METAB LEARNING OBJECTIVES

What are the key components of the human diet?

Carbohydrates, proteins, lipids, vitamins, minerals, and water — all essential for energy, growth, repair, and body function.

Why are carbohydrates important?

Main energy source; broken into glucose for ATP production.

Why are proteins important?.

Needed for tissue repair, enzyme and hormone production

Why are lipids important?

Energy storage, cell membranes, insulation, hormone synthesis.

How do you calculate Body Mass Index (BMI)?

A: BMI = weight (kg) / height² (m²)

What factors affect long-term body weight regulation?

Genetics, hormones (like leptin & ghrelin), metabolism, physical activity, diet, environment.

What is body homeostasis?

Maintenance of stable internal conditions (like temp, pH, glucose)

What regulates body homeostasis?

Negative feedback loops (e.g., insulin/glucagon, thermoregulation).

How is energy obtained from food?

Food → macronutrients → broken down in cellular respiration → ATP.

What are the main pathways for carbohydrate metabolism?

Glycolysis, Krebs cycle (TCA), and oxidative phosphorylation.

What’s the key function of glycolysis?

Breaks down glucose → pyruvate → ATP (anaerobic or aerobic).

How are lipids metabolised?

β-oxidation of fatty acids → acetyl-CoA → ATP via TCA cycle.

How are proteins metabolised?

Deamination of amino acids → carbon skeletons enter TCA → urea.

Why are these pathways clinically important?

Defects can cause energy deficits, toxic build-up (e.g., PKU, MSUD).

How are drugs metabolised in the body?

Mainly in the liver by enzymes (esp. cytochrome P450) → Phase I (modification) & Phase II (conjugation) → excretion.

What can affect drug metabolism?

Genetics, liver function, age, other drugs, diet.

What happens in anaerobic metabolism?

Glucose → pyruvate → lactate (instead of acetyl-CoA), less ATP.

Clinical issue with lactate build-up?

Lactic acidosis — can cause confusion, weakness, rapid breathing.

How is glucose transported?

Via GLUT transporters (e.g., GLUT4 in muscle/adipose, insulin-dependent).

How is glucose stored?

As glycogen (in liver & muscle) via glycogenesis.

How are lipids transported?

As lipoproteins: chylomicrons, VLDL, LDL, HDL

How are lipids stored?

As triglycerides in adipose tissue.

What are clinical effects of defects in transport/storage?

Diabetes (glucose issues), hyperlipidemia (lipid transport errors), glycogen storage diseases.

What are ketone bodies?

Acetoacetate, β-hydroxybutyrate, acetone — alt. energy source.

Why do they (ketone bodies) matter clinically?

Can cause ketoacidosis — life-threatening in uncontrolled T1DM.

What is marasmus?

Severe calorie deficiency → muscle wasting, stunted growth.

What is kwashiorkor?

Protein deficiency → oedema, fatty liver, distended belly.

Name a condition caused by defective galactose metabolism..

Galactosemia — leads to liver damage, cataracts

What’s G6PD deficiency?

Enzyme defect → hemolysis under oxidative stress (e.g., fava beans).

What’s the metabolic issue in PKU?

Deficient phenylalanine hydroxylase → phenylalanine build-up.

Homocystinuria: key issue?

Homocysteine build-up → ↑ clotting risk, developmental delay.

What is a glycogen storage disease?

Enzyme defects → abnormal glycogen storage (e.g., von Gierke’s disease).

What’s a key cause of hypoglycaemia?

Insulin overdose, fasting in children, enzyme defects.

What’s the primary metabolic role of the central nervous system?

Uses glucose (and ketones when fasting); high energy demand; no energy storage.

What does the liver do metabolically?

Glucose homeostasis (stores/releases glycogen)
detoxifies
makes plasma proteins
produces ketones
lipid & amino acid metabolism hub.

Role of cardiac muscle in metabolism?

Constant high energy use — mainly uses fatty acids for fuel.

What about skeletal muscle?

Uses glucose (active) & fatty acids (rest); stores glycogen; major protein reserve.

What does adipose tissue do?

Stores triglycerides; releases fatty acids during fasting; responds to insulin.

What’s the red blood cell metabolism like?

only does anaerobic glycolysis (no mitochondria); needs glucose.

Which hormones regulate metabolism?

insulin, glucagon, cortisol, adrenaline, thyroid hormones, GH.

What does insulin do?

Lowers blood glucose; promotes storage (glycogen, fat), protein synthesis.

What does glucagon do?

Raises blood glucose; stimulates glycogenolysis, gluconeogenesis.

What’s cortisol’s metabolic role?

Stress hormone; promotes gluconeogenesis, fat breakdown, protein catabolism.

How does adrenaline act?

Fight/flight: ↑ glucose & fatty acid availability via glycogenolysis & lipolysis.

What do thyroid hormones (T3/T4) do?

Boost basal metabolic rate; enhance metabolism globally.

What about growth hormone (GH)?

Stimulates growth, lipolysis; opposes insulin in glucose metabolism.

What happens during feeding?

Insulin ↑ → glucose uptake, glycogen & fat synthesis.

What happens during fasting?

Glucagon ↑ → glycogen breakdown, gluconeogenesis, lipolysis.

What happens during starvation?

Protein sparing; fatty acids used; ketone bodies ↑ for brain fuel.

Metabolic change in pregnancy?

Insulin resistance ↑, lipolysis ↑, ketone production ↑ for foetus.

What changes during exercise?

Short-term: glycogen used; Long-term: fatty acids used; insulin sensitivity improves.

Main regulators of these states?

Insulin & glucagon balance; plus cortisol, adrenaline, GH depending on stress/activity.

Why is blood glucose relatively stable?

Tightly regulated by insulin and glucagon; liver balances glucose input/output.

What happens in type 1 diabetes?

Autoimmune destruction of β-cells → no insulin → hyperglycaemia, ketoacidosis.

What happens in type 2 diabetes?

Insulin resistance ± impaired insulin secretion → hyperglycaemia, metabolic syndrome.

What metabolic issue might cause abdominal distension/mass?

hepatomegaly from glycogen storage disease, fatty liver in obesity or kwashiorkor.

Abnormal development/delay — metabolic link?

Inborn errors (PKU, homocystinuria, galactosemia) → brain impact.

Abnormal eating/exercise behaviour — think?
A: Anorexia → hypoglycaemia, electrolyte imbalance; excessive exercise → muscle protein loss.

Blackouts/faints in metabolism?
A: Hypoglycaemia (insulin overdose, fasting, metabolic enzyme defects).

What’s a metabolic cause of bone pain?
A: Rickets/osteomalacia (vitamin D def.), hyperparathyroidism.

Breathlessness in metabolic conditions?
A: Lactic acidosis (e.g., mitochondrial disorders), diabetic ketoacidosis (Kussmaul breathing).

Chest pain metabolic links?
A: Electrolyte imbalances → arrhythmias; metabolic syndrome → atherosclerosis.

Constipation or diarrhoea and metabolism?
A: Seen in hypothyroidism (slow motility), lactose intolerance, G6PD crisis.

Fatigue — think?
A: Anaemia, hypothyroidism, diabetes, chronic metabolic acidosis.

Failure to thrive / decreased appetite — causes?
A: Inborn errors (e.g., galactosemia), chronic hypoglycaemia, cortisol deficiency.

Jaundice and metabolism?
A: Seen in galactosemia, G6PD deficiency (hemolysis), liver failure.

Palpitations from metabolic causes?
A: Hypoglycaemia, hyperthyroidism, pheochromocytoma.

Peripheral oedema — metabolic causes?
A: Kwashiorkor (low albumin), liver failure, nephrotic syndrome.

Polydipsia/polyuria points to?
A: Diabetes mellitus (glucose osmotic diuresis), diabetes insipidus.

Tremor or muscle pain?
A: Hypoglycaemia (tremor), hypothyroidism or statins (myalgia).

Weight loss — think?
A: Hyperthyroidism, uncontrolled diabetes, starvation states.

Weight gain — think?
A: Hypothyroidism, Cushing’s syndrome, insulin therapy.

Electrolyte disturbance — examples?
A: Hyponatraemia (SIADH, adrenal insuff.), hypercalcaemia (hyperparathyroidism).