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CACP > Applied Physiology and Pathophysiology of Thromboembolic Disorders > Flashcards

Applied Physiology and Pathophysiology of Thromboembolic Disorders Flashcards

1
Q

what are the Direct thrombin inhibitors

A

Dabi, argatroban, bilvilruidin, desirudin

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2
Q

what are the Factor Xa inhibitors

A

Apixaban, Rivaroxaban, edoxaban (enoxaparin does it too)

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3
Q

what are the indirect thrombin inhibitors

A

heparin, fondaparinux (ATRIXA) , enoxaparin

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4
Q

what are the 1/2 lives of protein C and S

A

8 hours (C) and 30 hours (S)

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5
Q

How does warfarin affect protein C and S

A

Warfarin inhibits the body’s own production of protein C and protein S. Therefore, initial treatment with warfarin alone in people with protein C or protein S deficiency may temporarily make clotting worse or precipitate a new clot or a severe skin rash known as skin necrosis

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6
Q

How do protein C and protein S inhibit coagulation?

A

Activated protein C (APC) together with its cofactor protein S inhibits coagulation by degrading FVIIIa and FVa on the surface of negatively charged phospholipid membranes.

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7
Q

Patient with HIT (caused by LMWH/Heparin) are at elevated risk for

A

venous/arterial thrombosis
myocardial infarction
skin lesions

all due to development of HIT antibodies

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8
Q

what are the clear signs of HIT?

A
  1. platelet count fall > 50% and Platelet nadir >20kg/ul
  2. clear onset between 5-14 days or platelet fall < 1 day (with prior heparin exposure in the past 30 days)
  3. new confirmed thrombosis, skin necrosis at heparin injection site, anaphylactoid reaction after IV heparin bolus, adrenal hemorrhage
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9
Q

what is Immune thrombocytopenia

A

platelets become coated with autoantibodies to platelet membrane antigens, resulting in splenic sequestration and phagocytosis by mononuclear macrophages (shortens lifespan of platelets) decrease number of platelets

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10
Q

What is secondary ITP

A

what immune thrombocytoenia does but it is assoicated with another condition like (HIV, HCV, SLE, CLL)

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11
Q

The condition caused by severely reduced activity of the von Willebrand factor cleaving protease ADAMTS13. (characterized by arteriolar platelet rich thrombi, kidney dsyfunction, thrombocytopenia) is known as what?

A

Thrombotic thrombocytopenia purpura

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12
Q

Can arterial flow cause platelet or fibrin based clots?

A

Platelet based (associatedw with atherscelerotic plaque, cause by turbulent blood flow that can damage arterial endothelium and activate platelets to initiate coagulation, can cause ischemia, infarction)

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13
Q

Venous flow is static and can cause _____ base clots

A

fibrin (emobolus like can morel likely to detach and travel)

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14
Q

what are the STRONG risk factors for VTE

A
  1. Hip/knee replacement/major surgery, SCR or major trauma (>10)
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15
Q

What are the moderate risk factors for VTE

A

arthroscopic knee, central venous lines, chemotherapy, congestive heart or respiratory failure, hormone replacement therapy, malignancy, OC therapy, paralytic stroke, pregnancy/postpardum, previous VTE, thrombophilia

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16
Q

what are the lowest risk factors for VTE

A 
bed rest greater than 3 days 
immobility due to sitting 
old age 
laparoscopic surgery, 
obestiy 
pregnancy and 
varicose veints
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17
Q

what are the sx/s of peripheral vascular deisease (thrombotic or emoblic causes of acute limb ischemia?)

A 
Six P 
pallor,
pain
paresthesia
payalsis 
pulselessness 
Poikilothermia (skin is cool-cold)
18
Q

what are some tests that will be done to dx DVT

A

compression US with doppler

19
Q

what are some tests that will be done to dx PE

A

CBC, Serum chemistireis, ABG, BNP, Troponin, d-dimer

20
Q

what is the Wells score?

A

is a number that reflects your risk of developing deep vein thrombosis (DVT)

21
Q

what is the Pulmonary Embolism Severity Index (PESI)?

A

is a risk stratification tool that has been externally validated to determine the mortality and outcome of patients with newly diagnosed pulmonary embolism (PE).

22
Q

what are the most frequent signs for Post thrombotic (post phlebitic syndrome)

A

Leg pain, leg heaviness, vein dilation, edema, skin pigmentation, and venous ulcers

23
Q

what are some treatments that can minimize the symptoms of post thrombotic/phelbitic syndrome?

A

Exercise, limb elevation, compression therapy

24
Q

what are the risk factors for AFIB, Aflutter?

A

HTN, CAD, valvular heart disease, cardiomyopathy, cogenitial heart disease, VTE disease, Obstructive sleep apnea , obesity, DM, metabolic syndrome, CKD

25
Q

what are the sx/s of AFIB/AFlutter

A

Fatigue, rapid heart beat, flutter/thumping in chest, dizziness, SOB, anxiety, weakness, faintness, confusion, sweating

26
Q

Define Paroxysmal AFIB

A

when heart returns to normal rythm on its own or w/intervention within 7 days.

(people w/this type may only have a few episodes throughout the yr, they are unpredictable and will usually turn into permanent)

27
Q

Define Persistent AFIB

A

irregular rhythm that lasts longer than 7 days, this type will not return to normal sinus rhythm and will require some form of treatment

28
Q

Long standing vs permanent AFIB

A

long standing = irregular rhythm that lasts longer than 12 months
permanent= last indefinitely and the patient/dr have not decided to continue further attempts to restore normal rhythm.

29
Q

what are the risk factors for ischemic stroke

A 
HTN
DM
Smoking 
dyslipidemia
physical inactivity
Sickle cell 
age/family 
afib and carotid artery stenosis
30
Q

what are the risk factors for hemorrhagic stroke

A

aneurysms, HTN, anthrombitic therapy, ETOH

31
Q

what is the major distinguishing characteristics of a TIA

A

blow flow returns on its own (bld flow is blocked from the brain for a short period of time less than 5 mins)

32
Q

what are the types of bioprosthetic valves?

A

Mosaic, hancock carpentier edwards perimount, biocor

mitorflow

33
Q

what are the types of mechanical valves?

A 
St jude (bileaflet mechanical valve) 
Medtronic hall (Monoleaflet) 
Cage ball valve (Starr edwards)
34
Q

what are the low Thrombogenic heart valves

A

st jude medical
ON-X
carbomedics
medtronic Hall

35
Q

what are the medium Thrombogenic heart valves

A

bileaflet

bjork shiley

36
Q

what are the high Thrombogenic heart valves

A

lillehei-kaster
omniscience
starr edwards

37
Q

what are the s/sx of Heart failure

A 
increase edema 
SOB 
DOE (Dyspnea on Exertion)
weight gain 
trouble sleeping (cant lie flat) 
loss of appetite
38
Q

how dose exacerbations of heart failures effect anticoag therapy

A

increase INR value due to an increase in hepatic congestion and decreased warfarin catabolism.

39
Q

what are the risk factors for CAD and cardiac ischemia/infarction.

A 
Smoking 
HTN
High cholesterol
obesity 
Hyperglycemia 
poor diet
40
Q

What are the sx/s of CAD and Cardiac ischemia/infarction

A

Angina, pain in upper body, DOE, Sweating, N/V, Dizziness, palpitations.

CACP (8 decks)

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