Intro Pathology & Cell adaption Flashcards

0
Q

when exposed to stress Mechanisms of adaption are

A
atrophy 
hypertrophy 
hyperplasia 
metaplasia 
dysplasia
neoplasia
age
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1
Q

etiology

A

cause

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2
Q

hyperplasia

A

increase in number of cells in any organ/tissue

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3
Q

examples of tissue that undergo physiologic hyperplasia when stressed?

A

uterus and prostate - hormone induced

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4
Q

What tissue exhibits compensatory hyperplasia?

A

skin calluses from trauma

ex: like digging with a shovel causes calluses to form

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5
Q

Pathologic hyperplasia

A

prolonged hormonal stimulation => BPH, fibroids

viral infection by papillomavirus => wart

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6
Q

Hypertrophy

A

increased size of cells and/or the organ

ex: heart

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7
Q

Hypertrophy due to pathogenesis

A

increased functional demand - running

Hormonal stimulation - thyroxin

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8
Q

Atrophy

A

shrinkage in size of the cell by loss of structural components

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9
Q

what can be some causes of atrophy?

A
decreased work load 
loss of innervation 
diminished blood supply 
inadequate nutrition
loss of endocrine stimulation
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10
Q

Metaplasia

A

reversible change in which one adult epithelial type is replaced by another adult type epithelium

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11
Q

Squamous metaplasia in uterine cervix …

A

is normal

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12
Q

Squamous metaplasia in bronchi

A

leads to chronic bronchitis in smokers

columnar going to sqaumous

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13
Q

Chronic irritation of the bronchus

A

increases risk of infection in lungs

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14
Q

If metaplasia is pathologic and prolonged can give rise to

A

dysplasia then squamous cell carcinoma

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15
Q

Dysplasia

A

epithelial or mesenchymal cells that have undergone metaplasia then atypical cytological alterations involving cell size, shape and orientation
evolution at cellular level detrimental to the host organism
can then lead to cancer (uncontrolled growth)
ex: snuff => cheek

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16
Q

Pt has RUQ pain. Stools are pale. Bilirubin 9.7
Normal Bilirubin 0.1-1.1
cholangiogram shows gallstone in bile duct
what change is seen on the skin?

A

Icterus

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17
Q
Pt smokes 2 pk/day and 30 yr 
chronic cough for past 3 yrs, worse in past 2 weeks 
Left pulmonary parenchymal lesion 
Biopsy shows squamous metaplasia 
what is most appropriate interpretation?
A

Irritant effect

this NOT cancer yet

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18
Q

Pt experiences blood loss from MVA
hypotensive for hours
Hematocrit is 12%
What tissues least resistant to impact of these events?

A

Skeletal muscle

19
Q

at end of menstrual cycle, endometrium sloughs off. Endometrium microspocially shows cellular fragmentation
What would trigger upregulation of BCL-2 in endometrial cells?

A

Decreased estrogen

BCL-2 involved in up regulation of cell death

20
Q

what break up abnormal proteins in cells?

A

chaperone ubiquitin protease

21
Q

environment accentuates aging by

A

intracellular accumulation of exogenous materials

22
Q

Antracosis

A

carbon pigment in the lung

goes to the hilar lymph nodes

23
Q

examples of intracellular accumulations

A
Lipofuscin
melanin
iron 
calcium 
fat 
bilirubin
24
Q

Why do bruises turn brown?

A

iron deposition and hemosiderin

25
Q

Hemolytic anemia can cause

A

iron deposits

26
Q

spleen and liver eat up RBCs and recycle

A

iron to the BM for new RBCs

27
Q

multiple transfusions cause

A

hemosiderin deposition in the kupfer cells of the liver

28
Q

While dystrophic calcification occurs in dead or injured tissues, metastatic calcification occurs in

A

normal tissues

29
Q

Conditions that cause reversible fatty liver

A

Fatty meal
Obesity
Alcoholism
rarely causes fibrosis

30
Q

Causes of Jaundice/Icterus

A

Results from accumulation of bilirubin

  • bile duct occulsion
  • alcoholism (late event)
  • drugs
  • hemolytic anemia
  • pancreatic tumors
31
Q

where are you likely to see coagulative necrosis?

A

myocardium and kidney

32
Q

Coagulative necrosis is not seen in

A

the brain

33
Q

coagulative necrosis is

A

wedge shaped

base and apex

34
Q

pathology of coagulative necrosis

A

anucleate eosinophilic fibers with PMNs

eosinophilic changes due to binding of eosin by denatured proteins, loss of glycogen, membrane disruption and debris

35
Q

Structure of brain

A

Fatty structure with some nerves

see Liquefactive necrosis

36
Q

Liquefactive necrosis

A

progressive degradation of cells by enzymes and denaturation of proteins either by autolysis or heterolysis

37
Q

Enzymatic degradation with liquefaction is characteristic of

A

bacterial/fungal infections due to massive infiltrates of PMN

38
Q

Fat necrosis

A

saponification of fat cells with calcification due to enzymatic breakdown by lipases
may be dystrophic calcification
feels hard because of the calcium soaps

39
Q

what is the most common cause of Fat necrosis?

A

trauma to a fatty structure
- Breasts
then its alcohol - causes pancreas to release enzymes

40
Q

Breast nodule

A

could be fat necrosis

could contain cancer too

41
Q

Caseous Necrosis

A

‘cheesy’, round
inflammatory reaction to bacteria
seen in TB
has distinct pattern of centralized amorphous debris and surrounding granuloma - chronic inflammatory cells

42
Q

Gangrenous Necrosis

A

not a distinct pattern
combination of coagulative (dry) and liquefactive necrosis (wet)
wet component from bacterial invasion

43
Q

Fibrinoid necrosis

A

accumulation of amorphous, basic, proteinaceous material in the tissue matrix with a staining pattern reminiscent of fibrin
fibrin has been deposited
due to immune reaction

44
Q

Reperfusion injury

A

inflammatory cells come in but then oxygen and nutrients return and released enzymes cause peripheral damage

45
Q

In the brain liquefactive necrosis with reperfusion can lead

A

hemorrhage

46
Q

Autophagocytosis happens during Atrophy

A

this is not necrotic