Patho Midterm One Flashcards
(128 cards)
1
Q
Describe the pacemaker potential. How are pace maker potentials produced
A
Pace maker potential is the gradual DP from -60mV and Na slowly enters the cardiac cell
As the pacemaker potential reaches the threshold, it stimulates Ca channels to open which cause DP
2
Q
Describe action potentials? How do they relate to heartbeats
A
Occurs when the threshhold is crossed (-40mV)
Causes depolarization (DP) - Ca channels open
Once at a max point, K channels open, causing repolarization until the potential drops to -60mV again
Pacemaker potential starts over again
Each DP causes one heart beat
3
Q
What is tetanus? How is it prevented?
A
Tetanus is prolonged contraction due to repeated stimulation of the heart muscle
Prevented by the repolarization phase
4
Q
What is the absolute refractory period?
A
A period of time which the heart muscle cannot be stimulated. Maintained by Calcuim channels being open. Allows the heart to fill properly
5
Q
What is the cardiac conduction system pathway?
A
SA node in the R atrium stimulates the AV node
Activates the bundle of HIS in the septum
Traevls through the bundle branches in the lower septum into the Purkinje fibres in the ventricles
6
Q
Describe what happens in the different stages of the ECG
A
P: SA node fires
Atrial Filling (DP)
. Atria Contract (atrial systole)
QRS: AV node fires. Ventricles begin to fill (DP). Atria relax (RP). Ventricles contract.
T: Ventricles relax (RP)
7
Q
How do valves operate>
A
Flaps of connective tissue that close due to the changes of pressure in the atrium and ventricles. They are anchored by the chordae tendonae to prevent backflow
8
Q
What are the two normal heart sounds. When do they occur
A
S1: lubb. Louder and longer. Due to closing of the AV valves because ventricles are contracting
S2: Dubb. Closure of the semilunar valves. Ventricles are relaxing causing the Vp < Ap
9
Q
Where would you place your stethescope to listen to the different heart sounds?
A
Semilunar valves: 2-3ribs
AV: 5-6th ribes
10
Q
What is Cardiac Output
A
CO = SV x HR
11
Q
What is stroke volume?
A
SV = EDV - ESV
Governed by Contractilty , preload and afterload
To increase SV, you want to increase EDV and minimizeESV
12
Q
What is preload? How does increasing preload affect SV?
A
Amound of tension in the ventricles due to the stretch of myocardium.
Increasing preload increases contraction strength
An increase in preload increases SV
13
Q
What is Contractility? How does it affect SV?
A
The strength of the contraction of the heart
Increased contractiliy increased SV
14
Q
What is afterload? How is it related to SV?
A
Afterload is the pressure that the heart has to exert to overcome the pressure in the arteries.
Affected by elasticity of vessel, periphery size
Inversly proportional to SV
15
Q
What is ejection fraction? What does it tell us?
A
EJ = SV / EDV x100%
Fraction of blood that ejected from heart every heartbeat. Measure of how well the valves are working, not if the heart is getting an adequate amount of O2
16
Q
What is blood pressure? What factors affect it?
A
BP = CO x TPR
CO:
Blood Volume: Increased Na/ H20 absorption, Renin, aldosterone
Cardiac: bpm, volume / beat
TPR:
Blood viscosity (RBCs, albumin)
Vessel radius( influenced by vasomotor tone)
17
Q
What is vasomotor tone? How does it increase/ decrease?
A
If the sympathetic nervous system is activated, epinephrine is released, causing vasoconstriction.
Walls thicken increasing the PVR - strong tone
When SNS stimulation deceases, smooth muscle relaxes, dilating the vessel, decreasing PVR - weak tone
18
Q
What is flow? How is it influenced?
A
Flow = volume/ time (mm3/s)
velocity x cross section
Influenced by viscosity of blood, vessel elasticity and vessel radium
19
Q
How does local control influence BP?
A
- Lactic acid (wastes) cause vasodilation
- Vasoactive substances (histamines) cause vasodilation
- Angiogenesis can increase blood flow to the area
20
Q
How does neural control affect blood pressure? What are the two pathways?
A
Changes in BP are noted in the baroreceptors (aortic arch, carotoid sinuses and aortic sinus)
ie. If the BP is increased, the arteries stretch and this is detected by the baroreceptors. They activate the cardio-inhibitory center and inhibit the vasomotor center
- Cardioinhibitory center- increases vagal tone which decreases HR
- Vasomotor - Reduces sympathetic tone which reduces vasomotor tone which causes vasodilation
21
Q
What hormones control BP?
A
angiotensinogenigenfloats around in the blood stream. When BP drops,Reninis released from the kidneys which converts angiotensinogen toangiotensin I. As Angiotensin I passes through the lungs, ACE converts it toangiotensin II which is a powerful vasocontrictor.
Angiotensin II stimulates the adrenal cortex to release aldosterone which promotes Na and water retention in the kidnets
22
Q
How is venous return promoted?
A
- Venous muscles contract, causing some pressure
- Gravity drains the head and neck
- Skeletal muscles in the limbs pump blood with movement
- Inhalation causes the thoracic cavity to expand, decreasing blood pressure and sucking blood up
- Cardiac suction of the atrial space
23
Q
What factors promote capillary volume and flow
A
- Hydrostatic pressure mores fluid, nutrients and O2 from capillaries to the tissue bed
- As nutrients are removed, plasma proteins in capillary pull wastes and CO2 back into the capillary - Colloid osmotic pressure
24
Q
What is the largest cause of cardiac disease?
A
Atherosclerosis
25
How does artherosclerosis form
1. Trauma to endothelium allows fat cells to get underneath
2. WBCs follow and try to get rid of them, oxidizing them into foam cells
3. WBCs release growth factors which cause a plaque to form in the vessel
4. Plaque blocks the artery
26
What are chylomicrons? How do they help with cholesterol?
Liproprotein particles that transport lipids from the GI tract to the blood to the liver
27
What are risk factors of atherosclerosis? What are protective factor/s
Risk factors that cannot be changed: age, gender, heredity, lack of LDL receptors
Risk factors that can be changed: Diet, obesity, DM II, HTN, increased clotting factors, **smoking**
Protective factors: estrogen, exercise
28
What are HDL and LDL cholesterol? Which are good and bad
LDLs are bad proteins because they lack the lipoproteins to attach to receptors, so instead they float around in the blood stream. They can also deliver fat to the body
HDLs have a lot of proteins in the surface and therefore bind easily. They go to tissues and pick up lipids
29
What is the difference between stable and unstable plaques?
Stable: have thick fibrous caps over the core and only partially block the vessels. Don't tend to form clots of emboli
Unstable: Only have thin, fibrous caps which can rupture. Rupture can form a clot and fully occlude the artery or may break free and become an embolus
30
What are syndromes of Coronary Heart disease?
Angina, acute coronaty syndrome (MI and unstable angina), chronic ischemic disease, sudden cardiac death
31
What is coronary heart disease?
Occlusion of the coronary arteries
32
What can ischemia of the coronary arteries cause?
* Angina
* Heart attack
* Cardiac arrythmias
* conduction deficits
* heart failure
* suddent death
33
When does angina occure? What does it feel like? How can you help treat it?
Angina occurs when there is too much demand on the heart and not enough supply of oxygen to the heart muscles
Feels like heartburn or a squeezing pain in the middle of the chest
Increase supply by applying O2
Decrease demand by resting, decreasing anxiety, medications to decrease HR
34
What are the different types of angina?
35
What are the functions of the plural fluid in the cavity?
Reduces friction
Creates a pressure gradient between the atmosphere and the lungs
Compartmentalized infections inside and outside of the lung
36
WHat is generally considered the upper and lower Resp tract?
Upper: nasal cavity, pharynx, oral cavity, larynx
Lower: Bronchi, broncioles and alveoli
37
What is the function of the upper resp tract?
Humidify and filter incoming air
38
How are foreign particles trapped when entering the resp center?
The tracheobronchial epithelium contains goblet cells which produce mucus which trap foreign particles such as dust
Ciliated cells conduct particles back up to the pharynx
39
What is the bronchial tree? What is it composed of?
23 orders of bronchioles which end in alveoli
Line by epithelium, walls are cartiledge (keeps airway open) and smooth muscle (controls airway conductance)
40
What is conductance?
The flow of air
41
What are the different cell types found in the respiritory membrane?
Type I alveolar cells - simple squamous epithelium
Type II - cuboidal cells which produce surfactant
Alveolar macrophages - engulf foreign particles
Capillary endothelium
42
What are the stages"normal respiritory function"
1. alveolar ventilation - air is drawn into lungs
2. Alveolar perfusion - cappillaries surround alveoli
3. Alveolar-capillary diffusion - air leaves alveoli and enters capillaries
4. Gas transport to the rest of the body
Changes in any of these can cause respiritory failure
43
What is compliance? What is it dependent on?
:How easily the lungs are inflated
Dependent on presence of elastin (stretch) and collagen (prevents over stretching), water content, and surface tension
44
How does surfactant reduce surface tension?
Surfactant breaks down the hydrogen bonds connecting H2O molecules to each other, therefore reducing the surface tension and making it easier for the alveoli to expand
45
What factors affect alveolar - capillary diffusion
1. Permeability of epithelium (thickness)
2. Surface area (more SA, more area for diffusion to occur)
3. Concentration gradient of gas (\> gradient = better diffusion)
46
What is lung ventilation? What does it depend on?
The act of driving air in and out of the lungs
Depends on the action of the respiritory muscles (chest compliance) and lung compliance
47
A man's lungs were damaged during a fire due to smoke inhalation. The damage destroyed some of his surfactant. What happened to his lung compliance? Why was he given positive pressure ventilation?
Compliance is decreased because surfactant is destroyed
Positive pressure aid room will help force air into the lungs
48
What are the primary respiritory muscles?
Diaphragm, external intercostal muscles
49
When are the accessory muscles used? What are the accessory muscles for inhalation and exhalation?
For forced or deep breathing
Inhalation: Scalene, sternocleidomastoid
Exhalation: internal intercostal, abdomonial muscles
50
What is tidal volume?
Air inhaled and exhaled in one quiet breath. Difficult to get an accurate measure
51
What is residual volume?
The air that remains in the lungs after maximum expirarion. Keeps alveoli inflated (1L)
52
What is vital capacity?
The amount of air that can be exhaled with maxiumum effort after maxium inspiration
Measure the amound of air that can pass through the lungs
Assess strength of thoracic muscles & pulmonary function
53
What is forced expiratory volume?
% of vital capacity exhaled over time
Health adult ~75-85%
COPD ~ 60-65%
54
What is the minute respiritory volume?
Tidal volume x respiritory rate
Rest = 6L/min
Max = 125-175L/m
55
How is O2 transported in blood? What is the normal PaO2?
some is dissolved (PO2 = \>80mm Hg)
Most is bound to hemoglobin
56
What is the normal PaCO2?
35-45mm Hg
57
What occurs as you exhale?
Exhaling removed CO2 from blood which reduces carbonic acid (H2CO3) and raises your blood pH
58
How do central chemoreceptors work?
Measure the PCO2 and pH in the cerebrospinal fluid
Increases resps when PCO2 increases or ph decreases (stimulated the breathing center in the medulla oblongata)
59
How do peripheral chemoreceptors work?
They measure the PO2 in arterial blood (aorta, carotoid arterties)
Increase respirations when PO2 \<60mmHg
More sensitive
60
You are caring for a patient with chronically high PCO2. He is being given lowe flow O2 and c/o needing more O2, so you turn up his O2.
When you check on him later, he is unconcious and not breathing.
What happened?
Pt has chronic increased PCO2 therefore his central chemoreceptors have been de-sensitized and no longer recognizes having high PCO2.
By increasing the O2, the peripheral chemoreceptors register that the pt is getting enough O2 therefore the resps don't increase or decrease.
61
How does a peanut allergy cause cardiovascular shock?
What would you measure.
How would you treat it
Histamines are released which cause vasodilation.
The decrease in peripheral causes blood pooling in the body which decreases the blood to the heart (CO decreases)
Measure BP
Stop histamine release c anti histamines. Epinephrine activates CNS causing vasoconstriction
62
What is repiritory failure?
inability to deliver adequate O2 to the body
63
What are causes of respiritory fialure
Hypoventilation - hypercapnia, hypoxia
Impaired diffusion - hypoxemia but not hypercapnia
Pleural disorders
64
Why does impaired diffifusion cause hypoxemia but not hypercapnia?
Thickening of the alveoli causes the inability for O2 and CO2 to pass through the endothelium
That causes hypoxia. However, excess build up of CO2 in the blood causes it to be converved to HCO3 which can excreted by the kidney
65
What are causes of hypoventilation?
Depression of repiritory center dt brain injury, blood clot, tumor
Dieases of the respiritory nerves or muscles - polio, MS, myesthenia gravis
Thoracic cage disorders (scoliosis, kyphosis)
66
What can cause impaired diffusion?
Interstitial lung disease
ARDS
Pumonary edema
Pneumonia
67
What is hypoxemia? What are S&S?
When PO2 \<60mmHg
Agitation,combative behaviour, euphoria, impaired judgement, convulsions, delirium, stupor & coma
Hypotension and bradycardia dt the heart not receiving enough O2
Results in SNS activation (short term solution)
68
What is hypercapnia? What can it cause?
When PCO2 is \>50mmHg
Causes increased RR (central chemoreceptors triggered), decreased nerve firing (dt elevation of blood acidity) - disorientation, coma, & decreased muscle contraction
69
What is plueral effusion?
When fluid builds up in the lungs. Severity depends amount of effusion and type.
Can be seroius, pus, lymph or blood
70
Hydrothorax,
empyema,
chylothorax
Hemothorax
serous fluid
pus
lymph
blood
71
What is pneumothorax? What categories are there?
Puncturing of the pleural cavity causing collapse of lung on damaged side
1. Spontaneous - air filled blister on lung ruptures
2. Traumatic - chest injury
72
What are the two types of traumatic pneumothorax?
Open: air enters the wound on inhalation and exits on exhalation
Tension: Air enters on inhalation but cannot exit on exhalation. Very painful on injured side. Makes ventillation diffifult dt less room. Extra air needs to be exacuated from thoracic cage
73
What are clinical features of pneumothorax?
Tracheal shift to the non injured side dt boyancy and being pushed
Cardiac compression
lung deflation
Decreased breath sounds to injured side
Area of density on a radiograph
74
What are obstructive diseases? What are some examples?
Disorders which decrease the conductance of air to the lungs
(Asthma, COPD)
75
What are restrictive disorders? What are some examples?
Disorders which affect the capacity of the lungs
dt. chest wall changes, pleural effusions or parenchymal changes
76
77
What are the different types of angina? How are they treated?
Stable - a fixed occlusion (stenosis). Pain occurs when O2 demand for heart is increased. Relieved with rest
Unstable: thromboemboli leads to MI. Tx c anti coagulants
Variant: Coronary artery spasms block blood flow. Usually in young males who use drugs. Tx c calcium channel blockers
78
S&S of an acute MI
Chest pain - severe burning or crushing sensation
SNS response - GI distress, N&V, tachycardia, vasoconstriction, anxiety, restlesness, doom
Hypotension and shock - weakness in arms and legs
79
Where do the majority of MIs occur
20% in the left circumflex artery (supplied by LCA)
50% in the LT anterior descending artery (supplied by LCA)
30% in RCA (posterior infarction)
80
Why do Lt sided coronary arterial vessels experience 70% of MIs?
More pressure is experienced by the LCA. Greater risk of injury which leads to atherosclerosis
81
What is the pathogenesis of Acute Coronary syndrome
Plaque is broken down
Tissue thromboplastim is exposed
Platelet aggregates to area, forming a clot
thrombus is formed
acute ischema
82
What are complications of an acute MI?
Heart failure
Cardiogenic shock (heart is so damged that it cannot pump blood to the other organs)
Pericarditis (dt rupture)
Thromboemboli dt stagnation of blood in ventricles dt ineffective pumping
Rupture of heart
Ventricular aneurysm
83
What are the common outcomes of an MI 1 day after the infarct?
Death (20%)
Arrythmia
84
What are the common outcomes of an MI one week after the infarct?
Arrythmias (90%)
CHF (60%)
Shock (12%)
Rupture (1%)
85
What are the common outcomes of an MI one year after the infarct?
CHF (70%)
Arrythmia (20%)
Aneurysm (10%)
Thromboemboli (10%)
86
What are the common outcomes of an MI ten years after the infarct?
CHF(70%)
Recurring infarcts
Arrythmias
Only about 30% are still alive
87
What are serum cardiac markers of acute coronary syndrome? Why are these markers used?
Incraese in Myoglobin, creatinine kinase (makes ATP), triponin
Cell death releases these proteins into the bloodstream
88
How would each of the following affect BP?
1. Vasodilation
2. Decreased stretching of baroreceptors
3. Hypoxemia
4. Inhibiting ACE
5. Beta blockers
6. Aplha 2 agonist
7. Calcium channel blockers
1. Decrease
2. Increase
3. increase
4. decrease
5. decrease
6. increase (causes constriction)
7. decrease
89
What is primary and secondary HTN?
Primary (essential): No identifiable cause. High Na suspected to be related. Most come 90-95%
Secondary: dt pheochromocytoma, adrenal cortex adenomas, atherosclerosis
90
What is Stage 1,2 &3 HTN?
1. Stage 1: 140-159/90-99
2. Stage 2: 160-179/100-109
3. Stage 3: \>180/110
91
What are complications of HTN?
Cardiac hypertrophy (Lt ventricle)
Nephrosclerosis: changes in glomeruli and blood vessels
Retinopathy - hemorrhages lead to blindness
Encephalopathy - rupture of aneruysms
92
What is the difference between hyaline and malignant nephrosclerosis?
Hyaline: scar tissue forms over the glomeruli in the afferent arterioles
Malignant: Changes occur in the kidney which activates the renin - angiotensin - aldosterone system causing a cycle of elevated BP. Tiny hemorrhages in the renal cortex
93
What is heart failure? What causes it?
Inability to effectively pump the blood delivered to the heart to the rest of the body.
MI, cardiomyopathy
94
How is systolic dysfunction different from diastolic dysfunction?
Systolic dysfunction: low ejection graction dt poor contractility. Often associated with MI, ischemia & cardiomyopathy
diastolic dysfunction: Near normal ejection fraction. Dt poor or slow relaxation . Often associated with aging bc of decreased elasticity
95
What are the effects of Lt sided heart failure?
Backwards: Back up of blood in the lungs. Results in crackles, infection, laboured breathing. Often results in rt sided failure
Forward: decreased CO leading to decreased perfusion
96
What are the effects of Rt. sided heart failure?
Backwards: Jugular vein distension, GI tract congestion (N&V, anorexia), edema
Forwards: Low cardiac output dt decreased contractility, decreased blood carrying O2 in lungs
97
Mr. M has heart failure. He c/o severe SOB and has fluid in his lungs. He has tachycardia, increased diastolic BP and says that he feels weak and anxious.
Which are dt the SNS?
Which side is failing
SNS: anxiousness, increased BP, tachycardia, anxiety
Side: Lt ventricular
98
What is pericarditis? What are clinical manifestations?
Inflammation of the pericardium (covering around the heart).
Causes pain dt prostaglandins
Exudate (serous - pericardial effusion), fibrinous (adhesions decreasing expansibility)
ECG changes (changes in QRS wave)
99
What are the consequences of pericardial effusion?
Restricts heart expansion
Lt side can't accept enough blood which decreases CO, which decreases BP leading to shock
Rt side can't accept enough blood, causing edema, jugular distension, increases venous pressure
100
What are examples of myocardial disorders? Do they result in systolic or diastolic disorders?
Ventricles are hypertrophic, can't fill properly - DD
Ventricles are too stiff to stretch - DD
Ventricles are too weak to pump blood - SD
101
What is hypertrophic cardiomyopathy?
Genetic disorder in which defects in actin and myosin make the cells weak. The heart has to work harder to pump blood to the body. Causes the muscles to hypertrphy. Heart requires more O2 to fxn properly, making the person more prone to heart failure.
102
What are the types of valve defects?
Stenosis
Regurgitation
103
What are the effects of Aortic valve stenosis and regurgitation?
Stenosis: Ventricular hypertrophy b/c heart has to pump harder to get blood into aorta
Regurgitation: Ventricle dialates to accomodate the backflow of the blood. Decreases contractility which decreases CO
104
What are the effects of Mitral valve stenosis and regurgitation?
Stenosis: dialation of the atria. Could cause pulmonary congestion
Regurgitation: dialation of the atria. Could cause pulmonary congestion
105
What is cardiogenic shock?
Occurs when the heart fails to pump blood adequately.
Decreased CO decreases BP, causing SNS response causing vasoconstriction which increases the workload of the heart
106
What is distributive shock? What causes it?
When the BV dialate and there is not enough blood in the circulatory system to fill it
blood flow decreases, less blood is brought to the heart and less is pumped to the body
DT decreased SNS activity dt injury to brain or spine, anesthetics, insulin shock, emotions
Vasodilators in blood (histamines, sepsis)
Vessel damage dt severe hypovolemia
107
What is systemic inflammatory response syndrome?
aka Septic shock
Vasodilation dt imflammatory mediators
108
What are examples of obstructive airway disorders?
Bronchial asthma
Chronic bronchitis, emphysema, bronchietasis, cystic fibrosis
109
What differences are there between extrathoracic & intrathoracic airway problems in children?
Extrathoracic - prolonged inspiration, inspirational stridor. Body walll does not move c inspiration
Intrathoracic: Prolonged expiration c wheezing. Rib cage moves but air doesn't leave lungs
110
What are upper and lower obstructive disorders in children?
Upper = croup, epiglottits
Lower - acute bronchiolitis
111
What is croup? How does it present? How do you treat?
Occurs mostly in young chldren. Occurs 3 mos - 3 years
Brought about by influenze or other viral infections
S&SL hoarsness, brassy cough, fever, resp stridor, ctanosis, pallow
Tx c cold air
112
How does Epiglottitis presesnt?
SImilar to croup
113
What are the causes of asthma?
Extrinsic: dt allergic reaction
Intrinsic: exercise, cold, physical factors, physhological stress, chemical irritants, aspirin, age
114
What is the pathogenesis of Extrinsic asthma?
Dt Type 1 hypersensitivity. May be genetic. Parents often have ecxema
Allergin is inhaled and enter the endothelium of airways
Mast cells from the connective tissues interact with the allergin and IgE.
IgE attaches to the mast cell and acts as a receptor for the allergin.
The mast cells contain histamine, and when the allergin contacts IgE, histamine is released.
Changes happen to the cell wall - airway thckens, increase mucous production
115
What histology changes occur in bonchials during asthma?
Mucus in lumen
Inflammation & basement membrane thickening
Enlarged mucous glands
Smooth muscle hyperplasia
116
How is Asthma controlled?
antihistamines, bronchodialators (Ventolin), managing environment, cortico-steroids
117
How do corticosteroids work against asthma? What is the risk of using improperly
Increase synthesis of beta receptors which boosts the effects of beta agonists
Overuse can break down bronchial endothelium which can lead to thrusth
Can lead to down regulation of B receptors
118
How do you treat intrinsic asthma?
Bronchodilators, antiocholinergics to prevent vagal reflex
119
How does COPD onset? What is the pathophysiology?
Onsets gradual changes in the airway to decrease conductance.
Muscus glad hypertrophy, loss of alveoli tissue of loss of eleasticity
120
What is the pathophysiology of emphysema? What is the Etiology?
Foreign particles entering the alveoli cause an influx of WBCs, especially neutrophils
Neutrophils try to digest particles with tripsin. However, tripsin can damage damage to alveoli endothelium which reduces elasticity.
Can be a genetic disease dt lack of antitripsin which inactivates tripsin
Smokers are also at high risk
121
What is radial traction?
stretching ability of parenchyma
122
What happens when radial traction decreaes?
Lose the ability to get rid of stale air in the lungs. Requires more effort to get rid of air. Strong accessory muscles
123
What is the difference between centrilobular and panacinar emphysema
Centrilobular - bronchioles are enlarged. Less dangerous than panacinar
Panacinar - Alveoli + broncioles expanded.
124
S&S of emphysema?
Barrel chest, pursed lip breathing
Good color, warm (no hypoxia)
125
What is chronic bronchitis?
Persistent cough of six mos over a two year period. Increased mucous secretions causing a productive cough
Hypoxic
126
What are the differences between blue bloaters and pink puffers?
Pink Puffers - Increased RR, dyspnea, increased temp dt increased metabolic needs, use of accessory muscles. Breath better upright
Blue bloaters: Cyanosis and polycythemia, cor pumonae
127
What is cor pulmonae
increased work load causing rt sided heart failure
128
