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APEX > Fluid, Blood, Coagulation > Flashcards

Fluid, Blood, Coagulation Flashcards

1
Q

Describe the distribution of body water

A

60% of TBW = 42 L
60/40/20 (15/5)

40% = intracellular
20% = extracellular
15% = interstitial
5% = plasma

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2
Q

What populations tend to have a greater percentage of TBW by weight?

A

neonates have the most
women, elderly, obese have the least

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3
Q

What are the 2 most important determinants of fluid transfer between capillaries and interstitial space?

A

starling forces
glycocalyx

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4
Q

Net filtration pressure

A

(Pc - Pif) - (iic - iiif)

<0 = reabsorption
> 0 = filtration

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5
Q

What is the glycocalyx - what disrupts it?

A

forms a protective layer on the interior wall of the blood vessel. it has anticoagulant properties. it is the gatekeeper.

DM, sepsis, ischemia, vascular surgery all disrupt it

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6
Q

how is lymph returned to the systemic circulation?

A

via thoracic duct at the juncture of the IJ and subclavian vein

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7
Q

what is osmotic pressure and what is its primary determinant

A

the pressure of a solution against a semipermeable membrane that prevents water from diffusing across that membrane

-it is a function of the number of osmotically active particles in a solution. not a function of their molecular weights!

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8
Q

osmolarity vs osmolality

A

osmolarity = osmoles per liter
osmolality = osmoles per kg

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9
Q

reference for plasma osmolarity? and what are the 3 most important contributors

A

it is 280 - 290 mOsm/L
most important determinatns: sodium, glucose, BUN

Nax2 + Glucose/18 + BUN/2.8

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10
Q

NaCl 0.45%

A

hypotonic @ 154

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11
Q

D5W

A

hypotonic @253

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12
Q

NaCl 0.9%

A

isotonic @ 308

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13
Q

LR

A

isotonic @ 273

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14
Q

plasmalyte

A

294

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15
Q

albumin 5%

A

300

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16
Q

nacl 3%

A

1026

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17
Q

d5 nacl 0.9% (0.45%)

A

560, 405

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18
Q

D5 LR

A

525

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19
Q

How do isotonic IV fluids distribute to the patient?

A

they expand plasma volume and ECF

remain intravascularly (crystalloids) for30 minutes before moving to the ECF

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20
Q

what is the fda black box for on synthetic colloids

A

risk of renal injury

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21
Q

coagulopathy risks with colloids

A

dextran > hetastarch > hextend

dont exceed 20 mL/kg
not a problem with voluven

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22
Q

colloid anaphylactic potential

A

dextran

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23
Q

albumin leads to what electrolyte abnormality

A

hypocalcemia

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24
Q

how does hyperkalemia affect the EKG?

A

5.5 - 6.5 = peaked T wave
6.5 - 7.5 = p wave flattening, PR prolong
7 - 8 = QRS prolonged
> 8.5 = sine wave, VF

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25
Q

discuss hypocalcemia s/s

A

nerve irritability - tetany
change in LOC = sz
long QT

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26
Q

hypercalcemia s/s

A

nausea, abdominal pain
HTN
psychosis, sz
short QT

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27
Q

treatment for hypercalcemia

A

0.9% NaCl
diuretic

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28
Q

Hypermagnesemia

A

DTR loss = 5.8 - 10 mEq/ 7 - 12 mg/dL
Resp. Depression = > 10 or > 12
Cardiac arrest > 10 or > 12

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29
Q

What is the treatment for hypermagnesemia

A

CaCl
Ca gluconate

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30
Q

Acidosis

A

hyperkalemia, increased ICP, increased SNS tone

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31
Q

Alkalosis

A

decreased coronary blood flow, decreased calcium and potassium

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32
Q

Anion gap

A

Na - Cl + HCO3

Normal = 8-12

Accumulation of acid = gap acidosis (>12)
Loss of bicarbonate or ECF dilution = non-gap acidosis

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33
Q

Possible causes of anion gap

A

MUDPILES
M-methanol
U-uremia
D- DKA
p- paraldehyde
I- isoniazid
L- lactate
E- ethanol
S- salicylates

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34
Q

Nongap acidosis

A

HARDUP
H-hypoaldosteronism
A-acetazolamide
R- renal tubular acidosis
D- diaarrhea
U-uretrosigmoid fistula
P-pancreatic fistula

LARGE VOLUME NACL CAN CAUSE THIS TOO

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35
Q

Etiology of metabolic alkalosis

A

-Sodium bicarb administration
-Massive transfusion (liver converts preservatives to HCO3)
-Loss of gastric fluid (NG, vomiting)
-Diuretics
-ECF depletion –> sodium reabsorption –> H+ and K+ excretion to maintain electroneutrality
-Cushings or hyperaldosteronism

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36
Q

What is the most common electrolyte d/o found

A

HYPOKALEMIA

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37
Q

Major intracellulaar ions

A

Potassium, magnesium, and phosphate

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38
Q

what are the 4 steps of hemostasis

A
  1. vascular spasm
  2. platelet adhesion (primary hemostasis)
  3. coagulation and formation of fibrin (secondary hemostasis)
  4. fibrinolysis
39
Q

where are platelets formed?

A

by megakaryocytes in the bone marrow. they are cleared by macrophages in the reticuloendothelial system and the spleen

40
Q

platelet valuess

A

< 50 k = increased surgical bleeding risk
< 20 k = increased spontaneous bleeding risk

41
Q

what are the 3 steps of plt plug formation?

A
  1. adhesion (d/t collagen exposure, vwf and tf release)
  2. activation
  3. aggregation

MADE IN 5 MINUTES

42
Q

list the 12 coagulation factors

A

1 - fibrinogen
2 - prothrombin
3 - tissue factor
4 - calcium
5 - cofactor (labile)
7 - stable factor
8 - cofactor (antihemophilic)
9 - christmas factor
10 - stuart-prower
11 - plasma thromboplastin
12 - hageman’s factor
13 - fibrin stabilizing

43
Q

what activates the extrinsic pathway?

A

vascular injury (tissue trauma liberates TF from subendothelium)
measured by PT, INR
inhibited by warfarin

44
Q

What activates the intrinsic pathway

A

blood injury or collagen exposure
PTT, ACT
inhibited by hepaarin

45
Q

what factors are in the extrinsic pathway

A

3, 7 (EXTRINSIC)
13, 10, 5, 2, 1 (COMMON)
12, 11, 9, 8 (INTRINSIC)

…can be purchased for 37 cents
….. if you can’t buy it from $12, you can buy it for $11.98

46
Q

describe the process of fibrinolysis

A

since the clot is a temporary fix - we need a process to break down the clot once the body has healed itself.

plasminogen is a proenzyme that is synthesized in the liver. it is incorporated into the clot but it lays dormant until it is activated. plasmin degreades fibrin into FDP

47
Q

what two enzymes are needed for the converison of plasminogen to plasmin

A

tpa
urokinase

48
Q

what is R time

A

the time it takes for the clot to start forming

normal = 6 - 8 minutes
measures clotting factors
replace with FFP

49
Q

what is K time

A

time it takes for the clot to reach a certain strength

normal = 5 - 7 minutes
measures fibrinogen
replace with cryo

50
Q

what is alpha angle

A

the rate of fibrin deposition. obviously measures fibrinogen then.

normal = 50 - 60 degrees

treat with cryo

51
Q

what is maximum amplitude

A

the strength of the clot
normal = 50 - 60 mm

if it is low, treat with ddavp or platelets

52
Q

what is A60

A

height of vertical amplitude 60 minutes after MA

normal = MA5
if it is abnormal, it is due to excess fibrinolysis. treat with txa

53
Q

MOA of heparin

A

it inhibits the intrinsic and final common pathway.

antithrombin III is a naturally occurring anticoagulant that circulates in the plasma. heparin binds to AT and accelerates its anticoagulant activity 1000x

heparin AT complex neutralizes 9, 10, 11,12

54
Q

what drugs can you give to someone who can’t have heparin but need CPB

A

bivalirudin - 2 - 3 hours
argatroban - 4 - 6 hours

55
Q

MOA for COXi

A

prevent platelet aggregation by blocking COX1. this stops conversion of arachidonic acid to PG and ultimately txA2

56
Q

name 2 antifibrinolytics and 4 fibrinolytics

A

antifibrinolytic - txa, amicar
*block conversion of plasminogen to plasmin, promote clot formation
fibrinolytic - tPa, urokinase, streptokinase, reteplase, alteplase
*facilitate conversion of plasminogen to plasmin. they break DOWN clots!! (MI, stroke)

57
Q

what are the 3 types of vwd

A

1- mild, moderate reduction
2 - vWF that is produced doesn’t work well
3 - severe reduction in the amount of vwf produced

58
Q

lab values with vwdx

A

prolonged PTT and bleeding time

59
Q

MOA of desmopressin … dose?

A

synthetic analogue of ADH. it facilitates the release of vwf and f8
dose = 0.3 mcg/kg
type 1 > type 2
type 3 it doesn’t work at all

causes hotn with administration

60
Q

other than desmopressin .. what are 3 other treatments for vwdx

A

factor 8
ffp
cryo - 8. 13. fibrinogen. vwf.

61
Q

describe pathophysiology of hemophilia a

A

x-linked recessive d/o.
factor 8 deficiency

62
Q

lab values associated

A

PTT prolonged only

63
Q

hemophilia A treatment

A

factor 8 before surgery and continued for 2 - 6 weeks after
half life = 8 - 12 hours
T&C prior to surgery
antifibrinolytics

64
Q

hemophilia b

A

factor 9 deficiency
factor 9 is the concentrate to treat it. otherwise, same as hemophilia a.

65
Q

describe the role of rf7 in the management of hemophilia A and B

A

BYPASSSSSSS factor 8 or 9.
dose = 90 - 120 mcg/kg

SE: thrombosis arterial and venous.

last ditch effort treatment for idiopathic bleeding (20 - 40 mcg/kg) off-label

66
Q

Lab Results for DIC

A

increased PT, PTT, D-dimer
Decreased plt, fibrinogen

67
Q

Name 3 conditions that are at risk for DIC

A

sepsis - gram negative
pregnant - pre-e, abruption, AFE
malignancy - adenocarcinoma, leukemia, lymphoma

68
Q

DIC management

A

coagulopathy - FFP - feed the beast (plt, cryo ok)
severe thrombosis - IV heparin or LMWH
hypovolemia - give fluids

69
Q

HIT vs HIT 2 pathophys.

A

HIT is heparin induced platelet aggregation after a large dose of heparin

HIT 2 - antiplatelet abs (IGG) attack factor 4 immune complexes –> platelet aggregation. They are resistant to heparin anticoag. occurs after any dose of heparin

70
Q

onset of HIT 1 & 2

A

1 - 1-4 days
2- 5 - 14 days

71
Q

Plt count of HIT 1 vs 2

A

1 - <100
2 - < 50

72
Q

treatment for HIT 1 vs 2

A

no treatment for HIT 1
HIT 2 - d/c heparin. anticoagulate with direct thrombin inhibitor (bivalirudin, hiruidin, argatroban)

73
Q

Protein C/S deficiency

A

hypercoagulable
*heparin –> warfarin
*may or may not need lifelong anticoagulation

74
Q

factor 5 Leiden

A

causes a resistance to the anticoagulant effect of protein C
-only pt w/thromboembolism require anticoagulation

75
Q

Pathophys sickle cell

A

Amino acid substitution (valine for glutamic acid) on beta globulin chain
spleen removes sickled cells at 12 - 17days, compared to 120days

76
Q

Treatment for vaso-occlusive crisis

A

hydroxyurea
analgesics
hydration

77
Q

discuss blood type, antigens, plasma antibodies

A

Blood type = specific glycoproteins present on the erythrocyte cell membrane. They have an antigenic potential.

If an antigen is expressed on the erythrocyte, then there will NOT be an antibody against that specific antigen in the plasma

If an antigen is NOT expressed on the erythrocyte, then there will be an antibody against that specific antigen in the plasma

78
Q

Universal donor vs universal acceptor of FFP

A

Donor = AB +
Acceptor = O -

(opposite of RBC stuff)

79
Q

Type only

A

tests for ABO and Rh-D antigens.

5 minutes

recipient blood is mixed with anti-A, anti-B, anti-Rh D antibodies. 0.2% chance of incompatibility after this test

80
Q

Type & Screen

A

Tests for most clinically significant antibodies

45 minutes

recipient blood mixed with COMMERCIALLY prepared O RBCs that contain known antigens. 0.06% incompatibility rxn after this test

81
Q

Type & Crossmatch

A

tests for compatibility btw recipient plasma and the actual blood unit to be transfused.

45 minutes

simulates transfusion in a test tube. 0.05% chance of incompatibility reaction after this.

specific units are assigned to the patient after this!

82
Q

what are the indications for FFp

A

PT x 1.5
warfarin reversal
antithrombin deficiency
massive tx
DIC
c1 esterase deficiency

83
Q

cutoff for plt tx

A

< 100 for eye or neurosurgery
< 50 for neuraxial, invasive procedures, most surgeries

84
Q

what is in cryo

A

factor 8, 13
vwf
fibrinogen

85
Q

cryo indications

A

fibrinogen < 80
vwb dx
hemophilia

86
Q

FFP dosing

A

warfarin reversal 5 - 8 mL/kg

coagulop. = 10 - 20 mL/kg

87
Q

Plt dosing

A

1 pack per 10 kg body weight

88
Q

cryo dosing

A

5 bag pool increases fibrinogen by 50 mg/dL

89
Q

What is leukoreduction

A

Removes WBCs from RBCs and platelets

Leukocytes are responsible for HLA alloimmunization, febrile rxn, CMV tx

90
Q

What is washing and why is it used

A

removes any remaining plasma and antigens in the donor blood

prevents anaphylaxis in IgA deficient patients

91
Q

What is irradiation

A

Exposes units to gamma radiation, disrupting WBC DNA, destroying donor leukocytes. This prevents GVHost dx in immunocompromised pt.

leukemia, lymphoma, digeorge pt, stem cell pt

92
Q

Most common infection complication of RBC

A

CMV
leukoreduction reduces this risk

93
Q

List 4 most common complications of RBC

A

CMV > Hep B > Hep C > HIV

APEX (18 decks)

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