Dr Meducci vet's blog

Hypovolemic shock (haemorrhagic)

3:43 PM | Labels: haemorrhagic shock, Hypovolemic shock

In this week, shock has becoming our main topic in every class. So, here's the thing about it

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What is shock??

A serious condition that occurs when the cardiovascular system is unable to supply enough blood flow to the body, causing inadequate tissue perfussion.

Major classes of shock include:

Cardiogenic Shock (associated with heart problems)
Hypovolemic Shock (caused by inadequate fluid volume)
Anaphylactic Shock (caused by allergic reaction)
Toxic Shock (associated with infections)
Neurogenic Shock (caused by damage to the nervous system)

Shock is a life-threatening condition that requires immediate medical treatment. Some degree of shock can accompany any medical emergency. Shock can get worse very rapidly.

Recognition of shock

Depending on the specific cause and type of shock, symptoms may include:

Anxiety or agitation
Bluish lips and fingernails
Chest pain
Confusion
Cool, clammy skin
Decreased or no urine output
Dizziness or light-headedness
Faintness
Low blood pressure (Hypotension)
Paleness (pallor)
Profuse sweating, moist skin
Rapid pulse
Shallow breathing
Unconsciousness
Weakness
Hyperventilating
Extended capillary refill time >2secs

**ONLY HYPOVOLEMIC SHOCK WILL BE DISCUSSED**

Hypovolemic shock

Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion. Most often, hypovolemic shock is secondary to rapid blood loss. (Hemorrhagic shock)

Example of severe blood loss

(sorry couldn't found nice pic)

Acute external blood loss secondary to penetrating trauma and severe GI bleeding disorders are 2 common causes of hemorrhagic shock. Hemorrhagic shock can also result from significant acute internal blood loss into the thoracic and abdominal cavities.

Two common causes of rapid internal blood loss are solid organ injury and rupture of an abdominal aortic aneurysm. Hypovolemic shock can result from significant fluid (other than blood) loss. Two examples of hypovolemic shock secondary to fluid loss include refractory gastroenteritis and extensive burns.

**Losing about 1/5 or more of the normal amount of blood in the body causes hypovolemic shock.

Pathophysiology of hypovolemic shock (you may read the summary ^^ )

The hematologic system responds to an acute severe blood loss by activating the coagulation cascade and contracting the bleeding vessels (by means of local thromboxane A2 release). In addition, platelets are activated (also by means of local thromboxane A2 release) and form an immature clot on the bleeding source. The damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of the clot. Approximately 24 hours are needed for

complete clot fibrination and mature formation.

The cardiovascular system initially responds to hypovolemic shock by;

increasing the heart rate
increasing myocardial contractility
and constricting peripheral blood vessels.

This response occurs secondary to an increased release of norepinephrine and decreased baseline vagal tone (regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and pulmonary vessels). The cardiovascular system also responds by redistributing blood to the

brain, heart, and kidneys and away from skin, muscle, and GI tract.

The pathophysiology of hypovolemic shock is that when fluid volume goes down a decrease in the circulating volume of blood is seen. When the circulating volume of blood occurs the preload to the heart is decreased. A decrease in preload causes a decrease in stroke volume which will cause a decrease in the cardiac output. With reduced cardiac output you will see decreased cellular oxygen perfusion. When cells don’t receive enough oxygen they die. In addition to hypovolemic shock there is cardiogenic shock.

The renal system responds to hemorrhagic shock by stimulating an increase in renin secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which subsequently is converted to angiotensin II by the lungs and liver. Angiotensin II has 2 main effects, both of which help to reverse hemorrhagic shock, vasoconstriction of arteriolar smooth muscle, and stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is responsible for active sodium reabsorption and subsequent water conservation.

The neuroendocrine system responds to hemorrhagic shock by causing an increase in circulating antidiuretic hormone (ADH). ADH is released from the posterior pituitary gland in response to a decrease in BP (as detected by baroreceptors) and a decrease in the sodium concentration (as detected by osmoreceptors). ADH indirectly leads to an increased reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle.

Some of the complication associated with hypovolemic shock include;

Kidney damage
Brain damage
Gangrene of arms or legs, sometimes leading to amputation
Heart attack

**The pathophysiology of hypovolemic shock is much more involved than what was just listed. To explore the pathophysiology in more detail, references for further reading are suggested. These intricate mechanisms list above are effective in maintaining vital organ perfusion in severe blood loss. Without fluid and blood resuscitation and/or correction of the underlying pathology causing the hemorrhage, cardiac perfusion eventually diminishes, and multiple organ failure soon follows.

Summary of hypovolemic shock

Animals at hypovolemic RISK

Traumatic causes can result from penetrating and blunt trauma. Common traumatic injuries that can result in hemorrhagic shock include the following: myocardial laceration and rupture, major vessel laceration, solid abdominal organ injury, pelvic and femoral fractures, and scalp lacerations.Vascular disorders that can result in significant blood loss include aneurysms, dissections, and arteriovenous malformations.

GI disorders that can result in hemorrhagic shock include the following: bleeding esophageal varices, bleeding peptic ulcers, Mallory-Weiss tears, and aortointestinal fistulas.

Pregnancy-related disorders include ruptured ectopic pregnancy,placenta previa, and abruption of the placenta. Hypovolemic shock secondary to an ectopic pregnancy is common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a negative urine pregnancy test is rare but has been reported.

Treatment

Don't be too panic when you see people or animal in hypovolemic shock (particularly if you knew it) This is what you can do;

Before medical arrive;

Keep the person/animal comfortable and warm (to avoid hypothermia).
Have them lie flat with the feet lifted about 12 inches to increase circulation. However, if the person has a head, neck, back, or leg injury, do not change the person's position unless he or she is in immediate danger.
Do not give fluids by mouth. (it may cause heart to stop immediately-die)
If person/animal is having an allergic reaction, treat the allergic reaction, if you know how.
If the person/animal must be carried, try to keep him or her flat, with the head down and feet lifted. Stabilize the head and neck before moving a person with a suspected spinal injury.

Do like this

After medical arrived;

The goal of hospital treatment is to replace blood and fluids. An intravenous (IV) line will be put into the person's arm to allow blood or blood products to be given.

Fluid administration can increase cardiac pre-load as well as help with overall perfusion. There are two types of fluids.

Crystalloids such as normal saline, D5W, and lactated ringers.
Colloids such as whole blood, plasma and hetastarch.

While colloids might be preferred in some situations because of affinity to intravascular restoration, the down side is cost, potential for allergic reaction and speed or lack of speed in type and cross matching in an emergency.

Medicines such as dopamine, dobutamine, epinephrine, and norepinephrine may be needed to increase blood pressure and the amount of blood pumped out of the heart (cardiac output). One of the method to monitor the status of the patient is to do heart monitoring as well as urinary cathether (to collect and monitor how much urine is produced)

Sources: Hypovolemic shock; PubMed health, Shock; AricRn, Hypovolemic shock; emedicine.medscape.com, Shock; ambulancetechnicianstudy.co.uk

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Old times..

2:59 AM |

Somebody had asked me on facebook, my international reader (he is currently 1st year student of vet school somewhere around Egypt). His question was;

"Do you really like veterinary course?"

His question made me sit and ponder for a while. Why, of all this while somebody asked me this? I admit, everytime I woke up very early in the morning, I always remind myself how lucky I am to be in this life; A life I'd ever wanted more than anything even when I was a very little girl. At that time, I barely know about veterinary. Little Aina Meducci only knows "Doktor Haiwan" which means "Animal Doctor" in english. How naive I was!

We lived in the state of Johor, southernpart of Peninsular Malaysia that time. I was born in Kuala Lumpur but later on moved to Johor. I was raised with other kids whom simply pick up death cats on the street and buried it down nearby electric generator nearby our residential area. I had no idea that my noble action finally brought me in this course.

I always wanted to be 'animal doctor'. When my primary school teacher asked what is my ambition, I leaped out with joy! I wanted to be 'Doktor Haiwan'!! Sometimes, quite often my aunties teasing me about how do I bear to touch pigs and dogs (these animal is forbidden in Islam), and I simply replied.." If they sick and need treatment who's going to do that?" But now I realised, I have better explanation to backfire them hahaha

Anyway, Islam is not about to forbid everything. Recite the Holy Quran, it did mentioned that indeed we have ways to 'clean' after touching those animals. I was ashamed how those people whose are very narrow minded to judge this situation. Up until now, their mentality never seemto grow..

I wasn't a good student during primary school. I hate maths. Other subjects too.I never got good grades in my exams. I was prone to English. My family speaks Malay, let alone foreign languages. But when we moved back to Kuala Lumpur when I was 9, my new school friends spoke Malay with English slang. I was determined to learn English, and filled with jealousy when they brought Enid Blyton's book and able to speak english although not fluently. I begged my parents to buy one for me. From that moment, I started to learn english in a hard way. I also learn to listen to english songs, reading Nancy Drew's novel and talking to my dolls in english. Haha

I made my first trip overseas when I was 8. To Mecca, Saudi Arabia performing Umrah. Later on, we went to China, Indonesia, S'pore, Thailand, Pakistan, Europe and Saudi Arabia again. I love travelling!

My life turned into miracle soon after performing Hajj on 2004, when I was 14. I dont know why, my academical record shows an outstanding result by years, and I got good result in final year secondary school, and sent me to the matriculation college for one year in Perak. Another miracle came and saved my breath during the 1st sem!! Until now I am still wondering how I managed to survive in those cold, dark time of my life.

When my sem 2 result came, I straight away applied vet course. I remember putting UPM as my first choice and UMK on 2nd. But I wasn't sure weather I can get it, because my result is not very good to apply vet, but I tried it. I believe Allah knows the best for me, I have deep faith on Allah as I sat my foot on Tanah Haram to kneel and pray, years ago.

Allah had answered my pray! I got UMK vet! even though it was very far from Kuala Lumpur, but the passion has breached the border and finally brought me here. I thanked my parents and friends for their supports and I laid my hands about to say thank you to Allah, who truly understand my needs.

Now, as I am typing this to share my vet journey to you, I must carry on to this veterinary program that shaped of the road of my incredible life journey, and still hungry to learn more. For me, veterinary is not about easy or not to master, but is the matter of fact of how far do you love to learn about animals and how willing are you to take challenges. Enjoy the day as sun could have not set, and I'm sure that you will never regret of choosing veterinary as something you will have to deal with the rest of your life.

To Mak, abah, my brother and my little Qullip. I am here because of you. Keep on supporting :)

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Clostridium Perfringens in horse

5:52 AM | Labels: Clostridia Perfringens in horses

Me and King (Talebreed horse)

Hey! I just started O-level in training horse! My dean introduced this to me and why not? Even if I am not into horses (they are super big and I'm just a 'ketot girl') but I took this opportunity to learn and suddenly fell in love with it. The class starts during weekend (so can u imagine how busy i am?) and damnn tired! but I enjoyed the my first day of class and hopefully can keep it up until I am good enough to ride. Maybe having an equine license can make u proud instead of a car license ..right?

Post today is about disease of horses, particularly in GIT. Actually this is part of my assignment during clinical biology class. Haha

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Clostridium Perfingens

Clostridium perfringens is an anaerobic, Gram-positive, sporeforming rod (anaerobic means unable to grow in the presence of free oxygen). It is widely distributed in the environment and frequently occurs in the intestines of humans and many domestic and feral animals. Spores of the organism persist in soil, sediments, and areas subject to human or animal fecal pollution.

C. Perfingens

Infections due to C. Perfingens causes tissue necrosis, bacteremia, emphysematous cholecystitis, and gas gangrene, which is also known as clostridial myonecrosis. The toxin involved in gas gangrene is known as α-toxin, which inserts into the plasma membrane of cells, producing gaps in the membrane that disrupt normal cellular function. C. perfringens can participate in polymicrobial anaerobic infections. Clostridium perfringens is commonly encountered in infections as a component of the normal flora. In this case, its role in disease is minor.

C. perfringens is an anaerobic bacterium, who acquires energy by performing anaerobic respiration using Nitrate as its electron acceptor. There is an increase in growth when this bacterium is grown in the presence of Nitrate, because this inorganic acceptor allows more metabolites molecules to undergo substrate-level phosphorylation reactions, leading to an increase yield in energy production. C. perfringens can also undergo anaerobic fermentation to produce gases, such as carbon dioxide, that may increase its survival by creating a preferred anaerobic habitat in host tissues. C. perfringens also has all the enzymes necessary to carry out glycolysis and glycogen metabolism. However, C. perfringens does not have a complete set of genes necessary for amino acid biosynthesis; in fact, only 45 enzyme-encoding genes were discovered. Therefore, C. perfringens cannot survive on media that are lacking an essential amino acid supply.

Pathology

C. perfringens is categorized into five serotypes—A, B, C, D, and E—depending on the types of extracellular toxins (alpha-, beta, epsilon-, and iota-toxins) they make and their forms of tropisms. C. perfringens is a pathogen whose primary targets are human and animals. The bacterium can be found in many different habitats, such as the normal flora of human gastrointestinal (GI) tract, and environment, such as sewage and soil. Several common diseases associated with C. perfringens are food-poisoning, gas gangrene, and many veterinary diseases. C. perfringens enterotoxin (CPE) is the main virulent factor that initiates many critical GI diseases. When food contaminated with C. perfringens is consumed, CPE begins its membrane action in a unique four-step mechanism.

1. Binding CPE to the target receptor on plasma membrane protein or claudin proteins, which leads to the formation of a small complex.

2. The complex then undergoes physical change when it binds to other membrane proteins and forms a larger complex in the membranes, which results in the disruption of the membrane’s permeability. This usually leads to cell death, because the osmotic equilibrium is not maintained due to the breakdown of the membrane’s permeability

3. CPE is capable of forming a larger complex in the membrane and its toxic level is greatly enhanced when the first 45 N-terminal amino acids are eliminated.

4. On the other hand, eliminating amino acids outside of residue 45 prohibits CPE from forming large complex, and thus loses its toxicity.

A range of veterinary enterotoxaemias are caused by toxins absorbed from the intestinal bacteria. These include; necrotic enteritis in poultry and fowl (type A), an enterotoxaemic jaundice in lambs (type A), lamb dysentery (type B), an enterotoxaemia in neonatal calves and foals (type B), a hemorrhagic enterotoxaemia in piglets, calves and foals (type C), Struck in adult sheep (type C), Pulpy kidney disease in sheep, goats and calves (type D) and a rare enterotoxaemia in calves and lambs (type E).

Clostridia-associated enterocolitis in horse

Clostridium difficile and C perfringens have been implicated in this acute, sporadic disease of horses characterized by diarrhea and colic. Because of uncertainty about the etiology, the condition has also been referred to as idiopathic colitis, but there is now good evidence that these organisms are responsible for enterocolitis in horses.

C difficile is found only infrequently and C perfringens is found in low concentrations in the feces of normal horses. Both organisms may be present in soil or the environment and be ingested by horses. The factors that trigger disease are not well known, but it is presumed that some alteration in the normal flora permits excessive multiplication of the bacteria, which produce toxins capable of causing intestinal damage and systemic effects.

Predisposing factors that have been suggested include change in diet and antibiotic therapy. Other host factors that may determine whether disease develops include age, immunity, and presence or absence of intestinal receptors for the clostridial toxins. C difficile produces protein toxin A or B or both in the intestine. Toxin A is an enterotoxin that causes hypersecretion of fluid into the intestinal lumen and also causes tissue damage. Toxin B is a potent cytotoxin that induces inflammation and necrosis.

Recent antibiotic therapy is a common feature of the history of horses with C difficile -induced diarrhea. Certain antibiotics, notably erythromycin, β-lactam antibiotics, and trimethoprim/sulfonamide, are more likely than others to be associated with C difficilecolitis. Mares with foals that are being treated with erythromycin appear to be at high risk.

Elimination of roughage from the diet prior to surgery is also reported to predispose to C difficile colitis.C perfringens type A is believed to cause diarrhea by elaboration of an enterotoxin (CPE), which is released during sporulation and stimulates intestinal epithelial cells to secrete excess fluid into the lumen. A novel necrotizing toxin, called β2, produced by some strains of C perfringens , has recently been strongly associated with colitis in horses.

The characteristic lesion is a necrotizing enterocolitis. There is severe loss of colonic and cecal mucosal epithelial cells, hemorrhagic colitis and typhlitis, and thrombosis in capillaries of the intestinal mucosa.

Clinical signs include sudden death, diarrhea with or without blood, colic, reduced feed intake, and lethargy. These clinical signs are also consistent with other causes of enterocolitis. Foals affected at <3 days old with C perfringens -associated enterocolitis often have bloody diarrhea and colic. C perfringens type C infection in neonatal foals has consistently been associated with severe GI disease. Several foals on a particular farm may be affected, but the disease is typically sporadic. The role of C perfringens type A in enterocolitis in neonatal foals is less clear; it has been reported that >90% of foals at 3 days of age shed this organism in their feces and that C perfringens type A is likely one of the first bacteria to colonize the intestinal tract of newborn foals, irrespective of hygiene protocols. C difficile has been associated with enterocolitis in newborn foals as well as in adult horses. It has been identified as a nosocomial infection in humans, and this may also be seen in horses.

Foals and adult horses may be affected. Typically there are signs of abdominal pain and diarrhea with or without blood. There may be abdominal distention, especially in cases of C difficile -induced diarrhea. Dehydration, toxemia, and shock may develop, and the mortality rate is variable. One or several animals on a farm may be affected.

Diagnosis

Clinical features of the disease are similar to those of acute salmonellosis, Potomac horse fever, or monocytic ehrlichiosis. The identification of C perfringens as the cause of diarrhea in horses depends on demonstration of the presence of enterotoxin or the gene for CPE in the feces or intestinal fluid and the absence of other likely etiologic agents. Most C perfringens found in the intestine of horses lack the gene for CPE. Demonstration of large numbers of bacterial spores or a high concentration of C perfringens in the feces are also aids to a diagnosis.

Control

Metronidazole and chloramphenicol for oral administration to high-risk horses is recommended. The sources of C difficile spores may be attacked by surface disinfection with a sporicidal disinfectant, and the spread may be reduced by hand washing and by isolation of infectious horses and foals. Supportive care by using IV polyionic fluids, supplemental electrolytes, antiinflammatories, and broad spectrum of antibiotics can be used if the horse is leukopenic and at risk of bacterial translocation across the compromised GI tract.

*Recent finding: The yeast of Saccharomyces boulardii has been shown to be protective in clostridia diarrhea by degrading C difficile toxins A and B.

Sources: Clostridia.net, C.Perfringens microbewiki.kenyon.edu, The Merck veterinary manual

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Pathology: Types of necrosis

3:13 PM | Labels: Pathology, types of necrosis

It's been a while since my last post. I was very busy last week so I dont have much time to update this blog. I'm just coming back from Ipoh, after attending Veterinary Association Malaysia congress and it was awesome. I can imagine myself standing there and present my research paper. Haha. Ok2, back to business!

Just started my pathology class and Prof Imad taught the first things about tissue injury and as well as necrosis.

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Types of necrosis

The death of cells in a living tissue is called Necrosis. Necrosis is commonly referred to as a bedsore. The degradation of the tissue starts with swelling within the cell and ultimately an interruption of the membranes of the cell. The organelles begin to breakdown and this spreads and causes an inflammation. Necrosis can be caused due to an injury or infection of some kind. If the infection is not tended to correctly, the chances of necrosis starting is more likely. Necrosis is more severe than other cell deaths in infections because once those cells die they can release chemicals that are harmful or will damage other cells.

example of necrosis: death tissue in LIVING cell

According to Prof Imad, there are 4 major types of necrosis namely; coagulative, liquefaction, caseous, and fat necrosis.

1. Coagulative necrosis

Coagulative: Caused by ischemia. Ischemia results in decreased ATP, increased cytosolic Ca++, and free radical formation, which each eventually cause membrane damage.

Decreased ATP results in increased anaerobic glycolysis, accumulation of lactic acid, and therefore decreased intracellular pH.
Decreased ATP causes decreased action of Na+ / K+ pumps in the cell membranes, leading to increased Na+ and water within the cell (cell swelling).
Other changes: Ribosomal detachment from endoplasmic reticulum; blebs on cell membranes, swelling of endoplasmic reticulum and mitochondria.
Up to here, the changes are reversible if oxygenation is restored by reversing the ischemia. If the ischemia continues, necrosis results, causing the cytoplasm to become eosinophilic, the nuclei to lyse or fragment or become pyknotic (hyperchromatic and shrunken). In the early stages of necrosis, the cells remain for several days as ghosts of their former selves, allowing one to still identify them and the tissue (in contrast to the other types of necrosis). The cellular reaction is polys, followed by a granulation tissue responses.

Coagulative necrosis

Characterised by preservation of tissue achitecture, increased cytoplasmic eosinophilia and nuclear changes. The cell may look pyknosis (chromatin clumping and shrinking: increased eosinophilia), karyorrhexis (fragmentation of chromatin), karyolysis (fading of chromatin material) and dissapearance of stainable nuclei

2. Liquefactive necrosis

Usually caused by focal bacterial infections, because they can attract polymorphonuclear leukocytes. The enzymes in the polys are released to fight the bacteria, but also dissolve the tissues nearby, causing an accumulation of pus, effectively liquefying the tissue (hence, the term liquefactive).

The result of hydrolysis. When the cells die, they are rapidly destroyed by lysosomal enzymes, either their own or those from neutrophilic leukocytes (i.e., bacterial infections), or clostridia or snake poison. Acid and lye burns represent the extreme of liquefaction. Also, if both neurons and glia are killed, dead brain liquefies rapidly.

Liquefactive necrosis that is caused by neurophilic leukocytes is called PUS. The term may also be used for an effusion that is full of dead neutrophils. Because of the extensive protein hydrolysis (i.e., more total molecules), there's a tremendous increase in the osmotic pull. This explains the familiar high-pressure in a ripened pimple -- and deep in the brain, for example, this is even more serious.

NOTE: The truism that "brain liquefies" is a common source of misunderstanding. Brain deprived of its oxygen for a few moments will suffer neuronal damage but not necrosis. Brain deprived of blood flow for a few moments longer will lose neuronal structure but not glia, and remain solid. The same is true of diseases in which neurons die off one at a time (i.e., Alzheimer's disease causes the brain to shrivel but not to liquefy). Only if the glia are killed does the brain melt away, and then only after several days.

Liquefactive necrosis in the brain

liquefactive necrosis of the brain demonstrates many macrophages at the right which are cleaning up the necrotic cellular debris.

3. Caseous necrosis

All of the cells in an area die, the tissue architecture is obliterated, and they turn into a crumbly ("friable"), readily-aerosolized powder.

A distinct form of coagulative necrosis seen in mycobacterial infections (e.g., tuberculosis), or in tumor necrosis, in which the coagulated tissue no longer resembles the cells, but is in chunks of unrecognizable debris. Usually there is a giant cell and granulomatous reaction, sometimes with polys, making the appearance distinctive.

Gross appearance of caseous necrosis in a hilar lymph node infected with tuberculosis. The node has a cheesy tan to white appearance. Caseous necrosis is really just a combination of coagulative and liquefactive necrosis that is most characteristic of granulomatous inflammation.

Found in granulomatous inflammation; manifestation of partial immunity of interaction T-Lymphocyte, macrophage, and cytokines associated with tubercolosis. Architecture is not preserved but tissue is not liquefied. Grossly soft and cheeselike. Histologically amorphous and acidophilic.

4. Fat necrosis

A term for necrosis in fat, caused either by release of pancreatic enzymes from pancreas or gut (enzymic fat necrosis) or by trauma to fat, either by a physical blow or by surgery (traumatic fat necrosis). The effect of the enzymes (lipases) is to release free fatty acids, which then can combine with calcium to produce detergents (soapy deposits in the tissues). Histologically, one sees shadowy outlines of fat cells (like coagulative necrosis), but with Ca++ deposits, foam cells, and a surrounding inflammatory reaction.

This is fat necrosis of the pancreas. Cellular injury to the pancreatic acini leads to release of powerful enzymes which damage fat by the production of soaps, and these appear grossly as the soft, chalky white areas seen here on the cut surfaces.

Fat necrosis adjacent to pancreas is seen here. There are some remaining steatocytes at the left which are not necrotic. The necrotic fat cells at the righthave vague cellular outlines, have lost their peripheral nuclei, and their cytoplasm has become a pink amorphous mass of necrotic material.

Other types of necrosis

5. Gangrenous necrosis

Due to cut off blood supply to lower extremities or bowel due to vascular occlusion.

GANGRENE ("gangrenous necrosis") is not a separate kind of necrosis at all, but a term for necrosis that is advanced and visible grossly. If there's mostly coagulation necrosis, (i.e., the typical blackening, desiccating foot that dried up before the bacteria could overgrow), we call it DRY GANGRENE. If there's mostly liquefactive necrosis (i.e., the typical foul-smelling, oozing foot infected with several different kinds of bacteria), or if it's in a wet body cavity, we call it WET GANGRENE.

Occur to most diabetic patients

Gangrenous necrosis at lower limb (dry gangrene)

wet gangrene (bacterial rich)

6. Fibrinoid necrosis

Due to the deposition of fibrin-like material on arterial walls due to immune-mediated vasculitis.

Fibroid necrosis: smudgy pink material in vascular walla with or without necrosis

Sources: USMLE wiki: Cell pathology; cell injury and death Ed Friedlander M.D pathologist; cell injury and necrosis www.uvm.edu; cell injury, library.med.utah.edu

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Hypovolemic shock (haemorrhagic)

Old times..

Clostridium Perfringens in horse

Pathology: Types of necrosis