Robbins Must Knows Flashcards by Jonathan Emmanuel Cancio

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

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Increased vascular permeability

Suppurative (Purulent) Infection

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Leukocyte infiltration (neutrophils)

Suppurative (Purulent) Infection

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Chemoattractants from bacteria

Suppurative (Purulent) Infection

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Formation of “pus”

Suppurative (Purulent) Infection

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Spectrum of Inflammatory Responses to Infection

Type of Response:

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

Suppurative (Purulent) Infection

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Spectrum of Inflammatory Responses to Infection

Type of Response:

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

Mononuclear and Granulomatous inflammation

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Spectrum of Inflammatory Responses to Infection

Type of Response:

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

Mononuclear and Granulomatous inflammation

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Formation of granulomata

Mononuclear and Granulomatous inflammation

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Spectrum of Inflammatory Responses to Infection

Type of Response:

Examples include:

Syphilis
Tuberculosis

Mononuclear and Granulomatous inflammation

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Viral transformation of cells

Cytopathic-cytoproliferative reactions

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Necrosis or proliferation (including multinucleation)

Cytopathic-cytoproliferative reactions

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Linked to neoplasia

Cytopathic-cytoproliferative reactions

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Spectrum of Inflammatory Responses to Infection

Type of Response:

Examples include:

Cervical cancer (human papillomavirus)
Chicken pox, shingles
Herpes

Cytopathic-cytoproliferative reactions

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Toxin- or lysis-mediated destruction

Tissue necrosis

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Lack of inflammatory cells

Tissue necrosis

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Rapidly progressive processes

Tissue necrosis

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Spectrum of Inflammatory Responses to Infection

Type of Response:

Examples include:

Gangrene (Clostridium perfringens)
Hepatitis (hepatitis B virus)

Tissue necrosis

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Repetitive injury leads to fibrosis

Chronic inflammation/ scarring

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Loss of normal parenchyma

Chronic inflammation/ scarring

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Spectrum of Inflammatory Responses to Infection

Type of Response:

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

Chronic inflammation/ scarring

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Spectrum of Inflammatory Responses to Infection

Type of Response:

-Severe immune compromise

No reaction

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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

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Three categories of Agents of Bioterrorism

Category A agents
Category B agents
Category C agents

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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

Robbins Must Knows Flashcards

(262 cards)