Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FoM > Pathology > Flashcards

Pathology Flashcards

1
Q
  • osis
A

disease/condition

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

inflammation of

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

Diverticulitis
diverticular disease

A

diease –> Digestive conditions that affects the large intestine (colon).
Small bulges or pockets (diverticula)develop in the lining of the intestine

X + itis, is when these pockets become inflamed or infected.

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

Causes of inflammation

A
  • Microbial infections
  • Hypersensitivity reactions (some parasitic infections + TB)
  • Physical agents (trauma, heat injury, radiation)
  • chemicals (Acids, bacterial toxins, corrosives)
  • tissue necrosis ( secondary to ischaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Bacterial Endotoxin

exotoxin

A

endo - associated with bacterial cell walls, stimualting inflamamtion

chemicals release by bacteria, stimualting inflammation

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

Cardinal signs of acute inflammation

A

R - Redness (Rubor)
H - Heat (calor)
S - Swelling (tumor)

P - Pain (dolor) –> due to release of some chemical mediators (PROSTAGLANDIN + BRADYKININ) ++ due to physical distortion of tissue
L - Loss of Function (functio laesa)

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

synonym for redness

A

rubor

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

synonym for heat

A

calor

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

synonym for swelling

A

tumor

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

synonym for pain

A

dolor

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

Stages of inflammation

A
  1. Release of chemical mediators
  2. Vasodilation
  3. Increased vascular permeability
  4. Fluid accumulation
  5. Cellular recruitment
  6. Phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

synonym for exudate

A

pus

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

exudate

A

fluid that leaks out of blood vessels into nearby tissues is named…

it is made up of cells, protein and solid materials.

it may ooze from cuts or from areas of infection or inflammation

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

process called exudation

A

name of process when vascular changes in acute inflammation includes:

increased vascular permeability +++ increased net flow of fluid and cells our of vessels

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

Margination

A

the adhesion of white blood cells to the walls of damaged blood vessels.

caused by the loss of intravascular fluid, which slows the flow to the site, thus allowing leukocytes e.g. neutrophils to marginate

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

Synonym for adhesion

A

Pavementing

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

the process of diapedisis

A
  1. marginatoin of neutrophiles
  2. pavementing of neutrophils (adhesion)
  3. pass between endothelial cells (emigration)
  4. pass through basal lamina and migratie into adventitia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

HIstamin functions

A
  1. regualtes sleep wake cycle + cognitive function
  2. role in allergies
  3. causes vascular dilation + permeability

released mainly by mast cells

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

function of prostaglandins

A

derived from arachidonic acid

some cause paltelet aggregation
some cause increased vascular permeability
PAIN

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

function of Seratoning

A

vasoconstrictor

released by platelets

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

leukotrienes function

A

vasoactive properties

often made in neutrophils from arachidonic acidfun

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

funciton of Bradykinin (plasma factor)

A

peptide mediation vasodilation + pain
activated by coagulation factor XII

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

Plasma factors
4 enzyme cascade systems in plasma

A

these 4 enzyme cascade systems in plasma are called X:

  1. Coagulation system ( fibrinogen to fibrin)
  2. Kinins (activated by caogulation factor XII), includes Bradykinin
  3. Fibrinolytic system (removes fibrin from the vascular system preventing clots from occluding the vessel.)
  4. COmplement system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Chemical mediators of acute inflammation

A
  1. Early chemical events
    - Histamine + - Thromin released by inflammatory stimulus

—> causing upregulation of P-SELECTIN on endothelial cells + PAF on endothelial cells

—> allowing ligands onthe neutrophil surface to engage with the P-SELECTIN, starting to roll along the endothelial wall

  1. PAF (platelets activating factor)
    – docks with corresponding receptor on neutrophil and promotes expression of otehr molecules —-> endresult is a firm adhesion onto the endothelial surface
  2. Histamine
    – vascular dilation + permeability
    – released by mast cells
  3. Lysosomal compounds
    – vascular permeability
    – stimualte histamine release from mast cells
    – released by neutriphils
  4. Leukotrienes
    – vasoactive properties
    – often made by neutrophils from arachidonic acid
  5. Prostaglandins
    – dervied from arachidonic acid
    – increased vascualr permeability
    – plateelt aggregation
  6. Seartonin
    – vasoconstrictor
    – released by platelets
  7. Chemokines
    – attarcting more WBCs to site of inflammation
    – IL-8 attracts neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

cellular senescence

A

when the cell stops dividing as it ages
ascribed to progressive shortening of telomeres

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

HeLa cell line

A

cervical cancer cells taken without consent from Henrietta Lacks.

have active version of tolomerase which copies telomeres and prevents shortening

No Hayflick limit = cellular immortality

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

Function of telomerase

A

RESTORES telomeres
(so not present in normal cells, which have Hayflick limit)

hTERT gene - human telomerase reverse transcriptase, upregulation means more telomerase

hTERT mutations associated with many cancers

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

Clinicopathological features of Ageing: SKIN

A
  • contains less elastin
  • less collagen
  • atrophy of dermis
  • sun damage;photoageing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Clinicopathological features of Ageing: CARDIO

A

Ratio of ellastin to collagen decreases
reduced ability of conduit arteries to distend = increased systolic bood pressure

(aorta and major branches need to be able to stretch in response to internal pressure(compliance) and go back again (elasticity))

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

Clinicopathological features of Ageing: immune cells

A

immunosenescence
more memory cells, less naive cells ( decreased abiltiy to respond when encountering novel pathogens)

Thymus atrophy
less naive T cells

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

Clinicopathological features of Ageing: osteoarticular ageing

A

Osteoporosis
Normal mineralisation of bone matrix, BUT trabeulae are thinned

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

Clinicopathological features of Ageing: nervous

A

Neurodegenerative
CNS damage as a result of hypoxia/haemorrhage

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

Cell Size Feature of Necrosis

A

Increased (swollen)

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

Cell Size Feature of Apoptosis

A

Reduced (celll shrunken(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Nucleus Feature of Apoptosis

A

Fragemtnation / Condensatoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Nucleus Feature of Necrosis

A

Pyknosis, Karyohexis, Karyolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Plasma Membrane Feature of Necrosis

A

Disrupted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Plasma Membrane Feature of Apoptosis

A

Intact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Nearby inflammation feature of Necrosis

A

almost always

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Nearby inflammation feature of Apoptosis

A

Never

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Causes of cell injury

A

Physical damage ( trauma)
Oxygen deprivation
Microbial
Immunological
Chemical

  • strong acid contact (coagulates tissue proteins(
  • CO inhalation (prevents O2 transport)
  • Paracetamol overdose (Metabolites bind to liver cell prtoeins and lipoproteins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How are cells damaged?

A

ATP depletion / reduced synthesis
Mitochondria damage
Intracellular calcium
Free radical (ROS) damage
Defective membrane permeability
Protein misfolding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Casues of Hypoxia

A

Ischaemia (most common cause – also compromises delivery of glyogen substrates, so double whammy)

Reduction in oxygen carrying capacity of the blood
Eg anaemia, CO poisoning

Inadequate blood oxygenation
Eg pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What happens in hypoxic Injury

A
  1. Reduction in intracellular generation of ATP
    Sodium pump activity is reduced, so sodium accumulates in the cell
    This causes isoosmotic gain of water and acute cellular swelling
  2. Increase in anaerobic glycolysis (bc of deceased ATP)
    Rapid depletion in glycogen stores
  3. Ribosomes detach from the rough ER
    Polysomes dissociate into monosomes
    Reduction in protein synthesis
  • cytoskeleton breaks down
  • loss of ultrastructural features
  • irreversible daamge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Causes of Mechanical Injury

A

Direct mechanical damage
Cell membranes rupture, cytoplasm spills out

Freezing
Intracellular and cell membranes perforated by ice crystals

Osmotic imbalance
Rupture as a result of rapid change in osmotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

hyperplasia
metaplasia
dysplasia
atrophy
hypertrophy

A

increased no, of cells

  • conversion from one type of normal adult cell to another type of normal adult cell. (The most common types of metaplasia observed by pathologists involve the conversion from squamous to glandular cells and vice versa)

-refers to the abnormal development of cells within tissues or organs.

47
Q

1.hyperplasia
2. metaplasia
3.dysplasia
4.atrophy
5. hypertrophy

A
  1. “Increase in the number of cells in an organ or tissue”
  2. “Reversible change in which one adult cell type is replaced by another adult cell type.”
  3. “Shrinkage in the size of a cell by the loss of cell substance”
  4. Increase in the size of cells and consequently an increase in the size of the organ”
48
Q

Coagulative necrosis
- what it is
- causes

A

Tissue with connective tissue  basic arrangement preserved

Caused by ischemia

Ischemia results in decreased ATP, increased cytosolic Ca++, and free radical formation, which each eventually cause membrane damage

e.g. Infarct: localized area of ischemic necrosis - myocardial infarct

49
Q

caseous necrosis
- what it is
- causes

A

Cheese’-like necrotic debris contained within

Coagulated tissue no longer resembles the cells, but is in chunks of unrecognizable debris

Usually giant cell and granulomatous reaction

Example: Tuberculosis

50
Q

colliquative necrosis
- what it is
- causes

A

Tissue with minimal connective tissue  ‘liquifies’

Often in brain because lack of supporting stroma predisposes to total liquefaction when necrotic

Usually caused by focal bacterial infections, because they can attract polymorphonuclear leukocytes (neutrophils)

The enzymes in the neutrophils are released to fight the bacteria, but also dissolve
the tissues nearby, causing an
accumulation of pus
effectively liquefying the tissue

51
Q

Gangrenous necrosis

A

DRY – sterile coagulative necrosis e.g. distal limb

WET – coagulative necrosis with superimposed infection

52
Q

Fat necrosis

A

Release of enzymes from pancreas or gut or traumatic

Enzymes (lipases) release free fatty acids, which with calcium produce soapy deposits in tissuesP

53
Q

Physiological examples of Apoptosis

A

Embryogenesis (shaping organs, eliianting webbing between fingers)
Menstrual cycle (elimination of cells from funtional layer of endometrium)
Immune system –>
- Death of post-inflammatory neutrophils
- Removal of self-reactive lymphocytes
- Death of virally infected cells

54
Q

Clinical diagnosis of myocardial infacrtion ( cell death)

A

Myocyte necrosis  enzymes released (troponins, CK-MB, LDH)

55
Q

Labile cells
(Regeneration

A

good capacity to regenerate ( e.g. surface peithelial cells(

56
Q

Stable cells
(Regeneration)

A

Divide at a slow rate, but can regenerate if needed (e.g. hepatocytes in liver)

57
Q

Permanent cells
(Regeneration)

A

no means of effective regeneration
e.g. nerve cells, striated muscle cells

58
Q

Suppuration

A

formation of pus
lots of neutrophils accummulating
mix of neutrophils, debris, bacteria

forms abscess if it gets walled off

59
Q

Outcomes of inflammation

A
  • Resolution
  • Suppuration
    -Scarring / Fibrosis
  • Chronic inflammation
60
Q

Granulation tissue

A

a new connective tissue with microscopic blood vessels and myofibroblasts that develop at the wound site in the process of healing. It grows from the base of the wound and helps in filling the wounds. It is important for the contraction of the wound and epithelial cell migration.

New capillaries, leading to more macrophages, leading to proliferation of fibroblasts, leading to fibrosis and/or scarring

61
Q

Skin Healing - primary intention

A

in x Fibrin joins the edges together weakly
Over time, epidermal regrowth and collagen synthesis makes a stronger join

62
Q

Skin healing - secondary intention

A

Tissue defect filled in by granulation tissue
Epithelial regrowth over the surface
Fibrous scar forms and contracts over time

63
Q

Bone Healing

A

Break
Haematoma / inflammatory response
Callus formation (woven bone)
Replaced eventually by stronger lamellar bone

64
Q

Which parts of the kidney can regenerate, and which parts not?

A

Epithelium can regenerate, architecture can’t
Similar to liver
Loss of tubular epithelium only can regenerate/repopulate cells
Destruction of glomerulus or damage to interstitium usually results in scarring / impaired function

65
Q

Which smooth muscle cells can regeneration?

A

Vascular smooth muscle cells can regenerate
Other smooth muscle cells … not so much
Damaged muscle is replaced by scar tissue

66
Q

Examples of primary granulomatous disease

A

Crohns
sarcoidosis

67
Q

Resistance of microorganism to phagocytosis and intracellular killing

examples

A

TB
Leprosy

68
Q

Macroscopic signs of chronic inflammation

A

Chronic ulcer
chronic abscess cavity
fibrosis/ thickening of tissueC

69
Q

cells of chronic inflamamtion

A

lymphocytes(B and T)
plasma cells
macrophages
sometimes eosinophils

70
Q

Histology - recognising a lymphocyte

A

Small purple dots

71
Q

Histology - recognising a plasma cell

A

fried eggs

72
Q

Histology - recognising a macrophages

A

bigger blobby ones

73
Q

Histology - recognising a eosinophils

A

tomatoes with sunglasses

74
Q

Which cytokine promotes apoptosis

A

TNF

75
Q

which cytokine promotes anti viral defences

A

interferon

76
Q

Granuloma

A

collection of histiocytes

77
Q

difference between granuloma + granualtion tissue

A

A granuloma is a small, organized collection of immune cells, primarily macrophages, that forms in response to chronic inflammation, particularly when the body tries to isolate and contain a substance or infection it cannot eliminate.
– Contains and isolates difficult-to-remove substances
e.g. TB, Crohns (inflammation of bowel disease), Sarcoidosis

Granulation tissue is new connective tissue and microscopic blood vessels that form on the surface of a wound during the healing process, particularly in open wounds
– Repairs tissue and promotes wound closure
e.g. skin wounds

78
Q

Giant cells - what are they, how they form

describe the types
- Langhans
- Foreign body type
- Touton type

A

when macrophages collide, ending up with huge multinucleated cells

Langhans - horsehow nuclei (seen in TB)

Touton type - neat little circles of nuclei , lipid breakdown and xanthoma

foreign body - nuclei randomyl scattered

79
Q

Xanthoma

A

a skin condition in which certain fats build up under the surface of the skin

80
Q

Intrinsic Pathway of Apoptosis

A
  1. Cytochrome C released during apoptosis
    (mitochondrial protein)
  2. Binds with other factors
    - ATP (Apoptotic Protease activating factor)
    - Pro-caspace 9
    (MAKING AN APOPTOSOME)
  3. Pro-caspase 9 -> cleaved into -> caspase 9
  4. Caspase 9 cleaves
    procaspase 3 -> caspase 3 (active form)
    CASPASE 3 triggers CELL DEATH
81
Q

Extrinsic pathway of apoptosis

A

TNF PATHWAY:
1. tumor necrosis factor BINDS to TNF receptor

  1. TNF receptor associates with death domain (TRADD)
    FADD (Fass associated death domain)
    - forms complex with procaspase 8
    - caspase activation, procaspase 8, caspase 3
    - triggers cell death

FAS PATHWAY:
1. first apoptotic protein
FAS Ligand + FAS receptr

  1. Formation of FADD complex
    procaspsase 8/10
    death inducing signalling complex ( DISC)
    leading to caspase activaton
    - triggers cell death
82
Q

Mesenchyme
Mesenchymal cells

A

Multipotent stem cells
Progenitor cell which differentiates to all types of connective tissue –> e.g. fibroblast, osteoblast, chondroblast, preadipocytes

produce ECM that consists mainly of a simple ground substance rich in hyaluronic acid.

ECM + mesenchymal cells = MESENCHYME

EMBRYO: type of embryonic conenctive tissue that gives rise to all other connective tissues of the body during early development.

ADULT: present in small quantities as part of loose connective tissue in
- umbilical cord
- bone marrow
- adipose tissue
serve to give rise to fibroblasts + new blood vessels

83
Q

synonym for neoplasia

A

tumour

84
Q

tumour meaning

A

swelling

85
Q

ONCO / OLOGY
oncology

A

study of tumours ( i.e. swellings)

86
Q

Malignant neoplasm

A

potentially lethal
has ability to invade and metastasise

exceptions e.g.
- malignang tumor (BASAL CELL CARCINOMA) does not metastasise

87
Q

Benign neoplasm

A

does NOT have ability to metastasise

  • does NOT always mean harmless - some can be v locally destructive
88
Q

anaplastic tumour

A

the least differentiated tumour

DIFFERENTIATION TOPIC: the extent to which neoplastic tissues resemble their corresponding normal tissue of origin

as tumors become less well differentiated, anaplastic features become more prominent

89
Q

Anaplastic/Undifferentiated tumorsq

A

BAD BOYS
cannot be identified by morpholgy alone
– immunohistochemistry needed, to look at their lineage
– subtyping important for diagnosis and treatment

90
Q

Features of poor differentiation
(Grade 3 classification)

A

NUCLEUS, abnormal:
- high nuclear: cytoplasmic ratio
- clumped chromatin
- prominent nucleoli

Nuclear pleomorphism:
- varibaility in nuclear size/shape

increased mitotic activtiy

Loss of polarity

NECROSIS - bad sign

91
Q

Dysplasia

A

earliest form of precancerous lesion, describing confined neoplastic change(mostly epithelia) , with nuclear plyomorphism /architectural disruption

confined withi nthe basement membrane

it is NOT cancer, but can sometimes become cancer
- can be low/high grade

can regress, not alway sleading to malignancy

92
Q

Carcinoma in-situ

A

severe form of dysplasia
WIHTOUT invasion ( basement membrane of dysplastic epithelium not penetrated)
full thickness of epithelium

93
Q

x happens when the tumour is growing so fast that the blood supply cannot keep up

A

Necrosis

94
Q

adjectives to describe BENIGN local invastion

A

well circumscribed
enapsualtoin (fibrous capsule)

slow growing
noninvasive -nonmetastatic

Exophytic growth direction

sometimes they are NOT harmless, they can be very locally destructive

95
Q

adjectives t odescribe MALIGNANT local invasion

A

infiltrative
invasive

karge
rapidly growing with hemorrhage + necrosis
metastatic

Endophytic growth direction (fown the way into connective tissue in an invasive manner)

96
Q

Benign tumours (not just epithelial)

A

Suffix “-OMA”

97
Q

Benign tumour of glandular / secretory epithelium

A

ADENOMA

98
Q

Benign tumour of non-glandular / surface epithelium

A

PAPILLOMA

99
Q

Mesenchymal tissues
benign mesenchymal tumours prefixes + suffix OMA:

Smooth muscle
skeletal muscle
adipose
blood vessel
bone
cartilage
fibrous

A

leiomyo
rhabdomyo
lipo
haemangio
osteo
chondro
fibro

100
Q

suffix for malignant epithelial tumors

A

CARCINOMAS

101
Q

suffix for benign epithelial tumors

A

OMA

102
Q

malignant mesenchyma tumours called

A

SARCOMAS

103
Q

benign mesenchyma tumours suffix

A

OMA

104
Q

malignant mesenchymas tumours suffix

A
  • sarcoma
105
Q

TERATOMAS

A

TUMORS COMPOSED of well-differentiated tissues e.g. bone, mnuscle , teeth, hair

contains cells representing ALL 3 germ cell layers

REMINDER: well differentiated, behave better
the anaplastic are the bad boys

106
Q

HAMARTOMA

A

NON-NEOPLASTIC DISORDERED OVERGRWOTH OF NORMAL TISSUE

indigenous to site of occurence

e.g. PORT WINE STAIN

107
Q

CHORISTOMA

A

heterotropic rests
bening normal tissue but seen in abnormal location

e.g. pancreas nodule in stomach

108
Q

Myeloma

A

malignancy of plasma cells

109
Q

LYMOHOMA

A

Malignancy of B / T cekk origin, often beginning in lymph nodes

110
Q

Leukemia

A

Malignancy of WBCs, beign in bone marrow

111
Q

Melanoma

A

malignancy of melanocytes (producing pigment in the skin/0

112
Q

Melanocytic naevus

A

benign proliferation of melanocytes

113
Q
A

FoM (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions