Module 2 Patho Flashcards
(171 cards)
1
Q
Neoplasia “new”
A
New growth
2
Q
Process of cancer
A
-Cell signals to a proliferation
-Unlimited replication
-Lose cell differentiation
-Genetically unstable
3
Q
Carcinogenesis
A
-Damage to DNA
-Cell replication is incomplete or with abnormalities
4
Q
Metastasis
A
Development of secondary malignant growths at a distance from a primary site of cancer.
5
Q
Grading and staging
A
Catscan, MRI, PET scan
6
Q
Grading and staging
TNM (tumor, node, metastasis)
A
I, II, III, IV
Limited, Local, Expansive, Metastasis
7
Q
7 Warning Signs
A
-Change in bowel or bladder habits
-Sore that does not heal
-Unusual bleeding or discharge
-Thickening of a lump in the breast or elsewhere
-Indigestion or difficulty swallowing
-Noticeable difference in wart or mole
-Nagging cough or hoarseness
8
Q
Infection
Microbiome
A
The genetic material of all microbes that live on and inside the human body
9
Q
Infection
Antibiotic resistance
A
germs like bacteria and fungi develop the ability to defeat the drugs designed to kill them
10
Q
Infection
Pathogen characteristics
Virulence
A
the potential of microorganisms to cause disease
11
Q
Infection
Pathogen characteristics
Evasion
A
outside coating developed to prevent phagocytosis
12
Q
Infection
Pathogen characteristics
Spores
A
resistant to heat, chemical agents, and desiccation
13
Q
Infection
Pathogen characteristics
Antimicrobial resistance
A
Enzyme inhibition
Reduced permeability
Altered target sites
Protection of target site
Overproduction of target
Pump out drugs
Molecules to bind antibiotics
14
Q
Transmission of infection
A
- Reservoir
- Portal of exit
- Mode of transmission
- Portal of entry
- Susceptible victim
15
Q
Transmission of infection
Reservoir
A
Human, Animal, Inset, Soil
16
Q
Transmission of infection
Portal of exit
A
Nasal mucosa, Oral mucosa
17
Q
Transmission of infection
Mode of transmission
A
Insect bite, Nasal droplets, Saliva, Semen
17
Q
Transmission of infection
Portal of entry
A
Nasal mucosa, Oral mucosa, Skin abrasion, Skin puncture
18
Q
Transmission of infection
Susceptible victim
A
Malnourished, Unimmunized, Immune compromised
19
Q
Pathogenic Organisms
A
Bacteria
Viruses
Fungal
Parasites
Culture and sensitivity
20
Q
Pathogenic Organisms
Bacteria
A
-Single-celled rigid wall, organisms that have no internal organelles
-Degrade dead tissue
-Gram + or Gram -
21
Q
Pathogenic Organisms
Parasites
A
live in the human body, on the skin, or in the GI tract (can be good or bad)
22
Q
The Cell Players
Leukocytes
A
-ALL white blood cells (first line of defense)
-Mature cells shift to the right
23
Q
The Cell Players
Lymphocytes
A
Natural Killer (NK), T and B cells work on adaptive immunity
24
The Cell Players
Neutrophils
-immature white blood cells (stored in bone marrow), Immature bands, and used as a lost resort
-Immature cells left shift
25
The Cell Players
B & T Cells
T CD4 (helper T *mark toxic cells*), CD8 (killer T *kill marked cell*)/ B cell produces antibodies, memory cells (knows what is toxic to the cell), and produce T cells
26
The Cell Players
Natural Killer Cells (NK)
Recognize anti-body coated target cell
27
Chemical Mediators of Immunity
Complement Cascade
-Proinflammatory condition
-Chemotaxis (attracts neutrophils and monocytes, “histamine response”)
-Kinins (cause vasodilation, pain response)
-Cytokines (inflammation, regulate immunity, a large group of proteins, aid cell in the communication)
28
Injury = Inflammation
*always occurs with infection but does not always involve infection*
Redness, Swelling, Heat, Pain, Loss of Function, Acute or Chronic
29
Inflammation
1. Vascular Permeability
2. Leukocyte Emigration
3. Phagocytosis
30
Inflammation
Vascular Permeability
Histamines
Vasodilation
31
Inflammation
Leukocyte Emigration
Pass through blood vessels to inflamed tissue
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Inflammation
Phagocytosis
Neutrophils and monocytes - eat away and destroy
32
Inflammation
Phagocytosis
Neutrophils and monocytes - eat away and destroy
33
Exudates
Fluids that leak out of blood vessels
34
Exudates
Serous
clear drainage
35
Exudates
Serosanguinous
watery, light pinkish color
36
Exudates
Sanguineous
bloody drainage
37
Exudates
Purulent
pus, thick *infection*
38
Cell-Mediated vs Humoral
T Cell
-CD4 (interchangeable, go after bacterias) vs. CD8 (suppressors, go after cancers/viruses)
-T helper vs T killer
39
B cell *recognize antigen*
-Memory vs plasma membrane (short-lived antibody producers)
-Cloning memory cells and secreting antibodies
40
Antibodies (GAME) (drag and drop questions, memorize all)
IgG
IgA
IgM
IgE
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Antibodies (GAME)
IgG
most abundant (IgG = gigantic) protection against previously exposed infection
42
Antibodies (GAME)
IgA
Alternative
43
Antibodies (GAME)
IgM
Main fighter, immediate response
44
Antibodies (GAME)
Environmental, allergies, triggered by environmentally
45
Antibodies (GAME)
Antibody functions
Binding, antitoxins, precipitate out of body fluids, a coat for recognition
46
Passive vs. Active Immunity
-Passive - passive transfer (ex: mother to child), injection of antibodies
-Active - immunization, active infection, the body creates antibodies
47
Hypersensitivity
I - Immediate *severe/anaphylaxis*
II (tissue) - Immediate *tissue response to allergic reaction*
III (tissue/organ) - Ongoing
IV - Delayed
48
The Players
-Hydrogen ions H+ (7.35 - 7.45pH)
-Carbon dioxide PCO2 (35 - 45)
-Kidneys HCO3 (22 - 26 bicarbonate)
49
Alkalotic
*High pH*
Too much base (bicarbonate)
50
Acidotic
*Low pH* - Too much acid (bicarb HCO3-), pH is below 7.35 *H+ increase pH decreases*
51
ROME *blood gas*
*R - respiratory acidosis/alkalosis *lungs / pregnancy*
O - trends opposite
*M - metabolic acidosis/alkalosis *kidneys*
E - trends equally, up or down *pH & Carbon Dioxide*
52
ROME *blood gas*
R - respiratory acidosis/alkalosis *lungs / pregnancy*
-Respiratory Acidosis Ex: COPD, opioid overdose
-Respiratory Alkalosis Ex: Hypercenelation, panic, pregnancy
53
ROME *blood gas*
M - metabolic acidosis/alkalosis *kidneys*
-Metabolic Acidosis Ex: Renal failure, diabetic ketoacidosis
-Metabolic Alkalosis Ex: Prolonged vomiting, diuretic use, antacid use
54
4 Cardiac Tissue Layers
-Intima “inner” - innermost layer
-Media “middle” - Thickest in arteries
-Adventitia “v=vein” - Thickest in veins
-Capillaries - Sing layer thickness
55
Cardiac Blood Flow Determinants
-Gradient
-Resistance
Viscosity = thickness
The ratio of RBSs to plasma=hematocrit (thickness of the blood)
-Ohm’s Law (when pressure changes our circulatory system will change with it)
-Total peripheral resistance
-Systemic vascular resistance
56
Microcirculation, Velocity, Turbulent Flow
Law of LaPlace
distending pressure/wall tension
-Wall in tension - high radius or distending pressure = high wall tension
-Pressure = Thickness(of blood) / Radius
57
Microcirculation, Velocity, Turbulent Flow
Coagulation
Blood changing to a solid or semi-solid state
58
Microcirculation, Velocity, Turbulent Flow
Microcirculation
-Arteries - away from the heart
-Veins - to the heart
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Microcirculation, Velocity, Turbulent Flow
Microcirculation
Smallest vessels
Arteries -> Arterioles -> capillaries -> Venules -> Veins -> Vena Cava
60
Hyperemia
excess blood in the vessels supplying an organ or other part of the body
61
Flow Control
Extrinsic
Outside of the organ they control, and can override intrinsic systems
62
Flow Control
Intrinsic
The organ is able to maintain homeostasis within itself
63
Altered Flow
Hypoxia
insufficient supply of O2
64
Altered Flow
Ischemia
decreased blood flow in arteries to supply adequate oxygenation
65
Altered Flow
Blood vessel obstructions
Thrombus
a stationary blood clot
66
Altered Flow
Blood vessel obstructions
Embolus
moving clot
67
Altered Flow
Blood vessel obstructions
Vasospasm
constriction of arterial smooth muscle (drastic temperature changes)
68
Altered Flow
Blood vessel obstructions
Compression
obstruction (arterial occlusion)
69
Altered Flow
Blood vessel obstructions
Inflammation
inflammation of the inner layer (autoimmune origin, vasculitis)
70
Altered Flow
Raynaud Syndrome
Extreme vasoconstriction producing cessation of flow to fingers and toes
71
Altered Flow
Diagnosis
doppler flow, angiography, exercise/stress test
72
Altered Flow
Treatment
-First-line treatment - non-pharmacologic interventions (weight reduction, smoking, exercise)
-If not successful - drug therapy, surgery (angioplasty, stent, CABG)
73
Alpha and Beta Receptor
Alpha
increase HR, BP, RR, and pupil size
74
Alpha and Beta Receptor
Beta 1
increases HR, renin(regulates BP) release, and lipolysis(release fatty acid)
75
Alpha and Beta Receptor
Beta 2
76
Alpha and Beta Receptor
Stroke Volume x Heart Rate = Cardiac Output
Starling's Law - The more significant the heart force, the greater the output
77
Structural Alterations
Superficial veins
varicose veins
78
Structural Alterations
Deep veins
chronic venous insufficiency
79
Structural Alterations
Aneurysms
weakness in the blood vessel wall, and usually branches
-Diagnostic tests - CT, MRI, TEE
-Treatment - dissecting aortic aneurysms, vasodilators, grafts
80
Structural Alterations
Arteriovenous fistulas
AVM (arteriovenous malformation)
81
Structural Alterations
Arteriosclerosis
hardening of the blood vessels
82
Coronary Artery Disease (CAD)
-This can lead to ischemia
-LDL (low-density lipoprotein, bad ones, cholesterol) attaches to the artery wall and builds up (plaque), which can cause a blood clot (thrombus), HDL (high-density lipoprotein, good ones)
83
Coronary Artery Disease (CAD)
Modifiable risk-factors
Physical activities
Stress
Mental health
84
Coronary Artery Disease (CAD)
Nonmodifiable risk-factors
Age
Gender
Family history of CAD
Ethnicity
85
Arterial Ulcers
damage due to lack of blood flow to the tissue
86
Venous Ulcers
damage due to insufficient return of blood back to the heart
87
Acute Arterial Occlusion
The absence of arterial circulation may result from thrombi/emboli or mechanical compression
88
Acute Arterial Occlusion
Classic signs and symptoms 6 P’s
Pallor
Paraesthesia (numbness)
Paralysis
Pain
Polar
Pulseless
89
Alterations in Venous Flow
Incompetent valves producing varicose veins, chronic venous insufficiency
90
Alterations in Venous Flow
Deep vein thrombosis (DVT)
Can be life-threatening
Cause by a thrombus in a deep vein of the lower extremity
Treated aggressively with anticoagulation therapy
91
Alterations in Venous Flow
Valvular Incompetence
-Overstretching of the valves resulting in backflow of blood
-Varicose veins
92
Chronic Venous Insufficiency
-Results when valvular incompetence involves the deep veins
-Venous stasis ulcers - turns skin brown (hemosiderin deposits)
93
Lymphatic Flow
Lymphedema
It occurs when the normal flow is obstructed or altered in some fashion
Normally affects the extremities
Common with mastectomies in women
94
Blood Pressure
Average blood circulation 4-6 liters
Systolic B/P - ventricular contraction
Diastolic B/P - ventricular relaxation
BP (measure in mmHG) = CO (cardiac output) x SVR (systemic vascular resistance)
95
Hypertension
Increases the heart's workload and can lead to stroke, renal failure, aneurysms, damage to microcirculation, etc.
96
Blood Pressure Regulators
Baroreceptors - Help regulate blood pressure, located in the carotid and aorta
Vasomotor center in the medulla (by brainstem)
97
Hypertensive Emergency
180/120 (leads to organ damage)
Causes
Renal disease
Pre-eclampsia
Obstructive sleep apnea
98
Hypotension (low blood pressure)
Causes
Change in position
Fluid volume deficit
Arrhythmias
Vasovagal reaction
Medication
99
Blood Flow
-Transport oxygen/nutrients and removes wastes
-Order
-Capillaries -> Vena Cava -> R. Atrium -> Tricuspid Valve -> R. Ventricle -> Pulmonic Valve -> Pulmonary Artery -> Lungs -> Pulmonary Veins -> L. Atrium -> Mitral Valve -> L. Ventricle -> Aortic Valve -> Aorta -> Body
100
Cardiac Basics
PMI
Point of maximal impulse
101
Cardiac Basics
Tissues
-connective and epithelial
-Endocardium -> Myocardium -> Epicardium -> Pericardium
102
Cardiac Basics
Ventricular Ejection
-EDV - Volume of blood in the ventricle prior to ejection
-ESV - Amount of blood that remains in the ventricle after ejection
103
Cardiac Basics
Coronary resistance
dependent upon artery diameter and external compression
104
Myocardial ischemia develops
with a lack of oxygen
105
Myocytes
Transmit electrical signals and are excitable
106
Conduction System of the Heart
SA Node (60-100)
AV Node (40-60)
Bundle of His (20-40)
Bundle branches
Purkinje fibers
107
Cardiac Output (CO)
Heart Rate x Stroke Volume
108
Ejection Fraction
% of blood ejected from left ventricle with each contraction
Standard 55-60%
109
Test of Cardiac Function
Electrocardiography(ECG)
provides a graphic illustration of electrical currents generated by cardiac cells
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Electrocardiography(ECG)
P wave
atrial depolarization
111
Electrocardiography(ECG)
PR
atrial contraction/relaxation
112
Electrocardiography(ECG)
QRS complex
ventricular depolarization
113
Electrocardiography(ECG)
T wave
ventricular repolarization
114
Electrocardiography(ECG)
QT
ventricular contraction/relaxation
115
Electrocardiography(ECG)
U wave
in slow heart rate and low potassium
116
Test of Cardiac Function
MRI/CT
imaging cardiac structures, and abnormalities and detecting plaque
117
Test of Cardiac Function
Nuclear Cardiography
Radioactive substances injected into the bloodstream are used to trace patterns of blood flow in the heart (cold spots = inadequate perfusion)
118
Chapter 18
Alteration in Cardiac Function
119
Coronary Heart Disease (CDH)
Insufficient delivery of oxygenated blood to the myocardium (heart muscle)
Also called ischemic heart disease and coronary artery disease (CAD)
120
Atherosclerosis
-Causes narrowing of the arterial lumen that can lead to cardiac ischemia
-Plaque formation due to endothelium injury
-Excess lipid and debris accumulate within the vessel wall into the lipid core (CLOT)
Vulnerable plaques = thin cap (pimple)
Stable plaques = stable cap (dried-up pimple)
121
Angina Pectoris
3 Patterns
-Stable (typical) angina
-Unstable (Crescendo) angina
-Prinzmetal (variant) angina
122
Angina Pectoris
3 Patterns
Stable (typical) angina
-Predictable
-Common
-Relieved by rest and nitroglycerin
123
Angina Pectoris
3 Patterns
Unstable (Crescendo) angina
-May progress to acute ischemia
-The narrowing can lead to occlusion
-Unpredictable
-Not relieved with rest or nitroglycerin
124
Angina Pectoris
3 Patterns
Prinzmetal (variant) angina
-Characterized by vasospasms
-Unpredictable
125
Acute Coronary Syndrome
Includes
-Unstable angina
-ST - elevation MI (STEMI)
-Non-ST elevation MI (NSTEMI)
-STEMI vs NSTEMI
STEMI - plaque blocks a major artery completely
NSTEMI - block in a minor artery or partial occlusion is a major artery
126
Acute Coronary Syndrome
Myocardial Infarction (MI)
-Occlusion that is long enough to cause permanent myocardial cell death
127
Acute Coronary Syndrome
Diagnosis
Severe radiating pain
Diaphoresis
SOB
Last more than 15 minutes and is not resolved by nitroglycerin
Increase in troponin
128
Acute Coronary Syndrome
ECG Changes
ST-segment elevation (always MI)
ST - segment depression (ischemia)
Large Q waves, and inverted T waves
129
Acute Coronary Syndrome
Treatment
MONA
Morphine
Oxygen
Nitroglycerin
Asprin
130
Sudden Cardiac Arrest
-Sudden cardiac death
-Unexpected death from cardiac causes within 1 hour of symptom onset
131
Endocardial and Valvular Disease
Endocardial and valvular structures damaged by:
Inflammation and scarring
Infection
Calcification
Malformation
132
Endocardial and Valvular Disease
-Hearts workload is increased
-Stenosis - failure of the valve to open completely
-Regurgitation - the inability of a valve to close completely
-Prolapse - the ballooning of the valve
-Murmurs are common
-Systole - atria fill and ventricles constrict
-Open - Aortic & Pulmonic
-Diastole - ventricles fill and atria constrict
-Open - Mitral & Tricuspid
133
Rheumatic Heart Disease
Inflammation after the infection of streptococci (common in children)
134
Endocarditis
Inflammation of the inner lining of heart ventricles and valves
135
Myocarditis
Inflammation of heart muscle
136
Chronic Ischemic Cardiomyopathy
Classified by cause of functional impairment
Primary - unknown cause
Secondary - known cause
137
Chronic Ischemic Cardiomyopathy
Different types
Dilated - little muscle and space in ventricles large
Hypertrophic - tons of muscle and little space for ventricles to fill
Restrictive - normal muscle but impaired diastolic filling
138
Pericardial effusion
Accumulation of noninflammatory fluid to the pericardial sac impairs heart filling
139
Pericarditis
Acute or chronic inflammation of the pericardium caused by a virus
140
Heart Failure
-The heart pump fails due to the inability to maintain cardiac output EF is less than 60%
-FACES Test (fatigue, activity limitation, congestion, edema, shortness of breath)
141
Heart Failure
L-sided
L for Lungs
Often leads to R
Pink frothy sputum
Pulmonary congestion
142
Heart Failure
R-sided
-Backward effects caused by congestion in the systemic venous system
-Forward effects cause low output to the left ventricle leading to low CO
-Can cause biventricular heart failure
143
Heart Failure
Preload
initial stretching of the heart muscle
144
Heart Failure
Afterload
force or load against which the heart has contracted or ejected the blood
145
Heart Failure
Diagnostic
chest x-ray, echocardiography, and B-type natriuretic peptide level(BNP)
146
Heart Failure
Treatment
improve CO, minimize cardiac workload, and manage BP
147
Dysrhythmias
-Also called arrhythmias, and abnormality of the cardiac rhythm of impulse generation or conduction
148
Dysrhythmias
3 types: fast, slow, none
-Abnormal rates
-The abnormal electrical signal coming from somewhere else
-Disturbances in conduction pathways
-NSR “Tachy (high) and Brady (low)*
149
Dysrhythmias
Sinus arrhythmia
Just irregular, and usually harmless
Atrial flutter (sawtooth pattern) / fibrillation
150
Dysrhythmias
Fatal (emergency)
Ventricular Tachycardia (shark fin)
Ventricular Fibrillation (erratic and irregular)
151
Acute Respiratory Failure
-State of disturbed gas exchange
-3 types
-Hypoxemia (low carbon dioxide levels)
-Hypercapnia (respiration failure)
-Combination of both
152
Pulmonary Function Test (PFT)
A noninvasive test that shows how well the lungs are working
153
Crackles in the Lungs
Small air sacs in the lungs are filled with fluid
154
Ronci in the Lungs
Gurgling or bubbling sounds during both inhalation and exhalation
155
Wheezing
Inflammation and narrowing of the airway in any location of the respiratory tract
156
Pulmonary Hypertension (HTN)
Sustained high pulmonary artery systolic pressure
157
Pleural Effusion
Excess fluid outside the lungs “water on the lungs”
158
Pulmonary Venous Thromboembolism (PE)
“Pulmonary Embolus”
Detached material that occludes blood vessels in the lungs
159
Chronic Obstructive Pulmonary Disease (COPD)
Increased resistance to airflow
160
Obstructive Pulmonary Disorder
Asthma
Antibodies lead to inflammation, wheezing, and SOB
161
Obstructive Pulmonary Disorder
Bronchitis
Inflammation of “big airways”, genetics = B for blue bloater, and chronic cough
162
Obstructive Pulmonary Disorder
Emphysema
Irreversible damage to alveolar air sacs, genetic alpha antitrypsin = P for the pink puffer
163
Peak Flow
Green Zone (80-100%)
Yellow Zone (50-80%)
Red Zone (<50%)
164
Adult Respiratory Distress Syndrom (ARDS)
Alveoli injury, pulmonary edema from fluid shifts, and triggers inflammation
165
Tension Pneumothorax
Air enters pleural space, increased hydrostatic pressure shift fluid in the pleural space and can contain different fluid types
166
Interstitial Lung Disease (Pulmonary Fibrosis)
Injury/inflammation to lung tissue and alveoli thickness
167
Tuberculosis (TB)
Respiratory infection that causes macrophages and inflammation
168
Pneumonia
-Bacterial infection due to aspiration, inhalation, sepsis, or spread from other infections
-Manifests as inflammation, fever, SOB, and exudative fluid
169
Covid 19
Caused by SARS-COV2, incubation 5-6 or 1-14 days
