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;
87 Cards in this Set
- Front
- Back
Cause of disease?
|
Etiology
|
|
Progression of the disease?
|
Pathogenesis
|
|
Signs and Symptoms?
|
Clinical manifestations of disease
|
|
Cell injury can either be?
|
Reversible of Irreversible
|
|
Irreversible cell injury leads to either?
|
Necrosis
Apoptosis (planned) |
|
Proliferative capacity of cells is variable?
|
Labile
Stable Perment |
|
continuously dividing cells ( epithelium, bone marrow)
|
labile cells
|
|
Quiescent (in GO stage; hepatocytes, smooth m., lymphocytes)
|
Stable cells
|
|
nondiving (neurons, skeletal and cardiac muscle)
|
Permanent cells
|
|
Cellular adaptions to
increased demand |
hyperplasia (increase #)
hypertrophy (increase size) |
|
Cellular adaptions to
decreased nutrients |
atrophy
|
|
Cellular adaptions to
Chronic Irritation |
Metaplasia
|
|
Cellular adaptions to
Hypozia (acute,limited) |
reversible changes
|
|
Cellular adaptions to
Hypoxia (severe) |
Death:
Necrosis or Apoptosis |
|
Increase in cell SIZE w/ subsequent increase in organ size
|
HYPERTROPHY
- can be physiologic or pathologic |
|
Causes of hypertrophy?
|
Increased functional demand
Hormonal stimulation |
|
Increase in the NUMBER of cells in an organ which may then increase in size
|
HYPERPLASIA
- physiologic or pathologic |
|
2 examples of physiologic hyperplasia?
|
1. Hormonal hyperplasia (f/m) breast at puberty and in pregnancy
2. Compensatory hyperplasia - liver regeneration after partial resection |
|
2 examples of causes of PATHOLOGIC hyperplasia (increase in cell #)?
|
1. Excess hormone - ENDOMETRIAL hyperplasia due to estrogens
2. Growth factors - Warts (HPV 6, 11) |
|
is HYPERPLASIA a neoplastic process?
|
NO
- but may be FERTILE SOIL for malignancy |
|
Atypical Hyperplasia bad b/c
|
in the endometrium carries an increased risk for development of endometrial adenocarcinoma (CA of the glands)
|
|
Decrease in the SIZE of a cell or organ by loss of cell substance
|
Atrophy
|
|
Causes of atrophy?
|
1. decreased workload
2. loss of innervation 3. Decreased blood supply 4. Inadequate nutrition 5. Loss of endocrine stimulation 6. Pressure |
|
Protein degradation is important in atrophy - 2 key processes?
|
1. lysosomes w/ hydrolytic enzymes
2. Ubiquitin-proteasome pathway |
|
Incomplete development of an organ so that it fails to reach adult size
|
HYPOPLASIA
(example, hypoplastic left ventricle) |
|
REVERSIBLE change in which one ADULT cell type is replaced by another ADULT cell type?
|
Metaplasia
|
|
Metaplasia is usually the change in what cell type to what cell type?
|
Columnar changes to squamous
|
|
Typical causes of metaplasia?
|
chronic irritation
Calculi in ducts Vitamin A deficiency Cervix Barret esophagus |
|
Cervix metaplasia?
|
COLUMNAR EPITHELIUM of the endocervic becomes SQUAMOUS (dysplasia and squamous CA may develop)
|
|
Barrett esophagus
|
Gastric reflux results in COLUMNAR epithelium REPLACING squamous epithelium in the ESOPHAGUS (dysplasia and adenocarcinoma may occur (cancer of the glands)
|
|
COLUMNAR --> SQUAMOUS
|
Cervix metaplasia
|
|
SQUAMOUS --> COLUMNAR
|
Barrett esophagus
|
|
Atypical proliferative changes due to chronic irritation or inflammation?
|
DYSPLASIA
|
|
What is key to remember about DYSPLASIA as opposed to METAPLASIA?
|
Dysplasia will become malignant if not Tx's (premalignant change), while Metaplasia is not malignant itself, but it may be a step in pathway
|
|
oxygen deprivation
physical agents chemical agents and drugs infectious agents Immunologic reactions Genetic dereangements Nutritional imbalances |
Causes of Cell Injury
|
|
Celular changes secondary to injury may be either
|
Reversible
Irreversible |
|
Cellular swelling
Cell membrane blebs Detached ribosomes Chromatin clumping |
Reversible cell changes secondary to injury
|
|
Lysosomes rupture
Dense bodies in mitochondria Cell membrane rupture Karyolysis, karyorrhexis Pyknosis |
IRReversible cell changes secondary to injury
|
|
Death of GROUPS of cells after INJURY; usually w/ INFLAMMATION
|
NECROSIS
|
|
genetically CONTROLLED, ATP and ENZYME-DEPENDENT death of INDIVIDUAL cells; usually NO INFLAMMATION
|
APOPTOSIS
|
|
Cell membrane doesn't rupture, phagocytosis occurs
|
Apoptosis
|
|
Neutrophils involved in cleaning up after cell death
|
Necrosis
|
|
the cellular response to injurious stimuli depends on
|
the type of injury, its duration, and its severity
|
|
The CONSEQUENCES of cell injury depend on th
|
type, state, and adaptability of the injured cell
|
|
Susceptibility of cells to ischemic necrosis
HIGH |
Neurons (3-4 min)
|
|
Susceptibility of cells to ischemic necrosis
INTERMEDIATE |
Myocardium, hepatocytes, renal epithelium (30 min-2hr)
|
|
Susceptibility of cells to ischemic necrosis
LOW |
Fibroblasts, epidermis, skeletal muscle (many hours)
|
|
The morphologic changes of cell injury become apparent only after some critical biochemical system w/ in the cell has be deranged
|
- manifestation of lethal damage tkae more time to develop than those of reversible damage
-ultrastructural alterations are visible earlier than light microscopic changes |
|
Reversible injury
|
Cellular swelling
Fatty change |
|
Myocardial infarction markers
- 2 hours |
Cardiac specific enzymes and proteins
|
|
Myocardial infarction markers
-4-12 hours |
Morphologic (light microscopic) changes
|
|
What is visible in coagulation necrosis of myocardium?
|
Lose nuclei first and anoxic
- 12-24 hours neutrophils come in to remove dead tissue |
|
Morphologic changes in GROUPS of cells that follow the death of living tissue; cells and PMNs leak lytic enzymes
|
Necrosis
|
|
necrosis of the cytoplasm
|
eosinophilia (pinker), vacuoles, calcification, myelin figures
|
|
necrosis of the nucleus
|
pyknosis (breaks apart), karyorrhexis, karyolysis
|
|
Patterns of necrosis
|
Coagulative
Liquefactive Caseous Fat Fibrinoid |
|
Hypoxic death (except brain)
|
Coagulative necrosis
|
|
Bacterial infections; also hypoxic death in brain tissue (infarction)
|
Liquefactive necrosis
|
|
Tuberculosis
|
caseous necrosis
|
|
enzymic or traumatic damage to fatty tissue; eg. Pancreatitis (enzymic)
|
Fat necrosis
|
|
What can tell you how the cells have died
|
the cytoplasm
|
|
Difference between coagulative necrosis and liquefactive necrosis of the kidney
|
coagulative necrosis - all cells die at the same time (no nuclei), kidney glomerulus
Liquefactive necrosis - glomeruli and tubules still present but abscess formation |
|
liquefactive necrosis typically observed with
|
bacterial infections
- BUT also w/ stroke in the brain will observe it too |
|
Characteristic of granulomatous inflammation w/ central necrosis
|
surrounded by MP's (nucleated giant cells)
Plus, also have T-cells to act as messengers |
|
What causes fat necrosis of the pancreas?
|
Damaged by trauma or a stone in duct --> enzymes leak out of pancras and begin to chew it up --> calcification and soap
|
|
Fibrinoid necrosis in an artery is characterized by
|
pinking ring going around blood vessel
|
|
Mechanisms of cell injury?
|
oxidative phophorylation
mitochondrial damage influx of Ca2+ Free radical formation Membrane damage DNA and protein damage |
|
Depletion of ATP causes
|
Na+ pump fails
Ca2+ pump fails Decreased protien synthesis (ribosomes detach) Unfolded protein response |
|
What happens when
Na+ pump fails? |
Na+ and water enter and K+ is lost; glycolysis depletes glycogen and lowers pH (loss of enzymic activity)
|
|
What happens when
Ca2+ pump fails? |
Ca2+ into cells (toxic)
|
|
What happens when
decreaessd protein synthesis |
ribosomes detach
|
|
Big problem when decreased ATP and energy source?
|
Increased anaerobic glycolysis
decreased pH b/c of lactic acid buildup Clumping of nuclear chromatin |
|
What can cause mitochondrial damage?
|
Increased cytosolic Ca2+
Decreased ATP (hypoxia) |
|
What is the Mitochondrial Permeability Transition? (MPT)
|
pore that allows cytochrome C to escape
-apoptosis is triggered and cell death occurs |
|
What is Cytochrome C
|
usually associated with pro-apoptotic proteins
|
|
What can result as a consequence of loss of Ca2+ homeostatsis
|
Extracell. Ca2+ is 15X higher than cytosolic Ca2+
-Loss of ATP increases intracellular Ca2+ - Increased Ca2+ activates phospholipases, proteases, endonucleases and ATPases - incrased Ca2+ also increases mitochondrial permeability triggering apoptosis |
|
What is a free radical?
|
Single unpaired electron; highly reactive
|
|
Normal metabolism produces what free radicals?
|
superoxide anion
hydrogen peroxide and hydroxyl ion |
|
What free radical is produced in neutrophils
|
superoxide
|
|
What can free radicals do that is bad?
|
Lipid peroxidation of cell membranes
-protein fragmentation -breaks in DNA |
|
What are some antioxidant enzymes
|
superoxide dismutase
catalase glutathione peroxidase |
|
What are some antioxidant vitamins?
|
A, E, ascorbic acid, glutathione
|
|
What are a few membrane permeabilty defects?
|
plasma membrane
mitochondrial membrane Lysosomal membrane (release of RNases, DNases and proteases) - membranes of organelles |
|
Deficiency of Oxygen; causes include cardiorespiratory failure, anemia, CO poisoning; cell injury and death
|
Hypoxia
|
|
loss of blood supply (OXYGEN AND NUTRIENTS)
|
Ischemia
|
|
Which more rapidly and severely injures tissues - hypoxia or ischemia?
|
Ischemia (loss of both oxygen and nutrients)
|
|
Loss of oxygen results in
|
anaerobic glycolysis
-- causes decreased cellular pH and clumping of nuclear chromatin |