Exam 2 Flashcards
1
Q
What does leukocytosis indicate?
A
Increased WBC count does not always indicate disease.
2
Q
What is monoclonal proliferation?
A
Dominance of one WBC type is often diagnostic of a specific disorder.
3
Q
What does plasma cell dominance suggest?
A
Plasma cell proliferation may indicate a cancerous condition with excessive single antibody production.
4
Q
What are common symptoms of plasma cell disorders?
A
Night sweats, fatigue, bone marrow tumor origin, cancer cells release acid causing bone degradation.
5
Q
How do plasma cell disorders cause bone degradation?
A
Cancer cells break down calcium phosphate, weakening bones and leading to fractures.
6
Q
Why do malignant WBC disorders impair immune function?
A
Many WBCs are immature and dysfunctional, impairing immune function despite high WBC count.
7
Q
What is the consequence of dysfunctional white blood cells?
A
Weakened immune system increases infection vulnerability.
8
Q
What are the characteristics of Hodgkin’s lymphoma?
A
young age, less than 30 y/o, better prognosis, presence of Reed-Sternberg cells.
9
Q
How does Non-Hodgkin’s lymphoma differ from Hodgkin’s?
A
Prognosis varies; some forms are aggressive, others slow-growing.
10
Q
What is plasma cell myeloma (multiple myeloma)?
A
Cancer of plasma cells, excessive single antibody production, causes bone pain, fractures, and marrow tumors.
11
Q
What is the most abundant blood cell in the body?
A
Red blood cell (RBC).
12
Q
What regulates red blood cell production?
A
Erythropoietin (EPO).
13
Q
Where is erythropoietin (EPO) produced?
A
The kidneys, in response to oxygen levels.
14
Q
How does high altitude affect erythropoietin production?
A
Lower oxygen levels increase EPO release, leading to more RBC production.
15
Q
Does erythropoiesis stop when oxygen levels normalize?
A
No, it is a continuous process with a baseline level of EPO always present.
16
Q
What percentage of oxygen in the blood is freely dissolved in plasma?
A
About 3%.
17
Q
What role does the 3% dissolved oxygen play in transport?
A
It acts as an intermediary, constantly moving between alveoli and RBCs.
18
Q
How soluble is carbon dioxide (CO₂) in blood compared to oxygen?
A
CO₂ is much more soluble, with 7-10% dissolved in plasma.
19
Q
What are the two definitions of anemia?
A
- Low hemoglobin concentration.
- Low RBC count.
20
Q
What hormone controls red blood cell production (erythropoiesis)?
A
Erythropoietin (EPO).
21
Q
Where is erythropoietin (EPO) primarily produced?
A
The kidneys, in response to oxygen levels.
22
Q
How does high altitude affect erythropoiesis?
A
Low oxygen levels at high altitudes (e.g., Denver) increase EPO production, leading to more RBCs.
23
Q
What happens to erythropoietin production after returning to lower altitudes?
A
EPO production decreases but remains at a baseline level.
24
Q
Is erythropoiesis an ‘on-off’ process?
A
No, it is a continuous process.
25
What percentage of oxygen in the blood is freely dissolved in plasma?
~3%.
26
What is the role of the 3% dissolved oxygen in plasma?
It acts as a temporary transport medium, constantly moving between alveoli, capillaries, and RBCs.
27
Why is the dissolved oxygen fraction important?
It is dynamic and continuously in flux rather than a fixed amount.
28
How soluble is carbon dioxide (CO₂) in blood compared to oxygen?
CO₂ is significantly more soluble, with 7-10% dissolved in plasma.
29
How does CO₂ transport differ from oxygen transport?
CO₂ has higher solubility and unique transport mechanisms.
30
What are the two definitions of anemia?
1. Low hemoglobin concentration. 2. Low RBC count (RBC deficiency).
31
What does hematocrit measure?
The volume percentage of RBCs in the blood.
32
How does hematocrit relate to hemoglobin levels?
It correlates with hemoglobin since 97% of oxygen is carried by hemoglobin.
33
Why is hemoglobin concentration the most critical factor in oxygen transport?
It directly determines oxygen-carrying capacity.
34
What factors lower hemoglobin’s affinity for oxygen?
pH (Bohr effect), increased CO₂, higher temperature, and increased 2,3-DPG levels.
35
How does pH (Bohr effect) influence oxygen affinity?
Lower pH (more acidic environment) reduces hemoglobin’s affinity for oxygen, promoting oxygen release.
36
What is an example of the Bohr effect in action?
During exercise, increased acid production lowers pH, leading to oxygen unloading in tissues.
37
How does CO₂ affect hemoglobin’s oxygen affinity?
Increased CO₂ levels lower hemoglobin’s oxygen affinity, enhancing oxygen release.
38
How does CO₂ contribute to oxygen unloading during exercise?
Active muscles produce more CO₂, which promotes oxygen release to those muscles.
39
How does temperature affect hemoglobin’s affinity for oxygen?
Higher temperatures reduce hemoglobin’s affinity for oxygen.
40
Why does increased temperature promote oxygen release?
Active muscles generate heat, which helps unload oxygen to tissues.
41
What is 2,3-DPG (2,3-BPG) and how does it affect hemoglobin?
It is a molecule in RBCs that lowers hemoglobin’s oxygen affinity, enhancing oxygen unloading.
42
How do conditions in the lungs favor oxygen binding?
Cooling of blood, lower CO₂ levels due to exhalation, and decreased acidity.
43
What is the primary form of CO₂ transport in the blood?
Most CO₂ exists as bicarbonate (HCO₃⁻).
44
Why is CO₂ converted into bicarbonate in the blood?
It acts as a critical buffer system for maintaining pH balance.
45
What do blood tests for CO₂ actually measure?
Bicarbonate (HCO₃⁻) concentration, not free CO₂.
46
What type of test measures actual CO₂ gas concentration?
Arterial blood gas (ABG) tests.
47
What is hemoglobin and where is it found?
A protein found in red blood cells.
48
What is the structure of hemoglobin?
Four subunits, each containing a heme group.
49
What allows hemoglobin to bind oxygen?
Iron (Fe²⁺) embedded within the heme group.
50
How many oxygen molecules can a fully saturated hemoglobin molecule carry?
Four.
51
Why does sickle cell disease persist in certain populations?
It provides a protective effect against malaria.
52
How does being heterozygous for sickle cell affect malaria resistance?
Carriers have some resistance to malaria without severe symptoms.
53
What happens to individuals who are homozygous for sickle cell?
They develop full-blown sickle cell disease.
54
How does sickle cell trait differ from other genetic diseases like cystic fibrosis?
Heterozygous individuals are usually asymptomatic.
55
What type of disorder is sickle cell disease?
A congenital disorder present from birth.
56
Why does sickle cell disease cause chronic anemia?
Sickled cells have a shorter lifespan and are rapidly removed by the spleen and liver.
57
How does sickle cell disease affect blood flow?
Sickled cells clog capillaries, leading to ischemia (blocked blood flow).
58
What complications arise from sickle cell disease?
Organ damage, pain crises, increased infection risk, and spleen destruction by adolescence.
59
Which populations are most affected by sickle cell disease?
Those from malaria-endemic regions, particularly in Africa.
60
What are the treatment options for sickle cell disease?
Limited treatments; anticoagulants provide some relief, but the only cure is bone marrow transplantation, which is not widely accessible.
61
What determines a person’s blood type?
Surface antigens (recognition factors) on red blood cells.
62
What antibodies does each blood type produce?
Type A: Anti-B antibodies.
Type B: Anti-A antibodies.
Type AB: No antibodies (universal recipient).
Type O: Both anti-A and anti-B antibodies (universal donor).
63
Why is Type O the universal donor?
It has no A or B antigens, preventing immune reactions in recipients.
64
Why is Type AB the universal recipient?
It has no anti-A or anti-B antibodies, allowing it to accept any blood type.
65
What is the Rh factor?
A surface antigen on red blood cells that determines Rh-positive or Rh-negative status.
66
How do Rh-negative individuals develop anti-Rh antibodies?
They do not automatically produce them but can develop them after exposure to Rh-positive blood (e.g., pregnancy or transfusion).
67
Why is the Rh factor less critical than ABO compatibility in emergency transfusions?
ABO mismatches cause immediate severe reactions, while Rh mismatches usually require prior sensitization.
68
Why is Type O blood considered safe for all recipients?
It lacks A and B antigens, preventing an immune response in recipients.
69
What is a concern when transfusing whole blood from a Type O donor?
The donor’s plasma contains anti-A and anti-B antibodies, which could potentially cause an immune reaction.
70
What is the rarest blood type?
AB-negative.
71
What two factors must be considered in blood transfusions?
Soluble immunoglobulins (antibodies) and surface antigens on red blood cells.
72
Why do antibodies and surface antigens matter in transfusions?
They affect blood compatibility and immune reactions in recipients.
73
How are anemias classified?
Based on red blood cell (RBC) size (MCV) and color (MCHC) rather than the underlying cause.
74
What does Mean Corpuscular Volume (MCV) measure?
RBC size.
75
What are the classifications of anemia based on MCV?
Normal MCV → Normocytic anemia.
Increased MCV → Macrocytic anemia (e.g., B12/folate deficiency).
Decreased MCV → Microcytic anemia (e.g., iron deficiency anemia).
76
What does Mean Corpuscular Hemoglobin Concentration (MCHC) measure?
Hemoglobin content and RBC color.
77
What are the classifications of anemia based on MCHC?
• Low MCHC → Hypochromic anemia (pale RBCs due to low hemoglobin, e.g., iron deficiency anemia).
• Normal MCHC → Normochromic anemia.
78
What is the most common type of anemia?
Iron deficiency anemia.
79
How is iron deficiency anemia classified?
Microcytic, hypochromic anemia (small, pale RBCs due to low hemoglobin).
80
What is polycythemia?
An increased concentration of red blood cells.
81
What is the most common cause of polycythemia?
Dehydration (relative polycythemia) due to fluid loss.
82
How does dehydration cause relative polycythemia?
Fluid loss increases RBC concentration without increasing RBC production.
83
What is polycythemia vera?
A malignancy causing uncontrolled RBC production due to a bone marrow disorder.
84
How does increased RBC concentration affect blood flow?
It increases blood viscosity, reducing flow and raising the risk of circulatory complications.
85
What is the role of Activated Factor X (Xa) in the clotting cascade?
Converts prothrombin into thrombin.
86
What is thrombin's function in clot formation?
Converts fibrinogen into fibrin, forming a stable clot.
87
How does liver disease affect clotting?
Impairs synthesis of clotting factors, including fibrinogen, leading to clotting disorders.
88
What test evaluates blood clotting ability before surgery or while on anticoagulants?
Thrombin time test.
89
Why must clots be removed after vessel repair?
To prevent unnecessary blockage and restore normal blood flow.
90
What enzyme is responsible for breaking down clots?
Plasmin.
91
How is plasmin activated?
Plasminogen is converted to plasmin by tissue plasminogen activator (tPA).
92
What does plasmin do to fibrin?
Cleaves fibrin polymers into fragments, allowing clot breakdown.
93
How do platelets assist in vessel repair?
They release growth factors that help regenerate endothelial tissue.
94
What is the clinical use of tissue plasminogen activator (tPA)?
Dissolves clots in heart attacks (MIs) and ischemic strokes.
95
Why is timing critical for thrombolytic therapy?
Clot busters are most effective within a specific time window before the clot contracts too much.
96
Why can clot busters not be given in an ambulance?
A hemorrhagic stroke must be ruled out via imaging to prevent worsening a bleeding stroke.
97
What hormone controls platelet production?
Thrombopoietin (TPO).
98
Where do platelets originate from?
Megakaryocytes in the bone marrow.
99
How are platelets formed?
Megakaryocytes fragment into platelets, which are then released into circulation.
100
Where is thrombopoietin primarily produced?
The kidneys, with some contribution from the liver.
101
What is the role of the liver in thrombopoietin production?
Unclear, but it may act as a backup mechanism.
102
What is the major risk of thrombocytosis (excessive platelets)?
Increased risk of clot formation (thrombosis).
103
What are possible complications of thrombocytosis?
Ischemic stroke, increased blood viscosity, and vascular blockages.
104
Why might thrombocytosis also lead to bleeding?
Excessive platelets can cause clotting issues that disrupt normal hemostasis.
105
What is hemophilia?
An X-linked recessive bleeding disorder primarily affecting males.
106
Can females have hemophilia?
They can be carriers but usually do not show symptoms unless they inherit two defective alleles.
107
What clotting factor is deficient in Hemophilia A?
Factor VIII.
108
What clotting factor is deficient in Hemophilia B?
Factor IX.
109
Why do hemophiliacs experience prolonged bleeding?
Platelets form a temporary plug, but fibrin formation is impaired, preventing clot stabilization.
110
What are common symptoms of hemophilia?
Prolonged bleeding, easy bruising, and spontaneous hemorrhages.
111
Why is hemophilia historically significant?
It was prevalent in European royal families and passed down through Queen Victoria’s lineage.
112
What is von Willebrand disease?
A bleeding disorder caused by von Willebrand Factor (vWF) deficiency or dysfunction.
113
What are the roles of von Willebrand Factor (vWF)?
Platelet adhesion to vessel walls and stabilization of Factor VIII.
114
How does von Willebrand disease affect clotting?
Leads to excessive Factor VIII destruction, causing bleeding similar to hemophilia.
115
How common is von Willebrand disease compared to hemophilia?
More common but less well-known outside medical circles.
116
What role does vitamin K play in clotting?
Essential for producing clotting factors II (prothrombin), VII, IX, and X.
117
Why is vitamin K named 'K'?
From 'Koagulation,' reflecting its role in blood clotting.
118
What happens with vitamin K deficiency?
Impaired coagulation and increased bleeding risk.
119
What is Disseminated Intravascular Coagulation (DIC)?
A condition where excessive clotting depletes clotting factors, leading to both clot formation and severe bleeding.
120
Why does DIC cause both clotting and bleeding?
The body continuously forms clots, consuming coagulation factors, and once depleted, uncontrolled bleeding occurs.
121
What are common triggers for DIC?
Sepsis, trauma (e.g., being run over by a forklift), and obstetric complications (e.g., fetal demise, placental abruption).
122
How is DIC treated?
Anticoagulants can be paradoxically used to prevent further clotting factor depletion.
123
Do parasympathetic nerves control vascular tone?
No, only the sympathetic nervous system regulates blood vessel constriction and dilation.
124
How does sympathetic activation affect blood pressure?
Causes vasoconstriction, leading to increased blood pressure.
125
How does sympathetic withdrawal affect blood pressure?
Causes vasodilation, leading to decreased blood pressure.
126
How do parasympathetics influence the heart?
They slow heart rate via the vagus nerve but do not control blood vessels.
127
What is an embolus?
Anything that moves through the bloodstream but shouldn’t be there.
128
What are examples of emboli?
• Fat embolism (from a fractured bone).
• Air embolism (from improper IV access or injected air).
• Amniotic fluid embolism (during childbirth).
129
Why is an air embolism dangerous?
The heart cannot effectively pump air, which can be fatal.
130
What is atherosclerosis?
The formation of plaques inside blood vessels, leading to narrowing and increased risk of heart disease and stroke.
131
What are plaques made of?
Lipids (fats), proteins, and mineral deposits (salts, calcium, etc.).
132
What is primary (essential) hypertension?
The most common form (95% of cases) with no clear cause, likely genetic and lifestyle-related.
133
What is secondary hypertension?
A rare form (~5% of cases) caused by an identifiable condition, such as renal artery stenosis or endocrine disorders.
134
What is preeclampsia?
Hypertension in pregnancy with significant edema, more than normal pregnancy swelling.
135
What can untreated preeclampsia progress to?
Eclampsia, a life-threatening condition.
136
How does chronic systemic hypertension affect the heart?
Leads to left ventricular hypertrophy (LVH).
137
What type of hypertrophy occurs in hypertension?
Concentric hypertrophy.
138
What are the effects of left ventricular hypertrophy (LVH)?
• Increased muscle thickness in the left ventricle.
• Decreased end-diastolic volume (less space for blood filling).
• Increased risk of heart failure over time.
139
How does the heart compensate for reduced diastolic volume in left ventricular hypertrophy (LVH)?
Increases heart rate (tachycardia) to maintain cardiac output.
140
What genetic disorder is linked to familial hypercholesterolemia?
Familial hypercholesterolemia due to defective LDL receptors.
141
What is the function of LDL (Low-Density Lipoprotein)?
Transports cholesterol in the blood since cholesterol is lipid-soluble.
142
How does a defective LDL receptor affect cholesterol levels?
Leads to high cholesterol, contributing to atherosclerosis and hypertrophy.
143
Why is diet alone ineffective in managing familial hypercholesterolemia?
Genetic mutations impair cholesterol regulation, making dietary control insufficient.
144
What is mitral stenosis, and how does it affect the heart?
Narrowing of the mitral valve leads to left atrial enlargement due to blood backup.
145
What are common symptoms of mitral stenosis?
Fatigue, shortness of breath (dyspnea), jugular vein distension (JVD), and peripheral edema.
146
What are key examination findings in mitral stenosis?
Distended neck veins (JVD) and hepatomegaly due to systemic venous congestion.
147
What causes rheumatic fever, and how does it damage the heart?
Untreated streptococcal infections (Strep A) damage cardiac valves, especially the mitral valve.
148
How is rheumatic fever managed to prevent valve damage?
Long-term antibiotics to prevent recurring strep infections.
149
Can valve damage from rheumatic fever be reversed?
No, it can only be managed, not reversed.
150
What happens in mitral regurgitation (incompetent mitral valve)?
Blood leaks back into the left atrium, increasing left atrial volume.
151
How does the left ventricle compensate for mitral regurgitation?
Left ventricular dilation occurs over time.
152
How do chronic valve disorders contribute to heart failure?
They lead to ventricular remodeling and increased strain on the heart.
153
What does the term 'dilation' refer to in heart disease?
Ventricular enlargement due to volume overload.
154
How does left ventricular hypertrophy (LVH) compensate for aortic regurgitation?
The ventricle dilates to accommodate extra blood and maintain cardiac output despite inefficient forward flow.
155
What is the difference between concentric and eccentric hypertrophy?
• Concentric hypertrophy → Thicker muscle, reduced chamber size (due to high pressure, e.g., aortic stenosis).
• Eccentric hypertrophy → Increased chamber volume (due to volume overload, e.g., aortic regurgitation).
156
What is a mnemonic to remember hypertrophy types?
• Pressure overload → Concentric hypertrophy.
• Volume overload → Eccentric hypertrophy.
157
How does aortic stenosis affect the left ventricle?
Increases resistance to blood ejection, requiring the ventricle to generate more force.
158
What compensatory change occurs in aortic stenosis?
Concentric hypertrophy (thickened left ventricle) due to increased workload.
159
What are the long-term effects of aortic stenosis?
Reduced compliance, diastolic dysfunction, and eventual heart failure.
160
What is endocarditis, and what does it affect?
An infection of the heart’s inner layer that primarily affects heart valves.
161
What are common causes of endocarditis?
Bacterial infection, IV drug use, poor dental hygiene, prosthetic valves.
162
What are complications of endocarditis?
Valve destruction (leading to regurgitation and heart failure) and septic emboli (spreading infection to other organs).
163
What is dilated cardiomyopathy (DCM)?
Dilation of all four heart chambers, leading to poor contractility.
164
What are potential causes of dilated cardiomyopathy?
Idiopathic (most common), chronic alcohol abuse, peripartum cardiomyopathy.
165
What is the prognosis for dilated cardiomyopathy?
Younger individuals (e.g., pregnancy-related cases) may recover. Older individuals (e.g., long-term alcoholics) often have irreversible damage.
166
What is restrictive cardiomyopathy (RCM)?
A condition where the myocardium becomes stiff and less compliant, preventing normal heart expansion.
167
What is the key problem in RCM?
Blood cannot enter the ventricles easily, leading to reduced preload and cardiac output.
168
Which side of the heart is more affected in RCM and why?
The right side, due to higher venous return from systemic circulation compared to pulmonary circulation.
169
How does loss of right ventricular expansion affect cardiac output?
Reduces preload, further limiting cardiac output.
170
Which condition can mimic restrictive cardiomyopathy?
Constrictive pericarditis, as both restrict ventricular filling.
171
What are the hemodynamic effects of RCM?
Reduced ventricular stretch decreases stroke volume and forward circulation.
172
What compensatory mechanism can occur in RCM?
Interventricular septal deviations.
173
What is preload?
The stretch of the ventricle before contraction, influencing Frank-Starling mechanics.
174
How does restrictive cardiomyopathy affect preload?
Reduces preload, limiting the heart’s ability to pump efficiently.
175
Why is right ventricular filling more affected in RCM?
Systemic venous return is typically higher than pulmonary return, making the right ventricle more dependent on normal expansion.
176
What is the foramen ovale?
A hole in the interatrial septum that allows right-to-left blood flow in utero, bypassing the lungs.
177
What happens if the foramen ovale fails to close after birth?
It results in a patent foramen ovale (PFO), which may cause left-to-right shunting postnatally.
178
What is the ductus arteriosus?
A vascular connection between the pulmonary artery and the aorta that bypasses the lungs in utero.
179
What happens to the ductus arteriosus after birth?
It normally closes and becomes the ligamentum arteriosum.
180
What is patent ductus arteriosus (PDA)?
A condition where the ductus arteriosus remains open, causing abnormal blood flow.
181
Why is the ductus arteriosus site clinically significant?
It is prone to weakness, leading to conditions like aortic coarctation (narrowing of the aorta) or aortic aneurysms.
182
How do prostaglandin inhibitors affect the ductus arteriosus?
NSAIDs like indomethacin can prematurely close the ductus arteriosus, which may be harmful in preterm infants.
183
What is the simple definition of heart failure?
The heart is unable to pump enough blood to meet the body's needs.
184
Why is heart failure called 'congestive heart failure' (CHF)?
Blood backs up in systemic circulation due to inefficient pumping.
185
What are signs of venous congestion in CHF?
Jugular vein distension (JVD), hepatic engorgement, ascites, peripheral edema, varicose veins due to chronic venous hypertension.
186
What are the most common causes of heart failure in the U.S.?
Survivors of myocardial infarctions (MIs) and chronic hypertension.
187
What does the Frank-Starling relationship describe?
How increased ventricular filling (preload) enhances cardiac output—but only up to a certain point.
188
How does the Starling curve change in advanced heart failure?
It plateaus, meaning increased filling no longer improves output.
189
Why does heart failure worsen despite increased preload?
The heart loses its ability to generate force, reducing stroke volume and worsening heart failure.
190
How is the Frank-Starling relationship altered in heart failure?
The slope of the curve decreases, meaning increased preload does not significantly improve cardiac output.
191
Why does the heart fail to respond effectively to volume increases in heart failure?
The failing heart cannot efficiently handle increased preload, leading to stagnant circulation and congestion.
192
Why doesn’t preload increase despite systemic congestion?
Blood backs up in systemic veins because it cannot enter the failing heart efficiently.
193
What is the challenge of balancing preload in heart failure treatment?
Increasing preload too much strains an already failing heart, while reducing preload too much decreases cardiac output.
194
How do diuretics help manage preload in heart failure?
They reduce fluid overload, preventing excessive strain on the heart.
195
What is the risk of excessive diuresis in heart failure?
It can dangerously reduce preload and impair cardiac function.
196
What is the primary goal of heart failure treatment?
Managing symptoms and slowing disease progression rather than curing the condition.
197
How do inotropes (e.g., digoxin) help in heart failure?
They increase contractility, helping the failing heart pump more effectively.
198
Why are beta-blockers (e.g., metoprolol, carvedilol) used in heart failure?
They prevent excessive sympathetic activation, reduce the risk of arrhythmias and heart damage, and shield the heart from overcompensation.
199
How do vasodilators (e.g., ACE inhibitors, ARBs) help in heart failure?
They reduce vascular resistance (afterload), making it easier for the heart to pump blood forward.
200
What is the ultimate goal of heart failure treatment?
Slow disease progression so patients live long enough to die from another cause rather than heart failure itself.
201
What is preload?
The amount of blood returning to the heart.
202
Why must preload be optimized in heart failure?
It needs to be adequate for stroke volume but not excessive to avoid overloading the heart.
203
What is afterload?
The resistance the heart pumps against.
204
Why is lowering afterload beneficial in heart failure?
It reduces the heart’s workload and improves forward blood flow.
205
What is the risk of lowering afterload too much?
It can reduce systemic blood pressure too much, impairing circulation.
206
Why is heart failure treatment an ongoing process?
Cardiologists must continually adjust preload, afterload, and contractility to optimize function without overwhelming the failing heart.
