Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
142 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Erythroid hyperplasia |
High altitude |
|
|
|
No hyperplasia |
Cardiac myocytes
Skeletal muscles
Nerve/neurons |
|
|
|
Increase in the size of cells resulting to increase in the size of the organ or tissue |
Hypertrophy |
|
|
|
Constitutes in an increase number of cells in an organ or tissue resulting into increased volume or size |
Hyperplasia |
|
|
|
Thickness of left Ventricular hypertophy |
> 1.5 cm |
|
|
|
Most common cause of sudden cardiac death |
Hypertrophic cardiomyopathy |
|
|
|
Shrinkage in the size of the cell by loss of cell substance |
atrophy |
|
|
|
1st mechanism in decrease in cell size |
Ubiquitin proteasome degradation of cytoskeleton |
|
|
|
2nd mechanism in decrease in size |
Mannose 6 phosphate (autophagy) |
|
|
|
Lysosomal storage disease associated with defective phosphotransferace |
Icell disease |
(mucolipidosis II) is a rare inherited metabolic disorder characterized by coarse facial features, skeletal abnormalities and mental retardation |
|
|
Reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type |
Metaplasia |
|
|
|
Most common metaplasia |
(Squamous metaplasia)
columnar to squamous due to smoking* |
|
|
|
Most common metaplasia |
squamous metaplasia |
|
|
|
Mechanism of metaplasia |
reprogramming of stem cells |
|
|
|
Example of Squamous to columnar metaplasia |
Barrett esophagous |
|
|
|
Length of gastro esophageal junction |
40 cm |
|
|
|
Treatment for acute promyelocitic leukemia (m3) |
ATRA (all trans retinoic acid)?? |
|
|
|
Retinaldehyde |
normal vision |
|
|
|
Tansloaction gene 15 or 17 pml rara Associated with DIC ?? |
Acute promyelocytic leukemia |
|
|
|
Mesenchymal tissue can undergo metaplasia
Inflammation of skeletal muscle results in a metaplastic production of bone
Muscle to bone |
Myosistis ossificans |
|
|
|
Disorganized cellular architecture
Pre malignant
Reversible |
Dysplasia |
|
|
|
Most common cause of cellular injury |
Hypoxia |
|
|
|
Lack of O2, failure of cell to synthesize suffecient ATP by aerobic oxidation |
Hypoxia |
|
|
|
Causes of hypoxia |
ischemia
Hypoxemia
Decrease oxygen carrying capacity |
|
|
|
Decrease in blood flow in an organ |
Ischemia |
|
|
|
2 ways of ischemia |
Arterial (atherosclerosis) or Venous |
|
|
|
Most common cause of budd chiarri syndrome |
Polycythemia vera |
|
|
|
Myeloproliferative dse
JAK 2 MUTATION ?? |
Polycythemia vera |
|
|
|
Low partial pressure of oxygen in the blood
PaO2 Less than 60mmhg, SaO2<90% |
Hypoxemia |
|
|
|
Binds to hemoglobin 100 times affinity compared to oxygen |
carbon monoxide |
|
|
|
PaO2 is normal and SaO2 is decreased Cherry red appearance Earliest sign is headache |
Carbon monoxide poisoning |
|
|
|
Iron binds to oxygen
PaO2 is normal , SaO2 is decreased
Associated with sulfonamides and nitrates |
Methhomoglobenimia ?? |
|
|
|
Consequences of hypoxia |
impaired oxidative phosphorylation
- decrease atp : cellular swelling - Aerobic glycolysis |
|
|
|
Reversible injury hallmark |
Cellular swelling |
|
|
|
Effects of cellular swelling |
Loss of microvilli
Membrane blebbing
Swelling of Rough endoplasmic reticulum |
|
|
|
Hallmark of irreversable damage |
Membrane damage |
|
|
|
Cytochrome responsible for apoptosis
Site: Mitochondria |
Cytrochrome c |
|
|
|
Programmed cell death |
Apoptosis |
|
|
|
In irreversable injury sequence of events |
Biochemical , Ultastructural, Light microscopy, Gross |
|
|
|
Hallmark of reversible injury |
Cellular swelling |
|
|
|
Morphologic hallmark of cell death |
Loss of nucleus |
|
|
|
End result of irreversible injury |
cell death |
|
|
|
Order to cell death |
pyknosis , karyorrhexis ,karyolysis |
|
|
|
Irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis |
pyknosis |
|
|
|
Needs energy Activation of enzyme caspases |
Apoptosis |
|
|
|
Inactive proenzymes or zymogens |
caspases |
|
|
|
2 phases of apoptosis initiation |
intrinsic: mitochondrial (cytochrom c) Extrinsic: death receptors (fas and TNF receptor) |
|
|
|
Major mechanism Intrinsic Leakage of cytorhrome c Activate of caspases |
Mitochondrial pathway |
|
|
|
Bcl2 , bcl xl ,mcl |
Anti apoptotic |
|
|
|
Bax, bak, bad |
pro apoptotic |
|
|
|
Death receptor , initiation |
Caspase 8 |
|
|
|
Mitochondrial, initiation |
caspase 9 |
|
|
|
Execution phase |
Caspase 3 and 6 |
|
|
|
Combination of both apoptosis and necrosis |
Necroptosis |
|
|
|
RECEPTOR ASSOSCIATED KINASE 1 (RIP) |
Necroptosis |
|
|
|
Pyroptosis |
IL1 |
|
|
|
Spectrum of morphologic changes that follow cell death in living tissue
Pathologic |
necrosis |
|
|
|
Architecture of dead tissues is presserved for a span of at least some days
All organs except brain Area of infarct is wedge shaped |
Coagulative necrosis |
|
|
|
Brain necrosis |
Liquefactive |
|
|
|
Digestion of dead cells resulting in the transformation if the tissue into a liquid viscous mass |
liquefactive necrosis |
|
|
|
3 circumstances of liquefactive necrosis |
Brain Abscess Pancreatitis |
|
|
|
Coagulative necrosis that resembles mummified tissue (dry)
Super imposed infection (wet) |
Gangrenous necrosis |
|
|
|
Cottage cheese like material
Combination of coagulative and liquefactive
Chronic granulomatous ??? |
Caseous necrosis |
|
|
|
Chalky white appearance due to deposition of calcium
Pancreas, breast |
Fat necrosis |
|
|
|
Immune reactions involving blood vessels
Leaking of protiens into vessel wall results in bright pink staining |
Fibrinoid necrosis |
|
|
|
Sequence of necrosis |
Pyknosis, karyorrhexis, karyolysis |
|
|
|
4 causes of intracellular accumulations |
Abnormal metabolism Defect in protien folding transport Lack of enzyme Exogenous |
|
|
|
Werner syndrome enzyme defect premature aging |
DNA helicase |
|
|
|
Calcification in nonviable or dying tissue Normal calcium serum levels |
Dystrophic calcification |
|
|
|
Elevated serum calcium or phosphate |
Metastatic calcification |
|
|
|
Caloric restriction increases longevity by |
Reducing the signaling intensity igf 1 pathway ( decreases igf1) Increasing sirtuins |
|
|
|
Destroy or wall off injurious agents |
Inflammation |
|
|
|
Cardinal signs of acute inflammation |
Rubor, calor, tumor, dolor, functio laesa |
|
|
|
Predominantly neutrophilic |
Acute inflammation |
|
|
|
Presence of fibrosis |
chronic inflammation |
|
|
|
Hallmark of acute inflammation |
Swelling or edema
Local decreased blood circulation |
|
|
|
Sensitizes sensory nerve endings causing pain (dolor) |
Bradykinin and PGE2 |
|
|
|
Cause of rubor |
Histamine, prostaglandin and kinins |
|
|
|
Inflammation on 30 seconds the vessel will |
vasoconstriction |
|
|
|
Inflammation upon 1minute the vessel will |
Vasodilation |
|
|
|
In lights criteria: Cellular
Rich protien
Specific gravity greater than 1.012
Usually from Infections |
Exudate |
|
|
|
Cellular event, Neutophils cling to the walls of the capillary |
Margination |
|
|
|
Cellular events |
Leukocyte extravasation Phagocytosis |
Please look for video of this |
|
|
chemotaxic factors |
C5a , c3b opsonins |
|
|
|
Pavementing (leukocyte line the ensothelial surface) |
Rolling |
|
|
|
Selectins (p and e) will attach to this upon rolling to slow down |
Sialyl lewis x |
|
|
|
Adhesion molecules on the surface of endothelium and Upregulated by |
Tnf and il 1 |
|
|
|
Integrins present in leukocytes and upregulated by |
C5a and ltb4 |
|
|
|
For adhesion arrest and transmigration |
Icam-1 endothelial molecule
Cd11 / cd8 integrins |
|
|
|
Autosomal recessive defect of integrins (Cd18 subunit /b2 integrin)
Delayed seperation of the umbilical cord
Increase circulating neutrophils
Recurrent bacterial infections |
Leukocyte adhesion defect 1 |
|
|
|
Uni-directional movement of leukocytes towards the site of injury |
Chemotaxis |
|
|
|
Chemotaxic factors |
bacterial products Complement system ( c5a) Arachidonic acidnmedabolism |
|
|
|
3 major opsonins |
Fc fragment of IgG antibodies
C3b (complement)
Plasma lectins |
|
|
|
Process of coating a particle by opsonins to target it for ingestion |
Opsonization |
|
|
|
Decreased leukocyte function of mutation affecting involved lysosomal membrane traffic
Giant granules
Increase risk for pyogenic infections
Primary hemostasis, Albinism
Microtubule system defect |
Chediak higashi syndrome |
|
|
|
Decreased oxidarive burst |
Chronic granulomatous disease |
|
|
|
Most effective mechanism for phagocytosis |
Oxygen dependent killing |
|
|
|
Needed for oxygen dependent killing |
nadph oxidase Sod Mpo |
|
|
|
Nadph oxidase defecr |
cgd |
|
|
|
Destroy using enzymes in secondary granules |
oxygen independent killing |
|
|
|
Preformed mediators |
Histamine (inflammation)
Serotonin (platelet aggregation)
Lysosonal enzymes (degredation) |
|
|
|
Grabulation tissue |
day 3 healing |
|
|
|
Grabulation tissuebfills are Maximal neurovascilarization |
Day 5-7 healing |
|
|
|
Fibrin clot formation |
day 1 healing |
|
|
|
Macrophages stage in healing |
Day 2 of healing |
|
|
|
Macrophage in skin and mucosa |
Langerhans cells |
|
|
|
Placenta macrophages |
hifbauer cells |
|
|
|
Central nervous system macrophages |
microglia |
|
|
|
End of first month the tensile strength |
10% |
|
|
|
End of 3 month the tensile strength |
80% Type 3 collagen turns into type1 |
|
|
|
Excess production of scar tissue localized to the wound |
hypertrophic scar |
|
|
|
Out of proportion to the wkund. Excess type 3 collage. |
Keloid |
|
|
|
Classic location of keloid |
Earlobe |
|
|
|
Exhuberant granulation tissue |
Proud flesh |
|
|
|
3 compartments of water |
Intra cellular 2/3 Extra cellular 1/3 -interstitial 95% -intravascular 5% |
|
|
|
Stasis Hypercoagulability Injury to blood vessel wall |
Virchows triad |
|
|
|
Accumulation of fluid within the extravascular compartment and the intracellular tissue spaces of the body Interstitium and body cavities |
Edema |
|
|
|
Edema that is with an increase vascular permeability |
Inflammatory edema |
|
|
|
Edema is transudate |
non inflammatory edema |
|
|
|
Amount in pleural effusion |
more than 15ml |
|
|
|
Changes is the hydrostatic pressure or incotic pressure |
Generalized edema |
|
|
|
Increased volume of blood in affexted organ or tissue |
Hyperremia or congestion |
|
|
|
Active process
Arteriolar circulation |
active hyperemia |
|
|
|
Passive process
Venous obstruction
Blue |
congestion |
|
|
|
zone of liver that is most for susceptible site of ischemia |
Zone 3
Area most distant |
|
|
|
zone of liver that is most for susceptible site of injury or toxins |
Zone 1 |
|
|
|
Extravasation of blood into the surrounding tissues usually due to ruptured blood vessels |
hemorrhage |
|
|
|
Hemorrhage 1- 2mm |
Petechiae Usually platelet |
|
|
|
Hemorrhage >3mm to 1cm |
Purpura |
|
|
|
Hemorrhage 1- 2cm |
Echymosis |
|
|
|
Hemorrhage large pools of blood |
Hematoma |
|
|
|
Pathologic process resulting to formation of a solid blood clot within a vessel |
thrombosis |
|
|
|
Intrinsic pathway lab exam |
Ptt |
|
|
|
Extrinsic pathway lab |
Pt Warfarin |
|
|
|
Def factor 11 |
hemophelia c |
|
|
|
Common pathway |
Factor 10 |
|
|
|
Intravascular mass in the vessel is carried by the circulation to a site distant from its point of origin Solid, liquid or gas |
Embolus |
|
|
|
Embolic material are fetal skin, lanugo hair, verbix caseosa, mucin, bile , amniotic fluid debris High mortaloty rate 80% |
amniotic fluid embolism |
|
|
|
Caused by fracture , trauma or burns Petechial rasshes Mortality 10% |
fat embolism |
|
|
|
Emboli traveling from venous to arterial corculation via communication. Asd vsd |
Paradoxical embolism |
|
|
|
Process of tissue necrosis resulting fron interference if blood supply |
Infarction |
|
|
|
Arterial occlusion
Solid tissues
Single blood supply |
Anemic infarct |
|
