LAB FINAL Flashcards
1
Q
What is myocardial infarction?
A
Process by which an infarct in the heart muscle develops
2
Q
What is an infarct?
A
Zone necrosis due to lack of oxygen/deficiency - doesn’t matter what is the source of oxygen deficiency
3
Q
What is atherosclerotic heart disease?
A
Zone of necrosis due to lack of oxygen - heart is very sensitive to hypoxia
4
Q
What is a transmural infarct?
A
Through the entire thickness of the wall
5
Q
What is an intramural infarct?
A
Patial/portion of the wall thickness involved - typically the inner area compared to the outer
6
Q
How does blood flow in the heart?
A
From the outer wall to the inner wall through the coronary artery
7
Q
What area of the heart is more susceptible to infarct?
A
Subendocardial area is more susceptible to infarction than subpericardial
8
Q
What type of necrosis is myocardial infarction?
A
Coagulative necrosis
9
Q
What is coagulative necrosis?
A
Maintains shape, size, strength of dead tissue - prevents the heart from collapsing while necrosis occurs - allows for formation of healing
10
Q
What happens during healing of a myocardial infarction?
A
Strengthening of the dead portion of the heart muscle = does NOT rupture
11
Q
What type of healing happens in the heart muscle?
A
Repair
12
Q
What is considered “Repair” of the heart?
A
Development of CT/scar tissue within several day to restore structural integrity of the tissue that was damaged (loss of function of tissue)
13
Q
What is the role of phagocytosis in MI?
A
Removes dead muscle tissue > fibroblasts bring cells to heal (ground substance and Procollagen)
14
Q
Can permanent tissue regenerate?
A
NO
15
Q
What is regeneration?
A
Healing of parenchyma - replacement of tissue by the same tissue that was destroyed
16
Q
What is an example of regeneration?
A
Drinking kills the liver, hepatocytes are able to regenerate from the surviving cells, adjacent hepatocytes (daughter cells)
17
Q
What is stable tissue?
A
Rapid healing up until adolescence, healing slows after (glands, liver, etc)
18
Q
What is labile tissue?
A
Allows for regeneration healing of tissue at any time (skin, bone marrow, mucosal linings etc)
19
Q
Why are thrombi formed near the area of tissue healing and nowhere else in the heart?
A
No direct contact to the blood in the chamber due to boundary so not platelet activation
20
Q
What will result in thrombi formation?
A
Reduction of speed of blood (healing tissue no longer contractile/functioning structure)
21
Q
What is the process of thrombosis?
A
Heart tissue is no longer functioning, not pumping > blood is static above the dead tissue > allows for thrombosis (REDUCED BLOOD FLOW)
22
Q
Why would an artery with sclerosis not be smooth?
A
It is due to atheroma/atherosclerotic plaque
23
Q
What is the #1 problem that leads to death in atheroma?
A
Thrombosis d/t turbulence (lack of proper blood flow) of the blood flow
24
Q
What happens during the development of thrombosis?
A
Platelets are in contact with the wall which leads to more chances for platelet activation / formation (forming plaque)
25
What are the 2 different kinds of infarcts?
Red and White
26
Where does white infarct develop?
In tissue with a single source of blood supply (artery or vein) it doesn’t matter
27
Where does a red infarct develop?
In tissue with more than one source of blood supply (artery or vein)
28
What is granulation tissue?
Associated with healing - angiogenesis that occurs on the 2nd post injury day of the wound > healing requires blood supply, if there’s no blood supply, there’s no healing
29
What type of tissue is not involved in a scab?
Granulation tissue
30
What happens during Arteriosclerotic heart disease?
Large MI - tissue has been replaced by CT - function of the left ventricle is worse due to loss of function (decrease pumping ability = heart failure)
31
What is a thrombus formed across the brown infarction?
Brown infarction
32
A MI closer to the conduction center can lead to _____
Arrythmia > deadly > one of the very serious complications of MI
33
What can arteriosclerotic heart disease cause?
Broken heart
34
What is a broken heart?
Hole in the heart - blood pushed into the pericardial cavity
35
What will happen to the patient who has a hole in the heart during systole?
Systole that normally goes into the aorta will now go into the pericardial cavity predominantly
36
What will happen to the patient who has hole in the heart during diastole?
Not enough room for the muscle to relax since there is fluid filling its surrounding (disruption of hydrostatic P) blood cannot flow back into heart for systole - DEATH
37
What is cardiac tamponade?
Prevention of heart diastole due to accumulation of fluid in the pericardial cavity
38
What is able to accumulate in the pericardial cavity?
1. Blood
2. Transudate
3. Exudate from Pericarditis
39
What is an example of “Transudate” in accumulation of pericardial cavity?
Pulmonary stenosis, congestive HF (right sided), anything that results in HYPOALBUMINEMIA:
- nephrotic syndrome
- Kwashiorkor
- Liver cirrhosis
40
What can happen to the ventricles in MI?
Rupture of the interventricular septum
41
What happens with rupture of the interventricular septum?
Oxygenated and deoxygenated blood mix in right ventricle due to left ventricle having stronger hydrostatic P
*** LEFT TO RIGHT ****
42
What is hypertension?
BP = > 140/90
43
What diseases can happen due to hypertension?
MI and stroke
44
Why does hypertension lead to MI and stroke?
Changes in blood vessels
- Hyaline Arteriosclerosis
45
How can hypertension cause problems?
Causes Hyaline Arteriosclerosis which causes increased thickness to arterial walls -> harden -> narrowing of lumen -> leads to total obstruction = MI/STROKE **
46
How does hypertension affect the blood vessels ?
Over time, Increased BP pushes proteins into the vascular wall this results in dramatic narrowing of blood vessels
47
Why does hypertension affect heavier set people?
More vessels for the blood to flow through, decreased resistance OR they don’t know they’re hypertensive
48
What are hypertensive symptoms?
- Occipital headaches
- nausea
- vomiting
49
Does hypertension have a specific manifestation?
NO, sometimes just high BP
50
What are the 2 types of Hypertension?
1) . Primary aka Essential Hypertension
| 2) . Secondary
51
What is primary aka Essential Hypertension?
The disease of high BP and associated with young age (normal everyday people)
52
What is secondary hypertension?
Associated with other disorders (5%)
53
What is a major disorder that is under secondary hypertension?
Pheochromocytoma
54
What is pheochromocytoma?
Tumor of the adrenal MEDULLA
55
What happens during Pheochromocytoma?
Overproduction of catecholamines:
(Nor) epinephrine , dopamine
56
What happens when there is overproduction of catecholamines?
Vasoconstriction (in arterioles because of presence of sphincter that can control the blood flow) -> INCREASES BP
57
What would you think if you have a young patient (below 40) with high BP?
Probably secondary hypertension, and most likely Pheochromocytoma
- Normally has HIGHEST BP, 150/100
58
Hypertension can be ______
Benign (95%)
Malignant 5%
59
What is Benign Hypertension?
- Hypertension develops in proper age of patient (>40) when there is hardening of arteries (hyaline arteriosclerosis)
- The arteries have to adjust > not adequate reaction to the blood wave
60
Can benign hypertension become under control?
YES
61
What is malignant hypertension?
Diseases develop at any age (young or old)
62
How long does patient have to live with Malignant hypertension?
Within 1-2 years patient dies due to progression
63
What is the minimal diastolic pressure in Malignant Hypertension?
120 mmHg
64
Can you help the patient in malignant hypertension?
NO
65
What is the pathomorphological foundation of malignant hypertension?
Hyperplastic Arteriosclerosis
“Onion Skinning”
66
BP =
Q* peripheral resistance
67
Cardiac output =
Q
The amount of blood pumped out per minute = SV * HR : Blood volume and cardiac factors
68
What is blood volume associated with?
With Na absorption of DCT of nephron
69
Increased absorption of Na causes ?
Increase in blood volume due to water following
70
What is blood volume under the control of?
Aldosterone (mineralocorticoid) + atriopeptin aka atrial atrium uremic hormone
71
What does aldosterone do?
Increases reabsorption of sodium and sodium increases osmotic P in the blood so water follows to even out the osmotic P
72
What is atriopeptin?
aka Atrial Natrium uremic horomone (balancing opposite to aldosterone)
- DECREASES sodium reabsorption
73
Where is atriopeptin aka atrial natrium produced?
In the right atrium
74
What does atriopeptin do?
Protect the heart from overloading from too much blood in heart
75
What would you do if a patient came to you and said they have a problem with blood volume causing hypertension?
Decrease salt intake, use diuretics, decrease the Na reabsorption in DCT
76
What are Lazics?
Within 10 min of injection results in dramatic relief
77
What are cardiac factors in regard to hypertension ?
Factors are contractility and HR
78
What is a disease that results in the sudden decrease in contractility ?
MI - cardiogenic shock
79
What is myocardial cardiogenic shock?
Heart pumping cannot maintain adequate BP - develops in 10% of MI patients and 40-50% will die from this
80
Why does MI > Cardiogenic shock develop?
Develops due to patient over exerting heart after the MI, due to ignoring the MI, exertion overloads the heart and Cardiomyopathies
Develops without cause resulting in death within several weeks
81
Where would you see increased heart contractility ?
Bodybuilding
82
What do bodybuilders have?
They have increased contractility due to increased musculature due to increased resistance of blood flow -> HYPERTROPHIES
83
What does increased hypertrophy mean?
Decreased ability to supply the heart with adequate oxygen
84
If there is increased HR, what happens to BP?
Increased BP due to increased mass of the heart will allow the heart to pump more effectively > INCREASES BP
85
What do body builders have to do when the heart is hypertrophied?
Have to maintain the load that the heart is used to, if you don’t use it you lose it, results in decrease faster > MI
86
How can MI happen in bodybuilders ?
From rapid shrinkage of hypertrophied areas of the heart > you need to decrease the load very slowly, then the shrinkage of the heart will be equal to the shrinkage of the new blood vessels
87
What do you do to decrease heart rate?
(More than 90 = Tachycardia)
- To decrease conduction of signals, you need Bet blocker
88
What does peripheral resistance to blood flow do?
Peripheral resistance is friction between the blood and vessel wall
89
Peripheral resistance to blood flow are controlled by what?
Humoral factors
90
What are humoral factors?
Constrictors and dilators
- Affect the arterioles more than venules
91
What are the humoral factors?
- angiotensin II
- catecholamines
- thromboxane, leukotrienes, endothelin
- Inflammation mediators
- prostaglandins and NSAIDs
92
What is angiotensin II?
Have to work against the production of angiotensin II either through preventing formation or destroying it > ACE inhibitors
93
What are catecholamines?
Vasodilator at low concentrations: Vasoconstrictor at high concentrations
94
What do thromboxaned, leukotrienes, and endothelin do?
Increase BP through vasoconstrictor - exception to prostaglandin dilation
95
What are inflammation mediators?
Vasodilator:
Prostaglandins; kinins; NO/EDRF
96
How do NSAID drugs effect prostaglandins?
Decrease the production of PGs > allows for constrictors to predominate > aspirin could be the cause of hypertension due to this/stomach irritation > replace with another drug
97
What are neural factors affected by?
(Nor)epinephrine - how do the same substances effect opposite functions - beta are stimulated by low levels of catecholamines and alpha are stimulated by high levels
98
What are 2 types of neural factors?
A-adrenergic
B-adrenergic
99
Which Neural factor constricts ?
Alpha adrenergic (normally not activated at rest, have high threshold)
- stress
100
Which neural factors dilate?
Beta - adrenergic
- stress is important for development, progression of primary hypertension
101
What are local factors?
Autoregulation (ionic) pH, hypoxia
102
What is the autonomic NS in relation to peripheral resistance to blood flow?
SANS and PANS > works antagonistically - regulation of normal function of organs
103
How do SANS affect blood vessels?
Vasoconstriction
104
How do PANS affect blood vessels?
Does NOT result in vasodilation
- PANS can lead to a decrease in BP potentially due to decreased HR, decreased contractility (neg. Ionotropic and Chronotropic effect)
105
What is the principal treatment to hypertension?
Limit salt intake; mild > mild - mod exercise may be good enough to keep under control - over time this will not be enough
106
What is the treatment to sedative therapy?
Decrease stress, valerian root extract
107
With severe hypertension, what can happen?
Major killer is sudden increase in BP (stable hypertension is better than sudden)
108
What can sudden hypertension be caused by?
Change in temp, sudden activity, change of mood, etc
109
What is an increase in granulation tissue?
Proud flesh
110
CNS infection development depends on:
1. Virulence of infection
2. Status of immune system
3. Presence / absence of predisposing factors
111
What is virulence of infection?
How bad/harmful infection is
112
What is the “Status of immune system” ?
How effective the immune system is at defending you
113
What are the predisposing factors in relation to CNS infection?
- exposure of head to cold
- sinusitis
- otitis media
- basal skull fracture
- chronic pneumonia
114
What does not covering your head to the cold result in?
- decrease local resistance > inflammation
| - must cover head so you don’t get meningitis
115
What is sinusitis in regard to CNS infection?
Sinus is empty spaces in the bone covered by soft tissue open to the surrounding that have orifices communicating with immune system
116
What are the 4 sinuses and what do they contain?
- Maxillary: Largest; middle branch of trigeminal n. Goes through here
- Frontal: Directly behind glabella
- Ethmoid: Within nasal septum
- Sphenoid: Within body of sphenoid bone
117
What are the most commonly affected sinuses?
Frontal and Maxillary
| PAIN
118
What would exposure to the cold do to the sinuses?
If there is a decrease in resistance (exposure to cold) in addition to having the common cold can lead to swelling of sinuses
119
What happens when there is swelling of sinuses?
Swelling could be so dramatic, it could lead to closure of the orifices from the external environment > pus could be trapped within the body > very close to cranial fossa (CNS) - separated by thin layer of bone
120
What is otitis media?
Inflammation of the middle ear - area that contains the small bone that transmits sounds from eardrum to inner ear (mechanical spread of sound)
121
What is significant about the middle ear ?
It communicates with pharyngeal cavity through Eustachian tube
122
What can inflammation of otitis media cause?
Inflammation can form pus and go into mastoid = MASTOIDITIS
- Thin layers of the mastoid can be digested by the pus
123
What is a basal skull fracture, and how can it affect the CNS?
Fracture of the skull results in cracks separating the sinus from CNS > could result in sinuses going straight to the brain
124
Meningitis aka
Leptomeningits
125
What is meningitis aka Leptomeningtis?
Infectious inflammation of the dura mater in the structures of the brain in the vicinity of the subarachnoid space
126
What are the 3 different types of meningitis?
1. Acute (purulent) leptomeningitis aka Acute Bacterial Meningitis
2. Acute Lymphocytic (viral) Meningitis aka Aseptic type
3. Chronic Meningitis
127
What is the cause of Acute (Purulent) Leptomeningitis aka Acute Bacterial Meningitis?
Bacterial infection due to pus
128
Who is affected primarily by Acute (purulent) Leptomeningitis aka Acute bacterial meningitis ?
Infants, young children, and elderly:
- Strep Pneumonia
129
Does Acute (Purulent) leptomeningitis aka Acute Bacterial Meningitis have a high mortality rate?
YES
- When people die from this, pathologies will find pus on the hemispheres on the brain or on the foundation of the brain
130
What are the 2 tests to confirm meningitis?
Kernig and Brudzinski
131
What are the manifestations of Acute (Purulent) Leptomeningitis aka Acute Bacterial Meningitis?
1. Headache
2. Stiff neck
3. Fever
4. Mental confusion
132
Why do you get a headache from acute (purulent) leptomeninigtis aka Acute Bacterial Meningitis?
Due to increased cranial pressure
133
Why is there increased intracranial pressure with meningitis?
There is inflammation of the meninges, anytime there is inflammation you will see 5 cardinal signs, one of which is tumor (swelling)
134
What is the mechanism of meningitis?
The meninges swell > swelling of arachnoid granulations > decrease in the reabsorption of CSF > hydrocephalus > increased intracranial pressure
135
Why would you have a stiff neck with acute (purulent) Leptomeningitis aka acute bacterial meningitis?
Due to loss of function from inflammation (5 cardinal signs)
- Muscle spasms due to patient hurting from head being in Flexion
136
What is a red flag with acute (purulent) Leptomeningitis aka acute bacterial meningitis?
FEVER
MC ominous sign in Chiro office
137
What is an example of how fever can be dangerous from acute (purulent) Leptomeningitis aka acute bacterial meningitis?
**EPIDURAL ABSCESS
- pus accumulation between the dura mater and Lamina > compresses the spinal cord > decreased function and pain
*** SPACE OCCUPYING LESIONS
138
What happens if you adjust a patient with Acute bacterial meningitis?
The pus will spread along the spinal cord canal and patient will die the same day
139
Mental confusion is associated with what disease?
Acute (purulent) Leptomeningitis aka Acute Bacterial Meningitis
140
How do you diagnose Acute (purulent) leptomeningitis aka acute bacterial meningitis?
Lumbar puncture
Needle in the spinal cord canal to obtain CSF for analysis
141
Where is the lumbar puncture done?
Between L3 and L4 because the spinal cord ends at L2
142
What do you analyze during the lumbar puncture when checking for meningitis?
Cells, proteins, glucose, viscosity - normally the CSF is watery and clear with no cells
143
What will you see in the CSF of Acute (purulent) Leptomeningitis aka acute bacterial meningitis?
EXCESS NEUTROPHILS
- Because neutrophils target bacteria
144
What other substances will be high/low in the CSF of a patient with acute (purulent) leptomeningitis aka acute bacterial meningitis?
- Increased protein exudate is always made in acute inflammation, and exudate is a protein rich fluid
- Decreased glucose (bacteria eats all the glucose)
145
How do you determine bacteria within CSF of patient with acute purulent leptomeningitis aka acute bacterial meningitis?
Spread the CSF on agar plate, patients are given a broad spectrum antibiotic to prolong patient’s life
146
What is acute lymphocytic (viral) meningitis aka aseptic type?
Aseptic because there aren’t any bacteria in the blood
147
What type of lymphocytes are present during acute lymphocytic (viral) meningitis aka aseptic type?
T8 Cytotoxic Lymphocytes
148
What are T8 Cytotoxic Lymphocytes?
Specifically designed to eliminate viral cells, anti-tumor, and anti-graft (these cells are the reason for graft rejection)
149
Are there any antibodies in acute lymphocytic (viral) meningitis aka aseptic type?
NO, it is only cell reacting, it is T-Cell mediated Cytotoxicity
- TYPE IV HYPERSENSITIVITY
150
What are the 2 subtypes of Type IV Hypersensitivity?
1. T cell mediated cytotoxicity (associated with acute lymphocytic (viral) meningitis aka aseptic type
2. Delayed type: NOT viral, example = TB
151
Mumps virus is associated with what type of meningitis?
acute lymphocytic (viral) meningitis aka aseptic type
152
What can mumps result in?
Viral meningitis or acute orchitis (acute inflammation of the testes, 60% cases leads to infertility)
153
Viral meningitis is :
BENIGN
- Same manifestations as bacterial, but less severe
154
What will you see in the lumbar puncture of acute lymphocytic (viral) meningitis aka aseptic type?
- Increased lymphocytes
- increased protein (exudate again)
- NORMAL glucose (viral cells don’t consume glucose)
155
What is chronic meningitis caused by?
- mycobacterium TB
- treponema pallidum
- brucella species
- cryptococcus neoformans
156
How does chronic meningitis develop ?
Insidiously with no severe swelling in the beginning
157
What are manifestations of chronic meningitis?
Symptoms are not as severe and don’t develop seriously
158
What will you see in the lumbar puncture of chronic meningitis?
- increased mononuclear cells
- increased proteins
- decreased glucose
159
What are mononuclear cells?
Monocytes > macrophages and lymphocytes
160
Is there exudate in chronic meningitis?
NO exudate is only in ACUTE INFLAMMATION
161
Why is lumbar puncture not clear fluid ?
Tissue debris and accumulation of cells and microorganisms
162
DISEASES OF JOINTS
NEW
163
Where can inflammation of the joints ONLY happen?
Where there is blood supply
164
What is the only structure with blood supply in the joint?
Synovial membrane
165
What happens with disease progression with inflammatory arthritis?
Involvement of the rest of the joint > destruction of cartilage, destruction of bone, destruction of soft tissue, loss of function of joint, and FULL FUSION of the ARTICULATING BONES OF JOINT
166
What is full fusion of the articulating bones of the joint?
Joint Ankylosis
167
What are the 3 types of inflammatory arthritis?
1. RA
2. Seronegative Spondyloarthritides
3. Infectious Arthritis
168
What do you see with Seronegative spondyloarthritides?
Inflammation of the peripheral and spinal joints
169
Spondyloarthritides =
Vertebral joint inflammation
| Spondylo=vertebral
170
What are the synovial joints of the spine?
- facet/Z/Zygapophyseal/apophyseal joints (atlantoaxial)
- atlanto-occipital
- atlanto-odontoid
- SI joint
- costotransverse
- costovertebral
171
What is important about the SI joint in regard to Seronegative spondyloarthritides?
ALWAYS 100% INVOLVED
- Specifically the lower 1/3 (synovial portion)
- Clinically manifested by buttock pain
172
Are uncinate joints synovial?
NO
173
What are the types of Seronegative spondyloarthritides?
PEAR
- Psoriatic arthritis
- arthritis associated with IBD (crohn’s disease and ulcerative)
- Ankylosing spondylitis
- Reiter’s syndrome
174
What is Ankylosing Spondylitis?
Autoimmune disease with no etiology (should be called idiopathic AS)
175
What are the aka’s of AS?
Marie-Strumpel-Bechterew
| Know any
176
What is a major clinical presentation of AS?
Bamboo spine
177
How does Bamboo spine develop?
1. Inflammation
2. Ossification
3. Development of CT
178
What is inflamed in AS particularly bamboo spine?
Attachment of annulus fibrosus
179
what is ossified in AS particularly bamboo spine?
Out layer of the annulus fibrosus > syndesmophytes
- forming bone where fibrous tissue should be
180
What is “development of CT” in AS particularly bamboo spine?
Between 2 Articular surfaces > full fusion of the synovial joints
- joint ankylosis
- COMPLETE LOSS of ROM
181
How do you suspect AS in patient?
Have patient bend over and touch toes with knees straight
- SPine will be flat and immobile
- Inability to move in any 3 planes
182
What posture is it called when all bones are fused together in AS?
Walter’s posture
183
What do you see with AS on x ray?
All joint spaces absent, cannot see separate vertebra, syndesmophytes, SI joints fused, pubic symphysis fused, they would have no knee joints
184
What are early manifestations of AS?
1. Severe low back pain predominantly 2nd 3rd decade males 4:1
2. Pain is more severe in morning , and minimal in the evening (usually accompanied by stiffness)
3. Pain can be relieved by motion and physical exercise
185
What is the difference between DJD and Inflammatory arth?
Degenerative = Deg. Of cartilage
- cartilage cant be inflamed cause there is NO blood supply
186
What happens as DJD continues its process?
There is cartilage metabolism impairment, bone and soft tissue destruction, but there is NO fusion of articulating bones
187
What is final outcome of DJD?
Osteophytosis
188
What are Degenerative diseases?
OA
Spondylosis
Hemarthrosis
Forestier’s Disease
