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Pathology-1 > Reaction to Injury: Cell Injury, Renewal & Repair > Flashcards

Reaction to Injury: Cell Injury, Renewal & Repair Flashcards

1
Q

What are 3 ways in which the cell will react to injury?

A
  1. Adaptive (maintain homeostasis)
  2. Reversible Injury
  3. Death
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2
Q

What are two ways the cells adapts to stress?

A

Hyperplasia and hypetrophy

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3
Q

What is hyperplasia? Is It resersible?

A

Increased cell number in response to increased deman. Reversible if stimulus is removed

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4
Q

What is physiologic hyperplasia?

A
  • Hormonal (lactation change of the breast)
  • Compensatory (liver regeneration, wound repair)
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5
Q

What is pathologic Hyperplasia?

A
  • excessive hormone/growth factor stimulation (Endometrial hyperplasia-monorrhagia)
  • BHP-chronic androgenic stimulatin
  • “fertile soil” for subsequent neoplastic transformation

*can progress to cancer except in BPH

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6
Q

What is hypertrophy?

A

increased cells (& organ) size

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7
Q

Example or physiologic hypertrophy

A
  • ex. skletal muscle- post mitotic, respond by hypertrophy, each sarcomere can do more work, avoids cell injury
  • uterus during fetal development
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8
Q

What are some limitation of physiologic hypertrophy?

A
  • compenstaes for increased workload up to a point
  • decompensation= cardiac failure
  • In cardiac failures:

*dehenerative myocyte changes/ fibrosis/cell death

*mechanism: insufficient vascular supply (ishemia), structural alteration of sarcomere?

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9
Q

Usually Hyperplasia and hypertrophy happen together. In what tissues is this not true?

A

Permanent tissues cannot make new cells. only undergo hypertrophy.

ex. cardiomyocytes, SKM, and nerves.

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10
Q

In increase stress the cell wil adapt, but when the stress is removed what can happen to the cells?

A

Atrophy- shrinkage of cells due to loss of substance after full development

  1. decrease in cell number (apoptosis)
  2. decrese in size (ubiquitin protosome degredation of cytoskeleton and autophagy of cellular components)
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11
Q

What is autophagy?

A

vacuoles within cells and cell components consumed and degraded by lysosome

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12
Q

What are some examples for physiologic vs pathologic atrophy?

A

physiologic:
- post partum uterus in

Pathologic:

  • decrease workload (disuse)
  • loss of innervation (SKM)
  • Decreased blood supply
  • malnutrition/aging/extrinsic compression
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13
Q

What is hypoplasia?

A

failure to develop fully

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14
Q

what is aplasia?

A

failure of primordium to develop

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15
Q

What is metaplasia?

A

**REVERSIBLE, **adaptive change in cell type in response to stress

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16
Q

Give example of metaplasia.

A

*occurs via reprogramming of stem cells

ex. squamous metaplasia in smokers’ respiratory tract 2 to chronic noxious stimuli, tougher cells, but mucociliary resistance is lost
- can progress to cancer like in Barretts metaplasia.

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17
Q

Examplain what happens in barretts metaplasis.

A

change to intestinal epithelium. adaptive change because acid reflux. protextive mucous, but get adenocarcenoma of th esophagus.

-change form squamous to columnar non ciliated mucinous epothelia

-

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18
Q

What occurs if stress exceeds cells ability to adapt?

A

injury

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19
Q

hypoxia

A

reduced o2 availability

-switch to anaerobic glycolysis (lead to lactic acid build up)

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20
Q

ishemia

A

reduced/inadequate blood flow

-will induce hypoxia

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21
Q

What are the hallmarks of reversible cell damage

A

-hallmark:

cellular swelling with h2o because Na/K atp pump no working

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22
Q

what is the damage of irreversible cell damage?

A

membrane damage:

  • cytosolic enzyme leak out
  • ca enters cell
  • cyto c leaks into cytosol= apoptosis
  • lysomome membrane damage will leak hydrolytic enzymes into cytosol, which are activated by high calcium
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23
Q

What are some causes of hypoxia?

A

ishemia, hypoemia, and decrease o2 carrying capacity in blood

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24
Q

What are some causes of ishemia?

A
  • obstruction
  • hypotension (blood loss, sepsis, blocks nutrient dilivery, no ox phos or glycosysis)
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25
Q

Which condition famages tissue faster ishemia or hypoxia?

A

ishemia

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26
Q

What are two pathways in cell death?

A
  1. Necrosis: (murder)
  2. Apoptosis (cell suicide)
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27
Q

necrosis:

A

follows from irreversible ingury

always pathologic

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28
Q

apoptosis:

A

preprgrammed cell death

normal part of development

removing ‘bad’ cells (immunity, cancer)

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29
Q

What is the hallmark of cell death? mechanism?

A

loss of nucleus

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30
Q

what are the nuclear chages in necrosis?

A
  1. pyknosis- nucleus shrinks, raisin like
  2. karyorrheis- breaks into pieces
  3. karyolysis- used as building blocks, loss of chromatin’s basophilia
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31
Q

Morphology of necrosis

A
  • results from denaturation of cell proteins
  • Eosinophilia due to loss of chromatin, RNA (-charged PO4’s bind hematoxylin, acidosis neutralizes, thse so loss of blue staining)
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32
Q

Coagulative necrosis

A
  • preservation of the outline of cells (everything denatured, including all the “-ases”
  • loss of basophilia
  • characteristic of hypoxic death (except brain)
33
Q

Liquefactive necrosis

A
  • complete digestion of dead cells into a gelatinous mass
  • seen in bacterial/fungal infections
  • if associated with acute inflam response: pus
34
Q

Coagulative vs liquefactive necrosis

A
35
Q

gangrenous necrosis

A
  • not technically subtype of necrosis
  • used in context of extremities sans blood supply
  • subdivided into dry and wet gangrene
36
Q

What is dry gangrene

A

coagulative necrosis

37
Q

what is wet grangrene

A

dry + bacteria infection; coag + liquefactive

38
Q

Casesour necrosis

A
  • found in TB, fungal infections
  • refers to chessy gross appearnce
  • distinct foci composed of necrotic core surrounded by granulomatous inflamm.
39
Q

Fat necrosis

A
  • technically no a subtype of necrosis
  • localized fat destruction due to acute pancreatitis (activated enzymes autodigest membrans; fatty acids + Ca2+= chalky deposits
  • also seen in traumatic injury to breast tissue
40
Q

Apoptosis

A

intentional programmed cell death

  • thightly regulated
  • cell die from within, fragments, membrane stays intact
  • no inflammatory response
  • eliminates unwanted, potentially harmful, or irreversibly damaged cells
41
Q

What are the key mediators in apoptosis? What is their fxn?

A

capsaes, activate proteases (break down cytoskeleton), also activate endonucleus (break down DNA)

42
Q

How are capsases activated?

A
  1. intrinsic mito pathway: cytochrome c
  2. extrinsic receptor ligand pathway: FAS ligand
  3. cyto CD8+ T cells–>perforin and granzymes
43
Q

What can alter homeostasis?

A
  • vessel wall intergrity/endo fxn
  • intravascular P
  • intravascular osmolarity
  • balance of pro and anti-clotting mechanisms
44
Q

Edema

A

excessive wayer in the interstitial space

synonyms: hdrothorax, hydroperitoneum (AKA ascities), anascrca

45
Q

Inflammatory edema

A

increases vascular permeability

-lead to protein rish fluid= EXUDATE

46
Q

non inflammatory edema

A

due to imbalances in hydrostatic and oncotic pressures

-leads to watery fluid=TRANSUDATE

47
Q

What are some things that lead to non-inflammatory edema?

A
  1. increaed hydrostatic presure (CHF/DVT)
  2. Decreased plasma oncotic P (nephrotic syndrome, cirrhosis)
  3. Lymphatic obstruction (s/p mastectomy)
  4. Sodium retention (renal insufficiency)
48
Q

Congestion and Hyperemia:

A

overfilling of small vascular spaces in a particular tissue

49
Q

Hyperemia

A

active process due to arterial dilation, increased inflow

-tissue is red (arterial)

50
Q

Congestion

A

passive, impaired vebous outflow

  • can be systemic (as in CHF), or local (venous obstruction)
  • tissue is blue (venous)
51
Q

What happens in chronic passive congestion in CHF

A

statis of deoxygenated blood (congestion) leads to hypoxia and cell death

outcome: centrilobular coagulative liver necrosis

clinicopathological correlate: the “nutmeg” liver

52
Q

Hemorrhage

A

extravasation of bloow due to rupture of blood vessels

  • in body cavities (hemoperitoneum, hemopericadium, hemothorax, hemarthrosis, etc. )
53
Q

hematoma

A

bleeding within a tissue (range form bruises to fatal)

54
Q

petechiae

A

(1-2mm)- secondary to low plately counts or fxn

55
Q

purpura

A

(3-10mm)- secondary to trauma, vaculitis

56
Q

Ecchymoses

A

(>1-2cm)- secondary to trauma

-color changes over time. Hb breakdown: Red-Blue-Green, Brown-Yellow

57
Q

What are some consequences of hemorrhage?

A

tissue destruction

jaundice (secondary to hemoglobin breakdown)

anemia

shock

death

58
Q

Thrombosis-

A

-inappropriate, pathologic clotthing of blood

59
Q

What are some risk factors for thrombosis?

A
  1. endothelia injury (most impt)- converts endothelium to prothrombotic state
  2. stasis (or turbulent blood)- anything that alters hemodynamics stresses can affect endothelial cell function
  3. Hypercoagulability- can still have thrombosis w/o endothelial disruption, “injury” can lead to imbalances in coagulation states
60
Q

Altered blood flow in thrombosis

A

turbulent (non-laminar) blood flow or stais- injuries/activates endothelium

61
Q

What are the results of turbulent blood flow or statis in thrombosis?

A
  1. allows platelets access to vessel wall
  2. prevents dilution of activated clotting factors
  3. blocks influx of clotting inhibitors
  4. promote endothelial activation, resulting in local thrombosis, leukocyte adhesion, etc .
62
Q

Turbulent flow contributes to what pathologies?

A

-thrmbosis in coronary arteries, aneurysms, post AMI endocardium, valve disease

63
Q

Hyperviscosity syndromes, and SS anemia gives rise to?

A

stasis

64
Q

Thrombosis- Hypercoagulable states

A
  • less common but sitll import
  • any alteration of the coafulation pathways that predispose to thrombosis
65
Q

What are some Primary (genetic) causes that predispose to thrombosis?

A
  1. factor V leiden Q506R (2-10% caucasians, but carrier freq= 60% in pt w/ DTV)(resistant to protein c, leads to uncheck coagulation)
  2. prothrombin G20210A- 3x risk of DVT
  3. hyperhomocysteinemia- thrombosis AND atherosclerosis
66
Q

What are some axuired hyperoagulable states?

A
  1. prolonged bedrest
  2. AMI
  3. atrial fib
  4. tissue damage
  5. cancer
  6. heparin induced thrmbocytopenia- pts develop Abs that activate platelets, thombosis. RX lovenox
  7. antiphopholipd syndrom- anti cardiolipin Abs causes multiple thrombi, miscarriages, valve vegetations
67
Q

Arterial Thrombosis

A

caused by thrombogenix atherosclerotic plaques (can also emboli to any organ)

also occur akinetic segments of heart post-MI (mural thrombi)

68
Q

Venous Thrombosis

A

vast majority occur in superficial (saphenous)/deep veins of leg

69
Q

Superficial venous thrombosis

A

congestion, pain, tenderness, rarely embolize

-predispose to cellulitis, varicose ulcer

(symptomatic, not too dangerous)

70
Q

Deep (femoral/popliteal/iliac)

at least half are asymptomatic

-risk of EMBOLIZATION!

A
71
Q

What are the fates of thrombi?

A
  • propagation, with vessel obstruciton
  • embolization (dislodge and migrate)
  • dissolution (only for young thrombi)
  • organizatoin/recanalization (blood flow will force new channels through thrombus)
72
Q

embolism

A

intravascular solid/liquid/gas that is carried a distance from its origin

73
Q

What is the most common type of thromboemboli? And other examples?

A

-thromboemboli

other types:

  • fat or bone marrow (trauma)
  • air (diving accidents)
  • tumore fragments
  • amniotic fluid
74
Q

Pulmonary Embolism

A
  • 60-80% clinically silen
  • 200,000 death/yr US
  • 95% from DVT above the knee
  • often multiple/serial
  • where it embolizes depends on size
  • saddle embolus: acute R. heart failure
  • If ASD/VSD, ‘paradoxical emboli’
75
Q

Infarction:

A

area of ishemic necrosis secondary to (mostly arterial) vascular occlusion

  • 99% infarcts are secondary to arterial thrombosis or embolization
  • rare causes- vasospasm, extrinsic compression by tumor, edema, torsion
76
Q

Red (hemorrhagic) infarcts

A
  • venous occlusion
  • loose tissue w/ space for hemorrhage
  • dual blood supplies (lung)
77
Q

white (anemic infarcts)

A

-solid end-organs

78
Q

Systemic embolism

A

usually due to thrmboembolus most common in the left heart–> travel down to systemic circulation to occlude flow to organs, most commonly lower extremities.

Pathology-1 (5 decks)

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