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First Aid > Pathology > Flashcards

Pathology Flashcards

1
Q

Is apoptosis an inflammatory process?

A

No

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2
Q

Does apoptosis require ATP?

A

Yes

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3
Q

What are the cell changes associated with apoptosis?

A
  1. Eosinophilic cytoplasm
  2. Cell shrinkage
  3. Pyknosis (nuclear shrinkage) + nuclear basophilia
  4. Membrane blebbing
  5. Karyorrhexis (nuclear fragmentation)
  6. Formation of apoptotic bodies
  7. Phagocytosis
  • memory: Think of someone that is having a breakdown. 1. First they turn red (eosinophilic cytoplasm)
    2. then they clench up (cell shrinkage)
    3. then their intestines clench up (nuclear shrinkage)
    4. then they lash out and punch you (membrane bleb)
    5. then their heart breaks (karryorrhexis)
    6. then they melt into pieces (apoptotic bodies)
    7. then you give them a hug (phagocytosis)
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4
Q

What is a sensitive indicator of apoptosis? Which phenomenon of apoptosis does this capitalize on?

A

DNA laddering showing multiples of 180 bp

Capitalizes on KARYORRHEXIS (nuclear fragmentation), when endonucleases cleave at internucleosomal regions, yielding multiples of 180 bp

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5
Q

By what mechanism does radiation therapy induce apoptosis?

A
  1. Free radical formation (–> Lipid peroxidation, protein modification, DNA breakage)
  2. dsDNA breakage
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6
Q

What are the 2 pathways for apoptosis?

A
  1. Intrinsic pathway
    • Signal is generated (ex: drop in IL-2, detection of DNA damage)
    • Bcl-2 is blocked
    • so BAX, BAK , and Apaf-1 become uninhibited
    • so mitochondrial permeability increases
    • cytochrome C is released from inside mitochondria
    • cytosolic caspases are activated
  2. Extrinsic pathway
    • FasL binds to FasR (CD95)
    • Multiple Fas molecules coalesce
    • A binding site for FADD is made
    • FADD activates cytosolic caspases
      OR
    • Killer T cells release granzyme B and perforin
    • these activate cytosolic capsases
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7
Q

What kind of cell death utilizes the instrinsic pathway? The extrinsic pathway?

A

Intrinsic:

  • Embryology
  • Loss of IL-2 after immune reaction completed
  • Radiation
  • Toxins
  • Hypoxia

*memory: BIE-BIE (Bad things, IL-2 loss, Embryology)

Extrinsic:

  • Killer T cells (release perforin and granzyme B)
  • Thymic medullary negative selection (Fas-FasL)
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8
Q

Autoimmune disorders can be caused by what error in the apoptosis pathway?

A

Mutation in Fas or defective Fas-FasL interactions This results in more self-reacting lymphocytes in the body, which can cause autoimmune disease

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9
Q

Is necrosis an inflammatory process?

A

yes, always!

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10
Q

What happens first in coagulative necrosis?

A

proteins denature…. THEN enzymes degrade

*memory: The proteins die and coagulate, so the cells are able to maintain their shape

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11
Q

What happens first in liquefactive necrosis?

A

enzymes digest tissue (from neutrophils)…. THEN proteins denature

*memory: If the enzymes get there first, everything will be chewed up

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12
Q

What kind of necrosis is seen in brain infarcts? Why?

What else exhibits this type of necrosis?

A

Liquefactive necrosis. Because of the high fat content, AND because microglial cells contain hydrolytic enzymes

Also seen in bacterial abscesses, because neutrophils have hydrolytic enzymes

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13
Q

What 3 kind of processes cause caseous necrosis?

A
  1. TB
  2. systemic fungy (ex: Histoplasma capsulatum)
  3. Nocardia
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14
Q

What does fat necrosis look like on H&E stain? What 2 situations is this seen in?

A

Looks like: Dark blue (calcium stains dark blue, sign of fat saponification)

  1. Acute pancreatitis, 2. Breast trauma
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15
Q

What is the pathogenesis of fibrinoid necrosis?

A

Immune rxn in the vessels:Immune complexes + Fibrin = Vessel wall damage, pink

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16
Q

In which type of necoriss do you see lymphocytes?

A

Caseous necrosis (TB, nocardia, systmeic fungi). Lymphocytes and macrophages surround the fragments cells and debris.

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17
Q

What is the difference between dry and wet gangernous necrosis on histology?

A

Dry = Coagulative necrosis, Wet = Liquefactive necrosis

*memory: Dry sky means no clouds (Dry, iSKemia, CCCoag)

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18
Q

Pathogenesis of follicular (and undifferentiated) lymphoma

A

Overexpression of BCL-2 —> overinhibition of Apaf-1 –> no cell death

*memory: BCL-2 takes care of YOU (its anti-apoptotic)

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19
Q

T cells undergo positive and negative selection in the thymus, and then go chill in the lymph nodes. In what part of the thymus does negative selection occur?

A

Negative selection: Medulla
*You can remember this because they do positive selection first in the cortex (must recognize self), and then move deeper into the medulla to do negative selection

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20
Q

How do overly self-reactive T cells get eliminated in the body?

Does the T cell get FasR or FasL stimulated?

A

T cells bind to self MHC but receive so co-stimulatory signal (B7 on a dendrite or CD40 on a B cell), so the Fas-FasL pathway is initiated

I guess the Fas-R (CD95) on the T cell is stimulated

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21
Q

What early changes are seen histologically in brain infarcts? Late changes?

A

Early: Cellular debris, macrophages

Late: Cystic spaces, cavitation

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22
Q

Diabetics with atherosclerosis in the popliteal artery are particularly susceptible to what kind of necrosis?

A

Gangraneous (this type of necrosis is typical for any kind of chronic ischemia in the distal extremity. If a superimposed infection occurs, it will become wet/liquefactive. If not, it will be dry/coagulative).

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23
Q

What is the hallmark of reversible cell injury (reversible with oxygen)?

A

Cellular swelling

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24
Q

What is the hallmark of irreversible cell injury?

A

Plasma membrane damage

and therefore leakage of troponin, amylase, etc

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25
Q

Reversible or not: Decreased glycogen

A

Yes

Think of the glycogen just being diluted out by water

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26
Q

Reversible or not: Fatty change

A

Yes

Side Note: CCl4 induces free radical injury and first causes cellular swelling and then fatty change/liver necrosis. –> apolipoproteins lacking because ribosomes popped off RER

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27
Q

Reversible or not: Mitochondrial swelling

A

Yes

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28
Q

Reversible or not: Mitochondrial vacuolization

A

No! This means mitochondrial permeability. Phospholipid amorphous densities accumulate within the mitochondria.

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29
Q

Reversible or not: Lysosomal rupture

A

No! Anything with a messed up membrane will be irreversible

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30
Q

Reversible or not: Membrane blebbing

A

Yes!

If it is associated w/ cells turning pink, shrinking, and nucleus shrinking or breaking then NO! This would go along with apoptosis

But if it is associated with just cell swelling, then YES

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31
Q

Reversible or not: Nuclear chromatin clumping

A

Yes (this is the only nuclear change that is allowed)

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32
Q

Reversible or not: ATP depletion

A

Yes!

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33
Q

Reversible or not: Nuclear pyknosis

A

No (pyknosis = shrinking)

34
Q

Which area in the BRAIN is most susceptible to systemic hypoperfusion?

A

Boundary areas between ACA/MCA/PCA

*These are watershed areas. They are protected against single-vessel blockage, but they will be the first to go in systemic hypoperfusion

35
Q

Which area in the HEART is most susceptible to hypoxia/ischemia?

A

Subendocardium (especially in the LV)

36
Q

Which 2 areas in the KIDNEY are most susceptible to hypoxia/ischemia?

A
  1. Proximal tubule (straight segment) - medulla

2. Thick ascending limb - also medulla

37
Q

Which area in the LIVER is most susceptible to hypoxia/ischemia?

A

Zone 3 (area around the central vein)

38
Q

Which areas in the COLON are most susceptible to systemic hypoperfusion?

A
  1. Splenic flexure

2. Rectum

39
Q

Hypoxic Ischemic Encephalopathy (HIE) will affect which 2 cells predominantly?

A
  1. Hippocampus: Pyramidal cells
  2. Cerebellum: Purkinje cells
  • memory: Will’s dad couldn’t REMEMBER (hippocampus) and he couldnt WALK (cerebellum)
  • memory: both cell types start with P because your brain is huffing and PPPPuffing for some O2
40
Q

What causes reperfusion injury?

A

Free radicals

41
Q

Which 3 organs are likely to get pale infarcts?

A
  1. Spleen
  2. Heart
  3. Kidney
    (Tissues with a single end-arterial blood supply)

*memory: pale as SHiK

42
Q

Which 3 organs are likely to get red infarcts?

A
  1. Liver
  2. Intestines
  3. Lung
    (Tissues with multiple blood supplies)

*memory: when you’re red you’re a LIL dead

43
Q

Will motor neuron damage cause atrophy or hypoplasia of muscle?

A

Atrophy

44
Q

What cellular changes will be seen in a kidney with nephrolithiasis?

A

Atrophy (from the increasedpressure)

45
Q

What are the 3 vascular changes seen in inflammation?

A
  1. Increased vascular permeability
  2. Vasodilation
  3. Endothelial injury
46
Q

What are the 3 cell types of acute inflammation?

A
  1. Neutrophils
  2. Eosinophils
  3. Antibody (although not as much I think)
47
Q

What is the hallmark of acute inflammation?

A

Edema

48
Q

What cytokines would macrophages secrete to resolve acute inflammation after a few min/days?

A

IL-10 and TGF-Beta

49
Q

What would macrophages do to turn acute inflammation into chronic inflammation?

A

Express antigen on MHC2

50
Q

What are the 2 cell types of chronic inflammation?

A
  1. Mononuclear cells (B and T cells)

2. Fibroblasts

51
Q

What is chromatolysis? How do we identify it on histology?

A

The change the neurons undergo in their cell body after their axon gets injured.

Histology:

  • Round cell/swollen cell
  • Nucleus displaced to periphery
  • Nissl substance dispreses throughout body (and eventually dissolves and disappears)
52
Q

What is a Nissl body?

A

A site of protein synthesis in the SOMA and DENDRITES of the neuron containing granules of RER and free RIBOSOMES

53
Q

What signaling molecules are responsible for maintaining acute inflammation (pathoma)?

A

Leukotrienes

54
Q

What do mast cells secrete in acute inflammation?

A

Histamine + Arachidonic acid

55
Q

By what 4 steps does fever occur?

A
  1. Macrophages release IL-1 and TNF
  2. IL-1 and TNF go to perivascular cells of hypothalamus
  3. COX activity increased
  4. Prostaglandins increase the temperature set point of the hypothalamus

*memory: Go up to T1 (Tnf, il-1) near the brain

56
Q

A patient has been sick for 8 weeks. They are coughing up pus. Do they have acute or chronic inflam?

A

Acute!

Inflammation is defined by the types of cells present. Pus = neutrophils = acute.

57
Q

What 5 conditions can exhibit dystrophic calcification? (Include the PSaMMoma)

What 4 phenomena can ALSO exhibit dystrophic calcification?

A
  1. TB (lungs, pericardium)
  2. Schistosomiasis (bladder)
  3. Monckeberg arteriolosclerosis (vessels “pipe steam”)
  4. Congenital CMV + toxoplasmosis
  5. Psamomma bodies (Papillary [thyroid], Serous [cystadenocarcinoma ovary], Meningioma, Mesothelioma [malignant])
    * memory: Thomas Sayre-McCord is a little Calcified Pssy
  6. . Liquefactive necrosis of chronic abscesses
  7. Infarcts
  8. Fat necrosis
  9. Thrombi
    * memory: these conditions take calcium for a LIFT
58
Q

What KEY conditions can result in metastatic calcification? (Due to hypercalcemia)

A
  • Sarcoidosis (increased 1alpha hydroxylase expression leads to more active vit D)
  • Chronic renal failure w/ secondary hyperPTH (due to high Ca-PO4 coupling)
  • Warfarin
59
Q

Does acidic or alkaline pH favor calcium deposition?

A

Alkaline

60
Q

Which tissues in the body usually are receptive to metastatic calcification because of their alkaline pH?

A
  1. Kidney
  2. Lung
  3. Gastric mucosa
61
Q

At what location does leukocyte extravasation mainly occur?

A

Postcapillary venule

62
Q

What are the 4 steps of leukocyte extravasation?

A
  1. Margination/rolling
  2. Tight binding
  3. Diapedesis
  4. Migration
63
Q

Which interaction mediates leukocyte margination and rolling?

A 
VASCULATURE: E-selectin, P-selection 
LEUKOCYTE: Sialyl-Lewis, x
or
VASCULATURE: glyCAM1, CD34
LEUKOCYTE: L-selectin

*memory: L-selectin is on the LLLeukocyte, but E and P are on the Endothelium/Periphery

64
Q

Which interaction mediates leukocyte tight binding?

A 
VASCULATURE: ICAM-1 (CD54)
LEUKOCYTE: CD11/8 integrins (LFA-1, MAC1)
or
VASCULATURE: VCAM-1 (CD106)
LEUKOCYTE: VLA-4 integrin
65
Q

Which interaction mediates leukocyte diapedesis?

A

PECAM-1 (CD31) — both on vasculature and leukocyte

66
Q

What things do neutrophil chemotaxis?

HIGH YIELD!

A
  1. C5a (raise your 5 fingers to hail a neutrophil)
  2. IL-8 (IL-8 to get a date with a neutrophil)
  3. LTB-4 (to arrive b4 others)
  4. Kallikrein (calling crazy in)
  5. Platelet-activating factor (platelets are my pals)
67
Q

What increases P-selectin levels? E-selectin levels?

What is P-selectin released by?

A

P-selectin: Histamine
E-selectin: IL-1 and TNF-alpha *the same ones that cause fever

P-selectin is released by Wiebel-Palade bodies (which also release vWF)

68
Q

What is the defect in LAD1? LAD2?

A

LAD1: No LFA-1 subunit on the CD18 integrin

  • can’t do tight binding (with ICAM1)
  • delayed separation of umbilical cord, recurrent bacterial infections w/ no pus, high levels of neutrophils in blood

LAD2: No Sialyl-lewis antigen on WBC
- can’t do margination/rolling with E or P selectin

69
Q

What is the defect in Chediak-Higashi syndrome? What are the symptoms?

A

Phagosomes and lysosomes can’t fuse
*memory: Think of 2 fat guys, chediak and higashi, who cant eat because one of them has the spoon and the other the plate

Get SStaph/strep infections, PPPancytopenia, AAlbisnism, an NNNeural degeneration (pg 215)
*memory: the symptoms SPAN a whole range of things, just like their large bodies

70
Q

Which free radicals do the following scavenging enzymes eliminate:

  1. Catalase
  2. Superoxide dismutase
  3. Glutathione peroxidase
A

Catalase (and myeloperoxidase) –> H2O2 (peroxide)

Superoxide dismutase –> O2- (superoxide)

Glutathione –> OH- *the most important. Memory: GlutathiONE gets the important ONE (hydroxyl)

71
Q

What are 6 pathologies related to free radical injury?

A
  1. Retinopathy of prematurity (premature babies put on excess O2 go blind)
  2. Bronchopulmonary dysplasia (babies put on O2)
  3. CCl4 (converted to CCl3- by p450 –> liver necrosis, fatty change)
  4. Acetaminophen overdose (hepatitis, renal necrosis)
  5. Hemochromatosis
  6. Reperfusion injury (esp. after thrombolytic therapy)
72
Q

What is the oxidative burst sequence?

A

O2 –>(NADPH ox) –> O2- –> (Superoxide dismutase) –> H2O2 –> (myeloperoxidase) –> HOCl

73
Q

Which cells of the body are permanent (dont regenerate)?

A
  1. Neurons
  2. Myocardium
  3. Skeletal muscle
74
Q

Which cells of the body are labile? Where are the stem cells for each?

A
  1. Small and large bowel (mucosal crypts)
  2. Skin (basal layer)
  3. Bone marrow (CD34+)
  4. Alveoli (Type 2 pneumocytes)
75
Q

How long after healing do we stop regaining tensile strength?

A

3 months (gain 80%)

76
Q

What is the difference between a hypertrophic scar and a keloid? What is the difference in treatment?

A

Hypertrophic scar: Type 1 collagen, parallel, confined to wound
Keloid: Type 3 collagen, disorganized, extend way past wound

Treatment: Can resect hypertrophic scars (they won’t recur), but need to do steroid injection for keloid

77
Q

Which race is susceptible to keloid formation?

A

African Americans

78
Q

Overexpression of which growth factor can lead to astrocytoma?

A

PDGF (induces SM cell migration and fibroblast growth… astrocyte stimulates itself)

*memory: P for PDGF and Pervy (self stimulation)

79
Q

What tissue mediators stimulate angiogenesis?

A

FGF, VEGF (weaker), TGF-beta

80
Q

Which tissue mediator receptor is expressed by ERBB2?

A

EGFR (responds to cell growth via tyrosine kinase)

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