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STEP 1 Pathoma > Chapter 1 > Flashcards

Chapter 1 Flashcards

1
Q

Hypertrophy = bigger cells, hyperplasia= more cells: Both are responses to cellular stress

A
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2
Q

How does hypertrophy occur?

A

gene activation, protein synthesis, and production of organelles

NOTE: Hypertrophy and hyperplasia typicall occur together

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3
Q

What tissues can only undergo hypertrophy (not hyperplasia)?

A

Cardiac muscle, skeletal muscle, and nerve

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4
Q

Note that pathologic hyperplasia (e.g. endometrial hyperplasia) can progress to dysplasia and eventually cancer. What is an exception?

A

BPH doesnt increase risk for prostate cancer

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5
Q

Overview of atrophy

A

Decreases ins tress cause a decrease in cell number via apoptosis and a decrease in cell size via ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular components (intermediate filaments are tagged with ubiquitin and destroyed by proteosomes)

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6
Q

Metaplasia= changing of cell type to another (e.g. Barrett’s Esophagus). What is the change in BE?

A

nonkeratinizing squamous to noncilitaed columnar

Remember that metaplasia is generally reversible with removal of the driving force (i.e. with GERD) BUT persistent metaplasia can progress to dysplasia (I.e. Barretts to adenocarcinoma; exception- apocrine metaplasia of the breast has no increased risk for cancer)

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7
Q

What else can cause metaplasia?

A

Vit A deficiency (VitA is needed for differentiation of specialized epithelial surface suchs as the conjuctiva covering the eye and in deficiency, the goblet cell/columnar epithelium of the conjunctiva undergoes metaplasia into keratinizing squamous epithelium)

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8
Q

Mesenchymal tissue can also undergo metaplasia as in myositis ossificans in which CT within muscle changes to bone during healing after trauam

A
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9
Q

Dysplasia often refers to proliferation of precancerous cells (e.g. CIN is dysplastic and can lead to cervical cancer)- often arises from longstanding metaplasia or hyperplasia

NOTE: Dysplasia is typially reversible

A
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10
Q

What is aplasia?

A

Failure of cell production in utero (whereas hypoplasia is a decrease in cell production in utero, resulting in a small organ)

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11
Q

When cells are highly susceptible in injury?

A

Neurons (whereas skeletal muscle is more resistant)

NOTE: Slow developing ischemia (i.e. renal artery stneosis) results in atrophy while acute ischemia (e.g. renal artery embolus) causes cell injury

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12
Q

What are some common causes of cellular injury?

A

inflammation, nutritional deficiency or excess, hypoxia, trauma, and mutations

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13
Q

What is hypoxia?

A

Low oxygen delivery to tissue (low O2= cant make ATP= cell injury)

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14
Q

Common causes of ischemia (decreased blood flow through an organ)?

A

decreased arterial perfuison (e.g. atherosclerosis)

decreased venous drainage (e.g. Budd Chiari)

shock

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15
Q

What is hypoxemia?

A

low partial pressure of oxygen in the blood (Pao2 less than 60 mm Hg, SaO2 less than 90%)

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16
Q

Common causes of hypoxemia?

A
  • High altitue
  • hypoventilation
  • diffusion defect (e.g. interstital pulmonary fibrosis)
  • V/Q mismatch (blood bypasses oxygenated lung due to shunt, etc. or oxygenated air cannot reach blood due to ventilation problems such as atelectasis)
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17
Q

Left ventricular hypertrophy

A

Dilated cardiomyopathy

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18
Q

Decreased O2 carrying capacity arises with Hb loss or dysfunction. Examples include:

A
  1. Anemia (decrease in RBC mass)- Pao2 and Sao2 normal
  2. CO poisoning (Pao2 normal but SaO2 decreased)
  3. Methamoglobinemia
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19
Q

How does CO poisoning appear clinically?

A
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20
Q

What is Methamoglobinemia?

A

When the iron in heme is oxidized to Fe3+ and cannot bind oxygen (Pao2 normal and Sao2 decreased)

-seen with oxidant stress (e.g. sulfa or nitrate drugs) or in newborns

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21
Q

How does Methamoglobinemia present?

A

cyanosis with chocolate colored blood

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22
Q

How is Methamoglobinemia tx?

A

IV methylene blue with helps reduce iron back to Fe2+

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23
Q

What cellular processes occur as a result of low ATP?

A

1- NaK pumps stop resulting in sodium and water buildup in the cell

  1. Ca2+ pumps fail resulting in Ca2+ buildup in the cytosol
  2. Switch to Anaerobic glycolysis. lactic acid builds up results in acidosis, whch denatures proteins and precipitates DNA
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24
Q

The hallmark of REVERSIBLE cellular injury is _________

A

cellular swelling - the cytosol swells resulting in loss of microvilli and membrane budding

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25
Q

The hallmark of IRREVERSIBLE cellular injury is _________

A

Membrane damage - results in cytosolic enzymes leaking into serum (e.g. cardiac troponins) and calcium entering the cells

26
Q

The morphologic hallmark of cell death is loss of the nucleus. How?

A

Pccurs via nuclear condensation (pyknosis), fragmentation (karorrhexis), and dissoultion (karylosis)

Two different processes: apoptosis and necrosis

27
Q

Necrosis

A
  1. Death of large grousp of cells followed by acute inflammation due to some underlying pathologic process (never physiologic)- divided into several parts
28
Q

What are the main types of necrosis?

A
  1. Coagulative
  2. Liquefactive
  3. Gangrenous
  4. Caseous
  5. Fat
  6. Fibrinoid
29
Q

Coagulative necrosis

A
  1. Necrotic tissue that remains firm; cell shape and organ structure are preserved by coagulation of protein, but the nucleus dissapears
  2. Characteristic of ischemic infract of any organ EXCEPT THE BRAIN
  3. Area of infarct is often wedge-shaped (pointing to focus of vascular occulsion and pale)
  4. red infarct arises if blood re-enters a loosely organized tissue
30
Q

Liquefactive necrosis

A
  1. Necrotic tissues that become liquefied, enzymatic lysis of cells and protein results in liquefaction
  2. characteristics of brain infarction (proteolytic enzymes from the microgial cells liquefy the brain), abscesses (proteolytic enzymes from neutrophils), and pancreatitis
31
Q

Gangrenous necrosis

A

`. Coagulatiev necrosis that resemble mummified tissue

2, Characteristics of ischemia of lower limb and GI tract

  1. If superimposed infection of dead tissues occurs, then liquefactive necrosis ensues (wet gangrene)
32
Q

Caseous necrosis

A
  1. Cottage cheese appearance (combo of coagulative and liquefactive necrosis)
  2. Characteristic of granulomatous inflammation due to TB or fungal infection
33
Q

Fat necrosis

A
  1. Necrotic adipose tissue with chalky white appearance due to deposition of calcium
  2. Characteristics of trauma to fat (e.g. breast) and pancreatits-meiated damage of peripancreatic fat
  3. Fatty acids released by trauma or lipase join with calcium via saponification
34
Q

Describe saponification

A

This is an ex of dystrophic calcification in which calcium depsoits in dead tissues. In dystrophic calcification, the necrotic tissue acts as a nidus for calcification in the setting of normal serum calcium and phosphate

NOTE: Metastatic calcification, as opposed to dystrophic calcification, occurs when high serum calcium or phosphate levels lead to calcium deposition in normal tissues (e.g. hyperPTHism leading to nephrocalcinosis)

35
Q

Fibrinoid necrosis

A

Necrotic damage to vessel walls causing leakage of proteins (including fibrin) into vessel walls, resulting in bright pink wall staining

-clasic of malignant HTN and vasculitis

36
Q

What is apoptosis?

A

Energy (ATP dependent) genetically programmed cell death involving single cells or small groups (e.g. endometrial shedding during menstrual cycle, removal of cells during embryogenesis, and CD8 mediated kills of virally infected cells)

37
Q

Apoptosis morphology

A
  1. Dysing cell shrinks, causing the cytoplasm to become more eosinophilic
  2. Ncuelus condenses and fragments
  3. Apoptotic bodies fall from the cell and are removed by amcrophages (no inflammation)
    4) Caspases activate proteases and endonucleuses to break down the cytoskeleton and DNA, respectively.
38
Q

Describe the intrisnic mitochondrial caspase pathway

A

Cellular injury, DNA damage, or decreased hormonal stimulation leads to inactivation of Bcl2, allowing cytochrome c to leak from the inner mitochondrial matrix into the cytoplasm and activate caspases

39
Q

Describe the extrinsic receptor-ligand pathway

A
  1. FAS ligand binds to FAS death receptor (CD95) on target cells, activating caspases or TNF binds to do the same
40
Q

Describe the CD8 T cell mediated apoptosis pathway

A

Porforins secreted by CD8 T cells create membrane pores and granzymes enter and activate caspases

41
Q

What are free radicals?

A

Chemical speceies with an unpaired electron in the outer orbit

42
Q

How are free radicals made?

A

Physiologically during oxidative phosphorylation when cytochrome c oxidase (Complex IV) transfers electrons to oxygen and partial reduction of O2 yields superoxide (O2*), hydrogen peroxide, and hydroxyl radicals

Pathologically with ionizing radiation, inflammation (NADPH oxidase generated superoxide ions during oxygen-dependent killing by neutrophils), metals (e.g. copper and iron; Fe2+ generates hydroxyl free radicals via the Fenton rxn), and CYP metabolism of drugs/chemicals

43
Q

How do free radicals cause cellular injury?

A

via peroxiation of lipid and oxidation of DNA and proteins

44
Q

How are free radicals eliminated?

A

Antioxidants (.e.g glutathione and vitA,C, and E)

Enzymes including superoxide dismutase (in mitochondria; superoxide to hydrogen peroxide), glutathione peroxidase (in mitochondria; 2GSH + free radical to GS-SG and H2O), and catalse (in peroxisomes; hydrogen peroxide to O2 and water)

Metal carrier proteins including transferring and ceruloplasmin

45
Q

Examples of free radical meidated injury

A
  1. Carbon tetrachloride (CCl4; organic solvent in dry cleaning)- converted to CCl3 free radicals by CYPP450 in the liver, resulting in cell injury and swelling of the RER
  2. Reperfusion injury- return of blood to ischemic tissue results in production of O2-derived free radicals, which further damage tissue
46
Q

What is amyloid?

A

Amyloid is a misfolded protein that deposits in the extracellular space thereby damaging tissues (can be systemic or localized)

NOTE: Multiple proteins can deposit as amyloid. Some shared features include a B-pleated sheet configuration, congo red staining and apple-green birefringence under polarized light

47
Q

What are the types of systemic amyloidosis?

A

Amyloid deposition in multiple organs, divided into primary and secondary amyloidosis

48
Q

What is primary amyloidosis?

A

Systemic deposition of AL amyloid, which is derived from immunoglobulin light cahins (associated with plasma cell dyscrasia such as multiple myeloma)

49
Q

What is secondary amyloidosis?

A

Systemic deposition of AA amyloid, which is derived from serum amyloid-associated protein (SAA)

50
Q

What is SAA?

A

An acute-phase reactant that is icnreased in chronic inflammatory states, malignancy, and Familial Meidterranean Fever (FMF)

51
Q

What causes Familial Meidterranean Fever (FMF)?

A

dsyfunction of neutrophils (AR) and occurs in mediterranean pts.

52
Q

How does FMF present?

A

Episodes of fever and acute serosal nflammation (can mimic appendicitis, arthritis, or MI)- the high SAA during attacks desposits as AA amyloid in tissues

53
Q

What are some classic findings of systemic amyloidosis?

A
  1. Nephrotic syndrome (kidney most commo organ invovled)
  2. Restrictive cardiomyopathy or arrhythmia
  3. Tongue enlargement, malabsorption, and HSM
54
Q

How is systemic amyloidosis diagnosed?

A

tissue biopsu (abdominal fat pad and rectum are good targets)

55
Q

T or F. Amyloid cannot be removed

A

T. Affected organs must be transplanted

56
Q

Describe localized amyloidosis

A

Amyoid in a single organ

57
Q

What are some types of localized amyloidosis?

A
  1. Senile cardiac amyloidosis
  2. Familial amyloid cardiomyopathy
  3. Non-insulin dependent DM type II
  4. Alzheimer disease
  5. Diaylsis-associated amyloidosis
  6. Medullary carcinoma of the thyoid
58
Q

What causes senile cardic amyloidosis?

A

Non-mutated serum transthyretin deposits in the heart- usually asymptomatic and present in 35+% of pts 80+ yo

59
Q

What causes familial amyloid cardiomyopathy?

A

Mutated serum transthyretin deposits in the heart leading to restrictive cardiomyopathy (common in AA)

60
Q

How is Alzheimer associated with amyloid?

A

AB amyloid (derived from B-amyloid precursor protein) deposits in the brain forming amyloid plaques

NOTE: The gene for B-APP is on chrom 21 (most individuals with Down syndrome develop Alzheimer by the age of 40)

61
Q

Dialysis associated amyloidosis is associated with what kind of amyloid?

A

B2-microglobulin (deposits in joints)

STEP 1 Pathoma (18 decks)

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