11/10/17 Flashcards

1
Q

Intestinal type of gastric carcinoma is associated with what?

A

H. Pylori, smoked foods, type A blood, smoking and older males

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2
Q

T/F Diffuse type of gastric carcinoma is not associated with H. Pylori

A

True

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3
Q

Autoimmune chronic gastritis caused Pernicious anemia affects which part of the stomach?

A

Fundus and body

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4
Q

Can chronic NSAID use cause chronic gastritis?

A

Yes

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5
Q

What type of toxin is vibrio cholera? How does it work?

A

It is an enterotoxin. It is a gram negative, flagellated oxiposittive comma shaped bacteria that increases Gs activity. This in turn activates the CFTR channel, allowing more Cl- to efflux and Na, H2O and HCO3 to influx into the lumen. This is why patients get water diarrhea.

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6
Q

Does salmonella typhi cause diarrhea?

A

No. All other salmonella species causes diarrhea (split pea soup or sometimes bloody)

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7
Q

Which salmonella species has a vaccine?

A

S. Typhi

- also causes rose colored spots on chest

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8
Q

Name 6 bacteria that cause bloody diarrhea?

A
  1. C. Jejuni
  2. E. coli (EHEC and EIEC)
  3. Salmonella spp (not typhi)
  4. Shigella
  5. Yersinia
  6. Entameoba
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9
Q

Mesenteric ischemia is a __ bowel ischemia that usually involves which artery?

A

small

SMA

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10
Q

Acute mesenteric ischemia can cause an embolism/occlusion of the ___. This can eventually lead to what? How do patients present?

A
SMA
Small bowel necrosis
Pain out of proportion to exam
Rebound tenderness
Epigastric pain and guarding
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11
Q

Complete bowel obstruction in a patient will present as what?

A

Nausea, vomiting, anorexia

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12
Q

Non-occlusive mesenteric ischemia is caused by?

A

Hypoperfusion usually in watershed areas.
Bowel necrosis can occur from hypo perfusion.

It occurs secondary to:

  1. Diminished intravascular volume as seen in shock of dehydrated patients
  2. Low perfusion pressure from congestive HF.
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13
Q

Which intestinal disorder is associated with

  • Marfan syndrome
  • Ehlers-Danlos syndrome
  • Adult polycystic kidney disease (ADPKD)
A

Diverticulosis

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14
Q

Symptoms of ____
#1 Cause of hematochezia!
- FEVER, INCREASED WBCs
- LLQ pain

A

DIVERTICULITIS!!!!

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15
Q

Patients with ____ present with:

  1. Elevated WBC
  2. Diarrhea followed by constipation
  3. Fever
  4. Tender mass on palpation
  5. Left lower quadrant pain (“left-sided appendicitis”)

Mnemonic: “Whoa! Don’t Forget The Left-sided diversion!

A

Diverticulitis

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16
Q
  1. What can cause a colovesicle fistula?

2. What can cause a enterovesicle fistula?

A
  1. Diverticulitis

2. Crohn’s disease

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17
Q

Can NSAIDs caused duodenal ulcers?

A

No. That is only in gastric ulcers. H. Pylori (90%) and ZES can cause duodenal ulcers.

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18
Q

Hypertrophy of Brunner’s Glands indicate what type of ulcer?

A

Duodenal Ulcer

Brunner’s glands are located int the duodenum in the submucosa

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19
Q

Are duodenal ulcers increase the risk for cancer?

A

No. It is generally benign.

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20
Q

Does smoking increased the risk of peptic ulcers (both types)?

A

Yes!!

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21
Q

Chronic ____ use can lead to either gastric or duodenal ulcers.

Duodenal ulcers are always associated with _____ of gastric acid. Gastric ulcers, by contrast, may or may not be associated with such ____. Thus, one would expect to see hyperplasia of the _____ in a patient with a duodenal ulcer, since these glands help ___ stomach acid.

A

Chronic NSAID use can lead to either gastric or duodenal ulcers.

Duodenal ulcers are always associated with hypersecretion of gastric acid. Gastric ulcers, by contrast, may or may not be associated with such hypersecretion. Thus, one would expect to see hyperplasia of the Brunner’s Glands in a patient with a duodenal ulcer, since these glands help neutralize stomach acid.

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22
Q

Peyer patches, which are lymphoid tissue found in __ in the last segment of the __ __

A

Peyer patches, which are lymphoid tissue found in submucosa in the last segment of the small intestine,. This makes sense since the last segment is closest to the bacteria laden colon.

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23
Q

____ can cause a long-term, smoldering infection of the small intestine resulting in few or no symptoms. The image shows the trophozoite form of the organism, which proliferates in the intestine. Symptoms occur due to loss of brush border enzymes and progressive blunting of villi. Lactase is one of the brush border enzymes that is lost with ____ infection and can cause secondary lactose intolerance.

A

The organism is Giardia lamblia. Giardia can cause a long-term, smoldering infection of the small intestine resulting in few or no symptoms. The image shows the trophozoite form of the organism, which proliferates in the intestine. Symptoms occur due to loss of brush border enzymes and progressive blunting of villi. Lactase is one of the brush border enzymes that is lost with Giardia infection and can cause secondary lactose intolerance.

24
Q

____ disease is a rare, systemic infectious disease caused by the bacterium Tropheryma whipplei. Whipple disease is characterized by fever, abdominal pain, diarrhea, weight loss, and migratory ____. The primary involvement is of the small intestine and mesenteric lymph nodes. Histologically there is prominent macrophage infiltration and fat deposition. Characteristic vacuoles within the macrophage that stain with periodic acid-Schiff (PAS) stain are pathognomonic of the disease; the intracellular and extracellular PAS-positive material are bacilli. Giardia is an extracellular organism.

A

Whipple disease is a rare, systemic infectious disease caused by the bacterium Tropheryma whipplei. Whipple disease is characterized by fever, abdominal pain, diarrhea, weight loss, and migratory polyarthralgia. The primary involvement is of the small intestine and mesenteric lymph nodes. Histologically there is prominent macrophage infiltration and fat deposition. Characteristic vacuoles within the macrophage that stain with periodic acid-Schiff (PAS) stain are pathognomonic of the disease; the intracellular and extracellular PAS-positive material are bacilli. Giardia is an extracellular organism.

25
Q

Several organisms have the ability to invade the lining of the intestine when they infect humans, such as __ and __. Giardia does not invade the intestinal mucosa.

A

Several organisms have the ability to invade the lining of the intestine when they infect humans, such as Cryptosporidium and Entamoeba histolytica. Giardia does not invade the intestinal mucosa.

26
Q

GIardia affects the ___ intestines, which can cause watery diarrhea after ingesting diary

A

Small

27
Q

GI infections cause reactive hyperplasia of Peyer’s patches which can then serve as ___ point for intussusception. Peyer patches are small masses of ___ tissue whose function is to survey intestinal bacterial populations and arm the body against overgrowth of pathogenic bacteria. __ cells contained within Peyer patches take up ____ and present them to __ cells.

B cells then form germinal centers and, following ____ stimulation from T cells, class switch to IgA and differentiate into plasma cells.

A
The correct answer is E. 41% chose this.
The vignette describes a child who is suffering from small bowel intussusception after a recent GI infection. GI infections cause reactive hyperplasia of Peyer's patches which can then serve as lead point for intussusception. Peyer patches are small masses of lymphatic tissue whose function is to survey intestinal bacterial populations and arm the body against overgrowth of pathogenic bacteria. M cells contained within Peyer patches take up antigens and present them to B cells. B cells then form germinal centers and, following CD40L stimulation from T cells, class switch to IgA and differentiate into plasma cells.
28
Q

What are four extra-intestinal manifestations you’d see in Crohn’s?

A
  1. Migratory Polyarthritis
  2. Calcium oxalate stones
  3. Gallstones (cholesterol and pigment)
29
Q

Medication for Crohn’s?

A

CAAAI

Corticosteroid
Azathioprine
Antibiotics
Adalimumab
Infliximumab
30
Q

Medication for UC?

A

SMIC

Sulfasalazine
6-MP
Influximab
Colectomy

31
Q

What is the auto-autoantibody associated with autoimmune hepatitis?

A

Anti-Smooth Muscle

32
Q

Polymyositis, dermatomyositis autoantibodies?

A

Antisynthetase (eg, anti-Jo-1), anti-SRP, anti- helicase (anti-Mi-2)

33
Q

1° biliary cirrhosis Autiantibody?

A

Antimitochondrial

34
Q

Pernicious anemia autoantibody?

A

Antiparietal cell and antiIF

35
Q

How long is the incubation period for Hep. A?

A

~30 days

36
Q

What is the incubation period of Hep-B?

A

1-4 months

37
Q

HBsAG is undetectable in plasma after __-__ months of exposure. If you convert from acute to chronic
- HBsAG persists and is present for more than 6 months

A

HBsAG is undetectable in plasma after 4-6 months of exposure
If you convert from acute to chronic
- HBsAG persists and is present for more than 6 months

38
Q

Hep-B Vaccine
Vaccine:
- a recombinant version of HBsAG
- vaccinated individuals will be (+)anti-____
- all other antibodies (HBc, HBe) should be negative because these people were never infected.

A

Hep-B Vaccine
Vaccine:
- a recombinant version of HBsAG
- vaccinated individuals will be (+)anti-HBsAG
- all other antibodies (HBc, HBe) should be negative because these people were never infected.

39
Q

HBeAG IS DETECTABLE IN SERUM, IT INDICATES SIGNIFICANT __ __

A

viral replication and infectious state

40
Q

What is the first detectable antibody in Hep B infection?

A

Anti-HBcAG

41
Q

Anti-HBc IgM rise in ____ infection

Anti-HBc IgG prior exposure or chronic infection.

A

Anti-HBc IgM rise in acute infection

Anti-HBc IgG prior exposure or chronic infection.

42
Q

Explain the Window Period

A

A brief period where level of HBsAG have fallen and are undetectable

Anti-HBsAG not high enough to be detectable yet

Can give false appearance of ABSENT infection!!!!

During this period, anti-HBcAG (IgM) is the SOLE MARKER OF INFECTION!

43
Q

What is the sole marker for Hep B infection during window period?

A

Anti-HBcAG

44
Q

Time 0 = patient exposed to virus
1st marker:

1st marker (month 1)

  • HBsAG - note it rises during the incubation period, before symptoms occur.
  • This level rises and falls if that infection is cleared.
2nd marker (2 months or so):
- HBeAG
Then shortly after Anti-HBcAG rise 
3rd marker (4.5 month)
- Anti-HBeAG rise
4th marker (6.5 month)
- Anti-HBsAG rise.
A

Time 0 = patient exposed to virus
1 months passes before anything is detectable in serum

First thing that rises: HBsAG - note it rises during the incubation period, before symptoms occur.
This level rises and falls if that infection is cleared.

Next marker (2 months or so) - HBeAG
Then shortly after Anti-HBcAG rise 

Around 4.5 month, Anti-HBeAG rise
Around 6.5 month, Anti-HBsAG rise.

45
Q

Which two biliary diseases have increased IgM

A

Primary Sclerosing Cholangitis

Primary Biliary Cirrhosis

46
Q

Cytomegalovirus (CMV) esophagitis has a presentation similar to that of herpes simplex virus esophagitis, with punched-out mucosal lesions and “owl’s-eye” inclusion bodies on light microscopy. It would not produce the physical exam findings described in this vignette, however. CMV is typically treated by ganciclovir; ganciclovir-resistant strains can be treated with foscarnet, a ___ analog.

A

Cytomegalovirus (CMV) esophagitis has a presentation similar to that of herpes simplex virus esophagitis, with punched-out mucosal lesions and “owl’s-eye” inclusion bodies on light microscopy. It would not produce the physical exam findings described in this vignette, however. CMV is typically treated by ganciclovir; ganciclovir-resistant strains can be treated with foscarnet, a pyrophosphate analog.

47
Q

Herpes simplex virus (HSV) stomatitis and esophagitis manifest with vesicular lesions and punched-out mucosal erosions characterized by intranuclear inclusion bodies on light microscopy. Acyclovir, a ____ analog, can be used to treat HSV by inhibiting DNA replication.

A

Herpes simplex virus (HSV) stomatitis and esophagitis manifest with vesicular lesions and punched-out mucosal erosions characterized by intranuclear inclusion bodies on light microscopy. Acyclovir, a nucleoside analog, can be used to treat HSV by inhibiting DNA replication.

48
Q

___ is an antifungal agent that binds tubulin, interfering with microtubule function. It effectively treats fungal infections of the skin (tinea capitis, corporis, pedis, and the like). It is not used to treat candidiasis.

A

Griseofulvin is an antifungal agent that binds tubulin, interfering with microtubule function. It effectively treats fungal infections of the skin (tinea capitis, corporis, pedis, and the like). It is not used to treat candidiasis.

49
Q

What is this?
- Less severe than pemphigus vulgaris. Involves IgG antibody against hemidesmosomes (epidermal basement membrane; antibodies are “bullow” the epidermis).
Tense blisters C containing eosinophils affect skin but spare oral mucosa. Immuno uorescence reveals linear pattern at epidermal-dermal junction D . Nikolsky sign ⊝.

A

Bullous Pemphigold

Less severe than pemphigus vulgaris. Involves IgG antibody against hemidesmosomes (epidermal basement membrane; antibodies are “bullow” the epidermis).
Tense blisters C containing eosinophils affect skin but spare oral mucosa. Immuno uorescence reveals linear pattern at epidermal-dermal junction D . Nikolsky sign ⊝.

50
Q

Carcinoid Tumors
- Secrete _____!

RESPONSIBLE FOR THE MAJORITY OF CLINICAL EFFECTS:

  1. _____
    - from serotonin stimulation of GI motility
  2. INCREASED FIBROBLAST GROWTH AND FIBROGENESIS which can cause VALVULAR LESIONS
    - -> the serotonin increases fibroblast growth and fibrogenesis of the valves of the heart, especially with pulmonic and tricuspid valve.
  3. FLUSHING
    - other mediators also

Main clinical effect of patients with CT have diarrhea and flushing of skin.

A

What do they do?
- Secrete SEROTONIN!!

RESPONSIBLE FOR THE MAJORITY OF CLINICAL EFFECTS:

  1. DIARRHEA
    - from serotonin stimulation of GI motility
  2. INCREASED FIBROBLAST GROWTH AND FIBROGENESIS
    - -> VALVULAR LESIONS
    - -> the serotonin increases fibroblast growth and fibrogenesis of the valves of the heart, especially with pulmonic and tricuspid valve.
  3. FLUSHING
    - other mediators also

Main clinical effect of patients with CT have diarrhea and flushing of skin.

51
Q

HCC spreads ___

A

hematogenousy

52
Q

Which macromolecule can cross freely across the epithelial cell apical membrane by simple diffusion?

A

Free fatty acids

Free fatty acids are nonpolar hydrophobic molecules and are thus able to cross the cell membrane by simple diffusion. The phospholipid bilayer of cell membranes prevents polar solutes (eg, amino acids, nucleic acids, carbohydrates, proteins, and ions) from diffusing across the membrane, but allows the simple diffusion of hydrophobic molecules. Pancreatic lipase and bile salts metabolize triglycerides into free fatty acids and monoglycerides. They cross the villous epithelial cell membrane of the small intestine via simple diffusion and specific transporters. Once inside the enterocyte, fatty acids and monoglyceride are re-esterified to triglycerides in the smooth endoplasmic reticulum. Processing continues in the Golgi apparatus, forming chylomicrons containing cholesterol, lipoproteins, and other lipids. Chylomicrons are transported into the lacteals and lymphatic vessels, and finally delivered into the systemic blood for use by the body.

53
Q

What are hepadenocarcinomas associated with?

A

birth control pillsa

anabolic steroids

54
Q

The SMA weaves between what two things?

A

It travels posterior to the pancreatic tail and anterior to the 3rd part of the duodnum

55
Q

Basal Layer Keratinocytes are attached to the basement membrane by ___

A

hemidesmosomes