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Krystan: Semester Two Nursing School > 2850 Pathophysiology Exam Two > Flashcards

2850 Pathophysiology Exam Two Flashcards

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1
Q

Tension headache pathophysiology

A

Stress induced, and often associated with muscle tension in neck, shoulders, and occipital area

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2
Q

Tension headache: clinical manifestations

A

Bifrontal or occipitofrontal pain with gradual onset
Pressure or band like pain
Vital signs and neuro exam normal

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3
Q

Tension headache: risk factor

A

Stress

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4
Q

Cluster headache: pathophysiology

A

Pathophysiology not entirely understood, but believed to be a neurovascular disorder

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5
Q

Cluster headaches: clinical manifestations

A 
Severe, unilateral pain that is usually periorbital and radiates into the jaw, face, etc
Eye tearing
Eye redness
Runny nose
Pupil constriction
Restlessness 
Eyelid edema
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6
Q

Cluster headache: risk factors

A 
Alcohol
Tobacco
Stress
Allergies
Weather changes
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7
Q

Migraine headaches: pathophysiology

A

Pathophysiology not totally understood, but could be due to low serotonin levels in the brain leading to constriction and dilation of blood vessels

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8
Q

Migraine headache: clinical manifestations

A 
Unilateral, vascular, throbbing pain that lasts for 4-72 hours
May be preceded by aura
Nausea and vomiting
Light sensitivity 
Noise sensitivity
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9
Q

Migraine headache: risk factors

A 
Low serotonin in brain
Stress
Hormones
Smoking
Weather
Food additives
Alcohol
Caffeine 
Fatigue
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10
Q

Lupus: pathophysiology

A

Formation of autoantibodies that form immune complexes that are deposited in organs and tissues, which triggers an inflammation response that damages organ membranes and microvasculature

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11
Q

Which organs and tissues are most commonly affected by lupus?

A

Skin
Synovium
Glomeruli
Lungs

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12
Q

Lupus: clinical manifestations

A 
Fatigue
Fever
Myalgias
Arthralgias
Butterfly rash
Joint inflammation 
Musculoskeletal pain
Splenic enlargement
Pleurisy and pleural effusion 
Vasculitis
Pericarditis
Anemia
Thrombocytopenia 
Headaches
Leukopenia
Nephrotic syndrome
Raynaud’s phenomenon
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13
Q

Nephrotic syndrome

A

Hypertension plus hematuria

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14
Q

Ranaud’s phenomenon

A

Tricolor change in the fingers due to vasospasm of blood vessels

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15
Q

Lupus: risk factors

A 
Genetic predisposition
EBV antibodies
Being a woman of childbearing age
African American, Asian, or Hispanic descent
Estrogen
Certain prescription medications 
Environmental elements
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16
Q

Fibromyalgia: pathophysiology

A

Unknown

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17
Q

Fibromyalgia: clinical manifestations

A

Long-term, body wide pain affecting joints, muscles, tendons, and soft tissues
Fatigue
Headache
Sleep problems
Depression
Anxiety
Pain at at least 11 out of 18 specific tender points

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18
Q

Fibromyalgia: risk factors

A

Can affect anyone, but especially women between 20 and 50 years of age

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19
Q

What is the most important function of hemoglobin?

A

Combining with oxygen in the lungs and releasing it to peripheral tissues

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20
Q

What happens with PaO2 drops below 60 mmHg?

A

Hemoglobin drops off oxygen molecules too quickly, leading to tissue hypoxia

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21
Q

What is the role of erythropoietin in the stimulation of RBC production?

A

When bloodstream oxygen gets too low, the kidneys secrete erythropoietin, which stimulates the bone marrow to make red blood cells, increasing the oxygen carrying capacity of blood

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22
Q

What is the ventilation-perfusion ratio (V-Q ratio)?

A

Ratio of amount of air reaching the alveoli to the amount of blood reaching the alveoli

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23
Q

What is ideal in terms of the VQ ratio?

A

Equal amounts of air and blood reaching alveoli

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24
Q

What is the built in compensatory mechanism of the lungs to try to match blood flow and ventilation?

A

When there is little ventilation, pulmonary arterial vessels constrict, redistributing blood flow to better ventilated areas

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25
Q

What is the primary stimulus to control rate and depth of breathing?

A

Central chemoreceptors

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26
Q

How do central chemoreceptors work?

A

They sense changes in CO2 levels and blood pH and adjust rate and depth of breathing

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27
Q

Give an example of how breathing will be adjusted based on CO2 and pH

A

If CO2 levels are high/pH is low, respiration rate and depth will increase

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28
Q

Hypercapnia

A

High levels of CO2

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29
Q

What is the role of hypercapnia in breathing?

A

Stimulate breathing process

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30
Q

What is the secondary stimulus of breathing?

A

Peripheral chemoreceptors

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31
Q

How do peripheral chemoreceptors work as a stimulus to breathing?

A

Receptors in the aortic arch and carotid artery respond to decreased arterial oxygen and stimulate respiration

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32
Q

Breathing stimulated by peripheral chemoreceptors is known as..

A

Hypoxic drive

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33
Q

What happens when central chemoreceptors are exposed to high levels of CO2 for long periods of time?

A

They become less responsive, and peripheral chemoreceptors take over as stimulus for respirations

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34
Q

At what level of SaO2 do peripheral chemoreceptors take over?

A

60 mmHg

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35
Q

Describe how mycobacterium tuberculosis is passed to other individuals

A

Inhalation of airborne droplets containing M. Tuberculosis bacilli, which settle in the bronchial tree and proliferate

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36
Q

What is the role of white blood cells in responding to infection with M. Tuberculi?

A

WBC’s wall off the infected area, forming a lesion called a tubercule (WBCs + bacilli+ fibrotic tissue) which scar tissue forms around, making the bacilli inactive

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37
Q

What happens when M. Tuberculi bacteria continue to multiply?

A

They break through the scar tissue tubercule and continue to proliferate and spread, becoming active again

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38
Q

What adverse effect happens in tuberculosis infection when macrophages degrade the bacteria?

A

Enzymes for killing the bacteria also damage the lung tissue, making lung tissue necrotic, and bacteria reinfect the bronchial tree (patient is contagious again)

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39
Q

What are presenting signs and symptoms of pulmonary TB?

A 
Chronic cough with purulent sputum
Hemoptysis 
Weight loss
Anorexia
Chest pain
Fever with night sweats
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40
Q

What are some additional findings in patients with pulmonary TB?

A

Lung crackles

Enlarged lymph nodes

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41
Q

What populations are at high risk for acquiring TB?

A 
Healthcare workers
Urban residents
Nursing home residents
Prisoners
Immunosuppressed patients
Those born/living/traveling outside US
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42
Q

What other lifestyle factors increase the risk of acquiring TB?

A 
Living in close quarters with other/infected people
Alcoholism
ESRD
Diabetes
Travel to areas where TB is common
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43
Q

What are the top causes/triggers of asthma?

A 
Allergies
Viral respiratory infections
Exercise 
Inhaled chemicals
Multiple episodes of asthma
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44
Q

What happens in the body (pertaining to asthma) when allergens trigger the immune system?

A

Bronchial constriction
Inflammation
Increase in size and number of goblet cells that secrete mucus

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45
Q

What is the role of T lymphocytes in the pathophysiology of asthma?

A

They assist B cells to turn into plasma cells that produce immunoglobin E, which triggers the release of histamines and leukotrienes

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46
Q

What is the role of leukotrienes during an asthma attack?

A

Responsible for development of bronchoconstriction, bronchial hyperreactivity, edema, and eosinophilia

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47
Q

What substance is stimulated during a viral respiratory infection that can trigger an asthma attack?

A

IgE directed towards viral antigens

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48
Q

What do viral and bacterial upper respiratory infections commonly cause in someone with asthma?

A

Bronchospasm and copious mucous production

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49
Q

How can exercise induce an asthma attack?

A

Provoking loss of heat and water from the tracheobronchial tree

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50
Q

What can exaggerate exercise-induced asthma?

A

Cold weather

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51
Q

How can inhaled chemicals induce bronchospasm?

A

They irritate receptors that stimulate a vagar reflex, which includes dizziness, sweating, nausea, fainting

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52
Q

What can multiple episodes of asthma cause in the airways?

A

Airway remodeling

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53
Q

Describe the process of airway remodeling

A

Proliferation of respiratory epithelium and hypertrophy of respiratory smooth muscle

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54
Q

What is the result of epithelial cell injury in patients with asthma?

A

It exposes airway to triggers for hyperreactivity, which can cause more frequent bronchospasm

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55
Q

What are clinical manifestations of asthma?

A 
Wheezing
Cough
Dyspnea
Chest tightness
Prolonged exhalation
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56
Q

What is an early sign of airway obstruction?

A

Prolonged exhalation

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57
Q

What are signs of a severe asthma attack?

A

Use of accessory muscles
Distant/diminished breath sounds
Diaphoresis

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58
Q

List the signs that a patient is going into respiratory failure

A

Inaudible breath sounds
Repetitive, hacking cough
Cyanosis

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59
Q

What is the most common etiology of asthma?

A

Allergy

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60
Q

Which employment settings have the highest risk for exposure to chemical agents that can cause asthma?

A 
Farming
Painting
Construction
Landscaping
Janitorial work
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61
Q

What are common triggers of asthma in children?

A

Viral infections, like rhinovirus or RSV

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62
Q

Define COPD

A

A combination of chronic bronchitis, emphysema, and hyperactive airway disease. It is a poorly reversible airflow limitation

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63
Q

What are characteristic features of COPD?

A

Mucus hypersecretion
Hypoxia
Cyanosis
Persistent cough

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64
Q

What are some characteristics of emphysema?

A

Overdistended alveoli with trapped air

Hyperreactivity in the airways

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65
Q

What is the consequence of overdistended alveoli with trapped air?

A

Obstruction of expiratory airflow
Loss of alveolar elastic recoil
High residual volume of CO2
Summary: breathing in is okay but breathing out is hard

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66
Q

What happens with hyper reactive airways in emphysema?

A

Extremely reactive to irritants, leading to episodes of bronchoconstriction

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67
Q

What pathological changes lead to airflow limitation in COPD?

A

Narrowing
Excessive mucus and fibrosis in airways
Loss of alveolar elastic recoil
Smooth muscle hypertrophy

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68
Q

How are pulmonary structures remodeled in COPD?

A

Bronchioles are remodeled due to chronic inflammation, thickened bronchiole walls, and constricted lumen

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69
Q

What factors cause the damages to lung structures in COPD?

A

Leukotrienes
Interleukins
Tumor necrosis

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70
Q

What happens when increased levels of CO2 become chronic in COPD?

A

Respiratory drive stimulus changes from PCO2 accumulation to low levels of PO2 instead. Hypoxia stimulates breathing

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71
Q

Why must administration of oxygen to patients with COPD be carefully controlled?

A

Oxygen can depress patient’s independent drive to breathe, leading to respiratory arrest

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72
Q

What are characteristic s/s of COPD?

A 
Dyspnea
Cough
Wheezing
Hypoxia
Cyanosis
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73
Q

What cardiac complication can be brought on by COPD?

A

Right sided heart failure

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74
Q

Why might individuals with COPD develop clubbing of the fingers?

A

Chronic hypoxia

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75
Q

What is a major cause of COPD?

A

Smoking

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76
Q

What are additional risk factors/causes of COPD?

A 
Occupational or environmental exposure to chemicals or dust
Secondhand smoke exposure 
Genetic predisposition 
Connective tissue diseases 
IV drug use
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77
Q

What is cystic fibrosis?

A

An inherited, autosomal recessive, multisystem disease

78
Q

Describe the disruption of cells that leads to CF

A

Disruption of exocrine gland function and chloride secretion in epithelial cells of respiratory tract, pancreas, sweat glands, salivary glands, intestines, and reproductive system

79
Q

What is the primary problem in CF?

A

Thick, viscous mucous secretions in multiple organ systems

80
Q

What is the consequence of mucous secretions in CF for the lungs and bronchioles?

A

Impaired oxygen/CO2 exchange at alveoli

Promotion of bacterial growth

81
Q

What are the consequences of CF mucous secretions on the GI tract?

A

Poor digestion due to increased mucous

82
Q

What are consequences of the CF mucous secretions on the pancreatic ducts?

A

Obstructed ducts, leading to deficiency of pancreatic enzyme and deficient digestion of protein, carbs, and fats

83
Q

What are respiratory signs and symptoms of CF?

A 
Cough
Excessive sputum
Chronic infection
Wheezing
Air trapping
Sinus disease
Pallor
84
Q

What are GI signs and symptoms of CF?

A 
Failure to thrive
Fat soluble vitamin deficiency 
Edema
Pancreatitis 
Rectal prolapse
Loose and fatty stools
85
Q

Why are women of childbearing age at higher risk for iron deficient anemia?

A

Menstrual blood loss

Increased iron needs in pregnancy/delivery/breastfeeding

86
Q

Why are infants and children at risk for iron deficient anemia?

A

Low iron in cows milk (after weaning from formula or breast milk)
Increased iron need during growth

87
Q

Why are elderly adults at risk for iron deficient anemia?

A

Poor diet
Dental issues
Lack of stomach acid (which is needed for iron absorption)

88
Q

What are some causes of GI bleeding?

A

Peptic ulcers
Esophageal varices
GI cancer

89
Q

What is the first thing to do when a man presents with iron deficiency?

A

Check for GI bleeding

90
Q

What is the RDA of iron intake for men and women?

A

Men: 8 mg/day
Women: 18 mg/day

91
Q

What are signs and symptoms of anemia in general?

A

Fatigue
Weakness
Exercise intolerance

92
Q

What are specific signs of iron deficiency?

A 
Har loss
Cheilitis 
Nail changes
Pica
Cold intolerance
Glossitis (tongue inflammation)
93
Q

Normal BP parameters

A

Less than 120/80

94
Q

Stage one hypertension parameters

A

140-159/90-99

95
Q

Stage two hypertension parameters

A

Greater than 160/100

96
Q

Primary hypertension

A

Also known as essential hypertension, it has no known cause

97
Q

Secondary hypertension

A

Hypertension that is a side effect of a systemic disorder

98
Q

What percentage of adults with HTN have primary HTN?

A

90-95%

99
Q

What are risk factors for hypertension?

A 
Age 
African American heritage
Obesity
Diabetes
Inactivity
Tobacco use
High sodium diet
Low potassium or vitamin D intake
Excess alcohol 
Stress
100
Q

Why are African Americans at higher risk for hypertension?

A

High sodium sensitivity

101
Q

What are two major negative effects of HTN on the cardiovascular system?

A

High damaging forces against the endothelial lining

High resistance against the left ventricle

102
Q

What are the effects of high aortic pressure?

A

Excessive workload in the left ventricle, which can lead to left ventricular failure

103
Q

How does HTN predispose systemic arteries to injury?

A

It creates a high shearing force against artery walls, which causes endothelial weakening and injury, which can specifically cause blindness, kidney failure, stroke, and lower extremity vascular issues

104
Q

What are signs and symptoms of target organ damage in HTN?

A 
Chest pain
Dsypnea on exertion 
Palpitations 
Headache
Vision problems
Dizziness
Weakness
Edema
Leg pain
105
Q

What symptoms may people with HTN complain of?

A

Often none

In extreme cases: headache, nosebleeds, blurred vision, palpitations

106
Q

What change serves as the precursor to atherosclerosis?

A

Endothelial injury

107
Q

What are common causes of endothelial injury?

A

Oxidizing free radicals
Shearing force of high BP
High blood glucose levels
Elevated LDL cholesterol

108
Q

Non-modifiable risk factors for atherosclerosis

A

Age
Gender (males earlier)
Race (African American)
Family history

109
Q

Modifiable risk factors for atherosclerosis

A 
Diet
Activity level
Obesity
Lifestyle
HTN
Diabetes
110
Q

What is the age difference between men and women in the risk of developing atherosclerosis?

A

Men over 45 are at higher risk

Women over 55 or post-menopausal are at increased risk

111
Q

Why are diabetic patients at higher risk for developing atherosclerosis?

A

Often have elevated triglyceride and LDL levels

Often have vascular changes

112
Q

Why does smoking increase atherosclerosis risk?

A

Smoke contains free radicals that cause endothelial injury

Smoke decreases HDL levels

113
Q

What lifestyle factors contribute to the development of atherosclerosis?

A

Tobacco use
Excess alcohol use
Stress

114
Q

What is the bodily process of atherosclerosis development?

A

Endothelial injury brings WBCs and platelets to injury site
WBCs ingest LDL cholesterol
These cholesterol-laden WBCs become foundation for atherosclerotic plaque

115
Q

What happens over time with atherosclerotic plaques?

A

It enlarges and becomes calcified and turns into a fibrous platelet cap (atheroma)
The expanding plaque stretches the vessel to its limit, and the vessel becomes stiff and hardened

116
Q

What signs and symptoms may be present when atherosclerosis has caused organ dysfunction?

A 
Chest pain
SOB
Palpitations 
Leg pain
Dependent edema
117
Q

What are signs and symptoms when atherosclerosis causes altered cardiac function?

A 
Obesity
SOB at rest
Pallor
Cyanosis
Weak pulses in lower extremities
Increased BP
Rapid pulse
S4 murmurs and bruits
Chest pain
Dyspnea upon exertion
118
Q

Cardiac output

A

Amount of blood pumped out of left ventricle each minute

119
Q

What is cardiac output based on

A

Heart rate times stroke volume

120
Q

What controls the heart rate?

A

SNS and PNS

121
Q

What influences stroke volume?

A

Preload
Afterload
Cardiac contractility

122
Q

Preload

A

Volume of blood in the heart at the end of ventricular diastole

123
Q

What does preload mean in the clinical setting?

A

Volume of blood that enters the right atrium from the venous system

124
Q

Afterload

A

Amount of resistance ventricles must overcome to pump blood out of the heart

125
Q

What creates high afterload for the right ventricle?

A

High pulmonary vascular resistance

126
Q

Cardiac contractility

A

Myocardium’s ability to stretch and contract in response to the heart filling with blood

127
Q

What conditions enhance contractility in a healthy heart?

A

Increased preload/SV

128
Q

What happens to contractility when afterload increases?

A

Contractility decreases, so less blood is ejected from the heart

129
Q

What does RAAS stand for?

A

Renin-angiotensin-aldosterone system

130
Q

Describe renin and its role in BP

A

Released from kidneys when renal perfusion decreases, triggering angiotensinogen to be released from the liver, which breaks down into angiotensin I, which triggers formation of angiotensin II when it encounters ACE in the lungs

131
Q

What is the role of angiotensin II?

A

Arterial vasoconstrictor that raises BP, triggers ventricular remodeling, and stimulates adrenal release of aldosterone

132
Q

Aldosterone and it’s mechanism of action

A

Acts at the nephron to increase sodium and water reabsorption from distal tubules to the bloodstream

133
Q

What are the net effects of the RAAS?

A

Elevated BP and BV, which leads to increased workload for left ventricle

134
Q

What problem does the RAAS create in left ventricular failure?

A

The increased BP and BV further weaken the heart muscles

135
Q

Parasympathetic nervous system effects on the heart

A

Stimulates cholinergic receptors to slow HR and decrease contraction force

136
Q

Sympathetic nervous system effect on the heart

A

Stimulates beta 1 adrenergic receptors to increase HR and contraction force

137
Q

What role does the posterior pituitary play in blood pressure and blood volume control?

A

It releases ADH, which causes water reabsorption at the nephron for increased BV and BP

138
Q

What does left ventricular diastolic dysfunction occur from?

A

Reduced relaxation or increased stiffness of ventricular muscle

139
Q

What is the common cause for development of left ventricle changes?

A

Increased afterload caused by HTN

140
Q

What does left ventricular systolic dysfunction occur from?

A

Reduced forward pumping strength of ventricle muscle, leading to decreased stroke volume and cardiac output

141
Q

What are the two major types of consequence of left ventricle systolic dysfunction?

A

Backwards effect and forward effect

142
Q

Backward effect of left ventricular dysfunction

A

Buildup of hydrostatic pressure in the left atrium and pulmonary vasculature, leading to fluid accumulation in pulmonary interstitial/intracellular spaces (pulmonary edema)

143
Q

Forward effect of left ventricle systolic dysfunction

A

Inadequate ejection of blood into the aorta and decreased perfusion through the arterial circulatory system

144
Q

What does left ventricle systolic dysfunction stimulate?

A

RAAS, ADH release, and SNS activation

145
Q

What are the effects of angiotensin II on the systemic arterial system?

A

Widespread vasoconstriction
Increased peripheral arterial resistance
Aldosterone release

146
Q

What are clinical manifestations of LVF?

A

Orthopnea
Paroxysmal nocturnal dyspnea (sudden SOB in middle of night)
Cerebral symptoms: headache, memory loss, insomnia, anxiety, disorientation
GI signs and symptoms

147
Q

Right ventricular failure is also known as

A

Cor pulmonale

148
Q

Backwards failure in right ventricular failure

A

Right ventricle is weak, leading to increased pressure in right atrium, which increases systemic venous pressure, leading to edema in the body

149
Q

What is the result of increased pulmonary arterial blood flow?

A

Hypoxemia (tissue hypoxia)

150
Q

What are clinical manifestations of right ventricular failure?

A

Jugular venous distension
Poor GI venous drainage
Peripheral edema

151
Q

What conditions are associated with poor GI venous drainage?

A 
Anorexia
Nausea
Early satiety 
Postprandial fullness 
Indigestion
Impaired absorption
152
Q

Stress incontinence: manifestations

A

Incontinence upon force, such as coughing, sneezing, or laughing

153
Q

Stress incontinence: causes

A

Poor pelvic support or sphincter weakness due to pregnancy, age, or low estrogen levels

154
Q

Urge incontinence: manifestations

A

Urgency and frequency of urination

155
Q

Urge incontinence: cause

A

Overactive detrusor muscle, though the exact mechanism is unclear

156
Q

Overflow incontinence: manifestations

A

Chronic overdistention and urinary retention

157
Q

Overflow incontinence: most common cause

A

BPH

158
Q

Neurogenic bladder: manifestation

A

Chronic bladder overdistention

159
Q

Neurogenic bladder: causes

A

Spinal cord injury or disorder causing interruption of sensory nerve fibers or afferent nerve pathways between bladder and spinal cord

160
Q

Mixed incontinence

A

Combination of stress and urge incontinence

161
Q

Functional incontinence: manifestation

A

Incontinence due to not being able to get to the bathroom in time

162
Q

Functional incontinence: causes

A

CNS damage, (stroke, dementia, immobility, cognitive impairment)

163
Q

BPH: pathophysiology

A

Excessive cell growth of the prostate gland

164
Q

BPH: etiology

A

Testosterone-sensitive cellular proliferation and lack of apoptosis in the prostate

165
Q

BPH: clinical manifestations

A 
Frequent urination but voiding only small amounts
Incontinence
Incomplete bladder emptying
Dribbling
Straining to urinate
Weak urine stream 
Increased UTI/risk
166
Q

By age 60, what percent of men have some degree of BPH?

A

50%

167
Q

Constipation: causes

A 
Lack of fiber or fluid
Lack of physical activity
Ignoring urge to defecate 
Drugs (especially opiates)
Diseases that slow GI tract
168
Q

Constipation: manifestations

A 
Hard stools
Pain and discomfort
Increased flatulence
Increased rectal pressure 
Hemorrhoids
Abdominal distinction and bloating
169
Q

What is the most common GI disorder in the US?

A

GERD

170
Q

GERD: pathophysiology

A

Lower esophageal sphincter is weak, allowing acid reflux into the esophagus, causing esophageal ulceration.
This causes metaplasia (esophageal epithelial cells turning into stomach-like columnar epithelium)
Delayed gastric emptying also contributes to discomfort and erosion

171
Q

GERD: signs and symptoms

A 
Dysphasia
Heartburn
Epigastric pain
Regurgitation
Respiratory complaints 
Bitter taste in mouth
172
Q

Who is most affected by GERD?

A

Infants and those over 40

173
Q

What is Barrett’s esophagus?

A

Changes in esophageal structure in GERD. Precancerous cellular changes

174
Q

GERD: risk factors

A 
Obesity
Pregnancy
Nicotine 
Alcohol use
Chocolate
Coffee
Fatty foods
Certain meds
175
Q

Peptic ulcer disease: description

A

Inflammatory erosion of stomach or duodenal lining

176
Q

Peptic ulcer disease: pathophysiology

A

Hypersection of hydrochloric acid, Ineffective GI mucous production, and poor cellular repair cause erosion of the mucous membranes in the stomach and duodenum. HCl leaks into the stomach wall and blood vessels, causing ulcers

177
Q

What often damages the protective mechanisms of the stomach in PUD?

A

H. Pylori bacteria (secretes urease, which breaks down urea and neutralizes stomach acid)

178
Q

What are some other causes of peptic ulcers?

A

Excessive NSAIDs
Alcohol abuse
Excess caffeine
Smoking

179
Q

Why does chronic NSAID use cause peptic ulcers?

A

NSAIDs counteract prostaglandin E secretion, which stimulates gastric mucous production

180
Q

Peptic ulcer disease: signs and symptoms

A 
Epigastric or abdominal pain occurring 2-3 hours after eating
Intense burning and gnawing pain
Pain that wakes patient up at night 
Nausea and vomiting
Blood in vomit or stool
181
Q

Peptic ulcer disease: complications

A

Bleeding from the ulcer
Perforation
Scarring of stomach lining
Pyloric stenosis

182
Q

Signs and symptoms of peptic ulcer perforation

A

Sudden, excruciating pain
Abdominal rigidity
Pallor
Cold sweats

183
Q

Signs of gastric peptic ulcers

A

Pain relief immediately upon eating food, then pain gets worse after acid secretion starts

184
Q

Signs of duodenal peptic ulcers

A

Pain that is not relieved by food, or food not relieving it until a while has passed after eating

185
Q

Crohn’s disease: definition

A

Chronic, uncontrolled immune response of the bowel that leads to bowl destruction and sometimes obstruction

186
Q

Crohn’s disease: pathophysiology

A

Mucosa of bowels is chronically inflamed with high levels of immunoglobins, T-cells, and macrophages. This causes inflammation and destruction of segments of the bowel

187
Q

What are some characteristic features of the bowel of someone with crohn’s?

A

Granulomas (large masses of immune cells)

Cobblestone appearance due to sporadic areas of bowel destruction

188
Q

Crohn’s disease: etiology

A

Unknown, but may be genetic or environmental

Higher SES or being female increase risk

189
Q

Peak onset for Crohn’s disease

A

Between 15 and 30 years old, or between 60 and 80 years old

190
Q

Crohn’s disease: signs and symptoms

A 
Diarrhea
Abdominal pain
Remissions and exacerbations
Blood in the stool
Weight loss 
Abdominal pain
Anorexia 
N/V/D
Increased bowel sounds
Arthritis
Cheilitis

Krystan: Semester Two Nursing School (13 decks)

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