Intro Pathology & Cell adaption Flashcards
when exposed to stress Mechanisms of adaption are
atrophy hypertrophy hyperplasia metaplasia dysplasia neoplasia age
etiology
cause
hyperplasia
increase in number of cells in any organ/tissue
examples of tissue that undergo physiologic hyperplasia when stressed?
uterus and prostate - hormone induced
What tissue exhibits compensatory hyperplasia?
skin calluses from trauma
ex: like digging with a shovel causes calluses to form
Pathologic hyperplasia
prolonged hormonal stimulation => BPH, fibroids
viral infection by papillomavirus => wart
Hypertrophy
increased size of cells and/or the organ
ex: heart
Hypertrophy due to pathogenesis
increased functional demand - running
Hormonal stimulation - thyroxin
Atrophy
shrinkage in size of the cell by loss of structural components
what can be some causes of atrophy?
decreased work load loss of innervation diminished blood supply inadequate nutrition loss of endocrine stimulation
Metaplasia
reversible change in which one adult epithelial type is replaced by another adult type epithelium
Squamous metaplasia in uterine cervix …
is normal
Squamous metaplasia in bronchi
leads to chronic bronchitis in smokers
columnar going to sqaumous
Chronic irritation of the bronchus
increases risk of infection in lungs
If metaplasia is pathologic and prolonged can give rise to
dysplasia then squamous cell carcinoma
Dysplasia
epithelial or mesenchymal cells that have undergone metaplasia then atypical cytological alterations involving cell size, shape and orientation
evolution at cellular level detrimental to the host organism
can then lead to cancer (uncontrolled growth)
ex: snuff => cheek
Pt has RUQ pain. Stools are pale. Bilirubin 9.7
Normal Bilirubin 0.1-1.1
cholangiogram shows gallstone in bile duct
what change is seen on the skin?
Icterus
Pt smokes 2 pk/day and 30 yr chronic cough for past 3 yrs, worse in past 2 weeks Left pulmonary parenchymal lesion Biopsy shows squamous metaplasia what is most appropriate interpretation?
Irritant effect
this NOT cancer yet
Pt experiences blood loss from MVA
hypotensive for hours
Hematocrit is 12%
What tissues least resistant to impact of these events?
Skeletal muscle
at end of menstrual cycle, endometrium sloughs off. Endometrium microspocially shows cellular fragmentation
What would trigger upregulation of BCL-2 in endometrial cells?
Decreased estrogen
BCL-2 involved in up regulation of cell death
what break up abnormal proteins in cells?
chaperone ubiquitin protease
environment accentuates aging by
intracellular accumulation of exogenous materials
Antracosis
carbon pigment in the lung
goes to the hilar lymph nodes
examples of intracellular accumulations
Lipofuscin melanin iron calcium fat bilirubin
Why do bruises turn brown?
iron deposition and hemosiderin
Hemolytic anemia can cause
iron deposits
spleen and liver eat up RBCs and recycle
iron to the BM for new RBCs
multiple transfusions cause
hemosiderin deposition in the kupfer cells of the liver
While dystrophic calcification occurs in dead or injured tissues, metastatic calcification occurs in
normal tissues
Conditions that cause reversible fatty liver
Fatty meal
Obesity
Alcoholism
rarely causes fibrosis
Causes of Jaundice/Icterus
Results from accumulation of bilirubin
- bile duct occulsion
- alcoholism (late event)
- drugs
- hemolytic anemia
- pancreatic tumors
where are you likely to see coagulative necrosis?
myocardium and kidney
Coagulative necrosis is not seen in
the brain
coagulative necrosis is
wedge shaped
base and apex
pathology of coagulative necrosis
anucleate eosinophilic fibers with PMNs
eosinophilic changes due to binding of eosin by denatured proteins, loss of glycogen, membrane disruption and debris
Structure of brain
Fatty structure with some nerves
see Liquefactive necrosis
Liquefactive necrosis
progressive degradation of cells by enzymes and denaturation of proteins either by autolysis or heterolysis
Enzymatic degradation with liquefaction is characteristic of
bacterial/fungal infections due to massive infiltrates of PMN
Fat necrosis
saponification of fat cells with calcification due to enzymatic breakdown by lipases
may be dystrophic calcification
feels hard because of the calcium soaps
what is the most common cause of Fat necrosis?
trauma to a fatty structure
- Breasts
then its alcohol - causes pancreas to release enzymes
Breast nodule
could be fat necrosis
could contain cancer too
Caseous Necrosis
‘cheesy’, round
inflammatory reaction to bacteria
seen in TB
has distinct pattern of centralized amorphous debris and surrounding granuloma - chronic inflammatory cells
Gangrenous Necrosis
not a distinct pattern
combination of coagulative (dry) and liquefactive necrosis (wet)
wet component from bacterial invasion
Fibrinoid necrosis
accumulation of amorphous, basic, proteinaceous material in the tissue matrix with a staining pattern reminiscent of fibrin
fibrin has been deposited
due to immune reaction
Reperfusion injury
inflammatory cells come in but then oxygen and nutrients return and released enzymes cause peripheral damage
In the brain liquefactive necrosis with reperfusion can lead
hemorrhage
Autophagocytosis happens during Atrophy
this is not necrotic
