Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PULM > PULM Week 5 Lectures > Flashcards

PULM Week 5 Lectures Flashcards

1
Q

what is plasma

A

obtained when blood is collected into an anticoagulant and the cells are removed (clotting factors still in inactive form)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is serum

A

obtained when blood is allowed to clot, clot separated into fibrin clot and serum (clotting factors activated and fibrinogen is depleted)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are platelets

A

“first defence”

formed from megakaryocytes (white blood cells synthesized in marrow)

non-nucleated

2-3 um in diameter

half life of 5-9 days

150-400 X 10^9 / L

activated by thrombin or ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what activates platelets

A

thrombin or ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

half life of platelets

A

5-9 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

where are platelets synthesized

A

formed from megakaryocytes in the marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is Virchow’s triad of normal hemostasis

A
  1. normal vascular epithelium
  2. normal blood flow
  3. correct hemostatic balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the mechanism of fibrin clot formation?

A

damaged endothelial layer–> platelets adhere–> platelet plug formation (aggregation) –> fibrin clot formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe a primary clot

A

“platelet plug”

3 As: ADHESION, AGGREGATION, ACTIVATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe a secondary clot

A

coagulation cascade + negative feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe the clotting cascade associated with a secondary clot

A

enzymes (proteases)–most of the facrors

coenzymes V and VIII

cofactors calcium and phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe the factors in negative feedback associated with a secondary clot

A
  1. anticoagulants: antithrombin–inhibits proteases; TFPI–inhibits proteases, mainly VIIa anf TF; thrombomodulin + protein C & S–breakdown coenzymes V and VIII
  2. fibrinolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 2 processes involved in thrombosis

?

A
  1. platelet plug formation

2. fibrin clot formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what leads to clotting? what is the pathway?

A

tissue damage leads to fibrin clot formation

initiator (tissue damage) –> activation of clotting factors–> FIBRINOGEN (soluble)–> [via THROMBIN]–> fibrin (insoluble) blood clot

initiator is TISSUE FACTOR (inside every cell)–lysis of cells leads to exposure of tissue factor (TF) which initiates the clot cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is thrombolysis

A

tissue repair and fibrin clot dissolution

blood clot–> [via PLASMIN] –> fibrin degredation products (soluble and cleared by liver–also called d-dimers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is fibrinogen

A

very complex protein made up of 6 polypeptides

shaped like a dumbbell

three globular domains linked by triple helices

activated by CROSS LINKING–introduced to factor XIIIa, which induces a covalent bond between lysine and glutamine residues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the role of vitamin K in thrombosis

A
  • some clotting factors require vitamin K dependent carboxylation during their biosynthesis to be biologically active
  • vitamin K is a fat soluble vitamin found in vegetable oils and green leafy veggies, also synthesized by gut flora
  • normally, gut bacterial synthesis is sufficient

i. e Carboxylatin of glutamic acid residues into gamma-carboxyglutamic acid (Gla)
1. Gla binds calcium leading to conformational change
2. Ca2+-Gla-proteins can bind to phospholipid membranes (supplied by activated platelets at the site of injury)
3. ensures fibrin formation occurs at injury site instead of in flowing blood
4. the Gla is absolutely REQUIRED for the membrane binding
5. non-carboxylated kitamin K dependent proteins are biologically inactive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

list Ca2+-Gla-proteins

where can they bind?

A

factor VII, X, IX, prothrombin (“vitamin K proteins”)

only these types of proteins can bind to platelet plug
(factors Va and VIIIa can also bind but not through Gla)

complexes allow for CONCENTRATION, ORIENTATION and LOCALIZATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is factor XII

A

factor XII deficient patients do not bleed–probably has non-coagulation functions

factor XIIa plays a minor role in hemostasis–activated by poly-phosphate on the activated platelet surface (negative charge)

resulting factor XIIa activates factor XI to factor XIa generating THROMBIN to further platelet activation after complex is formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

describe the termination of clotting

A
  1. dilution of flowing blood
  2. trapping of proteases in growing fibrin clot
  3. serine protease inhibitors (SERPINS) such as ANTITHROMBIN binds to active site of thrombin and forms inactive complex
  4. antithrombin deficiency can lead to risk of thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what initiates the coagulation system

A

tissue injury that exposes TF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do platelets play a role in clotting

A

support and enhance activation of the coagulation system by providing a surface onto which clotting factors assemble and by releasing stored clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is TF

A

membrane protein present on the subendothelial cellular components of the vessel wall (i.e smooth muscle cells and fibroblasts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what clotting pathway does TF activate?

A

the extrinsic pathway, which then in turn activates the intrinsic pathway

both pathways meet at the common pathway–> THROMBIN activation–> fibrin activation and crosslinking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what compounds are produced by endothelial cells that play a role in termination of clotting

A

thrombomoduling
antithrombin
TFPI

endothelial cells also activate fibrinolytic mechanisms through production of tissue plasminogen activator 1, urokinase, plasminogen activator inhibitor and annexin 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what does thrombomodulin do

A

binds to thrombin, activates proteins C & S, and inactivates factors Va and VIIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does antithrombin do

A

inhibits the proteases VIIa, IXa, IIa (thrombin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what does TFPI do

A

inhibtis proteases, mainly VIIa, TF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what does plasminogen do

A

plasminogen–>plasmin–>cleaves fibrin to FDPS, D dimers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

describe the extrinsic pathway

A

vascular injury–>TF –>factor VII-TF–> factor VIIa-tissue factor –> factor IX converts to factor IXa and factor X to factor Xa, both of which feed into the intrinsic pathway

the two pathways meet at Factor Xa production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

describe the intrinsic pathway

A

factor XI–>factor XIa–>converts Factor IX to factor IXa, which works with Factor VIIIa to convert Factor X to factor Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

describe the common pathway

A

starts with the meeting of the intrinsic and extrinsic pathways at factor Xa, which then converts prothrombin to thrombin

thrombin converts fibrinogen to fibrin which then goes on to be cross linked fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are clot busters

A

break up fibrin polymer network to restore normal blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how is plasminogen activated?

A

the inactive plasminogen form is activated due to plasminogen activator–tPA, uPA, streptokinase

after activation it becomes plasmin which is an enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

uPA

A

urokinase plasminogen activator

converts plasminogen to plasmin through TISSUE REMODELLING

not most important enzyme to make plasmin for clot busting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

tPA

A

tissue plasminogen activator

interacts with cofactor molecule (actual clot)

problems with tPA result in stroke due to too much bleeding

> 40% of patients clots are resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what does plasmin do?

A

it is a protease and it cleaves the triple helix of the fibrin polymer –produces d dimers that are soluble and cleared by the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what can be used as a marker for thrombosis

A

d dimer presence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

describe the protein C-protein S pathway

A
  1. thrombomodulin appears on endothelial cell plasma membranes
  2. once enough thrombin has accumulated, it interacts with thrombomodulin
  3. through negative feedback mechanisms, converts thrombin from procoagulant to anti-coagulant
  4. does this by exposing a new active site on the thrombin molecule and blocking procoagulant binding site
  5. leads to activation of protein C (a protease) with protein S
  6. this leads to inactivation and cleavage of factor Va, VIII (cofactors on platelet membranes)

deficiency of protein C or S results in increased risk of thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how does antithrombin work?

A

it is a glycoprotein that is found free floating in the blood

produced by the liver

most important and prevalent

particularly inhibits THROMBIN/Xa

negative feedback–binds to active site of thrombin and forms and inactive complex–does not allow thrombin to activate fibrin formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how does heparin work

A

accelerates the antithrombin-thrombin association

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

list the tests used to monitor coagulation

A
  1. D-dimer test
  2. prothrombin time (PT)
  3. activated partial thromboplastin time (aPTT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

d dimer test

A
  • detects for the presence of a THROMBUS

- normal values are

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Prothrombin time (PT) test

A
  • used to monitor coagulation state when patient is on WARFARIN
  • measures the time required for coagulation from the EXTRINSIC and common pathways
  • involves addition of thromboplastin and Ca2+ into plasma sample
  • now given as the International Normalized Ratio
  • measurement of clotting time
  • prothrombin time (in seconds) for a normal individual varies from lab to lab, country to country–caused problems
  • INR created to standardize the test–each manufacturer assigns an ISI value
  • normal INR = 1
  • on anticoagulant drugs, INR is >1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Activated partial thromboplastin time (aPTTT)

A

used to monitor coagulation state when patient is on HEPARIN

measures the time required for coagulation from the INTRINSIC and common pathways

involves addition of partial thromboplastin and Ca2+ and kaolin into plasma sample

also called partial thromboplastin time

thromboplastin is a crude brain extract of phospholipid and tissue factor

partial thromboplastin consists of phospholipid but no tissue factor

46
Q

what are the important hereditary risk factors for venous thrombosis?

  1. gain of function factor
  2. loss of function factor
A
  1. factor V Leiden
    prothrombin gene mutation
    increased factor VIII
  2. protein C deficiency
    antithrombin deficiency
    increased homocysteine
47
Q

what are the three overall groups of acquired risk factors for venous thrombosis

A
  1. stasis
  2. vascular injury
  3. hypercoagulative state
48
Q

what risk factors for venous thrombosis are associated with stasis

A
  1. obesity
  2. pregnancy
  3. age
  4. immobility–usually inpatients; rarely due to airline travel
  5. hospitalization
49
Q

what risk factors for venous thrombosis are associated with vascular injury

A
  1. surgery–hip and knee replacements
  2. trauma
  3. malignancy
  4. inflammation
50
Q

what risk factors for venous thrombosis are associated with hypercoagulative state

A
  1. pregnancy
  2. age
  3. malignancy
  4. hyperviscosity–i.e due to rare cancer of RBCs
  5. meds–Oral contraceptives
  6. post-partum–natural increase in factor VIII post-labor to prevent excessive bleeding can upset the pro/anticoagulant balance and result in thrombosis
51
Q

what are some other risk factors for venous thrombosis

A
  1. hormonal–> estrogen is a stronger risk factor than progesterone
  2. antiphospholipid antibody syndrome (APLS)–>body forms autoantibodies towards phospholipids; lupus anticoagulant, anticardiolipin antibodies; B2 glycoprotein antibodies–> interferes with PTT test so it looks like theyre at greater risk of bleeding but actually are at greater risk of clotting
52
Q

what % of people with first unprovoked VTE have a hereditary disorder?

A

50%

53
Q

how do hereditary and acquired risk factors come together to provide total risk for VTE?

A

if an individual has both, the effects are supra-additive, in that the relative risk due to having both is more than the sum of the individual risks

54
Q

what are hypercoagulable states

A

increased clotting factors, decreased anticoagulants and fibrinolysis

occur in the setting of:

  1. hereditary thrombophilias
  2. pregnancy
  3. post partum period
  4. age
  5. malignancy
  6. hyperviscosity (polycythemia)
  7. meds (oral contraceptives)
55
Q

name two hereditary thrombophilias

A
  1. factor V leiden

2. AT-III deficiency

56
Q

list 5 lab tests used to test for hypercoagulable states

A
  1. dRVVT (dilute Russell venom viper test)
  2. testing for antiphospholipid antibodies
  3. prothrombin time
  4. aPTT
  5. thrombin time
57
Q

what does the dRVVT test?

A
  • assessed presence of LUPUS anticoagulant (antiphospholipid syndrome)
  • mixing studies–> distinguish between clotting factor deficiency and presence of lupus anticoagulant
  1. if prolonged dRVVT coagulation time, mix patients blood with normal blood (which has clotting factors)
  2. if coagulation time is now corrected, patient has deficiency in clotting factors
  3. if the coagulation time is NOT corrected, patient likely has lupus anticoagulant
    - -> antiphospholipid syndrome
58
Q

how do you test for antiphospholipid antibodies

A

ELISA–> detect Ab to phospholipids (CARDIOLIPIN) or phospholipid binding proteins (B2-MICROGLOBULIN)

when antibodies interfere with phospholipid-dependent coagulation tests–> lupus anticoagulants

59
Q

what are you measuring when you test thrombin time

A

you incubate the plasma with thrombin (IIa) and this measures FIBRINOGEN FUNCTION only

60
Q

when do you test for hereditary factors?

A
  • unprovoked +/- recurrent VTE
  • strong family Hx
  • purpura fulminans in neonates and children–requires URGENT protein C&S testing
61
Q

what is the definition of acute heart failure

A

(acute decompensated HF)

defined as a short term or rapid change in heart failure signs and symptoms resulting in need for urgent therapy

examples include MI, arrhythmias, or sudden loss of valve function

62
Q

how does acute left ventricular failure affect pulmonary pathophysiology

A

in acute HF, there is a sudden shift of blood volume from systemic to pulmonary circulation

this causes:

  1. dilation of vessels
  2. heavy, wet, frothy lungs when cut
  3. hyaline granular fluid
  4. acute pulmonary edema–acute build up of fluid in the lungs
  5. potential pneumonia because it is an ideal culture medium
  6. frothy sputum because of surfactant
63
Q

what is the pathogenesis of chronic left ventricular failure

A

incapacity of the left heart to pump away all blood presented to it by RV

64
Q

what are diagnostic features of chronic LV failure

A

fluid accumulation in alveolar spaces

congestion
rales
microhemorrhages
rusty sputum

65
Q

what are the typical etiologies of chronic pulmonary congestion

A
  • moderate LV failure

- stenotic mitral valves

66
Q

what is the pathology of chronic LV failure in the pulmonary system?

  1. gross
  2. microscopic
A 
chronic lesions
1. i.e rheumatic fever' heavy wet lungs
2. congested capillaries
microhemorrhages
3. "heart failure" cells (macrophages engulf hemoglobin)
4. lower lobe edema
5. CAPILLARIES UNDER PRESSURE
67
Q

what happens as a result of obstruction in the pulmonary vasculature

A

whether due to something like a pulmonary embolus or anything else–> may result in changes within the right ventricle as well as the left ventricle secondarily

an increase in the afterload for the right ventricle will cause the right ventricle to first dilate (if acute) and then overtime/chronically hypertrophy (pressure overload, so concentric hypertrophy)

the hypertrophy will ultimately increase the O2 demand of the right heart

the dilation will cause a number of different malformations–i.e tricuspid regurgitation or deviation of the interventricular septum into the left ventricular chamber, reducing its volume

68
Q

what is the result of a deviated interventricular septum as a result of RV hypertrophy from pulmonary obstruction?

A

reduces the LV chamber size

this will decrease the amount of filling for the LV, which compounds the problem of less filling due to pulm obstruction

also means there is less blood to pump out to rest of body, making exercise more difficult

would also decrease coronary blood flow–> less perfusion leads to problems in overworked RV

69
Q

what is cor pulmonale

A

right sided heart failure due to pulmonary hypertension

70
Q

symptoms of cor pulmonale

A

breathlessness
peripheral edema
JVC distension
hepatomegaly

71
Q

causes of cor pulmonale/pulmonary obstruction

A
  1. PULM EMBOLISM–acute and massive–very serious
  2. acute pulmonary infection–may lead to rapid worsening of cor pulmonale
  3. chronic obstructive pulmonary disease–chronic bronchitis, emphysema (MOST COMMON CAUSE)
  4. diseases of the pulmonary vasculature (chronic thromboembolic disease)
  5. diffuse interstitial lung disease (pulm fibrosis)
  6. obstructive sleep apnea
  7. obesity hypoventilation syndrome
72
Q

name an antiplatelet agent

A

aspirin

73
Q

name an anticoagulant that is a calcium ion chelator

A

citrate

EDTA

74
Q

name an anticoagulant that accelerates inhibition of thrombin and factor Xa by antithrombin

A

heparin

75
Q

name an anticoagulant that inhibits liver carboxylation of Gla proteins

A

coumarol drugs (warfarin)

aka blood thinners

76
Q

name an anticoagulant that directly inhibits thrombin and factor Xa

A

new oral anticoagulants

77
Q

name a thrombolytic agent

A

tPA (clot busters)

78
Q

MOA of unfractionated heparin

A

-amplifies the anticoagulant effect of antithrombin III
(which is a natural plasma protease inhibitor of thrombin and factor Xa)
-inhibits factor Xa by binding only antithrombin III
-inhibits thrombin by binding antithrombin III and thrombin

79
Q

pharmacokinetics of of unfractionated heparin

A
  • very complex
  • dose-response curve is difficult to predict, therefore Tx must be individualized and monitored with aPTT
  • reduced bioavailability because it binds to a variety of plasma proteins
  • shorter half life
  • administered via IV or SC
80
Q

side effects of both unfractionated and low molecular weight heparin

A
  1. heparin-induced thrombocytopenia (HITS)–> antibodies against heparin/platelet factor 4 complex–> platelets become activated and sticky leading to thrombocytopenia, bleeding due to this, +/- thrombosis (greater chance with unfractionated heparin due to increased plasma protein binding)
  2. hemorrhage–unfractionated heparin is reversible with protamine sulfate
  3. osteoperosis
  4. hyperkalemia
  5. fever
81
Q

MOA of LMW heparin

A
  • amplifies the antigoaculant effect of antithrombin III
  • most molecules are too small to bind both antithrombin III and thrombin at the same time
  • mediates most of the anticoagulant effects through inhibition of factor Xa which minimal effects on factor IIa
82
Q

pharmacokinetics of LMW heparin

A
  • more predictable dose response curve than unfractionated
  • does not need to monitor with aPTT
  • less plasma protein binding
  • longer half life
  • administered SC
83
Q

indications for both heparin types

A
  1. treatment and prevention of inappropriate thrombosis such as VTE, PE, DVT caused by stasis, endothelial damage, or a hypercoagulable state
  2. treatment and prevention of arterial thrombosis
  3. initial management of: unstable angina, acute MI, coronary angioplasty or stent placement, cardiac surgery requiring bypass machine
  4. disseminated intravascular coagulation (DIC)
84
Q

which type of heparin is best for

  1. sick inpatients?
  2. outpatients?
  3. concern of bleeding risk and need for invasive procedures
  4. stable inpatients?
A
  1. unfractionated
  2. LMW
  3. unfractionated because is rapidly reversible protamine sulfate
  4. LMW
85
Q

which type of heparin should be used in the context of renal failure

A

unfractionated (because LMW accumulates in renal failure)

86
Q

what are the two new oral anticoagulants

A

rivaroxaban

dibigatran

87
Q

what does rivaroxaban do

A

inhibits factor Xa

88
Q

what does dibigatran do

A

inhibits thrombin

89
Q

advantages of the new oral anticoagulants

A

do not require continuous monitoring of clotting time

90
Q

disadvantage of new oral anticoagulants

A

no current antidote (bind very tightly–requires 10 hrs to clear from patient or treat with fresh frozen plasma)

91
Q

what does warfarin do? (generally)

A

inhibits liver carboxylation of Gla proteins

i.e inhibits prothrombin, factor IX, factor X, factor VII, protein C&S

92
Q

will warfarin break down already formed clots?

A

no

93
Q

MOA of warfarin

A
  • vitamin K is a key factor in hepatic activation of 4 coagulation factors (II, VII, IX, and X)
  • to act as a cofactor vitamin K must be in the reduced form (converted by VKOR
  • warfarin inhibits VKOR by blocking formation for reduced vitamin K and inhibiting activation of the 4 clotting factors
  • highly plasma protein bound–fat soluble vitamin
  • warfarin is a vitamin K analogue, so it competitively inhibits the vitamin K epoxidase (VKOR?)
  • this means that the vitamin K dependent clotting factors cant get the gamma-carboxylate group and they are unable to be activated
94
Q

pharmacokinetics of warfarin

A
  • readily and completely absorbed from the GI tract
  • inactivated by the liver and excreted through the kidneys
  • takes around 3 days to work since the relative turnover of these clotting factors is about 72 hours on average
  • it is metabolized by many different CYP450 enzymes (hence the large number of side effects)
95
Q

how is warfarin administered

A

orally (100% bioavailable)

96
Q

how is warfarin reversed

A

replacement of drug with vitamin K

97
Q

SEs of warfarin

A
  1. hemorrhage
  2. skin necrosis
  3. purple toe syndrome
  4. microembolization
  5. teratogenicity
  6. less common: agranulocytosis, leukopenia, diarrhea, nausea, vomiting
98
Q

drug interactions with warfarin

A

MANY

99
Q

indications for warfarin

A
  1. prophylaxis and treatment of VTE
  2. prophylaxis and treatment of atrial fibrillation
  3. valvular stenosis
  4. heart valve replacement
  5. MI
  6. antiphospholipid syndrome
  • replaces heparin at discharge
  • most common treatment for PE or DVT
100
Q

contraindications for warfarin

A
  1. pregnancy
  2. recent events that predispose to bleeding (stroke,surgery)
  3. platelet disorder
  4. hypersensitivity
  5. vitamin K deficiency
  6. non-steroidal anti-inflammatory drugs
101
Q

give 3 examples of thrombolytic agents

A
  1. tPA (tissue plasminogen activator)
  2. streptokinase, staphylokinase (bacteria)
  3. uPA (urokinase)
102
Q

indications for thrombolytic therapy

A

submassive PE (hypotension, severe hypoxemia, right heart failure)

selective cases of massive DVT

ischemic stroke

103
Q

MOA of thrombolytic agents

A

activate plasminogen–> plasmin

fibrin–> D2E/d dimer

104
Q

limitations of thrombolytic agents

A

bleeding risk is 3X higher than anticoagulant therapy, especially intracranial bleeding

105
Q

DDx for DVT

A
  1. varicose veins
  2. ruptured baker’s cyst
  3. muscle or tendon
  4. joint
  5. peripheral edema

*need to distinguish between deep (iliac, femoral, popliteal, tibeal) and superficial (greater/lesser saphenous vein)

106
Q

Well’s criteria for DVT

clinical likelihood for having a DVT

A
  1. active cancer
  2. paralysis or casting
  3. bedridden >3d or surgery within 3 months
  4. Hx of DVT
  5. likely alternative diagnosis (-2)
  6. calf swelling >3cm
  7. superficial veins
  8. unilateral edema
  9. swelling of entire leg
  10. localized pain over deep venous system

high risk = >4

107
Q

imaging to evaluate VTE/DVT

A

doppler ultrasound

indicated when low clinical probability with + d dimer

indicated when moderate to high Wells score

+ confirms Dx

  • repeat in 5-7 days
108
Q

DDx for pulmonary embolism

A
  1. MI
  2. pericarditis
  3. pneumonia
  4. pneumothorax
  5. chest wall pain
  6. CHF
  7. pleuritis
  8. pericardial tamponade
109
Q

what is the PE imaging protocol

A

CT scan

VQ scan can also be performed

110
Q

which anticoagulants are immediate acting? delayed acting?

A

immediate = heparin

delayed = warfarin

111
Q

which patients with diagnosed venous thromboembolism should be investigated for hypercoagulable states

A
  1. idiopathic VTE

2. VTE at young age (

PULM (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions