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Pathology > Hemodynamics and Shock > Flashcards

Hemodynamics and Shock Flashcards

1
Q

edema in the living

A

too much interstitial fluid in the tissues and outside the individual cells for whatever reason

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2
Q

intracellular edema

A

cloudy swelling we see in injured (but not necessarily killed) cells

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3
Q

Anasarca

A

generalized, severe edema

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4
Q

effusion

A

liquid in the pericardial, pleural, peritoneal or joint cavities

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5
Q

Ascites

A

effusion in the peritoneal cavity

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6
Q

hydrothorax

A

watery fluid in the pleural space

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7
Q

empyema

A

pus/purulent effusion in the pleural cavity - less often “pyothorax” (Ringo Starr)

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8
Q

Hydropericardium

A

watery fluid in the pericardial cavity

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9
Q

Hydrocephalus

A

too much cerebral spinal fluid for whatever reason

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10
Q

Hydrocele

A

extra fluid within the membrane around the testis

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11
Q

hydrosalpinx

A

too much fluid in the fallopian tube (oviduct)

often follows gonorrheal or other salpingitis

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12
Q

ileus

A

too much fluid in the small bowel for whatever reason

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13
Q

seroma

A

non-infected fluid in the surgical incision

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14
Q

loculated effusion

A

more than one compartment, due to scarring. Harder to drain

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15
Q

blister

A

fluid in the epidermis, or between the epidermis and dermis

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16
Q

bulla

A

big blisters

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17
Q

vesicles

A

little blisters

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18
Q

edema spreads ______ and _____

A

collagen and smooth muscle

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19
Q

Five mechanisms by which edema can form

A
  1. excess body fluid
  2. increased pressure in the small veins of the body (“vascular problems/ edema”)
  3. Decreased total plasma protein/albuim content
  4. lymphatic vessel obstruction
    THESE will give you a TRANSUDATE, salt water without very much protein in it. These can be interconnected.
  5. Leaky vessels, usually from inflammation
    THIS will give you an EXUDATE, with plenty of protein in it.
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20
Q

Excess total body water

A 
iatrogenic fluid overloading
kidney failure (heart failure, after shock, antihypertensive Rx/Cach blockers, kidney dz)
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21
Q

increased venous pressure

A

ALL SYSTEMIC VEINS - R CHF, pericardial dz
PULMONARY VEINS - L CHF
LEG VEINS - Pregnancy, valve failure, standing up a lot
PORTAL VEIN - certain liver diseases, famously cirrhosis
OBSTRUCTED/NARROWED VEIN - thrombus, pressure

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22
Q

Decreased blood protein content

A

malnourished, malabsorption, liver failure, nephrotics

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23
Q

lymphatic obstruction

A

filariasis, surgery, radiation, cancer

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24
Q

hard to place

A

BRAIN - trauma, lead poisoning

MICROCIRCULATION/ANGIOEDEMA (genes, ace inhib)

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25
Q

dependent edema seen in patients with failing heart pumps

A

excess total body water and increased venous hydrostatic pressure contribute

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26
Q

edema will pit if the cause is

A

something other than inflammation or obstructed lymph vessels

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27
Q

cardiac edema tends to be worse in the ____ in those who are

A

feet, sacral region
up and about, bedridden

the reason is that gravity adds to hydrostatic pressure

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28
Q

increaed pressure in veins can result from

A

inadequate valves, internal obstruction by a thrombus, external compression by a mass (even the pregnant uterus)

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29
Q

Medusas head (kaput)

A

distended veins over the abdomen in liver failure/ ascites

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30
Q

Edema in liver is often a combination of

A

increased portal venous pressure and low serum albumin levels –> ascites

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31
Q

edema around the eyes

A

when generalized edema is due only to total body water overload (renal failure/other sodium retention)

because this tissue is very loose

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32
Q

renal wasting of protein

A

blood volume drops and the kidneys retain Na to keep BP adequate, very severe edema often results

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33
Q

lymphedema is most often due to

A

cancer. surgery and radiation therapy are also important causes. there is a filarial disease that still causes epidemic elephantiasis in many tropical regions

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34
Q

original mastectomies

A

took far too much tissue for no reason, and left thousands of women with lifelong lymphedema

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35
Q

podoconiosis (dust foot)

A

dessert dwellers who do not have shoes. may develop this from sand getting into and plugging the lymphatics

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36
Q

Milroy’s dz

A

lymphatics are malformed, producing lifelong lymphedema. worst in the legs

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37
Q

orange peel skin “peau d’orange:

A

ominous sign in the breast, signifying cancer plugging the dermal lymphatics

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38
Q

chylous effusions

A

result from damaged lymphatics, usually the thoracic duct. turbid, lipid rich fluid

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39
Q

non inflammatory exudates occur in

A

neovascularization, as deep wounds heal (granulation tissue) or cancers grow

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40
Q

generalized edema can develop in

A

dengue, in burn patients, and patients with sepsis/ “systemic inflammatory response” (IL-1/a TNF) without any localized infection

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41
Q

edema appearing first in the feet after standing

A

consider heart failure

CARDIAC EDEMA

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42
Q

edema appearing first around the eyes

A

consider total body water overload and/ or low blood albumin

RENAL EDEMA

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43
Q

edema appearing first as excess fluid in the abdomen

A

consider low blood albumin plus increased resistance to the portal venous flow

consider primary LIVER DISEASE

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44
Q

Dilated arteries by themselves

A

DONT cause edema.

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45
Q

Listening for pulmonary edema

A

warning of both heart failure and pneumonia - crackles, little bubbles of edema that pop
snap crackle pop

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46
Q

The reason for the snap crackle and pop of pulmonary edema is

A

the little bubbles air makes with the water and surfactant. surfactant has the physical properties of soap

crackles= rales

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47
Q

You might have experienced mild pulmonary edema

A

when you push yourself to your limit as a tuner, especially if you’re just getting into shape

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48
Q

Heroin and opiate overdose

A

froth from the mouth, typical gush of pulmonary edema

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49
Q

pulmonary edema only shows well on histology if its

A

an exudate

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50
Q

Cerebral edema is especially problematic because

A

it can push the brainstem out of the bottom of the skull

can get it from injury, poisoning, or a variety of other causes

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51
Q

Angioedema

A

poorly understood syndrome, blood vessels suddenly becoming extra-permeable

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52
Q

angioedema is best known in

A

hereditary C1-esterase deficiency
it’s also a rare but serious side effect of drugs like captopril (ace inhibitor)

in C1 esterase deficiency, edema of the larynx can kill

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53
Q

Hyperemia

A

increased blood flow to the organ. Hyperemia is generally RED and THROBS

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54
Q

Congestion

A

decreased bloos flow from the organ. congestion is typically PURPLE and doesn’t throb

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55
Q

both hyperemia and congestion increase

A

the amount of blood in the organ

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56
Q

what happens to your liver when you die?

A

unless your last few heartbeats are as strong as they are in health, or you bleed out, your blood will pool in you liver, causing congestion nearest the veins that drain it

NUTMEG LIVER

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57
Q

Describe blood flow and effects based on shape of liver lobule

A

blood pools around a hepatic central vein. The central liver cells die of lack of good blood flow over several hours.

liver cells die first in the central areas because they are furthest away from where thee fresh blood ethers.

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58
Q

Nutmeg liver with portal areas _____ and central areas_____

A

alive

dead

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59
Q

________ runs with hydrostatic lung edema, especially if

A

pulmonary congestion
the left ventricle can’t pump adequately

remember that in the lungs, the arteries and veins don’t run together

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60
Q

in pulmonar congestion, which runs with hydrostatic lung pressure, little bleed can leave behind

A

“heart failure cell”

little iron pigments of hemosiderin

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61
Q

Congestion can result form

A

any of the vascular problems that produce a transudate.

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62
Q

blood that is to viscous

A

(too much IgM, cyroglobulin, way high Hgb/Hct, sickles)

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63
Q

cryoglobulin precipitates

A

when you get too cold (it’s only marginally soluble)

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64
Q

hemorrhage

A

blodd cells that have escaped from a blood vessel. Can be trivial. Can be deadly

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65
Q

what determine whether a hemorrhage is serious

A

quantity and location

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66
Q

hematoma

A

enough blood in the tissues for you to be able to palpate it

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67
Q

cauliflower ear results from

A

the organization of a hematoma (transformation of mass of blood to mass of fibrous tissue, scar tissue)

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68
Q

Hemothorax

A

blood in pleural cavity

common, especially in trauma or thoracic aortic ruptruer, to bleed to heath iNTO your pleural cavities - each can hold maybe two quarts of fluid and you have only 5 quarts of loud.

fluid compressing the lungs also prevents people from taking deep breaths

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69
Q

Hemopericardium

A

blood in the pericardial sack

hard fro heart to pump bc it has pressure around it. hard for blood to get to the heart to supply it

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70
Q

hemoperitoneum

A

blood in the peritoneal cavity

71
Q

hemarthrosis

A

bleed(s) into a joint

common in hemophilia

72
Q

Petechiae

A

little bruiss

73
Q

purpura

A

bigger than petechia, bruises

74
Q

ecchymoses

A

largest bruises, might be defined to be over 10 mm, or due to injury, or either

75
Q

suction contusions may be

A

petechiae or purpura

76
Q

Tourniquet test

A

to see if a person has fragile blood vessels
(dengue)
appearance of many little petechiae confirms exaggerated capillary fragility

77
Q

petechiae on lower eyelid warn of

A

endocarditis.
can also confirm the impression of strangulation in forensic cases

little bits of pieces of infection in the heart break off, will end up getting suck in places with small blood vessels. fiber and bacteria are more dense than blood, shot straightt up from heart to carotid, external carotid, lower eyelids–> get infected, neutrophils come in and tear up blood vessels leading to petechiae

78
Q

purpura commonly seen in older folks results from

A

old sun exposure/loss of tissue support rendering the capillaries more fragile/likely to break.

no valves here as compared with legs.

79
Q

Dengue

A

complex viral infection involving the microvasculature

the virus damages the vessels
in addition to hemorrhage, systemic edema is common

targets endothelial cells, carried by mosquitos - bug that has the fastest access to blood vessels. can have a lot of bleeding

80
Q

After removal of IV lines, we should

A

apply pressure, especially in patients on anticoagulants

81
Q

peticeiae on the epicardium

A

sever thrombocytopenia

82
Q

hemoptysis

A

coughing up blood

83
Q

hematemesis

A

throwing up blood

84
Q

hematochezia

A

bright red blood from the rectum

85
Q

melena

A

blood digested during passage through the gut (upper gut)

86
Q

thrombus

A

blood that has solidified within a vascular lumen or cardiac chamber

87
Q

clot

A

blood that has solidified anywhere else

88
Q

The instant you’re hurt, hemostasis starts with

A

VASOCONSTRICTION. reflex vasoconstriction.

89
Q

vaso constriction in injury is followed by

A

primary hemostasis

90
Q

primary hemostasis is carried out by

A

platelets plugging up any little injuries in seconds

91
Q

Platelet adhesion is followed by

A

aggregation and release of platelet granule contents

92
Q

specific deficiencies in platelets (low numbers, poor function) may produce

A

petechiae at first. when severe, GI and brain bleeding are the most fears consequences

93
Q

secondary hemostasis

A

the clotting cascade turning liquid blood solid. this takes minutes

94
Q

Thrombin does a lot of things

A

thrombin bound to thrombomodulin on intact endothelium stops activating fibrinogen and starts activating protein C instead, preventing/stopping clotting

95
Q

thrombi form when

A

over time
when pro-thrombotic factors overshadow antithrombotic mechanisms (which prevent their formation and or remove them afterwards)

96
Q

it takes a few hours for factor XIII to

A

cross-link/polymerize the fibrin, making the thrombus more firm and crumbly

97
Q

Virchow’s Triad

A
  1. injured endothelium
  2. altered blood flow (turbulance/stasis)
  3. hyper coagulable blood

need only to have one component to be at risk for a thrombus, often you have multiple

98
Q

antemortem clot

A

lines of sahn.

all thrombi form chaotically, with some areas incorporating more red cells than others

99
Q

The most thrombogenic thing that you can have in your circulatory system is

A

a thrombus. THROMBI PROPOGATE

100
Q

in an organized thrombus,

A

the thrombus turns into a scar.

101
Q

what breaks down thrombi

A

plasmin

102
Q

recanalization

A

thrombi usually turn into granulation tissue, and contraction opens many little channels (scar contracts)

103
Q

post mortem thrombus

A

red cells on bottom, liquid on the top.
chicken fat and currant jelly
rubbery rather than crumbly. don’t adhere to the wall, and are not propagated distally

104
Q

the most common site for venous thrombi

A

the legs

problematic when it embolizes to lungs

105
Q

mural thrombus

A

on the wall of a heart. can overlie an old MI. keeps chamber from filling, prone to embolize. one of the most dreaded side effects of MI

106
Q

atheroclerotic plaques often often cause

A

overlying thrombi

107
Q

Vegetations

A

thrombi on a valve (mitral valve)

108
Q

thromboembolus

A

is both a thrombus and an embolus

109
Q

Virchow’s triangle: INJURED ENDOTHELIUM causes

A

on top of a ruptured atherosclerotic plaque
myocardial infarcts/myocardidtis
cardiac jet lesion (abnormal flow)
inflamed heart valves/prosthetic heart valves
radiation injury
after an electrical injury (gangrene can result)
tumor in a vessel or cardiac chamber
sclerosing htrapy for varicose veins
indwelling lines in veins/heart
smoking
high blood pressure itself

110
Q

Virchow’s triad: ALTERED BLOOD FLOW causes

A

myocardial infarcts (dead awl balloons out)
quivering/fibrillating cardiac atria
overruptured athererosclerotic plaques
in dilated heart chambers (valve or muscle disease)
in weakened arteries that have ballooned (aneurysms)
at arterial branch points (why there;s more plaques there)
over-viscous blood (more prone to stasis)
Sicklers, polycythemia (high RBC mass), IgM, cryoglobin
vascular malformations. why hemagiomas often regress
prolonged bed rest/immobilization

111
Q

Virchow’s triad: HYPERCOAGULABLE BLOOD causes

A

GENETIC
common: factor V leiden, prothrombin G20210A
less common: deficiencies of AT-III, protein S, protein C
rare: very high homocysteine

Pregnancy/ after childbirth
after sever trauma, burns, surgery, maybe even tissue necrosis, as during heart attack
nephrotic syndrome (lose small anticoagulant proteins)
tumors making prothrombotic substances
antiphopholipid syndrome (lupis anticoagulant)
old age
smokers, obesity, lack of exercise

112
Q

White thrombi

A

arterial thrombi. blood flow in arteries is faster and more laminar, thus fewer red cells are trapped in the fibrin.

113
Q

white clot syndrome/ “heparin induced thromocytopenia”

A

this is a dread illness caused by antibodies against a complex of heparin and platelet factor 4.
masses of platelets become the white clots existing thrombi extend, and moderate thrombocytopenia occurs

114
Q

Fibrinolysis

A

thrombi begin breaking down as soon as they are made. –> balance

115
Q

violin strings

A

thrombi that embolize to the lung and organize over months, leaving the lumen almost fully patent

116
Q

DIC results whenever

A

blood clotting is activated through the circulating bloodstream

117
Q

In DIC

A

platelets and clotting factors are consumed - consumption coagulopathy - then plasmin is activated

see schistocytes and thrombocytopenia. little fibrin thrombi
progression to bleeding from many places, including mucosal surfaces

118
Q

DIC is both

A

“too much clotting” and “too much bleeding”

Death Is Coming

119
Q

Fragmented red cells

A

=schistocytes

120
Q

schistocytes and thrombocytopenia (too few platelets)

A

consider DIC

121
Q

black plague got its nickname from

A

the DIC that’s often seen, producing gangrene

122
Q

meningococcemia

A

DIC is part (not all) of the picture in meningococcemia

123
Q

if this morning’s venipuntrue site/ your current IV site starts to bleed, consider

A

DIC

the mechanism is that plasmin has destroyed the fibrin holding the “injury” together

124
Q

Tests for DIC

A

D-dimer, fibrin spli products

125
Q

Causes of DIC:

thromboplastin gets into the blood

A 
various obstetrical catastrophes
disseminated cancers
acute promyelocytic leukemia
large infarcts
really bad intravascular hemolysis (think of bad malaria)
snakebite
126
Q

Causes of DIC:

damaged endothelim

A

reickettsial disease
meningococcemia
vasculitis
toxemia of pregnancy

127
Q

Causes of DIC

thromboplastin in blood AND damaged endothelium

A 
bad trauma, 
big infarcts
shock
gram negative sepsis
burns 
heat stroke
ebola, marburg, and probably other emerging infections
128
Q

pulmonary thromboembolus

A

thrombus–> embolizes and gets stuck in the lungs can be fatal

129
Q

paradoxical embolus

A

from venous side, through foramen oval and out to systemic circulation

130
Q

amniotic fluid embolus

A

from placenta–> lungs see keratin from unborn child in lungs

131
Q

air embolus

A

about 100 ml of air is sufficient to kill

132
Q

gas emboli have many causes

A

decompression sickness (most feared hazard of scuba diving)

133
Q

fat embolization

A

most often follow fracture of a long bone

from broken ribs during CPR

134
Q

in the brain with massive fat emolisation,

A

petechia occur throughout the with matter, no body knows why.

135
Q

bone marrow embolus

A

from broken ribs during CPR

136
Q

atheroembolie

A

choleterol embolic from an atherosclerotic plaque. spindle like.

trash foot

137
Q

Heroin is often cut with other substances such as

A

talc

138
Q

Intravenous heroin users may have ______ in lungs.

A

talc granulomas. the talc is inside the vessels, hence injected, not inhaled

139
Q

what can embolize

A

lots of things. silicone. peanut butter. fat. air. thrombi

140
Q

White infarcts

A 
arterial insufficiency
and 
not reperfused
and 
single blood supply
141
Q

Red infarcts

A

venous insufficiency
or
Reperfused
or Dual blood supply

142
Q

infarct

A

area of ischemic necrosis caused by loss of the blood supply

143
Q

arterial infects can result form

A 
thromboemboli
thromb formin in situ
atheroemboli
hemorrhage into an atherosclerotic plaque (small artery)
tumor in an artery (rare)
144
Q

venous infarcts can result from

A

any cause of congestion

remember twisting of a vascular supply

145
Q

lung infants are always _____ . Why

A

red

dual blood supply

146
Q

Bowel infarct always ____ because

A

red

usually venous, and always reperfused

147
Q

strangulated hernia

A

compromise of the venous return causes bowel infarction

148
Q

_____ and _____ have dual blood supplies. If you aren’t in shock already, it’s practically impossible to infarct them

A

lung and liver

149
Q

brainstem infarcts are mostly ____

A

pale

150
Q

are kidneys easy or hard to infarct

A

easy. only have one blood supply

151
Q

testicular torsion leads to a

A

venous infarct

152
Q

decubitus pressure ulcers are

A

basically infarcts, since the tissue dies because of ischemia. infection and other factors keep the process going
weight of the person keepl the blood from getting to the area, occluding the veins.

153
Q

Watershed infarcts

A

necrosis at the places that are farthest from the arterial supply

after shock (systemic hypo perfusion)

154
Q

Shock

A

whenever there is widespread under perfusion of the body, for whatever reason.

our bodies have a limited ability to deal with a damaged heart, loss of blood/ water, or loss of vascular tone.

if the underlying problem is not or cannot be fixed, shock is self perpetuating, further damaging the body until death results.

155
Q

Three main categories of the causes of shock

A

hypovolemic
cardiogenic
loss of vascular tone

156
Q

Causes of shock - cardiac

A

big MI, rupture, diphtheria, some poisons, tamponade, PULMONARY EMBOLI

157
Q

causes of shot - hypovolemic

A 
hemorrhage (internal, external)
other fluid (sweat, vomiting, diarrhea, burns, 3rd space)
158
Q

causes of shock - lost vascular tone

A

septic/total body inflammation/ Toxic shock syndrome (superantigens, etc)
anaphylacitic (capillaries relax and leak)
neurogenic (poisons, war gas, cord injury, vasovagal)
meds (especially some anesthetic agents)
other leaky capillary syndromes (dengue, ebola, more)

159
Q

lactic acidosis

A

poor perfusion, too little oxygen to tissue
a host of poorly understood chemical mediators, there have been attempts to target some of these molecules, but so far there has been little success

160
Q

Compensated shock

A

you are shunting blood.
the body sends what blood is available to brain and heart first. measured blood pressure is maintained, but the kidneys, gut liver, skin are probably under perfused

pale, cold
don’t look that bad. might have a fast pulse and or respirations, and you’ll die soon unless the underlying problem is corrected

161
Q

progressive shock/ decompensated shock

A

you are going anaerobic

kidney and liver cells are probably mostly dead, the anaerobic metabolism has shot the lactate levels up and the pH down, and other things are being released into blood from oxygen deprived tissues

the acidity in much of your body DILATES arteries that would better be constricted, and blood pools in them. and pH drop interferes with heart function and much more.

look horrible, vital signs are bad. If and only if, we fix the cause of shock can we still save you

162
Q

irreversible shock

A

you will be dead soon

there has been sufficient damage to your body from lack of perfusion that NO intervention can save you

lysosomes are digesting your cells, and your gut mucosa is probably permeable to bacterial products

you can still make your will ,make decisions involving your care, etc, but you WILL die within a few hours

163
Q

shock not only _______ but ______

A

stops the machine, but wrecks the machinery

164
Q

after a few hours in shock, expect to see

A

diffuse hypoxic brain injury
subendocardial necrosis
contraction bnd necrosis in the myocardium
acute tubular necrosis in the kidneys
“stress lesions” in the adrenal cortex (thick, lost lipid)
“stress ulcers”/ bleeds in the stomach and duodenum
Necrosis of the small intestine (if dopamine used)
fatty change/ necrosis in the centers of liver lobules
congested liver (unless much hemorrhage)

days later :shock lung” often develops - hyaline membranes

165
Q

Sepsis

A

bacteria actually flourishing in the blood stream

is rapidly fatal if not Rx’d quickly and successfully

166
Q

Gram ____ _____ are the most common causes of sepsis, but _________ can also cause sepsis

A

gram positive cocci

gram negatives, fungi, and viruses

167
Q

Most shock patients feel _____

septic patients may feel _______ because

A

cold

warm, widespread arterialdilation

168
Q

Watershed infarction of ______ is part of the downward spiral of shock

A

subendocardium

169
Q

some people will survive shock. One sign of a previous bad episode of shock is

A

widespread scarring of the subendocardium, where the infarcts have healed. scarring can provide long survival, even if only a few cells didn’t die

170
Q

Late lung changes that follow shock ar probably caused by

A

cytokines and neutrophil products.

171
Q

late lung changes following shock

A

fibrin leaking from vessels, plastered over the air space

172
Q

cyanosis

A

blue color. when theres >5gm of unoxygenated hemoglobin in the blood it’ll look bluish. This could be because of poor oxygenation (lung disease), poor systemic perfusion (shock - all the oxygen’s being taken), or just a part of your body surface bing cold (no need to send extra blood to cold area)

173
Q

____ is basic to caring for the patient in shock, and provides support while we are preparing for definitive treatment of whatever’s the underlying cause

A

proper fluid management

Pathology (15 decks)

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