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652 Cards in this Set
- Front
- Back
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most common cause of intestinal obstruction
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small intestine ileus
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pathology of simple intestinal obstruction
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dilation, hypersecretion, and bacterial overgrowth
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pathology of closed loop obstruction
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single constrictive lesion occludes both proximal and distal end of intestinal loop
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most common causes of simple intestinal obstruction
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adhesions, tumors, strictures
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most common cause of closed loop obstructions
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hernias, adhesions, volvulus
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mechanical obstruction vs ileus
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1. location - mechanical = middle of abdomen, ileus = diffuse
2. severity: mechanical = severe; ileus = mild 3. character: mechanical = pain increases and decreases as muscle fatigues; ileus = constant |
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history: how to distinguish proximal from distal intestinal obstruction
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proximal = short periodicity
distal = longer periodicity |
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history questions to ask ppl with sx of intestinal obstruction to build risk for adhesions and cancer
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1. prior episodes of bowel obstruction 2. previous surgeries 3. h/o intraabdominal inflammation 4. h/o cancer
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what type of proteins are HLA antigens
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glycoproteins
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what does G1 stage of cell cycle correspond to
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protein synthesis and growth
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what is the variable stage of the cell cycle
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G1
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what does s stage of cell cycle correspond to
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chromosomal duplicaiton
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what does g2 stage of cell cycle correspond to
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mitosis
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what does m stage of cell cycle correspond to
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nucleus division
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what are the 4 stages of mitosis
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prophase - centromeres attach, spindle form, nucleus dissolves
metaphase - lining up of chromosomes anaphase- splitting apart of chromosomes telophase- reformation of nucleus |
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where do steroid hormone receptors exist
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cytoplasm
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where do thyroid hormone receptors live
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nucleus
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what is generated in glycolysis from 1 molecule of glucose
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2 atp, 2 pyruvate
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how much atp produced from 1 molecule of glucose from aerobic respiration
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36
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Three initial responses to vascular injury
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vasoconstriction, platelet adhesion, thrombin generation
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what are the initial components involved in the intrinsic pathway
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exposed collagen, prekallikrein, HMW kininogen, factor XII
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what are the initial components involved in the extrensic pathyway
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tissue factor, factor vii
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what is the prothrombin complex (convergence of intrinsic and extrensic pathways)
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factor X, V, calcium, PF 3, prothrombin
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what inhibits factor X
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tissue factor pathway inhibitor
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what links platelets together and binds GpIIb/IIIa molecules
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fibrin
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what factor helps in crosslinking fibrin
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xiii
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3 functions of thrombin
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converts fibrinogen to fibrin
activates factors 5, 8 activates platelets |
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2 functions of at3
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binds and inhibits thrombin
inhibits factors 9, 10, 11 |
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what molecule activates at3
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heparin
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function of protein c
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degrades 5 and 8, degrades fibrinogen
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what is a cofactor for protein c
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protein s
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where is tpa normally released from, what does it do
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endothelium, converts plasminogen to plasmin
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function of plasmin
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degrades 5 and 8, fibrinogen, and fibrin
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what is alpha 2 antiplasmin
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inhibitor of plasmin, released from endothelium
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what coag factor has the shortest half life
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7
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does factor 5 and 8 lose activity in whole blood? ffp?
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yes, no
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which coag factor is not made in liver
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8 (made in endothelium)
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what are the vitamin k dep factors
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2 7 9 10 c s
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how long does vit k take to have effect? how long does ffp take to have effect, how long does it last?
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6 hrs, immediate but lasts 6 hrs
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what is another name for factor 2
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prothrombin
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what is the normal half life for rbc? plt? pmn?
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120d, 7d, 2d
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what does pgi2 do, where is it released from?
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decreases platelet aggregation
promotes vasodilation from endothelium |
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what does txa2 do, where is it released from?
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increaes platelet aggregation
promotes vasoconctriction releases calcium in platelets and exposes GpIIb/IIa AND Gp1a |
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GpIIb/IIIa vs Gp1b
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GPIIb/IIIa = platelet platelet binding
GP1b = platelet collagen binding |
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what does cryoprecipitate contain
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vWF, factor 8, fibrinigoen
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what does ffp contain
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all coag factors, protein c & s, at3
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what medications can cause release of 8 and vwf from endothelium
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ddavp, estrogens
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what coag factors does pt measure, what does it represent
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2, 5, 7, 10, fibrinogen. liver synthetic function
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what coagfactors does ptt measure
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everything except 7 and 13
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what should ptt be for routine anticoagulation
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60-90s
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what is act, what should it be
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activated clotting time
150-200 sec for routine anticoagulation >460s for cardiopulmonary bypass |
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what should inr be for general surgery, CL placement, needle biopsies, eye surgery
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< 1.5, < 1.3
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what is the most common cause of surgical bleeding
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incomplete hemostasis
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inheritance of vWD
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1, 2 = AD
3 = AR |
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what does vWF do
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link Gp1b on plts to collagen
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what type of vWD is most common
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I
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what are the 3 types of vWD, how to tx each type
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I = less vWF, DDAVP
II = defect in vWF or doesn't work well, cyro III = complete vWF deficiency, cryo & DDAVP useless |
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lab abnormalities in vWD disease
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PT normal, PTT either way, long bleeding time esp with ristocetin test
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inheritance of hemophilia
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X linked recessive
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lab abnormalities in hemophilia
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prolonged ptt, normal PT (for both types)
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hemophilia a vs b
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a = 8 deficiency
b = 9 deficieny |
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planning of surgery for hemophiliacs
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for hemophilia a, need 8 levels at 100% before surgery, at least 80% for 2 weeks after surgery
for hemophilia b, need 9 levels at 100% preop, at least 30% 2-3d after |
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how to tx hemophilia
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hemearthrosis - DO NOT ASPIRATE, ice, ROM, either factor 8 or cryo
otherwise, factor 8 or cryo |
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what meds can cause acquired thrombocytopenia
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h2 blockers, heparin
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what is glanzmann thrombocytopenia, how do you tx
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gp2b/3a receptor deficiency, tx w/ plts
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what is bernard soulier, how do you tx
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gp1b receptor deficiency, tx with plts
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what kind of clots are associated with HIT
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white clots
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tx for HIT
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stop heparin, use argatroban
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how long to stop asa prior to surgery
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7d
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how long to stop plavix prior to surgery? mechanism? tx?
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7d
ADP receptor antagonist PLTs |
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perioperative plt goal
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>50k prior to surg
>20k postop |
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what coagulation d/o can occur with prostate surgery? how to tx
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release of urokinase -> thrombolysis. tx with amicar (aminocaproid acid)
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what is the most sensitive way to pick up on bleeding d/o
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h&p -- history of
abnormal bleeding with tooth extraction or tonsillectomy |
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most common congenital hypercoagulability d/o
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factor 5 leiden
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what is factor v leidin? tx?
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defect in factor 5 that causes it to resist activated protein c. tx with heparin & warfarin
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tx of hyperhomocysteinemia
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folic acid, b12
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how to tx protein c & s deficiency
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heparin, warfarin
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how to tx at3 deficiency
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at3 or ffp, then hep + warf
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surgery in polycythemia vera
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hct < 48, plt< 400 preop
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name causes of acquired hypercoagulability
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malignancy
inflammatory states infections OCP pregnancy postop myeloproliferative |
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are pts on cardiopulmonary bypass hypocoagulable?
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hypercoagulable cuz 12 activated, use heparin to prevent
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pathogenesis of venous vs arterial thrombosis
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venous has virchow's triad - injury, stasis, hypercoagulability
arterial is just what set at home |
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indications for ivf filter
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CI to anticoagulations, PE on anticoagulation, more proximal DVTs (i.e. deep femoral or iliofemoral)
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PEs most commonly caused by
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iliofemoral DVT
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mechanism of aminocaproid aci
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inhibits plasmin
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mechanism of warfarin
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prevents vitamin k dependent decarboxylation of glutamic residues
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how to reverse heparin
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protamine
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long term heparin causes
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osteoporosis, alopecia
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what is protamine rxn
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hypotension, bradycardia, decreased heart function
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LMWH -- what factors does it act on
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Xa, thrombin
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half life of argatroban
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50 min
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metabolism of bivalirudin
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proteinase enzymesi n blood
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what direct thrombin inhibitor is irreversible
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hirudin
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what needs to be trended with thrombolytics (streptokinase, urokinase, tpa)
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fibrinogen levels > 100
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absolute CI to thrombolytics
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active internal bleeding, recent CVA or neurosurgery <3mo, recent GI bleed, closed head or facial trauma < 3mo, uncontrolled HTN, AVM, thrombocytopenia
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which blood products do not have risk of viral transmission
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albumin, globulins
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respiratory effects of stored blood
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low in 2,3-dpg -- causes left shift of hgb curve
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lab abnormalities after acute hemolysis after abo mismatch
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haptoglobin < 50, free hgb > 5, increased indirect bili
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an anesthetized pt recently transfused with diffuse bleeding
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abo mismatch
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why do people get fever after transfusion (nonhemolytic)
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antibodies against donor leukocytes
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mechanism of trali
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donor ab's to recipient wbcs
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cause of poor clotting after massive transfusion
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dilutional thrombocytopenia
hypocalcemia |
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what parasite can be transmitted with blood transfusion
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chagas
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most common blood product that is contaminated
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plts
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most common bacteria in blood products
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gnr - e coli
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function of il2
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maturation of cytotoxic t cells
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function of il4
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maturation of b cells into plasma cells
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3 functions of helper t cells
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release il2, il4, and delayed type hypersensitivity
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what molecule is used to target cytotoxic t cells
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mhc class 1
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what cells is mhc1 present on
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all nucleated cells
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what activates cd4 vs cd8 cells
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mhc2 vs mhc1
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mhc1 vs mhc2: how many domains
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1 has single chain with 5 domains
2 has 2 chains with 4 domains each |
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viral infections -- how do they get detected
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presentation of viral epitopes on mhc1, recognized by cd8
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bacterial infection -- how do they get detected
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presentation of bacterial epitopes on mhc2, recongized by cd4 which raise b cells
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what cells do nk cells recognize
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ones without self-mhcs
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which ig's are opsonins
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igm, igg
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which ig's fix complement
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igm, igg
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what are the 4 hypersensitivity rxnx
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1 = immediate, ige based
2 = cytotoxic, igm or igg based 3 = immune complex 4 = delayed |
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what is major source of histamine in blood vs tissue
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basophils vs mast cells
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primary lymphoid vs secondary lymphoid organs
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liver, bone thymus vs
spleen and lymph nodes |
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what converts lymphocytes to lymphokine activated killer cells
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il2
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what converts lymphocytes into tumor infiltrating lymphocytes
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il2
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when to give tetanus shot vs toxoid
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give toxoid, if <3 doses or if unknown
give globulin if tetanus prone and not immunized or unknown (>6h old, obvious contamination, crush, burn, frostbite) |
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microflora in stomach, proximal small bowel, distal small bowel, and colon
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nothing, some yeast and gpc's
10^5, gpcs 10^7 gpc, gpr, gnr 10^11 - anaerobes bacteroides fragilis most common anaerobe, e coli most common aerobe |
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most common fever by pod2, by pod5, after pod5
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atalectasis, UTI, wound infection
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insulin and glucose in GNR sepsis
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first decreased insulin and increased glucose (due to impaired utilization), then increased insulin and glucose both (due to insulin resistance)
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optimal glucose level in septic pt
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100-120
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when do you need abx for abscess
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pts with dm, celulitis, signs of sepsis (SIRS), or bioprosthetic hardware
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SSI rates by type of wound: clean, clean contaminated, contaminated, grossly contaminated
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2%, 5%, 10%, 30%
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when do you stop periop ppx abx
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24 hours, unless cardiac which is 48h
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most common organism in ssi? most common gnr? most common anaerobe?
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coag + staph (staph aureus). e coli. b fragilis
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how much bacteria is needed to cause wound infection
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>10^5
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risk factors for wound infection
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long operation
hematoma or seroma age chronic disease (copd, renal, liver, dm) malnutrition immunosuppressive drugs |
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most common organisms in ICU pneumonia
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S aureus (1), pseudomonas (2)
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MCC line infections
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s epidermis > s aureus > yeast
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how many cfu's needed to call a central line infection
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>15 cfu's from a central line cx
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usual cause of nec fac
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GAS (group a strep, beta hemolytic)
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toxin in GAS? c perfringens
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exotoxin. alpha toxin
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how to tx necrotizing infections
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early debridement, high dose penicillin
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what is fournier's gangrene
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severe necrotizing infection of perineal and scrotal region
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when do you need to cover for fungal infection
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+ blood cx
2 cx that are not blood, 1 site if severe sx prolonged bacterial abx with failure to improve |
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how to tx nocardia? actinomyces?
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snap
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how to tx candida?
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fluconazole, anidalafungin if severe
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how to tx aspergillosis
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voriconazole if severe
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how to tx histo
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liposomal amphotericin
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how to tx crytococcus
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liposomal amphotericin
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how tx coccidioidomycosis
|
liposomal amphotericin
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risk factor for sbp
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low protein in peritoneal fluid
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usual causes of sbp
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e coli, strep, klebsiella
strep in kids, e coli in adults |
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how to dx sbp. tx?
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pmn>500 in intraperitoneal fluid, 3g ceph like rocephin
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when do you have to r/o intraabdominal source for sbp?
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if not getting better on abx,
if cx are polymicrobial |
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how to ppx sbp
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fluoroquinalone esp norfloxacin
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mcc of secondary bacterial peritonitis
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intra ab source so b fragilis, e coli, enterococcus
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exposure risk for hiv blood transfusion? infant from + mother? needle stick from + pt? mucous membrane exposure?
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70% 30% .3% .1%
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post exposure ppx for hiv
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azt, ritonivir 1-2hrs after exposure
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mcc for laparotomy in hiv pts
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opportunistic infections > neoplastic dz > *
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mc neoplasm in aids pts
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kaposi sarcoma
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mc location for lymphoma in hiv pt
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stomach > rectum
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mc kind of lymphoma in hiv pt
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NHL (B cell)
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causes of lower gi bleed in hiv pt? upper gi? which one more common
|
lower gi more common
upper = kaposi, lymphoma lower = cmv, bacterial, hsv |
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what cd4 count does hiv become symptomatic
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350ish
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how to tx brown recluse spider bites
|
dapsone, may require resection
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how to tx acute septic arthritis, what are causes
|
gonococcus, staph, hib, strep
drain -> 3g ceph and vanc |
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causes of diabetic foot infection, how to tx
|
polymicrobial - staph, strep, gnr, anaerobe
tx: bs abx like unasyn |
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bacteria in human bites, pathogmnemonic
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eikenella
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cause of furuncle
|
s epidermidis, s aureus
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what is a carbuncle vs furuncle
|
furuncle = boil
carbuncle = loculated furuncle |
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cause of pd cath infection
|
s aureus, s epidermidis
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how to tx pd cath infection
|
intraperitoneal vanc and gentamicin with increased dwell time and intraperitoneal heparin
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when to remove pd cath for infection
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peritonitis that lasts 4-5 days
|
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risk factors for sinusitis
|
nasoenteric tubes
intubation pts with severe facial fractures |
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preop- razors vs clippers
|
clippers have less chance of wound infections
|
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CHG vs betadine
|
chg good for everything, betadine doesn't work v fungi
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list some cell wall inhibitors
list some 30s inhibitors list some 50s inhibitors list some dna helicase inhibitors list some rna polymerase inhibitors list some oxygen radical producers list some purine synthesis inhibitors |
penicillins, cephalosprins, carbapenams, monobactams, vanc
cyclines, aminoglycosides, linezolid macrolides, clinda, streptogramins (-pristins) fluoroquinolones rifampin metronidazole TMP (DHFR inhibitor), sulfomamides (PABA analogue) |
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bacteriostatic vs bacteriocidal abx
|
ECSTaTIC about bacteriostatics - erythromycin, clindamycin, SMX, TMP, tetracycline, chloramphenicol
Very Finely Proficient at Cell Murder (vanc, fluoroquinolones, penicillin, aminoglycoside, cephalosporin, metronidazole) |
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mechanism of resistance for MRSA
|
mutation of cell wall binding protein
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mechanism of resistance for VRE
|
mutation in cell wall binding protein
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mechanism of gentamicin resistance
|
decrease in active transport of gentamicin into bacteria
|
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appropriate vanc level
|
peak 20-40, trough 5-10
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appropriate gent level
|
peak 6-10, trough <1
|
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what to do if peak dose of abx too high? if trough too high?
|
decrease dose, decrease frequency
|
|
|
spectrum for penicillin
|
GPC, GPR, syphilis. not good vs staph or enterococci
|
|
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spectrum of ampicillin/amoxicillin
|
same as pen + enterococci as well
|
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what is unasyn/augmentin not good vs
|
pseudomonas, acinetobacter, serratia
|
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side effect of ticarcillin/piperacillin
|
PLT inhibition
|
|
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spectrum of the 3 cephalosporins
|
1g: good vs GPC only, doesn't work vs enterococcus
2g: GPC+GNR, not as good vs GPC as 1g. Good for community acquired GNR 3g: GNR+ anaerobes. CAN KILL PSEUDOMONAS |
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side effect of 3g ceph
|
cholestatic jaundice
|
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what has longest half life in 2g ceph
|
cefotetan
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spectrum of monobactam
|
GNR + pseudomonas, acinetobacter, serratia
|
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spectrum of carbapenams
|
GPC, GNR, anerobes. NOT GOOD FOR GPC, GNR, anaerobes
|
|
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side effect of carbapenams
|
seizures
|
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spectrum of bactrim
|
GNR + GPC. NOT GOOD FOR ENTEROCOCCUS, PSEUD, ACINETOBACTER, SERRATIA
|
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spectrum of quinolones
|
MOSTLY GNR, some GPC. Can kill acinetobactera and serratia. NOT GOOD FOR ENTEROCOCCUS
|
|
|
dosing timing of cipro vs levo
|
cipro = bid, levo = qd
|
|
|
spectrum of aminoglycosides
|
GNR, incl serratia, acinetobacter, pseudomonas
|
|
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are aminoglycosides good vs anaerobes
|
no needs o2 to work
|
|
|
mechanism of resistance to aminoglycosides
|
modifiying enzymes, decreased active transport
|
|
|
side effect of aminoglycoside
|
reversible nephrotoxicity, irreversible ototoxicity
|
|
|
side effects of erythromycin
|
nausea if po
cholestasis if iv |
|
|
what is stretogramins good for
|
GPC incl MRSA and VRE
|
|
|
what is linezolid good for
|
GPC incl MRSA and VRE
|
|
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spectrum of tetracycline
|
GPC, GNR, syphilis
|
|
|
side effect of clinda
|
pseudomembranous colitis
|
|
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what is good abx for aspiration pna
|
clinda
|
|
|
side effects of flagyl
|
disulfram like rxn, peripheral neuropathy if long term use
|
|
|
side effects of ampho
|
nephrotox, fever, hypokalemia, hypotension.
liposomal type has fever side effects |
|
|
mechanism of ampho
|
binds sterols in wall and alters permeability
|
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mechanism of conazoles
|
inhibit ergosterol which is needed for cell membrane
|
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|
mechainsm of anidulafungin
|
inhibits cell well glucan synthesis
|
|
|
mechanism of isoniazid
|
inhibits myocolic acids
|
|
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side effects of isoniazid
|
hepatotox, b6 deficiency
|
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side effect of pyranzinamide
|
hepatotoxicity
|
|
|
side effect of ethambutol
|
retrobulbar neuritis
|
|
|
what is acyclovir used for, gancyclovir
|
gancyclovir is for CMV
|
|
|
side effects of gancyclovir
|
bone marrow suppresion, CNS toxicity
|
|
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what abx to use for enterococcus
|
vanc
timentin/zosyn ampicillin/amoxicillin gent/ampicilli n |
|
|
what abx to use for pseudomonas, acinetobacter, serratia
|
ticarcillin/piperacillin
timentin/zosyn 3g ceph aminoglycoside penams fluoroquinolones |
|
|
why is sulfonamides bad in newborns
|
displaces indirect bili from albumin
|
|
|
where is tetracycline and heavy metals stored
|
in bone
|
|
|
0 order kinetics vs 1st order kinetics
|
constant amount of drug eliminated regardless of dose vs certain proportion of dose eliminated per time
|
|
|
how many half lives to reach steady state
|
4-5 (5 on test)
|
|
|
what is bioavailablity
|
fraction of unchanged drug reaching circulation (100% for iv)
|
|
|
ed50 vs ld 50
|
ed 50 = level at which desired effect occurs in 50%
ld 50 = level at which death occurs in 50% |
|
|
what is tachyphlaxis
|
tolerance after only a few doses
|
|
|
drug metabolism phase 1 vs phase 2
|
phase 1 = demethylation, oxidation, reduction, hydrolysis
phase 2 = glucourinidation, sulfation (makes water soluble) |
|
|
cyp inducers vs inhibitors
|
inducers = Queen Barb steals phenphen and refuses carbs, alcohol, and glucose (quinidine, barbituates, st john wart, phenytoin, rifampin, carbamezepine, chronic alcohol, glucocorticoids)
inhibitors = PiCK EGS (protease inhibitors, isoniazid, cimetidine, ketoconazole, erythromycin, grapefruit, sulfonamide) |
|
|
mechanism of colchicine
|
binds tubulin, inhibits migration of wbc
|
|
|
mechanism of cholestyramine
|
binds bile acids in gut, forces body to resynthesize bile acids from cholesterol
|
|
|
side effect of cholestyramine
|
ADEK deficiency
|
|
|
side effect of statins
|
rhabdo, live dysfunction
|
|
|
mechanism of promethazine in nausea
|
dopamine inhibitor
|
|
|
mechansm of octreotide
|
somatostatin anlogue
|
|
|
effects of digoxin
|
inhibits na/k atpase, increasing intracellular calcium -> ionotrope
slows av conduction |
|
|
check level of what before giving digxoin
|
k
|
|
|
what antiarrythmic has been implicated in causing mesenteric ischemia
|
digoxin
|
|
|
best single agent for mortality after MI
|
bb
|
|
|
best single agent for mortality with CHF
|
acei
|
|
|
what drugs to use for inhibition of adrenal steroid synthesis
|
metyrapone, aminoglutethimide
|
|
|
what drug to use to inhibit progression of metastatic prostate ca
|
leuprolide (inhibits lh and fsh when given continuously)
|
|
|
electrolyte abnormalities with ASA
|
respiratory alkalosis > metabolic acidosis
|
|
|
mc side effect with gadolinium
|
nausea
|
|
|
mc side effect with iodine contrast
|
nausea > dyspnea
|
|
|
mallampati class
|
1 = see entire uvula
2 = partial obstruction of uvula 3 = base of uvula visible 4 = only hard palate |
|
|
what is MAC
|
minimum alveolar concentration -- smallest concentration of inhalational agent that 50% people will not move
|
|
|
MAC vs lipid solubility
|
low MAC = more lipid soluble = more potent
|
|
|
speed of induction for inhalational vs solubility
|
inversely proportional, so faster agents are less potent
|
|
|
physiological effects of inhalational agents
|
myocardial depression, increased cerebral blood flow, decreased renal blood flow
|
|
|
side of halothane
|
hepatitis -- fever, eosinophilia, jaundice, increased lfts
|
|
|
which inhalational agent has highest cardiac depression/arythmias
|
halothane
|
|
|
which inhalational agent has termors at induction
|
NO2
|
|
|
which inhalational agent is least pungent
|
halothane
|
|
|
which inhalational agent is good for mask induction
|
sevoflurane cuz less laryngospasm and fast
|
|
|
which inhalational agent is good for neurosurgery
|
isoflurane, lowers brain o2 consumption, no increase in cp
|
|
|
which inhalational agent is associated with seizures
|
enflurane
|
|
|
side effects of sodium thiopental
|
decreased cerebral blood flow and metabolic rate, hypotension
|
|
|
side effects of propofol
|
hypotension, respiratory depression
|
|
|
allergy with propofol
|
egg
|
|
|
does propofol provide analgesia
|
no
|
|
|
benefit of ketamine
|
no respiratory depression
|
|
|
side effects of ketamine
|
hallucinations, catecholamine release, increased airway secretions, and increased cerebral blood flow
|
|
|
what is ketamine ci in
|
patients with head injury
|
|
|
benefits of etomidate
|
fever hemodynamic changes and fast acting
|
|
|
negatives of etomidate
|
continouous infusions can lead to adrenocortical supression
|
|
|
indications for RSI
|
recent oral intake, GERD, delayed gastric emptying, pregancy, bowel obstruction
|
|
|
what are the first and last mm to go down after paralytics? how about when recovering?
|
diaphragm last to go down, first to recover
neck muscles and face 1st to go down, las tto recover |
|
|
which paralytic is depolarizing
|
succinylcholine
|
|
|
side effects of succ
|
malignant hyperthermia , conversion of open angle glaucoma to closed angle
|
|
|
what dose of dantrolene to use for malignant hyperthermia
|
10 mg / kg
|
|
|
signs of malignant hyperthermia in OR after succ
|
(increased end tidal o2, fever, tachycardia, rigidity, acidosis and hyperkalemia)
|
|
|
which nondepolarizing agent can be used in liver and renal failure
|
cis-atracurium (hoffman degradation)
|
|
|
which nondepolarizing agent is fast? slow? long acting?
|
rocuronium is fast. pancuronium is slow and long lasting
|
|
|
metabolism - rocuronium vs pancuronium
|
hepatic vs renal
|
|
|
how to reverse nondepolarizing agents
|
neostigmine, edrophonium + atropine or glycopyrrolate
|
|
|
mechanism of nondepolarizing paralytics
|
competitively inhibits acetylcholine receptors
|
|
|
why do you use atropine and glycopyrrolate with reversal of nondepolarizing
|
blocks the muscarinic receptors so avoid the parasympathetic effects of neostigmine etc
|
|
|
why are infected tissues hard to anesthetize
|
acidosis prevents action of the agent
|
|
|
when is epinephrine ci in local anesthesia
|
arrythmia
unstable angina uncontrolled hypertension poor collaterals ureteroplacental insufficiency |
|
|
which local anesthetics tend to have allergic reactions
|
esters
(amides have two i's in their name) |
|
|
metabolism of narcotics
|
liver met, renal excretion
|
|
|
what can use of narcs in pts on MAOIs cause
|
hyperpyrexic coma
|
|
|
hemodynamic effect of histamine release
|
hypotension
|
|
|
morphine effect on cough
|
decreases cough
|
|
|
side effects of demerol
|
tremors, fasciculations, convulsions, seizures
|
|
|
avoid use of demerol in which pts
|
renal failure
|
|
|
is there histamine release with morphine? demerol?
|
yes, no
|
|
|
cross rxn with morphine and fentanyl?
|
no
|
|
|
what are the fastest acting narcs
|
sufentanil, remifentanil
|
|
|
what is the most potent narc
|
sufentanil
|
|
|
do benzos have analgesia
|
no
|
|
|
can you use versed in pregnants
|
no
|
|
|
how to tx overdose of benzos
|
flumazenil
|
|
|
ci of flumazenil
|
elevated ICP or status epilepticus
|
|
|
morphine in epidural can cause
|
respiratory depression
|
|
|
lidocaine in epidural can cause
|
bradycardia and hypotension
|
|
|
how to tx acute hypotension and bradycardia with epidural
|
fluids, phenylephrine, atropine
|
|
|
who is epidural contraindicated in
|
hypertrophic cardiomyopathy, cyanotic heart disease (sympathetic denervation causes decreased afterload)
|
|
|
where does injection occur in spinal anesthesia
|
subarachnoid space
|
|
|
complications of epidural, spinal anesthesia
|
hypotension, bradycardia, respiratory depression if high spinal, HA, urinary retention, abscess/hematoma
|
|
|
tx for spinal HA with epidural
|
rest, fluids, caffeine, analgesics
|
|
|
what preop conditions is assoc with most postop mortality
|
renal failure, CHF
|
|
|
risk factors for postop MI
|
age > 70
DM previous MI CHF unstable angina |
|
|
sudden transient rise in ETCO2 during surgery
|
hypoventilation, increase tidal volume or respiratory rate
|
|
|
sudden drop in ETCO2 during surgery
|
vent disconnect, PE (look for hypotension in PE)
|
|
|
where should ET tube be placed
|
2cm above carina
|
|
|
MC PACU complication
|
NV
|
|
|
what determines osmotic gradient between plasma and interstitium? between intracellular and extracellular?
|
protein, sodium
|
|
|
first sign of volume overload
|
weight gain
|
|
|
ionic composition of LR
|
130 na
4 k 2.7 Ca 109 Cl 28 Bicarb |
|
|
how to calculate plasma osmolarity
|
2*Na + glucose/18 + BUN/2.8
|
|
|
how much fluid loss in open abdominal cases
|
0.5-1L /h
|
|
|
how much insensible losses, where are they from
|
10cc/kg/day
75% skin, 25% respiratory |
|
|
benefit of using D5 in mIVF
|
stimulates insulin release which results in amino acid uptake and prevents catabolism
|
|
|
normal daily na requirement? k requirement?
|
1 meq/kg/day
.5 meq/kg/day |
|
|
what lytes are lost in
sweat saliva stomach pancreas bile small intestine large intestine |
hypotonic
k h, cl bicarb bicarb bicarb, k k |
|
|
how to replace gastric losses
|
D5 1/2NS +K
|
|
|
how to replace losses from pancreas/biliary/small intestine
|
LR with bicarb
|
|
|
how to replace large intestine losses
|
LR + K
|
|
|
ekg sign of hyperkalemia
|
peak t wave
|
|
|
how to tx hyperkalemia
|
calcium gluconate acutely
bicarb insulin + D50 kayexalate |
|
|
ekg change with hypokalemia
|
flat t waves
|
|
|
what 2 fluid and electrolyte things need to be checked for hypokalemia
|
overdiuresis leads to hypokalemia
check mag |
|
|
how to tx symptomatic hypernatremia
|
slow infusion of D5
|
|
|
how to tx hyponatremia
|
water restriction, then diuresis
|
|
|
how slow to correct hyponatremia
|
no more than 1meq/hr
|
|
|
how to correct for glucose in hyponatremia
|
each 100 glucose above normal, add 2 to Na
|
|
|
MC malignant cause of hypercalcemia
|
breast cancer
|
|
|
MC benign cause of hypercalcemia
|
hyperPTH
|
|
|
what to avoid in hypercalcemia
|
no LR, no thiazide diuretics
|
|
|
how to tx hypercalcemia of malignancy
|
mithramycin, calcitonin, alendronic acid, dialysis
|
|
|
how to tx hypercalcemia
|
fluids (NS) and lasix
|
|
|
symptoms of hypocalcemia
|
hyperreflexia
Chvostek sx perioral tingling Trousseau sx prolong QT interval |
|
|
how to calculate corrected calcium
|
(4- albumin) *.8 + Ca
|
|
|
what lyte do you need to check before correcting Ca
|
Mg
|
|
|
how to tx hypermag
|
calcium
|
|
|
usual cause of hypermag
|
renal failure pts on mag
|
|
|
usual cause of hypomag
|
massive diuresis, chronic TPN, EtOH abuse
|
|
|
how to calc AG
|
Na - (bicarb + Cl)
|
|
|
causes of AG MA
|
MUDPILES
methanol uremia DKA paraldehydes isoniazid lactate ethylene glycol salicylates |
|
|
mechanism of contraction alkalosis
|
usually associated with metabolic alkalosis
loss of water leads to Na reabsorption in exchange for K leading to hypokalemia Na/H exchanger leads to paradoxical aciduria |
|
|
FeNa in prerenal
|
<1%
|
|
|
how much renal mass must be damaged before increase in Cr and BUN
|
70%
|
|
|
what is myoglobin converted to that is toxic to renal cells
|
ferrihemate
|
|
|
what lytes accumulate in tumor lysis syndrome? which ones are decreased
|
phosphate, uric acid. decreased calcium
|
|
|
how to tx tumor lysis syndrome
|
hydration
rasburicase (converts uric acid to allantoin which is harmless) allopurinol diuretics alkalinization |
|
|
transferrin vs ferritin
|
transferrin is a transporter of iron, whereas ferritin is storage form
|
|
|
approx caloric need
|
20 cal/kg/day
|
|
|
how many calories in fat? protein? oral carbs? dextrose?
|
9cal/g
4 cal/g 4cal/g 3.4cal/g |
|
|
nutritional requirements for adult healthy male - protein, fat, carbs
|
20% protein (1g protein/kg/day, 20% are essential amino acids)
30% faat 50% carbs |
|
|
how much does pregnancy increase kcal req by? how about lactation
|
300 kcal/day
500 kcal/day |
|
|
increased caloric requirement in burns in addition to maintenance
|
30 kcal/day * BSA
3g * BSA |
|
|
how much does fever increase basal metabolic rate
|
10% for each degree above 38c
|
|
|
what is energy source in central TPN vs PPN
|
glucose vs fat
|
|
|
what is form of energy used by colonocytes
|
short chain fatty acids
|
|
|
what is form of energy used by small bowel enterocytes
|
glutamine
|
|
|
what is form of energy used by most neoplastic cells
|
glutamine
|
|
|
metabolism of glutamine
|
release of ammonia in kidney
|
|
|
half life of albumin? transferrin? prealbumin
|
18d, 10d, 2d
|
|
|
how to calculate ideal body weight
|
men = 106 lbs + 6 lbs for each inch over 5 ft
women = 100 + 5 lbs for each inch over 5 ft |
|
|
3 signs of poor preop nutritional status
|
weight loss > 10% in 6mo
weight <85% of IBW albumin < 3 |
|
|
what is respiratory quotient and how to use it for nutrition
|
ratio of co2 produced to o2 consumed
RQ>1 = overfeeding, decrease carbs and calories RQ<.7 = starving, increase carbs and calories |
|
|
significance of respiratory quotient range
|
RQ .7 = fat use
RQ .8 = protein use RQ 1 = carb use |
|
|
timelines for diuresis, catabolic phase, anabolic phase
|
catabolic = POD0-3
anabolic = POD3-6 diuresis = POD2-5 |
|
|
how long does it take glycogen stores to deplete
|
24-36h
|
|
|
what is the primary substrate for gluconeogenesis, what are some others
|
amino acids esp alanine
lactate, pyruvate, glycerol |
|
|
where does gluconeogenesis occur in late starvation
|
kidney
|
|
|
main source of energy in starvation? trauma?
|
fat
mostly fat, but more protein |
|
|
how many days w/o eating
|
7d
|
|
|
benefits of enteral feeding
|
avoid bacterial translocation (bacterial overgrowth, increased gut permeability, bacteremia)
avoid TPN complications |
|
|
when do you consider gastrostomy for lack of feeding access
|
>4w
|
|
|
energy source for brain
|
glucose>ketones
|
|
|
cause of refeeding syndrome
|
occurs with feeding after starvation, results in decreased k,mg, and phosphate
|
|
|
what things besides brain use exclusively glucose
|
peripheral nerves, adrenal medulla, RBC, WBC
|
|
|
major molecule in cachexia
|
tnf alpha
|
|
|
1 g of nitrogen corresponds to how much protein
|
6.25
|
|
|
how to calculate nitrogen balance
|
protein ingested/6.25 - (24 hour urine nitrogen + 4g)
|
|
|
normal protein synthesis for healthy male
|
250g/day
|
|
|
amino acids in skeletal muscle mostly broken down to...
|
glutamine and alanine
|
|
|
how do long chain FFA enter circulation vs short and medium chain
|
short and medium chain get in by diffusion and go thru portal system
long chain enters via micelles and get sent through lymphatics |
|
|
use for saturated vs unsaturated fatty acids
|
saturated fats = fuel, esp for colonocytes, liver, heart, and skeletal mm
unsaturated fats = cellular structural components |
|
|
lipoprotein lipase vs hormone sensitive lipase
|
lipoprotein lipase = in liver and adipose, clears chylomicrons and TAGs
HSL = in adipose, breaks down TAGs to fatty acids and glycerol and releases to bloodstream |
|
|
what is hormone sensitive lipase resond to
|
growth hormone, glucocorticoids, catecholeamines
|
|
|
what are essential fatty acids
|
linolenic , linoleic acids
|
|
|
absorption of glucose, galactose, fructose into gut
|
glucose, galactose = active transport
fructose = facilitated diffusion |
|
|
sucrose vs lactose vs maltose
|
maltose = 2x glucose
lactose = galactose = glucose sucrose = fructose + glucose |
|
|
in which pts do you have to limit protein intake
|
liver failure, renal failure -- avoid hyperammonia
|
|
|
what are branched chain amino acids, where are they metabolized, why is that significant
|
leucine, isoleucine, valine
muscle can be preferentially used in liver failure pts |
|
|
essential amino acids
|
TV FILM HWRK = threonine, valine, pheynlalanine, isoleucine, leucine, methionine, histidine, tryptophan, arginine, lysine
|
|
|
central TPN composition
|
10% AA
50% Dextrose lytes minerals vitamins |
|
|
how many cals in TPN lipids
|
10% lipids = 1.1kcal/cc
|
|
|
what is cori cycle
|
glucose converted to lactate in muscle
lactate goes to liver and is converted to pyruvate and glucose (gluconeogensis) |
|
|
what molecule does PET detect
|
fluorodeoxyglucose
|
|
|
what neoplasm is AFP assoc with
|
liver ca
|
|
|
what neoplasm is ca 19 9
|
pancreas
|
|
|
what neoplasm is ca 125 assoc with
|
ovarian
|
|
|
what neoplasm is beta hcg assoc
|
testicular, choriocarcinoma
|
|
|
what neoplasm is NSE (neuron specific enolase) assoc with
|
small cell lung ca, neuroblastoma
|
|
|
what marker is carcinoid assoc with
|
chromogramin A
|
|
|
what marker is thyroid medullary ca assoc with
|
ret oncogene
|
|
|
half life of CEA, PSA, AFP
|
18d, 18d, 5d
|
|
|
what translocation assoc with Burkitt
|
8-14
|
|
|
most vulnerable stage of cell cycle for xrt
|
m phase
|
|
|
higher energy radiation effect on skin
|
skin preserving
|
|
|
benefits of fractionate xrt doses
|
repair of normal cells
reoxygenation of tumor (to allow more free radicals) redistribution of tumor cells in cell cycle |
|
|
what are radioresistant tumors
|
epithelial, sarcomas
|
|
|
are large or small tumors more sensitive to xrt
|
small, cuz large ones don't have o2
|
|
|
killing ability of cell cycle specific agents vs nonspecific agents
|
plateau in killing ability vs linear response
|
|
|
risk, benefit of tamoxifen
|
decreases short term risk of breast ca by 50%
1% risk of blood clot .1% risk of endometrial cancer |
|
|
mechanism of taxol
|
stabilizes microtubules
|
|
|
toxicity of cisplatin
|
nephro, neuro, oto
|
|
|
tox of carboplatin
|
BM suppression
|
|
|
tox of binblastine
|
BM suppresion
|
|
|
mechanism of vincristine/vinblastine
|
microtubule inhibitors
|
|
|
tox of vincristine
|
peripheral neuropathy, neurotox
|
|
|
mechanism of alkylating agents
|
transfer alkyl agents and form covalent bonds to DNA
|
|
|
what drug to use for hemorrhagic cystitis caused yb cyclophosphamide
|
mesna
|
|
|
tox of cyclophosphamide
|
gonadal dysfunction , SIADH, hemorrhagic cystitis
|
|
|
what drug can stimulate immune system against cancer
|
levamisole
|
|
|
mechanism of MTX
|
inhibition of DHFR
|
|
|
tox of MTX
|
renal tox
|
|
|
how to reverse effect of MTX
|
leucovorin rescue (folinic acid)
|
|
|
mechanism of 5FU
|
inhibits thymidylate synthetase
|
|
|
effect of leucovorin with 5FU
|
increases tox
|
|
|
mechanism of doxorubicin
|
dna intercalator and o2 former
|
|
|
tox of coxorubicin
|
cardiotox, doses >500
|
|
|
mechanism of etoposide
|
inhibits topoisomerase
|
|
|
which neoplastic agents have least myelocuppression
|
bleomycin, vincristine, busulfan, cisplatin
|
|
|
what is sweet syndrome, when do you see it
|
acute febrile neutropenic dermatitis seen when using GCSF for neutrophil recovery after chemo
|
|
|
when do you do mastectomy with normal breast
|
BRCA I or II + with strong famhx
|
|
|
when do you do thyroidectomy with normal thyroid
|
RET proto oncogene with fam hx
|
|
|
which chromosome assoc with rb1? p53? apc? DCC?
|
13, 17, 5, 18
|
|
|
function of dcc protein
|
cell adhesion
|
|
|
function of bcl protein
|
apoptosis
|
|
|
what are each of these a defect in?
ras src sis erb B myc |
G protein
tyrosine kinase PDGF receptor EGF receptor transcription factors |
|
|
initial gene mutation on pathway to colorectal ca
|
apc
|
|
|
what do each of these carcinogens lead to
coal tar beta naphthylamine benezene asbestose |
larynx, skin, bronchial ca
urinary tract/bladder ca leukemia mesothelioma |
|
|
suspicious axillary node which cancers
|
lymphoma, breast, melanoma
|
|
|
suspicious supraclavicular node which cancers
|
neck, breast, lung, stomach (virchow) pancreas
|
|
|
suspicous periumbilical node
|
pancreas (sister mary joseph)
|
|
|
ovarian met
|
stomach ca (krukenberg), colon
|
|
|
mc mets to bone
|
breast, prostate
|
|
|
mc met to skin
|
breast, melanoma
|
|
|
mc sb met
|
melanoma
|
|
|
4 phases of clinical trails
|
1 = safe, what dose?
2 = effective? 3 = better than existing? 4 = implementation |
|
|
different types of ca tx -- induction, primary, adjuvant, salvage
|
induction = sole tx, used for advanced disease or if no other tx exists
primary = 1st chemo, followed by secondary adjuvant = combined with other modality salvage = fail to respond |
|
|
when to do palliative surg for ca
|
tumor of hollow viscus causing obstruction or bleeding
breast ca with skin or chest wall involvement |
|
|
can you do sentinal node bx in pts with palpable nodes
|
no need to dissect them
|
|
|
rate of colon met to liver survival rate
|
35% 5-yr survival if successfully resected
|
|
|
5 positive prognostic factors for survival after resection of hepatic colorectal mets
|
disease free interval > 1yr
tumor number <3 CEA< 200 size < 5cm negative nodes |
|
|
most successfully cured mets with surg
|
colon cancer in liver
sarcoma to lung |
|
|
which type of ca does surgical debulking help chemo
|
ovarian ca
|
|
|
which solid tumors can cure with chemo only
|
hodgekins, NHL
|
|
|
name some t cell lymphomas
|
htlv -1, mycosis fungoides (sezary cells)
|
|
|
which growth factor implicated in angiogenesis
|
VEGF
|
|
|
most important HLA's in recipient/donor matching in order of importanc
|
HLA-DR>HLA-A~HLA-B
|
|
|
what kind of transplantation is ABO blood compatiblity not required in
|
liver
|
|
|
what things are tested against one another in a cross match
|
recipient serum vs donor lymphocytes
|
|
|
what is panel reactive antibody
|
detection of preformed recipient antibodies by mixing them against panel of HLA cells
|
|
|
is low or high PRA a contraindication to txp
|
high
|
|
|
tx of mild rejection vs severe rejection
|
pulse steroids vs
steroids and antithymoglobulin or daclizumab |
|
|
mc malignancy after transplant
|
skin cancer (squamous cell) > PTLD (post transplant lympho-proliferative disorder)
|
|
|
what is post transplant lympho proliferative disorder thought to be due to?
|
EBV
|
|
|
how to tx post transplant lympho proliferative d/o
|
withdraw immunosuppression, maybe chemo/xrt
|
|
|
mechanism of mycophenolate
|
inhibits purine synthesis
|
|
|
which txp meds require a WBC goal
|
mycophenolate, ATG
|
|
|
2 anti-inflammatory functions of steroids
|
inhibit macrophages
inhibit genes for cytokine synthesis (il1, il6) |
|
|
given these txp antirejection drugs, which are induction, maintenance, and acute:
mycophenolate steroids cyclosporin fk 506 (prograf) sirolimus ATG zenapax (daclizumab) |
mycophenolate - maintenance
cyclosporin - maintenance fk 506/prograf - maintenance sirolimus - maintenance ATG - induction and acute rejection zenapax - induction and acute rejection steroids - induction, maintenance, acute rejection |
|
|
mechanism of cyclosporin
|
binds cyclophilin
inhibits cytokine synthesis (il2, il4) |
|
|
trough goal for cyclosporin
|
200-300
|
|
|
side effects of cyclosporin
|
nephrotox, hepatotox, tremor, seizure, HUS
|
|
|
excretion of cyclosporin
|
biliary
|
|
|
mechanism of fk 506, what is another name
|
prograf
binds fk binding protein (similar to cyclosporine but stronger) |
|
|
side effects of prograf compared to cyclosporin
|
nephrotox
more gi and mood sx than cyclosporine less enterohepatic recirculation less rejection in kidney txps |
|
|
goal trough for prograf
|
10-15
|
|
|
mechanism of sirolimus
|
binds fk binding protein, BUT INHIBITS mTOR UNLIKE PROGRAF
this inhibits T & B cell response to IL2 |
|
|
what kind of antibody is ATG
|
horse or rabbit POLYCLONAL
|
|
|
wil ATG work in someone who is complement deficient
|
no it is complement dependent
|
|
|
side effects of ATG
|
cytokine release syndrome (fever, pulmonary edema, shock)
GIVE STEROIDS AND BENADRYL PRIOR TO DRUG TO PREVENT |
|
|
mechanism of daclizumab (zenapax)
|
monoclonal ab against il2
|
|
|
accelerated rejection vs acute rejection
|
< 1 week vs 1 week to 1 month
|
|
|
tx for hyperacute rejection
|
emergent retransplant or removal if kidney
|
|
|
tx for acute/accelerated rejection
|
increase immunosuppression, pulse steroids, antibody tx
|
|
|
tx for chronic tx
|
increase immunosuppression
|
|
|
how long can you store kidney
|
2d
|
|
|
compatibility tests for kidney
|
ABO, crossmatch
|
|
|
can you do kidney txp if uti
|
yes
|
|
|
can you do kidney transplant if acute rise in cr
|
yes
|
|
|
which vessels are txp kidneys attached to
|
iliac vessels
|
|
|
#1 complication of renal transplant, how to tx
|
urine leaks, drainage and stenting
|
|
|
how to dx and tx renal artery stenosis assoc with kidney transplant
|
u/s, pta w/ stent
|
|
|
mcc external ureter compression s/p kidney transplant, how to tx, what if that fails
|
lymphocele, perc drain if that fails, peritoneal window
|
|
|
what is postop oliguria due to after kidney txp
|
atn
|
|
|
what is postop diuresis due to after kidney txp
|
urea and glucose
|
|
|
new proteinuria after kidney transplant suggestive of
|
renal vein thrombosis
|
|
|
what is postop dm2 after kidney txp due to
|
csa, fk, steroids
|
|
|
how to tx cmv vs hsv
|
gancyclovir vs acyclovir
|
|
|
kidney rejection workup (increased cr, poor UOP)
|
u/s with duplex, biopsy
decrease csa/fk pulse steroids |
|
|
tx for chronic rejection
|
no good tx
|
|
|
5 year graft survival for kidney
|
cadaver = 65%, living = 75%
|
|
|
mc complication of living kidney donation? most common cause of death?
|
wound infection
PE |
|
|
how long can you store liver txp
|
24h
|
|
|
contraindications for liver txp
|
current ETOH abuse, acute ulcerative colitis
|
|
|
mc reason for liver txp in adults
|
chronic hep c
|
|
|
factors in MELD score
|
Cr, INR, TB
|
|
|
what MELD score benefits from liver TXP
|
>15
|
|
|
criteria for urgent liver txp
|
fulminant hepatic failure
|
|
|
how to prevent reinfection in ppl with hep b after liver txp, how much does it lower rate
|
HBIG
lamivudine reduces rate to 20% |
|
|
reinfection rate of hep b vs hep c
|
with hbig and lamivudine, hep b is 20%
hep c is ~100% |
|
|
is portal vein thrombosis a CI to txp liver
|
no
|
|
|
what is recidivism (start drinking again) rate after liver txp
|
20%
|
|
|
if >50% of liver txp cross section is macrosteatatic, what is rate of primary non function
|
50%
|
|
|
what kind of anastamosis for liver txp
|
duct to duct, hepaticojejunostomy in pediatrics
|
|
|
what drains placed in liver txp
|
r subhepatic, r+l subdiaphragmatic
|
|
|
blood supply of biliary system
|
hepatic a
|
|
|
mc common arterial anomoly seen in liver txp
|
replaced r hepatic
|
|
|
mc complication of liver txp, how to tx
|
bile leak
place drain -> ERCP with stent across leak |
|
|
what is primary nonfunction after liver txp
|
1st 24h -- tb >10, bile output < 20cc/12h, elevated pt/ptt
after 96h -- AMS, increased LFT, renal failure, respiratory failure |
|
|
early hepatic a thrombosis vs late hepatic a thrombosis after liver txp
|
early = fulminant liver failure with lfts elevated and low bile output
late = biliary strictures and abscesses |
|
|
sx of ivc thrombosis/stenosis after liver txp? tx? is it common?
|
edema, ascites, renal failure
thrombolytics/IVC stent not common |
|
|
early vs late portal vein thrombosis after liver txp
|
early = abd pain
late = UGIB, acites |
|
|
tx for early portal vein thrombosis after txp
|
reoperation -- thrombectomy, revise anastamosis
|
|
|
histology of cholangitis after liver txp
|
pmns around portal triad
|
|
|
pathology of acute rejection after liver txp vs chronic rejection
|
portal triad lymphocytosis, endotheliitis, bile duct injury
disappearing bile ducts, bile duct obstruction with increased ALP, portal fibrosis |
|
|
what is retransplantation rate after liver txp
|
20%
|
|
|
what is 5yr survival rate after liver txp
|
70%
|
|
|
what donor vessels are needed for pancreas txp
|
celeiac and sma arteries
portal vein |
|
|
what vessels are attached in pancreas txp
|
iliac vessels
|
|
|
where does pancreatic duct anastamosis go in pancreas txp
|
duodenoenterostomy (donor duodenum to recipient bowel)
|
|
|
does pancreas txp help with retinopathy? gastroparesis? vascular disease?
|
yes yes no
|
|
|
#1 complication of pancreas txp
|
venous thrombosis
|
|
|
how to dx rejection in pancreas txp
|
difficult
increased glucose or amylase fever leukocytosis |
|
|
how long can heart be stored for txp
|
6h
|
|
|
what blood tests needed for heart txp
|
abo compatibility, crossmatch
|
|
|
what is pulmonary complication of heart txp, what is it assoc with, tx
|
pulmonary hypertension, early mortality, NO+ECMO
|
|
|
pathology of acute rejection in heart txp
|
perivascular lymphocytic infiltrate with varying grades of myocyte inflammation and necrois
|
|
|
mcc of late death death overall following heart txp
|
chronic allograft vasculopathy (progressive diffuse coronary atherosclerosis)
|
|
|
how long can you store lung for txp
|
6h
|
|
|
#1 cause of early mortality after lung txp, how to txp
|
reperfusion injury, similar to ARDS
|
|
|
indication for bilateral lung txp
|
cystic fibrosis
|
|
|
exclusion criteria for lung txp
|
aspiration
moderate to large contusion infiltrate purulent sputum P/F ratio < 350 with PEEP of 5 |
|
|
pathology of acute vs chronic rejection in lung txp
|
peripvascular lymphocytosis vs bronchiolitis obliterans
|
|
|
mcc death after lung txp
|
chronic rejection
|
|
|
how to ppx PCP
|
bactrim
|
|
|
what are the fungal opportunistic infection
|
aspergillus, candida, cryptococcus
|
|
|
who, in order of priority, can decide to donate body for organ donation
|
spouse>adult children> parents>siblings>guardian>any other person authorized
|
|
|
what things are released by endothelium in response to injury
|
collagen, platelet activating factor, tissue factor
|
|
|
what cytokines do platelets release once they bind collagen
|
PDGF
|
|
|
what are the most important leukocyte in wound healing, what do they release
|
macrophages
growth factors (PDGF) and cytokines (IL1, TNFalpha) |
|
|
what does PDGF do
|
activates leukocytes -- PMNs, macrophages
activates fibroblasts promotes angiogenesis promotes epithelialization |
|
|
how does EGF differ from PDGF
|
both activate fibroblasts and promote angiogenesis and epithelialization
PDGF also activates leukocytes |
|
|
how does FGF differ from PDGF
|
both activate fibroblasts and promote angiogenesis and epithelialization
PDGF also activates leukocytes |
|
|
what is platelet activating factor
|
a phospholipid that is chemotactic for inflammatory cells and increases amount of adhesion molecules
|
|
|
what are the main chemotactic factors for inflammatory cells
|
PDGF, IL8, LTB4, C5a, C3a, PAF
|
|
|
what are the main chemotactic factors for fibroblasts
|
PDGF, EGF, FGF
|
|
|
what are the main factors for angiogenesis
|
PDGF, EGF, FGF, IL8, hypoxia
|
|
|
what are the main factors for epithelialization
|
PDGF EGF, FGF
|
|
|
how long do PMNs last
|
1-2 days in tissues, 7 days in blood
|
|
|
how long do platelets last
|
7-10d
|
|
|
which cells release major basic protein? what does it do
|
stimulates basophils and mast cells to release histamine
|
|
|
which immune cells have ige receptors
|
eosinophils
|
|
|
which immune cells release histamine in blood? in tissues?
|
basophil
mast cell |
|
|
effects of histamine
|
vasodilation, capillary leakage
|
|
|
effects of bradykinin
|
peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction
|
|
|
what is the precursor for NO, what molecule processes it
|
arginine, guanylate cyclase (increases cGMP)
|
|
|
what is endothelin
|
causes vascular smooth muscle contraction
|
|
|
what is initial cytokine response to injury and infection
|
tnf alpha and il1
|
|
|
what is the largest producer of tnf? il1?
|
macrophage
|
|
|
what does tnf alpha do
|
increase adhesion molecules, procoagulant
causes cachexia activates PMNs and macrophages high concentrations can cause circulatory collapse |
|
|
what cytokine is responsible for raising set point
|
il1
|
|
|
what molecule do alveolar macrophages release when collapsed
|
il1, mechanism of atalectasis
|
|
|
which cytokine increases hepatic acute phase protien production
|
il6
|
|
|
what kind of leukocyotes does interferon activate
|
NK, macrophages, cytotoxic T cells
|
|
|
function of crp
|
opsonin that activates complement
|
|
|
what are the hepatic acute phase reactants
|
crp, amyloid A&P, fibrinogen, haptoglobin, ceruloplasmin, a1at, c3
|
|
|
what hepatic proteins are decreased in an acute phase rxn
|
albumin, prealbumin, transferrin
|
|
|
what are selectins involved in, where are they found
|
rolling adhesion.
NOTE: l = leukocytes, e = endothelial, p = platelet |
|
|
what are beta 2 integrins, where are they found, what is another name, what do they do
|
cd11/18
bind ICAMS found on leukocytes anchoring adhesion (vs rolling) |
|
|
what is ICAM/VCAM/PECAM/ELAM
|
binds integrins on leukocytes and plts, help to mediate transendothelial migration
|
|
|
classic pathway vs alternative pathway iin complement cascade
|
classic = antibodies, involves C1,C2,C4 (which aren't in alt)
alternative = endotoxin, or other stimuli, involves factors B,D,P C3 is common to both |
|
|
what metal cofactor is required for complement
|
Mg
|
|
|
which factors in complement pathway increase vascular permeability and cause bronchoconstriction; activate mast cells and basophils
|
C3a, 4a, 5a
|
|
|
what complement proteins responsible for MAC
|
C5b-9b
|
|
|
what complement proteins responsible for opsonization
|
C3b, C4b
|
|
|
which complement proteins mediate chemotaxis
|
C3a, C5a
|
|
|
what step in the arachadonic acid pathway do steroids block
|
blocks phospholipase, which converts phospholipids into arachidonic acid
|
|
|
what do each of the following cause: ltc4, ltd4, lte4, ltb, 4
|
ltc-e are slow reacting substances of anaphylaxis -- bronchoconstriction, bronchoconstriction, increased vascular permeability
ltb4 = chemotaxis |
|
|
when do catechols peak after injury
|
24-48h
|
|
|
what is the neuroendocrine response to injury
|
CRF, ACTH, ADH, GH, epinephrine, norepinephrine
|
|
|
what are CXC cytokines? what do they do, what are the main examples
|
cysteine - X - cysteine
chemotaxis, angiogenesis, wound healing IL8, PF4 |
|
|
what enzyme makes superoxide anion radical? what makes hydrogen peroxide
|
NADPH oxidase
xanthine oxidase |
|
|
what enzyme neutralizes superoxide anion radical? hydrogen peroxide
|
superoxide dismutase (converts to H2O2)
glutathione peroxidase, catalase |
|
|
what leukocyte is responsible for most of the ill effects of reperfusion injury
|
PMNs
|
|
|
what enzyme is defective in chronic granulomatous disease
|
NADPH oxidase
|
|
|
3 stages of wound healing & timeline
|
inflammation -> proliferation -> remodeling
0-1 week 1-3 weeks 3 weeks+ |
|
|
what stage of wound healing does epithelialization occur? at what rate?
collagen cross linking? how about collagen deposition? neovascularization? formation of granulation tissue? replacement of type 3 collagen with type 1? |
inflamation. 1-2mm/day
remodeling proliferation proliferation proliferation proliferation |
|
|
how does amount of collagen change in remodeling stage of wound healing
|
does not change, but production and degradation occur
|
|
|
what is rate of healing for peripheral nerves
|
1mm/day
|
|
|
list these cells in order of when they arrive to wound, earliest first.
lymphocytes PMNs PLTs macrophages fibroblasts |
platelets
PMNs macrophages lymphocytes fibroblasts |
|
|
what are the most predominant cells in a wound on day 1
day 3 day 5 |
PMN
macrophage fibroblast |
|
|
function of fibroblasts
|
replace fibronectin/fibrin with collagen
|
|
|
function of fibronectin
|
chemotaxis for macrophages, and anchors fibroblasts
|
|
|
what do macrophages do in wound healing
|
releases growth factors and cytokines, act as director and organizer
|
|
|
platelet plug vs provisional matrix
|
plt + fibrin vs plt + fibrin + fibronectin
|
|
|
does reopening wound result in slower healing?
|
no faster cuz healing cells are there
|
|
|
most important factor in healing open wounds
|
epithelialization (i.e. healing by secondary intention)
|
|
|
where does migration occur mostly from during epithelialization? what does it depend on
|
hair follicles>wound edges~sweat glands
depends on granulation tissue |
|
|
most important factor in healing closed incisions? what does that depend on
|
tensile strength (i.e. healing by primary intention)
collagen deposition and cross linking |
|
|
what is the strength layer of the bowel, what is the weakest point for an anastomsosi
|
submucosa
3-5d |
|
|
what cells are involved in wound contraction and healing by secondary intention? how do they communicate
|
myofibroblasts
gap junctions |
|
|
what is required for hydroxylation and cross linking of proline residues in collagen
|
alpha keto gluterate, vitamin C, oxygen, iron
|
|
|
how does dm inhibit wound healing
|
hyperglycemia causes poor leukocyte chemotaxis
|
|
|
what can be given to counteract effects of steroids on wound healing
|
25000 IU qday of vitamin A
|
|
|
effect of smoking on wound
|
wound hypoxia/ischemia
|
|
|
what is epidermolysis bullosa? caused by? how to tx?
|
poor wound healing
excessive fibroblasts phenytoin |
|
|
where do diabetic foot ulcers usually occur
|
charcot's joint (2nd MTP)>toes
|
|
|
what are most leg ulcers due to
|
VENOUS (not arterial) insufficiency
|
|
|
when should you do a scar revision
|
1yr to allow for maturation and to see if it improves with age
|
|
|
what glycosaminoglycan do scars contain
|
hyaluronic acid
|
|
|
what is blood supply to cartilage
|
none, gets nutrients by diffusion
|
|
|
when does chemotherapy stop having an effect on wound healing
|
14d
|
|
|
keloid formation - is it genetic?
|
autosomal dominant
|
|
|
how to tx keloids? hypertrophic scar tissue
|
steroid INJECTION, silicone, pressure garments, XRT
steroids, silicone, pressure NO XRT |
|
|
keloids vs hypertrophic scar tissue
|
in keloids collagen goes beyond the original scar, in hypertrophic, stay in the original scar
|
|
|
risk factor for hypertrophic scar tissue
|
dark skin
flexor surfaces of upper torso |
|
|
what are alpha granules, where are they
|
granules of PF4, beta thrombomodulin, PDGF, and TGF beta
platelets |
|
|
what are dense granules
where are they |
adenosine, serotonin, calcium
platelets |
|
|
what are the major platelet aggregation factors
|
txa2, thrombin, PF4
|
|
|
function of tgf beta
|
modulates platelet alpha granules
|
|
|
when are the 3 peaks for trauma related deaths
what are they due to |
1st peak = <30min - severe vascular or neurological injury
2nd = <4h - head injury>hemorrhage (golden hour) 3rd = days- weeks (multisystem organ failure/sepsis) |
|
|
most common organ injury in blunt trauma
|
liver
|
|
|
biggest factors in predicting mortality from falls
|
age, body orientation
|
|
|
ld50 for mortality from falls
|
4 stories
|
|
|
mc organ injury in penetrating injury
|
small bowel
|
|
|
classes of shock
|
I - normotensive, generally normocardic, <15%
II - tachycardic <30%, anxiety III - tachy and hypotension, AMS with confusion <40% IV - |
|
|
mc cause of death after reaching ER alive in trauma
|
head injury
|
|
|
mc cause of death in long term for trauma pts
|
infection
|
|
|
mc cause of upper airway obstruction in trauma pts
|
tongue
|
|
|
when to give blood for resuscitation
|
after 2l crystalloid
|
|
|
seat belts cause what kind of injury
|
small bowel perf, lumbar spine fx, sternal fx
|
|
|
indication for dpl
|
blunt trauma with hypotension
|
|
|
when is dpl positive
|
>10cc blood, >100k rbc/cc, gross contaminants, >500 wbc/cc
|
|
|
what does DPL miss
|
retroperitoneal bleeds, contained hematomas
|
|
|
what is minimum amount of free fluid for fast that it can detect
|
<50cc
|
|
|
what does fast scan miss
|
retroperitoneal bleeds, hollow viscus injury
|
|
|
what does ct scan miss in trauma pt
|
diaphragm injury, hollow viscus injury
|
|
|
do you need laparotomy for small evisceration? diaphragm injury? liver lac? extraperitoneal bladder injury?
|
yes, yes, no no
|
|
|
sign of abd compartment syndrom
|
bladder pressure > 25
|
|
|
mechanism of abd compartment syndrome
|
IVC compression
|
|
|
when to perform ER thoracotomy
|
blunt trauma -- if came in with vital signs but lose in ER
penetrating -- if had vitals, but lost ON THE WAY or IN ER |
|
|
gcs motor
|
6 = follows commands
1 = no response 4 = withdraws 3 = flexion with pain 2 = extension with pain 5 = localizes pain |
|
|
verbal gcs
|
5 = oriented
1 = no response 4 = disoriented/confused 3 = inappropriate word usage 2 = garbled |
|
|
eye gcs
|
4 = sponteanously open
3 = to command |
|
|
indication for intubation off gcs
|
<=8
|
