pathology MNI Flashcards

1
Q

what are the two types of cerebral edema

A

vasogenic bc of disruption of BBB which will make fluid go to the extracellular space. often bc of trauma or meningitis

cytotoxic bc of cell injury such as ischemia, causing inc in intracellular fluid

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

presenting sx of ex vacuo hydrocephalus vs NPH

A

ex vacuo presents like dementia or stroke causing loss of brain volume

NPH- whacky wet wobbly (reason unset but probably bc of high CSF volume at one point causing ventricles to large)

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

increased intracranial pressure characterised by headache
(positional), diplopia (CN-6 palsy), vomiting, and papilledema potentially leading to
vision loss.

epidemiology?

A

Pseudotumor Cerebri
( Idiopathic Intracranial Hypertension)

usually seen in obese women of child bearing age

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

lewy body

A

parkinsons

cytoplasmic inclusions

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

what are the presentation of the various types of herniations

A

subfalacine: crushes the anterior cerebral artery causing lock of sense or motor in the lower limbs.

transtetorial herniation: Ipsy down and out, spy blown pupil, hemiparalysis

tonsils: press of cardiac or breathing centers

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

Kernohan Phenomenon

A

continuous displacement from transtetorial herniation causes contralateral down and out blown pupil,

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

parenchymal braininjury

A

concussion
Chronic Traumatic Encephalopathy (multiple concussions)

croup and contecroup contusions

diffuse axonal injury(neurons stretch beyond elastic point separating grey and white matter)

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

protein accumulation is of hyperphosphorylated tau protein only

A

Chronic Traumatic Encephalopathy

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

linear flame shaped hemorrhages due to stretching of median and paramedian
pontine arteries. Pontine arteries branch from basilar artery running on anterior surface of pons. caused by?

A

duret hemmorage

caused by herniations/ inc in ICP

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

foamy macrophages

A

found in lipohyalinosis of the lenticulostraie arteries

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

vascular brain injury

A

epidermal hemmorage(hit the pterion, middle meningeal artery doesn’t cross culture, biconvex, LOC, then fine, then dead

subdural bc of rupture of the bridging veins. prominent in infants and elders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  • Swollen brain with wide
    gyri & narrowed sulci
  • Poor demarcation
    between gray & white
    matter
  • Eventually tissue
    liquefies leaving a fluid
    filled cavit
A

ischemic infracts

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

which intraparenchymal hemmorages are bc of HTN

location?

A

-charciod bouard(lenticulostriae)
-slit hemmorages
-primary intraparenchymal hemorrhage

location: basal ganglia

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

subarachnoid hemorage

A

berry aneurysm(non traumatic rupture)

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

tangled network of arteries and veins with no interposing capillaries

cuases

A

AV malformation
“tangled worms”

causes non htn hemmorage, in newborns causes high output congestive heart failure because of the shunting

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

fusiform vs saccular ansursym

A

fusiform is charcoal bouard

saccular is berry(no muscular or internal elastic leaving just hyalinized intimate and adventitia)

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

Affects larger non-penetrating vessels
supplying the cortex and is therefore typically superficial/ lobar in location, unlike small
penetrating vessels affected by hypertension which are typically subcortical/deep

A

non htn
amyloid antipathy

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

associated with
autosomal dominant polycystic kidney
disease, Ehler-Danlos syndrome and other
congenital diseases which can affect
connective tissue of blood vessels.

A

berry aneurysm

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

subarachnoid hemmorage complication and how to prevent if possible

A

-rebleed

-vasospasm give Nimodipine

-healing process causes fibrosis and can obstruct CSF resorption= hydrocephalus

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

Lumbar puncture: shows high number
of RBCs or xanthochromia (yellowish
CSF due to release of bilirubin after
RBC lysis

A

berry

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

alzheimers lobes affected and common cause of death

A

frontal, parietal, and temporal lobes affecting spacial awareness, character and memory

pneumonia or infection is common cause of death

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

alzheimer plaque mutations

A

ab extracellular plaques are APP gene

the tau just comes in after

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

tau protein cause what kind of plaques and how are they made

A

normally binds microtubules but after phosphorylation by AB plaque will be unable to bind causing *neurofibrilary tangles inside cells!! the tangles outside the cell are called neuritic plaques

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

early onset alz mutations

vs late onset

A

APP (downs 21)
the gamma secretase gene is coded on chromosome 1 and 14 in the presillin 1 and 2

late onset: Apo E4

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

Narrowing of gyri and widening of cerebral sulci

A

alzheimers dizease (opposite of ischemia occlusion)

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

what are the two types of FTLD

A
  1. Pick disease. Tau neurofibrillary tangles with pick bodies also intracellular (just tau intracellular)
  2. intracellular accumulation of TDP-43 a DNA/RNA binding protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Death of Striatal
Cholinergic Interneurons & Death of Striatal GABAergic Neurons

A

huntington

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

Death of
pigmented dopaminergic neurons in Substantia Nigra

A

parkinsons

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

Alpha Synuclein aggregates normal and abnormal

A

parkinsons

normal:Alpha Synuclein is expressed at presynaptic neurons and binds to
presynaptic secretory vesicles containing dopamine and causes
exocytosis of dopamine into synaptic cleft.

abnormal:aggregates are toxic to
dopaminergic neurons in substantia nigra
and cause neurons to undergo programmed
cell death.

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

Lewy body dementia

A

when dementia sx arise within 1 year of motor symptoms

if more than one year called dementia secondary to parkinsons disease

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

autosomal dominant movement disorder associated with degeneration of the
striatum (Caudate and Putamen) causing

A

huntington

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

Huntington disease mutation

A

AD gain of function of HTT causes trinucleotide repeats of CAG (glutamine) which will impare mitochondrial and the synthesis of proteins like Ach and GABA

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

characteristic Ubiquitinated-Mutant protein intranuclear fragments
made of?

A

huntingtons disease

Ubiquitinated-Mutant protein and impaired proteolysis

when staining stain for ubiquity

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

hallmark of HD

A

the intraNUCLEAR inclusions of ubiquinated huntingtin

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

chorea and Athetosis

A

huntington

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

als mutations

A

Chromosome 9 hexanucleotide repeat and Superoxide
dismutase gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is spared with ALS

A

intelect, sphincter control, and eye movement, sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

degeneration of
corticospinal tract in the lateral portion of the spinal

A

ALS

its not demyelination but actual nerve degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

autoimmune demyelinating disorder characterized by disease
activity separated in time, that produce white matter lesions that are
separated in space

A

MS

commonly statics with optic neuritis

plaques are often periventricular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

MS genetic risk factor and non genetic

A

Genetic HLA DRB1

smoking and low Vitamin D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

inc igG in CSF but not in blood

A

MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

names of post infection demyelinations

A

Acute Disseminated Enecephalomyelitits

Acute Necrotizing Hemmoragic Encephalomyelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

non-immune damage to oligodendrocytes

A

Central Pontine Myelinolysis/Osmotic Demyelination

typically after sudden
correction of hyponatremia that may result in a rapidly evolving quadriplegia and bulbar
palsy bc of oligodendrocyte contraction and apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

confusion
* Ocular palsies
* Ataxia

if left untreated

A

Wernicke encephalopathy

if left untreated can cause causes korsacoff syndrome where no new memories can be made and will have confabulations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

typical brain tumors in kids vs adults

A

kids: medulloblastoma, pilocytic astrocytoma, ependemoma

adults: glioblastoma(astrocytoma), oligocondroma, meningioma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

genetic for the astrocytomas

A

pilocytic is BRAF

glioblastoma is IDH 1 and 2

35
Q

Bipolar cells with thin hair like
(“pilo”) processes in a fibrillary
meshwork with eosinophilic rod like
structures called

A

Rosenthal fibers

pilocytic ast rocytoma

36
Q

Infiltrating tumor with hemorrhage and
necrosis and crossing the midline producing a

A

producing a butterfly glioma

glioblastoma

37
Q

Microvascular proliferation with areas of
“pseudo”-palisading necrosis

A

glioblastoma

38
Q

IHC GFAP

A

for all glial cancers

astrocytoma, oligodendroglioma, ependemoma

39
Q

insidious seizure presentation

A

oligodendroglioma

40
Q

Regular cells, round to oval nuclei &
abundant granular chromatin

Cells may form rosettes with long
delicate processes extending into the
lumen- “canals”
* Also seen are “pseudo”-rosettes
which are perivascular: tumor cells
are around vessels

A

ependymonoa

40
Q

association with neurofibromatosis 2

A

adult spinal ependymomas,
meningioma, 8th nerve shwannoma

41
Q

oligodendroglioma genetics

A

Codeletion of 1p and 19q: good prognosis

will have IDH 1 mutation

42
Q

Cells with round nuclei, clear cytoplasm forming
halos; and thin-walled capillaries

A

oligodendoglioma

43
Q

neuroectoderm cerebral tumor genetics

IHC marker?

A

medulloblastoma

Wnt-β catenin pathway(better orognosis), MYC overexpression

IHC is a neuronal and glial markers

44
Q

Sheets of small round blue anaplastic cells
* Hyperchromatic nuclei, abundant mitosis,
scant cytoplasm
* Rosettes

A

medulloblastoma

45
Q

Chromosome 22q

A

schwannoma

46
Q

where do the most common brain metastases come from

A

Breast
Lung
Skin
Kidneys (kids)
GIT (geriatrics)

47
Q

what kind of bone resists movement in all directions

A

woven bone

lamellar bone is unidirectional force for weight bearing

48
Q

which bones undergo intramembranous ossification

A

flat bones of face, skull, and clavicle

48
Q

FGFR3

mutation type?
what normally happens

A

achondroplasia
\
AD gain of function

normally inhibits endochondrial ossification but with GOF there’s no getting it uninhibited

48
Q

short extremeties, normal trunk, large head/buldging fontanells

A

achondroplasia

48
Q

OI sx besides brittle bones

A

blue sclera, hearing loss, yellow/blue teeth, bruise easily

49
Q

Defective Osteoblasts and Matrix Production

A

osteogenesis imperfects 2

“accordion like shortening of the limbs”

49
Q

what is not affected in achondroplasia

A

intelegence, life expectancy, sex repor

49
Q

deficient osteoclast development or function, which leads to diffuse, symmetric skeletal sclerosis

A

osteoporosis

Mutations interfere with acidification of the osteoclast resorption pit,

49
Q

Erlenmeyer flask deformity

A

long bones lack the medullary canal in osteoporosis

49
Q

decrease in type I collagen synthesis

A

osteogenesis imperfecta

49
Q

osteogenesis imprtfecta mutation

A

genes encoding α1 and α2 chains of type I collagen…
Glycine residue replaced by another amino acid causing the helix not to form properly and be defective

dominent negative effect(will effect the normal produced proteins)

50
Q

Bone is osteopenic, kyphoscoliosis, spondylolisthesis

A

elder dances syndrom

50
Q

severe AR osteopetrosis

A

pancytopenia, hepatospleenomegaly
compressed cranial nerves
renal tubular acidosis

51
Q

marfan mutation

A

fibril 1 on chrom 15

52
Q

loss of horizontal trabeculae and thickened
vertical trabeculae

A

osteoporosis

thin trabeculae and loss of apposition

52
Q

what does RANKL do and what up regulates it
where does it bind

A

RANKL promotes the conversion of osteoblasts to clasts and is promoted by IL-11, PTH, Vit D and malignancies

RANKL bind to RANK on the osteoclasts(decoyed by osteoprogestin)

53
Q

examples of secondary osteoporosis

A

vit D/C def
steroids
hyperthyroid/parathyroid

54
Q

Normal calcium, phosphate and alkaline phosphatase levels

A

osteoporosis

55
Q

Initiated by unregulated osteoclastic activity
➔ increased resorption
➔ stimulates increased osteoblastic activity
➔ abnormal bone deposition

A

pagets disease

56
Q

phases of pagets disease

A
  1. osteolytic, osteoclast dominent
  2. mixed= woven bone
  3. blastic phase= jigsaw mosaic
57
Q

increased hat size and deafness

A

pagets disease

58
Q

Increased Serum Alkaline Phosphatase
* Increased ….

A

Urinary Hydroxyproline

pagets

59
Q

pagets disease complications

A

cardiac failure heart disease, osteosarcoma, giant cell tumors, extra osseous hemapoisis

60
Q

reason for renal tubular dysfunction to cause osteopenia

A

renal tubular acidosis causes the hydroxyapatite to disolve

61
Q

bone changes in end stage renal failure

A
  1. high turnover with lots of resportiona nd formation
  2. aplastic disease more like osteomalacia than remodeling
  3. mixed
62
Q

Frontal bossing and
squared appearance
of forehead
* Persistent hyaline
cartilage and overgrown
costochondral junctions called

A

Rachitic rosary: where the palisade of cartilage is absent(stack of coins)

rickets

also comes with Harrison groove and pigeon chest deformity

poorly calcified osteoid

63
Q

Newly formed osteoid matrix laid down by
osteoblasts is inadequately mineralized
➔producing the excess of persistent
osteoid

A

osteomalacia

64
Q

Subperiosteal haemorrhages

Microfractures and bony deformities

A

scurvy

poor crosslinginging

65
Q

which bone tumors are commonly in adults

A

Echocondroma(within medullary cavity/ no stalk)
giant cell tumors,
chondrosarcoma

66
Q

Slow growing, bone islands, in paranasal sinuses and calvaria, associated
with

A

with FAP colonic adenomas in Gardner syndtom

osteoma

67
Q

site of:
1.osteoid osteoma
2.osteoblastoma
3. osteosarcoma
4. osteochondroma
5. enchondroma
6. chondrosarcoma
7. osteoclastoma

A
  1. CORTEX of femur/tibia
  2. vertebrae lamina and pedicle
  3. MEDULLA of long bones near knee
  4. near the knee
  5. small bones of hands and feet
  6. Axial skeleton- pelvis, shoulder, ribs
  7. knee
68
Q

which one is bigger osteoid osteoma
or osteoblastoma

which one has nocturnal pain
which one can be relieved by NSAIDS
which one has reactive scoliosis

A

osteoblastoma is greater than 2 cm

osteoid osteoma has nocturnal pain bc of release of PGE2 , can be relieved by NSAIDs, and has sclerosis

69
Q

bimodal age peaks

A

osteosarcoma
1 young bc de novo mutations
2. old bc of pagets

70
Q

osteosarcoma mutations

A

Rb
CDNK2
MDM2
p53
CDK4

71
Q

genes involve in the cartilage bone tumors

A

osteochondroma= ext 1 and 2

enchondroma is IDH 1 and 2

chondrosarcoma: EXT 1/2, IDH 1,2 CDKN2

72
Q

Olliers and Mafucci syndromes

A

enchondroma

73
Q

chondrocytes and cartilage matrix surrounded by
ring of reactive bone tissue in medullary cavity of tubular bone

A

enchondroma

74
Q

where do chondrosarcoma metastitize

A

lungs

75
Q

Develops in epiphysis and spreads to metaphysis

A

osteoclastoma/ giant cell tumor

76
Q

Onion skin appearing because of periosteal bone reaction

A

ewig sarcoma

77
Q

11:22 translocation

A

ewig sarcoma

Primitive round cells without any obvious differentiation

78
Q

Homer-Wright rosettes
rounded cell clusters with a
central fibrillary core

A

indicative of attempted neuroectodermal differntiation

Ewing

79
Q

bence jones proteinuria

A

multiple myeloma
light chains K and L found in urine

80
Q

adult and kid metastizises to bone

A

ADULT:
breast, lung, thyroid, kidney, prostate

KIDS:
Osteosarcoma, wilms tumor , neuroblastoma, ewig, rhabdo

81
Q

starts with chondrocyte injury

A

osteoarthritis

then causes fibrillation of articular cartiledge

82
Q

features of osteoarthritis

A

eburnation,
subchonral reactive sclerosis, subchondral cysts, osteophytes

83
Q

HLADR4

A

rheumatoid arthritis

can also be caused by smoking or infection

84
Q

CD4+T-cellmediatedproliferationofsynovialcellswith“pannus”formation leading to joint erosion

A

RA

85
Q

Periarticular Osteopenia and Ankylosis

A

cause of morning stiffness in RA

shows absent reparative activity unlike OA that has sclerosis and osteophytes

86
Q

Ulnar aspect of forearm, elbow

A

RA

87
Q

antibody found in RA

A

ACPA

88
Q

HLA B27

A

seronegative Spondyloarthropathies:
Ankylosing Spondylitis,
Reactive Arthritis

89
Q

Insidious onset back pain in the lower lumbar or buttock region i.e Lumbar Spine and Sacroiliac joints
* Prolonged morning stiffness lasting >1hr -> improves with activity

Pleuritic chest pain and limited chest expansion -> secondary to inflammation of costovertebral or costochondral junctions.

A

Ankylosing Spondylitis

90
Q

reactive arthritis sx

A

conjunctavitis, uveitis, arthritis

esp after salmonella, or chlamydia