1
Q
Gastric glands
A
at the base of the gastric pits, contain endocrine cells that secrete hormones and exocrine cells that secrete an acidic, enzyme containing fluid called gastric juice
2
Q
mucous neck cells
A
Secrete acidic mucus
3
Q
parietal cells
A
Secrete hydrochloric acid (HCl)
Produce intrinsic factor - required for absorption of vitamin B12
Pepsinogen - enzyme that HCl activates
4
Q
chief cells
A
Secrete inactive pepsinogen
When it encounters an acidic environment (HCl) it activates into the enzyme pepsin (begins protein digestion)
5
Q
DNES cells
A
Endocrine cells
G cells - secrete hormone gastrin - gastrin stimulates the parietal cells to secrete HCl
6
Q
3 phases of acid secretion in the stomach
A
- cephalic phase
- gastric phase
- intestinal phase
7
Q
cephalic phase
A
Mediated by sight, smell, taste, thought of food
Prepares the stomach to receive food by increasing the release of hydrogen ions into it
These stimuli trigger the vagus nerve and result in 4 effects
- Direct stimulation of H+ release (from parietal cells)
- Stimulation of gastric secretion (from G cells)
- Stimulation of histamine secretion (from DNES cells)
- Inhibition of somatostatin secretion (from DNES cells)
- Somatostatin inhibits acid secretion (inhibit the inhibiter)
8
Q
gastric phase
A
- Begins when food enters the stomach and continues the stimulation from the cephalic phase
- Two stimuli trigger acid secretion
- Presence of food in the stomach → distension of the stomach wall → stimulates the ENS and vagus nerve (same effects as above)
- Presence of partially digested proteins stimulate G cells to produce and secrete gastrin → stimulates acid secretion → which activates pepsin → catalyzing protein digestion (positive feedback loop)
9
Q
intestinal phase
A
- Triggered by the presence of partially digested proteins in the fluid entering the duodenum
- Partially digested proteins trigger duodenal DNES cells (G cells) to release intestinal gastrin
- Enterogastric reflex - as chyme enters the duodenum, the declining pH and presence of lipids trigger this which decreases vagal activity and acid secretion
- Low pH of the duodenum also triggers the production of secretin and gastric inhibitory peptide (both hormones reduce acid secretion)
10
Q
3 types of folds in intestines
A
- circular folds
- intestinal villi
- microvilli
11
Q
migrating motor complex
A
- during fasting, the small intestine, exhibits slow rhythmic contractions along its length
- These contractions clear any remaining material
- Takes about 2 hours for digesting food to get from ileocecal valve
- Controlled by ENS and motilin (produced by cells of duodenal mucosa)
12
Q
bacteria in the large intestines
A
Produce vitamins (K & B)
Metabolize undigested materials (eg. soluble fibers → byproduct = flatus)
Deter the growth of harmful bacteria/pathogens
Stimulate the immune system
Induce immune tolerance body’s own antigens
Stimulate production of MALT and antibodies
13
Q
Cholecystokinin (CCK)
A
- a hormonal mediator of pancreatic secretion
- produced by duodenal DNES cells in response to the presence of lipids and partially digested proteins in the duodenum
- It acts on acinar cells to trigger the secretion of digestive enzymes and other proteins
14
Q
secretin
A
Released by duodenal cells in response to acids and lipids in the duodenum. Primarily triggers duct cells to secrete bicarbonate ions
15
Q
Porta Hepatis
A
Indentation where numerous blood vessels enter and exit the liver (including the hepatic artery, hepatic portal vein) also nerves, lymphatic vessels, and common hepatic duct
16
Q
The Gallbladder and Its Relationship to the Liver
A
- Gallbladder stores bile, concentrates it (removes water), and releases it when stimulated
- Secretin triggers bile production and release from hepatocytes
- CCK triggers contraction of gallbladder
- This causes the gallbladder to release bile into the cystic duct
- Cystic duct + common hepatic duct = common bile duct
- Common bile duct + main pancreatic duct = hepatopancreatic ampulla
17
Q
Digestion and Absorption of Carbohydrates
A
1) Polysaccharides are broken into oligosaccharides and disaccharides in reactions catalyzed by pancreatic amylase
2) Brush border enzymes (lactase, maltase, and sucrase) catalyze the breakdown of disaccharides into monosaccharides
3) The Na+/K+ pump creates a gradient for Na+ absorption from the fluid in the lumen
4) This gradient drives the secondary active transport of glucose and galactose via the Na+/glucose cotransporter
5) Fructose is absorbed by facilitated diffusion
6) All 3 monosaccharides cross the basal side of the enterocyte membrane and then diffuse into the blood
18
Q
digestion and absorption of proteins
A
1) Oligopeptides are broken down into free amino acids in reactions catalyzed by pancreatic and brush border enzymes
2) The Na+/K+ pump creates a Na+ gradient
3) This gradient drives the secondary active transport of certain amino acids into the enterocyte
4) Amino acids cross the basal enterocyte membrane by facilitated diffusion and enter the blood
19
Q
digestion and absorption of lipids
A
1) Lipids are broken apart by the stomach churning and broken down in reactions catalyzed by gastric lipase
2) Lipids enter the small intestine and are emulsified by bile salts
3) Pancreatic lipase catalyzes reactions that digest the lipids into free fatty acids and monoglycerides
4) Bile salts remain associated with the digested lipids to form micelles
20
Q
lipid absorption
A
1) Micelles escort lipids to the enterocyte plasma membrane
2) Lipids diffuse through the phospholipid bilayer and enter the cytosol
3) Lipids are reassembled into triglycerides and packaged into chylomicrons
4) Chylomicrons are released into the interstitial fluid by exocytosis and then enter a lacteal
21
Q
absorption of vitamins
A
Water soluble vitamins - polar
- Absorbed by small intestine dy diffusing through enterocytes plasma membranes
- Vitamin B12 - must bind to intrinsic factor to be absorbed in the ileum
- vitamin B & C
Fat soluble vitamins - non polar/lipid based
- Packaged into micelles with fats and lipids and are absorbed with them
- vitamin A, D, E, K
22
Q
nutrient pool
A
anabolic activities require amino acids, some lipids, and few carbohydrates
Catabolic reactions break down carbohydrates first, then lipids, and rarely amino acids
23
Q
glucose catabolism, 2 main stages
A
glycolysis
citric acid cycle
24
Q
glycolysis
A
- series of reactions in the cytosol that split glucose
- Energy investment phase: requires “spending” of 2 ATP for every 6 carbon glucose, producing two 3 carbon glucose sugars (pyruvate)
- Energy payoff phase: phosphate groups of the 3 carbon sugars are transferred to ADP to produce ATP (net total of 2), and the compounds are oxidized to produce NADH
- Net gain: 2 ATP & 2 NADH
25
citric acid cycle
- series of reactions in the mitochondrial matrix that breaks down glucose further
- Starts and ends with the same compound, oxaloacetate
- Overall yield per glucose molecule
- 10 NADH (2 from glycolysis, 2 from pyruvate oxidation, 6 from citric acid cycle)
- 2 FADH2
- 4 ATP (2 from glycolysis, 2 from citric acid cycle)
26
oxidative phosphorylation
occurs after glycolysis and citric acid cycle. series of oxidation-reduction reactions that use the energy released by glucose catabolism. Involves the transfer of electrons between electron carriers known as the electron transport chain (ETC)
1) Transfer of electrons between electron carriers
2) Generation and maintenance of a hydrogen ion concentration gradient
3) Use of the steep electrochemical gradient to drive the release of ATP
- produces 34 ATP
27
substrate level phosphorylation
involves the transfer of a phosphate group directly from the phosphate containing chemical (substrate) to ADP to form ATP
28
how many ATP can 1 glucose molecule yield
38 ATP
29
fatty acid catabolism
- 3 fatty acid + glycerol
- glycerol goes to glycolysis then citric acid cycle
- fatty acids oxidized through beta oxidation
- produces:
- FADH2 → ETC
- NADH → ETC
- Acetyl-CoA → citric acid cycle
Oxidation of fats releases twice as much energy as carbohydrates or proteins
30
amino acid catabolism
- Amino acid = “carbon skeleton” + nitrogen-containing amino group
- Amino group removed via transamination → carbon skeleton + glutamate
- Carbon skeleton → undergo oxidation via glycolysis or citric acid cycle
- Glutamate undergoes oxidative deamination → ammonia (NH3)
31
vitamin B1
coenzyme in many catabolic pathways
32
vitamin B9 (folic acid)
coenzyme in many metabolic pathways
| deficient during pregnancy
33
Very low density lipoproteins (VLDL)
bad
Contain a higher % of lipids than protein
Deliver triglycerides to adipose tissue for storage, and muscle tissue for immediate use
Lipids are removed from VLDL particles via reactions that convert them into free fatty acids and monoglycerides
Free fatty acids and monoglycerides diffuse into cells where they are either oxidized for fuel or reassembled into triglycerides
34
Low density lipoproteins (LDL)
bad
After VLDL’s unload triglycerides, they have a slightly higher density of protein
Main way cholesterol is delivered to peripheral tissue cells
35
High density lipoprotein (HDL)
good
Synthesized by the liver and released into circulation or the small intestine
Transfer lipids from the cells in peripheral tissues to the liver
In the liver, cholesterol is taken up by hepatocytes and excreted from the body in bile
36
blood supply to kidneys
Renal artery → segmental artery → interlobar artery → arcuate artery → interlobular (cortical radiate) artery → afferent arteriole → glomerulus → efferent arteriole → peritubular capillaries
37
macula densa
- Macula densa - tightly packed group of cells at the transition point between the ascending limb of the nephron loop and the distal tubule
- The macula densa comes into contact with with modified smooth muscle cells in the afferent and efferent arterioles, known as juxtaglomerular (JG) cells
38
Juxtaglomerular apparatus (JGA)
macula densa and JG cells together form a structure that regulates blood pressure and the glomerular filtration rate
39
collecting system
- cortical collecting duct
- medullary collecting system
- medullary collecting duct
- papillary duct
40
capsular hydrostatic pressure
- The fluid in the capsular space can only drain into the renal tubule so quickly
- Filtrate will accumulate inside the capsular space of a nephron which builds up its own hydrostatic pressure
- About 10 mm Hg
- Opposes filtration and tries to push water into the glomerular capillaries
41
autoregulation of GFR
Myogenic mechanism
| Tubuloglomerular feedback
42
myogenic mechanism
- An increase in systemic blood pressure stretches the afferent arteriole and leads to an increase in GFR → this causes muscles cells to contract, constricting the arteriole → decreases blood flow through the glomerulus (turns down the faucet) → decreases GHP and GFR back to normal
- A decrease in systemic blood pressure causes the afferent arteriole to be less stretched → decreases the GFR → smooth muscle cells relax → dilation of the arteriole → increases blood flow → increases GHP (turns up the faucet) → GFR increases back to normal
43
tubuloglomerular feedback
1) If the GFR increases, the volume of filtrate flowing through the renal tubule increases
2) The increased filtrate volume leads to an increased delivery of sodium and chloride ions to the macula densa cells in the distal tubule causing them to absorb more of these ions from the filtrate
3) The macula densa cells release ATP into the interstitial fluid. Some ATP is converted to the nucleoside adenosine, which leads to constriction of the afferent arteriole
4) The GFR decreases back toward normal range
- Increased ion delivery and absorption (due to increased GFR) leads to release of ATP which gets converted to adenosine, triggering afferent arteriole constriction, decreasing the GFR back to normal range
- Decreased ion delivery and absorption (due to decreased GFR) triggers dilation of afferent arteriole, increasing the GFR back to normal
44
RAAS
- can be triggered by 1) Stimulation from neurons of the sympathetic nervous system 2) low blood pressure 3) Stimulation from the macula densa cells in response to low sodium and chloride ion concentration in the filtrate
1) Systemic blood pressure decreases, causing a decrease in GFR
2) JG cells release renin
3) Renin converts angiotensinogen to angiotensin-I
4) ACE converts angiotensin-I to the active angiotensin-II
5) Effects of angiotensin-II
- Promotes vasoconstriction of efferent arterioles
- Promotes vasoconstriction of systemic blood vessels
- Promotes reabsorption of sodium and chloride ions from the proximal tubule and water follows
- Promotes aldosterone secretion, leading to increased sodium ion and water reabsorption (from distal tubule)
- Stimulates thirst → increased fluid intake
Compex system with a primary function of maintaining systemic blood pressure; it preserves the GFR as a secondary effect
45
ANP - kidneys
- dilates afferent arteriole and constricts efferent arteriole (increases GFR)
- inhibits release of ADH and aldosterone
46
components of countercurrent mechanism
- countercurrent multiplier
- urea recycling
- countercurrent exchanger
47
body water gains
- metabolic water = 250mL/day
- food = 750mL/day
- liquids = 1500mL/day
48
electrolyte normal ranges
```
Sodium (135-145 mmol/L)
Potassium (3.5-5 mmol/L)
Calcium (2.1-2.5 mmol/L)
Phosphate (1-1.5 mmol/L)
Chloride (96-106 mmol/L)
Magnesium (0.65-1.05 mmol/L)
```
49
hyponatremia
Can lead to problems with electrophysiology (reduces the Na+ gradient → slows depolarization → slows action potential generation)
50
hyperkalemia
- Alters the resting membrane potential (cell retains more K+ cause there is more in the ECF so less leak out cause no gradient exists)
- Resting membrane potential becomes more positive than normal (it is slightly depolarized at rest)
- An action potential is more easily generated and cells are more excitable
- With severe hyperkalemia → the cells can become so depolarized at rest that they are no longer excitable → this shuts down all excitable cells (including neurons and muscle cells) → can result in instantaneous death
51
hypokalemia
Makes the resting membrane potential more negative (cells are hyperpolarized)
Cells become difficult to stimulate → leads to muscle weakness, mental status changes, slowed heart rate
52
hypercalcemia
- Elevated Ca+ concentration in the ECF makes neurons less permeable to Na+ → diminishes the neurons ability to depolarize → decrease neuron activity → mental sluggishness, reduced reflex activity, weak muscle activity
- Ca+ are responsible for the plateau phase of cardiac action potentials → when there is to much Ca+ the plateau phase is shortened → makes contractions shorter and weaker → decreased cardiac output
- Digestive system - decreased activity of GI smooth muscle → constipation, decreased appetite
53
hypocalcemia
Neurons become hyperexcitable
When hypocalcemia is severe neurons begin firing spontaneously
Repetitive stimulation of skeletal muscles → carpopedal spasm
54
pampiniform venous plexus
- Pampiniform venous plexus - network of veins that drains blood from the testes into the testicular veins
- Right side = gonadal veins drain directly into inferior vena cava
- Left side = gonadal veins drain into the renal veins
55
Crura
- at the base of the penis the two corpora cavernosa split to form the two crura of the penis that attach to the ischial rami
- The bulb sits between the 2 crura (together these make up the root of the penis and connect it to the pelvic bones)
56
seminal vesicles
- produce seminal fluid, contains:
- Fructose - nourishes semen
- Prostaglandins - stimulate smooth muscle contraction
- Coagulating proteins and enzymes - helps sperm clot in the female reproductive tract
-Seminal fluid makes up about 60-70% of total semen volume
57
prostate gland
- Prostatic secretions makes up about 20-30% of semen volume, contains
- Citrate - sperm utilizes for ATP production
- Prostate specific antigens (PSA) and other enzymes - helps dissolve semen clot in female reproductive system
- Antimicrobial chemicals - inhibit bacterial growth (reduces risk of infection in female reproductive system)
58
bulbourethral glands
In response to sexual stimulation the bulbourethral glands secrete a thick alkaline mucus like fluid that helps neutralize any acidic urine remaning on the urethra prior to ejaculation
59
sustentacular cells functions
- Provide structural support for spermatogonia development by maintaining the environment around the cells
- Provide nutrients to dividing cells
- Secrete testicular fluid
- Phagocytose damaged spermatogenic cells and excess cytoplasm
- Produce androgen binding protein (ABP) and inhibin, which helps regulate spermatogenesis
60
oogenesis
Before birth
- Oogonia (stem cells of females) undergo mitosis from 2-7 months
- Oogonia begin meiosis 1
- At this point they are primary oocytes
- Proceed to prophase 1, then their development is suspended
Childhood
- Primary oocytes remain in prophase 1 and do not develop further until puberty
Puberty to menopause
- About once a month after puberty 20-30 oocytes are stimulated to continue development
- Usually one oocyte will complete meiosis 1 to produce two haploid cells that are different in size. (1 large, one very small - polar body)
- The smaller cell (the first polar body) contains DNA but very little cytoplasm and often degenerates
- The larger cell (the secondary oocyte) contains DNA and most of the cytoplasm
- As the ovarian cycle progresses the secondary oocyte begins meiosis 2, but its development is arrested in metaphase 2
- If the secondary oocyte is fertilized it will complete meiosis 2 and divide to form an ovum and the second polar body
- If fertilization does not occur the secondary oocyte will remain in metaphase 2 and eventually be shed with menses
61
phases of the ovarian cycle
Follicular phase
1) primordial follicle
2) primary follicle
3) secondary follicle
4) vesicular follicle
Ovulation phase
5) ruptured follicle
Luteal phase
6) corpus luteum
7) corpus albicans
62
primordial follicle
primary oocyte surrounded by a single layer of squamous follicle cells
63
primary follicle
- Follicle cells become cuboidal granulosa cells
- Microvilli develop
- thecal cells develop
64
secondary follicle
- Primary oocyte surrounded by multiple layers of granulosa cells (wall thickens)
- Follicular fluid found in small cavities around the oocyte (increases size of follicle)
- Granulosa cells enlarge and stimulate nearby cells to form a layer of thecal cells around the follicle
65
vesicular follicle
- Primary oocyte finished meiosis 1 to become secondary oocyte
- Surrounded by granulosa cells and a fluid filled antrum (pockets of follicular fluid merge to form antrum large fluid filled cavity)
66
ruptured follicle
- Secondary oocyte is released from the vesicular follicle (pierces the tunica albuginea)
- Cona radiata (secondary oocyte and associated granulosa cells) are released from the ovary
- After oocyte is released the vesicular follicle collapses and ruptured vessels bleed into the antrum
- Fraternal twins occur when more than one vesicular follicle releases secondary oocyte
- Identical twins results from fertilization of a single oocyte by a single sperm, followed by separation of dividing cells during development
67
corpus luteum
- Remnant of the ruptured follicle (becomes an endocrine organ)
- Secrete progesterone and some estrogen
- Persists for 3 months and then will degrade if pregnancy does not occur
68
corpus albicans
Remnant of the corpus luteum after it ceases hormone secretion (scar tissue)
69
what does estrogen do to the follicles
- Stimulates the dominant follicle to continue developing into a vesicular follicle
- The new vesicular follicle produces large amounts of estrogen, triggering an LH surge
- The LH surge and FSH trigger ovulation
70
phases of the uterine cycle
- Menstrual phase (days 1-5)
- Proliferative (preovulatory) phase (days 6-14)
- Secretory (preovulatory) phase (days 15-28)
71
menstrual phase
uterus sheds the stratum functionalis, resulting in menstruation
72
proliferative phase
a new stratum functionalis develops with endometrial glands and spiral arteries and veins
73
secretory phase
- spiral arteries convert the stratum functionalis to secretory mucosa and endometrial glands secrete uterine milk
- If pregnancy does not occur, the cells of the stratum functionalis die and on day 28 the menstrual cycle begins again
- If pregnancy does occur the secretory phase will continue and the uterus will continue to develop
74
relaxin
secreted by the placenta, helps suppress uterine contractions until the birth process begins, loosens connective tissue around pubic symphysis and pelvic bones
75
placental hormones
- Human placental lactogen (hPL)
- Melanocyte stimulating hormone (MSH)
- Corticotropin releasing hormone (CRH)
76
human placental lactogen
Helps stimulate breast development and prepare mammary glands
77
melanocyte stimulating hormone
Darkens the areolae and nipples
| Changes skin tone in some women
78
corticotropin releasing hormone
Important in the length of pregnancy and timing of childbirth
79
parturition
1) The fetal adrenal cortex produces cortisol which stimulates the placenta to secrete high levels of estrogen
2) The high estrogen level stimulates the uterus to form oxytocin receptors
3) Both the fetal hypothalamus and maternal hypothalamus secrete oxytocin which stimulates the placenta to secrete prostaglandins
4) Prostaglandins dilate the cervix, and along with oxytocin, increase the strength of uterine contractions
5) A positive feedback mechanism begins when cervical stretching triggers the release of more oxytocin and prostaglandins
80
dilation stage
- Time from onset of labour until the cervix is fully dilated (10 cm)
- Longest stage of labour (usually 8-48 hours for first child and 4-12 hours for next children)
- Contractions begin in the upper part of the uterus and moves towards the vagina
- As labour continuous contractions become stronger and move to the lower uterus
- Vertex position - fetus is head first against the cervix, cervix thins and dilates
- Water breaking happens when the amnion ruptures and releases amniotic fluid
81
milk let down reflex
1) Infant suckling triggers the maternal hypothalamus to produce oxytocin and the maternal anterior pituitary gland to produce and release prolactin
2) Oxytocin stimulates myoepithelial cells of the breast to contract
3) Prolactin stimulates the mammary glands to produce additional milk
4) A positive feedback mechanism is responsible for the continued production of milk which occurs as long as the infant is suckling
82
lactation
- In the last months of pregnancy increased levels of placental estrogen, progesterone, and human placental lactogen stimulate the production of prolactin
- Estrogen and prolactin stimulate alveoli in mammary glands to grow and lactiferous ducts to branch
- estrogen and progesterone levels decrease when the placenta is expelled and prolactin stimulates milk production
- Oxytocin is responsible for the ejection of milk (let down reflex)
Nurs 1080
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