Robbins Must Knows Flashcards
Spectrum of Inflammatory Responses to Infection
6 types of response
- Suppurative (Purulent) Infection
- Mononuclear and Granulomatous inflammation
- Cytopathic-Cytoproliferative reactions
- Tissue necrosis
- Chronic inflammation/scarring
- No reaction
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Increased vascular permeability
Suppurative (Purulent) Infection
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Leukocyte infiltration (neutrophils)
Suppurative (Purulent) Infection
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Chemoattractants from bacteria
Suppurative (Purulent) Infection
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Formation of “pus”
Suppurative (Purulent) Infection
Spectrum of Inflammatory Responses to Infection
Type of Response:
Examples include:
-Pneumonia (Staphylococcus aureus)
-Abscesses (Staphylococcus spp., anaerobic and other
bacteria)
Suppurative (Purulent) Infection
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Mononuclear cell infiltrates (monocytes, macrophages, plasma cells, lymphocytes)
Mononuclear and Granulomatous inflammation
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Cell-mediated immune response to pathogens (“persistent antigen”)
Mononuclear and Granulomatous inflammation
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Formation of granulomata
Mononuclear and Granulomatous inflammation
Spectrum of Inflammatory Responses to Infection
Type of Response:
Examples include:
- Syphilis
- Tuberculosis
Mononuclear and Granulomatous inflammation
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Viral transformation of cells
Cytopathic-cytoproliferative reactions
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Necrosis or proliferation (including multinucleation)
Cytopathic-cytoproliferative reactions
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Linked to neoplasia
Cytopathic-cytoproliferative reactions
Spectrum of Inflammatory Responses to Infection
Type of Response:
Examples include:
- Cervical cancer (human papillomavirus)
- Chicken pox, shingles
- Herpes
Cytopathic-cytoproliferative reactions
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Toxin- or lysis-mediated destruction
Tissue necrosis
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Lack of inflammatory cells
Tissue necrosis
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Rapidly progressive processes
Tissue necrosis
Spectrum of Inflammatory Responses to Infection
Type of Response:
Examples include:
- Gangrene (Clostridium perfringens)
- Hepatitis (hepatitis B virus)
Tissue necrosis
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Repetitive injury leads to fibrosis
Chronic inflammation/ scarring
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Loss of normal parenchyma
Chronic inflammation/ scarring
Spectrum of Inflammatory Responses to Infection
Type of Response:
Example include:
-Chronic hepatitis with cirrhosis (hepatitis B and C viruses)
Chronic inflammation/ scarring
Spectrum of Inflammatory Responses to Infection
Type of Response:
-Severe immune compromise
No reaction
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)
No reaction
Three categories of Agents of Bioterrorism
- Category A agents
- Category B agents
- Category C agents
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
Category A agents
What category does this agents of Bioterrorism belong?
- Small pox
- B. anthracis,
- Yersinia pestis, and
- Ebola virus
Category A agents
Agents of Bioterrorism
-relatively easy to disseminate, produce moderate morbidity but low mortality, and require specific diagnostic and disease surveillance.
Category B agents
Agents of Bioterrorism
-Many of these agents are food-borne or water-borne
Category B agents
Agents of Bioterrorism
Examples include:
- Brucella spp. and
- V. cholerae.
Category B agents
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
Category C agents
Agents of Bioterrorism
Examples include:
- Hanta virus
- Nipah virus
Category C agents
STI caused by HSV in Both males and females (2)
- Primary and recurrent herpes
- Neonatal herpes
STI caused by HBV in Both males and females
Hepatitis
STI caused by HPV ONLY in males
Cancer of Penis
STI caused by HPV ONLY in females (2)
- Cervical dysplasia and cancer
- Vulvar cancer
STI caused by HPV in Both males and females
Condyloma acuminatum
STI caused by HIV in Both males and females
AIDS
STI caused by Chlamydia trachomatis ONLY in males (3)
- Urethritis
- Epididymitis
- Proctitis
STI caused by Chlamydia trachomatis ONLY in females (5)
- Urethral syndrome,
- cervicitis,
- bartholinitis,
- salpingitis, and
- sequelae
STI caused by Chlamydia trachomatis Both in males and females
Lymphogranuloma venereum
STI caused by Ureaplasma urealyticum ONLY in males
Urethritis
STI caused by Neisseria gonorrheae ONLY in males (3)
- Epididymitis
- Prostatitis
- Urethral stricture
STI caused by Neisseria gonorrheae ONLY in females (5)
- Cervicitis,
- endometritis,
- bartholinitis,
- salpingitis, and
- sequelae (infertility, ectopic pregnancy, recurrent salpingitis)
STI caused by Neisseria gonorrheae Both in males and females (4)
- Urethritis,
- proctitis,
- pharyngitis,
- disseminated gonococcal infection
STI caused by Treponema pallidum Both in males and females
Syphilis
STI caused by Haemophilus ducreyi Both in males and females
Chancroid
STI caused by Klebsiella granulomatis Both in males and females
Granuloma inguinale (donovanosis)
STI caused by Trichomonas vaginalis ONLY in males (2)
- Urethritis
- Balanitis
STI caused by Trichomonas vaginalis ONLY in females
Vaginitis
critical mediator that activates macrophages and enables them to contain the M. tuberculosis infection
Interferon-gamma
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
Immediate (type I) hypersensitivity
Type of Hypersensitivity Reaction
Histopathologic Lesion: Vascular dilation, edema, smooth muscle contraction, mucus production, tissue injury, inflammation
Immediate (type I) hypersensitivity
Type of Hypersensitivity Reaction
Prototypical Disorders: Anaphylaxis; allergies; bronchial asthma (atopic forms)
Immediate (type I) hypersensitivity
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
Antibody-mediated (type II)
hypersensitivity
Type of Hypersensitivity Reaction
Histopathologic lesion: Phagocytosis and lysis of cells; inflammation; in some diseases, functional derangements without cell or tissue injury
Antibody-mediated (type II)
hypersensitivity
Type of Hypersensitivity Reaction
Prototypical disorder:
- Autoimmune hemolytic anemia
- Goodpasture syndrome
Antibody-mediated (type II)
hypersensitivity
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
Immune complex– mediated (type III) hypersensitivity
Type of Hypersensitivity Reaction
Histopathologic lesion: Inflammation, necrotizing vasculitis (fibrinoid necrosis)
Immune complex– mediated (type III) hypersensitivity
Type of Hypersensitivity Reaction
Prototypical disorders:
- Systemic lupus erythematosus
- some forms of glomerulonephritis
- serum sickness
- Arthus reaction
Immune complex– mediated (type III) hypersensitivity
Type of Hypersensitivity Reaction
Immune mechanism: Activated T lymphocytes → (1) release of cytokines, inflammation and macrophage activation; (2) T cell–mediated cytotoxicity
Cell-mediated (type IV) hypersensitivity
Type of Hypersensitivity Reaction
Histopathologic lesion: Perivascular cellular infiltrates; edema; granuloma formation; cell destruction
Cell-mediated (type IV) hypersensitivity
Type of Hypersensitivity Reaction
Prototypical disorders:
- Contact dermatitis
- multiple sclerosis
- type 1 diabetes
- tuberculosis
Cell-mediated (type IV) hypersensitivity
represent primary errors of morphogenesis, in which there is an intrinsically abnormal developmental process
Malformations
result from secondary destruction of an organ or body region that was previously normal in development
Disruptions
represent an extrinsic disturbance of development rather than an intrinsic error of morphogenesis
Deformations
a cascade of anomalies triggered by one initiating aberration
Sequence
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
Malformation syndrome
What Syndrome?
Associated CHD:
-pulmonary artery stenosis or tetralogy of Fallot
Gene defect:
-Signaling proteins or receptors (JAG1 or NOTCH2)
Alagille syndrome
What Syndrome?
Associated CHD:
-PDA
Gene defect:
-Transcription factor (TFAP2B)
Char syndrome
What Syndrome?
Associated CHD:
-ASD, VSD, PDA, or hypoplastic right side of the heart
Gene defect:
-Helicase-binding protein (CHD7)
CHARGE syndrome
What Syndrome?
Associated CHD:
-ASD, VSD, or outflow tract obstruction
Gene defect:
-Transcription factor (TBX1)
DiGeorge syndrome
What Syndrome?
Associated CHD:
-ASD, VSD, or conduction defect
Gene defect:
-Transcription factor (TBX5)
Holt-Oram syndrome
What Syndrome?
Associated CHD:
-pulmonary valve stenosis, VSD, or hypertrophic cardiomyopathy
Gene defect:
-Signaling proteins (PTPN11, KRAS, SOS1)
Noonan syndrome
Type of Leukemia/Lymphoma
Genotype:
-Diverse chromosomal translocations; t(12;21) involving RUNX1 and ETV6 present in 25%
B-cell acute lymphoblastic leukemia/lymphoma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Predominantly children; symptoms relating to marrow replacement and pancytopenia; aggressive
B-cell acute lymphoblastic leukemia/lymphoma
Most common leukemias/lymphomas in children (2)
- B-cell acute lymphoblastic leukemia/lymphoma
- Burkitt lymphoma
Cell of origin of B-cell acute lymphoblastic leukemia/lymphoma
Bone marrow precursor B cell
Type of Leukemia/Lymphoma
Genotype:
-Diverse chromosomal translocations; NOTCH1 mutations (50%–70%)
T-cell acute lymphoblastic leukemia/lymphoma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Predominantly adolescent males; thymic masses and variable bone marrow involvement; aggressive
T-cell acute lymphoblastic leukemia/lymphoma
Cell of origin of T-cell acute lymphoblastic leukemia/lymphoma
Precursor T cell (often of thymic origin)
Type of Leukemia/Lymphoma
Genotype:
-Translocations involving MYC and Ig loci, usually t(8;14); subset EBV-associated
Burkitt lymphoma
Type of Leukemia/Lymphoma
Genotype:
-Diverse chromosomal rearrangements, most often of BCL6 (30%), BCL2 (10%), or MYC (5%)
Diffuse large B-cell lymphoma
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
Extranodal marginal zone lymphoma
Type of Leukemia/Lymphoma
Genotype:
-t(14;18) creating BCL2-IGH fusion gene
Follicular lymphoma
Type of Leukemia/Lymphoma
Genotype:
-Activating BRAF mutations
Hairy cell leukemia
Type of Leukemia/Lymphoma
Genotype:
-t(11;14) creating cyclin D1–IGH fusion gene
Mantle cell lymphoma
Type of Leukemia/Lymphoma
Genotype:
-Diverse rearrangements involving IGH; 13q deletions
Multiple myeloma/solitary plasmacytoma
Type of Leukemia/Lymphoma
Genotype:
-Trisomy 12, deletions of 11q, 13q, and 17p; NOTCH1 mutations; splicing factor mutations
Small lymphocytic lymphoma/chronic lymphocytic leukemia
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Adolescents or young adults with extranodal masses; uncommonly presents as “leukemia”; aggressive
Burkitt lymphoma
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
Diffuse large B-cell lymphoma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Arises at extranodal sites in adults with chronic inflammatory diseases; may remain localized; indolent
Extranodal marginal zone lymphoma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Older adults with generalized lymphadenopathy and marrow involvement; indolent
Follicular lymphoma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Older men with pancytopenia and splenomegaly; indolent
Hairy cell leukemia
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Older men with disseminated disease; moderately aggressive
Mantle cell lymphoma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-older adults with lytic bone lesions, pathologic fractures, hypercalcemia, and renal failure; moderately aggressive
Multiple myeloma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-isolated plasma cell masses in bone or soft tissue; indolent
Solitary plasmacytoma
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
Small lymphocytic lymphoma/chronic lymphocytic leukemia
Cell of origin of Burkitt lymphoma
Germinal center B cell
Cell of origin of DLBCL
Germinal center of post-germinal center B-cell
Cell of origin of Extranodal MZL
Memory B cell
Cell of origin of FL
Germinal center B cell
Cell of origin of Hairy cell leukemia
Memory B cell
Cell of origin of MCL
Naive B cell
Cell of origin of Multiple myeloma/solitary plasmacytoma
Post-germinal center bone marrow homing plasma cell
Cell of origin of CLL/SLL
Naive B cell or Memory B cell
Most common leukemias/lymphomas in adults (3)
- DLBCL
- FL
- MM/Solitary plasmacytoma
Type of Leukemia/Lymphoma
Genotype:
-HTLV-1 provirus present in tumor cells
Adult T-cell leukemia/lymphoma
Type of Mature T-cell or NK cell Leukemia/Lymphoma (2)
Genotype:
-No specific chromosomal abnormality
- Peripheral T-cell lymphoma, unspecified
- Mycosis fungoides/Sézary syndrome
Type of Leukemia/Lymphoma
Genotype:
-Rearrangements of ALK (anaplastic large cell lymphoma kinase) in a subset
Anaplastic large-cell lymphoma
Type of Leukemia/Lymphoma
Genotype:
-EBV-associated; no specific chromosomal abnormality
Extranodal NK/T-cell lymphoma
Type of Leukemia/Lymphoma
Genotype:
-Point mutations in STAT3
Large granular lymphocytic leukemia
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
Adult T-cell leukemia/ lymphoma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Mainly older adults; usually presents with lymphadenopathy; aggressive
Peripheral T-cell lymphoma, unspecified
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Children and young adults, usually with lymph node and soft tissue disease; aggressive
Anaplastic large-cell lymphoma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Adults with destructive extranodal masses, most commonly sinonasal; aggressive
Extranodal NK/T-cell lymphoma
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Adult patients with cutaneous patches, plaques, nodules, or generalized erythema; indolent
Mycosis fungoides/Sézary syndrome
Type of Leukemia/Lymphoma
Salient Clinical Features:
-Adult patients with splenomegaly, neutropenia, and anemia, sometimes accompanied by autoimmune disease
Large granular lymphocytic leukemia
Cell of origin of Adult T-cell leukemia/ lymphoma
Helper T-cell
Cell of origin of Peripheral T-cell lymphoma, unspecified
Helper or cytotoxic T-cell
Cell of origin of Anaplastic large-cell lymphoma
Cytotoxic T-cell
Cell of origin of Extranodal NK/T-cell lymphoma
NK-cell (common) or cytotoxic T cell (rare)
Cell of origin of Mycosis fungoides/Sézary syndrome
Helper T-cell
Cells of origin of Large granular lymphocytic leukemia (2)
Two types:
- Cytotoxic T cell
- NK cell
Four major categories of Diarrhea
- Secretory
- Osmotic
- Malabsorptive
- Exudative
Category of Diarrhea
-characterized by isotonic stool and persists during fasting
Secretory diarrhea
Category of Diarrhea
-occurs with lactase deficiency, is due to the excessive osmotic force exerted by unab- sorbed luminal solutes
Osmotic diarrhea
Category of Diarrhea
-The diarrhea fluid is more than 50 mOsm more concentrated than plasma, and diarrhea abates with fasting
Osmotic diarrhea
Category of Diarrhea
-follows generalized failure of nutrient absorption, is associated with steatorrhea, and is relieved by fasting
Malabsorptive diarrhea
Category of Diarrhea
-due to inflammatory disease is character- ized by purulent, often bloody stools that continue during fasting.
Exudative diarrhea
Major herniation syndromes of the brain (3)
- Subfalcine (cingulate) herniation
- Transtentorial (uncal, mesial temporal) herniation
- Tonsillar herniation
Brain herniation:
-occurs when unilateral
or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the falx
-Subfalcine (cingulate) herniation
Brain herniation:
-This may lead to compression of the anterior cerebral artery and its branches, resulting in secondary infarcts.
-Subfalcine (cingulate) herniation
Brain herniation:
-occurs when the medial aspect of the temporal lobe is compressed against the free margin of the tentorium
-Transtentorial (uncal, mesial temporal) herniation
Term for secondary hemorrhagic lesions in the midbrain and pons accompanying the progression of transtentorial herniation
Duret hemorrhages
Brain herniation:
-refers to displacement of the cerebellar tonsils through the foramen magnum
-Tonsillar herniation
Brain herniation:
-This pattern of herniation is life-threatening because it causes brainstem compression and compromises vital respiratory and cardiac centers in the medulla
-Tonsillar herniation
Macroscopic Skin Lesion
-Traumatic lesion breaking the epidermis and causing a raw linear defect (i.e., deep scratch); often self-induced.
Excoriation
Macroscopic Skin Lesion
-Thickened, rough skin (similar to lichen on a rock); usually the result of repeated rubbing.
Lichenification
Macroscopic Skin Lesion
-Circumscribed, flat lesion distinguished from surrounding skin by color that are 5 mm in diameter or less
Macules
Macroscopic Skin Lesion
-Circumscribed, flat lesion distinguished from surrounding skin by color that are greater than 5 mm in diameter.
Patch
Macroscopic Skin Lesion
-Separation of nail plate from nail bed.
Onycholysis
Macroscopic Skin Lesion
-Elevated dome-shaped or flat-topped lesion that are 5 mm or less across
Papule
Macroscopic Skin Lesion
-Elevated dome-shaped or flat-topped lesion that are greater than 5 mm in size.
Nodule
Macroscopic Skin Lesion
-Elevated flat-topped lesion, usually greater than 5 mm across (may be caused by coalescent papules)
Plaque
Macroscopic Skin Lesion
-Discrete, pus-filled, raised lesion
Pustule
Macroscopic Skin Lesion
-Dry, horny, plate-like excrescence; usually the result of imperfect cornification
Scale
Macroscopic Skin Lesion
-Fluid-filled raised lesion 5 mm or less across
Vesicle
Macroscopic Skin Lesion
-Fluid-filled raised lesion greater than 5 mm across
Bulla
Macroscopic Skin Lesion
-Itchy, transient, elevated lesion with variable blanching and erythema formed as the result
of dermal edema
Wheal
Common term for Vesicle and Bulla
Blister
Microscopic skin lesion
-Diffuse epidermal hyperplasia
Acanthosis
Microscopic skin lesion
-Abnormal, premature keratinization within cells below the stratum granulosum
Dyskeratosis
Microscopic skin lesion
-Discontinuity of the skin showing incomplete loss of the epidermis
Erosion
Microscopic skin lesion
-Infiltration of the epidermis by inflammatory cells
Exocytosis
Microscopic skin lesion
-Intracellular edema of keratinocytes, often seen in viral infections
Hydropic swelling (ballooning)
Microscopic skin lesion
-Hyperplasia of the stratum granulosum, often due to intense rubbing
Hypergranulosis
Microscopic skin lesion
-Thickening of the stratum corneum, often associated with a qualitative abnormality of the keratin
Hyperkeratosis
Microscopic skin lesion
-Linear pattern of melanocyte proliferation within the epidermal basal cell layer
Lentiginous
Microscopic skin lesion
-Surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae
Papillomatosis
Microscopic skin lesion
-Keratinization with retained nuclei in the stratum corneum. On mucous membranes, it is normal
Parakeratosis
Microscopic skin lesion
-Intercellular edema of the epidermis
Spongiosis
Microscopic skin lesion
-Discontinuity of the skin marked by complete loss of the epidermis revealing dermis or subcutis
Ulceration
Microscopic skin lesion
-Formation of vacuoles within or adjacent to cells; often refers to basal cell–basement membrane zone area
Vacuolization
Nevus variant
Diagnostic Architectural Features:
-Deep dermal and sometimes subcutaneous growth around adnexa, neurovascular bundles, and blood vessel walls
Congenital nevus
Nevus variant
Diagnostic Architectural Features:
-Non-nested dermal infiltration, often with associated fibrosis
Blue nevus
Nevus variant
Diagnostic Architectural Features:
-Fascicular growth
Spindle and epithelioid cell nevus (Spitz nevus)
Nevus variant
Diagnostic Architectural Features:
-Lymphocytic infiltration surrounding nevus cells
Halo nevus
Nevus variant
Diagnostic Architectural Features:
-Coalescent intraepidermal nests
Dysplastic nevus
Nevus variants (2)
Cytologic Features:
-Identical to ordinary acquired nevi
- Congenital nevus
- Halo nevus
Nevus variant
Cytologic Features:
-Highly dendritic, heavily pigmented nevus cells
Blue nevus
Nevus variant
Cytologic Features:
-Large, plump cells with pink-blue cytoplasm; fusiform cells
Spindle and epithelioid cell nevus (Spitz nevus)
Nevus variant
Cytologic Features:
-Cytologic atypia
Dysplastic nevus
Nevus variant
Clinical significance:
-Present at birth; large variants have increased melanoma risk
Congenital nevus
Nevus variant
Clinical significance:
-Black-blue nodule; often confused with melanoma clinically
Blue nevus
Nevus variant
Clinical significance:
-Common in children; red-pink nodule; often confused with hemangioma clinically
Spindle and epithelioid cell nevus (Spitz nevus)
Nevus variant
Clinical significance:
-Host immune response against nevus cells and surrounding normal melanocytes
Halo nevus
Nevus variant
Clinical significance:
-Potential marker or precursor of melanoma
Dysplastic nevus
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Location: Antrum
H. pylori-Associated Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Inflammatory infiltrate: Neutrophils, subepithelial plasma cells
H. pylori-Associated Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Acid production: Increased to slightly decreased
H. pylori-Associated Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Gastrin secretion: Normal to increased
H. pylori-Associated Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Other lesions: Hyperplastic/inflammatory polyps
H. pylori-Associated Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Serology: Antibodies to H. pylori
H. pylori-Associated Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Sequelae: Peptic ulcer, Adenocarcinoma, MALToma
H. pylori-Associated Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Associations: Low socioeconomic status, poverty, residence in rural areas
H. pylori-Associated Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Location: Body
Autoimmune Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Inflammatory infiltrate: Lymphocytes, macrophages
Autoimmune Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Acid production: Decreased
Autoimmune Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Gastrin secretion: Increased to markedly increased
Autoimmune Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Other lesions: Neuroendocrine hyperplasia
Autoimmune Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Serology: Antibodies to parietal cells (H+,K+-ATPase, intrinsic factor)
Autoimmune Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Sequelae: Atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor
Autoimmune Gastritis
H. pylori-Associated Gastritis vs. Autoimmune Gastritis
Associations: Autoimmune disease: thyroiditis, diabetes mellitus, Graves disease
Autoimmune Gastritis
Hypertrophic Gastropathies and Gastric Polyps
Mean patient age, years: 30-60
Menetrier Disease (Adult)
Hypertrophic Gastropathies and Gastric Polyps
Mean patient age, years: 50 (2)
- Zollinger-Ellison syndrome
- Fundic gland polyps
Hypertrophic Gastropathies and Gastric Polyps
Mean patient age, years: 50-60 (2)
- Inflammatory and Hyperplastic polyps
- Gastric adenomas
Hypertrophic Gastropathies and Gastric Polyps
Mean patient age, years: Variable
Gastritis cystica
Hypertrophic Gastropathies and Gastric Polyps
Location: Body and Fundus (2)
- Menetrier Disease (Adult)
- Fundic gland polyps
Hypertrophic Gastropathies and Gastric Polyps
Location: Fundus
-Zollinger-Ellison Syndrome
Hypertrophic Gastropathies and Gastric Polyps
Location: Antrum > Body (2)
- Inflammatory and Hyperplastic Polyps
- Gastric Adenomas
Hypertrophic Gastropathies and Gastric Polyps
Location: Body
Gastritis Cystica
Hypertrophic Gastropathies and Gastric Polyps
Predominant cell type: Mucous (2)
- Menetrier Disease (Adult)
- Inflammatory and Hyperplastic Polyps
Hypertrophic Gastropathies and Gastric Polyps
Predominant cell type: Parietal > mucous, Endocrine
-Zollinger-Ellison Syndrome
Hypertrophic Gastropathies and Gastric Polyps
Predominant cell type: Mucous, cyst-lining
Gastritis Cystica
Hypertrophic Gastropathies and Gastric Polyps
Predominant cell type: Parietal and Chief
Fundic Gland Polyps
Hypertrophic Gastropathies and Gastric Polyps
Predominant cell type: Dysplastic, intestinal
Gastric adenomas
Hypertrophic Gastropathies and Gastric Polyps
Inflammatory infiltrate: Limited, Lymphocytes
-Menetrier Disease (Adult)
Hypertrophic Gastropathies and Gastric Polyps
Inflammatory infiltrate: Neutrophils
-Zollinger-Ellison Syndrome
Hypertrophic Gastropathies and Gastric Polyps
Inflammatory infiltrate: Neutrophils and Lymphocytes (2)
- Inflammatory and Hyperplastic Polyps
- Gastritis Cystica
Hypertrophic Gastropathies and Gastric Polyps
Inflammatory infiltrate: None
Fundic gland polyps
Hypertrophic Gastropathies and Gastric Polyps
Inflammatory infiltrate: Variable
Gastric adenomas
Hypertrophic Gastropathies and Gastric Polyps
Symptoms: Hypoproteinemia, weight loss, diarrhea
-Menetrier Disease (Adult)
Hypertrophic Gastropathies and Gastric Polyps
Symptoms: Peptic ulcers
Zollinger-Ellison Syndrome
Hypertrophic Gastropathies and Gastric Polyps
Symptoms: Similar to chronic gastritis (3)
- Inflammatory and Hyperplastic Polyps
- Gastritis Cystica
- Gastric adenomas
Hypertrophic Gastropathies and Gastric Polyps
Symptoms: None, nausea
Fundic Gland Polyps
Hypertrophic Gastropathies and Gastric Polyps
Risk Factors: None
Menetrier Disease (Adult)
Hypertrophic Gastropathies and Gastric Polyps
Risk Factors: Multiple endocrine neoplasia
Zollinger-Ellison Syndrome
Hypertrophic Gastropathies and Gastric Polyps
Risk Factors: Chronic gastritis, H. pylori
Inflammatory and Hyperplastic Polyps
Hypertrophic Gastropathies and Gastric Polyps
Risk Factors: Trauma, prior surgery
Gastritis cystica
Hypertrophic Gastropathies and Gastric Polyps
Risk Factors: PPIs, FAP
Fundic Gland Polyps
Hypertrophic Gastropathies and Gastric Polyps
Risk Factors: Chronic gastritis, atrophy,
intestinal metaplasia
Gastric adenomas
Hypertrophic Gastropathies and Gastric Polyps
Association with Adenocarcinoma: YES
Menetrier Disease (Adult)
Hypertrophic Gastropathies and Gastric Polyps
Association with Adenocarcinoma: NO
- Zollinger-Ellison Syndrome
- Gastritis Cystica
Hypertrophic Gastropathies and Gastric Polyps
Association with Adenocarcinoma: Occasional
Inflammatory and Hyperplastic Polyps
Hypertrophic Gastropathies and Gastric Polyps
Association with Adenocarcinoma: Syndromic (FAP) only
Fundic Gland Polyps
Hypertrophic Gastropathies and Gastric Polyps
Association with Adenocarcinoma: Frequent
Gastric adenomas
Necrosis vs. Apoptosis
Cell size: Enlarged (swelling)
Necrosis
Necrosis vs. Apoptosis
Nucleus: Pyknosis, Karyorrhexis, Karyolysis
Necrosis
Necrosis vs. Apoptosis
Plasma membrane: Disrupted
Necrosis
Necrosis vs. Apoptosis
Cellular contents: Enzymatic digestion; may leak out of cell
Necrosis
Necrosis vs. Apoptosis
Adjacent inflammation: Frequent
Necrosis
Necrosis vs. Apoptosis
Physiologic or Pathologic role: Usually pathologic (culmination of irreversible cell injury)
Necrosis
Necrosis vs. Apoptosis
Cell size: Reduced (shrinkage)
Apoptosis
Necrosis vs. Apoptosis
Nucleus: Fragmentation into nucleosome-size fragments
Apoptosis
Necrosis vs. Apoptosis
Plasma membrane: Intact; altered structure, especially orientation of lipids
Apoptosis
Necrosis vs. Apoptosis
Cellular contents: Intact; may be released in apoptotic bodies
Apoptosis
Necrosis vs. Apoptosis
Adjacent inflammation: No
Apoptosis
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
Apoptosis
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
O2• , superoxide anion
Properties of the Principal Free Radicals involved in Cell injury
Mechanism of inactivation: Conversion to H2O2 and O2 by SOD
O2• , superoxide anion
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
O2• , superoxide anion
Properties of the Principal Free Radicals involved in Cell injury
Mechanism of production: Generated by SOD from
O2• and by oxidases in peroxisomes
H2O2, hydrogen peroxide
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)
H2O2, hydrogen peroxide
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
H2O2, hydrogen peroxide
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•
OH, hydroxyl radical
Properties of the Principal Free Radicals involved in Cell injury
Mechanism of inactivation: Conversion to H2O by glutathione peroxidase
OH, hydroxyl radical
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
OH, hydroxyl radical
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)
ONOO−, peroxynitrite
Properties of the Principal Free Radicals involved in Cell injury
Mechanism of inactivation: Conversion to HNO2 by peroxiredoxins (cytosol, mitochondria)
ONOO−, peroxynitrite
Properties of the Principal Free Radicals involved in Cell injury
Pathologic effects: Damages lipids, proteins, DNA
ONOO−, peroxynitrite
Type I vs. Type II
Endometrial Carcinoma
AGE: 55-65 yo
Type I Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
CLINICAL SETTING:
- Unopposed Estrogen
- Obesity
- HTN
- Diabetes
Type I Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
MORPHOLOGY: Endometrioid
Type I Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
PRECURSOR: Hyperplasia
Type I Endometrial Carcinoma
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)
Type I Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
BEHAVIOR:
- Indolent
- Spreads via lymphatics
Type I Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
AGE: 65-75 yo
Type II Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
CLINICAL SETTING:
- Atrophy
- Thin physique
Type II Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
MORPHOLOGY:
- Serous
- Clear Cell
- MMT
Type II Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
PRECURSOR:
-Serous EIC
Type II Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
MUTATED GENES/GENETIC ABNORMALITIES:
- TP53
- Aneuploidy
- PIK3CA (PI3K)
- FBXW7 (regulator of MYC, cyclin E)
- CCNE1
- PPP2R1A (PP2A)
Type II Endometrial Carcinoma
Type I vs. Type II
Endometrial Carcinoma
BEHAVIOR:
- Aggressive
- Intraperitoneal and lymphatic spread
Type II Endometrial Carcinoma
