Exam 2 Flashcards
(180 cards)
1
Q
Allergy
A
- how our immune system responds to exposure to antigens
2
Q
medical term for allergy
A
- hypersensitivity
3
Q
antigen
A
- substance that can generate an immune response
4
Q
Type 1 Hypersensitivity (Name)
A
- Immediate hypersensitivity
5
Q
Type 1 Hypersensitivity (Immediate Sensitivity)
A
- develops within minutes of exposure
- “allergic rxn”
- Mast Cell (explain other slide)
- Symptoms: edema and itching locally, runny nose, congestion, coughing
- can cause anaphylaxis
6
Q
Mast Cell
A
- Type 1 hypersensitivity
- specialized type of white blood cell
- have granules with histamine
- binding sites for IgE protein made by B-Cells
- displayed and when antigen binds, cell releases all histamine (causes mucus production, edema, inflammation, bronchoconstriction)
7
Q
Anaphylaxis
A
- type 1 hypersensitivity
- hypotension (decreased vasomotor tone) and respiratory distress (bronchoconstriction & edema)
- treat with epinephrine
8
Q
Type II Hypersensitivity (Name)
A
Antibody-Mediated
9
Q
Type II Hypersensitivity (Antibody Mediated)
A
- immune rxn due to binding of antibodies to antigens
- antibodies coming from B-Cells
- autoimmune (antibodies bind host cells)
- complement system
10
Q
Complement System
A
- Type II hypersensitivity activates this
- set of proteins that punch holes into cells when it is activated
11
Q
Two diseases associated with Type II Hypersensitivity
A
- Autoimmune hemolytic anemia
- Goodpasture Syndrome
12
Q
Goodpasture Syndrome
A
- Associated with Type II hypersensitivity
- antibodies bind to the basement membrane of the lungs and kidneys
- respiratory and renal failure
13
Q
Type III Hypersensitivity (Name)
A
- Immune Complex Mediated
14
Q
Type III Hypersensitivity (Immune Complex Mediated)
A
- immune complex deposited onto blood vessel walls and in tissues
- immune complex: antibody bound to protein that contains the target antigen
- injury to vessel walls and tissues b/c of thrombosis
15
Q
Three examples of Type III hypersensitivity diseases
A
- Lupus: auto-antibodies bind proteins expressed in nucleus of cells.. cell damage releases these complexes and they are deposited around the body
- Arthus Rxn: skin necrosis at vaccination site b/c immune complexes bind foreign antigens found in the vaccine.
- Serum Sickness: immunized with one serum, build antibodies against it, immunized again with same serum immune complexes form
16
Q
Type IV Hypersensitivity (Name)
A
- Cell Mediated
17
Q
Type IV Hypersensitivity (Cell-Mediated)
A
- initiated by T-Cells
- delayed hypersensitivity
- T-Cells are primed against certain agents (viruses, fungi, bacteria..) they have been exposed to
- When seen again, creates inflammation to destroy cells
- Ex) TB skin test, Poison Ivy
18
Q
Uncontrolled Granulomas
A
- Sarcoidosis
19
Q
Antigens (5)
A
IgM IgG IgA IgE IgD
20
Q
IgM
A
- 5 individual igM antibodies together
- seen in early response to infection
21
Q
IgG
A
- primary antibody in antibody response to infection
- appears soon after IgM
- monomer
22
Q
IgA
A
- found in secretions and mucosal surfaces
23
Q
IgE
A
- antibody associated with immediate hypersensitivity
- found on surface of mast cells
- when antigens bind IgE, mast cells release histamine
24
Q
IgD
A
- found on surface of developing B-Cells as a receptor molecule
25
rapid red cell destruction
- hemolysis
- can be from inherited/aquired abnormality of red cell
- or abnormality of blood or blood vessels that causes injury to cell
26
hypochromia
- pale RBC (b/c of decreased hemoglobin)
27
abnormal shape of RBC
- poikilocytosis
28
Aplastic Anemia
- decreased number of stem cells
- macrocytic or normocytic
- bone marrow is empty (just adipocytes)
- all marrow cells affected
- treatment: transfusion, bone marrow transplant, immunosuppresion
29
"Anemia of Chronic Disease"
- inflammatory anemia
- iron held in macrophages, cannot be used for RBC production
- bone marrow usually normal
- microcytic or normocytic
30
Iron Deficiency
- most common form of anemia world wide
- from chronic blood loss (GI Bleed), menstruation, pregnancy
- just drinking cow's milk as an infant
- microcytic and hypochromic
- Treatment: Iron supplements, find source of bleeding
31
Pernicious Anemia
- Vitamin B-12 deficiency
- needed for DNA synthesis during RBC production
- Macrocytic with delayed maturation (megaloblastic)
- Often due to stomach disorder causing decreased production of factor needed for B-12 absorption
- Treatment: B-12 injections
32
Folic Acid Deficiency
- needed for DNA synthesis of red cells
- macrocytic /megablastic
- poor diet/alcohol abuse, use of drugs/ malabsorption
- Treatment= oral folic acid supplements
33
Thalassemia
- inherited disorder of hemoglobin production
- alpha thalassemia/beta thalassemia
- microcytic
- thalassemia minor: slightly decreased production
- thalassemia major: severe/no production
- need transfusions
34
Hemolytic Anemia General Features
- INCREASED production of RBC, increased # RBC precursors in blood, increased numbers of newly made cells
- high billirubin in blood
- destroyed either in spleen by being taken up by macrophages or while still in the blood stream
35
Sickle Cell Anemia
- type of hemolytic anemia
- inherited structural abnormality
- repeated cycles of hemoglobin polymerization causes cells to become rigid and clog small blood vessels causing tissue damage/death
- recessive inheritance... if one allele.. sickle cell trait
36
Autoimmune Hemolytic Anemia
- Production of antibodies against one's own RBC
- eaten by macrophages in the spleen and destroyed
- can be detected by the Coombs test
- Treatment: Immunosupression
37
Transfusion Rxn
- Hemolytic Anemia
- antibodies are made against other types of blood
- immediate massive hemolysis and severe or fatal immune reaction
38
Erthroblastosis Fetalis
- Hemolytic disease of the newborn
- mother (Rh-) previously exposed to RH antigen on fetal cells and makes antibodies to it
- in next pregnancy, can cross placenta and destroy RBC of fetus.. high billirubin, misscarries
- need to give anti-Rh serum to Rh- mother at time of delivery to destroy Rh+ cells that get into mother's circulation
39
Polycythemia
- too many RBCs
| - blood too thick, slow flow, risk of thrombosis
40
Polycythemia Vera
- primary polycythemia
| - no negative feedback on erythropoiten
41
Secondary Polycythemia
- RBC production in response to increased erythropoiten
| - usually caused by chronic low O2 levels in blood due to lung or cardiac disease
42
Neutropenia
- Decreased neutrophils production
- aplastic anemia or other forms of marrow failure
- also caused by chemotherapy
- Increased neutrophil consumption
- autoimmune
- severe infection
- enlargement of spleen
43
Increased risk of ______ with Neutropenia?
- Bacterial or Fungal Infection
44
Neutrophilia
- Increased Neutrophils
1. increased production of neutrophils in response to stimuli like infection
2. take corticosteroid drugs to fight infection, makes neutrophils less sticky on blood vessel wall surface
- more in blood, "higher count" but less to fight infection
3. unregulated production (leukemia)
45
Demargination
- when neutrophils stick less on blood vessel walls and more in blood
46
Lymphadeopathy
- enlargement of lymph nodes
| - from cancer or infection or inflammation
47
Splenomegaly
- Enlargement of Spleen
- many causes
- may cause low platelet counts b/c spleen soaks up these cells
48
Asplenia
- absence of spleen
| - lowers resistance to certain infections b/c spleen acts as a filter to remove bacteria from blood
49
Thrombocytopenia
- low platelet count
50
qualitative platelet disorders
- # normal, function abnormal
51
Leukemia definition
- Neoplastic (cancerous) proliferation of leukocyte precursors (blasts)
- cancerous cells replace normal bone marrow, spread via blood to other tissues
- caused by genes, infections, exposure to substances
52
Acute vs Chronic Leukemia (General)
- Acute: proliferation of immature leukocytes precursors that have lost the ability to differentiate.. never stop dividing, accumulate rapidly
- Chronic: proliferation of leukocyte precursors that retain the ability to differentiate, cells stop dividing when they differentiate, slower progressing
53
Manifestations of Leukemia
- accumulation of leukemic cells in bone marrow (marrow failure)
- accumulation of leukemic cells in blood
- accumulation of leukemic cells in tissues (spleen and lymph nodes)
- release of toxic substances from leukemic cells (tissue damage and clotting)
54
Acute Lymphoblastic Leukemia (ALL)
- either B or T-Cell precursors (blasts)
- most common form of leukemia in children (but adults too)
- rapidly progressing, often curable esp. in children with chemo and/or marrow transplant
55
Acute Myelogenous Leukemia (AML)
- most common adult leukemia
- proliferation of granulocyte precursors (blasts)
- treatable, occasionally curable with chemo and/or bone marrow transplantation
56
Chronic Myelogenous Leukemia (CML)
- malignant proliferation of myeloid stem cell with overproduction of white cells and platelets
- causes enlarged spleen, fever, fatigue, weight loss, circulatory problems
- treatable but can transform into fatal acute leukemia (Blast crisis)
- rare in children
- Philadelphia Chromosome : fusing of two parts of chromosomes and causes uncontrolled growth of myeloid cells
- targeted therapy
57
Chronic Lymphocytic Leukemia (CLL)
- B-cell proliferation.. SLOWLY GROWING
- primarily affects older people over 40
- enlarged lymphnodes and spleen
- may be asymptomatic for years
- gradual decrease in marrow function
- treatable but not curable
58
Lymphomas
- cancerous proliferation of lymphocytes and their precursors
- generally behave as "solid tumors" but malignant cells in blood as well
59
Non-Hodgkin's Lymphomas (2 types and what they cause)
- Low Grade: slowly growing, mature appearing cells. generally incurable but treatable , survive for many years
- High Grade: faster growing, less mature cells. potentially curable, very fast acting
- Cause enlargement of lymph nodes, spleen, infiltrate bone marrow, some types cause leukemia
60
Hodgkin's Lymphoma
- Distinctive microscopic appearance, multinucleated cells
(Reed-Sternberg Cells.. owl eyed)
- one of more common types of cancer in adolescents and young adults
- almost always originates in lymph nodes, spreads to spleen, bone marrow, liver, other organs
- moderate growth rate
- most patients can be cured if in early stages
61
Stages of Hodgkin's Lymphoma
- Stage 1: disease confined to single lymph node or group of nodes
- Stage 2: disease in two or more lymph node groups on same side of diaphragm
- Stage 3: disease in lymph nodes on both sides of diaphragm
- Stage 4: spread outside of lymph nodes
62
Multiple Myelomas
- cell of origin: plasma cell
- often secrete monoclonal immunoglobulin
- causes bone destruction, damage to kidneys and nerves, predispose to infection
- treatable but not curable with average survival 3-4 years
- >40 yrs old
63
Cells of Circulatory System (2)
- Endothelial Cells: maintain homeostasis of blood, secrete substances to control vascular tone
- Smooth Muscle Cells: respond to substances secreted by endothelial cells, distributes blood flow as needed
- Connective Tissue: forms matrix of blood vessel
64
Structure of Blood Vessel (3 types)
- Intima
- Media
- Adventitia
65
Intima
- thin portion of inner lining of blood vessel
| - predominantly endothelial cells
66
Media
- middle layer
- mainly smooth muscle cells
- absorbs pulsatile force
67
Adventitia
- outermost structure of the blood vessel
| - acts as a protective coat
68
Large Arteries
- Elastic
| - control flow, absorb pulsatility
69
Arterioles
- thin layer smooth muscle
70
Capillaries
- single layer vessels of endothelial cells
| - leaky into lymph nodes
71
Venule System
- low pressure, low flow system
- one way valves keep blood from going backwards
- veins more stiff
72
Atherosclerosis
- buildup of atherosclerosis plaque of foam cells
- growth outward first, then inward
- lipoprotein buildup on surface of vessel allows WBC to congregate at surface which evolve into macrophages
73
Risk Factors for Atherosclerosis
- Diet
- Smoking
- Hypertension
- High Cholesterol
- Low Physical Activity
- Overweight/Obese
- Diabetes Melilitus
- Alcohol
- Male gender, menopause, age, chronic inflammation
74
Coronary Artery Disease
- Plaques build up and reduce blood flow through artery gradually
- blood flow eventually significantly reduced
- get angina
- unstable plaque can then rupture producing myocardial infarction
75
Atherosclerosis Carotid Artery Disease
- plaques become severely compromised, stroke-like symptoms occur
- could be multiple paths to one area, not as bad
- Transient ischemic attacks.. stroke like symptoms coming and going over minutes to hours
76
Peripheral Artery Disease
- plaques severe enough to reduce blood flow to certain muscle groups
- acute onset of pain and weakness during exercise
- may need amputation if whole vessel is blocked and downstream isn't getting any bloodflow
77
Aneurysms
- areas of enlargement of an artery to a diameter >50% above normal size.
- expand gradually
- usually not due to plaques, more likely focal inflammation
- berry aneurysm: brain aneurysm
- can be congenital (cerebral) or acquired (syphilis, atherosclerosis, infections)
78
Aortic Dissection
- tear in intimal layer of an artery
| - patients with aneurysms are more likely to have dissection
79
Vasculitis
- local inflammation of artery which can cause deterioration of vessel, bleeding, and compromise of lumen.
80
telangelectasias
- localized dilations of veins and loss of integrity of valves
81
varicose veins
- dysfunction of larger superficial veins
82
Chronic Venus insufficiency
- disease of the larger veins and deeper veins
| - failure of valves resulting in stasis, edema, ulceration and deterioration of skin.
83
Venous Thrombosis
- Occurs in patients who do not move very much
| - blood clot develops in vein in leg
84
Typical Angina
- chest discomfort from low blood flow to heart
- increased demand for flow from overexertion or emotional symptoms
- when these stop, pain stops
- pain can radiate outward
85
What can be taken to make angina go away faster?
- nitroglycerin
86
atypical/non-cardiac chest pain
- chest pain that does not have symptoms of angina
87
Ischemic Cascade (5)
- Use stress test to see if symptoms can be induced
- on treadmill, hooked up to EKG
- echo or MRI also may be used before/after test to see mechanical function
- nuclear perfusion agent: perfusion abnormality (ischemic cells do not take up this agent)
- metabolism scan: see abnormal metabolism
- angiogram: find location of blockages
88
Bypass surgery usual artery
- left mammary artery b/c resistant to atherosclerosis
| - otherwise use vein from leg
89
Acute Coronary Artery Disease
- pain >20 minutes results in permanent damage to heart
- 95% of heart attacks are caused by activation of a plaque
- rupture damages tissue which attracts platelets which attracks RBC to clot... get a thrombus
90
Acute Myocardial Infarction Facts
- 30% mortality rate
- half occur before patient reaches the hospital
- occurs because heart goes into v fib, cardiac arrest
- upon reaching hospital, given fibrinolytic agent to dissolve clot or emergency catheterization
91
Blockages at beginning of coronary arteries
- cause large heart attacks, substantial damage, often heart failure
92
Complications of myocardial infarction
- heart failure
- rupture of wall in heart
- rupture of papillary muscle, which results in mitral valve failure
- aneursym formation
- sudden death
93
average mortality rate of patients who survive MI one year post attack
4%
94
Long term therapy after MI
- modify as many risk factors as possible
- aspirin to prevent clots
- beta blockers to decrease risk of heart failure
- cholesterol lowering agents
- antiotensin converting enzyme inhibitors: prevent heart enlargement over time
95
Valvular Stenosis
- poor opening of valve
- results in hypertrophy of cardiac muscle
- pressure overload hypertrophy to push enough blood out of left ventricle to body.. chamber stays same size
- increase in diameter and density of myocytes in wall of left ventricle
96
Valvular Insufficiency
- poor closing of valve
- blood leaks back into left ventricle
- increased workload causes an enlarged chamber in order to make sure correct amt of blood is still being pumped out
- called eccentric hypertrophy
- myocytes lengthen to accompany volume overload
97
problem with adaptive changes in heart for valve problems
- muscle eventually exhausts ability to hypertrophy further
| - heart muscle will fail
98
Aortic Stenosis (etiology)
- congenital bicuspid valve
- rheumatic heart disease
- senile calcific aortic stenosis
99
Aortic Stenosis (mechanism)
- only rheumatic disease causes direct injury and inflammation to valve
- LDL buildup on valves prevents opening
- cells transformed from fibrocytes to osteoblasts
100
Aortic Stenosis (Symptoms) (3)
- Exertional Angina Pectoris: consequence of inadequate blood flow to left ventricular myocardium during exercise
- Exertional Syncope: fainting because blood vessels dilate during exercise and reflex responses to increased pressure in left ventricle dilates vessels even more
- Heart Failure: increased pressures of filling cause congestion in lungs
101
Aortic Stenosis (Treatment)
- no cure by medication
- only way to fix is by replacement of valve with prosthetic device
- mechanical valve
- biological valve
- homograft
102
Mechanical Valve (Aortic Stenosis)
- St. Jude Valve/ Medtronic valve
- made of titantalum
- increase risk of blood clots on valve, must take warfarin
103
Biological Material Valve (Aortic Stenosis)
- from porcine or bovine pericardium strung over metal frame
- works well but has tendency to deteriorate or calcify over time
- given to people who can't handle anticoagulants or that are elderly
104
Homograft (Aortic Stenosis)
- heart valve harvested from human cadaver
| - does not require immuno-supression
105
Aortic Insufficiency (Etiology)
- Rhuematic Heart Disease
- Destruction of leaflets by endocarditis
- Bicuspid Valve
- Abnormalities of the aorta causing dilation of the annulus of the valve
106
Aortic Insufficiency (Symptoms)
- shortness of breath from exertion
| - slowly progressing
107
Aortic Insufficiency (Treatment)
- valve replaced with prostethic and sometimes aorta repaired or reinforced with Dacron conduit.
108
Mitral Stenosis (Etiology)
- most caused by rheumatic heart disease
- causes fusion of mitral leaflets
- later stages calcification
109
Mitral Stenosis (Symptoms)
- progressively increasing severity of shortness of breath
| - causes cardiac dyspnea
110
Cardiac Dyspnea
- high pressure in lungs from high pressure in left atrium
- fluid leaks out which lymphatic system picks up
- lymphatic system becomes overwhelmed, blood backs up into alveolar space and collapses sacs
111
Mitral Stenosis (Treatment)
- balloon catheter or prosthetic
112
Mitral Insufficiency (Etiology)
- rheumatic heart disease
- mitral valve prolapse
- disease which cause papillary muscle or chordae tendineae to rupture
113
Mitral Insufficiency (Symptoms)
- gradually develop shortness of breath with exertion
| - acute sudden development is medical emergency
114
Mitral Insufficiency (Treatment)
- surgical repair or prosthetic
115
Right Sided heart valve problems (3)
- pulmonic stenosis (congenital)
- tricuspid stenosis (rheumatic heart disease)
- Tricuspid insufficiency (very common, occurs secondary to enlargement of right ventricular or atrial chambers)
116
Heart Sounds Lub, Dub
| Murmurs
Lub: mitral valve closing
Dub: aortic valve closing
Whistle: Stenotic valve
Gurgle: Insufficient valve
117
Endocarditis (Etiology)
- bacterial normally present in the flora of the GI tract
| - acute endocarditis: caused by staphylococcus aureus or beta hemolytic streptococcal species
118
Endocarditis (Symptoms)
- inflammation of the endocardium
- common cause of valvular insufficiency
- significant heart failure if insufficiency becomes severe
119
Endocarditis (Diagnosis)
- culturing the organism
- identifying abnormal cardio waves
- using transesophageal echocardiography
120
Endocarditis (Treatment)
- can have surgery to correct if makes valvular insufficiency
- homograft
- antibiotics
121
Neoplasia
- New Growth
| - heritably altered, relatively autonomous growth of tissue
122
Growth Advantage
- either higher replicative rate or slower death rate than surrounding cells
- creates genetically unstable cells which can accumulate more mutations to give even more growth advantage
123
relative autonomy
- grow without some consideration to signals, still respond to their environment
- can't get too big or won't be able to get adequate nutrients from environment
- still responsive to growth hormones
- sometimes can grow own vessels
124
Benign Neoplasms
- slowly growing do not spread to other tissues
| - still can be harmful as they grow, causing pain, inducing bleeding, erosion, can produce hormones
125
Malignant Neoplasms
- rapidly growing, ability to spread to other organs
126
suffix "-oma"
- "growth"
127
Carcinoma
- malignant neoplasm in which cells arise from epithelium and differentiating towards epithelial cells
- most common forms of cancer
- breast, lung, colon, prostate
128
Sarcoma
- less common
- from mesenchymal cells
- connective tissues
129
Invasion
- contiguous (touching) growth of neoplastic cells beyond site of origin
- requires enzymes that can degrade surrounding tissues
130
dysplastic
- features of malignancy even though benign, risk for behaving malignant in the future
131
3 types of enzymes that degrade surrounding tissue for malignant neoplasms
- metalloproteinases
| - serine & cystine proteinases
132
Metalloproteinases
- attack basement membrane where epithelial cells are anchored.
133
serine and cystine proteinases
- attack extracellular matrix proteins in the tissues through which malignant cells migrate
134
Metastasis
- non-contiguous (not touching) spread of malignant cells through the body
- ex. brain cancer spreading to lymph nodes, breast cancer growing in lung
- occurs fairly late in course of neoplasms
135
Metastatic Cascade (6 steps)
- invade (surrounding tissues)
- intravasation (grow through wall of vessel)
- intravascular circulation (establish platelet coat to evade immune system, travel through circulation)
- extravasation (adhere to vessel wall, migrate back out)
- establish in new location
- angiogenesis (growth of own blood supply)
136
Differentiation
- degree of resemblance of a neoplasm to its tissue of origin
137
Anaplastic
- cells showing no differentiation at all, impossible to tell what tissue of origin is
138
Malignant lesions by definition are ______
- invasive
139
Benign lesions by definition are ______
- not metastatic
140
Mitotic Figures
- what you see when chromatids line up to divide
- indicative of active replication of cells
- grade of neoplasms measured by how many mitotic figures present
141
Grade of neoplasm measurement
- how many mitotic figures present
142
N:C ratio
- Nucleus cytoplasmic ratio
143
Stage/TNM
- how widely the malignancy has spread by invasion or metastasis
144
3 criteria to "stage" of neoplasm (TNM)
- extent of local growth of tumor (T)
- extension to lymph nodes (N)
- presence of distant organ metastases (M)
145
Why is stage important in neoplasia?
- determines course of treatment
| - correlates with survival
146
4 generalizations about malignant neoplasms
- cancer is a disease of genes
- cancer is clonal
- development of cancer (carcinogenesis) is a multistep process
- basic physiological functions in cells are commonly corrupted in pathway to cancer
147
8 functions of cells that are commonly corrupted in pathway to cancer
- Self-sufficiency in growth signals
- insensitivity to growth-inhibition
- evasion of apoptosis
- defective DNA repair
- limitless replicative potential
- angiogenesis
- ability to invade/metastasize
- evasion of immune system
148
Familial Cancer Syndromes
- altered gene expression that can be passed through generations
- patient inherits one allele of a defective gene, something then happens to other allele
149
Chemical Carcinogenesis
- types of chemicals linked to "hits"
150
3 steps required for development of cancer after chemical exposure
- initiation: appearance of permanent DNA damage in a cell
- promoters: agents that stimulate proliferation
- progression: when promoter comes at correct time after initiation, path to cancer progresses
151
Damage by radiation is ______ _______
dose dependent
152
UV light causes formation of what?
- pyrimidine dimers in DNA
153
UV lights causes what type of cell cancer?
-squamous and basal cell carcinoma
154
Ionizing Radiation causes what?
- leukemia, breast, lung, thyroid
155
Microbes and cancer
- helicobacter pylori (only bacterium)
| - many viruses
156
microbial oncogenesis involves: (3)
- insertion of viral DNA
- expression of viral proteins that drive DNA transcription
- stimulation of chronic inflammation (drives rapid host cell turnover)
157
most new cases of cancer/yr M&F
| causes of deaths/yr M&F
- new cases M: prostate, F: breast
| - causes of death: M&F: lung
158
Factors that effect cancers
- Age of patient
- Sex
- Race
- Geography
- Risk factors
- Genetic Predispositions
- Rate and pattern of growth and spread (ex. prostate cancer very slow growing)
159
Most cancers treated with combination of (3)
- surgery, radiation therapy, chemotherapy (kills all rapidly dividing cells)
160
Targeted or molecular therapy
- only cells expressing certain dysregulated protein are hit with drug
161
Major types of congenital heart disease (5)
- inadequate development of a cardiac chamber or major blood vessels leading from the heart.
- heart valve abnormality
- failure of development of a complete dividing partition between two major chambers
- abnormal connections of vessels to cardiac chambers
- combination of multiple above
162
Failure of dividing partition to fully form
- cardiac shunt forms
- shortcut through partition
- normally left-right b/c of high to low pressure
- blood through shunt is wasted
- greater amt of flow must pass to get same output
163
Atrial Septal Defect
- hole in atrial septum dividing two atrial chambers
- 7% all congenital defects
- hypertrophy of L&R atrium, R ventricle
- many no symptoms and not detected until later in life
- shortened lifespan with large defect
- lesions corrected with surgery
164
Ventricular Septal Defect
- hole between left and right ventricle
- 20% all congenital heart defects
- discovered shortly after birth b/c of loud murmur
- small holes usually close within first year
- large holes can cause symptoms of heart failure and congestion early in life
- large require surgery
- if not treated, shortens lifespan
165
Patent Ductus Arteriosus
- aorta and pulmonary artery don't separate after birth
- 8% all congenital defects
- large shunts results in heart failure
- vessel closed surgically or plugged
166
Cyanotic Heart Disease
- right to left shunt
- results in non-oxygenated blood out to body.. "blue baby"
- much more severe and often in combo with other things
- complex surgical repairs
167
Tetralogy of Fallot
- most common cause of cyanotic disease
- 4 abnormalities
- obstruction of outflow of blood from right ventricle to lungs
- right ventricular hypertrophy
- ventricular septal defect
- abnormal positioning of aorta
168
Normal Pericardium
- tough,thick, fibrous structure which surrounds heart
- protects from excessive motion and friction
- can function with no pericardium or open pericardium
169
Pericarditis
- localized inflammation of pericardial sac
- commonly caused by viral infection
- causes chest pain and production of fluid
- most situations, goes away with anti-inflammatory medication
170
Pericardial Effusion
- fluid accumulation within pericardial space
- most is a benign process that runs its course
- if severe, pressure rises on right side of heart, reduces volume
- heart failure, shock, death
171
Constrictive Pericarditis
- chronic inflammation --> chronic fibrosis
- forms shell around heart
- larger and thicker the shell, greater the amount of "constriction"
- reduced cardiac output
- treatment is removal of pericardium
- fungal infection or TB can cause
172
Primary Cardiomyopathy
- abnormality of myocytes of ventricular chambers
173
Secondary Cardiomyopathy
- result of a response of the myocytes to other disease processes
- ex. ischemic heart disease, toxins
174
Dilated Cardiomyopathy
- most common type of cardiomyopathy
- systolic dysfunction
- ventricular enlargement
- cardiac remodeling
175
Hypertrophic Cardiomyopathy
- disorder of the sarcoplasmic reticulum
- 50% family history
- genetic screening available
- asymmetry of hypertrophy
- septum thinned
- ventricular chambers lower vlume
- myocardial disarray (disordered myocardial architecture)
176
Restrictive Cardiomyopathy
- stiffened heart b/c of abnormal material between heart cells
- amyloid protein
- abnormality of diastole (filling)
- cuts into reserve
- transplantation only cure
177
Arrhythmogenic right ventricular cardiomyopathy
- right ventricle myocytes replaced by fatty tissue
| - fatal arrhythmia common
178
Heart Failure
- impaired ability of the heart to fill or eject blood
- most common symptoms are dysnpea and fatigue, fluid retention in lungs or circulation
- 5 million in US
179
Treatment of Heart Failure- Diuretic
- eliminate fluid
180
Angiotensin converting enzyme inhibitors
-
