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Clin Med > Heme/Onc Exam > Flashcards

Heme/Onc Exam Flashcards

1
Q

4 Grades of Anemia

A

Mild: 10-12 female or 10-13.5 male
Moderate: 8 and up
Severe: 6.5 and up
Life-Threatening: below 6.5

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2
Q

Normal RBC life span? How do they die, and how often normally?

A

100-120d

Senescence (phagocytized in liver/spleen/marrow) and hemolysis (<0.5% per day)

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3
Q

Normal CBC c diff (Hgb, Hct, rets, MCV, plt, WBC, neutros, lymphos, monos)

A 
Hgb: 12-16 female/13.5-17.5 male
Hct: 36-46 female/41-53 male
Rets: 0.5-1.5% or 35,000-85,000
MCV: 80-100
Plt: 150,000-400,000
WBC: 4,500-11,000
Neutros: 40-60%
Lymphos: 20-40%
Monos: 4-11%
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4
Q

What does EPO do and what triggers its release?

A

Causes proliferation/maturation of erythroid progenitors into rets and proerythroblasts
Released by KIDNEY in response to anemia and hypoxia (Hypoxia-Inducible Factors)

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5
Q

What do hemopexin and haptoglobin do?

A

Bind free heme and free Hgb respectively so that they can be recycled in new RBCs

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6
Q

What vitamins/minerals are needed to make an RBC?

A

Iron
Folate
B12

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7
Q

Most adult Hgb is ___. What are the other two?

A

HgbA (α2β2)
HgbA2 (α2δ2) is like 2 percent
HgbF (α2γ2) is less than 1 percent

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8
Q

What are some generic common Sx of anemia?

A

Fatigue
Decreased exercise tolerance
Dyspnea
Palpitations

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9
Q

What are some generic common exam signs of anemia?

A

Pallor
Tachycardia
Murmurs
Jaundice/splenomegaly if hemolytic

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10
Q

What use are rets in lab diagnostics of anemia?

A

Anemia –> inc EPO –> inc rets

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11
Q

A LOW ret count would make me look at __.

A

MCV!

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12
Q

A HIGH ret count would make me suspect ___ or ___.

A

Bleeding or hemolysis

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13
Q

A low ret count with a low MCV brings what 4 DDxs to the table?

A 
[this means they have a MICROCYTIC ANEMIA]:
Iron-def anemia
Thalassemia
Anemia of chronic disease
Sideroblastic anemia
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14
Q

A low ret count with a normal MCV brings what 3 anemia DDxs to the table?

A

[this means they have a NORMOCYTIC ANEMIA]:
Aplastic anemia
Anemia of chronic disease
Early stages of iron-def anemia

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15
Q

A low ret count with a high MCV is highly suspicious for what kind of anemia?

A

[this means they have a MACROCYTIC ANEMIA]:
Megaloblastic anemia!
(often d/t folate or B12-def)

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16
Q

Describe the transformation process of an HSC to an RBC. Where does this occur?

A

HSC –> proerythroblast –> erythroblast –> normoblast –> reticulocyte –> RBC

In red bone marrow until [Hgb] hits about 34%, then in the bloodstream

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17
Q

What is bilirubin?

A

The waste product of Hgb once the heme part has been recycled

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18
Q

If I suspect any type of anemia, what labs do I order?

A

CBC with diff

Peripheral blood smear

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19
Q

Microcytic means MCV ___; normocytic is MCV ___; and macrocytic means MCV is ___.

A

Micro <80
Normo 80-100
Macro >100

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20
Q

What is the difference between an MCV and an RDW?

A

MCV is avg RBC size; RDW is how much variation there is in RBC size

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21
Q

What is the difference between an MCH and an MCHC?

A

MCH is the avg wt of Hgb in an RBC

MCHC is the avg [Hgb] in an RBC (‘chromia’)

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22
Q

Spherocytes on a peripheral blood smear suggest…

A

Hereditary spherocytosis

Autoimmune hemolytic anemia (will also have reticulocytosis)

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23
Q

Schistocytes on a peripheral blood smear suggest…

A

DIC (will also have abnormal coag)
TTP
HUS (hemolytic-uremic syndrome)

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24
Q

Dacrocytes on a peripheral blood smear suggest…

What do they look like?

A

Myelofibrosis (a type of leukemia)

Teardrops!

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25
Q

What do stomatocytes on a peripheral blood smear suggest? What does a stomatocyte look like?

A

Hereditary stomatocytosis
Acute EtOH intoxication
Chemo Rxs like vinblastine
Normal variant of drying if not widespread

Like a slit in the middle of the RBC

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26
Q

What do codocytes on a peripheral blood smear suggest? What does a codocyte look like?

A

Liver disease
HbC (should also have splenomegaly)
Thalassemias
Splenectomy - surg or autosplenectomy (d/t SCA)

Like a target!

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27
Q

What do echinocytes on a peripheral blood smear suggest? What does an echinocyte look like?

A

Uremia
PK-def

Like a burr - ‘echino’ means ‘like a hedgehog’ in Greek

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28
Q

You find a leptocyte on a pt’s peripheral blood smear. What did it look like? What two hematological differentials are now on your DDx?

A

Kind of like a large, very thin target cell.

Iron-def anemia + thalassemia

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29
Q

You find a Cabot ring on a pt’s peripheral blood smear. What did it look like? What caused that?

A

Like a thread in the shape of a loop or an 8 inside the RBCs.

Leftover mitotic spindle from dyserythropoeisis.

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30
Q

What’s a Howell-Jolly body?

A

Leftover nuclear fragments often d/t splenectomy (or autosplenectomy of SCA).

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31
Q

Why would basophilic stippling occur?

A

That’s ribosomes/mitochondria chillin’ around the periphery of an RBC. Could be d/t lead poisoning or sepsis.

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32
Q

Polychromasia reflects what hematologic change in the body?

A

Inc production of rets

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33
Q

In order to be effective, an RBC needs heme + porphyrin ring + globins. What disorders happen when each of these ingredients is taken away? What would labs show once they are past the early stages?

A

No heme - iron-def anemia
No porphyrin - sideroblastic anemia
No globin - thalassemias

Microcytic hypochromic! (low MCHC, low MCV)

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34
Q

What is the most common cause of iron-def anemia? What are some clues that someone has iron-def?

A

BLEEDING (GI/period) - 100cc lost = 50mg iron lost
PICA/phagophagia, angular cheilitis, glossitis, koilonychia
+ general anemia s/s

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35
Q

What labs should you automatically order if you suspect iron-def anemia (which, like, you always should suspect)?

A

SrFe
Transferrin
Ferritin
TIBC

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36
Q

So just to be clear, what will the labs of a non-early-stage iron-def anemic show?

A 
LOW rets, MCV, MCHC
LOW SrFe, Transferrin, Ferritin (false high in inflam)
HIGH TIBC (can false low in inflam)
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37
Q

I am positive my patient has iron-def anemia. How should I treat it?

A

FeSO4 325mg titrating up from qhs to tid, c VitC x3-6mo

Repeat labs in 2-3wks

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38
Q

Bad news, my patient with iron-def anemia has uncontrollable bleeding or otherwise cannot do po meds. What should I do?

A

Venofer (iron sucrose) IV push 2-5min
or
Ferrlecit (sod ferr gluconate) IV drip 30mins

NOT iron dextran! ==> hypersensitivity rxn!

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39
Q

Again, the 4 MICROCYTIC anemias are:

A

Iron-def anemia (early stage = normocytic)
Thalassemia
Anemia of chronic disease (can be normocytic)
Sideroblastic anemia

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40
Q

Why does anemia of chronic disease occur? What are the chronic diseases that can cause it?

A

ILs blocking response to EPO + IL-6 increasing hepcidin (vault access denied!)

Endocrine, infection, chronic inflam, CA. (things that inc IL.)

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41
Q

Is anemia of chronic disease associated with CHF, DM, COPD, or HTN?

A

NOOOOO.

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42
Q

Is anemia of chronic kidney disease the same as anemia of chronic disease?

A

Kind of, but no. CKD = dec EPO production, not dec EPO response.

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43
Q

What do the labs of a person with anemia of chronic disease look like? Think this through.

A 
LOW rets, SrFe
LOW to NORMAL TIBC
NORMAL MCV, MCHC
NORMAL to HIGH Ferritin 
HIGH ESR/CRP
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44
Q

How do you treat anemia of chronic disease?

A

You treat the chronic disease.

+/- supplemental iron or EPO (aka ESA, a CSF+ESF)

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45
Q

ESAs include __, __, and __. What pt popn is best for each?

A

Epogen, Procrit (aka epogen alfa) = CKD pts

Aranesp (aka darbepoetin alfa) = CA pts who are NOT getting transplants

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46
Q

What are the downsides of ESA treatment?

A

BBW: inc VTE, CA mortality, HTN, and a slew of other S/E like HA and myalgia

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47
Q

What monitoring is needed before and during ESA treatment?

A

Baseline Hgb <10; also baseline Hct and Fe

Get Hgb qwk and stop once >12

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48
Q

What is the difference between α-thalassemia and β-thalassemia?

A 
α-thalassemia = chromosome 16 deletions (up to 4)
β-thalassemia = point mutations in β-globins
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49
Q

Who gets α-thalassemia? What is it called when there are 3 functioning chains? 2? 1? None?

A 
Chinese/SE Asians
3 good = silent carrier
2 good = α-thalassemia minor
1 good = HgbH disease
None left = hydrops fetalis (will die at birth)
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50
Q

HgbH disease would show what on peripheral blood smear? How do you treat this type of α-thalassemia?

A

Target cells and Heinz bodies

Might need transfusions or chelation. Unusually bad = splenectomy + stem cell transplant

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51
Q

In general, α-thalassemia s/s are __, __, and __, and these pts are treated with…

A

Fatigue, pallor, splenomegaly

Folic acid and iron supps, genetic counseling

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52
Q

Besides a peripheral blood smear, what labs should a suspected α-thalassemia pt get? What would they show?

A

CBC c diff - Microcytic hypochromic with normal ferritin (this r/o’s iron-def)
Hgb Electrophoresis - to determine how many αs are left

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53
Q

Homozygous β0-thalassemia (major) means no β-globins, which means…

A

No HgbA

Relatively high α-chains which –> hemolysis –> severe hemolytic anemia

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54
Q

What is β+-thalassemia? What are the two types of it?

A

Some β-globins, some HgbA
β+/β+ or β+/β0 = moderate (intermedia)
β+/β or β+/β0 = mild (minor)

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55
Q

All β-thalassemia is microcytic hypochromic, and will show what on peripheral blood smear? What special smear finding would β-thalassemia major have?

A

Target cells, dacrocytes, and basophilic stippling

+ POIKILOCYTOSIS for β-thalassemia major

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56
Q

Besides a peripheral blood smear, what labs should a suspected β-thalassemia pt get? What would they show?

A

CBC c diff - Microcytic hypochromic with normal ferritin (this r/o’s iron-def) and NORMAL RDW
Hgb Electrophoresis - to determine how many βs are left

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57
Q

Sideroblastic anemia is a microcytic hypochromic anemia associated with __, caused by genetics, drugs like __, or ___.

A

Copper-def (will have neutropenia)

Chloramphenicol, Linezolid; EtOHism

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58
Q

Labs of sideroblastic anemia would show…

A

CBC c diff - Microcytic hypochromic with HIGH SrFe, Transferrin, Ferritin, and RDW
LOW TIBC
+/- LFT/kidney fxn changes
Check lead and copper levels too

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59
Q

What four peripheral smear findings are consistent with sideroblastic anemia?

A

Sideroblasts, basophilic stippling, target cells, Pappenheimer bodies

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60
Q

How do you treat sideroblastic anemia?

A

Chelate, transfuse, give copper/B6 as needed

If severe: bone marrow transplant

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61
Q

What treatment options are useless in sideroblastic anemia?

A

EPO supplementation - won’t respond

Splenectomy - C/I in congenital sideroblastic anemia

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62
Q

What are some anemias that fall under the category of intrinsic hemolytic anemia?

A

Hereditary sphero/elliptocytosis
G6PD-def
SCA
Thalassemia MAJOR

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63
Q

What are some anemias that fall under the category of extrinsic hemolytic anemia?

A

Autoimmune (IgG = warm; IgM = cold)
Drug-induced (ABx, antimalarials, antiTBs, methyl/levodopa)
Microangiopathy like DIC, TTP, HUS
Infection/burns etc.

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64
Q

What are some generic s/s of hemolytic anemia?

A

Pallor or jaundice/icterus
Dark urine
Petechiae, purpura, ecchymosis
Abd +ttp

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65
Q

Direct bilirubin is __.

A

Conjugated

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66
Q

What are the big three lab findings of hemolytic anemia?

A

Inc LDH
Inc bilirubin
Dec haptoglobin

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67
Q

Besides the big three findings, what 4 other lab findings are consistent with hemolytic anemia? What would be present in urine?

A

Inc rets, indirect bilirubin, methemalbuminemia, hemoglobinemia
Urine hemosiderin

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68
Q

What does a direct Coombs test test for?

A

RBCs coated with antibodies/complement

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69
Q

What does an indirect Coombs test test for?

A

Anti-RBC antibodies in the serum

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70
Q

How do you treat moderate to severe hereditary spherocytosis?

A

Splenectomy!

+ folic acid and/or transfusions

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71
Q

How do you treat G6PD?

A

D/C offending drug (nitrofurantion, sulfa, dapsone) if that’s what’s causing it
Tx an infection if that’s what’s causing it

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72
Q

What are the 3 most significant LAB findings for G6PD?

A

Spherocytes + rets on smear
Hyperchromic
Coombs neg

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73
Q

Why does PNH occur?

A

No CD55/59 –> complement system lyses RBCs

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74
Q

Alright there’s a lot of systemic s/s of PNH but I’m down to the wire. Name three clear Sx of PNH.

A

Episodic hemoglobinuria
Erectile dysfxn
Thrombosis –> death

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75
Q

Main lab to diagnose PNH?
Coombs would be __.
LDH would be __.
Everything else is variable.

A

CD55 FLOW CYTOMETRY
neg
high

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76
Q

We give PNH pts to hematologists, but mild ones (most) don’t need intervention. How do we treat moderate/severe PNH pts?

A

Eculizumab + steroid + transfusions PRN

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77
Q

If a PNH pt has SEVERE Sx/thrombosis, how do we treat them?

A

Allogenic stem cell transplant

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78
Q

G6PD is a __ disorder that causes ___, most often in what pt popn?

A

X-linked recessive; episodic hemolytic anemia

AAM

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79
Q

During an episode, what would the labs of a G6PD pt show? When would you do them?

A

NOTHING

@6-8wks post-hemolysis episode: high rets/bilirubin; Heinz bodies and bite cells on smear

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80
Q

What is warm AIHA?

A

IgG:RBC at room temp, usually idiopathic

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81
Q

What are three big Sx of AIHA?

A

Angina + Jaundice + Splenomegaly

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82
Q

In warm AIHA, direct Coombs would be __ and indirect Coombs would be __.
What other three lab values are good to note?

A

POSITIVE!!
either + or -
Inc rets + inc indirect bili + dec haptoglobin

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83
Q

How do you distinguish between AIHA and hereditary spherocytosis, since both have the same smear? (What does that same smear show?)

A

Direct Coombs!! + for AIHA, - for HS

Smear for both = rets + spherocytes

84
Q

We will give AIHA pts to a hematologist, but in general, what 4 treatment options are we looking at?

A

Transfusions (hard)
Therapeutic plasma pheresis
Prednisone
Splenectomy

85
Q

Cold AIHA is called that because…

A

IgM:RBCs at cold temperatures which looks kinda like Raynaud’s in the extremities but with hemoglobinuria when it’s cold out

86
Q

What would the Coombs for cold AIHA show? What about the smear?

A

Coombs + for complement, - for antibodies

Rets on smear

87
Q

How do you treat cold AIHA?

A

Rituximab/immunosuppression if bad

Or more often just supportive stuff

88
Q

Sickle-cell disease is a __ disorder due to a __ mutation in what? How long do RBCs with sickle-cell live?

A

Autosomal recessive
V6E for β-globins –> HgbS
10-20d

89
Q

A sickle-cell crisis can be __ (like __), __ (like __), or __ (like __).

A

Vasoocclusive (CVA, MSK)
Hematologic (hemolytic crisis)
Infectious (PNA)

90
Q

How do you treat adult SCA when they are not in a crisis?

A

Get the pneumococcal vax
Avoid triggers
Folic acid 1mg po qd

91
Q

How do you treat SCA during a crisis?

A

Generous pain meds

Supportive measures

92
Q

What will a SCA smear show?

A

Sickled cells
Rets
Howell-Jolly bodies
Target cells if autosplenectomy

93
Q

How do you treat kids with SCA?

A

Hydroxyurea can inc HgbF
Long-term transfusions to reduce CVAs
Allogenic HSCT

94
Q

What are the risks associated with sickle-cell trait?

A

VTE

Rhabdo/MI after heavy exercise

95
Q

If LDH, T.Bili, and Haptoglobin are all NORMAL, what do you suspect?

A

Bleeding –> if not, CA, check smear

96
Q

If LDH and T.Bili are high, but hapto is low, what do you suspect?

A

Hemolysis –> look at smear

97
Q

What’s the difference between macrocytic and megaloblastic anemia? (think: labs + causes)

A

Macro - MCV > 100 (d/t EtOHics, hypothyroid, anti-HIV/hydroxyurea)
Megalo - MCV > 115 (and d/t vit-def)

98
Q

What is aplastic anemia?

A

Welp it ain’t anemia

It’s pancytopenia d/t injury to pluripotent stem cells

99
Q

Aplastic anemia is most common in…

A

East Asians

People with other marrow issues

100
Q

Aplastic anemia can be ACQUIRED:
From Rxs like…
Or from chemicals/toxins like…
Or from viruses, pregnancy, or anorexia.

A

Carbamazepine, phenytoin, indomethacin, gold, PTU, methimazole, sulfonamides, chloramphenicol

Benzene, solvents, and huffin’ glue

101
Q

What are two autoimmune causes of aplastic anemia?

A

Idiopathic autoimmune

SLE

102
Q

What are two congenital causes of aplastic anemia?

A 
Fanconi anemia
Dyskeratosis congenita (telomere length issue in HSC)
103
Q

Aplastic anemia presents as __ and __, and leads to …

A

Bleeding from everywhere (=petechiae) and cardiopulm compromise
Infections = death

104
Q

Aplastic anemia does NOT present with __, __, or __!

A

Hepatosplenomegaly!!
LAD
Bone pain

105
Q

3 big findings on labs of aplastic anemia? What would a smear show?

A

Pancytopenia
Anemia
Low rets

Smear - no weird shapes!

106
Q

Moderate aplastic anemia would show __ on a bone marrow Bx.

What about severe aplastic anemia?

A

<30% cellularity

<25% or <50% with really low plt, ANC, or rets

107
Q

What do you need to diagnose someone with very severe aplastic anemia?

A

Severe Aplastic Anemia + ANC under 200!

108
Q

How do you treat nonsevere aplastic anemia?

A

Treat the underlying cause, prevent infection, give EPO/myeloid GF

109
Q

How do you treat severe aplastic anemia?

A

Allogenic HSCT!

Or immunosuppression Horse AtG + CsA (can cause other hem/onc issues though)

110
Q

Fanconi anemia is a __ disorder that presents with fish hands and can only truly be treated by…

A

Autosomal recessive

Allogenic HSCT

111
Q

What do megaloblastic RBCs look like? What do megaloblastic neutros look like?

A

Macroovalocytic

Segmented

112
Q

What are the most common causes of megaloblastic anemia?

A

Poorly prepped foods

Folate-def in pregnancy

113
Q

Intrinsic factor is made by __ and helps B12 get absorbed in __.

A

Gastric parietal cells

The terminal ileum!

114
Q

What two pathways need B12 to do the thing?

A 
DNA synth (/RBC synth)
Myelination
115
Q

Pernicious anemia is an autoimmune disorder in which antibodies attack …
What can that eventually lead to?

A

Intrinsic factor and gastric parietal cells

Gastric CA

116
Q

B12-def is a macrocytic anemia with LOW __ and __, and HIGH __, ___, and __.

A

LOW B12 and rets

HIGH MMA, homocysteine, indirect bili

117
Q

Pernicious anemia would have LOW __, but HIGH __; also, antibodies. What special test can you do?

A

LOW pepsinogen
HIGH SrGastrin
Schilling test, but it kinda sucks.

118
Q

How do we treat B12 deficiency? And don’t just say ‘giving B12.’

A

B12 100mcg SC or IM qd x 1wk, then qwk x 1mo, then qmo for life
-or-
Methylcoabalamin 1mg SL or PO qd for life
+ folic acid x1mo

119
Q

Besides B12 level, what should you probably monitor in your B12-def pt you’re treating and why?

A

CBC - HypoK+ risk with supplemental B12

120
Q

Your body has enough B12 in storage for __ and enough folate in storage for __.

A

3yrs

2-3mos

121
Q

Where does folic acid get absorbed?

A

Whole sm intestine

122
Q

Normal plts are above __. Most thrombocytopenics are ASx until it’s under __.

A

150,000

100,000

123
Q

Plts come from __ cells and are stored in __. How long do they last?

A

Megakaryocytes (each makes like 10,000 plt)
Spleen (1/3 of all plts are in storage)
5-9d

124
Q

What causes stored plts to be released?

What phagocytizes plts?

A

Sympathetic nervous system

Kupffer liver cells and the spleen

125
Q

What is dilutional thrombocytopenia, and how do you prevent it?

A

In pts getting packed RBC - give plt to pt receiving >20 U in 24 hours.

126
Q

Bleeding difference between thrombocytopenics and coag disorder pts?

A

Thrombocytopenics bleed immediately, coag issues bleed more slowly

127
Q

Petechiae do not …

A

Blanch!

128
Q

Spontaneous bleeds occur below…

A

10-20,000 plts!

129
Q

What is vWF?

What is vWD?

A

A factor in plt aggregation

An autosomal dominant bleeding disorder

130
Q

What are the three types of vWD? Briefly describe each.

A

I - not enough vWF
II - the vWF is not effective
III - ZERO vWF, no Factor VIII, basically hemophilia A

131
Q

Heart valve disease, DIC, and hypothyroidism can all cause vWD. How?

A

Valves - ADAMTS-13 shearing
DIC - degradation of vWF
Hypothy - dec vWF synthesis

132
Q

What are the two treatment options for vWD?

A

Types I/II - desmopressin

Type III - transfusion

133
Q

Why is ITP called ‘idiopathic’ if we know why it happnes…? Why DOES it happen?

A

Cause the bone marrow looks normal

Anti-IIb/IIIa antibodies attack plts and anti-IgG attack megakaryocytes (also low TPO..?)

134
Q

Who gets ITP? What does it look like?

A

Peds s/p infection

Purpuric!

135
Q

How do you treat ITP?

A

IV steroid + IVIg + Anti-DIg
+/- plt transfusion right after
If emergency: splenectomy

136
Q

What is TTP?

A

Like the anti-vWD: inhibited ADAMTS-13 –> inc vWF –> plt adhesion –> thrombosis
But also: using up all that plt –> thrombocytopenia

137
Q

Besides primary ADAMTS-13 issues, how can you get TTP?

A

Meds: quinine, acyclovir, immunosuppressants, antiplatelets
Preg
CA/HIV

138
Q

What is the Pentad of TTP? (3+ needed with schistocytes for Dx)

A 
FAT RN
Fever
Anemia (microangiopathic hemolytic aka.. schistocytes!!)
Thrombocytopenia
Renal failure
Neuro Sx
139
Q

How to treat TTP?

A

Pass it onnnnnnn
They will do: plasmapheresis daily!
+/- immunosuppressant/steroid

140
Q

Hemophilia A is a __ genetic disorder caused by a deficient functional factor ___.
Hemophilia B is a __ genetic disorder caused by a deficient functional factor ___.
Hemophilia C is a __ genetic disorder caused by a deficient functional factor ___.

A

Recessive X-linked; VIII
Recessive X-linked; IX
Autosomal; XI

141
Q

Moderate hemophilia means a pt has ___% of clotting factor.

A

1-5% (less = severe, more = mild)

142
Q

In what three cases could a woman have symptomatic hemophilia A or B?

A

1) Dad has it, Mom carries it.
2) Turner Syndrome.
3) X-inactivation.

143
Q

What labs should I order to diagnose hemophilia?

A

aPTT for intrinsic pathway (will be high if they have it)

Factor VIII/IX

144
Q

What’s a common MSK Sx of hemophilia?

A

Target joint for hemarthrosis

145
Q

For hemophilia ppx, we give factor VIII/IX replacement. What about for acute bleeds?

A

Get clotting >50%!
1 U/kg of factor VIII gtt when corrected for goal [(% desired - % actual)/2] x wt in kg

rVIIa might be better to avoid antibodies making Tx useless!

146
Q

VitK (aka _) is a _-soluble vitamin needed to make…

A

Phylloquinone
Fat-soluble
II, VII, IX, X, and protC/S

147
Q

What are the three causes of VitK-def?

A

Not in diet (esp. neonates)
Too much Warfarin
Bile obstruction –> can’t absorb it

148
Q

DIC is a bleeding AND clotting condition resulting from overactivated __. What is the cutaneous Sx of DIC called?

A

Tissue factor!

Purpura fulminans

149
Q

What five labs would be ELEVATED in DIC?

A 
aPTT
PT
D-dimer
LFTs
Thrombin
150
Q

What five labs would be DECREASED in DIC?

A 
plt
Iron
Fibrinogen
AT
prot C/S
151
Q

Okayyy so how do we treat DIC?

A 
ABCs
plts
FFP
AT
\+/- heparin
\+/- protC
152
Q

Polycythemia Vera is caused by a __ mutation that leads to…

A

JAK2

Myeloproliferation of everything esp RBCs –> very high Hct, volume, and viscosity

153
Q

What’s the difference between primary and secondary polycythemia vera?

A

Primary is EPO-independent inc RBC synthesis.

154
Q

What are the five causes of secondary polycythemia vera?

A 
HEART
Hypoxemia
EPO-secreting tumors
Adrenal
Renal
Testosterone
155
Q

To diagnose polycythemia vera, you need how many criteria to be met? What are the major criteria?

A

1 major + 2 minor or 2 major + 1 minor
Hgb > 18.5/16.5 men/women
+JAK2 mutation

156
Q

Five ways polycythemia vera COMMONLY presents clinically…?

A 
HEENT stuff (d/t high blood vol)
Thrombotic stuff
Hepatosplenomegaly
Gout
Aquagenic pruritis
157
Q

What is an uncommon but pathognomic Sx of polycythemia vera?

A

Erythromelalgia

158
Q

General treatment of polycythemia vera is __ and __.

A

lo-ASA qd

Phlebotomy to release blood til Hct is <0.45

159
Q

If the polycythemia vera is bad or the risk is high, treat it by…

A

Hydroxyurea!!!

or interferon if that isn’t possible

160
Q

Ventilate if pt is __ or __, or for general anesthesia, or by your best judgement. Define each.

A

Hypoxemic: O2 <90% FiO2 (60%+)
Hypercapnic: pH <7.3 or pCO2 >50

161
Q

ETT tube size? What Rxs can you use to place one?

A

7-8mm minimum
Rocuronium or succinylcholine
+
Propofol or etomidate

162
Q

Where is the correct placement of an ETT on XR?

A

3-5cm ABOVE CARINA or else you might end up in R main stem

163
Q

Complications of an ETT include ___, __, __, and more rarely, ___.

A

ETT migration, larynx damage, dental damage

Tracheoesophageal fistula

164
Q

Trach someone who…

A

…you don’t expect to extubate within a week.

165
Q

Name four complications of a trach.

A

Tracheal stenosis (usually ASx)
Accidental decannulation
Aspiration
Cuff leaks

166
Q

Name the four most commonly used ventilator modes.

A

1) Volume control
2) Pressure control
3) Pressure Support
4) BiPAP (noninvasive)

167
Q

PEEP is normally __ mmHg, normal tidal volume is ___L, and an RSBI of ___ is a go for extubation.

A

5-20mmHg
6-8L
<100 (RR:TV)

168
Q

PEEP is used in most ventilation pts to __. In what two specific populations is it most useful?

A

Prevent alveolar collapse

Atelectasis pts + PNA pts (to dec supplemental O2 needed)

169
Q

In whom should we NOT use PEEP and why?

A

Hypovolemic pts - they already have dec cardiac output and PEEP further dec venous return –> dec CO

170
Q

Volume control is __ or __ and is used by setting ___ on the machine.

A

SIMV or AC

Set volume of air a set number of times a minute

171
Q

In whom would I prefer AC volume control? What is its main disadvantage?

A

Pts who are sedated/newly intubated

Auto-PEEP upon tachpynea

172
Q

In whom would I prefer SIMV volume control? What is its main disadvantage?

A

Pts who I’m gonna start to wean because they take some of their own breaths between ventilated ones
Dyssynchrony on tachypnea

173
Q

What do you preset in pressure control ventilation? What does that affect?

A

Set the driving pressure, which determines the TV

174
Q

Pressure control is good for…

A

Pts who have new sutures/you want to control how much their chest expands but are sedated (it’s uncomfy)

175
Q

The ideal ventilation mode for weaning pts is __. How does it work?

A

Pressure Support Ventilation (PSV)

Assists pts with their own breaths via 5-15mmH2O PRN

176
Q

What’s the main disadvantage for PSV?

A

No preset TV or RR = can hypoventilate if pt isn’t ready

177
Q

When is BiPAP the best option?

A

In impending respiratory failure

178
Q

Process for deciding to extubate?

A

1) Underlying cause treated?
2) Hemodynamically stable?
3) PaO2>60 on an FiO2 40-50%, and PEEP <10?

Cool, then challenge with SBT 30’.

4) Did they pass without strugglin’?
5) Is the RSBI <100 after 30’?

179
Q

An elevated Aa-gradient means…

A

Oxygen is NOT effectively transferred from the alveoli to the blood.
Low pO2 in arteries compared to inc alveolar pO2.

180
Q

Hypoxemia with an elevated Aa-gradient that IMPROVES on FiO2 is d/t…
If it does NOT improve with FiO2, the problem is…

A 
V/Q mismatch! (FYI ex: low in COPD/asthma, pulm edema; high in PE)
A shunt (ex: ARDS)
181
Q

3 identifying characteristics of ARDS?

A

Progressing resp distress
Not improved by FiO2
Bilateral infiltrates on CXR

182
Q

Phases of ARDS?

A

Exudative –> Proliferative –> maybe Fibrotic

183
Q

How do you treat ARDS?

A 
Treat the underlying cause!!!
Get paO2 to 55 using minimal settings
Get pH >7.3
Carefully use diuretics to get CVP <4, PCWP <8 
Supportive stuff
184
Q

Place a central line __, __, or __ using what technique?

A

IJ, fem, SC

Seldinger: U/S (except SC), guidewire, confirm CXR (except for fem - use gravity test or ABG)

185
Q

Get CVP when pt is __; normal is __ and highest during…

A

Supine!
0-20mmHg
Expiration

186
Q

Place a central line with pt ___ to avoid…

A

Trendelenberg - venous air embolism!!

187
Q

Three other big complications of a central line?

A

Thrombosis (tPA ppx)
PTX
Infection (vanco +/- zosyn while waiting on C&S)

188
Q

Three locations of arterial lines? Why would I give that over a central line?

A

Rad, fem, axillary

Unstable pts who require vasopressor support, or patients with severe HTN

189
Q

Bad arterial waveforms like __ or __ can tip you off to a lame arterial line placement. What are some complications/drawbacks of arterial lines?

A

Dampened, exaggerated/fling

Occlusions, limited ROM, infection

190
Q

A Swan-Ganz cath can tell you directly…

A

RA CVP, PAP

LA PCWP when balloon is inflated

191
Q

Three complications of a Swan-Ganz cath?

A

Damaging pulm a.
Ventr. arrythmia
Infection

192
Q

A WBC > ___ should make you think CA. What cells would be more specific to a myeloid leukemia on bone marrow Bx? What about a lymphoid leukemia?

A

60,000
Myeloid = PMNs
Lymphoid = lymphocytes

193
Q

A FUO with LAD and wt loss is ___ til proven otherwise.

A

Lymphoma

194
Q

AML occurs in __ pts, will show __ & __ on bone marrow Bx, and is treated by…

A

Old
Auer rods + >20% blasts
Chemo +/- BM transplant (M3= VitA)

195
Q

CML occurs in __ pts, is d/t __, and is diagnosed by

A

Old

9:22 BCR-ABL (Philadelphia chromosome) - diagnosed by cytogenics

196
Q

CML has three stages. What are they?

How do you Tx CML?

A

Chronic - Accelerated (>15% blast) - Blast (>30%, extramedullary so it’s becoming AML)
Imatinib + chemo +/- HSCT

197
Q

CLL occurs in __ pts, is d/t ___, and the most common Sx are __ and ___.

A

Very old
Hypermutation of Ig heavy chain
LAD, Well’s Syndrome (itchy eosinophilia)

198
Q

Two diagnostic labs for CLL?

A

Less than 55% atypical cells + B-surface antigens CD5/CD20

199
Q

How do you treat CLL?

A

Watch and wait!

Once progressive, chemo and SCT stuff

200
Q

ALL occurs in __ pts, has __ Sx that other leukemias don’t, and is diagnosed via __.

A

Peds
CNS Sx
LP

201
Q

How do you treat ALL (hint: 4 phases)?

A

Induction - 4-6wk inpt
Consolidation - 6-12mo
Maintenance - lo-dose chemo + prednisone 18-24mo
CNS ppx - LP/IT chemo

202
Q

Hodgkin’s lymphoma is better than NHL, and is characterized by __ & __ cells. What are the two subtypes?

A

Reed-Sternberg & Popcorn

Classic & Nodular Lympho-Predominant

203
Q

Biggest Sx of HL?

How do you treat HL?

A

Painless LAD above diaphragm!

Chemo + rad + ABVD Rxs 3-4 cycles

204
Q

Bence-Jones proteins, lytic bone lesions, and Rouleaux formations should all make you think…
What disorder might that be preceded by?

A

Multiple myeloma

MGUS

205
Q

Lymphoplasmacytic lymphoma includes __. How is it different than multiple myeloma?

A

Waldenstrom’s Macroglobulinemia

No lytic bone lesions!

206
Q

Modified Ann Arbor Staging I-IV:

A

I: one lymph node
II: two, on same side of diaphragm
III: two, one on each side of diaphragm
IV: an actual organ is now involved

Clin Med (4 decks)

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