B&l: Taube : High Yeild

Front 1

What is the importance of Mean Corpuscular Volume (MCV)? MUST KNOW THESE VALUES

**** ON TEST

Back 1

Can classify cells and types of anemia based on size:

Normocytic: 80-100fl
Microcytic: <80
Macrocytic >100

Front 2

What does a Mean Corpuscular Hemoglobin Concentration (MCHC) show?

Back 2

Measures the average conc. of Hb in a given volume of packed red cells

Just as MCV relates to cell size, MCHC relates to the color of the cells
Defines normochromic, and hypochromic cells relating to anemia classification.

Front 3

What are POIKILOCYTOSIS and ANISOCYTOSIS?

Back 3

POIKILOCYTOSIS: Nonspecific variation in shape.

ANISOCYTOSIS: Nonspecific variation in size.

seen in a smear reveiw

Front 4

if you see a lot of round macrocytes, what 2 things should you be thinking?
***

Back 4

Liver disease
alcoholism

Front 5

DNA replication problems should make you think what type of macrocyte?

Back 5

Oval

Front 6

Acanthocytes are seen with what 3 problems?

**

Back 6

Advanced Liver Disease:

due to neonatal hepatitis
metastatic disease
alcoholism.

Front 7

Most common cause of Echinocytes? (what were they again)

Back 7

Most common cause is an artifact of improperly prepares smears (slow drying, thick smears, aged blood) or “glass effect” causing an elevated ph in the medium surrounding the cell.

they are cells with spikes evenly distributed on a RBC membrane, maintain central pallor

Front 8

What produces schistocytes?

**

Back 8

when coagulation is increased

fibrin is increased

when RBC hits one of these filaments, the cell is sheared

Front 9

What causes Tear drop cells?

*

Back 9

either abnormal inclusion in the RBC (after splenic filtering)

more commonly when there is fibrosis of the bone marrow or the spleen that causes the red blood cell to get squeezed, and a portion of it is pulled off leaving a pear shape

Front 10

Possible associated diseases with high teardrop cell levels?

Back 10

Myelofibrosis
Myelofibrosis with myleloid metaplasia (MPS)
BM infiltration by hematologic or carinomatous malignancy.

Front 11

this cell is Round, thicker than normal, and without central pallor.

it is often smaller than a normal RBC

the MCV is normal to slightly reduced

***

Back 11

Spherocyte

Front 12

How do Spherocyte form?

Back 12

fibrin strand in perpheral circulation

it gets sheared in half

(or can be due to thermal problem, or immune hemolysis, where macrophage takes a bite out of the RBC)

Front 13

Spherocytes are associated with what? what is the MAJOR one to remember

Back 13

Hereditary Spherocytosis: intrinsic deficit of spectrin. (High MCHC reflecting cell dehydration).
Immune hemolytic anemia
Thermal injury (burns)

Microangiopathic hemolytic anemias***

Front 14

There are 2 types of Basophilic Stippling, what are they? Which is important ? Why?

Back 14

Coarse and Fine

COARSE: suggests impaired Hb synthesis

Front 15

Spherical intracytoplasmic inclusion that is iron stain negative.

associated with Abnormal cell division seen in Megaloblastic anemias or MPS

Back 15

Howell-Jolly Body

Front 16

if you see a multiple myeloma or lymphoma, how do you expect your RBCs to look? what will your MCV be like?

***

Back 16

Rouleaux formation (stack of coin)

your MCV is sky high because it sees the stack of coins as ONE BIG CELL

Front 17

HTLV-1 is associated with what?

*

Back 17

Adult T-Cell leukemia (ATL)

due to infection of CD4 T cells

Front 18

HTLV-2 is associated with what?

*

Back 18

Hairy cell leukemia (CD8 cells infected)

Front 19

Flower cells are seen in what? What are they?

*

Back 19

T-cell infected with HTLV1

the nucleus divides, but the cell does not

Front 20

what is different about HTLV infection and HIV?

***

Back 20

not due to free virus

goes in, integrates, but almost NEVER makes new virus

not passing along the virus, you are passing along T cells

Front 21

How does a 2nd pt get infected with HTLV?

Back 21

T cell transfer (IV drug use, sex)

graft versus host rxn activates the foreign T cell, that leads to making more virus (after that replication, it does not make more virus in the 2nd person)

Front 22

in pts who obtain HTLV, it mostly remains silent (even to the point where a pt can die before any problems occur). What will cause it to be activated leading to cancer?

Back 22

after a long period of time there is a demethylation

The TAX gene is then expressed-->targets IL2 gene and receptor gene

thus it is seen in old people

Front 23

in HTLV, what gene eventually gets turned on? What does this do? 2 major things happen...
**

Back 23

1) The TAX gene is then expressed-->targets IL2 gene and receptor gene

get self stimulation leading to lymphocytosis

2) Later get blockage of p53 and the Cyclin dependent kinase pathway (CKD)--> leads to adult t-cell leukemia

Front 24

Can you use HIV drugs to help with HTLV? (Reverse Transcription/Protease inhibitors)

Back 24

not a disease of viral replication like HIV

so no.

Front 25

There are 4 groups of adult t-cell leukemia that can result from HTLV...what are they...which is most common? which is gonna be most fatal?

Back 25

Acute: most common, most fatal
Lymphomatous
Chronic
Smoldering

Front 26

Circulating HTLV-1 infected CD4 T-lymphocytes invade CNS, primarily in spinal cord, at thoracic level. Possible infection of astrocytes. Eventual spread to brain stem.

what is this?

Back 26

HTLV-1 Associated Myelopathy/Tropical
Spastic Paraparesis (HAM/TSP).

Front 27

normal range for CD4 cells in HIV?

Back 27

normal range - 500 to 1,500 cells/ml

Front 28

CD4 levels of what predicts complications?

Back 28

CD4 < 200 predicts complications

Front 29

CD4 levels of what predicts death?

Back 29

CD4 < 50 predicts death

Front 30

What is the FDA approved method for HIV diagnosis?

Back 30

Antibody testing

note: Usually positive within 3 months of Primary HIV (PHIV) Infection but can take as long as 1 year

Front 31

What is the confirmatory diagnosis method for HIV?

Back 31

RNA Testing - Viral Load by molecular method

Front 32

Who should be HIV tested? 3

Back 32

Yearly “opt-out” HIV screening for all patients ages 13 - 64 years*.

All patients with positive PPD or initiating treatment for TB.

All patients seeking treatment for STIs, including all patients attending STI clinics, should be screened routinely for HIV.

Front 33

As a HCW, what is your greatest risk for HIV exposure?

Back 33

outside the hospital!!

Sexual contact, sharing needles, pregnancy

aka thinks you aren't (or shouldn't be) doing in the hospital!

Front 34

Please describe primary HIV (seroconversion illness)

When does it happen?
Symptoms?
Viral Load?
HIV antibody test?

Back 34

this is a flu like syndrome that pts get

7 to 30 days after initial exposure

Fever, headache, rash

Very high Viral Load (>100,000 copies)

HIV antibody negative (thus if you suspect HIV you have to do an RNA test)

Front 35

What is the fastest growing group with new HIV infections? 2

Back 35

Teenagers and older people

Front 36

Ppl with hiv are?:

living longer

have increased risk of co-morbitieis comparied to HIV neg

Can get life insurance

Will eventually die of AIDs

Can give blood transfusions

Back 36

living longer

have increased risk of co-morbitieis comparied to HIV neg

Can get life insurance

Front 37

What is going on with the life expectancy for pts with HIV?

Back 37

A 20-year-old HIV-positive person starting antiretroviral (ARV) therapy today can expect to live, on average, to the age of 69

Front 38

what % of babies with HIV will be infected

Back 38

25% of babies will be born HIV +

Front 39

What % of babies born to an HIV mom will have HIV antibodies when born?

Back 39

ALL OF THEM

passive immunity

so you have to have RNA testing to see if they have it or not

Front 40

There are a number of resistant mechanisms to antiretrovirals...please describe the reverse transcriptase

Back 40

Reverse transcriptase is error prone and 10 billion virions produced per day

Front 41

There are a number of resistant mechanisms to antiretrovirals...please describe the number of point mutations

Back 41

Every possible single point mutation (SPM) produced every day

Front 42

what does the single point mutation RT M184V do with respect to HIV resistance?

Back 42

get drug resistance to lamivudine (drug name not important)

then Monotherapy leads to replacement of wild type virus with highly resistant virus within days to weeks

Front 43

what type of adherence do pts have to exhibit who take HIV drugs...

Back 43

you have to be 90 to 95% adherence to your drug treatment or you WILL NOT STOP REPLICATION

thus you will NOT STOP ERRORS

and you will get further resistantance

Front 44

Who’s Best at Predicting Adherence?

Physician
Nurse
Pharmacist
Family Member

Back 44

Family Member

Front 45

Which of the following is best at predicting adherence to HIV drugs

Race
Gender
Disease stage
Active IDU

Back 45

Active IDU

but note this will have a NEGATIVE IMPACT

all of the others are not predictive

Front 46

must remember that taking your medicine and not missing a dose is SUPER IMPORTANT...this is for sure gonna show up on a test

**

Back 46

if you miss a dose, the virus can replicate and change (remember the reverse transcriptase will make errors with each replication)

Front 47

if you do an AB test and it is pos or negative what is the next test you should do?

***

Back 47

RNA TESTING

Front 48

what drugs were introduced in the mid 90s that lowered viral loads and subsequently deaths?

Back 48

Protease inhibitors

Front 49

If your CD4 count is <350, what co-morbidity must you consider for your patient?

Back 49

Cardiovascular disease

this is one of the pressures to treat ppl with HIV earlier

Front 50

In the case of a needle stick, when is the best time to start Post-Exposure Prophylaxis (PEP)

As soon as possible after the incident
Once you have been diagnosed HIV+
In less than 7 days
One hour before needle stick

Back 50

As soon as possible after the incident

Front 51

Post Exposure Prophylaxis is best done when? How effective is it? Can it be applied after sexual exposure?

***

Back 51

Works best if done immediately
Is very effective in preventing HIV infection
Can be applied to parenteral as well as sexual exposure

Front 52

When you have HIV and Hep C, which one do you treat?

Back 52

Whichever one is causing them the biggest issues

(hepatic fibrosis-->hep C; low CD4--> HIV)