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biochemistry iii > LECTURE 2 (Lipid Metabolism) > Flashcards

LECTURE 2 (Lipid Metabolism) Flashcards

1
Q

What are Lipids?

A

Macromolecules that contain carbon, hydrogen and oxygen atoms

[however, unlike carbohydrates lipids contain a lower proportion of oxygen]

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2
Q

what are examples of lipids?

A
  • Fatty acids
  • Triglycerides
  • Cholesterol
  • Phospholipids
  • Steroids
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3
Q

What is a fatty acid composed of?

A

Carboxylic group and hydrocarbon chain

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4
Q

What is the bond between a glycerol molecule and a fatty acid called?

A

An ester bond

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5
Q

Describe the enzymes involved in fat digestion

A

Fat breakdown begins in the mouth with LINGUAL LIPASE -> Partially digested lipids are broken down by GASTRIC LIPASE in the stomach -> Fat droplets and acidity stimulate small intestinal cells activation of CHOLECYSTOKININ (CKK) and SECRETIN

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6
Q

Describe fat digestion in the mouth

A
  • Mechanical digestion
  • Mixing with saliva
  • Limited enzymatic digestion (lingual lipase)
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7
Q

Describe fat digestion in the stomach

A
  • Mixing/churning
  • Limited enzymatic digestion (gastric lipase)
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8
Q

Describe fat digestion in the small intestine

A
  • Emulsification (bile)
  • Enzymatic digestion (pancreatic lipases)
  • Micelles help with absorption
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9
Q

What does Cholecystokinin (CKK) do?

A
  • Bile production and secretion
  • Pancreatic juice release (contains pancreatic lipase)
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10
Q

What does Secretin do?

A
  • Bicarbonate secretion from the pancreas
  • Increase pH
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11
Q

What are the properties of Pancreatic lipase?

A
  • Secreted by the pancreas and transferred to the duodenum
  • Participates in the hydrolysis and digestion of fat, cholesterol esters and fat-soluble vitamins
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12
Q

Where are monoglycerides and fatty acids absorbed mainly?

A

In proximal 2/3 of the jejunum

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13
Q

Where are bile salts absorbed?

A

In the terminal ileum and enter portal circulation (ENTEROHEPATIC CIRCULATION)

[95% are absorbed and recycled, 5% excreted in stool]

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14
Q

What are the properties of Bile?

A
  • Produced in liver
  • Stored in gallbladder
  • Secreted into duodenum after meal
  • Consists of water, phospholipids and electrolytes
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15
Q

What is the difference between Bile salts and Bilirubin?

A

Bile salts = necessary for lipid absorption

Bilirubin = mode of excretion from body

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16
Q

What is Emulsification?

A

A process in which large lipid globules are broken down into several small lipid globules

17
Q

What is the importance of Emulsification?

A

Mediated by bile salts which surround lipid particles and dissolve them in water creating a larger surface area for PANCREATIC LIPASE to work

18
Q

How are Bile acids synthesised?

A

Bile salts are synthesised from bile acids (Cholic acid, Chenodeoxycholic acid) synthesised from Cholesterol in liver -> Bile acids are conjugated with TAURINE (organic acid) and GLYCINE which are hydrophilic -> One end is hydrophobic and the other end is hydrophilic

19
Q

What are the functions of Bile Salts?

A
  • Emulsificaton of fats
  • Excretion of cholesterol
  • Antimicrobial
20
Q

Explain how Bile salts excrete cholesterol

A

Cholesterol is not soluble in water -> cannot be excreted in urine -> Incorporated into CONJUGATED BILE which is water soluble -> excreted in stool

21
Q

Explain how Bile salts are antimicrobial

A

Small intestine has few bacteria -> Loss of bile salts leads to bacterial overgrowth (in liver diseases) -> Bile salts disrupt bacterial cell membrane

22
Q

How are fatty acids absorbed into the lymph bloodstream?

A

In GI TRACT fatty acids are converted into TRIGLYCERIDES by combining with GLYCEROL -> Triglycerides are combined with lipoprotein molecules called CHYLOMICRONS by intestinal cells -> Chylomicrons + lymphatic fluid form a milky white CHYLE inside lymph vessels -> Chylomicrons are secreted into the lymph bloodstream

23
Q

How is cholesterol absorbed into the lymph bloodstream?

A

Cholesterol is converted into CHOLESTERYL ESTERS in enterocytes via ACYL-COA CHOLESTEROL ACYLTRANSFERASE (ACAT) -> Cholesterol esters are packaged into CHYLOMICRONS by intestinal cells -> To lymph bloodstream

24
Q

What is found within a Chylomicron?

A
  • Triglycerides
  • Cholesteryl esters
  • Vitamins A, D, E & K
25
Q

What is Cystic Fibrosis?

A

An autosomal recessive genetic defect in the CFTR (Cystic Fibrosis Transmembrane Regulator) gene on chromosome 7 leading to a misfolded protein resulting in thick, sticky mucus in lungs and GI tract

CAUSES:
Misfolded protein is retained in RER and not transported to cell membrane -> Causing decreased Cl- and H2O secretion -> CFTR ion transporter is supposed to secrete Cl- in lungs & GI tract and reabsorbs Cl- in sweat glands

SYMPTOMS:
- Recurrent respiratory infections
- Failure to thrive
- Meconium ileus (bowel occlusion due to thick and sticky stool)
- Biliary disease (Bile duct obstruction, pale or clay coloured stool, elevated LFTs, hepatomegaly, cirrhosis, gallstones)
- Infertility (95% males infertile, SUBFERTILITY in females)
- Digital clubbing
- Nasal polyps

DIAGNOSIS:
- Sweat chloride test
- DNA testing (If sweat chloride test is abnormal)
- Nasal transepithelial potential difference (if mild symptoms + -ve sweat test)

TREATMENT:
- Chest physiotherapy
- Albuterol
- Aerosolised DORNASE ALFA (Dnase)
- Hypertonic inhaled saline
- N-acetylcysteine (cleaves disulphide bonds in mucous glycoproteins -> can induce bronchospasm in some children)
- Enzyme that breaks down DNA strands in airway secretions -> hydrolyses DNA present in sputum/mucous in CF patients -> reduces viscosity & prevents airway infection & damage to lung parenchyma

PROGNOSIS:
- avg life span 37 years
- death from lung complications

26
Q

What is the common cause of chronic lung disease in children?

A

Cystic Fibrosis

27
Q

What is the CFTR function in Epithelial cells and Sweat glands?

A

EPITHELIAL CELL FUNCTION
- Pumps Cl- out of epithelial cells against concentration gradient (uses ATP)
- Creates a membrane potential that draws out Na/H2O -> hydrates mucosal surface in lungs & GI

SWEAT GLANDS
- Removes NaCl from sweat (makes sweat hypotonic) -> CF patients have high NaCl in sweat

28
Q

What do thick mucous in lungs of CF patients cause?

A
  • Recurrent pulmonary infections
  • Chronic bronchitis
  • Bronchiectasis
29
Q

What do which mucous in GI tract of CF patients cause?

A
  • Impaired flow of bile and pancreatic secretions (chronic pancreatitis, CF-related diabetes)
  • Malabsorption especially fats
  • Loss of fat-soluble vitamin (ADEK)
  • Steatorrhea (frequent, foul-smelling, greasy, floating stools)
30
Q

Describe the Sweat chloride test

A

PILOCARPINE GAUZE is placed on skin -> small electrical current drives pilocarpine into skin -> sweating -> sweat collected on filter paper -> chloride content analysed
-> high chloride level suggests CF

31
Q

Describe the Nasal transepithelial potential difference

A

Measures nasal voltage -> CF patients have more -ve voltage due to abnormal sodium processing

32
Q

What is the treatment for patients with Phe508 deletion?

A
  • LUMACAFTOR = corrects misfolded proteins and improves their transport to cell surface
  • IVACAFTOR = opens cl- channels -> improved chloride transport
33
Q

What are other options for treatments of CF?

A
  • Exacerbations treated with antibiotics (AZITHROMYCIN used as anti-inflammatory agent)
  • Ibuprofen slows disease progression
  • Lung transplantation
  • Pancreatic enzyme treatment
  • Vitamins (ADEK)
  • Vaccinations
34
Q

Describe newborn screening for CF

A
  • Increased blood levels of IMMUNOREACTIVE TRYPSINOGEN (IRT)
  • TRYPSINOGEN is a zymogen synthesised in pancreas
  • Blood test if +ve sweat test
35
Q
A

biochemistry iii (12 decks)

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