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Pathology > Lab Final > Flashcards

Lab Final Flashcards

1
Q

What is the difference between a transmural infarct and and intramural infarct?

A 
Trans = necrosis all the way through the wall 
Intra = necrosis within the wall
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2
Q

T or F

The inner portion of muscle is more susceptible to infarction than the outer

A

True

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3
Q

Why is the inner portion of muscle more susceptible to infarction than the outside?

A

Blood flows through the walls from the outside in.

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4
Q

T or F

The sub-pericardium is more susceptible than the sub-endocardium

A

False

Sub-endo more susceptible

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5
Q

This type of necrosis is characterized by preservation of size, shape and strength of necrotic tissue for several days

A

Coagulative

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6
Q

Coronary artery is sensitive to what hormone?

A

Epinephrine

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7
Q

T or F

Healing of an MI takes place by regeneration

A

False

Repair

  • replacement of dead tissue with connective tissue
  • Fibrosis
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8
Q

What is a white Infarct?

A

When you lose blood supply from ONE vessel. This is very typical for a MI

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9
Q

T or F

Granulation tissue will develop in the wound 24hrs

A

False

Second post-injury day

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10
Q

Angiogenesis is what? Where will it typically take place in the heart after an MI?

A

Formation of new blood vessels within the MEDIA

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11
Q

What cells produce pro collagen? What cells keep the collagen strands together?

A

Fibroblasts

Muccopolysaccharides

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12
Q

T or F

Eldery ppl are more vulnerable to death from MI than younger people

A

False

Other way around. Younger people do not have as many anastomoses on their heart as older people from atherosclerosis.

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13
Q

The blood from a rupture infarct will flow where?

A

Into the pericardial sack

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14
Q

What is Cardiac Tympanate?

A

Prevention of heart diastole due to accumulation of fluid in the pericardial cavity.
- pus can also accumulate

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15
Q

T or F

Pericarditis is when transudate accumulates in pericardial cavity

A

False

EXUDATE!

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16
Q

Transudate can accumulate in the heart as well which is similar to what other conditions?

A

Hypoalbuminemia due to Nephrotic syndrome (Kwashiorkor) or from right sided heart failure.

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17
Q

If there is a rupture of the inter ventricular septum where in the heart will the blood accumulate?

A

Right ventricle because the pressure is higher in the left ventricle.

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18
Q

Hypertension is a condition when the blood pressure is greater than ???

A

140/90

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19
Q

What is the only way to dx hypertension?

A

Blood pressure

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20
Q

What % of americans suffer from hypertension?

A

25%

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21
Q

What is a Pheochromocytoma?

A

Benign tumor of adrenal medulla that can cause very high blood pressure.
Adrenal releases wayyyyy to much Catecholamines: epi, norepi, and dopamine.

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22
Q

Too much dopamine can give what type of disease characteristics?

A

Parkinsonism Syndromes

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23
Q

A benign tumor of the adrenal cortex causing primary hyperaldosteronism is known as?

A

Conn’s Syndrome

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24
Q

What hormone are produced in the Adrenal Cortex?

A

Aldosterone, cortisol and androgens

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25
Q

What is the natural age for development of hypertension?

A

40-50

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26
Q

What is the name of the hormone that is the same as atrial natriuretic hormone and where is it produced?

A

Atriopeptin

Right Atrium

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27
Q

T or F

Atriopeptin works synergistically with aldosterone

A

False

Antagonistically

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28
Q

What is the minimal diastolic pressure for Malignant hypertension?

A

120

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29
Q

What is the pathomorphological foundation for malignant hypertension?

A

Hyperplastic Arteriolosclerosis

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30
Q

What is cardiac output?

A

blood pumped by heart per minute

SV x HR

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31
Q

What are some management strategies for benign hypertension?

A

Reduce sodium in diet to help lower bp

Prescribe diuretics to help remove fluid from body

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32
Q

T or F

Malignant Hypertension can be managed with diuretics

A

False

Cannot be controlled by any medical approach

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33
Q

Name some factors resulting in decrease of heart contractility

A

Cardiogenic Shock
Myocardiopathies
Myocarditis

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34
Q

T or F

Arteries account for TPR

A

False

Arterioles because they have sphincters

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35
Q

What is the most powerful vasconstrictor in the body?

A

Ang II

36
Q

What are some of the effects of Ang II on the body?

A

Narrows lumen of blood vessels
Increase blood volume
Stimulates aldosterone production and release

37
Q

T or F

Epi/Norepi/Dopamine are humeral factors causing dilation

A

False

Constriction

38
Q

T or F

Alpha adrenergic lower bp

A

False

Raise

39
Q

T or F

Catecholamines stimulate alpha receptors more than beta receptors

A

True

40
Q

Do beta adrenergic factors raise or lower bp?

A

Lower

41
Q

T or F

Parasympathetic stimulation will cause vasodilation

A

False

Does not affect peripheral blood vessels

42
Q

What does a negative chronotropic effect mean?

A

Decreased stimulation of the heart

43
Q

Decreased contractility of the heart is termed…

A

Negative Inotropic effect

44
Q

Inflammation of dura mater and structures within the subarachnoid space is known as?

A

Meningitis aka Leptomeningitis

45
Q

T or F

Acute Leptomeningitis affects the gyri of the brain how?

A

Flattened gyri due to intracranial pressure and hydrocephalus (communicating)

46
Q

How does the CSF change in meningitis?

A

Usually is clear, watery fluid, in meningitis its cloudy
Increased protein (exudate)
Decreased glucose

47
Q

What causes the cloudy CSF in meningitis?

A

Neutrophilia due to the bacterial infection

48
Q

Aseptic Meningitis akas?

A

Acute Lymphocytic

Viral Meningitis

49
Q

What is the cause of the viral form of meningitis?

A

Mumps virus aka Epidemic Parotiditis

50
Q

What other condition can cause Parotiditis?

A

Sjogrens Syndrome

51
Q

How will the CSF be with Aseptic Meningitis

A

Lymphocytosis
Increased protein
Normal glucose

52
Q

Why will the glucose be normal in the CSF with viral meningitis?

A

Virus do not consume glucose

53
Q

What will the CSF be with Chronic Meningitis

A

Mononuclear cells
Increased protein - no exudate but tissue debris and blood cells
Decreased glucose

54
Q

Pott’s Disease aka?

A

Tuberculosis Spondylitis (inflammation of vertebrae)

55
Q

What type of necrosis is associated with Pott’s Disease?

A

Casseous

56
Q

What is the main function of cartilage in synovial joints?

A

Ensures congruency of the articulating surfaces so there is uniform distribution of pressure.

57
Q

What are the categories of joint diseases?

A

Inflammatory - aka Arthritis = inflammation of synovial membrane
Degenerative - degeneration of cartilage, no inflammation
Metabolic - crystal

58
Q

T or F

Ankylosing is common in people with DJD

A

False

RA

59
Q

What is ankylosing?

A

Full fusion of bones

60
Q

What is Ochronosis?

A

Homogentesic acid in connective tissue.

61
Q

What does Seronegative mean?

A

There is NO Rheumatoid Factor present

62
Q

What does Spondyloarthritide mean?

A

Inflammation of the vertebral joints

63
Q

List the Seronegative Spondyloarthritides

A

Ankylosing Spondylitis
Psoriatic Arthritis
Reiter’s Syndrom
Arthritides characterized by IBD

64
Q

RA is ____% Seropositive

A

80

65
Q

What is the only common factor between the seronegative spondyloarthritides and RA?

A

Presence of inflammation

66
Q

What are the synovial joints associated with the spine?

A 
Z-joints aka Facets
Costotransverse
Costovertebral
SI join (lower 1/3) 
Atlanto-Co
Atlando-odontoid
67
Q

With the seronegative spondyloarthritides where do the pathological changes begin? Ligamentous attachments or the synovium?

A

Ligamentous Attachments

68
Q

What is the name of the area of insertion of any fibrous structure into bone?

A

Enthesis

69
Q

T or F

In SSA there is often Enthesopathy in multiple locations

A

True

70
Q

with SSA was is the % of involvement of the SI joints?

A

100

71
Q

What is the clinical manifestation of SSA in the SI joints?

A

Buttock Pain

72
Q

What percent of SSA patients develop Peripheral joint arthritis?

A

50%

73
Q

There is the presence of another blood marker in the majority of patients with SSA. What is the blood marker?

A

HLA-B27

74
Q

HLA-B27 is present in 95-97% of patients with what condition?

A

Ankylosing Spondylitis

75
Q

What are the aka’s for AS?

A

Bechtereu’s Disease

Marie-Stumpell-Bechtereu’s Disease

76
Q

What is the significant clinical feature of AS?

A

Bamboo spine

  • end stage
  • cannot do anything about it
77
Q

What is the anatomical location of the inflammation of the enthesis in AS?

A

Where the outer layer of the annulus fibrous or IVD attaches tot he corners of the vertebral bodies above and below.

78
Q

What is the name of the boney debris that replaces the annulus in AS??

A

Syndesmophytes

79
Q

T or F

Syndesmophwytes are calcification NOT Ossification

A

False

Ossification

80
Q

What is Fibrous Ankylosis?

A

The development of connective tissue between adjacent vertebrae

81
Q

T or F

In late stage of AS the patient will still have relatively good mobility in both the coronal and sagittal planes

A

False

NO ROM in the spine.
- spine will not curve, and patient will not be able to touch their toes.

82
Q

What is the diagnostic criteria for AS?

A

Measure the circumference of the patients chest.
If expansion is less than 6cm = abnormal
If expansion is less than 3cm = dx criteria for AS

83
Q

What is the posture seen in AS called?

A

“Waiter’s Posture”

  • Kyphosis with atrophy of the chest muscles
  • Knees bent
  • belly sticks out (ankylosing of CT and CV joints)
84
Q

T or F

In AS only the SI joints and Facet joints will fuse

A

False

EVERY SINGLE joint in the body can fuse.

85
Q

T or F

With AS pain will be best in the morning and will get worse during the day

A

False

Pain in the morning
Relieved by activity

86
Q

T or F

AS M:F = 1:4

A

False

M:F
4:1

87
Q

What is the involvement of the EYE in Ankylosing Spondylitis?

A

Iritis - inflammation of the eye and adhesions between the iris and lens
- irregular borders of the pupil

Pathology (6 decks)

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