Robbins Basic Pathology: Path: Hemodynamics Flashcards


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1

what causes fluid to exit the capillary and what side is this from

hydrostatic pressure pushing out the arterial side of capillary

2

what causes fluid to return to the capillary and on what end

oncotic pressure on the venous end

3

what can go wrong with fluid inside BVs

hemodynamic disorders
thromboembolic disease
shock

4

what is edema

increased fluid in the ECF

5

what is hyperemia

increased blood flow

6

what is congestion

increased backup

7

what is hemorrhage

extravasation

8

what is hemostasis

opposite of thrombosis

9

what is thrombosis

clotting blood

10

what is embolism

downstream travel of a clot

11

what is infarction

death of tissues without blood

12

what is shock

circulatory failure and collapse

13

what combats hemostasis

thrombosis (clots blood)

14

what are the 4 possible causes of edema

increased hydrostatic pressure
reduced oncotic pressure
lymphatic obstruction
sodium/water retention

15

how much of the body is water

60%

16

how much of body water is intracellular

2/3

17

how much of body water is interstitial

1/3

18

how much of body water is intravscular

5%

19

what is edema in general

shift to the interstitial space of fluid

20

what is another name for hydrothorax

pleural effusion

21

what is an increase in fluidin the pericardium

pericardial effusion or hydropericardium

22

where does pericardial effusion take placue

between visceral and parietal pericardium

23

what is another name for hydroperitoneum

ascites

24

what is anasarca

total body edema

25

what are some potential causes to increase hydrostatic pressure

impaired venous return
congestive heart failure
constrictive pericarditis
ascites (liver cirrhosis)
venous obstruction or compression
thrombosis
external pressure (mass)
lower extremity inactivity with prolonged dependency
arteriolar dilation
heat
neurohormonal dysregulation

26

how does ascites increase hydrostatis pressure

filter gets stuck between portal and venous output so there is backup

27

what can reduce plasma oncotic pressure (hypoproteinemia)

protein losing glomerulopathies (nephrotic syndrome)
liver cirrhosis
malnutrition
protein-losing gastroenteropathy

28

what three major vital organs are causes of edema

heart liver kidneys

29

what is considered mostly when we talk about loss of "protein"

albumin

30

what can cause lymphatic obstruction

inflammatory
neoplastic
postsurgical
postirradiation

31

what can cause Na over-retention

excessive salt intake with renal insufficiency

increased tubular reabsorption of sodium

renal hypoperfusion: increased renin-angiotensin-aldosterone system

32

what types of inflammation stages are possible

acute
chronic
angiogenesis

33

what will areas of increased vascular permeability or areas of increased blood vessels appear

edematoous

34

what is the equation relating net fluid flux and hydrostatic and oncotic pressures

Jv = ([Pc − Pi] − σ[πc − πi])

(starling-landis law)

35

what end of the capillary has higher hydrostatic pressure

arterial end (pushes fluid out)

36

what end of the capillary has higher oncotic pressure

venous end (pulls fluid back in)

37

what are two large consequences of CHF edema

increased venous pressure due to failure

decreased renal perfusion, triggering of renin-angiotensin-aldosterone complex, ultimately resulting in sodium retention

BOTH OF THESE ARE IMPORTANT

38

when do you get systemic edema

right ventricle backup

39

when do you get pulmonary edema

left ventricle backup

40

how does CHF edema cause problems

increased venous pressure due to failure

decreased renal perfusion triggering renin-angiotensin-aldosterone complex, resulting ultimately in sodium retention

41

how does CHF cause edema mechanically

failing ventricles can't keep up with fluid given to them, pressure rises and can surpass osmotic pressure going into the venule end of the capillaries and you get edema

42

what does ascites cause

portal hypertension

hypoalbuminemia

43

what will portal hypertension cause

edema of organs and tissues with portal circulation

44

what will hypoalbuminemia cause

systemic edema

45
card image

if you push on this stomach and there is a fluid wave what is this

ascites

46

what are some ways the kidneys can cause edam

sodium retention

protein losing glomerulonephropathies (nephrotic syndrome)

47

what do people with nephrotic syndrome have usually

hypoalbuminemia and hyperlipidemia because body tries to use fats to pull water back into capillaries

48

how can edema manifest itself

subcutanoues pitting
dependent legs
anasarca
periorbital edema
cerebral edemas

49

what are some ways cerebral edema can be manifest

herniation of cerebellar tonsils
herniation of hippocampal uncus over tentorium
subfalcine herniation

50

what does a LH backup lead to

pulmonary edema

51

what does a RH backup lead to

systemic edema

52

does transudate or exudate have a higher specific gravity

exudate

53

does transudate or exudate have a higher protein content

exudate

54

does transudate or exudate have a higher LDH (lactate dehydrogenase)

exudate

55

what does transudate come from

disturbance of starling forces

56

what does exudate come from

damage to capillary wall

57

what is hyperemia vs. congestion

hyperemia: increased inflow

congestino: decreased outflow

58

is hyperemia or congestion an active process

hyperemia is actie

59

what does chronic congestion usually imply

necrotic or damaged tissue due to lack of adequate perfusion

60

is congestino or hyperemia more associated with edema

congestion

61

what is congestion more associated with edema than hyperemia

because decreased venous flow, not increased arterial flow, is the prime feature that differentiates congestino from hyperemia

62

is edema or congestion more severe

edema

63

what wil be present in lung congestion

water in lung's alveoli and hemosiderin in MPs

64

what will acute congested liver show

predominance of central part of lobule because it is closest to caval/hepatic blood flow

65

what will chronic congested liver show

central lobular necrosis

66
card image

whats wrong here

acute passive congestion of the lung

67

what does acute passive congestino of the lung preced

acute pulmonary edema

68

what will be present in a picture of acute pulmonary edema

congested alveolar vessels with transudate in hte alveoliw

69

when does pulmonary edema happen (pressure-wise)

when pulmonary capillary pressure rises to values exceeding plasma colloid osmotic pressure (28 mm Hg in humans)

70

will pulmonary edema develop easily

no, there is a lot of safety because normal pulmonary capillary pressure is 8-12 mm Hg

71
card image

where is the Kerley B line

card image
72

what do chronic pulmonary edema cells look like histologically

hemosiderin laden MPs common

73

how does blood escape into the alveolar space for chronic pulmonary edema

chronic congestion causes the thin walled alveolar capillaries to burst

74

what happens to the alveolar septae in chronic pulmonary edema?

thickens

75
card image

diagnosis

chronic pulmonary edema

76

what is characteristic of chronic (passive) hyperemia of the lung?

congestion laden MPs due to breakdown of RBCs

77

what is the stain for the hemosiderin pigment

prussian blue

78

what is used to stain collagen in the lab

trichormoe, stains collagen green

79
card image

what are the red things on this liver and what condition is this

this ia acute passive congestion and the red dots are congested central veins

80
card image

what condition and tissue is this

acute passive congestion, liver

81

what is another name for chronic passive congestion (hyperemia) of the liver

nutmeg liver

82
card image

what condition is this

nutmeg liver/chronic passive congestion of the liver

83

what is chronic passive congestion of the liver associated with

necrosis in the central part of the hepatic lobule

84

what can chronic passive congestion of the liver lead to

cirrhosis; if cardiac in origin, cardiac cirrhosis

85

what are flattened gyri on the brain a signal of? why is this so

edem;a due to compression against the calvarium

86

what three parts of the brain are most likely to herniate

card image

subfalcine herniation up top

hippocampal cingulate gyrus (between cerebellum and cerebrum)
cerebellar tonsillar (through foramen magnum)

87

which herniation in the brain might not be apparent

subfalcine because they would push up against one another on opposite sides

88

what is hemorrhage

extravasation beyond a vessel

89

what does a hematoma imply

mass effect, pressing around neighbors

90

what is hemorrhagihic diathesis

abnormal bleeding due to something

91

what is a dissecting hemorrhage

used in resepsect to large arterial vessels (aorta) where blood goes into the planes of walls of the blood vessels

92

what are petechiae

pinpont spots

93

what are purpura

bigger than petechiae but same spots

94

what are petechiae usually due to

blood disorder

95

what is ecchymoses

bruise

96

what color will an acute hemorrhage appear

red

97

what color will chronic hemorrhage appear

MP with hemosiderin

98

how do hemorrhages evolve in terms of classification

acute to chronic

99

how do hemorrhages evolve in terms of color

purple to green to brown

100

how do hemorrhages evolve in terms of content

hemoglobin to bilirubin to hemosiderin (purple to green to brown)

101
card image

what are in eithe picture

left: petechial rash in colon

right: hematoma in brain

102

what type of hematoma is usually associated with skull fractures

epidural

103

what hematomas are associated with closed head trauma

subdural

104

besides epidural and subdural hematomas what else is indicated by bleeding in the brain

intraventricular or intraparenchymal hemorrhages or subarachnoid hemorrhage

105
card image

what type of image is this

CT (because bone densest)

106

what can CT show with hematomas

density

107

what can MRIs show with hematoma

chemistry and evolution

help estimate time

108

T/F premortem clots have texture and adhere to a BV wall

true

109

how do you know if a clot is post-mortem

they have a jelly or chicken fat consistency

110

what is the homeostasis of blood between

hemostasis and thrombosis

111

what is hemostasis

opposite of thrombosis, preserves liquidity of blood

112

what does hemostasis do

plugs the sites of vscular injury

113

what are the three components of hemostasis

vascular wall
platelets
coagulation cascade

114

what are the main events following a vsscular injury

arteriolar vasoconstriction
thrombogenic ECM at injury site
tissue factor released by endothelium and platelets
fibrin polymerization, TPA limits plug

115

what causes arteriolar vasoconstriction in response to vascular injury

reflex neurogenic constrictoin

endothelin from endothelial cells

116

what does thrombogenic ECM at the injury site do in response to vascular injury

adhere and activate platelets

platelet aggregation (primary hemostasis)

117

what does tissue factor do following vascular injury

activates coagulation cascade to thrombin to fibrin (secondary hemostasis)

118

what are the players following vascular injury and the onset of hemostasis

endothelium

platelets

coagulation cascade

119

what is the normal action of the endothelium

antiplatelet, anticoagulant, and fibrinolytic properties

120

what is the action of endotheilum in injury

pro-coagulant properties

121
card image

what is the dark thing?

what are the F's?

RBC

fenestrations

122

how does the endothelium act as an anti-platelet cell

protection from subendothelium ECM

degrades ADP (inhibits aggregation)

123

how does the endothelium act as an anti-coagulant

membrane has heparin like molecules

makes thrombomodulin which acts on protein C

tissue factor pathway inhibitor

124

besides anti platelet and anti coagulant properties, how does the endothelium act

fibrinoLYTICally (TPA)

125

how does the endothelium act prothrombotically

makes vWF
makes Tissue factor
makes plasminogen inhibitors

126

what does the von willebrand factor do

binds platelets to collagen

127

besides endothelium what makes tissue factor

platelets

128

what activates endothelium

infectious agents
hemodynamics
plasma
anything that disrupts it

129

what are the types of granules that platelets have

alpha and delta

130

what is in the alpha granules of platelets

fibrinogen
fibronectin
factor V and factor VIII
platelet factor 4 and TGF-beta

131

what is in the delta granules (or dense bodies) of platelets

ADP/ATP
Ca
histamine
serotonin
epinephrine

132

besides alpha and delta granules what do platelets make

tissue factor

133

what does TGF beta control

proliferation, cellular differentiation, and other functions in most cells

134
card image

where in this picture are the delta granules? what is in these granules?

the dense circles

ADP/ATP
Ca
histamine
serotonin
epinephrine

135

what are the phases of platelet aggregatino

adhesion
secretion
aggregatoin

136

what is involved in platelet "secretion" phase

release/activation/degranulation

137

where do platelets adhere to

primarily to subendothelial ECM

138

what is platelet adhesion regulated by

von willebrand factor

139

what does vWF do

bridges platelet surface receptors to ECM collagen

140

what granules are secreted in the platelet secretion phase

alpha and delta

141

what of the secreted material of platelets is bound? what does it bind to? what happens inside the platelets?

agonists bind to pletele surface receptors and intracellular protein phosphorylation

142

what substances play a role in platelet aggregation

ADP
Thromboxane A2
thrombin
fibrin

143

where does thrombin for platelet aggregation come from

coagulation cascade

144

what does fibrin do to the platelet plug

strengthens and hardens and contracts the platelet plug

145

where is ADP stored in platelets

delta/dense bodies

146

what family of ADP receptors does ADP interact with in platelet activation

P2Y1, P2Y12, P2X1

147

what converts ADP to adenosine

ecto-ADPases

148

what is the role of ecto ADPases converting ADP to adenosine

inhibit further platelet activation via adenosine receptors

149

what does plavix do

anti-platelet drug that inhibits P2Y12 receptor

150

what does thromboxane do

stimulates activation of new platelets and increases platelet aggregation

151

what is the overall sequence of platelet events

adherence to ECM, secretion of ADP and TXA2, exposure of phospholipid complexes and expression of tissue factor

primary plug becomes a secondary plug and this is strengthened by fibrin

152

what initiates the intrinsic coagulation cascade

contact with negative surfaces

153

what initiates the extrinsic coagulation cascade

tissue factor

154

what are the key events in the coagulation cascade (common)

prothrmbin to thrombin, then fibrinogen to fibrin

155

what are the cofactors involved in the coagulation cascade

Ca2+, phospholipid and vitamin K dependence (2, 7, 9, prothrombin

156

how does tissue factor pathway inhibitor inhibit coagulation

by stopping activation of factor 7, which needs tissue factor to help activate factor 10

157

what is another name for tissue factor

factor III or CD142

158

what is tissue factor present in

subendothelial tissue, platelets, and leukocytes

159

what is the time important for calculating the intrinsic coagulation cascade

aPTT

160

what are patients that take heparin best monitored with

aPTT

161

what is the time important for calculating hte extrinsic coagulation cascade

PT

162

what are patients that take coumadin best monitored with

PT

163

what is bleeding time a measure of

platelet function

164

what is a normal bleeding time

2-9 minutes

165

what is a normal platelet count

150k to 400k per mm3

166

what is the triangle of thrombosis

abnormal non laminar flow
endothelial injury
hypercoagulation

167

what is considered an endothelial "injury" to disrupt endothelium

any perturbation, not just physical damage

168

what is abnormal flow exampled by

nonlaminar flow
turbulence
eddies
stasis
disrupted endothelium

all of which may bring platelets into contact with endothelium and/or ECF

169

what is primary hypercoagulability usually a defect of

factor V and prothrombin

170

what are the most common types of primary hypercoagulability

mutation in prothrombin gene or methyleneTHF gene

171

what is a rarer form of primary hypercoagulability cause

antithrombin III deficiency, protein C deficienty, protein S deficiency

172

what is a very rare form of primary inherited hypercoagulability

fibrinolysis

173

is secondary hypercoagulability inherited or aquired

acquired

174

how do you get secondary hypercoagulability

prolonged bed rest or immobilization
MI
a fib
tissue damage
cancer
prosthetic cardiac valves
DIC
heparin-induced thrombocytopenia
antiphospholipid Ab syndrome

175

how does secondary hypercoagulability happen

IgG antibodies form a complex with heparin and PF4 in the bloodstream and the tail of the Ab then binds Fcylla receptor, a protein on the surface of the platelet which results in activation of the platelets and formation of platelet microparticles which initiate the formation of blood clots and the platelet count falls, leading to thrombocytopenia

176

what is lupus anticoagulant

Ig that binds to phospholipids and proteins associated with cell membrane

177

what is weird about the lupus anticoagulant name

it is actually a prothrombotic agent (presence of lupus anticoagulant antibodies precipitates the formation of thrombi in vivo

178

what is trousseau syndrome

venous thrombosis in cancer patients due to glycoproteins causing hypercoagulability

179

what is DIC hand in hand with

shock

180

what type of vessel wall can a thrombus adhere to

heart (mural)
artery (occlusive/infarct)
vein

181

are all thrombi obstrcutive

no, some are unobstructive

182

what color are acute thrombi

red

183

what color are organizing thrombi

yellow

184

what color are old thrombi

grey/white

185

do thrombi have to adhere to be considered thrombi

yes

186

whey are organizing thrombi yello

MPs come in and chew up fat

187

in addition to the thrombus color changing whwat else goes through changes

infarcted tissue

188

what do most systemic arterial thrombi come from

mural thrombi

189

about how many of the systemic arterial thrombi come form the aorta

20%

190

what all can happen to thrombi

propagation (downstream)
embolization
dissolution
organization
recanalization

191

which relative directions would propagation and embolization go

same

192

what is recanalization

where a thrombus has occluded a vessel but a new endothelial surface can grow into an older thrombus like a tube going through a pipe

193

what is the source of most pulmonary emboli

deep pelivic vein thrombus

194

do superficial vein thromboses embolize to the lungs

not usually

195
card image

what is the black squiggly line on the right and what stain is used here?

what are the majority of cells in this occlusive arterial thrombus

intenral elastic lamina, elastic stain

mostly MPs (NOT fibroblasts)

196
card image

what is the difference between the left and right here

left is a clotted vein, right is a clotted artery

197

where do deep vein thromboses come from (location in the body)

calf, thigh, pelvic veins

198

what is a huge factor in deep vein thrombosis

congestive heart failure

199

what is the most common form of DVT (deep vein thrombosis)

inactivity

200

what besides CHF and inactivity can cause DVTs

trauma and surgery and burns and injury to vessels and procoagulant substances from tissues and reduced tPA

201

what is the major source of PE

deep vein thrombosis

202

what combines to create an acute MI

old atheroosclerosis and fresh thrombosis

203

what can arterial thrombi do

send fragments downstream, probably have flecks of calcified or cholesterol plaque also

204

what is lodging of cardiac thrombi proportional to

cardiac output the organ receives

205

will venous thormbi have flecks of calcified or cholesterol plaques

NO

206

what are atheroemboli

chonesterol cleft comtaining arterial thrombi, which will NOT be present in venous thrombi

207
card image

what are these large white streaks

cholesterol clefts

208

what causes DIC

obstetric complications
advanced malignancy
shock

209

is DIC a primary disease

no

210

where does DIC usually occur

in capillaries

211

what is the idea of DIC

peopole use up all their clotting factors so they can't use them elsewhere

212
card image

what is going on here

clotting in glomerular capillaries

213

if someone clots in glomerular capillaries, what is probabl true

they are probably making clots in all capillaries

214

what types of general emboli exist

pulmonary
systemic

215

what can be the substance of the emboli

fat
air
amniotic fluid
thrombus

216

what do pulmonary emboli usually come from

venous circulation

217

what do systemic emboli usually come from

arterial circulation

218

what is a general rule with PEs

generally silent

219

what are the symptoms of a pulmonary embolism

chest pain
low PO2
SOB

220

how much of an occlusion of pulmonary vasculatoure presents a high risk for sudden death (acute coronary pulmonale or acute RHF)

60% or higher

221

are saddle emboli usually worse or better than others

worse

222

what do premortem blood clots look like

friable, adherent, lines of zahn

223

what do postmortem emboli look like

currant jelly or chicken fat

224

what does a saddle emoblism do in the vessel

flops form main pulmonary artery to left and right

225

what are lines of zahn from

fibrin productino

226
card image

what is depicted

lines of zahn

227
card image

what is depicted

lines of zahn

228
card image

what is shown here

saddle embolism

229

what is another name for systemic emboli that form in veins

paradoxical emboli

230

how many systemic emboli come from cardiac muscle and how many from aorta

80/20

231

what is embolization lodging site probability proportional to

degree of flow that that organ gets

232

what are systemic emboli usually from

arterial sources

233

how can paradoxical emboli happen

thrombus forms in vein and ends up in systemic circulation

234

how can paradoxical emboli happen

if there is a right to left shunt

235

how could a clot in the renal artery come from the vein in the pelvis

paradoxical embolus through right to left shunt

236

do most occluding emboli infarct

no, think about how you get V/Q mismatch instead

237

how do fat emboli happen

long bone fractures, also bones within marrow

238

how do air emboli happen

Scuba bends

239

what causes amniotic fluid emboli and are they fatal

very prolonged or difficult delivery, yes very high mortality

240

what are squames

epithelial cells that line fetal lungs

241

what do squames give proof of

amniotic fluid embolism in small pulmonary BV because they line amniotic sac

242
card image

what is shown here

amniotic fluid embolism

243
card image

what is this

normal bone marrow (50% fat, 50% cells)

244
card image

what is shown here

fat (marrow) embolism in a pulmonary artery

245

could a fat embolism be from an adult long bone fracture

no because they are not hematopoetic

246

what are fat emboli usually from in adults

axial skeleton fracture

247

what is an infarction

area of necrosis secondary to decreased blood flow

248

what types of infacritons are possible

hemorrhagic and anemic

249

are hemorrhagic areteries white or red

red

250

what color are anemic arteries

white

251

what color are infarcts to end arteries

white

252

what color are infarcts to dual artery supply arteries

red

253

what is the progression of healing in infarcts

acute to organization to fibrosis

254

will liver infarcts be white or red

red

255

what will happen in acute infarct

leukocyte infiltration

256

what will happen in organizing infarct

BV and MPs infiltrate

257

what will happen in a fibrosing infarct

fibroblasts infiltrate

258

what are the factors in infarct

nature of the area's vascular supply
rate of development
vulnerability to hypoxia
CHF vs. no CHF

259

is a slow developing or fast developing infarct better

slow

260

would a myocyte or fibroblast be more vulnerable to hypoxia

myocyte

261
card image

what are these things on the left and right

left: red (hemorrhagic) infarct (lung)
right: white (anemic) infarct (spleen)

262

why are many infarcts wedge-shaped

they outline or delineate the area of arterial distribution

263

where are lung infarcts usually

peripheral

264
card image

what is the organ here and what is wrong

kidney, wedge shaped infarct due to the blockage of an end renal artery branch

265
card image

how old is this infarct

months to years (fibrosis present)

266
card image

what does the white area show is present

this is area of acute infarct because you have neutrophils

267
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what stage of infarct is this

acute

268

what are the types of shock

cardiac
septic
hypovolemic

269

what is the definition of shock

cardiovascular collapse

270

what are the common pathophysiologic features of shock

inadequate cardiac output and/or inadquate blood volume

271

what are the general results of shock

inadequate tissue perfusion
cellular hypoxia
fatality if not corrected

272

what causes cardiogeneic shock? is it acute or chronic?

CHF
acute

273

what causes hypovolemic shock

hemorrhage or leakage

274

what is another name of endotoxic shock

septic shock

275

what is the number one killer in the ICU

septic shock

276

what are two less common causes of shock

neurogenic
anaphylactic

277

what is neurogenic shock due to

loss of vascular tone

278

what is anaphylacitc shock due to

IgE mediated systemic vasodilation

increased vascular permeability

279

what can cause cardiogenic shock

MI
ventricular rupture
arrhythmia
cardiac tamponade
pulmonary embolism (acute RHF or cor pulmonale)

280

how big would an acute PE have to be if someone were to go into cardiogenic shock

very big

281

if right heart fails, what will happen to the left heart

it will fail also

282

what is the ultimate cause of hypovolemic shock

vascular compartment loses fluid

283

what are four causes of hypovolemic shock

hemorrhage
vomiting
diarrhea
burns

284

how can loss of fluid from the vascular compartment proceed

directly or indirectly

285

what is the middle compartment in indirect fluid loss from the vascular compartment

ECF

286

good or bad to take fluid from the vascular compartment into intracellular fluid

very bad

287

what causes septic shock

overwhelming infection
endotoxins (LPS)
gram positive bacteria
fungal infections
superantigens

288

what is most septic shock due to

gram negative bacteria

289

what is gram positive shock due to

superantigens

290

what are superantigens

polyclonal T lymphocyte activators that induce systemic inflammatory cytokine cascades similar to those occuring downstream in septic shock (toxic shock super antigens by staph are the prime example)

291

what are the septic shock events after infection

peripheral vasodilation
pooling
endothelial activation
DIC

292

what can shock be thought of as

total body inflammatory response/infarct

293

what are endotoxins usually from

gran negative bacterial cell walls

294

what is another name for endotoxin

LPS

295

what do endotoxins attach to

cell surface antigen CD 14

296

what cytokines lead and control the cascade of cytokines

TNF and IL1

297

what are the septic shock events (more detailed)

systemic vasodilation (hypotension)
decreased contractility
diffuse endothelial activation
leukocyte adhesion
alveolar damage (adult respiratory distress syndrome)
DIC
vital organ failure (CNS)

298

what way would people normally die

shock

299

what is ARDS

adult respiratory distres syndrome

300

what is characteristic of non cardiogenic pulmonoary edema

fibrin, cells, proteins

301

what are the clinical stages of shock

nonprogressive
progressive
irreversible

302

what happens during the nonprogressive clinical stage of shock

compensatory mechanisms

303

what happens during the progressive clinical stage of shock

acidosis and early organ failure

304

what type of things go on during nonprogressive shock

compensatory mechanisms, catecholamines

vital organs are still perfused

305

what happens during progressive shock

hypoperfusion
early "vital" organ failure
oliguria
acidosis

306

do hemodynamic corrections work in irreversible shock

no

307

what can start as a pathologic response to shock

multiple organ failure
subendocardial hemorrhage
acute tubular necrosis
diffuse alveolar damage
GI mucosal hemorrhages
liver necrosis
DIC

308

what is DAD

diffuse alveolar damage: shock lung

309

what happens in subendocardial hemorrhage

inner part of myocardium perfused by blood from inside ventricle, preferentially coronary arteries perfuse the outer poortion of the myocardium

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what is acute tubular necrossi

toxins involved usually, but just means that there is a lack of blood flow and tubules will die before glomeruli do

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what happens in liver necrosis

clotting and catecholamines released

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what part of the GI mucosa is the first to become infarcted

mucosa

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what is damaged mostly in DAD

alveolar damage reacting to inadequate perfusion

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what is this

DAD (shock lung)

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what can shock lung be thought of as

pulmonary edema with alveolar septal damage and leakage of cells and esudate

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how is acute pulmonary edeema different from DAD histologically

DAD: septal damage and exudate leakage

acute pulmonary edema: no septal damage, alveolar transudate

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what is shown here in the upper field

coagulatin necrosis of myocardium

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in shock where is hypoperfusion greatest in the heart

subendocardium

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when is the subendocardium perfused mainly

diastole

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what is shown here?

how can you tell?

acute tubular necrossi (look at sparing of the glomeruli)

no nuclei in tubules

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what usually causes acute tubular necrosis

ischemia or drugs

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what plugs up the glomerular capillaries in DIC

fibrin

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what is shown here and what kind of stain is on the right

DIC in the glomerulus

right is fibrin stain

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what is the clinical progression of symptoms in shock

hypotension to tachycardia to tachypnea to warm skin to cool skin to cyanosis to renal insufficiency to obtudance to death

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what tissue is this

kidney

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what is wrong here

acute tubular necrossi

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how can you tell acute tubular necrosis vs renal infarct

in ATN just tubules damaged, in renal infarct the glomeruli are damaged too

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what are most tubules seen histologically

proximal tubules

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are proximal tubules more or less likely to be necrotic than other types of tubules

more likely

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what type of tissue is this

brain tissue

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what are most cells in brain tissue

glial cells

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what will be around neurons in brain tissue

white halos

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what is strange about this section of brain tissue

many glial cells (gliosis) and some edema

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what is this tissue

brain tissue

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what is going on in this picture

liquefactive necrosis

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what causes liquefactive necrosis

ischemia
stroke
infarct
hypoxia

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what organ is this and why is it weird

diagnosis?

liver with abnormally arranged lobules

cirrhosis

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what will cirrhosis cause

portal hypertension and ascites and edema (elsewhere due to lower albumin making ability)

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what is going on in this tissue

organizing stage of acute hemorrhage

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what are most brain infarcts

non-hemorrhagic

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where will blood collect if large cerebral BV is ruptured

subarachnoid space

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what is shown here? what is the white at the bottom? what is outside the white?

cardiac muscle cells with pericardial fat at the bottom and visceral pericardium outside

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what is going on here

inflammatory cells going into pericardial fat and pericardium

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what is what above and below the white line

myocardium below, thrombus at top

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what is true of the inflammatory response in all tissues

same general pattern of acute, organinzing, necrosis

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why are mural thrombi hard to detect

because all tissues are going to follow the same pattern of necrosis

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how are the left and right sides of these images different

right side more organizing, left side more acute (inflammatory steps)

this is probably an organizing blood clot with a recent component

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what is this

large pulmonary artery vessel

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is this a pre or post mortem blood clot and why

pre due to adherence and lines of zahn

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what type of tissue is this and what are the stratifications

anterior pitutary on bottom (glandular)
intermediate lobe on right (circle)
posterior pituitary on top (neural tissue)

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what are the dark things on the bottom of the screen

basophils

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how do you know that this is a partial infarct

because there are still some viable cells present with nuclei