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Pathology Pre-Midterm > Module 2-Path Continued > Flashcards

Module 2-Path Continued Flashcards

1
Q

What is cholestasis?

A

Accumulation of bilirubin in bile canaliculi of hepatocytes

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2
Q

What are the components of bile?

A

Bilirubin, bile salts, phospholipids, cholesterol and electrolytes

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3
Q

What are some causes of cholestasis?

A 
Obstruction of bile duct 
Cholecystitis 
Bile duct collapse 
Liver Failure 
Gall stones (Cholelithiasis) 
Biliary Atresia
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4
Q

When looking at an H and E stain of cholestasis is the bilirubin intracellular or extracellular?

A

Extracellular because it is not in the hepatocytes but it can become intracellular

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5
Q

Cholestasis can be due to obstruction of common bile duct by gallstones, what kind of bilirubin will you find built up in the patient?

A

Conjugated/direct bilirubin (product of hemoglobin catabolism)
Endogenous pigment found extracellularly
Skin (yellow), gallbladder (Green) and intestine (Brown)

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6
Q

How does a patient present with cholestasis usually?

A

Jaundice (icterus), steatorrhea (pale b/c no stercobilin), dark urine and malabsorption of fat soluble vitamins

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7
Q

Malabsorption of fat soluble vitamins, A/D/E/K result in what direct effects?

A

A –> causes night blindness
D–> causes hypocalcemia/arrhythemias
E –> no antioxidants
K –> causes bleeding

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8
Q

What are hemosiderin deposits?

A

Endogenous pigment from catabolism of hemoglobin
Denatured form of ferritin
Normally stores in RES (Spleen, bone marrow and Kupffer cells of the liver)

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9
Q

What is the pathogenesis for hemosiderin deposits?

A
  1. Excessive intracellular iron (Hemosiderosis) due to: excess intestinal iron absorption, hemolysis of RBCs and blood transfusions
  2. Hemochromatosis: extreme iron overload
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10
Q

Another pathogenesis for hemosiderin deposits is left ventricular hypertrophy, explain this

A

Aortic Stenosis –>Left Ventricular Hypertrophy –> left heart failure –> blood backs up into alveolar space –> pulmonary edema –> at 2 weeks hemosiderin laden macrophages in alveolar space (heart failure cells) with alveolar fibrosis (due to collagen) if less then 2 weeks(Acute) then transudate and RBCs in alveolar space (Driving force of transudate is hydrostatic pressure)

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11
Q

How does one present with these hemosiderin laden macrophages

A

Dyspnea
Orthopnea b/c fluid in alveolar space when laying down
Paroxysmal nocturnal dyspnea

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12
Q

What investigations would you use for hemosiderin deposits?

A

Stain blue on Prussian Blue and golden-brown on H and E b/c hemosiderin contains iron

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13
Q

Most common cause of left heart failure?

A

right heart failure (distended jug veins, hepatomegaly, ascites, peripheral edema)

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14
Q

In regards to hemochromatosis, what are the primary and secondary causes?

A

Primary: C282Y mutation of HFE gene (regulates iron absorption)
Secondary: Excess intestinal iron absorption, hemolysis of RBCs, or blood transfusions

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15
Q

What is the pathogenesis for hemochromatosis?

A

Excessive absorption of iron – >saturation of iron binding protein –> deposition of hemosiderin in tissue

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16
Q

What are the 6 organs that hemochromatosis can affect?

A 
Heart --> heart failure cells 
Liver --> cirrhosis 
Pancreas --> diabetes (bronze) 
Skin --> bronze appearance
Kidney --> kidney failure 
Brain --> anterior pituitary (testical atrophy, adrenal atrophy, thyroid atrophy)
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17
Q

What is the etiology of pulmonary antharcosis?

A

Inhalation of coal dust or carbon particles

and remember because its inhalation its an exogenous pigment) (intracellular

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18
Q

What is the pathogenesis for pulmonary antharcosis?

A

Phagocytized by alveolar macrophages/dust cells (incapable of digesting the pigment) –> travels to regional lymph nodes and accumulates

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19
Q

What is the presentation for pulmonary antharcosis?

A

Asymptomatic/no inflammation

seen in urban dwellers, smokers and coal miners

20
Q

When coal workers develop pneumoconiosis (Black lung) what happens?

A

carbon mixed with silica

patients would be SOB

21
Q

In regards to Tattoos, is the pigment innert?

A

Yep which means no inflammation

22
Q

what is the etiology of a tattoo?

A

Injection of insoluble metallic vegetable pigments into skin

23
Q

What is the pathogenesis for tattoos?

A

Remember it is exogenous but intracellular
engulfed by dermal macrophage –> unable to digest pigments –> remain in the dermis for life
Note —> Langerhans cells are another name for dermal macrophages

24
Q

When you get a tattoo what is the reason for acute inflammation?

A

needle causes acute inflammation

25
Q

What viruses can you get from tattoo?

A

HIV, HEP B and C (Those are the blood borne heps)

26
Q

Melanin is produced and stored where?

A

Produced –> by melanocytes
Stored -> in organelle (melanosome)
black in color

27
Q

What are some characteristics of melanin?

A

Acts as a protective barrier from UV light
Freckles: melanin accumulates in basal epithelial cells of skin
Can also accumulate in nevus cells or dermal macrophages (langerhans cells)
Can become tumors of the skin contain melanin (malignant melanoma)

28
Q

Lipofusion is considered what kind of pigment?

A

Wear and Tear Pigment; hallmark of aging

light-brownish in color

29
Q

Lipofuscin is an insoluble pigment produced due to what?

A

Free radical damage associated with again

30
Q

Where is lipofusion stored?

A

In lysosomes; does not interfere with cell function

31
Q

In what organs is lipofusion most visible?

A

Liver
Cardiac
Brain

32
Q

What are three ways in which tissues can be restored?

A
  1. removal of exudate
  2. removal of cellular and tissue debris
  3. replacement of cells and lost tissues
33
Q

Replacement of lost cells involves two processes, regeneration and repair, what are some differences between the two?

A

Regeneration: new cells are identical to the ones they are replacing
Repair: new cells are the same kind or simpler form than those being replaced

34
Q

what are the three 3 groups of regeneration cells?

A

Labile: follow cell cycle from 1 mitosis to the next ( epithelium, blood cells)
Stable: Low normal levels of replication, but still able to divide in response to stimuli: G0 –> G1 (glands and mesenchymal cells)
Permanent: can NOT divide in postnatal life
(CNS and cardiac muscle)

35
Q

Growth of new cells is best accomplished by what?

A

Recruitment of stable G0 cells into cell cycle

  1. growth/stimulatory factors
  2. loss of growth inhibitors normally present (neg feedback)
  3. cell -cell or cell-matrix interactions
36
Q

What are some mechanisms involved in repair?

A
  1. Control of cell proliferation
  2. Stimulatory hormones and growth factors
  3. Inhibitory Factors: Chalones (hormone life mitosis inhibitors -> epidermal, granulocyte and lymphocyte)
  4. Cell cell interactions
  5. Cell Matrix interactions
  6. Fibronectin –> most important glycoprotein in healing
37
Q

What are the three steps involved in repair process?

A
  1. Angiogenesis –> mediated by growth factors VEGF and b-FGF
  2. Fibrosis –> proliferation of fibroblasts and deposition of ECM=scar formation
  3. Maturation and Organization: scar ECM continues to be modified and remolded (mediated by metalloproteinases and collagenases)
38
Q

What are the steps in repair?

A
  1. Crust –> forms only if blood is available and conditions permit drying
  2. Removal of Debris: sloughing and phagocytosis
  3. Replacement of lost cells: cell migration and division (fibroblasts migrate after 8 hours, endothelium migrate in arcs after a lag period and epithelium migrates in sheets)
39
Q

What is granulation tissue?

A

Meshwork of capillaries, fibroblasts, inflammatory cells, ECM
formed during repair, after 3-5 days
acts as a scaffold that scar can form on

40
Q

Does brain tissue form a scar?

A

Nope just a hole

41
Q

Keloid is a lesion that consists of what?

A

Irregularly arranged, broad, homogenous, hyalinzed and basophilic collagen fibers
type III collagen

42
Q

What is primary healing ?

A

edges of wound in apposition, may be the case when it mimics closely restitution ad intergrum
superficial wound w/o bleeding: heal quickly by regeneration of epithelium
deeper cuts with retraction

43
Q

What is secondary healing?

A

Considerable loss of tissue; edges of wound can not be approximated
Large wound, abscess formation, ulceration
loss tissue is replaced with granulation tissue –> forms a scar

44
Q

What are some factors influencing the rate of healing?

A

Age, size of wound, secondary infection, dietary status (Vit C, D, protein)

45
Q

What are some local factors modifying the inflammatory response (factors relating to host)?

A

Adequacy of blood supply: well vascularized tissues are resistant to infections and capable of containing them
Location of injury: densely compact tissues resist spread of infections
Presence of infection
Presence of foreign bodies
Immobilization of wounds

46
Q

what are some systemic factors modifying the inflammatory response (factors relating to host)?

A

Physiolgoic condition of the host
Immunity
Hormones
Cortisone, hydrocortisone, corticosterone, ACTH: decrease inflammatory response

Pathology Pre-Midterm (35 decks)

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