Exam 1 Flashcards

1
Q

What is pathology

A

Study and diagnosis of disease through examination of organs, tissues, cells, and bodily fluids

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2
Q

What is pathophysiology

A

the study of abnormalities of physiologic functioning of living beings

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3
Q

What is etiology

A

the cause or reason for a phenomena. Identification of causal factors that acting together provoke a disease or injury

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4
Q

What is pathogenesis

A

development of disease in cells, tissues, and organs. Dynamic interplay of changes in cell, tissue, organ, and systemic function

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5
Q

What is idiopathic

A

Cause is unknown

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6
Q

What is iatrogenic

A

Cause is a result of unintended or unwanted medical treatment

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7
Q

What is a risk factor

A

Probability of development of disease when factor is present

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8
Q

Compare symptom vs. signs

A

Symptom is subjective that the patient reports (nausea) signs are objective (witnessed vomiting).

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9
Q

Give 8 stages and clinical course of a disease

A

Latent or incubation period, prodromal period, manifest illness or acute phase, subclinical stage, acute or chronic, exacerbations and remissions, convalescence, sequela

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10
Q

Give four physiologic processes affecting disease

A

Age, gender, genetic and ethnic background, and geographic area

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11
Q

Give 6 factors affecting disease to think about when treating someone

A

Cultural considerations, socioeconomic and lifestyle, age differences, gender differences, situational differences, and time variations

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12
Q

Give four types of primary prevention and give its other name

A

Prevention of disease: improved nutrition, housing, and sanitation. Immunizations. Education. Safety precautions (seat belts, speed limits, chemicals).

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13
Q

Give 3 types of secondary prevention and give its other name

A

Screening: physical examinations and routing screening. Self breast exams. Amniocentesis.

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14
Q

Give 2 types of tertiary prevention and give its other name

A

Treatment: Once a disease is established medical and surgical treatment. Rehabilitation.

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15
Q

How are large molecules such as proteins brought through membrane

A

Ingested via endocytosis (either pino or phago) and secreted via exocytosis.

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16
Q

Describe receptor mediated endocytosis

A

Chemicals bind to a receptor on the outside of membrane, the membrane with bound chemicals pinches inwards carrying the molecules inside the cell.

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17
Q

What is cellular edema

A

Excess fluid can enter the cell’s internal environment causing swelling.

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18
Q

Describe the Na-K pump and what happens if it fails

A

Maintains low Na and high K concentrations in the cell. This maintains cell volume by controlling solute concentration and therefore osmotic forces across the membrane. If Na is continually allowed in the cell it will burst.

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19
Q

What does the Na-K pump exchange every time ATP is bound

A

3 Na out and 2 K in

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20
Q

Where does aerobic vs anaerobic metabolism take place

A

Aerobic happens inside the mitochondria and requires oxygen while anaerobic metabolism happens outside of the mitochondria and consists of just glycolysis

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21
Q

Describe mitochondrial DNA

A

Only organelles with their own DNA. Mitochondrial DNA is subject to mutation by oxygen-derived free radicals.

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22
Q

Describe free radical effect on structures

A

Free radicals oxidize cell structures and can be called oxidants. They disrupt the integrity of the cell membrane and damage organelles and DNA, causing cell dysfunction. Worst place for this to occur is in muscles, cerebrum, and nerves.

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23
Q

Name some antioxidants

A

vitamins A, E, C, and beta-carotene counteract free radicals.

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24
Q

Describe lysosomes

A

contain digestive enzymes. They digest particles brought in by endocytosis, pinocytosis, or phagocytosis. Also digest worn out cell parts. In cell death autolysis occurs and enzymes rupture from lysosome and digest the whole cell.

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25
Q

What types of cells have many lysosomes

A

White blood cells (macrophages that constantly survey body for antigen)

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26
Q

How do lysosomes play a roll in myocardial infarction

A

In myocardial infarction cardiac muscle cell death leads to autolysis leading to lysosome enzymes spilling out to digest dead cardiac muscle cells. It is screened for by drawing blood and looking for lysosomal enzymes.

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27
Q

Describe ribosomes

A

They are the factories of protein synthesis. The nucleus gives directions on what proteins to make.

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28
Q

What is a clinical concept that involves ribosomes

A

Some antibiotics interfere with the function of bacterial ribosomes, thereby inhibiting bacterial protein synthesis.

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29
Q

What is a chromosome

A

Chains of genes

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30
Q

Describe cellular adaptations and maladaptive changes

A

All diseases result in some alteration of cell function because the cell responds to stressors in the environment. In circumstances of overwhelming insult, cell injury or cell death can occur. Cell injury can be reversible but if the injurious agent is persistent or severe enough, cell injury can lead to cell death.

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31
Q

What is histology

A

The microscopic study of tissues and cells.

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32
Q

What is a biopsy

A

Cell sample from an organ or mass of tissue to allow for histological examination.

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33
Q

What are pathogonomic changes

A

Unique histological findings that represent distinct disease processes.

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34
Q

What is atrophy

A

Decreased cell size

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35
Q

What is hypertrophy

A

Increased cell size

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36
Q

What is hyperplasia

A

Increased cell number

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37
Q

What is metaplasia

A

conversion of one cell type to another

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38
Q

What is dysplasia

A

disorderly cell growth

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39
Q

Give 6 causes for atrophy

A

Disuse or diminished workload. Lack of nerve stimulation (paralysis). Loss of hormonal stimulation. Inadequate nutrition. Decreased blood flow (ischemia). Aging.

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40
Q

Describe hypertrophy of cells and the natural effects it brings.

A

Individual cells become larger which can either be physiologic (lifting weights) or pathologic (disease caused). Hypertrophy necessarily brings a greater metabolic demand and greater energy needs

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41
Q

Give a pathologic hypertrophy example

A

The heart hypertrophies in response to hypertensions (greater workload because of greater peripheral resistance).

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42
Q

Give a physiologic hypertrophy example

A

Weight lifters develop hypertrophied muscles because of increased workload and use.

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43
Q

Describe causes of hyperplasia

A

Can be hormonal such as pregnancy of benign prostatic hyperplasia. Or can be compensatory cellular changes. Excessive cells can be a good adaptive response or they could be detremental.

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44
Q

Give an example of hormonal hyperplasia

A

Pregnancy increases demand of milk production (lactation) which causes hyperplasia of breast milk glands and tissue mass.

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45
Q

Give some cause for metaplasia

A

Metaplasia is replacement of one cell type by another cell type. Response to a change in environment. Typically occurs with chronic inflammation. The substitution of cells enables the survival of the tissue.

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46
Q

Give an example of metaplasia

A

In esophagitis, the cells of the lower esophagus change to be able to cope with the stomach acid that constantly irritates the cells. This leads to a disease called gerd. The flat epithelium of the esophagus change to become more columnar like stomach cells.

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47
Q

Describe dysplasia and what must be watched for

A

Deranged cellular growth. Cells vary in size, shape, and organization compared to healthy cells. It is a precancerous condition that must be watched carefully becaues very often will develop into neoplasia.

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48
Q

Describe neoplasia

A

New growth that usually refers to disorganized, uncoordinated, uncontrolled, proliferative cell growth that is cancerous. Tumor and neoplasm are often used interchangeably.

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49
Q

Describe some dysfunctions of the Na-K pump

A

Insufficient ATP, normal osmotic balance altered. Increased intracellular Na draws water in causing swelling. If an organ is swollen and enlarged it is termed megaly. Increased extracellular K also if calcium pump fails calcium accumulates in the cell leading to cell degradation and calcifications often accumulate in areas of cell injury and death. An example is a mammogram

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50
Q

Describe the effects of loss of plasma membrane integrity

A

Guardian of organelles is damaged, injurious agents can now affect any organlle. Water can enter causing swelling. The mitochondria can be damaged and halt energy production. Organelles can swell and deteriorate and the nucleus is now vulnerable to injury

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51
Q

Describe the effects of defects in protein synthesis

A

Cells low in energy, decreased ATP. Protein synthesis begins to fail and the lack of proteins can begin the process of cell degradation and death.

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52
Q

Describe what can happen with genetic damage and give an example

A

Injury to DNA causes mutations. The cell structure and function is changed. RNA can become damaged which produces abnormal proteins. These changes will often be incompatible with life. An example is exposure to high doses of radiation can trigger cancerous cell changes due to DNA damage.

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53
Q

Describe intracellular accumulations and give a clinical concept that is tied to these

A

Cells can accumulate excessive amounts of substances through cellular constituents, acquired from the environment, abnormal metabolic function, exposure, and aging. Possibly reversible if brought under control. Jaundice is tied to this.

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54
Q

Give two other examples of abnormal intracellular accumulations

A

Anthracosis (coal miner’s lung) and fatty liver

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55
Q

What is hypoxic cell injury and give 7 most common causes

A

Hypoxia is oxygen deprivation most commonly caused by ischemia, anemia, anaerobic metabolism, low concentrations of oxygen in the environment, inadequate oxygen diffusion, suffocation, and airway obstruction.

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56
Q

What is anemia

A

A condition that happens when your body is producing or has less red blood cells than it should

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57
Q

Describe free radical injury and give a clinical concept

A

Reactive oxygen molecules are produced as by-products of energy metabolism as well as present in cigarette smoke, pesticides, and other toxins. They disrupt the internal organelles and damage nucleus. Antioxidants can counteract this free radical injury.

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58
Q

Give 3 examples of mechanical trauma

A

laceration, gsw, falls

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59
Q

Give four examples of temperature causes of injury

A

Frostbite, radiation, electrical shock, sunburn

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60
Q

Describe 3 types of chemical injury and give examples of each

A

Endogenous (diabetes), biological (electrolyte imbalance) and exogenous (drugs, pollution, and poison). They injure plasma membrane and gain access to cell’s interior

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61
Q

What is an immunological reaction injury and give two examples

A

Immune system overreacts and attacks itself such as with allergies and autoimmune diseases like rheumatoid arthritis

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62
Q

What are required for enzymatic reactions

A

amino acids, glucose, fats, and minerals

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63
Q

What is needed for ALL cellular functions

A

carbohydrates

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64
Q

What are the basic building blocks of ALL cells

A

proteins

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65
Q

What is the significance of endothelial cell injury

A

Endothelial cells line the artery walls. Endothelium are a blanket of cells covering the inside of all arteries. Endothelial injury causes an inflammation reaction an initiates the process of atherosclerosis

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66
Q

Give 3 functions of endothelial cells aside from providing structural integrity of artery walls

A

Secrete nitric oxide (vasodilator). Secrete endothelin (vasoconstrictor), and secrete thrombogenic substances (help form platelet plugs)

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67
Q

Give four causes of endothelial cell injury

A

Hypertension, free radicals, high glucose, and hyperlipidemia

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68
Q

Describe hypertension in the context of endothelial cell injury

A

High shearing force against the wall of the artery damaging the endothelium. Aneurysm becomes more likely due to the weakening of the walls.

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69
Q

Describe free radicals in the context of endothelial cell injury

A

substances in the environment that attack endothelium and disrupt its integrity such as free radicals from cigarettes

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70
Q

Describe high glucose in the context of endothelial cell injury

A

in uncontrolled diabetes, glucose attaches to endothelial cells and disrupts their integrity. Development of arteriosclerosis throughout the body.

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71
Q

Describe hyperlipidemia in the context of endothelial cell injury

A

Low density lipoproteins (LDLs) in the bloodstream combine with WBCs in the endothelial artery wall to initiate the beginnings of atherosclerosis

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72
Q

Describe irreversible cellular injury and give two examples

A

Injury is too severe or prolonged to allow adaptation or repair and reversal. Apoptosis is genetically programmed cell death over a specific time span and has no adverse effects on the body. One example is ovaries undergo apoptosis in females at age 55. WBCs undergo apoptosis after their participation in an inflammatory reaction.

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73
Q

Describe necrosis and give an example

A

Tissue and cell death stressors overwhelm the cells ability to survive. Intracellular contents are released into bloodstream such as in myocardial infarction and an elevated troponin level (this is ischemic necrosis)

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74
Q

What happens with a failure of apoptosis and give an example

A

Cells that fail to undergo apoptosis can give rise to certain cancers, tumors, and detrimental hyperplastic cell changes. An example is prostate cancer is theorized to arise from cells that lose their apoptotic function.

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75
Q

Describe excessive apoptosis and give an example

A

Some disorders are associated with increased cellular apoptosis, which results in excessive cell death rates. An example is some degenerative neurological diseases such as spinal muscular atrophy are thought to arise from nerve cells that undergo increases apoptotic rates and die prematurely

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76
Q

Describe gangrene and give 3 causes

A

Necrosis of tissues as cells die. The dead tissue is a medium for certain types of bacteria. Causes are prolonged ischemia, infarction, and typically patients with peripheral arterial disease (PAD)

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77
Q

Describe clinical interventions to reverse cell injury and give 3 clinical examples

A

Removing the injurious stimuli is the first priority as well as restoring circulation or nerve stimulation. Examples are acid suppression treatment can resolve the metaplasia of barrett’s esophagus. Neoplastic growths can be surgically removed. Intracellular accumulations can usually be eradicated by resolving the etiology of the metabolic derangement

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78
Q

Give four interventions to treat permanent cell injury

A

Transplantation, restoration with stem cells, reproductive cloning, and therapeutic cloning.

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79
Q

What are embryonic stem cells

A

Cells taken from an embryo in the blastocyst stage. Cells have potential to become any new organ and since blastocyst cells don’t have surface antigens there are no incompatibility problems.

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80
Q

Give 5 proposed future treatments where stem cells could be used

A

Sickle cell anemia, diabetes, parkinson disease, tissue repair of skin, and replacement organs

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81
Q

Describe therapeutic cloning

A

This is another potential use for stem cells. Pluripotent stem cells offer the possibility of a renewable source of replacement cells and tissues to treat a myriad of diseases, conditions, and disabilities including parkinson’s disease, amyotrophic lateral sclerosis, spinal cord injury, burns, heart disease, diabetes, and arthritis.

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82
Q

Compare eustress and distress and name 3 theorists in this realm

A

Eustress is a stressor that positively motivates a person. Distress is stress that negatively affects a person’s well-being. Theorists are Hans Selye, Walter cannon, and Bruce McEwen

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83
Q

Describe stressor according to the selye stress response theory

A

A challenging demand on the body that arouses a response from multiple organ systems. Stressors can be positive or negative experiences for the individual and have the potential to cause adverse health effects.

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84
Q

Give 8 conditioning factors for an individual’s reaction to a stressor according to selye stress response theory

A

Age, gender, genetics, pre-existing health conditions, life experiences, developmental level, educational level, social support

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85
Q

What is adaptive ability according to selye stress response theory

A

the way in which the individual manages stress and reduces the effect of the stressor on his or her life

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86
Q

Describe the alarm stage of the general adaptation syndrome and give 3 characteristics

A

Fight or flight, the alarm stage is state of arousal characterized by stimulation of CNS, SNS, and adrenal gland

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87
Q

Describe the resistance stage of stress

A

The body attempts to stave off the effects of stress through continual hormone and catecholamine secretion. It is a time-limited stage. When stress subsides, then the SNS and adrenal stimulation abate, and the PNS responses resume a state of relaxation

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88
Q

Describe the exhaustion stage of stress

A

If the stressor does not subside and the stress is prolonged, the high levels of hormone and catecholamine secretion cannot be sustained and the exhaustion ensues. Stress overwhelms the body’s ability to defend itself. Resources are depleted and signs of systemic dysfunction occur. During this stage an individual can feel run-down, unable to cope, depressed, anxious, and can feel physically ill

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89
Q

Describe allostasis according to McEwen’s long term stress theory

A

a dynamic state of balance that changes according to exposure to stressors

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90
Q

Describe allostatic load according to McEwen’s long term stress theory

A

The wear and tear on body systems caused by stress reactions. Allostatic load is not only determined by the stressor, but also by how well the individual adapts to the stressor. Elderly individuals have less resiliency to stress because the body requires more time to recover from stressful event

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91
Q

Give four reasons that allostatic load can accumulate

A

repeated stressful experiences, inability of the individual to adapt to stress, prolonged reaction to a stressor, and inadequate response to a stressor.

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92
Q

According to McEwen what happens when stress exceeds the body’s ability to adapt

A

allostatic overload ensues and the initiation of pathophysiological disorders happens

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93
Q

Give 5 treatments for stress originating issues

A

reduce caffeine intake, engage in yoga, increase exercise, ensure sufficient sleep, and achieve proper nutrition

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94
Q

Give four other treatments of stress originating pathologies

A

Stress management programs, psychotherapy, alternative medicine, and pharmacology

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95
Q

Give 7 interventions to counteract immobility

A

Active range of motion, passive range of motion, isometric exercise, aerobic exercise, positional changes such as side-lying and to a chair (at least every 2 hours), special mattresses, and antithromboembolic stockings

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96
Q

Describe the four stages of pressure injuries

A
  1. Erythema and irritation of skin 2. Loss of skin layer 3. loss of skin and dermal layer with ulceration 4. loss of skin, dermis, muscle, down to the bone
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97
Q

What is erythema

A

superficial reddening of the skin usually in patches as a result of injury

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98
Q

Name the 6 areas that are most susceptible to pressure injuries

A

Occiput, shoulders, elbows, sacral region, calf region, and heels

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99
Q

Describe a cancerous neoplasm

A

Grows in an uncoordinated manner and looks different from normal cells. Doesn’t function like the tissue or origin and competes with normal cells for space, blood supply, oxygen and nutrition. Proliferates independently and FAST. Large numbers of cancers have a genetic link. Can arise from proto-oncogenes and faulty cellular apoptosis

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100
Q

Give the benign tumor suffix with two examples and name 3 exceptions that are all highly malignant

A

suffix is “Oma” such as lipoma and adenoma. Exceptions are lymphomas, hepatomas, and melanomas

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101
Q

Describe four types of malignant tumors

A

Adenocarcinoma (glandular tissue), carcinoma (epithelial tissue MOST human cancers are this type), sarcoma (mesenchymal tissue like nerve, bone, and muscle), and leukemia (WBC)

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102
Q

Describe how cancer cells don’t obey the rules

A

Ignore growth controlling signals and proliferate excessively becoming immortal. Lose their features and contribute poorly or not at all to tissue. Invade local tissue and overrun neighbors. Travel away from origin to invade distant sites. Genetically unstable, and are able to establish new colonies.

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103
Q

Describe benign neoplasia

A

Resemble healthy cells of tissue of origin (well-differentiated). Don’t metastasize. Stay local and are often encapsulated.

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104
Q

Describe malignant neoplasia

A

Appear very different from tissue of origin. Secrete inappropriate enzymes, hormones, clotting substances, and tumor angiogenesis factor. Tend to break away and lack normal cell function.

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105
Q

Describe the epidemiology of cancer

A

Leading COD behind heart disease. Men more than women. In men prostate, in women breast. Most cancer deaths occur in people older than 65. Many cancers are preventable with lifestyle and avoiding carcinogens

106
Q

Name 7 risk factors for cancer

A

Age, tobacco use, nutrition (too much fat, lack of fiber, too much alcohol, lack of antioxidants), obesity, occupation, sun exposure, sexual exposure

107
Q

Describe the immune system as it relates to cancer

A

constantly surveying for foreign substances (non-self antigens). Recognizes and attacks to destroy mutated cells. Immunocompetence decreases with age and older adults are more susceptible to tumor development

108
Q

Describe genetics as it relates to cancer

A

All cancers originate from changes in DNA. Tumor suppressor genes function to restrain cell growth, almost half of all cancers come from defective TP53 gene. Oncogenes regulate cell growth and proliferation, when mutated they stimulate constant cell growth

109
Q

What are the role of viruses in cancer

A

virus genes are inserted into the host cell which then manufactures the virus. Activation of growth promoting pathways and inhibition of tumor suppressors can arise due to the virus

110
Q

Give 3 examples of viruses playing an etiological role in cancer

A

HPV with cervical cancer, Eptstein-Barr virus with Burkitt’s lymphoma, and Hep B and C with Hepatocellular carcinoma (HCC)

111
Q

Describe 8 areas where carcinogenic embryonic antigen (CEA) a tumor marker can be found in the context of tumor markers

A

Colorectal, pancreatic, lung, breast, stomach, thyroid, liver, and ovarian

112
Q

Where is alpha-fetoprotein found in the context of tumor markers

A

liver and testicular

113
Q

Where is prostate surface antigen (PSA) found

A

prostate

114
Q

Describe two screening tests for prostate cancer

A

PSA and DRE

115
Q

Describe screening for cervical cancer

A

Papanicolou (pap) smear

116
Q

Describe screening for breast cancer

A

mammogram

117
Q

Describe screening for colon cancer

A

colonoscopy and FOBT

118
Q

Describe screening guidelines for ovarian cancer

A

CA-125 test with transvaginal ultrasound in women at risk

119
Q

Describe screening guidlines for breast cancer

A

After age 40 begin mammography (earlier if risk factors) MRI women with BRCA1 and/or BRCA2 gene

120
Q

Describe screening guidelines for cervical cancer

A

Women 21 and older Pap/HPV test

121
Q

Describe colorectal screening guidelines

A

Women and men 45+ colonoscopy, sigmoidoscopy and stool DNA test.

122
Q

Describe prostate screening guidelines

A

Men 50+ PSA and DRE

123
Q

Describe the spread of cancer in metastasis

A

Survival of tumor cell must find somewhere to stick before its destroyed in circulation. Fewer than 1 in 10,000 cancer cells that enter circulation will survive to metastasize. Tumor cells seem to “home” in on specific targets and are spread through bloodstream or lymphatics

124
Q

Describe grading and staging of cancers

A

Grading is a histological characterization of tumor cells. Usually 3 or 4 classes. Staging is the location and pattern of spread. TNM stands for Tumor size, lymph node affected, and degree of metastasis

125
Q

Describe the effects of cancer on the body

A

Asymptomatic, pain, cachexia, immune suppression, infection, bone marrow suppression (leukopenia, thrombocytopenia, anemia). Opportunistic infections and once chemotherapy has begun hair loss and sloughing mucosal membrane

126
Q

What is cachexia

A

Muscle mass loss sometimes associated with fat loss as well likely due to cancer cells being incredibly energetically hungry

127
Q

What do chemotherapy drugs most negatively affect

A

Cells that rapidly divide such as bone marrow, intestinal epithelia and hair follicles

128
Q

Describe the caution acronym for early signals of cancer

A

Change in bowel or bladder habits. A sore throat that doesn’t heal. Unusual bleeding or discharge. Thickening or a lump in breasts, testicles, or elsewhere. Indigestion or difficulty in swallowing. Obvious change in the size color, shape, or thickness of a wart, mole, or mouth sore. Nagging cough or hoarseness

129
Q

Describe the children acronym for cancer warning signs in children

A

Continued, unexplained weightloss. Headaches with vomiting in the morning. Increased swelling or persistent pain in bones or joints. Lump or mass in abdomen, neck or elsewhere. Development of whitish appearance in pupil of the eye. Recurrent fevers not caused by infections. Excessive bleeding or bruising. Noticeable paleness or prolonged tiredness

130
Q

What does hem/hemat prefix mean

A

blood

131
Q

What does blast suffix mean

A

make

132
Q

What does clast suffix mean

A

destroy

133
Q

What does emia suffix mean

A

blood

134
Q

What does penia suffix mean

A

lack

135
Q

What does rhage or rhagia suffix mean

A

Break out/discharge

136
Q

what does osis suffix mean

A

abnormal condition

137
Q

What is a hematocrit

A

test that measures percentage of red blood cells

138
Q

What are petechiae

A

Red brown or purple little spots on the skin caused by bleeding

139
Q

What is ecchymoses

A

Bleeding under the skin usually more like a bruise than petechiae

140
Q

What is hepatomegaly

A

Enlargement of the liver

141
Q

Describe cell lifespans for wbc/leukocytes, rbc, and platelets

A

in WBC it varies by cell type but neutrophils (60-80% of wbc count) have half life of 4-10 hrs in tissue and 6 hrs in blood once released from bone marrow. RBC live 80-120 days once released from bone marrow. Platelets live 4-10 days once released from bone marrow

142
Q

Describe myeloid cells and give four examples

A

Originate from myeloid stem cells. Neutrophils, monocytes, RBCs and Megakaryocytes (that give way to platelets) are examples

143
Q

Describe lymphoid cells and give 3 examples

A

Originate from lymphoid stem cells. T-cells, B-cells, and natural killer cells are examples

144
Q

Describe myeloid neoplasm

A

Originate in bone marrows stem cells and are released into blood stream. Stimulate overproduction of one or more cell types. Produced cells may be normal or abnormal in appearance or function

145
Q

Give etiology of chronic myeloid leukemia

A

Median age is 50 years old. More common in males than females. Ionizing radiation is a risk factor

146
Q

What is the philadelphia chromosome

A

Overproduction of mature granulocytes carrying the philadelphia chromosome leads to reduced apoptotic cell death and is a hallmark of chronic myeloid leukemias (CML)

147
Q

Give signs and symptoms of CML

A

Increased granulocyte count, fatigue, weight loss, bleeding, splenomegaly with abdominal pain and/or fullness. Extremely high WBC counts (150,000 cell/u)

148
Q

Give four general facts about CML

A

Onset usually 40-50 years, can convert to AML, stem cell transplant is a treatment and it has a 90% survival rate if caught

149
Q

What is etiology of AML

A

Previous chemotherapy or radiation therapy

150
Q

What is the pathophysiology of AML

A

Group of malignancies of varying myeloid stem cells. Presentation of affected cells vary in differentiation and maturation with increased blasts. Prolonged apoptosis

151
Q

Describe signs and symptoms of AML

A

They have an abrupt onset and consist of bone pain, anemia, thrombocytopenia, and frequent infections especially of skin, gi, gu and respiratory tract

152
Q

Give four general facts about AML

A

80% of adult leukemias are AML. Onset usually in 6th decade of life. Survival is 40-50% for children and 20-30% for adults. Prescription is chemotherapy and new monoclonal antibody modalities

153
Q

Describe lymphoid neoplasms

A

Malignant transformation of the lymphoid stem cells: t-cells b-cells and NK. Lymph tissue solid tumors are lymphoma and in the blood it’s leukemia

154
Q

Describe the etiology of CLL

A

Exposure to any agent that can disrupt DNA. Twice as likely in males. More common with family history of any B cell malignancy. Exposure to herbicides and insecticides or agent orange used in Vietnam.

155
Q

Describe pathophysiology of CLL

A

Usually due to a malignant b-cell precursor that invades lymphoid tissue and brone marrow leading to prolonged apoptosis and b-cells that do not mature

156
Q

Give signs and symptoms of CLL

A

In the bone marrow we see anemia (and therefore fatigue), thrombocytopenia (and therefore bleeding tendencies). In lymphoid tissues we see enlarged painless lymph nodes and/or spleen. Fever, elevated WBC count, ANOREXIA, weight loss, and frequent infections

157
Q

Describe treatment of CLL

A

Usually diagnosed by accident on routine lab draws. Chemotherapy is used and it has a 70-90% survival depending on particular cells involved

158
Q

Describe etiology of ALL

A

Common in children, survival rate of 80% in kids and 20-40% in adults. Risk factors are prenatal radiation exposure in children

159
Q

Describe the pathophysiology of ALL

A

Malignant transformation of t or b-cells in the bone marrow causing cells to not mature appropriately. Presents as lymphoblastic leukemia. Lymphoblasts crowd the bone marrow and suppress the formation of blood cells

160
Q

Describe signs and symptoms of ALL

A

Bone pain. Bruising, epistaxis or other bleeding issues. Fever/chills. Night sweats. Enlarged lymph nodes. Anorexia. Fatigue, pallor and dyspnea due to anemia. Abdominal pain. Activity avoidance. Frequent infection due to abnormal WBCs

161
Q

What is treatment for ALL

A

chemotherapy, bone marrow transplant, and monoclonal antibodies. Early treatment leads to 65-70% 5 year event free survival rate

162
Q

Describe plasma cell myeloma (multiple myeloma)

A

Malignancy of b-cells leading to increased antibody fragments called Bence Jones proteins. Twice as common in males and african americans. Risk factors include agent orange and radiation exposure

163
Q

Describe signs and symptoms of plasma cell myeloma (multiple myeloma)

A

Associated with deposition of the antibody fragments in bone and kidneys: High Ca in blood and urine, renal failure, honeycomb bone, bone pain, fractures, anemia, bleeding tendencies, frequent infections

164
Q

Give Plasma cell myeloma onset and treatment

A

Onset starts at 50 years and rate increases with age. Treatment is chemotherapy, bone marrow transplant, and stem cell transplant

165
Q

Describe etiology and pathophysiology of Hodgkin’s lymphoma

A

Malignancies of lymph nodes that produce reed sternberg cells from b-cells in association with Epstein-Barr virus. Exist in four forms. Predictable metastatic pattern. Overproduction of abnormal antibodies and underproduction of other blood cells. Most common in males with an onset of between 20-40 years

166
Q

Give some risk factors for Hodgkin’s lymphoma

A

60 years or older. Immune disorders. H. pyolori. Hep C. Immunosuppression. Toxic chemicals like pre 1980 hair dye, pesticides, herbicides, and benzene or other solvents.

167
Q

Give hodgkin diseases signs and symptoms

A

Painless lymphadenopathy of liver, spleen, tonsils, and thymus. Night sweats. Pruritus due to cytokine deposits in the skin. Weight loss and anorexia. Chest pain if the thymus is involved

168
Q

Describe Hodgkin diseases treatment and survival

A

Chemotherapy or radiation. 85% survival at 5 years for those under 65 and 50% survival at 5 years for those over 65

169
Q

Describe non-hodgkin diseases

A

Etiology is similar to Hodgkin’s lymphoma. Malignancies arising in lymph nodes that originate in any lymph tissue and do not have the reed-sternberg cells. Spread early and in unpredictable paths. Thought to be associated with some viruses.

170
Q

Describe non-hodgkin disease signs and symptoms

A

Lymphadenopathy (painless), fever, night sweats, weight loss, pruritus, infections, joint effusions, and local signs and symptoms.

171
Q

What is pruritus

A

Itchiness

172
Q

What are joint effusions

A

fluid buildup on joints

173
Q

Describe survival of non-hodgkin diseases and treatment

A

Survival ranges from 26-70% depending on number of risk factors present and the stage of disease at diagnosis. Stage III and IV are most common presentation with poorest prognosis. Treatment is chemotherapy, radiation, bone marrow transplant, and monoclonal antibodies

174
Q

What is mononucleosis and how is it spread

A

Epstein-Barr virus infection, most individuals have been exposed and have developed some immunity. Spread through contact with saliva

175
Q

Give signs and symptoms of mononucleosis

A

4-6 week incubation period, pharyngitis, lymphadenopathy, fever, spleenomegaly, hepatomegaly

176
Q

What is lymphadenopathy

A

Swelling of the lymph nodes

177
Q

How long does mono last

A

Dormant or latent for life. Signs and symptoms last from 1-4 months

178
Q

What is the etiology for neutropenia

A

Infections
Certain Drugs
Vitamin deficiencies
Bone marrow diseases
Radiation therapy
Hemodialysis
Hyperspleenism
Some autoimmune disorders

179
Q

What is the pathophysiology of Neutropenia

A

Low (<500cells/µL) neutrophils
Results in increased infections
Infections can be life threatening
Requires protection of individuals – neutropenic precautions

180
Q

Describe polycythemias

A

Excessive RBC, WBC and platelet production
Increased blood viscosity
Hypertension
Thrombosis
Mucosal hemorrhage

181
Q

Describe the 3 different types of polycythemias

A

Polycythemia Vera – malignant
Secondary Polycythemia – chronic hypoxemia
Relative Polycythemia - dehydration

182
Q

Give the signs and symptoms of polycythemias

A

HA (headache) Visual disturbances
Weight loss
Paresthesia
Dyspnea
Joint discomforts
Epigastric pain
Splenomegaly

Back pain
Weakness
Fatigue on exertion
Pruritus
Dizziness
Sweating

183
Q

What is the treatment for polycythemias

A

Contingent on cause
Remove the cause
Phlebotomy
Chemotherapy
Myelosuppressive therapy

184
Q

Name 3 bleeding disorders

A

Thrombocytopenia
Hemophilia
Von Willebrand Disease

185
Q

What is the etiology of thrombocytopenia

A

A long list of drugs
Cancers of the bone marrow
Recent viral infection
Liver or spleen disorders
Deficient Platelets due to:
Decreased production
Decreased survival time
Splenic Sequestration
Platelet Dilution

186
Q

Give second set of etiology for thrombocytopenia

A

Folate/B12 ↓
Radiation
Chemotherapy
Artificial heart valves
Hypothermia
Massive blood transfusions
Infections
DIC

187
Q

Give signs and symptoms and treatment for thrombocytopenia

A

S&S
Petechiae
Purpura
Intracranial hemorrhage
Prolonged bleeding time
Epistaxis
Rx – Remove the cause and transfuse. Administer pro clotting agents – vitamin K for example

188
Q

What is thrombocytosis and name signs and symptoms

A

Excess release of preformed platelets (transient)
S&S
Paradoxical hemorrhage
Peripheral ischemia
Pulmonary emboli

189
Q

What do coagulation disorders result from

A

Inappropriate activation of the clotting cascade
Inappropriate formation or stabilization of the fibrin clot

190
Q

Describe hemophilia A and B

A

Inherited X-linked recessive bleeding disorder (A&B)
Due to Factor VIII deficiency (A)
Due to Factor IX deficiency (B)
Inability to form a fibrin clot
Hemophilia A is most common

191
Q

What are the signs and symptoms of hemophilia A and B

A

S&S related to excessive bleeding
Prolonged bleeding from trauma
Spontaneous bleeding
Bruising
Hematomas
Hemarthrosis
Hematuria
GI bleeding
Intracranial bleeding

192
Q

Describe diagnosis and treatment of hemophilia A and B

A

Dx – based on history, bleeding times and factor assay
Rx –
Lifestyle changes
Replacement therapy
Factor replacement

193
Q

Describe von willebrand disease and the signs and symptoms

A

Autosomal dominant lack of a carrier protein for Factor VIII
S&S
Epitaxis
Rarely hemarthrosis
Menorrhagia
GI bleeding

194
Q

What is epistaxis

A

A nose bleed

195
Q

What is the diagnosis method and treatment for Von Willebrand disease

A

Medical history, bleeding times and factor assay
Rx- Desmopressin, hormonal suppression, replacement therapy

196
Q

Describe vitamin K deficiency

A

Vitamin K is necessary for several clotting factors
Infants are deficient due to a sterile gut (bacteria produce vitamin k), liver immaturity (processes vitamin k) and low dietary intake of vitamin K

197
Q

Give signs and symptoms and treatment for vitamin K deficiency

A

Melena
Hematuria
Intracranial hemorrhage
GI bleeding
Menorrhagia
Rx – Vitamin K replacement

198
Q

What is melena

A

Black stool

199
Q

What is hematuria

A

Blood in the urine

200
Q

What is menorrhagia

A

Abnormally heavy bleeding at menstruation

201
Q

Describe Disseminated Intravascular Coagulation (DIC)

A

Widespread intravascular thrombosis →widespread hemorrhage due to consumption of coagulation factors
Occurs 2ndary to malignancies, sepsis, snake bite, abruptio placenta, trauma, crush injuries, burns, shock, severe liver disease, incompatible blood transfusion, rickettsial infections

202
Q

Give signs and symptoms of DIC

A

Petechiae
Ecchymoses
Orifice bleeding
Needle stick site bleeding
Dyspnea
Hemoptysis
Renal

203
Q

What is dyspnea

A

Shallowness of breath

204
Q

What is hemoptysis

A

Coughing up of blood

205
Q

Describe the diagnosis and treatment of DIC

A

Clinical presentation and a series of coagulation studies
Rx-
Remove/correct cause
Replacement of clotting factors
Drug therapies

206
Q

Describe anemia and give compensatory mechanisms

A

Disease indicator
Low hemoglobin
Low RBC
Diminished O2 carrying capacity
Tissue hypoxia thus fatigue, weakness, angina, pallor
Headache (HA)
Hypotension, lightheadedness, tinnitus
Compensatory mechanisms
↑HR, Palpitations,↑RR, ventricular hypertrophy
Bone pain

207
Q

Describe the two classification structures for anemias

A

-cytic – morphology - size
normo
macro
micro
-chromic – color
normo
hypo
hyper

208
Q

Name the 3 types of anemia

A

Hemolytic
Blood loss
Hemoglobinopathies

209
Q

Name the 3 types of both acute and chronic blood loss anemia

A

Acute:
Normocytic
Normochromic
Dilutional
Chronic:
Iron-deficiency from depletion of iron
Microcytic
Hypochromic

210
Q

Give the etiology of hemolytic anemia

A

Hemoglobinopathies
Blood transfusion reaction
Certain drugs:
Cephalosporins
Quinidine
Penicillin
Levodopa
Methyldopa
NSAIDs

211
Q

What is a hemolytic anemia and what can it result in

A

Premature destruction of RBC
Primarily in the spleen
Also in the vascular space
Results in:
Retention of the by products of RBC lysis – jaundice & and bilirubin gallstones
Increase erythropoiesis
Results in splenomegaly

212
Q

Name the two types of inherited hemolytic anemia

A

Sickle Cell Anemia
Thalessemia

213
Q

What is sickle cell anemia, who is it most common in, and what triggers it

A

Autosomal Recessive Disorder
Abnormal Hg – HgS which is protective of malaria
Common in African, Middle Eastern & Mediterranean ancestry
RBCs sickle under stress/triggers:
Low oxygen
Low vascular volume
Cold stress
Infections
Acidosis
Extreme physical exertion

214
Q

What causes the severe pain in sickle cell anemia and name the organ dysfunction it causes

A

Vaso-occlusion from cells that clump – severe pain.

Organ dysfunction
Extremities - necrosis
Joints – infarcts
Long bones
Kidneys
Lungs – acute chest syndrome
Spleen - ↑infections

215
Q

Name 11 Signs and Symptoms of sickle cell anemia

A

Hemolysis of sickled cells
Splenomegaly
Asplenia
Hyperbilirubinemia
Sludging of RBCs
Necrosis from occlusions/infarcts
Infection leading cause of morbidity
Acute chest syndrome
Priapism in male
Retinal ischemia
Infections from necrosis and mortality especially before three years of age

216
Q

Describe the treatments for sickle cell disease

A

avoid triggers
Hydroxyurea – stimulate HgF production
Oxygen
Hydration
Pain meds
Prophylactic antibiotics

217
Q

Describe Thalassemia, who its most common in, and what happens

A

Autosomal Recessive
Individuals of *Mediterranean, Asian, or African American descent
Deficient Hg production & hypochromic microcytic anemia
Heinz bodies in the bone marrow impair RBC production
Accompanying hypercoagulability leads to strokes and pulmonary emboli

218
Q

Give 7 signs and symptoms of thalassemia

A

Growth retardation without blood transfusions begun early
↑hematopoiesis → bone marrow expansion → bony abnormalities (chipmunk faces, fractures)
Splenomegaly
Hepatomegaly
Iron toxicities
Bone pain
Hyperbilirubinemia

219
Q

What is the leading cause of morbidity in thalassemia

A

Infection

220
Q

What is the treatment for thalassemia

A

Mostly preventative
Prevent infection
Blood transfusions to replace hemolyzed cells

221
Q

Describe the etiology for acquired hemolytic anemia

A

Lysis of RBCs due to exogenous factors
Blood transfusions
Drugs
Chemicals
Venoms
Certain Infections
Prosthetic heart valves
Burn injuries
Vaculitis

222
Q

Name 6 anemias of deficient RBC production

A

Iron deficiency anemia
Megaloblastic Anemia
Vitamin B12 deficiency
Folic Acid Deficiency
Aplastic Anemia
Chronic Disease Anemias

223
Q

Describe iron deficiency anemia

A

Iron is recycled when RBCs are broken down
Chronic blood loss most common cause
Occurs also during growth spurts and pregnancy
Infants and children with high cow’s milk intake
Vegetarians
Elderly adults
Patients with GI disorders

224
Q

Describe signs and symptoms of iron deficiency anemia

A

Fatigue
Weakness
Palpitations
Dyspnea
Angina
Brittle hair and nails
Increased HR
Waxy pallor
Low H & H (Hemoglobin and hematocrit)
Low iron stores
Low RBC count
Microcytic hypochromic RBCs
Pica

225
Q

What is angina

A

Pain in the chest due to reduced bloodflow to the heart

226
Q

What is pica

A

Compulsive swallowing of non-food items (ice is iron deficiency anemia)

227
Q

Give etiology of megaloblastic anemia

A

Pregnancy
Breast Feeding
Alcohol Abuse
Certain Drugs
Advanced Age
GI disorders
Vitamin B12 deficiency

228
Q

Give megaloblastic anemia pathophysiology and signs and symptoms

A

Folate deficiency results in a defect in DNA synthesis impacting rapidly dividing cells in the bone marrow
Open neural tube
S&S:
As to be expected for anemia

229
Q

Give etiology of pernicious anemia (a type of megaloblastic anemia)

A

Alcoholics
Pregnant women
Anorexia
Lack of intrinsic factor
Achlorhydria
Vegetarians

230
Q

Give pathogenesis of pernicious anemia

A

Large RBCs owing to Folic Acid deficiency or Vitamin B12 deficiency
Folic Acid and Vitamin B12 are necessary for DNA synthesis
Results in weak RBCs
Vitamin B12 deficiency anemia is accompanied by neuronal changes that lead to dementia and other neurological impairment

231
Q

What are the signs and symptoms of pernicious anemia

A

Similar to Blood loss anemia
Additionally neurological manifestations:
Unsteady gait
Numbness and tingling
Balance problems
Memory impairment
Depression

232
Q

Give etiology of aplastic anemia

A

Bone marrow depression leads to low RBCs, WBCs & platelets
Causes
Radiation
Drugs
Chemicals
Toxins
Infection
Autoimmune reactions

233
Q

Describe clinical manifestations of aplastic anemia

A

Sudden or insidious onset
Weakness
Fatigue
Pallor
Petechiae
Eccochymoses
Bleeding
Frequent infections

234
Q

What is the treatment for aplastic anemia

A

Rx – Bone marrow transplant
Graft vs Host reactions
RBC transfusions
Antibiotics
Immunosuppresion

235
Q

Describe the causes of chronic disease anemia

A

Renal failure
Cancer
Chronic infection
AIDS
Rheumatoid arthritis
Systemic Lupus erythematosus
Hodgkins Dz

236
Q

What does autosomal mean in the context of recessive and dominant genes

A

Autosomal simply means its on one of the numbered (non-sex) genes

237
Q

What is macroorchidism

A

An increase in testicular size of twice what is normal for the age

238
Q

Describe the human genome project

A

Research study from 1990-2003
Mapped the Human genome
Link thousands disease to specific genes
Opened the door for pharmacogenomics

239
Q

compare dna to genes

A

DNA – composed of genes
Genes –carry directions for proteins and enzymes

240
Q

Describe genes

A

The same in every cell (23,000).
Not all are active or expressed in all cells.
Mutations occur during duplication.
The effect of the mutation depends on when the mutation occurs.
Multiple genes reside together and form chromosomes.

241
Q

Describe chromosomes

A

Store the genetic information created by DNA and RNA.
Arranged in pairs (one from Mom and one from Dad) in every cell.
Have specific structure
23 pairs
22 pairs are autosomes
1 pair is the sex chromosome
Karyotype is a picture of the 23 pairs of chromosomes

242
Q

Describe gene regulation

A

Every cell contains all of a person’s DNA & genetic information.
Only active genes are expressed in cells.
Mutations occur when the gene code is damaged or changed.
Mutations of somatic cells cause disease.
Mutations of germ cells are passed to offspring.

243
Q

Describe recombinant DNA technology

A

DNA is split
DNA may be altered
DNA is inserted into a one cell organism
The DNA replicates in the organism
Extraction

244
Q

Compare congenital to genetic

A

Congential – present at birth.
Genetic – due to a genetic mutation.

245
Q

Compare penetrance to expressivity

A

Penetrance refers to the likelihood your phenotype will reflect your genotype.
i.e., If you inherit the gene for colon cancer how likely are you to develop colon cancer.
Expressivity refers to how pronounced the phenotype will be.
i.e., If you inherit hypercholesterolemia just how high will your cholesterol be?

246
Q

Describe x-linked disorders

A

Usually affect males – No extra X to balance
Fathers pass the defective gene to all of their daughters and none of their sons.
Mothers have a 1 in 2 chance of producing affect male offspring and a 1 in 2 chance of producing a carrier female child
Females are rarely affected – have to have 2 affected Xs

247
Q

Describe marfan syndrome (autosomal dominant disorder)

A

Marfan Syndrome-Dz of connective, skeleton, eye, and cardiovascular systems
Skeleton – exaggerated length and thin extremities; Chest –pectus excavatum
Eyes- bilateral dislocation of the lens; myopia; and tendency to retinal detachment
*Cardiac – valvular abnormalities; rupture of the aorta
Nervous system – dura mater of the spinal cord

248
Q

What are some physical manifestations of marfans

A

Long arms
Long fingers
Protruding sternum
Hypeflexible joints
Long narrow face
Small jaw
Overcrowded teeth

249
Q

Describe huntington disease (autosomal dominant disorder)

A

Huntington Disease
Delayed neurological decline begins to appear around age 40.
Mental deterioration and involuntary arm and leg movement.
Onset – 35ish years & Fatal at 55ish years

250
Q

Name four autosomal recessive disorders

A

Phenylketonuria
Tay-Sachs
Albinism
Cystic Fibrosis

251
Q

Describe PKU

A

Phenylketonuria (PKU)
Lack an enzyme that degrades phenylalanine to a non toxic form.
Causes slow onset of mental retardation, microcephaly, delayed speech.
All babies have a blood test before hospital discharge to check for the enzyme.
Those lacking the enzyme need dietary (avoid protein, artificial sweeteners, diary) modifications.

252
Q

Describe Tay-Sachs disease

A

Enzyme to metabolize fat is missing
Accumulation of lipids in neurological tissue
Displacement of neurological tissue
Appear normal for the first few months of life
Relentless neurological deficits appear – cherry red spot on the retina*, blind, deaf, paralysis, dementia, seizures, exaggerated startle response, dysphagia
Death near age 4 years
Highest risk in Jewish populations

253
Q

Describe fragile x syndrome

A

Fragile X Syndrome – most common cause of inherited cognitive impairment
Mental retardation – slight or gross autistic-like behaviors (shyness, avoiding eye contact, attention deficits)
Long face with large mandible
Macroorchidism
Everted ears
Mitral valve prolapse
Hyper extensible joints
1 in 1,550 in males and 1 in 8,000 females births

254
Q

Describe chromosomal disorders

A

Result during meiosis
Chromosome does not split correctly
Most frequently – abnormal numbers of chromosomes

255
Q

Describe trisomy 21 (down’s syndrome)

A

THE most common chromosomal disorder
Risk increases as maternal age increases
Features
Rather square head
Upward slant of the eyes
Malformed, low set ears
Fat pad at back of neck
Open mouth
Protruding tongue
Increased risk of leukemia and Alzheimer Disease development

256
Q

Describe turner syndrome (monosomyx)

A

Short statue
Webbed neck – elastic neck
Puffy hands and feet at birth
Coarctation of the aorta
No puberty, no ovaries, sterile
Abnormal kidney, heart
Hypothyroidism
Scoliosis

257
Q

Describe klinefelters syndrome (polysomy x)

A

Extra X chromosome
Males develop some female secondary sex characteristics
Breasts
Lack of facial & chest hair
Statue (short torso, long extremities)- tall overall
High pitched voice
Lack of testicular development

258
Q

What is multifactorial inheritance

A

Inherit a predisposition to develop various disorders and the a triggers in the environment contribute to disease development.
No direct gene linkage

259
Q

Give examples of multifactorial inheritance

A

Coronary artery dz
Diabetes mellitus
Hypertension
Cancer
Manic depression
Schizophrenia
Cleft lip/cleft palate

260
Q

What is an environmentally influenced disorder

A

Exposure during the first 60 days post conception has the most pronounced effect.

261
Q

Give 5 types of prenatal diagnosis techniques

A

Ultrasonography – visual exam of structure and function
Alpha fetoprotein – maternal blood test -open neural tube or open ventral wall
Amniocentesis – amniotic fluid sample -chromosomal defects
Chorionic Villus Sampling – placental biopsy - genetic defects
Percutaneous umbilical blood sampling- collection of cord blood to determine genetic defects

262
Q
A