Exam 2 Flashcards

1
Q

phases of biliary and pancreatic secretion

A
  1. cephalic (5-10%)
  2. gastric (10-20%)
  3. intestinal (70-85%)
  4. STIM. BY SECRETIN AND CCK
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2
Q

leptin

A

ob gene product in adipocytes (binds to cytokine receptors); levels correlate with BMI

induces alpha-MSH in POMC neurons, reduces AGrP (anorexogenic) to supress appetite/stim. energy expenditure

high in obese people

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3
Q

amylin

A

co-secreted with insulin from β cells

slows gastric emptying and secretion, dec. pancreatic exocrine secretion and bile secretion, stimulates satiety

reduces post prandial glucose spike

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4
Q

B12 absorption

A
  • B12 released in stomach by pepsin, B12 combines with R protein (saliVary gland)
  • in SI R protein is degraded, B12 combines with intrinsic factor
  • B12/intrinsic factor absorbed in ileum by Na cotransporters
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5
Q

niacin

reactions its used for, deficiency disease/cause, source

A

(B3) NAD and NADPH

*has the highest RDA of all B vitamins

  • reactions: redox (electron acceptor/donor)
  • deficiency: pellagra - dermititis, diarrhea, dementia, death - due to corn diet/isoniazid TB tx
  • sources: humans can make from Trp, corn has to be treated with alkali, meat, fish, yeast
  • toxicity: facial flushing/hepatitis
  • use: lower TG and LDL/raise HDL
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6
Q

space of disse

A

in hepatocytes; microvilli sit in there (kind of beneath endothelial cells) - perisinusoidal

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7
Q

hepcidin

A

made by liver, for Fe absorption

IL6/high hepatocyte Fe releases hepcidin; binds to FP transporter to inhibiti release of Fe, downregulates DMT1 and inhibits release of Fe from macrophages

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8
Q

ascorbic acid

reactions its used for, deficiency disease/cause, source

A

vit C

  • rxn: cofactor in collagen and catecholamine synthesis, anti-oxidant, inc. absorption of non-heme iron
  • deficiency: scurvy (bad collagen cross linking), loose teeth, bruising, poor wound healing, petechiae
  • sources: citrus fruits, tomatoes
  • use in septic shock
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9
Q

law of the intestine

A

frequency of BER is greater in the proximal portion than distal portion of small bowel (12/min vs 8/min)

higher proximal motor activity pushes chyme distally

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10
Q

what is accomodation?

A

tension falls off in time but the muscle stays stretched due to internal rearrangement of microfibrils (because no Z lines)

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11
Q

pantothenic acid

reactions its used for, deficiency disease/cause, source

A

(B5) - coenzyme a

  • reaction: carboxylation and carb energy reactions as a carrier for acyl chains, ach synthesis, adrenal hormone synthesis
  • deficiency: (rare) fatigue, depression, irritability, neuropathy
  • sources: unprocessed foods (meat, veggies, whole grains, microbiota)
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12
Q

iron deficiency symptoms

A

pica (ice chewing), leg cramps, fatigue, pale

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13
Q

pyridoxine/pyridoxal, pyridoxamine

reactions its used for, deficiency disease/cause, source

A

(B6) PLP

  • reaction: in AA metabolism rxns (transamination and decarboxylation, glycogen phosphorylase)
  • deficiency: (rare alone) poor diet/alcoholics
    • symptoms:irritability, condusion, depression, stomitis
  • sources: meat, starchy veggies (potatoes), non citrus fruits (bananas/avo), fortified in pasta
  • toxicity: pain and numbeness
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14
Q

entero gastric reflex

A

decreases stomach emptying and increases duodenal activtiy distal to stimulus

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15
Q

gastroparesis

A

slowed gastric emptying

may be due to vagal nerve dysfunction, nNOS synthesis malfunction / loss of ICCs

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16
Q

where is gastrin secreted from and what does it do?

A

secreted by antral G cells from stretch/distension/AA

G cells release GRP

Gastrin binds to CCKB receptors to activate Gαq

(CCKA receptors inhibit gastric acid secretion)

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17
Q

what is an implication of loss of villus tips?

A

gluten enteropathy - autoimmune fur to HLA that sensitize T-cells to gluten

loss results in diarrhea and malnutrition

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18
Q

mechanism for secretory diarrhea

A

toxins increases cAMP which activates PKC, increases Cl flux by opening channels already present and makes new channels, inhibits Na H exchanger

HCO3 can’t compensate as more Cl is in enterocyte than plasma so more HCO3 into lumen to compensate for loss of anions, any excess H is removed by HCO3 combining ↑ acidosis

increases K loss in exchange for Na into enterocyte

⇒dehydration, metabolic hyperchloremia, hypokalemia acidosis

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19
Q

mechanisms for insulin release

A
  1. cephalic phase
  2. digestive phase
  3. absorptive phase - glucodetectors in blood and liver tell pancreas to release inulin, info travels via nucleus of the solitary tract (NST) into hypothalamus
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20
Q

low flow vs. high flow saliva formation

A

low flow: very hypotonic, low volume, low pH (6.8)

high flow: stimulated by Cl channel (basolateral) - slaiva with higher HCO3, Na, pH (8.4), low K

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21
Q

what does bile interfere with and how is that overcome?

A

bile interferes with pancreatic lipase, but is overcome by secreting co-lipase

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22
Q

what is ferroportin disease

A

mutations in ferroportin so hepcidin can’t bind ⇒ too much Fe in plasma

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23
Q

entero-enteric reflex

A

increases motor activity distal to distending/irritating stimulus, decreases proximal motor activity

(in abnormal distension/irritation, clears offending stimulus from bowel, doesn’t add material to stimulated portion)

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24
Q

events for defectation

A
  1. stim. of defecation reflex - contraction of distal colon, relaxation of internal anal sphinceter
  2. changing ano-rectal angle
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25
ENS is _______ in its resting state
inhibitory! chemical denervation increases small bowel motor activity
26
talk to me ab starch digestion
begins with salivary alpha amylase (which is inactivated by stomach gastric acid) then pancreatic amylase digests to alpha limit dextrins and maltooligosaccharides, eventually to glucose which enters cell thru SGLT1
27
unstirred water layer
layer of hypothetical water that coats mucosa of villi (from capillary effect) - **barrier to absorption** of all materials (espec. fats) ex. there is less absorption in non-motile bowel
28
kernicterus
bile pigment pathology; unconjugated bilirubin causes irreversible CNS damage as BBB still permeable; combines with neural cell nuclei / disrupts function
29
pectinate line lymph drainage, innervation
above: superior rectal → preaortic nodes OR middle rectal nodes, visceral innervation (not painful) below: superficial inguinal, somatic innervation (v painful)
30
HIF-2 dependent proteins
CYBRD1 (Fe3+ →2+ thru DMT-1) DMT-1 heme oxygenase (Fe3+→2+ thru HT) ferroportin - gets Fe out of cell
31
PP cell (F cell)
secrete pancreatic polypeptide in response to protein, fasting, exercise, and acute hypoglycemia
32
coordination of defecation
ano rectal angle due to contraction of puborectalis mucle - causes valvular like resistance in colon, prevents defecation een with internal anal sphincter inhibition has to move from (90-110 degrees to 130-140) - gets more **obtuse** and pelvic floor lowers
33
gastrocolic reflex
filling stomach increases distal motor activity in the colon (infants diapers have to be changed soon after feeding)
34
portal lobule
describes exocrine function of liver (bile secretion) - portal triad at center, central veins points of triangles
35
ferritin
holds up to 4500 Fe atoms - has ferroxidase converts Fe3+ to Fe2+ and then internalized; in most teissues (liver, spleen, BM) degraded by lysosomal proteases to mobilize iron. marker of inflammation
36
why are crypt cells immature
they secrete water and Nacl and Kcl rather than absorb them
37
EPO
glycoprotein hormone sec. by liver and kidneys - is a cytokine that stimulates erythrocyte precursors in BM to mature into erythrocytes liver synthesis in fetal period (up to 32 weeks gestation), kidney synthesis after EPO binds to EpoR which activates JAK2
38
riboflavin reactions its used for, deficiency disease/cause, source
(B2) FMN and FAD * reactions: redox reactions as cofactors (dehydrogenase, amino oxidase, decarboxylation pyruvate) * deficiency: inflammation (dermitis, stomatitis, cheliosis), photophobia * sensitive to light, can be depleted from sun exposure (phototherapy bilirubin) * sources: plants and yeast, enriched breads, liver/kidney
39
liver and GB development
come as ventral outgrowths of foregut. liver comes from development of hepatic cords, liver grows cranially and GB grows caudally. are both endoderm derivatives
40
migrating myoelectric complexes (MMCs)
bursts of intense motor activity to "clean out" stomach post emptying 4 phases: I: quiesence II: building waves of contraction III: crescendo of activitve IV: return to normal quiesence
41
wilson's disease
kayser-fleischer corneal rings with Cu deposits - mutation in ATP7B so Cu can't get into ceruloplasmic (Fe problems with oxidation coming out of liver) and excrete Cu in bile give cu chelator (penicillamine and trientine) factitious smile, pseudo-laughter/open mouth dull look, staring expression. hand and nuchal dystonia
42
what are the 3 phases of salivation?
1. cephalic - neurally stimulated by sight/smell/thought 2. oral - (largest volume) mechanical stimulation of oral cavity from food/gum 3. esophageal (gastric): distension of esophagus/stomach, cleans out dentition
43
where does most nutrient absorption occur?
jejunum! then duodenum, then ileum and colon act as reserve
44
AI vs. EAR vs. RDA vs UL
AI: approximates safe levels EAR: 50% of population safe levels RDA: safe levels for 97-98% of population UL: highest upper limit with no adverse effects
45
stomach development
rotates clockwise 90° during week 4-6, posterior side enlarges (LARP)
46
meckel's diverticulum vitilline cyst vitilline fistula
MD: vitilline duct stays attached to ileum (2% of population, within 2 feet of ileocecal junction, 2 inches, 2% symptomatic, detected by age 2) VC: ileal tissue suspended by vitelline ligaments VF: remains patent; feces could leak out of umbilicus
47
what things stimulate 5HT3 receptors?
stimuli from viscera, uvula, and pericardia (inc bowel obstruction) stimulates emesis
48
black arrow
bile canaliculi (hepatocytes) lined by cholangiocytes
49
is defecation voluntary or involuntary?
voluntary! external anal sphincter under voluntary control via skeletal muscle / pudendal nerve
50
glucose into β cell
glucose gets into β cell by GLUT2 results in K channel closure (due to ATP being formed), membrane depolarizes voltage gated Ca channels open, insulin gets released
51
black star
hepatic artery simple squamous epithelium, know its a BV
52
TNFα and IL-6
pro-inflammatory cytokine, pos. correlated with BMI. increases lipolysis and release of FFA, down regulates GLUT4. inhibits adiponectin
53
transthyretin TTR
involved in transport of thyroxine (T4) to target tissues, carries RBP and retinol bc too small for GFR
54
how does Cu enter/exit cell?
enter: DMT1 or Ctr1 exits: ATP7A (ATPase) - everywhere in body except liver circulates bound to albumin (excess goes into bile by ATP7B and excreted) - liver specific
55
what happens in SUVSM when there is increased intracellular calcium?
4 Ca bind to a calmodulin (weak bond) CAM activates MLCK myosin head gets phosphorylated which forms cross bridge with actin when ADP and Pi come off, swivels from 90 to 45 degrees = power stroke
56
how do glucose and galactose get into cell?
SGLT1-Na co-transport, influenced by insulin
57
PepT-1
brush border peptidase for oligopeptides; req. H co-transport, then get hydrolyzed to AA in the cell Na H exchanger to maintain pH
58
what is receptive relaxation?
the inhibition of the LES and resultant lowering of tension during swallowing. requires functional myenteric plexus
59
what are the 3 phases of swallowing, and what cranial nerves mediate each phase? in which state does dysphagia occur?
1. oral phase (voluntary) 1. CN V, VII, IX, X, XII 2. pharyngeal phase (involuntary) 1. CN IX, X 3. esophageal phase (involuntary) 1. CN X dysphagia can occur in any of the stages
60
3 things modulate the rate of gastric emptying of chyme. what are they?
1. pressure gradient between antrum and duodenum 2. if food is in solid/liquid form 3. chemicals that are affecting gastric emptying 1. 5HT3 and M3 inc. gastric emptying 2. CCK and 5HT1 slow gastric emptying
61
folate/folic acid reactions its used for, deficiency disease/cause, source
(B9) tetrahydrofolate FH4 * reaction: carrier for single C metabolism (homocysteine →methionine), synth of nucleic acids \*necessaery for fetal dev. * deficiency: (slow/rare) defective cell proliferation. during pregnancy ⇒ spina bifida * symptoms: megaloblastic anemia * sources: dark leafy greens * excess: can mask megaloblastic anemia bc vitamin B12 deficiency = demyelination/irriversible damage * methotrexate - cancer tx, blocks DHFR preventing FH4 synthesis
62
EC cells
* secretin: inc. HCO3 secretion in pancreas and pancreatic enyzme secretion * motilin: gastric and intestinal motiltity * substance P: nt, inc. pancreatic flow and HCO3 and amylase secretion
63
black arrow
in liver kuffer cell (hepatocyte macrophage)
64
hemochromatosis
mutation of genes regulating hepcidin (less hepcidin being made) so high ferroportin, low levels of Fe stores (its all in the body) HFE (hemochromatosis assoc gene product) binds to transferrin recpetor TfR2 (liver) so it can't adequately regulate hepcidin expression types 1-3 hepcidin problems, type 4 ferroportin problem. type 2 is worst
65
H+ preferentially releases
secretin (an enterogastrone) from S cells
66
constapation
inappropriate decreases from normal frequency of defecation - starvation, dehydration, surgery, antihypertensive drugs
67
omega acids
α linoleic (LA) - omega 6 → arachidonic acid, precursos to bioactive lipids in inflammation (PGs, leukotrienes) α linolenic (ALA) - omega 3, in oils/flax. converted to EPA then DHA. fatty fish high content
68
thrombopoietin
(from liver) reg. number of whole platelets in blood (300k). also made in BM, kidney, striated muscle liver predominants post 32 weeks gestation rate of TBO production changed by **IL-6** presence once TBO bound to platelets, gets catabolized
69
70
kallikrein
forms vasodilator bradykinin to inc. bf to salivary glands
71
IGF-1 and 2
made 1° by liver IGF-2 main during gestation - maternal IGF-2 doesn't cross placental barrier (from imprinted gene). stimulates IGF-1 in paracrine manner IGF-1 important post gestation most (98%) IGF-1 is bound (to IGF-BP-3) IGFR is RTK → AKT signaling pathway
72
PP cells
in islet of langerhans pancreatic polypeptide; inhibits enzyme and bicarb release
73
AMDR for adults
protein 10-35% (0.8 g/kg/day) fat 20-35% carbohydrates 45-65%
74
sequence of events in pharyngeal phase: (of swallowing)
1. internal nares sealed off 2. epiglottis covers trachea 3. oral cavity closes as base of tongue touches soft palate 4. UES opens 5. eustachian tubes open then close as bolus passes
75
hirschsprungs disease
congenital aganglionic megacolon - motor disorder of gut from failure of NC migration
76
ghrelin
secreted by stomach and hypothalamus, increased during fasting, decreased by presence of food in stomach. stimulates NPY/AgRP neurons role in body weight regulation GHS-R acylated - necessary to cross BBB
77
omphalocele vs gastroschisis
omphalocele: intestine protrudes into covered umbilical cord gastroschisis: structures not in peritoneal layer
78
Fe absorption
dietary Fe bound to iron solubulized by gastric acid, occurs in duodenum (damaged duodenum = microcytic anemia) Fe3+ in plasma absorbed by enterocytes and converted to Fe2+
79
midgut development
primary intestinal loop rotates around SMA (CCW 270 total) 2 phases: 1. gut herneates into umbilical cord at week6 (90 CCW) 2. returns to abdominal cavity week10 (180 CCW)
80
ID
gall bladder looks like coral reef
81
menkes disease
X-linked neurodegenerative disease due to ATP7A mutation (everywhere except adult liver) so Cu can't get released into blood most die by 3y. failure to thrive, cerebral degeneration, joint hypermobility, hypopigmentation, twisted hair (pili torti)
82
heme catabolism (dietary vs non heme iron)
dietary heme gets converted Fe3+→2+ by **heme oxygenase**, goes thru HT transporter bilirubin is byproduct nonheme iron solubilized by **ferric reductase** to Fe2+ which gets absorbed by DMT1 (Ca competitively inhibits)
83
colonic motor activtiy consists of:
1. segmentation (mixing and packing contractions) - apperance of haustra 2. mass peristalsis - simultaneous contraction of large areas of distal colon, squeezes feces into distal colon and rectum
84
primary vs secondary bile acids vs bile salts
**primary**: made in liver from cholesterol → cholic & deoxycholic acids **secondary**: 1° metabolized by bacteria → deoxycholic & lithocholic acids **bile salts**: 1° and 2° bile acids get conjugated with glycine and taurine - are more water soluble
85
system B not
Na dependent neutral AA transporter (to transport specific AAs, others for specific acidic/basic AAs)
86
fate of SCFA (\>12 C) vs LCFA (\<12 C)
SCFA diffuse right into hepatic portal circulation LCFA are re-esterified bto TGs, coated with beta lipoprotein and form chylomicrons which diffuse into lacteals to general circulation
87
what is normal BAO? normal MAO? ratio?
1.5-2.5 mmol/hr 15-25 mmol/hr ratio normally 1:5 (0.2)
88
R protein (haptocorrin)
binds with B12 (cyanocobalamine) after B12 freed by pepsin is partially digested by pancreatic enzymes, allowing intrinsic factor to bind B12
89
what pathway does Ach stimulate?
Gαq → inc. Ca, stimulates the H K pump stimulates M3 receptors on parietal cells and histamine releasing EC cells
90
what creates the post prandial alkaline tide?
basolateral parietal cell HCO3 is exchanged for Cl
91
chemoreceptor trigger zone (CTZ)
2nd level of receptors that supplement emetic center stim. by meningitis, spoled foods, chemo, toxins, hypoxia, acidosis, radiation therapy, pregnancy these stimulate 5HT3 receptors
92
adiponectin
secreted by white sc cells - much higher circulating levels than leptin! inversely correlated with BMI (skinny people have more adiponectin) signals AMPK, increases glucose uptake and FA oxidation in muscle, dec. liver gluconeogenesis and dec. BGL (inhibits energy consuming, anabolic pathways), promotes catabolism
93
phasic vs. tonic contractions
phasic - rhythmic contractions (SI and LI), req. AP to initiate Ca influx (ICCs) - BER tonic - baseline tension maintined at sphincters; doesn't require APs for Ca influx or ICCs
94
yellow arrow
in liver hemocydrin - liver takes care of worn out RBCs. complexes of ferritin
95
enterokinase
converts trypsinogen to trypsin secreted by **intestinal crypts** in active form, bound to mucosal BB but is freed from presence of bile salts and activated from trypsinogen presence \*the important enzyme that initiates activation of **pancreatic enzymes**
96
pancreas development
from 2 endodermal buds, ventral bud moves dorsally around the duodenum and becomes uncinate process (dorsal bud becomes neck, body, tail) ventral bud leads to main pancreatic duct
97
whats the diff between tone and tonus
tone: in SkM due to discharge of α motor neurons tonus: latch bridge formation/sustained muscular tension, a high efficiency contraction as no ATP needed (SUVSM)
98
vitelline duct
connect gut stube to disappearing yolk sac (week 4)
99
3 phases of gastric secretion:
1. cephalic 2. gastric 3. intestinal
100
what does excess DCA (deoxycholic acid) in the colon stimulate?
excess chloride secretion → secretory diarrhea in short bowel syndrome, colitis, defective bile transporters, IBS
101
red star
common bile duct low columnar epithelium
102
what is BAO/MAO in duodenal ulcers? Zollenger-Ellison syndrome? gastric ulcer atrophy/pernicious anemia
duodenal ulcers: 6:20 (0.3) ZE syndrome: 40/65 (0.62) + gastric ulcer: 0.75/10 (0.075) pernicious anemia/severe gastric mucosal atrophy: 0
103
biotin reactions its used for, deficiency disease/cause, source
(B7) * reaction: carboxylation reactions - CO2 binding factor, post translational modification of proteins * deficiency: rare, caused by raw egg whites (avidin) * symptoms: hair loss, rash, neurological * sources: egg yolks/liver, microbiota synthesize
104
what is key ENS transmitter?
serotonin (5HT); stim. by stretch receptors/efferent vagal stimulation in front of bolus, inhibits circular muscle and stimulates longitudinal muscle contraction
105
what do D (delta) cells release and what does that do?
somatostatin - inhibits gastric acid secretion (inh. parietal cells and gastrin secreting cells and EC cells) \*during digestion, D cells inhibited by vagal stimulation from Ach or GRP stimulated by pH \<2
106
hepatic zone 1 vs zone 3
zone 1 higher O2 and toxin content
107
salivary amylase (ptyalin)
begins starch digestion
108
GLP-1
secreted by intestinal L cells and CNS solitary tract - distal ileum and colon. secretion biphasic (first from neuro and gut hormones, then from digested nutrients) fx: increases insulin secretion to decrease post prandial glucose spikes, gets rapidly degraded. also increases brain satiety, dec. gastric motility/secretion, inc. tissue glucose uptake
109
2 fates of Fe2+ once it enters the cell
1. synthesized to ferritin (storage) 2. transported into plasma by FP transporter (basolateral) 1. **hepaestin** is bound to FP transporter and makes Fe3+ so it can be pumped out bound to **transferrin**
110
ito cell / hepatic stellate cell
stores vitamin A and lipid (vit A req. for sperm development, CV outflow - orientation of cardaic NC cells during septation - without, can lead to congenital heart defects/persistent truncus arteriosus) can differentiate into myofibroblasts in disease state → liver fibrosis, active in cancer - breaks down ECM to help cells metastasize
111
bile salt dependent vs independent fractions
**dependent**: resecretion of recycled bile salts and de novo bile acids which osmotically draw water and electrolytes into bile canaliculus **independent**: secretion of water, bicarb, electrylytes, stim. by secretin to neutralize acid
112
what neurons are in the arcuate nucleus, and how do they differ?
1. NPY/AgRP - appetite stimulating (orexogenic) 2. POMC/CART release αMSH - appetite suppressing (anorexogenic) NPY is MC3/4 antagonist, POMC is MC3/4 agonist
113
lateral hypothalamus
dopamine stimulates hunger
114
types of capillaries in pancreas
endocrine pancreas (islets) - fenestrated exocrine pancreas (acini/ducts) - non fenestrated
115
xeropthalmia
differentiation of epithelium (due to retinoic acid)
116
GLP-1
secreted from L cells in distal intestine rapidly after eating carbs and fat - is an incretin homrone, increases insulin secretion/inhibits glucagon decreases food intake/appetite
117
how is dietary Ca absorbed
mostly paracellular (espec when high Ca content), some transcellular occurs mainly in duodenum (some j/i) **transcellular:** req. calcitriol - low serum Ca stimulates PTH which will convert to active form (1 alpha hydroxylase), then calcitriol inserts TRPV6 channels into apical membrane, makes calbindin-D in absorptive cells, Ca H ATPase pump, Na Ca exchanger
118
retropulsion
from mid SI thru to stomach via pyloric sphincter during emesis; accounts for bitter bile like taste (can extend down to proximal colon in infants)
119
what is ferroxidase
converts Fe2+ →Fe3+ in enterocytes = hephaestin in hepactocytes/macrophases = ceruloplasmin
120
bile secretion
lipids [and protein] stimulate CCK release from I cells, stimulates CCKA receptors to * contract GB * relax sphincter of oddi * pancreatic enzyme secretion * inh. gastric acid secretion
121
types of diarrhea (2)
1. **secretory**: enterotoxins from viruses/bacteria/parasites - damaged mucosa, can't absorb fluids and electrolytes 2. **osmotic**: laxative abuse, malabsorption of osmotically active agents 3. **inflammatory** 4. **abnormal motility**
122
thiamine: reactions its used for, deficiency disease/cause, source
B1 (thiamine pyrophosphate TPP) * reactions: oxidative decarboxylation reactions (pyruvate dehydrogease, αKG dehydrogenase, transketolase * defiency - in areas sensitive to energy deprivation (CNS, heart, muscle) * disease: **beriberi** (dry = neuropathy, wet = CFH) * **wernicke-korsakoff syndrome**: psychosis/ataxis from chronic alcoholism/morning sickness * source: whole grain cereals, legumes, nuts, enriched bread
123
what is potentiated secretion?
stimulation of 2 secretory pathways: Gastrin-Ach pathway via Gαq GTP binding protein histamine pathway via Gαs
124
vitamin E (α tocopherol) reactions its used for, deficiency disease/cause, source
* reaction: antioxidant, inserts in PM to protect from ROS, traps free radicals * deficiency: severe ataxia, neuropathy/myopathy/retinopathy, impaired immunity, hemolytic anemia in infants * sources: nuts, seeds, vegetable oils, green veggies * toxicity: hemorrhaging/impaired blood clotting
125
why is vitamin C used in septic shock?
* counters ROS * recycles α tocopherol (Vit E) and BH4 which helps bring NO * inhibits NFKβ (pro-inflammatory) * cofactor for monooxygenase rxns (catecholamines and vasopressin pdtn) * increases catecholamine sensitivity
126
what is the principal activity of the small and large bowel?
NaCl and water resporption (97.8% recovery) - jejunum is major site for water, electrolyte, nutrient
127
ghrelin
released 90% from stomach and from pancreatic epsilon cells in response to low nutrients assoc. with GH stimulates hunger centers (NPY and AgRP) to generate appetite
128
how are SM cells joined to one another
physically - intermediate junctions electrically - gap junctions
129
where does gastric lipase come from and what does it do?
from chief and mucous neck cells of fundus hydrolyzes 15-20% of dietary lipid
130
what things stimulate 5HT1 and D2 receptors?
(emesis) vestibular system by inappropriate mtion/infections
131
where is R protein and what does it do
saliva; for B12 absorption
132
4 mechanisms to control the GI tract
1. ENS 2. endocrine 3. paracrine 4. SUVSM
133
NaK2Cl transport (NKCC1)
in ileum, colon and crypt cells electroneutral
134
ID
pancreatic islet pale with lots of BV
135
where are bile salts recovered
ileum; Na coupled transporter into enterocyte
136
what molecules inhibit precapillary sphincter smooth muscle, opening capillaries?
PaCO2 and adenosine
137
BMI calculation
weight/(height)^2 kg/(m)^2 \<18.5 = underweight 18.5-24.9 = desired weight 25-29.9 = overweight \>30 = obese
138
CFTR
cystic fibrosis chloride channel on apical side of pancreatic duct cell allows lumen to be flushed - maintains electro and osmoneutrality. without ⇒ pancreatitis
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primary peristaltic wave
generated in SkM portion of esophagus (upper 1/3); then contraction coordinated in the swallowing center, nucleus ambigious and non-vagal nuclei **myenteric plexus** intitiates spread down lower 2/3 upon efferent output from X dorsal motor nucleus **peristalsis**: wave of relaxation then wave of contraction
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where are the ICCs int he stomach
body
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what pathway is for the secretion of mucus
COX-1, stimulates PGE3 → mucus secretion
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D1 cell
secretes VIP: inhibits release of gastrin/gastric HCl stimulates secretion of water/electrolytes by small and large intestine - relax GI sphincters, slows intestinal transit time
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somatostatin
released by delta cells in response to glucagon and elevated BGL, inhibited by insulin \*acts paracrine to inhibit insulin and glucagon
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what regulates centroacinar cells?
secretin (HCO3 release)
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adaptive thermogenesis
metabolic adaptation to weight changes - changes in energy expenditure 10% reduction ing body weight accompanied by 20-25% decline in energy expenditure
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cobalamin reactions its used for, deficiency disease/cause, source
(B12) * reactions: methyl transfer rxns (homoxysteine →met, MM-CoA →SU-CoA) * deficiency: pernicious anemia (lack of intrinsic factor) from autoimmune/strict vegans * symptoms: **megaloblastic anemia** (from FH4 trapping), neuro disorders (demyelination) * elevated MM-CoA specific for B12 def
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what is pepsin activated by?
HCl
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what gets absorbed in the: * duodenum * jejunum * ileum * colon
* **duodenum**: nutrients, water, nacl, folate, Fe, Ca * **jejunum:** water, nacl, K, HCO3, nutrients (main) * **ileum**: water, nacl, nutrients (reserve), bile, B12 * **colon:** water, nacl, nutrients (reserve)
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black arrows
kupffer cells (liver macrophages) come from monocytes from BM, differentiate in target tissues. are APCs with MHC II, secrete cytokines and chemokines
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N balance equation
N balance = intake - excretion intake = .16 x itake positive N balance in pregnancy, low in sepsis
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what is derived from lateral mesoderm
Ct and viscera tissue, serous membranes
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of the LES: what is the function? innervation?
**function:** prevent material in stomach from refluxing back into esophagus **inn:** efferent vagal inn is inhibitory
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two stage hypothesis
**primary saliva:** secretion from acinar portions (fluid, ions, enzymes, mucous + blood borne hormones) - isotonic **secondary saliva**: interaction with ductal cells (striated duct) - hypotonic (more ions reabsorbed than water)
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fats preferentially release
CCK (an enterogastrone) from I cells
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what does histamine stimulate and where does it come from?
secreted by EC cells and acts paracrine EC cells stim. by Ach, gastrin, or distension histamine stim. h2 receptors on parietal cells which activates Gαs (cAMP → PKA → proton pump)
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acalasia
lack of receptive relaxation at the LES; if ENS or vagus doesn't work. causes regurguitation/mega esophagus
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brown adipose (and mechanism?)
higher in lean individuals, localized to supraclavicular and anterior cervical areas. allows for non-shivering thermogenesis based on **UCP-1** and **DIO2** UCP-1 has lots of mitochondria for energy storage mechanism: βAR → cAMP → DIO2 →T3→UCP-1 →leakage of protons, dissipation of energy as heat
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lingual gland lipase
iniitates lipid digestio of 10% of ingested fat (important when intenstinal digestion abnormal)
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gastritis
inflammation of gastric mucosa - sometimes by H. pylori, sometimes by NSAIDs
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pelvo-pelvic reflex
required for voiding; stimulus increased (\>18 mmHg) from stretching colonic and rectal receptors
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what nerve mediates receptive relaxation
vagus
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where are retinyl esters mainly absorbed
upper duodenum
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when is hepcidin released? what does it do? what is the control paradigm?
high Fe plasma, high hepatocyte Fe, or inflammation (IL6) binds to FP transporter, downregulates DMT-1, inhibits Fe release from macrophages control paradigm: in times of low iron, there is low hepcidin so more Fe uptake and release → anemia of chronic inflammatory diseases
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glucagon
secreted by α cells of pancreatic islets in response to low BGL; promotes mobilization of metabolic substrates. LIVER is prinicpal target (inc. cAMP, IP3, Ca)
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ventromedial hypothalamus
serotonin stimulates satiety
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erythroferrone
suppresses hepcidin expression in the liver to generate enough/sufficient RBC
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secretory acinar cells vs centroacinar cells (pancreas)
secretory acinar cells make exocrine secretions centroacinar cells make bicarb - reg. by secretin
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GERD
incompentent LES lets gastric juice reflux back into esophaugus could be caused by hiatal hernia, obesity, pregnancy (progesterone weakens LES contractions), Ca channel blockers, overfilling stomach/exercise after large meal, weak LES
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talk about IBP and what it does in high and low iron states
low iron: IBP not bound to Fe so it binds to 5' UTR of ferritin to block translation and to 3' UTR of TfR to protect from endonucleases high iron: IBP bound to Fe so 5' UTR free to translate ferritin, 3' UTR subject to endonucleases so TfR not translated
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how do ICCs depolarize SUVSM
open LTCCs depolarizations due to increases in gCa, gNa, and decreased gK
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calponin and caldesmin
interfere with actin phosphorylation, inc. rate of relaxation
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peptide YY (PYY)
from L cells in lower intestine, **co-releasd with GLP-1** to inhibit NPY/AgRP and stimulate POMC (anorexogenic)
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choleretic effect
hepatocyte reupatake and release of preformed bile; recycled bile used until theres not enough then 7αhydroxylase has to make new bile which breaks the positive feedback loop
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progression of bilirubin
bilirubin (70% from heme products) → \*bilirubin → conj. with glucuronic acid → urobilinogen → stercobilinogen → stercobilin (colors feces) \*by bilirubin reducatase
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water transport digestive vs interdigestive period
**digestive period**: 2/3 paracellular, 1/3 transcellular **interdigestive period**: 1/3 paracellular, 2/3 transcellular
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stool osmotic gap
differentiates secretory from osmotic diarrhea SOG = [290-(stool Na + stool K)] normal = 100-150 secretory = \<100 osmotic = \>150
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angiotensinogen
secreted by liver, an α2 globulin; renin from kidneys converts to ATI which gets to ATII from ACE (lungs) stim. by GCs, TH, estrogens, cytokines, ATII
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disaccharides: trehalose, lactose, sucrose
trehalose: 2 glucose molecules joined lactose: galactose and glucose sucrose: fructose and glucose
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steric hindrance of bile salts
there is steric hindrance to bile salts and pancreatic lipase, gets overcome by **pancreatic co-lipase**
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spleen development
grows in dorsal mesogastrium posterior to stomach, suspended by gastrolienal ligamtand and lienorenal ligament
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diarrhea
inappropriate increases in fecal water content
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hepatic (portal) acinus
smallest functional unit, is a rhombus with PT on short edges, CVs on long edges
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vitamin K (phylloquinone K1 or menaquinones K2) reactions its used for, deficiency disease/cause, source
* reaction: Co enzyme for carboxylases, post translational modification of glutamate, req. for clotting factors (prothrombin) and osteocalcin * deficiency: impaired clotting/bruising/hemorrhaging * in infants: VKDB (Im injection at birth) * sources: gut bacteria * phylo: dark leafy veggies * mena: fermentated foods/cheese/liver * warfarin is anti clotting drug that inh. vit K reactions
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succus entericus
secretions from the SI mucosa and mucosal glands