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Pathology 1 > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

Pathogenesis?

A

Developing a disease

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2
Q

Cellular response to injury depends

A

on the type, the duration and the severity of the injury

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3
Q

Consequences depend on

A

the type, the condition and the adaptability of the cell

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4
Q

The most important attack points in the cell:

A

plasma membrane, aerobic respiration, protein synthesis, genome

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5
Q

What follows the functional changes of a damaged cell?

A

Morphological changes

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6
Q

What kind of tissue or damage can a cell undergo?

A

Causes:

  1. Physical agents (mechanic, irradiation, electric, burn, thermic etc.)
  2. Chemical agents (toxins, drugs, bacterial toxins)
  3. Biological agents (microbes)
  4. Genetic defects
  5. Nutritional effects (qualitative/ quantitative malnutrition)
  6. Oxigen and nutrition deficiency (ischemia, hypoxia)
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7
Q

Difference between ischemia and hypoxia?

A

Ischemia: deficient blood supply
Hypoxia: deficient oxygen supply
Ischemia leads to nutrition deficiency and of course oxygen deficiency
Then again anaemia can reduce the oxygen transport by the blood and be a reasons as well

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8
Q

what biological function is turn off in ischemia?

A

Aerobic function is turned off and glycolysis/anaerobic function are turned on (2 ATP instead of 34 ATP per glucose)

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9
Q

What can we see in necrotic cells?

A

Lipids and fatty acid release leading to calcification of necrotic cells

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10
Q

Difference between reversible and irreversible injury

A

The reperfusion won’t aid

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11
Q

Reperfusion injury

A

ROS are produced during hypoxia that then destroy more tissue

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12
Q

Necrosis

A

Pathological, irreversible cell or tissue death in a living organism

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13
Q

Morphology of necrosis

A

Swelling: Transport mechanisms that require ATP are not working as intended and the build up of ions lead to increased water uptake
Eosinphilic: more acidic compounds are created e.g. lactate, the mitochondria swell and break leaking lysosomes that break down other parts of the cell leading to neutral and eventual acidic pH in the cytoplasm staining eosine
The ER also swell leading to removal of membranes and clumping of chromatin

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14
Q

Karyorrhexis

A

Fragmentation of nucleus

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15
Q

Pyknosis

A

Shrinkage of nucleus

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16
Q

Karyolysis

A

lysis of nucleus

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17
Q

Irreversible signs

A

Autolysis, heterolysis, and karyolysis cause by lysosome enzymes

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18
Q

Reversible damage

A

The nucleus is swollen but still present.

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19
Q

Necrosis at the level of an organ

A

Infraction

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20
Q

Coagulative necrosis

A

See a yellow wedge area in e.g. spleen and kidney surrounded by a hyperaemic are due to dilated capillaries. The yellow are neutrophil granulocytes.
Also firm and dry.

21
Q

Congestion

A

Reduced outflow leading to hemorrhagic infraction

22
Q

Double blood supply and infraction

A

Double blood supply can save the organ, but if not, the area will be red rather than yellow. Lungs and Bowels have double blood supply e.g.

23
Q

Liquefactive necrosis

A

Release of enzymes liquifying the organ e.g. brain and pancreas.

24
Q

Different stroke mechanisms

A

Infraction and aneurism

25
Q

Abscess

A

Typical bacterial infection leading to accumulation of neutrophils that then leave an empty cyst e.g. liver

26
Q

What forms the brown coloured inside macrophages?

A

breakdown of haemoglobin to haemosiderin

27
Q

Caseating necrosis

A

Granular resembles cheese, don’t see the border of the destructed tissue but you see T cells and other inflammatory cells around the area

28
Q

Fat necrosis

A

Damage to organs containing a lot of fat, acute pancreatitis, see tiny soap like lesions with blurred borders

29
Q

Fibrinoid necrosis

A

Necrosis of the vessel wall insudated plasma proteins into the vessel wall

30
Q

Apoptosis

A

Programmed cell death occurring in normal or pathological individual cells and is regulated by pro and anti apoptotic proteins

31
Q

2 pathways:

A
  • Intrinsic (mitochondrial) pathway– Bcl-2 family proteins

* Extrinsic (death-receptor) pathway– Fas and Fas-L interactions

32
Q

Morphology of apoptosis

A 
Cytoplasmic eosinophilic 
condensation of chromatin 
Karyorrhexis
apoptotic bodies 
Phagocytosis with inflammatory response
33
Q

Adaptation of cellular growth and differentiation

A

atrophy
hypertrophy
hyperplasia
metaplasia

34
Q

Atrophy

A

pathological or physiological cellular/organ shrinkage

35
Q

Physiological atrophy

A

removal of embryonic structures e.g thyroglossal duct and thymus

36
Q

Pathological atrophy

A

ischemia./hypoxia leading to renal atrophy. Short time reversible, longer leads to replacement with fat and connective tissue

37
Q

Hypertrophy

A

Enlargement of an organ or tissue due to increase in cell size
e.g. heart and skeletal muscle

38
Q

physiological atrophy

A

Working out, uterus enlargement

39
Q

Pathological hypertrophy

A

enlargement of heart due to chronic hypertension

40
Q

Hyperplasia

A

Enlargement of an organ or tissue due to increase in cell number

41
Q

Physiological hyperplasia

A

uterus during pregnancy (both hyperplasia and hypertrophy)

42
Q

Pathological hyperplasia

A

imbalance of hormones, inflammation, or following surgical resection e.g. adrenal cortex

43
Q

Metaplasia

A

Adaptive process of a tissue characterised by transformation to another type of matured tissue. e.g. bronchial squamous metaplasia due to chronic irritation of the tissue by smoking

44
Q

Intracellular accumulation

A

abnormal synthesis/metabolism leads to more product, accumulation of exogenous substances, pigments. E.g. the metabolism isn’t enough and the overload causes damage.
e.g. Excess triglycerides in the liver and inhibition of fatty acid oxidation
Alpha 1 antitrypsin deficiency
accumulation of Tau protein in Alzheimer’s disease, glycogen storage disease in diabetes mellitus

45
Q

Pigments

A

Anthracosis (exogenous pigments), Tattoos

Hemosiderin (endogenous pigments)

46
Q

Amyloidosis

A

Abnormal accumulation of specific extracellular proteins causing firmness, enlargement and malfunction of the involved organs
associated with chronic and hereditary diseases
can be due to abnormal folding of proteins

47
Q

Amyloid material

A

Fibril proteins that bind to proteoglycans glycosaminoglycan and plasma protein diagnosed with Congo red staining

48
Q

Systemic amyloidosis

A 
chronic inflammation (reactive systemic amyloidosis)
hemodialysis
49
Q

localised amyloidosis

A

Alzheimer’s diseases, atrial, endocrine amyloid in medullar carcinoma or type 2 diabetes

Pathology 1 (2 decks)

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