Reduction in size and/or number of cells in an organ or tissue with accompanying decrease in function
atrophy
Four causes of atrophy?
- decreased workload
- loss of innervation
- chronic ischemia
- loss of endocrine stimulation
Increase in size of cells within organs/tissues with overall increase in size of organ
Hypertrophy
Two causes of hypertrophy?
- demand for increase in function of organ
- hormonal stimulation
Increase in number of cells within organ/tissue
Hyperplasia
Two causes of physiologic hyperplasia?
- hormonal
- compensatory
Replacement of one type of tissue with another, different type of tissue
Metaplasia
What metaplasia is caused by cigarette smoke?
Squamous metaplasia - normal columnar cells that line lumens of bronchi are replaced by squamous cells which better tolerate toxic chemicals
- Squamous cells lift columnar cells up and out into the airway
What is disordered cell growth called?
Dysplasia
What is carcinoma-in-situ? (CIS)
abnormal cells occupy full thickness of epithelium but have not broken through the basement membrane
How do mild, moderate and severe dysplasia differ?
Mild = lower 1/3 of epithelium Moderate = lower 2/3 Severe = full thickness
What causes most cases of dysplasia in the uterine cervix?
HPV
Dysplastic tissue is still under control of ______ and ______.
Growth factors and ECM proteins
What are two characteristics of persistent viral infections?
- permissive
- non-destructive
10 viruses that can produce persistent infections?
HSV, CMV, EBV, VZV, Adenovirus, Polyomaviruses, T cell leukemia viruses, Measles (brain), HIV
Two examples of self-limiting acute infections?
- Influenza and polio
- not infectious during recovery
What are two viruses that manifest as slow progressive infections following an acute infectious phase of disease?
Measles, HTLV
- Different from latency by presence of infectious virus following recovery phase of disease
What causes slow, progressive diseases with no acute or recovery phase?
prions - Creutzfeld-Jacob
What is the extreme example of persistence?
Examples?
Latency - virus typically in non-infectious form
- viral genome either in episome or integrated into host DNA
- ALL HHV
What are three models on establishment/maintenance of HSV latency?
- Immune modulation model
- Immune elimination model
- Non-permissive model
How does the immune modulation model of latency work?
- Ganglion cells are permissive for HSV
- Once virus travels up axon to ganglion, Ab production begins
- Immune response modulates so that a non-lytic latent infection is established from the productive infection
How does the immune elimination model of latency work?
- non-permissive cells develop latent infection
- permissive cells develop productive infection
- host immune response eliminates the productively infected cells
How does the non-permissive model of latency work?
- All ganglion cells are non-permissive
- Replication of virus/inflammation signal ganglion cells to become permissive
- Host immune response shuts down signal by eliminating viral replication at entry site
- Ganglion cells return to non-permissive state and latency is established
- Reactivation mimics epithelial signal and reverts ganglion cells to permissive, productive cells
What are the two phases of reactivation? Causes?
- A: primary reactivation events lead to resumption of viral activity (early gene expression)
- B: immune response events cause replication and migration of viruses
