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Pathology > Pathoma 1. Growth Adaptations > Flashcards

Pathoma 1. Growth Adaptations Flashcards

1
Q

What are the 2 permanent tissues that only undergo Hypertrophy (no hyperplasia)

A

Cardiac Myocytes, Skeletal muscle, Nerve

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2
Q

Pathologic hyperplasia can lead to dysplasia and cancer. Give 1 example and 1 exception

A

Endometrial hyperplasia leads do Ca.

BPH (Benign Prostatic hyperplasia) does not)

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3
Q

How can atrophy decrease cell size?

A

Ubiquitin Proteosome degradation of cytoskeleton
and
Autophagy of cell components (thru lysosome)

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4
Q

What is the change of epithelium in Barrett’s Esophagous?

A

Squamous to Columnar

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5
Q

Metaplasia is reversible, but can progress to dysplasia and Ca. Cite example and exception

A

Barrett’s Esophagus progresses

Apocrine Metaplasia in breast is still reversible

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6
Q

What’s the mechanism of metaplasia?

A

Reprogramming of stem cells

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7
Q

Name the metaplasia that results from Vit.A deficiency, and other conseq of this deficiency

A

Keratomalacia (bc there’s an inability to maintain conjunctiva specialized tissue)
Acute Promyelocytic leukemia (due to 15-17 translocation)
Nightblindness

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8
Q

What is a common mesenchymal tissue metaplasia?

A

Myositis ossificans (bone grows in muscle due to trauma

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9
Q

WHat is dysplasia?

A

Disorded cellular growth. ALways the pre-step of Cancer (arises after longstanding pathologic hyperplasia or metaplasia)
Ex: CIN 1, 2, 3

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10
Q

What is Aplasia? + example

A

failure of cell production during embryogenesis Ex. Unilateral renal agenesis

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11
Q

Describe Hypoplasia and example

A

decrease in cell production during embryogenesis. Ex: streak ovary in Turner’s Sme

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12
Q

What is hypoxia and the 3 mains causes:

A

Decreased O1 flow to tissues.

  1. Ischemia
  2. Hypoxemia
  3. Decreased O2 carrying capacity of blood
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13
Q

What are the 3 mais causes of ischemia?

A
  1. Atherosclerosis,
  2. Vein Blockage (budd chiari sme= thrombossis of hepatic vein, due to 1. Policytemia Vera or Lupus hypercoagulable state)
  3. Shock
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14
Q

What is Hypoxemia and Examples?

A

Low Partial pressure of O2 in Blood (PaO2<60mmHg, and SaO2<90%)

Main causes:
LOW FiO2 (P of O2 in the atm)-due to High Altitude
LOW PAO2(bc of high PACO2, when there's hypoventilation, COPD and intersticial fibrosis of lungs

All leads to hypoxemia and then to hypoxia

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15
Q

3rd cause of Hypoxia is: and give examples

A

Decreased O2-carrying capacity of blood

  1. Anemia (hemoglobin LOSS)= SaO2 stays normal.
  2. CO Poisoning (Hb DYSFUNCTION)= SaO2 is decreased bc O2 is displaced.
  3. Methemoglobinemia: iron in Heme is oxidized from Fe2+ to Fe3+, and doesn’t bind O2 anymore. LOW SaO2.
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16
Q

Describe etiology of CO poisoning and features

A

smoke from fires, exhaust, gas heaters.

Headache and cherry red appearance of skin….coma nad death

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17
Q

WHat’s the etiology of Methemoglobinemia? and features

A

Oxidant stresses (sulfa/nitrate drugs) or newborns
Cyanosis + chocolate colored blood
TTM: IV methylene blue helps reduce Fe back to 2+

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18
Q

Hypoxia impairs oxydative phosphorylation. WHat are the consequences of this.

A
  1. low ATP.= impaired Na/K Pump=Swelling. IMpaired Ca2+ pump and it stays in cell, activating enzymes. Impaired AEROBIC glycolysis
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19
Q

What is the hallmark of cell injury while it’s still reversible?

A

SWELLING. Leads to loss of microvilli, membrane blebbing.

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20
Q

What’s the hallmark of irreversible damage? and the consequences:

A

Membrane Damage.

  1. Find Ez in blood (Troponins, CPK)
  2. Damage to mitochondrial membrane (Citocrome C leaks and causes APOPTOSIS.
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21
Q

What is the mechanism of cell death?

A

LOSS OF NUCLEUS. Thru Pyknosis, karryorexis, karyolysis.

22
Q

Differ nECROSIS AND APOPTOSIS

A

Necrosis is the death of a large number of cells followed by INFLAMMATION.

Apoptosis is ATP dependent and genetically programmed. Involves single cells and causes no inflammation.

23
Q

What are the 6 types of necrosis?

A

Coagulative, Liquefactive, Gangrenous, Caseous, Fat, Fibrinoid

24
Q

Coagulative necrosis: what do u know?

A

Tissue is firm, cell structure is perfect, but nucleus disappears. Area of infarcted tissue is wedge shaped. Red infarction arises is vein colapses but not artery- like TESTICULAR TORSION.

25
Q

Liquefactive necrosis: what do u know?

A

Total structure loss. Characteristic of Brain infarction, pancreatitis, abscess

26
Q

Gangrenous necrosis: what do u know?

A

Characteristic of lower limb/GI tract.
If it involves Coagulative necrosis=DRY gangrene
If it involves Liq necrosis= WET gangrene

27
Q

Caseous necrosis: what do u know?

A

Characteristic of granulomatous infection by TB/fungus. Friable, cottage cheese appearance. Combination of coag+Liq necrosis.

28
Q

Fat necrosis: what do u know?

A

Characteristic of Trauma to Fat (breasts) + Pancreatitis mediated damage to peripancreatic fat (though this is diff. from the liq necrosis that happens in Pancreatitis. Chalky white adipose tissue, due to deposition of Ca2+.= this is SAPONIFICATION (fatty acids released by trauma/lipase join w/ Ca+) =

29
Q

What is one of the effects of Saponificaiton?

A

Dystrophic calcification= dead fat picks up Ca2+= psamoma bodies.

30
Q

What is the mechanism of Psamoma Bodies and where do we find them?

A

Tumor cells outgrow their blood supply, die and calcification occurs there.

  1. Papillary Carcinoma of Thyroid
  2. Meningioma
  3. Papillary serous carcinoma of Ovary
31
Q

Metastatic calcification

A

Hight serum Ca or P precipitates Ca into tissues

32
Q

Fibrinoid necrosis: what do u know?

A

Characteristic of Malignant HTN or Vasculitis. Necrotic damage to blood vessel wall

33
Q

What is the most important example of fibrinoid necrosis??

A

Placenta, during preeclampsia.

34
Q

Examples of Apoptosis:

A

a) Endometrial shedding during menstrual cycle
b) removal of cells during embryogenesis
c) CD8+ mediated killing during viral inf

35
Q

Morphology of cells in apoptosis:

A

Cell shrinks and becomes deeply eosinophylic with basophylic nucleus, nucleus condenses and fragments, apoptotic bodies fall from cells and are removed my macrophages

36
Q

HY: Apoptosis is mediated by CASPASES. WHAT DO THEY DO?

A

1) Activate proteases (to break down cytoskeleton)

2) Endonucleases (to break down DNA)

37
Q

VERY HY: what are the 3 Pathways for CASPASE Activation?

A
  1. Extrinsic (death rcp) Pathway: FAS ligand on target cell binds FAS death recp and Caspase cascade starts!
  2. Intrinsic (Mitochondrial) Pathway: cell injury blocks Bcl2 (antiapoptotoc ptn), BAX and BAK (proapoptotic) form pores on mb and this leaks Cytocrome C out and starts Caspase cascade. BCL2 overexpresison decreases caspase activation, prevents apoptosis and increases tumorigenesis
38
Q

Of all of the free radicals the ___ free radical is the most damaging

A

OH-

39
Q

Explain the physiologic synthesis of free radicals:

A

It occurs during oxidative phosphorylation, and O2 accepts 4e to yield H2O.

40
Q

Explain the pathologic synthesis of free radicals:

A

happens when there is a PARTIAL reduction of O2. If it only accepts
1e=yields O2- (superoxide)
2e=yields H2O2 (hydrogen peroxide)
3e=OH- (hydroxyl)

41
Q

WHAT are the 4 mechanisms for path generation of FR:

A
  1. Ionizing Radiation
  2. Inflammation (O2————O2- thru NADH oxidase)
  3. Metals: In Hemochromatosis, the excess Fe2+ goes thru Fenton Feaction and generates FR (H2O2 into OH-), Happens with Cu+ also in Wilson’s disease)
  4. Drugs (acetaminophen, CCl4=CTC)
42
Q

What are the 3 mechanisms of free radical elimination?

A
  1. Antioxidants
  2. Metal Carrier Proteins
  3. Enzymes
43
Q

What are the enzymes that eliminate these free radicals?

A

superoxide (SOD= superoxide dysmutase)
H2O2 (CAT=catalase)
OH- (GP= glutathione peroxidase)

44
Q

What is the damage that free radicals cause?

A
  1. Peroxidation of Lipids
  2. Oxidation of DNA Ptns

this favors cancer and aging

45
Q

2 main Free Radical Injuries

A

VIGNETTE= Pct with MI has high Ez. but the enzymes continue elevating even after cath (after reperfusion)!`

  1. HY! P450 system in Liver converts Dry Cleaning chemical CCl4 to CCl3. This damages hepatocytes and protein synthesis. If there’s no ptn syn, there’s no Apolipoproteins to mtb fat = Fat accumulates= Fatty change of Liver!!!
  2. REPERFUSION INJURY: Tissue is dying due to Ischemia/MI, but if blood is returned, the combo of O2 and inflammatory cells produces FR, and further damages tissue!
46
Q

What is amyloid?

A

It’s a misfolded ptn that deposits in EC space and causes damage. mULTIPLE PROTEINS can deposit as amyloid

47
Q

3 main characteristics

A
  1. B-pleated sheet
  2. Congo red stain and Apple green birrefringent under polarized light
  3. Tend to deposit around Blood Vessels
48
Q

Deposit can be Systemic of Localized. Describe Systemc

A
  1. PRIMARY: systemic deposition of AL amyloid= associated with Plasma Dyscrasias.
  2. SECONDARY: systemic deposition of AA amyloid (derived from SAA- acute phase reactant present in chronic inflam states (LES, RA, Crohns, Chr Osteomielitis) and Familial Mediterranian Fever
49
Q

Describe the traits of Familial Mediterranean Fever

A
  1. Dysfunction of Neutrophils leads to
  2. Episodes of Fever and Acute serosal inflammation (mimics MI/Appendicitis)
  3. The high levels of SAA deposit as AA AMyloid
50
Q

Classic clinical findings of Systemic amyloidosis and Dx

A
  1. Nephrotic sym
  2. Restrictive Cardiomyopathy/Arrhythmias
  3. Tongue enlargement, melabsorption, hepatoslpenomegaly

DX: BIOPSY!
TTM: Transplant (Amyloid cannot be removed!!!)

51
Q

the 6 types of LOCALIZED AMyloidosis

A
  1. SENIL CARDIAC AMYLOIDOSIS
  2. Familiam Amyloid cardiomyopathy
  3. NIDDM 2 (Non insulin dependent DM type2)
  4. Alzheimer’s: Abeta-amyloid in brain
    HY 5. Dialysis associated amyloidosis: b2-Microglobulin is a structural component of MHC1 and deposits in JOINTS!
  5. Medullary carcinoma of Thyroid (find tumor cells in amyloid background)

Pathology (5 decks)

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