Chapter 1 ( Cell ) Flashcards

1
Q

How decrease in cell size occurs ?

A

1- ubiquitin proteasome degradation of intermediate filaments of cytoskeleton
2- autophagy of cellular components

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2
Q

Causes of methemoglobinemia ?

A

Oxidant stress ex : sulfa and nitrate drugs

New borns

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3
Q

How decreased ATP causes cellular dysfunction ?

A

1- Na-K pump leads in sodium and water build up
2- Ca pump leads in Ca build up
3- Aerobic glycolysis leads in lactic acids build up and low pH which denatures proteins and precipitates DNA

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4
Q

Hall mark of reversible cellular injury ?

A

Cellular swelling resulting in
1- loss of microvilli
2- membrane blebbing
3- dissociation of ribosomes from RER and decreased protein synthesis

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5
Q

Hall mark of irreversible cellular injury ?

A

Membrane damage :
1- Plasma membrane damage : cytosolic enzymes leaking to serum and Ca leaks into cells
2- Mitochondrial membrane damage : loss pf ETC and Cytochrome C leaking to cytosol which activates apoptosis
3- Lysosomal membrane damage : hydrolytic enzyme leaks to cytosol which is activated by high Ca

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6
Q

Steps of loss of nucleus during cell death ?

A

1- Pyknosis : nuclear condensation
2- Karyorrhexis : fragmentation
3- Karyolysis : dissolution

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7
Q

Appearance of caseous necrosis ?

A

Cottage cheese like appearance

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8
Q

Examples of pathological disorders that show Sammoma bodies ?

A

1- Papillary carcinoma of the thyroid
2- Meningiomas
3- Papillary serous carcinoma of the ovary

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9
Q

Examples for apoptosis ?

A

1- endometrial shedding during menstrual cycle
2- removal of cells during embryogenesis
3- CD8+ T cell mediated killing of virally infected cells

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10
Q

Pathways of activating Caspases ?

A

1- intrinsic mitochondrial pathway :
Cellular damage , DNA damage , decreased hormonal stimulation —> ATM activation —> P53 activation —> Bcl-2 inactivation —> BAC activation —> pores in the mitochondria —> leakage of cytochrome C —> form complex with APAF-1 —> activation of cspase cascade ( caspase 9 )
2- Extrinsic pathway : FAS ligand binds FAS death receptor ( CD95 ) activating caspases
TNF binds TNF receptor activating caspases ( caspase 8 )
3- Cytotoxix CD8 T cell mediated pathway : CD8 T cells secret perforins —> creates pores in cell membrane —> Granzymes enter cells trough the pores —> activate caspases

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11
Q

Examples for pathologic generation of free radicles ?

A

1- Ionizing radiation : water hydrolyzed to hydroxyl free radicle
2- Inflammation : NADPH oxidase generates syperoxide ions
3- Metals : generates hydroxyl free iron ( Fenton reaction )
4- drugs and chemicals : metabolized by P450 system of liver generating free radicles

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12
Q

How free radicles cause cellular injury ?

A

Peroxidation of lipids

Oxidation of DNA and proteins

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13
Q

Mechanisms of free radicals elimination ?

A

1- Antioxidants as Vit A,C,E
2- Enzymes as
Superoxide dismutase ( superoxide O2’ )
Glutathione peroxidase ( different free radicles )
Catalase (H2O2)
3- Metal carrier proteins as transferrin and ceruloplasmin

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14
Q

CCL4 ?

A

Organic solvent used in dry cleaning industry
Converted to CCl3 free radicle by P450 system of liver which cases cell injury and impaired protein synthesis
Decreases apolipoproteins leads to fatty liver

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15
Q

Features of Amyloid ?

A

Beta-pleated sheet configuration

Congo red staining and apple green birefringence when viewed microscopically under polarized light

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16
Q

Primary amyloidosis ?

A

Systemic deposition of AL amyloid which is derived from immunoglobulin light chain
With plasma cell dyscrasias as MM

17
Q

Secondary amyloidosis ?

A

Systemic deposition of AA amyloid which is derived from Serum Amyloid Associated protein (SAA)

18
Q

SAA ?

A

Acute phase reactant that is increased in chronic inflammatory state , malignancy and familial mediterranean fever

19
Q

FMF mechanism ? Presentation ?

A

Autosomal recessive
Dysfunction of neutrophils
Presents by : episodes of fever and acute serosal inflammation ( can mimic appendicitis , arthritis , MI )
High SAA during attacks deposits as AA amyloid in tissues

20
Q

Clinical findings of systemic amyloidosis ?

A

1- Nephrotic syndrome
2- Restrictive cardiomyopathy or arrhythmia
3- Tongue enlargement , malabsorption , hepatosplenomegaly

21
Q

Amyloid in serum cardiac amyloidosis ? Presentation ?

A

Non mutated serum transthyretin

Usually Asymptomatic

22
Q

Amyloid in familia amyloid cardiomyopathy ? Presentation ?

A

Mutated serum transthyretin

Restrictive cardiomyopathy

23
Q

Amyloid in NIDDM ?

A

Amylin in islets of pancreas

24
Q

Amyloid in Alzheimer disease ?

A

A Beta amyloid derived from Beta-amyloid precursor protein ( Beta-APP ), gene of which present on chromosome 21

25
Q

Amyloid in dialysis associated amyloidosis ?

A

Beta2-microglobulin deposits in joints

26
Q

Amyloid in medullary carcinoma of the thyroid ?

A

Calcitonin