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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
(that is # that is most sensitive to recently having eaten something
TG | measure of sugar in the diet (that is # that is most sensitive to recently having eaten something)
26
transportation of TG to mitochondria occurs on
carnitine Hydrolysis of FA
27
Fatty acid depends on _______to split acetyl CoA
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
28
what organ is responsible for ketone production? how does this occur?
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
29
fat sparing energy source
carbs
30
Carbs provide/builds _______ stabilizing TG, little FFA available
Carbs provide/builds alpha glycerophosphate stabilizing TG, little FFA available
31
how is AA moved in and out of the cell
facilitated transport
32
how does the body utilize proteins for energy
a. Deamination in liver (Removal of amino group) transamination or shifting of amino group nitrogen removed by demamination into urea
33
appendx is retro or intra peritoneal?
retroperitoneal and contains all layers of the cecum
34
common infections of the appendix
usually ficolith CMV, adenovirus, histoplasmosis, collagen vascular dz, IBD
35
average age of appendicitis
Average age 10-30 yrs Occurs in 10% of population, 20% have perforation and peritonitis: high fever, abdominal pain, leukocytosis
36
MCC of pancreatitis
``` 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
how does pancreatitis present
Epigastric pain, radiates to back - "boring" pain releaved with leaning forwards fetal position N /V/F
38
Labs for the pancrease
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
grave outcome for pancreatitis seen with these symptoms
Severe hypovolemia, ARDS, tachycardia > 130= grave outcome
40
Ranson Criteria for poor outcomes (IMPORTANT)
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
dx test of choice for pancreatitis
abd CT abd ULS to rule out gallstones
42
tx of acute pancreatitis
usually supportive NPO and IV fluid restriction with analgesics ERCP if biliary suspicion
43
how to interprit ransons
greater than 3 likely 0-2: 2% mort 3-4: 15% 5-6 40% 7-8 100%
44
pathophysiology of pancreatitis
acinar injury that leads to intracellular activation of pancreatic enzymes and auto-digestion this leads to edema and hemorrhage
45
PE for pancreatitis
epigastric tenderness decreased bowel sounds due to adynamic ileus tachycardia dehydration if shock
46
cullen's sign
burising around the belly button that is indicative of pancreatitis
47
grey turner
bruising around the flank that is consistent with acute pancreatitis
48
when do we usually see a rise in amylase with pancreatitis
6-12 hours rise in lipase seen 4-8 hours
49
which cells are responsible for secretions of enzymes in the pancrease
acinar this occurs through injury to pro enzymes in the duodenum or direct injury to the cells themselves
50
to digest a meal zymogens are released into the pancreatic duct and delivered to the SI where they are activated by
trypsin (active) trypsinogen (inactive) activated in the duadenum
51
describe the pathophysiology of alcohol abuse and pancreatitis
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
gallstone cause pancreatitis
gallstones block reaction of pancreatic juices
53
complications of acute pancreatitis
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
triad of chronic pancreatitis
calicifications steatorrhea DM 20% of pts
55
chronic pancreatitis dx
AXR calcified pancreas mangement is pancreatic enzymes and no ETOH 2% cancer no elevated enzymes
56
alpha-glycerophosphate role
role in stabilization of triglyceride (glycolysis step)
57
what will your alpha-glycerophosphate levels going to be if you're active vs inactive
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
albumin interaction with FA
Fatty acids released from triglycerides ionize in plasma, bind albumin through ionized portion
59
other than binding to protein how else are fatty acids mobilized
Esters of glycerol can move in the bloodstream Cholesterol can move in the bloodstream If liver failure, then hard to do fat metabolism
60
density when talking about fat refers to
Density refers to protein content
61
high protein, less TG & cholesterol
High density lipoprotein
62
(that is # that is most sensitive to recently having eaten something
TG | measure of sugar in the diet (that is # that is most sensitive to recently having eaten something)
63
transportation of TG to mitochondria occurs on
carnitine Hydrolysis of FA
64
Fatty acid depends on _______to split acetyl CoA
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
what organ is responsible for ketone production? how does this occur?
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
fat sparing energy source
carbs
67
Carbs provide/builds _______ stabilizing TG, little FFA available
Carbs provide/builds alpha glycerophosphate stabilizing TG, little FFA available
68
how is AA moved in and out of the cell
facilitated transport
69
how does the body utilize proteins for energy
a. Deamination in liver (Removal of amino group) transamination or shifting of amino group nitrogen removed by demamination into urea
70
appendx is retro or intra peritoneal?
retroperitoneal and contains all layers of the cecum
71
common infections of the appendix
usually ficolith CMV, adenovirus, histoplasmosis, collagen vascular dz, IBD
72
average age of appendicitis
Average age 10-30 yrs Occurs in 10% of population, 20% have perforation and peritonitis: high fever, abdominal pain, leukocytosis
73
MCC of pancreatitis
alcohol abuse and cholelithiasis. Others include hypercholsterolemia, trauma, PUD, hypercalcemia,
74
how does pancreatitis present
Epigastric pain, radiates to back - "boring"
75
Labs for the pancrease
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
grave outcome for pancreatitis seen with these symptoms
Severe hypovolemia, ARDS, tachycardia > 130= grave outcome
77
Ranson Criteria for poor outcomes (IMPORTANT)
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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