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Goljan Path > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Dystrophic and metastatic calcification

A

Dystrophic is normal serum Calcium in damaged tissue. Atherosclerosis, aortic stenosis (e.g. bicuspid valve). Hypercalcemia or hyperphosphatemia –> deposition of ca in normal tissue, which is “metastatic calcification.”

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2
Q

Hereditary spherocytosis

A

Cannot see a central area of pallor, then it’s a spherocytes. e.g. absence of spectrin

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3
Q

Ubiquitin

A

A stress protein. When intermediate filaments are damaged, they are ubiquinated for destruction. MALLORY bodies in fatty change in alcoholic hepatitis (keratin damaged!). Tau protein is ubiquinated neurofibrillary. Lewy body.

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4
Q

Three types of cells

A

Labile - NEVER in G0, short G0 (e.g. tissues with stem cells - bone marrow, intestine bottom of crypts, skins). Stable cells - G0 phase and needs stimulus to divide (liver, spleen, kidney, SMOOTH muscle). Permanent - can’t get into the cell cycle (striated, cardiac, neurons). With a permanent cell, can’t go through hyperPLASIA. G1 phase is most variable (e.g. proliferative phase of menstrual cycle are more variable). Cancer cells tend to have variable G1 phase.

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5
Q

Glucagon is a phosphorylator

A

loll

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6
Q

Cyclin-D dependent kinase

A

Activated by Cyclin D in G1 phase. G1 to S is MOST IMPORTANT checkpoint. Two suppressor genes = Rb (Chromosome 13). Active Cyclin-D dept kinase phosphorylates Rb to allow to get from G1 to S. p53 INACTIVATES that cyclin-d dependent kinase (chromosome 17). HPV inactivates Rb (E7 protein) and p53 (E6 protein). Rb - retinoblastoma.

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7
Q

S phase

A

4N at this point. G2 phase make tubulin for mitotic spindles (bleomycin). M phase - divides (griseofulvin, MTX, colchicine, paclitaxel - Yew tree) G0 or go into G1.

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8
Q

Growth alterations

A

Atrophy - decreased in tissue MASS. Cell decreases in size. Less mitochondria than normal. e.g. Increased pressure (hydronephrosis). e.g. brain atrophy - AD, atherosclerosis.. Hypopituitary –> adrenal gland (fasciculata - cortisol and reticularis - sex hormones; but glomerulosa is OK b/c aldo NOT stimulated by ACTH release). CF in Pancreas has blocked exocrine ducts –> back pressure -> atrophy. Renal vascular stenosis -> atrophic kidney -> increased renin.

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9
Q

Hypertrophy

A

Increase in size NOT NUMBER. Cardiac muscle hypertrophy - block is before the G2, the cells have 4N?.

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10
Q

Hyperplasia

A

Increase in NUMBER of cells. (Endometrial hyperplasia). However, prostate hyperplasia does NOT go into prostate cancer. All the other ones predispose to cancer. ALL HORMONE-stimulated GLANDS undergo hyperplasia.

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11
Q

Gravid uterus

A

Hypertrophy AND hyperplasia. 50:50

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12
Q

Psoriasis

A

Hyperplasia. Excess of stratum corneum. MTX works.

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13
Q

Metaplasia

A

Replaces one cell type to another. e.g. Barrett’s esophagus (glandular stroma where should be squamous epithelium)

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14
Q

Two parasites that produce cancer

A

Clonorchis sinesis - cholangiocarcinoma. Shistosoma hemtobium: transitional epithelium -> squamous metaplasia in the bladder

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15
Q

Actinic keratosis –>

A

Squamous cell carcinoma

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16
Q

Rubor, calor, tumor

A

HISTAMINE-mediated. Tumor from inc. permeability (venule) -> exudate.

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17
Q

Dolor

A

Bradykinin - activated by XII, increases vessel permeability and edema; and cough. Bradykinin is degraded by ACE. (Angioedema complication of ACEi). PGE2.

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18
Q

Directed chemotaxis

A

C5a, LTB4, (IL-8)

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19
Q

Opsonization

A

IgG, C3b; Neutrophils must have receptors for these opsonins.

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20
Q

Chronic inflammation

A

Macrophage/monocyte

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21
Q

Oxygen-dependent Myeloperoxidase system

A

Mol O2 (NADPH oxidase in cell membranes of neutrophils and monocytes but NOT macrophages w/ NADPH - HMP shunt, G6Pd, glutathione) –> superoxide. This respiratory burst measured by radiation detectors (nitro blue tetrazolium). NBT is a dye that goes into test tube. Free radical oxygen will cause a BLUE color. Superoxide dimutase –> peroxide. MPO (Myeloperoxidase from red granules in Neutrophils and Monocytes): peroxide + Cl- –> BLEACH. Macrophages lose this system.

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22
Q

G6Pd deficiency

A

Susceptible to infection b/c low MPO system function –> hemolysis

23
Q

Chronic Granulomatous Disease

A

X-linked recessive. Missing NADPH oxidase + respiratory burst. Don’t have superoxide, peroxide. HAVE MPO + Cl. If some bacteria makes peroxide that stays (Catalase NEG) —> system available. They can’t kill Staph (Coagulase AND Catalase +). But CAN kill Strep.

24
Q

MPO deficiency

A

Have a respiratory burst (normal dye) but can’t make bleach. Autosomal Recessive.

25
Q

Umbilical cord doesn’t come off.

A

Integrin (adhesion) molecule defect.

26
Q

Anaphylotoxins

A

C3a, C4a, C5a

27
Q

Nitric oxide

A

Mostly made in endothelial cells –> vasodilator. Pulm HTN treatment.

28
Q

IL-1

A

Pyogen. Stimulates hypthalamus to make prostaglandins which stimulates thermoregulatory center to make fever.

29
Q

Corticosteroids

A

Inhibits PLA2. Stops Arachnoid. Stop prostaglandins and leukotrienes. Decrease adhesion molecule synthesis —-> INCREASED neutrophil count (50% of neutrophils are already stuck on endothelium - “demargination.”). Lymphocytoxic - apoptosis via caspases. Eosinophils decreased.

30
Q

Dipyrimadole

A

Blocks thromboxane synthase (makes TXA2)

31
Q

PGE2

A

Patent ductus. Mucous barrier in stomach. Dysmenorrhea (inc. uterine contractility)

32
Q

Addison’s disease

A

NO cortisol. Decreased Neutrophils. Increased eosinophils and lymphocytes.

33
Q

EM of lymphocyte

A

All nucleus.

34
Q

EM plasma cell

A

Lots of RER = FINGER print. PLASMA cells

35
Q

Eosinophil

A

Only inflammatory cell that has crystals in granules. Charcot-Leyden crystals in sputum of asthmatics. IgE Ab connections -> Major Basic Protein for helminthic (Type II hypersensitivity). Purpose of eosinophils in Type I hs is to stop chemical mediators (histamines, etc.)

36
Q

Histiocyte marker

A

CD1

37
Q

Marker for most common leukemia in children

A

CD10 - ALL.

38
Q

CD21

A

EBV - B-cells

39
Q

Fever

A

IL-1. PGE2 (made by hypothalamus). RIGHT-shifts O2 curve (increased oxygen) –> Oxygen-dependent MPO system.

40
Q

Types of inflammation

A

Suppurative inflammation.

41
Q

Diptheria

A

Makes a toxin that leads to damage –> pseudomembrane

42
Q

Fibrinous inflammation

A

Inc. vessel permeability. e.g. lupus

43
Q

Granulation tissue

A

Fibronectin - adhesion agent, chemotactic agent (dy 3-5). COLLAGEN type III initially (blood vessels). Collegneases break down type III over time. Converts it into type I (Zinc). Max tensile strength = 80% in 3 mo.

44
Q

Keloid vs hypertrophic scar

A

Both excess type III collagen deposition. Keloid - blacks, 3rd degree burn –> scar –> squamous cell ca. Also from chronically draining sinus tract –> hyperplasia -> squamous cell carcinoma

45
Q

Acute vs chronic inflammation

A

IgM is primary in acute. Most potent activator of complement system in IgM. Pentamer –> boom classical pathway. Pus (exudate). IgG requires two events for complement and doesn’t go beyond C3. 10 days -> isotope switching -> splice out mu heavy chain -> puts in GAMMA heavy chain = IgG. IgG is main in chronic. Monocytes and macrocytes and plasma cells in chronic.

46
Q

Granuloma formation

A

Multi-nucleated giant cells. T-IV hypersensitivity (e.g. poison ivy). Alveolar MACROPHAGE holds TB and moves around (lympho-hematogenous spread) and processes that organisms’ antigen. After a week, presents to helper T-cell (Th1 via MHC-II) —> IFN-gamma, macrophage inhibitory factor, IL-2 —> IFN-g is activation for killing by macrophage. Caseous necrosis b/c of lipid. Epithelioid cell = activated macrophage. Fuse –> multi-nucleated giant cells. IL-12 makes memory of Ag experience -> Th1 cell. Often dystrophic calcification. TB stays alive.

47
Q

Positive PPD

A

Inject PPD into skin. Langerhans cell = dendritic cell (CD1). Burbick granules. Presents to Th1 w/ memory of previous exposure via MHC-II -> release cytokines –> inflammatory reaction (induration). Older people have less immune response. AIDS patients might not have any + PPD (Can’t make granulomas at all, 5mm +).

48
Q

Which part of kidney is most specific to ischemia?

A

Medulla. In nephron, the straight portion of proximal tubule. Second is medullary segment of thick ascending limb (Na-K-2Cl).

49
Q

Repair cell of lung

A

Type II pneumocyte - Also makes surfactant

50
Q

Repair cell of CNS

A

Astrocyte (stable cell) and can proliferate (gliosis)

51
Q

ESR

A

Whole blood into perpendicular cylinder.

52
Q

Cold agglutunins

A

IgM antibodies. Agglutination of RBC’s –> Raynaud’s.

53
Q

Cryoglobulins

A

Congeal in the plasma —> Raynaud’s. High associated with Hepatitis C.

54
Q

Acute appendicitis

A

Absolute neutrophilic leukocytosis. Toxic granulation (More azurophilic granules - MPO’s in here - in neutrophils). Left-shift: means LESS mature neutrophils. Greater than 10% BAND neutrophils.

Goljan Path (9 decks)

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