Nbme 7 Block 3 Answers
Nbme 7 Block 3 Answers
Nbme 7 Block 3 Answers
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
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&he 'ugular fora#en #ay be subdi(ided into three co#part#ents, each with their own contents.
&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
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 %%%%
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.
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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$
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