Exam 1 Flashcards
Virchow’s triad
stasis
vessel wall injury
hyper-coagulability
3rd most common cardiovascular illness
VTE
3rd most common cause of hospital related death
VTE
most common preventable cause of hospital related death
VTE
D Dimer
positive in presence of fibrin clot, good to rule out
test of choice for DX of DVT
compression ultrasonography
compression ultrasonography result if DVT
loss of vein compressibility, no blood flow with droppler tech
gold standard for DVT Dx
contrast venography
when do we do venography
in low risk pt with abnormal compression ultra
in high risk pt with normal compression ultra
when do we repeat compression ultra
in moderate risk pt with normal 1st compression ultra
the purpose of DVT tx
prevent PE
complication of DVT
post thrombophlebitic syndrome
chronic venous insufficiency
major difference in clinical presentation of DVT vs superficial thrombophlebitis
edema of extremity is uncommon in superficial thrombophlebitis
major difference in tx of DVT vs superficial thrombophlebitis
anticoagulation rarely required in superficial thrombophlebitis. local heat, NSAIDs are tx.
most common cause of PE
DVT (50-60% of proximal DVT embolize vs isolated calf DVT rarely embolize)
PE classifications
massive PE
submassive PE
massive PE
PE a/w SBP=40 for 15 min (that is not explained by hypovolemia, sepsis, acute MI, tension pneumothorax, new arrhythmia)
==> acute RV failure and death
most common PE symptom
dyspnea
PE signs
tachypnea, tachycardia, rales, decreased breath sounds, accentuated pulmonic component of the 2nd heart sound, JVD, sum/signs of LE DVT
most common PE sign
tachypnea
97% of pt with PE had one or more of three findings :
dyspnea, pleuritis chest pain, tachypnea
labs for PE
same as DVT, consider troponin and BNP
EKG of PE
S1Q3T3
PE signs on CXR
hamptons hump and wester mark
gold standard for PE dx
pulmonary angio
tx of VTE
anticoag med, thrombolytics, thrombectomy/embolectomy, IVC filter, prophylactics
prophylactics for VTE
TED hose, sequential compression devices (SCDs), low dose SQ heparin & Lovenox
anti coag meds
IV unfractionated heparin, LMW heparin, warfarin, fondaparinux, oral factor Xa inhibitors, oral direct thrombin inhibitors
indication for IV unfrac. Heparin
initial tx of VTE
side effects of IV unfrac. heparin
bleeding, thrombocytopenia
indication of LMWH-Lovenox
FDA approved for output tx of DVT and stable PE
side effects of LMWH-Lovenox
bleeding, thrombocytopenia
indication of warfarin
long term tx of VTE
contraindication of lovenox-LMWH
CrCl<30. elderly, obese
contraindication of warfarin
pregnancy category x
side effects of warfarin
bleeding
factor Xa inhibitors are
fondaparinux, rivaroxaban,
oral direct thrombin inhibitors
dabigatran (not approved in US), argatroban, desirudin, lepirudin
duration of anti coag tx if underlying thrombophilia
indefinite
duration of anti coat tx if cancer
as long as cancer is active
thrombolytics used for ..
unstable pt with PE, massive PE and cardiogenic shock, sever hypoxemia, substantial perfusion deficit on V/Q scan, RV dysfunction, entensive DVT
examples of thrombolytics
streptokinase, urokinase, rt-PA
IVC filter purpose
preventing DVT from propagating to lungs
absolute contraindication of IVC filter
active bleeding, anticoag
consideration of inpt vs outpt
pt is : ambulatory and stable w/ nl vitals low bleeding risk no renal insufficiency plan for LMWH/warfarin w/monitoring monitoring &tx of recurrent VTE and bleeding complications
prognosis for VTE
mortality 10-30% within 30 days
20-25% of PE cases present as sudden death
risk for recurrent and chronic morbidity
quality of life: long term anti coag
RBC life span
120 days
Hgb levels in anemia
wm <14
Hgb to Htc level ratio
1:3
reticulocytes
immature RBCs
retic count
indication of RBC production (blue on smear)
normal retic count
.5-2.5%
polychromasia
reticulocytosis (lots of blue)
causes of anemia
decreased RBC production, Increased RBC destruction, Blood loss
decreased RBC production causes
iron def, B12, folate def, chronic dz
increased RBC destruction causes
hemeolysis
nl MCV
80-100fl
nl MCH
26-34
RDW indicator of what
indicator of the degree of variation in the size of RBC
nl RDW
11-15%
anisocytosis
variation in size
anemia not noticeable till
Hgb <7-8
three main categories of anemia
hypochromic, microcytic
normochromic, normocytic
macrocytic (megablastic)
hypochromic, microcytic anemia examples
iron deg, thalassemias, sideroblastic
normo anemia example
hypothyroidsm, liver dz, chronic dz
macro anemia examples
folate def and B12 def, hemolysis
ret count in hemolysis and hemorrhage
increased
retic count in B12 /folate def
normal
most common cause of micro, hypo anemia
fe def
most common causes of fe def anemia (IDA)
menstrual blood loss, pregnancy, GI blood loss
RDW in IDA is
elevated
special tests for IDA
serum ferritin (dec), serum Fe(dec), TIBC (inc),bone marrow biopsy
major iron storage and first to fall when IDA
serum ferritin <10ng/ml
dignostic of IDA
serum ferritin <10ng/ml
determining of the cause of IDA is very important because for example
occult malignancy like colon, upper GI CA commonly present w/anemia
tx of IDA
replace iron store blood transfusion (maybe)
transfusion for IDA?
only if cerebrovascular or cardiopulmonary compromise, not recommended for iron replacement
thalassemias definition
inherited disorders of hgb production : alpha and Beta
thalassemia minor
dysfunction of one beta globulin chain, asymptomatic, hypochromic, microcytic
thalassemia major
cooley’s anemia,
severe dysfunction of both beta globulin chains, most die before 30
thalassemia lab eval
poikilocytosis (abnormal shapes), target cells, nucleated RBCs, NORMAL RDW (all RBCs are small)
thalassemia vs IDA RDW
nl is thalassemia, elevated in IDA
thalassemia tx
transfusion, splenectomy, iron chelation
why hgb should be >9 in thalassamia?
to prevent skeletal deformities and fractures
approach to micro anemia
check serum ferritin:
if low–>IDA
if nl–>check serum Fe nad TIBC
anemia of chronic dz (ACDz)
common in longstanding inflammatory dz, malignancy, autoimmune, chronic infection
etiology of ACDz
abnl iron metabolism, impaired erythropoeitin production
lab tests for ACDz
normo, nl or elevated ferritin, no dx lab test
tx of ACDz
treat cause, erythropoetin
myelodysplastic syndrome
acquired disorder of hematopoietic stem cells, resulting in a refractory anemia may lead to leukemia
etiology of myelodysplastic anm
idiopathic, 2 to radiation, chemotx, toxin exposure
sideroblastic anm
heterogenous group of disorders with abnl RBC iron metabolism
lab findings of sideroblastic anm
anisocytosis, poikilocytosis, ringed sideroblast, iron deposits
fe low, TIBC elevated, ferritin low
iron def
fe and TIBC nl, ferritin nl
no iron def
fe and TIBC low, ferritin nl/elevated
ACDz
fe high, TIBC nl, ferritin elevated
thalassemia
increased ret count due to ?
prior of recent hemorrhage, recent hemolysis
normal ret count due to?
normal bone marrow: with anemia of chronic dz, hypothyroidism, liver dz
abnormal bone marrow: myelofibrosis, leukemia, myeloma, matastases, renal failure
megablastic anemias
B12 and folate def, hemolysis (can be normo)
falsy elevated MCV due to?
large number of reticulocyte, RBC clumping
if B12 not replaced?
subacute combined degeneration of the spinal cord
daily B12 requirement
1-2 microg
pernicious anemia
def in IF –> B12 malabsorbtion and megablastic anemia due to autoantibodies against parietal cells
neuro findings in PA
dec. vibratory and position sense, ataxia, paresthesias, confusion, dementia
peripheral smears of PA
hypersegmentated neutrophils, anisocytosis, poikilocytosis, macro-ovalocytes, low platlets
lab findings of PA
low serum B12, positive Schilling test or antibodies to IF, elevated serum methylmalonic acid and homocysteine levels
Tx of PA
parenteral vitamin B12, Do not tx B12 def with folic acid alone
folic acid daily requirement
200 microg/day (400-800 for pregnants)
how long does it take to show folic acid def macro anemia?
4-5 months
folate def is common in
alcoholism, end of pregnancy, anticonvulsant therapy (enzyme inhibition reduces folate absorption), malabsorption syndromes, hemolytic anemias including sickle cell.
lab findings in FA def anemia
low serum folate level, homeosystein level is elevated but serum methylmalonic is normal
normal marrow can sustain RBC production ….nl
2-5 times
marrow cannot compensate for RBC survival time less than …
20 days
clinical findings of H anemia
jaundice, gallstones, increased risk of salmonella and pneumococcus
classifications of hemolysis
intravascular: destruction w/in blood stream
extravascular: destruction in the reticuloendothelia system like spleen
lab findings in hemolysis
elevated retic count (polychromasia), increased unconjugated bilirubin, elevated serum LDH, plasma hgb increased (hemoglobinuria)
serum haptaglobin is low in …
intravascular helysis
peripheral smear in hemolysis anemia
immature RBCs, nucleated RBCs, possible schistocytes
polychromasia ?
reticulocytosis, lots of blue –> lots of new
intravascular hemolysis classification
1.fragmentation syndromes 2. red cell enzyme defects 3.paroxysmal nocturnal hemoglobinuria
fragmentation syndrome
- traumatic (macroangiopathic) from prosthetic valve 2. microangiopathic caused by RBC disruption from fibrin strands in vessles
red cell enzyme defects
G6PD def (Heinz bodies)
Heinz bodies a/w
G6PD
schistocyte a/w
fragmentation syndrome
extravascular hemolysis
1.hereditary spherocytosis 2. sickle cell anemia 3. autoimmune hemolytic anemia 4. incompatible blood transfusion 5. drug-induced hemolytic anemia
positive osmotic fragility test for ?
hereditary spherocytosis
positive coombs test (also called DAT)
autoimmune hemolytic anemia
RBCs in Hereditary Spherocytosis
normal MCV, smaller surface area, dense, globular appearance, lack central pallor , poorly deformable , trapped in splenic sinusoids, phagocytized by splenic macrophages
clinical features of HS
mild jaundice, scleral icterus, splenomegaly,
why need for increased folate in HS
chronic hemolysis
what test for HS
osmotic fragility test : increased hemolysis in hypotonic fluid
HS Tx
1.splenectomy : RBC lifespan to normal, remove risk of bilirubin gallstones 2. pnemococcal vaccine
sickle cell anemia
- homeozygos form : sickle cell Dz with symptoms
2. heterozygos form: sickle cell trait no symp but carriers
male and female affected equally in …
sickle cell anemia
RBCs in sickle cell anemia
sickle shaped when deoxy causing pain
sign and symptoms of sickle cell anemia
delayed growth, increased susceptibility to infections, dehydration, hypoxia, high altitude, intense exercise
clinical features are due to..
- chronic hemolysis: aplastic crisis and dec in Hb, bilirubin gallstone
- vaso-occlusive ischemic tissue injury: pain crises, osteonecrosis of femoral and humeral heads, CVA, MI, Splenic infarct, leg ulcers
most common feature of SS dz ?
pain in back, ribs, limbs lasting 5-7 days, tx with analg and fluid
lab finding of SS
low Hb,normo RBCs, elevated retic count, Hb electrophoresis reveals Hb S
screen SS with …test
sickledex
peripheral smear in SS
few sickled RBCs, nucleated RBCs, target cells, howell-jolly bodies, thrombocytosis
tx of SS dz
RBC transfusion PRN, analgesics, fluid, O2, hydroxurea, bone marrow tp
chemotx
hydroxyurea suppresses bone marrow function of all cell lines
auto immune hemolytic anemia
RBCs with antigen-antibody complex are phagocytized by macrophages, and spherocytes are formed, they become smaller and destroyed in spleen.
smear of AI HA
polychromasia, spherocytosis, nucleated red cell
tx of Hemolysis
cause, corticosteroids, splenectomy, folic acid
incompatible blood transfusion
results in hemolysis
what test for incompatible BT
coombs test can detect antibodies
hemolytic dz of new born is a
incompatible BT (erythroblastosis)
aplastic anemia
acquired abnormality of bone marrow stem cells selective or total RBC, WBC, platelets
causes of aplastic anemia
chemical exposure, viral, ionizing radiation
hallmark of aplastic anemia
pancytopenia (anemia, leukopenia, thrombocytopenia)
clinical features of aplastic anemia
pancytopenia, absence of precursors for normoblasts, ganulocytes, megakaryocytes in bone marrow, weakness, infections, bleeding.
tx of aplastic anemia
cause, r/o other infections, hematology referral for blood component replacement, bone marrow transplant, immunosuppressive tx
preferred tx for aplastic anemia
bone marrow tp
infections resembling aplastic anemia
acute leukomia, myelodysplasia, PNH, granulomatous infxn such as TB
leading cause of disability in US
stroke
80% of strokes are
ischemic, rest is hemorrhagic
stroke risk factors
hx of neuro symp, degree of carotid stenosis, plaque charachteristics
symptomatic pt for stroke
contralateral weakness, contralateral sensory deficits, amaurosis fugax or hollenhorst plaque.
high risk groups for imaging of carotid bifurcation dz
> 60 yo and one of : HTN, CAD, current smoking, 1st degree relative with Hx of stroke
management of asymptomatic carotid stenosis
tx HTN, Hyperlipidemia, DM, smoking, aspirin
indication for surgery/intervention
- carotid endarterectomy (CEA)
2. carotid artery stenting (CAS)
chronic aorto-illiac occlusive dz
- younger female 2. smoker with hyperlipidemia 3. small infrarenal aorta 4.chronic lower limb ischemia
tx of chronic aorto-illiac occlusive dz
- aortic bypass 2. endovascular angio +/- stenting
acute aortic occlusive dz
1.vascular emergency 2. saddle embolism 3. in situ thrombosis of already diseased segment
presentation of acute aortic occlusive dz
neuro def (paralysis), absent femoral pulses
tx of acute aortic occlusive dz
quick imaging and operation
aneurysm definition
abnormal vessel dilation
dissection
a tear in intima and blood penetrates into media which splits longitudinally
aortic aneurysmal dz
degenerative and remodeling of aortic wall,
causes of aortic aneurysmal dz
genetic predisp, atherosclerotic, infection (TB, Syphilis), Marfans, Ehlers-Danlos
atherosclerotic aneu. 95% affects
abdominal aorta
AAA dx
UTZ: dx and size
CT/MRI: plan endovascular therapy
AAA management
follow up if 5.5 cm, symptomatic, rapid expansion
AAA
majority asymptomatic
most common complaint in AAA
back pain
ruptured AAA a/w
abd pain, pulsatile abd mass, tenderness, hypotension
surgical repair of AAA
w/ dacron graft, percutaneous endovascular stent grafts,
aortic dissection can occur secondary to ?
connective tissue dz,aneurysm, HTN, trauma
type of pain in aortic dissection
acute onset of tearing pain in either chest or abd
aortic dissection medical management
- beta blockers, 2. add vasodilators like Nipride
complication of aortic dissection
aortic rupture, cardiac tamponade, acute aortic regurg, acute coronary ischemia
Peripheral vascular dz
arterial (PAD)
venous
PAD
asymptomatic, intermittent claudication, critical leg ischemia-limb threat
intermittent claudication is a/w
PAD
peripheral venous dz
venous thrombosis, varicose veins, chronic venous insufficiency
most common form of PAD
chronic arterial insufficiency
chronic arterial insufficiency is most common in
elderly
underlying cause of chronic arterial insufficiency is
atherosclerosis
physical exam inspection finding in PAD
- pallor w/raised extremity 2. dependent rubor 3. HAIR LOSS ON LEG/FOOT 4.ATROPIC SKIN/NAIL CHANGES 5.ulcers 6.necrosis/gangrene
PE palpation findings in PAD
- pulses: femoral, popliteal, dorsalis pedis, posterior tibial 2. temp: cool 3. capillary refill: delayed
ABI (ankle-brachial index) is a/w
PAD , >1 nl
most common sites of PAD
superficial femoral and popliteal
atherosclerotic plaques frequently occur at ?
bifurcation: aortic, iliac, femoral
main symptom of PAD
claudication : ischemic pain in lower legs when walking resolve when standing or rest
claudication is more common in
calves (less frequent in buttocks and thighs)
Leriche syndrome
aortoiliac dz
Leriche syndrome vs venous dz
leg/foot pain usually improves when leg in dependent position; worsen when leg is raised. the opposite of venous dz.
rest pain?
with sever Leriche syndrome.
claudication worse prognosis
smoking and diabetes with overall amputation risk of 20%
non invasive testing for PAD
treadmill test/ABI, duplex ultrasound, magnetic resonance angio
claudication medical therapy
- stop-start walking regimen 2. SMOKING CESSATION 3.lipid lowering, 4. aspirin 5. clopoidogrel 6. pentoxifylline 7. cilostazol
indications for intervention claudication
impacting life style despite therapy, rest ischemia, limb threat
claudication surgical approaches
- endarterectomy 2.percutaneuos transluminal angioplasty(PTA) 3. stents 4. revascularization
endarterectomy
removal of atherosclerotic plaque
PTA
for localized dz w/short segments of obstructing plaque
stent for claudication
alternative to simple angioplasty
revascularization for claudication
aortofemoral bypass graft, femoral-popliteal, axillary-femoral
balloon angioplasty
one approach to limited PVD
bypass grafts are used for
aortoiliac and femoral-popliteal
Goretex grafts are most common for
fem-pop
claudication is a marker for..
systemic atherosclerosis
focal aortoiliac or iliac dz should be treated w/
angioplasty /stenting
occlusion longer than 5 cm, concomitant aneurysm, or in common femoral a. are better treated w/
surgery
initial tx in fem-pop dz
prolonged course of medical therapy
acute arterial obstruction
sudden cessation of blood flow to an extremity due: Acute Emergency
cases of acute arterial obstruction
embolism ( usually, from heart or aorta), thrombus in situ
5 Ps of acute obstruction
pain, pallor, paresthesia, paralysis, pulselessness
tx of acute obstruction
emergency: thrombectomy/embolectomy-dissolve via thrombolytic infusion-anricoag (heparin)-surgical bypass
raynaud’s phenomenon
episodic digital schemia on exposure to cold or emotional stress
triphasic response in raynauds
pallor, cyanosis, rubor
cause of raynaud
arterial vasospasm followed by arteriolar and capillary dilation
2 categories of raynaud
- raynaud dz: primary /idiopathic when 2ndary causes are excluded ~50%
- 2ndary raynauds phenomenon
drug tx for raynauds
ca channel blockers (nifedipine, diltiazem), reserpine (adrenergic blocker), prazosin (alpha 1 adrenergic blocker)
varicose vein sx
aching/burning sensation, tired/heavy, worse w/standing, better by elevation (UNLIKE ARTERIAL DZ)
varicose veins signs
prominent surface veins, superficial thrombosis, rupture/local bleeding, stasis dermatitis (dark pigmentation), ulceration esp. NEAR ANKLE, edema
