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Question 1

6 types of necrosis

src: wikipedia

Answer 1

Coagulative necrosis is characterized by the formation of a gelatinous (gel-like) substance in dead tissues in which the architecture of the tissue is maintained,[6] and can be observed by light microscopy. Coagulation occurs as a result of protein denaturation, causing albumin to transform into a firm and opaque state.[5] This pattern of necrosis is typically seen in hypoxic (low-oxygen) environments, such as infarction. Coagulative necrosis occurs primarily in tissues such as the kidney, heart and adrenal glands.[5] Severe ischemia most commonly causes necrosis of this form.[7]
    Liquefactive necrosis (or colliquative necrosis), in contrast to coagulative necrosis, is characterized by the digestion of dead cells to form a viscous liquid mass.[6] This is typical of bacterial, or sometimes fungal, infections because of their ability to stimulate an inflammatory response. The necrotic liquid mass is frequently creamy yellow due to the presence of dead leukocytes and is commonly known as pus.[6] Hypoxic infarcts in the brain presents as this type of necrosis, because the brain contains little connective tissue but high amounts of digestive enzymes and lipids, and cells therefore can be readily digested by their own enzymes.[5]
    Gangrenous necrosis can be considered a type of coagulative necrosis that resembles mummified tissue. It is characteristic of ischemia of lower limb and the gastrointestinal tracts. If superimposed infection of dead tissues occurs, then liquefactive necrosis ensues (wet gangrene).[8]
    Caseous necrosis can be considered a combination of coagulative and liquefactive necrosis,[5] typically caused by mycobacteria (e.g. tuberculosis), fungi and some foreign substances. The necrotic tissue appears as white and friable, like clumped cheese. Dead cells disintegrate but are not completely digested, leaving granular particles.[5] Microscopic examination shows amorphous granular debris enclosed within a distinctive inflammatory border.[6] Some granulomas contain this pattern of necrosis.[9]
    Fat necrosis is specialized necrosis of fat tissue,[9] resulting from the action of activated lipases on fatty tissues such as the pancreas. In the pancreas it leads to acute pancreatitis, a condition where the pancreatic enzymes leak out into the peritoneal cavity, and liquefy the membrane by splitting the triglyceride esters into fatty acids through fat saponification.[6] Calcium, magnesium or sodium may bind to these lesions to produce a chalky-white substance.[5] The calcium deposits are microscopically distinctive and may be large enough to be visible on radiographic examinations.[7] To the naked eye, calcium deposits appear as gritty white flecks.[7]
    Fibrinoid necrosis is a special form of necrosis usually caused by immune-mediated vascular damage. It is marked by complexes of antigen and antibodies, referred to as immune complexes deposited within arterial walls[6] together with fibrin.[6]

gangrene is usually a dry or coagulative type of necrosis, except when

Question 2

clostridium genus

FERMENTATION

____________

COMPARTMENT SYNDROME

src: wikipedia

Answer 2

gram positive
rod-shaped
motile
endospore forming
obligate anaerobes

found in soil, decaying organic matter, and the lower digestive tract of humans

-clostridium tenani - causes (all cases of) tetanus
axon damage
-c dificile
-c baccilus - botulism
-c perfingens - gas gangrene. shortest generation of any known organism 6.3 mins

Clostridium species produce more toxins and exhibit higher degrees of virulence than any other bacterial taxon

Clostridium infections are usually opportunistic, and occur in individuals with serious preexisting medical conditions. However, Clostridium infections are also known to occur in healthy individuals.

FERMENTATION
___________________

COMPARTMENT SYNDROME

• caused by physical trauma
• anatomical compartments (surrounded by deep aka investing fascia – fascia are collagen-dense connective tissues)
• fascial layers are generally less flexible than other types of connective tissue although they still have elastin; they’re less flexible due to dense collagen

Question 3

gas gangrene
etiology

src: wikipedia

Answer 3

Clostridium botulinum, Clostridium perfringens, Clostridium tetani, and Clostridium sordelli

Question 4

questions

Answer 4

examine how the gases produced by fermentation don’t poison the bacteria (O2 being a by-product – I assume they’re protected by either tissue compartments or biofilms but I’m not sure), but if I found nothing specific to C. perfringens et al., I would broaden my search to look at the ischaemic effects of gas bubbles in deep tissues (gas gangrene being a species of myonecrosis).

here I only have an implicit argument with how this topic is viewed: the so-called virulence factors e.g. toxins are secretions, whereas fermentation is basic sustenance, this is true, BUT trapped gases also happen to exert pressure on tissues which can lead to ischaemia – that is to say, if you can’t clearly see a design, it’s silly to exclude factors which might facilitate it, incidental or not. Plus I’m not seeing any timeline of disease progression so who’s to say the opportunistic infection isn’t actually instrumental to necrosis? It doesn’t make sense to assume a chance side-effect can’t also be a survival mechanism.