Cardiovascular, Lymphatic and Systemic DiseasesReineer Jalon College of Nursing Western Mindanao State University

y Cardiovascular &

Lymphaticy Bacterial y Septic shock y Rheumatic fever y Parasitic y Schistosomiasis y Elephantiasis/Filariasis

y Systemic y Bacterialy Anthrax y Plague y Lyme disease

y Viral y Dengue fever y Parasitic y Malaria

Septic Shocky Sepsis or septic shock is a systemic inflammatory response

secondary to a documented infection. Consequently, sepsis is a continuum of detrimental host responses to infection that ranges from sepsis to septic shock and Multiple Organ Dysfunction Syndrome(MODS). y Shock refers to a state of inability to maintain adequate tissue perfusion and oxygenation, ultimately causing cellular, and then organ system dysfunction.

Septic Shocky Pathophysiologyy inflammatory mediators are the key players in the pathogenesis. y The gram-positive and gram-negative bacteria induce a variety

of proinflammatory mediators, including cytokines. Such cytokines play a pivotal role in initiating sepsis and shock. The bacterial cell wall components are known to release the cytokines; these include lipopolysaccharide (gram-negative bacteria), peptidoglycan (gram-positive and gram-negative bacteria), and lipoteichoic acid (gram-positive bacteria) y An imbalance of homeostatic mechanisms lead to disseminated intravascular coagulopathy (DIC) and microvascular thrombosis causing organ dysfunction and death

Septic Shocky The predominant hemodynamic feature of septic shock is

arterial vasodilation. Diminished peripheral arterial vascular tone may result in dependency of blood pressure on cardiac output, causing vasodilation to result in hypotension and shock if insufficiently compensated by a rise in cardiac output y Vasoactive mediators cause vasodilatation and increase the microvascular permeability at the site of infection. Nitric oxide plays a central role in the vasodilatation of septic shock. Impaired secretion of vasopressin also may occur, which may permit the persistence of vasodilatation

Septic Shocky Etiologyy Most patients who develop sepsis and septic shock have underlying

circumstances that interfere with the local or systemic host defense mechanisms. The most common disease states predisposing to sepsis are malignancies, diabetes mellitus, chronic liver disease, chronic renal failure, and the use of immunosuppressive agents. In addition, sepsis also is a common complication after major surgery, trauma, and extensive burns. y Respiratory tract infection and urinary tract infection are the most frequent causes of sepsis, followed by abdominal and soft tissue infections. y The use of intravascular devices is a notorious cause of nosocomiallyacquired sepsis. y Multiple sites of infection may occur in 6-15% of patients

Septic Shocky Etiologyy Lower respiratory tract infections are the cause of septic shock

in 25% of patients. The following are common pathogens:y Streptococcus pneumoniae y Klebsiella pneumoniae y Staphylococcus aureus y Escherichia coli y Legionella species y Haemophilus species y Anaerobes y Gram-negative bacteria y Fungi

Septic Shocky Etiologyy Urinary tract infections are the cause of septic shock in 25% of

patients, and the following are the common pathogens:y E coli y Proteus species y Klebsiella species y Pseudomonas species y Enterobacter species y Serratia

Septic Shocky Etiologyy Soft tissue infections are the cause of septic shock in 15% of patients, and the

following are the common pathogens:y y y y

S aureus Staphylococcus epidermidis Streptococci Clostridia

y GI tract infections are the cause of septic shock in 15% all patients, and the

following are the common pathogens:y y y y y y y

E coli Streptococcus faecalis Bacteroides fragilis Acinetobacter species Pseudomonas species Enterobacter species Salmonella species

Septic Shocky Risk factorsy Extremes of age ( 70 y) y Primary diseases y Liver cirrhosis y Alcoholism y Diabetes mellitus y Cardiopulmonary diseases y Solid malignancy y Hematologic malignancy y Immunosuppression y Neutropenia y Immunosuppressive therapy y Corticosteroid therapy y Intravenous drug abuse y Compliment deficiencies y Asplenia

Septic Shocky Risk factorsy Major surgery, trauma, burns y Invasive procedures y Catheters y Intravascular devices y Prosthetic devices y Hemodialysis and peritoneal dialysis catheters y Endotracheal tubes y Prior antibiotic treatment y Prolonged hospitalization y Other factors - Childbirth, abortion, and malnutrition

Septic Shocky s/sxTemperature greater than 38C or less than 36C Heart rate greater than 90 Respiratory rate greater than 20 per minute WBC count more than 12,000/L, Chills are a secondary symptom associated with fever, which is a consequence of increased muscular activity that produces heat and raises the body temperature. y Sweating occurs when the hypothalamus returns to its normal set point and senses the higher body temperature, stimulating perspiration to evaporate excess body heat. y Alteration in mental function often occurs: apprehension, anxiety, agitation, and, eventually, coma are manifestations of severe sepsis. y Hyperventilation with respiratory alkalosis is a common feature of patients with sepsis secondary to stimulation of the medullary respiratory center by endotoxins and other inflammatory mediators.y y y y y

Septic Shocky Dxy PE, v/s y Observe patients for systemic signs of inadequate tissue

perfusion. In the early stages of sepsis, cardiac output is well maintained or even increased. The vasodilation may result in warm skin, warm extremities, and normal capillary refill (warm shock). As sepsis progresses, stroke volume and cardiac output fall, the aeg start to manifest signs of hypoperfusion(cool skin, cool extremities, and delayed capillary refill or cold shock) y CBC w/ dif count (Hgb, WBC, plt) y Assess renal and hepatic functions (serum creatinine, BUN, ALT, AST, albumin)

Septic Shocky Tx y The principles in the management of septic shock, based on

current literature, include the following components:Early recognition Early and adequate antibiotic therapy Source control Early hemodynamic resuscitation and continued support Corticosteroids (refractory vasopressor-dependent shock) Proper ventilator management with low tidal volume in patients with ARDS y Vasopressor drugs: Dopamine, Epinephrine, Norepinephriney y y y y y

Septic Shocky Nsg interventiony Assist Dr in mgt y Meds as ordered y Admin oxygen as ordered y Assist in intubation y Aseptic technique

Rheumatic Fevery Rheumatic fever causes

chronic progressive damage to the heart and its valves. y The association between sore throat and rheumatic fever was not made until 1880. y The dramatic decline in the incidence of rheumatic fever is thought to be largely owing to antibiotic treatment of streptococcal infection

Rheumatic Fevery Pathophysiologyy Acute Rheumatic Fever(ARF) is a sequela of a previous group A

streptococcal infection, usually of the upper respiratory tract. y The disease involves the heart, joints, CNS, skin, and subcutaneous tissues. It is characterized by an exudative and proliferative inflammatory lesion of the connective tissue, especially that of the heart, joints, blood vessels, and subcutaneous tissue

y Epidemiologyy As a sequela of beta-streptococcal exposure, ARF occurs during

school years when streptococcal pharyngitis is most prevalent. Similarly, prevalence is higher in the colder months of the year when streptococcal pharyngitis is most likely to occur.

Rheumatic Fevery s/sxy Guidelines of diagnosis used by the American Heart Association

include major and minor criteria (ie, modified Jones criteria). In addition to evidence of a previous streptococcal infection, the diagnosis requires 2 major Jones criteria or 1 major plus 2 minor Jones criteria.

y Major criteriay Carditis: This occurs in as many as 40% of patients and may

include cardiomegaly, murmur, congestive heart failure, and pericarditis, with or without valvular disease. y Migratory polyarthritis: This condition occurs in 75% of cases and is polyarticular, fleeting, and involves the large joints.

Rheumatic Fevery Subcutaneous nodules (ie,

Aschoff bodies): These nodules occur in 10% of patients and are edematous, fragmented collagen fibers. They are firm, painless nodules on the extensor surfaces of the wrists, elbows, and knees.

Rheumatic Fevery Erythema marginatum: This

condition occurs in about 5% of cases. The rash is serpiginous and long lasting. y Chorea (also known as Sydenham chorea and "St Vitus dance"): This characteristic movement disorder occurs in 5-10% of cases. Sydenham chorea consists of rapid, purposeless movements of the face and upper extremities. Onset may be delayed for several months and may cease when the patient is asleep

Rheumatic Fevery Minor criteriay Clinical findings include arthralgia, fever and previous history of

ARF y Laboratory findings include elevated acute phase reactants (eg, erythrocyte sedimentation rate, C reactive protein), a prolonged PR interval, and supporting evidence of antecedent group A streptococcal infections (ie, positive throat culture or rapid streptococcal screen and an elevated or rising streptococcal antibody titer).

Rheumatic Fevery Dx y Jones criteria y Streptococcal antibody tests disclose preceding streptococcal infection. y Isolate group A streptococci via throat culture y cx y Mitral stenosis; carditis; CHF y Tx y Penicillin G benzathine IM y Prednisone (glucocorticoid) y Naproxen (NSAID) y Haloperidol may be helpful in controlling chorea

Rheumatic Fevery Nsg interventions y Antibiotics as ordered; completing the course of antibiotics minimizes the risk of developing ARF (and subsequently rheumatic heart disease) y Salicylates and anti-inflam agents y Emphasize importance of long-term cardiac reevaluation and regular prophylactic antibiotics y Maintain hydration y Control joint pain and inflam w/ massage y Limit physical exercise in child w/ carditis y Monitor sx of cx (pulmonary HPN, CHF, thromboemboli, valvular dse, arrhythmias

Schistosomiasisy Also Bilharziasis or snail fever, is a

human disease syndrome caused by infection from one of several species of parasitic trematodes of the genus Schistosoma. This is a major source of morbidity and mortality for developing countries in Africa, South America, the Caribbean, the Middle East, and Asia. y Most human schistosomiasis is caused by Schistosoma haematobium, Schistosoma mansoni, or Schistosoma japonicum.

Schistosomiasisy Pathophysiologyy Acute schistosomiasis (ie, Katayama fever) is a serum sicknesslike

illness that develops after several weeks in some, but not most, individuals with new schistosomal infections. It may correspond to the first cycle of egg deposition and is associated with marked peripheral eosinophilia and circulating immune complexes. It is most common with S japonicum and S mansoni infections and is most likely to occur in heavily infected individuals after primary infection. Symptoms usually resolve over several weeks, but the syndrome can be fatal. Early treatment with cidal drugs may exacerbate this syndrome and necessitate concomitant glucocorticoid therapy.

Schistosomiasisy Pathophysiologyy Mild maculopapular skin lesions may develop in acute

infection within hours after exposure to cercariae. Significant dermatitis is rare with the major human schistosomal pathogens, probably because the invading and developing cercariae are minimally immunogenic. However, abortive human infection with schistosomal species that rely on other primary hosts may cause marked dermatitis or swimmer's itch. This self-limited process may recur more intensely with subsequent exposures to the same species.

Schistosomiasisy Epidemiologyy Highly endemic in Regions VIII, X, XI and XII

y Inc periody 2-6wk

y MOTy skin penetration of infective cercariae through

wading, swimming in infested waters y Not transmissible from person to person

Schistosomiasisy s/sxy Swimmers itch: itchiness w/in 24h; redness; and

pustule formation at the point of entry of cercariae lasting 2-3d y diarrhea; abdominal pain y Katayama fever: fever; generalized lymphadenopathy; hepatosplenomegaly 2-3wk after initial infx and last for 1-2mo

Schistosomiasisy Dx y S/E: ID of eggs y Liver & rectal bx y Cx y portal cirrhosis; cor pulmonale (hypertrophy of LV resulting fr lung dse); myocardial damage y Tx y Praziquantel PO y Nsg interventions y Proper disposal of excreta y Avoid wading in infested waters y Elimination of intermediate host y Maintain nutrition

Elephantiasisy or Lymphatic Filariasis, is a rare disorder of the lymphatic

system caused by parasitic worms such as Wuchereria bancrofti and Brugia malayi, all of which are transmitted by mosquitos(Aedes poicilus, Culex fatigans, Anopheles flavirostris). y Inflammation of the lymphatic vessels causes extreme enlargement of the affected area, most commonly a limb or parts of the head and torso. It occurs most commonly in tropical regions.

Elephantiasisy Pathophysiology y larvae from the mosquito migrate to the

lymphatics, where they develop into threadlike adult worms within 6 to 12 mo. Gravid adult females produce microfilariae that circulate in blood.

Elephantiasisy Epidemiologyy Phil stat: 2.5/100,000 pop y Distribution: Cam norte/sur, Sorsogon, Quezon,

Albay, Mindoro, Bohol, Samar, Palawan, Sulu, TawiTawi, Basilany MOTy Bite of mosquito

y Dxy Fresh blood smear y Bentonite Flocculation Test

Elephantiasisy s/sxy Acute: fever, malaise,

chills y Chronic: lymphadenitis, swelling of scrotum, lymphatic channel affected; eosinophilia

Elephantiasisy Txy Diethylcarbamazine

citrate (Beltrazan) y AH or corticosteroid y Surgicaly Nsg interventionsy Meds as ordered y Vector control y Health education in

endemic areas

Anthraxy The term anthrax means coal in

Greek, and the disease is named after the appearance of its cutaneous form. Anthrax is described in the Old Testament, by the poet Virgil, and by the Egyptians. At the end of the 19th century, Robert Koch's experiments with anthrax led to the original theory of bacteria and disease. y Anthrax is caused by inhalation, skin exposure, or gastrointestinal (GI) absorption. Disease caused by inhalation is usually fatal, and symptoms usually begin days after exposure. This delay makes the initial exposure to Bacillus anthracis difficult to track

Anthraxy Can be grown in

laboratories and is a potential biowarfare agent

Anthraxy Pathophysiology y Virulence depends on the bacterial capsule and the toxin complex. The capsule is a poly-D-glutamic acid that protects against leukocytic phagocytosis and lysis. Anthrax toxins are composed of 3 entities: a protective antigen, a lethal factor, and an edema factor. The protective antigen is an 83-kd protein that binds to cell receptors within a target tissue. Once bound, a fragment is cleaved free to expose an additional binding site. This site can combine with edema factor to form edema toxin or with lethal factor to form lethal toxin. Edema toxin acts by converting adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). Cellular cAMP levels are increased, leading to cellular edema within the target tissue. Lethal factor is not well understood, but recent work suggests that it may inhibit neutrophil phagocytosis, lyse macrophages, and cause release of tumor necrosis factor and interleukin 1.

Anthraxy Epidemiology y A zoonotic dse; spores can remain viable in soil for yrs y Livestock can become infected and can transmit infx to humans on contact w/ infected animals or animal products (hides, hair, wool, meat) y Inc period y Less than 2 wk y MOT y Ingestion, inhalation or ingestion

Anthraxy s/sxy Cutaneous: pruritic papule

or vesicle which enlarges and ulcerates in 1-2d; a central black aschar forms (malignant pustule); lesion is painless but w/ surrounding edema y Inhalational: fever; chills; non-productive cough; chest pain; headache; myalgia; malaise; pleural effusion; septic shock y GI: N&V; anorexia; abdominal pain; ascites; hematemesis; bloody diarrhea

Anthraxy Dxy CXR y G/S and culture of blood, pleural fluid, CSF, skin

discharges, tissue bx specimeny Txy Penicillin y Ciprofloxacin

Anthraxy Nsg interventions/considerationsy Standard precaution y Meds as ordered y Post-exposure prophylaxis y Anthrax vaccine

y Prognosisy high mortality for inhalational and GI anthrax

Plaguey The plague has caused more fear and terror than perhaps any other

infectious disease in the history of humankind. It has laid claim to nearly 200 million lives and has brought about monumental changes, such as the end of the Dark Ages and the advancement of clinical research in medicine. y AlexandreYersin isolated the plague bacillus, developed an antiserum to combat the disease, and postulated its connection with fleas and rats during the epidemic of 1894. The plague bacillus was named Yersinia pestis in his memory. y Although, the plague has been considered a disease of the Middle Ages, recent interest has been spurred by concerns over its use as a potential biological weapon. Aerosolized Y pestis, causing primary pneumonic plague, has been recognized by bioterrorism experts as having one of the highest potentials for adverse public health impacts.

Plaguey In addition to the concern over its use in acts of terrorism, there

are further reasons that may cause a dramatic increase in the number of plague cases worldwide in the years to come. One reason may be the climatic change brought about by global warming. This change is ideal for increasing the prevalence of Y pestis in the host population. A recent study has estimated a more than 50% increase in the plague host prevalence with an increase of 1 degree centigrade of the temperature in spring.Another reason may be the increasing population explosion worldwide, which is bringing humans into ever-increasing contact with wildlife. Lastly, the dramatic population increase will contribute to conditions of overcrowding and poor sanitationconditions ripe for plague hosts and vectors to flourish in.

Plaguey Pathophysiology y Three forms of the plague exist: bubonic plague,

pneumonic plague, and septicemic plague. The bubonic form of the plague involves the pathognomonic "bubo" and is caused by deposition of the bacillus in the skin by the bite of an infected vector. If the vector is a flea, bacillus proliferates in the flea's esophagus, preventing food entry into the stomach. To overcome starvation, the flea begins a blood-sucking rampage. Between its attempts to swallow, the distended bacillus-packed esophagus recoils, depositing the bacillus into the victim's skin.

Plaguey Pathophysiology y The bacillus invades nearby lymphoid tissue,

producing the famous bubo, an inflamed, necrotic, and hemorrhagic lymph node. Spread occurs along the lymphatic channels toward the thoracic duct, with eventual seeding of the vasculature. Bacteremia and septicemia ensue. The bacillus potentially seeds every organ, including the lungs, liver, spleen, kidneys, and rarely even the meninges

Plaguey Pathophysiologyy The most virulent form, pneumonic plague, results from direct

inhalation of the bacillus, which occurs from close contact of infected hosts or from aerosolized bacteria such as may occur if used as a biological weapon. A severe and rapidly progressive multilobar bronchopneumonia ensues with subsequent bacteremia and septicemia. Secondary pneumonic plague is caused when an infected patient seeds his or her lungs and airways. y The third type of plague is a primary septicemic plague. This is hypothesized to occur when the bacillus is deposited in the vasculature, bypassing the lymphatics. Early dissemination with sepsis occurs but without the formation of a bubo. This usually is observed in bites to the oral, tonsillar, and pharyngeal area and is believed to occur because of the vascularity of the tissue and short lymphatic distance to the thoracic duct.

Plaguey Epidemiology y From 1967-1993, the World Health Organization has reported an annual average of 1666 cases of the plague. y MOT y Bite of vector, rat flea Xenopsylla cheopis y Contact w/ infected tissue or body fluid y inhalation

Plaguey s/sx y Fever ; chills; myalgias; sore y y y y y y y

throat; malaise Enlarged, painful, swollen lymph node(bubo) Abdominal pain Nausea, vomiting (bloody at times) Constipation, diarrhea, and black or tarry stools Cough, which may be productive of bloody sputum Shortness of breath Stiff neck

Plaguey Dx y CBC: elevated WBC y U/A: hematuria, proteinuria y ABG: hypoxia and/or acidosis y G/S, culture of blood, sputum or bubo aspirate y Tx y Gentamicin IV/IM y supportive y Nsg considerations y Meds as ordered y Universal precaution (goggles, gloves, gown; mask if pneumonic)

Lyme Diseasey is a multi-system infection

commonly affecting the skin, CNS, heart and joints caused by the spirochete Borrelia burgdorferi.The bacterium is inoculated into the skin by a tick bite. The tick is almost always of the genus Ixodes.

Lyme Diseasey Pathophysiologyy Once in the skin, the spirochete can (1) be overwhelmed and

eliminated by host defense mechanisms; (2) remain viable and localized in the skin where it produces the pathognomonic skin lesion, or erythema migrans (EM); or (3) disseminate through the lymphatics or blood. Hematogenous dissemination can occur within days to weeks of initial infection; the organism can travel to the skin, heart, joints, CNS, and other parts of the body.

Lyme Diseasey Epidemiologyy In 2001, the CDC reported

17,029 cases and, in 2002, that number rose to 23,763a 40% increase.Year-to-year variation can be significant. More than 95% of cases come from 12 states (Connecticut, Delaware, Maine, Maryland, Massachusetts, Minnesota, New Hampshire, New Jersey, New York, Pennsylvania, Rhode Island, and Wisconsin). Even within these states, incidence can be quite variable from county to county and even neighborhood to neighborhood.

y MOTy Vector-borne

Lyme Diseasey s/sxy Bulls eye rash (EM) usually

found in moist parts of the body, usually ascribed as rounded rings of rash

Lyme Diseasey Dxy Aeg hx y Dermatologic findings:Classic EM is an erythematous papule or

macule that occurs at the site of the tick bite (1-33 d later; average, 7-10 d). Often, a central punctum is found at the site. The size varies enormously (as large as 70 cm; average, 16 cm) and depends on disease duration. EM usually is flat, round, or oval and monocyclic but non-pruritic. y Elevated IgM

Lyme Diseasey Txy y y y

Amoxicillin Doxycycline Cefuroxime Erythromycin

y Nsg interventionsy Ascertain if the aeg was exposed to deer ticks y Instruct aeg to wear light colored clothing when going to the

forest/ woods or have himself/herself vaccinated y When bitten by a tick, remove it by exerting slow steady upward pull and avoid squeezing it

Denguey Dengue has been called the most important mosquito-

transmitted viral disease in terms of morbidity and mortality. Dengue fever is a benign acute febrile syndrome occurring in tropical regions. In a small proportion of cases, the virus causes increased vascular permeability that leads to a bleeding diathesis or disseminated intravascular coagulation (DIC) known as dengue hemorrhagic fever (DHF). In 2030% of DHF cases, the patient develops shock, known as the dengue shock syndrome (DSS). Worldwide, children younger than 15 years comprise 90% of DHF subjects; however, in the Americas, DHF occurs in both adults and children

Denguey Dengue is a homonym for the

African ki denga pepo, which appeared in English literature during an 1827-28 Caribbean outbreak. The first definite clinical report of dengue is attributed to Benjamin Rush in 1789, but the viral etiology and its mode of transmission via mosquitoes were not established until the early 20th century. y EA: DEN-1, DEN-2, DEN-3, DEN-4, Chikungunya virus

Denguey Pathophysiology y Dengue viral infections frequently are not apparent. Classic

dengue primarily occurs in nonimmune, nonindigenous adults and children. Symptoms begin after a 5- to 10-day incubation period. DHF/DSS usually occurs during a second dengue infection in persons with preexisting actively or passively (maternally) acquired immunity to a heterologous dengue virus serotype. Illness begins abruptly with a minor stage of 2-4 days' duration followed by rapid deterioration. Increased vascular permeability, bleeding, and possible DIC may be mediated by circulating dengue antigen-antibody complexes, activation of complement, and release of vasoactive amines. In the process of immune elimination of infected cells, proteases and lymphokines may be released and activate complement coagulation cascades and vascular permeability factors.

Denguey Epidemiology y Phil stat: 29.8/100,000 pop y Source: infected persons y Common during rainy season y Infants and children mostly affected generally 0-9yo y Inc period y 4-6d (min 3d, max 10d) y MOT y Day biting female mosquitoes (Aedes aegypti, Aedes albopictus)

Denguey s/sx y Grade Iy Fever; (+) tourniquet test; non-specific sx; abdominal sign; Hermans

sign (petechiae)

y Grade II y Grade I + bleeding (epistaxis, melena, gingival bleeding, coffee ground vomitus) y Grade III y Grade II + circulatory collapse (hypotension, rapid & weak pulse, cold clammy skin y Grade IV y Grade III + shock w/ undetectable BP & P

DengueA child with dengue hemorrhagic fever or dengue shock syndrome may present severely hypotensive with disseminated intravascular coagulation (DIC), as this severely ill PICU patient did. Crystalloid fluid resuscitation and standard DIC treatment are critical to the child's survival

DengueDelayed capillary refill may be the first sign of intravascular volume depletion. Hypotension usually is a late sign in children. This child's capillary refill at 6 seconds was delayed well beyond a normal duration of 2 seconds.

Denguey Dx y Tourniquet test y CBC: leukopenia, thrombocytopenia, low hct y Dengue blot test y Tx y Symptomatic and supportive y No specific antiviral tx y Avoid aspirin

Denguey Nsg interventions y Monitor for signs of bleeding and fall in BP y Epistaxis: lean forward y Gingival bleeding: ice chips y Hematemesis: NPO y Prognosis y Grade I & II: good y Grade III: guarded y Grade IV: serious, high mortality rate

Malariay Term malaria is derived fr Lt mal(bad) and aria(air) y Infection transmitted by female Anopheles mosquito, caused y y y y y y

by Plasmodium falciparum(most fatal), P. vivax, P. ovale, P. malariae. at high risk are pregnant women and children Sexual cycle in mosquito; asexual cycle in human rbc Pf: malignant tertian malaria Pv: benign tertian malaria Po: benign tertian malaria Pm: quartan malaria

Malariay Pathophysiologyy The degree of damage to the tissue depends mainly on the

parasitic concentration y Red cell changes:y Low deformability y High adhesion y High fragility y Low oxygen transport

y Hemolysis leading to anemia y Rupture of infected and non-infected RBC (blackwater fever) y Organ damage: spleen, liver, brain, kidneys

MalariaEpidemiologyPhil stat: 52/100,000 pop

Inc periodPf: 10-13d Pm: 27-37d or up to yrs Po: 11-26d Pv: 12-21d

MOTbite of female Anopheles

Malariay s/sxy Stages y Cold: chilling: 10-15min (hot water bath on soles) y Hot: 41deg fever (TSB, antipyretics) y Diaphoretic (increase fluids, rest)

y Dxy symptomatic y Malarial smear (peak of fever) y IFA

Malariay Txy Chloroquine + Sulfadoxine/Pyrimethamine (CQ+SP) 1st line

drug in the tx of probable malaria and confirmed Pf y Artemether-Lumefantrine (Co-ArtemTM) 2nd line drug; given only to microscopically confirmed Pf which did not respond to CQ+SP y Quinine + Tetracycline/Doxycycline 3rd line drug; should be given to those who did not respond to Co-Artem or if CQ+SP is not available y N.B.: Tetracycline and Doxycycline are conrtaindicated for pregnant women and children under 8yo; instead give Quinine w/ Clindamycin