Pathology E3 Flashcards
1
Q
tissue edema
A
intercellular fluid
2
Q
anasarca
A
severe generalized edema
3
Q
pulmonary edema
A
intraalveolar fluid
4
Q
pleural effusion
A
fluid accumulation in pleural space
5
Q
ascites
A
fluid accumulation in peritoneal cavitiy
6
Q
transudate
A
increased hydrostatic pressure
clear
sterile
few benign cells
specific gravity <1.012
low protein content =<1 g/dl
fluid glucose ~ serum glucose
7
Q
pleural effusion
A
hydrothorax
8
Q
exudate
A
malignancy/inflammation
turbid/bloody
inflammatory cells
+ bacteria/other malignant cells
specific gravity >1.02
protein content >1g/dl
fluid glucose < serum glucose
9
Q
hyperemia
A
increased blood flow (perfusion)
10
Q
congestion
A
decreased blood outflow
11
Q
hyperemia and congestion both can be considered as a ….
A
local increase in blood volume
can be acute and chronic
12
Q
acute pulmonary congestion
A
sudden/acute pulmonary capillary engorgement and dilatation
leakage of fluids –> alveolar edema and filling of alveolar spaces with edema fluid
May be seen in sudden cardiac/ventricular arrhythmia w/ LV insufficiency
13
Q
chronic pulmonary congestion
A
chronic capillary engorgement –> slow leaking of edema fluid into alveolar spaces and alveolar microhemorrhages
hemosiderin-laden macrophages –> heart failure cells
may be seen w/ ongoing LV insufficiency
14
Q
hemosiderin-laden macrophages
A
heart failure cells
15
Q
Petechiae
A
small punctate bleedings from capillaries
thrombocytopenia
16
Q
Purpura
A
small bleedings slightly larger than petechiae, associated w/ blood extravasation from small arterioles
vasculitis
17
Q
Ecchymoses
A
lg cutaneous bleedings
trauma
suspect abuse
18
Q
hematoma
A
collection of blood in soft tissue or body cavities
19
Q
shock
A
disordered microcirculation leading to
tissue hypoperfusion and ischemia
referring to end of capillary and venous
20
Q
hypOperfusion
A
decreased flow of oxygenated blood due to obstruction of artery
21
Q
ischemia
A
blood flow insufficient for metabolic requirements
22
Q
infarct
A
ischemic necrosis
23
Q
most common causes of hypOperfusion and ischemia
A
atherosclerosis
thrombosis/embolism
dec of arterial blood flow resulting from narrowing (stenosis/thrombosis) of arteries, can be acute and chronic
24
Q
syndromes of acute ischemia
A
myocardial - angina pectoris
cerebral - TIA
leg muscles - claudicatio intermittens
25
Myocardial ischemia
(Angina Pectoris)
ischemic pain of heart muscle
coronary blood flow does not meet myocardial oxygen demand
most freq cause --> coronary artery stenosis
26
cerebral ischemia
transient ischemic attack (TIA)
most freq cause --> dec arterial blood supply due to arterial occlusion
presentation=short temporary dysfunction of brain (neurologic deficit)
27
ischemia of leg muscles
claudicatio intermittens
peripheral vascular disease (PVD)
dec. blood flow to lower extremity
28
chronic ischemia
organ atrophy
| reduction in organ size due to apoptotic cell loss
29
fx influencing outcome of ischemia
```
Duration of hypoxia or anoxia
Tissue tolerance
Capacity of cells to regenerate
Systemic Factors
Type of arterial supply
Collateral circulation
```
30
infarct
ischemic necrosis of tissue
caused by occlusion of arterial supply or venous drainage
most frequently via thrombosis or thromboembolic event
31
progression of tissue during MI
early MI (6-12 hr) - loss of cross striations, nuclei not present. Extensive hemorrhage at border of infarction (accounts for hyperemic border)
(12-2 hr)
(3 days): neutrophilic infiltrates w/ prominent necrosis and hemorrhage. extensive acute inflammatory cell infiltrates. myocardial fibers so necrotic that outlines are barely visible
1-2 weeks: granulation tissue. healing of infarct becomes more prominent, w/ capillaries, fibroblasts, macrophages (filled w/ hemosiderin)
More weeks: scar tissue
32
Hemostasis
response to vascular injury resulting in formation of a hemostatic plug
a well balanced well-regulated process.
1. maintains blood fluidity in normal vessels
2. provides hemostatic plug thrombus at the site of vascular injury. Clot is designed to seal the mural defect as a part of hemostasis.
33
response to vascular injury phases
1. Arteriolar vasoconstriction
2. Activation of platelets (primary hemostasis)
3. Activation of coagulation cascade (secondary hemostasis)
4. Activation of fibrinolytic system
34
endothelium functions
innermost cellular lining of blood vessels
```
Regulation of blood pressure
Regulation of immune factors
Regulation of inflammation
Regulation of tissue fluid homeostasis
Hormone synthesis
Produces procoagulant and anticoagulant factors (regulation of blood clotting)
```
35
magacaryocytes
fragments of magacaryocytes --> platelets
36
platelet contents
ADP/ATP
epinephrine
serotonin
^ via dense bodies
fibrinogen von willebrand factor
^ via alpha granules
37
intrinsic coagulation cascade
activation by Factor XII present in the plasma
38
coagulation cascade
Set of enzymes that lead to formation of fibrin (insoluble) out of fibrinogen (soluble)
fibrinogen cleavage by THROMBIN --> insoluble molecules form (fibrin --> end of coagulation cascade)
39
extrinsic coagulation cascade
activation by Tissue Factor (TF)
40
thrombosis
pathologic activation of clotting mechanism w/ formation of thrombus (clot)
in uninjured vasculature (could be venous or arterial)
results in vascular occlusion after minor injury
thrombus --> NOT a hemostatic plug
small can be resolved via fibrinolytic mechanisms
41
hemostasis
Activation of platelets + humoral coagulation system (clotting factors)
42
Virchow's triad
endothelial injury
abnormal blood flow
hypercoagulability
lead to thrombosis
43
risk fx for arterial thrombosis
coronary artery and MI
44
endothelial injury
exposes ECM --> activation of platelets and coagulation cascade
physical disruption not req. Endothelial dysfunction can be via DM, smoking, hypercholesterolemia
45
turbulence
at vascular bifurcation sites or areas of arteriosclerotic plaques
46
stasis
slowing of blood
47
hyperviscosity
increased cellular elements of blood
48
hypercoagulability
(thrombophilia)
disordered in coagulation pathways --> predisposed to thrombosis
caused by abnormal factor of coagulation cascade
49
Inherited and acquired thrombophilia
```
suspect if ...
over 60 y/o (or earlier) or FHx
spontaneous and/or massive DVT/VTE
cerebral/visceral vein thrombosis
VTE provoked by pregnancy/OCP/HRT
```
can be primary (hereditary) or secondary (acquired)
less important than endothelial injury/stasis
rare
50
Risk fx of hereditary thrombophilia
```
Mutation in Factor V = Factor V Leiden
Prothrombia G20210A Gene Mutation
Antithrombin III Deficiency
Protein C Deficiency
Protein S Deficiency
Hyperhomocystinemia
```
51
Protein C
Protein S
deficiencies can lead to...
natural anticoagulant system
degrade factor V, factor VIII
undegradable coagulation factor
52
Acquired Risk Factors for Thrombosis
```
immobilization
major surgery, fracture, burns
Malignancy
Myocardial Infarct
Heparin
Antiphospholipid antibody syndrome
Pregnancy, contraceptives/estrogen
Smoking
```
53
Fate of thrombi (3)
Thrombolysis
- If thrombus lyses in 1-5 days, clots removed by fibrinolytic system
Organization
- If thrombus has not lysed in 1-5 days
- Remodeling and recanalization of thrombus
Embolization
- Detachment and travel within circulation
(Embolus: detached intravascular mass carried by the blood to distant sites)
54
embolization
embolus trey transported until lodges in blood vessel
emboli can originate from venous or arterial circulation
55
pulmonary embolsm
Venous thrombi --. emboli that lodge in the pulmonary arterial tree
Over 80% of patients with PE have proven DVT
Most PEs originate from the lower limbs
Over 50% patients with DVT have silent PEs
DVT is a serious cause of morbidity and mortality
56
paradoxical embolism
emboli that cross from venous--> arterial circulation via septal heart defects
patent foramen ovale: hole in the wall between the heart's upper chambers
57
arterial thromboembolism
Emboli originating within arterial circulation
| Arise from chambers of the heart or heart valves 80% of the time
58
Other Examples of Emboli
Amniotic fluid emboli
Septic emboli (cardiac valve vegetations)
Air emboli
Fat emboli (trauma; motor vehicle accidents)
59
gangrene
infarct frequently affects structures like digits, extremities or sacral skin (nose)
dry coagulative necrosis --> dry gangrene
bacteria colonizing lesion --> wet gangrene
involves gas prod bacteria --> gas gangrene
60
infarct resolution process
necrosis - inflammation - repair
1. 6-12 hr post injury --> nuclear and cytoplasmic changes of necrosis become visible
2. 12-24 hr --> acute inflammatory rxn (neutrophil influx) develops pat infarct margin in the viable connective tissue
3. By 1 week, macrophages and new capillaries invade the infarct from margins establishing granulation tissue, begins to lay down collagen
4. 2-3 mo. infarct is converted to loose scar tissue which gradually matures to dense/contracted
61
Major risk fx of atherosclerosis
```
Age
Sex (females more protected)
Family history
Genetic abnormalities
Hyperlipidemia
Hypertension
Smoking
Diabetes
C-reactive protein
```
62
Minor risk fx of atherosclerosis
Obesity Physical inactivity Stress
Homocysteine (plasma >100 umol/L) Postmenopause Alcohol Lipoprotein (a) (alt form of LDL)
Unsat. Fat intake
63
non-modifiable risk fx of atherosclerosis
age
sex (men>women)
genetic
64
Modifiable risk fx for atherosclerosis
1. HLD (high LDL, low HDL)
genetic defects in lipoprotein metabolism/genetic or acquired disorders like diabetes or hypothyroidism
2. HTN
3. smoking
4. DM
5. C-reactive protein
65
A 44-year-old woman has a family history of heart disease. Her father and mother both developed congestive heart failure and myocardial infarction as a result of extensive coronary atherosclerosis. A dietary modification to include consumption of which of the following is most likely to reduce her risk for ischemic heart disease?
A. 40% of total caloric intake as fat
B. A diet high in saturated fat
C. 10% of total caloric intake as saturated fats
D. Fat found in beef products
E. Trans-fats
C.
66
An increased incidence of atherosclerosis has been correlated with all of the following except:
A. hypertension
B. diabetes mellitus
C. increased serum high-density lipoprotein (HDL) concentration
D. hyperuricemia
E. Use of oral contraceptives
C.
67
Principal point of physiologic resistance to blood flow
Arterioles
68
describe longitudinal section through the normal aorta with an elastic tissue stain
intima is at the top, while the thick aortic media demonstrates parallel dark elastic fibers
smc fibers are between the elastic fibers
69
vascular wall components
```
Endothelial cells
Smooth muscle cells
Extracellular matrix:
-Elastic elements
-Collagen
-Proteoglycans
```
70
Weibel-palade bodies
3 mm long membrane-bound bodies that represent the storage organelle for von Willebrand factor
71
Endothelial Cell Properties and Functions
Maintenance of permeability*
Regulation of thrombosis,
thrombolysis and platelet adherence*
^most important
Extracellular matrix production (collagen, proteoglycans)
Modulation of blood flow and vascular reactivity
Regulation of inflammation and immunity
Regulation of cell growth
Metabolism of hormones
ECM is part of clot
72
smc functions
Vasoconstriction and dilation
Synthesis of collagen, elastin and proteoglycans (for matrix)
Elaboration of growth factors and cytokines
Migration to the intima and proliferation
73
Smooth muscles form which layer of arterial wall?
A- INTIMA
B- MEDIA
C- ADVENTITIA
74
endothelial cells form which part of arterial wall?
intima
75
Arteriosclerosis = hardening of the arteries
| Used to describe 3 distinct patterns:
1. Atherosclerosis
2. Mönckeberg medial calcific stenosis
3. Arteriolosclerosis
76
Mönckeberg medial calcific stenosis
in medium-sized muscular arteries (>50 years old)
(media)
calcifications in the media; note that the lumen is unaffected by this process
when calcified muscular arteries show up on a radiograph of the pelvic region in an older person
most clinically INsignificant
77
Atherosclerosis (where are plaques comm. found?)
formation of intimal lipid rich fibrous plaques
Plaques commonly found at bifurcation points of arteries
(Turbulent flow/eddy currents vs. smooth,
laminar flow
Shear stress at high flow rates)
78
Arteriolosclerosis (which diseases associated w/?)
disease of SMALL arteries and arterioles, association with hypertension and diabetes mellitus
79
Atherosclerosis affects largely
elastic and muscular arteries
80
Hypertension and Diabetes affect primarily
small arteries and arterioles
81
hyperplastic arteriolosclerosis
Leakage of plasma proteins, excessive extracellular matrix production. Arteriolar wall is markedly thickened.
Narrowed lumen impairs glomerular blood supply.
ONION-SKIN appearance
more comm. in benign HTN, DM, elderly
82
Hyaline Arteriolosclerosis
Lamellar re-duplication of intimal smooth muscle cells. ECM goes out of lumen and deposits in wall
Severe benign hypertension, accelerated hypertension
May be accompanied by fibrinoid necrosis
more comm. in diabetic kidneys
(does not have layer of cells like hyper plastic, instead just has thick pink material)
83
MALIGNANT HYPERTENSION
Extremely high blood pressure (typically >180/120) that develops rapidly, causes organ damage + papilledema.
Tx: medical emergency
```
Causes:
h/o Hypertension, missing dose of medication
Collagen vascular disease
Renal disease
Tumors of adrenal glands
Cocaine
```
```
Complications:
Aortic dissection
Coma
Pulmonary edema
Heart failure
Renal failure
```
84
Which type of vessels are most affected by atherosclerotic changes?
1. Elastic arteries
2. Small arteries
3. Capillaries
4. Muscular arteries
A. 2 and 3
B. 4 and 1
C. 1 and 2
D. 1 and 3
B.
85
Precursors of Atheromatous Plaque
1. Fatty streaks
2. Intimal thickening (intimal cell mass)
- white, at branch points
- contain smc and CT but NOT lipid (trying to heal trauma)
86
Fatty streaks
Appear in aorta of children younger than 1 year of age and all children older than 10 years
Flat
Multiple yellow, flat spots (<1 mm), later elongated streaks
Precursors of atheromatous plaques
Composed of lipid filled foam cells with T lymphocytes and extracellular lipid (low density and very low density lipoproteins)
87
Foamy macrophages
macrophages w/ fat
precursors of Atheromatous Plaque
88
Progression of Atherosclerotic Lesions
Isolated Macrophage --> Fatty Streaks
| Intimal Thickening --> Extracellular Lipids --> Atheroma --> Fibroatheroma --> complex lesion
89
Precursor lesion for atheroma is –
```
A Thrombus
B Fatty streak
C Calcification
D Hemorrhage
E Exudate
F Ulceration
```
B
90
Atheromatous Plaque
Characteristic lesion of atherosclerosis
Raised focal plaque within the intima with a lipid core and a covering fibrous cap
Form 0.3-1.5 cm, sometimes larger masses
More common in abdominal aorta and its major branches
91
Atheromatous Plaque 3 principal components
Cells: Smooth muscle cells, macrophages, leukocytes
CT, ECM – collagen, elastic fibers, proteoglycans
Intracellular and extracellular lipid deposits
92
CHL clefts indicate
an acute injury not a chronic injury
93
SEQUELAE OF ATHEROSCLEROSIS
- Nothing happens
- Slowly decreasing blood supply
- Fibrous cap breaks causing thrombo embolism
- Hemorrhage from vaso vasorum in adventitia causing lumen occlusion
- Ulceration of surface
- Calcification
- Aneurysm/arterial rupture (balloon shaped protrusion of vessel wall)
94
clinical phases of atherosclerosis
aneurysm and rupture
occlusion by thormbus
critical stenosis
95
anterior descending coronary artery w/ marked atherosclerosis with narrowing. In general, the worst atherosclerosis is _____, where arterial blood flow is _______________.
worst atherosclerosis is proximal, where arterial blood flow is more turbulent
96
Which arterial layer is involved in atherosclerosis?
intima and media
97
What type of arteriosclerosis is least significant clinically?
Mönckeberg medial calcific stenosis
98
What is the early pathological lesion of atherosclerosis?
intimal thickening
99
What are the two risk factors for arteriolosclerosis?
HTN, DM
100
Where is arteriolosclerosis usually found?
kidneys
101
What is the most common cause of aneurysms?
atherosclerosis
102
Where do atherosclerotic aneurysms occur?
abd aorta
103
vasculitis
Inflammation of and damage of vessel wall, typically arteries are involved
104
vasculitis etiologies
```
Autoimmune processes ( immune complex deposition, ANCA, or antibodies against endothelial cell antigens )
Infection
```
105
```
Giant cell temporal arteritis
sx
causes
location
tx
```
large cell
Arteries, esp. cranial
Cause unknown. Poss immunologic basis, responds to steroids
Pain and tenderness over temporal area of head and may include jaw pain
Involvement of branches of the ophthalmic artery may lead to sudden loss of vision
Usually >50-60 yrs old
Associated with polymyalgia rheumatica; elev. ESR (60)
Giant cells and lymphocytes; intimal fibrosis
TX: 60mg prednisone
106
Polyarteritis nodosa
medium vessel
Necrotiz inflamm of renal arteries
30% of those with PAN have Hep B antigen in serum
Immune cells mistake antigens on blood vessel for hep B
Systemic (multi-organ) and segmental involvement of small and medium arteries
Usually young adults, most commonly males
107
Thromboangiitis obliterans (Buerger’s Disease)
Intermediate and small arteries, sometimes veins typically of the extremities (hands and feet)
Usually young adults, before age 35
Strong association with heavy cigarette SMOKING
Occlusive thromboses with microabscesses
108
Abdominal Aortic Aneurysm (AAA)
Intrinsic or acquired defect in wall
Most comm assoc with atherosclerosis
Typically involves aorta below renal arteries and above iliac bifurcation
Other forms:
Vasculitis
Trauma
Infections (mycotic)
109
Risk of AAA rupture is directly related to the size...
- Nil for 4cm AAA
- 1% per year for 4-5cm AAA
- 11% per year for 5-6cm
- 25%per year for 6cm and larger
110
AAA RUPTURE TRIAD
- Abrupt onset of severe back pain
- Hypotension
- Pulsative mass
111
Berry Aneurysms
Bifurcations of circle of Willis
0.5 - >3 cm
May be multiple
Etiology...
Genetic factors
Cigarettes
Hypertension
112
Syphilitic Aneurysm
| cardiovascular manifestation of tertiary syphilis
Typically affects ascending aorta and arch in males 40-55 y/o
Obliterative endarteritis of vasa vasorum leads to ischemic fibrosis of aortic media
Vasculitis with prominent plasma cell infiltrate
Compression/erosion of airways, esophagus, bone; rupture
113
Aortic Dissection
Entry of blood into wall of the aorta through a tear in the tunica intima and the subsequent pushing apart of the wall layers (tunica media)
Occurs in weakened aortic wall
presenting sx: abrupt onset of severe chest pain and/or back pain between the shoulder blades, pair described as “tearing pain”
114
Aortic Dissection Risk Factors
1. Older age
2. CHRONIC Hypertension
3. Connective tissue disorders
- Association with Marfan syndrome(defect in fibrillin), Ehler-Danlos syndrome(defect in collagen), coarctation, bicuspid aortic valve
4. Cystic medial degeneration- most frequent pre-existing histologically detected lesion
115
Most frequent pre-existing abnormality in aortic dissection
Cystic Medial Degeneration
116
Cystic Medial Degeneration
Separation and loss of elastic elements in aortic media; cyst-like spaces filled with mucopolysaccharide rich matrix
117
Sequelae of aortic dissection
```
Rupture into surrounding soft tissues
Rupture into pericardial space (hemopericardium)
Rupture into pleural space (hemothorax)
Re-entry into aortic lumen
Compression of branch ostia
```
