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Step 1 > Pathology- Growth, Celluar injury, Cell death > Flashcards

Pathology- Growth, Celluar injury, Cell death Flashcards

0
Q

Hyperplasia

A

Increase in cell number; involves production of new cells from stem cells

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1
Q

Hypertrophy

A

Increase in cell size; involves gene activation, protein synthesis, and organelle production.

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2
Q

What is the clinical significance of hyperplasia?

A

Hyperplasia can progress to dysplasia and eventually cancer

EXCEPTION: BPH–> not associated with increased risk of cancer

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3
Q

What is the mechanism of atrophy?

A
  1. Decrease in cell number- apoptosis
  2. Decrease in cell size- ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular contents
    - ubiquitin-proteosome: ubiquitin tagged on intermediate filaments & proteosome destroys
    - autophagy: vacuoles of cellular contents fuse with lysosomes
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4
Q

Metaplasia

A

: A change in stress is met with a change in cell type that is better able to handle new stress

  • occurs via a reprogramming of stem cells to new cell type
  • REVERSIBLE
  • If persistent can progress to dysplasia and eventually cancer
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5
Q

Barrett’s esophagus is a classic example of what? Explain.

A

Metaplasia; esophageal stratified squamous epithelium changes to stomach simple columnar with goblet cels

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6
Q

What is the significance of apocrine metaplasia?

A

Apocrine metaplasia is seen in fibrocystic changes of the breast but DOES NOT have an increased risk of cancer!

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7
Q

What is the significance of vitamin A?

A

Vitamin A has several functions:

  1. Important in immune cell maturation –> PML
  2. Vitamin A deficiency (VAD) can be secondary to iron deficiency; iron is necessary ti uptake vitamin A
  3. Vitamin A is necessary for maintenance of specialized epithelia = so if VAD can develop metaplasia of those epithelium
    - Conjunctiva: thin squamous epithelium maintained by vit. A; if VAD = metaplasia to stratified keratinized squamous epithelium called Keratomalacia
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8
Q

How is myositis ossificans and example of metaplasia?

A

: myositis ossificans usually occurs after skeletal muscle injury/trauma
-in the healing process connective tissue within the muscle undergoes metaplasia to bone

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9
Q

Aplasia

A

: failure of growth during embryogenesis resulting in no organ/structure

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10
Q

Hypoplasia

A

decreases in cell production during embryogenesis resulting in smaller organs

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11
Q

Dysplasia

A

: disordered cell growth; loss of cellular orientation, shape, and size

  • often refers to proliferation of precancerous cells
  • often arises in the setting of long-standing hyperplasia or metaplasia
  • REVERSIBLE
  • can progress to carcinoma
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12
Q

Hypoxia

A

Low delivery of oxygen to tissue

-causes of hypoxia include: ischemia, hypoxemia, and decreased oxygen carrying capacity of the blood.

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13
Q

Ischemia

A

:decreased flow of blood through an organ

-Arises in (1) decreased arterial perfusion, (2) decreased venous drainage, (3) shock= hypotension

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14
Q

Hypoxemia

A

: a low partial pressure of oxygen in the blood

-Arises with (1) high altitude, (2) hypoventilation, (3) diffusion defect, (4) V/Q mismatch

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15
Q

What is the process of reversible cellular injury?

A

: Hypoxia = impairs oxidative phosphorylation= decreased ATP

  • low ATP –> Na/K pump and Ca2+ pump failure
  • retained Na+ and water follows= cellular swelling –> loss of microvilli, membrane blebbing, ribosomal RER detachment (decreased protein synthesis)
  • increased cytosolic Ca2+–> can activate harmful enzymes
  • switch to anaerobic respiration = lactic acid = decreased pH –> denature proteins and DNA
  • REVERSED WITH OXYGEN
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16
Q

What is the process of irreversible cellular injury?

A

: hallmark is membrane damage

  • Plasma membrane damage: cytosolic enzymes leak into ECF, additional Ca2+ leaks into cell
  • Mitochondrial membrane: loss of electron transport chain, cytochrome c leaks into cytosol –>apoptosis
  • lysosome membrane: hydrolytic enzymes leak into cytosol and in turn activated by Ca2+
  • end result is cell death
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17
Q

Necrosis

A

:aka cellular murder! Never physiologic, always caused by exogenous injury/underlying pathologic process, followed by acute inflammation

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18
Q

What morphologic changes constitute cell death?

A

:Loss of the cell nucleus!

  1. Pyknosis: nuclear condensation
  2. Karyorrhexis: nuclear fragmentation
  3. Karyolysis: dissolution (disappear) as DNAases and RNAases degrade chromatin
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19
Q

Coagulative necrosis

A

: cell shape and organ structure are preserved
-proteins denature and coagulate preserving cellular architecture but nucleus disappears, very eosinophilic
- Characteristic of heart, kidney and liver infarction but can occur in any organ EXCEPT BRAIN
-

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20
Q

Pale Infarct

A

occur in solid tissues with a single blood supply (heart, kidney, spleen)
-infarcted is often wedge-shaped

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21
Q

Red Infarction

A

occur in loose tissues with multiple blood supplies (liver, lungs, intestine)
-result of reperfusion

22
Q

Liquefactive necrosis

A

: necrotic tissue that becomes liquefied; enzymatic lysis of cells and proteins

  • Brain: enzymes from microglial cells
  • abscess: enzymes from neutrophils
  • pancreatitis: pancreatic enzymes liquefy parenchyma
23
Q

Gangrenous necrosis

A

: Coagulative necrosis that resembles mummified tissue; common in limbs (DM patients) and GI tract

  • dry gangrene: ischemic coagulative
  • wet gangrene: superimposed infection of dead tissue, liquefactive necrosis ensues
24
Q

Caseous necrosis

A

:soft friable necrotic tissue, cottage-cheese like appearance. combination of coagulative necrosis and liquefactive necrosis
-characteristic of granulomatous inflammation (TB) or fungal infection

25
Q

Fat necrosis

A

:necrotic adipose tissue with chalky white appearance d/t deposition of calcium
-Characteristic of pancreatitis (saponification) and breast (trauma)
Recall: Saponification –> pancreatic enzymes released including lipase = degrade surrounding fat cells –> triglycerides + Ca2+ = saponification (dystrophic calcification)

26
Q

Fibrinoid necrosis

A

:necrotic damage to blood vessel wall

  • leaking of proteins including fibrin into blood vessel wall = bright pink staining of the wall
  • characteristic of malignant hypertension and vasculitis
27
Q

Apoptosis

A

Programmed cell death; ATP dependent

  • Characterized by pyknosis, membrane blebbing, karyorrhexis, and formation of apoptotic bodies that are then phagocytosed.
  • dying cell shrinkage leads to more eosinophilic cytoplasm
28
Q

DNA laddering

A

sensitive indicator of apoptosis; during karyorrhexis endonucleases cleave at internucleosomal regions = 180 bp fragments

29
Q

What is the mechanism of cell death in radiation therapy?

A

Causes apoptosis in tumor and surrounding tissue via hydroxyl free radial formation and dsDNA breakage
-note: rapidly dividing cells are susceptible to radiation therapy (skin, GI tract)

30
Q

Caspases

A

:mediate apoptosis; present in the cytoplasm

  1. activate proteases–> breakdown cytoskeleton
  2. activate endonucleases–> break down DNA
31
Q

Intrinsic mitochondrial pathway

A

:activated in cellular injury; DNA damage, or decreased hormonal stimulation

  • BAX & BAK = pro-apoptoic proteins; inactivate Bcl-2
  • Bcl-2= anti-apoptotic protein
  • Bcl-2 normally binds to Apaf-1 which prevents the release of cytochrome c from mitochondrial matrix
  • when Bcl-2 inactivated in apoptosis Apaf stimulates the release of cytochrome c
32
Q

What is the consequence of over-expression of Bcl-2?

A

Over-expression of Bcl-2 leads to over inhibition of Apaf-1 = decreases caspase activation = tumorogenesis
-Ex. follicular lymphoma

33
Q

Extrinsic apoptotic pathways

A
  1. FAS-FAS ligand: FAS ligand binds to FAS receptor (CD95) on target cell
    - binding causes multiple FAS molecules to come together forming a death domain + FADD
    - FADD activates caspases
    - necessary in thymic negative selection; CTLs can express Fas ligand
  2. Immune CTL release of perforin and granzyme B = activation of caspases
  3. TNF (tumor necrosis factor) binds TNF receptor and activates caspases
34
Q

What is the significance of defective FAS-FAS ligand interactions?

A

basis for autoimmune disorders

pg 220 FA

35
Q

How do free radicals cause damage?

A
  1. peroxidation of lipids in cellular membrane

2. oxidation of protein and DNA = protein modification & DNA damage

36
Q

Name the antioxidants.

A

Vitamin A,C, E & glutathione

37
Q

What enzymes eliminate free radicals?

A 
Superoxide dismutase (in mito): superoxide --> H2O2
Catalase (in peroxisomes): H2O2 --> O2 + H2O
Glutathione peroxidase (in mito): 2GSH + free radical --> Gs-SG and H2O
38
Q

How are transitional metals kept from creating free radicals?

A

carrier proteins - eg. transferrin and ceruloplasmin

39
Q

Pathologic generation of free radicals

A
  1. Ionizing radiation: water hydrolyzed to OH (most damaging free radical)
  2. Inflammation: NADPH oxidase generates superoxide = respiratory burst
  3. Transition metals: Fe2+ and Cu2+ (hemocromatosis & Wilson’s disease); fenton rxn
  4. Drugs/chemicals - acetaminophen overdose
40
Q

Carbon Tetrachloride (CCl4)

A

:solvent in dry cleaning industry
CCl4 converted to CCl3 free radical in p450 system in liver = reversible cell damage –> RER swelling and ribosomal dissociation = decrease in apolipoproteins
- decrease in apolipoproteins = fatty liver change

41
Q

How is damage mediated in reperfusion injury?

A

: return of blood also brings oxygen –> free radical generation which further damages tissue

  • seen esp after thrombolytic therapy
  • in cardiac injury this is why there is continued increase in cardiac enzymes
42
Q

Basic characteristics of amyloidosis

A

: amyloid is a misfolded protein that deposits in extracellular space = damage tissues

  • caused by multiple proteins but all; (1) B-pleated sheet configuration, (2) stain congo red, and (3) show apple green birefringence under polarized light
  • diagnosis requires biopsy that shows microscopic features
  • damaged organs must be transplanted, amyloid cannot be removed
43
Q

Primary amyloidosis

A

:deposition of AL in tissues; AL is derived from Ig light chains
- associated with plasma cell disorder or multiple myeloma

44
Q

Secondary amyloidosis

A

:deposition of AA (amyloid A )derived from SAA in multiple tissues
-SAA is an acute phase reactant so secondary amyloidosis seen in states of chronic inflammation: IBD, spondyloarthropathy, RA, SLE

45
Q

What organs tend to be affected in systemic amyloidosis? What are the manifestations?

A

Primary and secondary amyloidosis = systemic amyloidosis

  • Kidney (most commonly effected): nephrotic syndrome
  • heart: restrictive cardiomyopathy or arrhythmia
  • GI: tongue enlargement, malabsorption, hepatosplenomegaly
  • Brain: neuropathy
46
Q

Familial Mediterranean Fever

A

:d/t dysfunction of neutrophils = inflammation w/o infection

  • autosomal recessive
  • presents as episodes of fever and acute serosal inflammation (can mimic appendicitis, arthritis, or myocardial infarction)
47
Q

Senile cardiac amyloidosis

A

: non-mutated/WT serum transthyretin deposits in heart

-usually asymptomatic; slow progression of cardiac dysfunction

48
Q

Familial amyloid cardiomyopathy

A

:mutated serum transthyretin in heart –> restrictive cardiomyopathy and eventual heart failure

49
Q

Where do you expect to find amyloid deposition in DM II patients>

A

: amylin deposition in pancreatic islets

-increased insulin production secondary to insulin resistance–> amylin derived from insulin

50
Q

What kind of amyloid is seen in Alzheimer’s disease?

A

: ABeta amyloid derived from Beta-amyloid precursor protein; forms amyloid plaques

51
Q

What is the significance of Beta-amyloid precursor protein being on chromosome 21?

A

Most individuals with Down syndrome (trisomy 21) develop alzheimers by age 21.

52
Q

Where do you expect to see amyloid deposition in ESRD patients or patients on dialysis?

A

: B2-microglobulin deposits in joints

-B2-microglobulin (MHC I) not filtered well from the blood

53
Q

“Tumor cells in an amyloid background” after fine needle aspiration of the thyroid?

A

Medullary carcinoma; c-cells of tumor produce calcitonin; calcitonin deposits as amyloid

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