Pathology Flashcards

1
Q

causes of fluctuating cognitive function

A

subdural hematoma
cerebral abscesses
meningioma
hypertensive encephalopathy
insulinoma producing hypoglycemia
acute aortic regurgitation
alcohol intoxication

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2
Q

difference between acute and chronic inflammation

A

acute is sudden onset, short duration, and resolves over time

chronic is slow onset, long duration, stays

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3
Q

Give examples of chronic inflammation that are not a result of acute inflammation

A

TB, leprosy, Chron’s disease, sarcoidosis
mononucleosis

Chron’s disease -> inflammatory bowel disease
Sarcoidosis -> granulomas all over body because immune system overreacts

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4
Q

which is the first cell at the site of inflammation

A

neutrophils

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5
Q

what are the two cells that appear at the site of inflammation?

A

neutrophils and macrophages

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6
Q

give a few characteristics of neutrophils

A

polylobed nuclei
many lysosomes
1st cells to arrive at site of inflammation
die at the site of inflammation

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7
Q

what is the relationship between macrophages and immunity?

A

macrophages present an antigen to lymphocytes to produce antibodies and create long-term immunity

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8
Q

which cells produce antibodies

A

plasma cells

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9
Q

what is the relationship between capillary sphincters and inflammation?

A

they open so that more blood flows at the site of inflammation –> capillary bed gets more activated –> b.p drops and you get more swollen

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10
Q

how do you treat acute inflammation?

A

depending on the cause ice, aspirin, ibuprofen, antihistamines, steroid creams, antibiotics

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11
Q

how does ice decrease inflammation?

A

shuts capillary sphincters so reduces redness and stops swelling

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12
Q

how does ibuprofen reduce inflammation?

A

inhibits prostaglandin synthase

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13
Q

what is prostaglandin synthase?

A

chemical mediator for inflammation

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14
Q

how do corticosteroids reduce inflammation?

A

up-regulate inhibitors of inflammation and downregulate mediators of inflammation

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15
Q

what cells are part of the reticuloendothelial system

A

alveolar macrophages
histocytes (connective tissue phagocytes)
Kupffer cells
Mesangial cells (macrophages of the renal system - phagocytes products from glomerular b. m.)
microglial cells

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16
Q

what is normal blood flow called

A

laminar blood flow

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17
Q

what causes clot formation

A

exposure of platelets to collagen

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18
Q

how does a clot affect blood flow?

A

creates turbulent flow

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19
Q

what is a thrombus?

A

solid mass of blood constituents in the vascular system

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20
Q

what are the three causes of thrombosis?

A

change in vessel wall
change in blood flow
change in blood constituents

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21
Q

what in the cigarette damages endothelial cells

A

nicotine

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22
Q

what do healthy endothelial cells produce to be less sticky

A

NO

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23
Q

why is aspirin used for people with a risk of infarction?

A

inhibits platelet aggregation

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24
Q

what is an embolus

A

mass of material lodged in the vessel

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25
Q

what is ischemia

A

reduction in blood flow

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26
Q

what is infarction

A

reduction in blood flow which leads to subsequent cell death

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27
Q

what are the different types of emboli?

A

thrombus
cholesterol crystals
air
tumour
amniotic fluid
fat

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28
Q

what organs have 2 blood supplies and identify those blood supplies

A

lungs (pulmonary art and bronchial art) and some parts of the brain (circle of Willis)

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29
Q

what is heparin

A

an anticoagulant

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30
Q

resolution vs repair

A

resolution - tissue can regenerate
repair - tissue can’t regenerate

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31
Q

which organs can regenerate

A

Liver
GI tract lining
skin
bones
lung pneumocytes

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32
Q

Can alveoli regenerate

A

no

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33
Q

what organs don’t regenerate

A

brain
heart
spinal cord

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34
Q

1st intention healing vs 2nd intention

A

1st - brings ends together
2nd - the wound is too deep so it can’t bring the end. the tissue has to start growing again from below up and blood supply needs to be brought from both sides

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35
Q

what do you call fibrosis in the brain

A

gliosis

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36
Q

what cells regenerate

A

hepatocytes
pneumocytes
all blood cells
gut epithelium
skin epithelium
osteocytes
bone marrow

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37
Q

what process plays a massive role in growth and development

A

apoptosis and cell migration

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38
Q

what is the difference between spina bifida occulta, meningocele, and myelomeningocele

A

spina bifida –> missing a spinous process
meningocele –> meninges sticking out in a sack
myelomeningocele –> cauda equina sticks out in the meningeal sack

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39
Q

what is a cleft lip

A

a split in the upper lip or roof of the palate

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40
Q

describe the possible cardiac congenital defects

A

non-closure of:
- PATENT foramen ovale –> it raises the risk for stroke. Usually symptomless in children. Blood clots can travel from the right atrium to the left atrium and out to blood vessels of the body. If the clot blocks a blood vessel in the brain, it can cause a stroke.
- VENTRICULAR SEPTAL DEFECT –> Ventricular septal defect is a common congenital heart defect. The baby may have no symptoms and the hole can close over time as the wall continues to grow after birth. If the hole is large, too much blood will be pumped to the lungs. This can lead to heart failure.
- PATENT DUCTUS ARTERIOSUS –> The PDA lets oxygen-rich blood (blood high in oxygen) from the aorta mix with oxygen-poor blood (blood low in oxygen) in the pulmonary artery. As a result, too much blood flows into the lungs, which puts a strain on the heart and increases blood pressure in the pulmonary arteries.

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41
Q

what are the facial characteristics of a baby born with fetal alcohol syndrome

A

small eye openings
thin upper lip
smooth philtrum (no cupid’s bow above mouth - the dip)

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42
Q

what protein is in excess in Down’s syndrome

A

beta-amyloid –> gene present on chromosome 21

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43
Q

what are homeobox genes

A

genes that control cell migration

44
Q

why are children with Down’s syndrome more susceptible to bacterial infections

A

gene for

45
Q

what is the most common type of hyperplasia in adult males and where does it take place specifically

A

prostatic hyperplasia from the core of the prostate –> the core is the one that enlarges

46
Q

how does a cell decide when to apoptose

A

-when it detects too much DNA damage in the cell

47
Q

what is p53 and how can mutations of it affect cancer

A

protein in cells which detects DNA damage and triggers apoptosis

mutations in p53 lead to problems in detecting DNA damage –> growth of the cancer

48
Q

what is the pathophysiological mechanism of HIV

A

induces apoptosis in CD4 T-helper cells –> immunodeficiency

49
Q

what is the name of enzymes which trigger apoptosis

A

caspases

50
Q

Complications of artherosclerosis

A

Cerberal infarction, Carotid artheroma ,myocardial infarction, Aortic aneurysm, peripheral, vascular disease, gangrene

51
Q

What type of inflammation is caused by infectious mononucleosis and why

A

Chronic because it is caused by a virus so triggers lymphocyte response

52
Q

How do you reduce the risk of NSAID-related gastritis

A

Prescribe selective COX-2 inhibitors and ppi

53
Q

How do you reduce the risk of NSAID-related gastritis

A

Prescribe selective COX-2 inhibitors and ppi

54
Q

What are the consequences of acute inflammation

A

redness, swelling, pain, heat and loss of function

55
Q

Why does chronic inflammation lead to cancer

A

Inflammation causes cellular changes to repair damaged tissue —> increased cellular proliferation increases risk of developing mutations

Chronic infl cells also generate a lot of ROS and Nitrogen species —> increase chances of mutations

Infl cells also interfere with cell replication

56
Q

What type of arthritis is a chronic inflammatory disorder

A

Rheumatoid arthritis

57
Q

What type of arthritis is a chronic inflammatory disorder

A

Rheumatoid arthritis

58
Q

What are carcinomas and sarcomas

A

Carcinomas - Malignant cancers of epithelium
Sarcomas - Malignant cancers of connective tissue

59
Q

Where do carcinomas and sarcomas most likely spread to

A

Carcinomas spread to the lymph nodes that drain their site
In advanced stages carcinomas can also spread through blood to the bone
Sarcomas spread to blood

60
Q

Which are the most common cancers which spread to the bone

A

Breast, prostate, lung, thyroid and kidney

61
Q

Do all tumours show up on a CT scan

A

Micro metastases do not if they are under 10mm

62
Q

What is adjuvant therapy

A

Extra treatment given after surgical excision
Ex.: radiotherapy after breast lumpectomy

63
Q

What is the HER 2 receptor

A

A growth factor receptor found in some breast cancer cells which is associated with a more aggressive tumour and resistance to some kinds of chemotherapy and tamoxifen

64
Q

What type of cancer is asbestos associated with

A

Mesothelioma

65
Q

What type of cancer H. Pylori and epsine-barr associated with

A

Lymphoma

66
Q

What cancer is HPV associated with

A

Cervical cancer

67
Q

what is a carcinoma?

A

malignant cancer of epithelium

68
Q

what is a sarcoma?

A

malignant cancer of connective tissue

69
Q

What are the carcinogens for lung and skin cancer?

A

polycyclic aromatic hydrocarbons
(They result from burning coal, oil, gas, wood, garbage, and tobacco.)

70
Q

what are the carcinogens for bladder cancer and breast cancer?

A

aromatic amines
(chemicals found in industrial and manufacturing plants, tobacco smoke, commercial hair dyes, and diesel exhaust.)

71
Q

what are the carcinogens for gut cancer?

A

nitrosamines
(formed during the fermentation of various foods and tobacco and by the in vivo reaction of nitrite preservatives with amines under the acidic conditions found in the gastrointestinal tract. –> found in meat products, processed fish, cocoa, beer and other alcoholic beverages)

72
Q

what are the carcinogens for leukaemia?

A

alkylating agents –> Actual chemotherapy or radiotherapy –> can cause patients to develop leukaemia
(Alkylating agents keep the cell from reproducing (making copies of itself) by damaging its DNA. These drugs work in all phases of the cell cycle and are used to treat many different cancers, including cancers of the lung, breast, and ovary as well as leukemia, lymphoma, Hodgkin disease, multiple myeloma, and sarcoma.)

72
Q

Kaposi sarcoma viral carcinogen

A

Human Herpes virus 8
Kaposi sarcoma is a disease in which cancer cells are found in the skin or mucous membranes that line the gastrointestinal (GI) tract, from mouth to anus, including the stomach and intestines

73
Q

Hepatocellular carcinoma viral carcinogen

A

Hep B virus

73
Q

Burkitt lymphoma and Nasopharyngeal carcinoma viral carcinogens

A

Epstein Barr Virus

73
Q

Squamous cell carcinomas of the cervix, penis, anus, head and neck viral carcinogen

A

Human Papillomavirus

74
Q

Merkle cell carcinoma viral carcinogen

A

Merkle cell polyomavirus

74
Q

What cancers are associated with Human T-lymphotropic virus and
Hep C virus and what kind of viruses are they

A

Adult T-cell leukaemia
and Hepatocellular carcinoma

RNA viruses

74
Q

Which carcinogens are associated with skin cancer

A

UV and Arsenic (metal)

74
Q

Which mycotoxin is associated with hepatocellular carcinoma

A

Aflatoxin B1

mycotoxin = toxin produced by moulds and fungi in food

75
Q

What type of cancer is asbestos associated with

A

mesothelioma

76
Q

what is an adenoma?

A

benign neoplasm of glandular tissue or secretory epithelium; looks like small mushrooms with a stalk and have a smooth surface

77
Q

what are papillomas?

A

benign neoplasm with a rough surface (think of ivan’s mole on his face which he removed in russia)

are non-glandular and from non-secretory epithelium

78
Q

what is the 2 hit hypothesis

A

you already have a mutation that puts you at risk of cancer and if you get a second mutation/hit the cancer is triggered

79
Q

what are the 2 viral risk factors for lymphoma?

A

H pylori and Epstein Barr

80
Q

what are proto-oncogenes

A

genes which promote cell growth and survival and prevent apoptosis

81
Q

what are tumour suppressor genes and how are they regulated in cancer

A

these genes inhibit cell growth and proliferation and in cancer they are down-regulated

82
Q

small cell carcinoma vs non-small cell carcinoma

A

small cell –> very aggressive, loads of necrosis and rapid division

non-small cell –> no very aggressive, growth doesn’t generally outdo angiogenisis so little to no necrosis and doesn’t grow as fast.

83
Q

what is myeloma

A

plasma cell cancer –> originates from lymphoid progenitor cells

84
Q

what is a carcinoma in-situ?

A

carcinoma which hasn’t gone through BM yet

85
Q

tumour grading vs tumour staging

A

Grading –> how much the tumour cells resemble the normal tissue –> very different = high grade

Staging –> how much the tumour has spread

86
Q

explain the TNM tumour staging

A

T = tumour size, depth and spread

N = nodes –> extent of lymph node metastasis

M = metastases –> extent of spread to other parts of the body

87
Q

define carcinogenesis

A

conversion of normal cells to neoplastic cells via genetic alterations/mutations

88
Q

define oncogenesis

A

formation of benign or malignant tumours

89
Q

what is diethylstilboestrol

A

medication which was used for morning sickness but increased risk of vaginal cancer

90
Q

micro-invasive carcinoma vs invasive carcinoma

A

micro-invasive = has breached BM but can still be fully excised

invasive = got through BM and has high potential to invade rest of body

91
Q

how do cancer cells invade BM

A

They produce:
- proteases
- collagenases
- cathepsin D
- urokinase-type plasminogen activator –> protease involved in cell migration

They also have cell motility –> invade ECM

92
Q

outline the steps of metastasis

A

formation of malignant tumour
breaching of BM

INTRAVASION
breaching of lymphatic vessel or blood vessel (lymphatic vessel more easy to breach than blood vessel cuz only 1 cell layer whereas vs thick muscle layer)

Evasion of host immune defence
the tumour hides from the immune system by aggregating platelets on top of it –> can’t be detected if it hides behind platelets

travelling of tumour cells to new site

EXTRAVASION
tumour has adhesion receptors –> attaches to a place in the vessel and breaches the wall again to exit in new site

growth factors released from tumour:
- VEGF
- fibroblast growth factor

Inhibition of angiogenesis inhibitors:
- angiostatin
-endostatin
-vasculostatin

tumour growth and angiogenesis beyond 1mm

93
Q

what type of cancers invade venules easily and where do they usually metastasize

A

sarcomas easily invade venules and they can metastasize to the lungs because they travel up the vena cava to the heart through the pulmonary artery and to the lungs where they can easily get lodged in the capillaries and grow

94
Q

would you give chemotherapy to someone going into liver failure?

A

NO

95
Q

Angiogenesis inhibitors

A
  • angiostatin
    -endostatin
    -vasculostatin
96
Q

tumour definition

A

any abnormal swelling

97
Q

neoplasm definition

A

a lesion resulting from abnormal and autonomous growth of cells which persists after the initiating stimulus has been removed

98
Q

what are borderline neoplasms?

A

between benign or malignant

99
Q

what is the relationship between neoplastic cells and the stroma?

A

stroma supports the neoplastic cells –> mechanical support and nutrition : metastatic cells hijack the stroma

100
Q

Name the benign and malignant neoplasm of striated muscle

A

Rhabdomyoma and Rhabdomyosarcoma