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Cell metabolism 3 Flashcards

1
Q

what is metabolic adaption?

A

when your metabolism changes depending on your nutritional state.

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2
Q

what are the two states of metabolic adaption?

A

absorptive and postabsorptive

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3
Q

why is it important to maintain steady blood glucose levels?

A

because nervous system and red blood cells depend upon glucose

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4
Q

what happens during the absorptive state?

A

ingested nutrients are entering the blood stream and glucose is readily available for ATP production

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5
Q

what do pancreatic beta-cells release?

A

insulin

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6
Q

what happens during the postabsorptive state?

A

absorption of nutrients from GI tract is complete.

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7
Q

Describe the absorptive state (principle metabolic pathways)

A
  • After a meal, nutrients enter body - glucose, amino acids and triglycerides in chylomicrons
  • 2 metabolic hallmarks :
  1. oxidation of glucose for ATP production in all body cells
  2. storage of excess fuel molecules in hepatocytes, adipocytes and skeletal muscle cells
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8
Q

Describe the postabsorptive state - how are normal blood glucose levels maintained?

A
  • About 4 hours after the last meal, absorption in the small intestine is nearly complete
  • Blood glucose level starts to fall
  • Main metabolic challenge to maintain normal blood glucose levels
  • Glucose production – Breakdown of liver glycogen, lipolysis, gluconeogenesis using lactate and/or amino acids
  • Glucose conservation – Oxidation of fatty acids, lactate, amino acids, ketone bodies and breakdown of muscle glycogen
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9
Q

optimal levels of nutrients

A

We do not know with certainty what levels and types of carbohydrates, fat and protein are optimal

• Different populations around the world each radically different diets

– Adapted to lifestyle

• We do know some don’ts

– Too much sugar – Too much saturated fat – Processed foods

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10
Q

What are minerals?

A

Inorganic minerals that occur naturally in Earth’s crust

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11
Q

What is the major role of minerals?

A
  • Enzyme reactions
  • DNA binding proteins
  • Oxygen binding

Haemoglobin

Cytochrome P450s

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12
Q

What happens to excess minerals?

A

• Excess minerals are excreted in urine and faeces

– Extremely toxic in high concentrations

– Build-up in disease

  • Freidrich’s ataxia (iron)
  • Wilson’s disease (copper)
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13
Q

What are vitamins?

A

Organic nutrients required in small amounts to maintain growth and normal metabolism

– “Vital amines”

  • Do not provide energy or serve as body’s building materials
  • Most are co-enzymes – Vitamin B6
  • Most cannot be synthesised by the body – Vitamin K produced in the GI tract by gut flora
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14
Q

What are the two groups of vitamins?

A

• 2 groups

– Fat-soluble – A, D, E, K

– Water-soluble – several B and C vitamins

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15
Q

What happens to excess vitamins?

A
  • Excess water-soluble are excreted in the urine
  • Excess fat-soluble build up in the body and cause significant toxicity
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16
Q

What happens as a result of vitamin deficiencies? + give examples

A

Deficiencies lead to disease

  • Rickets (vitamin D)
  • Scurvy (vitamin C)
17
Q

What is metabolic syndrome and how is it diagnosed?

A

Caused by an underlying disorder of energy usage and storage

  • Unknown cause
  • Diagnosed by the clustering of at least three of the following:

– Central obesity

– High blood pressure

– High blood sugar

– High serum triglycerides

– Low HDL

  • Between 25 - 35% of the US adult population are classed as having metabolic syndrome
  • Closely related to insulin resistance and prediabetes
18
Q

What is inborn error of metabolism?

A
  • A large class of genetic diseases involving congenital disorders of metabolism
  • Defects in single genes for enzymes
  • Affect all metabolic pathways
  • Symptoms vary due to the nature of the genetic mutation
19
Q

What is disorder of carbohydrate metabolism? + Give examples

A

• Glycogen storage disease

– Von Gierke’s disease

Glucose-6-phosphatase deficiency

• 1:50,000

– Forbe’s disease

  • Glycogen debranching enzyme deficiency
  • 1:100,000

– Andersen disease

  • Glycogen branching enzyme deficiency
  • 1:500,000
20
Q

What is disorder of amino acid metabolism and how is it treated?

A

Phenylketonuria

– Due to a deficiency in phenylalanine hydroxylase (PAH)

– Autosomal recessive

– Treatment with food low in phenylalanine

– Aspartame is metabolised into Phe so should be avoided

21
Q

What are the consequences of amino acid disorder?

A

Lack of treatment can cause significant developmental problems

– Intellectual disability

– Seizures

– Behaviour problems

– Microcephaly

• Build-up of Phe competes for the LNAA transporter in the blood-brain-barrier

– Reduces entry of key amino acids which are used to synthesise neurotransmitters and neuronal proteins

• Lack of PAH also reduces Tyr synthesis

– Reduced dopamine, norarenaline and adrenaline synthesis

22
Q

What is disorder of fatty acid oxidation? Symptoms?

A

• Medium-chain acyl-coenzyme A dehydrogenase deficiency

– MCADD

– Prevention of the breakdown of fatty acids into acetyl-CoA

– Hypoglycaemia and sudden death

• Brought on by periods of fasting or vomiting

23
Q

What is incidence? Treatment?

A

Autosomal recessive

– ACADM gene

– Dehydrogenation step of fatty acids between C6-C12

• Common in Northern European caucasians

– 1:4,000 – 1:17,000

• Treatment is by the avoiding of fasting

– During illness, need to supplement using glucose

• Patients have potentially reduced survival – Needs to be diagnosed as an infant

24
Q

What is diabetes? Symptoms? Long term problems?

A
  • High blood sugar levels over a prolonged time due to the pancreas not producing, or the body not responding to insulin
  • Onset of a variety of symptoms

– Frequent urination

– Increased thirst

– Increased hunger

– Diabetic ketoacidosis

• Long-term problems

– Cardiovascular disease

– Kidney disease

– Foot ulcers

25
Q

What are the three types of diabetes?

A

– Type 1

  • Pancreatic failure to produce insulin due to loss of beta-cells
  • No known cause
  • Treated using insulin injections

– Type 2

  • Insulin resistance
  • Can lead to lack of insulin
  • Caused by obesity and insufficient excercise
  • Treated using diet

– Gestational diabetes

• Occurs in pregnant women

26
Q

Symptoms of diabetes

A
27
Q

What is diabetic ketoacidosis?

A

Arises from the lack of insulin pushing metabolism towards fatty acid oxidation

– Mainly in Type I diabetics

• Oxidation of fatty acids producing ketone bodies

– β-dihydroxybutyrate (most common)

– Acetoacetate

28
Q

Mechanism of diabetic ketoacidosis

A
29
Q

What are the symptoms of diabetic ketoacidosis?

A

Symptoms develop over 24 hours

– Nausea and vomiting

– Thirst

– Excessive urination

• Rapid, deep gasping

– Kussmaul breathing

– Associated with severe DKA

– Fruity breath smell

• Cerebral oedema (in children)

– Coma

– Death

30
Q

What are the stages of diabetic ketoacidosis?

A

Three stages

– Mild

  • pH 7.2 – 7.3
  • Serum bicarbonate 10 – 15 mM
  • Person is alert

– Moderate

  • pH 7.1 – 7.2
  • Serum bicarbonate 5 – 10 mM
  • Person is mildly drowsy

– Severe

  • pH < 7.1
  • Serum bicarbonate < 5
  • Patient is in a coma
31
Q

Treatment of diabetic ketoacidosis

A

• Treatment

– IV fluids

– IV insulin

– Potassium

• Replacement of potassium lost due to osmotic diuresis

• Prognosis

– 4% of type I diabetic patients develop DKA each year

– Risk of death is 1 – 4% with adequate treatment

– 20 - 50% of children with cerebral oedema will die

32
Q

What stage of diabetic ketoacidosis is characterised by a blood pH < 7.1 and a serum bicarbonate < 5 mM?

A

severe

33
Q

What is the incidence of Forbe’s disease?

A

Disorder of carbohydrate metabolism

Forbe’s disease

• Glycogen debranching enzyme deficiency

• 1:100,000

BBT (3 decks)

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