Armando Hasudungan's Medicine and Biology videos

armando hasudungan

Here's a compilation of videos made by Armando Hasudungan which are available on his YouTube channel.

Cancer - Introduction I

Cancer is the uncontrolled proliferation of cells that arise from virtually any cell type in the body.

Tumour = neoplasia. Tumours can be benign or malignant. Cancer refers to malignant tumour.

Benign tumours are slow growing, localised, and has well definied capsule. Benign tumours can grow big and press on nerves producing pain but are relatively harmless compared to malignant tumours.

Malignant tumours generally grow rapidly, are uncapsulated, and consist of different cells. Malignant tumours can break off and cause tumours on different sites a.k.a metastasis.

Commonly diagnosed cancer. Females: breast, lung, colorectal. Males: prostate, lung, colorectal.

Cancer - Introduction II

Video is describing a malignant tumour. Normal cells undergo transformation which progresses into dysplasia, neoplasia, and invasive neoplasia. Differentiation can be caused by genetic factor, environmental factor, or infection.

Cancer cells are characterised by anaplasia and autonomy. Anaplasia is the loos of differentiation and organisation. Autonomy is independence from normal cellular control.

Angiogenesis is the formation of blood vessels to supply nutirents to the tumour cells.

Cancer - Metastasis

Metastasis is the spread of cancer cells from the primary site to the secondary site. For example, in breast cancer, the primary site is the breast and the secondary site can be the lung, brain, and bone. Spread can occur via blood vessels or lymph.

Normal cells become dysplastic then becomes an in situ neoplasia followed by invasive neoplasia. Cancer cells can enter the blood and travel to the secondary site by anhering to the vessel wall, extravasation, and proliferation and angiogenesis at the secondary site.

Oma means growth. Different tumours are named differently based on the type of cell involved.

  • Melanoma - tumour of melanocytes
  • Lymphoma - tumour of lymph node
  • Carcinoma - tumour of epithelial cells
  • Adenocarcinoma - tumour of glandular epithelial cells

Breast cancer is a carcinoma.

Osteoporosis pathogenesis

Important cells:

  • Osteoblast - stimulates bone formation
  • Osteoclast - stimulates bone resorption

Important molecules:

  • TNF-alpha - stimulates osteoclast activity
  • RANK-L (Receptor activator of nuclear factor kappa-Β ligand) - secreted by osteoblast, stimulates osteoclast activity
  • M-CSF (macrophage colony stimulating factor) - secreted by osteoblast, stimulates proliferation of osteoclast
  • OPG (osteoprotegerin) - binds to RANK-L, lowring its activity

Oestrogen supresses RANK-L and M-CSF activity. During menopause, oestrogen levels fall which increases RANK-L and M-CSF activity. Hence, bone resorption is faster than bone formation.

In those taking glucocorticoids (steroids), OPG is inhibited hence increased RANK-L activity, increasing bone resorption.

Drugs used to treat osteoporosis include bisphosphonates, vitamin D and calcium.

Neurodegenerative Disorders Part I - Dementia, Alzheimer's, MND, MS

Degenerative disorders of the CNS are caused by the accumulation of proteins in the brain due to failure of these proteins to be broken down by the proteosome system.

Dementia presents mainly as memory impairment. There are many types of dementia including Alzheimer's Dementia, Pick's dementia, CJD, Dementia of Lewy body, etc.

Motor neurone disease or ALS is characterised by the degeneration of motor neurones particularly those in the brainstem and spinal cord.

Multiple sclerosis is characterised by autoimmune destruction of the myelin sheeth in the white matter.

Neurodegenerative Disorder II - Parkinson's and Huntington's

Parkinson's disease is caused by low dopamine in the pars compacta of the nubstantia nigra. Lack of dopamine in the nigrostriatal pathway causes the symptoms of parkinsons. Clinical manifestation include bradykinesia, resting tremor and rigidity.

Huntington's disease is caused by low GABA (gamma-Aminobutyric acid) which acts as the inhibitory neurotransimitter in our brain. Lack of GABA causes symptoms of Huntington's disease such as uncontorolled movements (chorea), irritability, and difficulty in decision making.

Eye disorders

List of eye disorders

  • Emmetropia - Normal vision
  • Hyperopia - far sightedness (eyeball too short or weak ciliary muscles or lens too thin)
  • Myopia - short sightedness (lens too curved)
  • Astigmatism - cuased by uneven curvature of the cornea
  • Conjunctivitis - inflammation of the conjunctiva caused by allergy, chemical irritants, virus or bacteria. Presesnts with red eye.
  • Trachoma - chlamydial conjunctivitis
  • Cataract - protein denaturation in the lens cuases it to be cloudy and opaque. Presents with blurry vision/ vision impairment. Cloudy pupil on physical examination.
  • Papilloedema - edema and inflammation of optic nerve, blocking nutrient flow to the retina. Caused by raised ICP (intracranial pressure), retrobulbar neuritis, and changes in retinal blood pressure.
  • Glaucoma - leading cause of blindness. Normal intraoccular pressure = 12 - 20 mmHg. In glaucoma, pressure can rise to 60 - 70 mmHg. Even 25 to 30 mmHg can cause retinal damage. Can cause a block in drainage of fluid in anterior chamber of the eye.
  • Retinal detachment - retina peels off. Caused by an injury where vitreous humour or blood seeping behind retina. Present as visual impairment or blindness.
  • Alterations in occular movement - Damage to cranial nerves III, IV and VI. Includes strabismus, nystagmus, and paralysis of individual extra occular muscles.
  • Retinopathies - retinal ischaemia, can be caused by diabetes or hypertension.

Muscular Dystrophy - Duchenne, Becker and Mytonic

Duchenne muscular dystrophy is an X linked, recessive disease where there is necrosis of the muscle cells due to defective gene leading to defective dystrophin protein synthesis. The dystrophin protein plays a role in holding the structure of the muscule cell membrane. When membrane is in tact, calcium stays outside the cell. In Duchenne muscular dystrophy, the membrane is compromised and calcium enters the cell causing necrosis.

Duchenne muscular dystrophy presents when the child is around 5 years old and the child usually becomes wheelchair bound by 10 to 12 years old. Clinical features include tiptoeing, thin weak thighs, weak stomach muscles, shoulders and arms heal back awkwardly, sway back, weak butt muscles, thick calves (fat), poor balance and awkward walking.

Myotonic dystrophy is the most common adult form of muscular dystrophy and is autosomal dominant, caused by repeat CTG sequence on chromosome 19. Patients have sustained involuntary muscle contraction. For example, there is difficulty in releasing the grip when the person does a handshake. Other features include a narrow face, prominent forehead, baldness, cataracts, and poorly developed chin.

Liver Disease Part 1

Cause of liver disease, unhealthy food, ethanol, drugs. Progression of liver damage: Healthy liver --> Simple Steatosis (fat accumulates in the liver, perivenular fibrosis) --> Steatohepatiits (fat accumulation, liver cell necrosis, inflammation, mallory bodies, fibrosis) --> cirrhosis (fibrosis, hyperplastic nodule). Steatosis and steatohepatitis are reversible but cirrhosis is irreversible.

Steatosis occurs when rate of fatty acid input exceeds rate of fatty acid output. Hepatic lipid content is the balance between uptake of free fatty acids in the liver, lipogenesis in the liver, oxidation of fatty acids in the liver and export of fatty acid within VLDL.

Process of fatty acid intake: lipoprotein containing triglycerides broken down into fatty acids by hepatic lipase and hormone sensitive lipase. Fatty acids in the liver is either oxidised or converted back into triglycerides and stored in the liver as lipid venules.

Oxidation of fatty acids in the liver is regulated by 2 molecules. PPAR-alpha (Peroxisome proliferator-activated receptor alpha) and PPAR-gamma. PPAR-alpha promotes oxidation while PPAR-gamma reduces oxidation. A defect in PPAR-alpha in the liver decreases oxidation of fatty acids in the liver, hence causing more conversion of fatty acids into triglycerids and stored as fat venules in the liver.

Liver Disease Part II

Alcoholic and non-alcoholic fatty liver disease.

The biochemical pathway of the conversion of fructose into fatty acids in the liver.

Metabolic syndrome is associated with NAFLD. Metabolic syndrome is when a patient has 3 out of 5 of the following:

  • Central obesity
  • Hypertension
  • Dyslipidaemia
  • Impaired glucose tolerance
  • Insulin resistance