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MD3 Pathology > Heme Pathology 2 > Flashcards

Heme Pathology 2 Flashcards

1
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HIV lymphadenopathy

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2
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Pneumocystis Pneumonia

Ground glass appearance (hazy) lung

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3
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Pneumocystis Pneumonia (progressed)

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4
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Pneumocystis Pneumonia

Heavy and filled with fluid

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5
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Pneumocystis Pneumonia

Lumen of alveolar space filled with bubbly material

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6
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Pneumocystis Pneumonia

Silver stain of cysts

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7
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Pneumocystis Pneumonia

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8
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Pneumocystis Pneumonia

Bronchoalveolar Lavage

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9
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Pneumocystis Pneumonia

Bronchoalveolar Lavage

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10
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CMV Pneumonia

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11
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CMV Pneumonia

Large cells with inclusions of replicating virus

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12
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CMV Pneumonia

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13
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CMV Pneumonia

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14
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CMV Pneumonia

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15
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CMV Pneumonia

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16
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Candida oral thrush

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17
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Candida Esophagitis

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18
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Candida Esophagitis

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19
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Candida Esophagitis

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20
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Candida Esophagitis

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21
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Candida Esophagitis

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22
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Candida Esophagitis

“Spaghetti and Meatballs” with yeast and pseudohyphy

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23
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Candida Esophagitis

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24
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Candida Esophagitis

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25
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Cryptococcal Pneumonia

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26
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Cryptococcus Pneumonia

Yeast has thick capsule

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27
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Cryptococcus Meningoencephalitis

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28
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Cryptococcus Meningitis

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29
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Crypotoccal Meningoencephalitis

“Soap Bubble Lesions”

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30
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Cryptococcal Meningoencephalitis

“Soap bubble lesions”

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31
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A

Cryptococcal Meningoencephalitis

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32
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Cryptococcal Meningoencephalitis

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33
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Cryptococcus Meningoencephalitis Silver Stain

Characteristic budding yeast and unequal narrow base budding

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34
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A

Cryptococcal Meningitis India Ink Stain (taken after lumbar puncture)

Yeast + capsule & narrow base budding

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35
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Cryptococcal Meningitis with narrow base budding

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36
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A

Cryptosporidium infection

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37
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A

Cryptosporidium infection (doesn’t invade tissue)

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38
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A

Cryptosporidium infection

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39
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Cryptosporidium infection

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40
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Cryptosporidium infection

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41
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Cryptosporidium infection (acid fast staining)

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42
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A

Toxoplasma Encephalitis

(Usually infects deeper regions of brain)

43
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Toxoplasma Encephalitis

44
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Toxoplasma Encephalitis

45
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Toxoplasma Encephalitis

Cysts with multiple tiny organisms (bradyzoites) that can rupture and release

46
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Toxoplasma Encephalitis

47
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Toxoplasma Myocarditis

Bradyzoites in the toxoplasma

48
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A

AIDs-related non-Hodgkin Lymphoma

49
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A

AIDS non-Hodgkin lymphoma (GI lymphoma)

50
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A

AIDS non-Hodgkin lymphoma

51
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A

AIDS non-Hodgkin lymphoma

Extranodal (GI)

52
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CNS AIDS non-Hodgkin lymphoma

53
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A

CNS AIDS non-Hodgkin lymphoma

54
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A

Burkitt Lymphoma “Starry sky”

Indicative of high grade lymphoma

55
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A

Burkitt Lymphoma

Usually a proto-oncogene (c-myc) on chromosome 8, but in lymphoma, transloacted to chromosome 14 (gene for immunoglobulin heavy chain, which is always on)

56
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A

Kaposi’s Sarcoma

57
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A

Kaposi’s Sarcoma

58
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A

Kaposi’s Sarcoma

59
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A

Kaposi’s Sarcoma

60
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A

Kaposi’s Sarcoma

Dermis-proliferating sarcoma, poorly formed BV

61
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A

Kaposi’s Sarcoma

62
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A

Kaposi’s Sarcoma

Caused by Human Herpes Virus 8

63
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A

Kaposi’s Sarcoma

64
Q

What are the main glycoproteins on HIV?

A
65
Q

Describe the pathogenesis of HIV –> AIDS

A
66
Q

What groups are at risk for HIV?

A
  1. Homosexual/bisexual men (>50%)
  2. IV drug abusers with no previous hx of homosexuality (25%)
  3. Hemophiliacs (esp. those who received large amounts of factor VII or IX before 1985) (0.5%)
  4. Recipients of blood and blood components - non-hemophiliacs (1%)
  5. Heterosexua contacts of high-risk groups (mostly IV abusers) (10%)
67
Q

What are the major routes of transmission of HIV/AIDS?

A

Sexual contact, parenteral inoculation, vertical transmission (mother to newborn)

68
Q

What is the immune dysfunction that results from HIV/AIDS?

A

Loss of CD4+ T cells –> inversion of CD4:CD8 ratio (normally 2)

Defect in cell-mediated immunity

Hypergammaglobulinemia (probably related to EBV stimulation of B cells)

69
Q

What are the clincal stages of HIV infection?

A

Acute retroviral syndrome

  • Initial or primary response of immuno-COMPETENT adult to HIV infection
  • High virus production, viremia, widespread seeding of lymphoid tissues
  • Self-limited acute illness & non-specific symptoms: sore throat, myalgia, rash, fever, adenopathy, weight loss, fatigue (similar to flu or mono)

Chronic (latent) phase

  • CD4 T cell count >500cell/uL
  • Contained virus, immune system largely intact but HIV still replicating, mostly in lymphoid tissue
  • Asymptomatic or persistent generalized lymphadenopathy. Minor opportunistic infections (thrush, herpes zoster)

Early symptomatic phase

  • CD4 T cells 200-500 cells/uL
  • Fever, weight loss, diarrhea, generalized lymphadenopathy

AIDS

  • HIV+ w/ CD4 <200 or AIDS-defining illness (PCP, systemic Candidiasis)
  • Breakdown of host defense, increasing viremia and clinical disease
  • Opportunistic infections, secondary neoplasms (Kaposi’s, cervical/anal SCC, primary CNS), or neurologic disease
70
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Opportunistic Infections

A
71
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AIDS-defining opportunistic infections and neoplasms

A
72
Q

What is PCP? Who does it affect? What are its clinical/lab features?

A

Pneumocystis Pneumonia is caused by Pneumocystis jirovecii (fungus, previously named P. carinii). Most common initial AIDS-defining infection (primarily opportunistic).

Usually affects patients with CD4 <200.

Clinical features: Fever, dyspnea, severe hypoxemia, diffuse alveolar/interstitial infiltrates

73
Q

What is the pathology of PCP?

A

Interstitial chronic inflammation (lymphocytes, plasma cells)

Diffuse alveolar foamy exudates

Silver stain: dark, ovoid, or cup-shaped cysts

Giemsa stain: Trophozoites (1-3 um) within exudates

74
Q

Lifecycle of P. jirovecii

A
75
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A
76
Q

What is CMV (type of virus? family?)

A

DNA virus, member of Herpes virus, ~10um

Most common opportunistic viral pathogen in AIDS patients, prob. due to reactivation

77
Q

What are some complications of CMV infection in AIDS patients?

A
  1. CMV penumonia
  2. Intestinal disease
  3. CMV mononucleosis
  4. CMV retinitis
78
Q

What is the clinical presentation of CMV pneumonia?

A

Fever, cough, hypoxemia, diffuse radiographic opacification (like PCP) that may progress to ARDS

79
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A
80
Q

What is the pathology of the CMV pneumonia?

A

Diffuse interstitial mononuclear infiltrate, sometimes with hemorrhage or necrosis

Enlarged pneumocytes, macrophages, & endothelial cells with inclusion bodies

  • ​Large intranuclear basophilic inclusions surrounded by clear zone
  • Smaller cytoplasmic inclusions
81
Q

What are some complications of CMV pneumonia?

A

Kidney impairment (from drugs used to treat condition)

Low WBC count (from drugs used to treat condition)

Overwhelming infection that doesn’t respond to treatment

Relapse of infection

82
Q

What is Candida esophagitis?

A

Fungal infection that can affect any organ

Most common cause of infectious esophagitis

Organism: Candida albicans (5 um=yeast, 20 um=pseudohyphae)

Oral candidiasis (thrush) common in HIV, but is NOT AIDS-defining

83
Q

When does Candida esophagitis appear?

A

As opportunistic infection in those with depressed immune system (rarely occurs in otherwise healthy individuals)

AIDS, hematologic disease, renal transplant, leukemia, chronic debilitating disease, DM, steroids, chemotherapy or radiotherapy

84
Q

What is the clinical presentation of candida esophagitis?

A

Dysphagia, odynophagia (painful swallowing) & retrosternal pain, associated with oral thrush (oropharyngeal moniliasis) in 20-80%

85
Q

Pathology of Candida esophagitis

A

Pale or white plaques involving mid to distal esophagus

Budding yeast or pseudohyphae (PAS stain positive)

86
Q

What organism causes Cryptococcus infection?

A

Cryptococcus neoformans

Fungus found in soil, pigeon droppings, etc.

Common infection in immunocompromised patients (esp. lung & CNS)

Exists as encapsulated yeast form in humans

87
Q

What is the pathology of cryptococcus infection?

A

Lung: Necrotizing granulomatous inflammation/solitary nodule

CNS: Meningitis w/ gelatinous bubbly exudates and encephalitis (inflammation of brain parenchyma) with perivascular extension into brain parenchyma -> soap bubble appearance

5-15 um round yeast with thick mucopolysaccharide capsule

Unequal narrow-based budding

88
Q

What is crytposporidiosis? How is it acquired?

A

Most common cause of diarrhea in AIDS patients

Acquired by ingesting oocysts of cryptosporidium parvum (protozoan shed in feces of infected humans/animals)

89
Q

What are the clinical manifestations of Cryptosporidiosis?

A

Severe watery diarrhea, sometimes with crapming abdominal pain and fever

90
Q

What is the pathology of cryptosporidiosis?

A

2-4 um round organisms found in intestine adherent to brush border

Chronic inflammation with lymphocytic infiltration fo epithelium common

91
Q

What is the life cycle of Cryptosporidium parvum?

A
92
Q

What causes toxoplasma encephalitis?

Who does it mostly affect?

A

Toxoplasma gondii

Affects immunocompromised patients, esp. AIDS

93
Q

What is the clinical presentation of Toxoplasma encephalitis?

A

Mass lesion (abscess-like), frequently multiple and deep seated (ring-enhancing lesions)

94
Q

What is the pathology of toxoplasma gondii?

A

Necrosis and inflammation (necrotizing encephalitis)

Vascular inflammation (vasculitis) and sometimes thrombosis

Cysts containing bradyzoites or free tachyzoites within parenchyma

95
Q

What is the lifecyle of toxoplasma encephalitis?

A
96
Q

What are the most common lymphomas that AIDS patients get?

A

May develop a number of B cell lymphomas, but Burkitt lymphoma and primary CNS lymphoma are characteristic

Typically have extranodal involves in AIDS patients

High grade, B-cell lymphoma

97
Q

What pathogen is AIDS non-Hodgkin lymphoma associated with?

A

Epstein Barr virus (EBV)

98
Q

What is the pathology of AIDS non-Hodgkin lymphoma?

A

Proliferation of monotonous small round blue cells

Burkitt lymphoma may have interspersed tingible body macrophages, imparting a starry-sky low power appearance

99
Q

What is the pathogenesis of Burkitt lymphoma?

A

Characteristic t(8,14) translocation, with translocation of c-myc gene from chromosome 8q24 to IG heavy chain gene on chromosome 14q32

100
Q

Pathogenesis of Burkitt’s Lymphoma

A
101
Q

What is Kaposi’s Sarcoma?

What organs does it affect?

A

Mesenchymal neoplasm caused by HHV 8 (human herpes virus 8)

May affect any organ, but mostly involves skin, mouth or GI tract

102
Q

What is the clinical presentation of Kaposi’s Sarcoma?

A

Raised, red, or violaceous non-pruritic skin path with becomes plaque-like and later nodular

103
Q

What is the pathology of Kaposi’s Sarcoma?

A

Poorly formed vascular spaces lined by plump spindle cells within dermis

Hemorrhage (extravasted RBCs) common

104
Q

Pathogenesis of Kaposi’s Sarcoma

A

MD3 Pathology (4 decks)

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