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Fundamentals of Patient Management > BSC Metabolism > Flashcards

BSC Metabolism Flashcards

1
Q

what are the 3 sections of the small intestine, their lengths, and characteristic features

A

1- duodenum, 10-12 inches, pyloric valve, arcs around head of pancreas, ends at duodenojejunal flexure/ junction
2- jejunum, 8ft, from duodenum to ileum
3- ileum, 12 ft, joins large intestine at ileocecal valve

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2
Q

what are the roles of the duodenum and ileum

A

d- receives stomach contents, pancreatic juice, and bile
i- regulates flow of contents

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3
Q

what do plicae circulares/ villi/ microvilli do

A

absorbs nutrients, electrolytes, and water in small intestine, NEEDS TO BE MAXIMAL SURFACE AREA

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4
Q

what happens to diet glucose

A
  • most of it is absorbed into bloodstream as glucose formed by hydrolysis of dietary starch and disaccharides
  • others are converted into glucose in the liver
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5
Q

what are carbohydrates/ sugars/ saccharides the precursor for

A

1- glycogen for storage
2- ribose & deoxyribose in nucleic acids
3- galactose for synth of lactose in milk

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6
Q

what are the 3 major carbohydrates and list examples for each category

A

1) monosaccharides, glucose, galactose, fructose
2) disaccharides, sucrose (gl & fr), lactose (ga &gl), and maltose (2xgl)
3) polysaccharides, glycogen stored in skeletal muscle (meat), starch, fiber (cellulose)

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7
Q

how do you regress from polysaccharide to disaccharide? from disaccharide to monosaccharide?

A
  • poly to di: salivary amylase and pancreatic amylase
  • di to mono: disaccharidases in small intestine and brush border enzyme near microvilli
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8
Q

how are glucose, galactose, and fructose absorbed into cells? how do they leave?

A
  • glucose and galactose: SGLT1, secondary active transport thru Na+ dependent cotransporter, high luminal [ ] against gradient
  • fructose: GLUT5, facilitated diffusion via glucose transporter
  • all leave through GLUT2 into capillaries
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9
Q

what happens when lactose is tolerated vs not tolerated

A

tolerated: lactase breaks down lactose to glucose and galactose -> normal poopie
not tolerated: lactase not present, only water, bacteria results and ferments -> gas, organic acids, osmotically active molecules irritation and motility -> back to more bacteria

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10
Q

what do insulin and glucagon do

A

insulin: stores fuel
glucagon: creates fuel by breaking down

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11
Q

what are the 4 fates of glucose

A

1) metabolized into pyruvate/ lactate via glycolysis
2) metabolized in the pentose phosphate pathway
3) stored as glycogen in the liver and skeletal muscle
4) stored as triglyceride in adipose tissue

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12
Q

what are the processes involved with metabolizing glucose into pyruvate/ lactate

A

glycolysis, krebs/tca/citric acid cycle, etc

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13
Q

what are the processes involved with metabolizing using the pentose phosphate pathway

A

glycolysis- alternate route: HMP -> glutathione

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14
Q

what are the processes involved with storing glycogen in the liver and skeletal muscle

A

glycogenesis

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15
Q

what are the processes involved with storing triglyceride in adipose tissue

A

fatty acid synthesis

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16
Q

what are the important features of glycolysis

A
  • 10 enzymatic rxns
  • occurs in cytosol
  • anaerobic (but w/ O2 can make 5 ATP in ETC)
  • aerobic, undergoes oxidative degradation in mitochondria to acetyl CoA
  • result sin 2 ATP and 2 NADH
  • 1 glucose = 2 pyruvate
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17
Q

what happens if glycolysis takes place in an anaerobic setting? what is another situation where this would occur

A
  • converts to lactate
  • w/ cells that have no mitochondria like RBCs
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18
Q

what is the process of pyruvate undergoing oxidative degradation during glycolysis

A

1) carboxyl group removed from pyruvate, releases CO2
2) NAD+ reduced to NADH
3) acetyl group transferred to coenzyme A -> acetyl CoA

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19
Q

what are the important features of krebs cycle? alternate names for this process?

A
  • occurs in mitochondria
  • doesn’t use O2 but will stop w/o it
  • forms: NADHx6, FADH2x2, GTPx2, waste- CO2
  • needs B1 (thiamine), B2 (riboflavin), B3 (niacin), B5 (pantothenic acid)
  • TCA (tricarboxylic acid), citric acid cycle
20
Q

describe the important features of ETC

A
  • inner mitochondrial membrane
  • requires lots of O2
  • converts NADH to NAD+ : generates 2.5 ATP& FADH2 to FADH generates 1.5 ATP
  • ATP synthase enzyme is key and what creates the H+ gradient to produce ATP
  • 4 complexes
21
Q

what are the important features of the alternate route of glycolysis

A
  • HMP
  • not ATP instead NADPH and pentoses important for ribose (RNA, DNA, and making proteins)
  • instead of glucose becoming pyruvate
  • occurs in cytosol, thus all cells
  • key enzyme: G6DP NEEDED
22
Q

what is NADPH used for

A
  • donates electrons (reducing agent) in anabolic rxns to make fatty acids and cholest. in liver and adipose tissue/ mammary glands/ synth steroids
  • indirectly eliminates toxic oxygen radicals
23
Q

what is glutathione and what are its states

A

major endogenous antioxidant produced by all cells
- participates directly in neutralizing free radicals
- maintains vitamin c& e in reduced forms
- reduced state- GSH, oxidized state- GSSG

24
Q

what are important features about glycogenesis

A

stores glucose in liver/ skeletal muscle for a rainy day

25
Q

compare and contrast liver hepatocytes and skeletal muscle in glycogenesis

A

liver
- glucokinase, stores 350-400 g of glucose
skeletal muscle
- hexokinase, stores 100g of glucose
BOTH use glycogen synthase (stim. by insulin) as key enzyme and if no room, stored as fat

26
Q

describe important features of fatty acid synthesis

A
  • synth. from acetyl-CoA
  • mainly in adipose tissue and liver
  • pathways between cytosol and mitochondria
27
Q

what are the 3 types of lipids and their roles

A

1) triglycerides- energy
2) phospholipds- plasma cell membrane, made of nitrogen compound, phosphate group, glycerol, and FA tails
3) cholesterol- building block of steroid hormones, travels in blood as LDL, HDL, used for plasma cell membrane

28
Q

what are the 6 stages of digestion/ absorption of lipids and relevant details of each step

A

1) emulsification: lipophilic and hydrophobic fat globule undergoes lecithin/ bile acid to become droplet
2) pancreatic lipase: hydrolyzes 1st and 3rd FA from triglycerides
3) colipase: is a co-enzyme that helps pancreatic lipase
4) micelles: lipids -> micelles coated w/ bile acid
5) chylomicrons- resynth’d and packaged triglyceride, cholesterol, and phospholipids, how intestinal cells absorb
6) lacteals: lymphatic capillary of the villus chylomicrons packaged into secretory vesicles and released from basal cell membranes into lacteal

29
Q

what is lipemia and when does it occur

A

w/in 1 hour of eating a fatty meal, chylomicrons are active in capillary endothelium.
- FAs into adipocytes and hepatocytes
- clears in a few hours
- contain lipoprotein lipase

30
Q

what are the types of lipoproteins and relevant features

A
  • synth by small intestine
    1) chylomicrons
    2) VLDL
    3) IDL
    4) LDL, bad cholesterol transports from liver to tissues
    5) HDL, good cholesterol transports excess tissues to liver
31
Q

what type of TG and cholesterol/ phospholipid content do VLDLs have?

A

high TGs, moderate C/P

32
Q

what type of TG and cholesterol/ phospholipid content do IDLs have?

A

moderate TGs, moderate C/P

33
Q

what type of TG and cholesterol/ phospholipid content do LDLs have?

A

low TGs, high C/P

34
Q

what type of TG and cholesterol/ phospholipid content do HDLs have?

A

low TGs, low C/P

35
Q

what are the treatments for high LDL?

A

statins
1) fluvastatin (lescol)
2) lovastatin (altoprev, mevacor)
3) atorrastatin (lipitor)
4) pitavastatin (livalo)
5) pravasttin (pravachol)
6) rosuvastatin (crestor)
7) simvastatin (zocor)

36
Q

what are the 2 modes of cholesterol de novo synthesis

A

dietary and synth by liver hepatocytes (amt determined by genetics)

37
Q

describe FA beta- oxidation

A
  • mitochondrial aerobic process
  • FA -> acetyl- CoA -> krebs (NADH, FADH2, GTP) -> ETC uses NADH, FADH2, ATP!
  • liver, skeletal muscle, and heart
38
Q

describe important features of ketone metabolism

A
  • synth in mitochondria of liver hepatocytes
  • ocurrs when fasting, oxaloacetate depletes in liver b/c gluconeogenesis -> impedes entry of acetly- CoA in Krebs
  • acetyl CoA accumulates -> liver converts to ketone bodies -> peripheral tissues (brain, skeletal muscle, kidneys -> acetyl CoA -> ATP via Krebs and ETC
39
Q

describe glucuneogenesis

A
  • synth glucose from non carb sources such as AAs (not leucine/ lysine), lactate, and glycerol
  • occurs primarily in liver hepatocytes
  • occasionally in epithelial cells of kidneys and small intestine
  • complex! NOT a reversal of glycolysis
40
Q

describe glycogenolysis

A
  • occurs during fasting state in liver and skeletal muscle
  • muscle provides G6P and begins glycolysis
  • liver breaks down glycogen into glucose preventing hypoglycemia
  • in both locations glucose is produced and fat is broken down
41
Q

what is the connection between glycogenolysis and gluconeogenesis

A

keeps you sustained in case liver and skeletal muscle run out of glycogen

42
Q

describe the cori and alanine cycles

A
  • involve gluconeogenesis in the liver and glycolysis in the muscle
  • cori: glucose -> pyruvate -> lactate in muscle -> blood -> liver, converted to pyruvate 0> gluconeogenesis -> glucose release and travels back to muscle
  • alanine: cori but pyruvate is transaminated after pyruvate then released into blood. in the liver-> transaminated back. xs alanine becomes urea
43
Q

how are AAs collected for energy

A
  • clear off brush border w/ aminopeptidases and proteases using active pancreatic enzymes
  • facilitated diffusion (GLUT5)
44
Q

how are AAs used for energy

A

1) gluconeogenesis (except leucine and lysine
2) ketone body (leucine and lysine)
3) directly fed into krebs

45
Q

can AAs be converted to TGs? how?

A

yes, krebs

46
Q

can AAs be broken down into waste

A

yes, amino groups cleaved into urea
- all urea synth in liver
- urea build up in blood leads to renal disease such as hepatic coma/ hepatic encephalopathy and azotemia and uremia which is TOXIC

Fundamentals of Patient Management (10 decks)

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