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105 Cards in this Set

  • Front
  • Back
h pylori is ass with what cancer?
primary B-cell gastric lymphoma - MALT LYMPHOMA!, gastric adenocarcinoma, etc

from chronic gastritis - no pmn, just lymphocytes
Monilial plaques
Candida - immunosuppress, raised white spots
Metaplastic atrophic gastritis can be due to what 2 origins?
1)Environment (DISTAL)- antrum, ass with H pylori, gastric cancer

2)Autoimmune (PROXIMAL)- body, Ab to PARIETAL CELLS, so ass w/ v gastric acid, Carcinoid tumors

Atropic gastritis MC in JAPAN
Hyperplastic gastrin-producing neuroendocrine cells (found in nodules) (carcinoid tumor develop)
pernicious anemia
tumor of intersittial cells of Cajal (induce peristalsis)
oropharyngeal dysphagia with Liquids better than solids
esophageal webs (Plummer-Vinson syn & Patterson-Kelly)
pharyngeal neoplasms
cervical osteoarthritis
cricopharyngeal dysfunction

mechanical d/o
oropharyngeal dysphagia with Solids better than liquids
Brainstem lesion
Myasthenia gravis

neuromuscular d/o, usually have many complicating systemic conditions
Individual that does not relax the upper esophageal sphincter
Cricopharyngeal Achalasia (neuromuscular problem)

difficulty initiating a swallow, PHARYNGEAL DILATION

over time -> Zenker's diverticulum
3 anatomical regions of esophageal compression

2)main stem bronchus

3)esophageal hiatus
Esophageal dysphagia where the person only intermittently experiences difficulty when swallowing solids
Progressive Esophagial Dysphagia ass with heartburn (3)

...not ass with heartburn
1)stricture of the esophagus



no heartburn, then CANCER
Esophageal dysphagia with both food and water

1) intermittent

2) progressive
1)Diffuse esophageal spasm (ass with angina-like chest pain)

2)Esophageal Achalasia (LES does not relax, loss of Meissner's and Auerbach's plexuses)
Two common locations for recurent herpes
2)hard palate
Major differences b/w aphthous ulcers and herpes labialas
1)aphthous ulcers do NOT start as vesicles (start as ulcers)

2)aphthous ulcers NEVER occur in the keratinized mucosa (start on thin mucosa such as buccal mucosa and ventral tongue)
What can inhibit aphthous ulcer formation

two diseases/syn ass with major aphthae


2)Behcet's syn
Angular cheilitis is cuased by what? predisposed by (3)?

Best way to dx?
MCC is candida

1)poorly fitting dentures


3)Vit B12 deficiency

also linked to Crohn's disease

dx: simple swab and smear
mucocele caused by
mucous retention in area secondary to trauma and irritation (salivary stone)

tx: must completely remove salivary gland
fordyce granules
ectopic sebaceous gland on lips or buccal mucosa

very discree yellowish-gold pinpoint granules
type of buccal lesion generally seen with certain syndromes, esp neurofibromatosis
Civatte bodies (orangeish thing in epithelium) & confined band of lymphocytes
Lichen planus

-a chronic, inflammatory AUTOIMMUNE dz

bilateral, t-lymphocyte mediated

potentially PRE-CANCEROUS
Candidiasis endocrinopathy syn
patients have a thyroid disorder and will not respond ot treatment until you correct the underlying endocrine disorder
cottage-chees like appearance that is scrapable, also ass with immunosuppressed patients
Pseudomembranous candidiasis
T/F nicotinic stomatitis pts are at high risk for cancer

ass with pip smokers

classic red dots on palate
Salivary Gland Tumors:

1)location of major gland tumors

2)location of minor gland tumors
1)MC major gland tumors = PAROTID

2)minor gland = palate
1)Benign Salivary gland tumor?

2) Malignant Salivary gland tumor? (2)
1)Pleomorphic adenoma (no ulceration)

2) Mucoepidermoid carcinoma (blueish hue reflecting the mucin component) & Adenoid cystic carcinoma (both have ulceration and pain)
Beningn migratory glossitis (geographic tonge) is ass with?

also perhaps Lyme disease and Lupus
Oral regions of high risk?

low risk?
high risk: vental tongue, floor of mouth, solf palate, lips

low risk: buccal mucosa, ginvival/mucobuccal fold areas
MC infections of colon

mech of dz?
viral infections like Rotaviuses (kids, self-limited, dehydration is biggest problem) and ass Norwalk strain of viruses (adults)

Parasites and bacteria (ie Amoebic colitis) have a > inceidence in developing countries

Infects the enterocytes in the duodenum and jejunum -> cells damaged and shed -> immature cell line do not have same fxn (diarrhea ie lactose intolerance)

Cholera mech
attach to enterocytes -> produce cGMP & alter permeability -> ^ peristalsis and diarrhea

Collagenous colitis & Lymphocytic colitis cause?
Watery diarrhea w/ NO HEMORRHAGE (if blood in diarrhea than not CC or LC)

CC - thick collagen band in lamina propria

LC - CD8 T-lymphocyte in lamina propria
how many days does it taek to clear out blood?
3-5 days
detect traces of blood in stool that are not necessarily visible by?

can remain psitive for how long?
hemeocccult/guaiac test

2 weeks! usual point of discharge is when stool turns brown
Shokc presents with ___ blood loss
Thrombocytosis and leukocytosis without infection may be caused by? a result of what?
Epinephrine and Cortisol


p.s. ADH released in shock will result in hyponatremia
Supine hypotension =

Postrural hypotention =
Supine hypotension = loss > 20% blood volume

Postrural hypotention = loss of 10-25% (sys drop > ~10 mg) of blood volume OR pulse ^ 20/min
Overtransusion will cause?

most significant in?
Recurrent bleeding

Cirrhotic patien
UGI Vessel that bleeds without a mark or ulcer
Dieulafoy's erosion

also Aortic graft
in UGI bleeds, BUN:creatinine >10x indicates (BUN > 40)
1)UGI bleed where the blood in the SMALl BOWEL is getting absorbed and being turned into urea and shows up in blood

2)Volume depletion
Iron is reabsorbed where?

Iron = Duodenum

Fats = ileum
Niacin deficiency
Pellagra: 4D's

Riboflavin deficiency
Glossitis & cheilitis
Thiamin (B1) deficiency?
parasthesisas (beriberi)
Folic Acid deficiency
Megaloblastic anemia

(microblastic = iron def)
**Ca deficiency?
carpopedal spasm
Seriology for celiac sprue
tTG (tissue transglutaminase, most specific)

anti-endomyseial antibody

anti-gliadin (less specific)
PAS stuffed macrophages
Whipple's Disease

fever, neruologic symptoms, arthritis, diarrhea, weight loss
if you see ulcer disease way down in the duodenum, past the ampulla, or in the jejunum think ____

(malignant cells make too much gastrin -> acid, but not as much as Pernicious anemia)
The way to diferentiate ZE and Pernicious anemia (atropic gastritis) is by?
pH of stomach

atrophic gastritis (PA): pH >4

ZE: pH = 2
most common treatable of of malabsorption
Giardiasis w/ metronidazole
genes involved in defective DNA mismatch repair system (microsatellite instability) of HNPCC (2)
what stain helps differentiate carcinoid from endocrie tumors?
If colorectal carcinoma is >50% coloid content then tumor is considered?

ass with?
Mucinous or Signet-cell type

ass with psedomyxoma pertoneum
When does separation of foregut into trachea and esophagus occur?

common error in this process called?
4th week gestation

Atresia (blind pouch)
Eosinophilic esophagitis is differentiated from relux esophagitis by?
eosinophils forming clusters @ surface epithelium
MC acquired abnormality in teh pediatric population is?
Congenital hypertrophic pyloric stenosis
MCC of nonsyndromic IHBA
A1 Antitrysin

also Trisomies 17,18 & 21
Trisomy 17 & 18

females & non-familial

(unlike neonatal/giant cell hepatitis)
MC liver tumor in 1st year of life
infantile hemangioendothelioma

F > M

very rarely can present with bleeding diathesis called Kasabach-Merrit syndrome

Benign (along wiht Mesenchymal hamartoma: firm, nontender mass in uper abdoman, often cystic and some hemorrhage & extramedullary hematopoiesis
what is used to Dx hepatobalstomas
AFP (+) (90% cases)

M > F

fetal type - clear cytoplasm, central nuclei w/nucleoli

Embryonal type - dark cytoplasm, cells arranged in ribbons and cords

Fetal type has better prognosis

^ AP (maybe in combe with GGT) =
^ AST/ALT = primary hepatocyte damage

^ AP (maybe in combe with GGT) = bilary tree disease/cholestatic hepatitis
thrombosis of hepatic vein
Budd-Chiari Syn

causes vascular changes leading to chronic passive congestion (nutmeg liver)
piecemeal necrosis hallmark of ?
piecemeal necrosis or interface hepatitis hallmark of chronic hepatitis

(a lot of lymphocytes going beyond the limiting plate area)
portal lymphoid aggreate with STEATOSIS indication of

other findings?
steatosis = HEP C

bile duct damage, protal LYMPHOCYTE, & lobular activity
Serology for autoimmune hepatitis

defining feature
ANA (anti-nuclear antibody)

ASMA (anti-smooth muscle actin)

LKM-1 (liver-kidney microsomal antigen 1)

defining feature: PLASMA CELL portal inflammation
Bilary disease:

primary biliary cirrhosis (PBC) vs primary sclereosing cholangitis (PSC) for 1)serology 2)sex 3)associations
PBC -> AMA; F>M; periductal GRANULOMAS

PSC -> ^IgM; M>F; ass with IBD ass (usually UC) & cholangiocarcinoma; onion-skinning
Chronic Hep Staging is measured by
degree of fibrosis
Primary (Hereditary) Hemochromatosis buzz words:
Chr 6p
HFE (heffer) gene
C282Y (chris & ylie)
H63D (herfat & deldar almost 69)

gold standard for Dx is Hepatic Iron Index >2

3 factors creating gallstones
1)superstaruation of cholesterol

2)hypomotility of GB

Cholangiocarnioma risk factors are (3)?

dx tumor marker

1) PSC
3)parasitic infection

CA 19-9

PAINLESS jaundice, weight loss, fever

arises from epithelial cells of intra and extra-hepatic bile ducts
Cholangitis is?

caused by?

bacterial infection of bile duct (enterobacter or gram neg are MC)


Charcot's Triad: fever, jaundice, RUQ pain
Gallbladdar cancer histology is mostly _____


1)RUQ pain, wight loss, jaundice
Cholecystitis has idential sx as?
Pathophysiology of fatty liver
1)increased lipolysis: adrenal/pituitary stim of breaking down triglycerides to FFA which go to liver

2)v mito fatty acid oxidation

3)make more NADH which is a cofactor for glycerol production

4)increased esterification (3GP + FFA -> TG )
difference b/w hepatic steatosis (fatty change) & steatohepatitis (alcoholic hepatitis) is ?
which the balloon hepatocytes in steatoheaptitis are 1)EOSINOPHILIC CYTOKERATIN & 2)MALLORY BODIES

also wire fibrosis in Zone 3
1st and 2nd hit of NAFLD
1st hit: insulin resistance

2nd hit: ROS

insulin ^ cAMP & stimulates hormone-sensitive lipase thereby ^ plasma FFA
Key difference d/w fatty liver from alcohol & insulin resistance?
Alcohol v FA oxidation while Obesity increases FA oxidation and liver cell is overwhelmed

both ^ FFA
both v VLDL export
both can result in steatohepatitis
a primary ademnocarcinoma that is very fibrous
Difference b/w Boerhaave's syn and Mallory-Weiss tear
Mallowry-Weiss tear - a mucosal (superficial) tear in esophagus (nontransmural)

Boerhaave's syn - transmural perforation (hole) of esophagus

both can be caused by vomitting/eating d/o
what vessels join to form the portal vein?
IMV, SMV and splenic vein
pateints on PPI long term can get
gastinomas or endocrine hyperplasia after many years
migratory necrolytic erythema on legs found with
Watery diarrhea found with
Only hepatitis that is DNA
Hep B
Which Hep's have fecal oral transmission (water)
Hep A & Hep E
Which Hep's have chrnicity
Hep B (chronic & acute)

Hep C (chronic onl)
Only Hep that can spread by semen and saliva
Hep B
Which Hep is mostly seen in 3rd world countries?
Hep E
MC cause of liver transplants in US?
Hep C
Incubation period for Hep A

Dx by
28 days

anti-Hep A IgM Ab

Self-limiting virus, ususlly does NOT cause fulminant liver failure

If you are leaving in less than 3 weeks, you should take what to prevent Hep A
immunoglobulin instead of vaccine
Incubation period for Hep B

Window Period b/w
120 days

HBsAg & HBsAb, use HBcAb IgM
best liver fxn test
first clinical sign of Hep C may be
throwing up blood

also look for:

prophyria cutanea tarda or palpable pupura


cryoglobulin in blood

arthralgias & arthritis
first lab sign of Hep C

anti-HCV appears?

RNA appears?
first: AST & ALT

anti-HCV: 2-3 months

RNA: 2 weeks
main blood screening test
EIA (enzyme immunoassay), tests for HepC Ab

if +, then perform quantitative HepC RNA by PCR to cover false positives
Hepatic Adenoma
Noncirrhtic liver solid liver lesion


ass with oral contaceptive and anabolic steroid use

absence of bile ducts or portal area with the proliferation of neoplastic haptocytes
noncirrhotic liver with characteristic CENTRAL SCAR
focal nodular hyperplasia
What is the one condition that can cause carcinoma without cirrhosis
anabolic steroids
Tumor Marker for Hepatocellular Carcinoma (HCC)
AFP (only seen in 60% of cases, so positive is useful but negative doesnt rule out HCC
Only morphologic varient of HCC that matters
Fibrolamellar Carcinoma

FAVORABLE prognosis! (HCC usually highly aggressive tumor with poor prognosis)

age <30

L side of liver (al others on R)

AFP not elevated but serum ferritin is
Bening cystic lesion of portal area nearly always found in famales and lined by mucinous epithelium with overian type stroma
Biliary cystadenoma
MC benign neoplasm of the liver
Hemangioma (tumor arising from blood vessels)
MC primary mesenchymal tumor of liver
MC primary malignant tumor in pediatric age group
MC malignant tumor in teh liver
Metastatic carcinoma