GI + Reproductive Physiology Flashcards
What is the function of the mouth for GI physiology?
- taste
- chewing (mixing food with saliva –> decreases size + mixes carbs w/salivary amylase) - bolus formation
- salivary glands: amylase (initial starch digestion) + lingual lipase (intial triglyceride digestion)
What is the function of the esophagus?
- transport
- during swallowing (involuntary - medullary swalling center): soft palate elevates, epiglottis covers glottis, UE sphincter relaxes + food goes down)
What is the function of the stomach?
- storage
- grinding
- mixing
- digestion
- secretion (acid)
- acid environment (pH1-2) enables activation of pepsinogen to pepsin
What gets secreted in the stomach?
- Mucus cells: secrete mucus
- Chief cells: secrete pepsinogen (–> pepsin –> protein digestion)
- Parietal cells (secrete HCL, IF)
- ECL cells: secrete histamine
- G cells (secrete gastrin; gastric lipase)
What are the digestive functions of the liver?
- metabolism
- detoxification
- catabolism of ammonia to urea (whole cycle)
- heme –> bilirubin –> +albumin
- bile production + secretion
(bile functions in lipid digestion + excretion)
What is the digestive function of the gallbladder?
- bile storage
What does the exocrine pancreas do?
- digestion
- HCO3 buffer
What does the small intestine do?
- digestion + absorption (proteins to aas, carbs to monosacchs, fats to chylomicrons)
- duodenum: neutralizes gastric contents (HCO3 –> inactivates pepsin), absorbs iron, Ca, carbs, fats, proteins
- jejunum: net absorption of NaHCO3, also carbs, fats + prots
- ileum: net absoprtion of NaCl, Vit B12, also fats + proteins
What does the large intestine do?
- fluid + electrolyte absorption
- segmented propulsion
- ascending (absorption of water + ion)
- transverse (fermentation)
- descending (storage of waste + indigestible materials)
General GI Wall Structure
LUMEN (microvilli)
- mucosa: epithelium, bm, lamina propria, muscularis mucosa
- submucosa (innervated by nerves)
- muscularis propria: circular muscles, myenteric plexus (innervated by nerves), longitudinal muscle
- mesothelium (serosal surface)
SEROSA
How is surface area increased in the gut?
- folds (3x)
- LI: villi (30X), crypts
- SI: microvilli (600x)
How does the autonomic NS regulate GI fcn?
Intrinsic
- enteric NS in M + SP (can direct all GI fcn): input from PS/S nerves (modulates activity), mechano + chemorec
Extrinsic
- PS: excitatory, vagus + pelvic nerves (long pre + short post-ganglionic fibers) –> M + SP –> smooth muscle, secretory cells, endocrine cells of GI
- S: inhibitory, short pre + long post ganglionic fibers that go to M + SP or directly to bvs + smooth muscle cells
What is the hormonal regulation of the GI system?
- endocrine: Gastrin, GIP, Secretin
- neurocine: Ach, vasoactive intesting polypetide, CCK
- paracrine: prostaglandins
What does Gastrin do?
coordinates H+ secretion by parietal cells
What does Secretin do?
- secreted by S cells of duodenum
- stimulated by H+, FA in duod.
- increases pancreatic secretion of HCO3
What does GIP do?
aka glc-dependent insulotropic peptide
- secreted by K cells of duod + jej
- stimulated by all carbs, fats, + prots (only GI hormone that is)
- increases insulin secretion from pancreas
- decreases gastric H+ secretion
What does CCK do?
- secreted by I cells of duod + jej
- stimulated by aas + FAs
- increases pancreatic secretions
- stims GB to contract (bile release)
- relaxes sphincter of Oddi
- inhibits gastric empyting
What happens when you eat?
food in stomach –> increased acid secretion + motility –> food + acid in duod
–> CCK + secretin secretion –> pancreatic + biliary secretion –> intestinal digestion of foods
–> GIP secretion –> insulin secretion
How is saliva regulated?
- PS: Ach –> IPs, Ca –> increases saliva
- S: NE –> cAMP –> increases saliva
How is gastric acid secretion regulated?
- increased H+ secretion (when parietal cells open)
- -> vagus –> ACh –> IPs/Ca –> inc H+
–> G cells –> gastrin –> IP3/Ca –> inc H+
–> ECL cells –> histamine –> cAMP –> inc H+
*** decreased H+ secretion d/t GI cells (somatostatin –> dec cAMP) or gastric mucosa (–> prostaglandins –> dec cAMP)
What controls bile secretions?
controlled by gallbladder contraction:
- CCK stims GB contraction (ACh release)
- ACh causes NO/VIP release –> acts on Sphincter of Oddi
What’s the deal with carbs?
- only monosacchs are absorbed
- starch digestion d/t amylase (salivary glands/pancreas), sucrase, isomaltase (SI)
- glc actively absorbed with Na+ dependent transporter (luminal side) + GLUT2 (blood side)
What’s the deal with proteins?
- only aas + di/tripeptides absorbed
- prots broken down by exopeptidase, endopeptidase, enterokinase, trypsinogen
- H+/peptide cotransport + basolateral aa transporter
What’s the deal with lipids?
- digestion requires emulsification by bile salts –> form micelles (outside hydrophilic, inside hydrophobic_
- lingual + gastric lipases break into glycerol + FAs
- slow gastric emptying aids in lipid digestion (CCK slows in response to lipids + stims bile rls from GB)
- broken down to go into cell –> re-esterified in cell (chylomicrons)
How are fat-soluble vitamins absorbed?
- A, D, E, K
- turn into micelles w/fat –> incorporated into chylomicrons
How are water-soluble vitamins absorbed?
- Vit B12 (absorbed in ileum via IF)
- Na-dependent co-transport
How is iron absorbed?
- body content regulated by rate of intestinal absorption in duodenum
- delivered from heme or as ferric iron via GI lumen
- transported/stored bound to proteins
What is the SRY?
- sex-determining region of Y chromosome
- alters transcription for genes
- Anti-Mullerian Hormone (AMH - growth factor) prevents formation of mullarian ducts (via apoptosis)
How is gender differentiated?
Indifferentiated gonhad
–> + SRY –> testes –> Sertoli Cells (AMH) + Leydig Cells (testosterone) –> male genital tract + external genitalia
–> - SRY –> ovaries –> - AMH + - testosterone –> female genital tract + external genitalia
What are some sex chromosomal abnormalities?
- XO: gonadal dysgenesis/Turner’s –> no sexual maturation, female external genitalia + phenotype
- XXX: superfemale
- YO: not compatible with life (no X)
- XXY: Kleinfelters –> small testes, reduced fertility, gynecomastia, behavioral deficits (born male but w/2º female sex characteristics)
What happens from in utero exposure of XX fetus to androgens?
- female pseudohermaphroditism
- typically male gender identity
- hormonal, not chromosomal
What happens in androgen resistance of XY fetus?
- male pseudohermaphroditism
- testicular feminization
- typically female gender identity
- congenital 5alpha-hydroxylase deficiency; congenital adrenal hyperplasia
What causes hypogonadism?
- impaired gonadotropin secretion –> decreased testosterone
- loss of T before puberty –> feminine characteristics, gynecomastia
- loss of T after puberty –> loss of libido
What form of testosterone may be used in the body?
- must be converted to estradiol via aromatase
- only free T is active
- most is bound in circulation to sex hormone binding globulin or ABP (androgen binding protein) in testes
- testosterone levels remain low until activation by pituitary gonadotropins in puberty
- testosterone stims sertoli cells to release inhibins (inh pituitary FSH biosyn + rls)
- inhibits GnRH release (after conversion to estradiol) + LH biosynthesis + release
What is GnRH? (in men)
- gonadotropin releasing hormone
- definition of puberty
- release is stimulated by NE, neuropeptide Y, leptin
- inhibited by melatonin, IL-1, DA, GABA, testosterone
- puberty initiated by pulsatile secretions of GnRH
What is LH? (in men)
stimulates T synthesis + release from Leydig cells in response to GnRH from hypothalamus)
What is FSH? (in men)
stimulates release of Androgen Binding Protein + inhibin from Sertoli Cells
What is inhibin?
inhibits pituitary production + release of FSH (made by Sertoli Cells)
What is Activin?
enhance RSH synthesis + secretion by blocking inhibin
inhibits inhibins har har har
Where is DHEA synthesized?
adrenal glands
Where is Androstenedione synthesized?
adrenal glands, gonads
Where is testosterone synthesized?
Leydig cells/testes
What are the three functions of testosterone and how are they carried out?
- Activates androgen receptor (internal genitalia, skeletal muscle, erythropoiesis)
- Conversion to DHT via 5alpha-reductase (external genitalia, hair, prostate growth)
- Conversion to estradiol (actual T effects): bone, libido
What is 17 hydroxysteroid DH?
key enzyme (last step) of testosterone synthesis
What is 5alpha-reductase?
- converts T to DHT (more potent androgen than T)
What is aromatase?
- converts T into estradiol (mostly produced in fat)
- -> estradiol mediates brain feedback on GnRH production + plays a role in epiphyseal closure/bone strength (if unresponsive to estradiol –> continued bone growth, osteoporosis)
What are the anabolic effects of androgens?
- increased protein synthesis
- block cortisol actions in breaking down proteins
- retention of Na, K, H2O, Ca, SO4, PO4
- increased kidney size
***cannot separate androgenic (virilizing) effects from anabolic effects
What are some of the bad effects of synthetic androgen abuse?
- gynecomastia
- liver damage (cholestasis, hepatitis, hepatic cysts)
- hepatocellular cancer
- suppression of gonadal fcn
- decreased T, sperm production, testicular size
- prostatic hyperplasia
- behavioral effects (dependence, aggressiveness)
What happens to male sexual characteristics with age?
- decreased testosterone (40yo)
- decreased sperm production (50yo)
- increased SHBG
- decreased E, libido, erectile capacity, muscle mess, cognitive fcn….AND SO MUCH MORE
What are the stages in ovarian follicle development?
1st stage: primordial follicle develops into a primary follicle (occurs w/conversion of oogonia to primary oocytes) –> arrested at this stage until puberty
2nd stage: takes place over 70-85d; only occurs during reproductive period (oocytes grow + mature)
3rd stage: one follicle becomes dominant (ova) over other follicles (15/28th day –> ovulation –> dominant follicle ruptures –> rls oocyte into peritoneal cavity)
What’s the deal with oogenesis?
- primordial germ cells (mitotic division until gestational wk 20-24)
- primary oocytes: completed 6m after birth
- oocytes decrease with age until menopause (all gone)
What is the corpus luteum?
- formed by residual elements of ruptured follicle
- if fertilization occurs –> continues hormone secretion until placenta takes over
- if fertilization doesn’t occur –> regresses during next 14d –> corpus albicans scar
What are theca cells?
- in the ovary
- synthesize + secrete progresterone
- express 17ß hydroxysteroid DH
- synthesize + secrete testosterone
What are granulosa cells?
- express aromatase
- convert T to estradiol
What does GnRH do in women?
- intermittent, pulsatile release important to follicular phase (frequent, small pulses; estrogen increases frequency) and luteal phase (larger, less freq pulses; progesterone decreases frequency)
- leads to synthesis + rls of LH and FSH
What does FSH do in women?
- stimulates growth of developing follicles
- induces expression of LH receptors on theca + granulosa cells
- regulates activity of aromatase (stims estradiol prdcn)
What does LH do in women?
- acts on theca cells to stim synthesis of androstenedione + T
- required for rupture of dominant follicle
- induces expression of FSH receptor on granulosa cells
What are the three stages of the menstrual cycle?
- follicular phase: build-up of endometrium tissue (dominant hormone is estrogen)
- ovulation: estradiol levels rise sharply (LH dominant)
- luteal phase: endometrium fully developed to receive fertilized embryo (progesterone dominant)
What’s so great about estrogen?
- maturation + maintenance of uterus, fallopian tubes, cervix, and vagina
- puberty (2º sex characteristics)
- blocks prolactin in breast/inh milk production
- maintenance of bone mast (decrease osteoclasts a lot, increase osteoblasts a little)
- proliferation of granulosa cells
- neg + pos feedback regulation of FSH + LH
What’s so great about progesterone?
- maintenance of secretory activity of uterus during luteal phase
- neg feedback of FSH + LH
- important for maintenance of pregnancy
- stimulates transient breast epithelial proliferation
- increases body temp
What’s the deal with estrogen receptors?
There are two:
- ER alpha (reproductive tract, lung, brain, vasculature) and beta (prostate, ovaries)
- products of separate genes but have 44% of the same aas
- shape determines function (bindings changes shape –> allows for dimerization –> attracts other proteins –> gets shit done)
What changes occur during puberty in females?
- it’s the only period in your life you want to shop at abercrombie and fitch (dark times)
- first sign: breast budding (estrogen), then pubic hair
- menarche (many of 1st cycles are anovulatory)
What changes occur during menopause?
- preceded by anovulatory cycles (decrease number of functioning follicles)
- estrogen levels decrease
- LH, FSH increase
- thinning of vaginal epithelium + decrease in vaginal secretions
- increased bone loss
- decreased breast mass
- vascular instability (hot flashes)
When does fertilization occur?
- w/in 24 hours of ovulation
- ovum begin to divide
When does implantation occur?
- after 5 days
- stuff happens
- meh
What hormones are involved in parturition?
- bunches
- physical: distension increases contractility
- estrogen/progresterone ration increases –> increase uterine sensitivity to contractile stimuli
- prostaglandins increase uterine contractility + softening/thinning of cervix
- oxytocin can stimulate uterine contraction + distension of cervix
What roles do estrogen + progesterone play during pregnancy + lactation?
- both: stimulate G&D of breast, block action of prolactin
–> at birth, decrease E/P levels –> relieve inhibition of prolactin on breasts
What role does oxytocin have on lactation?
- suckling stimulates oxytocin release –> contraction of myoepithelial cells –> milk ejection
What role does prolactin have on lactation?
- stimulated by sucking, TRH
- prolactin at higher levels (lactation) inhibits GnRH release –> decreased fertility while breastfeeding
