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Full Fiser ABSITE review > Basic Science > Flashcards

Basic Science Flashcards

Master basic science surgical principles

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 following

1) adhesion mlq (cell to cell and cell to extracellular
2) cell to cell occluding junctions (impermeable)
3) permeable jnc allow communication bw cells

A

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

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5
Q

How do the following work

1) g-protein
2) ligand-triggered protein kinase

A

1) intramembrane, transduce signal from receptor to response enzyme
2) 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 antigens
2) HLA-type antigens

A

1) glycolipids on cell membrane

2) glycoproteins (Gp) on cell membrane

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7
Q

Cell cycle:

1) which part determines cell cycle length
2) protein synthesis
3) chromosome duplication
4) mitosis
5) nucleus division

A

1) G1 most variable
2) S
3) S
4) M
5) M

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8
Q

What phase of mitosis do the following occur in:

1) chromosome alignment
2) separate nucleus reforms around each set of chromosomes
3) centromere attachment, spindle formation, nucleus disappears
4) chromosomes pulled apart

A

1) metaphase
2) telophase
3) prophase
4) 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 transcription
Transcription factors:
2) where do steroid hormones bind
3) where do thyroid hormones bind
4) what are initiation factors
A

1) DNA-template for RNA polymerase-> makes mRNA
2) bind in cytoplasm then enter nucleus
3) bind receptor in nucleus
4) 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) Purines
2) Pyrimidines
3) what has the strongest bond and why

A

1) Adenine, Guanine
2) 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 reticulum
2) smooth endoplasmic reticulum
3) golgi apparatus
4) phagosomes
5) 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 lysosomes
4) engulf large particles and take to lysosome
5) same but for small particles

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23
Q

Protein Kinase C

1) what activates it
2) 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_ Keratin
2_ desmin
3_ vimentin

A

1) hair/nails
2) muscle
3) 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 components

where does it form

A

X, V, Ca, platelet factor 3, prothrombin

forms 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 work

1) Vitamin K
2) FFP and what is 1/2 life

A

1) 6 hours

2) immediate, 1/2 life is 6 hr

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50
Q

Normal 1/2 life for:

1) RBC
2) platelets
3) PMNs

A

1) 120 days
2) 7 days
3) 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 for

1) PTT
2) ACT (activated clotting time)

A

1) PTT 60-90 sec

2) ACT 150-200sec (>460sec for cardiopulmonary bypass)

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59
Q

At what INR is

1) relative contraindication for surgery
2) relative CI for central line, biopsy of eye surgery

A

1) >1.5

2) >1.3

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60
Q

what is most common congenital bleeding disorder

A

vonWillibrands

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61
Q

VonWillibrands disease

1) inheritance pattern
2) role of vWF
3) affect on PT/PTT/INR
4) difference bw type 1-3
5) treatment

A

1) Types I and II are AD, type III is AR
2) links GpIb receptor on platelets to collagen
3) 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 deficiency
5) 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 A

1) inheritance
2) deficiency, coags
3) why don’t pts with dz always bleed at circumcision
4) how high does factor level need to be pre op, post op?
5) treatment

A

1) sex-linked recessive
2) factor VIII, prolonged PTT, nl PT
3) VIII can cross the placenta from mother
4) 100% preop, 80-100% for 10-14days postop
5) 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 B

1) inheritance
2) deficiency, coags
3) what factor level do you need preop, postop?
4) treatment

A

1) sex-linked recessive
2) IX, increased PTT, nl PT
3) 100% pre-op, 30-40% for 2-3days postop
4) recombinant factor IX or FFP

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64
Q

factor VII deficiency

1) coags
2) treatment

A

1) increased PT, nl PTT

2) recomb factor VII or FFP

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65
Q

1) causes of acquired thrombocytopenia
2) deficiency in glanzmann’s thrombocytopenia
3) deficiency in Bernard Soulier disease
4) treatment for the above

A

1) ranitidine (H2-blockers), heparin
2) GpIIb/IIIa receptor deficiency (platelets can’t bind each other)- rx with platelets
- -fibrin normally links receptors together
3) 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

HIT

1) cause of thrombocytopenia
2) what is HITT
3) treatment
4) is lovenox or heparin more likely to cause?

A

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

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68
Q

DIC (disseminated intravascular coagulation)

1) what is decreased? increased
2) coags?
3) what initiates it
4) rx

A

1) platelets, fibrinogen are decreased; fibrin split products and D-dimer are increased
2) inc PT and PTT
3) tissue factor
4) 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) ASA
2) Clopidogrel (Plavix)
3) coumadin

A

1, 2 and 3 are all 7 days

1) 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 mutation

1) mechanism of action
2) rx

A

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

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73
Q

Hyperhomocysteinemia

1) effect on clotting
2) rx

A

1) hypercoagulability

2) 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 vera

1) defect
2) what level to keep Hct and platelets before surgery
3) rx

A

1) platelet function defect–> thrombosis
2) Hct< 400 before surgery
3) 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 syndrome

1) coags
2) mechanism of hypercoagulability
3) Dx
4) rx

A

1) hypercoagulable but prolonged PTT
2) antibodies to cardiolipin and lupus anticoagulant (phospholipids), so seen in ppl with lupus but also others
3) false positive RPR, prolonged PTT (not corrected with FFP), positive Russel Viper venom time
4) 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 necrosis

1) cause
2) 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 state
2) pts with relative protein C deficiency

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80
Q

Key elements in developement of:

1) venous thrombus
2) arterial thrombus

A

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

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81
Q

Post-op DVT treatment
1_ 1st DVT
2_ 2nd DVT
3) 3rd DVT or significant PE

A

1) 6months
2) 1 year
3) 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 action

1) Warfarin
2) SCDs
3) Heparin vs. LMWH
4) Argatroban
5) Bivalirudin (Angiomax)
6) Hirudin (from leeches)

A

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

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86
Q

AC reversal

1) Warfarin
2) heparin/ LMWH

A

1) Vit K, FFP

2) 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) cause
2) symptoms/signs
3) labs (haptoglobin, free hemoglobun, bilirubin)
4) treatment
5) how can it present in anesthetized patients

A

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

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104
Q

Delayed hemolysis

1) cause
2) rx

A

1) antibody-mediated against minor antigens

2) 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 cells

1) Which CD?
2) what IL do they release and effect
3) type of hypersensitivity reaction that they mediate

A

1) CD4
2) IL-2-> maturation of cytotoxic T cells
IL-4-> B-cell maturation into plasma cells
3) delayed type hypersensitivity (brings in inflam cells by chemokine secretion)

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114
Q

Suppressor T cells

1) which CD?
2) role

A

CD8, regulate CD4 and CD8 cells

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115
Q

cytotoxic t cells

1) which CD
2) 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 I

1) effect
2) where found
3) structure

A

1) CD8 cell activation, target or cytotoxic T cells
2) on all nucleated cells
3) single chain with 5 domains

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120
Q

MHC class II

1) effect
2) where found
3) structure

A

1) CD4 activation, activates helper T cells (binds T cell receptor), stimulates antibody formation after interaction with B cell surface
2) 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 Cells

how 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 wound
2) 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 type

1) type I
2) type II
3) type III
4) 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 release
2) 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) stomach
2) Proximal small bowel
3) Distal small bowel
4) Colon

A

1) virtually sterile, some GPCs and some yeast
2) 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 48hrs
2) 48hrs to 5 days
3) after 5 days

A

1) atelectasis
2) UTI
3) 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 sepsis
2) late gm-neg sepsis
3) 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 resistance
3) 100-120 mg/dL

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152
Q

C. diff treatment:

1) oral
2) IV

A

1) vanc/flagyl
2) 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 surgery
2) clean contaminated
3) Contaminated
4) 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) GNR
2)anaerobe (and if present what does it imply)
… in SSI

A

1) E. Coli

2) . 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 factor
2) organisms that cause it
3) labs/diagnostic study results
4) rx
5) prophylaxis

A

1) low protein (500 cells/cc
4) ceftriaxone or other 3rd generation cephalosporin
5) Flouroquinolones (Norfloxacin

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183
Q

Secondary bacterial peritonitis

1) source
2) organisms
3) rx

A

1) intra-abdominal ie-perf viscus
2) 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 transfusion
2) Infant from positive mother
3) needle stick from positive patient
4) 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 pts

1) type
2) where
3) rx

A

1) non-Hodgkins
2) stomach most common, then rectum
3) rx- chemo. Surgery if significant bleeding or perforation

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191
Q

ddx for HIV +

1) UGIB
2) LGIB (more common)

A

1) kaposi’s sarcoma, lymphoma

2) CMV, bacterial, HSV

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192
Q

CD4 counts

1) normal
2) symptomatic HIV
3) opportunistic infections (AIDS)

A

1) 800-1200
2) 300-400
3) <200

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193
Q

Hepatitis C

1) chance of transmittion with blood transfusion
2) prevalence
3) rx
4) prevalence of sequelae

A

1) <0.0001%
2) 1-2%
3) interferon
4) 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 arthritis

1) cause
2) rx

A

1) Gonococcus, staph, H. flu, strep

2) drainage, ceftriaxone (or 3rd gen cyclosporin) + vanc until cx returns

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196
Q

lerktlnea. dialysis cather infection
1) organism
2) rx

A

1) S> aureus and s. epidermidis

2) intra peritoneal vanc and gentamicin, removal of catheter if pritonitis >5day, fecal peritonitis-> ex-lap

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197
Q

Difference between:

1) Antiseptic
2) Disinfectant
3) Sterilization

A

1) Kills and inhibits organisms on body
2) kills and inhibits organisms on inanimate objects
3) all organisms killed

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198
Q

Common antiseptics in surgery- what are they and what are they good for

1) Iodophors
2) Chlorhexadine gluconate

A

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

2) 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

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202
Q

Mechanism of Action of monobactams (aztreonam)

A

inhibit cell wall synthesis

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203
Q

Mechanism of Action of vancomycin

A

inhibit cell wall synthesis

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204
Q

Mechanism of Action of tetracycline

A

inhibitor of the 30s ribosome and protein synthesis

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205
Q

Mechanism of Action of Aminoglycosides (tobramycin, gentamycin)

A

inhibitor of the 30s ribosome and protein synthesis

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206
Q

Mechanism of Action of linezolid

A

inhibitor of the 30s ribosome and protein synthesis

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207
Q

Mechanism of action of erythromycin and clindamycin and synercid

A

Inhibitors of 50s ribosome and protein synthesis

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208
Q

mechanism of action of quinolones

A

inhibitor of DNA helicase (gyrase)

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209
Q

mechanism of action of rifampin

A

inhibitor of RNA polymerase

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210
Q

mechanism of action of metronidazole

A

produces oxygen free radicals that breakup DNA

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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) Vancomycin
2) Gentamicin
3) what to do if peak too high
4) what to do if trough too high

A

1) peak 20-40, trough 5-10
2) peak 6-10, trough <1
3) decrease amount of dose
4) 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 zosyn

1) what makes up the abx
2) coverage
3) side effects
4) zosyn dosing frequency

A

1) Timentin is ticarcillin/clavulanic acid and Zosyn is piperacillin/sulbactam
2) GPC (staph and strep), GNRs and anaerobes, enterococci, pseudomonas, acinetobacter, serratia
3) inhibits platelets and high salt load
4) QID dosing

227
Q

First generation cephalosporins

1) abx
2) coverage
3) which is the best for prophylaxis and why
4) does it penetrate the CNS

A

1) cefazolin (ancef) and cephalexin
2) GPC- staph and strep. *not effective for enterococcus
3) ancef- longest T1/2
4) no

228
Q

Second-generation cephalosporins

1) abx
2) coverage
3) which is best for prophylaxis

A

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

229
Q

third-generation cephalosporins

1) abx
2) coverage
3) side effects

A

1) ceftriaxone, ceftazidime, cefepime, cefotaxime
2) 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) Coverage
2) 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 T1/2
3) seizures.

232
Q

Bactrim (Trimethoprim/sulfamethaxazole)

1) coverage
2) 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

Quinolones

1) coverage
2) dosing of cipro
3) dosing of levofloxacin
4) MRSA sensitivity and IV vs. PO efficacy.

A

1) GNRs, +/-GPCs, pseudomonas, acinetobacter, serratia. *doen’t cover enterococcus
2) BID
3) QD
4) 40% MRSA sensitive (IV and PO same efficacy)

234
Q

Aminoglycosides

1) abx
2) coverage
3) cause of resistance
4) what abx is it synergistic with
5) Side effects

A

1) gentamicin, tobramycin
2) GNRs, pseudomonas, acinetobacter, serratia. *doesn’t cover anaerobes
3) modifying enzymes lead to decreased active transport
4) beta-lactams (ampicillin, amoxicillin) facilitate aminoglycocide penetration. Good for enterococcus coverage
5) reversible nephrotoxicity, irreversible ototoxicity

235
Q

Erythromycin (macrolides)

1) Coverage
2) Side effects
3) other action

A

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

236
Q

Vancomycin (glycopeptides)

1) coverage
2) mechanism of action
3) how resistance develops
4) side effects

A

1) GPCs, Enterococcus, C. diff (P.O. intake), MRSA
2) binds cell wall proteins
3) from a change in cell wall-binding protein
4) 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 def
Rifampin- inhibits RNA polymerase. SE- hepatotoxicity, GI symptoms, high resistance rate
Pyrazinamide- hepatotoxicity SE
Ethambutol- SE is retrobulbar neuritis

250
Q

mech of action and what it rxs and SE for

1) acyclovir
2) Ganciclovir

A

both inhibit viral DNA polymerase

1) HSV and EBV
2) 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 systems
2) Phase I of drug metabolism
3) Phase II of drug metabolism

A

1) hepatocyte smooth endoplasmic reticulum, P-450system
2) 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-450

1) Inhibitors
2) Inducers

A

1) Cimetidine, isoniazid, ketoconazole, erythromycin, cipro, flagyl, allopurinol, verapamil, amiodarone, MAOIs, disulfiram
2) 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 
Gout
1) what builds up
2) mechanism of the following treatments
a-Colchicine
b-indomethacin
c-Allopurinol
d-Probenecid
A

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

277
Q

Lipid lowering drugs- actions and side effects

1) Cholestyramine
2) Statins
3) 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 rhabdomyolysis
3) inhibits cholesterol synthesis. Can cause flushing (rx- ASA)

278
Q

GI drugs- brand name, action, mechanism, S/E

1) promethazine
2) Metoclopramide
3) Odansetron
4) Octreotide

A

1) phenergan, antiemetic, inhibits dopamine receptors. S/E- tardive dyskinesia, rx with benadryl
2) Reglan, prokinetic, inhibits dopamine receptors, can increase gastric and gut motility
3) Zofran, antiemetic, central-acting serotonin receptor inhibitor
4) long-acting somatostatin analogue, decreases gut secretions

279
Q

Anti-reflux medications

1) Omeprazole
2) Cimetidine/ranitidine

A

1) PPI, blockes H/K ATPase in stomach parietal cells

2) 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) symptoms
2) first metabolic abnormality
3) second metabolic abnormality

A

1) tinnitus, headaches, nausea, vomiting
2) respiratory alkalosis
3) metabolic acidosis

296
Q

what is the MC side effect of Gadolinium

A

nausea

297
Q

Iodine contrast

1) MC side effect
2) MC side effect requiring treatment

A

1) nausea

2) dyspnea

298
Q

treatment of tylenol overdose

A

N-acetylcysteine

299
Q

components of the standard airway exam for nonanesthesiologists and what is concerning

1) BMI
2) mouth opening
3) mallampati classification
4) mandibular protrusion
5) neck anatomy
6) cervical spine mobility
7) beard

A

1) BMI>31
2) Interincisor or intergingival distance >3cm
3) Class III-IV
4) inability to protrude lower incisors to meet or extend past upper incisors
5) radiation changes or thick obese neck
6) limited extension or possibly unstable cervical spine
7) 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/e

1) sodium thiopental
2) 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 bp
2) 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 cholinesterases
3) fast acting, fewer hemodynamic changes. s/e-continuous infusions can lead to adrenocortical suppression

311
Q

IV induction agents: Ketamine

1) effect
2) major benefit
3) s/e
4) 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 depression
3) hallucinations, catecholamine release (inc CO2, tachycardia), inc airway secretions, and inc cerebral blood flow
4) pts with head injury
5) good for children

312
Q

Rapid Sequence Intubation

1) when is it indicated
2) what do you give

A

1) recent oral intake, GERD, delayed gastric emptying, pregnancy, bowel obstruction
2) 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

succinylcholine

1) speed of action and effect
2) side effects
3) who can’t you use it in

A

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

317
Q

Malignant hyperthermia

1) medication indicated
2) cause
3) symptoms
4) treatment

A

1) succinylcholine
2) caused by a defect in calcium metabolism, calcium released from sarcoplasmic reticulum causes muscle excitation-contraction syndrome
3) inc end-tidal CO2, fever, tachycardia, rigidity, acidosis, hyperkalemia
4) 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 gravis
examples are: cis-atricurium, rocuronium, pancuronium

319
Q

Cis-atracurium

1) how is it degraded
2) good for what pts?
3) what is released 2/2 use?

A

1) Hoffman degradation
2) renal and liver failure pts
3) histamine

320
Q

speed of onset, duration and site of metabolism for:

1) Rocuronium
2) Pancuronium (and most comon side effect)

A

1) fast onset, intermediate duration, hepatic metabolism

2) 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 anesthetics

1) how do they work
2) how much 1%lido can you use
3) why are infected tissues hard to anesthetize
4) what is the longest, shortest acting and which is in between
5) side effects

A

1) increase action potential threshold, preventing Na influx
2) 0.5cc/kg of 1% lido (4.5mg/kg) with epi it is 7mg/kg
3) they are acidotic
4) length of action: bupivacaine>lidocaine>procaine
5) 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

Nacotics

1) drugs
2) mechanism of action
3) where are they metabolized/excreted
4) rx for overdose
5) what pts shouldn’t get

A

1) morphine, fentanyl, demerol, codeine
2) act on mu-opioid receptors-> profound analgesia, respiratory depression ( dec CO2 drive), no cardiac effects, blunt sympathetic response
3) metab in liver, excreted by kidney
4) 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 release
  • can 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

benzodiazepines

1) uses, where it is metabolized, side effect
2) shortest acting to longest acting ones
3) 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 depression
2) Versed (midazolam)- shortest acting (C/I in pregnancy bc crosses the placenta); Valium(diazepam)- intermediate acting; ativan (lorazepam)- long acting
3) Flumazenil (comptetive inhibitor). May cause seizures and arrhythmias, C/I in pt with elevated ICP or status epilepticus

334
Q

Epidural anesthesia

1) how it works
2) s/e if morphine used
3) s/e if lidocaine used
4) how is motor function spared

A

1) analgesia by sympathetic denervation
2) respiratory depression
3) decreased HR and BP
4) 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 classes
describe class 1-6 and E
A

1)healthy
2) mild dz, no limitation
3) 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) Donor
E) 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 electrolytes

1) Na and Cl in 0.9% and 3% NS
2) LR electrolytes
3) 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 28
3) (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) stomach
2) biliary system
3) pancreas
4) duodenum

A

1) 1-2L

2,3,4) 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 composition

1) sweat
2) Saliva
3) stomach
4) pancreas
5) Bile
6) large intestine
7) 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 replace

1) gastric losses
2) pancreatic/biliary/small intestine losses
3) large intestine losses
4) repletion ratio for GI losses
5) fluid for dehydration resuscitation
6) minimal UOP and should you replace it

A

1) D5 1/2NS +20KCl
2) LR with HCO3-
3) LR with K+
4) 1:1
5) NS
6) 0.5 cc/kg/hr, don’t replace

375
Q

1) normal K+ level
2) EKG changes of hyper and hypo K+
3) rx for hyperkalemia and when do you often see it
4) rx for hypokalemia

A

1) 3.5-5
2) hyper-peaked t-waves, hypo- T waves disappear
3) 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, dialysis
4) usually seen with overdiuresis. may need to replete Mg before K

376
Q

1) normal Na
2) hypernatremia: cause, sx, and how to correct
3) hyponatremia: cause; sx and how to correct
4) how to correct for hyperglycemia when evaluating Na level

A

1) 135-145
2) cause-dehydration; sx- HA, restless, irritable, seizures. rx- D5W slowly to avoid brain swelling
3) 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 Ca
2) levels of Ca when symptoms of hyperCa noted
3) what fluids should you NOT give in hyperCa
4) What diuretics should you NOT give
5) causes of hyperCa
6) rx of hyperCa

A

1) 8.5-10 or iCa 4.4-5.5
2) Ca>13 (iCa>6-7), sx- lethargy
3) LR
4) Thiazide diuretics (retain Ca)
5) breast cancer ismost common malignant cause, hyperparathyroidism is most common benign cause
6) NS at 200-300cc/hr + lasix. If malignant give mithramycin, calcitonin, alendronic acid and dialysis

379
Q

1) levels of Ca in hypoCa and sx
2) cause
3) rx
4) how to adjust Ca for protein (albumin level)

A

1) Cas sign (carpopedal spasm), prolonged QT
2) parathyroidectomy
3) replace Mg before you can correct Ca
4) for every 1g decrease in protein add 0.8 to Ca

380
Q

1) Normal Magnesium level
2) hypermagnesemia sx and pt’s it is seen in. and rx
3) hypomagnesemia- when do you see it and sx

A

1) 2.0-2.7
2) renal failure pts taking magnesium containing products. sx-lethrgic. rx- Calcium
3) in pts with massive diuresis, chronic TPN without mineral replacement or ETOH abuse. similar sx to hypoCa

381
Q

Metabolic acidosis

1) equation for calculating Anion Gap (what is nl)
2) causes of high anion gap acidosis
3) causes of nl anion gap acidosis
4) rx of acidosis

A

1) AG= Na - (HCO3+Cl), nl is 10-15
2) MUDPILES: methanol, uremia, DKA, par-aldehydes, Isoniazid, lactic acidosis, ethylene glycol, salicilates
3) 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 alkalosis

1) causes
2) 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 for

1) FeNa, urine Na and BUN/Cr ratio and urine osmolality if prerenal prbm

A

(urine Na/Cr)/ (plasma Na/Cr) best test for azotemia

1) 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 syndrome

1) what is released
2) effect on organ systems
3) rx

A

1) purines and pyrimidines-> inc PO4 and uric acid, dec Ca
2) inc BUN and Cr (renal damage), EKG changes
3) 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 how
2) where does it go from there and where is it converted into active form
3) effect of active form of vit D
4) effect of renal failure on levels

A

1) skin (UV sunlight converts 7-dehydrocholesterol to cholecalciferol
2) Goes to liver for (25-0H) and then to Kidney for (1-OH) which creates active form of vit D
3) increases Ca-binding protein-> inc intestinal Ca absorption
4) 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 in

1) fat
2) protein
3) oral carbohydrates
4) dextrose

A

1) 9cal/g
2) 4cal/g
3) 4cal/g
4) 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 required
2) 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) TPN
2) PPN

A

1) glucose

2) 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) Albumin
2) Transferrin
3) Prealbumin
4) nl protein level
5) nl albumin level

A

1) 18 days
2) 10days
3) 2 days
4) 6-8.5
5) 3.5-5.5

410
Q

what are acute indicators of nutritional status

A

retinal binding protein, prealbumin, transferrin

411
Q

Ideal body weight for

1) men
2) women

A

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

2) 106lb + 5lb for each inch over 5 ft

412
Q

preop signs of poor nutritional status

A

weight loss >10% in 6months

weight <3 (strong risk factor for morbidity and mortality after surgery)

413
Q

1) what is the respiratory quotient
2) RQ>1 signifies what State and how to treat
3) RQ <0.7 signifies what state and how to treat?
4) RQ=0.7
5) RQ=0.8
6) RQ-1.0

A

1) CO2 produced/O2 consumed= measure of energy expenditure
2) lipogenesis (overfeeding). rx- decrease carbs and caloric intake bc high carbs intake can lead to CO2 buildup and ventilator problems
3) ketosis and fat oxidation (starving). rx- inc carbs and caloric intake
4) pure fat utilization
5) pure protein synthesis
6) pure carb utilization

414
Q

Postoperative phases: when do they occur and nitrogen balance

1) Diuresis phase
2) catabolic phase
3) anabolic phase

A

1) POD 2-5
2) POD 0-3 (negative nitrogen balance)
3) POD 3-6 (positive nitrogen balance)

415
Q

Metabolic Differences bw starvation / injury

1) basal metabolic rate
2) presence of mediators (ie-TNF-a and IL-1)
3) major fuel oxidized
4) Ketone body production
5) gluconeogenesis
6) Protein metabolism
7) negative nitrogen balance
8) hepatic ureagenesis
9) muscle proteolysis
10) 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 stores

1) how quickly are they depleted in starvation and what does body switch to after
2) 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 fat
2) only in liver (skeletal muscle lacks it)
3) stays in muscle after breakdown from glycogen and is utilized

418
Q

1) gluconeogenesis precursors
2) which is the primary substrate and simplest aa precursor
3) which are the only aa’s to increase during times of stress
4) where does gluconeogenesis occur during late starvation

A

1) aa’s (esp alanine), lactate, pyruvate, glycerol
2) Alanine
3) kidney

419
Q

starvation:

1) when do you not see protein-conserving mechanisms
2) when do you see protein conserving mechs?
3) main source of energy
4) how much weight loss can most pts tolerate without major complications? how many days?

A

1) trauma due to catecholamines and cortisole
2) starvation
3) fats, however in trauma also use protein
4) 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 syndrome

1) when does it occur
2) electrolyte inbalances and s/e’s
3) how to prevent

A

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

424
Q

Cachexia

1) definition
2) mediating factor

A

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

425
Q

1) Kwashiorkor

2) Marasmus

A

1) protein deficiency

2) starvation

426
Q

Hemostatic adjustments initiated after injury

1) response of hypothalamus
2) pancreatic response
3) cardiac response
4) adrenal reponse
5) injured tissue and muscle results
6) kidney response
7) peripheral vessel response

A

1) elaboration of ACTH, ADH, GH
2) inc glucagon, dec insulin
3) inc stroke volume and HR
4) inc cortisol and catecholamine release
5) RELEASE of local infalmmatory mediators (cytokines, prostaglandins, platelet activating factor), and mobilization of aa’s from skeletal muscle
6) volume conserving mechs (aldosteronem ADH), humoral cascades-> complement and kinins
7) peripheral vasoconstriction to redistribute blood to vital organs

427
Q

Nitrogen balance

1) equation
2) how much protein is needed for 1g Nitrogen
3) significance of positive/negative Nitrogen balance
4) total protein synthesis in nl healthy 70kg male per day

A

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

1) Triacylglycerides (TAGs)
2) cholesterol
3) lipids (and break down products)

A

1) pancreatic lipase
2) cholesterol esterase
3) phospholipase (breaks it down into micelles and free fatty acids)

432
Q

FAT DIGESTION

1) what are micelles made of
2) how do they enter the enterocyte
3) purpose of bile salts
4) putpose of cholesterol
5) what are the fat-soluble vitamins and how are they absorbed
6) how are medium and short-chain fatty acids absorbed

A

1) aggregates of bile salts, long-chain free fatty acids and monoacylglycerides
2) fuse with enterocyte membrane
3) increase absorption area for fats, helping form micelles
4) used to synthesize bile salts
5) A, D, E, K- absorbed in micelles
6) simple diffusion

433
Q

FAT Digestion

1) what happens after micelles and other fatty acids enter enterocytes
2) 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 lymphatics
3) portal system (same as aa’s and carbs)

434
Q

lipoprotein lipase

1) where is it found
2) function

A

1) on endothelium in liver and adipose tissue

2) clears chilomicrons and TAGs from the blood, breaking them down to fatty acids and glycerol

435
Q

Free fatty acid-binding protein

1) where is it found
2) function

A

1) on endothelium in liver and adipose tissue.

2) binds short- and medium- chain fatty acids

436
Q

Saturated fatty acids

1) what are they used for
2) what cells are fatty acids the preferred source of energy for?

A

1) fuel by cardiac and skeletal muscles
2) (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 found
2) what does it do
3) what signaling factors is it sensitve to

A

1) fat cells
2) breaks down TAGs (storage form of fat) to fatty acids and glycerol, which are released into the bloodstream
3) 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 DIGESTION

1) 3 enzymes resonsible
2) how are glucose and galactose absorbed and where do they go after
3) how is fructose absorbed and where is it released after
4) what is sucrose
5) what is lactose
6) what is maltose

A

1) 1st- salivary amylase, then pancreatic amylase and disaccharidases
2) secondary active transport, released into portal vein
3) facilitated diffusion, released into portal vein
4) fructose+glucose
5) galactose +glucose
6) glucose+glucose

441
Q

Protein digestion

1) 4 enzymes responsible and order of action
2) where is trypsinogen released from
3) what activates trypsinogen and where is it released from
4) role of Trypsin
5) what breaks down protein and breakdown products
6) how is protein absorbed and where is it released

A

1) 1st-stomach pepsin, then trypsin, chymotrypsin and carboxypeptidase
2) from pancreas
3) activated by enterokinase which is released from the duodenum
4) activates other pancreatic protein enzymes and can autoactivate other trypsinogen molecules
5) proteases-> aa’s, dipeptides and tripeptides
6) 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’s
2) where are they metabolized?
3) what are the essential amino acids?

A

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

444
Q

What is the general composition of TPN

1) % aa’s
2) % dextrose
3) electrolytes
4) other
5) amount of kcal/cc in 10% and 20% lipid solution

A

1) 10%
2) 50%
3) Na, Cl, K, Ca, Mg, PO4, acetate
4) mineral and vitamins and lipids (given ceperately from TPN
5) 10% has 1.1 Kcal/cc, 20% has 2kcal/cc

445
Q

CORI cycle

1) what is it and where does it occur

A

1) glucose utilized and converted into lactate in MUSCLE
2) lactate goes to liver and converted back to pyruvate and eventually glucose via GLUCOneogenesis
3) Glucose then transported back to muscle

446
Q

Mineral and vitamin deficiencies- name the one that correlates to the symptoms below

1) hyperglycemia, encephalopathy, neuropathy
2) cardiomyopathy, weakness
3) pancytopenia
4) poor wound healing
5) weakness (failure to wean off ventilator), encephalopathy, decreased phagocytosis

A

1) Chromium
2) selenium
3) Copper
4) Zinc
5) Phosphate

447
Q

Mineral and vitamin deficiencies- name the one that correlates to the symptoms below

1) Wernicke’s encephalopathy, cardiomyopathy
2) sideroblastic anemia, glossitis, peripheral neuropathy
3) megaloblastic anemia, peripheral neuropathy, beefy tongue
4) megaloblastic anemia, glossitis
5) pellagra (diarrhea, dermatitis, dementia)

A

1) Thiamine (B1)
2) Pyridoxine (B6)
3) Vit B12 Cobalamin
4) folate
5) Niacin

448
Q

Mineral and vitamin deficiencies- name the one that correlates to the symptoms below

1) dermatitis, hair loss, thrombocytopenia
2) night blindness
3) coagulopathy
4) Rickets, osteomalacia, osteoporosis
5) neuropathy

A

1) essential fatty acids
2) Vit A
3) Vit K
4) Vit D
5) Vit E

449
Q

what is 2nd most common cause of death in US

A

CANCER

450
Q

MC cancer in

1) women
2) cancer-related death in men and women
3) men
4) how does PET work

A

1) breast
2) lung
3) prostate
4) positron emission tomography identifies mets by detecting fluorodeoxyglucose molecules

451
Q

1) difference in how cytotoxic T cells and natural killer cells attack tumor
2) T/F: tumor antigens are random only in viral induced tumors
3) 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 attack
2) false- Ag are random in all tumors except viral induced
3)hyperplasia- increased # of cells
metaplasia- 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 cancer

1) CEA and T1/2
2) AFP and T1/2
3) CA 19-9
4) CA 125
5) Beta-HCG (2 cancers)
6) PSA and T 1/2
7) NSE (2 cancers)
8) Chomagranin A
9) Ret oncogene

A

1) Colon CA, 18 days
2) HCC (liver CA)- 5 days
3) pancreatic CA
4) ovarian CA
5) choriocarcinoma, testicular CA
6) prostate CA, 18days
7) small cell lung CA, neuroblastoma
8) carcinoid tumor
9) 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 tumor
2) stage in which carcinogen acts with DNA
3) stage that follows tumor initiation
4) stage in which cancer cell become clinically detectable tumor

A

1) latency period
2) initiation
3) promotion of cancer cells
4) 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 example
2) 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) cervical
2) Gastric
3) HCC
4) nasopharyngeal CA
5) Burkitt’s lymphoma
6) other lymphomas

A

1) HPV
2) H. pylori
3) HBV and HCV
4) EBV
5) EBV
6) HIV

458
Q

radiation therapy (XRT)

1) what cell phase is most vulnerable
2) how is most damage done
3) main target (ie-what is damaged)
4) type of radiation associated with skin-preserving effect and why?

A

1) M phase
2) formation of oxygen radicals-> max effect with high O2 levels
3) DNA- O2 radicals and XRT itself damage
4) 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 tumors

2) very radioresistant tumors

A

1) seminomas, lymphomas

2) 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 disadvantage
2) effect of cell-cycle nonspecific agents

A

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

464
Q

CHEMO:

1) Tamoxifen- mechanism of action, what it treats, risk of using
2) Taxol- mechanism
3) Bleomycin and busulfan S/E
4) Cisplatin- mechanism and S/E’s
5) 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 rupture
3) pulmonary fibrosis
4) platinum alkylating agent- S/E: nephrotoxic, neurotoxic, ototoxic
5) platinum alkylating agent)- bone (myelo) suppression

465
Q

CHEMO:

1) Vincristine mech and S/E
2) Vinblastine mech and S/E
3) Levamisole mech
4) alkylating agents- how they work, what drug is ex, S/E
5) what can you give to help with hemorrhagic cystitis 2/2 cyclophosphamide

A

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

466
Q

Chemo:

1) methotrexate- mechanism, S/E and how to reverse
2) 5-FU mechanism
3) what increases toxicity of 5-FU
4) doxorubicin- mechanism and how does it cause heart toxicity
5) 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 folate
2) inhibits thymidylate syntehesis-> inhibit DNA/purine synthesis.
3) leucovorin
4) DNA intercalator. heart tox 2/2 O2 radicals at doses >500mg/m2
5) 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 13
2) p53
3) ras
4) APC
5) src
6) sis

A

1) tumor suppressor gene involved in cell-cycle regulation
2) tumor suppressor, chrom 17, nl induces cell cycle arrest and apoptosis
3) proto-oncogene- G protein defect
4) tumor suppressor, chrom 5, cell cycle regulation and movement
5) proto-oncogene- tyrosine kinase defect
6) proto-oncogene- platelet-derived growth factor receptor defect

471
Q

Mineral and vitamin deficiencies- name the one that correlates to the symptoms below

1) erb B
2) myc
3) DCC
4) bcl
5) BRCA

A

1) proto-oncogene- epidermal growth factor receptor defect
2) proto-oncogenes (c-, n-, l-), transcription factors
3) tumor suppressor- chrom 18, involved in cell adhesion
4) tumor suppressor involved in apoptosis
5) tumor suppressor

472
Q

What is Li-Fraumeni syndrome

1) defect
2) cancers

A

1) p53 gene

2) childhood sarcoma, breast CA, brain tumor, leukemia, adrenal CA

473
Q

Colon cancer

1) initial step in evolution of colorectal CA
2) other genes involved
3) does it met to bone?

A

1) APC mutation
2) p53, DCC, K-ras
3) not usually

474
Q

Carcinogens- what type of cancer risk

1) coal tar
2) Beta-naphthylamine
3) Benzene
4) asbestos

A

1) larynx, skin, bronchial CA
2) urinary tract CA (bladder CA)
3) leukemia
4) mesothelioma

475
Q

what cancers may spread to

1) suspicious supraclavicular node
2) axillary node
3) periumbilical node
4) ovaries
5) bone
6) skin
7) small bowel

A

1) neck, breast, lung, stomach (Virchow’s node), pancreas
2) lymphoma (#1), breast, melanoma
3) pancreas (sister mary joseph node)
4) stomach (krukenberg tumor), colon
5) breast #1, prostate
6) breast, melanoma
7) melanoma #1, lung and breast

476
Q

Clinical trials- what do the following phases evaluate

1) phase I
2) phase II
3) phase III
4) phase IV

A

1) is it safe and at what dose
2) is it effective
3) is it better than existing therapy
4) implementation and marketing

477
Q

describe the various types of chemo

1) induction
2) primary (neoadjuvant)
3) Adjuvant
4) salvage

A

1) sole treatment, used for advanced disease or when no other treatment exists
2) chemo given first, followed by another (secondary) therapy
3) given after other therapy is used
4) 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 has

1) skin lesions
2) Sezary cells

A

1) HTLV-1

2) 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 immunology

1) most important immune marker in recipient/donor matching
2) 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 treatment

1) mild rejection
2) severe rejection

A

1) pulse steroids

2) 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 level
5) 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 10-15
5) FK has less rejection episodes in kidney TXPs

500
Q

Transplant drugs:

6) Sirolimus
- mechanism and use
7) 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 therapy
7) 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

501
Q

Transplant drugs:

8) Zenapax (Daclizumab)
- mechanism
- T/F- is cytolytic

A
  • human monoclonal Ab against IL-2 receptors
  • used for induction and acute rejection episodes
  • false: Is NOT cytolytic
502
Q

Types of rejection- when it occurs, cause and rx

1) Hyperacute

A

1) minutes to hours; caused by preformed Abs that should have been picked up by cross match-> activates compliment cascade-> vessel thrombosis. Rx- emergent re-transplant (if kidney just remove organ)

503
Q

Types of rejection- when it occurs, cause and rx

2)Accelerated rejection

A

occurs in <1wk; caused by sensitized T cells to donor Ags. Rx- increase immunosuppression, pulse steroids, possible Ab Tx

504
Q

Types of rejection- when it occurs, cause and rx

3) Acute rejection

A

1 wk to 1 month; Caused by T cells (cytotoxic and helper). Rx- increase immunosuppression, pulse steroids, possibly Ab tx

505
Q

Types of rejection- when it occurs, cause and rx

4) Chronic rejection

A

months to years; partially a type IV hypersensitivity reaction (sensitized T cells) + Ab formation has a role-> graft fibrosis
Rx- increase immunosuppresion, but really no effective rx

506
Q

Kidney transplant

1) how long can kidney be stored
2) what compatibility do you need
3) can you still use a kidney that had UTI
4) can you still use a kidney that had an acute increase in Creatinine (1.0-3.0)
5) what do you attach the kidney to
6) primary causes of mortality after TXP

A

1) 48hr
2) cross-match and ABO
3, 4) yes
5) Iliac vessels
6) Stroke and MI

507
Q

Complications of kidney txp

1) MC complication and how to rx
2) renal artery stenosis- how to dx and rx
3) lymphocele- rx

A

1) urine leak- rx with drainage and stenting best
2) ultrasound to dx, rx with PTA (percutaneous transluminal angioplasty) with stent
3) MC cause of external ureter compression- 1st try percutaneous drainage. if that fails do peritoneal window so lymph fluid drains into peritoneum and is reabsorbed

508
Q

complications of kidney txp

1) cause of postop oliguria
2) cause of postop diuresis
3) what does new proteinuria raise concern for
4) cause of postop diabetes
5) common viral infections and rx

A

1) ATN (path shows hydrophobic changes)
2) urea and glucose
3) renal vein thrombosis
4) side effect of cyclosporin, FK and steroids
5) CMV- rx with ganciclovir; HSV- rx with acyclovir

509
Q

Kidney rejection workup

1) symptoms that make you start w/u
2) studies to rx
3) empiric treatments
4) path seen in acute rejection
5) chronic rejection- when do you see and rx
6) 5-year graft survival

A

1) inc Cr or poor UOP
2) US with duplex to r/o vascular prbm and ureteral obstruction; and bx
3) pulse steroids, and decrease in CSA (cyclosporin) or FK as they can be nephrotoxic
4) tubulitis (vasculitis with more severe form)
5) usually after 1 yr. no good rx
6) 70% (cadaveric 65%, living donors 75%)

510
Q

Living kidney donors

1) MC complication
2) MC cause of death
3) what happens to remaining kidney

A

1) wound infection (1%)
2) fatal PE
3) hypertrophies

511
Q

liver transplant

1) how long can you store liver
2) C/I to liver TXP
3) MC reason for liver TXP
4) components of MELD score
5) MELD at which pt benefits from liver TXP

A

1) 24hr
2) current ETOH abuse, acute ulcerative colitis
3) chronic hep C
4) creatinine, INR, bilirubin- used to predict if pts with cirrhosis will benefit more from TXP than from medical therapy
5) MELD>15

512
Q

1) criteria for urgent TXP
2) what can you rx pts with Hep B antigenemia be treated with after liver txp to help prevent reinfection
3) how much is the hep B reinfection rate reduced

A

1) fulminant hepatic failure (encephalopathy- stupor, coma)
2) Lamivudine (protease inhibitor) and HBIG (heb B immunoglobulin)
3) reduced to 20%

513
Q

1) disease most likely to recur in new liver allograft
2) when can you consider txp in pts with HCC
3) is portal vein thrombosis a C/I to liver TXP
4) percent of ETOH abusers who will start drinking again after txp

A

1) hep C
2) if no vascular invasion or mets
3) no
4) 20%

514
Q

Macrosteatosis in liver txp

1) what is it
2) what is it a risk factor for

A

1) extracellular fat globules in the liver allograft
2) primary non-function if 50% of cross-section is macrosteatatic in potential donor liver, there is a 50% chance of primary non-function

515
Q

liver txp surgery

1) when is duct to duct anastamosis performed in liver transplant
2) what drains are placed
3) most common arterial anomaly
4) what dose biliary system depend on for blood supply

A

1) hepaticojejunostomy in kids
2) right subhepatic, right and left subdiaphragmatic drains
3) right hepatic coming off of SMA
4) hepatic artery

516
Q

Liver txp complications

1) MC complication and rx
2) what is going on in a pt with:
- sx/signs in 1st 24 hours-total bili >10, bile output

A

1) bile leak (#1)- Tx: place drain, then ERCP with stent across leak
2) Primary nonfunction. rx- usually requires retransplantation

517
Q

liver txp complications:

1) MC early vascular complication
2) pt with inc LFTs, dec bile output, fulminant hepatic failure s/p txp
3) pt with biliary strictures and abscesses but no fulminant hepatic failure
4) treatment for early hepatic artery thrombosis

A

1, 2) Early hepatic artery thrombosis

3) late (chronic) hepatic artery thrombosis
4) MC will need emergent re-transplantation for ensuing fulminant hepatic failure but can try to stent or revise anastomosis

518
Q

liver txp complications:

1) pt with edema, ascites, renal insufficiency s/p txp. complication and how to rx
2) portal vein thrombosis- early and late signs and rx
3) cholangitis- cause

A

1) IVC stenosis/thrombosis (rare)- rx with thrombolytics, IVC stent
2) early- abd pain; late- UGI bleed, ascites, asx. rx- if early do re-op thrombectomy and revise anastamosis
3) get PMNs around the portal triad (NOT mixed infiltrate)

519
Q

liver txp rejection

1) acute rejection: a- what mediates it, b- clinical signs/labs, c-path, d-time of onset
2) Chronic rejection- how common is it, signs/sx

A

1) a- t-cell mediated against blood vessels; b-fever, jaundice, dec bile output, leukocytosis, eosinophilia, inc LFTs, inc total bili, and inc PT; c- portal triad lymphocytosis, endotheliitis (mixed infiltrate) and bile duct injury; d- 1st 1-2 months
2) unusual; get disappearing bile ducts 2/2 Ab and cellular attack-> bile duct obstruction with inc alk phos and portal fibrosis

520
Q

liver txp

1) retransplantation rate
2) 5-year survival

A

1) 20%

2) 70%

521
Q

Pancreas txp

1) what arteries and veins do you need from donor
2) where do you attach it to
3) where do you attach pancreatic duct and what do you need to take from donor to do this
4) benefits of successful pancreas/kidney and what does it not reverse

A

1) donor celiac artery and SMA for arterial supply and donor portal vein for venous drainage
2) iliac vessels
3) most use enteric drainage. Take second portion of duodenum from donor along with ampula of vater and pancreas, then perform anastamosis of donor duodenum to recipient bowel
4) stabilization of retinopathy, dec neuropathy, inc nerve conduction velocity, dec autonomic dysfnc (gastroparesis), dec orthostatic hypoTN
- no reversal of vascular disease

522
Q

Complications of pancreas transplant

A 
venous thrombosis (#1)- hard to treat
rejection- can see inc glucose or amylase, fever and leukocytosis
523
Q

heart transplant

1) how long can you store
2) what compatibility do you need
3) which pts do you do it in
4) rx for persistent pulm HTN after heart transplant
5) acute rejection path findings
6) what is the MCC of late death and death overall following heart txp

A

1) 6hours
2) ABO compatibility and cross match
3) life expectancy

524
Q

lung txp:

1) how long can you store
2) compatibility testing required
3) in which pts
4) #1 cause of early mortality and how to rx
5) indication for double lung txp
6) exclusion criteria for using lungs

A

1) 6hr
2) ABO and crossmatch
3)

525
Q

lung txp rejection

1) path in acute rejection
2) chronic rejection
3) what is MCC of late death and death overall

A

1) perivascular lymphocytosis
2) bronchiolitis obliterans
3) chronic lung rejection

526
Q

Oportunistic infections in txp patients

1) viral
2) protozoan and ppx treatment
3) fungal

A

1) CMV, HSV, VZV
2) Pneumocystis jiroveci pneumonia (reason for Bactrim ppx)
3) Aspergillis, Candida, Cryptococcus

527
Q

hierarchy for permission for organ donation from Next of Kin

A

1) Spouse
2) adult son or daughter
3) either parent
4) adult brother or sister
5) guardian
6) any other person authorized to dispose of body

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