1. ACDEC 6. AEBDC 11. ACCBB 16. AEDBB 21. DBAAD 26. EBACA 31. ECBAD 36. DACAE 41.

CABAB 46. DEDAE

1.AA

If there is no other bias in the study, statistical significance guarantees that there is a 95 percent chance that the studys result reflects what is happening in the population at large. 2.CC

Opioid receptors are a group of

protein!coupled receptors with opioids as ligands.

"orphine is shown to bind to #u receptors.

$.%%

&he 'ugular fora#en #ay be subdi(ided into three co#part#ents, each with their own contents.

&he anterior co#part#ent trans#its the inferior petrosal sinus.

&he inter#ediate trans#its the glossopharyngeal, (agus, and accessory ner(es )a*a cranial ner(es nu#ber I+, +, and +I respecti(ely,. &he posterior trans#its the sig#oid sinus )beco#ing the internal 'ugular (ein, and so#e #eningeal branches fro# the occipital and ascending pharyngeal arteries.

In this case the -ternocleido#astoid #. and &rape.oid are iner(ated by Accessory n.....+I 2 !!AA /afirlu*ast and #ontelu*ast are antagonist at 0&%1 receptors with slow onset of acti(ity used prophylactically for different for# of asth#a for e2a#ple the e2ercise or drugs li*e A-A Ipatropiu# cause bronchodilation in acute asth#a!!!!used in CO3% and safer than 4 agonist in patients wit C5 disease &heophyline !!!!bronchodilates (ia inhiubition of 3hosphodiesterase 3%6 !!!!increased cA"3 and also by antagonist of adenosine)bronchoconstrictor, &he final step of this $ groups of #edicine is wor* o(er the bronchospas# 1.66

&he anti#icrobial resistance to all #entioned antibiotics ....4eta!lacta# antibiotics)3enicillin and its generation, is caused by production of e2tended!spectru# beta lacta#ase 5.CC77

+!lin*ed recessi(e inheritance is a #ode of inheritance in which a #utation in a gene on the + chro#oso#e causes the phenotype to be e2pressed )1, in #ales )who are necessarily he#i.ygous for the gene #utation because they ha(e only one + chro#oso#e, and )2, in fe#ales who are ho#o.ygous for the gene #utation )i.e., they ha(e a copy of the gene #utation on each of their two + chro#oso#es,....so it is 281

5! AA 777 this 9 don:t ha(e all the infor#ation re;uiered to gi(e the answer, don:t says nothing about her husband< but CA==I6= fe#ale has half of the son affected and half of the daughters carrier then 5>?5> )1.1, &he 9 is about the e2pected ratio of carrier #other (iable fe#ale to #ale children for +! lin*ed recessi(e disease...the fe#ale child #ust get another affected + fro# daddy..to beco#e sic* so she needs to recei(e two genes,but #ale child 'ust needs one + that it co#es fro# her carrier #other to get the disease...so the ratio of getting affected + between fe#ale and #ale children is 281

@ ! AAA had it:s origen than the renal artery, no -uperior #esenteric bc it:s origen is superior to the top of the *idneys &he Inferior "esenteric Artery )I"A, branches off the anterior surface of the abdo#inal aorta below the renal artery branch points, and appro2i#ately #idway between these and the aortic bifurcation )into the co##on iliac arteries,. -upplies the large intestine fro# the left colic )or splenic, fle2ure to the upper part of the rectu#, which includes the descending colon, the sig#oid colon, and part of the rectu#. 3ro2i#ally, its territory of distribution o(erlaps )for#s a watershed, with the #iddle colic artery, and therefore the superior #esenteric artery. &he -"A and I"A anasto#ose (ia the #arginal artery of the colon )artery of %ru##ond,. &he territory of distribution of the I"A is #ore or less e;ui(alent to the e#bryonic hindgut. http8??en.wi*ipedia.org?wi*i?InferiorA#esentericAartery

B 6 Cartagener syndro#e, sinusitis, bronchiectasis, infertility, is Autoso#al =, there is abnor#al ciliary #otion and i#paired #ucociliary clearence, reason for the clinical signs

D. 4 Autoi##une "etaplastic Atrophic astritis )A"A , is an inherited for# of atrophic gastritis characteri.ed by an i##une response directed toward parietal cells and intrinsic factor.E1F &he presence of seru# antibodies to parietal cells and to intrinsic factor are characteristic findings. &he autoi##une response subse;uently leads to the destruction of parietal cells, which leads to profound hypochlorhydria )and ele(ated gastrin le(els,. &he inade;uate production of intrinsic factor also leads to (ita#in 412 #alabsorption and pernicious ane#ia. A"A is typically confined to the gastric body and fundus.

9. % Co#ple#ent co#ponent D is a protein in(ol(ed in the co#ple#ent syste#. A hereditary deficiency of CD can result in increased susceptibility to Geisseria infections, such as #eningitis and gonorrhea. %eficiency of C5!CD leads to Geisseria bactere#ia.

1>. C &he Hrachus is the part of the allantoids duct between the bladder and the u#bilicus. &he #edian u#bilical liga#ent is a structure in hu#an anato#y. It is a shri(elled piece of tissue that represents the re#nant of the e#bryonic urachus. It e2tends fro# the ape2 of the bladder to the u#bilicus, on the deep surface of the anterior abdo#inal wall. It is unpaired. It is co(ered by the #edian u#bilical fold 0ateral to this structure are the #edial u#bilical liga#ent )which is a different structure, not to be confused, and the lateral u#bilical liga#ent.

11. A Addison %isease8 Chronic adrenal insufficiencydue to adrenal atrophy or destruction by disease )Autoi###une, &4, #etastasis,. 1I deficiency of aldosterone and cortisol causing hypotension, and s*in hyperpig#entation. )JA page 291, 4ecause pri#ary hypocortisolis# is #anifested as a deficiency in glucocorticoid release fro# the adrenal corte2, increased AC&K will be released by the pituitary in order to trigger release of the absent glucocorticoid< it is because of this o(ersti#ulation of AC&K that bron.ing of the s*in occurs. In secondary or tertiary hypocortisolis#, there is a deficiency of either C=K or AC&K release by the hypothala#us or pituitary gland, respecti(ely. &he for#er will #anifest as no AC&K release while the latter will #anifest as physiologic )nor#al, AC&K release< neither will cause an o(erproduction of AC&K. On e2a#ination, the following #ay be noticed8E2F L0ow blood pressure that falls further when standing )orthostatic hypotension, LIn long!standing Addison:s %isease, the pinna of the ear #ay beco#e calcified L"ost people with pri#ary Addison:s ha(e dar*ening )hyperpig#entation, of the s*in, including areas not e2posed to the sun< characteristic sites are s*in creases )e.g. of the hands,, nipple, and the inside of the chee* )buccal #ucosa,, also old scars #ay dar*en.

&his occurs because #elanocyte!sti#ulating hor#one )"-K, and adrenocorticotropic hor#one )AC&K, share the sa#e precursor #olecule, 3ro!opio#elanocortin )3O"C,. After production in anterior pituitary gland, 3O"C gets clea(ed into a##a!"-K, AC&K and 4eta!lipotropin. &he subunit AC&K undergoes further clea(age to produce Alpha! "-K, the #ost i#portant "-K for s*in pig#entation. In secondary and tertiary for#s of Addison:s, s*in dar*ening does not occur. L"edical conditions such as type I diabetes, autoi##une thyroid disease )Kashi#oto:s thyroiditis and goiter, and (itiligo often occur together with Addison:s )often in the setting of Autoi##une polyendocrine syndro#e,. Kence, sy#pto#s and signs of any of the for#er conditions #ay also be present in the indi(idual with Addison:s.

http8??en.wi*ipedia.org?wi*i?Addison:sAdisease

12. C 6thanol )ethyl alcohol, and isopropanol )isopropyl alcohol, are alcohols that *ill bacteria. Alcohols *ill bacteria by first #a*ing the lipids that are part of the outer protecti(e cell #e#brane of each bacteriu# cell #ore soluble in water so that the cell #e#brane begins to lose its structural integrity and fall apart. As the cell #e#brane disintegrates, alcohol can then enter the cell and denature proteins within each bacteriu#.

1$. C Geisseria are fastidious ra#!negati(e cocci that re;uire nutrient supple#entation to grow in laboratory cultures. -pecifically, they grow on chocolate agar with carbon dio2ide Infection of the genitals in fe#ales with G. gonorrhoeae can result in pel(ic infla##atory disease if left untreated, which can result in infertility. 3el(ic infla##atory disease results if G. gonorrhoeae tra(els into the pel(ic peritoneu# )(ia the cer(i2, endo#etriu# and fallopian tubes,. Infertility is caused by infla##ation and scarring of the fallopian tube. Infertility is a ris* to 1> to 2>M of the fe#ales infected with G. gonorrhoeae.

11. 4 5aricella .oster (irus )5/5, is one of eight herpes (iruses *nown to infect hu#ans )and other (ertebrates,. It co##only causes chic*en!po2 in children and Kerpes .oster )shingles, in adults and rarely in children. 3ri#ary 5/5 infection results in chic*enpo2 )(aricella,, which #ay rarely result in co#plications including encephalitis or pneu#onia. 6(en when clinical sy#pto#s of chic*enpo2 ha(e resol(ed, 5/5 re#ains dor#ant in the

ner(ous syste# of the infected person )(irus latency,, in the trige#inal and dorsal root ganglia.E1F In about 1>N2>M of cases, 5/5 reacti(ates later in life producing a disease *nown as shingles. -erious co#plications of shingles include postherpetic neuralgia, .oster #ultiple2, #yelitis, herpes ophthal#icus, or .oster sine herpete. Kerpes .oster )or si#ply .oster,, co##only *nown as shingles and also *nown as .ona, is a (iral disease characteri.ed by a painful s*in rash with blisters in a li#ited area on one side of the body, often in a stripe. &he initial infection with (aricella .oster (irus )5/5, causes the acute )short!li(ed, illness chic*enpo2 which generally occurs in children and young people. Once an episode of chic*enpo2 has resol(ed, the (irus is not eli#inated fro# the body but can go on to cause shinglesOan illness with (ery different sy#pto#sOoften #any years after the initial infection. http8??en.wi*ipedia.org?wi*i?KerpesA.oster

15. 4 Cardiac ta#ponade is caused by a large or uncontrolled pericardial effusion, i.e. the buildup of fluid inside the pericardiu#.E2F &his co##only occurs as a result of chest trau#a )both blunt and penetrating,,E$F but can also be caused by #yocardial rupture, cancer, urae#ia, pericarditis, or cardiac surgery,E2F and rarely occurs during retrograde aortic dissection. http8??en.wi*ipedia.org?wi*i?CardiacAta#ponade 1@. A An acetylcholinesterase inhibitor )often abbre(iated ACh6I, or anti!cholinesterase is a che#ical that inhibits the cholinesterase en.y#e fro# brea*ing down acetylcholine, increasing both the le(el and duration of action of the neurotrans#itter acetylcholine. -o#e #a'or effects of cholinesterase inhibitors8 Actions on the autono#ic ner(ous syste#, that is parasy#pathetic ner(ous syste# will cause bradycardia, hypotension, hypersecretion, bronchoconstriction, I tract hyper#otility, and decrease intraocular pressure. -0H% 6 syndro#e. Actions on the neuro#uscular 'unction will result in prolonged #uscle contraction. http8??en.wi*ipedia.org?wi*i?AcetylcholinesteraseAinhibitor 1B. 6 I0 28 -ecreted by &h cells. -ti#ulates growth of helper and cytoto2ic & cells ) JA page 2>5,

is an interleu*in, a type of cyto*ine i##une syste# signaling #olecule, which is a leu*ocytotrophic hor#one that is instru#ental in the body:s natural response to #icrobial infection and in discri#inating between foreign )non!self, and self. I0!2 #ediates its effects by binding to I0!2 receptors, which are e2pressed by ly#phocytes, the cells that are responsible for i##unity. http8??en.wi*ipedia.org?wi*i?Interleu*inA2 1D. % 3eripheral (ascular disease )35%,, co##only referred to as peripheral arterial disease )3A%, or peripheral artery occlusi(e disease )3AO%,, refers to the obstruction of large arteries not within the coronary, aortic arch (asculature, or brain. 35% can result fro# atherosclerosis, infla##atory processes leading to stenosis, an e#bolis#, or thro#bus for#ation. It causes either acute or chronic ische#ia )lac* of blood supply,. Often 3A% is a ter# used to refer to atherosclerotic bloc*ages found in the lower e2tre#ity.E1F 35% also includes a subset of diseases classified as #icro(ascular diseases resulting fro# episodal narrowing of the arteries )=aynaud:s pheno#enon,, or widening thereof )erythro#elalgia,, i.e. (ascular spas#s.3eripheral artery occlusi(e disease is co##only di(ided in the Jontaine stages, introduced by =enP Jontaine in 1951 for ische#ia8E2FE$F 1. "ild pain when wal*ing )claudication,, inco#plete blood (essel obstruction< 2. -e(ere pain when wal*ing relati(ely short distances ) inter#ittent claudication ,, pain triggered by wal*ing Qafter a distance of R15> # in stage IIa and after 19. 4 A&G8 "ost co##on cause of acute renal failure in the hospital. -elf re(ersible, but fatal if left untreated )pro(ide supporti(e dialysis,. Associated with renal ische#ia. &o2ic A&G can be caused by free he#oglobin or #yoglobin, by #edication such as antibiotics and cytostatic drugs, or by into2ication )ethylene glycol, Qanti!free.eQ,. Kistopathology8 &o2ic A&G is characteri.ed by pro2i#al tubular epitheliu# necrosis )no nuclei, intense eosinophilic ho#ogeneous cytoplas#, but preser(ed shape, due to a to2ic substance )poisons, organic sol(ents, drugs, hea(y #etals,. Gecrotic cells fall into the tubule lu#en, obliterating it, and deter#ining acute renal failure. 4ase#ent #e#brane is intact, so the tubular epitheliu# regeneration is possible. lo#eruli are not affected http8??en.wi*ipedia.org?wi*i?AcuteAtubularAnecrosis 19.4 A&G, It #ay be classified as either to2ic or ische#ic. &o2ic A&G occurs when the tubular cells are e2posed to a to2ic substance )nephroto2ic A&G,. Ische#ic A&G occurs when

the tubular cells do not get enough o2ygen, a condition that they are highly sensiti(e and susceptible to, due to their (ery high #etabolis#. Acute tubular necrosis is classified as a QrenalQ )i.e. not pre!renal or post!renal, cause of Acute renal failure. %iagnosis is #ade by a JeGA )fractional e2cretion of sodiu#, R $M and presence of #uddy casts in urinalysis. On histopathology, there is usually tubulorrhe2is, that is, locali.ed necrosis of the epithelial lining in renal tubules, with focal rupture or loss of base#ent #e#brane. 3ro2i#al tubule cells can shed with (ariable (iability and not be purely QnecroticQ. 2>. 4 0eish#ania is a genus of &rypanoso#atid proto.oa, and is the parasite responsible for the disease leish#aniasis. It is spread through sandflies of the genus 3hleboto#us in the Old Sorld, and of the genus 0ut.o#yia in the Gew Sorld. &heir pri#ary hosts are (ertebrates< 0eish#ania co##only infects hyra2es, canids, rodents, and hu#ans. Cutaneous leish#aniasis )locali.ed and diffuse, infections appear as ob(ious s*in reactions. &he #ost co##on is the Oriental -ore )caused by Old Sorld species 0. #a'or, 0. tropica, and 0. aethiopica,. In the Gew Sorld, the #ost co##on culprits is 0. #e2icana. Cutaneous infections are #ost co##on in Afghanistan, 4ra.il, Iran, 3eru, -audi Arabia and -yria. http8??upload.wi*i#edia.org?wi*ipedia?co##ons?e?e>?0eish#aniasisAlifeAcycleAd...ra#Ae n.s(gn 21.%% !-eru# 4HG?cr ratio is greater than 15 and this is prerenal a.ote#ia....which is caused by a decrease in cardiac output)e(idenced by the increase in heart rate and decreased 43 in the ;uestion ste#,....the decreased cardiac output causes hypoperfusion of the *idneys ...and these causes A decrease in J= ...this in turn causes An increase in 4HG and Cr

22.44 Ke#iballis#us is usually characteri.ed by in(oluntary flinging #otions of the e2tre#ities. &he #o(e#ents are often (iolent and ha(e wide a#plitudes of #otion.&hey are continuous and rando# and can in(ol(e pro2i#al and?or distal #uscles on one side of the body. -o#e cases e(en include the facial #uscles. It is co##on for ar#s and legs to #o(e together. &he #ore a patient is acti(e, the #ore the #o(e#ents increase. Sith rela2ation co#es a decrease in #o(e#ents.

&he subthala#ic nucleus essentially pro(ides the e2cite#ent needed to dri(e the globus pallidus. In'ury to this area or its efferent or afferent connections can induce this disorder. &he structure itself is a regulator of #otor function and is also in(ol(ed in associati(e and li#bic functions. It was traditionally thought that the disorder was only caused by in'ury to the subthala#ic nucleus, but new studies are showing that da#age to other areas of the brain can also be responsible for causing this disorder. Ke#iballis#us caused by lesions in the subthala#ic nucleus is #ore se(ere than other for#s of the disorder

2$.AA

for ; 2$...0egally, a patient is inco#petent if unable to do the following8 !! )1, respond *nowingly and intelligently to ;uestions about reco##ended treat#ent< !!)2, participate in treat#ent decisions by #eans of rational thought processes< and !! )$, understand the ite#s of #ini#u# basic #edical treat#ent infor#ation with respect to that treat#ent !!hence the paranoid schi.ophrenic patient is legally co#petent and able to decide and refuse treat#ent....

it could be said that e(en a patient whose :delusions are plainly irrational :#ay be co#petent to #a*e a treat#ent decision if he or she fulfills the following criteria 1!co#prehending and retaining infor#ation relating to the decision 2!belie(ing the infor#ation pro(ided by the treating physician $!weighing it in the balance when #a*ing a choice....

21.AA

A.athioprine is an i##unosuppressi(e agent. It is first #etabolised to @!#ercaptopurine, which in turn is con(erted to inacti(e products by 2anthine o2idase. Allopurinol inhibits the second step of #etabolis#, and higher @!#ercaptopurine plas#a le(els result, with associated to2ic effects on the bone #arrow and other tissues. &he resulting blood

dyscrasias, leucopenia, thro#bocytopenia or pancytopenia, can be life threatening.

25.%% -taphylococcus aureus 8is a facultati(e anaerobic, ra#!positi(e coccus, and is the #ost co##on cause of staph infections. It is fre;uently part of the s*in flora found in the nose and on s*in. About 2>M of the hu#an population are long!ter# carriers of -. aureus -. aureus can cause a range of illnesses fro# #inor s*in infections, such as pi#ples, i#petigo, boils )furuncles,, cellulitis folliculitis, carbuncles, scalded s*in syndro#e, and abscesses, to life!threatening diseases such as pneu#onia, #eningitis, osteo#yelitis, endocarditis, to2ic shoc* syndro#e )&--,, chest pain, bactere#ia, and sepsis. 2@.66

; 2@!!Shen the patient ca#e to the clinic to be fitted for the diaphrag#...she is gonna be gi(en infor#ed consent before the procedure....and one part of the infor#ed consent is ...infor#ing the patient about alternati(e treat#ent benefits and disad(antages....

!!si#ply put...before any procedure ...infor#ed consent....part of that is e2plaining alternati(es... 2B.%% u dont ha(e to *now the e2act che#ical reaction...and the e2act inter#ediates and the en.y#es...!!the ;uestion is about regulation of #etabolis# by inter#ediates

!!!in the ;uestion co#pund 5 is produced fro# co#pund 1 by the en.y#e % ....and when this reaction produces #ore co#pund 5 ...co#piund 5 inturn regulates 6n.y#e % by negati(e feed bac*....#y answer is 6n.y#e %...which is %%%%

2B...% is wrong for sure.......

the answer *ey is ....4 waiting for e2planation 2D.A -ic*le!cell disease #ay lead to (arious acute and chronic co#plications, se(eral of which are potentially lethal.

-ic*le cell crisis -ic*le cell disease results in anae#ia and crisis that could be of #any types including the (aso!occlusi(e crisis, aplastic crisis, se;uestration crisis, hyper hae#olytic crisis and others. "ost episodes of sic*le cell crises last between fi(e and se(en days. 5aso!occlusi(e crisis 3ain crisis, or sic*le crisis ! when the flow of blood is bloc*ed to an area because the sic*led cells ha(e beco#e stuc* in the blood (essel. &hese are also called Q(asoocclusi(e crises.Q &he pain can occur anywhere, but #ost often occurs in the chest, ar#s and legs. 3ainful swelling of the fingers and toes, called dactylitis, can occur in infants and children under $ years of age. 3riapis# is a painful sic*ling that occurs in the penis. Any interruption in blood flow to the body can result in pain, swelling and possible death of the surrounding tissue not recei(ing ade;uate blood and o2ygen. 29.C Geuroleptic #alignant syndro#e )G"-, is a life! threatening neurological disorder #ost often caused by an ad(erse reaction to neuroleptic or antipsychotic drugs. It generally presents with #uscle rigidity, fe(er, autono#ic instability and cogniti(e changes such as deliriu#, and is associated with ele(ated creatine phospho*inase )C3C,. Incidence of the disease has declined since its disco(ery )due to changes in prescription habits,, but it is still a potential danger to patients being treated with antipsychotics. 4ecause of its unpredictability, there is no one set course of action to treat the syndro#e, but generally, re#o(al of the antipsychotic drug treat#ent, along with supporti(e #edical #anage#ent, lead to a positi(e outco#e. $>.A Jerritin ser(es to store iron in a non!to2ic for#, to deposit it in a safe for#, and to transport it to areas where it is re;uired. &he function and structure of the e2pressed ferritin protein (aries in different cell types. &his is controlled pri#arily by how #uch #=GA is translated, and how stable the #=GA is. #=GA concentration is further twea*ed by changes to how it is stored and how efficiently it is transcribed.&he presence of iron itself is a #a'or trigger for the production of ferritin, with so#e e2ceptions )such as the yol* ferritin of the gastropod 0y#naea, which lac*s an iron!responsi(e unit,. Jree iron is to2ic to cells as it acts as a catalyst in the for#ation of free radicals fro# reacti(e o2ygen species (ia the Jenton =eaction. Kence (ertebrates use an elaborate set of protecti(e #echanis#s to bind iron in (arious tissue co#part#ents. Sithin cells, iron is stored in a protein co#ple2 as ferritin or he#osiderin. Apoferritin binds to free ferrous iron and stores it in the ferric state. As ferritin accu#ulates within cells of the reticuloendothelial syste#, protein aggregates are for#ed as he#osiderin. Iron in ferritin or he#osiderin can be e2tracted for release by the =6 cells although he#osiderin is less readily a(ailable. Hnder steady state conditions, the seru# ferritin le(el correlates with

total body iron stores< thus, the seru# ferritin J=5=l is the #ost con(enient laboratory test to esti#ate iron stores.

$1.66 Geuroblasto#a..."ost co##on tu#or of the adrenal #edulla in children. can occur anywhere along the sy#pathetic chain K5A...itis abrea*down product of %opa#ine in urine G!"TC...oncogene less li*ely to de(elop K&G

$2.CC "ost #alignant )cancerous, li(er tu#ors arise when cancer spreads )#etastasi.es, fro# another part of the body to the li(er, #ost co##only fro# the colon.

$1. 6 Geuroblasto#a is the #ost co##on e2tracranial solid cancer in childhood and the #ost co##on cancer in infancy. Close to 5> percent of neuroblasto#a cases occur in children younger than two years old. It is a neuroendocrine tu#or, arising fro# any neural crest ele#ent of the sy#pathetic ner(ous syste# or -G-. It #ost fre;uently originates in one of the adrenal glands, but can also de(elop in ner(e tissues in the nec*, chest, abdo#en, or pel(is. Geuroblasto#a is one of the few hu#an #alignancies *nown to de#onstrate spontaneous regression fro# an undifferentiated state to a co#pletely benign cellular appearance. It is a disease e2hibiting e2tre#e heterogeneity, and is stratified into three ris* categories8 low, inter#ediate, and high ris*. 0ow!ris* disease is #ost co##on in infants and good outco#es are co##on with obser(ation only or surgery, whereas high! ris* disease is difficult to treat successfully e(en with the #ost intensi(e #ulti!#odal therapies a(ailable. &he first sy#pto#s of neuroblasto#a are often (ague #a*ing diagnosis difficult. Jatigue, loss of appetite, fe(er, and 'oint pain are co##on. -y#pto#s depend on pri#ary tu#or locations and #etastases if present.

$$.4 &he #uscular branches of the radial ner(e supply the &riceps brachii, AnconUus, 4rachioradialis, 62tensor carpi radialis longus, and 4rachialis, and are grouped as #edial, posterior, and lateral. http8??en.wi*ipedia.org?wi*i?Jile8Ku#erusAspiralAfracture.png http8??upload.wi*i#edia.org?wi*ipedia?co##ons?e?e2? rayD1D.png

$1. A A co#plete #ole is caused by a single sper# co#bining with an egg which has lost its %GA )the sper# then redupplicates for#ing a Qco#pleteQ 1@ chro#oso#e set, &he genotype is typically 1@,++ )diploid, due to subse;uent #itosis of the fertili.ing sper#, but can also be 1@,+T )diploid,. In contrast, a partial #ole occurs when an egg is fertili.ed by two sper# or by one sper# which reduplicates itself yielding the genotypes of @9,++T )triploid, or 92,+++T );uadraploid,. Co#plete hydatidifor# #oles ha(e a higher ris* of de(eloping into choriocarcino#a !! a #alignant tu#or of trophoblast cells !! than do partial #oles. Choriocarcino#a is a #alignant, trophoblastic and aggressi(e cancer, usually of the placenta. It is characteri.ed by early he#atogenous spread to the lungs. It belongs to the far end of the spectru# of gestational trophoblastic disease ) &%,, a subset of ger# cell tu#ors.

$5.% 3yelonephritis is an ascending urinary tract infection that has reached the pyelu# )pel(is, of the *idney. If the infection is se(ere, the ter# QurosepsisQ is used interchangeably )sepsis being a syste#ic infla##atory response syndro#e due to infection,. It re;uires antibiotics as therapy, and treat#ent of any underlying causes to pre(ent recurrence. It is a for# of nephritis. It can also be called pyelitis. -e(ere cases of pyelonephritis lead to sepsis, a syste#ic response to infection characteri.ed by fe(er, a raised heart rate, rapid breathing and decreased blood pressure )occasionally leading to septic shoc*,. Shen pyelonephritis or other urinary tract infections lead to sepsis, it is ter#ed urosepsis. "ost cases of Qco##unity!ac;uiredQ pyelonephritis are due to bowel organis#s that enter the urinary tract. Co##on organis#s are 6. coli )B>!D>M, and 6nterococcus faecalis. Kospital!ac;uired infections #ay be due to colifor#s and enterococci, as well as other organis#s unco##on in the co##unity )e.g. Clebsiella spp., 3seudo#onas

aeruginosa,. "ost cases of pyelonephritis start off as lower urinary tract infections, #ainly cystitis and prostatitis.

$@.% &he posterior inferior cerebellar artery )3ICA,, the largest branch of the (ertebral artery, is one of the three #ain arterial blood supplies for the cerebellu#.

It winds bac*ward around the upper part of the #edulla oblongata, passing between the origins of the (agus and accessory ner(es, o(er the inferior cerebellar peduncle to the undersurface of the cerebellu#, where it di(ides into two branches.&he #edial branch continues bac*ward to the notch between the two he#ispheres of the cerebellu#< while the lateral supplies the under surface of the cerebellu#, as far as its lateral border, where it anasto#oses with the anterior inferior cerebellar and the superior cerebellar branches of the basilar artery. 4ranches fro# this artery supply the choroid ple2us of the fourth (entricle.%iseases Infarction of this artery due to thro#bosis or a stro*e leads to lateral #edullary syndro#e, also *nown as 3ICA syndro#e or Sallenberg syndro#e. -e(ere occlusion of this or (ertebral arteries could lead to Korner:s -yndro#e as well. http8??upload.wi*i#edia.org?wi*ipedia?co##ons?2?2e?CircleAofASillisAen.s(g

$5.% Acute pyelonephritis is a potentially organ! and?or life!threatening infection that characteristically causes so#e scarring of the *idney with each infection and #ay lead to significant da#age to the *idney )any gi(en episode,, *idney failure, abscess for#ation )eg, nephric, perinephric,, sepsis, or sepsis syndro#e?shoc*?#ultiorgan syste# failure. "ost cases of Qco##unity!ac;uiredQ pyelonephritis are due to bowel organis#s that enter the urinary tract. Co##on organis#s are 6. coli )B>!D>M, and 6nterococcus faecalis. Antibiotics are the #ainstay of treat#ent. "ild cases #ay be treated with oral therapy, but generally intra(enous antibiotics are re;uired for the initial stages of treat#ent. &he type of antibiotic depends on local practice, and #ay include fluoro;uinolones )e.g. ciproflo2acin,, beta!lacta# antibiotics )e.g. a#o2icillin or a cephalosporin,, tri#ethopri# )alone or in co#bination with sulfa#etho2a.ole,. A#inoglycosides are generally a(oided due to their to2icity, but #ay be added for a short duration.

$B.A 0a#bert!6aton #yasthenic syndro#e )06"-, #ain causal cancer s#all!cell lung cancer In 06"-, antibodies against 5 CC, particularly the 3?9!type 5 CC, decrease the a#ount of calciu# that can enter the ner(e ending, hence less acetylcholine can be #obili.ed to the neuro#uscular 'unction. Apart fro# s*eletal #uscle, the autono#ic ner(ous syste# also re;uires acetylcholine neurotrans#ission< this e2plains the occurrence of autono#ic sy#pto#s in 06"-. 3?9 (oltage!gated calciu# channels are also found in the cerebellu#, e2plaining why so#e e2perience proble#s with coordination. Antibodies #ay also bind other 5 CCs. "any people with 06"-, both with and without 5 CC antibodies, ha(e detectable antibodies against the "1 subtype of the acetylcholine receptor< it is thought that their presence participates in a lac* of co#pensation for the slow calciu# influ2.

$D.C lycogen storage disease type I ) -% I, or (on ier*e:s disease, is the #ost co##on of the glycogen storage diseases. &his genetic disease results fro# deficiency of the en.y#e glucose!@!phosphatase. &his deficiency i#pairs the ability of the li(er to produce free glucose fro# glycogen and fro# gluconeogenesis. -ince these are the two principal #etabolic #echanis#s by which the li(er supplies glucose to the rest of the body during periods of fasting, it causes se(ere hypoglyce#ia. =educed glycogen brea*down results in increased glycogen storage in li(er and *idneys, causing enlarge#ent of both. 4oth organs function nor#ally in childhood but are susceptible to a (ariety of proble#s in the adult years. Other #etabolic derange#ents include lactic acidosis and hyperlipide#ia. Jre;uent or continuous feedings of cornstarch or other carbohydrates are the principal treat#ent. Other therapeutic #easures #ay be needed for associated proble#s.

$9.AA

AC6 inhibitors reduce the progress of diabetic nephropathy independently fro# their blood pressure!lowering effect.&his action of AC6 inhibitors is used in the pre(ention of diabetic renal failure. AC6 inhibitors bloc* the con(ersion of angiotensin I to angiotensin II. Hnder nor#al conditions, angiotensin II will constrict the efferent arterioles of the *idney leads to increased perfusion pressure in the glo#eruli....Rinc J=.

1>.66

&hro#bo2ane A2 )&+A2,, produced by acti(ated platelets, has prothro#botic properties, sti#ulating acti(ation of new platelets as well as increasing platelet aggregation.

11.CC

A%69HA&6 %O-6- OJ "A G6-IH" &=I-I0ICA&6 "AT CAH-6 %IA==K6A %H6 &O &K6 AC&IOG OJ -O0H406 "A G6-IH" -A0&- IG &K6 6G&6=IC &=AC&.

"agnesiu# trisilicate is an inorganic co#pound that is used as a food additi(e. It can also be used in oral phar#aceutical for#ulations and food products as a glidant. It is also used therapeutically as an antacid, and also for the treat#ent of ciproflo2acin o(erdose or to2ic 12.AA Geisseria #eningitidis, the #eningococcus, is a diplococcus. ra#!negati(e, o2idase!positi(e

identical in its staining and #orphological characteristics to Geisseria gonorrhoeae. Kowe(er, at an ultrastructural le(el, G. #eningitidis has a pro#inent polysaccharide capsule not seen in the gonococcus. &he capsule is antiphagocytic and is an i#portant (irulence factor in #eningococcal disease. G. #eningitidis strains are grouped on the basis of their capsular polysaccharides, into 12 serogroups, so#e of which are subdi(ided according to the presence of outer #e#brane protein and lipopolysaccharide antigens.

1$.66 Co#pensated =espiratory acidosis.........low 3K,low 4icarbonate ,and low 3co2 while Hnco#pensated =espiratory acidosis .....low 3K, low 4icarbonate and high 3co2 12.A Geisseria #eningitidis is a heterotrophic gra#!negati(e diplococcal bacteriu# best

*nown for its role in #eningitis and other for#s of #eningococcal disease such as #eningococce#ia.

0ipooligosaccharide )0O-, is a co#ponent of the outer #e#brane of G. #eningitidis which acts as an endoto2in which is responsible for fe(er, septic shoc*, he#orrhage due to the destructions of red blood cells.E9F Other (irulence factors include a polysaccharide capsule which pre(ents host phagocytosis and aids in e(asion of the host i##une response< and fi#briae which #ediate attach#ent of the bacteriu# to the epithelial cells of the nasopharyn2

11.AA In nor#al patients, after a s#all a#ount of gas has been e2haled, the flow is li#ited by airway co#pression and deter#ined by the elastic recoil of the lung and resistance upstrea# of that point. In restricti(e diseases, the #a2i#u# flow rate is reduced, as is the total (olu#e e2pired. &he flow is abnor#ally high in the latter part of e2piration because of increased recoil. In obstructi(e diseases, the flow rate is (ery low in relation to lung (olu#e, and a scooped out appearance is often seen following the point of #a2i#al flow.

http8??www.frca.co.u*?article.asp27articleidV1>>>2$

15. 4, I need e2planation please .....

1@. % -e(ere co#bined i##unodeficiency )-CI%,, )also *nown as QAly#phocytosis,Q Q lan.#annN=ini*er syndro#e,Q Q-e(ere #i2ed i##unodeficiency syndro#e,Q and Q&hy#ic aly#phoplasiaQ, is a genetic disorder in which both Qar#sQ )4 cells and & cells, of the adapti(e i##une syste# are i#paired due to a defect in one of se(eral possible genes. -CI% is a se(ere for# of heritable i##unodeficiency. It is also *nown as the Qbubble boyQ disease because its (icti#s are e2tre#ely (ulnerable to infectious diseases and so#e of the#, such as %a(id 5etter, beco#e fa#ous for li(ing in a sterile en(iron#ent.

-CI% is the effect of a highly co#pro#ised, so #uch it is al#ost considered absent, i##une syste#. &he gene #utations that cause -CI% are not 'ust for the disorder. &he buildup of dA&3, which induces the cell to #a*e cytochro#e c, destroys and signals for apoptosis in all rapidly proliferating cells. &his includes cells in the I tract, i##une syste# ly#phocytes, and sper# cells. Chronic diarrhoea, ear infections, recurrent 3neu#ocystis 'iro(ecii pneu#onia, and profuse oral candidiasis co##only occur. &hese babies, if untreated, usually die within 1 year due to se(ere, recurrent infections unless they ha(e undergone successful Ke#atopoietic ste# cell transplantation.

1$. 4 =espiratory acidosis with #etabolic acidosis. Hsing the winter:s for#ula, calculate the 3CO2 3CO2V 1.5 W KCO$ XD )X?!2, 1.5 W 12 X D )X?!2, V2@ )X?!2,

&herefore there is no co#pensation and thus since 3co2 is high and Kco$ is low,it is both respiratory acidosis with #etabolic acidosis. nor#al KCO$ range is 22! 2@ and in this case it is 12 thus it is also #etabolic acidosis.

15.44 6#pyse#a...per#anent enlarge#ent of all part of the respiratory unit...respiratory bronchioles,al(eolar,al(eoli Causes8 cigarette s#o*ing alpha1 antitrypsin deficiency &here are 2 types.... 1.Centriacinar...is charachteri.ed by trapping of air in the respiratory bronchiole...elastic

fibers of the distal &4 are destroyed,causing obbstruction to airflow...this causes the trapped air to distend the =4s,whose elastic tissue support is destroyed. 2.panacinar...is charachteri.ed by trapping of air in the entire respiratory unite behindd the collapsed &4

http8??www.google.co#?i#gres7 i#gurlVhttp8??www.#eddean.luc.edu?lu#en?#eded?=a...>C4s9996wAg 1B.66 1D.%% ...&he study design is Case Control and in case control studies u can only deter#ine the pre(alence of the disease...In this case the duration is one year and it is period pre(alence rather than point pre(alence

19.AA &he sarcoplas#ic reticulu# ser(es as a repository for CaXX. 1.In rested #uscle, CaXX is found in high concentration in the cisternae at the triad. 2.In recently acti(e #uscle, the calciu# is found in the narrowed, longitudinal portion fro# which it #o(es to the triad as ti#e passes. $.%uring contraction, CaXX is found in high concentration outside the sarcoplas#ic reticulu# a#ong the #yofila#ents

5>.66

%iphtheria to2oid the for#aldehyde!inacti(ated to2in of Corynebacteriu# diphtheriae, used as an acti(e i##uni.ing agent against diphtheria, usually in #i2tures with tetanus to2oid and pertussis (accine )%&3 or %&a3, or with tetanus to2oid alone )%& for pediatric use and &d, which contains less diphtheria to2oid, for adult use,.

1@ -CI% deficiencies in 4 and & cells!!!!!!!!!!this defect is early in the ste# Vcell differentition. 3resents with recurrents (iral, bacterial , fungal and proto.oal infections, "ay ha(e #ultiple causes )failure to synthesi.e "KCII antigens, defects I0!2 receptors or adenosine deficiency