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Block 1 > Cell Bio 3 > Flashcards

Cell Bio 3 Flashcards

1
Q

characteristics of ETOH

A

lipid and water soluble, absorbed in GI tract via passive diffusion –> metabolized in liver –> becomes acetaldehyde via alc dehydrogenase in cyto –> acetaldehyde to acetate via acetaldehyde dehydrogenase in mito –> NADH produced to go to ETC to make ATP

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2
Q

acetaldehyde vs acetate in blood

A

low levels in blood = fine, high chronic levels = bad b/c toxic intermediate (ROS) vs enters blood –> taken up by muscle and other tissues –> acetyl CoA go to TCA

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3
Q

acute vs chronic alc effects

A

inc NADH/NAD+ ratio (for q ETOH –> you make NADH) –> inhibits TCA –> FA catabolism to acetyl CoA –> excess acetyl CoA –> ketone bodies –> ketogenesis –> ketoacidosis; inc NADH –> inhibits FA [O] –> FA synthesis –> TAG –> VLDL –> hyperlipidemia; inc NADH –> pyru to lactate –> inhibits gluconeogenesis –> lactic acidosis, hypoglycemia; inc NADH –> inhibits glycolysis –> hyperglycemia. REVERSIBLE EFFECTS vs alc-induced liver dz, alc-induced hepatitis, hepatic steatosis aka fatty liver, cirrhosis, inc acetald and free radicals. IRREVERSIBLE EFFECTS

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4
Q

Class I alc dehydrogenase (ADH)

A

highest affinity to ETOH, located in liver, ETOH –> acetald + 1 NADH

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5
Q

ALDH I vs II

A

in cyto, picks up excess acetald vs in mito, [O] 80% of acetald to acetate and makes 1 NADH

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6
Q

Microsomal Ethanol Oxidizing System (MEOS)

A

[O] ETOH to acetald w/o making NADH in cyto –> make more ROS and acetald –> bad; binds to ETOH if [ETOH] = high; part of liver detox

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7
Q

cytochrome P450

A

can release more superoxide if induced by drugs, alc, chemical toxins (b/c superoxide can escape); O2 binds to Fe center and takes 1 e- from Fe –> superoxide binds w/ substrate

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8
Q

how much ATP = gained w/ ADH/ALDH vs MEOS?

A

12 ATP + 1 GTP per ETOH oxidized vs 7 ATP + 1 GTP

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9
Q

how can acetald dmg body?

A

bind to glutathionine –> cell loses primary defense mechanism; bind to free radical defense proteins –> inactivates them; dmgs ETC –> uncouples ETC from ATP synthase –> no FA [O] –> FA inc; dmg ALDH –> inc acetald levels (vicious cycle)

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10
Q

endogenous toxicants

A

toxic agents produced inside body, may be harmful as xenobiotics; caused by inborn error of metabolism (protein structure-fxn error d/t gene abnmllity)

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11
Q

liver detox has 2 phases

A

Phase I: [O], [H], or hydrolysis = bioactivation; carried out by cyt P450 mixed-fxn oxidases; prepares cmpds for phase II rxns
Phase II: conjugation w/ H2O soluble molec; specific rxns w/ specific enzymes; allows excretion via blood-kidney-urine or bile-feces

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12
Q

CYP2B1/2

A

phenobarbitol inc CYP2B2 –> ppl have dec sensitivity to phenobarbitol –> they take more. ethanol = inhibitor of CYP2B1/2 so if you take phenobarbitol + ethanol –> dec phenobarbitol metab –> high lvls of barbituates in blood

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13
Q

liver vs muscle w/ glycogen

A

controls blood glu lvl, can break down glycogen whenever vs keeps glycogen for its own use (not released in blood), lots of glycogen for fast twitch muscles

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14
Q

liver vs muscle w/ fasting

A

liver has 12-24hr glycogen supply during fasting, completely depleted post 30hrs; glycogen degraded to glu vs glycogen degraded to G1P to G6P for glycolysis –> muscle ctx and meet ATP demands

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15
Q

glycogen structure

A

branched glu polysacch (alpha1,4 w/ branched alpha1,6 q 8-10 residues); only has 1 reducing end and it’s attached to glycogenin protein, nonreducing end attaches to the glu; branching allows for tight packing of glu, rapid synth/degrad, mult enzymes working at same time

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16
Q

in glycolysis, glu = phosphorylated to G6P by hexokinase

A

PHOSPHORYLATED –> traps glu in cell

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17
Q

hexokinase vs glucokinase

A

in tissue (liver & skel muscle), higher affinity for glu –> do glycolysis even if [glu] = low vs in liver and pancreatic beta cells, lower affinity for glu –> do glycolysis when [glu] = high

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18
Q

glycogen degrad in liver vs muscle (specific process)

A

nor/epi or glucagon –> inc glycogenolysis –> activate glycogen phosphorylase and debranching enzyme –> G6Pase (only present in liver & kidney) deP G6P –> glu vs glycogen breaks down to G1P via glycogen phosphorylase –> G1P to G6P via phosphoglucosemutase –> G6P goes glycolysis to make ATP; AMP and nor/epi = big signal for glycogen degrad in fast twitch (glucagon does nothing)

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19
Q

debranching enzyme

A

4:4 transferase activity (break alpha1,4), or 1,6 glucosidase activity (break alpha1,6)

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20
Q

signal transduction by glucagon

A

operates via cAMP-directed phosphorylation cascade: glucagon receptor is G-protein-coupled –> activates adenylate cyclase –> cAMP prod –> cAMP binds to inactive PKA –> activates PKA –> PKA phosphorylates target proteins –> phosphorylates glycogen synthase => inactive –> stops glycogen synthesis OR phosphorylates glycogen phosphorylase => active –> starts glycogen breakdown

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21
Q

signal transduction by insulin

A

operates via tyrosine kinase activated phosphorylation cascade: insulin receptor autophosphorylates –> activates its kinase activity and phosphorylates targets –> phosphorylated targets activate phosphatase –> phosphatase dephosphorylates glycogen synthase –> start glycogen synthesis/stop glycogen breakdown

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22
Q

glycogen phosphorylase a vs glycogen phosphorylase b. glycogen synthase I/a vs glycogen synthase D/b

A

when glycogen phosphorylase = phosphorylated/active vs when glycogen phosphorylase = not phosphorylated/inactive. when glycogen synthase = not phosphorylated/active vs when glycogen synthase = phosphorylated/inactive

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23
Q

exer for glycogen degrad

A

muscle contraction –> ATP to ADP –> adenylate cyclase –> cAMP –> PKA –> phosphorylates glycogen phosphorylase –> glycogen breakdown

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24
Q

epinephrine on metab

A

signals for more glu need for brain, blood, muscle -> similar effects of glucagon. Epinephrine binds to β-adrenergic receptors (G couple protein receptor) or liver alpha receptors –> stimulates adenylate cyclase –> PKA activation –> glycogen degrad for more glu –> more ATP for quick rxn => f/light

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25
Q

glycogen storage dz vs therapy

A

inability to make/break glycogen nmlly –> pt’s liver can’t produce glu to release in blood –> hypoglycemia or muscle cramps d/t low energy vs small freq snacks to maintain glu (for liver); reduce exer or muscle fatigue to prevent cramps or supplement w/ higher dietary glu and aa (for muscle)

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26
Q

What does NADPH do?

A

key metabolite: help with FA synthesis, chol synthesis, neurotransmitter synthesis, nucleotide synthesis, glutathione defense system against ROS esp in RBC, NADPH oxidase uses NADPH to make superoxide –> help mac kill, drug detox

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27
Q

Irreversible (3) vs reversible (5) steps of PPP

A

oxidative phase: net 2 NADPH made, 1st and 3rd steps = inhibited by NADPH/activated by NADP+; G6P = [O] to 6-phosphogluco-delta-lactone via G6P dehydrogenase (rate limiting step) –> 6-phosphogluco-delta-lactone to 6-phosphogluconate –> 6-phosphogluconate = decarboxylated to Ru5P via 6-phosphogluconate dehydrogenase vs non-oxidative phase: Part 1 = 2 isomerizations of Ru5P and Part 2: pentose molec converted to glycolysis/gluconeogenesis intermediates

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28
Q

sucrose vs lactose vs maltose vs isomaltose

A

(glu-α-1,2-fru) vs (gal-β-1,4-glu) vs (glu-α-1,4-glu) vs (glu-α-1,6-glu)

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29
Q

fru metab mainly in liver vs other tissue. what happens if there is aldolase B defic?

A

fru = phosphorylated at C1 by fructokinase using 1 ATP –> F1P = cleaved by aldolase B to make DHAP + glyceraldehyde (if defic in aldolase B –> F1P inc –> bad) –> glyceraldehyde = phosphorylated by triose kinase and used 1 ATP –> G3P vs fru = phosphorylated at C6 by hexokinase to make F6P to do glycolysis. aldolase B defic –> high F1P –> bad –> ppl need to avoid fru

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30
Q

how to make fru from glu?

A

glu = reduced to sorbitol –> sorbitol = oxidized at C2 to make fru

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31
Q

gal metab

A

gal = phosphorylated at C1 by galactose kinase using 1 ATP to make gal1P –> gal1P reacts w/ UDP-glu to make G1P and UDP-galactose –> UDP galactose = converted to UDP-glu by epimerase

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32
Q

classical vs nonclassical galactosemia

A

can’t form UDP-gal or make molec dependent on UDP-gal –> gal1P inc in liver –> bad vs galactokinase = deficient or can’t be processed

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33
Q

fates of UDP-galactose

A

UDP-gal and UDP-glu help w/ synthesis of glycoproteins, glycolipids & proteoglycans; UDP =-gal also help form lactose in mammary gland

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34
Q

UDP-glucuronate

A

UDP-glu = oxidized to UDP-glucuronate –> has stable b/c of neg charge –> help inc solubility of molec it’s attached to; ex: bilirubin = insoluble but becomes soluble by adding 2 glucuronides. glucuronate can be modified to final form like GAGs or amino sugars

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35
Q

fed vs fasting vs starving state

A

glu from food enters blood via gut vs liver uses glycogen/precursor to make glu and send out to blood vs liver uses precursor (glycerol from adipose to FA, lactate from anaerobic glycolysis in muscle or RBC, aa from protein degrad in skel muscle esp ala) to make glu and send out to blood => gluconeogenesis

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36
Q

how does lactate vs ala become pyru? how does glycerol participate in gluconeo?

A

lactate to pyru via lactate dehydrogenase and NAD+ (becomes NADH when forming pyru) vs ala to pyru via ala transferase. glycerol to DHAP via glycerol kinase

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37
Q

1st bypass and its key point

A

PEP to pyru = irreversible –> can’t go pyru to PEP –> pyru to oxalo in mito via pyru carboxylase –> oxalo uses mal/asp shuttle to go to cyto –> oxalo to PEP via PEP carboxykinase + GTP. key point: can bypass irreversible step but requires energy

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38
Q

2nd bypass

A

FBP = dephosphorylated to F6P via FBPhosphatase –> F6P to G6P

39
Q

pos vs neg modulator for PFK-1

A

high AMP, F2,6P, insulin vs high ATP

40
Q

3rd bypass

A

G6P = dephosphorylated to glu via G6Phosphatase, rxn = inside ER lumen

41
Q

where to do glycogenolysis vs gluconeo?

A

liver does glycogenolysis to make glu for body, muscle does glycogenolysis to make glu for itself vs brain and RBC does gluconeo to make glu for blood stream

42
Q

what happens if there is excess glu?

A

liver makes glycogen and FAs, adipose takes FA and stores as TAGs; muscle makes glycogen

43
Q

describe need/intake relationship

A

intake > need –> wt gain
intake < need –> wt loss

44
Q

simple vs complex carbs. examples of dietary carbs

A

digest quickly, mono (glu, fru, gal), disacch (su, lac, malt) vs digest slowly, oligo/polysacch (starch, glycogen, dietary fiber). fruits, starch, milk

45
Q

where do you get largest calories from?

A

carb (40-60%)

46
Q

3 classifications of starch: rapidly digestible vs slowly digestible vs resistant

A

rapid effects on blood glu lvl vs slower effects on blood glu lvl –> glu doesn’t rise fast enough vs more like nondigestible fiber than starch, glu homeostasis -> glu doesn’t rise fast enough, reduce postprandial inulin requirement

47
Q

carb digestions from where to where?

A

mouth (salivary alpha amylase breaks alpha1,4 glu bonds) thru stomach (HCl inactivates salivary alpha amylase) to sm intestines (pancreatic alpha amylase produces malt, isomalt, oligosacch)

48
Q

2 types of dietary fiber: soluble vs insoluble

A

dec transit time thru sm intestines (ie. moves faster) –> inc fecal bulk, help intestinal flow vs no effect on transit time thru sm intestines –> create gelatinous mold, delay gastric emptying, dec absorption of chol and glu, soft stool d/t H2O absorption

49
Q

recommended Nat’l Cancer Institute of fiber intake vs adult avg intake

A

25-38g/d vs 10g/d

50
Q

why is dietary fiber good for you?

A

slow sugar absorption –> slow rise in blood glu, promote good microbiota, bacteria breaks down complex carbs, uses monosacch for ATP prod, produces short chain FA

51
Q

glycemic index. higher vs lower

A

value for single food item based on how slowly or quick it causes an inc in blood glu lvls after eating, reference = usually white bread. higher glycemic response –> sugar high –> crash vs lower glycemic response –> less dramatic effect on blood glu

52
Q

Describe FA synthesis (in cyto)

A

Acetyl CoA can’t diffuse from mito to cyto, but citrate can. Citrate diffuses from mito to cyto —> citrate lyase breaks cit into acetyl CoA (starting material) and oxalo —> oxalo can be converted back to pyruvate and yield NADPH in the process. acetyl CoA carboxylase (irreversible/committed/rate limiting step), ATP, and CO2 converts acetyl CoA to yield malonyl CoA and ADP + Pi —> FA synthase + acyl carrier protein/ACP and 2 NADPH converts malonyl CoA to yield palmitic acid (C16H32O2), water, and CO2
cycle rpts 7x

53
Q

what happens if there is PPP defic?

A

malic enzyme can supply NADPH

54
Q

purpose of ACP?

A

malonyl CoA attaches to -SH of ACP

55
Q

pos vs neg regulation of acetyl CoA carboxylase

A

high insulin dephosphorylates enzyme –> active, high cit vs AMP-activated protein kinase phosphorylates enzyme –> inactive, high palmitoyl CoA

56
Q

what’s the issue w/ human desaturases? how can we add more 2x bonds?

A

can’t introduce 2x bonds after C10, and ONLY do them at C5/6/9. start w/ essential FA linoleic acid –> add 2x bonds as much as we can –> elongase will lengthen chain 2C’s at a time via malonyl CoA condensation and reduction –> add more 2x bonds as much as we can; happens in cyto face of ER

57
Q

fxns of chol vs sources of chol

A

stabilizes cell membrane, precursor for bile salts and steroids; can make ubiquinone, dolichol for glycoprotein synthesis, cholecalciferol (active vit D) vs from acetyl CoA in liver/intestine, from animal products like egg/red meats/liver

58
Q

describe chol synthesis (in cyto)

A

Acetyl CoA can’t diffuse from mito to cyto, but citrate can. Citrate diffuses from mito to cyto —> citrate lyase breaks cit into acetyl CoA (starting material) and oxalo —> oxalo can be converted back to pyruvate and yield NADPH in the process. 2 acetyl CoAs condense to make acetoacetyl CoA –> 3rd acetyl CoA added => HMG-CoA –> HMG-CoA reductase (committed/rate limiting) + 2 NADPH reduce HMG-CoA to mevalonate –> mevalonate to isopentenyl pyrophosphate to squalene

59
Q

pos vs neg regulation of HMG-reductase

A

high insulin –> phosphatase deP HMG-CoA reductase –> active –> HMG-CoA to mevalonate –> chol vs high glucagon –> AMP mediated protein kinase phosphorylates HMG-CoA reductase –> inactive –> no chol; high AMP/low ATP or high sterol –> HMG-CoA reductase = inactive

60
Q

describe transcpxn control of chol synthesis

A

in ER. high chol –> chol bind to SCAP –> SREBP inactive. low chol –> chol doesn’t bind to SCAP –> SREBP active –> S2P cleaves DNA binding domain of SREBP –> DNA transcpxn –> chol synthesis

61
Q

2 enzymes that esterify chol

A

Acyl:chol acyltransferase (ACAT) –> store chol for steroid synth, in cells. lecithin:chol acyltransferase (LCAT) –> esterifies chol associated w/ HDL, in blood. -OH group at C3 of chol = esterified to be FA –> inc hydrophobicity of chol –> inc solubility in lipoproteins

62
Q

describe bile acid/salt synthesis. CCK

A

bile acid/salt = more polar/hydrophilic than chol; emulsify dietary lipids in sm intestines for digestion; cyt P450 monooxygenase + NADPH and 7-alpha-hydroxylase incorporates -OH (committed/rate-limiting). cholecystokinin signals gallbladder to release bile

63
Q

primary vs secondary bile acid/salt

A

in liver and sent to gallbladder, has all hydroxy groups (3 for cholic acid, 2 for chenodeoxycholic acid) vs modified by gut bacteria, lack -OH at C7. lithocholic acid = only -OH at C3 –> least soluble –> excreted

64
Q

examples of steroid hormones. what is the starting material?

A

aldosterone, cortisol, estrone, estradiol. CHOL = STARTING MATERIAL; tissue dependent synthesis

65
Q

chylomicrons vs VLDL vs LDL vs HDL vs IDL

A

made in gut –> carry dietary TAG from intestine to peripheral/muscle/adipose tissue; deliver chol and phospholipids to liver; HAS APO B48 vs made in liver –> carry endogenously synthesized TAG, chol, and chol esters from liver to muscle/adipose tissue; smaller than chylomicrons –> higher density; HAS APO B100 vs low protein, high fat (chol + chol-esters) => low density; made from VLDL after TAG removed; deliver chol from liver to blood vs high protein, low fat => high density (smallest blood lipoprotein); deliver chol from blood to liver or esterify chol via LCAT to IDL vs as VLDL loses TAGs, they become intermediate density lipoproteins => smaller and higher protein –> high density –> IDL taken up by liver to become LDL or HDL

66
Q

LDL receptor. describe endocytosis of LDLs

A

recognizes apoE and apoB100 –> binds V/LDL, HDL, IDL, chylomicrons and bring them into cell by endocytosis to deliver chol/esters. receptor mediated process: endosome fuse w/ lysosome –> lipoprotein degraded to chol –> some chol move to ER or re-esterified to minimize chol in cell –> receptors = recycled to Golgi to plasma membrane

67
Q

HDL synthesis

A

in liver and intestine; apoA-1 made and released to blood –> recruits phospholipid and chol from tissues. liver makes other proteins HDL carries –> HDL picks up chol from tissue to make chol-ester via Cholesterol Ester Transferase Protein (CETP) and puts them deep in HDL particle –> returns to liver

68
Q

HDL in Reverse Chol Transport

A

nascent HDL made in liver and intestine –> HDL picks up chol in tissue –> chol = esterified via LCAT and moved to interior of HDL particle –> chol-esters can be converted to LDL or delivered to liver

69
Q

can HDLs be a protein reservoir?

A

yes in the blood; they provide apoproteins apoC-I/II/III and apoE to nascent HDLs and nascent chylomicrons

70
Q

how to atherosclerotic plaques form?

A

minor dmg to blood vessel wall –> macs = recruited and uptake LDLs –> macs = filled w/ lipids => foam cells –> foam cells accumulate –> chemical signals induce PLT aggregation –> clot forms –> cells take up more LDL –> fat builds up –> fibroblasts excrete fibrous proteins –> cells die and leave debris –> more macs recruited –> cycle rpts until blood vessel = blocked

71
Q

what are eicosanoids?

A

cmpds made from 20C FA; arachidonic acid = most common, prostaglandins (5C rings w/ 2x bond at C13&14), thromboxanes (6C ring, sometimes w/ O at C9 and C11), leukotrienes (3 2x bonds, sometimes w/ O bound as OH or epoxide)

72
Q

Arachidonic acid Liberation: Direct vs Indirect Pathway

A

AA bound to C2 of glycerophospholipid –> G protein receptor activated –> phospholipase A2 cleaves glycerol-FA ester at C2 –> free AA enters eicosanoid pathway w/n membrane environ vs G protein receptor activated –> phospholipase C –> IP3 –> Ca2+ enter IP3 channel in ER –> Ca2+ inc –> PLA2 –> cleaves glycerol-FA ester at C2 –> free AA enters eicosanoid pathway w/n membrane environ; if AA bound to DAG –> DAG lipase liberates it then AA goes to eicosanoid pathway

73
Q

cyclooxygenase 1 vs 2 vs 3

A

COX1 = constitutive enzyme in gastric mucosa, PLTs, vascular endothelium, kidneys vs COX2 = mainly expressed in macs –> inducible and made in inflamm response vs variant of COX1 –> does same fxn

74
Q

cyclooxygenase pathway

A

O2 = added to AA to make 5C ring PG via COX –> PG converted to other PGs or TXs. PGH2 can be converted to TXA2 via COX in thromboxane synthesis pathway. AA = MAIN SUBSTRATE, PGH2 = MAIN PRODUCT (AA MOSTLY LEADS TO SERIES 2)

75
Q

what makes PG/TX active vs inactive?

A

-OH attached to C15 vs peroxyl attached to C15 or -OH at C15 = [O] to ketone –> half life = seconds to minutes –> stops signal –> breakdown products excreted in urine

76
Q

lipoxygenase vs cyt P450 pathway

A

AA to HPETE via lipoxygenase by incorporating O2 molec to a C in a 2x bond –> HPETE = [H] to HETE, or metabolized to LT or lipoxins vs AA to epoxide –> epoxide to diHETE or HETE (prevalent in ocular, vascular, endo and renal system)

77
Q

how to name series of eicosanoids. example of series 1 vs 2 vs 3

A

look at 2x bonds in nonring portion of cmpd; # of 2x bonds = # of series. dihomo-gamma-linoleic acid vs AA vs eicosapentoanoic acid; DGLA and EPA compete w/ AA binding to COX (COX favors 1 & 3)

78
Q

how do NSAIDs vs acetaminophen vs SAIDs inhibit COX

A

mostly inhibit COX1 –> inhibit PG formation (ASA acetylate ser in active site; ibu binds competitively inhibits COX) –> dec pain/inflamm vs competitively inhibit COX –> dec pain but not inflamm. THEY STOP PG FORMATION VIA COX (IE. FREE AA CAN FORM OTHER EICOSANOIDS VIA OTHER PATHWAYS) vs inhibit PG formation by downregulating or inhibiting immune responses leading to inflamm

79
Q

how is ASA diff from other NSAIDs?

A

ASA covalently modifies COX1 of PLTs –> irreversibly inhibits TXA2 formation for the entire PLT life span (other NSAIDS noncovalently inhibit and will reverse as drug lvl drops)

80
Q

can NADH inhibit ADH and ALDH?

A

weak inhibitor tho

81
Q

lipoprotein lipase (LPL) vs hormone sensitive lipase (HSL)

A

in adipose and muscle (muscle has higher affinity to LPL –> use fat even if [fat] = low; adipose stores fat when [fat] = high); insulin/fed state –> protein receptor OUTSIDE of adipose/muscle cell binds to apoCII on micelle of chylomicron/VLDL –> protrudes into lipoprotein –> binds/takes TG –> TG hydrolyzed into 3 FAs and transported across membrane while glycerol goes to liver vs in adipose; glucagon/fasting –> G protein –> adenylate cyclase –> cAMP –> PKA –> HSL = phosphorylated => active INSIDE of adipose cell –> cleave TAG –> release FA and glycerol into blood –> albumin picks them up. insulin –> HSL = dephosphorylated => inactive

82
Q

why and how does adipose make TAG?

A

for storage; glu –> DHAP –> gly3P + FA via LPL –> TAG; can also do gluconeo to get DHAP and then make TAG from there. adipose doesn’t have glycerol kinase

83
Q

why does liver make and store FA and TAG?

A

liver can’t store fat; liver phosphorylates glycerol via glycerol kinase –> gly3P –> add 2 FA –> phosphatidic acid –> package it into VLDL –> go to Golgi –> released in blood –> go to adipose for storage or muscle for energy use

84
Q

sphingosine vs ceramide vs cerebroside vs ganglioside vs sphingomyelin

A

always located in membranes and myelin sheaths; NO glycerol backbone –> sphingosine backbone (palmitate + serine; palmitate w/ amino and alc group) vs sphingosine structure but amino group is amide (thanks to a fatty acid binding w/ amino group) vs 1 sugar bound to alc group vs mult sugars bound to alc group vs phosphate + N group bound to alc group

85
Q

sphingolipids are degraded by what?

A

lysosomes

86
Q

factors dec vs inc HDL

A

obesity/high TAG, inflamm, inactivity, smoking vs exer/loss of body fat, moderate alc consumption, estrogen

87
Q

MNT for cholelithiasis vs pancreatitis vs gastroparesis

A

eat high sat fat –> fat malabsorption –> gallbladder doesn’t ctx –> block bile release; fasting, wt cycling, and very low calorie diets inc likelihood; MNT includes high fiber, low fat, plant based diet to prevent gallbladder ctx vs acute: NPO, no enteral feeds –> IV fluids; PO feeds: low fat digestible foods, 6 sm meals/d, adeq protein and calories; if you can’t start PO w/in 5-7d –> tube feeding. chronic: oral diet or tube feeding vs delayed gastric emptying d/t vol, liquids v solids, fiber, fat, osmolarity, hyperglycemia; MNT: sm freq meals, avoid high sugar meals, low fiber intake, moderate to low fat diet

88
Q

lingual lipase vs pancreatic lipase vs esterase

A

impt for babies to digest milk fat, impt for adults to overtake bile salt fxn vs cofactor = colipase that both hydrolyze C1 and C3 of TAG to 2 free FA + 2-monoacylglycerol (more soluble than TAG) –> form mixed micelles w/ bile salts; hydrolyzes all FA chain lengths vs removes FA esterified w/ other cmpds (ex: chol-esters)

89
Q

micelles. what happens inside enterocyte?

A

contain chol, fat-soluble vit, monoglycerides, phospholipids, bile acids; travel to apical membrane of enterocytes; products of fat digestion enter cell by simple diffusion. TGs = remade (2 free FA + 2-monoacylglycerol) in SER, apoB48 made in RER –> micrsomal triglyceride transfer protein (MTTP) attaches TAG to apoB48 –> goes to Golgi –> TAG packaged to chylomicrons for transport thru lymph to thoracic duct (bypass liver)

90
Q

simple lipids vs complex lipids. fxns

A

FA, TG, wax vs phospholipids (sphingomyelins, plasma membrane), glycolipids, lipoproteins. energy prod, fat storage, structure like cell membrane, cofactors like vit

91
Q

MNT for surgically altered gut vs wt management vs ca vs insoluble fibers

A

avoid added sugars vs choose right carbs to feel fuller vs dietary fibers = preventative effect vs bind to fat soluble carcinogens and remove them from gut

92
Q

SGLT-1

A

coupled transport of glucose and galactose into cell

93
Q

what happens if PEP can’t become glu?

A

gluconeo fails

Block 1 (20 decks)

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