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Pathophysiology > Patho Exam 3 > Flashcards

Patho Exam 3 Flashcards

1
Q

the production of blood cells

A

hematopoiesis

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2
Q

what is the order of hematopoiesis?

A

begins in yolk sac > liver and spleen > then taken to bone marrow

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3
Q

blood cell production in the bone marrow

A

medullary hematopoiesis

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4
Q

blood cell production in other places (liver, spleen)

A

extramedullary hematopoiesis

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5
Q

the hematopoiesis process starts with pluripotent stem cells. what do they develop into?

A

erthrocyte (red cell); myelocyte (monocyte and granulocyte); lymphocyte (T and B cells); and megakaryocyte (thrombocyte)

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6
Q

what is the growth of cells controlled by?

A

colony-stimulating factors (CSF) and other cytokines and chemical mediators

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7
Q

what do cytokines control the regulation of?

A

hematopoiesis

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8
Q

what are the normal lab values for RBCs in males and females?

A

males: 4.7-6.1 million/uL
females: 4.2-5.4 million/uL

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9
Q

what are the normal lab values for WBC?

A

5,000-10,000 mm1

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10
Q

what are the normal lab values for Hgb in males and females?

A

males: 14-18 g/dL
females: 12-16 g/dL

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11
Q

what are the normal lab values for Hct in males and females?

A

males: 42%-52%
females: 39%-47%

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12
Q

what are the normal lab values for platelets?

A

150,000-400,000 mm1

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13
Q

what is the normal erythrocyte sedimentation rate (ESR)?

A

less than 20 mm/hr

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14
Q

the stoppage of blood flow

A

hemostasis

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15
Q

what are the three stages of hemostasis?

A
  1. vascular constriction
  2. formation of platelet plug
  3. blood coagulation
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16
Q

platelet deficiency

A

thrombocytopenia

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17
Q

what are the causes of thrombocytopenia?

A

decreased platelet production; decreased platelet survival; splenic sequestration (pooling); intravascular dilution of circulating platelets

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18
Q

what are the lab features of thrombocytopenia?

A

low platelet count; prolonged bleeding time; normal coagulation

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19
Q

what are the clinical manifestations of thrombocytopenia?

A

bruising, prolonged bleeding, petechia, purpura; bleeding from mucous membranes; spontaneous bleeding, hemorrhaging

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20
Q

what is the treatment of thrombocytopenia?

A

focus in cause

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21
Q

blood thickens

A

hypercoagulability (Virchow’s triad)

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22
Q

what is Virchow’s triad?

A

venous stasis (sluggish blood flow); hypercoagulability; damage to vessel wall

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23
Q

breakdown of the RBC and the release of hemoglobin; generally normocytic and normochromic

A

hemolytic anemia

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24
Q

someone has hemolytic anemia. what two things will be increased?

A

reticulocyte count and serum count

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25
Q

what are the common causes of hemolytic anemia?

A

drug reactions and wrong blood received

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26
Q

breakdown of RBC and release of hemoglobin

A

RBC hemolysis

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27
Q

genetically determined, most common heritable hematologic disease in the world

A

sickle cell anemia

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28
Q

what are the lab features of sickle cell anemia?

A

Hgb S presence in blood; hemoglobin electrophoresis (homozygous, heterozygous for hgb S); anemia, decreased survival time of sickled cells; increased reticulocytes (immature RBC); increase of bilirubin (product of RBC breakdown)

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29
Q

what are the clinical maifestations of sickle cell anemia?

A

fatigue; exercise intolerance; hemolysis in spleen; vaso-occlusive events; pain (obstruction of vessels, tissue hypoxia, tissue death); hyperbilirubinemia

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30
Q

what does hyperbilirubinemia lead to?

A

jaundice

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31
Q

where do vaso-occlusive events occur? what do they do/cause?

A

occur in chest, abdomen, long bones, joints; block perfusion (cap stasis, venous thrombosis, arterial emboli (storke)); acute chest syndrome (pain, fever, pulmonary infarction, respiratory failure)

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32
Q

loss of iron containing red blood cells

A

blood loss anemia

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33
Q

loss of vascular volume (loosing blood); RBC normal in size and color

A

acute blood loss anemia

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34
Q

what are the clinical manifestations of acute blood loss anemia?

A

depends on the circumstance but hypovemoia is common

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35
Q

does not effect vascular volume due to compensatory mechanisms; often asymptomatic

A

chronic blood loss anemia

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36
Q

what can chronic blood loss anemia lead to?

A

microcytic hypochromic anemia (low hemoglobin due to depletion of iron stores)

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37
Q

common cause of anemia

A

iron deficiency anemia

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38
Q

what are the causes of iron deficiency anemia?

A

diet (not enough meat); bleeding; increased demand

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39
Q

what can lack of iron cause?

A

decreased hemoglobin synthesis in WBC causes impaired O2 delivery

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40
Q

presence of small RBCs in a peripheral blood smear; usually characterized by a MCV

A

microcytic anemia

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41
Q

circulating RBCs are smaller than usual size and have decreased red color

A

hyochromic anemia

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42
Q

what are the clinical manifestations of iron deficiency anemia?

A

hair loss; glossitis; pica

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43
Q

what are the treatments of iron deficiency anemia?

A

controlling chronic blood loss; increase iron intake (through diet or supplements)

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44
Q

size of cell

A

cytic

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45
Q

normal size

A

normocytic

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46
Q

small size

A

microcytic

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47
Q

large size

A

macrocytic

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48
Q

color of the cell

A

chromic

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49
Q

normal color

A

normochromic

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50
Q

decreased color

A

hypochromic

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51
Q

cancerous malignant neoplasms arise from single blood line of precursor hemtopoietic stem cells in bone marrow; immature malignant cells found in large numbers in blood marrow, infiltrate blood stream and organs

A

leukemia

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52
Q

disease if lymphoid stem cell line b and t cells; most common type of leukemia in children and adults

A

acute lymphocytic (ALL)

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53
Q

disease of the myeloid stem cells, blast cells in bone marrow accumulate and result in neutropenia, anemia, and thrombocytopenia

A

acute myelocytic (AML)

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54
Q

what are the clinical manifestations of acute leukemia?

A

insufficient production of normal WBC, RBC, and platelets (results in low grade fever, night sweats, and weight loss)

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55
Q

1/3 of all leukemias, disorder of older adults; malignancy of b lymphocytes; asymptomatic; lymph node enlargement, fever, pain, weight loss; no treatment (chemotherapy with stem cell transplant)

A

chronic lymphocytic (CLL)

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56
Q

excessive proliferation of granulocytes, RBC precursors and megakaryocytes

A

chronic myelogenous (CML)

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57
Q

what are the three phases of chronic myelogenous (CML)?

A

chronic, accelerated, and acute

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58
Q

what are the symptoms of chronic myelogenous (CML)?

A

fatigue, dyspnea, low grade fever, night sweats, bone pain, and bleeding

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59
Q

malignancy of cells in peripheral lymphoid tissues

A

lymphoma

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60
Q

malignant disorder characterized by reed sternberg cells, begin with single lymph one and then spread to other lymph nodes

A

hodgkin

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61
Q

all types of malignant lymphoma that do not have reed sternburg cells, neoplastic lymphoid cells that originate from t and b cells during differentiation in peripheral lymphoid tissues, begins with several enlarged lymph nodes in various locations

A

non hodgkin

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62
Q

what are the symptoms of lymphoma?

A

painless, progressive lymph node enlargement; fever; night sweats; weight loss; increased infections

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63
Q

deficiency in the normal number of neutrophils, a type of leukopenia

A

neutropenia

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64
Q

what is the normal neutropenia level?

A

3,000-7,000

65
Q

what does the level have to be in order to be diagnosed?

A

1,500

66
Q

what does the level have to be in order of it to be considered severe?

A

less than 500

67
Q

born with neutropenia

A

congenital

68
Q

autoimmune, drug related, infection related

A

acquired

69
Q

movement of gases from the atmosphere into the airway

A

ventilation

70
Q

flow of blood

A

perfusion

71
Q

reduction in arterial oxygen (PaO2), can lead to hypoxia

A

hypoxemia

72
Q

inadequate supply of O2 to tissues

A

hypoxia

73
Q

what are the causes of hypoxemia and hypoxia?

A

inadequate O2; respiratory disease; dysfunction of neurogical; alterations in perfusion

74
Q

what is the normal arterial PaO2 range?

A

75-100

75
Q

what are the respiratory defense mechanisms?

A

cilliary mucous membrane; cough reflux; macrophages

76
Q

what are the control centers of the respiratory system?

A

pons and medulla

77
Q

moves air, warms it, filters, humidifies

A

trachea

78
Q

smallest unit of lung, gas exchange site, produces surfactant

A

alveoli

79
Q

membrane lining

A

pluera

80
Q

what are the three pluera components?

A

visceral pluera; plueral space; parietal pluera

81
Q

what are the normal lab values for pH?

A

7.35-7.45

82
Q

what are the normal lab values for PaCO2?

A

35-45 mm Hgc

83
Q

what are the normal lab values for PaO2?

A

80-100 mm HgD

84
Q

what are the normal lab values for
HCO3 (bicarbonate)?

A

21-28 mEq/L

85
Q

what are the normal lab values for SaO2?

A

95-100%

86
Q

relationship of oxygen to hemoglobin

A

oxyhemoglobin dissociation curve

87
Q

what does it mean when the oxyhemoglobin dissociation curve shifts to the left?

A

increased affinity of hemoglobin to O2 (hemoglobin hold onto O2)

88
Q

what does it mean when the oxyhemoglobin dissociation curve shifts to the right?

A

decreased affinity (hemoglobin gives up O2 to the tissues)

89
Q

viral infection; affects upper and lower rest; three types: A, B, C; transmits through droplet

A

influenza

90
Q

what are the symptoms of influenza?

A

fever, chills, malaise, and sore throat

91
Q

entry of food/fluids into airways causing inflammation

A

aspiration

92
Q

bacterial

A

typical

93
Q

viral, fungal

A

atypical

94
Q

infection can be lobar (1 lobe) or bronchopenumionia (several lobes); community or hospital acquired

A

pneumonia

95
Q

infectious disease; airborne droplets; most commonly affects pulmonary system but can occur anywhere; lives in WBC and can cause scar tissue;

A

tuberculosis

96
Q

when it comes back out of where it lives in the WBCs and reinfects host

A

secondary tuberculosis

97
Q

what are the ways to test for tuberculosis?

A

skin test; chest x-ray; sputum; DNA techniques; genotyping

98
Q

what are the ways to treat tuberculosis?

A

multiple antibiotics; treatment can be prolonged; drug resistance is a problem

99
Q

leading cause of cancer death for men and women in the US; high mortality; primary tumors arise from lung tissue; aggressive; locally invasive; metastatic; crab protrusions;

A

lung cancer

100
Q

what are the six classifications of lung cancer?

A
  1. small cell (20-25%)
  2. non-small cell (75%)
  3. squamous cell (25-40%)
  4. adenocarcinoma (20-40%)
  5. large cell carcinoma (10-15%)
  6. small cell carcinoma (20-25%)
101
Q

strongest association with cigarette smoking; highly malignant; infiltrate early

A

small cell

102
Q

where does small cell lung cancer originate?

A

bronchiole epithelium

103
Q

common in men with smoking history

A

squamous cell

104
Q

where does squamous cell lung cancer originate?

A

central bronchi

105
Q

most common in north america; women and non smokers; weaker association with cigarette smoking

A

adenocarcinoma

106
Q

where does adenocarcinoma originate?

A

bronchioles or alveolar tissues

107
Q

highly anaplastic

A

large cell

108
Q

where does large cell lung cancer originate?

A

lung periphery

109
Q

what are the clinical manifestations of lung cancer?

A

dyspnea; cough; wheezing; chest pain; hemoptysis; increased sputum; hoarseness; anorexia (weight loss); paraneoplastic disorders; superior vena cava syndrome

110
Q

what are the diagnostic tests of lung cancer?

A

history/physical; pulmonary function; positive cytologic or histologic findings; bronchoscopy; tissue biopsies; pleural fluid samples; CXR; CT; MRI; PET scans

111
Q

inflammation and fibrosis or bronchial wall; hypertrophied mucus glands; loss of alveolar tissue; loss of elastic lung fibers

A

COPD

112
Q

hypersecretion of mucus and chronic cough, obstructive airflow

A

hypertrophied mucus glands

113
Q

decreased surface area for gas exchange

A

loss of alveolar tissue

114
Q

airway collapse, obstructed inhalation, air trapping

A

loss of elastic lung fibers

115
Q

airway obstruction of major and small airways caused by chronic inflammation and excessive bronchial secretions; bronchial wall fibrosis; mismatch of ventilation/perfusion; can’t compensate, hypoxemia and cyanosis; blue bloater

A

bronchitis

116
Q

what are the symptoms of bronchitis?

A

chronic productive cough for 3 months in 2 consecutive years

117
Q

hypersecretion of mucus in large airways (why the patient coughs)

A

hypertrophy of submucosal glands

118
Q

what happens in the small airways?

A

increase in goblet cells and excess mucus production

119
Q

what does loss of lung elasticity lead to?

A

CO2 retention

120
Q

enlargement of air sacs distal to the terminal bronchioles

A

air trapping/barrel chest

121
Q

destruction of alveolar walls and cap beds; smoking is main cause; hyperinflated lungs; bleb; airway collapse; mismatch of ventilation/perfusion; overventilated to maintain blood gas; pink puffer

A

emphysema

122
Q

what are the ways to diagnose emphysema?

A

H&P; pulmonary function; chest x-ray; labs

123
Q

what are the ways to treat emphysema?

A

no more smoking; bronchodilators, anticholinergics expectorants; steroids (anti-inflammatory); nutrition; immunizations

124
Q

blood borne substances lodge in pulmonary artery and obstruct bf; travel toward the heart and lungs; lodge in the pulmonary vasculature; hypotension

A

pulmonary embolism (PE)

125
Q

blood clots that develop in thighs and legs (MOST COMMON SOURCE OF PE)

A

thrombus

126
Q

secondary to fx (long bones, pelvis)

A

fat globules

127
Q

collections of fluid or debris related to a complicated factor

A

amniotic fluid

128
Q

something that has traveled from one area to another, like a bc/air/fluid, foreign object

A

embolism

129
Q

increase pulmonary artery pressure

A

vasoconstriction

130
Q

increase workload for right ventricle

A

right sided heart failure

131
Q

what are the risk factors of a pulmonary embolism?

A

development of DVT; immobility; trauma; spinal cord injury; fx; surgery

132
Q

what are the clinical manifestations of a pulmonary embolism?

A

restlessness; anxiety; tachycardia; tachypnea; sudden dyspnea; chest pain; hemoptysis; heart failure; shock; respiratory arrest

133
Q

what are the diagnostic tests of a pulmonary embolism?

A

V/Q scan; ABGs; pulmonary arteriography (primary use); D-dimer; lung scans

134
Q

what are the treatments of a pulmonary embolism?

A

improve respiratory and vascular status; pharmacologic therapy; surgical intervention

135
Q

what is the Virchow’s triad of a pulmonary embolism?

A

venous status: pulling of blood, sluggish blood flow
hypercoagulability: clot easy, dehydration, thick blood
drainage of vessel wall: trauma/surgery

136
Q

obstructive disorder, chronic disease, prevalence for disease has increased, airway obstruction, bronchial hyperresponsiveness, airway inflammation, airway remodeling, narrowing of airway

A

asthma

137
Q

what are the clinical manifestations of asthma?

A

cough, wheezing, chest tightness, prolonged expiration, tachycardia, tachypnea, dyspnea, hypoxemia, hypercapnia, anxiety

138
Q

what are the diagnostic tests of asthma?

A

history/physical, clinical findings, ABGs, pulmonary function test, determination of allergens (skin testing), CBC

139
Q

what is the management of asthma?

A

stepwise approach: prevent symptoms, reduce triggers, maintain pulmonary function, maintain normal activity, prevent exacerbations

140
Q

what are the 4 classifications of chronic asthma?

A

intermittent, mild, moderate, severe

141
Q

alveolar collapse; incomplete expansion of the lung or portion of

A

atelectasis

142
Q

what are the causes of atelectasis?

A

intra-op high dose supplemental O2; anesthesia; mucus plug; external compression by fluid, mass, exudate

143
Q

what specific population of people are at risk for atelectasis?

A

post op

144
Q

what is the patho of atelectasis?

A

decreased ciliary function > secretion retention > airway obstruction > impaired cough reflexes > hypoventilated alveoli > hypoxemia > acute respiratory failure

145
Q

what are the clinical manifestations of atelectasis?

A

cough; sputum production; low-grade fever; dyspnea; tachypnea; tachycardia; anxious; cyanosis; decreased breath sounds

146
Q

what are the treatments of atelectasis?

A

prevention (pre-op education, turn, cough, deep breathe, incentive spirometry); improve ventilation and remove secretions; adequate oxygenation; bronchoscopy (to remove mucous plugs)

147
Q

lung collapse, accumulation of air in the pleural cavity, breach in the lung or pleura, allows air to enter the pleura space and the lung or a portion of the lung collapses

A

pneumothorax

148
Q

what is the normal pressure in the pleural space?

A

negative

149
Q

why does the pressure need to be negative?

A

to keep the lungs inflated

150
Q

a subtype and an emergency, air enters and cannot leave, lung collapses, trach shifts to unaffected side

A

tension pneumothorax

151
Q

what are the clinical manifestations of a pneumothorax?

A

tachycardia, decreased or absent breath sounds, dyspnea, tachypnea, chest asymmetry, hypoxamia

152
Q

what are the diagnostic tests of a pneumothorax?

A

chest x-ray, CT scan, ABGs

153
Q

what are the treatments for a pneumothorax?

A

supplemental O2, evacuation of the air from the pleural space, chest tube insertion

154
Q

placed to chest drainage system that provide water-seal and suction

A

chest tube insertion

155
Q

abnormal collection of fluid in the pleural cavity as a result of a disease process

A

pleural effusion

156
Q

what are the 4 types of pleural effusion?

A

transudates or exudates, empyema (pus), blood; chyle (lymph fluid)

157
Q

what are the clinical manifestations of pleural effusion?

A

vary based on cause, dullness to percussion, absence of breath sounds over affected area, dyspnea, pleuritic pain, hypoxemia, fever (infections)

158
Q

what are the diagnostics of a pleural effusion?

A

CXR, CT, ultrasound; thoracentesis; analysis of pleural fluid; elevated WBC (infections)

159
Q

what are the treatments of pleural effusion?

A

thoracentesis (GOLD STANDARD); chest tube drainage (effusions)

Pathophysiology (1 decks)

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