Patho final Flashcards
(140 cards)
1
Q
infective endocarditis
A
Aortic Valve with bacterial endocarditis
2
Q
Pericarditis
A
The pericardium (lining of the heart) becomes inflamed.
3
Q
three types of cardiomyopathy
A
Hypertrophic CM-thickened left ventricular wall
Congestive or Dilated CM- Dilated Left Ventricle (Enlarged heart)
Restrictive: myocardial fibers become infiltrated with abnormal substances(toxins) causing ventricular dysfunction
4
Q
Stenosis
A
Occurs in the Aortic and Mitral valves. Valve opening does not open all the way, not enough blood passes through.
5
Q
structure that delivers oxygenated blood from the placenta to the fetus
A
ductus venous
6
Q
higher vascular resistance in the arterial systematic circulation would most likely lead to
A
Increased workload of the right ventricle
7
Q
The lowest pressure is in the
A
Right Atrium of the adult cardiopulmonary circulation
8
Q
Transposition of the great vessels has a
A
Right to left shunt
9
Q
Which Blood Lipid is considered to be protective against the development of coronary artery disease
A
HDL, high density lipoprotein
10
Q
After a myocardial infarction, which area does not heal?
A
Infarction
11
Q
Which of the following is considered a lethal dysrhythmia or arrhythmia
A
ventricular fibrillation
12
Q
Clinical manifestations of Left Ventricular Heart Failure include:
A
Dyspnea, Pink frothy sputum, Fatigue, Crackles
13
Q
Clinical manifestations of Right Ventricular Heart Failure include:
A
Edema, weight gain, neck vein distention, enlargement of liver and spleen
14
Q
Left ventricular heart failure(CHF) can lead to movement of fluid from capillaries to alveoli. This can lead directly to:
A
Crackles for lung sounds
15
Q
Left ventricular heart failure can lead to right ventricular heart failure and result in:
A
Peripheral edema
16
Q
In the development of coronary artery disease CAD, what usually happens first?
A
Endothelial damage and lips deposition
17
Q
Risk factors for CAD do not include:
A
female gender
18
Q
With myocardial infarction, the zone of infarction:
A
does not heal/becomes scar tissue
19
Q
clinical manifestations of myocardial infarction does not include:
A
warm, flushed skin
20
Q
Ventricular septal defect may cause
A
increased pressure in the Right ventricle
21
Q
With coarctation of the aorta, why is pre ductal worse than post ductal
A
Post ductal allows some blood to shunt thru the patent ductus arterioles
22
Q
Cyanosis is likely to be seen in
A
Tetralogy of ballot
23
Q
If a patient has normal O2 levels in the right Atrium, Right Ventricle, and left atrium, what is likely occurring?
A
blood shunting from the Right Ventricle to the Left Ventricle
24
Q
Regurgitation, like stenosis occurs in the aortic and mitral valves, it is when
A
the valve does not close all the way, so blood leaks backwards.
25
fetal circulation structures include the
dusts, venous, foramen ovale, ductus arteriosus
26
Cardiac shunt-- Left to right:
oxygenated blood from the left side goes into the right side and is (ASYNOTIC)
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Cardiac shunt right to left :
less oxygenated blood from the right side goes into the left side or the systemic circulation(CYANOTIC)
28
Acyanotic conditions include
ASD, Atrial Septal Defect, VSD, Ventricular Septal Defect, PDA Patent Ductus Arteriosus, COA, Coarctation of Aorta
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Atrial Septal Defect
An atrial septal defect (ASD) is a hole in the wall between the two upper chambers of your heart (atria)
30
Ventricular Septal Defect
A ventricular septal defect (VSD), a hole in the heart, is a common heart defect that's present at birth (congenital). The hole occurs in the wall that separates the heart's lower chambers (septum) and allows blood to pass from the left to the right side of the heart.
31
PDA, Patent Ductus Arteriosus
Patent ductus arteriosus (PDA) is a persistent opening between two major blood vessels leading from the heart. The opening, called the ductus arteriosus, is a normal part of a baby's circulatory system before birth that usually closes shortly after birth.
32
Coarctation of the Aorta
Coarctation of the Aorta (CoA or CoAo), also called aortic narrowing, is a congenital condition whereby the aorta is narrow, usually in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts. The word “coarctation” means narrowing. Coarctations are most common in the aortic arch.
33
cyanotic conditions include:
Tetralogy of Fallot
| Transposition of Great Vessels
34
Development of atherosclerosis: (CAD)
Inflammation starts things, damages the epithelium allowing lipids to deposit in the intima. The lipids are oxidized and attract monocytes which enter the intima and become macrophages. Macrophages ingest LDL then are transformed into foam cells. Foam cells release cytokines which cause further inflammation and injury to the
intima, A fatty streak is formed in intima (collection of foam cells)-(yellow, filled with lipids), starts to cause narrowing, fibrous plaque forms (fatty streak collected collagen, fibers, ect., , complicated lesion(advanced)- fibrous plague hemorrhages causing a clot formation and obstruction.
35
The three most dangerous risks for CAD or Coronary Artery Disease are:
Cigarette smoking, Hypertension, and hyperlipidemia
36
Clinical manifestations for ischemia (to the heart)
Transient 3-20 minutes, sub-sternal pain, discomfort, heaviness, pressure,tightening, squeezing, or aching. May Radiate to neck, left-arm, jaw, teeth, back.
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clinical manifestations for a Myocardial Infarction:
Include the same symptoms as Ischemia, but also include: Indigestion, nausea, vomiting, diaphoresis, cool, clammy skin, Change in BP and or HR and Rythym
* during an MI, Nitroglycerin does not usually relieve
38
What similar problem does backward effects of LVF lead to that is the SAME as what the back ward effects of RVF leads to.
Increased volume, pressure in the venous system, edema
39
What different problem does backward effects of of RVF lead to that backwards effects of RVF leads to.
Increased volume/pressure in the pulmonary system.
40
Tetralogy of Fallot is Cyanotic and is cause by
Right to Left shunting through Ventricular Septal Defect, and RV to Aorta
41
Four steps of PAthophys of infective endocarditis are:
1. Endocardium is "prepared" to be colonized by having endothelial damage
2. Colonization can then occur(because of NBT and 1 above)
3. Infective vegetation forms
- clotting cascade, fibrin ect.
4. Valve Dysfunction, emboli ect.
42
Transposition of Great vessels is cyanotic and is caused by
two circulations, the systemic circulation does not have 02 which can be a bit of a problem
43
Normal pressure in the right atrium is about
5mmHg
44
What about cigarette smoking leads to decreased 02 delivery to tissues
Carbon Monoxide
45
What starts the process of CAD development
Inflammation damaging the epithelium
46
Which is a clinical manifestation of Myocardial Infarction, but not of Myocardial Ischemia?
Diaphoresis(sweating)
47
Which two valves are closed during systole
mitral and tricuspid
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Which two valves are closed during diastole
aortic, and pulmonic
49
Backward effect of Left Ventricular Heart Failure first leads to:
Increased pulmonary artery pressure
50
What clinical manifestations are due to the forward effects of left ventricular failure.?
exercise intolerance
51
sensory perception is
the body's ability to receive sensory stimuli and to consciously translate that data into meaningful information.
52
In rheumatic fever, the systemic inflammation effect on the nervous system causes:
Syndenham's chorea
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cyanosis would most likely be seen with
Tetralogy of Fallot
54
Aortic valve regurgitation is least likely to produce
A systolic murmur
55
Strabismus
"Crossed eyes" deviation of one eye from the other when looking at an object. Most commonly caused by weak hypertonic muscle in affected eye, normal up to age 4 months. Clinical manifestations are deviation of eye, and diplopia (double vision).
56
Cataracts
Development of opacities(cloudiness) of ocular lens. Caused by old age mostly, lens becomes more stiff and opaque with age. Clinical manifestations include: decreased visual acuity, increase in glare, decreased color perception, white light reflex(instead of red) in pupil area
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Glaucoma
Increased intraocular pressure in anterior eye above normal of 13-22, increased risk between ages 45-60. Second leading cause of blindness. -obstruction to outflow of aqueous humor with resulting increase in amount of fluid and pressure in eye. Pressure in eye impairs blood flow to retina with subsequent loss of acuity
58
Otitis Media
Inflammation of middle ear....two kinds are
| Supportive(Infection) and Effusion(Fluid)
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Risk factors for CAD include:
Cigarette smoking, Hypertension, Hyperlipidemia, Advanced age, Male gender under 60, then male/female risk equal, Genetic predispositions
60
Hyperlipidemia increases risks of CAD and is described as
increased serum lipoproteins caused by increased dietary fat intake, diabetes and genetics. Lipoproteins=lipids, phospholipids , cholesterol and triglycerides bound to carrier proteins.
61
Hypertension
causes increased blood pressure, increases peripheral vascular resistance, which increases workload of heart and accelerates the process of atherosclerosis
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Hypoglycemia
BS level less than 60mg/dl. Resulting from overdose of insulin, inadequate food intake, increased amounts of exercise
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Clinical Manifestations of Hypoglycemia
Neurogenic reactions occur when the hypothalamus senses decreased glucose levels:the brain is the only organ that doesn't store glucose, it needs a new supply constantly. Hypoglycemia causes Increased HR and Respiration, Diaphoresis, pallor, tremors, cool skin
Cellular malnutrition results in dizziness, irritability, confusion, fatigue, vision changes, hunger, seizures, coma
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Clinical manifestations of Diabetic Ketoacidosis (Diabetic Coma)
Hyperglycemia, Ketonuria, polyuria, polydipsia, polyphagia, abdominal pain due to upsetting nerve endings in GI tract, Kussmauls respirations(fast, hard, deep), breathe smells sweet(like juicy fruit gum
Can lead to hypotension, tachycardia, shock, and cardiac arrhythmia due to potassium K alteration(exchange of K+ for H+)
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Diabetic Ketoacidosis is
Extreme hyperglycemia w/ketonuria. BS 300-800, caused by not enough insulin, illnesses, psychological stress
66
In diabetic Ketoacidosis there is a decrease in insulin which means
glucose can't get into the cells. (starvation in the midst of plenty.)The body senses the lack of cellular fluid and starts to break down stored glycogen(glycogenolysis and glycogenesis) The high BS leads to osmotic diurisis, Increased volume in blood stream, more volume into kidneys, and increased fluid loss that leads to dehydration. (osmotic action leads to polyuria/polydipsia
67
In Diabetic Ketoacidosis
there is increased lipolysis which leads to ketone production and accumulation(ketones are acids) Ketone Production leads to Ketonuria(Ketones in the Urine) and Acidosis.Excretion of Ketone acids by the lungs causes hard, fast, deep respirations
Acidosis is caused by the exchange of K for H
Increased proteolysis happens which is an increase in gluconeogenisis from non-carbohydrate substances.
68
Pulmonary Emboli is
an occlusion of a pulmonary artery by an emboli(blood clot) . An emboli is a thrombus that travels( usually travels in pulmonary artery.
69
Types of pulmonary emboli:
Most common:blood clot/thrombus(usually originate from deep calf veins
Tissue Fragment
Fat emboli
Air bubble
70
Pulmonary emboli are often caused by
venous stasis-prolonged bedrest, obesity, chronic atrial fibrillation without anticoagulation, heart failure, or central venous catheters.
Also vessel injuries like trauma or surgery
And History of prior embolus/thrombus
71
Pathophysiology of a pulmonary embolus:
thrombus clot formation
dislodgment of thrombus
occlusion of part of pulmonary circulation
increased pulmonary artery pressure
Right Ventricular failure resolutionofclot
severe shock absorbed/disolv
death
can lead to infarction(scar tissue/death of tissue)
72
With a pulmonary emboli, symptoms can vary from
silent(no symptoms) to
| dyspnea SOB, Fever, cough, Tachycardia, Hemotysis, Chest pain, hypoxemia, hypoxia
73
Pulmonary Edema is
Accumulation of fluid in the pulmonary interstitial space and into the alveoli, caused by Left ventricular heart failure(most common), mitral stenosis, alveolar capillary damage, or volume overload
74
Pathophysiology of pulmonary Edema
Increase in Pulmonary capillary hydrostatic pressure
causing fluid to leak into pulmonary interstitium
fluid goes into alveoli
which dilutes surfactant and
causes atelectasis
75
Clinical manifestations of Pulmonary Edema
dyspnea, orthopnea, paroxysmal nocturnal dyspnea(wakes person up), crackles in lungs, Hemoptysis(pink frothy sputum), and Hypoxia
76
Hypercalcemia is
Excess serum calcium levels which can be caused by hyperparathyroidism, excess vitamin D intake, or cancers with bony metastes -CA++resorption(loss from) bone
77
Clinical manifestations of Hypercalcemia
- cells less excitable
- anorexia, constipation
- kidney stones
- ECG changes
78
Hypocalcemia is
Low Serum Ca++ levels which can be caused by inadequate intestinal absorption, nutritional deficiency of CA++ or Vitamin D
Excess Dietary PO4
malabsorption of fat
hypoparathyroidism
79
Clinical manifestations of hypoglycemia include
```
increased neuromuscular excitability
confusion
facial twitching
muscle spasms/convulsions
diarrhea/cramping
cardiac rhythm problems
```
80
Cigarette smoking increases risk for CAD because
Nicotine causes release of epinephrin, which causes increased HR and Vasoconstriction
and increased platelet stickiness and increased clot formation
Carbon Monoxide attaches to Hgb molecules causes less 02 to be carried to the tissues
81
CAD occurs earlier and more severely with
diabetes. increased blood glucose accelerates CAD.
82
Women have higher mortality rates after
Acute myocardial infarctions. CAD is the number one killer of American Women
83
Cocaine and Methamphetamines are risks factor for CAD because it
increases blood pressure, heart rate, and causes vasoconstriction of coronary arteries
84
CAD detection is more difficult in women because
they have smaller coronary arteries, delay treatment, and have less favorable outcomes. CAD is considered a silent killer
85
Hyperhomocysteinemia
amino acids broken down by the liver with the help of vitamins B6, B12, and folic acid, acids causes injury to arteries walls.....treat with folic acid
86
Classical(typical) manifestations of Myocardial ischemia
transient lasting from 3-20 minutes
sub-sternal pain, discomfort, heaviness, pressure, tightening, squeezing, aching, may radiate to neck, left arm, jaw, teeth, or back
87
non-classical (Atypical) manifestations of Myocardial Ischemia:
Indigestion, upper back pain, jaw pain only, increasing fatigue
88
Classical(typical) manifestations of Myocardial infarctions
changes in Bp, HR, rhythm, (not relieved by nitroglycerin), sub-sternal pain, discomfort, heaviness, pressure, tightening, squeezing, aching...may radiate to neck, left arm, jaw, teeth, back, indigestion, nausea, vomiting, diaphoresis.
89
non-classical (Atypical) manifestations of Myocardial Infarction
weakness, fatigue, dyspnea SOB, upper back pain, No symptoms
90
Zone of Ischemia
collateral circulation causes healing
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zone of injury
collateral circulation also causes healing
92
zone of infarction
does not heal, becomes scar tissue
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P-wave
impulse from SA (normal pacemaker) through atria and atrial contraction
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PR interval
beginning of P to beginning of QRS (impulse from SA) through AV
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QRS
impulse through ventricles (contraction)
96
T-wave
repolarization of ventricles
97
Backward effects of LVF
- decreased emptying of the left ventricle
- leads to increased volume(preload)in left ventricle
- leads to increased volume (preload) to left atrium
- increased volume in pulmonary veins
- increased volume in pulmonary capillary bed
- movement of fluid from capillaries to alveoli activation
- leads to rapid filling of alveolar spaces
- pulmonary edema
- leads to (R) ventricular failure
98
Forward effects of LVF
- decreased cardiac output
- decreased perfusion of tissues of body
- leads to decreased blood pressure
- decreased blood pressure
- decreased GFR(glomerular filtration rate)
- decreased urine output
- decreased Renin-Angiotensin-aldosterone
- decreased sodium and water retention
99
Right Ventricular Heart Failure Backward Effects
- decreased emptying of the RV
- increased volume(preload) in the RV
- increased volume(preload) in the right atrium,
- increased volume in the vena cava
- increased volume in the systemic venous circulation
- increased volume in distendable organs(hepatomegaly,splenomegaly)
- increased capillary pressure
- peripheral, dependent edema
100
Myocardial ischemia
Local and temporary deficiency of blood supply due to obstruction of coronary circulation
101
CAD is a progressive disease that leads to
myocardial ischemia which causes angina(chest pain and discomfort)
102
Myocardial Ischemia is an imbalance between supply(decreased blood flow to myocardium) and
demand (myocardium's need for 02 and nutrients)
```
Myocardial cells become ischemic within
10 seconds(myocardial 02 deficit)
Anaerobic metabolism(without 02) leads to lactic acid accumulating which leads to chest pain(angina)
```
103
stable (angina)
predictable, similar events initiate attack,like stress/activity
similar type of sensation with each heart attack
aliened with rest and nitrates
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acute coronary syndrome-
sudden coronary artery obstruction due to thrombus formation over atherosclerotic plaque
unstable angina-indicate advanced CAD(impending MI)
MI may be associated with sudden death
105
Lab data value that you would see change in case of an MI would be
increased CPK(creatinine photokinase)
Troponin (cardiac muscle cell)
WBC(reflects inflammatory response)
Glucose(Blood sugar elevates with stress)
106
Myocardial infarction(Left Ventricle)
CAD leads to myocardial ischemia which leads to irreversible hypoxia na cellular death.
Cause is narrowed coronary artery(CAD) + clot formation(coronary artery 100% occluded
107
In a MI there is Cellular injury and the cellular death:
Cellular injury occurs in the first 30-60 seconds of hypoxia and causes EKG changes because myocardial cells are deprived of 02 and nutrients and lose contractility
and cellular death(myocyte)-after 20 minutes cellular death and necrosis(infarction)
Remodeling leads to scar formation, loss of functional cardiac cells, thin, poorly contracting ventricular walls
cell membranes rupture intracellular enzymes spill out into the bloodstream
*zone of infarction is weak and mushy for 10-14 days post MI, strong scar forms after 6 weeks
108
MI can lead to
decreased ejection fraction(%of blood from LV)
| and arrhythmia/dysryhtmias
109
Clinical manifestations of Right ventricular Heart failure:
jugular vein distention, increased central venous pressure in Right Atrium, peripheral edema, weight gain, fatigue, exercise intolerance, abdominal distention caused by hepatomegaly, and splenomegaly
110
Right ventricular Heart Failure(for Pulmonate) is commonly caused by
Left ventricular HF and pulmonary artery hypertension, COPD, pulmonary emboli
111
Left ventricular Heart failure(CHF) is caused by
MI (CAD), hypertension, increased systemic vascular resistance, and aortic stenosis
112
compensatory mechanisms for Heart failure include:
ventricular hypertrophy(enlarged heart)
SNS
ADH
Renin Release
113
Heart Failure is the inability of the heart to maintain adequate cardiac output(perfusion) to support body functions. The heart fails as a pump(LV) Ejection fracture becomes less than
40%, and results in ventricular remodeling(here chamber walls become thin, dilated and poorly contract. Mortality rate 60-80%
114
Preload:
the load coming to the heart, is affected by blood volume
115
afterload:
the load against which the heart(LV) must pump out against, affected by vasoconstriction
116
Acyonotic heart defects
defects that still have good 02 levels, Left to Right shunt...caused by abnormal opening between the atria, leads to increased pressure and 02 on the right side of the heart. 90% occur at the foramen ovale
usually are asymptomatic
117
congenital heart defects can be caused by
drugs, alcohol, genetics, and environment
118
cyanotic heart disease has
a right to left shunt, lower 02 levels because desaturated venous blood flows into the left side of the heart, bypassing the lungs, because the pressure on the right side is greater that the left, or the vessels are misplaced.
119
Atrial Septal Defect
caused by an opening between the atrium, asyanotic with L to R shutting,
Increased oxygen and pressure in R atrium and R ventricle,also increased pulmonary blood flow.
120
Ventral Septal Defect
opening between the ventricles, is asyonitc with L to R shunting, Increased oxygen and pressure in R atrium and R ventricle,also increased pulmonary blood flow.
121
Patent Ductus Arterioles
Ductus does not close, asyonotic with L to R shunting
increased pressure in Left atrium and L ventricle
increased pulmonary blood flow
122
ASD, VSD, PDA, all have
Increased pulmonary blood flow
123
ASD and VSD both have
Increased oxygen and pressure in R atrium and R ventricle,also increased pulmonary blood flow.
124
Coarctation of aorta
Narrowing of Aorta, asyonotic but with no shunting, causes increased blood flow to upper body
125
Tetralogy of Fallot
cyanotic, R to L shunting caused by VSD, pulmonary stenosis overriding aorta, Right Ventricular hypertrophy.
Increased oxygen to Right ventricle and pulmonary artery, increased pressure in right Ventrical.
126
Transposition of Great vessels:
2 separate circulations, cyanotic, must have defect for necessary shunting
127
Acute rheumatic fever
inflammatory disease involving the heart, joints, subcutaneous tissue, CNS, and skin.
Has 2 possible causes
may be autoimmune reaction or cross-reactivity of the streptococcal antigens and other tissues
or could be damage to the tissue may be a result of antibodies against streptococcal organism attacking the individuals own tissues.
Usually occurs in school aged children
128
One major manifestation of rheumatic fever is
rheumatic heart disease(endocarditis): strep causes bacterial vegetation to to form on the valve leaflets causing swelling and on the myocardium causing it to become fibrotic and necrotic (called Aschoff bodies) Valves lose elasticity and may stick)
129
other major manifestations of rheumatic fever include:
- migratory polyarthritis: Large joint to joint every day or two, or 2 or more joints in succession or at the same time
- syndenhams chorea:inflammation in CNS, causes purposeless movements, self-limiting
- subcutaneous nodules: small, painless nodules located over bony prominences
- Erythema marginatum-Transient, non-pruritic rash on the trunk and proximal extremities
130
minor manifestation of rheumatic fever:
fever, documented history of strept throat(creative protein, ASO titer),Arthralgia(just regular overall joint discomfort), Increased Sedimentation Rate(test for inflammation)
131
Micro emboli that look like splinters in the nail beds are called
splinter hemorrhages and occur due to infective endocarditis
132
Micro emboli-
splinter hemorrhages, oilers nodes, Janaway Lesions
133
In dilated congestive cardiomyopathy,
heart ballots out, causing immense cardiomegaly(enlarged heart) RVF and LVF
134
In hypertrophic cardiomyopathy,
altered shape of chambers leads to poorly coordinated contractions, leads to LVF
135
In restrictive cardiomyopathy
ventricular dysfunction leads to both RVF and LVF
136
Valve disorders incude stenosis and regurgitation(insufficiency) can be caused by
inflammation, infections, trauma, degenerative connective tissue disorder
137
stenosis
valve orifice(opening) is narrowed and constricted, flow through the valve is impeded, increased pressure and workload of the chamber that is trying to eject blood through that valve.
138
regurgitation
valve leaflets fale to close completely, blood can leak back through the valve when it is supposed to be closed. Increased volume to pump, usually increased workload of both the chamber getting more volume, and the chamber trying to pump out.
139
In Aortic Valve Stenosis
LV tris to push to Aorta, causes increased LV pressure, hypertrophy, and workload. Causes narrowed pulse pressure and a systolic murmur
140
In Aortic Regurgitation
LV-Aorta(Leaks back to LV) causes increased volume to pump, LV volume overload due to back flow, LV hypertrophy, and increased LV workload
