Buzzin Flashcards

Question

mallory-wess laceration

Answer 1

retching/violent vomiting = lengwise tears

Answer 2

perforation of esophagus due to increased pressure

Answer 3

metaplasia (replacement): squamous cell to intestinal glandular mucosa w/ goblet cells ADCA risk - length is most imp. risk factor >3cm

Answer 4

cervical LNs

Answer 5

SCC - mediastinal, paratracheal,, tracheobronchial nodes

Answer 6

think ADCA - spread gastric/celiac nodes

Answer 7

burns/trauma - proximal D

Answer 8

intracranial disease - see gastric, duodenal, esophageal ulcers

Answer 9

antrum / duodenum | spiral shaped, curved bacilli

Answer 10

drugs/alcohol

Answer 11

due to urease in H. pylori infection

Answer 12

ADCA, MALT lymphoma

Answer 13

AI gastritis AutoAbs to parietal cells and IF - loss of parietal cells

Answer 14

defective gastric acid secretion

Answer 15

acid producing mucosa - parietal cells

Answer 16

think PU that punctured through stomach

Answer 17

bright red blood in stools

Answer 18

upper GI endoscopy

Answer 19

metetrier disease: xs secretion of TGF alpha: body/fundus ; w/l diarrhea, Peripheral edema ZE syndrome : gastrin secreting tumor - see chronic diarrhea , multiple peptic ulcers

Answer 20

benign gastric adenoma/ a type of polyp

Answer 21

think gastric adenocarcinoma

Answer 22

1. Intestinal type (non signet ring) - usual type - assoc. w/ H. pylori APC/WNT pathway - occur in gastric antrum/pulorus - form bulky ulcerative tumors 2. Diffuse-type (signet ring) - not assoc. w/ h. pylori germline loss of fn. in E-cadherin (CDH1 gene) - infiltrate diffusely in wall of stomach - linitis plastica

Answer 23

marginal zone B cell lymphoma - H. pylori related arise in site of previous inflammation CD19/20 + see lyymphoepithelial lesions

Answer 24

mesenchymal gastro-intestinal stromal tumor arise from interstitial cells of cajal C-KIT/CD117 or PDGFRA mutations see spindle cell features

Answer 25

mesenchymal GIST

Answer 26

``` direct = occur medial to epigastric indirect = lateral to epigastric ```

Answer 27

think intussuscpetion

Answer 28

intussusception

Answer 29

Ischemic bowel disease, mural infarction, angiodysplasia, hemorrhoids

Answer 30

ischemic bowel disease also think CMV and E. coli

Answer 31

ischemic bowel disease - think splenic flexure, sigmoid colon, rectum ** most often colon!!!

Answer 32

painful bloody diarrhea

Answer 33

persist during fasting - think infectious; viral or enterotoxin

Answer 34

hypertonic fluid - abates w/ fasting - think lactase defic.

Answer 35

due to mucosal damage --> purulent bloody stoools that persist w/ fasting - think bacterial or IBD

Answer 36

abates w/ fasting : see improper absorption --> bulky stools w/ xs fat ex. celiac, giardia, CF, chronic pancreatitis

Answer 37

HLA-DQ2/DQ8 diffuse/severe blunting of villi in D/J malabsorption

Answer 38

subepidermal blistering of skin seen in 10% of celiac pts.

Answer 39

seen in Celiacs

Answer 40

mutated in abetalipoproteinemia:

Answer 41

abetalipoproteinemia:

Answer 42

abetalipoproteinemia:

Answer 43

campylobacter enterocoloitis most common bacterial pathogen in developed countries and travelers diarrhea see watery/blood diarrhea

Answer 44

shigellosis

Answer 45

maculopapular rash on chest and abdomen - typhoid fever - salmonella typhi may mimic appendicitis

Answer 46

watery/secretory noninflamm. diarrhea

Answer 47

O157:H7 --> HUS + bloody diarrhea

Answer 48

nonbloody diarrhea, prolonged in AIDS

Answer 49

Whipple disease - se w/l, diarrhea/steatorrhea, and polyarthritis see dense accum. of foamy macrophages in SI lamina propria --> accumulate in nodes and joints ** only one affecting lymphatic transport

Answer 50

rotovirus - causes severe wtery diarrhea

Answer 51

thik cryptosporidium spp. also MAI - can detect w/ acid fast stain

Answer 52

dysentery and liver abscess - caued by entamoeba histolytica seen in india, mexico, colombia --> go to liver, brain and lungs

Answer 53

deacreased expression of brush border enzymes --> steatorrhea

Answer 54

colon and rectum --> retrograde, no skips mucosa/submucosa - superficial broad based ulcers can cause megacolon and pseudopolyps NO granulomas/strictures bloody mucoid diarrhea risk of ADCA

Answer 55

``` regional enteritis unaffected, skip areas transmural linear mucosal ulcers - deep ulcers granulomas!!! fissureing/fistula creeping fat relatively mild diarrhea, ab. pain, RLQ (ileocecal) *** erythema nodosum ADCA fat + vit malabsorption ```

Answer 56

polyps w/ stalk

Answer 57

sessile - no malignant potential - most common

Answer 58

seen in chronic IBD - see rectal bleeding ad mucus discharge - not malignant

Answer 59

pedunculated - think PJ syndrome of juvenile polyposis

Answer 60

Peutz-Jeghers syndrome - see hamartomatous polyps, mucocutaneous hyperpigmentation increased risk of cancer

Answer 61

think juvenil polyposis age <5 see hamartomatous polyps - congenital malformations - digital clubbing - cancer by age 50

Answer 62

neoplastic polyps that are not yet malignant - size >4cm has increased malignancy

Answer 63

Familial adenomatous polyposis - see numerous adenomas >100 to make ddx colon cancer by age 30 if not treated autosomal dominant

Answer 64

think hereditary non-polyposis colorectal cancer HNPCC see sessile serrated adenomas autosomal dominant right sided ADcarcinoma - mucinous subtypes + endometrial cancer

Answer 65

predominantly on right side - has to do with DNA mismatch repair genes or hypermethlaition: MSH2, MLH1, BRAF --- think HNPCC or sporadic colon cancer

Answer 66

think typical tubular/villous ADCA with APC/WNT pathway defect change in bowel habits, rectal bleding, melena, LLQ pain : presents w/ obstruction and is caught more quickly

Answer 67

presents w/ fatigue, w/l, anemia : they don't often present w/ obstruction mucinous ADCA due to MSH2, MLH1, BRAF mutations and DNA mismatch repair problems

Answer 68

regional LNs, lungs, bones, liver *** most common

Answer 69

carcinoid tumor ** midgut most aggressive carcinoid syndrome = serotonin release - episodic skin flushing, diarrhea, bramping, asthma

Answer 70

upper zone = columnar epi. (see ADCAs) middle zone = transitional zone = cloacogenic carcinoma (behaves like SCC but doesn't make keratin) lower zone = squamous epi. - see condyloma papilliform - HPV 16/18, mutated E6/E7

Answer 71

perirectal and paravertral nodes

Answer 72

superficial inguinal /femoral nodes

Answer 73

Vacuolating cytotoxin (VacA) causes cell injury characterized by vacuolization. Another H. pylori gene from a pathogenicity island encodes cytotoxin-associated antigen (CagA) and is present in many patients with chronic gastritis and peptic ulcers and increases their risk for gastric cancer.

Answer 74

diffuse gastric ADCA - signet rings are seen

Answer 75

leather bottle stomach - diffuse gastric ADCA - signet rings are seen

Answer 76

UC sometimes CD

Answer 77

Shigella dysenteriae and Entamoeba histolytica. with E. histolytica can see liver abscess

Answer 78

fundic gland polyps

Answer 79

Salmonella typhi abdominal pain and diarrhea during week 1 of their illness. By week 2, these patients had splenomegaly and elevations in serum AST and ALT levels. By week 3, they were septic and had leukopenia. At autopsy, the patients who died were found to have ulceration of Peyer's patches.

Answer 80

zone 3 - acetiminophen toxicity

Answer 81

pregnancy, Reye syndrome, tetracycline/salicylate toxicity, alcohol

Answer 82

obesity, diabetes, hep C, EToH

Answer 83

jaundice, palmer erythema, spider angiomata, terry nails, finger clubbing, "fector hepatis"" - sweet/musty breath, edema/ascities, hypogonadism/gynecomastia

Answer 84

hepatic enceophalopathy - "flapping" tremor of hands - jerky irregular flexion patterns - due to ammonia accumulation and liver failure

Answer 85

think viral

Answer 86

think ethanol

Answer 87

hep C * most common alcohol * also really common hep B* sometimes

Answer 88

PDGF (migration of stellate cells) and TNF activates stellate cells TGF beta --> stimulates fibrinogenesis in myofibroblasts stellate cells secrete VEGF/ANG1 --> vascular remodeling

Answer 89

due to liver cirrhosis - b/c of fibrosis and sinusoidal remodeling of myofibroblasts --> intrahepatic vascular reistance pre-hepatic: portal occlusion Intra-hepatic: due to liver cirrhosis: alcohol + hep post hepatic: RSHF, hepatic v. outflow obstruction see varices, ascites, congestive splenomegaly, heptic encephalopathy

Answer 90

TB, carcinoma = exudate

Answer 91

transudate = albumin loss

Answer 92

think cholestasis - inability to excrete bile - backs up showing jaundice no bile salts to break down fats --> cholesterol retention and xanthomas bile salts deposit in skin --> pruritis

Answer 93

uridine diphosphatase = conjugates/ makes direct bilirubin

Answer 94

dark colored urine - due to bilirubin excretion

Answer 95

mpaired biliary excretion of bilirubin glucuronides is due to a mutation in the canalicular multidrug resistance protein 2 (MRP2) see elevated conjugated bili/jaundice w/out AST/ALT elevation DJ has black liver

Answer 96

think Gilbert/Crigler Najar - due to UDP problems

Answer 97

meausres hepatocyte membrane disruption ALT found in liver most common cause of just ALT/AST elevation = NASH higher AST/ALT ratio is likely ETOH see very high levels w/ viral infection

Answer 98

induced enzymes - think biliary things seen w/ cholestasis and EtOH isolated elevated GGT = EtOH isolated ALK Phos: must rule out bone and placenta

Answer 99

alcoholic liver disease

Answer 100

cirrhosis, AI hep

Answer 101

primary biliary cirrhosis

Answer 102

F-O contamination 1 mos. incubation third world epidemic - shellfish in US ACUTE ONLY - does not cause chronic disease see spike in fecal HAV see anti-HAV Ab in those having had vacc. see IgM- anti-HAV after 1 month in those that have been infected

Answer 103

ACUTE and CHRONIC (only minority go to chronic) - horizontal transmission: sex most common - vertical: seen in Asia! - 5% progresses to chronic hepatitis, 1% of total gets cirrhosis, .5% of total gets hepatocellular carcinoma 3 mos incubation histo: "gorund glass appearance" of HBsAg portal inflatmmion, apopostis w/ acidophil bodies

Answer 104

incomplete dsDNA - think HBV

Answer 105

see HBsAg, IgG Anti-HBc, IgM Anti-HBc****

Answer 106

see HBsAg, IgG Anti-HBc - don't see Anti-HBc IgM!!!

Answer 107

IgG Anti-HBc

Answer 108

IgG Anti-HBs - shows immunity to HBV

Answer 109

IgM - anti-HBc won't see anything during 3 mos. incubation gap

Answer 110

persistence of HBsAg for more than 6 mos, along with HBeAg and HBV-DNA ::: see it waver

Answer 111

presence of HBeAg and high levels of HBV DNA

Answer 112

age - younger age at time of infection = larger chance of increased chronicity

Answer 113

ACUTE and CHRONIC!!!! - most parenteral transmission 2 mos incubation no vaccine - genome is unstable see HCV RNA - in case of infection - stays w/ chronicity see anti-HCV in case of resolution * * most common cause of Hep C = Stable chronic hepatitis (not cirrhosis) * * only 15% of total go to cirrhosis Histo: portal inflammation, bridging fibrosis, lobular inflammation

Answer 114

Acute infection 3 mos incubation parenteral Absolutely dependent on HBV infection --> superinfection or co-infection

Answer 115

"hepatitis A of india" 1 mos incubation F-O route same serology as hep A: Fecal HEV seen during infection Anti-HEV Ab indicates vaccine / clearance IgM- anti-HEV - indicates infection - DDx

Answer 116

think cholangiocarcinomas - these are helminths

Answer 117

primary biliary cirrhosis (PBC) (a scarring of liver tissue, confined primarily to the bile duct drainage system of the liver).

Answer 118

think AI hepatitis histology same as viral hep - see cluster of periportal plasma cells Female = Type 1 Children = Type 2 sometimes also 80% have associated high titers of various autoantibodies, including (Type 1) ANA, ASMA, but negative for AMA (Type 2) ALKM1, ACL-1* Increased frequency HLA-B8 or HLA-DRw3 60% have other forms of autoimmune disease

Answer 119

angiosarcoma

Answer 120

think FE overload, Allyl alcohol

Answer 121

think CCl4 (carbon tetrachloride), acetaminophen, ethanol aceta: give n-acetyl cystein as antidote - toxicity due to NAPQ1 --> depletion of GSH

Answer 122

used to tx. psoriasis/ RA | see periportal fibrosis and cirrhosis

Answer 123

anti-TB metabolite --> causes liver damage with increased ALT

Answer 124

all changes begin in zone 3 --> portal tracts 1. Fatty liver: micro/macrovesicular 2. alcoholic hepatitis: ballooning and mallory bodies - see neutrophils surrounding necrotic hepatocytes - see fever, jaundice, RUQ pain, high AST:ALT, high alk phos and GGT 3. cirrhosis

Answer 125

metabolic syndrome; hyperlipidemia with high TG's, insulin resistance, high BP see aST cirrhosis (non alcoholic steatohepatitis)

Answer 126

mutations in these genes --> genetic adult hereditary hemochromatosis (autosomal recessive) --> causes gene defect in HFE hepatocytes unable to recognize iron thus don't make hepcidin = iron overload! --> ** cirrhosis, bronze skin, ARTHRALGIA *** prussian blue stain ***

Answer 127

chronic inflammm -- IL6 --> activates production of hepcidin

Answer 128

high copper levels! ATP7B deficiency (controls copper excretion in bile duct) levels accumulate in liver (cirrhosis/hepatitis), brain (parkinsonian/CNS disorders), eyes (Kayser-Fleischer rings) on labs see increased urine copper

Answer 129

Wilson Disease- high copper levels!

Answer 130

Menkes disease = copper deficiency = "kinky hair disease" --> severe neuro disease

Answer 131

Autosomal recessive Pizz gene mutation --> A1AT is a protease normally inhibits neutrophil elastase (this protein is made in liver --> accumulates in liver and causes disease ) seen in neonatal hepatitis and cirrhosis in 40's assoc. w/ smoking

Answer 132

extrahepatic biliary atresia idiopathic neonatal hep A1AT

Answer 133

primary biliary cirrhosis = cholestatis liver disease of destruction of small/medium bile ducts in liver AMA+ : directed against PCD-E2 in herings canal seen in middle aged women: pruritis and jaundice ** destruction of midde bile ducts --> periportal hepatocellular damage

Answer 134

primary sclerosing cholangitis = cholestasis w/ obliterative fibrosis of intra and extrahepatic bile ducts seen in IBD!!! UC - 90% male disease - see acute ascending cholangitis pANCA and ANA elevated!!! "beading" on ERCP and onion skin fibrosis

Answer 135

mutation in polycystin Pc1/Pc2 --> bile duct cystic changes/ fibrosis Von Meyenberg complex and caroli disease (autosomal recessive) think about ADPKD and manifestations in brain and kidneys

Answer 136

acute liver congestion at zone 3

Answer 137

obstruction of more than 2 hepatic vv or IVC sen in polycythemia or clotting disorders see RUQ pain, ascites, hepatomegaly zone 3 congestion

Answer 138

hemolysis, elevated liver enzymes, low platelets - seen in pregnancy

Answer 139

most common benign hepatic mask that isn't vascular - see central scar of stellate cells assoc. w/ osler-weber-rendu disease

Answer 140

commonest hepatic tumor/mass bleed when disrupted and are benign neoplasms

Answer 141

rounded smooth borders, no central scar seen in women on OC's: prone to rupture

Answer 142

think HBV, HCV, alcohol elevated AFP!!! see liver failure, cachexia, varices, hemorrhage

Answer 143

fibrolamellar variant of hepatocellular carcinoma - seen in young females and males, not assoc. w/ HBV, HCV, or cirrhosis see single large mass w/ malignant hepatocyes

Answer 144

arises from perihilar region of bile duct eptihelium

Answer 145

gallstones

Answer 146

cholesterol stones - female, fat, flatulent, fertile, forty

Answer 147

1. Increased production/saturation → supersaturatiohn 2. Crystallization (nidus) 3. Flow (volume, turbulence) – hypomotility leads to sludge 4. Accretion (matrix/sludge) – sludge gives nidus something to crystalize on → accretion of cholesterol forming stones

Answer 148

Cholesterolosis of the Gallbladder: cholesterol in mucosa - supersaturated bile and ↑mucosal uptake…can present clinically like acute/chronic cholecystitis - usually with stones (mechanism unknown if stone absent) - often called “strawberry gallbladder” o can cause gallbladder biliary pain o accumution of cholesterol in mucosa gives it the white/yellow dot background in the pattern of red

Answer 149

unconj bilirubin - due to chronic hemolysis, SS, thalassemia , CD

Answer 150

bili + cholelsterol e. coli infection, liver flukes (C. sinensis )

Answer 151

stones in gallbladder

Answer 152

inflamm. of gallbladder

Answer 153

stones in bile duct

Answer 154

seen in ill - HIV pts - no stones

Answer 155

acute cholecystitis see necrosis, hemorrhage, inflammation/edema

Answer 156

- obstruction of cystic duct without inflammation | - results in mucin filled gallbladder

Answer 157

``` radioactive dye (given IV) is excreted by the liver (GB not seen in acute cholecystitis …even up to 3 hrs…stone blocks duct) a. pt injected w/ die into vein – fills gallbladder and later will be seen in small bowel – if there is obstruction then die won’t go into gall bladder and will continue into small bowel ---- + study means there is a stone ```

Answer 158

used to evaluate the biliary tree a. tube is inserted down esophagus, into small bowel – at tip of scope there is alight to visualize the ampulla – can pass a needle into the ampulla and send it up into the biliary tree → inject die into biliary tree and examine for causes of obstruction b. can also go in a grab stones and pull them out of the ampulla of vater c. can also use ECRP to place a stent

Answer 159

• Cholangitis = bacterial infection superimposed on an obstruction of the biliary tree most often due to gallstone → ascending cholangitis - There is secondary bacterial infection…organism is typically from duodenum - E. coli, Klebsiella, enterobacter …. • Infection moves up the biliary tree into the liver bile duct system…sometimes resulting in multiple small liver abscesses • Typically causes: 1)Fever, 2)Jaundice, 3)Abdominal pain (Charcot’s Triad) - with Hypotension, Mental status changes (Reynold’s Pentad)….increased mortality – watch out! • Histology: shows inflamm. process due to stone, will see bile ducts are expanded and filled with pus → spills out into liver parenchyma and forms microabscesses and enzymes skyrock → super elevated ALT/AST

Answer 160

Chronic Cholecystitis: • >90% associated with gallstones (same epidemiology) • Pathophysiology: repeated bouts of acute inflammation, chemical or bacterial • Pathology: stiff, thickened wall with variable inflammation and Rokitanski-Aschoff sinuses • R-A sinus (seen on right) = areas where gallbladder has constricted and surface mucosa is pulled down into wall • Clinical: highly variable symptoms of pain and "dyspepsia" • Pathologic findings and clinical symptoms do not correlate well • Porcelain gallbladder: chronic cholecystitis with calcified wall, higher risk of adenocarcinoma → mandatory surgery • see fibrotic thickened gray-white wall due to fibrosis and inflammation with many gallstones present in the lumen • see calcified wall prominently on the CXR/ CT scan • Have high risk for developing ADCA, MUST COME OUT!

Answer 161

• 2 Xs more common in women, peaks in 7th decade • Native Americans and Hispanics • Usually assoc. with gallstones • Rarely diagnosed preop. or when resectable – no symptoms until advanced disease – rare ddx in time • Vast majority are Adenocarcinoma • Terrible prognosis; <10% 5 year survival! • ERBB2 (Her-2/neu) overexpressed (2/3) • can results in direct liver invasion!

Answer 162

cholangiocarcinoma located at jn. or right and left hepatic ducts

Answer 163

code for a variant of trypsin that is resistant to inhibitor deactivation

Answer 164

ducts do not fuse - - predisposes to chronic pancreatitis o see that tail and body (dorsal portion) drains through minor sphincter through the “minor duct of santorini” o Duct of Wirsung does not develop and very little drains out of papilla of vater (when use ERCP and inject into duct of wirsung – see no flux into the pancreas, only up into the biliary tree)

Answer 165

- - normal pancreas encircles 2nd part of duodenum - - presents with obstruction and other developmental defects - presents with “double bubble sign” : stomach and proximal duodenum fill w/ air - see bilious green tinged vomit – due to bile still entering into the small bowel (obstruction is usually below the ampula) o – may or may not be complete obstruction, and less commonly may present later in adulthood

Answer 166

* PRSS1: mutated trypsinogen resistant to antitrypsin * SPINK1: SPINK 1 protein is a trypsin inhibitor * CFRT: some cystic fibrosis variants get pancreatitis

Answer 167

alcohol: seen in males, 40 biliary stones: seen in women, 70 - Alcohol → damage of ductule that’s producing HCO3- - Drugs → damage of acinus: CCK → zymogens, lipase, amylase

Answer 168

DDx of Acute Pancreatitis: clinical DDX! - epigastric pain radiating to the back - fever, nausea, vomiting - elevated serum amylase and lipase*** Morphology: - Early stages: see diffuse swelling from edema with redness from vasodilation, but no necrosis - Mid stages: see areas of hemorrhage and peripancreatic fat along with fat necrosis= “saponification” - Later stages: see complete fat necrosis = complete saponification

Answer 169

alcohol see excruciating pain, diabetes, ascities, fat malab, pseudocyts formation and duct obstruction

Answer 170

- Have an epithelial lining. - As all epithelia secrete fluid, the cyst will continue to grow in size, and impinge on adjacent anatomical stuctures (a type of neoplasm) - Treatment must include excision of epithelium, or they will recur - Squamous cysts fill with keratin (because keratin is greasy, they were named as though the contents were fatty (i.e. sebaceous cyst of skin and cholesteatoma are misnomers) o epidermal inclusion cyst of skin, keratocyst of jaw, cholesteatoma of external ear canal/mastoid bone - Serous cysts secrete a watery clear fluid, mucinous cysts mucin

Answer 171

- Have no epithelial lining Will not grow in size unless connected to a duct - Treatment is by drainage - examples include pancreatic pseudocyst, adrenal pseudocyst and old abscess - represents 75% of all pancreatic cysts – usually occur after a bout of acute pancreatitis - histology: there is smooth borders no lining of the epithelium – instead is lined by fibrin and granulation tissue

Answer 172

cyst mass w/out atypica- seen in elderly females, straw colored serous yellow fluid in it neg. mucin stain

Answer 173

slow growing, painless mass in adult females makes mucinous fluid see smooth borders w/ cysts lined by columnar mucinous epithleium

Answer 174

• Typically arise in the main duct of the head of pancreas of males • May be benign, borderline or malignant • presents w/ obstruction, that is not a stone • histology: – see papillary neoplasm that distends the pancreatic duct – neoplasms behave like a stone and continue to grow and expand – must be removed in order to keep them from progressing to chronic pancreatitis – considered “intraductal neoplasm”

Answer 175

• 4th leading cause of Cancer Death in US – Median survival 9 months; 5% 5 year survival – only 20% completely resectable → s shelf: rectal pouch mass – metastasis • Diagnosis – Imaging: CT scan commonest, endoscopic US best (can do biopsy at the same time with US) – Tissue ddx: FNA cytology or needle core biopsy – Laboratory: CA 19-9 only for monitoring (classically elevated in pancreatic cancer – a marker to follow tx) • CANCER IS A TISSUE DIAGNOSIS • Pathology – Typically metastasize regional lymph nodesà then liverà then lungs – Direct local invasion (along nerves, duodenum, stomach, colon, vessels) – Peritoneal spread with ascites • Staging for possible surgery

Answer 176

pancreatic cancer

Answer 177

think pancreatic cancer

Answer 178

peutz-jeghers syndrome = inherited risk of pancreatic carcinoma

Answer 179

- KRAS – growth factor signal transducer | - p16/CDKNA: (cell cycle regulator: tumor suppressor)

Answer 180

chronic hepatitis. Mild steatosis is seen in HCV infection. The incidence of chronic hepatitis is highest with HCV infection.

Answer 181

characteristic, however, of liver cell injury associated with chronic alcoholism

Answer 182

Ceruloplasmin is an α2-globulin that carries copper in plasma. Because copper cannot be secreted into plasma, ceruloplasmin levels are low. in Wilson's disease

Answer 183

K-RAS mutations are found in more than 90% of pancreatic adenocarcinomas

Buzzin Flashcards

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