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MHD2 > Block 7 (GI) - L9 to L11 > Flashcards

Block 7 (GI) - L9 to L11 Flashcards

1
Q

Which type of GI bleed is more common (upper vs. lower)?

A

Upper (1.5-2x more common)

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2
Q

What anatomical structure separates the upper GI tract from the lower GI tract?

A

Ligament of Treitz

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3
Q

What are the structures of the upper GI tract?

A

Esophagus, stomach, duodenum (until ligament of Treitz)

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4
Q

What are the symptoms of upper GI bleeding?

A
  1. Hematemesis (coffe ground or bright red blood)
  2. Melena (black, tarry school)
  3. Occult blood
  4. Sometimes hematochezia (BRBPR)
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5
Q

What is the differential diagnosis for upper GI bleeding?

A
  1. Peptic ulcer
  2. Esophageal varices
  3. Erosive esophagitis
  4. Mallory-Weiss tear
    (uncommon: erosion, tumor, esophageal ulcer, portal gastropathy, Dieulafoy lesion, Cameron lesion)
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6
Q

Where are peptic ulcers found?

A

Stomach or duodenum

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7
Q

What are the two major causes of peptic ulcer disease?

A
  1. H. pylori infection

2. NSAIDs/ASA

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8
Q

What are the symptoms of peptic ulcer disease?

A

Epigastric abdominal pain, pain improved with eating, nausea, bloating, and early satiety

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9
Q

How is peptic ulcer disease evaluated?

A

EGD

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10
Q

What are complications of peptic ulcer disease?

A
  1. GI bleeding (acute leads to hematemesis, melena, orthostasis; chronic leads to iron-deficiency anemia)
  2. Perforation (sudden-onset abdominal pain, guarding, rigidity = acute abdomen)
  3. Obstruction (nausea, vomiting)
  4. Penetration (erode into adjacent organs)
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11
Q

How is peptic ulcer disease treated?

A
  1. Reduce NSAID/ASA use
  2. H2 blockers
  3. PPIs
  4. H. pylori eradication (PPI + amoxicillin + clarithromycin)
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12
Q

What causes esophageal varices?

A

Portal HTN inducing collateral circulation

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13
Q

90% of ___ patients develop esophageal varices.

A

Cirrhotic

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14
Q

How are esophageal varices treated?

A
  1. Aggressive fluid resuscitation
  2. Transfusion
  3. Sengstaken-Blakemore tube
  4. Octreotide
  5. Antibiotics
  6. EGD for variceal banding
  7. TIPS (transjugular intrahepatic portosystemic shunt)
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15
Q

What are some causes of erosive esophagitis?

A
  1. Reflux
  2. Pill-induced
  3. Infection (candida, CMV, HSV)
  4. Radiation
  5. Eosinophilic esophagitis
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16
Q

How does erosive esophagitis appear on endoscopy?

A

Linear “burns”

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17
Q

What is a Mallory-Weiss tear?

A

Hematemesis after violent retching/vomiting, usually self-limited

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18
Q

What is a Dieulafoy lesion?

A

Lesion of a large submucosal artery in the gastric cardia

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19
Q

What is a Cameron lesion?

A

Linear ulcerations found within hiatal hernias

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20
Q

How can the severity of a UGI bleed be assessed?

A
  1. Look for comorbid disease
  2. Hematemesis
  3. Hemodynamic instability
  4. Assess Hgb levels
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21
Q

Why might an NG aspiration be useful for differentiating between UGI and LGI?

A

Positive (for UGI) result: return of blood/coffee grounds
Negative (for UGI) result: return of bile without blood
Indeterminate result: return of saline without blood or bile

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22
Q

How should UGI bleeding be managed?

A
  1. Assess severity of bleed
  2. H&P
  3. ICU monitoring if needed
  4. 2 large bore IV’s for aggressive IV hydration
  5. PRBCs if needed
  6. Pre-endoscopic IV PPI
  7. Endoscope
  8. Assess risk for rebleeding
  9. Post-endoscopic IV PPI x 72 hours (decreases recurrent bleeding, need for surgery, mortality)
  10. Consult surgery/interventional radiology for severe bleeding
  11. Eradicate H. pylori if present
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23
Q

If you see a clean based ulcer with a flat, pigmented spot on endoscopy, what is recommended?

A

Change IV PPI to PO PPI, no endoscopic therapy needed

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24
Q

If there is an ulcer with an adherent clot, what is recommended?

A

Dislodge the clot with irrigation, endoscopically treat as low or high risk depending on ulcer characteristics, IV PPI

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25
Q

If there is an ulcer with a visible vessel, what is recommendd?

A

Endoscopic therapy and IV PPI

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26
Q

What factors increase risk for rebleeding?

A
  1. Active bleeding during endoscopy
  2. Ulcer >2cm
  3. Ulcer location (posterior duodenum, high lesser curvature of stomach)
  4. Age >60
  5. Comorbid illnesses
  6. Hgb < 10
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27
Q

What are the symptoms of LGI bleeding?

A

BRBPR

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28
Q

What is the differential diagnosis for LGI bleeding?

A
  1. DiverticulOsis
  2. Colitis (ischemic, IBD, radiation)
  3. Hemorrhoids
  4. Post-polypectomy
    (uncommon: colon polyps or cancer, rectal ulcer, angiodysplasia)
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29
Q

What is diverticulosis?

A

Asymptomatic mucosal outpouchings that cause acute, painless bleeding

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30
Q

Where is diverticulosis common?

A

Sigmoid colon

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31
Q

How is diverticulosis treated?

A

Colonoscopy

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32
Q

What are the symptoms of ischemic bowel colitis?

A

Abdominal pain and rectal bleeding

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33
Q

Where is ischemic bowel colitis common?

A

Splenic flexure, transverse colon

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34
Q

What are the two types of IBD?

A
  1. Crohn’s disease

2. Ulcerative colitis

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35
Q

What are the symptoms of ulcerative colitis?

A

Bloody diarrhea, abdominal pain

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36
Q

What are the symptoms of Crohn’s disease?

A

Abdominal pain, diarrhea, bleeding (less likely)

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37
Q

What are hemorrhoids?

A

Dilated anal and perianal collateral vessels, leading to pain and bleeding (small volume, red blood on toilet paper)

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38
Q

How are hemorrhoids treated?

A

Sclerotherapy and band ligation

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39
Q

How is LGI bleeding managed?

A
  1. H&P
  2. IVFs and PRBCs if needed
  3. EGD if hemodynamic instability to rule out upper GI bleed
  4. Colonoscopy
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40
Q

5% of GI bleeding occurs where?

A

Between the papill and the ileocecal valve

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41
Q

What is the most common cause of lower GI bleeding in children?

A

Meckel’s diverticulum

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42
Q

What is the first line step after a negative EGD or colonoscopy in the setting of bleeding?

A

Capsule endoscopy

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43
Q

What is on the differential diagnosis for upper GI bleeding in neonates?

A
  1. Swallowed maternal blood
  2. Vitamin K deficiency
  3. Coagulopathy
  4. Milk protein intolerance
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44
Q

What is on the differential diagnosis for upper GI bleeding in infants/children/adolescents?

A
  1. Mallory-Weiss syndrome
  2. Foreign body
  3. PUD
  4. Pill esophagitis
  5. Esophageal varices
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45
Q

What is the most common cause of severe bleeding in children?

A

Esophageal varices

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46
Q

What is on the differential diagnosis for lower GI bleeding in neonates?

A
  1. Anal fissures
  2. Swallowed maternal blood
  3. Necrotizing enterocolitis
  4. Malrotation with midgut vovulus
  5. Hirschprung disease
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47
Q

Necrotizing enterocolitis is generally seen in ___ and it has an unclear etiology.

A

Premature

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48
Q

What are the symptoms and imaging findings of necrotizing enterocolitis?

A

Non-specific symptoms (fever, lethargy), abdominal distention, vomiting, diarrhea, bleeding

Pneumatosis intestinalis (air in colon/wall of colon)

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49
Q

How does malrotation with midgut vovulus present?

A

Abdominal distension, emesis, melena, or hematochezia, bilious emesis

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50
Q

What is on the differential diagnosis for lower GI bleeding in infants/toddlers?

A
  1. Anal fissures
  2. Milk or soy-induced colitis
  3. Intussusception
  4. Meckel’s diverticulum
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51
Q

What is intussusception?

A

Telescoping of part of the intestine into itself

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52
Q

How does intussusception present?

A

Severe abdominal pain with passage of bloody/mucoid stool (currant jelly appearance), sausage shaped abdominal mass

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53
Q

Meckel’s diverticulum involves incomplete obliteration of the ___.

A

Omphalomesenteric duct

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54
Q

What is on the differential diagnosis for lower GI bleeding in older children?

A
  1. HUS (microangiopathic hemolytic anemia, E.coli 0157)
  2. HSP
  3. Infectious colitis
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55
Q

What are the two types of human parasites?

A
  1. Protozoa

2. Helminths

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56
Q

What are the 5 species of Plasmodia?

A
  1. P. vivax
  2. P. falciparum
  3. P. malariae
  4. P. ovale
  5. P. knowlesi
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57
Q

What is sporogony?

A

The sexual cycle of reproduction that takes place in mosquitos. Gameocytes form a zygote, which becomes an oocyst, which becomes a sporozoite.

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58
Q

What is schizogony?

A

The asexual cycle of reproduction that takes plan in man.

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59
Q

What is the exoerythrocytic cycle?

A

Schizogony that takes place in the liver shortly after infection; Sporozoites enter the bloodstream and are carried to the liver where they invade hepatocytes. Schizonts form, and reproduce asexually, bursting the hepatocytes and releasing merozoites into the blood.

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60
Q

What is the erythrocytic cycle?

A

Schizogony that takes place in RBCs. Merozoites infect circulating red cells. These become trophozoites, which form RBC schizonts. These reproduce asexually and burst red cells, repeating the cycle. Merzoites can also progress to gametocytes.

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61
Q

What are some diagnostic characteristics of malaria?

A
  1. P. vivax and P. ovale - Schuffne’rs dots (vesicle complexes in red cells)
  2. P. falciparum - electron dense knobs (facilitate binding to endothelium and uninfected RBCs)
  3. Pigment-degraded hemoglobin
62
Q

What happens to people with sickle cell anemia and malaria?

A

S hemoglobin impairs falciparum growth

63
Q

Which two species of plasmodium stay dormant in the liver?

A

P. vivax and P. ovale

64
Q

Discuss the pathogenesis of malaria.

A
  1. Fever is associated with schizont rupture
  2. Anemia can lead to hemolysis, which can cause renal failure
  3. Tissue hypoxia is caused by sludging of parasitized RBCs
  4. Immunopathologic events (cytokine release, immune complex nephritis)
65
Q

Describe the clinical manifestations of malaria.

A
  1. Prodrome - flu-like illness
  2. Chills, cyclic fever, headache, myalgias, nausea, splenomegaly, hemolytic anemia, thrombocytopenia
  3. Organ dysfunction with P. falciparum (cerebral malaria, renal failure, pulmonary edema)
66
Q

What are the unique clinical feature of P. falciparum?

A
  1. High level of parasitemia
  2. Microvascular events due to high parasitemia and sludging
  3. Cerebral malaria
  4. Pulmonary edema (vascular events and severe anemia)
  5. Renal failure (severe hemolysis and shock)
67
Q

What are the unique clinical feature of P. vivax and P. ovale?

A
  1. Moderate parasitemia
  2. NO microvascular events
  3. Hypnozoites in liver can lead to relapse
68
Q

What are the unique clinical feature of P. malariae?

A

Low parasitemia, mild symptoms, prolonged infection

69
Q

What is P. knowlesi?

A

Parasite of monkeys, but some human cases have been seen; it has a unique 24-hour cycle, no sludging

70
Q

How is malaria diagnosed?

A
  1. Demonstration of parasite stages in the blood (blood smear)
  2. PCR
  3. Rapid diagnostic tests
  4. Serology
71
Q

How is erythrocytic malaria treated?

A
  1. Chloroquine (falciparum has resistance)
  2. Quinine/quinidine
  3. Others
72
Q

How is exoerythrocytic malaria treated?

A
  1. Primaquine
73
Q

How is malaria transmitted?

A

Mosquitos

74
Q

What is the vector of Babesiosis?

A

Ixodes scapularis (tick)

75
Q

What is the reservoir of Babesiosis?

A

Small rodents

76
Q

Babesiosis can be co-transmitted with ___.

A

Lyme borreliosis

77
Q

Describe the life cycle of Babesiosis.

A
  1. Tick takes a blood meal from a mouse and infects the mouse (gametes produced)
  2. Tick takes a second blood meal from an infected mouse (gametes ingested and fertilized)
  3. Tick takes a blood meal from human (introduces sporozoites)
  4. Transmitted from human-to-human via blood transfusion
78
Q

What are the clinical features of Babesiosis?

A
  1. Majority are asymptomatic
  2. Can have fever, headache, fatigue, hemolytic anemia
  3. Severe sepsis can occur in the immunocompromised or splenectomized
79
Q

How is Babesiosis diagnosed?

A
  1. Blood smear (small rings to tetrads = cross-like)
  2. PCR
  3. Serology
80
Q

How is Babesiosis treated?

A

Atovaquone + azithromycine OR Clindamycin + quinine

81
Q

What are the reservoirs of Toxoplasma gondii?

A

Cats primarily (also sheep, pigs, cattle)

82
Q

How is Toxoplasma gondii transmitted?

A
  1. Ingestion of cat feces containing an oocyst
  2. Ingestion of inadequately cooked meat containing cysts
  3. Intrauterine
  4. Blood transfusion/organ transplant
83
Q

Describe the life cycle of Toxoplasmosis.

A
  1. Sexual reproduction in the gut of a cat.
  2. Feces excreted contains oocysts
  3. These can be ingested by others.
84
Q

What are the three clinical syndromes of toxoplasmosis?

A
  1. Acute: fever and generalized lymphadenopathy (mononucleosis-like)
  2. Congenital: multisystem disease including CNS and chorioretinitis
  3. Immunocompromised: encephalitis
85
Q

When is the baby at greatest risk of acquiring toxoplasmosis from the mother during pregnancy, and when are manifestations most severe?

A

Greatest risk: when acquired by mom in 3rd trimester

Severe manifestations: 1st trimester

86
Q

How is toxoplasmosis diagnosed?

A
  1. Tissue biopsy (can see cysts or tachyzoites)

2. Serology (IgG or IgM responses)

87
Q

How is toxoplasmosis treated? In pregnanct women?

A

Pyrimethamine + sulfadiazine

Spriamycin in pregnant women

88
Q

How is toxoplasmosis prevented in people with HIV/AIDs?

A

Bactrim

89
Q

Cryptosporidium is a coccidian protozoan which carries out its life cycle entirely in the ___ of animals and man.

A

Intestinal villi (on the surface)

90
Q

What is the reservoir of Cryptosporodium?

A

Domestic animals and humans

91
Q

How is Cryptosporidium transmitted?

A

Fecal-oral ingestion of cysts or sexually

92
Q

Describe the clinical features of Cryptosporidiosis in the immunocompetent.

A

Explosive, watery diarrhea and abdominal pain lasting 1-2 weeks

93
Q

Describe the clinical features of Cryptosporidiosis in the immunocompromised.

A

Severe, watery diarrhea with malnutrition and biliary disease; continues until immunity is restored

94
Q

How is Cryptosporidium diagnosed?

A
  1. Acid-fast stain of cysts in feces
  2. Direct fluorescence
  3. PCR
  4. Biopsy
95
Q

How is Cryptosporidium treated?

A

Nitazoxanide

96
Q

What are the reservoirs of amebiasis?

A

Infected humans

97
Q

How is amebiasis transmitted?

A

Fecal-oral, sexually

98
Q

How can amebiasis be distinguished as pathogenic from commensals?

A

Markers of pathogenicity: Zymodene, DNA analysis, monoclonal staining

Ab formation

99
Q

What are the virulence factors of amebiasis?

A
  1. Endocytic capacity
  2. Adherence via galactose-specific lectin
  3. Lytic capacity
  4. Extracellular proteinases
100
Q

What are the pathologic features of infection with Entamoeba histolytica?

A
  1. Flask ulcers
  2. Ameboma (mass of granulation tissue)
  3. Abscess-metastatic spread to liver, pleura, pericardium, lung, brain
101
Q

What are the symptoms of amebiasis?

A
  1. Intermittent diarrhea, flatulence, pain
  2. Dysentery (tenesmus, bloody diarrhea, severe pain)
  3. Abscesses in liver, lungs, pericardium, brain
  4. May be asymptomatic
102
Q

How is amebiasis diagnosed?

A
  1. Stool exam for trophozoites and cysts
  2. Serology
  3. PCR (to distinguish pathogenic from non-pathogenic)
103
Q

How is amebiasis treated?

A

When invasive - metronidazole, tinidazole

When cyst - lodoquinol, paromomycin, diloxanide, furoate

104
Q

Under the microscope, E. histolytica trophozoites have ___.

A

Pseudopods

105
Q

What can Naegleria fowleri cause and how is it acquired?

A

Encephalitis in a healthy person

Acquired by swimming in brackish water

106
Q

What can Acanthamoeba cause?

A

Encephalitis in immunocompromised and eye infections with trauma or contact lenses

107
Q

What can Balamuthia cause and how is it transmitted?

A

Rare encephalitis; soil, associated with organ recipients

108
Q

What is Giardia duodenalis (lamblia)?

A

Intestinal flagellate that causes food, water, and sexually-transmitted diarrhea

109
Q

What is the metabolically active form of G. duodenalis and its structural features?

A

Trophozoite - has two nuclei, four pairs of flagella, and a sucking disc

110
Q

What is the inactive form of G. duodenalis and its structural features?

A

Cyst - has a clear cyst wall, four nuclei, and can survive in cold water for 2 months

111
Q

Describe the pathogenesis of Giardia.

A

Attach to villi by sucking disc, cause malabsorption diarrhea (stool has increased fat and carbs), flattening of microvilli and inflammation (seen on jejunal biopsy)

112
Q

Describe the symptoms of Giardia.

A
  1. Often asymptomatic
  2. Diarrhea (foul-smelling, bulky, watery, non-bloody)
  3. Crampy abdominal pain
  4. Fever (20%)
  5. May become chronic or relapse
113
Q

How is Giardia diagnosed?

A
  1. Trophozoites and cysts in stool
  2. Direct fluorescence antibody test
  3. PCR
114
Q

How is Giardia treated?

A

Tinidazole, nitazoxanide

115
Q

Describe the morphology of Trichomonas vaginalis.

A

Oval shaped with an axostyle, four flagella, and an undulating membrane

116
Q

How is Trichomonas vaginalis transmitted?

A

Sexually

117
Q

Discuss the pathogenesis of trichomonas.

A

Damages squamous mucosa of the female genital tract leading to neutrophilic inflammatory reactions and petechial hemorrhage

118
Q

What are the clinical manifestations of trichomonas?

A
  1. Persistent vaginitis (frothy discharge, itching, burning, vaginal erythema)
  2. Associated with preterm births
119
Q

How is trichomonas diagnosed?

A
  1. Wet mount of vaginal discharge (see motile organisms)
  2. Urinalysis
  3. Culture
  4. DFA
120
Q

How is trichomonas treated?

A

Metronidzole or tinidazole + treat male partner

121
Q

What is the vector for Leishmania?

A

Sand fly

122
Q

What is the vector for African trypanosomiasis?

A

Tsetse fly

123
Q

What is the vector for American trypanosomiasis?

A

Triatomid bug

124
Q

What are the 4 morphologic forms of blood and tissue flagellates?

A
  1. Amastigote (intracellular form found in human - Leishmania, T. cruzi)
  2. Promastigote (extracellular form found in gut and mouth of insect - Leishmania)
  3. Epimastigote (extracellular form in gut and mouth of insect - Trypanosoma)
  4. Trypomastigote (extracellular form in human and insect - Trypanosoma)
125
Q

Describe the life cycle of Leishmania.

A
  1. Sandfly takes a blood meal from a human and injects promastigote
  2. Promastigotes are phagocytosed by macrophages, where they transform into amastigotes
  3. Amastigotes multiply in cells of various tissues
  4. Sandfly takes a blood meal, ingesting macrophages with amastigates
  5. Amastigotes transform into promastigotes in the gut
126
Q

Describe the pathogenesis of Leishmaniasis.

A

Injected promastigotes are opsonized with complement, taken up by macrophages, released to another cell or fly

127
Q

Describe the clinical manifestations of cutaneous Leishmaniasis.

A
  1. Cutaneous (papule - self-limited ulcer)
  2. Diffuse cutaneous (multiple lesions)
  3. Mucocutaneous (local lesion heals or enlarges, can cause metastatic destructive lesions of face and perineum)
128
Q

Describe the clinical manifestations of disseminated/visceral Leishmaniasis.

A
  1. 3-12 months after the bite, fever develops
  2. Dissemination to liver, spleen, bone marrow, lymph nodes (RES system)
  3. Anemia, leukopenia, thrombocytopenia, elevated IgG
  4. Progressive weakness, emaciation
129
Q

How is Leishmaniasis diagnosed?

A

For localized: biopsy, smear, culture, Ag detection

For visceral: aspirates, DNA detection, serology

130
Q

How is visceral Leishmaniasis treated?

A

Lipo. amphotericin b, antimony, miltefosine

131
Q

How is cutaneous/mucocutaneous Leishmaniasis treated?

A
  1. None or topical for mild

2. Pentavalent antimony, ketoconazole, fluconazole, lip amphotericine b, miltefosine

132
Q

What are the two major types of African Trypanosomiasis?

A

T. brucei gambiense and T. brucei rhodesiense

133
Q

What is the life cycle of African Trypanosomiasis?

A
  1. Fly ingests trypomastigotes which develop in the midgut
  2. Migrate to salivary gland and become epimastigotes, then infectious trypomastigotes
  3. Fly inoculates trypomastigates, which multiply and invade the bloodstream
  4. Fly infected with blood meal
134
Q

Describe the pathogenesis of African Trypanosomiasis.

A
  1. Change Ag structure of surface glycoprotein (immune evasion)
  2. Localize in endothelium (vasculitis in heart and CNS)
  3. Hemorrhage, demyelination
135
Q

What are the clinical manifestations of African Trypanosomiasis?

A
  1. Local chancre
  2. Fever lymphadenopathy, rash, itching
  3. Headache, impaired mentation
  4. Rhodesian = CHF, coma, death (rapid in east)
  5. Gambian = slow progression to coma (slow in west)
136
Q

How is African Trypanosomiasis diagnosed?

A
  1. Blood smear
  2. Elevated IgM
  3. Serology
137
Q

How is African Trypanosomiasis treated?

A

Pentamidine, Melarsoprol (CNS)

138
Q

What is Chagas’ disease?

A

Acute illness with chronic heart, esophagus, and colon involvement

139
Q

What causes Chagas’ disease (American Trypanosomiasis) and where is it found geographically?

A

Trypanosoma cruzi

Central and South America (~Southern US)

140
Q

What are the reservoirs of T. cruzi?

A

Rat, cat, dog, opossum, armadillo

141
Q

What is the vector of T. cruzi?

A

Reduviid (triatomid) bug (transmitted via its feeces)

142
Q

Discuss the pathogenesis of American Trypanosomiasis.

A
  1. Chagoma caused by local inflammation
  2. Dissemination to heart, muscle, smooth muscle, nerve, adherence, endocytosis, escape, multiplication, rupture, inflammation
  3. Affects blood vessels, muscle conduction, nerves of heart
  4. Affects nerve, smooth muscle of GI tract
143
Q

What are the symptoms of Chagas’ disease?

A
  1. Chagoma
  2. Fever, rash, splenomegaly, lymphadenopathy, edema (acute)
  3. Chronic illness (haert, megaesophagus, megacolon)
144
Q

How is Chagas’ disease diagnosed?

A
  1. Blood smear

2. Gene amplification

145
Q

How is Chagas’ disease treated?

A

Nifurtimox or Benznidazole

146
Q

How is Pneumocystis jiroveci (carinii) classified?

A

Not sure - has ribosomal RNA sequences like fungi, but other features like sporozoa

147
Q

How is P. jiroveci transmitted?

A

Respiratory aerosol

148
Q

Describe the morphology of Pneumocystis.

A
  1. Cysts (5-8 microns, contain 2-8 sporozoites)
  2. Sporozoites (released with cyst rupture, combine and mature)
  3. Trophozoites (matured form, make cysts)
149
Q

What are the clinical manifestations of Pneumocystis?

A
  1. Interstitial pneumonia in immunocompromised (fever, dry cough, severe dyspnea)
  2. CXR - diffuse interstitial infiltrates
  3. Low blood oxygen level
150
Q

How is Pneumocystis diagnosed?

A
  1. Cysts in lung tissue and secretions with silver stain and DFA
151
Q

How is Pneumocystis treated?

A

Bactrim, pentamidine

MHD2 (34 decks)

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