Intro Pathology & Cell adaption Flashcards by Amanda Romeu

when exposed to stress Mechanisms of adaption are

atrophy 
hypertrophy 
hyperplasia 
metaplasia 
dysplasia
neoplasia
age

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etiology

cause

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hyperplasia

increase in number of cells in any organ/tissue

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examples of tissue that undergo physiologic hyperplasia when stressed?

uterus and prostate - hormone induced

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What tissue exhibits compensatory hyperplasia?

skin calluses from trauma

ex: like digging with a shovel causes calluses to form

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Pathologic hyperplasia

prolonged hormonal stimulation => BPH, fibroids

viral infection by papillomavirus => wart

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Hypertrophy

increased size of cells and/or the organ

ex: heart

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Hypertrophy due to pathogenesis

increased functional demand - running

Hormonal stimulation - thyroxin

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Atrophy

shrinkage in size of the cell by loss of structural components

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what can be some causes of atrophy?

decreased work load 
loss of innervation 
diminished blood supply 
inadequate nutrition
loss of endocrine stimulation

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Metaplasia

reversible change in which one adult epithelial type is replaced by another adult type epithelium

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Squamous metaplasia in uterine cervix …

is normal

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Squamous metaplasia in bronchi

leads to chronic bronchitis in smokers

columnar going to sqaumous

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Chronic irritation of the bronchus

increases risk of infection in lungs

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If metaplasia is pathologic and prolonged can give rise to

dysplasia then squamous cell carcinoma

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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

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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

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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

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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