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== Hyperventilation ==
{| class="wikitable"
! rowspan="3" |Organ system
! rowspan="3" |Diseases
! colspan="9" |Clinical manifestations
! colspan="5" rowspan="2" |Diagnosis
! rowspan="3" |Other features
|-
! colspan="4" |Symptoms
! colspan="5" |Physical exam
|-
!Chest pain
!Dyspnea
!Fever
!Palpitations
!Cyanosis
!Tachypnea
!JVD
!Peripheral edema
!Auscultation
!ABGs
!Lab findings
!Imaging
!PFT
!Gold standard


|-
! rowspan="8" |Pulmonary system
!Pneumothorax
!+
!+
!+
!+
!+
!+
!_
!_
!
* Decreased breath sounds
!
-
!
Decreased Vt
!X- ray -
*Mediastinal shift
*Deep sulcus sign
*Hydropneumothorax
*CT-scan- Bullae
!
Decreased Vt
! CT-scan
!
*Hypoxia,
*Hypercapnia
* Hyperesonance to percussion,
* Vocal resonance
*Tactile fremitus decreased
|-
!Pulmonary embolism
!+
!+
!+
!+
!+
!+
!-
!-
!
* S3 gallop
*S4 gallop
!
Respiratory alkalosis
!
* Increased D- dimers
*Increased Troponins
!
* Duplex ultrasound
*EChocardiography
* Ventilation-perfusion scanning
!
Normal
!
CT angiography
!
* Hemoptysis
*History of coagulation abnormalities
* Malignancy
|-
!Pneumonia
!+
!+
!+
!+
!+
!+
!-
!-
!
*Bronchial breath sounds
*Crepitations
*Bronchophony
*Egophony
*Whispering pectoroloqy
!
Normal
!
*CBC
*Blood culture
*Mantoux test
*Serology (mycoplasma, viruses)
*Sputum: Gram stain and culture
!
*CXR- Lobar consolidation, Air bronchogram;
*Atypical pneumonia: Diffuse interstitial infiltrates
!
Normal
!
*CXR- Lung infiltrates
* Blood culture
!
* Productive cough
*Altered mental status
* Tachycardia
* Central cyanosis


|-
*C3 [[glomerulopathy]] must be differentiated from other [[diseases]] that cause [[inflammatory]] [[glomerulonephritis]] with [[glomerular]] [[complement]] deposition such as:
!Exacerbation of asthma/COPD
:*[[Infection]]-related [[glomerulonephritis]]
!-
:*[[Lupus nephritis|Lupus nephr]]<nowiki/>itis
!+
:*[[Paraprotein]] related [[glomerulonephritis]].
!-
!+
!+
!+
!-
!-
!
*Decreased breath sounds
*Wheezing
*Coarse crackles
 
!
*Increased PaCo2
*Decreased PaO2
!
*CBC- Increased hematocrit from chronic hypoxia
*Sputum evaluation, BNP( to rule out heart failure)
!
*X- ray:
*Hyperinflated lungs
*Flattening of the diaphragm
*Narrow heart shadow
*Cardiomegaly
!
*Increased TLC
*Increased RV
*Decreased Vital capacity
*Decreased DLco ( Emphysema)
*Normal DLco ( Chronic bronchitis)
!
*HRCT ( High resolution computed tomography of the lung)
!
*Productive cough
*Exercise intolerance
*Altered mental status
*Cor-pulmonale
*Hyperresonance on percussion
|-
!Interstitial lung disease
!+
!+
!-/+
!+
!+
!+
!-/+
!-
!
* Fine crackles
* Loud P2
!
* Increased A-a gradient
*Decreased PaO2
*Increased PaCo2
!-
!
* Chest X-ray- Reticular infiltrates
* Honey combing
!
*FEV1 decreased
*FVC decreased
*TLC decreased
* RV decreased
*DLco decreased
*FEV1/FVC normal
 
!
* HRCT -more accurate than chest xray
* Most accurate test is lung biopsy
!
*Physical examination shows clubbing
*Decreased pulmonary compliance
|-
!Intrapulmonary shunt
!+/-
!+
!-
!-
!+
!+/-
!-
!-
!Diminished breath sounds
! * Decreased O2
*Increased CO2
!
*CBC- Anemia, polycythemia
!
* Chest X-ray and CT : Smooth nodule with a feeding artery and a draining vein
!
* Decreased Vt, increased residual volume ( physiological)
!
CT angiography
!
* Chronic hypoxemia
* Clubbing
|-
!Upper airway obstruction
!-/+
!+
!-
!-/+
!-/+
!+
!-/+
!-
!Inspiratory stridor
!
* Increased PaCo2
* Decreased PaO2
!
-
!
*Plain radiograph of the neck
*Steeple sign (Croup in pediatric population)
*Thumb sign ( Epiglottitis)
*CT
*MRI
!Decreased vital capacity
!
* HRCT
* Bronchoscopy
!
* Hoarseness
* Accessory muscle use during respiration
*Chest retractions
|-
!High altitude sickness
!-
!+
!+/-
!+
!+/-
!+
!-
!+
!-/+
* Crackles
!
* Respiratory alkalosis
!
*CBC
*EKG- Right sided heart strain
!
*CXR- Bilateral patchy infiltrates
*Brain Ct scan
!
Decreased FVC
!
Test in hypobaric chamber with and without supplemental oxygen
!
* Headache
* Altered mental status
* Pulmonary edema
*Peripheral edema
*Epistaxis
*Rapid pulse
|-
! rowspan="4" |Cardiovascular system
!Acute coronary syndrome
!+
!+
!-
!+/-
!+/-
!+/-
!+/-
!+/-
!
* S3
*Systolic murmur
*Rales
!-
!
*Cardiac enzymes
*EKG
*CBC
*BNP
!
*Chest radiograph:
* Cardiomegaly
* Pulmonary edema
*Echo cardiography
*Myocardial perfusion imaging
*Cardiac angiography
!-
!
* Cardiac troponin
*Coronary angiography
!
* Diaphoresis
*Nausea
*Vomiting
*Presyncope
*Displacement of apical impulse
|-
!Heart failure
!+
!+
 
!-
!
+/-
!
+/-
!
+/-
!
+
!
+
!S3
! Respiratory alkalosis
!
* Increased BNP
* Hyponatremia
* Hypoalbuminemia
*EKG: To know the underlying cause( such as Afib, old MI)
!
* Chest X-ray: Increased cardio thoracic ratio, pulmonary edema, cardiomegaly, pleural effusion
!
Decreased Vt
!
* B-type natriuretic peptide
!
* Exertional dyspnea
*Orthopnea
* Paroxysmal nocturnal dyspnea
* Fatigue
* Hepatojugular reflex
* Hepatomegaly
|-
!Dysrhythmias
!+/-
!+
!-
!+
!-
!+/-
!-
!-
!Tachycardia
!Normal
! Abnormal BMP
!Normal
!Normal
!EKG
! Etiology:
* Cardiac
* Throtoxicosis
*Electrolyte abnormalities
*Psychiatric
* Medication induced
|-
!Shock
!+/-
!+/-
!+
!+/-
!+/-
!+/-
!+/-
!+/-
!
*Wheezing
*Stridor
!
* Mixed acid base disorders
!
Leukocytosis
!
Chest X-ray
!
Decreased Vt
!
Depends on the cause of shock
!
*Hypotension
*Pulsus paradoxus
*Altered mental status
*Oliguria
|-
! rowspan="3" |Metabolic/Systemic disorders
!Diabetic ketoacidosis
!-
! +
!-
!-
!-
!+
!-
!-
!-
! Metabolic acidosis
!
* Anion gap metabolic acidosis
*Serum Beta- hydroxy butyrate
*Acetone
* acetoacetate
* Urine ketones
*Hyponatremia
*Hyperkalemia
*Azotemia
* Hyperosmolality
*EKG
!
-
!
Normal
!
Blood test: Acidosis, hyperglycemia, ketonemia
!
* Hyperventilation (Kussumal's breathing)
*Hyperkalemia(But,depletion of total body potassium)
*Increased anion gap
* Abdominal pain
*"Acetone" odor on breath
*Polydypsia
*Polyuria
-
|-
!Hypocalcemia
!-
!-/+
!-
!+
!-/+
!-/+
!-/+
!-/+
!
* Inspiratory/expiratory wheezes
*S3
!
Respiratory alkalosis
!
* BMP
*LFT
* Serum albumin
*Coagulation markers
* Serum inonized calcium
*Serum 25 hydroxy Vitamin D
*Serum PTH ( Para thyroid hormone)
* EKG: QT prolongation
!
-
!
Normal
!
Serum ionized calcium
!
*Chvostek sign
*Trousseausign
*Tetany
*Seizures
|-
!Hypoglycemia
!-
!-
!-
!+
!-
!-
!-
!-
!-
!-
!
* BMP
*Oral glucose tolerance test
*72 hr fasting plasma glucose
*Serum Insulin level
* Serum Pro insulin
*Plasma C- Peptide
*Serum Cortisol
*Serum Thyroid hormone levels
* Urine analysis
* Blood culture
Liver function tests
!
*Chest X-ray: to rule out any infectious cause
*MRI : To rule out tumors like Insulinoma
* CT scan : To rule out any tumors producing Insulin like growth factors
!
-
!
* Glucose tolerance test
!
* Adrenergic symptoms: Sweating, tachycardia, anxiety
* Neuroglycopenic symptoms: Weakness, dizziness, confusion, blurry vision, coma in extreme cases
|-
! rowspan="2" |Endocrine system
!Hyperthyroidism
!-/+
!+
!-/+
!+
!-
!+/-
!-/+
!-/+
!
* Systolic hypertension with wide pulse pressure
!
* Respiratory acidosis
!
*Serum freeT3
*Serum freeT4
*Serum TSH
*Radioactive iodine uptake (RAIU)
*Antithyroglobulin antibodies
*Antimicrosomal antibodies
!
* Diffuse/ nodular uptake on thyroid scanning
!
Normal
!
* Serum TSH level
!
*Tremors
*Heat intolerance
*Excessive sweating
*Atrial fibrillation
*Exopthalmos
|-
!Pheochromocytoma
!-
!+
!-/+
!+
!-
!-/+
!-
!-
!
-
!
Normal
!
* Increased Plasma and urinary catecholamines and metanephrines
*Increased Urinary Vanillylmandelic acid level
!
* Non contrast CT
*MRI
*Nuclear Imaging: Meta Iodo-benzyl guanidine(I-123 MIBG)
 
!
Normal
!
* 24 hr urine test for metanephrines, catechoalmines and Vanillyl mandelic acid
!
* Von-Hippel Lindau syndrome
*MEN-I and MEN-II syndromes
*Hereditary paraganglionic syndromes
* Neurofibromatosis-I
|-
! rowspan="2" |CNS
!Central nervous system tumor
!-
!-/+
!-/+
!-
!-
!-/+
!-
!-
!Normal
!Respiratory acidosis
!
* CSF analysis- tumor cella
* Evoked potentials
* Audiometry
!
*MRI with contrast
*CT scan
!Normal
!Contrast enhanced Magnetic resonance imaging
!
*Headaches
*Focal neurological deficits
*Seizures
*Diplopia
*Gait ataxia
*Personality changes
|-
!Anxiety/panic attacks
!+/-
!+
!-
!+/-
!-
!-
!-
!
Normal
!
Normal
!
Normal
!
*CBC
*BMP
*TSH
*Blood alcohol level
*Serum drug screen
*Urine toxicology
*Urine metanephrines ( In refractory cases)
*EKG- sinus tachycardia
!
Normal
!Normal
!
* Psychiatric mental status examination
* General medical and neurologic examination
!
*Restlessness
*Easy fatiguability
*Difficulty concentrating
*Irritability
*Sleep problems
*Muscle tension
|-
! rowspan="3" |Others
!Pregnancy
!-/+
!+
!-
!-
!-
!-
!-
!-/+
!
* Normal
*Systolic murmur in some women
*S3 heard in some women
!
Respiratory  alkalosis
!
*CBC
*Rh type and screen
*Urine analysis
*Beta-HCG
*Glucose tolerance test
*Cervical cultures for Gonorrhea and Chlamydia
!
*Ultrasound
!
* Decreased Vt
* Increased residual volume
!
* Beta- HCG
* Ultrasound
!
* Amenorrhea
* Hypercoagulability
* Hyperemesis gravidarum
*Hemodilution
* Chloasma
* Striae gravidarum
|-
!Hepatic failure
!-
!-/+
!-/+
!-/+
!-/+
!+
!+
!+
!
*Right ventricular gallop
* Abdominal venous hum (portal vein hypertension)
*Hepatic arterial bruit( Alcoholic hepatitis, Cancer)
* Hepatic friction rub(Cancer, Fitz-Hugh-Curtis syndrome)
!
Respiratory alkalosis
!
* CBC
*Blood culture
* Abnormal liver function tests
*Abnormal prothrombin time
*Abnormal Serum ammonia levels
*Gamma glutamyl transpeptidase(GGT)
*Serum ceruloplasmin level
*Serum alpha-1 antitrypsin levels
*Serum alpha- feto protein levels
*Serum cholesterol levels
 
!
* Doppler ultrasound establishes patency and direction of blood flow in hepatic and portal veins
*Ultrasound- ascites
* CT scan with contrast( in evaluation of parenchymal disease)
* Magnetic resonance imaging
* Magnetic resonance cholangio pancreatography (MRCP: for visualizing intra and extra hepatic bile ducts)
!
Normal
!
Liver biopsy
!
* Jaundice
*Encephalopathy
*Ascites
*Hepatomegaly
*Splenomegaly
*Gynecomastia
|-
!Sepsis
!-
!+
!+
!-/+
!-
!-
!-
!-
! Normal
!Respiratory acidosis
!Leukocytosis
!Normal
!Normal
!SIRS criteria
!
* Fever
* Altered mental status
*Chills
* Hypotension
* Tachycardia
|}
 
== SChizophrenia==
 
Causes: (original)
 
 
__NOTOC__
{{Schizophrenia}}
{{CMG}};{{AE}}{{Vbe}}
 
==Overview==
[[Schizophrenia]] is a [[psychiatric]] [[diagnosis]] that describes a [[mental illness|mental disorder]] characterized by impairments in the [[perception]] or expression of [[reality]] and by significant [[Social anxiety|social]] or occupational dysfunction.
 
The causes of [[schizophrenia]] have been the subject of much debate over many decades with various factors proposed and discounted. To date none has been fully elucidated, but evidence suggests that [[genetic]] vulnerability and [[Environmental Health Perspectives|environmental]] stressors act in combination to result in schizophrenia.
 
Studies suggest that [[genetics]], early environment, [[neurobiology]] and [[psychological]] and [[Social anxiety|social]] processes are important contributory factors. Current [[psychiatric]] research into the [[development]] of the disorder often focuses on the role of neurobiology, although a reliable and identifiable [[Organic Chemistry|organic]] [[Cause system|cause]] has not been found. In the absence of a confirmed specific [[pathology]] underlying the [[diagnosis]], some question the legitimacy of schizophrenia's status as a [[disease]]. Furthermore, some propose that the perceptions and feelings involved are meaningful and do not necessarily involve impairment. Although no common cause of [[schizophrenia]] has been identified in all individuals diagnosed with the condition, currently most researchers and clinicians believe it results from a combination of both [[human brain|brain]] vulnerabilities (either inherited or acquired) and stressful life-events. This widely-adopted approach is known as the 'stress-vulnerability' model, and much scientific debate now focuses on how much each of these factors contributes to the development and maintenance of schizophrenia.
 
It is also thought that processes in early [[neurodevelopment]] are important, particularly [[prenatal]] processes. In adult life, importance has been placed upon the function (or malfunction) of [[dopamine]] in the [[mesolimbic pathway]] in the brain. This theory, known as the [[dopamine hypothesis of schizophrenia]] largely resulted from the accidental finding that a [[Medication|drug]] group which blocks dopamine function, known as the [[phenothiazine]]s, reduced [[psychotic]] [[symptoms]]. However, this theory is now thought to be overly simplistic as a complete explanation. These [[drugs]] have now been developed further and [[antipsychotic]] [[medication]] is commonly used as a first-line [[Treatment-resistant depression|treatment]]. Although effective in many cases, these [[medications]] are not well tolerated by some patients due to significant [[adverse drug reaction|side-effects]]. The [[Positive-sense RNA|positive]] [[symptoms]] are more responsive to [[medications]]; negative [[symptoms]] being less so.
 
Differences in [[brain]] structure have been found between people with [[schizophrenia]] and those without. However, these tend only to be reliable on the group level and, due to the significant variability between individuals, may not be reliably present in any particular individual. Significant [[brain]] [[atrophy]] and enlarged [[ventricular system|ventricles]] are the most conspicuous of such differences.
 
==Causes==
While the reliability of the [[schizophrenia]] [[diagnosis]] introduces difficulties in measuring the relative effect of [[genes]] and [[Environment, Health and Safety|environment]] (for example, symptoms overlap to some extent with severe [[bipolar disorder]] or major depression), evidence suggests that [[Genetics|genetic]] vulnerability and environmental stressors can act in combination to result in diagnosis of schizophrenia.<ref name="fn_12">Harrison PJ, Owen MJ. (2003). Genes for schizophrenia? Recent findings and their pathophysiological implications. ''[http://www.thelancet.com/ Lancet]'', 361(9355), 417&ndash;9. PMID 12573388</ref>
 
The extent to which these factors influence the likelihood of being diagnosed with schizophrenia is debated widely, and currently, controversial. Schizophrenia is likely to be a [[diagnosis]] of complex inheritance. Thus, it is likely that several [[genes]] interact to generate [[Risk-free interest rate|risk]] for schizophrenia or for the separate components that can co-occur to lead to a diagnosis.<ref name="fn_75">Owen MJ, Craddock N, O'Donovan MC. (2005). Schizophrenia: genes at last? ''Trends in Genetics'', 21(9), 518–25. PMID 16009449</ref> This, combined with disagreements over which research methods are best, or how data from genetic research should be interpreted, has led to differing estimates over genetic contribution.
 
It is thought that causal factors can initially come together in early [[neurodevelopment]], including during pregnancy, to increase the risk of later developing schizophrenia. One curious finding is that people diagnosed with schizophrenia are more likely to have been born in [[winter]] or [[spring (season)|spring]]<ref name="fn_21">Davies G, Welham J, Chant D, Torrey EF, McGrath J. (2003). A [[systematic review]] and meta-analysis of Northern Hemisphere season of birth studies in schizophrenia. ''Schizophrenia Bulletin'', 29 (3), 587&ndash;93. PMID 14609251</ref> (at least in the [[northern hemisphere]]). However, the effect is not large. Some researchers postulate that the correlation is due to viral infections during the third trimester (4–6 months) of pregnancy. There is now significant evidence that [[prenatal]] exposure to infections increases the risk for developing schizophrenia later in life, providing additional evidence for a link between in utero developmental pathology and risk of developing the condition.<ref name="fn_73">Brown, A.S. (2006). Prenatal infection as a risk factor for schizophrenia. ''Schizophrenia Bulletin'', 32 (2), 200–2. PMID 16469941</ref>
 
 
Schizophrenia is most commonly first diagnosed during late adolescence or early adulthood suggesting it is often the end process of childhood and adolescent development. Studies have indicated that genetic dispositions can interact with early environment to increase the risk of developing schizophrenia, including through global neurobehavioral deficits,<ref>Hans SL, Marcus J, Nuechterlein KH, ''et al'' (1999). Neurobehavioral deficits at adolescence in children at risk for schizophrenia: The Jerusalem Infant Development Study. ''Arch Gen Psychiatry''. 56(8):741–8. PMID 10435609</ref> a poorer family environment and disruptive school behaviour,<ref>Carter JW, Schulsinger F, Parnas J, Cannon T, Mednick SA. (2002). A multivariate prediction model of schizophrenia. ''Schizophrenia Bulletin'' 28(4):649–82. PMID 12795497</ref> poor peer engagement, immaturity or unpopularity<ref>Hans SL, Auerbach JG, Asarnow JR, Styr B, Marcus J. (2000). Social adjustment of adolescents at risk for schizophrenia: the Jerusalem Infant Development Study. ''J Am Acad Child Adolesc Psychiatry''. 39(11):1406–14. PMID 11068896 </ref> or poorer social competence and increasing schizophrenic symptomology emerging during adolescence<ref>Dworkin RH, Bernstein G, Kaplansky LM, ''et al'' (1991). Social competence and positive and negative symptoms: a longitudinal study of children and adolescents at risk for schizophrenia and affective disorder. ''Am J Psychiatry. '' Sep;148(9):1182–8. PMID 1882996 </ref> These developmental problems have also been linked to socioeconomic disadvantage or early experiences of traumatic events.<ref>Read J, Perry BD, Moskowitz A, Connolly J (2001). The contribution of early traumatic events to schizophrenia in some patients: a traumagenic neurodevelopmental model. ''Psychiatry'', 64, 319-45. PMID 11822210[http://www.childtrauma.org/CTAMATERIALS/Psychiatry_02.pdf Full text]) (PDF), Retrieved on [[2007-05-16]]</ref>
 
There is on average a somewhat earlier onset for men than women, with the possible protective influence of the female hormone [[Estrogen|oestrogen]] being one hypothesis made and sociocultural influences another.
 
===Genetic===
Substantial evidence suggests that the diagnosis of schizophrenia has a heritable component (some estimates are as high as 80%). Current research suggests that environmental factors play a significant role in the expression of any genetic disposition towards schizophrenia (i.e. if someone has the genes that increase risk, this will not automatically result in a diagnosis of schizophrenia later in life). A recent review of the genetic evidence has suggested a more than 28% chance of one identical twin obtaining the diagnosis if the other already has it<ref name="fn_9">[[E. Fuller Torrey|Torrey, E.F.]], Bowler, A.E., Taylor, E.H. & Gottesman, I. I (1994) ''Schizophrenia and manic depressive disorder''. New York: Basic books. ISBN 0-465-07285-2</ref> (see [[twin study|twin studies]]), but such studies are not noted for pondering the likelihood of similarities of social class and/or other socio-psychological factors between the twins. The estimates of heritability of schizophrenia from twin studies varies a great deal, with some notable studies<ref name="fn_10">Koskenvuo M, Langinvainio H, Kaprio J, Lonnqvist J, Tienari P (1984). Psychiatric hospitalization in twins. ''Acta Genet Med Gemellol (Roma)'', 33(2),321–32. PMID 6540965</ref><ref name="fn_11">Hoeffer A, Pollin W. (1970). Schizophrenia in the NAS-NRC panel of 15,909 veteran twin pairs. ''Archives of General Psychiatry'', 1970 Nov; 23(5):469–77. PMID 5478575</ref> showing rates as low as 11.0%&ndash;13.8% among monozygotic twins, and 1.8%&ndash;4.1% among dizygotic twins. However, some scientists criticize the methodology of the twin studies, and have argued that the genetic basis of schizophrenia is still largely unknown or open to different interpretations. The genetic disposition does not always express in twins being the same disorder as cases of one identical twin having schizophrenia and the other having bipolar disorder have been reported.<ref name="fn_23">Dalby, JT, Morgan D & Lee, M (1986). Schizophrenia and mania in identical twin brothers. ''Journal of Nervous and Mental Disease'' 174, 304–308. PMID 3701318</ref>
 
There is currently a great deal of effort being put into [[molecular genetics|molecular genetic]] studies of schizophrenia, which attempt to identify specific genes which may increase risk. Because of this, the genes that are thought to be most involved can change as new evidence is gathered. A 2003 review of [[Genetic linkage|linkage]] studies listed seven genes as likely to increase risk for a later diagnosis of the disorder.<ref name="fn_12" /> Two more recent reviews<ref name="fn_75" /><ref name="fn_79">Riley B, Kendler KS (2006). Molecular genetic studies of schizophrenia. ''Eur J Hum Genet'', 14 (6), 669–80. PMID 16721403</ref> have suggested that the evidence is currently strongest for two genes known as dysbindin (DTNBP1) and [[neuregulin]] ([[NRG1]]), with a number of other genes (such as [[COMT]], [[RGS4]], PPP3CC, ZDHHC8, [[DISC1]], and AKT1) showing some early promising results that have not yet been fully replicated.
 
In 2007, British researches have identified seven different genetic variations that are associated with schizophrenia and which all lie within or very near a gene [[FXYD6]].<ref>[http://www.schizophreniaforum.org/new/detail.asp?id=1326 Getting Crowded on Chromosome 11q22—Make Way for Phosphohippolin.] Schizophrenia Research Forum, [[14 March]] [[2007]].  Retrieved on [[2007-05-16]]</ref><ref>Choudhury K, McQuillin A, Puri V, Pimm J, ''et al'' (2007). ''Am J Hum Genet.'' Apr;80(4):664-72. PMID 17357072</ref> A genetic association study of chromosome 11q22-24 in two different samples implicates the FXYD6 gene, encoding phosphohippolin, in susceptibility to schizophrenia.  This gene, which lies on the long arm of chromosome 11, plays an important role in regulating Na/K homeostasis.
 
Please note that there are 3 generally-accepted after-conception causes for increase in schizophrenia-rate in a population, and 1 conception cause:
Lack of sunshine, in the 3rd trimester of gestation ( in the temperate regions a Spring birth, but also El Nino years in Australia, and a particularly overcast 3-month stretch in, IIRC, Brazil, all followed by birth of increased schizophrenia-rate population ).
Medical X-Rays, ( IIRC, also in the 3rd trimester of gestation ).
Influenza in the mother, during later pregnancy.
Older fathers ( poorer-quality genetic contribution )
 
Therefore, it is likely a ''genetic activation'', rather-than simple-possession of specific genes, that is the true cause of it ( simply having the genes would be Required, but Not Sufficient: having 'em activated might be the sufficient bit ).
 
===Emotional===
A number of [[emotional]] factors have been implicated in [[schizophrenia]], with some models putting them at the core of the disorder. It was thought that the appearance of blunted affect meant that sufferers did not experience strong emotions, but more recent studies indicate there is often a normal or even heightened level of emotionality, particularly in response to negative events or stressful social situations.<ref>Cohen & Docherty (2004). Affective reactivity of speech and emotional experience in patients with schizophrenia. ''Schizophr Res'', 1;69(1):7–14. PMID 15145465 </ref>  Related studies suggest that the content of [[delusional]] and [[psychotic]] beliefs in [[schizophrenia]] can be meaningful and play a causal or mediating role in reflecting the life history or social circumstances of the individual.<ref>Birchwood M, Meaden A, Trower P, Gilbert P, Plaistow J (2000). The power and omnipotence of voices: subordination and entrapment by voices and significant others. ''Psychol Med''. Mar;30(2):337–44. PMID 10824654</ref>
 
===Environmental===
Considerable evidence indicates that stressful life events cause or trigger schizophrenia.<ref name="fn_15">Day R, Nielsen JA, Korten A, Ernberg G, ''et al'' (1987). Stressful life events preceding the acute onset of schizophrenia: a cross-national study from the World Health Organization. ''Culture, Medicine and Psychiatry'', 11 (2), 123&ndash;205. PMID 3595169</ref> Childhood experiences of abuse or trauma have also been implicated as risk factors for a diagnosis of schizophrenia later in life.<ref>Harriet L. MacMillan, Jan E. Fleming, David L. Streiner, ''et al'' (2001). Childhood Abuse and Lifetime Psychopathology in a Community Sample. ''American Journal of Psychiatry'',158, 1878–83. PMID 11691695<br />* Schenkel LS, Spaulding WD, Dilillo D, Silverstein SM (2005). Histories of childhood maltreatment in schizophrenia: Relationships with premorbid functioning, symptomatology, and cognitive deficits. ''Schizophrenia Research'' Jul 15;76(2–3):273–286. PMID 15949659[http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TC2-4FWT420-3&_user=10&_coverDate=04%2F08%2F2005&_rdoc=1&_fmt=summary&_orig=browse&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=a75a0204ebb590104747e8115cddd64a Full-text available for purchase,] Retrieved on [[2007-05-16]]<br />* Janssen I, Krabbendam L, Bak M, Hanssen M, ''et al'' (2004). Childhood abuse as a risk factor for psychotic experiences. ''Acta Psychiatrica Scandinavica'', 109, 38–45. PMID 14674957</ref>
 
Evidence is also consistent that negative attitudes towards individuals with (or with a risk of developing) schizophrenia can have a significant adverse impact. In particular, critical comments, hostility, authoritarian and intrusive or controlling attitudes (termed 'high expressed emotion' by researchers) from family members have been found to correlate with a higher risk of relapse in schizophrenia across cultures.<ref name="fn_70">Bebbington PE, Kuipers E (1994). The predictive utility of expressed emotion in schizophrenia: an aggregate analysis. ''Psychological Medicine'', 24, 707–718. PMID 7991753</ref> It is not clear whether such attitudes play a causal role in the onset of schizophrenia, although those diagnosed in this way may claim it to be the primary causal factor. The research has focused on family members but also appears to relate to professional staff in regular contact with clients.<ref name="fn_71">Van Humbeeck G, Van Audenhove C. (2003). Expressed emotion of professionals towards mental health patients. ''Epidemiologia e Psychiatria Sociale'', 12(4), 232–235. PMID 14968481[http://www.psychiatry.univr.it/page_eps/docs/2003_4_humbeeck.pdf Full text] PDF, Retrieved on [[2007-05-16]].</ref> While initial work addressed those diagnosed as schizophrenic, these attitudes have also been found to play a significant role in other mental health problems.<ref name="fn_66">Wearden AJ, Tarrier N, Barrowclough C, Zastowny TR, Rahill AA. (2000). A review of expressed emotion research in health care. ''Clinical Psychology Review'', 20, 633–66. PMID 10860170</ref> This approach does not blame 'bad parenting' or staffing, but addresses the attitudes, behaviors and interactions of all parties. Some go as far as to criticise the whole approach of seeking to localise 'mental illness' within one individual — the patient — rather than his/her group and its functionality, citing a [[scapegoat]] effect.
 
Factors such as [[poverty]] and [[discrimination]] also appear to be involved in increasing the risk of schizophrenia or schizophrenia relapse, perhaps due to the high levels of stress they engender, or faults in diagnostic procedure/assumptions. Racism in society, including in diagnostic practices, and/or the stress of living in a different culture, may explain why minority communities have shown higher rates of schizophrenia than members of the same ethnic groups resident in their home country. The "social drift hypothesis" suggests that the functional problems related to schizophrenia, or the stigma and prejudice attached to them, can result in more limited employment and financial opportunities, so that the causal pathway goes from mental health problems to poverty, rather than, or in addition to, the other direction. Some argue that [[unemployment]] and the long-term unemployed and homeless are simply being stigmatised.
 
One particularly stable and replicable finding has been the association between living in an [[Urbanization|urban]] environment and schizophrenia diagnosis, even after factors such as [[drug use]], [[ethnic group]] and size of [[social group]] have been controlled for.<ref name="fn_19">Van Os J. (2004). Does the urban environment cause psychosis? ''British Journal of Psychiatry'', 184 (4), 287&ndash;288. PMID 15056569</ref> A recent study of 4.4 million men and women in [[Sweden]] found an alleged 68%&ndash;77% increased risk of diagnosed [[psychosis]] for people living in the most urbanized environments, a significant proportion of which is likely to be described as schizophrenia.<ref name="fn_20">Sundquist K, Frank G, Sundquist J. (2004). Urbanisation and incidence of psychosis and depression: Follow-up study of 4.4 million women and men in Sweden. ''British Journal of Psychiatry'', 184 (4), 293&ndash;298. PMID 15056572</ref>
 
A number of [[cognitive bias]]es or deficits have been found in people diagnosed with schizophrenia. These include jumping to conclusions when faced with limited or contradictory information; specific biases in reasoning about social situations, for example assuming other people cause things that go wrong (external attribution); difficulty distinguishing inner speech from speech from an external source (source monitoring); difficulty in adjusting speech to the needs of the hearer, related to [[theory of mind]] difficulties; difficulties in the very earliest stages of processing visual information (including reduced [[latent inhibition]]); difficulty with attention e.g. being more easily distracted, [[attentional bias]] towards threat. Some of these tendencies have been shown to worsen or appear when under emotional stress or in confusing situations. As with the related neurological findings, they are not shown by all individuals with a diagnosis of schizophrenia and it is not clear how specific they are to schizophrenia or to particular symptoms.<ref>Broome MR, Woolley JB, Tabraham P, Johns LC, ''et al'' (2005). What causes the onset of psychosis? ''Schizophr Res'', 79(1), 23–34. PMID 16198238</ref> However, the findings regarding cognitive difficulties in schizophrenia are reliable and consistent enough for some researchers to argue that they are diagnostic.<ref>Lewis R (2004). Should cognitive deficit be a diagnostic criterion for schizophrenia? ''Journal of Psychiatry and Neuroscience'' March; 29(2): 102–113. PMID 15069464 </ref> Impaired capacity to appreciate one's own and others' mental states has been reported to be the single-best predictor of poor social competence in schizophrenia.<ref>Brune M, Abdel-Hamid M, Lehmkamper C, Sonntag C (2007). Mental state attribution, neurocognitive functioning, and psychopathology: What predicts poor social competence in schizophrenia best? ''Schizophr Res.'' Mar 6 PMID 17346931 </ref> Similar cognitive features have been identified in close relatives of people diagnosed with schizophrenia.<ref>Sitskoorn MM, Aleman A, Ebisch SJH, Appels MCM, Khan RS (2004). Cognitive deficits in relatives of patients with schizophrenia: a meta-analysis. ''Schizophrenia Research'', Volume 71, Issue 2, Pages 285–295. PMID 15474899 </ref>
 
A number of emotional factors have been implicated in schizophrenia, with some models putting them at the core of the disorder. It was thought that the appearance of blunted affect meant that sufferers did not experience strong emotions, but more recent studies indicate there is often a normal or even heightened level of emotionality, particularly in response to negative events or stressful social situations.<ref>Cohen & Docherty (2004). Affective reactivity of speech and emotional experience in patients with schizophrenia. ''Schizophr Res'', 1;69(1):7–14. PMID 15145465 </ref> Some theories suggest positive symptoms of schizophrenia can result from or be worsened by negative emotions, including depressed feelings and low [[self-esteem]]<ref>Smith B, Fowler DG, Freeman D, ''et al'' (2006). Emotion and psychosis: links between depression, self-esteem, negative schematic beliefs and delusions and hallucinations. ''Schizophr Res''. Sep;86(1–3):181–8. PMID 16857346</ref> and feelings of vulnerability, inferiority or [[loneliness]].<ref>Beck, AT (2004). [http://www.atypon-link.com/SPC/doi/abs/10.1891/jcop.18.3.281.65649?cookieSet=1&journalCode=jcop A Cognitive Model of Schizophrenia,] ''Journal of Cognitive Psychotherapy'', 18 (3), 281–288. Retrieved on [[2007-05-16]]. </ref> Chronic negative feelings and maladaptive coping skills may explain some of the association between psychosocial stressors and symptomology.<ref>Horan WP, Blanchard JJ (2003). Emotional responses to psychosocial stress in schizophrenia: the role of individual differences in affective traits and coping. ''Schizophr Res.'' April 1;60(2–3):271–83. PMID 12591589</ref> Critical and controlling behaviour by significant others (high [[expressed emotion]]) causes increased emotional arousal<ref>Tarrier & Turpin (1992). Psychosocial factors, arousal and schizophrenic relapse. The psychophysiological data. ''Br J Psychiatry''. 161:3–11. PMID  1638327</ref> and lowered self-esteem<ref>Barrowclough C, Tarrier N, Humphreys L, Ward J, Gregg L, Andrews B (2003). Self-esteem in schizophrenia: relationships between self-evaluation, family attitudes, and symptomatology. ''J Abnorm Psychol''. 112(1):92–9. PMID 12653417</ref> and a subsequent increase in positive symptoms such as unusual thoughts. Countries or cultures where schizotypal personalities or schizophrenia symptoms are more accepted or valued appear to be associated with reduced onset of, or increased recovery from, schizophrenia.
 
Related studies suggest that the content of delusional and psychotic beliefs in schizophrenia can be meaningful and play a causal or mediating role in reflecting the life history or social circumstances of the individual.<ref>Birchwood M, Meaden A, Trower P, Gilbert P, Plaistow J (2000). The power and omnipotence of voices: subordination and entrapment by voices and significant others. ''Psychol Med''. Mar;30(2):337–44. PMID 10824654</ref> Holding minority or poorly understood sociocultural beliefs, for example due to ethnic background, has been linked to increased diagnosis of schizophrenia. The way an individual personally understands and attributes their delusions or hallucinations (e.g. as threatening or as potentially positive) has also been found to influence functioning and recovery.<ref>Honig A, Romme MA, Ensink BJ, Escher SD, Pennings MH, deVries MW (1998). Auditory hallucinations: a comparison between patients and nonpatients ''J Nerv Ment Dis''. Oct;186(10):646–51. PMID 9788642</ref>
 
[[Image:Schizophrenia PET scan.jpg|frame|Data from a [[Positron emission tomography|PET]] study<ref name="fn_25">Meyer-Lindenberg A, Miletich RS, Kohn PD, ''et al'' (2002). Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia. ''Nature Neuroscience'', 5, 267–71. PMID 11865311</ref> suggests that the less the [[frontal lobe]]s are activated (<font color="red">red</font>) during a [[working memory]] task, the greater the increase in abnormal [[dopamine]] activity in the [[striatum]] (<font color="green">green</font>), thought to be related to the [[neurocognitive deficit]]s in schizophrenia.]]
 
===Infective===
One theory put forward by psychiatrists [[E. Fuller Torrey]] and R.H. Yolken is that the parasite ''[[Toxoplasma gondii]]'' leads to some, if not many, cases of schizophrenia.<ref name="fn_58">Torrey EF, Yolken RH (2003). Toxoplasma gondii and schizophrenia. ''Emerging Infectious Diseases'', 9 (11), 1375–80. PMID 14725265</ref> This is supported by evidence that significantly higher levels of Toxoplasma antibodies in schizophrenia patients compared to the general population.<ref>Wang HL, Wang GH, Li QY, Shu C, Jiang MS, Guo Y (2006). Prevalence of Toxoplasma infection in first-episode schizophrenia and comparison between Toxoplasma-seropositive and Toxoplasma-seronegative schizophrenia. ''Acta Psychiatrica Scandinavica'', 114 (1), 40–48. PMID 16774660</ref>
 
=== Substance use ===
The relationship between schizophrenia and drug use is complex, meaning that a clear causal connection between drug use and schizophrenia has been difficult to tease apart. There is strong evidence that using certain drugs can trigger either the onset or relapse of schizophrenia in some people. It may also be the case, however, that people with schizophrenia use drugs to overcome negative feelings associated with both the commonly prescribed antipsychotic medication and the condition itself, where negative emotion, [[paranoia]] and [[anhedonia]] are all considered to be core features.
 
The rate of substance use is known to be particularly high in this group. In a recent study, 60% of people with schizophrenia were found to use substances and 37% would be diagnosable with a substance use disorder.<ref name="fn_74">Swartz MS, Wagner HR, Swanson JW, ''et al'' (2006). Substance use in persons with schizophrenia: baseline prevalence and correlates from the NIMH CATIE study. ''Journal of Nervous and Mental Disease'', 194(3), 164–72. PMID 16534433</ref>
 
==== Amphetamines ====
 
As amphetamines trigger the release of dopamine and excessive dopamine function is believed to be responsible for many symptoms of schizophrenia (known as the [[dopamine hypothesis of schizophrenia]]), amphetamines may worsen schizophrenia symptoms.
 
==== Hallucinogens ====
Schizophrenia can sometimes be triggered by heavy use of [[Psychedelics, dissociatives and deliriants|hallucinogenic]] or stimulant drugs,<ref>Mueser KT, Yarnold PR, Levinson DF, ''et al'' (1990). Prevalence of substance abuse in schizophrenia: demographic and clinical correlates. ''Schizophrenic Bulletin'', 16(1), 31–56. PMID 2333480</ref> although some claim that a predisposition towards developing schizophrenia is needed for this to occur. There is also some evidence suggesting that people suffering schizophrenia but responding to treatment can have relapse because of subsequent drug use. Some widely known cases where hallucinogens have been suspected of precipitating schizophrenia are [[Pink Floyd]] founder-member [[Syd Barrett]] and [[The Beach Boys]] producer, arranger and songwriter [[Brian Wilson]].
 
Drugs such as [[ketamine]], [[Phencyclidine|PCP]], and [[LSD]] have been used to mimic schizophrenia for research purposes. Using LSD and other [[psychedelics]] as a model has now fallen out of favor with the [[scientific research community]], as the differences between the drug induced states and the typical presentation of schizophrenia have become clear. The dissociatives ketamine and PCP are still considered to produce states that are remarkably similar however.
 
Hallucinogenic drugs were also briefly tested as possible treatments for schizophrenia by psychiatrists such as [[Humphry Osmond]] and [[Abram Hoffer]] in the 1950s. It was mainly for this experimental treatment of schizophrenia that LSD administration was legal, briefly before its use as a [[recreational drug]] led to its criminalization.
 
==== Cannabis ====
There is evidence that [[cannabis (drug)|cannabis]] use can contribute to schizophrenia. Some studies suggest that cannabis is neither a [[Causality#Necessary and sufficient causes|sufficient nor necessary]] factor in developing schizophrenia, but that cannabis may significantly increase the risk of developing schizophrenia and may be, among other things, a significant causal factor. Nevertheless, some previous research in this area has been criticised as it has often not been clear whether cannabis use is a cause or effect of schizophrenia. To address this issue, a recent review of studies from which a causal contribution to schizophrenia can be assessed has suggested that cannabis statistically doubles the risk of developing schizophrenia on the individual level, and may, assuming a causal relationship, be responsible for up to 8% of cases in the population.<ref name="fn_48">Arseneault L, Cannon M, Witton J, Murray RM (2004). Causal association between cannabis and psychosis: examination of the evidence. ''British Journal of Psychiatry'', 184, 110-7. PMID 14754822 [http://bjp.rcpsych.org/cgi/content/full/184/2/110 Full text available.]</ref>
 
An older [[longitudinal study]], published in [[1987]], suggested six-fold increase of schizophrenia risks for high consumers of cannabis (use on more than fifty occasions) in [[Sweden]].<ref>Andreasson S, Allebeck P, Engstrom A, and Rydberg U (1987). Cannabis and schizophrenia. A longitudinal study of Swedish conscripts. ''Lancet'', 1987, Dec 26, 2(8574), 1483–6. PMID 2892048</ref>
 
==== Tobacco ====
People with schizophrenia tend to smoke significantly more tobacco than the general population. The rates are exceptionally high amongst institutionalized patients and homeless people. In a [[UK]] census from 1993, 74% of people with schizophrenia living in institutions were found to be smokers.<ref name="mcneill">{{cite paper | author = McNeill, Ann | title = Smoking and mental health — a review of the literature | publisher = SmokeFree London Programme | date = 2001 | url = http://www.ash.org.uk/html/policy/menlitrev.pdf | format = [[PDF]] | accessdate = 2006-12-14 }}</ref><ref name="ocps">{{cite paper | author = Meltzer H, Gill B, Petticrew M, Hinds K. | title = OPCS Surveys of Psychiatric Morbidity Report 3: Economic Activity and Social Functioning of Adults With Psychiatric Disorders. | publisher = London, Her Majesty’s Stationery Office | date = 1995}} [http://www.statistics.gov.uk/STATBASE/Product.asp?vlnk=7993&More=Y Available for fee.]</ref> A 1999 study that covered all people with schizophrenia in [[Nithsdale]], [[Scotland]] found a 58% prevalence rate of cigarette smoking, to compare with 28% in the general population.<ref name="kelly_mccreadie">{{cite journal | last = Kelly | first = C | coauthors = McCreadie RG | title = Smoking Habits, Current Symptoms, and Premorbid Characteristics of Schizophrenic Patients in Nithsdale, Scotland | journal = [[American Journal of Psychiatry|The American Journal of Psychiatry]] | volume = 156 | pages = 1751–1757 | publisher = [[American Psychiatric Association]] | date = 1999 | url = http://ajp.psychiatryonline.org/cgi/content/abstract/156/11/1751 | accessdate = 2006-12-14 | pmid = 10553739 }}</ref> An older study found that as much as 88% of outpatients with schizophrenia were smokers.<ref name="hughes_et_al">{{cite journal | last = Hughes | first = JR | coauthors = Hatsukami DK, Mitchell JE, Dahlgren LA | title = Prevalence of smoking among psychiatric outpatients | journal = [[American Journal of Psychiatry|The American Journal of Psychiatry]] | volume = 143 | pages = 993–997 | publisher = [[American Psychiatric Association]] | date = 1986 | url = http://ajp.psychiatryonline.org/cgi/content/abstract/143/8/993 | accessdate = 2006-12-14 |pmid = 3487983}}</ref>
 
Despite the higher prevalence of tobacco smoking, people diagnosed with schizophrenia have a much lower than average chance of developing and dying from [[lung cancer]]. While the reason for this is unknown, it may be because of a genetic resistance to the cancer, a side-effect of drugs being taken, or a statistical effect of increased likelihood of dying from causes other than lung cancer.<ref name="fn_49">"''Conditions in Occupational Therapy: effect on occupational performance.''" ed. Ruth A. Hansen and Ben Atchison (Baltimore: Lippincott Williams & Williams, 2000), 54&ndash;74. ISBN 0-683-30417-8</ref>
 
A recent study of over 50,000 [[Sweden|Swedish]] conscripts found that there was a small but [[Statistical significance|significant]] protective effect of smoking cigarettes on the risk of developing schizophrenia later in life.<ref name="fn_50">Zammit S, Allebeck P, Dalman C, Lundberg I, Hemmingsson T, Lewis G (2003). Investigating the association between cigarette smoking and schizophrenia in a cohort study. ''American Journal of Psychiatry'', 160 (12), 2216&ndash;21. PMID 14638593</ref> While the authors of the study stressed that the risks of smoking far outweigh these minor benefits, this study provides further evidence for the 'self-medication' theory of smoking in schizophrenia and may give clues as to how schizophrenia might develop at the molecular level. Furthermore, many people with schizophrenia have smoked tobacco products long before they are diagnosed with the illness, and some groups advocate that the chemicals in tobacco have actually contributed to the onset of the illness and have no benefit of any kind.
 
It is of interest that cigarette smoking affects liver function such that the [[antipsychotic drugs]] used to treat schizophrenia are broken down in the blood stream more quickly. This means that smokers with schizophrenia need slightly higher doses of antipsychotic drugs in order for them to be effective than do their non-smoking counterparts.
 
The increased rate of smoking in schizophrenia may be due to a desire to self-medicate with [[nicotine]]. One possible reason is that smoking produces a short term effect to improve alertness and cognitive functioning in persons who suffer this illness.<ref name="compton_2005">{{cite web | last = Compton | first = Michael T. | title = Cigarette Smoking in Individuals with Schizophrenia | publisher = Medscape Psychiatry & Mental Health | date = [[2005-11-16]] | url = http://www.medscape.com/viewarticle/516304_print | accessdate = 2007-05-17 }}</ref> It has been postulated that the mechanism of this effect is that people with schizophrenia have a disturbance of nicotinic receptor functioning which is temporarily abated by tobacco use.<ref name="compton_2005" />
 
===Other===
[[Calcium channel]] abnormalities are currently being explored as a factor in schizophrenia. Related to this, three small studies have found some improvements on some measures, in schizophrenia with tardive dyskinesia, with the calcium channel blocking agent [[nilvadipine]] added to an existing antipsychotic regimen<ref>Yamada K, Ashikari I, Onishi K, Kanba S, Yagi G, Asai M. (1995). Effectiveness of nilvadipine in two cases of chronic schizophrenia. ''Psychiatry Clin Neurosci.'' Aug;49(4):237–8. PMID 9179944</ref>
 
Currently, there is growing evidence of the crucial role of [[autoimmunity]] in the etiology and pathogenesis of schizophrenia. This can be seen as a study of the statistical correlation schizophrenia with other [[list of autoimmune diseases|autoimmune diseases]]<ref name="fn_211">Eaton WW, Byrne M, Ewald H, Mors O, Chen CY, Agerbo E, Mortensen PB (2006). Association of Schizophrenia and Autoimmune Diseases: Linkage of Danish National Registers. ''American Journal of Psychiatry'' 163, 521–528. PMID 16513876</ref> and the recent work on the direct detailed study immune status of patients with schizophrenia.<ref name="fn_212">Jones AL, Mowry BJ, Pender MP, Greer JM. (2005). Immune dysregulation and self-reactivity in schizophrenia: do some cases of schizophrenia have an autoimmune basis? ''Immunol Cell Biol'', 83 (1), 9–17. PMID 15661036</ref><ref name="fn_215">Strous RD, Shoenfeld Y (2006). Schizophrenia, autoimmunity and immune system dysregulation: a comprehensive model updated and revisited. ''Journal of Autoimmunity'' 2006 Sep;27(2):71–80. PMID 16997531</ref>
 
==References==
{{Reflist|2}}
 
{{WH}}
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[[Category:Disease]]
[[Category:Psychiatry]]
[[Category:Mature chapter]]
[[Category:Primary care]]

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_NOTOC _ Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]


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