24 STROKE
● Stroke - abrupt onset of focal neurologic deficit that lasts at least 24 hrs; vascular
origin
● Transient ischemic stroke - focal ischemic neurologic deficit lasting <24 hrs usually
<30 mins
● Ischemic stroke - due either to thrombus formation or emboli occluding cerebral
artery
● Cardiogenic embolism - stasis of blood flow in the atria or ventricles to formation of
local clots that can travel through aorta to cerebral circulation
● Hemorrhagic Stroke - include subarachnoid hemorrhage (SAH), intracerebral
hemorrhage, subdural hematomas
● SAH - result from trauma or rupture of intracranial aneurysm
● Intracerebral hemorrhage - when ruptured blood vessel in the brain causes
hematoma
● Subdural hematomas - caused by traumas
● Hemorrhage Stroke - result in abrupt increased intracranial pressure
● clinical presentation: symptoms - unilateral weakness, cant speak, loss vision,
vertigo, falling
● Ischemic is not painful, hemorrhagic stroke has headache
● Posterior circulation - vertigo and diplopia
● Anterior circulation - result in aphasia
● Protein C, S, and antithrombin III - vest measured in steady state rather than acute
stage
● CT and MRI - reveal areas of hemorrhage and infarction
● CD, ECG, TTE, TCD - provide diagnostic info
● Short acting parenterals (labetalol, nicardipine, nitroprusside) - preferred for
treating BP in acute phase
● Non pcol for acute ischemic stroke - Surgical decompression to reduce
intracranial pressure; carotid Endarterectomy and stenting for secondary prevention
● Non Pcol for hemorrhagic Stroke - surgical intervention to clip or ablate the
vascular abnormality reduces mortality from rebleeding
● alteplase - plasminogen activator; reduces disability from IS
● Aspirin - started 24-48 hrs after alteplase completion reducing long term death and
disability
● Secondary prevention of IS
○ use antiplatelet therapy in noncardioembolic stroke (first line agents are clopi,
asa, ER dipyridamole plus asa); cilostazol also first line but lacks data; Limit
combi of clopi and asa in px with recent M
○ oral anticoagulation is reco for AFib and presumed cardiac source of
embolism; Warfarin (vit k anta is first line), dabigatran may be for some px
● Statins - reduce risk of stroke in px with CAD and elevated plasma lipids; treat IS px
regardless of baseline cholesterol with high intensity statin therapy to reduce 50%
LDL for secondary stroke prevention
● LMW heparin or low dose SC unfractionated heparin for prev of deep vein
thrombosis in hospi px with decreased mobility due to stroke
● There are no standard pcol strat for treating intracerebral hemorrage
● CCB nimodipine - reco for reducing incidence and severity of neurologic deficits from
delayed ischemia
● Inclu for alteplase use: >_ 18, <4.5hrs symptom onset
● IS tx: alteplase, asa, clopi, warfarin, dabigatran, ERdp+asa
● HS tx: Nimodipine (for SAH)
● ALLPX tx: heparins for DVT prophylaxis
25 VENOUS THROMBOEMBOLISM
● VTE - results from clot formation in the venous circulation; manifested as DVT and
pulmonary embolism (PE)
● Normal hemostasis - maintains integrity of normal circulatory system after blood
vessel dmg
● Pathologic venous thrombosis - occurs in absence of gross vein disruption
● Thrombin - converts factors 5 and 8 to their active cofactor forms; mediates
conversion of fibrinogen to fibrin
● Hemostasis - controlled by antithrombotic substances secreted by intact endothelium
adjacent to damaged Tissue
● Virchow triad:
○ Vascular injury occurs with trauma
○ Hypercoagulable states include malignancy
○ Stasis can result from damage to venous valves
● Symptoms of dvt: unilateral leg swelling, erythema, warmth, palpable cord, positive
homan sign
● PE symptoms: cough, chest pain, tachypnea
● Radiographic contrast - most accurate and reliable method for VTE diagnosis
● Noninvasive tests - for initial eval of px with suspected VTE
● Elevated d-dimer blood levels - negative test excludes vte but positive test is not
conclusive for vte diagnosis
● Anticoagulation - primary tx for VTE
○ Initially injectable anticoagulant and then warfarin for maintenance therapy;
oral rivaroxaban can be initiated as alternative
● Rapidly acting anticoagulants - for acute phase required to prevent thrombus
extension and embolization
● Anticoagulation Beyond 3mos is aimed for long term secondary prevention of
recurrent VTE
● Grafuated compression stockings and Intermittent pneumatic compression device -
improve venous blood flow and reduce risk of VTE
● Inferior vena cava filters , short term protection against PE in very high risk px with
conra indic to anticoag
● Thrombectomy - in Life threatening DVT
● catheter based embolectomy - for acute PE in px contrainc for thrombolytic therapy,
failed
● Surgical embolectomy - reserved for massive PE
● UFH - prevents growth and propagation of a formed thrombus
● Weight based SC UFH is less costly option
● Bleeding - primary AE for anticoagulants
● Protamine sulfate - for major bleeding due to UFH or LMWH
● HIT - a serious immune mediated problem
● Four Ts Score -
● LMWH has similar efficacy with IV UFH for VTE tx
● Measuring Antifactor Xa activity - most widely used method to monitor LMWH
● Fondaparinux sodium - indirectly inhibit factor Xa; for prev of VTE ff orthopedic and
abdo surgery; alt to lmwh tx for DVT AND PE; does not require CBC
● Rivaroxaban and apixaban are selective inhibitors of Xa;
● Rivaroxaban - approved for prev of VTE ff hip or knee replacement surgery
● Warfarin - inhibit enzyme for interconversion of Vit K in liver
● Reduced vitamin K - cofactor required for carboxylation of the Vitamin k dependent
coagulation proteins
● Asymptomatic elevated INR and INR greater than 4.5 without bleeding can withhold
warfarin and provide vit k
● If inr is 5-9 warfarin withhold Warfarin or combine with oral phytonadione
● Thrombolytic agents - proteolytic; convert plasminogen to plasmin
31 ANEMIA
● Anemias - group of diseases with decreased Hb or rbc <13 in mean or <12g/dL in
women
● Macrocytic cells - larger; b12 or folic acid deficiency
● Microcytic - smaller; iron deficiency
● Normocytic anemia - recent blood loss or chronic disease
● Deficiency of intrinsic factor - reduced Absorption of B12
● Folic acid deficiency anemia - caused by hyperutilization due to pregnancy or others
● Phenytoin - reduce absorption of folate
● Methotrexate - folate antagonism
● Anemia of inflammation - describe both anemia of chronic disease and critical illness;
hypoproliferative anemia
● Pediatric anemia - due to primary hematologic abnormality
● Risk Of IDA is increased by rapid growth spurts and dietary Deficiency
● acute onset anemia is characterized by cardiorespiratory symptoms
● Chronic anemia is characterized by symptoms of heart failure, cold sensitivity
● IDA is characterized by glossal pain, smooth tongue and Hb conc is less than 9 g/dL
● Decreased Serum ferritin - earliest and sensitive Lab change for IDA
● Oral iron therapy - not enteric coated or slow or SR
● Iron is poorly absorbed from veg, grain, dairy, and eggs. Iron is best absorbed from
emats, fish, and poultry. Administer at least 1hr b4 meals
● Parenteral iron for px with iron malabsorption
● Oral b12 is as effective as parenteral but parenteral acts more rapidly and is reco if
neurologic symptoms are present (IM cyanocobalamin)
● Oral folate for folate deficiency
● Iron is not effective when inflammation is present
● ESAs off label use for anemia Of inflammation
● Anemia in prematurity is treated with RBC transfusion
28 CHRONIC KIDNEY DISEASE
● CKD - abnormalities in kidney structure or fxn For 3mos or longer
● CKD stage 5 or ESRD - when gfr falls below 15ml/min/1.73m2 or px receiving RRT
● Susceptibility factors - increase risk for kidney disease but no direct cause of kidney
damage
● Initiation factors - directly result in kidney damage and a modifiable by drug therapy
● Progression factors - hasten the decline in kidney fxn after initiation of kidney
damage
● Stage 1 and 2 usually do not have symptoms or metabolic derangements as seen
with stages 3-5
● Uremic symptoms are absent in stage 1 and 2, minimal in 3 and 4, common in stage
5
● If high urine albumin excretion, initiate acei or arb. Add thiazide diuretic in combi with
ARB if additional Reduction in proteinuria is needed; nondihydropyridine ccb are
second line as antiproteinuric when acei or arb are contraindicated
● No acei is superior to another
● ESA for all ckd px with Hb is between 9 and 10 g/dL
● Iron deficiency - primary cause of resistance to treatment of anemia with ESA
● Parenteral Iron therapy improves Response to ESA therapy
● SC epoetin Alfa is preferred
● Darbepoetin alfa has longer half life than epoetin alfa
● Hypertension - esa common ae
● Phosphate binding agents - decrease phosphorus absorption in the gut and are first
line for controlling bot serum phosphorus and calcium conc
● Aluminum binders - cns toxicity
● Magnesium binders - hypermagnesemia and hyperkalemia
● Calcitriol - directly suppresses pth synthesis and upregulates vitamin d receptors
● Paricalcitol - less hyperphosphatemia
● Doxercalciferol - less hypercalcemia
● Cinacalcet - reduces pth secretion by increasing sensitivity of calcium sensing
receptor
● Prevalence Of hyperlipidemia increases a renal function declines
● Statins for hyperlipidemia in adults aged 50 and older with stage 1 to 5 ckd bot on
dialysis
23 SHOCK
● Shock - acute state of inadequate perfusion of critical organs that can lead to death
● Shock - systolic BP less than 90mmhg or reduction of at least 40mmhg from baseline
● Hypovolemic shock - intravascular volume deficit
● Cardiogenic shock - myocardial pump failure
● Septic, anaphylactic, neurogenic shock - peripheral vasodilation
● CBC is normal in absence of infxn
● Red cell count, Hb m, and hematocrit decrease In hemorrhagic shock
● Pulmonary artery (swan-ganz) catheter - used To determine CVP, PAP, CO, PAOP
● Supplemental O2 initiated At early signs of shock
● Fluid resuscitation for maintaining circulating blood volume
● Crystalloids: isotonic (normal saline or lactated ringer solution) are fluid of choice
● Colloids: hydroxyethyl starch, dextran, and albumin have advantage of prolonged
intravascular retention time compared with crystalloid solution
● Blood products: to ensure maintenance of O2 carrying capacity as well as clotting
factors and platelets for hemostasis (whole blood, platelet, fresh frozen plasma,
packed rbc)
Pharmacologic therapy for shock
● Hypovolemic shock: inotropic agents and vasopressors are not indicated (may
increase resistance and stop circulation). Vasoactive peptides that dilate peripheral
vasculature are preferred like dobutamine if bp Is high enough to tolerate dilation.
● Vasopressors - used only as temporizing measure or last resort
● Septic shock: administer IV fluid. Crystalloids are preferred over colloids
● NE is preferred initial vasopressor in septic shock not responding to fluid
administration; first line for septic shock because it increase MAP. STRONG a1
agonist and less b1 agonist
● Epi is Added when suboptimal Response to NE; combine a and b agonist;
acceptable choice for hemodynamic support of septic shock because of it combined
vasoconstrictor And inotropic effects
● Phenylephrine tried as initial vasopressor in severe tachydysrhythmias; pure a1
agonist, it improves MAP by increasing cardiac index
● Dobutamine is used in low CO states despite fluid resuscitation; an inodilator;
increases cardiac index
● Vasopressin as ajunct in px refractory to catecholamine vasopressors
● DA not as effective as epi and NE for achieving goal MAP in px with septic Shock
● Corticosteroids initiated in septic shock when adrenal insufficiency is suspected
22 ISCHEMIC HEART DISEASE
● IHD - lack of O2 and decreased or no blood flow
● Major determinants of MVo2 - HR, contractility, intramyocardial wall tension during
systole
● Double product - HR x SBP
● Variant (prinzmetal) angina - more likely to experience pain at rest and in early
morning hours
● Episodes of ischemia may be painless or silent
● Nonselective beta and alpha blockade with labetalol may be useful in px with
marginal LV reserve
● Nitrates - reduce mvo2 secondary to venodilation and arterial-arteriolar dilation,
leading to reduction In walk stress from reduced ventricular volume and pressure
● Nitroglycerin half-life is 1 to 5 minutes; ISMN is 5hrs
● Nitrate therapy - used to prevent acute anginal attack
● SL nitroglycerin relieves pain within 3 mins. Pain Persisting beyond 20-30 minutes
after use of two or three nitroglycerin suggests ACS and need emergency aid
● Chewable, oral, and transdermal are acceptable for long-term prophylaxis
● Verapamil and diltiazem cause less peripheral vasodilation than dihydropyridines
such as nifedipine but greater decrease i AV node conduction
● MVo2 is reduced with all CCBs primarily
● Amlodipine - probably the CCB of choice in severe ventricular dysfunction
● Ranolazine reduce calcium overload in ischemic myocytes through inhibition of late
sodium current; indicated for chronic angina; prolongs QT interval
● Beta blockers - preferable for chronic prophylaxis because of less frequent dosing; px
with high resting HR and fixed anginal threshold respond well to b blockade
● CCB are as effective as b blockers and are useful in px who have variable threshold
for exertional angina
● Nitrates - mainstay therapy for coronary artery spasm And variant angina pectoris
● B blockers have little or no role in mgt of variant angina
● Nifedipine, verapamil, diltiazem are all equally effective as single agents for initial mgt
