World MALARIA Day     

               April 25

Malaria is a protozoal disease caused by infection with parasites of the genus Plasmodium and transmitted to man by certain species of infected female Anopheline mosquito.

A typical attack include 3 stages

·         COLD STAGE

·         HOT STAGE

·         SWEATING STAGE

ETIOLOGY

Caused by

·         P.vivax

·         P. falciparum

·         P.malariae

·         P.ovale (rare)

LIFE CYCLE OF MALARIAL PARASITE

They undergo two cycles of development

·         Human cycle/asexual cycle/endogenous phase

·         Mosquito cycle/sexual cycle/exogenous phase

Man is the intermediate host and mosquito is the definite host

The asexual cycle has (– the asexual cycle begins when infected mosquito bites and injects “sporozoites”)

1.   HEPATIC PHASE – the sporozoites disappear within 60 minutes from peripheral circulation, most of them are destroyed by phagocytes, some reaches liver cell. After two weeks they become hepatic schizonts which eventually burst releasing a number of merozoites

2.   ERYTHROCYTE PHASE-significant merozoites penetrate the RBC and pass through the stages of trophozoites and schizont. The erythrocyte phase ends with the liberation of merozite, which infects fresh RBC.

3.   GAMETOGENY-some erythrocyte forms don’t divide but become male and female gametocyte.

The sexual cycle

The mosquito cycle begins when gametocytes are ingested by the vector when feeding on an infected person. Exflagellation of the male gametocyte is the first vent taking place in mosquito’s stomach, where 4-8 thread like filaments called “micro gametes” are developed.

Female gametocyte matures and becomes “macro gametes”. The resulting zygote is at first immotile and then becomes motile in 18-24 hours, which is known as OOKINETE which develops into oocyst and then to sporozoites. Many sporozoites migrate to the salivary gland and mosquito becomes infective.

EXTRINSIC INCUBATION PERIOD- the time period required for the development of parasite from gametocyte to sporozoite stage (10-20 days)

MODE OF TRANSMISSION

·         Vector transmission

·         Direct transmission

·         Congenital malarial

SYMPTOMS AND DIAGNOSIS

 Early and accurate diagnosis of malaria is essential for effective disease management and malaria surveillance. High-quality malaria diagnosis is important in all settings as misdiagnosis can result in significant morbidity and mortality.

WHO recommends prompt parasitological confirmation of diagnosis either by microscopy or malaria rapid diagnostic test (RDT) in all patients with suspected malaria before treatment is administered. On World Malaria Day 2012, WHO launched a new initiative called T3: Test. Treat. Track

CLINICAL FEATURES

·         COLD STAGE  - temperature rises to 39-41⁰c

                     Headache, nausea, vomiting

                     Skin is initially cold and later becomes hot

                        Stage lasts for ¼-1 hour

·         HOT STAGE – feels burning hot

                     Skin is hot and dry to touch

                     Intense headache and no vomiting

                     Lasts for 2-6 hours

·         SWEATING STAGE – fever

                            Skin is cold and moist

                            Patients feel relief and often fall asleep

 PREVENTION

MEDICATION 

HAEMOPHILIA

HAEMOPHILIA

THE WORLD HAEMOPHILIA DAY--- 17 APRIL

Hemophilia A—Factor VIII Deficiency

Hemophilia A is the most common hereditary cause of serious bleeding. It is an X-linked recessive disorder caused by reduced factor VIII activity. It primarily affects males. Much less commonly excessive bleeding occurs in heterozygous females, presumably due to preferential inactivation of the X chromosome carrying the normal factor VIII gene (unfavorable lyonization). Approximately 30% of cases are caused by new mutations; in the remainder, there is a positive family history. Severe hemophilia A is observed in people with marked deficiencies of factor VIII (activity levels less than 1% of normal). Milder deficiencies may only become apparent when other predisposing conditions, such as trauma, are also present. The varying degrees of factor VIII deficiency are explained by the existence of many different causative mutations. As in the thalassemias, several types of genetic lesions (e.g., deletions, inversions,splice junction mutations) have been identified. In about 10% of patients, the factor VIII concentration is normal by immunoassay, but the coagulant activity is low because of a mutation in factor VIII that causes a loss of function. In symptomatic cases there is a tendency toward easy bruising and massive hemorrhage after trauma or operative procedures. In addition, “spontaneous” hemorrhages frequently are encountered in tissues that normally are subject to mechanical stress, particularly the joints, where recurrent bleeds (hemarthroses) lead to progressive deformities that can be crippling. Petechiae are characteristically absent. Specific assays for factor VIII are used to confirm the diagnosis of hemophilia A. Typically, patients with hemophilia A have a prolonged PTT that is corrected by mixing the patient’s plasma with normal plasma. Specific factor assays are then used to confirm the deficiency of factor VIII. In approximately 15% of those with severe hemophilia A replacement therapy is complicated by the development of neutralizing antibodies against factor VIII, probably because factor VIII is seen by the immune system as a “foreign” antigen. In these persons, the PTT fails to correct in mixing studies. Hemophilia A is treated with factor VIII infusions. Historically, factor VIII was prepared from human plasma, carrying with it the risk of transmission of viral diseases. Before 1985 thousands of hemophiliacs received factor VIII preparations contaminated with HIV. Subsequently, many became seropositive and developed AIDS. The availability and widespread use of recombinant factor VIII and more highly purified factor VIII concentrates have now eliminated the infectious risk of factor VIII replacement therapy.

Hemophilia B—Factor IX Deficiency

Severe factor IX deficiency is an X-linked disorder that is indistinguishable clinically from hemophilia A but much less common. The PTT is prolonged. The diagnosis is made using specific assays of factor IX. It is treated by infusion of recombinant factor IX. It is clinically similar to hemophilia A.The severity of symptoms can vary. Bleeding is the main symptom. It is often first seen when the an infant is circumcised. Other bleeding problems usually show up when the infant starts crawling and walking. Mild cases may go unnoticed until later in life. Symptoms may first occur after surgery or injury. Internal bleeding may occur anywhere.

Symptoms can include:

• Bleeding into joints with associated pain and swelling
• Blood in urine or stool
• Bruising
• Gastrointestinal tract and urinary tract hemorrhage
• Nosebleeds
• Prolonged bleeding from cuts, tooth extraction, and surgery
• Spontaneous Bleeding

MNEMONICS:-

Hemophilia C- Factor XI deficiency

Low levels of factor XI (FXI) cause hemophilia C. FXI plays an important role in tissue factor-dependent thrombin generation on the surface of activated platelets.The formation of the initiating complex, TF-FVIIa-FXa, results in the generation of a small amount of thrombin. This is insufficient to produce a stable fibrin clot but stimulates a number of reactions in the amplification loop, including the activation of FXI. Subsequent formation of the tenase complex (FIXa-FVIIIa), followed by the prothrombinase complex (FXa-FVa), leads to a large burst of thrombin. For a schematic of these processes, Hemophilia C is also known as plasma thromboplastin antecedent (PTA) deficiency or Rosenthal syndrome. Like the other hemophilias, hemophilia C is associated with bleeding, but it differs from hemophilia A and B in some ways.

BRACHIAL PLEXUS --- MNEMONICS

BRACHIAL PLEXUS --- MNEMONICS

Introduction

The Brachial Plexus is a network of nerve fibers that run from the spine, passing through the cervico-axillary canal to reach axilla.  It is formed by the ventral rami of the lower four cervical and first thoracic nerve roots (C5-C8, T1). Sometimes C4 may also be involved.

Function

The brachial plexus is responsible for cutaneous and muscular innervation of the entire upper limb, with two exceptions: the trapezius muscle innervated by the spinal accessory nerve (CN XI) and an area of skin near the axilla innervated by the intercostobrachial nerve.

Description

Path

The brachial plexus is divided into Roots, Trunks, Divisions, Cords, and Branches. There are five "terminal" branches and numerous other "pre-terminal" or "collateral" branches that leave the plexus at various points along its length.

• The five Roots are the five anterior rami of the of the lower four cervical and first thoracic nerve roots (C5-C8, T1), after they have given off their segmental supply to the muscles of the neck.
• These Roots merge to form three Trunks:
  • Upper Trunk (C5-C6)
  • Middle Trunk (C7)
  • Lower Trunk (C8, T1)

• Each Trunk then splits into anterior and posterior divisions, to form six Divisions.   The anterior/ posterior divisions innervate flexor groups versus extensor groups:
  • anterior divisions of the upper, middle, and lower trunks
  • posterior divisions of the upper, middle, and lower trunks
• These six Divisions will regroup to become the three Cords. The Cords are named by their position with respect to the axillary artery.
  • The Posterior Cord is formed from the three posterior divisions of the trunks (C5-C8,T1)
  • The Lateral Cord is the anterior divisions from the upper and middle trunks (C5-C7)
• The Medial Cord is simply a continuation of the anterior division of the lower trunk (C8,T1)

MNEMONICS----

LATERAL CORD:-  (LML)

1.LATERAL PECTORAL

2.MUSCULOCUTANEOUS

3.LATERAL ROOT OF MEDIAN NERVE

POSTERIOR CORD:- (ULNAR)

1.UPPER SUBSCAPULAR

2.LOWER SUBSCAPULAR

3.NERVE TO LATISSIMUS DORSI

4.AXILLARY 

5.RADIAL

MEDIAL CORD:- (M4U)

1.MEDIAL PECTORAL NERVE

2.MEDIAL ROOT OF THE MEDIAN NERVE

3.MEDIAL CUTANEOUS NERVE OF ARM

4. MEDIAL CUTANEOUS NERVE OF FOREARM

5.ULNAR

Some more mnemonics for remembering the branches:

Posterior Cord Branches:-
STAR - subscapular (upper and lower), thoracodorsal, axillary, radial.
ULTRA - upper subscapular, lower subscapular, thoracodorsal, radial, axillary

Lateral Cord Branches:-
LLM "Lucy Loves Me" - lateral pectoral, lateral root of the median nerve, 
                    musculocutaneous

Medial Cord Branches:-
MMMUM "Most Medical Men Use Morphine" - medial pectoral, medial
                     cutaneous nerve of arm, medial cutaneous nerve of forearm, ulnar, 
                     medial root of the median nerve.

COAGULATION CASCADE---MNEMONICS

COAGULATION CASCADE/CLOTTING FACTORS --- MNEMONICS

Clotting factors are substances in the blood that act in 

sequence to stop bleeding by forming a clot.

Here's a mnemonic to help you remember them.

I Fibrinogen

II Prothrombin

III Tissue factor

IV Calcium

V Proaccelerin, Labile factor

VI  Unassigned – Old name of Factor Va

 
VII Stable factor, proconvertin

VIII Antihemophilic factor A

IX Antihemophilic factor B or Christmas factor

X Stuart-Prower factor

XI Plasma thromboplastin antecedent

XII Hageman factor

XIII Fibrin-stabilizing factor

Mnemonics:-

"Fresher's Party Tonight, Come Let's Sing And Call Seniors, Please Have Fun"

"Foolish People Try Climbing Long Slopes After Christmas, Some People Have Fallen"

"Fit Pants, Tight Collars, Loose American Shirts Are Cool Says Pretty Heroine Farah"


Here is how you draw the coagulation cascade:-

Intrinsic pathway is activated by subendothelial collagen.

Extrinsic pathway is activated by tissue thromboplastin.

Another mnemonic:
1972 WEPT

1972: Factors 10, 9, 7 & 2
W: Warfarin
E: Extrinsic
PT: Prothrombin Time

Factors X, IX, VII, II are Vitamin K dependent.
Warfarin acts on extrinsic pathway, prothrombin time used to check it.

Heparin acts on intrinsic pathway, partial thromboplastin time is used to check it.

Here is one MNEMONIC for hemophilia.
Remember in hemophilia, bleeding time is normal, PTT is increased.