Module 2-Path Continued Flashcards Preview

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

Flashcards in Module 2-Path Continued Deck (46):

What is cholestasis?

Accumulation of bilirubin in bile canaliculi of hepatocytes


What are the components of bile?

Bilirubin, bile salts, phospholipids, cholesterol and electrolytes


What are some causes of cholestasis?

Obstruction of bile duct
Bile duct collapse
Liver Failure
Gall stones (Cholelithiasis)
Biliary Atresia


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

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


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

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


How does a patient present with cholestasis usually?

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


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

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


What are hemosiderin deposits?

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


What is the pathogenesis for hemosiderin deposits?

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


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

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)


How does one present with these hemosiderin laden macrophages

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


What investigations would you use for hemosiderin deposits?

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


Most common cause of left heart failure?

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


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

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


What is the pathogenesis for hemochromatosis?

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


What are the 6 organs that hemochromatosis can affect?

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


What is the etiology of pulmonary antharcosis?

Inhalation of coal dust or carbon particles
(and remember because its inhalation its an exogenous pigment) (intracellular)


What is the pathogenesis for pulmonary antharcosis?

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


What is the presentation for pulmonary antharcosis?

Asymptomatic/no inflammation
seen in urban dwellers, smokers and coal miners


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

carbon mixed with silica
patients would be SOB


In regards to Tattoos, is the pigment innert?

Yep which means no inflammation


what is the etiology of a tattoo?

Injection of insoluble metallic vegetable pigments into skin


What is the pathogenesis for tattoos?

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


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

needle causes acute inflammation


What viruses can you get from tattoo?

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


Melanin is produced and stored where?

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


What are some characteristics of melanin?

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)


Lipofusion is considered what kind of pigment?

Wear and Tear Pigment; hallmark of aging
(light-brownish in color)


Lipofuscin is an insoluble pigment produced due to what?

Free radical damage associated with again


Where is lipofusion stored?

In lysosomes; does not interfere with cell function


In what organs is lipofusion most visible?



What are three ways in which tissues can be restored?

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


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

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


what are the three 3 groups of regeneration cells?

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)


Growth of new cells is best accomplished by what?

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


What are some mechanisms involved in repair?

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


What are the three steps involved in repair process?

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)


What are the steps in repair?

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)


What is granulation tissue?

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


Does brain tissue form a scar?

Nope just a hole


Keloid is a lesion that consists of what?

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


What is primary healing ?

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


What is secondary healing?

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


What are some factors influencing the rate of healing?

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


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

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


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

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