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Foundations 2 > 9/21 > Flashcards

9/21 Flashcards

1
Q

Morphological Types of Acute Inflammation

A

Neutrophils appear first then macrophages come, neutrophils have nuclei with multiple lobes

  1. Serous Fluids: clear fluid with few/no cells, transudate, erythematous vesicles or blisters
  2. Fibrinous: bread and butter pericarditis, Cell poor and protein rich
  3. Purulent: cloudy exudate, cell/protein rich
    Has cell debris, fibrin, bacteria, neutrophils
    Staphylococcus bacteria like pneumonia and the clap

Bronchopneumonia has exudate (fibrin and neutrophils) in alveoli, leptomeningitis

  1. Pseudomembranous: colitis from C. difficile, fibrino-purulent yellow/gray exudate mushrooms on colon/pharanyx, neutrophil/macrophages and fibrin on top of epithelial cells
  2. Ulcers: epithelial surface that is excavated by shedding of inflamed necrotic tissue, can be due to acute/chronic inflammation

Common in skin, GIT, bladder, can also be on cornea

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2
Q

Leptomeningitis

A

Fever, headache, vomit, stiff neck, photophobia, confusion

Purulent exudate in the subarachnoid space, see neutrophils and macrophages

Lumbar puncture shows increased protein content and neutrophils (exudate)

E. Colinfor infants, Strep. pneumoniae for infant/elderly, N. meninglitidis for teens/young adults

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3
Q

Pulmonary Abscess

A

Liquefactive necrosis rich in cell debris, fluid, macrophages, neutrophils

Nice round red nodule surrounded by blue

Necrosis is walled off by a fibrin wall, forms circle

Caused by Staph, Strep, and fungi

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4
Q

Infiltrative Inflammation (Non-Granulomatous)

A

Dominated by humoral adaptive immune response

  1. Macrophages: very light purple, pale chromatin and red nucleolous
  2. Lymphocytes: mainly dark purple, scant cytoplasm and dark round nuclei with prominent nucleoli
  3. Plasma Cells: light purple cytoplasm and dark purple nucleus, clock-face nuclear chromatin, amphophilic cytoplasm
  4. Eosinophils: bunch of bright pink cytoplasm dots and dark purple nucleus
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5
Q

Viral/bacterial Pneumonia Histology

A

Viral: Edema in the alveoli, light pink spaces instead of white, few mononuclear cells

Death of epithelial cells lining the alveoli results in cell poor exudate that coagulates into dark pink hyaline membrane

Bacteria: fibrin and neutrophils fill alveoli, more purple cell things filling alveoli than viral

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6
Q

Granuloma Histology

A

Macrophages form outer ring around epithelioid cells, lymphocytes near macrophages as well, fibroblast cells on the outside

Large pink oval surrounded by sea of purple dots

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7
Q

Granulomatous Inflammation

A

Noncaseating: foreign body, fungus, parasite, immune

Caseating: M. tuberculosis, Bartonella henselae

Necrotizing: fungus, immune

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8
Q

Different Types of Granulomas

A

Caseating: from bacteria, Langerhans type giant cells have pearl necklace of nuclei, foreign body giant nuclei if all bunched up in middle

Sarcoidosis: non-caseating granuloma Inflammation that lacks a known etiologic agent

Necrotizing Granuloma: coin lesion in chest, from fungal infections, light purple circle surrounds pinkish purple circle in middle

Granulomas from Fungus: use methenamine silver to identify yeast

Parasitic Schistosomiasis: form non-caseating granuloma, ova in tissue

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9
Q

Acute Phase Response

A

Collection of endocrine, metabolic, or neurological changes that are shortly observed after infection, microbial products, and inflammation

Characterized by fever, increased/decreased synthesis of plasma proteins by liver, behavioral changes, and increase in leukocytes

IL-1, IL-6, TNFalpha, and IFN activate immune cells and also act on liver to produce certain acute phase proteins

IL-6 is main cytokine mediator of acute phase response

Hypothalamus starts endocrine to make glucocorticoids that increase liver response to IL-6

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10
Q

Acute Phase Response Proteins

A

C-reactive protein

Serum amyloid protein

Mannose-binding lectin

Alpha-2 macroglobulin

Proteins that reduce iron availability: hepatoglobulin, ferritin, hepcidin, ceruplasmin

Alpha1 anti-trypsin/chymotrypsin

Coagulation proteins

Complement proteins

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11
Q

C-Reactive Protein

A

Produced in liver, no specific marker of inflammation

Binds to bacteria/fungi cell wall, also to PCs on dead/damaged human cells

Activates classical/alternative pathways of the complement system

Bind to Fc receptors and act as opsonin, activates macrophages to produce cytokines

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12
Q

Serum Amyloid A

A

Made in liver, associates with HDL

Binds to TLR to activate cells, chemotactic to neutrophils/mast cells

Stimulate cytokine synthesis, involved in pathogenesis of amyloid A-type amyloidosis and chronic inflammation

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13
Q

Random Acute Phase Response Proteins

A
  1. Alpha-2-Macroglobulin: inhibits proteases involved in coagulation and fibrinolysis

Iron limiting proteins- prevent bacteria from getting iron since needed for growth

  1. Haptoglobin: binds Hemoglobin
  2. Ferritin: binds iron
  3. Hepcidin: prevents iron release from ferritin in macrophages and intestines
  4. Ceruloplasmin: oxidizes iron

6/7. Alpha 1 Anti-trypsin/chymotrypsin: downregulate inflammation

  1. Coagulation Proteins: prothrombin, von Wilbrand Factor, fibrinogen, plasminogen
  2. Complement Proteins
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14
Q

Erythrocyte Sediment Rate

A

Increased fibrinogen levels during acute Phase Response causes RBCs to adopt Rouleaux formation and stack

ESR above 20 mm/hr denotes inflammation, is no specific indicator of inflammation though like C-reactive protein levels

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15
Q

Normal vs. Fever

A

Body temp. is controlled by hypothalamus

Diurnal variation: low 6 AM, high 4-6 PM

Fever: increase in body temp. That exceeds diurnal variation and occurs in conjunction with increase in hypothalamic set point, pyrogens reset the set point

Hyperpyrexia: temp. above 40 °C, severe infections and CNS hemorrhage

Hyperthermia (heat stroke): no intrinsic body pyrogens or altered set point

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16
Q

Mechanism of Fever

A

Infection/Inflammation activates NF-kappaB in leukocytes/endothelial cells, makes secrete pyrogenic cytokines (IL-1beta, IL-6, TNF-alpha, IFN) into circulation

Pyrogenic cytokines induce PGE2 synthesis, binds to EP3 receptors on neurons and causes glial cells to release cAMP to activate neuronal endings from the thermoregulatory center of the hypothalamus

Thermostatic set point raised, heat conservation and fever ensue

17
Q

Phases of Fever

A

Initiation Phase: elevation of set point brings chills, shivering, rigor

Plateau Phase: core body temperature equals set point and minimal chills, shivering, and rigors

Defervescence: core body temperature is above set point, patients feel warm and are sweating, recovery phase

18
Q

Impact of a Fever

A

Positive:
Increase IFN-gamma production
Stimulate antibody synthesis
Stimulate leukocyte motility and phagocytosis
Inhibit bacterial growth by limit Fe, Cu, Zn
Increase cell death in virally infected cells

Negative:
Heart rate increases but decreased cardiac output
Decreased blood flow to brain, seizures and CNS damage
Acidosis from higher respiratory rate, oxygen consumption, and metabolic rate

19
Q

Behavioral Responses to Fever

A

Mediated by IL-1, IL-6, TNF-alpha, IFN-gamma

Malaise
Pain (PGE2)
Sleepiness (PGD2)
Anorexia (PGE2)

20
Q

White Blood Cell Count

A

Normal WBC level: 5-10k/uL

Leukocytosis: increase in WBCs (15-25k/uL)

Leukemoid Reaction: markedly increased leukocyte count (40-100k+), resembles leukemia

Neutrophilia: increase in neutrophils, from bacterial infections

Eosinophilia: seen in asthma, hay fever, parasites

Lymphocytosis: viral infections, chronic inflammatory states

Leukopenia: decreased WBCs from certain infections/diseases like viruses, Rickettsia, Protozoa, TB, and cancers

Left Shift: bacterial infection/acute inflammation increase neutrophils, bands appear in blood and are precursor cells to the mature neutrophils

Bone marrow sends bands into blood stream that mature to neutrophils there, also called bandemia

21
Q

Leukocyte Adhesion Deficiency

A

Recessive disease, defects in leukocyte Adhesion to endothelial cells, presented in kids

Delayed umbilical cord detachment, omphalitis

Severe recurrent bacterial infections to skin/mucosal surfaces, no pus formation, gingivitis and periodontitis common

Neutrophilia from labs, neutrophils can’t transmigrate

Treatment: antibiotics and bone marrow transplant if severe LAD 1

LAD I: structural defects in neutrophil integrins, mutation in CD18

LAD II: absence of selectin on surface, Golgi GDP-fucose transporter defect

LAD III: defect in integrin activation process

22
Q

Chronic Granulomatous Disease

A

Mutations in genes for NADPH oxidase, phagocytes can’t make hydrogen peroxide or superoxide to kill microbes via oxidative burst

Genetically heterogenous with 70% X-linked recessive and 30% autosomal recessive, rare

Infections-
Common sites: lung, skin, lymph nodes, liver

Normal response to viral infections

Staph aureus are common bacterial infections, Aspergillus (fungi) commonly infect but make only a little sick so hard to diagnose

Diagnosis-
Tissue biopsy: look for granulomata
Oxidative burst test (Flow cytometry), Nitroblue tetrazolium test is old method, confirm via genetic testing

Treatment: antibiotics/antifungal prophylaxis, INF-gamma or bone marrow transplant

Foundations 2 (18 decks)

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