosterone

Front 122

Mineralocorticoids

Back 122

Aldosterone (Synthesis and release stimulated by Angiotensin)

Front 123

Glucocorticoids

Back 123

Cortisol - • imp. for normal gluc. levels. Only hormone stim. synth. of new gluc. through the conversion of AA

Front 124

Dehydroepiandrosterone (DHEA)

Front 125

in males Adrenal cortex source of estrogens (cortex possesses enzyme to convert testosterone to estradiol. Testes very little of the enzyme)

Front 126

Females: Adrenal cortex source of testosterone (enzyme converts testosterone to estradiol much lower concentration (not as active) in adrenal cortex than in ovaries)

Front 128

Effects of insulin.

Back 128

Insertion of transport prot. called gluc 4 in muscle. absence of insulin gluc. absorb into skel. muscle is sig. impaired. Stims. conv. of gluc.to glyc. Stims adipocytes to produce glycerol from glucose to remake triglyc. from fatty acids.

Front 129

insulin stims adipocytes to produce glycerol from glucose to remake triglycerides from fatty acids.

Front 130

intracellular lipase (hormone sensetive lipase)

Back 130

Responds to glucagon to break up fat for energy

Front 131

ENDOCRINE 3

Front 132

Somatostatin GHIH

Back 132

stimmed by IGF-1

Front 133

Draw the feedback control loop on slide 2 of endo 3

Front 134

Excess Growth Hormone Prior Puberty & Prior to Closure of the Growth Plates in the Long Bones

Back 134

gigantism

Front 135

Excess Growth Hormone Post Puberty

Back 135

Acromegaly – Growth of Soft Cartilaginous Tissue – Enlarged, Protruding Cheek Bones; Enlarged, Protruding Sternum and Ribs; Enlarged hands and Feet (Fig. 18-14)

Front 136

Deficiency Growth Hormone Prior to Puberty

Back 136

Dwarfism – small body size, may have poor muscle development, subcutaneous fat – baby fat (pudgy). • occurs because of deficiency Growth Hormone, or normal Growth Hormone but lack of Growth Hormone receptors, or normal Growth Hormone but low leves of IGF-1.

Front 137

why is a pygmy small

Back 137

Normal GH levels but lower than normal IGF-1 levels

Front 138

Broad Range of General Metabolic Effects of thyroid hormone

Back 138

• Permissive Action – Establishes metabolic conditions for synthesis and action other hormones. • Regulates Metabolism • Stimulates mitochondrial oxidative phosphorylation. Required for normal energy production. • Stimulates normal synthesis of enzymes and proteins. • Required Normal Growth and Development • Prolactin and Growth Hormone both require normal levels of T3. • Pre and postnatal neural development requires normal levels of T3. • Bone Growth

Front 139

Three Steps in the Synthesis of Thyroid Hormones – T3 & T4

Back 139

1. Uptake of Iodine by the Follicle Cells & conversion to iodine to iodide by peroxidase . 2. Iodination of tyrosine within thyroglobulin - occurs within the Lumen of the Follicle. Iodination produces two products: • Monoiodotyrosine (MIT) & Diiodotyrosine (DIT). 3. Coupling within the Lumen of the Follicle of MIT + DIT  T3, and DIT + DIT T4

Front 140

Long Loop Negative Feedback of thyroid hormone. Which one and the process

Back 140

• T3 inhibits TSHRH by Neurosecretory Neurons in Hypothalamus • T3 inhibits the Synthesis and Secretion of TSH by Thyrotrophs in Anterior Pituitary

Front 141

Hypothyroidism in adult and children and affects.

Back 141

kids - Cretinism – poor neuro. dev.if low T3 in first few years of life.
Adult - Myxedema, decreased contract., decreased respons. to symp. activity, decrease mobilize lipid stores + other effects

Front 142

Cause of Hypothyroidism

Back 142

• Also may have lack of TSHRH receptors in Anterior Pituitary Thyrotrophs.

Front 143

Absence of Iodine in diet

Back 143

Cause of Hypothyroidism - can't make T3 & T4 no Negative Feedback on TSHRH & TSH  High TSHRH and TSH. • TSH stimulates follicle hypertrophy  Goiter

Front 144

Lack of Receptors in the Follicles of the Thryoid Gland

Back 144

Cause of Hypothyroidism - unresponsive to TSH  no neg. feedback to Hyp. and Ant. Pit. by T3. High TSHRH & TSH but No Goiter because no stim. of thyroid follicles.

Front 145

How would you expect circulating levels of TSHRH and TSH to change in absence of TSHRH receptors?

Front 146

Hypersecretion of TSHRH, TSH or T3 –T4 Secreting Tumors

Back 146

Large excess T3 – T4 is a major medical emergency – increase sensitivity of norepinephrine and epinephrine leads to fatal cardiac arrhythmias, very high blood pressure, stroke.

Front 147

Hyperthyroidism

Back 147

Immune system synthesis of Thyroid Stimulating Hormone Immunoglobulin (TSI) • Same affects as TSH but TSI not under feedback control leads to constant stimulation of Thyroid and T3 and T4 production.

Front 148

What would you expect to happen to the levels of TSHRH and TSH in the presence of TSI? Would you expect a goiter?

Front 149

Exophthalmos

Back 149

protruding eyeballs (Fig. 19-5 textbook) as a consequence of high levels of TSI because of accumulation of mucopolysaccharide behind the eye. Edema around eyes. Lid retraction  drying of the cornea.

Front 150

Inability Synthesize or Secrete Corticoids

Back 150

Addison’s Disease • no Aldosterone • Can't maintain NA+ H2O balance. inadequate volume regulation. • Reduced secretion H+ and K+. • Death from reduced capacity for Gluconeogenesis • can't get glucose under stress or when low. • reduced activity of Glucagon – mobilization of glucose dependent on glucocorticoids.

Front 151

Excess Cortisol

Back 151

Cushing’s Disease • Decrease fat in limbs but more in trunk and face – moon face. • Muscle and bone Wasting.

Front 152

Two Functions of the Gonads

Back 152

Gametogenic Function Endocrine Function

Front 153

Spermatogenesis

Back 153

Sertoli Cells in seminiferous tubules

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Sperm are stored

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in Epididymis, and early segments of the Vas Deferens.

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Cells of Leydig

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between the Sertoli cells in the wall of the seminiferous tubules. Leydig Cells synthesize and secrete Testosterone.

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Theca and Granulosa Cells

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in the wall of the Ovarian Follicle synthesize and secrete Estrogens and Progestins.

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Three Levels in Classification of Gender

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genetic, gonadal, and phenotypic • Genetic Sex – Presence of X or Y sex chromosome. • Gonadal Sex – Presence of Ovaries or Testes. • Genital Sex (Phenotypic Gender) – Presence of Female or Male External Reproductive Structures

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Maleness – Requires

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Y Chrom.& Functioning SRY Which controls dif. of gonads to testes. (codes for signaling molecule). Need X chromosome for full diff. (1)synth. testosterone; (2) T recept (3) enzymes to convert T to DHT (4) Mullarian Inhibiting Substance (MIS)

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Femaleness –

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When no Y chrom., or non-funct. SRY or absence of any coding for functional maleness

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hormones prepuberty

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everything low and constant

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Puberty Male

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GNRH –pulsatile throughout
FSH and LH puls. with FSH higher
Test. high and constant.

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Puberty Female

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GNRH –cycling monthly FSH & LH – cycling monthly with LH higher before ov.

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Changes in Secretion of CRH and ACTH

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increasedadrenal sex steroid secretions leads to increased hair growth in both males and females observed at onset of Puberty. Other secondary sex characteristics observed with onset of puberty produced by gonadal testosterone and estrogens.

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Change in Feedback Regulation of GNRH. FSH & LH Secretions, and Sex Steroid Secretions

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Pub. changes Sex Ster. Synth.and Secretion, and Dev. of Prim. and Sec. Sex Char. • Decrease responsiveness of GNRH, and FSH & LH to negative feedback from estrogens leads to increase GNRH, FSH and LH, Secr. • Change from constant, low GNRH secretion to pulsatile secr. in male and cyc. secr. in female. • Increase resp. of gonads to FSH and LH  increase T in males and E2 in females • Change to postpubertal higher & pulsatile testosterone secretion, & monthly cyclical changes in estrogens and progesterone secretions.

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Secondary male Sex Characteristics

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• Male Pattern Hair Growth • Bone Growth and Closure of the Growth Plates • Increase Protein Synthesis  Increase Muscle Mass • Decrease in Body Fat and Increase Lean Body Mass • Increase RBC Production – Male Hemoglobin and Hematocrit greater than Female. • Increase in VLDL and Decrease Synthesis LDL and HDL • Enlargement of Larynx and Thickening Vocal Cords  Deepening Voice

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Effects of Estrogen and Progesterone Synthesized and Secreted by Cells within the Ovaries

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Reproductive Structures • Breast Development including development of Ductile System • Enlargement of the Labia • Changes in Lining and Secretions of the Vagina Oogenesis – Formation of the Follicles, Initiates the 2nd meiotic division of the ova, and ovulation. Secondary Sex Characteristics • Stimulation of Hair Growth • Bone Growth and Earlier (compared to male) Closure Growth Plates • Promotes Female Distribution of Fat – subcutaneous fat storage. • Decreases Sensitivity of Tissues to Insulin – Diabetogenic Effect

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oogenesis

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completion of first meiotic division