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Emma III > Pathology E3 > Flashcards

Pathology E3 Flashcards

1
Q

tissue edema

A

intercellular fluid

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2
Q

anasarca

A

severe generalized edema

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3
Q

pulmonary edema

A

intraalveolar fluid

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4
Q

pleural effusion

A

fluid accumulation in pleural space

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5
Q

ascites

A

fluid accumulation in peritoneal cavitiy

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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

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7
Q

pleural effusion

A

hydrothorax

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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

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9
Q

hyperemia

A

increased blood flow (perfusion)

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10
Q

congestion

A

decreased blood outflow

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11
Q

hyperemia and congestion both can be considered as a ….

A

local increase in blood volume

can be acute and chronic

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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

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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

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14
Q

hemosiderin-laden macrophages

A

heart failure cells

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15
Q

Petechiae

A

small punctate bleedings from capillaries

thrombocytopenia

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16
Q

Purpura

A

small bleedings slightly larger than petechiae, associated w/ blood extravasation from small arterioles

vasculitis

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17
Q

Ecchymoses

A

lg cutaneous bleedings

trauma
suspect abuse

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18
Q

hematoma

A

collection of blood in soft tissue or body cavities

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19
Q

shock

A

disordered microcirculation leading to
tissue hypoperfusion and ischemia

referring to end of capillary and venous

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20
Q

hypOperfusion

A

decreased flow of oxygenated blood due to obstruction of artery

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21
Q

ischemia

A

blood flow insufficient for metabolic requirements

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22
Q

infarct

A

ischemic necrosis

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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

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24
Q

syndromes of acute ischemia

A

myocardial - angina pectoris
cerebral - TIA
leg muscles - claudicatio intermittens

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25
Q

Myocardial ischemia

A

(Angina Pectoris)
ischemic pain of heart muscle

coronary blood flow does not meet myocardial oxygen demand

most freq cause –> coronary artery stenosis

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26
Q

cerebral ischemia

A

transient ischemic attack (TIA)

most freq cause –> dec arterial blood supply due to arterial occlusion

presentation=short temporary dysfunction of brain (neurologic deficit)

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27
Q

ischemia of leg muscles

A

claudicatio intermittens

peripheral vascular disease (PVD)

dec. blood flow to lower extremity

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28
Q

chronic ischemia

A

organ atrophy

reduction in organ size due to apoptotic cell loss

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29
Q

fx influencing outcome of ischemia

A 
Duration of hypoxia or anoxia
Tissue tolerance
Capacity of cells to regenerate
Systemic Factors
Type of arterial supply
Collateral circulation
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30
Q

infarct

A

ischemic necrosis of tissue

caused by occlusion of arterial supply or venous drainage

most frequently via thrombosis or thromboembolic event

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31
Q

progression of tissue during MI

A

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

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32
Q

Hemostasis

A

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.
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33
Q

response to vascular injury phases

A
  1. Arteriolar vasoconstriction
  2. Activation of platelets (primary hemostasis)
  3. Activation of coagulation cascade (secondary hemostasis)
  4. Activation of fibrinolytic system
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34
Q

endothelium functions

A

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)
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35
Q

magacaryocytes

A

fragments of magacaryocytes –> platelets

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36
Q

platelet contents

A

ADP/ATP
epinephrine
serotonin
^ via dense bodies

fibrinogen von willebrand factor
^ via alpha granules

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37
Q

intrinsic coagulation cascade

A

activation by Factor XII present in the plasma

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38
Q

coagulation cascade

A

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)

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39
Q

extrinsic coagulation cascade

A

activation by Tissue Factor (TF)

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40
Q

thrombosis

A

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

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41
Q

hemostasis

A

Activation of platelets + humoral coagulation system (clotting factors)

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42
Q

Virchow’s triad

A

endothelial injury
abnormal blood flow
hypercoagulability

lead to thrombosis

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43
Q

risk fx for arterial thrombosis

A

coronary artery and MI

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44
Q

endothelial injury

A

exposes ECM –> activation of platelets and coagulation cascade

physical disruption not req. Endothelial dysfunction can be via DM, smoking, hypercholesterolemia

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45
Q

turbulence

A

at vascular bifurcation sites or areas of arteriosclerotic plaques

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46
Q

stasis

A

slowing of blood

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47
Q

hyperviscosity

A

increased cellular elements of blood

48
Q

hypercoagulability

A

(thrombophilia)

disordered in coagulation pathways –> predisposed to thrombosis

caused by abnormal factor of coagulation cascade

49
Q

Inherited and acquired thrombophilia

A 
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
Q

Risk fx of hereditary thrombophilia

A 
Mutation in Factor V = Factor V Leiden
Prothrombia G20210A Gene Mutation
Antithrombin III Deficiency
Protein C Deficiency
Protein S Deficiency
Hyperhomocystinemia
51
Q

Protein C
Protein S

deficiencies can lead to…

A

natural anticoagulant system

degrade factor V, factor VIII

undegradable coagulation factor

52
Q

Acquired Risk Factors for Thrombosis

A 
immobilization
major surgery, fracture, burns
Malignancy
Myocardial Infarct
Heparin 
Antiphospholipid antibody syndrome
Pregnancy, contraceptives/estrogen
Smoking
53
Q

Fate of thrombi (3)

A

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
Q

embolization

A

embolus trey transported until lodges in blood vessel

emboli can originate from venous or arterial circulation

55
Q

pulmonary embolsm

A

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
Q

paradoxical embolism

A

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
Q

arterial thromboembolism

A

Emboli originating within arterial circulation

Arise from chambers of the heart or heart valves 80% of the time

58
Q

Other Examples of Emboli

A

Amniotic fluid emboli
Septic emboli (cardiac valve vegetations)
Air emboli
Fat emboli (trauma; motor vehicle accidents)

59
Q

gangrene

A

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
Q

infarct resolution process

A

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
Q

Major risk fx of atherosclerosis

A 
Age		
Sex (females more protected)			
Family history				
Genetic abnormalities	
Hyperlipidemia			       
Hypertension				
Smoking		 			
Diabetes 				
C-reactive protein
62
Q

Minor risk fx of atherosclerosis

A

Obesity Physical inactivity Stress
Homocysteine (plasma >100 umol/L) Postmenopause Alcohol Lipoprotein (a) (alt form of LDL)
Unsat. Fat intake

63
Q

non-modifiable risk fx of atherosclerosis

A

age
sex (men>women)
genetic

64
Q

Modifiable risk fx for atherosclerosis

A
  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
Q

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

A

C.

66
Q

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

A

C.

67
Q

Principal point of physiologic resistance to blood flow

A

Arterioles

68
Q

describe longitudinal section through the normal aorta with an elastic tissue stain

A

intima is at the top, while the thick aortic media demonstrates parallel dark elastic fibers

smc fibers are between the elastic fibers

69
Q

vascular wall components

A 
Endothelial cells
Smooth muscle cells
Extracellular matrix:
-Elastic elements
-Collagen
-Proteoglycans
70
Q

Weibel-palade bodies

A

3 mm long membrane-bound bodies that represent the storage organelle for von Willebrand factor

71
Q

Endothelial Cell Properties and Functions

A

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
Q

smc functions

A

Vasoconstriction and dilation

Synthesis of collagen, elastin and proteoglycans (for matrix)

Elaboration of growth factors and cytokines

Migration to the intima and proliferation

73
Q

Smooth muscles form which layer of arterial wall?

A

A- INTIMA

B- MEDIA

C- ADVENTITIA

74
Q

endothelial cells form which part of arterial wall?

A

intima

75
Q

Arteriosclerosis = hardening of the arteries

Used to describe 3 distinct patterns:

A
  1. Atherosclerosis
  2. Mönckeberg medial calcific stenosis
  3. Arteriolosclerosis
76
Q

Mönckeberg medial calcific stenosis

A

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
Q

Atherosclerosis (where are plaques comm. found?)

A

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
Q

Arteriolosclerosis (which diseases associated w/?)

A

disease of SMALL arteries and arterioles, association with hypertension and diabetes mellitus

79
Q

Atherosclerosis affects largely

A

elastic and muscular arteries

80
Q

Hypertension and Diabetes affect primarily

A

small arteries and arterioles

81
Q

hyperplastic arteriolosclerosis

A

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
Q

Hyaline Arteriolosclerosis

A

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
Q

MALIGNANT HYPERTENSION

A

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
Q

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

A

B.

85
Q

Precursors of Atheromatous Plaque

A
  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
Q

Fatty streaks

A

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
Q

Foamy macrophages

A

macrophages w/ fat

precursors of Atheromatous Plaque

88
Q

Progression of Atherosclerotic Lesions

A

Isolated Macrophage –> Fatty Streaks

Intimal Thickening –> Extracellular Lipids –> Atheroma –> Fibroatheroma –> complex lesion

89
Q

Precursor lesion for atheroma is –

A Thrombus 
B Fatty streak 
C Calcification 
D Hemorrhage 
E Exudate 
F Ulceration
A

B

90
Q

Atheromatous Plaque

A

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
Q

Atheromatous Plaque 3 principal components

A

Cells: Smooth muscle cells, macrophages, leukocytes
CT, ECM – collagen, elastic fibers, proteoglycans

Intracellular and extracellular lipid deposits

92
Q

CHL clefts indicate

A

an acute injury not a chronic injury

93
Q

SEQUELAE OF ATHEROSCLEROSIS

A
  • 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
Q

clinical phases of atherosclerosis

A

aneurysm and rupture

occlusion by thormbus

critical stenosis

95
Q

anterior descending coronary artery w/ marked atherosclerosis with narrowing. In general, the worst atherosclerosis is _____, where arterial blood flow is _______________.

A

worst atherosclerosis is proximal, where arterial blood flow is more turbulent

96
Q

Which arterial layer is involved in atherosclerosis?

A

intima and media

97
Q

What type of arteriosclerosis is least significant clinically?

A

Mönckeberg medial calcific stenosis

98
Q

What is the early pathological lesion of atherosclerosis?

A

intimal thickening

99
Q

What are the two risk factors for arteriolosclerosis?

A

HTN, DM

100
Q

Where is arteriolosclerosis usually found?

A

kidneys

101
Q

What is the most common cause of aneurysms?

A

atherosclerosis

102
Q

Where do atherosclerotic aneurysms occur?

A

abd aorta

103
Q

vasculitis

A

Inflammation of and damage of vessel wall, typically arteries are involved

104
Q

vasculitis etiologies

A 
Autoimmune processes ( immune complex deposition, ANCA, or antibodies against endothelial cell antigens )
Infection
105
Q 
Giant cell temporal arteritis
sx
causes
location 
tx
A

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
Q

Polyarteritis nodosa

A

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
Q

Thromboangiitis obliterans (Buerger’s Disease)

A

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
Q

Abdominal Aortic Aneurysm (AAA)

A

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
Q

Risk of AAA rupture is directly related to the size…

A
  • 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
Q

AAA RUPTURE TRIAD

A
  • Abrupt onset of severe back pain
  • Hypotension
  • Pulsative mass
111
Q

Berry Aneurysms

A

Bifurcations of circle of Willis
0.5 - >3 cm
May be multiple

Etiology…
Genetic factors
Cigarettes
Hypertension

112
Q

Syphilitic Aneurysm

cardiovascular manifestation of tertiary syphilis

A

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
Q

Aortic Dissection

A

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
Q

Aortic Dissection Risk Factors

A
  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
Q

Most frequent pre-existing abnormality in aortic dissection

A

Cystic Medial Degeneration

116
Q

Cystic Medial Degeneration

A

Separation and loss of elastic elements in aortic media; cyst-like spaces filled with mucopolysaccharide rich matrix

117
Q

Sequelae of aortic dissection

A 
Rupture into surrounding soft tissues
Rupture into pericardial space (hemopericardium)
Rupture into pleural space (hemothorax)
Re-entry into aortic lumen
Compression of branch ostia

Emma III (28 decks)

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