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Anatomy Step1 Buzzwords > Pathoma > Flashcards

Pathoma Flashcards

1
Q

Tumors with psamomma bodies

A

Serous papillary endometiral carcinoma
pappillary thyroid
mesothelioma
meningoma

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2
Q

Tumor mutation in serous papillary endometrial carcinoma

A

p53

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3
Q

What is CD14?

A

A TLR on macrophages that recognizes LPS (a PAMP) on all gram negative bacteria

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4
Q

What happens after TLR activation?

A

NF Kappa B is activated; turns on acute inflam response (activates immune response genes and immune mediators)

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5
Q

What releases arachidonic acid, what acts on it?

A

released: phospholipase A2 (from phospholipid cell membrane), acted on: COX or lipooxygnease

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6
Q

Function of PGI2, PGD2, PGE2, produced by?

A

all three: vasodilation (ARTERIOLE level), vascular permeability (POST CAPILLARY VENULE)

PGE2: also fever and pain

produced by cycloxygenase

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7
Q

Function of LTB4, LTC4, LTD4, LTE4 produced by?

A

LTB4: attract and activate neutrophils (others? IL8, C5a, bacterial products)

other three (C-e): mediate vasoconstriction (arteriole), bronchospasm, increased vascular permeability (post cap venule) (basically contract smooth muscle)

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8
Q

What is the pericyte?

A

thing underlying endothelial cells; can pull them apart and open up space and allow for fluid leakage.

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9
Q

How can mast cells be activated? Response?

A

tissue trauma, via C3a and C5a, Cross linking of cell surface by IgE (type I hypersens)

Dump histamine granules-> vasodilation of arterioles, increase vasc permeability (Immediate)

Delayed: Produce arachidonic acid metabolites, PARTICULARLY LEUKOTRIENES (like the second phase)

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10
Q

Three pathways of complement activation? Result?

A

Classical: C1 binds to IgG or IgM (bound to antigen–GM makes classic cars)
Alternative: microbial products directly activate complement
Mannose Binding lectin pathway: MBL binds mannose on microrganisms and activates complement

Result: C3 convertase is generated, C5 convertase generation, formation of MAC (which forms hole in membrane for lysis)–so key products are C3a and C5a (mast cell degranulation), C5a: chemotaxis for neutrophils, C3b: OPSONIN for phagocytosis, MAC: lyses microbes by creating holes in cell membrane

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11
Q

What is Hageman Factor? What does it do?

A

inactive proinflam protein produced in liver
activated upon exposure to subendothelial or tisuse collagen

REALLY IMPORTANT IN DIC
Activates:
Coagulation and fibrnolytic system, complement, kinin system (Cleaves HMWK to bradykinin->vasodilate, increase vasc permeability and pain—its like histamine with pain)

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12
Q

What creates pain?

A

PGE2, Bradykinin

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13
Q

What causes the cardinal signs of inflammation

A

Rubor/Calor: Vasodilation, increased blood flow (relaxation of arterioal smooth muscle—-histamine, PG, bradykinin)

Swelling (tumor: leakage of lfuid from postcap venule into interstital space (histamine—separate endothelial cells, tissue damage)

Pain: Brady kinin, PGE2, SENSITIZE SENSORY NERVE ENDINGS

Fever: Pyrogens cause MACROPHAGES to release IL-1 and TNF
then increase COX activity in perivascualr cells of hypothalamus
increased PGE2 raises tmperature set point in hypothalamus

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14
Q

What are the steps of the neutrophils arriving at inflammation and the important mediators?

A

1: Margination vasodilation slows blood flow in postcapillary venules, cells marginate frmo center of flow to periphery
2: Rolling: —selectins expressed by vessels, cause neutrophils to slow (P-selectin: Weibel-Palade bodies in endothelial cells , mediated by histamine, E-selectin: induced by TNF and IL1)
3: adhesion: cellular adhesion molecules upregulated by TNF and IL1—integrins upregulated on leukocytes/neutrophils by C5A and LTB4 (both things that are calling neutrophils)—interactions result in firm adhesion to vessel wall

Step4: transmigration and chemotaxis: Leukocytes (neutrophils) transmigrate across endothelium of postcap venules, move toward chmeical attracts (C5a, LTB4, IL8, bacterial products)

Step 5: Phagocytosis- consumption of pathogens or necrotic tissue—ENHANCED BY OPSONINS (IgG and C3b)

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15
Q

What do selectins do?

A

bind siayl Lewis X on leukocytes–results in rolling of leukocytes along vessel wall (usually neutrophils, also macrophages)

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16
Q

What is Leukocyte adhesion deficiency?

A 
autosomal recessive defect of integrins---defect of adhesion (CD18 subunit)
get neutrophillia (the marginated pool that is normally there can't bind so they just circulate so artifically high)
delayed separation of umbilical cord
recurrent baterial infections that lack pus formation
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17
Q

How does phagocytosis occur

A

Pseudopods from leukocytes extend to form phagosomes, internalized and merged with lysosomes to form phagolysosomes
(neutrophils doin this, macrophages, yeah)

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18
Q

What is Chediak Higashi Syndrome

A

Protein tracking defect; autosomal recessive; IMPAIRED PHAGOLYSOSOME FORMATION—the microtobules can’t carry to it (its kind of a microtubule issue)

Increased irsk of pyogenic infections
neutropenia (can't really divide well in the marrow)
Giant granules in leukocytes
defective priamry hemostasis
peripheral neuropathy
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19
Q

Describe the oxygen dependent neutrophil function

A

More offective- occurs in phagolysosome
Oxygen->Super oxide (via NADPH Oxidase—this is oxidative burst)
Super oxide->Hydrogen Peroxide (Superoxide dismutase)
Hydrogen Peroxide-> HOCl/Bleach (via myeloperoxidase)

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20
Q

What is the issue in CGD

A

CGD: no NADPH Oxidase (X linked or autosomal recessive)

can’t generate bleach—get infections with catalase + (most bacteria can generate hydrogen peroxide, and so we can use that to make bleach—but if they are catalase + they destroy hydrogen peroxide made by bacteria. So no bleach production.
organisms (S. Aureus, Nocardia, Aspergillius, Psuedomonas Cepacia, Serratia Merrescans)

Testing: Again nitroblue (if NADPH works can maek oxygen to superoxide and it turns blue, if we don’t have NADPH oxidase it will stay clear.)

other one is that green one

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21
Q

What disease is related to the last step of generating bleach?

A

MPO is fucked up (myeloperoxidase deficiecny)-can’t make bleach. They get candida infections (most are asymp though)

NORMAL NBT (first step of NADPH oxidase still works)

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22
Q

Describe oxygen independent killing for neutrophils

A

Less effective; occcurs via enzymes in leukocyte secondary granuels (Lysozyme, Mjoar basic protein)

23
Q

Final step of neutrophil arrival?

A

Resolution–neutrophils undergo apoptosis (this is what generates pus)
Disappear within 24 hours after resolution of inflammatory stimulus

24
Q

What occurs after neutrophils are done?

A

Macrophage phase! 2-3 days after inflammation begins

Derived from monocytes in blood, arrive exact same way as neutrophoils

25
Q

How do macrophages kill?

A

Ingest via phagocytosis; destroy phagocytosed material using enzymes in secondary granules (esp lysozyme).
Basically they use oxygen independent killing

26
Q

What do macrophages do besies phagocytosis?

A

Manage then ext step of procss. Do resolution and healing (generate iL-10 and TGF-B—THESE SHUT DOWN INFLAMMATORY PROCESS)
If necessary, continue acute inflammation (via generating IL-8) (this is how pus would form, have a continuing process, it is still acute inflammation even if its been months)
Abscess (recognize we gotta wall off, generate wall of fibrosis, trap inflammation, neutrophils really manage this process)
Chronic inflammation (say it was a virus; neutrophils can’t handle this; so we need helper T cells)

27
Q

What do you need to activate a T cell

A

1) binding of antigen and MHC complex

2) B7 on antigen presenting cell (dendritic cell of macrophage) binds CD28 on CD4+ T cells

28
Q

What do Th1 T cells produce

A 
Helps CD8 positive T cells
generate IL2 (t cell growth facotr, CD8+ T cell activatior)
IFN gamma (macrophage activator)
29
Q

What do Th2 cells produce

A

Helps B cells
Create IL4 (generate IgG and IgE)
IL5(eosinophil chemotaxis and activaiton, maturation of B cells to plasma cells, IgA generation)
produce IL-10 (to inhibit Th1)

30
Q

What is the second signal for CD8 T cells?

A

IL2 from CD4 TH1 cell
(the first is the MHC complex obviously)
then active for killin!

31
Q

How do CD8 positive T cells kill

A

Secretion of perforins and granzyme; induce apoptosis of target cell (CASPASE MEDIATED)
Expression of FasL binds Fas on target cell-> activate apoptosis

32
Q

3 ways to activate caspases

A 
intrinsic mitochondrial pathway; cytochrom c leaking
extrinsic receptor (FasL, TNF binding either or)
CD8 positive mediated (dumping enzymes)
33
Q

Naive B cell expression, activation?

A

IgM IgD

antigen binding->become plasma cell (if it was IgM cell would become IgM plasma cell)

or B cell antigen presented to CD4+ helper T cell vai MHC class II (then second signal is CD40 receptor on B cell binds CD40L on helper T cell)
(T CELLS THEN SECRETE IL4 AND IL5 ALLOWING FOR SWITCHING AND BECOMING PLASMA CELLS)
34
Q

What is granulamotus inflammation, describe process?

A

subtype of chornic inflam

KEY CELL, DEFINING FEATURES: Epithelioid histocytes (macrophages with abundant pink cytoplasm normally macrophages have foamy inside, but this is activation)
surrounded by giant cells and rim of lymphocytes
divided into noncaseating and caseating subtypes

35
Q

Diseases with noncaseating granulomas

A

Reaction to foreign material (breast implants? could even be in lymph nodes)
sarcoidosis
Beryillum exposure
Crohns disease (DONT FORGET THAT UC is CRYPT ABSCESSES)
cat scratch disease (STELLATE shaped often in neck)
there are others

There will still be nuclei present in the histocytes in the middle—won’t be dead.

36
Q

Diseaes with caseating granuloma

A

This is Caseating necrosis. TB and Fungus.
Can do AFB stain for TB, Silver stain for Fungus
—do in granulomas to make sure

37
Q

Describe granuloma formation

A

Macrophages present antigen via MHC II to CD4+ helper T cells
macrophages secrete IL-12, induce CD4+ helper tells to become TH1
TH1 secrete iFN gamma, converts macrophages to epitheloid histocytes and giant cells

IL12, IFN gamma , macrophages, CD4 Th1 really important

This happens in BOTH types of granuloma formation

38
Q

What is tissue regeneration?

A

baiscally replacing dead tissue with native tissue

39
Q

What is marker for hematopoetic stem cells in bone marrow?

A

CD34+

40
Q

What tissues are labile tissues and why for regeneration?

A

Labile Tissues: Continously cycle to regenerate tissue (Small bowel and large bowel—stem cells in mucosal crypts), (Skin- stem cells in basal layer), Bone marrow (hematopoetic stem cells), (Lung: Type II pneumocytes)

41
Q

What tissues are stable tissues and why for regeneration?

A

These are quiescent, can reenter cell cycle

Hepayocytes
Liver regnerations by compensatory hyperplasia after partial resection
Each hepatocyte proiduces additional cells and then enters quiescence

Proximal Renal Tubule (hence regeneration in ATN)

42
Q

What are permenant tissues, how do they regneerate?

A

myocardium, skeletal muscle, neurons

They don’t really very well. They lack significant regenerative properties. So they do REPAIR —generate a fibrous scar

43
Q

When does repair occur instead of regeneration?

A

If you have a permenant tissue, OR when you go far enough that regneerative stem cells are lost (like you stab yourself far enough to damage basaslis)

44
Q

What are the phases of repair and mediators

A

initial: granulation tissue: Fibroblasts (deposit Type III collagen), capillary (give nutrients), myofibroblasts (contract wound). THIS IS NOT GRANULOMA, seperate thing

Scar formation: Type III collagen replaced with type I collagen. Collagenase REMOVES type III collagen and requires ZINC as a cofactor

45
Q

Type I collagen locations

A

bone, scars—it is REALLY STRONG

46
Q

Type II Collagen locations

A

Cartilage

47
Q

Type III Collagen locations

A

Pliable; vessels (need to stretch), granulation tissue, embryonic tissue

48
Q

Type IV collagen locations

A

Basement membrane (lung, kidney)

49
Q

What is the mechanism of regneration and repair?

Examples?

A

paracrine signaling via growth factors (interact with receptors and shit)

TGFalpha: epithelial and fibroblast growth factor
TGFbeta: imporatnt fibroblast growth factor, inhibit inflammation
PDGF: endothelium, smooth muscle, fibroblast growth factor
FGF: angiogenesis, skeletal development (keep in mind even though its fibroblast growth factor it does angiogenesis)
VEGF: angiogenesis

50
Q

Intention types for scar healing

A

primary: wound ends broguht together, minimal scar formation
secondary: edges not approximated, granulation tissue fills in defect. CONTRACTION (MYOFIBROBLAST MEDIATED—these are the contractile guys and they are what makes wounds smaller)

Delayed wound healing: Infection most common cause), Vit C issue (hydroxylation—need to hydroyxlate proline or lysine procollagen before we can form the triple helix), copper (lysyl oxidase—cross links lysine and hydroxylysine, cant cross link collagen) or zinc deficiency (needed to convert type III collagen->type I collagen because Collagenase needs it)
others: foreign body, ischemia, diabetes, malnutrition

Dehiscence: rupture of wound, most common after abdominal surgery

51
Q

What do you hydroxylate on procollagen–why do you need it

A

proline or lysine—cross linking occurs via the OH groups added on them (so without it we cant get that triople helix)

52
Q

Describe a hypertrophic scar

A

a big scar. Made mostly of Type I collagen, but there is excess production.

53
Q

Describe a kelodi

A

excess prodcution of scar tisssue WAY otu of portion to wound
EXCESS OF TYPE III COLLAGEN
Genetic predposition (african americans)
Earlobes, upper extremeities, face (could for example happen after an ear piercing)

Anatomy Step1 Buzzwords (11 decks)

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