Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

FPP > Pearls Review > Flashcards

Pearls Review Flashcards

(102 cards)

Start Studying
1
Q

Metaplasias: Smokers transition

A

ciliated columnar epithelium -> squamous.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Metaplasias: GERD transition

A

squamous -> intestinal type
= Barrett Esophagus
(predisposes to carcinoma).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Metaplasia: HPV transition

A

columnar -> squamous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

swelling, karyorrhexis, leakage, inflammation, ALWAYS pathological.

A

Necrosis:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

shrinkage, fragmentation/condensation, either path or physiological.

A

Apoptosis:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Apoptotic Pathway: Instrinsic; Injury ->

A

Bcl-2 stops inhibiting -> mitochondria -> Cytochrome C -> caspases -> endonuclease activation and breakdown cytoskeleton.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Apoptotic Extrinsic

A

Fas + TNF receptor -> caspases -> etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathologic Calcification: Dystrophic;

A

damaged tissue, normal serum Ca (ex. Heart valves, atherosclerosis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathologic Calcification:Metastatic;

A

normal tissue, hypercalcemia (ex. PTH, Vit D intoxication, Bone destruction, renal failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

TRECs (T cell Receptor Excision Circles)

A

are circular pieces of DNA generated during T cell receptor editing. Absent in SCID (hence the screening test)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is absent in SCID that you can test for

A

TRECs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

obstructive lung disease due to inflammation/swelling and fibrosis of the lung. Some primary causes and also from recurrent infection

A

Bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

IgE mediated, requires sensitization, not dose dependent.

A

Allergen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Not IgE mediated, dose dependent, will affect everyone at high dose.

A

Irritant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

only made by Mast cells = best marker for Mast cell activation

A

Tryptase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Regulatory Tcells express_____ and suppress immune responses - disease is IPEX

A

Foxp3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Foxp3 messed up in this disease… thus no Tregs

A

IPEX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Acute inflammation dominant cell

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Chronic inflammation dominant cells =

A

Monocytes & Lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

_______recognize PAMPs -> release TNF -> increase thrombogenicity.

A

TLRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

______ recognize dead cells (uric acid, ATP crystals) -> release IL-1 -> activates fibroblasts

A

Inflammasome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

low protein/cells (SG <1.012) minimal flow.

A

Transudate -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

high in protein/cells (SG > 1.020) high flow.

A

Exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Adhesion:_______ loose on endothelial, platelets, and leukocytes.
_______ tight, only on leukocytes.

A

Selectins

Integrins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Selectins present on
endothelial cells, platelets, leukocytes
26
Integrins present on
leukocytes
27
movement of leukocytes through vessel wall by CD31 (PECAM1)
Diapedesis:
28
How do leukocytes move through vessels wall?
CD31 or PECAM
29
Histamine present in:
mast cells, basophils platelets
30
Action of Histamine
vasodilation, increase permeability.
31
NO present in:
endothelium, macrophages
32
NO action:
vasodilation
33
Bradykinin present in:
(Liver - plasma)
34
Bradykinin action
Increase permeability, pain.
35
IL-1, TNF present in
(macrophages, endothelium, mast cells):
36
Action of IL-1 and TNF
chemotaxis, FEVER
37
Chronic granulomatous inflammation contains
Multinucleated giant cells (from monocyte fusions) caused by IFN-y
38
What causes giant cell fusion
IFN-y
39
Systemic Inflammatory Reponse Syndrome (SIRS):
1. fever. 2. elevated plasma levels of acute phase proteins. 3 leukocytosis
40
Fever due to pyrogens (___,____,_____) -> production of PGE2 -> reset hypothalamus
(LPS, or IL-1, TNF)
41
; C reactive protein, fibrinogen, serium amyloid A.
Elevated acute phase proteins:
42
What induces acute phase proteins
From liver (IL-6 induced)
43
_______ causes RBC stacking = sedimentation = Erythrocyte sedimentation rate (ESR)
Fibrinogen
44
(stimulate by TNF, IL-1) incerase in WBCS (to 15-20k) 4 types
Leukocytosis:
45
What stimulates leukocytosis?
TNF and IL-1
46
bacterial infection (causes left shift)
Neutrophilia:
47
Lymphocytes signal a:
viral infection
48
allergies, asthma, parasites will cause
Eosinphilia:
49
typhoid, rickettsiae, some protozoa will cause
Leukopenia:
50
defect in collagen. hyperflexible skin, joints, easily ruptured organs
Ehlers-Danlos Syndrome (EDS):
51
specialized tissue seen in healing (present by 3-5 days)
Granulation Tissue:
52
4 steps of scar formation:
1) angiogenesis. 2) fibroblast proliferation. 3) ECM deposition. 4) Remodeling of fibrous tissue
53
Growth factors for fibroblasts: | Fibrogenic agent & inhibits lymphocytes.
TGF-B:
54
Growth factors for fibroblasts: | migration/proliferation of fibroblasts, SMCs, macrophages. FGF
PDGF:
55
``` Primary union (wound healing): Immediate - ```
fill w/ blood. W/ in 24 hrs-neutrophils, begin reepitheliazation.
56
``` Primary union (wound healing): Day 3- ```
neutrophils out macrophages in, granulation tissue present.
57
``` Primary union (wound healing): Day 5- ```
maximum granulation tissue, collagen fibers begin to bridge gap.
58
``` Primary union (wound healing): Weeks - ```
scar formation, decreased vessels.
59
Secondary union:
More extensive damage (not a clean cut) - everything more intense. Substantial scar. More wound contracture by myofibroblasts
60
reopening of wound.
Dehiscence
61
too much collagen (African Americans).
Keloid -
62
too tight around joint
Contracture -
63
Wound strength:
10% at first week. | 3 months - plateaus at 70-80%
64
Why does having HSV2 or syphillis put you at higher risk of contracting HIV?
Having HSV-2 or syphillus puts you at higher risk for contracting HIV, as HIV prefers activated T cells (CCR5, etc)
65
Acute HIV infection:
HIV virus can be detected, but Abs are not yet present.
66
Symptoms at 1-4wks after exposure to HIV-
fever, lymphadenopathy, rash, joint pain, myalgia, anorexia, etc.
67
We make Abs to HIV, but they don't work, why?
Because HIV-1 Reverse Transcriptase make 1 in 10,000 errors. 10,000 is the size of its genome (1 error/each replication, and 1 billion replications/day = 1 billion mutations/day)
68
- a PARADOXICAL deterioration in status after immune system recover from HAART (typically w/ in 8 wks)
Immune Reconstituion Inflammatory Syndrome (IRIS)
69
What happens to GALT in HIV patient?
lack of CD4 in the gut increases permeability to bacteria (LPS). ***This early insult is permanent! Continues even after HAART
70
Direct recognition of alloantigen (acute rejection):
Recipient T cells reacts to Donor MHC.
71
Indirect recogniton (chronic rejection):
Recipient T cell reacts to a peptide derived from the donor MHC.
72
minutes, preformed Abs from blood transfusion, pregnancy, or prior transplantation (barrier to xeno).
Hyperacute rejection:
73
Rejection that takes days to weeks, mostly by T cells (some Abs).
Acute:
74
Type of rejection that takes months to years, fibrosis of the graft (the major problem in kidney grafts now).
Chronic:
75
Sources of Hematopoietic Stem Cells (for HSCT).
1) BM. 2) umbilical cord. 3) Mobilized Peripheral Blood (PBSC) induced by G-CSF and GM-CSF
76
Host Disease (GVHD): 4 grades
(1-4, 4 being worst). | Based on amounts of rash, bilirubin, diarrhea (more = worse for all)
77
: benign mass of disororganized but well differentiated tissue. ex) lung hamartoma contains cartilage, BVS, SMCS, alveoli, but all disorganized
Hamartoma
78
ecptopic tissue in a foreign location
Choriostoma:
79
Grade/differentiation (different than staging):
how well differentiated it is. Benign are well differentiated. Malignant can vary. Metestatic: well to poorly differentiated (anaplastic = complete lack of differentiation)
80
Metastasis pathway:
1) Hematogenous; veins over arteries (sacromas). 2) lymph (carcinomas). 3) body cavities.
81
Carcinomas IG metastisize by
lymph
82
Sarcomas IG metastisize by
hematogenous and VEINS more than arteries
83
Clinical Stage is based on what three criteria
TNM Tumor size, Nodal involvement, Metastasis
84
differentiation and is based on HISTOLOGY. as opposed to stage.
Grade
85
Non-hormonal or hormonal effect of tumor, UNRELATED to local spread or mets. ex) a lung cancer which secretes ACTH causing Cushings.
Paraneoplastic syndromes**
86
Tumor cells attempt to downregulate the immune response via
TGF-B, CTLA-4, PD1, IL-10, and recruiting Tregs
87
have a modified receptor on them which directly binds an Ag on the tumor cell. No need for APC, MHC, or other peptides.
CAR (Chimeric Antigen Receptor) T cells (artificial)
88
Possible problems with CAR
1) too much proliferation -> toxic shock. | 2) autoimmunity
89
Histology prep:
cassestes fixed in formalin, embedded in parafin. at 5 mm thick. stained with hematoxylin and eosin (H&E): H stains the nucleus blue. E stains the proteins orangeish
90
What color does Hematoxylin stain the nucleus
blue
91
What color does eosin stain proteins?
pink/orange
92
Whats the difference between direct acting and indirect acting carcinogens? How are they simular?
Direct acting carcinogens - electrophilic, direct. Indirect - must be P450 activated. Both target nucleic acids
93
Polycyclic hydrocarbons result in lots of bad shit such as:
-> SCC of lungs, larynx, oral cavity; esophagus, pancreas, bladder CAs
94
Alkylating agents cause
-> Hematolymphoid malignancies
95
metabolizes polycyclic aromatic hydrocarbons. 10% caucasians have a highly induced form -> more carcinogen
CYP1a1 -
96
_______-> causes mutated DNA ->_______ -> causes replication of that mutated DNA
initiator | promoter
97
EBV prefers______
B cells:
98
in an immunosuppressed patient it mulitplies in B cells. Then a t(8;14) can lead to Burkitt Lymphoma
EBV
99
Killing of tumors follows
First Order Kinetics | Constant fraction. Not constant number. Log Kill (1=.9, 2=.99, 3=.99)
100
To be curative you must have _____log kill for ____cycles.
2-4 (2-4 is necessary to double expected lifespan) | 4-12
101
VEGF, FGF, MMPs.
Angiogenic factors:
102
PDGF, Angiopoetin, TGFB, Thrombospondin, Endostatin
Angiogenic Inhibitors

FPP (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions