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ILOs For Nutrition, Bodyweight And > Carbohydrates > Flashcards

Carbohydrates Flashcards

1
Q

General Formula

A

(CH2O)n

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2
Q

General structure

A

Have aldehyde groups (C=O), ketone groups
(-C=O-C)
And lots of hydroxyl groups

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3
Q

Carbs function

A

Glucose main metabolic fuel
Essentially:
Carbohydrate ——> Monosaccharides ——> Pyruvate ———> Acetyl CoA

Acetyl CoA can then enter into the KREBS Cycle or into Fatty Acid Synthesis

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4
Q

3 main monosaccharides

A

Glucose
Fructose (Fruit sugar)
Galactose

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5
Q

Disaccharides

A

Sucrose (Glucose-Fructose)
Lactose (Galactose-Glucose)
Maltose(Glucose-Glucose)

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6
Q

Polysaccharides

A

Glycogen (Storage polymer of glucose in animals)
Starch (Storage polymer of glucose in plants)

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7
Q

Cellulose not digestible in humans why?

A

Don’t posses enzyme to break the Beta 1-4 glycosidic bond

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8
Q

Lactose Intolerance

A

Due to low activity of ENZYME LACTASE

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9
Q

Lactose Intolerance Symptoms

A

Diarrhoea
Bloating
Discomfort

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10
Q

Lactose Intolerance Symptoms Explained

A

Lactose moves into large intestine. Osmotic pressure increases so water moves into large intestine (diarrhoea). Bacteria begin breaking it down releasing gases (bloating/discomfort)

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11
Q

Dietary Polysaccharide metabolism

A

Starch and Glycogen hydrolysed by category of enzymes called glycosidase enzymes in mouth and duodenum
Produce glucose, maltose and Dextrins
Maltose and Dextrins and dietary Lactose and sucrose digested in duodenum and jejenum

AMYLASE IN SALIVA
LACTASE, SUCRASE, PANCREATIC AMYLASE (BREAKS a 1-4 bonds) , ISOMALTASE (BREAKS a 1-6 bonds)

The enzymes are found attached to brush border membrane of epithelial cells in small intestine

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12
Q

Primary Lactase Deficiency

A

Absence of Lactase persistence allele in adults
So LACTASE ENZYME not produced

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13
Q

Secondary lactase deficieny

A

Caused by injury to small intestine:
Gastroenteritis
Coeliac Disease
Ulcerative colitis
Chron’s Disease

The transmembrane enzymes damaged

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14
Q

Congenital lactase deficiency

A

AUTOSOMAL RECESSIVE defect in lactase gene. Cant digest breast milk

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15
Q

Glycolysis main features

A

Is anaerobic
Oxidation of glucose IS EXERGONIC
2 NADH produced per glucose
4 ATP produced Net production of 2 ATP
2 ATP used in substrate phosphorylation of glucose
Finishes with 2 pyruvate molecules

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16
Q

Glycolysis Key Regulatory enzymes

A

Hexokinase(glucokinase in liver)
Converts glucose to glucose 6 phosphate

Phosphofructokinase-1 (key control enzyme of glycolysis) Fructose 6 phosphate to Fructose 2-6 bisphosphate

Pyruvate Kinase converts phosphoenolpyruvate to pyruvate

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17
Q

Cells/tissues requiring glucose

A

RBCs
Neutrophils
Inner cells of kidney medulla
Lens of eye
Either have low 02 environment or lack mitochondria

18
Q

1-3 bis phosphoglycerate important from glycolysis

A

2-3 bis phosphoglycerate is derived from it and it regulates oxygen affinity of haemoglobin

19
Q

Dihydroxyacetone = important glycolysis metabolite

A

Undergo reaction to produce Glycerol Phosphate.
Important to make Triacylglycerols (Triglycerides)

20
Q

Phosphofrucktokinase Regulates Glycolysis

A

Allosterically controlled:
High ATP INHIBITS, High Citrate INHIBITS, STIMULATED By High AMP

Hormonal controlled: Insulin STIMULATES, GLUCAGON INHIBITS

21
Q

Lactate Dehydrogenase (LDH) Importance

A

Converts Pyruvate to Lactate and Lactate to Pyruvate
Replenishes the amount of oxidised NAD+ when pyruvate is converted to Lactate
Uses up NADH oxidising it
ESSENTIAL WHEN NO 02 FOR OXIDATIVE PHOSPHORYLATION SO REDUCING POWER CANT BE REGENERATED SO GLYCOLYSIS WOULD CEASE

22
Q

[Blood Lactate] Controlled By

A

Rate of production
Rate of Utilisation
Rate of disposal by kidney

23
Q

Fructose and Galactose metabolism

A

They get metabolised so that they end up as G-3-P which can be converted to pyruvate so the normal metabolic pathway can resume

24
Q

Galactosaemia

A

Unable to utilise Galactose as a result of a deficiency in 1 of 2 enzymes:
-Galactokinase
-Galactose-1P uridyltransferase or just uridyl transferase

25
Q

Galactokinase deficient galactosaemia

A

Milder form than uridyl transferase deficient
Only galactose accumulates
Leads to galactose entering ALDOSE REDUCTASE PATHWAY PRODUCES galactitiol

26
Q

ALDOSE REDUCTASE PATHWAY

A

Galactose converted into galactitol (reduced alcohol)
This depletes the NADPH stores in the eye lens damaging the crystallin protein in the eye
The denatured protein makes the lens cloudy

27
Q

Galactose-1P Uridyl Transferase Deficient Galactosaemia

A

Common worse form of Galactosaemia
Both Galactose and Galactose-1-P
Galactose-1-P affects liver, kidney and brain (organ damage)

28
Q

Galactosaemia Treatment

A

NO LACTOSE IN DIET

29
Q

Galactosaemia Symptoms

A

Cataracts
Enlarged Liver
Vomiting
Diarrhoea
Galactose in Urine

30
Q

Pentose Phosphate Pathway

A

Starts with Glucose-6-Phosphate
Important source of NADPH for: Biosynthesis, detoxification, maintains GSH levels
Makes 5 Carbon sugar ribose (Needed for making. Nucleotides, DNA/RNA)

31
Q

Glucose-6-phosphate dehydrogenase

A

Rate limiting enzyme in Pentose Phosphate Pathway

32
Q

Glucose-6-Phosphate dehydrogenase (G6PDH) deficiency (ENZYME ESSENTIAL IN PROTECTING AGAINST OXIDATIVE STRESS/ROS since NADPH needed to maintain high GSH levels)

A

In RBCs affected. NADPH levels fall, so cell vulnerable to ROS, disulphide bridges form in RBC denaturing the haemoglobin, Heinz bodies present, haemolysis

33
Q

G6pd found in RBCs

A

It protects RBCs
Without it RBCS become damaged meaning less RBCs can take oxygen around the body making you anaemic and therefore tired/lacking energy

34
Q

GSH (Glutathione)

A

Protects cell against oxidative damage

35
Q

Why is NADPH important for GSH

A

Its needed to recycle GSH back into its active reduced form

36
Q

Active Glutathione Role (GSH)

A

Prevent damage from free radicals on cells

37
Q

RBCs vulnerable in G6PD deficiency

A

Pentose Phosphate Pathway only source of NADPH (NO MITOCHONDRIA SO NON KREBS CYCLE), vulnerable to oxidative damage. Haemoglobin gets cross linked by disulphide bonds, causing oxidative damage forming Heinz bodies. Cells get destroyed (haemolytic)

38
Q

Pyruvate Dehydrogenase

A

Catalyses conversion of pyruvate into acetyl CoA so the Krebs Cylcle (TCA Cycle) can happen

39
Q

Phosphofructokinase regulation

A

Stimulated by AMP (Low energy signal, when ratio of ATP:ADP is low, cell needs to make more ATP)

Inhibited by ATP (High energy signal also is product inhibition)

40
Q

Absorption of monosaccharides from small intestine into blood

A

Active Transport via Sodium GLucose Transporter 1 (SGLT1) into intestinal epithelial cells

Facilitated Diffusion Via GLUT2 transporter into BLOOD

41
Q

5 Glucose Transporters

A

GLUT 1
GLUT 2
GLUT 3
GLUT 4
GLUT 5

42
Q

All c

A

ILOs For Nutrition, Bodyweight And (2 decks)

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