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Human Pathophysiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Four Classification of Immune Disease

A
  • hypersensitivity
  • immunodeficiency
  • autoimmune disease
  • malignancy
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2
Q

Hypersensitivity

A

too much immune response

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3
Q

Immunodeficiency

A

too little immune response

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4
Q

Autoimmune Disease

A

inappropriate immune response

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5
Q

Malignancy

A

aggressive and harmful immune response

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6
Q

Hypersensitivity Reactions

A

an inappropriate immune response to a ‘foreign’ particle

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7
Q

How many types of hypersensitivities are there?

A

Type 1-4

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8
Q

Type 1-3 reactions are all mediated by….

A

B cells

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9
Q

Type 4 reactions are mediated by…

A

T cells

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10
Q

Type 1 Hypersensitivity catch phrase.

A

“immediate, rapid responses”

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11
Q

Main class of antibodies in Type 1 Hypersensitivity?

A

IgE

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12
Q

T/F: A person has already encountered antigen when having a Type 1 Hypersensitivty reaction.

A

TRUE – preformed antibodies already exist in the body due to sensitization

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13
Q

What are the main cells involved in a Type 1 Hypersensitivity?

A
  • mast cells
  • basophils
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14
Q

T/F: Mast cells are the main cell type to cause anaphylaxis.

A

TRUE – mast cells release granules the cause anaphylactic symptoms

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15
Q

T/F: IgE antibodies are attached to mast cells surfaces.

A

TRUE

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16
Q

What do mast cells do in an allergic reaction?

A
  • a rapid and intense release of various inflammatory substances
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17
Q

What inflammatory substances do mast cells release?

A

histamine, leukotrienes, and serotonin

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18
Q

What 3 major effects do granules have on surrounding areas?

A
  • vasodilation
  • increased capillary permeability
  • accumulation of edema
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19
Q

Describe the components of the 1st and 2nd wave of mast cell reactions.

A

1st: histamines and serotonin
2nd: derivatives of arachidonic acid

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20
Q

What is arachodonic acid made from?

A

part of the plasma membrane

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21
Q

What are the phases of Type 1 Hypersensitivty?

A
  • immediate and late
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22
Q

What are characteristics of the immediate phase of a Type 1 reaction?

A
  • “wheal and flare”
  • wheal: raised, red itchy skin lesion
  • flare: surrounding redness and increased warmth
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23
Q

What are characteristics of the late phase of a Type 1 reaction?

A

inflammation caused by eosinophils
- attached to flare
- release of cytokines causes edema

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24
Q

Allergens

A

particles triggering an immune response

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25
Q

Atopy

A

genetic predisposition that increases an individual’s susceptibility to develop allergic reactions, often characterized by a heightened immune response to common environmental allergens.

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26
Q

What is the most common allergen?

A

dust mites

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27
Q

Give examples of Allergic Diseases?

A
  • Hay Fever
  • Urticaria (hives)
  • Atopic dematitis (eczema)
  • Systemic Anaphylaxis
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28
Q

Describe the Hygiene Hypothesis.

A

the immune system is untrained and reacts to the wrong things more often
- IgE is typically meant to fight off parasites

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29
Q

Characteristics of places with higher rates of allergic disorders.

A
  • westernized countries
  • small family size
  • affluent, urban homes
  • stable intestinal microflora
  • high antibiotic use
  • low or absent helminth burden
  • good sanitation

places with low rates = opposite of list above

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30
Q

How are Type 1 Hypersensitivities treated?

A
  • avoidance
  • pharmacological management
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31
Q

List some Pharmacologic managements.

A
  • anti-histamines
  • corticosteroids
  • anti-IgE therapy
  • beta adrenergics
  • desensitization
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32
Q

Type 2 Hypersensitivity catch phrase.

A
  • “cytotoxic hypersensitivity”
  • tissue specific antibody directly attaches to antigen in target tissue
  • B cells
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33
Q

Main class of antibodies in Type 2 Hypersensitivity?

A

IgG, IgM

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34
Q

T/F: Type 2 Reactions target host cells rather than foreign antigen.

A

TRUE

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35
Q

Types of interaction for a Type 2 Reaction.

A
  • death of target cell
  • antibodies block receptor function
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36
Q

What does ‘death of target cell’ mean?

A

a cell being killed by other components of immune system

  • phagocytes
  • macrophages
  • neutrophils
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37
Q

What does ‘antibodies block receptor function’ mean?

A

blocking of the normal interaction between the receptor and its intended ligand, preventing the receptor from carrying out its usual signaling or regulatory function

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38
Q

T/F: Myasthenia Gravis is an example of ‘antibodies block receptor function’.

A

TRUE – antibodies against acetyl-choline receptor (NMJ)

  • causes weakness, atrophy
  • autoimmune disease
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39
Q

Examples of Type 2 Hypersensitivities.

A
  • transfusion reaction
  • hemolytic disease of the newborn
  • autoimmune reactions
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40
Q

Type 3 Hypersensitivity catch phrase.

A

immune complex hypersensitivity
- B cells

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41
Q

Main class of antibodies in Type 3 Hypersensitivity?

A

IgG, IgM

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42
Q

Immune complex

A

antigen and antibody combine to form immune complex

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43
Q

Describe the normal clearance of immune complexes.

A
  • RBCs drop off immune complex
  • kupfer cells (macrophages) in the liver removes immune complex
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44
Q

What locations are typically affected by failure to clear complexes?

A
  • blood vessels
  • kidney
  • joints
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45
Q

Failure to clear immune complexes results in…

A

a deposition-induced inflammatory response

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46
Q

T/F: Immune complex deposition can be distant from initial site.

A

TRUE – immune complexes can circulate to different site from formation

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47
Q

T/F: Immune complexes deposition can be local.

A

TRUE – complexes can remain at the site

Ex. farmers lung

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48
Q

T/F: Type 3 Reaction tend to be ongoing, with variations in symptoms based on antibody to antigen ratios.

A

TRUE – Type 3 Reactions are influenced by…
- size of complexes
- vascular permeability

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49
Q

Small immune complexes tend to….

A

circulate for longer, increasing length of immune response

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50
Q

Increased vascular permeability allows…

A

immune complexes to leak out into tissues to be deposited

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51
Q

Type 4 Hypersensitivity catch phrase.

A
  • cell mediated
  • delayed response
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52
Q

Main class of antibodies in Type 4 Hypersensitivity.

A
  • NONE; does not depend on antibodies
  • T cell mediated
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53
Q

What are the reaction steps of a Type 4 Hypersensitivity?

A
  1. Antigen uptake (hapten); presentation by APC
  2. Presentation to Helper T cell
  3. Memory T cells migrate to site
  4. Second Exposure = release mediators, attract other cells
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54
Q

Hapten

A

particle that is a partial antigen by itself

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55
Q

Examples of Type 4 Hypersensitivity.

A
  • Poison Ivy
  • Metallic injury (jewelry)
  • Tb test
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56
Q

Autoimmune Disease catch phrase.

A
  • “we have the enemy, and he is us”
  • self becomes foreign
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57
Q

Examples of Autoimmune Diseases.

A
  • Systemic Lupus Erythematosus
  • Rheumatoid Arthritis
  • Myasthenia Gravis
  • Type 1 Diabetes
  • Multiple Sclerosis
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58
Q

What are the 7 reasons the body turns on itself?

(be able to explain each one)

A
  • imperfect B and T cell programming
  • Inaccessible self-antigens
  • altered antigen
  • molecular mimicry
  • infection or inflammation
  • decrease suppressor T cell function
  • Genetic susceptibility (MHC protiens)
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59
Q

molecular mimicry

A
  • resemblance of pathogen and host antigen
  • immune response initiated by microbe becomes directed at self cells
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60
Q

Give a clinical example of molecular mimicry.

A

rheumatic fever = streptococci bacteria infection

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61
Q

Give 2 systemic Autoimmune Disease examples.

A
  • SLE
  • Rheumatoid Arthritis
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62
Q

Give 3 organ specific Autoimmune Disease examples.

A
  • Multiple Sclerosis
  • Hashimoto Thyroiditis
  • Myastenia gravis
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63
Q

What are the symptoms of SLE?

A
  • butterfly rash
  • women (20 - 40 yrs)
  • fever
  • weakness
  • photosensitivity
  • arthritis
  • kidney dysfunction
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64
Q

What type of Hypersensitivity if SLE?

A

Type 3
- binding of antibodies forms soluble immune complexes

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65
Q

Which organ is attacked most by SLE?

A

kidneys

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66
Q

What is the pathology of SLE?

A
  • Circulating antibodies specific for constituents of nucleus
  • Antinuclear Antibodies (ANA) in blood

Deposition:
- initiate further inflammation (arteries = vasculitis)
- chronic inflammatory disease (affects all tissues of the body)

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67
Q

How is SLE diagnosed?

A
  • blood work
  • presence of ANA
  • High ESR (cell count) and CRP (inflammation)
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68
Q

Most common clinical findings of SLE?

A
  • cytopenia
  • vasculitis
  • skin lesions
  • myocarditis
  • glomerunephritis
  • arthritis
  • brain (microinfarcts, psychosis, dementia)
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69
Q

What is the typicaly clinical outcome of SLE?

A

variable and unpredictable

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70
Q

T/F: SLE has a 30% mortality rate in the first 10 years.

A

TRUE – eventual death is due to organ failure of kidneys and brain

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71
Q

Treatment of both mild and severe SLE?

A

mild = NSAIDS
- inhibits arachadonic acid derivatives to stop inflammation

severe = corticosteroids, antineoplastic
- inhibits t cell division

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72
Q

T/F: Autoimmune disease inducing Lupus-like symptoms following exposure to certain drugs.

A

TRUE – only about 10% of lupus cases

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73
Q

What are common symptoms of Rheumatoid Arthritis?

A
  • immune system attacking synovial joints
  • 20- 40 yrs
  • episodic
  • 1- 3% of population
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74
Q

What type of Hypersensitivity is Rheumatoid Arthitis?

A

Type III Hypersensitivity

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75
Q

What does systemic Rheumatoid Arthitis attack?

A
  • lungs
  • bone
  • cartilage
  • pericardium
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76
Q

Rheumatoid Factor

A

autoantibody

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77
Q

Sjorgren Syndrome

A

autoimmune disease of lacrimal and salivary glands

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78
Q

What are symptoms of Sjogren Syndrome?

A
  • dry irritated red eyes
  • dry mouth
  • difficulty swallowing
  • extraglandular (vasculitis, neuropathy, lymphoma)
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79
Q

Amyloidosis

A

group of diseases in which amyloid proteins are abnormally deposited

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80
Q

Amyloid

A

extracellular, insoluble protein aggregates

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81
Q

Primary Amyloidosis

A
  • no cause is known
  • antibodies form amyloid (light chain)
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82
Q

Secondary Amyloidosis

A

secondary to some other condition (SLE, RA)
- signs and symptoms depends on the tissue/organ

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83
Q

Types of transplantation

A
  • autograft
  • homograft
  • allograft
  • xenograft
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84
Q

T/F: transplantation rejection is mediated by immune system.

A

TRUE – caused by mismatch of MHC

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85
Q

Types of Rejection

A
  • hyperacute organ rejection
  • acute organ rejection
  • chronic transplant rejection
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86
Q

Hyperacute Organ Rejection

A

preformed antibodies react with graft endothelial cells; people affected include…
- past transplant recipient
- pregnant woman
- blood transfusion recipient

timeframe = immediate

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87
Q

Acute Organ Rejection

A
  • within weeks
  • T cell mediated
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88
Q

Chronic Transplant Rejection

A
  • months to years
  • T cell mediated
  • ischemia and hypoperfusion of organ
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89
Q

Graft vs Host Reaction (GVH): Mechanism

A
  • immune cells in graft recognize host as foreign
  • transplanted graft lymphocytes attack host cells
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90
Q

Graft vs. Host Reaction (GVH): Tissues Affected

A
  • liver, skin, GI tract
  • tissues under most attack bc dividing frequently
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91
Q

Graft vs. Host Reaction (GVH): Minimization

A
  • matching graft as best as possible
  • immune suppression
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92
Q

T/F: GVH is commonly found with bone marrow transplantation.

A

TRUE – recipient must undergo pretransplant treatment

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93
Q

T/F: Bone marrow transplants are the most common type of transplantation.

A

FALSE – blood transfusions are the most common

blood typing is done to match donors and recipients

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94
Q

What antigens do Type A people have?

What antibodies do they produce?

A
  • A antigens
  • B antibodies
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95
Q

What antigens do Type B people have?

What antibodies do they produce?

A
  • B antigens
  • A antibodies
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96
Q

What antigens do Type O people have?

What antibodies do the produce?

A
  • no antigens
  • A and B antibodies
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97
Q

What antigens do Type AB peple have?

What antibodies do they produce?

A
  • A and B antigens
  • no antibodies
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98
Q

Major Transfusion Reaction

A
  • hemolysis
  • thrombosis
  • life threatening
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99
Q

Minor Transfusion Reaction

A
  • not life threatening
  • fever, chills
  • not due to ABO mismatch
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100
Q

Rh Incompataility

A
  • D/d antigens
  • Hemolytic Disease of the Newborn
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101
Q

Crossmatch

A

donor blood is compatible with recipient blood

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102
Q

Major Crossmatch

A
  • Donor RBC to recipient serum (paslma w/ clotting factor)
  • checking for preformed antibodies in recipient serum against donor RBC
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103
Q

Minor Crossmatch

A
  • donor serum to recipient RBC
  • checking fo rpreformed antibodies in donor serum that could hemolyse recipient
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104
Q

Severe Combined Immundeficiency Disease

A

deficiency of T cells
- caused by mutations
- prone to infections and cancer

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105
Q

Primary Immunodeficiency

X-Linked Agammaglobulin (XLA)

A
  • deficiency in tyrosine kinase
  • prevents development of mature B cells
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106
Q

Primary Immunodeficiency

XLA Clinical Presentation

A
  • males more often affected
  • bacterial infections more frequently
  • blood tests show no B cells
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107
Q

Primary Immunodeficiency

DiGeorge Syndrome

A
  • 22 q deletion
  • TBX1 is important for thymus formation
  • no thymus = no T cells SCID
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108
Q

Secondary (Acquired) Deficiency

A

Secondary to something else:
- nutrition
- infection
- radiation
- age

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109
Q

Secondary Deficiency

HIV

A

human immunodeficienct virus

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110
Q

Secondary Deficiency

AIDs

A

autoimmunedeficiency disorder

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111
Q

Secondary Deficiency

How are AIDs and HIV related?

A

HIV causes AIDS
- not exactly the same

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112
Q

Secondary Deficiency

Characteristics of AIDS

A
  • low Helper T cell count
  • recurrent infections that are not normally observed
  • certain kinds of neoplasms
  • cachexia (wasting away; skinny)
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113
Q

T/F: AIDs transmission is transmitted through skin to skin contact.

A

FALSE – transmission is through blood and bodily fluids

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114
Q

What groups are at higher risk of AIDs in the US?

A
  • gay and bisexual males
  • IV drug user
  • patients with hemophilia
  • recipients of transfusion of human blood
  • heterosexual contacts of the above
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115
Q

Retrovirus

A

a virus that uses RNA as its genetic material

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116
Q

HIV Pathogenesis

A
  1. HIV contributes its RNA to helper T
  2. Reverse transcriptase: RNA makes DNA
  3. Abnormal DNA becomes part to T cell DNA
  4. Synthesis of new HIV RNA
  5. New HIV virus buds from infected T cell
  6. Death of infected T cell
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117
Q

HIV entry depends on….

A
  • CD4 receptor
  • CCR5 (CXCR4) co-receptor
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118
Q

What are the 3 stage progressions of HIV?

A
  • Acute
  • Latent
  • Crisis
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119
Q

Acute HIV Syndrome

A
  • primary infection
  • sore throat, fever, rash
  • wide spread dissemination of virus
  • seeding of lymphoid organs
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120
Q

Latent HIV

A

infections still present but lack of symptoms
- can still be transmitted

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121
Q

Crisis HIV

A
  • AIDs
  • opportunistic diseases
  • low helper T cell count
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122
Q

What are the clinical features of the crisis period (AIDs) of HIV infection?

A
  • opportunistic infections
  • neoplasms
  • neurological symptoms
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123
Q

Examples of opportunistic infections during AIDs.

A
  • candidasis
  • tuberculosis
  • salmonella
  • herpes
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124
Q

Examples of neoplasms during AIDs.

A
  • kaposi sarcoma
  • lymphoma brain
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125
Q

Examples of neurological symptoms during AIDs.

A
  • dementia
  • seizures
  • mood swings
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126
Q

HIV resistant mutation?
Homo- vs Heterozygous?
Ethnicity?

A
  • mutation in CCR5 (co-receptor w/ CD4)
  • homo won’t be infected; hetero will cause infection to move slower
  • caucasian population
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127
Q

Diagnosis of HIV and AIDS

A
  • Anti-HIV antibodies
  • HIV antigens in blood
  • Saliva
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128
Q

Clinical Diagnosis AIDS

Definitive w/out confirming lab data.

A

kaposis’s sarcoma < 60 yrs old

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129
Q

Clinical Diagnosis AIDS

Definitive w/ confirming lab data.

A

CD4+ < 200 cells/ml

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130
Q

Clinical Diagnosis AIDS

Presumptive w/ confirming lab data.

A

recurrent pneumonia

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131
Q

T/F: The goals of HIV treatment is complete clearance of infection.

A

FALSE – HIV cannot be cured; goals include:
- control virus
- control other infections

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132
Q

HAART

A

Highly Active Antiretroviral Therapy

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133
Q

HAART Effects on HIV

A
  • suppress virus repilcation
  • act on different stages of life cycle of HIV
  • increases latency period, may be indefinitely
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134
Q

What different stages of HIV life cycle does HAART act on?

A
  • entry inhibitors
  • nucleotide reverse transriptase inhibitors
  • protease inhibitors
  • chemokine receptor
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135
Q

microflora

A

microorganisms normally living in or on your body

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136
Q

T/F: All microflora are beneficial.

A

FALSE – some are useful; many have no effect

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137
Q

pathogens

A

cause disease

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138
Q

T/F: Only pathogens are capable of causing disease if your health and immunity are weakend.

A

FALSE – both microflora and pathogens are capable of causing disease when normal health is weakend.

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139
Q

opportunistic pathogens

A

normally does not cause disease but could in a weakend immune system

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140
Q

T/F: Pathogens vary in where they live and replicate.

A

TRUE

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141
Q

T/F: Pathogens vary in how they damage host cells.

A

TRUE

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142
Q

T/F: All pathogens have the same ability to persist outside the body.

A

FALSE – pathogens vary in ability to live outside the body

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143
Q

Virulence

A
  • ability to cause damage and disease in host
  • “how much harm can it cause?”
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144
Q

Why are some pathogens more virulent than others?

A
  • secrete toxins
  • adhesion factors
  • evasive factors
  • host factors
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145
Q

Virulence variability: secrete toxins

A

exotoxins and endotoxins

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146
Q

Virulence variability: adhesion factors

A

help infective organism colonize

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147
Q

Virulence variability: evasive factors

A

help keep immune system from killing infective agent

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148
Q

Virulence variability: host factors

A
  • genetics
  • malnutrition
  • age
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149
Q

Contagion

A
  • how easily spread from one organism to another
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150
Q

Indirect contagion

A
  • sickness passed fomite before passing to another person
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151
Q

Direct contagion

A
  • from one person to another person
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152
Q

Mode of transmission

A
  • direct contact
  • ingestion
  • indirect contact (fomite)
  • droplets
  • vectors
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153
Q

Fomite

A

inanimate objects carrying pathogen

154
Q

Vectors

A

diverse modes of transmission through which infectious agents spread from one host to another
- encompassing direct contact
- airborne particles
- contaminated surfaces
- mosquitoes

155
Q

Agents of Infectious Disease

A
  • prions
  • virus
  • bacteria
  • fungus
  • parasites
156
Q

T/F: Prions are small infectious abnormally folded proteins.

A

TRUE – infection induces normal proteins to convert to abnormal prion form
- ‘scrapie’

157
Q

Prions primarily affect…

A

the nervous system

158
Q

Transmission of Prions

A
  • genetics (creutzfeldt jakob disease)
  • eating infected tissue (mad cow disease)
159
Q

T/F: Viruses have a protein coat surrounding nucleic acid core.

160
Q

T/F: Viruses have metabolic enzymes of their own.

A

FALSE – viruses lack metabolic enzymes and depend on host

161
Q

T/F: Viruses insert their genome into a host cell’s DNA.

162
Q

T/F: Viruses use host cell’s metabolic machinery to make new virsues.

163
Q

How does a virus effect cells?

A
  • alter cell physiology
  • inhibit synthesis of host cell macromolecules
  • genotoxic
  • alter cell’s antigenic properties
164
Q

What cell physiology could a virus alter?

A
  • ion movement
  • second messengers
165
Q

Genotoxic

A

alteration of DNA

166
Q

Types of viral infections

A
  • acute
  • latent
167
Q

Acute Viral Infection

Examples?

A
  • transient
  • rhinovirus, norovirus, measles, influenza
168
Q

Latent Viral Infections

A

some viruses cause persistent infection

169
Q

T/F: Anti-viral inhibits some stage of viral replication cycle without toxicity to cell.

170
Q

Antiviral Agents kill viruses by…

A
  • blocking viral RNA or DNA synthesis
  • blocking viral binding to cells (entry inhibitors)
  • blocking production of the protein coats (capsids) of new viruses
171
Q

Describe bacteria

A
  • prokaryotes
  • can live independently
  • use infected organism for food and shelter
172
Q

T/F: Bacterial infections are typically latent infections.

A

FALSE – typically acute infections

173
Q

Bacterial infections are typically characterized by….

A
  • shape
  • gram stain
174
Q

Examples of bacteria shape

A
  • cocci
  • baccili
  • spirochetes
175
Q

Gram Positive

A
  • staphylococci and streptococci
  • commonly found on skin
176
Q

Gram Negative

A
  • cause intestinal and respiraotory infections (pneumonia)
177
Q

Sepsis

A
  • blood is infected, typically bacteria
  • whole body inflammation
  • leads to septic shock
178
Q

Septic Shock

A
  • high mortality
  • wide spread organ damage
  • low BP
179
Q

Antibiotics kill bacteria by targeting…

A
  • cell wall synthesis
  • protein synthesis
  • nucleic acid synthesis
  • bacterial metabolism
180
Q

Bacteria fight antibiotics by…

A
  • inactivating antibiotics
  • changing antibiotic binding sites
  • using different metabolic pathways
  • changing their walls to keep antibiotics out
181
Q

Describe fungi

A
  • most require cooler temp than human core body temp
  • most infections are on body surfaces (skin, hair)
182
Q

Examples of fungus infections

A
  • candidiasis (yeast infection)
  • tinea pedis (athletes foot)
183
Q

Vector-borne infections: Malaria

184
Q

Vector-borne infections: Rocky Mountain spotted fever

A

ticks, lice, chiggers

185
Q

Vector-borne infections: Lyme disease

A

deer ticks

186
Q

Vector-borne infections: Plague

A

rodent fleas

187
Q

T/F: Emerging diseases are/were previously unknown or undetected.

A

TRUE – infections that have recently appeared

188
Q

Examples of emerging diseases

A
  • SARS
  • Zika
  • Swine Flu
  • COVID
189
Q

Why is China a common place of origin for these diseases?

A
  • highly populated areas
  • daily wildlife trade with close human contact
190
Q

Zoonosis

A

disease transfer from animal to human

191
Q

Describe coronavirus

A
  • large group of viruses that cause disease in humans and animals
  • enters via ACE2 receptor
  • genomic sequence similar to bat coronavirus
192
Q

T/F: Infection causes injury.

193
Q

T/F: Inflammation is the usual response to infection.

194
Q

T/F: Infectious agents spread in a certain way.

195
Q

T/F: Infection runs a natural course.

A

TRUE
- incubation
- prodromal
- illness
- convalescence
- recovery

196
Q

Incubation period

A

no symptoms; infectious cells are multiplying

197
Q

Prodromal period

A

nonspecific symptoms; feeling ‘under the weather’

198
Q

Illness period

A

specific signs and symptoms

199
Q

convalescence period

A

symptoms fading away

200
Q

Recovery period

A

no symptoms

201
Q

What immune cells respond to bacteria?

A

neutrophils

202
Q

What immune cells respond to viruses?

A

lymphocytes, macrophages

203
Q

What immune cells respond to mycobacteria and fungi?

A

lymphocytes, macrophages

204
Q

What immune cells respond to parasitic worms?

A

eosinophils

205
Q

What immune cells respond to protozoa?

A

lymphocytes, macrophages

206
Q

Tuberculosis is caused by…

A

mycobacterium
- typically infects lungs but can also affect any part of the body

207
Q

Transmission of Tuberculosis

A

airborne droplets

208
Q

Common Symptoms of Tuberculosis

A
  • cough
  • coughing up blood
  • chest pains
  • fever
  • night sweats
  • feeling weak and tired
  • losing weight without trying
  • decreased or no appetite
209
Q

T/F: 98% of Tuberculosis related deaths occur in developing countries.

A

TRUE – most common in southeast asia and africa

210
Q

T/F: Most of the US tuberculosis cases occurred in Florida, Texas, California, and New York.

A

TRUE – more populated areas

211
Q

Explain the respiratory route of TB spread.

A
  • Causitive agent (mycobacterium tuberculosis)
  • reservoir (infected patient)
  • Portal of exit (infected lungs)
  • Mode of transmission (sneeze/cough)
  • portal of entry (healthy lungs)
  • susceptible host (person not immune to TB)
212
Q

What does it mean when TB is described as ‘hardy’?

A

can exist outside of hosts for months

213
Q

TB infection begins with…

A

phagocytosis into macrophage

214
Q

T/F: TB can remain inside the host in a dormant form and reactivate later.

215
Q

T/F: In response to TB infection, immune system forms tubercules.

A

TRUE – granuloma formation

216
Q

Granuloma

Type of necrosis?

A

bacteria trapped in tissues, surrounded by immune cells

  • causeous
217
Q

Tuberculosis diagnosis is based on…

A
  • symptoms
  • medical history
  • TB tests
  • Chest X-rays
  • diagnositc microbiology
218
Q

What are the 2 types of TB tests?

A
  • TB skin test
  • blood tests
219
Q

What is diagnostic microbiology for TB?

A

sputum smear – look for acid-fast bacteria

220
Q

Latent Tuberculosis Infection (LTBI)

A

individuals harbor the tuberculosis bacteria without active symptoms or spreading the disease, but there is a risk of it reactivating into active tuberculosis in the future.

221
Q

What are the predisposing factors of activating LTBI?

A
  • HIV infection
  • Other illnesses
  • Weak immune system
  • Stress
  • Being homeless
222
Q

Latent TB Treatment

A
  • not symptomatic or contagious
  • positive skin test
  • usually treated with isoniazid for 6-12 months
  • chest x-ray is negative
223
Q

Infectious TB Treatment

A
  • treatment is very expensive
  • treated in phases
224
Q

T/F: A person with infectious TB is allowed to be around everyone.

A

FALSE – person must be isolated until non-infectious

225
Q

T/F: Directly observed therapy to assure adherence/completion recommended for TB treatment.

226
Q

STI acronym

A

sexually transmitted infection

227
Q

definition

STI

A

general term for any disease that can be spread by intimate or sexual contact

228
Q

Common signs and symptoms of STIs

A
  • hematuria, urinary frequency, incontinence, purulent discharge, burning, itching on urination
  • pelvic or genital pain
  • any skin ulcerations, especially in genital areas
  • fever, malaise
229
Q

Hematuria

A

blood in urine

230
Q

Incontinence

A

peeing on accident

231
Q

What are the types of STIs?

A
  • bacterial
  • viral
  • protozoal
  • parasitic
  • fungal
232
Q

What type of STI is Gonorrhea?

A

caused by bacteria

233
Q

T/F: 1 in every 20 college aged females is infected with gonorrhea.

234
Q

Gonorrhea transmission generally requires…

A

contact of epithelial surfaces

235
Q

T/F: Humans are the only natural hosts of gonorrhea.

236
Q

Symptoms of gonorrhea

A
  • pain
  • discharge (not bloody)
  • asymptomatic
237
Q

T/F: Gonorrhea bacteria can only grow in the genital region.

A

FALSE – can grow in the mouth, throat, eyes and anus

238
Q

T/F: A gonorrhea infected mother can infect an infant during vaginal delivery.

239
Q

T/F: Gonorrhea can lead to infertility.

240
Q

Gonorrhea Treatment

A

antibiotics

241
Q

What type of STI is syphilis?

A

caused by bacteria

242
Q

T/F: Syphilis can infect any body tissue.

243
Q

T/F: Syphilis is less common but more deadly.

A

TRUE – syphilis becomes a systemic disease shortly after infection

244
Q

Congenital Syphilis

A

maternal-fetal transmission can occur as early as 9 weeks gestation

245
Q

What are the stages of syphilis infection?

A
  • primary
  • secondary
  • latent
  • tertiary
246
Q

Describe the primary stage of syphilis

A

local manifestations
- chancre
- painless, can go unnoticed
- resolves spontaneously
- highly contagious

247
Q

Describe the secondary stages of syphilis

A

systemic manifestations
- fever, malaise, sore throat, hoarseness, anorexia, joint pain, skin rash, and lesions
- highly contagious

248
Q

Describe the latent stage of syphilis

A
  • medical evidence of the infection, but patient is asymptomatic
  • unlikely contagious
249
Q

Describe the tertiary stage of syphilis

A
  • may emerge 5-20 yrs following latency
  • most severe stage
  • formation of gummas
  • destructive systemic manifestations
  • neurosyphilis
250
Q

Gummas

A

destructive skin, bone, and soft tissue lesions

251
Q

Syphilis treatment

A

antibiotics

252
Q

T/F: The immune system has memory when it comes to STIs.

A

FALSE – the immune system does not have memory bc STIs typically affect a limited range of immune cells

253
Q

What type of STI is chlamydia?

A

caused by bacteria

254
Q

T/F: Chlamydia is rare.

A

FALSE – chlamydia is extremely prevalent

255
Q

T/F: Chlamydia is one of the most potentially damaging STDs in the US.

256
Q

Chlamydia hallmarks

A
  • urinary frequency
  • abdominal pelvic discomfort
  • discharge
257
Q

Chlamydia signs and symptoms

A
  • silent STD; asymptomatic; transmission occurs unknowingly
  • burning, itching in genitalia
  • mucopurulent vaginal discharge
  • discharge from penis
  • burning on urination
  • swollen scrotum
258
Q

Chlamydia prognosis

A
  • good with early treatment

If untreated, such complications as:
1. Pelvic Inflammatory DIsease
2. infertility in females
3. epididymitis in males
4. sterility in both

259
Q

What type of STI is herpes?

A

caused by virus

260
Q

T/F: Genital herpes is a highly contagious viral infection of genitalia.

261
Q

T/F: Genital herpes recurs spontaneously.

262
Q

T/F: Genital herpes is life-threatening in infants during vaginal birth.

263
Q

What are the two stages of genital herpes?

A
  • active with skin lesions
  • latent without symptoms
264
Q

What are the two types of herpes?

A
  • HSV-1 (cold sores)
  • HSV-2 (genitalia)
265
Q

T/F: 98% of initial herpes infections are type 2.

A

FALSE – only 80% of initial infections are type 2; but 98% of recurrent infections are type 2

266
Q

T/F: Herpes is transmitted through contact with a person who is shedding the virus.

A

TRUE – the skin can look normal, but virus is still being shed

267
Q

Genital herpes signs and symptoms

A
  • multiple shallow ulcerations, pustules, on genitales, mouth, and anus
  • vesicles rupture causing pain, itching
268
Q

Genital herpes treatment

A
  • managed not cured
  • anti-viral medication
269
Q

T/F: 80% with primary genital herpes have recurrence within 12 months

270
Q

HPV acronym

A

human papillomavirus

271
Q

T/F: HPV is the most common STI.

A

TRUE – HPV can spread without actually seeing them

272
Q

HPV (genital warts) signs and symptoms

A
  • soft skin-colored, whitish pink to reddish brown bengn growths
  • found on genitals, including vagina, cervix and anus
  • very contagious
  • may not be visible to naked eye
273
Q

HPV (genital warts) treatment

A

may go away without treatment
- sometimes immune system fights and can resolve

274
Q

HPV etiology

A
  • spread by intimate contact
  • pregnant women can pass the virus to the fetus during childbirth
  • has an incubation of 1 to 6 months
275
Q

What is HPV a risk factor for?

A
  • cervical cancer (women)
  • oral/throat cancer (everyone)
276
Q

How do you prevent HPV?

A

HPV vaccination

277
Q

Genital herpes physical description

A

blistery sores causing pain, itching

278
Q

Genital warts physical description

A

small, painless, do not open and pus

279
Q

T/F: Genital herpes come and go without treatment, but genital warts come but do not always go away without treatment.

280
Q

How to prevent STIs?

A
  • vaccines (HPV)
  • safe sex
281
Q

Cancer is a name given…

A

too a group of more than 100 related diseases

282
Q

Cancer is characterized by…

A

uncontrolled cell growth

283
Q

Lifetime probability of developing cancer for women?
For men?

A
  • 1 in 2 women
  • 1 in 3 men
284
Q

Most diagnosed cancers for women?
For men?

A
  • breast
  • prostate
285
Q

Most cancers caused deaths for women?
For men?

A
  • lung and bronchus
286
Q

There has been an overall negative trend in cancer mortality, this can most likely be accredited to…

A

an increase in screening tests

287
Q

Hyperplasia

A

increase in number

288
Q

Hypertrophy

A

increase in size

289
Q

neoplasm

A

uncontrolled growth of cells, benign or malignant

290
Q

tumor

A

a non-specific term meaning lump or swelling

291
Q

T/F: Neoplasm and tumor are synonymous.

292
Q

Metastasis

A

discontinous spread of a malignant neoplasm to distant sites

293
Q

Malignant

A

capable of metastasis

294
Q

cancer

A

any malignant neoplasm or tumor

295
Q

T/F: Metastasis, malignant and cancer can be considered synonymous.

296
Q

What is the difference between neoplasia and hyperplasia?

A

neoplasia is cell proliferation in the absence of a stimulus

297
Q

T/F: Neoplasia and hyperplasia can be differentiated from eachother by just looking at the mass as a whole.

A

FALSE – can only be distinguished from eachother by histological examination (cell and tissue structure)
- biopsy
- fine needle aspiration

298
Q

Hyperplasia treatment

A
  • remove stimulus
  • removal of hyperplastic tissue
299
Q

Neoplasm treatment

A
  • depends on benign (will not metasize) or malignant
  • depends on site of neoplasm

malignant neoplasm:
- curative therapy
- pallitative therapy

300
Q

What are examples of curative therapy?

A
  • chemotherapy
  • radiation
  • surgery
301
Q

Benign Neoplasms

A
  • grow slowly
  • capsule
  • do not metastasize
  • well differentiated
302
Q

Malignant neoplasms

A
  • grow rapidly
  • can metastasize
  • less differentiated
303
Q

What does it mean is cancer cells are dedifferentiated?

A

the most cancerous cells are less differentiated

304
Q

T/F: “-oma” does not distinguish between benign or metastatic.

A

TRUE – more often used in conjunction with malignant neoplasms

305
Q

Carcinoma

A

malignancy of epithelial cells

306
Q

sarcoma

A

malignancy of connective tissue

307
Q

melanoma

A

malignancy of connective tissue

308
Q

lymphoma

A

malignancy of lymphoid tissue

309
Q

Etiology of Cancer

A

loss of genetic integrity
- large or small scale
- damaged DNA due to mutations
- occur in germline or somatic cells

310
Q

How are mutations acquired?

A
  • carcinogens
  • inherited
  • spontaneous
311
Q

Environmental Carcinogens

A
  • ionizing radiation
  • virus
  • UV
  • dietary carcinogens
  • chronic inflammation
  • environment (smoking, pollution, diet)
312
Q

Hallmarks of Cancer

A
  • self sufficiency in growth signals
  • insensitivity to growth-inhibitory signals
  • evasion of apoptosis
  • limitless replicative capacity
  • sustained angiogenesis
  • tissue invasion and metastasis
  • evade immune surveillance
313
Q

Driving mutations

A
  • oncogenes
  • tumor suppressor genes
  • DNA repair genes
314
Q

Proto-oncogene

A

usually involved in normal cell growth and cell division

315
Q

Oncogene

A

proto-oncogene that has been activated by mutation
- growth factors, growth factor receptors, kinases, G-proteins
- gene amplification

316
Q

What are two examples of oncogenes?

317
Q

HER2 acronym

A

human epithelial growth factor receptor 2

318
Q

HER2 gene

A

encodes for growth factor receptors

319
Q

T/F: HER2 overexpression and amplification occur frequently in breast and ovarian cancer.

320
Q

Ras function

A
  • relays signals from cell surface
  • active when GTP bound
  • inactive and GDP bound
321
Q

What type of mutation causes Ras to always be on?

A

point mutation

322
Q

Tumor Suppressor Genes function?
Example?

A
  • halt cell cycle
  • p53
323
Q

Describe p53 activity during cell cycle

A
  • active at G1/S checkpoint
  • levels are normally low
324
Q

p53 nickname

A

Gaurdian of the Genome

325
Q

What state is p53 found in more than 50% of all cancers?

A

mutated (inactivated)

326
Q

p53 regulates (activates or inhibits) ?? of more than 50 different genes.

A

transcription

327
Q

When do activated p53 levels rise?

A
  • DNA becomes damaged
  • repair intermediates accumulate
328
Q

How are cancers resistant to apoptosis?

A
  • inactivate pro-apoptotic proteins
  • activate anti-apoptotic proteins
  • upregulate telomerase
329
Q

What is the significance of Bcl-2 anti-apoptosis genes?

A

overexpression prevents cells from undergoing apoptosis

330
Q

DNA repair genes function?
Examples?

A

correct errors that arise during DNA replication
- BRCA1 and BRCA2

331
Q

What is a common characterisitic of many cancers?
(60-80%)

A

chromosomal instability (CIN)

332
Q

CIN typically has…

A

poor prognosis

333
Q

CIN imbalance

A

instead of two copies, cancer cells had 1- 6

334
Q

CIN imbalances…
1. ?? number of chromsomes that have oncogenes
2. ?? chromosomes that bear TSG
3. ?? inflammation

A
  1. increase
  2. minimize
  3. increase
335
Q

T/F: Inflammation is a hallmark of cancer.

A

TRUE – Role of Immune System in Tumorigenesis

  • chronic inflammation contributes to cancer development
  • paradox
336
Q

How does chronic inflammation contribute to cancer development?

A

creates a microenvironment promoting genomic lesions and tumor initiation

337
Q

How is the immune system a paradox during tumorigenesis?

A

immune system protects host against tumor growth AND promotes tumor growth

338
Q

T/F: One mutation in DNA can cause cancer.

A

FALSE – one mutation is not enough to cause cancer

  • if one mutation caused cancer then the rate would be constant independent of age
  • percentage of people with cancer increases with age
339
Q

Biology of Neoplastic Growth

Dysplasia

A
  • premalignant state
  • tissue is atypical
  • usually epithelium
  • does not necessarily progress to malignancy
340
Q

Biology of neoplastic growth

Carcinoma in situ (CIS)

A
  • cancer in place
  • not invasive = basement membrane intact
  • curable by complete excision
341
Q

Biology of neoplastic growth

progression to invasion

A

invasion of blood vessels or lymphatics with metastasis

342
Q

Biology of neoplastic growth

What makes cancer so difficult to treat?

A
  • cells start as monoclonal
  • end result is tumor cell heterogeneity
  • tumor cells all have different number of mutations
  • becomes “survival of the fittest”
343
Q

biology of neoplastic growth

T/F: Not all tumor cells are actively dividing.

A

TRUE –

  • tumor growth ratio
344
Q

biology of neoplastic growth

Tumor Growth Fraction =

A

ratio of proliferating cells to total cells
- those with highest tumor growth fractions are most affected by chemotherapy

345
Q

T/F: People with high tumor growth fractions have better success rates with chemotherapy.

A

TRUE – large number of highly proliferative cells are easier to attack

346
Q

Paraneoplastic tumor

A

effects of cancer mediated by humoral factors

347
Q

Examples of paraneoplastic tumor

A
  • hormones released by a cancer cell (cushing syndrome = too much cortisol)
  • cross-reacting antibodies
348
Q

Paraneoplastic tumors are more common in

A
  • lung
  • breast
  • ovaries
  • lymphatics
349
Q

What is immune surveillance?
what cells are involved?

A
  • destruction of altered host cells
  • natural killer cells
  • cytotoxic T cells
350
Q

In regards to immune surveillance, immunodeficient patients…

A

are more likely to get cancer

351
Q

T/F: Cells need to be studied to confirm cancer.

352
Q

cytology

A

study of cells

353
Q

How are cells obtained for cytology?

A
  • biopsy (piece of tissue)
  • resection (larger piece of tissue)
  • fine needle aspiration (suction of some cells)
354
Q

What does cancer treatment depend on?

A

grading and staging

355
Q

cell grading

A

microscopic assessment
- how abnormal do they look?
- undifferentiated?

356
Q

cell staging

A

behavioral assessment
- size and extent of metastasis
- help plan the treatment

357
Q

Tumor Staging (TNM) system

A
  • Tumor: level 0-3
  • Nodes: level 0-2
  • Metastasis: level 0-2
358
Q

Gleason Grading system

A

levels 1-5
- 1 = differentiated
- 5 = completely undifferentiated

359
Q

Tumor Grading

Stage 0:

360
Q

Tumor grading

Stage 1:

A

not spread into surrounding tissues, but larger than stage 0

361
Q

tumor grading

Stage 2:

A

may extend into nearby tissue

362
Q

tumor grading

Stage 3:

A

spread to nearby lymph nodes, but not other parts of the body

363
Q

tumor grading

stage 4:

A

spread to distant tissues and organs

364
Q

Tumor markers

A

substances that appear in blood that can be used as a marker of neoplasm

365
Q

Are tumor markers used for cancer diagnosis?

A

no, need to look at cells for diagnosis

366
Q

What are tumor markers useful for?

A
  • confirmation of diagnosis
  • monitor therapy
367
Q

What are examples of Tumor markers?

A
  • prostate specific antigen; PSA
  • breast cancer-CA-15-3
368
Q

Lung cancer screening

A

chest radiographs (low sensitivity)

369
Q

Prostate cancer screening

A

PSA (controversial)

370
Q

breast cancer screening

A

mammogram at age 40

371
Q

cervical cancer screening

372
Q

colorectal cancer screening

A

fecal occult blood test, colonoscopy at 45 yrs

373
Q

Does early detection translate to decrease in deaths?

A

yes, otherwise whats the point in screening

374
Q

Cancer treatment

A
  • surgery
  • radiation
  • chemotherapy
  • hormone therapy
  • immunotherapy
  • angiogenesis therapy
375
Q

cancer treatment

surgery

A
  • to prevent cancer
  • removal of abnormal tissue
  • biopsy for diagnosis and staging
  • lymph node sampling
  • debulking surgery
  • palliative surgery
376
Q

cancer treatment

hormone therapy

A
  • receptor activation or blockage
  • interferes with cellular growth and signaling
  • doesn’t cure but works to prolong life
377
Q

cancer treatment

ionizing radiation

A

goals:
- eradicate cancer without excessive toxicity
- avoid damage to normal structures

  • ionizing radiation damages that cancer cell’s DNA
378
Q

cancer treatment

chemotherapy

A
  • use of nonselective cytoxic drugs that target vital cellular machinery or metabolic pathways critical to both malignant and normal cell growth replication

side effects:
- hair loss
- GI issues
- loss of appetite
- anemia
- frequent infections

379
Q

cancer treatment

immunotherapy

A
  • stimulating own immune system to work harder or smarted to attack cancer cell
  • giving immune system components to attack cancer (antibodies)
380
Q

What life style choices reduce risk of cancer?

A
  • don’t use tobacco products
  • sun safety
  • diet
  • drink alcohol in moderation
  • exercise regularly
  • vaccination (HPV)
  • safe sex practices
  • self-examination

Human Pathophysiology (4 decks)

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