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APEX > Fluids, Blood, Acid Base > Flashcards

Fluids, Blood, Acid Base Flashcards

1
Q

Difference between gap and non gap metabolic acidosis

A

Gap = accumulation of H+ (acid gain)
→ ketoacidosis, lactic acidosis, renal failure, methanol, uremia, paraldehyde, isoniazid, salicylates

Non-gap = Loss of HC03 (bicarbonate loss) OR chloride gain
→ diarrhea, renal tubular acidosis, hypoaldosteronism, fistula, acetazolamide, excessive NS admin (excessive Cl- pushes too much HC03 out of kidneys

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2
Q

Major intracellular ions

A

K+

Mg2+

P04 (2-)

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3
Q

Major extracellular ions

A

Na+, Ca2+, Cl-, HC03-

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4
Q

FFP

A

-ALL coag factors + fibrinogen, plasma proteins

INDICATIONS: warfarin reversal, coagulopathy, AT III deficiency, massive transfusion, DIC, C1 esterase deficiency (hereditary angioedema)

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5
Q

Cryoprecipitate

A

-Fibrinogen, Factor 8, Factor 13, vWF

INDICATIONS: Fibrinogen deficiency, Hemophilia A+B, vWB disease all types

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6
Q

Desmopressin (DDaAVP)

A

Synthetic analogue of ADH

  • Stimulates endogenous release of vWF
  • ↑ Factor 8 activity

Dose 0.3-0.5mcg/kg IV

INDICATIONS: vWB Disease (Type 1>Type 2), mild to moderate Hemophilia A

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7
Q

Appropriate treatments for Hemophilia A

What will labs show

A

All must restore Factor 8.

-FFP, Cryo, Factor 8 Concentrate, Recombitant Factor 7

PTT prolonged, normal PT

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8
Q

Appropriate treatments for Hemophilia B

What will lab values show

A

If severe, factor 9-prothrombin concentrate, but it has serious thromboembolic risks

Prolonged PTT, normal PT

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9
Q

Appropriate treatments for von Willebrand’s disease

A

Desmopressin 0.3 mcg/kg (works well for type 1, ok for type 2, doesn’t for type 3)

Cryo (can be used for all types)

Purified VIII-vWF concentrate for type III

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10
Q

Maximum ABL

A

EBV x [(Start Hct - allowed Hct)/Start Hct]

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11
Q

Change of Hgb/Hct one can expect with PRBC admin

How do you guesstimate Hct from Hgb?

A

-For each 1 unit PRBC given….
——Hgb should ↑ 1g/dL
——Hct should ↑ 2-3%

-Hgb can be estimated as 1/3 of Hct

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12
Q

Signs of hypercalcemia, TX

A 
HTN
Shortened QT
Hypotonia
Kidney stones
Polyuria
Dehydration
Bone pain
NV
ABD pain, pancreatitis
Cognitive dysfunction

TX: 0.9%NS and LOOP diuretic

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13
Q

Which hematocrit level (high) is a threat to life

A

60% → impaired organ perfusion

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14
Q

Warfarin reversal options

A

Non urgent: Phytonadione

Urgent: FFP, Recombitant Factor 7, prothrombin complex concentrate

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15
Q

Reversal agent for dabigatran (Pradaxa)

A

Idarucizumab

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16
Q

Determinants of plasma osmolarity

A

Sodium, glucose, BUN

280-290mOsm/L

Sodium is most important determinant
Hyperglycemia and uremia can ↑

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17
Q

Presentation of hypermagnesemia

A

Loss of deep tendon reflex = 10mg/dL or 4mEq/L
Resp depression = >18mg/dL or 6.5mEq/L
Cardiac arrest =>25mg/dL or 10 mEq/L

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18
Q

Where are platelets formed? Where are they metabolized?

A
  • formed by megakaryocytes in bone marrow

- cleared by macrophages in the reticuloendothelial system and spleen

19
Q

What does injured tissue initially express to attract platelets?

A

Tissue factor and vWF

20
Q

12 factors

A 
1 Fibrinogen
2 Prothrombin
3 Tissue factor
4 Calcium
5 Labile factor
7 Stable factor
8 Anti Hemophilic Factor
9 Christmas factor
10Stuart-Prower factor
11 Plasma thromboplastin antecedent
12 Hageman factor 
13 Fibrin stabilizing factor
21
Q

Extrinsic pathway

A

3, 7
Activated by vascular injury (tissue factor release)
Fast, only about 15 seconds

Measured by PT/INR
Inhibited by Coumadin

22
Q

Intrinsic pathway

A

8, 9, 11, 12

Activated by blood injury or exposure to collagen
Measured by PTT and ACT
Longer, about 6 mins
(Not 11.98, but 12)

Inhibited by heparin

23
Q

Final common pathway

A

1, 2, 5, 10, 13

Think of dollar denominations

24
Q

Describe fibrinolysis

A

Plasminogen is a proenzyme synthesized by liver.

(TPA/urokinase) turns plasminogen into plasmin, which is a proteolytic enzyme that degrades fibrin into FDP

25
Q

Heparin MOA

A

Inhibits intrinsic and final common pathways

ATIII is a naturally occurring anticoagulant that circulates in plasma but heparin binds to it and makes it 1000x more powerful

26
Q

Normal ACT

A

90-120 seconds

Should be >400 seconds before CPB

27
Q

Heparin and protamine CPB doses

A

Heparin =300-400units/kg

Protamine = 1mg for q 100 u heparin predicted to be in circulation

28
Q

Reasons for hypercalcemia

A

Cancer, Hyperparathyroidism, Thyrotoxicosis, Thiazide diuretics, immobilization

TX: loop diuretics, NS.
N/V, ABD pain, mental status change, HTN, shortening QT

29
Q

Reasons for hyponatremia

A

Cushing’s, SIADH, CHF, cirrhosis, TURP syndrome

30
Q

Platelet membrane glycoproteins

A

Repelled by healthy endothelium, attach to injury

  • GpIb → platelet to vWF
  • GpIIb-IIIa complex → links platelets together
31
Q

Possible SE of protamine

A 
Hypotension (histamine release, give >5 mins)
Pulmonary HTN (TxA2 and serotonin release)
Allergic RXN (fish allergy, vasectomy, previous NPH insulin use)
32
Q

ADP receptor inhibitors and when to stop before procedure

A

Plavix 7 days
Ticlodipine 14 days
Prasugrel 3 days
Ticagrelor 2 days

33
Q

GIIB/IIIa receptor antagonists

A

Abciximab 3 days
Eptifibatide 1 day
Tirofiban 1 day

34
Q

Thrombin inhibitors

A

Hirudin
Argatroban
Bivalirudin

All <8 hr stop time before surgery
Pts who have antithrombin III deficiency who are heparin non responders or who have HIT get these drugs

35
Q

Factor X inhibitor

A

Fondaparinux

Stop 4 days before surgery

36
Q

Lab values seen with vWF disease

A

↑ bleeding time, PTT

Others normal

37
Q

Labs seen with DIC

A

↑ PT/PTT
↑ d-dimer
↓ platelets
↓ fibrinogen

Eccymosis, petechaie, mucosal bleeding, can happen in OB

38
Q

Patients at risk for DIC

A

Sepsis
OB (preeclampsia, placental abruption, AFE)
Malignancy (↑ risk: adenocarcinoma, leukemia, lymphoma)

TX: IVF, FFP, platelets, Cryo, heparin or lovenox for severe microvascular thrombosis

39
Q

Universal acceptors

A

AB blood can accept all types
Plasma O negative

O has no erythrocyte antibodies because it doesn’t have A or B in it so it can go anywhere

40
Q

Universal donors

A

Blood O
Plasma AB +

Because 85% of the population is Rh-positive, O+ can be used as emergent in acute bleed if the patient is not a woman of child bearing age and has not received a prior transfusion

41
Q

What Rhogam does

A

Prevents Rh-negative mom from being sensitized against Rh-positive fetus, if this didn’t happen a subsequent pregnancy could trigger erythroblastosis fetalis

42
Q

Most common infectious complication of transfusion

A

CMV, leukoreduction greatly ↓ risk so anyone immunocompromised should get leukoreduced blood

CMV > Hep B > Hep C > HIV

43
Q

Most common cause of transfusion related mortality in US

A

TRALI

Critically ill, sepsis, burns, post CPB at high risk

APEX (11 decks)

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