Combo Part Ii

Front 1

What embryologic origin does the spleen come from?

Back 1

Mesoderm along the left side of the dorsal mesogastrium.

Front 2

What is the arterial blood supply of the spleen?

Back 2

Via the splenic artery off the celiac trunk, as well as the short gastrics (contained in the gastrosplenic ligament).

Front 3

In regards to physiology, what does the red pulp (85% of the spleen) do?

Back 3

Made up of cords of Billroth, blood is filtered and senescent or abnormal red blood cells (misshaped, have cellular inclusions like Heinz bodies, Howell-Jolly bodies, or Pappenheimer bodies, or are tagged with auto-antibodies) are removed by macrophages. Heinz Bodies: denatured hemoglobinHJ Bodies: nuclear remnantPappenheimer bodies: iron granules

Front 4

In regards to physiology, what does the white pulp do?

Back 4

Serves as the lymphoid immune response, including generating primary antibody responses. Antigen presentation occurs via macrophage or dendritic cell processing of antigens, primarily in T-cell dominated peri-arterial sheathes. Germinal centers form and make antibodies (IgM).

Front 5

Beyond the red pulp and white pulp, what are other functions of the spleen?

Back 5

Production of properdin (helps activate the alternative pathway of complement) and tuftsin (augments activity of phagocytic cells). Production of monocytes/lymphocytes Site of hematopoiesis during early development.

Front 6

What is the most common infection causing splenomegaly/splenic rupture in tropical regions of the world? How about the developed world?

Back 6

Malaria. In the developed world infectious mononucleosis.

Front 7

What causes the splenic atrophy in severe sickle cell disease?

Back 7

Auto-infarction due to vascular occlusion by distorted RBCs, causing atrophy.

Front 8

What diseases cause reactivation of the hematopoietic function of the spleen?

Back 8

Myeloproliferative disorders (including polycythemia very, myelogenous leukemia, idiopathic thrombocytosis), which causes fibrous replacement of bone marrow.

Front 9

What is Felty Syndrome?

Back 9

Rheumatoid arthritis accompanied by splenomegaly and neutropenia. Associated with antibiodies against granulocytes and responds well to splenectomy. Performed when patients get leg ulcers, have profound thrombocytopenia, and transfusion-dependent anemia.

Front 10

What mutation is primarily responsible for the RBC defects of Hereditary Spherocytosis, and what is its treatment?

Back 10

Defective erythrocyte membranes due to defective Spectrin. RBCs are fragile and are destroyed after only a few passes through the splenic cords --> anemia, jaundice, intractable leg ulcers and increased incidence of gallstones. Splenectomy.

Front 11

In hemolytic anemia, what antibiodies characterize both the warm and cold variants?

Back 11

Warm = IgG Cold = IgM. Hemolytic anemia is auto-Ab against RBCs after exposure to meds (Quinidine, PCN, methyldopa), during collagen vascular disease or infection. Best treatment is steroids. Splenectomy indicated only for patients with warm antibodies in whom steroids have failed or are contraindicated.

Front 12

What role does the spleen play in idiopathic thrombocytopenic purpura?

Back 12

It both MAKES the antibiotics attacking platelets, but also sequestration of Ab-coated platelets. The spleen is often NOT enlarged in this condition.

Front 13

What are the indications for splenectomy in ITP patients?

Back 13

Failure to respond to steroids in 6-8 weeks of treatment or who relapse after withdrawal of steroids. Roughly 75-85% of patients will have sustained response following surgery.

Front 14

What is a sensitive method for detecting accessory spleen in patients who will or have undergone splenectomy and haven't had a durable response?

Back 14

Technetium scan.

Front 15

What is the pentad of symptoms that mark Thrombotic Thrombocytopenic Purpura?

Back 15

1. Fever 2. Thrombocytopenic purpura 3. Hemolytic anemia 4. Neurologic manifestations 5. Renal dysfunction Plasmapheresis and FFP the most effective treatment.

Front 16

What lab abnormalities are often noted in post-splenectomy patients?

Back 16

Leukocytosis and thrombocytosis, present 1-2 days after splenectomy and can last for weeks. Aspirin is often considered for treatment IF the platelet count increases beyond 61 x 10

Front 17

What bacteria are the most common causes of overwhelming post-splenectomy infection (OPSI).

Back 17

Encapsulated: includines Strep pneumonia, H. flu and Neisseria meningitidis. Pediatric patients are most at risk, and are therefore frequently treated with prophylactic antibiotics post-splenectomy.

Front 18

Where are accessory spleens most commonly found?

Back 18

At the splenic hilum (20%).

Front 19

In regard to splenic artery aneurysm, what population is most at risk?

Back 19

Females (4x more likely), patients with fibromuscular dysplasia or atherosclerosis.

Front 20

What is the risk of rupture for splenic artery aneurysms?

Back 20

3-9%. These patients often experience a double-rupture phenomenon, wherein they have a herald bleed and subsequent major bleed.

Front 21

In regard to splenic artery aneurysms, what are the indications for treatment?

Back 21

If patients are symptomatic, if they are pregnant or INTEND to get pregnant, show pseudoaneurysms, or are asymptomatic > 2 cm

Front 22

How does treatment of a splenic artery aneurysm vary depending on where it is located along the splenic artery: - Proximal

Back 22

Exclusion with a proximal and distal ligation

Front 23

How does treatment of a splenic artery aneurysm vary depending on where it is located along the splenic artery: - Middle

Back 23

Excision of the lesion

Front 24

How does treatment of a splenic artery aneurysm vary depending on where it is located along the splenic artery: - Distal

Back 24

Splenectomy

Front 25

What antibodies are associated with ITP, and what lab abnormalities will you find?

Back 25

Anti-GP IIb/IIIa (IgG) causing peripheral platelet destruction. Patients show increased bleeding time, decreased platelet count and increased metamyelocytes (similar findings in TTP).

Front 26

What is the defect that causes thrombotic thrombocytopenic purpura?

Back 26

Deficiency of ADAMTS (vWF metaloprotease) causing decreased degradation of vWF multimers. This increases platelet aggregation and thrombosis. On labs you'll see increased schistocytes, increased LDH.

Front 27

In a child with ITP, but platelets > 30,000, what is the treatment?

Back 27

Observation (many children under 10 show spontaneous resolution of symptoms).

Front 28

What is the appropriate timing of platelet administration during splenectomy for ITP?

Back 28

DUring the case following ligation of the splenic pedicle (will prevent consumption).

Front 29

What subset of splenectomy patients have increased risk of OPSI?

Back 29

Those who had it for hemolytic disorders or for malignancy.

Front 30

What is the most dangerous time following splenectomy for developing OPSI?

Back 30

Within two years of surgery.

Front 31

What is the most common benign spleen tumor?

Back 31

Hemangioma, also the most common benign tumor (duh).

Front 32

What is the most common MALIGNANT splenic tumor?

Back 32

Non-Hodgkins Lymphoma.

Front 33

What does a pyruvate kinase deficiency cause?

Back 33

Congenital hemolytic anemia, altered glucose metabolism. RBC survival is increased following splenectomy. It is the MOST COMMON non-membrane protein congenital hemolytic anemia requiring splenectomy.

Front 34

In patients with Hodgkin's Lymphoma, what cell anomalies are seen?

Back 34

Reed-Sternberg Cells: binucleated/lobed (Owl's Eye), made of up B-cells.

Front 35

In regard to cell population, what portents a favorable prognosis and what a worse prognosis?

Back 35

Lymphocyte predominant = best Lymphocyte depleted = worst Nodular sclerosis is the most common, and has good prognosis.

Front 36

What is the chemotherapeutic regiment for Hodgkin's Lymphoma?

Back 36

CHOP therapy = Vincristine, Cyclophosphamide, Prednisone and Procarbazine

Front 37

What is the chemotherapy treatment of choice for Hairy Cell Leukemia?

Back 37

Leustatin (Cladribine)

Front 38

What are lab findings associated with hyposplenism?

Back 38

Infection with encapsulated organisms, thrombocytosis/leukocytosis, Howel Jolly Bodies, increased target cells. Hyposplenism can occur with sickle cell disease, radiation, celiac disease, cancers, EtOH/drug abuse, SLE, Fanconi anemia, HIV, trauma, amyloidosis.

Front 39

In regards to the dorsal and ventral buds that become the pancreas, what does the ventral bud give rise to?

Back 39

The uncinate and a portion of the head of the pancreas.

Front 40

What are the two embryologic ducts of the pancreas, and what are their ultimate forms?

Back 40

The main duct (duct of Wirsung) is made by the fusion of the ventral bud duct and the distal portion of the dorsal bud duct. This drains into the common bile duct. The accessory duct (duct of Santorini) derives itself from the proximal portion of the dorsal bud duct and empties via the minor papilla.

Front 41

What vertebral level does the pancreas live?

Back 41

At the first and second lumbar vertebrae.

Front 42

Describe the uncinate process's position in regards to blood vessels?

Back 42

It lies posterior to the SMA and SMV, but ANTERIOR to the inferior vena cava and aorta.

Front 43

Where do the superior pancreatoicduodenal arteries arise from?

Back 43

Off the gastroduodenal artery that branches off the celiac trunk common hepatic artery.

Front 44

What arterial systems supply the body and tail of the pancreas?

Back 44

Branches of the splenic and left gastroepiploic arteries (the largest branches being the dorsal pancreatic and transverse pancreatic arteries)

Front 45

Where does the portal vein form in relation to the pancreas?

Back 45

Posterior to the neck, as the confluence of the splenic and superior mesenteric vein.

Front 46

What conditions are annular pancreas associated with?

Back 46

Down syndrome, intracardiac defects, or intestinal malrotation in kids.

Front 47

1. What is the overall architectural structure of the pancreatic islets? 2. How do regions of the pancreas vary in makeup?

Back 47

1. A core of Beta cells, and peripheral mantle composed of alpha, delta and pancreatic polypeptide cells. 2. The head is rich in PP cells, while alpha cells predominate the body and tail (beta and delta cells are evenly distributed throughout the pancreas).

Front 48

In regards to the exocrine pancreas, what cells are responsive for enzymatic production, and which for fluid composition?

Back 48

Acinar cells produce enzymes, while ductal cells make the fluid and electrolytes under vagal and humoral control.

Front 49

How do pancreatic digestive fluids alter in composition, depending on varying factors?

Back 49

At low secretory rates concentrations of chloride and bicarbonate equal plasma, but as rate increases (with neurohumoral stimulation) bicarbonate levels increase and chloride decreases (most potently stimulated by Secretin) Both sodium and potassium concentrations remain the same, and reflect plasma.

Front 50

How does Secretin (the most potent stimulator of bicarbonate secretion) affect the pancreas (pathway)?

Back 50

Mucosal S cells in the proximal small bowel's Crypts of Lieberkuhn are released in the presence of luminal acid and bile, which goes into blood and binds selective receptors on ductal cells. The increased bicarbonate neutralizes stomach acid that enters the duodenum.

Front 51

What does Lipase do, and how is it secreted from the pancreas?

Back 51

Cleaves fatty acids. Active.

Front 52

What does Trypsinogen​ do, and how is it secreted from the pancreas?

Back 52

A protease (active form trypsin) that activates OTHER digestive enzymes (chymotrypsin, elastase, carboxypeptidase, etc.). It is secreted in the INACTIVE form, and activated by Enterokinase in the duodenum.

Front 53

What does Colipase​ do, and how is it secreted from the pancreas?

Back 53

Prevents lipase inactivation by bile acids in the duodenum. Active form.

Front 54

What does Cholesterol esterase​ do, and how is it secreted from the pancreas?

Back 54

Cleaves cholesterol ester bonds for cholesterol/FA absorption. Active form.

Front 55

What does amylase​ do, and how is it secreted from the pancreas?

Back 55

Cleaves complex carbs. Active form.

Front 56

What are the three major phases of pancreatic contribution to digestion?

Back 56

1. Cephalic: vagal efferent signal trigger enzyme-rich, bicarbonate-poor secretions 2. Gastric: antral distention, protein delivery triggers gastrin release, which weakly stimulates pancreatic enzyme secretion. Acidification of the duodenum cuases secretin release, which stimulates bicarbonate production/release. 3. Intestinal phase: CCK and Secretin continue to work together to stimulate release of enzymes

Front 57

What does the following cell type secrete? What are it's stimulators and inhibitors? Function? Alpha cells.

Back 57

Release: Glucagon (glycogenolysis, gluconeogenesis, lipolysis, increased blood sugar) Release Stimulants: hypoglycemia, arginine, alanine Inhibitor: Hyperglycemia, insulin, somatostatin

Front 58

What does the following cell type secrete? What are it's stimulators and inhibitors? Function? Beta cells.

Back 58

Release: Insulin (Protein synthesis and glucose uptake by cells) Release Stimulants: Hyperglycemia, glucagon, CCK, GIP, choliergic stimulation, B-adrenergic input Inhibitor: Somatostatin, amylin, panreatin, alpha adrendergic input

Front 59

What does the following cell type secrete? What are it's stimulators and inhibitors? Function? Delta cells.

Back 59

Release: Somatostatin (inhibit acid production, pancreas/GB secretions, regulates pancreatic endocrine function) Release Stimulants: Acid in duodenum Inhibitor: None

Front 60

What does the following cell type secrete? What are it's stimulators and inhibitors? Function? PP cells.

Back 60

Release: Pancreatic polypeptide (decreases GB, pancreatic secretions, inhibits food intake) Release Stimulants: food, vagal stimulation, ghrelin Inhibitor: Somatostatin

Front 61

What does the following cell type secrete? What are it's stimulators and inhibitors? Function? Delta 2 cells.

Back 61

Release: Vasoactive Inhibitory Peptide aka VIP (Increases gut motility and secretions) Release Stimulants: Fat in diet, acetylcholine Inhibitor: Somatostatin

Front 62

What are physical manifestations of hemorrhage with pancreatitis?

Back 62

Turner's Sign: flank ecchymosis Cullen's Sign: periumbilical ecchymosis Fox's Sign: ecchymosis below inguinal ligament and/or involving scrotum

Front 63

What percentage of pancreatitis is caused by EtOH or stones?

Back 63

80-90%

Front 64

What percentage of symptomatic cholelithiasis patients will potentially develop pancreatitis?

Back 64

3-8%

Front 65

What autoimmune diseases are linked with pancreatitis?

Back 65

SLE, Sjogren's Syndrome

Front 66

What percentage of pancreatitis is idiopathic?

Back 66

10-15%

Front 67

What admission variables are included in Ransom's criteria?

Back 67

AgeWBC countGlucoseLDHAST < 3 (1%), 3-4 (15%), 5-6 (50%), ≥ 7 (100%)

Front 68

What variables are included at 48 hours in Ransom's Criteria?

Back 68

Hematocrit decreaseBUN increaseSerum calciumPaO2Base deficitFluid requirement < 3 (1%), 3-4 (15%), 5-6 (50%), ≥ 7 (100%)

Front 69

In gallstone pancreatitis what is the early recurrence rate if cholecystectomy is not performed?

Back 69

35%

Front 70

What are the major infection-related complications of pancreatitis that may require operation?

Back 70

Infected pseudocyst, necrosis or abscess

Front 71

What is the gene mutation in hereditary pancreatitis?

Back 71

In the cationic trypsinogen gene.

Front 72

What is a simple test to evaluate exocrine pancreatic function in the setting of chronic pancreatitis?

Back 72

Sudan stain of feces, or levels of fecal elastase.

Front 73

By what percentage would endogenous enzyme secretion in chronic pancreatitis have to be reduced to create malabsorption?

Back 73

90%

Front 74

What percentage of acute pancreatitis patients develop pseudocyts?

Back 74

Up to 10%

Front 75

What is the actual definition of a pancreatic pseudocyst?

Back 75

Collection of fluid containing pancreatic enzymes that persist beyond 4 weeks of onset of acute pancreatitis (if before that they are termed acute fluid collections).

Front 76

What percentage of patients see spontaneous resolution of pancreatic pseudocysts?

Back 76

Up to 60%. Pseudocyst size correlates with eventual need for surgery. Of those with lesions > 6 cm, 67% will need surgical intervention. A trial of 6 weeks - 3 months is usually given before intervention is considered (allows wall to mature). Lesions < 5 cm most likely to resolve. Surgery is USUALLY an internal drainage procedure (cyst jejunostomy or cyst gastrostomy).

Front 77

What are risk factors in development of pancreatic adenocarcinoma?

Back 77

Increasing agebeing blackmalesmoking (NUMBER ONE RISK FACTOR!!!!)HNPCC / FAP / Peutz-Jahger Syndromeataxia-telangiectasia syndromeBRCA2 mutationFAMM (familial atypical multiple mole melanoma syndrome)hereditary pancreatitischronic pancreatitiscystic fibrosisexogenous estrogen intakepernicious anemiahigh meat and fat in diet.

Front 78

Beyond Virchow's nodes (left supraclavicular), Sister Mary Joseph's nodes (periumbilical), what is the name of metastatic lymph nodes found in drop metastases in the pelvis (palpable on rectal exam)? All indicative of intra-abdominal metastases.

Back 78

Blumer Shelf nodes

Front 79

Of the pancreatic endocrine tumors, which are almost always malignant?

Back 79

Glucagonomas, somatostatinomas. Insulinomas are rarely malignant (85-95% benign)

Front 80

If someone is diagnosed with a pancreatic endocrine tumor, what other work up is required?

Back 80

Serum calcium (concerning for MEN syndrome). Gastrinomas (25%), Insulinomas (10%) are most commonly associated with MEN syndrome.

Front 81

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found? - Insulinoma

Back 81

Symptoms: Whipple's Triad (hypoglycemia while exercising/fasting, plasma glucose level lower than 50 mg/dL, resolution of symptoms with administration of IV glucose). Diagnosis: Closely monitored fasting exam measuring glucose and insulin levels. EUS is the most sensitive study to locate the insulinoma. Can also perform portal venous sampling (usually for when operation has failed to ID and remove the tumor) Octreotide scans miss ≥ 40% (BAD TEST). Location: evenly distributed Treatment: enucleation if < 2 cm, resection if > 2 cm

Front 82

What is a radiographic sign of an annular pancreas?

Back 82

Double bubble sign (distended stomach, pylorus, and distended early portion of duodenum). Usually the second portion of the duodenum is trapped. Treatment includes a duodenojejunostomy or duodenoduodenostomy and sphincteroplasty. PANCREAS IS NOT RESECTED.

Front 83

Describe Tropical Pancreatitis.

Back 83

Type of chronic pancreatitis, found in young patients. Associated with SPINK1 mutation, and ingestion of casava root.

Front 84

What is the defective mutation in Hereditary Pancreatitis? What is their overall risk of developing pancreatic cancer?

Back 84

AD mutation in Trypsinogen gene (PR551), that presents in childhood and causes progressive decrease in pancreatic function. Roughly 40% cancer risk.

Front 85

What are primary treatments for a pancreatic fistula?

Back 85

TPN, allow drainage and Octreotide. If those fail can perform ERCP, sphincterotomy and stent placement (decreases flow resistance into the duodenum).

Front 86

What is a common ERCP finding in patients with chronic pancreatitis?

Back 86

Chain of lakes.

Front 87

What is the most common cause of splenic vein thrombosis?

Back 87

Chronic pancreatitis. This leads to Sinistral HTN (gastric varices without esophageal involvement). Treat with splenectomy.

Front 88

What percentage of pancreatic endocrine tumors are nonfunctional? What percentage of those are malignant? Most common medical treatment?

Back 88

1. Thirty percent. 2. Ninety percent. 3. 5-FU, Streptozocin

Front 89

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found? - Gastrinoma (Zollinger-Ellison Syndrome). Roughly 50% are multiple, roughly 50% malignant.

Back 89

Symptoms: persistent reflux despite medical treatment, reflux associated with diarrhea. Diagnosis: Elevated gastrin (> 1000, not extremely reliable), Secretin stimulation test (Gastrin levels increase with administration of Secretin). Somatostatin receptor scintigraphy (aka Octreotide scan) single best study to localize tumor or mets. Location: Gastrinoma triangle (most likely to be extra-pancreatic). Treatment: Enucleation if < 2 cm, formal resection if > 2 cm.

Front 90

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found? - Somatostatinoma

Back 90

Symptoms: diabetes, gallstones, steatorrhea, hypochlorhydria Diagnosis: fasting somatostatin levels Location: Pancreatic head Treatment: E

Front 91

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found? - Glucagonoma

Back 91

Symptoms: Diabetes, stomatitis (inflammation of oral mucus membranes), dermatitis (necrolytic migratory erythema) Diagnosis: Fasting glucagon levels Location: Distal pancreas Treatment: Zinc, amino acids, or fatty acids can treat skin manifestations.

Front 92

What are common presenting symptoms, and diagnostic modalities for the following pancreatic endocrine tumor? Where are they most commonly found? - VIPoma (Verner-Morrison Syndrome)

Back 92

Symptoms: Watery diarrhea, hypokalemia, achlorhydria (WDHA). Diagnosis: R/O other lesions, elevated VIP levels. Location: Tail Treatment: Treat with octreotide.

Front 93

What is the #1 hepatic artery variant?

Back 93

right hepatic artery off SMA, courses behind pancreas, posterolateral to the common bile duct

Front 94

What variant of the left hepatic artery is found in about 20% of the population?

Back 94

left hepatic artery off left gastric artery

Front 95

What is the most common variant of the common hepatic artery?

Back 95

off SMA

Front 96

What lobes of the liver does the falciform ligament separate?

Back 96

medial and lateral segments of the left lobe

Front 97

What does the falciform ligament carry?

Back 97

remnant of the umbilical vein

Front 98

What carries the obliterated umbilical vein to the undersurface of the liver?

Back 98

ligamentum teres

Front 99

What separates the right and left lobes of the liver?

Back 99

cantle's line drawn from the gallbladder fossa to the IVC

Front 100

What is the peritoneum that covers the liver called?

Back 100

Glisson's capsule

Front 101

The portal triad enters and the gallbladder lies under what two segments of liver?

Back 101

IV and V

Front 102

What are liver macrophages called?

Back 102

Kupffer cells

Front 103

What is the orientation of the contents of the hepatoduodenal ligament?

Back 103

CBD lateral, hepatic artery medial and portal vein posterior

Front 104

What is clamped in the Pringle maneuver?

Back 104

portal hepatis

Front 105

What are the four borders of the foramen of Winslow?

Back 105

anterior - portal triad, posterior - IVC, inferior - duodenum, superior - liver

Front 106

What 3 vessels form the portal vein and what is their configuration?

Back 106

IMV enters the splenic vein, SMV joins the splenic vein

Front 107

How many portal veins in the liver? and what % of the blood supply do they provide?

Back 107

2 portal veins in the liver, 2/3 of the blood supply

Front 108

What are the hepatic arteries? and veins?

Back 108

right, left and middle, same as the veins

Front 109

In 80% of the population what is the configuration of the hepatic veins entering the IVC?

Back 109

Middle hepatic vein joins left hepatic vein before going into the IVC. In the other 20%, all 3 go directly into the IVC.

Front 110

What is unique about the blood supply and drainage of the caudate lobe?

Back 110

Caudate lobe – receives separate right and left portal and arterial blood flow; drains directly into IVC via separate hepatic veins

Front 111

What membrane of the liver does nutrient uptake occur?

Back 111

sinusoidal membrane

Front 112

What is the usual energy source for the liver?

Back 112

ketones

Front 113

What is the only water soluble vitamin stored in the liver?

Back 113

B12

Front 114

What are the 2 most common problems with hepatic resection?

Back 114

bleeding and bile leak

Front 115

Which hepatocytes are most sensitive to ischemia?

Back 115

central lobular (acinar zone III)

Front 116

What % of the liver can be safely resected?

Back 116

75%

Front 117

Bilirubin is conjugated to what in the liver which improves water solubility?

Back 117

glucuronic acid

Front 118

What comprises 85% of bile? what is the main phospholipid in bile?

Back 118

bile salts, lecithin

Front 119

In bile, what is used to make bile acids?

Back 119

cholesterol

Front 120

What two molecules are bile acids conjugated to in order to make them more water soluble?

Back 120

taurine or glycine

Front 121

What are the two primary bile acids? the two secondary (dehydroxylated primary acids by bacteria in gut)?

Back 121

primary - cholic and chenodeoxycholicsecondary - deoxycholic and lithocholic

Front 122

What level of bilirubin is necessary for jaundice?

Back 122

>2.5

Front 123

What is the maximum bilirubin possible (unless pt has underlying renal disease, hemolysis or bile duct-hepatic vein fistula)?

Back 123

30

Front 124

What disease is the abnormal uptake of bilirubin resulting in mildly high unconjugated bilirubin?

Back 124

Gilbert's disease

Front 125

What disease is the inability to conjugate bilirubin; deficiency of glucuronyl transferase; high unconjugated bilirubin -> life threatening disease.

Back 125

Crigler-Najjar disease

Front 126

Physiologic jaundice of newborn has high unconjugated bilirubin and is the result of which immature enzyme?

Back 126

glcuronyl transferase

Front 127

There are two syndromes that have a high conjugated bilirubin. Which one is a deficiency in storage ability and which one is a deficiency in secretion ability?

Back 127

Rotor's syndrome is a deficiency in storage ability. Dubin-Johnson syndrome is a deficiency in secretion ability.

Front 128

In hep B which Ig dominates in the first 6 months? which one then takes over?

Back 128

IgM then IgG

Front 129

In Hep B which Anti-HB rises 10-12 weeks after infection? and 12-14? and 14-16?

Back 129

10-12 weeks Anti HBc12-14 weeks Anti-HBe14-16 weeks Anti-HBs

Front 130

What Ab is elevated in a pt who is vaccinated against Hep B

Back 130

Anti-HBs

Front 131

If a pt has elevated anti-HBc and elevated anti-HBs antibodies and no HBs antigens, what does that mean?

Back 131

pt had infection with recovery and subsequent immunity

Front 132

What is the most common viral hepatitis leading to liver TXP?

Back 132

Hep C (long incubation period)

Front 133

Hepatitis D is a cofactor for which other Hepatitis?

Back 133

Hep B

Front 134

What does Hepatitis E cause?

Back 134

fulminant hepatic failure in pregnancy, most often in 3rd trimester

Front 135

What is the most common cause of liver failure?

Back 135

cirrhosis

Front 136

What is the best indicator of synthetic function in pts with cirrhosis?

Back 136

prothrombin time (PT)

Front 137

What is the mortality of acute fulminant hepatic failure? The course of what sx determines the outcome?

Back 137

80% mortality, encephalopathy

Front 138

What is the main medical tx for hepatic encephalopathy and how does it work?

Back 138

lactulose is a cathartic that gets rid of bacteria in the gut and acidifies the colon preventing NH3 uptake by converting it to ammonium (titrate to 2-3 stools per day)

Front 139

What should you limit the protein intake to in hepatic encephalopathy?

Back 139

<70 g/day

Front 140

Other than the mainstay, lactulose, name three other medical treatments for hepatic encephalopathy.

Back 140

Neomycin, L-dopa, bromocriptine

Front 141

When you do a paracentesis for ascites what do you need to replace and what is the dose?

Back 141

albumin, 1g for every 100cc removed

Front 142

What is increased aldosterone caused by in ascites?

Back 142

impaired hepatic metabolism and impaired GFR

Front 143

Hepatorenal syndrome has the same appearance as prerenal azotemia what is the tx (2)?

Back 143

stop diuretics, give volume

Front 144

What is the cause of postpartium liver failure with ascities and how do you dx?

Back 144

hepatic vein thrombosisDx: SMA arteriogram with venous phase contrast

Front 145

Sx of SBP include fever, abdominal pain, positive cultures and PMNs greater than what level in the fluid?

Back 145

250

Front 146

SBP is most commonly mono-organism; if it is not then you need to worry about what?

Back 146

bowel perforation

Front 147

What is the most common organism in SBP?

Back 147

E. coli

Front 148

What is a risk factor for SBP in children?

Back 148

SLE

Front 149

What is the tx for SBP?

Back 149

3rd -generation cephalosporin; pts usually respond within 48 hrs

Front 150

What is 90% effective at treating esophageal varices?

Back 150

sclerotherapy

Front 151

Name 2 medical treatments for esophageal varices and how they work.

Back 151

vasopressin (splanchnic artery constriction)octreatide (decreased portal pressure by decreased blood flow)

Front 152

In pts with esophageal varices who are on vasopressin and have CAD should get what additional medical tx?

Back 152

NTG

Front 153

What is the name of the tube for esophageal varices that has a risk of esophageal rupture and is hardly used anymore?

Back 153

Sengstaken-Blakemore

Front 154

What is the role for propanolol in esophageal varices?

Back 154

may help prevent rebleeding; no good role acutely

Front 155

Pts who develop strictures after sclerotherapy for esophageal varices are easily managed with what tx? what if they develop refractory variceal bleeding, what tx?

Back 155

dilatation, TIPS for refractory bleeding

Front 156

What does TIPS stand for?

Back 156

transjugular intrahepatic portosystemic shunt

Front 157

What is the mortality of bleeding varices with 1st episode? What % will rebleed and what is the mortality with each subsequent bleeding episode?

Back 157

33%, 50%, 50%

Front 158

50% of portal hypertension in children is caused by what?

Back 158

portal vein thrombosis

Front 159

What is the normal port vein pressure?

Back 159

<12 mmHg

Front 160

What procedure would you do for a Child's A cirrhotic that just has bleeding as a symptom?What if the pt is Child's B or C with indication for shunt (bleeding, progression of coagulopathy, visceral hypoperfusion, refractory ascites)?

Back 160

splenorenal shunt (more durable) for ATIPS for B or C

Front 161

Pts with TIPS are at risk for developing what?

Back 161

encephalopathy

Front 162

What is the most common cause of massive hematemesis in children?

Back 162

portal HTN due to extrahepatic thrombosis of the portal vein

Front 163

What is the tx for Budd-Chiari syndrome?

Back 163

portacaval shunt (needs to connect to the IVC above the obstruction)

Front 164

Isolated gastric varices without elevation of pressure in the rest of the portal system can be caused by what?

Back 164

Splenic vein thrombosis

Front 165

What is most often the cause of splenic vein thrombosis?

Back 165

pancreatitis

Front 166

What is the treatment for splenic vein thrombosis?

Back 166

splenectomy

Front 167

What is the organism in amebic liver abscesses?

Back 167

Entamoeba Histalytica

Front 168

Risk factors for Entamoeba histalytica include ETOH and travel to Mexico. How do you dx?

Back 168

CT characteristics, elevated LFTs, white count, serology (cultures are often sterile since the protozoa exists only in peripheral rim)

Front 169

What is the tx for amebic liver abscesses?

Back 169

Flagyl; aspiration if refractory of contaminated; surgery only for free rupture

Front 170

What is the organism in hydatid liver cysts?

Back 170

Echinococcus

Front 171

How do you dx echinococcus infections (2 tests)?

Back 171

Positive Casoni skin test, positive indirect hemagglutination

Front 172

Abdominal CT shows liver lesion with ectocyst (calcified) and endocyt. What is that characteristic of?

Back 172

hydatid cyst

Front 173

What is the tx for hydatid cyst?

Back 173

preop albendazole, surgical removal (may wan to inject cyst with alcohol at time of removal to kill organsims) need to get all of cyst wall

Front 174

Why don't you aspirate hydatid cysts?

Back 174

can leak out and cause anaphylactic shock

Front 175

Pt with hydatid cyst has jaundice, elevated LFTs or cholangitis. What do you need to do preop?

Back 175

ERCP to check for communication with the biliary system

Front 176

Maculopapular rash, increased eosinophils. Sigmoid colon has fine granulation tissue, petechiae, ulcers and can cause variceal bleeding. What is the dx and what is the tx?

Back 176

SchistosomiasisTx: praziquantel and control variceal bleeding

Front 177

80% of liver abscess are what type? what is the number one organism?

Back 177

pyogenic, E. coli

Front 178

What artery does the cystic artery branch off of?

Back 178

Right hepatic artery.

Front 179

1. What arteries supply the hepatic and common bile duct? 2. What is the orientation?

Back 179

1. the right hepatic artery (lateral) and the retroduodenal branches of the GDA (medial). 2. In the 3- and 9-o'clock positions. The blood supply is longitudinal.

Front 180

Which branch of the Vagus supplies the liver and gallbladder?

Back 180

The left (anterior) branch.

Front 181

What common medications relax and constrict the sphincter of Oddi?

Back 181

Morphine constricts it, Glucagon relaxes it.

Front 182

What hormone stimulates the gallbladder's contraction, and where do the cells that make it PREDOMINANTLY live?

Back 182

CCK and secretin, found in the duodenum.

Front 183

What morphologically develops as a sign of chronic cholecystitis, and why does it develop?

Back 183

Rokitansky-Aschoff sinuses - invaginations of the epithelium of the wall of the gallbladder, due to increased GB pressure. Due to atrophy of mucosa, leading to epithelium protruding through into the muscular layer.

Front 184

1. What is the likelihood someone with typical GB pain, WITHOUT stones and LOW EF having lap chole help symptoms? 2. With atypical symptoms?

Back 184

1. 90% 2. 20%

Front 185

1. What increases biliary secretion? 2. What decreases biliary secretion?

Back 185

1. CCK (causes constant, steady tonic contraction), secretin (both found in the duodenum primarily), vagal input. 2. VIP, somatostatin, sympathetic stimulation

Front 186

How does the gallbladder alter the content of bile? What does it secrete?

Back 186

It actively utilizes Na/K ATPases to passively reabsorb water. It secretes mucus and H+ ions (causing bile to be more lithogenic).

Front 187

What is the difference in absorption of conjugated and unconjugated bile acids in the GI tract?

Back 187

Conjugated bilirubin is ACTIVELY reabsorbed, primarily in the terminal ileum (50%). Non-conjugated bile acids are PASSIVELY reabsorbed in the small bowel (45%), and colon (5%). Remember bile salt pools cycle 4-5 times / day.

Front 188

What breakdown product of bilirubin ends up in urine? What is the process?

Back 188

Urobilin. Conjugated bilirubin is broken down by gut bacteria, reabsorbed and released in urine.

Front 189

What is the metabolic pathway for synthesis of bile acids?

Back 189

HMG CoA --> (HMG CoA reductase) -->Cholesterol --> (7-alpha-hydroxylase) --> Bile acids. HMG CoA Reductase is the RATE LIMITING STEP.

Front 190

What causes non-pigmented stones?

Back 190

1. Increased cholesterol insolubilization - due to stasis, calcium nucleation by mucin glycoproteins and increased water reabsorption from the GB. 2. Decreased lecithin and bile acids. Most common stone found in the US!

Front 191

What causes pigmented stones?

Back 191

Solubilization of unconjugated bilirubin with precipitation of calcium bilirubinate and insoluble fats. Most common stones found WORLDWIDE (in US is non-pigmented stones).

Front 192

What causes black stones?

Back 192

Hemolytic disorders or cirrhosis. Can also occur with chronic TPN use or ileal resection. The most important factor is increased bilirubin load, decreased hepatic function and bile stasis.

Front 193

What causes brown stones, where do they commonly form?

Back 193

Due to infection causing deconjugation of bilirubin, mostly in the CBD, with precipitation of calcium bilirubinate. E. coli the most common offender (makes beta-glucuronidase).

Front 194

What are the most common bacteria causing sepsis in cholecystitis?

Back 194

E. coli, Klebsiella, Enterococcus

Front 195

What's the most common cause of CBD stricture?

Back 195

Occurs after a lap cholecystectomy, due to ischemia. Can also be caused by chronic pancreatitis or stricture of a biliary enteric anastomosis. ERCP will show stricture. Treat with sphincterotomy and possible stent placement to decompress, PTC tube if that fails.

Front 196

1. What are the most common causes of hemobilia? 2. How is it diagnosed?

Back 196

Due to a fistula between the bile duct and the hepatic arterial system (usually a pseudoaneurysm). Usually trauma (50% of the time). Can also be because of infection, primary gallstones, aneurysms and tumors. Treat with angiography with embolization.

Front 197

1. What is a common finding in patients with gallbladder adenocarcinoma, which is more common than common duct cancers? 2. What risk of cancer does porcelain gallbladder carry?

Back 197

90% have have a singular large stone. Usually more common than having multiple small stones. 2. Your risk is 10-20%, and you NEED a cholecystectomy.

Front 198

What region of the liver (the most common site of metastases) does gallbladder cancer first metastasize to?

Back 198

Segment IV and V.

Front 199

What is the staging that differentiates your treatment of gallbladder cancer? On a micro level?

Back 199

T1a (Stage I disease) lesions (into the lamina propria, NOT muscularis) can undergo laparoscopic cholecystectomy. T1b or greater (invading the muscular layer, aka Stage II disease), will require greater dissection (including RIGHT cystic duct nodes). Most present with stage IV disease due to late presentation. Overall 5 year survival is 5%.

Front 200

What is a unique finding of patients previously treated for gallbladder cancer?

Back 200

HIGH incidence of trochar site tumor implants following laparoscopic cholecystectomy. Hence laparoscopic approaches to gallbladder cancer are CONTRAINDICATED!

Front 201

1. What is the patient population for cholangiocarcinoma? 2. Risk factors? 3. What finding in symptomatic patients without a diagnosis is HIGHLY suggestive of cholangiocarcinoma?

Back 201

1. Elderly, males. 2. Clonorchis senensis infections, typhoid, ulcerative colititis, choledochal cysts, congenital hepatic fibrosis, chronic bile duct infections. 3. Focal bile duct stricture in patient WITHOUT history of biliary surgery or pancreatitis.

Front 202

How does treatment for cholangiocarcinoma vary depending on location along the bile duct?1. Upper 1/3 (also known as)?2. Middle 1/3?3. Lower 1/3?

Back 202

1. Klatskin tumors: the most common type, owrst prognosis, usually unresectable. Can attempt lobectomy and stenting of the contralateral bile duct if localized to right or left lobe. 2. hepaticojejunostomy 3. Whipple (pancreaticoduodenectomy)

Front 203

What is the overall cancer risk for cholangiocarcinomas?

Back 203

15%.

Front 204

What other disease are associated with primary sclerosing cholangitis?

Back 204

Retroperitoneal fibrosis, Riedel's thyroiditis, pancreatitis, ulcerative colitis and diabetes. Removing the colon in UC does NOT change the course of disease in PSC.

Front 205

What is the primary radiographic finding associated with primary sclerosing cholangitis on ERCP (the best diagnostic test)?

Back 205

Multiple strictures and dilations.

Front 206

What are medications useful for treatment of side effects of primary sclerosing cholangitis?

Back 206

Cholestyramine --> decreases bile acids by binding in the GI tract, preventing re-absorption. UDCA (urodeoxycholic acid): can decrease bile acids and improve liver enzymes

Front 207

What are the antibodies associated with primary biliary cirrhosis?

Back 207

Antimitochondrial antibodies

Front 208

When describing symptoms of cholangitis, what is Charcot's Triad? Reynold's Pentad?

Back 208

CT: RUQ pain, fever, jaundice RP: Charcot's triad with mental status changes and shock (suggesting sepsis)

Front 209

What is oriental cholangiohepatitis? Ultimate treatment?

Back 209

Associated with Asia, recurrent cholangitis from primary CBD stones (due to infection from C. sinensis, A. lumbricoides, T. trichiura, and E. coli) Hepaticojejunostomy and anti-parasitic medications.

Front 210

What is granular cell myoblastoma?

Back 210

A BENIGN neuro-ectoderm tumor of the gallbladder, or in the biliary tract with signs of cholecystitis. Treated with cholecystectomy.

Front 211

What are the GENERAL rules regarding size and age when dealing with GB polyps?

Back 211

If > 1 cm or patient > 60 worry about malignancy and TAKE IT OUT!

Front 212

What is Mirizzi Syndrome?

Back 212

Compression of the CBD by a stone in the infundibulum of the GB or inflammation arising from the gallbladder or cystic duct extending to the contiguous hepatic duct, causing stricture and hepatic duct obstruction.

Front 213

What antibiotic is associated with GB sludging or cholestatic jaundice?

Back 213

Ceftriaxone.

Front 214

What are the most common cause of GB polyps? Second most common?

Back 214

Usually cholesterol polyps (found in cholesterolosis, aka speckled cholesterol deposits on the GB wall). Adenomyomatosis, which are thickened nodules of mucosa and muscle associated with Rokitansky-Aschoff sinuses. Inflammatory polyps are the third most common.

Front 215

What are the three layers of an artery?

Back 215

Tunica intima - inner most layerTunica media - smooth muscle layerTunica adventitia - adipose and other CT support All layers are separated by an elastic lamina

Front 216

What is the composition of the tunica intima?

Back 216

Endothelial cells overlying subendothelial connective tissue. Via influence of vasoactive mediators (cytokines, antithrombotic agents) endothelial cells modulate vascular tone and blood flow, playing an integral role in hemostasis, coagulation and inflammation.

Front 217

What are the Vaso Vasorum and where on an artery are they found?

Back 217

Feeding blood vessels that supply large arteries, found in the adventitia.

Front 218

What are lymphatic channels lined with?

Back 218

Endothelium.

Front 219

What are non-modifiable risk factors for atherosclerosis?

Back 219

Age, gender, family history, genetic predisposition

Front 220

How do low-density lipoproteins contribute to the inflammatory state?

Back 220

Undergo oxidative modification in blood (to ox-LDLs), which induce adhesion molecule expression by endothelial cells and is a potent macrophage chemokine, promoting its migration into the tunica intima.

Front 221

How does hypertension contribute to atherosclerosis?

Back 221

1. Causes endothelial damage, inciting atherogenic inflammatory pathways 2. Hypertensive patients have elevated Angiotensin II (vasoconstrictor) levels, and promotes production of superoxide anions by endothelial cells and vascular SM cells. They operate synergistically to cause endothelial injury and promote inflammation.

Front 222

How do diabetics have altered vasodilation?

Back 222

1. Dysfunction of endothelial nitric oxide synthase. 2. They also have concurrent excess Endothelin-1 production (a potent vasoconstrictor). 3. Hyperglycemia increases formation of reactive oxygen species and advaned glycation endproducts, promoting inflammation.

Front 223

How does having Diabetes modify your risk for MI, and for gangrene of the lower extremity?

Back 223

1. MI - twofold increased risk 2. Gangrene - 8- to 15- fold increased risk

Front 224

What is the initial step in formation of atherosclerosis, and what does this inciting event trigger?

Back 224

Endothelial injury. This causes increased expression of adhesion molecules (E-selectin, intercellularl cell adhesion molecules, etc.). This promotesbinding, activation and diapedesis of circulating platelets and lymphocytes.

Front 225

Once initial endothelial injury occurs and platelet/leukocytes are attracted/activated, what occurs to progress atherosclerosis?

Back 225

Inflammatory cytokines attract monocytes that differentiate into macrophages, which engulf lipids, creating foam cells.

Front 226

What cell type in atherosclerosis promotes functional change (secretory to proliferative) of smooth muscle cells in the lesion, creating the atheromatous plaque.

Back 226

Lymphocytes.

Front 227

What is the makeup of an atheromatous plaque?

Back 227

Necrotic core, containing foam cells and extracellular lipids, covered by a fibrous cap of smooth muscle cells, lymphocytes and CT. Complicated plaques have calcification, ulceration, plaque rupture with subsequent hemorrhage and thrombosis.

Front 228

In regard to atheromatous disease causing neurologic symptoms, what are the various diagnoses based on time duration?

Back 228

TIA: < 24 hours duration of symptoms Reversible Ischemic Neurologic Deficits: 24 hours to 3 days duration. Stroke: > 3 days REMEMBER that hypertension is the most important risk factor for stroke in asymptomatic patients.

Front 229

What is the most common cause of embolic disease of the brain?

Back 229

Carotid arteries, which are atherosclerotic. Most often site of stenosis is the bifurcation.

Front 230

What is the sensitivity and specificity of a carotid bruit being associated with carotid artery disease, as foudn by the North American Symptomatic Carotid Endarterectomy Trial (NASCET)?

Back 230

63% and 61%, respectively.

Front 231

What are limitations for utilizing carotid duplex US to evaluate carotid stenosis vs. the gold standard (contrast angiograpy)?

Back 231

Not precise with stenoses > 50%, cannot reliably distinguish very high grade stenosis from occlusions. Cannot evaluate intracranial portions

Front 232

What are criteria for providing medical therapy for patients with carotid stenosis (and not surgery)?

Back 232

1. Symptomatic disease with < 50% stenosis 2. Asymptomatic disease and less than 60% stenosis 3. Patients at risk for surgical complications outweigh potential benefits of CEA

Front 233

What percent stenosis prompts CEA for carotid stenosis, both symptomatic and asymptomatic?

Back 233

Symptomatic: 50-69%. These patients have approximately 5% annual risk reduction with CEA. This came per the NASCET study. Asymptomatic: 70% (60% if patient has a low surgical complication risk) If they had a recent stroke wait 4-6 weeks.

Front 234

When performing a CEA on an intubated patients, what should be performed if EEG monitoring changes after clamping the artery? What standard care should be performed if no EEG is beign used?

Back 234

Temporary shunt should be placed. If being performed without EEG, a shunt should be used if the internal carotid artery stump pressure is < 50 mmHg.

Front 235

How does hypertension occur in patients following CEA?

Back 235

Manipulation of the carotid body. Occurs in 20% of patients. This puts patients at high risk for cerebral hemorrhage 2/2 vasoplegia induced by low flow states preoperatively.

Front 236

What nerve is most commonly injured in CEA?

Back 236

Vagus nerve causing hoarseness and increased risk of post-op aspiration.

Front 237

According to the Thrombolysis or Peripheral Artery Surgery (TOPAS) trial, what percentage of acute lower extremity ischemia is due to thrombosis?

Back 237

85% of cases. The others are embolic.

Front 238

What are the six "P"s of acute limb ischemia

Back 238

Pain (most common) Pallor Paresthesias Poikilothermia Paraylsis (late finding indicating advanced ischemia) Pulselessness

Front 239

In acute limb ischemia what is the first step of treatment?

Back 239

Heparinization, preventing clot propagation to distal circulation and decreases morbidity/mortality.

Front 240

What are common symptoms of CHRONIC lower limb ischemia?

Back 240

Intermittent claudication, rest pain, ischemic ulcers, frank gangrene.

Front 241

After heparinization, what is the decision regarding treatment for acute limb ischemia?

Back 241

Amenable to thrombectomy (if not, go straight to a bypass graft +/- fasciotomy).

Front 242

By what degree of drop in pressure signifies occlusive disease when comparing two regions of the body?

Back 242

30 mmHg.

Front 243

What symptoms are associated with an ABI 0.5 - 0.84?

Back 243

Intermittent claudication.

Front 244

What symptoms are associated with an ABI < 0.5?

Back 244

critical ischemia (rest pain, tissue loss, gangrene).

Front 245

In diabetics, why are pulse volume recordings (PVRs) used rather than ABIs, to measure limb ischemia?

Back 245

Diabetics have calcified arteries that are non-compressible, and therefore lead to artificially high pressure readings (similar to patients with renal failure). This affects tibial vessels, less so toe vessels. Can use Doppler waveforms in these patients.

Front 246

What is the 5 year patency for aortobifemoral bypass grafting with Dacron?

Back 246

88% patency.

Front 247

In regards to patency rates of PTFE vs. venous grafts, how do they compare in the lower extremity?

Back 247

Above the knee: vein grafts have only slightly higher patency rates. Below the knee: vein grafts have MUCH higher patency rates for below the knee targets

Front 248

What is the timeline of common failure for bypass grafts?

Back 248

Early (within 30 days), intermediate (30 days to 2 years) and late (> 2 years). Early failure often due to technical aspects. Intermediate failure = most often because of neointimal hyperplasia within vein grafts Late failure: natural progression of atherosclerotic disease

Front 249

What is the most common cause of aneurysms? How about in the Ascending aorta?

Back 249

Atherosclerosis. In the ascending aorta it is cystic medial necrosis, connective tissue disorders like Marfan's or Ehlers-Danlos.

Front 250

What size of AAA represents an indication for repair?

Back 250

4.5 - 5.5 cm. Below 4.5 cm there is no survival advantage.

Front 251

What anatomic requirement is there for consideration of EVAR?

Back 251

An adequate aneurysmal neck length of ≥ 15 mm, which allows proper fixation of the device without compromising renal artery flow.

Front 252

Describe the following endoleak: Type I

Back 252

Failure to seal the endograft to the native vessels. Tx: proximal or distal extension cuffs

Front 253

Describe the following endoleak: Type II

Back 253

Filling of the aneurysm sac by collateral vessels. Tx: Perc coil embolization. You can also observe as it may close (most common).

Front 254

Describe the following endoleak: Type III

Back 254

Disjunction between graft components, causing leak. Tx: secondary endograft

Front 255

Describe the following endoleak: Type IV

Back 255

Porosity of graft fabric. Tx: secondary stenting (nonporous stent) or observe

Front 256

What types of aneurysms are often NOT caused by atherosclerosis?

Back 256

Visceral aneurysms, as well as ascending aorta.

Front 257

In regard to splenic artery aneurysms, who require repair?

Back 257

Pregnant women (or those going to get pregnant), or those larger than 2 cm, or symptomatic. Usually will rupture in the 3rd trimester in pregnant women.

Front 258

How does treatment of a proximal hepatic and splenic aneurysms differ from more distal lesions?

Back 258

Proximal lesions can be simply ligated due to high collateral flow. Otherwise renal, hepatic and splenic aneurysms are treated with exclusion and bypass grafting.

Front 259

What criteria are used to repair iliac artery aneurysms?

Back 259

If they are symptomatic, ≥ 3 cm or mycotic. Repaired with a covered stent or bypass graft with exclusion.

Front 260

What criteria are used to repair femoral artery aneurysms?

Back 260

Symptomatic, ≥ 2.5 cm or mycotic. Tx: bypass and exclusion

Front 261

What criteria are used to repair popliteal artery aneurysms (the most common peripheral aneurysm)?

Back 261

Symptomatic, ≥ 2 cm, or mycotic. Tx: exclusion and bypass

Front 262

What are the common causes of renovascular hypertension?

Back 262

The majority are due to atherosclerotic plaques (70%) while the rest fibromuscular dysplasia (younger women and is either bilateral or has a predilection for right-sided disease). On imaging looks like a "string-of-beads". Tx: TPA (first choice) or bypass

Front 263

What diagnostic tests are useful for renovascular hypertension?

Back 263

Captopril renal flow scanning, duplex, MRI, arteriography. Confirmation is renal vein renin assay (measures renin activity in the renal vein compared to the systemic renin activity).

Front 264

What is Subclavian Steal Syndrome?

Back 264

When there is a proximal stenosis of the subclavian artery, and blood delivery to the limb is dependent on reversed flow through the ipsilateral vertebral artery via the Circle of Willis. With increased activity the patient has ischemic pain. This can lead to neurological symptoms of vertebrobasilar insufficiency (syncope).

Front 265

What region do the brachial plexus and subclavian artery leave the neck?

Back 265

Posterior to the anterior scalene, anterior to the posterior scalene, and the first rib.

Front 266

What is a clue for venous compromise of thoracic outlet syndrome?

Back 266

Effort-induced thrombosis (Paget-von Schrotter Disease). Presents as painful swelling of the affected arm. Diagnosed via duplex and venography. Primary treatment is thrombolytics and anticoagulation.

Front 267

What are the 4 broad types of mesenteric ischemia?

Back 267

1. Acute embolic: 50% of acute mesenteric ischemia, usually affects the SMA, often from cardiac source 2. Non-occlusive: 20% of acute mesenteric ischemia, usually in critically ill patients with dec. CO and splanchnic vasospasm. 3. Thrombotic: Cause in 25% of cases. Occlusion often at or near the ostium of the SMA without sparing jejunal vessels 4. Venous thrombosis: 5%. Affects younger patients, usually when they have hypercoagulable disorderUsually starts in distal vessels then propagates to larger.

Front 268

What is the TOC for nonocclusive mesenteric ischemia?

Back 268

Correcting the decreased cardiac output, potentially direct injection of vasodilators like papaverine in to the mesenteric vessels.

Front 269

What are classic symptoms of chronic mesenteric ischemia?

Back 269

Post-prandial pain, severe enough to deter eating, causing weight loss. Diagnosed with angiography. Treated with either PTA with or without stenting, bypass or endarterectomy.

Front 270

What are the characteristic findings (and related pathogenesis) of fibromuscular dysplasia?

Back 270

The media degenerates causing fibrous constrition with alternating aneurysmal dilation causing a "string of beads" appearance on angiography. Most often in women, affecting renal arteries, then carotid and iliac.

Front 271

What is the other name for thomboangiitis obliterans, and what is it?

Back 271

Buerger disease: severe progressive arterial occlusive disease affecting young male smokers, starting with lower extremity claudication and rapidly progressing to rest pain and ischemic ulceration.. On imaging shows corkscrew collaterals on angiogram. It also has skip lesions (making it impossible to bypass). There is NOT ATHEROSCLEROTIC DISEASE! Smoking cessation resolves most cases! PT to develop collaterals is essential.

Front 272

What is Takayasu arteritis?

Back 272

An autoimmune vasculitis often affecting the aorta and major branches, usually in women < 35 yo. Treat with immunosuppression (steroids), chemo for refractory symptoms.

Front 273

What autoimmune vasculitis affects women older than 50, and includes the temporal, occipital, subclavian and axillary arteries and can cause blindness?

Back 273

Temporal arteritis (aka Giant cell arteritis, granulomatous disease), involves large vessels (can include branches of the aorta and pulmonary arteries). Symptoms include fever, arthralgia, myalgia, anorexia. Diagnosed via temporal artery biopsy, steroids for treatment.

Front 274

What is phlegmasia cerulea dolens, and how does it differ from phlegmasia alba dolens?

Back 274

In iliofemoral venous thrombosis there is massive swelling, pain and cyanosis that develops (blue, swollen, painful). Phlegmasia alba dolens (swollen, white, painful) is the progressive form when arterial supply is compromised.

Front 275

What percentage of PEs are from DVTs?

Back 275

75%

Front 276

What is duration of treatment of anticoagulation for a first time DVT?

Back 276

6 months, and if it occurs again one year. At another incidence, or PE, they have lifelong anticoagulation.

Front 277

Worldwide, what is the most common cause of secondary lymphedema? In the US?

Back 277

Filariasis, a parasitic infection that obstructs lymphatics. Here it's due to malignancy.

Front 278

What pharmacologic therapy, along with conservative management, has been used to treat lymphedema?

Back 278

Benzopyrones increase the number of macrophages, enhancing proteolysis and causes removal of protein and edema.

Front 279

What is the communicating artery between the internal and external carotid artery?

Back 279

The ophthalmic artery (1st branch of the ICA) and internal maxillary artery (off the ECA).

Front 280

Based on the location of the lesion, what are suspected symptoms when someone has a stroke? Anterior cerebral artery:Middle cerebral artery:

Back 280

Anterior: mental status changes, slowing Middle: contralateral motor and speech (if dominant side), contralateral facial droop. This is the MOST COMMONLY DISEASED INTRACRANIAL ARTERY.

Front 281

Why do patients who undergo carotid endarterectomy require antiplatelet therapy post-op?

Back 281

It strips endothelium, which leaves a raw media for platelets to activate.

Front 282

What are patient risk factors that make someone a more ideal candidate for carotid artery stenting vs. endarterectomy?

Back 282

Age > 80CADRecent MI (w/in 4 weeks), CABG within 6 monthsCHF, EF < 30%Dialysis dependent renal failureSevere COPDContralateral internal carotid artery occlusionContralateral laryngeal nerve palsyRadiation-induced internal carotid artery stenosisPrior neck dissection

Front 283

In patients who develop vertebral artery disease (usually bilateral), what are common symptoms and how do you treat it?

Back 283

Vertebrobasilar insufficiency: diplopia, dysarthria, vertigo, tinnitus, drop attacks, incoordination, binocular vision loss. PTA, vertebral artery transposition to subclavian, transsubclavian endarterectomy, osteophyte resection, unroofing of transverse process foramina all options

Front 284

When thoracic aortic transection occurs due to trauma, where does it usually tear?

Back 284

At the ligamentum arteriosum, just distal to the left subclavian

Front 285

What are indications to repair an ascending aortic aneurysm?

Back 285

Acutely symptomatic (local compression or heart failure due to aortic insufficiency) ≥ 5.5 cm (same as AAA), ≥ 5.0 cm if Marfan's Diameter 2x normal Rapidly increasing size

Front 286

What are the Stanford and DeBakey classifications of aortic dissection?

Back 286

Type A: Has ANY ASSENDING component Type B: ONLY descending component

Front 287

What layer of the aorta is affected when dissection occurs?

Back 287

The media layer

Front 288

What causes aortic insufficiency in patients with aortic dissection?

Back 288

Occurs in 70% of acute disease, caused by annular dilatation or when the aoric valve cusp is sheared off. Death with ascending aortic dissections is most often due to cardiac failure from aortic valve insufficiency.

Front 289

What are indications for repairing both ascending and descending aortic dissections?

Back 289

Ascending: repair all Descending: if involves visceral, renal or leg ischemia, persistent pain, large size.

Front 290

As a complication of operating on thoracic aortic dissections, what causes paraplegia?

Back 290

Due to ischemia from occlusion of intercostal arteries and artery of Adamkiewicz during repair. The artery of Adamkiewicz arises from the left posterior intercostal, supplies the lower 2/3 of the spinal cord via the anterior spinal artery.

Front 291

What are the risk factors for identifying a AAA on screening ultrasound?

Back 291

Smoking (OR 5.1!!!)Family history (1.9)Older age (1.7)CAD (1.5)

Front 292

In regard to risks of rupture of a AAA, what risk is conferred by the following findings: - AAA > 5 cm

Back 292

15-20% five year risk of rupture

Front 293

In regard to risks of rupture of a AAA, what risk is conferred by the following findings: - AAA > 8 cm

Back 293

100% rupture risk in 5 years

Front 294

When do you decide to reimplant the inferior mesenteric artery in a AAA repair?

Back 294

- Poor IMA back bleeding- IMA stump pressure < 40 mmHg- Large meandering mesenteric artery- Absent doppler signal on bowel during repair- Previous colonic surgery- SMA stenosis

Front 295

What is the most common embolic site in someone with embolic acute mesenteric ischemia?

Back 295

At the origin of the middle colic artery, distal to the first jejunal branches.

Front 296

What percentage of patients experience impotence from aortic aneurysm repair (open)?

Back 296

1/3, due to disruption of autonomic nerves and blood flow to the pelvis

Front 297

What's the #1 cause of acute death after AAA repair?

Back 297

MI

Front 298

What's the #1 cause of late death after AAA repair?

Back 298

renal failure

Front 299

What is the rate of graft infection after AAA repair?

Back 299

1%

Front 300

What is the most common late complication after aortic graft placement?

Back 300

atherosclerotic occlusion

Front 301

What are you worried about in someone who recently had a AAA repair and is having bloody diarrhea?

Back 301

Ischemic colitis. Diagnose with procto-sigmoidosopy. The risk of this goes up with increased pre-operative sock. Age, time to operation, pre-op heart disease do NOT predict this.

Front 302

What are measurements of a AAA that qualify the patient for endovascular repair?

Back 302

> 15 mm neck length< 30 mm neck diameter< 60 degrees neck angulation> 35 mm common iliac artery length< 22 mm common iliac artery diameter

Front 303

What are common associated symptoms in patients with inflammatory aneurysms (not associated with infection)?

Back 303

Adhesion to the 3rd or 4th portion of duodenum. Ureteral entrapment (usually don't have to treat, just treat the aneurysm).

Front 304

What is the most common organism causing mycotic aneurysms

Back 304

Salmonella (Staph is second).

Front 305

What is the usual treatment for mycotic aneurysms?

Back 305

Extra-anatomic bypass (ax-fem with fem-fem crossover) and resection of infrarenal abdominal aorta clear of the infection.

Front 306

What is the most common organism causing aortic graft infection?

Back 306

Staph (E. coli second).

Front 307

What is the treatment of choice for infected aortic graft following AAA repair?

Back 307

Resect the graft and bypass through a non-contaminated field.

Front 308

What is a major delayed complication of AAA repair (seen over 6 months out), and where does it involve? Treatment?

Back 308

Aortoenteric fistula, usually involving the distal duodenum (3rd or 4th portion) near the proximal suture line. Patients often have a herald bleed and then blood per rectum. Tx: noncontaminated field bypass, resect the graft with aortic stump closure.

Front 309

What are the indications for repair of renal artery stenosis?

Back 309

- sudden worsening of HTN- refractory HTN despite 3 medications- worse renal function after giving an ACE inhibitor- unexplained atrophy of one kidney- HTN causing end-organ damage (renal insufficiency or recurrent decompensated HF)

Front 310

What is the most common peripheral artery that experiences aneurysm (vs. aortic and iliac that are the most common OVERALL), and what associated findings require further screening?

Back 310

Popliteal artery. They need screening for AAA (30% of patients with popliteal artery aneurysms have a AAA).

Front 311

Indications for repair of a popliteal artery aneurysm (consisting of bypass with proximal ligation)?

Back 311

1. Any > 2 cm 2. Any with intraluminal clot 3. Symptomatic

Front 312

In regard to this leg compartment, what nerve is involved and what are its functions? Artery? - Anterior compartment?

Back 312

Deep peroneal nerve - dorsiflexion, sensation between 1st and 2nd toe. Artery: Anterior tibial artery.

Front 313

In regard to this leg compartment, what nerve is involved and what are its functions? - Lateral compartment?

Back 313

Superficial peroneal nerve - eversion, lateral foot sensation

Front 314

In regard to this leg compartment, what nerve is involved and what are its functions? Artery? - Deep posterior compartment?

Back 314

Tibial nerve - plantarflexion Posterior tibial arteryPeroneal artery

Front 315

In regard to this leg compartment, what nerve is involved and what are its functions? - Superficial posterior compartment?

Back 315

Sural nerve

Front 316

What is the number one pharmacologic therapy to prevent atherosclerosis?

Back 316

Statins (particularly Lovastatin)

Front 317

What is homocystinuria linked with increased risk of, and what is treatment of choice?

Back 317

Atherosclerosis Folate, B12, B6 (lowering homocysteine levels may NOT decrease your risk of CVA or stroke!)

Front 318

Beyond aspirin, smoking cessation (most important), and exercise until pain occurs to improve collaterals, what is another medical therapy for the treatment of claudication?

Back 318

Cilostazol - inhibits platelet aggregation and SM proliferation, increases vasodilation, lowers HDL and triglycerides. Shown to increase walking distance by 50%. Contraindicated in patients with heart failure!

Front 319

Based on location of symptoms, where is the most likely vascular compromise? - Buttock claudication

Back 319

Aortoiliac disease

Front 320

Based on location of symptoms, where is the most likely vascular compromise? - Mid-thigh claudication

Back 320

external iliac

Front 321

Based on location of symptoms, where is the most likely vascular compromise? - Calf claudication

Back 321

Common femoral artery or proximal superficial femoral artery

Front 322

Based on location of symptoms, where is the most likely vascular compromise? - foot claudication

Back 322

Distal superficial femoral artery or popliteal artery

Front 323

What is the most common site of atherosclerotic occlusion in lower extremities?

Back 323

Hunter's canal (sartorius anteriorly, adductor longus posteromedially, lateral vastus medialis), where the distal superficial femoral artery exits.

Front 324

When venous grafting what are the two techniques utilized and what are the overall benefits?

Back 324

Reversed saphenous vein grafting: 5 year 1˚ and 2˚ patency 75 and 85% (best). In situ saphenous vein graft: vaso vasorum is maintained (prevents endothelial layer ischemia), allows caliber matching (prevents distal kinking), allowing smaller caliber saphenous vein. More likely to have technical error.

Front 325

What are recommendations regarding surveillance for native vein grafts vs. synthetic grafts, and what measurement confers higher thormbosis risk?

Back 325

Vein: active surveillance beneficial (IDs stenosis before progression to symptoms). Opening up an already thrombosed graft is very difficult. Synthetic: no benefit to surveillance (they can occlude without preceding stenosis. Highest thrombosis risk = peak systolic velocity > 300 cm/sec.

Front 326

What is the 5 year patency of femoral to distal target graft (including peroneal, anterior tibial, etc.)?

Back 326

50% five year patency, not influenced by level of distal anastomosis.

Front 327

What are the only indications for operating on a femoral pseudoaneurysm?

Back 327

It it is infected or rapidly expanding. Most < 2 cm will thrombose with compression (unless anticoagulated). Dirct thrombin injection also works.

Front 328

Why do we use vein grafting for bypasses below the knee?

Back 328

Synthetic grafts have decreased patency below the knee.

Front 329

What arteries are often affected in HIV-related aneurysms?

Back 329

The vasa vasorum. HIV-related aneurysms are often multiple at random sites like the common carotid and SFA. On US they look like pseudoaneurysms.

Front 330

What is a malperforans ulcer, who is it associated with and what is its treatment?

Back 330

At the metatarsal head (2nd MTP most common), often affecting diabetics (can get osteomyelitis). Tx: nonweightbearing, debridement of metatarsal head (remove cartilage), antibiotics, assess need for revascularization.

Front 331

What compartment of the leg is most often affected by reperfusion causing compartment syndrome?

Back 331

The Anterior. Occurs when pressures > 20-30 mmHg

Front 332

When are arterial autografts utilized?

Back 332

In children, using internal iliac artery for kids needing renal artery repair Radial grafts for CABG, IMA for CABG.

Front 333

What is the three-year mortality for patients who undergo either above- or below-knee amputation?

Back 333

50%

Front 334

What is the most common site of peripheral emboli to lodge in the lower extremity?

Back 334

Common femoral artery. Emboli to the periphery are treated with embolectomy if able. Consider fasciotomies in patients with ischemia for longer than 4-6 hours.

Front 335

What is blue toe syndrome?

Back 335

Flaking atherosclerotic emboli off an abdominal aorta or branches. Patients usually have good distal pulses. Most commonly from aorto-iliac disease.

Front 336

What are clinical signs of renovascular hypertension?

Back 336

BruitsDiastolic HTN > 115 mmHgWorsening HTNChildrenPremenopausal womenRapid onset after age 50HTN resistant to drugs

Front 337

What is seen on angiography that is suggestive of fibromuscular dysplasia as a cause of renovascular hypertension?

Back 337

String of beads lesions.

Front 338

What is the cause of hypertension in someone with renovascular hypertension?

Back 338

Increased angiotensin II mediated vasoconstriction. Increased aldosterone has no effect secondary to having a normal functioning kidney.

Front 339

What is Adson's test, and what disease process is it used in?

Back 339

Decreased radial pulse with head turned ipsilateral side (subclavian artery compression). Thoracic outlet syndrome.

Front 340

What is Tinsel's test, and what disease process is it used in?

Back 340

Tapping reproduces symptoms.

Front 341

What are contraindications to thrombolytic therapy when treating a thrombosed vessel?

Back 341

Recent stroke/TIAActive/recent bleedCoagulopathy Relative contraindications:- recent major surgery- recent major trauma- intracranial tumors- poorly controlled hypertension Patients with both motor and sensory deficits should NOT get TPA (too slow) and require OR.

Front 342

In thoracic outlet syndrome neurlogic involvement (most common), what nerves are most affected?

Back 342

Lower brachial plexus branches (C8 and T1) causing ulnar nerve involvement.

Front 343

What medication can be useful when performing embolectomy for mesenteric ischemia, that acts as a free radical scavenger, reducing reperfusion injury?

Back 343

Mannitol.

Front 344

What disease process causes celiac axis compression?

Back 344

Median arcuate ligament syndrome, evident by a bruit near the epigastrum, chronic pain, weight loss, diarrhea. Tx: divide the median arcuate ligament, may need arterial reconstruction.

Front 345

Most common complication of aneurysms above the inguinal ligament? Below?

Back 345

Above: rupture Below: thrombosis and emboli

Front 346

What population is affected by Kawasaki's disease, and what is treatment?

Back 346

Children get dilated coronaries and brachiocephalic vessels, can die of arrhythmias. Tx: steroids, possible CABG

Front 347

What are the three time-related symptoms that are seen with Radiation arteritis?

Back 347

Early - sloughing and thrombosis (obliterative endarteritis). Late (1-10 years): fibrosis, scar, stenosis Late Late (3-30 years): advanced atherosclerosis

Front 348

What is the medical treatment for Raynaud's disease?

Back 348

Calcium channel blockers (like Nifedipine).

Front 349

What is the most common cause of AV graft failure in dialysis patients?

Back 349

Venous obstruction due to intimal hyperplasia!

Front 350

What is hypothenar hammer syndrome?

Back 350

Repetitive use of the hand causes fibromuscular dysplasia of the ulnar artery causing aneurysm formation. This could clot or embolize. Tx: Resect the aneurysm, graft vein!

Front 351

In regard to venous insufficiency, what is the Trendelenburg Test?

Back 351

1: elevate the leg, occlude the greater saphenous vein junction and lower leg. Ifrapid filling of the GSV occurs there are valvular incompetencies. 2. If first part didn't fill the GSV, then release pressure on the saphenofemoral junction, if rapid filling have valve incompetency.

Front 352

What is the treatment for superficial thrombophlebitis, which is a NON-bacterial inflammation of veins?

Back 352

NSAIDs, warm packs, ambulation

Front 353

What is the treatment for suppurative thrombophlebitis?

Back 353

Resecting the vein

Front 354

What does someone suffereing from migrating thrombophlebitis possibly have?

Back 354

Pancreatic cancer.

Front 355

What is Mondor's disease?

Back 355

Self-limiting thrombophlebitis of the breast.

Front 356

How, beyond helping circulate blood, do SCDs help prevent clots?

Back 356

Help releast AT-III, tPA, and increase fibrinolysis.

Front 357

What are acquired hypercoagulable states?

Back 357

smoking, obesity, OC use, pregnancy, malignancy.

Front 358

In trauma patients what is the HIGHEST risk factor for VTE?

Back 358

Spinal cord injury

Front 359

What is May Thurner syndrome?

Back 359

Iliac vein clot on the left leg, due to compression by the iliac artery. You can usually treat with direct thrombolytics.

Front 360

What is Stewart-Treves Syndrome, in patients who've had breast cancer?

Back 360

Following axillary dissection, patients develop lymphangiosarcoma (raised blue/red coloring). Can occur 1-30 years post op. Very poor prognosis. Treat with WLE (chemoradiation shows poor response).

Front 361

For patients who develop lymphoceles following surgery (often for femoral to popliteal bypasses), what are the TOC?

Back 361

Inject isosulfan blue dye into the foot to ID lymphatic channels supplying the lymphocele, and resect the supplying lymphatic channel.

Front 362

What is white clot syndrome?

Back 362

Heparin-induced thrombosis, where you first develop thrombocytopenia and then clots (platelet rich, fibrin poor).

Front 363

What antibody complex causes HIT?

Back 363

IgG against platelet + PF-4 complexes, which can lead to thrombotic complications. Must use direct thrombin inhibitors after that (argatroban, lepirudin).

Front 364

When a child has a right to left shunt, what can they do to decrease it?

Back 364

Squating compresses femoral arteries, increasing systemic vascular resistance, decreasing the shunt.

Front 365

What is Eisenmenger's Syndrome?

Back 365

A shift in shunting direction (left to right to right to left), which is a sign of increasing pulmonary vascular resistance and pulmonary HTN.

Front 366

What is the first sign of CHF in children?

Back 366

Hepatomegaly!

Front 367

What are diseases causing kids to get L --> R shunting (symptoms of CHF)?

Back 367

VSD, ASD, PDA

Front 368

What are diseases causing kids to get R --> L shunting (symptoms of cyanosis)?

Back 368

Tetralogy of Fallot, transposition of great vessels, truncus arteriousus (aka a common trunk).

Front 369

What in infants keeps the ductus arteriosus open, and what can be given to help close this?

Back 369

Prostaglandins keep it open, aided by NSAIDs. Closure is aided by Indomethacin.

Front 370

What is the most common cardiac defect?

Back 370

Ventricular septal defect.

Front 371

What are medical therapies for patients with large VSDs/ASDs, who if not treated can develop CHF with failure to thrive (the most common reason repair is sought), tachypnea, tachycardia, and eventually a risk for endocarditis?

Back 371

Diuretics and Digoxin (decreases HR, but increases contractility by increasing intracellular calcium).

Front 372

Beyond failure to thrive, what peripheral vascular resistance number is an indication for repair?

Back 372

PVR > 4-6 Woods units If PVR 10-12 W.U. attempt vasodilators to see if reversible

Front 373

What is the most common form of atrial septal defect?

Back 373

Ostium secundum: centarlly located, has a patent foramen ovale (80%), can have anomalous pulmonary venous return (to the right atrium or IVC), and the IVC can connect to the left atrium.

Front 374

Describe the Ostium Primum defect.

Back 374

An atrioventricular septal defect or endocardial cushion defect found more inferiorly than an ostium secundum. Can get mitral valve and coronary sinus defects. The most common heart defect associated with Down Syndrome!!!

Front 375

What are the defects found in Tetralogy of Fallot?

Back 375

1. VSD2. Pulmonic stenosis3. Overriding aorta4. Right ventricular hypertrophy A R --> L shunt, it is the most common cardiac defect causing cyanosis!

Front 376

What is the medical management of Tetralogy of Fallot?

Back 376

Beta blockers

Front 377

What is the most common cyanotic cardiac defect discovered in the first week of life?

Back 377

Transposition of great vessels, a R --> L shunt. Patient survival dependent on mixing due to ASD, possibly VSD or PDA.

Front 378

Medical therapy for transposition of great vessels?

Back 378

Atrial septostomy, PGE1 (to keep PDA open).

Front 379

What type of shunting occurs with a truncus arteriosus, and what major complication occurs as a result?

Back 379

Right to left shunt, ultimately develop mixing that causes arterial saturations around 85-90%. Patients will go on to develop CHF (80% of kids die within the first year of life).

Front 380

What is the most common location of coarctation in patients with aortic involvement/

Back 380

Just distal to the left subclavian artery, so patients will show rib notching from the internal mammary artery and intercostal collaterals.

Front 381

What is the associated syndrome in patients with coarctation of the aorta?

Back 381

Turner Syndrome (gonadal dyskinesia, causing short, broad chested kids with webbed necks, and low set ears).

Front 382

What is the most common form of vascular rings (congenital defects of abnormal aorta/surrounding blood vessel formation, sometimes the trachea and esophagus are encircled making a ring) seen?

Back 382

Double aortic arch. Can manifest as recurrent pulmonary infections or dysphagia. Divide the smaller arch through a left thoracotomy.

Front 383

What is the first seen pathologic abnormality in the pathway of CAD?

Back 383

Fatty streaking (can be seen in children).

Front 384

In regards to posterior descending artery, what is the most common variant?

Back 384

RIGHT dominant circulation (posterior descending artery coming off the right coronary artery).

Front 385

When are you most likely to see papillary muscle rupture/free wall rupture in patients with recent MI?

Back 385

3-7 days post-event.

Front 386

What is the rate of restensosis after percutaneous transluminal coronary angioplasty for CAD?

Back 386

20-30% within one year.

Front 387

What is the 5 year patency rate of saphenous vein graft to treat CAD/MI?

Back 387

80-90% five year patency.

Front 388

What is the best conduit for bypass in cardiac disease?

Back 388

Internal mammary artery (> 90% 10 year graft patency).

Front 389

What are indications for CABG procedure?

Back 389

1. Left main disease2. Left main equivalent disease (LAD > 7)% and proximal left complications)3. 3 vessel disease4. 2 vessel disease with proximal LAD stensosis and either LVEF < 50% or extensive ischemia on noninvasive imaging5. One or 2- vessel disease with stable angina, large area of viable myocardium and high risk criteria on non-invasive testing, OR disease causing life-threatening arrhythmias OR disabling stable angina despite meds6. Nonstable angina

Front 390

What are the risk factors for mortality in patients undergoing CABG?

Back 390

Emergent surgery (MAJOR), age, reoperation, low EF, female sex, history of stroke/COPD/cardiogenic shock, recent MI

Front 391

What is the most common valvular lesion, and what are its causes?

Back 391

Aortic stenosis. Due to calcification (most common), congenital bicuspid aortic valve, rheumatic heart disease (MITRAL VALVE IS STILL THE MOST COMMONLY INVOLVED).

Front 392

What are indications for repair of aortic stenosis?

Back 392

Symptomatic (exertional dyspnea, syncope, angina, HF) OR valve area < 0.5 cm2 OR poor ventricular function

Front 393

What are medical therapies used for unstable angina?

Back 393

ASA, BBs, and statins. Heparin, Plavix and GIIb/IIIa inhibitors may also help. * abciximab (ReoPro)* eptifibatide (Integrilin)* tirofiban (Aggrastat) Calcium channel blockers are NOT used!

Front 394

What are the indications for patients to get valve replacement with a TISSUE valve (that does NOT require anticoagulation)?

Back 394

1. patients seeking pregnancy2. contraindications to anticoagulation3. are older and unlikely to require another valve4. have frequent falls

Front 395

What are contraindications for patients to get valve replacement with a TISSUE valve (that does NOT require anticoagulation)?

Back 395

Children, young patients (due to rapid calcification), and chronic renal dialysis.

Front 396

What are indications for repair of a mitral valve stenosis?

Back 396

Sympatomatic (usually occurs when valve < 1 cm2)

Front 397

What is the most common site of prosthetic valve infections?

Back 397

aortic valve

Front 398

What is the most common valve involved in native valve endocarditis?

Back 398

Mitral valve

Front 399

What bacteria is responsible for 50% of endocarditis?

Back 399

Staph aureu

Front 400

What are indications for surgery in patients with endocarditis?

Back 400

Failure of anti-microbial treatment, valve failure, perivalvular abscess, pericarditis.

Front 401

What are indications for peri-procedural endocarditis prophylaxis?

Back 401

1. Prosthetic valve2. rheumatic heart disease3. congenital cardiac malformations (VSD)4. Mitral valve prolapse with regurgitation5. Previous history of endocarditis Use first generation cephalosporins (Cephalexin, Cefazolin).

Front 402

What are the most common benign, malignant and metastatic cardiac tumors?

Back 402

Benign: Myxoma, mostly in the RA (75%). can cause mitral valve stenosis. Malignant: angiosarcoma Metastatic: lung cancer

Front 403

What veins have the lowest oxygen tension of any tissue in the body due to high extraction?

Back 403

Coronary veins.

Front 404

What is the first sign of cardiac tamponade on echo?

Back 404

Decreased right atrial diastolic filling, due to equilization of pressures across all heart chambers.

Front 405

Where do the superior parathyroid originate? and inferior?

Back 405

4th pharyngeal pouch, 3rd pharyngeal pouch

Front 406

Where are the superior parathyroids in relation to the RLNs? and the inferior?

Back 406

lateral, medial

Front 407

Where are the superior parathyroids in relation to the inferior thyroid artery? and inferior parathyroids?

Back 407

above, below

Front 408

What is the blood supply to the parathyroids?

Back 408

inferior thyroid artery

Front 409

What is the most common ectopic site for parathyroids?

Back 409

tail of the thymus

Front 410

What is a normal Ca level range?

Back 410

8.5-10.5

Front 411

What is a normal PTH level range?

Back 411

5-40

Front 412

What is the most common cause of hypoparathyroidism?

Back 412

previous thyroid surgery

Front 413

What is the name form bone lesions from Ca resorption; characteristic of hyperparathyroidism?

Back 413

Osteitis firbrosa cystica (brown tumors)

Front 414

Indications for parathyroid surgery include symptomatic disease or asymptomatic disease with Ca above what level?

Back 414

13

Front 415

What percentage of pts with hyperparathyroid have single adenoma? multiple adenomas? diffuse hyperplasia?

Back 415

single adenoma 80%multiple adenomas 4%diffuse hyperplasia 15%

Front 416

Hyperparathyroidism in pregnancy carries a risk of still birth. In what trimester do you operate?

Back 416

2nd

Front 417

What is the half-life of PTH?

Back 417

10 minutes

Front 418

What should be done if parathyroid CA is found?

Back 418

radical parathyroidectomy and take ipsilateral thyroid

Front 419

What are the three causes of postop hypocalcemia after parathyroid surgery?

Back 419

bone hunger, hypomagnesmia, failure of parathyroid remnant or graft

Front 420

Hypocalcemia postop after parathyroid surgery. What will the levels of PTH and HCO3- be if the cause is bone hunger? and what if it is aparathyroidism?

Back 420

Bone hunger – normal PTH, decreased HCO3− Aparathyroidism – decreased PTH, normal HCO3−

Front 421

What is the study that is used in hyperparathyroidism that is good for picking up adenomas and ectopic glands but not 4-gland hyperplasia?

Back 421

sestamibi-technetium-99

Front 422

What is the most common indication for surgery in secondary hyperparathyroidism?

Back 422

bone pain

Front 423

What diagnosis should you consider if pt has Ca 9–11, normal PTH (30–60), ↓ urine Ca?

Back 423

Familial hypercalcemic hypocalciuria

Front 424

What is the cause of familial hypercalcemic hypocalciuria?

Back 424

Caused by defect in PTH receptor in distal convoluted tubule of the kidney that causes ↑ resorption of Ca

Front 425

What is the tx for familial hypercalcemic hypocalciuria?

Back 425

Nothing, no parathyroidectomy because Ca generally not that high

Front 426

What is the most common location for metastases of parathyroid cancer?

Back 426

the lung

Front 427

List the MEN syndromes and components?

Back 427

MEN I: parathyroid hyperplasia, pancreatic islet cell tumors, pituitary adenomasMEN IIa: parathyroid hyperplasia, pheochromocytoma, medullary CA of the thyroidMEN IIb: pheochromocytomas, medullary CA of thyroid, mucosal neuromas, marfan's habitus

Front 428

Name the drug used in the management of hypercalcemia that inhibits osteoclasts (used with malignancies or failure of conventional treatment); has hematologic, liver, and renal side effects.

Back 428

Mithramycin

Front 429

When breast CA metastases to bone, what causes hypercalcemia?

Back 429

release of PTHrp

Front 430

What hormone is responsible for duct development of the breast? and lobular development? and what hormone synergizes those two?

Back 430

estrogen, progesterone, prolactin

Front 431

What nerve innervates serratus anterior; injury results in winged scapula?

Back 431

long thoracic

Front 432

What artery supplies serratus anterior?

Back 432

lateral throacic artery

Front 433

What nerve innervates latissimus dorsi?

Back 433

thoracodorsal nerve

Front 434

What artery supplies latissimus dorsi?

Back 434

thoracodorsal artery

Front 435

What innervates pectoralis major and minor? what innervates pectoralis major only?

Back 435

Medial pectoral nerve – innervates pectoralis major and pectoralis minor • Lateral pectoral nerve – pectoralis major only

Front 436

What nerve?:Lateral cutaneous branch of the 2nd intercostal nerve; provides sensation to medial arm and axilla; encountered just below axillary vein when performing axillary dissection. Can transect without serious consequences.

Back 436

intercostobrachial nerve

Front 437

Branches of 4 arteries supply the breast?

Back 437

internal thoracic artery, intercostal arteries, thoracoacromial artery, and lateral thoracic artery

Front 438

What is the valveless vein plexus that allows direct hematogenous metastasis of breast CA to spine?

Back 438

Batson's plexus

Front 439

What is the number 1 cause of axillary adenopathy?

Back 439

lymphoma

Front 440

What is the term used to describe breast cysts filled with milk; occurs with breast-feeding? Tx: ranges from aspiration to incision and drainage.

Back 440

Galactocele

Front 441

Dilated mammary ducts, inspissated secretions, marked periductal inflammation • Symptoms: noncyclical mastodynia, nipple retraction, creamy discharge from nipple; can have sterile subareolar abscess • Patients have a history of difficulty with breast-feeding • Tx: if typical creamy discharge is present that is not bloody and not associated with nipple retraction, may be able to reassure; otherwise need to rule out malignancy.

Back 441

Periductal mastitis (mammary duct ectasia or plasma cells mastitis)

Front 442

What syndrome is described by hypoplasia of chest wall, amastia, hypoplastic shoulder, no pectoralis muscle?

Back 442

Poland's syndrome

Front 443

Name the disease and treatment described by superficial vein thrombophlebitis of breast; feels cordlike, can be painful • Associated with trauma and strenuous exercise • Usually occurs in lower outer quadrant.

Back 443

Mondor's disease, tx NSAIDs

Front 444

What are the two types of fibrocystic breast disease that have a cancer risk?

Back 444

atypical ductal or lobular hyperplasia

Front 445

What type of fibrocystic disease can manifest as a cluster of calcifications on mammogram without a mass or pain → can look like breast CA? • Is differentiated from breast CA by regularity of nuclei and absence of mitoses

Back 445

sclerosing adenosis

Front 446

What is the most common cause of bloody discharge from nipple?

Back 446

intraductal papilloma

Front 447

Are intraductal papillomas premalignant?

Back 447

no

Front 448

How to locate a intraductal papilloma and what is the tx?

Back 448

→ can get contrast ductogram to find papilloma • Tx: resection (subareolar resection usually curative)

Front 449

What is the most common breast lesion in adolescents and young women?

Back 449

fibroadenoma

Front 450

How do you diagnose a fibroadenoma in a pt <30? and >30?

Back 450

In patients < 30 years: • Mass needs to feel clinically benign (firm, rubbery, rolls, not fixed) • Ultrasound or mammogram needs to be consistent with fibroadenoma • Need fine-needle aspiration (FNA) or core needle biopsy showing the lesion (not just normal breast tissue.In patients > 30 years → excisional biopsy to ensure diagnosis

Front 451

What is the difference in workup for nipple discharge that is spontaneous vs nonspontaneous?

Back 451

Spontaneous discharge – no matter what the color or consistency is worrisome for cancer • All these patients need some sort of biopsy in the area of the duct causing the dischargeNonspontaneous discharge (occurs only with pressure, tight garments, exercise, etc.) – not as worrisome but may still need excisional biopsy (i.e., if bloody)

Front 452

What two things do all pts with nipple discharge need?

Back 452

H and P and bilateral mammogram

Front 453

What is the usual cause of green nipple discharge and tx?

Back 453

Usually due to fibrocystic disease. Tx: if cyclical and nonspontaneous, reassure pt

Front 454

What are two possible causes of bloody nipple discharge and their workup?

Back 454

Bloody discharge – most commonly intraductal papilloma; occasionally ductal CA • Tx: need galactogram and excision of that ductal area

Front 455

What is the concern with serous nipple discharge and the tx?

Back 455

Serous discharge – worrisome for cancer, especially if coming from only 1 duct or spontaneous • Tx: excisional biopsy of that ductal area

Front 456

■ Affects multiple ducts of both breasts ■ Papillomas are larger than when they occur solitarily ■ Usually have serous discharge ■ Mammogram shows Swiss cheese appearance ■ ↑ risk of breast CA (40% get breast CA)

Back 456

Diffuse Papillomatosis

Front 457

■ Malignant cells of the ductal epithelium without invasion of the basement membrane ■ 50%–60% get cancer if not resected (ipsilateral breast); 5%–10% get cancer in contralateral breast ■ Considered a premalignant lesion ■ Usually not palpable and presents as a cluster of calcifications on mammography

Back 457

Ductal Carcinoma In Situ

Front 458

What size margin is needed for ductal carcinoma in situ?

Back 458

2-3 mm

Front 459

What is the most aggressive subtype of ductal carcinoma in situ; has necrotic areas • High risk for multicentricity, microinvasion, and recurrence • Tx: simple mastectomy

Back 459

Comedo pattern

Front 460

What is the tx for ductal carcinoma in situ with a small focus? and if high grade (ie comedo type, multicentric, multifocal)?

Back 460

small focus: lumpectomy and XRT; possibly tamoxifensimple mastectomy if high grade or large tumor; no ALND

Front 461

■ 40% get cancer (either breast) ■ Considered a marker for the development of breast CA, not premalignant itself ■ Has no calcifications; is not palpable ■ Primarily found in premenopausal women, usually incidental finding

Back 461

Lobular carcinoma in situ

Front 462

What are three treatment options for lobular carcinoma in situ?

Back 462

Tx: nothing, tamoxifen, or bilateral subcutaneous mastectomy (no ALND)

Front 463

What country has the lowest rate of breast CA worldwide?

Back 463

Japan

Front 464

Is breast CA increased or decreased in economically poor areas?

Back 464

decreased

Front 465

What is the breast CA risk for women?

Back 465

1 in 8 (12%)

Front 466

What is the median survival for untreated breast CA

Back 466

2-3 years

Front 467

What percentage of breast CAs have negative mammogram and negatie ultrasound?

Back 467

10%

Front 468

Symptomatic breast mass in a pt <30 years old, what next?

Back 468

ultrasound

Front 469

Symptomatic breast mass in a pt <30 years old, gets ultrasound and it shows it is solid, what next?

Back 469

FNA

Front 470

Symptomatic breast mass in a pt <30 gets ultrasound, shows solid, has FNA, it comes back nondiagnostic, what next? what if FNA comes back fibroadenoma

Back 470

excisional bx, fibroadenomas need excisional bx if enlarges

Front 471

Symptomatic breast mass in pt 30-50 years what next?

Back 471

bilateral mammograms and FNA; excisional bx if FNA nondiagnostic

Front 472

Symptomatic breast mass in a pt >50 years what next?

Back 472

bilateral mammograms and excisional or core needl bx

Front 473

What is the difference in FNA and core needle bx.

Back 473

Core needle bx gives architecture, FNA gives cytology (just the cells)

Front 474

Symptomatic breast mass is cystic, fluid is bloody what next? what if is clear and recurs? what if complex cyst?

Back 474

excisional bx for all three: bloody, recurs, or complex

Front 475

What size does a mass need to be in order to be detected on mammogram?

Back 475

>5mm

Front 476

What are the general screening mammogram guidelines? and for high risk?

Back 476

Every 2-3 years after age 40, yearly after 40High risk: 10 years before the youngest age of dx in first-degree relative

Front 477

What is the next step if mammogram shows suspicious or indeterminate calcifications or architecture?

Back 477

perform localized stereotactic needle excisional biopsy

Front 478

Name the BI-RADS level:Highly suggestive of malignancy. High probability of cancer; appropriate action should be taken.

Back 478

5

Front 479

Name the BI-RADS level:Suspicious abnormality. Definite probability of malignancy; consider biopsy

Back 479

4

Front 480

Name the BI-RADS level:Probably benign finding Short-interval follow-up

Back 480

3

Front 481

What muscle divides the three axillary lymph node levels and what are they?

Back 481

Pec Minor I – lateral to pectoralis minor muscleII – beneath pectoralis minor muscleIII – medial to pectoralis minor muscle

Front 482

What is the most important prognostic staging factor in breast CA? list 4 others?

Back 482

nodestumor size, tumor grade, progesterone and estrogen status

Front 483

What is the most common distant metastasis for breast CA? list 3 others?

Back 483

bonelung, liver, brain

Front 484

With breast cancer, how long does it take to go from one malignant cell to a 1 cm tumor?

Back 484

5-7 years

Front 485

Central and subareolar tumors have an increased risk of what?

Back 485

multcentricity

Front 486

What type are 85% of breast CAs? and the next 10%?

Back 486

ductal CA, lobular CA

Front 487

What is the median survival for inflammatory breast cancer?

Back 487

36 months

Front 488

What causes the peu d'orange appearance in inflammatory breast cancer?

Back 488

dermal lymphatic invasion

Front 489

Subcutaneous (simple) mastectomy preserves the nipple and leaves 1-2% of breast tissue. Not indicated for breast CA treatment. Used for what two conditions?

Back 489

DCIS and LCIS

Front 490

What size margins for lumpectomy?

Back 490

1 cm

Front 491

Clinically positive nodes not a candidate for SLND, needs what?

Back 491

ALND

Front 492

During SLND, if no radiotracer or dye is found, what do you do?

Back 492

ALND

Front 493

A complication of axillary lymph node dissection, sudden early, postop swelling could be do to what? what about slow swelling over 18 months?

Back 493

Axillary vein thrombosis, Lymphatic fibrosis

Front 494

A complication of axillary lymph node dissection: hyperesthesia of inner arm and lateral chest wall; most commonly injured nerve after mastectomy; no significant sequelae. What nerve could be injured?

Back 494

Intercostal brachiocutaneous

Front 495

How long to leave drains after axillary lymph node dissection?

Back 495

until drainage < 40cc/day

Front 496

Indications for XRT after mastectomy include:?skin or chest wall involvementpositive marginstumor > what size?extracapsular node invasioninflammatory CAfixed nodes or internal mammary nodes

Back 496

>4 nodes>5 cm tumor

Front 497

Lumpectomy with XRT pts need what before starting XRT?

Back 497

negative margins

Front 498

Two indications for chemo in breast CA

Back 498

• Positive nodes – everyone gets chemo except postmenopausal women with positive estrogen receptors → tamoxifen • >1 cm and negative nodes – everyone gets chemo except patients with positive estrogen receptors → tamoxifen • <1 cm and negative nodes – no further treatment

Front 499

With paget's disease of the breast, pts will have what 2 other conditions?

Back 499

DCIS or ductal CA

Front 500

What is the tx for Paget's disease of the breast?

Back 500

MRM if CA present otherwise simple mastectomy

Front 501

Cystosarcoma phyllodes, 10% are malignant, how can it mets?

Back 501

hematogenous (rare), no nodal mets

Front 502

What is the tx for Cystosarcoma phyllodes?

Back 502

WLE with negative margins, no ALND

Front 503

What is the name for the syndrome which is lymphangiosarcoma from chronic lymphedema following axillary dissection (MRM) • Patients present with dark purple nodule or lesion on arm 5–10 years after surgery

Back 503

Stewart-Treves syndrome

Front 504

What is the position of the phrenic nerve and vagus nerve in the hilum?

Back 504

■ Phrenic nerve – runs anterior to hilum ■ Vagus nerve – runs posterior to hilum

Front 505

What percentage of total lung volume is from the right lung?

Back 505

55%

Front 506

What percentage of quiet inspiration is from the diaphragm? and the intercostals?

Back 506

80%, 20%

Front 507

Which pneumocytes produce surfactant?

Back 507

Type II

Front 508

What structures direct air exchange between alveoli?

Back 508

Pores of Kahn

Front 509

How much pleural fluid is produced per day?

Back 509

1-2 L

Front 510

Which layer of the pleura produces pleural fluid and which layer has the lymphatics that clear the fluid?

Back 510

parietal pleura produces pleural fluid cleared by lymphatics in the visceral pleura

Front 511

What is the most common single site of lung CA mets?

Back 511

brain

Front 512

What is the overall 5 year survival rate for lung CA? and with resection?

Back 512

10%, 30%

Front 513

What is the most common type of lung CA?

Back 513

adenocarcinoma

Front 514

Local recurrence is increased with which type of lung CA? and distant metastases?

Back 514

local recurrence, distant metastases

Front 515

What percentage of pts with small carcinoma are surgical candidates?

Back 515

<5% (most get just chemo and XRT)

Front 516

What is the most common paraneoplastic syndrome?

Back 516

Small cell ACTH

Front 517

What is the most malignant lung tumor?

Back 517

mesothelioma

Front 518

Name two chemotherapy agents used for small cell lung CA

Back 518

cisplatin, etopside

Front 519

What is the name of the procedure used to assess aortopulmonary window nodes; goes through left 2nd rib cartilage?

Back 519

Chamberlain procedure

Front 520

In addition to Horner's syndrome, what other nerve can have sx with Pancoast tumor?

Back 520

ulnar

Front 521

Coin lesions are overall 5-10% malignant. Age <50 what percent are malignant? and age >50?

Back 521

<5%, 50%

Front 522

What type of tumor is carcinoids? what is the tx?

Back 522

neuroendocrine, tx: resection; treat like CA

Front 523

Name the lung mass: • Submucosal glands; spread along perineural lymphatics, well beyond endoluminal component; XRT sensitive • Slow growing; can get 10-year survival with incomplete resection • Tx: resection; if unresectable, XRT can provide good palliation

Back 523

Adenoid cystic adenoma

Front 524

What is the most common benign adule lung tumor?

Back 524

hamartoma

Front 525

Popcorn lesion on chest CT, dx? tx?

Back 525

hamartoma, Do not require resection ■ Repeat chest CT in 6 months to confirm diagnosis

Front 526

What type of tumor is the most common mediastinal tumor in adults and children, usually in posterior mediastinum?

Back 526

neurogenic tumors

Front 527

What is the most common site for mediastinal tumor?

Back 527

anterior (thymus)

Front 528

What are 5 types of tumors found in the anterior mediastinum?

Back 528

Thymoma,Thyroid CA and goiters,T-cell lymphoma,Teratoma,Parathyroid adenomas

Front 529

What is the tx for all thymomas?

Back 529

resection

Front 530

What is the tx for mediastinal teratoma? and seminoma?

Back 530

resection and chemo for teratoma; seminoma is very XRT sensitive, chemo for positive nodes or residual disease; surgery for residual disease after that

Front 531

90% of nonseminoma mediastinal germ cell tumor have elevations in what two markers? and what is the tx?

Back 531

beta-HCG and alpha-fetoproteinTx: cisplatin-based chemo and XRT; surgery for residual disease

Front 532

Benign tumor of the trachea seen in adults? and in children? malignant is usually what?

Back 532

adults papilloma; children hemangioma; malignant squamous cell carcinoma

Front 533

What is the most common late complication after tracheal surgery? and early complication?

Back 533

late - granulation tissue formationearly - laryngeal edema

Front 534

Postintubation stenosis – at stoma site with tracheostomy, at cuff site with ET tubeMay be able to treat with ___ or ___ May need resection with end-to-end anastomosis if severe.

Back 534

serial dilatation or with laser

Front 535

Tracheostomy – needs to be between the 1st and 2nd tracheal rings not >3 rings → risk what?

Back 535

tracheoinnominate fistula

Front 536

What is the tx for tracheoinnominate fistula?

Back 536

overinflate balloon to plug hole or stick your finger in hole and depress innominate artery. Resect innominate and place graft. Leave trachea alone. Use new tracheostomy site

Front 537

■ Tracheoesophageal fistula: • Use large-volume cuff below fistula • May need decompressing gastrostomy • Tx: tracheal resection, reanastomosis, ___ flap

Back 537

sternohyoid

Front 538

Lung abscess are most commonly associated with what?

Back 538

aspiration

Front 539

Tx for lung abscess is abx which are 95% successful, what next if abx fails? and if that fails?

Back 539

CT guided drainagesurgery if fails or cannot rule out CA (>6 cm, failure to resolve after 6 weeks)

Front 540

What are the three phases of empyema seen in 1-3 weeks respectively?

Back 540

Exudative phase - 1st weekFibroproliferative phase - 2nd weekOrganized phase - 3rd week

Front 541

What is the tx of empyema during the 1st and 2nd weeks? and 3rd week (3 options)?

Back 541

abx and chest tube in 1st and 2nd week3rd week - Tx: likely need decortication; fibrous peel occurs around lung • May need Eloesser flap (direct opening to external environment) for chronic unresolving empyema • Can also place a chronic chest tube that is gradually pulled out

Front 542

50% of chylothorax is secondary to what cause? and the other 50%

Back 542

50% secondary to tumor, 50% secondary to trauma or iatrogenic injury

Front 543

What is the most common tumor to cause chylothorax?

Back 543

lymphoma due to tumor burden on lymphatics

Front 544

The thoracic duct runs along the right side and dumps into the left sublavian vein at junction with internal jugular. Where does it cross? Why is this location significant in chylothorax?

Back 544

T4-5Injury above T5–6 results in left-sided chylothorax ■ Injury below T5–6 results in right-sided chylothorax

Front 545

Tx for chylothorax is 3-4 weeks of conservative therapy * chest tube, octreotide, low-fat diet or TPN). What if that fails for chylothorax secondary to trauma or iatrogenic injury? and for malignant cases?

Back 545

If that fails, surgery with ligation of thoracic duct on right side low in mediastinum (80% successful) if chylothorax secondary to trauma or iatrogenic injury For malignant causes of chylothorax, can perform mechanical or talc pleurodesis (less successful than above)

Front 546

What stain can be used to stain fat in chylothorax?

Back 546

sudan red stain

Front 547

Does the milky white fluid in chylothorax that is high in lymphocytes and TAGs get infected?

Back 547

chylothorax is fluid resistant to infection

Front 548

Massive hemoptysis (>600 cc/24 h), bleeding is from high pressure bronchial arteries. Most commonly secondary to infection. What type is most common?

Back 548

mycetoma (fungal)

Front 549

What is the tx for massive hemoptysis (>600cc in 24 hrs)?

Back 549

place bleeding side down if know; rigid bronchoscopy to identify site; mainstem intubation to side opposite of bleeding to prevent drowning in blood; to OR for lobectomy or pneumonectomy; brochial artery embolization if not suitable for surgery

Front 550

Spontaneous pneumothorax seen in tall, healthy, thin, young males. Recurrence risk after 1st pneumothorax is what percent? after 2nd? after 3rd?

Back 550

20%, 60%, 80%

Front 551

Which side is spontaneous pnuemothorax most common?

Back 551

right

Front 552

What is the tx for spontaneous pneumothorax?

Back 552

chest tube

Front 553

When is surgery indicated for spontaneous pneumothorax?

Back 553

recurrence, large blebs on CT scan, air leak >7 days, nonreexpansion.Also need surgery for high-risk profession (airline pilot, diver, mountain climber) or pts who live in remote areas

Front 554

What is the most common cysts of the mediastinum and their usual location?

Back 554

bronchiogenic cysts, usually posterior to the carina

Front 555

What type of pneumothorax occurs in temporal relation to menstruation. Caused by endometrial implants in visceral lung pleura?

Back 555

catamenial pneumothorax

Front 556

Residual hemothorax despite 2 good chest tubes. What next?

Back 556

OR for thorascopic drainage

Front 557

Clotted hemothorax - surgical drainage if >25% of lung, air-fluid levels, or signs of infection; surgery in 1st week to avoid what?

Back 557

avoid peel

Front 558

Whiteout on CXR: Midline shift toward whiteout is most likely collapse. Needs what tx?No shift - do CT to figure it outMidline shift away from whiteout likely effusion. Needs what tx?

Back 558

collapse needs bronchoscopy to remove plugeffusion needs chest tube

Front 559

Bronchiectasis is acquired from infection, tumor or what other condition?

Back 559

cystic fibrosis

Front 560

Noncaseating granulomas are seen in what lung condition?

Back 560

sarcoidosis

Front 561

What is the pleural fluid protein to serum ratio seen in an exudate? and the pleural fluid LDH to serum ratio seen in exudate?

Back 561

> 0.5> 0.6

Front 562

Recurrent pleural effusions can be treated with what?

Back 562

mechanical pleurodesis (talc pleurodesis for malignant pleural effusions)

Front 563

Airway fires are usually associated with the laser. What is the tx?

Back 563

stop gas flow, remove ET tube, reintubate for 24 hrs; bronchoscopy

Front 564

AVMs, connections between the pulmonary arteries and pulmonary veins; usually occurs in the lower lobes and in pts with what disease?

Back 564

Osler-Weber-Rendu disease

Front 565

What is the tx for AVMs in the lung?

Back 565

embolization

Front 566

What is the most common benign chest wall tumor? and malignant?

Back 566

benign - osteochondromamalignant - chondrosarcoma