Step 1 General Review Flashcards

1
Q

Squamous metaplasia from smoking injury

___ in mediastinal LN
__ in lung parenchyma

metastatic disease in brain req

A

noncaseating granulomas
caseating granulomas

invasive disease

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

Reversible injury is indicated by ___

may see __ in cytoplasm, representing __ segments of __

sometimes called __ or __

may have inc ___, becoming more pronounced w __

A

cellular swelling

clear vacuoles, distended, ER

hydropic change, vacuolar degen

eosinophilic staining, necrosis

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

Reversible cell injury

__ alterations, such as B and loss of __
__ changes, such as ___

Dilation of ___, __ may be present w detached __

__ alterations, w disaggregation of __/__ elements

A

plasma membrane, blebbing, microvilli
mitochondrial, amorphous densities

ER, myelin figures, polysomes

nuclear, granular/fibrillar

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

Progressive injury and cellular destruction is ___

cell fragmentation and phagocytosis is ___

A

necrosis

apoptosis

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

__ involves sequestration of cellular organelles into cytoplasmic autophagic vacuoles

eventually fuse w __ and __ material

enhanced during ___, allowing cell ___

acts in __/__ manner

dysreg can occur in __, ___ and ___

can defend against

A

Autophagy

lysosomes, digest

nutrient deprivation, survival

coordinated/sequential

cancer, IBD, neurodeg dz

microbes

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

Recurrent bacterial infections, impaired/delayed wound healing, marked leukocytosis dz

PMN lack ___
lueks cannot adhere to __

A

leukocyte adhesion disorder

CD18
endothelium

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

best strategy to prevent PMN infilitration blocks __

A

integrins

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

__ is induced by chem mediators such as __, causing __ and __ of blood

inc vasc permeability by __, __, other __ produces __ bw endothelial cells

inc passage of __ to endothelium

allows __/__ to enter site of __/__
fluid leak results in __

__ and __ also involved, showing __/___

A

vasodilation, histamine, erythema, stasis

histamine, kinins, mediators, gaps

fluids

plasma proteins/leuks, injury/host damage
edema

Lymph vessel/nodes
erythema, swelling

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

__ activates macrophages

__/__/__ stimulates macrophage to promote leuk recruitment and inflamm

T lymph that is activated to __/__ can also induce __/__ by releasing ))/__

A

IFN Y

TNF, IL1, chemokines

TH1, TH17, leuk recruitment/inflamm
IL17, TNF

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

Cough, fever, fatigue, wl, hilar adenopathy w granuloma formation dz is

distince, wll formed __ w concentric ___

__ distribution
exclusively ___
coalescent ___

A

sarcoidosis

granulomas, fibrosis

lymphangitic
interstitial
nodules

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

Broad based budding yeast

narrow bud yeast, smaller

halo yeast

A

blasto

histo

cryptococcus

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

Acute inflammation leads to __ recruitment

chronic leads to __ formation

A

PMN

fibrosis/scar

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

Apoptosis due to lack of __
results in ___
antagonizes ___
activates ___ channel

leakage of ___
activates __
eventually ___

A

survival signal
dna damage
BCL2
BAX/BAK

Cytochrome C
caspases
apoptosis

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

Fragile X syndrome mechanism ___ leads to loss of ___

Fragile X ataxia mechaism __ leads to accumultion of ___

repeat is ___

location is ___

A

trxn silencing, protein fxn

trxn dysreg, toxic mRNA

CGG

untranslated region

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

Freidrich ataxia mechanism ___ leads to loss of ___

triplet is __

location is ___

A

trxn silencing, protein fxn

GAA

intron

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

Huntington dz mechanism is __ w ___

toxic __ mutation

triplet is __

location

A

polyglutamine expansion, misfolding

gain of fxn

CAG

exon

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

atherosclerosis caused by excessive __ w loss of __

A

LDL, laminar blood flow

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

Virchow-s thrombosis triad

Abnormal blood flow such as __ and __

Hypercoag inherited __ or acquired ___

endothelial injury such as __ and ___

A

stasis, turbulence

factor 5 leiden, disseminated cancer

hypercholesterolemia, inflam

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

__ contributes to arterial/cardiac thrombosis by causing __ or __

fomrs __ contributing to local pockets of __

normal blood flow is __, so __ flow centrally away from endothelium

stasis/turbulence promote ___ enhancing procoag/leuk adhesion
disrupt __ and cause __/__ interaction
prevent washout/dilution of __ by __ and inflow of ___

A

turbulence, endothelial injury/dysfxn

countercurrents
stasis

laminar, platelets

endothelial activation
laminar flow, platelet/endothelium

clotting factors, new blood, clotting factor inhibs

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

atherosclerotic plaques expose __ and __ and cause __

aneurysms result in __

AMI assc w __ and __

dilated atrium is site of __

hyperviscosity inc __ to flow, resulting in ___

SCA impedes blood flow through ___

A

vWF/tissue factor, turbulence

stasis

stasis, flow abnorm

stasis

resistance, stasis

small vessels

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

substance derived from ___ complexes w coagulant protein to activate protein C to cleave factors 5/8

__ interacts w __ on endothelial membrane to activate ___ to inactive factor __/__

A

endothelial cells

thrombin, thrombomodulin, Protein C, 5a/8a

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

DIC

intravascular access of procoagulant
\_\_ comps, such as \_\_
\_\_ such as \_\_/\_\_ adenocarcinomas/mucins
\_\_ such as \_\_ or \_\_, tissue factor
S\_\_, \_\_
Diffuse endothelial injury
\_\_ infection, \_\_ tropic
\_\_ infect
\_\_/\_\_ toxin, \_\_\_
\_\_ disorders
A

obstetric, amniotic fluid
cancer, panc/other
trauma, crush injury/CNS
sepsis/endotoxin

ricketsial, endothelial
meningococcal
endothelial/shiga, E coli
immune complex

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

Healing process of uninfected skin does not include __ at infection site

cells that can heal in sunburn

A

dermal appendages

hair follicle epithelial

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

Apoptosis is __ of cell death to eliminate __/__ cells

characterized by __ of protein/DNA
initiated by __
removal via __

Mito (intrinsic) path- loss of __ + __ or __
assc w leakage of __ into mito membrane

process inhibited by __ indued by __ from GF

A

programmed, unwanted/damaged

enzymatic
caspases
phagocytes

survival signals, DNA damage/misfolded proteins
pro-apoptotc proteins

BCL2, survival signals

25
Q

Apoptosis death receptor
eliminates __ and damage by __

initiated by engagement of __ such as __/__ by __ on adjacent cells

A

self reactive lymphs/cytotoxic T lymphs

death receptors, TNF/FAS
ligand

26
Q

early genetic lesions of cancer is unlikely to involve ___

unless assc w ___

A

loss of p53

Li Fraumeni syndrome

27
Q

endometrial biopsy shows endometrial hyperplasia wout atypia is

A

granulosa/theca cell tumor

28
Q

EGFR inhibitors do not work on tumors assc w ____

A

KRAS activation

29
Q

histologic appearance alone can only be assc w

may be _ or _ or __

prognosis is best determined by ___

A

grade

anaplastic, moderate, well dff

tumor stage

30
Q

which cell removes red cells from circulation

mechanism is ___, via __ response

A

NK cells

complement dependent, type 2

31
Q

overlapping involvement of inflammatory disorders due to structural ___

major influencers are characteristics of ___ and local ___

complexes are __ size, formed w __ excess, most __

concentrated sites include organs where blood is __ at high pressure to form other fluids (__/__)

often affects __ and __

A

vulnerability to immune complex deposition

complex, vasc alterations

medium, antigen, pathogenic

filtered, urine/synovial fluid

glomeruli/joints

32
Q

drug to inhibit Type 1 reaction without inhibiting immediate mediator targets __

A

phospholipase a2

33
Q

swelling/cyanosis in minutes of transplant is a result of

rejection mediated by ___ recognizing foreign __ on graft
can be directly via __ or indirectly after __ and presentation by ___

tx of graft rejection relies on ___ to inhibit __ to graft

trasnplanting __ requires matching of __/__ and is complicated by __

A

preformed antibody

Host t cells, HLA antigens
APC in graft
uptake, host APC

immunosuppressives, immune response

HSC, donor/host, GVHD

34
Q

Hyperacute rejection- preformed __ bind to graft endothelium _ after transplant
leads to __/__ and __ failure

Acute cell reject- t cells destroy ___ by __/__ rxns

acute humoral reject- __ damage graft vasculature

chronic reject- dominated by \_\_
caused by \_\_ and \_\_
T cells secrete \_\_ to proliferate vasc SM cells
ab cause \_\_
eventually leads to \_\_\_
A

antidonor antibodies, immeditely
thrombosis, ischemic damage, rapid graft failure

graft parenchyma, cytotoxicitiy/inflam rxn

ab

arteriosclerosis
t cell activation/ab
cytokines
endothelial injury
parenychmal fibrosis
35
Q

Anemia
SLE- D, I, __ on red cells

HS- D, N, __ defect

Mycoplasma- D, I, __ on red cells

PA- __ deficit, __ due to impaired DNA synth,

Parvo- __ deficit, pure __ aplasia

A

destructive, immune mediated, IgG

destructive, nonimmune, red cell

prodxn, megaloblastic

prodxn, RBC

36
Q

Microcytic/hypochromic due to ___
Iron def due to __, __, __
Globin def due to __/__
porphyrin def due to __

A

failed Hb synth
diet, rapid growth, chonic loss
hemoblobinopathies, thal
porphyrias

37
Q

Failed DNA synth anemia appears __
__/__ def
could be __/__

A

macrocytic/megaloblastic
B1/folate
MDS/chemo

38
Q

Stem cell failure/destrxn anemia appears __/__

due to __/___

A

normochromic/normocytic

aplastic anemia, infiltrative disorders

39
Q

Pancytopenia, nuclear/cytoplasmic dyssynchrony, some myeloblasts

__ syndrome

A

myelodysplastic syndrome

40
Q

T12, 21 __ prog, __ dz

T15, 17 __ prog, __ dz

T 8,21 __ prog, dz

Del 5/7 or trisomy 8 dz

T8,14 dz

Inversion of 16 __ prog, __

T9,22 dz, prog

11q23 translocation dz, prog __

A

good, ALL

good, APL

good, AML

myelodysplastic syndrome

Burkitt lymphoma, leukemia

good, AML

bad

MLL, bad

41
Q

Epidural bleed is __, impact to __ area
affects ___
clinical pic is __ w __ progression

Sudbural is __, onset is __
affects ___
seen in __/__/___

A

arterial, temporal
MMA
biphasic, rapid

venous, insidious
bridging veins
infant/elderly/alcoholics

42
Q

Subarachnoid hemorrhage
such as ___, or __
bleed is __, __ progression
___ and __ signs

Intracerebral- ___
__ aneurysm
___ location, __ prog
affects __/__/____

A

congenital Berry anuerysm, PC kidney
arterial, rapid
pounding HA, global

hyperTN
charcot houchard
arterial, rapid
thalamus/cerebellum/cerebral white matter

43
Q

movement of PMN through tissue mediated by __

A

chemokines

44
Q

acidosis promotes ___

A

hyperK

45
Q

trisomy, hCG slightly elevated

mom w vaginal bleeding
multicystic mass
small, grape like masses
minimal troph proliferation

dx is

A

partial hydatidiform mole

46
Q

recurrent N meningitidis infections seen w

A

terminal complement defic

47
Q

__ is intact, indicates __ and not ___

__ have eosinopgilic cytoplasm

surrounded by __

A

BM, metaplasia, dysplasia

epithial macros

fibrotic ring

48
Q

lots of energy req to miantain correct ___

w nutrient dep, cell struggles to ___

difficulties seen in __ and __

cells round up w injury to keep low ___ ratio

A

cellular structure

maintain shape

neurons, renal podocytes

SA to V

49
Q

Cellular swelling induces uptake of __ to maintain __

cells drop microvilli becomes important in __ w __

A

water, electron pumps

GI dz, celiac dz

50
Q

Irreversible processes
Nuclear ___/___
Lysosome __ and release of __/___

A

frag, pyknosis

rupture, lytic proteins/endonucleases

51
Q

CGD def in ___

__ allow for PMN adherence
__ damages endothelium, released from ___

A

NADPH oxidase

integrins
TNF, macros

52
Q

Acute inflam response
predominant cell type

stops __ as macros release __/__ to upregulate receptors on __/___

A

PMNs
laminar flow, chemokines/cytokines
endothelium/leuks

53
Q

chronic infam cell type

takes __

A

monocytes/T lymphs

long time

54
Q

Apoptosis w __/__

Intrinsic occurs following __
__ is anti-apoptotic
__ regulates caspases, which eventually destroy material

Extrinsic pathway- __ mediated
includes ___

A

nuclear fragmentation/condensation

injury
BCL2
p53

receptor
PD1

55
Q

most common cause of mental retard in males

A

Fragile x syndrome

56
Q

regulation of coag factors occurs from ___

Thrombin cleaves __ to __

w intact endothelium
Thrombin binds to

thrombomodulin, generates ___

interacts w __/__ to inhibit __

A

endothelial cells

F5/8, F5a/8a

thrombomodulin receptor
anti-thrombin 3

PGI2/TXA2, F5a/8a

57
Q

__ mutation inc risk of clots
always __ thrombosis

__ mutation is venous thrombosis

A

Factor V leiden
venous

Prothrombin

58
Q

DIC- widespread, multiple __ w immediate __

inc __, __/__, __
__ in smear, low __/__

A

microthrombi, lysis

D dimer, PT/PTT, thrombi
schistocytes, platelets/fibrinogen

59
Q

cells tht __ are apoptotically programmed

__ most cancerous mutation

early lesions active __, inactive __ or alter genes for ___

Pathway- GF to __ to ___ to __

__ most common signal transduction cancer

A

constantly replicating

p53

signal transducre, tumor suppressor, apoptosis

receptor, signal transduction, cell cycle

RAS