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Exam 2 Flashcards

1
Q

Allergy

A
  • how our immune system responds to exposure to antigens
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2
Q

medical term for allergy

A
  • hypersensitivity
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3
Q

antigen

A
  • substance that can generate an immune response
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4
Q

Type 1 Hypersensitivity (Name)

A
  • Immediate hypersensitivity
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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
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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)
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7
Q

Anaphylaxis

A
  • type 1 hypersensitivity
  • hypotension (decreased vasomotor tone) and respiratory distress (bronchoconstriction & edema)
  • treat with epinephrine
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8
Q

Type II Hypersensitivity (Name)

A

Antibody-Mediated

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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
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10
Q

Complement System

A
  • Type II hypersensitivity activates this

- set of proteins that punch holes into cells when it is activated

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11
Q

Two diseases associated with Type II Hypersensitivity

A
  • Autoimmune hemolytic anemia

- Goodpasture Syndrome

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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
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13
Q

Type III Hypersensitivity (Name)

A
  • Immune Complex Mediated
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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
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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
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16
Q

Type IV Hypersensitivity (Name)

A
  • Cell Mediated
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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
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18
Q

Uncontrolled Granulomas

A
  • Sarcoidosis
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19
Q

Antigens (5)

A 
IgM
IgG
IgA
IgE
IgD
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20
Q

IgM

A
  • 5 individual igM antibodies together

- seen in early response to infection

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21
Q

IgG

A
  • primary antibody in antibody response to infection
  • appears soon after IgM
  • monomer
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22
Q

IgA

A
  • found in secretions and mucosal surfaces
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23
Q

IgE

A
  • antibody associated with immediate hypersensitivity
  • found on surface of mast cells
  • when antigens bind IgE, mast cells release histamine
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24
Q

IgD

A
  • found on surface of developing B-Cells as a receptor molecule
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25
Q

rapid red cell destruction

A
  • hemolysis
  • can be from inherited/aquired abnormality of red cell
  • or abnormality of blood or blood vessels that causes injury to cell
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26
Q

hypochromia

A
  • pale RBC (b/c of decreased hemoglobin)
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27
Q

abnormal shape of RBC

A
  • poikilocytosis
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28
Q

Aplastic Anemia

A
  • decreased number of stem cells
  • macrocytic or normocytic
  • bone marrow is empty (just adipocytes)
  • all marrow cells affected
  • treatment: transfusion, bone marrow transplant, immunosuppresion
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29
Q

“Anemia of Chronic Disease”

A
  • inflammatory anemia
  • iron held in macrophages, cannot be used for RBC production
  • bone marrow usually normal
  • microcytic or normocytic
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30
Q

Iron Deficiency

A
  • 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
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31
Q

Pernicious Anemia

A
  • 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
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32
Q

Folic Acid Deficiency

A
  • needed for DNA synthesis of red cells
  • macrocytic /megablastic
  • poor diet/alcohol abuse, use of drugs/ malabsorption
  • Treatment= oral folic acid supplements
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33
Q

Thalassemia

A
  • inherited disorder of hemoglobin production
  • alpha thalassemia/beta thalassemia
  • microcytic
  • thalassemia minor: slightly decreased production
  • thalassemia major: severe/no production
  • need transfusions
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34
Q

Hemolytic Anemia General Features

A
  • 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
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35
Q

Sickle Cell Anemia

A
  • 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
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36
Q

Autoimmune Hemolytic Anemia

A
  • 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
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37
Q

Transfusion Rxn

A
  • Hemolytic Anemia
  • antibodies are made against other types of blood
  • immediate massive hemolysis and severe or fatal immune reaction
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38
Q

Erthroblastosis Fetalis

A
  • 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
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39
Q

Polycythemia

A
  • too many RBCs

- blood too thick, slow flow, risk of thrombosis

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40
Q

Polycythemia Vera

A
  • primary polycythemia

- no negative feedback on erythropoiten

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41
Q

Secondary Polycythemia

A
  • RBC production in response to increased erythropoiten

- usually caused by chronic low O2 levels in blood due to lung or cardiac disease

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42
Q

Neutropenia

A
  • Decreased neutrophils production
    • aplastic anemia or other forms of marrow failure
    • also caused by chemotherapy
  • Increased neutrophil consumption
    - autoimmune
    - severe infection
    - enlargement of spleen
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43
Q

Increased risk of ______ with Neutropenia?

A
  • Bacterial or Fungal Infection
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44
Q

Neutrophilia

A
  • 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)
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45
Q

Demargination

A
  • when neutrophils stick less on blood vessel walls and more in blood
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46
Q

Lymphadeopathy

A
  • enlargement of lymph nodes

- from cancer or infection or inflammation

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47
Q

Splenomegaly

A
  • Enlargement of Spleen
  • many causes
  • may cause low platelet counts b/c spleen soaks up these cells
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48
Q

Asplenia

A
  • absence of spleen

- lowers resistance to certain infections b/c spleen acts as a filter to remove bacteria from blood

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49
Q

Thrombocytopenia

A
  • low platelet count
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50
Q

qualitative platelet disorders

A
  • # normal, function abnormal
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51
Q

Leukemia definition

A
  • 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
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52
Q

Acute vs Chronic Leukemia (General)

A
  • 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
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53
Q

Manifestations of Leukemia

A
  • 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)
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54
Q

Acute Lymphoblastic Leukemia (ALL)

A
  • 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
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55
Q

Acute Myelogenous Leukemia (AML)

A
  • most common adult leukemia
  • proliferation of granulocyte precursors (blasts)
  • treatable, occasionally curable with chemo and/or bone marrow transplantation
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56
Q

Chronic Myelogenous Leukemia (CML)

A
  • 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
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57
Q

Chronic Lymphocytic Leukemia (CLL)

A
  • 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
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58
Q

Lymphomas

A
  • cancerous proliferation of lymphocytes and their precursors
  • generally behave as “solid tumors” but malignant cells in blood as well
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59
Q

Non-Hodgkin’s Lymphomas (2 types and what they cause)

A
  • 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
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60
Q

Hodgkin’s Lymphoma

A
  • 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
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61
Q

Stages of Hodgkin’s Lymphoma

A
  • 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
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62
Q

Multiple Myelomas

A
  • 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
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63
Q

Cells of Circulatory System (2)

A
  • 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
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64
Q

Structure of Blood Vessel (3 types)

A
  • Intima
  • Media
  • Adventitia
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65
Q

Intima

A
  • thin portion of inner lining of blood vessel

- predominantly endothelial cells

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66
Q

Media

A
  • middle layer
  • mainly smooth muscle cells
  • absorbs pulsatile force
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67
Q

Adventitia

A
  • outermost structure of the blood vessel

- acts as a protective coat

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68
Q

Large Arteries

A
  • Elastic

- control flow, absorb pulsatility

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69
Q

Arterioles

A
  • thin layer smooth muscle
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70
Q

Capillaries

A
  • single layer vessels of endothelial cells

- leaky into lymph nodes

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71
Q

Venule System

A
  • low pressure, low flow system
  • one way valves keep blood from going backwards
  • veins more stiff
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72
Q

Atherosclerosis

A
  • 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
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73
Q

Risk Factors for Atherosclerosis

A
  • Diet
  • Smoking
  • Hypertension
  • High Cholesterol
  • Low Physical Activity
  • Overweight/Obese
  • Diabetes Melilitus
  • Alcohol
  • Male gender, menopause, age, chronic inflammation
74
Q

Coronary Artery Disease

A
  • 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
Q

Atherosclerosis Carotid Artery Disease

A
  • 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
Q

Peripheral Artery Disease

A
  • 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
Q

Aneurysms

A
  • 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
Q

Aortic Dissection

A
  • tear in intimal layer of an artery

- patients with aneurysms are more likely to have dissection

79
Q

Vasculitis

A
  • local inflammation of artery which can cause deterioration of vessel, bleeding, and compromise of lumen.
80
Q

telangelectasias

A
  • localized dilations of veins and loss of integrity of valves
81
Q

varicose veins

A
  • dysfunction of larger superficial veins
82
Q

Chronic Venus insufficiency

A
  • disease of the larger veins and deeper veins

- failure of valves resulting in stasis, edema, ulceration and deterioration of skin.

83
Q

Venous Thrombosis

A
  • Occurs in patients who do not move very much

- blood clot develops in vein in leg

84
Q

Typical Angina

A
  • 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
Q

What can be taken to make angina go away faster?

A
  • nitroglycerin
86
Q

atypical/non-cardiac chest pain

A
  • chest pain that does not have symptoms of angina
87
Q

Ischemic Cascade (5)

A
  • 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
Q

Bypass surgery usual artery

A
  • left mammary artery b/c resistant to atherosclerosis

- otherwise use vein from leg

89
Q

Acute Coronary Artery Disease

A
  • 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
Q

Acute Myocardial Infarction Facts

A
  • 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
Q

Blockages at beginning of coronary arteries

A
  • cause large heart attacks, substantial damage, often heart failure
92
Q

Complications of myocardial infarction

A
  • heart failure
  • rupture of wall in heart
  • rupture of papillary muscle, which results in mitral valve failure
  • aneursym formation
  • sudden death
93
Q

average mortality rate of patients who survive MI one year post attack

A

4%

94
Q

Long term therapy after MI

A
  • 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
Q

Valvular Stenosis

A
  • 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
Q

Valvular Insufficiency

A
  • 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
Q

problem with adaptive changes in heart for valve problems

A
  • muscle eventually exhausts ability to hypertrophy further

- heart muscle will fail

98
Q

Aortic Stenosis (etiology)

A
  • congenital bicuspid valve
  • rheumatic heart disease
  • senile calcific aortic stenosis
99
Q

Aortic Stenosis (mechanism)

A
  • only rheumatic disease causes direct injury and inflammation to valve
  • LDL buildup on valves prevents opening
  • cells transformed from fibrocytes to osteoblasts
100
Q

Aortic Stenosis (Symptoms) (3)

A
  • 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
Q

Aortic Stenosis (Treatment)

A
  • no cure by medication
  • only way to fix is by replacement of valve with prosthetic device
  • mechanical valve
  • biological valve
  • homograft
102
Q

Mechanical Valve (Aortic Stenosis)

A
  • St. Jude Valve/ Medtronic valve
  • made of titantalum
  • increase risk of blood clots on valve, must take warfarin
103
Q

Biological Material Valve (Aortic Stenosis)

A
  • 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
Q

Homograft (Aortic Stenosis)

A
  • heart valve harvested from human cadaver

- does not require immuno-supression

105
Q

Aortic Insufficiency (Etiology)

A
  • Rhuematic Heart Disease
  • Destruction of leaflets by endocarditis
  • Bicuspid Valve
  • Abnormalities of the aorta causing dilation of the annulus of the valve
106
Q

Aortic Insufficiency (Symptoms)

A
  • shortness of breath from exertion

- slowly progressing

107
Q

Aortic Insufficiency (Treatment)

A
  • valve replaced with prostethic and sometimes aorta repaired or reinforced with Dacron conduit.
108
Q

Mitral Stenosis (Etiology)

A
  • most caused by rheumatic heart disease
  • causes fusion of mitral leaflets
  • later stages calcification
109
Q

Mitral Stenosis (Symptoms)

A
  • progressively increasing severity of shortness of breath

- causes cardiac dyspnea

110
Q

Cardiac Dyspnea

A
  • 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
Q

Mitral Stenosis (Treatment)

A
  • balloon catheter or prosthetic
112
Q

Mitral Insufficiency (Etiology)

A
  • rheumatic heart disease
  • mitral valve prolapse
  • disease which cause papillary muscle or chordae tendineae to rupture
113
Q

Mitral Insufficiency (Symptoms)

A
  • gradually develop shortness of breath with exertion

- acute sudden development is medical emergency

114
Q

Mitral Insufficiency (Treatment)

A
  • surgical repair or prosthetic
115
Q

Right Sided heart valve problems (3)

A
  • pulmonic stenosis (congenital)
  • tricuspid stenosis (rheumatic heart disease)
  • Tricuspid insufficiency (very common, occurs secondary to enlargement of right ventricular or atrial chambers)
116
Q

Heart Sounds Lub, Dub

Murmurs

A

Lub: mitral valve closing
Dub: aortic valve closing
Whistle: Stenotic valve
Gurgle: Insufficient valve

117
Q

Endocarditis (Etiology)

A
  • bacterial normally present in the flora of the GI tract

- acute endocarditis: caused by staphylococcus aureus or beta hemolytic streptococcal species

118
Q

Endocarditis (Symptoms)

A
  • inflammation of the endocardium
  • common cause of valvular insufficiency
  • significant heart failure if insufficiency becomes severe
119
Q

Endocarditis (Diagnosis)

A
  • culturing the organism
  • identifying abnormal cardio waves
  • using transesophageal echocardiography
120
Q

Endocarditis (Treatment)

A
  • can have surgery to correct if makes valvular insufficiency
  • homograft
  • antibiotics
121
Q

Neoplasia

A
  • New Growth

- heritably altered, relatively autonomous growth of tissue

122
Q

Growth Advantage

A
  • 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
Q

relative autonomy

A
  • 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
Q

Benign Neoplasms

A
  • slowly growing do not spread to other tissues

- still can be harmful as they grow, causing pain, inducing bleeding, erosion, can produce hormones

125
Q

Malignant Neoplasms

A
  • rapidly growing, ability to spread to other organs
126
Q

suffix “-oma”

A
  • “growth”
127
Q

Carcinoma

A
  • malignant neoplasm in which cells arise from epithelium and differentiating towards epithelial cells
  • most common forms of cancer
  • breast, lung, colon, prostate
128
Q

Sarcoma

A
  • less common
  • from mesenchymal cells
  • connective tissues
129
Q

Invasion

A
  • contiguous (touching) growth of neoplastic cells beyond site of origin
  • requires enzymes that can degrade surrounding tissues
130
Q

dysplastic

A
  • features of malignancy even though benign, risk for behaving malignant in the future
131
Q

3 types of enzymes that degrade surrounding tissue for malignant neoplasms

A
  • metalloproteinases

- serine & cystine proteinases

132
Q

Metalloproteinases

A
  • attack basement membrane where epithelial cells are anchored.
133
Q

serine and cystine proteinases

A
  • attack extracellular matrix proteins in the tissues through which malignant cells migrate
134
Q

Metastasis

A
  • 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
Q

Metastatic Cascade (6 steps)

A
  • 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
Q

Differentiation

A
  • degree of resemblance of a neoplasm to its tissue of origin
137
Q

Anaplastic

A
  • cells showing no differentiation at all, impossible to tell what tissue of origin is
138
Q

Malignant lesions by definition are ______

A
  • invasive
139
Q

Benign lesions by definition are ______

A
  • not metastatic
140
Q

Mitotic Figures

A
  • 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
Q

Grade of neoplasm measurement

A
  • how many mitotic figures present
142
Q

N:C ratio

A
  • Nucleus cytoplasmic ratio
143
Q

Stage/TNM

A
  • how widely the malignancy has spread by invasion or metastasis
144
Q

3 criteria to “stage” of neoplasm (TNM)

A
  • extent of local growth of tumor (T)
  • extension to lymph nodes (N)
  • presence of distant organ metastases (M)
145
Q

Why is stage important in neoplasia?

A
  • determines course of treatment

- correlates with survival

146
Q

4 generalizations about malignant neoplasms

A
  • 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
Q

8 functions of cells that are commonly corrupted in pathway to cancer

A
  • 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
Q

Familial Cancer Syndromes

A
  • altered gene expression that can be passed through generations
  • patient inherits one allele of a defective gene, something then happens to other allele
149
Q

Chemical Carcinogenesis

A
  • types of chemicals linked to “hits”
150
Q

3 steps required for development of cancer after chemical exposure

A
  • 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
Q

Damage by radiation is ______ _______

A

dose dependent

152
Q

UV light causes formation of what?

A
  • pyrimidine dimers in DNA
153
Q

UV lights causes what type of cell cancer?

A

-squamous and basal cell carcinoma

154
Q

Ionizing Radiation causes what?

A
  • leukemia, breast, lung, thyroid
155
Q

Microbes and cancer

A
  • helicobacter pylori (only bacterium)

- many viruses

156
Q

microbial oncogenesis involves: (3)

A
  • insertion of viral DNA
  • expression of viral proteins that drive DNA transcription
  • stimulation of chronic inflammation (drives rapid host cell turnover)
157
Q

most new cases of cancer/yr M&F

causes of deaths/yr M&F

A
  • new cases M: prostate, F: breast

- causes of death: M&F: lung

158
Q

Factors that effect cancers

A
  • Age of patient
  • Sex
  • Race
  • Geography
  • Risk factors
  • Genetic Predispositions
  • Rate and pattern of growth and spread (ex. prostate cancer very slow growing)
159
Q

Most cancers treated with combination of (3)

A
  • surgery, radiation therapy, chemotherapy (kills all rapidly dividing cells)
160
Q

Targeted or molecular therapy

A
  • only cells expressing certain dysregulated protein are hit with drug
161
Q

Major types of congenital heart disease (5)

A
  • 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
Q

Failure of dividing partition to fully form

A
  • 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
Q

Atrial Septal Defect

A
  • 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
Q

Ventricular Septal Defect

A
  • 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
Q

Patent Ductus Arteriosus

A
  • 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
Q

Cyanotic Heart Disease

A
  • 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
Q

Tetralogy of Fallot

A
  • 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
Q

Normal Pericardium

A
  • tough,thick, fibrous structure which surrounds heart
  • protects from excessive motion and friction
  • can function with no pericardium or open pericardium
169
Q

Pericarditis

A
  • 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
Q

Pericardial Effusion

A
  • 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
Q

Constrictive Pericarditis

A
  • 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
Q

Primary Cardiomyopathy

A
  • abnormality of myocytes of ventricular chambers
173
Q

Secondary Cardiomyopathy

A
  • result of a response of the myocytes to other disease processes
  • ex. ischemic heart disease, toxins
174
Q

Dilated Cardiomyopathy

A
  • most common type of cardiomyopathy
  • systolic dysfunction
  • ventricular enlargement
  • cardiac remodeling
175
Q

Hypertrophic Cardiomyopathy

A
  • 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
Q

Restrictive Cardiomyopathy

A
  • stiffened heart b/c of abnormal material between heart cells
  • amyloid protein
  • abnormality of diastole (filling)
  • cuts into reserve
  • transplantation only cure
177
Q

Arrhythmogenic right ventricular cardiomyopathy

A
  • right ventricle myocytes replaced by fatty tissue

- fatal arrhythmia common

178
Q

Heart Failure

A
  • 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
Q

Treatment of Heart Failure- Diuretic

A
  • eliminate fluid
180
Q

Angiotensin converting enzyme inhibitors

A

-

Path 404 (5 decks)

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