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PATHOLOGY > Robbins Must Knows > Flashcards

Robbins Must Knows Flashcards

1
Q

Spectrum of Inflammatory Responses to Infection

6 types of response

A
  1. Suppurative (Purulent) Infection
  2. Mononuclear and Granulomatous inflammation
  3. Cytopathic-Cytoproliferative reactions
  4. Tissue necrosis
  5. Chronic inflammation/scarring
  6. No reaction
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2
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Increased vascular permeability

A

Suppurative (Purulent) Infection

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3
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Leukocyte infiltration (neutrophils)

A

Suppurative (Purulent) Infection

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4
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Chemoattractants from bacteria

A

Suppurative (Purulent) Infection

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5
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Formation of “pus”

A

Suppurative (Purulent) Infection

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6
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

Examples include:
-Pneumonia (Staphylococcus aureus)
-Abscesses (Staphylococcus spp., anaerobic and other
bacteria)

A

Suppurative (Purulent) Infection

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7
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Mononuclear cell infiltrates (monocytes, macrophages, plasma cells, lymphocytes)

A

Mononuclear and Granulomatous inflammation

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8
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Cell-mediated immune response to pathogens (“persistent antigen”)

A

Mononuclear and Granulomatous inflammation

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9
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Formation of granulomata

A

Mononuclear and Granulomatous inflammation

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10
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

Examples include:

  • Syphilis
  • Tuberculosis
A

Mononuclear and Granulomatous inflammation

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11
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Viral transformation of cells

A

Cytopathic-cytoproliferative reactions

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12
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Necrosis or proliferation (including multinucleation)

A

Cytopathic-cytoproliferative reactions

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13
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Linked to neoplasia

A

Cytopathic-cytoproliferative reactions

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14
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

Examples include:

  • Cervical cancer (human papillomavirus)
  • Chicken pox, shingles
  • Herpes
A

Cytopathic-cytoproliferative reactions

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15
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Toxin- or lysis-mediated destruction

A

Tissue necrosis

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16
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Lack of inflammatory cells

A

Tissue necrosis

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17
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Rapidly progressive processes

A

Tissue necrosis

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18
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

Examples include:

  • Gangrene (Clostridium perfringens)
  • Hepatitis (hepatitis B virus)
A

Tissue necrosis

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19
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Repetitive injury leads to fibrosis

A

Chronic inflammation/ scarring

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20
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Loss of normal parenchyma

A

Chronic inflammation/ scarring

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21
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

Example include:
-Chronic hepatitis with cirrhosis (hepatitis B and C viruses)

A

Chronic inflammation/ scarring

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22
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

-Severe immune compromise

A

No reaction

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23
Q

Spectrum of Inflammatory Responses to Infection

Type of Response:

Examples include:

  • Mycobacterium avium in untreated AIDS (T-cell deficiency)
  • Mucormycosis in bone marrow transplant patients (neutropenia)
A

No reaction

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24
Q

Three categories of Agents of Bioterrorism

A
  • Category A agents
  • Category B agents
  • Category C agents
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25
Q

Agents of Bioterrorism

-pose the highest risk and can be readily disseminated or transmitted from person to person, can cause high mortality, might cause public panic, and might require public health preparedness

A

Category A agents

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26
Q

What category does this agents of Bioterrorism belong?

  • Small pox
  • B. anthracis,
  • Yersinia pestis, and
  • Ebola virus
A

Category A agents

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27
Q

Agents of Bioterrorism

-relatively easy to disseminate, produce moderate morbidity but low mortality, and require specific diagnostic and disease surveillance.

A

Category B agents

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28
Q

Agents of Bioterrorism

-Many of these agents are food-borne or water-borne

A

Category B agents

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29
Q

Agents of Bioterrorism

Examples include:

  • Brucella spp. and
  • V. cholerae.
A

Category B agents

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30
Q

Agents of Bioterrorism

-include emerging pathogens that could be engineered for mass dissemination because of availability, ease of production and dissemination, potential for high morbidity and mortality, and great impact on health

A

Category C agents

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31
Q

Agents of Bioterrorism

Examples include:

  • Hanta virus
  • Nipah virus
A

Category C agents

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32
Q

STI caused by HSV in Both males and females (2)

A
  • Primary and recurrent herpes

- Neonatal herpes

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33
Q

STI caused by HBV in Both males and females

A

Hepatitis

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34
Q

STI caused by HPV ONLY in males

A

Cancer of Penis

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35
Q

STI caused by HPV ONLY in females (2)

A
  • Cervical dysplasia and cancer

- Vulvar cancer

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36
Q

STI caused by HPV in Both males and females

A

Condyloma acuminatum

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37
Q

STI caused by HIV in Both males and females

A

AIDS

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38
Q

STI caused by Chlamydia trachomatis ONLY in males (3)

A
  • Urethritis
  • Epididymitis
  • Proctitis
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39
Q

STI caused by Chlamydia trachomatis ONLY in females (5)

A
  • Urethral syndrome,
  • cervicitis,
  • bartholinitis,
  • salpingitis, and
  • sequelae
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40
Q

STI caused by Chlamydia trachomatis Both in males and females

A

Lymphogranuloma venereum

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41
Q

STI caused by Ureaplasma urealyticum ONLY in males

A

Urethritis

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42
Q

STI caused by Neisseria gonorrheae ONLY in males (3)

A
  • Epididymitis
  • Prostatitis
  • Urethral stricture
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43
Q

STI caused by Neisseria gonorrheae ONLY in females (5)

A
  • Cervicitis,
  • endometritis,
  • bartholinitis,
  • salpingitis, and
  • sequelae (infertility, ectopic pregnancy, recurrent salpingitis)
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44
Q

STI caused by Neisseria gonorrheae Both in males and females (4)

A
  • Urethritis,
  • proctitis,
  • pharyngitis,
  • disseminated gonococcal infection
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45
Q

STI caused by Treponema pallidum Both in males and females

A

Syphilis

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46
Q

STI caused by Haemophilus ducreyi Both in males and females

A

Chancroid

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47
Q

STI caused by Klebsiella granulomatis Both in males and females

A

Granuloma inguinale (donovanosis)

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48
Q

STI caused by Trichomonas vaginalis ONLY in males (2)

A
  • Urethritis

- Balanitis

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49
Q

STI caused by Trichomonas vaginalis ONLY in females

A

Vaginitis

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50
Q

critical mediator that activates macrophages and enables them to contain the M. tuberculosis infection

A

Interferon-gamma

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51
Q

Type of Hypersensitivity Reaction

Immune Mechanism: Production of IgE antibody → immediate release of vasoactive amines and other mediators from mast cells; later recruitment of inflammatory cells

A

Immediate (type I) hypersensitivity

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52
Q

Type of Hypersensitivity Reaction

Histopathologic Lesion: Vascular dilation, edema, smooth muscle contraction, mucus production, tissue injury, inflammation

A

Immediate (type I) hypersensitivity

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53
Q

Type of Hypersensitivity Reaction

Prototypical Disorders: Anaphylaxis; allergies; bronchial asthma (atopic forms)

A

Immediate (type I) hypersensitivity

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54
Q

Type of Hypersensitivity Reaction

Immune Mechanism: Production of IgG, IgM → binds to antigen on target cell or tissue → phagocytosis or lysis of target cell by activated complement or Fc receptors; recruitment of leukocytes

A

Antibody-mediated (type II)

hypersensitivity

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55
Q

Type of Hypersensitivity Reaction

Histopathologic lesion: Phagocytosis and lysis of cells; inflammation; in some diseases, functional derangements without cell or tissue injury

A

Antibody-mediated (type II)

hypersensitivity

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56
Q

Type of Hypersensitivity Reaction

Prototypical disorder:

  • Autoimmune hemolytic anemia
  • Goodpasture syndrome
A

Antibody-mediated (type II)

hypersensitivity

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57
Q

Type of Hypersensitivity Reaction

Immune Mechanism: Deposition of antigen-antibody complexes → complement activation → recruitment of leukocytes by complement products and Fc receptors → release of enzymes and other toxic molecules

A

Immune complex– mediated (type III) hypersensitivity

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58
Q

Type of Hypersensitivity Reaction

Histopathologic lesion: Inflammation, necrotizing vasculitis (fibrinoid necrosis)

A

Immune complex– mediated (type III) hypersensitivity

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59
Q

Type of Hypersensitivity Reaction

Prototypical disorders:

  • Systemic lupus erythematosus
  • some forms of glomerulonephritis
  • serum sickness
  • Arthus reaction
A

Immune complex– mediated (type III) hypersensitivity

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60
Q

Type of Hypersensitivity Reaction

Immune mechanism: Activated T lymphocytes → (1) release of cytokines, inflammation and macrophage activation; (2) T cell–mediated cytotoxicity

A

Cell-mediated (type IV) hypersensitivity

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61
Q

Type of Hypersensitivity Reaction

Histopathologic lesion: Perivascular cellular infiltrates; edema; granuloma formation; cell destruction

A

Cell-mediated (type IV) hypersensitivity

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62
Q

Type of Hypersensitivity Reaction

Prototypical disorders:

  • Contact dermatitis
  • multiple sclerosis
  • type 1 diabetes
  • tuberculosis
A

Cell-mediated (type IV) hypersensitivity

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63
Q

represent primary errors of morphogenesis, in which there is an intrinsically abnormal developmental process

A

Malformations

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64
Q

result from secondary destruction of an organ or body region that was previously normal in development

A

Disruptions

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65
Q

represent an extrinsic disturbance of development rather than an intrinsic error of morphogenesis

A

Deformations

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66
Q

a cascade of anomalies triggered by one initiating aberration

A

Sequence

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67
Q

a constellation of congenital anomalies, believed to be pathologically related, that, in contrast to a sequence, cannot be explained on the basis of a single, localized, initiating defect

A

Malformation syndrome

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68
Q

What Syndrome?

Associated CHD:
-pulmonary artery stenosis or tetralogy of Fallot

Gene defect:
-Signaling proteins or receptors (JAG1 or NOTCH2)

A

Alagille syndrome

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69
Q

What Syndrome?

Associated CHD:
-PDA

Gene defect:
-Transcription factor (TFAP2B)

A

Char syndrome

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70
Q

What Syndrome?

Associated CHD:
-ASD, VSD, PDA, or hypoplastic right side of the heart

Gene defect:
-Helicase-binding protein (CHD7)

A

CHARGE syndrome

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71
Q

What Syndrome?

Associated CHD:
-ASD, VSD, or outflow tract obstruction

Gene defect:
-Transcription factor (TBX1)

A

DiGeorge syndrome

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72
Q

What Syndrome?

Associated CHD:
-ASD, VSD, or conduction defect

Gene defect:
-Transcription factor (TBX5)

A

Holt-Oram syndrome

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73
Q

What Syndrome?

Associated CHD:
-pulmonary valve stenosis, VSD, or hypertrophic cardiomyopathy

Gene defect:
-Signaling proteins (PTPN11, KRAS, SOS1)

A

Noonan syndrome

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74
Q

Type of Leukemia/Lymphoma

Genotype:
-Diverse chromosomal translocations; t(12;21) involving RUNX1 and ETV6 present in 25%

A

B-cell acute lymphoblastic leukemia/lymphoma

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75
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Predominantly children; symptoms relating to marrow replacement and pancytopenia; aggressive

A

B-cell acute lymphoblastic leukemia/lymphoma

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76
Q

Most common leukemias/lymphomas in children (2)

A
  • B-cell acute lymphoblastic leukemia/lymphoma

- Burkitt lymphoma

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77
Q

Cell of origin of B-cell acute lymphoblastic leukemia/lymphoma

A

Bone marrow precursor B cell

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78
Q

Type of Leukemia/Lymphoma

Genotype:
-Diverse chromosomal translocations; NOTCH1 mutations (50%–70%)

A

T-cell acute lymphoblastic leukemia/lymphoma

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79
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Predominantly adolescent males; thymic masses and variable bone marrow involvement; aggressive

A

T-cell acute lymphoblastic leukemia/lymphoma

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80
Q

Cell of origin of T-cell acute lymphoblastic leukemia/lymphoma

A

Precursor T cell (often of thymic origin)

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81
Q

Type of Leukemia/Lymphoma

Genotype:
-Translocations involving MYC and Ig loci, usually t(8;14); subset EBV-associated

A

Burkitt lymphoma

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82
Q

Type of Leukemia/Lymphoma

Genotype:
-Diverse chromosomal rearrangements, most often of BCL6 (30%), BCL2 (10%), or MYC (5%)

A

Diffuse large B-cell lymphoma

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83
Q

Type of Leukemia/Lymphoma

Genotype:
-t(11;18), t(1;14), and t(14;18) creating MALT1-IAP2, BCL10-IGH, and MALT1-IGH fusion genes, respectively

A

Extranodal marginal zone lymphoma

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84
Q

Type of Leukemia/Lymphoma

Genotype:
-t(14;18) creating BCL2-IGH fusion gene

A

Follicular lymphoma

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85
Q

Type of Leukemia/Lymphoma

Genotype:
-Activating BRAF mutations

A

Hairy cell leukemia

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86
Q

Type of Leukemia/Lymphoma

Genotype:
-t(11;14) creating cyclin D1–IGH fusion gene

A

Mantle cell lymphoma

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87
Q

Type of Leukemia/Lymphoma

Genotype:
-Diverse rearrangements involving IGH; 13q deletions

A

Multiple myeloma/solitary plasmacytoma

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88
Q

Type of Leukemia/Lymphoma

Genotype:
-Trisomy 12, deletions of 11q, 13q, and 17p; NOTCH1 mutations; splicing factor mutations

A

Small lymphocytic lymphoma/chronic lymphocytic leukemia

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89
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Adolescents or young adults with extranodal masses; uncommonly presents as “leukemia”; aggressive

A

Burkitt lymphoma

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90
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-All ages, but most common in older adults; often appears as a rapidly growing mass; 30% extranodal; aggressive

A

Diffuse large B-cell lymphoma

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91
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Arises at extranodal sites in adults with chronic inflammatory diseases; may remain localized; indolent

A

Extranodal marginal zone lymphoma

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92
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Older adults with generalized lymphadenopathy and marrow involvement; indolent

A

Follicular lymphoma

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93
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Older men with pancytopenia and splenomegaly; indolent

A

Hairy cell leukemia

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94
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Older men with disseminated disease; moderately aggressive

A

Mantle cell lymphoma

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95
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-older adults with lytic bone lesions, pathologic fractures, hypercalcemia, and renal failure; moderately aggressive

A

Multiple myeloma

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96
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-isolated plasma cell masses in bone or soft tissue; indolent

A

Solitary plasmacytoma

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97
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Older adults with bone marrow, lymph node, spleen, and liver disease; autoimmune hemolysis and thrombocytopenia in a minority; indolent

A

Small lymphocytic lymphoma/chronic lymphocytic leukemia

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98
Q

Cell of origin of Burkitt lymphoma

A

Germinal center B cell

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99
Q

Cell of origin of DLBCL

A

Germinal center of post-germinal center B-cell

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100
Q

Cell of origin of Extranodal MZL

A

Memory B cell

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101
Q

Cell of origin of FL

A

Germinal center B cell

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102
Q

Cell of origin of Hairy cell leukemia

A

Memory B cell

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103
Q

Cell of origin of MCL

A

Naive B cell

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104
Q

Cell of origin of Multiple myeloma/solitary plasmacytoma

A

Post-germinal center bone marrow homing plasma cell

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105
Q

Cell of origin of CLL/SLL

A

Naive B cell or Memory B cell

106
Q

Most common leukemias/lymphomas in adults (3)

A
  • DLBCL
  • FL
  • MM/Solitary plasmacytoma
107
Q

Type of Leukemia/Lymphoma

Genotype:
-HTLV-1 provirus present in tumor cells

A

Adult T-cell leukemia/lymphoma

108
Q

Type of Mature T-cell or NK cell Leukemia/Lymphoma (2)

Genotype:
-No specific chromosomal abnormality

A
  • Peripheral T-cell lymphoma, unspecified

- Mycosis fungoides/Sézary syndrome

109
Q

Type of Leukemia/Lymphoma

Genotype:
-Rearrangements of ALK (anaplastic large cell lymphoma kinase) in a subset

A

Anaplastic large-cell lymphoma

110
Q

Type of Leukemia/Lymphoma

Genotype:
-EBV-associated; no specific chromosomal abnormality

A

Extranodal NK/T-cell lymphoma

111
Q

Type of Leukemia/Lymphoma

Genotype:
-Point mutations in STAT3

A

Large granular lymphocytic leukemia

112
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Adults with cutaneous lesions, marrow involvement, and hypercalcemia; occurs mainly in Japan, West Africa, and the Caribbean; aggressive

A

Adult T-cell leukemia/ lymphoma

113
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Mainly older adults; usually presents with lymphadenopathy; aggressive

A

Peripheral T-cell lymphoma, unspecified

114
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Children and young adults, usually with lymph node and soft tissue disease; aggressive

A

Anaplastic large-cell lymphoma

115
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Adults with destructive extranodal masses, most commonly sinonasal; aggressive

A

Extranodal NK/T-cell lymphoma

116
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Adult patients with cutaneous patches, plaques, nodules, or generalized erythema; indolent

A

Mycosis fungoides/Sézary syndrome

117
Q

Type of Leukemia/Lymphoma

Salient Clinical Features:
-Adult patients with splenomegaly, neutropenia, and anemia, sometimes accompanied by autoimmune disease

A

Large granular lymphocytic leukemia

118
Q

Cell of origin of Adult T-cell leukemia/ lymphoma

A

Helper T-cell

119
Q

Cell of origin of Peripheral T-cell lymphoma, unspecified

A

Helper or cytotoxic T-cell

120
Q

Cell of origin of Anaplastic large-cell lymphoma

A

Cytotoxic T-cell

121
Q

Cell of origin of Extranodal NK/T-cell lymphoma

A

NK-cell (common) or cytotoxic T cell (rare)

122
Q

Cell of origin of Mycosis fungoides/Sézary syndrome

A

Helper T-cell

123
Q

Cells of origin of Large granular lymphocytic leukemia (2)

A

Two types:

  • Cytotoxic T cell
  • NK cell
124
Q

Four major categories of Diarrhea

A
  • Secretory
  • Osmotic
  • Malabsorptive
  • Exudative
125
Q

Category of Diarrhea

-characterized by isotonic stool and persists during fasting

A

Secretory diarrhea

126
Q

Category of Diarrhea

-occurs with lactase deficiency, is due to the excessive osmotic force exerted by unab- sorbed luminal solutes

A

Osmotic diarrhea

127
Q

Category of Diarrhea

-The diarrhea fluid is more than 50 mOsm more concentrated than plasma, and diarrhea abates with fasting

A

Osmotic diarrhea

128
Q

Category of Diarrhea

-follows generalized failure of nutrient absorption, is associated with steatorrhea, and is relieved by fasting

A

Malabsorptive diarrhea

129
Q

Category of Diarrhea

-due to inflammatory disease is character- ized by purulent, often bloody stools that continue during fasting.

A

Exudative diarrhea

130
Q

Major herniation syndromes of the brain (3)

A
  • Subfalcine (cingulate) herniation
  • Transtentorial (uncal, mesial temporal) herniation
  • Tonsillar herniation
131
Q

Brain herniation:

-occurs when unilateral
or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the falx

A

-Subfalcine (cingulate) herniation

132
Q

Brain herniation:

-This may lead to compression of the anterior cerebral artery and its branches, resulting in secondary infarcts.

A

-Subfalcine (cingulate) herniation

133
Q

Brain herniation:

-occurs when the medial aspect of the temporal lobe is compressed against the free margin of the tentorium

A

-Transtentorial (uncal, mesial temporal) herniation

134
Q

Term for secondary hemorrhagic lesions in the midbrain and pons accompanying the progression of transtentorial herniation

A

Duret hemorrhages

135
Q

Brain herniation:

-refers to displacement of the cerebellar tonsils through the foramen magnum

A

-Tonsillar herniation

136
Q

Brain herniation:

-This pattern of herniation is life-threatening because it causes brainstem compression and compromises vital respiratory and cardiac centers in the medulla

A

-Tonsillar herniation

137
Q

Macroscopic Skin Lesion

-Traumatic lesion breaking the epidermis and causing a raw linear defect (i.e., deep scratch); often self-induced.

A

Excoriation

138
Q

Macroscopic Skin Lesion

-Thickened, rough skin (similar to lichen on a rock); usually the result of repeated rubbing.

A

Lichenification

139
Q

Macroscopic Skin Lesion

-Circumscribed, flat lesion distinguished from surrounding skin by color that are 5 mm in diameter or less

A

Macules

140
Q

Macroscopic Skin Lesion

-Circumscribed, flat lesion distinguished from surrounding skin by color that are greater than 5 mm in diameter.

A

Patch

141
Q

Macroscopic Skin Lesion

-Separation of nail plate from nail bed.

A

Onycholysis

142
Q

Macroscopic Skin Lesion

-Elevated dome-shaped or flat-topped lesion that are 5 mm or less across

A

Papule

143
Q

Macroscopic Skin Lesion

-Elevated dome-shaped or flat-topped lesion that are greater than 5 mm in size.

A

Nodule

144
Q

Macroscopic Skin Lesion

-Elevated flat-topped lesion, usually greater than 5 mm across (may be caused by coalescent papules)

A

Plaque

145
Q

Macroscopic Skin Lesion

-Discrete, pus-filled, raised lesion

A

Pustule

146
Q

Macroscopic Skin Lesion

-Dry, horny, plate-like excrescence; usually the result of imperfect cornification

A

Scale

147
Q

Macroscopic Skin Lesion

-Fluid-filled raised lesion 5 mm or less across

A

Vesicle

148
Q

Macroscopic Skin Lesion

-Fluid-filled raised lesion greater than 5 mm across

A

Bulla

149
Q

Macroscopic Skin Lesion

-Itchy, transient, elevated lesion with variable blanching and erythema formed as the result
of dermal edema

A

Wheal

150
Q

Common term for Vesicle and Bulla

A

Blister

151
Q

Microscopic skin lesion

-Diffuse epidermal hyperplasia

A

Acanthosis

152
Q

Microscopic skin lesion

-Abnormal, premature keratinization within cells below the stratum granulosum

A

Dyskeratosis

153
Q

Microscopic skin lesion

-Discontinuity of the skin showing incomplete loss of the epidermis

A

Erosion

154
Q

Microscopic skin lesion

-Infiltration of the epidermis by inflammatory cells

A

Exocytosis

155
Q

Microscopic skin lesion

-Intracellular edema of keratinocytes, often seen in viral infections

A

Hydropic swelling (ballooning)

156
Q

Microscopic skin lesion

-Hyperplasia of the stratum granulosum, often due to intense rubbing

A

Hypergranulosis

157
Q

Microscopic skin lesion

-Thickening of the stratum corneum, often associated with a qualitative abnormality of the keratin

A

Hyperkeratosis

158
Q

Microscopic skin lesion

-Linear pattern of melanocyte proliferation within the epidermal basal cell layer

A

Lentiginous

159
Q

Microscopic skin lesion

-Surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae

A

Papillomatosis

160
Q

Microscopic skin lesion

-Keratinization with retained nuclei in the stratum corneum. On mucous membranes, it is normal

A

Parakeratosis

161
Q

Microscopic skin lesion

-Intercellular edema of the epidermis

A

Spongiosis

162
Q

Microscopic skin lesion

-Discontinuity of the skin marked by complete loss of the epidermis revealing dermis or subcutis

A

Ulceration

163
Q

Microscopic skin lesion

-Formation of vacuoles within or adjacent to cells; often refers to basal cell–basement membrane zone area

A

Vacuolization

164
Q

Nevus variant

Diagnostic Architectural Features:

-Deep dermal and sometimes subcutaneous growth around adnexa, neurovascular bundles, and blood vessel walls

A

Congenital nevus

165
Q

Nevus variant

Diagnostic Architectural Features:

-Non-nested dermal infiltration, often with associated fibrosis

A

Blue nevus

166
Q

Nevus variant

Diagnostic Architectural Features:

-Fascicular growth

A

Spindle and epithelioid cell nevus (Spitz nevus)

167
Q

Nevus variant

Diagnostic Architectural Features:

-Lymphocytic infiltration surrounding nevus cells

A

Halo nevus

168
Q

Nevus variant

Diagnostic Architectural Features:

-Coalescent intraepidermal nests

A

Dysplastic nevus

169
Q

Nevus variants (2)

Cytologic Features:

-Identical to ordinary acquired nevi

A
  • Congenital nevus

- Halo nevus

170
Q

Nevus variant

Cytologic Features:

-Highly dendritic, heavily pigmented nevus cells

A

Blue nevus

171
Q

Nevus variant

Cytologic Features:

-Large, plump cells with pink-blue cytoplasm; fusiform cells

A

Spindle and epithelioid cell nevus (Spitz nevus)

172
Q

Nevus variant

Cytologic Features:

-Cytologic atypia

A

Dysplastic nevus

173
Q

Nevus variant

Clinical significance:

-Present at birth; large variants have increased melanoma risk

A

Congenital nevus

174
Q

Nevus variant

Clinical significance:

-Black-blue nodule; often confused with melanoma clinically

A

Blue nevus

175
Q

Nevus variant

Clinical significance:

-Common in children; red-pink nodule; often confused with hemangioma clinically

A

Spindle and epithelioid cell nevus (Spitz nevus)

176
Q

Nevus variant

Clinical significance:

-Host immune response against nevus cells and surrounding normal melanocytes

A

Halo nevus

177
Q

Nevus variant

Clinical significance:

-Potential marker or precursor of melanoma

A

Dysplastic nevus

178
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Location: Antrum

A

H. pylori-Associated Gastritis

179
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Inflammatory infiltrate: Neutrophils, subepithelial plasma cells

A

H. pylori-Associated Gastritis

180
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Acid production: Increased to slightly decreased

A

H. pylori-Associated Gastritis

181
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Gastrin secretion: Normal to increased

A

H. pylori-Associated Gastritis

182
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Other lesions: Hyperplastic/inflammatory polyps

A

H. pylori-Associated Gastritis

183
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Serology: Antibodies to H. pylori

A

H. pylori-Associated Gastritis

184
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Sequelae: Peptic ulcer, Adenocarcinoma, MALToma

A

H. pylori-Associated Gastritis

185
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Associations: Low socioeconomic status, poverty, residence in rural areas

A

H. pylori-Associated Gastritis

186
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Location: Body

A

Autoimmune Gastritis

187
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Inflammatory infiltrate: Lymphocytes, macrophages

A

Autoimmune Gastritis

188
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Acid production: Decreased

A

Autoimmune Gastritis

189
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Gastrin secretion: Increased to markedly increased

A

Autoimmune Gastritis

190
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Other lesions: Neuroendocrine hyperplasia

A

Autoimmune Gastritis

191
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Serology: Antibodies to parietal cells (H+,K+-ATPase, intrinsic factor)

A

Autoimmune Gastritis

192
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Sequelae: Atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor

A

Autoimmune Gastritis

193
Q

H. pylori-Associated Gastritis vs. Autoimmune Gastritis

Associations: Autoimmune disease: thyroiditis, diabetes mellitus, Graves disease

A

Autoimmune Gastritis

194
Q

Hypertrophic Gastropathies and Gastric Polyps

Mean patient age, years: 30-60

A

Menetrier Disease (Adult)

195
Q

Hypertrophic Gastropathies and Gastric Polyps

Mean patient age, years: 50 (2)

A
  • Zollinger-Ellison syndrome

- Fundic gland polyps

196
Q

Hypertrophic Gastropathies and Gastric Polyps

Mean patient age, years: 50-60 (2)

A
  • Inflammatory and Hyperplastic polyps

- Gastric adenomas

197
Q

Hypertrophic Gastropathies and Gastric Polyps

Mean patient age, years: Variable

A

Gastritis cystica

198
Q

Hypertrophic Gastropathies and Gastric Polyps

Location: Body and Fundus (2)

A
  • Menetrier Disease (Adult)

- Fundic gland polyps

199
Q

Hypertrophic Gastropathies and Gastric Polyps

Location: Fundus

A

-Zollinger-Ellison Syndrome

200
Q

Hypertrophic Gastropathies and Gastric Polyps

Location: Antrum > Body (2)

A
  • Inflammatory and Hyperplastic Polyps

- Gastric Adenomas

201
Q

Hypertrophic Gastropathies and Gastric Polyps

Location: Body

A

Gastritis Cystica

202
Q

Hypertrophic Gastropathies and Gastric Polyps

Predominant cell type: Mucous (2)

A
  • Menetrier Disease (Adult)

- Inflammatory and Hyperplastic Polyps

203
Q

Hypertrophic Gastropathies and Gastric Polyps

Predominant cell type: Parietal > mucous, Endocrine

A

-Zollinger-Ellison Syndrome

204
Q

Hypertrophic Gastropathies and Gastric Polyps

Predominant cell type: Mucous, cyst-lining

A

Gastritis Cystica

205
Q

Hypertrophic Gastropathies and Gastric Polyps

Predominant cell type: Parietal and Chief

A

Fundic Gland Polyps

206
Q

Hypertrophic Gastropathies and Gastric Polyps

Predominant cell type: Dysplastic, intestinal

A

Gastric adenomas

207
Q

Hypertrophic Gastropathies and Gastric Polyps

Inflammatory infiltrate: Limited, Lymphocytes

A

-Menetrier Disease (Adult)

208
Q

Hypertrophic Gastropathies and Gastric Polyps

Inflammatory infiltrate: Neutrophils

A

-Zollinger-Ellison Syndrome

209
Q

Hypertrophic Gastropathies and Gastric Polyps

Inflammatory infiltrate: Neutrophils and Lymphocytes (2)

A
  • Inflammatory and Hyperplastic Polyps

- Gastritis Cystica

210
Q

Hypertrophic Gastropathies and Gastric Polyps

Inflammatory infiltrate: None

A

Fundic gland polyps

211
Q

Hypertrophic Gastropathies and Gastric Polyps

Inflammatory infiltrate: Variable

A

Gastric adenomas

212
Q

Hypertrophic Gastropathies and Gastric Polyps

Symptoms: Hypoproteinemia, weight loss, diarrhea

A

-Menetrier Disease (Adult)

213
Q

Hypertrophic Gastropathies and Gastric Polyps

Symptoms: Peptic ulcers

A

Zollinger-Ellison Syndrome

214
Q

Hypertrophic Gastropathies and Gastric Polyps

Symptoms: Similar to chronic gastritis (3)

A
  • Inflammatory and Hyperplastic Polyps
  • Gastritis Cystica
  • Gastric adenomas
215
Q

Hypertrophic Gastropathies and Gastric Polyps

Symptoms: None, nausea

A

Fundic Gland Polyps

216
Q

Hypertrophic Gastropathies and Gastric Polyps

Risk Factors: None

A

Menetrier Disease (Adult)

217
Q

Hypertrophic Gastropathies and Gastric Polyps

Risk Factors: Multiple endocrine neoplasia

A

Zollinger-Ellison Syndrome

218
Q

Hypertrophic Gastropathies and Gastric Polyps

Risk Factors: Chronic gastritis, H. pylori

A

Inflammatory and Hyperplastic Polyps

219
Q

Hypertrophic Gastropathies and Gastric Polyps

Risk Factors: Trauma, prior surgery

A

Gastritis cystica

220
Q

Hypertrophic Gastropathies and Gastric Polyps

Risk Factors: PPIs, FAP

A

Fundic Gland Polyps

221
Q

Hypertrophic Gastropathies and Gastric Polyps

Risk Factors: Chronic gastritis, atrophy,
intestinal metaplasia

A

Gastric adenomas

222
Q

Hypertrophic Gastropathies and Gastric Polyps

Association with Adenocarcinoma: YES

A

Menetrier Disease (Adult)

223
Q

Hypertrophic Gastropathies and Gastric Polyps

Association with Adenocarcinoma: NO

A
  • Zollinger-Ellison Syndrome

- Gastritis Cystica

224
Q

Hypertrophic Gastropathies and Gastric Polyps

Association with Adenocarcinoma: Occasional

A

Inflammatory and Hyperplastic Polyps

225
Q

Hypertrophic Gastropathies and Gastric Polyps

Association with Adenocarcinoma: Syndromic (FAP) only

A

Fundic Gland Polyps

226
Q

Hypertrophic Gastropathies and Gastric Polyps

Association with Adenocarcinoma: Frequent

A

Gastric adenomas

227
Q

Necrosis vs. Apoptosis

Cell size: Enlarged (swelling)

A

Necrosis

228
Q

Necrosis vs. Apoptosis

Nucleus: Pyknosis, Karyorrhexis, Karyolysis

A

Necrosis

229
Q

Necrosis vs. Apoptosis

Plasma membrane: Disrupted

A

Necrosis

230
Q

Necrosis vs. Apoptosis

Cellular contents: Enzymatic digestion; may leak out of cell

A

Necrosis

231
Q

Necrosis vs. Apoptosis

Adjacent inflammation: Frequent

A

Necrosis

232
Q

Necrosis vs. Apoptosis

Physiologic or Pathologic role: Usually pathologic (culmination of irreversible cell injury)

A

Necrosis

233
Q

Necrosis vs. Apoptosis

Cell size: Reduced (shrinkage)

A

Apoptosis

234
Q

Necrosis vs. Apoptosis

Nucleus: Fragmentation into nucleosome-size fragments

A

Apoptosis

235
Q

Necrosis vs. Apoptosis

Plasma membrane: Intact; altered structure, especially orientation of lipids

A

Apoptosis

236
Q

Necrosis vs. Apoptosis

Cellular contents: Intact; may be released in apoptotic bodies

A

Apoptosis

237
Q

Necrosis vs. Apoptosis

Adjacent inflammation: No

A

Apoptosis

238
Q

Necrosis vs. Apoptosis

Physiologic or Pathologic role: Often physiologic, means of eliminating unwanted cells; may be pathologic after some forms of cell injury, especially DNA damage

A

Apoptosis

239
Q

Properties of the Principal Free Radicals involved in Cell injury

Mechanism of Production: Incomplete reduction of O2 during oxidative phosphorylation; by phagocyte oxidase in leukocytes

A

O2• , superoxide anion

240
Q

Properties of the Principal Free Radicals involved in Cell injury

Mechanism of inactivation: Conversion to H2O2 and O2 by SOD

A

O2• , superoxide anion

241
Q

Properties of the Principal Free Radicals involved in Cell injury

Pathologic effects: Stimulates production of degradative enzymes in leukocytes and other cells; may directly damage lipids, proteins, DNA; acts close to site of production

A

O2• , superoxide anion

242
Q

Properties of the Principal Free Radicals involved in Cell injury

Mechanism of production: Generated by SOD from
O2• and by oxidases in peroxisomes

A

H2O2, hydrogen peroxide

243
Q

Properties of the Principal Free Radicals involved in Cell injury

Mechanism of inactivation: Conversion to H2O and O2 by catalase (peroxisomes), glutathione peroxidase (cytosol, mitochondria)

A

H2O2, hydrogen peroxide

244
Q

Properties of the Principal Free Radicals involved in Cell injury

Pathologic effects: Can be converted to OH and OCl−, which destroy microbes and cells; can act distant from site of production

A

H2O2, hydrogen peroxide

245
Q

Properties of the Principal Free Radicals involved in Cell injury

Mechanism of production: Generated from H2O by hydrolysis (e.g., by radiation); from H2O2 by Fenton reaction; from O2•

A

OH, hydroxyl radical

246
Q

Properties of the Principal Free Radicals involved in Cell injury

Mechanism of inactivation: Conversion to H2O by glutathione peroxidase

A

OH, hydroxyl radical

247
Q

Properties of the Principal Free Radicals involved in Cell injury

Pathologic effects: Most reactive oxygen- derived free radical; principal ROS responsible for damaging lipids, proteins, and DNA

A

OH, hydroxyl radical

248
Q

Properties of the Principal Free Radicals involved in Cell injury

Mechanism of production: Produced by interaction of O2• and NO generated by NO synthase in many cell types (endothelial cells, leukocytes, neurons, others)

A

ONOO−, peroxynitrite

249
Q

Properties of the Principal Free Radicals involved in Cell injury

Mechanism of inactivation: Conversion to HNO2 by peroxiredoxins (cytosol, mitochondria)

A

ONOO−, peroxynitrite

250
Q

Properties of the Principal Free Radicals involved in Cell injury

Pathologic effects: Damages lipids, proteins, DNA

A

ONOO−, peroxynitrite

251
Q

Type I vs. Type II
Endometrial Carcinoma

AGE: 55-65 yo

A

Type I Endometrial Carcinoma

252
Q

Type I vs. Type II
Endometrial Carcinoma

CLINICAL SETTING:

  • Unopposed Estrogen
  • Obesity
  • HTN
  • Diabetes
A

Type I Endometrial Carcinoma

253
Q

Type I vs. Type II
Endometrial Carcinoma

MORPHOLOGY: Endometrioid

A

Type I Endometrial Carcinoma

254
Q

Type I vs. Type II
Endometrial Carcinoma

PRECURSOR: Hyperplasia

A

Type I Endometrial Carcinoma

255
Q

Type I vs. Type II
Endometrial Carcinoma

MUTATED GENES/GENETIC ABNORMALITIES:
-PTEN
-ARID1A (regulator of chromatin) 
-PIK3CA (PI3K)
-KRAS
-FGF2 (growth factor) 
-MSI
-CTNNB1 (Wnt signaling) 
-POLE
-TP53 (progressed
tumors)
A

Type I Endometrial Carcinoma

256
Q

Type I vs. Type II
Endometrial Carcinoma

BEHAVIOR:

  • Indolent
  • Spreads via lymphatics
A

Type I Endometrial Carcinoma

257
Q

Type I vs. Type II
Endometrial Carcinoma

AGE: 65-75 yo

A

Type II Endometrial Carcinoma

258
Q

Type I vs. Type II
Endometrial Carcinoma

CLINICAL SETTING:

  • Atrophy
  • Thin physique
A

Type II Endometrial Carcinoma

259
Q

Type I vs. Type II
Endometrial Carcinoma

MORPHOLOGY:

  • Serous
  • Clear Cell
  • MMT
A

Type II Endometrial Carcinoma

260
Q

Type I vs. Type II
Endometrial Carcinoma

PRECURSOR:
-Serous EIC

A

Type II Endometrial Carcinoma

261
Q

Type I vs. Type II
Endometrial Carcinoma

MUTATED GENES/GENETIC ABNORMALITIES:

  • TP53
  • Aneuploidy
  • PIK3CA (PI3K)
  • FBXW7 (regulator of MYC, cyclin E)
  • CCNE1
  • PPP2R1A (PP2A)
A

Type II Endometrial Carcinoma

262
Q

Type I vs. Type II
Endometrial Carcinoma

BEHAVIOR:

  • Aggressive
  • Intraperitoneal and lymphatic spread
A

Type II Endometrial Carcinoma

PATHOLOGY (26 decks)

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