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deck_1522518 Flashcards

1
Q

what increases cell membrane fluidity

A

cholesterol

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2
Q

What gradient is used for co-transport of glucose, proteins and other mlq?

A

Na+ gradient

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3
Q

Are cells more negative inside or outside and why?

A

negative inside compared to outside bc of Na/K ATPase (3Na+ out/ 2K+ in)

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4
Q

What are the following1) adhesion mlq (cell to cell and cell to extracellular2) cell to cell occluding junctions (impermeable)3)permeable jnc allow communication bw cells

A

1)desmisomes (cell-cell), hemidesmisomes (cell-matrix)2)tight junctions3) gap junctions

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5
Q

How do the following work1) g-protein2) ligand-triggered protein kinase

A

1) intramembrane, transduce signal from receptor to response enzyme2) receptor and response enzyme are single transmembrane protein

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6
Q

What kind of cell surface receptors are:1) ABO blood-type antigens2)HLA-type antigens

A

1) glycolipids on cell membrane2) glycoproteins (Gp) on cell membrane

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7
Q

Cell cycle:1) which part determines cell cycle length2) protein synthesis3) chromosome duplication4) mitosis5) nucleus division

A

1) G1 most variable2) S3) S4)M5) M

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8
Q

What phase of mitosis do the following occur in:1) chromosome alignment2) separate nucleus reforms around each set of chromosomes3) centromere attachment, spindle formation, nucleus disappears4) chromosomes pulled apart

A

1) metaphase2) telophase3) prophase4) anaphase

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9
Q

1) describe nucleus membrane

A

double, outer membranse continuous with rough endoplasmic reticulum

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10
Q

Where are ribosomes made

A

in nucleolus (within the nucleus, no membrane)

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11
Q

1_ what is used for transcriptionTranscription factors:2) where do steroid hormones bind3) where do thyroid hormones bind4) what are initiation factors

A

1) DNA-template for RNA polymerase-> makes mRNA2)bind in cytoplasm then enter nucleus3) bind receptor in nucleus4) bind RNA polymerase to initiate transcription

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12
Q

uses oligonucleotides to amplify specific DNA sequences

A

DNA polymerase chain reaction

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13
Q

1) Purines2) Pyrimidines3) what has the strongest bond and why

A

1) Adenine, Guanine2) cytosine, thymidine(DNA), uracil(RNA)3) Cytosine-Guanine (3 hydrogen bonds… T-A only has two)

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14
Q

Translation

A

mRNA used as template by ribosomes for protein synthesis

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15
Q

How ribosomes work

A

small and large subunits read mRNA then bind appropriate tRNAs that have amino acids and eventually make proteins

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16
Q

glycolysis

A

1 glucose -> 2ATP + 2 pyruvate

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17
Q

Where does Krebs cycle occur

A

mitochondria inner matrix

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18
Q

Krebs cycle

A

2 pyruvate (from 1 glucose) -> NADH and FADH2 -> electron transport chain -> 36 ATP from 1 glucose

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19
Q

Gluconeogenesis

A

lactic acid (Cori cycle- opposite of glycolysis) + aa => glucose

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20
Q

why can’t fat and lipids be used in gluconeogenesis

A

acetyl CoA (breakdown product of fat metabolism) can’t be converted back to pyruvate

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21
Q

Where does Cori cycle occur

A

in liver, pyruvate has key role, converts lactate into new glucose

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22
Q

Functions of 1) Rough endoplasmic reticulum2) smooth endoplasmic reticulum3) golgi apparatus4) phagosomes5) endosomes

A

1) makes proteins (increased in pancreatic acinar cells)2) lipid/steroid synthesis, detoxifies drugs (increased in liver and adrenal cortex)3) modifies proteins with carbs then transported to cell membrane, secreted or targeted to lysosomes4)engulf large particles and take to lysosome5) same but for small particles

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23
Q

Protein Kinase C1) what activates it2) what does it do

A

1) calcium and diacylglycerol (DAG)2) phosphorylates other enzymes and proteins

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24
Q

Protein Kinase A- what activates it and what does it do

A

activated by cAMP, same as PKC in action

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25
Q

muscle thick filaments

A

myosin, uses ATP to slide along actin

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26
Q

muscle thin filamints

A

actin

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27
Q

Where are the following found?1_ Keratin2_ desmin3_ vimentin

A

1) hair/nails2) muscle3) fibroblasts

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28
Q

microtubules

A

form specialized cellular structures such as cilia, neuronal axons and mitotic spindles, , also involved in transport organelles in the cell

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29
Q

centriole

A

specialized microtubule in cell division (forms spindle fibers which pull chromosome apart)

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30
Q

Intrinsic coagulation pathway

A

exposed collagen +prekallikrein +HMW kininogen+ factor XII->activates XI +VIII->activates X + V-> prothrombin (II) converted to thrombin-> fibrinogen to fibrin

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31
Q

Extrinsic coagulation pathway

A

Tissue factor from injured cells + factor VII-> activates X + V->prothrombin (II) to thrombin-> fibrinogen to fibrin

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32
Q

prothrombin complex componentswhere does it form

A

X, V, Ca, platelet factor 3, prothrombinforms on platelets and catalyzes formation of thrombin

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33
Q

where do intrinsic and extrinsic pathways converge

A

factor X

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34
Q

role of tissue factor pathway inhibitor

A

inhibits factor X

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35
Q

role of fibrin

A

links platelets together (binds Gpiib/iiia) to form platelet plug

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36
Q

role of factor XIII

A

crosslinks fibrin

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37
Q

role of thrombin

A

converts fibrinogen to fibrin and fibrin split products, activates factors V and VIII, activates platelets

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38
Q

role of antithrombin III

A

key to anticoagulation, binds and inhibits thrombin, also inhibits factors IX, X, XI,

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39
Q

how does heparin work

A

activates antithrombinIII-> up to 1000x nl activity

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40
Q

Role of protein C

A

degrades factors V and VIII, degrades fibrinogen

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41
Q

Role of protein S

A

protein C cofactor

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42
Q

Vit K-dependent factors

A

II, VII, IX, X, proteins C and S

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43
Q

Role of tissue plasminogen activator

A

released from endothelium and converts plasminogin to plasmin for fibrinolysis

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44
Q

Role of Plasmin

A

degrades factors V and VIII, fibrinogen and fibrin-> lose platelet plug

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45
Q

Alpha-2 antiplasmin role

A

released from endothelium, natural inhibitor of plasmin

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46
Q

which clotting factor has the shortest half life

A

VII

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47
Q

which factors activity is lost in stored blood? in what product is it not lost in?

A

Factors V and VIII. Not lost in FFP

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48
Q

which factor is not synthesized in the liver

A

VIII, synthesized in endothelium

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49
Q

how long do the following take to work1) Vitamin K2) FFP and what is 1/2 life

A

1) 6 hours2) immediate, 1/2 life is 6 hr

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50
Q

Normal 1/2 life for:1) RBC2)platelets3) PMNs

A

1)120 days2)7 days3) 1-2 days

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51
Q

actions of prostacyclin (PGI2) and where is it released from

A

from endothelium-> decreases platelet aggregation and promotes vasodilation (antagonist to TXA2)

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52
Q

Actions of thromboxane (TXA2) and where it is released from

A

from platelets->increases platelet aggregation and promotes vasoconstriction, Triggers release of Ca in platelets-> exposes Gpiib/iiia receptror-> platelet to platelet binding and platelet to collagen binding via Gp1b receptor

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53
Q

Cryoprecipitate-which factors and when to use

A

Factors VIII-vWF and fibrinogen, use in hemophilia A and von Willibrands disease

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54
Q

FFP- which factors

A

all coag factors+ proteins C and S + AT-III

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55
Q

how DDAVP and conjugates estrogens work

A

cause release of VIII and vWF from endothelium

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56
Q

What does PT measure

A

II, V, VII, X, fibrinogen

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57
Q

What does PTT measure

A

all factors except VII, also measures fibrinogen

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58
Q

Anticoagulation goals for1) PTT2) ACT (activated clotting time)

A

1) PTT 60-90 sec2) ACT 150-200sec (>460sec for cardiopulmonary bypass)

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59
Q

At what INR is 1) relative contraindication for surgery2) relative CI for central line, biopsy of eye surgery

A

1) >1.52) >1.3

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60
Q

what is most common congenital bleeding disorder

A

vonWillibrands

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61
Q

VonWillibrands disease1) inheritance pattern2) role of vWF3) affect on PT/PTT/INR4) difference bw type 1-35) treatment

A

1) Types I and II are AD, type III is AR2) links GpIb receptor on platelets to collagen3) PTT can be prolonged, otherwise nl, long bleeding time (ristocetin test)4) type 1- reduced vWF quantity, type 2- defect in vWF (wont work well), type 3- complete vWF deficiency5) for all you can give cryoprecipitate and recombinant VIII-vWF, for type 1 you can also give DDAVP

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62
Q

Hemophilia A1) inheritance2)deficiency, coags3) why don’t pts with dz always bleed at circumcision4) how high does factor level need to be pre op, post op?5) treatment

A

1) sex-linked recessive2) factor VIII, prolonged PTT, nl PT3) VIII can cross the placenta from mother 4) 100% preop, 80-100% for 10-14days postop5)recombinant factor VIII or cryoprecipitate, if joint bleed DO NOT aspirate, also can give ice and keep mobile

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63
Q

Hemophilia B1) inheritance2) deficiency, coags3)what factor level do you need preop, postop?4) treatment

A

1) sex-linked recessive2) IX, increased PTT, nl PT3) 100% pre-op, 30-40% for 2-3days postop4) recombinant factor IX or FFP

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64
Q

factor VII deficiency1) coags2) treatment

A

1) increased PT, nl PTT2) recomb factor VII or FFP

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65
Q

1) causes of acquired thrombocytopenia2) deficiency in glanzmann’s thrombocytopenia3) deficiency in Bernard Soulier disease4) treatment for the above

A

1)ranitidine (H2-blockers), heparin2) GpIIb/IIIa receptor deficiency (platelets can’t bind each other)- rx with platelets–fibrin normally links receptors together3) GpIb receptor def (plt can’t bind collagen), rx with platelets–vWF normally links GpIb to collagen

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66
Q

Platemet disorder in Uremia and rx

A

inhibits platelet function. rx- hemodialysis (1st), DDAVP, platelets

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67
Q

HIT1)cause of thrombocytopenia2) what is HITT3) treatment4) is lovenox or heparin more likely to cause?

A

1) antiplatelet antibodies (IgG PF4 antibody) -> platelet destruction2) when there is also platelet aggregation and thrombosis (white clot)3) stop heparin/lovenox, start argatroban4) risk of lovenox is less than heparin

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68
Q

DIC (disseminated intravascular coagulation)1) what is decreased? increased2) coags?3)what initiates it4) rx

A

1) platelets, fibrinogen are decreased; fibrin split products and D-dimer are increased2)inc PT and PTT3) tissue factor4) treat underlying cause (ie- sepsis)

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69
Q

how far in advance prior to surgery to stop and what they inhibit:1) ASA2) Clopidogrel (Plavix)3)coumadin

A

1, 2 and 3 are all 7 days1) inhibits cycloxygenase-> decreased TXA2 (platelets lack DNA so can’t regen cyclooxygenase)2)ADP receptor antagonist (tx with platelets)3) inhibits vit-K dep factors, consider starting heparin while awaiting surgery

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70
Q

level that you want platelets before and after surgery

A

> 50,000 before surgery, >20,000 after surgery

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71
Q

how does prostate surgery affect clotting and how to treat

A

can release urokinase which activates plasminogen-> thrombolysis. Treat with Amicar (E-aminocaproic acid)

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72
Q

Factor V leiden mutation1)mechanism of action2) rx

A

1) causes resistance to activated protein C (defect in factor V)2) heparin, warfarin

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73
Q

Hyperhomocysteinemia1) effect on clotting2) rx

A

1) hypercoagulability2) folic acid and B12

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74
Q

Antithrombin III deficiency treatmetn

A

recombinant AT-III or FFP then heparin and warfarin. heparin alone won’t work

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75
Q

polycythemia vera1) defect2) what level to keep Hct and platelets before surgery3) rx

A

1) platelet function defect–> thrombosis2) Hct< 400 before surgery3)phlebotomy, ASA

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76
Q

most common factor causing aquired hypercoagulability

A

tobacco

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77
Q

Anti-phospholipid antibody syndrome1) coags2) mechanism of hypercoagulability3)Dx4) rx

A

1) hypercoagulable but prolonged PTT2) antibodies to cardiolipin and lupus anticoagulant (phospholipids), so seen in ppl with lupus but also others3) false positive RPR, prolonged PTT (not corrected with FFP), positive Russel Viper venom time4) heparin, warfarin

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78
Q

effect of cardipulmonary bypass on coagulation and treatment

A

factor XII (Hageman factor) activated-> hypercoaguable state. rx with heparin to prevent

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79
Q

Warfarin-induced skin necrosis1) cause2) which pts are most susceptible

A

1) pt on coumadin without being heparinized first. bc proteins C and S have shortest half-lives, they decrease first->relative hyperthrombic state2) pts with relative protein C deficiency

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80
Q

Key elements in developement of:1) venous thrombus2) arterial thrombus

A

1) virchow’s triad: venous stasis, endothelial injury and hypercoaguability2) endothelial injury

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81
Q

Post-op DVT treatment1_ 1st DVT2_ 2nd DVT3) 3rd DVT or significant PE

A

1) 6months2) 1 year3) lifetime

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82
Q

When to put in IVC (Greenfield) filter

A

contraindication to AC, documented PE while on AC, free-floating IVC, ilio-femoral or deep femoral DVT, recent pulmonary embolectomy

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83
Q

most common site of origin for PE and rx

A

ileofemoral embolism, if pt in shock despite ionotropes in pressors go to OR, otherwise give heparin or suction catheter-based intervention

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84
Q

what is a procoagulant agent and when to use

A

E-aminocaproic acid (Amicar). inhibits plasmin_> inhibits fibrinolysis. used in DIC, persistent bleeding after CP bypass, thrombolytic overdose

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85
Q

AC mechanisms of action1) Warfarin2) SCDs3) Heparin vs. LMWH4) Argatroban5) Bivalirudin (Angiomax)6) Hirudin (from leeches)

A

1) prevents vit K-dependent decarboxylation of glutamic residues on vit-K dep factors2) improve venous return and induce fibrinolysis with compression via release of tPA from endothelium3) Heparin binds AT-III, LMWH (enoxaparin and fondapariunx) binds AT-III and increases neutralization of Xa and thrombin4 and 5)reversible direct thrombin inhibitor6) irreversible direct thrombin inhibitor

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86
Q

AC reversal1) Warfarin2) heparin/ LMWH

A

1) Vit K, FFP2) Protamine (doesn’t work for LMWH)

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87
Q

half life of heparin

A

60-90 minutes

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88
Q

how is heparin cleared?

A

by reticuloendothelial system

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89
Q

complications of long-term heparin

A

alopecia, osteoporosis

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90
Q

can Heparin or warfarin be used in pregnancy?

A

heparin can bc it doesn’t cross placental barrier, but warfarin crosses so can’t be used

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91
Q

Cross-recation of protamine

A

with NPH or previous protamine exposure. 1% get protamine reaction (hypotension, bradycardia, decreased heart function)

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92
Q

Where is argatroban metabolized and T1/2

A

liver, T1/2= 50minutes

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93
Q

Where is bivalirudin metabolized and T1/2

A

proteinase enzymes in blood, T1/2=25min

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94
Q

what is most potent direct inhibitor of thrombin

A

Hirudin

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95
Q

Ancrod

A

Malayan pit viper venom-> tPA release

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96
Q

what are thrombolytics and mechanism of action and reversal

A

streptokinase, urokinase, tPA-> activate plasminogen (follow fibrinogen levels); fibrinogen <100 worry about bleed. reverse with Amicar (E-aminocaproic acid)

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97
Q

absolute contraindications to thrombolytic use

A

active internal bleed, recent CVA or neurosurg (<3mo), intracranial pathology or recent GI bleed

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98
Q

major but not absolute CI to thrombolytic use

A

surgery <10d ago, organ biopsy or obstetric delivery, L heart thrombus, active PUD, recent major trauma, uncontrolled HTN, recent eye surgery

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99
Q

which blood products don’t carry risk of HIV and hepatitis? why?

A

albumin and serum globulins (they are heat treated)

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100
Q

What is donated blood screened for

A

HIV, Hep B and C, HTLV, Syphilis, West Nile virus

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101
Q

who should you give CMV-negative blood too

A

low-birth-weight infants, bone marrow transplant patients, other transplant patients

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102
Q

1 cause of death from transfusion

A

ABO incompatibility from clerical error

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103
Q

Acute hemolysis with transfusion:1) cause2) symptoms/signs3) labs (haptoglobin, free hemoglobun, bilirubin)4) treatment5)how can it present in anesthetized patients

A

1) ABO incompatibility, antibody mediated2) back pain, chills, tachycardia, fever, hemoglobinuria, can lead to ATN, DIC, shock3) haptoglobin 5g/dL increase in unconjugated bilirubin4)fluids, diuretics, HCO3-, pressors, histamine blockers (Benadryl)5) diffuse bleeding

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104
Q

Delayed hemolysis1)cause2)rx

A

1) antibody-mediated against minor antigens2) observe if stable

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105
Q

Nonimmune hemolysis- rx

A

fluids and diuretics (from squeezed blood)

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106
Q

what is the most common transfusion reaction and why does it occur and treatment

A

febrile nonhemolytic transfusion reaction (recipient antibody against donor WBC), rx- d/c transfusion and use WBC filters for subsequent transfusions

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107
Q

Cause of anaphylaxis with blood transfusion and treatment

A

recipient antibodies against donor IgA in IgA deficient patient, rx- fluids, lasix, pressors, steroids, epinephrine, histamine blockers (Benadryl)

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108
Q

Cause of urticaria from blood transfusions and treatment

A

recipient antibodies against donor plasma proteins or IgA in an IgA deficient patient, rx- histamine blockers (benadryl), supportive

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109
Q

Cause of TRALI (transfusion-related acute lung injury)

A

caused by donor antibodies to recipient’s WBC-> clot in pulmonary capillaries

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110
Q

when does dilutional thrombocytopenia occur?

A

after 10units of pRBCs

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111
Q

effect of Ca on clotting

A

required for clotting cascade, hypoCa-> poor clotting, see this with massive transfusion

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112
Q

most common bacterial contaminate and what type of blood product is most commonly affected

A

GNRs (E. Coli), affects platelets bc not refridgerated

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113
Q

Helper T cells1) Which CD?2) what IL do they release and effect3) type of hypersensitivity reaction that they mediate

A

1) CD42) IL-2-> maturation of cytotoxic T cellsIL-4-> B-cell maturation into plasma cells3) delayed type hypersensitivity (brings in inflam cells by chemokine secretion)

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114
Q

Suppressor T cells1) which CD?2) role

A

CD8, regulate CD4 and CD8 cells

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115
Q

cytotoxic t cells1) which CD2) job

A

CD8, recognize and attack non-self-antigens attached to MHC class I receptors (ie- viral gene products)

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116
Q

what does the intradermal skin test PPD measure?

A

cell-mediated immunity (T-cells)

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117
Q

which infections are associated with defects in cell-mediated immunity

A

intracellular pathogens (TB and viruses)

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118
Q

Humoral (antibody) mediated immunity- how are B cells stimulated to become plasma (antibody secreting) cells

A

IL-4 from helper T cells (CD4) stimulates B cells to become plasma cells

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119
Q

MHC class I1)effect2) where found3) structure

A

1) CD8 cell activation, target or cytotoxic T cells2) on all nucleated cells3) single chain with 5 domains

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120
Q

MHC class II1) effect2) where found3) structure

A

1) CD4 activation, activates helper T cells (binds T cell receptor), stimulates antibody formation after interaction with B cell surface2) on antigen-presenting cells (monocytes, dendrites)3) 2 chains with 4 domains each

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121
Q

basic sequence of events of immune response in viral infection:

A

endogenous viral proteins produced-> bound to MHC class I-> cell surface->recognized by CD8 cytotoxic T cells

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122
Q

basic sequence of events of immune response in bacterial infection:

A

endocytosis ->proteins bound to class II MHC-> cell surface->recognized by CD4 T helper cells-> B cell activation-> Ab production and memory B cell formation

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123
Q

Natural Killer Cellshow they work and why we have them

A

do not require MHC, Ag presentation or previous exposure, not T or B cells. They recognize cells that lack self-MHC which is part of the body’s natural immunosurveillance for cancer

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124
Q

what is the initial Ab made after exposure to antigen

A

IgM

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125
Q

what is the largest antibody

A

IgM (5 domains, 10 binding sites)

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126
Q

what Ab is most abundant in body

A

IgG

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127
Q

what Ab is resonsible for secondary immune response

A

IgG

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128
Q

what Ab can cross the placenta/provides protection in newborn period

A

IgG

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129
Q

Where is IgA found

A

in secretions, peyer’s patches in gut and in breast milk (additional source of immunity in newborn)

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130
Q

role of IgA

A

helps prevent microbial adherence and invasion in gut

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131
Q

IgE role

A

allergic reactions, parasite infections, immediate hypersensitivity reactions

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132
Q

Which Abs are opsonins

A

IgM and IgG

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133
Q

which Abs fix complement

A

requires 2 IgG or 1 IgM

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134
Q

which region of Ab recognizes Ag

A

variable region

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135
Q

which region of Ab is recognized by PMNs and macs

A

constant region (Fc fragment doesn’t carry variable region)

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136
Q

diff bw polyclonal antibodies and monoclonal antibodies

A

poly have multiple binding sites to the Ag at multiple epitopes, monoclonal Ab have only 1 binding site to 1 epitope

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137
Q

what cell is major source of histamine in blood

A

Basophils

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138
Q

what cell is major source of histamine in tissue

A

Mast cells

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139
Q

what are the primary lymphoid organs

A

liver, bone, thymus

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140
Q

what are the secondary lymphoid organs

A

spleen and lymph nodes

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141
Q

what does immunologic chimera mean

A

2 different cell lines in 1 individual (ie- bone marrow tx pts)

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142
Q

Role of IL-2 and what dz can it be used to treat?

A

converts lymphocytes to lymphokine-activated killer cells by enhancing their immune response to tumor and into tumor-infiltrating lymphocytes. Can be used with some success for melanoma. (causes maturation of cytotoxic t cells)

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143
Q

When to give tetanus toxoid:1) non-tetanus prone wound2)wounds >6hr old, obvious contamination, devitilized tissue, crush, burn, frosbite or missile injuries (all are tetanus prone)3)when to give tetanus immune globulin

A

1) give tetanus toxoid only if pt has received

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144
Q

Describe the 4 types of hypersensitivity reactions and diseases/reactions for each type1) type I2) type II3) type III4) type IV

A

1) immediate hypersensitivity reaction (allergy), eosinophils have IgE receptors for the Ag->release major basic protein-> mast cells converted to basophils-> histamine, serotonin and bradykinin release2) IgG or IgM reacts with cell-bound Ag (ABO blood incompatibility, Graves, Myasthenia Gravis)3) Immune complex depositions (serum sickness, SLE)4)Delayed-type hypersensitivity- Ag stim of previously sensitized T cells (PPD, contact dermatitis)

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145
Q

sterility of/microflora in:1)stomach2)Proximal small bowel3) Distal small bowel4) Colon

A

1)virtually sterile, some GPCs and some yeast2) 10^5 bacteria (GPCs)3) 10^7 bacteria (GPCs, GPRs, GNRs)4) 10^11 bacteria (almost all anaerobes, some GNR, GPCs)

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146
Q

most common immune deficiency

A

malnutrition

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147
Q

most common organisms in GI tract

A

Anaerobes (esp bacteroides fragilis) are 1000:1 times more common that aerobes

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148
Q

most common aerobic bacteria in the colon

A

E. Coli

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149
Q

MC fever source:1)within 48hrs2) 48hrs to 5 days3)after 5 days

A

1) atelectasis2) UTI3) wound infection

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150
Q

What part of E. Coli causes gm neg Sepsis and how

A

Endotoxin (lipopolysaccharide A) released->triggers TNF-a release->activates complement-> activates coagulation cascade

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151
Q

Insulin and glucose in 1)early gm-neg sepsis2) late gm-neg sepsis3) optimal glucose in septic pts

A

1) decreased insulin, increased glucose (impaired utilization causes hyperglycemia just before clinical signs of sepsis)2) increased insulin, increased glucose 2/2 insulin resistance3)100-120 mg/dL

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152
Q

C. diff treatment:1) oral2) IV

A

1) vanc/flagyl2)flagyl *lactobacillus can help

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153
Q

Most common type of organism in abscesses

A

90% have anaerobes, 80% have both anaerobic and aerobic bacteria

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154
Q

When do abscesses usually occur

A

7-10 days postop

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155
Q

When do you need to give abx for abscesses

A

DM, cellulitis, clinical signs of sepsis, fever, elevated WBC or bioprosthetic hardware (mechanical valves, hip replacements)

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156
Q

incidence of wound infection in surgery:1) clean surgery2) clean contaminated3) Contaminated4) gross contamination

A

1) 2% (ie-hernia)2) 3-5% (ie- elective colon resection with prepped bowel)3) 5-10% (ie-gunshot wound to colon with repair)4) 30% (ie-abscess)

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157
Q

What is the purpose of prophylactic abx and how long to give

A

prevent surgical site infection, stop within 24hrs postop, except for cardiac surgery stop within 48hrs)

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158
Q

Most common organism in surgical wound infections

A

Staph aureus (coagulase-positive) is most common; Staph epidermidis is coagulase negative

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159
Q

what do staph organisms release

A

exoslime- a exopolysaccharide matrix

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160
Q

most common…1) GNR2)anaerobe (and if present what does it imply)… in SSI

A

1) E. Coli2). B. fragilis (implies translocation from gut

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161
Q

how much bacteria is needed to create SSI

A

10^5 (less if foreign body present)

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162
Q

risk factors for SSI

A

long operation, hematoma/seroma, old age, chronic disease (COPD, renal failure, liver failure, DM), malnutrition, immunosuppresive drugs

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163
Q

What should you think about if there is a surgical infection within 48hrs of procedure

A

Injury to bowel with leak, invasive soft tissue infection with Clostridium Perfringens and beta-hemolytic strept infections (bc they produce exotoxins).

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164
Q

most common infection in surgery pts, risk factor and orgnaism

A

UTI, foley, E. Coli

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165
Q

leading cause of infectious death after surgery and risk factors

A

nosocomial pneumonia, risk factors are length of ventilation, aspiration from duodenum

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166
Q

most common organisms in ICU pneumonia

A

1) S. aureus; 2)Pseudomonas; (GNR is most common class of organism)

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167
Q

most common organisms in line infection

A

1) S. epidermidis, 2) S. aureus, 3) yeast

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168
Q

most dirty line and line salvage rate with abx

A

femoral line; salvage rate is 50% with abx except less likely for yeast infection

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169
Q

what constitutes a positive central line culture and actions

A

> 15 colony forming units=line infection-> move line, also move if line site has signs of infection, never forget to dc line and place PIVs if line no longer needed

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170
Q

Signs/symptoms of necrotizing fasciitis

A

pain our of proportion to skin findings, WBC>20, thin gray drainage, skin blistering/necrosis, induration and edema, crepitus or soft tissue gas on x-ray

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171
Q

most common cause of nec fasciitis and treatment

A

Beta-hemolytic (group B) strep (exotoxin). rx- early debridement, high-dose PCN vs. broad spectrum if suspect polymicrobial

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172
Q

toxic part of C. perfingins and where it sets up and rx

A

alpha toxin, sets up in necrotic tissue bc decreases oxidation-redux potential, rx- early debridement and high-dose PCN

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173
Q

Fornier’s Gangrene0 cause and rx

A

mixed organisms (GPCs, GNRs, anaerobes) in DM or immunocompromised. rx- early debridement, try to preserve testicles, abx

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174
Q

when do you need fungal coverage for suspected infection

A

positive blood cultures, 2 sites other than blood, 1 site with severe sx, endophthalmitis, or pts on prolonged bacterial antibiotics with failure to improve

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175
Q

Actinomyces- what does it cause and rx

A

pulmonary sx (not a true fungus), tortuous abscesses in cervical, thoracic and abdominal areas. rx- drainage of PCN G

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176
Q

Nocardia- what does it cause and rx

A

pulmonary and CNS symptoms most common. rx- drainage and sulfonamides

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177
Q

what is the most common fungal inhabitant of the respiratory tract and rx

A

Candida- rx with fluconazole or anidulafungin for severe infections

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178
Q

Apergillosis rx

A

Voriconazole

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179
Q

Histoplasmosis- what does it cause, what regions is it found in, and rx

A

pulm sx- Missisippi and Ohio River valleys. rx- liposomal amphotericin if severe

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180
Q

cryptococcus- sx and rx

A

CNS sx most common (often in AIDs pt). rx- amphotericin

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181
Q

coccidioidomycosis- sx and rx and region

A

pulm sx, found in southwest, rx with amphotericin

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182
Q

Spontaneous Bacterial Peritonitis (SBP, primary)1) what is a risk factor2) organisms that cause it3) labs/diagnostic study results4) rx5) prophylaxis

A

1) low protein (500 cells/cc4)ceftriaxone or other 3rd generation cephalosporin5) Flouroquinolones (Norfloxacin

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183
Q

Secondary bacterial peritonitis1)source2) organisms3)rx

A

1) intra-abdominal ie-perf viscus2) polymicrob (B. fragilis, E. coli, enterococcus)3) laparotomy to find source

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184
Q

risk of contracting HIV from the following exposures:1) HIV blood transfusion2) Infant from positive mother3)needle stick from positive patient4)mucous membrane exposure

A

1) 70%2)30%3)0.3%4) 0.1%

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185
Q

How long after exposure dose HIV seroconversion occur

A

6-12 weeks

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186
Q

What treatment regimen should you get after exposure

A

AZT (Zidovudine- reverse transcriptase inhibitor) and ritonavir( protease inhibitor), give within 1-2hr after exposure

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187
Q

most common cause for laparotomy in HIV-positive pt

A

opportunistic infections (esp CMV); 2nd most common is neoplastic disease

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188
Q

most common intestinal manifestation of AIDS

A

CMV colitis (presents as bleeding or perforation sometimes)

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189
Q

most common neoplasm in AIDS pt

A

Kaposi’s Sarcoma

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190
Q

Lymphoma in HIV pts1) type2) where3)rx

A

1) non-Hodgkins2) stomach most common, then rectum3) rx- chemo. Surgery if significant bleeding or perforation

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191
Q

ddx for HIV +1) UGIB2) LGIB (more common)

A

1) kaposi’s sarcoma, lymphoma2) CMV, bacterial, HSV

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192
Q

CD4 counts1) normal2) symptomatic HIV3) opportunistic infections (AIDS)

A

1) 800-12002) 300-4003) <200

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193
Q

Hepatitis C1) chance of transmittion with blood transfusion2) prevalence3) rx4) prevalence of sequelae

A

1) <0.0001%2)1-2%3) interferon4) 60% chronic infection, 15% cirrhosis, 1-5% HCC, fulminant hepatic failure is rare

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194
Q

brown recluse spider bite rx

A

Dapsone (possible graft later)

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195
Q

Acute septic arthritis1) cause2) rx

A

1) Gonococcus, staph, H. flu, strep2) drainage, ceftriaxone (or 3rd gen cyclosporin) + vanc until cx returns

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196
Q

lerktlnea. dialysis cather infection1) organism2) rx

A

1) S> aureus and s. epidermidis2) intra peritoneal vanc and gentamicin, removal of catheter if pritonitis >5day, fecal peritonitis-> ex-lap

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197
Q

Difference between:1) Antiseptic2) Disinfectant3) Sterilization

A

1) Kills and inhibits organisms on body2) kills and inhibits organisms on inanimate objects3) all organisms killed

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198
Q

Common antiseptics in surgery- what are they and what are they good for1)Iodophors2)Chlorhexadine gluconate

A

1) Betadine- good for GPCs and GNRs, poor for fungi2)Hibiclens- good for GPCs, GNR and fungi

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199
Q

Mechanism of Action of Penicillins

A

inhibit cell wall synthesis

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200
Q

Mechanism of Action of Cephalosporins

A

inhibit cell wall synthesis

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201
Q

Mechanism of Action of carbapenems

A

inhibit cell wall synthesis

202
Q

Mechanism of Action of monobactams (aztreonam)

A

inhibit cell wall synthesis

203
Q

Mechanism of Action of vancomycin

A

inhibit cell wall synthesis

204
Q

Mechanism of Action of tetracycline

A

inhibitor of the 30s ribosome and protein synthesis

205
Q

Mechanism of Action of Aminoglycosides (tobramycin, gentamycin)

A

inhibitor of the 30s ribosome and protein synthesis

206
Q

Mechanism of Action of linezolid

A

inhibitor of the 30s ribosome and protein synthesis

207
Q

Mechanism of action of erythromycin and clindamycin and synercid

A

Inhibitors of 50s ribosome and protein synthesis

208
Q

mechanism of action of quinolones

A

inhibitor of DNA helicase (gyrase)

209
Q

mechanism of action of rifampin

A

inhibitor of RNA polymerase

210
Q

mechanism of action of metronidazole

A

produces oxygen free radicals that breakup DNA

211
Q

mechanism of action of sulfonamides

A

inhibits purine synthesis (PABA analogue)

212
Q

mechanism of action of Trimethoprim

A

inhibits dihydrofolate reductase-> inhibits purine synthesis

213
Q

What antibiotics are bacteriostatic

A

tetracycline, clindamycin, erythromycin (all have reversible ribosomal binding), bactrim

214
Q

what abx have irreversible binding to 30s ribosome and are considered bactericidal

A

aminoglycosides

215
Q

Mechanism of action of PCN resistance

A

plasmids for beta-lactamase

216
Q

most common method of antibiotic resistence

A

transfer of plasmids

217
Q

Cause of MRSA resistance

A

mutation of cell wall-binding protein

218
Q

Cause of VRE (vanc-resist-enterococcus) resistance

A

mutation of cell wall-binding protein

219
Q

Gentamicin resistance cause

A

modifying enzymes lead to a decrease in active transport of gentamicin into the bacteria

220
Q

Appropriate drug level:1) Vancomycin2) Gentamicin3) what to do if peak too high4) what to do if trough too high

A

1) peak 20-40, trough 5-102) peak 6-10, trough <13) decrease amount of dose4) decrease dose frequency

221
Q

PCN coverage

A

GPCs (strept, syphilis, Neisseria meningitides (GPR), Clostridium perfringens (GPR), beta-hemolytic strept, anthrax)***doesn’t work on Staph or Enterococcus

222
Q

Oxacillin and naphcillin coverage

A

cover staph only

223
Q

Ampicillin coverage

A

same as PCN + enterococci

224
Q

Unasyn and Augmentin-what abx make them and coverage

A

Unasyn is ampicillin/sulbactam; Augmentin is amoxicillin/clavulanic acid. Sulbactam and clavulanic acid are beta-lactamase inhibitors. These are broad spectrum and cover GPCs (staph and strep), GNRs, enterococci and some anaerobes. * not effective for Psudomonas, Acinetobacter or Serratia

225
Q

Ticarcillin and piperacillin coverage and side effects

A

GNRs- enterics, Pseudomonas, Acinetobacter, Serratia. S/E- inhibit platelets and high salt load.

226
Q

Timentin and zosyn1) what makes up the abx2) coverage3) side effects4) zosyn dosing frequency

A

1)Timentin is ticarcillin/clavulanic acid and Zosyn is piperacillin/sulbactam2)GPC (staph and strep), GNRs and anaerobes, enterococci, pseudomonas, acinetobacter, serratia3) inhibits platelets and high salt load4) QID dosing

227
Q

First generation cephalosporins1) abx2) coverage3) which is the best for prophylaxis and why4) does it penetrate the CNS

A

1) cefazolin (ancef) and cephalexin2) GPC- staph and strep. *not effective for enterococcus3) ancef- longest T1/24) no

228
Q

Second-generation cephalosporins1)abx2)coverage3) which is best for prophylaxis

A

1) cefoxitin, cefotetan, cefuroxime2)GPCs, community-acquired GNRs, some anaerobic coverage, lose some staph coverage. *not effective for enterococcus, pseudomonas, acinetobacter or serratia3) cefotetan- longest T1/2

229
Q

third-generation cephalosporins1) abx2) coverage3) side effects

A

1) ceftriaxone, ceftazidime, cefepime, cefotaxime2) GNRs mostly + some anaerobic coverage. Covers Pseudomonas, Acinetobacter, Serratia. *doesn’t cover enterococcus.3) cholestatic jaundice, sludging in gallbladder (Ceftriaxone)

230
Q

Aztreonam (monobactam) coverage

A

GNRs, picks up Pseudomonas, Acinetobacter and Serratia

231
Q

Carbapenems (meropenem and imipenem)1) Coverage2) what do you give it with and why?3) side effects

A

1) broad spectrum- GPCs, GNRs, anaerobes. *not effective for MEP (Mrsa, Enterococcus, Proteus)2) Cilastatin- prevents renal hydrolysis of the drug and increases T1/23) seizures.

232
Q

Bactrim (Trimethoprim/sulfamethaxazole)1) coverage2) side effects

A

1) GNRs with some GPC coverage. Not effective for Enterococcus, Pseudomonas, Acinetobacter and Serratia, but does cover staph.2) teratogenic, allergic reactions, renal damage, Stevens-Johnson syndrome (erythema multiforme), hemolysis in G6PD-deficient pt

233
Q

Quinolones1) coverage2)dosing of cipro3) dosing of levofloxacin4) MRSA sensitivity and IV vs. PO efficacy.

A

1) GNRs, +/-GPCs, pseudomonas, acinetobacter, serratia. *doen’t cover enterococcus2)BID3) QD4) 40% MRSA sensitive (IV and PO same efficacy)

234
Q

Aminoglycosides1) abx2) coverage3) cause of resistance4) what abx is it synergistic with5) Side effects

A

1) gentamicin, tobramycin2) GNRs, pseudomonas, acinetobacter, serratia. *doesn’t cover anaerobes3) modifying enzymes lead to decreased active transport4) beta-lactams (ampicillin, amoxicillin) facilitate aminoglycocide penetration. Good for enterococcus coverage5) reversible nephrotoxicity, irreversible ototoxicity

235
Q

Erythromycin (macrolides)1) Coverage2) Side effects3) other action

A

1) GPCs- best for community-acquired pneumonia and atypical pneumonias2)nausea (PO), cholestasis (IV)3) also binds motilin receptor (prokinetic for bowel)

236
Q

Vancomycin (glycopeptides)1) coverage2) mechanism of action3)how resistance develops4) side effects

A

1) GPCs, Enterococcus, C. diff (P.O. intake), MRSA2) binds cell wall proteins3) from a change in cell wall-binding protein4) HTN, Redman syndrome (from histamine release), nephrotoxicity, ototoxicity

237
Q

Synercid coverage (streptogramin-quinupristin-dalfopristin)

A

GPCs including MRSA and VRE

238
Q

Linezolid coverage

A

GPCs including MRSA and VRE (oxazolidinones)

239
Q

Tetracycline coverage and side effects

A

GPCs, GNRs, syphilis. S/E- tooth discoloration in children

240
Q

Clindamycin coverage and side effects

A

anaerobes, some GPCs including C. perfringens, good for aspiration pneumonia. side effects- pseudomembranous colitis

241
Q

Metronidazole coverage and side effects

A

anaerobes, disulfiram-like reaction, peripheral neuropathy from long-term use

242
Q

Amphotericin- coverage and mechanism

A

antifungal, binds sterols in wall and alters membrane permeability. S/E- nephrotoxic, fever, hypokalemia, hypotension, anemia. The liposomal type has fewer side effects

243
Q

Voriconazole and itraconazole coverage and mechanism

A

antifungals, inhibit ergosterol synthesis needed for cell membrane

244
Q

Anidulafungin (Eraxis)- coverage and mech

A

antifungal, inhibits synthesis of cell wall glucan

245
Q

what to give if pt has prolonged broad-spectrum abx and fever

A

itraconazole

246
Q

rx for invasive aspergillosis

A

voriconazole

247
Q

rx for Candidemia

A

anidulafungin

248
Q

rx for fungal sepsis other than candida and aspergillosis

A

liposomal amphotericin

249
Q

Name the anti-tuberculosis drugs, mechanisms of action and side effects

A

Isoniazid- inhibits mycolic acids (give with pyridoxine). SE- hepatotoxicity, B6 defRifampin- inhibits RNA polymerase. SE- hepatotoxicity, GI symptoms, high resistance ratePyrazinamide- hepatotoxicity SEEthambutol- SE is retrobulbar neuritis

250
Q

mech of action and what it rxs and SE for1) acyclovir2) Ganciclovir

A

both inhibit viral DNA polymerase1) HSV and EBV2) CMV. SE- decreased bone marrow, CNS toxicity

251
Q

complication of broad-spectrum abx

A

superinfection

252
Q

Abx effective for enterococcus

A

vanc, Timentin/Zosyn, ampicillin/amoxicillin, or gent with ampicillin

253
Q

Abx effective for psuedomonal, Acinetobacter and Serratia-

A

ticarcillin/piperacillin, Timentin/Zosyn, third-gen cephalosporins, aminoglycosides (Gentamicin and tobramycin), meropenem/imipenem, floroquinolones

254
Q

how to rx pseudomonas

A

double cover

255
Q

when should perioperative abx be given and what they prevent

A

give within 1 hr before incision. prevent SSI.

256
Q

what medication routes avoid first-pass liver metabolism

A

sublingual and rectal

257
Q

What is skin absorption for drugs based on

A

lipid solubility through the epidermis

258
Q

what drugs are absorbed in the CNS (properties)?

A

nonionized, lipid-soluble drugs

259
Q

what mlq binds drugs

A

albumin (PCNs and warfarin are 90% bound)

260
Q

why can’t you give newborns sulfonamides?

A

will displace unconjugated bilirubin from albumin in newborn-> hyperbilirubinemia

261
Q

Where are tetracyclines and heavy metals stored?

A

bone

262
Q

0 order kinetics

A

constant amount of drug is eliminated regardless of dose

263
Q

1st order kinetics

A

drug eliminated proportional to dose

264
Q

how many T1/2 does it take for a drug to reach its steady state?

A

five T1/2’s

265
Q

volume of distribution of a drug

A

amount of drug in the body divided by the amount of drug in plasma/blood. high volume of distribution means higher [] in extravascular compartment (ie- fat tissue) compared with intravascular compartment

266
Q

bioavailability

A

fraction of unchanged drug reaching the systemic circulation (100% for IV drugs, less for other routes)

267
Q

ED50

A

Drug level at which desired effect occurs in 50% of pts

268
Q

LD50

A

drug level at which death occurs in 50% of pts

269
Q

hyperactive drug rx

A

effect at an unusually low dose of drug

270
Q

Tachyphylaxis

A

drug tolerance after only a few doses

271
Q

Drug metabolism:1) 2 systems2) Phase I of drug metabolism3) Phase II of drug metabolism

A

1) hepatocyte smooth endoplasmic reticulum, P-450system2) demethylation, oxidation, reduction, hydrolysis reactions (mixed fnc oxidases, requires NADPH/ oxygen)3) glucuronic acid (#1) and sulfates attached (forms water-soluble metabolite); usually inactive and ready for excretion. Biliary excreted drugs may become deconjugated in intestines with reabsorption, some in active form (called enter-hepatic recirculation, ie-cyclosporin)

272
Q

Cytochrome P-4501) Inhibitors2) Inducers

A

1) Cimetidine, isoniazid, ketoconazole, erythromycin, cipro, flagyl, allopurinol, verapamil, amiodarone, MAOIs, disulfiram2) cruciform veggies, ETOH, insecticides, cigarette smoke, phenobarbital (barbituates), Dilantin, theophylline, warfarin

273
Q

what is most important organ for eliminating most drugs

A

kidney (glomerular filtration and tubular secretion)

274
Q

Polar drugs and how they are excreted

A

water soluble drugs; more likely to be eliminated in an unaltered form

275
Q

nonpolar drugs and how excreted

A

non-ionized, fat soluble; more likely metabolized before excretion

276
Q

Gout1) what builds up2) mechanism of the following treatmentsa-Colchicineb-indomethacinc-Allopurinold-Probenecid

A

1) uric acid, end product of purine metabolism2) a-anti-inflammatory, binds TUBULIN and inhibits migration of WBCsb-NSAID, inhibits prostaglandin synthesis (reversible cyclooxygenase inhibitor)c-xanthine oxidase inhibitor, blocks uric acid formation from xanthined-increases renal secretion of uric acid

277
Q

Lipid lowering drugs- actions and side effects1) Cholestyramine2) Statins3) Niacin

A

1) binds bile acids in gut so body has to resynthesize bile acids from cholesterol-> lowers body cholesterol. can bind vit. K and cause bleeding.2)HMG-CoA reductase inhibitors. Can cause liver dysfunction and rhabdomyolysis3) inhibits cholesterol synthesis. Can cause flushing (rx- ASA)

278
Q

GI drugs- brand name, action, mechanism, S/E1) promethazine2) Metoclopramide3)Odansetron4) Octreotide

A

1) phenergan, antiemetic, inhibits dopamine receptors. S/E- tardive dyskinesia, rx with benadryl2) Reglan, prokinetic, inhibits dopamine receptors, can increase gastric and gut motility3) Zofran, antiemetic, central-acting serotonin receptor inhibitor4) long-acting somatostatin analogue, decreases gut secretions

279
Q

Anti-reflux medications1)Omeprazole2) Cimetidine/ranitidine

A

1) PPI, blockes H/K ATPase in stomach parietal cells2) blocks H2 histamine receptors, decrease acid in stomach

280
Q

Digoxin-mechanism-action-S/E’s

A

-inhibits Na/K ATPase and increases myocardial Ca-slows AV conduction, inotrope-can decrease blood flow to intestines-> mesenteric ischemia, visual changes (yellow hue), fatigue, arrhythmias

281
Q

what increases sensitivity of heart to digitalis and can precipitate arrhythmias or AV block

A

hypokalemia

282
Q

is digoxin cleared with dialysis

A

NO

283
Q

Amiodarone-what does it treat-S/Es

A

-acute atrial and ventricular arrhythmias-pulm fibrosis with prolonged use, hypo- and hyperthyroidism

284
Q

what cardiac condition is magnesium used to treat

A

Ventricular tachycaria/ torsades de pointes

285
Q

ACE-inhibitors-Mechanism-Uses-S/E

A

-antiotensin-converting enzyme inhibitors-can prevent CHF after myocardial infarction, can prevent progression of renal dysfunction in pts with HTN and DM-S/E- can precipitate renal failure in pts with renal artery stenosis

286
Q

what is the best single agent shown to improve survival in patients with CHF

A

ACE-inhibitors

287
Q

what medication may prolong life in pts with severe LV failure, and reduce risk of MI and a-fib post op

A

beta-blocker

288
Q

what is the best single agent shown to improve survival after and MI

A

beta-blocker

289
Q

Atropine mechanism and action

A

acetylcholine antagonist, increases heart rate

290
Q

metyaprone and aminoglutethimide-action-used for?

A

-inhibit adrenal steroid synthesis-used in pts with adrenocortical CA

291
Q

Lueprolide-mechanism-should it be given continuously or intermittently?-use

A
  • analogue of GnRH and LHRH-don’t give continuously bc will get paradoxic inhibition of LH and FSH-used in pts with metastatic prostate CA
292
Q

NSAIDS-mechanisms and se

A

inhibit prostaglandin synthesis and lead to decreased mucus and HCO3- secretion and increased acid production (mech of ulcer formation)

293
Q

Misoprostol- mechanism and use

A

PGE1 derivative, protective prostaglandin used to prevent peptic ulcer disease (consider use in pts on chronic NSAIDs)

294
Q

Haldol- meachnism, use and S/E (and how to rx)

A

antipsychotic, inhibits dopamine receptors, can cause extrapyramidal manifestations (rx with Benadryl)

295
Q

ASA poisoning 1) symptoms2) first metabolic abnormality3) second metabolic abnormality

A

1) tinnitus, headaches, nausea, vomiting2) respiratory alkalosis3) metabolic acidosis

296
Q

what is the MC side effect of Gadolinium

A

nausea

297
Q

Iodine contrast1) MC side effect2) MC side effect requiring treatment

A

1) nausea2) dyspnea

298
Q

treatment of tylenol overdose

A

N-acetylcysteine

299
Q

components of the standard airway exam for nonanesthesiologists and what is concerning1)BMI2) mouth opening3) mallampati classification4) mandibular protrusion5) neck anatomy6) cervical spine mobility7)beard

A

1) BMI>312) Interincisor or intergingival distance >3cm3) Class III-IV4) inability to protrude lower incisors to meet or extend past upper incisors5) radiation changes or thick obese neck6) limited extension or possibly unstable cervical spine7) full beard

300
Q

MAC (minimum alveolar concentration)

A

smallest concentration of inhalational agent at which 50% of patients will not move with incision

301
Q

Small MAC-lipid solubility and potency

A

more lipid soluble=more potent

302
Q

relation of speed of induction to solubility

A

inversely proportional

303
Q

what inhalation agent has the fastest onset and what is the relative MAC

A

Nitrous oxide- high MAC (low potency)

304
Q

result of inhalational agents

A

unconsciousness, amnesia and some analgesia- most have some myocaridal depression-increase cerebral blood flow-decrease renal blood flow

305
Q

Pros of using nitrous oxide

A

fast, minimal myocardial depression, tremors at induction

306
Q

Halothane pros and cons and who it is good for

A

slow onset/offset with highest degree of cardiac depression and arrhythmias; least pungent= good for children

307
Q

Sevoflurane- pros and who to use it for

A

fast, less laryngospasm and less pungent, good for mask induction

308
Q

Isoflurane- what it is good for and why?

A

good for neurosurgery (lowers brain O2 consumption, no increase in ICP)

309
Q

s/e of enflurane

A

seizures

310
Q

IV induction agents- speed of action and s/e1)sodium thiopental2) propofol (and what pts can’t have it and where ist it metabolized)3)Etomidate

A

1) fast acting barbituate. s/e- decreases cerebral blood flow and metabolic rate, decrease bp2)rapid distribution and on/off. gives amnesia/sedative but no analgesia. s/e- hypotension, respiratory depression. can’t use if egg allergy. metabolized in liver and by plasma cholinesterases3) fast acting, fewer hemodynamic changes. s/e-continuous infusions can lead to adrenocortical suppression

311
Q

IV induction agents: Ketamine1) effect2) major benefit3) s/e4) C/I in what pts?5)who is it good for

A

1) dissociation of thalamic/limbic systems; places pt in cataleptic state (amnesia, analgesia)2) no respiratory depression3) hallucinations, catecholamine release (inc CO2, tachycardia), inc airway secretions, and inc cerebral blood flow4)pts with head injury5) good for children

312
Q

Rapid Sequence Intubation1) when is it indicated2) what do you give

A

1) recent oral intake, GERD, delayed gastric emptying, pregnancy, bowel obstruction2) pre-oxygenate, etomidate, syccinylcholine typical sequence

313
Q

what is the last muscle to go down and the 1st muscle to recover from paralytics

A

diaphragm

314
Q

what are the 1st mucles to go down and last to recover from paralytics

A

neck and face muscles

315
Q

what is the only depolarizing agent of the muscle relaxants

A

succinylcholine

316
Q

succinylcholine1) speed of action and effect2) side effects3) who can’t you use it in

A

1) fast, short acting paralytic2) malignant hyperthermia, hyperkalemia (depolarization releases K), open-angle glaucoma, atypical pseudocholinesterases, prolonged paralysis in pts (asians) with atypical psudocholinesterases3) pts with severe burns, neuro injury, neuromuscular disorders, spinal cord injury, massive trauma, or acute renal failure

317
Q

Malignant hyperthermia1) medication indicated2) cause3) symptoms4) treatment

A

1)succinylcholine2) caused by a defect in calcium metabolism, calcium released from sarcoplasmic reticulum causes muscle excitation-contraction syndrome3) inc end-tidal CO2, fever, tachycardia, rigidity, acidosis, hyperkalemia4) dantrolene (10mg/kg) inhibits Ca release and decouples excitation complex, cooling blankets, HCO3, glucose, supportive care

318
Q

How do nondepolarizing muscle relaxants/paralytics work and in what pts may their effect be prolonged.- what drugs are in this category

A

inhibit neuromuscular jnc by competing with acetylcholine; prolonged effect in myasthenia gravisexamples are: cis-atricurium, rocuronium, pancuronium

319
Q

Cis-atracurium1) how is it degraded2) good for what pts?3) what is released 2/2 use?

A

1) Hoffman degradation2) renal and liver failure pts3) histamine

320
Q

speed of onset, duration and site of metabolism for:1) Rocuronium2) Pancuronium (and most comon side effect)

A

1) fast onset, intermediate duration, hepatic metabolism2) slow onset, long duration, renal metabolism, s/e-tachycardia

321
Q

Reversing drugs for nondepolarizing agents (Cis-atracurium, rocuronium, pancuronium) and mechanism of action-what should you give with them

A

neostigmine and edrophonium- block acetylcholinesterase increasing acetylcholine*give atropine and glycopyrrolate in addition to counteract effects of generalized acetylcholine overdose

322
Q

local anesthetics1) how do they work2) how much 1%lido can you use3) why are infected tissues hard to anesthetize4) what is the longest, shortest acting and which is in between5) side effects

A

1) increase action potential threshold, preventing Na influx2)0.5cc/kg of 1% lido (4.5mg/kg) with epi it is 7mg/kg3)they are acidotic4) length of action: bupivacaine>lidocaine>procaine5)tremors, seizures, tinnitus, arrhythmias (CNS symptoms occur before cardiac)

323
Q

benefit of adding epi to local and what pts can’t you use them in

A

allows higher doses to be used, don’t give epi to pts with arrhythmias, unstable angina, uncontrolled HTN, poor collaterals (penis and ear), uteroplacental insufficiency

324
Q

which class of local rarely causes allergic reactions

A

amides- lidocaine, bupivacaine, mepivacaine

325
Q

which class of local anesthetics has increased incidence of allergic reactions

A

Esters-tetracaine, procaine, cocaine (inc allergic rx due to PABA analogue)

326
Q

Nacotics1) drugs2) mechanism of action3) where are they metabolized/excreted4) rx for overdose5) what pts shouldn’t get

A

1) morphine, fentanyl, demerol, codeine2) act on mu-opioid receptors-> profound analgesia, respiratory depression ( dec CO2 drive), no cardiac effects, blunt sympathetic response3)metab in liver, excreted by kidney4) Narcan (naloxone)5) avoid in pts on MAOIs bc can cause hyperpyrexic coma

327
Q

morphine side effects

A

analgesia, euphoria, respiratory depression, miosis, constipation, histamine release-> hypoTN, dec cough

328
Q

Demerol side effects and what pts to avoid using it in

A

analgesia, euphoria, respiratory depression, miosis, tremors, fasciculations, convulsions no histamine releasecan cause seizures (avoid in pts with renal failure and careful with total amount) 2/2 buildup of normeperidine

329
Q

methadone- action

A

simulates morphine, less euphoria

330
Q

fentanyl- onset time, strength, histamine released?

A

fast acting, 80x strength of morphine, but no cross reaction in pt with morphine allergy. no histamine release

331
Q

Sufentanil and remifentanil- onset and half-life

A

very fast acting, short half-lives.

332
Q

what is most potent narcotic

A

sufentanil

333
Q

benzodiazepines1)uses, where it is metabolized, side effect2) shortest acting to longest acting ones3) rx of overdose (how it works, adverse effects, and who this rx is contraindicated in)

A

1) anticonvulsant, amnesic, anxiolytic. metabolized in liver. s/e-respiratory depression2)Versed (midazolam)- shortest acting (C/I in pregnancy bc crosses the placenta); Valium(diazepam)- intermediate acting; ativan (lorazepam)- long acting3) Flumazenil (comptetive inhibitor). May cause seizures and arrhythmias, C/I in pt with elevated ICP or status epilepticus

334
Q

Epidural anesthesia1) how it works2) s/e if morphine used3) s/e if lidocaine used4) how is motor function spared

A

1) analgesia by sympathetic denervation2) respiratory depression3) decreased HR and BP4) use dilute concentrations

335
Q

rx for acute hypotension and bradycardia in epidural/spinal anesthesia

A

turn epidural down, IVF, phenylephrine, atropine

336
Q

S/e of T5 epidural

A

can affect cardiac accelerator nerves

337
Q

In what pts are epidurals and spinal anesthesia contraindicated in

A

hypertrophic cardiomyopathy or cyanotic heart disease bc sympathetic denervation decreases afterload which worsens these conditions

338
Q

what space is injected in spinal anesthesia

A

1) subarachnoid space- spread determined by patient position and baricity. Neurologic blockade> motor blockade

339
Q

what is a caudal block used for

A

through sacrum, good for pediatric hernias and perianal surgery

340
Q

epidural and spinal complications

A

hypotension, headache, urinary retention, abscess/hematoma formation, respiratory depresion (with high spinal)

341
Q

spinal headaches- cause and symptoms and treatmetn

A

caused by CSF leak, HA that is worse with sitting up. rx- fluids, rest, caffeine, analgesics, blood patch to site if persists >24hours

342
Q

what surgical pre-op risk factors/comorbidities are associated with the most postop hospital mortality

A

renal failure (#1) and CHF

343
Q

what pts need a cardiology workup preop:

A

angina, previous MI, SOB, CHF, walks 5/min, high grade heart block, age>70, DM, renal insufficiency, patients undergoing major vascular surgery

344
Q

what surgeries are considered high risk

A

aortic, major vascular and peripheral vvascular surgeries

345
Q

what risk category is carotid endarterectomy

A

moderate

346
Q

what are the biggest risk factors for postop MI

A

age>70, DM, previous MI, CHF, unstable angina

347
Q

ASA classesdescribe class 1-6 and E

A

1)healthy2) mild dz, no limitation3) severe disease (angina, prev MI, poorly controlled HTN or DM, mod COPD)4) severe constant threat to life (unstable angina, CHF, renal failure, liver failure, severe COPD)5) Moribound (ruptured AAA, saddle pulm embolus)6) DonorE) emergency

348
Q

what non cardiac surgical procedures are considered high risk (>5%)

A

emergent (esp in elderly), aortic, peripheral and other major vascular (except carotid endarterectomy), long procedure with large fluid shift

349
Q

what noncard procedures are intermediate cardiac risk (<5%)

A

CEA, head and neck surgery, intraperitoneal and thoracic surgery, orthopedic and prostate surgery

350
Q

what is the best determinant of esophageal vs tracheal intubation

A

end-tidal CO2 (ETCO2)

351
Q

cause and rx of intubated pt undergoing surgery with sudden transient rise in ETCO2

A

hypoventilation, rx- inc tidal volume or respiratory rate

352
Q

Cause of intubated pt with sudden drop in ETCO2

A

disconnected from vent, pulmonary embolism is also has hypotension

353
Q

correct ET tube position

A

2cm above the carina

354
Q

MC PACU complication

A

nausea and vomiting

355
Q

what procedures are higher volume hospitals associated with lower mortality for?

A

abdominal aortic aneurysm repair and pancreatic resection

356
Q

total body water-% of weight and how has a little more water and a little less water

A

2/3 of total body weight, more in infants, less in women

357
Q

how much of water is intracellular (where) and extracellular (where)

A

2/3 intracell *muscle, 1/3 extracell (2/3 interstitial, 1/3 plasma)

358
Q

what determines plasma/intersitial compartment osmotic pressures

A

proteins

359
Q

what determines intracellular/extracelluar osmotic pressure

A

Na

360
Q

MC cause of volume overload and sign

A

iatrogenic (weight gain)

361
Q

cellular catabolism- what is released

A

H2O

362
Q

fluids and electrolytes1) Na and Cl in 0.9% and 3% NS2) LR electrolytes3) plasma osmolality- how to calculate and what is normal osmolality

A

1) 0.9% (154, 154), 3% (513 and 513)2) has the ionic composition of plasma Na 130, K 4, Ca 2.7, Cl 109, bicarb 283) (2xNa) + (glucose/18) + (BUN/2.8); nl is 280-295

363
Q

quick maintenance IVF calculation

A

40 + weight in Kg (from 4/2/1 rule)

364
Q

what is the best indicator of adequate volume replacement

A

urine output

365
Q

what is the fluid loss during open abdominal operations

A

0.5-1 L/hr

366
Q

when should you replace blood loss

A

> 500cc

367
Q

Insensible fluid losses- how much from where

A

10cc/kg/day 75% skin, 25%respiratory

368
Q

what fluids to use in 1st 24hr postop? after that?

A

LR/NS/p-lyte, then switch to D5 1/2NS with 20KCL

369
Q

what is the purpose of D5 in IVF

A

stimulates insulin release-> aa uptake and protein syntesis (also prevents protein catabolism

370
Q

How much fluid is excreted daily by 1) stomach2) biliary system3) pancreas4) duodenum

A

1) 1-2L2,3,4) 0.5-1L

371
Q

normal K+ requirement per day

A

0.5-1mEq/kg

372
Q

normal Na+ requirement per day

A

1-2 mEq/kg

373
Q

GI electrolyte loses- describe electrolyte composition1) sweat2) Saliva3) stomach4) pancreas5) Bile6) large intestine7) small intestine

A

1) hypotonic (Na [] 35-65)2)K+ (highest concentration of K in body)3) H+ and Cl-4) HCO3-5) HCO3-6) K+7) HCO3-, K+

374
Q

best IVF to replace1) gastric losses2) pancreatic/biliary/small intestine losses3) large intestine losses4) repletion ratio for GI losses5) fluid for dehydration resuscitation6) minimal UOP and should you replace it

A

1) D5 1/2NS +20KCl2) LR with HCO3-3) LR with K+4) 1:15) NS6) 0.5 cc/kg/hr, don’t replace

375
Q

1) normal K+ level2) EKG changes of hyper and hypo K+3)rx for hyperkalemia and when do you often see it4) rx for hypokalemia

A

1) 3.5-52) hyper-peaked t-waves, hypo- T waves disappear3) renal failure. rx- Ca gluconate- stabilizes heart membrane; Sodium bicarb (alkalosis-> K+ enters cell in exchange for H+); 10u insulin and 1 ampule of 50% dextrose (K driven into cells); Kayexalate, lasix, dialysis4) usually seen with overdiuresis. may need to replete Mg before K

376
Q

1) normal Na2) hypernatremia: cause, sx, and how to correct3) hyponatremia: cause; sx and how to correct4) how to correct for hyperglycemia when evaluating Na level

A

1) 135-1452) cause-dehydration; sx- HA, restless, irritable, seizures. rx- D5W slowly to avoid brain swelling3)fluid overload; sx-HA, N/V, seizures. rx- 1st water restriction then diuresis. Correct slowly to avoid central pontine myelinosis (no more than 1mEq/hr)4) can cause psuedohyponatremia, for each 100increment of glucose over normal add 2 points to the Na value

377
Q

electrolyte abnormality in SIADH

A

hyponatremia

378
Q

1) normal Ca and ionized Ca2) levels of Ca when symptoms of hyperCa noted3) what fluids should you NOT give in hyperCa4) What diuretics should you NOT give5) causes of hyperCa6) rx of hyperCa

A

1) 8.5-10 or iCa 4.4-5.52) Ca>13 (iCa>6-7), sx- lethargy3) LR4) Thiazide diuretics (retain Ca)5) breast cancer ismost common malignant cause, hyperparathyroidism is most common benign cause6) NS at 200-300cc/hr + lasix. If malignant give mithramycin, calcitonin, alendronic acid and dialysis

379
Q

1) levels of Ca in hypoCa and sx2) cause3) rx4) how to adjust Ca for protein (albumin level)

A

1) Cas sign (carpopedal spasm), prolonged QT2) parathyroidectomy3) replace Mg before you can correct Ca4) for every 1g decrease in protein add 0.8 to Ca

380
Q

1) Normal Magnesium level2) hypermagnesemia sx and pt’s it is seen in. and rx3) hypomagnesemia- when do you see it and sx

A

1) 2.0-2.72) renal failure pts taking magnesium containing products. sx-lethrgic. rx- Calcium3) in pts with massive diuresis, chronic TPN without mineral replacement or ETOH abuse. similar sx to hypoCa

381
Q

Metabolic acidosis1) equation for calculating Anion Gap (what is nl)2) causes of high anion gap acidosis3) causes of nl anion gap acidosis4) rx of acidosis

A

1) AG= Na - (HCO3+Cl), nl is 10-152) MUDPILES: methanol, uremia, DKA, par-aldehydes, Isoniazid, lactic acidosis, ethylene glycol, salicilates3) usually Na/HCO3 loss (ileostomies, small bowel fistula, massive bile leak)4) rx underlying cause, keep pH>7.2 with bicarb, severely decreased pH can affect myocardial contractility

382
Q

metabolic alkalosis1) causes2) NG suction electrolyte effects and Rx

A

1) usually contraction (diarrhea, vomiting, NG suction)2) hypochloremic, hypokalemic metabolic alkalosis with paradoxical aciduria-lose Cl and H from stomach 2/2 NGT-> hypoCl and alkalosis-lose water-> kidney reabsorbs Na in exchange for K via Na/K ATPase exchanger (hypokalemia)-Na/H- exchanger activated in an effor to reabsorb water and K/H exchanger in effor to reabsorb K -> paradoxical aciduria-Rx- Normal saline to correct the Cl- deficit

383
Q

how long does it take for respiratory compensation of metabolic abnormalities

A

minutes

384
Q

how long does it take for renal compensation of metabolic abnormalties

A

HCO3- regulation takes hours to days

385
Q

how to calculate FeNa and what is it the best test for1) FeNa, urine Na and BUN/Cr ratio and urine osmolality if prerenal prbm

A

(urine Na/Cr)/ (plasma Na/Cr) best test for azotemia1) FeNa20, urine osmolality >500mOsm)

386
Q

how to preven renal damage from contrast dyes

A

prehydration is best, aso HCO3- and n-acetylcysteine

387
Q

Myoglobin- why is it toxic to kidney and how to rx

A

converted to ferrihemate in acidic environment-> toxic to renal cells. rx- alkalinize urine.

388
Q

Tumor lysis syndrome1) what is released2) effect on organ systems3) rx

A

1) purines and pyrimidines-> inc PO4 and uric acid, dec Ca2) inc BUN and Cr (renal damage), EKG changes3) hydration (best), rasburicase (converts uric acid in inactive metabolite allantoin), allopurinol ( dec uric acid production), diuretics, alkalinization of urine

389
Q

Vitamin D (cholecalciferol)1) where is it made and how2) where does it go from there and where is it converted into active form3) effect of active form of vit D4) effect of renal failure on levels

A

1) skin (UV sunlight converts 7-dehydrocholesterol to cholecalciferol2) Goes to liver for (25-0H) and then to Kidney for (1-OH) which creates active form of vit D3) increases Ca-binding protein-> inc intestinal Ca absorption4) decreased active vitamin D (dec 1-OH hydroxylation)-> decreased Ca reabsorption from gut

390
Q

why do pts with CKD have anemia

A

decreased erythropoeitin

391
Q

difference of transferrin and ferritin

A

transferrin= transporter of iron; ferritin= stored iron

392
Q

average caloric need

A

20-25 calories/kg/day

393
Q

Calories in1) fat2) protein3) oral carbohydrates4) dextrose

A

1) 9cal/g2) 4cal/g3) 4cal/g4) 3.4 cal/g

394
Q

nutritional req for average healthy adult make% protein, fat and carbs

A

20% protein (1gprotein/kg/day 20% should be essential aa’s), 30% fat (imp for essential fatty acids), 50% carbohydrates

395
Q

how much do trauma/surgery/sepsis increase caloric requirements

A

20-40%

396
Q

how much does pregnancy increase the caloric requirement and lactation?

A

pregnancy- 300kcal/day, lactation 500kcal/day (protein requirement also increases)

397
Q

Burns:1) calories required2) protein required

A

1) 25kcal/kg/day + (30kcal/day x %burn)2) 1-1.5 g/kg/day + (3g x %burn)

398
Q

what is most of energy expenditure used for

A

heat production

399
Q

how much does fever increase basal metabolic rate

A

10% for each degree above 38.0 C

400
Q

how to calculate caloric need for overweight patients

A

[(actual body weight- ideal body weight) x 2.5] + ideal body weight

401
Q

what does the harris-benedict equation use to calculate basal energy expenditure

A

weight, height, age, and gender)

402
Q

maximum glucose administration in central line TPN

A

3gm/kg/hr

403
Q

what is the base of 1) TPN2) PPN

A

1) glucose2) fat

404
Q

what is the fuel for colonocytes

A

short-chain fatty acids (ie- butyric acid)

405
Q

what is the feul for small bowel enterocytes

A

Glutamine

406
Q

what is the most common aa in blood stream and tissue

A

Glutamine

407
Q

role of glutamine

A

releases NH4 in kidney to help with nitogen excretion, can be used for gluconeogenesis

408
Q

what is the primary fuel for most neoplastic cells

A

Glutamine

409
Q

T 1/2 of:1) Albumin2) Transferrin3) Prealbumin4) nl protein level5) nl albumin level

A

1) 18 days2) 10days3) 2 days4) 6-8.55) 3.5-5.5

410
Q

what are acute indicators of nutritional status

A

retinal binding protein, prealbumin, transferrin

411
Q

Ideal body weight for1) men2) women

A

1) 106lb + 6lb for each inch over 5ft2) 106lb + 5lb for each inch over 5 ft

412
Q

preop signs of poor nutritional status

A

weight loss >10% in 6monthsweight <3 (strong risk factor for morbidity and mortality after surgery)

413
Q

1) what is the respiratory quotient2) RQ>1 signifies what State and how to treat3) RQ <0.7 signifies what state and how to treat?4) RQ=0.75) RQ=0.86) RQ-1.0

A

1) CO2 produced/O2 consumed= measure of energy expenditure2) lipogenesis (overfeeding). rx- decrease carbs and caloric intake bc high carbs intake can lead to CO2 buildup and ventilator problems3) ketosis and fat oxidation (starving). rx- inc carbs and caloric intake4)pure fat utilization5) pure protein synthesis6) pure carb utilization

414
Q

Postoperative phases: when do they occur and nitrogen balance1) Diuresis phase2) catabolic phase3) anabolic phase

A

1) POD 2-52) POD 0-3 (negative nitrogen balance)3) POD 3-6 (positive nitrogen balance)

415
Q

Metabolic Differences bw starvation / injury1) basal metabolic rate2) presence of mediators (ie-TNF-a and IL-1)3) major fuel oxidized4) Ketone body production5) gluconeogenesis6) Protein metabolism7) negative nitrogen balance8) hepatic ureagenesis9) muscle proteolysis10) hepatic protein synthesis

A

1) - / ++2) - / +++3) fat/ mixed (fat and proteins)4) +++ / can be + or -5, 6, 7, 8, 9, 10) +/ +++

416
Q

true/false: the magnitude of metabolic response is proportional to the degree of injury

A

true

417
Q

Glycogen stores1) how quickly are they depleted in starvation and what does body switch to after2) where is glucose-6-phosphatase found?3) where is glucose-6-phosphate?

A

1) 24-36hours (2/3 skeletal muscle, 1/3 liver)-> body then switches to fat2) only in liver (skeletal muscle lacks it)3) stays in muscle after breakdown from glycogen and is utilized

418
Q

1) gluconeogenesis precursors2)which is the primary substrate and simplest aa precursor3) which are the only aa’s to increase during times of stress4) where does gluconeogenesis occur during late starvation

A

1) aa’s (esp alanine), lactate, pyruvate, glycerol2) Alanine3) kidney

419
Q

starvation:1) when do you not see protein-conserving mechanisms2) when do you see protein conserving mechs?3) main source of energy4) how much weight loss can most pts tolerate without major complications? how many days?

A

1) trauma due to catecholamines and cortisole2) starvation3) fats, however in trauma also use protein4) 15%, 7 days. If longer need to start TPN or Dobbhoff tube

420
Q

what are the benefits of feeding via the gut

A

avoid bacterial translocation (bacterial overgrowth, increased permeability due to starved enterocytes, bacteremia) and TPN complications

421
Q

Indications for PEG

A

when regular feeding not possible (CVA) or predicted not to occur for >4wk

422
Q

Source of energy for brain normally and during starvation?what about peripheral nerves, adrenal medulla, RBCs and WBCs

A

brain- glucose normally but can use ketones with progressive starvation. The others are obligate glucose users

423
Q

refeeding syndrome1) when does it occur2) electrolyte inbalances and s/e’s3) how to prevent

A

1) when feeding after prolonged starvation/malnutrition2) results in decreased K, Mg, PO4-> cardiac dysfnc, profound weakness, encephalopathy3) start to re-feed at low rate 10-15kcal/kg/day

424
Q

Cachexia1) definition2) mediating factor

A

1) anorexia, weight loss, wasting. glycogen breakdown, lipolysis protein catbolism2)TNF-alpha

425
Q

1) Kwashiorkor2) Marasmus

A

1) protein deficiency2) starvation

426
Q

Hemostatic adjustments initiated after injury1) response of hypothalamus2) pancreatic response3) cardiac response4) adrenal reponse5) injured tissue and muscle results6) kidney response7) peripheral vessel response

A

1) elaboration of ACTH, ADH, GH2) inc glucagon, dec insulin3) inc stroke volume and HR4) inc cortisol and catecholamine release5) RELEASE of local infalmmatory mediators (cytokines, prostaglandins, platelet activating factor), and mobilization of aa’s from skeletal muscle6) volume conserving mechs (aldosteronem ADH), humoral cascades-> complement and kinins7) peripheral vasoconstriction to redistribute blood to vital organs

427
Q

Nitrogen balance1) equation2) how much protein is needed for 1g Nitrogen3) significance of positive/negative Nitrogen balance4) total protein synthesis in nl healthy 70kg male per day

A

1) (Nin-Nout)=([protein/6.25]-[24hr urine N +4g])2) 6.25gm protein3) positive- more protein ingested than excreted (anabolism)negative- catabolism, more protein excreted than taken in4) 250g/day

428
Q

what organ is responsible for aa production and breakdown

A

liver

429
Q

what is majroity of protein breakdown from skeletal muscle

A

glutamine and alanine

430
Q

purpose of urea production

A

used to get rid of ammonia from amino acid breakdown in liver

431
Q

What enzyme breaks down1) Triacylglycerides (TAGs)2) cholesterol3) lipids (and break down products)

A

1) pancreatic lipase2) cholesterol esterase3) phospholipase (breaks it down into micelles and free fatty acids)

432
Q

FAT DIGESTION1) what are micelles made of2) how do they enter the enterocyte3) purpose of bile salts4) putpose of cholesterol5) what are the fat-soluble vitamins and how are they absorbed6) how are medium and short-chain fatty acids absorbed

A

1) aggregates of bile salts, long-chain free fatty acids and monoacylglycerides2) fuse with enterocyte membrane3) increase absorption area for fats, helping form micelles4) used to synthesize bile salts5) A, D, E, K- absorbed in micelles6) simple diffusion

433
Q

FAT Digestion1) what happens after micelles and other fatty acids enter enterocytes2) where do chylomicrons and long-chain fatty acids go?3) where do medium and short-chain fatty acids go? what other nutrients go to the same place?

A

1) chylomicrons formed (90%TAG, 10%phospholipid/proteins/cholesterol)2) thoracic duct to lymphatics3) portal system (same as aa’s and carbs)

434
Q

lipoprotein lipase1) where is it found2) function

A

1) on endothelium in liver and adipose tissue2) clears chilomicrons and TAGs from the blood, breaking them down to fatty acids and glycerol

435
Q

Free fatty acid-binding protein1) where is it found2) function

A

1) on endothelium in liver and adipose tissue.2) binds short- and medium- chain fatty acids

436
Q

Saturated fatty acids1) what are they used for2) what cells are fatty acids the preferred source of energy for?

A

1) fuel by cardiac and skeletal muscles2) (ketones- acetoacetate and beta-hydroxybutyrate) are preferred nrg source for colonocytes, liver, heart and skeletal muscle

437
Q

what are unsaturated fatty acids used for

A

structural components for cells

438
Q

Hormone-sensitive lipase (HSL)1) where is it found2) what does it do3) what signaling factors is it sensitve to

A

1) fat cells2) breaks down TAGs (storage form of fat) to fatty acids and glycerol, which are released into the bloodstream3) growth hormone, catecholamines, glucocorticoids

439
Q

What are the essential fatty acids, what are they needed for

A

linolenic, linoleic. needed for prostaglandin synthesis (long-chain fatty acids). Imp for immune cells.

440
Q

CARBOHYDRATE DIGESTION1) 3 enzymes resonsible2) how are glucose and galactose absorbed and where do they go after3) how is fructose absorbed and where is it released after4) what is sucrose5) what is lactose6) what is maltose

A

1) 1st- salivary amylase, then pancreatic amylase and disaccharidases2) secondary active transport, released into portal vein3) facilitated diffusion, released into portal vein4) fructose+glucose5) galactose +glucose6) glucose+glucose

441
Q

Protein digestion1) 4 enzymes responsible and order of action2) where is trypsinogen released from3) what activates trypsinogen and where is it released from4) role of Trypsin5) what breaks down protein and breakdown products6) how is protein absorbed and where is it released

A

1) 1st-stomach pepsin, then trypsin, chymotrypsin and carboxypeptidase2) from pancreas3) activated by enterokinase which is released from the duodenum4) activates other pancreatic protein enzymes and can autoactivate other trypsinogen molecules5) proteases-> aa’s, dipeptides and tripeptides6) secondary active transport, then released as free aa’s into the portal vein.

442
Q

In which patients should you limit protein intake and why

A

liver and renal failure to avoid ammonia buildup and possible worsening encephalopathy

443
Q

1)What are the branched chain aa’s2) where are they metabolized?3) what are the essential amino acids?

A

1) leucine, isoleucine, valine (LIV)2) muscle3) all branched chain aa’s (leucine, isoleucine, valine) + argenine, histidine, lysine, methionine, phenylalanine, threonine and tryptophan

444
Q

What is the general composition of TPN1) % aa’s2) % dextrose3) electrolytes4) other5) amount of kcal/cc in 10% and 20% lipid solution

A

1) 10%2) 50%3) Na, Cl, K, Ca, Mg, PO4, acetate4) mineral and vitamins and lipids (given ceperately from TPN5) 10% has 1.1 Kcal/cc, 20% has 2kcal/cc

445
Q

CORI cycle1) what is it and where does it occur

A

1) glucose utilized and converted into lactate in MUSCLE2) lactate goes to liver and converted back to pyruvate and eventually glucose via GLUCOneogenesis3) Glucose then transported back to muscle

446
Q

Mineral and vitamin deficiencies- name the one that correlates to the symptoms below1) hyperglycemia, encephalopathy, neuropathy2) cardiomyopathy, weakness3) pancytopenia4) poor wound healing5) weakness (failure to wean off ventilator), encephalopathy, decreased phagocytosis

A

1) Chromium2) selenium3) Copper4) Zinc5) Phosphate

447
Q

Mineral and vitamin deficiencies- name the one that correlates to the symptoms below1) Wernicke’s encephalopathy, cardiomyopathy2) sideroblastic anemia, glossitis, peripheral neuropathy3) megaloblastic anemia, peripheral neuropathy, beefy tongue4) megaloblastic anemia, glossitis5) pellagra (diarrhea, dermatitis, dementia)

A

1) Thiamine (B1)2) Pyridoxine (B6)3)Vit B12 Cobalamin4) folate5) Niacin

448
Q

Mineral and vitamin deficiencies- name the one that correlates to the symptoms below1) dermatitis, hair loss, thrombocytopenia2) night blindness3) coagulopathy4) Rickets, osteomalacia, osteoporosis5) neuropathy

A

1) essential fatty acids2) Vit A3) Vit K4) Vit D5) Vit E

449
Q

what is 2nd most common cause of death in US

A

CANCER

450
Q

MC cancer in1) women2) cancer-related death in men and women3) men4) how does PET work

A

1) breast2) lung3) prostate4) positron emission tomography identifies mets by detecting fluorodeoxyglucose molecules

451
Q

1) difference in how cytotoxic T cells and natural killer cells attack tumor2) T/F: tumor antigens are random only in viral induced tumors3) diff bw hyperplasia, metaplasia, and dysplasia. use GERD for example

A

1) cytotoxic T cells need MHC complex to attack tumor. NK cells can indivudually attack2) false- Ag are random in all tumors except viral induced3)hyperplasia- increased # of cellsmetaplasia- replaccement of one tissue with another (ie- GERD squamous epithelium in esophagus changed to columnar gastric tissue in Barret;s esophagus)dysplasia- altered size, shape and organization (ie- Barrett’s dysplasia

452
Q

tumor markers: name the cancer1) CEA and T1/22) AFP and T1/23) CA 19-94) CA 1255) Beta-HCG (2 cancers)6) PSA and T 1/27) NSE (2 cancers)8) Chomagranin A9) Ret oncogene

A

1) Colon CA, 18 days2) HCC (liver CA)- 5 days3) pancreatic CA4) ovarian CA5) choriocarcinoma, testicular CA6) prostate CA, 18days7) small cell lung CA, neuroblastoma8) carcinoid tumor9) thyroid medullary CA

453
Q

2 steps necessary for cancer transformation

A

1) heritable alteration in genome 2) loss of growth regulation

454
Q

define the following stages of tumor growth:1) time between exposure and formation of clinically detectable tumor2) stage in which carcinogen acts with DNA3) stage that follows tumor initiation4) stage in which cancer cell become clinically detectable tumor

A

1) latency period2) initiation3) promotion of cancer cells4) progression

455
Q

3 mechanisms from which cancer can arise

A

carcinogenesis (ie-smoking), viruses (ie-EBV) or immunodeficiency (ie-HIV)

456
Q

1) what are oncogenes, where are they found and give an example2) what are proto-oncogenes

A

1) contained in retroviruses like EBV- associated with Burkitt’s lymphoma (8:14 translocation) and nasopharyngeal CA (c-myc)2) human genes with malignant potential

457
Q

Viruses associated as the infectious agent in the following cancers:1) cervical2) Gastric3) HCC4) nasopharyngeal CA5) Burkitt’s lymphoma6) other lymphomas

A

1) HPV2) H. pylori3) HBV and HCV4) EBV5) EBV6) HIV

458
Q

radiation therapy (XRT)1) what cell phase is most vulnerable2) how is most damage done3) main target (ie-what is damaged)4) type of radiation associated with skin-preserving effect and why?

A

1) M phase2) formation of oxygen radicals-> max effect with high O2 levels3) DNA- O2 radicals and XRT itself damage4) high-energy radiation bc maximal ionizing potential not reached until deeper structures

459
Q

why do we fractionate XRT doses

A

allows repair of normal cells, allows re-oxygenation of tumor, allows redistribution of tumor cells in cell cycle

460
Q

1) very radiosensitive tumors2) very radioresistant tumors

A

1) seminomas, lymphomas2) epithelial, sarcomas

461
Q

why are large tumors less responsive to XRT

A

lack of O2 in tumor

462
Q

how does brachytherapy work

A

source of radiation in or next to tumor delivers high, concentrated doses of radiation

463
Q

CHEMO:1) what are cell-cycle specific agents and disadvantage2) effect of cell-cycle nonspecific agents

A

1) 5FU and methotrexate- exhibit plateau in cell-killing ability2) have linear reponse to cell killing

464
Q

CHEMO:1) Tamoxifen- mechanism of action, what it treats, risk of using2) Taxol- mechanism3) Bleomycin and busulfan S/E4) Cisplatin- mechanism and S/E’s5) Carboplatin- mechanism and S/E’s

A

1) blocks estrogen receptor-> decreases short term (5-yr) risk of breast CA 45% (1% risk of clot, 0.1% risk of endometrial CA)2) promotes microtubule formation and stabilization that cannot be broken down-> cells rupture3) pulmonary fibrosis4) platinum alkylating agent- S/E: nephrotoxic, neurotoxic, ototoxic5) platinum alkylating agent)- bone (myelo) suppression

465
Q

CHEMO:1) Vincristine mech and S/E2) Vinblastine mech and S/E3) Levamisole mech4) alkylating agents- how they work, what drug is ex, S/E5) what can you give to help with hemorrhagic cystitis 2/2 cyclophosphamide

A

1) microtubule inhibitor, peripheral neuropathy, neurotoxic2) microtubule inhibitor, bone (myelosuppression): vinBlastine B=bone3) anthelminthic drug though to stimulate immune system against cancer4) transfer alkyl groups-> form covalent bonds to DNA. Ie- Cyclophosphamide (acrolein is active metabolite). S/E- gonadal dysfnc, SIADH, hemorrhagic cystitis5) Mesna

466
Q

Chemo:1) methotrexate- mechanism, S/E and how to reverse2) 5-FU mechanism3) what increases toxicity of 5-FU4) doxorubicin- mechanism and how does it cause heart toxicity5) Etoposide mechanism

A

1) inhibits dihydrofolate reductase (DHFR)-> inhibits purine and DNA synthesis. S/e- nephrotoxic, radiation recall. Leucovorin rescue (foloinic acid) reverses effects by re-supplying folate2) inhibits thymidylate syntehesis-> inhibit DNA/purine synthesis.3) leucovorin4) DNA intercalator. heart tox 2/2 O2 radicals at doses >500mg/m25) inhibits topoisomerase (which normally unwinds DNA)

467
Q

which chemo agents are the least myelosuppressive

A

bleomycin, vincristine, busulfan and cisplatin

468
Q

Why do we use GCSF (granulocyte colony-stimulating factor) after chemo and what are the S/E’s

A

1) used for neutrophil recovery after chemo. S/E- Sweet’s syndrome (acute febrile neutropenic dermatitis)

469
Q

When do we resect a normal organ to prevent cancer

A

breast with BRCA I/II or strong fam hx; Thyroid with RET proto-oncogene and fam h/o thyroid CA

470
Q

Are the following tumor suppressor genes or proto-oncogenes and what is the defect associated with CA:1) Rb1 (Retinoblastoma) on chromosome 132) p533) ras4) APC5) src6) sis

A

1) tumor suppressor gene involved in cell-cycle regulation2) tumor suppressor, chrom 17, nl induces cell cycle arrest and apoptosis3) proto-oncogene- G protein defect4) tumor suppressor, chrom 5, cell cycle regulation and movement5) proto-oncogene- tyrosine kinase defect6) proto-oncogene- platelet-derived growth factor receptor defect

471
Q

Mineral and vitamin deficiencies- name the one that correlates to the symptoms below1)erb B2) myc3) DCC4) bcl5) BRCA

A

1) proto-oncogene- epidermal growth factor receptor defect2) proto-oncogenes (c-, n-, l-), transcription factors3) tumor suppressor- chrom 18, involved in cell adhesion4) tumor suppressor involved in apoptosis5) tumor suppressor

472
Q

What is Li-Fraumeni syndrome1) defect2) cancers

A

1) p53 gene2) childhood sarcoma, breast CA, brain tumor, leukemia, adrenal CA

473
Q

Colon cancer1) initial step in evolution of colorectal CA2)other genes involved3) does it met to bone?

A

1) APC mutation2) p53, DCC, K-ras3) not usually

474
Q

Carcinogens- what type of cancer risk1) coal tar2) Beta-naphthylamine3) Benzene4) asbestos

A

1)larynx, skin, bronchial CA2) urinary tract CA (bladder CA)3) leukemia4) mesothelioma

475
Q

what cancers may spread to 1) suspicious supraclavicular node2) axillary node3) periumbilical node4) ovaries5) bone6) skin7) small bowel

A

1) neck, breast, lung, stomach (Virchow’s node), pancreas2) lymphoma (#1), breast, melanoma3) pancreas (sister mary joseph node)4) stomach (krukenberg tumor), colon5) breast #1, prostate6) breast, melanoma7) melanoma #1, lung and breast

476
Q

Clinical trials- what do the following phases evaluate1) phase I2) phase II3) phase III4) phase IV

A

1) is it safe and at what dose2) is it effective3) is it better than existing therapy4) implementation and marketing

477
Q

describe the various types of chemo1) induction2) primary (neoadjuvant)3) Adjuvant4) salvage

A

1) sole treatment, used for advanced disease or when no other treatment exists2) chemo given first, followed by another (secondary) therapy3) given after other therapy is used4) for tumors that fail to respond to initial therapy

478
Q

T/F: lymphnodes have good barrier function and should not be viewed as signs of metastasis

A

False- poor barriers, view as signs of met

479
Q

When to use en bloc multiorgan resection

A

aggressive local invasivenes (not metastatic disease) ie- colon into uterus, adrenal into liver, gastric into spleen

480
Q

when to use palliative cancer surgery

A

tumors of hollow viscus causing obstruction or bleeding (ie-colon CA), breast CA with skin or chest wall involvement

481
Q

when should you not do sentinel LN bx

A

when clinically palpable nodes- for these pts go after and sample these nodes

482
Q

survival rate for colon mets to liver

A

35% 5-year survival if completely resected

483
Q

good prognostic indicators after resection of heaptic colorectal mets

A

tumor number 12mo

484
Q

most successfully cured metastases with surgery

A

colon to liver, sarcoma to lung, but still low overall survival

485
Q

for which tumor does surgical debulking improve chemotherapy

A

ovarian CA

486
Q

which tumors are curable solid tumors with chemo only

A

hodgkin’s and non-Hodgkin’s lymphoma

487
Q

T cell lymphomas- which type has1) skin lesions2) Sezary cells

A

1) HTLV-12) mycosis fungoides

488
Q

HIV-related malignancies

A

Kaposi’s sarcoma, non-Hodgkin’s lymphoma

489
Q

V-EGF- role in cancer

A

vascular epidermal growth factor- causes angiogenesis, involved in tumor metastasis

490
Q

transplant immunology1) most important immune marker in recipient/donor matching2)which type of transplant does not require ABO blood compatibility?

A

1)HLA-DR is most important overall, but HLA-A and -B also v. imp (human leukocyte antigen)2)liver transplant

491
Q

purpose of cross-match for transplant- what does it detect and how is it done (what is mixed together), what is likely to occur with TXP if positive-cross match

A

detects preformed recipient antibodies to the donor organ by mixing recipient serum with donor lymphocytes. If Abs are present-> positive cross match and hyperacute rejection

492
Q

what is panel reactive antibody-what result is a C/I to transplant-what H&P factors can increase PRA

A

-identical technique to cross-match, but detects preformed recipient Abs using a panel of HLA typing cells and gives a percentage of cells that the recipient serum reacts with-high PRA (>50%) is C/I to transplant due to risk of hyperacute rejection-transfusions, pregnancy, previous transplant and autoimmune diseases

493
Q

Transplant rejection treatment1) mild rejection2) severe rejection

A

1) pulse steroids2) steroid and Ab therapy (ATG=anti-thymocyte globulin or daclizumab)

494
Q

1 malignancy following transplant

A

squamous cell skin cancer

495
Q

2 malignancy following transplant-what virus is it related to-how to treat

A

post-transplant lympho-proliferative disorder (PTLD)-EBV related-withdrawal of immunosuppression, may need chemo and XRT for aggressive tumor

496
Q

Transplant drugs:1) Mycophenolate (MMF, Cellcept)-mechanism-S/E-when is it used-what other drug has similar action

A

1)- inhibits de novo purine synthesis-> inhibits growth of T cells-S/E-myelosuppression, must keep WBC>3-maintenance therapy to prevent rejection-Azathioprine (Imuran) has similar action

497
Q

Transplant drugs:2) Steroids-mechanism-when is it used

A

-inhibit inflammatory cells (macrophages) and genes for cytokine synthesis (IL-1 and IL-6)-used for induction after transplant, maintenance and acute rejection episodes

498
Q

Transplant drugs:3) Cyclosporin (CSA)-mechanism-when is it used-side effects-what trough level do you want-where is it metabolized/excreted

A

calcineurin inhibitor-binds cyclophilin protein and inhibits genes for cytokine synthesis (IL-2, IL-4, etc)-used for maintenance therapy-S/E- nephrotoxicity, hepatotoxicity, tremors, seizures, hemolytic-uremic syndrome-trough 200-300-hepatic metabolism with biliary excretion (reabsorbed in gut, get entero-hepatic recirculation)

499
Q

Transplant drugs:4) FK-506 (Prograf, tacrolimus)-mechanism-when is it used-S/E- what is goal tough level5) does FK-506 or cyclosporin have less rejection episodes in kidney transplants

A

4)calcineurin inhibitor -Binds FK-binding protein and inhibits genes for cytokine synth (like CSA)-maintenance therapy-nephrotoxicity, more GI sx and mood changes than CSA but less enterohepatic recirculation than CSA-trough 10-155) FK has less rejection episodes in kidney TXPs

500
Q

Transplant drugs:6) Sirolimus-mechanism and use7) Anti-thymocyte globulin (ATG)-mechanism-use-T/F: is cytolytic so depends on complement-S/E and how to prevent

A

6) binds FK-binding protein like FK-506 but inhibits mammalian target of rapamycin (mTOR)-> inhibits T and B-cell response to IL-2-used as maintenance therapy7) Equine (ATGAM) or rabbit (Thymoglobulin) polyclonal Ab against T cell Ags (CD2, CD3, CD4)- used for induction and acute rejection episodes-True-cytokine release syndrome (fever, chills, pulm edema, shock). Give steroids and benadryl before drug to try to prevent

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