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Difference between skin cancer and warts
1. Differences between different diseases
Clinical pharmacy
Assignment submitted by Ifsha Akhlaq 528
Difference between skin cancer and warts.
SKIN CANCER WARTS
Skincancer alsoknownas melanomaisacancer
that beginsinthe melanocytes.Because mostof
these cellsstill make melanin,melanomatumors
are oftenbrownorblack.
Warts are raisedbumpsonthe skincausedby the
humanpapillomavirus(HPV).
EPIDEMIOLOGY
- In 2007 inunitedstate 56940 casesof
melanomareported.
- In 1996 2 per100000 patient.
- In 2001 2.7 per100000 patientreported.
- Worldwide frequencyisunknownbut
estimatedapproximately7-12% of the
population.
- In school agedchildren10-20% reported.
SIGNS & SYMPTOMS
- Unusual sores
- Lumps
- Blemishes
- Marking changesincolor.
- Roughsurface
- Roundor oval warts
- Spotwhere wartsmay be lighteror
darkerthan otherskin
- Some wartscause pain
PATHOPHYSIOLOGY
Sun light exposure cause formation of thymine
dimers. DNA repair removes most UV induced
damage. Cumulative DNA damage leads to
mutation. The sunlight depresses the local immune
system and decreasing immune surveillance of new
tumor cells.
The Human papillomavirusinfectsthe epithelium
and systemicdisseminationof the virusnot
occurs. Virusreplicate inthe epidermislayer.
DIAGNOSTIC TEST
- Physical examine
- Skin biopsy
- Sentinel lymph node biopsy
- CT scan
- MRI
- Immunohistochemical detectionof HPV
structural proteins.
- Polymerase chain reactionmaybe used
to amplifyviral DNA
TREATMENT
- Interferon
- Interleukin-2
- Othermedicinessuchasipilimumab
- Chemotherapysuchasdacarbazine
- Topical agents
- Intralesionalinjections
- Photodynamictherapy
- Systemicagents
Difference between Asthma and Chronic obstructive pulmonary disease.
2. ASTHMA CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
Is a chronicdisease characterizedbyrecurrent
attacks of breathlessnessandwheezing varyingin
severityane-frequencyfrompersontoperson.
Chronicobstructive pulmonarydiseaseisalung
disease characterizedbychronicobstructionof
lungsairflow thatinterfereswithnormal
breathing.
EPIDEMIOLOGY
- In 2001 7.3% increased.
- In 2010 8.4% increased.
From2001 – 2009 asthmaper
- Worldwide deathsbyasthmais180,000 annually.
- COPDis thirdleadingcause of deathinAmerica.
- In 2010
- 12.1 millioninU.S
- 10.1 millionAmericans
- 4 percentinWashington
- 9 percentinAlbania
Reported.
Worldwide:-
- 64 millionin2004 worldwide.
- 3 millionin2005.
- 90% die inlow and middle income
countries.
SIGNS & SYMPTOMS
- Wheezing
- Whistlingsoundwhenbreathe
- Shortnessof breath
- Chestpain
- Chroniccoughing
Asthmasymptomsalsoknownasasthma flare-ups
or asthma attacks.
- Ongoingcough
- Increasedmucus
- Shortnessof breath
- Wheezing
- Fatigue
- Frequentflare-ups
PATHOPHYSIOLOGY
Involve in three components:-
1) Airway inflammation.
2) Intermittent airflow obstruction.
3) Bronchial hype responsiveness.
Airway inflammation
Mechanism of inflammation may be acute, sub
acute or chronic.
The airway edema and mucus secretion also
involve in this bronchial reactivity.
Intermittent airflow obstruction
Mucus hyper secretion, desquamation of
epithelium, hyperplasia of smooth muscles and
remodeling of airway cause air flow
obstruction.
The airway obstruction causes increased
resistance of airflow and decreased expiratory
flow rates. These changes causes decreased
The most commoncause of COPDis chronic
exposure tocigarette smoke directlyorbyair
pollutionoccupational exposure.
The smokingorotherirritantso fairwayscause
neutrophils,T-lymphocytesandother
inflammatorycellswhichare accumulate in
airways.
3. ability of expel air and hyperinflation occurs.
Bronchial hype responsiveness
Due to airflow obstruction the uneven changes
of airflow occur which is results in hypoxia,
hyper carbia is prevented by the ready diffusion
of carbon dioxide across alveolar capillary
membranes. The acute episode in early stage
has hypoxemia in the absence of carbon dioxide
retention.
Hyperventilation triggered by the hypoxic drive
which causes decrease in carbon dioxide. In
early stages the respiratory alkalosis occurs
from hyperventilation.
After this metabolic acidosis occurs due to
increased cardiac output, work of breathing,
oxygen consumption. Respiratory failure leads
to respiratory acidosis.
DIAGNOSTIC TEST
- Medical histories.
- Breathing tests.
- Spirometry test.
- Allergy test for those who have allergy with
asthma.
- X-raysor CT Scans of the chest.
- Pulmonaryfunctiontesting.
- Oximetryorarterial bloodgastesting.
TREATMENT
It requirescontinuousmedicalcare.Moderate to
Severe asthmarequire longtermmedicationsdaily
like anti inflammatorydrug.Suchas corticosteroids,
budesonide,mometasone,flunisolide.If symptoms
occur short termmedications(Inhaledshortacting
beta) agonistsanticholinergics.
There are several pathsfortreatmentof COPD.
- Avoidinginfections
- Medications
-Bronchodilators
-Anti inflammatory
-Antibiotics
- Oxygentherapy
- Pulmonaryrehabilitation
- Lung volume Reductionsurgery.
Difference between Jaundice and Hepatitis B.
JAUNDICE HEPATITIS B
Yellowingof the skinandeyesconditionoccurs
whentoomuch bilirubinispresentinbody.
HepatitisBis a viral infectionthatattacksthe liver
and can cause both acute and chronicdisease.
EPIDEMIOLOGY
- In Unitedstates
6.1% infantsin1986
4.3 % in2003
2.9% in 1994 reported.
- In Turkey10.5% reported.
- 780,000 people die inayeardue to
hepatitisB.
- In Middle Eastand Indiansubcontinent2-
5 % chronicallyinfected.
- Lessthan 1 % of the populationof
westernEurope andNorthAmericanis
4. chronicallyinfected.
SIGNS & SYMPTOMS
- Yellowtintedskinandeye
- Whitesof eye turnbrownbut in severe
condition
- Dark urine
- Pale stool
- Excessive fatigue
- Vomiting
- Dark urine
- Jointpain
- Loss of appetite
- Fever
- Abdominal discomfort
- Weakness
- Yellow skinandeyes
PATHOPHYSIOLOGY
Bilirubin is produced by breakdown of
hemoglobin into unconjugated bilirubin. Un
conjugated bilirubin binds to albumin in the
blood and transport to liver. In liver the enzyme
uridine diphosphogluconurate
glucuronasyltransferase (UGT) conjugated this
bilirubin with glucronic acid which is taken up
by hepatocytes. This conjugated bilirubin
excreted in bile. In patients or neonates the
conjugated bilirubin is deconjugates and
recycled into the circulation and not excreted
from body.
Bloodbecome exposedtoHBV the bodycell
mediatedimmuneresponse sendingcytotoxicT
cellsandnaturallykillercellsagainstthe virusand
release inflammatorycytokines.
As the hepatocytesare attackedandinfiltrated
by the HBV.Because hepatocytesare continually
proliferatingthe virusisconstantlybeingshed
intothe bloodwhichleadstothe chronic illness.
DIAGNOSTIC TEST
- CBCs
- Liver function test
- Imaging test
Abdominal ultrasounds
Computed tomography scans
Magnetic resonance imaging
- Liver biopsies
- HepatitisBsurface antigentest
- HepatitisBcore antigentest
- AntibodyHepatitisBsurface antigentest
- Liverfunctiontests
TREATMENT
- Supportive care
- Jaundice causedbymedication/drugsthe
antidote isrequired.
- Steroidsinwhichhave autoimmune
diseaseswithjaundice.
- Diureticsandlactulose isusedinjaundice
withcirrhosis.
- Antibioticsforinfectiouscausesof jaundice.
- Blood transfusionsmaybe requiredin
individualswhohave anemiafrom
hemolysis.
- Surgeryisrequiringforjaundice with
gallstones.
- Jaundice withliverfailure needliver
transplant.
- HepatitisBimmune globulin
Within24hours incontact withHBV
- Antiviral medication
- Livertransplant
5. Difference between Hepatitis A and Hepatitis C.
HEPATITIS A HEPATITIS C
Hepatitis A is a liver disease caused by the
hepatitis A virus. The virus is spread when an
uninfected person ingest food or water that is
contaminated with the faeces of an infected
person.
A liver disease caused by hepatitis C virus.
Virus can cause both acute and chronic
hepatitis infection.
EPIDEMIOLOGY
- 1.4 millioncasesof hepatitisA everyyear.
- In Shanghai in1988 about300,000 people
reportedwithhepatitisA.
- In developingcountriesabout90%childrenare
affected.
- 130-150 million people have chronichepatitisC.
- 350000 to 500000 people die inayear.
Most affectedregionsare Central andEastAsia
and NorthAfrica.
SIGNS & SYMPTOMS
- Flulike symptoms(fever,fatiguebodyaches)
-Abdominal pain
-Lightcoloredstool
-Dark urine
-Lossof appetite
-Unexplainedweightloss
-Jaundice
-Malaise
-Diarrhea
80% patienthave nosymptomsbutsome
complainof mildtosevere systemssuchas
-Fever
-Dark urine
-Lossof appetite
-Abdominal pain
-Jointpain
-Jaundice
PATHOPHYSIOLOGY
HAV virus acquired by mouth and replicate in
liver. After 10-12 days virus present in blood
and excreted in the biliary system into are feces.
Virus is present in serum and virus excretion
begins to decline in at the onset of clinical
illness.
The natural targetsof HCV are hepatocytesandB-
lymphocytes.Viral clearance isassociatedwith
the developmentandpersistenceof strongvirus-
specificresponsesbyTlymphocytesandhelperT
cells.
DIAGNOSTIC TEST
-Detection of HAV-specific IgM and IgG
antibodies
-Reverse transcriptase polymerase chain
reaction
-CBCtest
-Serological test
-Nucleicacidtest
-Genotypingtest
-Liverfunctiontest
-Liverbiopsy
TREATMENT
No specifictreatmentsforhepatitisA but
symptomsare treated.
Therapyusedto maintaincomfortsuchas
replacementof fluidswhichare lostfromvomiting
and diarrhea.
-Antiviral treatment
Bedrest isrecommended
-Antiviral combinationtherapywithinterferon
and ribavirin.
6. Difference between Infection and Disease.
INFECTION DISEASE
The invasionandmultiplicationof microorganism
such as bacteria,virusandparasitesthatare not
normallypresentwithinthe body.
Illnessorsicknesscharacterizedbyspecificsigns
and symptoms
EPIDEMIOLOGY
- In unitedstate 2 millionsnosocomial
infectioninhospitalizedpatient.
- 3-21 % in2002 survey
- Annually 1billionpoundscostinUnited
kingdom10% patient
- The 95% of the worldwide population
measuredindisease.
SIGNS & SYMPTOMS
- Fever
- Warm
- Painful swollenwound
- Bloodor puscomingfrom the wound
- Dizziness
- Fast heartbeat
- Disease maybe acute,chronic,malignant
or benign.
- Acute disease symptomsare nausea,
vomitingandpain.
- Chronicdisease have severe pains,
diarrhea,swelling,breathingtroublesetc.
PATHOPHYSIOLOGY
the normal host cell response to infection is a
complex process that localizes and controls
bacterial invasions, and initiating the repair of
any injured tissues.
Involves
- Activation of circulating and fixed
phagocyte cells,
- The generation of pro inflammatory and
inflammatory mediators.
- Sepsis results when the response to
infection becomes generalized and
involves normal tissues from the site of
injury or an infection.
Functional changesinthe bodythatoccurs in the
body.
A disease wouldchange the conformationof an
enzyme;something wouldnotbe spiltoraltered
insome way thenleadstosymptoms.
DIAGNOSTIC TEST
- Blood tests
- X-rays
- C T scan
- MRI scan
- Wound culture
- Differenttype of diagnostictestsare
- Bloodtests
- Computedtomographyscan
- X-rays
- TREATMENT -
- Woundcleaning
- Antibiotics
- NSAIDS
- Life style changes
- Follow ahealthydiet
- Exercise regularly
- Manage stress
- Medicines
- Surgeries
7. References
1) Skincancer melanomabyMichael RHoltel,MD
http://www.emedicine.medscape.com/article/846566-overveiw#a11
Access date 9th
October2014
2) Woundinfections
www.drugs.com/cg/wound-infection.html.
Accessdate 9th October2014
www.medicinenet.com/script/main/art.asp?articlekey=12923
accessdate 9th
October2014
3) Pathophysiologyof sepsisbyRemi Neviere,MD
http://www.uptodate.com/contents/pathophysiology-of-sepsis?Source=outline-linkand
view=textandanchor=H544041.
Date of access13th
October2014
4) Human diseaseswrittenbyJonathanH.RobbinsM.D
www.bratanmica.com/EBchecked/topic/275628/human-disease.
Date of access9th
October2014
5) HepatitiswrittenbyVinodKDhavan,MD,FACP,FRCP( C) ,FIDA
www.emedia.medscape.com/article/177792-overview#aw2aab6b2b3aa
Date of access8th
October2014
6) Hepatitis Cwittenbyapril Kalm
www.healthline.com/health/hepatits-c
Date of access8th
October2014
7) HepatitisA
Epidemiologyandpreventionof vaccine-preventable diseases.
The pinkbookcourse textbook12th
editionsecondprintingMay2012
www.cdc.gov/vaccines/pubs/pinkbook/hepa.htm
8. Date of access 9th
0ctober
8) HepatitisA writtenbyRichardK Gilroy,MBBS,FRACP
www.emedicine.medsacpe.com/article/177484-overview#ao104
Date of access 9th
0ctober 2014
9) Definitions
www.who.int/mediacenter/factsheets/fs164/en/
www.who.int/mediacenter/factsheets/fs328/en/
www.who.int/mediacenter/factsheets/fs204/en/
www.who.int/mediacenter/factsheets/fs315/en/
www.who.int/mediacenter/factsheets/fs307/en/
Date of access 7th
October2014
10) AmericanAcademyof allergy,AsthmaandImmunology
http://www.aaaai.org/conditions -and-treatments/asthma.aspx
Date of access 5th
October2014
11) Pathophysiologyof asthmawrittenbyMicheal JMorris,MD,FACP,FCCP
www.emedicine.medscape.com/article/296301-overview#aw2aab6b2b4
Date of access 7th
October2014
12) Americanlungsassociationfightingforair
www.lung.org/lung-disease/copd/resources/facts-figures/copd-fact-sheet.html
Date of access 8th
October2014
13) COPDwrittenbyRobinMadele MedicallyReviewedbyGeorge Kruik,MD.MBA/publishedon27th
February2013
www.healthlin.com/health-slideshow/copd-symptoms
Date of access 8th
October2014