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Laura ESA2 - To remember > Random Things To Remember > Flashcards

Random Things To Remember Flashcards

(47 cards)

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1
Q

What are the most common sites that a tumour can metastasise to bone from?

A

Kidney, thyroid, prostate, Breast and bronchus

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2
Q

How does a carcinoma spread?

A

Fost by the lymphatics, then via the blood stream

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3
Q

How does a sarcoma spread?

A

By the blood stream

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4
Q

What do platelets produce which is proangiogenic?

A

VEGF

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5
Q

What is angiogenesis inhibited by?

A

Radiation - link - cancer.

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6
Q

What are the 2 processes of cell regeneration exploited by cancer cells?

A

Angiogenesis and contact inhibition

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7
Q

What is granulation tissue?

A

A specialised tissue only seen in areas of chronic inflammation and fibrous repair, in response to local hypoxia.

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8
Q

What are the components of granulation tissue?

A

Myo/fibroblasts
Blood vessels
Extracellular matrix

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9
Q

What does it mean if the edges of a wound are opposed?

A

They are close to each other

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10
Q

What are examples of thrombin inhibitors?

A

Anti-thrombin 3
Alpha 1 antitrypsin
Protein C/S

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11
Q

How does heparin act?

A

It is a co factor for anti thrombin 3

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12
Q

How does oral warfarin act?

A

It interferes with synthesis of vitamin K dependent clotting factors, but has a slower effect than heparin

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13
Q

Give an example of a widely used fibrinolytic therapy and how it works.

A

Streptokinase. It activates plasminogen, converting it to plasmin. Plasmin causing the breakdown of fibrin.

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14
Q

What is virchow’s triad?

A

It states that thrombosis depends on 3 things:

Changes in blood flow, changes in vessel wall and changes in blood components.

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15
Q

What are the outcomes of thrombosis?

A 
LORPE
Lysis
Organisation
Recanalisation
Propogation
Embolism
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16
Q

How do fat embolisms most commonly occur?

A

Due to fractures of long bones

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17
Q

What are the most common causes of cerebral embolisms?

A

Atrial fibrillation - stasis - thrombus.

If in left heart, can go to the brain and cause a stroke or TIA

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18
Q

What are the most common sites of blood metastasis?

A

Bone, liver, kidney, lungs, brain

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19
Q

How does increased rate of proliferation occur?

Study These Flashcards
A

By shortening the cell cycle

Conversion of quiescent cells to proliferating cells

20
Q

What is the role of checkpoints?

Study These Flashcards
A

They aim to prevent abnormalities in newly formed daughter cells.
Without checkpoints metaplasia and dysplasia would be much more common, leading to a greater likelihood of cancerous formation

21
Q

How is the cell cycle regulated?

Study These Flashcards
A

By cyclins and cyclin dependent kinases

22
Q

What stimulates the production of cyclins?

Study These Flashcards
A

Many growth factors

23
Q

What regulates the formation of CDk-cyclin complexes?

Study These Flashcards
A

CDK inhibitors. These inhibitors can be shut off by various growth factors

24
Q

What is the most commonly altered checkpoint of the cell cycle in cancer cells?

Study These Flashcards
A

The checkpoint between G1 and S

25
If the checkpoint between G1 and S is activated what happens?
The cell cycle is delayed and this triggers the DNA repair mechanisms or cell apoptosis via the p53 protein.
26
What is hyperplasia? What type of cell populations can it occur in?
Increase in cell number | Labile and stable populations
27
What is the difference between hyperplasia and neoplasia?
Hyperplasia is a normal process. Abnormal conditions but a normal response. Neoplasia is an abnormal growth of cells.
28
What is the difference between pathological and physiological hypertrophy?
Pathological is due to disease where as physiological is due to normal body function.
29
Why can hyperplasia lead to cancer?
Because it can become neoplasia or repeated mutations can accumulate
30
Give an example of pathological and physiological hypertophy.
Pathological-cardiac muscle in response to hypertension | Physiological-skeletal muscle growth or a pregnant uterus.
31
What are the 6 hallmarks of cancer?
``` ALARMS Angiogenesis Limitless division Apoptosis resistance Resistance to growth stop signals Metastasise Self sufficiency of growth signals ```
32
What are the 2 main differences between liquefactive and coagulation necrosis?
Liquefactive is caused by enzyme release and the cellular architecture is lost. Coagulative is caused by protein denaturation and the cellular architecture is maintained.
33
What type of process is apoptosis?
It is an active process. ATP is required.
34
What are the 3 stages of apoptosis?
Initiation, execution, degradation and phagocytosis
35
What are the intrinsic and extrinsic methods of initiation of apoptosis?
Intrinsic-DNA damage is detected by p53 proteins which induce apoptosis Extrinsic - death signal ps such as TRAIL and FAS bind to death receptors in the cell.
36
What are the enzymes called that mediate the cellular effects of apoptosis?
Caspases
37
What are the 2 main cell types in chronic inflammation?
Macrophages and lymphocytes
38
What is the main role of lymphocytes
They present antigens and secrete antibodies
39
When assessing differentiation what are some of the features you look T?
Nucleus to cytoplasm ratio Presence of mitotic figures Nuclear pleomorphism
40
What effect does NA have on myocardial cells?
Increases opening of Ca2+ channels. | Increases affinity of pumps in the SR so increases store of Ca2+
41
Why are individuals whose coronary blood flow is compromised treated with beta adrenoreceptor antagonists? What effect do these drugs have on the heart at rest/when the individual is excited or stressed?
Beta adrenoceptor antagonists reduce the heart rate, force of contracion and therefore the workload of the heart when the individual is excited or stressed. There is no effect at rest because the SNS is not active.
42
What type of channels do anaesthetics block?
Inactivated fast Na+ channels.
43
What are the different ECG changes seen during a STEMI ahpnd what causes each of them?
T wave inversion: Ischaemia ST segment elevation: Injury Q waves: necrosis, present after MI
44
What drugs are used to treat heart failure?
``` BAD OCC beta blockers Ace inhibitors Diuretics Organic nitrates Cardiac glycosides Ca2+ channel blockers ```
45
Why can bone fracture cause fat embolisms?
Because yellow bone marrow is fat storage so fat is released when bone marrow is broken.
46
When ACh binds to M2 receptors what is the effect?
Decreases the production of adenylyl cyclase when increases the opening of K+ channels. Slowing if cardiac pacemaker cells.
47
Normally, what is the side effect of stimulated adenylyl cyclase receptors?
Hydrolyses ATP to cAMP which stimulates production of PKA. | PKA phosphorylates many kinases.

Laura ESA2 - To remember (1 decks)

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