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Digestive > 4B A&P and Pathology of the Small Intestine (Part 2) > Flashcards

4B A&P and Pathology of the Small Intestine (Part 2) Flashcards

1
Q

What is emulsification?

A

Taking big globules of fat and dispersing them into smaller droplets

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2
Q

What is responsible for emulsification?

A

Bile

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3
Q

What is the benefit of emulsification?

A

Increasing surface area of exposed of fat

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4
Q

After emulsification, which two pancreatic enzymes begin digestion on the emulsified fat droplets?

A

Pancreatic lipase and his friend colipase

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5
Q

What are micelles?

A

Lipids coated with bile acids to protect and sequester it from water, so the lipids could travel thru the water

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6
Q

Where do micelles go after they form?

A

To the brush border

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7
Q

How do the micelles get inside the brush border cells?

A

They merge with the phospholipid bilayer of the brushborder and the fatty contents are uptaken into the inside of the absorptive enterocyte

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8
Q

What happens to the fatty products brought into the cells from the micelles?

A

Inside they cell they get repackaged with protein-coated chylomicrons

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9
Q

What happens to the chylomicrons?

A

They go to the lymph vessels - lacteals (lymphatic capillaries) first, then thoracic ducts before going into the blood when the lymph empties into the subclavian veins

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10
Q

Which is bigger lacteals or blood capillaries?

A

Lacteals (lymphatic capillaries)

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11
Q

Where does the thoracic duct empty into the venous circulation?

A

At the juncture of the jugular and subclavian veins

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12
Q

What is Lipemia? When does it occur?

A

Lipid in the blood.

W/in an hour after eating a fatty meal

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13
Q

What is the half-life of chilomicrons?

A

Less than 60 minutes, so plasma usually becomes clear within a few hours

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14
Q

What is the fate of chilomicrons?

A

Removed from blood as they pass thru the capillaries of adipose tissue and the liver

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15
Q

What enzyme does adipose tissue and the liver contain large quantities of?

A

Lipoprotein lipase

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16
Q

Where is lipoprotein lipase especially active?

A

In the capillary enthothelium

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17
Q

What does lipoproteinn lipase do?

A

Hydrolyzes the TGs of chylomicrons into FAs and glycerol, which diffuse into adipocytes (storage) & hepatocytes (re-packaged into lipoproteins and exported to blood)

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18
Q

Can tissues use the contents of chylomicrons?

A

Yes, sir!

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19
Q

What are the five general types of lipoproteins?

A 
Chylomicrons
VLDL
IDL
LDL
HDL
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20
Q

Where are chylomicrons synthesized?

A

By the enterocytes of the small intestine.

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21
Q

What lipoproteins does the liver synthesize?

A

VLDL, IDL, LDL and HDL

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22
Q

What do VLDLs contain?

A

High TGs, moderate cholesterol and phospholipids

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23
Q

What do IDLs contain?

A

Moderate TGs, cholesterol and phospholipids

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24
Q

What do LDLs contain?

A

Low TGs, high cholesterol and phospholipids

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25
Q

What do HDLs contain?

A

Lows TGs, cholesterol and phospholipids

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26
Q

What are the only two lipoproteins routinely monitored clinically to screen for atherosclerosis, MI and stroke risk, and heart disease?

A

LDL-C and HDL-C

27
Q

What are the most effective drugs currently in use for treating elevated LDL-C?

A

Statins (Lipitor, Crestor, Lescol, Mevacor, etc)

28
Q

What are the adverse effects of statins?

A

Myopathy

29
Q

What is Myalgia? Myositis? Rhabdomyolysis?

A

Myalgia is muscle pain/weakness w/o inreased creatine kinase VS Myositis also includes elevated CK.
Rhabdomyolysis has very high CK (>10 times the upper normal limit), increased serum creatinine, often with dark urine and myoglobinuria

30
Q

What does dark urine and myoglubinuria indicate?

A

Muscle damage

31
Q

T/F all statins have been associated with myopathy?

A

T

32
Q

How many pts out of 10 report having muscle complaints?

A

1 in 10

33
Q

What are risk factors for myopathy?

A

Being elderly, small size, high statin dose, liver or renal disease, diabetes, uncontrolled hypothyroidism, and interacting medications

34
Q

What was the first lipid lowering agent?

A

Niacin (Vit B3)

35
Q

What are the three basic preparations of niacin?

A

Immediate release, sustained release, and extended release

36
Q

What is no-flush niacin? Does it work?

A

Inositol hexaniacinate/niacinamide. No, it is worthless

37
Q

What is the mechanism of action of Niacin?

A

Reduces production of VLDL, which leads to a secondary reduction of LDL

38
Q

What is the most potent agent for raising HDL?

A

Niacin

39
Q

Is intolerance to Niacin common?

A

Yes, only 50-60% of pts may be able to take full doses

40
Q

What are the adverse effects of Niacin? How can this be mitigated?

A

Flushing. Take ASA or NSAIDs 30-45 minutes prior to each niacin dose (blunts this prostaglandin-mediated effect)

41
Q

Why are Bile Acid binding resins taken?

A

Some take when statins do not lower the LDLs enough

42
Q

What do Bile Acid binding resins do?

A

Bind bile acids in your gut

43
Q

What happens if you bind bile acids with resins?

A

Can’t emulsify fats, means you can’t digest/absorb fat as well

44
Q

Do resins affect HDL or TGs?

A

No, not much. Will lower LDLs

45
Q

What happens if you don’t breakdown/absorb fat?

A

It stays in your gut and becomes part of the stool

46
Q

What are the consequences of fat remaining in stool?

A

Constipation

47
Q

What can relieve constipation and bloating?

A

Increased dietary fiber or fiber supplement (Metamucil)

48
Q

What are the drug interactions of bile binding resins?

A 
Interfere with:
Fat soluble vitamins.
Folate
Thiazides
Tetracyclines
Warfarin
Propanolol
Penicillin
49
Q

What is one way of avoiding some of the drug-drug interactions of resins?

A

Take resins a few hours AFTER taking the affected medications

50
Q

All H2O absorption in the small intestine is what type?

A

Passive and secondary to solute movement

51
Q

What stimulates water absorption in the small intestine?

A

Solutes such as Na+, glucose, amino acids

52
Q

How is most K+ absorbed?

A

Passively when luminal [K+] rises b/c of absorption of water (solvent drag)

53
Q

Where does calcium absorption occur? What is it primarily regulated by?

A

In the Duodenum and jejunum.

Regulated by Vitamin D3

54
Q

What does vitamin D do?

A

Stimulates synthesis of Ca++binding proteins called calbindins in enterocytes

55
Q

How are fat soluble vitamins (ADEK) absorbed in the small intestine?

A

Similar to fat

56
Q

How are more water-soluble vitamins absorbed in the small intestine?

A

By simple diffusion

57
Q

What water soluble vitamin requires intrinsic factor?

A

B12

58
Q

What cells absorb IF-B12 complexes across the brush border?

A

Ileal cells

59
Q

What does atrophy of gastric mucosa result in?

A

Deficiency of IF and acid secretion that causes VitB12 deficiency

60
Q

Where do peristaltic contractions occur?

A

Esophagus, stomach, and small intestine

61
Q

How long does it take chyme to move across the entire Small Intestine via peristalsis?

A

3-5 hours

62
Q

What is segmentation?

A

A series of contractile and relaxation periods that mechanically digests food

63
Q

What is peristalsis and segmentation controlled by?

A

Autonomic nervous system - SNS generally inhibit, while paraSNS generally excite muscular activity

Digestive (15 decks)

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