Pathology Flashcards
Pyknosis
irreversible condensation of chromatin in the nucleus of a cell undergoing apoptosis
Karyorrhexis
destructive fragmentation of a dying cell (cell undergoing apoptosis); irreversible
Karyloysis
Dissolution of the chromatin/Fading of the nucleus of a dying cell; part of apoptosis; irreversible
Apoptosis vs Necrosis
Apoptosis–>no inflammation; form apoptotic bodies, which are phagocytosed
Necrosis –> swelling and inflammation; intracellular components extravasate
Cell injury that’s reversible with oxygen:
- decreased ATP synthesis
- Cellular swelling (ie no ATP –> impaired Na/K pump)
- Nuclear chromatin clumping
- decreased glycogen
- fatty change
- ribosomal detachment (decreased protein synthesis)
Cell injury that’s irreversible
- Nuclear pyknosis, karyolysis, karyhorrhexis (all processes involved in apoptosis)
- Calcium influx–> caspase activation
- plasma membrane damage
- lysosomal rupture
- mitochondiral permeability (ie with intrinsic pathway of apoptosis)
Areas that are susceptible to hypoxia:
- Watershed areas –> Splenic flexure and ACA/MCA
- Subendocardial tissue of heart
- Proximal Tubule in cortex of Kidney
- Thick Ascending limb in medulla of kidney
- Neurons
- Area around central vein of liver
Red vs Pale Infarcts
Red = hemorrhagic; happens in tissues with loose collaterals, like liver, lungs, intestine; or, after reperfusion of an area
Pale happen in solid tissues with old one blood supply (like heart, kidney, spleen)
What causes reperfusion injury?
Damage by free radicals
Hypovolemic/Cardiogenic Shock vs Septic Shock findings:
Hypovolemic/Cardiogenic:
- LOW-output failure
- increased TPR
- Low cardiac output
- Cold, Clammy pt
Septic Shock:
- HIGH-output failure
- decreased TPR
- dilated arterioles, high venous return
- Hot patient
Mediators of fluid exudation in inflammation:
- Histamine
- Serotonin
- Bradykinin
Acute phase cytokines associated with inflammation?
IL-1
IL-6
TNF-alpha
Metalloproteinases:
Enzymes involved in remodeling of ECM following injury
–> require ZINC! this is why Zinc deficiencies result in delayed wound healing!
Why is vitamin C important for wound healing?
–>fibrosis, need collagen for deposition of ECM; need vitamin C for collagen!
Two supplements given to pts who are healing:
- Vitamin C (for collagen)
- Zinc (for metalloproteinases)
5 steps of Leukocyte Extravasion:
1) Rolling (E- and P-Selectins and Sialyl Lewis leukocyte)
2) Tight binding (ICAM and Integrin)
3) Diapedesis (PECAM)
4) Migration (Bacterial products and chemotactic signals = C5a, IL-8, LTB4, Kallikrein)
5) Phagocytosis
signals for neutrophil chemotaxis?
C5a
IL-8
Leukotriene B4
Kallikrein
Delayed separation of umbilicus, and abnormal integrin:
Leukocyte Adhesion Deficiency
Which vitamins are anti-oxidants (can eliminate free radicals)?
A, C, E
3 phases of wound healing: When does each phase occur? which cells are the mediators? characteristics?
1) Inflammatory
2) Proliferative
3) Remodeling
1) Inflammatory:
- ->occurs immediately
- ->Mediators: platelets, neutrophils, macrophages
- ->form clot, neutrophils go into tissue, macrophages clean up
2) Proliferative:
- ->2-3 days after wound
- ->Mediators: fibroblasts, myofibroblasts, endothelial cells, keratinocytes
- ->granulation tissue, collagen, angiogenesis, epithelial cell proliferation, dissolve clot, wound contraction
3) Remodeling:
- ->1 week after wound
- -> Mediators: Fibroblasts
- -> Type I collagen replaces type III collagen (type I is for late wound repair; type III is for granulation/early wound repair)
Type of collagen involved in early wound healing? late wound healing?
-Early wound healing –> granulation tissue –> Collagen Type III
Late wound repair –> Scar tissue –> Type I collagen (stronger)
Pathogenesis of granuloma formation:
Th1 cells secrete IFN-gamma –> activate macrophages –> macrophages secrete TNF-alpha –> induces and maintains granuloma formation
***If give pt with a granuloma an anti-TNF drug –> drug can break down granulomas, leading to disseminated disease
Transudate vs Exudate:
- Transudate:
- Hypocellular
- Protein poor
What is the ESR?
- -> Erythrocyte sedimentation rate
- -> inflammatory products, like fibrinogen, coat RBCs, causing them to aggregate. So, when put in test tube, aggregated RBCs fall at a faster rate….
3 conditions with DECREASED ESR?
- Sickle Cell (weird RBC shape!)
- Polycythemia (too many RBCs!)
- CHF (not sure why…)
5 states in which have increased ESR?
- inflammation
- infection
- cancer
- pregnancy
- SLE
Bence Jones
=amyloid seen in multiple myeloma; derived from Ig light chains
Beta-amyloid
amyloid protein in Alzheimer’s deases
Beta-2-microglobulin
protein seen in dialysis-associated amyloidosis
*note: have B2-microglobulin on MHC I; this amyloid is derived from MHC-I proteins
Transthyretin
protein seen in senile cardiac amyloidosis
A-CAL protein
protein seen in Medullary Carcinoma of the thyroid
–>derived from Calcitonin
Carcinoma in situ =
Pre-invasive
- ->cells have not yet invaded basement membrane, but neoplastic cells encompass entire thickness
- ->have high nuclear/cytoplasmic ratio and clumped chromatin
What enzymes do neoplastic cells use to invade the basement membrane?
Collagenases and Hydrolases (metalloproteinases)
Hamartoma =
mass of MATURE tissue ENDOGENOUS to site from where it originates (similar to hyperplasia…)
Hyperplasia = Metaplasia = Dysplasia = Anaplasia = Neoplasia = Desmoplasia =
Which of these processes are reversible? irreversible?
Hyperplasia–> increased # of cells
Metaplasia–> one adult type replaced by another
Dysplasia–> abnormal growth, loss of cellular orientation, shape, size; commonly pre-neoplastic
Anaplasia–>abnormal cells, lack differentiation; very primitive; little/no resemblance to tissue of origin
Neoplasia–> uncontrolled, excessive, clonal proliferation of cells
Desmoplasia–> fibrous tissue formation in response to neoplasm
Features of Anaplastic cells:
- high nucleus:cytoplasm ratio
- prominent nucleoli
- nuclear chromatin clumpin
- lots of mitotic figures
Are mature teratomas benign or malignant?
in women–> benign
in men–> malignant
