Ch 1 Pathoma

Question 1

Hypertrophy

Answer 1

an increase in size of cells

Question 2

Hyperplasia

Answer 2

an increase in number of cells (production of new cells form stem cells)

Question 3

_______ involves gene activation, protein synthesis, and production of organelles

Answer 3

Hypertrophy

Question 4

Permanent tissues such as these 3, cannot make new cells and can only hypertrophy

Answer 4

Cardiac muscle, skeletal muscle, and nerve

Question 5

An exception to pathologic hyperplasia progressing to dysplasia and eventually cancer

Answer 5

Benign prostatic hyperplasia (BPH) - does not increase risk for prostate cancer

Question 6

_____ occurs via a decrease in size and number of cells

Answer 6

Atrophy

Question 7

Decrease in cell number occurs via ______. And decrease in size occurs via ______ and ______

Answer 7

Apoptosis; Ubiquitin proteosome degradation of the cytoskeleton; Autophagy

Question 8

Metaplasia

Answer 8

A change in stress on an organ leads to a change in cell type (most commonly involves surface epithelium) - metaplastic cells are better able to handle new stress

Question 9

Barrett’s Esophagus

Answer 9

normal esophagus is lined by nonkeratinizing squamous epithelium –> acid reflux causes metaplasia to non-ciliated mucin-producing columnar cells

Question 10

Metaplasia and dysplasia are both (reversible/irreversible)

Answer 10

Reversible with removal of driving stressor - if stress persists can become irreversible (carcinoma) - apocrine metaplasia of breast carries no increased risk for cancer

Question 11

Vitamin A deficiency can result in _____

Answer 11

Metaplasia

Question 12

______ is necessary for differentiation of specialized epithelial surfaces such as the conjuctiva covering the eye

Answer 12

Vitamin A - in deficiency, conjuctiva can undergo metaplasia into keratinizing squamous epithelium

Question 13

Keratomalacia

Answer 13

destruction of the cornea due to vitamin A deficiency induced metaplasia of the conjuctiva

Question 14

Example of mesenchymal (connective) tissue metaplasia

Answer 14

Myositis Ossificans - CT w/in muscle changes to bone during healing after trauma

Question 15

Dysplasia

Answer 15

disordered cellular growth (ex: cervical intraepithelial neoplasia CIN) - often a precursor to cancer - often arises from longstanding hyperplasia (endometrial hyperplasia) or metaplasia (Barrett’s esophagus)

Question 16

Aplasia and Hypoplasia

Answer 16

failure of cell production during embryogenesis (unilateral renal agenesis) and decrease in cell production during embryogenesis (streak ovary in Turner syndrome)

Question 17

______ occurs when a stress exceeds the cell’s ability to adapt

Answer 17

cellular injury - likelihood depends on type of stress, severity, and type of cell affected; slowly developing ischemia results in atrophy and acute ischemia results in injury

Question 18

5 common causes of cellular injury

Answer 18

inflammation, nutritional deficiency/excess, hypoxia, trauma, genetic mutations

Question 19

3 causes of hypoxia

Answer 19

ischemia (decreased blood flow through an organ), hypoxemia (low partial pressure of O2 in blood), decreased O2-carrying capacity of blood

Question 20

3 causes of ischemia

Answer 20

decreased arterial perfusion (atherosclerosis), decreased venous drainage (Budd-Chiari syndrome), shock (generalized hypotension –> poor tissue perfusion)

Question 21

4 causes of hypoxemia (low partial pressure of O2 in blood)

Answer 21

high altitude (decreased PAO2), hypoventilation (decreased PAO2), diffusion defect (normal PAO2 - ex: fibrosis), V/Q mismatch (right to left shunt or alveolar dead space)

Question 22

3 causes of decreased O2 carrying capacity (normal PaO2)

Answer 22

Anemia (normal SaO2), CO poisoning (decreased SaO2), methemglobinemia (decreased SaO2)

Question 23

Classic finding of CO poisoning and methemglobinemia (and tx)

Answer 23

cherry red appearance of skin (early sign of exposure is headache); cyanosis with chocolate-colored blood (tx is intravenous methylene blue which helps reduce Fe3+ back to Fe2+ –> Fe2 binds O2) - seen with oxidant stress (sulfa and nitrate drugs) or in newborns

Question 24

Low ATP disrupts these 3 key cellular functions

Answer 24

Na/K pump (leads to Na buildup and water buildup/swelling), Ca2+ pump (results in Ca buildup in cytosol which can lead to enzyme activation), aerobic glycolysis (leads to anaerobic glycolysis, increasing lactic acid and lower pH –> denatures proteins and precipitates DNA)

Question 25

The hallmark of reversible injury is _______

Answer 25

cellular swelling - results in loss of microvilli and membrane blabbing, and dissociation of ribosomes (RER swelling) and decreased protein synthesis

Question 26

The hallmark of irreversible injury is _______

Answer 26

membrane damage - results in cytosolic enzymes leaking in to serum (cardiac troponins), additional Ca entering cell, mitochondrial membrane damage results in loss of ETC chain and leakage of cytochrome c causing apoptosis; lysosome membrane damage results in hydrolytic enzymes leaking (further activated by additional Ca in cell)

Question 27

Morphologic hallmark of cell death is ______ and the three phases this occurs.

Answer 27

Loss of the nucleus; occurs via nuclear condensation (pyknosis), fragmentation (karyorrhexis), and dissolution (karyolysis)

Question 28

Two mechanisms of cell death

Answer 28

necrosis (murder) and apoptosis (suicide)

Question 29

Necrosis and the 6 types

Answer 29

death of large groups of cells followed by acute inflammation. Due to some underlying pathologic process (never physiologic). Coagulative, liquefactive, gangrenous, caseous, fat, and fibrinoid

Question 30

In _____ necrosis, the tissue remains firm and cell shape and organ structure are preserved by _______ of proteins, but the nucleus disappears

Answer 30

coagulative; coagulation

Characteristic of ischemic infarction of any organ except the brain

Question 31

In ______ necrosis, area of infarcted tissue is often wedge-shaped and pale

Answer 31

coagulative; wedge points to focus of vascular occlusion; red infarct occurs when blood re-enters loosely organized tissue (seen in organs with dual blood supply)

Question 32

Liquefactive necrosis is characteristic of these three instances

Answer 32

brain infarction (proteolytic enz from microglial cells liquefy the brain), abscess (prot enz from neutrophils liquefy tissue), pancreatitis (prot enz from pancreas liquefy parenchyma)

Question 33

Gangrenous necrosis is characteristic of

Answer 33

ischemia of lower limb (and GI tract) - dry gangrene resembles mummified tissue; wet if superimposed infection of dead tissue occurs

Question 34

_____ necrosis is soft and friable necrotic tissue with cottage cheese like appearance

Answer 34

Caseous - combination of coagulative and liquefactive (soup like)

Question 35

Caseous necrosis is characteristic of

Answer 35

granulomatous inflammation due to TB or fungal infection

Question 36

Fat necrosis appearance

Answer 36

necrotic adipose tissue with chalky white appearance due to deposition of calcium

Question 37

Fat necrosis is characteristic of

Answer 37

trauma to fat (e.g. breast) and pancreatitis-mediated damage of peripancreatic fat; fatty acids released by trauma or lipase (pancreatitis) join with calcium via saponification

Question 38

Saponification can occur via dystrophic calcification or metastatic calcification - what’s the difference?

Answer 38

DC occurs when calcium deposits on dead tissues in the setting of normal serum calcium and phosphate. MC occurs when high serum calcium or phosphate levels lead to calcium deposition on normal tissues (ex: hyperparathyroidism leading to nephrocalcinosis)

Question 39

Fibrinoid necrosis is characteristic of

and appearance

Answer 39

malignant hypertension and vasculitis; it causes necrotic damage to bv wall - leaking of proteins (including fibrin) into vessel wall results in bright pink staining of wall microscopically

Question 40

Three major examples of apoptosis

Answer 40

endometrial shedding during period, removal of cells during embryogenesis (de-webbing), CD8+ T cell mediated killing of virally infected cells

Question 41

Apoptosis morphology

Answer 41

dying cell shrinks (cytoplasm becomes more eosinophilic since it’s more concentrated), nucleus condenses and fragments, apoptotic bodies fall from the cell and are removed by macrophages - NOT followed by inflammation

Question 42

Apoptosis is mediated by ___ that activate ____ and ____

Answer 42

caspases; proteases (break down cytoskeleton) and endonucleases (break down DNA)

Question 43

3 pathways by which caspases are activated

Answer 43

intrinsic mitochondrial pathway (injury, dan damage, or dec hormonal stim leads to inactivation of Bcl2 which allows cytochrome c to leak), extrinsic receptor-ligand pathway (FAS ligand binds FAS death receptor on target cell - negative selection of thymocytes in thymus), cytotoxic CD8+ T cell mediated pathway (perforin secreted by t cells create pores in membrane and releases granzyme through pores to activate caspase)