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MEH corrections > metabolism > Flashcards

metabolism Flashcards

1
Q

what is the function of glycerol-3-phosphate dehydrogenase?

A

converts Dihydroxyacetone phosphate (an intermediate of glycolysis) to glycerol phosphate
* Dihydroxyacetone phosphate is essential in triglyceride and phospholipid formation in liver

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2
Q

what causes galactosaemia?

A

deficiency in galactokinase, UDP-galactose epimerase or uridyl transferase
galactokinase = accumulation of galactose
UDP-galactose epimerase = accumulation of UDP-galactose
uridyl transferase = accumulation of galactose-1P and galactose

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3
Q
  1. what is basal metabolic rate?
  2. what factors affect BMR?
A
  1. energy to sustain life
  2. factors that affect it:
    * body weight
    * body temperature
    * gender
    * thyroid function
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4
Q

what are the consequences of excess paracetamol?

A

formation of NAPQI
direct hepatocyte damage
depletes glutathione levels which increases cells risk of oxidative damage

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5
Q

how are uncouples involved in heat generation in the body?

A
  • uncouplers cause H+ to leak across inner mitochondrial membrane
  • this decreases PMF
  • ATP synthase is uncoupled from ETC so no ATP is synthesised
  • UCP1 is expressed in brown adipose tissue + is involved in thermogenesis
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6
Q
  1. where is glycogen stored in the body and what is its function in each tissue?
  2. where is the most glycogen stored in the body?
  3. what enzyme is involved in glycogen synthesis?
  4. what enzyme is involved in glycogen hydrolysis?
A
  1. skeletal muscle - provides glucose 6-phosphate to be catabolised + livere - maintain blood glucose levels
  2. skeletal muscle
  3. glycogen synthase
  4. glycogen phosphorylase
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7
Q

which enzyme is involved in the hydrolysis of TAG?

A

lipase

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8
Q

what is normal blood glucose range?

A

3.3 - 6.0 mmol

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9
Q

which enzymes are measured to assess liver function?

A

ALT + AST
ALT = alanine aminotransferase
AST = aspartate aminotransferase

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10
Q

which hormones regulate calcium levels?

A

PTH - short term regulation
calcitrol - long term regulation

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11
Q
  1. what is the regulatory enzyme in lipogenesis?
  2. what factors increase lipogenesis?
  3. what factors decrease lipogenesis?
A
  1. Acetyl-CoA carboxylase
  2. insulin + citrate
  3. glucagon/adrenaline + AMP
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12
Q
  1. what is phenylketonuria?
  2. what method of inheritence is PKU?
  3. what are the symptoms of PKU?
  4. how is PKU treated?
A
  1. phenylalanine hydroxylase is deficient so phenylalanine isnt converted to tyrosine. This means phenylalanine is converted to phenylpyruvate which results in the accumulation of phenylketones
  2. autosomal recessive
  3. severe intellectual disability, developmental delay, seizures, hypopigmentation
  4. low phenylalanine diet with lots of tyrosine, avoid artificial sweetners, avoid high protein foods
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13
Q
  1. what is homocystinurias?
  2. what is method of inheritence of homocystinurias?
  3. what are the symptoms of homocystinurias?
  4. how is homocystinurias treated?
A
  1. defect in cystathione beta-synthase causes problems in breaking down methionine which causes excess homocystine to accumulate which is excreeted in urine
  2. autosomal recessive
  3. cardiovascular disease
  4. low methionine diet, avoid milk, meat, chees and eggs, cysteine, Vit B6 and B12 supplements
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14
Q
  1. what is von gierkes disease?
  2. what are the symptoms of von gierkes disease?
  3. how is von gierkes disease treated?
A
  1. glucose 6-phosphatase deficiency which results in excess glycogen accumulation in tissues, however, glycogen is not broken down properly so causes hypoglycaemia
  2. constantly hungry, fatigue, irritability, puffy cheeks
  3. diet rich in carbohydrates, eat regularly
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15
Q
  1. what is McArdle disease?
  2. what are the symptoms of McArdle disease?
A
  1. muscle glycogen phosphorylase deficiency
  2. muscle cramps, fatigue, weakness, exercise intolerance
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16
Q
  1. what is cushings syndrome?
  2. what causes cushings syndrome?
  3. what are symptoms of cushings syndrome?
  4. how is cushings syndrome treated?
A
  1. hyperactivity of adrenal cortex results in excess cortisol secretion
  2. chronic use of glucocorticoids, primary cortisol-producing adrenal adenoma or excess secretion of ACTH due to a pituitary adenoma
  3. polydipsia, polyuria, hyperglycaemia, thin arms and legs (due to increased proteolysis), moon shaped face. and central obesity (due to increased fat deposition), purple striae on lower abdomen (due to catabolic effects on protein structure in skin)
  4. drugs to lower cortisol or surgery to remove lesion
17
Q
  1. what are the causes of too litle cortisol secretion?
  2. what is addisons disease caused by?
  3. what is secondary adrenal insufficiency caused by?
  4. what are the symptoms of too little cortisol?
A
  1. primary adrenal insufficiency (or Addisons disease) or secondary adrenal insufficiency
  2. failure of the adrenal gland to produce cortisol usually due to autoimmune disease
  3. failure of ACTH production, inadequate CRH production
  4. muscle weakness, increased skin pigmentation, decreased BP (due to Na+ and fluid depletion), hypoglycaemic episodes
18
Q
  1. what is an addisonian crisis?
  2. how is an addisonian crisis treated?
A
  1. addisons disease causes a loss of both cortisol and mineralcorticoids when stressed symptoms worsen causing vomitting, severe dehyrdation, hypotension, confusion
  2. IV cortisol and fluid replacement
19
Q

what are the different anabolic processes that the TCA cycle produces precursors for?

A

amino acid synthesis
fatty acid synthesis
glucose synthesis
haem synthesis

20
Q

which molecule in skeletal muscle acts a small store of energy which is used up rapidly during first few seconds of vigorous exercise?

A

creatine phosphate

21
Q
  1. which enzyme is involved in the hydorlysis of glycogen?
  2. what effect does adrenaline have on this enzyme in skeletal muscle?
  3. what effect does glucagon have on this enzyme in skeletal muscle?
A
  1. glycogen phosphorylase
  2. increases
  3. no effect (glucagon has no effect on this enzyme in skeletal muscle but does increase its activity in liver)
22
Q

what is the use of pyruvate in the body?

A

lactate circulates in blood before being taken up by liver, heart and kindey
lactate is converted to pyruvate by lactate dehydrogenase
1. pyruvate is used by the heart for energy production
1. pyruvate is used as precursor for gluconeogenesis in liver
1. pyruvate is used as precursos for gluconeogenesis in kidney

MEH corrections (3 decks)

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