Pathology - First Aid / Pathoma Flashcards
Apoptosis
Programmed cell death. ATP required.
No inflammation.
Intrinsic: mitochondrial pathway (due to cell injury, DNA damage, or decreased hormonal stimulation) leads to inactivation of Bcl2
Extrinsic: rs ligand pathway
- FAS ligand binds FAS death rs (CD 95) on target cells which activates caspases
- TNF binds TNF rs on target cell and activates caspases
Cytotoxic CD8+ T cell mediaited pathway:
Perforins secreted and create holds in membrane through which granzymes enter to activate caspases.
Proapopotic proteins
BAX
BAK
Apaf-1
Anti-apoptotic proteins
Bcl-2
ex. follicular lymphoma w/ t(14;18) and overly expressed Bcl-2 which inhbits Apaf-1
Types of Necrosis
Coagulative. Liquefactive. Gangrenous (dry and wet). Caseous. Fat (saponification/dystrophic calcification seen) Fibrinoid.
Reversible cell injury Characteristics
Cell/mitochondrial swelling - loss of microvilli and membrane blebbing.
Swelling of RER - dissociation of ribosomes and decreased protein synthesis.
Fatty change.
ATP depletion.
Glycogen decreased.
Irreversible cell injury Characteristic
Nuclear pyknosis, karyorrhexis, karyolysis.
Hallmark of irreversible injury is : any type membrane damage.
-PM damage
-mitochondiral membrane damage
-lysosomal membrane damage
Chromatolysis
Process involving neuronal cell body following axonal injury (first aid 225)
Leukocyte extravasation
- Margination and Rolling
- Adhesion/Tight binding
- Transmigration/Diapedesis @ post-cap venule
- Migration/Chemotaxis
- Phagocytosis
- Destruction of phagocytosed material
*first aid 227
How does Free Radical Injury arise?
Ionizing radiation.
Inflammation (ex. WBC NADPH oxidase).
Metals.
Drugs and chemicals (P450 etc).
How to Eliminate Free Radicals?
Antioxidants (glutathione; Vitamins ACE)
Metal Carrier Proteins (transferrin, ceruloplasmin)
Scavenging enzymes (Superoxide dismutase, catalase, glutathione peroxidase)
Two tissue mediators that stimulate angiogenesis…
FGF. “fibroblast growth factor”
VEGF. “vascular endothelial growth factor”
Phases of wound healing
Inflammatory
Proliferative
Remodeling
Primary amyloidosis
Systemic deposition of AL amyloid.
Derived from Ig light chain
Associated with plasma cell dsycrasias (ex. multiple myeloma)
Secondary amyloidosis
Systemic deposition of AA amyloid which is derived from the acute phase reactant SAA
Chronic inflammatory states.
Familial Mediterranean fever (FMF).
Classic findings of Systemic Amyloidosis
Diverse involvement since almost any tissue can be involved:
Nephrotic syndrome (kidney is mc involved).
Restrictive cardiomyopathy or arrhythmia.
Tongue enlargement, malabsorption, hepatosplenomegaly.
- Amyloid can’t be removed - organs must be transplanted
- Diagnose via tissue biopsy (ex. abdominal fat pad or rectum) - congo red stain/apple green biorefringence
Localized Amyloidosis
Senile cardiac amyloidosis. Familial amyloid cardiomyopathy. T2DM. Alzheimer disease. Dialysis-associated amyloidosis. Medullary carcinoma of the thyroid.
What’s a benign/malignant name for neoplasm of connective tissue?
Fibroma.
Fibrosarcoma.
Carcinomas spread via…
Lymphatics.
Exceptions: Renal cell carcinoma Hepatocellular carcinoma Follicular carcinoma of the thyroid Choriocarcinoma
Diseases assoc. w/neoplasms: Acanthosis nigricans
rare paraneoplastic indicator of visceral malignancy
but more commonly assoc. with insulin resistance
Diseases assoc. w/neoplasms: Barrett esophagus
Esophageal ADC
Diseases assoc. w/neoplasms: Chronic atrophic gastritis, postsurgical gastric remnants
Gastric carcinoma
Tuberous Sclerosis
Rare multisystem genetic disease that causes benign tumors to grow in the brain and on other vital organs such as the kidneys, heart, eyes, lungs, and skin.
A combination of symptoms may include seizures, intellectual disability, developmental delay, behavioral problems, skin abnormalities, and lung and kidney disease.
TSC is caused by a mutation of either of two genes, TSC1 and TSC2, which code for tumor growth suppressor proteins hamartin and tuberin, respectively.
Ex. A child presents w/mental retardation, seizures, and facial angiofibromas. What 3 tumors is this child at risk for?
Often manifests w/multiple hamartomatous (benign) tumors including giant cell astrocytoma, renal angiomyolipoma, and cardiac rhabdomyomas; the tumors may become malignant
Plummer-Vinson syndrome
AKA Paterson–Brown–Kelly syndrome or sideropenic dysphagia.
Rare disease characterized by difficulty in swallowing, iron deficiency anemia, glossitis, cheilosis and esophageal webs. Treatment with iron supplementation and mechanical widening of the esophagus generally provides an excellent outcome.
Nowadays, extremely rare. Generally occurs in postmenopausal women.
Increased risk of squamous cell carcinomas of the esophagus and pharynx
