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IPAP > Pathology: Block 1 > Flashcards

Pathology: Block 1 Flashcards

1
Q

Cell injury depends on what 3 things?

A

Type of injury
Duration/severity
Type of cell

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2
Q

List 4 examples of cell systems that are vulnerable to injuries

A

Membrane- integrity
Mitochondria- ATP supply
RER- protein synthesis
Nucleus- genetics

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3
Q

Define Ischemia, Hypoxia, and Anoxia

Difference between the 2?

A

Ischemia- insufficient blood flow, lacks O2 and nutrients
Hypoxia- reduces O2
Anoxia- complete lack of O2, impedes cell respiration, NaK pump failure= 0 ATP

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4
Q

Of the 3 forms of reduced O2 supply to tissues, which one is fastest?

A

Ischemia causes injury faster than hypoxia

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5
Q

How/why does ischemia-reperfusion injury cause damage?

A

Returning O2 to site activates free radicals which releases MORE radicals and cytotoxic enzymes

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6
Q

What are the 5 types of cellular adaptations that can occur from adverse/prolonged stimuli?

A 
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
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7
Q

Define Hyperplasia and what causes it

A

Increased size due to an increase in the NUMBER of cells

Hormone / chronic injury

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8
Q

Define Metaplasia

A

Reversible change in TYPE of cell

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9
Q

What is the sequence of changes from metaplasia to cancer if a stimulus is not removed?

A

Metaplasia
Dysplasia
Neoplasia
Cancer

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10
Q

Define Dysplasia

A

Disorderly arrangement/layering of cells

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11
Q

Define Necrosis

A

Premature/unnatural death of organs/tissue which then release inflammatory factors

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12
Q

What are the 3 types of necrosis

A

Coagulative- most common form
Liquefactive
Caseous

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13
Q

What causes coagulative necrosis?

What part of this process allows the superficial tissue to retain it’s shape/structure?

A

Rapid hypoxia or anoxia

Rapid inactivation of hydrolytic enzymes prevents tissue lysis

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14
Q

Where does coagulative necrosis most commonly occur?

A

Solid organs

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15
Q

Where does liquefactive necrosis commonly occur?

A

Brain, lytic enzymes change tissue to pus

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16
Q

What causes casous necrosis?

A

TB/Fungal infections cause cells to fall apart

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17
Q

What is the difference in final events between necrosis and apoptosis?

A

Necrosis- non membrane= inflammation

Apoptosis- membrane= phagocytosis

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18
Q

Define Dystrophic Calcification

Give two examples

A

Pathological calcification that occurs in dead/dying tissue from any type of necrosis
(atheromas of athersclerosis)

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19
Q

Define Metastatic Calcification

Give two examples

A

Pathological calcification that occurs in normal tissue other disease process causes secondary hypercalcemia
(hyperparathyroidism, multiple myeloma, Vitamin D toxicity, renal failure)

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20
Q

What are 4 processes found in the pathogenesis of inflammation/

A

Circulation
Permeability
WBC response/activation
Mediators

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21
Q

What step of the inflammation pathogenesis process does chemotaxis occur?

A

3- WBC response/activation

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22
Q

What step of the pathogenesis process does WBC adhesion get activated?

A

4- by cytokines (mediators)

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23
Q

Acute/immediate inflammation response brings in what WBC?

A

Neutrophils- granulocytic cells in blood circulation

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24
Q

Chronic inflammation includes what physiological changes and what kind of WBCs?

A

Vascular proliferation and tissue changes/scars

Lymphocytes and macrophages- agranulocytic cells in tissues

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25
Q

What are the cardinal signs of inflammation?

A

Redness- erythema/rubor
Heat- calor
Pain- dolor
Swelling- tumor

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26
Q

What are the 3 major steps of acute inflammation?

A

Dilation
Increased permeability
Emigration of leukocytes

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27
Q

What is the body’s first response to injury?

What causes this reaction?

A

Dilation- induced mostly by histamine

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28
Q

What are 3 types of mediators that would be found during the second step of the acute inflammation process?

A

Histamine
Bradykinin
Leukotrienes

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29
Q

During what step of the acute inflammation process do WBCs accumulate and become active?

A

3- emigration of leukocytes

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30
Q

What are the sequence of signs/symptoms of the acute inflammation process?

A

Warmth
Erythema
Edema

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31
Q

What are the 2 classes of inflammation mediators?

A

Plasma derived- from liver

Cell derived- cells

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32
Q

What are the 3 types of plasma-derived mediators?

A

Acute-phase proteins
Factor 7 (Hageman factor)
Complement proteins

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33
Q

What are the two types of cell-derived mediators?

A

Preformed (Mast, Platelets, Neutrophil macrophages)

Newly synthesized (leukocytes, leukocyte macrophages, endothelial macrophage lymphocytes)

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34
Q

Histamine is what type of mediator?

Where does it come from?

A

Cell derived

Mast, Basophil, Platelet

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35
Q

Leukotrienes and prostaglandins are what type of mediators?

A

Cell-Derived Arachidonic acid derivatives

Arise from membranes to be metabolized through either LOX or COX pathways

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36
Q

What does the Lipoxygenase pathway produce?

A

Leukotrienes- chemotaxis and permeability

Lipoxins- phagocytosis

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37
Q

What does the Cyclooxygenase pathway produce?

A

Prostaglandin
Thromboxane
Prostacyclin

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38
Q

What are the functions of prostaglandins?

A

Vasodilation
Vascular permeability
Pain
Fever

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39
Q

What are the functions of thromboxane?

A

Platelet aggregation
Thrombosis
Vasoconstriction

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40
Q

What are the functions of prostacyclin?

A

Counteracts Prostaglandins and Thromboxane so effects don’t become too extreme

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41
Q

Why are anti-inflammatory drugs taken?

A

COX inhibitors

Inhibit prostaglandin and thromboxanes

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42
Q

What are the functions of bradykinins?

A

Same as histamine but at slower pace
Amplifly/prolong inflammatory response
Begins coagulation
Creates pain

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43
Q

How are bradykinins formed?

A

Activation of hageman factor (coagulation factor 7)

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44
Q

What 2 things comprise the complement system?

A

Innate and Adaptive immunity

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45
Q

What are the 3 functions of the complement system?

A

Prolongs inflammation
Phagocytosis via opsonization
Cell lysis- membrane attack complex

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46
Q

Define the Complement System

A

Cascade of proteins acting through separate pathways to end in Membrane Attack Complex to destroy a cell

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47
Q

Define the Complement System Alternate Pathway?

A

Bacterial/fungal endotoxins/snake venom

Does NOT use Ag-Ab complex

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48
Q

What sequence of events starts the Complement’s Alternate Pathway?

A

IgA and properdin activate complement B and D to influence C3

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49
Q

Define the Complement Lectin pathway

A

Starts w/ carbohydrate binding on bacterial surface

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50
Q

How are Plymorphonuclear Neutrophils visually identified?

A

Segmented nucleus and cytoplasm w/ granules

“neutrophilic granulocytes”

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51
Q

What are 4 unique characteristics of PMNs?

A

1st to appear in acute inflammation
Phagocytic
Granules kill w/ O2 radicals
Produces cytokines, promotes fever

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52
Q

PMNs make up ? % of circulating WBCs?

Eosinophils make up ? %

A

60-70%

2-3%

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53
Q

Eosinophils are associated with ? activity?

A

Interact w/ basophils during Allergic reactions

and Parasitic infections

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54
Q

What are 2 unique characteristics about eosinophils?

A

Slower to sites than PMNs but survive longer (seen w/ chronic inflammation)
Have mobility, phagocytic and bactericidal actions similar to PMNs

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55
Q

Basophils are predominant in allergic reactions mediated by what?

A

IgE

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56
Q

Basophils are precursors of what cells?

A

Mast cells

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57
Q

What is the other 2 names of macrophages?

A

Tissue mononuclear cells

Histiocytes

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58
Q

Where are macrophages derived from?

A

Blood monocytes

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59
Q

How are macrophages visually identifiable?

A

One large nucleus

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60
Q

What two cells are longer living than PMNs and are seen in chronic infectious states?

A

Eosinophils

Macrophages

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61
Q

Platelets contain granules with what 4 substances?

A

Histamine
Coagulation proteins
Cytokines
Growth factors

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62
Q

Acute inflammatory reactions have what 3 outcomes?

A

Complete resolution
Healing by scar/fibrosis
Chronic inflammation

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63
Q

Chronic inflammation is characterized by what 3 characteristics?

A

Mononuclear infiltration
Tissue destruction
Repair

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64
Q

What 4 things can cause chronic inflammation?

A

Resistant microbes
Immune responses
Toxic substances
Foreign bodies

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65
Q

Systemic inflammation is AKA ?

A

Acute phase reaction

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66
Q

What are the 3 acute-phase proteins?

What are they indicative from?

A

CRP
Fibrinogen
Serum amyloid
Acute-Phase Reaction

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67
Q

What are the clinical S/Sx of systemic inflammation?

A 
Fever from PMN released pyrogens
Leukocytosis
Inc HR/BP
Decreased sweating
Anorexia
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68
Q

Fever during systemic inflammation triggers what reaction to occur in the brain?

A

Prostaglandin synthesis in hypothalamus

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69
Q

Systemic inflammation that presents with anorexia, somnolence and malaise are secondary to what event?

A

Cytokine impact on brain cells

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70
Q

Define Serous Inflammation

A

Mildest form of inflammation

Caused by physical agents

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71
Q

Define Fibrinous Inflammation

A

Exudate w/ fibrin and cellular debris

Bacterial infection

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72
Q

Define Purulent Inflammation

A

Yellow fluid of dead PMNs/tissue debris

Bacterial infection

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73
Q

What is the difference between fibrinous and purulent inflammation locations?

A

Purulent can be on mucosa, skin or internal organs

Abscesses

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74
Q

Define Ulcerative Inflammation

A

Surface tissues broken down from underlying inflammation

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75
Q

Define Pseudomembranous Inflammation

A

Combined ulcerative inflammation w/ fibrino-purulent exudate

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76
Q

C. Diff is an example of what type of inflammation?

A

Pseudomembranous

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77
Q

Define Granulomatous Inflammation

A

Chronic inflammation, not acute

Macrophage and fibroblasts create barrier

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78
Q

TB, histoplasmosis, sarcoidosis and parasites are what type of inflammation?

A

Granulomatus

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79
Q

What starts the wound healing and tissue repair process that is critical to the survival of an organism?

A

Inflammatory response

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80
Q

What are the two types of wound healing/tissue repair reactions?

A

Regeneration

Scar formation

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81
Q

Define the Regeneration Reaction of wound healing

A

Proliferation of residual/uninjured cells and tissue replacement by stem cells

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82
Q

Define the Scar Formation reaction of wound healing

A

When injured tissues are incapable of regeneration or severe damage has occurred to supporting structures

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83
Q

Scar formation occurs from what type of tissue?

A

Fibrous connective

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84
Q

What does scar tissue have and what does it lack?

A

Structure stability for integrity

Cannot replace function of lost cells

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85
Q

What are the 4 steps of the wound healing process?

A

Hemostasis
Inflammatory
Proliferative
Remodeling

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86
Q

Wound resolution and consequences depend on what?

A

Type of cells injured

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87
Q

Define Labile Cells and their wound healing capabilities

A

Continuously divide and self-replace

Easily regenerate for wound healing

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88
Q

What type of cells are most affected by chemo/radiation therapy?

A

Labile- skin, GI tract, hematopoietic

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89
Q

Give 3 examples of Labile Cells

A

Skin
GI tract
Hematopoietic

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90
Q

Define Stable Cells and their wound healing capabilities

A

Rarely self-divide but can be stimulated to replicate

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91
Q

Where are Stable Cells found?

A

Kidney proximal renal tubule

Liver

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92
Q

Define Permanent Cells and their wound healing capabilities?

A

Non dividing cells that lack the capacity to replicate

No new cells form, only fibrous scarring

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93
Q

Where are Permanent Cells found within the body?

A

Neurons

Myocardium

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94
Q

What cells are least affected by chemo/radiation therapy?

A

Neurons
Myocardium
Permanent cells

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95
Q

Define Angioblasts and when do they arrive during the wound healing process?

A

Precursors to blood vessels

Appear 2-3 days after injury

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96
Q

When do Fibroblasts arrive during the wound healing process and what is their function?

A

Several weeks later

Re-establishes the extracellular matrix by producing fibrinoectin and collagen

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97
Q

Myofibroblasts are hybrid properties of what two things?

A

Smooth muscles

Fibroblasts

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98
Q

What are myofibroblasts purpose during the wound healing process?

A

Contract pulling margins inward

Reduces wound size allowing proliferating epithelium to fill in the injured site

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99
Q

What events happen during the Hemostasis phase of wound healing?

A

Vasoconstriction then dilation
Platelet activation
Coagulation
Fibrin + platelet + RBC=clot

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100
Q

What events happen during the Inflammation phase of wound healing?

A

Vessels leak into wound and cause localized swelling

Controls bleeding and prevents infection

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101
Q

What events happen during the Proliferation phase of wound healing?

A

New tissue from collagen and fibronectin
Epithelialization
Wound contracts and new vessels are formed

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102
Q

During epitheliazation, what layer of the skin differentiates?

A

Deep basal differentiate into layers

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103
Q

What events happen during the Tissue Remodeling phase of wound healing?

A

Maturation phase
Begins 21 days after injury
Collagen is remodeled and wound fully closes

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104
Q

Define Stricture

A

Tubular structures are narrowed by the healing process

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105
Q

Define First/Primary Intention

A

Clean, uninfected laceration that is healed by epitherlial regeneration as the principal mechanism

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106
Q

During what part of wound healing does tensile strength increase with time?

A

First/Primary intention

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107
Q

Define Secondary Intention

A

Large/complex wound healing for dirty/ulcerated wounds

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108
Q

Secondary intention includes what two processes?

A

Regeneration

Scarring

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109
Q

During what phase of wound healing is a large scar and inflammatory reaction more intense?

A

Secondary intention due to abundant granulation tissue

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110
Q

What type of medication/mineral must be avoided during wound healing?

A

Glucocorticoids- anti-inlfammatory affect weakens scar

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111
Q

What are 3 types of wound healing complications?

A

Dehiscence- separation of margins due to tension or infection
Hypertrophic- thicker than expected
Keloid- Taller and wider scar than original wound (more common in dark skin individuals)

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112
Q

List 4 parts of Inate Immunity

A

Mechanical Barriers- skin/cilia
Phagocytic cells- neutrophil, macrophage
NK Cells- special t-lymphocytes
Protective Proteins- lysozyme, properdin

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113
Q

Where are Lysozyme and Properdin proteins found and what are their purpose?

A

Lysozyme- body fluid protective protein

Properdin- alternate complement

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114
Q

Acquired immunity is the “learned” immunity and is based off of responses to ?

A

Ags- any chemical/biological substance that induces a specific immune response

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115
Q

Acquired Immunity words towards what end goal?

A

Immunocompetence- body’s ability to mount appropriate immune responses now and for future events

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116
Q

Difference between Primary and Secondary Lymphoid tissue?

A

Primary- B/T lymphocytes production

Secondary- B/T colonized in lymph nodes

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117
Q

Tonsils, adenoids and spleens are heavily colonized by which lymphocyte?
What colonizes GI/Bronchial mucosa?

A

B Lymphocytes

MALT

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118
Q

70% of circulating lymphocytes are ?

A

T-cells

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119
Q

Function of CD4 cells

A

Part of Ag response

Help B lymphocytes produce Abs

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120
Q

What cell secretes cytokines?

A

CD4- secrete interleukin

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121
Q

What does interluekin cause once it’s secreted?

A

Stims macrophages to become phagocytic

Triggers IgE/immunoglobulins to activate eosinophil and basophils

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122
Q

Function of CD8 cells?

A

Suppress unwanted Ab production

Mediates killing of foreign cells

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123
Q

CD4 cells are AKA?

CD8 cells are AKA?

A

4- Helper-T cells

8- Suppressor/cytotoxic cells

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124
Q

Function of NK cells?

A

Subset of T-cell that lacks an Ag receptor

Recognizes cells infected by viruses

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125
Q

What does the CD in CD4 or CD8 cells stand for?

A

Cluster Differentiation

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126
Q

What cell is essential for Ab production?

A

B Cells

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127
Q

Why are B cells essential for Ab production?

A

Congegrate in nodes/spleen and activate Ab production gene to form Ag receptors on cell surfaces

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128
Q

What is triggered when Ag attaches to B cell surfaces?

A

Plasma Cells

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129
Q

Define Plasma Cell

A

Fully differentiated decendents of B cells w/ numerous ER

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130
Q

Function of Plasma Cells

A

Mass Ab production and release into circulation

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131
Q

Abs are AKA and have what two parts?

A

Immunoglobulins w/ heavy and light chains

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132
Q

What are the Heavy and Light Chains of Abs?

A 
Heavy- determines Ab property/function that is specific and unique to each class
Light- variable for targeted Ag
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133
Q

RBCs have _____ and serum has _____

A 
RBC= Ag
Serum= Ab
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134
Q

What Ag and Abs does Group A blood have?

A 
RBC= A Ag
Serum= anti-B Abs
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135
Q

What Ag and Abs does Group B blood have?

A 
RBC= B Ag
Serum= anti-A Abs
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136
Q

What Ag and Abs does Group O blood have?

A 
RBC= No Ags
Serum= anti-A and anti-B Abs
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137
Q

What Ag and Abs does Group AB blood have?

A 
RBC= both A and B Ags
Serum= No Abs
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138
Q

What blood type if the universal RBC donor?

What blood type is the universal RBC recipient?

A

O- donor

AB- recipient

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139
Q

What is the Rh factor?

A

D antigen on surface of RBCs

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140
Q

How/when are Anti-D antibodies formed since they’re not naturally occurring?

A

Rh neg PT exposed to Rh pos

Female birthing Rh pos baby or transfusion of Rh pos blood

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141
Q

What happens to Rh factors of a mother during pregnancy?

A

Rh neg exposed to Rh pos forms IgG Abs that can cross placenta
1st Rh pos baby- not harmed due to lack of Rh Abs in mother
2nd Rh pos baby will be killbed by Anti-D Abs

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142
Q

What is the purpose/use of RhoGam?

A

Given to mother w/ing 12hrs of deliver to destroy fetal Rh pos RBC and prevents her from forming Anti-D Abs

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143
Q

Define Cross-Match blood transfusion

A

Type and Cross
Donor serum mixed w/ recipient RBCs
Recipient serum mixed with donor RBCs

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144
Q

Define Type and Screen blood transfusion

A

PT blood is typed but not cross-matched

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145
Q

What type of blood transfusion locks in donor blood for a specific recipient/PT?

A

Cross-Match/ Type and Cross

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146
Q

What type of blood transfusion identifies a “soft reserve” and allows for greater blood bank flexibility?

A

Type and Screen

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147
Q

During a Emergency Release blood trasnfusion what type of blood is pushed out?

A

Type O RBCs

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148
Q

What are the 3 types of blood transfusions?

A

Cross-Match
Type and Screen
Emergency Release

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149
Q

What type of transfusion reaction has the highest risk?

A

Whole blood

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150
Q

What is a “minor” transfusion reaction?

A

Reaction to preservative

Urticaria, fever, bronchospasms

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151
Q

Minor transfusion reactions can be reduced by using ?

A

Leukocyte-poor RBCs

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152
Q

What is a “major” transfusion reaction?

A

ABO mismatch

Fever/chills, back pain, dyspnea, renal failure

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153
Q

What steps are take and what things are given to a PT after a “major” transfusion reaction?

A

Stop transfusion
IV fluids
IV BiCarb
Donor and PT blood to lab

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154
Q

Define Hypersensitivity reaction

A

Abnormal immune response to exogenous Ag or endogenous auto-antigens

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155
Q

What are the 4 classifications of hypersensitivity reactions?

A

1- anaphylactic/atopic
2- cytotoxic Ab-mediated
3- immune complex
4- cell mediated/delayed type

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156
Q

Type I hypersensitivity reaction is what type of response?

A

IgE mediated response

Allergin sensitized B cells->Plasma Cells->IgE

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157
Q

Which hypersensitivity reaction requires a prior exposure for the reaction to take place?

A

Type I

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158
Q

What happens during a Type I hypersensitivity reaction if PT is re-exposed?

A

Ag-Ab complex form on Basophils or Mast Cells

Histamine released and increases permeability->edema->emigration of inflammatory cells

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159
Q

What are the inflammatory cells involved in a Type I hypersensitivity?

A

Eosinophils

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160
Q

Give four clinical examples of Type I hypersensitivities?

A

Anaphylaxis
Asthma
Atopic dermatitis
Allergic Rhinitis

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161
Q

What events occur during a Type II hypersensitivity

A

IgG or IgM mediated Ag-Ab complex

Ab bind to Ag in basement membrane and activates complement system->MAC->Cytotoxicity

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162
Q

During what type of hypersensitivity do Abs target a specific tissue or cell of the body?

A

Type 2

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163
Q

What are the intrinsic or extrinsic causes of a Type 2 hypersensitivity?

A

Intrinsic- autoimmune

Extrinsic- Drug, Virus, Chemical are seen a foreign and mimics an autoimmune response

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164
Q

What are 5 clinical examples of Type 2 Hypersensitivities

A 
Transfusion Reaction
Graves Disease
Goodpasture's Syndrome
Myasthenia Gravis
Hemolytic Anemia
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165
Q

Define and explain Graves Disease

A

Hyperthyroidism AKA thyrotoxicosis

Auto-Abs bind to TSH receptor and stims over production of thyroid hormone

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166
Q

Define and explain Goodpasture’s Syndrome

A

Auto-Ab attacks collagen in lungs and kidneys

Causes damage to renal glomeruli (blood and protein) and SOB/bloody cough

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167
Q

Define and explain Myasthenia Gravis

A

Auto-Abs attach to Ach receptors on striated muscle cells blocking Ach stimulation leading to severe muscle weakness

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168
Q

Define and explain hemolytic anemia

A

Auto-Abs against RBC Ags
Results in clumping/destruction of RBCs w/ the fragments collecting in spleen (splenomegaly), hemolyzed RBCs cause bilirubin and jaundice

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169
Q

What is the less common hypersensitivity reaction?

A

Type 3

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170
Q

Define and explain Type 3 hHypersensitivy?

A

Ag-Ab complex mediation that incorrectly deposit on structure and become trapped on semi-permeable membranes where they accidentally activate complement systems to recruit WBCs leading to cell damage

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171
Q

What are 3 clinical examples of Type 3 hypersensitivity?

A

Systemic Lupus Erythematosus
Post Strep Glomerulonephritis
Polyarteritis nodos

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172
Q

What mediates Type 4 Hypersensitivity?

A

Previously sensitives T Cells or macrophages

NO Ab involvement

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173
Q

Define and explain Type 4 hypersensitivity?

A

No Ab involvement
Macrophages take up Ag and presents to T cells causing cytokine release transforming macrophages to epithelioid cells and formation of granulomas

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174
Q

What are 2 clinical examples of Type 4 Hypersensitivity?

A

Contact dermatitis

Granulomatus reactino from TB, Fungi or sarcoidosis

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175
Q

What does contact dermatitis result in?

A

Wheal formation

Vesicles

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176
Q

What type of hypersensitivity is a TB test?

A

Delayed type

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177
Q

Autoimmune diseases can be diagnosed when what 3 situations exist?

A

Auto-Abs documented
Immune mechanism causes pathologic lesion
Disorder has an immune origin

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178
Q

What are the two forms of autoimmune diseases?

A

Systemic- multi-organ

Specific- limited to one organ

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179
Q

What are examples of systemic autoimmune diseases?

A 
Lupus Erythematosus
Rheumatic fever
RA
Systemic sclerosis
Polyarteritis nodosa
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180
Q

What are examples of organ-specific diseases?

A 
Brain- MS
Thyroid- Hashimotos
Blood- AI hemolytic anemia
Kidney- glomerulonephritis
Muscle- myastenia gravis
Skin- pemphigus vulgaris
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181
Q

What are some characteristics of Systemic Lupus Erythematosus?

A

Common in women
Type 3 hypersensitivity
Triggers synthesis of more self cells
Anti-Nuclear Abs to nuclear proteins

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182
Q

What are the criteria for diagnosing Systemic Lupus Erythmatosus?

A 
Arthritis
Renal disorder
Dermatitis
Serositis
Neurologic disorder
Vasculitis
Hematologic disorder
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183
Q

What are skin S/Sx of Systemic Lupus Erythmatosus?

A

Malar rash (butterfly rash that spares nasolabial folds)
Discoid rash
Oral/pharyngeal ulcer
Photosensitivity

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184
Q

Define Immunodeficiency/Immune Compromise

A

Inadequate immune response causing reduces resistance to infections

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185
Q

What is lymphopenia a disease example of?

A

Immunodeficiency

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186
Q

What are the two types of immunodeficiency diseases?

A

Primary- congenital: T/B cell differentiation affected

Acquired- more common: immunosuppression, marrow dysfunction, diabetes, AIDS

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187
Q

What kind of virus is HIV?

A

Retrovirus- replicating by reverse transcriptase in T Cells

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188
Q

What is the CD4:CD8 ratio in HIV?

A 
4:8= 2:1
AIDS= .5:1
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189
Q

Crisis phase symptoms of HIV occur when CD4 counts drop below?

A

Less than 200

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190
Q

What are the opportunistic infections seen in AIDs?

A 
Cytomegalovirus
Candida
Crytpococcus
TB
Herpes simplex
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191
Q

What kind of tumors are seen in AIDS PTs?

A

Kaposi sarcoma

Lymphoma

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192
Q

Define Neoplasia

A

New Growth

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193
Q

How are tumors named?

A

-oma suffix

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194
Q

What kind of origin does carcinoma and sarcoma have?

A

Carcinoma- epithelial

Sarcoma- mesenchymal

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195
Q

What are the 3 exceptions to tumor name appearing benign but is not?

A

Melanoma
Lymphoma
Leukemia

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196
Q

What are the benign types of epithelial tumors?

A

Pailloma

Adenoma

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197
Q

What is the malignant type of epithelial tumor?

198
Q

What are the benign and malignant mesenchymal tumors?

A

Benign: oma suffix
Malignant: - sarcoma suffix

199
Q

What is the hallmark S/Sx of anaplasia?

A

Anaplasia- lack of differentiation

200
Q

Due to slow growth, benign tumors retain what characteristic?

A

Encapsulated- makes tumor mobile, discrete and palpable

201
Q

Due to rapid growth, malignant tumors generally possess what 2 characteristics?

A

Poorly demarcated from surrounding normal tissue

Locally invasive allowing for metastases

202
Q

What is the most reliable feature that separates malignant from benign tumors?

A

Locally invasive

203
Q

What characteristic marks a tumor as malignant?

A

Metastasis

204
Q

Metastasis risk increases with what 4 things?

A

Non-differentiated
Aggressive local invasion
Rapid growth
Large size

205
Q

What are the three pathways that tumor metastasis spread?

A

Hematogenous spread
Lymphatic spread
Seeding of body cavities/surfaces

206
Q

What 2 organs and what part of the organ are most frequently involved in hematogenous spreading?

A

Liver
Lungs
Veins penetrated easier

207
Q

Define sentinel lymph node

A

First node to receive lymphatic drainage from primary tumor site

208
Q

What procedure is often used to detect metastatic cells?

A

Biopsy of sentinel nodes

209
Q

Where is malignancy seeding often seen?

A

Peritoneal cavity

210
Q

What is the criteria used to determine the extent a tumor has spread?

A

Staging- based on clinical exam, radiology, biopsy and surgery offers more prognostic value than grading

211
Q

What procedure/method is better for predicting a PTs outcome

212
Q

What is the most common method of staging?

A

TNM System
T- Tumor size T1T2T3T4
N- number of lymph nodes w/ cancer NXN0N1
M- metastasis MOM1

213
Q

How is cancer grading conducted?

A

Histologic exam of tumor

214
Q

What method/procedure is used for treatment planning of certain cancers?

215
Q

Cancer grading reflects the degree of _______

A

Differentiation

Less differentiation= aggressive

216
Q

What is the Cancer Grading system?

A 
X- unknown
I- well differentiated, low grade
II- Moderate diff, intermediate
III- poor diff, high grade
IV- undifferentiated, high grad
217
Q

What are examples of chemical carcinogens?

A 
Asbestos
Nitrosamines
Naphthylamine dyes
Arsenic
Aflatoxin
218
Q

What are examples of carcinogen microbes?

A

H. Pylori

S. Haematobium

219
Q

What are examples of viral carcinogens?

A

Oncovirus
HPV
Epstein-Barr Virus
Hep B

220
Q

UV light radiation causes what three types of cancer?

A

SCC
BCC
Melanoma

221
Q

What types of ionizing radiation are carcinogens?

222
Q

What is the link between skin damage from radiation and treatment?

A

Tissues easily damaged by radiation can be readily treated by radiation therapy

223
Q

What type of cells are most sensitive by ionizing radiation?

A 
Stem Cells
Hematopoietic
Reproductive
Epidermis- skin/intestine
1st trimester fetus
224
Q

What tissues are least sensitive to ionizing radiation?

A

Nerve cells
Bone
Muscle

225
Q

Define proto-oncogenes?

A

Normal cellular genes that regulate cell growth and differentiation

226
Q

Define Oncogenes?

A

Mutated/damaged proto-oncogene leading to uncontrolled cell growth

227
Q

Proto-oncogenes can be changed into oncogenes by what 4 mechanisms?

A

Point Mutation
Gene Amplification- more copies=inc malignancy
Translocation- causes over-expression of adjacent gene
Insertion of viral genome

228
Q

Define Tumor Suppressor Gene

A

Anti-oncogene w/in normal cells due to protective action against oncogene activation

229
Q

Name 3 examples of genetic causes of cancer?

A

Familial adenomatous polyposis coli
Neurofibromatosis Type 1
Wilms’ tumor (nephroblastoma)

230
Q

What are Cafe Au Lait spots associated with?

A

Neurofibromatosis Type 1

231
Q

Where can tumor markers be isolated from?

A

Blood
Urine
Stool
Cancerous tissue

232
Q

What are malignant cell tumor markers?

A

Retention of functions essential for survival

Regression to fetal/embryonic functions

233
Q

Tumor markers may be used for what 4 things?

A

Diagnosis
Predict response
Assess treatment response
Monitoring

234
Q

Tumor marker do not generally recommended for routine screening with what exception?

A

Prostate Specific Antigen

235
Q

What is Alpha-fetoprotein tumor marker used for detecting?

A

Liver
Testicles
Ovaries

236
Q

What is CA-125 tumor marker used for detecting?

A

Ovarian
Lung
Breast

237
Q

What is Carcinoembryonic Antigen tumor marker used for detecting?

A

Colon
Lung
Breast
Ovary

238
Q

What is Human Chorionic Gonadotropin tumor marker used for detecting?

A

Testicular

Breast

239
Q

Most cancer occur during _____ of life and are caused by _____?

A

Mid-later

Environmental causes

240
Q

What are the dominant risk factors for most cancers?

A

Environmental influences

241
Q

What are the top two environmental factors of cancer epidemiology?

A

Smoking

Alcohol

242
Q

What does the CAUTION acronym mean for cancer?

A 
Change in bowel/bladder
A sore that doesn't heal
Unusual bleeding/discharge
Thickening lump on breast
Indigestion
Obvious wart/mole change
Nagging cough/hoarseness
243
Q

Define Cachexia

A

Common Sx in cancer PTs
Wasting away of body fat/muscle
Weak, anorexia, anemia

244
Q

Define Paraneoplastic Syndrome

A

Earliest sign of occult neoplasm
Hypercalcemia
Hypercoagulability

245
Q

What is the most common S/Sx in Paraneoplastic Syndrome?

A

Hypercalcemia

246
Q

Define Hereditary Disorder
Define Familial Disorder
Define Congenital disorder

A 
H= derived from parents
F= through generations
C= present at birth but are NOT genetic
247
Q

__% of pediatric pediatric inpatients have a genetic disorder?

248
Q

Define Morphogenesis

A

Evolution/development of organ/body part

249
Q

What happens with errors of morphogenesis?

A

Incompatible w/ life

Spontaneous abortion during 1st trimester

250
Q

Define Agenesis

A

Absence of organ

Organ contain primordial tissue

251
Q

Define Aplasia

A

Entire organ mass is comprised of primordial tissue

252
Q

Define Atresia

A

Absence/closure of a body opening

253
Q

Define Hypoplasia

A

Underdevelopment of tissue/organ/body

254
Q

Define Involution Failure

A

Persistence of embryonic structures long into development

255
Q

What types of morphogenesis errors usually result in non-viable births?

A

Agenesis

Aplasia

256
Q

__% of congenital defects are idiopathic

257
Q

Define Teratogens

A

Agents known to cause fetal malformations

258
Q

What are the 3 types of teratogens

A

Physical- radiation
Chemical- ETOH (most preventable teratogen)
Microbial- TORCH

259
Q

Define TORCH syndrome

A 
Toxoplasmosis
Other
Rubella- german measles
Cytomegalovirus
Herpes
260
Q

Define Genome

A

Complete set of chromosomes

261
Q

Define Keryotype

What can it be AKA?

A

Full chormosome set contained w/in a nucleus

AKA- chromosomal count/code

262
Q

Define Genotype

A

Genetic form

Set of instructions that may/not be expressed

263
Q

Define Phenotype

A

Physical form

Unique appearance that can be effected by environment

264
Q

What two parts make up the observed phenotype?

A

Expressed genotype

Environmental influence

265
Q

What are the 3 types of chromosome structural abnormalities?

A

Deletion
Inversion/breakage
Translocation

266
Q

Define Numerical Abnormality

A

Loss/gain of chromosome

267
Q

Define Aneuploid

A

Cells possessing abnormal numbers of chromosomes

268
Q

Define Euploid

A

Normal number of chromosomes

269
Q

Define 47XXY

Define 45XO

A 
Klinefelters syndrome (male)
Turners syndrome (female)
270
Q

What are the odds of females delivering a baby w/ Downs?

A

Over 45y/o= 1:25

271
Q

Prenatal counseling is required for women older than __y/o

272
Q

What are the clinical characteristics of Down’s Sydrome?

A 
Retardation
Epicanthal folds
Macroglossia
Simian Crease
Internal organ defects
Hematologic disorders
273
Q

What is the incidence reate of Klinefelters Syndrome?

A

1:700
Little/no sperm production
Rarely passed/inherited

274
Q

What are the clinical characteristics of Klinefelters?

A

2* characteristics not fully developed at puberty
Body habitus
Learning disability

275
Q

What are the incidence rates of Turner’s Syndrome?

A

1:3000

Ovaries don’t mature or atrophy

276
Q

What are the clinical characteristics of Turner’s Syndrome?

A

2* characteristics not developed at puberty
Body habitus
Heart defects

277
Q

What are the 3 main patterns of single gene disorders?

A

Autosomal dominant
Autosomal recessive
Sex-linked

278
Q

Define Autosomal Dominant

A

Homozygous AA or heterozygous Aa
Dominant traits expressed
A will over ride a in heterzygous pairing

279
Q

Define Autosomal Recessive

A

Homozygous aa

Recessive trait might be expressed in phenotype

280
Q

Define Sex-Linked Disorder

A

Primarily recessive disorders w/ X-linked chromosomes

X and Y are not direct alleles of each other

281
Q

What are examples of autosomal dominant disorders?

A 
Marfans
Familial hyperchoesterolemia
Polycystic kidney disease
Huntingtons
Osteogenesis imperfecta
282
Q

What is the incidence rate and characteristics of Marfan’s Sydrome?

A

1:5000

CT issue of fibrillin

283
Q

Why is the lack of fibrillin in Marfan’s Syndrome important?
What happens without it?

A

Glue for CT structure

Heart failure/Aortic rupture

284
Q

What are the clinical characteristics of Marfan’s Syndrome?

A

Tall/slender habitus w/ elongated head
Elongated fingers, loose joints
Aortic aneurysms
Cataracts/lens detachments

285
Q

What is the most important and frequently encountered autosomal disorder in the US?

A

Familial Hypercholesterolemia

Mutated gene the encodes LDL

286
Q

What are the clinical characteristics of Familial Hypercholesterolemia?

A

Atherosclerosis/heart disease
Xanthomas- lipid rich nodules
Eyelid deposits

287
Q

What are the characteristics of Polycystic Kidney Disease?

A

Abnormal flank pain
PAINLESS hematuria
UTI
Hypertension

288
Q

When do Huntington’s Disease symptoms start?

What is the life expectancy after diagnosis?

A

30-40

10-15yrs after due to pneumonia, fall, suicide

289
Q

What is the pathogenesis of Huntington’s Disease?

A

Progressive neurological disorder of involuntary movements leading to premature brain death and atrophy

290
Q

What are the clinical characteristics of Huntington’s Disease?

A

Chloreiform movements- gyrating movement of trunk and limb

Grimacing face

291
Q

What is Osteogenesis Imperfects AKA and what is the cause of the disease?

A

Brittle Bone Disease

Defected Type I Collagen

292
Q

What are the clinical characteristics of Osteogenesis Imperfecta

A

Multiple, easy Fx
Can be confused w/ abuse
Blue sclera

293
Q

What is the largest group/variety of genetic disorders?

A

Autosomal recessive

294
Q

Why are autosomal recessive disorders so large/common?

A

Encoded by genes on on eo f 22 autosomes and NOT the 23rd sex-linked gene

295
Q

What are the basic features of autosomal recessive disorders?

A

Only in homozygous w/ both recessive genes present and usually w/ unaffected heterozygous parents

296
Q

What are the common Autosomal Recessive Disorders?

A 
CF
SCA
Phenylketonuria
Wilson's Disease
Hemochromatosis
297
Q

What PT population is CF most common in?

A

Caucasian/Norther European

298
Q

What autosomal recessive disorder is the most lethal?

299
Q

What is the pathogenesis for CF?

A

Abnormally thick mucus blocks airway and pancreatic ducts

300
Q

What are the clinical characteristics of CF?

A

Pulmonary infections

Pancreatic insufficiency

301
Q

How is CF diagnosed?

A

Pilocarpine test- sweat test for excess NaCl in sweat

302
Q

What is the pathogenesis of SCA?

A

Hgb defect causes sickling when O2 is low

303
Q

Define a Sickle Cell Crisis?

A

Fever
Respiratory disease
Hemolysis of RBCs causing anemia and jaundice

304
Q

Define Splenic Sequestrian Crisis?

A

Spleen over removes sickling RBCs causing acute anemia and spleen damage

305
Q

PKU is the lack of what enzyme?

A

Phenyalanine hydroxylase- metabolizes phenylalanine into tyrosine

306
Q

What are the clinical characteristics of PKU?

A

Excess phylalanine causes melanin synthesis inhibition, PT have fair skin/hair and blue eyes
Continued build up leads to retardation and seizure

307
Q

What kind of diet do PKU PTs have to follow?

A

Avoid- meat, fish, nuts, legumes, dairy products and aspartame

308
Q

What are the X-linked recessive diseases?

A 
Hemophilia
Duchenne Muscular Dyst.
Fragile X Syndrome
Color blindness
G6PD Deficiency
309
Q

How are X-linked recessive diseases passed along?

A

Mother->son

Only fertile male-> daughters

310
Q

What form of hemophilia is more rare?

311
Q

What is the pathogenesis for Hemophilia?

A

Coagulation factor 8 (A) or 9 (B)

312
Q

What are the clinical characteristics of hemophilia?

A

B s/sx always severe

Easy nose/oral bleeding

313
Q

How is hemophilia treated?

A

Infusion of man-made recombinant clotting factors

314
Q

Who does Duchenne Musc. Dystrophy effect?

A

1:3300 males

315
Q

What is the pathogenesis of Duchenne Muscular dystorphy?

A

Defected dystophin protein which normally interacts w/ contractile proteins to maintain shape

316
Q

What are the clinical characteristics of Duchenne Muscular Dystrophy

A

Affects skeletal muscle

Progressive muscle weakness/wasting

317
Q

What is the difference between male and females inheritting Fragile X Disease?

A

Males= mental deficiency

318
Q

What is the pathogenesis of Fragile X Syndrome?

A

Amplification of fragile portion of X-chromosome

319
Q

What are the clinical characteristics of Fragile X Syndrome?

A

Mental retardation

Macro-orchidism in 90% of prepubertal males

320
Q

Define Multifactorial Inheritance

A

Familial disorders don’t follow Mendelian genetic rules

321
Q

What are the traits/disease features of multifactorial inheritance?

A

Product of several genes
Ex/endogenous influences
Genes encoding error exhibit dose effect
Sibling risk determined from familial data

322
Q

What are examples of multifactorial inheritance?

A

Dwarfism
Hypertenstion
Diabetes
Gout

323
Q

What are increased/decreased levels of Alpha-Fetoprotein indicative of?

A 
Inc= brain/kidney abnormalities
Dec= Down's
324
Q

What is Chorionic Villus Biopsy used for?

A

Tissue sample of placenta for chromosomal and enzyme analysis

325
Q

When is an amniocentesis performed?

A

12 - 18wks for chemical/chromosomal analysis

326
Q

Extracellular fluid is a combination of what two liquids and what majority ions?

A

Interstitial and plasma

High Na, Low K

327
Q

Intracellular fluid is made up of what ions?

A

Low Na, High K

328
Q

How much liquid is required per day to clear byproducts of metabolism?

A

500-800ml/day

329
Q

Define Edema

A

Excess fluid collection in interstitial spaces and body cavities

330
Q

Interstitial space is AKA ?

A

Third space

331
Q

Edema results form an imbalance between what things?

A

Permeability
Oncotic pressure
Venous pressure- obstruction or overload
Lymphatic obstruction- or inadequate drainage

332
Q

High permeability causes leakage to where?

A

Interstitial space

333
Q

What helps maintain oncotic pressure?

A

Albumin holds fluid inside of blood vessels

334
Q

What happens to bodily fluids if there is an increase in hydrostatic pressure?

A

Pushes fluid outside of vessels

335
Q

Define Localized Edema

A

Excess fluid in tissue, organs or body cavities

336
Q

What is the difference in naming tissue/organ edma and body cavity edema?

A 
Tissue/organ= location + edema
Body= hydro + location
337
Q

Define Generalized Edema

A

Excess fluid accumulation through out the body

338
Q

Generalized edema is generally due to one of three things

A

Heart, liver, kidney failure

339
Q

Generalized edema is AKA ?

340
Q

Define Pleural Effusion

A

Hydrothorax

Fluid in chest

341
Q

What is the difference between pleural effusion and pulmonary edema?

A

Pulmonary edema is inside of lung tissue

Pleural effusion is in thoracic cavity/pleural space outside of lung tissue

342
Q

What are the specific gravities of transudates and exudates?

A

Trans- low, clear

Ex- high, pus

343
Q

Transudate can arise from what three things?

A

Increased hydrostatic pressure- DVT
Decreased oncotic pressure- hypoalbuminemia
Decreased lymph drainage- lymph obstruction

344
Q

Exudates tend to arise from what process?

A

Increased permeability, usually from inflammatory process

345
Q

Pitting edema is usually caused by one of three things?

A

Hypoalbuminemia- nephrotic syndrome, malnutrition
CHF
Fluid overload- renal disease

346
Q

How does CHF lead to pitting edema/pulmonary edema?

A

Insufficient blood from heart
Hyp-perfused kidneys
Renin->aldosterone
Inc Na/water retention from tubules
Inc intravascular press increases hydrostatic press in lungs
Fluid pushed from pulmonary capillaries to lung tissue

347
Q

Define Hemothorax

A

Blood between lung and chest wall

348
Q

Define Hemopericardium

A

Blood in pericardial sac

349
Q

Define Hematoma

A

Blood collection in tissue

350
Q

Define Hemoptysis

A

Coughing up blood

351
Q

Define Hemodynamically Stable

A

Maintaining adequate blood flow to vital organs

352
Q

Whats the difference between hematochezia and melena?

A

Melena- dark blood

Hematochezia- bright red blood in stool

353
Q

What are 3 superficial skin signs of bleeding?

A

Petechiae
Purpura- nonblanching bruises
Ecchymosis

354
Q

Thrombi are made up of what three things?

A

Platelet
Fibrin
RBCs

355
Q

Why are thrombi created?

A

Prevent extravascular blood loss

356
Q

In normal homeostasis, what balances clotting factors and platelets?

A

Endothelial cells

Plasmin

357
Q

Define Virchows Triad

A

Injury to endothelium
Hemodynamic change
Hypercoagulate state

358
Q

Where do DVTs usually form?

A

Leg
Pelvis
Axillary vein
Mesenteric vein

359
Q

What are risk factors for developing DVTs?

A 
Inactivity
Smokers
Pregnancy
Oral contraceptives
Cancer
DVT history
Aging
360
Q

What are 4 forms of embolus

A

Thromboemboli- most common
Liquid
Gas
Solid particle- marrow/fat

361
Q

What is the most significant result of venous emboli?

362
Q

Most PEs develop from what/where?

A

DVTs in leg or pelvis

363
Q

What are the S/Sx os large emboli?

A

Sudden chest pain
Sudden SOB
Hemopytsis

364
Q

Where do arterial emboli usually originate?

A

Heart

Large arteries

365
Q

Aortic aneurysms release clots to what 3 locations?

A

Intestine
Kidney
Leg

366
Q

What happens if an embolus stops in the brain or intestined?

A

Brain- ischemic stroke/infarct

Intestine- bowel ischemia/infarct

367
Q

What happens if an embolus stops in a kidney?

A

Infarct w/ hematuria

368
Q

What happens if an embolus stops in a lower extremity?

A

Small emboli- blue toe necrosis

Large- ischemia, cold pulseless leg

369
Q

What is the first symptom of ischemia?

370
Q

Define White Infarct

A

Arterial inflow obstruction causing paleness

Necrosis occurs downstream of blockage

371
Q

Where are White Infarcts usually found?

A

Solid organs

372
Q

Define Red Infarct

A

Venous outflow obstruction causing necrosis upstream of blockage

373
Q

Where do Red Infarcts normally occur?

A

Intestine

Testes

374
Q

Define Shock

A

Decreased tissue perfusion by blood

375
Q

What are the 3 mechanisms of shock?

A

Pump failure- cardiogenic
Fluid Loss- hypovolemic
Loss of tone- Hypotonic/distributive shock

376
Q

What are the 3 types of Distributive Shock?

A

Neurogenic
Anaphylactic
Septic

377
Q

What are 4 causes of cardiogenic shock?

A

MI
C-fib
Pericardial tamponade
Tension pneumo

378
Q

What is Beck’s Triad

A

Hypotension
Muffled heart sounds
JVD

379
Q

What are symptoms of a pneumothorax?

A

Inc respiration/air hunger
Dec breath sound on affected side
JVD
Tracheal deviation (late)

380
Q

What are 3 causes of JVD?

A

Heart Failure
Cardiac tamponade
Tension Pneumo

381
Q

What are 2 causes of hypovolemic shock?

A

Hemorrhage

Water loss

382
Q

What are the symptoms of hypvolemic shock?

A 
Tachycardia
Tachypnea
Cold and clammy
Increased thirst 
Light headedness
Hypotension
Confusion/Altered
383
Q

What does a decrease in body fluids do to Hct levels?

A

Hemotoconcentration

Hemodilution if fluids added

384
Q

Neurogenic shock is due to loss of what part of the NS?

A

Sympathetic

385
Q

What are the 3 stages of shock?

A

Early/compensated
Decompensated
Irreversible

386
Q

What are the S/Sx of early/compensated stages of shock?

A

Tachcardia
Vasoconstriction
Reduced urine output
Normal BP

387
Q

What are the S/Sx of decompensated stage of shock?

A 
Compensation begins to fail
Hypotension
Tachy and SOB
Oliguria
Acidosis
388
Q

What are the S/Sx of irreversible stage of shock?

A

Circulatory collapse

389
Q

What kind of response is a vasovagal syncope?

A

Neurocardogenic response

Mild form of neurogenic/cardiogenic shock

390
Q

What causes a vasovagal syncope?

A 
Tigger stimuli
Enhanced PNS vagal tone, bradycardia
Dec sympathetic tone, 
dilation
Brain is under perfused and faints
391
Q

What are the clinical characteristics of a vasovagal syncope?

A

Prodrome- light head, N/V, tunnel vision, pale
Brief LOC
Supine-restoration
Immediate regain of consciousness w/out amnesia or post-ictal symptoms

392
Q

What are the two progenitor cells that give rise to blood cell lines?

A

Myeloid cells

Lymphoid cells

393
Q

Define Myeloid Cells

A

Granyles w/ complex nucleus
Neutrophils
Eosinophils
Basophils

394
Q

Define Lymphoid Cells

A

Lack granules w/ large, dense nucleus
T/B-Cells
NKCs

395
Q

Why do RBCs have a biconcave shape?

A

Increased SA for O2/CO2

396
Q

What is the structural make up of Hgb?

A

4 heme groups
4 globins
Arranged in 4 pyrrole rings w/ central Fe molecule

397
Q

How are the 4 globin chains of Hgb designated?

398
Q

Normally adult heme is Hgb __

399
Q

What are the 4 RBC indices?

A

MCV- avg volume/size per RBC
MCH- avg Hgb per RBC
MCHC- avg Hgb concentration per RBC
RDW- variation of RBC volume

400
Q

What measurement is not a part of RBC indices?

A

Reticulocyte Count (Retic)- number of immature RBCs in sample

401
Q

What is the Reticulocyte Count a measurement of?

A

Reflection of bone marrow production of new RBCs

Distinguishes between inadequate production vs anemic RBC destruction

402
Q

How to tell between marrow or anemic cause for Reticulocyte Counts?

A

Marrow responds to anemic state by increasing production (inc Retic count), anemia is not from inadequate production

403
Q

What are the two anemia classifications?

A

Etiological/pathogenesis- decreased/abnormal production, inc loss/destruction of RBCs
Morphological- looks or content

404
Q

What are the clinical features of anemia?

A

Dec O2 causes hypoxic symptoms
Palesness
SOB
Drowsiness

405
Q

What are anemia levels for M/W?

A

M- less than 13g

F- less than 11.5g

406
Q

Define Decreased Hematopoiesis

A

Bone marrow failure- aplastic anemia/myelophthisic anemia

Nutrient Deficiency- Fe, B12, protein

407
Q

Define Aplastic Anemia

A

Loss of stem cells from bone marrow causing pancytopenia

408
Q

Define Myelophthisic Anemia

A

Replacement of bone marrow by cancers/fibrosis/granulomas

Leukemia, multiple myeloma

409
Q

What are the two causes of Aplastic Anemia?

A

Idiopathic

Secondary- marrow suppressed by drugs/virus

410
Q

What is the pathogenesis of Aplastic Anemia?

A

Marrow becomes hypocellular

Stem cells replaced by fat

411
Q

What are the clinical features of Aplastic Anemia?

A

Uncontrolled infections/bleeding

Insidious fatigue/pallor/weakness

412
Q

What is the treatment for Aplastic Anemia?

A

Bone marrow transplant

413
Q

Most PTs that die from Aplastic Anemia die from what?

414
Q

What is the most common form of anemia?

A

Fe defficiency

415
Q

What is the etiology of Iron Deficiency Anemia

A

Inc Fe loss
Inadequate Fe uptake
Increased Fe requirements

416
Q

What is the pathology of Iron Deficiency Anemia?

A

Microctyic/hypchromic

Target cells- abnormal heme distribution

417
Q

What are the clinical features of Iron Deficiency Anemia

A

More common in females

Males- secondary to occult bleeding (GI ulcer, cancer)

418
Q

How is Iron Deficient Anemia treated?

A

Fe supplements but with investigation to underlying cause

419
Q

Define Megaloblastic Anemia

A

B12/Folic acid deficiency

420
Q

What is the pathology for Megaloblastic Anemia?

A

Large/hyperchromic RBCs

Hypersegmentation of WBCs

421
Q

Lack of B12 leads to what specific anemia and caused by what?

A

Pernicious Anemia
Bowel disease
Stomach surgery

422
Q

What causes folic acid anemia?

A

Pregnancy
Lactation
ETOH abuse

423
Q

What are the clinical features of megaloblastic anemia?

A

Fatigue
Palor
SOB
Weak

424
Q

Pernicious anemia has what unique clinical features?

A 
Dec vibratory sense
Dec reflexes (permanent)
425
Q

How is megaloblastic anemia treated?

A

B12 shots

Folate supplements

426
Q

What is usually the cause of abnormal hepatopoiesis?

What are 3 examples?

A

Genetics
Sickle Cell
Thalassemia
Hereditary Spherocytosis

427
Q

What causes Thalassemia?

A

Defect in Hgb A, A or B chain

428
Q

What causes Hereditary Spherocytosis?

A

RBC structural protein error

429
Q

What causes Sickle Cell?

A

Defect during AbA Synthesis causing HbS production

430
Q

What kind of genetic disorder is Sickle Cell?

A

Autosomal Recessive

431
Q

People with HbS below __ % are asymptomatic

432
Q

What is the pathology of Sickle Cell?

A

Multiple Organ infarcts

433
Q

What are the clinical features of Sickle Cell?

A

Fetal HgF -> adult HbA
Abnormal cell lysis->jaundice
Splenic sequestration crisis

434
Q

Sickle Cells affects what part of the Hgb chain?

435
Q

Sickle Cell affects ? population?

Thalassemia affects ? population?

A

African/Mid-Eastern

Mediterranean/SE Asia

436
Q

Define Alpha Thalassemia and Beta Thalassemia

A

A- A chain defect, less severe

B- B chain defect, severe/lethal

437
Q

What is the pathology of thalassemia?

A

RBCs are microcytic and hypochromic with target cells

Hbg electrophoresis IDs subtype HbA2

438
Q

Thalassemia pathology is similar to what other blood disorder?

A

Iron deficiency

439
Q

Define Hereditary Spherocytosis

A

Structural protein defect of RBC cytoskeleton

Causes dec in RBC flexibility, leading to RBCs lyses and capture in spleen

440
Q

What is the pathology of Hereditary Spherocytosis?

A

RBCs are small spherical, not biconcave

Microcytic and hyperchromic (normal Hgb on smaller RBC)

441
Q

What are the clinical characteristics of Hereditary Spherocytosis

A

Hemolytic/aplastic crisis if RBC destruction exceeds production

442
Q

What is the treatment method for Hereditary Spherocytosis?

A

Splenectomy

443
Q

Destruction of RBCs usually occur from ?

A

Hemolytic anemia

444
Q

What are some common causes of destruction of RBC leading to hemolytic anemia?

A 
Malaria
Autoimmune hemolytic anemia
Mismatched transfusion
Hemolytic disease in newborn
Drugs: anti-malarial, sulfa trigger lysing event in PTs w/ G6PD
445
Q

Define Lymphadenopathy

What is a red flag here?

A

Enlarged lymph node w/out not specific cause

Slowly enlarging, persistent and non-tender- early cancer

446
Q

Define Lymphadenitis

A

Infected lymph node

Enlarged and tender w/ possible abscess

447
Q

Define Lymphangitis

What are some S/Sx that would be seen

A

Infection of lymph vessels
Red streaking- blood poisoning
Fever, chills, leukocytosis

448
Q

What are the two forms of plycythemia?

A

Primary- vera, myeloproliferative disorder considered neoplastic. Hematopoietic stem cell proliferation w/out external stimuli
Secondary- over production of RBCs w/ increase stimulation by increased erythropoietin

449
Q

Secondary polycythemia is usually caused by what event?

A

Prolonged hypoxia

450
Q

What are the clinical features of polycythemia?

A

Splenomegaly
Red/flushed skin
Hyperviscous blood w/ easy clotting
Headache, hypertension

451
Q

What is the treatment for polycythemia?

A 
Cytotoxic drugs
Therapeutic phlebotomy (blood letting)
452
Q

What are some causes of leukopenia?

What are these PTs at risk for?

A

Cytotoxins- chem/rad PTs

Overwhelming infections

453
Q

Define Leukocytosis

A

Normal response to inflammation/infection

454
Q

Prolonged leukocytosis may represent what other disease?

A

Malignancy

455
Q

Neutrophilia is indicative of ?
Eosinophilia is indicative of ?
Lymphocytosis is indicative of ?

A

Bacterial
Allergy, parasitic
Viral, chronic TB

456
Q

What are 3 malignant disease of WBCs?

A

Leukemia
Lymphoma
Multiple Myeloma

457
Q

What are the 4 types of leukemia

A

ALL/CLL

AML/CML

458
Q

What are the two types of lymphomas?

A

Non-Hodgkins

Hodgkins

459
Q

What is the most common form of leukemia in children, especially under the age of five?

A

Acute lymphoblastic leukemia

460
Q

What is the pathogenesis of Acute Lymphoblastic Leukemia

A

Bone marrow w/ immature blast (lymphoid) cells

Malignant lymphoid cells in peripheral blood

461
Q

What are the clinical features of Acute Lymphoblastic Leukemia?

A

Enlarged lymph nodes
Splenomegaly
Rapid- recurrent infections, malaise, bleeding into skin

462
Q

How is Acute Lymphoblastic Leukemia treated?

A

Chemo

W/out chemo= fatal in 3-6mon

463
Q

What PT population is Acute Myelogenous Leukemia common in?

A

Most common acute leukemia in +65y/o

464
Q

Acute Myelogenous Leukemia is linked to what environmental factors?

A

Radiation

Benzene

465
Q

What is the pathogenesis of Acute Myelogenous Leukemia?

A

Proliferation of myeloblasts

Blast cells take over marrow and smother normal stem cells

466
Q

What are the clinical features of Acute Myelogenous Leukemia?

A

Enlarged spleen/nodes

467
Q

What is the treatment for Acute Myelogenous Leukemia

A

Chemo/radiation/BMT

High recurrence rate

468
Q

Chronic Meylogenous Leukemia usually infects what PTs?

A

Adults over 30y/o

469
Q

What is the pathogenesis of Chronic Myelogenous Leukemia?

A

Bone marrow over run by malignant cells

470
Q

Chronic Myelogenous Leukemia PTs usually have what genetic abnormality?

A

Philadelphia chromosome abnormality on #22

471
Q

What are the clinical features for Chronic Myelogenous Leukemia?

A

Slow onset fatigue, infections, splenomegaly

472
Q

What are the 3 phases of progression of Chronic Myelogenous Leukemia

A

Chronic- 2/3yrs w/ leuko/thrombocytosis
Accelerated- inc blast production in marrow
Blast Crisis- death

473
Q

What is the treatment method for Chronic Myelogenous Leukemia?

A

Radiation w/ chemo

474
Q

What is the PT population for Chronic Lymphocytic Leukemia

A

Older adults above 50y/o

475
Q

Why is Chronic Lymphocytic Leukemia hard to diagnose?

A

Lymphocytes are indistinguishable from normal lymphocytes

476
Q

What are the clinical features of Chronic Lymphocytic Leukemia

A

Slow progression of increase infections

477
Q

What is the treatment method for Chronic Lymphocytic Leukemia?

478
Q

What is the pathogenesis of lymphoma?

A

B-cell phenotypes

479
Q

What are the clinical features of lymphoma?

A

Painless lymph nodule
Extra nodule tumor spread
Fatigue/malaise/fever

480
Q

What are the 3 subtypes of lymphoma?

A

Follicular- older population has slow growing tumor, least response to treatment
Diffus large B cell- most aggressive but most responsive to treatment
Burkitts- Common in Africa, endemic in kids w/ EBV

481
Q

What part of the body does Burkitt’s Lymphoma effect?

A

Mandible, face

482
Q

What is the incidence of Hodgkin’s Lymphoa?

A

Bi-modal peaks at 25 and 55

483
Q

What are the clinical features of Hodgkin’s Lymphoma?

A

Large nodes- neck, mediastinum

Reed-Sternberg cells

484
Q

What is the pathogenesis of Multiple Myeloma?

A

Malignant plasma cells proliferate in bone marrow casuing punched-out look

485
Q

What are the clinical features of Multiple Myeloma?

A

Serum protein electrophoresis

Bence-Jones proteins

486
Q

How is Multiple Myeloma treated?

A

Ineffective to chemo, death from renal failure

487
Q

Characteristics of Idiopathic Thrombocytopenic Purpura?

A

Auto-Abs to platelets destroy them in spleen
Acute to children post-viral infection
Easy bleeding from gums/nose
Chronic ITP needs splenectomy

488
Q

Characteristics of Thrombotic Thrombocytopenic Purpura

A

Abnormal clotting in small cells
Primary- Abx breaks up Von Willebrand clotting factor
Secondary- from cancer, pregnancy, HIV
Easy bleeding gums, nose, hemolytic anemia

489
Q

How is TTP treated?

A

Plasmapheresis to remove Abs

490
Q

What are the inherited Bleeding Disorders?

A

A- 8 disorder
B- 9 disorder
Von Willebrands Disease- autosomal dominant
Easy/ecess bleeding
Tx w/ infusion of concentrated blood-clotting factors

491
Q

What medication is contraindicated in PTs with Von Willebrand’s?

A

Aspirin- due to inhibitory affect on platelets

IPAP (212 decks)

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