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NURS 316 > Midterm > Flashcards

Midterm Flashcards

1
Q

Pathophysiology

A

the study of the physical and functional changes that occur during a disease process

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2
Q

Etiology

A

study of the causes and reason for a particular disease or injury

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3
Q

Idopathic

A

cause is unknown

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4
Q

Iatrogenic

A

resulting from medical treatment

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5
Q

Risk Factor

A

Increase likelihood of disease

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6
Q

Latent Period

A

Time between exposure and first appearance of S & S

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7
Q

Prodromal Period

A

When S&S first appear, indicating onset of disease

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8
Q

Acute Phase

A

Disease/illness is at full intensity
-May be short-lived but intense manifestation

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9
Q

Chronic Illness

A

May last months to years, sometimes after acute course

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10
Q

Exacerbation

A

A sudden increase in severity of disease or Signs and symptoms

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11
Q

Remission

A

Decrease in severity, S&S: may indicate disease is cured

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12
Q

Convalescent

A

Stage of recovery after a disease, injury or surgey

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13
Q

4 Factors that Affect Health and Disease

A

Cultural Consideration
Age Difference
Gender Differences
Situational Differences

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14
Q

Epidemiology

A

Study of the patterns of disease involving populations
- Examines the occurance, incidence, prevalence, transmission, and distribution of disease in large groups of populations/people

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15
Q

Endemic disease

A

Consistently present within a particular geographic area or population
Often associated with specific environmental or social factors

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16
Q

Epidemic

A

Sudden increase in the number of cases of a disease above what is normally expected in a specific region or population
- Can be caused by a new strain of a pathogen, changes in the environment or lapses in vaccination coverage

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17
Q

Pandemic

A

Epidemic that has spread across multiple countries or continents, affecting a large portion of the global population
- Involves a new pathogen to which most people have little or no immunity

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18
Q

Levels of Organiztion

A

Nucleus - Heart muscle cell - Heart muscle - Heart - Circulatory system

Organelles - Cell - Tissue - Organ - System

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19
Q

Cell Structure (3 Main Parts)

A

Cell Membrane: Encase the cell and regulates the movement of substances in and out of the cell

Nucleus: Houses the majority of the cells DNA/genetic material

Cytoplasm: Gel-like fluid inside the cell that contains various cell components with specific functions (DOES NOT INCLUDE NUCLEUS)

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20
Q

5 Stages of Cell Cycle

A

G-0 (Resting Stage)
G-1
S (Synthesis)
G-2 (Pre-mitotic Phase)
M (mitosis)

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21
Q

G-0 (Resting Stage)

A

Phase where cells conduct their everyday activities specific to cell type (Eg, metabolism, contraction etc)
- Cells spend most of their lifetime in this phase**

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22
Q

G-1 Phase

A
  • First Step after receiving signal to divide
  • Cell synthesizes ribonucleic acid (RNA), proteins, and other components needed for DNA duplication
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23
Q

S (Synthesis)

A

Cells duplicate its DNA

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24
Q

G-2 (Pre-Mitotic Phase)

A

Cell makes additional proteins and the components necessary for cell division/mitosis

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25
Q

M (mitosis) Phase

A

Cell undergoes mitosis (prophase, metaphase, anaphase, & telophase)
- Results in the cell splitting into 2 identical cells

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26
Q

Cell Proliferation

A

Cells multiply through mitosis where one cell divides to make two new daughter cells identical to the parent cell
- Allows the body to grow, repair, and replace cells
- Tightly regulates to ensure that cells divide only when necessary

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27
Q

Cell Differentiation

A

Process by which a cell becomes more specialized with distinct functions and characteristics
- Ensures cells can perform specialized functions necessary for organisms survival
- Stem Cells: are special cells with the ability to develop into various cell types
- They receive signals directing them to become a specific type of cell

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28
Q

Cell Types

A

Labile
Stable
Permanent

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29
Q

Labile Cells

A

Constantly dividing and replacing cells that are lost
Eg. the skin, intestinal epithelial cells

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30
Q

Stable Cells

A

Do not divide under normal conditions but can be stimulated to divide after injury
Eg. Hepatocytes and liver regeneration (Zeus vs Prometheus)

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31
Q

Permanent Cells

A

Lack regeneration ability
Eg, cardiac, neural, and skeletal cells
- Cardiac tissues don’t heal after MI, causing reduced cardiac capacity

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32
Q

4 Types of Tissues

A

Epithelial
Muscular
Connective
Nervous

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33
Q

Epithelial Tissues

A

Line all internal and external surfaces

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34
Q

Muscular Tissues

A

Specialized for contraction, allowing movement and force generation in the body

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35
Q

Connective Tissue

A

Supports, connects, or separates different types of tissues and organs in the body

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36
Q

Nervous Tissue

A

Specialized tissues that transmit electrical impulses to coordinate bodily functions by facilitating communication between different body parts

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37
Q

Cellular Adaption

A

A cells ability to adjust in response to different stimuli and challenging environmental conditions that threaten their structure or function
- Stimuli can be Physiological (breast during pregnancy), or pathological (aging)
- Cells may change in size, number, or type, to adapt
- If stress is too severe or the adaptations are not effective, the cell may become injured or die

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38
Q

5 Cellular Adaptations

A

Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia

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39
Q

Atrophy

A
  • Decreases in cell size leading to tissue degeneration
  • Atrophied cells = decrease in cell content = reduced oxygen consumption
  • Caused by: Disuse, denervation, loss of endocrine stimulation, inadequate nutrition, ischemia
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40
Q

Hypertrophy

A

Enlargement of cells increase in size and functional components
Eg. Bigger muscle = more ATP, more actin and myosin filaments
- Results from increased functional demands or specific hormonal stimuli
- Caused by: Exercise & muscle mass, uterus enlargement in pregnancy (physiological), myocardial hypertrophy from hypertension (pathological)

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41
Q

Hyperplasia

A
  • “plasia” = Cell formation or growth
  • Controlled increase in the number of cells in an organ or tissue
  • Occurs in wound healing with proliferation fibroblasts of connective tissues
  • Different from hypertrophy BUT may occur TOGETHER (Eg. uterus)
  • Cause by: Stimulation of endometrium in the follicular stage of menstrual cycle (physio), Benign prostate hyperplasia (patho), endometrial hyperplasia (patho)
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42
Q

Metaplasia

A

Reversible replacement of mature, differentiated cell-type by another cell-type that is better suited to tolerate a particular stimuli or environment
- Reprogramming of undifferentiated stem cells present in tissue, but conversion of cell type remains within boundaries of primary tissue (epithelial cells CANNOT be converted to cardiac cell)
- Caused by: Barret’s Oesophagus (in response to reflux), replacement of ciliated pseudostratified columnar epithelium in bronchi w/ stratified squamous epi (smoking)

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43
Q

Neoplasia

A

When signals cause metaplasia to persist, they frequently lead to the development of neoplasia

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44
Q

Dysplasia

A

Disordered growth in tissue, resulting in cells that vary in size, shape and organization
- Caused by irritation (smoke), or inflammation (radiation causes damage to cell DNA)
- Mild-moderate cases may regress if underlying cause if alleviated but severe dysplasia can be a precursor to irreversible malignancy

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45
Q

Intracellular Accumulation

A
  • Describes the build-up of substance that the cells cannot immediately use or eliminate
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46
Q

Normal Body Substance

A

Substance is produced faster than it can be metabolized or excreted
Eg. Obesity = high delivery of free fatty acids from adipose tissues to the liver = accumulation of FFA = Fatty liver

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47
Q

Abnormal Endogenous Products

A

May result from disorders that disrupt metabolism due to abnormal or missing enzyme
Eg, Von Gierke disease where a deficiency in Glucose-6-phosphatase leads to accumulation of glycogen in the liver and kidneys

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48
Q

Exogenous Products

A

Environmental agents and pigments
Eg. Accumulation of carbon dust blackens the lung tissue and may cause serious lung disease

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49
Q

Pathological Calcifications

A

2 Types: Dystrophic & Metastatic

Involve abnormal tissue deposition of calcium salts, and other minerals in tissues

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50
Q

Dystrophic Calcification

A

Occurs in damaged or necrotic tissues despite normal calcification levels in the blood
- Happens in areas of tissue like damaged heart valves, atherosclerotic plaques, or areas of chronic inflammation

51
Q

Metastatic Calcification

A

Occurs in healthy tissues due to elevated levels of calcium in the blood (hypercalcemia)

52
Q

Physical Agents of Cellular Injury

A

Can generally be reversed up to a specific point, after which the damage becomes irreversible, leading to cell death
- MECHANICAL FORCE: Trauma due to body’s impact w/ external force (split and tear tissues, fracture bones, disrupt blood flow etc)
- EXTREMES OF TEMP: Heat (burns) disrupt cell membrane. Cold may lead to hypoxic tissue injury due to vasoconstriction
- ELECTRICAL INJURIES: Extensive tissue injury. Disruption of neural and cardiac impulses

53
Q

Radiation of Cellular Injury

A

ULTRAVIOLET RADIATION: Photon is a particle of electromagnetic radiation energy
- UV radiation contain high energy photons that can disrupt release free radicals, damage DNA and damage melanin-producing processes in skin cells

IONIZING RADIATION:
-Radiation energy above the UV range
- L.R. photons cause ionization of molecules and atoms in the cell by knocking off elections from them
Eg. Localized irradiation in cancer treatment

NONIONIZING RADIATIONS:
- Radiation energy BELOW the UV range (Eg. Ultrasound, welding, microwaves)
- Uses energy from vibration of atoms and molecules o generate thermal energy
- Resulting thermal energy can disrupt the cell depending on duration and extent of exposure

54
Q

Cell Injury (Chemical and Biologic)

A

CHEMICAL INJURY:
- May injure cells membrane, block enzymatic pathways, disrupt cell metabolism etc
- Air and water pollutants. tobacco smoke, drugs and alcohol, CO, Lead toxicity, mercury toxicity

BIOLOGIC INJURY:
- Viruses incorporate themselves into a cell’s DNA machinery
- Bacteria may release toxins that increase cardiac permeability, interfere with ATP production or other cellular processes

55
Q

Mechanisms of Cell Injury

A

FREE RADICAL INJURY:
- Highly reactive with molecules in their vicinity and can convert other molecules into additional free radicals
Reactive Oxygen Species (ROS) = Free radical in the body

56
Q

Oxidative Stress

A

When the generation of free radicals exceeds the ability of the body to neutralize it
- High blood sugar can cause oxidative stress on blood vessels
- In cancer, oxidative stress damages the DNA in healthy cells
- Also linked to Aging neurodegenerative disease

57
Q

Antioxidants

A

Vit A,C,E, Zinc, Beta-carotene

58
Q

Hypoxic Cell Injury

A

Oxygen Deficiency: lack of O2 in the air, respiratory disease, anemia, ischemia

Deprives the cell of O2 thereby interrupting the generation of ATP

59
Q

Genetic Defect

A

Cause cell injury due to deficiency in function proteins or the accumulation of damaged DNA or misfolded proteins (both trigger cell death)
EG, sickle cell anemia

60
Q

Reversible Cell Injury

A

Cellular Swelling
Fatty Changes

61
Q

Cellular Swelling

A

Impairment of the sodium-potassium-ATPasepump leads to accumulation of Na and water inside the cell
- Hydropic degeneration. Change is reversible if O2 delivery resumes alongside ATP production

62
Q

Fatty Changes

A

Intracellular accumulation of fat, causing small vacuoles of fat disperse throughout the cell
-Increased fat load (obesity)
-Impairment of fat metabolism

63
Q

Apoptosis

A

Highly selective process that controls tissue regeneration by eliminating injured and aged cells. Cellular suicide
- Does NOT trigger the inflammatory process
- Responsible for several physiologic processes: Programmed destruction of cells during embryonic development (separates webbed-toes and fingers in embryo), Hormone-dependent involution of tissue, Control immune cells

64
Q

Necrosis

A

Refers to cell death in an organ or tissue that is still part of a living tissue
- Usually due to ischemia or toxic injury
- Interferes with cell replacement and tissue regeneration
- Triggers inflammatory process**

65
Q

Gangrene

A

When a considerable mass of tissue undergo necrosis

66
Q

Neoplasm

A

Cels regulate growth (proliferation) by turning growth-promoting and growth suppressing genes on and off

67
Q

Neoplasia

A

Abnormal cell proliferation/tissue growth caused by damage or mutation of regulators

68
Q

Metastasis

A

Movement of abnormal cells to other parts of the body, where they populate new tumors

69
Q

Benign (Non-cancerous)

A

Uncontrolled cell proliferation enclosed in a fibrous capsule and does not infiltrate or affect tissue of origin directly
- Slow growing and localized
- Does not metastasize and can be removed
Eg. Benign prostatic hyperplasia

70
Q

Malignant Tumors (cancerous)

A

Rapid and uncontrolled cell proliferation that invades the tissue of origin and can invade other remote tissues via lymph or blood
- Always requires treatment

71
Q

Cancer Cells

A

Uncontrolled proliferation
- De-differentiation (loss of normal function)
- Invasiveness
- Metastases: Cancer cells break away, travel through the blood or lymph system, form new tumors, metastatic tumor is the same type of cancer as the primary tumor

72
Q

Angiogenesis

A

Formation of new capillaries out of existing blood vessels
- Cancer cells establish their own blood supply to bring nutrients and escape during metastasis

73
Q

Telomere

A

Section of DNA that safeguards the chromosome ends from damage and entanglement
- They shorten with each cell division and eventually become too short for proper cell division = cell death

74
Q

Telomerase

A

An enzyme that lengthens the telomere chains and allow continued replication
- Found in stem cells
- Cancer cells produce large amounts = Indefinite replication

75
Q

Types of Cancer

A

Solid - Abnormal tissue mass, difficult to assess in blood at 1st, Eg. Breast, prostate, lung CA

Hematological - Formed in the blood or bone marrow, not a mass (liquid), Eg. Leukemia, lymphoma

76
Q

Types of Carcinogens

A

Chemical: Tobacco smoke & Asbestos = Lung CA

Physical: Sun’s UV rays = Skin carcinoma, Xrays = Leukemia

Biological: Genetic predisposition to damaged growth promoter/suppressor, viruses/HPV = Cervical CA

77
Q

Diagnostic Tools

A

Blood Test: CBC & Differential (Hb, WBC, blood smears)

Imaging: Ultrasound, CT scan, MRI, PET, Mammogram

Others: Biopsy, Colonoscopy

78
Q

CA Staging

A

Identifies the location and extent of cancer invasion within the body
- Assessed at initial diagnosis to help understand the disease’s prognosis and the most effective treatment options
- CA is assigned values for the tumor (T), node (N), Metastasis (M) and then a stage
- Assigned stage does not change even if CA progresses***

79
Q

4 Stages of CA

A

Stage 1: Least Invasive, most favourable outlook. No lymph involvement, no metastasis, tumors are less than 2 cm in size

Stage 2: Local lymph involvement, no metastasis, tumors are less than 5 cm in size

Stage 3: Nodal involvement, no metastasis, tumors over 5 cm

Stage 4: (Most aggressive = least favourable outlook), nodal involvement, metastasis tumors greater than 5 cm

80
Q

CA Grading aka Biopsy

A

Involves examining cancer cells under microscope and comparing their appearance to that of normal, mature cells it came from

G1 = differentiated and very similar to the parent cells
G4 = Very abnormal and different from normal cells. Aggressive CA cells with worst prognosis

Grading can change as the tumor evolves

81
Q

Clinical Manifestations

A

Obstruction: Anorexia and necrosis of tissue leading to loss of function

Hematologic Alterations: Impairs functions of blood cells. Leukemia, GI tumors, Renal cell carconoma

Anorexia-cachexia Syndrome: “wasting syndrome” - malnutrition, weight loss, neoplastic cells divert nutrition to own use

Paraneoplastic Syndromes: malignant tumor secretes hormones or proteins that affects organ systems away from tumor sites (symptoms occur away from tumor site)

Psychological Stress

Pain

82
Q

Drugs Targeting DNA Formation/Repair (Anti-neoplastic Agents)

A

Alkylating Drugs: Non-cycle specific

Anti-metabolites (-ate/purine, bine): Interrupts S-phase

Cytotoxic Antibiotics (-mycin/bicin): Block DNA replication enzymes or produce free-radicals

Vinca Alkaloids (Vin-): Targets Mitosis-phase

83
Q

Hormonal Anti-neoplastic Agents

A

Used to treat cancers that are linked to hormonal stimulation
- Prevents cell proliferation by disrupting testosterone/estrogen/progesterone

84
Q

Immunotherapy

A

Immuno-stimulants: Stimulate immune system against certain tumor cells

Antibodies

85
Q

Improving Success of Chemotherapy

A

Combination Drugs
Dosing Schedule
Route of Administration

86
Q

Chemo Toxicity

A

Growth Fraction: ratio of replicating cells (growth) to resting cells in a tissue
- Anti-neoplastic drugs are more toxic to tissues and tumors with high growth fractions

87
Q

Neutrophils

A

Very sensitive to chemo due to need for constant replacement. short life span 7-12hrs
Neutropenia: Diagnosed when neutrophil count is below 1500 cells/mL
- Requires reverse iso
- Colony Stimulating factors

88
Q

Platelets

A

Lifespan = 7-8 days (needs constant replenish)
- Thrombocytopenia: diagnosed when platelet count drops below 100,000/milliletre of blood
- Low platelets can cause increased bleeding

89
Q

Erthythrocytes

A

Lifespan = 90-120 days (anemia appears later in chemo)
- Anemia affects O2 delivery to tissues
- RBC infusions and medications like epoetin alfa can be administered

90
Q

Extravasation

A

Unintended leakage of blood, lymph, or other fluids (including chemo drugs) from a blood vessel or catheter into the tissue surrounding IV site

91
Q

Vesicants

A

Drugs that have the potential to cause blistering, severe tissue injury or necrosis when they infiltrate into surrounding tissue

92
Q

Irritants

A

Agents that may cause inflammation and/or pain at venipuncture site or along the vein
- DO NOT cause tissue necrosis

93
Q

Stress

A

Any physical or psychological stimuli that disrupts homeostasis

94
Q

Sympathetic NS

A

Fight or flight

95
Q

Parasympathetic NS

A

Rest and Digest

96
Q

Synaptic Transmission

A
  • Pre-synaptic neuron initiates signal that is received by the post-synaptic neuron
  • Pre-synaptic neurons contain neurotransmitters (stored in vesicles) that are released into the synaptic cleft when stimulated by action potential
  • Binding of neuroT’s to receptors on post-synaptic neuron or target tissues at neuroeffector junction induces response (Activate or inhibit AP)
97
Q

Synaptic Transmission

A

Termination of neurotransmitter action
- NeuroT separates from receptor, returning it to baseline activity
- NeuroT is removed from synapse through: Reuptake back into pre-synaptic neuron OR Degradation in synaptic cleft by enzymes
- Acetylcholine degraded by AchE
- Norepinephrine degraded by MAO or COMT in synapse

98
Q

What do ANS Drugs do?

A
  • Alter synthesis of the neurotransmitter in the preganglionic nerve
  • Prevent storage of neurotransmitter in vesicles within the preganglionic nerve
  • Influence release of the neurotransmitter from the preganglionic nerve
  • Bind to the neurotransmitter receptor site on the postganglionic nerve
  • Prevent the normal destruction or reuptake of the neurotransmitter
99
Q

ANS Receptors

A
  • Cholinergic Receptors (Respond to Ach)
  • Adrenergic Receptors (Responds to Epin and Norepin)
100
Q

Cholinergic Receptors

A

Nicotinic:
- Found on postganglionic neurons in ANS
- Promotes sympathetic and parasym. effects
- Found at neuromuscular junction of skeletal muscle cells

Muscarinic:
- Found on parasymp. target tissues
- Promotes parasymp. effects

101
Q

Adrenergic Receptors

A

Alpha and Beta Subtypes
- Found on target tissues of sympathetic nervous system
**Promotes sympathetic effects

102
Q

3 Responses to Stress

A

Alarm Reaction
Resistance/Adaptation
Exhaustion

103
Q

Alarm Reaction

A

Stressor = activation of Symp NS (fight or flight)
- SNS = Norepin and Epin
= Increased Symp NS functions and decrease in parasymp innervation

104
Q

Resistance/Adaptation

A

Persistant stress activates the Hypothalamus-pituitary-Adrenal (HPA) axis which promotes the secretion of ACTH (which stimulates adrenal cortex to make Cortisol

Cortisol: helps body deal with long-term stress by increasing blood sugar, enhancing metabolism and suppressing non-essential functions like digestion and immune response

105
Q

Exhaustion

A

HPA axis may become dysregulated
- Sustained elevation of BP and HR may lead to cardiovascular diseases
- Prolonged inhibition of digestive and urinary functinons = GI and Renal disorders
- Decreased muscle mass and fat = weight loss
Bad immune system

106
Q

Cortisol

A

Helps body deal with stress by increasing energy supply

Liver: promotes metabolism
Muscle: reduces glucose uptake and promotes breakdown of muscle proteins into amino acids to make energy

Fat Cell: promotes lipid breakdown for additional energy

Pancreas: decreases insulin and increases glucagon to increase blood glucose

Others: Increase BP by upping vasoconstriction
and reduces inflammation and suppresses immune system

107
Q

Innate Immunity

A

Physical barriers: skin and mucous membranes

Cellular Barriers: phagocytes, cytokines

Process barriers: inflammation, opsonins, fever

108
Q

Adaptive/Acquired Immunity

A
  • Memory (Remembers immune response)
  • Relies on Lymphocytes (B cells and T cells) to recognize specific antigens presented by pathogens
    (antigens are the foreign substance that provokes the immune response)
  • B cells produce the antibodies and T cells directly attack infected cells or help regulate the immune response
109
Q

Plasma

A

55% of whole blood volume
- Contains 90% water, blood protein and solutes (electrolytes and nutrients)

110
Q

Cells Contain…

A

45% of whole blood
- RBCs, WBCs, platlets
- Synthesized via Hemopoiesis

111
Q

WBCs and Types

A

-Synthesized from hematopoietic stem cells
- Migrate out of blood vessels into tissues and towards stimulus
- 2 Types:
Granulocytes and Agranulocytes

112
Q

Granulocytes

A

Neutrophils:
-First order at the site of injury (within 90min)
- Make up 50-70% of WBC (short-lived)
- Phagocytose and digest pathogens then apop

Eosinophils:
- Respond to parasites involved in allergic reactions

Mast Cells:
- Localized in tissue for allergic responses (player in anaphylaxis)

Basophils:
- Amplifies allergic response

113
Q

Agranulocytes

A

Monocytes:
- Inactively circulate bloodstream until chemotaxis signal is received about damage
- Move into interstitial space as macrophages
- **Macrophages phagocytose invaders and produce signals to prolong immune response

Lymphocytes:
- Involved in systemic response
- T Lymphs = kill infected or damaged cels and stores memory
- B Lymphs = secrete antibodies which physically interest with antigens to neutralize or mark them for destruction

114
Q

Inflammation

A

Reaction of vascular tissues to harmful stimuli
- Eliminate the initial cause of cell injury, remove the damaged tissue, and generate new tissue

115
Q

Cells of Inflammation

A

Endothelial Cells: for a selective permeable barrier between the circulating blood in vessels and the surrounding tissues

Platlets: Release potent inflammatory mediators which increase vascular permeability

Neutrophils and Macrophages:

Eosinophils, Basophils and Mast Cells

116
Q

Mast Cells

A

Mostly found in con tissue and blood vessels (skin, mucosa)
- Degranulation may be caused by injury, temp, allergens
- Primary secretors of histamine (primary mediator associated with inflammation assoc w/ allergies)

117
Q

RSHPL

A

Redness (rubor)
Swelling (tumor)
Heat (colour)
Pain (dolor)
Loss of function (functio laesa)
Signs of Swelling

118
Q

Blood Tests in inflammation

A

Neutrophils

Lymphocytes

Eosinophils

C- Reactive Protein

118
Q

Inflammation in Tissue Injury

A

Endothelium, tissues, and mast cells:
-release inflammatory mediators (histamine)
- Release pro-inflammatory mediators (cytokines etc)

119
Q

Non-Sterodial Anti-Inflammatory Drugs (NSAIDS)

A

Selective COX Inhibitors:
- Target COX-2-MOA
- Analgesic, anti-inflam, and anti-pyretic actions typical of older NSAIDS

Non-Selective COX Inhibitors:
- First gen - block both COX 1&2
- Side effects of bleeding, gastric upset and reduced kidney function from blocking COX-1
- Eg ASA, Ibuprofen etc

120
Q

Histamine

A

Primary mediator of inflammation assoc with allergic reaction
- Released upon mast cells’ contact with allergen… bind to H1 receptors

Histamine + H1 = Smooth muscle contraction, vasodilation & increased permeability, swelling and flare (redness), Increased sensitivity and pain and wakefulness

121
Q

Anti-Histamines 1st & 2nd Gen

A

1st:
-block histamine
-receptors, very lipid soluble (causes drowsiness)
- Benadryl

2nd:
- Block H1 - histamine receptor
- Less lipophilic = decreased CNS distribution (non drowsy)
- Eg. Cetrizine (Reactine), Loratadine (Claritin)

122
Q

Challenges in Drug Development

A

Local Response:
-Patient touches something
- localized hives, itching, no vital sign changes etc

Systemic: Patient comes to a friends house and a cat is present
- Watery eye, itchy eyes, runny nose, sneezing

Systemic Life-Threatening:
- The cat allergy worsens
- Itching, diffused urticaria throughout, difficulty breathing, tachy
- Anaphylaxis

NURS 316 (3 decks)

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