Lecture 1-3 Pathology - Inflam and healing Flashcards
Balance between with two things determines whether you increase demand or get injured (as a cell)
So yeah, stress causes a normal cell to either increase demand and get adaptaion or it will get injured - with injury, it can either die or adapt.
What are examples of causes of cell stress or injury?
Hypoxia, agents, genetic and nutritional imbalance
What is a common cause of hypoxia (starts with I)? Explain what it is and how it causes hypoxia
What is a common cause of ischaemia? (3)
What are the results of ischamia? (4)
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What are other causes of hypoxia? (3)
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What happens at molecular level for hypoixia?
- Decrease ATP bc mitochondria’s membrane damaged
- Membrane damage so lysosome, plasma, mito all sorta go blitz
- Can get reactive O2 species - damage DNA
How do you recognise these changes?
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What is steatosis?
When the liver cells are under stress/injured from alcohol - they accumulate triglycerides. The accumulation of these small lipid droplets in cytoplasm is steatosis
With stress or reversible injury, what are the 4 types of cell adaptations/changes?
Hyperplasia - increase in cell number (cells response to the demand by dividing). Like in goitre - increase in cells in thyroid to make up for thyroxine caused by iodine deficiency
Hypertrophy - increase cell size. Like in pregnancy, uterus cells grow bigger - not more. Cells can’t divide so they increase cellular components in response to demand. Or like hypertension. BUT continued demand leads to necrosis!
*Can get both hypertrophy and hyperplasia at the same time.
Atrophy - cells decrease in size. Diminished size and function but not dead. Might be because like decreased WORKLOAD or less BLOOD or not enough nutrition (like less protein) or loss of INNERVATION or like reduced ENDOCRINE stimulation (e.g. breasts and endometrium after menopause).
Metaplasia - replace cell type. It’s a reversible change in adult cell type (reprogramming of stem cells). Tougher type e.g pseudostratefied changed to squamous for smokers but loss of function too since no cilia. Can become dysplastic if prolonged but yeah.
Dysplasia - we didn’t get told
What are the 4 immediate or acute consequences of myocardial cell death?
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What are the two main types of cell death? What’s the difference between them? (slide 47)
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What are the two types of apoptosis?
Physiological e.g. cell removal during embrogenesis or hormone-dependent involution e.g. lactating breast after weaing
Pathological e.g. viral infections, cell death by Cytotoxi T cells
What is necrosis and what are the 4 types? Well, the two main types?
Distinct morphological patterns of necrosis can be seen after the initial phases which are a balance between _______ ______ and ______ _______.
What does protein denaturation favour? What about enzyme action favours?
It’s enzymatic digestion and leakage of cellular contents. Get swelling bc ATP-type pumps aren’t working. Finally cell ruptures and spills stuff everywhere. This will induce inflam response (innate and adaptive)
Innate - clears mess away and start healing process
Explain coagulative necrosis
Explain ischaemic coagulative necrosis
- Protein denaturation favours this
- You get preservation of basic structural outline for several days
- Can regenerate tissue if have labile cells in like liver, kidney or lung (but slide 113 says they’re stable)
- Ultimately necrotic material removed by phagocytosis
- Frequently it’s of a limb or digit. Wet gangrene if have infection too this a liquefactive component
Explain liquefactive necrosis
What if it happens in the CNS?
- Transformation of necrotic tissue into a liquid viscous mass.
- If done by infection then will have pus (neutrophils)
- Also done by phagocytosis
If in CNS, no scar formation - just a cavity.
What’s an abscess?
An abscess (Latin: abscessus) is a collection of pus that has built up within the tissue of the body. Signs and symptoms of abscesses include redness, pain, warmth, and swelling. The swelling may feel fluid filled when pressed.
