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Pathophysiology 1 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Define stress

A

a state of real or perceived threat to homeostasis

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2
Q

Which two body systems control homeostasis?

A

neuro and endocrine

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3
Q

What is the major regulator of homeostasis?

A

hypothalamus

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4
Q

Why is homeostasis important?

A

maintains optimum cell structure and function

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5
Q

Define stressor

A

any external or internal stimulus (variable) that causes a change in the internal homeostatic balance (creates imbalance)

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6
Q

What are the two types of stressors? (this will be a question on the exam)

A

Distress– bad stress, ex. genetic, congenital or acquired stress that damages the body

Eustress– good stress, ex. exercising, which energizes and motivates the body

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7
Q

What is the difference between signs and symptoms?

A

signs– measurable

symptoms– subjective

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8
Q

Define allostasis

A

the process of the body trying to adapt to change– is a compensatory mechanism caused by chronic change to the homeostatic set point of a variable

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9
Q

Describe allostatic overload

A

when the body is not able to adapt to stress– from chronic or severe stress

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10
Q

Describe General Adaptation Syndrome (GAS)

A

-how our body responds to a stressor
-described by Dr Hans Selye in 1946
-a more thorough version of the fight-or-flight response
2 main factors determine an individual’s response to a specific stressor:
-the specific event or environmental stressor
-the conditioning of the individual experiencing the stress–
including how they cope with the stressor

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11
Q

What are the 3 stages of GAS?

A

1) alarm reaction (fight or flight)– norepinephrine was released during a sympathetic NS response
2) resistance reaction– allostasis/adaptation/allostatic load
3) exhaustion stage (allostatic overload)– onset of stress-related issues occurs

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12
Q

What are the physiological effects of NE and epi?

A

increase perfusion/mobilize resources (ex. glucose) to organs vital to survival; those deemed non-vital to survival have perfusion decreased

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13
Q

What are the categories of stressors?

A

chemical, physical, and psychological

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14
Q

What reaction does prolonged stress trigger?

A

the resistance reaction by the HPA

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15
Q

What does hypothalamic CRH trigger?

A

anterior pituitary ACTH and then adrenal cortex cortisol

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16
Q

Name some stress related diseases

A

HTN, cancer, diabetes, allergies

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17
Q

Name some coping strategies

A

meditation, deep breathing, exercise

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18
Q

What is the formula for cardiac output?

A

CO=SVxHR

CO is cardiac output (volume of blood pumped per minute)
SV is stroke volume (volume of blood pumped)
HR is heart rate (beats per minute)

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19
Q

What affects stroke volume?

A

3 variable: preload, contractility, and afterload

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20
Q

Describe preload

A

the “fill”; the volume of blood that fills the ventricle during ventricular diastole (ventricles at rest)– it is related to the rate of venous return and is equal to the end diastolic volume (EDV)

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21
Q

Describe contractility

A

the “push”; the force of contraction produced by cardiac muscle cells– Frank-Starling’s Law of the Heart states that contractility is directly affected by preload and thus directly affects SV and CO

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22
Q

Describe afterload

A

the “squeeze”; this is the resistance cardiac muscle must overcome to pump blood through the aortic valve->aorta->aortic branches– afterload opposes forward flow of blood and thus inversely affects SV and CO
Increase in afterload is a sign aortic valve disorder or an issue with the aorta itself

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23
Q

What is the purpose of the surfactant secreted by type II alveolar cells?

A

to coat the inside of the alveoli as an oil to reduce surface tension so that the cell doesn’t break when it expands during inspiration

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24
Q

What is between the inner and outer layers of the capillary?

A

type 4 collagen (egg shaped cell)– this is the collagen that is destroyed during emphysema in COPD patients

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25
Q

Explain the V/Q ratio

A

ventilation (air coming in) divided by perfusion (blood flow)– should equal to close to 1 for maximum amount of respiratory gas exchange

expresses the effectiveness of gas exchange

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26
Q

What is the pH of blood?

A

between 7.35 and 7.45– controlled by the amount of bicarbonate in the blood and the amount of carbon dioxide given off by your lungs

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27
Q

What happens if blood pH is off?

A

protein misfolding, enzyme damage, DNA damage, etc.

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28
Q

What compromises respiratory function?

A
  1. inadequate blood flow to pulmonary capillaries
  2. inadequate airflow to the alveoli
  3. inadequate exchange of respiratory gases between pulmonary capillaries and alveoli
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29
Q

What are the three basic causes of respiratory disease?

A
  1. hypoperfusion
  2. hypoventilation
  3. inadequate gas exchange
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30
Q

Define hypoperfusion

A

too little blood flow through the lungs– main causes are heart failure and pulmonary embolism

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31
Q

Define hypoventilation

A

too little gas diffusion in the alveoli– main causes are airway obstruction and restricted lung expansion

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32
Q

What is an acceptable V/Q ratio?

A

ideal is as close to 1 as possible– so between 0.8 and1.2

<0.8 means more perfusion than ventilation
>1.2 means more ventilation than perfusion

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33
Q

Describe dead-space ventilation

A

-decreased perfusion (low Q) and normal ventilation
-results in V/Q ration >1
-ventilating a “dead” area where little or no blood is going through
-ex. blockage in pulmonary artery
-builds up CO2

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34
Q

What is cor pulmonale?

A

an abnormal enlargement of the right side of the heart caused by the heart struggling to pump out blood

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35
Q

Describe physiological shunting

A

-normal perfusion and decreased ventilation
-results in a V/Q ratio <1
-something is blocking the airway
-results in mixed blood leaving lung tissue and not just oxygenated blood
-risk of acidosis from lack of CO2

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36
Q

Describe silent unit

A

-decreased perfusion and decreased ventilation
-hypoventilation triggers reflex vasoconstriction and hypoperfusion
-an attempt to maintain V/Q ration = 1
-usually seen in pneumothorax (collapsed lung) and ARDS (acute respiratory distress syndrome)
-not sustainable long term

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37
Q

What are the signs and symptoms of respiratory disease?

A

-cough
-dyspnea
-cyanosis

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38
Q

Define dyspnea

A

-shortness of breath reported by patients
-result of obstruction or reduced lung compliance
-normal during heavy exertion but not normal long term

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39
Q

Where is cyanosis visible?

A

only lighter skin tones it can be visible on the surface of the skin but on darker skin tones check the mucous membranes and whites of the eyes

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40
Q

What causes peripheral cyanosis? central cyanosis?

A

peripheral– due to peripheral vasoconstriction and reduced blood flow to tissue so it is a perfusion issue

central– due to failure of the lungs to oxygenate the blood so it is a ventilation/perfusion imbalance

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41
Q

What are the two clinical heart failure?

A

right-sided heart failure and left-sided heart failure

both result in hypoperfusion

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42
Q

Describe right-sided heart failure

A

-weakened right ventricle cannot maintain adequate output so reduced blood flow
-V/Q mismatch
-results in dead-space ventilation and decreased efficiency of gas exchange

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43
Q

Describe left-sided heart failure

A

-weakened left ventricle results in decreased CO
-blood backs up in pulmonary circulation-> pulmonary HTN-> hypoperfusion

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44
Q

What is pulmonary edema?

A

-when plasma and RBCs break through the very thin capillary layers as soon as the pulmonary artery pressure rises too high
-often accompanies heart failure
-abnormal accumulation of fluid in lungs
-patient may cough up pink, frothy fluid and can drown in their edema
-always have dyspnea

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45
Q

Describe thromboembolism

A

-arise in deep calf or thigh veins and lodge in pulmonary vessels, blocking blood flow
-associated with pulmonary HTN upstream from occlusion
-pulmonary HTN results in hypoperfusion
-can lead to right-sided heart failure

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46
Q

Clinical examples of hypoperfusion

A

-heart failure
-pulmonary edema
-thromboembolism

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47
Q

Describe bronchial asthma

A

-obstructive lung disease results in hypoventilation
-result of exposure to inhaled irritant
-mucosal swelling, bronchoconstriction, mucus hypersecretion
-productive cough, dyspnea and wheezing

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48
Q

What is the difference between bronchial asthma and chronic bronchitis?

A

-diagnostically similar
-difference in rapidity of the onset and the speed of resolution if treated properly

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49
Q

Describe chronic obstructive pulmonary disease (COPD)

A

-a group of respiratory disorders characterized by chronic and recurrent obstruction of airflow in the pulmonary airways
-progressive but may be partially reversible
-hyperreactive to an irritant, usually smoking
-diagnosed on the basis of 2 consecutive years in which a productive cough is present for at least 3 months
-currently the third leading cause of death in North America and the second leading cause of disability
-encompasses chronic obstructive bronchitis and pulmonary emphysema

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50
Q

Describe chronic obstructive bronchitis

A

-part of COPD
-increased mucus production, obstruction of small airways, and a chronic productive cough
-symptoms similar to bronchial asthma
-swelling of mucosa caused by the irritation from the inhaled particulate matter

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51
Q

Describe pulmonary emphysema

A

-enlargement of air space and destruction of lung tissue
-the continuous activation of neutrophils in the lungs which release an elastase enzyme which destroys type 4 collagen in the alveolar cells walls which causes them to collapse
-barrel-shaped chest, dyspnea, wheezing

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52
Q

Describe restrictive lung disease

A

-diverse category of lung disease causing the same problem of restricted lung expansion
-reduced lung expansion b/c of changes in pulmonary interstitium (support structure of the lungs) and/or respiratory structures external to the lungs
-NOT due to airway obstruction

53
Q

What are the two categories of restrictive lung disease?

A

1) extrinsic restriction– caused by changes to respiratory system structures external to the lungs
2) intrinsic restriction– caused by changes to the lung tissue itself

54
Q

Describe intrinsic restrictive lung disease

A

disorders that produce alterations in pulmonary interstitium

two forms:
1) acute respiratory distress syndrome
2) pulmonary fibrosis

55
Q

What can be caused by perfusion or ventilation disorders?

A
  • Hypoxia
  • Anoxia
  • Hypoxemia
  • Ischemia
  • Infarction
56
Q

What’s the difference between a thrombus and a blood clot?

A

A thrombus is inside the vessel and a blood clot is outside the vessel

57
Q

What are some causes of impaired circulation?

A
  • Endothelial damage
  • Abnormal blood flow pattern
  • Obstructions
58
Q

What are some causes of inadequate cardiac output?

A
  • Weak ventricular pump
  • Structural heart defect
  • Dysrhythmias
  • Sudden decrease in vascular resistance
59
Q

Which type of blood vessel has elastic fibers?

A

Elastic arteries–a property called compliance

60
Q

What is the purpose of Arterioles?

A

regulate blood flow into capillary beds
- Vasoconstriction will decrease perfusion
- Vasodilation will increase perfusion

61
Q

Describe arterial remodeling

A

When a chronically high arterial BP causes structural changes

62
Q

How does stress effect blood flow?

A
  • Chronic stress leads to increase NE/epi and increase RAAS activity -> chronic systemic vasoconstriction -> chronic increased PR -> chronic endothelial damage
  • Chronic stress leads to increased cortisol -> hyperglycemia -> high BG causes chronic irritation of endothelial cells -> cell damage
63
Q

Where is the highest normal capillary BP?

A

In the Kidneys

64
Q

If you increase capillary BHP what happens to IFHP?

A

It increases–IFHP manifests as tissue edema

65
Q

Why is slow blood flow rate a potential problem?

A

Platalets will automatically start clotting

66
Q

What can you do right now to promote YOUR venous return?

A
  • Gravity
  • Valves
  • Skeletal muscle pumps
  • Respiratory pumps
67
Q

What is a common disease in veins?

A

Varicose veinsssssssssss

68
Q

Define myopathy

A

A heart muscle disease

69
Q

What 3 aspects make up stroke volume?

A
  • Preload
  • Afterload
  • Contractility
70
Q

If there is an increase in afterload what does this signal?

A

A problem with the aorta

71
Q

Which two variables directly affect cardiac workload?

A
  • Contractility
  • Heart rate
72
Q

What is orthostatic hypotension?

A

Hypotension with change of position

73
Q

What causes a change in BP?

A

A change in blood volume and change in peripheral resistance

74
Q

Define Oliguria

A

almost no pee

75
Q

What are the patterns of blood flow?

A
  • Normal :)
  • Turbulent :(
  • Sluggish :(
  • Stasis (stopped) :( :(
76
Q

What happens when platelets and collagen interact?

A

Coagulation cascade

77
Q

Name the 3 components of a blood clot? (Definitely on the EXAM)

A
  • Fibrin
  • Platelets
  • Red Blood Cells
78
Q

Define Thrombosis

A

The formation of a thrombus

79
Q

Define Sepsis

A

Blood borne infection

80
Q

Define Arteritis and Phlebitis

A

Arteritis: Inflammation of an artery (most likely due to infection)
Phlebitis: Inflammation of a vein (most likely due to IV)

81
Q

Define Axial streaming

A

Cells go down the center of the blood vessel (axial zone) – while plasma surrounds them in the plasmatic zone

82
Q

Where is the highest blood pressure?

A

Aorta

83
Q

Define Bifurcations

A

sites of vessel branching – occurs as blood is forced into a new direction of flow creating turbulence

84
Q

Define Stenosis

A

The narrowing of a vessel; could be a structural abnormality or cause by trauma

85
Q

Describe the types of arterial remodeling

A
  • T. intima -> Endothelial damage
  • T. media -> Vascular smooth muscle hypertrophy
  • Vascular Fibrosis -> Fibroblasts make collagen (decreased compliance)
86
Q

Define Hypovolemia

A

A decrease in blood volume
example: dehydration, hemorrhage, or endocrine disorder

87
Q

What can result from blood stasis?

A

No blood flow leads to ulcerations and necrosis

88
Q

What is the difference between a Thrombus and an Embolus?

A

A Thrombus is a blood clot that forms in a vein and an Embolus is anything that moves through the blood vessels until it reaches a vessel that is too small to let it pass.

89
Q

Define Atherosclerosis

A

A progressive inflammatory arterial disorder that only occurs in arteries and arterioles.
2 Major etiologies:
- Hypercholesterolemia
- Inflammation

90
Q

What happens as a result of partial occlusion compared to complete occlusion?

A

Partial occlusion -> causes ischemia (tissue hypoxia)
Complete occlusion -> Infarction (tissue anoxia / tissue necrosis)

91
Q

Define Collateral Circulation

A

The addition of extra microvasculature due to chronic hypoxia
- Protective mechanism when arterial occlusion is a slow process
- Helps perfusion
- Not in pulmonary vessels

92
Q

What is Artheroma?

A

Fatty plaques
- Made of triglycerides, cholresterol, fatty acids and may include calcium
(only in arteries!)

93
Q

What is the chronological order of Atherogenesis? (EXAM)

A
  1. Injury to endothelial cells lining artery wall -> chronic inflammation -> artery wall remodeling
  2. Fatty streak formation
  3. Fibrous atheromatous plaque formation (Fibrosis)
  4. Development of complicated lesions (hard fatty plaque or thrombus)

DECREASES LUMEN SIZE

94
Q

Describe Fatty streak formation

A
  • Migration of WBC’s
  • Lipid accumulation and oxidation promotes inflammatory response
  • Macrophages -> phagocytize lipids -> become LDL laden foam cells
  • Fibroblast and smooth muscle cell proliferation
95
Q

Define occlusion

A

blockage of a vessel– can be estimated in percentages

96
Q

What serious complications can result from atherosclerosis?

A

-hypertension
-partial or complete occlusion
-formation of a complicated lesion (stable or unstable plaque)
-aneurysm or ruptured aneurysm weaken the artery wall and thrombosis or hemorrhage can occur at site of lesion

97
Q

Describe Virchow’s triad

A

the triad describes the 3 major causes of thrombosis in arteries, veins or heart chambers

  1. endothelial cell injury
  2. alterations in blood flow
  3. hypercoagulability
98
Q

What are the two methods of classifying thrombi?

A
  1. by location– occlusive, intrmural or vegetations
  2. by vessel type– arterial or venous
99
Q

Where are (intra)mural thrombi found?

A

-attached to the lining of the heart wall or aorta
-high embolization rate
-post-cardiac arrest

where are murals found? on walls

100
Q

Where are vegetation thrombi found?

A

-attached to damaged or infected heart valve or artificial heart valves
-may include bacteria or fibrous scar tissue (a complication of rheumatic heart disease)

101
Q

What is a complicated lesion?

A

It is a combination of atherosclerotic fatty plaque and thrombus

102
Q

What is Homan’s sign?

A

when there is pain in the calf muscle with dorsiflexion of the foot– seek immediate medical intervention

103
Q

Where is the risk of embolism for an arterial occlusion? for a venous occlusion?

A

arterial occlusion has a risk of embolism in the specific tissue that the artery serves

venous occlusion has a risk of embolism in the lungs

104
Q

What are the types of emboli?

A

-thromboemboli
-air (gaseous)
-neoplasm
-microorganisms (septic)
-amniotic fluid
-fat
-foreign body

NOT ALL EMBOLI ARE BLOOD CLOTS

105
Q

What should you ask yourself when trying to locate a potential embolic site?

A

1) where did the embolus form?
2) where will the embolus travel to until it reaches a vessel too small to pass through? this is where it will lodge and block blood flow

106
Q

What is the difference between ischemia and infarction?

A

ischemia is a lack of blood supply to an area and infarction is the process of obstructing blood flow (resulting in death of cells)

107
Q

What are the two categories of infarcts?

A

based on appearance
1) white or pale infarcts– arterial occlusion
2) red infarcts– venous occlusion

108
Q

Define aneurysm

A

weakened blood vessel or heart wall; outpouchings develop

-if the wall ruptures then it is called a ruptured aneurysm-> sudden hemorrhage
-clinical manifestations depend on the location of the aneurysm

109
Q

Define varicosity

A

a weakened/distended “tortuous” vein which results in the blood back-flowing and pooling
-can be genetic, congenital or acquired (mechanical compression)
-localized distended purplish veins, edema, skin discoloration, etc.
-can result in varicose veins
-can also be found in the esophagus and rectum/anus

110
Q

What are hemorrhoids?

A

genetic or acquired varicose veins of the rectum and/or anus; sitting too long “straining a stool”, constipation and pregnancy can cause hemorrhoids

111
Q

What are the 4 major etiologies of inadequate CO?

A

1) impaired ventricular pumping
2) conduction defects that cause arrhythmias/dysrhythmias
3) structural heart defects
4) decreased peripheral (systemic) vascular resistance (decreased PR)

112
Q

Define etiology

A

the cause of a disease

113
Q

What are the two types of myocardial remodeling?

A

1) myocardial hypertrophy– thickening of muscle
2) myocardial dilation– muscle fibers stretched

the result of the ventricles trying to maintain tissue perfusion

114
Q

What is the difference between stable angina and unstable angina?

A

stable– pain due to myocardial ischemia that occurs most commonly during or immediately following exercise/exertion but may occur due to another physiological trigger

unstable– pain due to myocardial ischemia without any obvious/probably cause

115
Q

What is the time frame difference between an ischemic attack and a myocardial infarction?

A

ischemic attack– O2 deficit for less than 20 min

myocardial infarction– O2 deficit for more than 20 min

116
Q

Why is Acute Coronary Syndrome serious?

A

-unstable plaque in a coronary artery causing unstable angina (high risk of myocardial infarction)

117
Q

Define myocardial stunning

A

the period of time when myocardial cells are alive, but injury is severe enough to prevent their normal depolarization and repolarization phases– the cells should return to normal function

118
Q

Define hibernating myocardium

A

these cardiac cells are either still feeling some ischemia or have adapted to survive but cannot do their normal function– they don’t contract (sleeping)

119
Q

What are the 3 zones of myocardial damage?

A

1) zone of infarction and necrosis– center of damage, where there is no blood flow
2) zone of hypoxic injury– uncertain the extent of permanent myocardial damage (many cells hibernating)
3) zone of ischemia– far from damaged area, no permanent deficit

120
Q

What does conduction defects mean in relation to the heart?

A

-defects in electrical signals (depolarization and repolarization) of cardiac conduction system– causes uncoordinated mechanical activity of cardiac muscle
-dysrhythmias and arrhythmias
-decrease CO and BP
-can result in cardiac arrest

121
Q

What are the effects of a cardiac dysrhythmia?

A

sluggish flow, decreased CO and decreased tissue perfusion

FOR ALL TYPES OF CARDIAC DYSRHYTHMIA

122
Q

Define tachycardia

A

-fast heart rate
-decreased ventricular filling with increased myocardial O2 needs

123
Q

Define bradycardia

A

-slow HR
-may impair blood flow to vital organs

124
Q

Define flutter

A

-rapid atrial ectopic tachycardia (240-450bpm)

125
Q

Define fibrillation

A

-heart chamber(s) vibrate instead of pumping effectively

126
Q

Define coarctation of the aorta

A

the severe narrowing (stenosis) of the aortic arch– makes the LV push very hard to pump blood through that highly resistant aorta

-high afterload

127
Q

Define regurgitation of the heart valve

A

blood leaks backwards

128
Q

Define prolapse of the heart valve

A

valve cannot close properly which can lead to regurgitation

Pathophysiology 1 (5 decks)

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