1-1 (Histology) (done perman) Flashcards by Heejae Yang

which deaths must be reported to medical examiner for autopsy

1 dead on arrival
2 trauma or substance use
3 death within 24 hrs of admission or procedure
4 less than 18 yrs old

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list out examples of anatomic pathology

1 surgical (piece of a human, like organ) 
2 cytology (scraping of a human, like a Pap smear)

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list of ex of clinical pathology

1 blood bank 
2 microbio (Ca level, Na level, etc)

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types of tissue samples

1 cytology (least invasive)

2 biopsy (read: looking at cells in their natural environ, so can see the architecture of the body)

3 resection (most invasive)

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cytology def

give ex

look at cells suspended in fluid

1 body fluid
2 scraping

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name the dif kinds of biopsies

rank them in terms of teh SIZE of tissue that is yielded

1 needle core (small) 
2 incisional (big) 
3 endoscopy (bigger) 
4 excisional (biggest)

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which biopsy uses a shape descriptor

incisional

read: shave, punch

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what’s the most common tissue specimen

endoscopy biopsy

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where are endoscopy biopsies done

GI
GU (urinary)
respiratory

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what’s the most commonly used fixative

10% formalin

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uses of formalin

prevents bacterial growth
keeps tissue moist
halts cell degeneration

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give 2 ex of what you take out for an excision/resection

1 non essential organ

2 organ with failing function

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what’s the purpose of ink

tells you where the outside of the organ is

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what’s the purpose of placing the sample in the wax machine

to make it firmer

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formalin makes proteins (verb)

cross link

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what kind of section is made during a surgery

why

turn around time

con

frozen section

why - directs surgeon’s decision

20 min

con
-thick section

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what’s the main distinguishing point about immunohistochemistry

it is specific

since it uses tagged Ab against antigens

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flow cytometry function

counts # of CD4 or 8

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elastin is shown via what stain

Verhoeff

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silver stain shows what

fungi

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hypertrophy results from increased what

hyperplasia results from what

trophy - inc demand

plasia - inc stimulation (via hormones)

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hyperplasia def

increase in cell #

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metaplasia def

reversible change in differentiation

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what can cause metaplasia

ciagarette smoking

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systemic hypertension will affect heart how

left ventricle hypertrophy

what is an example of a muscle that cannot undergo plasia so has to undergo hypertrophy

myocardial muscle

steps of autophagy

1 things to be thrown out are placed in autophagic vacuole | 2 vacuole fuses with lysosome

when does autophagy occur

- when person is starved - immobilized (leading to atrophy)

metaplasia occurs in response to what kind of signal

exogenous signal (ie tobacco smoke)

example of metaplasia

- occurs in bronchial epithelium - chronic smoking will trigger metaplasia - norm, columnar to abnorm, stratified squamous

why does squamous metaplasia predispose smoker to repeated lung infections

squamous epi means cilia is gone

% of adult smokers started before age 18

90%

ER function

protein and lipid synthesis

Golgi apparatus function

protein packaging and sorting

cytoskeleton function

protein transport | cell shape

mitochondria function

ATP synthesis | fatty acid oxidation

what are the two forms of cell death are these reversible which form of death has a reversible stage

necrosis apoptosis no rev stage = necrosis

reversible types of cell injury

1 cloudy swelling/hydropic degeneration 2 fatty change

cloudy swelling - where - mec

where - mito and ER mec - impaired Na/K ion pump -> water and ions accumulate

K Na Ca in vs out [ ]

k - greater in na - greater out ca - greater out

ATPase pumps # Na (in/out) | how about K

pumps 3 Na out pumps 2 K in

where is fatty change most common (organ)

liver

cause of fatty change

1 drug toxicity (ethanol) | 2 obesity and diabetes

official term for fatty change

steatosis

official term for cloudy swelling

hydropic degeneration

liver makes what kinds of fat and it transports it to other organs in body how is the lipid transported

phospholipid cholesterol ester triglycerides lipid + apoprotein = transported as LIPOPROTEIN

mec of fatty change each mec is linked to a specific scenario

1 increased uptake of free fatty acids (obesity) 2 decreased catabolism of free fatty acids by mito (drugs, anoxia, pregnancy) 3 dec secretion of lipoproteins (chem or malnutrition)

what is the most common liver disease worldwide predisposing condition

non alcoholic fatty liver disease (NAFLD) obesity and diabetes

sign of cirrhosis in the liver color what is colored

color - blue | collagen

describe the two pathways NAFLD can take

80% - isolated fatty liver (no progression to cirrhosis and no inc risk of death) 20% - NASH (non alcoholic steatohepatitis) -> NASH cirrhosis -> liver cancer

time line of cell death

1-2 hrs after injury - cell death occurs 12 hrs - gross morphologic changes (things that the pathologist can detect via microscope)

main dif bt apoptosis and necrosis (2)

n - always pathological n - elicits inflammatory rxn ap - can be physiological (natural) ap - not accompanied by inflammation

necrosis is result of (non/specific) activation of nucleases

non sp

in apoptosis, how are DNA cleaved

endonucleases selectively cleave DNA at sites between nucleosomal units (linker DNA)

read: physiological apoptosis - during embryonic development - normal tissues always have some death going on (renew) - hormonally sensitive tissues, like endometrial lining during period

ionizing radiation (is an apoptotic stimulus) it targets

1 thymic lymphocytes | 2 intestinal epithelium

what's the other apoptotic stimulus describe mec

give Finestride -> leads to hormonal/DHT withdrawal -> apoptosis of prostate -> prostate dec in size

what's the consequence of a larger prostate

compress urethra (urinate frequently)

describe the intrinsic pathway to triggering apoptosis

injury or hormone withdrawal -> mito releases cytochrome C -> activates caspase -> activates executioner caspase -> apoptosis

describe the EXtrinisic pathway to triggering apoptosis

FAS or TNF bind to death receptor -> activates caspase -> activates executioner caspase -> result in apoptosis

necrosis: mec for transition from reversible to irreversible injury IS result of these mec

mito plasma mem damage = accumulation of Ca in injured cells

read: bc of plasma mem damage, Ca and phosphate goes into the cells

name the pathways that initiate apoptosis

1 mito/intrinsic pathway | 2 death receptor/extrinsic pathway

read: several biochemical pathways involving oxidases may generate reactive oxygen metabolites (ROS)

these pathways generate ROS (naturally in body) 1 ETC 2 peroxisome - in liver, metabolize fatty acids and as byproduct, generate H202 3 NADPH oxidase 4 Cytochrome P450 oxidase

reperfusion to cure ischemia - what have to be careful about

this generates oxidants from the phagocytic cells in restored circulation

which type of antioxidant defense is MOST effective against damage to lipids initiated by OH dot?

vitamins

what things bind to Fe and Cu to turn OFF their redox active state

Bind Fe: transferrin and ferritin Bind Cu: ceruloplasmin