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Pathophysiology II > Week 2 > Flashcards

Week 2 Flashcards

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
Q

HDL comes from where?

A

“nascent HDL” comes from LV and SI

26
Q

ApoA1 in bloodstream activates Lecithin-Cholesterol Acyltranserase (LCAT) does what?

A

converts NaSCENT HDL into Mature HDL that carries ApoE and ApoC2 on its surface

27
Q

how long do glycogen stores last?

A

1 day

28
Q

how long do fat stores last?

A

3 days

29
Q

how long do protein stores last?

A

1+ week

30
Q

after 1-3 days, what is the fuel source?

A

Hepatic gluconeogenesis, driven by Alanine and Lactate fort the brain

31
Q

since RBCs have no mitochondria, the cannot use what

A

keynotes

32
Q

insulin drives what state?

A

“Fed” state (storage of protein, carbohydrates, fat)

33
Q

priority targets for fuel sources

A

Brain and RBCs

34
Q

what is most common Gi diagnosis in primary care visits?

A

GERD

35
Q

Definition of GERD

A

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
Q

Sx of GERD

A
  • 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
Q

Defensive factors in GERD

A

Lower Esophageal Sphincter
Upper Esophageal Sphincter
Peristalsis
Saliva
Bicarbonate

38
Q

Aggressive factors in GERD

A

Hiatus Hernia
Acid
Pepsin
Bile acids
Trypsin
Alcohol
Acidic foods

39
Q

Nervous activity in GERD

A
40
Q

Hallmark Sx of GERD is

A

Heartburn

41
Q

in GERD, LES is

A

Transiently relaxed, has decreased resting tone

42
Q

Two typical complications of GERD

A

Erosive Esophagitis
Barrett’s Esophagus

43
Q
A

Erosive Esophagus

44
Q
A

Barrett’s Esophagus, replacement of squamous cells to columnar cells, beginning of potential malignancy

45
Q

Problem with sympathetic stimulation from GERD?

A

Sympathetic stops digestion, stomach stagnates, acidity goes up, reflux happens, gastric emptying is delayed.

46
Q
A

Esophageal Adenocarcinoma

47
Q

Alarm Sx of GERD

A
  • Weight loss
  • Bleeding
  • Dysphagia
  • Family history of esophageal or gastric cancer
48
Q

EGD (upper endoscopy) prompted by?

A
  • Refractory to treatment
  • Long duration of symptoms
  • Atypical symptoms, dysphagia
49
Q

EGD (upper endoscopy) sees normal esophagus in how many patients with heartburn and regurgitation?

A

2/3

50
Q

Presence of erosive esophagus confirms GERD?

A

Yes

51
Q

Relationship b/t GERD and BMI

A

Positive correlation

52
Q

Surgical solutions to GERD

A

Bariatric Surgery
Sleeve Gastrectomy

53
Q

Bariatric surgery

A

Roux-en-Y Gastric Bypass. Make stomach pouch, connect to duodenum. Connect duodenum to middle LI.

Reduces Reflux
Clinical trial shows big success

54
Q

Sleep Gastrectomy

A

Increases Reflux, LES is modified, provoking a decrease in LES resting pressure

55
Q

Major Histamine Producing Cells, Study This!

A
56
Q

Histamine 1

A
57
Q

Histamine 2

A
58
Q

Two types of medications

A

H2 Receptor Antagonists
PPI (Proton Pump Inhibitors)

59
Q

What do H2R receptor antagonists and PPIs do?

A

Pathophysiology II (5 decks)

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