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Boards > Pathoma Ch. 1-2 Basics > Flashcards

Pathoma Ch. 1-2 Basics Flashcards

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
Q

6 types of localized amyloidosis

A
  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)
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26
Q

Anaphylatoxins…function?

A

C3a and C5a – activate mast cells –> histamine release

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27
Q

PGI2, PGD2, PGE2

LTC4, LTD4, LTE4

Histamine

A

PGs = vasodilation, permeability

LTDs = vasoconstriction, bronchospasm, vascular permeability

Vasodilation, permeability

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28
Q

C3b

C5a

A

Opsonin for phagocytosis

Neutrophil chemoattractant

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29
Q

Classical activation of complement

A

IgM or IgG on antigen –> C1 activation

“GM makes CLASSIC cars”

30
Q

Hageman factor…fxns?

A

Factor XII – when exposed to COLLAGEN…

  1. Activates intrinsic clotting cascade
  2. Activates complement
  3. Activates kinin system (bradykinin)
31
Q

Bradykinin…fxns?

A

Vasodilation and permeability (w/ histamine)

Pain (w/ PGE2)

32
Q

Redness and warmth…mediators?

A

Bradykinin, histamine, and PGs

33
Q

Swelling…mediators?

A

Histamine, tissue damage

34
Q

Pain…mediators?

A

PGE2, bradykinin (sensitize free nerve endings)

35
Q

Fever…pathway?

A

Pyrogen (ex. LPS) –> macrophage –> IL-1/TNF –> COX in hypothalamus –> PGE2 –> raised temp set point

36
Q

Weibel-Palade bodies…fxns?

Via what?

How to remember?

A

Release vWF and P-selectin

Histamine causes it’s release

W-P = vWf and P-selectin

37
Q

E-selectin - upregulation signal

A

TNF, IL-1

38
Q

Sialyl-Lewis X

A

Selectin receptor on leukocytes

39
Q

ICAM and VCAM - upregulation signal

A

TNF, IL-1

40
Q

Integrins - upregulation signal

A

C5a, LTB4 (on leukocytes)

41
Q

CD18

A

Integrin deficiency on leukocytes

42
Q

Pyogenic infections, neutropenia, giant granules in neutrophils, albinism, peripheral neuropathy, mucosal bleeding

Issues?

A

Chediak-Higashi syndrome

Defective protein trafficking –> impaired phagolysosome, melanin movement, cell granule movement, neurotransmitter movement, platelet granule movement

43
Q

What is the oxidative burst?

A

O2 to O2- by neutrophils (via NADPH oxidase)

44
Q

Catalase positive organisms (5)

A

Staph, Pseudomonas, Serratia, Nocardia, Aspergillus

45
Q

NBT test

A

Catalase converts O2 to O2-

Negative in CGD (colorless/yellow)

46
Q

Many Candida infections
NBT test turns blue
Respiratory burst intact

A

MPO deficiency (no HOCl-)

47
Q

Oxygen-independent killing…mechanisms?

A

Lysozyme (macrophages)

Major basic protein (eosinophils)

48
Q

Resolution of inflammation…what happens to neutrophils?

A

APOPTOSIS

49
Q

How do macrophages kill?

A

Lysozyme (oxygen-independent)

50
Q

4 potential functions of macrophages once they arrive (2-3 days)

A
  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
Q

5 stimuli for chronic inflammation

A
  1. Persistent infection (via macrophages, CD4 cells)
  2. Virus, mycobacteria, parasites, fungi
  3. Autoimmune disease
  4. Foreign material
  5. Cancers
52
Q

4 = 28/7

A

CD4 co-stimulatory = CD28 (T cells) and B7 (APC)

53
Q

Co-stimulation for CD8-MHC1 interaction

A

IL-2 (from CD4 T cell)

54
Q

Macrophages with abundant pink cytoplasm surrounded by giant cells and a rim of lymphocytes

What are the central cells called?

A

Granuloma

Epithelioid histiocytes

55
Q

Caseating granuloma…options?

A

TB, Fungi

56
Q

Noncaseating granuloma…options? (5)

A

Foreign body, sarcoidosis, beryllium, Crohn’s disease, cat-scratch disease

57
Q

Stellate-shaped non-caseating granuloma

A

Cat-scratch disease

58
Q

Formation of a granuloma (pathway)

A

Macrophage (antigen) –> CD4 cell (via MHC2 and IL-12) –> Th1 cell –> IFN-gamma –> macrophage conversion to epithelioid histiocyte and giant cells

59
Q

Labile cells

A

Bowel stem cells in MUCOSAL CRYPTS
Skin stem cells in BASAL LAYER
Hematopoietic stem cells (CD34+)

60
Q

Stabile cells

A

Hepatocytes

Proximal renal tubules

61
Q

***Permanent cells

A

Myocardium
Skeletal muscle
Neurons

62
Q

When will a SCAR form?

Initial phase of this process?

A

When the regenerative stem cells are lost or absent

GRANULATION TISSUE (NOT granuloma)

63
Q

***Granulation tissue…components

A

Fibroblasts, Capillaries, Type 3 collagen, Myofibroblasts

64
Q

Main component of scar

What happens to the precursor? What is required?

A

Type 1 collagen

Collagenase removes type 3 (ZINC COFACTOR)

65
Q

Patient has a zinc deficiency and gets a deep skin wound. What type of collagen will be present?

Why?

A

Type 3 (Collagenase cannot remove the type 3 w/o zinc)

66
Q

***Mediators of tissue regeneration and repair (w/ functions)

A

TGF-alpha – epithelial and fibroblast GF
TGF-beta – fibroblast GF + inhibits inflammation
PDGF – endothelial, smooth muscle, and fibroblast GF
FGF – angiogenesis
VEGF - angiogenesis

67
Q

**Primary vs. secondary intention

A

Primary = wound edges brought together

Secondary = granulation tissue fills defect, myofibroblasts contract the wound (SCAR)

68
Q

Vitamin C - function

A

Hydroxylation of proline and lysine (procollagen) – needed for eventual CROSS-LINKING

69
Q

Copper - function

A

Lysyl oxidase (CROSS-LINKING lysing and hydroxylysine)

70
Q

Keloid - made of what?

Most common locations?

A

Type 3 collagen

Earlobes, Face, Upper Extremities

71
Q

Hypertrophic scar

A

Excess scar tissue LOCALIZED TO WOUND

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