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Pathoma Ch. 1-2 Basics Flashcards

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1
Q

Conjunctival –> stratified keratinizing squamous

A

Vitamin A deficiency –> Keratomalacia (metaplasia)

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2
Q

Pieces of bone in muscle after trauma

A

Myositis ossificans (metaplasia)

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3
Q

Streak ovary in Turners…type of tissue failure

A

Hypoplasia

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4
Q

Cyanosis w/ chocolate-colored blood

PaO2 and SaO2

Causes?

Tx?

A

Methemoglobinemia (Fe2+ –> Fe3+)

SaO2 low

Oxidant stress (sulfa drugs, nitrates)
Newborns

IV methylene blue (Fe3+ reducing agent)

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5
Q

Pre-eclampsia…see what on biopsy of placental BVs?

A

Fibrinoid necrosis (via the HTN)

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6
Q

Fibrinoid necrosis…classic examples

A

Vasculitis, Malignant hypertension

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7
Q

Cellular injury, DNA damage, etc —> apoptosis…

What protein/gene is down-regulated to allow for apoptosis? What happens?

A

BCL-2 decreases –> cytochrome C can leak out of mitochondria and activate caspases

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8
Q

Caspases activate what?

A

Proteases and endonucleases

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9
Q

Negative selection of T cells in thymus is via what?

A

Fas-FasL –> apoptosis

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10
Q

CD95

A

Fas receptor on target cells for apoptosis

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11
Q

How does a T cell kill a cell? (2)

A
  1. Via perforins and granzyme (pores –> caspase activation)

2. Via Fas-FasL

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12
Q

Cytochrome C oxidase

A

Complex 4 in ETC (final step)

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13
Q

3 free radicals and the enzymes that destroy them

A
  1. Superoxide (O2-) - Superoxide dismutase
  2. Hydrogen peroxide - Catalase
  3. Hydroxyl (OH-) - glutathione peroxidase
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14
Q

Oxygen-dependent killing in neutrophils (2)

A
  1. NADPH oxidase (O2 to O2-)

2. Myeloperoxidase (O2- to H2O2)

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15
Q

Mechanism of damage in hemochromatosis and wilsons

How to prevent this normally?

A

Metals –> free radical damage (Fenton reaction)

Metal carrier proteins (transferrin, ceruloplasmin)

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16
Q

Mechanism of damage in acetaminophen damage

A

P450 metabolism –> free radicals –> hepatic necrosis

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17
Q

How do free radicals cause damage?

A

Peroxidation of lipids

Oxidation of DNA and proteins

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18
Q

Dry cleaning industry –> fatty change in liver…cause and pathway?

A

Carbon tetrachloride –> P450 –> CCl3 (free radicals) –> cell injury/swelling of RER –> decreased protein (apolipoprotein) synthesis –> fatty change

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19
Q

Continued rise in cardiac enzymes after MI treatment w/ tPA

A

Free radical damage (reperfusion injury)

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20
Q

2 steps of T-cell selection in thymus

A
  1. Positive selection (EFFECTIVE self-binding)

2. Negative selection (TOO MUCH self-binding)

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21
Q

All amyloid has what 2 shared features?

A
  1. Beta-pleated sheet

2. Congo red stain and apple-green birefringence

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22
Q

Mediterranean ancestry
Episodes of fever + appendicitis/arthritis/MI SYMPTOMS
Congo red staining within tissue
Familial pattern

Cause?
Amyloid type?

A

Familial Mediterranean Fever

Neutrophil dysfunction

SAA (Secondary amyloidosis)

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23
Q

Systemic amyloidosis…2 types

A
  1. Primary (AL - Ig light chains) - plasma cell dyscrasias

2. Secondary (AA - SAA) - chronic inflammation

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24
Q

Nephrotic syndrome
Restrictive cardiomyopathy/arrhythmia
Tongue enlargement, malabsorption, HSM

A

Secondary amyloidosis

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25
6 types of localized amyloidosis
1. Senile cardiac amyloidosis (normal transthyretin) 2. Familial amyloid cardiomyopathy (mutated transthyretin -- restrictive cardiomyopathy) 3. Type 2 DM (amylin --> islets) 4. Alzheimers (A-beta from APP --> brain) 5. Dialysis (beta-2 microglobulin --> joints) 6. Medullary thyroid carcinoma (calcitonin)
26
Anaphylatoxins...function?
C3a and C5a -- activate mast cells --> histamine release
27
PGI2, PGD2, PGE2 LTC4, LTD4, LTE4 Histamine
PGs = vasodilation, permeability LTDs = vasoconstriction, bronchospasm, vascular permeability Vasodilation, permeability
28
C3b C5a
Opsonin for phagocytosis Neutrophil chemoattractant
29
Classical activation of complement
IgM or IgG on antigen --> C1 activation | "GM makes CLASSIC cars"
30
Hageman factor...fxns?
Factor XII -- when exposed to COLLAGEN... 1. Activates intrinsic clotting cascade 2. Activates complement 3. Activates kinin system (bradykinin)
31
Bradykinin...fxns?
Vasodilation and permeability (w/ histamine) | Pain (w/ PGE2)
32
Redness and warmth...mediators?
Bradykinin, histamine, and PGs
33
Swelling...mediators?
Histamine, tissue damage
34
Pain...mediators?
PGE2, bradykinin (sensitize free nerve endings)
35
Fever...pathway?
Pyrogen (ex. LPS) --> macrophage --> IL-1/TNF --> COX in hypothalamus --> PGE2 --> raised temp set point
36
Weibel-Palade bodies...fxns? Via what? How to remember?
Release vWF and P-selectin Histamine causes it's release W-P = vWf and P-selectin
37
E-selectin - upregulation signal
TNF, IL-1
38
Sialyl-Lewis X
Selectin receptor on leukocytes
39
ICAM and VCAM - upregulation signal
TNF, IL-1
40
Integrins - upregulation signal
C5a, LTB4 (on leukocytes)
41
CD18
Integrin deficiency on leukocytes
42
Pyogenic infections, neutropenia, giant granules in neutrophils, albinism, peripheral neuropathy, mucosal bleeding Issues?
Chediak-Higashi syndrome Defective protein trafficking --> impaired phagolysosome, melanin movement, cell granule movement, neurotransmitter movement, platelet granule movement
43
What is the oxidative burst?
O2 to O2- by neutrophils (via NADPH oxidase)
44
Catalase positive organisms (5)
Staph, Pseudomonas, Serratia, Nocardia, Aspergillus
45
NBT test
Catalase converts O2 to O2- | Negative in CGD (colorless/yellow)
46
Many Candida infections NBT test turns blue Respiratory burst intact
MPO deficiency (no HOCl-)
47
Oxygen-independent killing...mechanisms?
Lysozyme (macrophages) | Major basic protein (eosinophils)
48
Resolution of inflammation...what happens to neutrophils?
APOPTOSIS
49
How do macrophages kill?
Lysozyme (oxygen-independent)
50
4 potential functions of macrophages once they arrive (2-3 days)
1. Resolution (IL-10, TGF-beta) 2. Continue inflammation (IL-8 --> more neutrophils) 3. Abscess (fibrogenic growth factors, cytokines) 4. Chronic inflammation (CD4 T cell activation)
51
5 stimuli for chronic inflammation
1. Persistent infection (via macrophages, CD4 cells) 2. Virus, mycobacteria, parasites, fungi 3. Autoimmune disease 4. Foreign material 5. Cancers
52
4 = 28/7
CD4 co-stimulatory = CD28 (T cells) and B7 (APC)
53
Co-stimulation for CD8-MHC1 interaction
IL-2 (from CD4 T cell)
54
Macrophages with abundant pink cytoplasm surrounded by giant cells and a rim of lymphocytes What are the central cells called?
Granuloma Epithelioid histiocytes
55
Caseating granuloma...options?
TB, Fungi
56
Noncaseating granuloma...options? (5)
Foreign body, sarcoidosis, beryllium, Crohn's disease, cat-scratch disease
57
Stellate-shaped non-caseating granuloma
Cat-scratch disease
58
Formation of a granuloma (pathway)
Macrophage (antigen) --> CD4 cell (via MHC2 and IL-12) --> Th1 cell --> IFN-gamma --> macrophage conversion to epithelioid histiocyte and giant cells
59
Labile cells
Bowel stem cells in MUCOSAL CRYPTS Skin stem cells in BASAL LAYER Hematopoietic stem cells (CD34+)
60
Stabile cells
Hepatocytes | Proximal renal tubules
61
***Permanent cells
Myocardium Skeletal muscle Neurons
62
When will a SCAR form? Initial phase of this process?
When the regenerative stem cells are lost or absent GRANULATION TISSUE (NOT granuloma)
63
***Granulation tissue...components
Fibroblasts, Capillaries, Type 3 collagen, Myofibroblasts
64
Main component of scar What happens to the precursor? What is required?
Type 1 collagen Collagenase removes type 3 (ZINC COFACTOR)
65
Patient has a zinc deficiency and gets a deep skin wound. What type of collagen will be present? Why?
Type 3 (Collagenase cannot remove the type 3 w/o zinc)
66
***Mediators of tissue regeneration and repair (w/ functions)
TGF-alpha -- epithelial and fibroblast GF TGF-beta -- fibroblast GF + inhibits inflammation PDGF -- endothelial, smooth muscle, and fibroblast GF FGF -- angiogenesis VEGF - angiogenesis
67
**Primary vs. secondary intention
Primary = wound edges brought together Secondary = granulation tissue fills defect, myofibroblasts contract the wound (SCAR)
68
Vitamin C - function
Hydroxylation of proline and lysine (procollagen) -- needed for eventual CROSS-LINKING
69
Copper - function
Lysyl oxidase (CROSS-LINKING lysing and hydroxylysine)
70
Keloid - made of what? Most common locations?
Type 3 collagen Earlobes, Face, Upper Extremities
71
Hypertrophic scar
Excess scar tissue LOCALIZED TO WOUND

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