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Summer AP II > EXAM 2 Study Guide Mo > Flashcards

EXAM 2 Study Guide Mo Flashcards

1
Q

In a healthy 45 years old male, red blood cells are formed in?

A

Vertebrae

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2
Q

How much of a whole blood sample is:
Plasma?
Formed elements (hematocrit)?

A

Plasma = 55%
Formed elements = 45% (this includes erythrocytes at 45% and the buffy coat which is leukocytes(WBC) and platelets which account for less than 1% of whole blood)

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3
Q

What are the 3 components that make up the Plasma portion of whole blood? (give me percents)

A

91.5% is H2O

7% is proteins

2% Other solutes
(ions, waste products, salts, lipids, enzymes, gas, and vitamins)

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4
Q

What are the 3 components that make up the Formed elements (hematocrit) portion of whole blood? (give me percents)

A

Erythrocytes 45%

Leukocytes/WBC and Platelets < 1%

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5
Q

Total body weight of a person is what percentage blood and what percentage body fluids and tissues?

A

8% blood

92% body fluids and tissues

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6
Q

Leukocytes/WBC are part of the formed elements of whole blood. What is the breakdown of Leukocytes/WBC with percentages?

A 
PMNs (Neutrophils) 40-70%
Lymphocytes 20-40%
Monocytes 2-10%
Eosinophils 1-6%
Basophils <1%
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7
Q

What is the most abundant and least abundant component of Leukocytes/WBC?

A

PMN (Neutrophils) are most abundant at 40-70%

Basophils are least abundant at less than 1%

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8
Q

Proteins make up 7% of plasma of whole blood. What is the component break down of Proteins with percentages?

A

albumin =55%
globulins = 38%
fibrinogen = 7%

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9
Q

In normal adult blood composition what is the formula for serum?

A

serum=plasma-clotting factors (e.g.,fibrinogen).

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10
Q

What components of blood is known as hematocrit - “crit”?

A

RBC, WBC, and platelets are known as hematocrit.

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11
Q

Tell me the Hematocrit difference between a normal person, anemia, and polycythemia?

A

anemia is less “crit” and polycythemia is more “crit” than normal blood.
Anemia = thin blood
Polycythemia = thick blood (more viscous)

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12
Q

Hb x 3 = ?

A

Hct

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13
Q

If someone is infant to 5 years old where does majority of their red blood cell production come from? (what bone(s))

A

Rib and Tibia

all bones but rib and Tibia is majority

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14
Q

20 year old throughout the remaining life span where does majority of the red blood cell production come from? (what bone(s))

A

Vertebra (then sternum then rib and hipbone)

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15
Q

Functions of RBC? (3 answers)

A

Transport of hemoglobin.
Transport of oxygen and carbon dioxide.
Acid-base buffer.

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16
Q

What regulates RBC production in response to hypoxemia (released from the kidneys mostly)

A

Erythropoietin

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17
Q

What two vitamins are needed to mature a RBC?

A

Vit B12 and folic acid

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18
Q

What destroys old RBCs and how?

A

Macrophages destroy old RBCs by phagocytosis.

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19
Q

Hb is excreted as?

A

bilirubin

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20
Q

iron is released as/to?

A

transferrin

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21
Q

Hypoxia is a stimulus to the kidneys to release erythropoietin from the kidneys mainly (10% from liver) which then does what?

A

erythropoietin stimulates red bone marrow and thus increases RBC counts. The more RBC the more oxygen that can be carried!

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22
Q

What are some ways hypoxia can develop and create a stimulus for the release of erythropoietin? (3 things)

A

decreased RBC count

decreased amount of hemoglobin

decreased availability of 02

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23
Q

If you are deficient in what three things it can cause anemia?

A

IRON
vitamin B12
folic acid

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24
Q

Where does the body store iron?

A

iron is stored in Hb (65%) and also in the liver, spleen, and bone marrow

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25
Q

Intracellular iron is stored in protein-iron complexes such as? (2)

A

ferritin and hemosiderin

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26
Q

Circulating iron is loosely bound to the transport protein?

A

transferrin-carrier protein

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27
Q

The life span of an erythrocyte is ?

A

100-120 days

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28
Q

“Old and senile” RBCs become rigid and fragile, and their hemoglobin begins to degenerate, they are trapped in ? (graveyard of RBC)

A

Spleen

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29
Q

Dying erythrocytes are engulfed by ?

A

macrophages

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30
Q

Heme and globin are separated and the WHAT is salvaged for reuse?

A

iron

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31
Q

Heme is degraded to a yellow pigment called ?

A

bilirubin

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32
Q

The liver secretes bilirubin into the intestines as ?

A

bile

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33
Q

The intestines metabolize bile into?

A

urobilinogen

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34
Q

This degraded pigment (heme-bilirubin-bile-urobilinogen) leaves the body in feces, in a pigment called ?

A

stercobilin (what makes poop brown)

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35
Q

what is free bilirubin’s solubility status? toxic or non toxic? transported by what?

A

Free bilirubin is NOT soluble in water, toxic to the CNS, and transported by albumin.

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36
Q

How is Free bilirubin removed?

A

Free bilirubin is removed from blood by the liver, conjugated with glucuronate and excreted in bile (not urine).

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37
Q

In the intestine, bacteria convert conjugated bilirubin to ?

A

urobilinogen (soluble).

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38
Q

What is responsible for the pink color of plasma?

A

Transferrin

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39
Q

Transferrin has how many iron binding sites?

A

two

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40
Q

30% of total iron “storage iron” is?

A

Ferritin

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41
Q

Hemosiderin, what is it?

A

iron-storage complex (water-soluble)

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42
Q

Methemoglobin means what in relation to iron form?

A

iron in ferric form (Fe+++)

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43
Q

What is the treatment for methemoglobinemia?

A

IV methylene blue (converts ferric to ferrous form)

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44
Q

Which iron form is the “GOOD” form?

A

Ferrous (Fe++)

“2 for us”

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45
Q

Does methemoglobin bind more readily to 02?

A

No, does not bind to 02 as readily, but has increased affinity for CN-

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46
Q

Because methomoglobin does not bind to 02 as readily, what does that mean for saturation?

A

defective 02 transport leads to low saturation.

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47
Q

What meds can cause methemoglobinemia? (3)

A

Nitrites, benzocaine*, metabolites of prilocaine

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48
Q

how will the fingernails of someone with methemoglobinemia look?

A

gray-blue discoloration

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49
Q

causes of cyanide poisoning? (4)

A

Nitroprusside (releases CN ions)
Bitter almond oil
KCN
Wild cherry syrup

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50
Q

S/S of cyanide poisoning?

A

Tachycardia, hypotension, coma , acidosis, increased venous O2, rapid death.

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51
Q

How do you treat cyanide poisoning?

A

To treat cyanide poisoning, use sodium nitrite and amyl nitrites to oxidize Hb to metHb (inducing methemoglobinemia) which binds cyanide, allowing cytochrome oxidase enzyme to go free and function.

Use thiosulfate to bind this cyanide, forming thiocynate, which is excreted by kidneys.

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52
Q

What is porphyria?

A

The porphyrias are conditions of defective heme synthesis that leads to the accumulation and increase excretion of heme precursors i.e. porphyrins

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53
Q

A similar condition to porhyria can be caused by what?

A

Lead

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54
Q

S/S of porphyria? (4)

A

Abdominal pain, N/V
Tachycardia, sustained hypertension
Muscular weakness
Seizures

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55
Q

If someone has porphyria what meds should you not give them (contraindicated) (2)

A

BARBITURATES

Benzo

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56
Q

What is the most common porphyria and what are the presenting symptoms?

A

Porphyria cutanea tarda
Blisters, photosensitivity
tea colored urine.

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57
Q

Which porphyria has the accumulated substrate ALA (aminolevulinic acid)?

A

Acute intermittent porphyria

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58
Q

“Anemia” would mean you have a decrease in what three components of blood?

A

decreased RBC, Crit, and Hb.

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59
Q

Hyper-segmented neutrophil is the hall mark of?

A

Megaloblastic anemia

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60
Q

Management of iron deficiency anemia in female and male patients?

A

give IRON, packed RBC

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61
Q

How do you treat megaloblastic anema (pernicious)?

A

Combination of folic acid and Vit B12 for life (never folic acid alone)

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62
Q

Pathogenesis of Sickle cell anemia?

A

Valine takes the place of glutamine in the 6th position of the Beta-hemoglobin chain (HbS).
(see slide 58, visual helps)

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63
Q

clinical manifestations of Sickle Cell Anemia?

A

sickling can lead to ischemia, thrombosis CVAs, and infections.
painful leg ulcers (vaso occlusive)
Hematuria
Necrosis of the spleen
Salmonella osteomylitis
Require vaccination against pneumococci, salmonella
Priapism
Cor pulmonale
Sickl “crisis” by decreased 02 and dehydration
Resistance to malaria (why?)

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64
Q

Treatment for sickle cell anemia?

A

Hydroxyurea is a myelosuppressive agent which increase HbF (fetal hemoglobin)

Bone marrow transplant (BMT)

HbF interferes with formation of HbS

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65
Q

What could you do to prevent a sickle cell crisis?

A 
Hydration
adequate 02 (low 02 30-40 mmHg triggers sickling)
maintain cardiac output
avoid stasis (you do not want the blood to sit and get stuck)
66
Q

Secondary Polycythemia vs Polycythemia vera?

A

Secondary polycythemia is physiological, due to hypoxia (people living in high altitude), increased EPO levels and NO treatment required.

vs.

Polycythemia vera is a stem cell disorder with low EPO levels, high hematocrit -60-70%, high WBC and platelet count, and treatment is required.

67
Q

Tell me everything you know about secondary polycythemia?

A 
Physiological 
Due to hypoxia such as people living in high altitude
increased EPO level
CHF
RBCs count > 6-7 millions/mm3
No treatment required
68
Q

Tell me everything you know about polycythemia vera?

A

Pathological- stem cell disorder
RBCs count > 6-7 millions/mm3
decreased EPO level
Crit ~ 60-70 %
High WBC and platelet count as well
increased viscosity (x10 times) leads to sluggish flow of blood
Treatment : Repeated phlebotomy to lower crit.

69
Q

What is the treatment for polycythemia vera?

A

Repeated phlebotomy to lower the hematocrit

70
Q

Hemostasis: step by step (12 steps)

A
  1. Vessel injury or atherosclerotic plaque rupture
  2. Subendothelial collagen layer exposes
  3. Platelets bind to injured subendothelial by vWF (glue)
  4. GP Ib is vWF receptor
  5. Platelets activate and release following chemical mediators that increase Ca++ and decrease cAMP within platelets
    a) Thromboxane A2, platelets activating factor (PAF) and ADP
    b) Thrombin
  6. Recruitment and activation of new platelets (+ feed back)
  7. Crosslinking of platelet aggregate by surface glycoprotein ( GP IIb/IIIa)
  8. Aggregation of platelets leads to Thrombus (temporary plug) formation
  9. Activation of clotting factors (by injured tissue factors )
  10. Formation of thrombin that convert fibrinogen to fibrin (thread)
  11. Fibrin tie up platelets together forming a stable, permanent platelet-fibrin plug
  12. Fibrinolysis ( plasmin formation ) to limit any further growth of clot
71
Q

MOA: NSAID?

A

reversibly inhibits COX

72
Q

Does APAP (tylenol) alter platelet function?

A

NO it DOES NOT alter platelet function.

73
Q

How does Ticlopidine work?

A

inhibit ADP- (ADP- mediates platelet aggregation) thus you are making the blood NOT clot.

74
Q

How does Plavix work?

A

inhibits ADP-mediated platelet aggregation.

75
Q

Which is good and which is bad when you are talking about not trying to clot? cAMP and ADP?

A

cAMP is good
ADP is bad

Thus you want to increase cAMP and decrease ADP if you want a lack of clotting.

76
Q

How does Dipyridamole (Persantine) work?

A

increases cAMP that prevents platelet aggregation.

77
Q

What are 3 examples of Anti-fibrinogen receptor (GPIIb/IIIa) drugs?

A

Abciximab (Reopro)
Tirofiban
Eptifibatide

78
Q

MOA of Anti-fibrinogen receptor (GPIIb/IIIa) drugs
which would be specifically the drugs Abciximab (Reopro)
Tirofiban
Eptifibatide

A

Cap and block the fibrinogen receptors on platelets leading to no linking which causes no aggregation

79
Q

vWF circulates with what other protein? (hand in hand circulation as one complex)

A

vWF:VIII

80
Q

Most common hereditary bleeding disorder?

A

von Willebrand’s dz

81
Q

vWF is synthesized by?

A

endothelium

82
Q

vWF is a carrier protein for what factor?

A

VIII (antihemophilic factor)

83
Q

What deficiency causes von W dz?

A

Due to deficiency of vWF or an abnormal vWF.

84
Q

Bleeding time and platelet count with Von W dz?

A

prolonged BT despite normal platelet count (platelets cannot stick to injured area.)
(you also have an increased PTT)

85
Q

Bleeding time and platelet count with Hemophilia

A

normal BT because of normal platelet count and vWF.

you have an increased PTT only (you also have increased PTT with von W dz

86
Q

Compare bleeding time and platelet count of von W dz to Hemaphilia?

A

hemophila is normal BT and normal platelet count.
von W dz has a prolonged bleeding time but normal platelet count.

(they both have increased PTT and normal PT)

87
Q

if you have abnormal vWF then what else will you have a functional deficiency of?
and what does that deficiency show up as clinically?

A

factor VIII, bc it is vWF carrier protein.

Deficiency is manifested clinically by prolonged PTT.

88
Q

Abnormal labs associated with von W dz?

A

prolonged BT, PTT

89
Q

What are some signs/symptoms of von Willebrand’s dz?

A

Nose and mucous membrane bleeding
Easy bruisability
Prolonged bleeding from wounds
Menorrhagia– very heavy period

90
Q

Tx for von W dz? (3 tx, (first line and two others))

A
  1. Desmopressin (dDAVP)
    First line treatment
    Increases vWF level
    Side effects of Desmopressin: hyponatremia, thrombocytopenia
  2. Cryoprecipitate is rich in factor VIII:vWF
  3. Estrogen and OCP
91
Q

thromboxane A2 and ADP both do what to platelets?

A

promote platelet aggregation.

92
Q

Vit K dependent Factors are?

A

II, VII, IX, X

93
Q

What proteins are vit. K dependent?

A

Protein C and S

94
Q

second most common x-linked coagulation defect?

A

Hemophilia A

95
Q

Hemophilia B is a deficiency in what factor?

A

IX

96
Q

What is the name for a deficiency in factor VIII?

A

Hemophilia A

97
Q

can you have deficient factor VIII and normal vWF?

A

yes, that is the bases of Hemophilia A, deficient in VIII but have normal platelets and vWF.

now vWF is a carrier protein for factor VIII, so if you have a problem with the vWF then you will have a functional deficiency of factor VIII.

98
Q

Hemophilia A clinical findings?

A

Soft tissue and joint bleeding
Dangerous CNS bleeding with minor trauma
Spontaneous hematuria leading to ureteral colic (clot formation in the urinary tract)

99
Q

Lab findings with Hemophilia A ?

A

Prolonged PTT (intrinsic pathway)

Low factor VIII

Normal BT b/c normal platelets and vWF

100
Q

Treatment for Hemophilia A?

A

FFP and cryo (low in VIII)

Factor VIII replacement

(Hepatitis C and HIV infection very common due to tinted blood transfusion)

101
Q

Does BT have something to do with the coagulation cascade?

A

NO!

BT measuresonlythe response of plateletsto a vascular injury. It has nothing to do with the coagulation cascade!

102
Q

What patients should you give vit K to always?

A

surgical patients with liver dz

103
Q

Almost all clotting factors are made in the liver except? (3)

A

Factor VIII:vWF

Factor III ( tissue factor thromboplastin)

Factor IV ( Ca++)

104
Q

Tell me the basics of DIC?

A

Abnormal bleeding and clot formation

Critically ill patients

Coagulation and clot lysis in uncontrolled manner

Due to massive tissue damage

Depletion of clotting factors

105
Q

pathophysiology of DIC?

A

widespread activation of the coagulation system leading to depletion of coagulation factors and platelets “global consumption” leading to bleeding

106
Q

with DIC you have thrombi formation in small vessels, what does that cause?

A

organ ischemia

107
Q

What are some possible causes of DIC? (4)

A

Obstetrics complications; retain dead fetus, abortion, eclampsia -MCC

Gram negative sepsis

Release of procoagulant tissue factors

Transfusion, trauma, malignancy, acute pancreatitis, nephrotic synd.

108
Q

Clinical manifestation of DIC?

A

Bleeding from tubes, wounds, vascular access sites

Shock, ischemia, infection

Multiple organ failure

109
Q

What change in labs will you see with DIC?

A

INCREASED:
PT, PTT, FDP (fibrin degradation products), D-dimer

DECREASED:
Fibrinogen and platelets (because they are used up ) “consumptional deficiency”

110
Q

Treatment for DIC?

A

Treat the underlying problem

Platelets , FFP and cryo

111
Q

When you give Heparin what lab do you monitor, what about Warfarin?

A 
Heparin = PTT
Warfarin = PT
112
Q

Which is intrinsic and which is extrinsic: PT, PTT?

A

PT=extrinsic pathway

PTT= intrinsic pathway

113
Q

Heparin onset of action vs Warfarin?

A 
Heparin= rapid, less than 1 min. 
Warfarin = slow, 8-12 hours.
114
Q

Structure of heparin vs warfarin?

A

heparin is large, acidic, anionic (neg. charged ion).

warfarin is small, lipid soluble.

115
Q

Route for heparin vs warfarin?

A

heparin is IV and S/C, warfarin is oral.

116
Q

site of action heparin vs warfarin?

A 
heparin= blood
warfarin= liver.
117
Q

MOA of heparin?

A

Increases the activity of antithrombin III ;1000 to 10000 times.
(antithrombin III is a powerful anticoagulant in blood)

118
Q

MOA Warfarin?

A

Impairs synthesis of Vit. K dependent clotting factors (II, VII, IX, X)

119
Q

DOA: Heparin vs warfarin?

A

Heparin: acute (hours)
warfarin: chronic (weeks to months)

120
Q

How do you treat an overdose of heparin?

A

protamine

121
Q

How do you treat an overdose of warfarin?

A

Vit. K, FFP

122
Q

Tell me what you know about LMWH? (what factor it inhibits, monitoring, and risk?)

A 
LMWHs inhibit factor Xa (common pathway)
It cannot be monitored by PT or PTT because it does not affect either.
Low risk (HIT), easy , no monitoring, cost effective
123
Q

Where is Heparin naturally in your body?

A

Heparin (present in basophil and mast cells)

124
Q

Tell me how histamine induced thrombocytopenia is caused by heparin?

A

Histamine released due to heparin, increases PA pressure, decreases BP, bronchoconstriction, anaphylaxis, heparin induced thrombocytopenia (HIT) leading to bleeding.

125
Q

how does the antidote to heparin work?

A

Protamine to neutralize heparin (strong base vs. strong acid)

126
Q

What pathway does heparin block?

A

intrinsic and common pathways

127
Q

activated coagulation time (ACT) what is that?

and what is an adequate ACT with heparin, and what must it be above?

A

to assess adequacy of heparinization; ‘bedside coagulation test’
Adequate heparinization if ACT > 400-450 sec
No case below 400 sec.

128
Q

PTT of someone on heparin should be what?

A

1.5 - 2.5 x normal (normal is 30 sec)

45-75 sec

129
Q

warfarin inactivates what?

A

vit. K dependent clotting factors.

130
Q

warfarin blocks what pathway?

A

extrinsic (VII) and common (II ,X) pathways.

131
Q

What do you monitor when someone is on warfarin? (2)

A

Monitor dose by checking PT “Pro time” and INR (Extrinsic Pathways)

132
Q

Can pregnant women use warfarin?

A

should be avoided

133
Q

how long before surgery should you stop using warfarin?

A

d/c 3-5 days preop

134
Q

Oral vitamin K or FFP is the antidote for what?

A

Warfarin overdose

135
Q

How many days does it takes to correct the effects of warfarin after you discontinue it?

A

5 days

136
Q

PTT:
assess?
monitor what med?
normal time?

A

Assesses intrinsic pathway+ common pathway

Monitor heparin dose

25-35 sec

137
Q

PT:
Assess?
monitors what med?
normal time?

A

Assesses extrinsic pathway+ common pathway

Monitor warfarin dose

12-14 sec

138
Q 
ACT:
Assess?
monitor what med?
Normal time?
What you want the time to be on the drug?
A

Assesses intrinsic pathway

Access adequacy of heparinization

80-150 sec

400- 450 sec suggest complete heparinization

139
Q

BT:
assess?
measures what?
normal?

A

Time for skin wound to stop bleeding

Best test to measure platelet function

3 to 10 min

140
Q

Aspirin, what does it do to bleeding time?

A

Aspirin alters platelet function for 7-12 days ( the life span of platelet), resulting prolong BT

141
Q

Platelet count:
normal?
significant bleeding time with minor trauma?
spontaneous bleeding?

A

Normal 150,000 to 400,000/ml

Significant bleeding with minor trauma < 50,000

Spontaneous bleeding < 20,000

142
Q

universal donor is?

A

O-

143
Q

universal recipient is?

A

AB+

144
Q

What is Erythroblastosis fetalis?

A

Hemolytic disease of newborn. Rh- mother having a Rh+ fetus.

145
Q

what happens with the first pregnancy of a Rh- mom and Rh+ baby?

A

Rh+ erythrocytes leak into mother’s circulation during delivery
Formation of anti-D antibodies in mother.

146
Q

What happens with 2nd pregnancy of Rh- mom and Rh+ baby?

A

Passage of mother’s antibodies to fetus through placenta
Anti-D antibodies will cause hemolysis of the baby’s RBCs
(Jaundice, kernicterus)

147
Q

Prophylaxis for an Rh- mom, Rh+ baby?

A

give Rh(D) immunoglobulins (RhoGAM®) to an Rh- mother during 3rd trimester and immediately after delivery of Rh+ child. These antibodies destroy fetal Rh+ erythrocytes.

148
Q

Which Ig type can cross the placenta?

A

IgG

149
Q

What is the function of protein C?

A

Degrade factor V and VII

150
Q

What is the function of Protein S?

A

Cofactor of Protein C

151
Q

what is the function of vWF?

A

adhesion

152
Q

what is the the function of antithrombin III?

A

is a nonvitamin K-dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin factor II, IX, X, XI, XII

153
Q

If someone is unresponsive to heparin what could be the issue?

what would be the treatment?

A

antithrombin III deficiency that is due to cirrhosis and nephrotic syndrome.

Tx: FFP that contains AT3

154
Q

Thrombophilia can be due to a deficiency of what?

A

antithrombin III

155
Q

Heavy bleeding after warfarin would make you think of what deficiency?

A

Protein C deficiency

156
Q

Vitamin K dependent anticoagulant that promotes fibrinolysis?

A

Protein C

157
Q

Warfarin interferes with what pathway?

A

extrinsic pathway

158
Q

PT and INR assess which pathway?

A

extrinsic

159
Q

Heparin interferes with what pathway?

A

intrinsic

160
Q

PTT and ACT assess what pathway?

A

intrinsic

161
Q

INR:
What is it measuring?
what pathway is it monitoring?
what drug does it monitor?

A

ratio of patient PT to a controlled PT obtained by standard method.
Monitors extrinsic pathway like PT.
Monitors warfarin dose.

162
Q 
Thrombin time (TT):
What does it evaluate?
what is normal?
A

Evaluate ability of thrombin to convert fibrinogen to fibrin.
normal is less than 30 sec.

Summer AP II (3 decks)

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