FA 2 Flashcards
1
Q
Diverticulisis - complications/treatment of complications
A
- abscess
- fistula (colovesical –> pneumaturia)
- obstruction (inflammatory stenosis)
- perforation (–> peritonitis)
treatment: percutaneous drainage or surgery
2
Q
Acute mesenteric ischemia - presentation
A
- abdominal pain out of proportion of physical findings
- red currant jelly stools
- decreased sounds
3
Q
Angiodysplasia - definition, presetation, location
A
acquired torturous dilation of vessels –> hematoscezia
MC often in cecum, terminal ileum, ascenidng colon
4
Q
Colonic polyps - histological types (neoplastic or not?)
A
- hyperplastic - nonneoplastic
- hamartomatous - non-neoplastic
- adenomatous - neoplastic
- serrated - premalignant
5
Q
Colonic polyps - Adenomatous - types and malignancy
A
tubular –> less malignant potential
villous –> more malignant potential
tubulovirous –> intermediate malignant potential
6
Q
Serrated - mechanism/biopsy
A
premalignant, via CpG hypermethylation phenotype pathway with microsatellite instability
biopsy: saw-tooth pattern of crypts
7
Q
Polyposis syndromes - types
A
- familiar adenomatous polyposis (FAP)
- Gardner syndrome
- Turcot syndrome
- Peutz-Jeghers syndrome
- Juvenile polyposis syndrome
8
Q
Gardner syndrome?
A
FAP + osseus and sot tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth
9
Q
Turcot syndrome
A
FAP + malignant CNS tumor
10
Q
Peutz-Jeghers syndrome - definition/mode of inheritance/presentation
A
AD syndrome featuring with numerous hamartomas throughout GI tract, along with hyperpigmented mounth, lips hands, genitalia
11
Q
Peutz-Jeghers syndrome - cancer
A
increased risk of breast and GI cancers (eg. CR, stoma, small, panceas)
12
Q
Juveniles polyposis syndrome - definition/mode of inheritance/presentation
A
AD syndrome in children (typically under 5) featuring with numerous hamartomatous polyps in large and small intestine, stomach
13
Q
Lynch syndrome - cancers?
A
- Colorectal (de novo, not drom adenomatous polyp_
- ovarian
- endometrial
- skin
14
Q
Colorectal cancer (CRC) - risk factors
A
- adenomatous polys
- serrated polys
- familiar cancer syndromes
- Inflammatory bowel disease
- tobacco use
- diet of processed meat with low fiber
15
Q
Colorectal cancer (CRC) - location (in order)
A
rectosigmoid>ascending>descending
16
Q
Colorectal Cancer - barium enema x-ray
A
“Apple core” lesion
17
Q
Colorectal Cancer - markers/characteristics
A
CEA tumor marker –> food for monitoring recurrence, should not used for screening
18
Q
γ-Glutamyl transpeptidase (γ-GT) - increased in
A
- increased in various liver and biliary disease (just as ALP but not in bone disease
- associated with alcohol use
19
Q
Functional liver markers
A
- Bilirubin
- Albumin
- Prothrombin
- platelets
20
Q
Functional liver markers - platelets (and mechanism)
A
- decreased in advanced liver disease (low thrombopoietin, liver sequestration)
- decreased in portal hypertension (splenomegaly/splenic sequestration)
21
Q
hepatic steatosis?
A
Macrovesicular fatty change, heavy greasy liver, that may be reversible with alcohol cessation
22
Q
alcoholic hepatitis - histology
A
- Swollen and necrotic hepatocytes with neutrophilic infiltration
- Mallory bodies
23
Q
Mallory bodies - appearance
A
intracytoplasmic eosniphhiic inclusions of damaged keratin filaments
24
Q
Hepatic encephalopathy - triggers example
A
- increased NH3 production and absorption –> dietary protein, GI bleed, constipation, infection
- decreased NH3 removal –> renal failire, diuretics, bypassed hepatic flow post-TIPS
25
Hepatic encephalopathy - treamtnet (and mechanism)
1. lactulose --> increases NH4+ generation
| 2. rifamixn or neomycin --> decreases NH4+ producing gut bacteria
26
GI bleeding increases ammonia - mechanism
RBCs contain proteins Significant bleeding (esp upper GI) --> increases the protein load in the intestine and the production of ammonia
27
Diuretic therapy ammonia
Decreased serum potassium levels and alkalosis may facilitate the conversion of ammonium (NH4) to ammonia (+NH3).
28
Constipation - ammonia
Constipation increases intestinal production and absorption of ammonia
29
Liver tumors - types (and MC)
1. Hepatocellular Carcinoma (hepatoma)
2. Cavrnous hemangioma
3. Hepatic adenoma
4. Angiosarcoma
5. Metastases (MC)
30
cancers that give metastasis to liver
1. GI malignancies (Collon>>stomach>pancreas)
2. breast
3. lung
31
A complication of Hepatocellular carcinoma (may lead to..)
| Hepatocellular carcinoma spreads ....
- Budd-Chiari syndrome
| - hematogenously
32
Hepatocellular carcinoma - diagnosis
1. increased a-fetoprotein
2. US or contrast CT/MRI
3. biopsy
33
Cavrnous hemangioma - frequency/behavior/epidimiology
common, benign liver tumor
typically occurs at 30 - 50
(NO BIOPSY--> hemorrhage)
34
Liver angiosarcoma - definition/risk factors
Malignant tumor of endothelial origin
| associated with arsenic, vinyl chloride
35
Hepatic adenoma - definition/risk factors
Rare, benign liver tumor, often related to oral contraceptive or anabolic steroid use
- may regress spontaneously or rupture (abdominal pain and shock)
36
α1-antitrypsin deficiency causes (and mechanism
1. misfolded gene product protein aggregates in hepatocellular ER --> Cirrhosis with PAS+ globules in liver
2. lings --> low α1-antitrypsin --> uninhibited elastase in alveoli --> low elastic tissue --> panacinar emphysema
(CONDOMINANT TRAIT)
37
bilirubin - levels
total: 0.1 - 1 mg/dL
direct: 0 - 0.3 mg/dL
indirect: 0.2 - 0.7 mg/dL
jaundice: more than 2.5 mg/dL
38
Causes of mixed (direct and inderect) hyperbilirubinemia
1. Hepatitis
| 2. Cirrhosis
39
Wislon disease (hepalenticular degeneration) - mechanism
AR mutation in hepatocyte copper transporting ATPase (ATP7B gene, ch13) --> inadequate copper excretion into bile and blood (low serum ceruloplasmin, low serum copper, high urine copper) --> accumulates in liver, brain, kidneys, joints, cornea
40
Wislon disease (hepalenticular degeneration) - copper accumulates in (organs)
1. liver 2. brain
3. kidneys 4. joints
5. cornea
41
Wislon disease (hepalenticular degeneration) - presentation
before 40 with
1. liver disease (eg. hepatitis, acute liver failure, cirrhosis),
2. neurologic disease (dysarthria, dystonia, tremor, parkinsonism
3. psychiatric disease
4. Kayser-Fleisher rings
5. Hemolytic anemia
6. renal disease (eg. Fanconi syndrome)
42
Hemochromatosis - iron accumulation especially in
1. liver 2. pancreas 3. skin
| 4. heart 5. pituitary 6. joints
43
Hemochromatosis - lab/diangosis
1. increased ferritin and iron, decreased TIBC --> increased transferrin saturation
2. Liver MRI
3. biopsy with Prussian blue stain
44
Hemochromatosis - clinical manigestation
classic triad: 1. cirrhosis 2. DM 3. Skin pigmentation (bronze diabetes). ALSO: 4. reversible dilated cardiomyopathy 5. hypogonadism 6. arthropathy 7. HCC
45
hemochromatosis - mechanism of arthropathy
calcium pyrophosphate deposition --> esp in metacarpophalangeal joints
46
common cause of death in hemochromatosis
HCC
47
wilson vs hemochromatosis according to age of presentation
wilson --> before 40
hemochromatosis --> after age of 40 when total body iron > 20g (iron loss through menstruation slows progression in women)
48
wilson vs hemochromatosis according to treatment
hemochromatosis --> 1. repeated phlebotomy 2. chelation with deferasirox 3. deferoxamine
4. oral deferiprone
Wilson --> 1. chelation with penicillamine or trientine
2. oral zinc
49
Hepatocellular carcinoma - paraneoplastic
EPO
50
Biliary tract disease - clinical presentation
1. pruritus
2. jaundice
3. dark urine
4. light-colored stool
5. hepatosplenomegaly
51
Biliary tract disease - labs
cholestatic pattern of LFTs:
1. increased CB
2. increased cholersterol
3. increased ALP
52
Biliary tract diseases - types and epidemiology (what type of patients
1. Priamary sclerosing cholangitis --> middle-aged men with IBD (UC)
2. Primary billiary cirrhosis --> middle aged women
3. Secondary biliary cirrhosis --> Patients with known pbstructive lesions (gallstone, biliary strictures, pancreatic carcnoma)
53
Priamary sclerosing cholangitis - appearance (histology and gross)
histology --> concentric "onion skin" bile duct fibrosis (intrahepatic and extrahepatic ducts) --> alternating strictures and dilation "beading" on ERCP and MRCP
54
Primary sclerosing cholangitis is associated with
1. ulcerative colitis
2. p-ANCA
3. high IgM
55
Primary sclerosing cholangitis can lead secondaty to
1. biliary cirrhosis
2. cholangiocarcinoma
3. gallbpaladder cancer
56
Primary biliary cirrhosis - mechanism
anti - mitochondrial antibodies --> autoimmune reaction --> lymphocytic infiltrate + granulomas --> destraction of intralobular bile ducts
57
Primary biliary cirrhosis - associated with
1. anti - mitochondrial antibodies
2. increased IgM
3. other autoimmune conditions (eg. Sjogren, CREST, Hashimoto, RA, celiac disease)
58
Secondary biliary cirrhosis - mechanism
extrahepatic biliary obstruction (gallstones,, biliary structures, pancreatic Ca) --> high pressure in intrahepatic ducts --> injury/fibrosis and bile stasis
59
Gallstones (cholelithiasis) - types (MC)
1. Cholesterol stones (MC - 80%)
| 2. Pigment stones
60
cholelithiasis - definition and types and radiolucent of radiopaque
cholelithiasis: solide round stone in gallbladder
1. Cholesterol stones --> radiolucent with 10-20% radiopaque due to calcifications
2. Pigment stones --> if black --> radiopaque (Ca2+ bilirubinate, hemlyisis), if brown (infection) --> radiolucent
61
cholelithiasis - cholesterol stones are associated with
1. estrogen (female, obesity, multiparity, estrogen therapy)
2. Crohn
3. advanced age
4. rapid weight loss
5. Native american origin
6. Fibrates
62
cholelithiasis - pigment stones are associated with
1. Crohn
2. chronic hemolysis
3. Alcoholic cirrhosis
4. advanced age
5. biliary infections (Ascaris lumbricoides, Clonarchis sinensis)
6. total partental nutrition
63
Mirizzi's syndrome is a rare complication in which
gallstone in cystic duct of gallbladder --> compression of the common bile duct common hepatic duct --> obstruction and jaundice
64
acute pancreatitis - diagnosis
2 of 3 critera
1. acute peigastric pain (often radiating to the back)
2. high serum amylase or lipase (more specific) to 3x upper limit of normal
3. characteristic imaging findings
65
pancreatic pseudocyst risk for
rupture --> enzymes in the abnominal cavity and hemorrhage
66
Pancreatic abscess - due to, presents with
due to E. Coli
| presents with abdominal pain, high fever, persistently elevated amylase
67
special clinical presentation in necrotic pancreatitis
Periublical (Cullen's sign) and flank (Grey Turner) hemorrhage
68
Chronic pancreatitis - serum enzymes
amilase and lipase may or may not be elevated
69
pancreatic adenocarcinoma - Risk factors
1. Tobacco 2. chronic pancreatitis (esp >20 years)
| 3. Diabetes 4. >50 age 5. Jewish and African amerinan males
70
pancreatic adenocarcinoma - clinical presentation
1. abdominal pain radiating to back
2. Weigh loss (malabsrorption and anorexia)
3. Migratory thrombophlibitis (Trousseau syndrome)
4. Obstrctive jaundice (and pale stool) with Courvoisier sign (if at head)
5. secondary DM (if at body or tail)
71
pancreatic adenocarcinoma - markers
1. CA 19-9,
| 2. CEA (not specific)
72
pancreatic adenocarcinoma - Courvoisier sign?
presence of a palpably enlarged gallbladder which is nontender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones
73
CEA as a marker
not specific
1. colorectal ca (70%)
2. pancreatic ca (70%)
3. gastric ca
4. breast ca
5. medullary thyroid ca
74
1. primary biliary cirrhosis - antibodies
2. antoimmue hepatitis type 1 - antibodies
3. Biliary tract disease associated with ulcerative colitis
1. antimitochondrial
2. anti smooth muscle
3. primary sclerosing cholangitis
75
H2 blockers - drugs
- TIDINE
| 1. Cimetidine 2. Ranitidine 3. Famotidine 4. Nizatidine
76
H2 blockers - clinical use
1. Peptic ulcer
2. gastritis
3. mild esophageal reflux
77
H2 blockers - adverse effect
1. cimetidine inhibits p-450
2. cimetidine has antiandrogenic effects (prolactin release, gynecomastia, impotence, low libido in males)
3. cimetidine can cross BBB (confusion, dizziness, headache) and placenta
4. Cimetidine and ranitidine --> decrease renal excretion of creatinine
other H2 blockers are relatively free ok all these effects
78
proton pump inhibitors (PPIs) - adverse effects
1. high risk for C. difficile infection
2. high risk for pneumonia
3. low serum Mg2+ with long-term use
79
Antiacid affect on other drugs - mechansim
Can affect asbsorption, biovailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastrinc emptying
80
Antiacids - drugs
1. Aluminium hydroxide
2. calcium carbonate
3. Magnesium hydroxide
81
Aluminium hydroxide - toxicity
- all antiacids can cause hypokalemia
| - constipation and hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures
82
calcium carbonate - toxicity
- all antiacids can cause hypokalemia
- hypercalcemia (milk-alkali syndrome
- rebound acid increasing
83
Magnesium hydroxide - toxicity
- all antiacids can cause hypokalemia
- diarrhea
- hyporeflexia
- hypotension
- cardiac arrest
84
Bismuth - similar drug/mechanism of action
Similar drug: sucralfate
Binds to ulcer base, providing physical protection and allowing HCO-3 secretion to reestablish pH gradient in the moucous layer
85
Bismuth, sucralfate - clinical use
1. increases ulcer healing
| 2. travelers diarrhea
86
Misoprostol - mechanism of action
A PGE1 analog --> 1. increases production and secretion of gastric mucous barrier
2. decreases acid production
87
Misoprostol - clinical use
1. Prevention of NSAID-induced peptic ulcers (NSAID block PDE1 production)
2. maintenance of PDA
3. off label for induction of labor (ripens cervix)
88
Misoprostol - adverse effect
1. Diarrhea
| 2. contraindicated in women of childbearing potential (abortifacient)
89
Octreotide - mechanism
- Long acting somatostatin analog
| - Inhibits secretion of various splanchnic vasodilatory hormones
90
Octreotide - clinical use
1. acute variceal bleeds
2. acromegaly
3. VIPoma
4. carcinoid tumors
5. gastrinoma
6. glucagonoma
91
Octreotide - adverse effects
1. nausea
2. cramps
3. steatorrhea
4. increased risk for cholelithiasis (inhibition of CCK)
92
Sulfasalazine - mechanism
A combination of sulfapyridine (antibacterial) and 5- aminosalicylic acid (anti-inflammatory) --> activated by colonic bacteria
93
Sulfasalazine - clinal use
1. Ulcerative colitis
2. Crohn disease
(colitis component)
94
Sulfasalazine - adverse effect
1. malaise 2. nausea 3. sulfonamide toxicity
| 4. reversible oligospermia
95
Osmotic lexatives - drugs
1. Magnesium hydroxide
2. magnesium citrate
3. polyethlene glycol
4. lactulose
96
Loperamide - mechanism of action
agonist at μ-opiodi receptor --> slows gut motility
| POOR CNS penetration --> low addictive potential
97
Loperamide - clinical use / SE
Diarrhea
| SE: 1. constipation 2. nausea
98
Ondansetron - mechanism of action
5-HT3 agonists -->a. decreases vagal stimualtion
| b. central acting antiemetic
99
Ondansetron - clinical use
control vomiting:
a. postoperatively
a. in cancer chemotherapy
100
Ondansetron - adverse effect
1. Headache
2. constipation
3. QT interval prolongation
101
Metoclopramide - mechanism
D2 receptor agonists --> increased resting tone, conractility, LES tone, motility (does not influence colon transport time)
102
Metoclopramide - clinical use
1. Diabetic and postsurgery gatroparesis
| 2. antiemetic
103
Metoclopramide - adverse effects
1. increased parkinsonian effects, tardtive dyskenisia
2. restlessness/fatique 3. drawsiness 4. depression
5. diarrhea 6. Interaxt with digoxin and diabetic agents
104
Metoclopramide - drug interactions
1. digoxin
| 2. diabetic agents
105
Metoclopramide - Contraindicated in
patients with small bowel obstruction or Parkinson disease
106
Orlistat - mechanism
inhibits gastric and pancreatic lipase --> decreases breakdown and absorption of dietary fats
107
Orlistat - clinical use
weight loss
108
Orlistat - adverse effects
1. steatorrhea
| 2. decreased absorption of fat-soluble vitamins
109
Ursodiol (ursodeoxycholic acid) - mechanism
nontoxic bile acid --> increases bile acid secretion and decreases cholesterol secretion and reabsorption
110
Ursodiol (ursodeoxycholic acid) - clinical use
1. primary biliary cirrhosis
| 2. gallostone prevention or dissolution
