Brainscape's Knowledge GenomeTM

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


See full index

FOUNDATION MEDICINE > Pathology Cameron McCloskey > Flashcards

Pathology Cameron McCloskey Flashcards

1
Q

What is cancer?

A

Uncontrolled cell division that can invade other tissue and impede their function

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

What is a tumour?

A

Any swelling Can be benign or malignant

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

What is a neoplasm?

A

New growth not in response to any stimulus

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

Define malignant

A

Metastatic potential is present This involves any neoplasm invading the basement membrane

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

What is metastasis?

A

The spreading of a neoplasm to a different part of the body

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

Give three pre-malignant stages

A
  1. Dysplasia - disordered growth with no stimulus (no invasion of basement membrane)
  2. Metaplasia - change of one cell type to another
  3. Hyperplasia - increase in cell number
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Metaplasia is a response to _____

A

Stress

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

What can initiate metaplasia?

A
  1. Injurious or noxious stimuli
  2. Cytokines and cell signals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why are post-menopausal obese women at risk to hyperplasia (and cancer)?

A

Oestrogen will cause proliferation of the endometrium as part of the menstrual cycle. Cholesterol is similar in structure to oestrogen Obese women have high cholesterol which can cause proliferation in the endometrium Due to increased (an unnecessary) proliferations, these women have more “chances” for cells to begin to grown autonomously and for hyperplasia to occur

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

What occurs in dysplasia that does not occur in either metaplasia or hyperplasia?

A

A genetic abnormality is developed

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

What is carcinoma in-situ?

A

This is the final stage a neoplasm goes through before becoming malignant (invading basement membrane and spreading by metastases) This is the same as high-grade dysplasia

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

How is the N:C (nuclear:cytoplasmic) ratio affected in malignant cells affected?

A

N:C ratio is high

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

List some causes of cancer

A
  1. Genes
  2. Smoking
  3. Alcohol
  4. UV radiation, and other rdiation types
  5. Drugs
  6. Infections
  7. Obesity
  8. Burnt toast…supposedly Etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are Weinberg Hallmarks?

A

These are “bad decisions” made by a cell that are key to becoming malignant.

  • Increased growth signals
  • Growth suppression removed
  • Avoiding apoptosis
  • Achieving immortality
  • Becoming invasive
  • Making own blood supply (angiogenesis)
  • Lose cellular DNA spellchecking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Li-Fraumeni syndrome?

A

Genetic condition affecting the tp53 gene which codes for p53. This means sufferers from LFS are unable to stop excessive growth and attempt DNA repairs (or activate apoptosis)

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

How does radiation cause cancer?

and What is Xeroderma pigmentosa?

A

Pyrimidine dimers are formed in DNA which are molecular lesions involving two consecutive bases on a single DNA strand to bind together ruining the normal base pairing Numerous instances can cause pyrimidine dimers in DNA to become overwhelmed

  • its a genetic defect in nucleotide excision repair NER, suffer from numerous skin cancers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe briefly the cell cycle

A
  1. Cyclin D activated CDK4 (cyclin dependent kinase)
  2. CDK4 phosphorylates Rb (retinoblastoma)
  3. Rb now unbinds from DNA allowing for DNA replication to occur - access to DNA is now possible
  4. Synthesis phase now occurs involving DNA replication
  5. M phase follows after G2 and the cell divides
  6. Cytokinesis is when the cell physically divided
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are oncogenes?

A

A gene with the potential to cause cancer It involves increased growth

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

What are tumour supressors?

A

These are genes preventing the pathway to cancer

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

How can neoplastic cells evade DNA spellchecking?

A

Destroying spellcheck proteins such as P53

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

What happens to a tumour in the bloodstream?

A

It will aggregate with platelets This means it will eventually slow down and stop within a blood vessel and grow in this new location

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

Name 2 growth factors that can aid angiogenesis (for neoplasms)

A
  1. VEGF (vascular endothelial growth factor)
  2. PDGF (platelet derived growth factor)
    (Angiogenesis is the formation of new blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the three stages involved in the pathway of mutations and neoplasm development?

A
  1. Initiation - first mutation
  2. Promotion - accumulation of mutations (dysplasia)
  3. Persistance - malignant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

FISH is better than PCR for _____ genetic abnormalities

A

Large

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

PCR is ideal for _____ genetic abnormalites

A

Small

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

What are the functions of p53? (4)

A
  1. Cell cycle arrest at G1
  2. Increase levels of p21 to inhibit CDKs preventing Rb phosphorylation and hence DNA replication
  3. Apoptosis activation when damage is too great
  4. Activate repair mechanisms when damage is minimal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are first principles in relation to identifying neoplasms?

A

These are quick decisions that can make an estimate as to whether the neoplasm appears malignant or not

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

How do benign tumour look?

A
  1. round and smooth
  2. homogenous (same type of cells)
  3. symmetrical, organised
  4. Normal N:C ratio
  5. Encapsulated: Slow growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do malignant tumours look?

A
  1. Not symmetrical
  2. Pleomorphism :jagged edges
  3. heterogenous
  4. High N:C ratio: Hyperchromatia darkly stained nuclei, usually due to increased DNA content
  5. Fast growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is differentiation?

A

The process by which stem cells develop into mature cells types

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

What can poor cell differentiation indicate?

A

Neoplasms Potentially malignant

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

What is pleomorphism?

A

cells grow in multiple shapes and size forms of the “same” cell type - poor differentiation has taken place

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

What is hyperchromasia?

A

A cell which has a nucleus that stains very darkly - highlights large amount of genetic material suggesting fast growth and malignancy

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

Why does rapid cell division in neoplasms impact the number of mutations developed?

A

The more divisions that take place, the more chances there is for mutation

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

What is a neoplasm of the epithelium called?

A

Carcinoma - always malignant

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

What is a benign neoplasm of glandular cells called?

A

Adenoma

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

What is a benign neoplasm of squamous cells called?

A

Papilloma

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

What is a neoplasm of bladder epithelial cells called?

A

Urothelial cell carcinoma - always malignant

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

What is a malignant neoplasm of glandular cells called?

A

Adenocarcinoma

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

What is a malignant neoplasm of squamous cells called?

A

Squamous cell carcinoma

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

What are malignant neoplasms of connective tissue (mesenchyme) called?

A

Sarcomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the names of benign/malignant neoplasms of fat tissue?

A

Benign - lipoma Malignant - liposarcoma

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

What are the names of benign/malignant neoplasms of bone?

A

Benign - osteoma Malignant - osteosarcoma

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

What are the names of benign/malignant neoplasms of cartilage?

A

Benign - enchondroma Malignant - chondrosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the names of benign/malignant neoplasms of skeletal muscle?

A

Benign - rhabdomyoma

Malignant - rhabdomyosarcoma

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

What are the names of benign/malignant neoplasms of smooth muscle?

A

Benign - leiomyoma

Malignant - leiomyosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the names of benign/malignant neoplasms of nerves?

A

Benign - neurofibroma (or schwannoma)

Malignant - peripheral nerve sheath tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the names of benign/malignant neoplasms of blood vessels?

A

Benign - haemangioma

Malignant - angiosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the names of benign/malignant neoplasms of the CNS?

A

Benign - gliomas

Malignant - named after benign version with malignant added in front

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the name of malignant neoplasms of the skin?

A

Melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are names for blood neoplasms?

A

All are malignant Leukaemia Lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

When referring to neoplasms what does “stage” refer to?

A

Distance from origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

In relation to neoplasms, what do karyotypes allow for?

A

Translocations to be discovered and defined

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

When referring to neoplasms what does “grade” refer to?

A

Level of differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the difference between neoplasia and dysplasia?

A

Neoplasia - autonomous growth Dysplasia - disordered growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What do cancers do to the body?

A
  1. Compression/blockage of vessels/airways or ducts
  2. Impacts tissue function
  3. Haemorrhage - by infiltration
  4. Infiltrating bone marrow can weaken the immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Tumours are very metabolically active using large amounts of energy, what is the name of the weight loss associated with this?

A

Cachexia

58
Q

In which two ways can growing occur?

A
  1. Hyperplasia - increase in cell number
  2. Hypertrophy - increase in cell size
  • e.g increase in size of myometrial smooth muscle cells increase in dimeters is more associate with hypertrophy.
  • e.g Breast lobules have an increased number of cells under hormonal influence (mainly progesterone) to provide for normal lactation this shows as slight increase in brest size which is associated with hyperplasia
59
Q

Whta causes hyperplasia?

A

An external stimulus

such as hormones

(when removed, growth is reversed)

60
Q

What is atrophy?

A

The decrease in cell size

opposite to hypertrophy

61
Q

What is metaplasia?

A

The reversible change from one mature cell type to another

62
Q

Metaplasia occurs in a response to signals delivered to stem cells. What can some of these signals be due to?

A
  • Cytokines
  • Growth factors
  • Other chemicals such as noxious stimuli
63
Q

What are the four main stages in the cell cycle?

A
  • G1
  • S
  • G2
  • M
64
Q

In the cell cycle what does G1 consist of?

A
  • The cell increases in size as protein synthesis increases
  • Cyclin dependent kinase 4 (CDK4) becomes activated by cyclin D due to phosphorylation and a complex is formed between the two
  • After sufficient CDK4 is activated the cycle can proceed
  • Retinoblastoma (Rb) can be phosphorlated by the complex and it comes free from E2F
  • E2F can now act as a transcription factor
65
Q

What is retinoblastoma?

A

A transcription inhibitor

(normally binds to E2F)

66
Q

What occurs in stage S of the cell cycle?

A

DNA replication occurs

67
Q

What occurs in stage G2 of the cell cycle?

A
  • The cell grows more due to increased protein synthesis
  • P53 checks for errors in DNA replication
  • It can attempt to fix errors or initiate apoptosis if the errors are too severe
68
Q

Some cells are terminally differentiated and cannot divide or repair (e.g. neurones). What is a term to describe this?

A

Replicative senescence

69
Q

What are telomeres?

A

They consist of a TTAGGG sequence at the end of a chain

They prevent the chromosome from degrading and “unravelling”

Telomere shortening is linked to ageing

70
Q

What does the term “resolution” mean in terms of wound repair?

A

Returns tissue completely to normal

(occur when injury is minimal, there is good vascualr supply and the injurious agent is easily removed)

71
Q

What is suppuration?

A

The production of pus

72
Q

In terms of tissue repair, what does the term “organisation” mean?

A

Resolution cannot occur, and despite healing, scar tissue is present

This often occurs when the injury goes beyond the basement membrane

(occur if there is necrosis, large quantities of fibrin produced or poor blood supply)

73
Q

What is granulation tissue?

A

When tissue becomes injured, the site is infiltrated with capillaries and myofibroblasts (muscle cells)

Collagen and smooth muscle are depositied

This tissue is ganulation tissue and has a red shiny appearance

74
Q

Why does scarring occur and what is the consequence?

A

It occurs when myofibroblasts mature and produce collagen which causes the scar

This therefore means the functioning of that tissue segment is lost

75
Q

Depending on what is found pathologically during autopsy, how can the recency or cause of death be determined?

A

Presence of neutrophils mean recent injury

Granulation tissue means there has been around 2 weeks since injury

Scarring can mean anything in excess of 6 weeks

76
Q

What is scarring of the liver called?

A

Cirrhosis

77
Q

What is the consequence of cirrhosis?

A

Liver failure

(toxins cannot be removed from the blood as efficiently, and proteins are not as easily synthesised)

78
Q

Stages of Acute inflammation ?

A

Vasoconstriction,

vasodilation,

increased permeability of vessels,

stasis of red blood cells,

neutrophil margination

79
Q

What are the cell types that are most dominant in both acute and chronic inflammation?

A

Acute - neutrophils polymorphs

Chronic - lymphocytes

80
Q

What are the two categories of foreign bodies?

A

Both can potentially lead to granuloma formation

  1. Exogenous - talc, asbestos, oil
  2. Endogenous - keratin, bone, crystals
81
Q

Which types of infections may lead to granuloma formation?

A
  • Parasites
  • Foreign bodies
  • cancer e.g keratin production
  • organ specific e,g Corhn’s , hypersensitivity pneumonitis
  • Mycobacterium (TB)
82
Q

Tb granuloma is cause by what?

A

Caseousكاسياس necrosis (cheesy)

83
Q

What are the two types of cell death?

A
  1. Apoptosis
  2. Necrosis
84
Q

What are the three types of necrosis?

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
85
Q

Describe coagulative necrosis

A
  • Dead cells are consumed by enzymatic processes and other cells
  • Ghost outlines exist since the nucleus is no longer present
  • Cells are therefore no longer living so do not degrade properly
86
Q

Describe liquefactive necrosis

A
  • No cell structure is maintained
  • Cells are liquefied
  • This is normally associated with bacterial or fungal infections
87
Q

Describe caseous necrosis

A
  • Associated with Tb
  • A Ziehl-Neelson stain can aid identification of caseous necrosis
  • Involves granulomatous inflammation with central necrosis
88
Q

What is the key difference between apoptosis and necrosis?

A

Apoptosis requires energy, necrosis does not

89
Q

Apoptosis is normally physiological, but when may it be pathological?

A
  • Injury
  • Radiation damage
  • Chemotherapy
  • Viral infections
  • Cancers
  • After transplant
90
Q

What are the two mechanisms for apoptosis?

A
  • Extrinsic
  • Intrinsic
91
Q

Describe the extrinsic pathway for apoptosis

A
  • It involves death receptor initiation
  • FasL binds to death receptor Fas which activates caspases
  • FADD, an adapter protein, bridges the gap between the Fas receptor and the caspases
  • It is the death inducing signalling complex that undergoes conformational change when the Fas receptor is bound to caspases
  • A caspase cascade occurs
92
Q

Describe the intrinsic pathway for apoptosis

A
  • Normally growth signals promote anti-apoptotic molecules in the mitochondrial membrane
  • Growth signals become deactivated
  • They are replaced by Bax and Bak - apoptotic regulators
  • This increases the permeability of the mitochondria
  • Proteins called cytochrome C escape inducing apoptosis
93
Q

After apoptosis is induced, what then happens to the cell?

A
  • Cells shrink by pyknosis (irreversible condensation of chromatin in the nucleus)
  • The nucleus clumps and break up
  • The cytoplasm breaks up forming blebs
  • Macrophages remove debris
94
Q

How is cellular ageing caused? (3)

A
  1. Oxidative stress by free radical damage
  2. Accumulation of metabolic by products such as lipofuscin (this accumaltes with age and is toxic to cells)
  3. Telomere shorting lead to Finite cell divisions
95
Q

What are telomeres?

A

Telomerase is a large ribonucleoprotein complex responsible for progressive synthesis of telomeric DNA repeats (TTAGGG) at the 3′ ends of linear chromosomes, thereby reversing the loss of DNA from each round of replication.

The TTAGGG sequence at the end of a chromosome

This prevents DNA unwinding

The number of repeats is reduced with each division and will eventually become depleted meaning cells can no longer divide

96
Q

Why do stem cells never die?

A

Telomerase continually renews the TTAGGG repeats

This maintains telomere length

Telomerase is not active in normal cells, but can be in cancerous cells conferring immortality

97
Q

After injury describe the vascular changes that occur

A
  • Vasodilatation occurs
  • Histamine and nitric oxide control this process
  • This causes calor and rubor
98
Q

What is the consequence of vasodilatation in vessels after injury?

A

Blood flow is slowed down (stasis) leading to white cell margination

99
Q

4 stages of Leucocyte extravasation

A

Chemoattraction, rolling, tight adhesion, transmigration

SEE MORE IN THE NOTES

100
Q

As a result of white cell margination, how do white cells interact with the endothelial wall?

A
  • They will bind, via carbohyrate groups, to selectins which are luminal proteins on the endothelial wall
  • This attraction has low affinity so the white cell rolls along the vessel wall
  • The release of chemokines, by macrophages will activate white cells allowing them to bind to selectins more strongly and also to the vessel wall via integrin to ICAM-1 and VCAM-1 which results in much stronger affinity
  • TNF and IL-1 will increase expression of ICAM-1 and VCAM-1
  • Histamine and thrombin are released from inflammatory cells which increase selectin expression
  • After coming to a halt, white cells undergo diapedesis
101
Q

During inflammation, why do vessels become leaky?

A

White cells need to undergo diapedesis and reach the site of inffection or injury

102
Q

“Leaky” vessels during inflammation is brought about by many mechanisms, what are these?

A
  • Endothelial cell contraction (muscle tissue) - this is caused by histamine, bradykinin, substance P and leukotrienes
  • Direct injury
  • White cells - self harm will release damaging toxins
  • Transcytosis - VEGF mediated, macromolecules are captured in vesicles on one side of the cell, drawn across the cell and ejected from the other side
  • New vessel formation - new vessels are weaker and leakier, their production is mediated by VEGF
103
Q

What is VEGF?

A

Vascular endothelial growth factor

104
Q

What is chemotaxis?

A

Movement of cells along a chemical gradient migrating to the source of injury

105
Q

What are the three phases of phagocytosis?

A
  1. Recognition and attachment
  2. Engulfment
  3. Killing and degredation
106
Q

Describe the recognition phase of phagocytosis

A

Bacterial surfaces express mannose receptors

Opsonins are antibodies or any other substance increasing suceptibility to phagocytes

The complement system will also surround foreign material

107
Q

Describe the engulfment phase of phagocytosis

A

Pseudopods (arms) of the phagocyte surround the foreign material forming a vesicle termed a phagosome

The phagosome will then join with a lysosome and form a phagolysosome

108
Q

Describe the killing an degredation phase of phagocytosis

A

Reactive oxygen species within lysomes kill pathogens

This ROS is created due to NADPH which oxidises oxygen

109
Q

What are the 4 clinical features of inflammation?

A
  1. Rubor (redness) / Erythema
  2. Calor (heat)
  3. Tumour (swelling)
  4. Dolor (pain)
110
Q

Why are neutrophils classed as polymorphs?

A

They have many lobes to their nucleus

111
Q

3 type of Adaptations to increase demand on cells

A
  • Increased demand – hyperplasia, hypertrophy
  • Decreased demand – atrophy
  • Altered stimulus - metaplasia (when body change its structure to try to adapt to the environment its in e.g squamous mucosa during Barrett’s metaplasia )
112
Q

when there is increase load on left ventricle what type of adaptation to increase demand on myofibers cells will happen

A

Hypertrophy

113
Q

How doses immune system recognize pathogens that are hidden inside the cells

A

Through interacting with TOOL-LIKE RECTORS which present on infected cell surface with an antigen

114
Q

How is endothelial contraction is involved in acute inflammation ?

A

Contraction of endothelial cells will lead to increase inter endothelial space which its the most important mechanism of vascular leakage.

during acute inflammation, the body’s immune system responds to tissue damage or infection by releasing various mediators, such as histamine and bradykinin, which can cause blood vessels to dilate and increase blood flow to the affected area.

At the same time, these mediators can also cause the endothelial cells that line the blood vessels to contract, which can increase the gaps between the cells and allow fluid, immune cells, and other substances to leak out of the blood vessels and into the surrounding tissues.

This process of increased vascular permeability is important for allowing immune cells to reach the site of infection or injury and to help repair the damaged tissue.

115
Q

what is the different between pathological hyperplasias and cancer ?

A

This where the growth control mechanisms become permanently dysregulated or ineffective and thus the process of pathological hyperplasias can not be reversed.

In many cases, pathologic hyperplasia could lead to cancers . For example, patients with hyperplasia of the endometrium are at increased risk of developing endometrial cancer

116
Q

autophagy

A

is the process in which the starved cell eats its own organelles in an attempt to survive

117
Q

what is Adaptation

A

is reversible changes in number , size phenotype metabolic activity or function of the cell.

it can be

Physiologic adaptations which is the response of cells to normal stimulations by hormones.

Pathologic adaptations are responses to stress that allow cells to modulate their structure and function, to escape injur.

e.g saving of nitrogen in the body instead of releasing it with urea when there is low level of it in the body

118
Q

irreversible cell injury is associated with —–?

A

loss of membrane integrity. This allows intracellular enzymes such as AST and ALT to leak into the serum

119
Q

what is the different between Hyperplasia and Hypertrophy ?

A

Increasing cell numbers requires activation of cell signalling pathways and the cell cycle

120
Q

examples of reversible and irreversible injury

A
  • Plasma membrane blebs, Ribosomal disaggregation, Chromatin clumping, and Mitochondrial swelling
  • Nuclear fragmentation
121
Q

What does coagulative necrosis mean

A

is a type of accidental cell death typically caused by ischemia or infarction. e,g Arterial thrombosis will lead to ischemia.

122
Q

why does necrosis require no energy

A

because it is cell death by a pathological response such as overwhelming chemical or physical insult.

123
Q

What process of cell death requires energy?

A

A

Apoptosis

124
Q

where does apoptosis usually happen in cell cycle

A

G1 phase

125
Q

G2 checkpoint?

M checkpoint?

A

Mitosis will not occur if DNA is damaged or not replicated

Mitosis stops if chromosomes are not properly aligned

126
Q

What part of the cell is involved in cell aging?

A

A

Telomere
Shortening

127
Q

What is a granuloma and when is it normally present?

A

A
  • Collection of macrophages (in response to foreign bodies eg bone, asbestos, TB, parasites, syphillis, malignancy)
  • FOUND in chronic inflammation
128
Q

Sarcoma is malignant. True or false?

A

A

TRUE

129
Q

Pathogenesis of atheroma?

A

A
  • Fatty streak
  • Fibrofatty plaque
  • Proliferative atheroma
  • Complicated atheroma
130
Q

Aetiology of atheroma?

A

A

Endothelial injury

  • Response to injury
  • Macrophages + platelets
  • Lipid accumulation
  • Smooth muscle proliferation
131
Q

Complications of atheroma?

A

A

Thrombosis
Aneurysm
Dissection
Embolism
Ischaemia

132
Q

Thrombus definition?

A

A

Solid mass of blood constituents, formed within blood vessels

133
Q

where is cytochrome c normally located ?

A

is located in the mitochondrial intermembrane/intercristae spaces

134
Q

What are the causes of biological ageing

A
  1. Oxidative stress free radical damage
  2. Accumulation of lipofuscin (yellow)
  3. Telomere shortening
135
Q

only two terms that describe melginancy

A

carcinoma or sarcoma

136
Q

mutation in the factor VIII gene that causes X-linked haemophilia causes what

A

Normal X-inactivation

mutation in the Factor VIII gene on the X chromosome causes hemophilia by impairing the body’s ability to clot blood, and the severity of the condition depends on the amount of functional Factor VIII produced.

137
Q

How does increased intracellular calcium contribute to cell death?

A

Hypoxia and reduced ATP can increase intracellular calcium levels, which can lead to cell death through apoptosis. Apoptosis can occur via an internal pathway (intrinsic) involving mitochondrial permeability or an external pathway (extrinsic) involving FAS. Small changes in calcium can activate the intrinsic pathway by releasing pro-apoptotic factors from mitochondria. Opsonisation and complement are involved in immune pathways that aid in phagocytosis and antibody activity.

138
Q

the difference between GRANULATION TISSUE and GRANULOMA .

A
  • two cell types are predominantly found in granulation tissue Endothelial cells and myofibroblasts
  • GRANULOMA (composed of macrophages/histiocytes).

https://www.mypathologyreport.ca/

139
Q

The form of necrosis that takes place in the CNS is termed

A

C. Liquefactive necrosis

140
Q

Coagulative necrosis where cellular outlines are retained is often found in

A

cardiac muscle.

141
Q

Resolution/restitution are forms of

A

repair

FOUNDATION MEDICINE (23 decks)

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