exam 1 pt 2 Flashcards

1
Q

what is dysplasia?

A

changes inc ell size, shape and organization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

chronic inflammation and irritation can trigger?

A

dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

is dysplasia reversible?

A

yes bc it is adaptive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

when is dysplasia a cancer precurser?

A

when it penetrates the basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

metaplasia is?

A

one cell replaced by another type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cigar cell changes?

A

ciliated columnar to strat squamous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Gerd cell change

A

strat squamous to ciliated columnar
*barret esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what causes cellular edema and power failure in cell>

A

hypoxic cell injury that deprives the cell of oxygen and stops metabolisms and atp generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what happens when aerobic metabolism stops

A

no nak pump/ transport, decrease intracellular k, na is stuck inside causing swelling and er dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

stopping aerobic metabolisms from hypoxic cell injury causes

A

ribosomes to detach from rer (no protein synth), vacuolation, lysosome swelling and mitochondria, ca accumulation in the cell that activates enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what happens when hypoxic cell injury uses anaerobic metabolism to get atp from glycogen?

A

lactic acidosis from ph decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what do free radicals bond with>

A

nucleic acids, proteins, lipids nad carbohydrates
-prevents oxidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is lipid peroxidation?

A

caused by oxidative stress
-destruction of polyunsat lipids
-damage the membrane and increase permability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is protein alteration?

A

the fragmentation of the polypeptide chain which causes protein loos, misfolding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

lipid peroxidation, dna damage, mitochondrial damage and protein alterations are all caused by?

A

oxidative stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what organs are affected by lead?

A

kidney, reproduction, musculoskeleta, nervous, RBC, GIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

does lead cross BBB?

A

yes

18
Q

how does lead cause anemia?

A

it inhibits enzymes in heme synthesis and decreases thier life span

19
Q

how does lead cause granuoles/ basophilic stippling

A

inhibits rRNA degredation in RBC

20
Q

what makes RBC microcytic and hypochromic?

A

lead

21
Q

“lead cholic”?

A

abdominal pain

22
Q

lead affect on kidney?

A

tubular dysfunction causing glycosuring, aminoaciduria and hyperphosphaturia
-increase bp

23
Q

what does lead do to NS?

A

demyelinates cerebral and cerebellar white matter and kills cortical cells

24
Q

adult lead NS symptoms?

A

peripheral demyelinating neuropathy that slows nerve conduction bc of impaired nt release

25
Q

exotoxins harm?

A

cell ability to make ATP

26
Q

endotoxin cause ?

A

cell injury and increase capillary permeability which causes edema/ diarrhea

27
Q

inability to repair UV damage?

A

xeroderma pigmentosum
-no nucleotide excision repair enzymes

28
Q

effects of X.P. on skin?

A

photosensitive (blister), freckles, checkered pigmentation, telangiectasis, increase skin cancer (basal cell carcinoma and melanoma)

29
Q

accumulation of lipids in liver cause?

A

steatosis (fatty changes in liver)

30
Q

what is the mechanism of lipid accumulation?

A

increase movement of fatty acid to liver, increase synth of triglycerides and decrease apoprotein synth

31
Q

function of apoproteins

A

accept lipids

32
Q

is cellular swelling reversible?

A

yes

33
Q

what happens in hypoxic injury?

A

no atp made, na stuck in cell, increase osmotic pressure moves water into cell, er distends and ruptures, cisternae make vacuoles (vacuolation)

34
Q

calcification mechanism?

A

ca leaves mitochondria, acid excreted, oh- made, calcium hydroxide and hydroxyapatite precipitated mixed into salt, ca salt harden and interfere with cell function. structure

35
Q

regular blood calcium levels are associated with>

A

dystrophic calcification

36
Q

where are the ca deposits in dystrophic calcification

A

necrotic/ dying tissue

37
Q

atheroscletoric plagues, heart valve damage and pulmonary tb commonly have>

A

dystrophic calcification

38
Q

where does metastatic calc. happen?

A

normal undamage tissue

39
Q

hyperthyroidism, phosphate retention in renal failure, vit d intoxication all cause?

A

hypercalcemia which can cause metastatic calc.

40
Q

low ATP, cell edema, fatty changes in liver, low glycogen store and low protein synths are all?

A

reversible cell injuries

41
Q
A