EXAM 2 Study Guide Mo Flashcards
1
Q
In a healthy 45 years old male, red blood cells are formed in?
A
Vertebrae
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)
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)
4
Q
What are the 3 components that make up the Formed elements (hematocrit) portion of whole blood? (give me percents)
A
Erythrocytes
Leukocytes/WBC
Platelets
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
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%
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%
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%
9
Q
In normal adult blood composition what is the formula for serum?
A
serum=plasma-clotting factors (e.g.,fibrinogen).
10
Q
What components of blood is known as hematocrit - “crit”?
A
RBC, WBC, and platelets are known as hematocrit.
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)
12
Q
Hb x 3 = ?
A
Hct
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
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)
15
Q
Functions of RBC? (3 answers)
A
Transport of hemoglobin.
Transport of oxygen and carbon dioxide.
Acid-base buffer.
16
Q
What regulates RBC production in response to hypoxemia (released from the kidneys mostly)
A
Erythropoietin
17
Q
What two vitamins are needed to mature a RBC?
A
Vit B12 and folic acid
18
Q
What destroys old RBCs and how?
A
Macrophages destroy old RBCs by phagocytosis.
19
Q
Hb is excreted as?
A
bilirubin
20
Q
iron is released as/to?
A
transferrin
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!
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
23
Q
If you are deficient in what three things it can cause anemia?
A
IRON
vitamin B12
folic acid
24
Q
Where does the body store iron?
A
iron is stored in Hb (65%) and also in the liver, spleen, and bone marrow
25
Intracellular iron is stored in protein-iron complexes such as? (2)
ferritin and hemosiderin
26
Circulating iron is loosely bound to the transport protein?
transferrin-carrier protein
27
The life span of an erythrocyte is ?
100-120 days
28
“Old and senile” RBCs become rigid and fragile, and their hemoglobin begins to degenerate, they are trapped in ? (graveyard of RBC)
Spleen
29
Dying erythrocytes are engulfed by ?
macrophages
30
Heme and globin are separated and the WHAT is salvaged for reuse?
iron
31
Heme is degraded to a yellow pigment called ?
bilirubin
32
The liver secretes bilirubin into the intestines as ?
bile
33
The intestines metabolize bile into?
urobilinogen
34
This degraded pigment (heme-bilirubin-bile-urobilinogen) leaves the body in feces, in a pigment called ?
stercobilin (what makes poop brown)
35
what is free bilirubin's solubility status? toxic or non toxic? transported by what?
Free bilirubin is NOT soluble in water, toxic to the CNS, and transported by albumin.
36
How is Free bilirubin removed?
Free bilirubin is removed from blood by the liver, conjugated with glucuronate and excreted in bile (not urine).
37
In the intestine, bacteria convert conjugated bilirubin to ?
urobilinogen (soluble).
38
What is responsible for the pink color of plasma?
Transferrin
39
Transferrin has how many iron binding sites?
two
40
30% of total iron "storage iron" is?
Ferritin
41
Hemosiderin, what is it?
iron-storage complex (water-soluble)
42
Methemoglobin means what in relation to iron form?
iron in ferric form (Fe+++)
43
What is the treatment for methemoglobinemia?
IV methylene blue (converts ferric to ferrous form)
44
Which iron form is the "GOOD" form?
Ferrous (Fe++)
| "2 for us"
45
Does methemoglobin bind more readily to 02?
No, does not bind to 02 as readily, but has increased affinity for CN-
46
Because methomoglobin does not bind to 02 as readily, what does that mean for saturation?
defective 02 transport leads to low saturation.
47
What meds can cause methemoglobinemia? (3)
Nitrites, benzocaine*, metabolites of prilocaine
48
how will the fingernails of someone with methemoglobinemia look?
gray-blue discoloration
49
causes of cyanide poisoning? (4)
Nitroprusside (releases CN ions)
Bitter almond oil
KCN
Wild cherry syrup
50
S/S of cyanide poisoning?
Tachycardia, hypotension, coma , acidosis, increased venous O2, rapid death.
51
How do you treat cyanide poisoning?
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.
52
What is porphyria?
The porphyrias' are conditions of defective heme synthesis that leads to the accumulation and increase excretion of heme precursors i.e. porphyrins
53
A similar condition to porhyria can be caused by what?
Lead
54
S/S of porphyria? (4)
Abdominal pain, N/V
Tachycardia, sustained hypertension
Muscular weakness
Seizures
55
If someone has porphyria what meds should you not give them (contraindicated) (2)
BARBITURATES
| Benzo
56
What is the most common porphyria and what are the presenting symptoms?
Porphyria cutanea tarda
Blisters, photosensitivity
tea colored urine.
57
Which porphyria has the accumulated substrate ALA (aminolevulinic acid)?
Acute intermittent porphyria
58
"Anemia" would mean you have a decrease in what three components of blood?
decreased RBC, Crit, and Hb.
59
Hyper-segmented neutrophil is the hall mark of?
Megaloblastic anemia
60
Management of iron deficiency anemia in female and male patients?
give IRON, packed RBC
61
How do you treat megaloblastic anema (pernicious)?
Combination of folic acid and Vit B12 for life (never folic acid alone)
62
Pathogenesis of Sickle cell anemia?
Valine substitutes with glutamine in the 6th position of the Beta-hemoglobin chain (HbS).
(see slide 58, visual helps)
63
clinical manifestations of Sickle Cell Anemia?
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?)
64
Treatment for sickle cell anemia?
Hydroxyurea (increase HbF), BMT
HbF interferes with formation of HbS
(this makes little sense to me, but it is what Mo has down)
65
What could you do to prevent a sickle cell crisis?
```
Hydration
adequate 02 (low 02 30-40 mmHg triggers sickling)
maintain cardiac output
avoid stasis
```
66
Secondary Polycythemia vs Polycythemia vera?
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
Tell me everything you know about secondary polycythemia?
```
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
Tell me everything you know about polycythemia vera?
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
What is the treatment for polycythemia vera?
Repeated phlebotomy to lower the hematocrit
70
Hemostasis: step by step (12 steps)
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
MOA: NSAID?
reversibly inhibits COX
72
Does APAP (tylenol) alter platelet function?
NO it DOES NOT alter platelet function.
73
How does Ticlopidine work?
inhibit ADP- mediated platelet aggregation.
74
How does Plavix work?
inhibits ADP-mediated platelet aggregation.
75
Which is good and which is bad when you are talking about clotting? cAMP and ADP?
cAMP is good
ADP is bad
Thus you want to increase cAMP and decrease ADP if you want a lack of clotting.
76
How does Dipyridamole (Persantine) work?
increases cAMP that prevents platelet aggregation.
77
What are 3 examples of Anti-fibrinogen receptor (GPIIb/IIIa) drugs?
Abciximab (Reopro)
Tirofiban
Eptifibatide
78
MOA of Anti-fibrinogen receptor (GPIIb/IIIa) drugs
which would be specifically the drugs Abciximab (Reopro)
Tirofiban
Eptifibatide
Cap and block the fibrinogen receptors on platelets leading to no linking which causes no aggregation
79
vWF circulates with what other protein? (hand in hand circulation as one complex)
vWF:VIII
80
Most common hereditary bleeding disorder?
von Willebrand's dz
81
vWF is synthesized by?
endothelium
82
vWF is a carrier protein for what factor?
VIII (antihemophilic factor)
83
What deficiency causes vWF dz?
Due to deficiency of vWF or an abnormal vWF.
84
Bleeding time and platelet count with Von W dz?
prolonged BT despite normal platelet count (platelets cannot stick to injured area.)
85
Bleeding time and platelet count with Hemophilia
normal BT because of normal platelet count and vWF
86
Compare bleeding time and platelet count of von W dz to Hemaphilia?
hemophila is normal BT and normal platelet count.
| von W dz has a prolonged bleeding time but normal platelet count.
87
if you have abnormal vWF then what else will you have a functional deficiency of?
and what does that deficiency show up as clinically?
factor VIII, bc it is vWF carrier protein.
| Deficiency is manifested clinically by prolonged PTT.
88
Abnormal labs associated with von W dz?
prolonged BT, PTT
89
What are some signs/symptoms of von Willebrand's dz?
Nose and mucous membrane bleeding
Easy bruisability
Prolonged bleeding from wounds
Menorrhagia– very heavy period
90
Tx for von W dz?
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
thromboxane A2 and ADP both do what to platelets?
promote platelet aggregation.
92
Vit K dependent Factors are?
II, VII, IX, X
93
What proteins are vit. K dependent?
Protein C and S
94
second most common x-linked coagulation defect?
Hemophilia A
95
Hemophilia B is a deficiency in what factor?
IX
96
What is the name for a deficiency in factor VIII?
Hemophilia A
97
can you have deficient factor VIII and normal vWF?
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
Hemophilia A clinical findings?
Soft tissue and joint bleeding
Dangerous CNS bleeding with minor trauma
Spontaneous hematuria leading to ureteral colic
99
Lab findings with Hemophilia A ?
Prolonged PTT (intrinsic pathway)
Low factor VIII
Normal BT b/c normal platelets and vWF
100
Treatment for Hemophilia A?
FFP and cryo (low in VIII)
Factor VIII replacement
(Hepatitis C and HIV infection very common due to tinted blood transfusion)
101
Does BT have something to do with the coagulation cascade?
NO!
| BT measures only the response of platelets to a vascular injury. It has nothing to do with the coagulation cascade!
102
What patients should you give vit K to always?
surgical patients with liver dz
103
Almost all clotting factors are made in the liver except? (3)
Factor VIII:vWF
Factor III ( tissue factor thromboplastin)
Factor IV ( Ca++)
104
Tell me the basics of DIC?
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
pathophysiology of DIC?
widespread activation of the coagulation system leading to depletion of coagulation factors and platelets “global consumption” leading to bleeding
106
with DIC you have thrombi formation in small vessels, what does that cause?
organ ischemia
107
What are some possible causes of DIC? (4)
Obstetrics complications; retain dead fetus, abortion, eclampsia -MCC
Gram negative sepsis
Release of procoagulant tissue factors
Transfusion, trauma, malignancy, acute pancreatitis, nephrotic synd.
108
Clinical manifestation of DIC?
Bleeding from tubes, wounds, vascular access sites
Shock, ischemia, infection
Multiple organ failure
109
What change in labs will you see with DIC?
INCREASED:
PT, PTT, FDP, dimer
DECREASED:
Fibrinogen and platelets (because they are used up ) “consumptional deficiency”
110
Treatment for DIC?
Treat the underlying problem
| Platelets , FFP and cryo
111
When you give Heparin what lab do you monitor, what about Warfarin?
```
Heparin = PTT
Warfarin = PT
```
112
Which is intrinsic and which is extrinsic: PT, PTT?
PT=extrinsic pathway
| PTT= intrinsic pathway
113
Heparin onset of action vs Warfarin?
```
Heparin= rapid, less than 1 min.
Warfarin = slow, 8-12 hours.
```
114
Structure of heparin vs warfarin?
heparin is large, acidic, anionic.
| warfarin is small, lipid soluble.
115
Route for heparin vs warfarin?
heparin is IV and S/C, warfarin is oral.
116
site of action heparin vs warfarin?
```
heparin= blood
warfarin= liver.
```
117
MOA of heparin?
Increases the activity of antithrombin III ;1000 to 10000 times.
(antithrombin III is a powerful anticoagulant in blood)
118
MOA Warfarin?
Impairs synthesis of Vit. K dependent clotting factors (II, VII, IX, X)
119
DOA: Heparin vs warfarin?
Heparin: acute (hours)
warfarin: chronic (weeks to months)
120
How do you treat an overdose of heparin?
protamine
121
How do you treat an overdose of warfarin?
Vit. K, FFP
122
Tell me what you know about LMWH? (what factor it inhibits, monitoring, and risk?)
```
LMWHs inhibit factor Xa
They cannot be monitored by PT or PTT because they do not affect either
Low risk (HIT), easy , no monitoring, cost effective
```
123
Where is Heparin naturally in your body?
Heparin (present in basophil and mast cells)
124
Tell me how histamine induced thrombocytopenia is caused by heparin?
Histamine released due to heparin, increases PA pressure, decreases BP, bronchoconstriction, anaphylaxis, heparin induced thrombocytopenia (HIT) leading to bleeding.
125
how does the antidote to heparin work?
Protamine to neutralize heparin (strong base vs. strong acid)
126
What pathway does heparin block?
intrinsic and common pathways
127
activated coagulation time (ACT) what is that?
| and what is an adequate ACT with heparin, and what must it be above?
to assess adequacy of heparinization; ‘bedside coagulation test’
Adequate heparinization if ACT > 400-450 sec
No case below 400 sec.
128
PTT of someone on heparin should be what?
1.5 - 2.5 x normal (normal is 30 sec)
129
warfarin inactivates what?
vit. K dependent factors.
130
warfarin blocks what pathway?
extrinsic (VII) and common (II ,X) pathways.
131
What do you monitor when someone is on warfarin? (2)
Monitor dose by checking PT “Pro time” and INR (Extrinsic Pathways)
132
Can pregnant women use warfarin?
should be avoided
133
how long before surgery should you stop using warfarin?
d/c 3-5 days preop
134
Oral vitamin K or FFP is the antidote for what?
Warfarin overdose
135
How many days does it takes to correct the effects of warfarin after you discontinue it?
5 days
136
PTT:
assess?
monitor what med?
normal time?
Assesses intrinsic pathway+ common pathway
Monitor heparin dose
25-35 sec
137
PT:
Assess?
monitors what med?
normal time?
Assesses extrinsic pathway+ common pathway
Monitor warfarin dose
12-14 sec
138
```
ACT:
Assess?
monitor what med?
Normal time?
What you want the time to be on the drug?
```
Assesses intrinsic pathway
Access adequacy of heparinization
80-150 sec
400- 450 sec suggest complete heparinization
139
BT:
assess?
measures what?
normal?
Time for skin wound to stop bleeding
Best test to measure platelet function
3 to 10 min
140
Aspirin, what does it do to bleeding time?
Aspirin alters platelet function for 7-12 days ( the life span of platelet), resulting prolong BT
141
Platelet count:
normal?
significant bleeding time with minor trauma?
spontaneous bleeding?
Normal 150,000 to 400,000/ml
Significant bleeding with minor trauma < 50,000
Spontaneous bleeding < 20,000
142
universal donor is?
O-
143
universal recipient is?
AB+
144
What is Erythroblastosis fetalis?
Hemolytic disease of newborn. Rh- mother having a Rh+ fetus.
145
what happens with the first pregnancy of a Rh- mom and Rh+ baby?
Rh+ erythrocytes leak into mother’s circulation during delivery
Formation of anti-D antibodies in mother.
146
What happens with 2nd pregnancy of Rh- mom and Rh+ baby?
Passage of mother’s antibodies to fetus through placenta
Anti-D antibodies will cause hemolysis of the baby’s RBCs
(Jaundice, kernicterus)
147
Prophylaxis for an Rh- mom, Rh+ baby?
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
Which Ig type can cross the placenta?
IgG
149
What is the function of protein C?
Degrade factor V and VII
150
What is the function of Protein S?
Cofactor of Protein C
151
what is the function of vWF?
adhesion
152
what is the the function of antithrombin III?
is a nonvitamin K-dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin factor II, IX, X, XI, XII
153
If someone is unresponsive to heparin what could be the issue?
what would be the treatment?
antithrombin III deficiency that is due to cirrhosis and nephrotic syndrome.
Tx: FFP that contains AT3
154
Thrombophilia can be due to a deficiency of what?
antithrombin III
155
Heavy bleeding after warfarin would make you think of what deficiency?
Protein C deficiency
156
Vitamin K dependent anticoagulant that promotes fibrinolysis?
Protein C
157
Warfarin interferes with what pathway?
extrinsic pathway
158
PT and INR assess which pathway?
extrinsic
159
Heparin interferes with what pathway?
intrinsic
160
PTT and ACT assess what pathway?
intrinsic
