CPR Test Answers

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’s 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’t 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’t 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’t 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

What is the rate for chest compressions per minute for any age?

100 compressions per minute

The compression-ventilation ratio for one or two rescuers for ADULT CPR is?

30 compression to 2 ventilation breaths

The compression-ventilation ratio for one or two rescuer CHILD or INFANT CPR is?

15 compressions to 2 ventilation breaths

Where should the hands be placed on the chest for adult CPR?

hands should be placed on the lower half of breast bone

What is the preferred hand technique for two rescuer infant CPR?

2 thumb – Thumb & encircling hand technique (compressions with thumbs)

What is the depth of compressions on an adult?

2 inches

What is the depth of compression on an infant?

⅓ the depth of the chest size or 4 cm

The rescuers knows its rescue breaths are effective when what happens?

When the chest rises

What is the first step in using an AED?

Turn it on

After an AED shock is delivered, what is the next step?

Check for breathing. If there isn’t an breathing occurring, begin compressions and respirations.

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.

When is scene safety assessed?

When you first arrive at the scene

Interruptions to CPR should take more than ___ seconds.

Chest compressions should be initiated within ___ seconds if identifying victim is not responsive and has no pulse.

In two rescuer CPR, the first rescuer starts ___________ _________________ while the seconds rescuers ____________ _ _ _.

starts chest compressions; call 911. (or activated AED and/or provides help with airway)

If a choking victim becomes unresponsive, the rescuer should first call for help (or EMS) and begin _____.

Rescue breaths for a CHILD or INFANT should be one breath every ________________.

3-5 seconds

Rescue breaths for an ADULT should be one breath every ____________.

5-6 seconds

How do you relive choking in an INFANT?

5 back slaps, 5 chest thrusts

How do you relieve choking in an ADULT?

abdominal chest thrust (Heimlich maneuver)

If any choking victim goes unresponsive, what additional step do you perform before breathing?

CPR, look, and remove if there is anything visible in the back of the victims airway

Blod smear

Gray platelets missing their typical granules

Microlytic anemias

siderblastic anemia, ACD, Lead posioning, Thalassemias, Irondeficiency late

Normocytic – nonhemolytic

Reticulocyte count is normal or decrease
Iron def. early. ACD. aplastic anemia. chronic kidney disease

Hemolytic — intrinsic

High reticulocyte count
RBC membrane defect — hereditary spherocytosis, G6pD, HbC sickle cell

Hemolytic extrensinc

Autoimmune, infections

Macrocytic -Megaloblast

folate deficiency, B12m orotic aciduria

Macrocytic — Non megaloblastic

liver disease, alcoholism, diamond blacking

Physical features of iron deficiency anemia

angular cheilitis, Plummer vinsons

Plummer vinson syndrome

Iron transport

Transferrin

Iron storage

Ferritin — may be false high if patient has an active infection or inflammation

What is iron used to make

Hemoglobin, myglobin, enzymes

Hemoglobin electrophoresis- sickle cell

megaloblastic anemias

megaloblasts in marrow as well
as macrocytes in the peripheral bloold

Rule of 3’s

Drug-Induced hemolysis

Penicillin the drug can bind to the RBC membrane so now the body sees it as a foreign antigen so. Now you’re destroying your own RBC that have this medication bound to it

Hereditary Spherocytosis

Abnormal cytoskeletal proteins (spectrin, ankyrin, band 3 and protein 4.2) are unstable and have less flexibility.
An impaired membrane with this permeability defects allows Na+ to accumulate in the cell, while allowing the escape of K+
Destruction of cells — jaundice
Cells will pop at lower water concentrations

G6PD deficiency: Hemolytic anemia due RBC Enzyme defect

maintains the level of the coenzyme nicotinamide adenine dinucleotide phosphate (NADPH).
NADPH restores the level of glutathione which protects the red blood cells against oxidative damage.
neonatal jaundice, favism, hemolysis by oxidant drugs

Hemoglobin concentration — the concentration of hemoglobin the blood

The concentration of RBC in the whole blood

Hematocrit — volume percentage of whole blood occupied by RBC
3 x HGB

Mean corpuscular volume
he average volume of a circulating erythrocyte.
80-100
higher in large cell

Mean corpuscular hemoglobin
The quantity of hemoglobin in the average circulating erythrocyte.
higher in larger cells

Mean corpuscular hemoglobin concentration
concentration of hemoglobin in the average RBC in circulation
same based on cell size

Observed reticulocyte count

Reticulocytes are typically reported as a percentage of the total erythrocytes.

CV — calculated by measuring the curve width at the point that is ∓1 standard deviation from the MCV, then dividing that number by the MCV. 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 — Reticulocytes have greater effect

Anemia due to premature red cell destruction

Corrected reticulocyte count

OR x patients HCT / mean normal HCT
Female hematocrit RR = 37% to 47%
Mean would be 37+47 / 2 —> 42

Anemia due to insufficient red cell production

Anemia due to insufficient hemoglobin synthesis

Anemia due to impaired DNA synthesis

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’ll result in microcytes
decreased reticulocyte count, B12 and folate deficiency

microcytic hypochromic

Anemia due to impaired HGB syntesis –> iron deficiency

macrocytic normochromic

Anemia due ti impaired DNA synthesis — Folate or B12 deficiency

Rule of three

RBC x 3 = HBG
HGB x 3 = HCT

Chronic iron defiecny

cause of limited protein synthesis , any stores of reticulocytes have been release but erthryopotein would be elevated

What vitamins are especially needed for adequate cell division?

Folic acid is converted to tetrahydrafolate which is essential for purine (G/A) and thymidine synthesis.
Vit. B12 Involved in the conversion of N5-methyltetrahydrafolate into THF.

Right Shift

No production of immature neutrophils in the bone marrow
Indicates bone marrow suppression
Hyper-segmented
Lymphocytes

Lift shift

Occurs when increased bands and less mature neutrophils are present in the blood, along with a lower average number of lobes in segmented cells

Neutrophils

Decreased in hereditary netropenia, bone marrow disease, viruses
Increased in bacterial infections, tumors (left shift)
TH17

Lymphocytes

Decreased — Congenital immunodeficiency diseases, severe infections, corticosteroids, HIV
Increase– Viral infections, some fungi/ parasites, pertussis (right shift)
important in viral infections — CD8 T cells

Eosinophils

Decreased in bacterial infections and ACTH
increased in parasitic infections, type 1 hypersensitive and asthma

Monocytes

Decreased in corticosteroids, hairy cell leukemia
Increased in mycobacterial infections and TB
TH1 response –intracellular bacteria

Basophils

Decreased with corticosteroids
Increased in hypersensitivity reactions (1)

Leukemia

When you have a ton of immature WBC in the periphery (left shift)

Hyperplasia

Higher than normal of cells, not abnormal shape

Hypoplasia

Incomplete or arrested development of an organ, below number o cells

Dysplasia

abnormal growth noted microscopically, might be premalignant

Aplasia

Congenital absence of an organ

Autoimmune

usually idiopathic

Autoimmune B cell autoantibodies

Neutropenia
Thrombocytopenia
Anemia

Aplastic Anemia

T-cell mediated, decreased neutrophils, platelets and reticulocytes
looks like tons of fat in the bone marrow

Idiopathic autoimmune treatment

Combination of immunosuppressive agents and bone marrow growth factors
Neupogen, cyclosporine, prednisone

Autoimmune disease associations

RA: rheumatoid arthritis, Felty’s syndrome
SLE: systemic lupus erythematosis
Aplastic Anemia

Neupogen

Colony stimulating factor for white cell growth and proliferation

Cyclosporine and prednisone

immuno suppressant to inhibit current white blood cells from attacking stuff

Radiation induced marrow aplasia

Lymphoid and bone marrow cannot handle are amounts of radiation, and the body remembers radiation forever —

Myelofibrosis

reticulin stain to bring out the black fibers

Impact of Dose fractionation

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’re proabably going to die from other radiation problems – without planed in one big dose

Myelophthisic Anemia

Due to marrow infiltration — solid tumors, liquid tumors, infection (TB, plotts)
Or due to myelofibrosis — new growth of fibrous tissue or new formation in marrow

Isolated anemia

Normal WBC and normal platelets

Luekopenia

Low WBC, neutropenia – lymphopenia

Thrombocytopenia

Low platelets

PK pathway

Enzyme in glycolysis that converts phosphoenolpyruvate to pyruvate with the generation of ATP
gene called PKLR
All ATP in RBC is via glycolysis

Phenotype and genotype for G6PDA-

most frequent in african populations
affects the stability of the G6PD enzyme. –> so it works fine just has a short half life so affects mostly older RBC
males have low penetrance –> asymptomatic

Phenotype and genotype G6PDB-

Mediterranean populations
affects both the stability of the enzyme and its catalytic activity.
Affects both young and old RBC
oxidant stress –> hemolysis much quicker

Principle pathway product that is deficient in RBCs of a person with PK deficiency

reduces RBC ATP production.
effects membrane pumps than maintain membrane flexibility and cell shape — so they get killed by spleen

Sickle cell gel technique

Normal will cut at the mstII site — 110 bp BRC product –> 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

Sickle mode of inheritance

Autosomal recessive disease caused by a very specific mutation in the β-globin gene (HBB gene).
Mutation causes an amino acid substitution of valine for glutamic acid at amino acid 6 of the β-globin protein.

hemoglobin C disease

Its a lysine now instead of a glutamic acid so its not as severe as sickle cell

Mode of inheritance of hereditary sperocytosis / population

75% autosomal dominant, (20% are due to new mutations)
25% autosomal recessive — more severe
Most common hemolytic anemia of Northern Europeans

Mode of inheritance of hereditary elliptocytosis / population

Mostly autosomal dominant
african and mediterranean populations

Most prevalent enzyme disorder in the world

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)

How HE mutations alter normal spectrin function.

α/β spectrin dimers cannot form into tetramers.
Mutations are sometimes seen in the genes coding for glycophorin and protein 4.1.
Elliptical cell

Metabolic pathway that G-6-PD is involved in

hexose monophosphate (HMP) shunt.
catalyzes the oxidation of glucose-6-P to 6-phosphogluconolactone (first step)

Product that is deficient in RBCs of a person with a G-6-PD deficiency.

NADPH –> reduced glutathione
without it –> hydrogen peroxide accumulates in the RBC.
This leads to oxidation of membrane components, fragility of the RBC and extensive hemolysis.

Diagram and explain the relationship between NADPH, glutathione and hydrogen peroxide in RBCs.

without reduce glutathione hydrogen peroxide accumulates in the RBC.
This leads to oxidation of membrane components, fragility of the RBC and extensive hemolysis.

Similarity between HS and HE

caused by defects in the linkage of the lipid bilayers of the cell membrane with the underlying cytoskeleton

normocytic anemias

Normocytic anemias are typically the result of enhanced RBC destruction or blood loss rather than a production problem.

Hereditary spherocytosis mutations

Ankyrin (ANK1)
Spectrin (SPT)
Band 3
protein 4.2
mutations lead to RBCs that lose cell membrane over time –> spherical cells that are more rigid

Hereditary Spherocytosis microvessicles

Don’t have band 3 — span 3/ protein 4.2 def
Have band 3 — Spectrin/ ankyrin def.

HS autosomal recessive

Alpha Spectrin SPTA1

Spectrin

The spectrin/actin network represents the cortical cytosketon of RBCs.
Spectrin binds to ankyrin which anchors specitrin to the membrane via band 3 – 4.2 regulates association of band 3 and ankyrin

HS autosomal dominant

Beta spectrin SPTB

Hemolytic Anemia cues

RBC had IgG and complement C3 on their surface –normally our RBC should not have these attached

PK Deficiency Genetics

PK is autosomal recessive.
PK deficiency produces a phenotype only in RBCs.
Typically, 5-25% of normal enzyme activity
Increased levels of 2-3 BPG allows for delivery to periphery

Location or RBC destruction

Extravascular –> spleen, splenic macrophages in white pulp play large ole
Intravascular –> in the blood, complement mediated direct killing

Pathogenesis of AIHA

Autoantibodies directed against RBC membrane antigens that lead to RBC destruction
Shortens RBC life span
develop sporadically, not familial

types of AIHA based on direct coombs test

DAT pattern
Optimal temperature that the autoantibodies react with the human RBCs Three types, warm, cold and mixed

Warm AIHA

70-80% of cases in adults, 90% in children
DAT pattern –> 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

Warm AIHA symptoms

similiar to anemia, fatigue, jaundice, dyspnea
Elevated serum levels of indirect bilirubin,

Cold AIHA symtoms

Almost always in adults over 50
similiar to anemia,
CAD
cold exposure –> acrocyanosis via massive agglutination of RBCs (blue/ yellow hands on heat image)

Causes of Warm AIHA

primary –> idiopathic
secondary –> lymphoproliferative disorder like leukemia, lymphoma and other autoimmune disorders like lupus

Causes of Cold AIHA

primary — idiopathic
secondary — underlying illnesses, infections , lymphoproliferative disorders
RARELY autoimmune
common after mycoplasma pneumoniae — can see their antibodies

Treatment options for Warm AIHA

Corticosteroids, splenectomy, blood transfusions

Incomplete phagocytosis results in wAIHA

Spherocytes
Sphere shaped RBCs rather than bi-concave disk shaped

Treatment options for cold AIHA

Treat Mycoplasma infection with antibiotics (underlying infection commonly)
Corticosteroids
blood transfussions

Pathogenesis of cAIHA

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)
Usually IgM
Activates classical complement pathway

Pathogenesis of wAIHA

~50% of DAT is positive for complement component
Mostly C3d
complement bound antibodies can also be cleared in the liver via Kupfer cells

Pathway of cAIHA

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)

Why do infections cause autoimmunity

Molecular mimicry — foreign antigens share sequences or structures similar with self antigens

Beta globin

146 amino acids
chromsome 11
Hgb A1

Alpha globin

141 amino acids
chromosomes 16
Hgb A1, A2 and fetal

Thalassemia genetics

Alpha — gene deletion
beta — gene mutation
microcytic, hypochromic

Alpha thalassemia – one deletion

Silent carrier
No way to really diagnose

Alpha thalassemia – two deletions

Thal trait; mild hypochromic microcytic anemia
MCV 7-=0-75
might be confused with iron deficiency
May be homozygous (-a/-a) or hetero (–/aa)

Hemoglobin H Disease

Live normal life; however, infections, pregnancy, exposure to oxidative drugs may trigger hemolytic crisis.
RBCs are microcytic, hypochromic with marked poikilocytosis
vulnerable to oxidation –> 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)

Alpha thalassemia – three deletions

Hgb H; variable severity, but less severe than Beta Thal Major
Hemoglobin II disease
(–/-a)
Results in accumulation of excess unpaired gamma or beta chains. Born with 10-40% Bart’s hemoglobin (γ4). Gradually replaced with Hemoglobin H (β4).

Alpha thalassemia – four deletions

Bart’s Hgb; Hydrops Fetalis; In Utero or early neonatal death —> incomparable with life
Hemoglobin Bart has high oxygen affinity so cannot carry oxygen to tissues.
Baby with HUGE stomach

Alpha Thalassemias — treatment

Nothing really, just don’t confuse them with needing iron treatment

Ferratin in thalassemia vs. iron deficiency

Low in iron deficiency

Silent Carrier State for
β-Thalassemia

Due to various heterogenous beta mutations
nearly normal beta/alpha chain ratio and no hematologic abnormalities.

β-Thal Minor

Have one normal beta gene and one mutated beta gene.
Fine unless under stress like pregnancy, infection or folic acid deficiency

β-Thal Intermedia

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. maintain hemoglobin 7 or else transfusions

Beta Thalassemia Major

Reduced or nonexistent production of β-globin
poor oxygen carrying
increased alpha global production and precipitation
Anemia, jaundice, splenomegaly
Hyperplastic Bone Marrow–Increase in extramedullary erythropoiesis
severe microcytic, hypochromic anemia.

Beta Thalassemia Major- appearance

X-ray looks like theres hair present
Have protruding upper teeth and Mongoloid facial features.
target cells, teardrop cells and elliptocytes.

Mentzer index for children (MCV/red blood cell count) for Thalassemia vs. iron

High in iron def.
low in thalassemia

Thalassemia electrophoresis

Quantitative defects of globin chain synthesis result in hemoglobinopathies

Thalassemia

Sideroblastic anemias

Defects involving incorporation of iron into the heme molecule
hypochromic cells in the peripheral blood and increased marrow iron;
may sideroblasts in bone marrow

Qualitative defects of globin chain synthesis result in hemoglobinopathies

Sickle cell

Ringed sideroblasts

Prushin blue stain in all erythro-precursors the iron is actually precipitating in the mitochondria — any iron in bone marrow means your not iron def.

Sideroblastic Anemia Etiology

Hereditary
X-linked (isolated / genetic syndromes)
Autosomal
or can be acquired through drugs and heavy metals

Causes of iron deficiency in infants and young children

Insufficient dietary iron

Causes of iron deficiency in infants and young women

Menstruation or pregnancy

Causes of iron deficiency in older adults

Excessive bleeding

The earliest lab result that might suggest an iron deficiency prior to anemia.

Anisocytosis

Contrast the functions of transferrin and ferritin.

Transferrin — extracellular iron transport
Ferritin — intracellular iron storage, highly expressed in macrophages of liver and spleen, hollow sphere to store iron

How does reduced hemoglobin production result in a microcytic anemia.

Limiting factor in size

Lab results for stage 1 iron deficiency

Tissue iron stores are reduced and serum ferritin levels decrease
Transferrin receptor levels on the cell surface increase
NOT anemic

Lab results for stage 2 iron deficiency

Serum iron levels decrease.
Transferrin levels increase
Fewer cells being produced (anemia) but most cells being made are normocytic and normochromic.
Beginning to see anisocytosis and increased RDW.
protoporphyrin levels increase because its the last intermediate in heme biosynthesis before you need iron

Diagram the distribution of iron in a healthy individual.

Lab results for stage 3 iron deficiency

Hemoglobin levels drop below 10 g/dL
Microcytic and hypochromic erythrocytes are seen.
MCV and RDW are better indicators than is MCHC for iron deficiency anemia.

Anisocytosis

Earliest lab findings, unequal size of RBC

Ferrous

Toxic unbound
so its always protein associated

Ferric

Fe3+ ) travels in the circulation bound to plasma transferrin.
excessive iron stored in this state

Target cell

RBC with a dark center and periphery with a clear ring between

% saturation

Serum iron/TIBC x 100
20-50% normal

Total iron binding capacity and is a measure of transferrin levels.

5’/3′ UTR

proteins for iron homeostasis are regulated postranscriptionally.
iron-response elements (IREs) 5′–> regulates translation
IRES 3′ UTR –> regulates mRNA stability

Erythrocyte Size

Quantity of hemoglobin dictates RBC size

IREs/ IRP

IREs form a stem-loop structure in the mRNA.
IREs are bound by iron regulatory proteins (IRPs) that respond to iron levels
IRP binding to 5′ — inhibits translation
IRP binding to 3′ enhances stability and translation

poikilocytosis

Abnormally shaped RBC
cause elevation in RDW, even through MCV goes down because cell size is shrinking, but a wider range of shapes now

Apoferritin

IRE in 5′
will be expressed in high levels in high iron.

Hepcidin

protein represses iron transport in the gut as well as iron release from macrophages and other cells.
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.

Transferrin receptor

IRE in 3′
will be expressed highly in low iron levels

Fe Salts

oral vs. IV

Low iron IRP

binding to apoferritin mRNA and inhibiting translation.
Apoferritin expression low.
5′ and tf receptor inhibitor degradation

High iron IRP

NO IRP binding to apoferritin mRNA and no inhibition of translation.
Apoferritin expression high.
and none to Tf receptor — Tf expresion low

Folate

def. –> inadequate dietary intake, high demands and low stores so it manifests much quicker
1mg PO daily
good prophylactically in pregnancy and alcoholics, hemolytic anemias

B12(hydroxocobalamin)

anemia — Neurologic Syndrome (parathesias), low demand in body so can take a way
100-1000ug IM 1-2 weeks

GM-CSF (sargramostim)

recombinant human GM-CSF.
Stimulates myelopoeisis
used in bone marrow transplantation
cancer adjuvant

Hydroxyurea

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)
bone marrow suppression and GI effects, teratogen during pregnancy

Thrombopoietin (romiplostim)

Stimulates megakaryopoiesis
Leads to long linear increases in platelet counts
used in idiopathic thrombocytopenia purpura, cancer chemotherapy adjuvant

IL-11 (oprelvekin)

Enhances megakaryocyte maturation.
Used in non myeloid cancers
Causes edema and many need diuretics concomitantly.

How are growth factors given

IM or IV or else digestive system would break them up
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

G-CSF (filgrastim)

Filgrastim- recombinant human G-CSF
Stimulates neutrophil production
Uses –> After autologous bone marrow transplants
Cancer chemotherapy adjuvant

Erythropoietin

Used to treat anemia that is secondary to chronic kidney disease.
Hypertension, thrombotic events

Pernicious anemia

Megaloblastic anemia due to vitamin B12 deficiency
When the body elicits an immune response against its own tissues against intrinsic factor needed for vitamin B12 absorption

Antibodies against parietal cells would

lead to ADCC, opsonization

What antibody effector function is used against IF?

Neutralization
Type 2 hypersensitivity, IgG or IgM because antibodies are not forming immune complexes

Causes of chronic gastritis

Autoimmune gastritis
Helicobacter pylori infection
type 1 diabetes or other autoimmune

How to diagnose pernicious anemia

1 it will be megaloblastic — increased MCV, oval RBC and hyperhsegmented neutrophils,

Intestinal metaplasia can be seen in pernicious anemia

Ectoparasites

Live on the surface of their host, usually arthropods

Treatment of pernicious anemia

IM injection of B12

Definitive host

A host in which the parasite reaches sexual maturity

Endoparasites

Live within the body of the host, mostly protozoa and helminths

Cestode

Tapeworm
Segmented bodies
Hermaphroditic
Absorb nutrients no GI system

Trematode

Fluke (complex flatworm
Non-segmented (leaf)
Hermaphroditic
Primitive gut

Pituitary and Adrenal gland

Growth hormone and adrenal hormones stimulate erythropoeitin production
Normocytic normochromic
anemia in patients affected with
Growth hormone deficiency or addisons disease

Reservoir host

Animal (definitive host) that serves to maintain the parasite’s life cycle in the environment

Three factors key to transmission of parasites

the source of infection; the mode of transmission; the presence of a susceptible host

Nematodes – roundworms

Non-segmented cylindrical bodies covered with cuticle
Separate sexes
complete GI

Hepcidin and inflammation

Increased because inflammation leads to IL6 which leads to its increased release
Increased erythropoietic activity (production of Red Cells)
suppresses Hepcidin production.
it inhibits iron transport across cell membranes, absorption and release of storage iron

Hypothyroidism anemia

chronic disease or
a Macrocytic anemia occurs

Anemia of Chronic Disease:

Also called “anemia of inflammation”
May follow both mild acute infection eg Otitis media or gastroenteritis or with more severe and chronic infections.
There is a fall in hemoglobin after an inflammatory reaction

Erythrocyte sedimentation rate

ESR= number of mm that Red blood cells fall in 1 hour in a vertical tube of anticoagulated blood
0-15 for males and 0-20 for females
Low – sickle cell
High — autoimmune, cancer, inflammation

Bacteremia

-Viable bacteria in the bloodstream
-clinical symptoms –> sepsis and speticemia
H. influenzae, Brucella, listeria, streptococcus pneumoniae

C Reactive protein

A non specific protein that rises quickly in inflammation and infections.

Clinical Manifestations of Sickle Cell Disease

Unpredictable severe pain episodes –>Pain due to tissue damage from lack of blood flow
Triggers –> cold, infection and low O2 levels
Reversing the triggers can help to reverse sickled cell to normal shape and restore flow
splenic palpation!

Viremia

-Virus in the blood
-Can either stay at entry or leave (first replicate at site of entry)

Infection-mediated Hemolytic Anemia

Infections that lead to the presentation of hemolytic anemia
Most common in malaria.
Clostridium perfringens
Mycoplasma pneumoniae

life cycle of Babesia microti

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 –> human dead end host

Clostridium perfringens

Occurs most often in patients who have undergone septic abortion or after acute cholecystitis
Neutrophils with two bacilli

How to diagnose and prevent Babesiosis.

Fever, chills, hemolytic anemia, elderly and immosurpressed at higher risk, many others are asymptomatic
Ring Forms –trophozoites
Maltese cross
avoid ticks

Carrion’s Disease 2 phases

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

Carrion’s Disease treatment

Ciprofloxacin
Wart –azithromycin, rifampin

Clostridium perfringens mechanism of infection

Alpha toxin, a lecithinase C that lyses erythrocytes (intravascular hemolysis), platelets, leukocytes and endothelial cells

Life cycle of malarial parasite

P. falciparum and P. vivax
Female mosquito is the specific vector — Human host –> mosquito
blood stage parasites –> clinical manifestations

Vectors for malarial parasite

Human and mosquito(sporozoites)

Maltese cross

Malaria prevention

Personal protection – use of insect repellents, bed-nets, and protective clothing

Chloroquine

Primarily a blood schizonticide, concentrates in vacuoles preventing proper heme breakdown. Buildup of free heme is toxic to the parasite.
Oral
Pruritus in africans
malaria

Differentiate malaria from babesiosis based on laboratory and clinical findings.

Verruga Peruana wart

B. bacilliformis
Carrion’s Disease

Atovaquone

Disrupts mitochondrial electron transport. Active against both tissue and blood schizonts, so can discontinue at one week post exposure.
Malaria and Babesis

Azithromycin

Macrolide antibiotic that targets the 50S ribosomal subunit and inhibits Protein Synthesis
Babesiosis
oral, mostly unchanged by liver
GI problems, increased QT interval

Clindamycin

similar to macrolides- binds 50S ribosomal subunit and blocks protein synthesis.
Oral
prodrug
C.Diff
Babesiosis, MRSA

Quinine

Depresses oxygen uptake and carbohydrate metabolism; intercalates into DNA, disrupting the parasite’s replication and transcription.
Oral
Prolonged QT
Babesiosis, malaria

LUMEFANTRINE

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].
oral
CYP3a4 metabolism
GI affects, QT interval

malarial paroxysm

(fever spikes, chills, and rigors at regular intervals) associated with the synchronous release of schizonts and the lysis of erythrocytes

MEFLOQUINE

nknown, but prophylaxis of malaria is due to the destruction of the asexual blood forms of the malarial pathogens.
oral
20 day half life
Behavioral disturbances and CNS dizziness
NOT FOR EPILEPTIC patients

PRIMAQUINE

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’t give to G6PD patients

TETRACYCLINES

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.
Oral or IV
short half life
Not for pregnant woman — discoloration of teeth in fetus
phototoxicity

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