Lipids Flashcards

1
Q

What are the Main Groups of Lipids?

A

Fatty Acids
Fatty Acid Derivatives
Steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are Fatty Acids? Expand on the 2 Types. (how it is at room temperature, how stable, order of chain)

A

Hydrocarbons with one terminal carboxyl group COOH

Saturated - single bonds only
- solid at room tep - butter, egg, coconut, animal fats
- very stable
- straight chains
- stack tightly

Unsaturated = 1+ double bonds
- mono/polyunsaturated
- liquid at room temperature - plant oils
- bent chains
- two configurations
= cis - carbons are on same side of double bond
= trans - carbons on opposite side of double bond, the shape doesn’t bend much

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the Fatty Acid Deratives? Expand on the 2 Types. (structure and function)
Triglycerides

A

Triglycerides
- Glycerol + 3FA
- efficient long term storage
- forms in the cytoplasm of adipocytes
- function: protect and cushion organs

Phospholipids
- phosphate + glycerol + 2FA
- functions:
- permeable barrier of cell membrane
- provide supporting matrix
- participate in signal transduction
- provide precursors for processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a Steroid, where is it produced, its functions, how does it travel in the blood and 2 types.

A

hydrophobic molecules characterised by a carbon skeleton of 4 fused rings

75% produced by liver, 25% diet

Functions
- maintain membrane fluidity
- involved in production of hormones and Vitamin D

Transported in Blood via Lipoproteins

LDL - low density (saturated makes up body cholesterol)
HDL - high density
= positive, removes cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the Functions of Lipids? (5)

A
  • source of energy
  • absorb fat-soluble vitamins
  • protect internal organs
  • insulate body from heat loss
  • support biosynthesis precursors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where are Lipids Digested in the GIT?

A
  • oral cavity
  • stomach
  • small intestine
  • large inestine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Role of Oral Cavity in Digestion

A

saliva contains lingual lipase
- emulsifies fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What 2 Enzymes does the Stomach Contain to bring about Digestion

A

contain lingual lipase and gastric lipase
- break down fat into diglycerides and FA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What gets Stimulated in the Small Intestine During Digestion (3) and what other Enzymes are Present? (3)

A

chime (digested food) = acidic

mucosal wall stimulated
- secrete cytokinin hormone

gall bladder and pancreas stimulated
- secrete bile salts and pancreatic lipase

Enzymes:
- cholesteryl ester hydrolase
- phospholipase A2
- lysophospholipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do Bile Salts Do?

A

hydrophobic side attach to fat droplets
= form micelles

  • outside is hydrophilic so allows solubility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the Role of the Large Intestine in Digestion?

A

Exretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How are Lipids Absorbed into the Blood Stream? (14)

A

intestinal lumen
- on the apical border
- micelles transport to the basolateral border via enterocytes
= simple diffusion

in the cells endoplasm’s reticulum
- packed into a chylomicron
- triglycerides combines with protein
- phospholipid and cholesterol also packaged
- chylomicron exits via exocytosis

epithelial cell
- on the basolateral side
- lymph vessels called lacteals
- take up chylomicron
- secrete into bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What Happens Once Chylomicrons Lose their Triglycerides?

A

left with LDL
= Low density lipoproteins
- back to liver for storage
- secrete when losing fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 2 Types of Lipoproteins and Implications?

A

LDL
- Low Density Lipoprotiens
- high risk
- large amount of cholesterol and cholesteryl esters
- deliver cholesterol to peripheral tissues

HLD
- High Density Lipoproteins
- less risk
- remove excess cholesterol and take back to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What Implications does Cholesterol have on Blood Pressure? (5)

A
  • cholesterol forms plaque on interior of blood vessels
  • harder and calcified
  • narrows lume
  • less blood flow
  • high blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is Hyperlipidaemia Treated?

A

Statins
- inhibit HMG-CoA Reductase
- mimics the natural substrate and bind to enzyme
- inhibit cholesterol synthesis in the liver

17
Q

Define Atheroma

A

the accumulation of intracellular and extracellular lipid in the initma of large and medium sized arteries

18
Q

Is Atheroma Common? When does it Begin? It is Reversible? What can Reduce it?

A

very common
early lesions begin 20/3s
not reversible but drugs can stabilise
- calcium antagonists can reduce foam cell production

19
Q

Define Atherosclerosis

A
  • thickening and hardening of arterial walls
  • increases blood pressure
  • consequence of atheroma
  • in response chronic endothelial cell damage
20
Q

How does Atheroma lead to Atherosclerosis, then Lead to Thrombus

A
  • atheroma ruptures
  • chronic endothelial cell injury
  • endothelial dysfunction
  • LDL’s enter intima
  • intimal macrophages engulf lipids
  • fatty streaks = early lesion
  • continued accumulation of lipid on smooth muscle wall
  • raised yellow lipid plaque
  • fibrous cap forms over lipid core - calcifies
  • ulceration - surface breaks
  • predisposition of thrombus formation
21
Q

What are Risk Factors for Atherosclerosis (6)

A

diet
hypertension
diabetes
obesity
smoking
sedentary lifestyle

22
Q

What is the Primary and Secondary Prevention for Atherosclerosis

A

primary - risk factor modification
- delaying formation in those who have never suffered a serious complication

secondary - regular medication
- prevent reccurent events in high risk patients

23
Q

How Does Atheroma Affect Different Parts of the Body? - aorta, coronary arteries, internal carotid arteries, iliac and popliteal artery

A

aorta
- weaken wall
- dilation = aortic aneurysm
- risk of rupture

corny artery
- narrow arterial lumen
- reduced blood flow
- angina - myocardial ischemia
- thrombus formation over plaque
- lumen occlusion
- myocardial infarction

internal carotid artery
- reduced blood flow
- embolism builds up and travels to the brain
- blocks blood flow
- if transient = ischemia, if stroke = infarction

iliac and popliteal artery
- arterial lumen narrows
- reduced blood flow
- ischaemia - intermittent claudication and gangrene

24
Q

Draw out Fatty Acid Synthesis

25
State 4 Essential Fatty Acids
a-linolenic acid linoleic acid y-linoleic acid arachidonic acid
26
Why is arachidonic acid important?
derivatives: prostaglandins, thromboxanes in inflammation etc
27
How Is arachidonic acid found?
20:4 = 20C with 4 Double bonds
28
Where are Double Bonds Only Formed in Fatty Acids
Δ4,5,6,9 - can't go past 9th carbon
29
Draw Lipolysis
30
Draw Beta-Oxidation
aceyl-CoA into Acetyl CoA
31
How is Lipase Activated and Inactivated?
activate - protein kinase phosphorylates ATP to ADP, activates cAMP inactivate - dephosphorylated by phosphatase
32
How can you Transport Liver Acetly CoA in the blood?
ketone bodies
33
Define Ketosis
normal physiological response to fasting or low carb diet
34
Define Ketoacidosis
abnormal high levels of ketone bodies in the blood
35
How are Ketone Bodies used?
if in fasting or uncontrolled type 1 diabetes, as an alternative source of energy - uses oxaloacetate to produce glucose - TCA slows down - Acetyl CoA increases - fatty acids use it making more ketone bodes
36
What is the Effect of Diabetic Ketoacidosis?
excess glucose - large osmotic loss, dehydrated kidney excess ketone bodies - reduces pH, coma and death
37
How does Diabetic Ketoacidosis Work?
BGC is high, cant take up no glucose - no insulin - liver thinks its fasting - gluconeogenesis - more glucose in the blood - b-oxidation - more ketone bodies