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Block 4: GI, Repro, Endocrine, Skin > Exam 2 > Flashcards

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
Q

ENS is _______ in its resting state

A

inhibitory!

chemical denervation increases small bowel motor activity

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26
Q

talk to me ab starch digestion

A

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

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27
Q

unstirred water layer

A

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

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28
Q

kernicterus

A

bile pigment pathology; unconjugated bilirubin causes irreversible CNS damage as BBB still permeable; combines with neural cell nuclei / disrupts function

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29
Q

pectinate line lymph drainage, innervation

A

above: superior rectal → preaortic nodes OR middle rectal nodes, visceral innervation (not painful)
below: superficial inguinal, somatic innervation (v painful)

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30
Q

HIF-2 dependent proteins

A

CYBRD1 (Fe3+ →2+ thru DMT-1)

DMT-1

heme oxygenase (Fe3+→2+ thru HT)

ferroportin - gets Fe out of cell

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31
Q

PP cell (F cell)

A

secrete pancreatic polypeptide in response to protein, fasting, exercise, and acute hypoglycemia

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32
Q

coordination of defecation

A

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

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33
Q

gastrocolic reflex

A

filling stomach increases distal motor activity in the colon (infants diapers have to be changed soon after feeding)

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34
Q

portal lobule

A

describes exocrine function of liver (bile secretion) - portal triad at center, central veins points of triangles

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35
Q

ferritin

A

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

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36
Q

why are crypt cells immature

A

they secrete water and Nacl and Kcl rather than absorb them

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37
Q

EPO

A

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

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38
Q

riboflavin

reactions its used for, deficiency disease/cause, source

A

(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
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39
Q

liver and GB development

A

come as ventral outgrowths of foregut.

liver comes from development of hepatic cords, liver grows cranially and GB grows caudally. are both endoderm derivatives

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40
Q

migrating myoelectric complexes (MMCs)

A

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

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41
Q

wilson’s disease

A

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

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42
Q

what are the 3 phases of salivation?

A
  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
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43
Q

where does most nutrient absorption occur?

A

jejunum! then duodenum, then ileum and colon act as reserve

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44
Q

AI vs. EAR vs. RDA vs UL

A

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

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45
Q

stomach development

A

rotates clockwise 90° during week 4-6, posterior side enlarges (LARP)

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46
Q

meckel’s diverticulum

vitilline cyst

vitilline fistula

A

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

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47
Q

what things stimulate 5HT3 receptors?

A

stimuli from viscera, uvula, and pericardia (inc bowel obstruction)

stimulates emesis

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48
Q

black arrow

A

bile canaliculi (hepatocytes)

lined by cholangiocytes

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49
Q

is defecation voluntary or involuntary?

A

voluntary! external anal sphincter under voluntary control via skeletal muscle / pudendal nerve

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50
Q

glucose into β cell

A

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

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51
Q

black star

A

hepatic artery

simple squamous epithelium, know its a BV

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52
Q

TNFα and IL-6

A

pro-inflammatory cytokine, pos. correlated with BMI. increases lipolysis and release of FFA, down regulates GLUT4. inhibits adiponectin

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53
Q

transthyretin TTR

A

involved in transport of thyroxine (T4) to target tissues, carries RBP and retinol bc too small for GFR

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54
Q

how does Cu enter/exit cell?

A

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

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55
Q

what happens in SUVSM when there is increased intracellular calcium?

A

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

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56
Q

how do glucose and galactose get into cell?

A

SGLT1-Na co-transport, influenced by insulin

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57
Q

PepT-1

A

brush border peptidase for oligopeptides; req. H co-transport, then get hydrolyzed to AA in the cell

Na H exchanger to maintain pH

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58
Q

what is receptive relaxation?

A

the inhibition of the LES and resultant lowering of tension during swallowing. requires functional myenteric plexus

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59
Q

what are the 3 phases of swallowing, and what cranial nerves mediate each phase? in which state does dysphagia occur?

A
  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

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60
Q

3 things modulate the rate of gastric emptying of chyme. what are they?

A
  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
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61
Q

folate/folic acid

reactions its used for, deficiency disease/cause, source

A

(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
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62
Q

EC cells

A
  • 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
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63
Q

black arrow

A

in liver

kuffer cell (hepatocyte macrophage)

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64
Q

hemochromatosis

A

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

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65
Q

H+ preferentially releases

A

secretin (an enterogastrone) from S cells

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66
Q

constapation

A

inappropriate decreases from normal frequency of defecation - starvation, dehydration, surgery, antihypertensive drugs

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67
Q

omega acids

A

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

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68
Q

thrombopoietin

A

(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

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69
Q
A
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70
Q

kallikrein

A

forms vasodilator bradykinin to inc. bf to salivary glands

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71
Q

IGF-1 and 2

A

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

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72
Q

PP cells

A

in islet of langerhans

pancreatic polypeptide; inhibits enzyme and bicarb release

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73
Q

AMDR for adults

A

protein 10-35% (0.8 g/kg/day)

fat 20-35%

carbohydrates 45-65%

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74
Q

sequence of events in pharyngeal phase: (of swallowing)

A
  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
Q

hirschsprungs disease

A

congenital aganglionic megacolon - motor disorder of gut from failure of NC migration

76
Q

ghrelin

A

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
Q

omphalocele vs gastroschisis

A

omphalocele: intestine protrudes into covered umbilical cord
gastroschisis: structures not in peritoneal layer

78
Q

Fe absorption

A

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
Q

midgut development

A

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
Q

ID

A

gall bladder

looks like coral reef

81
Q

menkes disease

A

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
Q

heme catabolism (dietary vs non heme iron)

A

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
Q

colonic motor activtiy consists of:

A
  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
Q

primary vs secondary bile acids vs bile salts

A

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
Q

system B not

A

Na dependent neutral AA transporter (to transport specific AAs, others for specific acidic/basic AAs)

86
Q

fate of SCFA (>12 C) vs LCFA (<12 C)

A

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
Q

what is normal BAO?

normal MAO?

ratio?

A

1.5-2.5 mmol/hr

15-25 mmol/hr

ratio normally 1:5 (0.2)

88
Q

R protein (haptocorrin)

A

binds with B12 (cyanocobalamine) after B12 freed by pepsin

is partially digested by pancreatic enzymes, allowing intrinsic factor to bind B12

89
Q

what pathway does Ach stimulate?

A

Gαq → inc. Ca, stimulates the H K pump

stimulates M3 receptors on parietal cells and histamine releasing EC cells

90
Q

what creates the post prandial alkaline tide?

A

basolateral parietal cell HCO3 is exchanged for Cl

91
Q

chemoreceptor trigger zone (CTZ)

A

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
Q

adiponectin

A

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
Q

phasic vs. tonic contractions

A

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
Q

yellow arrow

A

in liver

hemocydrin - liver takes care of worn out RBCs. complexes of ferritin

95
Q

enterokinase

A

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
Q

pancreas development

A

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
Q

whats the diff between tone and tonus

A

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
Q

vitelline duct

A

connect gut stube to disappearing yolk sac (week 4)

99
Q

3 phases of gastric secretion:

A
  1. cephalic
  2. gastric
  3. intestinal
100
Q

what does excess DCA (deoxycholic acid) in the colon stimulate?

A

excess chloride secretion → secretory diarrhea

in short bowel syndrome, colitis, defective bile transporters, IBS

101
Q

red star

A

common bile duct

low columnar epithelium

102
Q

what is BAO/MAO in duodenal ulcers?

Zollenger-Ellison syndrome?

gastric ulcer

atrophy/pernicious anemia

A

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
Q

biotin

reactions its used for, deficiency disease/cause, source

A

(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
Q

what is key ENS transmitter?

A

serotonin (5HT); stim. by stretch receptors/efferent vagal stimulation

in front of bolus, inhibits circular muscle and stimulates longitudinal muscle contraction

105
Q

what do D (delta) cells release and what does that do?

A

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
Q

hepatic zone 1 vs zone 3

A

zone 1 higher O2 and toxin content

107
Q

salivary amylase (ptyalin)

A

begins starch digestion

108
Q

GLP-1

A

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
Q

2 fates of Fe2+ once it enters the cell

A
  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
Q

ito cell / hepatic stellate cell

A

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
Q

bile salt dependent vs independent fractions

A

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
Q

what neurons are in the arcuate nucleus, and how do they differ?

A
  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
Q

lateral hypothalamus

A

dopamine

stimulates hunger

114
Q

types of capillaries in pancreas

A

endocrine pancreas (islets) - fenestrated

exocrine pancreas (acini/ducts) - non fenestrated

115
Q

xeropthalmia

A

differentiation of epithelium (due to retinoic acid)

116
Q

GLP-1

A

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
Q

how is dietary Ca absorbed

A

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
Q

retropulsion

A

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
Q

what is ferroxidase

A

converts Fe2+ →Fe3+

in enterocytes = hephaestin

in hepactocytes/macrophases = ceruloplasmin

120
Q

bile secretion

A

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
Q

types of diarrhea (2)

A
  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
Q

thiamine:

reactions its used for, deficiency disease/cause, source

A

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
Q

what is potentiated secretion?

A

stimulation of 2 secretory pathways:

Gastrin-Ach pathway via Gαq GTP binding protein

histamine pathway via Gαs

124
Q

vitamin E (α tocopherol)

reactions its used for, deficiency disease/cause, source

A
  • 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
Q

why is vitamin C used in septic shock?

A
  • 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
Q

what is the principal activity of the small and large bowel?

A

NaCl and water resporption (97.8% recovery) - jejunum is major site for water, electrolyte, nutrient

127
Q

ghrelin

A

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
Q

how are SM cells joined to one another

A

physically - intermediate junctions

electrically - gap junctions

129
Q

where does gastric lipase come from and what does it do?

A

from chief and mucous neck cells of fundus

hydrolyzes 15-20% of dietary lipid

130
Q

what things stimulate 5HT1 and D2 receptors?

A

(emesis)

vestibular system by inappropriate mtion/infections

131
Q

where is R protein and what does it do

A

saliva; for B12 absorption

132
Q

4 mechanisms to control the GI tract

A
  1. ENS
  2. endocrine
  3. paracrine
  4. SUVSM
133
Q

NaK2Cl transport (NKCC1)

A

in ileum, colon and crypt cells

electroneutral

134
Q

ID

A

pancreatic islet

pale with lots of BV

135
Q

where are bile salts recovered

A

ileum; Na coupled transporter into enterocyte

136
Q

what molecules inhibit precapillary sphincter smooth muscle, opening capillaries?

A

PaCO2 and adenosine

137
Q

BMI calculation

A

weight/(height)^2

kg/(m)^2

<18.5 = underweight

18.5-24.9 = desired weight

25-29.9 = overweight

>30 = obese

138
Q

CFTR

A

cystic fibrosis chloride channel on apical side of pancreatic duct cell

allows lumen to be flushed - maintains electro and osmoneutrality. without ⇒ pancreatitis

139
Q

primary peristaltic wave

A

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

140
Q

where are the ICCs int he stomach

A

body

141
Q

what pathway is for the secretion of mucus

A

COX-1, stimulates PGE3 → mucus secretion

142
Q

D1 cell

A

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

143
Q

somatostatin

A

released by delta cells in response to glucagon and elevated BGL, inhibited by insulin

*acts paracrine to inhibit insulin and glucagon

144
Q

what regulates centroacinar cells?

A

secretin (HCO3 release)

145
Q

adaptive thermogenesis

A

metabolic adaptation to weight changes - changes in energy expenditure

10% reduction ing body weight accompanied by 20-25% decline in energy expenditure

146
Q

cobalamin

reactions its used for, deficiency disease/cause, source

A

(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
147
Q

what is pepsin activated by?

A

HCl

148
Q

what gets absorbed in the:

  • duodenum
  • jejunum
  • ileum
  • colon
A
  • 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)
149
Q

black arrows

A

kupffer cells (liver macrophages)

come from monocytes from BM, differentiate in target tissues. are APCs with MHC II, secrete cytokines and chemokines

150
Q

N balance equation

A

N balance = intake - excretion

intake = .16 x itake

positive N balance in pregnancy, low in sepsis

151
Q

what is derived from lateral mesoderm

A

Ct and viscera tissue, serous membranes

152
Q

of the LES:

what is the function?

innervation?

A

function: prevent material in stomach from refluxing back into esophagus

inn: efferent vagal inn is inhibitory

153
Q

two stage hypothesis

A

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)

154
Q

fats preferentially release

A

CCK (an enterogastrone) from I cells

155
Q

what does histamine stimulate and where does it come from?

A

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)

156
Q

acalasia

A

lack of receptive relaxation at the LES; if ENS or vagus doesn’t work. causes regurguitation/mega esophagus

157
Q

brown adipose (and mechanism?)

A

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

158
Q

lingual gland lipase

A

iniitates lipid digestio of 10% of ingested fat (important when intenstinal digestion abnormal)

159
Q

gastritis

A

inflammation of gastric mucosa - sometimes by H. pylori, sometimes by NSAIDs

160
Q

pelvo-pelvic reflex

A

required for voiding; stimulus increased (>18 mmHg) from stretching colonic and rectal receptors

161
Q

what nerve mediates receptive relaxation

A

vagus

162
Q

where are retinyl esters mainly absorbed

A

upper duodenum

163
Q

when is hepcidin released? what does it do? what is the control paradigm?

A

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

164
Q

glucagon

A

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)

165
Q

ventromedial hypothalamus

A

serotonin

stimulates satiety

166
Q

erythroferrone

A

suppresses hepcidin expression in the liver to generate enough/sufficient RBC

167
Q

secretory acinar cells vs centroacinar cells (pancreas)

A

secretory acinar cells make exocrine secretions

centroacinar cells make bicarb - reg. by secretin

168
Q

GERD

A

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

169
Q

talk about IBP and what it does in high and low iron states

A

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

170
Q

how do ICCs depolarize SUVSM

A

open LTCCs

depolarizations due to increases in gCa, gNa, and decreased gK

171
Q

calponin and caldesmin

A

interfere with actin phosphorylation, inc. rate of relaxation

172
Q

peptide YY (PYY)

A

from L cells in lower intestine, co-releasd with GLP-1 to inhibit NPY/AgRP and stimulate POMC (anorexogenic)

173
Q

choleretic effect

A

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

174
Q

progression of bilirubin

A

bilirubin (70% from heme products) → *bilirubin → conj. with glucuronic acid → urobilinogen → stercobilinogen → stercobilin (colors feces)

*by bilirubin reducatase

175
Q

water transport digestive vs interdigestive period

A

digestive period: 2/3 paracellular, 1/3 transcellular

interdigestive period: 1/3 paracellular, 2/3 transcellular

176
Q

stool osmotic gap

A

differentiates secretory from osmotic diarrhea

SOG = [290-(stool Na + stool K)]

normal = 100-150

secretory = <100

osmotic = >150

177
Q

angiotensinogen

A

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

178
Q

disaccharides: trehalose, lactose, sucrose

A

trehalose: 2 glucose molecules joined
lactose: galactose and glucose
sucrose: fructose and glucose

179
Q

steric hindrance of bile salts

A

there is steric hindrance to bile salts and pancreatic lipase, gets overcome by pancreatic co-lipase

180
Q

spleen development

A

grows in dorsal mesogastrium posterior to stomach, suspended by gastrolienal ligamtand and lienorenal ligament

181
Q

diarrhea

A

inappropriate increases in fecal water content

182
Q

hepatic (portal) acinus

A

smallest functional unit, is a rhombus with PT on short edges, CVs on long edges

183
Q

vitamin K (phylloquinone K1 or menaquinones K2)

reactions its used for, deficiency disease/cause, source

A
  • 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
184
Q

succus entericus

A

secretions from the SI mucosa and mucosal glands

Block 4: GI, Repro, Endocrine, Skin (2 decks)

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