Metabolism Flashcards

(42 cards)

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?

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
How is cortisol secretion controlled?
HPA axis
26
What is addison's disease and why does it result in hyperpigmentation? What other symptoms are associated?
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
What is cushings syndrome? What are the symptoms?
Overproduction of glucocorticoids. Muscle proteolysis, hyperglycaemia, moon face, hypertension, immunosuppresion (cortisol is immunosuppressive)
28
How can a dexamethasone test distinguish between cushings and an ademona?
Dexamethasone suppresses secretion of ACTH and therefore corisol High dose suppresses cushings. No dose can suppress adenoma.
29
How can a synacthen test be used to diagnose addisons?
Synacthen increases plasma cortisol but not in addisons.
30
symptoms and treatment of graves
symptoms - exophthalmos, osteoporosis, decrease weight, heat intolerance treat - carbimazole, thyroidectomy
31
cause of hypothyroid, symptoms, treat
cause - iodine deficiency, thyroidectomy symptom - alopecia, lethargy, cold intolerance, increase wight treat - thyroxine
32
pathway of Vit D
absorbed in skin then hydroxylated in liver then hydroxylated in kidney
33
what is cushings syndrome and disease
syndrome - increased cortisol disasese - increase cortisol due to tumour
34
what cells need glucose absolutely
blood cells, eye lens, kidney medulla
35
how galactose converted to galactitol
aldose reductase
36
what happens in phase 1 and 2 drug metabolism
phase 1 - exposes reactive groups phase 2 - conjugation by addition of a water soluble group phase 1 uses CYP enzymes
37
how and where is appetite controlled
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
how is pOMC, ghrelin, PYY and leptin released
POMC - stomach full ghrelin - stomach empty PYY - small intestine stretched leptin - adipocytes release
39
thyroid histology
follicular (simple cuboidal) with colloid filled lumens. inbetween follicles is CT and parafollicular cells
40
thyrophin and growth hormone releasing pathways
TRH to TSH to T3 + T4 GHRH to GH
41
where is circadian clock found. influenced by?
suprachiasmatic nucleus in hypothalamus influenced by melatonin
42
what is barkers hypothesis
prenatal conditions predispose baby to later life diseases