Week 2 Flashcards

(59 cards)

1
Q

Cholesterol esters and Triglycerides are located in the hydrophobic core of the macromolecule, surrounded by phospholipids and apoproteins

A

Lipoproteins

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2
Q

Chylomicrons
VLDL
LDL
HDL

A

Four types of lipoprotein

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3
Q

Relationship of proteins to density

A

The more protein, the more dense, as protein is more dense than lipids

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4
Q

first step of chyloformation

A

diary fat eaten, salivary lipase secreted, presence of free fatty acids, monoglycerides, cholesterol.

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5
Q

Presence of fat globules, hard to break up, what is secreted?

A

bile salts

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6
Q

what do bile salts do?

A

make surface-optimized fat droplets

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7
Q

what breaks up surface-optimized fat droplets into micelles?

A

pancreatic lipase

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8
Q

what breaks up micelles into chylomicrons?

A

enterocytes

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9
Q

name three apoproteins that bind to chylomicrons in the lymphatic system

A

ApoB48, ApoC2, ApoE

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10
Q

what does ApoB48 do?

A

Micelles secretion of chylomicrons from GI to lymph

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11
Q

what does ApoC2 do?

A

Hydrolyzes conversion of TG to Fatty Acids for absorption (LPL)

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12
Q

What does ApoE do?

A

Mediates reuptake of multiple remnants

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13
Q

what organ secretes VLDL?

A

Liver

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14
Q

what does VLDL carry?

A

Triglycerides and cholesterol

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15
Q

ApoC2 activates LPL which then does what?

A

cut and cleave TG and FA, converts VLDL into IDL that carries TG and cholesterol in it with ApoB100 and ApoE bonded on its surface

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16
Q

low density lipoprotein

A

chylomicrons

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17
Q

medium low density lipoprotein

A

VLDL

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18
Q

medium high density lipoprotein

A

LDL

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19
Q

high density lipoprotein

A

HDL

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20
Q

How does lipoprotein change in the small intestine?

A

from low density to high density

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21
Q

which is “bad” type of lipoprotein that forms plaques and causes arteriosclerosis?

A

LDL

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22
Q

what is main component in low density lipoproteins?

A

triglycerides

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23
Q

Main component in “bad” lipoprotein?

A

cholesterol (50%)

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24
Q

Main component in “good” lipoprotein?

A

Protein (50%)

25
HDL comes from where?
"nascent HDL" comes from LV and SI
26
ApoA1 in bloodstream activates Lecithin-Cholesterol Acyltranserase (LCAT) does what?
converts NaSCENT HDL into Mature HDL that carries ApoE and ApoC2 on its surface
27
how long do glycogen stores last?
1 day
28
how long do fat stores last?
3 days
29
how long do protein stores last?
1+ week
30
after 1-3 days, what is the fuel source?
Hepatic gluconeogenesis, driven by Alanine and Lactate fort the brain
31
since RBCs have no mitochondria, the cannot use what
keynotes
32
insulin drives what state?
"Fed" state (storage of protein, carbohydrates, fat)
33
priority targets for fuel sources
Brain and RBCs
34
what is most common Gi diagnosis in primary care visits?
GERD
35
Definition of GERD
a condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications Reflux that is not troublesome is not GERD “Troublesome”: mild symptoms 2 or more times/week or severe symptoms 1 or more times/week
36
Sx of GERD
* Chest pain * Chronic cough * Chronic laryngitis * Asthma * GERD often not the sole cause of atypical symptoms * Atypical symptoms without concomitant heartburn/reflux unlikely to be due to GERD
37
Defensive factors in GERD
Lower Esophageal Sphincter Upper Esophageal Sphincter Peristalsis Saliva Bicarbonate
38
Aggressive factors in GERD
Hiatus Hernia Acid Pepsin Bile acids Trypsin Alcohol Acidic foods
39
Nervous activity in GERD
40
Hallmark Sx of GERD is
Heartburn
41
in GERD, LES is
Transiently relaxed, has decreased resting tone
42
Two typical complications of GERD
Erosive Esophagitis Barrett's Esophagus
43
Erosive Esophagus
44
Barrett's Esophagus, replacement of squamous cells to columnar cells, beginning of potential malignancy
45
Problem with sympathetic stimulation from GERD?
Sympathetic stops digestion, stomach stagnates, acidity goes up, reflux happens, gastric emptying is delayed.
46
Esophageal Adenocarcinoma
47
Alarm Sx of GERD
* Weight loss * Bleeding * Dysphagia * Family history of esophageal or gastric cancer
48
EGD (upper endoscopy) prompted by?
* Refractory to treatment * Long duration of symptoms * Atypical symptoms, dysphagia
49
EGD (upper endoscopy) sees normal esophagus in how many patients with heartburn and regurgitation?
2/3
50
Presence of erosive esophagus confirms GERD?
Yes
51
Relationship b/t GERD and BMI
Positive correlation
52
Surgical solutions to GERD
Bariatric Surgery Sleeve Gastrectomy
53
Bariatric surgery
Roux-en-Y Gastric Bypass. Make stomach pouch, connect to duodenum. Connect duodenum to middle LI. Reduces Reflux Clinical trial shows big success
54
Sleep Gastrectomy
Increases Reflux, LES is modified, provoking a decrease in LES resting pressure
55
Major Histamine Producing Cells, Study This!
56
Histamine 1
57
Histamine 2
58
Two types of medications
H2 Receptor Antagonists PPI (Proton Pump Inhibitors)
59
What do H2R receptor antagonists and PPIs do?