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SMART 2 > Pathology > Flashcards

Pathology Flashcards

1
Q

ATP dependent program cell death

A

Apoptosis

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2
Q

What enzyme is involved in both Intrinsic and Extrinsic pathways of apoptosis

A

Caspases

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3
Q

What happens to the cell membrane during apoptosis

A

Intact without significant inflammation

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4
Q

What is sensitive indicator of apoptosis

A

DNA laddering

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5
Q

What is DNA laddering

A

Fragments in multiples of 180bp

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6
Q

What regulates the Intrinsic pathway

A

Bcl-2 family proteins

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7
Q

Which proteins are the PRO-apoptotic proteins

A

BAX and BAK

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8
Q

What are the ANTI-apoptotic proteins

A

Bcl-2 and Bcl-x

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9
Q

Which anti-apoptotic protein keeps the mitochondrial outer membranes impermeable preventing CYTOCHROME C release from the inner mitochondrial matrix

A

Bcl-2

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10
Q

Over expression of Bcl-2 can lead to

A

Follicular lymphoma ( t[14;18] )

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11
Q

What is involved in the Extrinsic pathway

A
  1. Ligand receptor interactions

2. Cytotoxic CD8+ T-cell mediated (Immune cell)

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12
Q

What happens in Ligand receptor interactions

A

FasL bind to Fas [CD95 death receptor] on target cell activating caspases or TNF-alpha binding to its receptor

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13
Q

What happens in Cytotoxic CD8+ T cell mediated (Immune cell) pathway

A

Cytotoxic T-cell release of perforin creates pores and Granzyme B–> activate caspases

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14
Q

Autoimmune Lymphoproliferative syndrome is caused by

A

Defective Fas-FasL interactions

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15
Q

The histology of this necrosis has cell outline preserved but NO nuclei and increased cytoplasmic binding to Eosin dye

A

Coagulative necrosis

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16
Q

Where can’t coagulative necrosis occur

A

Brain

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17
Q

What necrosis is seen in bacteria abscesses and BRAIN infarct

A

Liquefactive necrosis

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18
Q

Fragmented cells and debris surrounded by lymphocytes and macrophages

A

Caseous Necrosis

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19
Q

What causes Fat necrosis

A

Damaged cells release LIPASE to break down triglyceride liberating Fatty acids to bind calcium—-> SAPONIFICATION

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20
Q

How does saponification appear on H&E

A

Dark blue

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21
Q

Necrosis which causes vessels walls to be THICK and PINK (type 3 HSR)

A

Fibrinoid

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22
Q

Liquefactive superimposed on coagulative

A

Wet Gangrenous

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23
Q

What infarct occurs in venous occlusion and tissues with multiple blood supply

A

Red infarct

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24
Q

Examples of tissue with red infarct

A

Liver, Intestine, Testes, reperfusion

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25
Q

What is the cause of Reperfusion injury

A

Free Radicals

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26
Q

Where does Pale (anemic) infarcts occur

A

Solid Organs with single blood supply (heart, kidney ad spleen)

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27
Q

What is cells are first released during Acute inflammation

A
  1. Neutrophile
  2. Eosinophil
  3. mast cells
    * * Basophil mediated
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28
Q

What are some outcome of acute inflmmation

A
  1. Complete resolution
  2. Abscess formation
  3. or Progression to chronic inflammation
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29
Q

What cells are first released during chronic inflammation

A

Mononuclear cells

  1. monocytes and macrophages
  2. lymphocytes
  3. plasma cells
    * * Fibroblast mediated
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30
Q

Persistent destruction and repair associated with blood vessel proliferation and fibrosis

A

Chronic inflammation

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31
Q

Nodular collection of epithelioid macrophages and giant cells

A

Granuloma

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32
Q

Calcium deposition in abnormal tissues which tend to be localized

A

Dystrophic calcification

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33
Q

Where does Leukocyte extravasation usually occur

A

Post capillary venules

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34
Q

Which tissues CANNOT undergo hyperplasia but can only undergo hypertrophy

A

Permanent tissue (cardiac muscle, skeletal muscle and nerve)

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35
Q

In what condition can a cell undergo hyperplasia but does not increase risk of cancer

A

Benign Prostatic Hyperplasia (BPH)

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36
Q

A decrease in cell number occurs via

A

Apoptosis

37
Q

A decrease in CELL SIZE occur via

A

Ubiquitin-proteosome and Autophagy

38
Q

In ubiquitin proteosome degradation what is tagged to be destroyed

A

Intermediate Filament

39
Q

What happens in autophagy cellular components

A

involves generation of autophagic vacuoles that fuse with lysosomes

40
Q

When a change in stress on an organ cause a change in cell type.

A

Metaplasia

41
Q

Thin squamous lining of the conjunctiva undergoes metaplasia into stratified keratinizing squamous epithelium. The change is called

A

Keratomalacia

42
Q

Failure of cell production during embryogenesis

A

Aplasia

43
Q

Example of Aplasia

A

Unilateral renal agenesis

44
Q

A decrease in cell production during embryogenesis (small organ)

A

Hypoplasia

45
Q

Example of Hypoplasia is

A

Streak ovary in Turner Syndrome

46
Q

Soft and friable necrotic tissue with cottage cheese-like appearance

A

Caseous Necrosis

47
Q

Which enzyme breaks down cytoskeleton in apoptosis

A

Proteases

48
Q

Which enzyme breaks down DNA in apoptosis

A

Endonucleases

49
Q

Pathological hyperplasia leads to ….

A

Dysplasia —> Cancer

50
Q

Which hyperplasia does not increase the pt’s risk for cancer?

A

BPH (does not increase risk for prostate cancer)

51
Q

Which vitamin deficiency can result in metaplasia

A

Vitamin A

52
Q

List 5 common causes of cellular injury

A
  1. Hypoxia
  2. Inflammation
  3. Nutritional deficiency/excess
  4. Trauma
  5. Genetic mutations
53
Q

What is hypoxia?

A

Low O2 delivery to tissues (MC/impt cause of cell injury)

54
Q

What is the end result of hypoxia?

A

Lack of ATP ===> Cell injury

55
Q

List causes of hypoxia

A
  1. Ischemia
  2. Hypoxemia
  3. Decreased O2 carrying capacity
56
Q

What decreases O2 carrying capacity?

A
  1. Anemia
  2. Carbon monoxide poisoning
  3. Methemoglobinemia
57
Q

What causes hypoxemia?

A
  1. High altitude
  2. Hypoventilation
  3. Diffusion defect
  4. V/Q mismatch
58
Q

What is diffusion defect?

A

Partial alveolar pressure of O2 unable to push O2 into blood d/t thick diffusion barrier (eg interstitial pulm. fibr)

59
Q

What is V/Q mismatch?

A
  1. Blood bypass oxygenated lung (circulatory issue: R –> L shunt)
  2. Oxygenated air unable to reach lung (ventilation issue: atelectiasis)
60
Q

What causes ischemia?

A
  1. Decrease arterial perfusion
  2. Decreased venous drainage
  3. Shock
61
Q

Pt with CO poisoning would present with ……

A
  1. Cherry red appearance of skin (flushed) - classic

2. Headache (early sign of exposure)

62
Q

What is the classical finding in methemoglobinemia?

A
  1. Cyanosis

2. Chocolate colored blood

63
Q

Pt presents with cyanosis and chocolate colored blood. What is the diagnosis?

A

Methemoglobinemia

64
Q

What is the mechanism associated with methemoglobinemia?

A

Inability of iron in heme to bind to O2 d/t the fact that it is Fe3+. Fe2+ only can bind O2.

65
Q

What is the Tx for methemoglobinemia

A

IV methylene blue. (reduce Fe3+ to Fe2+)

66
Q

What are the morphological signs of cell death?

A

LOSS OF NUCLEUS via

  1. pyknosis - nuclear condensation
  2. kayorrhexis - fragmentation
  3. karyolysis - dissolution
67
Q

What is amyloid?

A

Misfolded proteins that deposit in xtracelluar space –> damage of tissues

68
Q

What are the types of systemic amyloidosis?

A

Primary & Secondary

69
Q

Systemic deposition of AL amyloid……

A

Primary systemic amyloidosis

70
Q

Systemic deposition of AA amyloid…..

A

Secondary amyloidosis

71
Q

What is AA amyloid derived from?

A

Serum amyloid associated protein (SAA)

72
Q

What is SAA (serum amyloid assoc protein)?

A

It is an acute phase reactant.

73
Q

When is SAA increased?

A
  1. Chronic inflammatory states
  2. Malignancy
  3. Familial Mediterranean Fever (FMF)
74
Q

What is Familial Mediterranean Fever (FMF)?

A
  1. Dysfunction of neutrophils (Autosomal Recessive) in a person of Mediterranean origin
75
Q

What is the clinical presentation of FMF?

A
  1. Episodes of fever (recurring fever)

2. acute serosal inflammation

76
Q

Who is normally affected by FMF?

A

Persons of Mediterranean descent

77
Q

What illnesses does FMF mimic?

A
  1. Appendicitis
  2. Arthritis
  3. MI
78
Q

What are the clinical findings of systemic amyloidosis?

A
  1. Nephrotic syndrome (MC organ = Kidney)
  2. Restr. cardiomyopathy/arrhythmia
  3. Tongue enlargement
  4. Malabsorption
  5. Hepatosplenomegaly
79
Q

Amyloidosis localized to one organ…

A

Localized amyloidosis

80
Q

Cause of senile cardiac amyloidosis?

A

Deposition of non-mutated serum transthyretin in the heart

81
Q

Cause of familial amyloid cardiomyopathy?

A

Deposition of mutated serum transthyretin in the heart –> restrictive cardiomyopathy

82
Q

List examples of localized amyloidosis..

A
  1. Senile cardiac amyloidosis
  2. Familial amyloid cardiomyopathy
  3. Non-insulin dependent DM2
  4. Alzheimer dz
  5. Medullary carcinoma of the thyroid
  6. Dialysis assoc. amyloidosis
83
Q

What area in the Brain is susceptible to ischemia?

A 
Boundary areas of 
ACA/MCA - anterior
MCA/PCA - posterior 
Purkinje cells of the cerbellum
Pyramidial cells of the HIPPOCAMPUS & Neocortex
84
Q

What area in the Heart in susceptible to ischemia?

A

Sub-endocardium (LV)

85
Q

What areas of the kidney are susceptible to ischemia?

A

Straight segment of the proximal tubule (medulla)

Thick ascending limb of loop of Henle (medulla)

86
Q

What area of the liver is susceptible to ischemia?

A

Zone III = Area around central vein

87
Q

What area of the Colon is susceptible to ischemia?

A

Splenic flexure

Rectum

88
Q

What area of Stomach is susceptible to ischemia?

A

Fundus

SMART 2 (7 decks)

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