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Pathoma > Chapter 1 > Flashcards

Chapter 1 Flashcards

1
Q

Which permanent tissue only undergo hypertrophy and not hyperplasia

A

Cardiac muscle, skeletal muscle, and nerve

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2
Q

How does hyperplasia lead to cancer

A

When hyperplasia occurs secondary to pathologic process

Pathologic hyperplasia (ex Endometrial hyperplasia ) can progress to dysplasia and eventually cancer

Exception : BPH no increase risk for prostate cancer

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3
Q

Name of process that results in decrease cell no.

A

apoptosis

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4
Q

Name of processes that results in decrease cell size

A

Ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular components

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5
Q

What is metaplasia

A

A change in stress on an organ leads to a change in cell type

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6
Q

Barrett Oesophagus is a classic example of which type of growth adaptation?

A

Metaplasia

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7
Q

What type of tissue changes occur most commonly in metaplasia

A

Changes of one type of surface epithelium( squamous,columnar,urothelial) to another

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8
Q

What type of metaplasia do you see with Barrett’s Oesophagus

A

non-keratinized squamous epithelium to mucin producing columnar cells

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9
Q

Metaplasia is reversible or irreversible

A

reversible - with removal of stressor

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10
Q

Can metplasia progress to cancer

A

Yes, under persistent stress
meatplasia—>dysplasia—>cancer
ex Barrett’s oesophagus—> adenocarcinoma of the Oesophagus
Exception: BPH

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11
Q

What vitamin deficiency can lead to metaplasia

A

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

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12
Q

How will a vitamin A deficiency manifest

A

Keratomalacia = thin squamous lining of the conjunctiva undergo metaplasia into stratified keratinizing squamous epithelium.
Night blindness

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13
Q

MYOSITIS OSSIFICANS is an example of what

A

Mesenchymal (connective) tissue undergoing metaplasia

muscle tissue changes to bone during healing after trauma (inflammation)

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14
Q

Define dysplasia in 3 words

A

dissordered cellular growth

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15
Q

Cervical intraepithelial neoplasia( CIN) is an example of what growth adaptation

A

Dysplasia

refers to a proliferation of precancerous cellls

is a precursor of cervical cancer

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16
Q

How does dysplasia arise?

A

often from longstanding pathologic hyperplasia (endometrial hyperplasia) or metaplasia (Barrett)

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17
Q

Is Dysplasia Reversible

A

Yes in theory, with alleviation of inciting stress

if stress persists and it progresses to carcinoma—> that is irreversible

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18
Q

Define aplasia

A

Failure of cell production during embryogenesis

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19
Q

Define hypoplasia

A

Decrease in cell production during embryogenesis resulting in relatively small organ (streak ovaries– turner’s syndrome)

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20
Q

What type of cells are highly succeptible to ischemic injury ?

A

Neurons (occurs after 3-5mins)

21
Q

What does slowly progressing ischemia result in

A

results in atrophy

in contrast to acute ischemia which results in cell injury

22
Q

Define Hypoxia

A

Low oxygen delivery to tissues

23
Q

what are three causes of hypoxia

A

Ischemia (decreased blood flow through an organ)
Hypoxemia (low partial pressure of oxygen in the blood)
Decreased O2 carrying capacity

24
Q

What are three causes of ischemia ?

A

Decreased arterial perfusion
decreased venous drainage (Budd Chiari Syndrome- from polycythemia vera or Lupus causing a thrombosis in hepatic vein)
Shock

25
Q

What lab values constitute hypoxemia

A

PaO2< 60 mmhg
SaO2<90%

26
Q

4 causes of hypoxemia

A

high altitude
v/q mismatch (right-to-left shunt; atelectasis)
Diffusion Defect (Interstitial pulmonary fibrosis)
hypoventilation (increased PACO2—> decreased PAO2)

27
Q

How does decreased O2 carrying capacity of the blood occur ?

A

Arises with hemoglobin (Hb) loss or dysfunction

28
Q

What are 3 examples of decreased O2 carrying capacity

A

Anemia
carbon monoxide posioning
Methhemoglobinemia (PaO2 normal; SaO2 decreased)

29
Q

What is the classic physical finding in CO poisoning

A

Cherry-red appearance of skin
Headache = early sign the lead to coma and death

30
Q

Explain Methhemoglobinemia

A

Iron in heme is oxidized to Fe3+ which cannot bind O2
seen with oxidant stress (sulfa and nitrate drugs) or in newborns (babies suck at reducing Fe3+ to Fe2+)

31
Q

What is a classic finding in methhemoglobinemia

A

cyanosis with chocolate coloured blood

32
Q

What is the treatment for methhemoglobinemia

A

Intravenous methylene blue
helps reduce Fe3+ to Fe2+ state

33
Q

What is the hallmark of reversible injury

A

Cellular swelling

34
Q

What is the hallmark of irreversible damage

A
  1. Plasma membrane damage
    cytosolic enzymes leaking into the serum (eg. cardiac troponin)
    additional calcium entering the cell
  2. Mitochondrial membrane damage
    Loss of electron transport chain (inner mitochondrial membrane)
    cytochrome c leaking into cytosol (activates apoptosis)
  3. Lysosome membrane damage
    resultsi in hydrolytic enzymes leaking into the cytosol , which in turn are activated by the high intracellular calcium
35
Q

what is the morphologic hallmark of cell death

A

loss of the nucleus ( occurs via nuclear condensation- pyknosis, fragmentation - karyorrhexis and dissolution - karyolysis

36
Q

Define coagulative necrosis

A

Necrotic tissue that remains firm
characteristic of ischemic infarction of any organ except the brain .

37
Q

What ir red infarction

A

if blood re-enters a loosely organized tissue after ischemic infarction (eg. pulmonary or testicular infarction)

38
Q

What is Liquefactive necrosis

A

Necrotic tissue that becomes liquefied ; enzymatic lysis of cells and protein results in liquefactin

39
Q

Liwuefactive necrosis is characteristic of what type of infarction(s)

A

Brain infarction: Proteolytic enzymes from microglial cells liquefy the brain
Abscess: Proteolytic enzymes from neutrophils liquefy tissue
Pancreatitis: Proteolytic enzymes from pancreas liquefy parenchyma

40
Q

what is gangrenous necrosis

A

Coagulative necrosis that resembles mummified tissue
characteristic of ischemia of lower limb and GI tract

41
Q

Caseous necrosis

A

Soft and friable necrotic tissue with @cottage cheese-like appearance
combination of coagulative and liquefactive necrosis
characteristic of granulomatous inflammation due to tuberculous or fungal infection

42
Q

What is fat necrosis

A

Necrotic adipose tissue with chalky-white appearance due to deposition of calcium
Characteristic of trauma to fat (eg. breast) and pancreatitis mediated damage of pancreatic fat

43
Q

What is saponification

A

Saponification is an example of dystrophic calcification in which calcium deposits on dead tissues. In dystrophic calcification, necrotic tissue acts as a nidus for calcification in the setting of normal serum calcium and phosphate

44
Q

what distinguishes dystrophic calcification from metastatic calcification

A

in metastatic calcification there is an increase in serum calcium or phosphate levels whilst in dystrophic calcification the serum calcium is normal

45
Q

What is Fibrinoid necrosis

A

Necrotic damage to blood vessel wall
leaking of proteins (including fibrin) into vessel wall results in bright pink staining of the wall microscopically
characteristic of malignant hypertension and vasculitis

46
Q

What is apoptosis

A

energy (ATP) dependent, genetically programmed cell death

47
Q

Apoptosis is mediated by what?

A

caspases that activate proteases and endonucleases

  1. Proteases break down the cytoskeleton
    Endonucleases break down DNA
48
Q

What are the pathways in which caspases are activated

A

1.Intrinsic mitochondrial pathway
cell injury, DNA damage or loss of hormonal stimulation (eg.menses) leads to inactivation of Bcl2 , lack of Bcl2 allows cytochrome c to leave the mitochondrial matrix activating caspases
2.Extrinsic receptor-ligand pathway
FAS ligand binds FAS death receptor(CD95) on the target cell activating caspase (eg. negative selection of thymocytes in thymus)
Tumor Necrosis Factor(TNF) binds TNF receptor on target cell, activating caspases
3. Cytotoxic CD8+ T-Cell mediated pathway
perforins secreted by CD8+ T cells enter pores and activates caspases
Granzymes from CD8+ T cell enters through the pores and activates caspases
CD8+ T cell killing of virally infected cells is an example

Pathoma (4 decks)

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