PATH 3810 Cell Issues

physiologic adaptations

response to normal stimulation by hormones or
endogenous chemical mediators

pathologic adaptations

responses to stresses that allow cells to modulate
structure and function and escape injury

hypertrophy

adaptive response of cells with limited capacity to divide. caused by increased functional demand, eventually reaches point of no return. may progress to degenerative changes in cells/cell injury

physiologic hypertrophy of the uterus during pregnancy

hyperplasia

increase in number of cells in a tissue/organ

hormonal physiologic hyperplasia

increases functional capacity of tissue

compensatory physiologic hyperplasia

increases tissue mass after damage or partial resection

pathologic hyperplasia

excessive hormonal/growth factor stimulation

hyperplasia is an important…

…response of connective tissue in wound healing

pathologic hyperplasia of the thyroid gland due to hyperthyroidism

atrophy

shrinkage of cells by loss of cell substance

causes of atrophy

• atrophy of disuse

• denervation atrophy

• ischemia

• inadequate nutrition

• loss of endocrine stimulation

• senile atrophy

• tissue compression

• protein degradation/decreased protein synthesis

atrophy is accompanied by…

increased autophagy, resulting in increased numbers of autophagic vacuoles (which are filled with dead cell parts)

normal brain vs atrophied brain

metaplasia is…

reversible

metaplasia

one cell type replaced with another cell type

metaplasia cause

cells sensitive to certain stressful stimuli will be replaced with a cell than can better withstand that stress. arises by altered differentiation pathway of stem cells. important protective features of normal epithelium are lost. may predispose malignant transformation is stimuli persist.

metaplasia

Question 1

Etiology is the term that refers to what element of pathology?

the cause of a disease of condition

Apoptosis differs from necrosis in that apoptosis is 

Energy dependent, not associated with inflammation, and can occur under physiologic conditions

Question 3

Which of the following is NOT a feature of necrosis?

partitioning of the cytoplasm to form membrane-bound vesicles of cytosol and organelles

two phenomena that consistently characterize irreversibility

(1) Inability to reverse mitochondrial dysfunction
(2) profound disturbances in membrane function

changes in cell injury diagram

yes i understand this

hypoxia

oxygen deficiency

ischemia

loss of blood supply

the two main morphologic correlates of REVRESIBLE cell injury are

1. cellular swelling

2. fatty change

Which of the following BEST characterizes the lesion in the images provided?​

Hyperplasia

Which of the following consistently characterize irreversible injury to cells?​ 

a and b

Which of the following is true for the histology image below?​ 

Squamous differentiation of respiratory epithelium in the bronchi of a habitual smoker

cellular swelling results from

inability to maintain ionic and fluid homeostasis

fatty change in cells occurs in

hypoxic, toxic, and metabolic injury to cells involved in fat metabolism

normal kidney tubules with viable epithelial cells

early (reversible) ischemic injury showing surface blebs, increased eosinophilia of cytoplasm, and swelling of occasional cells

necrotic (irreversible) injury of epithelial cells, with loss of nuclei and fragmentation of cells and leakage of contents

necrosis

morphologic changes that accompany cell death: unable to maintain membrane integrity

features of necrosis

• increased eosinophilia

• nuclear changes

pyknosis

nuclear shrinkage with DNA condensation

karyorrhexis

nuclear fragmentation

karyolysis

nuclear dissolution

i looked at this diagram regarding necrosis and i understand what i am looking at

coagulative necrosis of the kidney (gross)

coagulative necrosis of the kidney (microscopic)

coagulative necrosis

tissue appears like solid mass in which proteins are denatured,
but the basic tissue architecture is preserved

liquefactive necrosis

dissolution of tissue, particularly common in hypoxic injury in
central nervous tissue

liquefactive necrosis of the brain

caseous necrosis

form of coagulative necrosis, tissue is yellow-white and crumbly, aka “cheesy”

caseous necrosis of the lung

fat necrosis

descriptive of focal areas of fat destruction, typically as result of lipolytic enzymes

fat necrosis of the pancreas

fibrinoid necrosis

special form seen in blood vessels involving necrosis of the vessel walls together with deposition of amorphous eosinophilic protein; frequently associated with Ag-Ab complex deposition in walls of blood vessels

fibrinoid necrosis of an artery

reperfusion injury

Restoration of blood flow to ischemic but
otherwise viable tissues results in
exacerbated and accelerated injury

• Increased production of reactive oxygen species leading to oxidative stress

• Reperfusion delivers more leukocytes and cytokines

apoptosis

programmed, intentional cell death where the plasma membrane remains intact

apoptosis is…

…energy dependent

blebbing is…

partitioning (imagine squeezing a stress ball)

i looked at this diagram relating to necrosis vs apoptosis and i understand

deposition of lipids often appears as…

…clear vacuoles within cytoplasm and parenchymal walls

fatty change is also called…

…steatosis.

steatosis is…

the accumulation of free triglycerides

xanthomas

aggregates of cholesterol-containing “foamy” macrophages in skin and tendons

steatosis of the liver

protein reabsorption droplets in the renal tubules

protein accumulation occurs because…

…excess is presented to cells, or because cells synthesize excessive amounts

lipofuscin pigment

insoluble brown-yellow pigment that accumulates in tissues (especially heart, liver, brain) as a function of age or atrophy. Insoluble products of free radical catalyzed peroxidaton of lipid of organelle membranes

lipofuscin accumulation in cardiac muscle

hemosiderin pigment

hemoglobin-derived granular pigment that accumulates during
conditions of local or systemic iron excess. Initial
accumulations begin in mononuclear phagocytes in liver, bone marrow, spleen

hemosiderin accumulation in the liver under H&E

hemosiderin accumulation in the liver under Prussian Blue reaction

pathologic calcification

abnormal tissue deposition of calcium salts

dystrophic calcification

deposition of calcium at sites of cell injury and necrosis, occurs under normal serum calcium

metastatic calcification

deposition of calcium in normal tissues, reflecting a derangement in calcium metabolism

calcification of the aortic valve