Which features of ionising radiation is incorrect?
X/gamma rays have energy to break bonds.
Damage to DNA bases.
Water is the main target for ionising radiation.
Water breaks into H and OH radical with OH and ionising radiation go on to break DNA strands.
What are all the effects of death of endothelial cells
Ulceration
Scarring
Atrophy (shrinkage) of surrounding tissue
Inflammation and chronic pain
Which is not a feature of UV radiation to damage of DNA?
Damage to DNA bases where adjacent C-T become linked.
The DNA strand will break.
Misrepair generates C to T point mutations leading to cancer development
More damage leads to death of keratinocytes (peeling sunburn)
The chemical factor to damage to DNA -Alkylation is:
Fungal product aflatoxin B1 accumulates in poorly stored food (in underdeveloped countries).
Metabolites react covalently (alkylate) with proteins to cause liver injury ; acutely at high doses.
Metabolites alkylate DNA hence G to T mutations = liver cancer= chronic and low doses.
Folic acid further damages the DNA.
The crystals puncture the membranes.
Which is a feature of biological dietary deficiency - DNA?
Autoimmune gastritis lack intrinsic factor prevents B12 absorption.
Proteins cause liver injury acutely
Inflammasomes generate severe inflammation.
Hydrogen peroxide will be detoxifed to catalase to oxygen and water.
Which is not a feature of chemical damage to lipids?
Cells take up crystals into lysosomes.
Crystals puncture lysosome membrane.
Damaged mitochondria cannot reduce oxygen completely.
Inflammasomes activated.
ROS and RNS are not free radicals?
Which is not an oxidative reaction in the chemical factor of damage to lipids?
Superoxide (O2-) - detoxed by superoxide dismutase
Hydrogen peroxide - detoxed by catalase
Oxygen therapy - exposure to premature babies
Hydroxyl radical - OH.
Which of these does not contribute to injury of cell via ROS?
Oxygen therapy
Inflammation
Megablastic anaemia
Damaged mitochondria
UV radiation
Radiotherapy
How does acute haemorrhagic pancreatitis occur? Biological lipase factor
Proteolytic cleavage of ECM proteins
The p53 transcription factor
Damage to exocrine cells which synthesise digestive enzymes or block ducts that these enzymes travel to duodenum by
Prolonged heat exposure
Which is not a consequence of heat exposure in proteins?
High fever
Heat stroke
Malignant hyperthermia
Acute haemorrhagic pancreatitis
Is the Maillard reaction the enzymatic addition of sugars to proteins?
Which of the following is not a result of the reaction occurring between reducing sugars and amino groups?
Reversible early stage Schiff bases
Irreversible rearrangements to Amadori products.
Further rearrangements to advanced glycation end products (AGE).
Nrf transcription factors.
How do AGE injure cells?
Inhibit protein function
Cross linking and precipitating proteins (blocking axon transport in neurons)
Generating ROS
Binding to receptors of AGE (RAGE) on vascular and inflammatory cells that reduce blood flow and cause inflammation.
The enzymatic addition of sugars to proteins.
Does AGE accumulate during ageing, diabetes, and chronic inflammation?
When and where does proteolytic cleavage occur during inflammation when proteins are damaged? Biological factor
Collagen in arthritis
Elastin in emphysema
Laminin during cancer invasion
Blood vessel damage behind eye during retinopathy
Which factor does acute intracellular oedema (hydropic change) not affect the cells regulation of ion concentration in cytoplasm?
Plasma membranes permeable to Na+ hence K+ leaks out (Na+ in) hence cell swells.
ATP synthesis disrupted, Na+/K+ ATPase inhibited
Na+ pump damaged
Cell shrinks due to excess water loss
Does abnormalities in capacity of cells to recycle components result in the non-accumulation of products such as fat and glycogen?
When there are fatty changes in liver cell what does not happen when the triglycerides accumulate?
In normal liver cells they cannot metabolise increased fatty acids conc. coming from adipose tissue (diabetes)
In abnormal liver cells they have a decreased ability to oxidise fatty acids (alcohol damage)
In abnormal liver cells have decreased ability to export triglycerides compounded with lipid-acceptor proteins i.e. VLDL leading to malnutrition, kwashiorkor - not enough proteins and more fat.
In normal liver cells they cannot transport more of the fat from the tissue to urine and therefore leading to blockage.
