Lung undergoing acute vasodilation.

Leads to outpouring of fluid with fibrin into alveolar space, along with PMN's.

Vasodilation(blood flow to area of inflammation leading to redness and heat)->vascular permeability(endothelial cells become "leaky" from direct endothelial cell injury or via chemical mediators)->exudation(fluid, proteins, RBC's, WBC's excape from intravascular space as a result of increased osmotic pressure extraascularly and increased hydrostatic pressure intravascularly)->vascular stasis(slowing of blood in the bloodstream w/vasodilation and fluid eudation to allow chemical mediators and inflammatory cells to collect and respond to stimulus)

Acute inflammation-later stage.

Fibrin mesh(stringy) in fluid with PMN's has formed in the area of inflammation. This fluid produces "tumor"/swelling of acute inflammation.

Neutrophils: Little black dots; arrive within 24 hours to take away microbes.

Macrophages: Bigger blobs; come in after neutrophils to end acute reaction and clean up other debris.

Meningitis.

Yellow-tan exudate of acute bacterial meningits obscures the sulci.

White stuff=neutrophils and fibrin, will be found in CNS fluid with spinal tap.

Vasculitis (acute inflammation of blood vessel).

Demonstrates the destruction that can accompany the acute inflammatory process and the interplay with the coagulation mechanism.

Arterial wall is undergoing necrosis, there's thrombus formation in the lumen.

Vasculitis: in a small vessel may present as a rash; can have infectious or non-infectious cause.

Arterial vasculitis-higher magnification.

Can see arterial wall necrosis, fragmented remains of neutrophilic nuclei(karyorrhexis), and scattered inflammatory cells. Neutrophils are  dying via apoptosis or disintegrating, so vasculitis is probably of non-infectious origin.

Acute inflammation is a non-selective process that can lead to tissue destruction.

Gall bladder-cuboidal grandular epithelium.

Neutrophils are infiltrating mucosa and submucosa of the gallbladder in a patient w/ acute cholecystitis.

Cholecystitis: often associated with gall stones that irritate the mucosa causing acute inflammation; may lead to chronic inflammation and fibrosis in gall bladder. Patients may or may not have jaundice (depending if bile duct's blocked), will often have nausea, vomiting, fever, pain. Surgery needed so cancer doesn't develop.

Lung with acute bronchopneumonia.

PMN's are in alveoli. Patient has productive cough b/c large amounts of purulent sputum(neutrophils form exudate in the alveoli) were produced. 

Likely bacterial b/c neutrophils are in alveolar space(in viral, they're in alveolar walls).

Alveolar walls intact->early infection or patient is getting treatment.

Lung with bronchopneumonia-gross.

It's abscessing(dark spots) and has numerous areas of raised, lighter tan appearance which are the areas containing the extensive neutrophilic infiltrates.

Dark spots could be necrotizing tissue, not necessarily abscesses.

Acute abscessing pneumonia.

You can see extensive neutrophilic exudate. 

No granulation tissue/fibrosis around neutrophils so it's not an abscess yet, but the tissue destruction and necrotizing pattern leads to abscess formation that can cause a scar and chronic inflammation.

Alveoli are collapsed and there's neutrophil and macrophage accumulation.

There's loss of alveolar walls and tissue destruction, so it's a necrotizing pattern.

Ulceration of gastric mucosa.

A consequence of acute inflammation on epithelial surfaces, submucosa and vasculature is exposed.

A large ulcer and several adjacent smaller ones w/ surrounding erythema appear left of center at the gastroesophageal junction.

Peptic ulcers are usually solitary and associated w/ H.Pylori and hyperacidity, while stress(illness, trauma, burns, etc) ulcers  involve hyperacidity and ischemia and result in many small ulcers.

Lung of a patient with influenza A.

Certain etiologic agents like viruses are more likely to lead to chronic inflammation.

Inflammatory infiltrates of chronic inflammation are more likely to be interstitial(within tissues) rather than exudative like acute inflammtion.

Potential space in the interstitium is widened due to lymphocyte accumulation, alveolar lumen is clear.

Patients tend to present with dry cough, hacking, and low-grade fever.

Rheumatoid arthritis.

Dark blue lymphocytes can be seen in the synovium. Synovium should be 1-2 cells thick, but in RA it proliferates and grows in joint spaces->can impinge joint space and erode bone.

Fingerlike projections occur when the immune cells aggregate and lymphocytes form lymphnoid nodules.

A variety of inflammatory cell types may present though 1 may predominate. Here are mainly neutrophils, but also plasma cells, lymphocytes, and macrophages.

Macrophages: phagocytose other cells and debris; one in this slide has "pigged out" by consuming a neutrophil, RBC, and a nuclear fragment.

Granulomatous inflammation-hilar lymph node granuloma

Granuloma tends to be a well-fromed focal lesion. Granulomas due to infection are often caseating b/c they have prominent caseous necrosis.

Epithelioid cells around the center of a granuloma.

Have pink cytoplasm similar to squamous epithelial cells and their nuclei tend to be long and stringy.

Can see some necrosis at the top and epitheloid or spindle shaped macrophages down below.

In TB: Patients may display a scar after TB bacteria is killed or could get primary progressive disease or can get secondary if TB reactivated later in life.

Sarcoidosis

Sarcoidosis is a hilar lympathopathy and granulomas tend to be well formed.Two pulmonary granulomas, consisting of epithelioid macrophages, giant cells, lymphocytes, plasma cells, and fibroblasts, maybe some neutrophils.

Granulomas are associated with multinuclear cells and can be immune type or non-immune type, caseating or non-caseating.

Foreign body type giant cell at upper left of center adgacent to vegetable material aspirated into lung(can cause pneumonia and infection if immune system doesn't clear it). Foreign body giant cells have nuclei scattered haphazardly arond cell.

There are lots of neutrophils so we can assume it's an acute infeciton, but there's some giant cells coming in.

IV drug user.

Bright crystals are talc, the talc was used to dilute the injected drug. The foreign material can produce a granulomatous reaction.

High magnificaton granulation tissue

Has capillaries, fibroblasts, and a variable amount of inflammatory cells(mostly mononuclear with the possibility of some PMN's).

Scarring

Inhaled silica in the lung persists indefinitely and produces an inflammatory reaction that's marked by prominent fibrosis.

Dense pink collagen is seen at the center of the nodule.

Healing biopsy site on the skin.

Skin surface has re-epithelialized the week following the excision.Below there's granulation tissue with small capillaries and fibroblasts forming collagen.

After a month, just a small collagenous scar will remain.