Unit 3 Flashcards
(454 cards)
1
Q
Heart beats per day
A
86,000
2
Q
Liters of blood circulated per day
A
6000L
3
Q
Right side heart pressure
A
Low
4
Q
Right side heart destination
A
Lungs
5
Q
Left side heart pressure
A
High
6
Q
Left side heart destination
A
Body
7
Q
Volume of blood pumped by both sides per unit time
A
Equal
8
Q
Preload
A
Pressure of venous flow back to the heart
9
Q
Afterload
A
Pressure of the heart generated to overcome systemic arterial pressure
10
Q
In a normal state, this is the relationship between preload and afterload
A
EQUAL
11
Q
What happens to blood demand as the heart works harder
A
It increases
12
Q
What happens to the heart muscle if it works harder over time
A
It gets bigger
13
Q
In adulthood, does the blood pressure to the heart increase?
A
NO
14
Q
What does heart disease do to conduction in the heart.
A
Any damage to the heart can interrupt conduction.
15
Q
Heart Failure Definitions
A
Heart cannot provide enough blood to meet the needs of the body
Heart cannot pump all the blood returned to it
16
Q
Forward Heart Failure
A
Not enough blood flow to tissue
Usually associated with the left heart
17
Q
Reverse Heart Failure
A
Backup of venous return
Usually associated with the right heart
18
Q
Right Sided Heart Failure Symptoms
A
Peripheral edema
Ascites
Pleural effusion
Stasis dermatitis
19
Q
Left Sided Heart Failure Symptoms
A
Pulmonary edema with dyspnea
Hemoptysis
Paroxysmal Nocturnal Dyspnea
Orthopnea
20
Q
Left Side Heart Failure Causes
A
Hypertension
Valvular Disease
Ischemic Heart Disease
Cardiomyopathies
21
Q
Right Sided Heart Failure Causes
A
Left side heart failure
Lung Disease
Congenital Heart Diseases
22
Q
Most Common Cause of Left Side Heart Failure
A
Ischemic Heart Disease
23
Q
Most Common Cause of Right Side Heart Failure
A
Left side heart failure
24
Q
Heart Failure Compensation Causes
A
Increased sympathetic tone
Increase contractile force
Increased preload return
Aldosterone release
Myocardial hypertrophy
25
Heart Failure Compensation General Point
Make the pump better
26
Heart Failure Decompensation Components
Excessive ventricular dilation
S3 heart sound
Impaired electrical conduction
27
What does heart dilation do to electrical conduction?
Heart dilation impairs electrical conduction
28
Cor Pulmonale Definition
Heart disease caused by lung disease
29
Diseases that cause cor pulmonale
Lung Disease
Pulmonary Vessel Disease
Diseases of Chest Wall Movement
Pulmonary Arteriol Constriction
30
Most common cause of cor pulmonale
COPD
31
Ischemic Heart Disease Definition
Damage to myocardium cause when blood supply does not meet demand
32
Most Common Cause of Ischemic Heart Disease
Atherosclerosis of coronary arteries
33
Other Causes of Ischemic Heart Disease
Drugs
Infection
Emboli
Hypovolemia
34
Which coronary artery feeds the conducting system?
Right coronary artery
35
How many vessels does atherosclerosis usually impact?
More than one
36
Leading cause of death for adult men and women
Ischemic heart disease
37
How many people have a myocardia infarction per year?:
1.5 million
38
How many people per year die of ischemic heart disease?
500,000
39
How many people per year die of ischemic heart disease before reaching the hospital?
250,000
40
Four Presentations of Ischemic Heart Disease
Sable and Unstable Angina
Acute Myocardial Infarct
Sudden Cardiac Death
Congestive Heart Failure
41
When do ischemic heart disease symptoms appear
Over 75% coronary artery lumen occlusion
42
Stable Angina Symptoms
Crushing Chest Pain
Associated with Diaphoresis
Brought on by exertion and relieved by rest
43
What does stable angina indicate generally?
Harolds the development of worse disease
44
What causes acute coronary syndromes?
Acute changes in artery plaque
45
Unstable Angina Symptoms
Longer duration
Brought on by less activity
Not relieved by rest
46
Myocardial Infarction Definition
Death of cardiac muscle cells due to inadequate blood supply
47
Myocardial Infarction Most Common Cause
Coronary artery thrombosis related to plaque rupture
48
What happens when cardiac cells die?
They release cardiac enzymes
49
Main Cardiac Enzymes
Troponin I
Creatine Kinase
50
Which muscle layer is the first to die in a myocardial infarct.
Inner layer of heart muscle
51
Timeline of vessel occlusion for reversible injury
About 30 minutes
52
Gross Features 30 minutes to 4 hours after infarct
None
53
Light microscope findings 30 minutes to 4 hours after infarct
Usually none, but sometimes variable myocyte waviness
54
Gross Features 4 to 12 hours after infarct
Occasional dark mottling
55
Light microscope findings 4 to 12 hours after infarct
Beginning of coagulation necrosis
Beginnings of Edema
Beginnings of Hemorrhage
56
Gross Features 12 to 24 hours after infarct
Dark mottling
57
Light microscope findings 12 to 24 hours after infarct
Ongoing coagulation with Pyknosis of nuclei
Myocyte hypereosinophilia
Marginal contraction band necrosis Beginning of PMNs
58
Gross Features 1 to 3 days after infarct
Mottling with yellow tan infarct center
59
Light microscope findings 1 to 3 days after infarct
Coagulation necrosis with loss of nuclei and striations
Interstitial infiltrate of PMNs
60
Gross Features 3 to 7 days after infarct
Hyperemic border with central yellow tan softening
61
Light microscope findings 3 to 7 days after infarct
Beginning disintegration of dead myofibers, with dying PMNs
Early phagocytosis of dead cells by macrophages at border
62
Gross Features 7 to 10 days after infarct
Maximally yellow tan soft sand core with depressed red tan margins
63
Light microscope findings 7 to 10 days after infarct
Well developed phagocytosis of dead cells with early formation of fibrovascular granulation at margin
64
Gross Features 10 to 14 days after infarct
red gray depressed infarct borders
65
Light microscope findings 10 to 14 days after infarct
Well established granulation tissue with new vessels and collagen deposition
66
Gross Features 2 to 8 weeks after infarct
Gray white scar that progresses from the border towards the core of the infarct
67
Light microscope findings 2 to 8 weeks after infarct
Increased collagen deposition with decreased cellularity
68
Gross Features greater than 3 months after infarct
Scaring complete
69
Light microscope findings greater than 3 months after infarct
Dense collagenous scar
70
How many patients suffer from complications after acute MI
80 to 90%
71
Sudden Cardiac Death
Fatal arrhythmia that can occur after a heart attack
72
How many MI patients suffer a myocardial rupture?
4 to 8%
73
When does a myocardial rupture happen after an MI
7 to 10 days
74
Pericarditis Definition
Inflammation of pericardium usually 2 to 3 days post MI
75
How many MIs are "silent"
20 to 30%
76
Clinical Features of Acute MI
Angina
Dyspnea
Tachycardia
Sweating
Acute onsent conjestive heart failure
Arrhythmias
Cardiogenic Shock
77
Acute MI EKG Changes
Q Waves
ST Elevation
T wave Inversion
78
Cardiac Enzyme Elevation Serial Measurements
Measured every 8 hours 3 times
79
When is troponin positive
4 to 6 hours
80
Features of Chronic Ischemic Heart Disease
Dilation of ALL CHAMBERS
Myocardial fibrosis
Hypertrophy
81
Sudden Cardiac Death Timeframe
Death within 24 hours of symptom onset
82
Sudden Cardiac Death Rule Out
Pulmonary Embolism
Ruptured Aortic Aneurysm
Ruptures Cerebral Aneurysm
83
Normal Blood Pressure
<120/80
84
Hypertension
>140/90
85
Hypertension mostly impacts this aspect of circulation
Afterload
86
Does blood supply grow with cardiac hypertrophy?
NO
87
S4 Sound Cause
Thickened ventricle unable to relax
88
Two Major Types of Valve Disease
Stenosis
Regurgitation
89
Two Major Effects of Valvular Heart Disease
Hemodynamic stress on chambers due to abnormal flow
Infection
90
What happens when hemodynamic stress is placed on a valve
Upstream ventricle dilates
91
Which valvulare lesions are more common and clinically significant?
Left sided valve disease
92
Major Cause of Mitral Stenosis
Rheumatic fever and subsequent fever
93
Rheumatic Fever Causative Organism
Strep A
94
Rheumatic Carditis Histology Finding
Aschoff Bodies
95
Rheumatic Carditis Pathology Finding
Verrucous endocarditis
96
Rheumatic Carditis Valvular Pathology
Thickened Leaflets
Fusion of Commissures
Thickened Chordae
Fish Mouth Opening
97
Effects of Mitral Stenosis
Dilated left atrium
Arrhythmias
98
Main Mitral Regurgitation Cause
Left ventricular dilation pushes the annulus apart, pushing the valve leaflets apart
99
Secondary Mitral Regurgitation Cause
Mitral prolapse
100
Mitral Valve Prolapse Heart Sound
Mid Systolic Click
101
Mitral Valve Prolapse Cause
Idiopathic increase in ground substance that causes a floppy valve
102
Most Common Valvular Abnormality
Aortic Stenosis
103
Two Entities of Aortic Stenosis
Senile Calcification
Calcification of the Abnormal Bicuspid Valve
104
Age of onset of calcification if you have a bicuspid instead of tricuspid aortic valve
About 10 years earlier than normal
105
Common Symptoms of Aortic Stenosis
Angina
Syncope
CHF
106
Aortic Regurgitation Causes
Chronic hypertension with dilated aortic root
Marfan Syndrome
Syphilis
107
Endocarditis Definition
Inflammation of the inner layer of heart
108
Two Main Types of Endocarditis
Non bacterial thrombotic
Bacterial
109
Non Bacterial Thrombotic Endocarditis Etiology
Clots form on the valve leaflets due to hypercoagulability
110
Most Common Site of Non Bacterial Thrombotic Endocarditis
Aortic Valve
111
Most Common Site of Bacterial Endocarditis
Left side valves EXCEPT in IV drug users
112
Acute Bacterial Endocarditis Causative Organism
Staph
113
Acute Bacterial Endocarditis Main Symptom
Fever and new onset murmur
114
Is acute bacterial endocarditis an emergency?
YES
115
Subacute Bacterial Endocarditis Causative Organisms
Oral Flora
Strep viridans
116
Subacute Bacterial Endocarditis happens most often in this type of valve
An already abnormal valve
117
Acute Bacterial Endocarditis Etiology
Inflammation punches holes in valves
118
Two Types of Prosthetic Valve
Bioprosthetic
Mechanical
119
Issues with Bioprosthetic Valves
Calcification
Perforation
Tearing
NO Anticoagulation
120
Issues With Mechanical Valves
Requires lifelong anticoagulation
121
Both types of prosthetic valves increase risk for what?
Subacute bacterial endocarditis
122
Primary Myocardial Disease General Definition
Disease of the heart muscle itself
123
Two Main Types of Myocardial Disease
Myocarditis
Cardiomyopathies
124
Myocarditis
Inflammation of the heart muscle
125
Most common cause of myocarditis
Coxsackie Virus
126
Other causes of myocarditis
Autoimmunity
Rejection
127
Viral myocarditis progression
Fever and flulike symptoms to sudden heart failure
128
Myocarditis Major Histological Finding
Lymphocytes in normal heart tissue
129
Cardiomyopathy General Definition
Issues with heart muscle cells themselves
130
Three Types of Cardiomyopathy
Dilated
Hypertrophic
Restrictive
131
Most Common Cause of Cardiomyopathy
Idiopathic
132
Hypertrophic Obstructive Cardiomyopathy Etiology
Asymmetric hypertrophy of the interventricular septum with obstruction of aortic outflow
133
Major Histological Finding of Hypertrophic Obstructive Cardiomyopathy
Myofiber disarray
134
Major Cause of Hypertrophic Obstructive Cardiomyopathy
Autosomal dominant beta myosin mutation
135
Restrictive Cardiomyopathy Definition
Myocardial process that makes the wall stiff
136
Major Causes of Restrictive Cardiomyopathy
Amyloidosis
Fibrosis due to radiation
Fibrosis after myocarditis
137
Congenital Heart Disease Occurence
8/1,000 births
138
Percentage of Congenital Heart Disease that Can be Linked to Definite Etiology
10%
139
Two main categories of congenital heart disease
Left to right
Right to left
140
Acyanotic Heart Defect Shunt Type
Left to right shunt
141
Cyanotic Heart Defect Shunt Type
Right to left shunt
142
What happens to the pulmonary vessels in left to right shunts
Hypertrophy due to the higher pressure
143
Most Frequent Congenital Heart Defects
Ventricular Septal Defect
Patent Ductus Arteriosus
Pulmonary Stenosis
Tetralogy of Fallot
144
Most common type of heart shunt
Left to right
145
Most common types of acyanotic heart defects
Atrial Septal Defect
Ventricular Septal Defect
Patent Ductus Arteriosus
146
Most common heart defect
Ventricular Septal Defect
147
Most common area of the heart impacted by ventricular septal defect
Membranous area
148
Patent Ductus Arteriosus Anatomy
Shunt between aorta and pulmonary artery
149
Patent Ductus Arteriosus Murmur
Machinery murmur
150
Most Common Right to Left Shunts
Tetralogy of Fallot
Transposition of Great Vessels
151
Components of Tetarology of Fallot
Ventricular Septal Defect
Overriding Aorta
Pulmonary Stenosis
Right Ventricular Hypertrophy
152
Tetralogy of Fallot Xray Finding
Boot shaped heart
153
Tet Spell Symptom
A running child will periodically squat
154
Transposition of Great Vessels Etiology
Aorta and pulmonary artery arise from the wrong ventricles
155
Babies with transposition of great vessels can only survive with this defect
Left to right shunt like patent ductus arteriosus
156
Major Causes of Pericarditis
Viral Infection
Autoimmune
Post MI
Renal Failure
157
Three Outcomes of Myocarditis
Resolution
Effusion
Constrictive pericarditis with fibrosis
158
Four Types of Pericardial Effusion
Serous
Serosanginous
Chylous
Pure Blood
159
Causes of Serous Pericardial Effusion
Congestive Heart Failure
Renal failure
160
Causes of Serosanginous Pericardial Effusion
Tumor
Trauma
161
Most common heart tumors are what?
Metastases
162
Two Types of Cardiac Tumor
Myxoma
Rhabdomyoma
163
Most common site of myxoma
Left atrium
164
Most common risk in myoma patients
Obstruction and emboli
165
Rhabdomyoma Age Group
Kids
166
Rhabdomyoma Components
Tumor of Heart Muscle
Associated with Tuberous Sclerosis
167
Main Risk Factors For Coronary Artery Disease
Hypertension
Smoking
Diabetes
Elevated Cholesterol
168
Main Storage Form of Lipid
Triglycerides
169
Main Energy Source for Cardiac Muscle
Lipids
170
Transport Form of Lipids
Lipoproteins
171
Types of Lipoproteins
Chylomicrons
VLDL
LDL
HDL
172
Where is most dietary fat absorbed?
The ileum
173
First organ dietary lipids encounter after absorption
The liver
174
Lipids exit the liver in the form of what?
VLDLs
175
LDLs are rich in what lipid
Cholesterol
176
How are lipids recycled and shuttled between cells?
In HDLs
177
What is the form of cholesterol that contributes to atherosclerosis?
LDLs
178
What is the "good" cholesterol?
HDLs
179
Familial Hypercholesterolemia Genetics
Mendelian autosomal dominant mutation in LDL receptors
180
Xanthalasmas
Deposits of fat in the skin and tendons
181
Xanthalasmas are strongly associated with what?
Familial hypercholesterolemia
182
Acceptable Limit for Blood LDL
200 mg/dL, but lower for diabetics and people with known heart disease
183
What causes LDL to enter the blood
Microscopic endothelial injury
184
What happens to LDL when it enters the blood?
Oxidation
185
What do macrophages do when they encounter oxidized LDLs?
They eat it, then die
186
What do macrophages signal as they eat oxidized LDLs?
Smooth muscle cell migration into vessel
187
How can we diagnose MI generally?
Clinical symptoms
EKG Changes
Lab value changes
188
Main MI EKG Change
ST Segment Elevation
189
Will an EKG show changes in the early stages of an MI?
Probably Not
190
When does CKMB rise?
3 to 6 hours after MI onset
191
When does CKMB peak?
12 to 24 hours
192
When does CKMB return to normal?
48 to 72 hours
193
CKMB Disadvantage
It does not stay in the blood for long
It is somewhat nonspecific
194
How long are troponin levels detectable in blood?
7 days after MI onset
195
When does troponin become elevated after MI?
6 hours after onset
196
ANP and BNP test for what?
Volume overload
197
Why are ANP and BNP released?
Excessive cardiac muscle stretch
198
Elevated ANP and BNP confirm what pathology?
Congestive heart failure
199
Neutrophil General Role
Fight acute infection
40 to 60% of WBC Count
200
Lymphocytes General Role
Produce antibodies
201
Monocyte General Role
Phagocytosis of Large Particles
202
Eosinophils General Role
Kills parasites
Associated with allergies
203
Basophils General Role
Inflammatory response and histamine release
204
Neutropenia General Definition
Low neutrophils and other WBCs
205
Neutropenia WBC Count
Less than 1000 cells
206
Agranulocytosis WBC Count
Less than 100 cells
207
Two general causes of neutropenia
Decreased production
Increased destruction
208
Leukocytosis General Definition
Increased number of WBCs
209
Types of Leukocytosis
Neutrophilic
Eosinophilic
Basophilic
Monocytosis
Lymphocytosis
210
Infectious Mononucleosis Organism
EBV
211
Infectious Mononucleosis Transmission
Virus shed through oral contact
212
Infectious Mononucleosis Key Symptoms
Massively enlarged lymph organs
213
Infectious Mononucleosis Immediate Antibody
IgM
214
Infectious Mononucleosis Long Term Antibody
IgG
215
When does IgG typically rise in infectious mononucleosis
About 2 weeks
216
What cell does EBV preferentially infect
B Cells
217
Two Causes of Lymphadenitis
Reactive
Neoplastic
218
Two Causes of Reactive Lymphadenitis
Trauma
Infection
219
Cat Scratch Disease Causative Organism
Bartonella henselae
220
Hemophagocytic Lymphohistiocytosis
When macrophages activate and phagocytose normal healthy cells
221
Two General Categories of Lymphoma
Hodgkins
Non Hodgkins
222
Two Origins of Lymphoma
Myeloid
Lymphoid
223
Hodgkin Lymphoma Cell Type
B Cells
224
Hodgkin Lymphoma Malignant Cell Type
Reed Sternberg Cells that look like owl eyes
225
Hodgkin Lymphoma Age Distribution
Bimodal, either young adults or old people
226
Single Type of Hodgkin Lymphoma
Nodular Sclerosing
227
Hodgkin Lymphoma Key Symptoms
Nodular nontender lymphadenopathy
Mediastinal Mass
Pruritis
Lymph nodes become tender with alcohol consumption
228
How to confirm Hodgkin Lymphoma
Excision biopsy of lymph node
229
Non Hodgkin Lymphoma Cell Types
Both B AND T
230
Non Hodgkin Lymphoma Spread
Can spread through the blood
231
Non Hodgkin Lymphoma Key Symptoms
Extranodal involvement
Spread to other organs
232
Burkitt Lymphoma Associated With These Organisms
HIV
EBV
233
Stage I Lymphoma
Localized
234
Stage II Lymphoma
Lymph nodes in two or more spots ABOVE the diaphragm
235
Stage III Lymphoma
Lymph nodes ABOVE AND BELOW the diaphragm
236
Stage IV Lymphoma
ORGAN INVOLVEMENT with or without lymph node involvement
237
Peripheral B Cell Lymphomas
Follicular Lymphoma
238
Peripheral B Cell Lymphoma Prevalence
About 40% of Non Hodgkins lymphomas
239
Mantle Cell Lymphoma Prognosis
Poor because the disease progresses quickly and is incurable
240
Extranodal Marginal Zone Lymphoma Cause
Sustained chronic inflammation
241
Diffuse Large B Cell Lymphoma Cause
ADD LATER
242
Diffuse Large B Cell Lymphoma Timecourse
Agressive
243
Burkitt Lymphoma Genetic Cause
MYC gene on chromosome 8
244
Burkitt Lymphoma Histology
Stary sky on bone marrow smear
245
Four Types of Leukemias
AML
ALL
CML
CLL
246
Myeloid Cell Suffix
phils
247
Lymphoid Cell Types
T and B cells
248
AML Prevalence
Most common leukemia in adults
249
AML APL Subtype Histology
Auer Rods
250
AML Key Symptom
Anemia
NO Hepatosplenomegaly
251
AML Key Histology
Greater than 20% myeloblasts
252
CML Genetic Cause
Translocation between chromosomes 9 and 22
253
CML Etiology
Uninhibited granulocyte proliferation
254
CML Treatment
Tyrosine Kinase Inhibitor
255
ALL Etiology
Uninhibited immature B cell proliferation
256
ALL Key Symptoms
Anemic
Lumpy
Limping
257
ALL Unique Symptoms
Petechiae and purpura
258
ALL Bone Marrow Biopsy Symptoms
Greater than 20% lymphoblasts
259
ALL Population
Mostly children
260
ALL Prognosis
95% Remission
75 to 80% Cure
261
CLL Population
Elderly adults
262
CLL Etiology
Accumulation of B Cells in the lymph nodes
263
CLL Histology
Smudge Cells, or Crushed Little Lymphocytes
264
Multiple Myeloma Population
Over 70 and male
265
Multiple Myeloma Key Symptoms
Widespread Lytic Lesions of Bone
Renal Disfunction with Bence Jones
Protein Cast
Bone Pain
266
Langerhans Cell Histiocytosis Etiology
Proliferation of dendritic cells
267
B Symtoms
fever, night sweats, weight loss
268
Malignancies That Present With B Symptoms
Hodgkin Lymphoma
CLL
269
Neutrophilic Leukocytosis Cause
Bacterial infection
270
Eosinophilic Leukocytosis Causes
Parasitic Infection
Allergic Reaction
Drugs
271
Basophilic Leukocytosis Cause
Myeloproliferative neoplasms
272
Monocytosis Causes
TB
Malaria
Rickettsia
Lupus
Endocarditis
IBD
273
Lymphocytosis Causes
Chronic immune stimulation with monocytes disorders
274
Infectious Mononucleosis Time Course of Recovery
4 to 6 weeks
275
Peripheral B Cell Lymphomas
Follicular
Mantle Cell
Extranodal Marginal Zone
Diffuse Large B Cell
Burkitt
276
Follicular Lymphoma Genetics
14:18 Gene Translocation
277
Mantle Cell Lymphoma Genetics
11:14 Gene Translocation
278
Extranodal Marginal Zone Lymphoma Cause
Sustained inflammation
279
Diffuse Large B Cell Lymphoma Genetics
BCL6 Rearrangement
14:18 BCL2 Translocation
280
Burkitt Lymphoma Genetics
MYC Translocation on Chromosome 8
281
Follicular Lymphoma Prevalence
Common ~40% of Non Hodgkin Lymphomas
282
Follicular Lymphoma Age
Over 50 years
283
Follicular Lymphoma Prognosis
Mean survival 10 years
284
Follicular Lymphoma Treatment
No cure but can treat the symptoms with cytotoxic drugs
285
Mantle Zone Lymphoma Prognosis
4 to 6 year survival
286
Mantle Zone Lymphoma Treatment
None, the cancer is aggressive and incurable
287
Extranodal Marginal Zone Lymphoma Prognosis
Indolent course
288
Extranodal Marginal Zone Lymphoma Treatment
Excision and radiation
289
Diffuse B Cell Lymphoma Prevalence
35% of all Non Hodgkin Lymphomas and the most common lymphoma in adults
290
Diffuse B Cell Lymphoma Age
60s
291
Diffuse B Cell Lymphoma Prognosis
Poor because the cancer is aggressive
292
Diffuse B Cell Lymphoma Treatment
High dose chemo or stem cell transplant
293
Leukemias of Bone Marrow
AML
CML
ALL
294
Two Parts of Hemoglobin
Two alpha and two beta polypeptide chains
295
This resides in each hemoglobin polypeptide chains
Heme with iron
296
Three Types of Hemoglobin
A
A2
F
297
Hemoglobin A Structure
Two Alpha Chains
Two Beta Chains
298
Hemoglobin A2 Structure
Two Alpha Chains
Two Delta Chains
299
Hemoglobin F Structure
Two Alpha Chains
Two Gamma Chains
300
When do humans express Hemoglobin F
Gestation months 3 thru 9 and the first 6 months of newborn life
301
Major Characteristics of Hemoglobin F
Higher affinity for oxygen
302
Two Major Abnormal Hemoglobins
H
S
303
Hemoglobin H Structure
Four Beta Chains
304
Hemoglobin S Structure
Two Alpha Chains
Two Beta S Chains
305
Major Disease Associated With Hemoglobin S
Sickle Cell Disease
306
Hemoglobin Decreased in What Disease
Macrocytic Anemia
Normocytic Anemia
Microcytic Anemia
307
MCV Signifies What
Average volume of red cells
308
MCH Signifies What
The amount of hemoglobin per RBC in absolute units
309
MCHC Signifies What
Average hemoglobin concentration in red blood cells
310
RDW Signifies What
Variations of red blood cell size in CBC
311
Reticulocyte Count Signifies What
Speed of release of immature red blood cells
312
Reticulocyte Count Increased in These Diseases
Blood Loss
Hemolytic Anemia
High Altitude
313
Anisocytosis Definition
Variations in red blood cell size
314
Poikilocytosis Definition
Variations in red cell shape
315
Most Common Cause of Anemia
Iron Deficiency Anemia
316
Most Common Cause of Iron Deficiency Anemia
Bleeding
317
Most Common Cause of Bleeding
Heavy menstruation or GI bleed
318
Symptoms of Anemia
Fatigue
Tachycardia
Palpitations
Dyspnea on exertion
319
Anemia SHOULD NOT present with these symptoms
Lymphadenopathy
Hepatosplenomegaly
Bone Pain
320
Anemia Physical Exam Findings
Palor of skin and mucosa
Smooth Tongue
Brittle Nails
Cheilosis of Lips
321
Older adults with new onset iron deficiency anemia should be screened for these pathologies
GI Bleed
Colon Cancer
322
Unique Symptom of Iron Deficiency Anemia
Pica
323
Iron Deficiency Anemia Cell Type
Microcytic
324
Anemia of Chronic Disease Causes
Chronic Inflammatory States
Organ Failure
Age Over 85
325
Anemia of Chronic Disease Cell Type
Normocytic
326
Anemia of Chronic Disease Characteristic Lab Findings
NONE
327
Thalassemia Cell Type
Microcytic
328
Alpha Thalassemia General Genetics
Gene deletions
329
Beta Thalassemia General Genetics
Point mutations
330
Alpha Thalassemia Population
Southeast Asia and Chinese
331
Alpha Thalassemia Specific Genetics
Number of deletions of alpha globin genes determines severity of disease
332
Number of deletions of Hemoglobin H disease
3
333
Beta Thalassemia Population
Mediterranean
334
Beta Thalassemia Specific Genetics
Heterozygosity and homozygosity determine severity of disease
335
Hemoglobin H Electrophoresis Finding
Fast migrating hemoglobin
336
Beta Thalassemia Electrophoresis Finding
Elevation of hemoglobin A2 and hemoglobin F
337
Required for B12 Absorption
Intrinsic factor from stomach parietal cells
338
Most Common Causes of B12 Deficiency Anemia
Pernicious Anemia
Gastric Surgeries
339
Key Symptoms of B12 Deficiency
Glossitis
Peripheral Nerve Paresthesias
Decreased vibration and position sense
340
B12 Deficiency Cell Size
Macrocytic
341
Pernicious Anemia Lab Findings
Increased Methylmalonic Acid
Increased Homocysteine
342
Most Common Cause of Folate Deficiency Anemia
Medications
Alcohol Abuse
343
Folate Deficiency Cell Size
Macrocytic
344
Aplastic Anemia Cause
Idiopathic
Bone Marrow Failure
345
Aplastic Anemia Key Symptoms
Anemia
Neutropenia
Low Platelets
346
Aplastic Anemia Physical Exam Findings
Palor
Purpura
Petechiae
347
Haptoglobin Function
Binds and clears free hemoglobin in the plasma
348
Three Hemolytic Anemias
G6P Deficiency
Sickle Cell
Autoimmune
349
G6P Deficiency Genetics
X Linked Recessive
350
G6P Deficiency Population
Black men
351
G6P Deficiency Key Symptoms
Infections or drugs cause hemolysis
352
Sickle Cell Anemia Genetics
Autosomal Recessive
353
Sickle Cell Anemia Lab Findings
Howell Jolly Bodies
Target Cells
Run electrophoresis to confirm
354
Test to Confirm Sickle Cell Anemia
Electrophoresis
355
Autoimmune Hemolytic Anemia Cause
Rapid development of antibodies against self red blood cells
356
Layers of Blood Vessels
Adventitia
Media
Intima
357
Intima cell Type
Endothelial
358
Capillary Structure
Single layer of endothelial cells with a basement membrane
359
Endothelial cells regulate what?
Vascular smooth muscle
Vascular resistance
Inflammation
360
Endothelia Cell Special Properties
Non thrombotic
Anticoagulant
Usually impermeable
361
Components of Endothelial Activation
Intimal Thickening
Hypercoagulability
Free Radial Production
Thrombogenesis
362
What can activate an endothelial cell?
Turbulent Blood Flow
Hypertension
Immune Activation
Cigarette Smoke
363
Preclinical Atherosclerosis Progression
Normal
Fatty Streak
Fibrofatty Plaque
Advanced Plaque
364
Clinical Atherosclerosis Components
Aneurysm and rupture
Occlusion by thrombus
Critical Stenosis
365
Components of Irreversible Intimal Thickening
Endothelial dysfunction
Smooth muscle recruitment
ECM Proliferation
Intimal Thickening
366
What can accumulate in a vessel after endothelial injury
LDL
367
What due macrophage become after they consume lipids?
Foam cells
368
What happens to smooth muscle cells when foam cells develop?
They migrate from the media to the intima
369
Fatty Streak
Intimal Accumulation of foam cells
370
Atheroma
Intimal accumulation of foam cells and extracellular lipid
371
Fibroatheroma
An atheroma with a fibrous cap
372
Fibrous Cap Components
Smooth muscle cells and extracellular matrix
373
These fibrous caps are stable
Thick
374
These fibrous caps are unstable
Thin
375
Nonmodifiable Atherosclerosis Risk Factors
Genetics
Middle age and older
Male sex
Menopausal Female Sex
376
Modifiable Atherosclerosis Risk Factors
Hypertension
Smoking
Diabetes
Hyperlipidemia
377
Hypertension increases the risk for ischemic heart disease by this much
60%
378
Smoking does this to the death rate of ischemic heart disease
Doubles it
379
Diabetes does this to the risk of ischemic heart disease
Doubles it
380
Other Risk Factors of Atherosclerosis
Inflammation
Chlamydia pneumoniae Infection
Homocysteine through low B12 or folate
381
Atherosclerosis Complications
Calcification
Rupture
Hemorrhage
Embolization
Aneurysm
Sudden Death
382
Untreated hypertension does this to life expectancy
Reduces it by 20 to 30 years
383
Nonmodifiable Risk Factors of Hypertension
Age
Family History
Race
384
Major Modifiable Risk Factor of Hypertension
High sodium diet
385
Primary Hypertension
Hypertension with no underlying cause
386
Secondary Hypertension
Hypertension with an underlying cause
387
Benign Hypertension
Slow clinical course
388
Malignant Hypertension
Rapid Clinical Course of 1 to 3 years
Often presents with retinal hemorrhage and renal failure
389
Blood Pressure Equation
Blood Pressure=(cardiac output)(peripheral resistance)
390
Source of Atrial Natriuretic Peptide
Heart
391
Renin Function
Converts Angiotensinogen to angiotensin 1
392
Source of Angiotensinogen
Liver
393
Two Types of Arteriosclerosis
Hyaline
Hyperplastic
394
Hyaline Arteriosclerosis Cause
Benign Hypertension
395
Hyperplasic Arteriosclerosis Cause
Severe Hypertension
396
Malignant Hypertension Histology
Necrotising arteriolitis
397
Malignant Hypertension Components
Hyperplastic arteriosclerosis
Fibrinoid Deposits
Vascular Wall Necrosis
398
Hyperplasic Arteriosclerosis Histology
Onion skin vessel wall
399
Internal Elastic Lamina Location
Separates the tunica intima from the tunica media
400
What happens to the elasticity of vessels with age?
It decreases
401
Percentage of Patients With Coronary Artery Anatomical Variation
1 to 5%
402
Berry Aneurysm
Aneurysm of Circle of Willis branching points
403
Arteriovenous Fistula
When an artery connects to a vein without first going through a capillary bed
404
Etiololgy of Arteriovenous Fistula
Developmental Defect
Ruptured Aneurysm
Vascular Necrosis
Penetrating Trauma
405
Fibromuscular Displasia
Abnormally thickened and fibrotic arterial media and intima
406
Fibromuscular Displasia Population
Young women with no other risk factors
407
Fibromuscular Displasia Clinical Correlations
Spontaneous Coronary Artery Dissection
Renovascular Hypertension
408
True Aneurysms include these structures
All three layers of the vessel wall
409
Fasle Aneurysms
Vessel defect leads to pulsatile hematoma against the outside of the vessel wall
410
Saccular Aneurysm
Discrete outpouchings of the vessel
411
Fusiform Aneurism
Encompasses full vessel circumference
412
Aneurysm General Etiology
Alterations in smooth muscle cell or extracellular matrix compromise the structural integrity of the vessel
413
Predisposing Conditions for Aortic Aneurysm
Atherosclerosis
Hypertension
414
Abdominal Aortic Aneurysm Risk Factors
Male Sex
Smoking
Genetics
415
AAA Rupture Risk
Less than 4cm never burst
Between 4 to 5cm 1% per year
Between 5 to 6cm 11% per year and requires surgery
Over 6 cm 25% per year
416
Thoracic Aortic Aneurysm Risk Factors
Hypertension
Bicuspid Aortic Valve
Marfans
Other Genetic Mutations
417
Thoracic Aortic Aneurysm Clinical Signs and Symptoms
Respiratory and feeding issues
Persistent Cough
Pain
Cardiac Disease
Aortic Dissection or Rupture
418
Arterial Dissection
When blood enters between the layers of the blood vessel and pushes them apart
419
Aortic Dissection Risk Factors
Male Sex
Age 50 and above
Hypertension
Connective Tissue Disorders
Rarely in Pregnancy
420
General Types of Aortic Dissection
Proximal and Distal
421
Debakey 1 Aneurysm
Involves the ascending and descending aorta
422
Debakey 2 Aneurysm
Involves only the ascending aorta
423
Debakey 3 Aneurysm
Involves only the descending aorta
Also called a Stanford Type B
424
Retrograde Aneurysm
When an aneurysm starts distal but progresses proximally
425
Type A Dissection Treatment
Intensive Antihypertensives
Surgical Repare
426
Type B Dissection Treatment
Majority can be managed conservatively
427
Two Types of Vasculitis
Infection
Autoimmune
428
Giant Cell Arteritis Etiology
T Cell Response to antigens in vessel walls
429
Giant Cell Arteritis Symptoms
Severe unilateral headache
General malaise
Low Fever
Vision Loss
430
Giant Cell Arteritis Treatments
Steroids
Anti TNF Therapy
431
Takayasu Arteritis Pathogenesis
Autoimmune scarring of medium and large vessels
432
Takayasu Arteritis Symptoms
Vision loss and weak pulse in the extremities as a young person
433
Polyarteritis Nodosa Main Association
Hep B
434
Polyarteritis Nodosa Clinical Presentation
Rapidly Accelerating High Blood Pressure
Abdominal Pain
Bloody Stools
Diffuse muscular pain
435
Polyarteritis Nodosa Treatment
Immunosupretion
436
Kawasaki Patient Population
Kids under 4
437
Kawasaki Main Problem
Coronary arteritis with infarct or dissections
438
Kawasaki Clinical Presentation
Red eyes
Swollen and red hands and feet
Cardiovascular Issues
439
Polyangiitis Effects These Vessels
Small vessels
440
Kawasaki Treatment
IV Immunoglobulin in the ICU
441
Polyangiitis Triggers
Penicillin Drugs
Strep Infection
442
Polyangiitis Symptoms
Hemoptysis
Hematuria or Protineuria
Abdominal Pain
Purpura
443
Allergic Granulomatosis and Angiitis Associations
Allergies
Asthma
Allergic Rhinitis
Lung Infiltrates
Elevated eosinophils
444
Thromboangiitis Obliterans Associations
Smoking
Young age
Indian, Japanese, or Mediterranean descent
445
Raynaud Phenomenon Etiology
Vasoconstriction of arteries and arterioles in the extremities
446
Thrombophlebitis and Phlebothrombosis Etiology
Deep vein thrombosis from venous stasis
HIGH RISK FOR PULMONARY EMBOLISM
447
SVC Syndromes
Neoplasms compress the superior vena cava
448
Lymphangitis
Acute inflammation due to bacterial seeding of lymph vessels that presents as a red streak
449
Lymphedema
Increased hydrostatic pressure leads to edema
450
Kaposi Sarcoma Causative Organism
Herpes
451
Kaposi Sarcoma Main Association
HIV patients
452
Retrograde Dissection Clinical Signs and Symptoms
Aortic root dissection
Fatal disruption of aortic valve
Coronary artery compression
Tamponade
Aortic Insufficiency
Myocardial Infarction
453
Malignant Tumors of Blood Vessels
Angiosarcoma
454
Angiosarcoma Survival Rate
30% at 5 years
