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Semester 3 > General Pathology (lectures 5-6) > Flashcards

General Pathology (lectures 5-6) Flashcards

1
Q

autoimmune diseases

A

break down of tolerance of AG on own cells (SELF-AG)

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2
Q

diagnosis of autoimmune disease

A

auto-Antibodies

immune mechanisms cause pathological lesions

can be difficult to find evidence of immune nature of disorder

“pathogenicity difficult to prove”

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3
Q

AI disease genetic factor

A

increased frequency via Family history

genetic component

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4
Q

more common in

A

women

E.g.
SLE
RA

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5
Q

systemic vs localized

A

can be systemic or local

how localized?

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6
Q

E.g. of systemic (multi-organ) AI disease

A

systemic lupus erythematosus

rheumatic fever

rheumatoid arthritis

systemic sclerosis

polyarteritis nodosa

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7
Q

E.g. of AI diseases limited to single organ (more localized)

A

multiple sclerosis (CNS)

Hashimoto’s thyroiditis (thyroid)

Grave’s disease (thyroid)

Autoimmune hemolytic anemia (blood)

Pemphigus vulgaris (skin)

Myasthenia Gravis (muscle)

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8
Q

Systemic Lupus Erythematosus

A

“prototype of AI disease”

multisystemic

1/2500 people

10x more common in women

genetic component (family history?)

more common in young adults

but can happen any age

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9
Q

signs symptoms

A

CNS symptoms

pattern baldness

butterfly rash

Endocarditis, Pericarditis

Pleuritis, Pneumonitis

lupus nephritis

raynaud’s phenomenon

myositis, arthritis

osteoporosis

splenomegaly

lymphadenopathy (lymph nodes, aka lymph glands)

anemia, neutropenia, thrombocytopenia

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10
Q

pathogenesis SLE

A

poorly understood

Malfunction of T suppressor cells which allows polyclonal activation of B cells

“Plasma cells derived from uncontrolled B cell clones secrete antibodies against autoantigens and foreign antigens”

“Many antibodies to DNA, RNA and nuclear proteins = called antinuclear antibodies (ANA)”

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11
Q

antinuclear antibodies (ANA)

A

“The antinuclear antibody (ANA) is a defining feature of autoimmune connective tissue disease. ANAs are a class of antibodies that bind to cellular components in the nucleus, including proteins, DNA, RNA, and nucleic acid-protein complexes.”

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12
Q

Agab complexes during SLE

A

Antigens that reach circulation form complexes with antibodies in the serum

“Circulating Ab-Ag complexes deposited in membranes e.g. synovial membrane, serous membranes, endocardium, choroid plexus, ant. eye chamber”

E.g.
synovial membrane (joints)

serous membranes (heart, lungs, abdomen)

endocardium

choroid plexus (brain)

anterior eye chamber (eyes)

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13
Q

atnerior eye chamber sle

A

“Anterior uveitis in patients with SLE is usually mild and rarely leads to a deterioration in visual acuity, and also may present as synechiae or a fibrinous inflammatory exudate in the anterior chamber of the eye.”

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14
Q

complement system activation vs immune complexes

A

“Immune complexes are large and retained and activate complement, which elicits an inflammatory reaction resulting in many organ-specific inflammatory diseases”

e.g.
glomerulnonephritis,
arthritis,
etc

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15
Q

clinical features sle

A

variable

Inflammation of joints (arthritis) – most common; redness, swelling, pain

Kidney involvement (75%)

Cutaneous lesions (butterfly rash) (30-60%)

Damage to RBCs causing anemia

Enlargement of lymph nodes and spleen

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16
Q

treatment sle

A

Corticosteroids

cyclophosphamide (immunosuppressive)

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17
Q

cyclophosphamide

A

“a synthetic cytotoxic drug used in treating leukemia and lymphoma and as an immunosuppressive agent.”

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18
Q

sle and kidneys

A

kidney transplant as treatment if kidneys severely affected

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19
Q

immunodeficiency

A

Primary (congenital) or

secondary (due to infections, metabolic diseases, cancer, or treatment/chemotherapy, etc.)

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20
Q

which type of immunodeficiency more common

A

secondary

cancer, infection, chemotherapy, metabolic disease

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21
Q

E.g. of secondary immunodeficiency

A

AIDS

acquired immunodeficiency syndrome

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22
Q

involvement of B/T cells vs entire immune system

A

Primary or secondary may involve just B cells or T cells

or may be generalized and involve the whole immune system

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23
Q

how are ID diseases characterized

A

All ID diseases are characterized by lymphopenia – low lymphocyte count in peripheral blood

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24
Q

lymphopenia

A

low lymphocyte count in peripheral blood

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25
Q

B cell deficiency

A

associated with low levels of serum antibodies

(low plasma, low AB production)

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26
Q

reduced resistance to infection

A

All ID disorders cause reduced resistance to infections

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27
Q

primary ID diseases

A

genetic disorders affecting differentiation and maturation of T cells and B cells

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28
Q

when occur?

A

Can occur at any step along the developmental sequence that leads from stem cells to fully differentiated cells

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29
Q

leads to

A

Leads to heterogenous group of disorders with mild or severe symptoms

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30
Q

e.g. primary ID disease

A

DiGeorge’s syndrome

T-cell deficiency related to aplasia of thymus, associated with aplasia of parathyroid glands

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31
Q

aplasia

A

the failure of an organ or tissue to develop or to function normally.

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32
Q

AIDS

A

Acquired immune deficiency syndrome

Set of symptoms and infections resulting from the damage to the human immune system caused by the human immunodeficiency virus (HIV)

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33
Q

what does AIDS do

A

Progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumours

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34
Q

HIV transmitted how

A

transmitted through direct contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV

Transmission can involve sex, blood transfusion, contaminated needles, exchange between mother and baby during pregnancy, childbirth, breastfeeding, or other exposure to bodily fluids

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35
Q

HIV how?

A

sex

blood transfusion

contaminated needles

between mother/baby during pregnancy

during childbirth

breastfeeding (virus in breastmilk)

exposure to bodily fluids (semen, pre-ejaculate, etc.)

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36
Q

direct contact?

A

direct contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV

certain bodily fluids

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37
Q

epidemiology

A

..

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38
Q

etiology HIV

A

RNA retrovirus

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38
Q

retrovrius define

A

RNA viruses that have an enzyme (reverse transcriptase) capable of making a complementary DNA copy of the viral RNA, which then is integrated into a host cell’s DNA. The family includes a number of significant pathogens, typically causing tumors or affecting the function of the immune system, e.g. HIV.

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39
Q

why called retrovirus?

A

While transcription was classically thought to occur only from DNA to RNA, reverse transcriptase transcribes RNA into DNA. The term “retro” in retrovirus refers to this reversal (making DNA from RNA) of the usual direction of transcription.

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40
Q

where highest prevalence?

A

Africa

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41
Q

how many worldwide

A

35 million

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42
Q

how many new cases per year

A

100,000 in US

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43
Q

percentage of college students

A

1% (18-25)

An estimated 3% to 6% of U.S. college students are HIV positive (different source)

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44
Q

HIV pathogenesis

A

Transmitted through the transfer of body fluids

Virus can’t survive outside host cell

HIV has affinity for T helper cells and monocytes (macrophage outside BV)

…
Macrophages can also become infected …

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45
Q

other cells infected

A

Fixed tissue phagocytic cells can also become infected (e.g. microglia)

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46
Q

what do infected cells do

A

Infected cells can serve as reservoir for virus

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47
Q

what happens to infected cells often/eventually

A

HIV virus is cytotoxic thus infected cells often die

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48
Q

hiv initial infection

A

Initial infection stimulates B cells to produce antibodies within weeks

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49
Q

hiv latent phase

A

The second stage of HIV infection is chronic HIV infection (also called asymptomatic HIV infection or clinical latency). During this stage, HIV continues to multiply in the body but at very low levels. People with chronic HIV infection may not have any HIV-related symptoms

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50
Q

hiv latency vs AIDS onset

A

Latent infection can persist for years

As virus replicates and destroys more helper T cells, symptoms of AIDS begin to appear

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51
Q

immunity during AIDS

A

Cell mediated immunity becomes depressed and humans cannot defend against infections (opportunistic infections)

Death generally occurs due to infection but can also occur due to tumours

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52
Q

phases of hiv

A

acute (inital infection)

chronic (latent)

crisis (AIDS)

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53
Q

acute

A

primary infection

sharp increase in presence of HIV virus in blood

sudden decrease in presence of CD4+ helper T cells in blood

acute stage lasts a few weeks

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54
Q

chronic/latent stage – and crisis stage

A

after immune system responds with antibodies to HIV

there is huge dip in presence of virus in blood

there is an increase in CD4+ helper cells (not to original amount, but close)

during actual clinical latency there is a relatively small presence of HIV virus in blood

presence of CD4+ helper cells very gradually declines throughout many many years

at the end of clinical latency, the amount of CD4+ helper cells decline to an extent that they can no longer contribute to defending against HIV virus (antibody production)

at this stage, virus overtakes immune system, and AIDS symptoms appear (crisis stage)

virus level increases and CD4+ level continues to decrease, until opportunistic infections/diseases lead to death

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55
Q

how long can latent stage be

A

chronic/latent stage = many many years

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56
Q

how long crisis stage

A

also can be few years

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57
Q

viremia

A

the presence of viruses in the blood.

“uncontrolled virus proliferation leads to chronic viremia”

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58
Q

4 phases of illness (hiv/aids)

A

..

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59
Q

Phase of acute illness (Group I)

A

Usually 3-6 wks after exposure

Symptoms typically non-specific, include fever, night sweats, nausea, myalgia, headache, sore throat, skin rash, lymph node enlargement

Symptoms last 2-3wks, then disappear

Pt. develop antibodies to HIV

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60
Q

Phase of asymptomatic infection (Group II)

A

Variable duration, months to years

theoretically can last a long time, and allow patient to live a relatively full life with currently available medicine/treatment

Asymptomatic patient carries virus and is infectious

Approx. 50% of HIV+ patients develop AIDS within 10 years of initial diagnosis if untreated

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61
Q

Phase of generalized lymphadenopathy (III)

A

Persistent lymphadenopathy develops in asymptomatic pts or early in disease

May persist for months or years

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62
Q

AIDS (Group IV)

A

Pt shows signs of AIDS which reflect opportunistic disorders including GI disorders, CNS involvement, neoplasia

Clinically, ratio of CD4+ /CD8+ cells decr.

In the last stages, almost no CD4+ cells present
–>
opportunistic diseases and death

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63
Q

AIDS define

A

AIDS is defined as HIV infection that leads to any of the disorders in clinical category B or C of HIV infection or a CD4+ T lymphocyte count of < 200/μL.

(less than 200 per cubic mm – aka microlitre)

The normal CD4 count range is between 500 and 1400 cells/microliters., taking into consideration laboratory variations.

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64
Q

disorders in clinical category B or C of HIV infection

A

Serious opportunistic infections

Certain cancers,
such as Kaposi’s sarcoma and
non-Hodgkin lymphoma,
to which defective cell-mediated immunity predisposes

Neurologic dysfunction

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65
Q

pathology..

A

Non-specific; vary with time, extent of viremia and degree of immunosuppression

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66
Q

@ lymph nodes

A

Initially lymph nodes enlarge and show hyperplasia

After time, lymph nodes become depleted of lymphocytes and eventually become infected

After time, lymph nodes become depleted of lymphocytes and eventually become infected (decreased CD4+)

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67
Q

@ brain

A

Microglia in the brain and multinucleated giant cells form nodules

Opportunistic infection leads to meningitis or encephalitis (CMV, herpes, fungi, protozoa)

May destroy part of the brain directly or through infarct

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68
Q

@ respiratory tract

A

Initially localized to URT but often progresses to LRT (pneumonia or TB)

–> Pneumocystis jiroveci/carinii (named after individuals)

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69
Q

cyst vs abscess

A

“While a cyst is a sac enclosed by distinct abnormal cells, an abscess is a pus-filled infection in your body caused by, for example, bacteria or fungi. The main difference in symptoms is: a cyst grows slowly and isn’t usually painful, unless it becomes enlarged.”

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70
Q

pneumocystis pneumonia define

A

fungal infection in one or both lungs. It is common in people who have a weak immune system, such as people who have AIDS.

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71
Q

@ GI tract

A

Infections are similar to respiratory tract and can also include parasites

Diarrhea and malabsorption of nutrients can also be present

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72
Q

@ skin

A

Can include dermatitis or infections (fungi, herpes, bacteria)

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73
Q

tumours

A

Often lead to mortality

Increased incidence of tumours esp. lymphomas (lymph nodes, spleen, liver, brain, etc.) and Kaposi’s sarcoma

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74
Q

pathologic findings in AIDS

A

meningitis
encephalitis
AIDS dementia

herpes labialis (more frequent/severe outbreaks)

thrush

pneumonia

malabsorption

colitis
proctitis (anus, rectum)

dermatitis
folliculitis
impetigo

Kaposi’s sarcoma

AIDS nephropathy

lymphomas

lymphadenopathy

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75
Q

Kaposi’s sarcoma

A

Malignant disease of endothelial cells

Caused by herpesvirus

Often occurs in skin and internal organs

Nodules composed of anastamosing vascular spaces filled with blood

Can cause bleeding or compress vital organs

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76
Q

diagnosis

A

Presence of HIV antibodies in blood (HIV+)

T cell count – decreased ratio of CD4+ /CD8+ (less than 200 per nanolitre of CD4+)

AIDS diagnosed by presence of opportunistic infection and tumours

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77
Q

treatment

A

Medications - replication inhibition (of virus)

Expensive & not readily available worldwide

Vaccines unsuccessful

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78
Q

Amyloidosis (disease)

A

Caused by deposition of a fibrillar substance called amyloid

Multi-factorial disease

Often related to abnormalities of the immune system or an abnormal response to chronic infection

Amyloid: any fibrillar protein that forms a beta-pleated sheet

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79
Q

where amyloid deposited

A

Amyloid is deposited in the extra-cellular spaces

Changes the function of tissues and cells

Deposits in blood vessels changes their permeability

Leads to proteinuria in kidney

Vessels in liver and adrenal glands becomes solid

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80
Q

amyloidosis – what happens

A

Atrophy and loss of cell function

Amyloid in heart causes weakened contractions

Amyloid in brain causes dementia

Clinical presentation is variable and depends on the organ system involved

No effective treatment
(treat symptoms as they appear)

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81
Q

Clinical Presentation of Amyloid Deposition

A

Systemic amyloidosis: usually caused by deposition of AA or AL amyloid in various organs (e.g., liver, kidneys, adrenals, spleen, heart)

Localized organ: specific amyloid deposits (e.g., Alzheimer’s disease)

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82
Q

LECTURE 6

A

..

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83
Q

neoplasm

A

new growth

“Uncontrolled cell growth whose proliferation cannot be adequately controlled by normal regulatory mechanisms”

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84
Q

neoplasm define

A

“An abnormal mass of tissue that forms when cells grow and divide more than they should or do not die when they should. Neoplasms may be benign (not cancer) or malignant (cancer).”

“Benign neoplasms may grow large but do not spread into, or invade, nearby tissues or other parts of the body.”

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85
Q

normal cell gorwth requires

A

genetic material, aka DNA and RNA

signals from one cell to another

growth inhibiting or growth promoting substances

1) genetic material
2) signaling
3) growth inhibiting/promoting substance

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86
Q

differentiating

A

Once a cell stops growing it needs to differentiate - to become specialized -

by activating some genes, and suppressing other genes

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87
Q

tumour cells vs differentiation

A

Tumour cells do not achieve the same level of differentiation as normal cells

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88
Q

neoplastic cell growth

A

Autonomous - independent of normal growth factors and inhibitors

Excessive - doesn’t respond to normal regulators

Disorganized – compared to the formation of normal tissues

1) independent
2) excessive
3) disorganized

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89
Q

benign/malignant neoplasm (tumour)

A

enign – limited growth potential and good outcome

Malignant – grow uncontrollably with poor outcome

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90
Q

histological classifcaiton of benign vs malignant based on

A

based on how cells look under the microscope

91
Q

benign tumours, macroscopic features

A

Sharply demarcated

Often encapsulated (by CT tissue)

Can have expansive growth which compresses adjacent tissue leading to atrophy and fibrosis

Can be easily removed by surgery

No hemorrhage or necrosis

92
Q

benign tumours microscopic features

A

Resemble the original tissue from which they have arisen

Show high levels of differentiation

93
Q

benign tumours – cellular features

A

Uniform cell populations (homogenous)

Regularly shaped/same sized nuclei

Well developed cytoplasm

Nucleus occupies a small portion of the cell

Nucleus has even distribution of chromatin

Nucleoli are not overprominent

94
Q

benign tumours – chromosomal & biological features

A

Has normal number of chromosomes

Retain normal complex functions

95
Q

Malignant tumours, macroscopic features

A

No clear margins from normal tissue

No encapsulation (CT)

Can have invasive growth

Cannot be removed easily by surgery

Hemorrhage and necrosis present

96
Q

malignant tumours microscopic features

A

Differ considerably from original tissues

Show anaplasia (cells take on new characteristics)

Undifferentiated

97
Q

anaplasia

A

the loss of the mature or specialized features of a cell or tissue, as in malignant tumors.

losing degree of differentiation (?)

98
Q

anaplasia..

A

“Anaplasia is a qualitative alteration of differentiation. Anaplastic cells are typically poorly differentiated or undifferentiated and exhibit advanced cellular pleomorphism.”

“In fact, anaplasia and pleomorphism are sometimes used incorrectly as synonyms. Pleomorphism refers to variation in the size and shape of cells.”

99
Q

anaplasia etymology

A

Ancient Greek: ἀνά ana, “backward” + πλάσις plasis, “formation”

100
Q

malignant tumours – cellular features

A

Don’t have uniform cell populations (heterogenous)

Cells vary in size and shape

Nuclei vary in shape and size

Variable amounts of cytoplasm

Nucleus is larger

Hyperchromatic (more chromatin, unevenly distributed, nucleoli prominent, multiple)

101
Q

hyperchromatic

A

Hyperchromatic (more chromatin, unevenly distributed, nucleoli prominent, multiple)

102
Q

hyperchromatic..

A

“the development of excess chromatin or of excessive nuclear staining especially as a part of a pathological process.”

103
Q

malignant tumours chromosome features

A

Aneuploid (abnormal number of chromosomes)

104
Q

aneuploid etymology

A

Greek
an- “not, without” (see an- (1))
+
euploid,
from Greek

eu “well, good” (see eu-)
+
-ploid, from -ploos “fold” (from PIE root *pel- (2) “to fold”)

105
Q

aneuploid

A

having an abnormal number of chromosomes in a haploid set.

106
Q

malignant tumours biological features

A

No specialization or differentiation

Metabolism is geared toward supporting growth and replication (metastasis?)

107
Q

beniign vs malginatn expansion rate

A

benign slow expansion (& limited)

malignant fast expansion (& more uncontrolled)

108
Q

metastases?

A

no benign

yes malignant

109
Q

metastasis

A

the development of secondary malignant growths at a distance from a primary site of cancer.

2) a metastatic growth.

110
Q

b vs m – external surface texture

A

benign smooth

malignant irregular

111
Q

encaspulated?

A

b YES

m NO

112
Q

Necrosis?

A

b NO

m YES

113
Q

hemorrhage

A

b NO

m YES

114
Q

“architecture”

A

benign = Resembles normal tissue of origin

malignant = does not

115
Q

cells?

A

b DIFFERENTIATED

m NOT

116
Q

nuclei?

A

uniform (size/shape)

vs

Pleomorphic

117
Q

“mitoses”

A

few

vs

many; irregular

118
Q

metastasis

A

A process by which cells move from one site to another in the body.

Only malignant tumours metastasize.

Benign tumours never metastasize.

Involves a spread of tumour cells from a primary location to another site in the body.

Spread can occur through 3 main pathways:

119
Q

how metastases SPREAD? (3 ways)

A

1) via lymphatics

2) via blood (hematogenous spread)

3) via body cavities

120
Q

hematogenous

A

“originating in or carried by the blood.”

121
Q

metastatic cascade

A

Not all malignant cells are capable of metastasis.

Cells must acquire the capacity to metastasize.

Cells then expand clonally.

Clone expands, cells reach lymphatics or blood vessels or body cavity.

122
Q

can all malignant cells metastasize?

A

no

must acquire the capacity to metastasize.

123
Q

how carried?

A

Fluid carries the cells from the primary site to distant locations where cells attach and begin forming a new tumour mass.

Metastatic cells must escape immune cells including macrophages, T cells, NK cells.

Malignant tumour must form new blood vessels (angiogenesis).

124
Q

what cells target metastatic cells?

A

immune cells, specific and non-specific (natural)

macrophages, T cells, NK cells

125
Q

angiogenesis and malignant tumours

A

Malignant tumour must form new blood vessels (angiogenesis).

126
Q

note tumour-induced angiogenesis

A

chemotactic factors

enzymes

tumour angiogenic factors (E.g. FGF – fibroblast growth factor ??)

127
Q

E.g. metastasis

A

tumour starts @ respiratory epithelial cells

grows into CT below

continues growing into smooth muscle further below

reaches deeper BV / lymph vessel structures

cells from tumour break off into LV & BV

E.g. = carcinoma of lung

128
Q

histological classification (how tumours named?)

A

Tumours are named for the cell type that they resemble the most.

129
Q

end in “-oma”

A

Benign tumours of mesenchymal cells (i.e. cells of CT, bone and muscle)

130
Q

e.g. benign tumours

A

Fibroma - from fibroblasts

Chondroma - from cartilage

Lipoma - from adipose

Leiomyoma - from smooth muscle cells

Osteoma – from bone

Rhabdomyoma - from striated muscle cells

131
Q

adenoma

A

from epithelial cells; composed of glands or ducts

132
Q

E.g. Adenoma

A

..

133
Q

1) Tubular or villous adenomas

A

from epithelial cells in the GI tract; aka polyps

134
Q

polyp

A

a small growth, usually benign and with a stalk, protruding from a mucous membrane.

135
Q

2) Papillomas (adenoma)

A

protuberant tumours of the skin, urinary bladder, mouth, larynx

136
Q

papilloma

A

“a benign tumor (as a wart or condyloma) resulting from an overgrowth of epithelial tissue on papillae of vascularized connective tissue (as of the skin) see papillomavirus”

“a small wartlike growth on the skin or on a mucous membrane, derived from the epidermis and usually benign.”

137
Q

3) Cystadenomas

A

cystic tumours composed of hollow spaces lined by neoplastic epithelium

138
Q

cystadenoma

A

Cystadenomas are rare cystic tumors of epithelial origin that arise in the liver, the majority in the right lobe, or less commonly in the extrahepatic biliary system. There are two histological variants, a mucinous type and a serous type.

139
Q

malignant tumours

A

Malignant tumours of mesenchymal cells are named for the root of the cell type plus the suffix “sarcoma”

140
Q

E.g.

A

Fibrosarcoma - from fibroblasts

Chondrosarcoma - from cartilage

Liposarcoma – from fat

141
Q

carcinomas vs sarcomas

A

Malignant tumours of epithelial cells are called carcinomas

E.g.
squamous cell carcinoma

142
Q

Adenocarcinomas (vs adenoma)

A

malignant tumours from glands and ducts

143
Q

note, some malignant tumours end in “-oma”

A

Lymphoma - malignant tumours of lymphoid cells

Glioma - malignant tumours of glial cells

Seminomas - malignant tumours of testicles

144
Q

why?

A

could just be for linguistic/phonetic reasons (?)

“seminsarcoma” / “glisarcoma” / “lymphsarcoma” does not sound as natural (?)

145
Q

nomenclature

A

Some tumours of the same name can be benign or malignant in which case we must designate “malignant”:

E.g.
Malignant islet cell tumour

146
Q

blastoma

A

malignant tumors composed of embryonic cells originating from embryonic primordia

147
Q

E.g. blastoma

A

Retinoblastoma: eye

Neuroblastoma: adrenal medulla or immature neural cells

Hepatoblastoma: liver

Nephroblastoma: kidney

148
Q

embryonic primordia

A

“Primordia are those primitive embryonic structures from which. various structures of the body develop. ▶ They are primarily derivatives of the Trilaminar Embryonic Germ. Disc layers i.e. Ectoderm, Mesoderm and Endoderm; which are one. of the outcomes of Gastrulation.”

149
Q

gastrulation define

A

Gastrulation is an early developmental process in which an embryo transforms from a one-dimensional layer of epithelial cells, a blastula, and reorganizes into a multilayered and multidimensional structure called the gastrula.

150
Q

teratomas

A

Benign tumours derived from germ cells (egg and sperm) are called teratomas.

151
Q

teratoma

A

teratogen

teratoma

“monstrous” and “tumor”

152
Q

teratoma..

A

Derived from germ cells; contain tissues formed from all three germ layers:

Ectoderm
Mesoderm
Endoderm

153
Q

Eponymous tumours – named after somebody

A

Hodgkin’s lymphoma

Ewing’s sarcoma

Kaposi’s sarcoma

154
Q

tumour staging

A

based on clinical assessment during gross examination, surgery, x-ray/imaging examinations, etc

155
Q

tumour grading

A

based on histologic examination

156
Q

tumour staging done to

A

to clinically assess the extent of tumour spread

Based on clinical exam, x-ray, biopsy, surgery

157
Q

TNM system of staging

A

TNM system of staging takes into account:

1) size of Tumor (T),

2) presence of lymph NODE metastases (N),

3) distant Metastases (M)

158
Q

staging 1-4 (or A-D)

A

TNM system of staging assigns a number to: tumour size, lymph node involvement and distant metastasis

E.g. T1, N1, M1

159
Q

grading based on histological examination (differentiation)

A

Grade I – well differentiated

Grade II – moderately well differentiated

Grade III – undifferentiated

160
Q

which used for prognosis?

A

Staging and grading used for prognosis.

161
Q

which better predictive value?

A

Staging has more predictive value.

162
Q

biochemistry of cancer cells

A

Metabolism of cancer cells is simpler

Require less oxygen

Better adapted for survival

Fewer mitochondria

Fewer enzymes

RER is simpler and less abundant

Simplified metabolism leads to loss of functional capacity

(loss of parenchyma?)

163
Q

anaplasia and (malignant) tumour cells

A

E.g. acquire fetal characteristics

Produce proteins such as alpha-fetoprotein (AFP)

164
Q

alpha-fetoprotein test (AFP test)

A

“An alpha-fetoprotein (AFP) test can be used to help diagnose and manage liver or germ cell tumours.”

“High levels of AFP may be a sign of cancer of the liver, ovaries, or testicles. But having a high AFP level doesn’t mean you have cancer “

165
Q

growth properties

A

Lack contact inhibition – tend to pile up forming aggregates and nodules

Do not require firm support for growth

Autonomous – do not depend on growth stimuli

Excessive and unregulated – do not respond to normal inhibitory influences

(disorganized)

166
Q

contact inhibition (lacking @ malignant tumours)

A

“CONTACT INHIBITION is cessation of cellular movement, growth, and division upon contact with other cells”

“Contact inhibition is the term used to describe the abrupt arrest of the cell cycle that occurs in cultures of rapidly proliferating epithelial cells”

167
Q

causes of cancer / risk factors

A

..

168
Q

carcinogen

A

Carcinogen – cancer causing agent

169
Q

exogenous carcinogen

A

Chemicals, physical agents, viruses

170
Q

engogenous carcinogen

A

Genetic

Oncogene – human cancer gene; can be identical to exogenous viral gene

171
Q

human carcinogens

A

uv rays = skin cancer

radiation = thyroid/skin

viruses –> lymphoma

metabolic carcinogen –> intestinal

contact caricinogen –> skin

metabolic liver/excretory carcinogens –> liver/bladder

172
Q

ID of carcinogens (3 elements)

A

1) Clinical studies – gathering data by practicing physicians observing cancer patients (case studies)

2) Epidemiologic studies – involve studying populations and families

3) Experimental studies – performed on animals and in labs (in vitro)

173
Q

epidemiology

A

the branch of medicine which deals with the incidence, distribution, and possible control of diseases and other factors relating to health.

174
Q

how do carcinogens act

A

Locally at the site of contact (e.g. skin and lungs)

At the site of digestion

At the site of metabolic activation in the liver

At the site of excretion in the urine

175
Q

carcinogenesis

A

1) Ingestion of the potentially harmful substance (procarcinogen) - activated metabolically in the liver

2) Starts initiation - induction of genetic changes in the exposed cells

3) Promotion - initiated cells are stimulated to proliferate

4) Conversion - convert to new cell (tissue?) type

5) Progression - acquisition of new genetic features

6) Clonal expansion - expansion of cell clones

Some will be dormant in new location, some will metastasize

Selection – the most adaptable and vital clones will survive

176
Q

carcinogenesis steps

A

1) ingestion

2) initiation

3) promotion

4) conversion

5) progression

6) clonal expansion

177
Q

physical carcinogen

A

UV light

X-rays

Radioactive isotopes

Atomic bombs

178
Q

biological carcinogens

A

Aflatoxin (fungi) on peanuts causes liver cancer especially in Africa and Asia

Parasites in Egypt cause bladder cancer

179
Q

aflatoxin

A

Aflatoxins are a family of toxins produced by certain fungi that are found on agricultural crops such as maize (corn), peanuts, cottonseed, and tree nuts.

180
Q

viral carcinogens

A

Classified as DNA or RNA viruses

RNA can be further classified:
a) acute-transforming or slow-transforming
b) Retrovirus
…

181
Q

retrovirus

A

“A retrovirus is a type of virus that inserts a DNA copy of its RNA genome into the DNA of a host cell that it invades, thus changing the genome of that cell”

“While transcription was classically thought to occur only from DNA to RNA, reverse transcriptase transcribes RNA into DNA. The term “retro” in retrovirus refers to this reversal (making DNA from RNA) of the usual direction of transcription.”

182
Q

Human DNA viruses

A

HPV

EBV

HBV

183
Q

Human RNA virus

A

HTLV-1

184
Q

HPV

A

human papillomavirus (HPV)

70 subtypes linked to human lesions such as warts

Can cause benign or malignant tumours

Some strains of HPV cause genital warts which is linked to invasive cervical carcinoma

185
Q

EBV

A

Epstein-Barr Virus
(note also INFECTIOUS MONONUCLEOSIS)

Human herpesvirus with a predilection for B cells

Extremely prevalent (90%)

Can be asymptomatic or can produce infectious mononucleosis (IM)

Related to Burkitt’s lymphoma and nasopharyngeal carcinoma

186
Q

ebv – B cells

A

EBV is transmitted from the carrier through the saliva and enters the host via the oropharynx region.

B cells are the principal targets of EBV infection, primarily due to their expression of CD21, the major receptor for the virus.

“Epstein-Barr virus (EBV) infection is known to convert resting B lymphocytes into immortal cells that continuously multiply, leading to posttransplant lymphoproliferative disorder (PTLD).”

“After Epstein-Barr virus (EBV) infection in vivo, B-cells with latent virus infection persist indefinitely through life. These cells grow in vitro on explanation and can be established as immortal B-cell lines.”

187
Q

EBV – Burkitt’s lymphoma

A

“Epstein-Barr virus (EBV) causes Burkitt’s lymphoma (BL), which is endemic in Africa, and, as we demonstrate, promotes survival of the tumor cells even long after their explantation.”

“Epstein–Barr Virus (EBV) can transform B cells and contributes to the development of Burkitt lymphoma and other cancers.”

188
Q

EBV – nasopharyngeal carcinoma

A

Nasopharyngeal carcinoma (NPC) and gastric carcinoma accounted for 82% of EBV-attributed malignancies and 89% of deaths attributed to EBV-associated neoplasms. EBV is known to cause lifelong persistent infection asymptomatically in over 90% of the global population.

“Nasopharyngeal carcinoma (NPC) is consistently associated with Epstein-Barr virus (EBV) infection in regions in which it is endemic”

189
Q

HBV

A

hepatitis B virus

Transmitted by blood

Associated with liver cancer

190
Q

HBV associated with

A

liver cancer

191
Q

HTLV-1 (RNA virus)

A

HUMAN T-CELL LYMPHOMA/ LEUKEMIA VIRUS 1

RNA retrovirus

Causes a rare form of adult T cell leukemia

192
Q

oncogenes, proto-oncogenes

A

Normal cellular genes, called proto-oncogenes, encode for proteins important for basic cell functions

Proto-oncogenes are transformed into oncogenes (mutated normal cellular genes) by four mechanisms:

193
Q

proto-oncogene

A

“Proto-oncogenes are normal genes which affect normal cell growth and proliferation, but which have the potential to contribute to cancer development if their expression is altered.”

“A variety of events may activate proto-oncogenes and convert them from benign genes to cancer genes.”

194
Q

4 mechanisms that can convert proto-oncogene to oncogene

A

1) point mutation
(change structure)

2) gene amplification
(change quanitity)

3) chromosomal rearrangement
(change location)

4) Insertion of viral genome

195
Q

1) Point mutation

A

single base substitution in the DNA chain

196
Q

2) Gene amplification

A

increased number of copies of the proto-oncogene

197
Q

3) Chromosomal rearrangement

A

translocations of one chromosomal fragment onto another or deletion of a fragment or insertion of a fragment

198
Q

4) Insertion of viral genome

A

..

199
Q

second contributing factor (if proto-oncogene becomes oncogene)

A

TUMOUR SUPRESSOR GENES

200
Q

Tumour suppressor gene

A

Cells regulatory genetic mechanisms to protect against activated or newly acquired oncogenes

“If a tumour cell is fused with a normal cell, the hybrid cell will be benign because the tTUMOUR SUPPRESSOR GENES of the normal cell will suppress the oncogenes of the malignant cell”

201
Q

what happens if Tumour suppressor genes don’t function

A

1st mutation = proto-oncogene –> oncogene
(I.e.
SUSCEPTIBLE CARRIER)

2nd mutation = defective Tumour Suppressor Genes

–> leads to cancer

Note cancer can also occur with Tumour Suppressor Genes
–> (more active oncogenes?)

202
Q

hereditary cancer

A

Certain cancers occurs more often in families.

family history, genetic component

“linked to an absence of a specific tumour suppressor gene.”

203
Q

hereditary cancer vs tumour supressor genes

A

linked to an absence of a specific tumour suppressor gene.

204
Q

Hereditary cancer – E.g.

A

Neurofibromatosis type I

Familial adenomatous polyposis coli

Wilms’ tumor

Skin tumors in xeroderma pigmentosum

Chromosomal fragility syndromes (Bloom’s syndrome, Fanconi’s syndrome)

205
Q

Wilm’s tumour

A

rare kidney cancer

mainly affects children

AKA nephroblastoma

the most common cancer of the kidneys in children

affects children ages 3 to 4

less common after age 5

can affect older children and even adults

206
Q

Familial adenomatous polyposis coli

A

Familial adenomatous polyposis (FAP) is an inherited disorder characterized by cancer of the large intestine (colon ) and rectum. People with the classic type of familial adenomatous polyposis may begin to develop multiple noncancerous (benign) growths (polyps ) in the colon as early as their teenage years.

207
Q

Neurofibromatosis Type I

A

common autosomal dominant disease in humans

numerous subcutaneous neural sheath tumours

also with pigmented lesions of the skin (café au lait spots)

E.g. “The Elephant Man”

208
Q

autosomal dominant

A

Autosomal dominant inheritance is a way a genetic trait or condition can be passed down from parent to child.

One copy of a mutated (changed) gene from one parent can cause the genetic condition.

A child who has a parent with the mutated gene has a 50% chance of inheriting that mutated gene.

209
Q

neurofibromatosus type 1 – clinical features

A

lisch nodules (nodular aggregate of dendritic melanocytes affecting the iris)

Neurofibromas (lumps on/under skin)

skin fold freckling

cafe au lait spots (pigmented lesions)

210
Q

immune response to tumours

A

Malignancy may alter tumour cells so much that they become “foreign” to the body’s immune system

211
Q

how does immune system respond to tumour cell antigens?

A

Tumour antigens will induce antibody production and cell-mediated immune response (T suppressor/cytotoxic cells)
–>
(ACQUIRED IMMUNITY)

Innate immunity – NK kills, macrophages

212
Q

what can immune response do to tumour

A

Ultimately, immune response can limit growth of tumour

Many small tumours are perhaps eliminated by immune system

Immunotherapy treatment can be successful in eliminating tumours

213
Q

immunotherapy

A

the prevention or treatment of disease with substances that stimulate the immune response.

214
Q

HIV/AIDS & cancer risk

A

People with HIV often have weakened immune systems, which means they will have a greater chance of getting cancer.

215
Q

CLINICAL MANIFESTATION OF NEOPLASIA

A

variable

signs include:
Change in bowel/bladder habits

A sore that won’t heal

Unusual bleeding or discharge

Thickening or lump in breast or elsewhere

Indigestion or difficulty in swallowing

Obvious change in wart or mole

Nagging cough or hoarseness

216
Q

clinical features of tumour depend on:

A

1) Type of tumour

2) Location of tumour

3) Histological grade of tumour

4) Clinical stage of tumour

5) Immune status of person

6) Sensitivity of tumour to therapy

217
Q

local symptoms

A

tumour growth compressing adjacent structures

Compression of brain causes epileptic seizures

Compression of lung causes coughing

Can cause atrophy
Can cause hemorrhage
Can cause obstruction

218
Q

systemic conditions

A

Cachexia - wasting

Anorexia – loss of appetite

Weight loss

Thrombosis

Paraneoplastic syndromes

219
Q

Paraneoplastic

A

Paraneoplastic comes from the Greek words for alongside (para), new (neo) and formation (plasis)

220
Q

Paraneoplastic syndromes

A

a consequence of the presence of cancer in the body,

NOT due to the local presence of cancer cells;

can be caused by substances secreted by cancer cells

221
Q

Paraneoplastic Syndromes, E.g.

A

Cushing’s syndrome: small-cell carcinoma of the lung

Hypercalcemia: squamous cell carcinoma of the lung

Polycythemia (erythrocytosis): renal cell carcinoma

Venous thrombosis: pancreatic carcinoma

Myasthenia gravis: thymoma

222
Q

Cushing’s syndrome risk factors

A

Risk factors for Cushing’s syndrome are adrenal or pituitary tumors, long-term therapy with corticosteroids, and being female.

223
Q

epidemiology (?)

A

Incidence – the number of new cases in a specific time period in a given population

Prevalence – the number of all cases within a given population at a given time

Mortality – the number of deaths attributed to a specific population during a specific period

224
Q

most common cancer with highest mortality rate

A

Lung cancer (“lung and bronchus”)

225
Q
A

Semester 3 (19 decks)

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