Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI and Liver > GI Deck 3 > Flashcards

GI Deck 3 Flashcards

1
Q

17 year old male presents to his PMD with yellow eyes. No recent sexual contact, IVDA, or ETOH. On no medications. Similar episode 2 yrs ago.

Physical exam: +Scleral icterus. No stigmata of chronic liver disease. No hepatosplenomegaly or ascites

Labs:

Normal CBC and SMA-7

AST=25 (normal)

ALT=30 (normal)

Alk phos= 50 (normal)

Total bilirubin= 5.0 (elevated) Indirect bilirubin = 4.5 (elevated)

A

Gilbert’s Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

45 year old female presents with intermittent right upper quadrant pain, nausea, vomiting for 2 days. Low grade fever. History of occasional RUQ pain in past but never so bad or associated with nausea and vomiting. Noticed that 2 days ago her stool become more pale and her urine got darker.

Physical exam: BP=150/90; HR=110; +Scleral icterus. No stigmata of chronic liver disease, normo-active bowel sounds, moderate RUQ tenderness. No rebound or guarding. No hepatosplenomegaly

Labs:

AST=50 (normal)

ALT=52 (normal)

Alk phos=290 (elevated)

Total bilirubin = 6.0 (elevated) Direct bilirubin = 5.0 (elevated)

A

Obstruction - alk phos elevated, conjugated hyperbilirubinemia

Most commonly a stone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

35 year old male presents with RUQ pain, nausea, and vomiting for 3 days. No associated diarrhea. Recent unprotected sexual contact.

Physical exam: No scleral icterus. Mild RUQ discomfort; otherwise normal.

Labs:

AST=2000 (markedly elevated)

ALT=3000 (markedly elevated)

Alk phos=99 (normal)

Total bilirubin=3.0 (slightly elevated)

A

Viral hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

40 year old male presents to the ER with fever and jaundice. He just lost his job and his wife left him.

Physical exam: +scleral icterus and jaundice, otherwise normal.

Labs:

WBC=20K (elevated)

AST=200 (elevated)

ALT=50 (slightly elevated)

Alk phos=150 (slightly elevated) GGTP=300 (elevated)

Total bilirubin=15 (elevated)

A

Alcoholic Hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the blood supply of the liver?

A

Dual - portal vein (60-70%) and hepatic artery (30-40%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the outflow blood supply of the liver?

A

IVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the path of the biliary system?

A

Drain bile fromed by hepatocytes that is secreted inot bile canaliculi

Into canals of Herig

Into intrehepatic and extrahepatic bile duts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the blood supply of the bile ducts?

A

Hepatic arteries via peribiliary plexus of capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the components of the portal tracts?

A

Bile duct, portal vein, hepatic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the central venules (terminal hepatic venules)?

A

Drain blood from sinusoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are kupffer cells?

A

Special macrophages of the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can precpitate hepatocellular injury?

A

Oxygen deprivation (hypoxic or ischemic)

Chemical or drug injury (e.g. acetaminophen)

Infection (hepatitis)

Immunoligcal (autoimmune)

Genetic misprograming (storage disorder)

Metabolic imbalance (Fatty liver disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is ballooning degeneration/

A

Hepatocyte swelling (Volume change)

The result of severe cellular injury, can cause cell death

Clumped cytoplasmic organelles and large clear spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do we see here?

A

Ballooning degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is steatosis?

A

Accumulation of triglyceride fat droplets within hepatocytes

Microvesicular - multiple tiny droplets that don’t displace nucleus (pregnancy, valproic acid toxicity)

Macrovesicular - single large droplet that displaces the nucleus (obesity, diabetes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does cholestasis look like pathologically?

A

Looks like ballooning degenration, but rather feathery

Bile flow impaired, results in jaundice

Have a foamy cytoplasm

Obstruction, bile duct disease, viral hepatitis, toxic injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do we see here?

A

Cholestasis. Note hte feathery appearacne

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are gross features of acute hepatitis?

A

Capsule is edematous and tense

Liver is swollen and red

Focal depressions due to subcapsular necrosis and collapse

Bright yellow or green

In fulmanant hepatitis, the liver is shunken and soft, and the capsule is wrinkled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What do we see here?

A

Acidophilic bodies that are indicative of apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What areas of the liver are most susceptile to necrosis in ischemic injury?

A

Centrilobular zones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What do we see pathologicallyi n hepatitis?

A

INjury associated with influx of acute or chronic inflammatory cells

Apoptotic hepatocytes, scavenger macrophages, lobular and portal inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What do we see here?

A

HEpatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the difference between fulminant and subfulminant hepatitis?

A

Fulminant - develops within 2-3 weeks and results in massive hepatic necrosis

Subfulminant - less rapid course may extend up to 3 months, submassive

most due to viral hepatitis, rest due to drug or chemical toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is interface hepatitis?

A

Inflammatory cells extend beyond the margins of the protal tract connective tissue - spill over into adjacent limiting plate nad beyond

Portal tract with irregular borders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the two mechanisms of liver regeneration?

A

Adult differentiated hepatocytes unergo division and replication

Extensive hepatic necrosis stimulates proliferation of progenitor cells (canal of herig = reserve compartment). In this way, you see the ductular reaction below

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are key events in liver fibrosis?

A

Stellate cells

Extracellular matrix deposition

Alteration of the parenchymal microvasculature

In cirrhosis, excess type I and III collagents are laid down not only in portal tracts but also in the lobule, creating delacate or broad septal tracts

Generally irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What collagents are laid down too much in cirrhosis?

A

Collagen I and III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is this?

A

Cirrhosis

Excess type I and III collagen laid down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

A 45 year old man was incidentally found to have elevated transaminases. Further work-up revealed +HCV antibodies. He reveals that he experimented with illicit drugs 25 years ago. A liver biopsy is performed.



A

Chronic hepatitis C, grade 2, stage 2

Steatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does the grade of chronic hepatitis indicate?

A

Degree of inflammation - foci of parenchymal necrosis and apoptotic bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What odes the stage of chronic hepatitis indicate?

A

Degree of fibrosis (portal fibrosis, fibrous septa, bridging fibrous septa, transition into cirrhosis, cirrhosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

48 yo female with abnormla liver enzymes:

 AST 350, ALT 270

 + ANA 1:320

 *Liver biopsy was performed



A

Autoimmune hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is a useful menomonic for remembering hte hepatitides?

A

A = always acute

B = bloodborne

C = chronic

D = double (requires B)

E = epidemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is ALD?

A

Alcoholic Liver Disease

Most common cause of cirrhosis in western world

MOre common in men than women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How does alcohol consumption relate to ALD

A

Continued alcohol ingestion once alcohol liver injury is present (converse is true, abstinence allows improvement)

Positve correlation between average per capita consumption of alchol and frequency of cirrhosis

Amount ingested and duration of intake correlate with incidence of ALD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does Gender play a role in ALD?

A

Gastric mucosal alcohol dehydrogenase activity is lower in women, so there is greater hepatic exposure to ingested alcohol in women

HCV or HBV infection worsens ALD

Risk of liver injury increases above a threshold level of 80 g/day for men and 20 g/day for women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How do you screen for alcohol problems?

A

CAGE questions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Does the type of alcohol consumed influence the likelihood of developing hepatotoxicity?

A

Nope!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are physical signs that can be seen in ALD?

A

Jaundice

Spider nevi

Hepatomegaly

Splenomegaly

Spider nevi are these:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is this?

A

Spider nevi - seen in ALD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What lies on the spectrum of liver disease in patients who drink alcohol?

A

Normal, fatty liver, alcoholic hepatitis, cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is alcoholic steatosis?

A

Consequence of alcohol oxidation

Excess lipid is stored in large droplets within individual hepatocytes

Generally considered a benign, reversible condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What od we see here?

A

Alcoholic steatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are features of alcoholic hepatitis?

A

COmbination of steatosis, hepatocellular necrosis, and acute inflammation

Most pronounced in zone 3 of hepatic acinus

Eosiniophilic fibrillar material (mallory’s hyaline bodies) in ballooned hepatocytes

Focally intense lobular infiltration of polymorphonuclear leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What do we see pathologically in cirrhosis/

A

Deposition of collagen around terminal hepatic veina dn along sinusoids

Characteristic chicken-wire pattern of scarring

Chronic alcohol use impairs normal regenerative response resultin gin small nodules of regenerating parenchymal and micronodular cirrhosis

Abstinence is associated with development of macronodular cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What do we see here?

A

Cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What do we see here?

A

Micronodular cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What therapy is available for patients iwth ALD?

A

Discontinue alcohol use and resume nutritious diet

Enroll pt in detox proram

Hospitalize for complications of electrolyte abnormalities, cardiac dysfunction, pacnreatitis, hemorrhagic gastropathy, major alcohol withdrawal syndromes, and infection

No specific drug therapies

Perhaps liver tranplant - if compliant and abstinent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is NAFLD?

A

Non-Alcoholic Fatty Liver Disease

Most common liver abnormality in US

mimics clinical nad histological features of ALD

Hepatic manifestation of metabolic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is along the spectrum of NAFLD?

A

NAFL - Steatosis

+ inflammation, ballooning, fibrosis, mallory’s hyaline, megamitochondria

NASH: Cirrhosis (cryptogenic, HCC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is necessary for a diagnosis of NASH?

A

Histology - steatosis, macro>micro, zone 3 predominant

Lobular inflamation
Hepatocellular ballooning, usually zone 3

May see perisinusoidal fibrosis, glycogenated nuclei, acidophil bodies, Mallory’s hyaline, iron, megamitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are outcomes of NASH?

A

16% improve

43% stable

41% progress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are diseases that are commonly associated with NAFLD?

A

Diabetes - 40%

Obesity - 40-100%
hyperlipidemia - up to 80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are pathophysiological features of NAFLD?

A

Insulin resistance

Increased adiposity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How can NAFLD present?

A

Asymptomatic with liver enzyme elevation or fatty liver on imaging (common)

Hepatomegaly, fatigue

Decompensated cirrhosis, HCC (rarely)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How do you diagnose NAFLD?

A

History- < 20g alchol per day

Labs - ALT> AST, elevated triglycerides, insulin resistance

Imagin - ultrasound, CT, MRI,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How do you treat NAFLD?

A

Control risk factors (weight loss, lipid control, diabetes control, abx for bacterial overgrowth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How do you distinguish ALD and NAFLD?

A

By history - NAFLD = < 20g alcohol consumption per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is PBC?

A

Primary biliary cirrhosis

Mostly women, mean age 50 years (wide range)

All races/nationalities

Variations in prevalence

Unknown etiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How do you diagnose PBC?

A

Elevated Alk/Phos/GGTP (cholestatic pattern)

Anti-mitochondrial antibodies (AMA) in 95%

Elevated serum IgM

Elevated cholesterol (in 75%)

Histologic confirmation - “florid duct lesion”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What do you see here?

A

Florid duct lesion

Indicative of PBC - primary biliary cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How do patients with PBC present?

A

Abnormal liver biochemistries

Symptoms of pruritis, fatigue

Signs and symptoms of advanced liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What physical exam findings do you see in primary biliary cirrhosis?

A

Hepatomegaly (50%)

Splenomegaly (30%)

Jaundice - late finding

Xanthomas

Xanthelasma

Butterfly pigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are diseases associated with PBC?

A

85% have other autoimmune diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is PSC?

A

Primary sclerosing cholangitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are secondary causes of sclerosing cholangitis?

A

AIDS cholangiopathy

Bile duct neoplasm
BIliary tract surgery

Choledocholithiasis

Congenital

Ischemic injury of duct

Caustic injruy (chemo)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Who gets PSC more?

A

Males, 25-45 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the pathogenesis of PSC?

A

Unknown - immune mediated (HLA-B8, HLA-DR3, HLA-Drw52A)

Hypersensitivity reaction - exposure to toxic bile acids within intestines or ischemic injury

CMV or cryptosporidium infection - inflammatory response to chronic or recurrent infection inp ortal circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How do patinets with PSC present?

A

Asymptomatic elevation of LFTs

Pruritis

Cholangitis (fever/chills/RUQ pain/jaundice)

Signs of advanced liver disease

Cholangiocarcinoma (as a result of chronic inflammatory process)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How do you diagnose PSC?

A

Elevated Alk Phos/GGTP

No specific antibody test (pANCA, anti SMA, positive ANA) not in ALL, but in most

Cholangiogrpahy - intrahepatic and extrahepatic ducts

Liver biopsy shows onion skin fibrosis around bile ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What disease has characteristic onion skin fibrosis around the bile ducts?

A

PSC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What do you see here?

A

PSC - primary sclerosing cholangitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What od you see here?

A

Onion skin fibrosis aroudn bile duts - Primary sclerosing cholangitis (PSC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What diseases are associated with PSC?

A

IBD - in many

Other immunoligcal diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are complicaitons of PSC?

A

Cholangitis

End stage liver disease

Cholangiocarcinoma

Risk of colon cancer increased 10x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How do you treat PSC?

A

Resect - avoid surgery

Dilate - dominant striture

Medication - ursodeoxycholic acid increases bile flow (Controversial)

Transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is autoimmune hepatitis and who gets it?

A

More in women than in men

Early adulthood/adolescence/ perimenopausal women

What it sounds like

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

How does autoimmune hepatitis present?

A

Acute hepatitis (fever, chills, RUQ pain, jaundice)

Insidious - abnormal LFTs fatigue, aches

Advanced liver disease/liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are diagnostic criteria for autoimmune hepatitis?

A

Serum ALT/AST abnormalities

Serum gamma gobulin (IgG > 1.5x nl)

ANA, SMA or LKM1 > 1:80 in adults

Liver biopsy to rule out other lesions

Normal levels of alpha-1-antitrypsin, ceruloplasmin

Seronegativity for infectious etiologies

No parenteral blood exposure

Low ethalnol ingestion

No use of hepatotoxic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

How do you treat autoimmune hepatitis?

A

Long term immunosuppression (mainstay) - prednisone, azathioprine, mycophenolate mofetil (cellcept)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What diseases are associated with autoimmune hepatitis?

A

SLE, MG, ITP, Pernicious anemia, other autoimmune disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is Wilson Disease?

A

Rare inherited autosomal recessive disorder of copper metabolism (ATP7B Gene)

Causes absent or reduced funciton of ATPase - decreased hepatocellular excretion of copper in bile, resulting in accumulation of copper in hepatocytes

Cellular death, release into blood where it can deposit in brain, kidneys, and cornea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What do oyu see here?

A

Copper deposition associated with Wilson Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is normal copper homeostasis?

A

Dietary copper is abosred by small intestine and transported to liver

Hepatocytes incorporate coppper into apoceruloplasmin to produce ceruloplasmin which gets secreted to blood

Copper also secreted to bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is copper homeostasis in wilson disease/

A

Mutaiton of ATP7B resutls in retention of copper in hepatocytes

Impaired incorporation of copper into ceruloplasmin so you get low serum ceruloplasmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

How does Wilson Dsease present?

A

Hepatic - 42% - Abnormal liver chemistries, Chronic hepatitis, Fulminant hepatic failure, cirrhosis

Neurologic - 34% - mild tremor, parkinson liek symptoms

Hematologic - 2% - hemolytic anemia

Psychiatric - 10% - depression, labile mood, frank psychosis

Rarely presents after 40 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are kayser Fleisher rings?

A

Deposition of copper in eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What do we see here?

A

Kayser Fleischer rings - Wilson’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

How do you diagnose Wilson Disease/

A

Low serum ceruloplasmin

Kayser Fleisher rings

Urinary copper > 100ug/24 hours

Hepatic copper > 250ug/g dry weight

Genetic testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How do oyu treat wilson disease?

A

First line - chelating agents (D penicillamine

Second line - zinc = blocks absorption

Diet - low copper

Liver transplant is curative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is HFE-Hereditary hemochromatosis?

A

Iron overload

Genetic - autosomal recessive

Mutation is most commonly occuring genetic abnormalities in american population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What causes HFE hereditary hemochromatosis?

A

HFE gene mutaitons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

WHat is the pathogenesis of HFE hereditary hemocrhomatosis?

A

Mutaiton in HFE causes altered HFE protein

Leads to impairment of iron sensing and absorption

Excess iron absorbed from GI tract

Iron deposits in liver, heart, pituitary and thyroid glands, pancreas, joints and gonads

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is normal iron homeostasis?

A

Dietary iron absorbed by duodenal enterocytes and exoprted itno blood by ferroportin

Circulates boudn to transferrin

Liver cell senses plasma iron and absorbs it via HFE/TFR2

HFE regulates synthesis of hepcidin

Hepcidin inhibits iron secretion by duodenum and release of iron by macrophages (neg feedback)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is hemochromatosis iron homeostasis?

A

Defect in HFE results in less hepcidin produciton

MOre iron is absorbed and stored in macrophages

MOre iron gets transported and deposited by plasma tranferrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is the classic triad of HFE hereditary hemochromatisis?

A

Cirrhosis, bronze skin, diabetes

Cirrhosis - deposition in liver

Bronze skin - pituitary

Diabetes - pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

WHat is a serious sequella of HFC hereditary hemochromatosis?

A

Deposition of iron in heart - can cause CHF, arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What do you see here?

A

Bronzed skin of HFC hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Why do women develop later onset of HFE Hereditary hemochromatosis?

A

Menstrual blood loss can artificailly deplete iron stores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

How do you diagnose Hereditary hemochromatosis?

A

Fasting transferrin saturation > 50% on two consecutive tests

Ferritin > 1000 ng/ml

Genetic testing

MRI with liver iron quantification

Liver biopsy - parenchymal iron distribution, 3+ to 4+ stainable iron in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is this a progression of?

A

Hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What do you see here?

A

Hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is a difference between hereditary/primary and secondary hemochromatosis?

A

Iron deposits in reticuloendothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What do ou see here?

A

Secondary hemochromatosis - deposition of iron in reticuloendothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

How do you treat hemochromatosis?

A

Screen family members

Phlebotomize blood once or twice per week to deplete iron stors

Maintenence phlebotomy to maintain low or low normal ferritin levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is the mortality associated with hereditary hemochromatosis?

A

Symptomatic have less survival rates

If phlebotomy is initiated before cirrhosis, can have simlar survivals

Liver transplats can help

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is cirrhosis?

A

end stage of any chronic liver diease

Characterized histologically by regenerative nodules surrounded by fibrous tissues

Clinically can be either compensated or decompensated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What lab results can suggest cirrhosis?

A

Liver insufficiency - low albumin, prlonged PT, high bilirubin

Portal hypertension (low platelet count)

AST/ALT ratio > 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What do you see on the right?

A

Cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is seen on the right?

A

Cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is hte progression/natural history of chronic liver dizease?

A

Chronic liver disease to compensated cirrhosis to decompensated cirrhosis to death

compensated to decompensated is characterized by development of complications (variceal hemorrhage, ascites, encephalopathy, jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is the most common source of complications from cirrhosis?

A

Portal hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What is significant about the coronary vein wrt portal hypertension?

A

Feeds upper stomach and esophagus - varices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What, from a vascular perspective, causes portal hypertension?

A

Increase in resistance ot portal flow, or increase in portal venous inflow (P = RxF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What occurs in cirrhosis that leads to portal HTN?

A

Increased intrahepatic resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are causes of portal HTN?

A

Cirrhosis is most common cause

Site of increased resistance is sinusoidal

Other causes are classified acording to site of increased resistance (pre-hepatic, presinusoidal, post sinusoidal, post hepatic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Where is the site of increased resistance in cirrhosis?

A

Sinusoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is the site of increased resistance in schistosomiasis?

A

Pre-sinusoidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the site of increased resistance in portal or splenic vein thrombosis?

A

Pre-hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is the site of increased resistance in veno-occlusive disease?

A

Post-sinusoidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is the site of increased resistance in budd-chiari syndrome?

A

Post-hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Why is portal hypertension a positive-feedback problem?

A

Backup causes splanchnic arterial vasodilation - this increases flow to the mesenteric veins and portal veins - causes hyperdynamic state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

How does a hyperdynamic circulatory state arise in cirrhosis?

A

Splanchnic and systemic vasodilation that decreases arterial blood volume seen by kidneys - causes RAAS system to activate and increase sodium and water retention, this expands plasma volume, leading ot hyperdynamic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is the relationship between state of cirrhosis and prevalence of esophageal varices?

A

Worse = greater risk of varices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Which varices are more likely to rupture?

A

Larger ones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What is the treatment of medium/large varices without hemmorrhage?

A

β-blockers indefinitely

Endoscopic variceal ligation in patients intolerant to β-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is the treatment of small varices with no hemorrhage?

A

Surveillance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is the treatment with variceal hemorrhage or recurren themorrhage?

A

Control hemorrhage

IV access and fluid resuscitation - don’t overtransfuse

Antibiotic prophylaxis

Pharmacological threapy

Endoscopic therapy

Shunt therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What is the efficacy of endoscopic variceal band ligation?

A

Controls bleeding in 90%

Rebleeding in 30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What is TIPS?

A

Transjugular Intrahepatic Portosystemic Shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What are gastric varices?

A

Bleedign in stomach - harder to manage, but still possible. Seen in portal hypertension

Endoscopic cyanoacrylate injection helps control bleeding (glue)

TIPS also controls bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is portal hypertensive gastropathy?

A

Endoscopic change seen in most portal HTN pts

May be mild or severe

Characterized by cobblestone appearance of mucosa

More proximal than distal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is type A hepatic encephalopaty?

A

Associated with Acute liver failure (tylenol toxicity, etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is type B hepatic encephalopathy?

A

Associated iwth porto-systemic Bypass without intrinsic hepatocellular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What is type C hepatic encephalopathy?

A

Associated with Cirrhosis and portosystemic shunting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Why does cirrhosis cause hepatic encephalopathy?

A

(Type C)

Translocation of substances across bowel - protein load and bacterial products

Failure to metabolize these substances in liver - delivered directly to brain, can cause damage

Ammonia is pretty useless test, though

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

How do you diagnose Hepatic encephalopaty/

A

Clinical findings and history

Ammonia levels are unreliable (poor correlation) - NOT necessary

Number connection test

Slow dominant rhythm on EEG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What are the stages of hepatic encephalopathy?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What is asterixis useful for?

A

Finding hepatic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What physical exam maneuvers are useful for evaluating hepatic encephalopathy?

A

Asterixis

Number connection test,

Draw a star

Sample handwriting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What is minimal hepatic encephalopathy?

A

Occurs in 30-70% of cirrhotic patients without overt hepatic encephalopathy

Detected by psychometric and neuro-psychological testing

May improve with lactulose or synbiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

How can you treat hepatic encephalopathy?

A

Identify and treat precipitating factor: Infection, GI hemorrhage, prerenal azotemia, sedatives,constipation

Lactulose (adjust to 2-3 bowel movements/day)

Protein restriction, short term if at all (not fully proven to be efficacious)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What is ascites?

A

Accumulation of fluid in the peritoneal cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What is the most common cause of ascites?

A

Cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What are causes of ascites?

A

Cirrhosis

Peritoneal Malignancy

Heart Failure

Peritoneal TB

Pancreas, Budd Chiari, Nephrogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Where does the fluid in ascites come from?

A

Weeping liver - from the liver itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Is portal vein obstruction enough to initiate ascites?

A

NO - need to have a bad liver

Portal HTN is not enough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Is hepatic vein obstruction enough for the initiation of ascites?

A

Yes, outflow block increases sinusoidal pressure which causes fluid to leak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

How does ascites develop?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What is the SAAG?

A

Serum Ascites Albumin Gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What is a SAAG > 1.1 indicate?

A

Source of ascites is hepatic sinusoids -> Sinusoidal HTN or postsinusoidal HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What does a SAAG < 1.1 indicate?

A

Peritoneal pathology (malignancy, TB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

How can you discern what the source of ascites is?

A

SAAG (< 1.1 = peritoneum, > 1.1 = hepatic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is a better therapeutic option for ascites, large volume paracentisis (LVP) or diuretics?

A

Both are equally efficacious - depends on lifestyle preferences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What is the most common iinfection in cirrhotic patients?

A

SBP - spontaneous bacterial peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What types of bacteria are responsible for SBP?

A

Gram negatives, more often than gram positives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Why does SBP occur?

A

Translocation of bacteria caused by:

Decreased immunity

Intestinal bacterial overgrowth (secondary to decreased transit time)

Increased permeability of intestinal mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

How do you diagnose SBP?

A

More than 250 PMN in ascitic fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

How do you treat SBP?

A

IV cefotaxime, amoxicillin

Oral ofloxoacin (in uncomplicated)

Avoid aminoglycosides

At least 5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What does the development of renal failure indicate for the prognosis for a patient with cirrhosis?

A

Increased mortality rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is hepatorenal syndrome?

A

Renal failure in patients with cirrhosis, advanced renal disease and severe sinusoidal portal HTN in the absence of histological changes in kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What are the two types of hepatorenal syndrome?

A

Type 1 - rapidly progressive, doubling of creatinine to > 2.5 or halving of creatinine clearance to < 20ml/min

Type 2 - more slowly progressive, creatinine > 1.5 mg/dl or clearance of creatinine < 40 ml/min (associated iwth refractory ascites)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What two things are always present in patients with hepatorenal syndrome?

A

Ascites and hyponatremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What do hyponatremia and ascites in the setting of liver disease and renal failure indicate?

A

Hepatorenal syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

How do you make a diagnosis of acute liver failure?

A

Coagulopathy (INR > 1.5)

Encephalopathy

Jaundice < 24 weeks duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What are the two main subdivisions of acute liver failure?

A

Fulminant

Subfulminant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What are major etiologies of fulminant hepatic failure?

A

Viral - HAV, HBV +/- HDV, HEV, HSV, CMV EBV, VZ, Adenovirus, Hemorrhagic fever viruses

Drugs/toxins - Acetaminophen, CCl4, mushrooms, ecstasy, TB meds, …

Vascular - Right heart failure, Budd-Chiari syndrome, shock liver, …

Metabolic - Wilson’s Disease, Pregnancy, Reye’s

Misc - malignant metastases, autoimmune

Intermediate - graft non-function in transplanted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What ist he most common cause of liver failure in the US?

A

Acetaminophen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Why do patients iwth acute liver failure die?

A

Multi-organ failure - CV dysfunction, renal failure, Hypoglycemia, coagulopathy, infection/sepsis, cerebral edemam secondary to hepatic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What is the basis of hepatic encephalopahty?

A

Nitrogen load to gut causes increased NH3 to liver, and other metabolites

Sent up to brain, causes damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What is the most dangerous sequellae of hepatic encephalopathy?

A

Cerebral edema - vasogenic and cytotoic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What is the cushing reflex?

A

Systemic hypertension with bradycardia - sign of cerebral edema (can be seen in acute hepatic failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What are signs of cerebral edema secondary to liver failure?

A

Cushing reflex

Decerebrate rigidity

Disconjugate eye movements

Loss of pupillary reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

How do you monitor cerebral edema in liver failure?

A

ICP

Cerebral perfusion pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What are coagulopathies seen in acute liver failure?

A

Decreased synthesiss of factors II, V, VII, IX, and X

Factor V has short halflife and is a good reflection of liver function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

Why do you have infection/sepsis in acute liver failure patients?

A

Kupffer cell malfunction, neutrophil malfunction and cell mediated immunity dysfunction

Risk increases with time in ICU

Gram + organisms more common than gram -

Fungal infections after 2 weeks in ICU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What is a cardiovascular sequellae of liver failure?

A

Low systemic resistance and pulmonary resistance

INcrease in Cardiac outupt increases metabolic rate which causes oxygen debt and relative hypotension and tachycardia –> lactic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

What are metabolic symptoms seen in acute liver failure patients?

A

Hypoglycemia - defective gluconeogenesis and inadequate uptake of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

How do you treat acute liver failure?

A

Depends on etiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What is the treatment for tylenol overdose?

A

N-Acetyl Cysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What is Hy’s Law?

A

Aminotransferase elevation accompanied by bilirubin elevation carries a worse prognosis than aminotransferase elevation alone

LFT elevation + bilirubin elevation = worse than LFT elevation alone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What are predictable vs idiosyncratic hepatotoxins?

A

Preidctable = dose dependent, reproducible, high incidence, short latency, absent extrahepatic involvement

Idiosyncratic = not dose dependent, poorly reproducible, low incidence, variable latency, can have extrahepatic involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What are the three phases of hepatic biotransformation of drugs?

A

Oxidation (Phase I) - CYP

Conjugation (Phase II) - Transferases

Excretion (Phase III)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What are CYP inducers?

A

Rifampin

Phenytoin

Carbamazepine

Phenobarbital

Dexamethasone
Alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What are CYP inibitors?

A

Grapefruit Juice
Erythromycin
Clarithromycin
Ketoconazole

RItonavir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What are three forms of alcoholic liver disease?

A

Hepatic steatosis

Alcoholic Hepatitis

Alcoholic cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What defines hepatic steatosis?

A

Large, fatty liver

Microvesicular or macrovesicular

Hepatomegaly, High serum bilirubin, alk. phos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What is microvesicular vs macrovesicular?

A

Macro - one single vacule with mucus pushed to the side

Micro - nucleus stays in the center, and you see multiple vacuoles

189
Q

What do you see here?

A

Hepatic steatosis

190
Q

What are symptoms of alcoholic hepatitis?

A

Non-specific or cholestatic

191
Q

what are lab findings in alcoholic hepatitis?

A

Hyperbilirubinemia, high alkaline phosphatase, leukocytosis

192
Q

What does hyperbilirubinemia, high alk. phos, and leukocytosis indicate?

A

Alcoholic hepatitis

193
Q

What do you find pathologically in alcoholic hepatitis?

A

Hepatocyte swelling adn necrosis (ballooning)

Mallory-Denk bodies - tangled skeins of cytokeratin filaments

Neutrophilic reaciton (lobular inflammation)

Fibrosis

194
Q

What do we see here?

A

Mallory-Denk bodies (Mallory’s hyalines)

Indicative of alcoholic hepatitis

195
Q

What is the final and irreversible stage of alcoholic liver disease?

A

Alcoholic cirrhosis

196
Q

What are findings in alcoholic cirrhosis?

A

Yellow-tan, fatty enlarged liver turns into a brown, shrunken, non-fatty liver

197
Q

What are vascular disorders of the liver?

A

Passive congestion (acute - failing heart in agonal period; chronic - CHF)

Shock

Infarction

198
Q

Where in the lobular architecture of the liver do you find ischemic necrosis?

A

Centrilobular hepatocytes

199
Q

What is veno-occlusive disease?

A

Fibrous occlusion of small hepatic venules < 1mm in diameter with secondary parenchymal congestion

200
Q

What do you see on the left?

A

Veno-occlusive disease

201
Q

What can cause veno-occlusive disease?

A

Pyrrolizidine alkaloids (>150 plants) - abdominal pain, ascites, hepatomegaly; chronic w/ portal HTN, or hepatic failure

After BM transplantation

Hepatic radiation adn chemotherapeutic drugs (azathioprine)

202
Q

What signs/symptoms will you see in a patient with veno-occlusive disease due to pyrrolizidine alkaloids?

A

Acutely - abdominal pain, ascites, hepatomegaly

Chronic - portal HTN, hepatic failure

203
Q

What signs/symptoms will you see in a patient with veno-occlusive disease after bone marrow transplantation?

A

54% are symptomatic

3 weeks after treatment, present wtih weight gain, thrombocytopenia, jaundice, hepatic failure

204
Q

What is on the differential diagnosis when considering veno-occlusive disease?

A

Constrictive pericarditis

CHF

Hepatic vein thrombosis (Budd-Chiari Syndrome)

Sickle cell disease

205
Q

What is caudate lobe (of the liver) hypertrophy indicative of?

A

Budd-Chiari Syndrome

Pretty reliable

206
Q

What can cause Budd-Chiari Syndrome?

A

Hypercoagulable states

Stasis or mass lesions (HCC, membranous obstruciton of IVC)

Vascular injury (trauma, vasculitis, sarcoidosis)

IBD, connective tissue disease, Multiple Myeloma, etc..

207
Q

What are features of hepatic adenoma?

A

Solitary, well-demarcated mass, encapsulated

Microscopically - resemble normal hepatocytes, BUT portal tracts, central venules are ABSENT, and arteries and veins traverse the tumor

Associated with oral contraceptive use

208
Q

What liver lesions are solitary, well-demarcated masses that are encapsulated. They also have absent portal tracts and central venules, and are associated with oral contraceptive use. More than 1 may be present?

A

Hepatic adenoma

Hepatic adenomatosis is if there are > 10 lesions

209
Q

What is focal nodular hyperplasia (FNH)?

A

Benign hepatocellular lesion

Can be of any size, and can be solitare or multiple

Can be associated with hemangiomas or hepatocellular adenomas

Doesn’t bleed or transform into HCC

can be seen in both normal or fatty liver

210
Q

Does FNH transform to HCC?

A

NO

211
Q

What do you see here?

A

Focal nodular hyperplasia

212
Q

What do you see here?

A

Focal Nodular Hyperplasia

213
Q

What is nodular regenerative hyperplasia (NRH)?

A

Can cause non-cirrhotic portal HTN

Compression of liver cell plates in between hyperplastic nodules (crowding of reticulin fibers)

Occurs in many systemic conditions - MPD, collagen vascular disease, medications (early antiretrovirals)

214
Q

What is a hemangioma?

A

Benign vascular tumor

Most common tumor in the liver

215
Q

What is this?

A

Hemangioma

Benign vascular tumor

MOst common ltumor in the liver

216
Q

What type of tumors are most common in the liver?

A

Secondary (mets)

217
Q

What is the most common metamstases to the liver?

A

Colon cancer

218
Q

This was taken from the liver, what do you suspect?

A

Metastatic colon cancer

219
Q

What are the primary liver tumors?

A

HCC (hepatocellular carcinoma)

Cholangiocarcinoma

Angiosarcoma

220
Q

What viral infection does HCC have a strong association with?

A

HCV

HBV

221
Q

What are common causeso fo HCC?

A

HBV

HCV

Aflatoxin B

Alcohol

Rare: contraceptive and anabolic steroids; metabolic disease; storage disease; vinyl chloride; old age

222
Q

What is this?

A

HCC

223
Q

What do HCC look like grossly?

A

Soft, hemorrhagic, tan masses

224
Q

What does HCC look like histologically?

A

Look like benign hepatocytes, but can be varying

Can produce Bile

225
Q

What is cholangiocarcinoma?

A

BIle duct carcinoma

Gland-forming (adenocarcinoma)

Arises from biliary epithelium

Strong association with PSC

226
Q

What is a klatskin tumor?

A

Hilar tumor of the biliary tree (cholangiocarcinoma

At the convergence of right and left hepatic ducts

Causes obstruction

227
Q

What is an intrahepatic cholangiocarcinoma?

A

Cholangiocarcinoma that occurs at more distal sites (not at the common biliary tree)

228
Q

What is an angiosarcoma?

A

Malignant vascular tumor

Multiple hemorrhagic nodules

229
Q

What is htis?

A

Angiosarcoma of liver

230
Q

What is this?

A

Bile duct cyst

231
Q

What is the most common presentation of cystic fibrosis patients in pediatric settings?

A

Failure to thrive

232
Q

Why do children typically fall off the weight curve (have poor weight gain)?

A

Not typically malabsorption

Typically poor caloric intake - picky eaters, parents feedign ‘low fat diet’

233
Q

When do you begin a malabsorption workup on a child?

A

When a child takes in more calories but still does not gain weight

234
Q

What are routine tests for malabsorption workup?

A

Calorie count

72 hour fecal fat

serum d-xylose

blood for CBC, chem screen, CRP, ESR, and celiac antibodies

235
Q

What are you thinking in a child with abnormal fecal fat and normal d xylose?

A

Pancreatic insufficeincy, such as cystic fibrosis

236
Q

What are you thinkin in a child with positive fecal fat with abnormal d-xylose?

A

Villous damage (Crohns, Celiac, allergy, autoimmune enteropathy, short gut syndrome)

237
Q

What is cystic fibrosis?

A

Autosomal recessive disease

1:2500 in caucasians

Chromosome 7

CFTR gene - transmembrane conductance regulator

238
Q

What is the most common Cystic Fibrosis mutation?

A

ΔF508

2/3 of mutations

239
Q

What is the funciton of CFTR?

A

Controls flow of H20 and ions in and out of cells

CFTR impaired function causes lack of ion flow

CFR is found in epithelial cells of lung, liver, pancreas, GI and reproductive

Moves chloride out and sodium in

240
Q

What is the result of CFTR mutations?

A

Cause epithelium to produce abnormally thick, sticky mucus that can cause obstructions

241
Q

What is a sweat test useful for?

A

CFTR defect identification -

CFTR mutations don’t allow for reabsorption of sodium in sweat glands - get sweatty salt

242
Q

How do most cystic fibrosis patients present?

A

Pancreatic insufficiency in 85%

243
Q

What are GI issues seen in Cystic Fibrosis?

A

Pancreatic insufficiency

Meconium ileus

Distal intestinal obstruction syndrome

INtestinal atresia

Rectal prolapse

244
Q

What is meconium ileus?

A

Bowel obstruction wihtin first 48 hours of life

Meconium obstructs the terminal ileum, resulting in abdominal distention and bilious vomiting

245
Q

What is distal intestinal obstuction syndrome?

A

In older patients, similar to meconium ileus

Can present as abdominal pain, constipation, bloating

246
Q

How does cystic fibrosis cause rectal prolapse?

A

Passage of large, bulky stools - can be due to pressing down and increased effort

Can often be presenting sign

247
Q

What are liver conditions seen in cystic fibrosis?

A

Biliary fibrosis/cirrhosis

Portal Hypertension

Cholestasis

248
Q

Why does cystic fibrosis cause liver disease?

A

Thickened secretions/bile blocks bile ducts leading to cholestasis

Cholestasis leads to inflammaiton, fibrosis and cirrhosis

Present with signs of portal HTN - hepatosplenomegaly, hypersplenism, variceal hemorrhage

249
Q

What is extra-hepatic biliary atresia?

A

Most common structural cause for neonatal jaundice

Abnormal LFTs

Abnormal physical exam: failure to thribe, jaundice, abndominal distension, +/- hepatosplenomegaly

250
Q

What is the most common structural cause for neonatal jaundice?

A

Extrahepatic biliary atresia (EHBA)

251
Q

What is the natural history of extrahepatic biliary atresia (EHBA)?

A

End stage liver disease - most common cause of transplants in children (liver)

252
Q

What casues extrahepatic biliary atresia?

A

Unknown - infectious? autoimmune? vascular accident?

253
Q

How do you diagnose extrahepatic biliary atresia?

A

Sonogram

hepatobiliary scan (HIDA) - most sensitive

Liver biopsy

Intraoperative cholangiogram

254
Q

What is HIDA?

A

Hepatobiliary scan - with technecium 99

Good to identify extrahepatic biliary atresia

255
Q

What do you see on biopsy of a patient with extrahepatic biliary atresia?

A

Cholestasis - bile plugs

Fibrosis with or without cirrhosis

Bile ductular proliferation

Inflammation

256
Q

How do you treat extrahepatic biliary atresia?

A

Portoenterostomy - excision of obliterated extrahepatic ducts and attachment of small bowel to porta hepatis to act as biliary conduit

A bridge to liver transplant

257
Q

What is the most common cause of constipation in children?

A

Stool witholding - control, fear

258
Q

What do you worry aobut if a pateint doesn’t respond to constipation treatment?

A

Hirschsprung’s Disease

Or if infant doesn’t pass meconium within first 24-48 hours of life, you must rule out Hirschsprung’s disease

259
Q

What is Hirschsprung’s Disease?

A

Most common cause of lower intestinal obstruciton in neonates

Males more than females

More commin in Down Syndrome

Delay of passage of meconium - constipation - abdominal distention - vomiting - perforation - enterocolitis

260
Q

What causes Hirschsprungs disease?

A

Failure of craniocaudal migration of ganglion cell precursors along GI tract

Absence of Meissner’s and Aurbach’s plexus causes lack of parasympathetic input - lack of relaxation

Results in obstructive symptoms

261
Q

How do you diagnose Hirshsprung’s disease/

A

Barium enema - look for transition zone

Rectal biopsy - check for presence or absence of ganglion cells

Normal biopsy:

262
Q

How do you treat Hirschsprung’s disease/

A

Surgery - resection of aganglionic segment and then pull through rest of bowel to rectum

Must make diagnosis early to prevent eneterocolitis - bacterial translocation

263
Q

What is the largest immune cell reservoir in the body?

A

The gut

264
Q

How does antigen uptake occur in the GI tract?

A

Direct sampling by dendritic cells

Particulate antigens sampled by M cells (Peyer’s patches)

Soluble antigen by transcellular (normal) or paracellular (inflammatory) mechanisms

265
Q

How do immune cells home to the gut?

A

Vitamin A is metabolized by resident GI dendritic cells, which induces integrin α4β7 on T and B cells during induction

They can then home back

Vitamin A deficiency leads to mucosal infections

266
Q

How do commensal bacteria fight off pathogenic bacteria?

A

Out competing

Inducing production of antimicrobial peptides

Inducing immune cell proliferation/specification

267
Q

What is oral tolerance?

A

Oral presentation before skin contact for immunization (tolerance development) causes less of a hypersensitivity reaction upon second exosure

268
Q

What is the major Ig in mucosal sites?

A

IgA

269
Q

What allelic variants are associated with Crohn’s Disease?

A

NOD2

270
Q

How do NOD2/ATG16L defects lead to increased inflammatory states of mucosa?

A

Lead to defective bacterial sensing, defective defensin production and persistent intracellular bacteria

271
Q

What infection are gut bacteria uniquely susceptible to?

A

HIV-1

CCR5 expressing cells

272
Q

What are mechanisms of GI defense against infection?

A

Gastric acid secretion (pH < 4 is bacteriocidal - PPIs may be increasing risk of C. diff)

Intact small bowel motility

Mucous secretion by enterocytes

Secretion of IgA

273
Q

What is a common feature of bacterial dysentery?

A

Enteroinvasion

274
Q

What are common features of enteroinvasion?

A

Bloody, mucopurulent stools

Signs and symptoms of inflammation (abdominal pain, fever, fecal leukocytes, leukocytosis)

275
Q

What are common organisms implicated in dysentery?

A

Shigella

Campylobacter

Yersinia

Enteroinvasive E. coli

Enteroinvasive salmonellosis

276
Q

What are features of toxin-induced diarrhea?

A

NO cellular invasion

Stools not bloody, not purulent, no fecal leukocytes

Toxins released by adherent organisms or preformed toxins (vibrio cholera, enterotoxigenic e. coli)

277
Q

What are mechanisms of action of toxin induced diarrhea?

A

cAMP

cGMP

Calcium channels

INterfere with Na driven absorption and stimulates chloride driven secretion

278
Q

What are mechanisms/examples of infection induced diarrhea?

A

C diff, enterohemorrhagic e. coli, enterotoxic e. coli

Features include cell injury, inflammation, intestinal secretion

279
Q

What is a difference between organisms with preformed toxins and those without, with respect to toxin-induced diarrhea?

A

Preformed toxins - do not require adhesion

280
Q

How does shigella present?

A

Invasive organism - mostly colonic, with scattered terminal ileal ulceration

Enteroadherence with release of toxin may precede enteroinvasion - may have watery diarrhea prior to teh dysentery

Doesn’t usually penetrate beyond mucosa - bacteremia is rare

281
Q

What is this?

A

Infectious colitis - not specific for given organism

282
Q

How do you get non-typhoid salmonella?

A

Five F’s

Food, fingers, feces, flies, fomites

283
Q

Where does salmonella typically infect?

A

Terminal ilieum, less likely colon

May present as gastroenteritis or dysentery

284
Q

What are risk factors for invasive non-typhoid salmonellosis?

A

immunosuppression

sickle cell anemia

schistosomiasis

reduced gastric acidity

Usually in terminal ileum, less frequently in colon

Bacteremia can lead to localized infections in joints, meninges, cardiac valves, bone

285
Q

What are features of salmonella typhi/typhoid fever?

A

Invades small bowel mucosa, lamina propria, lymphatics, blood stream

Minimal intestinal systems

Systemic toxicity - high fevers, headaches, toxemia, mental status changes

Then pain localizes to right lower quadrant as organisms localize to Peyer’s patches of ileum, which preceds diarreha, bleeding and perhaps even perforation

286
Q

What is campylobacter jejunii?

A

Most frequent cause of bacterial infections

Chicken, human and other animals are most frequent carriers

Asymptomatic, watery diarrhea, dysentery

Highest diagnostic yield is with stool cultures

287
Q

What is yersinia enterocolitica?

A

Favors invasion in right lower quadrant with acute onset that may mimic Crohn’s

Most common in children, may mimic appendicitis

Source - milk, ice cream, pets, animal food products

Enteroinvasive pattern, diagnosis with stool patterns

288
Q

What are features that can distinguish yersinia enterocolitica from Crohn’s, and from appendicitis?

A

From crohns - acute onset

From appendicitis - diarrhea

289
Q

What are major causes of enterotoxic diarrhea?

A

Vibrio cholerae, enterotoxic e coli

Never invasive - watery stool, often voluminous, often dehydrating

Caused by infected water or food

Organisms adhere to enterocytes, followed by elaboration of a toxin

290
Q

How does vibrio cholerae cause waterry diarrhea?

A

A and B subunits of enterotoxin

B unit Binds enterocytes - in small bowel

A unit Activates intracellular Adenylate cyclase, which stimulates secretion

Colon not involved

291
Q

What is enterotoxigenic e coli?

A

Most common cause of travelers diarrhea

Non-invasive

2 toxins - heat labile - resembels cholera toxin A (actiavtes Adenylate cyclase)

heat stable - activates guanylate cyclase

292
Q

What is enterotoxigenic e coli O1:H157

A

May be epidemic

Adheres to distal small bowel

Shiga-like toxin causes mucosal destruction, allowing toxin to enter circulation and bind to blood cells

Causes hemolytic uremic syndrome (HUS)

293
Q

How does staph aureus produce GI symptoms?

A

Preformed toxin - usually in dairy or cream products

Inadequate heating ot kill spores

Typical presentation is very early onset of upper GI symptoms (1-4 hours)

Followed by diarrhea - whole episode resolves in 24 hours

294
Q

What is the pathogenesis of clostridium perfingens?

A

May be epidemic

Almost always inadequately heated meat

Spores survive and organism proliferates rapidly, if not adquately cooled immediately

Diarrhea starts about 8-24 hours after ingestion, self limited after about 24 hours

295
Q

What is the most common source of traveler’s diarhea?

A

Enterotoxigenic e coli

296
Q

What is the most common type of community acquired gastroenteritis

A

Viral

297
Q

What is the most common cause of diarrhea in young children?

A

Viral

298
Q

What is the main culprit of viral gastroenteritis?

A

Rotavirus - double stranded RNA virus

Proliferation of secretory crypt cells - secretory diarrhea

Destruciton of mature enterocytes in small bowel

BBM enzymes reduced - undigested disaccharides - osmotic component

Fecal-oral, respiratory secretions, contaminated surfaces

299
Q

What is the most common cause of community acquired infectious diarrhea in adults?

A

Norovirus - norwalk virus

300
Q

What is significant about hte pathogenicity of norovirus?

A

Need very small inoculum

Non-invasive

Reversible lesions in upper jejunum - loss of BBM enzynems - can lead ot osmotic diarrhea

Abrupt onset - lasts 12-60 hours

301
Q

What are risk factors for C. diff?

A

Typically after exposure to antibiotics, or nosocomial exposure

Highest risk is clindamycin

Most commonly used in patients treated with penicillins, cephalosporins, and early generation quinolones

INcreased risk with age and PPI use

302
Q

What antibiotic has the highest risk of c. diff?

A

Clindamycin

303
Q

How does c. diff cause disease?

A

part of normal flora - becomes pathogenic when normal flora disturbed

304
Q

What are presentations of c. diff?

A

Asymptomatic, diarrhea, pseudomembranous colitis, severe fulminant oclitis,

(Broad spectrum)

305
Q

What do we see here?

A

Pseudomembranes from C. diff colitis

Volcanic eruptions

306
Q

What is giardiasis?

A

More common in IgA deficient patients

Watery diarrhea

More likely to produce upper GI symptoms

307
Q

What infeciton is common in patients with IgA deficiency?

A

Giardiasis

308
Q

What are differences between IBD and IBS?

A
309
Q

What are causes of colitis?

A

Ulcerative colitis

Crohns

Radiation, ischemia, infection, antibiotics, NSAIDS, diversion colitis, diverticular colitis

310
Q

How do you differentiate between acute infection and IBD?

A

Duration of symptoms, onset of symptoms, platelets, Hgb and biopsy

311
Q

Where is the inflammation in ulcerative colitis?

A

Only in colon - Mucosal only

Pan colitis

312
Q

Where is the inflammation in crohn’s disease?

A

Transmural inflammation that can be in the proximal colon (ileitis, ileocolitis, colitis)

313
Q

What are environmental risk factors for IBD?

A

Smoking, appendectomy, high sanitation level in childhood, high intake of refined carbohydrates, perinatal infection

314
Q

What is the role of bacteria in the pathogenesis of IBD?

A

Germ free models do not develop colitis

315
Q

Which IBD affects rectum?

A

UC - Starts at rectum, and works its way back. May have abrupt cutoff. Continuous

CD - patchy, transmural inflammation at any part of GI tract

316
Q

What are features of UC?

A

Colon only

Mucousal inflammation

Continuous distribution

Rectal involvement

317
Q

What are potential extents of UC?

A
318
Q

What are we looking at?

A

Spectrum of disease - UC

319
Q

What are complications of ulcerative colitis?

A

Toxic colitis - megacolon

Dilatation of large bowel - gas

Prelude to perforation

320
Q

What are features of Crohns Disease?

A

Transmural, patchy inflammation

Can affect any part of the GI tract

321
Q

Where is Crohn’s Disease commonly presenting?

A
322
Q

What does Crohn’s Disease look like on the gut wall?

A

Transmural inflammation

323
Q

What is this?

A

Aphthae - how inflammation begins in Crohn’s Disease

324
Q

What are complications of Crohn’s Disease?

A

Inflammation, Fistulization, Obstruction, Microperforation

325
Q

This is an ileum, what is this?

A

Crohn’s Ileitis - Cobblestone ulceration

326
Q

What do we see here?

A

Cobblestoning, Cookie cutter ulcers, deep ulcers

Crohn’s Disease

327
Q

What is this?

A

Cobblestone appearance of Crohn’s Disease

328
Q

What is this? When does it occur?

A

Granuloma - Hallmark of Crohn’s Disease, but only seen in < 30% of pts

329
Q

What is a hallmark of Crohn’s that differentiates from Ulcerative colitis, that surgeons often see?

A

Creeping mesenteric fat

330
Q

What are symptoms of strictures/obstructions that are often seen as complications of Crohn’s Disease?

A

Post-prandial cramps

Distention

Borborygmi - loud bowel sounds

Vomiting

Weight loss

331
Q

Where can fistulas occur in Crohn’s Disease?

A

Enteroenteric - can be asymptomatic

Enterovesical - can present as UTIs

Retroperitoneal - abscess signs, if affets psoas

Enterocutaneous - drainage via scar

Perianal - pain, drainage

Rectovaginal - drainage

332
Q

What are the most common fistulas seen in crohn’s disease?

A

Perianal

333
Q

Which IBD classically involves the rectum?

A

UC

CD doesn’t typically

334
Q

What are some extra-GI features of IBD (Both UC and CD)?

A

Aphthous stomatitis, episcleritis and uveitis, arthritis, vascular, E. nodosum, p. gangrenosum

335
Q

How does the arthritis of IBD typically present?

A

Monoarticular, asymmetrical, large joints, no synovial destruction, seronegative

336
Q

What are long term copmlications of IBD?

A

Neoplasms - UC and CD: colorectal cancer; CD: small bowel adenocarcinoma

Nutritional and metabolic distrubances

337
Q

What are long term sequellae of IBD?

A

Gallstones, malabsorption, renal disease

338
Q

How do children with IBD present?

A

Fever

Anemia

Arthritis

Failure of growth and development

339
Q

How do you treat IBD?

A

Anti-inflammatory (5-aminosalicylates, corticosteroids)

Immunomodulators (azathioprine, 6-mercaptopurine, MTX)

Biologics (infliximab, adalimumab, certolizumab, golimumab)

Antibiotics (Crohn’s more than UC)

Surgical therapy

340
Q

What surgery is used for UC vs Crohn’s?

A

UC = total proctocolectomy with end-ileostomy

Crohn’s - Segmental resection with primary anastamosis

341
Q

When you have collar-button ulcers, what are you thinking?

A

Entameoba hystolitica

342
Q

What antibiotic can be used to increase gastric emptying?

A

Erythromycin - motilin receptor agonist

343
Q

What is the activity of metoclopramide?

A

Dopamine receptor antagonist, seratonin receptor agonist

Prokinetic

344
Q

What is domperidone?

A

D2- receptor antagonist (peripheral)

Not available in US - prokinetic therapy

345
Q

How does Nausea and Vomiting occur physiologically?

A
346
Q

What are classes of anti-emetics?

A

Central muscarinics, Dopaminergic (D2), histaminergic (H1), serotinergic (5-HT3)

347
Q

What are phentothiazines?

A

D2 receptor blockers in the CTZ that are anti-emetics

Also have anithistamine and anticholinergic effects

Adverse = parkinson-like symptoms

E.g. prochlorperazine, chlorpromazine

348
Q

What are the buytrophenones?

A

Haloperidol, droperidol

Dopaminergic receptor inhibitors

Used for anti-emesis

Toxicity = parkinson-like effects

349
Q

What are the 5-HT3 antagonist anti-emetics?

A

the -setrons (ondansetron, tropisetron, granisetron)

Acts at 5-HT3 receptor in CTZ

Mild gastric prokinetic effects

350
Q

What are anti-diarrheals?

A

Anti-motility agents used in clinical conditions of reduced absorptive surface, or diarrhea of other etiology

E.g. loperamide, diphenoxylate with atropine, codeine, opium drops

351
Q

What is octreotide?

A

Synthetic analogue of somatostatin - used in inhibiting release of secretory hormones in secretory tumors

Gastrinomas, carcinoid tumors, VIPomas

352
Q

What is clonidine used for in GI?

A

Adrenergic stimulation increases electrolyte absorption and inhibits fluid secretion

Use limited by hypotension, drowsiness and depression

353
Q

What cells typically release 5-HT in the motility pathway?

A

enterochromaffin cells

354
Q

What is alosetron?

A

5-HT3 receptor antagonist used in treatment of IBS-Diarrhea

Block serotonin efect on myenteric plexus acetylcholine release, leads to reduced chloride secretion and decreased motility

355
Q

What do you want to do to treat a constipated patient?

A

Increase secretion - chloride transport is curcial in regulation of fluid secretion

Activation of apical chloride channels and arriers leads to secretion of Cl ions which is the major determinant of mucosal hydration throughout GI tract

356
Q

What is lubiprostone?

A

Chloride-induced secretion stimulatnt

Prostaglandin derivative that is highly selective to type 2 Cl channel

Exerts secratoggue effects through activation of CFTR to increase Cl secretion

357
Q

What is linactolide?

A

Agonist of guanylate cyclase C receptors on luminal surface of intestinal goblet and enteroendocrine cells

INcreases intracellular cGMP leading to activation fo CFTR

358
Q

37 year old successful stock broker, entertains clients 4 nights weekly for last 6 years. Typically drinks about 5 mixed drinks each dinner. Develops 5 BMs/day, greasy and particularly foul smelling.

Treat with?

A

Presentation consistent with chronic alcoholism and pancreatic insufficiency: Treat with pancreatic enzymes

359
Q

27 year old NYC diamond dealer with 6 year history of ileitis undergoes resection of 35 cm of terminal ileum .Within 2 weeks of surgery develops 6 loose BMs daily

A

Pt has had resection of site of bile salt reabsorption and bile salts are spilling into colon causing an irritant effect leading to watery diarrhea. Treatment: use cholestyramine or other bile salt binding agent

360
Q

59 year old develops epigastric pain. Self treats himself with OTC omeprazole for 8 weeks without success. Endoscopy reveals 2 large gastric ulcers and multiple ulcers in duodenal bulb. He develops 8 watery bowel movements daily that do not diminish with decrease in fasting.

A

Symptoms are consistent with gastrinoma and a secretory diarrhea, ie. gastrinoma. Treatment: Attempt location of tumor for resection if possible, and use octreotide to reduce the gastrin- stimulated diarrhea.

361
Q

66 year old woman has just had a colectomy for Crohn’s disease and has had 3 prior small bowel (SB) resections. She has 160 cm of residual SB. She has over 2 liters of ileostomy output daily.

A

She has lost her colonic water absorptive capacity. Her length of residual small bowel is adequate to avoid malabsorption as a cause of her diarrhea. Treatment: Use agents to slow intestinal motility to increase absorbtive time (e.g. loperamide, diphenoylate, codeine)

362
Q

19 year old college freshman half marathon state champion, drinks approximately 3 liters of caffeine-free diet soda daily, often before long training runs. She has 6 watery BMs daily with near incontinence during long training runs.

A

In her diet soda she is ingesting large amounts of non-absorbed osmotic artificial sweeteners e.g. sorbitol

363
Q

61 year old ER nurse, develops diarrhea consisting of up to 8 watery BMs daily. She has developed flushing that reminds her of her months of emerging menopause 8 years ago.

A

Combination of watery diarrhea in combination with flushing should suggest the diagnosis of carcinoid tumor. As with gastrinoma, described above, surgical management is the primary option and octreotide is used to reduce the secretory diarrhea

364
Q

71yearold,livinginanursinghomeisfebrile to 101.0F is admitted to the hospital for treatment of pneumonia with amoxacillin-clavulinic acid. 3 days after admission she develops 8 watery BMs daily and spikes a fever to 102.9F.

A

New onset of diarrhea in the hospital, especially with antibiotic use strongly suggests the diagnosis of Clostridium difficile. Treatment: Metronidazole or vancomycin and try to limit antibiotic use.

365
Q

A 29 year old is addicted to oxycontin and is admitted for in-patient detoxification. He develops, nausea, vomiting, and 8 watery BMs/day during the first 48 hours of narcotic withdrawal.

A

Symptoms are consistent with narcotic withdrawal syndrome. This form of diarrhea is treated with clonidine. Use is often limited by hypotension.

366
Q

What do we see here?

A

Normal colon

367
Q

What do you see here?

A

Ulcerative colitis - we know because:

  • Affects colon and rectum only
  • Continuous inflammaiton
  • Retrograde spread from rectum
  • partial or pancolitis
  • Circumferential inflammation
368
Q

What do we see here?

A

Ulcerative colitis - Mucosal inflammation only

369
Q

Normal on left, what is on right?

A

Distorted crypts, dense mononuclear inflammatory cells

UC or Crohn’s

370
Q

Why do IBD have deformities of crypts?

A

Destruction and reconstruction, allows deformation to occur

371
Q

What do we see here?

A

Crohn’s disease, we can tell because:

  • Any part of Gi tract
  • Thickened bowel wall
  • Stenosis
  • Discontinuous
  • Cobblestoning andulcers
  • Non-circumferential
372
Q

What do we see here?

A

Thick mesentery, creeping fat

Crohn’s Disease

373
Q

What is significant about hte inflammation seen in Crohn’s disease vs in UC?

A

Transmural!

374
Q

What do we see here?

A

Transmural inflammation seen in Crohn’s Disease

375
Q

What is a pathological feature of Crohn’s Disease that can clinch a diagnosis?

A

Granulomas

376
Q

What feature of Crohn’s Disease is this?

A

Granulomas

377
Q

What is a potential complication of crohn’s disease shown here?

A

Penetrating fissures, leading to peritonitis

378
Q

When can this occur?

A

Severely active Ulcerative Colitis or Crohns Disease

379
Q

What do we see here?

A

Atrophic mucosa after long IBD course (“burned out IBD”)

Everything becomes flat and featureless

380
Q

What do we see here?

A

Inflammatory polyps

Can indicate UC or CD

381
Q

What sequellae of IBD is characterized by massive dilation and potentially perforation of the colon?

A

Toxic Megacolon

382
Q

Where does toxic megacolon typically present?

A

Transverse colon

383
Q

What is a dangerous risk of IBD?

A

Dysplasia and then cancer

384
Q
A

C. diff- associated colitis

385
Q

What do we see here?

A

Pseudomembranous colitis

Likely Clostridium difficile-associated colitis

386
Q

What do we see here?

A

Pseudomembranes

Surface necrosis, dilated crypts, volcano like acute inflammatory exudates

Likely from C. Difficile Colitis

387
Q

What is clostridium difficile?

A

Gram positive, spore-forming rod

Endemic in healthcare settings

Easy transmission

Altered colonic microlfora due to broad spectum antibiotics and chemo

Treat with metronidazole, vancomycin, fecal transplant

388
Q
A

Colonic ischemia

389
Q

What factors can predispose a patient to colonic ischemia?

A

Low blodo flow relative to tissue mass

Poor collaterals

Watershed regions (SMA-IMA, IMA-hypogastric

Sensitivity to vasoconstrictors

Long vasa recta

Reduced blood flow during mechanical activity

Countercurrent blood flow

390
Q

What are the watershed areas of blood flow of the colon?

A
391
Q

What is the significance of countercurrent blood flow in the colon?

A

Can cause colonic ischemia - veins can draw oxygen from arteries in colon

392
Q

Who gets colonic ischemia?

A

Elderly patients (heart dx, vascular dx, low-flow states)

Shock

Young patients (heavy exercise, oral contraceptives, vasoconstrictive drugs, usually limited to mucosa and resolves completely)

393
Q

What do we see here?

A

Colonic ischemia

394
Q

What occurs in colonic ischemia?

A

Edema of colon - engorged blood vessels followed by leakage of plasma and rbcs into tissue

395
Q

Which disease has characteristic “thumbprinting” in the colon on barium enema?

A

Colonic ischemia

396
Q

What is this?

A

Diverticular disease

397
Q

What do we see here?

A

Diverticular disease

398
Q

What are presentations of diverticular disease?

A

Painless bleeding

Inflammation (diverticulitis) - can cause perforation and peritonitis

Fever, LLQ tenderness, rope-like mass

399
Q
A

Can be collagenous colitis - need biopsy to know

400
Q

What do we see here?

A

Collagenous colitis

401
Q

What do we see here?

A

Lymphocytic colitis

402
Q

What are differences between collagneous and lymphocytic colitis

A

Both have chronic watery diarrhea, grossly normal mucosa, microscopic chronic inflammation

403
Q

What geographic regions get colon cancer?

A

Well-developed countries

404
Q

What are the strongest risk factors for developing colon cancer?

A

Advancing age (>50)

Country of birth

Hereditary syndrome (FAP, Lynch)

Longstanding IBD

405
Q

What are the strongest protective factors for colon cancer?

A

Physical activity

Aspirin, NSAIDs

Colonoscopy

406
Q

How does colon cancer develop?

A

Normal -> Adenomatous polyp -> cancer

During 5-10 years

407
Q

What defines stage III colon cancer?

A

spread to lymph nodes

408
Q

What defines stage IV colon cancer?

A

Spread to other organs

409
Q

What defines stage II colon cancer?

A

Breach of mucosal layers

410
Q

What determines prognosis of colon cancer?

A

staging

411
Q

What do patients present with when they have colon cancer?

A

Constipation/difficulty passing stool, bleeding, GI pain/discomfort

Desmoplastic reaction can casue narrowing of lumen

412
Q

What is this?

A

Pedunculated tubular adenoma

413
Q

What defines invasive vs non-invasive cancer in colon cancer?

A

If it passes through the muscularis mucosa

414
Q

What is this?

A

Sessile serrated polyp

415
Q

What are the molecular pathways of colon carcinogenesis?

A

APC, then k-ras, then DCC/18q genes, then p53

416
Q

What is microsatelite instability?

A

Mutation/loss of DNA mismatch repair genes

Mutations of key target genes (TGFβRII)

e.g. Lynch Syndrome

417
Q

What is CpG Island Methylation (CIMP)?

A

DNA methylation inhibits key gene expression

BRAF oncogene mutation

Mechanism of sessile serrated polyp leading to cancer

418
Q

What are common symptoms of colon cancer?

A

NO SYMPTOMS

Change in nature of stool (color - red/black/tar; caliber - thinner; frequency - less often, more often)

Abdominal discomfort or cramps

Unexplained weight loss

Loss of apetite

Anemia

419
Q

What are hte most common signs of colon cancer?

A

Abdominal mass, tenderness, distention

Enlarged liver (if metastatic)

Abnormal rectal exam - mass, fecal occut blood test positive

May not have signs

420
Q

What symptoms occur when a patient has a cancer on their right side of the colon?

A

Occult bleedign, anemia

Left - obstructive symptoms, overt bleedign

421
Q

What symptoms occur when a patient has a colon cancer on their left side of the colon?

A

Obstructive symptoms, overt bleeding

Right - occult bleedign, anemia

422
Q

Who is at average risk of colon cancer?

A

Men + women older than 50 years old

423
Q

What are high risk colon cancer groups?

A

Hereditary syndromes

IBD

Family history

Personal history

424
Q

What is the gold standard of colon cancer screening?

A

Colonoscopy

425
Q

What is a radiographic technique that can be used for screening for colon cancer?

A

Barium enema - can see the “apple core” lesion

426
Q

How do you change colon cancer surveillance for patients with family histories?

A

Start screening 10 years earlier

427
Q

What is the lifetime risk of cancer in FAP?

A

100%

428
Q

What is this?

A

FAP

429
Q

What is the genetics of FAP?

A

Autosomal dominant inherited syndrome

430
Q

Where can lesions occur in FAP?

A

Anywhere in GI tract

431
Q

What gene is mutated in FAP?

A

APC gene

432
Q

Do you need a family history to have FAP?

A

No - up to 30% are de novo mutations

433
Q

What is lynch syndrome?

A

(hereditary non-polyposis colon cancer)
Autosomal dominant Germline mutations in DNA mismatch repair genes (MSH2, MLH1, PMS1, PMS2, MSH6)

434
Q

What are genetic features of colon cancers from lynch syndrome?

A

Microsatellite instability

435
Q

What are clinical features of lynch syndrome?

A

Colonic neoplasms (few adenomas, proximal locaiton, multiple simultaneous cancers, typical histology - signet ring cell, mucinous)

Extraintestinal cancers (endometrium, GU, Small bowel, Brain, Stomach, OVary, pancreas)

436
Q

What test do you do on colon cancers that would be positive in Lynch syndrome?

A

MSI - microsatellite instability

Done on tissue, not blood

95% of lynch syndrome tumors are MSI+, 10-15% of sporadics are MSI+

437
Q

How do you know if a patient ahs lynch syndrome?

A

Family history

3,2, 1 rule

3 or more HNPCC-associated cancers - two of whom are first-degree relatives

2 or more generations

1 person affected before age 50

438
Q

What is this?

A

Colorectal adenoma

Most common polyp wherever colorectal cancer is common

Usually after 40 years old

Anywehre in colon or rectum

1/2-2 cm in size, but can be smaller or larger

Benign, but potential origin of cancer

439
Q

How does one define a colorectal adenoma?

A

benign neoplasm containing dysplastic colorectal epithelium

440
Q

What do we see here?

A

Colorectal adenoma - benign neoplasm consisting of dysplastic colorectal epithelium

441
Q

What are differences between dysplastic colorectal epithelium and normal epithelium?

A

Nuclei are elongated, darkly stained, crowded, overlapping

Cytoplasm is blurred distinction between enterocytes and goblet cells, reduced or excessive mucin

442
Q

What is tubular adenoma vs villous adenoma?

A

Tubular - tubules in adenoma

Villous - Finger-like prongs

Distinction made on lower magnification

443
Q

What do we see here? howd o you know?

A

Pedunculated tubular adenoma

  • smooth gross appearance is characteristic of tubular adenomas
444
Q

What do you see here?

A

Villous adenoma

Typically presenting as large and sessile (not pedunculated)

445
Q

What do you see here?

A

villous adenoma

They are rarely huge and carpet-like

May cause watery diarrhea, hypokalemia

446
Q

What is a difference between the sizes of villous and tubular adenomas?

A

Villous can be very very large - can cause watery diarrhea, hypokalemia

447
Q

What is a hyperplastic polyp?

A

Tiny (<1cm)

Clinically insignificant

Hard to distinguish from adenoma, similar to adenomas in age adn geographic distribution and may harbor genetic mutations

Taken out anyways (because you can’t really tell)

448
Q

What are these?

A

Hyperpastic polyps

Elongated, serrated, not dysplastic

449
Q

What is a sessile serrated polyp?

A

Precuror of microsatellite unstable CRC

Can be seen with narrow band imaging

450
Q

What are differences between hyperplastic polyps and sessile serrated polyps?

A
451
Q

What do we see here?

A

Adenoma glands

Organized, tubular or villous shapes, no stromal reaction

452
Q

What do we see here?

A

Cancer glands

Disorganized

Sharp angulations

Desmoplastic stroma

453
Q

What is the most important prognostic indicator of colorectal cancer?

A

Tumor stage

454
Q

What parameters are used in tumor staging?

A

Depth of tumor invasion

Lymph node metastases

455
Q

What are prognostic indicators of CRC that arent involved in staging?

A

Completeness of resection

Histologic grade (differention)

Venous invasion

Distribution of nodal mets

Molecular features

456
Q

What about differentiation of colorectal cancers is a prognostic feature?

A

Poor differentiatino - worse

457
Q

Which of htese colon cancers is owrse?

A

On the right - worse

458
Q

Is mucinous adenocarcinoma an important prognostic feature?

A

NO

459
Q

What features do MSI cancers often have that can be identified histologically via immunostain?

A

Lymphocyte infiltration (CD3 immunostain)

This is a favorable prognostic finding

460
Q

What is a common, small appendiceal tumor that occurs in the tip and is rarely malignant?

A

Appendiceal carcinoid

461
Q

This is in the appendix, what is htis?

A

Appendiceal carcinoid - nesting tumor pattern, round nuclei, speckled chromatin

462
Q

When you see evenly spaced, round nuclei in a histologic section of the appendix, what are you thinking?

A

Appendiceal carcinoid

463
Q

What is a mucinous cystadenoma?

A

Benign tumor of the appendix<!–anki–>

464
Q

What is this?

<!–anki–>

A

Mucinous cystadenoma - benign

465
Q

What is this?

A

Mucinous cystadenocarcinoma - malignant tumor

466
Q

How do you know if an appendix mucninous tumor is benign or malignant?

A

If you see it outside of the appendix

Outsdie = mucinous cystadenocarcinoma

Inside = mucinous cystadenoma

467
Q

What is this?

A

Anal cancer

468
Q

What are most anal cancers found to be histologically?

A

Usually squamous

Spreads locally to rectal sphincter, prostate nad vagina

MEts to iliac and inguinal lymph nodes

They are very radiosensitive

469
Q

What are treatment options for anal cancers?

A

Chemo and radiation can be as effective as surgery- so start with non-surgical options

GI and Liver (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions