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ASDOH Clinical Pathology > Test 2 > Flashcards

Test 2 Flashcards

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1
Q

This type of Massive thromboembolus are often lethal because they prevent the entry of blood into the lungs and cause acute anoxia. They block both branches.

A

saddle emboli

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2
Q

Emboli that originate in the left atrium or ventricle, aorta, and the major arteries and carried by arterial blood

A

● Arterial emboli

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3
Q

Liquid emboli are?

A

fat emboli that occur after bone fracture, and amniotic fluid emboli caused by the entry of amniotic fluid into the uterine veins during delivery

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4
Q

what is a Fat embolism?

A

Describes the release of emboli of fatty marrow into damaged blood vessels following severe trauma to fat-containing tissue, particularly with bone fractures

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5
Q

appear 1-3 days after injury, and in its most severe form is characterized by respiratory failure

A

fat embolism syndrome

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6
Q

Occurs in 90% of patients with severe skeletal injuries, and less than 10% have clinical findings

A

fat embolism syndrome

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7
Q

What is the fat embolism Triad?

A

○ Respiratory issues (ARDS)
○ Neurological problems
○ Thrombocytopenia

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8
Q

What is Amniotic Fluid Embolus

A

Refers to entry of amniotic fluid containing fetal cells and debris into the maternal circulation through a tear in the placental membranes and rupture of the uterine and cervical veins

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9
Q

Describe Gaseous emboli

A

an air embolism produced by injected air into the veins; or air that is liberated under pressure, as in decompression sickness

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10
Q

What is Hyperemia ?

A

● Denotes an accumulation of blood in the peripheral circulation
● Resultant influx of blood into the capillaries
● Typically occurs in acute inflammation, blushing, or exercise
● Separated into two types:

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11
Q

What is Active hyperemia

A

■ Consequence of dilation of the arterioles mediated by neural signals that lead to the relaxation of arteriolar smooth muscle

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12
Q

Describe Passive congestive Hyperemia

A

■ Caused by increase in venous back pressure and most often occurs in a chronic form
■ Typically a consequence of congestive heart failure, where the stagnation of venous oxygenated blood contributes to a bluish discoloration of the tissues (cyanosis)
■ Often associated with peripheral or pulmonary edema

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13
Q

in the lungs, leads to formation of edema and extravasation of RBC in the alveoli…

A

In chronic form of Passive congestive hyperemia

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14
Q

Leads to NUT MEG lung

A

Chronic form of Passive congestive hyperemia Disintegration of RBC are taken up by the alveolar macrophages and the hemoglobin of the RBC is degraded into a brown pigment (hemosiderin) that accumulates in the lysosomes of the macrophages

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15
Q

The transformation of the fluid blood into a solid aggregate encompassing blood cells and fibrin

Fibrin is polymerized fibrinogen and forms a meshwork of thin filaments that bind together the cellular elements of the blood, forming a…

A

thrombus or CLOT

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16
Q

■ Attached to the mural endocardium of the heart chambers

■ Found overlying a myocardial infarction

A

Intramural thrombi

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17
Q

■ Are composed of tightly intermixed RBCs and fibrin

■ Thrombi in small vessels tend to be red

A

○ Red thrombi

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18
Q

○ Layered thrombi

A

■ Show distinct layering of cellular elements and fibrin
● The white layer in these are called Lines of Zahn
● Thrombi in larger arteries, veins, and mural thrombi tend to be layered

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19
Q

○ With time, the thrombus stimulates ingrowth of inflammatory cells and vessels, producing granulation tissue that provides more firm anchorage:
■ This process is called …

A

organization

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20
Q

■ Results from a pump failure of the heart (congestive heart failure), most often secondary to an MI that destroys a large part of the functioning myocardium
● Similar results from myocarditis, valvular heart disease

A

○ Cardiogenic Shock: pump failure of the heart

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21
Q

■ Results from loss of circulatory volume, attributed to massive hemorrhage or water loss related to massive burn, vomiting, or diarrhea

A

○ Hypovolemic Shock: loss of fluid from the circulation

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22
Q

results from a loss of vascular tone and pooling of blood in peripheral blood vessels

A

■ Hypotonic shock

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23
Q

■ Hypotonic shock Can also occur when…

A

● Occurs in anaphylactic shock caused by exposure to an allergen and in neurogenic stimuli, such as pain caused by trauma or a spinal cord injury

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24
Q

resulting from the spread of bacteria from a severe localized infection in the blood stream
● Abscesses, pneumonia, or peritonitis
■ Can occur with gram positive and fungal infections
● Staph aureus, candida

A

○ Septic Shock: from severe Gram Negative Bacteremia

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25
■ Gram negatives involved include:
``` ● E. Coli→ number 1!! ● Proteus ● Serratia ● Pseudomonas ● K. pneumoniae ● Bacteroides ```
26
● Complex binds to receptors on WBC and tissue cells, causing the release of inflammatory mediators
Gm- Bacteria that all have LPS
27
● Stages of Shock:
○ Non-Progressive Stage ○ Progressive Stage ○ Irreversible Stage
28
○ Non-Progressive Stage of shock
■ An initial phase during which the reflex compensatory mechanisms are activated and perfusion of vital organs is maintained ■ Vasoconstriction of the renal blood vessels results in renal hypoperfusion, decreased GFR, and activation of RAS for conservation of fluid ● This increases cardiac output and blood pressure ■ This stage is reversible and treatable
29
○ Progressive Stage of shock
■ Characterized by tissue hypoperfusion and the onset of worsening circulatory and metabolic imbalances (acidosis) ■ Low pH also has depressive effect on HR, potentiating pump failure ● Left ventricular insufficiency raises the intrapulmonary venous pressure, causing stagnation of blood in the pulmonary circulation ● Forms pulmonary edema and ARDS aka Shock Lungs ■ Urinary output begins to fall, marking the transition between reversible and irreversible stages
30
○ Irreversible Stage of shock
■ Sets in after the body has incurred cellular and tissue injury so severe that even if treatment is instituted, survival is not possible ■ Cellular injury is widespread, affecting all organs ● Kidneys most serious: renal shutdown ● Intestines show necrosis, perforation, and peritonitis ● Brain exhibits ischemic encephalopathy, confusion, and coma ○ Patients in great distress or unconscious ● Marked hypotension, respiratory distress, acidosis, anuria
31
● Waterhouse-Friderichsen Syndrome...
entire adrenals fill up with blood, terminal events in Gram Negative shock all because of DIC
32
○ Accounts for 95% of oral cancers
Squamous Cell Carcinoma
33
● In general, oral cancer accounts for approximately___% of all malignant tumors in men and__% of all malignant tumors in women
5% | 2%
34
○ Leukoplakia
■ White plaques ■ Asymptomatic white patch on the surface of a mucous membrane ■ Not a tumor, but can result in malignant transformation to squamous cell carcinoma ● Superficial cancer in 10% of the cases ● Invasive cancer in 8% of cases ● Eventually, 20% become malignant
35
○ Erythroplakia
■ Much less common but way more cancerous than leukoplakia ■ Red or dysplastic leukoplakia ■ Red, velvety, and eroded area within the oral cavity mucosa ■ Epithelial changes tend to be markedly atypical, incurring a much higher risk of malignant transformation (>50%) ■ Same risk factors as Leukoplakia
36
■ Strong link between HPV___ and___ causing oral and cervical cancers
16 and 18
37
■ Most cases or oral cancer due to HPV have a history of past or present of...
tobacco use
38
Among the most common sites due to reverse smoking ■ Lit end held inside a mouth This results in...
○ Southern India Cancer on Hard Palate
39
● Buccal Mucosa
○ Accounts for 2% of oral cancers ○ Early lesions may present as irregular leuko- or erythroplakic plaques, whereas more advanced lesions appear ulcerative and infiltrative exophytic masses ○ Majority arise in the middle to posterior portion of cheek buccal mucosa with spread to alveolar ridge, upper and lower jaw, tonsils, and palate ○ Etiology relates to smoking and chewing tobacco, snuff dipping, and alcohol use
40
Oral cancer Prognosis:
○ Approximately 75% of intraoral squamous cancers are advanced stages at diagnosis negatively affecting prognosis ○ Increased incidence of a secondary primary tumor (squamous cell) in lungs and esophagus
41
Septic shock in the Progressive Stage Forms...
pulmonary edema and ARDS aka Shock Lungs
42
● Sites where arteriole emboli will cause infarction know most common
``` ○ Brain 70% (from lecture, rest 30%) ○ Spleen ○ Kidneys ○ Messentery ○ Extremities with peripheral vasculature ```
43
● Remember in pulmonary embolism, starts on the _____ side and ends in the _____ artery
○ Venous | ○ Pulmonary
44
● Pathogenesis of a fat embolism- what is the underlying issue?
○ Broken bone- a huge one
45
● The vast majority of arteriole emboli start where?
○ The heart
46
● Most common emboli
○ Thromboembolis
47
● Major site of septic emboli
○ The heart- bacterial endocarditis
48
● Components of thrombosis
○ Red thrombi | ○ Layered thrombi
49
○ Red thrombi
■ Are composed of tightly intermixed RBCs and fibrin, low platelets ■ Thrombi in small vessels tend to be red
50
○ Layered thrombi
■ Show distinct layering of cellular elements and fibrin ● Many platelets, low RBCs ● The white layer in these are called Lines of Zahn ● Thrombi in larger arteries, veins, and mural thrombi tend to be layered
51
Lungs characteristics associated with Shock
ARDS
52
Kidney characteristics associated with Shock
anuria
53
Liver characteristics associated with Shock
congested, enlarged, blood oozing from the cut surface
54
intestines characteristics associated with Shock
necrosis, perforation, peritonitis
55
Brain characteristics associated with Shock
ischemic encephalopathy
56
Define chronic passive congestive hyperemia
Heart failure cells: nutmeg cells the blood pools in the veins, eventually in the pulmonary alveoli, and as pulmonary macrophages take up the RBC, they get characteristic brown
57
○ Lines of Zahn
seen in pulmonary embolism, platelets mixed with fibrin
58
● Definition of a paradoxical embolis?
○ An embolism that develops in the venous circulation but enters the arterial circulation via the foramen ovale or a rupture of the interventricular septum
59
● Know 4 possible fates of thrombus
○ Recanalization ○ Lysis ○ Organization ○ Embolization
60
○ Source of white infarcts | and what's affected
arterial side | ■ Solid organs: heart and kidneys
61
○ Sources of red infarcts
dual blood supply, venous ■ Liver and lungs ■ Testes and intestines
62
● Possible complications of septic emboli wherever they lodge?
○ Infarcts caused by infected thrombi or emboli (septic infarcts) show signs of inflammation and may transform into an abscess that tends to heal poorly because of inadequate blood supply to the infarcted area
63
characteristics and causes for Cardiogenic shock
MI, myocarditis, valvular heart disease
64
characteristics and causes for Hypovolemia shock
burns, massive diarrhea, vomiting
65
● General features of amniotic fluid emboli.
■ Rare maternal complication of childbirth, but when it occurs it is often catastrophic ■ Usually occurs at the end of labor ■ Classic finding are the presence of epithelial squamous cells shed from fetal skin, lanugo hair, and fat from vernix caseosa within the pulmonary vasculature
66
○ Ecchymosis
large and bruised
67
Venus hemorrhage Purpura
1mm- 1cm
68
○ Peticchia
less than 1mm | ■ All resulting from venous internal hemorrhage
69
○ Congestion
chronic passive congestion is hyperremia, back up of blood flow in the peripheral circulation, venous back flow
70
○ Hyperremia
accumulation of blood in the peripheral circulation, acute would be due to dilation of blkmood vessels
71
● Underlying condition for a bone marrow embolis?
CPR occurrence
72
● Blushing is a good example of what?
○ Active hyperemia
73
○ Leukoplakia possible locations and size
■ Most often in buccal mucosa, tongue, floor of mouth | ■ May be solitary or multiple, vary in size, and cannot be removed via scraping

ASDOH Clinical Pathology (3 decks)

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