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Foundations of Pathology > Foundations > Flashcards

Foundations Flashcards

1
Q

Blood volume and percent body weight?

A

5 Liters, 5 % BW

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2
Q

ECM for blood?

A

Plasma

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3
Q

Peripheral Blood is…

A

All blood that’s not in the bone marrow

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4
Q

plasma componenets

A

90% water, 10% protein

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5
Q

Plasma is made how

A

Fluid phase after centrifugation in the presence of heparin to prevent clotting

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6
Q

Serum

A

The fluid portion after coagulation and centrifugation. It is done to remove the clotting factors and cells

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7
Q

Most clinical blood work is done on which fraction of blood?

A

Serum

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8
Q

normal RBC range

A

4.6 to 6.1 million per mcL men, 4.2-5.4 mil per mcL women

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9
Q

normal WBC range

A

4 to 10 thousand per mcL

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10
Q

Differential count

A

A count that tells the wbc distribution

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11
Q

Neutrophil

A

34-71%

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12
Q

Eosinophils

A

0-7%

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13
Q

Basophils

A

0-1%

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14
Q

Monocytes

A

5-12%

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15
Q

Lymphocytes

A

19-53%

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16
Q

RBC diameter

A

7.5 microns

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17
Q

HbF

A

2 alpha, 2 chi

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18
Q

band-3

A

pumps bicarbonate out of the RBC… also binds ankyrin, which binds spectrins, to maintain biconcavity

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19
Q

What is normal hematocrit

A

40-51%

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20
Q

Hemoglobin is..

A

33% of RBC

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21
Q

Chronic Granulomatous Disease (CGD)

A

Young person, liver abscess with low virulence bacteria. Caused by no NADH oxidase in PMNs… x linked or recessive autosomal.

Treat with TM-Sulfa prophylaxis and itraconazola (for bacteria and fungi). Give prednisone for granulomas that will form. Hepatosplenomegaly and pneumonia common.

Cured with BMT

Diagnosed by testing for respiratory burst with fluorescent DHR… also detects carries, who have two populations which is visible upon stimulation

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22
Q

Leukocyte Adhesion Deficiency-1

A

Loss of beta unit of CD18, which binds… needed to adhere to integrins on epithelium.

BMT for sever cases, otherwise aggressive antibiotic treatment

Present with pyogenic infections, delayed umbilical cord detachment… Cannot form pus, and have leukocytosis during infection

Tested with flow cytometry with anti-CD18 fluorsenet antibody… ULCERS without PUS

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23
Q

Leukocyte Adhesion Deficiency-2

A

Deficiency is fucosylation (Fuct1) a fructose transporter. also called CD15. Tested using flow cytometry with an anti-FUCT1 fluorescent antibody.

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24
Q

MyD88/IRAK-4 Deficiency

A

All TLRs that use common pathway will be busted. TLR3/4 can still work via TRIF, a separate activator. Phenotype is the same for both MyD88 and irak-4. Manifest with similar PID.

high mortality until age of 8, at which point they can fend off infection on their own. Very susceptible to strep, staph, pseudomonas… meningitis, sepsis, and arthritis. ALL BACTERIAL

Susceptiblity not predicted based on mice models

IVIG and Abx prophylaxis until 8.

Bad infections but with no elevation in white counts or c reactive protein? suspect this

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25
Q

TLR3/4? or TLR3 Signaling defect

A

Defect in TRIF or in TLR 3 directly

Causes herpes virus encephalitis, recurrent

Not 100% penetrance

26
Q

Late Complement Deficiency

A

Onset later in life, with variable penetrance. Usually adolescent. Must be homozygous, and susceptible to adolescent-onsite mengococcal disease, which becomes recurrent through adulthood. Homozygous null C5-C9, which form the membrane attack complex (MAC)

27
Q

Early Complement Deficiency

A

C2 deficiency is the most common. Autosomal recessive. Causes collagen vascular diseases (SLE), recurrent bacteria. Best screening test CH50. A CH50 of 0 suggests individual complement deficiency. A low, but non-zero, CH50 score suggests consumption.

28
Q

Sever Combined Immunodeficiency

A

SCID. Profound cellular and humoral immunity defects. P. jirovecii, otitis media, thrust, diarrhea, failure to thrive

100% mortality unless BMT. Need to do a genetic screening test using CBC, and detect a lymphopenia less than 1500 per mcl

Definitive Testing: is with TRECs!

29
Q

TRECs are a marker for

A

NORMAL, NAIVE T cells! Measured using real time PCR

30
Q

DiGeorge Syndrome (22qDS deletion syndrome)

A

CATCH22… Cardiac Defects; Abnormal face; Thymic hypoplasia; Cleft palate; Hypocalcemia; 22nd chromosome.

Low set ears, chin inward, fish shaped mouth, chola brow. Issues with swallowing, liquid comes back out of nose. Heart issues were common during childhood. Recurrent infections (thrust, otitis media, pneumonia)

Up to 30% have low T cell counts, with many abnormal. Need monthly IVIG supplementation, since B cells are dysfunctional without T cells. Autoimmunity, likely due to abnormal thymus (incomplete negative selection)

Test chromosome microarray or RT PCR for haploinsufficiency of TBX1

31
Q

X-Linked Agammaglobulinemia

A

No B cells. Very low immunoglobulins IgG/A/M. Frequent recurrent respiratory sickness, otitis media, pneumonia as early as first year.

Treat with gamma globulin in order to prevent bronchiectasis…

Also able to get vaccine- related polio, and other enteroviral infections and encapsulated bacteria infections (mycoplasma, h. influenzae)

Screen all Ig’s (will be pan-hypogammaglobulinemia) in newborns is best.

Btk or BLNK in cell signaling is abolished. This is what mediate survival signals in B cells after cross linking.

32
Q

Common Variable Immunodeficiency

A

Often presents with Bronchiectasis and interstitial lung disease

Leads to abnormal function of bronchi and cilia, making them susceptible to bronchitis and pneumonia. Progresses even with IVIG treatment

Similar therapy to CF. Physiotherapy, vests, chest pumping, hypertonic saline, hospitalizations with Abx for severe cases. Prophylaxis with Ab? possible

Very low IgG, with lower IgA and IgM also

Onset is greater than 4 years old
Exclude primary Ab deficiency (Ab), and secondary Ab deficiency, such as BCL, corticiosteroids, rituximab

Increases risk for B cell lymphomas

Later onset common, low FEV1/FVC (less than 50%)

Diffuse parenchymal disease, including GLILD… 10% of patients, with hepatomegaly and lung disease, due to multisystemic lymphoproliferative disorder

33
Q

Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED)

A

Adrenal, parathyroid disease, and other endocrine dysfunction. Autoimmune disease, hypogonadism, vitiligo, pernicious anemia… all because AIRE is missing. Central negative selection fails.
Central tolerance failure

34
Q

Autoimmune lymphoproliferative syndrome (ALPS)

A

Widespread lymphadenopathy and splenomegaly, with autoimmune cytopenias (anemia, thrombocytopenia)

FAs or Fas ligand busted, very high gamma globulin titers, many double negative T cells, leading to peripheral tolerance failure

35
Q

Factor that allows T cell self antigens survive neg selection

A

Foxp3

36
Q

Immune Dysregulation Polyendocrinopathy, X-linked (IPEX)

A

Infant boys affected, IBD, eczema, very high IgE, foxp3 is busted with no Tregs functioning

37
Q

CD25 Deficiency

A

IPEX-like disease, with eczema, hypothyroidism, anemia, neutropenia, diarrhea, hepatosplenomegaly, lymphadenopathy, respiratory illness

Excessive amounts of gabba globulins. CD25 is a receptor Tregulatory cells that binds IL-2, leading to T cell reg dysfunction

38
Q

Acute Rheumatic Fever

A

Joints, heart, nodules, erythema marginatum, sydeham’s chorea are major

Fever, arthralgia, elevated acute phase reactants and prolong PR interval are minor

two major or 1 major with two minor for diagonsis.

Give PCN prophylaxis for life once one bout of rheumatic fever occurs to prevent another strep infection

5 year prophylaxis or til 21 if carditis
10 year prophylaxis or til 21 if valvular disease
IF both… then 10 year prophylaxis or til 40, whichever longer

M protein in strep has mimicry with cardio cells

Example of Type II, with disease breaking self-tolerance

39
Q

Systemic Lupis Erythematousous

A

Fatigue, fevers, rash, butterfly rash, high ANAs, low complement levels

Arthritis, serositis, cerebritis, nephritis, pleuritis, carditis

Early onset SLE can be caused by early complement defects, especially C2 (also C1q and C4)

40
Q

rheumatoid arthritis

A

Proximal joint

Synovial fibroblasts activated by T cells, released IL1 IL6, TNF, all are inflammatory cytokines
B cells aggregated in synovium, and autoantibodies such as ANAs present in many
Both cell and humoral mediated immunity, but this is generally thought of as a type IV hypersensitivity

Treat with NSAIDs

41
Q

Ehlers Danlos Syndrome

A

Hyperextensible skin, easily traumatized
Joints and ligaments hypermobile

Rupture of internal organs, especially colon and large arteries

Collagen with very low tensile strength

42
Q

Five reasons for elevated eosinophil count

A 
Neoplasia
Asthma
Allergy
Connective Tissue Disease
Parasitic Disease
43
Q

Senstivity for farmer’s lung

A

Alveolitis, Type III against spores or dust

44
Q

Systemic antigen excess

A

Type III if it is against viral hepatitis or bacterial endocarditis antigen in sera

45
Q

Pernicious anemia sensitivity

A

Megaloblastic anemia is a Type II specificity… intrinsic factor bound to gastric parietal cells

46
Q

Goodpasture syndrome

A

Causes nephritis. Type II sens. Type IV collagen binds basement membrane in lung and glomeruli attack

47
Q

Acute rheumatic fever

A

Type II cross reaction with M protein from strep and heart

48
Q

Bullous pemphigoid

A

Skin vesicles as epidermal basement membrane gets attacked. This is a type 2 sensitivity

49
Q

Vasculitides

A

Neutrophil cytoplasmic antibodies

50
Q

Antiphospholipid antibodies

A

These thrombotic phenomena are Type II

51
Q

What cells involved in type iv hypersensitivity?

A

CD4 TH1 and CD8 T cells

52
Q

Tuberculin response

A

Th1 mediated response causes swelling at site in 48-72 hours. Hypersensitive skin reactions same deal. Rhus dermatitis/poison ivy

53
Q

Which hypersensitive reactions are soluble and which aren’t

A

Th1 mediated ones are soluble, but CD8 mediated ones are cell associated

54
Q

IL-4 and IL-13 purpose

A

Th2 release these to stimulate isotype switching of B cells

55
Q

IL-3, IL-5, GM-CSF

A

promote survival and eosinophilia

56
Q

RANTES and Eotaxin

A

Chemokines for T cells and eosinophils. CCR3 on eosinophils bind it. Eotaxin is always found at allergic inflammatory sites

57
Q

MIP-1alpha

A

chemtaxis for macrophages and everything else

58
Q

Platelet activating factor

A

Actives mononuclear and polymorphonuclear cells, attracting agent

59
Q

Steroids do what to IL-5

A

Decrease its release

60
Q

Effector mechanisms for allergy

A

Type !: mast cell activation

2: FcR regions
3: FcR regions and complement
4: Macrophage activation (for Th1), but directly cytotoxic for CD8

Foundations of Pathology (1 decks)

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