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GI > Metabolism > Flashcards

Metabolism Flashcards

1
Q

how many calories are there per a phosphate bond

A

12,000 calories per phosphate bond

Every time you liberate a phosphate, you give off that much energy

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2
Q

only thing we start to break down in our mouth chemically

why is this the case

A

carbs

Have to break down carbs into glucose, fructose, or galactose and get it in the glycolytic pathway to -

Motherload of ATP

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3
Q

what role do carbs play in the Krebs cycle

A

form pyruvate and acetyl CoA and ultimately the ETC which is where we make huge amounts of ATP.

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4
Q

what role do fats play in the Krebs cycle

A

You can take fats and break them down to long chains of fatty acids (long chains of carbons on a glycerol backbone) and then break those chains down, break off 2 carbon blocks from that - that’s acetyl CoA (dump it into the citric acid cycle and ETC and convert fat for energy

no preferred

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5
Q

what role do proteins play in the Krebs cycle

A

macronutrient; important ingredient for us to build up amino acids for the construction of proteins

Not a very effective energy source b/c not very efficient

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6
Q

how do most cells transport glucose

A

c. Active cotransport with sodium in gut, most somatic cells use facilitated diffusion to move glucose

The gut uses ATP to move glucose out of the gut

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7
Q

what are Glucokinase and hexokinase responsible for

A

converting to Glucose-6-phosphate to sequester and traps the glucose molecule in the cell and polarity around the membrane repels it so it stays in the cytoplasm

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8
Q

what occurs with sugars if metabolically active

what happens if you’re not metaboliccaly active

A

If metabolically active, you will run the sugars through the glycolytic pathway and then through the krebs cycle. If not, then will store the sugar molecule as glycogen

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9
Q

what’s the benefit of it being a 10-step process?

A

you convert more of that energy that you liberate to make ATP. When you metabolize sugar, you lose energy to heat.

40-60% of energy in the glucose molecule is lost to heat (to the process)
If you did it all at once, it would be worse

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10
Q

Every time you release CO2, the enzyme

A

decarboxylase enzyme

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11
Q

where does Oxidative Phosphorylation occur

A

Occurs in mitochondria membrane

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12
Q

describe oxidative phosphorylation

A

in the mitochondrial membrane electrons are moved down the chain and then using that energy/current from flow of protons in complex 5 to generate enough of an energy release to put a phosphate on an ADP and store that as 12,000 calories

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13
Q

describe the different forms of lipids

A

neutral TG

phospholipids and cholesterol

can be saturated

monounsaturated
or polyunsaturated

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14
Q

one double bond in a carbon chain is indicative of what kind of fat

A

monosaturated fat

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15
Q

how are lipids transported

A

Enter lymph as TG in chylomicrons

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16
Q

role of apo b in lipid transport

A

Apoprotein B adsorbed to surface with protein projecting into aqueous medium providing stability to the chylomicron

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17
Q

Lipoprotein lipas acts on TG where

A

Lipoprotein lipase in adipose and liver hydrolyzes TG at endothelium

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18
Q

what happens after the hydrolization of TG by lipoproteins

A

Fatty acids from the hydrolyzed triglyceride absorbed and reconstituted into TG

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19
Q

alpha-glycerophosphate role

A

role in stabilization of triglyceride (glycolysis step)

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20
Q

what will your alpha-glycerophosphate levels going to be if you’re active vs inactive

A

If you are active and doing a lot of oxidative phosphyraltion, your alpha glycerophosphate are going to be low and your TG are going to be less stable and easier to break fat down.

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21
Q

albumin interaction with FA

A

Fatty acids released from triglycerides ionize in plasma, bind albumin through ionized portion

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22
Q

other than binding to protein how else are fatty acids mobilized

A

Esters of glycerol can move in the bloodstream

Cholesterol can move in the bloodstream

If liver failure, then hard to do fat metabolism

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23
Q

density when talking about fat refers to

A

Density refers to protein content

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24
Q

high protein, less TG & cholesterol

A

High density lipoprotein

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25
Q

(that is # that is most sensitive to recently having eaten something

A

TG

measure of sugar in the diet (that is # that is most sensitive to recently having eaten something)

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26
Q

transportation of TG to mitochondria occurs on

A

carnitine

Hydrolysis of FA

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27
Q

Fatty acid depends on _______to split acetyl CoA

A

c. Fatty acid depends on beta oxidation to split acetyl CoA

Acetyl CoA dumped into citric acid cycle and you can support ATP production that way

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28
Q

what organ is responsible for ketone production?

how does this occur?

A

e. Liver can convert acetyl coA to acetoacetic acid for transport (ketone production)

when we are starving, then ketones become the byproduct of fatty acid metabolism. It is a threat in DM patients b/c they can become ketoacidotic

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29
Q

fat sparing energy source

A

carbs

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30
Q

Carbs provide/builds _______ stabilizing TG, little FFA available

A

Carbs provide/builds alpha glycerophosphate stabilizing TG, little FFA available

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31
Q

how is AA moved in and out of the cell

A

facilitated transport

32
Q

how does the body utilize proteins for energy

A

a. Deamination in liver
(Removal of amino group)

transamination or shifting of amino group

nitrogen removed by demamination into urea

33
Q

appendx is retro or intra peritoneal?

A

retroperitoneal and contains all layers of the cecum

34
Q

common infections of the appendix

A

usually ficolith

CMV, adenovirus, histoplasmosis, collagen vascular dz, IBD

35
Q

average age of appendicitis

A

Average age 10-30 yrs

Occurs in 10% of population, 20% have perforation and peritonitis: high fever, abdominal pain, leukocytosis

36
Q

MCC of pancreatitis

A 
Idiopathic
Gallstones
ETOH
Trauma (knife)
Steroids
Mumps infx
Autoimmune dz
Scorpion! 
Hyper-tryglyceride hylercalcemia 
ERCP
Drugs (sulfa and reverse transcriptase inhibitors an protease inhibitors)
37
Q

how does pancreatitis present

A

Epigastric pain, radiates to back - “boring”

pain releaved with leaning forwards

fetal position

N /V/F

38
Q

Labs for the pancrease

A

Amylase - made by salivary gland (ULN X3)

Lipase (more sensitive b/c liver makes it)

Liver enzymes with biliary obstruction (3X suggest gallstone pancreatitis)

WBC elevated as pancreatic cells degrade

Mild hyper bilirubinuria, hyperglycemia, hypocalcemia

39
Q

grave outcome for pancreatitis seen with these symptoms

A

Severe hypovolemia, ARDS, tachycardia > 130= grave outcome

40
Q

Ranson Criteria for poor outcomes (IMPORTANT)

A

admission:

G: >200mg/dL
A: >55
L: LDG: >350 IU/L;
A: >250 
W: WBC >16,000

within 48 hours

Ca <8
Hemato >10%
Oxygen<60
BUN >5
Base deficit >4
Sequestration of fluid >6L

GA
LAW

cows down (Ca decreased due to fat necrosis )

blood down
oxygen down
base down
fluid up

41
Q

dx test of choice for pancreatitis

A

abd CT

abd ULS to rule out gallstones

42
Q

tx of acute pancreatitis

A

usually supportive NPO and IV fluid restriction with analgesics

ERCP if biliary suspicion

43
Q

how to interprit ransons

A

greater than 3 likely

0-2: 2% mort
3-4: 15%
5-6 40%
7-8 100%

44
Q

pathophysiology of pancreatitis

A

acinar injury that leads to intracellular activation of pancreatic enzymes and auto-digestion

this leads to edema and hemorrhage

45
Q

PE for pancreatitis

A

epigastric tenderness decreased bowel sounds due to adynamic ileus

tachycardia

dehydration if shock

46
Q

cullen’s sign

A

burising around the belly button that is indicative of pancreatitis

47
Q

grey turner

A

bruising around the flank that is consistent with acute pancreatitis

48
Q

when do we usually see a rise in amylase with pancreatitis

A

6-12 hours

rise in lipase seen 4-8 hours

49
Q

which cells are responsible for secretions of enzymes in the pancrease

A

acinar

this occurs through injury to pro enzymes in the duodenum or direct injury to the cells themselves

50
Q

to digest a meal zymogens are released into the pancreatic duct and delivered to the SI where they are activated by

A

trypsin (active)

trypsinogen (inactive)
activated in the duadenum

51
Q

describe the pathophysiology of alcohol abuse and pancreatitis

A

alcohol increase productions of enzymes and decrease production of bicarb and fluid
leading to thick pancreatic juices and blocked ducts

backed up juices and distension

causes the enzymes to come in contact with zymogens

and they become activated trypsin

auto-digestion

ETOH also stimulate acinar to release inflammatory cytokines and immune creations

52
Q

gallstone cause pancreatitis

A

gallstones block reaction of pancreatic juices

53
Q

complications of acute pancreatitis

A

swelling, digestion, bleeding

liquefactive hemorrhagic necrosis

or pancreatic pseudocysts (fills up with juice)

ARDS
leaky blood vessels hard to breath LCD with acute pancreatitis

54
Q

triad of chronic pancreatitis

A

calicifications
steatorrhea
DM

20% of pts

55
Q

chronic pancreatitis dx

A

AXR calcified pancreas
mangement is pancreatic enzymes and no ETOH

2% cancer

no elevated enzymes

56
Q

alpha-glycerophosphate role

A

role in stabilization of triglyceride (glycolysis step)

57
Q

what will your alpha-glycerophosphate levels going to be if you’re active vs inactive

A

If you are active and doing a lot of oxidative phosphyraltion, your alpha glycerophosphate are going to be low and your TG are going to be less stable and easier to break fat down.

58
Q

albumin interaction with FA

A

Fatty acids released from triglycerides ionize in plasma, bind albumin through ionized portion

59
Q

other than binding to protein how else are fatty acids mobilized

A

Esters of glycerol can move in the bloodstream

Cholesterol can move in the bloodstream

If liver failure, then hard to do fat metabolism

60
Q

density when talking about fat refers to

A

Density refers to protein content

61
Q

high protein, less TG & cholesterol

A

High density lipoprotein

62
Q

(that is # that is most sensitive to recently having eaten something

A

TG

measure of sugar in the diet (that is # that is most sensitive to recently having eaten something)

63
Q

transportation of TG to mitochondria occurs on

A

carnitine

Hydrolysis of FA

64
Q

Fatty acid depends on _______to split acetyl CoA

A

c. Fatty acid depends on beta oxidation to split acetyl CoA

Acetyl CoA dumped into citric acid cycle and you can support ATP production that way

65
Q

what organ is responsible for ketone production?

how does this occur?

A

e. Liver can convert acetyl coA to acetoacetic acid for transport (ketone production)

when we are starving, then ketones become the byproduct of fatty acid metabolism. It is a threat in DM patients b/c they can become ketoacidotic

66
Q

fat sparing energy source

A

carbs

67
Q

Carbs provide/builds _______ stabilizing TG, little FFA available

A

Carbs provide/builds alpha glycerophosphate stabilizing TG, little FFA available

68
Q

how is AA moved in and out of the cell

A

facilitated transport

69
Q

how does the body utilize proteins for energy

A

a. Deamination in liver
(Removal of amino group)

transamination or shifting of amino group

nitrogen removed by demamination into urea

70
Q

appendx is retro or intra peritoneal?

A

retroperitoneal and contains all layers of the cecum

71
Q

common infections of the appendix

A

usually ficolith

CMV, adenovirus, histoplasmosis, collagen vascular dz, IBD

72
Q

average age of appendicitis

A

Average age 10-30 yrs

Occurs in 10% of population, 20% have perforation and peritonitis: high fever, abdominal pain, leukocytosis

73
Q

MCC of pancreatitis

A

alcohol abuse and cholelithiasis. Others include hypercholsterolemia, trauma, PUD, hypercalcemia,

74
Q

how does pancreatitis present

A

Epigastric pain, radiates to back - “boring”

75
Q

Labs for the pancrease

A

i. Amylase - made by salivary gland
ii. Lipase (more sensitive b/c liver makes it)
iii. Liver enzymes with biliary obstruction
iv. WBC elevated as pancreatic cells degrade
v. Mild hyper bilirubinuria, hyperglycemia, hypocalcemia

76
Q

grave outcome for pancreatitis seen with these symptoms

A

Severe hypovolemia, ARDS, tachycardia > 130= grave outcome

77
Q

Ranson Criteria for poor outcomes (IMPORTANT)

A

i. Leukocytosis >16k
ii. Glucose >200
iii. LDH 350
iv. AST 230
PO2 <60
v. Base deficit >4
vi. Calcium Falling
vii. BUN Rising
viii. The more criteria they meet, the worse their prognosis

GI (13 decks)

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