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Pathophysiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is surfactant?

A

Active Surface Agent produced by the alveoli.

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2
Q

What does surfactant do?

A

Reduces surface tension in the alveoli allowing them to stay open

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3
Q

Definition of Perfusion

A

movement of oxygen to and into the cells

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4
Q

Definition of Diffusion

A

movement of oxygen across alveolar walls into pulmonary capillaries

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5
Q

Where is pulmonary interstitium located?

A

Between alveoli and capillary

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6
Q

What does the pulmonary capillaries of alveolar(capillary membrane) do?

A

form a network around each alveolus so dense that an almost continuous sheet of blood covers the alveoli.

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7
Q

lungs are covered by what?

A

double layered membrane called pleura

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8
Q

visceral pleura is attached to

A

lungs

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9
Q

parietal pleura is attached to

A

chest wall cavity

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10
Q

How large is each capillary?

A

Interior diameter of each capillary is just large enough to allow red blood cells to squeeze by in single file so that their cell membranes touch the capillary walls

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11
Q

CO2 and O2 do not pass through plasma when

A

diffusing in and out of the alveoli

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12
Q

Each RBC stays in the pulmonary capillary bed for about how long?

A

1 second

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13
Q

Each RBC exchanges gases with how many alveoli per second.

A

2-3 alveoli

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14
Q

What does surfactant do?

A

lowers surface tension of alveolar walls, increases lung compliance(elasticity), and eases the work of breathing

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15
Q

How often must surfactant be replenished?

A

continuously

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16
Q

What stimulates surfactant replacement?

A

normal ventilation

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17
Q

Hypoventilation leads to what?

A

decreased surfactant/alveolar collapse/atelectasis

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18
Q

What does a normal unit look like: alveoli/capillary

A

Normal ventilation, normal perfusion

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19
Q

What does a dead space unit look like?

A

Normal ventilation, no perfusion

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20
Q

What does Shunt unit look like?

A

No ventilation, normal perfusion

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21
Q

What does a silent unit look like

A

No ventilation, no perfusion

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22
Q

pulmonary embolism is an example of what kind of space

A

Dead space unit

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23
Q

How many oxygen molecules can one RBC carry?

A

1200

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24
Q

If any of the 7 steps of oxygenation get interrupted, what happens?

A

tissue becomes hypoxic (low oxygen levels)

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25
Q

What is hypoxemia?

A

decreased oxygenation of arterial blood

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26
Q

What is Hypoxia?

A

decreased oxygenation of the cell

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27
Q

List the seven steps required to transfer oxygen from environmental air into the lungs

A
  1. Ventilation
  2. Transport of O2 from alveoli into plasma and red blood cells
  3. Reversible chemical combination of O2 and CO2 with Hemoglobin(HGB)
  4. Circulation of blood from pulmonary venous capillaries to systemic capillaries
  5. Diffusion of O2from capillary blood into interstitial fluid
  6. Diffusion into cells
  7. Diffusion of O2 into mitochondria where(in combination of glucose) it helps synthesize ATP
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28
Q

Definition of oxygenation:

A

steps required to transfer O2 from environmental air into cells

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29
Q

Explain step one of oxygenation

A

ventilation of lungs-brings O2 to alveolar capillary membrane(exchange surface)

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30
Q

Explain step two of oxygenation

A

Transport of O2 from alveoli into plasma and RBCs-one RBC contains 300 HGB, Each HGB molecule can carry 4 O2 molecules, so each RBC can carry 1200 O2 molecules

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31
Q

Explain step three of oxygenation

A

Reversible chemical combination of O2 and CO2 with HGB (this is due to pressure changes)

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32
Q

Explain step four of oxygenation:

A

circulation of blood from pulmonary venous capillaries to systemic capillaries

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33
Q

Explain step 5 of oxygenation

A

Diffusion of O2 from capillary blood into interstitial fluid

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34
Q

Step 6 of oxygenation

A

Diffusion into cells

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35
Q

Step 7 of oxygenation

A

Diffusion of O2 into mitochondria where(in combination with glucose) it helps to synthesize ATP

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36
Q

Etiologies of hypoxia include:

A
  • reduced transfer of O2 from alveolar(atmospheric) air to blood(hypoxemia)
  • Impaired transport of O2 across alveolar membrane
  • ventilation/perfusion mismatch
  • decreased HGB concentration
  • decreased inspired oxygen
  • Ischemia
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37
Q

One cause of hypoxia is reduced transfer of O2 to blood, an example of this is hypoventilation, define and give some causes of hypoventilation

A

Hypoventilation is decreased rate and/or decreased depth of respirations. Some causes of hypoventilation include drug overdose, anesthesia, chest or abdominal pain, surgery, and trauma

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38
Q

Another cause of Hypoxia is impaired transport of O2 across the alveolar membrane. This diffusion capacity of alveolar membrane can be affected by what three things?

A
  • Whether surface area is available or not
  • the thickness of the membrane
  • interstitial space issues
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39
Q

Another cause/etiology of hypoxia is ventilation/perfusion mismatch. Explain this

A

Ventilation or (air into alveoli) and perfusion (pulmonary capillary blood flow) are mismatched. They should match well normally. Being mismatched causes dead space unit or shunt space unit or silent space unit.

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40
Q

Another etiology of hypoxia is Low HGB concentration also known as Anemia. Causes of anemia include:

A

blood loss, decreased production of RBCs, and decreased iron intake

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41
Q

Carbon monoxide(CO) poisoning can also cause Hypoxia by decreasing Hemoglobin production, explain CO poisoning:

A

CO combines with HGB at same site as O2

*Hemaglobin is 210x more likely to go for CO molecule that for an O2 molecule. (HGB has an affinity for CO.)

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42
Q

Another etiology of hypoxia is decreased inspired oxygen. Two examples of this include:

A
  • breathing high altitude air (in the mountains, there is not as much O2 in the air.
  • breathing air from which O2 has been removed.
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43
Q

Breathing air while on vacation in the rocky mountains could cause you to become:

A

Hypoxic

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44
Q

Being trapped in a building where there is a fire and inspiring low O2 concentrated air can cause you to become what?

A

Hypoxic

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45
Q

Two causes of low hemoglobin concentration are what?

A

anemia and CO poisoning

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46
Q

What happens during CO poisoning

A

CO combines with Hemoglobin at the same site as Oxygen does.

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47
Q

If you have Carbon monoxide in your home this may cause you to become what?

A

Hypoxic

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48
Q

If you lose a lot of blood, you may become what?

A

Anemic/Hypoxic

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49
Q

If your production of red blood cells decreases your hemoglobin level will decline and you may become?

A

Hypoxic

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50
Q

You must get enough iron in your diet so you do not become anemic in order to prevent what?

A

Low Hemoglobin levels that can lead to hypoxia

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51
Q

What is Ischemia?

A

Ischemia is decreased blood flow to tissues(O2 cannot get to where it is going)

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52
Q

Ischemia can be caused by what three things?

A
  • vasoconstriction
  • obstruction in blood vessel(blood clot in artery)
  • decreased cardiac output
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53
Q

Ischemia can be either…

A

local/regional or general/systemic

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54
Q

Local/regional ischemia is

A

local-something is blocking artery, for example:atherosclerosis of iliac arteries leading to decreased blood flow to the legs.

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55
Q

general/systemic ischemia is

A

decreased perfusion of O2 to tissues(overall), example: heart failure leading to decreased cardiac output.

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56
Q

two clinical manifestations of Hypoxia include:

A 
Increased pCO2 (percent of Carbon monoxide)
and decreased pH (respiratory acidosis)
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57
Q

To assess for Hypoxia, you would check the what?

A

Arterial blood gases-SaO2, PaO2

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58
Q

SaO2 means

A

percent of available HGB that is saturated with O2. (95-100) is good.

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59
Q

PaO2 means

A

partial pressure of O2 in arterial blood

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60
Q

early signs of Hypoxia include:

A

changes in behavior, levels of consciousness, confusion, lethargy, increased heart rate,

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61
Q

middle signs of Hypoxia include: dyspnea(shortness of breath)

A

dyspnea(shortness of breath), decreased urine output, prolonged capillary refill

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62
Q

A late sign of hypoxia is:

A

blue tinted lips, tongue, mucous membranes

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63
Q

Approximately how many alveoli do we have?

A

300 million

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64
Q

This involves the transfer of gases between air-filled spaces in the lungs and blood?

A

diffusion

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65
Q

In emphysema patients the urge to breathe is stimulated by what?

A

decreased oxygen

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66
Q

The two processes that occur during respiration are?

A

inspiration and expiration

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67
Q

In what area of the lung does respiration occur?

A

alveoli

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68
Q

What does the hypoxic drive do?

A

It stimulates a person to breathe on the basis of low oxygen levels.

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69
Q

Dyspnea is most accurately defined as?

A

shortness of breath or difficulty breathing

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70
Q

A pleural effusion is most accurately described as

A

fluid accumulation outside the lung

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71
Q

A blood clot lodged in a pulmonary artery is referred to as a

A

pulmonary embolism

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72
Q

The oxygen-carbon dioxide exchange takes place in the

A

alveoli

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73
Q

If carbon dioxide levels drops too low, the person automatically breathes:

A

slower and less deeply

slow/shallow

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74
Q

If the level of carbon dioxide in the arterial blood rises above normal, the patient breathes:

A

rapidly and deeply

fast/deep

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75
Q

The rate of breathing typically increases when?

A

carbon dioxide levels increase

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76
Q

Altered mental status is an example of?

A

Hypoxia to the brain

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77
Q

An obstruction to the exchange of gases between the alveoli and the capillaries may result from:

A

pneumonia

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78
Q

pulmonary edema can develop quickly after a major

A

heart attack

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79
Q

pulmonary edema may also be produced by

A

inhaling toxic chemical fumes

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80
Q

The loss of the elastic material around the air spaces as a result of chronic stretching of the alveoli is

A

Bronchitis

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81
Q

A patient with COPD usually presents with

A

a green, yellow, or rusty productive cough

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82
Q

A pneumothorax is a complete accumulation of air in the:

A

pleural space

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83
Q

A collection of fluid outside the lungs on one or both sides of the chest is called a

A

pleural effusion

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84
Q

Over breathing to the point that the level of arterial carbon dioxide falls below normal is

A

hyperventilation

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85
Q

Pulse oximeters measure the percentage of hemoglobin saturated with

A

oxygen

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86
Q

With a pneumothorax, the lung collapses because

A

the negative vacuum pressure in the pleura space is lost.

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87
Q

Patients with Carbon monoxide poisoning initially complain of

A

headache, fatigue, and nausea

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88
Q

Pulmonary edema is commonly associated with

A

congestive heart failure

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89
Q

COPD most often results from

A

cigarette smoking

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90
Q

Signs and symptoms of pulmonary emboli include:

A

dyspnea, hemoptysis, and tachycardia

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91
Q

What passes from blood through capillaries to tissue cells

A

oxygen

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92
Q

What are the sounds of air trying to pass through fluid in the alveoli

A

rales or crackles

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93
Q

A patient with a barrel chest and a “puffing” style of breathing most likely has

A

emphysema

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94
Q

An acute or chronic inflammation of the major lung passageways

A

bronchitis

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95
Q

accumulation of air in the pleural space

A

pneumothorax

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96
Q

Fluid build up within the ALVEOLI AND LUNG TISSUE

A

Pleural effusion

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97
Q

An infection of the lung that damages lung tissue

A

pneumonia

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98
Q

disease in the lungs in which the alveoli lose elasticity due to chronic stretching

A

emphysema

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99
Q

fluid outside the lung

A

pleural effusion

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100
Q

condition in which the body;s cells and tissues do not have enough oxygen

A

hypoxia

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101
Q

the exchange of oxygen and carbon dioxide

A

respration

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102
Q

a disease that can lay dormant in the lungs for decades, then reactivate

A

tuberculosis

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103
Q

movement of O2 to and into the cells is called

A

perfusion

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104
Q

pulmonary embolism most likely leads to a

A

dead space unit

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105
Q

surfactant does what in the alveoli?

A

decreases surface tension of alveolar walls that helps keep alveoli open

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106
Q

CO poisoning leads to

A

fewer spots for O2 to attach the the heme

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107
Q

two early signs of hypoxia

A

change in behaviorLOC/ increased HR

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108
Q

two late signs of hypoxia

A

decreased BP/cyanosis

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109
Q

The pressure in the pleural space is normally:

A

A bit less than atmospheric pressure

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110
Q

What is the term for “collapse of alveoli”? What to things would you expect to hear for lung sounds?

A

Atelectasis- crackles/diminished lung sounds

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111
Q

List four labs you might seek out if you were worried about oxygenation…

A

pO2, pCo2, SaO2, HGB

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112
Q

Pleural effusion includes

A
  • fluid in pleural space
  • usually a disease process(fluid, blood,pus)
  • pushes on lung tissue
  • atelectasis
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113
Q

pneumothorax includes

A
  • air in pleural space
  • destroys negative pressure
  • lung collapses
  • atelectasis to full collapse
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114
Q

Both pneumonia and tuberculosis have a

A

vaccine

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115
Q

pneumonia and TB both are transmitted via

A

respiratory droplet route

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116
Q

pneumonia can be caused by any bacteria or virus but TB is specifically caused by

A

mycobacterium tuberculosis

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117
Q

Tuberculosis facts

A

infected get a tubercle lesion, can be dormant or active. symptoms are similar of that of pneumonia, but they also consist of night sweats, and a cough that starts out non-productive and ends up productive after a few weeks. Must get CXR

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118
Q

A pulmonary emboli is usually seen in someone at risk for

A

blood clots

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119
Q

What is the most common etiology of pulmonary edema?

A

Left ventricular heart failure

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120
Q

In pulmonary edema, fluid enters the interstitial space due to which pressure change?

A

increased pulmonary capillary hydrostatic pressure

121
Q

Chronic bronchitis

A

increased thick mucous
inflamed thick bronchial walls
wheezing
purulent sputum production

122
Q

emphysema

A 
alveolar destruction/loss of recoil
air trapping/alveolar deadspace
extreme dyspnea
little cough or sputum
-barrel chest
-pursed lip bleeding
123
Q

Esophageal atresia:

A

food can’t get down

124
Q

trachea-esophageal fistula

A

high risk for aspiration into the lungs

125
Q

pyloric stenosis

A

constipation, vomiting(and aspiration), fluid and electrolyte imbalances

126
Q

Transmural:penetrate the entire wall. Examples:

A

skip lesions, fissures, fistulas, strictures, intestinal obstruction

127
Q

Which usually starts in the rectum and extends into the sigmoid colon?

A

ulcerative colitis

128
Q

Explain why very sick patients in ICUs are at risk for stress ulcers.

A

Acute major body “insult” leads to blood being shunted away from the mucosal lining of the gut…also known causing ischemia ..Mucosal cells then degenerate leading to erosions

129
Q

Which peptic ulcer disease does not have excess acid production?

A

Gastric ulcers(problem is the barrier(mucosal lining) is broken down

130
Q

which peptic ulcer disease has a predictable pattern of pain?

A 
duodenal ulcers(high acid production)
pain, then food, then relief
131
Q

Rhabdomyolysis or myoglobinuria pathophysiology:

A

muscle cell damage, leads to myoglobin released(into bloodstream), it passes through kidney nephrons, can either pass through the urine, or cause intratubular obstruction that leads to kidney damage.

132
Q

there are two kinds of atelectasis, they are:

A

compression atelectasis and absorption atelectasis

133
Q

compression atelectasis is

A

external pressure usually caused by tumor or fluid

134
Q

absorption atelectasis is

A

internal obstruction usually caused by secretions or fluid in the alveoli

135
Q

clinical manifestations of atelectasis include

A 
rales/crackles
decreased breath sounds
dyspnea, cough, fever
decreased pO2and SaO2
Increased pCO2
136
Q

Etiologies and pathophysiology of pleural effusion(fluid in pleural space)

A

transudate(hydrothorax)-water accumulation(usually under the visceral pleura)-caused by cardiac, liver, and kidney disease
exudate-fluid is increased in proteins, caused by infection, can be malignancy
pus(empyema)-infection
blood(hemothorax)-caused by trauma or thoracic surgery

137
Q

Clinical manifestations of Pleural effusion

A

atelectasis-fluid displaces lung tissue
dyspnea, chest pain, mediastinal shift(if large amounts of fluid)
mediastinal organs(heart, trachea, great vessels-pushed to opposite side of fluid.

138
Q

pneumothorax is

A

the presence of air in the pleural space

139
Q

some causes of a pneumothorax include

A

fractured ribs, ruptured bleb(COPD), thoracotomy, or can be spontaneous

140
Q

pathophysiology of a pneumothorax is

A

-air enters the pleural space
-negative pressure is destroyed
lung collapses

141
Q

clinical manifestations of a pneumothorax include

A

dyspnea
chest pain
hypoxia
absent breath sounds in affected lung area

142
Q

Tension pneumothorax is usually caused by

A

trauma

143
Q

Pathophysiology of Tension Pneumothorax

A

air enters the pleural space on aspiration and then can’t escape on expiration
(wound acts as a one way valve)
Air continues to build up in pleural space

144
Q

Clinical manifestations of a tension pneumothorax include:

A

mediastinal shift(like in pleural effusion)
hypoxia
dyspnea
decreased blood pressure

145
Q

Definition of pneumonia

A

acute infection in lungs caused by bacteria, viruses, or fungi. (caused by LOWER respiratory infection)

146
Q

Pathophysiology of pneumonia

A

aspiration of microbial agent(bacteria/virus/fungus), which causes an inflammatory response, causing alveoli to fill with excavate, then there is phagocytosis in the alveoli that results in the resolution of the infection

147
Q

Manifestations of pneumonia include:

A

fever, chest pain, increased respiratory rate, Rusty brown or yellow colored sputum, increased WBC, CXR infiltrates

148
Q

A pulmonary emboli is a

A

thrombus that travels(also known as a blood clot)

149
Q

A pulmonary emboli usually travels in in a

A

pulmonary artery

150
Q

Definition of pulmonary emboli is

A

an occlusion that lodges in a pulmonary artery….it is a blockage of an artery in the lungs by a substance that has traveled from elsewhere in the body through the bloodstream (embolism).

151
Q

the four types of emboli are

A 
1.blood clot(thrombus)-most common type
(usually thrombus originates in deep calf veins
2. tissue fragment
3. fat emboli
4. air bubble
152
Q

Causes of pulmonary emboli include:

A
  1. venous stasis-prolonged bedrest, obesity, chronic atrial fibrillation without anticoagulation, heart failure, central venous catheter
  2. vessel injury such as trauma or surgery
  3. history of prior embolus/thrombus
153
Q

Pathophysiology of a pulmonary emboli

A

thrombus(clot formation), then dislodgment of thrombus, which leads to occlusion of part of pulmonary circulation, which can then go one of two ways: resolution of clot-it is absorbed/dissolved(fibrinolytic system), sometimes leaving scar tissue also known as an infarction caused by tissue death OR it can cause increased pulmonary artery pressure that can lead to R ventricular failure, severe shock and even sudden death.

154
Q

Clinical manifestations of a pulmonary emboli depends on the severity of pulmonary emboli:

A 
there could be no symptoms(silent)
sudden dyspnea
fever
cough
tachycardia
hemoptysis(coughing up of blood)
chest pain
hypoxemia/hypoxia
155
Q

Definition of acute respiratory failure:

A

Inadequate gas exchange(to meet tissue oxygenation needs at rest) A term applied to a pulmonary disease that meets the criteria of pO2 less than 50mmHg
or pCO2 more than 50 mmHg

156
Q

Acute Heart failure leading to pulmonary edema(flash) definition:

A

accumulation of fluid in the pulmonary interstitial space and into the alveoli

157
Q

causes of Acute heart failure are

A

Left ventricle heart failure(most common cause)
-mitral stenosis
-alveolar capillary damage
volume overload

158
Q

Pathophysiology of Acute Heart Failure(Flash)

A
  • increase in pulmonary capillary hydrostatic pressure

- fluid leaks into pulmonary interstitial space , then go into alveoli, which dilutes surfactant and causes atelectasis

159
Q

Manifestations of AHF include

A

dyspnea-labored difficult breathing
orhtopnea-SOB that occurs when lying flat
paroxysmal nocturnal dyspnea-SOB attack when asleep-a sensation that wakes the person up
crackles(rales),rhonchi
Hemoptysis/pink, frothy sputum
Hypoxia

160
Q

Tuberculosis:

A

Lung infection caused by mycobacterium tuberculosis bacteria.

161
Q

All three of these are necessary for definite diagnosis of TB.

A

positive skin test, positive sputum culture, positive chest X-ray

162
Q

clinical manifestations of TB include:

A

fatigue, weight loss, low grade fevers, night sweats, cough-non-productive to productive in a few weeks, becomes very purulent (a lot of sputum)

163
Q

TB skin on test is negative it can mean

A

person has never been exposed OR exposed, but not infected(TB is dormant)

164
Q

TB skin test that is positive can mean

A

has been infected, but has no disease OR has active TB disease

165
Q

pathophysiology of TB:

A

TB transmitted via airborne respiratory droplets(laughing, sneezing, coughing), it is inhaled into lung and TB starts to multiply, inflammation occurs(neutrophils and macrophages migrate to area)
a tubercle lesion forms causing necrosis of infected tissue lead to dormant or active TB. Dormant TB still needs treated but is not contagious like active TB is.

166
Q

Chronic Obstructive Pulmonary Disease

A

obstruction of Air flow that causes difficulty of expiration(breathing out)

167
Q

two types of COPD include

A

chronic bronchitis and emphysema

168
Q

Chronic bronchitis

A

hypersecretion of mucous and chronic cough

169
Q

Causes of Chronic Bronchitis

A

chronic inhaled irritation, cigarette smoking, air pollutions, infections

170
Q

Pathophysiology of Chronic bronchitis:

A

inhalation of irritants,increases development of thick mucous, this causes ciliary function to become decreased, which makes you not be able to clear mucous, causing increased susceptibility to infection, causes inflamed and thick bronchial walls, which leads to airway obstruction(especially during expiration)

171
Q

Manifestations of Chronic Bronchitis are:

A

wheezing, dyspnea, productive cough, decreased exercise tolerance, repeated respiratory infections, yellow, green, rusty sputum, hypoxia with respiratory acidosis, cyanosis

172
Q

Emphysema:

A

Emphysema is the destruction of alveolar walls, loss of elastic recoil, obstruction from changes in lung tissue rather than mucous production and inflammation

173
Q

the two causes of emphysema include

A

cigarette smoking or Alpha Antitrypsin deficiency(genetic deficiency of enzyme that keeps lung tissue from breaking down)

174
Q

Pathophysiology of emphysema:

A

alveolar destruction, increased air in alveoli,(air trapping), leads to collapse of small airways which leads to decreased alveolar diffusing surface, which causes decreased gas exchange between O2 and CO2

175
Q

manifestations of Emphysema

A 
dyspnea-SOB(especially on exertion) DOE
hypoxia with respiratory acidosis
cyanosis
no cough/little sputum production
Increased anterior/posterior to lateral diameter of chest "barrel chest" 
frequent respiratory infection
176
Q

tendon

A

fibrous connective tissue that attaches skeletal muscle to bone

177
Q

ligaments

A

fibrous connective tissue that connects bones where they meet at joint

178
Q

A tear or rupture in a tendon(may be accompanied by a fracture)

A

Strain

179
Q

A tear or rupture of a ligament

A

sprain

180
Q

a complete separation of a tendon or a ligament from the bone

A

avulsion

181
Q

clinical manifestations of strain, sprains, and avulsions include:

A

sharp localized pain and tenderness

soft tissue swelling

182
Q

local muscle damage from sudden, forced motion, causes muscle to to be stretched beyond normal capacity

A

muscle strain

183
Q

Etiologies of muscle strains

A

sports injuries/trauma

184
Q

Pathophysiology of a muscle strain is

A

Hemorrhage into surrounding tissue and inflammation present. Manifestations include pain and bruising

185
Q

Rhabdomyolysis or Myglobinuria is defined as

A

A life threatening complication of severe muscle trauma.

186
Q

Causes of Myglobinuria include

A

burns, trauma such as crush syndrome, or compartment syndrome, extreme exertion

187
Q

Pathophysiology of Myglobinuria/Rhabdo:

A

Increased pressure within the muscle fibers
edema, muscle ischemia, muscle infarction,
Muscle cell damage(rupture of the sarcelomma) releases myoglobin(an intracellular protein)
Myoglobin is detected in the urine where it is not normally found.

188
Q

Clinical manifestations of Myglobinuria include

A

Dark, reddish brown urine,

can lead to acute renal failure (intratubular obstruction)

189
Q

Adult forms of muscular dystrophy include

A
  • Becker’s
  • limb/girdle
  • facioscapulohumeral
  • myotonic
190
Q

Duchenne Muscular Dystrophy is

A

a genetic disorder characterized by progressive muscle degeneration due to no production of the protein dystrophin

191
Q

Etiology(cause) of DMD is

A

AN X-linked recessive disorder that affects 1 in 3500 male births.

192
Q

Pathophysiology of DMD is

A

there is a gene defect causes no production of dystrophin (protein that controls calcium release that is necessary for muscle fiber contraction)
this causes a decrease of and necrosis of muscle fibers, increase of connective tissue(causing fibrosis) and fat(causing fatty infiltration) which replace muscle fibers: pink or yellowish pink replaces dark red staining of muscle fibers
Elevated serum enzymes(CPK,Creatine phosphokinase test, LDH, Lactate dehydrogenaseSGOT)SGOT: Serum glutamic oxaloacetic transaminase)muscle cell membranes

193
Q

Clinical manifestations of DMD

A

-onset is 3 years of age
-progression: rapid lower extremity weakness, progresses up to chest and head muscles
-waddling gait, delayed sitting and walking, falls
-Shoulder girdle muscle weakness 3-5 years after onset
kyphoscoliosis causes pulmonary dysfunction(muscle weakness causes twisting of mediastinal organs)
-cardiac dysfunction(chronic congestive failure) common
death usually in 20’s and 30’s due to respiratory and cardiac involvement.

194
Q

Digestion

A

the process takes substances in one form and breaks them down into molecules small enough to pass through the intestinal wall

195
Q

Mouth

A

the mouth is the beginning point, with ingestion of food. Major functions include chewing and saliva secretion(a liter to a liter and a half of saliva is secreted each day)

196
Q

What enzyme in the mouth starts some of the carbohydrate breakdown?

A

salivary amylase(ptyalin)

197
Q

Pharynx

A

In the pharynx, food is swallowed and moved into the esophagus, at this time the trachea is closed off.

198
Q

Esophagus

A

The esophagus, a muscular tube which lies behind the trachea, initiates peristalsis

199
Q

Pyloric sphincter

A

The sphincter allows the stomach to empty and prevents back flow into the stomach from the small intestine.

200
Q

Small intestine

A

small intestine includes the duodenum, jejunum, and ileum, the major function of the small intestine is absorption of nutrients:approximately 90% of the available nutrients are absorbed into the blood stream in the small intestine

201
Q

Large intestine

A

Large intestine includes ascending, transverse, descending, and sigmoid colon.. Major functions of the large intestine are absorption(mostly of water and electrolytes) and the formation of wastes.)

202
Q

Rectum and anal canal

A

primary function is excretion of wastes

203
Q

Tracheo-esophageal fistula

A

cells of the embryonic foregut fail to differentiate during the developmental period. Normally the trachea separates from the esophagus during weeks 4 through 6 of embryonic development, while in TEF, the foregut fails to separate into a totally separate esophagus and trachea, resulting in a patent fistula(open connection) between the two structures.

204
Q

Clinical manifestations of TEF:

A

Manifestations relate to the fact that there is no normal pathway from the esophagus down to the stomach, and that there is an opening between the trachea and either the esophagus or the stomach. Manifestations usually occur very soon after birth(especially with the first feeding)

205
Q

Clinical manifestations of TEF continued

A
  • Infants are unable to handle oral secretions(swallowing leaves nowhere to go)and they appear to have increased oral secretions.
  • coughing, choking, spitting up of feedings
  • aspiration into lungs is a potential complication
  • abdominal distention with the type in example c (they swallow air)
206
Q

Pyloric stenosis

A

a genetically -influenced abnormal narrowing of the pyloric sphincter that connects the stomach and the small intestine:the condition occurs between 1 and 200 male infants, and 1 in 1000 in female infants

207
Q

Stress ulcers usually occur

A

after a major insult to the body (shock, burns, drug ingestion, severe infection)
-the development of stress ulcers is acute instead of chronic.

208
Q

The pathophysiology of stress ulcers is

A

related to ischemia, the major insult to the body leads to shunting of blood away from the gut. this leads to decreased metabolism of mucosal cells, and then degeneration of the mucosal lining. The mucosa is then unable to protect itself from the acid in the GI tract.

209
Q

Stress ulcers tend to be

A

superficial gastric erosions, they tend to be multiple and diffuse, and can occur in the stomach and duodenum. A characteristic is that they DO NOT penetrate the muscular.

210
Q

Ulcerative colitis is a

A

chronic inflammatory disease that causes ulceration of the colonic mucosa usually in the rectum and sigmoid colon; onset usually takes place between 20 and 40 years of age.

211
Q

causes of ulcerative colitis include:

A 
genetic/familial
infectious
immunologic
psychosomatic
dietary
212
Q

pathophysiology of ulcerative colitis

A
  • Inflammatory process begin
  • mucosa becomes hyperemic and edematous
  • causes mucosal hemorrhages
  • leads to ulcerations/mucosal destruction
  • leads to sloughing off of the mucosa
  • there are periods of exacerbations and remissions
213
Q

Clinical manifestations of ulcerative colitis

A
  • cramping abdominal pain
  • bloody, mucousy diarrhea
  • fluid and electrolyte imbalances
  • weight loss
  • anemia
214
Q

Chron’s disease is a

A

chronic, inflammatory disorder that can affect both the large and small intestines

215
Q

Pathophysiology of Crohns

A

an inflammatory process starts in the submucosa
it spreads inward and outward
causes skip lesions/transmural lesions(lesions that affect the entire width of the wall, but affect certain segments and not others.)
strictures-can lead to obstruction/occlusions
fissures can extend inflammation

216
Q

clinical manifestations of Crohns (Regional Enteritis)

A
  • individuals may have non-specific diarrhea for several years
  • non-bloody diarrhea
  • abdominal pain usually in the RLQ
  • fluid and electrolyte imbalance
  • vitamin deficiencies and hypoproteinemia
  • weight loss
  • a complications that occur related to strictures is intestinal obstruction
  • a complication that can occur related to formation of fissures is fistulas, and possible peritonitis
217
Q

affects mucosa, is extensive but superficial, does not have skip lesions and is not a small intestinal disease…surgery-cure

A

ulcerative colitis

218
Q

effects entire wall of intestine(transmural), is patchy but deep, has skip lesions, is a small intestinal disease, and has frequent recurrence even after surgery, with no cure

A

Crohn’s disease

219
Q

There are two types of peptic ulcer disease

A 
gastic ulcers(less common/more chronic)
and
duodenal ulcers(pain goes away after eating)
220
Q

Gastric ulcers are

A

ulcers of the gastric mucosa(the stomach) and are less common then duodenal ulcers;they occur equally in men and women, and most frequently occur between 55 and 65 years of age

221
Q

Gastric ulcer risk factors include:

A
  • smoking
  • meds(non-steroidal anti inflammatory drugs)
  • alcohol
  • chronic disease
  • psychological stress
  • infection(H. pylori) is found in most ulcers
222
Q

Pathophysiology of Gastric ulcer

A

mucosal barrier has increased permeability to H+
this leads to back-diffusion of acid
this leads to ulceration

223
Q

clinical manifestations of gastric ulcers include:

A

usually upper abdominal pain that is normally intermittent, but has no particular pattern.
Gastric ulcers seem to be more chronic(last longer)

224
Q

duodenal ulcers

A

occur more frequently than gastric ulcers, usually affect younger people than gastric ulcers, men and women are equally affected

225
Q

cause of duodenal ulcers is

A

the hypersecretion of acid and/or pepsin (pepsin is a hormone of digestion that is a proteolytic enzyme)

226
Q

Pathophysiology of duodenal ulcers

A

increased acid concentrations
penetrate the mucosal barrier
leads to ulceration

227
Q

clinical manifestations of duodenal ulcers include:

A

chronic intermittent epigastric pain that usually follows a particular pattern of “pain-food-relief”
pain occurs and is usually relieved after eating
pain may reoccur 2 to 3 hours after eating.
can cause hemorrhage/perforation

228
Q

Bones have three major functions:

A
  • give form to the body
  • support tissues
  • permit movement
229
Q

Twelve major bone disorders include:

A

fractures, paget’s disease(osteitis deforming), gout, osteomyelitis, osteoporosis, degenerative joint disease/osteoarthritis,osteogenic sarcoma
scoliosis, osteomalacia(rickets), congenital hip dysplasia, talipes equinovarus, dislocation/subluxation

230
Q

definition of a fracture is

A

a break in a bone due to a force that exceeds the strength of the bone

231
Q

the highest incidence of fractures occurs in

A

young males from trauma and the elderly from osteoporosis

232
Q

bone is broken all the way through

A

complete fracture

233
Q

a bone is damaged but is still in one piece

A

incomplete greenstick fracture

234
Q

bone breaks through the skin

A

open(compound) fracture

235
Q

skin is not broken by the bone is an example of

A

closed(simple) fracture

236
Q

when several pieces of bone get fractured it is called

A

comminuted fracture

237
Q

parallel to bone

A

linear fracture

238
Q

45 degree angle to shaft of the bone

A

oblique fracture

239
Q

encircles bone, displaced by twist

A

spiral fracture

240
Q

straight across(horizontal)bone

A

transverse fracture

241
Q

fracture at the site of disease(tumor or osteoporosis)

A

pathologic fracture

242
Q

from repeated stress on a bone(athletes)

A

stress fracture

243
Q

fractures of the what in children can interrupt normal growth?

A

epiphysis

244
Q

Functions of the Gi tract include

A
  • ingestion of food
  • motility(propulsion of food and wastes) (peristalsis) Neural control of motility is mostly through the parasympathetic nervous system via the vagus nerve and some intrinsic control
  • secretion of mucous, H2O, and enzymes
  • mechanical digestion of food particles
  • chemical digestion of food particles
  • absorption of digested food
  • elimination of waste products(defecation)
245
Q

Pathophysiology of fractures

A
  • bleeding of broken ends of bones
  • hematoma(clot)>fibrous network
  • osteoblasts(bone forming cells), collagen strands and deposit calcium
  • callus formation(new bone)
  • remodeling(excess callus is resorbed and mature bone is formed
246
Q

manifestations of fractures include:

A
  • abnormal alignment
  • immediate pain
  • loss of function/sensation
  • swelling
  • spasm
  • blood loss
  • crepitus(audible clicking sounds of fractured bone with movement)
247
Q

a potentially lethal problem after long bone fracture(fat globules are released from bone marrow and travel in the blood and lodge in the lung.

A

Fat emboli

248
Q

Localized abnormal and excessive bone remodeling(bone formation and resorption0which eventually enlarges and softens the affected bone:commonly affects the vertebrae, skull, sacrum, sternum, and pelvis

A

paget’s disease(osteitis deformans)

249
Q

causes of Paget’s disease

A

unknown for the most part(may follow inflammation, virus bone tumors, autoimmune dysfunction)

250
Q

pathophysiology of Paget’s disease

A
  • excessive resorption of spongy bone
  • fibrous tissue replace bone marrow
  • abnormal new bone forms
251
Q

Manifestations of Paget’s disease

A
  • Bone deformity (barrel chest, bowing of legs, and kyphosis(hunch back)
  • bone pain
  • fractures
252
Q

A disorder that disrupts the body’s control of uric acid production or excretion, that may follow traumatic injury or joint strain

A

GOUT

253
Q

Etiology of Gout

A
  • Excessive serum uric acid (lack of execution or excessive production):
  • increased production of uric acid
  • increased rate of purine (end product of nucleoprotein digestion) synthesis
  • purines break down to uric acid
  • increased production of uric acid
  • Decreased excretion of uric acid
  • renal failure(decreased exception of uric acid) causes urate crystals
  • form and deposit in kidneys
254
Q

Pathophysiology/manifestations of gout

A
  • when uric acid reaches a certain concentration, it crystallizes
  • urate crystals cause joint inflammation and renal stones
  • increased serum uric acid (rate)
  • hot, red, tender joint(usually peripheral)(outer edges of joints)
255
Q

bacterial, fungal, parasitic or viral bone infection

A

osteomyelitis

256
Q

Osteomyelitis is caused by

A

open bone from surgery or trauma

blood bourne from other sites of infection

257
Q

Pathophysiology of osteomyelitis

A
  • pathogen in bone causes inflammatory response
  • abscesses form (lifts periosteum off underlying bone
  • pressure from abscess causes decreased blood supply to bone which causes necrosis
  • osteoblasts form new bone
258
Q

Manifestations of osteomyelitis

A

acute: fever,chills, bone pain, weight loss
chronic: if inadequate antibiotics: drug-resistant bacteria

259
Q

reduced bone density

A

osteoporosis

260
Q

Osteoporosis Incidence

A
  • most common metabolic bone disease
  • incidence increases with age
  • most common in caucasian females
261
Q

Causes of osteoporosis

A
  • decreased estrogen after menopause(estrogen normally inhibits bone resorption)
  • decreased dietary calcium and vit. D.(decreased absorption of these in elderly)
  • increased caffeine, nicotine, alcohol(causes loss of calcium from bone)
  • Renal Failure(nephrons unable to remove excess PO4)
    • increased PO4(PO4 binds with calcium)
    • decreased calcium(stimulates increased production of parathyroid hormone(PTH)
    • PTH overstimulates osteoclaststo remodel (loss of CA++ from bone)
262
Q

Pathophysiology of osteoporosis

A
  • increased rate resorption by osteoclasts
  • decreased rate of bone formation by osteoblasts
  • net decrease in bone density
263
Q

Manifestations of osteoporosis

A

bone pain, bone deformity such as kyphoscoliosis (hunch back), fractures, and loss of height

264
Q

Degenerative Joint Disease (osteoarthritis)

A

degeneration and loss of articular surfaces in synovial joints

265
Q

Osteoarthritis or DJD is caused by

A

mechanical joint stress, trauma, age, wear and tear

266
Q

Pathophysiology of osteoarthritis (DJD)

A
  • loss of articular cartilage(flakes off and becomes thin or absent)
  • bone becomes dense and hard
  • bone spurs form and (grow outward from bone)
267
Q

Manifestations of Osteoarthritis include:

A
  • joint pain and stiffness
  • -swelling
  • decreased range of motion of joint
  • deformity
268
Q

Large, destructive malignant bone tumor found in the metaphyses of long bone(femur). Can be rapidly fatal with lung metastasis . usually in adolescents, can be overlooked as a sports injury

A

Osteogenic Sarcoma

269
Q

Pathophysiology of Osteogenic Sarcoma

A
  • bone marrow has a moth eaten pattern of destruction
  • anaplastic cells (atypical/abnormal cells)
  • tumor destroys bone
  • tumor breaks through periosteum and can form a soft tissue mass
  • bone pain worsens at night
  • causes increased alkaline phosphate(enzyme produced by osteoblasts)
270
Q

impaired absorption of fats, carbohydrates, proteins, vitamins, minerals, H2O, and/or electrolytes over into the bloodstream

A

malabsorption

271
Q

Many malabsorption disorders are also called:

A

inflammatory bowel disorders because with many of these, there is an inflammatory reaction in the intestines that is causing the malabsorption of nutrients

272
Q
  • Incomplete digestion of nutrients. An example of this is if there is deficient enzymes of digestion(like lactase), if this is the case, lactose cannot be broken down into monosaccharides
  • Abnormalities of the absorptive surface
  • bochemical or genetic. (celiac enteropathy)
  • inflammatory or infectious disorders causing abnormalities with the absorptive surfaces (Crohns is an example of inflammatory disorder)
  • Lack of absorptive surface area(necrotizing enterocolitis)
A

General causes of malabsorption

273
Q

The intestinal wall is made up of many villi(tiny folds), these folds greatly increase the absorptive surface area which helps with absorption over into the bloodstream of the broken down products.

A

Absorption

274
Q

In the grooves between the villi are the crypts of lieberkuhn which contain two types of cells:

A

cells that secrete intestinal juices

absorptive cells

275
Q

Excess serum sodium levels Na+

A

Hypernatremia

276
Q

Etiologies of Hypernatremia

A

1) Acute Na+ gain-
- H20 is redistributed to ECF
- ICF dehydration
2) H2O loss
- both ECF and ICF dehydration

277
Q

Manifestations of Hypernatremia

A
  • Hyperosmolarity in the blood
  • Intracellular dehydration
  • If Acute NA+gain, fluid moves from ICF to ECF, this causes HYPERVOLEMIA
278
Q

Severe muscle trauma leads to release of myoglobin, a protein, into the bloodstream. Renal threshold for myoglobin is low. Excess myoglobin in the kidney tubules causes tubular obstruction, this can lead to

A

Renal failure

279
Q

What is the difference between a ligament and a tendon? .

A

Both are connective tissue. A ligament connects two bones together at a joint. A tendon connects a skeletal muscle to bone.

280
Q

The first component of Paget’s disease is excess resorption of spongy bone (old bone is broken down faster than new bone can be built). The second component is generation of new bone at a faster than normal, new collagen fibers are disorganized. Last, abnormal new bone forms, but the body uses fibrous tissue to replace bone marrow, so the bones are softer and weaker, and susceptible to fractures and deformities.

A

Paget’s Disease

281
Q

Ways to prevent osteoporosis include

A

(1) Weight bearing exercises require the use of muscles and tendons. So they pull on the bones, and this (a) decreases bone and calcium resorption (loss) and (b) stimulates osteoblasts to form new bone. These exercises also strengthen muscles to prevent fractures and falls.
(2) The hormone estrogen stimulates osteoblast activity and depresses osteoclast activity. Without the hormone estrogen, there is an increase in bone resorption (loss).
(3) Calcium decreases bone resorption and stimulates osteoblast function.
(4) Vitamin D is needed for gastrointestinal absorption of calcium. A deficiency of Vitamin D is also associated with increased PTH levels which stimulates bone resorption.

282
Q

Gout summarized

A

The excessive production of serum uric acid is due to an increased rate of purine synthesis. Purines break down into uric acid so uric acid would elevate. Lack of excretion generally occurs in renal failure. Uric acid can crystallize and deposit in and obstruct the tubules possibly leading to renal failure.

283
Q

Example of a shunt unit (no ventilation/normal perfusion)

A

pulmonary edema-fluid on lungs collapsing alveoli causing abnormal ventilation/another example is Tumor

284
Q

Example of a dead space unit(normal ventilation/no perfusion)

A

pulmonary embolism because the clot would block perfusion

285
Q

Low serum sodium levels is

A

Hyponatremia

286
Q

Causes of hyponatremia include

A
  • Na+ loss(sweating/vomiting)
  • restricted intake
  • Excess water gain
287
Q

manifestations of hyponatremia include:

A

hypoosmolarity
altered cellular depolarization and repolarization
might see lethargy or confusion

288
Q

Dysfunctional wound healing can be caused by

A
  • Ischemia-lack of oxygen delivery
  • wound infection
  • excessive bleeding(low platelets)
  • diabetes mellitus
  • malnutrition
  • medications
  • dehiscence(pulls apart at the sutured incision line
289
Q

risks for dehiscence include:

A

infected incision, excessive strain, obesity

290
Q

The three phases of wound healing are:

A

Phase 1:Inflammation
Phase 2:Proliferation and New tissue formation
Phase 3:Remodeling and maturation

291
Q

Phase one of wound healing:Inflammation:

A
  • Occurs first 1-2 days
  • Involves the recruitment of :
  • platelets(clot formation)
  • neutrophils for (clearing necrotic debree and bacteria out
  • macrophages
292
Q

Phase two if wound healing:Proliferation and New Tissue Formation:

A
  • Occurs from day 3 or 4 to two weeks
  • Involves recruitment of fibroblasts/growth factors
  • Granulation of tissue/collagen
293
Q

Phase three: Remodeling and maturation

A
  • Occurs weeks after injury to to years
  • Tissue regeneration
  • fibroblasts and collagen activity continue
  • End result is either normal tissue structure or scar formation
294
Q

Excess serum potassium levels

A

Hyperkalemia

295
Q

etiologies(causes) of hyperkalemia include:

A
  • increased intake of potassium
  • renal failure
  • shift from ICF to ECF
  • burns/trauma-cells lice(break up)
  • acidosis-H+ build up in the blood(needs to get rid of H+ to get PH balanced
296
Q

manifestations of hyperkalemia:

A
  • cells are more excitable
  • restlessness
  • intestinal cramping/diarrhea
  • muscle weakness
  • cardiac rhythm problems
297
Q

Low serum Potassium levels

A

Hyponatremia

298
Q

Hyponatremia is caused by

A
  • decreased intake
  • increased loss(vomiting/diarrhea) -GI/Renal
  • shift from ECF to ICF
  • Alkalosis
  • to few H+ in the blood
299
Q

manifestations of hyponatremia:

A

decreased neuromuscular excitability
loss of smooth muscle tone
cardiac rhythm problems

Pathophysiology (4 decks)

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