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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
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
megaloblasts in marrow as well as macrocytes in the peripheral bloold
Rule of 3’s
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
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
Anemia due to impaired HGB syntesis –> iron deficiency
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.
No production of immature neutrophils in the bone marrow Indicates bone marrow suppression Hyper-segmented Lymphocytes
Occurs when increased bands and less mature neutrophils are present in the blood, along with a lower average number of lobes in segmented cells
Decreased in hereditary netropenia, bone marrow disease, viruses Increased in bacterial infections, tumors (left shift) TH17
Decreased — Congenital immunodeficiency diseases, severe infections, corticosteroids, HIV Increase– Viral infections, some fungi/ parasites, pertussis (right shift) important in viral infections — CD8 T cells
Decreased in bacterial infections and ACTH increased in parasitic infections, type 1 hypersensitive and asthma
Decreased in corticosteroids, hairy cell leukemia Increased in mycobacterial infections and TB TH1 response –intracellular bacteria
Decreased with corticosteroids Increased in hypersensitivity reactions (1)
When you have a ton of immature WBC in the periphery (left shift)
Higher than normal of cells, not abnormal shape
Incomplete or arrested development of an organ, below number o cells
abnormal growth noted microscopically, might be premalignant
Congenital absence of an organ
Autoimmune B cell autoantibodies
Neutropenia Thrombocytopenia 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
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 —
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
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
Normal WBC and normal platelets
Low WBC, neutropenia – lymphopenia
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 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
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
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
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
146 amino acids chromsome 11 Hgb A1
141 amino acids chromosomes 16 Hgb A1, A2 and fetal
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.
Have one normal beta gene and one mutated beta gene. Fine unless under stress like pregnancy, infection or folic acid deficiency
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
Quantitative defects of globin chain synthesis result in hemoglobinopathies
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
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
The earliest lab result that might suggest an iron deficiency prior to anemia.
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.
Earliest lab findings, unequal size of RBC
Toxic unbound so its always protein associated
Fe3+ ) travels in the circulation bound to plasma transferrin. excessive iron stored in this state
RBC with a dark center and periphery with a clear ring between
Serum iron/TIBC x 100 20-50% normal
Total iron binding capacity and is a measure of transferrin levels.
proteins for iron homeostasis are regulated postranscriptionally. iron-response elements (IREs) 5′–> regulates translation IRES 3′ UTR –> regulates mRNA stability
Quantity of hemoglobin dictates RBC size
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
Abnormally shaped RBC cause elevation in RDW, even through MCV goes down because cell size is shrinking, but a wider range of shapes now
IRE in 5′ will be expressed in high levels in high iron.
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.
IRE in 3′ will be expressed highly in low iron levels
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
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
anemia — Neurologic Syndrome (parathesias), low demand in body so can take a way 100-1000ug IM 1-2 weeks
recombinant human GM-CSF. Stimulates myelopoeisis used in bone marrow transplantation cancer adjuvant
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
Stimulates megakaryopoiesis Leads to long linear increases in platelet counts used in idiopathic thrombocytopenia purpura, cancer chemotherapy adjuvant
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
Filgrastim- recombinant human G-CSF Stimulates neutrophil production Uses –> After autologous bone marrow transplants Cancer chemotherapy adjuvant
Used to treat anemia that is secondary to chronic kidney disease. Hypertension, thrombotic events
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
Live on the surface of their host, usually arthropods
Treatment of pernicious anemia
IM injection of B12
A host in which the parasite reaches sexual maturity
Live within the body of the host, mostly protozoa and helminths
Tapeworm Segmented bodies Hermaphroditic Absorb nutrients no GI system
Growth hormone and adrenal hormones stimulate erythropoeitin production Normocytic normochromic anemia in patients affected with Growth hormone deficiency or addisons disease
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
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
-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!
-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
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)
Personal protection – use of insect repellents, bed-nets, and protective clothing
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
Disrupts mitochondrial electron transport. Active against both tissue and blood schizonts, so can discontinue at one week post exposure. Malaria and Babesis
Macrolide antibiotic that targets the 50S ribosomal subunit and inhibits Protein Synthesis Babesiosis oral, mostly unchanged by liver GI problems, increased QT interval
similar to macrolides- binds 50S ribosomal subunit and blocks protein synthesis. Oral prodrug C.Diff Babesiosis, MRSA
Depresses oxygen uptake and carbohydrate metabolism; intercalates into DNA, disrupting the parasite’s replication and transcription. Oral Prolonged QT Babesiosis, malaria
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
(fever spikes, chills, and rigors at regular intervals) associated with the synchronous release of schizonts and the lysis of erythrocytes
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
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
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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