Module 1-Path Continued Flashcards Preview

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

Flashcards in Module 1-Path Continued Deck (57):
1

What is Steatosis?

Intracellular accumulation of lipid in hepatocytes (hepatic steatosis)

2

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

Micro --> nucleus is central
Maco --> nucleus is pushed to the periphery of cell

3

What is the etiology of hepatic steatosis?

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

4

What is the only irreversible fatty change in the liver?

CCL4 due to CCL3 free radicals --> lipid peroxidation
(aka antifreeze ingestion)

5

What is the pathogenesis for hepatic steatosis?

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

6

what is the presentation for hepatic steatosis?

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

7

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

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

8

Explain the complications of hepatic steatosis..

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

9

What other organs can undergo fatty changes?

Heart
Kidney

10

What are the staining for fat?

Oil red O
Sudan Black
Osmic Acid (EM)

11

What are the staining for glycogen?

PAS

12

Coagulative Necrosis is almost always due to what?

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

13

What is the etiology of coagulative necrosis?

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

14

How does coagulative necrosis appear on H and E stain?

No nuclei with eosinophilic appearance (proteins are dentaured)

15

What are some examples of coagulative necrosis?

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

16

What organs undergo coagulative necrosis?

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

17

What is Gangrenous Necrosis?

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

18

Necrosis always accompanied by what?

Inflammation

19

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

PMNs/Neutrophils

20

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

Macrophages

21

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

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

22

In regards to inflammation, what does cicatrization mean?

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

23

Liquefactive necrosis can be from what?

Hypoxia in the brain (Stroke) or
Bacterial / Fungal Infections (most common lung)

24

Is architecture maintained in liquefactive necrosis?

No

25

Explain the process of liquefactive necrosis in the brain

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

26

What are gitter/foam cells?

When microglia become loaded with fat/necrotic debris
(this is liquefactive necrosis)

27

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

Well this would be chronic inflammation now
so you see astrocytes (which are fibroblasts of brain) and gliosis (fibrosis of the brain)

28

What are some complications of liquefactive necrosis of the brain?

Stroke (paralysis and slurred speech)

29

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

Pyogenic (neutrophils/pus/debris)

30

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

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

31

What is another common organ for liquefactive necrosis?

Pancreas in acute pancreatitis

32

What is the etiology in breast fat necrosis?

Trauma, non enzymatic and NO HYPOCALCEMIA
Dystrophic calcification --> normal calcium levels as well

33

What is the etiology in the pancreas for fat necrosis?

Enzymatic, alcoholism and gallstones

34

Are the calcium levels normal for acute pancreatitis fat necrosis?

NOPE
hypocalcemia due to saponification

35

Are the calcium levels normal for chronic pancreatitis fat necrosis?

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

36

What is the pathogenesis of fat necrosis in acute pancreatitis?

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

37

Fat necrosis, key word?

Chalky Cheesy

38

What is the investigation for fat necrosis?

Interlobular space of fat upon microscopy

39

What are the complications of fat necrosis?

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

40

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

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

41

In acute pancreatitis what enzyme acts first?

Trypsin the amylase and lipase

42

Does amylase or lipase come out first in the blood?

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

43

Caseous necrosis is a combination of what necrosis?

Coagulative + liquefactive

44

What is the etiology of caseous necrosis

TB

45

What is the pathogenesis for caseous necrosis?

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

What is a caseating granuloma?

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

What are Langhans giant cells/?

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

48

How does TB present clinically?

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

49

What is the investigation of caseous necrosis?

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

50

What make Caseous necrosis cheesy-milky?

The mycolic acid due to the waxy cell wall

51

What is the key word for caseous necrosis?

Cheesy-milky

52

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

Histoplasma
Batman's Disease

53

Does caseous necrosis in TB go through an acute phase?

nope straight to chronic

54

What kind of hypersensitivity reaction is caseous necrosis?

type IV hypersensitivity (Cell mediated)

55

How is a granuloma formed?

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

TGFbeta recruits what?

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

57

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

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