Lipids Flashcards

1
Q

What are the Main Groups of Lipids?

A

Fatty Acids
Fatty Acid Derivatives
Steroids

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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

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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

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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

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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
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6
Q

Where are Lipids Digested in the GIT?

A
  • oral cavity
  • stomach
  • small intestine
  • large inestine
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7
Q

Role of Oral Cavity in Digestion

A

saliva contains lingual lipase
- emulsifies fats

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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

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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

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10
Q

What do Bile Salts Do?

A

hydrophobic side attach to fat droplets
= form micelles

  • outside is hydrophilic so allows solubility
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11
Q

What is the Role of the Large Intestine in Digestion?

A

Exretion

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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

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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

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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

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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
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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

A
25
Q

State 4 Essential Fatty Acids

A

a-linolenic acid
linoleic acid
y-linoleic acid
arachidonic acid

26
Q

Why is arachidonic acid important?

A

derivatives: prostaglandins, thromboxanes in inflammation etc

27
Q

How Is arachidonic acid found?

A

20:4 = 20C with 4 Double bonds

28
Q

Where are Double Bonds Only Formed in Fatty Acids

A

Δ4,5,6,9

  • can’t go past 9th carbon
29
Q

Draw Lipolysis

A
30
Q

Draw Beta-Oxidation

A

aceyl-CoA into Acetyl CoA

31
Q

How is Lipase Activated and Inactivated?

A

activate
- protein kinase phosphorylates ATP to ADP, activates cAMP

inactivate
- dephosphorylated by phosphatase

32
Q

How can you Transport Liver Acetly CoA in the blood?

A

ketone bodies

33
Q

Define Ketosis

A

normal physiological response to fasting or low carb diet

34
Q

Define Ketoacidosis

A

abnormal high levels of ketone bodies in the blood

35
Q

How are Ketone Bodies used?

A

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
Q

What is the Effect of Diabetic Ketoacidosis?

A

excess glucose - large osmotic loss, dehydrated kidney

excess ketone bodies - reduces pH, coma and death

37
Q

How does Diabetic Ketoacidosis Work?

A

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