Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

8 PATH 2 > LAB FINAL > Flashcards

LAB FINAL Flashcards

1
Q

What is myocardial infarction?

A

Process by which an infarct in the heart muscle develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is atherosclerotic heart disease?

A

Zone of necrosis due to lack of oxygen - heart is very sensitive to hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a transmural infarct?

A

Through the entire thickness of the wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is an intramural infarct?

A

Patial/portion of the wall thickness involved - typically the inner area compared to the outer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does blood flow in the heart?

A

From the outer wall to the inner wall through the coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What area of the heart is more susceptible to infarct?

A

Subendocardial area is more susceptible to infarction than subpericardial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What type of necrosis is myocardial infarction?

A

Coagulative necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens during healing of a myocardial infarction?

A

Strengthening of the dead portion of the heart muscle = does NOT rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of healing happens in the heart muscle?

A

Repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the role of phagocytosis in MI?

A

Removes dead muscle tissue > fibroblasts bring cells to heal (ground substance and Procollagen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Can permanent tissue regenerate?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is regeneration?

A

Healing of parenchyma - replacement of tissue by the same tissue that was destroyed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is stable tissue?

A

Rapid healing up until adolescence, healing slows after (glands, liver, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is labile tissue?

A

Allows for regeneration healing of tissue at any time (skin, bone marrow, mucosal linings etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What will result in thrombi formation?

A

Reduction of speed of blood (healing tissue no longer contractile/functioning structure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Why would an artery with sclerosis not be smooth?

A

It is due to atheroma/atherosclerotic plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the 2 different kinds of infarcts?

A

Red and White

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Where does white infarct develop?

A

In tissue with a single source of blood supply (artery or vein) it doesn’t matter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Where does a red infarct develop?

A

In tissue with more than one source of blood supply (artery or vein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is granulation tissue?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What type of tissue is not involved in a scab?

A

Granulation tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What happens during Arteriosclerotic heart disease?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is a thrombus formed across the brown infarction?

A

Brown infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

A MI closer to the conduction center can lead to _____

A

Arrythmia > deadly > one of the very serious complications of MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What can arteriosclerotic heart disease cause?

A

Broken heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is a broken heart?

A

Hole in the heart - blood pushed into the pericardial cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What will happen to the patient who has a hole in the heart during systole?

A

Systole that normally goes into the aorta will now go into the pericardial cavity predominantly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What will happen to the patient who has hole in the heart during diastole?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is cardiac tamponade?

A

Prevention of heart diastole due to accumulation of fluid in the pericardial cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is able to accumulate in the pericardial cavity?

A
  1. Blood
  2. Transudate
  3. Exudate from Pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is an example of “Transudate” in accumulation of pericardial cavity?

A

Pulmonary stenosis, congestive HF (right sided), anything that results in HYPOALBUMINEMIA:

  • nephrotic syndrome
  • Kwashiorkor
  • Liver cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What can happen to the ventricles in MI?

A

Rupture of the interventricular septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What happens with rupture of the interventricular septum?

A

Oxygenated and deoxygenated blood mix in right ventricle due to left ventricle having stronger hydrostatic P

*** LEFT TO RIGHT **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is hypertension?

A

BP = > 140/90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What diseases can happen due to hypertension?

A

MI and stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Why does hypertension lead to MI and stroke?

A

Changes in blood vessels

  • Hyaline Arteriosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How can hypertension cause problems?

A

Causes Hyaline Arteriosclerosis which causes increased thickness to arterial walls -> harden -> narrowing of lumen -> leads to total obstruction = MI/STROKE **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How does hypertension affect the blood vessels ?

A

Over time, Increased BP pushes proteins into the vascular wall this results in dramatic narrowing of blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Why does hypertension affect heavier set people?

A

More vessels for the blood to flow through, decreased resistance OR they don’t know they’re hypertensive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are hypertensive symptoms?

A
  • Occipital headaches
  • nausea
  • vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Does hypertension have a specific manifestation?

A

NO, sometimes just high BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the 2 types of Hypertension?

A

1) . Primary aka Essential Hypertension

2) . Secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is primary aka Essential Hypertension?

A

The disease of high BP and associated with young age (normal everyday people)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is secondary hypertension?

A

Associated with other disorders (5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is a major disorder that is under secondary hypertension?

A

Pheochromocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is pheochromocytoma?

A

Tumor of the adrenal MEDULLA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What happens during Pheochromocytoma?

A

Overproduction of catecholamines:

(Nor) epinephrine , dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What happens when there is overproduction of catecholamines?

A

Vasoconstriction (in arterioles because of presence of sphincter that can control the blood flow) -> INCREASES BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What would you think if you have a young patient (below 40) with high BP?

A

Probably secondary hypertension, and most likely Pheochromocytoma

  • Normally has HIGHEST BP, 150/100
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Hypertension can be ______

A

Benign (95%)

Malignant 5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is Benign Hypertension?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Can benign hypertension become under control?

A

YES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is malignant hypertension?

A

Diseases develop at any age (young or old)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How long does patient have to live with Malignant hypertension?

A

Within 1-2 years patient dies due to progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the minimal diastolic pressure in Malignant Hypertension?

A

120 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Can you help the patient in malignant hypertension?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the pathomorphological foundation of malignant hypertension?

A

Hyperplastic Arteriosclerosis

“Onion Skinning”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

BP =

A

Q* peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Cardiac output =

A

Q

The amount of blood pumped out per minute = SV * HR : Blood volume and cardiac factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is blood volume associated with?

A

With Na absorption of DCT of nephron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Increased absorption of Na causes ?

A

Increase in blood volume due to water following

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is blood volume under the control of?

A

Aldosterone (mineralocorticoid) + atriopeptin aka atrial atrium uremic hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What does aldosterone do?

A

Increases reabsorption of sodium and sodium increases osmotic P in the blood so water follows to even out the osmotic P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is atriopeptin?

A

aka Atrial Natrium uremic horomone (balancing opposite to aldosterone)

  • DECREASES sodium reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Where is atriopeptin aka atrial natrium produced?

A

In the right atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What does atriopeptin do?

A

Protect the heart from overloading from too much blood in heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What would you do if a patient came to you and said they have a problem with blood volume causing hypertension?

A

Decrease salt intake, use diuretics, decrease the Na reabsorption in DCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are Lazics?

A

Within 10 min of injection results in dramatic relief

77
Q

What are cardiac factors in regard to hypertension ?

A

Factors are contractility and HR

78
Q

What is a disease that results in the sudden decrease in contractility ?

A

MI - cardiogenic shock

79
Q

What is myocardial cardiogenic shock?

A

Heart pumping cannot maintain adequate BP - develops in 10% of MI patients and 40-50% will die from this

80
Q

Why does MI > Cardiogenic shock develop?

A

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
Q

Where would you see increased heart contractility ?

A

Bodybuilding

82
Q

What do bodybuilders have?

A

They have increased contractility due to increased musculature due to increased resistance of blood flow -> HYPERTROPHIES

83
Q

What does increased hypertrophy mean?

A

Decreased ability to supply the heart with adequate oxygen

84
Q

If there is increased HR, what happens to BP?

A

Increased BP due to increased mass of the heart will allow the heart to pump more effectively > INCREASES BP

85
Q

What do body builders have to do when the heart is hypertrophied?

A

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
Q

How can MI happen in bodybuilders ?

A

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
Q

What do you do to decrease heart rate?

A

(More than 90 = Tachycardia)

  • To decrease conduction of signals, you need Bet blocker
88
Q

What does peripheral resistance to blood flow do?

A

Peripheral resistance is friction between the blood and vessel wall

89
Q

Peripheral resistance to blood flow are controlled by what?

A

Humoral factors

90
Q

What are humoral factors?

A

Constrictors and dilators

  • Affect the arterioles more than venules
91
Q

What are the humoral factors?

A
  • angiotensin II
  • catecholamines
  • thromboxane, leukotrienes, endothelin
  • Inflammation mediators
  • prostaglandins and NSAIDs
92
Q

What is angiotensin II?

A

Have to work against the production of angiotensin II either through preventing formation or destroying it > ACE inhibitors

93
Q

What are catecholamines?

A

Vasodilator at low concentrations: Vasoconstrictor at high concentrations

94
Q

What do thromboxaned, leukotrienes, and endothelin do?

A

Increase BP through vasoconstrictor - exception to prostaglandin dilation

95
Q

What are inflammation mediators?

A

Vasodilator:

Prostaglandins; kinins; NO/EDRF

96
Q

How do NSAID drugs effect prostaglandins?

A

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
Q

What are neural factors affected by?

A

(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
Q

What are 2 types of neural factors?

A

A-adrenergic

B-adrenergic

99
Q

Which Neural factor constricts ?

A

Alpha adrenergic (normally not activated at rest, have high threshold)

  • stress
100
Q

Which neural factors dilate?

A

Beta - adrenergic

  • stress is important for development, progression of primary hypertension
101
Q

What are local factors?

A

Autoregulation (ionic) pH, hypoxia

102
Q

What is the autonomic NS in relation to peripheral resistance to blood flow?

A

SANS and PANS > works antagonistically - regulation of normal function of organs

103
Q

How do SANS affect blood vessels?

A

Vasoconstriction

104
Q

How do PANS affect blood vessels?

A

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
Q

What is the principal treatment to hypertension?

A

Limit salt intake; mild > mild - mod exercise may be good enough to keep under control - over time this will not be enough

106
Q

What is the treatment to sedative therapy?

A

Decrease stress, valerian root extract

107
Q

With severe hypertension, what can happen?

A

Major killer is sudden increase in BP (stable hypertension is better than sudden)

108
Q

What can sudden hypertension be caused by?

A

Change in temp, sudden activity, change of mood, etc

109
Q

What is an increase in granulation tissue?

A

Proud flesh

110
Q

CNS infection development depends on:

A
  1. Virulence of infection
  2. Status of immune system
  3. Presence / absence of predisposing factors
111
Q

What is virulence of infection?

A

How bad/harmful infection is

112
Q

What is the “Status of immune system” ?

A

How effective the immune system is at defending you

113
Q

What are the predisposing factors in relation to CNS infection?

A
  • exposure of head to cold
  • sinusitis
  • otitis media
  • basal skull fracture
  • chronic pneumonia
114
Q

What does not covering your head to the cold result in?

A
  • decrease local resistance > inflammation

- must cover head so you don’t get meningitis

115
Q

What is sinusitis in regard to CNS infection?

A

Sinus is empty spaces in the bone covered by soft tissue open to the surrounding that have orifices communicating with immune system

116
Q

What are the 4 sinuses and what do they contain?

A
  • 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
Q

What are the most commonly affected sinuses?

A

Frontal and Maxillary

PAIN

118
Q

What would exposure to the cold do to the sinuses?

A

If there is a decrease in resistance (exposure to cold) in addition to having the common cold can lead to swelling of sinuses

119
Q

What happens when there is swelling of sinuses?

A

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
Q

What is otitis media?

A

Inflammation of the middle ear - area that contains the small bone that transmits sounds from eardrum to inner ear (mechanical spread of sound)

121
Q

What is significant about the middle ear ?

A

It communicates with pharyngeal cavity through Eustachian tube

122
Q

What can inflammation of otitis media cause?

A

Inflammation can form pus and go into mastoid = MASTOIDITIS

  • Thin layers of the mastoid can be digested by the pus
123
Q

What is a basal skull fracture, and how can it affect the CNS?

A

Fracture of the skull results in cracks separating the sinus from CNS > could result in sinuses going straight to the brain

124
Q

Meningitis aka

A

Leptomeningits

125
Q

What is meningitis aka Leptomeningtis?

A

Infectious inflammation of the dura mater in the structures of the brain in the vicinity of the subarachnoid space

126
Q

What are the 3 different types of meningitis?

A
  1. Acute (purulent) leptomeningitis aka Acute Bacterial Meningitis
  2. Acute Lymphocytic (viral) Meningitis aka Aseptic type
  3. Chronic Meningitis
127
Q

What is the cause of Acute (Purulent) Leptomeningitis aka Acute Bacterial Meningitis?

A

Bacterial infection due to pus

128
Q

Who is affected primarily by Acute (purulent) Leptomeningitis aka Acute bacterial meningitis ?

A

Infants, young children, and elderly:

  • Strep Pneumonia
129
Q

Does Acute (Purulent) leptomeningitis aka Acute Bacterial Meningitis have a high mortality rate?

A

YES

  • When people die from this, pathologies will find pus on the hemispheres on the brain or on the foundation of the brain
130
Q

What are the 2 tests to confirm meningitis?

A

Kernig and Brudzinski

131
Q

What are the manifestations of Acute (Purulent) Leptomeningitis aka Acute Bacterial Meningitis?

A
  1. Headache
  2. Stiff neck
  3. Fever
  4. Mental confusion
132
Q

Why do you get a headache from acute (purulent) leptomeninigtis aka Acute Bacterial Meningitis?

A

Due to increased cranial pressure

133
Q

Why is there increased intracranial pressure with meningitis?

A

There is inflammation of the meninges, anytime there is inflammation you will see 5 cardinal signs, one of which is tumor (swelling)

134
Q

What is the mechanism of meningitis?

A

The meninges swell > swelling of arachnoid granulations > decrease in the reabsorption of CSF > hydrocephalus > increased intracranial pressure

135
Q

Why would you have a stiff neck with acute (purulent) Leptomeningitis aka acute bacterial meningitis?

A

Due to loss of function from inflammation (5 cardinal signs)

  • Muscle spasms due to patient hurting from head being in Flexion
136
Q

What is a red flag with acute (purulent) Leptomeningitis aka acute bacterial meningitis?

A

FEVER

MC ominous sign in Chiro office

137
Q

What is an example of how fever can be dangerous from acute (purulent) Leptomeningitis aka acute bacterial meningitis?

A

**EPIDURAL ABSCESS

  • pus accumulation between the dura mater and Lamina > compresses the spinal cord > decreased function and pain

*** SPACE OCCUPYING LESIONS

138
Q

What happens if you adjust a patient with Acute bacterial meningitis?

A

The pus will spread along the spinal cord canal and patient will die the same day

139
Q

Mental confusion is associated with what disease?

A

Acute (purulent) Leptomeningitis aka Acute Bacterial Meningitis

140
Q

How do you diagnose Acute (purulent) leptomeningitis aka acute bacterial meningitis?

A

Lumbar puncture

Needle in the spinal cord canal to obtain CSF for analysis

141
Q

Where is the lumbar puncture done?

A

Between L3 and L4 because the spinal cord ends at L2

142
Q

What do you analyze during the lumbar puncture when checking for meningitis?

A

Cells, proteins, glucose, viscosity - normally the CSF is watery and clear with no cells

143
Q

What will you see in the CSF of Acute (purulent) Leptomeningitis aka acute bacterial meningitis?

A

EXCESS NEUTROPHILS

  • Because neutrophils target bacteria
144
Q

What other substances will be high/low in the CSF of a patient with acute (purulent) leptomeningitis aka acute bacterial meningitis?

A
  • Increased protein exudate is always made in acute inflammation, and exudate is a protein rich fluid
  • Decreased glucose (bacteria eats all the glucose)
145
Q

How do you determine bacteria within CSF of patient with acute purulent leptomeningitis aka acute bacterial meningitis?

A

Spread the CSF on agar plate, patients are given a broad spectrum antibiotic to prolong patient’s life

146
Q

What is acute lymphocytic (viral) meningitis aka aseptic type?

A

Aseptic because there aren’t any bacteria in the blood

147
Q

What type of lymphocytes are present during acute lymphocytic (viral) meningitis aka aseptic type?

A

T8 Cytotoxic Lymphocytes

148
Q

What are T8 Cytotoxic Lymphocytes?

A

Specifically designed to eliminate viral cells, anti-tumor, and anti-graft (these cells are the reason for graft rejection)

149
Q

Are there any antibodies in acute lymphocytic (viral) meningitis aka aseptic type?

A

NO, it is only cell reacting, it is T-Cell mediated Cytotoxicity

  • TYPE IV HYPERSENSITIVITY
150
Q

What are the 2 subtypes of Type IV Hypersensitivity?

A
  1. T cell mediated cytotoxicity (associated with acute lymphocytic (viral) meningitis aka aseptic type
  2. Delayed type: NOT viral, example = TB
151
Q

Mumps virus is associated with what type of meningitis?

A

acute lymphocytic (viral) meningitis aka aseptic type

152
Q

What can mumps result in?

A

Viral meningitis or acute orchitis (acute inflammation of the testes, 60% cases leads to infertility)

153
Q

Viral meningitis is :

A

BENIGN

  • Same manifestations as bacterial, but less severe
154
Q

What will you see in the lumbar puncture of acute lymphocytic (viral) meningitis aka aseptic type?

A
  • Increased lymphocytes
  • increased protein (exudate again)
  • NORMAL glucose (viral cells don’t consume glucose)
155
Q

What is chronic meningitis caused by?

A
  • mycobacterium TB
  • treponema pallidum
  • brucella species
  • cryptococcus neoformans
156
Q

How does chronic meningitis develop ?

A

Insidiously with no severe swelling in the beginning

157
Q

What are manifestations of chronic meningitis?

A

Symptoms are not as severe and don’t develop seriously

158
Q

What will you see in the lumbar puncture of chronic meningitis?

A
  • increased mononuclear cells
  • increased proteins
  • decreased glucose
159
Q

What are mononuclear cells?

A

Monocytes > macrophages and lymphocytes

160
Q

Is there exudate in chronic meningitis?

A

NO exudate is only in ACUTE INFLAMMATION

161
Q

Why is lumbar puncture not clear fluid ?

A

Tissue debris and accumulation of cells and microorganisms

162
Q

DISEASES OF JOINTS

A

NEW

163
Q

Where can inflammation of the joints ONLY happen?

A

Where there is blood supply

164
Q

What is the only structure with blood supply in the joint?

A

Synovial membrane

165
Q

What happens with disease progression with inflammatory arthritis?

A

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
Q

What is full fusion of the articulating bones of the joint?

A

Joint Ankylosis

167
Q

What are the 3 types of inflammatory arthritis?

A
  1. RA
  2. Seronegative Spondyloarthritides
  3. Infectious Arthritis
168
Q

What do you see with Seronegative spondyloarthritides?

A

Inflammation of the peripheral and spinal joints

169
Q

Spondyloarthritides =

A

Vertebral joint inflammation

Spondylo=vertebral

170
Q

What are the synovial joints of the spine?

A
  • facet/Z/Zygapophyseal/apophyseal joints (atlantoaxial)
  • atlanto-occipital
  • atlanto-odontoid
  • SI joint
  • costotransverse
  • costovertebral
171
Q

What is important about the SI joint in regard to Seronegative spondyloarthritides?

A

ALWAYS 100% INVOLVED

  • Specifically the lower 1/3 (synovial portion)
  • Clinically manifested by buttock pain
172
Q

Are uncinate joints synovial?

A

NO

173
Q

What are the types of Seronegative spondyloarthritides?

A

PEAR

  • Psoriatic arthritis
  • arthritis associated with IBD (crohn’s disease and ulcerative)
  • Ankylosing spondylitis
  • Reiter’s syndrome
174
Q

What is Ankylosing Spondylitis?

A

Autoimmune disease with no etiology (should be called idiopathic AS)

175
Q

What are the aka’s of AS?

A

Marie-Strumpel-Bechterew

Know any

176
Q

What is a major clinical presentation of AS?

A

Bamboo spine

177
Q

How does Bamboo spine develop?

A
  1. Inflammation
  2. Ossification
  3. Development of CT
178
Q

What is inflamed in AS particularly bamboo spine?

A

Attachment of annulus fibrosus

179
Q

what is ossified in AS particularly bamboo spine?

A

Out layer of the annulus fibrosus > syndesmophytes

  • forming bone where fibrous tissue should be
180
Q

What is “development of CT” in AS particularly bamboo spine?

A

Between 2 Articular surfaces > full fusion of the synovial joints

  • joint ankylosis
  • COMPLETE LOSS of ROM
181
Q

How do you suspect AS in patient?

A

Have patient bend over and touch toes with knees straight

  • SPine will be flat and immobile
  • Inability to move in any 3 planes
182
Q

What posture is it called when all bones are fused together in AS?

A

Walter’s posture

183
Q

What do you see with AS on x ray?

A

All joint spaces absent, cannot see separate vertebra, syndesmophytes, SI joints fused, pubic symphysis fused, they would have no knee joints

184
Q

What are early manifestations of AS?

A
  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
Q

What is the difference between DJD and Inflammatory arth?

A

Degenerative = Deg. Of cartilage

  • cartilage cant be inflamed cause there is NO blood supply
186
Q

What happens as DJD continues its process?

A

There is cartilage metabolism impairment, bone and soft tissue destruction, but there is NO fusion of articulating bones

187
Q

What is final outcome of DJD?

A

Osteophytosis

188
Q

What are Degenerative diseases?

A

OA
Spondylosis
Hemarthrosis
Forestier’s Disease

8 PATH 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions