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STEP2 > Heme/Onc > Flashcards

Heme/Onc Flashcards

1
Q

Manifestations of CO poisoning

A

CO displaces oxygen on hemoglobin

treat with 100% oxygen, possibly in a hyperbaric chamber

AMS
Cherry-red lips
Pulse-ox normal

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2
Q

microcytic anemias

A 
IDA
lead poisoning
chronic disease
sideroblastic
thalassemia
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3
Q

normocytic anemias

A

hemolytic anemia
chronic disease
hypovolemia

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4
Q

macrocytic anemia

A

folate deficiency
B12 deficiency
liver disease
alcohol abuse

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5
Q

Mean RBC lifespan

A

120 days

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6
Q

hemolysis

A

intrinsic- defect intrinsic to cell
extrinsic

H and P:
pale, jaundice, hepatosplenomegaly, brown urine

Labs:
decreased H/H
increased retic count
increased indirect bilirubin
increased LDH
normal MCV
decreased serum haptoglobun

Coombs test for autoimmune abs

Peripheral blood smear:
schistocytes
spherocytes
Burr cells

Types of hemolytic anemia
Drug- induced
immune
mechanical 
G6PD deficiency
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7
Q

COOMBs test

A

coomb’s reagent is rabit IgM against human IgG or complement, so that red cells that are bound by auto-immune factors will agglutinate in presence of reagent

direct test looks at patient red cells (reagent mixed with patient RBCs, agglutination- RBCs coated with IgG and complement)
antibodies on the RBCs may be due to warm or cold agglutinins
Warm= IgG (agglutinate at body temp)
Cold= IgM (mycoplasma, EBV), only agglutinate in cold environment

indirect test looks at patient plasmsa: mix serum with type O RBCs, and then with Coombs’ reagent. Agglutination if anti-RBC antibodies in serum

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8
Q

Drug- induced (coombs positive) hemolytic anemia

A
  • PCN
  • methyldopa
  • quinidine (and quinine)
  • cephalosporins
  • NSAIDs
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9
Q

Immune hemylotic anemia

A

warm agglutinins or cold agglutinins

Associations:
EBV, mycoplasma pneumoniae, HIV

Treatment:
avoid cold exposure
steroids
splenectomy

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10
Q

Mechanical hemolytic anemia

turbulent blood flow

A

prosthetic heart valve

schistocytes

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11
Q

Hereditary spherocytosis

A

Genetic defect of red cell membranes, resulting in spherical red cells

characteristic findings:

  • jaundice and gallstones
  • splenomegaly
  • anemia with reticulocytosis and increased MCHC (mean corpuscular hemoglobin concentration)
  • high incidence of pseudohyperkalemia as RBCs lyse after blood draw and intracellular potassium leaks
  • peripheral smear reveals spherocytes
  • positive osmotic fragility test

What is the treatment?

  • folic acid 1mg daily
  • red cell transfucions in cases of extreme anemia
  • splenectomy in moderate to severe disease
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12
Q

G6PD deficiency

Spleen Purges Nasty Inclusions From Damaged Cells

A

G6PD repairs oxidative damage to RBCs. Without it the body is prone to hemolysis

Spleen Purges Nasty Inclusions From Damaged Cells

Sulfonamides
Primaquine
Nitrofurantoin
ING
Fava beans
Dapsone
Chloroquine

PBS:
bite cells
Heinz bodies

Diagnosis:
decreased G6PD activity
fatigue begins within days of ingesting oxidants

Treatment:
antioxidants
transfusions

severer form affects mediterranean patients
milder affects blacks

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13
Q

Why is serum haptoglobin decreased in hemolytic anemia

Why is LDH increased

A

Haptoglobin binds free hemoglobin in the blood

Haptoglobin-hemoglobin complex is removed from circulation by the spleen

LDH is found inside RBCs

When RBCs lyse, LDH is released into circulation

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14
Q

G6PD

A

enzyme involved in pentose phosphate pathway
maintains glutathione in RBCs, which is neded to protect RBCs from oxidative damage

deficiency is x- linked recessive non-immune hemolytic anemia

stressors include infection, drugs, fava beans

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15
Q

Iron deficiency anemia

A

most common anemia
blood loss
poor iron intake
poor iron absorption

acutely, after blood loss the H/H will be normal. H/H won’t drop until after dilution

The new red cells have less iron, so they’re smaller than normal (hypochromic and microcytic with central pallor)

pregnancy
kids can have iron- fortified cereal after 6 months of age due to inadequate intake

history: fatigue, weakness, dyspnea, pica, restelss legs
exam: pallor, tachycardia, tachypnea. angular chelitis, spooning of the nails (concave)

Treatment: iron supplements
determine cause of iron loss
elderly, suspect colon cancer and pursue colonoscopy

Labs:
low serum iron
low serum ferritin
increased TIBC (directly proportional to transferrin), which is the iron transport protein

iron:TIBC ratio is decreased (

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16
Q

ferritin

A

storage form of iron, low in IDA
elevated in hemochromatosis
increased or elevated in anemia of chronic disease

normal in lead poisoning

increased in sideroblastic anemia

normal in thalassemia

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17
Q

transferrin

A

protein that transports iron in the blood
high in iron deficiency anemia, when your body wants to bind up iron and transport it where it needs to go

decreased in anemia of chronic disease

normal in lead poisoning

decreased in sideroblastic anemia

normal in thalassemia

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18
Q

Anemia of chronic disease

A

decreased serum iron
increased or normal ferritin
decreased TIBC

iron:TIBC ratio is normal or high (>18%)

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19
Q

Lead poisoning

A

serum iron is normal or increased

ferritin and TIBC are normal

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20
Q

Sideroblastic anemia

A

increased serum iron
increased serum ferritin
decreased TIBC

ringed sideroblasts build up in erythroblast, RBC precursors

seen in the bone marrow

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21
Q

Thalassemia

A

increased serum iron
normal ferritin
normal transferrin and TIBC

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22
Q

lead poisoning anemia

A 
fatigue, weakness
crampy abdominal pain
joint pain
HA
short-term memory loss
lead lines on gums
peripheral neuropathy

Labs:
decreased MCV

peripheral blood smear:
basophilic stippling (basophilic dots, granules of denatured RNA all over the cell)
-lead poisoning
-thalassemia
-alcohol use

no central pallor

Treatment:
adults- EDTA, succimer
children- EDTA, succimer, dimercaprol if severe

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23
Q

Megaloblastic anemia

A 
impaired DNA synthesis
B12 deficiency
folate deficiency (suspect in elderly with poor nutrition, and alcoholism, drug induced- phenytoin)
hypersegmented PMN (more than 6 lobes)
H and P:
poor nutrition
inflammation of the tongue (glossitis)
no neurologic symptoms
How do we diagnose folate deficiency anemia?

Just give PO folate supplements anyway
To look at folate levels over time, check RBC folate level

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24
Q

What test gives a measure of RBC folate level over time

A

RBC folate level

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25
Q

B12 deficiency anemia

A

pernicious anemia- autoantibodies attack gastric parietal cells in the stomach
so that the body can’t make IF

inadequate B12 intake (vegetarian)

Note: folate insufficiency develops a lot more quickly than B12 deficiency

Resection of the ileum

Bacterial overgrowth

Diphyllobothrium latum infection (fish tapeworm)

H and P
peripheral neuropathy
paresthesias
ataxia
loss of vibration sense
dementia

labs:
megaloblastic anemia
decreased B12 levels
high serum MMA and homocysteine (intermediate byproducts that build up with B12 is insufficient)

Schilling test (out-dated)

Treatment:

  • IM B12
  • dietary B12 supplements
  • Intranasal B12
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26
Q

Anemia of chronic disease

A

Anemia in patients with chronic inflammatory states

DM

defect in iron mobilization and utilization

total body iron content is normal

serum iron levels may be low

Treatment:
treat the underlying disorder
supplemental erythropoietin to hgb 11 or 12

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27
Q

Aplastic anemia

A

pancytopenia from bone marrow failure (leuopenia and thrombocytopenia as well)

Causes:
radiation
drugs
toxins
viral infection (EBV, HIV, parvovirus)
SCD- parvo B19 aplastic crisis
idiopathic
congenital

H and P
anemia (weakness, pallor, fatigue)
leukopenia (persistent infections)
thrombocytopenia (poor clotting, easy bruising, petechiae)

Labs: pancytopenia
hypocellularity
IH: fatty infiltration, with aplastic anemia

Treatment:
address underlying cause
bone marrow transplant

worse the older you get

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28
Q

What conditions are associated with schistocytes (fragmented RBCs)

A

hemolytic anemia

DIC, TTP, HUS

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29
Q

Acanthocytes (spur cells)

A

abetalipoproteinemia

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30
Q

Echinocytes (burr cells)

A

uremia, hemolysis

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31
Q

Bite cells

A

G6PD deficiency

it’s macrophages that bite the Heinz bodies

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32
Q

Basophilic stippling of RBCs

A

lead poisoning

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33
Q

peripheral neuropathy + ringed sideroblasts

A

lead poisoning

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34
Q

hypersegmented PMNs

A

megaloblastic anemia

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35
Q

Heinz bodies (denatured hgb in RBC)

A

G6PD deficiency

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36
Q

Sideroblastic anemia

A

anemia due to defects in the heme synthesis pathway

May be inherited (genetic)
or acquired (alcohol abuse, INH, lead poison, zinc tox, copperdeficiency)

High RDW
MCV low, hypochromic

sideroblasts are normal nucleated RBC precursors with visible iron granules in their cytoplasm, found in the bone marrow

Ringed sideroblasts, which have iron granules surrounding the nucleus, are NOT normal.

Treatment: 
Supplement vitamin B6 (pyridoxine)
Address underlying cause, stop alcohol
Transfusions
Erythropoietin
Deferoxamine or phlebotomy if patient is iron-overloaded

myelodysplasia with ringed sideroblasts also exists and can progress to acute leukemia

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37
Q

Alpha Thalessemia

A

alpha thalessemia- defect in alpha globin

more prevalent in patients of African and Asian descent

alpha thalessemia minima: 1 mutated allele, asymptomatic

alpha thal minor or trait: 2 mutated alleles, asymptomatic

HbH disease: 3 mutated alleles
a ton of beta globin
made of 4 beta globin molecules
microcytosis
chronic hemolysis

Hemoglobin Bart’s: 4 mutated alleles, incompatible with life
made of 4 gamma globins
hydrops fetalis (leads to death)

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38
Q

Beta thalessemia

A

defect in beta globin
mediterranean populations

beta thal minior:

  • decreased amounts of beta- globin
  • minimal anemia
  • increased HbA2, made of alpha globin and gamma globin

Beta thal major:
no beta globins at all
HbA2 and HbF
more severe anemia

target cells: central darkening, surrounded by pallor, then more darkening on the outside

39
Q

thalassemia complications:

A

iron overload due to transfusions: iron chelator (deferoxamine) for iron overload

rule out thalessemia before starting iron supplements on an anemic patient. Rule out can be done with hemoglobin electrophoresis

40
Q

How long does HbgF stick around for?

A

6 months

41
Q

SCD

A 
H and P
sickle cell pain episodes
infection
hypoxia 
trauma
bone pain/infarction: fish vertebrae (middle infarcts, so the vertebrae get narrow in the center)

osteonecrosis of the femoral head or humoral head

hair on end on skull xray

chest pain
stroke
painful swelling of hands and feet

dyspnea
priapism
splenomegaly
jaundice
leg ulcers
labs:
anemia
sickling
HbS
increased HbF
Treatment:
hydration
oxygen
analgesics
folate
longterm management with hydroxyurea, increased HbF
avoid triggers, stay healthy
Treatment: 
pneumococcal vaccine especially if asplenic
HiB 
Meningococcal vaccine
hep B vaccine
annual flu vaccine

prophylactic penicillin until age 5
Transfusions
Stem cell transplant
Gene therapy

Complications:

  • chronic anemia
  • pulmonary htn because of occlusion of pulmonary vasculature
  • heart failure
  • aplastic crisis
  • acute chest syndrome (cp, hypoxemia, pulm infiltrates)
  • stroke
  • osteonecrosis
  • autosplenectomy

vaccinate against Hib, pneumococcus, meningococcus, influenza, hep B

  • increased risk of infection
  • salmonella osteomyelitis
  • strep pneumo
  • h, influenzae
  • meningococcus
  • klebsiella
42
Q

What complication occurs in 10% of patients with sideroblastic anemia?

A

acute leukemia

43
Q

Osteomyelitis in a sickle cell patient

A

salmonella

44
Q

What can cause lymphopenia without immunodeficiency?

A

increased cortisol levels
chemotherapy
radiation
lymphoma

45
Q

What can cause eosinophilia?

A

Collagen-vascular disease
Atopic diseases (allergies, asthma, Churg-strauss, allergic bronchopulmonary aspergillosis)
Neoplasm
Adrenal insufficiency (Addison disease)
Drugs (NSAIDs, penicillins, cephalosporins)
Acute interstitial nephritis

Parasites (strongyloides, ascaris- loffler eosinophilic pneumonitis) other causes include HIV, hyper IgE syndrome, coccidiomycosis, etc)

46
Q

Neutropenia

A

viral infections: viral hepatitis, HIV, EBV

certain drugs
chemotherapy
aplastic anemia

H and P
recurrent infections

Treatment:
G-CSF
GM-CSF
Steroids

47
Q

How do we manage neutropenic fever? in a cancer patient

A

admit the patient for observation
culture blood, urine, CSF
broad-spectrum abx
narrow down abx after you’ve isolated an organism

48
Q

Type 1 hypersensitivity

A

mediated by IgE antibodies, cross-link antibodies on mast cells

mechanism: degranulation of mast cells

hives, pruritis, bronchospasm, oropharyngeal angioedema, allergic rhinitis, asthma, anaphylaxis

Treatment:
antihistamines
leukotriene inhibitors
bronchodilators
corticosteroids
49
Q

Type II hypersensitivity

A

mediated by IgM and IgG antibodies directed towards self cells

bind to specific antigens, and activates the complement cascade

examples:

  • drug- induced hemolytic anemia
  • immune hemolytic anemia
  • hemolytic disease of the newborn
  • immune thrombocytopenia
  • acute rheumatic fever
  • Goodpasture syndrome
  • Bullous pemphigoid
  • Pemphigus vulgaris
  • Graves disease
  • Myesthenia gravis

Treat:
anti-inflammatories
immunosuppressive agents
plasmapheresis

50
Q

Type III hypersensitivity

A

mediated by IgM and IgG immune complexes against soluble antigens (soluble in the blood)

The immune complexes deposit in tissues, and there they initiate complement cascade

Examples:
Arthus reaction
serum sickness
glomerulonephritis

Treatment:
anti-inflammatories

51
Q

Type IV hypersensitivity

A

T cells and macrophages
delayed-type hypersensitivity

mechanism:
T cells present antigens to macrophages

examples:
Transplant rejection, contact dermatitis, PPD testing

Treatment: steroids, immunosuppressants

52
Q

Anaphylaxis SU138

A 
severe type 1 hypersensitivity
MCC drugs
also,
insect stings
latex
eggs, nuts, seafood

H and P
si/sx 5-50 minutes after exposure

tingling in the skin
pruritis
chest tightness
angioedema (can't breath, can't swallow)
syncope 
tachycardia
wheezing
urticaria
hypotension
treatment:
ABCs, intubate if necessary
stop the offending agent
epinephrine
H1/H2 blockers, helps with itching but not airway
bronchodilators
steroids (maybe)
IV fluids if hypotension because you are trying to fill up the vascular space that opens up 2/2 vasodilation
53
Q

Thrombocytopenia

A

PLT

54
Q

Thrombocytopenia may be due to impaired platelet production

A 
drugs
infections
aplastic anemia
folate and B12 deficiency
alcohol, toxic to the bone marrow

bone marrow will show reduced or abnormal megakaryocytes

Treatment: stop the offending agent, initiate bone marrow transplant if needed

55
Q

drugs that cause thrombocytopenia

A 
Heparin, abciximab
carbamazepine, phenytoin, valproate
cimetidine
acyclovir, rifampin
sulfonamides (eg sulfasalazine, TMP-SMX)
procainamide, quinidine
quinine, gold compounds
56
Q

Splenic sequestration of platelets

A

splenomegaly
normal one marrow biopsy

Splenectomy can be curitive

57
Q

HIT

A

Thrombosis plus thrombocytopenia (sudden decrease in platelet count by at least 50%)

  • heparin forms complexes with platelet factor 4
  • antibodies against the complex cause platelet activation and aggregation (hypercoagulable thrombopenic state)
  • platelets are removed from circulation

Labs:

  • serotonin release assay (gold standard, but expensive)
  • immunoassay (ELISA) detects platelets
  • heparin- induced platelet aggregation assay (specific, but not sensitive)

Treatment: stop heparin, get labs to confirm the diagnosis

anticoagulate with direct thrombin inhibitor like argatroban until PLT gets about 100,000 or so
Then switch to warfarin for 3 months, or direct thrombin inhibitor

These patients should avoid heparin

58
Q

Immune thrombocytopenia

A

anti-platelet antibodies

platelet count

59
Q

TTP-HUS

A

thrombotic thrombocytic purpura and hemolytic uremic syndrome

deficiency of metalloprotease, leading to excessive platelet aggregation

associated with E.COli O157:H7

HUS triad:
hemolysis,
uremia,
thrombocytopenia

TTP pentad:
hemolysis, 
uremia,
thrombocytopenia 
neurologic sequelae
fever

Fever, Anemia, Thrombocytopenia, Renal, Neuro symptoms (FAT RN)
all features do not have to be present at once

Treatment:
steroids
plasmapheresis
FFP

60
Q

Antiphospholipid syndrome

A

antiphospholipids against specific phospholipids, increasing risk of thrombocytopenia and hypercoagulability

seen in
pregnancy
lupus
other autoimmune diseases

61
Q

HELLP syndrome

A

sequelae of eclampsia/pre-eclampsia

HELLP:
Hemolysis
Elevated Liver enzymes
Low Platelets
(Hypertension)

Treat by inducing labor, and delivering the baby

62
Q

vWF disease

A

autosomal dominant deficiency of vWF and sometimes factor 8

MC inherited bleeding disorder

vWF is released into local circulation from endothelial cells
1. It helps platelets adhere to vessel walls and crosslink with one another
2. it stabilizes factor VIII
This is important for formation of fibrin clot

Labs:
increased PTT due to factor 8 dysfunction
increased BT
decreasd RISTOCETIN COFACTOR activity
decreased vWF antigen
normal platelet count, platelets are normal too, they just won’t work

H and P:
easy bruising
mucosal bleeding
menorrhagia

Tx:
Desmopressin (induces vWF secretion), first-line for acute bleeding
Cryoprecipitate or factor VIII concentrates for severe or refractory bleeding

OCP for menorrhagia

avoid aspirin and other platelet inhibitors

63
Q

What are the only 2 factors not synthesized by the liver

A

vWF
factor 8

these remain at normal levels even when there is liver failure

64
Q

Vitamin K deficiency

A

10,9,7,2,c,s

poor intake (green leafy vegetables)
malabsorption
eradication of gut flora that produce vitamin K

H and P:
easy bruising
mucosal bleeding
melena
hematuria
delayed clot formation
macrohemorrhage

Labs:
increased PT, INR

Treatment:
PO or IM vit K
FFP for acute bleeding

RF:
ESRD

65
Q

Hemophilia B (factor 9) “Benign”

Hemophilia A “Eight”

A 
H and P
uncontrolled bleeding that is spontaneous, following minimal trauma, after surgery
hemarthrosis
IM bleeding
GI and GU bleeding

This is a macrohemorrhage, fibrin clot issue

Labs:
increasd PTT
normal PT
normal BT

Treatment: 
Hemophilia A- give factor VIII
Hemophilia B- give factor IX
Desmopressin can induce factor VIII release
Transfusions may be needed

Complications: hemophilia can lead to death from severe uncontrolled bleeding

66
Q

Disseminated intravascular coagulation SU 141

A

excess clotting leads to hypocoagulability

STOP Making Thrombi
Sepsis
Trauma
OB complications
Pancreaitis
Malignancy
Transfusions
H and P
uncontrolled bleeding
hemoptysis
jaundice
distal cyanosis
hypotension especially with sepsis
Labs:
decreased platelets
increased bleeding time
increased PT
increased PTT
everything is messed up
decreasd fibrinogen (all being used up)
increased D-dimer

Schistocytes

Treatment:
treat the underlying cause
if platelets are diminished, replace platelets

If PT and PTT are increased, give FFP or cryoprecipitate

+/- heparin

67
Q

Hypercoagulable states

A

due to coag cascade defects

Factor V Leiden mutation (most common)
Antithrombin deficiency
Protein C deficiency
Protein S deficiency

Prothrombin gene mutation (prothrombin G20219A)

Screen if patient has recurrent DVT or fhx of DVT

anticoagulate for life only if they’ve had thrombotic event(s)

68
Q

What’s the teratment for vWF disease?

A

DDAVP
for severe bleeding, cryoprecipitate or factor VIII concentrates
OCPs
avoid aspirin and other platelet inhibitors

69
Q

most common mutation leading to venous thrombosis in white patients?

A

factor V Leiden mutation

70
Q

How do we treat the hemotologic infection known as sepsis?

A
  1. secure the airway, give oxygen
  2. give IV fluids
  3. Give vasopressors (NE is choice)
  4. Colloid can help bulk up intravascular volume
  5. If the pressors aren’t working, consider adrenal insufficiency and glucocorticoids as treatment
  6. Broad spectrum antibiotics initially. Avoid antibiotics before culturing to avoid false negative cultures
  7. glycemic control between 140 and 180. If you gave glucocorticoids or the patient has DM, consider giving insulin
71
Q

Malaria medications

A 
chloroquine
primaquine
quinine
atovaquone/proguanil
mefloquine
72
Q

Abnormal T cells fighting off infected B cells

A

Infectious mononucleosis
Downey cells

Teenagers and young adults get this infection

90-95% of adults are seropositive

symptoms appear 2-5 weeks after infection

H and P:
3-6 months of fatigue
sore throat
malaise
lymphadenopathy- posterior primarily
splenomegaly
fever
tonsillar exudates

can have comorbid strep throat

Labs: 
positive heterophil abs
positive Epstein-Barr serology
elevated LFTs
hemolytic anemia
thrombocytopenia
increased lymphocytes

Tx:
supportive care
self- limited
reassurance
there is no antiviral medication available
NSAIDs or acetaminophen for fever, sore throat, malaise
Encourage rest and plenty of fluids
Return to sport (risk of splenic rupture)
-may return gradually to noncontact sports 3 weeks after symptom onset
-may return gradually to contact sports 4 weeks after symptom onset
Steroids only helpful if impending airway compromise due to enlarged tonsils or if life- threatening sequelae develop (fulminant liver failure, hemolytic anemia, thrombocytopenia)

Complications:
splenic rupture
aplastic anemia
DIC
HUS-TTP
73
Q

SIRS criteria

A

38.390

RR>20

12,00010% bandemia

74
Q

Acute phase HIV presentation

“acute retroviral syndrome”

A 
fever, myalgias, fatigue
HA
sore throat
rash
lymphadenopathy
mucosal ulcers
persistent high fevers
75
Q

What does latent phase HIV look like?

A

several years without symptoms while the virus is destroying lymphocytes

76
Q

Late phase HIV (AIDS)

A 
opportunistic infections
AIDS-defining illnesses
weight loss 
night sweats
neurological changes
recurrent/unusual infections
77
Q

wasting syndrome

A

CD410% of baseline

H and P:
chronic diarrhea
weakness
fever

Tx: HIV meds and supportive care, antiretroviral therapy, appetite stimulants (megestrol)

78
Q

AIDS dementia

A

CD4 may be over 200
intellectual decline, ataxia, apathy due to virus. Treat with antiretroviral therapy

diagnosis: cerebral atrophy on CT or MRI

79
Q

Bacterial pneumonia

A

streptococcus pneumoniae
haemophilus influenzae
nocardia

severe symptoms:
productive cough
high fever
hypoxia

diagnosis: sputum gram stain, lobar consolidation on CR, diffuse, nodular infiltrates on CXR

Treatment: pathogen specific

80
Q

Candida esophagitis

A

an AIDS- defining illness

CD4

81
Q

Pneumocystis jirovecii pneumonia

A

CD4 35 mmHg

82
Q

Tuberculosis

A

also AIDS- defining

CD4

83
Q

Histoplasmosis

A

CD4

84
Q

Toxoplasmosis

A

AIDS- defining

H and :
HA, confusion, fever, focal neurological symptoms, seizures

Dx:multiple ring- enhancing lesions on CT or MRI
Tx:
pyrimethamine + sulfadiazine+ leucovorin

or pyrimethamine + clindamycin

85
Q

Lymphomas (esp CNS or non-Hodgkin)

A

CD4

86
Q

Progressive multifocal leukoencephalopathy (JC virus)

A

a demyelinating disease

CD4

87
Q

Cryptococcal meningitis

A

CD4

88
Q

CMV

A

CD4

89
Q

Mycobacterium avium intracellulare complex (MAC)

A

CD4

90
Q

HIV screening

In what way do we capture all the true positives and then weed out the false positives

A

99% sensitive for HIV antibodies

If positive, then repeat ELISA is performed

Preliminary positive= both screening tests were positive

Confirm with specific western blot to screen out false positive

91
Q

HIV screening tests:CD4 count, significance

A

tracks disease progression

clinical improvement during HIV treatment- how is HIV affecting the immune system?

92
Q

HIV viral load, significance

A

measures viral replication in the blood

PCR- amount of virus in a sample of blood

how useful is the antiretroviral regimen

may show evidence of acute infection prior to ab response

93
Q

What combination of drugs do you give for HIV prevention after a needle stick?

A

emtricitabine+ tenofovir+raltegravir

STEP2 (34 decks)

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