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NURS 311: Pathophysiology > Exam 1: Chapters 1-6 > Flashcards

Exam 1: Chapters 1-6 Flashcards

1
Q

The study of functional changes in the body caused by injury, disorder, or disease is called what?

A

Pathophysiology

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2
Q

A disease is a _______ _________ of cells, tissues, organs, or organ systems

A

Functional impairment

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3
Q

Pathogenesis encompasses the point at which disease process begins to when?

A

The point when the disease presents itself

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4
Q

a disease-causing microorganism is what?

A

A pathogen

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5
Q

When a disease has an unknown cause, it is called what?

A

Idiopathic

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6
Q

When a disease is caused inadvertently by medical treatment, this is known as what?

A

Iatrogenic

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7
Q

These types of diseases are caused by an infection received in a healthcare environment

A

Nosocomial

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8
Q

What is the difference between incidence and prevalence?

A
  • Incidence is the rate** **of new cases of a disease occurring in a specific population over a particular period of time.
  • Prevalence the number of cases of a disease in a specific population at a particular timepoint or over a specified period of time.
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9
Q

A dramatic increase in disease incidence in a POPULATION is called what?

A

Epidemic

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10
Q

When epidemic spreads across continents, it is known as what?

A

Pandemic

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11
Q

A disease outbreak that is consistently present, but limited to within a certain area is known as what?

A

Endemic

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12
Q

How are Nosocomial disease prevented?

A

appropriate hand hygiene and infection control measures

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13
Q

The presenting signs and symptoms of the disease are known as what?

A

Clinical manifestations

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14
Q

Subjective data reported by the ill individual are known as what?

A

Symptoms

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15
Q

“At your health screening, you describe the following: achiness, lethargy, and vague abdominal discomfort. These are categorized as what?”

A

systemic manifestations

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16
Q

Identify the difference between a signs and symptoms.

A
  • Signs are the observable or measurable expression: manifestations that can be seen or measured by the healthcare professional: 99 degree fever, blisters, rash, etc.
  • Symptoms are self-reported by the patient, subjective manifestations: fatigue, tingling, discomfort, etc.
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17
Q

___ Encompasses when the disease process first starts to the point when the disease presents itself

A

Pathogenesis

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18
Q

What is the difference between morbidity and mortality?

A
  • morbidity is the negative outcome with disease complications that can impact the quality of life
  • motility = death
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19
Q

The decrease in size of a cell is considered what?

A

Atrophy

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20
Q

When a cell increases in size, this is known as what?

A

Hypertrophy

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21
Q

When the number of cells increase, this can be labeled as what?

A

Hyperplasia

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22
Q

When a cell changes from one type to another, this is considered what?

A

Metaplasia

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23
Q

When a cell changes in size, shape, arranged, uniformity, and structure, it is labeled as what?

A

Dysplasia

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24
Q

What Am I:

Reduction is size of the cells in the cerebrum of the brain, resulting in reduction in brain tissue itself.

A

Cerebral Atrophy

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25
Q

In brief terms, why does cerebral atrophy occur?

(Pathophysiology)

A

Loss of neuron function / neural death leads to atrophy

  • As atrophy occurs, distance between neurons increases, making communication between other neurons more difficult
  • Decreased stimulation leads to further atrophy
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26
Q

What are some causes of cerebral atrophy?

A
  • Decreased stimulation resulting from reduction in physical and intellectual activities
  • Low levels of Vitamin B
  • Mechanical injury – TBI
  • Loss of neurons and neurotransmitter production in one region, resulting in atrophy elsewhere (communication issues)
  • Reduced oxygen and nutrient delivery
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27
Q

What are some clinical manifestations of cerebral atrophy?

A
  • Can be localized to certain region in the brain
  • Can be global and affect entire brain
  • Clinical manifestations depend on what part of the brain is impacted
  • Ex: Cognitive impairment from frontal and temporal lobes. Atrophy in basal ganglia results in movement impairment
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28
Q

Atrophy in what region is associated with Alzheimers?

A

Hippocampus and cerebral cortex (frontal and temporal lobes)

  • Condition affecting memory and comprehension → REMEMBER: cognitive impairment associated w/ frontal and temporal atrophy
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29
Q

Movement disorders are associated with atrophy where? Why is this important?

A
  • Basal ganglia
  • Region responsible for production of dopamine (required for motor function)
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30
Q

The clinical manifestations associated with cerebral atrophy depends on what?

A
  • The degree of atrophy
  • The location of atrophy
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31
Q

Which condition am I?

  • Occurs because of neuronal insult during a critical time in brain development
  • Manifestations vary but many involve motor skills, coordination, balance, and seizure activity
A

Cerebral palsy

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32
Q

Cellular atrophy results in:

a. Increase in tissue volume due to increase in cell number
b. Increase in tissue volume due to increase in cell size
c. Decrease in tissue volume due to decrease in cell size
d. No change in tissue volume

A

Cellular atrophy results in:

C. Decrease in tissue volume due to decrease in cell size

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33
Q

Why is early diagnosis critical with cerebral atrophy?

A

Because there is limited ability to restore function that has been lost by the time the diagnosis is made

Once neuron death has occurred, it cannot be reversed. WANT TO PREVENT FURTHER DEATH INSTEAD.

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34
Q

What is the goal with cerebral atrophy diagnosis?

A

To determine the underlying cause of atrophy to initiate appropriate treatment early.

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35
Q

Why can atrophy be difficult to identify early?

A

The signs are slow and subtle

  • May be observed by others rather than the affected individual first
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36
Q

What are some ways to determine atrophy?

(Diagnostic testing)

A
  • Physical assessment for neurologic deficits
  • Brain imaging MRI, PET, SPECT, CT to determine location and severity of atrophy
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37
Q

Treatment for cerebral atrophy is targeted towards what?

A

Prevention or slowly of continued atrophy

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38
Q

What are some treatment options for cerebral atrophy?

A
  • There is no cure: neurons cannot replicate
  • Treatment is individualized based on specific diagnosis and type of atrophy → goal is to maximize function and minimizing atrophy
  • PT, OT, SPEECH CRITICAL FOR PROMOTION OF OPTIMAL FUNCTION
  • PHARM OPTIONS MAY HAVE W/ NEUROLOGICAL SIGNAL TRANSMISSIONS
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39
Q

I am a condition cellular hyperplasia. What am I?

A

Acromegaly

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40
Q

What is the cause of Acromegaly

A
  • Secretion of excessive growth hormone
  • Increase in insulin-like growth factor 1 (IGF-1)
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41
Q

What condition results in exaggerated skeletal and organ growth after epiphyseal plate closure

A

Acromegaly

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42
Q

What are some clinical manifestations of Acromegaly

A
  • Soft tissue swelling: difficult getting rings on/off
  • Altered facial features: prominent jaw, brow, nasal bone
  • Pain, numbness in hands
  • Voice deepening
  • Skin changes: course hair growth, body odor, skin tags, oily appearance, sweating
  • Breast discharge, impotence, menstrual cycle changes
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43
Q

Why is Acromegaly difficult to diagnose?

A
  • Due to slow and insidious onset of clinical manifestations
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44
Q

How is Acromegaly diagnosed?

A
  • Confirmed w/ elevated IGF-1
  • Measurement of growth hormone
  • Imaging to determine if pituitary adenoma is present
  • Glucose tolerance test
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45
Q

What are some treatments for Acromegaly?

A

Drug Therapy

Radiation therapy

Surgical removal adenoma

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46
Q

What is treatment designed to do for Acromegaly?

A

Reduce overproduction of IGF-1 and growth hormone

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47
Q

What are the drug classes used in Acromegaly treatment?

A
  • Somatostatin analogs
  • Dopamine agonists
  • Growth factor antagonist
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48
Q

Acromegaly drug therapy: Somatostatin analogs

A
  • First choice
  • inhibits growth hormone secretion and reduction in the pituitary adenoma size
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49
Q

Acromegaly drug therapy: Dopamine agonists

A
  • second choice: less effective
  • reduce the hormone growth hormone and subsequent IGF-1 secretion
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50
Q

Acromegaly drug therapy: Growth hormone antagonist

A

binds to the growth hormone receptor

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51
Q

What are some non pharmacological treatment options for Acromegaly?

A
  • radiation therapy to promote death in growth hormone hypersecreting cells
  • Surgical: removal of tumor (adenoma) causing hypersecretion of growth hormone
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52
Q

What size does the adenoma have to be for surgery to be an option in Acromegaly?

A

less than 40 ng/mL

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53
Q

Cardiac Hypertrophy can be described as…

A

Heart muscle becomes thickened due to excessive workload and functional demand

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54
Q

What is the cause of Cardiac Hypertrophy?

A
  • Primary hypertrophic cardiomyopathy: know specific cause, often result of inherited genetic autosomal-dominant trait
  • Secondary hypertrophy: often caused by underlying condition that causes an increase in ventricle workload
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55
Q

Cardiac Hypertrophy that occurs in the right ventricle is due to

A

increased pressure in the pulmonary circulation

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56
Q

Cardiac Hypertrophy that occurs in the left ventricle is due to

A

increased pressure in the systemic circulation (i.e, HTN)

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57
Q

How does Cardiac Hypertrophy affect pumping and filling of the heart?

A
  • Not able to pump as well due to rigidity of the ventricles, leading to “pump failure”
  • Muscle becomes less effective @ contracting despite increased size, impacting pumping ability
  • Increased muscle doesn’t allow as much blood in
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58
Q

How does left sided Cardiac Hypertrophy impact the rest of the body?

A

Left ventricle responsible for pumping blood from lungs → providing oxygen rich blood to body

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59
Q

What are some clinical manifestations of Cardiac Hypertrophy

A
  • Variable in its expression: some develop signs, others do not
  • Symptoms of pump failure: SOB, chest pain, syncope
  • Irregular heart rate and rhythm,
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60
Q

How is Cardiac Hypertrophy diagnosed?

A
  • Genetic testing (primary hypertrophic)
  • Routine screenings to determine HTN, exercise tolerance, presence of ventricular arrhythmia
  • EKG: evaluate electrical activity of the heart
  • Ultrasound: measures ventricles, heart valves, blood vessels
  • Exercise stress testing
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61
Q

What is normally heard during cardiac contraction w/ Cardiac Hypertrophy?

A

Heart murmur

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62
Q

What are some treatments for Cardiac Hypertrophy?

A
  • Strategies: target symptom relieve and prevent sudden death
  • Antihypertensives (ARBs drug of choice followed by ACE)
  • Surgery to reduce left ventricular mass or repair heart valve
  • Activity restrictions may be required
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63
Q

What are the medications used with Cardiac Hypertrophy

A
  • ARBs - “tan”
  • ACE - Benazepril, Lisinopril
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64
Q

When does cervical metaplasia occur?

A

When there is an external issue with the cervix that causes damage to the squamous epithelial cells

  • Infection
  • Irritation
  • Trauma
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65
Q

When does cervical dysplasia occur?

A
  • When there is abnormal cell growth that happens during breakdown of existing cell tissues
  • Internal issue
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66
Q

What are the clinical manifestations of cervical metaplasia and dysplasia?

A

There are no signs

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67
Q

What increases your risk for cervical metaplasia and dysplasia

A
  • Early onset sexual activity
  • Multiple (more than 3) sexual partners
  • Exposure to HPV
  • Smoking
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68
Q

What are some lab and diagnostic tests associated w/ cervical metaplasia and dysplasia

A
  • Routine screening (PAP) smears help identify characteristics of cells
  • Colposcopy: visually see cervix with use of speculum
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69
Q

How often should you get PAP smear?

A

Initial screening begins at 21, every 3 years after that until 30, then 5 years until 65

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70
Q

What are some treatment options for cervical metaplasia and dysplasia?

A
  • Cryosurgery: cold therapy destroys the mildly dysplastic cells
  • Liquid nitrogen: used for the dysplastic cells on the exocervix
  • CO2 laser ablation: directing a laser toward the cervical lesion vaporizing tissue
  • Ablation
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71
Q

Dyspnea is a frequent complaint that may indicate either an underlying ______ or _____ condition

A

Cardiovascular or Pulmonary

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72
Q

Cool, pale, and painful extremities may indicate the presence of a ____ or _____

A

clot or peripheral vascular disease

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73
Q

Blood pressure and heart rate will do what with smoking?

A

Increase

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74
Q

What are some laboratory studies that may indicate markers of CVD?

A
  • Decreased HLD
  • Increase LDL
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75
Q

What is our body’s first line of defense?

A
  • Skin
  • Eyes: lashes
  • Tears
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76
Q

What is our body’s second line of defense?

A
  • Inflammatory mechanisms activated
  • Vasodilation & capillary permeability
  • Phagocytes move in to engulf and destroy
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77
Q

What is our body’s third line of defense?

A
  • Immune response
  • Immune cells recognize and destroy harmful substance
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78
Q

What are the 3 main goals of inflammation?

A
  1. Increase blood flow to site (vascular response)
  2. Increase healing cells at site (cellular response)
  3. Remove injured tissue and prepare for tissue repair and healing
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79
Q

What are the 5 cardinal signs of inflammation?

A

heat, incapacitation (loss of function), pain, edema, redness

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80
Q

What are some Systemic manifestations of inflammation?

A

fever

increased circulating leukocytes (leukocytosis= elevated WBC) and plasma proteins (C-Reactive Proteins)

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81
Q

What is the treatment of inflammation?

A

Reduce blood flow (elevate, ice)

Decrease swelling (compression, rest)

Block the action of chemical mediators

Decrease pain

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82
Q

What are the 3 stages of wound healing?

A
  1. Inflammatory
  2. Proliferative
  3. Maturation
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83
Q

Stages of Wound Healing: Inflammatory

A
  • Immediate, 2-5 days
  • Bleeding stops, clots begins
  • Formation of a scab
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84
Q

Stages of Wound Healing: Proliferative

A
  • 5 to 3 weeks
  • New granulation tissue forms
  • Wound edges pull together
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85
Q

Stages of Wound Healing: Maturation

A
  • 3 weeks to 2 years
  • Collagen forms, strengthens wound
  • Only 80% as strong as original tissue
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86
Q

What condition am I?

“Inflammation of the lining of the paranasal sinuses lasting 4-12 weeks”

A

Acute sinusitis

  • Acute lasts 4-8weeks
  • Subacute lasts 8-12 weeks
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87
Q

When does recurrent acute sinusitis occur?

A

When the patient has had up to four episodes per year, with sinus inflammation completely resolving between episodes

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88
Q

What can cause acute sinusitis?

A
  • When ostia and outfow of mucus are blocked
  • Impaired clearance of the mucus by protective cilia or altered mucus quality or quantity
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89
Q

What is the role of the ostia in the sinus?

A

Provide outflow of drainage and prevent backflow and contamination of sinuses

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90
Q

What is the primary etiology of acute sinusitis?

A

Viral infections transmitted via respiratory droplets:

  • rhinovirus
  • adenovirus
  • coronavirus
  • Influenza A and B
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91
Q

What are some clinical manifestations of acute sinusitis?

A
  • Facial pain over sinus regions of face increasing w/ straining or bending down
  • Fever
  • Nasal congestion and/or excessive nasal discharge
  • Persistant cough
  • Fatigue
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92
Q

What are some diagnostic criteria for acute sinusitis?

A
  • Physical examination: have clinical manifestation
  • General inflammatory labs: WBC, CRP, ESR
  • Sinus radiographs when dx is in question (will reveal opaque, mucus filled thickened sinus)
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93
Q

An acute sinusitis follows a what many times?

A

Upper respiratory infection

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94
Q

What are some treatments for acute sinusitis?

A

It can resolve on its own

Pharmacologic

  • Antibiotics for 10 to 14 days
  • Antihistamines
  • Decongestants
  • Nasal sprays → oxymetazoline hydrochloride-

Surgical

  • If antibiotic treatment is unsuccessful and continues to have thick purulent drainage
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95
Q

Acute sinusitis treatment: oxymetazoline hydrochloride

A
  • Nasal spray
  • Helps w/ vasoconstriction
  • Only use for 5 days, can cause rebound congestion
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96
Q

What condition am I

“Persistent low-grade inflammation the paranasal sinuses lasting over 12 weeks with or without flares .”

A

Chronic sinusitis

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97
Q

What is the pathophys of Chronic sinusitis

A

Multifactorial

  • Environmental: persistent infection/allergens
  • Genetics: Metabolic abnormalities or immune deficiencies
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98
Q

How do the multifactorial triggers result in chronic sinusitis?

A

(environmental - infections, allergens, genetics; immune, metabolic issues)

  • Disrupt mucociliary clearance and result in mucus stagnation → creates environment conducive to bacterial growth and chronic inflammation
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99
Q

What are some clinical manifestations of chronic sinusitis?

A
  • Nasal congestion
  • Nasal discharge
  • Sore throat
  • Foul breath, unpleasant taste
  • Low-grade fever
  • Chronic cough
  • Hyposmia: reduced ability to smell
  • Facial fullness, discomfort, headache
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100
Q

What is the diagnostic criteria

A

Persistence of obstructed and mucus-filled sinuses over 12 weeks or longer

Two of the following must be present

  • Anterior or posterior mucopurulent drainage
  • Nasal obstruction
  • Facial pain, pressure fullness
  • Hyposmia

Confirmed by the presence of mucosal thickening, changes to the surrounding bone, and changes in the air fluid levels by a CT scan

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101
Q

What are some treatment options for chronic sinusitis

A

GOAL: reduce mucosal swelling, promote sinus drainage, clear infections

Pharmacologic

  • Glucocorticoids- oral or topical through a nasal spray
  • Antibiotics

Nonpharamcologic

  • Nasal saline irrigation
  • If ineffective, consider surgical internvention*
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102
Q

All burns cause an acute _____ response

A

Inflammatory

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103
Q

Burns: Superficial partial-thicknes

A
  • known as first degree
  • Damage to epidermis
  • Mild sunburn
  • Does not result in necrosis or scaring
  • Healing occurs in about a week
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104
Q

Burns: Deep partial-thickness

A
  • Known as second degree
  • Damage epidermis and penetrate the dermis layer
  • Scalding with hot liquids, chemical burn
  • Blisters present
  • Healing occurs in 2 to 4 weeks
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105
Q

Burns: Full-thickness

A
  • Know as third degree
  • Damage to epidermis, dermis and subcutaneous layers
  • Scarring is often extensive
  • Loss of elasticity- contractures can occur
106
Q

What type of burn am I?

“Erythema, heat, swelling, pain, redness, loss of function”

A

Superficial partial-thickness burns

(first degree)

107
Q

What type of burn am I?

“Blistering, redness, heat, pain, edema, serous exudate of clear fluid that seeps from the tissues”

A

Deep partial-thickness burns

(second degree)

108
Q

What type of burn am I?

  • “Destroys the nerve endings, sweat glands and hair follicles
  • Destruction of nerve endings= decreased pain response
  • Redness, eschar, edema, exudate”
A

Full-thickness burns

(third degree)

109
Q

Rule of 9’s: Arms (each side) and Head

110
Q

Rule of 9’s: Legs

A

Each side 9%

111
Q

Rule of 9’s: torso, back

A

18% each side

112
Q

Rule of 9’s: groin

113
Q

Rule of 9’s: Buttock

114
Q

After removing source of injury, what is next priority intervention w/ burns?

A

ABC’S

  • Then administer IV fluids to replenish water and Na losses
115
Q

Why are fluids important w/ burns?

A

help restore circulating blood volume and improves perfusion to organs

116
Q

Why do you often times place pt with significant burns in isolation?

A

At high risk for infection

117
Q

What might wound management include w/ burns?

A
  • Cleaning with sterile saline- removing blisters or necrotic tissue
  • Dressings changed every 1 to 2 days
  • Hydrotherapy-soaking in a tub every day or bid to remove dead tissue
  • Skin grafting- can use self donor to cover and protect the exposed areas
118
Q

Chronic inflammation of synovial membranes and synovial hyperplasia is what condition?

A

Rheumatoid Arthritis

119
Q

What is thought to be cause of RA?

A

Exact cause is unknown

Likely a combination:

  • Genetic susceptibility
  • Immune trigger event
  • Subsequent development of autoimmunity against synovial cells
120
Q

In RA, there is an excess ____ response

A

Inflammatory, acts on joints

121
Q

What are some clinical manifestations of RA?

A
  • Mild to debilitating
  • Symmetrical joints
  • Pain (can be chronic)
  • Stiffness
  • Most noticeable early in the morning when immobile for periods of time
  • Redness, heat, swelling
  • Decreased mobility
122
Q

Malalignment is of the joints in RA are caused by what?

A

Combination of:

  • Cartilage and bone erosion,
  • fibrosis,
  • muscle spasms and muscle atrophy
123
Q

What is some diagnostic criteria for RA?

A
  • No definitive test exists: based on history and physical exam (stiff joints, pain symmetrical joints)
  • Elevated ESR (normal 0-22m, 0-29w)
  • CRP (normal less than 1)
  • Positive ANA
  • Positive RF (high levels found in blood)
  • X-rays showing joint damage
124
Q

What are some treatments for RA?

A

Involves careful balance of pharm and nonpharm strategies

Pharmacology: to induce remission

  • Anti inflammatory
  • Immunosuppressive

Nonpharmacology: involve

  • balance of activity & rest
  • physical therapy to promote joint mobility
  • splints: prevent deformities
  • heat and cold therapy
  • surgical: total joint replacement
125
Q

Ingestion of irritating substances and/or poor gastric perfusion results in inflammation of the gastric mucosa is known as what condition?

A

Acute gastritis

126
Q

What irritants are most often the cause of acute gastritis

A

Aspirin

Alcohol

Certain microorganisms

127
Q

What is the pathophys of acute gastritis

A

Exposure to gastric irritants inhibits production of gastric mucosa and makes it more vulnerable to stomach contents

  • Can lead to erosion and perforation
  • Necrotic cells
  • Hemorrhaging
128
Q

What are some clinical manifestations of acute gastritis

A
  • Indigestion (heart burn)
  • Loss of appetite
  • N&V
  • Hiccups
  • Hematemesis: vomiting blood
  • Anemia may result from gastric hemorrhage
129
Q

What are some diagnostic criteria for acute gastritis

A

Physical examination

  • Usually shows hx of aspirin/NSAID use, excessive alcohol intake, recent contaminated food, etc
  • Abdominal tenderness

Direct visualization of stomach w/ endoscope to visualize ulcers

Stool analysis may show occult blood

Hemoglobin and Hematocrit levels = anemia

130
Q

Treatment for acute gastritis

A
  • Begins w/ removal of gastric irritants
  • Antacids to buffer or decrease production of gastric acid
131
Q

What bacteria is most often the cause of chronic gastritis?

132
Q

What are some diagnostic tests that can be performed w/ chronic gastritis?

A
  • Gastric tissue biopsy to determine presence of H. Pylori
  • Breath test to measure presence off enzyme given off by bacterium
  • Blood test for protein antibodies against H. Pylori
133
Q

Treatments for chronic gastritis

A
  • Multiple antibiotics (H. Pylori deep in stomach mucosa)
  • Proton pump inhibitors or bismuth → antimicrobial properties & increase gastric pH
  • Immunosuppressive drugs for autoimmune processes
  • Vitamin B12
134
Q

What are some common causes of pancreatitis?

A
  • Duct blockage by gallstones
  • Excessive alcohol use
135
Q

What are some clinical manifestations of acute pancreatitis?

A
  • Upper abdominal pain w/ sudden onset → dull, aching RADIATING TO BACK
  • Nausea, vomiting, anorexia, and/or diarrhea
136
Q

What is a tale-tell sign of acute pancreatitis

A

Dull, steady, ache that RADIATES to the back

137
Q

What is the diagnostic criteria for acute pancreatitis

A
  • History and physical → presence of clinical manifestations
  • Laboratory testing: CBC, ESR, CRP
  • Serum amylase and lipase → excessive released w/ pancreas inflammation
  • AST and ALT → expected to be elevated w/ pancreatitis caused by gallstones
138
Q

Diagnostic testing w/ acute pancreatitis: Lipase

A

Normal: 0 to 160 units per liter (U/L)

Expected to be elevated w/ inflammation of pancreas

139
Q

Diagnostic testing w/ acute pancreatitis: Amylase

A

25-126 U/L

Expected to be elevated w/ inflammation of pancreas

140
Q

Diagnostic testing w/ acute pancreatitis: AST & ALT

A

Expected to be elevated w/ pancreatitis caused by gallstones

141
Q

What are some treatments associated acute pancreatitis?

A
  • Receive aggressive IV hydration in first 24 hrs
  • NPO to reduce pancreatic secretion
  • Surgical removal of gallstones
  • Medications
142
Q

What are some medications that can be used with acute pancreatitis

A

Narcotic: to bloc pain receptor

Antacids: neutralize gastic secretion

Proton pump inhibitor : inhibit pancreatic secretion

143
Q

In Chrons disease, the exact cause is unknown but what can play a role?

A

Family history

144
Q

Which condition am I?

Chronic inflammation anywhere throughout the GI tract but most commonly in small intestine

A

Crohn’s Disease

145
Q

What are some clinical manifestations associated w/ Crohn’s disease?

A

RELATED TO RAPID STOOL TRANSIT TIME

  • Symptoms are based on the location of the affected area
  • Abdominal pain- relieved with defecation
  • Diarrhea- non bloody but can contain mucus or hidden blood
  • Malnutrition - due to impaired intestinal absorption
  • Occult blood in stool
  • Systemic manifestations (fever, weight loss, fatigue)
146
Q

What are some diagnostic criteria for Crohn’s disease

A
  • History and physical examination
  • Direct visualization w/ endoscope or radiograph
  • CT scans to visualize complications → abscesses, fistulas
  • Stool culture to rule out infection
147
Q

Treatment for Crohn’s disease

A
  • Symptom management
  • Pharmacologic treatment - immunosepressants to decrease inflammatory response
  • Dietary changes → Avoid spicy foods, have High calories and protein, Low in fat and fiber during exacerbations
  • Surgical treatment: Remove damaged bowel or repair fistulas
148
Q

What is Natural active immunity

A
  • Your body produces antibodies to a live pathogen
  • ACTUALLY EXPERIENCE IT AND PRODUCE ANTIBODIES
149
Q

What is Artificial active immunity

A

your body produces antibodies in exposure to a vaccine

150
Q

What are the two types of active immunity

A

Natural and artificial

151
Q

What are the two types of Passive immunity

A

Natural and passive

152
Q

What is Natural passive immunity

A
  • You receive antibodies that were originally creased in a response to disease agent.
  • Example: mother passes immunity to child through breast milk.
153
Q

What is Artificial passive immunity

A
  • You receive antibodies that were created in exposure to a vaccine
  • Example: bit by an animal, you will get a rabies shot so you don’t get infected with rabies.
154
Q

Type 1 immediate hypersensitivity reaction

A

IMMEDIATE ALLERGY:

  • anaphylaxis, asthma, urticaria
155
Q
  • Type II antibody-mediated hypersensitivity reaction
A
  • IgG antibodies, incompatible blood
156
Q
  • Type III immune complex-mediated reaction
A

Immune system

  • Antigen/antibody, RA or Lupus
157
Q
  • Type IV cytotoxic T lymphocyte-mediated hypersensitivity reaction
A
  • Delayed hypersensitivity reaction
  • Poison Ivy, PPD, contact dermatitis
158
Q

Chronic inflammation anywhere throughout the GI tract but most commonly in small intestine is what disease?

A

Crohn Disease

159
Q

Chronic inflammation that begins in rectum and ascends the descending colon is what disease?

A

Ulcerative Colitis

160
Q

How does Crohn’s disease and Ulcerative colitis differ?

A
  • UC is continuous is superficial areas of ulceration that usually starts near rectum and works its way back up
  • Crohn’s is more sporadic
161
Q

What are some clinical manifestations of Ulcerative Colitis

A
  • Bloody diarrhea
  • Frequent bowel movements
  • Electrolyte imbalances
  • Abdominal pain
  • Fever
  • Weakness, fatigue
  • Anemia
162
Q

Ulcerative Colitis Diagnostic Criteria

A
  • History and physical examination
  • Endoscopic examination → Will show mucosal erythema
  • Radiographs (imaging) to show narrowing in colon (Colonic dilations), ulcers, perforations or obstructions
  • Complete blood count (anemia)
163
Q

Ulcerative Colitis Treatment

A

Pharmacologic treatment

  • Anti-inflammatory
  • Antidiarrheal
  • Immunosuppressive medication

Dietary changes

  • Healthy and increase fluids
  • Avoid: milk, caffeine and spicy foods

Surgical treatment

  • To remove obstructions or perforations
164
Q

The skin is the first life of defense. What is the second?

A

inflammatory response

165
Q

What are the two Specific immune response

A

Cell mediated immunity - relies on cells to attack vs antibodies (t-cells)

Humoral immunity – ALL ABOUT ANTIBODIES (B-LYMPHOCYTES)

166
Q

Cytotoxic cells in the immune system have what role?

A

attack tumor cells and cells infected with viruses

167
Q

Helper T cells have what role in the immune system

A

go to the site of inflammation

168
Q

B lymphocytes produce what?

A

Antibodies

169
Q

What are the components of WBC with Differential

A
  • Neutrophils 50-70% of all WBC → seen w/acute bacterial infections
  • Monocytes: Clean up committee, older bacterial infections
  • Lymphocytes: Elevate with viral conditions
  • Eosinophils → Allergic response
  • Basophils → Inflammation and hypersensitivity reactions (responsible for allergic reaction)
170
Q

HIV life cycle

A
  1. HIV attaches itself to CD4 cell and enters
  2. HIV copies itself to make more virus
  3. Young HIV leaves CD4
  4. HIV grows mature and goes off to invade more CD4 cells
171
Q

Initial infection and symptom development for AIDS is what?

A

2-4 weeks, can extend to several months

172
Q

AIDS Clinical Manifestations

A
  • Fever
  • Sore throat
  • Enlarged lymph nodes
  • Skin rash
  • Joint paint
  • Headaches
173
Q

Kaposi sarcoma is associated with what?

A

HIV/AIDS

  • Must common cancer w/ HIV
  • Tumors attach to small blood vessels
  • Purplish lesions on the skin
  • Becomes painful as disease progresses
174
Q

Diagnostic tests w/ AIDS

A
  • Enzyme-linked immunosorbent assay (ELISA)
  • Ora Quick HIV-1 Antibody Test
  • Western blot assay
  • HIV viral load test
  • CD4+ cell count
  • CBC
175
Q

Diagnostic tests w/ AIDS: ELISA

A
  • First screening used to determine the presence of HIV antibodies
176
Q

Diagnostic tests w/ AIDS: Ora Quick Rapid HIV-1 Antibody Test

A
  • Results in 20 minutes
  • Blood sample from finger prick
  • If positive must be confirmed w/ Western Blot assay
177
Q

Diagnostic tests w/ AIDS: Western Blot assay

A

reliable test used to confirm that the client is HIV seropositive

178
Q

Diagnostic tests w/ HIV: HIV viral load test

A
  • Measures the amount of HIV viral activity.
  • Used to monitor for disease progression and response to antiretroviral medications
  • Levels greater than 5,000-10,000 copies/mL indicate need for tx
179
Q

Diagnostic tests w/ HIV: CD4 + cell count

A

use to confirm the progression from HIV infection to AIDS

180
Q

Diagnostic tests w/ HIV: CBC

A

detects:

anemia,

leukopenia - low wbc

thrombocytopenia - low platelet

181
Q

What are some tx for HIV/AIDS

A
  • Antiretroviral therapy (ART)
  • Drugs used in combination: reduce development of drug resistance
182
Q

If exposed TO HIV, 2-3 antiretroviral medications are used ASAP but not more than _____ after exposure

A

3 days

(continue them for 28 days)

183
Q

AIDS medications: Antiretroviral

A
  • Reduce viral load
  • Maintain CD4+ cell counts above 500 (normal range is 500 to 1500)
  • Treat opportunistic infections & malignancies
184
Q

AIDS medications: NRTI’s

A

Generic: zidovudine

  • Inhibits action of reverse transcriptase to prevent HIV reproduction (prevents RNA to be transcripted to DNA)
185
Q

AIDS medication: NNRTI’s

A

generic: nevirapine, delavirdine
* Blocks HIV reproduction

186
Q

AIDS medication: Protease inhibitors

A

generic name of medications: nelfinavir, saquinavir

  • Block production of HIV protease enzyme which is need to mature virions (mature needed to infect other cells)
187
Q

AIDS medications: Fusion Inhibitors

A

generic name of medication: enfuvirtide

  • Prevent virus from entering CD4+ cells
188
Q

AIDS medications: HAART (Highly active antiretroviral therapy)

A

combines 3 or 4 of the drugs

prevents drug resistance

189
Q

When the body comes into contact with something it is allergic to the immune system reacts by sudden release of mast cells and mediators into the circulation of the blood resulting in what?

A

Anaphylaxis

190
Q

What are some clinical manifestations of Anaphylaxis

A

Severe bronchospasm

Skin flushing, urticaria

Angioedema

Low blood pressure

191
Q

Treatment of Anaphylaxis

A
  • Immediate administration of epinephrine to relax smooth muscle
  • Airway management: supplemental o2
  • Antihistamines to help reduce symptoms stimulated by histamine release
  • Fluids
192
Q

Diagnostic testing w/ Anaphylaxis

A
  • Allergy testing to determine pathogen
  • blood test to measure the amount of serum and plasma
193
Q

SLE is what type of reaction?

A

Type III hypersensitivity reaction

194
Q

Typical clinical manifestations of SLE

A
  • Joint pain and swelling
  • Skin rashes
  • Fatigue
  • pericardial effusion (swelling around the heart)
  • Pleural effusion (swelling around the lungs)
195
Q

Diagnostic Criteria for SLE

A

four of which must be present to obtain a diagnosis of SLE.

  1. Butterfly rash over cheeks
  2. Ulcers or open areas in mouth or nasopharynx
  3. Arthritis, associated w/ tenderness swelling or fluid buildup
  4. Pleuritis (inflammation of lining of lungs) or pericarditis (inflammation of heart lining)
  5. Proteinuria (protein in urine) greater than 5 g/dL or +3 on a dip stick
  6. Seizures or psychosis, suggesting neurologic involvement
  7. Anemia, leukopenia, or thrombocytopenia (abnormally low number of platelets), suggesting hematologic involvement
  8. Lab values including anti-DNA antibody, anti-Sm (antibody to Smith nuclear antigen), or a false-positive test for syphilis
  9. Abnormal antinuclear antibody (ANA)
196
Q

What are some treatments for SLE?

A

Anti-inflammatories: NSAIDS or corticosteroids

DMARDS - delay profess and resulting damage

Antimalarial - slows dx progress: Plaquenil

Immunosuppressants: reserved for more aggressive → Cyclophosphamide, Ritumaxid, mycophenolate

197
Q

What are the mechanisms for causing disease

A
  • Direct destruction of host cell by pathogen
  • Interference with host cell’s metabolic function
  • Exposing host cell to toxins produced by pathogen
198
Q

The potency of the pathogen is known as what?

199
Q

The proportion of exposures needed to cause the infection is called what?

A

Infectivity

200
Q

The ability to produce harmful toxins is known as what?

A

Toxigenicity

201
Q

_____ is viewed by the immune system as foreign

A

Antigenicity

202
Q

A pathogen that is Obligate requires a what?

A

Host: for metabolism & reproduction

203
Q

Facultative pathogens may live ____ or ____

A

on the host OR independently

204
Q

What type of pathogen cannot replicate outside the cell? What type can?

A

Virus CANNOT replicate outside of cell

Bacteria CAN replicate outside of cell

205
Q

Aerobic vs Anaerobic

A
  • Aerobic: require oxygen
  • Anaerobic- does not require oxygen
206
Q

What is the chain of infection?

A
  1. Infectious agent
  2. Source of infection
  3. Portal of exit
  4. Mode of transmission
  5. Portal of entry
  6. Susceptible host
207
Q

How can chain of infection be broken?

A
  1. Infectious agent - STERILIZATION: kills agent
  2. Source of infection - SANITIZING ENVIRONMENT, ANTIMICROBIAL DRUGS → prevents spread
  3. Portal of exit: HAND WASHING, TRASH DISPOSAL, COVERING SECRETIONS
  4. Mode of transmission → ISOLATION, AIRFLOW CONTROL, STERILIZATION, HAND WASHING
  5. Portal of entry → COVERING POTENTIAL ENTRY POINTS
  6. Susceptible host → RECOGNITION OF HIGH-RISK PTS, TX OF UNDERLYING DISEASE
208
Q

What are the 5 main routes of transmission?

A
  1. Contact
  2. Vehicle
  3. Airborne
  4. Droplet
  5. Vector
209
Q

Routes of transmission: Contact

A
  • Direct: physical transfer of organism → Bathing, dressing change, foley catheter insertion, shaking hands
  • Indirect: susceptive host is exposed to a contaminated object → blood pressure cuff, thermometers, etc.
210
Q

Mode of transmission: vehicle

A

Food can carry salmonella

Blood = hepatitis

211
Q

Mode of transmission: Airborne

A
  • Fine particles that are suspended in the air.
  • Air disperse the organism and can be inhaled or deposited on the skin
212
Q

Mode of transmission: Droplet

A
  • large moist droplets during sneezing, talking or coughing
  • Seldom travel more than 3 feet
213
Q

Mode of transmission: Vector borne transmission

A
  • Transmission living animals- rats and insects example mosquitoes can carry malaria, rats= bubonic plague
214
Q

What phase of acute infection is at greatest risk for transmission

A

Incubation b/c don’t know they have it

215
Q

5 phases of acute infection

A
  1. Exposure
  2. Incubation
  3. Prodromal - onset of nonspecific s/s (fatigue, low grade fever weakness)
  4. Acute clinical illness - onset of s/s specific to disease
  5. Convalescence - full recovery (Fatigue is common during this time )
216
Q

What mode of transmission does Influenza A have?

A

Respiratory droplet transmission

217
Q

What are some clinical manifestations of Influenza A?

A
  • Cough
  • Sore throat
  • Nasal congestion/drainage
  • Chills, body aches
  • Fever
  • Weakness, malaise
218
Q

How can Influenza A be diagnosed?

A
  • History and physical examination: S/s → severe abrupt onset
  • Rapid viral assays: identifies A & B, Use nasopharyngeal secretions- 10 to 20 minutes results
219
Q

Hepatitis A is transmitted how?

A

Fecal-oral (contaminated food and water supplies

220
Q

What are the three stages of Viral Hepatitis Clinical Manifestations

A
  1. Prodrome
  2. Icterus
  3. Recovery
221
Q

Viral Hepatitis Clinical Manifestations: Prodrome

A

FIRST TWO WEEKS FOLLOWING EXPOSURE

  • Fatigue
  • Anorexia
  • Headache
  • Low-grade fever
222
Q

Viral Hepatitis Clinical Manifestations: Icterus

A

TWO WEEKS AFTER EXPOSURE AND LASTS TO 6 WEEKS

  • Jaundice → eyes, palm
  • Hepatomegaly- (enlarged liver)
  • Clay stool
  • Dark urine
223
Q

Viral Hepatitis clinical manifestation: Recovery

A

ABOUT 8 WEEKS AFTER INITIAL EXPOSURE TO VIRUS

  • Improvement with residual hepatomegaly
  • Liver will remain enlarged for an additional 1-4 weeks → Avoid deep percussion
224
Q

Diagnostic criteria for Viral Hepatitis

A

Detection of viral antibodies in blood

  • Anti-HAV
  • Anti-HCV
  • Anti-HDV
  • Anti-HEV

Labs

  • Clotting time prolonged (platelet count, PTT, PT, & INR = if high, impaired liver failure – if high, can bleed to death
  • Urine bilirubin
  • Serum bilirubin
    • More than 30 mg/dL= more sever
225
Q

What condition am i: bacterial infection that attacks the lung

226
Q

What causes TB?

A

Inhalation of infected aerosolized droplets

227
Q

What are some clinical manifestations of TB?

A
  • Most cases asymptomatic
  • Night sweats
  • Malaise, fatigue
  • Severe chronic cough w/ hemoptysis
  • Weight loss, anorexia
228
Q

What are some diagnostic testing for TB

A
  • TB skin test
  • Chest X-ray
  • Sputum culture → needs to be done first thing AM
229
Q

What kind of isolation will a TB patient be in?

A

Airborne → N95, isolation gown, mask, goggles, gloves

230
Q

What is the common tx for TB?

A

Multiple antimicrobial medications over several months

  • Rifampin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol
231
Q

Bacterial infection of the renal parenchyma is associated with what disease?

A

Pyelonephritis

  • Bacteria travels thru lower urinary tract and triggers inflammatory response
232
Q

What are some signs and symptoms of Pyelonephritis

A
  • Fever
  • CVA pain
  • Dysuria
  • Frequent urination
  • Blood in urine
233
Q

What are some diagnostic criteria for Pyelonephritis

A
  • UA to screen for bacterium
  • Imaging can show renal abnormalities
  • CBC can show infection
234
Q

What is the tx for Pyelonephritis

A

Medications

  • IV fluids, antibiotics, pain meds → in ER
  • Oral antibiotics when @ home

Surgery to remove any abscesses or obstructions, correct abnormalities

235
Q

Inflammation of the meninges of the brain and spinal cord is known as what?

A

Bacterial Meningitis

236
Q

What is the common cause of Bacterial Meningitis

A

N. meningitidis → respiratory droplet transmission

237
Q

What are some clinical manifestations of Bacterial Meningitis?

A

Rapid and severe onset → less than 24 hrs

Severe headache, photophobia

Nuchal rigidity

Decreased alertness, LOC, mental status change

Seizure

238
Q

What are some diagnostic criteria for Bacterial Meningitis?

A
  • Kernig’s sign
  • Brudzinski’s sign
  • CSF analysis and cultures, blood culture for infection
239
Q

Bacterial Meningitis: Kernig’s sign

A
  • supine position with knees bent and hips flexed
  • lift, and extend one knee upward-
  • (+) if the moving leg in the upward position causes pain → grimacing
240
Q

Bacterial Meningitis: Brudzinski’s

A
  • Bring neck towards the chest.
  • In a positive patient, their knees will bend upward, at same time instead of staying flat
241
Q

What are some treatments for Bacterial Meningitis?

A

Medications

  • IV antibiotics
  • IV corticosteroids
  • IV fluids

Immunization: Haemophilus influenzae and meningococcal di

242
Q

A ___ ____ is characteristics such as height or skin color that is influenced by two or more genes

A

Polygenic trait

243
Q

TORCH

A
  • A group of diseases that cause damage to the fetus if exposed

T - Toxoplasmosis

O - other hepatitis

R - rubella

C - cytomegalovirus

H - herpes

244
Q

Deficiency in what leads to neural tube defects

A

Folic acid

  • Cleft left
  • Spinabifida
245
Q

A Progressive degenerative neurologic disorder with an autosomal dominant inheritance pattern leading to defect on chromosome 4 is called what?

A

Huntington Disease

246
Q

What are some clinical manifestations of Huntington Disease?

A
  • Personality changes
  • Loss of memory
  • Antisocial and impulsive behaviors & emotional lability
  • Dyskinesia → difficulty performing voluntary movements
  • Chorea (HALLMARK SIGN): Rapid, involuntary, non-repetitive movement of the face, trunk and limbs
247
Q

What are some diagnostic criteria for Huntington Disease

A
  • Family, personal hx: autosomal dominant → anyone else have it
  • Physical exam: Mental, cognitive, and emotional evaluation
  • Genetic testing
  • CT, MRI, PET: can detect abnormalities, shrinkage, etc.
248
Q

Tx of Huntington Disease

A

NO CURE.

  • Supportive care → OT, PT, Speech
  • Nutritional management
  • Assist with ADL
  • Pharm: meds to help w/ movement
249
Q

What condition am I

  • Single gene mutation with autosomal recessive inheritance located on gene 11
250
Q

What is sickled shape known as?

A

hemoglobin S (HbS)

  • The blood cell life span is reduced from 120 days to 16 days → leads to anemia
251
Q

How does shape of RBC w/ sickle cell impact blood flow?

A
  • Abnormal shape makes it hard to pass thru small blood vessels → leads to TRAPPING and decreased o2
252
Q

What are some clinical manifestations of sickle cell?

A
  • Jaundice
  • Anemia → Loss of RBC’s- making it difficult to oxygenate tissues
  • Pain
  • Organ damage → Spleen, kidneys and liver
  • Infection
  • Tissue ischemia → decreased o2, leads to PAIN
253
Q

What are some diagnostic criteria for Sickle Cell disease?

A

Lab Analysis

  • Hemoglobin electrophoresis (HbA, HbS)
  • If no complications (crisis from trapping) perform yearly tests →
    • CBC
    • UA (kidney function)
    • Retinal exam
  • Test liver and kidney function q2-3yrs
    • AST, ALT
    • BUN, Creatinine
254
Q

What is treatment with Sickle Cell aimed at?

A
  • Preventing complications
    • Prevention of infection (antibiotic)
    • Immunizations (flu, pneumonia, meningitis)
    • Pain management w/ opioids
  • Blood transfusions for anemia
255
Q

How much folic acid should be taken during pregnancy to prevent neural tube defects?

256
Q

What are the two neural tube defect diseases?

A
  • Spinal bifida
  • Anencephaly
257
Q

incomplete closure of vertebrae is called what?

A

Spina bifida

258
Q

What type of spina bifida is this

  • a dimple with a little tuff of hair at the base of the spinal cord
  • small gap in the spine, but no opening or sac on the back.
A

Spina Bifida Occulta

  • a failure of the vertebral arch to close
  • Without protrusion of meninges or spinal cord
259
Q

incomplete closure of skull with exposure of the brain and meninges is called what?

A

Anencephaly

260
Q

What type of Spina Bifida is this:

  • Sac of fluid that comes through opening in baby’s back
  • Does not contain spinal cord or nerves
A

Spina Bifida: Meningocele

  • Little disability
261
Q

What type of Spina Bifida is this:

  • Sac of fluid that comes through opening in baby’s back
  • Spinal cord and nerves are in sac and damaged
A

Spina Bifida: Myelomeningocele

Can impact ability to go to bathroom, loss of feeling in extremities, leg function

NURS 311: Pathophysiology (2 decks)

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