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Boards 23' > Pathology (Gen Principles) > Flashcards

Pathology (Gen Principles) Flashcards

1
Q

Hypertrophy

A

increase in size
involves gene activation and *protein synthesis, and production of organelles (for cellular fxn - mitochondria)

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2
Q

Hyperplasia

A

increase in cell number
production of new cells from stem cells - classic response to hormone stimulation

Ex: breast growth at puberty, liver regeneration (donation) and bone marrow (anemia)

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3
Q

physiologic changes of the uterus during pregnancy

A

smooth muscle undergoes hypertrophy and hyperplasia

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4
Q

Important note about permanent tissues

A

canNOT make new cells - so cannot undergo hyperplasia - hypertrophy ONLY

3 permanent tissues:
cardiac myocytes
skeletal muscle
nerves

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5
Q

3 permanent tissues

A

“terminally differentiated”
cardiac myocytes
skeletal muscle
nerves

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6
Q

pathologic hyperplasia

A

hyperplasia that progresses to dysplasia and cancer

ex: endometrial hyperplasia - due to estrogen

exception: benign prostatic hyperplasia (BPH) - due to androgens - not related to cancer and no increase in cancer risk

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7
Q

Atrophy

A

decrease in stress on the organ (less stress) - decrease in size and number

Mechanism:
apoptosis (decrease # of cells)
ubiquitin-proteasome degradation (decrease in cell size)

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8
Q

mechanism of atrophy

A
  1. decrease in # - apoptosis
  2. decrease in size
    a. ubiquitin-proteasome degradation pathway - destroying the cytoskeleton
    b. autophagy of cellular components and then destroyed by lysosomes
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9
Q

Metaplasia

A

change cell type in response to stress

most common involves surface epithelium

metaplastic cells are better to handle the new stress

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10
Q

Mechanism of metaplasia

A

REVERSIBLE reprogramming of stem cells - can progress to cancer

ex: Barrett esophagus and respiratory epithelium w/ cigarette smoke (to stratified squamous cell epithelium)

exception: apocrine metaplasia (fibrocystic change of the breast - does not increase the risk of breast cancer)

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11
Q

the exception to metaplasia as an increased risk to cancer

A

apocrine metaplasia (fibrocystic change of the breast - does not increase the risk of breast cancer)

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12
Q

Which vitamin deficiency can lead to metaplasia?

A

Vitamin A deficiency
- night blindness
- also necessary for immune cell maturation (PML - trapped in blast state (derivative of Vitamin A is a tx)
- can result in metaplasia (necessary for maintenance of specialized epithelial - conjunctival and upper respiratory tract - pulmonary infections)

ex: keratomalacia

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13
Q
A

keratomalacia - clouding and drying (xerophthalmia) of the eye caused by a Vitamin A deficiency

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14
Q

Mesenchyme tissues

A

Connective tissues
- blood vessels, bone, fat, cartilage

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15
Q

presence of bone within skeletal muscle

A

myositis ossificans (ex of an mesenchyme metaplasia) - muscle going to bone

bone is normal - look careful and see that there is a distinct separation between the bone and muscle (is not growing off the bone - so not a bone issue like osteosarcoma)

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16
Q

Dysplasia

A

REVERSIBLE disordered cellular growth

proliferation of precancerous cells (ex: CIN) - arises from long standing hyperplasia (endometrial hyperplasia) or metaplasia (Barrett esophagus)

if stress persists - leads to cancer IRREVERSIBLE

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17
Q

Aplasia

A

failure of growth/cellular production during embryogenesis

ex: unilateral renal agenesis (fails to develop one kidney)

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18
Q

Hypoplasia

A

decrease in cell production during embryogenesis - results in small organ

Ex: streak ovary in Turner syndrome

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19
Q

Characteristic changes that indicate dysplasia

A

pleomorphism, abnormal nuclei (hyperchromatic or large), and mitotic figures (clumped chromatin)

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20
Q

Hypoxia

A

low oxygen delivery to tissues - O2 final electron acceptor - needed for ATP/energy - impairs oxidative phosphorylation -cellular injury (Na+/K+ failure)

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21
Q

CO poisoning

A

carbon monoxide is an odorless gas that binds Hb more tightly than 02; PaO2 will be normal but SaO2 will be decreased - (O2 is in the blood, just not bound to Hb)

Ex: smoke from fires, exhaust from cars (suicide) and gas heaters

Clinical manifestation: cherry red appearance of the skin, early sign of *headache and then confusion until it gets to coma and death

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22
Q

Methemoglobinemia

A

iron in heme is oxidized to Fe3+ (normally in Fe2+ state) - so now Hb can no longer bind O2

PaO2 is normal, SaO2 decreased - (O2 is in the blood, just not bound to Hb)

Seen in oxidant stresses (sulfa and nitrate drugs) and in newborns

Clinical manifestation: chocolate-colored blood w/ cyanosis Tx: IV methylene blue (reduce Fe3+ to Fe2+)

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23
Q

Low ATP in cells

A

ATP needed for Na+/K+ pump (pushes Na+ out to maintain gradient) w/ failure Na+ will build up inside the cell - H20 follows - swelling (first signs of cellular injury)

Also:
Ca2+ pump - high cyclic Ca2+ (enzyme activator) and aerobic glycolysis

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24
Q

Initial phase in reversible injury

A

hallmark = cellular swelling
leads to loss of microvilli, membrane blabbing and swelling of the RER (ribosomes pop pff the ER - decreased protein synthesis)

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25
Q

Hallmark of irreversible cell injury

A

membrane damage (there are 3 membranes):
1. plasma membrane - cytosolic enzymes will leak out into the blood (serum testing - liver and cardiac damage)
2. mitochondrial membrane - Cystochrome C can leak out and cause apoptosis
3. Lysosomes - digestive enzymes are released to cause intracellular damage

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26
Q

Where is ETC is located in the mitochondrial?

A

inner mitochondrial membrane

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27
Q

Hallmark of cell death

A

loss of the nucleus
pyknosis (shrinking of nucleus), karyorrhexis breaking up the nucleus) and karyolysis (breaking down of those nuclei pieces)

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28
Q

Necrosis

A

death of a large group of cells and is followed by inflammation; NEVER PHYSIOLOGIC, always pathologic (some problem is present)

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29
Q

Coagulative necrosis

A

necrotic tissue that remains firm - cell shape and organ structure are preserved however the nucleus disappears

Note: caused by ischemic infarction of any organ BUT the brain!

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30
Q

Liquefactive necrosis

A

necrotic tissue becomes liquified due enzymatic lysis of cells and proteins; occurs in 3 main circumstances:

  1. brain infarction (mediated by microglia cells)
  2. abscess - neutrophil enzymes
  3. pancreatitis - pancreatitis enzymes
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31
Q

Gangrenous necrosis

A

resembles mummified tissue (dry gangrene); characteristic ischemia over the lower limb and GI tract

if infection occurs (superimposed) on dead tissue, then liquefactive necrosis aka “wet gangrene”

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32
Q

Caseous necrosis

A

soft, friable necrotic with “cottage cheese-like appearance; characteristic of TB and fungal infection

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33
Q

Fat necrosis

A

necrotic adipose tissue with a chalky-white appearance due to deposition of Ca2 (saponification)

  • trauma to breast (car accident) - giant cells and calcifications on mammography and also pancreatitis in peripancreatic fat
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34
Q

Fibrinoid necrosis

A

necrotic damage to blood vessel wall; leaking proteins into vessel walls results in bright pink staining

Malignant HTN and vasculitis

35
Q

In what circumstance would a 30 yr woman present with fibrinoid necrosis?

A

preeclampsia (HTN in 3rd trimester in pregnancy) - fibrinoid necrosis is seen in blood vessel irreversible injury typically due to long-standing HTN

36
Q

CD8+ T cell-mediated killing of virally infected cells is an example of what type of cell death?

A

apoptosis; T cells release Granzyme B (enters pores) and perforin (perforates/creates pores) - activates executioner caspases

37
Q

Intrinsic (mitochondrial) pathway

A

cellular injury, DNA damage or decreased hormonal stimulations which inactivates BCL2 (anti-apoptotic/don’t wanna die) - functions to keep mitochondrial membrane impermeable to cytochrome C so it is not released

release of cytochrome C initiates cell destruction

38
Q

Extrinsic (death receptor) pathway

A

*FASL binds FAS death receptor (CD95) on target cell - occurs in negative selection in the thymus

TNF binds TNF receptor on target cells

39
Q

Free radicals

A

chemical species with unpaired electron in their outer orbit - this unpaired electron has the ability to cause injury in the cell

40
Q

pathological generation of free radicals

A

ionizing radiation (hydroxyls)
inflammation
metals (copper and iron)
drugs and chemicals (acetaminophen - converted by p450 enzymes and generate free radicals in the process) carbon tetrachloride (CCl4) is another big one

41
Q

free radical damage

A

perioxidation of lipids
oxidation of DNA and proteins (damages DNA)

42
Q

Elimination of free radicals

A

Antioxidants (ex: vitamin A,C, E)
Enzymes (SOD, Glutathione peroxidase and Catalase)
Metal carrier proteins (ferritin)

43
Q

Enzymes that eliminate free radicals

A

O2 to O2- to H2O2 to OH- to H2O

  1. Superoxide dismutase (SOD) handles O2-/superoxide
  2. Catalase handles H2O2/peroxide
  3. Glutathione peroxidase handles OH-/hydroxyl (most dangerous free radical)
44
Q

CCl4 free radical injury

A

typically exposure from dry cleaning industry

converted to CCl3 in the P450 enzymes of the liver - free radical damages the hepatocytes - cellular swelling - protein synthesis is reduced (decrease Apolipoprotein synthesis) - fatty change of the liver

45
Q

Amyloid

A

misfolded protein that deposits in the *extracellular space and damages tissues

not one protein - broad characteristic of proteins that can be folded in a characteristic way - beta-pleated sheet configuration and picks up Congo red staining and apple-green birefringence under polarized light

46
Q

apple-green birefringence under polarized light

A

characteristic of amyloid deposition

47
Q

Primary amyloidosis

A

systemic deposition (throughout the body) of *AL amyloid derived from Ig light chain

associated with plasma cell dyscrasias (abnormality of plasma cells - overproduction of the light chains)

48
Q

Secondary amyloidosis

A

systemic deposition (throughout the body) of *AA amyloid derived from SAA

SAA is an acute phase reactant (Increased in chronic inflammatory states, malignancy and familial Mediterranean fever)

49
Q

Familial Mediterranean fever

A

dysfunctional neutrophils AR that occurs in a person of Mediterranean origin
presents with episodes of fever and *acute serosal inflammation

High SAA during attacks and these deposit as AA amyloid

50
Q

Which organ is the most commonly involved in amyloid deposition?

A

the kidney
results in nephrotic syndrome (large loss of protein in the urine)

51
Q

Senile cardiac amyloidosis

A

localized non-mutated *serum transthyretin deposits in the heart; usually asymptomatic; presents in elderly (80yrs)

52
Q

Familial amyloid cardiomyopathy

A

localized mutated *serum transthyretin deposits in the heart; usually symptomatic and results in restrictive cardiomyopathy (5% of Blacks)

53
Q

Acute inflammation

A

edema and neutrophils - key immune cell

54
Q

TLRs

A

toll-like receptors present on innate immune cells and recognize PAMPs

Ex: CD14 on macrophages can recognizes LPS on gram (-) bacteria and activates immune genes NF-kB - leads to multiple immune mediators

55
Q

Arachidonic Acid

A

released from cell membrane by phospholipase A2 acted on by COX or 5-lipooxygenase

COX produces prostaglandins - mediate vasodilation (at the arteriole) and increased vascular permeability (at the post-cap venule) (PGE2) - also mediates fever and pain

5-lipooxygenase products leukotrienes (LTE) - attract and activate neutrophils (LTB4)

56
Q

Role of leukotriene B4 (LTB4)

A

produced by the 5-lopoxygenase pathway from Arachidonic Acid; functions to attract and activate neutrophils for acute inflammation

57
Q

Role of prostaglandin E2 (PGE2)

A

produced by the COX pathway from Arachidonic Acid; functions to mediate vasodilation (at the arteriole) and increased vascular permeability (at the post-cap venule) and also mediates fever and pain

58
Q

Role of leukotrienes C4, D4, and E4 (LTC4, LTD4, LTE4)

A

basically cause contraction of smooth muscle

vasoconstriction (arteriole), bronchospasm (bronchus) and increased vascular permeability

59
Q

Mast cell activation

A
  1. tissue trauma
  2. complement proteins C3a and C5a
  3. cross-linking of cell-surface Ice by antigen
60
Q

Immediate response of activation of mast cells

A

dumping/releasing of histamine - vasodilation (arteriole)

61
Q

Delayed response on the activation of mast cells

A

production of arachidonic acid metabolites, particularly leukotrienes - attract and activate neutrophils (LTB4) - vasoconstriction (arteriole), bronchospasm (bronchus) and increased vascular permeability (LTC4, LTD4, LTE4)

62
Q

Classical complement pathway

A

“GM makes classic cars”

C1 binds IgG or IgM that is bound to antigen

63
Q

Alternate complement pathway

A

microbial products directly activate complement

64
Q

Mannose-binding lectin pathway

A

MBL binds mannose on microorganism and activates complement

65
Q

Key products of complement

A

C3a and C5a - trigger mast cell degranulation

C5a - chemotactic for neutrophils

C3b - opsonin for phagocytosis

MAC - lyses microbes by creating holes in the cell membrane

66
Q

Hageman factor

A

inactive proinflammatory protein produced in liver and activated upon exposure to sub endothelial or tissue collagen

*plays an important role in DIC

66
Q

Hageman factor

A

inactive proinflammatory protein produced in liver and activated upon exposure to sub endothelial or tissue collagen

*plays an important role in DIC

67
Q

Mediators of pain

A

PGE2 and bradykinin -they sensitive nerve endings

68
Q

Mediators of fever

A
  1. macrophage release of IL-1 and TNF
  2. increased COX in perivascular cells of hypothalamus
  3. increased PGE2 raised temp set point
69
Q

Healing

A

begins when inflammation occurs; occurs via regeneration and repair

70
Q

Labile tissues

A

tissues that are constantly regenerating: small and large bowel (stem cells in mucosal crypts), skin (stem cells in the basal layer) and bone marrow (hematopoietic stem cells - CD34+)

71
Q

Stable tissues

A

tissues that are quiescent but can re-enter the cell cycle; regeneration of the liver by hyperplasia - each hepatocytes produces additional cells and then enters quiescence; also the proximal renal tubule

72
Q

Permanent tissues

A

terminally differentiated tissues - myocardium, skeletal muscle and neurons; major healing is repair w/ fibrous (not regeneration)

73
Q

Initial phase of repair

A

granulation tissue
fibroblasts deposit type III collagen, capillaries provide nutrients and myofibroblasts contract the wound

74
Q

Granuloma

A

subtype of chronic inflammation w hallmark = epitheloid histiocytes
MOA: IL-12 from macrophages hits CD4+ converts into Th1 cell secretes IFN-gamma that gives macrophages an epitheloid histiocytes appearance

75
Q

Granulation tissue vs a scar in healing

A

granulation tissue is from type III collagen by fibroblast; in a scar type III collagen is replaced w/ type I collagen (stability)

collagenase removes the type III collagen and requires a *zinc cofactor

76
Q

Molecules that are important for healing and repair

A

TGF-alpha: epithelial and fibroblast growth factor

TGF-beta: important fibroblast growth factor and inhibits inflammation

PDGF: endothelium, smooth muscle, fibroblast growth factor

FGF: angiogenesis and skeletal development

VEGF: angiogenesis

77
Q

The two cytokines that are secreted by macrophages that function to shut down inflammation and start the healing process

A

IL-10 (anti-inflammatory) and TGF-beta

78
Q

pt has a large wound that has healed via secondary intention and 6 weeks later you notice that the wound is significantly reduced in size? What the mechanism that the wound reduces in size?

A

via myofibroblast - they have the ability to contract the wound and make it smaller

79
Q

Delayed wound healing

A

prolonged healing of a wound; #1 cause is infection, then Vitamin C deficiency (scurvy) - necessary for strengthening of collagen, also lack of copper or zinc

Others: foreign body, ischemia, diabetes and malnutrition

80
Q

Dehiscence

A

rupture of a wound; most commonly seen after abdominal surgery (the wound tears open)

81
Q

Hypertrophic scar

A

excess production of scar tissue; predominantly made up of type I collagen

82
Q

Keloid

A

excess production of scar tissue that is out of proportion to the wound; excess type III collagen; predisposition to Blacks; classically affects the earlobes

Boards 23' (29 decks)

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