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31 Cards in this Set

  • Front
  • Back
Speed, duration, and types of cells involved in Acute inflammation
Rapid onset (minutes), short duration (hours days), leukocytes, neutrophils.
What types of things cause acute inflammation
1) Infection and microbial toxins
2) Necrosis via ischemia, trauma, or injury
3) Foreign body
4) Hypersensitivity Rx
What type of things cause chronic inflammation without ever being acute first
1) Rheumatoid arthritis
2) Atherosclerosis
4) TB
5) Persistent infection from certain organisms and viruses
6) Immune mediated inflammatory (autoimmune/allergic)
7) Prolonged exposure to toxic agents.
Serous inflammation
Type of acute inflammation. Thin fluid from plasma or secreted mesothelial cells lining a cavity (effusion). Blister is an ex.
Fibrinous Inflammation
Type of acute inflammation. Increased vasc permiability, allows large molecules like fibrinogen to get into extravascular space and deposit fibrin. Occurs with large vascular leak or procoagulant stimulus (ex cancer cells). Fibrin over time makes scar.
Suppurative inflammation
Type of acute inflammation. Purulent. Lots of pus, neutrophils, liquefactive necrosis, and edema. Bacteria usually gram + cocci or gram - rod via release of chemo-attractants. An abscess is this type of inflammation.
Abscess
Type of suppurative acute inflammation. Is a localized collection of purulent inflammatory tissue. Have central necrosis of leukocytes and tissue surrounded by neutrophils and vascular dilation and fibroblastic proliferation. Will heal with fibrosis and scar.
Ulcer
Type of acute inflammation. Produced by shedding of inflamed necrotic tissue. Occur near a surface like mouth, gut, GI, skin.
Granulomatous Inflammation
Type of chronic inflammation. Is a circumscribed collection of epitheliod histiocytes. Can have surrounding lymphocytes and giant cells. Can be caused by:
-TB and leprosy
-Sarcoidosis
-cat scratch disease
-lymphogranuloma inguinale
-brucellosis
-syphilis
-histoplasma
-berrylliosis
-Rx to lipids
-Foreign body
-Chron disease
-Shistosome egg
Causes of pneumonia in aids patients
Most common cause is Pneumocystis jiroveci. Can also be caused by:
-candida
-cytomegalovirus
-Crypto
-histoplama
-herpes
-mycobacteria
-Toxo
-papoviruses
Candidas infection in aids patients
Most common fungal infection in aids patients. Usually in mouth (get flush), vagina, and esophagus.
Cytomegalovirus in aids patients
Causes retinitis, esohphagitis, colitis, and multiple mucosal ulcerations.
Herpes simplex virus in Aids patients
Causes mucocutaneous ulcerations of the mouth, esophagus, external genitalia, or perianal region.
Mycobacterial infections in aids patients
Can get infected with M.avium. 1/3 of all AIDs deaths are due to TB.
CNS infection in AIDS patients
Cryptococcus can cause meningitis.
Toxo can cause meningitis and CNS mass lesions.
JC virus (a papovirus) can cause progressive multifocal leukoencephalopathy.
What causes tumors in aids patients
An ocogenic DNA virus. Infection cant be contained in aids patients.
What causes Kaposi Sarcoma in AIDS patients
HHV-8 infection, found in all types if KS. Virus encodes for proteins which interfere with p53 and RB suppressor pathways. However, HHV-8 needs a cofactor, which HIV provides.
What is present in Kaposi sarcoma in aids patients
Prolif of spindle-shaped cells with features of endothelial and smooth muslces cells with vascular spaces. Cells produce pro-inflammatory and angiogenic factors. Unlike reg KS, aids kind have wide spread skin, mucus, GI, lymphnode, and pulmonary disease. More aggressive in general.
Non-hodgikins lymphoma in aids patients
120x more common in aids patients than general pop, especially if CD4 is low.
Systemic lymphoma in aids patients.
Caused by EBV, is 80% of aids related lymphomas. Hits lymph nodes, CNS, GI, salivary glands, and lungs
Primary CNS lymphoma in aids patients
Caused by EBV, 1000x more likely in aids patients than general pop.
Body cavity based primary effusion lymphoma in aids patients
Rare, linked to KSHV. Patients present with pleural, peritoneal, and pericardial effusion.
Amyloid definition
Randomly oriented protein fibrills that share physical and chemical properties. Are proteins misfolded into beta pleated sheets and deposited in the extracellular space. This can be because of excessive production of a protein (AL, AA) or it can be a mutated protein (TTR).
AL
Amyloid light chain. Called a primary amyloidosis, is most common. Caused by protein excess. Derived from Ig light chains made from a monoclonal plasma cell pop. Usually lambda light chains.
AA
Amyloid associated. Caused by protein excess. Made from a unique protein called SAA made by the liver. Protein production increases during inflammation as part of acute phase response of chronic. Associated with rheumatoid arthritis, ankylosing spondylitis, Crohn disease, ulcerative colitis, and in skin-poppers.
TTR
Also called familial or hereditary amyloidosis. Amyloid caused by mutated Transthyretin, a serum protein that binds and transports thyroxine and retinol. Deposits in peripheral nerve. Can also get cardiac symptoms.
There is also a senile cardiac amyloidosis where amyloid is deposited in the heart but TTR has normal conformation. Get restrictive cardiomyopathy and arrhythmia.
Amyloidosis presentation via light and electron microscope
By light, extracellular hyaline pink deposits stain with congo red stain and if viewed with polarized light, have apple green appearance.
By electron microscopy, made of continuous, non branching fibrils
Amyloidosis gross appearance of organs involved
Organ is firm and waxy
Organs often involved in amyloidosis
Kidney, if glomerulus, get protienuria.
Heart leads to congestive heart failure, restrictive cardio myopathy, and arrhythmias.
Tongue becomes enlarged (teethmarks on the periphery are a giveaway) can affect speach and swallowing.
GI can cause malabsorbtion, diarrhea, and disturbance.
Also can involve liver, spleen, and thyroid.
How is amyloidosis diagnosed?
Based on histology.
Why is amyloidosis harmful
Deposits itself in the place of normal tissue. Damage can also be related to interaction with receptors for advanced glycation end-products (RAGE), oxidative stress, and apoptosis.