Metabolism Flashcards

1
Q

What are the 3 irreversible steps of glycolysis? Name the enzymes used.

A

Steps 1, 3 and 10

1) Glucose –> Glucose 6-Phosphate

Hexokinase and glucokinase

3) Fructose 6-phosphate –> Fructose 1,6 BP

PFK

10) PEP –> Pyruvate

Pyruvate Kinase

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2
Q

How would you overcome the irreversible steps of glycolysis in gluconeogenesis? State the reactions.

A

10) Pyruvate –> PEP

PEP carboxykinase

3) F-1,6-BP –> F 6-P

F-1,6-BPase

1) G-6P –> Glucose

G-6Pase

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3
Q

Why does lactate build up in anaerobic respiration?

A

NADH + H+ + pyruvate –> NAD+ + lactate

Enzyme - LDH

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4
Q

What is lactose made up of?

A

Galactose + glucose

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5
Q

What is galactosaemia? What is the rare and common forms of it? What is the result of galactosaemia? How is it treated?

A

Inability to convert galactose to glucose.

Rare - Lack of galactokinase

Common - Lack of transferase

Results in galactose –> Galactitol via Aldose reductase. Depletes NADPH

NADPH prevents cross linking of proteins in eye, results in cataracts.

Treatment is to avoid lactose.

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6
Q

What does the pentose phosphate pathway produce? What enzyme is necessary?

A

Produces NADPH and C5 sugars for nucleic acid synthesis.

Needs G-6-P DHase

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7
Q

Give 2 examples of uncouplers

A

Dinitrophenol and dinitrocresol

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8
Q

How is TAG stored in adipose tissue and how does this system ensure that fatty acids are released in times of low serum glucose?

A

TAGs constantly being converted from TAG to FAs and back.

Conversion back to TAG requires extracellular glucose to enter cell and reform TAG.

Lack of glucose in ECF results in FA reslease from cell.

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9
Q

How is fat broken down for energy in the mitochondria?

A

FA links to CoA and taken into matrix using carnitine shuttle.

Oxidative reaction cycles produce FADH2 and NADH. Lose 2 Carbons for every cycle.

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10
Q

Describe the steps in glycogen synthesis

A
  1. Glucose –> G-6-P via glucokinase
  2. G-6-P –> G-1-P via phosphoglucomutase
  3. G-1-P + UTP –> UDP-Glucose
  4. Glycogen + UDP-glucose –> Glycogen + UDP via glycogen synthase.
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11
Q

Describe the steps for glycogen breakdown.

A
  1. Glycogen –> G-1-P via glycogen phosphorylase
  2. G-1-P –> G-6-P –> glycolysis
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12
Q

What is phenylketonuria? What enzyme is deficient? What is its pattern of inheritance?

A

Inability to convert phenylalanine to tyrosine which is needed to create dopamine. Phenylketones excreted in urine

Phenylalanine hydroxylase

Autosomal recessive

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13
Q

What is homocysteinuria? What enzyme is deficient? What is its pattern of inheritance?

A

Inability to convert homocysteine to cystathionine, which goes on to make cysteine. Results in connective tissue defects.

CBS

Autosomal recessive.

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14
Q

How do statins function?

A

Inhibit HMG-CoA reductase which synthesises cholesterol

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15
Q

What happens in an overdose of paracetemol?

A

Drug spills over from phase 2 into phase 1 of drug metabolism.

Results in generation of NAPQI intermediates which exhausts glutathione reserves and leaves hepatocytes open to ROS.

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16
Q

How is alcohol metabolised?

A

1) Alcohol –> acetaldehyde via Alcohol DHase
2) Acetaldehyde –> Acetate via Aldehyde DHase

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17
Q

What is type 1 and type 2 diabetes?

A

Type 1 - autoimmune destruction of Beta cells

Type 2 - Disorder of insulin secretion or insulin resistance.

18
Q

What are the normal ranges of glucose in the blood?

A

3 - 7 mmol/l

19
Q

How is T3 and T4 synthesised?

A
  1. Thyroglobulin secreted into lumen of follicular cell
  2. Iodide attaches to either 1 or 2 sites on tyrosine R chains to form MIT or DIT
  3. When needed, thyroglobulin endocytosed into follicular cell, cleaved, and T3 and T4 enter blood.
20
Q

What are the effects of T3 and T4? What does absence of T3 and T4 from birth result in?

A
  • Increase metabolism of glucose, fats and proteins
  • Increase BMR, heat and o2 consumption
  • Needed for neurological, bone, heart development

Absence results in cretinism

21
Q

What are the symptoms of hypothyroidism? Name a disease associaed with hypothyroidism.

A

Hashimoto’s disease

  • Cold intolerance and weight gain
  • Lethargy
  • Bradycardia
  • Alopecia and xeroderma
22
Q

What are the symptoms of hyperthyroidism? Name a disease associated with hyperthyroidism.

A

Grave’s disease

  • Heat intoleranc
  • Weight loss
  • Tachycardia
  • Hyperactivity
23
Q

Symptoms of hypo and hypercalcaemia?

A

Hypo - tetany, hyperexcitability of nervous system

Hyper - Kidney stones, depression and dehydration (moans, stoans and groans)

24
Q

State the 4 layers of the adrenal gland and what is produced in each layer.

A
  1. Zona glomerulosa - Mineralocorticoids
  2. Zona fasciculata - Glucocorticoids
  3. Zona Reticularis - Androgens
  4. Medulla - Adrenaline
25
Q

How is cortisol secretion controlled?

A

HPA axis

26
Q

What is addison’s disease and why does it result in hyperpigmentation? What other symptoms are associated?

A

Insufficeint glucocorticoid production.

Low cortisol production, therefore no negative feedback of ACTH. ACTH has MSH like activity when present in excess.

Weight loss, hypoglycaemia, muscular weakness.

27
Q

What is cushings syndrome? What are the symptoms?

A

Overproduction of glucocorticoids.

Muscle proteolysis, hyperglycaemia, moon face, hypertension, immunosuppresion (cortisol is immunosuppressive)

28
Q

How can a dexamethasone test distinguish between cushings and an ademona?

A

Dexamethasone suppresses secretion of ACTH and therefore corisol

High dose suppresses cushings. No dose can suppress adenoma.

29
Q

How can a synacthen test be used to diagnose addisons?

A

Synacthen increases plasma cortisol but not in addisons.

30
Q

symptoms and treatment of graves

A

symptoms - exophthalmos, osteoporosis, decrease weight, heat intolerance

treat - carbimazole, thyroidectomy

31
Q

cause of hypothyroid, symptoms, treat

A

cause - iodine deficiency, thyroidectomy

symptom - alopecia, lethargy, cold intolerance, increase wight

treat - thyroxine

32
Q

pathway of Vit D

A

absorbed in skin then hydroxylated in liver then hydroxylated in kidney

33
Q

what is cushings syndrome and disease

A

syndrome - increased cortisol

disasese - increase cortisol due to tumour

34
Q

what cells need glucose absolutely

A

blood cells, eye lens, kidney medulla

35
Q

how galactose converted to galactitol

A

aldose reductase

36
Q

what happens in phase 1 and 2 drug metabolism

A

phase 1 - exposes reactive groups

phase 2 - conjugation by addition of a water soluble group

phase 1 uses CYP enzymes

37
Q

how and where is appetite controlled

A

appetit controlled by arcuate nucleus in hypothalamus

vagus nerve stimulates hunger in arcuate nucleus.

Vagus inhibited by POMC which is activated by leptin and insulin

Vagus stimulated by (NPY and AgRP) which is stimulated by ghrelin but inhibited by PYY and leptin and insulin

38
Q

how is pOMC, ghrelin, PYY and leptin released

A

POMC - stomach full

ghrelin - stomach empty

PYY - small intestine stretched

leptin - adipocytes release

39
Q

thyroid histology

A

follicular (simple cuboidal) with colloid filled lumens. inbetween follicles is CT and parafollicular cells

40
Q

thyrophin and growth hormone releasing pathways

A

TRH to TSH to T3 + T4

GHRH to GH

41
Q

where is circadian clock found. influenced by?

A

suprachiasmatic nucleus in hypothalamus influenced by melatonin

42
Q

what is barkers hypothesis

A

prenatal conditions predispose baby to later life diseases