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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

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51
Q

Metastatic Calcification

A

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

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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

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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

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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

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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

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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

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57
Q

Antioxidants

A

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

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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

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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

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60
Q

Reversible Cell Injury

A

Cellular Swelling
Fatty Changes

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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

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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

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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

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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**

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65
Q

Gangrene

A

When a considerable mass of tissue undergo necrosis

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66
Q

Neoplasm

A

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

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67
Q

Neoplasia

A

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

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68
Q

Metastasis

A

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

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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

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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

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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

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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

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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

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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

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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

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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

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77
Q

Diagnostic Tools

A

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

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

Others: Biopsy, Colonoscopy

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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***

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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

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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

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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

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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

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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

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84
Q

Immunotherapy

A

Immuno-stimulants: Stimulate immune system against certain tumor cells

Antibodies

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85
Q

Improving Success of Chemotherapy

A

Combination Drugs
Dosing Schedule
Route of Administration

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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

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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

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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

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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

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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

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91
Q

Vesicants

A

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

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92
Q

Irritants

A

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

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93
Q

Stress

A

Any physical or psychological stimuli that disrupts homeostasis

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94
Q

Sympathetic NS

A

Fight or flight

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95
Q

Parasympathetic NS

A

Rest and Digest

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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)
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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

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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
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99
Q

ANS Receptors

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

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101
Q

Adrenergic Receptors

A

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

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102
Q

3 Responses to Stress

A

Alarm Reaction
Resistance/Adaptation
Exhaustion

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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

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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

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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

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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

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107
Q

Innate Immunity

A

Physical barriers: skin and mucous membranes

Cellular Barriers: phagocytes, cytokines

Process barriers: inflammation, opsonins, fever

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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
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109
Q

Plasma

A

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

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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

123
Q

Pancreas Types and Functions

A

ACINI:
- Secrete digestive juices into the duodenum

ISLETS OF LANGERHANS:
- Secrete hormones into the cell
- Composed of beta cells that secrete insulin, alpha cells that secrete glucagon and delta cells that secrete somatostatin

124
Q

Endocrine Pancreas

A

Islets of Langerhans
Scattered in exocrine pancreas
Made up of 4 cell types
Distribution of cell type varies w/ region of pancreas

125
Q

Pancreas Cell Composition

A

Alpha Cell = 10% and 0.5% (Glucagon) In response to low blood glucose and to activity of sympathetic nervous system

Beta Cell = 70-80% and 15-20% (Insulin, Amylin), In response to HIGH bl. glucose and activity of the parasymp. nervous system

Delta Cell = 3-5% and <1% (Somatostatin)

F Cell = <2% and 80-85% (Pancreatic polypeptide)

126
Q

Pancreas Functions

A
  • Located beneath LIVER and tucked into the curvature of the duodenum
  • Has ENdocrine AND EXOcrine functions

EXOCRINE:
- Secretes enzymes into duodenum to support digestion of macromolecules
- Secretes bicarbonate into the duodenum to raise pH of chyme

ENDOCRINE:
- Islets of Langerhans includes Alpha and Beta cells to secrete hormones

127
Q

3 Metabolic Processes That Ensure Glucose Supply for Body Fuel

A

1) GLYCOLYSIS = process through which glucose is broken down into water and CO2 w/ the release of energy

2) GLYCOGENOLYSIS = breakdown of stored glycogen (from liver or skeletal muscles)
- Controlled by 2 hormones = Epinephrine (Break down glycogen in muscle) and Glucagon (breaks down glycogen in the liver. Can be directly released into blood stream and used by nervous system)

3) GLUCONEOGENESIS = building of glucose from new sources
- Hormones that stimulate = Glucagon, Glucocorticoid hormones, Thyroid hormones
- Process usually occurs in the liver

128
Q

Physiology of Serum Glucose Control

A

Glucose is preferred source of energy to produce ATP by cells of body

  • Normal range for serum glucose = 3.3-5.5 mmol/L BUT body usually regulates between 4.4-5

Insulin:
- Promotes formation of glucose transporters that bring glucose from the blood into cells, lowering glucose
- Promotes conversion of monosaccharides, lipids, and amino acids into storage forms of polysaccharides, triglycerides and proteins
- Insulin secretion increases during fed state

Glucagon:
- Promotes conversion of glycogen, proteins and lipids into glucose and release glucose into blood
- Glucagon secretion increases during fasted state

129
Q

Actions of Insulin on Glucose

A
  • Increases glucose transport into skeletal muscle and adipose tissue
  • Increases glycogen synthesis
  • Decreases glyconeogenesis
130
Q

Actions of Glucagon on Glucose

A

Promotes glycogen breakdown
Increases gluconeogenesis

131
Q

Actions of Insulin on Fats and Proteins

A
  • Anabolic in nature
  • Promotes glucose uptake by target cells and provides for glucose storage as glycogen
  • Prevents fat and glycogen breakdown
  • Inhibits gluconeogenesis and increases protein synthesis
132
Q

Actions of Glucagon on Fats and Protein

A
  • Catabolic in nature
  • Increases transport of amino acids into hepatic cells
  • Increases breakdown of proteins into amino acids for use in gluconeogenesis
  • Increases conversion of amino acids into glucose precursers
133
Q

Other Hormones Affecting Blood Glucose

A

CATECHOLAMINES:
- Epinephrine and norepinephrine
- Help to maintain blood glucose levels during periods of STRESS
- Inhibiting insulin release and decreasing movement of glucose into cells
- Promoting glycogenolysis by converting muscle and liver glycogen to glucose
- Increasing lipid activity, conserving energy, Causes mobilization of fatty acids and conserves glucose
- Conversion of bl. glucose mediated by these actions is important in the homostatic effect

GH:
- Increases protein synthesis in all cells of the body
- Mobilizes fatty acids from adipose tissue and anatagonizes the effects of insulin

GLUCOCORTICOIDS:
- Critical to survival during periods of fasting and starvation
- Stimulate gluconeo. by the liver

134
Q

Control of Insulin Release

A

Normally released in small increments when food is ingested

  • Consists of 2 polypeptide chains
  • Check amount a person is releasing by testing the C Peptide
  • Rise in plasma insulin after a meal stimulates storage of glucose as glycogen in the liver and muscle
  • Also inhibits gluconeo. and enhances fat deposition in adipose tissue
  • Fall in insulin levels during the night when you’re eating facilitates the release of stored glucose from the liver, protein from the muscle and fat
135
Q

Counter-Regulatory Hormones

A

Glucagons
Epinephrine
GH
Cortisol

136
Q

Amylin

A

2nd Beta Cell Hormone

Effects:
- Amylin and insulin together suppress the secretion of glucagon by the liver
- Amylin slows the transfer of nutrients to the intestine

137
Q

Glucagon

A

Produced in alpha cells
Transported via the portal veins to the liver
Acts in opposition to insulin
Stimulates breakdown of glycogen and fats to glucose and promotes gluconeo. from fats and proteins

138
Q

Somatostatin

A

Produced in the pancreas by the delta cells
- Inhibits secretion of insulin, glucagon, GH

139
Q

Diabetes Mellitus

A

Major disease affecting pancreas

Occurs when there is insufficient secretion of insulin from the pancreas or when target tissues do not respond to circulating insulin in the appropriate manner

Hyperglycemia is a symptom of underlying problem

Disorder of carb, protein, and fat metabolism (Results from an imbalance between insulin availability and insulin need)

Can represent:
- Absolute insulin deficiency
- Impaired release of insulin by the pancreatic beta cells
- Inadequate or defective insulin receptors
- Production of inactive insulin or insulin that is destroyed before it can carry out its action

140
Q

Prediabetes

A

Impaired fasting plasma glucose and impaired glucose tolerance

141
Q

Risk Factors and Causes of Diabetes

A

Family Hx.
Obesity esp. abdominal and visceral adiposity
BMI >27%
Race/ethnicity
GDM or babies >9lbs (mom is more at risk of developing if she has big babies)
HTN </= 140/90 mmHg
Triglycerides >200mg/dL
Prev. impaired glucose tolerance

Causes:
- Genetics
- Autoimmune
- Viral
- Environmental

142
Q

3 Poly of Diabetes

A

Polyuria = Excessive urination

Polydipsia = Excessive thirst

Polyphagia = Excessive hunger

143
Q

4 Types of Diabetes

A

Type 1 = Loss of Beta cell function, Absolute insulin deficiency

Type 2 = Impaired ability of the tissues to use insulin, relative lack of insulin or impaired release in relation to blood glucose levels

Gestational
Secondary

144
Q

Type 1 DM

A

aka “Insulin-dependent DM (IDDM)

  • Pancreas cannotproduce insulin
  • Represents 5-10% of all cases of DM
  • Usually underweight
  • Treated w/ insulin replacement therapy
  • Disease usually appears during childhood through early adulthood
  • Rapid onset

Characteristics:
- Little to no C Peptide
- Autoimmune process
- Weak family history
- Obesity uncommon
- Diabetic Ketoacidosis (DKA) often present
- Insulin mandatory (Exercise and diet help)

S&S:
- Frequent urinations
- Unusual thirst
- Extreme hunger
- Unusual weight loss
- Extreme fatigue
- Irritability
- Ketoacidosis

145
Q

Complications of Type 1 DM

A

Not treating it**

DKA:
- Extreme hyperglycemia, osmotic diuresis
- Body metabolizes lipids to ketone bodies to create source of energy for cells
- Ketone bodies reduce pH of blood causing metabolic acidosis
- Fruity breath (Due to presence of ketones)
- Treated w/ Insulin and fluid replacement

146
Q

Type 2 DM

A

aka “Non-insulin dependent (NIDDM)”

Pancreas does not produce enough insulin to meet needs of body or receptors are not sensitive to insulin that is produced

Represents 90-95% of DM

Clients are usually overweight*
- Treated w/ appropriate diet and exercise, then w/ oral hyperglycemic drugs and then insulin if needed
- Usually appears in the middle adulthood though children w/ sedentary lifestyles are developing disease
- Gradual onset

Characteristics:
- Strong family history
- Obesity common
- DKA rare
- Insulin resistance
- Varying levels of insulin (hyperinsulinemia not uncommon)

S&S:
- Frequent infections
- Blurred vision
- Cuts/bruises slow to heal
- Tingling/numbness in hands and feet
- Recurring skin, gum or bladder infections
- Any of the type 1 signs
- Often no symptoms occur

147
Q

Type 2 Risk Factors

A

Previously identified IFG (Impaired fasting glucose) or IGT (Impaired glucose tolerance)
(Aka “Prediabetes”)
- Hypertension (>/= 140/90)
- HDL cholesterol level >/=40 mg/dL
- History of GDM or delivery of babies over 9lbs

148
Q

Subdivisions of Type 1 Diabetes

A

Type 1A = Immune-mediated diabetes

Type 1B = Idiopathic diabetes

149
Q

Idiopathic Type 1B Diabetes

A

No evidence of autoimmunity is present

  • Only a small number of people
  • Usually African or Asian decent
  • Strongly inherited
  • Have episodic ketoacidosis due to varying degrees of insulin deficiency w/ periods of absolute insulin deficiency that may come and go
150
Q

Metabolic Abnormalities Contributing to Hyperglycemia in Type 2 DM

A

Impaired beta cell function and insulin secretion
Peripheral insulin resistance
Increased hepatic glucose production

151
Q

Causes of Beta Cell Dysfunction in Pts w/ DM

A
  • Initial decrease in beta cell mass
  • Increased beta cell apoptosis/decreased regeneration
  • Long-standing insulin resistance leading to beta cell exhaustion
  • Chronic hyperglycemia can induce beta cell desensitization (“glucotoxicity”)
  • Chronic elevation of free fatty acids can cause toxicity to beta cells (“Lipotoxicity”)
  • Amyloid deposition in beta cell can cause dysfunction
152
Q

Metabolic Syndrome and Type 2 DM

A

Metabolic Syndrome:
- Triglycerides
- HDL
- Hypertension
- Systematic inflammation
- Fibrinolysis
- Abnormal function of the vascular endotheluim
- Macrovascular disease
- Obesity and insulin resistance
- Increased resistance to the action of insulin
- Impaired suppression of glucose production by the liver
- Hyperglycemia and hyperinsulinemia

153
Q

Gestational Diabetes

A

Higher risk of C-section
Perinatal death
Neonatal complications
Risk of developing type 2 DM in 5-10yrs increased

Any degree of glucose intolerance during pregnancy

Hyperglycemia develops during pregnancy - secretion of placental hormones (Which causes insulin resistance)

-High risk women should be screened at 24-28weeks of gestation
-Need oral glucose tolerance test or glucose challenge
- 2hr Fasting level after 100mL glucose load of 155 would indicate GDM

154
Q

Secondary Diabetes

A

Causes:
- Damage/injury/interference or destruction of pancreas

Conditions:
- Cushing’s
- Hyperthyroidism
- Recurrent pancreatitis
- Use of parenteral nutrition

Medications:
- Corticosteroids
- Thiazides
- Dilantin
- Atypical antipsychotics

*Resolves when treatment of underlying condition is treated

155
Q

Chronic Conditions of DM

A

Macrovascular disease
Microvascular disease
Ocular disease
Neuropathy
Nephropathy

156
Q

Other Symptoms of Hyperglycemia

A

Weight loss
Recurrent blurred vision
Fatigue
Paresthesias
Skin infections

157
Q

Blood Tests for GLucose

A
  • Fasting Blood glucose test
  • Casual blood glucose test
  • Capillary blood tests and self-monitoring of cap. blood glucose levels
  • Glycated hemoglobin testing
158
Q

Treatment Plans for DM

A

Nutrition therapy
Exercise
Anti-diabetic agents

159
Q

Primary Control of DM

A

Diet
Exercise
Self-monitored blood glucose
Medications
Other monitoring/tests

160
Q

Complication Control DM

A

Controlling complications and target organ damage:

  • Bl. glucose/glycosylated hemoglobin
  • BP
  • Dyslipidemia
  • Weight management
  • Smoking
  • Dental/foot/eye care
  • Vaccinations
161
Q

Oral Antidiabetic Agents

A

Sulfonylureas
Repaglinide and Nateglinide
Biguanides
α-Glucosidase Inhibitors
Thiazolidinediones

162
Q

3 Principle Types of Insulin

A

RAPID-ACTING:
-Clear in appearance
Onset = 10-15min
Peak = 1-2hr
Duration = 3-5hr
Eg)
- Lispro (Humalog)
- Glulisine (Apidra)
- Aspart (NovoRapid)

INTERMEDIATE ACTING:
- Cloudy in appearance
Onset = 1-3hr
Peak 3-8hr
Duration = up to 18hrs
Eg)
NPH (Humulin-N, Novolin-NPH)

SLOW OR LONG ACTING:
- Clear in appearance
Onset = 90min
Peak = None
Duration = up to 24hrs
Eg)
Glargine (Lantus)
Detemir (Levemir)
Zinc

163
Q

Acute Complications of DM

A

Diabetic Ketoacidosis
Hyperglycemia
Ketosis
Metabolic acidosis
Hyperosmolar hyperglycemic state
Hypoglycemia
Hypoglycemia Abnormally low bl. glucose level (<70)

Causes:
- Too much insulin or oral hypoglycemic agents
- Too little food or excessive exercise
- Delayed or skipped meals

164
Q

Hypoglycemia

A

MILD = sympathetic nervous system is stimulated (Surge of epinephrine and norep.)
S&S = sweating, tremor, tachycardia, palpitations, nervousness, and hunger

MODERATE = Deprives the brain cells of needed fuel for functioning
S&S = inability to concentrate, headache, lightheadedness, confusion, memory lapse, numbness of lips and tongue, slurred speech, impaired coordination, emotional changes, irrational or combative behaviour, double vision and drowsiness

EMERGENCY MEASURES = for pts. who are unconsciousness or cannot swallow = Glucagon 1mg injection can be given IM

165
Q

Hypoglycemia Unawareness

A

No warning S&S
Increase risk of dangerously low BS
Related to autonomic neuropathy

166
Q

DKA

A

Caused by absence of markedly inadequate amounts of insulin and disorders in the metabolism of fats CHO and proteins

3 Main Clinical Features:
- Hyperglycemia
- Dehydration nad electrolyte loss
- Acidosis, Brunner & Suddath (Insulin deficiency leads to breakdown of fat (Lipolysis) into free fatty acids and glycerol and free fatty acids are converted into ketone bodies by the liver)

Diagnosis:
- Bl. glucose levels >250mg/dL
- Low bicarbonate (<15)
- Low pH (<7.3)
- Ketonemia (positive at 1:2 diluation)
- Moderate ketonuria

167
Q

Ketoacidosis

A

S&S = Nausea & vomiting, rapid breathing, extreme tiredness and drowsiness, weakness, acidosis (Fruity breath, tachy, hypotension)

168
Q

3 Main Causes of DKA and Treatment

A

1) Decreased or missed dose of insulin
2) Illness or infection
3) Undiagnosed or untreated diabetes

Treatment:
- IV fluid and electrolyte replacement
- Correct acidosis
- Provide adequate insulin
- Est. cause
- Can be mild or severe

169
Q

Monitoring and Managing Potential Complications

A

Fluid Overload = administering fluids rapidly to treat DKA or HHNS

Hypokalemia = due to treatment of DKA loss of potassium

Cerebral Edema = cause unknown, may be rapid correction of hyperglycemia resulting in fluid shift

170
Q

Hyperglycemia Hyperosmolar Nonketotic Syndrome (HHS)

A
  • Serious condition - Bl. glucose 800-1000
  • Ketosis usually minimal or absent
  • Defect is usually lack of effective insulin (insulin resistance)
  • Presistent hyperglycemia causes osmotic diuresis which results in losses of water and electrolytes
  • To maintain osmotic equilibrium, water shifts from intracellular fluid space to extracellular fluid space
  • With glycosurea and dehydration, hypernatremia and increase osmolarity occurs
  • Usually occurs in older adults
171
Q

Characteristics of HHS

A

Bl. Glucose = >600

Plasma osmolarity = >310

Dehydration

Absence of ketoacidosis

Depression of the senorium

172
Q

Causes, S&S and Treatment of HHS

A

Acute illness
Medications that exacerbate hyperglycemia
Dialysis treatment

S&S:
- Hypotension
- Profound dehydration
- Tachy
- Variable neurological signs
- Morality rate 10-40%

Treatment:
- Fluid replacement and correct electrolytes

173
Q

DKA vs HHS

A

DKA:
- More common in Type 1 DM**
- Lower mortality rate
- Onset = hours
- Treatment = fluid replacement, IV insulin, K replacement

HHS:
- More common in Type 2 DM**
- Higher mortality rate
- Onset = Days
- Treatment = NO INSULIN**, replace fluid/electrolyte

174
Q

Chronic Complications of DM

A

Disorders of the microvasculature
- Neuropathies (impaired sensation or pain, carpal tunnel, slowed digestion), nephropathies (damage to small vessels that supply glomeruli of kidney. Leading cause of end-stage renal disease), retinopathies (leading cause of acquired blindness)
- Distal symmetric neuropathy and foot ulceration

Macrovascular complications:
- Diseases of large and medium sized vessels
- Atherosclerosis = from altered lipid met.
- Cerebral vascular
- Peripheral vascular disease
- Adults w/ DM = 2-4x increased risk

Heart disease and stroke account for majority of deaths in DM clients
Poor circulation

175
Q

Pathologic Changes Observed w/ Diabetic Peripheral Neuropathies

A

Thickening of the walls of the nutrient vessels that supply the nerve
- Leading to the assumption that vessel ischemia plays a major role in the development of neural changes

Segmental demyelinization process that affects Schwann Cells

Accompanied by slowing of nerve conduction

176
Q

Classification of Diabetic Peripheral Neuropathies

A

SOMATIC:
- Polyneuropathies (Bilateral sensory)
- Mononeuropathies
- Amyotrophy

AUTONOMIC:
- Impaired vasomotor function
- Imparied GI function
- Impaired GU function
- Cranial nerve involvement

177
Q

Microvascular Diseases (+ 2 Areas Affected)

A

Unique to Diabetes

Capillary Basement membrane thickening
- Surrounds the endothelial cells of the cap
- Believed that increased bl. glucose levels react through series of biochemical responses to thicken basement membrane to several times its normal thickness

2 Areas Affected:
- Retina
- Kidneys

178
Q

DM Retinopathy Proliferative Vs Non-Proliferative

A

Pro = Most SEVERE form
Non = Most COMMON form

179
Q

Treatment of DM Nephropathy

A

Hypertension Control = Lower BP <120/80

Antihypertensive agents:
-ACE Inhibitors (“-pril”)= CaptoPRIL, EnalaPRIL, lisinopril, benazepril, fosinopril etc
- ARB (Angiotension Receptor Blocker) = CandesarTAN, cilexetil, irbesarTAN, losarTAN, potassium, telmisarTAN,
- Beta blockers

Glycemic control:
- Pre-prandial plasma glucose 90-130
- A1C <7.0%
- Peak postprandial plasma glucose <180
- Self-monitoring of Bl. Glu. (SMBG)
- Medical Nutrition Therapy

Restrict dietary protein to RDA of 0.8g/kg body weight per day

180
Q

3 Primary Treatments of End-Stage Renal Disease (ESRD)

A

1) Hemodialysis
2) Peritoneal Dialysis
3) Kidney Transplant

181
Q

Pathogenesis of DM Neuropathy

A

Metabolic Factors:
- High Bl. Glu.
- Advanced glycation end products
- Abnormal Bl. fat levels

Ischemia
Nerve fibre repair mechanisms

182
Q

Autonomic Neuropathy

A

Affects the autonomic nerves controlling internal organs:
- Peripheral
- GU
- GI
- Cardiovascular

Is classified as clinical or sub-clinical on the presence or absence of symptoms

Hypoglycemic unawareness

Sudomotor neuropathy = absence of sweating of the extremities w/ compensatory increase in upper body sweating

Sexual dysfunction

183
Q

Treatment of Foot Ulcers

A

Bed Rest
Antibiotics
Debridement

Good control of Bl. Glu.

*If pt has PVD, ulcers may not heal due to the decreased ability of O2 nutrients and antibodies to reach injured tissue

184
Q

Acanthosis nigricans

A

Dark, course, thicken skin on the neck

185
Q

Diabetic dermatopathy

A

Red-brown flat-topped papules

186
Q

Granuloma Annulare

A

Type 1
Autoimmune
Partial rings of papules often in dorsal surface of hands and feet

187
Q

Pharmacotherapy of Type 2 DM

A

Most common drugs promote release of insulin (secretagogues) OR increase receptor sensitivity to insulin

SECRETAGOGUES:
- Sulfonylureas (also decreases insulin resistance, can cause hypoglycemia, GI disturbances, rash, cross sensitivity w/ sulfa drugs and thiazide diuretics)
- Meglitinides (Administer slightly before meals, well tolerated)

SENSITIVITY INCREASE:
- Biguanides (Decreases production and release of glucose from liver, increase cellular uptake of glucose, lower lipid level, Risk of lactic acidosis, avoid alcohol, low risk of hypoglycemia)
- Thiazolidinediones (Increases insulin sensitivity to fat and muscle tissue, can cause fluid retention and worsening heart failure. Therapeutic effects take several days to develop. NO hypoglycemia)

ALPHA GLUCOSIDASE INHIBITORS:
- Reduce absorption of glucose by preventing digestion of carbs
- Hypoglycemia can occur if combined w/ another oral drug, insulin or sulfonylurea (treat w/ glucose NOT sucrose)

INCRETIN ENHANCERS:
- Reduce met. of insulin
- Decreases rate of digestion of carbs
- Well tolerated
- Minor nausea, vomiting, and diarrhea
- Some weight loss
- LOW risk hypoglycemia

188
Q

Incretin Enhancers

A

GLP-1 acts rapidly to produce:
- Increased amount of insulin by pancreas
- Decreased amount of glucagon secreted by pancreas
- Delayed gastric emptying
- Decreased food intake

2 CLASSES:
- Activating GLP-1 receptor
- Inhibiting dipeptidyl peptidase 4 (DPP-4)

189
Q

Sulfonylureas

A
  • Divided into 1st and 2nd Gen. categories
  • Stimulate release of insulin from pancreatic islet cells
  • Increase sensitivity of insulin receptors on target cells
190
Q

Diabetes Monitoring

A

Blood:
- Glucose
- Hemoglobin A1C
- Fructosamine
- Lipid Profile
- Creatinine
- BUN

Urine:
- Ketones (Type 1)
- Glucose
- Protein

Weight
BP

191
Q

Problems Assoc. W/ Urine Glucose Testing

A

Not easily interpreted (some tests are qualitative instead of quantitative)

Potential false positive readings depending on test used

Lack of direct correlation between urine glucose and bl. glu. levels

Results are technique dependent

192
Q

Frequency of Bl. Glu. Monitoring

A

Minimum Recommendation:
- Diet/exercise or oral meds = 2-3times/day to 2-3times/week

Fixed-dose Insulin:
- 3-4x/day to 3 days/week

Intensive Insulin Therapy:
- 3-4x/day everyday
- 3am measurement weekly

Additional measurements needed when:
- sick
- Change in exercise habits
- Travel
- Change in treatment plan
- Symptoms of hypo/hyperglycemia

193
Q

Factors Affecting Accuracy of Bl. Glu. Tests

A

User variability
Hematocrit >60% or <25%
Defective strips (temp, moisture, time)
Very high TG and/or cholesterol
Extreme environmental temps
Hypoxia
Altitude
Uric acid
Ascorbic acid
Improper cleaning and maintenance

194
Q

Glycosylated Hemoglobin (HbA1c)

A

Formed when glucose reacts w/ hemoglobin (concentration-dependent reaction)

Usually constitutes 4-6% of total hemoglobin

Level reflects ave. bl. glu. over 3 months

Level canbe drawn any time of day (regardless of meals)

Best indicator of overall degree of glycemic control

195
Q

Monitoring Hemoglobin A1C

A

Gold Standard for monitoring long term

Should be performed every 3-6months
(3 = therapy has changed or goals not met)
(6 = if meeting goals)

196
Q

Interpreting HbA1c Levels

A

> 8% = always warrants changes in therapy**

May experience hyperglycemia for 2-4 weeks before HbA1c will rise

197
Q

Conditions Affecting Results

A

Anything affecting ave. life span of RBC can cause misleading HbA1c results:
- Bleeding
- Hemolysis
- Sickle cell anemia

198
Q

DM & Dyslipidemia

A

Type 2 have a 2-4 increase risk of coronary Heart Disease

Most common pattern:
- Increased TGs + Decreased HDL
(While LDL seem to be similar to non diabetics)

Weight loss and exercise will DECREASE TGs and INCREASE HDL without need for drugs

Also decreased saturated fats in diet

199
Q

Dm & HTN

A

HTN contributes to the development and progression of chronic complications of DM

Decreasing BP will slow the rate of progression of neuropathy, reduce CV disease and cerebrovascular complications

Goal BP = <140/90

ACE-1 or ARB first line = renal protective

200
Q

Elements of the Hematopoietic System

A

All blood cells and their precursers

Bone marrow (where blood cells are born)

Lymphoid tissues (where some blood cells circulate as they develop and mature)

201
Q

Composition of Blood

A

Fluid/Dissolved Components:
- Water
- Proteins
- Small molecular substances

Cellular Elements:
- RBCs
- Thrombocytes or platelets
- WBCs (lymphocytes and leukocytes)

202
Q

Function of Plasma Components of Blood

A

Carry cells that transport gases

Aid in body defenses

Prevent blood loss

203
Q

3 Plasma Proteins

A

ALBUMIN:
- 54% of plasma proteins
- Contributes to plasma osmostic pressure and maintenance of blood volume
- Serves as a carrier for certain substances

GLOBULINS:
- 38%
- Alpha globulins transport bilirubin and steroids
- Beta Globulins transport iron and copper
- Gamma “ constitute the antibodies of the immune system

FIBRINOGEN:
- 7%
- Converted to fibrin in the clotting process

204
Q

Neutrophils (“first responders”)

A

50-60% of WBCs

Maintaining normal host defenses against invading substances

  • 1st cells to arrive at the site of infection (first responder)
  • Origins in myeloblasts (bone marrow)
  • Move to the tissue for approx. 1-3 days (die in the tissue discharging phagocytic function OR die of senescence)
205
Q

Eosinophils

A

1-3% of WBCs

Increase in number during allergic reactions and parasitic infections

  • Assoc. w/ allergic reactions**
  • In parasitic reactions, they use surface markers to attach themselves to the parasite and then release hydrolytic enzymes
206
Q

Basophils

A

0.3-0.5% of total LEUKOCYTES

Involved in allergic reactions and hypersensitivity

  • Consist of heparin (anticoagulant), histamine (vasodilator), and other mediators of INFLAMMATION**

Similar to mast cells

207
Q

Lymphocytes

A

20-30% of LEUKOCYTES

Defend against microorganisms through IMMUNE RESPONSE

Function in the spleen or lymph nodes

3 Types:
1) B lymphocytes
2) T lymphocytes
3) NK Cells

208
Q

Monocytes and Macrophages

A

3-8% total LEUKOCYTE

Important role in CHRONIC inflammation

Involved in IMMUNE RESPONSE:
- Activating lymphocytes**
- Presenting antigen to T cells

Cells survive for months to years in the tissues

209
Q

Thrombocytes (Platelets)

A

Circulating cell fragments of the large megakaryocytes

Function to form platelet PLUG that helps CONTROL BLEEDING

8-9 days in circulation

210
Q

Hematopoiesis

A

Blood cells originate from pluripotent stem cells in the bone marrow

Proliferation, differentiation, and functional abilities of various blood cells are controlled by cytokines (hormone-like growth factors)

211
Q

Hemato. Growth Factors

A
  • Increase peripheral stem cells for transplantation
  • Accel. cell proliferation after bone marrow engraftment

Eg)
EPO
TPO
G-CSF
GM-CSF

212
Q

Conditions Responding to Use of Hemato. Growth Factors

A

Bone marrow failure caused by chemotherapy or aplastic anemia

Anemia of kidney failure

Hemato. neoplasms

Infectious diseases such as AIDS

Congenital and myeloproliferative disorders

Some sold tumors

213
Q

Complete Blood Count (aka CBC)

A

Provides info regarding the number of blood cells and their structural and functional characteristics

White cell differential count is the determination of the relative proportions (%’s) of individual white cell types

214
Q

Ways to Obtain Blood Specimens

A

Skin puncture (capillary blood)

Venipuncture (Vein blood)

Arterial puncture (artery blood)

Bone marrow aspiration

215
Q

Types of Diagnostic Tests for Blood

A

CBC
Erythrocyte sedimentation rate
Bone marrow aspiration and biopsy

216
Q

Clinical Terms for Blood

A

Anemia = Low RBC
Polycythmia = High RBC

Leucopenia = Low WBC
Leucocytosis = High WBC

Thrombocytopenia = Low Platelets
Thrombocytosis = High Platelets

217
Q

Anemia =

A

Blood loss (hemorrhage) = HEMORRHAGIC Anemia

Bone marrow failure (from radiation, toxin, tumor, fibrosis) = APLASTIC Anemia

Erythropoietin deficiency (secondary to renal disease, Iron, folic acid, Vit B12 deficiency) = NUTRITIONAL Anemia

Hemolysis (RBC destruction) = HEMOLYTIC Anemia

218
Q

Polycythmia (High RBC)

A

Low O2 tension in blood (CHD, Cor pulmonale, pulmonary fibrosis)

Polycythemia rubra vera

Dehydration (from severe diarrhea)

Renal Disease w/ high erythro. production

219
Q

Leucocytosis (High WBC)

A

Infectious diseases
Inflammatory Disease (Eg RA or allergy)
Leukemia
Severe emotional or physical stress
Tissue damage (Eg burns)
Low O2
Dehydration
Diarrhea

220
Q

Leukopenia (Low WBC)

A

Bone marrow failure (Eg. b/c of infection, tumor or fibrosis)

Presence of cytotoxic substance

Autoimmune/collagen-vascular diseases (Eg. lupus erythematosus)

Diseases of liver or spleen

Radiation exposure

221
Q

Thrombocytosis (High Platelet)

A

Chronic myeloid Leukemia

222
Q

Thrombopenia (Low Platelet)

A

Aplastic anemia
Chemotherapy

223
Q

Packed Cell Volume (PCV) Hematocrit

A

Ratio of volume of RBCs to volume of Blood

HIGH Hematocrit = Polycythemia

LOW Hematocrit = Anemic

224
Q

5 Stages of Hemostasis

A

1) Vessel Spasm (Vascular Constriction)
2) Formation of platelet Plug
3) Blood coagulation or dev. of an insoluble fibrin dot
4) Clot retraction
5) Clot dissolution

225
Q

2 Categories of Disorders of Hemostasis

A

THROMBOSIS:
- inappropriate formation of clots within vascular system

BLEEDING:
- Failure of blood to clot in response to appropriate stimulus

226
Q

1) Vascular Constriction

A

Vessel spasm constricts the vessel and reduces blood flow (transient event lasting min-hr)
Vessel spasm is initiated by endothelial injury and caused by local and humoural mechanisms

227
Q

2) Platelet Plug Formation

A

Adhesion and aggregation

1) Attracted to damaged vessel wall
2) Activation by subendothelial tissue
3) Changes from smooth disks to spiny spheres
4) Exposing glycoprotein receptors on their surfaces

228
Q

3) Requirements for Blood Clotting Process

A

Presence of platelets produced in bone marrow

Von Willebrand factor generated by the vessel endothelium

Clotting factors synthesized in liver using Vit K

229
Q

4) & 5) Clot Retraction/Dissolution

A

Interaction of substrates, enzymes, protein cofactors, and calcium ions that circulate in the blood or are released from platelet cells in the vessel wall

230
Q

Intrinsic and Extrinsic Coagulation Pathways

A

Terminal steps in both pathways are the same:
- Calcium, factors X&V, platelet phospholipids combine to form prothrombin activator
- Prothrombin activator converts prothrombin to thrombin
- Causes conversion of fibrinogen in fibrin strands that create the insoluble blood clot

231
Q

Thrombin System

A

Calcium ions must be present for the thrombin system to begin

Consists of several blood proteins that activate when bleeding occurs

Activated clotting proteins engage in a cascade of chemical reactions that finally produce a substance called “fibrin”

Fibrin strands stick to the exposed vessel wall, clumping together and forming a web-like complex of strands

RBCs become caught up in the web causing a clot

232
Q

Regulation of Blood Coagulation

A

Antithrombin III inactivates coagulation factors and neutralizes thrombin

When antithrombin III is complexed w/ naturally occurring heparin, its action is accelerated and provides protection against uncontrolled thrombus formation on the endothelial surface

Protein C (plasma protein) acts as an anticoagulant by inactivating factors V and VIII

Protein S accelerates the action of Protein C

Plasmin breaks down fibrin into fibrin degradation products that act as anticoagulants

233
Q

Conditions that Create Increased Platelet Function

A

Atherosclerosis
DM
Smoking
Elevated blood lipoid and cholesterol levels
Increased platelet levels

234
Q

Conditions that Cause Accel. Activity of the Coagulatory System

A

Pregnancy and the puerperium
Use of oral contraceptives
Postsurgical state
Immobility
CHF
Malignant diseases

235
Q

Hypercoagulability States

A

Increase risk of clot or thrombus formation in the arterial or venous circulations

Arterial thrombi are assoc. w/ conditions that produce turbulent blood flow and platelet adherence

Venous thrombi are assoc. w/ conditions that cause stasis of blood flow w/ increased concentrations of coagulation factors

236
Q

Causes of Bleeding

A

Decrease in the # of Circulating Platelets:
- Depletion of platelets must be relatively severe before hemorrhagic tendencies of spontaneous bleeding occur

Impaired Platelet Function:
- Bleeding resulting from platelet deficiency commonly occurs in small vessels and is characterized by petechiae and purpura

237
Q

Increased Platelet Function

A

Hypercoagulability due to increased platelet function results in platelet adhesion, formation of platelet clots and disruption of blood flow

Causes of increased platelet function are disturbances in flow, endothelial damage and increased sensitivity of platelets to factors that cause adhesiveness and aggregation

238
Q

Atherosclerotic Plaques and Platelets

A

Plaques disturb blood flow, causing endothelial damage and promoting platelet adherence

Platelets that adhere to vessel wall release growth factors which cause proliferation of smooth muscle and thereby contribute to the development of atherosclerosi

Smoking, elevated blood lipids and cholesterol, hemodynamic stress, and DM predispose vessel damage, platelet adherence and eventual thrombosis

239
Q

Platelet Defects

A

Thrombocytopenia:
- Low Platelets, increased sequestration of platelets in spleen or decreased platelet survival
Types:
- Drug-induced Thrombocytopenia:
- Idiopathic Thrombocytopenia purpura
- Thrombotic Thrombocytopenia purpura

Impaired Platelet Function

240
Q

Manifestations of Thrombocytopenia

A

Bleeding:
- Mucus membranes (nose, mouth, GI tract and uterine cavity)
- Commonly occurs in small vessels (Petechiae = pinpoint purplish red dots & Purpura = purple areas of bruising)

241
Q

Coagulation and Vit K

A

Vit K is an essential cofactor for synthesis of clotting factors

Fat-soluble vitamen synthesized by intestinal bacteria

In Vit K deficiency, the liver produces inactive clotting factor resulting in abnormal bleeding

242
Q

Coagulation Defects

A

Deficiencies can arise b/c of defective synthesis, inherited disease, or increased consumption of the clotting factors

Eg) Hemophilia A
Hemophilia B
Von Willebrand Disease
Any genetic disruption of the production of the clotting factor

243
Q

Vascular Disorders that Cause Bleeding

A

HEMORRHAGIC TELANGIECTASIA:
- Uncommon autosomal dominant disorder characterized by thin-walled, dilated capillaries and arterioles

VIT C DEFICIENCY:
- “Scurvy”
- Results in poor collagen synthesis and failure of the endothelial cells to be cemented together properly, causing fragile wall

CUSHING DISEASE:
- Causes protein wasting and loss of vessel tissue support because o the excess cortisol

SENILE PURPURA:
- Bruising in elderly persons
- Caused by the aging process

244
Q

Conditions Assoc. W/ Disseminated Intravascular Coagulation

A

Obstetric conditions
Cancers
Infections
Shock
Trauma or surgery
Hematologic conditions

245
Q

RBC Development

A

Continuously being formed from the pluripotent stem cells in bone marrow

Move through a series of divisions to develop into mature RBCs

Normoblast to reticulocyte, the RBC accumulates hemoglobin as the nucleus condenses and is lost

Red cell loses its mitochondria and ribosomes

246
Q

Function of RBCs

A

Transportation of O2 to the tissues

Hemoglobin bind some CO2 and carry it from the tissues to the lungs

Hemoglobin molecule is comprised of two pairs of structurally different polypeptide chains

Each of the four polypeptide chains consists of globin (protein) and a heme unit (Which surrounds an atom of iron that binds to O2)

Each molecule of hemoglobin can carry 4 molecules of O2

The production of each type of globin chain is controlled by individual structural genes with 5 different gene loci

Mutations can occur anywhere in these 5 locations

247
Q

Erythropoiesis

A

Red cells are produced in the red bone marrow after birth

Until Age 5, almost all bones produce Red cells to meet growth need
- After 5, bone marrow activity gradually declines

After 20yrs red cell production takes place mainly in the membranous bones of the vertebrae, sternum, ribs and pelvis

With this reduction in activity of red bone marrow is replaced with fatty yellow bone marrow

248
Q

Hemoglobin Structure

A

Globin Chains = α & β

Heme = Iron & Porphyrin

O2 Binding

249
Q

RBC Destruction

A

Lifespan = 120 days
- Broken down in the spleen
- Degradation products (Iron and amino acids) are recycled

Heme molecule is converted to bilirubin and transported to the liver:
- It is removed and rendered water soluble for elimination in the bile

250
Q

Bilirubin

A

Heme unit is converted to bilirubin

Insoluble in plasma and attaches to plasma proteins for transport (unconjugated)

Removed from blood by liver and conjugated w/ glucuronide to render it water soluble (conjugated)

Jaundice

251
Q

RBC Lab Tests

A

RBC Count:
- measures total # of RBC in 1mm3 of blood

% of Reticulocytes (normally 1%ish):
- Provides an index of the rate of Red cell production

Hemoglobin (grams per 100mL of blood):
- Measures the hemoglobin content in blood

Hemacrit:
- Measures volume of red cell mass in 100mL of plasma volume

252
Q

Transfusion Therapy

A

Provides the means for replacement of RBCs and other blood components

4 Major ABO blood types are determined by the presence or absence of 2 red cell antigens (A & B)

The presence of D antigen = Rh-positive type
The absence of D antigen = Rh-negative type

253
Q

RBC Components Used in Transfusion Therapy

A

Whole blood
RBCs
Leukocyte-reduced blood cells
Washed RBCs
Frozen RBCs

254
Q

Immediate Hemolytic Transfusion Reaction

A

Intravascular lysis of transfused RBCs by complement, IgM

Causes:
- Transfusion of ABO-incompatible blood
- Transfusion of ABO-incompatible plasma
- Non-ABO antibodies

Clinical Manifestations:
- Fever (but most febrile reactions not hemolytic)
- Back pain
- Dark or red urine
- Bronchospasm
- Shock
- DIC
- Organ failure
- Death

S&S of Transfusion Reactions:
- Sensation of heat along vein where blood is being infused
- Flushing of face
- Urticaria (Hives)
- Headache, pain in lumbar
- Chills, fever, constricting pain in chest
- Cramping pain in abdomen
- Nausea and vomiting
- Tachy, hypotension and dyspnea

Treatment:
- Stop transfusion
- IV crystalloid or colloid
- Maintain BP, HR
- Maintain airway
- Diuresis (fluid, loop diuretic, mannitol may cause volume overload)
- Monitor renal and coagulation status

255
Q

After Stopping Blood Transfusion

A

Check blood product/paperwork to ensure correct product given

Notify blood bank/transfusion service

Obtain blood and urine samples
- Plasma and urine hemoglobin
- Direct Coombs test
- Repeat crossmatch/antibody screen
- Repeat ABO/Rh typing

256
Q

Delayed Hemolytic Transfusion Reaction

A

IgG-mediated lysis of transfused red cells (usually extravascular, non-ABO)

Usually begins 5-10 days after transfusion

Jaundice, falling Hct, positive direct Coombs test, fever

Not generally life-threatening

257
Q

Febrile, Non-Hemolytic Transfusion Reaction

A

Cause:
- Cytokines released by leukocytes during storage, antibodies to HLA antigens on transfused or donor PMNS

Incidence:
- </= 0.5% of units transfused

More common in multiple transfused recipients

Fever, chills, res distress in severe reactions

Reduced incidence/severity w/ leukocyte-poor product

258
Q

Transfusion Related Acute Lung Injury (TRALI)

A

Hypoxemia w/ bilateral pulmonary infiltrates

No increase in central venous or pulmonary artery pressures

Usually begins acutely within 6hrs of transfusion

Clinical = acute res distress, fever, chills

Pathophysiology:
- Underlying lung injury (Eg. sepsis, pneumonia) causes PMNs to adhere to pulmonary caps
- Mediators in transfused blood product (neutrophil antibodies, cytokines) activate PMNs w/ resistant cap injury

Risk = FFP > Platelets > RBC

Treatment:
- Stop transfusion
- O2
- Ventilatory support
- Pulse corticosteroids

259
Q

G6PD

A

Hereditary deficiency of glucose-6-phosphate dehydrogenase predisposes to oxidative denaturation of hemoglobin, w/ resultant red cell injury lysis

260
Q

Extravascular Hemolysis Vs Intravascular Hemolysis

A

Extravascular = When RBCs become LESS DEFORMABLE making it difficult for them to transverse the splenic sinosoids

Intravascular = Result of complement fixation in transfusion reactions, mechanical injury or toxic factors

261
Q

Sickle Cell Disease

A

Inherited disorder in which an abnoraml hemoglobin (Hemoglobin S [HbS]) leads to the chronic hemolytic anemia, pain and organ failure

262
Q

Thalassemias

A

Group of inherited disorders ofhemoglobins synthesis leading to the decreased synthesis of either the α- or β-globin chains of HbA

263
Q

Iron Deficiency Anemia

A

Common worldwide cause of anemia affecting people of all ages

Results from dietary deficiency, loss of iron through bleeding or increased demands

B/C iron is a component of heme, a deficiency leads to a decreased hemoglobin synthesis and consequent impairment of O2 delivery

264
Q

Vit B12 Deficiency

A

aka Megaloblastic Anemia

Red cells are produced abnormally large b/c of excess cytoplasmic growth and structural proteins

265
Q

Primary vs Secondary Polycythemia

A

Primary = Proliferative disease of the bone marrow w/ an absolute increase in total RBC mass accompanied by elevated white cell and platelet counts

Secondary = results from increased erythropoietin levels caused by hypoxic conditions such as chronic heart and lung disease

266
Q

Neonatal Blood

A

Hemoglobin concentrations at birth are high, reflecting the high synthetic activity in utero to provide adequate O2 delivery

HbF vs HbA = affinity of F vs A

Hyperbilirubinemia = Unconjugated vs conjugated, phototherapy

Hemolytic disease

267
Q

Aging and RBCs

A

Age-Assoc. Decline in the hemto. reserve

  • Reduction in hemato. progenitors
  • Reduced production of hemato. growth factors
  • Inhibition of erythro.
  • Inflammatory cytokines interfere w/ erythro. interaction w/ its receptors

Anemia:
- Hb decreases
- RBC production decreases w/ age
- CBC = peripheral blood smear and reticulocyte count and index
- Studies rule out comorbid conditions such as malignancy, GI conditions that cause bleeding and pernicious anemia

268
Q

Process of Hemostasis

A

“stopping blood flow”

Proceeds in a series of steps using clotting factors:

  • Intrinsic and extrinsic pathways both lead to formation of prothrombinase
  • Prothrombinase converts to prothrombin to thrombin
  • Thrombin converts to fibrinogen to fibrin
  • Fibrin strands trap RBCs forming clots

Cofactors = Ca+2 and Vit K are critical for synthesis of clotting factors

Fibrinolysis = Plasmin breaks down fibrin network

Pharmacotherapy focuses on manipulating these elements

269
Q

Process of Fibrinolysis

A

“removal of blood clot, proceeds in cascading steps”

Initiated by release of enzyme ‘tissue plasminogen activator (tPa)’
- Converts inactive plasminogen enzyme in the clot to active form plasmin enzyme

Plasmin digests fibrin strands to remove clot

270
Q

Diseases of Hemostatis

A

Thromboembolic disorders:
- Thrombus = stationary clot
- Embolus = clot that moves to another location
- Deep Venous Thrombosis (DVT) = venous clots often develop in the legs as a DVT but can migrate to lungs creating pulmonary embolism
- Clots migrating from left atrium can cause strokes
- Coronary artery clots cause MI

Platelet Disorders:
- Due to decreased production resulting in low Platelet counts
- Bone marrow suppression
- Folic acid and B12 deficiency
- Decreased thrombopoietin in liver failure

Hemophilia and von Willeband’s disease:
- Genetic conditions resulting in absence of clotting factors = difficulty clotting

271
Q

Anticoagulants

A

Used to prolong bleeding time in order to prevent blood clots from forming

Eg) Heparin
- Enhances antithrombin III (AT-III) activity
- Decreases thrombin activity (active factor IIa)
- Decreases prothrombinase (Active factor Xa)

Low molecular weight heparin:
- Also enhances AT-III activity but more specific to prothrombinase (active factor X)
- Fewer adverse effects than heparin (Less risk of thrombocytopenia compared to heparin)

272
Q

History of Anticoagulants

A

Warfarin has been the drug of choice for the prevention and treatment of arterial and venous thrombotic disorders for more than 40yrs

It was initially marketed as a pesticide against rats and mice and is still popular for this purpose

NURS 316 (5 decks)

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