Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology Exam III > GI + Reproductive Physiology > Flashcards

GI + Reproductive Physiology Flashcards

1
Q

What is the function of the mouth for GI physiology?

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the function of the esophagus?

A
  • transport
  • during swallowing (involuntary - medullary swalling center): soft palate elevates, epiglottis covers glottis, UE sphincter relaxes + food goes down)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the function of the stomach?

A
  • storage
  • grinding
  • mixing
  • digestion
  • secretion (acid)
  • acid environment (pH1-2) enables activation of pepsinogen to pepsin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What gets secreted in the stomach?

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the digestive functions of the liver?

A
  • metabolism
  • detoxification
  • catabolism of ammonia to urea (whole cycle)
  • heme –> bilirubin –> +albumin
  • bile production + secretion
    (bile functions in lipid digestion + excretion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the digestive function of the gallbladder?

A
  • bile storage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does the exocrine pancreas do?

A
  • digestion

- HCO3 buffer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does the small intestine do?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the large intestine do?

A
  • fluid + electrolyte absorption
  • segmented propulsion
  • ascending (absorption of water + ion)
  • transverse (fermentation)
  • descending (storage of waste + indigestible materials)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

General GI Wall Structure

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is surface area increased in the gut?

A
  • folds (3x)
  • LI: villi (30X), crypts
  • SI: microvilli (600x)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does the autonomic NS regulate GI fcn?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the hormonal regulation of the GI system?

A
  • endocrine: Gastrin, GIP, Secretin
  • neurocine: Ach, vasoactive intesting polypetide, CCK
  • paracrine: prostaglandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does Gastrin do?

A

coordinates H+ secretion by parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does Secretin do?

A
  • secreted by S cells of duodenum
  • stimulated by H+, FA in duod.
  • increases pancreatic secretion of HCO3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does GIP do?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does CCK do?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What happens when you eat?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is saliva regulated?

A
  • PS: Ach –> IPs, Ca –> increases saliva

- S: NE –> cAMP –> increases saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is gastric acid secretion regulated?

A
  • 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What controls bile secretions?

A

controlled by gallbladder contraction:

  • CCK stims GB contraction (ACh release)
  • ACh causes NO/VIP release –> acts on Sphincter of Oddi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What’s the deal with carbs?

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What’s the deal with proteins?

A
  • only aas + di/tripeptides absorbed
  • prots broken down by exopeptidase, endopeptidase, enterokinase, trypsinogen
  • H+/peptide cotransport + basolateral aa transporter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What’s the deal with lipids?

A
  • 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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How are fat-soluble vitamins absorbed?

A
  • A, D, E, K

- turn into micelles w/fat –> incorporated into chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How are water-soluble vitamins absorbed?

A
  • Vit B12 (absorbed in ileum via IF)

- Na-dependent co-transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How is iron absorbed?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the SRY?

A
  • sex-determining region of Y chromosome
  • alters transcription for genes
  • Anti-Mullerian Hormone (AMH - growth factor) prevents formation of mullarian ducts (via apoptosis)
29
Q

How is gender differentiated?

A

Indifferentiated gonhad

–> + SRY –> testes –> Sertoli Cells (AMH) + Leydig Cells (testosterone) –> male genital tract + external genitalia

–> - SRY –> ovaries –> - AMH + - testosterone –> female genital tract + external genitalia

30
Q

What are some sex chromosomal abnormalities?

A
  • 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)
31
Q

What happens from in utero exposure of XX fetus to androgens?

A
  • female pseudohermaphroditism
  • typically male gender identity
  • hormonal, not chromosomal
32
Q

What happens in androgen resistance of XY fetus?

A
  • male pseudohermaphroditism
  • testicular feminization
  • typically female gender identity
  • congenital 5alpha-hydroxylase deficiency; congenital adrenal hyperplasia
33
Q

What causes hypogonadism?

A
  • impaired gonadotropin secretion –> decreased testosterone
  • loss of T before puberty –> feminine characteristics, gynecomastia
  • loss of T after puberty –> loss of libido
34
Q

What form of testosterone may be used in the body?

A
  • 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
35
Q

What is GnRH? (in men)

A
  • 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
36
Q

What is LH? (in men)

A

stimulates T synthesis + release from Leydig cells in response to GnRH from hypothalamus)

37
Q

What is FSH? (in men)

A

stimulates release of Androgen Binding Protein + inhibin from Sertoli Cells

38
Q

What is inhibin?

A

inhibits pituitary production + release of FSH (made by Sertoli Cells)

39
Q

What is Activin?

A

enhance RSH synthesis + secretion by blocking inhibin

inhibits inhibins har har har

40
Q

Where is DHEA synthesized?

A

adrenal glands

41
Q

Where is Androstenedione synthesized?

A

adrenal glands, gonads

42
Q

Where is testosterone synthesized?

A

Leydig cells/testes

43
Q

What are the three functions of testosterone and how are they carried out?

A
  • 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
44
Q

What is 17 hydroxysteroid DH?

A

key enzyme (last step) of testosterone synthesis

45
Q

What is 5alpha-reductase?

A
  • converts T to DHT (more potent androgen than T)
46
Q

What is aromatase?

A
  • 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)
47
Q

What are the anabolic effects of androgens?

A
  • 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

48
Q

What are some of the bad effects of synthetic androgen abuse?

A
  • 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)
49
Q

What happens to male sexual characteristics with age?

A
  • decreased testosterone (40yo)
  • decreased sperm production (50yo)
  • increased SHBG
  • decreased E, libido, erectile capacity, muscle mess, cognitive fcn….AND SO MUCH MORE
50
Q

What are the stages in ovarian follicle development?

A

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)

51
Q

What’s the deal with oogenesis?

A
  • primordial germ cells (mitotic division until gestational wk 20-24)
  • primary oocytes: completed 6m after birth
  • oocytes decrease with age until menopause (all gone)
52
Q

What is the corpus luteum?

A
  • 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
53
Q

What are theca cells?

A
  • in the ovary
  • synthesize + secrete progresterone
  • express 17ß hydroxysteroid DH
  • synthesize + secrete testosterone
54
Q

What are granulosa cells?

A
  • express aromatase

- convert T to estradiol

55
Q

What does GnRH do in women?

A
  • 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
56
Q

What does FSH do in women?

A
  • stimulates growth of developing follicles
  • induces expression of LH receptors on theca + granulosa cells
  • regulates activity of aromatase (stims estradiol prdcn)
57
Q

What does LH do in women?

A
  • acts on theca cells to stim synthesis of androstenedione + T
  • required for rupture of dominant follicle
  • induces expression of FSH receptor on granulosa cells
58
Q

What are the three stages of the menstrual cycle?

A
  • 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)
59
Q

What’s so great about estrogen?

A
  • 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
60
Q

What’s so great about progesterone?

A
  • 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
61
Q

What’s the deal with estrogen receptors?

A

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)
62
Q

What changes occur during puberty in females?

A
  • 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)
63
Q

What changes occur during menopause?

A
  • 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)
64
Q

When does fertilization occur?

A
  • w/in 24 hours of ovulation

- ovum begin to divide

65
Q

When does implantation occur?

A
  • after 5 days
  • stuff happens
  • meh
66
Q

What hormones are involved in parturition?

A
  • 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
67
Q

What roles do estrogen + progesterone play during pregnancy + lactation?

A
  • both: stimulate G&D of breast, block action of prolactin

–> at birth, decrease E/P levels –> relieve inhibition of prolactin on breasts

68
Q

What role does oxytocin have on lactation?

A
  • suckling stimulates oxytocin release –> contraction of myoepithelial cells –> milk ejection
69
Q

What role does prolactin have on lactation?

A
  • stimulated by sucking, TRH

- prolactin at higher levels (lactation) inhibits GnRH release –> decreased fertility while breastfeeding

Physiology Exam III (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions