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7 Flashcards

1
Q

What are the 2 branches of adaptive immunity?

A

Humoral (B-cells) and Cell-mediated (T-cells - CD4, CD8)

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2
Q

Humoral immunity

A

Antibody production, Main defence against bacteria and bacterial toxins

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3
Q

Cell-mediated Immunity

A

Formation of a population of lymphocytes that attack and destroy infected cells (CD8), Main defense against viruses, fungi, parasites, cancers, and some bacteria, rejection of transplanted organs,

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4
Q

Chain of events when a foreign antigen enters the body

A
  • Recognition of foreign antigen
  • Proliferation of individual lymphocytes that are programmed to respond to the antigen form a large group (clone) of cells
  • Destruction of pathogen /infected cells by the responding lymphocytes
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5
Q

T lymphocyte Response

A

Unable to respond to a foreign antigen (TCR) until a macrophage or dendritic cell (APC) cell has phagocytosed the antigen, digested it, and displayed on its cell membrane the antigen fragments combined with its own MHC proteins

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6
Q

B Lymphocyte Response to antigen

A
  • Have immunoglobulin molecules (BCR) on their cell membranes that function as antigen receptors, and they can bind entire antigen molecules to their receptors (do not require MHC presentation)
  • Processed into fragments
  • Fragments displayed on the cell’s membrane with MHC class ll proteins for presentation and recognition by CD4 T-cells to enhance antibody production
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7
Q

Antibodies

A

Globulins produced by plasma cells and can only recreate to specific antigen that induce its formation

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8
Q

Antibody function

A
  • Activation of complement
  • Neutralization
  • Agglutination
  • Opsonization
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9
Q

Types of antibodies

A
  • Immunoglobulin G (IgG)
  • Immunoglobulin A (IgA)
  • Immunoglobulin M (IgM)
  • Immunoglobulin E (IgE)
  • Immunoglobulin D (IgD)
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10
Q

IgG

A
  • Smaller antibody
  • Principal antibody molecule in response to majority of infectious agents
  • Monomer shape
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11
Q

IgM

A
  • Large antibody; a macroglobulin – early production before IgG is produced
  • Responsible for immune control in early response
  • Expressed on surface as monomer – secreted form (pentamer)
  • Very efficient combining with fungi
  • Pentamer
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12
Q

IgE

A
  • Found in minute quantities in blood; binds to mast cells, basophils/eosinophils
  • Concentration is increased in allergic individuals
  • Important in controlling parasitic infections
  • Monomer
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13
Q

IgA

A
  • Produced by antibody-forming cells located in the respiratory and gastrointestinal mucosa (GI/respiratory and urogenital tract)
  • Combines with harmful ingested or inhaled antigens, forming antigen–antibody complexes
  • Dimer
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14
Q

IgD

A
  • Found on cell membrane of B lymphocytes (Functions mainly as BCR) - no plasma cell
  • Present in minute quantities in blood
  • Monomer
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15
Q

What type of immunoglobulins are on Naïve B cells on their cell surface?

A

IgM and IgD

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16
Q

What do plasma cells do?

A
  • Proliferation/Increased Ab production
  • Class switching – specialized effector functions.
  • Affinity Maturation – competition/ mutation
  • Memory (travel to spleen/BM)
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17
Q

Why do B-cells need T-cells?

A

Ab production is weak and short lived with no memory

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18
Q

Methods of adaptive immunity control

A
  • Cytokines (direct/control immune response)
  • Tolerance (central/peripheral)
  • Regulatory cells
  • Activation vs. Anergy/Apoptosis
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19
Q

Loss of control of Adaptive Immunity

A

Hypersensitivity or Autoimmunity

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20
Q

Cytokine for cell-mediated immunity

A

IL-2

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21
Q

Cytokines for Humoral immunity

A

IL-4 and IL-5

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22
Q

IL-2

A
  • Interleukin 2 is produced by T cells, It is the major growth factor for T cells. Also promotes the growth of B cells
  • IL-2 acts on T cells in paracrine/autocrine fashion.
  • Activation of T cells results in expression of IL-2R and the production of IL-2. promotes cell division.
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23
Q

IL-4

A
  • Interleukin 4 is produced by macrophages and Th2 cells.
  • stimulates the development of Th2 cells from naïve Th cells and it promotes the growth of differentiated Th2 cells resulting in the production of an antibody response.
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24
Q

IL-5

A

Interleukin 5 is produced by Th2 cells and it functions to promote the growth and differentiation of B cells and eosinophils. It also activates mature eosinophils.

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25
Q

TGF-Beta

A
  • Transforming growth factor beta is produced by T cells and many other cell types. It is primarily an inhibitory cytokine.
  • It inhibits the proliferation of T cells and the activation of macrophages. It also acts on cells to block the effects of pro-inflammatory cytokines.
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26
Q

INF-y

A
  • Interferon gamma is an important cytokine produced by primarily by Th1 cells, although it can also be produced by Tc and NK cells to a lesser extent.
  • It has numerous functions in both the innate and adaptive immune systems.
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27
Q

Th1 pathogens

A
  • (cell based) geared towards viral/ bacterial attacks in blood/ tissues
  • Polarize cells of adaptive and innate immunity to promote cellular immunity most effective against these invaders –PROINFLAMMATORY
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28
Q

Th2 pathogens

A
  • (humoral-antibody) geared towards parasitic/mucosal infections.
  • ANTIIFLAMMATORY
  • Antibody based
  • basis of hygiene
  • Hypothesis, Allergy IgE
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29
Q

Cytokine Positive feedback

A

Th1/2 cytokines enhance and encourage Th1/2 functions and uncommitted cells (IL-2/IL-4)

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30
Q

Cytokine Negative feedback

A

Th1 inhibits Th2 functions and vice versa (IFNgamma/IL-10)

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31
Q

Central Tolerance

A

T and B cells must not react to self antigens and be restricted to self MHC molecules

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32
Q

Where do Immature T-cells go?

A

They go from bone marrow to the thymus from the blood

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33
Q

How do TCRs remain diverse?

A

They proliferate and rearrange gene segments

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34
Q

Positive selection - MHC

A

Cells that recognize MHC-peptide complexes receive rescue signals that prevent apoptosis

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35
Q

Negative Selection - self cells

A

Cells that survive positive selection exit the thymic cortex to the medulla where they are tested for tolerance to self-antigens

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36
Q

AIRE(autoimmune regulator) gene

A

Causes transcription of a wide selection of organ-specific genes that create proteins that are usually only expressed in peripheral tissues

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37
Q

Fetal development

A

Full complement when born, activity of thymus decreases over time with large drop in thymic function after puberty

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38
Q

B-cells central tolerance

A

Decreased stringency of central tolerances mechanism compared to T-cells. B-cells continue to develop throughout life

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39
Q

Positive B-cell selection

A

Activate B-cell maturation

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40
Q

Negative B-Cell selection

A

Reaction to self

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41
Q

Peripheral Tolerance

A

Naïve T-cells stay in circulation, don’t stay in LN, or tissues so they only encounter a portion of the antigens in our body (compartmentalization)

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42
Q

Cell Anergy

A

Apoptosis; shut off the immune response (indirectly and directly)

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43
Q

Indirect cell anergy

A

Fewer antigens present to stimulate an immune response (DCs die after a few days, without continued support from macrophages and DC activated cells will doe off)

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44
Q

Direct anergy

A

Apoptosis and by molecular inhibition of immune functions (activated T cells are inherently pro apoptotic)
*Tim-3
*PD1/ PD1L
*CTLA-4
All deactivate the immune response

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45
Q

CTLA4-B7 binding

A

Makes less B7 molecules available for interaction with CD28; CTLA:B7 binding represses activation and block CD28 signalling (repression will shut down immune response)

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46
Q

What does the lack of co-receptor signals mean?

A

Anergy/death or compartmentalization

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47
Q

T reg cells

A

T cells that regulate activation of other T cells and necessary to maintain peripheral tolerance to self antigens; Produce cytokines that shut down the immune system

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48
Q

Natural T ref (nTreg)

A

Turn down immune response to self antigens

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49
Q

Inducible or adaptive Treg cells

A

Generated to self and foreign antigen after an inflammatory immune response

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50
Q

Hypersensitivity reactions

A

Allergy (Environment) and Autoimmunity (Self)

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51
Q

Types of hypersensitivity reactions

A
  • Type I: Allergy (immediate)
  • Type II: Cytotoxic
  • Type III: Immune complex
  • Type IV: Delayed hypersensitivity or cell-mediated hypersensitivity
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52
Q

Allergy response

A

IgE loading on mast cells, basophils, and eosinophils (mild reaction; rash, itching, swelling)

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53
Q

Allergy treatment

A

Environmental control, antihistamines, steroids, leukotriene inhibitors, allergen immunotherapy. Antihistamine drugs often relieve many allergic symptoms; histamine is one of the mediators released from IgE-coated cells

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54
Q

Anaphylaxis

A

Hypersensitivity reaction that may be life-threatening (fall in blood pressure and severe respiratory distress); Systemic response: peanuts, Bee sting, penicillin allergy
Require epinephrine to treat

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55
Q

Biphasic anaphylaxis reaction

A

Have a less severe initial reaction and 24hrs later have a much worse one

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56
Q

Atopic person

A

Allergy prone individual

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57
Q

Environmental susceptibility

A

Hygiene hypothesis (overly clean can make you more susceptible to illness)

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58
Q

Type 2: Cytotoxic

A

Antibody dependent (IgM, IgG) that combine with tissue or cell antigen creating lysis of cell or other membrane damage (examples: Autoimmune hemolytic anemia, blood transfusion reactions, Rh hemolytic disease, autoimmune glomerulonephritis)

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59
Q

Type 3: Immune complex

A

Ag-Ab immune complexes deposited in tissues activate complement pathway; Neutrophils attracted to site, causing tissue damage (examples: Rheumatoid arthritis, systemic lupus erythematosus (SLE), some types of glomerulonephritis)

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60
Q

Type 4: Cell-mediated, delayed hypersensitivity

A

Typically after 24-48 hours T lymphocytes are sensitized and activated on second contact with same antigen which induces inflammation and activates macrophages through lymphokines (Example: contact dermatitis, Diabetes Mellitus (T1), Rheumatoid arthritis)

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61
Q

Treatment for autoimmune disease

A

Various immune suppressing drugs/therapies (Corticosteroids, cytotoxic drugs, NSAIDS, immunotherapy with various biologics, antibody treatments (monoclonal – blocking or IVIG), symptomatic)

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62
Q

When can autoimmunity occur?

A

-Individual express MHC molecules that efficiently present self peptides (Two particular types of MHCII increase chance of type1 diabetes by 20 fold)
-Production of T and/or B cells that have receptors that recognize self (Random mix match, even identical twins will not share TCR repertoires (chance))
-Breakdown of tolerance mechanisms designed to eliminate these cells

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63
Q

Potential causes of Autoimmunity

A

*Defects in central tolerance deletion/ survival
*Defects in T Reg function/ numbers
*Defective apoptosis mechanisms (+ve/-ve)
*Inadequate inhibitory receptor functions (CTLA/ Fas)
*Chronic activation of APC’s, excessive T cell activation

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64
Q

Autoimmunity development

A
  1. Genetic susceptibility
  2. Failure of self tolerance/immune control
  3. Infection/ injury
  4. Activation of APC’s
  5. Recruitment of auto-reactive
    lymphocytes
  6. Activation of auto-reactive Lymphocytes
  7. Tissue injury from auto immune attacks
  8. Auto immune disease
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65
Q

Insulin dependent diabetes mellitus

A

Immune system targets insulin producing Beta cells in the pancreas (Islets of Langerhans) which is mediated by CTL activity, Dysfunctional natural Treg cells.

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66
Q

Myasthenia Gravis

A

Self reactive antibodies bind to acetylcholine receptors which results in muscle weakness and paralysis

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67
Q

Multiple Sclerosis

A

CNS inflammatory disease that is initiated by reactive T cells/ Macrophages causing chronic inflammation destroys myelin sheath protein, causing defect in sensory inputs

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68
Q

Rheumatoid Arthritis

A

Systemic autoimmune disease; Cartilage protein targeted causing chronic joint inflammation (IgM, IgG antibody complexes form in joints)

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69
Q

Lupus Erythematosus

A

Systemic: rash (forehead/ cheeks), inflammation of lungs, kidneys, joints, paralysis, convulsions; Breakdown in both T an B cell tolerance (lack of activation cell death may play a role)

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70
Q

Genetic mutations associated with Autoimmune disorders include dysregulation of

A

-Treg (FoxP3)
-Cell activation (IL-2, IL-12, CD2/58, Blk)
-Activation inhibitors (IL-10, CTLA4)
-Apoptosis (Bim, Fas)
-HLA alleles (MHC)

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71
Q

Which gender usually has an autoimmune disease

A

Women (80%), when makes get it they’re more severe

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72
Q

Autoimmune treatment

A

Symptomatic/ Immunosuppression Drugs:
-Corticosteroids/anti-inflammatory
-Chemical T cell/ B cell inhibitors/Cytokine blockers (IL-2)
-mAb to block immune receptors on T/B cells or cytokines (TNFa)
-Pain control/physical therapy
-IVIG – block Fc receptors on cells

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73
Q

Communicable disease

A

Disease transmitted from person to person

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74
Q

Endemic

A

Communicable diseases in which a small number of cases are continually present in the population

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75
Q

Epidemic

A

Communicable diseases concurrently affecting large numbers of people in a population (contained to a defined geographic area)

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76
Q

Pandemic

A

Global, world-wide outbreak across several countries or continents

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77
Q

Direct Transmission

A

Direct physical contact (sex) and Droplet spread (coughing, sneezing)

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78
Q

Indirect transmission through an intermediary mechanism

A

Contaminated food or water
Insects (vector)

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79
Q

Methods of Disease Control

A

Immunization (Active), Plasma containing antibodies/Maternal transmission (Passive), Identification, Isolation, treatment, controlling means of transmission (mask wearing), controlling indirect transmission for contaminated food or water

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80
Q

Isolation

A

Promptly carried out to shorten the time in which others may be infected, Isolation prevents contact with susceptible persons and stops spread

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81
Q

Food or water contamination control

A

Chlorination of water supplies, Effective sewage treatment facilities, Standards for handling, manufacturing, and distributing commercially prepared foods, Eradication and/or control of animal sources and vectors, Physical barriers - nets

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82
Q

Bubonic Plague

A

The black death has a 70% death rate without treatment, and 10% with treatment, one of the most deadly diseases, carried by rodents

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83
Q

STIs

A

Spread primarily by sexual contact (examples: Syphilis, Gonorrhea, Herpes, Chlamydia)

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84
Q

Primary Syphilis

A

Penetrates mucous membranes of the genital tract, oral cavity, rectal mucosa, or through the break in skin; multiplies rapidly throughout the body; forms a chancre (small ulcer) found on the penis, vulva, vagina, oral cavity, or rectum; occurs for 4-6 weeks and can heal without treatment

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85
Q

Secondary Syphilis

A

Systemic infection with skin rash and enlarged lymph nodes (develops after 4-10 wks typically lasts 2-3 years); begins after the chancre has healed and is accompanied with fever, lymphadenopathy, skin rash, shallow ulcers on mucous membranes of oral cavity and genital tract; can subside without treatment

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86
Q

Tertiary Syphilis

A

Late destructive lesions in internal organs (3-15y develops in 15-40% of cases); not generally communicable, Organisms remain active, causing irreparable organ damage due to chronic inflammation; Neuro and ocular syphilis are common in this stage

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87
Q

How to diagnose syphilis

A

Microscopic exam (Detection of Treponema from fluid squeezed from chancre) and Serologic tests (antigen–antibody reactions; Turns positive soon after chancre appears and remains positive for years)

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88
Q

Congenital Syphilis

A

Transmission from mother to child could cause the death of the fetus

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89
Q

When do gonorrhea symptoms occur?

A

A week later

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90
Q

Gonorrhea

A

Neisseria gonorrhoeae infection; Primarily infects mucosal surfaces: Urethra, genital tract, pharynx, rectum

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91
Q

Gonorrhea in females

A

Infects mucosa of the uterine cervix and urethral mucosa; profuse vaginal discharge from cervical infection; can be asymptomatic; Infection may spread to fallopian tubes (Salpingitis)

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92
Q

How does gonorrhea manifest

A

Abdominal pain and tenderness, Fever, Leukocytosis

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93
Q

Gonorrhea in males

A

Acute inflammation of the mucosa of anterior urethra, Purulent urethral discharge, Pain on urination, Less likely to be asymptomatic in males than females

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94
Q

Extragenital gonorrhea

A

In the rectum; Pain and tenderness; purulent bloody mucoid discharge (anal sex) or Pharynx and tonsils (Oral-genital sex acts)

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95
Q

Disseminated gonococcal infection

A

Organisms gain access to the bloodstream and spread throughout body; Fever; joint pain; multiple small skin abscesses; infections of the joints, tendons, heart valves, meninges

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96
Q

Diagnosis and treatment

A

Culture swab (Suspected sites: Urethra, cervix, rectum, pharynx, Blood in disseminated infections)
Nucleic acid amplification test: Based on the identification of nucleic acids in the organism
Treatment: Antibiotics - cefriaxone (some strains are penicillin resistant

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97
Q

Type 1 Herpes simplex virus infection

A

Infects oral mucous membrane and causes blisters; usually infected in childhood, most adults have antibodies to the virus; It may cause genital infections

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98
Q

Type 2 Herpes simplex virus infection

A

Infects genital tract and infections usually occur after puberty; Causes 80% of infections – a higher rate of recurrence, 20% of type 1 due to oral-genital sexual practices and may infect oropharyngeal mucous membranes

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99
Q

Herpes Manifestation

A

Vesicles (Small external painful blisters) and shallow ulcers following sexual exposure, Men (Glans or shaft of the penis), Women (Vulva - painful, Vagina or cervix - little discomfort)

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100
Q

Herpes diagnosis

A

Intranuclear inclusions in infected cells, Viral cultures from vesicles or ulcers most reliable diagnostic tests, and Serologic tests in some cases

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101
Q

Herpes Treatment

A

Antiviral drug shortens the course and reduces the severity, but does not eradicate the virus (orally, per IV, or topically), Cold compress and pain relievers, Deliveries should be done by cesarean section

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102
Q

Chlamydia trachomatis infection

A

Most common STD, 3 to 4 million cases per year

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103
Q

Chlamydia clinical manifestations

A

Similar to gonorrhea (infection can spread to fallopian tubes to have similar effects), many are asymptomatic

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104
Q

Chlamydia in Women

A

Cervicitis and urethritis, involving the uterine cervix, and urethra; moderate vaginal discharge (Major complications: sterility)

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105
Q

Chlamydia in Men

A

Nongonococcal urethritis, acute urethral inflammation with frequency and burning on urination (Major complications: epididymitis)

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106
Q

Chlamydia Diagnosis

A

Detection of chlamydial antigens in cervical or urethral secretions, Fluorescence microscopy
Cultures (swabs), Nucleic acid amplification tests: based on chlamydial nucleic acids

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107
Q

Chlamydia Treatment

A

Antibiotics (azithromycin/doxycycline)

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108
Q

Condylomata

A

Anal and genital warts - HPV

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109
Q

Trichomonal vaginitis

A

Trichomonas vaginalis infection (protozoan parasite)

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110
Q

Scabies and crabs

A

Microscopic mites

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111
Q

HIV Virus

A

Attacks the immune system, specifically destroying CD4 T cells, leads to the development of Acquired Immuno Deficiency Syndrome which increases susceptibility to pathogens and opportunistic infections.

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112
Q

Genetic material and Proteins in the HIV virus

A

9 kb Genome, ssRNA retrovirus (+ve), codes for 9 proteins, 2 structural proteins (Gag and Env), 1 enzymatic protein (Pol), 6 regulatory proteins (Tat, Rev, Nef, Vif, Vpr, and Vpu)

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113
Q

HIV Transmission

A

Sexual contact, Blood and body fluids (seminal, vaginal), Mother to infant (HIV primarily infects CD4 T-cells through interactions with CD4 receptors on the cell surface and GP120 spikes on virus

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114
Q

HIV Direct inoculation

A

Intimate sexual contact, linked to mucosal trauma from rectal intercourse

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115
Q

HIV Transfusion

A

Contaminated blood or blood products, lessened by routine testing of all blood products, Sharing of contaminated injection needles, Transplacental or postpartum transmission via cervical or blood contact at delivery and in breast milk

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116
Q

HIV steps of infection

A
  1. HIV cannot multiply alone. It must be inside a cell before it can make copies of itself.
  2. When HIV infects a cell, it hijacks its machinery.
  3. In the host cell, HIV makes copies of itself.
  4. These newly created virus particles can then go infect other cells.
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117
Q

HIV life cycle

A

Binds to CD4 and enters the cell, reverse transcriptase converts RNA into DNA (errors and mutations occur in this step), DNA is then transported into the nucleus, intergrase integrates the viral DNA into the host cell’s genome (can be inactive), once activated genes are transcribed and viral RNA is transported to the cytoplasm, proteins are translated and cleaved by a protease, virions are released at the membrane, T-cells are activated and support the infection

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118
Q

HIV replication and Genetic Variability

A

Fast replication and high mutation rate (1/cycle). This provides an adaptive advantage to HIV

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119
Q

What mutants are immune to infection with HIV?

A

CCR5 (highly expressed in macrophages)

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120
Q

CD4 T-cells abnormalities

A

Depletion/cell death, reduced proliferation /regeneration, destruction by infection, indirect and direct destruction by viral proteins

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121
Q

HIV to AIDS

A

A healthy individual has between 800 and 1500 CD4T cells in 1 µL of blood. Immune deficits start to emerge below 500 (HIV/other autoimmune diseases), Once this number drops below 200, the individual is described as having AIDS.

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122
Q

Cytopathic effects of HIV

A

Cell-cell fusion, accumulation of unintegrated viral DNA, alteration of cell permeability lipids, apoptosis, the release of toxic cytokines by infected cells, destruction of immune responses, inhibition of growth factors, degradation of RNA which reduces protein synthesis

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123
Q

CD8 T-cells are destroyers using…)

A

Cell-to-cell contact and secreted factors destroy infected cells (Perforin/Granzyme A, B) and inhibit virus production/promote immune activation (IFNy, TNFa, IL-2, MIP1a/b, RANTES)

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124
Q

What is CTL dysfunction caused by?

A

Cytokine/ receptor dysregulation, Direct effect of HIV soluble factors, Cell death/ apoptosis, Other immune cell dysfunction, Anergy

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125
Q

What is Anti-HIV CTL (CD8) activity associated with?

A

LTNP/Elite controllers (some control of the HIV infection and slower disease progression)

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126
Q

Early vs. Late Manifestations of HIV infection

A

Early (Asymptomatic, mild febrile illness) and Late (Generalized lymph node enlargement, nonspecific symptoms, fever, weakness, chronic fatigue, weight loss, thrombocytopenia, AIDS)

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127
Q

Antibody response to HIV

A

Antibodies are formed within 1 to 6 months, Detection of antibodies provides evidence of HIV infection, Antibodies do not eradicate virus, Virus is detectable by laboratory tests (viral RNA)

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128
Q

Signs and Symptoms of AIDS

A

An infected person usually experiences a mononucleosis-like syndrome that may be attributed to the flu or another virus (may be asymptomatic for years)

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129
Q

Non-specific symptoms of AIDS

A

Weight loss, fatigue, night sweats, and fever

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130
Q

Viral replication

A

Measure the amount of viral RNA in the blood (Virus replicates in lymph nodes, but the amount of viral RNA in blood reflects extent of viral replication in lymphoid tissue)

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131
Q

Treatment for HIV and AIDS

A

No cure for AIDS, antiretroviral agents inhibit HIV viral replication

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132
Q

HIV Treatment groups

A

Nonnucleoside reverse transcriptase inhibitors, Nucleoside reverse transcriptase inhibitors (nucleoside analogs), Protease inhibitors, Integrase inhibitors

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133
Q

Protease Inhibitors

A

Block the action of viral protease in viral replication; cut viral protein into short segments to assemble around viral RNA to form infectious particles

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134
Q

PrEP

A

HIV prevention treatment

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135
Q

Pathogenic Organism types

A

Bacteria, Viruses, Fungi

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136
Q

Bacteria types

A

Chlamydiae, Rickettsiae and Ehrlichiae, and Mycoplasma

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137
Q

Classification of Bacteria

A
  • Shape and arrangement(coccus, bacillus, spiral), Gram strain reaction (Gram-positive and Gram-negative)
  • Biochemical and growth characteristics (Aerobic and anaerobic, spore formation, and biochemical profile)
  • Antigenic structure (antigens in the cell body, capsule, flagella (motility)
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138
Q

Bacteria Genomic Sequence

A

16S ribosomal RNA, proteins and peptides are seen

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139
Q

Coccus (Spherical) Bacteria

A

Clusters: Staphylococci
Chains: Streptococci
Pairs: Diplococci
Kidney bean-shaped (in pairs: Neisseriae)

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140
Q

Bacillus (rod-shaped) Bacteria

A

Square ends: Bacillus anthracis (anthrax)
Rounded ends: Mycobacterium tuberculosis (TB)
Club shaped: Corynebacterium (Diptheria)
Comma shaped: Vibrio (Cholera)

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141
Q

Spiral Organisms

A

Tightly coiled: Treponema pallidum (Syphilis)
Relaxed coil: Borrelia (Lyme)

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142
Q

Steps of Gram-Staining

A

Step 1: Crystal violet (purple dye) – stains peptidoglycan
Step 2: Gram iodine (acts as a mordant)
Step 3: Alcohol or acetone (rapid decolorization)
Step 4: Safranin (red dye)

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143
Q

How do gram positives stain?

A

Resists decolorization and retains the purple stain (cell wall is composed of multiple peptidoglycan layers combined with teichoic acid; lipopolysaccharide absent)

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144
Q

How do gram negatives stain?

A

Can be decolorized and stained red (the cell wall is composed of a thin peptidoglycan layer and lacks teichoic acid; lipopolysaccharide present)

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145
Q

True or False: All bacteria can be stained

A

False; Mycobacterium has no cell wall and is unable to be stained

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146
Q

Cocci Gram-Positive

A

Staphylococci, Streptococci, Pneumococci

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147
Q

Cocci Gram-Negative

A

Gonococci and Meningococci

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148
Q

Bacilli Gram-Positive

A

Corynebacteria, Listeria, Bacilli, Clostridia (Oxygen and spore forming)

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149
Q

Bacilli Gram-Negative

A

Haemophilus, Gardnerella, Francisella, Yersinia, Brucella, Legionella, Salmonella, Shigella, Campylobacter, Cholera bacillus, Colon bacillus (E. coli + related organism)

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150
Q

Spiral organisms (Gram-Negative only)

A

Treponema pallidum and Borrelia burgdorferi

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151
Q

Acid-fast organisms (Gram-Positive only)

A

Tubercle bacillus and Leprosy bacillus

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152
Q

Staphylococci

A

Gram-positive cocci in Grapelike clusters found in the skin (epidermis) or the nasal cavity (aureus); normally not pathogenic but opportunistic

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153
Q

Staphylococci pathogenic strains cause

A

Vomiting and diarrhea, toxic necrosis, tissue necrosis, hemolysis, inflammation (distinguished by culture on blood agar plates)

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154
Q

Staphylococci Infections

A

Impetigo, boils, nail infection, cellulitis, surgical wound infection, eye infection, postpartum breast infections, Abscess

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155
Q

A drug-resistant strain of Staphylococci

A

Methicillin-resistant Staphylococcus aureus, or MRSA (antibiotic-resistant)

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156
Q

Streptococci are found…

A

Gram-positive cocci arranged in chains or pairs, normal inhabitants of skin, mouth, pharynx (Streptococcus viridans), gut, female genital tract (peptostreptococci); opportunistic organisms

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157
Q

Streptococci Diseases

A

3 types: pyogenic, toxigenic, and immunologic

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158
Q

Pyogenic Streptococci Diseases

A

Pharyngitis, cellulitis, endocarditis, urinary tract infection

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159
Q

Toxigenic Streptococci Diseases

A

Scarlet fever, toxic shock syndrome

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160
Q

Immunologic Streptococci Diseases

A

Rheumatic fever, glomerulonephritis (induce hypersensitivity)

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161
Q

Streptococci Classification

A

Lancefield classification groups A to V (Most significant: A, B, D)

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162
Q

Group A Streptococci

A

Many pathogenic strains (Streptococcus pyogenes): cause pharyngitis, strep throat, tissue infections (necrotizing fasciitis, gangrene)

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163
Q

Group B Streptococci

A

(Streptococcus agalactiae): Anal/Genital tract of women, neonatal transmission risk, meningitis, sepsis

164
Q

Group D Streptococci

A

Enterococcus faecalis, Streptococcus bovis): Urinary, biliary, and cardiovascular infections – difficult to treat and Ab resistant

165
Q

Beta hemolysis

A

Complete lysis of red cells

166
Q

Non-beta hemolysis (2 types)

A

Alpha hemolysis: Incomplete lysis of red cells (Streptococcus pneumoniae, Strep mutans (tooth decay)
Gamma hemolysis: Nonhemolytic, no lysis

167
Q

Non-pathogenic Gram-positive bacilli

A

Corynebacteria are found in the skin except for C. diphtheria (Ulcers in the throat and injured heart + nerve tissue)
Listeria monocytogenes (a food contaminant found in nature - can cause systemic illness leading to meningitis)

168
Q

Pathogenic Gram-positive bacilli

A

Bacillus anthracis (Anthrax); Spores are spread through inhalation (can remain as spores) and spread rapidly in alveoli, germinate in the lymph nodes, and produce toxins (fever, chest pain, 20% fatality without treatment in days)

169
Q

Bacillus anthracis (Anthrax) Treatment

A

Requires long courses AB treatment

170
Q

Gas gangerne (Clostridium perfringens)

A

Contaminate wounds, proliferate in dead/necrotic muscle tissue (ferment necrotic tissue), releasing tissue-destroying toxins with systemic effects (sepsis). Toxins also cause neutrophil lysis

171
Q

Tetanus (C. Tetani)

A

Produces neurotoxin that causes sustained muscular contractions (bone fractures), Symptoms days to weeks after exposure, Fatal due to effect on respiratory muscles

172
Q

Botulism (C. botulinum)

A

Food poisoning from toxin ingestion of improperly cooked/ stored food, infants particularly susceptible, produces neuroparalytic toxins – pathology not caused by infection

173
Q

Intestinal infection (C. Diff)

A

Hard to get rid of due to antibiotic resistance (broad spectrum Ab use)

174
Q

Hemophilus Influenzae

A

Gram -ve; Variety of infections lung, CNS, Skin, blood

175
Q

Yersinia pestis

A

Gram -ve; Plague

176
Q

Salmonella, Shigella, Campylobacter

A

Gram -ve; Food poisoning - GI infection

177
Q

Legionella (Legionnaire’s disease)

A

Gram -ve; severe pneumonia

178
Q

Vibrio Cholerae (Cholera)

A

Gram -ve; severe, acute watery diarrhea

179
Q

Helicobacter pylori

A

Gram -ve; stomach inflammation - Ulcers

180
Q

E.coli

A

Gram -ve; Common to GI tract residents but some strains that are ingested by raw/uncooked animal products (typically can develop toxic effects including inflammation, anemia, bloody diarrhea and abdominal pain.

181
Q

Spiral organisms diseases

A

Syphilis (Tremponema pallidium), Lyme disease, Acid-fast bacteria, and Leprosy

182
Q

Lyme disease (Borrelia burgdorferi) + how does it spread?

A

Transmitted though infected tick bite to spread throughout the body
3 stages:
Stage 1: circular “bulls eye” rash accompanied with flu like symptoms
Stage 2: cardio (heart palpitations), neuro (meningitis, facial paralysis) and joint pain
Stage 3: chronic arthritis and neuro deficits (memory, fatigue, insomnia)

183
Q

Acid-fast bacteria

A

Hard to stain due to waxy coat; causes granulatomas inflammation (Macrophage infection) and TB (Mycobacterium tuberculosis) which primarily infects lungs

184
Q

Leprosy (Mycobaterium leprae)

A

The infection leads to skin lesions, peripheral nerve damage (lack of sensation, muscle weakness, vision loss); low infectivity and pathogenicity; inflammation of Schwann cells causes most of the damage

185
Q

Chlamydiae

A

Gram-negative, nonmotile bacteria, obligate intracellular parasites, rigid cell wall, no vaccine available for treatment

186
Q

Chlamydial Diseases

A

Psittacosis (pneumonia): Inhalation of dried bird feces
Trachoma (Chlamydia trachomatis A, B, C): Chronic conjunctivitis, blindness
Nongonococcal urethritis (men): Spread to other areas
Cervicitis (women): Lead to salpingitis, pelvic inflammatory disease, infertility, ectopic pregnancy
Neonatal inclusion conjunctivitis: Newborn from infected mother

187
Q

Rickettsiae and Ehrlichiae

A

Obligate intracellular parasites (typically endothelial cells)– both transmitted by insect bites and respond to some antibiotics

188
Q

Rickettsia Disease

A

Infects, proliferates endothelial cells in small blood vessels of skin - causing damage, leakage of blood into surrounding tissues (rash and edema)

189
Q

Rocky Mountain Spotted Fever (ticks)

A

East Coast spring and early summer; flu-like and Rash after 2 to 6 days on hands and feet then the trunk, affects CNS

190
Q

Rickettsialpox (mites from mice) symptoms

A

flu like symptoms, full-body rash

191
Q

Typhus symptoms and illnesses

A

Flu-like, rash (epidemic: lice; endemic: fleas, mites)

192
Q

Ehrlichiosis Transmission and Symptoms

A

Transmitted via the bite of an arthropod vector (ticks, mites, lice, fleas), Infect and multiply in neutrophils or monocytes, Cause febrile flu-like (muscle aches, chills) illness with skin rash, Transmission enhanced by poor hygiene, overcrowding, wars, poverty

193
Q

Primary atypical pneumonia (+Symptoms and treatment)

A

Mycoplasma pneumoniae; Most common in winter, young adults, outbreaks in groups; Cough, sore throat, fever, headache, malaise, myalgia, Resolves spontaneously in 10 to 14 days and responds to antibiotics: Tetracycline and erythromycin

194
Q

Viruses’ Nucleic acid structure

A

Either DNA or RNA (ss,ds, +/-ve), enclosed in a capsid, with an outer envelope made of lipoprotein (often from host cell)

195
Q

Virus size

A

Smaller than cells (20 to 300 nm diameter) and cannot be seen under a light microscope

196
Q

Nucleoid

A

Genetic material, DNA or RNA, not both (centre of virus)

197
Q

Capsid

A

Protective protein membrane surrounding genetic material in virus

198
Q

Coat/Envelope

A

Surrounds the virus (combination of host membrane and viral proteins (retrovirus)) - non-enveloped viruses, adenovirus, exist

199
Q

True or False: Viruses lack metabolic enzymes

A

True, they rely on the host’s metabolic processes for survival

200
Q

HIV

A

destruction of the immune system

201
Q

HPV

A

proliferation and neoplasia

202
Q

Ebola

A

acute cell necrosis and degeneration

203
Q

HCV

A

slowly progressive cell injury

204
Q

HSV, VZV: Herpes Zoster/Shingles

A

Invades a susceptible cell, Asymptomatic latent viral infection

205
Q

Modes of action in various viruses

A

Invades a susceptible cell, Asymptomatic latent viral infection (HSV, VZV: Herpes Zoster/Shingles) – dormant in neural cells
Acute cell necrosis and degeneration (Ebola)
Cell hyperplasia
Proliferation and Neoplasia(HPV)
Slowly progressive cell injury (HCV)
Destruction of the immune system (HIV)

206
Q

Bodily defences against viral infections

A

(Innate/Adaptive) formation of interferons: Broad-spectrum antiviral agent inhibits viral replication (non-specific), activates immune cells
- Cell-mediated Immunity
- Humoral defences

207
Q

What do anti-viral agents do?

A

Block viral replication (HIV/HCV), prevent the virus from invading cells (HIV) - the best defence is a vaccination for community and personal immunity

208
Q

Fungi

A

Plantlike organisms without chlorophyll, are obligate aerobes

209
Q

Types of Fungi

A

Yeast (small ovoid/spherical), mold - spoilage of foods (branching/filamentous), Bread, cheese, wine, and beer production

210
Q

Fungi cell wall vs. bacteria cell wall

A

Chitin vs. peptidoglycan

211
Q

Fungi vs. bacteria cell membrane

A

Erogosterol and zymosterol vs. cholesterol

212
Q

Fungi growth factors

A

High humidity (moist), heat, dark areas with oxygen supply

213
Q

How can Fungi cause disease

A

Present in natural habitat and can cause chronic disease, become opportunistic in immunocompromised, lose regular flora due to antibiotics, cause superficial skin infections

214
Q

Fungi treatment

A

Antifungal drugs or topical treatment in mild cases

215
Q

Mucous membranes (Candida albicans)

A

Common in immunocompromised patients with
fungal infection on tongue, mouth, esophagus (thrush)

216
Q

Aspergillus fumigatus

A

Spores from decaying plant matter can result in severe pulmonary and systemic disease in immunocompromised, asthma can develop

217
Q

Histoplasmosis, coccidioidomycosis, blastomycosis, cryptococcosis

A

Inhaled spores from dust; usually acute, self limited respiratory infection, involve blood vessels in severe cases (systemic disease)

218
Q

Antibiotics mechanism

A

Inhibits synthesis of the bacterial cell wall (leads to swelling-rupture), inhibits bacterial metabolic functions, and cell membrane(injury-death)

219
Q

Penicillin family

A

Penicillin, methicillin, nafcillin, oxacillin, amoxicillin, ampicillin, piperacillin, ticarcillin

220
Q

Cephalosporins

A

Cephalexin, cefoxitin, ceftazidime, ceftriaxone; vancomycin, bacitracin

221
Q

Chloramphenicol

A

Tetracycline; macrolide; erythromycin, azithromycin, clarithromycin; clindamycin, gentamicin, netilmicin, streptomycin

222
Q

Antibodies that inhibit bacterial DNA synthesis

A

Ciprofloxacin, norfloxacin, ofloxacin

223
Q

Antibiotic Sensitivity Tests: Tube dilution

A

Measures the highest dilution that inhibits growth in test tube

224
Q

Antibiotic Sensitivity Tests: Disk method

A

Inhibition of growth around the disk indicates sensitivity to antibiotic

225
Q

Antibiotic Sensitivity Tests: MALDI-TOF-MS

A

Identification of strains with known antibiotic-resistance characteristics

226
Q

What do tetracycline levels test?

A

Kidney Function

227
Q

Adverse effects antibiotics

A

Toxicity, hypersensitivity (allergy), alteration of normal bacterial flora (resistance)

228
Q

Development of resistant bacteria

A

Spontaneous mutation and Plasmid-acquired resistance

229
Q

Mechanisms for circumventing effects of antibiotics

A

Develop antibiotic enzymes (penicillinase), Change cell wall structure (repel Ab), and change internal metabolic machinery (Ab loses function/binding)

230
Q

Cause of antibiotic resistance

A

Over-prescribing of antibiotics, patients not finishing their treatment, poor infection control in hospitals and clinics, over-use of antibiotics in livestock and fish farming, lack of hygiene and poor sanitation, lack of new antibiotics being developed

231
Q

Mechanisms of control for cell growth

A

Constant renewal (Hair follicles, gut lining), Stable, but can renew when stimulated (T-cells), Permanent, therefore, no renewal (cardiac muscle)

232
Q

How is cancer developed?

A

Loss of control of cell division/ mutation of a gene

233
Q

Characterization of Cancer tumours

A

Benign vs. Malignant
Solid vs. Invasive
In situ vs. Infiltrating

234
Q

Benign Tumor characteristics (Growth rate, Character of growth, Tumor spread, Cell differentiation)

A

Growth rate: Slow
Character of growth: Expansion
Tumor spread: Localized (Brain tumors can do damage while being benign)
Cell differentiation: Well differentiated

235
Q

Malignant Tumor characteristics (Growth rate, Character of growth, Tumor spread, Cell differentiation)

A

Growth rate: Fast
Character of growth: Infiltration
Tumor spread: Metastasis by bloodstream and lymphatics (establish secondary sites)
Cell differentiation: Poorly differentiated

236
Q

Benign tumor classification

A

The cell of origin (Prefix-) and -oma (suffix)

237
Q

Malignant tumor classification

A

3 groups (carcinoma, sarcoma, leukemia/lymphoma)

238
Q

Carcinoma cancer

A

Most common (85% of tumors); Epithelial tissue (arises from the surface, glandular or parenchymal epithelium) and spreads through lymph nodes

239
Q

Adenocarcinoma

A

Subtype of carcinoma cancer (ex. pancreas - glandular/ secretory cells)

240
Q

Squamous cell carcinoma

A

Subtype of carcinoma cancer found on skin

241
Q

Sarcoma cancer

A

Less common; Arise from connective tissue, endothelium, and mesothelium and spreads rapidly through the bloodstream

242
Q

Fibrosarcoma

A

A subtype of sarcoma cancer affects fibroblasts

243
Q

Myosarcoma

A

A subtype of sarcoma cancer affects muscles

244
Q

Leukemia

A

Neoplasm of blood cells; non-solid tumors and overgrows and crowds out normal blood-forming cells

245
Q

What happens if neoplasm cells populate LN and spleen

A

Lymphoma (T cell/ B cell)

246
Q

Neoplasm development

A

A stepwise process that involves ongoing series of genetic changes over time (activation of oncogenes, loss of function of one or more tumor suppressor genes, and additional random genetic changes)

247
Q

What does cancer in stem cells cause?

A

A tumor with a high degree of heterogeneity

248
Q

True or False: Fast-growing neoplasms may outgrow the blood supply

A

True, this can be used as a therapeutic target

249
Q

True or False: Tumors have their own blood supply

A

False, tumors derive blood supply from tissues they invade

250
Q

Angiogenesis

A

Malignant tumors frequently induce new blood vessels to proliferate in adjacent normal tissues to supply the demands of the growing tumor

251
Q

Necrosis in parts of malignant tumors

A

When the tumor outgrows its blood supply part with the poorest blood supply undergoes necrosis

252
Q

The blood supply in tumors in the lung

A

Blood supply is best at the periphery of the tumor and poorest at the center (central necrosis)

253
Q

The blood supply in tumors growing outward from an epithelial surface (ex. colon)

A

The best blood supply is at the base and the poorest at the surface (peripheral necrosis)

254
Q

How can genetic change occur in cancer-causing genes?

A

Radiation, carcinogens, viruses – failure of DNA repair/fidelity mechanisms, Failure of Immune defences, over time these can accumulate (age-dependent), can also be inherited susceptibilities to developing cancer

255
Q

Proto-oncogene

A

Philadelphia chromosome – seen in chronic granulocytic leukemia (translocation of pieces of chromosome 9 and 22); a very aggressive cancer

256
Q

Loss of apoptotic control leads to…

A

Uncontrolled cell growth and cells eventually form a tumor

257
Q

Tumor-suppressor genes

A

Genes (expressed in pair of homologous chromosomes) that inhibit/control cellular division/proliferation; prevent DNA replication (ex. APC, DCC, p53)

258
Q

What virus causes leukemia and lymphoma?

A

T cell leukemia–lymphoma virus (HTLV-1) that is related to the AIDS virus (tax onocogene)

259
Q

What virus causes Kaposi sarcoma?

A

Human herpesvirus 8 (HHV-8)

260
Q

What virus causes Condylomas (warts)

A

Papilloma virus (HPV); predisposes to cervical carcinoma

261
Q

What virus causes Chronic viral hepatitis

A

Hepatitis B and C viruses (chronic inflammation/repair)

262
Q

What virus causes Nasopharyngeal carcinoma

A

Epstein-Barr virus also causes infectious mononucleosis

263
Q

Which immune cells detect and destroy cancerous cells?

A

CD8 T-cells and NK cells

264
Q

Which cancers do those with severe immunodeficiency have an increased risk of?

A

Blood and skin cancers

265
Q

True or False: All mutations that cause cancers are directly related

A

False, Most mutations that cause cancer are not directly inherited (it can influence it, ex. only 10% of breast cancer cases linked to genetic mutations)

266
Q

Which abnormal gene causes an 80% risk of breast cancer by age 90

A

BRCA1/2 DNA repair genes

267
Q

Neurofibromatosis

A

increased production of benign tumours of the nerves that have an increased risk of malignancy (autosomal dominant)

268
Q

Actinic keratoses

A

Small, crusted, scaly patches that develop on sun-exposed skin; may develop into cancer if untreated

269
Q

Lentigo maligna

A

The freckle-like proliferation of melanin-producing cells that may develop on sun-exposed skin; may transform into melanoma

270
Q

Leukoplakia

A

Thick white patches in the mucous membranes of the mouth from exposure to tobacco tars from pipe or cigar smoking or smokeless tobacco (may give rise to squamous cell cancers of the oral cavity)

271
Q

Diagnosis of Tumors

A

Recognize early warning signs and symptoms, Complete medical history and physical examination, screening early (need to consider invasiveness/severity, cost/benefits), Surface – Visual, Orifice (opening) – Endoscopy, Internal – CT scan/MRI, Lab procedures

272
Q

Cytologic diagnosis

A

Fine needle aspiration, biopsy (many organs – precise location of tumor by CT, Xray or US)

273
Q

Histology

A

Frozen section Slides prepared and stained – rapid histological diagnosis in minutes

274
Q

Abnormal smear

A

Slides of abnormal cells shed from surface of tumors

275
Q

Tumor-associated antigen tests

A

Some cancers secrete substances that can be detected in the blood by lab tests (Carcinonembryoic antigen, Alpha-fetoprotein, Human chorionic gonadotropin, Acid phosphatase)

276
Q

Carcinoembryonic antigen (CEA)

A

Produced by most malignant tumors of the GI tract, pancreas, breast

277
Q

Alpha-fetoprotein

A

Normally produced by fetal tissues in the placenta but not adult cells

278
Q

Human chorionic gonadotropin

A

Normally produced by the placenta in pregnancy

279
Q

(PSA test) Acid phosphatase

A

Normally produced by prostate epithelial cells

280
Q

Treatments of tumor

A

Surgery, TNM Classification, Staging I-IV, Radiotherapy, Hormones (Corticosteroids), Chemotherapy (anti-cancer drugs), Adjuvant chemotherapy,

281
Q

TNM Classification

A

T- size 1-4, N spread to regional LN 1-3, M distant metastasis 0-2

282
Q

Staging I-IV

A

Early, localized, regional spread, distant spread

283
Q

Chemotherapy

A

Lasts 3-6 months (4-8 cycles of 3-4 weeks), 3 stages: Induction (1 month intensive) /Consolidation (few months) / Maintenance (2-3 years); Normal cells recover quickly, side effects disappear gradually (prognosis of the patient depends on their overall health and the type of anticancer drugs used)

284
Q

Alkylating agents

A

Inhibit DNA synthesis, structure or function (DNA replication)

285
Q

Side effects of chemotherapy

A

Anemia, Constipation, Depression, Diarrhea, Hair loss (alopecia), Infection, Loss of appetite (anorexia), nausea and vomiting, Mouth, gum, and throat problems; sores, and sexual problems

286
Q

External Radiation Therapy

A

Damages DNA to disrupt growth of cancer, targeted external bean for 15 min 5x/week for 3-9 weeks

287
Q

Internal Radiation Therapy

A

Tablet, liquid (IV) or brachytherapy (implant to deliver radioactive dose directly to tumor); fewer side effects compared to external

288
Q

Considerations for Surgery (PROO)

A

Patient health/survivability (risks)
Resectability of tumor
Operability of tumor
Other treatment options

289
Q

Immune system cancer control (CNMA)

A

CD8 (Cytotoxic) T cells destroy cancer antigens presented by MHC I
NK cells can destroy cells expressing stress signals, deficient MHC I expression
Macrophages can destroy tumor cells by phagocytosis
Antibodies to tumor antigens can tag tumor cells for destruction by Macrophages/ complement

290
Q

Immunotherapy (Non-specific or Specific types)

A

Stimulating the body’s immune response to attack cancer
Nonspecific: Cytokines
Specific: Tumor-infiltrating lymphocyte therapy, Tumor vaccines, Tumor antibody therapy

291
Q

IFN alpha

A

Has general antiviral effects, inhibition of tumor growth, useful in leukemia, multiple myeloma

292
Q

IL-2

A

Stimulates NK cells and Cytotoxic CD8 T cells
and used in metastatic melanoma, renal cell carcinoma

293
Q

CAR-T therapy

A

Specific Immunotherapy; Genetic TCR alteration

294
Q

Dendritic cell therapy

A

Activation of dendritic cells in presence of tumor antigens

295
Q

Anti-tumor vaccines

A

Tumor antigens from patient used to immunize patient against recurring disease after resection

296
Q

Anti-tumor antibodies

A

Specific antibodies directed against tumor, sometimes linked with antitumor drug (chemo) or toxin (radioactive)

297
Q

Drugs to remove blockades that are inhibiting immune function

A

Prevents tumor immune suppression functions (CTLA-, PD1, PD-L1)

298
Q

Oncolytic viruses (Vaccinia, Vesicular stomatitis virus)

A

Infects and kills cancer cells, stimulate anti-tumor immunity - Attenuation

299
Q

Thyroid cancer survival rate

A

95% (5-year rate)

300
Q

Pancreatic cancer survival rate

A

4% (5-year rate)

301
Q

Most common cancers in males and females

A

Lung cancer (males) and Breast cancer (females)

302
Q

Plasma

A

Fluid component of blood

303
Q

Blood composition and function

A

Red cells, leukocytes, and platelets; carries antibodies, oxygen, nutrients, hormone , and CO2 plus other waste products

304
Q

Red blood cell function

A

Oxygen/Carbon Dioxide exchange
(the more red blood cells the more oxygen you can carry); Most numerous cells in the blood

305
Q

Leukocytes (WBC) function and types

A

Immune functions; Neutrophils (Most numerous – first line), Monocytes (Phagocytic Macrophages), Eosinophils (Allergy, parasitic infections), Lymphocytes (Adaptive Immunity), and Basophils (Parasitic infections)

306
Q

Platelet function

A

Hemostasis

307
Q

Stem cells

A

Precursor cells in bone marrow that differentiate to form red cells, white cells, and platelets (any cell) - Hematopoietic stem cells differentiate into any blood cell type

308
Q

Erythroblast

A

Precursor cells in bone marrow

309
Q

Hemoglobin

A

An oxygen-carrying protein formed by the developing red cell

310
Q

Ganulocytes/ Polymorphpnucleargraulocytes

A

PMN - Eosinophils, Basophils, Neutrophils

311
Q

Where are Lymphocytes produced?

A

Mainly in lymph nodes and spleen; some are produced in bone marrow

312
Q

Neutrophils

A

The first line of defence (Most numerous in adults,
Makeup 60-70% of total circulating WBC, Actively phagocytic, Predominant in inflammatory reactions)

313
Q

Monocytes

A

3-5% of leukocytes (Increased in certain types of chronic infection, Circulate to sites of inflammation, Transition to Macrophages (APC), Infection/tissue repair)

314
Q

Eosinophils/Basophils

A

Present in low numbers (Increased in allergic reactions and Increased in presence of animal–parasite infections)

315
Q

Lymphocytes

A

15-20% of leukocytes (T/B cells, seen predominantly in children, Mostly located in lymph nodes, spleen, and lymphoid tissues (some in circulation plus lymphatic system), cell-mediated and humoral defence reactions)

316
Q

Platelets

A

Essential for blood coagulation, Much smaller than leukocytes, Represent bits of the cytoplasm of megakaryocytes, the largest precursor cells in bone marrow, Short survival, about 10 days

317
Q

Hematopoiesis

A

Formation and development of blood cells; bone marrow replenishes blood cells (damage/age)

318
Q

Substances necessary for hematopoiesis

A

Protein, Folic Acid, Vitamin B12 (required for DNA synthesis), Iron (Decreased RBC production if any of these are lacking)

319
Q

How is RBC production regulated

A

Oxygen content in blood which stimulates hormone (epo) release from kidneys

320
Q

True or False: High reticulocyte count indicates the body is creating a lot of RBC

A

True, they leave bone marrow and differentiate into RBC in circulation

321
Q

Red cell production

A

Regulated by oxygen content of the arterial blood – stimulated by erythropoietin

322
Q

White cell production

A

Regulated by Interleukin levels/ response to infection – complex

323
Q

Hemoglobin

A

96% of RBC content Tetramer is composed of four subunits, each one consisting of heme and globin

324
Q

Heme

A

Porphyrin ring that contains an iron atom

325
Q

Globin

A

The largest part of hemoglobin; forms different chains designated by Greek letters such as alpha, beta, gamma, delta, and epsilon

326
Q

Porphyrin ring

A

Produced by the mitochondria; iron is inserted to form heme

327
Q

Reticulocyte

A

A young red cell without a nucleus, but retains some organelles; identified by special strains found in bone marrow (matures in 24-48)

328
Q

Globin chains

A

Produced by ribosomes; joined to heme to form a hemoglobin unit (4 subunits to complete hemoglobin tetramer)

329
Q

Red blood cell degradation

A

Worn-out red cells are removed in the spleen, Hemoglobin is degraded and excreted as bile by the liver, The porphyrin ring cannot be salvaged, Globin chains break down and are used to make other proteins, and Iron is extracted and saved to make new hemoglobin

330
Q

Reduced oxygen supply stimulates

A

Erythropoiesis (erythropoietin)

331
Q

High partial pressure oxygen in lungs

A

Promotes binding

332
Q

Low partial pressure oxygen in tissues

A

Promotes release

333
Q

Methemoglobin Iron

A

Fe 3+, not in ferrous state, can’t bind oxygen, inherited disorder or response to toxic agents

334
Q

Carboxyhemoglobin

A

Binds CO with high affinity (200x stronger than oxygen), blocks oxygen binding, products of incomplete combustion

335
Q

Where are Iron reserves stored?

A

Liver, bone marrow, and spleen

336
Q

What do Duodenal cells produce?

A

Hepcidin to block uptake by duodenal cells and interferes with iron transport

337
Q

Hemochromatosis

A

Common genetic disease transmitted as an autosomal recessive trait – chronically absorbs too much iron

338
Q

Reasons for Iron overload

A

Patients who take iron supplements chronically, or have blood disorders where there is a loss of RBC destruction (sickle cell), overload due to inability to reduce iron levels

339
Q

Treatment for Hemochromatosis

A

Periodic removal of blood (phlebotomy) until iron stores are depleted, and use of iron chelation treatment to remove iron

340
Q

Anemia causes

A

Insufficient raw materials (Iron deficiency, vitamin B12 deficiency, Folic acid deficiency), Inability to deliver adequate red cells into circulation due to marrow damage or destruction (aplastic anemia), excessive loss of red cells

341
Q

Hemorrhage

A

External blood loss

342
Q

Sickle cell, thalassemia

A

Shortened survival of red cells in circulation

343
Q

Hereditary hemolytic anemia

A

Defective red cells

344
Q

Normocytic anemia

A

Normal size and appearance

345
Q

Macrocytic anemia

A

Cells larger than normal impaired (folic acid and Vitamin B12 deficiency)

346
Q

Microcytic anemia

A

smaller cells (thalassemia)

347
Q

Hypochromic anemia

A

Reduced hemoglobin content

348
Q

Hypochromic microcytic anemia

A

Smaller than normal and reduced hemoglobin content

349
Q

Iron-deficiency Anemia

A

The most common type; Hypochromic microcytic anemia (not enough iron);

350
Q

When does Iron-deficiency Anemia happen

A

This happens when there are a lack of iron in the diet, rapids periods of growth in infants, inadequate reutilization of iron, chronic infection/inflammation, cancers, and loss of blood (GI tract, excessive menstrual bleeding, too frequent blood donations)

351
Q

Laboratory tests in blood for iron deficiency

A

Serum ferritin (low), Serum iron (low), and Serum iron-binding capacity (high)

352
Q

Iron-Deficiency Anemia Treatment

A

Learning the cause of anemia, treatment on cause than symptoms, administering supplementary iron

353
Q

Vitamin B12 deficiency anemia

A

Those who are vegetarian are at risk; found in meat, milk, and foods rich in animal proteins; For structural and functional integrity of the nervous system; deficiency may lead to neurologic disturbances

354
Q

Folic acid

A

Green leafy vegetables and animal protein foods; are required for normal hematopoiesis and normal maturation of many other types of cells

355
Q

Absence or deficiency of vitamin B12 or folic acid

A

Mature red cells are larger than normal or macrocytes; corresponding anemia is called macrocytic anemia, Leukopenia (low WBC), thrombocytopenia (low platelets), Abnormal red cell maturation or megaloblastic erythropoiesis

356
Q

Folic Acid Deficiency Anemia Pathogenesis

A

Inadequate diet: Encountered frequently in chronic alcoholics
Poor absorption caused by chronic intestinal disease
Occasionally occurs in pregnancy with increased demand for folic acid

357
Q

Pernicious Anemia (macrocytic anemia)

A

Lack of intrinsic factor (B12); causes included gastric mucosal atrophy, Autoantibodies directed against gastric mucosal cells and intrinsic factor, Surgery to remove sections of the stomach, and Chronic intestinal diseases (Crohn’s, IBD)

358
Q

Pernicious Anemia treatment

A

Increased oral dose (B12 supplements) or Intramuscular injections

359
Q

Conditions that depress bone marrow function

A

Anemia of chronic disease: Mild suppression of bone marrow function (parvoirus B19), Aplastic anemia (Marrow injured by radiation, anticancer drugs or chemicals, Autoantibodies, CTL autoimmunity)

360
Q

What does bone marrow suppression affect?

A

WBC and platelets - Pancytopenia (anemia, leukopenia, thrombocytopenia)

361
Q

Bone marrow treatment

A

Depends on the cause; Blood and platelet transfusions, Immunosuppressive drugs, Hemopoietic stem cell transplant in highly selected cases of aplastic anemia, or no specific treatment

362
Q

Hereditary hemolytic anemia

A

Genetic abnormality prevents normal survival, Abnormal shape (Hereditary spherocytosis; These cells have no central pallor), Abnormal hemoglobin (Hemoglobin S (sickle hemoglobin) or hemoglobin C), Defective hemoglobin synthesis (Thalassemia minor and major; globin chains are normal, but synthesis is defective)

363
Q

Thalassemia

A

Defective synthesis of alpha or beta globulin

364
Q

Alpha – (4 genes)

A

1- no change 2 -trait with mild disease, 3 severe disease, 4 – incompatible with life (hydrops fetalis)

365
Q

Unstable Beta tetramers

A

Defective Oxygen exchange; formed by lack of alpha and excess beta chains

366
Q

Beta – (2 genes)

A

Heterozygous-mild, homo-severe

367
Q

Sickle cell

A

Hemoglobin S (beta Hgb point mutation); Present in areas where Malaria is/was common; Constant sickling wears out cells and sickled cells are targeted for early destruction by the spleen, cells can also form blockages, chronic joint pain also occurs

368
Q

Sickle cell trait vs. Sickle cell disease

A

Trait: heterozygous, generally asymptomatic, Disease: homozygous, chronic health problems

369
Q

Vaso-occlusive crisis

A

Severe, abdominal pain (kidney, liver spleen infarction)

370
Q

Acquired Hemolytic Anemia

A

Normal red cells that are unable to survive due to a hostile environment; Attacked and destroyed by antibodies and Destruction of red cells by mechanical trauma

371
Q

Clotting Disorders

A

Disseminated intravascular Coagulation (DIC), Thrombotic Thrombocytopenic Purpura TTP –clots form in small blood vessels damaging RBC

372
Q

Diagnostic Evaluation of Anemia

A

History and physical examination, Complete blood count to assess the degree of anemia, leukopenia, and thrombocytopenia, Blood smear to determine if normocytic, macrocytic, or hypochromic microcytic, Reticulocyte count to assess the rate of production of new red cells, lab tests, bone marrow study, and evaluation of blood loss

373
Q

Secondary polycythemia

A

Common, Reduced arterial oxygen saturation leads to a compensatory increase in red blood cells (increased erythropoietin production)

374
Q

Primary or polycythemia vera

A

Rare, Manifestation of diffuse marrow hyperplasia of unknown etiology (cause), an overproduction of red cells, white cells, and platelets; can evolve into granulocytic leukemia

375
Q

Polycythemia Complications

A

Clot formation due to increased blood viscosity and platelet count

376
Q

Polycythemia Treatment (both types)

A

Primary polycythemia: Treated with drugs that suppress marrow function
Secondary polycythemia: Periodic removal of excess blood

377
Q

Secondary thrombocytopenic purpura

A

Damage to bone marrow from drugs or chemicals; Bone marrow infiltrated by leukemic cells or metastatic carcinoma

378
Q

Primary/ Immune thrombocytopenic purpura (ITP)

A

Associated with platelet antibodies where the bone marrow produces platelets, but they are rapidly destroyed, chronic in adults (immune suppression for treatment)

379
Q

Lymphatic System function

A

Provide immunologic defenses against foreign material via cell-mediated and humoral defense mechanisms and provides return of lost circulatory volume to vascular system

380
Q

Lymph nodes

A

Bean-shaped structures consisting of a mass of lymphocytes supported by a meshwork of reticular fibers that contain scattered phagocytic cells

381
Q

Where is lymphoid tissue

A

Present in thymus, tonsils, adenoids, lymphoid aggregates in intestinal mucosa, respiratory tract, and bone marrow

382
Q

Thymus

A

Overlies base of the heart; large during infancy and childhood; undergoes atrophy in adolescence (essential in the prenatal development of the lymphoid system and in the formation of body’s immunologic defence mechanisms ( T cell development/ selection))

383
Q

Spleen

A

Specialized to filter blood (Macrophages, antibodies, lymphocytes and sinusoids to detect and remove pathogens in blood)

384
Q

Reasons for splenectomy

A

Traumatic injury: To prevent fatal hemorrhage
Blood diseases: Excessive destruction of blood cells in the spleen (hereditary hemolytic anemia)
Prevent chronic splenomegaly
Cancer – Leukemia, Lymphoma

385
Q

Effects/risks of a splenectomy

A

Less-efficient elimination of bacteria (especially if blood-borne)
Impaired production of antibodies
Predisposed to systemic infections
Risk of increased platelet/RBC

386
Q

Which infections are splenectomy patients at risk of?

A

Streptococcus pneumoniae, Haemophilus influenzae, and meningococcus infections

387
Q

Treatment for Splenectomy

A

Vaccines and antibiotic prophylaxis

388
Q

Infectious mononucleosis

A

Lymphatic System disease; usually caused by Epstein-Barr virus (EBV-B-cell 90%) or CMV – Tcell/macrophages (5-7%)
Risk: spleen may rupture during high-contact sports and in those with compromised immune systems (give rise to B cell lymphoma)

389
Q

Enlarged LN cancers

A

Metastatic tumors: Breasts, lung, colon, other sites, Malignant lymphoma (Hodgkin lymphoma
and Non-Hodgkin lymphoma), and Lymphocytic leukemia

390
Q

Leukemia

A

A neoplasm (Cancer) of hematopoietic tissue; Leukemic cells diffusely infiltrate the bone marrow and lymphoid tissues, spill over into the bloodstream, and infiltrate throughout various organs of the body

391
Q

Aleukemic leukemia

A

Condition in which white cells are confined to the bone marrow such that their number in the peripheral blood is normal or decreased

392
Q

Myelodysplasia (Preleukemia)

A

A disturbed growth and maturation of marrow cells; 3 types: Anemia (Reduced number of erythrocytes), Leukopenia (Reduced number of white cells), Thrombocytopenia (Reduced number of platelets)
Not all patients develop leukemia

393
Q

Common types of hematopoietic cells that give rise to leukemia

A

Granulocytic, Lymphocytic, and Monocytic

394
Q

CLL, CML, ALL, AML

A

chronic lymphocytic leukemia, chronic myelogenous leukemia, acute lymphocytic leukemia, and acute myeloid leukemia

395
Q

Splenomegaly

A

Enlarged spleen

396
Q

Hepatomegaly

A

Enlarged liver

397
Q

Lymphadenopathy

A

Enlarged lymph nodes

398
Q

Bone pain in Leukemia

A

Expansion of cells in bone marrow

399
Q

Chronic leukemia

A

The evolution of disease proceeds at a relatively slow pace and often can be controlled

400
Q

Acute leukemia

A

A rapidly progressive disease, more difficult to control

401
Q

Diagnosis Leukemia

A

flowcytometry (phenotyping) bone marrow biopsy, Karyotyping (numbers, disease-specific risk genes – BCR/ABL fusion)

402
Q

Lymphoma

A

When cancerous cells form solid tumors in LN; mostly diseased B-cells or some T-cells which disrupt immune function

403
Q

Hodgkin Lymphoma

A

young adults, start in single LN and spreads to others and eventually other parts of the body. Usually detected early as a single or group of enlarged LN

404
Q

Reed-Steinberg cells

A

(large atypical B-cells) that act as nucleus of tumor and secrete cytokines to attract other tumor cells

405
Q

Non-Hodgkin

A

Older adults, variable in appearance an progression, often not detected until widespread dissemination has occurred

406
Q

Treatment of Leukemia and Lymphoma + survival rate

A

Destruction of malignant cells by chemotherapy or radiation to produce remission (3 phases: Induction/Consolidation/Maintenance)
Other treatments:
- Hematopoietic Stem Cell Therapy (BMT, peripheral, cord blood): replaces malignant cells (must use immune suppression drugs)
50% 5 year survival rate if HLA match is found

407
Q

HCV

A

slowly progressive cell injury

H (2 decks)

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