Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

Cell response to change in homeostasis?

A

Deviation from homeostasis results in adaptation to a certain point and then injury occurs and cell death follows

Eg high blood pressure to thicker walls to pump against increased resistance to increased oxygen demand to eventual death

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

What are the two forms of cell injury?

A

Reversible and irreversible. Irreversible leads to cell death

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

What causes cell injury?

A 
Bacteria 
Hypoxia 
Radiation
Trauma 
Toxins 
Temperature changes 
Immune mechanisms 
Dietary deficiencies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is pus?

A

Collection of dead neutrophils

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

Global vs local hypoxia?

A

Global is whole body eg cardiac arrest

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

Hypoxia vs ischemia?

A

Hypoxia is oxygen deprivation whereas ischaemia is lack of blood supply

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

Causes of hypoxia?

A

Hypoxaemic= reduced absorption of O2 due to lung disease or running at altitude (arterial O2 content is low)

Anaemic= decreased ability of haemoglobin to carry O2

Histiocytic= cant use oxygen due to disabled oxidative phosphorylation enzymes like cyanide poisoning

Ichaemic= lack of blood supply

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

How does immune system damage body’s cells?

A

Hypersensitivity where host tissue injured due to overly vigorous immune reaction

Autoimmune reactions where body fails to distinguish self from non self

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

What happens in reversible hypoxia cellular injury?

A

Oxidative phosphorylation ceases, happens with cyanide poisoning also.

ATP levels drop and ATPases fail to function. Sodium, calcium and water enter cell and cause it to swell.

Glycolysis is increased and so pH decreases and nuclear chromatin clumps

Ribosomes detach from rough Er and protein synthesis ceases and results in lipid deposition and intracellular accumulations

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

What marks irreversible hypoxia damage?

A

Inability to use glycolysis.

Calcium enters cell from outside and breakdown of mitochondria and ER.

Calcium is a co factor for ATPase, phospholipase, protease and endonuclease which causes lots of damage and leads to cell death

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

What are the three free radicals of significance in cells?

A

Hydroxyl OH

O2- superoxide

H2O2 hydrogen peroxide

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

How are free radicals produced?

A

Oxidative burst of neutrophils

Radiation

Oxidative phosphorylation etc

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

Role of heat shock proteins?

A

Mend mis folded proteins due to heat. Eg unfoldases or chaperonins like ubiquitin

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

What is pyknosis?

A

Shrinkage of cell nucleus

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

Karyorrhexis?

A

Fragmentation of cell nucleus

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

Karyolysis?

A

Dissolving of nucleus

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

What do lysosomes do during cell injury?

A

Consume damage and then rupture and release contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Oncosis vs necrosis?

A

Both are definitions of cell death

Oncosis is cell death with swelling and the spectrum of changes that occur in injured cells prior to death

Necrosis in a living organism refers to the morphological changes that occur after a cell has been dead some time 12-24 hours

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

What are the four types of necrosis?

A

Coagulative

Liquefaction

Caseous

Fat necrosis

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

What causes coagulative?

A

Protein denaturation resulting in solid mass of dead cells eg ischaemia of solid organs

Liquefactive resulting from breakdown by enzymes eg ischaemia in loose tissues

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

Appearance of coagulative and liquefactive necrosis

A

Coagulative leaves the ghost outline of cells and appears white. There will be no nuclei and plenty of neutrophils

Liquefactive cells appear like blobs and pus as enzymatic digestion has occurred

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

Caseous and fat necrosis?

A

Caseous appears like cottage cheese

Fat necrosis results from damage to adipose tissue. Often seen in pancreatitis when lipases are released. Looks like candle wax

23
Q

What would an ischaemia tissue develop?

A

An infarct

24
Q

What is an infarct?

A

An area of necrosis caused by reduction in arterial blood flow (ischaemia)

Action is infarction

25
Q

What is gangrene?

A

Necrosis visible to the naked eye

26
Q

Dry vs wet gangrene?

A

Dry= coagulative (exposed to air)

Wet= modified by infection (liquefactive (bacteria))

27
Q

What is gas gangrene?

A

Wet gangrene but with bacteria that produce a gas resulting in bubbles.

Caused by anaerobic bacteria and can lead to sepsis

28
Q

What are the two most common causes of infarction?

A

Thrombosis and embolism

29
Q

Why are some infarcts red?

A

If there is bleeding into the tissue eg lung has a dual blood supply

Numerous anastomoses

Sometimes tissues partly perfused so has red colour but not enough to prevent necrosis

30
Q

How do you treat stroke?

A

First talk a CT scan of head to see if there is a bleed. If no bleed use drug to break clot and re perfuse

31
Q

Consequence of infarction?

A

Depends on blood oxygen content

Speeed of ischaemia (if slow can develop new vessels)

Tissue involved

Availability of alternative blood supply

32
Q

Implications of leaky membrane?

A

Local inflammation

Toxic effects such as arrhythmias due to disruption of resting membrane potential

High concentrations in blood can aid in diagnosis

33
Q

What is the implication of potassium leaking from cell?

A

If too high you get atrial fibrillation and tachycardia which can often result in death

34
Q

What usually kills a patient with ischaemia or infarct?

A

High potassium leakage which causes atrial fibrillation and tachycardia

35
Q

What leaks from damaged cells?

A

Potassium
Enzymes (troponin)
Myoglobin

36
Q

Implication of myoglobin leakage?

A

Caused by rhabdomyolysis. Can block renal tubules and cause renal failure

37
Q

Apoptosis?

A

Suicide as opposed to murder. DNA and proteins are broken down in a controlled manner. Lysosomes are not broken down like in necrosis. Can have a physiological role eg making glands or a pathological role eg when cells are damaged

38
Q

Why is apoptosis very important?

A

Control!

There is no inflammatory response initiated. Surrounding cells are not damaged as contents are not leaked. Instead they are destroyed by macrophages

39
Q

What are the three phases of apoptosis?

A

Initiation
Execution
Degradation and phagocytosis

40
Q

What two ways can apoptosis be triggered?

A

Either an intrinsic or extrinsic mechanism

Intrinsic= irreparable DNA damage

Extrinsic= initiated by extracellular signals to the cells that are a danger such as tumour cells and virus infected cells

41
Q

Cascades?

A

Proteins that play a key role in apoptosis

42
Q

Oncosis/necrosis vs apoptosis?

A

See grid in lecture

43
Q

Where do abnormal cellular accumulations come from?

A

Usually seen when metabolic processes dont happpen as they should

Eg water
Protein
Lipids 
Pigments 
Carbohydrates
44
Q

When does fluid accumulate in cells?

A

Hydroponic swelling

When energy suppplies cut off eg hypoxia so no oxidative phosphorylation meaning sodium and water flood in

Particular problem in brain

45
Q

What is steatosis?

A

Lipids accumulating in the cells

46
Q

When do lipids accumulate in cells?

A

Generally cholesterol. Can accumulate in macrophages (foam cells) and form atherosclerotic plaque.

Can be seen as xanthomas (white lumps around eyelids and elbows)

47
Q

When do pigments appear in cells?

A

Carbon, coal dust, soot etc inhaled and phagocytosed by alveolar macrophages

Also in tattooing consumed by macrophages and remains

48
Q

Accumulation of endogenous pigments in cells?

A

Haemosiderin which is an iron storage molecule which forms when there is excess iron

49
Q

Hereditary haemochromatosis?

A

Genetic disorder resulting in increased intestinal absorption of dietary iron.

Accumulates in skin, liver pancreas etc

Treat by bleeding to remove iron

50
Q

What accumulates in jaundice?

A

Bilirubin a breakdown product of heme

Excreted through bile but if duct blocked will accumulate in blood and get deposited in tissues

51
Q

Why do we get intracellular accumulations?

A

Abnormal metabolism

Alteration in protein folding and transport

Deficiency of critical enzymes

Inability to degrade phagocytosed particles

52
Q

Dystrophic vs metastatic calcium deposition?

A

Dystrophic is localised while metastatic is generalised

53
Q

What causes metastatic calcification?

A

Hypercalcaemia due to increased secretion of parathyroid hormone, renal failure (retention of phosphate) and destruction of bone eg cancer or immobilisation

54
Q

Which cells can liver forever?

A

Germ cells and stem cells as they have telomerase which maintains telomere length

Pathology (11 decks)

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