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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
Which condition famages tissue faster ishemia or hypoxia?
ishemia
26
What are two pathways in cell death?
1. Necrosis: (murder) 2. Apoptosis (cell suicide)
27
necrosis:
follows from irreversible ingury always pathologic
28
apoptosis:
preprgrammed cell death normal part of development removing 'bad' cells (immunity, cancer)
29
What is the hallmark of cell death? mechanism?
loss of nucleus
30
what are the nuclear chages in necrosis?
1. pyknosis- nucleus shrinks, raisin like 2. karyorrheis- breaks into pieces 3. karyolysis- used as building blocks, loss of chromatin's basophilia
31
Morphology of necrosis
- 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)
32
Coagulative necrosis
- preservation of the outline of cells (everything denatured, including all the "-ases" - loss of basophilia - characteristic of hypoxic death (except brain)
33
Liquefactive necrosis
- complete digestion of dead cells into a gelatinous mass - seen in bacterial/fungal infections - if associated with acute inflam response: pus
34
Coagulative vs liquefactive necrosis
35
gangrenous necrosis
- not technically subtype of necrosis - used in context of extremities *sans* blood supply - subdivided into dry and wet gangrene
36
What is dry gangrene
coagulative necrosis
37
what is wet grangrene
dry + bacteria infection; coag + liquefactive
38
Casesour necrosis
- found in TB, fungal infections - refers to chessy gross appearnce - distinct foci composed of necrotic core surrounded by granulomatous inflamm.
39
Fat necrosis
- 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
Apoptosis
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
What are the key mediators in apoptosis? What is their fxn?
capsaes, activate proteases (break down cytoskeleton), also activate endonucleus (break down DNA)
42
How are capsases activated?
1. intrinsic mito pathway: cytochrome c 2. extrinsic receptor ligand pathway: FAS ligand 3. cyto CD8+ T cells--\>perforin and granzymes
43
What can alter homeostasis?
- vessel wall intergrity/endo fxn - intravascular P - intravascular osmolarity - balance of pro and anti-clotting mechanisms
44
Edema
excessive wayer in the interstitial space synonyms: hdrothorax, hydroperitoneum (AKA ascities), anascrca
45
Inflammatory edema
increases vascular permeability -lead to protein rish fluid= EXUDATE
46
non inflammatory edema
due to imbalances in hydrostatic and oncotic pressures -leads to watery fluid=TRANSUDATE
47
What are some things that lead to non-inflammatory edema?
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
Congestion and Hyperemia:
overfilling of small vascular spaces in a particular tissue
49
Hyperemia
active process due to arterial dilation, increased inflow -tissue is red (arterial)
50
Congestion
passive, impaired vebous outflow - can be systemic (as in CHF), or local (venous obstruction) - tissue is blue (venous)
51
What happens in chronic passive congestion in CHF
statis of deoxygenated blood (congestion) leads to hypoxia and cell death outcome: centrilobular coagulative liver necrosis clinicopathological correlate: the "nutmeg" liver
52
Hemorrhage
extravasation of bloow due to rupture of blood vessels - in body cavities (hemoperitoneum, hemopericadium, hemothorax, hemarthrosis, etc. )
53
hematoma
bleeding within a tissue (range form bruises to fatal)
54
petechiae
(1-2mm)- secondary to low plately counts or fxn
55
purpura
(3-10mm)- secondary to trauma, vaculitis
56
Ecchymoses
(\>1-2cm)- secondary to trauma -color changes over time. Hb breakdown: Red-Blue-Green, Brown-Yellow
57
What are some consequences of hemorrhage?
tissue destruction jaundice (secondary to hemoglobin breakdown) anemia shock death
58
Thrombosis-
-inappropriate, pathologic clotthing of blood
59
What are some risk factors for thrombosis?
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
Altered blood flow in thrombosis
turbulent (non-laminar) blood flow or stais- injuries/activates endothelium
61
What are the results of turbulent blood flow or statis in thrombosis?
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
Turbulent flow contributes to what pathologies?
-thrmbosis in coronary arteries, aneurysms, post AMI endocardium, valve disease
63
Hyperviscosity syndromes, and SS anemia gives rise to?
stasis
64
Thrombosis- Hypercoagulable states
- less common but sitll import - any alteration of the coafulation pathways that predispose to thrombosis
65
What are some Primary (genetic) causes that predispose to thrombosis?
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
What are some axuired hyperoagulable states?
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
Arterial Thrombosis
caused by thrombogenix atherosclerotic plaques (can also emboli to any organ) also occur akinetic segments of heart post-MI (mural thrombi)
68
Venous Thrombosis
vast majority occur in superficial (saphenous)/deep veins of leg
69
Superficial venous thrombosis
congestion, pain, tenderness, rarely embolize -predispose to cellulitis, varicose ulcer (symptomatic, not too dangerous)
70
Deep (femoral/popliteal/iliac) at least half are asymptomatic -risk of EMBOLIZATION!
71
What are the fates of thrombi?
- propagation, with vessel obstruciton - embolization (dislodge and migrate) - dissolution (only for young thrombi) - organizatoin/recanalization (blood flow will force new channels through thrombus)
72
embolism
intravascular solid/liquid/gas that is carried a distance from its origin
73
What is the most common type of thromboemboli? And other examples?
-**thrombo**emboli other types: - fat or bone marrow (trauma) - air (diving accidents) - tumore fragments - amniotic fluid
74
Pulmonary Embolism
- 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
Infarction:
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
Red (hemorrhagic) infarcts
- venous occlusion - loose tissue w/ space for hemorrhage - dual blood supplies (lung)
77
white (anemic infarcts)
-solid end-organs
78
Systemic embolism
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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