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TxPlan/MedComplex/SpecNeeds > MedComplex-Exam 2 Part 3 (IBD,Liver,Pancreas) > Flashcards

MedComplex-Exam 2 Part 3 (IBD,Liver,Pancreas) Flashcards

1
Q

What is another name for CJ Crohn’s disease?

A

Regional Enteritis

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2
Q

What is the BASIC etiology of Inflammatory Bowel Disease? What are two possible secondary explanations?

A

Basically Unknown…1)emotional 2)genetic

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3
Q

CUC vs Crohns LET’S GO!!! Which one is 3x more common than the other?

A

CUC is 3x more common than Crohn’s

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4
Q

CUC vs Crohns LET’S GO!!! more common in whites than blacks (esp. E. Euro Jews)

A

BOTH

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5
Q

CUC vs Crohns LET’S GO!!! Peak in the 3rd decade of life

A

BOTH

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6
Q

CUC vs Crohns LET’S GO!!! Familial predisposition

A

BOTH

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7
Q

CUC vs Crohns LET’S GO!!! Extra intestinal complications

A

BOTH

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8
Q

CUC vs Crohns LET’S GO!!! In the early stages, both diseases have _________ changes often indistinguishable from one another.

A

morphologic

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9
Q

CUC vs Crohns LET’S GO!!! Peter’s Patches

A

Crohn’s Disease

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10
Q

CUC vs Crohns LET’S GO!!! transmural inflammation

A

Crohn’s

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11
Q

CUC vs Crohns LET’S GO!!! rubber-hose fibrosis

A

Crohn’s

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12
Q

CUC vs Crohns LET’S GO!!! creeping fat

A

Crohn’s

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13
Q

CUC vs Crohns LET’S GO!!! cobblestone

A

Crohn’s

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14
Q

CUC vs Crohns LET’S GO!!! skip Holladay lesions

A

Crohn’s (Cj is a skippy/spotty hitter)

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15
Q

CUC vs Crohns LET’S GO!!! The fibrotic intestines may be narrowed, causing intestinal stricture, and the inflammation of the serosa leads to adhesions with adjacent intestinal loops and the formation of “Fistulas”

A

Crohn’s

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16
Q

CUC vs Crohns LET’S GO!!! Fistulas

A

Crohn’s

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17
Q

CUC vs Crohns LET’S GO!!! Diffuse

A

CUC

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18
Q

CUC vs Crohns LET’S GO!!! backwash ileitis

A

CUC

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19
Q

CUC vs Crohns LET’S GO!!! Since we know Crohn’s is transmural, what layers are involved in CUC?

A

mucosa and submucosa

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20
Q

CUC vs Crohns LET’S GO!!! Prone to bleeding

A

CUC (Uhh. fucking chronic ULCERATIVE colitis)

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21
Q

CUC vs Crohns LET’S GO!!! surface of a football

A

CUC

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22
Q

CUC vs Crohns LET’S GO!!! Crypt Abscesses

A

CUC

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23
Q

CUC vs Crohns LET’S GO!!! Inflammatory Pseudopolyps

A

CUC

24
Q

____________ is the most significant late complication of CUC…what do they start from?

A

malignant transformation…start from pseudopolyps

25
Q

What % of CUC pt’s are unlucky and need an entire colon replacement? What % are lucky and the CUC goes away after a single episode?

A

20% unlucky…10% lucky

26
Q

CUC vs Crohns LET’S GO!!! left side of the colon

A

CUC

27
Q

CUC vs Crohns LET’S GO!!! right side of colon and ileum

A

Crohn’s

28
Q

CUC vs Crohns LET’S GO!!! Granulomas are diagnostic

A

Crohn’s

29
Q

CUC vs Crohns LET’S GO!!! Toxic Megacolon

A

CUC

30
Q

IMPORTANT POINT** CUC vs Crohns LET’S GO!!! extraintestinal complications ( arthritis, eye lesions, and skin lesions)

A

IDENTICAL FOR BOTH

31
Q

CUC vs Crohns LET’S GO!!! Risk of cancer

A

CUC

32
Q

CUC vs Crohns LET’S GO!!! Exacerbations and remissions

A

BOTH

33
Q

What are the 4 major consequences of portal HTN?

A

1.Hepatic Encephalopathy 2.Ascites 3.Splenamegaly 4.Esophageal Varices (2 up from liver, 2 down/around from liver)

34
Q

Caput Medusae is a result of what?

A

Portal-Systemic Shunts in Portal HTN

35
Q

Ascites c/o portal HTN: ______ cannot be produced in a cirrhotic liver

A

Albumin

36
Q

Splenomegaly c/o portal HTN: The enlarged spleen has a tendency to sequester and destroy blood cells which can result in a _________.

A

pan-cytop-enia (pandemic broo)

37
Q

Why in the world did that God awful hemorrhoids picture show up?

A

c/o hepatic HTN

38
Q

Hepatic Encephalopathy: What is the chemical that the liver cannot handle?

A

ammonia

39
Q

How does the liver get FAT? Alcohol has a high caloric content and serves as a substrate for new fat formation in the liver cells ( called ___________)

A

neolipogenesis

40
Q

COME ON! YOU GOT THIS!! What are the 4 ways the liver becomes fat c/o EtOH?

A

1.Accumulation of Fat 2.EtOH is fuel for new fat 3.EtOH inhibits beta oxidation 4. no LDL/HDL export

41
Q

What is the first of the sequence to liver Cirrhosis?

A

fatty liver

42
Q

What is it called when the liver becomes enlarged, tan-yellow, fatty and greasy?

A

Steatosis

43
Q

Over 80% of Acute Pancreatitis is caused by which 2 factors?

A

1.Gall Stone obstruction 2.EtOH constriction

44
Q

In Acute Pancreatitis: Obstruction could also lead to the reflux of bile into the pancreas. ______ normally activates pancreatic proenzymes in the intestines and could activate enzymes prematurely in the ducts

A

BILE

45
Q

All these describe…. diabetes, fibrosis, entrapment of celiac nerve, calcifications, poor vitamin absorption

A

Chronic Pancreatitis

46
Q

1 reason for chronic pancreatitis

A

surviving acute pancreatitis

47
Q

1 pathogenesis in acute pancreatitis

A

autodigestion

48
Q

What is the enzyme that is activated to then spur auto digestion?

A

trypsinogen

49
Q

What two enzymes will show up in the blood within the first 24hrs of acute pancreatitis?

A

amylase and lipase

50
Q

Hepatits associations!! Hep A

A

fecal/oral route

51
Q

Hepatits associations!! co-infection/superinfection

A

Hep D (with Hep B)

52
Q

Hepatits associations!! Hep C

A

Blood Transfusion (non-a, non-b)

53
Q

Hepatits associations!! Fecal/oral route

A

A

54
Q

Hepatits associations!! Necrosis of the liver DURING PREGNANCY

A

Hep E…Get it PregnancEEEEE

55
Q

Hepatits associations!! Which is the only DNA virus?

A

Hep B!

56
Q

What is the only antibody that covers the “WINDOW PERIOD” of Hep B?

A

The Hep B Core Antibody (aka Anti-HBc) (window period is 5-6 mo post exposure

TxPlan/MedComplex/SpecNeeds (21 decks)

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