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FMS Week 5 > Cellular Pathology > Flashcards

Flashcards in Cellular Pathology Deck (29):
1

Robbins List Causes of Cell Injury

Oxygen Deprevation (Vascular)

Chemical Agents (Intoxication) 

Infectious Agents (Infectious)

Immunologic Reactions (Inflammatory)

Genetic Factors (Congenital)

Nutritional Imbalances (Environmental, Metabolic)

Physical Agents (Trauma) 

2

4 types of adaptions 

Hypertrophy

Hyperplasia

Atrophy

Metaplasia

3

Hypertrophy

Increase in cell size

4

Hyperplasia

Proliferation

5

Atrophy

Decrease in cell size 

6

Metaplasia

change of one type of differentiated cell into another type of differentiated cell 

7

Hx GERD. What cellular change might you see at the gastroesophageal junction

Protective metaplasic changes result in intestinal epithelium at lowe GE junction 

8

45 year old M with barretts esophagus. What might you see?

 

A small region of red, velvet-like mucosa in the lower esophagus

9

27 year old M with N x 1 week, scleral icterus, and elevated AST and ALT

Defect in cell membrane 

10

19 year old previously healthy collapeses playing bball. Died. 

Age related atheromatous plaque buildup

MI due to CAD

Septal hypertrophy (congenital)

Congenital narrowing of the aorta with poor blood flow to the legs 

Cardiac myxoma (pedunculated tumor within the L atrium) 

 

Septal Hypertrophy 

11

6 types of necrosis 

Coagulative 

Liquefactive 

Gangrenous 

Caseous 

Fat necrosis: Saponification 

Fibroid necrosis 

12

Coagulative Necrosis 

Seen in ischemia/ infarcts in most tissues (except brain)

Due to ischemia or infarction: proteins denature, then enzyme degredation 

13

Liquefactive necrosis 

Seen in bacterial abcesses, brain infarcts (due to increased fat content) 

Due to neutrophil release lysosomal enzynes that digest tissue. Enzymatic degredation first, then proteins denature

14

Gengrenous Necrosis 

Seen in distal extremity after chronic ischemia 

Due to:

Dry: ischemia

Wet: superinfection 

15

Caseous Necrosis 

Seen in TB, systematic fungi

Due to macrophages wall off the infecting microorganisms lead to granular debris

16

Fat necrosis 

Seen in enzymatic acute pancreatitis (saponification of pancreatic fat) and nonenzymatic traumatic (eg breaest injury) 

Damaged cells release lipase which breaks down triglycerides in fat cells 

Chalkiness 

17

Fibrinoid necrosis 

Immune reaction in vessels

Immune complexes combine with fibrin leading to vessel wall damage 

18

Diseases due to misfolded proteins (think neurodegenerative) 

Huntingtons

Parkinsons

Alzheimers 

19

Failure to degrade a metabolite due to inherited enzyme deficiencies

storage diease 

20

Cellular accumulation of normal substance

most neurodegenerative dz, fatty liver: acquired by inadequate removal of a normal substance 

21

Cellular accumulation of abnormal endogenous substance

cystic fibrosis, alpha1antitrypsin, other. Accumulation of an abnormal endogenous substance as a result of genetic or acquired defect

22

Failure to degrade a metabolite 

inborn errors of metabolism/ storage dz. Failure to degrade a metabolite due to inherited enzyme deficiencies

23

accumulation of abnormal exogenous substance 

pneumoconioses, scoliosis, asbestosis, berylliosis. deposition and accumulation of an abnormal exogenous substance 

24

Dystrophic calcification 

dystrophic calcification is encountered in areas of necrosis of any type. It is virtually inevitable in the atheromas of advanced atherosclerosis, associated with intimal injury in the aorta and large arteried and is characterized by the accumulation of lipids 

25

Metastatic calcification

deposition of calcium salts in normal tissues is known as metastatic calcification and is almost always secondary to some derangement in calcium metabolism (hypercalcemia) 

26

54 year old F. Fatigue, C, HTN, kidney stones, PE/nl, PTH, Ca/PO4 elevated

widespead calcifation of the interstitial tissue in her kidneys, lungs, and GI tract. What type of calcification

metastatic calcification 

27

SLE 

Positive anti-ds-DNA antibodies 

28

68 year old M smoker dies of chron bronchitis. No other medical problems. What is least likely to be observed in the lungs?

Patchy squamous metaplasia

Thickened bronchial walls 

Granulomatous inflammation

neutrophil infiltration

mucoid gland enlargement

granulomatous inflammation

29