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Biology Of Disease > Unit 3 > Flashcards

Unit 3 Flashcards

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1
Q

Heart beats per day

A

86,000

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2
Q

Liters of blood circulated per day

A

6000L

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3
Q

Right side heart pressure

A

Low

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4
Q

Right side heart destination

A

Lungs

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5
Q

Left side heart pressure

A

High

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6
Q

Left side heart destination

A

Body

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7
Q

Volume of blood pumped by both sides per unit time

A

Equal

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8
Q

Preload

A

Pressure of venous flow back to the heart

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9
Q

Afterload

A

Pressure of the heart generated to overcome systemic arterial pressure

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10
Q

In a normal state, this is the relationship between preload and afterload

A

EQUAL

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11
Q

What happens to blood demand as the heart works harder

A

It increases

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12
Q

What happens to the heart muscle if it works harder over time

A

It gets bigger

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13
Q

In adulthood, does the blood pressure to the heart increase?

A

NO

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14
Q

What does heart disease do to conduction in the heart.

A

Any damage to the heart can interrupt conduction.

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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

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16
Q

Forward Heart Failure

A

Not enough blood flow to tissue
Usually associated with the left heart

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17
Q

Reverse Heart Failure

A

Backup of venous return
Usually associated with the right heart

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18
Q

Right Sided Heart Failure Symptoms

A

Peripheral edema
Ascites
Pleural effusion
Stasis dermatitis

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19
Q

Left Sided Heart Failure Symptoms

A

Pulmonary edema with dyspnea
Hemoptysis
Paroxysmal Nocturnal Dyspnea
Orthopnea

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20
Q

Left Side Heart Failure Causes

A

Hypertension
Valvular Disease
Ischemic Heart Disease
Cardiomyopathies

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21
Q

Right Sided Heart Failure Causes

A

Left side heart failure
Lung Disease
Congenital Heart Diseases

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22
Q

Most Common Cause of Left Side Heart Failure

A

Ischemic Heart Disease

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23
Q

Most Common Cause of Right Side Heart Failure

A

Left side heart failure

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24
Q

Heart Failure Compensation Causes

A

Increased sympathetic tone
Increase contractile force
Increased preload return
Aldosterone release
Myocardial hypertrophy

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25
Q

Heart Failure Compensation General Point

A

Make the pump better

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26
Q

Heart Failure Decompensation Components

A

Excessive ventricular dilation
S3 heart sound
Impaired electrical conduction

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27
Q

What does heart dilation do to electrical conduction?

A

Heart dilation impairs electrical conduction

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28
Q

Cor Pulmonale Definition

A

Heart disease caused by lung disease

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29
Q

Diseases that cause cor pulmonale

A

Lung Disease
Pulmonary Vessel Disease
Diseases of Chest Wall Movement
Pulmonary Arteriol Constriction

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30
Q

Most common cause of cor pulmonale

A

COPD

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31
Q

Ischemic Heart Disease Definition

A

Damage to myocardium cause when blood supply does not meet demand

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32
Q

Most Common Cause of Ischemic Heart Disease

A

Atherosclerosis of coronary arteries

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33
Q

Other Causes of Ischemic Heart Disease

A

Drugs
Infection
Emboli
Hypovolemia

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34
Q

Which coronary artery feeds the conducting system?

A

Right coronary artery

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35
Q

How many vessels does atherosclerosis usually impact?

A

More than one

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36
Q

Leading cause of death for adult men and women

A

Ischemic heart disease

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37
Q

How many people have a myocardia infarction per year?:

A

1.5 million

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38
Q

How many people per year die of ischemic heart disease?

A

500,000

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39
Q

How many people per year die of ischemic heart disease before reaching the hospital?

A

250,000

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40
Q

Four Presentations of Ischemic Heart Disease

A

Sable and Unstable Angina
Acute Myocardial Infarct
Sudden Cardiac Death
Congestive Heart Failure

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41
Q

When do ischemic heart disease symptoms appear

A

Over 75% coronary artery lumen occlusion

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42
Q

Stable Angina Symptoms

A

Crushing Chest Pain
Associated with Diaphoresis
Brought on by exertion and relieved by rest

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43
Q

What does stable angina indicate generally?

A

Harolds the development of worse disease

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44
Q

What causes acute coronary syndromes?

A

Acute changes in artery plaque

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45
Q

Unstable Angina Symptoms

A

Longer duration
Brought on by less activity
Not relieved by rest

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46
Q

Myocardial Infarction Definition

A

Death of cardiac muscle cells due to inadequate blood supply

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47
Q

Myocardial Infarction Most Common Cause

A

Coronary artery thrombosis related to plaque rupture

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48
Q

What happens when cardiac cells die?

A

They release cardiac enzymes

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49
Q

Main Cardiac Enzymes

A

Troponin I
Creatine Kinase

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50
Q

Which muscle layer is the first to die in a myocardial infarct.

A

Inner layer of heart muscle

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51
Q

Timeline of vessel occlusion for reversible injury

A

About 30 minutes

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52
Q

Gross Features 30 minutes to 4 hours after infarct

A

None

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53
Q

Light microscope findings 30 minutes to 4 hours after infarct

A

Usually none, but sometimes variable myocyte waviness

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54
Q

Gross Features 4 to 12 hours after infarct

A

Occasional dark mottling

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55
Q

Light microscope findings 4 to 12 hours after infarct

A

Beginning of coagulation necrosis
Beginnings of Edema
Beginnings of Hemorrhage

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56
Q

Gross Features 12 to 24 hours after infarct

A

Dark mottling

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57
Q

Light microscope findings 12 to 24 hours after infarct

A

Ongoing coagulation with Pyknosis of nuclei
Myocyte hypereosinophilia
Marginal contraction band necrosis Beginning of PMNs

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58
Q

Gross Features 1 to 3 days after infarct

A

Mottling with yellow tan infarct center

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59
Q

Light microscope findings 1 to 3 days after infarct

A

Coagulation necrosis with loss of nuclei and striations
Interstitial infiltrate of PMNs

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60
Q

Gross Features 3 to 7 days after infarct

A

Hyperemic border with central yellow tan softening

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61
Q

Light microscope findings 3 to 7 days after infarct

A

Beginning disintegration of dead myofibers, with dying PMNs
Early phagocytosis of dead cells by macrophages at border

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62
Q

Gross Features 7 to 10 days after infarct

A

Maximally yellow tan soft sand core with depressed red tan margins

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63
Q

Light microscope findings 7 to 10 days after infarct

A

Well developed phagocytosis of dead cells with early formation of fibrovascular granulation at margin

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64
Q

Gross Features 10 to 14 days after infarct

A

red gray depressed infarct borders

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65
Q

Light microscope findings 10 to 14 days after infarct

A

Well established granulation tissue with new vessels and collagen deposition

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66
Q

Gross Features 2 to 8 weeks after infarct

A

Gray white scar that progresses from the border towards the core of the infarct

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67
Q

Light microscope findings 2 to 8 weeks after infarct

A

Increased collagen deposition with decreased cellularity

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68
Q

Gross Features greater than 3 months after infarct

A

Scaring complete

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69
Q

Light microscope findings greater than 3 months after infarct

A

Dense collagenous scar

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70
Q

How many patients suffer from complications after acute MI

A

80 to 90%

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71
Q

Sudden Cardiac Death

A

Fatal arrhythmia that can occur after a heart attack

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72
Q

How many MI patients suffer a myocardial rupture?

A

4 to 8%

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73
Q

When does a myocardial rupture happen after an MI

A

7 to 10 days

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74
Q

Pericarditis Definition

A

Inflammation of pericardium usually 2 to 3 days post MI

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75
Q

How many MIs are “silent”

A

20 to 30%

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76
Q

Clinical Features of Acute MI

A

Angina
Dyspnea
Tachycardia
Sweating
Acute onsent conjestive heart failure
Arrhythmias
Cardiogenic Shock

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77
Q

Acute MI EKG Changes

A

Q Waves
ST Elevation
T wave Inversion

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78
Q

Cardiac Enzyme Elevation Serial Measurements

A

Measured every 8 hours 3 times

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79
Q

When is troponin positive

A

4 to 6 hours

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80
Q

Features of Chronic Ischemic Heart Disease

A

Dilation of ALL CHAMBERS
Myocardial fibrosis
Hypertrophy

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81
Q

Sudden Cardiac Death Timeframe

A

Death within 24 hours of symptom onset

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82
Q

Sudden Cardiac Death Rule Out

A

Pulmonary Embolism
Ruptured Aortic Aneurysm
Ruptures Cerebral Aneurysm

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83
Q

Normal Blood Pressure

A

<120/80

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84
Q

Hypertension

A

> 140/90

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85
Q

Hypertension mostly impacts this aspect of circulation

A

Afterload

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86
Q

Does blood supply grow with cardiac hypertrophy?

A

NO

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87
Q

S4 Sound Cause

A

Thickened ventricle unable to relax

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88
Q

Two Major Types of Valve Disease

A

Stenosis
Regurgitation

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89
Q

Two Major Effects of Valvular Heart Disease

A

Hemodynamic stress on chambers due to abnormal flow
Infection

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90
Q

What happens when hemodynamic stress is placed on a valve

A

Upstream ventricle dilates

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91
Q

Which valvulare lesions are more common and clinically significant?

A

Left sided valve disease

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92
Q

Major Cause of Mitral Stenosis

A

Rheumatic fever and subsequent fever

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93
Q

Rheumatic Fever Causative Organism

A

Strep A

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94
Q

Rheumatic Carditis Histology Finding

A

Aschoff Bodies

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95
Q

Rheumatic Carditis Pathology Finding

A

Verrucous endocarditis

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96
Q

Rheumatic Carditis Valvular Pathology

A

Thickened Leaflets
Fusion of Commissures
Thickened Chordae
Fish Mouth Opening

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97
Q

Effects of Mitral Stenosis

A

Dilated left atrium
Arrhythmias

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98
Q

Main Mitral Regurgitation Cause

A

Left ventricular dilation pushes the annulus apart, pushing the valve leaflets apart

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99
Q

Secondary Mitral Regurgitation Cause

A

Mitral prolapse

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100
Q

Mitral Valve Prolapse Heart Sound

A

Mid Systolic Click

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101
Q

Mitral Valve Prolapse Cause

A

Idiopathic increase in ground substance that causes a floppy valve

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102
Q

Most Common Valvular Abnormality

A

Aortic Stenosis

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103
Q

Two Entities of Aortic Stenosis

A

Senile Calcification
Calcification of the Abnormal Bicuspid Valve

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104
Q

Age of onset of calcification if you have a bicuspid instead of tricuspid aortic valve

A

About 10 years earlier than normal

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105
Q

Common Symptoms of Aortic Stenosis

A

Angina
Syncope
CHF

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106
Q

Aortic Regurgitation Causes

A

Chronic hypertension with dilated aortic root
Marfan Syndrome
Syphilis

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107
Q

Endocarditis Definition

A

Inflammation of the inner layer of heart

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108
Q

Two Main Types of Endocarditis

A

Non bacterial thrombotic
Bacterial

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109
Q

Non Bacterial Thrombotic Endocarditis Etiology

A

Clots form on the valve leaflets due to hypercoagulability

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110
Q

Most Common Site of Non Bacterial Thrombotic Endocarditis

A

Aortic Valve

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111
Q

Most Common Site of Bacterial Endocarditis

A

Left side valves EXCEPT in IV drug users

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112
Q

Acute Bacterial Endocarditis Causative Organism

A

Staph

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113
Q

Acute Bacterial Endocarditis Main Symptom

A

Fever and new onset murmur

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114
Q

Is acute bacterial endocarditis an emergency?

A

YES

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115
Q

Subacute Bacterial Endocarditis Causative Organisms

A

Oral Flora
Strep viridans

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116
Q

Subacute Bacterial Endocarditis happens most often in this type of valve

A

An already abnormal valve

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117
Q

Acute Bacterial Endocarditis Etiology

A

Inflammation punches holes in valves

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118
Q

Two Types of Prosthetic Valve

A

Bioprosthetic
Mechanical

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119
Q

Issues with Bioprosthetic Valves

A

Calcification
Perforation
Tearing
NO Anticoagulation

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120
Q

Issues With Mechanical Valves

A

Requires lifelong anticoagulation

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121
Q

Both types of prosthetic valves increase risk for what?

A

Subacute bacterial endocarditis

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122
Q

Primary Myocardial Disease General Definition

A

Disease of the heart muscle itself

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123
Q

Two Main Types of Myocardial Disease

A

Myocarditis
Cardiomyopathies

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124
Q

Myocarditis

A

Inflammation of the heart muscle

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125
Q

Most common cause of myocarditis

A

Coxsackie Virus

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126
Q

Other causes of myocarditis

A

Autoimmunity
Rejection

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127
Q

Viral myocarditis progression

A

Fever and flulike symptoms to sudden heart failure

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128
Q

Myocarditis Major Histological Finding

A

Lymphocytes in normal heart tissue

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129
Q

Cardiomyopathy General Definition

A

Issues with heart muscle cells themselves

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130
Q

Three Types of Cardiomyopathy

A

Dilated
Hypertrophic
Restrictive

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131
Q

Most Common Cause of Cardiomyopathy

A

Idiopathic

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132
Q

Hypertrophic Obstructive Cardiomyopathy Etiology

A

Asymmetric hypertrophy of the interventricular septum with obstruction of aortic outflow

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133
Q

Major Histological Finding of Hypertrophic Obstructive Cardiomyopathy

A

Myofiber disarray

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134
Q

Major Cause of Hypertrophic Obstructive Cardiomyopathy

A

Autosomal dominant beta myosin mutation

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135
Q

Restrictive Cardiomyopathy Definition

A

Myocardial process that makes the wall stiff

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136
Q

Major Causes of Restrictive Cardiomyopathy

A

Amyloidosis
Fibrosis due to radiation
Fibrosis after myocarditis

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137
Q

Congenital Heart Disease Occurence

A

8/1,000 births

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138
Q

Percentage of Congenital Heart Disease that Can be Linked to Definite Etiology

A

10%

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139
Q

Two main categories of congenital heart disease

A

Left to right
Right to left

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140
Q

Acyanotic Heart Defect Shunt Type

A

Left to right shunt

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141
Q

Cyanotic Heart Defect Shunt Type

A

Right to left shunt

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142
Q

What happens to the pulmonary vessels in left to right shunts

A

Hypertrophy due to the higher pressure

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143
Q

Most Frequent Congenital Heart Defects

A

Ventricular Septal Defect
Patent Ductus Arteriosus
Pulmonary Stenosis
Tetralogy of Fallot

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144
Q

Most common type of heart shunt

A

Left to right

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145
Q

Most common types of acyanotic heart defects

A

Atrial Septal Defect
Ventricular Septal Defect
Patent Ductus Arteriosus

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146
Q

Most common heart defect

A

Ventricular Septal Defect

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147
Q

Most common area of the heart impacted by ventricular septal defect

A

Membranous area

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148
Q

Patent Ductus Arteriosus Anatomy

A

Shunt between aorta and pulmonary artery

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149
Q

Patent Ductus Arteriosus Murmur

A

Machinery murmur

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150
Q

Most Common Right to Left Shunts

A

Tetralogy of Fallot
Transposition of Great Vessels

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151
Q

Components of Tetarology of Fallot

A

Ventricular Septal Defect
Overriding Aorta
Pulmonary Stenosis
Right Ventricular Hypertrophy

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152
Q

Tetralogy of Fallot Xray Finding

A

Boot shaped heart

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153
Q

Tet Spell Symptom

A

A running child will periodically squat

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154
Q

Transposition of Great Vessels Etiology

A

Aorta and pulmonary artery arise from the wrong ventricles

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155
Q

Babies with transposition of great vessels can only survive with this defect

A

Left to right shunt like patent ductus arteriosus

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156
Q

Major Causes of Pericarditis

A

Viral Infection
Autoimmune
Post MI
Renal Failure

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157
Q

Three Outcomes of Myocarditis

A

Resolution
Effusion
Constrictive pericarditis with fibrosis

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158
Q

Four Types of Pericardial Effusion

A

Serous
Serosanginous
Chylous
Pure Blood

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159
Q

Causes of Serous Pericardial Effusion

A

Congestive Heart Failure
Renal failure

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160
Q

Causes of Serosanginous Pericardial Effusion

A

Tumor
Trauma

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161
Q

Most common heart tumors are what?

A

Metastases

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162
Q

Two Types of Cardiac Tumor

A

Myxoma
Rhabdomyoma

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163
Q

Most common site of myxoma

A

Left atrium

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164
Q

Most common risk in myoma patients

A

Obstruction and emboli

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165
Q

Rhabdomyoma Age Group

A

Kids

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166
Q

Rhabdomyoma Components

A

Tumor of Heart Muscle
Associated with Tuberous Sclerosis

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167
Q

Main Risk Factors For Coronary Artery Disease

A

Hypertension
Smoking
Diabetes
Elevated Cholesterol

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168
Q

Main Storage Form of Lipid

A

Triglycerides

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169
Q

Main Energy Source for Cardiac Muscle

A

Lipids

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170
Q

Transport Form of Lipids

A

Lipoproteins

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171
Q

Types of Lipoproteins

A

Chylomicrons
VLDL
LDL
HDL

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172
Q

Where is most dietary fat absorbed?

A

The ileum

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173
Q

First organ dietary lipids encounter after absorption

A

The liver

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174
Q

Lipids exit the liver in the form of what?

A

VLDLs

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175
Q

LDLs are rich in what lipid

A

Cholesterol

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176
Q

How are lipids recycled and shuttled between cells?

A

In HDLs

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177
Q

What is the form of cholesterol that contributes to atherosclerosis?

A

LDLs

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178
Q

What is the “good” cholesterol?

A

HDLs

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179
Q

Familial Hypercholesterolemia Genetics

A

Mendelian autosomal dominant mutation in LDL receptors

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180
Q

Xanthalasmas

A

Deposits of fat in the skin and tendons

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181
Q

Xanthalasmas are strongly associated with what?

A

Familial hypercholesterolemia

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182
Q

Acceptable Limit for Blood LDL

A

200 mg/dL, but lower for diabetics and people with known heart disease

183
Q

What causes LDL to enter the blood

A

Microscopic endothelial injury

184
Q

What happens to LDL when it enters the blood?

A

Oxidation

185
Q

What do macrophages do when they encounter oxidized LDLs?

A

They eat it, then die

186
Q

What do macrophages signal as they eat oxidized LDLs?

A

Smooth muscle cell migration into vessel

187
Q

How can we diagnose MI generally?

A

Clinical symptoms
EKG Changes
Lab value changes

188
Q

Main MI EKG Change

A

ST Segment Elevation

189
Q

Will an EKG show changes in the early stages of an MI?

A

Probably Not

190
Q

When does CKMB rise?

A

3 to 6 hours after MI onset

191
Q

When does CKMB peak?

A

12 to 24 hours

192
Q

When does CKMB return to normal?

A

48 to 72 hours

193
Q

CKMB Disadvantage

A

It does not stay in the blood for long
It is somewhat nonspecific

194
Q

How long are troponin levels detectable in blood?

A

7 days after MI onset

195
Q

When does troponin become elevated after MI?

A

6 hours after onset

196
Q

ANP and BNP test for what?

A

Volume overload

197
Q

Why are ANP and BNP released?

A

Excessive cardiac muscle stretch

198
Q

Elevated ANP and BNP confirm what pathology?

A

Congestive heart failure

199
Q

Neutrophil General Role

A

Fight acute infection
40 to 60% of WBC Count

200
Q

Lymphocytes General Role

A

Produce antibodies

201
Q

Monocyte General Role

A

Phagocytosis of Large Particles

202
Q

Eosinophils General Role

A

Kills parasites
Associated with allergies

203
Q

Basophils General Role

A

Inflammatory response and histamine release

204
Q

Neutropenia General Definition

A

Low neutrophils and other WBCs

205
Q

Neutropenia WBC Count

A

Less than 1000 cells

206
Q

Agranulocytosis WBC Count

A

Less than 100 cells

207
Q

Two general causes of neutropenia

A

Decreased production
Increased destruction

208
Q

Leukocytosis General Definition

A

Increased number of WBCs

209
Q

Types of Leukocytosis

A

Neutrophilic
Eosinophilic
Basophilic
Monocytosis
Lymphocytosis

210
Q

Infectious Mononucleosis Organism

A

EBV

211
Q

Infectious Mononucleosis Transmission

A

Virus shed through oral contact

212
Q

Infectious Mononucleosis Key Symptoms

A

Massively enlarged lymph organs

213
Q

Infectious Mononucleosis Immediate Antibody

A

IgM

214
Q

Infectious Mononucleosis Long Term Antibody

A

IgG

215
Q

When does IgG typically rise in infectious mononucleosis

A

About 2 weeks

216
Q

What cell does EBV preferentially infect

A

B Cells

217
Q

Two Causes of Lymphadenitis

A

Reactive
Neoplastic

218
Q

Two Causes of Reactive Lymphadenitis

A

Trauma
Infection

219
Q

Cat Scratch Disease Causative Organism

A

Bartonella henselae

220
Q

Hemophagocytic Lymphohistiocytosis

A

When macrophages activate and phagocytose normal healthy cells

221
Q

Two General Categories of Lymphoma

A

Hodgkins
Non Hodgkins

222
Q

Two Origins of Lymphoma

A

Myeloid
Lymphoid

223
Q

Hodgkin Lymphoma Cell Type

A

B Cells

224
Q

Hodgkin Lymphoma Malignant Cell Type

A

Reed Sternberg Cells that look like owl eyes

225
Q

Hodgkin Lymphoma Age Distribution

A

Bimodal, either young adults or old people

226
Q

Single Type of Hodgkin Lymphoma

A

Nodular Sclerosing

227
Q

Hodgkin Lymphoma Key Symptoms

A

Nodular nontender lymphadenopathy

Mediastinal Mass

Pruritis

Lymph nodes become tender with alcohol consumption

228
Q

How to confirm Hodgkin Lymphoma

A

Excision biopsy of lymph node

229
Q

Non Hodgkin Lymphoma Cell Types

A

Both B AND T

230
Q

Non Hodgkin Lymphoma Spread

A

Can spread through the blood

231
Q

Non Hodgkin Lymphoma Key Symptoms

A

Extranodal involvement
Spread to other organs

232
Q

Burkitt Lymphoma Associated With These Organisms

A

HIV
EBV

233
Q

Stage I Lymphoma

A

Localized

234
Q

Stage II Lymphoma

A

Lymph nodes in two or more spots ABOVE the diaphragm

235
Q

Stage III Lymphoma

A

Lymph nodes ABOVE AND BELOW the diaphragm

236
Q

Stage IV Lymphoma

A

ORGAN INVOLVEMENT with or without lymph node involvement

237
Q

Peripheral B Cell Lymphomas

A

Follicular Lymphoma

238
Q

Peripheral B Cell Lymphoma Prevalence

A

About 40% of Non Hodgkins lymphomas

239
Q

Mantle Cell Lymphoma Prognosis

A

Poor because the disease progresses quickly and is incurable

240
Q

Extranodal Marginal Zone Lymphoma Cause

A

Sustained chronic inflammation

241
Q

Diffuse Large B Cell Lymphoma Cause

A

ADD LATER

242
Q

Diffuse Large B Cell Lymphoma Timecourse

A

Agressive

243
Q

Burkitt Lymphoma Genetic Cause

A

MYC gene on chromosome 8

244
Q

Burkitt Lymphoma Histology

A

Stary sky on bone marrow smear

245
Q

Four Types of Leukemias

A

AML
ALL
CML
CLL

246
Q

Myeloid Cell Suffix

A

phils

247
Q

Lymphoid Cell Types

A

T and B cells

248
Q

AML Prevalence

A

Most common leukemia in adults

249
Q

AML APL Subtype Histology

A

Auer Rods

250
Q

AML Key Symptom

A

Anemia
NO Hepatosplenomegaly

251
Q

AML Key Histology

A

Greater than 20% myeloblasts

252
Q

CML Genetic Cause

A

Translocation between chromosomes 9 and 22

253
Q

CML Etiology

A

Uninhibited granulocyte proliferation

254
Q

CML Treatment

A

Tyrosine Kinase Inhibitor

255
Q

ALL Etiology

A

Uninhibited immature B cell proliferation

256
Q

ALL Key Symptoms

A

Anemic
Lumpy
Limping

257
Q

ALL Unique Symptoms

A

Petechiae and purpura

258
Q

ALL Bone Marrow Biopsy Symptoms

A

Greater than 20% lymphoblasts

259
Q

ALL Population

A

Mostly children

260
Q

ALL Prognosis

A

95% Remission
75 to 80% Cure

261
Q

CLL Population

A

Elderly adults

262
Q

CLL Etiology

A

Accumulation of B Cells in the lymph nodes

263
Q

CLL Histology

A

Smudge Cells, or Crushed Little Lymphocytes

264
Q

Multiple Myeloma Population

A

Over 70 and male

265
Q

Multiple Myeloma Key Symptoms

A

Widespread Lytic Lesions of Bone

Renal Disfunction with Bence Jones
Protein Cast

Bone Pain

266
Q

Langerhans Cell Histiocytosis Etiology

A

Proliferation of dendritic cells

267
Q

B Symtoms

A

fever, night sweats, weight loss

268
Q

Malignancies That Present With B Symptoms

A

Hodgkin Lymphoma
CLL

269
Q

Neutrophilic Leukocytosis Cause

A

Bacterial infection

270
Q

Eosinophilic Leukocytosis Causes

A

Parasitic Infection
Allergic Reaction
Drugs

271
Q

Basophilic Leukocytosis Cause

A

Myeloproliferative neoplasms

272
Q

Monocytosis Causes

A

TB
Malaria
Rickettsia
Lupus
Endocarditis
IBD

273
Q

Lymphocytosis Causes

A

Chronic immune stimulation with monocytes disorders

274
Q

Infectious Mononucleosis Time Course of Recovery

A

4 to 6 weeks

275
Q

Peripheral B Cell Lymphomas

A

Follicular
Mantle Cell
Extranodal Marginal Zone
Diffuse Large B Cell
Burkitt

276
Q

Follicular Lymphoma Genetics

A

14:18 Gene Translocation

277
Q

Mantle Cell Lymphoma Genetics

A

11:14 Gene Translocation

278
Q

Extranodal Marginal Zone Lymphoma Cause

A

Sustained inflammation

279
Q

Diffuse Large B Cell Lymphoma Genetics

A

BCL6 Rearrangement
14:18 BCL2 Translocation

280
Q

Burkitt Lymphoma Genetics

A

MYC Translocation on Chromosome 8

281
Q

Follicular Lymphoma Prevalence

A

Common ~40% of Non Hodgkin Lymphomas

282
Q

Follicular Lymphoma Age

A

Over 50 years

283
Q

Follicular Lymphoma Prognosis

A

Mean survival 10 years

284
Q

Follicular Lymphoma Treatment

A

No cure but can treat the symptoms with cytotoxic drugs

285
Q

Mantle Zone Lymphoma Prognosis

A

4 to 6 year survival

286
Q

Mantle Zone Lymphoma Treatment

A

None, the cancer is aggressive and incurable

287
Q

Extranodal Marginal Zone Lymphoma Prognosis

A

Indolent course

288
Q

Extranodal Marginal Zone Lymphoma Treatment

A

Excision and radiation

289
Q

Diffuse B Cell Lymphoma Prevalence

A

35% of all Non Hodgkin Lymphomas and the most common lymphoma in adults

290
Q

Diffuse B Cell Lymphoma Age

A

60s

291
Q

Diffuse B Cell Lymphoma Prognosis

A

Poor because the cancer is aggressive

292
Q

Diffuse B Cell Lymphoma Treatment

A

High dose chemo or stem cell transplant

293
Q

Leukemias of Bone Marrow

A

AML
CML
ALL

294
Q

Two Parts of Hemoglobin

A

Two alpha and two beta polypeptide chains

295
Q

This resides in each hemoglobin polypeptide chains

A

Heme with iron

296
Q

Three Types of Hemoglobin

A

A
A2
F

297
Q

Hemoglobin A Structure

A

Two Alpha Chains
Two Beta Chains

298
Q

Hemoglobin A2 Structure

A

Two Alpha Chains
Two Delta Chains

299
Q

Hemoglobin F Structure

A

Two Alpha Chains
Two Gamma Chains

300
Q

When do humans express Hemoglobin F

A

Gestation months 3 thru 9 and the first 6 months of newborn life

301
Q

Major Characteristics of Hemoglobin F

A

Higher affinity for oxygen

302
Q

Two Major Abnormal Hemoglobins

A

H
S

303
Q

Hemoglobin H Structure

A

Four Beta Chains

304
Q

Hemoglobin S Structure

A

Two Alpha Chains
Two Beta S Chains

305
Q

Major Disease Associated With Hemoglobin S

A

Sickle Cell Disease

306
Q

Hemoglobin Decreased in What Disease

A

Macrocytic Anemia
Normocytic Anemia
Microcytic Anemia

307
Q

MCV Signifies What

A

Average volume of red cells

308
Q

MCH Signifies What

A

The amount of hemoglobin per RBC in absolute units

309
Q

MCHC Signifies What

A

Average hemoglobin concentration in red blood cells

310
Q

RDW Signifies What

A

Variations of red blood cell size in CBC

311
Q

Reticulocyte Count Signifies What

A

Speed of release of immature red blood cells

312
Q

Reticulocyte Count Increased in These Diseases

A

Blood Loss
Hemolytic Anemia
High Altitude

313
Q

Anisocytosis Definition

A

Variations in red blood cell size

314
Q

Poikilocytosis Definition

A

Variations in red cell shape

315
Q

Most Common Cause of Anemia

A

Iron Deficiency Anemia

316
Q

Most Common Cause of Iron Deficiency Anemia

A

Bleeding

317
Q

Most Common Cause of Bleeding

A

Heavy menstruation or GI bleed

318
Q

Symptoms of Anemia

A

Fatigue
Tachycardia
Palpitations
Dyspnea on exertion

319
Q

Anemia SHOULD NOT present with these symptoms

A

Lymphadenopathy
Hepatosplenomegaly
Bone Pain

320
Q

Anemia Physical Exam Findings

A

Palor of skin and mucosa
Smooth Tongue
Brittle Nails
Cheilosis of Lips

321
Q

Older adults with new onset iron deficiency anemia should be screened for these pathologies

A

GI Bleed
Colon Cancer

322
Q

Unique Symptom of Iron Deficiency Anemia

A

Pica

323
Q

Iron Deficiency Anemia Cell Type

A

Microcytic

324
Q

Anemia of Chronic Disease Causes

A

Chronic Inflammatory States
Organ Failure
Age Over 85

325
Q

Anemia of Chronic Disease Cell Type

A

Normocytic

326
Q

Anemia of Chronic Disease Characteristic Lab Findings

A

NONE

327
Q

Thalassemia Cell Type

A

Microcytic

328
Q

Alpha Thalassemia General Genetics

A

Gene deletions

329
Q

Beta Thalassemia General Genetics

A

Point mutations

330
Q

Alpha Thalassemia Population

A

Southeast Asia and Chinese

331
Q

Alpha Thalassemia Specific Genetics

A

Number of deletions of alpha globin genes determines severity of disease

332
Q

Number of deletions of Hemoglobin H disease

A

3

333
Q

Beta Thalassemia Population

A

Mediterranean

334
Q

Beta Thalassemia Specific Genetics

A

Heterozygosity and homozygosity determine severity of disease

335
Q

Hemoglobin H Electrophoresis Finding

A

Fast migrating hemoglobin

336
Q

Beta Thalassemia Electrophoresis Finding

A

Elevation of hemoglobin A2 and hemoglobin F

337
Q

Required for B12 Absorption

A

Intrinsic factor from stomach parietal cells

338
Q

Most Common Causes of B12 Deficiency Anemia

A

Pernicious Anemia
Gastric Surgeries

339
Q

Key Symptoms of B12 Deficiency

A

Glossitis
Peripheral Nerve Paresthesias
Decreased vibration and position sense

340
Q

B12 Deficiency Cell Size

A

Macrocytic

341
Q

Pernicious Anemia Lab Findings

A

Increased Methylmalonic Acid
Increased Homocysteine

342
Q

Most Common Cause of Folate Deficiency Anemia

A

Medications
Alcohol Abuse

343
Q

Folate Deficiency Cell Size

A

Macrocytic

344
Q

Aplastic Anemia Cause

A

Idiopathic
Bone Marrow Failure

345
Q

Aplastic Anemia Key Symptoms

A

Anemia
Neutropenia
Low Platelets

346
Q

Aplastic Anemia Physical Exam Findings

A

Palor
Purpura
Petechiae

347
Q

Haptoglobin Function

A

Binds and clears free hemoglobin in the plasma

348
Q

Three Hemolytic Anemias

A

G6P Deficiency
Sickle Cell
Autoimmune

349
Q

G6P Deficiency Genetics

A

X Linked Recessive

350
Q

G6P Deficiency Population

A

Black men

351
Q

G6P Deficiency Key Symptoms

A

Infections or drugs cause hemolysis

352
Q

Sickle Cell Anemia Genetics

A

Autosomal Recessive

353
Q

Sickle Cell Anemia Lab Findings

A

Howell Jolly Bodies
Target Cells
Run electrophoresis to confirm

354
Q

Test to Confirm Sickle Cell Anemia

A

Electrophoresis

355
Q

Autoimmune Hemolytic Anemia Cause

A

Rapid development of antibodies against self red blood cells

356
Q

Layers of Blood Vessels

A

Adventitia
Media
Intima

357
Q

Intima cell Type

A

Endothelial

358
Q

Capillary Structure

A

Single layer of endothelial cells with a basement membrane

359
Q

Endothelial cells regulate what?

A

Vascular smooth muscle
Vascular resistance
Inflammation

360
Q

Endothelia Cell Special Properties

A

Non thrombotic
Anticoagulant
Usually impermeable

361
Q

Components of Endothelial Activation

A

Intimal Thickening
Hypercoagulability
Free Radial Production
Thrombogenesis

362
Q

What can activate an endothelial cell?

A

Turbulent Blood Flow
Hypertension
Immune Activation
Cigarette Smoke

363
Q

Preclinical Atherosclerosis Progression

A

Normal
Fatty Streak
Fibrofatty Plaque
Advanced Plaque

364
Q

Clinical Atherosclerosis Components

A

Aneurysm and rupture
Occlusion by thrombus
Critical Stenosis

365
Q

Components of Irreversible Intimal Thickening

A

Endothelial dysfunction
Smooth muscle recruitment
ECM Proliferation
Intimal Thickening

366
Q

What can accumulate in a vessel after endothelial injury

A

LDL

367
Q

What due macrophage become after they consume lipids?

A

Foam cells

368
Q

What happens to smooth muscle cells when foam cells develop?

A

They migrate from the media to the intima

369
Q

Fatty Streak

A

Intimal Accumulation of foam cells

370
Q

Atheroma

A

Intimal accumulation of foam cells and extracellular lipid

371
Q

Fibroatheroma

A

An atheroma with a fibrous cap

372
Q

Fibrous Cap Components

A

Smooth muscle cells and extracellular matrix

373
Q

These fibrous caps are stable

A

Thick

374
Q

These fibrous caps are unstable

A

Thin

375
Q

Nonmodifiable Atherosclerosis Risk Factors

A

Genetics
Middle age and older
Male sex
Menopausal Female Sex

376
Q

Modifiable Atherosclerosis Risk Factors

A

Hypertension
Smoking
Diabetes
Hyperlipidemia

377
Q

Hypertension increases the risk for ischemic heart disease by this much

A

60%

378
Q

Smoking does this to the death rate of ischemic heart disease

A

Doubles it

379
Q

Diabetes does this to the risk of ischemic heart disease

A

Doubles it

380
Q

Other Risk Factors of Atherosclerosis

A

Inflammation
Chlamydia pneumoniae Infection
Homocysteine through low B12 or folate

381
Q

Atherosclerosis Complications

A

Calcification
Rupture
Hemorrhage
Embolization
Aneurysm
Sudden Death

382
Q

Untreated hypertension does this to life expectancy

A

Reduces it by 20 to 30 years

383
Q

Nonmodifiable Risk Factors of Hypertension

A

Age
Family History
Race

384
Q

Major Modifiable Risk Factor of Hypertension

A

High sodium diet

385
Q

Primary Hypertension

A

Hypertension with no underlying cause

386
Q

Secondary Hypertension

A

Hypertension with an underlying cause

387
Q

Benign Hypertension

A

Slow clinical course

388
Q

Malignant Hypertension

A

Rapid Clinical Course of 1 to 3 years
Often presents with retinal hemorrhage and renal failure

389
Q

Blood Pressure Equation

A

Blood Pressure=(cardiac output)(peripheral resistance)

390
Q

Source of Atrial Natriuretic Peptide

A

Heart

391
Q

Renin Function

A

Converts Angiotensinogen to angiotensin 1

392
Q

Source of Angiotensinogen

A

Liver

393
Q

Two Types of Arteriosclerosis

A

Hyaline
Hyperplastic

394
Q

Hyaline Arteriosclerosis Cause

A

Benign Hypertension

395
Q

Hyperplasic Arteriosclerosis Cause

A

Severe Hypertension

396
Q

Malignant Hypertension Histology

A

Necrotising arteriolitis

397
Q

Malignant Hypertension Components

A

Hyperplastic arteriosclerosis
Fibrinoid Deposits
Vascular Wall Necrosis

398
Q

Hyperplasic Arteriosclerosis Histology

A

Onion skin vessel wall

399
Q

Internal Elastic Lamina Location

A

Separates the tunica intima from the tunica media

400
Q

What happens to the elasticity of vessels with age?

A

It decreases

401
Q

Percentage of Patients With Coronary Artery Anatomical Variation

A

1 to 5%

402
Q

Berry Aneurysm

A

Aneurysm of Circle of Willis branching points

403
Q

Arteriovenous Fistula

A

When an artery connects to a vein without first going through a capillary bed

404
Q

Etiololgy of Arteriovenous Fistula

A

Developmental Defect
Ruptured Aneurysm
Vascular Necrosis
Penetrating Trauma

405
Q

Fibromuscular Displasia

A

Abnormally thickened and fibrotic arterial media and intima

406
Q

Fibromuscular Displasia Population

A

Young women with no other risk factors

407
Q

Fibromuscular Displasia Clinical Correlations

A

Spontaneous Coronary Artery Dissection
Renovascular Hypertension

408
Q

True Aneurysms include these structures

A

All three layers of the vessel wall

409
Q

Fasle Aneurysms

A

Vessel defect leads to pulsatile hematoma against the outside of the vessel wall

410
Q

Saccular Aneurysm

A

Discrete outpouchings of the vessel

411
Q

Fusiform Aneurism

A

Encompasses full vessel circumference

412
Q

Aneurysm General Etiology

A

Alterations in smooth muscle cell or extracellular matrix compromise the structural integrity of the vessel

413
Q

Predisposing Conditions for Aortic Aneurysm

A

Atherosclerosis
Hypertension

414
Q

Abdominal Aortic Aneurysm Risk Factors

A

Male Sex
Smoking
Genetics

415
Q

AAA Rupture Risk

A

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
Q

Thoracic Aortic Aneurysm Risk Factors

A

Hypertension
Bicuspid Aortic Valve
Marfans
Other Genetic Mutations

417
Q

Thoracic Aortic Aneurysm Clinical Signs and Symptoms

A

Respiratory and feeding issues
Persistent Cough
Pain
Cardiac Disease
Aortic Dissection or Rupture

418
Q

Arterial Dissection

A

When blood enters between the layers of the blood vessel and pushes them apart

419
Q

Aortic Dissection Risk Factors

A

Male Sex
Age 50 and above
Hypertension
Connective Tissue Disorders
Rarely in Pregnancy

420
Q

General Types of Aortic Dissection

A

Proximal and Distal

421
Q

Debakey 1 Aneurysm

A

Involves the ascending and descending aorta

422
Q

Debakey 2 Aneurysm

A

Involves only the ascending aorta

423
Q

Debakey 3 Aneurysm

A

Involves only the descending aorta
Also called a Stanford Type B

424
Q

Retrograde Aneurysm

A

When an aneurysm starts distal but progresses proximally

425
Q

Type A Dissection Treatment

A

Intensive Antihypertensives
Surgical Repare

426
Q

Type B Dissection Treatment

A

Majority can be managed conservatively

427
Q

Two Types of Vasculitis

A

Infection
Autoimmune

428
Q

Giant Cell Arteritis Etiology

A

T Cell Response to antigens in vessel walls

429
Q

Giant Cell Arteritis Symptoms

A

Severe unilateral headache
General malaise
Low Fever
Vision Loss

430
Q

Giant Cell Arteritis Treatments

A

Steroids
Anti TNF Therapy

431
Q

Takayasu Arteritis Pathogenesis

A

Autoimmune scarring of medium and large vessels

432
Q

Takayasu Arteritis Symptoms

A

Vision loss and weak pulse in the extremities as a young person

433
Q

Polyarteritis Nodosa Main Association

A

Hep B

434
Q

Polyarteritis Nodosa Clinical Presentation

A

Rapidly Accelerating High Blood Pressure
Abdominal Pain
Bloody Stools
Diffuse muscular pain

435
Q

Polyarteritis Nodosa Treatment

A

Immunosupretion

436
Q

Kawasaki Patient Population

A

Kids under 4

437
Q

Kawasaki Main Problem

A

Coronary arteritis with infarct or dissections

438
Q

Kawasaki Clinical Presentation

A

Red eyes
Swollen and red hands and feet
Cardiovascular Issues

439
Q

Polyangiitis Effects These Vessels

A

Small vessels

440
Q

Kawasaki Treatment

A

IV Immunoglobulin in the ICU

441
Q

Polyangiitis Triggers

A

Penicillin Drugs
Strep Infection

442
Q

Polyangiitis Symptoms

A

Hemoptysis
Hematuria or Protineuria
Abdominal Pain
Purpura

443
Q

Allergic Granulomatosis and Angiitis Associations

A

Allergies
Asthma
Allergic Rhinitis
Lung Infiltrates
Elevated eosinophils

444
Q

Thromboangiitis Obliterans Associations

A

Smoking
Young age
Indian, Japanese, or Mediterranean descent

445
Q

Raynaud Phenomenon Etiology

A

Vasoconstriction of arteries and arterioles in the extremities

446
Q

Thrombophlebitis and Phlebothrombosis Etiology

A

Deep vein thrombosis from venous stasis
HIGH RISK FOR PULMONARY EMBOLISM

447
Q

SVC Syndromes

A

Neoplasms compress the superior vena cava

448
Q

Lymphangitis

A

Acute inflammation due to bacterial seeding of lymph vessels that presents as a red streak

449
Q

Lymphedema

A

Increased hydrostatic pressure leads to edema

450
Q

Kaposi Sarcoma Causative Organism

A

Herpes

451
Q

Kaposi Sarcoma Main Association

A

HIV patients

452
Q

Retrograde Dissection Clinical Signs and Symptoms

A

Aortic root dissection
Fatal disruption of aortic valve
Coronary artery compression
Tamponade
Aortic Insufficiency
Myocardial Infarction

453
Q

Malignant Tumors of Blood Vessels

A

Angiosarcoma

454
Q

Angiosarcoma Survival Rate

A

30% at 5 years

Biology Of Disease (5 decks)

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