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Pathology Pre-Midterm > Module 1-Path Continued > Flashcards

Module 1-Path Continued Flashcards

1
Q

What is Steatosis?

A

Intracellular accumulation of lipid in hepatocytes (hepatic steatosis)

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2
Q

In regards to hepatic steatosis there is microvesicular and macrovesicular, what is the difference between the two?

A

Micro –> nucleus is central

Maco –> nucleus is pushed to the periphery of cell

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3
Q

What is the etiology of hepatic steatosis?

A 
Alcohol Consumption 
Metabolic Syndrome (obesity, hypertension, diabetes, dyshyperlipidemia), Reyes Syndrome, CO poisoning
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4
Q

What is the only irreversible fatty change in the liver?

A

CCL4 due to CCL3 free radicals –> lipid peroxidation

aka antifreeze ingestion

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5
Q

What is the pathogenesis for hepatic steatosis?

A

Alcohol dehydrogenase consumes NAD+ and makes NADH (acetylaldehyde) which gets converted to acetic acid which also uses NAD+
NAD+ is also needed for beta oxidation of FA –> which leads to accumulation of FAs in the hepatocytes
Increase in NADH production means no apolipoproteins are being made

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6
Q

what is the presentation for hepatic steatosis?

A

Incidental finding on autopsy/imaging is most common because it is asymptomatic until turns into hepatitis (fever, vomiting, RUQ pain and jaundice)

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7
Q

In regards to AST and ALT levels what are they for hepatic steatosis?

A

AST > ALT with a ratio of 2
elevated ALT- if viral hepatitis
ALP/GGT –> bile

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8
Q

Explain the complications of hepatic steatosis..

A

Fatty change (reversible) –> hepatitis (reversible) –> cirrhosis (irreversible ) –> hepatocellular carcinoma (irreversible)

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9
Q

What other organs can undergo fatty changes?

A

Heart

Kidney

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10
Q

What are the staining for fat?

A

Oil red O
Sudan Black
Osmic Acid (EM)

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11
Q

What are the staining for glycogen?

A

PAS

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12
Q

Coagulative Necrosis is almost always due to what?

A

Ischemia leading to hypoxia; overall architecture of the organ is still preserved

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13
Q

What is the etiology of coagulative necrosis?

A

Anything that causes ischemia/hypoxia (Atherosclerosis/embolus/gunshot wound)

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14
Q

How does coagulative necrosis appear on H and E stain?

A

No nuclei with eosinophilic appearance (proteins are dentaured)

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15
Q

What are some examples of coagulative necrosis?

A 
Rental Artery Stenosis
Sickle cell anemia (vaso-occlusive event) 
Volvulus in the GI 
Embolus of SMA 
Coagulative necrosis in lung by PE 
MI
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16
Q

What organs undergo coagulative necrosis?

A

Any organ

remember the brain in the first 24 hours (acute ischemic stroke)

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17
Q

What is Gangrenous Necrosis?

A

Ischemic Coagulative necrosis + superimposed infection (wet gangrene) –> seen with diabetes and vasculitis

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18
Q

Necrosis always accompanied by what?

A

Inflammation

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19
Q

In regards to inflammation what are the first cells on the scene (first 24 hours), due to bacteria. (remember viral is different)

A

PMNs/Neutrophils

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20
Q

Past 24 hours until about day 3 what cell predominates in acute inflammation?

A

Macrophages

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21
Q

After 2 weeks the inflammation becomes chronic, what kind of tissue forming

A

Collagen initially type III with granulation tissue (That includes blood vessels and angiogenesis)

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22
Q

In regards to inflammation, what does cicatrization mean?

A

Type III to type I collagen (remember 3,2,1)

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23
Q

Liquefactive necrosis can be from what?

A

Hypoxia in the brain (Stroke) or

Bacterial / Fungal Infections (most common lung)

24
Q

Is architecture maintained in liquefactive necrosis?

A

No

25
Q

Explain the process of liquefactive necrosis in the brain

A

Ischemia or Hypoxic event -> microglia releasing hydrolytic enzymes which digest brain parenchyma

26
Q

What are gitter/foam cells?

A

When microglia become loaded with fat/necrotic debris

this is liquefactive necrosis

27
Q

After 2 weeks of liquefactive necrosis what cells do you see?

A

Well this would be chronic inflammation now

so you see astrocytes (which are fibroblasts of brain) and gliosis (fibrosis of the brain)

28
Q

What are some complications of liquefactive necrosis of the brain?

A

Stroke (paralysis and slurred speech)

29
Q

Another cause of liquefactive necrosis is bacterial/fungal infection that results in an abscess. what kind of bacteria is involved with these abscesses?

A

Pyogenic (neutrophils/pus/debris)

30
Q

Liquefactive necrosis of the lung, would include what kind of symptoms?

A

SOB
Cough
Fever (due to IL-1 and TNF)
Smelly Sputum

31
Q

What is another common organ for liquefactive necrosis?

A

Pancreas in acute pancreatitis

32
Q

What is the etiology in breast fat necrosis?

A

Trauma, non enzymatic and NO HYPOCALCEMIA

Dystrophic calcification –> normal calcium levels as well

33
Q

What is the etiology in the pancreas for fat necrosis?

A

Enzymatic, alcoholism and gallstones

34
Q

Are the calcium levels normal for acute pancreatitis fat necrosis?

A

NOPE

hypocalcemia due to saponification

35
Q

Are the calcium levels normal for chronic pancreatitis fat necrosis?

A

Fibrosis (because its chronic)
dystrophic calcification with hypocalcemia because of malabsorption of fat soluble vitamins –> no vit D –> cant take up Ca2+

36
Q

What is the pathogenesis of fat necrosis in acute pancreatitis?

A

Pancreatic Injury —> release of amylase and lipase –> released FAs combine with Ca2+ –> saponification

37
Q

Fat necrosis, key word?

A

Chalky Cheesy

38
Q

What is the investigation for fat necrosis?

A

Interlobular space of fat upon microscopy

39
Q

What are the complications of fat necrosis?

A

Fever, nausea, vomiting, epigastric pain, spasms and tetany due to decrease in serum Ca2+

40
Q

Describe fat necrosis calcium levels for chronic inflammation, dystrophic calcification, and metastatic calcification

A

Chronic inflammation –> hypocalcemia
Dystrophic calcification - normal except (except pancreatitis)
Metastatic Calcification- hypocalcemia

41
Q

In acute pancreatitis what enzyme acts first?

A

Trypsin the amylase and lipase

42
Q

Does amylase or lipase come out first in the blood?

A

Amylase comes out in the first 24 hours in the blood (specific not sensitive)

43
Q

Caseous necrosis is a combination of what necrosis?

A

Coagulative + liquefactive

44
Q

What is the etiology of caseous necrosis

A

TB

45
Q

What is the pathogenesis for caseous necrosis?

A

TB inhalation –> macrophages try to engulf microbe but can’t so they release IL-12 which converts CD4+ T cells –> TH1 cells –> TH1 cells secrete IFN gamma to activate macrophages to epithelioid cells (no phagocytic function/only secrete IL-1/TNF/TGF) –> Granuloma (complex mixture of chronic inflammatory cells and dead tissue)

46
Q

What is a caseating granuloma?

A

central area of caseous necrosis (no nuceli in the center) –> walled off by chronic inflammatory cells (macropges, T cells, plasma cells, fibroblast, giant cells, epitheliod cells, but NO PMNs)

47
Q

What are Langhans giant cells/?

A

Collection of epithelioid cells) only in TB with horseshoe shaped arrangement of nuceli

48
Q

How does TB present clinically?

A

Cough, low grade fever, SOB, night sweats and fever (patient will be an african-american or asian immigrant)

49
Q

What is the investigation of caseous necrosis?

A

Acid fast and cottage cheese like appearance due to mycolic acid
(acid fast stain of the sputum) (Ziehl-Nielsen stain)

50
Q

What make Caseous necrosis cheesy-milky?

A

The mycolic acid due to the waxy cell wall

51
Q

What is the key word for caseous necrosis?

A

Cheesy-milky

52
Q

If a patient has a caseous necrosis but based off a fungal infection what parasite is this from and what is the disease called?

A

Histoplasma

Batman’s Disease

53
Q

Does caseous necrosis in TB go through an acute phase?

A

nope straight to chronic

54
Q

What kind of hypersensitivity reaction is caseous necrosis?

A

type IV hypersensitivity (Cell mediated)

55
Q

How is a granuloma formed?

A

macrophages that secrete IL-12 and then IL12 converts CD4 T cells from THknot to TH1 these then secrete IFNgamma and they convert those macrophages to the epitheliod histocites (called activated macrophages –> no phagocytic activity –> secretory –> make IL1,TGFB and TNFalpha)

56
Q

TGFbeta recruits what?

A

fibroblasts (in periphery) and these lay down collagen so this caseous necrosis becomes a fibroid scar (so its heals by fibrosis)

57
Q

In summary what is IL-1, TNF and TGFbeta responsible for?

A 
TNFalpha = fever and weight loss
IL-1= fever 
TGFbeta = fibrosis

Pathology Pre-Midterm (35 decks)

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