We thoroughly check each answer to a question to provide you with the most correct answers. Found a mistake? Tell us about it through the REPORT button at the bottom of the page. Ctrl+F (Cmd+F) will help you a lot when searching through such a large set of questions.<\/p>\n\n\n\n
Due to the essential nature of washing your hands, how much time is recommended to wash your hands?
10 seconds
20 seconds
1 minute
4 minutes
Before responding to a first aid scenario, what is the first question you should ask at the scene?
Age of the injured or ill person
Safety of the scene
Nature of the injury
Time of the injury
You come upon a person who has lost a significant amount of blood, has a very pale skin color, and is confused. What do you suspect the cause to be?
Seizure
Stroke
Low blood sugar
Shock
Personal protective equipment consists of the following items:
Gloves
Mask
Eye shield
All of the above
While dining out in a restaurant you hear a mother cry out that her six-month-old child, who was given some marbles by an older child, is gagging. His mouth area is turning blue and he\u2019s unable to take a breath or cry out. What would you do first in this scenario?
Begin CPR
Attempt rescue breaths then compressions
Deliver back blows and chest thrusts
Blind finger Sweep
A stroke consists of which following signs?
ConfusionIncorrect response
Chest pain
Facial droop
Nausea
While performing CPR on an infant, another rescuer appears on the scene, what do you do next?
Immediately transport the patient
Wait until exhausted, then switch
Have the second rescuer help with CPR, to minimize fatigue
Have the second rescuer begin ventilations; ratio 30:2
What would be the most likely scenario if a 20-year-old dove headfirst off a dock and once they reached the surface of the water didn\u2019t appear to be moving?
Heart attack
Low blood sugar
Neck injury
Mammalian diving reflex
Where should you place the AED pads when treating an infant for pediatric cardiac arrest?
Chest and back
Do not use an AED on an infant
Upper chest and mid abdomen
Wherever they fit
You are first to the scene and you find an unresponsive person with no pulse that has thrown up. You feel CPR is not something you are comfortable giving them. What would be the next best thing for you to do?
Wipe off the face or cover with a shirt
Compression only CPR
Go and get help
Do not initiate resuscitation
How long should you check for breathing while performing CPR?
Do not check for breathing, continue chest compressions
2 seconds
5 seconds
No longer than 10 seconds
What would your next step be after you are performing single-person CPR and the AED (Automatic External Defibrillator) advises a shock?
Call for help
Resume CPR with chest compressions
Check for a pulse
Resume ventilation
After finding an unresponsive child, yelling for help, and confirming the child isn\u2019t breathing what would be your next course of action?
Leave the child and search for an AED
Deliver rescue breaths as most cardiac arrest occur due to breathing problems
Begin back blows and chest thrusts
Deliver 30 chest compressions
As a daycare provider that is working alone, one of your three-year-old children isn\u2019t feeling well and lays down for a nap. After checking on the child, you notice they are not breathing and are blue in color. What would be the best step to take?
Do back blows.
Do a blind finger sweep.
Call 911.
Deliver two minutes of CPR
When you try to give an unresponsive adult a rescue breath and the chest does not appear to rise, what would you do next?
Perform abdominal thrusts
Begin CPR
Go call 911
Repeat the head tilt\/chin lift maneuver and attempt the breath again
What do you do if an infant is choking and while trying to assist them they become unresponsive?
Leave the infant to get help.
Do a blind finger sweep
Begin CPR.
Do abdominal thrusts.
After finding someone who is unresponsive, has a pulse but does not appear to be breathing, you find you are unable to give them CPR, what do you do next?
Begin CPR
Repeat the head tilt\/chin lift maneuver and attempt the breath again
Abdominal thrusts
Heimlich maneuver
AED pads can be used for children at what age?
17
16
14
Up until puberty
Arriving first to the scene, you find an unresponsive person with no pulse that has thrown up. You feel CPR is not something you are comfortable giving them. What would be the next best thing for you to do?
Wipe off the face or cover with a shirt
Compression only CPR
Go and get help
Do not initiate resuscitation
Properly operating an AED include the following steps:
Power on the AED, attach electrode pads, shock the person, and analyze the rhythm
Power on the AED, attach electrode pads, analyze the rhythm, and shock the person
Go and gePower on the AED, analyze the rhythm, attach electrode pads, and shock the person
Power on the AED, shock the person, attach electrode pads, and analyze the rhythm
Read Also: CPR Pretest<\/p>\n\n\n\n
What is the rate for chest compressions per minute for any age?
100 compressions per minute<\/p>\n\n\n\n
The compression-ventilation ratio for one or two rescuers for ADULT CPR is?
30 compression to 2 ventilation breaths<\/p>\n\n\n\n
The compression-ventilation ratio for one or two rescuer CHILD or INFANT CPR is?
15 compressions to 2 ventilation breaths<\/p>\n\n\n\n
Where should the hands be placed on the chest for adult CPR?
hands should be placed on the lower half of breast bone<\/p>\n\n\n\n
What is the preferred hand technique for two rescuer infant CPR?
2 thumb \u2013 Thumb & encircling hand technique (compressions with thumbs)<\/p>\n\n\n\n
What is the depth of compressions on an adult?
2 inches<\/p>\n\n\n\n
What is the depth of compression on an infant?
\u2153 the depth of the chest size or 4 cm<\/p>\n\n\n\n
The rescuers knows its rescue breaths are effective when what happens?
When the chest rises<\/p>\n\n\n\n
What is the first step in using an AED?
Turn it on<\/p>\n\n\n\n
After an AED shock is delivered, what is the next step?
Check for breathing. If there isn\u2019t an breathing occurring, begin compressions and respirations.<\/p>\n\n\n\n
Why is high quality CPR and compressions necessary?
High quality CPR is necessary because is provides adequate blood flow and oxygen circulation throughout the body when done correctly.<\/p>\n\n\n\n
When is scene safety assessed?
When you first arrive at the scene<\/p>\n\n\n\n
Interruptions to CPR should take more than _<\/em> seconds. Chest compressions should be initiated within _<\/em> seconds if identifying victim is not responsive and has no pulse. In two rescuer CPR, the first rescuer starts ______<\/strong><\/em><\/strong><\/em> while the seconds rescuers _<\/em><\/strong><\/em><\/strong> _ _. If a choking victim becomes unresponsive, the rescuer should first call for help (or EMS) and begin _<\/strong>. Rescue breaths for a CHILD or INFANT should be one breath every ____<\/em><\/strong><\/em><\/strong>. Rescue breaths for an ADULT should be one breath every __<\/strong><\/em><\/strong>. How do you relive choking in an INFANT? How do you relieve choking in an ADULT? If any choking victim goes unresponsive, what additional step do you perform before breathing? Blod smear Microlytic anemias Normocytic \u2013 nonhemolytic Hemolytic \u2014 intrinsic Hemolytic extrensinc Macrocytic -Megaloblast Macrocytic \u2014 Non megaloblastic Physical features of iron deficiency anemia Iron transport Iron storage What is iron used to make Hemoglobin electrophoresis- sickle cell<\/p>\n\n\n\n megaloblastic anemias Rule of 3\u2019s<\/p>\n\n\n\n Drug-Induced hemolysis Hereditary Spherocytosis G6PD deficiency: Hemolytic anemia due RBC Enzyme defect\u200b HGB RBC HCT MCV MCH MCHC Observed reticulocyte count RDW Anemia due to premature red cell destruction<\/p>\n\n\n\n Corrected reticulocyte count Anemia due to insufficient red cell production<\/p>\n\n\n\n Anemia due to insufficient hemoglobin synthesis<\/p>\n\n\n\n Anemia due to impaired DNA synthesis microcytic hypochromic macrocytic normochromic Rule of three Chronic iron defiecny What vitamins are especially needed for adequate cell division?\u200b Right Shift Lift shift Neutrophils Lymphocytes Eosinophils Monocytes Basophils Leukemia Hyperplasia Hypoplasia Dysplasia Aplasia Autoimmune Autoimmune B cell autoantibodies Aplastic Anemia Idiopathic autoimmune treatment Autoimmune disease associations Neupogen Cyclosporine and prednisone Radiation induced marrow aplasia Impact of Dose fractionation Myelophthisic Anemia\u200b Isolated anemia Luekopenia Thrombocytopenia PK pathway Phenotype and genotype for G6PDA- Phenotype and genotype G6PDB- Principle pathway product that is deficient in RBCs of a person with PK deficiency Sickle cell gel technique Sickle mode of inheritance hemoglobin C disease Mode of inheritance of hereditary sperocytosis \/ population Mode of inheritance of hereditary elliptocytosis \/ population Most prevalent enzyme disorder in the world How HE mutations alter normal spectrin function.\u200b Metabolic pathway that G-6-PD is involved in Product that is deficient in RBCs of a person with a G-6-PD deficiency.\u200b Diagram and explain the relationship between NADPH, glutathione and hydrogen peroxide in RBCs.\u200b Similarity between HS and HE normocytic anemias Hereditary spherocytosis mutations Hereditary Spherocytosis\u200b microvessicles HS autosomal recessive Spectrin HS autosomal dominant Hemolytic Anemia cues PK Deficiency Genetics\u200b Location or RBC destruction Pathogenesis of AIHA\u200b types of AIHA based on direct coombs test Warm AIHA Warm AIHA symptoms Cold AIHA symtoms Causes of Warm AIHA Causes of Cold AIHA Treatment options for Warm AIHA Incomplete phagocytosis results in wAIHA Treatment options for cold AIHA Pathogenesis of cAIHA Pathogenesis of wAIHA\u200b Pathway of cAIHA Why do infections cause autoimmunity Beta globin Alpha globin Thalassemia genetics Alpha thalassemia \u2013 one deletion Alpha thalassemia \u2013 two deletions Hemoglobin H Disease Alpha thalassemia \u2013 three deletions Alpha thalassemia \u2013 four deletions Alpha Thalassemias\u200b \u2014 treatment Ferratin in thalassemia vs. iron deficiency Silent Carrier State for\u200b \u03b2-Thal Minor\u200b \u03b2-Thal Intermedia\u200b Beta Thalassemia Major\u200b Beta Thalassemia Major- appearance Mentzer index for children (MCV\/red blood cell count) for Thalassemia vs. iron Quantitative defects of globin chain synthesis result in hemoglobinopathies Sideroblastic anemias Qualitative defects of globin chain synthesis result in hemoglobinopathies Sideroblastic Anemia Etiology Causes of iron deficiency in infants and young children Causes of iron deficiency in infants and young women Causes of iron deficiency in older adults The earliest lab result that might suggest an iron deficiency prior to anemia.\u200b Contrast the functions of transferrin and ferritin. How does reduced hemoglobin production result in a microcytic anemia.\u200b Lab results for stage 1 iron deficiency Lab results for stage 2 iron deficiency Diagram the distribution of iron in a healthy individual.<\/p>\n\n\n\n Lab results for stage 3 iron deficiency Anisocytosis Ferrous Ferric Target cell % saturation TIBC 5\u2019\/3\u2032 UTR Erythrocyte Size IREs\/ IRP poikilocytosis Apoferritin Hepcidin Transferrin receptor Fe Salts Low iron IRP High iron IRP Folate B12(hydroxocobalamin) GM-CSF (sargramostim) Hydroxyurea Thrombopoietin (romiplostim) IL-11 (oprelvekin) How are growth factors given G-CSF (filgrastim) Erythropoietin Pernicious anemia Antibodies against parietal cells would What antibody effector function is used against IF?\u200b Causes of chronic gastritis How to diagnose pernicious anemia Ectoparasites Treatment of pernicious anemia\u200b Definitive host Endoparasites Cestode Trematode Pituitary and Adrenal gland Reservoir host Three factors key to transmission of parasites Nematodes \u2013 roundworms Hepcidin and inflammation Hypothyroidism anemia Anemia of Chronic Disease:\u200b Erythrocyte sedimentation rate Bacteremia C Reactive protein Clinical Manifestations of Sickle Cell Disease\u200b Viremia Infection-mediated Hemolytic Anemia life cycle of Babesia microti Clostridium perfringens How to diagnose and prevent Babesiosis.\u200b Carrion\u2019s Disease 2 phases Carrion\u2019s Disease treatment Clostridium perfringens mechanism of infection Life cycle of malarial parasite Vectors for malarial parasite Malaria prevention Chloroquine Differentiate malaria from babesiosis based on laboratory and clinical findings.\u200b<\/p>\n\n\n\n Verruga Peruana wart Atovaquone Azithromycin\u200b Clindamycin\u200b Quinine\u200b LUMEFANTRINE malarial paroxysm MEFLOQUINE PRIMAQUINE TETRACYCLINES\u200b We thoroughly check each answer to a question to provide you with the most correct answers. Found a mistake? Tell us about it through the REPORT button at the bottom of the page. Ctrl+F (Cmd+F) will help you a lot when searching through such a large set of questions. 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10<\/p>\n\n\n\n
10<\/p>\n\n\n\n
starts chest compressions; call 911. (or activated AED and\/or provides help with airway)<\/p>\n\n\n\n
CPR<\/p>\n\n\n\n
3-5 seconds<\/p>\n\n\n\n
5-6 seconds<\/p>\n\n\n\n
5 back slaps, 5 chest thrusts<\/p>\n\n\n\n
abdominal chest thrust (Heimlich maneuver)<\/p>\n\n\n\n
CPR, look, and remove if there is anything visible in the back of the victims airway<\/p>\n\n\n\n
Gray platelets missing their typical granules<\/p>\n\n\n\n
siderblastic anemia, ACD, Lead posioning, Thalassemias, Irondeficiency late<\/p>\n\n\n\n
Reticulocyte count is normal or decrease
Iron def. early. ACD. aplastic anemia. chronic kidney disease<\/p>\n\n\n\n
High reticulocyte count
RBC membrane defect \u2014 hereditary spherocytosis, G6pD, HbC sickle cell<\/p>\n\n\n\n
Autoimmune, infections<\/p>\n\n\n\n
folate deficiency, B12m orotic aciduria<\/p>\n\n\n\n
liver disease, alcoholism, diamond blacking<\/p>\n\n\n\n
angular cheilitis, Plummer vinsons
Plummer vinson syndrome
Plummer vinson syndrome<\/p>\n\n\n\n
Transferrin<\/p>\n\n\n\n
Ferritin \u2014 may be false high if patient has an active infection or inflammation<\/p>\n\n\n\n
Hemoglobin, myglobin, enzymes<\/p>\n\n\n\n
megaloblastic anemias
megaloblasts in marrow as well \u200b
as macrocytes in the peripheral bloold<\/p>\n\n\n\n
Penicillin the drug can bind to the RBC membrane so now the body sees it as a foreign antigen so. Now you\u2019re destroying your own RBC that have this medication bound to it \u200b<\/p>\n\n\n\n
Abnormal cytoskeletal proteins (spectrin, ankyrin, band 3 and protein 4.2) are unstable and have less flexibility.\u200b
An impaired membrane with this permeability defects allows Na+ to accumulate in the cell, while allowing the escape of K+
Destruction of cells \u2014 jaundice
Cells will pop at lower water concentrations<\/p>\n\n\n\n
maintains the level of the coenzyme nicotinamide adenine dinucleotide phosphate (NADPH).\u200b
NADPH restores the level of glutathione which protects the red blood cells against oxidative damage.\u200b
neonatal jaundice, favism, hemolysis by oxidant drugs<\/p>\n\n\n\n
Hemoglobin concentration \u2014 the concentration of hemoglobin the blood<\/p>\n\n\n\n
The concentration of RBC in the whole blood<\/p>\n\n\n\n
Hematocrit \u2014 volume percentage of whole blood occupied by RBC
3 x HGB<\/p>\n\n\n\n
Mean corpuscular volume
he average volume of a circulating erythrocyte.\u200b
80-100
higher in large cell<\/p>\n\n\n\n
Mean corpuscular hemoglobin
The quantity of hemoglobin in the average circulating erythrocyte.\u200b
higher in larger cells<\/p>\n\n\n\n
Mean corpuscular hemoglobin concentration
concentration of hemoglobin in the average RBC in circulation
same based on cell size<\/p>\n\n\n\n
Reticulocytes are typically reported as a percentage of the total erythrocytes.\u200b<\/p>\n\n\n\n
CV \u2014 calculated by measuring the curve width at the point that is \u22131 standard deviation from the MCV, then dividing that number by the MCV.\u200b Minimize effects of small population of abnormal cells
SD is calculated by measuring the curve width at the point where 20% of cells have that volume \u2014 Reticulocytes have greater effect<\/p>\n\n\n\n
OR x patients HCT \/ mean normal HCT
Female hematocrit RR = 37% to 47%\u200b
Mean would be 37+47 \/ 2 \u2014> 42\u200b<\/p>\n\n\n\n
Insufficient supply of nucleotides will slow down the rate of DNA synthesis which means slower cell cycle progression
No problem in protein syntehsis so you\u2019ll result in microcytes
decreased reticulocyte count, B12 and folate deficiency<\/p>\n\n\n\n
Anemia due to impaired HGB syntesis \u2013> iron deficiency<\/p>\n\n\n\n
Anemia due ti impaired DNA synthesis \u2014 Folate or B12 deficiency<\/p>\n\n\n\n
RBC x 3 = HBG
HGB x 3 = HCT<\/p>\n\n\n\n
cause of limited protein synthesis , any stores of reticulocytes have been release but erthryopotein would be elevated<\/p>\n\n\n\n
Folic acid is converted to tetrahydrafolate which is essential for purine (G\/A) and thymidine synthesis.\u200b
Vit. B12 Involved in the conversion of N5-methyltetrahydrafolate into THF.\u200b<\/p>\n\n\n\n
No production of immature neutrophils in the bone marrow\u200b
Indicates bone marrow suppression \u200b
Hyper-segmented
Lymphocytes<\/p>\n\n\n\n
Occurs when increased bands and less mature neutrophils are present in the blood, along with a lower average number of lobes in segmented cells\u200b<\/p>\n\n\n\n
Decreased in hereditary netropenia, bone marrow disease, viruses
Increased in bacterial infections, tumors (left shift)
TH17<\/p>\n\n\n\n
Decreased \u2014 Congenital immunodeficiency diseases, severe infections, corticosteroids, HIV
Increase\u2013 Viral infections, some fungi\/ parasites, pertussis (right shift)
important in viral infections \u2014 CD8 T cells<\/p>\n\n\n\n
Decreased in bacterial infections and ACTH
increased in parasitic infections, type 1 hypersensitive and asthma<\/p>\n\n\n\n
Decreased in corticosteroids, hairy cell leukemia
Increased in mycobacterial infections and TB
TH1 response \u2013intracellular bacteria<\/p>\n\n\n\n
Decreased with corticosteroids
Increased in hypersensitivity reactions (1)<\/p>\n\n\n\n
When you have a ton of immature WBC in the periphery (left shift)<\/p>\n\n\n\n
Higher than normal of cells, not abnormal shape<\/p>\n\n\n\n
Incomplete or arrested development of an organ, below number o cells<\/p>\n\n\n\n
abnormal growth noted microscopically, might be premalignant<\/p>\n\n\n\n
Congenital absence of an organ<\/p>\n\n\n\n
usually idiopathic<\/p>\n\n\n\n
Neutropenia
Thrombocytopenia
Anemia<\/p>\n\n\n\n
T-cell mediated, decreased neutrophils, platelets and reticulocytes
looks like tons of fat in the bone marrow<\/p>\n\n\n\n
Combination of immunosuppressive agents and bone marrow growth factors
Neupogen, cyclosporine, prednisone<\/p>\n\n\n\n
RA: rheumatoid arthritis, Felty\u2019s syndrome\u200b
SLE: systemic lupus erythematosis\u200b
Aplastic Anemia<\/p>\n\n\n\n
Colony stimulating factor for white cell growth and proliferation<\/p>\n\n\n\n
immuno suppressant to inhibit current white blood cells from attacking stuff<\/p>\n\n\n\n
Lymphoid and bone marrow cannot handle are amounts of radiation, and the body remembers radiation forever \u2014
Myelofibrosis
Myelofibrosis
reticulin stain to bring out the black fibers<\/p>\n\n\n\n
Give in smaller doses over 6 weeks so that they can tolerate a larger amount
If your total body is exposed to over 800 you\u2019re proabably going to die from other radiation problems \u2013 without planed in one big dose<\/p>\n\n\n\n
Due to marrow infiltration \u2014 solid tumors, liquid tumors, infection (TB, plotts)
Or due to myelofibrosis \u2014 new growth of fibrous tissue or new formation in marrow<\/p>\n\n\n\n
Normal WBC and normal platelets<\/p>\n\n\n\n
Low WBC, neutropenia \u2013 lymphopenia<\/p>\n\n\n\n
Low platelets<\/p>\n\n\n\n
Enzyme in glycolysis that converts phosphoenolpyruvate to pyruvate with the generation of ATP
gene called PKLR
All ATP in RBC is via glycolysis<\/p>\n\n\n\n
most frequent in african populations
affects the stability of the G6PD enzyme. \u2013> so it works fine just has a short half life so affects mostly older RBC
males have low penetrance \u2013> asymptomatic<\/p>\n\n\n\n
Mediterranean populations
affects both the stability of the enzyme and its catalytic activity.\u200b
Affects both young and old RBC
oxidant stress \u2013> hemolysis much quicker<\/p>\n\n\n\n
reduces RBC ATP production.\u200b
effects membrane pumps than maintain membrane flexibility and cell shape \u2014 so they get killed by spleen<\/p>\n\n\n\n
Normal will cut at the mstII site \u2014 110 bp BRC product \u2013> 56 and 54 bp bands
Affected will not be able to cut so they will have 110 bp gel
heterozygote will have 3 bands
cut with MSTII restriction enzyme<\/p>\n\n\n\n
Autosomal recessive disease caused by a very specific mutation in the \u03b2-globin gene (HBB gene).\u200b
Mutation causes an amino acid substitution of valine for glutamic acid at amino acid 6 of the \u03b2-globin protein.\u200b<\/p>\n\n\n\n
Its a lysine now instead of a glutamic acid so its not as severe as sickle cell<\/p>\n\n\n\n
75% autosomal dominant, (20% are due to new mutations)
25% autosomal recessive \u2014 more severe
Most common hemolytic anemia of Northern Europeans<\/p>\n\n\n\n
Mostly autosomal dominant
african and mediterranean populations<\/p>\n\n\n\n
G-6-PD deficiency, x linked so mainly in males, in mediterranean countries, africa and china.
Female carriers are resistant to malaria
avoid oxidant drugs, fauvism, infections (oxidant stress)<\/p>\n\n\n\n
\u03b1\/\u03b2 spectrin dimers cannot form into tetramers.
Mutations are sometimes seen in the genes coding for glycophorin and protein 4.1.\u200b
Elliptical cell<\/p>\n\n\n\n
hexose monophosphate (HMP) shunt.\u200b
catalyzes the oxidation of glucose-6-P to 6-phosphogluconolactone (first step)<\/p>\n\n\n\n
NADPH \u2013> reduced glutathione
without it \u2013> hydrogen peroxide accumulates in the RBC.\u200b
This leads to oxidation of membrane components, fragility of the RBC and extensive hemolysis.\u200b<\/p>\n\n\n\n
without reduce glutathione hydrogen peroxide accumulates in the RBC.\u200b
This leads to oxidation of membrane components, fragility of the RBC and extensive hemolysis.\u200b<\/p>\n\n\n\n
caused by defects in the linkage of the lipid bilayers of the cell membrane with the underlying cytoskeleton<\/p>\n\n\n\n
Normocytic anemias are typically the result of enhanced RBC destruction or blood loss rather than a production problem.\u200b<\/p>\n\n\n\n
Ankyrin (ANK1)
Spectrin (SPT)
Band 3
protein 4.2
mutations lead to RBCs that lose cell membrane over time \u2013> spherical cells that are more rigid<\/p>\n\n\n\n
Don\u2019t have band 3 \u2014 span 3\/ protein 4.2 def
Have band 3 \u2014 Spectrin\/ ankyrin def.<\/p>\n\n\n\n
Alpha Spectrin SPTA1<\/p>\n\n\n\n
The spectrin\/actin network represents the cortical cytosketon of RBCs.\u200b
Spectrin binds to ankyrin which anchors specitrin to the membrane via band 3 \u2013 4.2 regulates association of band 3 and ankyrin<\/p>\n\n\n\n
Beta spectrin SPTB<\/p>\n\n\n\n
RBC had IgG and complement C3 on their surface \u2013normally our RBC should not have these attached<\/p>\n\n\n\n
PK is autosomal recessive. \u200b
PK deficiency produces a phenotype only in RBCs.\u200b
Typically, 5-25% of normal enzyme activity
Increased levels of 2-3 BPG allows for delivery to periphery<\/p>\n\n\n\n
Extravascular \u2013> spleen, splenic macrophages in white pulp play large ole
Intravascular \u2013> in the blood, complement mediated direct killing<\/p>\n\n\n\n
Autoantibodies directed against RBC membrane antigens that lead to RBC destruction
Shortens RBC life span
develop sporadically, not familial<\/p>\n\n\n\n
DAT pattern \u200b
Optimal temperature that the autoantibodies react with the human RBCs \u200bThree types, warm, cold and mixed<\/p>\n\n\n\n
70-80% of cases in adults, 90% in children
DAT pattern \u2013> IgG postive or IgG and C3 postive
antibodies major players
Autoantibodies bind and react with RBC at 37
extracellular hemolysis
Does not lead to hemoglobinemia and hemoglobinuria<\/p>\n\n\n\n
similiar to anemia, fatigue, jaundice, dyspnea
Elevated serum levels of indirect bilirubin,<\/p>\n\n\n\n
Almost always in adults over 50
similiar to anemia,
CAD
cold exposure \u2013> acrocyanosis via massive agglutination of RBCs (blue\/ yellow hands on heat image)<\/p>\n\n\n\n
primary \u2013> idiopathic
secondary \u2013> lymphoproliferative disorder like leukemia, lymphoma and other autoimmune disorders like lupus<\/p>\n\n\n\n
primary \u2014 idiopathic
secondary \u2014 underlying illnesses, infections , lymphoproliferative disorders
RARELY autoimmune
common after mycoplasma pneumoniae \u2014 can see their antibodies<\/p>\n\n\n\n
Corticosteroids, splenectomy, blood transfusions<\/p>\n\n\n\n
Spherocytes \u200b
Sphere shaped RBCs rather than bi-concave disk shaped<\/p>\n\n\n\n
Treat Mycoplasma infection with antibiotics \u200b (underlying infection commonly)
Corticosteroids
blood transfussions<\/p>\n\n\n\n
DAT pattern for IgG is negative and C3 positive
complement is the major player
Cold antibodies typically react with RBCs at below 30oC (optimum, 4oC)\u200b
Usually IgM \u200b
Activates classical complement pathway<\/p>\n\n\n\n
~50% of DAT is positive for complement component \u200b
Mostly C3d\u200b
complement bound antibodies can also be cleared in the liver via Kupfer cells<\/p>\n\n\n\n
Autoantibodies bind RBC in periphery when cold and eventually the antibodies come off and the complement stays
hemolysis is both extra and intravascular ( can lead to hemoglo binemia and hemoglobinuria)<\/p>\n\n\n\n
Molecular mimicry \u2014 foreign antigens share sequences or structures similar with self antigens<\/p>\n\n\n\n
146 amino acids
chromsome 11
Hgb A1<\/p>\n\n\n\n
141 amino acids
chromosomes 16
Hgb A1, A2 and fetal<\/p>\n\n\n\n
Alpha \u2014 gene deletion
beta \u2014 gene mutation
microcytic, hypochromic<\/p>\n\n\n\n
Silent carrier
No way to really diagnose<\/p>\n\n\n\n
Thal trait; mild hypochromic microcytic anemia
MCV 7-=0-75
might be confused with iron deficiency
May be homozygous (-a\/-a) or hetero (\u2013\/aa)<\/p>\n\n\n\n
Live normal life; however, infections, pregnancy, exposure to oxidative drugs may trigger hemolytic crisis. \u200b
RBCs are microcytic, hypochromic with marked poikilocytosis
vulnerable to oxidation \u2013> heinz like bodies, golf ball like and stained with brilliant cresyl blue (have dots in the middle of RBC and with blue look like they have granules)<\/p>\n\n\n\n
Hgb H; variable severity, but less severe than Beta Thal Major\u200b
Hemoglobin II disease
(\u2013\/-a)
Results in accumulation of excess unpaired gamma or beta chains. Born with 10-40% Bart\u2019s hemoglobin (\u03b34). Gradually replaced with Hemoglobin H (\u03b24).<\/p>\n\n\n\n
Bart\u2019s Hgb; Hydrops Fetalis; In Utero or early neonatal death \u2014> incomparable with life
Hemoglobin Bart has high oxygen affinity so cannot carry oxygen to tissues. \u200b
Baby with HUGE stomach<\/p>\n\n\n\n
Nothing really, just don\u2019t confuse them with needing iron treatment<\/p>\n\n\n\n
Low in iron deficiency<\/p>\n\n\n\n
\u03b2-Thalassemia\u200b
Due to various heterogenous beta mutations
nearly normal beta\/alpha chain ratio and no hematologic abnormalities. \u200b
\u200b<\/p>\n\n\n\n
Have one normal beta gene and one mutated beta gene. \u200b
Fine unless under stress like pregnancy, infection or folic acid deficiency<\/p>\n\n\n\n
May be either heterozygous from mutations causing mild decrease in beta chain production, or may be homozygous causing a more serious reduction in beta chain production. \u200bmaintain hemoglobin 7 or else transfusions<\/p>\n\n\n\n
Reduced or nonexistent production of \u03b2-globin\u200b
poor oxygen carrying
increased alpha global production and precipitation
Anemia, jaundice, splenomegaly\u200b
Hyperplastic Bone Marrow\u200b\u2013Increase in extramedullary erythropoiesis\u200b
severe microcytic, hypochromic anemia. \u200b<\/p>\n\n\n\n
X-ray looks like theres hair present
Have protruding upper teeth and Mongoloid facial features. \u200b
target cells, teardrop cells and elliptocytes.<\/p>\n\n\n\n
High in iron def.
low in thalassemia
Thalassemia electrophoresis
Thalassemia electrophoresis<\/p>\n\n\n\n
Thalassemia<\/p>\n\n\n\n
Defects involving incorporation of iron into the heme molecule
hypochromic cells in the peripheral blood and increased marrow iron;\u200b
may sideroblasts in bone marrow<\/p>\n\n\n\n
Sickle cell
Ringed sideroblasts
Ringed sideroblasts
Prushin blue stain in all erythro-precursors the iron is actually precipitating in the mitochondria \u2014 any iron in bone marrow means your not iron def.<\/p>\n\n\n\n
Hereditary \u200b
X-linked (isolated \/ genetic syndromes)\u200b
Autosomal
or can be acquired through drugs and heavy metals<\/p>\n\n\n\n
Insufficient dietary iron<\/p>\n\n\n\n
Menstruation or pregnancy<\/p>\n\n\n\n
Excessive bleeding<\/p>\n\n\n\n
Anisocytosis<\/p>\n\n\n\n
Transferrin \u2014 extracellular iron transport
Ferritin \u2014 intracellular iron storage, highly expressed in macrophages of liver and spleen, hollow sphere to store iron<\/p>\n\n\n\n
Limiting factor in size<\/p>\n\n\n\n
Tissue iron stores are reduced and serum ferritin levels decrease
Transferrin receptor levels on the cell surface increase
NOT anemic<\/p>\n\n\n\n
Serum iron levels decrease.\u200b
Transferrin levels increase
Fewer cells being produced (anemia) but most cells being made are normocytic and normochromic.\u200b
Beginning to see anisocytosis and increased RDW.\u200b
protoporphyrin levels increase because its the last intermediate in heme biosynthesis before you need iron<\/p>\n\n\n\n
Hemoglobin levels drop below 10 g\/dL\u200b
Microcytic and hypochromic erythrocytes are seen.\u200b
MCV and RDW are better indicators than is MCHC for iron deficiency anemia.\u200b<\/p>\n\n\n\n
Earliest lab findings, unequal size of RBC<\/p>\n\n\n\n
Toxic unbound
so its always protein associated<\/p>\n\n\n\n
Fe3+ ) travels in the circulation bound to plasma transferrin.
excessive iron stored in this state \u200b<\/p>\n\n\n\n
RBC with a dark center and periphery with a clear ring between<\/p>\n\n\n\n
Serum iron\/TIBC x 100\u200b
20-50% normal<\/p>\n\n\n\n
Total iron binding capacity and is a measure of transferrin levels.<\/p>\n\n\n\n
proteins for iron homeostasis are regulated postranscriptionally.\u200b
iron-response elements (IREs) 5\u2032\u2013> regulates translation
IRES 3\u2032 UTR \u2013> regulates mRNA stability<\/p>\n\n\n\n
Quantity of hemoglobin dictates RBC size<\/p>\n\n\n\n
IREs form a stem-loop structure in the mRNA.\u200b
IREs are bound by iron regulatory proteins (IRPs) that respond to iron levels
IRP binding to 5\u2032 \u2014 inhibits translation
IRP binding to 3\u2032 enhances stability and translation<\/p>\n\n\n\n
Abnormally shaped RBC
cause elevation in RDW, even through MCV goes down because cell size is shrinking, but a wider range of shapes now<\/p>\n\n\n\n
IRE in 5\u2032
will be expressed in high levels in high iron.<\/p>\n\n\n\n
protein represses iron transport in the gut as well as iron release from macrophages and other cells.\u200b
released from liver
When iron levels in the body are high, hepcidin levels increase (negative control)
inhibits ferroportin and prevents iron transport out of enterocytes and macrophages.\u200b<\/p>\n\n\n\n
IRE in 3\u2032
will be expressed highly in low iron levels<\/p>\n\n\n\n
oral vs. IV<\/p>\n\n\n\n
binding to apoferritin mRNA and inhibiting translation. \u200b
Apoferritin expression low.\u200b
5\u2032 and tf receptor inhibitor degradation<\/p>\n\n\n\n
NO IRP binding to apoferritin mRNA and no inhibition of translation. \u200b
Apoferritin expression high.\u200b
and none to Tf receptor \u2014 Tf expresion low<\/p>\n\n\n\n
def. \u2013> inadequate dietary intake, high demands and low stores so it manifests much quicker
1mg PO daily
good prophylactically in pregnancy and alcoholics, hemolytic anemias<\/p>\n\n\n\n
anemia \u2014 Neurologic Syndrome (parathesias)\u200b, low demand in body so can take a way
100-1000ug IM 1-2 weeks\u200b<\/p>\n\n\n\n
recombinant human GM-CSF.\u200b
Stimulates myelopoeisis\u200b
used in bone marrow transplantation
cancer adjuvant<\/p>\n\n\n\n
blocks ribonucleotide reductase which converts RNA bases into DNA bases. In Sickle cell anemia, it somehow causes an increased production of HbF (2 alpha and 2 gamma chains)\u200b
bone marrow suppression and GI effects, teratogen during pregnancy<\/p>\n\n\n\n
Stimulates megakaryopoiesis\u200b
Leads to long linear increases in platelet counts
used in idiopathic thrombocytopenia purpura, cancer chemotherapy adjuvant<\/p>\n\n\n\n
Enhances megakaryocyte maturation.\u200b
Used in non myeloid cancers
Causes edema and many need diuretics concomitantly.\u200b<\/p>\n\n\n\n
IM or IV or else digestive system would break them up \u200b
Peptide proteins
glycosylated do not pass through membrane so the receptors for these growth factors are on the surface so they signal through the JAK \/ STAT pathway<\/p>\n\n\n\n
Filgrastim- recombinant human G-CSF\u200b
Stimulates neutrophil production\u200b
Uses\u200b \u2013> After autologous bone marrow transplants\u200b
Cancer chemotherapy adjuvant \u200b<\/p>\n\n\n\n
Used to treat anemia that is secondary to chronic kidney disease. \u200b
Hypertension, thrombotic events<\/p>\n\n\n\n
Megaloblastic anemia due to vitamin B12 deficiency \u200b
When the body elicits an immune response against its own tissues against intrinsic factor needed for vitamin B12 absorption<\/p>\n\n\n\n
lead to ADCC, opsonization<\/p>\n\n\n\n
Neutralization
Type 2 hypersensitivity, IgG or IgM because antibodies are not forming immune complexes<\/p>\n\n\n\n
Autoimmune gastritis
Helicobacter pylori infection
type 1 diabetes or other autoimmune<\/p>\n\n\n\n
1 it will be megaloblastic \u2014 increased MCV, oval RBC and hyperhsegmented neutrophils,
Intestinal metaplasia can be seen in pernicious anemia
Intestinal metaplasia can be seen in pernicious anemia<\/p>\n\n\n\n
Live on the surface of their host, usually arthropods<\/p>\n\n\n\n
IM injection of B12<\/p>\n\n\n\n
A host in which the parasite reaches sexual maturity<\/p>\n\n\n\n
Live within the body of the host, mostly protozoa and helminths\u200b<\/p>\n\n\n\n
Tapeworm
Segmented bodies\u200b
Hermaphroditic\u200b
Absorb nutrients no GI system\u200b<\/p>\n\n\n\n
Fluke (complex flatworm
Non-segmented (leaf)\u200b
Hermaphroditic\u200b
Primitive gut\u200b<\/p>\n\n\n\n
Growth hormone and adrenal hormones stimulate erythropoeitin production
Normocytic normochromic \u200b
anemia in patients affected with \u200b
Growth hormone deficiency\u200b or addisons disease<\/p>\n\n\n\n
Animal (definitive host) that serves to maintain the parasite\u2019s life cycle in the environment\u200b<\/p>\n\n\n\n
the source of infection; the mode of transmission; the presence of a susceptible host\u200b<\/p>\n\n\n\n
Non-segmented cylindrical bodies covered with cuticle\u200b
Separate sexes
complete GI<\/p>\n\n\n\n
Increased because inflammation leads to IL6 which leads to its increased release
Increased erythropoietic activity (production of Red Cells)\u200b
suppresses Hepcidin production.
it inhibits iron transport across cell membranes, absorption and release of storage iron<\/p>\n\n\n\n
chronic disease or \u200b
a Macrocytic anemia occurs\u200b
\u200b<\/p>\n\n\n\n
Also called \u201canemia of inflammation\u201d\u200b
May follow both mild acute infection eg Otitis media or gastroenteritis or with more severe and chronic infections.\u200b
There is a fall in hemoglobin after an inflammatory reaction<\/p>\n\n\n\n
ESR= number of mm that Red blood cells fall in 1 hour in a vertical tube of anticoagulated blood\u200b
0-15 for males and 0-20 for females
Low \u2013 sickle cell
High \u2014 autoimmune, cancer, inflammation<\/p>\n\n\n\n
-Viable bacteria in the bloodstream
-clinical symptoms \u2013> sepsis and speticemia
H. influenzae, Brucella, listeria, streptococcus pneumoniae<\/p>\n\n\n\n
A non specific protein that rises quickly in inflammation and infections.\u200b<\/p>\n\n\n\n
Unpredictable severe pain episodes\u200b \u2013>Pain due to tissue damage from lack of blood flow\u200b
Triggers \u2013> cold, infection and low O2 levels
Reversing the triggers can help to reverse sickled cell to normal shape and restore flow\u200b
splenic palpation!<\/p>\n\n\n\n
-Virus in the blood
-Can either stay at entry or leave (first replicate at site of entry)<\/p>\n\n\n\n
Infections that lead to the presentation of hemolytic anemia
Most common in malaria.
Clostridium perfringens
Mycoplasma pneumoniae<\/p>\n\n\n\n
Transmitted via young nymph of deer tick, rodents serve as rosorvoir where it undergoes asexual reproduction. The definitive host is the tick
so tic bites mouse, parasite grows, tic bites again \u2013> human dead end host<\/p>\n\n\n\n
Occurs most often in patients who have undergone septic abortion or after acute cholecystitis
Neutrophils with two bacilli<\/p>\n\n\n\n
Fever, chills, hemolytic anemia, elderly and immosurpressed at higher risk, many others are asymptomatic
Ring Forms \u2013trophozoites
Maltese cross
avoid ticks<\/p>\n\n\n\n
Human bartonellosis, also called the Oroya fever
Transmitted by sand fly
An acute hematic phase characterized by a systemic febrile illness and a chronic phase with skin lesions known as Verruga Peruana wart<\/p>\n\n\n\n
Ciprofloxacin
Wart \u2013azithromycin, rifampin<\/p>\n\n\n\n
Alpha toxin, a lecithinase C that lyses erythrocytes (intravascular hemolysis), platelets, leukocytes and endothelial cells\u200b<\/p>\n\n\n\n
P. falciparum and P. vivax\u200b
Female mosquito is the specific vector \u2014 Human host \u2013> mosquito
blood stage parasites \u2013> clinical manifestations<\/p>\n\n\n\n
Human and mosquito(sporozoites)
Maltese cross
Maltese cross<\/p>\n\n\n\n
Personal protection \u2013 use of insect repellents, bed-nets, and protective clothing\u200b<\/p>\n\n\n\n
Primarily a blood schizonticide, concentrates in vacuoles preventing proper heme breakdown. Buildup of free heme is toxic to the parasite.\u200b
Oral
Pruritus in africans
malaria<\/p>\n\n\n\n
Verruga Peruana wart
B. bacilliformis
Carrion\u2019s Disease<\/p>\n\n\n\n
Disrupts mitochondrial electron transport. Active against both tissue and blood schizonts, so can discontinue at one week post exposure. \u200b
Malaria and Babesis<\/p>\n\n\n\n
Macrolide antibiotic that targets the 50S ribosomal subunit and inhibits Protein Synthesis
Babesiosis
oral, mostly unchanged by liver
GI problems, increased QT interval<\/p>\n\n\n\n
similar to macrolides- binds 50S ribosomal subunit and blocks protein synthesis.\u200b
Oral
prodrug
C.Diff
Babesiosis, MRSA<\/p>\n\n\n\n
Depresses oxygen uptake and carbohydrate metabolism; intercalates into DNA, disrupting the parasite\u2019s replication and transcription.\u200b
Oral
Prolonged QT
Babesiosis, malaria<\/p>\n\n\n\n
but possibly inhibits the formation of b-hematin ( a storage structure that the parasite uses to get rid of the high levels of heme inside the parasite)[hemozoin].\u200b
oral
CYP3a4 metabolism
GI affects, QT interval<\/p>\n\n\n\n
(fever spikes, chills, and rigors at regular intervals)\u200b associated with the synchronous release of schizonts and the lysis of erythrocytes\u200b<\/p>\n\n\n\n
nknown, but prophylaxis of malaria is due to the destruction of the asexual blood forms of the malarial pathogens. \u200b
oral
20 day half life
Behavioral disturbances and CNS dizziness
NOT FOR EPILEPTIC patients<\/p>\n\n\n\n
DOC for eradication of dormant liver forms of vivax and ovale. Active against hepatic, dormant, and gamete stages, not effective against erythrocytic stage
Oral
hemolytic anemia so don\u2019t give to G6PD patients<\/p>\n\n\n\n
Competitively blocking the binding of tRNA to the A site of the 30S subunit, preventing addition of new amino acids to the growing peptide chain.\u200b
Oral or IV
short half life
Not for pregnant woman \u2014 discoloration of teeth in fetus
phototoxicity<\/p>\n","protected":false},"excerpt":{"rendered":"