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First Aid Pathology Flashcards

1
Q

Apaptosis

A

programmed cell death
ATP required
no significant inflammation (unlike necrosis)
characterized by deeply eosinophilic cytoplasm, cell shrinkage, nuclear shrinkage (karyorrhexis), and formation of apoptotic bodies

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2
Q

Intrinsic pathway

A

involved in tissue remodeling in embryogenesis

occurs when a regulating factor is withdrawn from a proliferating cell population or after exposure to injurious stimuli

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3
Q

Extrinsic pathway

A

2 pathways:

  • ligand receptor interactions (FasL binding to Fas)
  • immune cell (cytotoxic T-cell release of perforin and granzyme B)
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4
Q

Necrosis

A 
enzymatic degradation and protein denaturation of cell due to exogenous injury resulting in leakage of intracellular components
inflammatory process (unlike apoptosis)
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5
Q

coagulative necrosis:
seen in
due to
histo

A
  • ischemia/infarcts in most tissues (except brain)
  • ischemia or infarction; proteins denature, then enzymatic degradation
  • cell outline preserved; incr. cytoplasmic binding of acidophilic dyes
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6
Q

liquefactive necrosis:
seen in
due to
histo

A
  • bacterial abscesses, brain infarcts (due to incr fat content)
  • neutrophils releasing lysosomal enzymes that digest the tissue; enzymatic degradation first, then protein denatures
  • early: cellular debris and macrophages; late: cystic spaces and cavitation (brain), neutrophils and cell debris seen with bact. infxn
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7
Q

caseous necrosis:
seen in
due to
histo

A
  • TB, systemic fungi
  • macrophages wall off infecting microbes (granular debris)
  • fragmented cells and debris surrounded by lymphocytes and macrophages
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8
Q

fat necrosis
seen in
due to
histo

A
  • enzymatic: acute pancreatitis; nonenzymatic: breats trauma
  • damaged cells release lipase, which breaks down fatty acids in cell membranes
  • outlines of dead fat cells without peripheral nuclei; saponification of fat (combined with Ca2+) appears dark blue on H&E stain
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9
Q

fibrinoid
seen in
due to
histo

A
  • immune reactions in vessels
  • immune complexes combine with fibrin (vessel wall damage)
  • vessel walls are thick and pink
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10
Q

gangrenous
seen in
due to
histo

A
  • distal extremity, after chronic ischemia
  • dry: ischemia; wet: superinfection
  • dry: coagulative (cell outline preserved); wet: liquefactive (early: cellular debris and macrophages; late: cystic spaces and cavitation)
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11
Q

cellular injury

reversible

A 
ATP depletion
cellular/mitochondrial swelling (decr. ATP, decr activity of Na+/K+ pump)
nuclear chromatin clumping
decr glycogen
fatty change
ribosomal/polysomal detachment
membrane blebbing
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12
Q

cellular injury

irreversible

A

nuclear pyknosis (shrinkage), karyorrhexis (fragmentation), karyolysis
plasma membrane damage (degradation of membrane phospholipid)
lysosomal rupture
mitochondrial permeability/vacuolization; phospholipid-containing amorphous densities within mitochrondria (swelling alone is reversible)

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13
Q

Ischemia
susceptible areas:
organ and location

A
  • brain (ACA/MCA/PCA boundary areas)
  • heart (Subendocardium, LV)
  • kidney (straight segment of proximal tubule (medulla), thick ascending limb (medulla)
  • liver (area around central vein (zone III)
  • colon (splenic flexure, rectum)
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14
Q

Infarcts

red

A 
red = hemorrhagic infarcts
occur in venous occlusion and tissues with multiple blood supplies, such such as liver, lung and intestine
Reperfusion injury (after angioplasty) is due to damage  by free radicals 
*think REd for REperfusion
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15
Q

Infarcts

pale

A

Pale = anemic infarcts

occur in solid organs with a single (end-arterial) blood supply, such as heart, kidney, and spleen

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16
Q

define atrophy

A

reduction in the size and/or number of cells

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17
Q

causes of atrophy

A
  • decr endogenous hormones (eg post-menopausal ovaries)
  • incr exogenous hormones (eg steroid use)
  • decr innervation (eg motor neuron damage)
  • decr blood flow/nutrients
  • decr metabolic demand (eg paralysis)
  • incr pressure (eg nephrolithiasis)
  • occlusion of secretory ducts (eg calculus/stones)
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18
Q

five characteristics of inflammation

A 
rubor (redness)
dolor (pain)
calor (heat)
tumor (swelling)
functio laesa (loos of function)
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19
Q

vascular component of inflammation

A

incr vascular permeability, vasodilation, endothelial injury

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20
Q

cellular component of inflammation

A

neutrophils extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator release

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21
Q

acute cellular component of inflammation

A

neutrophil, eosinophil, and antibody mediated
acute inflammation is rapid onset (sec - min) and of short duration (min - days)
outcomes include complete resolution, abscess formation, or progression to chronic inflammation

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22
Q

chronic cellular component of inflammation

A

mononuclear cell and fibroblast mediated
characterized by persistent destruction and repair
assoc with blood vessel proliferation, fibrosis
granuloma: nodular collections of epitheliod macrophages and giant cells
outcomes include scarring and amyloidosis

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23
Q

what is chromatolysis?

A

process involving the neuronal cell body following axonal injury
changes reflect incr protein synthesis in effort to repair the damaged axon
characterized by:
round cellular swelling
displacement of the nucleus to the periphery
dispersion of Nissl substance throughout cytoplasm

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24
Q

define dystrophic calcification

A

Ca2+ deposition in ABNORMAL TISSUE, secondary to injury or necrosis
tends to be localized (eg calcific aortic stenosis)
seen in TB (lungs and pericardium), liquefactive necrosis of chronic abscesses, fat necrosis, infarcts, thrombi, schistosomiasis, Monchkeberg arteriolosclerosis, congenital CMV + toxoplasmosis, psammoma bodies
*is not directly assoc with serum Ca2+ levels (pt usually normocalcemic)

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25
Q

define metastatic calcification

A

widespread deposition of Ca2+ in NORMAL TISSUE secondary to hypercalcemia or high calcium-phosphate product levels
Ca2+ deposits predominantly in interstitial tissues of kidney, lung, and gastric mucosa (these tissues lose acid quickly, incr pH favors deposition)
*pt is usually not normocalcemic

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26
Q

Leukocyte extravasation

A

WBCs exit from blood vessels at sites of tissue injury and inflammation in 4 steps

1) margination and rolling (defective in leukocyte adhesion deficiency type 2), involves E-selectin, P-selectin, and GlyCAM-1, CD34
2) tight-binding (defective in leukocyte adhesion def. type 1), involves ICAM-1 (CD54)
3) diapedesis (WBC travels btwn endothelial cells and exits blood vessel), involves PECAM-1 (CD31)
4) migration (WBC travels through interstitium to site of injury or infection guided by chemotactic signals released in response to bacteria (C5a, IL-8, LTB4, kallikrein, platelet-activating factor)

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27
Q

what is free radical injury?

A

free radicals damage cells via membrane lipid peroxidation, protein modification, and DNA breakage

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28
Q

when are free radicals initiated?

A

radiation exposure, metabolism of drugs (phase I), redox reactions, nitric oxide, transition metals, WBC (neutrophils, macrophages) oxidative burst

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29
Q

how are free radicals eliminated?

A
  • scavenging enzymes such as catalase, superoxide dismutase, glutathione peroxidase
  • spontaneous decay
  • antioxidants (Vit A, C, E)
  • metal carrier proteins (transferrin, ceruloplasmin)
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30
Q

Pathologies that involve free radical injury

A
  • retinopathy of prematurity
  • bronchopulmonary dysplasia
  • carbon tetrachloride, leading to liver necrosis (fatty change)
  • acetaminophen overdose (fulminant hep, renal papillary necrosis)
  • iron overload (hemochromatosis)
  • reperfusion injury (superoxide), esp after thrombolytic therapy
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31
Q

what’s an inhalation injury?

A

pulmonary complication associated with smoke and fire

caused by heat, particulates (

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32
Q

sx of inhalation injury?

A 
chemical tracheobronchitis
edema
pneumonia
ARDS
many pts present secondary to burns, CO inhalation, or arsenic poisoning
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33
Q 
hypertrophic scars vs keloid scars in terms of
collagen synthesis
collage arrangement
extent
recurrence 
notes
A 
hypertrophic: 
has moderate collagen synth
collagen is parallel
scar confined to borders of original wound
infrequently recur following resection 
keloid:
high levels of collagen synth
collagen is disorganized
scar extends beyond borders of original wound
frequently recur following resection
higher incidence in african americans
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34
Q

wound healing:

tissue mediators and their functions

A

PDGF- secreted by activated plalets and macrophages, induces vascular remodeling and smooth muscle cell migration, stimulates fibroblast growth for collagen synth
FGF- stimulates angiogenesis
EGF- stimulates cell growth via tyrosine kinases
TGF-beta- angiogenesis, fibrosis, cell cycle arrest
metalloproteinases- tissue remodeling
VEGF- stimulates angiogenesis

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35
Q

phases of wound healing
inflammatory (up to 3 days after wound)
mediators and characteristics

A

-platelets, neutrophils, macrophages

clot formation, incr vessel permeability and neutrophil -migration into tissue; macrophages clear debris 2 days later

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36
Q

phases of wound healing
proliferative (day 3- weeks after wound)
mediators and characteristics

A
  • fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages
  • deposition of granulation tissue and collagen, angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (mediated by myofibroblasts)
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37
Q

phases of wound healing
remodeling (1 week- 6+ mo after wound)
mediators and characteristics

A
  • fibroblasts

- type III collagen replaced by type I collagen, incr tensile strength of tissue

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38
Q

Granulomatous disease

A
  • Bartonella henslae (cat scratch disease)
  • Berylliosis
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
  • Crohn disease (noncaseating granuloma)
  • Foreign bodies
  • Francisella tularensis
  • Fungal infections (caseous necrosis)
  • Granulomatosis with polyangiitis (Wegener)
  • Listeria monocytogenes (granulomatosis infantiseptica)
  • M. leprae (leprosy; Hansen disease)
  • M. tuberculosis (caseous necrosis)
  • Treponema pallidum (tertiary syphilis)
  • Sarcoidosis (noncaseating granuloma)
  • Schistosomiasis
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39
Q

pathogenesis of granuloma formation

A

Th1 cells secrete IFN-gamma, activating macrophages

TNF-alpha from macrophages induces and maintain granuloma formation

40
Q

what drugs can cause disseminated disease?

A

Anti-TNF drugs can, as a side effect, cause sequestering granulomas to break down, leading to disseminated disease
Always test for latent TB before starting anti-TNF therapy!

41
Q

Exudate

A 
think THICK
cellular
protein rich
specific gravity > 1.020
Due to: lymphatic obstruction, inflammation/infxn, malignancy
42
Q

Transudate

A

think THIN
hypocellular
protein-poor
specific gravity

43
Q

what is ESR (erythrocyte sedimentation rate)?

A

products of inflammation (eg fibriongen) coat RBCs and cause aggregation
the denser the RBC aggregates fall at a faster rate within a pipette tube. Often co-tested with CRP levels

44
Q

things that cause increased ESR?

A 
most anemias
infections
inflammation (eg, temporal arteritis)
cancer (eg, multiple myeloma)
pregnancy
AI disorders (eg SLE)
45
Q

things that cause decreased ESR?

A 
sickle cell anemia (altered shape)
polycythemia (inc RBCs "dilute" aggregation factors)
HF
microcytosis
hypofibrinogenemia
46
Q

describe amyloidosis

A

abnormal aggregation of proteins (or their fragments) into beta-pleated sheets. leads to damage and apoptosis

47
Q

types of amyloidosis:

AL (primary)

A

due to deposition of proteins from Ig Light chains
can occur as a plasma cell disorder or associated with multiple myeloma
often affects multiple organ systems: renal (nephrotic syndrome), cardiac (restrictive cardiomyopathy, arrhythmia), hematologic (easy bruising, splenomegaly), GI (hepatomegaly), and neurologic (neuropathy)

48
Q

types of amyloidosis:

AA (secondary)

A

fibrils composed of serum Amyloid A
often multisystem
seen with chronic inflammatory conditions such as RA, IBD spondyloarthropathy, protracted infection

49
Q

types of amyloidosis:

Dialysis-related

A

fibrils composed of beta2- microglobulin
seen in patients with ESRD and/or on long-term dialysis
may present in carpal tunnel syndrome

50
Q

types of amyloidosis:

Heritable

A

heterogeneous group of disorders, including familial amyloid polyneuropathies due to transthyretin gene mutation

51
Q

types of amyloidosis:

Age-related (senile) systemic

A

due to deposition of normal (wild-type) transthyretin in myocardium and other sites
slower progression of cardiac dysfunction relative to AL amyloidosis

52
Q

types of amyloidosis:

Organ-specific

A

Amyloid deposition localized to a single organ
most important form is amyloidosis in Alzheimer disease due to deposition of beta-amyloid protein cleaved from amyloid precursor protein (APP)
Islet amyloid polypeptide (IAPP) is commonly seen in DM type 2 and is caused by deposition of amylin in pancreatic islets

53
Q

What’s lipofuscin?

A

a yellow-brown “wear and tear” pigment associated with normal aging

54
Q

how is lipofuscin made?

A

formed by oxidation and polymerization of autophagocytosed organellar membranes

55
Q

hyperplasia

A

cells incr in number

56
Q

dysplasia

A

abnormal proliferation of cells with loss of size, shape, and orientation

57
Q

carcinoma in situe/preinvasive

A

neoplastic cells have not invaded intact basement membrane
incr nuclear/cytoplasmic (N/C) ratio and clumped chromatin
neoplastic cells encompass entire thickness

58
Q

invasive carcinoma

A

cells have invaded basement membrane using collagenases and hydrolases (metalloproteinases)
cell-cell contacts lost by inactivation of E-cadherin

59
Q

metastasis

A

spread to distant organ
“seed and soil” theory of METS
seed= tumor embolus
soil= target organ is often the first-encountered capillary bed
the cancer cells being the “seeds” and the specific organ microenvironment​s being the “soil.”

60
Q

what’s P-glycoprotein?

A

AKA multidrug resistance protein 1 (MRP1)
classically seen in adrenal cell carcinoma but also expressed by other cancer cells
used to pump out toxins, including chemotherapeutic agents (one mechanism of decr responsiveness or resistance to chemotherapy over time)

61
Q

carcinoma implies

A

epithelial origin

62
Q

sarcoma implies

A

mesenchymal origin

63
Q

carcinoma and sarcoma both imply

A

malignancy

64
Q

most carcinomas spread via

A

lymphatics

65
Q

most sarcomas spread via

A

blood

66
Q

non-neoplastic malformation

A

hamartoma (disorganized overgrowth of tissue in their native location)
choristoma (normal tissue in a foreign location)

67
Q

benign epithelial tumors

A

adenoma

papilloma

68
Q

benign blood vessel tumor

A

hemangioma

69
Q

benign smooth muscle tumor

A

leiomyoma

70
Q

benign striated muscle tumor

A

rhabdomyoma

71
Q

benign connective tissue tumor

A

fibroma

72
Q

benign bone tumor

A

osteoma

73
Q

benign fat tumor

A

lipoma

74
Q

malignant epithelial tumor

A

adenocarcinoma

papillary carcinoma

75
Q

malignant blood cell tumors

A

leukemia

lymphoma

76
Q

malignant blood vessel tumor

A

angiosarcoma

77
Q

malignant smooth muscle tumor

A

leiomyosarcoma

78
Q

malignant striated muscle tumor

A

rhabdomyosarcoma

79
Q

malignant connective tissue tumor

A

fibrosarcoma

80
Q

malignant bone tumor

A

osteosarcoma

81
Q

malignant fat tumor

A

liposarcoma

82
Q

description of benign tumor

A 
well differentiated
well demarcated
low mitotic activity
no METS
no necrosis
83
Q

description of malignant tumor

A 
poor differentiation
erratic growth
local invasion
METS
decr apoptosis 
upregulation of telomerase prevents chromosome shortening and cell death
84
Q

description of cachexia

A 
weight loss
muscle atrophy
fatigue
occurs in chronic dz (CA, AIDS, HF, TB)
mediated by TNF-alpha, IFN-gamma, IL-1, and IL-6
85
Q

Oncogene
description
need damage to

A

gain of function -> incr CA risk

need damage to only 1 allele

86
Q

Tumor suppressor
description
need damage to

A

loss of function -> incr CA risk

need damage to both alleles

87
Q

what should tumor markers be used for? what shouldn’t they be used for?

A
  • used to monitor tumor recurrence and response to tx

- shouldn’t be used as primary tool for CA dx or screening

88
Q

what are psammoma bodies? what diseases are they associated with?

A

-laminated, concentric spherules with dystrophic calcification
PSaMMoma
P=papillary carcinoma of thyroid
S= serous papillary cystadenocarcinoma of ovary
M=meningioma
M=malignant mesothelioma

89
Q

Cancer incidence in men

A
  1. prostate
  2. lung
  3. colon/rectum
90
Q

Cancer incidence in women

A
  1. breast
  2. lung
  3. colon/rectum
91
Q

Cancer mortality in men

A
  1. lung
  2. prostate
  3. colon/rectum
92
Q

Cancer mortality in women

A
  1. lung
  2. breast
  3. colon/rectum
93
Q

what’s the primary leading cause of death in US? 2nd?

A
  • hear disease

- cancer

94
Q

common METS to brain from tumors in:

A

lung > breast > prostate > melanoma > GI

95
Q

common METS to liver from tumors in:

A

colon&raquo_space; stomach > pancrease

96
Q

common METS to bone from tumors in:

A

prostate/breast > lung/thyroid/kidney

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