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178 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
factors that when increased, increase risk
APOB48, APOB100, APOCIII, APOE-4,PCSK9, APO Lp(a), OLTP
factors that when increased, decrease risk
LDLR,HDLc,PCAT, ABCA1, CETP, APOCII, APOA5, APOE-2, LPL, ACAT
THROMBIN
topical, arrest minor bleeding
GELFOAM
absorbable collagen, surgery/trauma
Heparin
IV/SC, potentiates ATIII,

sides: bleeding

used DVT, PE, lab samples

protamine sulfate antagonist
lepirudin
hirudin derivative

irreversible thrombin inhibitor

used when heparin contraindicated

monitor aPTT

sides:decreased Hgb, BP
bivalirudin
hirudin derivative

reversible thrombin inhibitor

use coronary angioplasty

bleeding at site of puncture

short acting
warfarin (coumadin)
vitamin K antagonist

(rescue: fresh plasma, konakion/aquamephyton vit K)

enzyme induction, increased clotting facotrs, increased VITK ingestion/absorption decrease warfarin effect
dabigatran etexilate
use atrial fibrillation, or following surgery

direct thrombin inhibitor
aspirin
decrease TXA2
clopidogrel
irreversible block ADP receptor on platelets

inhibits binding of fibrinogen to platelet

sides: TTP
ticlopidine
irreversible inhibition adp binding fibrinogen to platelet

thrombasthenia like state

use for acute cerebral ischemia

sides: severe neutropenia
prasugrel
inhibits platelet aggregation by PalphaY12 receptor ADP

used before angioplasty

significant and fatal bleeding
TTP
ticagrelor
inhibits platelet aggregation by PalphaY12 receptor ADP reversibly

faster onset

more minor bleeding and respiratory conditions
dipyridamole
increased [cAMP] in plateleys, inhibits phosphodiesterase, inhibits metabolism

not used as monotherapy, used with warfarin

prophylaxis for prosthetic heart valves
prostacyclin (PGI2)
increase [cAMP] in platelet
stimualtes adenylate cyclase
increased cAMP
decreased platelet activity
decreased cAMP
increased platelet activity
streptokinase
short half life
complexes with plasminogen and activates

systemic plasminogen activation
fibrinolysis
urokinase
cleaves arg-arg peptide bond in plasminogen
systemic
t-PA
activates BOUND plasminogen (bound to fibrin)

clot specific, not systemic
aminocaproic acid
binds to lysine binding sites on plasminogen, prevents plasmin binding fibrin

antifibrinolytic

reduces OD of fibrolytic agents

new clots not lysed

sides: muslce weakness/myopathy
platelet activation
adp, serotonin, collagen, thrombin, TXA2
TTP
disorder of vWF
deficiency in ADAMSTS13 (cleaves vWF into Fx form)
inherited:protease def
acquired: autoimmune
vWF
complexes with factor VIII

stored in alpha granules and weibel-palade bodies (endotheliall cells)

made by endothelial cells
vWD
most common inherited bleeding disorder
HIT heparin induced thrombocytopenia
hypercoagulable
immune rxn to IgG to heparin bound PFIV

fab portion IgG binds to PFIV-HEPARIN and Fc binds to platelet receptor activating platelet

microvascular thrombi, PE, gangrene, stroke, MI

more likely with unfractionated heparin

less with LMWH

usually give patients chance to correct, can give protamine
platelet storage pool disorders
def. in alpha granules(fibrinogen, PDGF, PFIV) or dense granules (serotonin, CA++, ADP) or both
bernard-soulier syndrome
GPIbIX/V deficiency,

vWF cannot attach to subendothelium
glanzmanns thrombasthenia
GPIIbIIIa
cannot aggregate
findings in coagulation disorder
delayed bleeding, hemarthrosis, deep hematomas
findings in platelet/vessel disorders
petechia, purpura, superficial bleeds, mucosal bleeding
vWD
VIII, bleeding time, vWF
hemophilia A
x linked recessive
hemarthrosis, delayed bleed
aPTT
VIII

most common severe congenital bleeding disorder
bleed everywhere
hemophilia B
x linked recessive, hemarthrosis, delayed bleeding
aPTT
IX
christmas disease
bleed everywhere
hemophilia C
aPTT
XI
autosomal recessive
jews
mild to moderate
aPTT
intrinsic, heparin
PT
extrinsic, coumadin
Vit K deficiency
nutritional, mutation in gene encoding y-glutamyl carboxylase
lupus anticoagulant
anti-phospholipid antibody syndromes
common acquired hypercoagulability
lab tests look like cant clot, clot quicker
Hx of miscarriages, odd thrombosis sites, no Hx of bleeding
hyperfibrinolysis
occurs with liver disease
secondary to DIC
increased DDIMERS
elongated PT
T-TM
thrombin-thrombomoduliin activate protein C cleaves V/VIII
factor V leiden
APC resistance
ATIII deficiency
serpin def.
autosomal dominant
DVT
high risk stasis, mi, dic,
localized pain, heat, redness, swelling

often asymptomatic

Dx ddimers, ultrasound
given warfarin to avoid newly synthesized clotting factors
clotting cascade
XII-XI-IX-VIII-X-V-II(thrombin)-FIBRIN

or

VII-X-V-II
immune complex vasculitis
systemic, immunological
IG and complement found in lesion
circulating complecces

in SLE anti-dna complexes found in vessels

some caused by hypersensitivity to drugs

viral infx as well
drug hypersensitivity vasculitis
Ig against drug modified proteins
skin is often a target
mild to fatal
viral infx vasculitis
Ig to viral proteins

30% of patients with PAN (polyarteritis nodosa) have Hep B related immunovascultitis)
ANCA
circulating Ig reacts with neutrophil granules
cANCA
antiPR3
pANCA
antiMPO
Anti Endothelial Cell Antibodies
SLE
KAWASAKI
Polyarteritis Nodosa
small/medium arteries (other vessels not involved)
renal/gi common
renal cause of death
young adults
HTN, wt loss, fatigue, melana, fibrous thickening vessel wall, lethal

lesions are different ages in same vessel

no glomnephritis, no pulmonary
microscopic polyangitis
arteries, caps, venules
lesions of same age
palpable purpura of skin
glomerulonephritis, pumlonary
hemoptysis, athralgia, proteinuria, hematuria
pANCA
most lesions devoid of immune complexrs
no granulomatous inflammation

immune rxn to drugs, tumor antigens, microorganisms
churg-strauss
allergic granulomatous angitis
pANCA
eosinophilia
neutrophilic infiltration
giant cell arteritis
temporal arteries, large and small arteries, thickened, tender, nodular,

most common vasculitis in elderly


granulomatous, nodular thickening intima, fragmentation of IEL
temporal, opthalmic, vertebral, aorta
permanent blindness
takayasu arteritis
granulomatous
med/large
ocular Sx
weakneed pulses upper extremities
neurodeficits, numb extremities
visual deficits
infectious arteritis
direct invasion of bacteria/fungi
mycotic aneurymss
kawasaki
children, infants
conjunctivitis
coronary
microcutaneous lymph node syndrome
skin rash, fever
transmural thickening
t-cell activation, secrete cytokins, b cell hyperactive, antibodies to SMC and EC
wegeners granulomatosis
necrotizing vasculitis
upper resp
mimics tb
renal involvement
more males that females, around 50 years old
cANCA
thromboangitis obliterans
buergers disease
medium/small arteries
male smokers under 35
hypersensitivity to tobacco compounds
distal finger/toes gangrene, necrosis, pain
cavernous hemangioma
von hippel lindau in brain stem retina, red-blue spongy lesions, large cavernous bloood filled spaces
skin mucosal surfaces
capillary hemangioma
capillaries/connective tissue
skin and usbcu
red to blue lesions
smaller generally
glomous tumor
from glomous body
red blue
painful
distal fingers and toes
branching vascular channels
under nails
hemangioendothelioma
well differentiated w channels, some malignant characteristics
angiosarcoma
virtually no vascular channels
anaplastic spindle cells
VAT
vinyl chlorida
arsenic
thorotrast
kaposis sarcoma
HHV8
aids
von hippel lindau
autosomal dominant
deletion UHC gene (tumor suppressor)

hemangioblastoma/cavernous hemangioma in brainstem or retina
liver, kindey, pancreas cyst
oslo weber rendu
autosomal dominant
mutation TGFb binding proteings
mormons
dilations and convolutions of capillaries
hemorrage, gi bleeds
sturge weber syndrome
congenital
ipsilateral port wine stain of face
glacuoma
meningeal hemangiomas
mr, seizures
retinal detachment
meds that cause immune thrombocytopenia
quinine, heparin, sulfonamides, gold salts, antibiotics, sedatives, antiinflammatory, antiplatelet, hairspray
meds that suppress platelet production
etoh, chemo, thiazide diuretics
ITP
autoimmune platelet destruction (gpIIbIIIa)
impaired megakaryocyte maturation
give corticosteroids, splenectomy

if doesnt work, immunotherapy, tpo mimetics

itp in children associated with vaccinations
resolve on own, no corticosteroids
gestational thrombocytopenia
during pregnancy
acquired platelet disorders
aspiring, uremia, liver disease, myeloma, cardiopulmonary bypass
platelet adhesion defect
bernard soulier, gpIb, vWF def.
platelet aggregation defect
gpIIbIIIa
scott's syndrome
factor X/V
antiprostaglandin antiplatelet
aspirin
antigpIIbIIIa
abciximab/epitfibatide
adp receptor PalphaY12 antagonist
clopidogrel
factor XII deficiency
will not show up with aPTT or PT
PT
tissue factor, extrinsic, heparin
aPTT
intrinsic, coumadin,
warfarin blocks
2,7,9,10, c,s
coumadin overdose cause
antibiotics decrease gi flora that produce vit k
coumadin od tx
vitk fresh frozen plasma prothrombin complex
heparin od tx
withold heparin, protamine sulfate
liver disease thrombocytopenia tx
mgt liver disease, fresh frozen plasma, cryoprecipitate, vit K
DIC
infx, shock, cancer, pregnancy triggers

innapropriate coagulation consumes factors V and VIII and platelets

lots of microemboli, lots of hemolysisi, increased fibrinolysis, thrombocytopenia,
primary fibrinolysis
snake bites, electrocution
abnormal fibrinolysis
secondary triggered by DIC
increased PT, increased DDIMERS

tx tPA and urokinase
TTP
neuro, febrile, hemolytic anemia, renal impair, thrombocytopenia

inhibition adamsts13

tx plasma
thrombin time
detetcts fibrinogenemia, dysfibrinogenemia, heparin, ddimers
ristocetin
Dx for vWD, antibiotic reacts with vWF, wont clump in pt deficient in vWF
hemophilia a mgmt
DDAVP (releases factor VIII)
viii concentrates
heme b management
factor IX concentrates
heme C tx
fresh frozen plasma
factor VIII inhibitor
IgG to factor VIII
catastrophic bleeding
preg, autoimmune, tumors, skin disease

if give factor VIII concetrates, will not improve much (because antibody present)
antiphospholipid synfdome
Ig reacts with phospholipids involved with coagulation

also called lupus anticoagulant

SLE, viral infx, cocaine, procainamide, quinine, antibiotics can cause

recurrent miscarriage, thrmobosis, stroke dementia, visual changes

PTT not corrected with plasma, PT prolonged too


no bleeding problems, thrombosis problems
TFPI
inhibits extrinsic pathway
atiii
inhibits thrombin activation
Factor V leidin
apc resistnace
thrombomodulin, protein C and S
prevent thrombin activation factor V
HIT
PFIV
alpha granules
binds heparin, generates anticomplex IgG
Fc binds platelet, activates, clumping, reduces platelets

tx with direct thrombin inhibitors and cooumadin after normal platelet counts
ddavp contrainidcated
if ristocetin clumps platelets
itp diagnosis
of exclusion
statins
HMG-coA reductase inhibitors
inhibits serum cholesterol
lowers BP
increases eNOS
ezetimibe
blocks chol reuptake form gut
bile acid resins
binds bile acids, prevents reabsorption
niacin
inhibit lipase activity
inhibit generation VLDL
increase HDL most
bile acid binding resins
colestipol, cholestyramine,

not used as monotherapy
lower ldl, increase HDL
impair absorption vitamins, gi problems

increased VLDL increased TG sythesis by liver
statins
force liver cells to import LDL from bloodstream
decrease absorption from meal, decreased LDL

increased synth LDLR

platelet inhibition
increased eNOS

elevated liver enzymes, elevated CPK (myopathy)

carcinogen, teratogenic
ezetimibe
used with statins
inh absorption choelsterol from gut
niacin
inhibit adipose lipolysisi
decreased FFA supply to liver, decreased LDL, increased HDL

GOUT, HYPERURICEMIA vasomotor flushing
fibric acid derivatives
increased transcription of LPL

gemfibrozil

activate receptor in liver and muscle that increases LPL?FA oxidation decrease TG synthesis

GALLSTONES
liver enzymes
myopathy

fenofibrate
lower myopatthy
statins and pregnancy
contraindicated
cholestyramine monotherapy bad
increased VLDL TG
EtOH
increased TG
FIBRATES
LPL, gallstones
statins
liver enzymes
antianginals decrease O2 demand
beta blockers, ca2 blockers, nitrates
increase o2 supply antianginals
vasodilators, ca2 blockers, statin, antithrombitcs, bypass
adenosine
reduce tachicardia
atropine
increase heart contraction
nitrates
pools blood in veins, decrease wall tension, relieves vasospasm, decreased platelet aggregation

nitrogylcerin patch-longer term

rebound tachycardia

dilation, dizziness, reflex tach
angina tx with nitrates
acute, unstable, stable, variant
ca2 channel blockers
inhibits contraction

verapimil/diltiazem-cardiac and vasodilator activity

high doses cause CHF (decreased HR, CO) be careful with beta blockers

nifedipine(dihydropyridines)only vasodilator (variant, stable angina) no cardiac effect\
reflex tach

arteriolar dilators

peripheral edema
angina tx with ca2 blockers
variant, stable
beta blockers
b1-metoprolol-decrease HR, SV, o2 demands, increase diastolic perfusion time

b2-propanolol-peripheral vasoconstriction


block tach reflext by nitrates and ca2blockers

not effective for vasospasm
beta blockers angina tx
stable, unstable
nitrates
meningeal headaches, increase HR, cardiac force
prophylactic for stable angina
diltiazem
diuretics
reduce sodium, water, filling pressure
digoxin
increase Ca++

heart failure

inotropic
dobutamine and milrinone
increase cAMP, PKC, CA++
inotropic

heart failure
ace inhibitors
prevent angI--angII
inhibit cardiac remodeling
metoprolol
stops aldosterone
ace inhibitor and potassium sparing diuretic
long term inotropic
digoxin
contraindicated in CHF
ca2blockers
digoxin milrinone dobutamine
increase CO, force contraction
diuretics/venodilators
decrease preload,
arterial vasoldilators
decrease afterload
increase cardiac output
ace II/ANG II blockers
decrease pre and afterload
low dose beta blockers
decrease SNS, bisprolol., carvediol, metoprolol
digoxin MOA
inhibts NA atpase

stimulates vagus nerv, decrease HR, od causes bradycardia and heart block
systolic dysfx, fix and cause antoarrythmia
dobutamine MOA
beta agonst, brings CA++ in
digoxin tox cure
K+ and Mg, reduced CA

increased quinidine increase dig toxicity because similar mechanisms
beta agonists
dobutamine for acute CHF
increase contraction
milrinone/inamrirone
increase contraction, vasodilator decreases pre and afterload

phosphodiesterase inhibitor


acute chf
beta blockers
stable chf
block RAAS, SNS
digtoxin bradycardia blocked by
atropine
gm-csf
increase neutrophils in response to kidneys
epo
released by kidney in response to hypoxia
b12 def
neural problems
b12, folate def
macrocytic
iron def
microcytic
iron tox
emesis, lavage, chelator, bicarb
etoh
increase VLDL
exacerbates gallstones
gemfibrozil
CPK affected
statins
raises HDL, lowers LDL
niacin
all angina tx
nitrates
stable unstable angina
beta blockers
variant and stable agina
ca2 blockers
nitrate side
reflect tach, contractility
cause orthostatic hypotension
nitroglycerin/prazosin
isoproterenol
increase o2 demand, worsen angina
nifedipine
exclusiveley reduces afterload
verapimil
variant angina

causes tach
metoprolol
decrease contractility
nitroglycerin
increase venous capacitance

rapid
chronic recurrent stable angina
metoprolol

esmolol has short half life
beta blockers reduce chf mortality and negative inotropic effect
carvediol, metoprolol ,bisprolol
digoxin
increase ef
atropine
counteracts dig bradycardia